key: cord-006870-f5w6fw6q
authors: nan
title: Abstracts Presented at the Neurocritical Care Society (NCS) 15th Annual Meeting
date: 2017-09-19
journal: Neurocrit Care
DOI: 10.1007/s12028-017-0465-9
sha: 
doc_id: 6870
cord_uid: f5w6fw6q

nan

External ventricular drain (EVD) management after subarachnoid hemorrhage (SAH) is thought to influence patient outcomes and complications. Evidence from single center randomized controlled trials suggest that an early clamp trial is safe and associated with shorter ICU stay and fewer EVD complications. However, a recent survey revealed that most neuro ICU's across the US still adopt a gradual wean and continuously draining EVD strategy. Therefore, we sought to determine the optimal approach at our institution.

We reviewed 200 consecutive patients admitted to our institution from 2012 to 2017 with nontraumatic SAH requiring an EVD. In 2015, our neurocritical care unit revised our internal EVD management guideline from a gradual wean to an early clamp trial approach. We performed a retrospective multivariate analysis to compare outcomes before and after our guideline change. Patients that were gradually weaned after institution of the new guideline were also included in the early clamp trial group.

We observed a significant reduction in ventriculoperitoneal shunt (VPS) rates after changing to an early clamp trial approach (13% early clamp vs 35% gradual wean, p=0.002, OR=0.208 on multivariateanalysis). There was no increase in delayed VPS placement at 3 months (8.6% vs 9.3%, p=0.41). An early clamp trial approach was also associated with a shorter mean EVD duration (10.2 vs 15.6 days, p<0.001), shorter ICU length of stay (14.2 vs 16.9 days, p=0.001), shorter hospital length of stay (18.2 vs 23.7 days, p<0.001), lower rates of non-functioning EVD (15% vs 30%, p=0.025), and fewer ventriculostomyassociated infections (1.3% vs 8.8%, p=0.039). We found no difference in symptomatic vasospasm rates between the groups (20.2% vs 24.6%, p=0.52).

An early clamp trial approach is associated with fewer complications and shorter length of stay compared to a gradual EVD wean. Prospective multicenter studies are needed to provide further insight into the best strategy.

Autoimmune encephalitis refers to rare sometimes paraneoplastic conditions in which the immune system attacks the brain, leading to altered function. Delayed diagnosis and treatment potentially leads to permanent neurological injury or death. The primary objective of this study was to analyze the admission and discharge modified Rankin Scale (mRS) assessments among patients diagnosed with autoimmune encephalitis, and to identify any effectiveness of immunosuppressive therapy on a subset of these patients.

Through retrospective chart review we identified patients that met currently accepted clinical and serological criterion for autoimmune encephalitis. Clinical data was obtained on these cases and a modified Rankin Score mRS was assessed on both hospital admission and discharge or subsequent 'best clinical' visit. Assessment of "improvement" from initial therapy was based on any decrease in mRS score and clinical neurological functional improvement in accordance with physician and patient affirmation by the time of discharge.

Seventy-seven patients met criterion for clinical or serological autoimmune encephalitis. Of these patients, 11 had cancer and 66 did not have known cancer. Fifty-seven (74%) patients underwent immunosuppressive therapy with corticosteroids, IVIg, and/or plasma exchange and 30 patients experienced a decrease in mRS score. Improvement from initial treatment was 21%, 71%, 58%, and 80% for admitting mRS scores or 2 through 5 respectively. The p-values for improvement from initial immune therapy based on an mRS of 3, 4, or 5 compared to an mRS of 2 were 0.0014, 0.035, and 0.013 respectively.

Immunosuppressive therapies for patients with an initial mRS score of 3, 4 or 5 may have a higher yield than for those with an mRS of 2. These therapies are generally reserved for those with an mRS of 2 or greater. Further study is needed to assess functional improvement in those with autoimmune mediated encephalitis treated with immunosuppressive therapies.

Many patient, family and hospital factors have been associated with obtaining consent for organ donation after brain death (BD). We evaluated potential factors that played a role in the consent rate in a large tertiary hospital over a period of 11.5 years.

We evaluated all declarations in our hospital's BD registry between January 2006 and June 2017 regarding consent for donation. We cross-matched the hospital electronic medical records with the records of the local organ procurement organization to identify this population.

254 patients were included in the registry (59. 5% African American) and 213 were approached for donation. There was a 71.8% consent rate for organ donation. There was no significant relationship between sex, admission diagnosis, ICU (neuro vs. medical vs. surgical), physician specialty (neurology vs. other), time from event to BD declaration or religion and decision to donate. Families were more likely to consent to donation if the patient was non-AA (88% vs 62% for AA, p<0.001), was younger (46.5 vs 52.4, p=0.026), had a lower creatinine at the time of death (1.7 ± 1.9 vs 2.4 ± 2.3 mg/dL, p=0.015), and had an apnea test completed (74% vs 50%, p=0.017). In a logistic regression model, only AA race and PaO2 independently predicted refusal of donation (odds, 95%CI, 5.3, p<0.001 and 0.84, p= 0.017, respectively) .

Although the majority of BD patients in this large series were AA, their families were 5 times less likely to consent for organ donation than non-AA families. There is an urgent need to explore the reasons for low donation rates in this population.

Post-anoxic myoclonus is seen in up to 20% of patients who remain comatose, and historically was felt to be a poor prognostic sign. Little distinction has been made in the literature between epileptic (cortical) vs subcortical myoclonus.

From 604 consecutive cardiac arrest patients that did not return to baseline (May 2007-May 2016) we identified 18% (N=111) patients with clinical myoclonus. Basic demographics and characteristics of their arrest were collected and EEG reports were reviewed. Raw EEG including video was reviewed by two epilepsy-trained neurologists, whenever available. Myoclonus was subcategorized into subcortical and cortical based on the presence of a preceding EEG correlate. Jerk-locked EEG back-averaging was performed on two representative patients.

The average age of patients with myoclonus was 63+/-17 years, and 29% (N=32) survived to discharge. Cortical myoclonus was twice as likely as subcortical myoclonus (59% vs 23%, respectively). Compared with 493 patients without myoclonus, patients with myoclonus were more likely to have longer, more severe arrests. Patients with subcortical myoclonus were at risk for electrographic seizures, although at a lower rate than those with cortical myoclonus (8% vs 43%, respectively). Mortality rates did not differ between patients with cortical and subcortical myoclonus (74% vs 76%). Patients with cortical myoclonus were more likely to be discharged in a vegetative state compared to those with subcortical myoclonus (82% vs 33%, respectively (OR 9.3; 95%CI 1.1-76.7). Amongst survivors, good functional outcome at discharge did not differ between cortical vs subcortical myoclonus (12 vs 16%, respectively). Jerk-locked EEG back-averaging was useful in distinguishing subcortical from cortical myoclonus.

Myoclonus is seen in every sixth patient with cardiac arrest. Cortical and subcortical myoclonus cannot be distinguished using clinical criteria. Both may have good outcomes when managed with targeted temperature management and an aggressive antiepileptic regimen.

Intoxication by central nervous system (CNS) depressant drugs can lead to anoxic brain injury by cardiac or respiratory arrest. We tested the hypothesis whether intoxication by these drugs contributes to mortality in acute anoxic brain injury

We utilized healthcare cost and utilization project databases (Nationwide Inpatient Sample and Kids' Inpatient Database) to obtain patients admitted with diagnosis of anoxic brain injury. Patients with drug intoxication (opioid, alcohol, sedative/hypnotic drugs) were identified. Regression analysis was used to assess relationship between drug intoxication status to in-hospital mortality. The regression model was adjusted for age, gender, chronic medical comorbidities, presence of cardiac arrest and hospital characteristics.

We analyzed a total of 12,319 patients with anoxic brain injury out of which 197 (1.6%) had drug intoxication and 35% were reported to have cardiac arrest. Median age was 58 years and 54% patients were males. In-hospital mortality was 57%. Among the survivors, 20% underwent feeding tube placement and 15% had tracheostomy. Drug intoxication was a significant positive predictor of inhospital mortality with adjusted odds ratio 1.5 (1.1 -2.1), p=0.01.

CNS depressant drug intoxication is associated with higher in-hospital mortality in patients with acute anoxic brain injury.

Cardiac arrest affects approximately 600,000 individuals every year and is the third most common cause of mortality in the US. Currently, there is no way of reliably risk stratifying survivors of cardiac arrest. Identifying early predictors of outcome is vital for triaging and clinical trial enrollment. We proposed to identify key clinical and laboratory parameters that can reliably predict long-term outcomes among comatose survivors of cardiac arrest.

This was a retrospective chart review of comatose survivors of cardiac arrest. We gathered data regarding several clinical (age, pre-arrest mRS, GCS on admission, 24 and 48 hours, presence/absence of shock and respiratory failure) and laboratory parameters (troponins, lactate, creatinine, and ALT at admission, and peak values within the first 24 and 48 hours) as well as characteristics of the cardiac arrest (duration, arrest rhythm, location, and bystander CPR). We used a dichotomized GOS (1-3 vs 4-5) at 6 months as the primary outcome. We performed univariate and multivariable analysis to identify predictors of poor outcome.

A total of 98 patients were enrolled. On univariate analysis, higher age, higher pre-arrest mRS, lower GCS at 48 hours, non VF/VT arrest rhythm, in-hospital arrest location, absence of bystander CPR, and shock were statistically significant (p <0.05) for poor outcome. In multivariable analysis, only higher prearrest mRS and lower GCS at 48 hours were independent predictors of poor outcome; no bystander CPR demonstrated a trend for being an independent predictor. None of the early laboratory data achieved statistical significance for predicting poor outcome.

We identified several clinical predictors of poor outcome in our small cohort of comatose survivors of cardiac arrest. The above variables need to be analyzed among a larger cohort that includes all survivors of cardiac arrest in order to develop an injury severity score that can help risk stratify cardiac arrest survivors.

After cardiac arrest, somatosensory evoked potentials (SSEPs), EEG characteristics, and MRI are routinely used to evaluate comatose patients. The relationship between structural hypoxic injury, absent cortical potentials and the generation of background reactivity or epileptogenic potentials is unclear. Here we evaluate a consecutive series of patients with cardiac arrest that were studied with SSEPs and evaluate clinical, EEG, and MRI measures to study the dissociation between hypoxia-induced thalamic disconnection and spontaneous cortical activity.

In this retrospective cohort study, all comatose patients post-cardiac arrest who received SSEPs were identified and reports were reviewed. 71 patients were found; one patient with a high cervical cord injury was excluded. We recorded presence of cortical (N20) and subcortical evoked responses (P14), whenever available. Based on the closest available EEG (maximum 2 days from SSEP recording) we determined reactivity, background characteristics (diffuse suppression or burst-suppression versus all other backgrounds), and presence of generalized periodic discharges (GPDs) or seizures. Diffusion weighted or T2 FLAIR abnormalities in the thalamus were evaluated based on available MRIs. Chi-square and Fisher's exact test were applied as applicable.

Of 70 patients with SSEP, 33 (47%) had absent N20s, and 29% of those (n=9) had absent P14. EEG reactivity was possible, albeit less common, in patients with absent N20s (10% vs 51%, p<0.001), but none of the patients with absent P14s had a reactive EEG. Those with absent N20s were more likely to have diffusely suppressed or burst-suppressed background (94% vs 51%, p=0.03) and to have abnormal thalamic signal on MRI (50% vs 12%, p=0.008). GPDs, stimulus-induced GPDs, and seizures were equally common in those with and without N20s.

The integrity of the somatosensory thalamo-cortical pathway does not appear to be necessary for presence of reactivity or generation of periodic epileptiform discharges.

All families of patients who have become brain dead (BD) should be offered the choice of donation. This does not always happen and the factors that lead to approaching them or not are not known. Our objective was to evaluate which factors influence the donation coordinators (DC) working for an organ procurement organization approach families after brain death

We evaluated all declarations in our hospital's BD registry between January 2006 and June 2017 regarding consent for donation and cross-matched the hospital electronic medical records with the records of the local organ procurement organization.

In order to refine neurologic prognosis in cardiac arrest patients we sought to incorporate heart rate variability into a multimodal prediction model. Heart rate variability has been shown in animal studies to be preserved in survivors of cardiac arrest.

In our preliminary study, we retrospectively analyzed patients admitted to the University of Virginia who had undergone a cooling protocol following cardiac arrest. Analysis of heart rate variability for each patient was done in the frequency domain using the fast Fourier spectral transform with spectral bands at 0.150-0.400 Hz for high frequency (HF) and low frequency (LF) power within the frequency band 0.040-0.150 Hz. The unit-less LF/HF ratio was considered a measure of balance between sympathetic and parasympathetic tone.

Over a 3-year period, a total of 167 patients were cooled. 45 patients (27%) had cEEG, 13 (8%) had routine EEGs and 17(10%) had SSEPs performed. Numerous patients (42, 25% of all arrests or 72% of all EEGs performed) had malignant patterns, defined as burst suppression, severe suppression, or generalized periodic discharges. Of the 17 SSEPS, 10 had an absent N20 (none survived to discharge) and 7 had an N20 that was present (3 survived to discharge). 2 patients with absent N20s and malignant EEGs had lower LF/HF ratios when compared to 2 survivors with present N20s (0.78 vs. 1.46).

The trend towards parasympathetic dominance following a severe neurologic injury and loss of normal sympathetic tone in those patients with absent N20s and malignant EEGs and may serve as an additional marker of poor prognosis following cardiac arrest.

Physicians often struggle with the intricacies of brain death determination and communication about end-of-life care. In an effort to remedy this situation, we introduced an educational initiative at our medical school to improve student comprehension and comfort dealing with brain death.

Beginning in July 2017, students at our medical school were required to attend a 90-minute brain death didactic and simulation session during their neurology clerkship. Students completed a test immediately before and after participating in the initiative.

Of the 145 students who participated in this educational initiative between July 2016 and June 2017, 124 (86%) consented to have their data used for research purposes. Students correctly answered a median of 53% of questions (IQR 47-58%) on the pretest and 86% of questions (IQR 78-89%) on the posttest (p<0.001). Comfort with both performing a brain death evaluation and talking to a family about brain death improved significantly after this initiative (18% of students were comfortable performing a brain death evaluation before the initiative and 86% were comfortable doing so after the initiative, p<0.001; 18% were comfortable talking to a family about brain death before the initiative and 76% were comfortable doing so after the initiative, p<0.001).

Incorporation of simulation in undergraduate medical education is high-yield. At our medical school, knowledge about brain death and comfort performing a brain death exam or talking to a family about brain death was poor prior to development of this initiative, but awareness and comfort dealing with brain death improved significantly after this initiative. This initiative was clearly a success and can serve as a model for brain death education at other medical schools.

Early withdrawal of life support (EWLS) is a major factor in deaths following hypoxic ischemic injury after cardiac arrest (CA) in patients receiving targeted temperature management (TTM). Appropriate timing of prognostication, and subsequent withdrawal of life support is recommended in recent guidelines, but is not always followed in clinical practice. We describe the impact of EWLS in a multicenter registry database.

Using data from the International Cardiac Arrest Registry (INTCAR), we defined EWLS as withdrawal in the first three days of hospitalization. Among all patients treated with targeted temperature management, we developed a logistic regression model to predict EWLS. We then performed a propensity score and evaluated the incidence of good outcome between deciles of risk for EWLS.

1311 patients entered into INTCAR from 2012-2016 from 16 different hospitals were included. Mean age was 62 (±16) years, mean CPR duration was 28 (± 21) minutes, 689 (53%) had a shockable rhythm, and 812 (62%) received bystander CPR. Support was withdrawn in 609, with 336 (55%) events classified as EWLS. (26% of total cohort). Among patients with support withdrawal, older age (p=0.002), nonshockable rhythm (p=0.003), increased ischemic time (p=0.03), and shock on admission (p<0.001) were associated with EWLS. Among propensity matched patients grouped into deciles of probability for EWLS, survival with good functional outcome occurred in 18% (6th decile), 30% (7th), 10% (8th), 6% (9th), and 12% (10th decile).

Early withdrawal of life support after cardiac arrest occurs frequently, and is associated with age, duration of CPR, a non-shockable rhythm, and shock at the time of admission. A cohort of patients propensity-matched to those with EWLS had 6-30% survival with favorable neurologic outcomes. These data support that in most patients receiving TTM, conservative and delayed prognostication after cardiac arrest is appropriate.

Brain herniation (BH) is a deadly event that requires immediate central venous access for infusion of hyperosmotic agents, especially 23.4% NaCl. Traditional venous catheters, whether peripheral or central, takes several minutes to place, and requires skill for successful placement, thus delaying critical treatment. Intraosseous (IO) cannulation has been shown, at least during cardiac arrest, to be a secure and rapid means of central vascular access that requires limited training. However, limited data exists on the use of IO in BH for administering 23.4%. The aim of study of this study is to measure changes in serum sodium and BH reversal after administering 23.4% via IO.

Retrospective chart review of patients with acute neurologic injury requiring 23.4% and IO placement due to a lack of central access. Demographics, diagnosis, GCS, sodium (Na+), and pupillary reactivity, and immediate and delayed complications were collected.

Results 9 patients included: 4 males, age range 33-84 yo. Diagnosis include intracerebral hemorrhage ( n=7), extra-axial hematoma (n=1) and SAH (n=1). GCS ranged 3 to 8. All patients were intubated. Most patients were co-treated with hyperventilation, NaBicarb, mannitol, and propofol. IO was placed in tibia (1) or humerus (8); all placed correctly on first attempt. Comparing 1 hr post-23.4% NaCl treatment to pretreatment: Na+ level increased in 6 of 9; GCS improvement in 4 of 9; and returned pupillary reactivity in 4 of 7. No adverse events reported, such as shock, cardiac arrest, tissue or limb injury.

Preliminary data suggest that during BH, IO cannulation results in safe and timely 23.4% administration in patients with no central access. Additional safety data is needed, particularly with regards to the potential for myonecrosis. However, if safe, IO cannulation should replace central line placement as the initial route of central venous access during BH.

The pupillary light reflex is associated with outcome after cardiac arrest as a dichotomous variable (present/absent) at various time points following resuscitation (ROSC). Infrared pupillometry provides quantitative measures including pupil diameter (PD), and Neurological Pupil Index (NPi) which ranges from 0 (nonreactive) to 5 (brisk) and reflects velocity and degree of pupil constriction in response to a standardized light stimulus. These measures may provide early prognostic information to guide therapy.

Comatose adult survivors of cardiac arrest treated with targeted temperature management were monitored with the Neuroptics NPi-200 pupillometer. Outcomes were defined as good (GO) if discharge Cerebral Performance Category score was 1-2, and poor (PO) if 3-5. Data are presented as median (IQR). Groups were compared using non-parametric statistical tests.

Fifty-one patients were enrolled; the median age was 57 (48.5-68.5), and 33 (65%) were male. Initial rhythm was VT/VF in 55%, asystole in 23%, and PEA in 20%. Outcome was good in 16 (31%) patients. The initial PD did not differ between outcome groups [3.1 (2-4.7) PO vs 3.0 (2-4.2) GO]. The initial NPi was lower in poor outcome patients [3.3 (1.5-4) vs 3.9 (2.4-4.2) GO, p=0.005] measured 4.5 (3.4-6.3) hours after ROSC. NPi dropped below 3 in more poor outcome patients [27(77%) vs 6(37.5%) GO, p=0 .015], and to zero in 18(51%) poor vs 1(6%) good outcome patients (p=0.005). Receiver operator characteristic curves confirmed that initial NPi predicted poor outcome better than pupil diameter (AUC 0.78 vs 0.61, p=0.016).

A low Neurological Pupil index predicted poor outcome 4-6 hours after resuscitation from cardiac arrest, and dropped to abnormal levels (<3) and to zero (reflecting a non-reactive pupil) more often in patients with poor outcomes. Additional research is needed to define potential confounders, optimal timing, and thresholds for different levels of neurological risk with pupillometry.

Prediction of death in a timely manner after withdrawal of life support (WLS) is essential during organ donation after cardiac death (DCD). We aimed to develop a modified version of the recently develop DCD-N score to improve the specificity of prediction and test it in a specific group of patients with catastrophic brain injuries referred for DCD.

We analyzed prospectively collected data by our local organ procurement agency on all consecutive adults with severe neurological injury evaluated for DCD across 18 centers in the USA from March 2015 to May 2017. We analyzed three variables used in the DCD-N score (corneal reflex, cough reflex and oxygenation index) and substituted the fourth variable for vasopressor support.

A total of 278 patients, mean age 50 (SD±13) years were included in the final analysis. Anoxic brain injury was the most common cause of death (55%) followed by stroke (27%). In multivariate logistic regression analysis adjusted for age and cause of death, absent corneal reflex (OR 3.2, 95% CI 1.6 to 6.0, p = 0.0005, 2 points), absent cough reflex (OR 2.2, 95% CI 1.1 to 4.2, p = 0.02, 1 point), vasopressor support at high doses (OR 4.9, 95% CI 2.3 to 10.5, p < 0.0001, 2 points) and O2 Ind CI 1.6 to 5.5, p = 0.0005, 2 points) were associated with the likelihood of death within 60 minutes of specificity 83% and AUC 0.81.

The modified DCD-N score has a greater specificity in predicting death within 60 minutes of WLS and is developed specifically from a cohort of patients evaluated for DCD. Future prospective studies are needed for further validation of this scoring system.

Significant number of the patients with anoxic brain injury have poor neurological recovery. This created a significant anxiety in families who often request early prognostication. This study was conducted to evaluate possible ultra-early prediction of good neurological recovery in patients undergoing hypothermic protocol for anoxic brain injury

Retrospective chart review of the patients with anoxic brain injury was conducted. All patient underwent standard evaluation and management in the early stages of ICU care, including initiating of hypothermic protocol with intravenous cooling device. All patients underwent evaluations with EEG and SSEP within first day after admission during hypothermia phase and MRI brain after re-warming.

Total of 65 charts were reviewed. 9 patient had normal SSEP and normal MRI. All patients had good neurological recovery, except for one patient who died secondary to severe cardiac failure EEG did not have any predictive value for the good neurological outcome when it was done during hypothermic protocol.

Normal SSEP may a reliable predictor for good neurological recovery.

Apnea test is the essential component to confirm brain death by stimulation of respiratory center in brainstem. Guidelines recommend that apnea testing should meet the criteria of disconnection from mechanical ventilator, and oxygen supplying by catheter. However, during the apnea test under this technique, disconnection from ventilator may induce hypoxia due to abrupt decruitment of alveoli and pulmonary barotrauma such as pneumothorax. There are some studies that suggest continuous positive airway pressure can be effective for patients with hemodynamically instability and respiratory impairment. We suggest a novel method of apnea test by using ambu bag with positive end-expiratory pressure (PEEP) valve to avoid abrupt change of PEEP during the apnea test.

Apnea testing was performed by using ambu bag with PEEP valve to 26 adult brain death patients. Ambu bag was not bagging during the testing and just connected to endotracheal tube with 10 L/min of 100% oxygen. PEEP valve was applied the same PEEP of previous mechanical ventilator. On the apnea testing, vital signs and EKG were monitored. Arterial blood gas analysis were measured 2 and 4 minutes after disconnection from mechanical ventilator.

There were no significant differences in mean PaO2 between before and after apnea test (275 ± 181 and 260 ± 178, P=0.7). Mean arterial blood pressure were 90 ± 17 mmHg and 90 ± 22 mmHg before and after the test, respectively. During the intervention and following observation, arrhythmia or pulmonary complications had not occurred.

We suggest a novel method of apnea testing which is a simple and easy technique by using ambu bag with PEEP valve to minimize decruitment of alveoli. This method shows vital signs and respiratory oxygenation of the patients remained stable during the test.

Declaration of brain death based on clinical exam has been plagued with challenges. As a result, ancillary testing such as nuclear scintigraphy cerebral blood flow (CBF) studies have been recommended. We present a case in which the apnea test could not be completed due to hemodynamic instability and where the nuclear scintigraphy CBF study resulted in a false declaration of brain death.

A 59 y/o male was admitted with bilateral hearing loss and confusion. On day two, the patient developed blurred vision, and an MRI confirmed bilateral cerebellar and pontine infarctions. By day four, he had developed diffuse cerebral edema in the cerebellum, brainstem, and bilateral occipital lobes, and we proceeded with the clinical exam for brain death. All cranial reflexes were absent; however the apnea exam could not be completed due to blood pressure instability. A nuclear scintigraphy CBF study revealed the complete absence of radiotracer activity, and the patient was pronounced dead. Two hours later, the patient regained a gag reflex. On the following day, the clinical exam, with the exception of apnea testing, was again consistent with brain death. A cerebral angiogram was performed and demonstrated normal blood flow to the anterior circulation. The patient was ultimately pronounced dead on day eight after two separate complete clinical brain death exams, including apnea testing, were performed.

Cerebral angiography showed essentially normal blood flow where nuclear scintigraphy showed no blood flow.

Nuclear scintigraphy CBF studies are commonly recommended when apnea testing cannot be completed. Given the dramatic differences in the results observed between these modalities, a reevaluation of this practice should be considered.

Patients' perceptions of recovery moderate outcomes, however studies exploring the specific cognitive, functional, and psychological domains associated with subjective perceptions of recovery at hospital discharge after cardiac arrest (CA) are lacking.

This is a prospective, observational cohort of patients admitted to Columbia University Medical Center after CA, and survived to hospital discharge between 9/2015-5/2017. Patients with sufficient mental status to perform a neuropsychological exam and a questionnaire at discharge were included. Subjective perceptions of recovery were assessed via responses to the forced-choice dichotomized question, "Do you feel that you have made a complete recovery from the arrest?"Objective outcome measures of recovery included: Repeatable Battery for Neuropsychological Status (RBANS), Modified Lawton Physical Self-Maintenance Scale (L-ADL), Barthel Index (BI), Cerebral Performance Category Scale (CPC), Center for Epidemiological Studies-Depression scale (CES-D), and Post traumatic stress disorder-checklist (PTSD-C). Chi-square, Wilcoxon-Rank Sum, and logistic regression were used to compare the respondents, and determine factors associated with subjective perceptions of recovery.

64 patients were included with mean age of 52±17 years; 58% were men and 48% were white. 67% responded not having made a complete recovery. No significant differences were found between respondents in terms of demographics, charlson comorbidity index, arrest-related variables, RBANS, L-ADL, BI, Pre-or post-arrest CPC scores. Those responding that they had not made a full recovery had higher rates of PTSD-C (45% vs 0%, p<0.001), and depression (51% vs 25%, p=0.05). Moreover, everyone that screened for PTSD (N=19) reported not having made a complete recovery. Patients with higher PTSD scores were more likely to report not having made a complete recovery (OR 1.25; p< 0.003) after adjusting for age, gender and depression scores.

Presence of post traumatic stress disorder symptomatology at discharge, and not neurocognitive or functional status, is highly associated with post-cardiac arrest patients' subjective perceptions of recovery.

Early EEG background reactivity is a strong predictor of neurological recovery after hypoxic-ischemic brain injury despite hypothermia and sedation. Unfortunately, expert interrater-agreement on visual scoring of EEG background reactivity ranges from 24-50%. Recent studies indicate that machine-learning approaches using quantitative EEG (QEEG) might yield equivalent or superior performance to current EEG reactivity assessment practices, however its ability to predict outcomes has not been tested. We hypothesized that a QEEG reactivity method can predict long-term functional outcome in hypoxic ischemic brain injury.

We retrospectively reviewed clinical and EEG data of cardiac arrest patients managed with hypothermia at two university hospitals. EEG reactivity was tested daily using a structured exam consisting of auditory, tactile, and visual stimulation. Our quantitative EEG method evaluated changes in EEG spectra, entropy, and frequency features during 30 seconds before and after each stimulation-step (30 QEEG features used). Only the first EEG reactivity assessment for each subject was used in the final analysis. Good outcome was defined as Cerebral Performance Category of 1-2 at six months. A penalized multinomial logistic regression was utilized for feature selection and a random-forest classifier was employed in the training and validation sets. Model performance evaluation metric was the area under ROC curve (AUC).

Outcome and EEG data was available for a total 77 subjects, and 30 cases were excluded due to presence of burst-suppression, periodic epileptiform discharges, or EEG artifact. Forty-seven subjects were included in the final analysis. Mean age was 57.8 (standard deviation 17.9) years and 29.8% had good outcome. The combination of four features provided best outcome prediction performance with an AUC of 0.87 (Kolmogorov-Smirnov test, skewness, Two-group test, and Renyi entropy).

Early QEEG reactivity is predictive of good outcome at six months. A quantitative approach to EEG reactivity analysis might facilitate accurate and individualized prognostication in hypoxic-ischemic brain injury.

Hypoxic-ischemic brain injury is the leading cause of morbidity and mortality following cardiac arrest, and the ability to predict neurologic recovery in comatose cardiac arrest survivors is limited. Functional MRI measures brain network connectivity and resting-state network connectivity can be measured in comatose patients. The default mode network (DMN) is one resting state network that has been correlated with consciousness. We hypothesized the degree of connectivity in the DMN and other resting-state networks would correlate with consciousness recovery in post-cardiac arrest coma.

Consecutive patients with hypoxic-ischemic coma were enrolled. Functional MRI was obtained on all patients on post-arrest day 2-5 on an inpatient 3 Tesla MRI. The connectivity in multiple resting-state networks was analyzed using Pearson's correlations between 30 component maps for each subject and 14 previously defined standard network maps. Connectivity in the default mode network and in additional resting-state networks was correlated with outcome. Good outcome was defined as consciousness recovery at any point in the acute hospitalization.

15 patients were included in this study. The mean age was 57±14 years (22-79) and 9 were male. 6 patients survived with good outcome. The primary arrest rhythm and the duration of cardiac arrest did not differ between groups (primary rhythm as VT/VF: 50% vs 44%, good vs poor, p= 0.8; cardiac arrest duration: 20.2±11.7 minutes vs 20.2±12.1 minutes, good vs poor, p=0.99). Patients with good outcome had significantly higher mean network connectivity (0.13±0.06 vs 0.07±0.04, good vs poor, p=0.03). DMN connectivity showed a trend towards significance (0.14±0.04 vs 0.09±0.06, good vs poor, p=0.1).

In comatose patients following cardiac arrest higher fMRI measured resting state connectivity correlated with consciousness recovery. Functional connectivity may be developed as a prognostic biomarker.

Sedative and analgesic infusions and neuromuscular blockade agents (NMBA) are commonly used for comfort, suppression of shivering, and reduction of metabolic activity during targeted temperature management (TTM) after cardiac arrest. The optimal sedation and analgesia regimens are unknown. We sought to describe variability in sedation and shivering management practices at US and European cardiac arrest receiving centers.

International Cardiac Arrest Registry (INTCAR) centers were surveyed regarding sedation protocols for TTM after cardiac arrest. The survey was administered via REDCap with a response rate of 48%.

Ten United States and 28 European centers completed the survey. Shivering is measured at 35 (92%) of centers and recorded at 14 (37%) centers. Ten centers use NMB to control shivering prophylactically, 12 centers use NMB only if shivering occurs, and 16 centers increase opioids or sedatives when shivering occurs, but do not use NMB. The most common sedative was propofol (31/38 centers), followed by midazolam (24/36) and the most common analgesic was fentanyl (25/38) followed by remifentanyl (17/25). 0, 18, and 21 centers report having a sedation target of light, moderate, or deep respectively. A sedation scale is used at 25 (66%) centers, targeted to patient comfort at 8 (21%) centers. Daily sedation lightening is protocolized when rewarming starts at 6 (16%) centers, when normothermia is reached at 28 (72%) and not specified in the remainder of groups. Of patients who awaken, centers report that they expect this to occur at 24 (17 centers), 48 (12 centers) and 72 (6 centers) hours respectively.

Among cardiac arrest receiving centers internationally, there is significant variability in TTM sedation and shivering management strategy.

Our hospital policy allows an optional SBD (with an apnea and a cerebral blood flow test) or a DBD (with an apnea test). We have evaluated the adoption of and reason for performing a single brain death exam (SBD) vs two (dual) brain death exams (DBD) and their impact on organ function and consent for organ donation.

We evaluated our hospital's BD registry between January 2006 and June 2017 regarding SBD or DBD. We also cross-matched our electronic medical records with the records of the local organ procurement organization.

Of 251 BD declarations, 115 (46%) were SBD and 136 (54%) DBD. During the 1st five years, 43% of all BD exams were SBD and during the second 57%. Patients with SBD were older (50.6±16.5 for SBD vs 46.5±17.1 years for DBD, p= 0.057), had a primary neurologic diagnosis (96% vs 47%, p< 0.001) and were admitted to the Neuro-ICU (74% vs 27%, p< 0.001). During the 2nd exam, 76.7% patients were on equal or higher dose of pressors. SBD patients had lower K+, BUN, creatinine and heart rate, but higher peak Na+ and apnea PaO2 (for all p<0.05), although apnea pH and PaCO2 were similar. The time between injury to BD pronouncement was shorter in SBD by 29.4 hours. There was no difference in consent rate between SBD and DBD (74% vs 70%, p=0.47).

At our institution, BD declaration was more often done by DBD exams, although the primary diagnosis and the unit of admission influenced the decision. An increased adoption of SBD exams was noted after the 2010 AAN BD Guidelines, supporting SBD exam, were published. Although the number of exams did not affect rate of consent for donation, surrogate markers indicated better function of organs after SBD, while DBD patients stayed in the ICUs over a day longer.

There are no data supporting better numbers or function of organs in donors after brain death (BD), if there is a shorter waiting period (as expected with single brain death exam [SBD] ) from the time that BD is declared to the time the patient arrives at the operating room (OR). Our goal was to find if the number of brain death exams, either SBD or dual (DBD), had any impact on the number of organs recovered and transplanted

We evaluated our hospital's BD registry between January 2006 and June 2017 regarding SBD or DBD and cross-matched our electronic medical records with the records of the local organ procurement organization

Out of 251 BD declarations, 150 led to consent, of which 74 (49.3%) after SBD and 76 (50.7%) after DBD. There was a trend for longer consent to OR time for DBD (41.7 ± 20.1 hours vs 36.4 ± 13.7 for SBD, p=0.07). There was no difference in the number of organs recovered or transplanted based on the number of exams (4.0 ± 1.8 vs 3.7 ± 1.8 organs/patient recovered and 3.2 ± 2.0 vs 2.8 ± 1.9 transplanted for SBD vs DBD, respectively, p>0.05). There was a trend for more lungs to be transplanted after SBD exam (62% vs 44%, p=0.06), but this was not found with kidneys, heart, liver, pancreas or intestines. In multiple logistic regression models, adjusting for variables pertinent to each individual organ function (for example, BUN or creatinine level for kidneys, blood gases for lungs etc), the number of exams was not an independent predictor for successful transplantation Conclusions SBD exam led to similar numbers of organs transplanted compared to DBD exam in this single center registry analysis. More rapid brain death declaration, as with SBD, is not a factor that influences organ transplantation

The Glasgow Coma Scale (GCS) is a standardized and commonly used way of assessing important aspects of neurological condition for critically ill patients. While it is a validated tool for prognostication, it is unclear whether serial measurements add value to this prognosis. We used a large set of serially collected GCS measurements to assess the impact of GCS score on the trajectory of neurological recovery as well as factors affecting score variance.

GCS total and subscores (483,041 time points from 5,456 patients) recorded hourly by registered nurses in the Neurosurgical Intensive Care Unit (NSICU) between January, 2012 and May, 2016 were analyzed retrospectively. K-means clustering provided groups with similar progression characteristics during NSICU stay. K-means clustering provided groups with similar progression characteristics during NSICU stay. Descriptive features for each cluster were binned into histograms and evaluated for similarity using 2 and Kruskal-Wallis tests.

Linear correlations of the sub-scores were very high (eye-verbal: 0.583, eye-motor: 0.686, verbal-motor: 0.583), while compositional variance was low for aggregate scores. Hour-to-hour variance in GCS correlates to significant NSICU activities such as nursing shift changes. Among patients with similar minimum GCS scores during their stay, those that recovered were significantly less likely to have deteriorated in the hospital ( 2, p<<0.0001). For patients with a minimum GCS<=8, those that arrived at their minimum score (i.e., did not deteriorate in NSICU) were 18.6% more likely to recover than those who deteriorated in-hospital (KW, p<<0.0001) . Patients that experienced recovery show significantly greater improvement as early as 2 hours after their minimum score (KW, p<<0.0001).

The GCS is unnecessarily complex for most NSICU patients and can be represented by fewer variables. Serial GCS measurements do provide value for prognosis and may be able to distinguish patients with potential to recover early in their hospital course.

Stroke is a major cause of death and disability, and common admission to neurological intensive care units. Preferences for cardiopulmonary resuscitation (CPR) are often discussed, but there is limited understanding of CPR outcomes among stroke patients.

Systematic review and meta-analysis of published literature from 1990 to 2016 among stroke patients undergoing in-hospital CPR. Preferred Reporting Items for Systematic Reviews and Meta-analysis, Metaanalysis of Observational Studies in Epidemiology, and Utstein guidelines were used to construct standardized reporting templates. Detailed searches of PubMed and Cochrane libraries were supplemented with hand-searched bibliographies. Primary data from studies meeting inclusion criteria at two levels were extracted, i) survival to hospital discharge after CPR, and stroke as a primary admitting diagnosis, and the less restrictive, ii) survival to hospital discharge after CPR with stroke listed as a comorbidity, were meta-analyzed to generate weighted, pooled estimates of survival to hospital discharge.

Of 818 articles screened, there were 176 articles (22%) that underwent full review. Three articles met primary inclusion criteria, specifically identifying patients with stroke as a primary admitting diagnosis. Twenty additional articles met secondary inclusion criteria, listing stroke as a comorbidity. There was an 8% (95% Confidence Interval (CI) 0.01, 0.14) rate of survival to hospital discharge rate from a combined sample of 561 patients that received in-hospital CPR. Among the more heterogenous population of inpatients with stroke listed as a comorbidity, there was 16% (95% CI 0.14, 0.19) rate of survival to hospital discharge. Adherence to Utstein reporting guidelines was poor, and neurological outcomes were measured in 6 (26%) of studies.

Survival to hospital discharge among stroke patients is lower relative to general hospital populations. These preliminary findings highlight the need for improving the quality of evidence to inform patient and provider discussions of CPR among stroke patients.

There is often a tendency to treat patients with traumatic brain injury (TBI) and a Glasgow Coma Scale (GCS) score of 3 on presentation less aggressively because of low expectations for a good outcome. Based on the CRASH trial database, a prognosis calculator has been developed for the prediction of outcome in TBI patients. Our aim was to investigate whether the CRASH calculator can be used for prognostication in patients with TBI and GCS of 3 on presentation.

We performed a retrospective review of patients with TBI and a GCS score of 3 from 1/12 to 9/16. The CRASH calculator has been validated to estimate mortality at 14 days and death and severe disability at six months (Glasgow Outcome Scale-GOS 1-3). The calculator uses country of origin (USA in our dataset), Age, GCS, pupils reactivity to light, presence of major extracranial injury, and findings on CT scan of brain (petechial hemorrhages, Obliteration of the third ventricle or basal cisterns, Subarachnoid bleeding, Midline shift, and Non-evacuated hematoma). The individual prognosis for mortality at 14 days and unfavourable outcome at 6 months was calculated and compared with the actual outcomes.

A total of 62 patients were included. A tend toward underestimation of the risk of mortality at 14 days was found (Estimated mortality was 66 % compared to actual mortality of 81%; Difference of 15%, p = 0.05). However, the estimation of outcome at 6 months was accurate (Estimated GOS 1-3 was 85.5 % compared to actual of 85.5 %, p = 1.0).

The CRASH prognosis calculator underestimated the risk of mortality, but accurately predicted unfavourable 6 month outcome in patients with TBI and GCS of 3 on presentation. Pending larger studies to validate our findings, we believe that CRASH calculator can only support -not replace -clinical judgment.

There are no nationally enforced standards regarding brain death. Few data exist on how brain death is determined across the U.S.

We used claims data from 2012-2015 from a nationally representative 5% sample of Medicare defined as ICD-9-CM code 348.82. The primary outcomes were evaluation by a neurologist or neurosurgeon, defined as a physician evaluation-and-management claim associated with the Medicare provider specialty codes for neurology or neurosurgery, during the dates of the hospitalization. CPT codes were used to ascertain ancillary testing: brain radionuclide imaging, transcranial Doppler ultrasound, or electroencephalography for brain death determination. Exact binomial confidence intervals (CIs) were used to report proportions.

We identified 312 patients with a brain death diagnosis. Common associated neurological diagnoses were stroke (122 patients; 39.1%), cardiac arrest (120; 38.5%), and traumatic brain injury (TBI) (45; 14.4%). Head CT or brain MRI was performed in 79.8%; this was true of 91.6% of cases of stroke or TBI versus 68.3% of cardiac arrests. Neurologists were involved in the care of 137 patients (43.9%; 95% CI, 38.3-49.6%). They were more commonly involved in the care of stroke (50.8%) or cardiac arrest (55.0%) than TBI (6.7%) or other conditions (24.0%). Neurosurgeons were involved in 98 cases (31.4%; 95% CI, 26.3-36.9%), mostly after TBI or stroke. Two hundred patients (64.1%; 95% CI, 58.5-69.4%) were seen by a neurologist or neurosurgeon. Twenty-nine patients (9.3%; 95% CI, 6.3-13.1%) underwent any ancillary testing. Two hundred and nine patients (67.0%; 95% CI, 61.5-72.2%) were seen by a neurologist or neurosurgeon or underwent ancillary testing.

In a nationally representative cohort of elderly patients, one-third of patients with a brain death diagnosis were not evaluated by a neurologist or neurosurgeon or by using ancillary tests.

Traumatic brain injury (TBI) is a major cause of death and disability in the US. Recent advances in 3D illustration (3DI) can precisely quantify intracranial pathology on computed tomography (CT). The current standard of measurement, ABC/2, demonstrates variability in precision with bleed phenotype. The aim of this project is to assess accuracy automated 3DI and compare it to standard ABC/2 measurements.

Baseline CT scans collected during the ProTECTIII multicenter clinical trial (n=881) were retrospectively reviewed by a central neuroradiologist. Subdural and epidural hematomas were identified (n260). The radiologist calculated ABC/2 score using OsiriX (Mac) and RadiAnt (PC) workstations. In a blinded fashion, research assistants concurrently generated 3DI using the following methods: DICOM data were resampled to 1.5 mm thickness slices and symmetrized using image analysis software (Aquarius TeraRecon Inc, 2012) . Lesions were then compiled into single volumetric regions of interest (3D Slicer v4.5, 2015) . Hemorrhages were divided into two groups for analysis: Group 1. volume of hemorrhage

Bland-Altman analysis. This study was IRB approved.

There is a significant difference between the results of the 3DI and ABC/2 methods. In Group 1. the estimated relative bias between the two measurements (after transformation) is 0.17 (SD 1.16; pvalue 0.044; 95% CI 0.005, 0.333). In Group 2, the relative bias is -0.712, SD 1.22, pvalue <0.0001, 95% CI (-1.013, -0.410).

The 3DI method calculates detailed surface area measurements in large and small volume hemorrhages, while ABC/2 averages cross-sectional area. The ABC/2 estimates vary by bleed phenotype and offer less topographical precision than 3DI. This is particularly true in extra-axial hemorrhages, which are

Numerous studies have shown a significant association between hypotension and poor outcome in patients with head injuries. Prior investigations have demonstrated that generation of negative intrathoracic pressure (ITP) in ventilated patients with brain injury improves mean arterial pressure (MAP) and lowers intracranial pressure (ICP). We hypothesized that augmentation of negative ITP by breathing through an impedance threshold device (ITD) with 7 cmH2O of inspiratory resistance would improve mean arterial pressure in a porcine model of intracranial hypertension.

Six spontaneously breathing female pigs (42.2 ± 3.7 kg), anesthetized with propofol, were subjected to focal brain injury through inflation of an 8 French Foley catheter placed in the epidural space. Once a stable injury was obtained, baseline data were collected for 20 minutes followed by 20 minutes of ITD use. Results are reported as mean ± SD.

The ITP without the ITD during inspiration was -1.0 ± 0.4 mmHg, compared to -9.0 ± 0.8 mmHg with the ITD, p<0.001. Following brain injury, MAP (mmHg) was significantly higher during ITD use (95 ± 11 vs. 89 ± 11; p<0.001). Cerebral perfusion pressure (mmHg) was also significantly higher during ITD use (75 ± 11 vs. 69 ± 10; p<0.05). ICP (mmHg) was not significantly different between groups (20.1 ± 3.4 vs. 19.9 ± 3.3; p=0.19) although end tidal carbon dioxide levels (mmHg) were significantly higher during ITD use (26 ± 3 vs. 20 ± 1; p<0.005) presumably due to lower respiratory rates during ITD use (29 ± 5 vs. 35 ± 7; p=0.21). Contralateral cerebral blood flow (ml/100gm/min) was similar between groups (34 ± 18 vs. 34 ± 17).

In this porcine model of intracranial hypertension, spontaneous respirations through an ITD significantly improved MAP and CPP. This approach could be utilized to prevent hypotensive episodes in the setting of brain injury.

The impact of applying nanotechnology and biomedical engineering to improve the management of patients with Spinal Cord Injuries (SCI) is still not accurately described, nor understood.

A systematic review of the literature was conducted, according to PRISMA criteria, to identify publications revolving around "SCI+nanotechnology" and "SCI+Biomedical Engineering" indexed on PubMed in the period 2007-2017. Furthermore, the database of clinicaltrials.gov was searched to highlight the stage of translation of this research into clinical practice through randomized clinical trials (RCT). Finally the USPTO database was interrogated to identify the number of pertinent patents filed in NorthAmerica in the same timeframe.

The literature on bioengineering and nanotechnology contributions to SCI is exponentially growing, with almost 50% of articles published between 2015 and 2016. Its quality and the interest of the scientific community are high, as confirmed by the average Impact Factor (14.9) and the average number of citations (5) of articles published in the last two years. This field still represents a niche of SCI research: the 56 articles reviewed represent only 1.2% of all articles on SCI published in the same decade. This trend is confirmed on clinicaltrials.gov: out of 886 RCT on SCI only few focus on the application of those technologies, furthermore 34 out of 40 articles spurring from the RCT identified were published after 2010, and 25% after 2016. Interestingly, with 119 patents registered by the USPTO, the interest in the commercial application of this research seems vivid.

Currently, the most promising areas of research are: nanofabrication/nanoscaffolding for structural repair, nanodrugs for regeneration, and design of neural interfaces for functional therapies. This review showed that both universities and independent research institutions (mostly from USA, China and European Union) are driving this research race; the figures provided above suggest its potential to become a successful example of translational medicine.

There are no neuroprotective and neuroregenerative treatments available for Traumatic Brain Injury (TBI). Clinical trials investigating potential treatments such as therapeutic hypothermia and progesterone have failed. Pre-clinical studies indicate there may be a role of stem-cells in promoting neuroprotection/neuroregeneration in-vivo in animal models of TBI. We aim to provide a pre-clinical literature review into stem-cells as a potential therapeutic option in TBI-animal models.

A literature search was conducted on Pubmed and Google Scholar using the terms "traumatic brain injury", "stem-cell", "preclinical", and "animal studies". Studies were included if there was an in-vivo animal model of TBI with either intravenous or intra-cortical stem-cell transplantation, along-with a control group, and investigated either motor or behavioral outcomes, or a combination.

Twenty-seven studies (n=1184 animals) satisfied the criteria. 774/1184 (65.4%) animals were investigated for outcomes. 17 studies harvested stem-cells from human-source, whereas 10 harvested stem-cells from animal-source. Bone-marrow stromal-cells (BMSC) were used in 17 studies, neural stemcells (NSC) in 7, and miscellaneous in 3. 450/774 (58.1%) animals received any stem-cell transplantation, whereas 324 were controls. Of animals receiving stem-cell transplantation (450), 339 (75.3%) showed significantly better outcomes relative to control animals in each individual study, with exception of one study. Amongst transplanted animals, functional outcomes did not differ significantly when grouped by stem-cell type (p=0.553), transplantation route (p=0.054), and source (p=0.784). Animals were followedup until 1 week (n=5 studies), 2 weeks (n=10), 4 weeks (n=5), or >4-weeks (n=7).

This pre-clinical data demonstrates that stem-cell transplantation may have treatment potential in TBI as shown by improvement in functional outcome in as many as three-quarters of all animals that were treated with stem-cells. This data provides a foundation for the design of clinical translational studies.

Age of trauma patients including those with aSDH is increasing as stated by national trauma registers. We were especially interested if age > 65 years significantly influences outcome compared to younger patients and if other factors like initial GCS have an influence too.

Methods midline shift, if aSDH was surgically removed, additional contusions, comorbidities and intake of anticoagulants. Outcome was analyzed using the Glasgow Outcome Scale (GOS) at hospital discharge (GOS 1) and if possible 6 months after discharge (GOS 2). Uni-and multivariate analysis (cox regression model) was performed using the Sigma Stat Softwar 0.05.

adverse outcome p=0.014. In addition, all patients > 65 years with an initial GCS 3 died whereas only 44% of younger patients with initial GCS 3 died (p<0.005). This was the only significant result in the multivariate analysis

The monovariate analysis of our data showed a significantly higher risk for adverse outcome after aSDH whe it should be considered if it is reasonable to transfer them from local hospitals to a specialized neurosurgical clinic, especially in times of limited resources.

Reported incidence of pulmonary edema in isolated head injury varies from 50-85%. Lung sonography is a potentially useful non invasive technique to detect extravascular lung water(EVLW). This study aimed to identify the presence of EVLW using lung ultrasound (B lines >3 per lung field) in chead injured patients admitted to ICU . Secondary objectives were to compare diagnostic accuracy and time to identification of EVLW using chest x ray versus lung ultrasound. Association of EVLW with duration of mechanical ventilation (MV)and ICU stay were observed

After Ethical clearance (IEC No. INT/IEC/2015/372), 120 patients with head injury requiring MV and critical care were enrolled in the study. Daily routine chest x ray and bedside lung ultrasound were done from the day of ICU admission until the patient was on mechanical ventilator support. Four inter costal spaces (ICS) were scanned in semi recumbent position; third and sixth ICS on either side of sternum till mid clavicular line. EVLW was reprted as > 3 B lines per lung field scan sonographically. Details of MV and ICU management were noted .

Evidence of EVLW at the time of admission using sonography and CXR was recorded in 32 and 6 patients respectively. During ICU stay 61.7% patients showed EVLW using lung USG (vs 43 patients on CXR). Mean delay in detection of EVLW on CXR after detection on ultrasound was 1.42±0.767 days. Patients with low GCS, S. Albumin, Pao2/Fio2 ratio and greater APACHE II and SAPS II had significantly higher incidence of EVLW. Duration of weaning, mechanical ventilation and ICU stay was significantly longer in patients with presence of EVLW (p <0.05)

Conclusions: Lung ultrasound appears promising in detecting EVLW earlier than chest X ray and may aid to minimize the duration of mechanical ventilation, weaning and ICU stay .

Antiepileptic drugs (AEDs) are recommended by guidelines for prophylaxis of early post-traumatic seizures (PTS) associated with traumatic brain injury (TBI). There has been an increased use of both phenytoin and levetiracetam for this indication. The purpose of this study is to determine the incremental cost-effectiveness of phenytoin compared with levetiracetam for early PTS prophylaxis in TBI patients.

A cost-effectiveness study was conducted comparing phenytoin and levetiracetam for early PTS prophylaxis during the 7 days post-TBI. Patients were included if they were 18 years or older, received a study drug, and had a diagnosis of TBI. Patients were excluded if they had a history of epilepsy, did not sustain a recent TBI, were initiated on both study drugs concurrently, or were switched to pentobarbital for elevated intracranial pressure. Data was collected via retrospective chart review using electronic medical records and publically reported costs. Effectiveness was measured as having a successful seizure prophylaxis regimen (SSPR), which was defined as 1) no clinical or electrographic seizure, 2) no discontinuation of study AED, 3) no cross-over of study AED to different AED, or 4) no addition of AED during the 7 days of therapy. The costs included costs of the study drugs, phenytoin level, and EEG. The data was used to calculate the primary endpoint, the incremental cost for the incremental change in SSPR or the incremental cost effectiveness ratio (ICER).

The phenytoin regimen (n=136) cost $371.76 and had an SSPR of 81.6%. The levetiracetam regimen (n=237) cost $628.85 and had an SSPR of 86.1%. The ICER was $57 for each 1% increase in SSPR with levetiracetam.

The SSPR of phenytoin and levetiracetam were similar. Because patients who received phenytoin may differ from those who received levetiracetam, further analysis is needed prior to drawing any conclusions about the cost-effectiveness of levetiracetam relative to phenytoin.

Augmented renal clearance (ARC) has been reported in up 85% of critically ill TBI patients and may impact therapeutic drug concentrations. Improved predictors of ARC are needed. Serum CysC, a validated marker of glomerular filtration, has not been examined as a marker for ARC in critically ill TBI patients. This pilot study tested the hypothesis that serum CysC concentrations are lower than reference values following TBI.

Adult TBI patients enrolled in the UKCCTS-UNCTracs prospective study of ARC effects on drug clearance, were eligible. CysC serum concentrations (ELISA -R & D CysC) were measured daily for up to 7 days and compared to reference values. Descriptive statistics and student t-test for continuous measures (Patient vs. reference lower range CysC) were calculated.

The first ten patients [7M/3F, mean age= 41.5years (18-59 y/o), median GCS=6 (IQR3-7)] provided a total of 49 serum CysC for analysis. Each patient provided at least 4 samples (range 4-7) for up to seven days. Measured serum CysC concentrations were below the reference range in 24 of 49 samples. The overall mean CysC concentration was 0.589 + 0.132 mg/L vs expected mean of 0.621 + 0.05. (NS) Measured values fell below the lower reference range in 5 patients (2M/3F) for the first 4 study days (Mean = 0.483 + 0.101 vs 0.622 + 0.067 p<0.05). The mean difference between measured concentration and reference value was 0.139 + 0.07 mg/L. After 4 days, four patients (2M/2F) remained below reference values with a mean difference of 0.14 + 0.06 mg/dl.

Preliminary results show CysC was not consistently below reference ranges in all TBI subjects. A subset of subjects showed significantly lower CysC within seven days of injury. The relationship between CysC and ARC needs to be further examined as analysis continues.

Functional connectivity of the default mode network (DMN) is believed to be necessary for recovery of consciousness after coma. However, DMN connectivity has not been comprehensively studied in patients with acute severe TBI. We hypothesized that DMN connectivity in patients with acute severe TBI is associated with level of consciousness.

We prospectively enrolled patients admitted to the intensive care unit for acute severe TBI and performed resting-state functional MRI (rs-fMRI) as soon as safely possible. DMN functional connectivity was assessed by rs-fMRI analysis of the blood-oxygen level dependent (BOLD) signal using a seed-based approach. Pearson's correlation coefficients were calculated between the mean BOLD time series within DMN nodes and all other regions in the brain. Level of consciousness was assessed at the time of the scan using the Coma Recovery Scale-Revised (CRS-R). Two-sample t-tests were performed to identify brain regions with connectivity differences between conscious and unconscious subjects. We then tested for associations between level of consciousness and DMN connectivity within these regions.

We enrolled 16 patients (12 male, mean+/-SD age 30+/-8 years) and 16 matched controls (11 male, age 28+/-8 years). RS-fMRI was performed 9.6+/-4.5 days post-injury. At the time of rs-fMRI, patients' levels of consciousness were coma (n=1), vegetative state (VS; n=4), minimally conscious state (MCS; n=7), and post-traumatic confusional state (PTCS; n=4). Connectivity within the medial prefrontal cortex and posterior cingulate was selectively reduced in unconscious patients (coma and VS) compared to conscious patients (MCS and PTCS; false discovery rate-corrected P < 0.05). When these regions were further interrogated, connectivity correlated with CRS-Conclusions DMN functional connectivity correlates with level of consciousness after acute severe TBI.

Traumatic brain injury (TBI) is a substantial source of death, disability, and healthcare utilization. Many older TBI patients present to community hospitals and are transferred to trauma centers for further care; however, little is known about the provision of care and patient outcomes at the final receiving hospital. We described trauma center care among geriatric transfer patients with TBI.

We conducted a secondary analysis on a sub-cohort from a prospective multi-center study focusing on ambulance and emergency department (ED) care of injured older adults transported via ambulance. The current analysis focused on TBI patients transferred to the region's Level I trauma center from another hospital. Transfer paperwork from the originating hospital was reviewed and we conducted a detailed medical record abstraction, including computed tomography (CT) findings, procedures, length of stay (LOS), and ED disposition.

Data were collected on 205 transfer patients. Thirty had confirmed abnormalities on head CT (14.6%). The mean age was 78 years (range: 55-91), 57% female, and the most frequent mechanism of injury was falls (93%). Average LOS was 13.5 days (range: 0-230, median LOS 4.5), with 8 patients staying one day or less. CT findings included subdural hematoma (60%), subarachnoid hemorrhage (50%), and intraparenchymal hemorrhage (36.7%). Five patients required neurosurgical intervention (17%), eight required ICU admission (27%), two were discharged from the ED (7%), and two transitioned to inpatient hospice (7%).

TBI is a frequent cause of transfers to trauma centers. In our sample, admission occurred in the majority of patients, but neurosurgical intervention was less common. However, for appropriately selected patients, strategies such as telemedicine may reduce transfers thus saving resources and improving continuity of care for patients and their families. This is an area in which future research is warranted.

The prospects and timing of decannulation may affect surrogate decision making regarding tracheostomy for traumatic brain injury (TBI) patients, yet predictors of decannulation are unknown.

Methods tracheostomy admitted to an affiliated acute rehabilitation hospital between January 2014 and December 2014. Patients who had life-sustaining measures withdrawn were excluded. Admission data, including injury characteristics and presence of lung injury on initial chest X-Ray, and inpatient complications were compared. Patients were followed throughout rehab and to the point of decannulation. Patients lost to follow up were eliminated from analysis. Time of decannulation was verified by inpatient physician notes. A Cox Proportional Hazards model was created to determine factors associated with the time to decannulation and reported as hazard ratios (HR).

There were 209 TBI patients admitted to the ICU during study period and 94 (79% men, mean 46 yearsold, median GCS 7) underwent tracheostomy after 10 ± 6 days of intubation, of which 79 were followed throughout rehabilitation. Overall cannulation time was 37 (29-65) days. 55 (70%) patients had their trach removed prior to discharge from rehab after 35 (27-49) days of cannulation. In a Cox Proportional model adjusting for sex, reintubation, aspiration pneumonitis, and presence of lung injury on admission chest X-ray; a higher hospital discharge GCS was associated with a shorter time to decannulation (HR, 1.147; 95% CI, 1.023-1.286; p =.019) while patients who required inpatient dialysis had a longer time to decannulation (HR: 0.281; 95% CI, 0.098-0.803; p = .018).

The majority of TBI patients that require tracheostomy will be decannulated prior to discharge from rehab. Longer durations of tracheostomy cannulatio hospital discharge and those that receive inpatient dialysis.

Goal Directed Therapy (GDT) is thought to be associated with outcome after traumatic brain injury (TBI). Our team applied GDT to standardize care in patients with moderate to severe TBI, who were enrolled in a large multicenter clinical trial.

Physiologic goals were defined a priori in order to standardize care across 42 sites participating in the ProTECT III trial. Data were collected hourly for all randomized subjects (n=882). Hours where GDT were not achieved were classified as "transgressions". These included: MAP1.4; Platelets180mg/dl; and SBP180mmHg. The proportion of hours spent in transgression was calculated for each parameter and grouped by quartile. Poor outcome was defined via stratified dichotomy of the GOS-E. Data were adjudicated electronically and via expert review. For each parameter, the association between outcome and either (1) occurrence of transgression or (2) cumulative duration of transgression was estimated via logistic regression model, and backward selection was used to identify the physiologic parameters associated with outcome. Subgroup analyses were performed in subjects with intracranial monitoring (tICP, n=480) . Parameters significant at alpha 0.01 are reported.

Prolonged duration of transgression was associated with poor outcome when: glucose>180mg/dl (p=0.0001); Hgb180mg/dl (p=0.0098) and inversely associated with MAP180 mg/dL (p=0.0015) or and was inversely associated with MAP<65mmHg (p=0.0055).

The ProTECT III clinical trial rigorously monitored compliance with GDT after TBI. Multiple significant associations between physiologic transgressions and patient outcome were found. The data suggest that reducing physiologic transgressions is important to minimizing patient morbidity after TBI.

The measurement and management of intracranial pressure (ICP) is a key component in the care of severe head injury. Extracranial ventricular drains (EVD) have remained the standard due to the ability to lower ICP with the drainage of cerebrospinal fluid (CSF). Placement of an EVD is a more invasive procedure than intraparenchymal ICP monitors (IPM) and it is unclear if the use of an EVD improves outcomes. We hypothesized that early placement of an EVD, in adult patients with severe head injury, would not affect outcomes.

Utilizing data from the Citicoline Brain Injury Treatment (COBRIT) trial, a prospective multicenter study, we identified 224 patients who met the inclusion criteria; 1) placement of an ICP monitoring device, 2) Glasgow coma score (GCS) less than 9, 3) EVD placement prior to arrival or within 6 hours of arrival at the study institution. Primary outcome was Glasgow outcome score-extended (GOSE) at 180 days post injury. Secondary outcomes included neuropsychological evaluations at 180 days post injury, mortality, and length of ICU stay. Logistic regression with forward-stepwise predictor adjustment and propensity score adjustment was performed to assess the independent association between EVD placement and outcomes.

Patients who received an EVD prior to or within 6 hours of arrival at the study institution had worse GOSE at 180 days (3.8 ± 2.2 vs 4.9 ± 2.2, p=0.007), higher in hospital mortality (23% vs 10%, p =0.021), and did worse on 4 out of 8 neuropsychological measures at 180 days. There was no difference in ICU length of stay (16.5 ± 9.0 vs 13.9 ± 10.8, p=0.289).

Early placement of EVDs in severe adult head injury is independently associated with worse outcomes and higher in hospital mortality.

Goal Directed Therapy (GDT) is thought to be associated with outcome after traumatic brain injury (TBI). Our team applied GDT to standardize care in patients with moderate to severe TBI, who were enrolled in a large multicenter clinical trial.

Physiologic goals were defined a priori in order to standardize care across 42 sites participating in the ProTECT III trial. Data were collected hourly for all randomized subjects (n=882). Hours where GDT were not achieved were classified as "transgressions". These included: MAP1.4; Platelets180mg/dl; and SBP180mmHg. The proportion of hours spent in transgression was calculated for each parameter and grouped by quartile. Data were adjudicated electronically and via expert review. For each parameter, the association between outcome and either (1) occurrence of transgression or (2) cumulative duration of transgression was estimated via logistic regression model, and backward selection was used to identify the physiologic parameters associated with mortality. Subgroup analyses were performed in subjects with intracranial monitoring (tICP, n=480). Parameters significant at alpha 0.01 are reported.

Mortality was 17.2% and 23.2% in the full and tICP cohorts. Prolonged duration of transgression was associated with increased mortality for: Hgb1.4 (p180mg/dl (p180mg/dl (p=0.0093), and SBP1.4 (p1.4 (p=0.0005). Covariates inversely related to mortality included single occurrence of MAP180mmHg (p<0.0032).

The ProTECT III clinical trial rigorously monitored compliance with GDT after TBI. Multiple associations between physiologic transgressions and mortality were observed. The data suggest that maintaining physiologic measures within GDT guidelines may be important in preventing deaths.

Current outcome models in moderate-severe traumatic brain injury (msTBI) include only admission characteristics. Yet, msTBI patients commonly have prolonged intensive-care-unit(ICU)-stays with high risks to develop ICU complications, lending to the hypothesis that these may be additionally associated with outcomes. The objective of this study was to examine the incidence rates of pre-specified medical and neurological ICU complications, and their impact on post-traumatic in-hospital mortality and 12month functional outcomes.

We analyzed 431 msTBI patients consecutively enrolled in the prospective observational OPTIMISMstudy at a level-1 trauma center between 11/2009-1/2017. Poor outcome was defined as Glasgow Outcome Scale 1-3. Multivariable logistic regression was employed to adjust for admission characteristics and ICU-length-of-stay.

The mean age was 52±22 years, 73% were men, and median motor Glasgow-Coma-Scale and Injury-Severity-Scores were 4 (IQR 1;5) and 27 (IQR 25;38), respectively. The three most common medical and neurological ICU complications were: hyperglycemia (83%), systemic inflammatory response syndrome (69%) and fever (66%); intracranial pressure crisis (ICP; [56% of n=162 with ICP-monitor]), brain edema requiring osmotherapy (46%), herniation (45%). Multivariable models were adjusted for age, Marshall-CT-classification, motor Glasgow-Coma-Scale, pre-admission hypotension, ICU-length-of-stay and Injury-Severity-Score. After adjustment, in-hospital mortality was significantly associated with in-ICU-cardiacarrest (OR 23;95%CI 3.5-152. 

Recent studies suggest benefits for early tracheostomy in patients with traumatic brain injury (TBI), yet data regarding who will require tracheostomy is lacking.

ad lifesustaining measures withdrawn were excluded. Admission and inpatient variables were compared. Multivariable logistic regression analyses were used to assess admission and inpatient factors associated with receiving a tracheostomy and to develop models predictive of tracheostomy.

There were 209 patients (78% men, mean 48 years-old, median GCS 8) meeting study criteria with tracheostomy performed in 94 (45%). Admission predictors of tracheostomy included GCS, Marshall score, injury mechanism, PaO2/FiO2 ratio, and number of quadrants on chest x-ray with consolidation. Inpatient factors associated with tracheostomy included the requirement for an external ventricular drain (EVD), number of operations, pneumothorax, inpatient dialysis, aspiration, reintubation, and the presence of hospital acquired infections. Multiple logistic regression analysis demonstrated that the development of hospital acquired infection (adjusted odds ratio [AOR], 4.78; 95% confidence interval [CI], 2.18-10.48; p < .001), number of operations (AOR, 1.47; 95% CI, 1.2-1.78; p < .001), pneumothorax (AOR, 2.64; 95% CI, 1.08-6.48; p = .034), reintubation (AOR, 7.18; 95% CI, 2.50-20.54; < .001), penetrating TBI (AOR, 0.14; 95% CI, 0.03-0.60; p=0.008) and placement of EVD (AOR, 6.73; 95% CI, 3.03-14.95; < .001) were independently associated with patients undergoing tracheostomy. A model of inpatient variables only was more strongly associated with tracheostomy than one with admission variables only (ROC AUC 0.90 vs. 0.72, P<0.001) and did not benefit from addition of admission variables (ROC AUC 0.91 vs 0.90, P=0.76).

Potentially modifiable inpatient factors have a stronger association with tracheostomy than do admission characteristics.

Existing traumatic brain injury (TBI) guidelines are designed primarily for the evaluation and management of TBI in tertiary care centers with advanced neuroscience capabilities. Military Special Operations medical providers, however, are often required to treat and sustain patients in austere environments with limited resources for up to 72 hours. TBI management guidelines directed specifically toward the care of these patients are needed.

A review of recent operational experiences involving TBI and a survey of Military Special Operations Medics prompted a multidisciplinary Expert Panel to develop draft clinical practice guidelines/recommendations for prolonged field management of TBI. The panel conducted an in-depth review of literature on TBI and related topics and adapted existing and emerging therapies to address the unique challenges encountered in prolonged field care.

TBI management while optimal management of PbtO2 is not fully established. The objective of this

-Coeur arterial blood gas was drawn (ICP, CPP, hemoglobin, temperature, PCO2 and PaO2). Probes were localized in normal appearing white matter. We used a was calculated.

A total of 1006 data sets were collected from 38 patients (mean age 44.5±20.0, median GCS 4, mortality range from 94 to 400). Mean PaO2 for the group as a whole was 178 mmHg (± 88) and mean CPP was 72 mmHg (± 12). Mean duration of PbtO2 monitoring was 6.5 days (± 3.7).

Taking into account all determinants of PbtO2 and using a protocolized approach to correct PbtO2, the mmHg for a few days. High PaO2 values are possibly required due to the fact that oxygen delivery to the brain is rate-limited by diffusion and impaired by oedema or microvascular ischemia. It should be noted that pulse oximetry is not sensitive to detect PaO2 below this level.

Traumatic Brain Injury (TBI) and stroke are extremely common causes of Acute Brain Injury (ABI), which cause long term disability and permanent neurological impairment. Coma and stupor are common manifestations of ABI, due to interruptions of the Ascending Reticular Activating System (ARAS). Neuro stimulants can improve functioning of the ARAS. Despite decades of research there is a paucity of prospective high-level evidence utilizing neuro stimulants to help with earlier awakening from coma and stupor in ABI. We reviewed the literature using the GRADE level of evidence (LOE) methodology.

We performed a preliminary literature search of the National Library of Medicine (NLM) using search terms ABI and stimulants. Within the literature we searched for timing of stimulant use among ABI studies and included all forms of ABI such as TBI, stroke, and anoxic injury.

We retrieved 508 total results, of which we excluded 474 since they did not meet GRADE high LOE criteria or were "n of 1" studies or aggregates. Only 34 high LOE randomized studies or meta-analyses were found. Among these various stimulants were investigated including methamphetamines such as methylphenidate and lisdexamfetamine, caffeine, armodafinil, galantamine, and amantadine. Methylphenidate had 10 randomized trials and a meta-analysis in subacute TBI but reported only attention as a main outcome. We were unable to draw broad-level recommendations about optimal timing, best stimulant, and patient centered outcomes from this data.

There is insufficient data to recommend optimal stimulant, timing, and dosing among heterogeneous ABI disease models. We propose conducting future homogenous ABI neuro stimulant trials in for safety, tolerability, dose-finding, optimal timing, and outcomes based efficacy. Neuro stimulants could play a role in earlier awakening and extubation in ABI which could improve outcomes similar to sedation/vacation bundles in ICU's currently if studied adequately.

TBI remains the leading cause of death and disability in young adults in the US and Europe. Thus far, pharmacological and non-pharmacological intervention studies did not confirm benefits on functional outcomes.

The inducible enzyme Nitric Oxide Synthase (iNOS) is upregulated in response to brain injury, causing excessive production of NO, a key driver of secondary injury after TBI. The antipterin VAS203 is a structural analogue of the endogenous NOS cofactor and a potent in-vivo selective inhibitor of iNOS. A randomized, placebo-controlled Phase 2 study examined 3 dose levels of VAS203 in 32 patients with acute moderate or severe TBI. Cerebral microdialysis showed pharmacologically relevant drug concentrations close to the injury and a tendency for VAS203 to increase the arginine/citrulline ratio, an indirect marker of NOS inhibition (Stover et al., J Neurotrauma 2014). VAS203 conferred a significant benefit on the extended Glasgow Outcome Scale Interview (eGOS-I) at 6 and 12 months after injury. No changes in systemic blood pressure or partial brain oxygen pressure were noted. A recent pharmacokinetics and pharmacodynamics study further corroborated the selective iNOS inhibition by VAS203.

The confirmatory NOSTRA Phase 3 trial (EudraCT no. 2013-003368-29; ClinicalTrials.gov identifier NCT02794168) was initiated in 2016. Adult patients with a nonrequiring intracranial pressure monitoring, are randomized 1:1 to VAS203 or placebo, administered in addition to standard of care, as intravenous continuous infusion for 48 hours, starting between 6 and 18 hours post TBI. The primary efficacy endpoint is eGOS-I at 6 months post injury. Additional endpoints include the daily therapy intensity level and TBI-specific quality of life measures. Continuous safety monitoring is performed by an independent committee.

NOSTRA III, the only ongoing registration study in acute moderate and severe TBI, is sponsored by vasopharm GmbH, and plans to recruit 232 patients by Q3 2018.

A Glasgow Coma Scale (GCS) score of 3 on presentation in patients with traumatic brain injury (TBI) portends a poor prognosis. Consequently, there is often a tendency to treat these patients less aggressively because of low expectations for a good outcome.

We performed a retrospective review of patients with TBI and a GCS score of 3. Demographics, APACHE IV scores , pupillary reactivity to light, intracranial pressure (ICP), ICP burden (the number of days with an ICP spike >25 mm Hg as a percentage of the total number of days monitored), and outcome (Mortality and Glasgow Outcome Scale-GOS at 6 months, with good outcome defined as GOS of 4-5). Patients were divided into 2 groups: Group 1 (GOS = 1-3) and Group 2 (GOS = 4-5).

A total of 62 patients were included. The overall mortality rate was 80.6 %. At 6-month, 9 patients (14.5 %) achieved a GOS 4-5. Compared to Group 2 (n = 9), Group 1(n = 53) had higher average APACHE IV score (104 ± 19 vs 89 ± 27, p = 0.04), more patients with bilateral fixed pupils (59 % vs 22 %, p = 0.04), and higher ICP burden ( 50 ± 34 vs 0 ± 0, p = 0.0001). GOS Score 4-5 was achieved in 41% of patients presenting with bilateral reactive pupils versus 6.9 % of patients presenting with bilateral fixed pupils (p = 0.005).

14.5 % of patients with TBI and a GCS of 3 at presentation achieved a good outcome at 6 months. APACHE IV scores, ICP burden, and pupillary reactivity were significant predictors of outcome. We believe that patients with severe TBI who present with a GCS of 3 should still be treated aggressively initially since a good outcome can be obtained in a significant proportion of patients.

Elevated circulating catecholamine levels are independently associated with functional outcome and mortality after isolated traumatic brain injury (TBI). We assessed the ability of peripheral catecholamine levels to improve the prognostic performance of the CRASH and IMPACT-TBI models.

Prospective, observational, multicenter cohort study, conducted at three Level 1 Trauma Centers in Canada and USA. Epinephrine (Epi) and norepinephrine (NE) concentrations were measured in the peripheral blood at admission (baseline), 6, 12 and 24h after trauma. Outcome was assessed at 6 months and dichotomized into favorable [Extended Glasgow Outcome Scale (GO -TBI models, which identified core prognostic markers of severe TBI. The baseline model (M1) included age, GCS and pupillary size/reactivity. The model 2 (M2) included M1 + hypoxia, hypotension and Marshall CT classification. Model 3 and 4 included M1 + Epi levels, and M1 + NE levels, respectively. The risk models performance was assessed by comparing receiver operating characteristic (ROC) curves, and by the use of integrated discrimination improvement (IDI) index.

M3 had significantly higher ROC and IDI than the baseline model (M1), to predict mortality. M3 had a ROC = 0.930 (0.891 -0.968, p = 0.012) and IDI = 0.14 (p = 0.0001). The prediction of mortality was not improved by including NE [M4 = ROC = 0.896 (0.848 -0.943, p = 0.245) and IDI = 0.02 (p=0.124)]. The integrated discrimination improvement index indicated the prediction of unfavourable outcome by the baseline model was improved by including EPi (IDI = 0.04, p=0.024), and NE (IDI = 0.08, p=0.0002) in the models.

Catecholamine levels improved risk models performance to predict mortality and unfavorable outcome after traumatic brain injury.

Following traumatic brain injury (TBI), depression is common and may influence recovery. Small trials demonstrated that various drugs are beneficial in managing depression following TBI, but no large, definitive study has been conducted. We performed a meta-analysis to estimate the potential benefit of anti-depressant medications following TBI.

Multiple databases were searched using the terms "anti-depressant TBI," and "depression treatment TBI" to find prospective pharmacologic treatment studies of depression following TBI. Studies were excluded if they did not measure depression as an outcome. Effect sizes for anti-depressant medications in post-TBI patients were calculated for within-subjects designs that examined change from baseline after receiving medical treatment and treatment-placebo designs that examined the differences between anti-depressants and placebo groups. A random effects model was used for both analyses.

Of 923 titles screened, 10 studies were included, with 288 total patients. Medications evaluated included selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, and tricyclic antidepressants. Pooled estimates showed significant reduction in depression scores for individuals after pharmacotherapy (mean change [MC] -11.7, 95% confidence interval [CI]: -15.5 to -8.0) and significant difference in reduction of depression scores between medications and placebo in the pooled estimate (standardized mean difference of four trials [SMD] -0.4, 95% CI: -0.7 to -0.1); however only one of the four treatment-placebo studies found medications significantly reduce depression scores more than placebo.

This meta-analysis found a significant benefit of pharmacotherapy for treatment of depression in patients with TBI. However, there was a high degree of bias and heterogeneity regarding TBI severity, time since injury, depression severity, and demographics. Larger prospective studies on the impact of anti-depressants on post-TBI depression are warranted to better understand treatment effects and the relationship of post-TBI depression and outcome more broadly.

Pleural effusion (PE) has been reported in 62% of medical ICU. There is little published data on the prevalence and clinical significance of PE in mechanically ventilated patients with traumatic brain injury.

Head injury patients admitted to ICU for mechanical ventilation (MV) within 48-72 hours and GCS > 5 were assessed for eligibility. Presence of PE was assessed by serial CXR on daily basis and volume of effusion was estimated and recorded. In case there was no evidence of PE on CXR, a bedside sonography in semi recumbent position was done within 72 h of ICU admission. Pleural fluid volume was estimated based on 4-point classifications on sonography. Details of mechanical ventilation and ICU management were recorded. Successful weaning was defined as ability to breath spontaneously for 48 h. Primary aim was to observe prevalence of PE in MV head injured patients. As secondary measure; impact of PE on duration of MV, weaning and length of ICU stay were compared.

Study enrolled 90 patients. Three baseline CXR showed PE. Total of 27(30%) patients developed PE in ICU. 9 patients had evidence of PE on both CXR and USG. 18 patients had only sonographic evidence of PE, which were not detected on CXR. Significantly more minimal effusions were detected on sonography (10/27, p=0.03). Duration of mechanical ventilation and duration of ICU stay were significantly more in patients with PE. (p= 0.009, Mann Whitney rank sum test) There was no significance difference in duration of weaning in patients with and without effusion (2.9±2.2, 2.1±1.3, p=0.084).

Chest ultrasonography increased the detection rate of pleural fluid. Patients with PE had longer duration of mechanical ventilation. Early detection may be associated with shorter period of mechanical ventilation and ICU stay

Spine surgery can trigger a systemic inflammatory response syndrome and lead to hypotension requiring vasopressors. As sepsis is a major differential diagnosis in the post-operative period, the objective of this study is to understand the prevalence of a true systemic infection in this setting.

Retrospective review of all consecutive adults with post-operative shock requiring vasopressors following spine surgery in an academic tertiary medical center.

A total of 43 patients, median age 69 years (IQR 57-74), were included in the final analysis. Comorbidities included a median BMI of 28 (IQR 23-33), coronary artery disease (28%) and diabetes mellitus (16%). Median estimated blood loss was 1200 cc (IQR 450 to 2150 cc). Circulatory volume was adequately replaced in a total of 72% patients within 6 hours post-op. All patients received crystalloids, and an additional 42% received multiple (>4) units of PRBCs transfusion. Adequate urine output was confirmed in 42 (98%) of the patients. The maximum median rate and duration of each vasopressor infusion was as follows: phenylephrine 100 mcg/min (IQR 60-150, n = 39), 21 hours (IQR 12-46), norepinephrine 40 mcg/min (IQR 20-95, n = 13), 16 hours (IQR 8-62), epinephrine 10 mcg/min (IQR 10-50, n = 3), 12 hours (IQR 8-16) and vasopressin 0.04 units/min, 23 hours (4-31, n = 3). Of the 43 patients, 34 (79%) met at least 2 SIRS criteria. Infection was confirmed in a total of 10 patients; positive respiratory or blood cultures in 7 (16%) patients and positive urinalysis or urine culture in 5 (12%). Two patients (5%) were diagnosed with myocardial infarction. No patients had pulmonary embolism.

Our study suggests that the risk of infection and sepsis in patients with persistent shock following spine surgery is small but not negligible. Larger multicenter studies are needed to confirm our findings and to identify the predictive factors.

Ischemic and hyperemic injuries may occur unnoticed after severe traumatic brain injury (TBI) and contribute to additional brain damage. Maintaining an adequate cerebral perfusion is considered crucial in preventing such injuries, as deviations from autoregulation-guided optimal cerebral perfusion pressure (CPPopt) are associated with greater mortality and disability. This makes reliable estimation of CPPopt an interesting diagnostic and treatment tool for monitoring.

CPPopt is defined as the cerebral perfusion pressure (CPP) at which the pressure reactivity index (PRx) is minimal. The leading method for estimating CPPopt automatically, by Aries et al. (2012) , fits a parabola to pairs of PRx and CPP data. The method uses preset heuristics to reject the fit as unreliable, namely when the parabola is too "shallow" or does not cover a certain CPP range. As a result, the 2012 CPPopt estimates could be generated only about 50-60% of the time. Moreover, the manually set heuristics potentially restrict the generality of the model.

Here, we propose an alternative method based on Bayesian inference. Treating PRx at each time as a function of CPP corrupted by noise serves as a "forward model" that can be inverted to yield, for a given data set, a temporally evolving posterior probability distribution over CPPopt. The mean of this distribution is a Bayesian estimate of CPPopt; we find that these estimates are generally consistent with those obtained from the classic method. Importantly, the width of the distribution at a given time serves as a metric of uncertainty about CPPopt estimation. We find that this uncertainty tends to be large at time points where the classic method with preset heuristics rejects the fitted parabola.

Our method makes manually setting rejection criteria unnecessary. Bayesian estimation of CPPopt holds promise as a tool for providing additional decision support in the care of individual TBI patients.

Quantitative parameters derived from continuous EEG (cEEG) have been useful to understand evolution of traumatic brain injury (TBI) and the impact on regional networks. These parameters are often interrogated at a global level rather than region-specific. The regional evaluation of quantitative EEG parameters may provide an objective assessment of regional network function, and be of predictive value for prognostication

Continuous EEG was performed in 54 patients with TBI, and MRI imaging was obtained during acute and chronic time points post injury (within 30 days and 6 months, respectively). The Extended Glasgow Outcome Scale (GOSE) assessed clinical recovery at 6 months, with good recovery defined as GOSE score 5-8 and poor as GOSE score 1-4. Volumetric measurements of selected brain regions, both cortical and subcortical, were obtained at acute and chronic time points. Quantitative parameters derived from cEEG, such as percent alpha variability (PAV) and hemispheric symmetry, were calculated continuously and anatomically (frontal, temporal, occipital) through the acute hospitalization course. We hypothesized that persistent regional variation in alpha power post injury would lead to brain regionspecific atrophy and may predict outcome at 6 months

Acute PAV within the first 48 hours post injury was poor in patients with poor outcome. In addition, patients with poor outcome had significantly more atrophy in the thalamus, hippocampus, and temporal and occipital lobes. Asymmetry of the hemisphere PAV values correlated with both brain atrophy and clinical outcome

Regional asymmetry of PAV within the first 48 hours post injury correlates with chronic brain atrophy and clinical outcome after TBI

After moderate and severe traumatic brain injuries (TBIs), individuals are often admitted to an intensive care unit (ICU), and later require intensive rehabilitation. Many neuro-ICUs engage therapists and physiatrists for rehabilitation and therapy during a patient's ICU admission. However, the optimal timing, intensity, and components of rehabilitation needed while in the ICU are not known and practice patterns are highly variable. The goal of this study is to describe the rehabilitation practices to identify whether there is consensus on best practices.

An electronic survey asking participants to describe TBI rehabilitation practices in their ICU was distributed via REDCap through the Neurocritical Care Society (NCS) and American Congress of Rehabilitation Medicine (ACRM) websites. Potential respondents were first asked if they cared for patients with TBI in the ICU, and if they answered "yes," they were invited to complete the survey. Two email reminders were sent to each group for completion. After 51 weeks, the data were extracted and analysis completed.

There were 47 respondents who reported that they cared for patients with TBI in the ICU (17 attending physicians, 6 advanced care practitioners, 15 therapists, 4 nurses, 4 fellows, and 1 other). Of these, 96% recommended early rehabilitative care. The most common reasons to wait for the initiation of physical therapy and occupational therapy were normalization of intracranial pressure (ICP) (86% and 89% respectively) and hemodynamic stability (66% and 69% respectively). Speech therapy was typically recommended after extubation (65%) and normalization of ICP (58%).

The majority of clinicians caring for patients with TBI in the ICU support early rehabilitation efforts, typically after a patient is extubated, intracranial pressure has normalized and the patient is hemodynamically stable. Prospective studies evaluating the merits of these self-reported rehabilitation initiation criteria are warranted.

High-dose methylprednisolone (HDMP) has been studied as a potential therapeutic option for acute SCI, with mixed results regarding efficacy and consistent suggestion of complications. We conducted a retrospective cohort study of acute SCI patients extracted from the Medical Information Mart for Intensive Care III (MIMIC-III) database to evaluate the hypothesis that steroid-related adverse drug events (ADEs) occur less often than in published clinical trials using HDMP.

Three groups of patients coded for acute SCI were identified from MIMIC-III from June 2001 to October 2012: HDMP recipients per NASCIS II/III protocols (HDMP, n = 55), patients who received some steroids but not per NASCIS II/III protocols (Non-HDMP, n = 47), and patients who did not receive steroids (No Steroids, n = 198) . Demographics and data on complications of steroid therapy were extracted. One-way ANOVA or Student's t test were used to evaluate continuous variables; chi-squared or Fisher's exact test were used for nominal or categorical variables.

There were no differences in steroid-related ADEs between the three groups. There were higher average blood glucose readings in recipients of any steroids compared with the No Steroids group, and more variation in blood glucose readings in HDMP recipients compared with the other two groups. There was a higher ICU LOS and ventilator time in the HDMP group compared with the other two groups. Compared with three other trials examining similar use of HDMP in acute SCI, there were higher rates of pneumonias overall, though lower rates of urinary tract infections, skin & soft tissue infections, pressure ulcers, and superficial thromboemboli/thrombophlebitis.

The results of this study are consistent with previous works related to the potential for harm regarding the use of HDMP or any steroids in acute SCI. Changes in selected adverse event profiles may be due to standardization of ICU supportive care over time.

Cervical spinal immobilization and clearance protocols are important steps in the minimization of secondary spinal cord injury. Patients with primary neurologic diseases are frequently found down and placed in rigid cervical collars despite sustaining minimal-to-no cervical injury. In these patients, neurologic dysfunction can complicate and delay cervical clearance. Decreasing time spent in cervical spinal immobilization could improve patient care by allowing greater access to / range-of-motion of the neck, increasing patient comfort, and decreasing skin breakdown.

Through retrospective chart review over a 28-month period, we collected the following: the rationale behind each MRI, any MRI evidence of cervical instability, the result of any CT imaging, and the basic mechanism of any trauma. For patients that were simply found down, any evidence of trauma either by history or physical exam was recorded.

During the study period, there were 306 instances where an MRI of the cervical spine was performed. Of those MRIs, 176 (58%), were performed for cervical spinal clearance. Sixty-one (35%) of MRIs were ordered without any CT imaging first. Of the patients with a normal CT, six (3.4%) were found to have MRI evidence of cervical instability. Notably, of the 62 patients who were found down, there was only one instance where the MRI demonstrated instability. That patient had extensive facial injuries suggestive of an unwitnessed fall. In the 40 patients that were found down with no history or evidence on physical exam of trauma, there was no MRI instability.

For patients that are found down without any history or evidence on physical exam of trauma, a CT of the cervical spine is likely sufficient for cervical spinal clearance.

Acute subdural hematoma (ASDH) represents a major clinical entity in severe traumatic brain (sTBI), approximately 60% are accompanied by various extents of ASDH. STBI has been reported to cause cerebral circulatory disturbances at an acute stage and had the worst circulatory disturbance among sTBI. In this study, we focused on the cerebral circulation of ASDH, evaluated the absolute left-right difference between cerebral hemispheres and compared the cerebral circulation between the favorable outcome group and the unfavorable group.

We retrospectively reviewed 31 patients with ASDH. They were admitted to our hospital from 2002 to2011. In these patients, we simultaneously performed xenon-computed tomography (Xe-CT) and perfusion CT to evaluate the cerebral circulation on post-injury days 1-3. We measured CBF using Xe-CT and mean transit time using perfusion CT and calculated the cerebral blood volume (CBV).

A significant absolute difference in cerebral circulation between the hemispheres among different types of TBI was observed in MTT. There was no significant difference in these parameters between left-right hemispheres with ASDH among the favorable outcome group and unfavorable group. Although there was no significant difference in age, GCS at the onset of treatment, CBF and CBV, there was significant difference only in MTT between the favorable outcome group and unfavorable group.

The circulatory disturbance in patients with ASDH occurs diffusely despite the focal injury. Additionally, in unfavorable patients, the circulatory disturbance is worse than in favorable patients. Because ASDH suffered ischemia more than other types of sTBI, we had to perform not only removal of the occupying lesions, but also neurointensive care, including whole-body management and hypothermia therapy for the ischemic brain after surgery. We have to adopt a treatment strategy appropriate to the pathophysiology of the different TBI types.

Kcentra is 4-factor prothrombin complex concentrate that is FDA approved for reversal of warfarin. There is limited research describing the use of Kcentra for coagulopathy in the setting of traumatic intracranial hemorrhage. Here, we show the largest ever retrospective review for the use of Kcentra in the setting of traumatic intracranial hemorrhage.

Retrospective chart review was performed from 2013-2016 for patients with intracranial hemorrhage who presented to the R Adams Cowley Shock Trauma Center. Patients who received Kcentra were identified. Basic clinical information was obtained including cardiac/stroke history, blood pressure, Glasgow Coma Score, medication history, and categorization of hemorrhage. Pre and post INR level was assessed. Hemorrhagic expansion was assessed with CT scan up to up to 24 hours. Disposition and thromboembolic events were recorded.

Forty-four patients were identified as receiving Kcentra in the setting of traumatic intracranial hemorrhage. Pre and post Kcentra dosing INR was found to be significantly different (p<0.001) across the two groups assessed (warfarin and TBI/NOAC coagulopathy). Seventeen patients (38.6%) had hemorrhagic expansion as determined on CT scan. Disposition (home vs rehab vs death) was found to have three significant variables: history of stroke, hemorrhagic expansion, and admission Glasgow Coma Score. Eight patients (18.2%) were found to have thromboembolic events.

Here, we show the largest retrospective review describing the clinical use of Kcentra for coagulopathy reversal in the setting of intracranial hemorrhage. Overall, Kcentra is shown to be a safe and effective drug for the reversal INR. Importantly, our reported hemorrhagic rate of 38.6% is lower than established rates reported in the literature for warfarin/coagulopathic patients with intracerebral hemorrhage (50-60%). The prognostic importance of hemorrhagic expansion was highlighted in the disposition analysis which showed that zero patients were discharge home if there was recorded expansion. 

Despite the impact of post-traumatic amnesia (PTA) duration on long-term functional outcome after traumatic brain injury (TBI), radiologic predictors of PTA duration are lacking. We hypothesized that the number of traumatic microbleeds (TMBs) detected by gradient recalled echo (GRE) magnetic resonance imaging (MRI) in neuroanatomic regions that mediate memory correlates more strongly with PTA duration than does the number of global TMBs.

Using a prospective outcome database of patients treated for mild-to-severe TBI at an inpatient rehabilitation hospital, we retrospectively identified 65 patients who underwent acute MRI with GRE. PTA duration was determined by the Galveston Orientation and Amnesia Test, Orientation Log or chart review. A rater blinded to PTA duration identified TMBs on the GRE datasets globally and in neuroanatomic regions that mediate memory, including the hippocampus, fornix, corpus callosum, thalamus, and the temporal lobe. Associations between global and regional TMBs (in the 5 mentioned locations) and PTA duration were tested using Spearman rank correlation coefficients.

The cohort was comprised of 25% ( 

Hippocampus and corpus callosum TMBs are associated with PTA duration, and thus may have greater utility for predicting functional outcomes than global TMB number. Validation of these findings in larger prospective studies is indicated.

Using a large two-center cohort of 413 penetrating traumatic brain injury (pTBI) patients, we previously developed the Survival after Acute Civilian Penetrating Brain Injuries (SPIN) Score, a logistic regressionbased parsimonious risk stratification scale for estimating survival after civilian pTBI. The objective of the present study was to externally validate the SPIN-Score.

Our multicenter validation cohort comprised 362 pTBI patients retrospectively identified from three U.S. Level-1 trauma center registries. The SPIN score variables (motor GCS [mGCS], sex, pupillary reactivity, self-inflicted pTBI, transfer status, Injury Severity Score [ISS] and INR) were collected from the trauma registries supplemented by chart review. Using the SPIN-score multivariable logistic regression model from the original study, receiver-operating-characteristic area-under-the-curve (ROC-AUC) analysis and Hosmer-Lemeshow Goodness-of-fit testing was performed.

The mean age was 32±15 years, and patients were predominantly male (85%), with 41% white and 28% black. In-hospital mortality was 52%, and 6-month mortality of discharge survivors was 3. 

In this multicenter external validation study, the full SPIN-model predicts in-hospital survival after pTBI with excellent discrimination and calibration. After removing INR from the model, discrimination remained excellent, but model calibration diminished. The full SPIN-score may provide important information to guide families and physicians after civilian pTBI.

Limited data has described alterations in vancomycin pharmacokinetic (PK) parameters in traumatic brain injury (TBI) patients that have resulted in sub-therapeutic concentrations. The primary objective of this study is to evaluate the PK parameters of vancomycin in TBI patients to determine if using the common clinical practice of capping creatinine clearance (CrCl) to 120 mL/min in determining dosing impacts achievement of therapeutic concentrations.

This was a single-center, retrospective study of patients at least 18 years of age with TBI who received vancomycin and one reported steady-state vancomycin serum level from April 2014 to December 2015. Predicted PK parameters based on population data using actual and capped creatinine clearance (CrCl) at 120mL/min were compared with calculated PK parameters based on serum trough concentrations at steady state. The difference was assessed using a two-sample Wilcoxon rank-sum test where p < 0.05 was considered statistically significant.

When using actual CrCl [median 167 mL/min 

Patients with TBI experienced CrCl that were greater than predicted. Based on the results of this study, actual CrCl is more accurate at predicting vancomycin PK than the common practice of capping CrCl at 120mL/min. Therefore, actual CrCl should be used when determining vancomycin dosing regimens in patients with TBI to achieve desired therapeutic concentrations.

Neurocritical care is traditionally provided within institutions in urban centers while access in rural communities has been limited. Transport to urban centers is not always favorable for a variety of reasons including critical patient condition, family wishes, weather, and geography. Our hypothesis is that tele-neurocritical (Tele-NCC) can extend access to this service with meaningful impact on ICU outcomes.

A Tele-NCC pilot study was initiated within Intermountain Healthcare. Starting 5/1/17, the study included all ischemic stroke patients admitted to the ICU of one primary stroke center in Utah. Tele-NCC consultations were provided by NCC physicians at our flagship hospital located three hundred miles from the spoke site. Tele-NCC consultations occurred via an existing telehealth platform developed inhouse. Primary outcomes for this pilot study were ICU and hospital lengths of stay (LOS). Secondary outcomes include stroke complication rates and results on a provider satisfaction questionnaire.

To date,12 Tele-NCC consultations have been performed with median hospital LOS = 3 days (IQR 2.8 -4.3) and ICU LOS = 1.6 days (IQR 1 -2). In the 12 months prior to the pilot, there were 109 admissions to the ICU for ischemic stroke with median LOS = 4 days (IQR 2.8 -5.8) and ICU LOS = 1.8 (IQR 1 -2.6). For this small sample size, the p-values for comparison of hospital and ICU lengths of stay before and after Tele-NCC are 0.39 and 0.78 respectively.

Tele-NCC care can have significant impact on ICU outcomes by expanding access to critical support from neurocritical care specialists. Tele-NCC expands access to not only consultation on critical neurological emergencies, but also on when to de-escalate from the ICU or in end of life discussions with which general ICU teams may not be comfortable. These impacts could be measured as important decreases in hospital and ICU LOS.

Hospital readmissions increase health care costs, increase patient exposure to nosocomial disease, and imply patients were not stable for discharge. Because readmissions are a target for hospitals and payers, several centers have developed predictive readmission scores in order to identify high-risk patients. We contend that these general readmission scores are not suitable for neurocritically ill patients and that specific predictive score must be developed to identify high-risk patients.

We conducted a retrospective chart review of 340 consecutive patients admitted to our neuroscience critical care unit. We recorded the readmission scores, reason for admission, length of stay,and if they were readmitted. We then compared the median readmission scores between the two groups.

After removing patients without readmission scores or died at the end of the original admission,we analyzed the records of 279 patients. Patients were more likely to be readmitted if they were initially emergently hospitalized or had malignancy. Readmitted patients had a longer original hospital length of stay. We found no difference median readmission score between those who were readmitted, and those who were not. Most readmitted patients (65.8%) had an original "low-risk" readmission score.

We found that our center's score was poor in predicting readmission for neurocritical care patients and that several components of the score do not apply to our patient population. We propose that to accurately predict readmission,centers should create their own unique readmission scores for more homogeneous admission populations.

Clinical evaluation of the level of consciousness in non-communicative patients can be very challenging.

In this study, we aimed to evaluate the nurses and nursing assistants' (NAs) perception of the consciousness on patients suffering from disorder of consciousness (DOC). Through their activities, nurses and NAs have an extended observation time of patient's behavior, and make repeated implicit assessments of patients' clinical state of consciousness. We hypothesized that even in the absence of a structured and explicit evaluation of consciousness (in contrast for instance with the Coma Recovery Scale Revised -CRS-R), nursing expertise could be a valuable measure to improve assessment of state of consciousness in DOC patients.

This was a prospective observational single-center study. Our primary objective was to correlate the nurses and NA's assessment of DOC-patients' consciousness quantified through an Analogic Visual Scale (the "DOC-feeling score") with the results of the standard methods (including CRS-R, fMRI, electrophysiology). The secondary objective was to identify elements which correlate with this assessment and/or with the expert's diagnosis (such as visual pursuit, patient's participation to nursing, motor responses to verbal command or adapted reactions to painful care). . Linear regression reveals a good correlation between the "DOC-feeling score" and the CRS-R gold standard (R2 = 0.37, p-value <0.0002, Figure 2 ).

Global assessment of the level of consciousness by all the caregivers interacting with the patient using the "DOC-feeling score" is reliable and can improve assessment of state of consciousness in DOC patients.

Investigating causes of deterioration in neurological patients is important to anticipate these complications and improve outcomes.

This is a prospective observational study performed at an academic tertiary care trauma, stroke and neurorehabilitation center. Data was collected over a year from Rapid Response System activations (RRSa).

In one year, our center had 5388 admissions. 169 RRSa were performed on 140 patients. Most common admission diagnosis was ischemic stroke 45 (32%). Most common RRSa organ system involvement was respiratory system (n=59, 34.8%). The only predictors of death or new limitation of care in those patients who had RRSa were age (67 years vs 58 years, p <0.01) and history of cancer 8 (26%) vs 11 (19%) p=0.02. 62.1% (n=105) of RRSa happened during day shift and 37.9% (n=64) during night shift. 20.7% (n=35) of RRSa happened around shift change and were more likely to result in an unplanned ICU admission. 37.7% (n=63) of RRSa happened within 24 hours of admission and were more likely to result in unplanned ICU admissions.

The most common reasons for in hospital decompensation in neurological inpatients are nonneurological. Most common organ system involvement responsible for RRSa is respiratory system. The only predictors of death or new limitation of care were history of cancer and age 67 and older. RRSa activations were more frequent during day shift. However, there was no different in the outcomes we evaluated between day and night shifts. RRSa happening around shift change wew more likely to result in unplanned ICU admission. RRSa within 24 hours of admission showed an increased risk of unplanned ICU admission when compared to RRSa happening after 24 hours of admission.

Neurocritical care is a growing field with an increasing number of dedicated neuroscience intensive care units. In this dynamic context, it is unclear which types of physicians provide neurocritical care across the United States.

We performed a retrospective cohort study using claims data from a nationally representative 5% within analyzed critical care procedures . The primary outcome was physician specialty, defined by Medicare provider specialty codes. In a sensitivity analysis, we excluded claims for services on the day of admission and claims associated with a diagnosis of cardiac arrest, since these activities may often occur outside of neuroscience intensive care units.

We identified 

Between 2009 and 2014, neurologists were responsible for approximately one-quarter of neurocritical care services among a nationally representative cohort of elderly patients.

Critically-ill patients on mechanical ventilation (MV) cannot verbally communicate. Research suggests several phenomena occur in patients during MV because of impaired communication including anxiety, loss of control, loneliness, and compromised interaction (Schou and Egerod, 2008) . For neurocritical care patients, this can be especially profound when coupled with cognitive and motor/sensory deficits. Currently, the BLOM® speaking valve (SV) is the only approved product available that allows phonation in ventilator-dependent patients with tracheostomy. SV trials are known to facilitate vent-weaning. The current standard of care (Passy-Muir speaking valve, 30 minute trials), is contra-indicated in patients who cannot tolerate cuff deflation. As such, the BLOM® SV was evaluated for clinical and quality efficacy.

We retrospectively evaluated clinical outcomes associated with BLOM® SV on MV during a trial in a neuroICU of a large tertiary center between 6/1/2014 and 5/31/2016. Baseline demographics, diagnoses, physiologic, sedation, delirium, mobility and swallowing parameters, length of stay, ventilator modes and settings, ventilator days, work of breathing and presence of pneumonia were abstracted along with patient, family and interdisciplinary staff satisfaction survey results.

28 patients were recommended for BLOM® tracheostomy. 22 patients received SV trials. Of the 185 trials were performed, 28% (52) were optimal/completed (30+ minutes); 36% (68) were suboptimal/completed trials (0-29 minutes); 14% (27) unable to complete. Satisfaction results from patients/families were positive compared to the interdisciplinary team survey results. Remaining parameters currently in analysis with results pending, to be completed by end of August, 2017.

Impaired communication during MV is suboptimal for neurocritical care patients. Our clinical experiences with BLOM® SV showed positive and negative outcomes. Positive benefits were enhanced patient/family engagement and family satisfaction. Unanticipated obstacles included significant increase in patient fatigue during SV trials, often delaying ventilator weaning. Further study is needed to determine efficacy in this population.

Patients with clinical signs of cerebral herniation require immediate intervention known as a "brain code". In our Neurosciences Critical Care Unit (NCCU), a rapid response program is in place to ensure the safety of 23.4% hypertonic saline's use (high risk medication) and to expedite its delivery to the bedside given the emergent need for this medication when ordered. Our institution, however, is lacking a more holistic and structured approach to cerebral herniation syndrome that include components of Tiers Zero to Three Emergency Neurological Life Support Elevated ICP or Herniation Protocol.

The Neurocritical Care Communication Council consists of bedside staff nurses, nursing leadership, Advanced Practice Providers (Nurse Practitioners and Clinical Nurse Specialist), Pharmacists, Respiratory Therapists and Physicians. The Council identified processes during neurological brain codes that could be improved as a result of using a bedside debriefing tool. The Unit Leadership Council of the NCCU reviewed literature on hospital debriefing tools and referenced this organizations current Resuscitation Debriefing Tool. From these sources, a Brain Code Debriefing form was constructed.

A clinical tool was developed with the expectation of standardizing the brain code process in this NCCU. The Brain Code Debriefing Form will be piloted to determine unit and system wide value. Pre-and postimplementation data will be collected to discover areas of improvement for optimized patient care.

Through the development of this debriefing tool, it was ascertained that a Clinical Practice Guideline for impending cerebral herniation would be beneficial to further guide and direct evidence-based care. Thus, a preliminary algorithm for identification and emergency treatment is in process.

The Americas Medical Center is a 212-bed tertiary hospital complex, located in the city of Rio de Janeiro. The center was elected by the International and the Brazilian Olympic Committees as the referral hospital for the Olympic Family (OF), comprised of athletes and their crews, support and technical personnel, credentialed media and credentialed governmental representatives from the participating countries. The Neurology and Neurocritical care teams were selected to head a comprehensive program of acute emergency neurology, including a 10-bed Neurocritical care unit (NICU), and 24-7 emergency neurology service. We hereby describe our experience during the 2016 Olympic Games in Rio de Janeiro, Brazil

Results 63 neurological assessments were conducted in patients from the OF, 22 of these involving athletes from 19 countries. The most common reason among athletes were traumatic brain injuries (TBI), with 6 politraumas (all involving cycling), 7 mild TBI (3 of boxing, 2 of field hockey, 1 of rowing and 1 of cycling) and 2 moderate TBI (cycling and water polo). Three patients were admitted to the NICU: 2 ischemic strokes and 3 politraumas with TBI. Motor vehicle accidents with associated TBI involving the OF were surprisingly frequent, with 10 assessments, none requiring admissions. Finally, 39 CT scans of head, 22 CT scans of the cervical spine and 14 MRI scans (3 brain and 11 spine MRI) were performed to assess the patients. Of note, cases of seizures, functional deficits, multiple sclerosis flare and psychiatric complaints were observed affecting the OF.

Not only that multiple sports-related injuries were observed, cases of diverse acute neurological issues were reported involving members of the OF. Olympic Games are complex events mobilizing thousands of people, and a comprehensive and detailed plan for neurological emergencies is of extreme importance

The term "handoff" has been defined as the "transfer and acceptance of responsibility for patient care that is achieved through effective communication, passing patient-specific information from one caregiver or team of caregivers to another to ensure the continuity and safety of the patient's care" (Patterson and Wears, 2010) . The Joint Commission reported that two-thirds of sentinel events occur at the time of patient handoff, which led to a National Patient Safety Goal, requiring standardized process for handoffs (The Joint Commission on Accreditation of Healthcare Organizations, 2006) . To support this NPSG, a NCCU specific handoff tool and timeout process were created to support the transition from OR to NCCU.

NCCU postoperative handoffs were identified as an area to enhance staff satisfaction and patient safety. Baseline data to evaluate the frequency of neurosurgery report was performed in May 2017. Using a Qualtrics survey in June 2017, staff satisfaction with current NS OR report was obtained from NCCU RNs, NPs, and fellows evaluating whether they felt they received: accurate medical history, accurate information about performed procedure, sufficient handoff for patient care, specific patient goals, recent pharmacological intervention, anticipated concerns regarding diagnosis/procedure, estimated blood loss, blood/fluid intake, airway concerns, complications and overall satisfaction with handoff. A taskforce of RNs, NPs, neurointensivists, and neurosurgeons was established, ending with the creation of a handoff tool and timeout process. The new tool and process were initiated and two months later, a repeat survey was sent to evaluate staff satisfaction and perceived effectiveness of the new process and handoff tool.

Currently being tabulated at time of submission.

Using standardized, open communication techniques including handoff tools and a timeout throughout the perioperative period is crucial to positive outcomes and can improve perioperative care in the NCCU patient and increase satisfaction and collaboration of all team member during OR handoff.

In the age of the Healthcare Reform and rising costs, it is important for strategic service lines to explore cost saving and care efficiency strategies. Beginning in September 2016, physician and administrative leadership within the Duke Neurosciences intensive care unit (NeuroICU) began investigating per patient cost to explore opportunities to decrease direct cost to the NeuroICU, cost to the patient, and reduce redundancy of care.

With assistance from Health System Finance, the team assessed the following data points within each cost group and compared these values to that of our peers within the US News and World Report Top Honor Roll: · Number of Units · Direct Cost per Unit · Total Direct Cost Our performance according to our peers in the following cost areas was: 1.Pharmacy-ranked 8th out of 15 2.Laboratories-ranked 12th out of 15 3.Radiology-ranked 14th out of 15 4.Cardiovascular-ranked 14th out of 15.

Based on these performance metrics, Neuroscience administrative and medical leadership developed a project grid of prospective initiatives and identified the following for each cost area: ·Stakeholder-led teams inclusive of providers, nursing, and administration ·Duration or impact of each initiative: short, medium, or long ·Activity phases based on duration The stakeholder-led groups would propose and validate projects based on scope and duration. At each group's meeting, members reviewed charge level financial data by activity code for the group's respective cost area to develop applicable initiatives.

Multiple initiatives are currently underway including those within the cost areas of Pharmacy, Laboratories, and Radiology. Included among these initiatives is a change in routine resistant organism screening and cervical spine clearance. Other initiatives will be target intravenous anti-hypertensive treatment and laboratory frequency. The total cost savings from these initiatives can only be estimated at this point but will likely be in excess of $50,000 for the calendar year.

It is uncertain whether dedicated neurocritical care units are associated with improved outcomes for critically ill neurologically injured patients in the era of collaborative protocol-driven care. We examined the association between dedicated neurocritical care units and mortality, and the effects of standardized management protocols for severe traumatic brain injury.

We surveyed trauma medical directors from centers participating in the American College of Surgeons Trauma Quality Improvement Program (TQIP) to obtain information about ICU structure and processes of care. Survey data were then linked to the TQIP registry, and random-intercept hierarchical multivariable modeling was used to evaluate the association between dedicated neurocritical care (NCC) units, the presence of standardized management protocols and mortality. We performed three sensitivity analyses reclassifying NCC units by restricting to closed units, under UCNS director leadership, and exclusion of neurotrauma units.

Data was analyzed from 9,773 adult patients with isolated severe traumatic brain injury admitted to 134 TQIP centers between 2011 to 2013. Fifty ICUs were dedicated neurocritical care units, whereas 84 were general ICUs. Rates of standardized management protocols were similar comparing dedicated neurocritical care units and general ICUs. Care in a dedicated neurocritical care unit was not associated with improved risk-adjusted in-hospital survival (OR 0.97; (95% CI 0.80-1.19; P= 0.79). The results from the model were robust in our sensitivity analyses. The presence of a standardized management protocol for these patients was associated with lower risk-adjusted in-hospital mortality (OR 0.77; 95% CI 0.63-0.93; P=0.009).

Compared to dedicated NCC models, standardized management protocols for severe traumatic brain injured patients are low-cost process-targeted intervention strategies that may improve clinical outcomes. Understanding the differences in processes of care within the context of ICU structure is necessary to better understand mortality differences observed between centers, and may help in the design of future trials for severe TBI patients.

Complex multidisciplinary care of patients in the neurocritical care unit requires reliable and effective communication to minimize medical errors. We implemented a structured rounding process that incorporates AHRQ-endorsed Team Strategies and Tools to Enhance Performance and Patient Safety (Team STEPPS) to improve interprofessional collaboration between team members.

We convened a project team of physicians, advanced practice providers (APPs), nurses, respiratory therapists, and pharmacists in a 16-bed NICU. We defined structured rounding processes and implemented Team STEPPS strategies to promote closed-loop communication between team members during daily rounds. The Assessment of Interprofessional Team Collaboration Scale (AITCS-II) was administered to team members at baseline and 16 months post-intervention. Impact on overall team collaboration and subscale domains of team partnership, cooperation and coordination was assessed. The possible range of the overall collaboration score is 23 to 115; higher scores indicate better collaboration.

The survey was completed by 61 (85%) staff at baseline, and 54 (77%) staff post-intervention. Overall team collaboration scores improved significantly pre and post-intervention (78.0 ± 18 vs 89.7 ± 15, p < .001), as did subdomain scores of team partnership (27.9 ±6.9 vs 31.9 ± 5.2, p < .001), collaboration (28.1 ± 6.3 vs 32.1 ± 5.7), and coordination (22.1 ±6.6 vs 25.7 ± 5.7., p < .001). Perceived shared understanding of patient daily goals between nurses and providers (physicians/APPs) increased from 58% to 91% (Chi-square 15.7; p < .001). 68% of staff reported that the intervention shortened or did not affect the duration of rounds. Of those who reported longer duration of rounds, 100% responded that the intervention was worthwhile.

Interprofessional team collaboration can be enhanced by structured rounding and communication workflows. By promoting closed-loop communication during daily rounds, shared understanding of patient daily goals between team members is increased, and may optimize quality and safety of patient care.

Advanced practice providers (APPs) are increasingly utilized to provide clinical care within neurocritical care units (NSICU) . Despite the complex issues in this patient population, the specific educational and orientation needs of these providers have not been established.

To meet the demands for rapidly and effectively training APPs to provide advanced neurocritical care (NCC), a structured educational curriculum was developed and integrated within the standard orientation and on-boarding process for newly-hired APP within our NSICU. This curriculum was designed with measurable learning goals, objective assessments of goal achievement, and opportunities for additional education and remediation at multiple steps within the program.

The curriculum has three phases with distinct goals and assessments. Phase I covers basic triage and resuscitation issues for the acutely-decompensating patient. Phase II covers general critical care principles in significantly greater depth. Phase III provides detailed experience and exposure to specific NCC issues. Each phase incorporates relevant reading assignments with a tailored study guide, as well as a multiple-choice question post-test to demonstrate knowledge acquisition. Phases II and III also include an oral exam incorporating hypothetical patient scenarios to allow the APP to demonstrate comprehension and application of the goals for each phase. Each phase lasts approximately 4 to 8 weeks with the expectation that the entire orientation curriculum will be completed within six months of employment. In addition to the educational curriculum, phases I and II include working alongside a more senior APP preceptor and providing bedside care for a progressively increasing number of patients. APPs not meeting minimum established standards on any aspect of the curriculum are provided additional remediation and instruction by the preceptor and NCC faculty based on an individualized learning plan.

A standardized educational curriculum provides a structured learning environment for new APPs in the field of neurocritical care.

Reimbursement changes from the Centers for Medicare and Medicaid Services and value based purchasing systems have made quality improvement linked to clinical outcomes more crucial than ever. In one neuroscience ICU, providers and nurses collaborate to address key infection parameters that impact patient outcomes.

Quality metric data in one neuroscience ICU was collected over a period of 3 fiscal years. Outcome measures, consisting of glycemic and temperature control, and ventilator weaning strategies, were obtained after certain parameters were enforced over two years and then compared to the initial year.

The urinary catheter utilization has decreased by over 10%, with catheter associated urinary tract infections decreased by 80% in 3 years (p-value <0.0001). Central line utilization decreased by 5%, with a 60% decrease in central line associated blood stream infections in 3 years (p-value 0.45). New ventilator weaning strategies were put into place utilizing adaptive support ventilation mode, which decreased total ventilator days by 1000 days/year . Successful weaning and extubations resulted in no recorded ventilator-associated pneumonia in the last 3 years. This neuroscience ICU maintains glucose below 180mg/dl more than 85% of the time. Regarding temperature control data, a normothermia protocol was implemented that utilizes aggressive temperature control coupled with bromocriptine administration. As a result, 95% of patients had a temperature less than 38°C. All of the quality initiatives that have been implemented have improved the observed/expected mortality ratio by 4.4%.

This study shows that by optimizing infection control, temperature management, glycemic control and ventilation strategies, there is an overall positive impact on the patient's morbidity and mortality. As evidenced by these results, this institution is now a top performer when compared in a national clinical database. This presentation will share the pragmatic strategies to create a culture of quality improvement in any neurocritical care unit or patient care organization.

Health care records are not accessible universally at point of care delivery. In developing countries like Thailand a large proportion of health care records are still paper based. Patients may not able to convey relevant information about their own medical problems and medications during patient-physician encounters or in the event of emergency. Our purpose was to create a simple platform for recording relevant basic healthcare information through a system that can be securely accessed even in countries like Thailand. Our vision is to improve healthcare communications and leverage social media in Thailand and other developing countries, particularly for patients with lower levels of education or socioeconomic status.

We created a cloud-based personal healthcare information platform 'MEiD' that uses a QR code scanned from wristbands and other products like stickers to access patient information. Conventional methods require a treating team to request medical records from a patients' prior hospital visits including visits at different medical facilities. Time lost during this process can potentially cause delay in treatment decisions. We also aim to improve health literacy in Thailand. Application name 'MEiDTH' is available in both apple store and google play.

We launched MEiD in Thailand in April of 2017. We have more than 1,000 active users and have sold more than 3000 wristbands. The MEiD Thailand Facebook page has received 20,367 likes. There are at least two patients that have already benefited from this product: one of these patients received intravenous tissue plasminogen and had a good outcome. Timely access to his past medical history and medications via MEiD was a key in this case.

Our cloud based personal healthcare information platform using QR codes from wristbands and stickers can help increase health literacy, decrease times to appropriate treatment, improve patient safety and decrease healthcare costs.

Clinical pharmacists have become an integral part of multidisciplinary medical teams. Expanding the role of pharmacists in the neurocritical care units has the potential to positively impact the quality of patient care and provide costs savings. This study examines these potential benefits at one neurocritical care unit.

We reviewed patient medication profiles and had formal rounds with a pharmacist four times per week.

For the purposes of this study, the focus was on minimization of a select number of high expense drugs. Nine months of baseline data was compared to three months of post intervention data. Interventions were performed at the time of rounding, which involved timely conversion to enteral formulas, changes to alternative medications or discontinuation of medications. We then performed a cost-benefit analysis to assess the net amount of money saved by reducing inappropriate pharmacy drug use following the interventions.

Average cost of nicardipine was $34,122 pre-intervention, compared to $23, 871 post-intervention (pvalue 0.0229). The cost of IV levetiracetam usage on average was $4,719 pre-intervention and $3,612 post-intervention (p-value 0.102), while the cost of IV dexmedetomidine was $2355 pre-intervention compared to $1800 post-intervention (p-value 0.5226). Average expense per month was reduced by approximately $11,900 per month compared to the average expense per month from the previous 9 months (p-value 0.0128). Appropriate use of stress ulcer prophylaxis was also positively impacted; patient days/month on famotidine was reduced by approximately 30% from baseline, 222 patient days (pre-intervention) vs 150 days post-intervention.

Pharmacist interventions within a neurocritical care unit are known to be beneficial clinically for patients, however this study also shows that their interventions offer substantial cost benefits and should justify creating collaborations between pharmacists and neurointensivists.

Multi-disciplinary rounds have been shown to improve patient outcomes. The objective of this study is to observe the effect on patient care, team dynamic, and nursing satisfaction before and after the implementation of a nursing-led rounding model in the Neurological ICU.

Prior to the implementation of the nursing-led rounds quality initiative, nurses in the neurointensive care unit (NICU) were asked to answer a brief survey on basic demographics and perceptions of team dynamics and satisfaction in the NICU. A multidisciplinary systems-based rounding sheet inclusive of the ABCDEF bundle and previous NICU checklist was created and revised with extensive bedside and senior nursing educator input. While rounding, nurses presented and clinicians were to in real-time come up with an assessment and plan and relay these to the nurse and other team members. Any questions, educational pearls or concerns by the clinician team or the bedside nurse were encouraged during these rounds. Nurses completed a 6 month post-implementation survey.

42 of the full-time NICU nurses (71%) responded to both the pre-implementation and postimplementation surveys. A bimodal distribution of nursing experience was noted with 41% new nurses (<1 year) and 31% experienced nurses (5 years+). More than half of the nurses (68%) reported doing both night and day shifts as opposed to being exclusive to only day or night. There was an increase in the nursing perceptions of participation during rounds as well as education during rounds. Nurses felt significantly more involved with patient decision making and felt that they were able to give input into the patients care.

The implementation of a nursing-led rounding structure may be beneficial to communication, education and overall patient care. As the project continues, we hope to further examine common ICU objective measures as well as other subjective measures such as patient satisfaction scores and communication perceptions.

With increased elective and non-elective volume, directing the flow of admissions has become essential to the efficient operation of inpatient strategic service lines. This is especially true in the Neurosciences where widespread acute ischemic stroke intervention has placed an especially high demand on Comprehensive Stroke Centers. As a result, an important collaboration was formed at Duke between the Health System, Transfer Center and Neurosciences to create an algorithm-driven multi-hospital triage and pre-hospital care system called PHAST (Pre-Hospital Acute Services Team). In this abstract, we present the formation and current state of this service.

This effort was formally begun in the Spring of 2015 with an initial focus on centralizing the admission process into the Duke Neurosciences Intensive Care Unit (NeuroICU) by an ICU physician. After some initial success, it was clear that the service line would benefit from a more formalized process. As a result, a successful multidisciplinary collaboration with a core group of physicians and administrators was formed to develop algorithms and to overcome multiple administrative and legal hurdles.

Over a period of 24 months, multiple algorithms were developed to systematize Neuroscience admissions including Acute Ischemic Stroke and Vascular and Non-Vascular Neuroscience emergencies.

In an effort to decrease door-to-intervention times as well as effectively mitigate the impact of limited bed-space availability, this system now serves 3 hospitals including 2 with acute neurointerventional services and the 3rd with a burgeoning Neurohospitalist program and incorporated rehabilitation services. In addition to systematizing the transfer and admission process, quality assurance, improvement, and educational processes are in a place.

The current state of PHAST is that of a young but maturing and now essential service for Duke Neurosciences.

Extubation involves removal of an endotracheal tube (ETT) and is a common intensive care unit (ICU) procedure. Extubation failure occurs in 8-20% of ICU patients and can be difficult to predict accurately. We hypothesized that a multivariate Re-Intubation Scale Calculation (RISC) model could predict extubation failure better than a single variable like Rapid Shallow Breathing Index (RSBI).

After IRB approval, we conducted a retrospective review of data on mechanically ventilated ICU patients above 18 years of age who were not receiving mechanical ventilation through a tracheostomy tube from January 1, 2006, through December 31, 2015 at Mayo Clinic Rochester. Various data points were gathered on these patients via electronic medical records search, and reintubations within 72 hours of extubation were identified. Univariate and multivariate logistic regression models were used to predict reintubation after extubation and construct a RISC estimate.

We included a total of 6161 patients which were randomly divided into a derivation set (N=3080) and validation set (N=3081). In the derivation set, patients had a mean age of 62±17 years, and 59% were men. Three hundred and ninety three extubation failures occurred within 72 hours. Predictors of extubation failure included underweight status, GCS score>=10, mean airway pressure at 1 minute=1500mL and total mechanical ventilation days>=5 in the final multivariable model. RISC score was calculated using the validation set and ranged from 0 to 8. Logistic model result shows that, as RISC increased by 1, the odds of having extubation failure was 1.6 fold higher (C-index=0.72). ROC analysis shows that the best cut off for RISC was >=4 vs. <4, which demonstrated a sensitivity of 0.80, specificity of 0.54 and AUC=0.67.

The current RISC model warrants further exploration in a prospective study to help critical care providers to decide when extubation can be done more safely.

This report presents results of the 2nd nationwide survey concerning neurocritical care units (NCUs) in China.

This is an observational cross-sectional survey and close-ended self-reported questions were used. The questionnaire was sent to 31 different provinces (autonomous regions and municipalities) across China from October 1st, 2015 to January 1st, 2016. Basic information, equipment and device information, and staffing and organization information were investigated.

In total, 101 questionnaires from 101 NCUs at 92 hospitals in 28 regions were received. Most of the hospitals with NCUs were large-scale (average hospital beds: 2150), teaching (84.8%), and tertiary hospitals (97.8%). The average number of NCU beds was 14, occupying 11.2% of the total number of beds in their department. Most of the equipment and devices (37/50) were available in over 80% of the 101 NCUs. However, some devices were centralized by hospital and operated with assistance from other departments. A total of 1250 full-time doctors and 1978 full-time nurses were employed at the NCUs. A few of the NCUs achieved a doctor-to-bed ratio of 0.5:1 (40.6%) and a nurse-to-bed ratio of 1:1 (37.6%). And respiratory therapists, clinical dieticians, clinical pharmacists, and physiotherapists were present in 5.9%, 32.7%, 36.6% and 49.5% of the 101 NCUs.

The number of NCUs increased, the availability of NCU equipment became more sufficient, and the staffing of NCUs improved. However, we should pay attention to the management of specialized NCU equipment, the shortage of NCU staff, and the need of NCU training.

Automated devices collecting quantitative measurements of pupil size and reactivity are increasingly used for critically ill patients with neurologic disease. However, there is limited data on the effect of ambient light conditions on pupil metrics. To address this issue, we we tested the range of pupil reactivity in healthy volunteers in both light and dark conditions.

We measured quantitative pupil size and reactivity in seven healthy volunteers with the Neuroptics-200 pupillometer in both bright and dark ambient lighting conditions. Bright conditions were created by overhead LED lighting in a room with ample natural light. Dark conditions consisted of a windowless room with no overhead light source. The primary outcome was the Neurologic Pupil Index (NPi), a composite metric ranging from 0-5 in which >3 is considered normal. Secondary outcomes included resting and constricted pupil size, change in pupil size, constriction velocity, dilation velocity and latency. Results were analyzed with multi-level linear regression to account for both inter and intra-subject variability.

Seven subjects underwent ten pupil-readings in bright and dark conditions, yielding 140 total measurements. Mean resting pupil sizes were 3.56 v. [13.8-16.4 ], p<0.001). All additional secondary outcomes except latency were also significantly different between conditions.

We found that ambient light levels impact pupil parameters in healthy subjects. However, changes in NPi are small and more consistent in varying lighting conditions than other metrics. Further testing of patients with poor pupil reactivity is necessary to determine if ambient light conditions could influence clinical assessment in the critically ill. Practitioners should standardize lighting conditions to maximize the reliability of their measurements.

Neural stem cells (NSCs) are known to have anti-inflammatory effect in strokes in previous studies. However, the mechanism of anti-inflammatory effect in direct co-culture with NSCs in hemorrhagic stroke remains unclear. The aim of this study was to investigate whether direct co-culture with NSCs modulates hemolysate-induced inflammation in Raw 264.7 cells.

We stimulated Raw 264.7 cells with hemolysate to induce hemorrhagic inflammation in vitro. Hemolysate-activated Raw 264.7 cells were co-cultured with HB1.F3 directly for 4 hours. Following direct co-culture, the production of cycloxygenase-2 (COX-2), Interleukin-signal regulated kinase (ERK) were assessed by western blotting, and tumor necrosis factor (TNFevaluated by enzyme-linked immunosorbent assay (ELISA).

Hemolysate generates an activation of inflammatory response in Raw 264.7 cells. Direct co-culture with HB1.F3 significantly suppressed the phosphorylation of ERK 1/2 in hemolysate-activated Raw 264.7 cells. The expression of inflammatory mediators such as COX-2, IL-by direct co-culture with HB1. F3 cell. In addition, the expression of COX-2, IL-attenuated by ERK inhibitor (U0126).

Our results demonstrated that direct co-culture with HB1.F3 cells reduced the inflammatory responses in hemolysate-activated inflammation via suppressing ERK1/2 pathway. This suggests that NSCs treatment can suppress the inflammatory response in hemorrhagic stroke.

No pharmacological intervention improves outcomes after primary intracerebral hemorrhage (ICH). We developed a novel therapeutic approach based on known biological function of endogenous apolipoprotein E (apoE). ApoE is a key mediator of neuroinflammatory responses and modifies recovery from a variety of acute and chronic brain injuries. Unfortunately, intact apoE holoprotein does not cross the blood brain barrier (BBB) and cannot be administered as a neurotherapeutic. We created apoEmimetic peptides that cross the BBB and down-regulate neuroinflammatory responses in vitro and in vivo. CN-105, our lead candidate, is a 5-amino acid apoE-mimetic peptide derived from apoE's receptorregion. CN-105 retains anti-inflammatory and neuroprotective effects of intact apoE, was well-tolerated in preclinical studies, readily crosses the BBB, and demonstrates excellent pharmacokinetic, safety, and tolerability profiles in Phase 1 studies.

This is a multicenter, open-label phase 2a trial of CN-105 in patients with acute primary supratentorial ICH. A total of 60 participants between the ages 30 and 80 years across 4 study centers, with a confirmed radiographic diagnosis of spontaneous, primary supratentorial ICH. Patients will be evaluated for eligibility within 12 hours of symptom onset. Eligible participants will receive CN-105 intravenously over 30--minute infusion every 6 hours up to 3 day maximum. Participants will be monitored daily throughout the Treatment phase and receive standard-of-care treatment for the duration of the study.

Primary: To assess safety of CN-105 administration in primary ICH. Secondary: To evaluate effects of CN-105 administration on 30--day mortality and functional outcomes. Exploratory: To investigate feasibility of radiographic surrogates of clinical outcomes using perihematomal edema measurements on serial brain CT and MRI, and investigate feasibility of serial biochemical markers of neuroinflammation as surrogate measure of perihematomal edema and clinical outcome.

CN-105 represents a first-in-class agent now entering Phase 2 clinical trials in patients with acute ICH.

Novel oral anticoagulant (NOAC) associated intracranial hemorrhage is a life-threatening condition for which activated prothrombin complex concentrate factor eight inhibitor bypassing activity (FEIBA) may be used for reversal. Few studies report its use in spontaneous or traumatic intracranial hemorrhage. Our institutional protocol is reversal with FEIBA 25 units/kg and escalating doses as needed. The safety and efficacy of this protocol was assessed.

We performed a retrospective review of adult patients presenting to a Level 1 trauma center between 2014-2016 with spontaneous or traumatic intracranial hemorrhage while on a NOAC . We evaluated the medication they presented on, indication for anticoagulation, location and size of the hemorrhage, presentation GCS, dosage of FEIBA recieved, change in size of hemorrhage on serial imaging as well as time between serial images, complications from reversal, and need for blood product transfusion.

We identified 19 patients with an acute intracranial hemorrhage while on NOACs. Patients underwent a baseline head CT documenting acute intracranial blood, were reversed with FEIBA (25 u/kg), and underwent repeat imaging 6 hours later per protocol. Ten (59%, 10/17) patients had no increase in hematoma volume on repeat imaging. Two underwent neurosurgical procedures (aneurysm coiling, sub-occipital craniectomy) without intra-operative bleeding complications. Five (29% 5/17) patients had clinically insignificant increase in size of hemorrhage. Of those, one underwent a subsequent neurosurgical procedure, which was already anticipated. Two (12%, 2/17) patients had clinically significant hematoma enlargement. Of those, one underwent urgent craniectomy (indicated based on initial presentation) and one required a ventriculostomy for hydrocephalus. Two patients had no repeat imaging.

Adjusted dose FEIBA (25 units/kg) may be an effective alternative to standard dose (50 unit/kg) for reversal of NOACs in acute intracranial hemorrhage. Our experience showed clinically significant hematoma expansion in 12% of patients and no increase in unplanned neurosurgical procedures after reversal with FEIBA.

Here we sought to determine if there is an association between recanalization success and rate of hemorrhagic transformation amongst patients who have undergone intra-arterial thrombectomy for ischemic stroke secondary to anterior circulation large vessel occlusion (LVO), many treated at extended time from last seen well (LSW) after MRI assessment.

Stroke patients with anterior circulation LVO treated with thrombectomy between April, 2011 to June, 2017 were studied. Group-wise comparisons were made between patients with post thrombectomy hemorrhage (as confirmed by a single, blinded neuro-radiologist reviewer) and patients without hemorrhage. Failed or incomplete recanalization was defined as mTICI < 2B. Symptomatic intracranial hemorrhage (SICH) was defined as validated hemorrhagic conversion or parenchymal hematoma plus 4 point decrease in NIHSSS. Pertinent baseline characteristics were recorded and analyzed.

SICH was more prevalent amongst patients with TICI<2B recanalization (OR 2.76 [95CI 1.33 -5.71]). Interestingly there was a low rate of SICH amongst patients with TICI=0 recanalization (2/12 [16.7%]). Although many patients were treated at advanced time LSW no excess rate of SICH was observed. Baseline characteristics including age, presentation NIHSS, and presentation ASPECTS were similar among the two groups.

Rates of SICH are low after successful MRI seleted thrombectomy regardless ot time LSW. Patients with poor recanalization show increased rates of SICH in keeping with past literature. Our data suggest that thrombectomy after MRI selection may be safe and effective for patients at extended time LSW of tor patients with unknown LSW.

CTA spot sign is associated with hematoma growth, a common complication of intracerebral hemorrhage (ICH) that portends worse outcomes. Magnesium and calcium are cofactors in the clotting cascade and for platelet aggregation. We tested the hypothesis that magnesium and calcium levels are associated with the presence of the CTA spot sign.

Patients with spontaneous ICH presenting to Northwestern Memorial Hospital were identified from a prospective observational registry. Inclusion criteria included CTA obtained within 24 hours of symptoms onset and admission magnesium and calcium levels. CTA spot sign (active contrast extravasation on CT angiography) was identified by a board-certified neurointensivist or neuroradiologist. Variables suggesting association with spot sign at p<0.1 were assessed for inclusion in a logistic regression model, and a parsimonious predictive model for CT spot sign was developed using backward stepwise variable selection.

146 patients (age 63 ± 14.5 years, 47% male, median ICH score 1 [IQR 1-3]) were included. Seventeen (11.6%) patients with CTA spot sign were identified. Admission magnesium was 1.96 +/-0.27 and calcium was 9.27 +/-0.56. Lower magnesium (OR 0.074, 95% CI 0.007-0.746, p 0.027), lower calcium (OR 0.390, 95% CI 0.156-0.973, p 0.044), and higher ICH Score (OR 1.98, 95% CI 1.28-3.07, p 0.002) were independently associated with CT spot sign.

Magnesium and calcium level on admission are associated with the presence of a CTA spot sign in patients with ICH. Magnesium and calcium supplementation may be attractive therapeutic targets for preventing harm from hematoma growth.

Cerebellar intraparenchymal hemorrhage (IPH) is a rare and likely underreported complication of subdural hematoma (SDH) evacuation.

We present two cases of post-operative IPH and review the literature.

Case 1. An 83-year-old man underwent craniotomy for evacuation of a chronic right frontoparietal SDH. Post-op CT showed pneumocephalus. The patient was extubated and clinically improved. Three days post-operatively, he became lethargic and a CT brain revealed a 4cc right cerebellar IPH. He was unable to safely swallow, declined a feeding tube and died under hospice care nine days later. Case 2. A 72year-old man underwent craniotomy for evacuation for a left convexity SDH. Routine post-op CT revealed an incidental left cerebellar IPH. He returned to baseline one month later. Only four such cases have been reported in the literature (1-4). Two cases led to death within one week and two recovered, one with significant deficits. Five more occurred following burr hole drainage of SDH and two others following drainage of subdural hygromas (2, 5-10). The incidence of cerebellar IPH following supratentorial craniotomy has been reported in up to 0.29% of cases with significant morbidity or mortality (3). It occurs irrespective of age, pre-existing coagulopathy or arteriovenous malformations. Size of insult and amount of CSF loss do not correlate to IPH, despite the fact that cerebral blood flow imaging shows over-drainage of cerebrospinal fluid (CSF), causes intracranial hypotension and subsequent damage to dural veins (3,11). IPH also occurs independently of operating room position, even though having the head turned is thought to compress venous drainage in the neck and cause congestion (3).

Cerebellar vasculature may be more sensitive to changes in intracranial pressure, though why this does not lead to complications more routinely is not clear. Cerebellar IPH should be considered in cases of neurological decline after SDH evacuation.

Intracerebral hemorrhage (ICH) location predicts outcome, but most studies have examined differences between deep, lobar, and infratentorial locations. This study aims to characterize specific deep ICH locations in a diverse cohort.

The Ethnic/Racial Variations of Intracerebral Hemorrhage (ERICH) study is a multi-center, prospective, U.S.-based study. 1345 subjects with supratentorial deep ICH, known ICH volume, and three-month follow-up data were included. Logistic regression was used to evaluate the association between location and poor outcome (mRS > 3). Receiver operating curve (ROC) analysis was performed to identify ICH volumes specific for poor outcome by location.

671 thalamic, 581 putaminal, and 83 caudate ICHs were included. Median ICH volume was largest in putamen (15 mL), followed by thalamus (9 mL) and caudate (4 mL, p<.001). Intraventricular hemorrhage (IVH) was most prevalent in caudate (94%), followed by thalamus (65%) and putamen (23%, p < 0.001). Subjects with thalamic ICH were older (62 vs 57 vs 58 years, p < 0.001) and more likely hypertensive (91% vs 85% vs 82%, p= 0.002) than those with putaminal and caudate ICH, respectively. Compared to thalamic, putaminal ICH had more ICH expansion (23% vs 15%, p < 0.001) and surgery (20% vs 14% p = 0.004) but fewer external ventricular drains (15% vs 27%, p < 0.001). Thalamic location predicted poor outcome (OR 2.25, 95% CI 1.35-3.73) at 90 days after adjustment for age, sex, premorbid disability, ICH volume, ICH expansion, IVH, and admission GCS. ROC analysis identified 10 mL for thalamic and 29 mL for putaminal ICH without IVH as having 95% specificity for poor outcome.

There are significant differences in characteristics and outcomes within deep ICH. Specificity estimates for the identified ICH volume thresholds require external validation. These findings may have implications for prognostication and clinical trial design.

Racial differences in outcome after intracerebral hemorrhage (ICH) among Asians, Native Hawaiians and other Pacific Islanders (NHOPI) have been inadequately studied since these racial groups have been historically aggregated into a single racial category.

A multiracial prospective cohort study of ICH patients was conducted from 2011 to 2016 at a tertiary center in Honolulu, HI to assess racial disparities in come after ICH. Favorable outcome was defined as 3month modified Rankin Scale (mRS) score £ 2. Patients with no available 3-month functional outcome, race other than Asians and NHOPI, and baseline mRS >0 were excluded. Multivariable analyses using logistic regression were performed to assess the impact of race on favorable outcome after adjusting for the ICH Score, early do-not-resuscitate (DNR) order and dementia/cognitive impairment.

A total of 220 patients (161 Asians, 59 NHOPI) were studied. Overall, 65 (29.5%) achieved favorable outcome at 3 months. NHOPI were younger than Asians (51.8±15.3 vs. 63.9±16.7 years respectively, p<0.0001), and had higher prevalence of diabetes (39.0% vs. 21.1% respectively, p=0.007), obesity (58.9% vs. 23.1 respectively, p<0.0001), and lower prevalence of early DNR order (3.4% vs. 24.2% respectively, p=0.0004) and advance directive presence (6.8% vs. 29.2% respectively, p=0.0005). NHOPI race was a predictor of favorable outcome in the unadjusted model (OR 2.47, 95% CI: 1.32, 4.62) and after adjusting for the ICH Score (OR 2.30, 95% CI: 1.06, 4.97) but not in the final model (OR 2.04, 95% CI: 0.94, 4.42) . In the final model, the ICH Score remained as the only independent negative predictor of outcome (OR 0.26, 95% CI: 0.17, 0.41 per point).

NHOPI are more likely to achieve favorable functional outcome after ICH compared to Asians even after controlling for ICH severity. However, this association was attenuated after adjusting for DNR status and baseline cognitive factors.

Intracerebral hemorrhage (ICH) patients often require continuous antihypertensive infusions. We sought to identify clinical and care process predictors of anti-hypertensive infusion duration, and tested whether infusion duration independently predicts intensive care unit length of stay (ICU LOS) after adjusting for validated measures of ICH illness severity.

We identified spontaneous ICH patients admitted 12/2013-9/2015 to a tertiary center, excluding those transitioned to comfort care within 24 hours. We abstracted demographic and clinical variables from the medical record. We calculated the total duration each patient received continuous infusion of an antihypertensive medication. We categorized Glasgow Coma Scale score as 14-15; 8-13; or < 8. Two reviewers independently classified ICH location and etiology. We determined univariate associations of clinical variables to anti-hypertensive infusion and performed regression analysis to determine the effect of continuous infusion on ICU LOS.

We identified 495 spontaneous ICH patients and excluded 50 for early comfort care. In the remaining 445, mean age was 70 [69-71] years, 45% were female, median ICH score was 1 [1-2], and 44% had lobar hemorrhages. Continuous infusion included nicardipine, clevidipine, labetalol and diltiazem. A total of 127 (28%) patients received anti-hypertensive infusions, mean 13 hours. Mean time to enteral antihypertensive administration medication was 32.5 hours, and mean ICU length of stay was 3.4 days [3.0 -3.8]. Predictors of longer antihypertensive infusion duration were male gender (p=0.003), non-lobar ICH (p=0.0002), non-caucasian race (p<0.001), younger age (p<0.0001), higher initial systolic (p=0.03) and diastolic BP (p=0.01), worse GCS category (p<0.001), and longer time to first enteral medication (p<0.0001). Anti-hypertensive infusion duration independently predicted ICU LOS (p<0.0001) after adjusting for age, race, GCS category, time to enteral antihypertensives, and ICH score.

Worse GCS category, younger age, non-lobar ICH location, and race are significant independent predictors continuous IV antihypertensive infusion duration, which is significantly associated with longer ICU stay.

Patients with sICH have a high risk of VTE. Pharmacological prophylaxis such as unfractionated heparin(UFH) has been demonstrated to reduce VTE. However, published datasets exclude patients with recent ICH out of concern for hematoma enlargement. AHA/ASA guidelines recommend UFH 1-4 days after hematoma stabilization while the ESO has no recommendations on timing of UFH. There are few data for patients who received UFH before 48 hours. Our institutional practice is to begin UFH following sICH after 24 hours of clinical and radiographic stability. We examine the impact of this practice on risk of hematoma expansion.

We performed a retrospective cohort analysis of 87 sICH patients admitted in 2012-2013 to a single US university hospital. Demographic and clinical characteristics were abstracted. ICH was measured via 3D volumetrics for an admission CT, a 24 hour follow-up, and a follow-up prior to discharge. Percent hematoma growth between 24-hour CT and discharge CT was calculated. Risk factors for expansion >5%, including early heparin use, were analyzed via oneway T-test and Chi-squared tests.

Results 87 sICH patients analyzed had a median ICH score of 2(IQR1-3) and median admission GCS of 10(IQR6-13). 39%(34/87) patients received early UFH. 18%(16/87) suffered hematoma expansion >5%. Overall mean hematoma growth was higher with early UFH (UFH24hr -15%,p=0.0007). In multivariate analysis, ICH score, GCS and initial hematoma size did not predict >5% hematoma expansion.

Early VTE prophylaxis at 24 hours from sICH had a statistically significant increase in hematoma size, but this increase is clinically insignificant. In this cohort, early UFH did not increase risk of significant hematoma expansion. Further prospective trials are warranted, given the high risk of VTE in this population.

Antiplatelet therapy at the time of spontaneous intracerebral hemorrhage (sICH) may increase the risk of hemorrhage expansion and mortality. Current guidelines recommend consideration of a single dose of desmopressin in sICH associated with cyclooxygenase-1 inhibitors or adenosine diphosphate receptor inhibitors. This study sought to compare outcomes in patients that received desmopressin for antiplatelet reversal in the setting of sICH to similar patients that did not receive desmopressin.

This retrospective chart review of the electronic medical record included adult patients admitted for sICH that were on antiplatelet agents at the time of diagnosis. Patients that received desmopressin were compared to similar patients that did not receive desmopressin. Exclusion criteria included traumatic brain injury, active coagulopathy and thrombocytopenia. The primary outcome was the incidence of hematoma expansion. Additional outcomes included average increase in hematoma volume, in-hospital mortality and functional outcome at hospital discharge.

Overall, 73 patients (36 received desmopressin, 37 did not receive desmopressin) were included for analysis. Incidence of hematoma expansion was not different between groups (36% with desmopressin vs 22% without desmopressin, p=0.17). Average largest increase in hematoma volume on follow-up imaging from baseline was not different (10.5±16.7 mL with desmopressin vs 10.2±26.7 mL without desmopressin, p=0.96. In-hospital mortality was significantly higher in the desmopressin group (20% vs 8% without desmopressin, p=0.016) as well as the incidence of a Modified Rankin Score of 4-6 at discharge (39% vs 28% without desmopressin, p=0.029).

Administration of desmopressin for antiplatelet reversal in sICH does not appear to reduce the incidence of hematoma expansion. Further studies assessing temporal relation of desmopressin administration and hematoma expansion are needed to confirm the results of this single-center retrospective study.

Clinical outcome after intracerebral hemorrhage (ICH) remains poor. Definitive phase-3 trials in ICH have failed to demonstrate improved outcomes with intensive systolic blood pressure (BP) lowering.We sought to determine whether other BP parameters-diastolic BP, pulse pressure (PP), and mean arterial pressure (MAP)-showed an association with clinical outcome in ICH.

We retrospectively analyzed a prospective cohort of 672 patients with spontaneous ICH and documented demographic characteristics, stroke severity, and neuroimaging parameters. Consecutive hourlyBP recordings allowed for computation of systolic BP, diastolic BP, PP, and MAP. Threshold BP values that transitioned patients from survival to death were determined from ROC curves. Using inhospital mortality as outcome, BP parameters were evaluated with multivariable logistic regression analysis.

Patients who died during hospitalization had higher mean PP compared to survivors (68.5 ±16.4mmHg vs. 65.4 ±12.4 mmHg; p=0.032). The following admission variables were associated with significantly higher in-hospital mortality (p < 0.001): poorer admission clinical condition, intraventricular hemorrhage, and increased admission normalized hematoma volume. ROC analysis showed that mean PP dichotomized at 72.17 mmHg, provided a transition point that maximized sensitivity and specific for mortality. The association of this increased dichotomized PP with higher in-hospital mortality was maintained in multivariable logistic regression analysis (OR 3.0; 95%CI 1.7-5.3; p < 0.001) adjusting for potential confounders.

Widened PP may be an independent predictor for higher mortality in ICH. This association requires further study.

A National Confidential Enquiry into Patient Outcome and Death (NCEPOD) report concerning management of aneurysmal subarachnoid haemorrhages in the UK suggested up to half of patients received suboptimal consideration for organ donation. As demand for organs continues to increase, so does the need to pursue all potential sources of donor organs. Subarachnoid haemorrhages have an estimated mortality of 50% and can potentially provide younger donor organs with less chronic pathology. This is a comprehensive picture of donation rates within a tertiary centre.

Retrospective data regarding all deceased patients on the Neuro-Intensive Care Unit during 2016 with aneurysmal subarachnoid haemorrhage as the cause of death was obtained from the NHS Blood and Transfusion team. The local audit committee provided ethical approval. Data regarding organ donation was extracted and compared to national data, then analysed using Fisher's Exact Test.

Referral rates were 100%. This is greater than the national average of 57.7% (p=0.001), yet only 30.8% of referred patients proceeded to organ donation. Consent was withheld in 52.8% of potential donors. Nationally 37.9% of donors are lost due to non-consent (p=0.235). 32.1% of consented patients were unable to donate organs, similar to national figures (p=1.00).

Referral rates within this centre are excellent; consent remains the main obstacle. Consent rates can be improved using a long contact model where specialist nurses in organ donation establish relationships with relatives prior to any discussion of donation. The ideal discussion is a pre-planned collaboration involving a senior doctor and a specialist nurse. Early brain stem testing may facilitate earlier acceptance of death by relatives whilst reducing the duration of the multi-systemic effects of the associated hyperresponsive cascade on donor organs. Neurosurgeons should be encouraged to suggest organ donation when declining referrals. Further work is needed to assess the barriers to instituting these measures and inspiring change.

Spontaneous brainstem hemorrhage has been historically associated with high mortality. However, updated data on the frequency and outcome of spontaneous brainstem hemorrhage is scarce vis-a-vis advances in neuro-critical care. The purpose of this study was to investigate the frequency and outcome of spontaneous brainstem hemorrhage.

Records of consecutive intracerebral hemorrhage (ICH) patients presenting to an urban academic medical center from January 2010 though December 2015 were reviewed. Cases with brainstem hematomas were isolated for analysis. Data on demographics and outcomes were collected and analyzed. Sub-group analysis was also done to look at outcomes based on location of hemorrhage in the brainstem.

Of 181 consecutive spontaneous ICH patients, 13 (7.18%) presented with brainstem hemorrhage; 7 (53.8%) were pontine, 2 (15.4%) mesencephalic, and 4 (30.8%) were located in both the pons and the midbrain. The average age was 52.92 years and (38.46%) were men. Median Glasgow Coma Scale on presentation was 6.5. Thirty-day mortality rate was 62.5%, with 6 in-hospital deaths and 2 deaths post discharge. Two and 3 patients were discharged home or a rehabilitation facility, respectively. In subgroup analysis, thirty-day mortality for midbrain, pons and combined pons/midbrain hemorrhage was 0%, 57% and 100%, respectively.

Spontaneous brainstem hemorrhage remains an uncommon but highly fatal clinical entity. More than one-half die within 30 days. Only a minority are discharged to rehabilitation or home. In sub-group analysis, location of brainstem hemorrhage was shown to influence outcome, with 100% mortality in case of combined pons/midbrain hemorrhage, and more than 50% mortality with pontine hemorrhage. Midbrain hemorrhage was associated with good outcome with 100% survival. 

Patients with intracerebral hemorrhage (ICH) frequently present with hypertension. It is unclear whether this is due to preexisting hypertension (prHTN) causing the bleed, an effect of the bleed, or both.

We retrospectively analyzed a single-institution cohort of ICH patients presenting between 2013 and 2016. Data included home antihypertensive use; aSBP; TTE, and EKG and imaging results; and nicardipine administration. The primary objective was to assess the relationship between prHTN and aSBP, while the secondary objectives were to assess the relationship between prHTN, imaging and acute antihypertensive requirements.

112 ICH patients met inclusion criteria. In our assessment for prHTN, we found that 46% of patients were on antihypertensives, 16% had LVH on EKG, and 15% had LVH on TTE. There was a significant relationship between LVH on TTE and LVH on EKG (p<0.001), but not between home antihypertensive use and presence of LVH using either modality. aSBP was higher for all patients with markers of pHTN, but this was only significant for patients with LVH on TTE (181mmHg, IQR 153-214 vs. 152mmHg, IQR 137-169, p < 0.001) and patients with LVH on EKG (195 mm Hg, IQR 155-216 vs. 147 mm Hg, IQR 129-163, p<0.001). All patients with markers of prHTN were more likely to require nicardipine, but this was only significant for patients with LVH on TTE (94% vs. 64%, p=0.016) and patients with LVH on EKG (83% vs. 52%, p=0.018). All patients with markers of prHTN were more likely to have deep bleeds (p=0.017 for patients with LVH on EKG vs. those without LVH on EKG). There was no relationship between any markers of prHTN and the presence of a spot sign.

In patients with ICH, prHTN is related to higher aSBP, deep bleed location, and increased acute antihypertensive requirements.

All spontaneous intracerebral hemorrhage (sICH) patients, including those with low severity are uniformly admitted to the intensive care unit (ICU) at our institution. Many may not benefit from this high-intensity observation and leave the ICU within 24 hours without experiencing any complications. Identifying low-risk characteristics could aid in triaging such patients to stroke units instead.

Retrospective data collection of all sICH patients admitted to our institution from June 1, 2013-June 30, 2016 included ICH score, need for surgical interventions, medical complications, and ICU/hospital LOS. We analyzed variables predicting short (< 24 hour) ICU LOS among low severity (LS-ICH) patients (defined as those with ICH score 0-1).

163 (52%) of 313 sICH patients had ICH scores of 0-1, of which just under half (78) had ICU LOS 24 hr. They also spent significantly fewer days in hospital (4 vs 9.7, p<0.001). We could not identify a clear ICH score cutoff that was sensitive enough to predict short ICU LOS. However, requirement for antihypertensive infusion and early clinical deterioration correlated strongly with longer ICU LOS p<0.001.

There appears to be a subset of mild ICH patients (ICH score 0-1) who do not require ICU observation. A risk assessment score incorporating GCS and ICH volume may be able to delineate this low-risk population who could instead be admitted to a stroke unit, with the potential for significant cost saving and hospital efficiency.

Obesity has been linked with relative longevity in several disease conditions. This relationship has been termed the "obesity paradox." In this study we sought to evaluate the impact of obesity on short-term outcomes in patients with intracerebral hemorrhage (ICH).

Patients admitted with a diagnosis of ICH were selected from the 2003-2014 Nationwide Inpatient Sample (NIS) database, using ICD-9 codes. Patients with ICH were dichotomized based on the presence of obesity as a coexisting diagnosis based on ICD-9 codes and diagnosis related groups. The primary outcome measure was in-hospital mortality. Length of stay and total charges were also examined as resource utilization measures.

Of 

Obesity is a major health care burden as evidenced by higher resources utilization. Counterintuitively, obesity appears to be associated with lower in-hospital mortality in ICH patients. One possible physiological basis for this could be that the higher LDL levels on presentation result in a lower likelihood of hematoma expansion.

Recent short-term outcome analysis indicates association of spontaneous intraventricular hemorrhage (IVH) related hydrocephalus with incontinence and gait dysfunction. We explore the association of hydrocephalus scores, intraventricular alteplase and clinical variables with these outcomes at long term follow up in survivors from the CLEAR III trial.

CLEAR III, a randomized, multi-center, double-blinded, placebo-controlled trial was conducted to determine if pragmatically employed external ventricular drainage (EVD) plus intraventricular alteplase improved outcome, in comparison to EVD plus saline in patients with IVH causing obstructive hydrocephalus. We assessed hydrocephalus scores on survivors at diagnosis, days 30 and 365. Incontinence and dysmobility were defined using 12-month Barthel Index subscores (<10 for bladder and <15 for mobility, respectively). Outcome measures were predictors of incontinence and gait dysmobility at 1 year after ICH. 

This prospective observational study analyzed consecutive ICH-patients (n=246) treated at the neurological and neurosurgical departments of the University-hospital Erlangen, Germany over a 21month inclusion period (05/2013-01/2015). We analyzed the influence of patient characteristics, inhospital measures and functional status on treatment recommendations and on OAC initiation during 12-month follow-up. 

Clear treatment recommendations by attending stroke physicians seem necessary to ensure OAC initiation after ICH. OAC showed beneficial associations; however data here suggests the presence of an indication bias introduced by treatment recommendations and outpatient care during follow-up. Therefore, observed association with age and functional status might affect unadjusted analyses.

Although recently, Non-vitamin K Antagonist Oral Anticoagulants (NOACs) therapy in patients with non valvular atrial fibrillation have half the incidence of intracerebral hemorrhage (ICH) compared to warfarin. However, it would be still controversial subject that outcome of NOAC-associated ICH (NICH) might be worse or better than warfarin-associated ICH (WICH). In this study, we investigated clinical outcome and radiological finding of ICH between two different anticoagulation treatments.

Retrospective review of medical records was performed for 1,197 patients who admitted with ICH from 2003 to 2016 in Seoul National University Bundang Hospital. Clinical characteristics, functional outcome, location and volume of ICH, and all-cause mortality within 90 days were analyzed.

Among those patients, 47 patients with WICH and 8 patients with NICH were included. Lesion location was common in supratentorial deep area (50.0%, 44.7%), lobar area (37.5%, 31.9%) and brainstem and cerebellum (12.5%, 23.4%) in the NICH and WICH group, respectively. No significant difference found in initial NIHSS (15.5 vs 10), discharge NIHSS (16.5 vs 8), mRS (0 to 2) at discharge (14.9% vs 25.0%), mRS (0 to 3) at discharge (36.2% vs 25.0), mRS (0 to 2) at 90 days (25.5% vs 12.5) and mRS (0 to 3) at 90 days (25.5% vs 12.5) in NICH and WICH group. We did not find any difference between NICH and WICH for allcause mortality at discharge (17% vs 0%), 90 days (27.7% vs 0%), and 1year (34% vs 25%). Median baseline ICH volume was not significant difference in two groups (3676.2 vs 1542.24).

In our study, functional outcome, mortality, and baseline ICH volume were similar following NICH and WICH. Because of low statistical power due to small sample size in our study, further studies with prospective larger patient cohorts will need to be conducted.

Novel Oral Anticoagulants (NOAC) are increasingly used as an alternative to vitamin-K antagonists (VKA) such as warfarin for anticoagulation and have shown lower rates of intracranial hemorrhage in several randomized clinical trials. It has been suggested that NOAC-IPHs might be particularly dangerous, yet the literature regarding hematoma characteristics and outcomes between NOAC-IPHs and VKA-IPHs is inconclusive. Given the lack of standardized reversal strategies and lack of information on outcomes following NOAC-associated IPH, the aim of this meta-analysis was to compare 1) mortality; 2) hematoma volume, and 3) risk of hematoma expansion in patients who developed an IPH on NOACs versus VKA.

A meta-analysis of the literature through December 2016 was conducted using PubMed, EMBASE and Cochrane databases in accordance with PRISMA guidelines. Pooled risk ratios (RR) were calculated for mortality and hematoma expansion and pooled mean difference (MD) was calculated for hematoma volume (ml) using random-effect (RE) and fixed-effect (FE) models.

NOAC-IPH was not associated with increased mortality (RE and FE: RR: 1.07; 95%-CI: 0.89;1.28, I2=0.00%, p-heterogeneity=0.29; 7 studies) and hematoma expansion (RE and FE: RR: 0.97; 95%-CI: 0.77;1.21, I2=0.00%, p-heterogeneity=0.48; 4 studies) compared to VKA-IPH. The hematoma volume of NOAC-IPH was smaller than VKA-IPH (RE: MD: -8.83ml; 95%-CI: -17.00; -0.67, FE: MD: -6.48ml; 95%-CI: -9.85; -3.10; 5 studies), but with considerable heterogeneity that could not be alleviated (I2=79.1%, p-heterogeneity0.05).

NOAC-IPH was not associated with increased mortality or hematoma expansion compared to VKA-IPH and may be associated with a smaller hematoma volume.

Controversy exists regarding blood pressure (BP) reduction and perihematomal ischemia (PHI). We investigated the association of acute BP reduction and presence of qualitative and quantitative PHI in a large prospective cohort of intracerebral hemorrhage (ICH).

Consecutive patients from the prospective NIH funded DASH1 study (> 18 years, primary spontaneous ICH) were included. PHE volume was outlined on T2/FLAIR and ICH volume on GRE; these and ADC were co-registered. Tissue characteristics was defined as: CE = ADC 1200 x 10-6 mm2/sec. The association of clinical, radiographic factors and BP at baseline and 24 hours with qualitative perihematomal and/or remote ischemia (i.e. DWI bright ADC dark) and quantitative CE on ADC were determined.

164 patients (50% female) with mean age 64 ± 15, and NIHSS 8 (IQR 3, 17) were included. MRI time was 34.6 hours (IQR 21, 60). 37% had lobar ICH. ICH volume was 12 cc (IQR 5, 33). 44% had perihematomal (33%) or remote ischemia (21%). 99% of patients had areas of perihematomal ADC 1 cc) was associated with higher absolute (52±30 mm Hg, p=0.05) and relative (38% ± 16% vs 33% ± 15%, p=0.058) MAP reduction, younger age (p=0.03), h/o TIA/stroke (p=0.04) and larger ICH volumes (32 vs 7 cc) (p<0.001).

In multivariate analysis, MAP reduction was not significantly associated with CE whereas ICH volume was (p=0.00).

Perihematomal and remote ischemia is frequently seen after ICH, but the severity of PHI is small and of unclear significance. BP reduction may be associated with PHI but this was not an independent predictor.

Introduction: Patients with Left Ventricular Assist Devices (LVADs) receive anticoagulation and antiplatelet therapy to prevent pump thrombosis. Consequently, neurological events including intracranial hemorrhage (ICH) are one of the most feared causes of morbidity and mortality in these patients. There is little evidence to guide initiation of anticoagulation after such ICH events.

Methods: This is a retrospective, single academic center analysis of LVAD patients from 2014-2017. The electronic medical record was reviewed after IRB approval for the physiologic, laboratory, and radiographic data of these patients as well as survival or cause of death by 30 days or by discharge.

Results: During the analysis, 51 patients were reviewed, 7 of which (13.7%) had intracranial hemorrhage. One patient was excluded from analysis after care was transitioned to hospice, thus follow-up scans were not obtained. The remaining 6 patients were receiving both aspirin (81-325mg daily) and warfarin (2-8mg daily) with an INR of 1.5-3.3 (mean=2.8) at the time of ICH. Aspirin (81-325mg daily) was resumed within 1-2 (mean=1.1) days post ICH. Warfarin was resumed 1-20 (mean=6.6) days post ICH at 2-8mg (mean=4mg) with goal INR (1.7-2)-(2-3) depending on device. There was 1 death due to withdrawal of life support in setting of multiple comorbidities, though follow-up scan 7 days post warfarin resumption revealed no evidence of rebleed. The remaining 5 patients showed no evidence of rebleed on CT scans at 2 months post warfarin resumption and were subsequently discharged to rehab facilities or home with Modified Rankin Scores 0-4 (mean=2.8).

Conclusion: In this review of 51 LVAD patients, about 13% suffered ICH, and of those 6 survivors aspirin was safely resumed within 2 days and warfarin was safely resumed as early as 7 days post-event.

Further studies are needed in order to establish safe practice guidelines and risk factors to prevent ICH.

Intracerebral hemorrhage (ICH) remains a devastating form of stroke, and perihematomal edema worsen outcomes after ICH. Recent studies have demonstrated the safety of minimally invasive surgery (MIS) for hematoma removal, but the efficacy of MIS in the treatment of ICH is controversial. This study aimed to evaluate the effect of MIS compared with medical treatment for basal ganglia ICH.

We retrospectively analyzed the clinical outcomes of prospectively collected data from two stroke centers. The treatment strategies of the two stroke centers for basal ganglia ICH are different; one stroke center underwent MIS and the other stroke center medically treated according to the current guidelines. We hypothesized that MIS could reduce perihematomal edema and improve functional outcomes compared to medical treatment. Primary outcome of this study was a modified Rankin scale (mRS) at 3 months after ICH occurrence.

A total of 155 patients with basal ganglia ICH were treated with different treatment strategies; 86 patients underwent MIS and 69 patients received medical treatment. No statistically significant differences were found in age, sex, hematoma volume, and Glasgow Coma Scale scores between the groups. A better functional recovery (mRS < 3) at 3 months was found in the medical treatment group than the MIS group (46.4% vs 14.0%, p <0.05). No significant differences were observed between groups in terms of mortality.

Our findings suggest that the best medical treatment improves functional recovery after basal ganglia ICH compared to MIS. These results are contrary to other studies of ICH, and further randomized trials are required.

Perihematomal edema (PHE) after intracerebral hemorrhage (ICH) is thought to be predominantly vasogenic. The presence and extent of cytotoxic edema (CE) is controversial. We investigated PHE diffusivity (PHED) and factors associated with CE.

Consecutive patients from the prospective NIH funded DASH1 study (> 18 years, primary spontaneous ICH) were included. PHE volume was outlined on T2/FLAIR and ICH volume on GRE; these and ADC were co-registered. Tissue characteristics was defined as: CE = ADC 1200 x 10-6 mm2/sec. Clinical and radiographic factors associated with CE were determined. 

Cytotoxic edema is detected in the perihematomal area, early after ICH and is associated with younger age, larger ICH and prior h/o TIA/stroke. Its clinical significance needs to be studied further.

Hemorrhagic stroke carries a high mortality rate and determining prognostic factors during initial presentation can aid redirecting intensive care unit (ICU) management. We described the physiological profile and clinical outcomes of hemorrhagic stroke patients in a Colombian ICU.

We retrospectively reviewed all hemorrhagic stroke patients admitted to our ICU from 2014-2017. Clinical characteristics, outcomes, available laboratory values and hourly vital signs from the first 48 hours in the ICU were retrieved and analyzed.

Our primary stroke center admitted 395 patients, 72 (18%) were hemorrhagic. Out of these, 47 required ICU management, representing 1 % of the total 4687 ICU admissions during this time frame. Intracerebral hemorrhage (ICH) was present in 32 patients while subarachnoid hemorrhage (SAH) was seen in 15. The latter had a median Fisher score of 4. For all patients, the most common risk factors were hypertension (61.7%), dyslipidemia (29.8%) and smoking (17.0%). ICU mortality was 25.5% (53.3% with ICH and 12.5% with SAH). Mean Sequential Organ Failure Assessment (SOFA) score was significantly greater in patients who died (8.8 vs. 1.8, p<0.05) and mean Glasgow Coma Scale was significantly lower (8.1 vs. 13.2, p<0.05). Vasopressors were required in 18 patients (38.3%), mechanical ventilation in 22 (46.8%), and half of the patients requiring either support therapy died. Only 5 patients (10.6%) had fever in the first 48 hours and all died. Mean coefficient of variation for systolic, diastolic and mean blood pressure was significantly lower in patients who survived. Mortality cases were more likely to have hypokalemia and hypomagnesemia than surviving patients (50.0% vs. 25.7% and 58.33% vs. 40%, respectively).

ICU-admitted hemorrhagic stroke patients have a poor prognosis. SOFA and GCS are accurate predictors of mortality. Certain electrolyte disturbances, fever and a higher variation of blood pressure during the first 48 hours were associated with a worse outcome.

The association between worsening cerebral edema and unfavorable outcome in ICH patients has been described in RCTs. The objective of this analysis was to compare hospitalized spontaneous ICH patients with and without perihematomal edema (PHE) expansion and to evaluate relationships between hypertonic saline (HTS) use, peak serum Na, PHE expansion, and short-term outcomes.

We conducted a cross-sectional study of consecutive spontaneous ICH patients admitted to a single center from 11/2014-11/2015. Head CTs during the first week of admission, use of HTS, and PHE (using ABC/2 method) were evaluated. PHE expansion of 10% or more was considered worsening edema.

Outcomes of interest included time to peak Na, poor disposition (not home or inpatient rehabilitation), discharge mRS 4-6, and in-hospital death.

Of 180 ICH patients, 43% experienced worsening PHE. There was no difference in age, race, sex, arrival BP arrival, or vascular risk factors in patients with or without worsening PHE. However, for each mm of midline shift (MLS) present on initial head CT, odds of PHE expansion was decreased by 16% (OR 0.84, 95%CI 0.73-0.97, p=0.014). MLS on initial head CT was the best discriminator of PHE expansion (AUC 0.811 (95%CI 0.663-0.958).

Although hampered by small sample size, our data indicates that finding that ICH patients with degree of MLS on initial head CT is the best radiographic predictor of had lower odds of PHE expansion. Those without MLS at presentation may be at risk of PHE expansion, and counterintuitively may be those most in need of aggressive medical management. may suggest a role for intensive osmotherapy in patients with favorable imaging at presentation.

Intracerebral hemorrhage (ICH) is a devastating stroke with high mortality rates. Previous studies have shown a potential role of immune cells as a prognostication method. A high neutrophil to lymphocyte ratio was associated with poor outcomes after ICH. We sought to determine whether absolute lymphocyte count(ALC) at admission was predictive of outcomes in patients with ICH.

We performed a retrospective chart review of all patients admitted to our hospital with a diagnosis of ICH from January 2012 to December 2016.We collected baseline demographic characteristics, medical history, ICH scores, differential leucocyte, platelet and total leucocyte(TLC) counts at admission. The functional outcomes after ICH were measured using modified rankin scale (MRS) at discharge. MRS of 5 and 6 were considered poor outcomes. Statistical analysis was done after grouping lab values into higher and lower groups with respect to the normal reference ranges

A total of 257 patients with ICH were admitted to our center during the study period. 111 patients were included in the study and the rest were excluded due to lack of differential leucocyte counts at admission. 34% (38 of 111) had poor outcomes. Univariate analysis using Fisher's exact test showed significant association between low ALC levels (10.5) were also found to be significantly associated with worse outcomes (p = 0.0036, 0.0001, 0.0022, respectively). However, after multivariate analysis, only low absolute lymphocyte counts retained significant association (p =0.0268).

Intracerebral hemorrhage patients with low absolute lymphocyte counts at admission have a higher probability of poor outcomes at discharge. Further studies are required to confirm our results.

Intraventricular hemorrhage (IVH) is a significant predictor of poor outcome after intracerebral hemorrhage (ICH), and may differentially predict hydrocephalus and mortality among blacks vs. nonblacks. We aimed to confirm these findings in a separate cohort of spontaneous ICH patients with severe IVH.

The CLEARIII-IVH trial was a randomized, multi-center placebo controlled trial examining the effect of intraventricular alteplase versus saline, on outcomes in patients with spontaneous IVH. We retrospectively analyzed data on all 500 patients, including self-reported race/ethnicity, medical comorbidities, presentation characteristics and functional outcomes.

Represented race/ethnic groups with >5 subjects per group were 252(50.4%) White/non-Hispanic (WNH), 53(10.6%) White/Hispanic (WH), 168(33.6%) Black/African American/non-Hispanic (BNH), and 14(2.8%) Asian. BNH were significantly younger than rest of the cohort with median age [interquartile range] 55 [46,60] years, had more hypertension(97%, p=0.056), and significantly higher rates of antihypertensive medication non-compliance (70.8%, p=0.048). WNH had more frequent coronary artery disease (14.7%, p<0.001), use of vitamin K antagonists (10.7%, p=0.002) and elevated INR on presentation (9.1%, p=0.002). BNH had significantly more frequent hydrocephalus on presentation (23.8%, p=0.003), and a higher rate of ventriculoperitoneal shunt placement (25%, p=0.015). Neither ICH nor IVH volume at enrollment, nor IVH remaining at end of treatment differed significantly between race/ethnic groups. However, BNH patients were more likely to have greater than 80% IVH reduction, a recognized endpoint for better functional outcomes in CLEARIII (26.8% vs. 25%-WH; 17.1%-WNH; 7.1%-Asian; p=0.019), and this difference persisted in those who received intraventricular alteplase (p=0.04) and after adjustment for diagnostic IVH volume (p=0.03). Race/ethnicity was not an independent predictor of mortality or poor outcome at 30 or 180 days on multivariable logistic regression.

Although functional outcomes did not differ significantly among race/ethnic groups, differences in risk factors, hydrocephalus/shunting post IVH and response to thrombolytic therapy warrant further exploration.

Investigators from the Randomized trial of Unruptured Brain Arteriovenous malformations (AVM) trial (ARUBA) reported in 2013 that interventions to obliterate unruptured AVMs resulted in greater morbidity and mortality compared to medical management. We investigated whether patterns of AVM treatment changed after ARUBA's publication.

We used inpatient and outpatient claims data from 2009-2015 from a nationally representative 5% sample of Medicare beneficiaries. Unruptured brain AVMs were identified using ICD-9-CM code 747.81. The date of first AVM diagnosis was coded as occurring before or on November 20, 2013 (online publication of ARUBA) versus after. Outcomes were referral to a neurologist or neurosurgeon, and interventional treatment. Interventional treatments were identified using CPT codes 61680-61692, 61623-61624, 61796, 61798, or 77371-77372. The likelihood of outcomes after versus before ARUBA was compared using survival analysis with log-rank tests and Cox proportional hazards models adjusted for age, sex, race, and the Charlson Comorbidity Index. We censored patients at diagnosis of intracranial hemorrhage.

We identified 1,444 patients with a mean 2.8 (±2.0) years of follow-up after diagnosis of unruptured brain AVM. Diagnosis was most often by neurologists (20.6%), neurosurgeons (14.4%), and internal medicine specialists (11.3%). After ARUBA publication, there were no changes in 1-year cumulative rates of referral to a neurosurgeon (26.9% after, 26.8% before; P = 0.99) or neurologist (46.8% after, 47.7% before; P = 0.97), but there was an increase in AVM treatment (7.0% after, 3.5% before; P = 0.0096). After adjustment for demographics and comorbidities, there was an increased likelihood of interventional management (HR 1.9; 95% CI, 1.1-3.2) after ARUBA's publication.

In a nationally representative cohort of elderly patients, we found an increase in interventional AVM management after publication of ARUBA. This is notable given that our data pertain to older patients who are generally seen as less suitable surgical candidates.

Elderly patients with severe intracerebral hemorrhage (ICH) are often projected to have future functional dependence but unclear degree of cognitive recovery. Surrogates for such patients frequently weigh multiple concerns when facing the difficult decision of whether to prolong life with tracheostomy and gastrostomy tube insertion versus pursue comfort care. We aimed to characterize distinct groups of surrogates in these situations, based solely on how they prioritize their concerns.

Subjects recruited from a probability-based US population sample completed an online best-worst survey that presented the above scenario and asked the respondent to prioritize concerns as the patient's surrogate. Clusters were identified with latent class analysis after weighting data to match the US Census demographic distribution. Class solutions were replicated 20 times from random starting seeds, with the solution chosen after factoring in Akaike's information criterion.

We identified 4 distinct decisional groups among 792 respondents (response rate = 44.6%). All groups reported multiple concerns as important, but Group 1 (34.4%) was more concerned than any other that the patient was too old to live with disability. Group 2 (26.4%) focused on ensuring agreement among other family members. Group 3 (20.7%) was concerned that the patient might suffer if tube feeding and IV fluids were stopped and that the prognosis could be incorrect. Group 4 (18.6%) had numerous considerations that were comparably important but prioritized paying for long-term care. Groups varied in whether they would actually request prolonging care for the patient (Group 1 = 5.20%, G2 = 9.46%, G3 = 31.13%, G4 = 23.12%, p<0.0001). In a multivariate model, religious affiliation and frequency of attending religious services were the only variables independently predicting group membership.

We identified 4 distinct profiles of decisional patterns for surrogates of severe ICH patients with uncertain prognosis. These data will inform development of strategically tailored decision aids.

Cerebral venous sinus thrombosis (CVST) represents an important cause of both ischemic and hemorrhagic strokes in young people. While recent guidelines recommend management in a stroke unit, the impact of Neurocritical care in this condition has not been studied. We aimed to assess whether the introduction of a Neurocritical Care program influenced clinical outcomes in CVST patients.

We retrospectively reviewed electronic medical records of adult patients admitted to Yale New Haven Hospital's Neuroscience ICU (NICU) between 2011 and 2017 with a diagnosis of CVST. Demographics, vascular risk factors, comorbidities, length of stay and discharge modified Rankin scale (mRS) were collected. Patients were excluded for age 24 hours of presentation. We compared two time periods, before (epoch 1, 2010-2012) and after (epoch 2, 2013-2017) the introduction of continuous staffing of CVST cases by neurointensivists in the NICU. Univariable and multivariable logistic regression were utilized to model the odds of poor outcome (dichotomized mRS 0-2 vs 3-6).

Fifty-three patients with CVST met the inclusion criteria during the study period (mean age 39 (+/-17) years, 51 % female). 20 patients were identified for Epoch 1 and 33 patients for Epoch 2. Overall, 40 patients (76%) had a good (mRS 0-2) outcome. For epochs 1 and 2, good outcomes were observed in 12 (60%) and 28 (85%) patients, respectively (p=0.04). In both univariable and multivariable regression analysis (adjusted for age and sex), admission during epoch 2 was associated with a significantly reduced odds of a poor outcome (OR 0.27, CI 0.07 -0.98; p =0.048) and (OR 0.27, CI 0.07-1; p=0.05), respectively.

In this small, single-center cohort of patients with CVST, most patients experienced a good outcome. The institution of continuous neurointensivist coverage was independently associated with better outcomes. Further validation in prospective, multicenter cohort studies is needed.

Thrombelastography (TEG) provides a dynamic assessment of clot formation, strength, and stability. We examined relationships between TEG parameters and outcomes from intracerebral hemorrhage (ICH).

We prospectively enrolled patients with spontaneous ICH between 2009 to 2017. TEG was performed at the time of admission. We divided patients into two groups based on the presence or absence of hematoma expansion (HE). Clinical characteristics, baseline TEG values, and outcomes were compared between the two groups. Multivariable regression analysis was conducted to compare the differences of TEG components between the two groups after adjusting for potential confounding effects.

We included 275 patients, 67 (24%) with HE and 210 (76%) without HE. Patients with HE were more often male and had higher rates of aspirin use, lower incidence of intraventricular hemorrhage, and larger baseline hematoma volumes. After controlling for potential confounders, mean R time was independently associated with HE (5.3 ± 0.4 vs. 4.8 ± 0.2 mi significantly higher risk of HE with OR 2.63 (95% CI: 1.49, 4.65), p=<0.001. Patients with hematoma expansion were more likely to have poor neurological outcome (mRS 4-6) at discharge (91% vs. 73%, p=0.002) and had higher mortality rates (28% vs. 14%, p=0.005). Overall, 47 patients (17%) died in the hospital. Following multivariable analysis, patients who died had significantly lower mean delta (0.4 ± 0.2 vs. 0.6 ± 0.2 mins.; p=0.04) and smaller angle (69.9 ± 3.1 vs. 66.1 ± 1.9 degrees; p=0.01) than those who lived.

Hematoma expansion and mortality from ICH are independently associated with slower clot formation on TEG. Baseline TEG identifies significant coagulation disturbances which may predict poor outcome and represent potential targets for therapeutic intervention.

Intracerebral hemorrhage (ICH) patients often present with acute hypertension requiring intravenous and enteral antihypertensive medications. We performed a cohort study to determine clinical predictors of time to enteral antihypertensive medication and its effect on ICU length of stay (ICU LOS).

We identified consecutive spontaneous ICH patients admitted from 12/2013 to 9/2015 to a tertiary center, and excluded those transitioned to comfort care (CMO) within 24 hours of admission. We calculated time from hospital admission to first enteral (oral or feeding tube) antihypertensive. We abstracted demographic and clinical variables. Two reviewers examined medical records and classified ICH location and etiology. We determined univariate and adjusted associations of clinical variables to time to enteral antihypertensive medication and performed regression analysis to determine effect on ICU LOS.

We identified 495 patients and excluded 50 for early transition to CMO. Endotracheal intubation (p=0.03), higher ICH score (p<0.001), no outpatient antihypertensive use (p=0.001), and non-lobar ICH location (p=0.005) predicted longer time to starting enteral antihypertensive in adjusted analysis. Presenting systolic or diastolic BP, time of ICU admission (day vs. night), sex, and race were not significant predictors of time to enteral antihypertensive. Time to enteral anti-hypertensive is the strongest predictor of ICU LOS (p<0.0001) after adjustment for age, GCS, ICH score, sex, race, and duration of IV antihypertensive infusion.

Patients with higher ICH scores, intubation, no prior antihypertensive use, and non-lobar ICH are at risk for increased time to enteral antihypertensive administration. Timely enteral antihypertensive administration is an important and potentially modifiable predictor of ICU LOS in acute ICH.

Overall mortality from intracerebral hemorrhage (ICH) represents a combination mortality from a potentially fatal disease as well as practice variation around treatment withdrawal of care. Early Do-Not-Resuscitate (DNR) rates are independently associated with in-hospital mortality and may serve as a proxy for withholding aggressive care. The 2007 American Heart Association (AHA) Guidelines recommended that DNR orders should not be applied before 24 hours out of a concern that less aggressive care would lead to a self-fulfilling prophecy and excess mortality.

We performed a retrospective analysis of temporal trends among primary ICH patients presenting to all nonfederal emergency departments in California from 1999 to 2014 using data from the Office of Statewide Health Planning and Development (OSHPD). Demographic information, clinical covariates (such as mechanical ventilation, craniotomy), and early DNR status within 24 hours were collected and analyzed using segmented regression to evaluate for differences in linear trends from 1999-2006 compared with 2007-2014.

Over a 

Use of early DNR orders for ICH patients has steadily decreased over the last 15 years, even after adjusting for age and disease severity. The pace of this downward trend did not significantly change around the time when recommendations on early DNR use for ICH in AHA guidelines were revised in 2007.

Spontaneous intracerebral hemorrhage (ICH) is a common form of stroke that often results in severe morbidity or death. For most ICH, there are no proven therapies for acute management. Evidence suggests minimally invasive surgical evacuation of ICH may result in improved patient outcomes. The ENRICH clinical trial is designed to determine the efficacy and economic impact of early ICH evacuation using minimally invasive, transulcal, parafascicular surgery (MIPS) compared to standard guideline-based management. In this abstract we present the trial design and rationale at the foundation of the ENRICH clinical trial.

ENRICH is an adaptive, prospective, multi-center clinical trial designed to enroll up to 300 patients with acute ICH. Patients are block-randomized based on hemorrhage location (lobar vs basal ganglia) 1:1 to MIPS or standard management. Included patients are 18 -80 years, GCS 5-14, baseline mRS 7, presenting within 24 hours from last known well and found to have a spontaneous, CTA-negative, supratentorial ICH (30-80 mL). Primary efficacy will be determined by demonstrating significant improvement in the mean utility-weighted mRS at 180 days after enrollment. Economic effect of MIPS will be determined by quantifying the cost per quality-adjusted life-years gained at pre-determined time points.

The rationale for early intervention is to interrupt the time-dependent ICH related pathophysiology caused by mechanical pressures and the pro-inflammatory secondary cascade that leads to worsened cellular injury and edema formation. The planned enrichment strategy acknowledges that hemorrhages in varied locations may have a differential response to MIPS. Study adaptation, in the form of enrichment, may occur if pre-determined futility rules are met for the primary outcome in either of the two locations.

ENRICH is designed to establish the clinical and economic value of early MIPS in the treatment of ICH. Enrollment was initiated in December 2016.

Early seizures (< 30 days) after intracerebral hemorrhage (ICH) may be associated with the presence and degree of perihematomal cytotoxic injury. We explored the association between perihematomal diffusivity (PHD) and early seizures after ICH.

Consecutive patients from the prospective NIH funded DASH study (> 18 years, spontaneous ICH) were included. All patients had multimodal MRI within 2 weeks. Perihematomal edema (PHE) volume was outlined on T2/FLAIR and ICH volume on GRE; these and ADC were coregistered to analyze PHD. EEG monitoring was performed for clinical suspicion of seizure. Mean ADC values of PHE and the percentage of PHE volume were compared between the seizure and no-seizure groups, with ADC values 1200 as vasogenic edema.

Results 26 (11%) of a total of 229 patients had early seizures at a median of day 2 post ICH. Mean ADC in the PHE region was higher in the seizure group (mean: 1169 +/-127 vs 1066 +/-154, p=0.001). ICH, absolute, and relative PHE volumes were not different between groups. The PHE of the seizure group had a lower percentage of cytotoxic edema (5% vs 8%, p=0.007) and a higher percentage of vasogenic edema (43% vs 30%, p 1300 was the most predictive of seizure with AUC = 0.73, though ADC thresholds between 1200-1400 had largely similar AUC's. PHE volume of >24% (of ADC > 1300) identified patients with seizure with sensitivity of 0.81, specificity of 0.63, and remained significant in multivariable analysis.

Patients with early post-ICH seizures have higher mean perihematomal ADC and a larger percentage of vasogenic edema in the perihematomal region. Vasogenic edema due to BBB breakdown and perihematomal inflammation rather than cytotoxic injury is associated with early post ICH seizures.

Novel neuroprotective treatments hold the promise to improve patient outcomes by broadening time windows of intervention and reducing hypoperfusion and reperfusion injury in the era of mechanical thrombectomy for acute ischemic stroke. Hibernating species, such as arctic ground squirrels (AGS), demonstrate remarkable resilience to ischemic and reperfusion injuries. Bioinformatic analyses of genomes of hibernating species reveals signatures of convergent evolution in genes regulating stability and formation of mitochondrial respirasomes. Hypoxia pre-conditioning (HPC) also leads to improved survival upon subsequent exposure to hypoxia, and is associated with increased stabilization of respirasomes. The respirasome is a macromolecule consisting of oligomers of complex I, III, and IV. Cox7a2l is a key mediator of respirasome stability via interactions with Complex I and III.

In this study, we explored the role of Cox7a2l in mediating respirasome stabilization in AGS neural stem and progenitor cells (NSC/NPCs) as well as mouse NSC/NPCs exposed to HPC. Respirasome stability was assessed using blue native gel electrophoresis and mitochondrial metabolism assessed by measuring oxygen consumption in vitro (Seahorse metabolic analyzer).

Exposure to mild hypoxia and induction of HIF leads to stabilization of respirasomes, upregulation of HIF, and modulation of mitochondrial metabolism. Interestingly, overexpression of the AGS isoform of Cox7a2l, which has amino acid substitutions in residues mediating respirasome stability, recapitulates the effects of hypoxia on respirasome stability and mitochondrial metabolism without altering HIF expression.

Targeting respirasome stability by modulating Cox7a2l is a potentially novel neuroprotective target for treatment of ischemic injuries. Testing of these hypotheses in pre-clinical models of stroke is on-going.

Acute stroke symptoms need timely diagnostics in order to ensure best outcomes. As a non-academic, community-based center located in rural Western NC, where we are the regions only Comprehensive Stroke Center, we developed a process to intake stroke patients quickly directly from CT to Interventional Radiology when applicable. A smooth transition reduces the quantity of time from imaging to interventional suite, ultimately reducing the time it takes to prepare to actively treat a patient.

Interventional Radiology Value Stream Mapping started in June 2016. Multidisciplinary team worked in multiple work groups to design and create "Code IR Stroke Now". Flow chart created to show multiple moving parts simultaneously, to streamline transition from ER (sometimes this includes triage from the region also) to IR. An IR "ready" criteria was made, ER and IR checklists, followed by post procedure debrief and treatment plans/order set to standardize care and documentation. First Mock Code IR was done 3/28/17, this was critiqued/perfected. "Go Live" date: 4/3/17. We continue process improvement today.

In first three months, 13 patients have gone through this process. Average compliance for goal Door to Puncture <90min went from 78.6% to 100%. Door to Groin times reduced from 72 minutes to 62minutes. Our performance is 26 minutes quicker than other Comprehensive Stroke Centers (88m avg GWTG database). Saved an average of 19 million neurons per patient. Total of 247 million neurons saved on average since 4/3/17!

Door to Groin times can be reduced with streamline approach to care. Multidisciplinary team approach, including House Supervisors, Anesthesia, Switch-board in addition to the bedside staff and providers can make a smooth transition from the time a large vessel occlusion is identified to getting the patient to the interventional suite. Activation of "Code IR Stroke Now" page activates this team 24/7.

It is unknown whether antithrombotics for secondary stroke prevention in patients with acute ischemic stroke (AIS) due to infective endocarditis (IE) reduce the rate of secondary AIS or increase major bleeding.

We conducted a multi-center, retrospective cohort study from 2007-2015 of patients with AIS secondary to left-sided IE, separated into two groups (antithrombotic vs no antithrombotic). Antithrombotics included antiplatelets and/or therapeutic anticoagulation. The primary outcome was a composite of recurrent AIS and major bleeding. Secondary outcomes included AIS and major bleeding individually. A binary logistic regression model adjusted for age and native vs prosthetic valve involvement was used for outcome evaluation.

The final analysis included 123 patients (91 antithrombotic vs 32 no antithrombotic). Median age was 61 years and 25 (20%) patients had prosthetic valve infections. Infecting organisms were mostly methicillin sensitive S. aureus (29%) or Streptococcus spp. (26%). Valve repair/replacement occurred in 34 (28%) patients. Aspirin with or without another antithrombotic (85%) was the most common antithrombotic treatment. The primary outcome occurred in 25.3% vs 15.6% of patients with antithrombotics vs no antithrombotics, respectively (OR 2.2; 95% CI 0.7 to 6.9). AIS (6.6% vs 2.9%; OR 2.2; 95% CI 0.2 to 20) and major bleeding (18.7% vs 12.5%; OR 2.3; 95% CI 0.7 to 8.1) were similar between groups. A subgroup analysis of aspirin monotherapy vs no antithrombotic yielded similar results for the primary outcome (28.6% vs 15.6%; OR 3.1; 95% CI 0.9 to 11.1) and AIS (7.1% vs 3.1%; OR 2.3; 95% CI 0.2 to 25.0). Major bleeding was increased, however (26.2% vs 12.5%; OR 4.1; 95% CI 1.01 to 16.7; p=0.048).

Antithrombotics after AIS secondary to IE were not associated with a decrease in recurrent AIS or an increase in major bleeding. Aspirin monotherapy was associated with an increase in major bleeding without any reduction in AIS.

Malignant Hemispheric Stroke (MHS) represents between 2-8% of all hospitalized ischemic stroke in the United States. Pooled analysis of 3 European studies has demonstrated that decompressive hemicraniectomy (DCHC) for MHS reduces mortality compared with conservative medical management and may also improve functional outcomes. These trials however, excluded patients with major medical comorbidities that might confound clinical outcomes. APACHE II and SOFA scores are validated ICU scoring systems to help characterize disease severity and estimated hospital mortality. This study aims to evaluate APACHE II and SOFA scores in predicting outcomes for patients undergoing DCHC for MHS.

This is a single center retrospective analysis of patients who underwent early DCHC for MHS between May 2010 through January 2017 at UNC Chapel Hill. APACHE II and SOFA scores were calculated for the date of admission or date of first presentation to neurologic care. Outcomes included mortality at discharge, mortality at 30 day, and functional outcome at last follow up, up to one year. Multivariate analysis included timing of surgery, age, laterality, presence of midline shift, hemorrhage or multiple territory infarction.

We identified 44 patients who met inclusion and exclusion criteria. The median age was 58 (25 to 78), -nine percent of patients received surgery by hospital day 2. Full statistical analysis is pending.

Our hypothesis is a positive correlation between ICU severity scores and mortality. Given APACHE II and SOFA scores capture the effects of acute and chronic disease that would affect patient recovery, we hope to provide a more comprehensive prognostication of outcomes following surgery to help guide physicians and family members of these patients in their decision-making process.

We conducted this study to investigate the effects of decompressive craniectomy (DC) combined with hypothermia on mortality and neurological outcomes in patients with large hemispheric infarction.

Within 48 hours of symptom onset, patients were randomized to one of the following three groups: DC group, DC plus head-surface cooling (DCSC) group and DC plus endovascular hypothermia (DCEH) group. We combined the data of the DCSC and DCEH group to DCH group during analysis. The primary endpoints were mortality and modified Rankin Scale (mRS) score at 6 months.

There were 9 patients in the DC group, 14 patients in the DCSC group and 11 patients in the DCEH group. For all patients, the mortality at discharge and after 6 months was 8.8% (3/34) and 35.3% (12/34), respectively. The DCH group had lower mortality, but the difference was not statistically significant (at discharge, 4.0% vs. 22.2%, P=0.098; 6 months, 32.0% vs. 44.4%, P=0.449). After 6 months, 22 patients survived, and 54.5% of the surviving patients had good neurological outcomes (mRS score of 1-3). The DCH group had better neurological outcomes, but this difference was also not statistically significant (10/17, 58.8% vs. 2/5, 40.0%; P=0.457). The total number of patients experiencing complications in the DC group and the DCH group was 15 (7.2%) and 59 (10.3%), respectively.

Treatment with hypothermia led to decreased mortality and improved neurological outcomes in LHI patients who received DC. A multi-center RCT is needed to confirm these results.

DESTINY II investigated hemicraniectomy in patients 61-years and older for the treatment of malignant cerebral edema. We sought to describe the treatment effect of early hemicraniectomy in DESTINY II, using number needed to treat to benefit (NNTB) and benefit per hundred (BPH) treated at 6 and 12months. As an mRS of 5 is generally undesirable, we also present NNTB and BPH excluding this outcome.

For all possible dichotomizations of the mRS, net NNTB was derived by taking the inverse of absolute risk difference, and net BPH by multiplying absolute risk difference by 100. For benefits simultaneously across all disability transitions on the mRS, NNTB, and BPH, estimates were derived using joint outcome tables: 1) algorithmic minimum and maximum and 2) four independent experts. The expert data is presented as geometric mean.

The algorithmic NNTB was 2.34 (range 1.89-2.78) at 6-months and 2.71 (2.38-3.03) at 12-months, while BPH was 44.5 (36-53) and 37.5 (33-42). The expert NNTB was 2.25 (2.08-2.56) at 6-months and 2.78 (2.63-2.94) at 12-months, and the BPH was 44.4 (39-48), and 35.9 (34-38) respectively. Excluding mRS 5 The algorithmic NNTB was 4.38 (range 4-4.76) at 6-months and 4.44 (3.35-4.55) at 12-months, while BPH was 23 (21-25) and 22.5 (22-23). The expert NNTB was 4.36 (4.0-4.76) at 6-months, and 4.4 (4.35-4.54) at 12-months, and BPH was 22.9 (21-25) and 22.7 (22-23) respectively.

Early systematic hemicraniectomy improves outcome (including mRS 5) for every 2-3 patients treated. Excluding patients with mRS 5, hemicraniectomy improves outcome for every 4.4 patients treated. The algorithmic range provides bounds to the data, while the expert geometric mean provides the most accurate point estimate. These data provide a powerful tool to describe the potential treatment outcomes to families during the first day following a malignant middle cerebral artery infarction.

Background Cerebral bypass surgery is performed to restore, or revascularize blood flow to the brain. Previous studies have not shown whether emergency surgical reperfusion therapy may be effective in acute ischemic stroke patients with large artery occlusion and hemodynamic deterioration. Objective To evaluate the effect of emergency STA-MCA bypass surgery on the outcome of hemodynamic compromised patients who had progressive or fluctuating stroke despite best medical treatments.

We retrospectively reviewed the clinical and radiological data of 57 consecutive patients treated by both emergency bypass surgery (31 cases, 54.4%) and elective bypass surgery (26 cases, 45.6%) due to large artery occlusion at a single center. The effect of surgical therapy was measured with the modified Rankin scale (mRS) at 3 months. Clinical severity was evaluated by the National Institutes of Health Stroke Scale (NIHSS) between pre-and post-operative state. Major perioperative complications were defined as any hemorrhagic stroke, myocardial infarction and death.

Results Occlusive sites were the cervical internal carotid artery in 32 (56.1%) patients and the middle patients in emergency surgery group and 24 (92.3%) patients in elective surgery group. Emergency bypass surgery improved NIHSS (preoperatively, 9 [4-16] ; 2 weeks postoperatively, 6 [2-11]). Major perioperative complications in 30 days were happened in three patients (9.7%) after emergency bypass surgery, and four patients (15.4%) after elective bypass surgery.

Emergency revascularization surgery may be effective alternative treatment for acute ischemic stroke patients with hemodynamic deterioration refractory to maximal medical treatments without significant complications. Larger randomized clinical study is needed to evaluate the effect of emergency revascularization surgery in acute hemodynamic deterioration.

Multiple studies have reported lower mortality rates in obese patients with various cardiovascular disorders, a phenomenon called as the 'obesity paradox'. Such relationship has been largely unreported in patients with neurological pathologies especially stroke. This study reports the effect of obesity on prognosis in patients with ischemic stroke.

Analysis of National Inpatient Sample data (2003-2013) showed a total of 1,168,847 patients discharged with primary diagnosis of IS, ICD-9 Code 433.xx and 434.xx. Patients with obesity were identified using Agency of Healthcare Research and Quality (AHRQ) criteria. We used binary regression to compare inhospital mortality between obese and non-obese patients with ischemic stroke.

From 2003-2013, 1,168,847 patients with ischemic stroke were identified of which 8.7% were found to be obese. Obese patients with ischemic stroke were more often younger, female, and African American as compared to Caucasian. After risk adjustment for demographics, and baseline comorbidities, obese patients with ischemic stroke had lower observed in hospital mortality as compared with non-obese patients with ischemic stroke (2.5% vs 4%, OR: 0.717 CI=0.681-0.756 p<0.001).

From an eleven year nationwide cohort of patients with ischemic strokes, we observed a significant protective effect of obesity and better prognosis including a lower mortality rate. More prospective studies are warranted to further analyze this counter-intuitive trend.

Very early mobilization of critical care patients improves outcome, length of stay, and patient satisfaction. Data for efficacy of very early mobilization for stroke patients have been mixed, and there is limited outcomes data for patients mobilized within 24 hours of receiving intravenous alteplase (IV tPA). The objective of this retrospective observational study was to determine if patients receiving IV tPA who were mobilized earlier were more likely to discharge home.

Medical records of ischemic stroke patients who received IV tPA between 2012 and 2016 at two urban facilities were reviewed for mobility protocol activities. Patients who received endovascular treatment, were placed on comfort care day zero or one, mobilized after the first 24 hours, and transferred out or left against medical advice were excluded. Multinomial regression was used to determine if there were significant differences in patients' discharge status by time first mobilized, adjusting for stroke severity using the National Institutes of Health Stroke Scale (NIHSS), age and gender.

Of the 268 patients included, 46.6 % (n=125) were female, mean age was 68.6 (±14.8), and the median admit NIHSS was 5.0 [IQR: 3.0, 10.0]. The median time first mobilized was 9.0 hours [IQR: 4.3, 15.0], 71.3% (n=191) of patients were discharged to home, 12.3% (n=33), a skilled nursing facility (SNF), 13.8% (n=37), an inpatient rehab facility (IRF), and 2.6% (n=7) hospice or expired. There was suggestive, but inconclusive evidence for a relationship between time first mobilized and discharged to SNF versus home (p=.071). For every one hour increase in time mobilized, patients were 1.07 (95% CI= 1.00 -1.15) times more likely to be discharged to SNF than home.

This study reveals very early mobility is potentially efficacious after IV tPA. Longer time to first mobility was associated with discharge to skilled nursing facility, although this was not statistically significant.

Medical management of cerebral edema after large volume stroke varies greatly across institutions. Hypertonic saline has emerged as a common treatment strategy to attempt to reduce edema and theoretically prevent the need for decompressive hemicraniectomy. There is no established protocol for hypertonic saline administration and there have been concerns regarding safety.

In a single-center, retrospective analysis we identified patients who received hypertonic saline for malignant edema after an ischemic stroke involving the entire hemisphere or diffuse middle cerebral artery (MCA) territory. We compared patients who received continuous infusions of 2% or 3% hypertonic saline to those who received continuous infusions with boluses of 23.4%. The primary endpoint was time to goal sodium (150). Secondary endpoints included the need for surgical decompression and adverse events.

We included 28 patients who received only continuous infusions of hypertonic saline and 20 patients who received a combination of continuous infusions and bolus doses. We found no significant difference between number of patients who reached goal sodium (14 vs 14 respectively, p=0.17) or time to goal sodium (20 hours vs 23.5 hours, p=0.68). There was a significant difference in the number of patients who underwent surgical decompression (4 vs 8, p=0.04). There was not a significant difference in the rate of acute kidney injury or development of acidosis between groups (5 vs. 5, p=0.55).

Both hypertonic strategies appear to be safe. Bolus dosing, on review, was more often instituted during clinical deterioration, accounting for the higher rate of surgical intervention. We feel we can safely be more aggressive earlier in the clinical course to potentially avoid surgical decompression. Furthermore, we may need to look more closely at our target sodium, evaluating whether it should be based on the patient's baseline sodium or a universal value.

Even though recanalization is strongly associated with improved functional outcomes and reduced mortality, clinical benefit from thrombolysis is reduced as stroke onset to treatment time increases. In the recent study, endovascular treatment(EVT) has been demonstrated to improve functional outcome in patients with acute ischemic stroke (AIS) within the time window of onset to 6 or 8 hours. However, beyond usual thrombolysis time window, early neurologic deterioration(END) related with proximal artery occlusion is not uncommon in AIS. With this, we report AIS case series treated with EVT because of END related proximal artery occlusion.

From January 2012 through March 2017, all 261 patients underwent IAT for AIS with anterior circulation stroke. Among them, twenty-four patients underwent EVT due to END. At admission, all twenty-four patients showed near to complete occlusion of a proximal artery and had diffusion-perfusion mismatch.

Mean age was 68. Initial median initial National Institutes of Health Stroke Scale (NIHSS) was 5 and NIHSS after END was 12. All patients had diffusion-perfusion mismatch over 200%. Seven patients treated with IV-tPA before EVT. Good recanalization (TICI 2b/3) was achieved in 91.7%. The hemorrhagic complication was seen in the follow-up computed tomography scan in 4 of 24 cases: three were hemorrhagic transformation, another was the subarachnoid hemorrhage. The thromboembolic mortality case.

In our report, EVT in AIS with END achieved safe and successful recanalization. And successful recanalization was associated with good clinical outcome. We think EVT could be a useful method in case of END in AIS patients with proximal artery near to complete occlusion, even beyond usual 6 to 8 hours time window for EVT.

Jugular bulb venous monitoring can provide information about cerebral hemodynamics and metabolism. We investigated the feasibility and clinical application of jugular bulb venous monitoring in acute ischemic stroke patients at neurocritical care unit.

From March 2015 to June 2017, we conducted jugular bulb venous monitoring in 33 patients in a tertiary referral hospital. Five patients were excluded; 3 without ventilator care and 2 other diseases than stroke. Jugular venous catheters were placed in internal jugular vein by ultrasound-guided method. Lactate, venous oxygen saturation (SjvO2), and arteriovenous oxygen saturation differnece (AVDO2) were monitored every 4 hours. Metabolic derangement was defined when lactate level was more than 2.0 mmol/l. Patients were divided according to presence of clinical deterioration. For long-term prognosis, modified Rankin Scale 5-6 at 3 months were defined as poor outcome.

Twelve patients (42.9%) showed metabolic derangement and they experienced more frequent clinical deteriorations compared to patients without metabolic derangement (n=9, 64.3% vs. n=3, 21.4%, p=0.022). Clinical deterioration was noted in 14 patients, and lactate level was significantly higher in the presence of clinical deterioration group (1.44±0.48 vs. 1.04±0.20mmol/l, p=0.009). Adjusting other potential variables (age, baseline stroke severity, SjvO2, and AVDO2), metabolic derangement was an independent factor associated with clinical deterioration (OR 6.60, 95% CI 1.23-35.44, p=0.028). Meanwhile, poor outcome group (n=12) showed no difference on lactate level, but AVDO2 were higher in poor outcome group (29.54±5.51 v. 24.95±5.65, p=0.041). AVDO2 remained an independent factor for poor outcome after multivariable logistic regression analysis (OR 3.68, 95% CI 1.08-12.55, p=0.038).

This study showed that lactate was associated with clinical deterioration during neurocritical care, whereas venous desaturation contributed to long-term prognosis. Jugular bulb venous monitoring is a feasible tool in patients with acute ischemic stroke at neurocritical care unit.

Swift recognition of stroke symptoms, immediate access to testing and timely treatment plays a vital role in functional outcomes (Middleton et al., 2015) . Delays can postpone treatment and complicate recovery. Delays at this facility included registration, order entry times, and imaging. PI included evaluating and eliminating interruptions, with a goal of reducing the time to treatment.

Process Improvement (PI) utilized an evidence-based algorithm to improve performance metrics and treatment of acute strokes. Setting was a suburban, ANCC Magnet recognized primary stroke center with 16 beds in the ED that experiences 24,010 ED visits and 6,619 admissions per year. Patients included in the acute stroke protocol presented with signs and symptoms of stroke and last known well within 12 hours of symptom onset. Participation included ED staff, and staff working in areas impacted by stroke care. Code Stroke was initiated for patients who fit the criteria. An overhead page was implemented notifying the team throughout the hospital. Radiology would prioritize CT and call the ED as soon as CT was ready. In the meantime, ED team continued assessments. With CT resulted, the physician would determine whether the patient was eligible for tPA. The acute stroke protocol included a list of inclusion/exclusion criteria for tPA administration. Other treatment requirements included reminders for frequency of vital signs, neuro checks and assessments.

Implementation began in May 2016 and the team began to see a significant decrease in CT times and better compliance of dysphagia screening and NIH assessments. CT TAT completed within 45 minutes increased from 62% to 83%. NIH Stroke Scale completion rose from 79% to 100%. Compliance with completing dysphasia screening increased from 86% to 93%.

Results stem from a commitment to excellence from the entire team. PI continues to further improve care for stroke patients.

Induced hypertensive therapy (IHT) has used to enhance cerebral perfusion pressure in subarachnoid hemorrhage and stroke, but there is no established indication for IHT in ischemic stroke. We report the usage of IHT in acute ischemic patients with hemodynamic instability caused by steno-occlusive disease of a main cerebral artery.

We reviewed acute ischemic stroke patients with cerebral perfusion deficit due to intracranial and extracranial steno-occlusive disease. IHT was applied for early neurological deterioration and maintained until hemodynamic instability was stabilized over 24 hours or neurointervention including angioplasty and extracranial intracranial arterial bypass surgery were performed.

52 patients were analyzed. Territories of stroke were 31 of anterior circulation of intracranial vessels, 11 of posterior vessels, and 10 of extracranial vessels. Mean duration of IH therapy was 4176.04 minutes. Pre and post NIHSS score of IH therapy was 8.19 and 7.35, respectively. 30 patients (57.7%) were showed improvement and 13 patients (25%) were stabilized without further aggravation. 16 patients revealed bradycardia. There was no fatal complication of therapy. 15 patients were performed further treatment include bypass surgery, angioplasty, and stenting after IH therapy. At 3 months follow up, 34 patients showed good outcomes (modified Rankin scale 0, 1, and 2).

IHT may be safe and effective for the neurologic deterioration or progression of acute ischemic stroke with hemodynamic instability due to severe steno-occlusive disease of major cerebral artery. Large randomized trials are needed to confirm this result.

Most patients with progressive stroke have a poor prognosis. The aim of our study was investigate the factors related with progressive neurologic deficit (PND) in the patients receiving recanalization therapy for acute ischemic stroke.

-month period, were enrolled. Blood pressures (BPs) at 0, 12, and 24 hours after admission and BP variation (BPV) for the first 24 hours were collected. Variables associated with PND were analyzed.

Among 216 enrolled patients, 68 patients showed PND. The patients with PND had higher systolic BPs at 0, 12, and 24 hours after admission and higher BPV than the others (p <0.05). Posterior circulation stroke was more prevalent in the patients with PND (p <0.01). In logistic regression analysis, PND was independently associated with posterior circulation stroke [odds ratio (OR) = 3.35, p <0.001] and systolic BP at 24 hours after admission (OR = 1.02, p = 0.03).

PND may be associated with elevated systolic BP for the first 24 hours after admission in the patients receiving recanalization therapy for acute ischemic stroke.

Telestroke has revolutionized stroke care delivery in the modern era. Massachusetts General Hospital (MGH) uses the most common model, the hub and spoke. The demonstration of superiority of endovascular therapy (ET) with intravenous tPA over tPA alone for acute stroke patients with large vessel occlusions prompts a thorough assessment of Telestroke's role in the delivery of ET, particularly in terms of transferring patients to hubs capable of ET. Our primary objective was to examine associations between transfer time and clinical outcomes.

Patients were selected from the Get with the Guidelines-Stroke registry who were transferred to MGH from Jan 2011 to Oct 2015 who had NIHSS>6 and last known well<12h on MGH arrival (n=618). We excluded patients for whom we could not calculate the primary predictor, transfer time (defined as the MGH arrival time minus the telestroke consult answered time, n=384). Several clinical outcomes were explored by linear and logistic regression to determine association with transfer time.

Of the 234 patients in the study, 120 (51%) were transferred by ambulance, 114 (49%) by helicopter, and 63 (27%) underwent ET at MGH. Median transfer time was 132 min, and median ASPECTS decrease was 2 during transfer. Longer transfer time was associated with decreased likelihood of undergoing ET (p=0.003). However, transfer time was not significantly associated with ASPECTS decrease during transfer. For those patients undergoing ET, transfer times bore no association to 90 day mRS.

This study identifies an association between longer transfer time and decreased likelihood of undergoing ET. Reasons are varied, and are not clearly related to imaging progression alone. Only 27% of transferred patients underwent ET. More efficient spoke triage and transfer may improve the ratio of patients treated with ET. These data provide an important perspective during this period of stroke triage evolution.

Intra-arterial thrombectomy (IAT) has been approved for acute treatment of ischemic strokes (IS). With the advent of several new devices for IAT, this procedure has become more widely utilized with better outcomes. We performed this analysis to evaluate trends and predictors of utilization of IAT over an 8 year period.

Analysis of Nationwide Inpatient Sample data (2006 to 2013) showed a total of 850,997 patients discharged with a primary diagnosis of IS, ICD-9 Code 433.xx, and 434.xx. IAT was ascertained by ICD-9 procedure code 39.74. Independent predictors of IAT were studied using binary logistic regression. The predictors included in the model were age, sex, race, teaching status, and insurance type.

Results 4903 or 0.6% of IS patients received IAT. Mean age of patients receiving thrombolysis was 71.01 years. Percentage of IS patients receiving IAT has consistently increased from 0.037% in 2006 to 1% in 2013. We also observed significant year to year decrease in mortality among patients receiving IAT. In 2006, 26.2% of IAT patients died as compared to 15.8% in 2013. Using binary logistic regression, the statistically significant independent predictors of IAT utilization were Age (OR= 0.978, p=0.000), Female gender (OR=1.120, p=0.019), Insurance type as compared to Medicare (Private insurance OR=1.199 p=0.006, and self-pay OR=0.778 p=0.05). As compared to Caucasians, African Americans were less likely to receive treatment (OR=0.531 p=0.000). Also, a teaching hospital was found to be more likely to administer IAT as compared to a non-teaching hospital (OR = 5.941, p=0.000).

IS patients with younger age, female gender, private insurance and patients admitted to teaching hospitals are more likely and African Americans are less likely to receive IAT. This study showed that IAT utilization has increased significantly since 2006 with a steep decline in the in-hospital mortality. This may point to improved IAT devices and better patients' selection.

Telestroke plays an integral role in stroke care. Nationally the most common model is the hub and spoke, which is used at our institution. Understanding Telestroke's role in the transfer of candidate patients for endovascular therapy (ET) is critical to minimizing delays. Our primary objective was to evaluate predictors of transfer delay.

Patients were selected from the Get with the Guidelines-Stroke registry who were transferred to MGH from Jan 2011 to Oct 2015 with NIHSS>6 and last known well<12h on MGH arrival (n=618). We excluded patients for whom we could not calculate transfer time (the MGH arrival time minus the telestroke consult answered time, n=384). Ideal time was calculated using Google Maps incorporating date/time information for ground transfers and straight line distance at 130mph for helicopter transfers. Ideal time was subtracted from actual time to calculate delay, accounting for distance, mode of transport, weather, and traffic. Analysis of covariance was used to explore 3 possible predictors of delay (night vs. day, weekend vs. weekday, tPA delivery at spoke).

Of the 234 patients in the study, 120 (51%) were transferred by ambulance, 114 (49%) by helicopter, and 63 underwent ET. A significant proportion of the variation in delay was explained by the predictors (F=6.43, p<0.0005). Nocturnal transfer (1800-0600hrs) was associated with significantly longer delay (20.53 additional minutes relative to daytime transfers, p<0.0005). Weekend vs. weekday transfer and tPA delivery at spoke hospital did not contribute significantly to model variance.

Our findings highlight the importance of refining protocol approaches. Nocturnal transfers were associated with substantial delay relative to daytime transfers. In contrast, delivery of tPA was not associated with delays, underscoring the impact of effective protocols that are in place. Metrics and protocols for transfer, especially at night, may have a positive impact on transfer times.

The use of anticoagulant therapy in the acute stage of ischemic stroke is controversial. Novel oral anticoagulant (NOAC) is effective in preventing recurrent embolism in patients with non-valvular atrial fibrillation (NVAF), but the risk of hemorrhagic transformation is the major concern for its early use in ischemic stroke. We aimed to study the use of NOAC in patients with acute ischemic stroke and NVAF.

Patients with acute ischemic stroke and NVAF, who were admitted to our acute stroke unit from 2014 to 2016, were recruited in this single-centre cohort study. The timing of initiation of NOAC is at the discretion of the treating physician based on the stroke severity and infarct size.

NVAF attributed to 32.5% (214/ 659) of all ischemic stroke cases. The early recurrent embolism rates were 1.4%, 3.3% and 4.7% at one week, two weeks and one month respectively. NOACs were prescribed in 105 patients. NOACs were initiated within one week in 47 patients (44.8%). The median time to NOAC initiation were five days (IQR 1.8 -18.0), nine days (IQR 6.3 -25.3) and 20 days (IQR 12.0 -37.0) for patients with no/small-sized infarct, moderate-sized infarct, and large-sized infarct respectively. At one month, two patients had recurrent ischemic stroke despite treated with NOAC. Only one patient, who had a large-sized infarct, developed symptomatic hemorrhagic transformation.

Early use of NOAC in ischemic stroke appears to be safe. Further large prospective studies are required to evaluate the risk and benefit of NOAC use in acute ischemic stroke.

Osmotherapy (hypertonic saline or mannitol) is the mainstay of available therapy to counter cerebral edema that can develop after large hemispheric infarction. In a post-hoc analysis of the GAMES-RP trial, we hypothesized that patients with large infarction, treated with intravenous glyburide, might require less osmotherapy than placebo treated patients.

GAMES-RP was a multi-center prospective, double blind, randomized, placebo controlled study which enrolled 84 patients with large anterior circulation infarction. Patients were randomized to IV glyburide administration (BIIB093; n=44) or placebo (n=40) with target time from symptom onset to drug infusion decompressive craniectomy (DC), or both. Total bolus osmotherapy dosing was quantified by an "osmolar load" (volume in L * osmolarity in mOsm/L).

Of the 84 subjects, the percentage of patients who received bolus osmotherapy did not differ between the glyburide and placebo treated subjects (51% v. 53%; p=0.89). There was no difference in mean total osmolar load received (mOsm) or hours from drug bolus to osmotherapy administration. Overall, 40 subjects received osmotherapy. The baseline DWI lesion volume (mL) was significantly larger in the osmotherapy treated group (170.2 ±53.3 v. 147.4 ±45.5; p=0.047). The presence of adjudicated malignant edema on imaging was more common in the osmotherapy group (63% v. 30%, p=0.004), as was DC (45% v. 8%; p<0.0001). Among patients with adjudicated clinical neurologic deterioration from edema, 31% (n=11) did not receive osmotherapy.

Treatment with IV glyburide was not associated with less osmotherapy, possibly due to a ceiling effect resulting from the large infarct volumes. However, osmotherapy use was associated with larger infarct volumes, malignant edema, and higher incidence of DC. Use of osmotherapy did not always follow the appearance of clinical or radiographic malignant edema.

Acute ischemic stroke patients receiving intravenous alteplase (IV-tPA) are placed on bedrest for 24 hours or longer due to provider fear of worsening stroke symptoms from decreased cerebral perfusion. This is based on medical uncertainty and lack of robust studies, despite American Stroke Association (ASA) recommendations for mobilization when hemodynamically stable. This retrospective observational study evaluates very early mobility in acute ischemic stroke patients post IV-tPA while evaluating for change in NIHSS.

Medical records of ischemic stroke patients who received IV-tPA between 2012 and 2016 at two urban hospitals were reviewed for mobility protocol activities. Patients who were given endovascular treatment, placed on comfort care on day zero or one, mobilized after the first 24 hours, transferred out or left against medical advice were excluded from the analysis. Multiple linear regression was used to determine if those patients mobilized earlier saw a greater change between NIHSS at admit and 24 hours post IV-tPA administration, adjusting for age and gender.

Of the 268 patients included in the final analysis, 46.6% (n=125) were female, mean age was 68. The multiple linear regression results showed no significant relationship between change in NIHSS from admit to 24 hours post IV-tPA and earlier mobilization, after adjusting for age and gender (ß= -0.065 change in NIHSS points per hour; p=0.181).

This study reveals early mobility does not worsen stroke symptoms or severity based on NIHSS. This suggests that very early mobility of patients after IV-tPA is safe as recommended by ASA.

Interhospital transfers to a Stroke Center following IV-tPA administration are increasingly common. However, no studies have evaluated ICU needs in these transfer patients and such understanding may have a significant impact on resource utilization. The aim of this study is to compare the frequency, timing, and nature of ICU-level needs in post-IV-tPA patients that were transferred versus those who present directly to the admitting hospital.

Retrospective chart review of consecutive, tPA-treated ischemic stroke patients admitted to the ICU at a Comprehensive Stroke Center servicing a large Telestroke referral network from 11/2013 to 7/2015 was performed. We evaluated patient demographics, stroke characteristics, and ICU needs between transfer and non-transfer patients before and after ICU admission.

Results 331 patients were admitted to the ICU post-tPA. 237 patients (71.6%) were transferred from an outside hospital, of which 123 patients had ICU needs (51.9%). This frequency of ICU needs was no different when compared to the non-transfer patients (47/94, 50.0%, p = 0.81). Similar ICU needs were observed for each specific ICU intervention between transfer and non-transfer patients (IV antihypertensive, vasopressor requirement, IV rate control, respiratory support, IA therapy, ICP monitoring, hypertonic therapy, and neurosurgical intervention, all p > 0 association with ICU needs (OR 11.9 in transfer patients, OR 9.7 in non-transfer; both p < 0.0001).

Transferring post-IV-tPA patients is not associated with increased ICU needs. About one-half of post-tPA patients do not have ICU needs, and these patients typically have milder stroke severity. Our data supports the safety of transferring post-tPA patients, and to potentially monitor a subgroup of these patients in a non-ICU setting. The ability to appropriately triage post-tPA patients may lead to more efficient and cost-effective stroke care.

Stroke patients requiring decompressive craniectomy remain at high risk of prolonged mechanical ventilation as well as ventilator associated pneumonia (VAP). Early tracheostomy placement may provide a reduction in the duration of mechanical ventilation however prediction of those who ultimately require a tracheostomy remains a clinical challenge. A preoperative assessment of tracheostomy dependence may help to guide decision making. The authors compare key outcome data after early versus late tracheostomy and develop a preoperative decision-making tool to predict postoperative tracheostomy dependence. A subsequent validation utilizing a decision tree analysis applied prospectively is ongoing and will be presented.

We performed a retrospective analysis of prospectively collected registry data and developed a propensity weighted decision tree analysis to predict tracheostomy requirement utilizing factors present prior to surgical decompression. Outcomes include probability functions for ICU LOS, Hospital LOS, and mortality based on data for early (10 day) tracheostomy. A subsequent validation of the decision tree is being applied prospectively to evaluate its predictive value.

A total of 168 surgical decompressions were performed on patients with acute ischemic or spontaneous hemorrhagic stroke between 2010-2015. Forty eight patients (28.5%) required a tracheostomy, whereas 35 (20.8%) developed VAP, and 126 (75%) survived hospitalization. Mean ICU and hospital LOS were 15.1 and 25.8 days respectively. Utilizing GCS, SOFA score and hydrocephalus presence, our decision tree analysis provided a 63% sensitivity and 84% specificity for tracheostomy prediction. Early tracheostomy conferred significantly fewer ventilator days (p<0.001) and shorter hospital LOS (p=0.014) with similar VAP and mortality rates between groups.

Early tracheostomy shortens duration of mechanical ventilation and length of stay following surgical decompression for stroke, however without a demonstrable impact in mortality or VAP rates. A preoperative decision tree awards a practical tool that may provide insight to guide preoperative decision-making with patient families.

Patients suspected acute stroke are critical in time delay of endovascular or intravenous thrombolytic therapy. Prehospital notification from emergency medical services (EMS) may shorten the door to recanalization time. The 'Brain Saver', web-based prehospital notification system could reduce the time interval from symptom onset to recanalization.

Beginning in March 2016, stroke team consisted of stroke specialized doctors, nurses and radiologists of multi departments received direct alarms via smart phone application from paramedics of EMS about transport information of patients with suspected stroke. We compared baseline characteristics and prehospital/ in-hospital delay time in stroke patients treated with intravenous thrombolysis or endovascular treatment for 12 months with and without EMS use Brain Saver Protocol.

167 patients (69 patients with protocol and 98 patients without protocol) were enrolled in this program. The patients who used Brain Saver had shorter median onset-to-arrival times (63 minutes versus 142 minutes, P < .001) and in in-hospital delay time (35 minutes versus 52 minutes, P<.001). Prehospital notification by Brain Saver was associated with shorter median door-to-imaging time (5 minutes versus 12 minutes, P<.001), door-to-needle time (20 minutes versus 31 minutes, P <.05), door to puncture time (55 minutes versus 137 minutes, P < .001)

We found that prehospital notification was associated with faster door-to-imaging time, door-to-needle time and door-to-puncture time in patients presenting within 6 hours of symptom onset. Close collaboration between stroke team in hospitals and the EMS system gives stroke suspected patients an in-time emergency care system.

Infection is a common complication in the acute phase after ischemic stroke. Furthermore, malnutrition is associated with unfavorable outcome in patients with stroke. Therefore, we investigated that premorbid undernutrition identified by objective and quantitative method, Nutritional Risk Index (NRI) was related to the risk of infection after ischemic stroke.

A consecutive 852 patients who were admitted within 7 days after ischemic stroke onset between October 2010 and October 2015 were included. We assessed initial nutritional status using NRI, and NRI formula as follows: NRI = (1.519 × serum albumin, g/dL) + {41.7 × present weight (kg)/ideal body weight (kg)}. The patients were categorized into three groups on the basis of NRI [No risk (NRI >97.5), Moderate risk (NRI 83.5-97.5), and Severe risk (NRI <83.5)]. We compared the clinical characteristics and NRI according to the presence of infection.

Among the included patients (mean age, 67.7 years, male, 60.6%), 85 (10.0%) patients experienced infection during hospitalization. The rate of pneumonia was 81.2% (n=69), and the rate of urinary tract infection was 11.8% (n=10) among total infection. The proportion of lower NRI patients (Moderate risk and Severe risk) was significantly greater in the infection group (45.9% vs. 17.9% and 10.6% vs. 2.7%, P <0.001). Moreover, higher NRI patients were less likely to be admitted to the intensive care unit (1.4% vs. 5.1% vs. 6.7%, P = 0.004). A multivariate analysis revealed that lower NRI groups had a higher risk of infection [Odds ratio (95% confidence interval); Moderate risk 3.98 (1.95 -8.13); Severe risk 4.21 (1.10 -16.14), P for trend = 0.001].

Our study demonstrated that the lower NRIs predicted infection complications and severe infections after ischemic stroke. This suggests that assessment of nutrition depletion could be a useful predictor and a modifiable risk factor for infection following stroke.

CYP2C19 plays a major role in the metabolism of the clop[idogrel. CYP2C19 generates an active oxidized metabolite of clopidogrel that exerts antipl;atelet activity by inhibiting P2Y12 reeceptor. The major alleles of the CYP2C19 gene are *1, *2, *3 and *17 and approximately 30% of Caucasians and 55% of Asians have one or more loss of function alleles

In this study, patients with at least two *2 or *3 allels were classified as poor metabolizer(PM), those with one *2 or *3 allele were classified as intermediate metabolizer(IM), and those without a *2, *3 or *17 alleles were classified as extensive metabolizer. In addition. those with (*2/*17 or *3/*17) were classified as unknown metabolizer.

784 stroke patients were enrolled for this trial. The mean age was 61 years, and 32% were women. 61% had a history of hypertension, 29% of DM and 28% of dyslipidemia. Of the participants, 37% were classifies as EM, 1% as UM, 45% as IM, 16% as PM and 1% as unknown metabolizer. 38% had good genotype for clopidogrel metabolism and 62% had poor genotype. There were no significant diffirences in the demographic and clinical findings between the good and poor genotype groups

The prevalence of CYP2C19 polymorphisms is different according to the ethnicity. The racial difference in platelet function may lead to diffrerences in the treatment as well as new targets for antiplatelet therapy

The social brain hypothesis is an evolutionary theory proposing that the number of contacts in a primate's social network is proportional to neocortical volume. We tested the hypothesis in a patient population with social network data before and after vascular events. We studied whether social network indices would decrease after stroke, but not after myocardial infarction (MI), as anticipated by the theory.

We examined trajectories of the Lubben Social Network Scale score (range 0-50, higher values indicating larger network) before and after vascular events in participants from the Cardiovascular Health Study. We used a repeated measures design with linear mixed models to compare the change in social network score before and after events in 382 persons with ischemic stroke and 395 with MI. Over a mean of 11.1 years of follow-up for stroke and 12.4 years for MI, we examined an average of 4 social network scores for each participant. We controlled for socio-demographics, baseline cognitive function, and comorbidities.

Social network scores declined significantly after stroke (an additional -0.14 points every year, 95% CI -0.27, -0.01, P=0.04), but not after MI (-0.06, 95% CI -0.16, 0.04, P=0.24) compared to the baseline slope in fully adjusted models.

Social network score declined more steeply after stroke than after MI, even after adjusting for potential confounders. These findings support the social brain hypothesis but do not address mechanism. Shrinkage of the social networks may be a specific target for interventions to optimize recovery in vascular diseases, particularly stroke.

Emergency Neurological Life Support (ENLS) protocols are an essential component to assessment and management of patients within the first hours of the neurological emergency. With increasing focus on emergent endovascular treatment for large vessel occlusion (LVO) in acute ischemic stroke our institution incorporated Stroke VAN assessment as part of the ENLS Acute Stroke Initial Assessment protocol.

Stroke VAN screening tool was taught to all nurses in the Emergency Department (ED) who triage stroke. All patients who presented to the ED with suspected stroke had a VAN assessment completed prior to ED physician evaluation and CT imaging. Patients with weakness in addition to visual changes, aphasia, or neglect were considered VAN + and triaged immediately to CT angiogram head/neck with immediate notification to the Neurointerventionalist.

A sample of 76 patients presenting to the ED as a stroke alert over an 8 month time period were utilized. Using the Stroke VAN assessment tool was found to improve time to identification of LVO by reducing time from arrival to CTA for VAN positive patients from 77 minutes pre-intervention (n=31) to 27 minutes post-intervention (n=35). This was a significant decrease in time to identification of patients presenting with LVO (p<0.05), improving time to endovascular treatment.

Incorporating Stroke VAN as part of the Acute Stroke Assessment Protocol improved identification of patients presenting with LVO, decreased time to CTA imaging and improved time to endovascular treatment which is well documented with improved neurological prognosis. Time is essential in neurological emergencies. The VAN assessment is quick and easy to perform, requires no scoring or calculations, and is the only LVO screening tool tested in the ED by ED nurse and physicians. We suggest incorporating Stroke VAN to the ENLS Acute Stroke protocol as a way to improve identification of LVO and improve time to endovascular treatment.

Elevated Blood pressure (BP) is known to be related to hemorrhagic transformation (HT) after ischemic stroke. However, the effect of BP variation on the HT remains unclear, especially in patients with successful recanalization after mechanical thrombectomy. Therefore, we investigated the relationship between BP and HT after mechanical thrombectomy following ischemic stroke.

A consecutive 141 patients with acute ischemic stroke and successful recanalization (TICI 2b or TICI 3) were included for the analysis between January 2013 and November 2016. The information on BP was obtained over the first 24 hours using various parameters including mean, maximum (max), minimum (CV), and successive variations (SV) for systolic, diastolic BP, and mean BP. We defined major HT as a parenchymal hematoma type 2 (PH2).

Among the included patients (age, 66.3; and male, 55.2%), 16 patients (11.3%) developed major HT over the first 24 hours after successful recanalization. Systolic BP max-min was significantly increased in patients with major HT compared to those without major HT (61.2 mmHg vs. 44.2 mmHg, P = 0.034) while other BP parameters were not. In addition, systolic BP max-min was significantly associated with symptomatic HT (n=11, 7.8%, P = 0.007). After adjusting for confounders, systolic BP max-min was independently associated with major HT (Odds ratio, 1.028; 95% confidence interval, 1.004-1.051).

Our results demonstrated that absolute change of systemic BP over the first 24 hours was associated with major and symptomatic HT after successful mechanical thrombectomy after acute ischemic stroke. This suggests that maintaining stable systolic BP is an important factor in possibly preventing major HT after successful recanalization.

The benefits of intravenous tissue-plasminogen activator in acute ischemic stroke are highly timedependent. However, there are so many cross-departmental tasks to eligible patent that many stroke centers have difficulty achieving the guideline recommended 1-hour door-to-needle (DTN) time. We have developed web based visual task management system called "Task Calc. Stroke" (TCS) by using information and communication technology. Herein, we performed a trial installation and preliminary evaluation of TCS.

The application software of TCS was designed to run on the Google Cloud Platform. TCS alerts the relevant hospital staff to the patient's arrival condition and time, and displayed tasks to be performed and its treatment status by changing color in real time on networked wall-mounted smart devices in the several relevant departments. We started a trial installation of TCS during the daytime from August 2015. We compared lead times before (August 2014 to July 2015) and after (August 2015 to July 2016) trial installation of TCS.

Trial installation of TCS in our hospital showed successful information sharing. A total of 33 patients included (pre: 13, post: 20) . After the installation, significant reductions occurred in the median time from door to complete blood count time [26.6 vs. 17.5 min, p < 0.001] and a trend toward a reduction from door to needle time [36.0 vs. 30.0 min, p = 0.175].

TCS may be useful tool to reduce the lead times of acute stroke patients. TCS is a new approach that has the potential to promote efficiency for acute stroke care.

Prior history of intracranial hemorrhage (ICH) has been considered a contraindication to administration of intravenous recombinant tissue plasminogen activator in acute ischemic stroke, per the original Activase FDA label and 2013 AHA/ASA guidelines. However, limited data are available on the risks of lysis in patients with prior ICH.

We performed a cross-sectional study of adult patients who received thrombolysis, using administrative claims data on admissions to acute care hospitals in California between 2005-2011. Diagnosis codes were used to identify patients who received thrombolysis, and to ascertain (1) a prior diagnosis of ICH, including intraparenchymal hemorrhage (IPH), subarachnoid hemorrhage (SAH), subdural hematoma (SDH), or epidural hematoma (EDH); and (2) relevant comorbidities, including hypertension, smoking, diabetes, heart failure, atrial fibrillation, renal disease, malignancy, and demographic data. We used univariable and multivariable logistic regression to model the odds of in-hospital mortality as a function of prior ICH, after adjusting for potential confounders.

60,142 patients received thrombolysis during the study period (mean age 65 [SD 15], female count 26,613 [44%]). Of these, 824 patients (1.4%) had a documented diagnosis of prior ICH on admission. Inhospital mortality was 7% overall, 6.9% for patients without prior ICH, and 33.1% for patients with prior ICH. In multivariable analysis, all prior ICH subtypes remained independently associated with in-hospital mortality, including IPH (OR 5.9, CI 4.9-7.1, P <2e-16); SAH (OR 6.5, CI 4.8-8.8, P <2e-16); and SDH (OR 3.8, CI 1.8-7.5, P=0.0002). Only 4 patients had EDH and testing was not possible.

1.4% of patients who received thrombolysis during the study period had prior diagnosis of ICH. Prior ICH was found to be significantly associated with in-hospital mortality regardless of ICH subtype.

We evaluated the association between early neurological improvement (ENI) after ERT and time spent from symptom onset to recanalization, according to the degree of collateral circulation measured using multiphase CTA.

Patients with anterior circulation occlusion who underwent ERT based on a non-contrast brain CT and multiphase CTA were evaluated. Collateral status was evaluated using a pial arterial filling score, which was developed into a six-point scale. ENI was defined as equal to more than 50%, or as an 8-point decrement in NIHSS from baseline. Neurological statuses at day 1 and at day 7 (or discharge) were determined by a certified neurologist using NIHSS.

The collateral circulation degree measured by multiphase CTA was inversely correlated with baseline stroke severity (p=0.02). The proportion of ENI at day 1 was significantly lower in patients with poor collateral status (score 0~4) according to the time from symptom onset to recanalization (0-180, 50.0%; 180-360, 14.8%; > 360, 14.3%; p=0.02). However, the proportion was similar in patients with a good -180, 57.1%; 180-360, 50.0%; 360-480, 50.0%; >480, 50.0%; p=0.97, day 7 or discharge; 0-180, 81.0%; 180-360, 71.4%; 360-480, 100.0%; >480, 66.7%; p=0.68). Collateral status was the best predictor for ENI after ERT. ENI was achieved in only 5 (14.3%) patients with poor collateral status, and their time from symptom onset to recanalization was more than 180 minutes.

The time window for ERT might differ according to baseline collateral status measured by multiphase CTA. The current time window for ERT within 6 hours from symptom onset to groin puncture could be

Atrial fibrillation (AF) is the most common cardiac arrhythmia among adults. Despite of the proven advantage in primary and secondary stroke prevention in patients with AF, antithrombotic therapy has been reported to be still underused in many countries. However, there is a little data about the incidence of AF and any changing pattern of antithrombotic therapy among patients with AF over the past decade in Korea.

Data source for this study were obtained from the nationwide sample cohort comprising 1,025,340 individuals (2% of entire population in Korea) which were established by Nationwide Health Insurance System.

During a 10-year follow-up period, there was 16, 273 developed AF (1.58%). the incidence of patients with AF remained relatively constant during study period (8.23% in 2004 vs 8.24% in 2013). The proportion of patients with antithrombotic therapy increased from 18.5% in 2004 to 36.5% in 2013 significantly (p for trends < 0.001). However, the proportion of patients with antiplatelet agents was higher than with oral anticoagulation.

AF steadily increased over recent 10 years in Korea. However, only 36.5% of AF patients were receiving antithrombotic therapy. Our study demonstrated that there was huge gap between the clinical practice and treatment guideline in antithrombotic medication for AF patients in Korea over the past decade.

OhioHealth (OH) possesses one of the nation's largest neuroscience programs and is the leading volume provider of stroke care in Ohio. OH is comprised of 12 hospital-based sites, 4 primary stroke centers, 1 comprehensive stroke center, and a virtual health (VH) stroke network that serves 24 hospitals throughout the state. In August 2016, stroke services at OhioHealth were restructured to enable dedicated clinical time for VH providers, require expertise, training, and quality review participation for stroke responders, streamline activation algorithms to limit hand-offs, and eliminate identified barriers to VH consultation. A 6 month interim analysis was planned to assess the impact of these changes (termed "Stroke 2.0").

Comparative analyses were performed between the first 6 months of Stroke 2.0 and the similar time period of the year prior to restructuring. Pre-defined metrics included consultation volume, VH response time, IV-tPA time to treatment, research enrollment volume, endovascular referral rate and time to treatment, ischemic stroke (IS) observed : expected (O:E) mortality data, and patient retention rate at associate VH sites.

During the first 6 months of Stroke 2.0, 2007 encounters were seen (historical 700) with a mean activation to VH log in of 4.3 minutes. Both volume of patients treated with IV-tPA (154 vs. 96, p< 0.05) and mean treatment times (63 vs. 86 minutes; p< 0.005) were significantly reduced. Mean time to endovascular intervention was less during Stroke 2.0 (98 vs. 140 minutes, p <0.05). System-wide O: E mortality was reduced after restructuring (0.513 vs. 0.704, p< 0.05), accounting for 21 additional lives saved. Acute stroke research enrollment doubled (77 vs. 38) during this same period. Transfer rates to VH hub were unchanged (59 vs. 59 %, p = 1.0).

Strategic changes in staffing, expertise, VH structure, and access can have profound and positive changes on a well-functioning stroke system.

Strokes due to CNS fungal infections (SCFI) are often misdiagnosed.

Retrospective study of electronically-extracted records in patients with strokes & positive fungal studies, from cerebrospinal fluid (CSF) or brain biopsy. Other stroke etiologies were excluded. Thirteen patients had SCFI by a priori exclusion & inclusion criteria.

Nine were males. Mean age was 53+17 years. Symptoms were mild [NIHSS 6 (2, 9.5) (median and IQR)]. Focal deficits & headaches (both 76.9%) were common. Seventy-percent were immuno-compromised (medications, malignancy, transplant recipients). Clinical course was indolent in 30.7%. Seventy-percent had poor outcome (2-LTAC, 4-SNF, 2-dead). Ninety-two percent had CSF pleocytosis (Range:27-471) while 61% had CSF glucose less than 40mg/dL (Range: 2-37). Seventy-five percent had lymphocytic predominance. Seven strokes were from yeasts (4-Cryptococcus, 1-Coccidiomycosis, 1-Histoplasma, 1-Candida) and 6 from molds (4-zygomycetes, 2-Aspergillus). Sixty-two percent had posterior circulation involvement (71.4% yeast vs 50% molds). There was lepto-meningeal enhancement in 83% of yeast vs. 0% of molds infections (p= 0.01). The basal ganglia (BG) was involved in 75% of intravenous-drug users (IVDU) vs. 0% of non-IVDU (p=0.01). One had abnormal CNS vessel imaging directly attributed to the ischemic lesions.

In this series, patients were young, immunocompromised or IVDU. Stroke sizes & clinical deficits were modest with no angiographic evidence of vasculitis. Majority had CSF pleocytosis & hypoglycorrhachia. Posterior circulation involvement was typical. Lepto-meningeal meningitis was only seen in yeast infections. The BG was spared in non-IVDU but common in IVDU. Mechanism of stroke in yeast infections is probably from meningitis & secondary involvement of small perforating branches. Mechanism in mold infections in immuno-competent IVDU is probably direct angio-invasiveness in small vessels of the BG. Outcomes are poor in spite of therapy. SCFI should be considered in selected cases of cryptogenic (recurrent or progressive) strokes with clinical, CSF and MRI features described.

Life-threatening bleeding requires prompt reversal of factor Xa (FXa) inhibitors. Their anticoagulant effects can be reversed with the antidote andexanet alfa. The efficacy of andexanet to reverse bleeding in an apixaban anticoagulated porcine trauma model was investigated.

After ethical approval, male pigs (n=15) were given apixaban for 3 days (20 mg daily); the sham group (n=5) received placebo. Standardized polytrauma by blunt liver injury and bilateral femur fractures were inflicted. 12 minutes post-trauma, animals were randomized (n=5 per group) to a single andexanet bolus (1,000 mg), a bolus (1,000 mg) + infusion (1,200 mg over 2 hours) regimen, or vehicle (control). Blood loss (BL) and hemodynamics were monitored over 6 hours or until death and analyzed by ANOVA (mean±SEM).

Apixaban anti-FXa levels were 183±26 ng/mL with no differences between anticoagulated groups prior to injury. BL in the sham animals was 494 ± 24 mL 12 minutes after injury (total BL 651±39 mL at "x" hours; 100% survival). Anticoagulation with apixaban significantly increased BL 12 minutes after injury (873±25 mL; P<0.01). Controls exhibited a total BL of 3,913±235 mL with 100% mortality (mean survival time = 165 minutes). Treatment with a bolus or bolus+infusion of andexanet was associated with a significant reduction in BL versus sham (P<0.05) and 100% survival. Two hours after injury, apixaban anti-FXa levels in bolus animals were 99±45 ng/mL, whereas the bolus+infusion regimen resulted in levels of 17±6 ng/mL (P<0.05). Hemodynamic parameters (e.g., cardiac output) and markers of shock (e.g., lactate) recovered to pre-trauma levels in andexanet-treated groups. Clinically and macroscopically, no adverse events were observed.

In this study, andexanet effectively and safely reversed apixaban anticoagulation and reduced BL induced by severe trauma under anticoagulation. The bolus alone had a similar impact on survival and BL as the bolus+infusion regimen in this lethal porcine model.

Current guidelines for management of pain, agitation, and delirium in mechanically ventilated patients in the intensive care unit (ICU) recommend an analgesia-first approach to sedation management. However, these guidelines are derived from non-neurologic patient populations leaving uncertainty in their generalization to this population. The purpose of this study was to evaluate implementation of an analgesia-first sedation clinical pathway in the neuroscience ICU.

A single-center cohort study was performed within the neuroscience ICU including patients mechanically ventilated for greater than 48 hours over a time period of three months before and after clinical pathway implementation. Providers were educated on the pathway with emphasis on frequent assessment of Richmond Agitation-Sedation Scales (RASS), Critical Care Pain Observation Tool (CPOT), and Confusion Assessment Method-ICU (CAM-ICU) scores and systematic de-escalation of sedatives through adequate pain and delirium management. Outcome measures included frequency and magnitude of RASS, CPOT, and CAM-ICU scores, analgesic and sedative medication prescription/administration per day of mechanical ventilation (MV).

A total of 107 patients met inclusion criteria (67 pre-pathway and 40 post-pathway). There was no statistically significant difference in the median frequency of RASS (4.8 vs. 4.1) and CPOT (6.7 vs. 6.4) assessments per day of MV or in median RASS (-3 vs. -3) and CPOT (0 vs. 0) scores. Mean acetaminophen usage increased from 85.1% to 100% (p< 0.001) post-pathway implementation. There was no statistically significant difference in mean opioid or propofol usage, however a trend toward increased morphine and decreased propofol usage was observed post-pathway.

Analgesia-first sedation pathway implementation trended towards increased opioid analgesic and decreased sedative use, however only increased acetaminophen usage was significant. This highlights challenges in changing unit-based practices and future directions include focus on the frequency and reliability of pain, agitation and delirium assessment. Interdisciplinary coordination and communication remains necessary for effective unit-based practice changes.

Andexanet alfa (andexanet), a modified, recombinant human factor Xa (FXa) molecule, binds and sequesters FXa inhibitors. In a phase 2 study of apixaban, rivaroxaban, edoxaban, and enoxaparin in healthy volunteers, andexanet rapidly reversed pharmacodynamic markers of anticoagulation. Here, the ability of andexanet to reverse the anticoagulant activity of betrixaban was investigated.

In a randomized, double-blind, phase 2 study in healthy subjects, andexanet (n=12) or placebo (n=6) was administered intravenously following 80mg PO QD betrixaban to steady state (7 days). In Cohort 1 (andexanet bolus only), subjects (n=6) received a 800-mg andexanet bolus 3 hours after the last betrixaban dose (Day 7) or placebo (n=3). In Cohort 2 (andexanet bolus plus 2-hour infusion), subjects (n=6) received a 800 mg andexanet bolus 4 hours after the last betrixaban dose, followed by a 2-hour infusion of andexanet (8mg/min) or placebo (n=3). Endpoints included safety and pharmacodynamic markers of anticoagulation reversal.

Following treatment with betrixaban in Cohort 1, andexanet rapidly decreased anti-FXa activity from 29.9±11.6 to 6.5±4.5ng/mL, while the anti-FXa levels following placebo were largely unchanged (45.2±44.8 to 43.6±37.7ng/mL). Unbound betrixaban plasma concentration decreased from 12.3±5.6 to 3.6±2.7ng/mL with andexanet, but remained constant following placebo administration (18.3±17.9 to 19.3±18.1ng/mL). Similar results were observed in Cohort 2 following andexanet bolus (2 minutes after bolus), and the effects were maintained during the 2-hour infusion of andexanet. For Cohort 1, thrombin generation was restored in 6/6 (100%) and 1/3 (33.3%) of andexanet-administered and placebo subjects, respectively. For Cohort 2, thrombin generation was restored in 5/6 (83.3%) of andexanet subjects versus 1/3 (33.3%) of placebo subjects. Andexanet was well tolerated; there were no thrombotic events or serious/severe adverse events.

Andexanet was well tolerated and rapidly reversed anticoagulation effects of betrixaban in healthy subjects. These and other studies indicate that andexanet could be a universal antidote for FXa inhibitors.

Andexanet alfa (AnXa), a recombinant human FXa molecule, reverses the anticoagulant activity of FXa inhibitors. In studies of healthy volunteers, AnXa showed dose-dependent reversal of direct and indirect FXa inhibitors in tissue factor (TF)-initiated thrombin generation (TG). We compared rivaroxabaninduced inhibition of TG initiated via the extrinsic pathway (TF) versus intrinsic pathway (non-TF).

TF-initiated TG was measured using a calibrated automated thrombogram (CAT) and PPP-reagent. Non-TF-initiated TG was measured using CAT and Actin FS. Anti-FXa activity was measured using an anti-FXa chromogenic assay. Pooled plasma was spiked with rivaroxaban or rivaroxaban+AnXa; TG, anti-FXa activity, and clot formation were measured. For low TF-initiated clot formation, thromboelastography profiles were measured.

AnXa alone had minimal effect on endogenous thrombin potential (ETP). AnXa fully reversed rivaroxaban-induced anticoagulation in the Actin FS assay, independent of AnXa-TFPI interaction. Modulation of TF activity was assessed by correlating ETP versus anti-FXa activity with rivaroxaban or rivaroxaban+AnXa. Rivaroxaban dose-dependently inhibited TF-initiated TG as anti-FXa activity increased. At similar anti-FXa levels, rivaroxaban+AnXa had higher ETP than rivaroxaban alone, but not in the Actin FS assay. Clot formation was studied in plasma using thromboelastography without rivaroxaban. AnXa did not affect thromboelastography parameters, with/without recombinant tissue plasminogen activator (rtPA). When low TF initiated clot formation without rtPA, AnXa reduced the thromboelastography-R parameter, but not maximum amplitude. The fibrin clot was lysed at low rtPA, resulting in well-segregated coagulation and fibrinolysis. With the optimal rtPA, fibrin clots formed at each TF concentration were compensated by the fibrinolytic activity of rtPA.

Without a FXa inhibitor, AnXa had minimal effect on TF or Actin FS-initiated TG with no direct effect on rtPA function. AnXa dose-dependently and completely reversed rivaroxaban-induced inhibition of TG initiated by intrinsic or extrinsic pathways, but had different effects on ETP due to the AnXa-TFPI interaction.

There is a growing body of evidence relating poor outcomes to off-hour management. Studies investigating the effect of overnight extubation (OE) have produced mixed results, and limited data is available for brain-injured patients. There may also be tendency to limit OE due to decreased staffing levels at night. We sought to determine the safety of OE and risk factor profiles associated with extubation failure (EF) in this cohort.

We conducted a retrospective review of mechanically ventilated patients admitted to a single-center in-house database. Exclusion criteria included limitations in care, tracheostomy placement, selfextubation, and death prior to extubation. The primary outcome was EF defined as non-elective endotracheal intubation within 72 hours. EF rates were compared between daytime (6AM -5:59PM) and overnight (6PM -5:59AM) extubation cohorts. In-hospital mortality served as a secondary outcome.

Amongst 997 identified patients, 783 (78.5%) underwent daytime extubation (DE) and 214 (21.5%) OE. EF was indifferent between DE and OE (10.1% and 8.4% respectively; p=0.46). However, multivariable adjustment for clinical severity indicators suggests higher EF for OE (OR: 1.16, CI: 0.65-2.06; p=0.61). Compared to DE, OE was more likely performed in elective post-operative patients (29.9% vs 21.1%; p=0.006) with lower APACHE-II scores (median 11 vs 13; p=0.002), and shorter durations of MV (median 0.3 vs 1.4 days; <0.001). Higher APACHE-II score, longer duration of MV, and admission diagnoses of acute vascular injury or neuromuscular disease were associated with EF. There was no difference in mortality (p=0.91).

In our cohort, OE was not associated with increased EF or mortality. Our results suggest that OE can be performed safely if standard extubation criteria are met in low-risk patients. These data provide a basis for subsequent more robust studies.

Case series have reported reversible left ventricular dysfunction, also known as stress cardiomyopathy or Takotsubo cardiomyopathy, in the setting of acute neurological diseases such as subarachnoid hemorrhage. The nature of the association between various neurological diseases and Takotsubo remains incompletely understood.

We performed a cross-sectional study of all adults in the National Inpatient Sample, a nationally representative sample of U.S. hospitalizations, from 2006-2013. Our exposures of interest were primary diagnoses of acute neurological disease, defined by ICD-9-CM diagnosis codes. Our outcome was a diagnosis of Takotsubo cardiomyopathy. Binary logistic regression models were used to examine the associations between our prespecified neurological diagnoses and Takotsubo cardiomyopathy after adjustment for demographics.

We identified 18,321,298 adults with a primary acute neurological diagnosis and 231,416,640 patients admitted to the hospital without a primary acute neurological diagnosis. Among neurological diagnoses, subarachnoid hemorrhage (odds ratio [OR], 9.20; 95%CI, , status epilepticus (OR, 6.31; 95% CI, 5.21-7.63), transient global amnesia (OR, 2.71; 95% CI, 1.66-4.43), and meningoencephalitis (OR, 2.36; 95% CI, 1.91-2.92) were most strongly associated with Takotsubo cardiomyopathy. Weaker associations were present for ischemic stroke (OR, 1.18; 95% CI, 1.08-1.30) and migraine headache (OR, 1.44; 95% CI, 1.31-1.59). Intracerebral hemorrhage and Guillaine-Barre syndrome were not significantly associated with Takotsubo cardiomyopathy. In our multivariable model, female sex was significantly associated with Takotsubo (OR, 5.09; 95% CI, 4.85-5.35).

We found associations with Takotsubo cardiomyopathy for several acute neurological diseases besides subarachnoid hemorrhage.

Gram-Negative Meningoventriculitis (GNMV) causes significant morbidity and mortality. In addition to intravenous antibiotics, intra-thecal (IT) or intraventricular (IV) antibiotics may be used to treat central nervous system (CNS) gram-negative infections, including multi-drug resistant GNMV. There are limited studies on the effect of direct CNS administration on cerebrospinal fluid (CSF) cultures, CSF routine parameters and other clinical outcomes.

We conducted a retrospective chart review of all patients who received IT or IV antibiotics for GNMV since 2009. Demographics, source of illness, severity of illness (SOFA), intravenous and IT/IV antibiotic choice and CSF microbiological, drug level and routine analysis were collected. Time to pathogen clearance from CSF culture was also measured.

There were 32 inpatient encounters where IV/IT antibiotics were given for GNMV during our study period, of which 24 were cared for in a neurosciences intensive care unit. Antibiotics utilized were: Gentamicin (20), Colistimethate sodium (7), Amikacin (4), and Tobramycin (1). The most common pathogens were P. aeruginosa (8), K. pneumoniae (8), Enterobacter sp. (7) and E. coli (5). Prior to dosing, median CSF white blood cell (WBC) count, protein and glucose was 2804/uL, 201 mg/dL and 25 mg/dL, respectively. IT/IV Antibiotics were dosed a median of 4 times per patient and clearance of CSF culture occurred in a median of 5 days. There were significant changes in CSF WBC (p< .001), protein (p<.001) and glucose (p<.001) between the first and last dose of IV/IT antibiotics. Twenty-five (78.1%) patients survived to discharge, 20 (62.5%) were confirmed alive at 6 months. Patients who survived to discharge went to rehabilitation (5), home (5), long-term acute-care (9) and skilled nursing facility (6).

IT and IV antibiotics significantly improve CSF WBC, protein and glucose profiles and clear CSF cultures in patients with GNMV. IT and IV administration may provide additional benefit to systemic therapy.

Gram-positive organisms are the most common cause of meningo-ventriculitis. Systemic antimicrobial therapy may fail to achieve adequate cerebrospinal fluid (CSF) concentrations, particularly against organisms with higher minimum inhibitory concentrations, such as MRSA and VRE. Direct intraventricular (IV) or intra-thecal (IT) administration may be beneficial as they can facilitate high CSF levels at the site of infection. There are limited studies on the effect of direct central nervous system (CNS) administration of antibiotics on CSF cultures, CSF routine parameters and other clinical outcomes.

We conducted a retrospective chart review of all patients who received IT/IV antibiotics for grampositive meningo-ventriculitis since 2009. Demographics, source of illness, severity of illness (SOFA), intravenous and IT/IV antibiotic choice and CSF microbiological, drug level and routine analysis were collected. Time to pathogen clearance from CSF culture was also measured.

There were 30 inpatient encounters where IV/IT antibiotics were given for gram-positive meningoventriculitis during our study period, of which 23 were cared for in a neurosciences intensive care unit. Antibiotics utilized were: Vancomycin (28) and Daptomycin (2). The most common pathogens were Staphylococcus sp. (15), Enterococcus sp (5), and Streptococcus sp (8). Prior to dosing, median CSF white blood cell (WBC) count, protein and glucose was 430/uL, 117mg/dL and 47mg/dL, respectively. IT/IV Antibiotics were dosed a median of 4 times per patient and clearance of CSF culture occurred in a median of 3 days. There were significant changes in CSF WBC (p< .001), protein (p<.001) and glucose (p=.045) between the first and last dose of IV/IT antibiotics. Twenty-nine (96.7%) patients survived to discharge, 19 (63.3%) were confirmed alive at 6 months.

IT and IV antibiotics significantly improve CSF WBC, protein and glucose profiles and clear CSF cultures in patients with gram-positive meningo-ventriculitis. IT and IV administration may provide additional benefit to systemic therapy.

Use of prothrombin complex concentrate (PCC) for urgent reversal of anticoagulant associated coagulopathy is increasing, and at the University of Illinois Hospital (UIH), an anti-thrombotic reversal guideline was developed in May 2016 in order to assist licensed practitioners in choosing the appropriate reversal agent, optimal dosing, and improve timely administration PCC. The current study examined the safety and efficacy of PCC used for the urgent reversal of anticoagulant associated coagulopathy before and after the development of the anti-thrombotic reversal guideline.

This was a retrospective chart review of adult patients who received PCC as the only hemostatic agent at the UIH from Jan 2008 to April 2017. The primary endpoint was hemostasis and secondary endpoints included thromboembolic events and time to PCC administration.

There were 21 and 17 patients who received PCC before and after the anti-thrombotic reversal guideline, respectively. Frequent cause of coagulopathy was warfarin (81% and 76%, respectively), and frequent indication for PCC was acute intracranial hemorrhage (81% and 76%, respectively). 3-factor PCC was more frequently used before the guideline and 4-factor PCC was more frequently used after the guideline. In patients presenting with warfarin induced major bleeding, target INR <1.4 was achieved in 71% and 62% of these patients before and after the guideline, respectively. Clinical assessment of bleeding cessation from direct oral anticoagulant (DOAC) therapy was difficult to assess. Thromboembolic event was observed in 38% and 6% of the patients, respectively. Median time to PCC administration from its initial order was 107 minutes and 80 minutes, respectively.

Hemostasis was similarly observed in the warfarin group before and after the development of reversal guideline, but more thromboembolic events were observed before the reversal guideline. In order to further reduce the PCC administration time, a change in workflow has been made to administer PCC in timely manner.

Dexmedetomidine, a selective alpha-2 adrenoreceptor agonist inhibiting sympathetic neuronal activity, is a mild sedation agent. Two recent case reports showed reduced norepinephrine (NE) requirement in septic shock with clonidine, a less selective alpha-2 agonist. Increased vasopressor responsiveness (VR) was also observed with dexmedetomidine in cardiovascular surgical settings.

Sympatholytic effects of the alpha-2 agonists reverse vascular desensitization due to high levels of sympathetic activity in sepsis. Depletion of intra-neuronal catecholamines with reserpine has shown to increase VR. In septic sheep infused with Escherichia coli, clonidine reduced renal sympathetic tone and restored VR. Additionally, alpha-2 agonists have shown to decrease pro-inflammatory cytokines and reduce mortality, improve capillary perfusion deficit, and lower arterial lactate in animal sepsis models. A prospective trial in human septic shock is in the pipeline. We report decreases in vasopressor requirement with initiation of dexmedetomidine in two patients with brain injury.

A 51-year-old woman presented with a high-grade subarachnoid hemorrhage and concomitant reverse Takatsubo cardiomyopathy. Her clinical course was complicated by septic shock secondary to aspiration pneumonia at admission. When dexmedetomidine was started after 36 hours of NE infusion, a steady decrease in NE dosage was observed until its discontinuation. Increased VR was also observed in a 33year-old man being treated for new onset refractory status epilepticus. On hospital day 10, the patient continued to have stimulus-induced seizures on ketamine, midazolam and pentobarbital infusions and required NE to maintain an adequate mean arterial pressure. When dexmedetomidine was added, a decrease in NE infusion was observed within an hour and continued for six hours until the patient no longer required vasopressor therapy.

These findings are consistent with aforementioned reports of restored VR by alpha-2 agonists in septic shock, and warrant further investigation of possible beneficial effects of attenuated hyperadrenergic state conferred by alpha-2 agonists in various neurocritical care settings.

Decreasing the amount of time a patient remains intubated has been shown to reduce multiple negative outcomes. By extubating these patients earlier, risk of infection, prolonged immobility, and delirium are reduced. In early 2016, this NSICU was chosen to participate in the Society of Critical Care Medicine's ICU Liberation Collaborative. The collaborative was focused on implementation of the ABCDEF Bundle or ICU Liberation. The successful implementation of the bundle led to a decrease in the amount of time neurocritically ill patients were intubated.

The bundle elements began to be rolled out in June 2016 (end of 1st quarter). Included in the bundle's roll out was the creation of a respiratory clinical specialist role to help the interprofessional team with the respiratory components of the bundle. This role was a full time respiratory care practitioner who was dedicated to the NSICU and helped to ensure standards were being met. Additionally, as a part of the bundle's implementation, a spontaneous awakening trial and spontaneous breathing trial algorithm was developed and initiated. This algorithm relied on interprofessional collaboration between nursing and respiratory therapy with communication to the provider and was rolled out in September 2016 (end of 3rd quarter).

Ventilator O/E for 2016: 1st quarter-0.953, 2nd quarter-0.989, 3rd quarter-0.827, 4th quarter-0.798 Ventilator O/E for 2017: 1st quarter-0.844, 2nd quarter-0.700

The bulk of the research conducted that proved the benefits of the bundle elements has been completed in medical and/surgical patient populations. The neurocritical care patient population is very specialized and has several nuances that may impact the way the various elements need to be implemented. Through this process, we have found that the techniques suggested within each element can positively impact the neurocritical care patient population.

The Cognitive Reserve Hypothesis refers to inter-individual differences in the ability of patients to cope with brain pathology. Cognitive reserve can be measured by surrogate markers such as education and occupation and has shown to be an important predictor of outcomes in Alzheimer disease, multiple sclerosis and traumatic brain injury. In this prospective longitudinal cohort study we determined whether cognitive reserve measured as number of years of education and employment status predicted 3-month functional outcome of NCC patients.

Demographic and clinical data, including number of years of education and occupational status, were collected. At three months after discharge, Glasgow Outcome Scales (GOS) were collected via telephone from patients or surrogate respondents. GOS scores were categorized into 'Good' or 'Poor' outcome (GOS 1-3).

From March 2016 to July 2016, 35/83 patients with 3-month follow-up data were included. Mean age was 56 ± 19 years, 12 (34%) were male, with stroke as the predominant admitting diagnosis.The two groups with good vs poor outcomes did not differ in age, gender or race in univariate analysis although employment status was statistically different in the two groups. In multivariate logistic regression neither employment nor education was a significant predictor of good vs poor outcome (P = 0.34, P = 0.88).

Prognostication in neurocritical care patients is difficult. The effect of cognitive reserve needs to be studied further. Our current sample size is small and as enrollment continues, we will determine the relationship between cognitive reserve and 3-month functional outcome.

Fever commonly occurs in patients with spontaneous intracerebral hemorrhage (sICH). However, it is non-infectious in the majority of cases. Blood cultures (BCx) are often obtained as part of a fever workup, yet their utility may be limited and false-positive results may potentially compromise patient care. We hypothesized blood cultures in the first 48 hours would more likely be false-positive.

We performed a retrospective chart review of patients admitted to a tertiary medical center with a diagnosis of spontaneous intracerebral hemorrhage. Patients with secondary causes of ICH as well as institution of comfort measures only were excluded. Data obtained included demographics, clinical parameters of ICH and blood culture results. Blood culture results and charts were reviewed for adjudication of false-positive and true-positive cultures.

Of 654 included patients with sICH, 226 patients (34%) had 1065 blood cultures obtained. 52 cultures were positive, of which 23 were classified as false-positive and 29 as true positive. False positive results were more common in the first 2 days (17 vs. 6), while true positive results were more common after the first 48 hours (12 vs. 17) (p= 0.018).

Early blood cultures in patients with sICH are more commonly non-infectious. In line with prior published data, our results demonstrate the high cost and limited yield for blood cultures within the first 48 hours.

Predictive energy expenditure (PEE) equations are commonly used in lieu of indirect calorimetry (IC) due to cost and limited resources; however, these equations may not be as accurate as IC in estimating resting energy expenditure (REE) in critically ill patients. The purpose of this study is to compare PEE and measured energy expenditure (MEE) in critically ill adults with acute brain injury.

This was a retrospective review of adult patients admitted with acute brain injury between May 1st, 2014 and April 1st, 2016 who had IC performed. Three predictive equations (PE), Harris Benedict (HBE), Penn State University, and Mifflin St Jeor (MSJ), were used in comparison to IC results. Subgroup analyses included a modified ASPEN weight-based equation, stratifying patients based on BMI and type of acute brain injury.

144 patients met inclusion criteria. Comparing the PEE estimated by the three predictive equations to the MEE from IC found no significant difference. High degrees of interpatient variability were discovered in each ANOVA analysis, with standard deviations ranging from 17 -29%. Despite no difference found among PEE and MEE, Pearson's correlations indicated weak associations when HBE, Penn State, and MSJ were individually compared to MEE (r-values = 0.372, 0.409, and 0.372, respectively). In patients with a BMI < 30 kg/m2, a significant difference was found (p-value=0.0006) with PEE underestimating the REE. Additionally, In aneurysmal subarachnoid hemorrhage a significant difference was observed between PEE and MEE( p-value=0.005).

The results of this study highlight the importance of using IC whenever feasible due to the interpatient variability of the REE of critically ill patients with acute brain injury. Although predicative equations appear to have similar estimations as IC, interpatient variability warrants more accurate measurement with IC to optimize nutrition in patients with acute brain injury.

Introduction 4-Factor prothrombin complex concentrate (PCC) should be administered as soon as possible for reversal of anticoagulation in the setting of life-threatening bleeding or urgent procedures. Limited information is available on the safety, efficacy, and time to administration of PCC when administered at high infusion rates.

On March 21, 2017 Grady Health System implemented a rapid PCC administration strategy while attempting to reduce times from order entry to administration as a quality improvement initiative. This IRB-approved, retrospective evaluation includes PCC administrations 90 days pre-and post-protocol implementation. After protocol implementation, PCC doses were prepared in up to four, 60-mL syringes, dependent on the ordered dose. Each syringe was administered over 2 minutes, not exceeding a rate of 750 IU/minute. The primary objective of this study is to evaluate the safety of a rapid administration strategy for PCC. Secondary objectives include turn-around times and effectiveness of INR reversal in patients previously on warfarin.

Results 52 unique PCC administrations were identified: 29 administrations in the pre-cohort and 23 in the postimplementation cohort. Most PCC administrations were in the setting of spontaneous or traumatic intracranial hemorrhage. There were no infusion-related adverse events documented with the exception of a possible PCC infiltration post-implementation which resolved with supportive care only. The median order entry to administration time was higher in the post-implementation group (52 vs. 42 minutes). 18 administrations in the pre-cohort and 11 administrations in the post-cohort were for warfarin reversal. A greater percent of patients previously on warfarin reversed to an INR < 1.4 in the post-cohort compared to the pre-cohort, 81.8% vs 72.2%, respectively.

This retrospective evaluation suggests that rapid intravenous push administration of 4-factor PCC is safe and effective. Time to administration was longer after implementation of rapid PCC administration and may have been due to operational limitations.

ICU readmission is defined as a return to the ICU during the same hospital admission. There are multiple studies related to medical and general surgical recidivism, however there is limited data on ICU readmissions following spine surgery. The aim of this study was to evaluate factors associated with ICU readmissions following spine surgery.

Patients requiring ICU admission following spine surgery from June 2013 to June 2017 were studied. Variables included age, gender, ICU and hospital disposition, ICU and hospital length of stay, BMI, comorbidities, surgical location, number of previous surgeries and vertebra manipulated, estimated blood loss, post op blood transfusions, and cause of readmission. A 1:1 matched control group based on age, BMI and location of surgery was identified.

Thirty-two patients required readmission following spine surgery during the study period. There was a higher prevalence of preoperative atrial fibrillation in the readmission group (20% vs. 5%, p=0.04). EBL (1041 vs 1214 ml, p=0.9) and lowest MAPs (60 vs 59.2 mmHg, p=0.7) were not significantly different in the two groups. We found a higher mortality rate (22% vs 0%, p=0.01), longer ICU (60.7 vs 39.5 hours, p=0.06) and hospital LOS (17.28 vs 7.87 days, p= 0.001) in the readmission group. Respiratory distress (25%) was the most common reason for readmission followed by cardiovascular instability (13%). Discharge rates to inpatient rehabilitation and nursing facilities were similar for both groups; however 42% of the control group went directly home as opposed to 19% of the readmission group.

Complex spine patients who experience ICU recidivism have a longer hospital stay and incidence of death within 5 years of their index procedure. They are less likely to be discharged home. Preoperative a-fib correlates with increased incidence of readmission to ICU post-operatively. Further studies are needed looking at post operative fluid and pain management.

To demonstrate the feasibility of exenatide infusion for hyperglycemia following acute brain injury.

Adult patients with acute brain injury and having two blood glucose concentrations >150 mg/dL and was administered within 48 hours of admission and continued per protocol for a maximum duration of 48 hours. The primary endpoint was feasibility (<25% of subjects experiencing severe hypoglycemia (<40 -180 mg/dL). Descriptive endpoints were also collected. Data is presented as medians [interquartile range] or percentages.

A total of eight patients received exenatide (age 64.0 years [58.8, 67.8], 87.5% male, 50.0% Caucasian, 50.0% history of diabetes, A1c 6.5% [5.5,7.3]). Admitting diagnoses were intracerebral hemorrhage (n=3), acute ischemic stroke (n=3), subarachnoid hemorrhage (n=1), and subdural hematoma (n=1). Glascow coma score was 10.5 [7.0, 14.0] and Sequential Organ Failure Assessment was 2.0 [1.0, 4.0]. Based upon predefined criteria, feasibility was met with 0% of subjects experiencing severe hypoglycemia, 87.5% achieving the blood glucose goal, and 0% experiencing nausea requiring discontinuation. Blood glucose was controlled during the 48-hour exenatide infusion ( 

Intravenous exenatide infusion is feasible for the treatment of hyperglycemia following acute brain injury.

Extubation failure remains a common complication in critical care patients, and is associated with increased intensive care unit and hospital length of stays, hospital costs, morbidity and mortality. The most common cause of reintubation is laryngeal edema, often identified by the presence of a high pitched inspiratory whistling sound known as post-extubation stridor (PES). Providers in the neurocritical care unit (NCCU) at a large urban academic medical center noted higher than normal rates of PES.

To reduce the rates of PES and reintubation without delaying extubation, a clinical pathway was created by an interdisciplinary team. The purpose of the pathway was to aid in the identification of patients expected to develop PES and guide prophylactic treatment. Prior to project implementation, all providers in the NCCU completed hands on training with practice in completing the pathway in the form of a checklist. During the 12 week implementation phase, checklists were completed on all intubated patients daily during rounds.

During the 12 week trial, there were a total of 606 ventilator days. There were 531 completed checklists, yielding an 87.62% compliance rate for utilization of the clinical pathway. Of the 56 patients who were extubated during the trial, 54 had a checklist completed, generating 96.43% compliance on the day of extubation. A chi-square analysis was performed to evaluate outcomes following all non-palliative extubations during the 12 week pre-implementation (n = 43) and post-implementation (n = 56) periods. Implementation of the pathway was associated with a statistically significant reduction in rates of PES (1, N = 99) = 6.16, p<0.02, reintubation (1, N = 99) = 5.54, p<0.02 and reintubation due to PES, (1, N = 99) = 8.32, p<0.005.

The clinical pathway implemented in our NCCU was safe and effective in reducing rates of PES, reintubation and reintubation due to PES.

Agency for Healthcare Research and Quality (AHRQ) identified postoperative deep vein thrombosis (DVT) or pulmonary embolism (PE), also commonly referred to as venous thromboembolism (VTE), as one of the complications acquired in the hospital and thus developed a mechanism to report its rate using administrative data. Postoperative VTE rate reduction became top priority for the University of Illinois (UIH) due to its high yearly rate, especially among patients in the Neurosciences Intensive Care Unit (NSICU). Therefore, a quality improvement team in the NSICU implemented VTE bundle and analyzed its effect on the VTE rate.

The VTE bundle was initiated on all neurosurgery and neurology patients admitted to the NSICU since March 2016. VTE bundle included lower extremity Doppler ultrasound within 24 hours of admission, VTE education provided to patient or family member within 48 hours of admission, and daily surveillance on proper use of mechanical sleeves and the mechanical device, low-dose heparin initiation and maintenance therapy, and documentation of activity status. The nursing staff were encouraged to follow the early mobilization protocol.

Mean VTE rate was 52.9 per 1000 cases approximately 1-year before and 33.6 per 1000 cases approximately 1-year after the implementation of VTE bundle. The rate of compliance was high on all aspects of VTE bundle, especially on correct placement of IPC sleeve >85%; functioning IPC device >90%; low-dose heparin >90%; documentation of activity status >94%. No adverse effects were noted (i.e., skin breakdown, major bleeding) during the study period.

This was the first time in 3 years at UIH, the postoperative VTE rate was reduced among NSICU patients based on the AHRQ reports. The reduction may partly be attributed to the implementation of VTE bundle; however further evaluation need to be performed to determine the effect size of VTE bundle.

Increasing evidence suggests that large volume infusions of 0.9% sodium chloride (NaCl) for resuscitation are associated with hyperchloremic metabolic acidosis and renal vasoconstriction leading to an increased risk of acute kidney injury (AKI). In patients with neurologic injury, hypertonic (1.5% or 3%) NaCl or sodium acetate (NaAcetate) may be required for therapeutic hypernatremia, treatment of cerebral salt wasting or elevated intracranial pressure. The primary aim of this study was to determine the incidence of AKI in neurologically injured patients receiving intravenous hypertonic NaCl and in those who were switched to hypertonic NaAcetate based on provider preference.

This single-center, retrospective study compared patients that received only hypertonic NaCl to patients that were switched to NaAcetate. Data was collected to assess renal function, hyperchloremia, and metabolic acidosis.

A total of 301 patients were screened and of those 142 were included. The patients who were switched from NaCl to NaAcetate (n=45) had a greater incidence of AKI (27% vs. 6%, p<0.001) and hyperchloremia (56% vs. 29%, p = 0.01) compared to patients who received only NaCl (n=97). The incidence of metabolic acidosis was increased but not statistically significant (15% vs. 11%, p = 0.791). On average, hypertonic NaCl was switched to hypertonic NaAcetate on day 3 of treatment with a mean chloride of 115.7 mEq/L at the time of the switch. There was no statistical difference in the administration of nephrotoxic antibiotics, mannitol, vasopressors, or contrast dye between the two groups. The receiver operating characteristic (ROC) analysis demonstrated that if a patient received greater than 2055 mEq of chloride over 7 days they were more likely to develop AKI (sensitivity 72%, specificity 70%, p=0.002, AUC 0.70).

Neurologically injured patients receiving hypertonic sodium therapy requiring a switch to hypertonic NaAcetate had an increased incidence of hyperchloremia and AKI.

In-hospital complications following acute neurological injury has been a topic of extensive research to help reduce the morbidity and mortality among the patients. However, the incidence and prevalence of in-hospital infections following an acute neurological injury at the national level has never been studied. The aim of our study is to determine the frequency and prevalence of in-hospital complications among different patient groups admitted following acute neurological injury.

We identified patients with primary diagnosis of ischemic stroke (IS), subarachnoid stroke (SAH), intracerebral hemorrhage (ICH), status epilepticus (SE), meningitis, encephalitis and traumatic brain injury (TBI) from nationwide inpatient database (2011-2014) through using the respective ICD-9 codes. Common in-hospital complications among the above-mentioned diagnoses through using their respective ICD-9 codes

Patients with primary diagnoses of IS (n=1855297), SAH (n=101576), ICH (n=254758), SE (n=190701), Meningitis (n=46067), Encephalitis (n=23839), TBI (n=1142155) were identified. In-hospital events such as myocardial infarction (MI), sepsis, pneumonia, deep venous thrombosis (DVT), pulmonary embolism (PE), urinary tract infections (UTI), and GI bleed were identified and compared among different patient groups. Patients with SE were noted to experience higher systemic complications, MI (3.6%), sepsis (11.2%), pneumonia (8.6%), DVT (1.7%), UTI (16.2%), GI bleed (0.41%). Patients admitted with meningitis had a higher incidence of sepsis (20.5%), pneumonia (9.0%), DVT (2.2%), PE (1.5%) and UTI (12.7%) compared to the other groups. UTI was the most common in-hospital complication observed.

Based on our analysis, we report a higher incidence of urinary tract infections among all patients admitted following acute neurological injuries. Patients with primary diagnosis of status epilepticus experienced more systemic complications compared to the other diagnoses.

Macroglossia is a phenomenon that has been documented in association with prolonged neurosurgical procedures, brainstem injury, phenobarbital administration, and venous/lymphatic congestion of the tongue. However, exact causation of this condition in the neurocritical care population remains unclear. Patients with macroglossia face significant risk for airway compromise. No interdisciplinary patient safety and management protocol exists.

Patients admitted to two Neuro ICU's within a single health system between 2012-2017 were reviewed. Twenty-five patients with macroglossia were identified. An interdisciplinary patient management protocol was created, instituting airway safety standards, oral care directives, and interventions to promote symptom resolution. Early consultation to Oral and Maxillofacial Surgery and consideration of early tracheostomy was recommended.

Seventeen patients (68%) were women. Age ranged from 20-81 years. The majority (16/25) of patients were African American. Primary diagnoses included status epilepticus (12/25) and stroke (1 SAH, 4 AIS, 6 ICH). Nineteen patients received antiepileptic medications before diagnosis. Average GCS at symptom onset was 5.8 [3] [4] [5] [6] [7] [8] [9] [10] [11] and at time of discharge was 8.9 [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] . Median symptom onset was hospital day 5 [0-39]. Twenty patients (80%) required tracheostomy. Nine (36%) experienced symptom resolution by hospital discharge. Two patients received botulinum toxin injection; both experienced symptom resolution. Lingual massage was performed in two patients; in both patients, tongue swelling resolved. Tongue lacerations occurred in 10/25 patients (40%), although most were observed following macroglossia onset, ruling out trauma as an inciting event. Chlorhexidine oral rinse was discontinued for all except five patients due to concern for angioedema. Endotracheal tube was dislodged in two patients, complicating reintubation, although successful. No trend in pre-existing allergies or antibiotic regimen was apparent.

Macroglossia is a relatively uncommon but high-risk condition in the Neuro ICU that warrants further study. Care of patients with macroglossia should be standardized in order to ensure airway safety. An interdisciplinary approach is recommended.

One of the biggest challenges of magnetic resonance imaging (MRI) examination is the acquisition of high-quality diagnostic images, as it requires the neurological intensive care unit (NICU) patients to keep still for a significant time. In situations with poor patient cooperation, unplanned sedation is inevitable, which can lead to complications such as desaturation and hypotension. We investigated the incidence and factors related to complicated MRI examinations (MRI-c) in patients admitted to the NICU.

We designed a retrospective study to review the data of 218 patients who had an attempt to undergo brain MRI during stay in the NICU between July 2014 and August 2016. The MRI-c group was defined when a patient met one of following criteria: 1) required sedation for MRI examination due to irritability 40 mmHg or required inotropic agents, 4) developed cardiac or respiratory arrest.

Of 218 patients, 66 (30.3%) developed MRI-c. The most common cause of MRI-c was unexpected irritability at the MRI room. Among patients with MRI-c, 62 (93.9%) patients required unplanned sedation; 9, desaturation; 6, hypotension; none, cardiac or respiratory arrest. Higher APACHE II scores (p = 0.031) and lower GCS scores (p = 0.047) on admission and use of sedative agents during critical care in the NICU were associated with MRI-c (p < 0.01). In addition, patients with MRI-c had longer MRI scan time than those without MRI-c (p = 0.004).

Many of neuro-critically ill patients undergo unsafe MRI scans. Our findings suggest that severity of illness and use of sedative agents during management in the NICU were factors related to MRI-c.

Introduction: Fulminant hepatic encephalopathy (FHE) with diffuse cerebral edema has dismal prognosis if transplantation is not performed. Novel therapeutic interventions may change this outcome.

We reviewed all cases with FHE admitted to our hospital since 2008. In 2010, we developed a multidisciplinary management protocol, mandating transfer of patients entering grade 3 from other ICUs to the Neurosciences-ICU (NICU) for intracranial pressure (ICP) management. Multiple interventions were utilized including coagulopathy reversal with Factor VII and prothrombin complex concentrate (PCC, Kcentra), ICP device placement, osmotherapy, aggressive ammonia lowering regimen with lactulose and rifaximin, early renal replacement therapy, mild hypothermia for refractory ICP, in conjunction with liver transplantation candidacy investigation.

Results: Twenty-four patients (19 women, mean age of all patients 40 years) were admitted; seven were managed in the MICU/SICU and 17 in the NICU. The etiology of FHE was acetaminophen toxicity in 72% of patients. The Model for End-Stage Liver Disease (MELD) admission scores and liver enzymes between the MICU/SICU and the NICU were not different (Mann-Whitney test). Although the NICU admission ammonia level was higher than the MICU/SICU (168.75 vs 99.50, p = 0.00), the lowest achieved ammonia was lower in the NICU (41.31 vs 78.13, p = 0.022, Mann-Whitney). Patients received ICP monitoring (all in the NICU plus 2 in the SICU) and the highest ICP recorded was 120 mm Hg. The preand post-coagulation reversal INR were 3.37 and 1.3, p=0.031, Wilcoxon test). Seven patients in the NICU received hypothermic treatment. Mortality in the MICU/SICU was 85.7% (6/7) and in the NICU 41.1% (7/17), p = 0.13 (chi square test).

Conclusion: A multidisciplinary approach centered around Anti-cerebral edema protocol-driven management based on novel interventions may improve the outcome of patients with FHE.

Catheter-associated urinary tract infections (CAUTI) are among the most common health-care associated infections (HCAIs), (Gould, 2016) . Neurological patients in the critical care setting are particularly at risk for CAUTI due to cognitive, motor, and sensory deficits. In the Neuro Intensive Care Unit, despite following recommended CAUTI reduction bundle guidelines, CAUTI rates continued to rise over the last five years with rates reaching 6.45 per 1000 catheter days. In January of 2017, the unit implemented a CAUTI Taskforce to perform a literature review of best practices and subsequent 1:1 peer training and education targeting CAUTI reduction.

In an analysis of organisms causing the infections, E. coli and Enterococcus bacteria accounted for more than 50% of CAUTIs on the unit. The taskforce (comprised of 13 staff nurses) focused on fecal management, proper cleaning technique, and proper indications of indwelling urinary catheter necessity. Using training videos, indwelling urinary catheter care checklists, and real-time feedback on technique, the taskforce performed 1:1 training with bedside staff over four weeks. To ensure undivided attention, the taskforce worked in pairs enabling one trainer to teach and observe the staff member receiving training while the second trainer provided the necessary clinical duties for the trainee's patients.

After implementation, the CAUTI rate decreased to 3.43 for January-March 2017 and 2.83 for April-June 2017, lowering total CAUTI events to 23 for FY17 compared to 32 for FY16.

Implementing a 1:1 training program focused on fecal management, cleaning techniques, and appropriately timed catheter removal can reduce CAUTI rates in the neuro critical care setting.

Brain aneurysms can be treated with coil embolization or flow-diverting devices. Thromboembolism is a major complication of aneurysmal coil embolization, with an incidence as high as 28% . New flowdiverting devices have been designed to have a mesh with high coverage area and high flexibility to facilitate the redirection of blood flow. These features can induce blood stagnation and thrombosis. To reduce the risk of thrombosis, the common but unproven practice of dual antiplatelet therapy with aspirin and clopidogrel has been implemented from the cardiac literature. Despite some favorable outcomes, clopidogrel, "non-responsiveness" has been reported to be present in as low as 5% to as high as 56% making this agent not optimal. This will leave practitioners with other oral P2Y12 alternatives such as prasugrel and ticagrelor that have not been studied widely in this setting. It is therefore likely that controversy exists among practitioners regarding the use of optimal antiplatelet agents in neurointerventional procedures. We hypothesized that practices in regards with the use of oral antiplatelets in neurointerventional procedures are likely heterogeneous and different from state to state. By using an electronic survey, we would like to identify different practices surrounding the use of oral anti-platelets in neuro-endovascular centers in the United States.

An electronic survey will be distributed via the Web using Survey Monkey (Seattle, WA). The survey will be posted on the neuro-critical care society (NCS) web page. All practicing neuro ICU or stroke physicians, pharmacists, physician assistants, or nurse practitioners are eligible to respond to this survey. This survey is approved by the Johns Hopkins Hospital IRB and the NCS research committee.

8 centers have completed the survey at this point. The results will be analyzed after the closing date of survey (9/4/2017).

To be completed

Myasthenia Gravis (MG) Crisis and Guillain-Barre Syndrome (GBS) are immune mediated diseases that may require mechanical ventilation as part of their management if severe. Comparative analysis of outcomes in terms of length of stay, disability, and mortality between these two disease entities at national level is not reported

Mechanically ventilated patients with primary diagnosis of Guillain-Barre Syndrome and Myasthenia Gravis were identified from the Nationwide In-Patient Sample (NIS) database for the years 2012 to 2014

Mechanically Ventilated MG patients (n=2330, mean= 62+/-19.5 years) were older compared to GBS patients (n=2060, mean= 55.9 +/-20.0 years, p=0.001). Medical Co-morbidities were significantly higher in MG patients (diabetes mellitus, congestive heart failure, coagulopathy, chronic lung disease and dyslipidemia) whereas significantly higher nicotine dependence and alcohol abuse were noted in GBS. Significantly higher in hospital complications of pneumonia and urinary tract infection were noted in GBS. Disease severity measured by APDRG severity index and rate of treatment with intravenous immunoglobulin and plasma exchange was comparable. Length of stay (25.3 ± 18.2 days , p < 0.0001 ); hospital charges ( $353361.2 ± 293863.2 vs 232160.12 ± 222881.3 p = 0.001) ; moderate to severe disability ( 86.6% vs 46.2% p < 0.001) were significantly higher for GBS patient compared to MG. Inhospital mortality was comparable ( 8.7% GBS vs 8.6 % MG, p =0.93). In multivariate analysis after adjusting for confounders including treatment, myasthenia gravis patients had significantly less disability (OR 0.06 (95% CI 0.03-0.10) and shorter length of stay (OR 0.32, 95% CI 0.16-0.61).

Mechanically ventilated GBS patients have higher in-hospital complications, length-of-stay, and disability compared to MG. This may reflect a delay in diagnosis of GBS at admission and poor response to immunotherapy in certain GBS variants.

Betrixaban is an inhibitor of factor Xa (FXa) for prophylaxis of venous thromboembolism (VTE) in at-risk patients hospitalized for acute medical illness. A phase 3 trial (APEX) compared extended-duration anticoagulation with betrixaban to enoxaparin in acute medically ill patients; the effect of patient characteristics on population pharmacokinetics and exposure-response relationships is analyzed here.

Patients received betrixaban (35-42 days; n=3,759) or enoxaparin (10±4 days; n=3,754). The primary efficacy and safety endpoints were composite occurrence of VTE events and incidence of major bleeding, respectively. Betrixaban dose was 80mg PO QD (40mg PO QD for patients with severe renal insufficiency/requiring concomitant P-glycoprotein inhibitor). Pharmacokinetic samples were collected -5 hours or 10-30 hours after the most recent dose of study medication. Patient characteristics included age, sex, race, region, body weight, CrCl category, and specific P-glycoprotein inhibitor.

3,146 pharmacokinetic samples were analyzed. At 80mg, the projected concentration was 18.8ng/mL at 2 hours post-dose and 16.1ng/mL at 20 hours post-dose, showing a stable daily concentration. Coadministration of 2 P-glycoprotein inhibitors on the day of sampling more than doubled betrixaban concentration to ~35ng/mL at 20 hours post-dose. At 40mg, the projected concentration was 7.2ng/mL at 20 hours post-dose, indicating a greater-than-dose-proportional exposure relationship. Patient age, sex, weight, CrCl category, P-glycoprotein inhibitors, and region were significant covariates affecting betrixaban pharmacokinetics. The exposure-response relationship for the primary efficacy endpoint was not significant, but the relationship between betrixaban concentration and major/clinically relevant nonmajor bleeding was significant in multivariate testing (P=0.011).

The betrixaban pharmacokinetic profile exhibited stable serum concentrations with QD dosing. Several covariates had a 15%-20% effect on betrixaban concentration, but no effect on efficacy/safety. Betrixaban dose should be adjusted to 40mg for patients taking amiodarone or clarithromycin, but not other P-glycoprotein inhibitors.

Andexanet alfa is being investigated for reversal of anticoagulation by factor Xa (FXa) inhibitors. A pharmacokinetic/pharmacodynamics model, developed in healthy subjects, predicted the andexanet regimen required to reverse anticoagulation by FXa inhibitors. The current analysis validated the pharmacokinetic/pharmacodynamic model using interim data from the ANNEXA-4 study in patients with acute major bleeding.

In ANNEXA-4, an ongoing prospective, open-label study, bleeding anticoagulated patients received IV andexanet bolus (400 or 800 mg) followed by 120-minute infusion (4 or 8 mg/min). Anti-FXa activity was measured before andexanet administration (baseline), at end of bolus (EOB), at end of infusion, and at 4, 8, and 12 hours after infusion. The relationship between baseline anti-FXa activity and reversal in healthy subjects was derived from the pharmacokinetic/pharmacodynamic model and used to predict percent reversal for patients with acute major bleeding.

From the first interim analysis of ANNEXA-4, 73 patients (apixaban, n=39; rivaroxaban, n=34) had plasma levels available for model qualification, although 7 did not meet criteria for inclusion into safety and 27 did not meet criteria for efficacy analysis. The mean observed percent reversal of anti-FXa activity for rivaroxaban and apixaban was well predicted by the healthy subject pharmacokinetic/pharmacodynamic model; the point estimates fell within the 90% confidence intervals of predicted values. The percent reversal at EOB for rivaroxaban and apixaban were 74.4 [58.3-90.7] and 83.9 [75.3-92.5], compared with 76.3 and 84.1 predicted by the model. The predicted reversal closely fit the observed confidence intervals through the first 4 hours for rivaroxaban and apixaban, and extended through all evaluated time points for rivaroxaban and slightly outside of post-4-hour time points for apixaban, possibly due to higher baseline anti-FXa activity levels for apixaban.

The pharmacokinetic/pharmacodynamic model in healthy subjects closely predicted the extent of reversal of anti-FXa activity for apixaban and rivaroxaban in patients with major bleeding.

Risk factors and methods to predict extubation failure are well established for patients in Medical ICUs and Surgical ICUs. Literature on patients who fail extubations in Neurological ICUs is limited. The intention of this study was to collect descriptive information from patients with neurological injuries who failed liberation from mechanical ventilation.

Retrospective review of all patients with acute neurological injury who were admitted to our Neuro ICU and who required reintubation within 72 hours of discontinuation of mechanical ventilation between January 2012 -February 2017.

We identified 60 patients intubated primarily due to neurological pathology who required reintubation within 72 hours after initial extubation over a 5-year study period. The majority of reintubated patients (n=43; 71.7%,) had a positive fluid balance prior to failed extubation. Twenty-six of the reintubated patients had a concurrent underlying chronic cardiac and/or pulmonary disease. Five patients were placed on noninvasive ventilation post extubation. Low Glascow Coma Scale and absence of basic brainstem functions (gag and cough reflexes) was only minimally predictive of extubation failure. Most of our reintubated patients did not have significant supratentorial midline shift nor an insult to the posterior circulation or dominant hemisphere.

In patients with primary brain injury who required reintubation, a positive fluid balance prior to extubation may confer a lower rate of successful extubation. Lesion location and supratentorial midline shift may not be tightly associated with extubation success. Overall, our reintubation rate is quite low. Early tracheostomy may play a small but significant role in the low rate of reintubation. Further studies may be useful in creating a scoring system to identify the likelihood of extubation success in patients with neurological injury.

Surgical prophylaxis guidelines for EVD insertion recommend peri-procedural antibiotics rather than prolonged antibiotic administration for the duration of EVD placement. Several small studies have shown that prolonged systemic antibiotic use does not reduce the incidence of catheter related ventriculitis. Prolonged use is also associated with a higher rate of multi-drug resistant (MDR) infections. This study aims to show that prolonged antibiotic administration following EVD insertion is potentially harmful.

This is a single center, retrospective, chart review. All 100 patients admitted to our hospital who had an EVD placed from January 2000 to March 2017 were identified. Patients with preceding infections, incomplete data or uncertain infection diagnosis were excluded. Sixty-nine patients were analyzed. Documented variables included demographics, comorbidities, indications for EVD, duration of antibiotic therapy, infections and organisms' sensitivities.

Eight patients (12%) did not receive any antibiotic therapy; the rest received Cefazolin following EVD insertion. Infections occurred in 22 of 69 (32%) patients; 13 of 22 (59%) were MDR bacteria. Ventriculitis occurred in 4 (6%) patients, and 2 of these were resistant to Cefazolin (MDR). Ventriculitis was not associated with the use or duration of antibiotic therapy. Graphical analysis showed that the probability of any infection decreased during the first 3 days of antibiotic prophylaxis. After 3 days, the longer patients remained on prophylactic Cefazolin, the higher the probability of infection (Spearman rank correlati patients who received antibiotics for > 3 days were 2.5 times as likely to develop MDR infections (95% CI,0.60 to 10.3; p=0.3).

Cefazolin may prevent infections for the first 3 days after EVD insertion. However, prolonged administration increased the risk of MDR bacterial infections. A randomized study comparing periprocedural (72hrs) antibiotic use is needed to resolve this controversy.

Each year more than 13,000 deaths are associated with urinary tract infections. Eighty percent of all UTIs are associated with an indwelling catheter. Neuroscience Intensive Care (neuro-ICU) units have the highest rates of catheter associated urinary tract infections. Catheter associated urinary tract infection (CAUTI) increases morbidity rates, length of stay, and costs among hospitalized patients. At an urban academic medical center, our neuro-ICU had the highest CAUTI cases among our ICUs. The purpose of this project was to reduce our CAUTI cases by 50%.

This quality improvement project used several strategies: (1) formed a multidisciplinary CAUTI Task Force that included nurses, physicians, infection control, management and supply chain personnel; (2) developed an action plan to update standard of practice by conducting a review of the literature and pilot testing new products; and, (3) educated staff using huddles, a bedside guide, and email blasts with CAUTI facts starting in August 2016. Additionally, CAUTI prevention was discussed during patient handoffs among nurses and physicians. Data were collected for all neuro-ICU patients from fiscal year (FY) 2016-2017. CAUTI cases are determined by utilizing CDC's National Healthcare Safety Network. Analysis included evaluation of trends across time.

We reduced our number of CAUTI cases from 5 in FY 2016 to 1 in FY 2017. As of the beginning of FY 2018, we have not had a CAUTI for 365 days.

A comprehensive approach with a strong commitment by clinicians is critical for sustaining a reduction in CAUTI. We reduced our cases and exceeded our goal. Our efforts to provide evidence-based care are ongoing as we continue to monitor the research and upcoming supplies aimed at making hospitalacquired CAUTI a never event.

Isophane insulin (NPH) is a commonly prescribed basal insulin to manage hyperglycemia in critically ill patients on continuous tube feeding due to its intermediate duration of action. However, the incidence of hypoglycemia may be higher given the duration of NPH can last between 14-24 hours and because of the potential for unexpected interruption in feeding. Using scheduled regular insulin (RI) instead of NPH may reduce this risk given its shorter duration of action. It may also improve glycemic control due to more frequent titration.

This was a single-center, retrospective, observational, cohort study from December 2016 to May 2017. Patients on continuous tube feeding who were prescribed scheduled RI were compared to those prescribed NPH. All patients continued to receive an insulin sliding scale. Choice of agent was determined by the bedside team. The primary endpoint was incidence of hypoglycemia while secondary endpoint assessed efficacy. 

In our patient population, a higher incidence of hypoglycemia was seen in those that received NPH.

Hypertonic saline bolus (HSB) is a proven intervention for neurological emergencies arising from cerebral edema and increased intracranial pressure. Safety of HSB administered via central venous catheters is well established. However, infusion of HSB through peripheral intravenous access raises concern for complications related to caustic nature of the solution. We aim to assess the safety of peripherally administered boluses of hypertonic saline (3% sodium chloride) at a regional Level 1 Trauma and Comprehensive Stroke Center.

We performed retrospective chart review of patients who received HSBs from January 1, 2014 to January 1, 2015 as part of a quality improvement project. We identified 167 instances of HSB administration. The cases were individually reviewed for IV gauge, location of the IV, whether central access was present at the time of administration, documentation of IV removal, and volume of boluses. Patients were excluded if there was concurrent central venous access catheter present at the time of HSB administration or unrelated death within 12 hours after administration of HSB. Adverse events were defined as line infiltration, erythema, or swelling at the site of HSB administration.

111 charts were excluded from the study because of presumed administration of HSB through central venous access, not peripheral IV. Two patients had adverse events (3.5%). None of the patients progressed toward limb threatening complications. The majority of patients (54/56) did not experience erythema or infiltration of the IV.

HSB administered through peripheral intravenous access does not pose significant risk of severe complications and may be safely used in emergency situations in the absence of central line access.

Routine screening of high risk asymptomatic trauma or surgical patients for venous thromboembolism(VTE) is controversial. Studies suggest against screening while others recognize that some patients at high risk may benefit. The purpose of this pilot study is to evaluate the outcome of routine screening in patients who underwent neuro-surgical interventions.

All adult patients admitted to a neuro-intensive care unit with a primary diagnosis of brain injury requiring surgical interventions were included. Data from April-June, 2017 were retrospectively collected on all subjects who had either spine or cranial surgery. Data collected include: incidence of VTE, number of times duplex ultrasonography and computed tomography of the chest was performed. On July 1st, prospective data collection began by screening for presence of deep vein thrombosis(DVT) on day 1, 7 and 14 from admission or surgery day. All patients received pharmacologic and mechanical VTE prophylaxis within 36-48 hours post-operatively.

A total of 101 (pre-pilot, n=91 and post-pilot, n=10) subjects were included in the study. In the pre-pilot group, the ages ranged from 18-70 and most were male. Majority, 73/91(80%) had either craniotomy/craniectomy while 18/91(20%) had spine surgery. About 30/91(33%) were admitted with primary diagnosis of traumatic brain injury. Of the 91 subjects, 35 had duplex screening for DVT and 8 had screening for pulmonary embolism(PE). The incidence of VTE was confirmed in 11/91(12%); (DVT-8% and PE-4%). Median hospital length of stay was 9 (IQR 4-15) days. 38/91(42%) were discharged home and 2/91(2%) death rate was attributed to PE. In the post-pilot group, one incidence of PE was identified on day 1 post surgery screening. The rest of the results are still pending.

In this preliminary report, post surgical patients have a higher incidence of VTE. Routine screening might benefit to lower the incidence of mortality caused by PE.

Epsilon aminocaproic acid (EACA) is an antifibrinolytic agent that crosses the blood-brain barrier and has shown benefit in decreasing bleeding in patients acutely. Its use in intracranial hemorrhage has uncertain benefit. We aimed to describe the administration and impact of EACA in a single-center Neurosciences Intensive Care Unit (NeuroICU) over one year.

We performed a single-center retrospective study of NeuroICU patients undergoing intravenous EACA administration over a one-year time period. Inclusion criteria included EACA administration over 24 hours for a diagnosis of acute traumatic hematoma. The dose and duration of EACA infusion was collected. We additionally collected and compared pre-administration and post-administration prolonged thromboplastin time (PTT) hematology assays and neuroimaging. Clinical outcomes were reviewed for survival at hospital discharge.

Over a 13-month period (April 2016-May 2017), 24 patients each received a 24-hour infusion of EACA. The most common indication for EACA was to prevent worsening of intracranial hemorrhage in patients in traumatic coma (GCS <8). 68% of patients underwent neurosurgical management. PTT assay values showed a significant difference before and after EACA administration. (PTT 30.3+/-SD vs. 28.6+/-SD; student's t test p<0.05, n=21). Stability of the intracranial hematoma burden was evident following EACA in 63% of patients. 29% of patients who received EACA survived to discharge.

Patients receiving EACA showed a significant reduction in PTT assay values 24 hours after completing their dose. CT neuroimaging demonstrated stable intracranial hemorrhage burden in most patients receiving EACA despite a high prevalence of acute operative neurosurgical management. However, only a modest number of patients receiving EACA survived to discharge. These results suggest that EACA may acutely reverse hematologic abnormalities and enable emergent neurosurgical management in patients with severe, acute traumatic hemorrhage, despite a limited role in affecting survival outcomes in these patients.

Prognostication is difficult for patients admitted to a neurocritical care unit (NCCU). Can serum biomarkers obtained as part of routine admission lab work help predict outcomes among patients

In this prospective cohort study, the following biomarkers were measured at admission: C-reactive protein (CRP), arterial lactate, neuron specific enolase (NSE), lactate dehydrogenase (LDH), albumin, and brain natriuretic peptide (BNP). We collected information about demographics, comorbidities, hospital procedures and complications and 30-day mortality. We compared these serological biomarkers in patients who were alive versus those who had died at 30 days.

A total of 112 patients were enrolled over 4 months from June to September 2016, 11 of which whom (9.8%) died within 30 days of admission. There were no statistically significant differences in age or gender between the two groups. The 30-day mortality group had a higher mean Charlson Comorbidity Index (CCI) (3.0 vs 1.6, p=0.027) as well as mean NSE (39.1 vs 13.9 ug/L, p=0.008) and BNP levels (590.2 vs 177.3 pg/mL, p=0.003). Mean CRP, lactate, and LDH were also higher in the 30-day mortality group (79.5 vs 51.8 mg/L, 2.3 vs 1.9 mmol/L, and 307.2 vs 274.2 U/L) while mean albumin was lower (3.0 vs 3.3 g/dL), although these differences were not statistically significant (p<0.35).

CCI and serological biomarkers may have utility in predicting 30-day mortality among patients admitted to the NCCU. As we continue enrollment, we plan to develop a predictive model for 30-day mortality on admission for patients admitted to the NCCU using serological biomarkers, CCI and admission characteristics.

Among hospitalized acutely ill medical patients, the risk for venous thromboembolism (VTE) is high. The goal was to examine VTE prophylaxis of at-risk patients and VTE risk during hospitalization and in the outpatient continuum of care.

Acutely ill medical patients were identified from the MarketScan Commercial and Medicare databases from 1/1/2012 to 6/30/2015. Inclusion criteria were hospitalization for heart failure, respiratory diseases, ischemic stroke, cancer, infectious diseases, and rheumatic diseases; 6 months of continuous insurance coverage prior to (baseline period) and after (follow-up period) the index hospitalization. Outcomes included the proportions of patients receiving inpatient and/or outpatient VTE prophylaxis, and the risk for VTE events.

years, and 55.4% were female. Patients were hospitalized for infectious diseases (40.6%), respiratory diseases (31.0%), cancer (10.7%), heart failure (10.4%), ischemic stroke (6.4%), and rheumatic diseases (0.9%). Mean hospital length of stay was 4.8 days. In total, 59.1% (n=10,581) of patients did not receive any VTE prophylaxis, and 7.1% (n=1,267) received both inpatient and outpatient VTE prophylaxis. During hospitalization, 38.2% (n=6,843) received VTE prophylaxis (enoxaparin, 76.7%; warfarin, 15.2%; enoxaparin and warfarin, 5.3%; a direct oral anticoagulant (DOAC), ~2%). Following discharge, 9.7% (n=1,738) received outpatient VTE prophylaxis (warfarin, 43.8%; DOAC, 13.7%; enoxaparin, 10.1%; enoxaparin and warfarin, 7.6%). Among the entire study population, the VTE event risk remained elevated up to 30-40 days after hospital admission.

Among hospitalized acutely ill medical patients, the risk for VTE was present in both the inpatient and outpatient settings, with significant VTE risk extending into the post-hospitalization period. Only a small portion of at-risk patients (7.1%) received VTE prophylaxis in both the inpatient and outpatient continuum of care, suggesting an unmet medical need for VTE prophylaxis in the post-hospitalization.

Brain edema is a good research target in various forms of neurologic injury. A real time measurement of brain edema is possible using thermal conductivity methods. However, this technique might be hard to apply in small rodents, which are commonly used as experimental brain edema models. We developed a new approach method for applying thermal conductivity methods in rodent brain edema model.

A 10-week-old Spraque-Dawley rats were used for brain edema model. Qflow 500 probe was inserted through a suboccipital burr hole, located 3mm left from the midline, then was advanced anteriorly 10mm from the occipital bone margin until probe place assistance value indicates valid values (ranging from 0 to 2.0). Probe was fixated using adhesive glues and tagging suture. In vivo brain water content was continuously calculated using thermal conductivity values. For validation, calculated brain edema was compared with standard methods (Dry/Wet brain weight ratio) in water intoxication models (intraperitoneal injection of distilled water, 20% of body weight) and drying effect of mannitol was validated in streptokinase induced intracerebral hemorrhage (ICH) models.

Calculated brain water content was 78.6±0.6% in thermal conductivity method and 78.4±0.5% using Dry/Wet weight ratio methods (P=0.43). In water intoxication model, brain water content started to increase 30 minutes after injection and reached up to 81.5±0.7% at 6 hours post injection. On wet/dry weight method, edema was measured as 81.0±0.8% (P=0.80). In ICH model, brain water content started to drop 30 minutes after administration of mannitol (0.5mg/kg) and drifted back 4 hours after injection of mannitol.

Thermal conductivity method in assessing brain edema is applicable in rodents using suboccipital approach through burr hole. This method may better reflect dynamic changes of brain edema.

In patients with critical brain injury, alterations of brain physiology with dialysis initiation are poorly understood.

From a consecutive series of brain-injured patients undergoing invasive multimodality monitoring between 2008 and 2016, 13 patients that underwent continuous veno-venous hemodialysis (CVVH-D) and 4 patients that underwent intermittent hemodialysis (iHD) were identified. Changes in mean arterial pressure (MAP), intracranial pressure (ICP), and brain tissue oxygenation (PbtO2), and microdialysis lactate-pyruvate ratio (LPR) were compared six hours prior to and twelve hours following dialysis initiation. High-resolution data was collected every 5 seconds, with the exception of LPR collected hourly. Data were normalized to patient maximum values, analyzed by fitted segmented regression, and checked for slope change-points by Davies' test. Values prior to dialysis initiation were averaged as a baseline for comparison.

Median values for patients undergoing CVVH-D were MAP 85 +/-12.77, ICP 9.8+/-9.61, pbtO2 21.7 +/-6.023 mmHg (n=5), and LPR 21.6 +/-22.13 (n=4). Normalized median values for patients undergoing iHD were MAP 94 +/-13.73, ICP 19 +/-5.32. For the CVVH patient segmented regressions with normalized data, there was no change in MAP (slope 0.0004) during the twelve hours. However, we found a change-point in ICP at 4.78 hours (CI 3.76-5.79, slope change 0.006 to 0.0006) and pbtO2 at 4.99 hours , slope change 0.006 to -0.023). LPR increased through CVVH (slope 0.036 +/-0.0097). Median values for patients undergoing iHD were MAP 94 +/-13.73, ICP 19 +/-5.315. There was no identified change-points in MAP or ICP in iHD patients, further parameters were limited by small sample size.

Initiation of CVVH in patients with neurologic multimodality monitoring showed change-points in ICP and PbtO2 in setting of stable MAP, with slight decrease in ICP and PbtO2. Initiation of HD in showed no change-points in ICP.

Data on the cerebral effects of antihypertensive agents are limited but potentially important in patients requiring blood pressure reduction in neurological emergencies. Our objective was to measure the effect of rapid-acting antihypertensive agents on cerebral blood flow (CBF) in patients with acute hypertension

We conducted a prospective, quasi-experimental study of patients with a SBP > 180 mmHg and planned rapid-acting antihypertensive treatment in the emergency department. Patients < 18 years or pregnant were excluded. Non-invasive hemodynamic and transcranial Doppler measurements of the middle cerebral artery mean flow velocity (MFV) were obtained prior to and post treatment. Analysis included descriptive statistics and generalized linear modeling to test the effect of four categories of antihypertensive agents on MFV. Categories included clonidine, IV labetalol, IV hydralazine and combination therapy.

We enrolled 35 patients (37% female) with a mean age of 49 ± 13 years. Eight (23%) patients received clonidine, 6 (17%) IV labetalol, 5 (14%) IV hydralazine and 16 (46%) combined therapy. The mean baseline SBP was 214 ± 24 mmHg and MFV 49 ± 13 cm/sec. The mean percentage fall in SBP by medication was: clonidine -12 ±7%, labetalol -13 ±12%, hydralazine -23 ±11%, and combination -23 ±16%. The overall change in MFV was -9 ±15%, and by medication was: clonidine -10% (95%CI -2 to -21%), labetalol -11% (95%CI -5 to -27%), hydralazine +1% (95%CI -18 to +21%), and combination -11% (95%CI -2 to -19%). Adjusting for baseline BP, hydralazine caused less change in MFV compared to other medications (difference between means +12%, 95%CI -3 to +26%, p=0.1).

In this study with modest BP reductions, rapid-acting antihypertensive medications had comparable effects on cerebral blood flow. These results hint that cerebral blood flow may be more stable with hydralazine administration, but further testing of hydralazine and infusions such as nicardipine is required.

Studies exploring correlations between non-invasive (oscillometric) blood pressure (NIBP) and intraarterial blood pressure (ABP) have excluded neurocritically ill patients with continuous infusion of vasoactive medications. Compared to ABP, NIBP monitors generally tend to over-read at low values and under-read at high values. This study examines the relationship between simultaneously measured NIBP and ABP recordings in these patients.

Following informed consent, prospective observation of patients (N=70) admitted to a Neurosciences ICU, with simultaneous ABP and NIBP monitoring and continuous vasopressor (n=21) or antihypertensive (n=49) infusion. Paired NIBP/ABP observations along with covariate and demographic data were abstracted via chart audit. Analysis was performed using SAS v9.4.

2,177 paired NIBP/ABP observations from 70 subjects (49% male, 63% white, mean age 59 years) receiving vasopressors (n=21) or antihypertensive agents (n=49). T-tests show significant difference between paired readings: ([SBP: m=137 vs 140mmHg respectively; p<.0001], [DBP: m=70 vs 68mmHg respectively, p<.0001], [MAP: m=86 vs m=90mmHg respectively, p<.0001]). The paired differences for specific medications were tabulated, with 50-70% of the differences <10mmHg, and 75-90% of the values with <20mmHg difference. Bland-Altman plots for MAP, SBP, and DBP demonstrate good intermethod agreement between paired measures (excluding outliers) and demonstrated marked NIBP-ABP SBP differences at higher blood pressures. Pearson Correlation Coefficients for paired measurements show strong positive correlation for MAP (+0.82), SBP (+0.84), and DBP (+0.73).

Despite a statistically significant difference between NIBP and ABP readings for patients on vasoactive medications, there may be no clinical significance. The relatively positive and linear correlation between paired values guide providers towards not being forced to use one over the other. The final manuscript will aim to detail whether there is a clinical significance in particular vasoactive medications.

Pathological activity in continuous electroencephalogram (cEEG) data of ICU patients is conventionally categorized into a small number of named rhythmic and periodic patterns. We aimed to develop a valid method to automatically discover a small number of homogeneous pattern clusters, to facilitate efficient interactive labeling by cEEG experts.

We extracted 576 time and frequency domain features from 12+ hour cEEG recordings from 10 different ICU patients. After removing artifacts, we applied principal component analysis (90% variance retained), then separated the data into 9 clusters (K-means). From each cluster we took 9 random samples plus the most central one, rendering 900 samples in total. Three expert electroencephalographers independently categorized all samples into one of 6 standard pattern categories (seizures, GPDs, LPDs, LRDA, GRDA, burst suppression, other). We compared two methods for labeling clusters: (1) "Labor intensive labeling" (LIL): assign the most frequent of 30 expert-provided labels; (2) "Labor efficient labeling " (LEL): assign the most frequent of the 3 expert labels for the central sample. We compared interrater agreement (IRA) among experts vs. between each expert and consensus labels using LIL vs. LEL. Finally, we used Laplacian Eigenmaps (LE) to visualize the data. 

This research suggests that large cEEG datasets can be automatically clustered into a small number of patterns described by standard ICU EEG pattern labels. We demonstrated efficient cluster labeling by inspecting only the central-most representative of each cluster. Furthermore, LE visualizations support the hypothesis of an interictal-ictal continuum.

Real time measurement of cerebral oxyhemoglobin (OxyHb) and deoxyhemoglobin (DeoxyHb) using near infrared spectroscopy (NIRS) may help us better understand the status of cerebral oxygenation and possibly cerebral blood flow (CBF) in patients with acute brain injury. We developed 48 multichannel functional NIRS (fNIRS) system and evaluated its role in patients with acute brain injury.

A 48 Channel fNIRS system (NIRSITTM) was used for measuring cerebral OxyHb and DeoxyHb in patients with brain injury. Measurement protocols were as follows; baseline measurement for 5 minutes with activation stimuli (nipple pinching for 5 seconds). Patients groups were categorized as follows; 1) Global cerebral ischemia with profound cerebral injury (N=40), 2) Large ischemic stroke or Decrease in CBF in the frontal lobe due to severe stenosis in the middle cerebral artery (MCA) or internal carotid artery (ICA) (N=74), 3) High grade Subarachnoid hemorrhage with a risk of vasospasm (N=14), Control groups did not have either cerebral lesion or CBF abnormality (N=22).

Global ischemia with good functional outcome group had better OxyHb level (rSO2) compared to those with poor outcome (67.4% vs. 59.5%, respectively, P = 0.003). Patients with poor perfusion in the MCA territory had low OxyHb level compared to mirror lead in the contralateral hemisphere. OxyHb level in patients with decreased vasomotor reactivity on Diamox SPECT had improved after carotid stenting. Three patients who underwent superficial temporal artery-middle cerebral artery bypass surgery had transient hyperperfusion syndrome. OxyHb and total Hb were elevated in the affected area. Patients with SAH and vasospasm had blunted oscillation pattern of OxyHb compared to those without vasospasm.

Bedside multichannel measurement of OxyHb and DeoxyHb using fNIRS might be useful in understanding hemodynamic changes occurring in patients with acute brain damage at the real time.

Multimodality monitoring (MMM), brain tissue oxygenation (PbtO2) and Microdialysis (MD) in SAH may be important to the treatment of delayed cerebral ischemia (DCI). Our hypothesis was that concordance between PbtO2 and MD occurs in the tissue bed displaying angiographic vasospasm.

This retrospective observational study includes 10 patients with SAH. The extent of angiographic vasospasm for each vessel was graded on angiography by the on call neuro-interventionalist and quantified as 0 (no spasm) to 6 (severe spasm). PbtO2 and MD probes were placed in the frontal lobe white matter. The severity of vasospasm was estimated by the weighted average of (1x ACA + 2 x MCA + 3 x ICA) / 6. Cases with score of 2 or more were considered to have clinically relevant vasospasm. Using a within-subjects design, epochs of baseline MMM were compared with during spasm using daily mean for PbtO2, LPR, glucose, ICP and CPP. Given the limited number of observations the simplifying assumption was made that the observations from all epochs are independent. The measurements from all patients were divided in the two groups with and without spasm and were compared using a twotailed non-paired student T-test.

Sixteen sets of baseline and vasospasm epochs were evaluated for PBTO2 and 18 for MD. Compared with baseline values, the average PbtO2 was significantly lower (15.1 vs 24.6mmHg, p=0.003), LPR was non-significantly higher (38.3 vs 28.4, p=0.07), and glucose was similar (0.9 vs 1.2 mmol/l, p= 0.5) during vasospasm epochs. There was no difference in ICP (9.7 vs 9.7mmHg, p=0.98). These differences were unaffected by induced hypertension, when CPP was augmented for treatment of DCI (120.4 vs 101.3 mmHg, p=0.07).

MMM during angiographic vasospasm after SAH suggests discordant changes in brain oxygenation and metabolism. These data suggests that DCI may be related to metabolic factors other than tissue oxygenation.

Multimodal monitoring including brain tissue oxygenation (PbtO2) is increasingly used for the management of acute TBI patients. The optimal management of PbtO2 is not fully established. Increasing FiO2 is efficacious to correct PbtO2 but may mask other oxygen delivery mechanisms which may be deficient. The objective of this study was to explore the clinical utility of a PbtO2/PaO2 ratio to detect overtreatment by FiO2.

Retrospective cohort stud were collected simultaneously whenever an arterial blood gas was drawn (ICP, CPP, hemoglobin, temperature, PCO2 and PaO2). Causes of cerebral hypoxia (PbtO2 < 20mmHg) were noted. PbtO2/PaO2 ratio <0.15 was considered abnormal and plotted over time for each patient individually.

1006 data sets were collected from 38 patients (mean age 44.5±20.0, median GCS 4, mortality 45%).

33.0% of the time and associated with a mean PaO2 of 250 mmHg. Measures within the low PbtO2-low ratio category had significantly lower CPP (64 vs 72 mmHg), higher PaO2 (242 vs 130 mmHg) than patients with normal PbtO2 or normal ratio respectively. Various causes of hypoxic PbtO2 were reported when the ratio was abnormal: hypocapnia, low CPP, low cardiac index, long equilibration time... Four patterns of evolution of the ratio over time were identified and associated with different mortality rate: 28.5%, 33.3%, 46.7% and 60%.

Conclusions associated with increased PaO2 and decreased CPP. This suggests clinicians often used FiO2 to compensate for deficient cerebral oxygen delivery. Indeed, various causes of hypoxia besides low PaO2 were identified and corrected. Pattern of temporal evolution of the ratio seems to correlate with mortality.

Pupillary light response (PLR) evaluates cranial nerves II, III, and midbrain function. Bedside quantitative infrared pupillometry provides reproducible assessment of the PLR, reported as the neurological pupillary index (NPI). Increased intracranial pressure results in decreases in NPI. Intracranial hypotension (IH) can also cause brainstem distortion. We therefore hypothesized that similar changes in NPI could be seen with IH. Here, we describe sequential changes in NPI in IH before and after treatment.

We identified four patients monitored with pupillometry for clinical care during IH diagnosis and treatment. IH was diagnosed with a compatible history, exam, and characteristic neuroimaging findings. Patients' NPI at baseline, during symptomatic IH, and after treatment were compared using related samples Friedman's two-way ANOVA and Wilcoxon signed ranks tests.

Two patients were male; causes of IH were CSF leak following lumbar instrumentation (n=3) and basilar skull fracture (n=1). Mean baseline NPI was normal (defined as >3) and declined in one or both eyes concurrent with clinical deterioration in the 24-48 hours preceding definitive diagnosis. All patients underwent treatment for CSF leak with epidural blood patch or fracture repair, with return of NPI > 3 within 5 hours of treatment. The baseline, symptomatic and post treatment NPI's differed significantly (3.55±0.35 vs 0.80±0.59 vs 3.65±0.24, mean +/-SD, pre-treatment vs nadir vs post-treatment, p=0.05). Both baseline and post treatment NPI's differed from the NPI nadir (p=0.068) but there was no difference between baseline and post-treatment NPI (p = 0.71).

Impairment of the PLR, as measured by NPI, occurred during symptomatic IH and resolved after treatment. Because management of intracranial hyper-and hypotension differ markedly, our results emphasize the importance of evaluating the clinical context before attributing pupillary/NPI changes to increased ICP. Automated pupillometry provides a non-invasive, bedside tool for monitoring progression and treatment of intracranial hypotension

The correlation of optic nerve sheath diameter (ONSD) as seen on ultrasonography (US) and directly measured intracranial pressure (ICP) has been well described. Nevertheless, differences in ethnicity and type of ICP monitor used are obstacles to the interpretation. Therefore, we investigated the direct correlation between ONSD and ventricular ICP and defined an optimal cut-off point for identifying increased ICP (IICP) in Korean adults with brain lesions.

This prospective study included patients who required an external ventricular drainage (EVD) catheter for ICP control. IICP was defined as an opening pressure over 20 mmHg. ONSD was measured using a 13 MHz US probe before the procedure. Linear regression analysis and receiver operator characteristic (ROC) curve were used to assess the association between ONSD and ICP. Optimal cut-off value for identifying IICP was defined.

A total of 62 patients who underwent ONSD measurement with simultaneous EVD catheter placement were enrolled in this study. Thirty-two patients (51.6%) were found to have IICP. ONSD in patients with IICP (5.95 ± 0.25 mm) was significantly higher than in those without IICP (5.17 ± 0.57 mm) (P 5.6 mm disclosed a sensitivity of 93.75% and a specificity of 86.67% for identifying IICP.

ONSD as seen on bedside US correlated well with directly measured ICP in Korean adults with brain lesions. The optimal cut-off point of ONSD for detecting IICP was 5.6 mm.

Impaired cerebral autoregulation following neurological insult has been established as a strong predictor of clinical outcome. Hypothermia may offer autoregulatory protection in these patients, although the effect of body temperature on autoregulatory status is unclear.

Retrospective analysis of data from an ongoing prospective study to evaluate multimodal monitoring using near infrared spectroscopy (NIRS) for bedside measurement of autoregulation. Ninety-one comatose patients (GCS <8) were continuously monitored for up to three days. NIRS derived cerebral oximetry index (COx) was used as a marker of autoregulation. COx was calculated as a moving, linear correlation coefficient between regional cerebral oxygenation saturation and MAP. Autoregulation improves as COx values approach 0, and is impaired as values approach 1. Patients were grouped by trend in temperature seen over the monitoring period: no change (<1oC temperature change, n=12), increase (n=6), decrease (n=7), increase followed by decrease (n=7), decrease followed by increase (n=6), and fluctuating (n=53). We performed multivariable logistic regression analysis to assess the association between temperature and outcomes. The association between hourly temperature and COx was assessed using mixed random effects models with random intercept.

In patients showing a sustained increase or decrease in temperature, a linear relationship between temperature and COx was seen; for every 1oC increase or decrease in temperature, COx changed by 0.045±0.010 (p<0.001) and -0.020±0.018 (p=0.15), respectively, after adjusting for pCO2, haemoglobin, MAP and temperature probe location. Mean temperature changes over the monitoring period for these groups were 2.52±1.07oC and -1.77±1.13oC, respectively. COx did not change significantly in other groups. There was no significant difference in mortality or poor outcome (mRS 4-6) at discharge and 3, 6, or 12 months between patients in each group.

In acute coma patients in the neurocritical care unit, increasing body temperature is associated with worsening cerebral autoregulation as measured by COx.

The historical tradition of examining the pupillary light reflex (PLR) required the examiner to score the size and reactivity of the pupil. A change in the PLR from brisk to sluggish or fixed may be a marker of a pathological process and a need for intervention. The PLR has been difficult to quantify and has poor inter-rater reliability. Handheld pupillometry provides several novel measures, such as the neurological pupillary index™ (NPi) and constriction velocity (CV) that may be more quantifiable than the PLR. The purpose of this analysis is to examine the relationship between CV and NPi in neurologically injured patients.

The END-PANIC Registry is a prospective registry of pupillometer values and variables associated with intracranial dynamics (e.g., ICP). This analysis from 946 adult (over 18 years) patients from 2 hospitals includes 42,568 pupillometer readings; left eye (20,943), and right eye (21,625).

Subjects had a mean age of 57.9 yrs and 48.1% were male. The primary admission diagnosis included neoplasm (241), ischemic stroke (169), SAH (82), ICH (81), TBI (9), and other (364). The left eye mean/s.d. CV (1.6/0.9) NPi (4.1/0.9) and Size (3.5/1.2) were similar to the right eye CV (1.6/0.9) NPi (4.1/0.9) and size (3.5/1.2); statistically significant difference related to large sample size. The correlation between left eye CV and NPi (r2=0.068, p<0.001) was significantly improved after controlling for size (r2=0.67, p<0.001). The correlation between right eye CV and NPi (r2=0.048, p<0.001) was significantly improved after controlling for size (r2=0.67, p<0.001).

Constriction velocity is highly dependent on size of the pupil. Further studies need to be undertaken to determine the sensitivity and specificity of abnormal NPi and CV in detecting pathological processes such as midline shift or 3rd nerve compression that effect pupillary reactivity.

Cerebral injury is increasingly described in adult recipients of extracorporeal membrane oxygenation (ECMO) therapy. We describe the association between regional brain tissue oxygenation (rSO2) measured by near infrared spectroscopy (NIRS), survival, and cerebral injury on neuroimaging.

A single-center retrospective chart review was conducted of adult patients who underwent veno-arterial (VA) ECMO from April 2016 to October 2016. All patients had received NIRS monitoring during ECMO therapy. Baseline demographics, in-hospital complications, and mortality were recorded. Desaturations of rSO2, defined as decline >25% below baseline or absolute value <40, were recorded and analyzed. Desaturation burden was calculated by area under the curve analysis and measured by rSO2*seconds.

Eighteen VA ECMO patients (9 females) underwent NIRS monitoring during the study period. Eleven patients experienced desaturations, while 7 did not. Patients with desaturations tended to be younger (50.2 vs. 64.7 years old), more likely female (8 vs. 1), had lower ejection fraction (28.6% vs. 46.4%) and experienced liver dysfunction (7 patients vs. 1). Patients with desaturations were more likely to have abnormalities on CT scan (6 vs. 0). Eleven of the 18 patients survived to discharge. Survivors tended to be younger (50.2 vs. 64.6 years old) and had lower initial ECMO sweep (4.1 vs. 6.7). Survivors had lower baseline rSO2 values at the beginning of NIRS monitoring (right -57 vs. 65, left -57 vs. 68), fewer desaturation events (7 vs. 14), lower desaturation burden, and spent less overall time desaturating (1:21 vs. 3:09 hours).

Desaturation on NIRS may be correlated with cerebral injury in the adult VA ECMO population and may have utility in triggering clinical investigation or determining prognosis. Further studies in larger patient populations are needed to determine its reliability and accuracy.

Pressure reactivity index (PRx) is the most validated index to measure cerebrovascular reactivity in patients after traumatic brain injury. The aim of this study is to identify the natural history of cerebral autoregulation measured by PRx in various forms of brain injury to monitor restoration or not of cerebral vasomotor reactivity in the acute phase.

Retrospective analysis of data from ongoing prospective study to evaluate multimodal monitoring using PRx for the measurement of cerebral autoregulation at the bedside. Thirty comatose patients (Glasgow Coma Scal used as a marker of autoregulation. PRx was calculated as a moving, linear correlation coefficient between ICP and MAP. Impaired cerebral autoregulation has been pre Standard maximal medical therapy was implemented to treat elevated ICP, cerebral edema, etc. Patients with withdrawal of care in the first 48 hours or brain death on neurological exam were excluded.

Thirty comatose patients from acute brain injuries (16 intracerebral hemorrhage, 6 TBI, 5 aneurysmal subarachnoid hemorrhage, 2 intraventricular hemorrhage, 1 hypoxic ischemic encephalopathy) were studied. The average PRx upon starting neuromonitoring using PRx was 0.3 ± 0.35 (impaired), whereas the average PRx at the end of day 3 of neuromonitoring was 0 ± 0.10 (restored). One third of the patients had ICP crisis during monitoring. The average opening ICP=8.3, average highest recorded ICP=26.9.

Impaired cerebral autoregulation has been implicated as a predictor of clinical outcome. Aggressive medical therapy instituted by the neurocritical care team (ICP and cerebral edema management, blood pressure control, etc.) may result in restoration of cerebral vasomotor reactivity measured by PRx by intensive care day 3-5. Restoration of cerebral vascular reactivity may be a necessary but not sufficient for favorable outcome.

Elevated intracranial pressure (ICP) is an important cause of death following acute liver failure (ALF). While invasive ICP monitoring (IICPM) remains the gold standard, the presence of coagulopathy increases the risk of bleeding in ALF. Measurement of optic nerve sheath diameter (ONSD) using Optic Nerve Ultrasound (ONUS) may accurately detect elevated ICP. Our goal was to study the ability of ONUS to detect sustained intracranial hypertension following ALF, and to predict death and Therapeutic Intensity Level (TIL), a quantitative measure of the intensity of treatment required to control ICP.

Consecutive patients with ALF admitted to our institution in a 6-year period underwent ONUS. Blinded measurement of ONSD was performed from deidentified ONUS videos. Patients underwent IICPM on the basis of an institutional protocol for selection of appropriate candidates, coagulopathy reversal and insertion of an intraparenchymal monitor. The TIL-basic for management of ICP during the ICU stay was recorded. The ability of highest ONSD to predict concurrent ICP>20mmHg at the time of measurement, sustained ICP elevation >20mmHg at any time and TIL-basic>2 was assessed in patients who underwent IICPM, while prediction of death was assessed in all patients. Receiver Operating Characteristic (ROC) curves were constructed for the outcomes of interest.

Thirty-nine patients with ALF were admitted during the study period, 29/39(74%) underwent ONUS, 25/39(64%) underwent IICPM and 19(49%) died. Of 25 patients who underwent IICPM, 13(52%) developed sustained ICP elevation and 7(28%) had a TIL-basic>2. The ROC Area Under the Curve (AUC) of ONSD for prediction of concurrent ICP>20mmHg was 0.63(95% Confidence-Interval 0.39-0.82, p=0.42 for null hypothesis of AUC=0.5), sustained ICP elevation at any time was 0.51(0.28-0.73,p=0.97), death was 0.56(0.36-0.74,p=0.59) and TIL>2 was 0.61(0.42-0.79,p=0.33).

In patients with ALF, ONSD measurement performed poorly for detection of ICP elevation, and was a poor predictor of TIL and death.

Limited literature exists regarding the neurochemical and physiologic events that occur as brain death develops. Using intracranial multi-modality monitoring, we identify physiological changes that signal the onset of brain death.

We measured intracranial pressure (ICP), brain partial oxygen tension (PbtO2), cerebral blood flow (CBF), and biochemical correlates of cerebral metabolism in 4 patients with diffuse hypoxic ischemic brain injury after cardiac arrest during the development of brain death. Monitoring probes were inserted into cerebral white matter through a burr hole using a CT compatible multi-lumen bolt. Brain tissue energy-related metabolites (Lactate, Pyruvate, Glutamate, Glucose, Glycerol) were measured using a bedside microdialysis analyzer. PbtO2 and temperature were measured via a Licox catheter. Cerebral perfusion was measured with a Hemedex Bowman Perfusion monitor. Brain death was confirmed in accordance with institutional guidelines.

A characteristic pattern of physiologic and neurochemical findings emerged as brain death occurred. Absolute loss of cerebral autoregulation, with a near perfect correlation between ICP and MAP was followed by equalization of MAP and ICP resulting in progressive drop in CPP to zero, followed by a progressive decline in PbtO2 that became unresponsive to a 100% FiO2 challenge. Cerebral perfusion decreased in tandem with PbtO2. Lactate/Pyruvate ratio (LPR), glutamate, and glycerol all increased precipitously, with LPR consistently >1000. Brain temperature decreased despite maintenance of a normal core temperature. Finally, intracranial compliance, while initially very low (evidenced by marked increase in the P2 component of the ICP waveform), appeared to paradoxically re-normalize as the recording continued.

Continuous neuromonitoring reveals a characteristic pattern of cerebrovascular physiologic changes that accompany brain death. These changes are consistent with a progressive cessation of cerebral perfusion caused by diffuse cerebral edema. Although not currently a part of the formal brain death determination process, such monitoring could be helpful to identify when brain death has truly occurred.

Automated devices that collect objective quantitative data on pupil size and reactivity are increasingly used for critically ill patients with neurologic disease. However, there is limited data on the normative range of pupillary reactivity in the critically ill, and the relationship between reactivity and traditional monitoring metrics. To determine pupil characteristics in this population, we prospectively collected quantitative pupillometry data in patients admitted to the Neuro ICU with an expected stay of at least 24 hours.

Trained nursing staff measured pupillary reactivity with the NeurOptics-200 pupillometer device every 2-hours. Measurements included the Neurologic Pupil Index, (NPi) a composite metric ranging from 0-5 in which >3 is considered normal, resting and constricted pupil size, constriction velocity, dilation velocity and latency. These recordings were compared with averaged intracranial pressure (ICP) and Glasgow Coma Scale (GCS) assessments within the same hour. We used univariate and spearman's rank tests to explore associations between pupil characteristics and clinical variables, followed by multi-level linear regression to account for intra-and inter-subject variability.

One-hundred patients underwent 4200 paired observations. Fifty-five patients had at least one recorded episode of anisocoria, 27 had low NPis in more than 10% of recordings, and 29 had normal pupil reactivity. Average and minimum NPi was correlated with average and minimum recorded hourly Glasgow Coma Score (GCS) (p values <0.001). Increased asymmetry in both pupil size (p=0.002) and dilation velocity (p=0.02) was associated with increased intracranial pressure (ICP). Anisocoria was associated with hyperosmolar therapy (p=0.002). The presence of low NPis in more than 10% of total pupil measurements was associated with death at discharge (p=0.02).

The range of pupillary metrics varies among critically ill neurologic patients and correlates with GCS and ICP. Further study is needed to establish whether change in pupil metrics predict specific clinical events.

Near infrared spectroscopy (NIRS) provides a non-invasive measurement of regional cerebral oxygen saturation (rSO2) that may be able to detect seizure activity. In this study, we explored the hypothesis that rSO2 is lower ipsilateral to seizures or epileptiform activity compared to the contralateral side in comatose patients.

Five patients (2 men and 3 women; mean age 69) underwent continuous electroencephalography (cEEG) monitoring and NIRS recording. cEEG data were classified as baseline, epileptiform activity or seizure, slowing, or burst suppression at hourly intervals over the course of the recoding period (mean duration 34.1 hours, range 24 to 85 hours). Three patients had idiopathic status epilepticus, two had intracranial hemorrhage, and one had a temporal meningioma. The relationship between rSO2 and epileptiform discharges was explored using scatterplots. The association was assessed using mixed random effects models with a random intercept. An independent within-subject residual structure was used.

There were 127 measurements with cEEG and NIRS from 5 patients. One patient was excluded as the NIRS sensors were potentially reversed. Epileptiform activity or seizures were observed in a median of 37% of the measurements (IQR 23-62%). rSO2 was significantly lower on the side ipsilateral to seizures -5.19, p <0.001) after adjusting for MAP. All patients only had partial seizures with no generalization. Partial seizures and/or epileptiform discharges were not associated with impaired autoregulation.

We found a significant lower cerebral oxygen saturation ipsilateral to seizures and/or epileptiform activity. The association was observed in patients with various etiologies of coma, and with either convulsive and non-convulsive seizures. Decreases of regional cerebral oxygen saturation at the bedside may alert the clinician of ipsilateral seizures.

Elevated intracranial pressure (ICP) and cerebral edema are common causes of mortality in neurocritical-care patients. Key monitoring techniques for ICP-elevation include neuroimaging and invasive ICP-measurement. Examination of the pupils is routinely performed to determine disturbances within cerebral physiology but shows high inter-rater variability. Portable infrared pupillometry is increasingly used for accurate measurements. The benefit of these technique remains to be established in patients with elevated ICP. Aim of this study was identify pupillary parameters associated with ICPcrisis in neurocritical-care patients.

We prospectively enrolled 31 critically-ill patients (subarachnoid hemorrhage/intracerebral hemorrhage/stroke/bacterial meningitis) admitted to our neurointensive care unit(07/2016-07/2017) who required placement of external ventricular drains. We recorded serial pupillometer readings [i.e. maximum/minimum apertures(mm), constriction/dilation velocities(mm/sec.), latency period(sec.)] and corresponding ICP values every 3 hours after admission. Neurological Pupil index(NPi), an algorithm that compares above mentioned pupillary parameters to a normative model of pupil reaction to light, grades pupil-function on a scale of 0(nonreactive) to 5(normal). Receiver Operating Characteristic(ROC) Curve Analysis was performed to investigate associations between pupillary parameters and presence of ICPcrisis(ICP>20mmHg).

In 31 

Our data suggest a relationship between non-invasively detected changes in NPi, CV or MCV and ICPcrisis. Yet, clinical benefit of these parameters is subject to future studies.

Lung injury is frequently observed in patients with severe, acute brain injury. While these patients often require mechanical ventilation, a lung protective ventilation strategy has not been extensively studied. This may be due, in part, to concerns that elevated positive end-expiratory pressure (PEEP) could adversely affect intracranial pressure (ICP) or cerebral perfusion pressure (CPP). We were interested in exploring this relationship as a first step towards understanding whether mechanical ventilation resulted in a transmission of pressure to the brain.

8) and received both mechanical ventilation and ICP monitoring were enrolled in this pilot study. An esophageal balloon was inserted to measure their transpulmonary pressure (Ptp). Fluid responsiveness was assessed prior to the intervention. Subjects underwent a step-wise increase in PEEP (increments of five) from 5 to 15 cmH2O. Airway pressure, Ptp and ICP were measured at each PEEP interval.

Of the planned twenty, three patients have been enrolled to date. Primary diagnoses included aneurysmal subarachnoid hemorrhage and intraparenchymal hemorrhage with a median GCS of 7. Patients were ventilated using either volume control or pressure support ventilation; median FiO2 was 0.35. Two patients were on vasopressors and the same two patients were determined to be fluid responsive. At baseline (PEEP 5), mean ICP, CPP, and Ptp were 6mmHg, 85mmHg, and -3.18cmH2O, respectively. When PEEP was increased to 10 cmH2O, the average change from baseline in ICP and CPP was -3.7% and -2.2%, respectively. When increased to 15 cmH2O the change from baseline in ICP and CPP was 3.0% and 0.5%. During the intervention ICP did not exceed 20 mmHg, nor did any patient experience hypotension.

Preliminary data suggests that intrathoracic pressure is not directly transmitted to the intracranial compartment. Continued enrollment is needed to confirm these findings.

Neurocritical care after severe traumatic brain injury (sTBI) is focused on detecting and preventing secondary brain injuries. In addition to intracranial pressure (ICP), measures of brain tissue oxygen (PbtO2), regional cerebral blood flow (rCBF), and electrocorticography (dEEG) may provide critical clinical data. Few studies have assessed the safety of such an approach and the reliability of data that is gathered. We describe here the placement, complications, and reliability of multimodality monitoring (MMM) data from a novel, single burr hole approach using a four-lumen bolt at our institution.

We included consecutive adult sTBI patients admitted to the Neuroscience Intensive Care Unit at the University of Cincinnati from April 2015 to March 2017 who underwent MMM as part of standard clinical management per institutional protocol. Data was obtained regarding device placement and complications. All data was visually inspected for errors and gaps in data.

40 patients were included. The mean age was 43+/-17 and 85% were men. Bolts were placed a median of 17.7 (IQR 8.3-16.9) hours from injury. No clinically significant complications occurred, although 37.5% had minor complications (e.g. small tract hemorrhage or pneumocephalus). Suboptimal placement of probes was noted in 13%. We monitored patients a median 103.5 (IQR 48.8-133.6) hours. ICP data was the most reliable, with data available 94.8% of the total monitoring time and only 1.2% error time. PbtO2 and dEEG data were reliable for > 90% of total monitoring time with < 2% error time. rCBF provided data for 77% of total monitoring time and had 17.9% error time.

MMM in sTBI may be carried out via a single burr hole without significant clinical complications and reliably yields continuous data to facilitate clinical decision making. This supports the feasibility of our approach as an alternative to ICP monitoring alone.

Intracranial hemorrhage patients with non-compliant ventricles may have high intracranial pressure (ICP) despite normal ventricle size. We aimed to assess the incidence of elevated ICP among those with no radiographic evidence of intracranial hypertension.

Prospectively enrolled primary intracranial hemorrhage patients (SAH, SDH and IPH) admitted to two tertiary-care centers between 4/2008-5/2016 were retrospectively reviewed. Among patients with external ventricular drainage (EVD), admission head CT (HCT) scans within 72h prior to EVD placement were reviewed for evidence of elevated intracranial pressure (ICP) including: ventricle size (bicaudate index, temporal horn size), basal cistern effacement, midline shift and global cerebral edema. When all of these features were absent, patients were classified as having normal-ICP HCT. The incidence of elevated ICP (>20mmHg) at the time of EVD placement and during hospital stay were recorded.

Of 741 intracranial hemorrhage patients enrolled, 253 (34%) had EVD. 23/253 (9%) had a normal-ICP HCT. Of these, 11/23 (48%) had elevated opening pressure at the time of EVD placement, and 13/23 (57%) had elevated ICP during their hospital stay. Among normal-ICP HCT patients with ICP>20mmHg, 92% had SAH, and the median GCS and Hunt-Hess scores were 14 (range 3-15) and 3 (range 2-5). The positive and negative predictive values of normal-re 52% 62%, respectively (AUC 0.471, P=0.648) The only radiographic feature that was associated with elevated ICP was global cerebral edema (OR 5.4, 95% CI 3.5-8.4, P<0.001).

Approximately half of intracranial hemorrhage patients without radiographic features of elevated ICP had ICP>20mmHg at the time of EVD placement and additional patients had elevated ICP during their hospital stay. Radiographic findings should not be relied upon to exclude the possibility of elevated ICP.

The measurement of intracranial pressure (ICP) is a cornerstone of intensive care management following severe traumatic brain injury (sTBI). It has been only recently that the time integral of ICP has been quantified in relation to outcome; the time integral of brain tissue oxygen (PbtO2) has not been studied.

We gathered time-locked intracranial monitoring data on s TBI patients at the University of Cincinnati over 2 years. Clinical management of all patients followed national standards. Raumedic PTO probe was used to measure ICP and PbtO2; accuracy was verified by visual inspection with automated data cleaning. Normalized data was mapped based on correlation with Glasgow Outcome Scale scores at 3-6 months.

We studied 43 patients aged 42+/-18 years (mean+/-SD); 84% were male. Initial post-resuscitation Glasgow Coma Scale score was median 6 (interquartile range: 4.5-7). 13/43 underwent craniectomy prior to monitoring. Among those with good (GOS4-5) and poor (GOS1-3) outcome, the average ICP was 13.2+/-5.6mmHg and 18.4+/-8.6mmHg (p=0.09); the average PbtO2 was 25.7+/-10.0mmHg and 31.1+/-21.5mmHg (both N.S.). The correlation with outcome was dependent on both ICP and time: an ICP > 27mmHg for > 5 minutes was associated with poor outcome, whereas an ICP < 23mmHg was associated with poor outcome only after 4 hours. In contrast, the PbtO2 level, but not the duration, correlated with poor outcome in those without craniectomy at a PbtO2 < 30mmHg, and particularly below 12mmHg. PbtO2 burden was less reliable in those following craniectomy.

We replicated the effects of ICP/time in a cohort of patients with severe TBI, both with and without craniectomy and subsequently demonstrated the burden of brain tissue hypoxia in those without craniectomy. The time integral of multimodality monitoring data may provide more accurate measures of secondary insult burden with implications for clinical care and prognosis.

Neurologists who work in neurocritical care (NCC) as neurointensivists may have critical care (CC) charges rejected for payment unless they are classified per Centers for Medicare Services (CMS) taxonomy codes in their systems as critical care providers. The Neurocritical Care Society and CMS created a new NCC code 2084A2900X to fix this issue. We polled the AAN CCEN section members for awareness of this problem.

We conducted a six question Google Forms survey using the AAN CCEN Synapse community website to assess knowledge of the NCC taxonomy code: We received 20 anonymous responses by the time we closed the poll on 7/13/17.

Question (Q1) and (Answers, A1): Are you a neurology or neurosurgery back grounded intensivist who does neurocritical care at your hospital? Y/N (yes/no). A1: 95% reported being neurologists. Q2: Were you aware of the new CMS Neurocritical care taxonomy code 2084A2900X ? Y/N A2: 55% were aware of the taxonomy code. Q3: Are you aware why the NCC taxonomy code was created? Y/N A3: 55% of respondents were unaware why this code was created. Q4: What is your primary department for revenue collection? A4: 85% reported Neurology, 15% Neurosurgery, 15% Critical care, and 15% blend. Q5: Are you aware that Medicare can reject critical care charges (99291 and 99292) can be rejected unless you are listed as a CMS 'critical care provider' or as a neurocritical care provider? A5: 20% reported rejected charges at their centers. Q6: Are you aware of rejection of critical care charges happening at your own institution due to this misclassification? Y/N A6: 20% of respondents reported rejected charges at their center.

Although limited in sample size, this survey revealed almost half of the respondents were unaware of the NCC code. We believe a larger study is warranted.

Arterial Subdural Hemorrhage (SDH) is a rare but potentially devastating neurologic entity. It has been associated with ruptured aneurysms. We report a case-series of five patients with arterial SDH and their outcomes.

A retrospective chart review of our institute's vascular database was conducted using a pre-defined search strategy including the terms "aneurysm", "Arterio-venous malformation", "subdural hemorrhage", and "dural Arterio-venous fistula" (dural-AVF).

Amongst 200 patients in the database, five cases were identified with ages ranging from 43 to 78 (four females). Four had SDH due to aneurysm (two internal-carotid, one middle-cerebral, and one posteriorcerebral artery; one had parieto-occipital dural AV-fistula. No patient had preceding head-trauma or anticoagulation. Of aneurysmal patients, one had no SAH. On admission CT-Head imaging, the mean-SDH size was 10.88mm (SD 3.24; range 7.4-15mm), and mean midline-shift (MLS) was 12.64mm (SD 2.49; range 9-15mm). The mean ratio between SDH-size and MLS was 1.16 (SD 0.25). In a historic cohort of acute subdural hemorrhage of non-arterial etiology ; the mean size of SDH was 8.0 mm and the mean MLS was 4.6 mm. Ratio of MLS: SDH size was 0.56. In our series, three patients with aneurysms had decompressive-craniectomy, one had mini-craniotomy for SDH evacuation; the patient with dural-AVF had coiling and mini-craniotomy for SDH evacuation. Four patients had died during hospitalization, whereas patient with dural-AVF recovered to baseline functional-status at 6-month follow-up.

Arterial SDH is a rare entity and may present without subarachnoid hemorrhage and any preceding head-trauma. The degree of midline-shift is usually out of proportion to SDH size. There should be a low threshold to obtain vessel imaging in cases of SDH with no clear trauma history. MLS: SDH ratio may be a useful screening tool for possibility of arterial SDH especially in absence of trauma and may reflect rate of bleeding.

Neurostimulant medications (amantadine and modafinil) are sometimes prescribed after acute nontraumatic brain injury to facilitate wakening and rehabilitation participation; the safety and effectiveness of this practice is unknown. Following a retrospective evaluation of our experiences, we characterized anticipated challenges to designing a prospective randomized trial of neurostimulant medications to promote rehabilitation participation after acute non-traumatic brain injury.

Retrospective chart review of patients over with subarachnoid hemorrhage (n=17), intracerebral hemorrhage (n=41) and ischemic stroke (n=30) who received neurostimulant medications over a period of 43 months. Data regarding clinical course and potential confounders to assessing response were collected. Continuous data are reported as median and interquartile range.

Neurostimulant medications were initiated in 88 patients at a median of 7 (5-13) days after hospital admission, for hypersomnolence 68 (77%), not following commands 28 (32%), lack of eye opening 25 (28%), and/or low GCS 15 (17%). Thirty-nine (44%) patients were receiving sedatives or opioids at the time of neurostimulant(s) initiation. Twenty-two (25%) patients received newly prescribed sedatives or opioids after neurostimulant(s) initiation. Potentially sedating antiepileptic medications were prescribed to 14 (16%) of patients. Twenty-two (25%) patients were intubated at the time of neurostimulant initiation confounding the GCS-V. Potentially confounding clinical factors included hydrocephalus 37 (42%), vasospasm 7 (8%), and seizures 4 (5%). Twenty-eight (32%) of patients had temporary cerebrospinal fluid diversion in place at the time of neurostimulant initiation.

Initiation and titration of neurostimulant medications after acute non-traumatic brain injury was common, but timing and indications varied widely. Confounders to assessing effectiveness included concomitant sedating medications, variable pathophysiology related to the type and location of the stroke, and clinical factors like seizures, vasospasm, and hydrocephalus. These confounders are likely to make prospective evaluation of neurostimulant medication effectiveness difficult in the period of initial therapy following acute non-traumatic brain injury.

Brain small vessel disease can cause cognitive impairment via ischemic or hemorrhagic mechanisms. Current imaging modalities, specifically magnetic resonance imaging allow for easier detection of different intracranial pathological processes including cerebral microhemorrhages (CMs). Research demonstrated that the number and location of CMs correlate with the type of cognitive impairment (memory, processing speed, executive function, and motor speed).

A retrospective analysis of 50 patients (age 44 to 87) seen at our neurology outpatient clinic from 2010 to 2017 who were identified by Linguamatics software to have "microhemorrhage" in their radiology MRI report. Additional information included age, sex, cognitive examination, presence of cardiovascular risk factors, MRI, and the number and location of CMs. Cognitive function was determined by Mini Mental State Examination (MMSE) score and diagnosis by a cognitive neurologist. Patients were grouped by presence of 1 CM or greater (2 to 10) and regression was used to determine a relationship with MMSE and vascular risk factors.

The number of microhemorrhages per patient were 1(17 patients), 2 (5 patients), 3 (8 patients), 4 (12 patients), 5 (3 patients), 6 (3 patients) and 10 (2 patients). Vascular risk factors included hypertension (16 patients), diabetes mellitus (25 patients) and smoking history (26 patients). Regression analyses indicated that the presence of more than 1 CM correctly predicted MMSE lower than 26 at 83% (p=0.003). Age was the only factor that influences this finding and increased this prediction to 90%.

This study provides novel evidence that the presence of multiple CMs on brain images predicts the presence of cognitive impairment. This study raises the need for more investigations.

Point-of-care ultrasound is a valuable tool in critical care, allowing timely and frequent beside assessment of clinical questions. Neurocritical care has long utilized transcranial Doppler but is still early in the adoption of other critical care ultrasounds. This study looked at the comfort level and competency of the participants at the point-of-care ultrasound workshop at the 2016 Neurocritical Care Society Annual Meeting.

The workshop comprised of didactics and hands-on small group practice using live models. Topics covered included ultrasound physics, lung, cardiac, optic nerve sheath ultrasounds, as well as case studies in neurocritical care. Participants were asked to complete an anonymous pre-and postworkshop assessment on a volunteer basis.

A total 41 pre-workshop and 33 post-workshop assessments were completed. The mean age of the participants was 40.7 ± 9.2 years. There were 21 (51.2%) attending physicians, 8 (19.5%) advance practice practitioners, 7 (17.0%) fellows, 4 (9.7%) residents, and 1 (2.4%) research scientist. Participants had limited ultrasound experience prior to the workshop, with 12 (29.2%) reported none, 16 (39.0%) reported < 1 year, and 10 (24.3%) reported 1 to 3 years. On a 1-5 scale on comfort using ultrasound with 1 being very uncomfortable and 5 being very comfortable, participants reported a median score of 2 (IQR 2-3) pre-workshop with an improvement to 4 (IQR 3-4) post-workshop. For 15 matched pre-and post-tests, all 15 participants had an improvement in their ultrasound knowledge.

While the majority of the participants at this workshop had prior ultrasound experience, many are still uncomfortable with their ultrasound competency. The format of didactics and hands-on small group practice improved the comfort level as well as overall ultrasound knowledge of these participants. Additional opportunities for point-of-care ultrasound training should be considered in neurocritical care fellowships and meetings.

Event Related potentials (ERPs) allow assessment of cognitive processing in unconscious brain-injured patients. Here we explored the diagnostic and prognostic value of ERPs obtained shortly after brain injury.

We prospectively collected a comprehensive ERP paradigm labeled "Local Global paradigm" from a consecutive series of unconscious patients with acute brain injury. This auditory paradigm allows the assessment of: 1) cortical responses, 2) unconscious cognitive processing, 3) unconscious focusing of attention, and 4) conscious processing of sounds. Levels of consciousness assessed with the Coma Recovery Scale-Revised (CRS-R) at the time of recording were correlated with the presence/absence of each ERPs component and functional connectivity/complexity measures. We tested the prognostic value of each measure for recovery of consciousness prior to discharge.

We analyzed 32 recordings from 15 patients (median recordings per patients 2[IQR 1,3]). Recordings were made 6 [IQR 4.25,10.75] days after brain injury and all patients were unconscious at the time of the initial recording. Underlying etiologies included ICH(N=6), SAH(N=4), TBI(2) and other (N=3). There were trends for higher CRS-R scores in patients with preserved ERP components. CRS-R scores correlated with the functional connectivity indexed (rho=0.44; p=0.01) but not with complexity measures. Five (33%) patients regained consciousness (within 6 to 42 days from brain injury). One of these patients had to be excluded due to poor quality recording. All the 4(100%) remaining patients had the three type of non-conscious responses preserved on at least one recording in comparison to only 3(30%) among patient who did not recover consciousness (Fischer p-value = 0.07). Similarly, connectivity was greater in patients who regained consciousness (0.0855 vs 0.0797; p=0.05) but the complexity was similar.

Simple bedside ERP responses indexing cognitive processing during the Local Global paradigm obtained shortly after brain injury correlate with the level of consciousness but, more importantly, the probability to recover consciousness.

Over a decade ago, the Institute of Medicine introduced Family-Centered Care (FCC) as a vital aspect of quality health care by strongly recommending that family members of intensive care unit (ICU) patients be actively involved in decision-making. While there are many resources to help ICU staff conduct meetings and provide information to families, the latest Society of Critical Care Medicine guidelines for FCC recommend the implementation of communication and decision support tools for family members to use. Electronic decision support tools such as My ICU Guide have been effective in pilot studies at allowing family members to customize information delivery and communicate their preferences to ICU staff. We sought to integrate a decision support and communication tool for families into an electronic patient portal.

We developed an electronic patient and family engagement checklist for the neurointensive care unit (NICU) using Doctella (Patient Doctor Technologies, Sunnyvale, CA), an existing patient engagement application. Checklist components included: identifying a spokesperson, developing an advance directive, understanding diagnosis and prognosis, access to helpful resources, and a family meeting guide and planner.

We presented the checklist to our hospital's Patient and Family Engagement steering committee for the ICUs and received useful feedback. The checklist will also be vetted by the hospital's Patient and Family Advisory Council. Usability testing will also be conducted.

A family engagement checklist using an electronic patient portal is a novel strategy to enhance communication in the NICU. Further validation of the tool is needed.

Applying painful stimuli to brain injured patients is a time-honored practice assumed to provide valuable clinical information for diagnosis, prognosis, and potential guidance for therapeutic interventions. However, there is limited literature that has evaluated and discussed the benefits and potential adverse effects related to repeated painful stimulation during bedside neurological examinations. Though providers intend to do no harm, the practice of repetitive painful stimulation can unintentionally damage patient's skin, muscle, and bone, as well as inflict emotional duress. In conjunction with basic ethical principles used to justify painful stimulation during patient examinations, we propose a revisiting of the practice of routine repetitive painful stimulation in neurologic bedside assessments.

1. Discuss the current literature regarding the use of painful stimulation and its beneficial and damaging effects, 2. Describe alternative strategies for neurologic assessments, 3. Propose guidelines to optimize accurate neurologic assessments while avoiding unnecessary repeated painful stimulation, 4. Propose the development of a graded methodology for delivering painful stimulation when necessary for neurologic assessments.

A summary of the literature will be outlined and discussed focusing on the ethical considerations and justification for the use of painful stimulation in the neurologic patient and the perception of pain in coma and minimally unconscious patients, 2. Alternative strategies will be presented to minimize bodily and emotional injury, 3. A proposed outline with a companion flow diagram "Easing the Pain Guidelines" implemented in a tertiary care neurocritical care unit will be presented.

There has been little attention paid to the burden of painful stimulation inflicted on patients in the neurocritical care unit. The guiding principle of nonmaleficence (do no harm) morally obligates clinicians to evaluate current practice standards using repetitive painful stimulation in routine neurologic assessments. Implementing standardized guidelines will limit unintended harm to patients without compromising accurate neurologic assessments.

Plasmapheresis is utilized in anti-N-methyl-D-aspartate receptor (NMDAr) encephalitis to remove autoantibodies. Antiepileptic drugs (AED), such as valproate, are often used to control seizures which may complicate anti-NMDAr encephalitis. It is important to prevent rapid reductions of AED levels to ensure proper seizure management in this setting.

We obtained total and free (active drug, unbound to plasma proteins) valproate levels intermittently throughout two 5-day courses of daily plasmapheresis. During the first course, trough levels were obtained. During the second course, levels were obtained before, during, and after plasmapheresis.

The patient was a 26 year old female, weighing 79 kg. Albumin was 2.6 g/dL. Her valproate regimen ranged from 1250 mg to 2250 mg every 8 hours (47 to 85 mg/kg/day), given intravenously or enterally. Prior to the first plasmapheresis, valproate dose was 1250 mg every 8 hours, resulting in a total level of 25 mcg/mL (reference range: 50-125 mcg/mL). Free valproate was 21 mcg/mL (reference range: 7-23 mcg/mL); free fraction was 86% (reference range: 5-18%). Four days later, prior to the 5th plasmapheresis, the total valproate level was 35.3 mcg/mL. Two days after the 5th plasmapheresis the total level was unchanged at 34 mcg/mL; free valproate was 8 mcg/mL and free fraction was 24%. During the second course of plasmapheresis, valproate total levels, free levels, and free fractions were 49 mcg/mL, 18 mcg/mL, and 36% before, 105 mcg/mL, 24 mcg/mL, and 23% during (valproate dose given upon initiation of plasmapheresis), and 59 mcg/mL, 24 mcg/mL, and 41% after plasmapheresis, respectively.

Valproate serum levels were not markedly influenced by plasmapheresis. Free valproate levels and the free fraction were highly elevated throughout the patient's hospital course, however. Future studies should evaluate critically ill patients' clinical response and toxicity correlations as the free fraction of valproate appears to be elevated in this setting.

The purpose of this study is to assess knowledge retention of Emergency Neurological Life Support (ENLS) after participation in the course via a prospective observational study.

Study subjects seeking ENLS certification consented for study participation (ENLS-VS) from the NCS website then took a closed-book, 70 multiple-choice question pre-test within 72 hours of ENLS course participation. After completion of the ENLS course, participants took the same closed-book, 70 multiplechoice question test (post-test). These tests consisted of novel questions from material presented in the course. Questions were not repeated from the ENLS certification exams.

Thirty participants enrolled in the study with 11 completing both the pre-test and immediate post-test. All 11 participants' scores improved on the post-test as compared to the pre-test. The mean percent correct on the pre-test was 63.5% with a median of 64.3% (range 34.5-85.7%). Of the participants who have completed both pre-and immediate post-test, the mean pre-test score was 72.4% with a median of 72.9% (range 61.4%-72.9%). The mean post-test score was 86.7% with a median of 88.6% (range 77.1%-94.3%). The improvement of scores was statistically significant on the post-test compared to the pre-test (86.7% vs. 72.4 % %, p< 0.005).

All participants in the Emergency Neurological Life Support course showed improved test scores immediately after participation in the standard ENLS course. This study will assess knowledge retention at 6-months following training, and is actively enrolling new participants.

Augmented renal clearance (ARC, defined as a creatinine clearance of > 150ml/min) has been demonstrated in neurocritical care disease states such as traumatic brain injury, intracranial hemorrhage, and subarachnoid hemorrhage. ARC may result in increased elimination of renallyeliminated medications, thereby reducing drug exposure with standard doses. The overall prevalence of ARC is not well described. The purpose of this study was to estimate the overall prevalence of ARC in a neurocritical care population.

This was a retrospective cohort study of adults > 18 years of age admitted to the intensive care unit on the neurosurgery service. Demographic and pertinent laboratory data were collected for patients admitted from January 1, 2016 thru December 31, 2016. An ARCTIC score was calculated for each patient (6 or greater suggests ARC). Parametric data was compared using one-sample Student's T-test, nominal data was compared using Fisher's exact test (alpha = 0.05). Statistical analysis was conducted using IBM SPSS version 24.

present in a total of 37.24% of patients. A broad spectrum of neurocritical care diagnoses was present. The mean age in years was significantly lower in patients with ARC [47.8 (14SD)] than without ARC [54 (17SD), p = 0.026], as was the serum creatinine [with ARC 0.55mg/dl (0.1SD) vs without ARC 1mg/dl (0.6SD), p < 0.001]. Mean hospital length of stay was greater in patients with ARC than without [10.1 (10SD) vs 6.5 (10SD), p < 0.001].

ARC occurs commonly in neurocritical care patients and likely merits proactive screening or direct measurement of creatinine clearance in select patients. Pharmacokinetic studies of commonly used renally-eliminated medications may be needed to establish population parameters in the neurocritical care population.

Education surveys demonstrate gaps in resident neurocritical care education and training. We assessed junior residents' baseline knowledge of neurologic emergencies, procedural competency, knowledge of available resources, and the impact of pre-rotation orientations.

Junior residents (neurosurgery PGY1s and neurology PGY2s) who had not previously rotated in the NeuroICU were surveyed. A three-part survey was administered: Part I, knowledge of ICU structure and personnel; Part II, procedural competency; Part III, comfort with common neurocritical care emergencies. The survey was comprised of selection responses. After the survey but prior to starting the rotation, each resident was oriented to the unit by a neuroICU attending and nursing director. This orientation reviewed rotation goals, ICU structure, personnel and rounding expectations. A survey was repeated to evaluate the orientation.

Of 15 residents who had not rotated in the ICU, 10 (66.7%) responded. None of the residents understood their specific role within the ICU team. 80% did not understand the role of the resource nurse and were unaware of where to find procedure equipment. 60% of residents were not comfortable placing an A-line; 30% were not comfortable performing a lumbar puncture. Over half of respondents said they "didn't know and could not easily find" the indications for hemicraniectomy after malignant MCA ischemia, the indications for ICP monitoring, or the initial workup of autoimmune encephalitis. 14 residents responded to post orientation surveys. 76% felt the orientation was helpful in explaining the roles of team members. 61% felt it was at least "somewhat helpful" in understanding the role of the resource nurse. 46% felt the orientation was "helpful" and 38% felt it was "somewhat helpful" in identifying the goals of the rotation.

These baseline measures underscore the importance of structured interventions, both before and during the NeuroICU rotation, to improve junior resident comfort and preparedness in managing neurologic emergencies.

Physician-staffed helicopter emergency medical services (HEMS) are a well-established component of prehospital care in Japan. However, there has been no report on HEMS and neurocritical care patients. We studied characteristics of neurocritical care patients who were transported by HEMS.

We retrospectively evaluated neurocritical care patients who were brought to our Emergency and Critical Care Medical Center (ECCMC) by HEMS between January, 2010 and March, 2017. We excluded patients in whom the outcome was unknown, those who were transported to other hospitals or between facilities.

Of 4216 

The most important role of HEMS is rapid transportation of a flight medical team to the scene to provide immediate, lifesaving medical treatment. We found that half of patients admitted to our hospital by HEMS were neurocritical care patients. As proposed in the ENLS of neurocritical care society, HEMS is considered useful to allow neuro-emergency patients to receive the best care in the first hour.

Optic Nerve Sheath Diameter (ONSD) measurement using ocular ultrasound has been shown to accurately detect elevated Intracranial Pressure (ICP), but does require specialized training. Variations in the optimal ONSD threshold for detection of elevated ICP in the literature limits clinical utility, and may reflect heterogeneity in manual measurement techniques. Our objective was to develop, and validate against expert measurement, an image-analysis algorithm for ONSD measurement to facilitate standardization and ease of use of this technique.

Consecutive patients with acute brain injury admitted to the neurointensive care unit underwent ocular ultrasound with a multipurpose point-of-care ultrasound machine. A 6-second video was recorded from each eye in the axial plane and downloaded in DICOM format. The ONSD measurement algorithm was as follows. An average of images was calculated using non-overlapped segments of the image sequence. A line integral was performed to estimate the border of the region of interest (ROI), the globe. The ROI orientation and globe point of the segmented region were established, then a point 3mm posterior to the globe point identified. The ONSD was measured at this point. Manual ONSD measurement was performed separately from the DICOM videos by an expert blinded to the algorithm measurement. An Intraclass Coefficient (ICC) was calculated for absolute agreement between highest ONSD measured by the algorithm and expert manual measurement.

A total of 27 patients with acute brain injury underwent ocular ultrasound. The ICC for absolute agreement between algorithm (median 0.66, Interquartile Range 0.61-0.71) and manual expert (median 0.63, 0.61-0.71) highest ONSD measurement was 0.68 (95% Confidence Interval 0.31-0.85).

An algorithm for automated measurement of ONSD was developed and demonstrated good inter-rater agreement with expert measurement, although further refinement is required. Automated measurement may help standardize and simplify a promising noninvasive bedside tool for the detection of elevated ICP.

After transition to electronic health record (EHR), transition to inpatient hospice required a separate encounter to account for change in insurance payer in our neuroICU. This negatively affected completed transitions and hence patient-centered care. The focus of this quality improvement project was to define the new process, improve outcomes, and identify further opportunities.

The Quality Improvement method "Plan-Do-Study-Act" was employed for this work within a 30-bed Neuro-ICU at a large Academic Medical Center. We assessed the current state (not enabling transition to inpatient hospice) and the desired state (enrollment in hospice during inpatient stay). A new process was created using an EHR Discharge Navigator, coordinating all relevant stakeholder groups (patient/caregiver, nurse, pharmacist, bed control, physician,). In addition, standard methodology for unit-based education, in-service, just-in-time training, and booster education was employed to identify process, outcome, and improvement opportunities.

After rollout of the new discharge navigator, 90% of all patient-facing staff successfully completed the Inpatient Hospice training. Process Improvements lead to increase in Palliative Care consults by 500% (16 to 96 annually) and Inpatient Hospice discharges up to 30% (68 to 88 annually). Furthermore, there was a statistically significant improvement in the Vizient Mortality Index R2 = .11, F(1,51 ) = 22.64, p < .05 and Length of Stay Index R2 = .10, F(1,51) = 12.64, p < .05 within the study population and period.

Ability to transfer patients to inpatient hospice is often limited and complicated. This study shows how employing standard Quality Improvement as well as Education and Implementation methods can result in improved process and outcome measures with sustainable success. Opportunities remain in further analyzing and optimizing 'Time to Palliative Care consult', 'Time to Admission to Hospice and Withdrawal of Artificial Support'.

ARNP and PA's are a rapidly growing part of the critical care workforce. Proper selection among a pool of APP candidates for the job is necessary to ensure the "right fit" and optimize patient safety. Conventional interview techniques may not be adequate when selecting critical care APP's. We hypothesized that use of a Simulation Center could be used to help select APP candidates based on their critical thinking skills in conjunction with contemporary interviewing skills.

From 2010 to 2013, we performed conventional interviews for APP's to staff critical care and neurocritical care patients. In 2014 we changed to an interview process consisting of the conventional interaction with the interviewee followed by simulation. After narrowing down the initial candidate pool, each was taken to the simulation center where they participated in a simulation of a decompensating patient. Proctors were able to view the simulation in a separate room and direct the simulation mannequin. During this time proctors were able to evaluate the interviewee's patient interaction, assessment and interventions. An evaluation tool was to grade APP candidates for their decision making skills, communication and thought.

From 2014 to 2017, we screened 40 candidates before selecting 21 for interviews and finally 10 of those for simulation. Over this timeframe, our center hired 6 APP's. Comparing the ratio of screen applicants to employment was 6.6 and ratio of interviewed to hired candidates was 3.5. These ratios show the competitive process and potential use of Simulation in selecting APPs. Compared to the time period of applicants prior to Simulation to after, retention went from 75 to 92%, and disciplinary action for practice deficiencies went from 16% to 0%.

The use of simulation based interviews for critical care APP's in our institution improved retention and decreased the number of disciplinary actions compared to conventional interview methods.

The contraindications for lumbar puncture (LP) in the setting of cerebral mass effect remain debatable. Limited retrospective data advocate its potential safety. Yet, high-quality guidelines specifically addressing this topic are not available. Specific patient populations (post-instrumentation & immunosuppressed) may benefit from CSF studies. We reviewed 1072 consecutive patients who underwent LP and cerebral imaging a week before or after LP from 2007-2014. All individuals with evidence of brain herniation, a component of midline shift, or mass effect were included. All subjects received a low volume LP (5-10 cc of CSF).

There were 132 patients with radiological increased ICP. Midline shift (average = 4 mm) was present in 39 patients. We also observed herniation: uncal (n=16), subfalcine (n=15), and a combination of both (n=10) , ventricular effacement (n=67) and cisternal compression with partial occlusion: Quadrigeminal cistern (n=3), cerebellar-pontine-angle cistern (n= 14), ambient cistern (n=24), crural cistern (n=14), prepontine cistern (n=7), suprasellar cistern (n=12), basal cistern (n= 2), suprachiasmatic cistern (n= 4), cisterna magna (n=3), interpeduncular cistern (n=3), medullary cistern (n=4). All patients tolerated the LP without complications. Most survived a week after the procedure (n=128, 97%). Notably, four individuals deteriorated for reasons unrelated to the LP and expired within a week because of withdrawal of care.

As brain compliance cannot yet be accurately determined radiologically, we believe anatomical involvement should drive decision-making regarding LP safety. Our data suggest that a low volume LP (5-10 cc) might be safe in individuals with subfalcine herniation, midline mass effect < 4 mm at foramen of Monro level, and partial cisternal effacement. We believe that while LPs might be safer in patients with supratentorial mass effect, individuals with posterior fossa involvement may tolerate it as well. These promising findings need further verification in larger sample populations.

The importance of neurocritical care has recently been recognized in Japan. However, to date, there has been no neurocritical care training program. We developed the Neurocritical Care Hands-on Seminar as a proposed training module, and here we report the satisfaction of participants.

We prepared a post-course questionnaire about participants' degree of satisfaction. The main concept of our seminar was "how to maintain cerebral oxygen demand and supply balance." Beginning with a short lecture about this concept, participants joined four hands-on scenarios: post-cardiac arrest syndrome (PCAS), subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), and states epilepticus (SE). In the PCAS scenario, participants learned how to trouble shoot regarding targeted temperature management, especially in regard to the management of shivering. In the SAH scenario, they learned about perioperative management, including delayed cerebral ischemia. In the TBI scenario, starting with actual insertion of an intracranial pressure (ICP) monitor in the simulator, they learned about ICP management through a scenario-based simulation. In the SE scenario, they learned about SE management, with actual continuous electroencephalogram monitoring.

This seminar was held twice in 2017. Most participants were middle-aged intensivists; 11% were in their twenties (6/54), 64.8% were in their thirties (35/54), 18.5% were in their forties (10/54), and 5.6% were in their fifties (3/54). Most of the participating physicians were specialists in emergency or intensive care medicine (74.1%; 40/54); nurses (13.0%; 7/54) and a clinical engineer (1.9%: 1/54) also participated. Most participants (81.5%; 44/54) were satisfied with the seminar, and almost all (98.1%; 53/54) improved their self-confidence in the ability to carry out clinical practice in neurocritical care.

We received positive, satisfied reactions from the Japanese intensivists who participated in our seminar. For further improvement, we need to collect objective data to assess the utility of our Neurocritical Care Hands-on Seminar.

Lumbar puncture in the presence of mass effect?

Ciro Ramos-Estebanez UHCMC, Case Western Reserve University/Neurology, Cleveland, Ohio, USA Introduction 1) We propose an international consortium that would prospectively confirm the safety of low volume lumbar puncture (LP) in the presence of mass effect in selected scenarios. 2) Welcome peers and advisors to join the effort. LP may be clinically necessary in the presence of cerebral mass effect. While empirical antibiotic therapy is generally successful, specific groups such as post-instrumentation patients and immunosuppressed individuals may benefit from cerebrospinal fluid (CSF) studies. In the absence of high-quality clinical recommendations, uncontrolled retrospective literature suggests that a small volume LP (5-10 cc) might be without complications in specific situations. Nevertheless, the ethical principle of non-maleficence and the liability risk prevent clinicians from performing LPs. In this scenario, an extended length of stay, poor outcomes, or a higher cost of care are legitimate concerns. Synthesize an external peer reviewed methodology to maintain rigour and transparency. 6.

Seek appraisal, approval and endorsement of national and international Quality Improvement Committees. 7.

Generate and assimilate the most current clinical evidence through:

A. Systematic review and meta-analysis. B. Prospective randomized controlled clinical trial. 8.

Construct a protocol to inform decision making amongst healthcare and non-healthcare personnel. 9.

Dissemination and implementation. 10. Schedule updates and/or revision.

15 centers across the globe (North America = 5, South America=4, Europe=2, and Asia=5) have agreed to establish an LP consortium so far.

Retrospective analyses suggest low-volume LP's relative safety in the presence of increased ICP. Thereby, an expert consortium trusted with prospective verification would potentially benefit specific patient populations.

Patient centered decision making in the NCCU requires family members understanding of their loved one's preferences and values as well as the complexities of their medical condition and treatments. Family-Centered Care (FCC) is essential so that family members are actively involved in decision-making. Stakeholders have reported their preference to receive prognostic information in smaller packets and recapitulated in different venues including rounds, bedside and care conferences. We examine implementation of a multimodal communication strategy on clinician utilization, family engagement and satisfaction in the NCCU.

An interdisciplinary team convened to develop a plan implementing a multimodal communication strategy. Pre-implementation survey of clinicians (MDs, NPs, RNs, etc.) and patient families was completed to determine the level of family engagement already in place in the NCCU. Four interventions were implemented: family communication boards were installed in patient rooms; family engagement pamphlets developed; a script and schedule for family care rounds was developed; nursing and provider staff were educated on inviting families to participate in patient care team rounds. Family involvement on patient care rounds and family conferences was compared before and after the implementation of the 4 best practice initiatives. Additionally, pre and post implementation patient satisfaction survey results were also compared to evaluate the project's success.

Pre-implementation data was collected from October -November 2016. Sixty-one clinician surveys and forty family surveys found that family more consistently participated on daily rounds. Baseline and postimplementation surveys demonstrated families feeling supported during the decision-making process.

The implementation of a multimodal communication framework to achieve consistent family engagement and communication has led to an appreciable change in utilization by clinicians. Its use is supported by consistent positive family attitudes towards communication and availability of information in the NCCU.

Neurocritical Care Society undertook initiatives to integrate social media in member engagement activities and initiated a Twitter Journal Club (#NCSTJC) in 2015 with the first Journal Club conducted in February 2015. Articles were chosen by a subgroup of the Communications Committee in consultation with Dr. Eelco Wijdicks, Chief Editor, Neurocritical Care Journal. These articles were chosen based on their overall importance and the interest bound to generate amongst the journal club attendees. The journal club occurs bimonthy over an hour and is unique in the participation of the authors. The journal club is registered with Healthcare Hashtag Project. Each article chosen for #NCSTJC is made available free to download 2 weeks before and after the scheduled date for the journal club courts Springer.

Analytics data on usage on article discussed in #NCSTJC was obtained from Sean Beppler, Editor, Clinical Medicine.

Between Feb 2015 and Apr 2017, 12 sessions were held with data available from 11. The NCC articles discussed had higher than average Altmetric scores (measuring social media activity). These articles represented 5% of all NCC articles discussed on Twitter since Feb 2015 but 15.3% of all tweets. Total Usage (number of times an article HTML page is accessed, or a pdf is downloaded ) was 12, 989 ( Mean 1082, n=11) representing 24.6% usage of all neurocritical care articles, a total of 39 citations and 3191 downloads ( mean 290) . The upper bound of the audience as assessed by the publisher was total of 111, 524 for all 1 articles (mean 9,294 per article)

Twitter is becoming an emerging platform for dissemination of information in medical education and academic activities. While the exact impact of the initiative on member engagement or outreach in enhancing journal impact or citations is hard to determine, we saw trends in enhanced engagement.

Neurostimulant medications have been studied in patients with traumatic brain injury, but few studies describe their use in patients with acute non-traumatic brain injury. Our objective was to describe neurostimulant medication prescribing patterns, clinical response, and potential adverse effects in this patient population.

Retrospective database review of patients with acute ischemic stroke, intracerebral hemorrhage, or subarachnoid hemorrhage who received amantadine or modafinil from December 2012 through June 2016. Neurostimulant selection, dosing regimen, and indication were recorded. Patients were classified as responders if they met two of the following three criteria within 7 days of neurostimulant initiation: 1) increase in average daily GCS of greater than 3 points, 2) neurological improvement documented in provider progress notes, or 3) increased participation in rehabilitation therapies documented in physical or occupational therapist progress notes. Safety data included need for a new anxiolytic or sleep aid or seizure. Continuous data are reported as median with interquartile range.

Eighty-eight patients received neurostimulants: intracerebral hemorrhage (n=41), ischemic stroke (n=30), subarachnoid hemorrhage (n=17). Median age was 66 (55-73) years and 57 (65%) were male. Amantadine (n=71), modafinil (n=13), or both (n=4) were initiated a median of 7 (5-13) days after hospital admission. The median initial daily dose of amantadine and modafinil were 200 mg and 100 mg, respectively. Reasons for initiation included somnolence (77%), not following commands (31%), lack of eye opening (28%), and low GCS (17%). Forty (45%) patients were responders, occurring at a median of 3 (2-5) days after neurostimulant initiation. Twenty-three (26%) patients required new prescription of an anxiolytic or sleep aid. Four (5%) patients developed seizure.

Neurostimulant medications may increase wakefulness and participation in rehabilitation therapies in patients with acute non-traumatic brain injury, with tolerable adverse effects. The role of neurostimulants in this population should be defined in prospective studies.

Difficulty in obtaining peripheral intravenous (PIV) access often necessitates central venous access placement in many critically ill patients. Central line placement exposes patients to potential complications such as pneumothorax, hemorrhage, catheter-related infection or deep venous thrombosis. Ultrasound-guided PIV placement has become common practice in emergency departments, but there is no systematic program to train and support routine use of ultrasound-guided PIV access in ICUs. We have developed a systematic program to train and support ICU nurses in becoming experts and clinical leaders in ultrasound-guided PIV placement. We hypothesize that implementation of this program will increase nurse confidence and chances of successful PIV placement subsequently decrease central line-related complications in 30-bed neurocritical care ICUs.

We have developed a video didactic training program for the neurocritical care nursing staff. The program discusses use and maintenance of the ultrasound machine and guided-technique for PIV placement including the short-and long-axis approaches. The training video is followed by a hands-on simulation session using mannequins. Standardized-surveys are administered to nurses before training and then at 3 and 6 months post training.

We are prospectively collecting data on nurse comfort level with ultrasound-guided PIV placement, total IV attempts, patient central line associated bacteremia (CLAB) rates and total number of patient central line days. We will compare this data for 6 months pre-and post program implementation. Comparisons will be made using t-test and Chi-square analyses or non-parametric equivalents depending on data distribution.

Central-line related complications are an important clinical problem in all ICUs. We have developed and implemented a systematic training program to support nursing-led ultrasound-guided PIV placement. We will determine if this program reduces the overall number of central lines placed, duration of indwelling central lines, and CLAB rates in a neurocritical care, and subsequently expand to additional ICUs and beyond.

Ultrasound measurement of optic nerve sheath diameter (ONSD) is a sensitive and specific non-invasive ultrasonographers. Despite clinical applications in the ICU, ER and outpatient settings, neurology residents lack experience and training. The aim of our project was to provide neurology residents with foundational skills in ocular ultrasound and ONSD measurement.

We designed a two-part workshop for neurology residents covering ultrasound basics, measurement of ONSD, and ultrasound appearance of papilledema. Workshop 1 was a 30 minute lecture and demonstration followed by 90 minutes of hands-on practice. Two weeks later, workshop 2 included 60 additional minutes of practice to consolidate learning. The practical portions were facilitated by emergency medicine attendings and residents with experience in performing ocular ultrasounds. Neurology residents tracked the number of practice ultrasounds performed. They also completed anonymous pre-and posttests to assess their knowledge of ocular ultrasound and their comfort level and likelihood to perform future procedures using a 6-point Likert scale.

Prior to the workshop, the majority (14/19) of neurology trainees had never performed an ocular ultrasound. One (1/19) was able to answer two basic questions about the procedure correctly, which increased to 100% on the posttest (n=16). Trainees performed an average of 5 ultrasounds total during the workshops. Resident self-assessment of comfort performing the procedure increased from a median of "very uncomfortable" to "moderately comfortable" on the 6-point Likert scale (p=0.001). Resident likelihood to perform the procedure in the future increased from a median of "very unlikely" to "moderately likely" on the 6-point Likert scale (p=0.002).

This session successfully increased basic knowledge, comfort, and likelihood to perform ocular ultrasound among neurology residents. Future directions include follow-up to gauge magnitude of practice changes and accuracy of procedural skills.

Reaching patients by telephone is a common method of assessing functional outcome, cognitive function, and quality of life after hospital discharge. However, when patients do not answer the phone, missing data creates bias and warrants strategies to increase follow-up rates. We hypothesized that we would have less follow up with patients discharged to long-term care facilities and sought to examine other potential sources of lost data.

Between 1/2016 and 3/2017, we identified all patients admitted to the University of Cincinnati Neuroscience Intensive Care Unit (NSICU). We excluded those with recurrent admissions, boarders, and those admitted < 24 hours or for uncomplicated post-op care. Telephone follow-up was attempted for each patient. Univariate analysis was used to identify associations with patients who did not answer the phone.

1103 critically-ill patients were included. Average age was 59.7+/-17.6 and 53% were men. The average hospital length-of-stay was 9.4+/-8.9 days. Major diagnoses were: ischemic stroke (25%), intracerebral hemorrhage (19%), traumatic brain injury (15%), seizures/status epilepticus (10%) and subarachnoid hemorrhage (9%). 271 (25%) died in the hospital; 130 (12%) died by follow-up. 702 survivors were assessed 133.2+/-25.6 days following admission. 462 calls were answered, 231 were not. There were no associations between rate of answered calls and age, gender, race, hospital length-of-stay, diagnosis, or hospital disposition. There were no differences in between morning vs. afternoon calls. Only the number of attempts differed: the probability of an answered call was 90% on the first attempt but declined to 14% by the third attempt (OR 0.13; p<0.01).

Our outcome assessment strategy captured data on 78% of neurocritically ill patients. Those who answer the phone are most likely to answer with the first call; the probability of a patient answering after a second phone call may not justify resources needed to continue calling these patients.

Posterior reversible encephalopathy syndrome (PRES) typically presents with vasogenic edema on neuroimaging. A subset of patient, however, can have "atypical findings" including restricted diffusion and intracranial hemorrhage. These atypical findings all suggest acute vascular injury, and may mark a distinct pathophysiological subtype of PRES. However, it is unknown whether atypical imaging findings are associated with differences in precipitating factors or outcome.

Patients with evidence of restricted diffusion, frank hematoma, microhemorrhage, or subarachnoid hemorrhage were classified as having atypical imaging findings. The demographics, risk factors, clinical outcomes, and degree of vasogenic edema for patients with typical (n = 109) vs atypical PRES findings of vascular injury (n = 75) were analyzed.

Patients with atypical PRES had a longer hospital stay (22.8 vs 15.4 days; p = 0.039) and were less likely to be discharged home (54.7% vs 69.7%; p = 0.036). Severity of vasogenic edema (graded using a standardized radiologic scale) was also higher in patients with atypical imaging findings (severe edema: 41.3% vs 21.1%; p = 0.003).

Restricted diffusion and hemorrhage are features of acute vascular injury that may mark a unique pathophysiological subtype of PRES. PRES patients with these atypical imaging features had longer hospital stays, greater degree of vasogenic edema, and were less likely to be discharged home. This may be due to the fact that bleeding and infarction lead to irreversible brain injury, prolonging hospital stay and contributing to overall disability.

In 2016, 16 deaths occurred in the neuro-oncologic critical care unit (NCCU). The impact of this event is significant for patients, families, and the staff that care for them. Brain and spinal pathology can be incredibly debilitating causing a rapid and impromptu decline of the patient's status. In order to better support patients, family, and staff throughout the dying process, the NCCU staff created formalized endof-life care interventions. These interventions include educational pieces and supportive approaches to aid all involved through the dying process.

Several interventions were created to help transition the family members during the dying process. These include the creation of: DNR-CC closet, homemade blankets, condolence cards, hygiene bags, educational packets, Word Clouds, and aromatherapies and massage items. Once the patient's code status is changed to comfort care, a blanket is given to the patient. Family members are provided with a bag of toiletries for those that remain at bedside. Education on the dying process are given to family members. Multidisciplinary resources are provided, such as religious support focused on patient/family beliefs, palliative care for symptom management, and dietary provision of light snacks to the family. Education for the physicians, nurse practitioners, nurses, and patient care associates was provided for those who wished to attend to further understand this end of life care program. A 29 item tool was created to collect before and after data on staff satisfaction and comfort with the end of life process.

Results from this process are currently in process.

Creating specific end-of-life care interventions for the NCCU have enabled staff to better care for patients and families. Through the creation of the interventions and utilization of the DNR-CC closet, this unit has been able to better provide comprehensive education and supportive pieces to patients and family members during such a difficult time.

Delirium is a neuropsychiatric syndrome, characterized by disturbance in awareness, with reduced ability to sustain attention, impaired cognition, perception, tends to fluctuate in severity during the day; In critical care is associated with longer stay and increase mortality. This study aimed to determine the incidence, prevalence, predictors, risk factors and outcomes of delirium in Critically ill Adult.

A historical cohort study was conducted in adult patients hospitalized in a polyvalent ICU from January 2016 until December 2016. Delirium was diagnosed using CAM-ICU. A bivariate and multivariable risk were analyzed and presented as odds ratio (OR) and 95 % confidence interval (CI).

A total of 1133 patients were enroll. Delirium developed in 276 patients.The incidence was 24.3%. Three independent predictors for delirium were identified, Sedation (OR 6 (95% CI, P < 0,001); alcohol dependence (OR 4,4; 95%CI, P < 0,001) and Glasgow coma Scale < 8 (OR 2,2; 95% CI, P < 0,001). Delirious patients had a significantly APACHE II (15 (11-21) vs 13 (8-19), P < 0.001), higher SOFA, (6 (3-8) vs 4 (2-7), P< 0.001) and higher SAPS III (56 (48-65) vs 50 (41-60), P< 0.001). Other risk factors were hyperlactatemia ( P<0.002), and Hypotension (MAP<65mmHg),(P< 0.035). Patients required prolonged mechanical ventilation, P< 0.001), and prolonged ICU-hospital stay.

The incidence of delirium in the period from January 1 to December 31, 2016 was 24.3% in a polyvalent intensive care unit. Exposure to sedative medications, alcohol dependence, and decrease Glasgow coma Scale minor 8 are independent predictors for the development of delirium. Similarly, the ICU stay was longer in the group that developed delirium; however, mortality was not affected by the presence of this condition.

It has been previously reported that the course of HSV-2 in the CNS is significantly more benign that HSV-1, and that it rarely causes encephalitis or significant morbidity in immunocompetent adults. The aim of our study was to investigate the claim that HSV-2 CNS infections are typically benign, and to assess for predictors of poor outcome in those patients who do suffer significant morbidity from HSV-2 CNS infections.

Restrospective chart reviews were completed on patients with a positive HSV PCR at our institution from July 2008 until July 2016. Patients with a HSV PCR positive for HSV-2 were selected in our analysis. Multiple clinical variables were evaluated in these patients and we assessed outcome in the patient population, dichotomizing outcome into two categories at the time of discharge: good outcome defined as home or inpatient rehabilitation versus those with poor outcome defined as death, hospice, or placement in a long term acute care facility. 21 patients with HSV-2 positive PCRs were identified. Their charts were evaluated for demographics, laboratory values (serum and CSF), imaging results, and outcome.

There were 3 patients with poor outcomes. It was noted that they were all female, their mean age was 59.6 (vs 47.2 in the good outcome group) and two of the three were immunocompromised (67% vs 44% in the good outcome group).

Statistical analysis was performed however due to the small sample size no statistical significance was found. However, age, sex, clinical presentation consistent with encephalitis and immune status seemed to have a trend towards poor outcome in this pilot study. Future study with larger sample size is warrented to further assess this trend, as HSV-2 may not be as benign as previously reported.

There is a high prevalence of non-traumatic illness in patients presenting to emergency departments as trauma team activations (TTA). We sought to determine the prevalence of neurologic emergencies within a population of patients receiving a TTA.

This was a retrospective review of prospectively-collected registry data capturing all TTAs in a highvolume, urban, academic level I trauma center. Records from June 2011 through June 2016 were reviewed to identify patients found to have a diagnosis of ischemic stroke, intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH) or status epilepticus. Further demographic, clinical, and outcomes data was then abstracted from the electronic medical record. A proportion of abstracted charts were reviewed by an independent reviewer to ensure data quality.

There were 18,859 trauma activations in the registry during the study period. 120 patients (0.6%) were found to have a nontraumatic neurologic emergency and were included in the analysis. Of these patients, there were 55 ischemic stroke (46%), 40 ICH (33%), 15 SAH (13%), and 10 status epilepticus (8%) patients. The mean age was 67, and 70 patients (58%) were male. The mean GCS on presentation was 10. About half of these patients (43%) were intubated in the emergency department. All patients received a head CT scan. 20 patients (16%) received intravenous thrombolysis.

Neurologic emergencies such as ischemic stroke, ICH, SAH or status epilepticus were common diagnoses in this population of trauma activation patients. Clinicians caring for patients in these settings must maintain a high index of suspicion for non-traumatic illnesses, and act quickly to mobilize appropriate resources when a diagnosis is made to avoid delays in care. Further research is needed to examine ways to improve both time to diagnosis and quality of care in this patient population.

Formalized communication strategies decrease post-traumatic stress disorder (PTSD) symptoms in caregivers in the intensive care unit (ICU). In one study, only 2% of family meetings met all shared decision-making criteria. However, much of the research has focused on family meetings, ignoring less formalized communication.

The decision maker (patient or caregiver) was interviewed for all patients admitted to the medical (MICU), neurosciences (NSICU), surgical (SICU), and cardiothoracic ICU (CTICU) for greater than 72 hours. Subjects who stated significant decisions had been made were asked to report on 10 aspects of shared decision making on a 5-point scale. They identified the lead provider, who was subsequently approached to complete the same questionnaire.

Overall, 121 eligible decision makers were identified, 47 (39%) in the MICU, 31 (26%) in the NSICU, 25 (21%) in the SICU, and 18 (15%) in the CTICU. Of these, 63 (52%) were unable to be contacted, 7 (6%) had insufficient English, and 13 (11%) reported no decisions made, with 38 (31%) enrolled. Nineteen (50%) provider interviews were completed. Topics most reported covered "Well" or "Thoroughly" by caregivers were assessment of understanding (36, 95%) and the nature of the decision (35, 92%), while those least covered were need for input from others (23, 61%) and the context of the decision (25, 66%). Topics reported most covered by providers were the nature of the decision (18, 95%) and opinions about the treatment decision (17, 89%), while those least covered were patient's values and preferences (12, 63%) and their preferred role in decision making (10, 53%). Eighteen (47%) caregivers and 5 (26%) providers described all topics covered "Well" or "Thoroughly."

These results demonstrate differences in perception of shared decision making by decision makers and providers. Further qualitative investigation is underway to elucidate the nature of these inconsistencies.

Organ donation is a life-saving medical intervention. The effect of race, insurance and economic status on organ donation and recipients has not been studied at a National level.

In our study, we analyzed Nationwide in-patient (NIS) database of years 2011-14 to select donors and recipients. Baseline demographics (i.e., Age, gender, race), insurance status and socio-economic status was compared between two groups.

We identified donors (n=26821) and recipients (n=108953) from 2011-14. Recipients were significantly older (Mean age ± SD, 50.3±16.3 Vs 41.5±13.5, p<0.001). Donors had higher (57.1% vs 38.3%, p<0.001) proportion of women compared to recipients. Both groups had a higher proportion of Whites compared to other races (67% and 57.9% respectively). Insured patients were largely represented in both groups with Private insurance predominating in donors (67%) and Medicare in Recipients (50.2%). Interestingly, Self pay represented 15.5% of Donors but only 0.8% of Recipients.

Race, insurance and socioeconomic status seem to be evenly similarly represented in Donors and Recipients. Interestingly Self pay insurance has a higher distribution among Donors than Recipients.

Central line-associated bloodstream infections (CLABSIs) are a common health care associated infection accounting for 30,100 infections annually in the intensive care and acute care areas (CDC,2014). According to the Center for Disease Control, CLABSIs result in thousands of deaths yearly and upwards of billions of health care dollars spent on preventable hospital acquired infections. Intensive care patients, especially the neurocritical care population, have an increased need for centrally placed catheters related to inadequacy of peripheral access, need for caustic IV medications, and fluid resuscitation. Our NeuroICU's goal was to decrease utilization and subsequently reduce number of CLABSIs. In February 2016, we initiated a patient-centered quality improvement effort with this goal in mind.

The NeuroICU Clinical Nurse leaders conducted rounds daily to evaluate the necessity and management of central lines. The Neurocritical care team and clinical nurse leaders collaborated in exploring alternatives if central lines were present. In addition to daily rounding, CLABSI bundles based on CDC guidelines for CLABSI prevention were initiated. Our NeuroICU developed checklist "Buster Cards" in September of 2016, prompting staff to the bundle interventions. The intent of the cards was to enhance nurse to nurse dialogue of bundle elements. The cards were evaluated monthly for trends in care.

From August 2015-June 2017, there was a 15% reduction in NeuroICU utilization of central lines. In addition, the mean number of CLABSIs per month decreased from 0.67 to 0.22. Trending of unit Buster Cards did not show care variances during this time period.

Implementing daily Clinical Nurse Leader rounds with enhanced team communication significantly reduced the NeuroICU's utilization of central lines and thereby decreased the rate of CLABSIs.

Percutaneous dilatational tracheostomy (PDT) is one of the most commonly performed procedures on critically ill patients. Many studies showed the safety and feasibility of PDT, but there is limited data of PDT in neurocritical care units. We have described our experience of PDT performed by neurointensivist.

PDTs were performed by neurointensivists at bedside using the Griggs guide wire dilating forceps technique. To confirm a secure puncture site, PDT was done under fiberoptic bronchoscopic guidance. From September 2015 to May 2017, procedural data were prospectively collected. The patients' demographic and clinical characteristics were retrospectively reviewed. We analyzed immediate complications of PDT as the primary outcome.

PDTs were performed for 46 patients; the mean age was 65.9 years, 26 (56.5%) were male, and mean acute physiology and chronic health evaluation II score was 20.5 ± 7.0. Overall, the procedural success rate was 100% and the mean procedural time was 19.7 ± 9.3 min. Periprocedural complications occurred in 13 patients; 10 had minor bleeding and 3 had tracheal ring fracture. There were no serious periprocedural complications of PDT.

From our experience, PDT performed by neurointensivist was safe and feasible and was implemented without serious complications.

The Neurocritical Care Unit (NCCU) is a fast paced setting with a multitude of providers and team members requiring optimal communication. It is also a high cost/high utilization environment, dictating the need for patients to be moved thru appropriate levels of care efficiently. All of this must be accomplished while providing support and opportunity for collaboration and decision making on the part of the patient/ family unit. There is great discussion in the case management world about the benefits of a unit based verses service based case management model. We looked at outcomes following the implementation of a unit based case manager in the NCCU.

A dedicated Case Manager (CM) was implemented in the NCCU to maximize assessment, advocacy, communication, education, identification of resources, and facilitation of services. Processes to support maximal contributions were created.Interventions included use of a discharge planning worksheet, implementation of a morning huddle, and space for the case manager to be physically available on the unit.

LOS of patients discharged from NCCU decreased from 7.2 to 5.1. ALOS for patients that passed thru the NCCU during their hospitalization decreased from 10.7 days to 9.2. There was a 38% increase in discharges from NCCU from 2015 to 2016. Average time from admission to CM assessment decreased from 51 hours to 32.2 hours. Progress notes indicating intervention and/or communication of the plan increased from 211 to 630. Staff questionnaire indicated increased awareness of LOS and dc plan needs.

In this Midwestern, academic medical center, integrating a dedicated, unit based CM resulted in improved LOS, increased discharges and improved staff awareness of DC plans.

High throughput genotyping technologies and large collaborative consortia have revolutionized the field of medical genetics. Open data access is the final barrier to be overcome to capitalize fully on the opportunities currently available in stroke genetics research. The International Stroke Genetics Consortium (ISGC) has created the Cerebrovascular Disease Knowledge Portal (CDKP), a comprehensive web-based resource to explore and freely access genetic data related to cerebrovascular diseases.

Funded by the NIH, the CDKP has been jointly developed by the ISGC and the American Heart Association (AHA) Institute for Precision Cardiovascular Medicine. The CDKP seeks to democratize access to genomic data and potentiate stroke genomics research by providing open access to genetic, phenotypic and imaging data on stroke. Within the CDKP, data are aggregated, integrated, and harmonized according to a pre-specified standardized pipeline. Any institution or investigator working with stroke genomic data is welcome to deposit their data or use available data.

The CDKP houses two types of data, each meeting different regulatory and analytical needs: summary level data and individual level data. The CDKP offers three main features: (1) a web-based graphical user interphase that allows the exploration of stroke genomics information through a wide menu of integrated tools for analysis and data visualization; (2) a repository of full sets of genome-wide summary statistics produced by published landmark studies in the field, available with a single mouse click ; and (3) a repository of individual level data, accessible through a secure cloud working space provided by the AHA Platform for Precision Medicine. The CDKP can be accessed at www.cerebrovascularportal.org.

The CDKP advances the ISGC's goal of liberal data sharing in stroke genomics and other areas of cardiovascular research that may benefit from genomic analyses. In the future, phenotypic datasets can be added to further enrich sharing of non-genetic data as well.

Hyperosmolar therapy using hypertonic saline is common in patients admitted to the Neurocritical Care Unit (NCCU) for the management of different type of cytogenic cerebral edema or increased intracranial pressure (ICP). Vancomycin is commonly prescribed in NCCU as empiric antimicrobial therapy. The purpose of the study is to evaluate the effects of hypertonic saline therapy on the pharmacokinetic parameters of vancomycin in critically ill patients with generalized or compartmental ICP.

This was a retrospective, observational study of adult patient consecutively admitted in the NCCU between February 2012 and February 2017 who received hypertonic saline (3% sodium chloride) and vancomycin dosing protocol managed by the pharmacist. Patients with serum creatinine > 1.4 mg/dL were excluded from the study. The estimation of vancomycin trough levels was done by using published pharmacokinetic equations and then compared to the measured trough levels with the Paired t test. The study protocol was approved by our Institutional Review Board.

Of forty-four patients who met the inclusion criteria, twenty-one patients (47.7%) were diagnosed with intracerebral hemorrhage, nine (20.5%) ischemic stroke, seven (15.5%) subarachnoid hemorrhage, four (9%) subdural hemorrhage, two with brain tumors, and one patient with chiari malformation. The mean dosing regimen was 13.8 ± 3.4 mg/kg every 12 (8 -24) h. The mean measured trough level was lower than the predicted trough level (9 ± 3.3 vs. 18.9 ± 6.2 mcg/mL; p < 0.0001). The mean serum sodium level was 147 ± 8 mEq/L and the mean serum osmolality was 317 ± 18 mOsm/kg.

Critically ill patients with cerebral edema or high ICP who were treated with hypertonic saline achieved a subtherapeutic vancomycin level that may lead to lower through level and possibly poor clinical response. Further research is warranted to evaluate the clinical response of vancomycin in this patient population.

Unnecessary telestroke activations are costly to emergency departments (ED), telestroke providers, and patients. Therefore it is important that ED nurses are well trained to effectively recognize stroke symptoms, and decrease the rate of false-positive stroke code activations.

The Nursing-driven Acute Stroke Care (NAS-Care) study aims to determine if implementing a standardized ED stroke program decreases door-to-needle times in emergency departments utilizing telemedicine. The NAS-Care intervention consists of ED nursing education including mock codes, NIHSS certification, and implementation of a standardized flow sheet. In this interim analysis from the first 4 (of 7) NAS-Care study hospitals, we examined ED admission and discharge diagnoses at each site for 3 months of blinded baseline data collection ("Control") and 6 months after standardized training ("Intervention"). False-positive encounters were defined as stroke code activations for which the patient diagnosis on leaving the ED was not stroke. 

Although hospitals trended toward a reduction in false-positive stroke code activations after implementation of the standardized stroke education, mock stroke codes, and flow sheet, none of the values were statistically significant. Further research is needed to determine whether intensive ED nursing education can improve telestroke resource utilization.

Pharmacist-driven intravenous (IV) to oral (PO) conversion protocols result in greater compliance, improved cost-savings, and better patient outcomes related to length of stay, re-admission, and duration of intravenous therapy. This study aims to determine the cost-savings and patient impacts of such a conversion protocol for anti-epileptic drugs (AEDs) including lacosamide, levetiracetam, phenytoin, and valproic acid.

A retrospective, observational phase was conducted to determine usual practice patterns concerning conversion to oral therapy between 11/1/2016 and 11/30/2016. The conversion protocol was approved in December 2016 and implemented in January 2017. A second retrospective phase observed conversion practices beginning 02/01/2017 and ending 03/02/2017. Length of intravenous and oral therapy, date eligible for conversion, and date of conversion were recorded. Hospital acquisition costs were utilized for medication expenditure calculations. This information was used to determine financial impact of the protocol and is presented as descriptive endpoints. Adverse drug events were collected via an institutional incident reporting system.

A total of 408 encounters were identified, resulting in 147 encounters in the pre-cohort and 121 postcohort encounters. Looking at the pre and post cohorts respectively, both cohorts had similar median lengths of stay (11 days vs. 9 days), 30-day readmission rates (6.8% vs 9.9%), and rates of conversion from oral back to intravenous therapy (6.8% vs 6.6%). The median length of intravenous therapy was 5 days prior to protocol implementation and decreased to 3 days in the post-cohort. The average cost per day of AED therapy was $10.36 in the pre-cohort but decreased to $4.46 in the post-cohort. Median missed opportunity costs, defined as the cost savings if conversion occurred at the earliest possible date, also decreased between the cohorts from $3.87 to $1.24.

Pharmacist involvement in AED conversion had a positive financial impact without compromising patient care.

The National Institute of Neurological Disorders and Stroke (NINDS) established the NIH StrokeNet to facilitate the rapid initiation and efficient implementation of multi-center exploratory and confirmatory clinical trials focused on promising interventions in stroke prevention, treatment, and recovery. StrokeNet was initiated in the Fall 2013, and involves over 350 hospitals across the US. The network is anchored by 25 Regional Coordinating Centers (RCCs), along with the National Coordinating Center (NCC) at the University of Cincinnati and National Data Management Center (NDMC) at the Medical University of South Carolina, as well as active participation by the NINDS. One of the primary goals of the StrokeNet is to serve as the primary infrastructure for conducting stroke clinical trials and pipeline for new potential treatments.

To maximize the impact of NIH StrokeNet, it is important for the larger community of stroke researchers and clinicians, including the neurocritical care specialists, to know its structure and the process and timeline by which stroke trials are developed and implemented.

Since the inception of the network, 49* proposal concepts have been submitted to the StrokeNet and are in different development stages. Among those evaluated to obtain NINDS permission to submit a grant application, 16 have submitted and 3 are in the process. Every application has been prepared and submitted for peer review within 3 months of the NINDS permission. Two* funded StrokeNet trials are now underway with brisk enrollment rates, and another is awaiting study initiation. (*As of abstract submission date)

The NIH StrokeNet has become a stable infrastructure and offers several distinct advantages to developing competitive clinical trial proposals, including scientific input from the StrokeNet Working Groups, comprehensive feasibility assessments (including site enthusiasm and patient availability), assistance with grant budgeting, and other requirements for grant submission that are likely to help refine and improve the application.

The Modified Early Warning Score (MEWS) is a physiological scoring system, validated in adult medicalsought to determine the value of MEWS to identify clinical deterioration or occurrence of sepsis in neuroICU patients.

We retrospectively reviewed all patients admitted to the neurological intermediate care unit (IMC) or neuroICU of a large tertiary care center from 7/2015presentation/during admission. Baseline characteristics, diagnoses, physiologic parameters, infections, treatment with antibiotics, neurological worsening and mortality were abstracted from the electronic medical record. Outcomes were defined as escalation of care and discovery of a new infection or sepsis.

Of 2556 p were male. 62% were intubated, and in-hospital mortality was 22% (versus 9% for all admissions). 182 (40%) were already treated with antibiotics for a known infec diagnosed in 19%. In reaction to the elevated MEWS score, antibiotics were added or broadened in 22%, and level of care was escalated in 2.7% from IMC to ICU. In 18.2%, there was neurological worsening, most frequently associated with increasing cerebral edema (34%) and midline shift/herniation (18%).

The MEWS score is not a valuable screening tool in the neuroICU population. It preferentially was triggered in known high acuity patients with ongoing or present infections with no change of management in the majority of patients. While associated with high mortality, its ability to indicate new infections or sepsis was poor. In 1 out of 5 patients, the MEWS score was associated with neurological worsening known at that time of the score. Other screening tools should be explored for early warning in the neuroICU.

Introduction: It is challenging to maintain neurosciences critical care nursing expertise in an environment of a rapidly expanding knowledge, changing evidence-based practices and technological advancements. To address the needs for neuroscience nursing expertise in a mixed Critical Care Unit, our institution developed a core group of nurses, known as "Neuro Champions", who have additional training and expertise in neurocritical care.

Methods: Nursing participation was voluntary and recruitment was via unit-wide announcements. The goal was to improve patient care by developing a core group of nurses who serve as resources and educators for all things neurosciences related. To develop content expertise, the nurses initially completed a set curriculum including: neuro anatomy and pathophysiology, cerebral hemodynamics and multimodal monitoring, pupillometry, EEG interpretation, temperature management, EVDs, and quality indicators. Bi-monthly meetings continued ongoing education, with content including clinical case studies and review of processes and protocols. Additionally, 6 beds staffed by Neuro Champions were designated as Critical Neurological Care Unit ("CNCU") beds to co-localize the highest acuity neurosciences patients. The Neuro Champions are responsible for educating and sharing neuro related practices with the entire ICU nursing staff.

Results: As a result of the implementation of the Neuro Champion role, our ICU has benefited from: 1) dedicated co-localized beds for the highest acuity neuro patients; 2) increased number of ENLS certified nurses; 3) improved collaboration between the medical team and nurses; 4) promoting care uniformity to maintain Comprehensive Stroke Center certification; 5) integration of multimodal monitoring advancements, all of which supports advances in patient care and research.

Conclusions: The Neuro Champion role has provided a platform for neurosciences-specific nursing expertise in a mixed critical care unit and has facilitated education dissemination to the entire staff via a core group of nurses. This expanded knowledge has improved the care of the neurologically critically ill patients.

The rate of cerebrovascular complications in patients treated with extracorporeal membrane oxygenation (ECMO) is about 7%. Transcranial Doppler (TCD) can be used to noninvasively monitor cerebral blood flow velocities (CBFVs) in patients undergoing ECMO. The aim of this study is to describe TCD-CBFV patterns in patients undergoing venovenous (VV) and venoarterial (VA) ECMO.

A neuro-surveillance protocol among ECMO patients was initiated as part of a quality improvement project at our institution. Daily neurological exam, daily TCD, brain-CT on days one and three and 24-hr continuous EEG were performed in all patients undergoing VV and VA-ECMO. Demographics, clinical and imaging data were collected for the duration of ECMO support. CBFVs, lindegaard ratios (LR), pulsatility index (PI) and resistance index (RI) on TCD were collected.

Total of 11 patients were included in the study [6 female (55%); 9 Caucasians (82%)]. Mean age was 62 years. 8 (73%) patients received VA-ECMO; 1 (9%) VV-ECMO; 2 (18.2%) received both VA and VV-ECMO. Median days on ECMO was 7 days. Median number of TCD studies performed was 2 (mean, 3.45 

We observed an overall pattern of low-normal flow CBFVs and reduced pulsatility in patients on VA-ECMO.

Nurse Practitioner (NP) and Physician Assistant (PA) roles continue to expand in the critical care setting. Single and multisite studies have examined various aspects of APP practice, but none have focused on role implementation within the Neurologic Critical Care Unit (NCCU). The purpose of this study was to obtain foundational knowledge about how NCCU APPs are implementing the role nationally

This was a voluntary, cross-sectional, descriptive study of Nurse Practitioners (NP) and Physician Assistant (PA) practicing in the US. APPs were invited to participate in this voluntary, 70 item survey. Distribution occurred initially through email inquiry via multidisciplinary, professional organization listservs (NCS, AACN, AANN) followed by snowball effect circulation. Enrollment occurred from March to June 2016. Data was collected in RedCap and analyzed using SPSS with descriptive statistics for demographic, institutional, practice, role characteristics of the sample and for each survey data element

172 APP participants completed the survey: 78% NP, 12% PA, 10% other. The majority of respondents were master's prepared (82.9%) acute care trained, (68.9%) and hospital employed (81.4%). Participants were either early in their career (38.7% 1-5 years as APP) or experienced (28.7% > 9 years). 81% work in a direct care role with 77% providing total care for their patients with an average daily caseload of 7.6 + 3.4 patients. 63% of providers believed 3-6 patients was a reasonable caseload for total care. In addition to the NCCU, 28% of participants care for patients in step-down or emergency department (36%) with 49% routinely bilingl for their work.

This study is the first to provide information regarding how NCC APPs are implementing the role in the United States. This study provides benchmarking data which may guide future research with this population as well as serve as a template for evaluation of other APP specialty roles.

Despite advances in treatment, the median survival for high grade gliomas (HGG) remains poor. There is a growing body of research showing that palliative care improves quality of life and survival in patients with advanced malignancies. We sought to examine our own practices in the Neurologic Intensive Care Unit (NICU) regarding palliative care consultation in this population. We hypothesized that the incidence of palliative care consultation is low and associated with a clarification of patient's wishes, measured by a change in code status.

We conducted a retrospective cohort review of patients with previously diagnosed HGG admitted to the NICU from 2011-2016 with a length of stay (LOS) greater than 48 hours. The primary outcome was the incidence of patients with an advanced directive or inpatient palliative care consult (PCC). Secondary outcomes included intensive care unit LOS, change in code status and location of death.

90 patients were identified with HGG. The mean age was 59.5 years (19-86years), 64% were male, 81% were white. Zero patients were admitted with an advanced directive on admission. PCC was obtained in 16 patients (18%). PCC was associated with increased NICU stay (254 hrs vs 63 hrs p=0.01), a change in code status to do not resuscitate (69% vs 11% p=0.00001), and an increased likelihood to not die in the hospital (92% vs 58% p=0.08).

At our large academic tertiary care facility intensivists underutilize palliative care services for HGG patients. Patients with fatal brain tumors are not having end of life discussions prior to admission, indicating a need for early palliative care intervention. Patients are six times more likely to change their code status and there is a trend towards dying outside of the hospital if they receive a palliative care consult.

Hypertonic saline (HTS), a hyperosmolar solution, is typically administered using a central venous catheter (CVC) due to concerns of extravasation, but a CVC is rarely readily available. In emergent situations, intraosseous (IO) access is used when peripheral intravenous access is not available. Existing literature does not address the administration of hypertonic saline using IO access for adult patients with brain injury. The administration of HTS is often delayed due to the time taken to obtain a central venous access. Insertion of an IO needle is typically much faster than a CVC.

We report the safety and tolerability of HTS using IO route. A prospective pilot study on the safety and tolerability of 3% HTS via IO is currently underway. Data on local complications at the site of injection, pain during insertion and during infusion, and serial serum sodium levels were collected. Additionally, we report a case of successful administration of 23.4% HTS using the IO route.

Preliminary data demonstrated that 3% HTS was well-tolerated, with no reports of severe pain, infections, extravasation, soft tissue injury or local infectious complications in our sample of patients with brain injury. Indications for use of hypertonic saline included patients with cerebral edema and mass effect from intracerebral hemorrhage. An appropriate rise of serum sodium levels by approximately 1 mmol/L/hr in was observed. In the case where 30 ml of 23.4% HTS, no local complications were observed and serum sodium levels rose appropriately.

Administration of HTS using IO route appears to be safe and feasible. Utilizing IO access for urgent administration of HTS may reduce the lag time to administration of the initial bolus, reduce the need for emergent placement or eliminate the placement of CVC in certain cases.

Optic nerve sheath diameter (ONSD) measurement is an emerging bedside tool to assess intracranial pressure (ICP) non-invasively in brain injury patients. Multiple studies demonstrate ONSD width from 4.5mm to 5.8mm correspond to an external ventricular device (EVD)-measured ICP >20mmHg. We sought to create a low cost, 3-D constructed, re-usable OSND teaching model to train neurology, neurosurgery, and critical care advanced practice providers and physicians.

We searched the National Library of Medicine using terms "optic nerve sheath diameter ultrasound" with combinations of "simulation" and "model." The literature was used in conjunction with a human non-contrast head CT head model to make an eye ball model which was then tested in our simulation center and compared to a live human model.

We identified 253 articles, of which 15 were associated with models and two with simulation. One gelatin model was reported, upon which we based our initial design. We could not validate the visual findings of this model. However, following construction of multiple beta models, the design most representative of human eye anatomy was a globe made of ballistics gel with either a 3mm, 5mm or 7mm 3-D printed "optic nerve" attached to a platform composed of ballistics gel and psyllium powder with a hollowed out core for ultrasound gel the globe rests upon. This model was taught to learners at a continuing medical education event prior to teaching OSND on a live human model. A 3-D printed skull from CT head data is being created to incorporate this model.

A simple 3-D ballistic ONSD model allows learners to learn proper hand placement, basic landmarks, ONSD measurement, and practice proper pressure on human eyes. This model can be replicated and utilized in a sustainable fashion given that the globe and platform are composed of ballistics gel.

Pressure measurements using pressure guide wires is an invaluable diagnostic tool in the management of many endovascular revascularization therapies. Its role is well established in coronary artery disease management such as use of fractional flow reserve (FFR) as a standard diagnostic tool to determine need for stenting, angioplasty or bypass. Renal fractional flow reserve remains an integral physiologic parameter used in endovascular revascularization therapy of renal artery stenosis. Despite the wide spread use of pressure wires in endovascular therapies, its application in the management of cerebral venous diseases remains vastly unexplored. We sought to evaluate the safety and applicability of pressure guide wires in several cerebral venous diseases.

Patients undergoing diagnostic angiography for possible venous outflow obstruction had pressures measured by pressure guide wires (Volcano Verrata® or Prestige PrimeWire®) across the following vessels: superior sagittal sinus, torcula, right and left transverse sinus, right and left sigmoid sinus, and right and left internal jugular vein. Venous pressures were also collected from patients undergoing venous thrombectomy, stenting, or an arteriovenous malformation embolization (AVM).

Five patients who underwent diagnostic angiography for pseudotumor cerebri showed no major variability in their pressures across the cerebral venous architecture which was confirmed by lack of stenosis or thrombi on intravascular ultrasound (IVUS). Four patients had a pressure difference above 10 which was suggestive of a stenosis and later confirmed by IVUS. Patients undergoing pressure measurements that had evidence of stenosis or thrombosis by IVUS showed improvement in pressure gradients post stenting or thrombectomy. No variability in pressure gradients were noted in a patient that underwent AVM embolization.

Pressure measurements using pressure guide wires can improve diagnostic accuracy and guide management of several diseases of the cerebral venous system. Further studies are necessary to understand the applicability of this approach in the management of venous disease.

Monitoring metrics is imperative for quality assurance and ongoing improvement in a developing clinical unit. A new Neurocritical care unit (NCCU), specializing in the treatment of critically ill, neurologicallyinjured patients opened in July 2013. This study examined quality metrics that correlate with the development and growth of a Neurocritical care program.

Data from patients with principle diagnoses of ischemic stroke (ISC), subarachnoid (SAH) or intracerebral (ICH) hemorrhage, seizure, or brain tumor, admitted to NCCU in 2014 and 2016 were used in the analyses. Quality metrics included overall and individual complication rates per 1,000 patient days of pneumonia, venous thromboembolism, pulmonary embolism, sepsis, septic shock, pulmonary edema, gastrointestinal bleeding, and catheter associated urinary tract infection, as well as hospital mortality and length of stay (LOS). Chi-squared and Mann-Whitney tests and Poisson regression were used to compare metrics between 2014 and 2016.

Patient volumes increased by 17.0% (439 to 515) from 2014 to 2016. The overall complication rate declined significantly from 3.94 to 2.33 per 1,000 patient days (p=0.031). The highest complication rate in 2014 and 2016 was pneumonia (1.45 and 0.85 per 1,000 patient days, respectively). The proportion of patients who expired decreased from 11.6% (n=51) in 2014 to 10.5% (n=54) in 2016, though not significantly (p=0.65). There were no significant differences in LOS among patients with ISC, brain tumor or seizure. However, those with SAH or ICH had significantly shorter stays in 2014 (median [interquartile range] =3.0 [2.0, 9.5]) versus 2016 (7.0 [2.0, 14.0]) (p=0.032).

Data suggest that over the initial 3-year period, complication rates among patients in the NCCU improved. LOS did increase for hemorrhage patients; however, this may be related to greater severity of illness in the patient population over time. Further analyses will be conducted to account for severity and other factors.

Delirium is a frequently seen but underestimated problem in critical care settings. Delirium screening is considered time consuming, which is one of the factors leading to under diagnosis. The CAM-ICU screening tool for delirium has been validated in medical and surgical ICUs. Among neurological patients, it has been validated in stroke patients but not in general neurocritical care population. This study was designed to validate CAM-ICU flow sheet in neurointensive care unit.

A prospective cohort study was conducted in a 16 bed neurointensive care unit of a university hospital. Patients meeting the inclusion criteria (all NICU patients) and exclusion criteria (comatosed, aphasic, psychotic, prior diagnosis of neurocognitive disease, persistently vegetative state, sedated) were screened for delirium by (1) a nurse practitioner using confusion assessment method (CAM-ICU) and (2) a physician reference rator using delirium screening criteria in Diagnostic and Statistical Manual of Mental Disorders-5. Assessments were done daily Monday through Friday for the ICU stay. Paired assessments were done less than 4 hours apart.

The study enrolled 50 patients (19 male, 31 female). 159 daily assessments were done. Mean age of the patients was 63.5 and mean SAP score was 23. Admitting diagnoses were ICH (8), SAH (10), ischemic stroke (5), tumor (9), spinal surgery(4), neurological infections(4), seizures(3),elective angiograms(4), hydrocephalus(1), transverse myelitis(1) and AV dural fistula(1). Using DSM-5 criteria, the reference rator identified delirium in 8 out of 50 (16%) patients during the ICU stay. 27 out of 159 assessments were positive for delirium according to DSM-5 and 29 according to CAM-ICU. CAM-ICU flow sheet had sensitivity of 96.43% (95%CI 81.65% -99.91%) and specificity of 98.51% (95%CI 94.71%-99.82%).

CAM-ICU has high sensitivity and specificity for diagnosing delirium in critically ill neurological population. It is a valid tool for diagnosing delirium.

A value stream mapping event (VSM) for general neurology inpatients, revealed multiple barriers related to videofluoroscopy swallow studies. There was a high volume of patients requiring instrumental swallow assessments, a limited number of radiology appointments, and transportation delays that were delaying feeding plans, discharge recommendations and goals of care discussions.

An Operations Engineer involved in the VSM event started the process by collecting observational data regariing timing. After meeting with the Chief Operating Officer, Director of Patient Transport, Director of Radiology, Speech Pathology Manager, Neuro Intensive Care Unit Manager and the Operations Engineer, a pilot program was agreed upon. The results for the three week pilot program were successful, and resulted in a permanent change in procedure.

The pilot data showed a decrease in test time by 5 minutes, a decrease in transport delays by 13 minutes, and a decrease in length of stay by 0.6 days. The number of patients waiting for the study dropped from 1.6 to 0.3 per week. By annualizing this data, the change has created 238 new available bed days, 38 additional patient encounters and an incremental annual contribution margin of $381, 425.

With the appointment time consistent, the nurse is able to plan patient care around the study, and ensure the patient is prepared and not delayed for the study. It has also allowed, if deemed safe for the patient to swallow, medications to be changed from the intravenous route to the oral route earlier, and earlier determination of safe feeding and diet restrictions.

We previously reported outcome for children with refractory and super-refractory status epilepticus in a cohort of 40 patients. Mortality was 30%. 25% of survivors required new tracheostomy and/or gastrostomy tubes. The majority of surviving patients experienced some degree of disability at discharge as determined by the Pediatric Cerebral Performance Category Scale (PCPC). Here, we aimed to identify patient factors in this cohort that were associated with a decline in functional neurologic outcome at discharge.

Retrospective chart review of children age 0-19 years who received pentobarbital infusion for status epilepticus in the pediatric intensive care unit of a large tertiary children's hospital from 2004-2015. Outcome was defined using PCPC at admission and discharge. Potential factors associated with outcome were evaluated using Fisher's exact test and Wilcoxon rank sum test.

40 children were included. PCPC score at admission (p=0.0006), etiology of status epilepticus (p=0.015), new tracheostomy (p=0.012), and new gastrostomy tube (p=0.012) were all significantly associated with children were more likely to have normal baseline neurologic function and more likely to have febrile encephalitis, stroke/trauma, or hypoxic ischemic encephalopathy as the etiology of status epilepticus. Duration of pentobarbital infusion (median = 8days vs. 3days) (p=0.005) and duration of hospital admission (median = 1.48months vs. 0.49months) (p=0.005) were both longer in patients who had an

Admission PCPC score, etiology of status epilepticus, new tracheostomy and gastrostomy tube as well as longer duration of pentobarbital infusion and longer hospital stay were significantly associated with a decline in functional neurologic outcome at hospital discharge in children with refractory and superrefractory status epilepticus.

Status epilepticus (SE) is the most common pediatric neurological, and super-refractory SE is a lifethreatening form of SE that continues or recurs for more than 24 hours despite multiple therapeutic interventions. This population-based study investigated pediatric SE and SRSE admissions in Germany.

Pediatric (age 0-18 years) admissions between 2008-2015 were identified in the Arvato Health Analytics database. SE, epilepsy, and febrile seizure cases were identified using a modification of a previouslypublished algorithm based on ICD-10 diagnosis codes (G40, G41, and R56) and coding for ventilator and intensive care unit use. Based on primary diagnosis, prior epilepsy status, and ventilation SE was subclassified as non-refractory, refractory (RSE), and super-refractory (SRSE). Inpatient mortality, costs, length-of-stay (LOS), and discharge disposition were assessed overall and for RSE and SRSE.

The algorithm identified 11,693 seizure-related admissions and classified 4% as SE, of which 22.9% were RSE and 13.1% were SRSE. The RSE frequency was highest among ages 1-6. The incidence of cases classified as SRSE peaked among newborns (age<1 year), decreasing between ages 1-7 years. Cases classified as SE accounted for 23.0% of total costs associated with seizure-related hospitalizations. SRSE exhibited the highest per case cost (mean €77,316), amounting to 58.0% of all SE costs, and these costs correlated with the highest LOS (median 44.5 days). SRSE was associated with greater mortality (11.7%)

Cases classified as SRSE accounted for 14.2% of all pediatric seizure-related costs, despite representing only 0.5% of admissions. SRSE was associated with the highest LOS and mortality rate. These results highlight the burden of illness associated with SRSE and suggest that optimization of SRSE management has the potential to improve outcomes and reduce costs.

Despite its more routine use and the recognition that MRI provides superior detection of traumatic brain injuries, there has been little written about how MRI might affect the acute management of trauma patients. We sought to describe MRI findings in a cohort of children admitted to the PICU with TBI and to extend comparisons between CT and MRI in acute trauma. A secondary aim was to quantify in what ways MRI findings influenced clinical management in this cohort.

We retrospectively identified 101 patients admitted to the PICU with an acute head injury between September 2010 and May 2016 who underwent head MRI within the first 96hrs. We compared MRI with CT findings, using the NIH Common Data Elements definitions of injury type. We determined by chart review the indication for MRI and if there was documentation that MRI led to a change in management, defined as either an escalation or a de-escalation of care.

Seven patients had MRI only, and MRI identified additional lesions in 60 of the 94 patients who had first undergone head CT. Of these, 49 patients had new intra-parenchymal lesions, 22 had new extra-axial lesions, and 11 had both a new intra-parenchymal and a new extra-parenchymal lesion identified. The most frequent new lesions were contusions and traumatic or diffuse axonal injury. Acute management was influenced by MRI in a majority of patients, leading to an escalation of medical or surgical management in nearly one third and a de-escalation of care in half.

Early MRI may have a beneficial role in the acute management of pediatric traumatic brain injury. MRI frequently identified clinically important lesions not appreciated on CT, and findings influenced management decisions. Future studies will assess whether early MRI improves patient outcomes or provides cost/benefit by reducing length of stay.

While adverse outcomes of decompressive hemicraniectomy (DH) including infection, disturbances of the CSF compartment, and sunken flap syndrome are well documented, there is a dearth of literature assessing outcomes related to the timing of cranioplasty.

While adverse outcomes of decompressive hemicraniectomy (DH) including infection, disturbances of the CSF compartment, and sunken flap syndrome are well documented, there is a dearth of literature assessing outcomes related to the timing of cranioplasty.

We identified 143 patients who received DH, 60 of whom underwent reconstructive cranioplasty at our institution. The post-cranioplasty complication rate was 20%, which was due in part to hemorrhage, infectious complications, or CSF compartment disturbances. Patients receiving early cranioplasty developed an increased rate of hemorrhagic complication (19% vs 0%; p = 0.01), increased median hospital length of stay (LOS) (10 vs 4 days; p = 0.002) and increased median ICU LOS (3 vs 1 days; p = 0.01). Of the patients who received DH surgery related to malignant cerebral edema from an acute ischemic stroke, total complication rates trended down for early compared to late cranioplasty surgery (8% vs 18%; p = 0.68).

Patients receiving DH surgery for any cause who underwent early reconstructive cranioplasty, experienced higher rates of hemorrhagic complications and increased hospital and ICU LOS. However, among those patients receiving DH surgery for the specific indication of malignant cerebral edema from acute ischemic stroke, significant differences did not exist between the early and late cranioplasty groups. The total complication rates in these patients trended lower in the early group. Another important and mainly unpublished finding is that a majority of DH patients are lost to surgical follow up and may therefore impact the complication rate of this not so benign surgery.

Postoperative antibiotics (PA) are often administered to patients after instrumented spinal surgery until all drains are removed to prevent surgical site infections (SSI). This practice is discouraged by numerous medical society guidelines, so our institutional Neurosurgery Quality Improvement Committee decided to discontinue use of PA for this population.

We retrospectively reviewed data for patients who had instrumented spinal surgery at our institution for seven months before and after this policy change and compared the frequency of SSI and development of antibiotic related complications in patients who received PA to those who did not (non-PA).

We identified 188 PA patients and 158 non-PA patients. Discontinuation of PA did not result in an increase in frequency of SSI (2% of PA patients vs. 0.6% of non-PA patients, p=0.4). Growth of resistant bacteria was not significantly reduced in the non-PA period in comparison to the PA period (2% vs. 1%, p=1). The cost of antibiotics for PA patients was $5,499.62, whereas the cost of antibiotics for the non-PA patients was $0. On a per patient basis, the cost associated with antibiotics and resistant infections was significantly greater for patients who received PA than for those who did not (median of $26.32 with IQR $9.87-$46.06 vs. median of $0 with IQR $0-$0; p<0.0001).

After discontinuing PA for patients who had instrumented spinal procedures, we did not observe an increase in the frequency of SSI. We did, however, note that there was a non-significant decrease in the frequency of growth of resistant organisms. These findings suggest that patients in this population do not need PA, and complications can be reduced if PA are withheld.

The development of flow-diverting stents has allowed for new treatment options for giant vertebrobasilar aneurysms. However, the expertise required to perform these procedures safely and concerns about complications continue to limit their use. We sought to identify common complications of this treatment that can be anticipated by neurointensivists, to optimize management in the postoperative period.

We retrospectively reviewed our hospital database of treated aneurysms to identify those with giant vertebrobasilar aneurysms. Medical and neurological complications were recorded.

Six patients (5 male, 1 female) underwent treatment of giant vertebrobasilar aneurysms with pipeline embolization devices. Five received adjunctive coiling. Frequently reported pre-procedure symptoms were dysphagia (n=4), diplopia (n=3), dysarthria (n=3), facial weakness (n=3), hemiparesis (n=2), gaze palsy (n=2), and nystagmus (n=2). Five patients ambulated normally. Due to concerns about necessary procedures after stenting when on antiplatelet therapy, three patients received prophylactic ventriculoperitoneal shunts, two underwent gastrostomy, and two underwent tracheostomy. Angiography confirmed successful aneurysm embolization in all patients. Postoperatively, all patients developed new or worsened symptoms attributed to brainstem edema, including hemiparesis (n=4), facial weakness (n=4), dysphagia (n=4), diplopia (n=4), nystagmus (n=3), gaze palsy (n=3), and dysarthria (n=3). Neurological symptoms were treated with steroids, with most symptoms subsiding by discharge. Five patients had medical complications, including pneumonia (n=2), respiratory failure (n=2), gastrointestinal bleeding (n=2), arrhythmia (n=2), urinary tract infection (n=1), and myocardial infarction (n=1). Two patients were re-intubated, three underwent gastrostomy, and one underwent tracheostomy. Functional status at 3-months was available for five patients. Three achieved modified Rankin Scale scores between 0-2, one regressed to a 5, and one died.

The treatment of giant vertebrobasilar aneurysms presents significant challenges. Practitioners should anticipate temporary postoperative neurological worsening and various medical complications. Prophylactic shunt placement, gastrostomy, and/or tracheostomy should be considered in patients anticipated to likely need these procedures after treatment.

Ventriculostomy-related infection (VRI) remains a major complication of external ventricular drain (EVD) placement. Historically, prophylactic antimicrobials are utilized to decrease the incidence of VRI after EVD placement. Recent guidelines for the insertion and management of EVDs recommend a single preoperative dose prior to EVD insertion and urges against the use of duration antibiotic prophylaxis. Prior to the publication of this guideline, we hypothesized that significant variations existed among institutions with respect to antibiotic prophylaxis practices in this setting. The purpose of this practice survey was to determine trends in antimicrobial prophylactic strategies utilized by various healthcare institutions for EVD placement prior to publication of the 2016 Neurocritical Care Society (NCS) evidence-based guidelines for the insertion and management of EVDs.

A seven-question practice survey on antimicrobial prophylaxis for EVD placement was distributed to active pharmacist members of the NCS by email and open for response from 12/22/15 to 1/25/2016. The following information was collected: antimicrobial prophylaxis regimen utilized, pharmacologic class, utilization of impregnated catheters, and institution guidance. Survey results were analyzed for trends in antimicrobial prophylaxis in the setting of EVD placement.

Respondents (43/105, 41% response rate) from 43 institutions completed a seven-question EVD management survey. Most institutions initiate a single dose of antibiotics prior to EVD insertion (31/43, 72%). Periprocedural antimicrobial therapy is the most common prophylactic strategy utilized by respondents (18/43, 42%). Of respondents who do not continue antimicrobial prophylaxis for the duration of EVD placement, 59% (10/17) utilize antimicrobial-impregnated catheters to reduce incidence of VRI.

The importance of antimicrobial prophylaxis to prevent infectious complications associated with EVD placement is widely accepted. Prophylactic strategies vary between institutions. Periprocedural antimicrobial therapy is the most common prophylactic strategy utilized by survey respondents. Antimicrobial-impregnated catheters are commonly utilized in institutions using periprocedural antimicrobial prophylaxis.

The postoperative course seen in critically ill neurosurgical patients is known to vary depending on the timing of the surgical procedure. This study seeks to compare the clinical characteristics, complications, and outcomes between elective or urgent surgery patients admitted to the intensive care unit (ICU).

Retrospective review of a two-year neurosurgical patients' cohort. The pre and postoperative conditions and outcomes were compared between elective (group A) and emergency (group B) surgery patients.

A total of 416 patients were evaluated, 262 in Group A and 154 in Group B. The most common diagnosis was intracranial tumor. The mean American Society of Anesthesiology (ASA) score was significantly higher in Group B than in group A (3.35 vs. 2.79, p<0.05). Mean Sequential Organ Failure Assessment (SOFA) score on admission was higher in Group B (2.47 vs. 0.83, p<0.001). These patients were more likely to require mechanical ventilation (OR 14.75, p<0 .001) and vasopressors (OR 5.76, p<0.001) . Group B had a higher probability of rebleeding (OR 5.29, p<0 .001), intracranial hypertension (OR 11.9, p<0.001), hydrocephalus (OR 6.45, p<0.001), and reintervention (OR 1.91, p=0.043). Post-operative nausea and vomiting were less likely in group B (1.9% vs. 9.9% and 0 vs. 3.4%, respectively). Mean hospital and ICU LOS were shorter in group A than in group B (9.1 vs. 15.4 and 2.8 vs. 5.7, p<0.001 respectively). Mortality rate during ICU stay was higher in Group B (9.74% vs. 1.52%; OR 6.96, p<0.001). The preoperative Glasgow Coma Scale (GCS) in patients who died, was below 8 in only a minority of them (14.28% in Group B; 0% in Group A).

In this cohort of neurosurgical patients, emergency, compared to elective operations, were associated with higher post-operative complications and mortality rates. Emergency surgery was associated with a higher severity of illness measured by the SOFA and ASA scores.

Intraprocedure rupture (IPR) is a rare but potentially serious complication of endovascular coiling of intracranial aneurysms. Potential complications include hemorrhage, ischemic stroke, vasospasm and hydrocephalus which can lead to increased morbidity and mortality. The clinical course for these patients is not well studied and characterized.

We performed a retrospective review of prospectively collected data for all unruptured aneurysms treated with endovascular coil embolization between July 2003 and March 2017 at a large universitybased hospital. Out of 998 cases of all unruptured aneurysms coil embolizations, 10 (1.002%) patients had IPR. We reviewed baseline data, procedure notes, clinical course, and outcomes at discharge and at 3, 6 and 12 months.

Among the ten patients, the location of the aneurysms included: 4 basilar apex, 3 internal carotid artery 1 anterior communicating artery, 1 posterior cerebral artery, and 1 posterior communicating artery aneurysm. Patients were monitored in the ICU for variable lengths of time and daily transcranial Doppler ultrasound detected no significant sonographic vasospasm. The large majority of the patients (8/10) were discharged to home at their baseline functional status assessed by Modified Rankin scale. One patient was discharged to inpatient rehabilitation for cognitive deficits from IPR of a basilar apex aneurysm. They were subsequently discharged home with supervision. There was a single mortality in a patient receiving retreatment of a proximal ICA aneurysm with prior stenting and coil embolization who developed massive subarachnoid hemorrhage with diffuse intraventricular hemorrhage with external ventricular drain placement.

The incidence of IPR is very low and potentially serious complications occur rarely in these patients. The location and factors associated with IPR are highly variable and without clear associations. Outcomes of such complications are overall favorable. A short observation period in the hospital is likely warranted with a benign clinical course the most likely outcome.

The standard treatment of Cerebral Venous-Sinus Thrombosis (CVST) is anticoagulation. However some patients clinically deteriorate secondary to mass-effect from infarct or Intracerebral-Hemorrhage (ICH). The role of decompressive-craniectomy (DC) in this patient population is unknown. We elucidate the baseline characteristics of patients treated with DC, and report their outcomes.

A retrospective chart review of our institutional database identified patients with CVST who were treated with DC. Demographic and clinical data were collected. Imaging variables collected from CT-Head or MRI-Brain immediately before DC were intracerebral-hemorrhage volume (ICH-V), combined volume of mass-effect from infarct/ICH and peri-lesional edema (ME-V), midline-shift at level of pinealgland (MDS-P), midline-shift at cranial-most portion of corpus-callosum (MDS-CC), and herniation-type. Favorable outcome was defined as Glasgow-Outcomes Scale of 4-5 upon last-known follow-up.

A total of 15 patients (females=10) treated with DC were identified with mean-age 46.7 (+/-17.4), mean Glasgow-Coma Scale (GCS) before surgery 8 (+/-3.9), mean-ICH-V 42.2 ml (+/-44.0), mean-ME-V 100.7 ml (+/-51.6), mean-MDS-P 6.1mm (+/-3.9), and mean-MDS-CC 7.4mm (+/-6.5). Transverse-sinus was most commonly involved (n=10). 14/15 patients had any herniation, most commonly cingulate (n=10). Meanchange in GCS from admission to before-surgery was -4.8 (+/-4.2). Ten patients were anticoagulated before surgery. On last-known follow-up, 9/15 patients had a favorable outcome. Four had died. On chisquare analysis, Superior-Sagittal Sinus thrombosis was associated with unfavorable outcomes (p=0.025), and mortality (p=0.039). On univariate binary-logistic regression, there was a non-significant trend towards unfavorable outcomes (p=0.082) and mortality (p=0.079) with every-point decrease in mean-GCS before surgery. The predictive-value of other factors towards outcomes is unknown given limited sample-size.

Decompressive-craniectomy might improve outcomes even in patients with CVST who have developed coma, cerebral herniation, have failed treatment with anticoagulation, and have large-volume masslesions causing midline-shifts of >5mm. A prospective multi-institutional observational-cohort would POSTER PRESENTATIONS better delineate outcomes in comparison to matched-patients who are not treated with decompressivecraniectomy.

Meningiomas are often benign and mostly asymptomatic, and the treatment approaches may include open surgical resection, radiosurgery, and/or watchful waiting. Reported morbidity and mortality rates for elderly patients undergoing meningioma resection vary widely. We sought to investigate mortality rates for elderly patients undergoing craniotomy for meningioma resection using the Nationwide Inpatient Sample (NIS).

The NIS datasets from 2003 to 2013 were used to identify patient admissions for meningioma resection based on the ICD-9-CM code 01.51. Age categories were defined as 70 years of age. Primary outcomes were in-hospital mortality, poor outcomes (defined as death or discharge to a facility other than home), cost and length of hospitalization.

A total of 24,953 patients were identified who underwent meningioma resection during 2003-2013 of which 20.4% were elderly (>70 years). Each of the primary outcomes was heavily influenced by the advancing age. In-hospital mortality was higher in the elderly as compared to the younger patients (3.5% vs 1% p<0.001), as was the rate of a poor outcome (64.8% vs 28.1%, p<0.001). Elderly patients also had a higher cost ($104425 vs $96012, p=0.013) and increased length of hospitalization (8.9 vs 6.8 days, p<0.001).

In our study, age > 70 was strongly associated with adverse outcomes after meningioma resection. This increased risk should be taken into account when considering surgical intervention in this subgroup. Based on this study, closer perioperative monitoring may be warranted in the elderly patient subgroup.

Treatment with anticoagulation improves outcomes in cerebral venous-sinus thrombosis (CVST). However patients who develop extensive infarcts and/or intracerebral-hemorrhage with mass-effect resulting in comatose-state are at risk of poor outcomes, and may benefit from decompressive craniectomy (DC). We evaluated the role of DC in the management of malignant CVST and its impact on outcomes.

Literature-search was conducted on Pubmed and Google-Scholar using terms "Craniectomy", and "cerebral venous-sinus thrombosis". We included studies that described any number of patients with CVST who underwent DC after clinical deterioration and reported their outcomes. A similar search strategy identified patients from our institute. Outcomes were reported as modified-Rankin Scale (mRS) or Glasgow-Outcomes Scale (GOS) and were classified as favorable (mRS 0-3; GOS 4-5), or unfavorable (mRS 4-6; GOS 1-3).

A total of 296 patients (females=164; males=74; unknown=58) who underwent DC for malignant-CVST were identified from 29 studies (n=281) and our institute (n=15). Age and GCS (before-surgery) were only available from 125 patients, with mean-age 36.74 (+/-13.52) and mean-GCS 7.58 (+/-3.03). 199 patients (67.2%) had favorable-outcomes, while 63 patients (21.3%) died. In the multi-variate binarylogistic regression-model, every point-drop in GCS decreased the odds of favorable-outcomes by 0.57times (p<0.001; 95%CI=0.423-0.775), and survival by 0.58-times (p=0.002; 95%CI=0.414-0.821). Thrombosis in Internal-jugular vein (IJV) (OR=10.39; 95%CI=1.36-79.30; p=0.024) and Deep-cerebral veins (DCV) (OR=8.94; 95%CI=1.33-60.17; p=0.024) predicted unfavorable-outcomes. IJV-thrombosis (OR=10.67; 95%CI=1.07-106.86; p=0.044) and DCV-thrombosis (OR=13.5; 95%CI=1.57-115.82; p=0.018) also predicted mortality. Interestingly, cortical-vein thrombosis was associated with lower odds of unfavorable outcomes (OR=0.217; 95%CI=0.051-0.921; p=0.038). Data regarding anticoagulation and long-term follow-up were not uniformly available.

For patients with malignant-CVST, craniectomy could potentially improve outcomes. Factors such as GCS before-surgery and CVST location can help predict outcome following DC and aid the decision-making process. A multi-institutional observational cohort should be designed to prospectively evaluate predictors for, timing of, and outcomes after craniectomy in CVST.

The external ventricular drain (EVD) is commonly used in the Neurocritical care unit to help monitor intracranial pressure (ICP) with the added advantage of therapeutically treating elevated ICP by diverting cerebrospinal fluid (CSF). Placement of an EVD can be complicated by hemorrhage surrounding the catheter insertion tract, which in some cases may prove to be fatal. This retrospective study was designed to look at the rate of tract hemorrhages after EVD placement that were performed at our institution as well as associated outcomes.

We conducted a retrospective review of all patients who underwent EVD placement during a 3 year period using our institutional database. Postinsertion computerized tomography (CT) scans of the head were analyzed independently by 2 physicians to identifying tract hemorrhages. Data on primary diagnosis, age, sex, length of ICU stay and mortality were collected and analyzed.

A total of 115 patients were identified as having had an EVD placed during their hospital course. 15 patients were excluded as there were no images of EVDs present in their records. 100 patients were analyzed, of which 43% were male. Mean age was 59.4 years. 50% of patients had a diagnosis of subarachnoid hemorrhage, 45% with intraparenchymal hemorrhage and 16% with ischemic stroke. Mortality was 15% among all EVD patients. The rate of tract hemorrhages among all patients with EVD images was 21%. Asymptomatic tract hemorrhages occurred in 19 patients (95.23%) with 1 patient (4.77%) dying due to the tract hemorrhage itself. Among patients with tract hemorrhages mortality was 14.3%.

The rate of tract hemorrhages was noted to be 21% with the majority being asymptomatic. There was no difference in mortality among patients with EVDs who developed tract hemorrhages compared to patients with no tract hemorrhages.

Verapamil is a phenylalkylamine calcium channel blocker that blocks the calcium ion influx through slow channels into conductile and contractile myocardial cells and vascular smooth muscle cells resulting in vascular relaxation and vasodilatation. Symptomatic hypotension and/or extreme bradycardia/asystole are often seen with intravenous verapamil administration requiring pharmacologic treatment. In Neuroendovascular field verapamil is mainly being used as a vasodilator agent. Current lack of pharmacokinetic/pharmacodynamics data of intra-arterial verapamil often makes very challenging to neurointerventionalists during endovascular procedures. The purpose of this study is to observe acute hemodynamic effects of intra-arterial verapamil administration as well as the safety of higher dose of the medication during endovascular treatment.

Ten patients who underwent endovascular treatment for acute ischemic stroke were evaluated pre and post procedure with vital signs. The dosage of intra-arterial verapamil was documented and tabulated along with the pre and post heart rate and systolic blood pressure.

The dose of intra-arterial verapamil varied from 1 to 5 mg in each Internal Carotid or Vertebral artery, total dose per patient per procedure varied from 2.5 to 10. The average dose of intra-arterial verapamil administered was 4.95 ± 2.0 mg or 59.7 ± 30.8 mcg/kg that were infused over 5 to 10 minutes. At the baseline before administration of intra-arterial verapamil, the mean systolic blood pressure (SBP) was 157.8 ± 24.4 mm Hg and the mean heart rate (HR) was 71.6 ± 16.2 bpm. After administration of intraarterial verapamil, SBP decreased by mean of 16.7 ± 0.8 mm Hg but we observed no symptomatic hypotension requiring any pharmacologic treatment. HR changed only by mean of 0.1 ± 5.4 bpm post intra-arterial verapamil.

We observed no acute significant changes in hemodynamic parameters with administration of verapamil in Carotid or Vertebral arteries. This may represent its safe use during Neuro-endovascular therapy.

Growing evidence suggests inflammation is critical in epileptogenesis. Endogenous brain apolipoprotein E protein (apoE) modulates neuroinflammatory responses to injury through downregulation of glial activation and secondary neuronal injury. We created a 5 amino acid peptide (CN-105) mimicking the binding face of apoE. CN-105 downregulates the inflammatory response in vitro and in vivo and improved histologic and clinical outcomes across several injury models in mice. We hypothesized that downregulation of inflammation by administration of CN-105 will reduce the development of epilepsy after pilocarpine induced status epilepticus in mice.

C57Bl/6 mice were intraperitoneally injected with pilocarpine to induce status epilepticus. Following induction of status, animals were randomized to receive two doses of CN-105 or vehicle at 45 minutes and 6 hours. Status was terminated by injection of benzodiazepine at 55 minutes. Epidural EEG leads were surgically placed at 3 weeks and continuous video-EEG (cvEEG) monitoring was performed for several days in a row at 4-6 weeks post status to determine spontaneous seizure development and frequency.

At 4-6 weeks following induction of status epilepticus, administration of 0.2 or 0.5mg/kg CN-105 reduced the development of epilepsy by approximately 50% compared to vehicle treated animals. Further, CN-105 treated animals that did develop seizures had significantly fewer seizures than vehicle mice. Similar results were seen with 7 daily doses of 1mg/kg starting at 45 minutes. Importantly, CN-105 is not an anticonvulsant as cvEEG monitoring during status induction clearly demonstrated that seizures were not stopped or reduced by injection of CN-105.

These results are consistent with the hypothesis that inflammation plays an important role in the development of epilepsy after injury and demonstrates treatments that target inflammation, like CN-105, can prevent and/or reduce the development of epilepsy. This represents the first therapy to prevent the development of epilepsy that has entered into clinical trials.

To determine the speed of brain entrance of the antiepileptic drugs (AEDs) brivaracetam (BRV) and levetiracetam (LEV) after single intravenous dosing in humans. BRV and LEV both bind to synaptic vesicle protein 2A (SV2A), but BRV has more rapid brain entry than LEV in mice and monkeys [1] . SV2A can be quantified in the living human brain using PET imaging with [11C]UCB-J[2].

PET scans (n=13) were performed with [11C]UCB-J administered by a bolus-infusion protocol in healthy volunteers (n=9). Therapeutic dosages of BRV (50mg, n=1; 100mg, n=4; or 200mg, n=2) or LEV (1500mg, n=6) were administered as 5-minute intravenous infusions 60 minutes after the start of the first PET scan. Tracer displacement half-times were determined by subtracting the radioligand clearance halftime from the radioligand displacement half-times estimated by exponential fitting of the post-AED drop in distribution volumes (VT). Data were also analyzed using an advanced mathematical model that described the relationship between brain [11C]UCB-J PET data and time-varying AED plasma curves to directly estimate brain entrance (K1) of both AEDs and [11C]UCB-J, free fraction of [11C]UCB-J in the brain, and VT values.

The radioligand clearance half-time was 8 minutes. Tracer displacement half-times were 1.7 and 2.1 minutes for BRV 200mg, and 20 ±6 minutes for LEV 1500mg. Lower BRV doses had longer half-times, but values were misleading as they assumed 100% SV2A occupancy. The advanced compartment model described well -dose scans. Using the advanced model, the BRV uptake rate (~50 uL/min/cm3) was found to be at least 8-fold higher than that of LEV (~6 uL/min/cm3).

The results demonstrate that BRV enters the human brain faster than LEV. The potential therapeutic benefit of this has yet to be determined. 

While intravenous anesthetic therapy (IVAT) represents the gold-standard for treatment of refractory status epilepticus (RSE), the optimal depth and duration of therapy is not known. The goal of this retrospective observational study was to describe the relationship between the depth of burst suppression and the ability to successfully wean IVAT during RSE treatment.

Fifty patients were identified with RSE who underwent continuous electroencephalography. Using Persyst, the suppression ratio (SR) was calculated up to 72 hours prior to weaning IVAT. The type and duration of IVAT was recorded, as well as complications. We compared these variables between successful and unsuccessful weans.

The mean SR for all patients was 19.0±26.3%, with a mean treatment duration of 63.3±42.1 hours. There was no difference in treatment duration between successful and unsuccessful weans(p=0.54), but SR was significantly lower in successful weans (10.0±15.2% vs 27.9±33.4%, p=0.01). The receiver operating curve (ROC) for the sensitivity and specificity of the mean SR to predict a successful weaning attempt did not identify a threshold to predict weaning success. The use of pentobarbital was associated with a significantly higher SR when compared to midazolam (69.1±18.9% vs 6.9±8.2%, p <0.001). Patients failed IVAT weaning a mean 24.5±22.6 hours after initiating the IVAT wean, which occurred after a mean decrease in the midazolam infusion rate of 68 ± 33%. Depth of SR was not associated with infection risk (p=0.74), but was associated with the need for tracheostomy (27.6±32.7% versus 10.2±17.2%, p=0.01). Vasopressors were required in 87.5% of patients while on IVAT.

Unsuccessful weaning of IVAT was associated with a higher depth of SR, which is likely a marker of disease severity. Depth of sedation was not associated with increased risk of infection, but was associated with the need for tracheostomy. Vasopressor requirements are common.

The primary objective of this study was to determine the sensitivity and specificity of real-time Neuro ICU nurse interpretation of quantitative EEG (QEEG) trends in the identification of recurrent nonconvulsive electrographic seizures in adult patients admitted to the Neuro ICU.

Thirteen adult patients admitted to the Neuro ICU that had nonconvulsive seizures on continuous EEG (cEEG) monitoring were included in the study. Neuro ICU nurses consented for their participation and underwent a brief, standardized QEEG training session. A 1-hour QEEG panel (rhythmicity spectrogram, left/right and amplitude-integrated EEG, left/right) printout containing the marked sentinel seizure(s) was displayed next to the bedside cEEG/QEEG monitor. At one-hour intervals, the nurses logged the number of seizures seen in the past hour based on their QEEG interpretation for the duration of their shift. Their answers were compared with the gold standard of neurophysiologist interpretation of seizure occurrence on raw EEG.

A total of 120 hours of QEEG data was reviewed for 13 patients. Average length of data collection was 9.5 hours. For the Neuro ICU nurses' ability to detect the presence of seizures on real-time QEEG the sensitivity was 70.0% (95% CI, 34.8-93.3%) and specificity was 90.0% (95% CI, 82.8-94.9%). The positive predictive value for seizure detection was 38.9% (95% CI, 24.2-56.0%) and the negative predictive value was 97.1% (95% CI, 92.7-98.8%). The false-positive rate was 0.075/hr.

A simplified panel of QEEG trends can be used by Neuro ICU nurses to screen for recurrent electrographic seizures in critically ill patients with a reasonable sensitivity, an excellent specificity and a very low false-positive rate. This may facilitate earlier identification of recurrent electrographic seizures by notifying the neurophysiologist who is not present in the ICU and not able to perform real-time cEEG interpretation.

Nonconvulsive status epilepticus (NCSE) is an indicator of poor outcomes in neurocritical care settings. However, because of unfamiliarity with continuous electroencephalography monitoring (cEEG), the diagnosis and treatment of NCSE remains challenging, and its clinical impact and prognostic factors have not been sufficiently reported in Japan.

We performed cEEG for 188 adult patients in our neurocritical care unit with coma or unexplained altered mental status from April 2013 to September 2015. We reviewed all cEEG records according to the American Clinical Neurophysiology Society's terminology (2012 version), and diagnosed patients with NCSE when the cEEG revealed spatiotemporally evolving or fluctuating periodic or rhythmic discharges and after considering clinical information based on the modified Salzburg consensus criteria. Patients with NCSE were aggressively treated with benzodiazepines, fosphenytoin, and levetiracetam. They were divided into a generalized convulsive status epilepticus (GCSE) group and a non-GCSE group. We compared mortality and outcomes between the two groups after 3 months using Fischer's exact test. Outcomes were defined as poor when the Glasgow Outcome Scale score was worse at the 3-month follow-up than at admission. We excluded 15 cases undergoing supportive care or lacking of follow-up.

Of 173 cases in the study, 61 cases were diagnosed with NCSE, including 18 cases with accompanying GCSE and 43 cases without. Mortality rates at the 3-month follow-up were significantly higher in the non-GCSE group than the GCSE group (19% vs. 0%, respectively; p = 0.0492). The rate of poor outcomes was significantly higher in the non-GCSE group than in the GCSE group (26% vs. 0%, respectively; p = 0.0138).

This study suggests that the absence of GCSE is associated with increased mortality and poor outcomes among NCSE patients. Limitations of this study include its retrospective design and small number of NCSE patients. Further studies are necessary to identify additional prognostic factors.

Super-refractory status epilepticus (SRSE) is a life-threatening condition in which status epilepticus recurs or continues for over 24 hours despite first-, second-, and anesthetic third-line agent (TLA) medications. No treatments are currently approved for SRSE. A randomized, double-blind, multi-center, placebo-controlled Phase 3 trial evaluated brexanolone (USAN; formerly SAGE-547 Injection), a synaptic and extrasynaptic GABAA receptor positive allosteric modulator as adjunctive therapy for SRSE (NCT02477618; "STATUS Trial").

Enrolled subjects underwent a qualifying TLA wean after at least 24 hours of seizure-or burstsuppression. SRSE subjects failing the qualifying wean were randomized 1:1 to a blinded infusion of brexanolone or placebo as adjunctive therapy following resumption of one or more TLA infusions. Subjects were administered the blinded infusion for 6 days, during which attempts were made to wean off TLA infusions. Clinical Standardization Guidelines (CSGs) facilitated standardization across sites by outlining EEG patterns for which TLA weaning should be continued, paused, or discontinued. An on-call Clinical Standardization Team provided real-time support. Safety was assessed via adverse events, laboratory testing, vital signs, and ECG parameters. The primary endpoint was defined as successfully

Super-refractory status epilepticus (SRSE) is a life-threatening neurological condition characterized by status epilepticus persisting over 24 hours despite treatment with first-, second-, and third-line agents (TLAs) or upon the weaning of TLAs. Currently, there is no consensus around treatment protocols for SRSE. This study aims to describe SRSE treatment patterns and related outcomes in a US population.

We retrospectively identified SRSE cases in Cerner HealthFacts®, a large, de-identified, US electronic health record database, using records from 2000-2015. Cases were classified as SRSE using a modified version of a previously published algorithm using ICD-9 and procedure coding for status epilepticus (345.00, 345.01, 345.1x, 345.3, 345.41, 345.51, and 345.81) , ventilator support, pharmacotherapies. Descriptive and univariate statistics were used to evaluate anesthetic treatment, anti-epileptic medications, and the association between Glasgow Coma Score (GCS) and mortality.

Using our algorithm, 1153 SRSE cases (1137 patients) were classified. Multiple TLAs were received in 89% of cases, and in 37%, >2 concurrent TLAs were received. The first post-admission TLAs were propofol, lorazepam and midazolam, respectively, in 38%, 38% and 18% of cases. Median anesthetic duration was 9.5 days. Mortality was higher in -8 (3.1 vs. 1.6 days; p<0.001).

SRSE patients identified in our analysis underwent variable treatment patterns, reflecting lack of co days of TLA treatment.

Nonconvulsive seizures (NCS) and nonconvulsive status epilepticus (NCSE) occur in approximately 20% of neurologically critically ill patients. The most effective antiepileptic drug (AED) regimen to treat NCS and NCSE is unknown. This study was designed to determine the efficacy of add-on clobazam, a unique 1,5-benzodiazepine with favorable pharmacokinetic properties, in the treatment of NCS and NCSE.

A retrospective chart review was performed on 17 adult patients who were admitted to the neurological intensive care unit between January 1, 2013 and June 1, 2017, were diagnosed with NCS or NCSE by continuous EEG monitoring and received clobazam as add-on therapy. The primary efficacy endpoint was defined as clobazam being the last AED added before NCS/NCSE cessation, regardless of latency between dosing and NCS/NCSE cessation.

Of the 17 patients included in this study, 7 (41%) had NCS vs. 10 (59%) with NCSE. The most common etiologies were autoimmune (n=6) and CNS tumor (n=5), with 7 patients (41%) having pre-existing epilepsy. Clobazam was the last AED added before cessation of NCS/NCSE in 12 of 17 (71%) subjects. Clobazam was chosen as the 3rd to 6th line agent. Clobazam was started at a median of 2 days from the onset NCS/NCSE (range 1-55 days). The median total daily dose of clobazam was 20 mg (range 10-60 mg).

This study suggests that clobazam may be effective at various time points in the treatment of NCS/NSCE and may prevent the need for addition of intravenous anesthetic drugs to control seizures. However, a prospective study is warranted to determine efficacy and optimal dosing.

Continuous electroencephalography monitoring(cEEGM) with international 10-20 system is essential for detect nonconvulsive status epilepticus (NCSE). In Japan, both cEEGM systems and human resources are lacking, and few facilities are able to conduct such advanced monitoring. The cEEGM headset, described in this report, is a novel and easy-to-use technology. We attempted to validate the novel cEEGM headset by comparing it with a conventional, international 10-20 cEEGM system (conventional cEEGM).

We completed this study at a single center, eight-bed neurocritical care unit, between January 2017 and June 2017. The new, cEEGM headset features eight electrodes (F, C, T, O), and is capable of simultaneously transmitting EEG data by Bluetooth. Patients with disturbed consciousness, of unknown etiology, underwent cEEGM headset followed by conventional cEEGM. We verified the concordance rate of the two systems for detecting EEG morphologies (e.g. periodic discharges, rhythmic delta activity, spikes and waves), and diagnosing NCSE. EEG morphologies were appreciated according to "American Clinical Neurophysiology Society's Standardized Critical Care EEG Terminology: 2012 version" and diagnosis of NCSE were done according to modified Salzburg consensus criteria.

Among this period, we enrolled thirty patients. Three patients were excluded because of not satisfying protocol. Final analyses included verified data from 27 patients. The mean age was 66 years old (range: 20-86), 59% were male, mean Acute Physiology and Chronic Health Evaluation (APACHE) II score was 15 (range: 5-27), and mean Full Outline of Unresponsiveness (FOUR) score was 10 (range: 6-16). We appreciated concordant EEG morphologies, and NCSE, in 78% (21/27), and 74% (20/27) of patients, respectively.

This easy novel cEEGM headset may be useful in settings with limited resources or access to conventional cEEGM technology. Further study is needed to validate the actual diagnostic ability of this novel headset.

The traditional approach to interpreting EEG requires physicians with formal training to visually assess the waveforms. This approach is less practical in critical settings when a trained EEG specialist is not readily available to diagnose subclinical seizures, such as non-convulsive status epilepticus, in patients with altered mental status. We have recently invented an algorithm for sonifying EEG, and in the current study, we explored whether individuals without EEG training can detect ongoing seizures by simply listening to one channel of sonified EEG.

We sonified 84 EEG samples (15-second long) that represented various conditions commonly seen in the ICU (7 seizures; 25 LPD, GPD, or burst suppression, and 52 normal or slowing). 34 Medical students and 30 nurses were asked to indicate each audio sample as "seizure" or "non-seizure". We then compared their performance with that of EEG experts [epilepsy attendings with >10 years of experience (n=2) and epilepsy fellows (n=7)] and some of the medical students (n=29) who also diagnosed the same EEGs on visual display.

Non-experts listening to single-channel sonified EEGs detected seizures with remarkable sensitivity (students: 98±5%; nurses: 95±14%) compared to experts or non-experts reviewing the same EEGs on visual display (attendings: 100%; fellows: 90±11%; students: 76±19%). If the EEGs contained seizures or seizure-like activity, non-experts listening to sonified EEGs rated them as seizures with high specificity (students: 85±9%; nurses: 82±12%) compared to experts or non-experts viewing the EEGs visually (attendings: 95±1%; fellows: 91±7%; students: 65±20%).

Our study confirms that individuals without EEG training can detect ongoing seizures or seizure-like rhythmic periodic activity by merely listening to short duration of sonified EEG. While sonification of EEG cannot replace the traditional approaches to EEG interpretation, it provides a meaningful triage tool for fast assessment of patients with suspected subclinical seizures.

Super-refractory status epilepticus (SRSE) is a life-threatening form of status epilepticus (SE) that continues despite, or recurs after, 24 hours of therapeutic interventions, including continuous intravenous anesthetic third-line agents (TLAs). No therapies are approved for SRSE, leading to substantial variation in both management and determination of treatment response. For the Phase 3 trial of brexanolone as adjunctive therapy for SRSE involving up to 180 international sites, we developed and implemented Clinical Standardization Guidelines (CSGs) for real-time support of TLA administration, weaning, and outcome assessment under EEG neuromonitoring.

A Clinical Standardization Team (CST), including investigators and SE experts, developed consensus CSGs defining acceptable EEG patterns for continuation, termination, or pausing the weaning of TLAs. CSG implementation was facilitated by training and CST call centers staffed internationally by physicians with critical care EEG expertise. In cases of disagreement, the local site retained final decision-making authority.

A "traffic light" system defined: 1)"green" tolerated EEG patterns (improving background, 3 seizures within 3 hours, discharges >3 Hz, or discharges 1-2.9 Hz with evolution and no improvement over 6 hours), and 3)"amber" EEG patterns not meeting the above, for which TLA weaning should be paused while optimizing anti-epileptic medications and monitoring for transitions to green/red EEG patterns. The initial 125 CST consultations yielded 97% CSG compliance; 83% of EEGs underwent CST review. Few CST consultations lasted >60 minutes (7%); most lasted <30 minutes (67%).

This Phase 3 trial demonstrates the feasibility of applying neuromonitoring CSGs for TLA weaning in SRSE patients, to ensure better consistency of clinical care and reliability of the primary outcome measure in clinical trials. CSGs were well accepted by investigators and may serve as a framework for future clinical trials or clinical therapies in SRSE.

Severe brain trauma is a leading cause of death and disability worldwide. Post-traumatic epilepsy (PTE) is a chronic complication that occurs in up to 40% of cases (Frey, 2003; Najafi et al., 2015) . Drugs and other interventions to prevent epileptogenesis would likely be most effective early after traumatic brain injury (TBI), but cannot be given indiscriminately. There is a critical need for tools that quantify those at high risk for PTE. Abnormal neural activity, in the form of ictal-interictal continuum abnormalities(IICAs) are increased acute brain injuries, and appear to differentiate patients at risk for secondary brain injury (e.g. Kim et al., 2017) . We hypothesized that IICAs acutely following TBI may be a marker of posttraumatic epilepsy risk.

We evaluated continuous EEG data from moderate to severe TBI patients who did and did not develop PTE, (any seizure 2-12 months post-TBI; n=50). Seizures <1month post-TBI were classified as symptomatic, not PTE. Conventional 10-20 scalp electrode placement was used and EEGs were reviewed by standard visual analysis, by the MGH neurophysiology service. Daily EEG reports were scored for the presence of IICAs and seizures. Demographic data including gender, age, TBI severity and type of brain injury were recorded. Univariate and multivariate regression analyses were performed to determine which IICA and demographic features correlated with PTE.

GCS (p=0.02) and TBI severity (p=0.02) were significantly associated with PTE, as expected. Seizures (p=0.002), epileptiform discharges (p=0.0003), generalized periodic discharges (0.0003) and lateralized rhythmic delta activity (p=0.04) independently predicted risk for post-traumatic epilepsy. Epileptiform discharges, in particular, were more prevalent acutely post-TBI in PTE patients.

Increased IICA prevalence is significantly associated with PTE and may be a predictive marker for identifying patients who may benefit from anti-epileptogenesis trials.

Rapidly obtaining EEG signals in the ED and ICU for at-risk patients can enhance diagnosis accuracy and speed, while cutting down time until treatment. Ceribell Inc has developed a portable EEG data recorder and electrode headset with rapid setup (~ 5 min) technology without any EEG technician required to overcome the inaccessibility of EEG in urgent situations when seizures are suspected. The purpose of this study is to evaluate the signal quality and performance of the Ceribell system compared to a reputable clinical EEG system.

We collected EEG samples in the laboratory and at Stanford University Medical Center. Laboratory collections on healthy volunteers included simultaneous collection of EEG using Ceribell and Nihon Kohden systems, and a split-signal that recorded EEG to both data recorders from the same electrodes.

In the ICU, EEG was recorded with the Ceribell system on 25 patients and subsequently with the clinical EEG system. Data was filtered and spectral densities, Mean Frequency (MF), Spectral Entropy (SE), and 75% Spectral Edge Frequency (SEF75) were computed.

In the split-signal test, the waveforms consistently appeared similar by visual inspection. The analysis of Ceribell data revealed (MF = 22.46 Hz, SE= 8.51, SEF75 = 21.56) similar to the commercial system (MF = 22.86 Hz, SE = 8.52, SEF75 = 21.58). In the simultaneous test, the Ceribell system produced (MF = 14.3 Hz, SE = 8.4, SEF75 = 17.36) similar to the commercial system (MF = 15.5 Hz, SE = 8.58, SEF75 = 18.84). In the clinical setting, the Ceribell system showed spectral density distributions comparable with the commercial system.

Our results indicate that the signal quality of the Ceribell system is similar to a commercially available EEG used widely in the clinical setting, while requiring less setup time and allowing more portability.

Status epilepticus (SE) is a life-threatening condition characterized by prolonged seizures without regaining consciousness between seizure events. When SE continues or recurs 24 hours or more after treatment with third line anesthetic agents, it is considered super-refractory SE (SRSE). There are few population-based studies on the descriptive epidemiology of SRSE at a national level. The objective was to estimate the incidence of SRSE in Canada in 2010-2012.

We analyzed standardized national administrative record-level data covering all provinces across Canada as provided by the Canadian Institute for Health Information. SRSE episodes were classified from two databases for acute care admissions (Discharge Abstract Database) and emergency visits (National Ambulatory Care Reporting System) over 3 fiscal years (2010/2011 to 2012/2013). Cases were identified as SRSE using a modification of a previously published algorithm using ICD-10-CA diagnostic codes for epilepsy (G40), status epilepticus (G41), or convulsions (R56) plus an intensive care unit stay of 2 days or more with mechanical invasive ventilation.

Using our algorithm, from 2010-2012, the mean annual number of cases classified as SRSE was 3,427 (9.98/100,000 persons per year). The annual incidence was higher in males (11.78/100,000 per year) than females (8.21/100,000 per year). The highest rates were in the age group 70-79 years: 20.7 and 32.9 per 100,000 per year for females and males, respectively. The mean age of SRSE patients was 52 years (SD=22 years), with 58% males. The most common comorbidities for SRSE included metabolic disturbances (39%), sepsis (32%), toxic withdrawal state (31%), cardiovascular disease (22%), and head trauma (13%). In-hospital mortality for SRSE was 21%.

This is the first study reporting estimates of SRSE incidence in Canada. These results suggest that SRSE is associated with a substantial disease burden. Interventions that improve patient outcomes and reduce mortality are required.

New-onset refractory status epilepticus (NORSE) is a condition characterized by prolonged pharmacoresistant seizures in a previously healthy individual with no identifiable etiology during initial evaluation. Typical magnetic resonance imaging (MRI) findings include bilateral limbic and neocortical T2-weighted hyperintense lesions. Fluorodeoxyglucose (FDG)-positron emission tomography (PET) findings have not been previously reported. This study sought to describe FDG-PET and MRI characteristics in patients with NORSE.

Methods 12 patients were retrospectively identified amongst a database of autoimmune-mediated encephalitis from 2008-2017, meeting diagnostic criteria for NORSE and having undergone MRI and PET over the course of their illness. Imaging findings were confirmed with a board-certified neuroradiologist.

Nine patients were autoantibody positive: three N-methyl-D-aspartic acid (NMDA) receptor, two glutamic acid decarboxylase (GAD), three voltage-gated potassium channel (VGKC)-complex with two having leucine-rich glioma-inactivated protein 1 IgG positivity, and one gamma-aminobutyric acid (GABA) B receptor. All patients had identifiable abnormalities on FDG-PET. Hypometabolism was most common, with 11 of 12 patients having diffuse, bilateral, or unilateral frontal, parietal, or occipital cortical hypometabolism. Nine patients also had bilateral (7) or unilateral (2) mesial temporal hypermetabolism. Two patients had multifocal hypermetabolism with bilateral or unilateral frontal abnormalities in addition to mesial temporal findings. Of the nine patients with FDG-PET hypermetabolism, concurrent MRI scans failed to show corresponding T2-weighted hyperintense lesions in the mesial temporal and medial frontal regions in two patients.

FDG-PET findings in NORSE include bilateral or unilateral mesial temporal or mesial frontal hypermetabolism with diffuse, bilateral, or focal cortical hypometabolism. Hypermetabolism may reflect regions predominantly involved in acute epileptogenesis. FDG-PET may improve sensitivity when compared to MRI alone.

While seizures are uncommon but reported in primary intraventricular hemorrhage (IVH), little evidence is available on the prevalence of hyperexcitable patterns on long term EEG monitoring.

We sought to determine the prevalence of hyperexcitable patterns and seizures in patients with primary IVH who were extracted from a cohort consisting of patients with spontaneous intracerebral hemorrhage (sICH) who underwent continuous electroencephalogram (cEEG) monitoring between January 2013 and December 2016 at Yale-New Haven Hospital. Indications for cEEG monitoring included fluctuation of or depressed mental status, abnormal movements and a limited clinical exam. We recorded demographics, radiologic hydrocephalus, duration of EEG recording and EEG findings. Hyperexcitable patterns comprised generalized, bilateral independent or lateralized periodic discharges (PDs), lateralized rhythmic delta activity (RDA), brief potentially ictal rhythmic discharges (B(I)RDs), and spike-and-wave discharges (SW).

Of 196 adults with sICH who had cEEG performed, 13 patients had primary IVH. Hydrocephalus was present in 9 patients (69%). Patients were monitored for a mean duration of 22.4 (± 14.7) hours. 9 patients had hyperexcitable patterns and/or electrographic seizures (70%): Electrographic seizures and co-existent hyperexcitable patterns were captured in 2 of 13 patients (16%) and hyperexcitable patterns without seizures in 7 of 13 patients (54%). Hyperexcitable patterns included periodic discharges (PDs) (4) (generalized, lateralized and bilateral independent, with and without rhythmicity), rhythmic delta activity (RDA) (5) (both lateralized and generalized, with and without sharps), brief potentially ictal rhythmic discharges(B(I)RDs) (1) and spike-and-wave discharges (SW) (1). There was no significant difference between patients with and without hydrocephalus and hyperexcitability or electrographic seizures (p= 0.76).

Both electrographic seizures and/or patterns of hyperexcitability on EEG are common in our selected cohort of primary IVH patients. This underscores the importance of continuous EEG monitoring in this patient population, since the detection of non-convulsive seizures may offer an opportunity for therapeutic intervention.

Patients with aneurysmal SAH (aSAH) frequently have ictal-interictal continuum (IIC) EEG patterns. While seizure burden can worsen outcomes, less is known about IIC burden. We investigated the impact of IIC burden and anti-epileptic drug (AED) treatment on aSAH outcomes.

We included patients with aSAH undergoing continuous EEG (cEEG) from 2011-2016. Patients with nonaneurysmal SAH or 90%, 50-89%, 10-49%, 1-9%, <1%. Age gender, admission GCS, APACHE II score, Fisher and Hunt and Hess (HH) scores, AED dosing and discharge GOS were ascertained by chart review. 

Presence of IIC patterns in aSAH independently predicts worse neurologic outcome, although maximum burden does not. Although nearly half of these patients receive AED treatment, our data suggest that AED treatment may not influence outcome. Prospective studies may further delineate the clinical risks and benefits of AED treatment.

Refractory status epilepticus (RSE) is defined by failure to control epileptic activity after the administration of 1st and 2nd line antiepileptic agents. Mortality associated with RSE has been estimated to be around 23-61% at hospital discharge. We conducted this study to analyze trends in the frequency and management of RSE.

We conducted a cross-Consortium (UHC) database from 2009 to 2016. This is a database from 120 academic medical centers and their 299 affiliated hospitals in the United States and consists of a sample of 12,366,264 patients. Data including age, sex, antiepileptics (AED) and length of stay was collected. Total mean age was 52.4 years and females were 48.83%. There was an increasing trend of using lorazepam as the first line AED (58.5% in 2009 to 60.5% in 2016) and a decreasing trend was noted of using midazolam as the first line AED (62.9% in 2009 AED (62.9% in to 55.4% in 2016 . Leviteracetam was the most common second line AED used throughout all years which was followed by propofol followed by phenytoin/fosphenytoin. Mean length of hospital stay was 10.8 days.

Between 2009 to 2016, the proportion of hospitalized patients in the United States diagnosed with RSE has increased. Lorazepam and leviteracetam have been the most common AEDs used. Mean length of hospital stay has not changed.

Status epilepticus is associated with high risk of multi-organ dysfunction. Ketamine for the treatment of super refractory status epilepticus (SRSE) has the benefit of a different mechanism and lack of cardiac depression when compared with other anesthetic agents. This study evaluated the improvement in Sequential Organ Failure Assessment (SOFA) score in patients treated with ketamine for SRSE.

This is a retrospective study of patients with SRSE from 2011 to 2016. The timing and dosage of anesthetic agents used in their treatment were abstracted. SOFA scores at admission and for the first 6 days after initiation of ketamine were calculated. The presence of shock prior to initiation of ketamine included septic shock and cardiogenic shock. Outcomes including mortality, organ failure, and hospital associated infections (HAIs) were also recorded.

A total of 47 patients were treated with ketamine after failure of seizure control using other anesthetic agents. Seventeen (36.2%) had an improvement of their SOFA score while 30 (63.8%) did not. The median SOFA score on admission was 5 (IQR 4-6) for those who had an improvement and 6 (IQR 6-8) for those who did not (p=0.11). Cardiac arrest was the etiology of SRSE for 6 (37.5%) patients who improved vs. 10 (62.5%) patients who did not (p=0.89). Patients required 0 to 3 vasopressors for hemodynamic support, with less needed for those who had an improvement (p=0.02). There was a higher rate of HAIs in patient who did not have an improvement of their SOFA score (p=0.04).

There is a subset of patients treated with ketamine for SRSE who have an improvement in their SOFA score, require less vasopressor support, and have a lower rate of HAIs. Further studies are needed to better understand which patient population may most benefit from the use of ketamine for treatment of SRSE.

The Ceribell EEG System (CES) is a novel 8 channel EEG device with instant sonification and visual display capability that can be set up quickly without an EEG technician. We hypothesized that by using CES, we can decrease time to EEG acquisition and improve diagnosis and treatment decisions in suspected nonconvulsive seizures (NCS).

Adult ICU patients (GCS < 12) who had continuous EEG (cEEG) as part of clinical care were enrolled. Once cEEG was ordered, consent was obtained and CES was placed by the treating physician (n=7) who listened to the left/right hemisphere signals for 30 seconds each. Suspicion for seizure (1=low, 5=high) and decision to treat (yes/no/not sure) were rated pre-and post-sonification. Three blinded epileptologists compared accuracy of sonification with visual CES EEG. Outcomes were difference in time to EEG acquisition, change in suspicion for seizure and decision to treat, and ease of use (1=challenging; 5=easy).

35 patients (mean age 61 +/-18, median GCS of 6 (IQR 4-8.5) were enrolled from 7:00 AM to 5:00 PM. Start of EEG acquisition was significantly faster for CES (23 minutes (IQR 14-46) vs 145 minutes (IQR 93-237) p<0.001), median difference 86 minutes (IQR 60-152). One patient had NCS during sonification and this was accurately identified and treated. Low suspicion for seizure (1) was more likely postsonification (63% vs 37%, p=0.029). Treatment decision changed in 40% after sonification, and this was in the correct direction 86% of the time. Inappropriate decision to treat decreased from 26% to 9% (p=0.07). Negative predictive value was 100% (95% CI 85-100%). CES was consistently rated easy to use.

The Ceribell EEG System is easy to use, speeds EEG acquisition, accurately identifies NCS, and enables appropriate treatment decisions. It has the potential to greatly enhance timely diagnosis and treatment of NCS in critically ill patients.

The aim of the study was to understand the efficacy of ketamine in refractory status epilepticus and identify the underlying factors affecting the effectiveness of ketamine. Moreover, we also studied the rate of complications in patients who underwent continuous midazolam ketamine dual therapy for treatment of refractory status epilepticus.

This is retrospective cohort study evaluating the efficacy of ketamine in patient with refractory status epilepticus in total of 52 patients admitted to University of Maryland Medical Center in either neuro intensive care unit /MICU during the last five years between (2011-2016). We established a standardized algorithm for managing refractory status epilepticus. Electrographic and clinical control of seizures was classified into four groups: likely response, possible response, permanent response and no response reviewed by a team of epileptologist and neuro intensivist. The effective doses of ketamine to abort RSE were studied. Complications intensive care unit stay while on therapy were reviewed.

Of the 52 patients, 29 were male, 23 were female. 22% of the patients had cardiac arrest as an etiology of seizures. Median loading dose was 1.5 mg/kg, median maintenance dosage was 4 mg/kg/hr. 25 % of the patients had no response to ketamine. 75% were responsive to ketamine of which, 12 patients had likely response to ketamine, 28 patients had possible response.38.5% of the patients had permanent response to ketamine. 67% patients had hospital acquired infections, 34 % patient had metabolic acidosis, 25% had ARDS.

This is one of the largest single center study illustrating the efficacy of ketamine in aborting RSE. Further study should address the difference in incidence of complications in patients with usage of ketamine versus groups alternative therapies. This study also demonstrates the etiology of seizures and its influence on efficacy of ketamine in aborting RSE.

Acute cardiopulmonary complications are frequently observed in convulsive status epilepticus but mechanism is poorly understood. Complications include tachy-arrhythmias, myocardial ischemia, Takotsubo cardiomyopathy and neurogenic pulmonary edema. Herein, we mapped evolution of cardiac dysautonomia as function of 5 sequential electrographic stages of SE in four subjects admitted to ICU. We hypothesize pathological co-activation of both arms of autonomic system contributes to cardiac complications. Heart rate variability (HRV) is considered a proxy for ANS tone on heart.

We analyzed HRV in time and frequency domain, complexity measure (Lempel Ziv-LZ) during SE and mapped changes as function of stages of SE as determined by scalp EEG. Conventional scalp EEG recording and lead I-EKG (sampled at 256 Hz) were analyzed using Kubios HRV software 2.1. Cardiac vagal index (CVI) and cardiac sympathetic index (CSI) were calculated using geometric Lorenz-plot method. Parasympathetic activity is expressed in RMSSD, pNN, CVI, and HF power

Four adults (range 22-59; M=3) were admitted to ICU following convulsive SE. Ictal HRV changes initially reflected high sympathetic system activation (high CSI) and reduced vagal tone (low HF, RMSSD) as reported previously with convulsive seizure. Earlier stages of SE (Stage I and II) were marked by dual activation of the ANS with sympathetic predominance (lower CVI/CSI ratio). Later stages of SE (Stage IV and V), demonstrated progressive increase in parasympathetic activity (HF power, RMSSD, CVI, CVI/CSI ratio). HF power and RMSSD at Stage V SE was three times higher than during discrete seizure. LZ complexity measure downtrended with the loss of fluctuations in late stages of SE. In one subject SE terminated with asystole

This case series highlights dynamic changes in sympatho-vagal imbalances with progressive SE. Dual activation of sympatho-parasympathetic system and loss of complexity measures are associated with increased cardiac complications. Therapies directed towards stabilization of cardiac dysautonomia might minimize complications

Super-refractory status epilepticus (SRSE) is a life-threatening neurological condition that is characterized by status epilepticus that persists for 24 hours despite treatment with first-, second-, and third-line agents (TLAs) or upon the weaning of TLAs. SRSE is associated with limited treatment options, and high morbidity and mortality. This study aims to describe and quantify inpatient SRSE treatment and its associated outcomes in the US.

SRSE cases were classified retrospectively using a modified version of a previously published algorithm applied to a large, de-identified, US electronic health record database (Cerner Health Facts®) covering >600 hospitals (2000) (2001) (2002) (2003) (2004) (2005) (2006) (2007) (2008) (2009) (2010) (2011) (2012) (2013) (2014) (2015) . Cases were classified utilizing ICD-9 and procedure coding for status epilepticus (345.00, 345.01, 345.1x, 345.3, 345.41, 345.51 and 345.81) , ventilator support or with LOS>180 days or missing age were excluded. Univariate statistics were used to describe mortality, hospital LOS, ICU LOS, and discharge disposition.

Our algorithm classified 1153 cases as SRSE (1137 patients). Most cases (61%) were to large (300+ beds) and/or teaching hospitals (86%). Mean hospital LOS was 24.4 days, and ICU LOS was 15.1 days. Both LOS and ICU LOS were significa Average mortality rate was 23.5%. Mortality rates increased with number of TLAs used (1-2 TLA=21.5%; 3-rged home (6% with tracheostomy), while 32% (N=285) were discharged to another facility.

Treatment of SRSE requires acute, intensive management in the hospital setting. LOS and mortality rates were high and increased with increasing use of TLAs. While good outcomes remain possible even after SRSE, additional interventions are needed that enable seizure control, liberation from anesthetic and ventilator management, and improved mortality.

Refractory status epilepticus (SE) carries an exceedingly high mortality and morbidity, often warranting an aggressive therapeutic approach. Initially used in childhood epilepsies, ketogenic diet (KD) has also accumulated supporting evidence in the treatment of pediatric SE. Recently, the implementation of KD in adults with refractory and super-refractory SE has been shown to be feasible and effective.

We describe our recent experience with a new onset refractory status epilepticus (NORSE) patient and the unexpected challenge of achieving and maintaining a ketotic target. Practical advice, a comprehensive review of offenders jeopardizing ketosis commonly used in the neurocritical care unit and alternatives is provided.

A previously healthy 29-year-old woman was admitted with cryptogenic NORSE following a febrile illness with a course complicated by prolonged super-refractory SE. A comprehensive work-up was notable only for mild cerebral spinal fluid (CSF) pleocytosis, elevated non-specific inflammatory serum markers, and edematous hippocampi with associated diffusion restriction on magnetic resonance imaging (MRI). Repeat CSF testing was normal and serial MRIs demonstrated resolution of edema and diffusion restriction with gradually progressive hippocampal and diffuse atrophy. She required an aggressive approach including high anesthetic infusion rates, 16 anti-seizure drug trials (in various combinations), empiric partial bilateral oophorectomy, and immunosuppression. Enteral ketogenic formula was started on hospital day 27, however, sustained beta-hydroxybutyrate levels > 2mmol/L were only achieved 37 days later following a careful comprehensive adjustment of the care plan. Notably, a significant response to KD was only achieved with beta-hydroxybutyrate levels > 3.5 mmol/L.

There are hidden carbohydrates in commonly administered medications for SE, antibiotics, and even electrolyte repletion formulations and solutions used for oral care -all challenging the use of KD in this setting. Tailoring comprehensive care and being aware of possible complications of KD are important for the successful implementation and maintenance of ketosis.

Early seizures are estimated to occur in 18-33% of patients with moderate to severe traumatic brain injury (TBI) (Herman 2015, Vespa 1999). Continuous EEG (cEEG) is essential for detection of nonconvulsive seizures (Claassen 2004) The University of California Davis protocol for TBI includes cEEG on a case by case basis, which we reviewed.

A retrospective review of patients admitted to ICU for TBI from 9/23/2016-3/13/2017 was performed for demographics, ICU length of stay (LOS), and cEEG. Patients with cEEG were assessed for demographics, TBI severity, GCS, cEEG indication and findings.

100 patients were identified. Twenty-one were monitored on EEG. Median age was 36, 24% were female. Indications for cEEG included seizure prior to admission (n=4), altered mental status (AMS) (n=13), AMS with paroxysmal events (n=4). Seizures were recorded in 2 patients. Median duration of cEEG was 26.8, 296.36, and 146.25 hours among the groups. Those with seizures prior to hospitalization were connected to cEEG earliest (median 14 .65 hours) but had the longest median ICU LOS (623.27 hours), followed by AMS (40.28 and 424.92 hours) and AMS with paroxysmal events (78.83 and 377.88 hours). Median GCS was 3, 6, and 5 respectively. Median LOS for patients without seizures or interictal epileptiform activity (IEA) was 380.63 hours, 483. 47 for those with IEA only, and 580.58 for those with seizures. Median GCS was 4.5, 6, and 4 among the EEG groupings.

Our data suggests seizures prior to hospitalization, cEEG recorded seizures, and IEA predict longer ICU LOS. Associated lower GCS likely indicates more severe injuries. TBI patients with AMS may have delay to seizure detection and treatment. Our rate of seizure detection is lower than expected. A more consistent protocol for cEEG will likely improve seizure detection. Prospective studies are needed to determine if cEEG can predict and influence outcomes.

Status epilepticus is a serious neurologic emergency. Although many studies have been published on incident status epilepticus, there are few data on the risk of recurrent status epilepticus.

We performed a retrospective cohort study using administrative claims data to identify all patients hospitalized with status epilepticus in California, New York, and Florida between 2005-2013. Our primary outcome was a recurrent hospitalization for status epilepticus. Survival statistics were used to calculate the cumulative rate of recurrence at 30 days, 1 year, and 5 years. In subgroup analyses, we compared rates of recurrence according to age, gender, race, and etiology (stroke, traumatic brain injury, acute and chronic central nervous system (CNS) infections, brain tumors, dementia, autoimmune CNS disease, or unspecified etiology).

We identified 37,418 patients with status epilepticus. During a mean follow-up of 2.9 (±2.0) years, 4,755 (12.7%; 95% CI, 12.4-13.0%) developed recurrent status epilepticus. The cumulative rate of recurrence was 2.7% (95% CI, 2.5-2.9%) at 30 days, 10.9% (95% CI, 10.5-11.3%) at 1 year, and 20.8% (95% CI, 20.2-21.5%) at 5 years. The 5-year cumulative rate of recurrence was 19.8% (95% CI, 18.9-20.6%) in women versus 21.9% (95% CI, 21.0-22.8%) in men, 16.8% (95% CI, 16.0-23.2% (95% CI, 22.4-24.0%) in patients <60, and 19.1% (95% CI, 18.4-19.9%) in white patients versus 23.0% (95% CI, 22.1%-24.0%) in non-white patients. The 5-year cumulative rate of recurrence was highest for status epilepticus associated with autoimmune CNS disease (30.3%; 95% CI, 25.4-35.9%) and chronic CNS infection (24.1%; 95% CI, 19.6-29.4%).

Approximately 1 in 5 patients with status epilepticus experienced a recurrent episode within 5 years. Recurrence was most often seen in younger patients, non-white patients, and patients with underlying autoimmune CNS disease or chronic CNS infection.

Super-refractory status epilepticus (SRSE) is a rare, life-threatening form of status epilepticus (SE) refractory to multiple therapies including anesthetic third-line agents (TLAs). Enrollment in a SRSE clinical trial is challenging because patients may present urgently before SRSE is confirmed or may dynamically improve before randomization. Pivotal clinical trials in SRSE require patient selection criteria accurately identifying SRSE at randomization. In this Phase 3 trial of brexanolone as adjunctive therapy for confirmed SRSE, the enrollment scheme enabled operationally confirming SRSE prior to randomization during a qualifying wean (QW) under real-time EEG neuromonitoring.

Informed consent was obtained for all subjects 1) admitted in SE having failed first-and second-line therapies; 2) transferred on TLAs in seizure-or burst-suppression; or 3) transferred without seizure-or burst-suppression or not receiving TLAs. Subjects were required to achieve seizure-or burst-suppression for 24 hours through continuous administration of one or more TLAs, followed by a post-enrollment QW of TLAs. Enrolled subjects failing the QW were randomized to concomitant brexanolone or placebo following reinstitution of one or more TLAs. Subjects not randomized after a successful QW underwent a 3-week follow-up.

The QW protocol and criteria for QW failure were developed and implemented utilizing EEG neuromonitoring to confirm SRSE after enrollment using the definition of Shorvon and colleagues. A QW was performed on over 100 evaluable subjects across 180 international sites to enable enrollment of patients with confirmed SRSE. Subjects with a successful QWs who were not randomized provided insight into outcomes associated with SE and avoided the randomization of patients who did not meet SRSE criteria following enrollment.

The use of neuromonitoring-guided diagnosis during a structured QW helped confirm SRSE, facilitating the enrollment of appropriate patients into this Phase 3 trial in a rare, critically ill, and dynamic SRSE patient population.

Autoantibodies to the 65 kDa isoform of gulutamic acid decarboxylase (GAD65 Ab), commonly found in T1DM patients, have been associated with drug resistant epilepsy. Ketosis prone diabetes is a heterogenous syndrome encompassing various forms of beta cell dysfunction culminating in diabetic ketoacidosis. Rates of epilepsy in patients with ketosis prone diabetes are not known.

We compared the prevalence of epilepsy in patients with ketosis prone diabetes in a multi-ethnic population with the prevalence of epilepsy in the type 1 diabetes population as well as the general population in a metropolitan medical center. Our study design is Prospective review of retrospectively collected sera of 500 patients admitted for diabetic ketoacidosis (defined as pH < 7.3, bicarb < 17, with ketonemia or ketonuria) for the presence of GAD65 Ab. All these sera were assessed separately for autoantibody presence or absence at Dr Hampe's lab in Washington, Seattle. We also reviewed patients medical records for neurological diagnoses. This done in a blinded fashion by two separate reviewers.

Out of our 500 patients with ketosis prone diabetes, 4.3% also had epilepsy. This is higher than the published rate in Type 1 Diabetics (1.35%) and the general population in the surrounding area (<0.05%). Antibody testing revealed 21% of patients with ketosis prone diabetes were GAD65 Ab positive with a rate of epilepsy of 1%. A two-tailed T test between the GAD65 Ab + group and GAD65 AB -group showed no statistically significant difference in prevalence of epilepsy in these two groups.

While prevalence of epilepsy is higher in the ketosis prone diabetes population than the general population of Houston, the difference is not related to titers of GAD65 Ab, and must be due to some other unknown factor in these patients

Management of refractory status epilepticus commonly involves the induction of seizure-or burstsuppression using anesthetic agents. However, the duration and endpoints of these therapies are not well defined. Specifically, weaning anesthetic agents is complicated by the emergence of EEG patterns on the ictal-interictal continuum (IIC), which have uncertain significance, given that IIC patterns may worsen cerebral metabolism and oxygenation, have a dissociation between scalp and depth EEG recordings, and indicate a late stage of status epilepticus itself. Determining the significance of IIC patterns in the unique context of anesthetic weaning is important to prevent the potential for unnecessarily prolonging anesthetic coma.

We identified a series of patients who underwent over 48 hours of burst-suppression therapy, multiple weaning attempts, and continued weaning despite the initial emergence of IIC patterns. Patients who experienced anoxic brain injury were excluded from the series.

We report 5 cases of patients who underwent successful weaning despite initial emergence of IIC patterns. EEG patterns following anesthetic weaning (including lateralized periodic discharges approaching 3 Hz frequency and lateralized rhythmic delta activity) as well as terminal EEG patterns are described in detail.

In these 5 patients, continuing weaning of anesthetic agents despite the emergence of IIC patterns did not result in relapse to status epilepticus. While the metabolic impact of these patterns on brain activity is uncertain, weaning strategies that treat IIC as a surrogate of recurrent status epilepticus risk further prolonging anesthetic management and its known toxicity. We speculate that IIC patterns are transitional and may have a context-specific association with status epilepticus relapse, with less risk conferred when these patterns are observed during the weaning of anesthetic agents after prolonged burst-suppression therapy. Other electrographic features aside from this clinical context may discriminate the risk of status epilepticus relapse, such as EEG background activity.

Brivaracetam (BRV) is approved as adjunctive therapy for focal (partialyears) with epilepsy. BRV is available as oral tablets, oral solution, and an intravenous (IV) formulation. The formulations are interchangeable. This abstract reports the safety and tolerability of IV BRV. During clinical development, 177 participants received IV BRV. We report pooled safety findings from 153 participants receiving BRV 25-150 mg doses. The therapeutic range of BRV is 25-100 mg twice daily.

In N01256, 24 healthy volunteers received IV BRV as a 15-minute infusion or 50 mg/min bolus (25, 50, 100, or 150 mg single doses; n=6 in all groups). In EP0007 (NCT01796899), 25 healthy volunteers received IV BRV 100 mg as a single 2-minute bolus injection or oral tablets. In N01258 (NCT01405508), 104 patients received 7 days of BRV oral tablets 100 mg twice daily or placebo, and then 4.5 days of IV BRV 100 mg twice daily either as a 2-minute bolus or 15-minute infusion for nine doses in total. Treatment-emergent adverse event (TEAE) data were pooled.

Data reported are for IV BRV 25-150 mg (n=153). Most frequent TEAEs were somnolence 30.1%, dizziness 15.7%, fatigue 15.0%, headache 7.2%, dysgeusia 6.5%, euphoric mood 3.9%, feeling drunk 3.9%, and infusion-site pain 3.3%. Infusion-site pain was specific to administration route. Most TEAEs were mild or moderate and occurred mostly in healthy volunteers.

IV BRV was well tolerated, with an AE profile consistent with oral administration except for routespecific injection-site AEs, dysgeusia, euphoric mood and feeling drunk. The interpretation of these data was complicated by the difficulty of pooling disparate studies involving healthy volunteers and epilepsy patients with heterogeneous medical histories and concomitant antiepileptic drug use. Further clinical trials or real-world experience are needed to understand potential clinical impact. UCB Pharma funded

Refractory status epilepticus (RSE) is a challenging condition that requires multiple antiepileptic drugs (AED) to treat. During RSE, the brain is under excessive excitation, which results in an increase in glutamate receptors such as alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and Nmethyl-Daspartate (NMDA).. Perampanel (PER), a novel, noncompetitive AMPA-receptor antagonist, may have a role in the treatment of RSE and there are positive results in different animal models with RSE.

We identified 8 adults patients over a 6 month period who were treated with PER for different forms of RSE. One was excluded as the etiology of RSE was anoxic brain injury and care was transitioned to comfort only within 24 hours of initiating PER. Three patients had a definite response to PER, which we defined as resolution of ictal patterns on electroencephalogram (EEG) within 48 hours of PER without adding a new AED. One had a possible response with significant improvement in EEG findings; however, there was some EEG improvement predating the initiation of PER. In observed several treatment factors that may have increased response to PER. Those who responded had it used earlier in the treatment cascade (sixth or seventh vs. ninth or tenthAED ), higher initial dose (8 mg vs 4mg), and were escalated to maximum dosage within 48 hours. They were also more likely be receiving continuous ketamine and midazolam, suggesting a possible synergy with PER. There were no documented adverse effects in any patient prior to discharge. One patient did experience a decline in phenytoin levels, which could be related to PER as there are reports of enzyme-inducing properties.

We observed efficacy of PER in several patients with focal and generalized RSE without a significant adverse effect profile. Further studies are needed to clarify the dosing, timing and appropriate indications in RSE treatment.

Topiramate is a potent broad-spectrum anti-epileptic drug (AED) with several mechanisms of action including blockage of the inotropic glutamatergic AMPA receptor, voltage-gated sodium channels, antagonism of non-NMDA glutamate receptors and enhancement of GABA mediated chloride conductance. We hypothesize that Topiramate is an effective adjunctive therapy in RSE and SRSE due to multiple mechanisms of action.

We performed a retrospective analysis of 11 patients admitted to the intensive care unit with status epilepticus (SE) at a tertiary referral center from 2013-2016. We reviewed demographics, age, seizure type, etiology, prior AED/Topiramate exposure, time to response to treatment, EEG reports and neuroimaging results. RSE was defined as failure of benzodiazepine and another conventional second line AED to stop SE. SRSE was defined as SE that continues or recurs 24 hours after being treated with an anesthetic agent.

6 (55%) were male, 6 (55%) had a history of seizures; mean age of patients with SE was 62.5 years. Of 11 treated patients, 6 (55%) had focal non-convulsive SE (NCSE), 1 (9%) had myoclonic SE, 1 had myoclonic, followed by generalized NCSE,1 (9%) had generalized NCSE, and 1 (9%) had focal and generalized nonconvulsive SE, prior to administration of Topiramate. 3 (27%) patients were treated with 2 AEDs, 8 (72%) patients with 3 AEDs prior to Topiramate. Electrographic seizures improved in 10 (91%) patients after receiving Topiramate. Resolution of electrographic seizures occurred within 12 hours in 2 (18%) patients, 24 hours in 4 (36%) patients, 48 hours in 2 (18%) patients and 72 hours in 2 (18%) patients.

Our findings suggest that Topiramate could be an effective adjunctive treatment in RSE and SRSE. However, prospective studies, including larger number of patients are needed to confirm these findings.

Patients with refractory status epilepticus (SE) require multiple antiepileptic drugs (AEDs) to abort seizures, and often barbiturates. There is a paucity of data on how to wean AEDs safely once seizures are controlled while minimizing medication side-effects or withdrawal symptoms.

A retrospective review of 160 patients admitted to Mayo Clinic in Rochester, Minnesota for SE between 2006 and 2016 was performed. Patient demographics, SE type (focal versus generalized, convulsive, and refractoriness), seizure etiology, AEDs in admission and at outpatient follow-up, AED side effects from use and withdrawal, and functional outcomes in terms of modified Rankin Scale were recorded.

44 of 160 (27.5%) patients had refractory SE, 24 (15.0%) patients had refractory non-convulsive status epilepticus (NCSE), 62 (38.8%) patients had convulsive SE, 18 (11.2%) patients had NCSE, and 12 (7.5%) patients had epilepsia partialis continua. Of the 122 patients with outpatient follow-up (ranging 1 to 50 weeks following hospital discharge with 68.0% patients following-up within one month), 120 patients were on an AED regardless of etiology. Patients were on a median of 1 AED in both refractory and nonrefractory SE at follow-up. 9 (5.6%) patients had withdrawal seizures after AEDs were weaned (3 had a prior stroke, 1 traumatic brain injury, 2 idiopathic, 2 multifactorial). None of the 13 patients completely weaned off a barbiturate had seizure recurrence at follow-up. 6-month mortality in refractory SE was 22/68 (32.4%) and 23/92 (25.0%) in non-refractory cases. Favorable functional outcome at follow-up was achieved in 17/68 (25.0%) patients with refractory SE versus 29/92 (31.5%) in non-refractory SE.

We found a low rate of late seizure recurrence after weaning AEDs in refractory and non-refractory SE, particularly in the case of barbiturates.

Spreading depolarizations (SD) are strongly associated with secondary brain injury after aneurysmal subarachnoid hemorrhage (SAH). However, studies to understand whether SDs play a causal role in secondary injury are hindered by existing SD induction methods which are invasive, cumbersome, and cause primary tissue injury.

We developed a method to study the role of SDs after experimental SAH using commercially available transgenic optogenetic mice which express channelrhodopsin (ChR2) in cortical neurons. We used in vivo laser speckle and Doppler flowmetry, intrinsic signal imaging, and local field potential (LFP) and extracellular potassium shifts to detect SDs.

We optogenetically induced SDs with light through intact and unaltered skull in multiple regions without causing primary brain injury. We found regional differences in thresholds for optogenetically-induced SDs (from lowest to highest threshold): (1) whisker barrel, (2) motor, (3) sensory, and (4) visual cortex. Lower thresholds were associated with higher ChR2 tissue expression. Changes in LFP and increased extracellular potassium concentrations at the site of stimulation preceded precipitation of an SD. Finally, we induced and detected SDs in the setting of SAH over several days through chronically implanted glass coverslips

Non-invasive optogenetic light stimulation can reliably induce SDs in the setting of SAH. Longitudinal optogenetic induction of SDs in ChR2 transgenic mice is a potentially useful tool to study the role of SDs in the pathogenesis of secondary brain injury after SAH.

Aneurysmal subarachnoid hemorrhage is a devastating neurologic injury with significantly prolonged hospital courses and high morbidity and mortality. When aneurysms are detected, they often require securement either via surgical clipping or endovascular techniques. A subset of intracranial aneurysms, given location, poor surgical approach, and wide neck are amenable to flow diversion which promotes thrombosis through redirecting of blood flow within an aneurysm leading to slow obliteration. Approximately 10% of treated aneurysms with flow diversion do not obliterate after 12 months, but currently there is no validated way to predict treatment failure. Computational models of blood flow of flow diverted aneurysms predict a significant difference in the hemodynamic energy loss across aneurysms between cases that resolve and those that do not. Energy loss could be estimated clinically during angiography, however, this hypothesis needs to be validated experimentally because computer models often over estimate hemodynamic parameters, poorly predict flow through stents, and may not have the resolution to fully describe intra-aneurysmal blood flow.

In this pilot study, four cases of giant fusiform intracranial aneurysms will be selected --two with resolution following flow diversion treatment, and two without resolution. Models of each vessel geometry will be fabricated using additive manufacturing techniques. Under fluoroscopy, within the model vessel, flow diverting stents will be placed within the aneurysm in the same configuration that was achieved clinically. Model blood, containing tracer particles will be pumped through model aneurysms and using particle image velocimetry, energy loss will be calculating within model vessels following treatment.

Energy loss between aneurysms successfully and unsuccessfully treated with flow diversion will be compared experimentally.

Hemodynamic energy loss may be a clinically measurable value which could predict treatment failure after flow diversion. Additive manufacturing techniques can be used to test patient specific hemodynamics to improve understanding of flow-diversion treatment success or failure.

The National Institute of Neurological Disorders and Stroke (NINDS) and the National Library of Medicine (NLM) initiated development of unruptured cerebral aneurysms and subarachnoid hemorrhage (SAH)specific Common Data Elements (CDEs) in 2015 as part of a joint project to develop data standards for funded neuroscience clinical research. Through the development of these data standards, the NINDS and NLM SAH joint CDE initiative strives to improve SAH data collection by increasing efficiency, improving data quality, reducing study start-up time, facilitating data sharing/meta-analyses and helping educate new clinical investigators.

The SAH CDE working group (WG) consisted of 83 international members with varied fields of SAHrelated expertise and was divided into domains such as subject characteristics and assessments and exams. The WG developed a set of SAH-specific CDE recommendations by selecting among, refining and adding to existing field-tested data elements, especially established Stroke CDEs. WG CDE recommendations were drafted into the NIH CDE Repository. Following an internal review of recommendations, the SAH CDEs were vetted during a public review on the NINDS website for 6 weeks and later posted on NLM and NINDS websites.

Version 1.0 of the SAH CDEs was available on the NINDS CDE website in April 2017. These new SAH CDEs and recommendations include those developed for unruptured intracranial aneurysms and long-term therapies. The website provides uniform names and structures for each data element, as well as guidance documents and template case report forms using the CDEs.

The NINDS encourages the use of CDEs by the clinical research community in order to standardize the collection of research data across studies. The NINDS CDEs are a continually evolving resource, requiring updates as research advancements indicate. These newly developed SAH CDEs will serve to be a valuable starting point for researchers and facilitate streamlining and sharing data.

Subarachnoid Hemorrhage (SAH) represents 5% of stroke admissions in the US. Aneurysmal hemorrhage represents the most dangerous etiology, however 10-15% of SAH have negative digital subtraction angiography (DSA). There is variation in practice with regards to repeat diagnostic studies and timing of such studies. It is not uncommon to repeat DSA in 7-10 days of the initial assessments. This study aims to describe the costs associated with prolonged ICU stay and repeat diagnostic studies this patient cohort.

Retrospective review of all patients admitted for spontaneous SAH between January 2011 and April 2017 at our single institution. Patients with at least one negative initial angiogram for suspected spontaneous SAH were included. Patients were categorized into diffuse patterns of SAH and nondiffuse. Cost estimates were based on standard costs as provided by our financial department and CDC estimates for costs of hospital acquired infections.

One hundred fifty-four patients were identified with initial negative DSA. Second angiograms were performed in 81% of patients, and potentially positive causal findings in 18/125 (14.4%). ICU LOS for angiogram negative diffuse SAH and non-diffuse were 10.1 and 6.5 days respectively. Other indications for ICU stay included vasospasm (8.5%), EVD placement (30.8%), and Intubation (22%). The excess cost estimates per patient for angiogram negative diffuse and non-diffuse SAH were $71,567 and $52,843 respectively. Hospital acquired complications were an additional total $57,422 for the cohort.

This is the first study to our knowledge attempting a cost analysis of the diagnosis and management of patients with angiogram negative SAH. We had a high frequency of patients requiring ICU admission for other indications, which should continue to dictate the level of care. However, there may be a cohort of lower risk patients in which de-escalation would not harm, and be of benefit in the reduction of morbidity and cost.

Purpose: To evaluate the feasibility and potential role of bedside optical coherence tomography (OCT) as a diagnostic protocol in Terson's Syndrome (TS) in patients with acute subarachnoid hemorrhage (aSAH). Background: 10% of SAH patients become permanently legally blind. The average cost of lifetime support and unpaid taxes for each blind person is approximately $900,000. TS presents as ocular bleeding commonly associated with aSAH. It can be diagnosed by fundoscopy, yet retinal haemorrhages, detachments and macular holes may be undetected. Early TS identification is critical since untreated it may lead to legal blindness, limit rehabilitation and impair quality of life.

Pilot study: 31 SAH patients were screened for TS with dilated fundoscopy and then with OCT. Mood assessments (PHQ-9, HDS), quality of life measures (NIH-PROMIS) and subjective visual function scales (VFQ-25) were performed.

There was a 22.6% (n=7) incidence of TS. Dilated retinal fundoscopy significantly failed to detect TS (n=4, 57.1% missed cases). IVH was significantly more in TS (85.7% vs. 25%). No participants experienced any complications from OCT examinations. Neither decreased quality of life visual scores nor a depressed mood correlated with objective OCT pathological findings at 6 weeks follow-up after discharge. There were no significant mood differences between TS cases and controls.

OCT is the gold-standard in retinal disease diagnosis. This pilot study showcases its bedside feasibility in aSAH. In our series, OCT was a safe procedure that enhanced TS detection by decreasing false negative/ inconclusive fundoscopic examinations. It allows early diagnosis of macular holes and severe retinal detachments, which require acute surgical therapy to prevent legal blindness. Besides, OCT aids ruling out potential false positive visual deficits in individuals with a depressed mood at follow up. A comprehensive study is underway to understand the impact OCT might exert on blindness prevention and quality of life.

Fever is common in patients with aneurysmal subarachnoid hemorrhage (aSAH), and blood cultures are commonly sent to diagnose etiology. Several studies have shown a low incidence of positive blood cultures, but no studies have assessed blood cultures in patients with aSAH.

We performed a retrospective analysis of patients admitted with aSAH between January 2013 to December 2015. Blood cultures were adjudicated as true positive (TP) or false positive (FP) based on speciation, time to positivity, number of cultures positive, and repeat culture results. TP patients were compared to all other patients. Age, gender, Hunt Hess, Modified Fisher, aneurysm treatment, incidence of delayed cerebral ischemia (DCI), length of stay (LOS), and neurological outcomes were analyzed.

324 patients with aSAH were included. Blood cultures were sent on 195 (60%). Sixteen were positive. Eleven were adjudicated TP and 5 FP. Thus, 3.4% (11/324) of patients had true bacteremia, and blood culture yield for true infection was 5.6% (11/195). FP rate was 2.6% (5/195). Eight TPs were gram negative (73%), and all contaminants were Staphylococcus non-aureus. Median post-bleed day for TP results was 23. Only 3 patients were TP within the first week of admission (0.9%). TP patients had higher admission WFNS (p=.015) and IVH score (p=.006), but age, gender, aneurysm treatment, and Fisher score did not differ. TP patients had longer ICU and hospital LOS and higher incidence of DCI (56% vs 27%, p=.026). Mortality did not differ in the two groups either.

The yield of blood cultures in aSAH patients is low. Even with a contamination rate under 3%, 31% of positive blood cultures are FP. Future studies should evaluate factors to identify patients at higher risk of bacteremia to reduce costs and improve care.

Intra-arterial verapamil therapy reduces cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). There is little literature that quantitatively describes its safety, required dosing, or efficacy. As a result, therapeutic outcomes need to be subjectively analyzed by experienced radiologists during the intervention and clinically correlated by cerebral perfusion pressure, intracranial pressures and Transcranial Dopplers. We present a novel imaging analysis to quantify cerebral perfusion in realtime and apply this technology to patients undergoing therapy for vasospasm.

We developed software to evaluate changes in contrast flow dynamics for digital subtraction angiography (DSA) scans performed pre-and post-intra-arterial therapy for vasospasm. Performing signal intensity curve deconvolution on a voxel by voxel basis provides quantitative 2D perfusion parameters including: time to peak, time to drain, area under the curve, root mean transit time, arrival time, tissue concentration, arterial input functions and cerebral blood flow at each voxel. After aligning perfusion studies, our software then displays and automatically creates regions of interests for changes in perfusion to visualize the effects of interventions.

Our software quantitatively measures perfusion from DSAs and can normalize two DSAs accounting for differences in volume and speed of contrast administration. Two applications of this technology are demonstrated. The first subtracts perfusion from pre-and post intra-arterial interventions quantifying exact changes in perfusion at each voxel. The second compares two DSA studies of the same patient at different dates to contour the territories susceptible to delayed cerebral ischemia. We compare this analysis to MRI imaging when applicable demonstrating ischemic changes aligning to the susceptible territories outlined by our analysis.

DSA based perfusion is an effective study to quantify the need for and the precise effects of endovascular interventions. Quantitative thresholds and analysis based on DSA perfusion may assist with real-time assessment of treatment efficacy for patients undergoing intra-arterial verapamil therapy.

We aim to characterize the clinical predictors of ventriculoperitoneal shunt (VPS) placement in aneurysmal subarachnoid hemorrhage (aSAH) patients. There has been no clear consensus as to effective measures of predicting VPS placement in these patients.

We reviewed the clinical data of patients with aneurysmal subarachnoid hemorrhage (aSAH) who were treated at our institution between 2011-2014. We eliminated patients who died or had withdrawal of care during admission. We recorded patient demographics and clinical predictors including admission/discharge Glasgow Coma Scale (GCS), Hunt Hess score, aneurysm size/location, modified Fischer score, modified Rankin scale (mRS), intracranial pressure (ICP) values during EVD clamp trial, and incidence of vasospasm requiring intra-arterial therapy.

There were 112 patients included in this study and 36% of patients required VPS (n=42/112). VPS patients had significantly worse mRS functional scores at discharge (2.7 vs 3.4; p=0.029), but this began to balance at 1 year (2.5 vs 3.3; p=0.08). Aneurysms were significantly larger in VPS patients (7.4cm vs 5.5cm; CI: 0.57 to 3.38; p=0.006). A greater percentage of VPS patients had posterior fossa aneurysms, but this was not found to be statistically significant (37% vs 52%; p=0.12). VPS patients had significantly lower GCS scores at admission (12.9 vs 14.1; p=0.02), and discharge (11.7 vs 9.4; p=0.01). There was no difference in modified Fischer score (p=0.36) or Hunt Hess (p=0.06), but both variables were higher in the VPS cohort. There was no difference in the frequency of vasospasm in the VPS cohort (p=1.0), or ICP values (p=0.15).

Patients presenting with large aneurysms and poor GCS scores had a significantly higher likelihood of requiring VPS during admission. These patients had significantly poorer mRS scores at discharge but not at 1 year.

Subarachnoid hemorrhage (SAH) affects a young population and results in death or disability in the majority of those who experience it. This epidemiology is very different from other forms of stroke. Consequently, patients with SAH and their families may have different priorities for recovery. Involving patient perspectives is encouraged in research and is often accomplished using patient-reported outcome measures (PROMs). However, whether PROMs reflect patient and family priorities is unclear given that (a) PROMs are often developed without their input; and (b) generic PROMs may not apply to specific conditions. We aimed to systematically review the SAH literature that has: a) involved patient, family or caregivers in evaluating existing outcome measures, b) developed novel outcome measures by incorporating their perspectives (including co-development), or c) described outcomes important to patients, families, or caregivers.

We searched Embase and Ovid MEDLINE from inception to December 19, 2016. Study eligibility and data extraction was performed independently and in duplicate. For each eligible citation, we abstracted the following: study population, design, type of patient involvement, and outcome measure(s), as applicable. We planned a qualitative summary of all included studies.

Our search yielded 4275 unique citations. Only four articles have met our eligibility criteria. In each, patients (N=235) self-report impairments resulting from SAH and their impact on their lives (aim c). None involve the evaluation of PROM applicability. Additionally, we found 8 articles that, although they did not meet our a priori eligibility criteria, discuss collecting PROMs (N=2), using PROMs to predict health outcomes (N=4), and comparing PROM applicability without patient perspectives (N=2) in SAH populations.

Based on our findings, there is alack of patient, family, or caregiver involvement in selecting or identifying outcomes after SAH with direct relevance to them. SAH research may be overlooking outcomes that are important to patients.

Early brain injury (EBI) after aneurysmal subarachnoid hemorrhage (aSAH) is defined as brain injury occurring within 72 hours of aneurysmal rupture. Although EBI is the most significant predictor of outcomes after aSAH, its underlying pathophysiology is not well understood. We hypothesize that EBI after aSAH is associated with an increase in peripheral inflammation measured by cytokine expression levels and changes associations between cytokines.

Methods aSAH patients were enrolled into a prospective observational study and were assessed for markers of EBI: global cerebral edema (GCE), subarachnoid hemorrhage early brain edema score (SEBES), and Huntassays to determine levels of 13 pro-and anti-inflammatory cytokines. Pairwise correlation coefficients between cytokines were represented as networks. Cytokines levels and differences in correlation networks were compared between EBI groups.

Of the 71 patients enrolled in t associated with high grade SEBES. Correlation network analysis suggests higher systematic inflammation Conclusions EBI after SAH is associated with increased levels of specific cytokines. Peripheral levels of IL10, IL6 and ession levels of individual cytokines may offer deeper insight into the underlying mechanisms related to EBI.

Few recent studies have evaluated health resource utilization and patient outcomes in aneurysmal subarachnoid hemorrhage (aSAH) in the United States. Empirical evidence implicates aSAH as one of the highest cost diseases treated in the hospital. We identified aSAH patients to determine hospital charge, length of stay (LOS) and patient disposition associated with care in U.S. hospitals using claims data from the 2013 National Inpatient Sample (NIS).

Patients within the International Classification of Disease, 9th Revision (ICD-9) 430 diagnosis code were identified; a secondary analysis of the NIS (2013) was conducted utilizing ICD-9 Clinical Modification codes excluding patients with traumatic and non-aneurysmal SAH. Population size, patient outcome, average charge and average LOS were calculated using subgroups including: aneurysmal clipping or endovascular coiling (n=5,925), aneurysmal clipping or coiling with external ventricular drain (EVD) (n=4,660), use of EVD only (n=2,355), other surgical procedures (n=880) and medically managed (n=1,545). Analyses were survey-weighted and adjusted for patient and hospital characteristics.

In 2013, aSAH resulted in an average per patient hospital charge of $308,139, an average LOS of 17 days, an average mortality of 20% and total, annual hospital charges of $4.7 billion. The highest average charge per patient ($417,042) and hospital LOS (22 days) were attributed to clipped or coiled patients with EVD, and highest mortality (47%) found in medically managed patients.

These data support the conclusion that aSAH is a high cost illness managed in U.S. hospitals, and help raise awareness to the potential economic benefits resulting from developing safer, more effective therapies. Additional analyses with updated datasets including lifetime burden of aSAH (e.g. physician fees, long term medical and care costs, hospital re-admission impact, quality of life, productivity loss, caregiver burden) should be explored to understand the full economic burden of aSAH and the potential cost effectiveness of new therapies.

External ventricular drain (EVD) placement is a mainstay of treatment for patients with aneurysmal subarachnoid hemorrhage with hydrocephalus or elevated intracranial pressures, but the optimal strategy for EVD management is still unclear. The goal of this study was to compare the impact of EVD clamping at three different levels on the duration of drain placement and the intensive care unit (ICU) length of stay.

We performed a retrospective analysis of patients admitted with aneurysmal subarachnoid hemorrhage to the neurological ICU from December 2015 to January 2017 and included all patients who had an EVD placed. Patients who died were excluded from the study. Patients were divided into three groups: patients whose EVD was clamped at 10 mmHg, patients whose EVD was clamped at 15 mmHg, and patients whose EVD was clamped at 20 mmHg. Duration of drain placement in days and ICU length of stay in days was compared among the 3 groups using an analysis of variance (ANOVA). Outcomes were adjusted for presenting Hunt-Hess score, modified Fisher grade, gender, and age.

There were 10 patients who had their EVD clamped at 10 mmHg, 23 who had their EVD clamped at 15 mmHg, and 25 who had their EVD clamped at 20 mmHg. There was no difference in duration of EVD placement among the three groups (adjusted p-value 0.36, unadjusted p-value 0.6) nor in ICU length of stay (adjusted p-value 0.18, unadjusted p-value 0.43).

EVD clamping at three different levels did not affect drain duration nor length of stay in ICU. This study was limited by the small number of patients enrolled. Further studies are need to clarify optimal strategies for EVD management in the ICU.

Headache is a presenting complaint in majority of patients with aSAH and is known to persist long after initial ICU care. Various medications have been used for control of headache with major emphasis on opiate use. History of a prescription for an opioid pain medication increases the risk for overdose and opioid use disorder. We looked at prevalence of opiate use at discharge and its associated factors.

Chart review of all patients admitted in a tertiary care center between Jan 2014 and March 2016 was carried out. Along with baseline demographic data, information about use of pain scores, CSF diversion, use of opiates, average morphine equivalent doses, use of opiates at discharge and destination at discharge was collected. Analysis was carried out using Microsoft Excel. The study was approved by hospital IRB.

52 patients were admitted with aSAH in above period (70% female, Average Age: 57 yrs). 45 (62% home, 25% SNF) survived to discharge. Among survivors, 40% required CSF diversion for hydrocephalus. All people complained of pain on presentation and were prescribed opiates during hospital stay. Average oral morphine equivalent doses used was 86 mg per day. 25 (56%) patients were prescribed opiates on discharge. Alternative regimens included (2 patients: tricyclic antidepressant (TCA), 2 opiate + TCA, 1 acetaminophen, 1 dexamethasone, TCA and opiates). Most common prescribed form of opiate was oxycodone. There was no significant association between opiate use/morphine dosing and age, gender, final disposition and CSF diversion,

Opiate prescription at discharge is common in patients with aSAH. No clinical characteristic seem to predict analgesic need at discharge. Little data exists about better alternatives leading to variety of treatment approaches. Further controlled trials are needed to decrease opiate use and prevent adverse effects

Delayed Cerebral Ischemia (DCI) in SAH has been associated with vasospasm-dependent and vasospasmindependent phenomena. For more than 40 years isolated hemostasis disorders have been reported in these patients. The objective of this systematic review is to describe the natural history of hemostasis in SAH.

We systematically reviewed the Medline, EMBASE, Cochrane and Lilacs databases using controlled language and the PRISMA statement and included studies on spontaneous SAH analyzing any hemostasis parameter. We screened 1794 titles, of which 57 observational were included. Evidence was evaluated following the STROBE Statement. No meta-analysis was attempted because of the methodological nature and heterogeneity of the studies.

Hemostasis is profoundly altered during the first hours after bleeding, with several alterations noted including a hypercoagulable state concomitant with increased fibrinolysis activation and reduced clot stability. Direct and indirect coagulation markers show a trend towards normalization of hemostasis in the first 2 to 3 days. Platelet count decreases with a nadir 4 to 6 days after bleeding and a recovery in the following weeks. A later nadir is associated with DCI. Platelet aggregability is consistently decreased in the first few days, regaining its normal function around the second week after bleeding. In addition, the persistence of these alterations or the presence of a second peak in pro-coagulatory activity is associated consistently with DCI and worse functional outcomes.

The hyperacute phase of SAH is characterized by a profound activation in hemostasis with reduced clot stability, probably due to an increase in the fibrinolytic pathways. On the second day post-bleeding, a slow trend towards normalization takes place, except in patients evolving towards DCI. Further research on the pharmacologic manipulation of hemostasis in SAH might be warranted to decrease DCI and improve outcomes in this population.

Hypertonic saline(HTS) is a treatment for SAH-related cerebral edema, administered to improve cerebral perfusion and reduce brain injury. HTS a supra-physiological chloride concentration that can contribute to acute kidney injury which can lead to a poor outcome. In a previously published single-center cohort of 1,267l SAH patients, 16.7% developed acute kidney injury (AKI). Hyperchloremia, but not hypernatremia, was correlated with an increased risk to develop AKI (O.R. 7.39 ). AKI was correlated with increased mortality.

A secondary analysis of the aforementioned SAH patient cohort (2009) (2010) (2011) (2012) (2013) (2014) , was analyzed. Trends of acute kidney injury were evaluated in relation to the burden of exposure to intravenous chloride, as well as serum levels of sodium and chloride.

The proportion of patients developing AKI with a maximal serum chloride concentration of 108 (p 109, will be randomized into one of two treatment groups: standard hypertonic saline solution (NaCl 23.4%) versus a solution of NaCl/Na-Acetate. We hypothesize that by reducing the IV chloride burden(baseline compared to post randomization exposure), the delta serum chloride level will decrease, and will subsequently reduce AKI occurrence (ACETATE trial, clinicaltrials.gov NCT03204955).

AKI is common in SAH patient population, and associated with worse outcomes. Serum chloride concentrations are a significant risk factor for the development of AKI. A prospective randomized clinical trial now underway examining the relationship between the hypertonic solution composition and serum chloride concentration, and to the development of acute kidney injury in aneurysmal SAH.

Spontaneous spinal subarachnoid hemorrhage (SSAH) is a rare but serious condition that can lead to a variety of medical complications. Literature to this point primarily includes isolated case reports, and none have looked at hyponatremia as a complication.

Patients were identified from the electronic medical record database at the Mayo Clinic in Rochester, Minnesota. The Advanced Cohort Explorer tool was used, searching from January 2000 to December 2015. Inclusion criteria were spinal subarachnoid blood products due to hemorrhage into the spinal subarachnoid space not due to (1) redistribution of blood from intracranial subarachnoid hemorrhage, (2) trauma, (3) medical procedures, or 4) predominant hematomyelia who experienced symptoms and received treatment at our facility.

Eight patients (median age 70 years, range 51-87) were identified as meeting the study criteria. Five of these eight patients experienced hyponatremia during hospitalization with a median value of 125 meq/L. All of these patients were treated with free water restriction and one patient briefly received 1.5% sodium chloride solution; in all cases the hyponatremia improved after free water restriction.

In all cases the hyponatremia improved with fluid restriction, and there was no documentation of increased urine output, suggesting that it was likely due to SIADH. Cord compression and hyponatremia were present together in two patients, and in these cases treatment of the hyponatremia was particularly useful to avoid worsening edema. To our knowledge this is the first compilation of cases of spontaneous SSAH highlighting hyponatremia as a complication.

There is significant morbidity and mortality associated with aneurysmal subarachnoid hemorrhage (SAH) and only about 20% of patients survive and resume their previous lifestyle after 3-6 months. Many randomized clinical trials (RCTs) have been conducted yet no treatment definitively improves outcome from SAH. Outcome is strongly related to baseline factors, yet imbalances are common in early trials. We developed a technique to identify promising treatments at early phase using a pooled control arm model (pPREDICTS: Kent, Shah, Mandava Neurology 2015) that compares early studies at their own baselines. We applied this method to SAH to develop a multi-dimensional model (pPREDICTS-SAH).

Models for functional outcome and mortality (dependent variables) were developed based on baseline variables (eg: WFNS grade 4-5 % and age) using methodology developed for ischemic stroke (Mandava, Kent, Stroke 2009 ). The outcome model is a 3-dimensional surface bounded on either side by +/-0.1 prediction interval surfaces. These prediction interval surfaces incorporate statistical variability to assess whether a treatment differs from expected outcome. Treatment arms from RCTs and single arm trials, of various treatments of SAH were compared against the pooled controlled arm.

The best model fit was for good outcome (modified Rankin Score 0-2 equivalents) based on % patients with WFNS 4-5 and age (R2=0.54; p<0.001). Seven trials of known negative drug tirilazad were superimposed on the model and fall within the +/-0.1 prediction interval surfaces confirming futility. Three trials were neutral and within the prediction interval surfaces while case series using implanted prolonged release nicardipine and a low dose heparin study were above the +p=0.1 surface showing promise. Models were also developed for mortality (R2=0.23, p=.02).

Outcome models based on percentage of high grade WFNS and age were successfully developed. This approach may be useful to prioritize treatments worthy of further study.

Oral nimodipine is recommended to improve outcome in treatment of aneurysmal subarachnoid hemorrhage (aSAH). FDA approved nimodipine liquid oral solution (NOS) in 2013 to reduce complications associated with administering nimodipine capsules (NC) to patients with impaired swallow. Experience with NOS at our center has been complicated by increased liquid bowel movements (LBM) prompting unnecessary testing for infectious diarrhea and exposure to invasive fecal management devices.

Study approved by local Qualtiy Improvement Review Committee. Data was collected prospectively in consecutive patients diagnosed with aSAH during intensive care unit (ICU) course. Formulations of nimodipine available were generic NC (Heritage Pharmaceutical) and NOS (Arbor Pharmaceuticals). We examined total ICU days exposed to NOS, ICU days with LBM, infectious diarrhea investigations, and fecal management device use. All statistical tests were performed using Minitab.

27 patients were studied from 3/6/2017 to 6/23/2017; 17 patients exposed to NOS for 143 ICU days, 71 ICU days with LBM, 7 infectious diarrhea investigations, and 5 required fecal management devices. 17 patients exposed to NC for 154 ICU days, 9 ICU days with LBM (all cases were also received NOS), no infectious diarrhea investigations, and no fecal management device requirements. Odds ratio for LBM with exposure to NOS was 15.9 (95% CI 7.5 to 33.5, p < 0.0001).

The high incidence of LBM with NOS resulted in more infectious diarrhea testing and fecal management device use. Uncontrolled diarrhea may increase risk for dehydration and delayed cerebral ischemia, although this is not explored in the current study. NOS can mitigate risks associated with needle aspiration of NC, however these issues coupled with higher cost may limit benefit of its use. Possible solutions may include compounding NC into a liquid formulation by pharmacists or pharmacy technicians. Possible safety and cost benefits require further investigation.

Headache (HA) management after subarachnoid hemorrhage (SAH) is challenging and lacks standardization. We hypothesized that inadequate inpatient HA pain management leads to the development of chronic HA (cHA) after SAH.

Prospective, observational study of non-traumatic Hunt and Hess (HH) grades I-III SAH patients admitted from 2/2014 to 12/2014. After informed consent we recorded demographics, clinical and radiographic features, analgesic and steroid doses, hospital course and inpatient pain scores using Numeric Rating Scale (NRS, 0-10) before (NRS-pre) and after each analgesic administration over post-bleed days 0-14. A phone survey administered 12-24 months after admission evaluated cHA burden. Inpatient HA control effectiveness was evaluated by percent pain resolution from initial pain score, using NRS-pre. The percentage of administrations yielding full pain resolution was compared between those with and without cHA. Chi-square and t-tests were used for statistical analyses.

29 patients, 69% female, mean age 54.8 ±11.4 years with HH grade I (6/29), II (16/29), and III (7/29) SAH were enrolled with 7 lost to follow-up. At follow-up, 27.3% patients (6/22) reported daily HA, 13.6% (3/22) occasional HA, and 59% (13/22) no HA. Full pain resolution after analgesic administration was associated with less cHA (57 [17.4%] vs. 80 [24.3%], p=0.029). Mean daily inpatient opioid dose (morphine equivalents) for patients with and without cHA was 14.9 mg and 8.9 mg, respectively (p=0.28). Mean NRS-pre were 4.94 vs 4.12 for patients with vs without cHA, respectively (p=0.05).

Inpatient analgesia for SAH-related HA is inadequate and may be associated with the development of chronic HA. Patients with cHA had higher mean inpatient pain score and fewer analgesic administrations resulting in complete pain resolution. Inpatient opioid dose per day was higher in cHA group, although not statistically significant. Additional research is needed to characterize the relationship between inpatient headache management and chronic headache after SAH.

Subarachnoid hemorrhage (SAH) remains a significant cause of neurological morbidity and mortality with few interventions to prevent delayed cerebral ischemia. Hypocapnia has been associated with worse outcomes in brain injury. SAH patients may be particularly susceptible to hypocapnia induced vasoconstriction. This study aims to describe the incidence of iatrogenic and spontaneous hyperventilation in SAH patients.

A descriptive analysis was performed on a retrospective cohort of adult SAH patients admitted to Beth Israel Deaconess Medical Center ICUs between 2008 and 2015 with GCS <9 who were treated with mechanical ventilation and an extraventricular drain, and had at least one ABG. Patients on chronic ventilator support were excluded. The lowest PaCO2 per ICU day was analyzed.

125 patients were included with 959 days with at least one documented PaCO2. Mean GCS on admission was 5.0 (SD 1.7). 70.3% of patients survived to hospital discharge. 61.6% of patients were exposed to severe hypocapnia (PaCO2 30mmHg, those with severe hypocapnia had similar PaO2 and PaO2/FiO2 ratios, but mildly increased leukocytosis (13.1 vs 12.3). 40.9% of PaCO2s <30mmHg occurred during spontaneous ventilation or over-breathing.

Prior studies have shown that hypocapnia causes decreased brain tissue perfusion and is associated with worse outcomes in SAH patients. These recent data demonstrate that severe hypocapnia is common in patients with SAH severe enough to warrant intubation, and is associated with both iatrogenic and spontaneous hyperventilation. Hypocapnia is not primarily compensatory or hypoxia driven, as suggested by mean pH and PaO2. Confirmation of this association and potential future interventions require further study.

Although delirium is associated with higher rates of hospital complications among critical care patients, limited data exist on risk factors for delirium in aneurysmal subarachnoid hemorrhage (SAH). A previous study identified older age, high Hunt Hess grade, intraventricular hemorrhage (IVH), and hydrocephalus as risk factors for delirium. We sought to identify risk factors for delirium during admission after SAH.

Retrospective review was performed of prospectively collected data for consecutive SAH patients enrolled into the University of Maryland Recovery After Cerebral Hemorrhage (REACH) Study. Baseline data and clinical complications during each admission, including delirium, were recorded. Statistical analysis was performed using univariate and multivariate logistical regression.

103 SAH patients from July 2014 to January 2016 were reviewed. While age was not singly associated with delirium during ICU admission, higher Hunt Hess grade, IVH, hydrocephalus, hospital-acquired infection, elevated troponin, and intubation were significantly associated with delirium on univariate analyses. Upon stepwise multivariate logistic regression, IVH (OR 9.6, p=0.04) and intubation (OR 6.4, p=0.01) remained significantly associated with delirium.

IVH and intubation predicts delirium during ICU admission for SAH. Further analyses are needed to determine if the relationship between IVH and delirium is primarily explained by risk of hydrocephalus, risk of fever, medication exposure, or through independent mechanisms.

Stroke triage scales are very important in order to expedite acute evaluation, assure quick door to neuroimaging time and decrease door to needle time in patients with ischemic stroke eligible to intravenous thrombolysis. Subarachnoid hemorrhage (SAH) is associated with a high mortality in the acute phase due to a particular risk of early and devastating re-bleeding. Therefore patients with SAH also need urgent assessment. The performance of classic triage stroke scales in the identification of patients with SAH was not previously evaluated. The objective of our work was to evaluate the performance of the Los Angeles Prehospital Stroke Screen (LAPSS) in identifying patients with SAH admitted to a tertiary hospital.

We evaluated consecutive patients admitted to a tertiary hospital with SAH from January 2009 to May 2016. At hospital admission, LAPSS was applied by trained nurse personnel to all noncomatose patients with complaints suggestive of neurological disease.

A total of 139 with SAH patients were evaluated (mean age 55.9 +/-15.6), 59.7% females). LAPSS was applied to 94 patients. LAPSS was positive in only 45 patients (32.4%). Patients with a positive LAPSS had higher NIHSS stroke score at admission ( 4, [2,23] versus 0, p<0.01), lower Glasgow coma Scores (14 [8, 15] versus 15, p<0.01) and a significant shorter door to neuroimaging time (p<0.01).

In patients with SAH and mild symptoms, LAPSS was not a sensitive screening tool in our series. Hospital and pre hospital services using LAPSS for triage of patients with stroke should be aware of this limitation and include in triage flowcharts specific questions evaluating SAH specific symptoms.

Spontaneous subarachnoid hemorrhage (SAH) is a neurological emergency, which despite current advances in management strategies and advent of institutional protocols, remains with significant rates of mortality due to poorly understood causes. Our objectives were to characterize in-hospital mortality by evaluating the primary cause of death and externally validate the HAIR score, a clinical score that prognosticates mortality.

In this retrospective cohort study, we reviewed all SAH patients admitted to our Neuro-ICU between April 1, 2010 and March 31, 2016. Univariate and multivariate logistic regressions were performed to identify predictors of in-hospital mortality, our primary outcome. To validate the HAIR score, the model's predictors were Hunt and Hess score at treatment decision, age, intraventricular hemorrhage, and re-bleeding within 24 hours. Discrimination was assessed by visualizing the receiver-operating curve and calculating the area under the curve (AUC).

Among 434 SAH patients with a median age of 56 years (interquartile range, 48 -65), 63.6% females, inhospital mortality was 14.1% (n=61). Of those, 54 (88.5%) had a neurological cause for death or withdrawal of care and 7 (11.5%) had a cardiac death. Median time from SAH to death was 6 days. The main causes of death were the primary effects of the initial hemorrhage, re-bleeding and refractory edema. Factors significantly associated with in-hospital mortality in the multivariate analysis were age, Hunt and Hess score, and intra-cerebral hemorrhage. Maximum lumen size was also a significant risk factor among aneurysmal SAH patients. The HAIR score had a satisfactory discriminative ability, with an AUC of 0.89.

Our in-hospital mortality is lower than previous reports, attesting to the continuing improvement of our protocolized subarachnoid hemorrhage care. The major causes are the same as previous reports. The HAIR score showed good discrimination and could be a useful tool for predicting mortality.

So far, scientific and therapeutic efforts mainly focused on the prevention of rebleeding and ischemic complications(DCI) in patients with subarachnoid hemorrhage(SAH). However, data regarding the impact of parenchymatous hemorrhage(PH) on longterm outcome in these patients is limited.

All consecutive patients with atraumatic SAH admitted to our hospital over a 5-year-period(2008-2012) were retrospectively analyzed. Extent of SAH as well as presence, localization and volume of PH were evaluated. Functional and health outcome were assessed after 12 months using the modified Rankin scale (unfavorable:3-6) and the EQ-5D. Propensity-score(PS)-matching was performed to minimize potential bias due to confounding variables between SAH-patients with and without PH.

Of overall 494 patients with atraumatic SAH, 85(17.2%) patients had PH on initial imaging. PH-patients had a worse clinical condition on admission (WFNS: PH 4(3-5) vs. ØPH 2(1-4);p<0.001) and a greater extent of SAH (modified Fisher: PH 3(2-4) vs. ØPH 2(1-3);p=0.001). Median PH-volume was 11.0(5.4-31.8)ml with largest volumes in patients with ruptured )ml). After successful PS-matching (parameters: age, WFNS, modified Fisher and Graeb score) patients with PH had worse functional and health outcome after 12 months compared to those without PH (mRS 3-6: PH 56/82(68.3%) vs. ØPH 33/78(42.3%);p=0.001; EQ-5D: PH 50(30-70) vs. ØPH 80(65-95); p<0.001). In multivariate analysis presence of PH was the strongest independent predictor of unfavorable outcome after 12 months followed by the occurrence of DCI (risk-ratio(95%CI): PH 4.5(2.0-10.0); p<0.001).

Parenchymatous hemorrhage is frequent and associated with functional and subjective impairments in patients with atraumatic SAH.

Aneurysmal subarachnoid hemorrhage (aSAH) is associated with early and delayed brain injury. Insulin growth factor (IGF1) is a potent cellular growth-promoting factor with demonstrated independent neuroprotective actions in stroke and neurologic disease but has not been well characterized after aSAH. This study sought to examine the relationship between plasma IGF1 levels and outcomes after aSAH.

This cohort of 128 aSAH patients was 50.6 years (SD 10.03) and female (66%) with a mean HH 3 (45%), WFNS 1 (41%) and Fisher 3 (48%). Initial and peak plasma IGF1 concentrations were measured in 268 plasma samples from a banked biorepository using a commercial sandwich solid-phase ELISA kit. Delayed neurological deterioration (DND) and delayed cerebral ischemia (DCI) were determined using radiologic and clinical information. IGF1 levels were log transformed due to non-normality. ANOVA, t-Tests, Pearson correlations and logistic regression analyses were completed using SPSS and SAS.

Older age was significantly associated with lower initial and peak plasma IGF1 levels (r=.37, p<.001; r=.41, p<.001). Men had higher initial and peak plasma IGF1 levels than women (p<.01; p=.002), and premenopausal women had higher initial and peak plasma IGF1 levels than post-menopausal women (p=.003; p=.004). Lower peak plasma IGF1 levels were associated with increased clinical severity by WFNS (p=.02) and Fisher grade (p=.03) as well as the development of DND (p=.04; p=.003). Lower peak IGF1 levels were associated with the presence of DCI (p=.009). Controlling for age and Fisher grade, log peak plasma IGF1 levels remained significantly associated with the presence of DND (p=.01; OR 0.27; CI: 0.1-.74) and DCI (p=.007; OR 0.29; CI: 0.12-0.7).

IGF1 levels have not been well characterized after aSAH. These results suggest lower plasma IGF1 are associated with clinical severity and outcomes after aSAH and provide impetus for future work to further examine these relationships.

Induced hypertension (IH) is the mainstay of medical management for delayed cerebral ischemia (DCI) after subarachnoid hemorrhage. However, using vasopressors to raise systemic blood pressure well above normal levels may be associated with systemic and neurological complications, of which posterior reversible encephalopathy syndrome (PRES) has been increasingly recognized. However, the frequency and risk factors for IH-induced PRES have never been systemically evaluated

We identified 68 patients treated with IH from 345 SAH patients admitted over a three-year period. PRES was diagnosed based on clinical suspicion (i.e. unexplained deterioration), confirmed by imaging. We conducted retrospective extraction of data on IH therapy, including baseline and highest target mean arterial pressure (MAP) and vasopressor dose/duration. We compared those with PRES to IHtreated controls and also described the clinical features and sequelae of all PRES cases.

Five SAH patients were diagnosed with PRES, with median time from initiation of vasopressors to diagnosis of 6.6 days (range 1-8 days). Baseline MAP did not differ between PRES and IH controls, but highest target MAP was greater (140 vs. 120 mm Hg, p=0.006). Magnitude of IH was similarly greater (54 vs. 34 mm Hg above baseline, p=0.004). All cases presented with lethargy, three had new focal deficits, and one had a seizure. One died from cardiac complications but the other four patients had complete resolution with IH discontinuation, without infarction or residual disability.

PRES was diagnosed in 7% of patients undergoing IH therapy and was most likely when MAP was raised well above baseline to levels exceeding the traditional limits of autoregulation (130-140 mm Hg). High clinical suspicion for this reversible disorder appears warranted when aggressive IH targets are maintained for several days or in the presence of unexplained neurological deterioration. Other interventions may be preferable for refractory DCI when moderate degrees of IH have been attempted.

Patients with aneurysmal subarachnoid hemorrhage (aSAH) may receive significant exposure to potentially harmful ionizing radiation exposure (PHIRE) from diagnostic tests and therapeutic procedures during their initial hospitalization. We hypothesized that risk factors to detect excessive PHIRE are present at the time of admission.

Following IRB approval, all patients admitted to our institution with documented aSAH over a 4-year period were retrospectively evaluated for inclusion and exclusion criteria. Patients were excluded if they died prior to discharge. All study data, including SAH-specific and patient-specific risk factors, were obtained from the electronic medical record. The total effective dose of ionizing radiation (TEDIR) per patient was calculated from previously published radiation exposure data. PHIRE was considered to have occurred if TEDIR was greater than 50 mSV, the annual PHIRE limit for radiation workers. Logistic regression models were then fit to the dataset to evaluate clinical variables that significantly the risk of PHIRE in these patients.

Data were collected from 108 patients (58.4% of all aSAH patients evaluated). The mean TEDIR in these patients was 47.8 mSv. Forty-two (38.9%) of patients met criteria for PHIRE. In multivariate logistic regression modeling, male gender (OR=3.2, CI=1.1-11.8), posterior circulation aneurysms (OR=3.7, CI=1.2-11.5) and ventriculostomy (OR=24.8, CI=3.7-164.7) were significantly associated with an increased risk of PHIRE.

In this study, approximately 40% of aSAH patients received PHIRE. Male gender, posterior circulation aneurysms and ventriculostomy were significantly associated with increased risk of PHIRE. These factors may serve as important predictors of patients who require additional or complex care necessitating repeated diagnostic or therapeutic procedures during their hospitalization. Alternative diagnostic or therapeutic modalities should be considered for patients with these risk factors to limit the risk of PHIRE. Future research should also evaluate the effect of PHIRE on neurologic outcomes in these patients.

It remains unclear whether patients with unruptured intracranial aneurysms (ICA) should be treated. Vessel wall enhancement (VWE) in high-resolution magnetic resonance vessel wall imaging constitutes a promising marker of aneurysm instability in this population. To find risk factors for aneurysm instability, we sought to identify predictors of VWE in patients with unruptured ICAs.

We conducted a retrospective analysis of prospectively collected data on patients with unruptured ICA evaluated by a single provider. All patients were evaluated using a previously validated algorithm to ascertain VWE using high-resolution magnetic resonance vessel wall imaging. Two different raters, blinded to the study data, categorized all observed aneurysms as VWE-positive or VWE-negative. Kappa statistics were used to evaluate the reproducibility of this approach. Univariable and multivariate logistic regression modelling was utilized to identify factors associated with VWE after adjusting for potential confounders.

94 patients with unruptured ICA were included in the analysis (mean age 59 [SD 14] , female sex 77 [82%]). Of these, 34 (36%) were VWE-positive and 60 (64%) were VWE-negative. Inter-rater reliability for VWE ascertainment was excellent (kappa 0.86, 95%CI 0.75, 0.97). 9 out of 10 (90%) patients presenting with cranial nerve palsy were VWE-positive. In univariable analysis, age (p=0.03), headache on presentation (p=0.004), and size (p<0.001, per additional millimeter) were associated with VWE-positive status. In multivariable analysis, headache on presentation (p=0.007) and size (p=0.003) remained independently associated with VWE.

Cranial nerve palsy is an established clinical marker of aneurysm instability; consequently, our results confirm the role of VWE as a marker of aneurysm instability. Headache on presentation and aneurysm size are independently associated with VWE; these risk factors for aneurysm instability could be used to select patients with unruptured ICAs that may benefit from vessel wall imaging.

Prognostication in subarachnoid hemorrhage (SAH) patients presenting in coma is crucial for surgical decision making. Indications for aggressive aneurysmal treatment are unlikely for those not demonstrating signs of neurological improvement chronologically or after ventricular drainage. Early neurological evaluation is, however, challenging in critically ill SAH patients requiring anesthesia and intubation for airway protection.

In this single-center retrospective study, we applied continuous amplitude-integrated EEG (aEEG) monitoring using a subhairline montage for WFNS Grade V patients who did not undergo emergency aneurysm treatment. Monitoring was initiated soon after admission to the ICU. Patterns of aEEG findings were classified according to Rundgren, et al. as follows: flat (F); suppression-burst (SB); electrographic status epilepticus (ESE); and continuous (C). Based on the aEEG findings, indications for aneurysm treatment were reevaluated. Outcome was assessed at six months using the Glasgow Outcome Scale.

Twenty-three patients, 8 men and 15 women, aged 68.3 ± 14.1 years (mean ± SD), were eligible since December 2012. All patients underwent prophylactic intravenous sedation. The population represented 28 % of all Grade V patients including those resuscitated after cardiac (n=9) or respiratory (n=2) arrest. The Glasgow Coma Scale scores were 3 (n= 21), 4 (n=1), and 5 (n=1), respectively. Aneurysms were located in the posterior fossa in 9 patients (39%). aEEG monitoring was initiated 11.8 ± 12.2 hours median 8.4, 1.03-41.7 hours after arrival. All patients showing early F (n=12) or SB patterns (n=3) died. One patient demonstrated ESE remained in a persistent vegetative state. Five out of 7 patients with a C pattern underwent aneurysm treatment; 4 clippings and 1 coil embolization. Moderate disability was attained in 3 and severe disability in 2. Two patients undergoing conservative therapy died.

Continuous aEEG provided useful prognostic information for identifying salvageable SAH patients undergoing sedation in the early phase.

Delayed cerebral ischemia (DCI) may result in focal neurological deficits and cerebral infarction after subarachnoid hemorrhage. While global cerebral blood flow (CBF) may be variably reduced, DCI is more likely related to regional impairments in CBF below critical perfusion thresholds. We applied volumetric methods to assess the proportion of brain exhibiting hypoperfusion (PBH) in those with clinical DCI and in the symptomatic hemisphere of those with focal deficits.

Methods 61 patients with aneurysmal SAH underwent 15O-PET and CT imaging during period of risk for DCI (median 8 days after SAH, IQR 7-10). We measured PBH as proportion of voxels with CBF < 25 ml/100g/min, after excluding regions of infarction/hematoma on CT. We compared PBH in patients with vs. without DCI at time of PET and, in those with focal deficits, we compared hypoperfusion between affected and unaffected hemispheres.

PBH was greater in the 23 (38%) with DCI compared to those without DCI (20%, (9) (10) (11) (12) (13) (14) (15) (16) p=0 .006) despite higher mean arterial pressure (MAP) and most being on active hemodynamic therapies. Global CBF was also lower in those with DCI (36.0 vs. 44.4 ml/100g/min, p=0.01) but did not differ between those remaining symptomatic and those whose deficits had resolved. While mean hemispheric CBF was not lower in the affected hemispheres of 13 with lateralizing deficits (40.2 vs. 41.1 ml/100g/min, p=0.15), there was greater PBH in the symptomatic hemisphere (21% vs. 18%, p=0.049).

SAH patients with DCI have a greater proportion of brain with hypoperfusion despite active hemodynamic therapy and higher MAP. There was also larger proportion of the symptomatic hemisphere with hypoperfusion despite no asymmetry of hemispheric CBF. Such measurements of hypoperfusion may better reflect the regional pathophysiology of DCI than global averaged measures of CBF. Further studies should determine whether burden of hypoperfusion correlates with tissue and patient outcomes.

Patients who survive aneurysmal subarachnoid hemorrhage (aSAH) are often burdened with lasting cognitive impairment due to a combination of sequelae including neuro-cardiac injury. The impact of neurocardiac injury after aSAH is poorly understood. This study sought to examine if neurocardiac injury detected by global longitudinal strain (GLS) is associated with poor performance in neuropsychological NP memory impairment after aSAH.

We studied 135 aSAH patients at 3 months and 112 at 12 months (SAHMII study R01NR04221) after hemorrhage. Speckle tracking GLS from 3 apical views were assessed days 0-5 from bleed from transthoracic echocardiograms. Neuropsychological (NP) outcomes covering 7 domains were completed at 3 and 12 months after hemorrhage by trained personnel. Memory tests included controlled oral word association (COWA), Wechsler memory scale (WMS) and Rey auditory (R-aud) and Complex Figure (ReyC). ANOVA and Kruskal-Wallis, Pearson and Spearman correlations and logistic regression were completed using SPSS and SAS.

There were 30 (22%) patients with abnormal GLS (defined as >-17%) and 27 (24%) in the 3 and 12 months groups respectively. GLS groups had similar age, gender and fisher grade. Abnormal GLS was associated with higher HH at 3 (p=.05) and 12 (p=.002) months. Abnormal GLS was significantly associated with decreased performance in R-aud memory domains at 3 months (p=.013) and 12 months (p=.027) after aSAH and even when controlling for age and HH at 3 months (p=.010). GLS<-17 was associated with poor memory performance 12 months after aSAH in COWA (p=.008) and the WMS (p=.02) even after adjusting for age and HH, COWA (p=.008) and WMS (.018).

Neuro-cardiac injury detected by GLS was associated with decreased performance in memory domains of NP function at 3 and 12 months after aSAH. While these relationships require further examination, neurocardiac injury may contribute to long term NP impairment after aSAH.

Delayed Cerebral infarction (DCI) is a frequent complication following high-grade aneurysmal subarachnoid hemorrhage (aSAH). Management of DCI includes maintaining hypertension, which is challenging in heavily sedate patients. Ketamine is a hemodynamically stable, analgesic sedative not studied in this population. We hypothesize that Ketamine infusion (K), as compared to traditional sedatives (control), will safely improve the hemodynamic profile in high grade ventilated aSAH patients

Retrospective review of aSAH patients admitted 1/2015 to 2/2017 requiring mechanical Delayed Cerebral infarction (DCI) is a frequent complication following high-grade aneurysmal subarachnoid hemorrhage (aSAH). Management of DCI includes maintaining hypertension, which is challenging in heavily sedate patients. Ketamine is a hemodynamically stable, analgesic sedative not studied in this population. ventilation >72 hrs, and without DNR within 48 hrs from admission. We assessed demographics, hemodynamics, pressor, DCI at 2 weeks, ventilator and ICU LOS, and mortality. Fisher Exact, Wilcoxon, and Paired T-Test applied.

Comparing K (n=16) vs control (n=19), median (Q1, Q3) results for: Age 59 (48, 67) vs 59 (48, 72); Hunt and Hess 4 (3, 5) vs. 4 (3, 4); MPM-3 30 day estimated mortality 27. 8% vs. 28.5%; and GCS 7 (6, 9) vs 7 (5, 8) . Ketamine initiated on day 4 (2, 5); ICU LOS 20 (17, 24) vs. 15 (7, 22); and Vent LOS 17 (12, 29) vs. 11 (8, 28) . Mean (SD +/-) for 8 hours before and after ketamine: MAP 93 (11) vs 99 (15), p 0.05, except where noted.

Ketamine infusion, as a second line sedative, had no effect on mortality or ICP, and improved MAP. However, there was a nonsignificant increase in DCI as well as vent LOS, without a greater rate of tracheostomy. Prospective studies are needed to study the effect on DCI and long term outcomes.

Seizures are a well-known complication of aneurysmal subarachnoid hemorrhage(aSAH) and occur most commonly in the immediate post-hemorrhagic period. Most commonly used antiepileptic drugs (AEDs) for seizure prophylaxis in aSAH include phenytoin and levetiracetam. There is no reliable data available on the safety and efficacy of restricting AED prophylaxis only till the aneurysm is secured.

We retrospectively chart reviewed patients admitted to our neurosciences intensive-care-unit with aSAH during the last two years. Seizure incidence was studied in patients treated with phenytoin versus levetiracetam and in patients treated for 3 to 7 days versus those where AED was discontinued immediately after aneurysm was secured.

In 28 patients AED prophylaxis was discontinued immediately after the aneurysm was secured, and in 21 patients it was continued for 3 to 7 days. Of th phenytoin was used in 20 patients and levetiracetam was used in 8 patients. In patients receiving AED prophylaxis for 3 to 7 days, phenytoin was used in 8 cases and levetiracetam was used in 13 cases. None of these patients had seizures reported during hospitalization or at three month follow-up.

Stopping the AED prophylaxis immediately after aneurysm coiling is not associated with increased risk of seizures. Seizures at presentation in patients with aSAH are not associated with development of epilepsy at 3 months. Both phenytoin and levetiracetam are well tolerated in patients with aSAH when limited to the immediate post-hemorrhagic period.

The main preceding factor of Delayed cerebral ischemia (DCI) in aSAH is cerebral vasospasm (CVS). Anticipating DCI can have major impact on patient outcomes. Studies have attempted to predict DCI in patients with aSAH by using various imaging modalities that measure CVS, ranging from transcranial Doppler ultrasonography, CTP, and MR perfusion. Few compare these imaging modalities to the accepted gold standard of DSA. We propose that MRI using ASL imaging can be used as a sensitive and specific measure of CVS and can be used as a marker to identify patients with aSAH who are at risk for developing DCI.

To support our hypothesis, we compare ASL results in patients with documented CVS on DSA who developed DCI. 165 patients in the academic years 2013 to 2016 with the diagnosis of aSAH were admitted to our NICU. The inclusion criteria for the patient population was the presence of aSAH confirmed by DSA, diagnosis of DCI by a neurointensivist, MRI with ASL, and a repeated DSA during the hospitalization after DCI was suspected. All patients underwent MRA with ASL on Day 8 in an attempt to capture the peak time of CVS.

Nine patients were included in this study. All cases with perfusion defects on ASL sequences had confirmed CVS on DSA except for one. The outlier in our cohort developed DCI with asymmetry on ASL that was not demonstrated on DSA.

To our knowledge, no studies have compared the specificity of ASL with DSA in detecting CVS. This study highlights the utility of ASL in detecting CVS in patients with aSAH. Our limited data suggests ASL can be utilized for detection of DCI and CVS with greater confidence than the conventional modalities. We also suggest that ASL approaches the utility of DSA in the detection of CVS.

Blood glucose dysregulation following aneurysmal subarachnoid hemorrhage is associated with serious complications and poor clinical outcome. An influence of hyperglycemia on the occurrence of delayed cerebral ischemia (DCI) is assumed, nevertheless the exact mechanism remains unclear. The goal of the present study aims to investigate the influence of systemic blood glucose level on cerebral perfusion measured by dynamic perfusion computed tomography (PCT) and outcome.

Daily serial blood glucose levels and PCT data sets of 206 patients treated at our neurointensive care unit after aSAH were retrospectively analyzed. Serial PCTs were performed between six hours and 21 days after aneurysm repair. Mean average of mean transit times (MTTs) was calculated for each perfusion scan. The maximum mean transit time (maxMTT) and outcome assessed with Glasgow Outcome Scale were correlated with defined blood glucose ranges as followed 1.) >180mg/dl (hyperglycemia) 2.) 140-180mg/dl (elevated glucose level) 3.) 110-140mg/dl (strict glucose control) and <110mg/dl (low glucose level).

Hyperglycemia (>180 mg/dl) was associated with prolonged maxMTT (p< .05, rs = .13) and was linked to an increased risk of infarction (p < .001) whereas strict glucose control (110-140 mg/dl) correlated significantly negative with maxMTT (p < .05, rs = -.17). Strict glucose control was also associated with a lower occurrence of cerebral infarction and good outcome (p < .001, rs = .47). In contrast, elevated blood glucose levels (140-180 mg/dl) and hyperglycemia showed a negative correlation with good outcome (p < .001, rs = -.26, rs = -.35).

The present analysis supports for the first time the assumption that dysregulation of blood glucose balance influences cerebral perfusion and thus may contribute to the occurrence of DCI and poor outcome. Therefore careful monitoring and prompt treatment of blood glucose levels after aSAH should be highly valued to avoid cerebral perfusion deficits correlated with poor outcome.

The aim of this study was to determine the correlation between Transcranial Doppler (TCD) velocities and angiographic vasospasm after Subarachnoid hemorrhage (SAH).

Methods 221 patients with SAH were evaluated with Spencer Technologies TCD Power M Mode from 2-14 days, following the SAH. Both the Temporal windows were insonnated to determine flow velocities in the middle (MCA) and anterior cerebral arteries (ACA) and the suboccipital widow was used to determine flow velocities in the vertebral (VA) and Basilar arteries (BA). The middle cerebral artery/ipsilateral extracranial internal carotid artery velocity ratio (Lindegaard ratio) was also correlated with vasospasm CT Angiography and conventional cerebral angiography was used to confirm TCD findings suggestive of Vasospasm. The sensitivity, specificity, likelihood ratios for positive and negative TCD results, positive

There was 131 males and 90 females and with mean age 42.72+-7.6 years. 88 % were Aneurysmal SAH. Delayed ischemic neurological deficits (DIND) developed in 48/221 patients (21.70 %). Interobserver ue of cm/s were useful (likelihood ratio for negative result = 0.15, likelihood ratio for positive result = 14.89). Lindegaard ratios correlated well with Vasospasm. TCD diagnosis of Vasospasm was more often present in the MCA, followed by ACA and Basilar arteries.

TCD is a good non invasive method to detect Vasospasm and predict the occurrence of DIND. Very high angiographic vasospasm. TCD is also useful to follow up patients with angiographically proved Vasospasm.

Aneurysmal Subarachnoid Hemorrhage (aSAH) is a significant cause of morbidity and mortality. The mortality rate approaches 50%. Nearly half of the survivors remain unable to care for themselves . DCI occurs in 29% of these patients . When present, it doubles the risk of poor outcome. -Several methods have been used to treat cerebral vasospasm and DCI, which is a major cause of morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (SAH). Milrinone safe and, potentially, effective treatment of DCI as reported in low level of evidence literature . However, the efficacy not compared in a randomized way to placebo. We will examine the effectiveness and safety of intra-venous injection of milrinone for the treatment of DCI following aneurysmal sub-arachnoid haemorrhage. Our intension is to study the outcome of using milrinone as an addition to current therapies such as hypertensive therapy are not effective enough, yet can not be replaced as it is Standard of care. As intravenous milrinone was not yet shown to have an affect in DCI in a randomized controlled trial. This pilot trial is a step towards that study.

The study is a pilot trial of a randomized placebo-controlled double blind trial testing the potential beneficial effect of Milrinone, a phosphodiesterase inhibitor, on clinical neurological outcome in patients with DCI after aneurysmal subarachnoid hemorrhage. The study drug will be given along with the standard therapy when DCI occurs.

The administration of milrinone increases cerebral blood flow most likely as a result Of cerebral vasodilation. As intravenous milrinone was not yet shown to have an affect in DCI in a randomized controlled trial. This pilot trial is a step towards that study.

Milirinone promising treatment for delayed cerebral ischemia following aneurysmal sub-arachnoid haemorrhage .particulary by using standardized protocol as a finding suggestive of good prognosis

Fever in the neurocritical care population is very common and is strongly associated with increased mortality and poor outcome. Fever is aggressively treated in the ICU due to its deleterious effects. Yet despite best efforts with standard antipyretic agents and even with aggressive cooling measures with endovascular cooling catheters some patients may still have refractory fevers. Celecoxib, a cyclooxygenase-2 (COX-2) inhibitor, has been used as an adjunctive antipyretic agent. This is a retrospective analysis to evaluate the effectiveness of celecoxib in lowering temperatures in patients with refractory fevers.

This is a retrospective chart review of patients admitted to a neurointensive care unit at a single institution with fevers (>38.3C) that do not respond to convention treatment with acetaminophen, endovascular cooling catheters and ibuprofen. 83 patients with severe traumatic brain injury, subarachnoid hemorrhages and intracerebral hemorrhages were included. Patient temperature recordings were obtained in the period of 24 hours before and 48 hours after administration to the first dose of celecoxib. The mean temperature of the before and after periods were compared and temperature difference was calculated.

83 patient records were included. The average of the mean temperatures in the before periods and after periods were 37.79 C (+/-SEM 0.0659) and 37.37 C (+/-SEM 0.062 respectively. There was a significant difference on Mann-Whitney-Wilcoxon Rank Sum test (p<0.000003). One average there was a drop of 0.41(+/-SEM 0.069) degree Celsius of the mean temperature after the start of treatment.

In neurocritically ill patients with fevers that are refractory to conventional treatments adding celecoxib, a COX-2 inhibitor seems to be effective at lowering the core body temperature. Further study is warranted to evaluate for adverse effects such as risk of cardiovascular events.

Achieving and maintaining normothermia (NT) after subarachnoid hemorrhage (SAH) or intracerebral hemorrhage (ICH) often requires temperature modulating devices (TMD). Shivering is a common adverse effect of TMD's that can lead to further costs and complications. We evaluated a new esophageal TMD, the EnsoETM (Attune Medical: Chicago, IL), to compare NT performance, shiver burden, and cost of shivering interventions with existing TMD's.

Patients with SAH or ICH and refractory fever were treated with the EnsoETM. Patient demographics, temperature data, shiver severity, and amount and costs of medication used for shiver management were prospectively collected. Control patients who received other TMDs were matched for age, gender, and body surface area (BSA) to EnsoETM recipients and similar retrospective data was collected. All patients were mechanically-ventilated. Fever burden was calculated as areas of curves of time spent above 37.5 or 38C. Demographics, temperature data, and costs of EnsoETM recipients were compared to recipients of other TMD's.

Eight EnsoETM recipients and 24 controls between October 2015 and November 2016 were analyzed. There were no differences between the two groups in demographics or patient characteristics. No difference was found in temperature at initiation (p = 0.4) and fever burden above 38°C (p = 0.47). EnsoETM recipients showed a non-significant trend in taking longer to achieve NT than other TMD's (p = 0.07). EnsoETM recipients required fewer shiver interventions than controls (p = 0.03). EnsoETM recipients incurred fewer costs than controls per day (p = 0.04).

The EnsoETM achieved and maintained NT in SAH and ICH patients and was associated with less shivering and lower pharmaceutical costs than other TMD's. Further studies in larger populations are needed to determine the EnsoETM's efficacy in comparison to other TMD's.

Targeted temperature management is an important aspect of care in neurologically impaired patients. However, achieving optimum temperature for a specific patient can be challenging; a patient's size, body composition, metabolism, and hypothalamic function contribute to his or her response to a given temperature management modality. The purpose of this study is to evaluate patient response to esophageal temperature management when continuously applied for at least 72h.

Deidentified core temperature data for 18 patients (a total of 1237 measurements) were obtained from three hospital sites where esophageal temperature management was used for at least 72h (range 72-452h). Indications for active temperature management included: cardiac arrest (7), refractory fever (4), subarachnoid hemorrhage (4), intracranial hemorrhage (2), and traumatic brain injury (1). Goal temperatures ranged from 33-38°C and initial patient temperatures ranged from 35-40°C. Deviation from goal was calculated by subtracting target temperature from actual temperature for each measurement which allowed the calculation of the mean and standard deviation for each time point across all temperature management protocols.

Across 129 time points, representing an average treatment time of 137.7h, 95.3% of mean deviations from goal were within ±1°C and 68.5% were within ±0.5°C. In interpreting these results, several limitations must be considered. This dataset reflects a wide range of temperature management protocols and clinical scenarios. For example, a larger than average deviation in measurements recorded in the 24-36h period was related to rewarming in cardiac arrest patients who rewarmed slowly. Also, the later time points were dominated by SAH, ICH, and refractory fever patients who often experience more pronounced fever spikes.

This analysis indicates that esophageal temperature management is a feasible option for patients who require active temperature management for 72 or more hours.

The role of therapeutic temperature management (TTM) in neurocritical care is uncertain. One question that has been inadequately addressed is the diversity of practice across multiple neurocritical care units (NCCU) throughout the world. A barrier to understanding this practice variance is a data collection method that would provide adequate understanding of how TTM is implemented in various NCCUs. The purpose of this pilot study is to test the efficacy of a data collection method that would provide unitlevel data on TTM practice.

The design of this study was prospective, observational, and cross-sectional study using quality assurance methodology. The study received Institutional Review Board approval. To reduce the risk of loss of confidentiality and promote privacy, individual patients were not consented. Data on temperature management was collected each day for 90 consecutive days.

Completed data was available for 90 days. Mean daily census of 15 patients included the following mean number of patients with SAH (2), ICH (1), ischemic stroke (2) and other (9). Of those, TTM was provided to at least one patient during 40 of 90 days (44.4%). The most common TTM method (Tylenol) was used on 112 patient days; surface cooling was used on 53 patient days. TTM was initiated for fever management (109 patient days) and normothermia (11 patient days). The most common associated complication was hypocalcemia (19) and hypokalemia (5).

The data collection form was easily and quickly filled completed on a daily basis, but provides limited data. Although the form captured a significant number of events surrounding the use of TTM, the primary limitation noted is the inability to link specific events (e.g., hypokalemia) to specific patients or diagnoses. This pilot study demonstrates the efficacy of data capture and provides insight towards refining a prospective observational study to describe TTM practice.

Brainstem tumors are exceedingly dangerous due to its proximity to the structures responsible for basic human survival in the neurocritical care setting. These lesions may cause autonomic dysregulation. We report on a rare case of a female with a past surgical history of ventriculoperitoneal shunt with a brainstem mass of Müllerian type epithelial tissue.

Methods 38 year old Caucasian female presented to our hospital status-post fall after episodes of lightheadedness, as well as, episodes of decreased respirations in her sleep. MRI showed a medullary contrast enhancing mass with calcifications measuring 2.8 x 2.7 x 1.5 cm and a small calcified lesion in the right lateral ventricle. Suboccipital craniectomy for biopsy and decompression was performed.

Intraoperatively, the heart rate and blood pressure dropped transiently due to the mass being firmly adhered with calcification to the medulla. The neuropathologist diagnosed the tissue as Mullerian Type Epithelium with estrogen receptors. Post-operatively, our patient encountered several instances of cardiac pauses on monitoring that required the need for cardiology to place a permanent pacemaker.

The above is a rare case of a calcified heterogeneously contrast enhancing brainstem mass that underwent neurosurgical biopsy. Histopathology results indicated Müllerian type epithelial tissue which is tissue that gives rise to female reproductive organs. The origin of a brainstem lesion from an embryologically gynecological site could be speculated to have traveled retrograde via the ventriculoperitoneal shunt catheter. Patient required postoperative cardiac management and intervention with a pacemaker for encroachment or mechanical conflict of the mass onto the rostral ventrolateral medulla. Oncology recommended PET CT scan and further consideration for tamoxifen chemotherapeutic regimen. This case is a reaffirmation of the importance of brain tumor location and tissue diagnosis for the purpose of adjuvant treatment of neurosurgical lesions in the neurocritical care setting.

Tranexamic acid (TXA) has been used off label in cardiovascular and orthopedic surgery, as well as in trauma resuscitation. The use of TXA has increased since the publication of CRASH-2 (2010) and

MATTERs (2012), demonstrating its efficacy in trauma patients to reduce bleeding. There remains concern about the thrombotic risk as well the reduction in the seizure threshold after TXA administration.

Case Description: We present a case of a 25-year-old female admitted to the surgical ICU after a motor vehicle accident with multiple traumatic pelvic and extremity fractures and soft tissue injury. She subsequently developed extensive arterial and venous thromboses with bilateral acute ischemic strokes with superimposed posterior reversible encephalopathy syndrome after TXA administration. A second case involved a 50-year-old female who had a fall from standing and given TXA in the field by EMS. Shewas admitted to the neurocritical care unit with status epilepticus and suffered a complicated course with cardiogenic shock due to stress induced cardiomyopathy.

Discussion: The risk-benefit balance of TXA administration is generally considered acceptable in severe bleeding. The cases presented here suggest the neurological risks of TXA administration may be poorly understood and demonstrate the need for better patient selection and heightened awareness for early identification and management of complications given the possible severity of neurologic sequelae.

Conclusion: TXA is an anti-plasmin drug that is increasingly used in the areas of trauma and postoperative bleeding. We aim to educate clinicians in the potential neurological complications that can arise with its use.

Cryptococcus Neoformans is normally an opportunistic infection known to cause meningoencephalitis and can present with stroke like symptoms. In imaging, CNS vasculitis can be identified, which can lead to cerebral infarcts. When involved, these cerebral vessels are small sized leading to lacunar infarcts. We present a case that involved a large vessel territory leading to patient mortality. Initial treatment with glucocorticoids, though beneficial in other meningoencephalitidies, may actually be harmful in fungal CNS infections.

Case: A 57 year old male with a presents with 2 weeks slurred speech and worsening headache. An enhancing lesion on brain MRI in left temporal lobe was concerning for vasculitis. Patient was treated with glucocorticoids, with a negative rheumatologic workup and discharged home. Patient subsequently presented 2 days later with worsening symptoms, with CT imaging showing completed infarcts. Blood cultures were positive for Cryptococcus Neoformans; patient died due to diffuse right MCA territory edema and brain herniation syndrome.

Discussion: It is important to consider CNS infection even in immunocompetent patients who present with any of the following: fever, nuchal rigidity, mental status change, and headache. CNS vasculitis in association with infection is caused by basilar meningeal exudates. These cause traversing vessels to become inflamed, leading to distal inflammation and subsequent thrombus and infarction. We present a right MCA territory infarct , presumed to be based on the aforementioned vasculitic process. When acute infarcts are associated with opportunistic CNS infections, they are usually not associated with large vessel infarction. We also examine the adjunctive use of glucocorticoid therapy for treatment of fungal CNS infections.

This is an infrequent case of Cryptococcus Neoformans causing a CNS infection in an HIV-seronegative patient not on chronic immunosuppressive medications. This case presents a unique complication of Cryptococcal infections, a CNS vasculitis leading to infarction in a large vessel territory.

We describe the baseline characteristics, continuous intravenous midazolam doses, seizure control, hospital course and outcomes in patients who received high dose continuous midazolam infusion for refractory status epilepticus

In this retrospective case series study, we evaluated adult patients with refractory status epilepticus treated with high continuous intravenous midazolam doses in an academic neurocritical care unit between August 2016 and June 2017.

Four patients were identified. The maximum midazolam dose for each patient was: Withdrawal seizures (occurring within 48 hours of discontinuation of continuous iv midazolam) occurred in Patient B. "Ultimate continuous iv midazolam failure" (patient requiring change to a different continuous intravenous antiepileptic drug despite maximum optimized dose) was not observed in any of the four patients. Hospital complications occurred in patient A and B due to infections. Hypotension related to continuous infusion midazolam occurred in patient A. Three out of four patients discharged alive to a skilled nursing facility; after a goals of care discussion with the family, the fourth patient had withdrawal of care due to the severity of his brain injury.

In this case series, we report the use of high dose continuous IV midazolam for treatment of refractory status epilepticus. There were no midazolam-related deaths.

Neurologic complications in Infective Endocarditis (IE) occur up to 35 % and are independent predictors of mortality. Infectious intracranial aneurysms known as "mycotic aneurysm" (MA) are rare constituting 2-5 %. Hemorrhaging rate is 50%. Mortality is 80% with rupture. Ruptured MA poses significant management conundrum due to lack of available solid prospective data guiding the order (cardiac vs neurosurgical) or timing (early vs delayed) of surgery.

A 34y/o male IV drug abuser presented with acute hypoxemic respiratory failure secondary to pneumonia and suspected meningitis. GSC 6 intubated on IV antibiotic. Hemodynamic instability prompted TEE showing Large aortic valve vegetation. Blood cultures positive MSSA fulfilled criteria for IE. Tests showed kidneys infarctions. CT brain showed R MCA territory infarct with SAH.CTA head revealed small MA along the distal R MCA M4 branch confirmed with cerebral angiogram. Acute heart failure and arrhythmia led discussion on cardiothoracic surgery for valve replacement. Due to ruptured MA, decision to secure it was made prior to cardiac surgery. After failed endovascular intervention, patient underwent surgical clipping. Post operative MRI brain showed new infarcts suggesting recurrent embolization. Due to risk of Intracranial bleeding, cardiac surgery was postponed for at least 2 weeks initially then to 6 weeks. Patient underwent AVR after completed 6 weeks of antimicrobial therapy with St Jude Mechanical Valve and discharged on anticoagulation with a Modified Rankin scale of 1.

This case reflects on how urgent surgical intervention should take place.Safety period between neurological event and cardiac surgery is largely debated because of lack of Controlled studies.

There has been no consensus on how to approach those cases as paucity of robust evidence. Given their rarity the best management modality remains unclear. This case stress the importance of multimodal therapy in achieving good outcome although the timing of surgery remains a matter of debate.

We present a patient with vertebral cerebral artery embolism (CAE) following blunt trauma.

Case Presentation: A 49 year-old male was admitted with a right vertebral artery dissection and occlusion with intraluminal air, widespread pneumocephalus, bilateral pneumothoraces, a pulmonary laceration, and multiple fractures including ribs, C3 transverse foramen (with normal alignment), and femur following a motor vehicle collision. His pupils were initially nonreactive, and he experienced one hour of witnessed generalized seizure activity on arrival despite aggressive treatment.

Management: Midazolam infusion, levetiracetam, and fosphenytoin were initiated for seizure control. Targeted temperature management to 36 Celsius was initiated on arrival out of concern for hypoxic brain injury. Computed tomography at 12 hours demonstrated resolution of vertebral and intracerebral air, diffuse edema, and diffuse loss of gray-white matter differentiation, thus a hypertonic saline infusion was initiated. The following day, an MRI demonstrated diffusion restriction in the areas adjacent to the air, including C3-4 and diffusely throughout bilateral cerebral hemispheres. Prognosis was thought to be poor. However, the following day, the patient awoke. By day four he followed commands. He was discharged to skilled nursing on day 17. At three months he had only minimal residual right hip weakness.

Discussion: There are only three case reports of CAE following blunt trauma, and only one involving the vertebral artery. Air migrates to the arterial circulation due to a positive gradient from low central venous pressure or high airway pressure. Pulmonary venous air then embolizes to cerebral vasculature. As little as 2mL of arterial air emboli can be fatal with the major cause of death being circulatory obstruction and arrest from air trapped in the right ventricular outflow tract. Conclusion: This patient developed pneumocephalus and CAE due to a pulmonary laceration. As the cerebral air reabsorbed, his seizures resolved and his exam improved.

Petrous ICA aneurysms are extremely rare1-2 and difficult to treat surgically, due to the inherent challenges of microsurgical access to the carotid canal of the petrous bone3-4. Endovascular approaches may also prove challenging, typically as the consequence of therapeutically-unamenable morphology, but occasionally due to size considerations as well.5

A 23-year-old male presented with headache and vertigo for the past 3 weeks. The patient was HIVpositive with medication noncompliance and denied any history of trauma or head injury. Head CT identified a 3.9 x 2.3 cm heterogeneous soft tissue density lesion in the right petrous bone. CT angiography revealed a 3.0 x 1.8 x 2.8 cm lobulated giant aneurysm of the right petrous ICA. MRI/MRA was performed to rule out thrombosis and showed giant partially thrombosed right petrous ICA aneurysm. The decision was made to treat using flow diversion.

The patient underwent catheter angiography, confirming a giant 3 x 3.5 cm right internal carotid artery petrous segment aneurysm. We proceeded with flow diversion pipeline endovascular device, placement of two pipeline endovascular devices (flex 5 x 30 and 5 x 25) successfully. Final angiographic runs showed significant stasis within the aneurysm and demonstrated the flow-diverter construct was well placed both proximal and distal to the aneurysm neck with no sign of endovascular leak. The patient was discharged home well.

We suggest that flow diversion is an ideal treatment for petrous ICA aneurysms, specifically un-ruptured lesions of complex morphology. Other options for treating petrous ICA aneurysms challenging, not possible, less effective, and/or carry substantial risks. Second, several of the disadvantages of PEDocclusion of side vessel branches and preclusion of future coil embolization, do not apply to the petrous segment of the ICA. Lastly, use of PED in petrous ICA aneurysms has proven effective in the vast majority of reports.

The spot sign is a focus of enhancement within the hematoma on CT angiogram (CTA) with unique characteristics. It has a spot-like appearance within the margin of a parenchymal hematoma without connection to an outside vessel. It should measure greater than 1.5 mm in diameter in at least one dimension. Its contrast density (Hounsfield units, HU) is at least double that of the background hematoma. Finally, there should be no hyperdensity at the corresponding location on non-contrast CT. It is a strong predictor of hematoma expansion and poor prognosis in intra-parenchymal hemorrhage. The pathogenesis of spot sign remains unclear. Some studies showed an association with faster rates of contrast leakage which indicates continued bleeding. A spot sign has not been reported with isolated intraventricular hemorrhage (IVH) before.

A case report of a 59-year-old man with a past medical history of hypertension who got admitted to the ER with acute encephalopathy and right-sided weakness.

Head CT-scan (HCT) revealed isolated IVH. CTA was notable for a spot sign. It measures 2.8 mm in diameter and 175 HU in density (surrounding hematoma measures 80 HU). It lies within the hematoma without connections to any adjacent vessel. A follow-up HCT after four hours showed expansion of the IVH.

Although seems uncommon, looking for a spot sign in isolated IVH can also anticipate expansion of the hemorrhage. A further study is needed to validate this observation and calculate the prevalence of the spot sign in isolated IVH.

West Nile neuroinvasive disease may present with nonspecific physical exam and imaging findings. To our knowledge, this is the first report of WNND involving the temporal lobe in adults with neuroimaging suggestive of limbic encephalitis. Our patient presented in winter and developed autonomic instability and sensory deficits, which are all rare findings in WNND.

73-year-old Texan with DM presented with acute confusion and seizure in November. Patient complained of headache, fever, diarrhea and lower extremity weakness after a fishing trip. Patient was febrile with mosquito bites on his arms. Neurological exam was significant for comatose state, absent brainstem and deep tendon reflexes, and flaccid paraparesis. He developed autonomic instability with labile blood pressures. LP revealed 13 WBC/mm3 (monocyte predominance), 23 RBC/mm3, glucose 99 mg/dL, elevated protein of 82 mg/dL, and a positive West Nile virus (WNV) IgM antibody; gram stain, HCV PCR, and the paraneoplastic and autoimmune panels were negative. EEG showed severe diffuse brain slowing. MRI brain had T2 Flair and DWI changes in right hippocampus and posterior limb of internal capsule. EMG described severe subacute sensorimotor axonal polyneuropathy without prolonged distal latencies and normal conduction velocities. He received 5 days of IVIG without improvement and was terminally extubated.

Our patient presented with both clinical entities of West Nile: WN fever and WNND (present in less than 1% of cases). Our patient had axonal polyneuropathy with paralysis which is due to inflammatory changes in the white matter tracts affecting spinal sensory pathways. Sympathetic ganglia involvement caused the autonomic instability, another very rare manifestation of WNND. November presentation was due to warmer Texas winter.

Recognize that West Nile fever and West Nile neuroinvasive disease may present together in winter.

Recognize that West Nile neuroinvasive disease can present with rare temporal lobe neuroimaging, sensory involvement, and autonomic instability.

Intracerebral hemorrhage (ICH) is a common pathology seen in the Neurocritical care setting that can be associated with significant morbidity and mortality. The use of sympathomimetic agents containing phenylpropanolamine (PPA) have been associated with ICH in the past which lead to the drugs' removal by the FDA as an over the counter medication in 2005. We report a case in which PPA was the etiology for a spontaneous ICH in a patient who was taking an appetite suppressant.

Case report and review of the literature

We report a case of a 40 year old female with no prior medical history, who presented with sudden onset left sided hemiparesis and hemianesthesia found to be due to a right striatocapsular intraparenchymal hematoma. Systolic blood pressures at presentation and throughout the hospital course were normal. Extensive work up including multiple CT scans of the head, MRI brain, CT angiography, MR angiography and Digital Subtraction Angiography were performed with no evidence of any vessel abnormality. Etiology of the ICH was attributed to the use of PPA.

In young patients with no known comorbidities, PPA use should be considered a primary etiology of ICH when no intracranial vessel abnormality can be detected.

Seizures have been known to cause sudden death, but reports in the literature of only cardiopulmonary failure in cases of sudden unexpected death in epilepsy (SUDEP). We present the case of a patient who presented post-seizure and developed sudden progressive and fatal cerebral edema within 14 hours after a second seizure.

A 22 year old female with a history of Down syndrome and epilepsy presented to the emergency department after a prolonged convulsive seizure. She received 2 doses of 2mg lorazepam and levatiracetam 6.7 mg/kg with cessation of seizure activity and return to baseline neurologic status within 5 hours of the initial event. Head CT showed lack of sulci throughout the cerebral hemispheres and basilar cistern effacement despite being at her baseline neurologic status. 8 hours after presentation the patient had another seizure, vomited, was intubated and an additional 15 mg/kg of levatiracetam given. 14 hours after presentation, the patient was admitted to the NeuroICU with absent brainstem reflexes and repeat head CT with worsened cerebral edema and tonsillar herniation. Formal brain death testing was performed approximately 24 hours after the patient's initial presentation.

Seizures are known to cause a hypermetabolic state in the brain. Uncontrolled neuronal firing leads to hyperemia, failure of Na+/K+ ATP pump, increased levels of neuronal chloride, and inability for cells to maintain homeostasis. In this case, the patient's initial head CT showed cerebral edema, likely from prolonged seizure activity. Once the second convulsive seizure occurred, a period of pre-intubation hypoxemia coupled with post-intubation hypotension allowed for progression of cerebral edema in an already compromised brain; similar to what is seen in post-cardiac arrest and traumatic brain injury. This case illustrates the importance of controlling for factors that can contribute to secondary brain injury in seizure patients.

Posterior reversible encephalopathy syndrome (PRES) is a clinico-radiographic syndrome characterized by seizure, headache, encephalopathy and neuroimaging findings of symmetric white matter edema in the posterior cerebral hemispheres. Cerebellar and brainstem involvement occurs rarely. Here, we report a patient who presented with severe PRES complicated by diffuse cerebellar edema and obstructive hydrocephalus requiring decompression with ventriculostomy placement.

This is a case report from a tertiary medical center. A 23-year-old woman with a history of migraine presented to the emergency room with 2-day history of fever, right upper quadrant abdominal pain, nausea and vomiting. On day two of hospitalization, the patient developed worsening headache, dizziness and lethargy and her blood pressure was elevated to 188/93 mmHg. CT of the brain showed cerebellar edema and bilateral occipital lobes with effacement of the fourth ventricles and associated hydrocephalus involving the lateral and third ventricle.

MRI obtained post-operatively revealed T2-weighted/FLAIR diffuse hyperintensities in the parietal, occipital lobes and cerebellum. There was no mass lesion or restricted diffusion in diffusion weighted images (DWI) suggestive of acute infarction. Cerebellar edema with compression of the fourth ventricles with hydrocephalus was slightly improved status post interval ventricular drain placement. Ventriculostomy was weaned off over the course of seven days. Follow up MRI showed improvement of the hydrocephalus with decreased in T2-weighted hyperintensities in posterior parietal and occipital lobes as well as within the cerebellum.

Severe cerebellar edema with obstructive hydrocephalus is an exceedingly rare complication of PRES; however, prompt recognition and surgical decompression in addition to usual medical management is critical to achieve a favorable outcome. While obstructive hydrocephalus may be successfully treated with medical management and blood pressure reduction, this case emphasizes that clinical evidence of brain herniation should prompt immediate consideration for emergent ventriculostomy placement or surgical decompression to redirect cerebrospinal fluid and reduce intracranial pressure.

One of the biggest uses of QEEG is the alpha delta ratio (ADR). ADR drops of 20% from baseline are associated with vasospasm (VSP/DIND). We describe a case in which subtle QEEG ADR change occurred in a poor grade SAH patient over a number of days, making it challenging to detect an acute ADR drop.

This is a case report and literature review. This study also compared hemispheric ADR values against the MCA values by TCD, DSA, CTA and clinical exam.

A 67 year old female with Hunt Hess III, WFNS IV, came in comatose with a ruptured ICA aneurysm. Over six days, she developed refractory VSP/DIND. The patient's ADR was gradually declining but their increased ICP required propofol sedation, which itself lowers ADR. Re-analysis over multiple days had to be performed, and that re-analysis showed a gradual ADR decline preceding the VSP/DIND. When looking at our cases, we found a sensitivity and specificity of (40,75%) when using the ADR nadir compared to CTA/DSA. Recent publications have shown the ADR method has less than ideal sensitivity and specificity of (65,43%).

QEEG ADR is a useful multimodal monitoring parameter in NeuroICU patients with relatively good baseline ADR. However, its ability to detect VSP and DIND in poor grade SAH patients who have ADR values that are already low (< 0.5) is challenging, particularly given the confounders in this population, such as EEG artifact which artificially raise ADR values, and sedation (e.g., propofol) which suppress ADR values. Based on this information, we would suggest neuroICU centers carefully use continuous EEG monitoring for other indications such as nonconvulsive seizures, unless they have sophisticated bedside protocols about sedation vacation (baseline daily ADR that is not) and EEG department resources (technicians who can fix EEG electrode artifacts).

Hypoxic-ischemic brain injury is a severe consequence of global cerebral hypoperfusion following cardiac arrest. Brain CT findings may include diffuse sulcal effacement, loss of cisternal spaces, poor differentiation of grey/white matter, and decreased densities in the basal ganglia and watershed territories. The connection between aggressive resuscitation, as seen with in-hospital cardiac arrest, and cerebral edema is unclear. Here we present the case of a hemodynamically unstable patient who developed transient reversible cerebral edema believed secondary to aggressive resuscitative efforts and pressor therapies.

A 55 year old female with a past medical history significant for diabetes and hypertension presented to the emergency department with headache and non-bilious vomiting. Workup revealed isolated ventricular hemorrhage secondary to a ruptured left Posterior Inferior Cerebellar Artery (PICA) aneurysm and cerebellar arteriovenous malformation, which underwent subsequent embolization. During her early hospital course she remained intubated due to pulmonary factors, but awake and alert with a non-focal neurologic examination. Her course was subsequently complicated by a severe metabolic acidosis requiring several doses of bicarbonate boluses and continuous infusion, CVVHD, intravenous crystalloids, hydrocortisone and multiple pressors to maintain stability. Over a 24 hour period she received 10 liters of volume while maintaining a mean arterial pressure above 60mm Hg and O2 saturations above 88%, without requiring CPR. Subsequent progressive encephalopathy developed, with a CT Brain revealing diffuse sulcal effacement prompting hyperosmolar therapy.

Gradually her encephalopathy began to improve, with repeat imaging showing improvement of cerebral edema and return of grey/white matter differentiation.

This case highlights a potential etiology of reversible cerebral edema that may confound early prognostication in patients with hemodynamic instability such as multi-organ failure and in-hospital cardiac arrest. Further investigations are warranted.

Langerhans cell histiocytosis (LCH) is a rare disease with an incidence of 0.2-2.0 cases per 1000,000 children under 15 years of age. Frequency in adults is unknown. The hypothalamic-pituitary manifestations of LCH (commonly diabetes insipidus) and hypernatremia are well known complications.

Here we present a case where a patient presented with poor mental status and the etiology remained unknown initially despite extensive testing.

Electronic medical record was reviewed regarding hospital course, sodium trends, and radiology images.

This patient is a 66 year old female with history of Langerhans' cell histiocytosis with biopsy-confirmed suprasellar metastases (complicated by pan-hypopituitarism) who was transferred to our institution for hypernatremia and hydrocephalus. She had undergone two cycles of chemotherapy, most recently one week prior to presentation, and five rounds of radiation completed three months earlier. Her presentation to the community hospital from a nursing facility was with unresponsiveness and she was intubated on arrival. Her sodium was 174 at that time; and had been 137 three days prior. Sodium was corrected from 174 to 139 over the course of four days with a drop from 174 to 157 within the first ten hours. Her mental status improved to the point where she was awake and following commands; however still remained intubated. When she presented to our institution her sodium was 139 and subsequently became unresponsive with a poor neurological exam limited to cranial nerve function only. She was evaluated with EEG monitoring and MRI brain; however both were unrevealing for a cause. She had an external ventricular drain placed for concern for hydrocephalus that did not change her exam. One week later repeat MRI brain revealed extrapontine myelinolysis.

This case highlights the complications associated with intracranial LCH and the need for repeat imaging in patients with rapid sodium correction to identify effects of osmotic demyelination.

Cangrelor is a rapid-acting, intravenous P2Y12 platelet receptor inhibitor with a plasma half-life of 3-6 minutes and full platelet recovery achieved within one hour after discontinuation. Because it is rapidly reversible, cangrelor is commonly used to bridge patients with recent coronary stents to CABG surgery. Oral P2Y12 inhibitors, such as clopidogrel, have a delayed onset and offset with platelet recovery occurring over 5-7 days, making their use challenging perioperatively or in the setting of an acute bleed. Safety and efficacy data of cangrelor in noncoronary stents are lacking.

We present two patients in whom cangrelor was used to maintain internal carotid artery (ICA) stent patency acutely.

Both patients presented with an ischemic stroke secondary to acute occlusions of the left ICA and left middle cerebral artery (MCA) and were taken emergently to the neurointerventional suite for carotid artery stenting (CAS) and mechanical embolectomy of the MCA clot. Heparin and eptifibatide were administered intraoperatively. Post-procedure DynaCT demonstrated intracranial hemorrhage complications. Dual antiplatelet therapy (DAPT) with clopidogrel and aspirin, typically initiated following CAS, was deferred given the difficulty of reversing their antiplatelet effect in hemorrhage expansion. Instead, cangrelor was initiated to maintain carotid stent patency at 0.75 mcg/kg/min in one patient and 0.5 mcg/kg/min in the other patient and infused for 5.5 and 25 hours, respectively. Platelet reactivity was trended with the VerifyNow® assay and used to adjust cangrelor dosing. Serial imaging was obtained to monitor hemorrhage expansion. One patient was transitioned to oral DAPT and discharged while the other patient deteriorated neurologically from malignant cerebral edema and expired.

Cangrelor may be useful following CAS complicated by intracranial hemorrhage when the need to maintain stent patency must be balanced with the risk of hemorrhage expansion. Further research is warranted to determine its safety and efficacy in noncoronary stents.

Cerebral amyloid angiopathy (CAA) although has been described in the literature, the different categories of this entity and its recognition and subsequent treatment are still elusive. It is important for neuro intensivists to recognize its variable presentation . We describe a single case report and perform a systemic review. CAA depending on pathology can be categorized as Inflammatory-CAA where perivasculitis is seen on biopsy. This causes a non-destructive perivascular inflammatory infiltration and amyloid deposition pattern. On the other hand, Amyloid beta related angitis (ABRA) results in a vasculitis and there is predominantly granulomatous angio-destructive inflammatory mediated disease affecting leptomeningeal and cortical vessels characterized by meningeal lymphocytosis and abundant amyloid-beta deposition within the vessel walls. CAA on the other hand results in no inflammation of vessels but rather just deposition of amyloid deposition in the walls of vessels.

We report a case of a 82 year old man with an extensive cardiac history, who presented with syncope. Initial computed tomography (CT) of head was negative. During admission, he acutely started having trouble answering questions including his name, and was unable to communicate his needs. Repeat CT head showed hypodensity in left frontal region which was attributed to a stroke. He than developed complex partial seizures requiring intubation and seizure management. Lumbar puncture showed mild pleocytosis. MRI brain showed edematous changes of the left subcortical and deep white matter frontal lobe region which on repeat imaging subsequently worsened. Biopsy was eventually performed which confirmed Inflammatory cerebral amyloid angiopathy. He was treated with steroids and immunosuppression with gradual improvement. 3 month follow up in clinic with continued improvement to independence.

Recognize the various subtypes of CAA in their pathology, presentation and potential treatment.

In acute emergency situations, intraosseous vascular access represents an alternative route of vascular access when peripheral vein insertion is difficult. We present the first documented case of intraosseous alteplase (tPA) administration in a patient with acute ischemic stroke symptoms.

Methods 57 year old male with past medical history of hypertension, end stage renal disease, and diabetes mellitus presented to the hospital with sudden onset expressive aphasia and right sided numbness 36 minutes prior to ED arrival. NIHSS was 3 and code stroke was activated. Patient blood pressure was 207/102. CT head did not show any acute intracranial hemorrhage. It was decided to proceed with thrombolytic therapy. One peripheral venous access was obtained through which nicardipine drip was started to lower the blood pressure however second peripheral venous access was attempted multiple times but was unable to be obtained. tPA is more effective the faster it is administrated, and there was no known contraindications to administering tPA via intraosseous access (IO).

We report the first known case of successful and safe administration of fibrinolytic therapy through the intraosseous route in a patient with acute ischemic stroke symptoms.

Intraosseous access has been considered to be more invasive than intravenous (IV) and carries theoretical risk of bleeding however we were able to demonstrate tPA administration through IO without any local or systemic complications. The bioavailability of alteplase through IO access has not been studied however it is considered to be close to IV infusion in case of morphine and vasopressors.

No studies negate or support the use of intraosseous access in stroke patients. Contraindications are few and complications are uncommon. The findings of our case report suggest that intraosseous cannulation may be safely used for fibrinolysis in acute ischemic stroke patients with difficult peripheral venous access in in-hospital or out-of-hospital setting.

Tufts Medical Center, Boston, Massachusetts, USA

We report a case of a pregnant patient with bilateral ovarian teratomas who presented with treatment refractory NMDA receptor encephalitis despite removal of bilateral teratomas, successfully treated with Rituximab.

Case report and discussion of treatment and outcome.

25 year old 22 weeks pregnant female with known ovarian cysts who presented with one week of confusion and subsequent status epilepticus. She was started on empiric treatment with IVIG while undergoing workup. NMDA receptor antibody was confirmed. Left oophorectomy and right ovarian cystectomy were performed, both of which confirmed ovarian teratoma. She was given high dose steroids. Her worsening condition prompted consideration of additional agents. Plasma exchange and Rituximab were initiated and then she was continued on Rituximab alone. She improved dramatically over six weeks and delivered at full term via spontaneous vaginal delivery. At one year follow up, the child was healthy and meeting appropriate milestones.

We report the use of rituximab for safe and successful treatment of NMDA receptor encephalitis in a gravid female.

Neovascular glaucoma (NVG) is a known complication of carotid endarterectomy in patients with carotid stenosis. There are no previous reports of acute NVG refractory to medical treatment following carotid artery stenting (CAS). We report a patient who needed surgical treatment for acute exacerbation of NVG following CAS.

A 56-year-old man with hypertension, diabetes, and hypercholesterolemia presented with recurrent transient weakness in his right hand. Fifteen days before presentation, he had experienced acute loss of vision on the left side because of central retinal artery occlusion. Magnetic resonance imaging of the brain was unremarkable. Conventional angiography showed an occlusion of the left proximal internal carotid artery. Ophthalmological evaluation before CAS showed neovascularization of the iris and a normal intraocular pressure (IOP) of 14 mm Hg in the left eye. CAS was uneventful, but the following morning, the patient developed pain in the left eyeball with an IOP of 49 mm Hg. Anterior chamber paracentesis followed by intraocular injection of bevacizumab, panretinal photocoagulation, and medical treatment failed to reduce the IOP below 32-36 mm Hg. Eighteen days following CAS, an Ahmed glaucoma valve was implanted in the left eye to treat the refractory NVG. IOP decreased to 6 mmHg and his ocular pain resolved completely post implantation.

Although NVG is a rare complication of CAS, it should be suspected in patients who develop acute ocular pain following CAS. NVG may respond to anterior chamber paracentesis, panretinal photocoagulation, and bevacizumab, but surgical treatment, such as implantation of an Ahmed glaucoma valve, should be considered in cases with refractory NVG.

Background: Cerebral amyloid angiopathy is a common cause of spontaneous lobar intracerebral hemorrhage. Convexal subarachnoid hemorrhage can be a manifestation of cerebral amyloid angiopathy. Whether focal amyloid burden predicts future hemorrhage is unclear.

Case: An 82-year-old man presented with transient left arm weakness and paresthesias in the setting of previous cognitive decline. MRI showed a convexal subarachnoid hemorrhage of the right central sulcus, as well as susceptibility weighted imaging findings consistent with superficial siderosis. Lumbar puncture revealed normal cell count with a mildly elevated protein. He had spontaneous resolution of his symptoms after several hours. One year later he presented with sudden onset confusion and imaging again showed a convexal subarachnoid hemorrhage over the posterior right frontal lobe. Susceptibility weighted MRI revealed hemosiderin over the right posterior frontal and anterior parietal lobes. An amyloid-PET, obtained one year prior to his first spell as a research participant, demonstrated asymmetric amyloid deposition in the right temporo-parietal region. 6 years after his initial episode he presented again with confusion, headache, and decreased level of alertness. A CT scan demonstrated a right-sided temporo-parietal intracerebral hemorrhage in the area of asymmetric amyloid deposition on PET. His family opted for comfort measures only, and he was discharged to hospice. Autopsy revealed severe amyloid angiopathy, as well as Alzheimer disease, Braak stage VI.

Discussion: This case illustrates the clinical course of a patient with amyloid angiopathy, including recurrent convexal subarachnoid hemorrhages, and superficial siderosis. Of importance, the amyloid PET scan predicted the location of his intracerebral hemorrhage 7 years later.

The case of a 23-year-old man, presenting with a past medical history of migraine headaches, dipola, vertigo, with symptoms later progressing to lethargy and confusion for 10 days. Brain MRI revealed a peripherally enhancing mass within the left thalamus with central restricted diffusion, which is consistent with a cerebral abscess.

Case report of congenital heart disease when discovered in adulthood is an interesting entity, especially when it is the source of brain abscesses.

Detailed history taking, physical examination and appropriate imaging can usually reveal the anomaly.

The diagnosis of brain abscess should promote the clinician to consider right to left shunts as a possible predisposing condition for brain abscess

Management of acute cerebral embolism in patients with implanted ventricular assist devices (VADs) is particularly challenging, since chronic anticoagulation often precludes the use of intravenous tissue plasminogen activator (IV-tPA). We describe a VAD patient who suffered cerebral embolization, and was successfully treated with thrombectomy, emphasizing the nuances particular to this clinical scenario in the context of limited historical experience.

A 54 year-old man with heart failure (ejection fraction 10%) and HeartWare II VAD implantation about 15 months prior, was found at the scene of a car accident with expressive aphasia, right homonymous hemianopia, extinction and right hemiplegia, with a National Institutes of Health Stroke Scale (NIHSS) score of 12. Upon arrival, his CT was unremarkable, but CTA revealed occlusion of the left middle cerebral artery (M1 segment). Since his INR was 2.1, he underwent emergent thrombectomy with the Solitaire device, resulting in complete revascularization (TICI = 3) 120 minutes from onset, with rapid deficit resolution (NIHSS = 0).

The procedural and clinical success was accompanied by lack of evidence of infarction in subsequent CT studies, and a modified Rankin score of 0 upon discharge. The removed thrombus displayed early organization, suggesting unexpected firmness, and underscoring the potential importance of mechanical removal rather than chemical lysis in VAD patients. Our case has attributes that set it apart from those previously reported: 1) The use of a hybrid (i.e. retrieval PLUS aspiration) endovascular retrieval technique, 2) The lack of concurrent use of thrombolytic drugs, and 3) The rapid, sustained and optimal clinical improvement.

The utilization of VADs continues to grow, yet the literature regarding endovascular techniques for managing these types of patients remain scarce. However, the increasing availability of centers capable of delivering this type of treatment, suggests that thrombectomy should be strongly considered in VAD patients with acute cerebral embolism.

Extreme cerebral oxygen changes has not been reported via monitoring of partial brain tissue oxygen levels. Here we present an aSAH patient with brain tissue oxygen (PbtO2) monitoring, who developed cerebral hypoxia due to cerebral vasospasm, then went on to develop cerebral hyperoxia with associated cerebral infarction.

Methods 54 yo female with HH5FG4 SAH with initial GCS of 3T underwent coiling of a ruptured basilar tip aneurysm. A PbtO2 monitor was inserted to guide therapy. This patient had multiple episodes of low PbtO2 (80 mmHg). This corresponded to infarction on follow up head CT and MRI with preservation of local arterial vessels on MRA, consistent with diagnosis of DCI.

In the present case, high PbtO2 is more likely resulted from a combined effect of 1) increased CBF from co-administration of ketamine at the time of milrinone infusion; 2) decreased cerebral metabolic demands in already infarcted left frontal lobe, resulting in reduced oxygen uptake; 3) accelerated reperfusion and thus hyperemia with milrinone. Restoration of flow with milrinone may have been too late to reverse the prolonged period of vasospasm induced ischemia, resulting in perfusion of infarcted tissue, or luxury perfusion.

Clinicians utilizing PbtO2 monitoring for DCI management should be cautious of high PbtO2 values, as it may herald cerebral infarction. Further studies are needed to better elucidate the mechanism of reperfusion injury and potential treatments.

Patients with acute brain injury, especially those with intracranial hemorrhages are at a higher risk for hemorrhage while on therapeutic anticoagulation. Unfractionated heparin (UFH) is frequently used as it is easily reversible and has a short half-life. Activated partial thromboplastin time (aPTT) is traditionally used to monitor its effect. Several disadvantages with aPTT monitoring include inability to reach therapeutic goal, over-or under-dosing and its associated complications. Anti-Xa level is reported to have better correlation with actual degree of anticoagulation using UFH.

Retrospective chart review of 3 patients with acute brain injury who required initiation of early therapeutic anticoagulation and monitored with anti-Xa level.

Case 1 -30 year-old-man with intracerebral hemorrhage (ICH) developed lower extremity deep vein thrombosis (DVT) and required therapeutic anticoagulation. Patient became therapeutic within six hours of titrating infusion based of anti-Xa levels and remained therapeutic. Asymptomatic rectal bleeding associated with fecal management system was noted. Case 2 -26 year-old-man with cerebral venous sinus thrombosis presented required therapeutic anticoagulation. UFH infusion was initially monitored using aPTT levels which had widely varied lab results, thus monitoring was switched to anti-Xa levels which provided a more consistent therapeutic range. However, patient developed thrombocytopenia in the setting of inflammatory bowel disease. Therefore, UFH infusion was changed to Argatroban infusion. Case 3 -22 year-old-man with lower medullary acute ischemic stroke due vertebral artery dissection required therapeutic anticoagulation to prevent recurrence. Patient became therapeutic within 27 hours of titrating based of anti-Xa levels.

To monitor therapeutic anticoagulation, anti-Xa level appears to achieve target anticoagulation level faster and without serial variation as compared to aPTT. However, anti-Xa level estimation is costlier as compared to aPTT and not widely available. By restricting it to special populations like those with acute brain injury might justify its use and underscore cost-effectiveness.

Neurological admissions presenting to the ICU benefit from a dedicated neurocritical care team but many community hospitals lack this subspecialty expertise. With an aging population and a neurointensivist shortage, more patients are transferred to designated neurocritical care units which increases healthcare spending and resource utilization. Recognizing this obstacle, we describe the management of a patient in status epilepticus via our novel "eNeuro-ICU" consult program in which a 'sub-hub' of the Northwell Health Tele-ICU was set up at the only hospital out of 19 in our health system that is staffed 24/7 by neurointensivists.

A 56-year-old man with history of a left frontal meningioma presented with multiple seizures to a hospital within our healthcare system. He received 6 mg of lorazepam and levetiracitam in the emergency department and was admitted to the ICU for further monitoring. There he was witnessed to have recurrence of clinical activity concerning for ongoing seizure. Levetiracitam was increased and phenytoin was added. Neither immediate neurological consult nor continuous EEG was available, thus an "eNeuro-ICU" consult was obtained. In this model, the bedside provider contacts the Tele-ICU that facilitates a conference call with the neurointensivist. AV technology was used to provide consultations and follow ups. The neurointensivist determined the patient was rapidly returning to baseline and recommended a head CT, lab studies and continuation of the anti-epileptic drugs. The eICU team monitored the patient overnight.

By leveraging the infrastructure in place for management of critically ill patients remotely, an additional level of subspecialty care was offered in a timely manner and allowed the patient to remain at their local facility.

Based on the success of the initial program we are currently in the process of extending the virtual consult service to various community hospitals' EDs/ICUs to improve outcomes for patients who would benefit from neurocritical care services.

Hypoglycemic encephalopathy is a potentially life-threatening manifestation of hypoglycemia, It is usually caused by metabolic change, hypoglycemic agents, and malignancy. Here, we report a patient with hypoglycemic encephalopathy caused by sleeve gastrectomy

A 34-year-old woman was admitted due to unconsciousness of acute onset. She showed normal corneal and vestibulo-ocular reflex but sluggish pupil light reflex and decerebrated posture by painful stimulation. She has taken severe medications for weight control including orthosiphon powder and hydrochlorothiazide after bariatric surgery. Laboratory studies showed significantly low blood glucose level (13mg/dL) with normal liver enzyme and creatinine. There was no evidence of adrenal insufficiency. Electroencephalography showed no epileptiform discharge. Initial and follow-up brain magnetic resonance imaging revealed diffuse high signal intensity on white matter expanded to cortex, corpus callosum and posterior limb of the left internal capsule, suggesting hypoglycemic encephalopathy. In abdomen-pelvic CT, there is no mass lesion like carcinomas or insulinoma.

The clinical diagnosis of hypoglycemic encephalopathy followed by sleeve gastrectomy was made by given history of bariatric surgery and the lack of evidence of hypoglycemic agent overdose, adrenal insufficiency, endogenous hyperinsulinism or malignancy. There are several hypotheses that sleeve gastrectomy can encourage hypertrophy of beta cells, hypersecretion of glucagon-like peptide, glucagon abnormality and increased insulin sensitivity, that may induce hypoglycemia.

We suggest that clinicians should consider sleeve gastrectomy itself as a possible cause of profound hypoglycemia

Pulmonary embolism (PE) is a fatal complication in neurological conditions with plegic extremities. Clinical presentations and supportive testing can be variable. We present a case of PE which presented with ST segment elevations 2 weeks after spontaneous intracerebral hemorrhage (sICH).

Case report and review of the literature

We present a case of a 68 year old female with a history of a recent sICH with resultant left hemiplegia who presented with a syncopal episode and chest pain. On physical examination, she was noted to be tachypneic and tachycardic with an unchanged neurological exam. 

Pulmonary embolism can present with a variety of EKG abnormalities including ST elevations after sICH and the treating physician should be aware of these idiosyncrasies. Anticoagulation should be cautiously initiated in such cases.

Infectious intracranial aneurysms (IIA) are rare neurovascular lesions associated with infective endocarditis. We present a case of a large IIA which developed within 24 hours of a negative CT angiogram and ruptured despite 4 weeks of appropriate antibiotic treatment.

A 66 year-old woman presented with fevers and malaise. Her initial workup revealed an aortic valve mass and blood cultures grew out Streptococcus. Three days after intravenous penicillin therapy was initiated for bacterial endocarditis, she developed a new headache and right hemianopsia. A head CT demonstrated a left occipital lobe stroke with hemorrhagic transformation. Further workup with CT angiography revealed a 5 mm outpouching along of the distal branch of the left PCA, consistent with an infectious intracranial aneurysm. On repeat imaging, this aneurysm demonstrated growth despite medical treatment, and required coil embolization/occlusion. Aortic valve replacement was planned after 4 weeks of antibiotic therapy because of continued severe aortic insufficiency and persistent valve vegetation. On the day of surgery, she developed acute word-finding difficulty followed by a rapid neurologic deterioration resulting in coma. A head CT demonstrated a new left frontal intraparenchymal and subarachnoid hemorrhage associated with the rupture of an 11mm x 11mm irregularly shaped aneurysm in the region of the left MCA bifurcation, which had been absent on a prior surveillance CT angiography just 23 hours prior. She underwent emergent coil embolization, extraventricular drain placement, and decompressive hemicraniectomy. Despite these measures, her exam did not improve. She was transitioned to comfort measures and life-sustaining therapies were withdrawn.

The development of IIA can occur despite appropriate medical treatment. These aneurysms may rapidly expand and rupture within hours, as shown by our case. Even with prior exonerating imaging, clinicians should have a high suspicion for IIA development in all infective endocarditis patients.

The corneomandibular reflex, also known as Wartenburg reflex or Von Solder phenomenon, is a rare pathological reflex signifying severe supranuclear trigeminal injury. It presents as contralateral jaw deviation to corneal stimulation. Etiologies include upper brainstem lesions, large hemispheric lesions with brainstem compression, as well as advanced amyotrophic lateral sclerosis and multiple sclerosis when corticobulbar pathways are affected. This clinical finding is useful in differentiating structural and metabolic causes of coma, as this examination finding would not be present in metabolic phenomena.

A middle aged man presents with a hypertensive right thalamic hemorrhage and a FOUR score of E0M0B0R1. The patient's cornea was stimulated with a cotton swab. The cornea was tested bilaterally to determine any lateralizing features. Recording on video was performed with patient's family written consent as patient was comatose.

Upon stimulation of the patient's cornea a contralateral jaw jerk was appreciated. This was replicated contralaterally.

This case describes a common patient with a rare physical examination finding. There is utility in recognizing this finding as it will aid in determination of the underlying cause of a comatose state. The corneomandibular reflex present at presentation rules out a metabolic cause. A structural cause was validated by imaging studies (shown). The reflex arc was researched and has been independently artistically rendered (shown), which demonstrates the pathway beginning with the afferent limb of the corneal stimulus (V1) which travels to the main trigeminal sensory nucleus via the trigeminal ganglion. Severe supranuclear trigeminal lesions will inhibit inhibitory interneurons within the mesencephalic nucleus, leading to activation of the motor nucleus of the trigeminal nerve. This causes activation of the ipsilateral external pterygoid muscle which produces a contralateral jaw jerk. Overall this patient fared poorly and expired several days after admission.

Pneumocephalus is when air enters and is contained inside the intracranial compartment. When intracranial pressure increases causing neurological decline, patients can experience nausea, vomiting, seizures, dizziness, and altered mental status. Here we present three cases of postoperative pneumocephalus which resolved quickly with humidified oxygen delivery via high-flow nasal cannula. We follow the cases with a review of the mechanisms and pathophysiology of pneumocephalus and its treatment, as well as future directions in management.

Case series of 3 patients with post-operative pneumocephalus who were treated with high-flow nasal cannula.

Case 1 describes a 78-year-old woman who underwent hemicraniotomy for removal of meningiomas, with focal postoperative neurological signs and 8mm of midline shift on head CT due to pneumocephalus. Case 2 describes a 57-year-old woman who underwent right anterior temporal lobectomy for seizures, who developed postoperative focal prefrontal lobe signs and Mount Fuji sign on head CT. Case 3 describes a 58-year-old man with bilateral subdural hematomas, status post bilateral burr hole evacuation. He was excessively somnalent postoperatively with bilateral pneumocephalus. With high-flow nasal cannula, they all returned to clinical, and near radiographic baseline within 8, 12, and 20 hours, respectively.

Recognizing the limitations of a small case series, we believe these cases support use of high-flow nasal cannula when treating patients with symptomatic pneumocephalus. Thsee patients showed more rapid clinical and radiographic improvement after implementation of HFNC oxygen therapy than previously described using other methods. High-flow nasal cannula may help washout nitrogen from the lungs, allowing a downward gradient from the nitrogen in the intracranial air bubble out the lungs. In addition, high-flow nasal cannula is more comfortable for the patient, allowing for more consistent treatment. Randomized studies are needed to confirm our findings.

The neurotoxin produced by Clostridium botulinum is the most lethal toxin known by weight. Early recognition and treatment of Botulism are crucial for full recovery. We present a case of progressive paralysis secondary to botulism toxemia following a gunshot wound (GSW).

A 27-year-old man suffered a GSW to the right lower extremity. He was treated in the emergency department where the wound was irrigated and closed. Some bullet fragments could not be retrieved due to close proximity to popliteal vessels and surrounding nerves. He returned ten days later with diplopia and nausea. He denied consumption of canned foods or illicit substances and had no preceding upper respiratory or gastrointestinal illnesses. On examination, he exhibited ptosis and symmetric bilateral motor weakness with diminished deep tendon reflexes. The GSW showed no signs of infection. Progressive respiratory insufficiency resulted in intubation and mechanical ventilation.

A lumbar puncture revealed normal opening pressures and cerebrospinal fluid analysis was unremarkable. Titers for acetylcholine receptor and anti-muscle specific kinase antibodies were negative, as was a tensilon test. Blood toxicology analysis showed no evidence of illicit substances or heavy metal poisoning. A high suspicion for wound botulism led to consultation with the regional poison center and CDC. Blood and anaerobic wound samples were obtained for toxin bioassay and culture. Empiric intravenous penicillin G therapy was started. Equine Heptavalent Antitoxin (H-BAT) was obtained and administered on hospital day 2. Serum toxin bioassay tested positive for botulinum neurotoxin type A. The patient required a gastrostomy tube due to persistent dysphagia. After one month of hospitalization, he was discharged home and continues outpatient physical therapy.

Wound botulism from traumatic injury is exceedingly rare with only one to two cases reported annually. Our case is the first reported incidence of wound botulism from a single gunshot wound.

Hyperammonemic cerebral edema (HCE) with brain herniation carries a dismal prognosis historically despite aggressive treatment. However, we report a case where a patient with severe HCE and herniation returned to her neurological baseline after aggressive medical management.

A 62-year-old woman became acutely comatose with a blown left pupil and required intubation several days after admission for encephalopathy. Head CT demonstrated diffuse cerebral edema with central and bilateral uncal herniation. Profound hyperammonemia (238ug/dL) was implicated, though hepatic function was normal. Her intracranial hypertension was ultimately controlled using hyperventilation, sedation, and osmotherapy, resulting normalization of her brainstem reflexes and improvement in her coma and imaging. Continuous veno-venous hemodialysis (CVVHD) normalized her ammonia and encephalopathy that was initially refractory. Multiple porto-hepatic shunts were identified on hepatic CT angiogram as the cause of her hyperammonemia, and were embolized. She was eventually weaned off CVVHD and extubated, without residual neurological deficits.

Our case demonstrates that, with contemporary management, clinical and radiographic reversal of HCE and herniation is possible and prognosis is not uniformly poor. Therefore, neurological prognostication in these patients should only be performed after assessing the clinical trajectory following cerebral resuscitation and ammonia reduction. Furthermore, our case provides an example of how CVVHD can be used to reduce refractory hyperammonemia quickly until the cause of the hyperammonemia can be ascertained and addressed. Finally, this is the first case reported of HCE secondary to primary portosystemic shunt in absence of hepatic disorder; vascular imaging of the liver should be considered in the work-up of patients with hyperammonemia.

A good neurological prognosis is possible for patients with HCE and cerebral herniation with aggressive management that includes reduction of ICP and ammonia. CCVHD is a useful adjunct to treat refractory hyperammonemia. A porto-systemic shunt should be considered as an etiology for hyperammonemia.

Cerebral venous sinus thrombosis (CVST) often presents with intracerebral hemorrhage and seizures. Extensive involvement of the cerebral sinuses can lead to comatose state due to cerebral edema and associated intracranial hypertension. If not reversed with early therapeutic anticoagulation, then mechanical thrombectomy and decompressive hemicraniectomy (DHC) may be necessary as life-saving measures. However, etiological diagnosis of associated hypercoagulable state is needed for successful long-term treatment.

Case report of a patient presenting with CVST requiring anticoagulation, DHC and total colectomy (to treat underlying ulcerative colitis) as treatment with full anticoagulation was associated with lifethreatening hematochezia.

Twenty-five year old man with one week history of diarrhea presented with left sided weakness. Imaging studies confirmed extensive CVST with minimal venous drainage through bilateral cavernous sinuses as well as right hemiparesis secondary to left post cingulate intracranial hemorrhage. Patient subsequently developed loss of vision and became encephalopathic, despite initiation of anticoagulation with heparin. Hence, mechanical thrombectomy was attempted but was unsuccessful. He also developed consumptive thrombocytopenia for which his anticoagulation was switched to argatroban. Progressive neurologic deterioration necessitated DHC. His neurological examination progressively improved upon re-initiation of anticoagulation resulting in restoration of vision and resolution of left hemiparesis. Later in the disease course, he developed symptomatic hematochezia associated with his primary disease, ulcerative colitis and required total colectomy. Subsequently he was transitioned to oral anticoagulation and transferred to inpatient rehabilitation facility due to deconditioning from prolonged hospitalization.

CVST can be life-threatening unless early treatment is initiated. Appropriate and timely treatment including etiological diagnosis can lead to favorable patient outcomes.

Adverse effects of intrathecal non-ionic contrast during myelography are rare but can include seizures and encephalopathy. To our knowledge, cerebral edema has only been reported in the literature in two previous cases. We report a case of malignant cerebral edema following intrathecal administration of non-ionic contrast who developed seizure like activity with radiographic evidence on a head computerized tomography (CT) scan of acute diffuse cerebral edema. An 80 year-old male underwent an elective spinal CT myelogram using 20mm of Isovue M 200 non-ionic contrast to evaluate chronic lumbar pain related to spinal stenosis. No complications were reported intra-procedurally and the patient was discharged home. The patient began to complain of progressive worsening headaches. The following morning he started complaining of nausea/vomiting, lost consciousness with posturing vs seizure like activity. A head CT revealed extensive brain edema and swelling with crowding of the brainstem and herniation ( fig. 1 ). This patient was intubated and given an IV mannitol, 23.4% hypertonic saline followed by an infusion of 3% hypertonic saline infusion. Serial CTs revealed complete resolution of his cerebral edema 48 hours after admission ( fig. 2 and 3) . The patient's mental status improved, was extubated, and then was discharged home 5 days after admission.

While significant adverse effects of non-ionic contrast following spinal myelography are rare, the potential life threatening severity of these incidents warrants further patient education following this routine outpatient procedure. We recommend close neurological monitoring after intrathecal administration of contrast media. Patients should be provided with detailed instructions about the potential side effects of non-ionic contrast and how to seek medical attention if symptoms of cerebral edema are noted post procedurally.

A large acute traumatic subdural hematoma with brain compression and midline shift is typically considered a neurological emergency necessitation surgery. Spontaneous resolution of a large subdural hematoma is considered a rare phenomenon with a few case reported in the literature. To our knowledge, we present the first case of spontaneous resolution of a traumatic acute subdural hematoma with brain compression and midline shift on dual antiplatelet therapy. A 71 year-old patient initially presented after being found down and unresponsive in his home. The patient was on aspirin and clopidigrel. He was found to have altered mental status, wasn't following commands, and had a Glascow Come Scale score of < 8. The patient's initial head CT revealed a large left acute subdural hematoma (SDH) measuring 1.8cm in diameter. Neurosurgery was consulted upon arrival for possible emergent evacuation. The patient's repeat head CT showed a decreased SDH to 1.1cm in diameter. Given the rapidly resolving SDH, surgery was postponed. Another repeat head CT the following day revealed a decrease in size of the SDH to 10mm in diameter.

Several theories have been proposed for the rapid resolution of an acute SDH including CSF leaking into the SDH through a tear in the arachnoid membrane with rapid reabsorption, redistribution of the hematoma in the subdural space, and acute fluctuations in ICP driving the spontaneous resolution of the SDH. Close neurological and repeat imaging may be helpful in managing these patients. As seen in our patient and others, a low density band in the subdural hematoma may indicate CSF and be a predictor for spontaneous resolution of an acute SDH. The features of this atypical case offer points of discussion regarding the surgical or non-surgical approach of these patients.

Early post-hypoxic myoclonus -or myoclonic status epilepticus -develops within 48 hours of the initial anoxic injury and is associated with poor outcomes per current AAN practice guidelines. Late posthypoxic myoclonus -or Lance-Adams syndrome -develops >48 hours after the anoxic injury, consciousness is regained, and is associated with relatively good outcomes.

The patient is a 46 yo man with a history of alcohol and cannabis use disorder, bipolar disorder, PNES who presented after attempted hanging for up to 15 minutes. Intial rhythm was PEA; he had 3 rounds of CPR, received 1mg epinephrine, and was intubated prior to ROSC. Myoclonic jerks were noted within 24 hours post arrest. Hypothermia protocol was initiated as GCS was 3T. CT Head showed subtle loss of grey-white differentiation. EEG initially showed that his generalized myoclonic jerks correlated with cortical activity. He was started on versed gtt, Keppra, VPA with improvement in the frequency of jerks. On post-arrest day 3, MRI brain showed mild cerebellar edema. MRI C-spine was negative for significant myelopathy, arguing against myoclonus as a spinal reflex. Mentation gradually improved; on post-arrest day 7 he opened his eyes to command. EEG evolved to show GPEDs and SIRPIDs and OXC and TPM were added. On post-arrest day 11 a paralytic challenge resolved electrographic spikes, suggesting subcortical origin of myoclonus. He continued to improve cognitively, but despite clonazepam, VPA, home OXC he continues to have severe intention myoclonus.

Despite the presumed poor prognosis, the patient's family pursued aggressive measures and his mentation gradually improved.

Early post-hypoxic myoclonus carries a poor prognosis, however, in this case, the patient survived with a good cognitive outcome likely owing to his age and relatively few comorbidities. Further studies are needed to differentiate early-onset Lance-Adams from myoclonic status since prognosis differs greatly.

Posterior reversible encephalopathy syndrome (PRES) can occur from multiple etiologies and often presents with rapid-onset headache, altered consciousness, seizures and/or visual disturbances. Vasogenic edema involving predominantly cerebral white matter is a key finding on imaging studies. Although seizures are a frequent presenting symptom of PRES, refractory status epilepticus (RSE) requiring multiple antiepileptic medications is very rare.

A case report of a patient presenting with PRES and clinical course complicated with RSE necessitating use of intravenous anesthesia, ketamine, and newly-available brivaracetam.

65-year-old woman with history of congestive heart failure, chronic iron deficiency anemia and uncontrolled hypertension was admitted for severe encephalopathy and convulsive status epilepticus (CSE) for longer than 30 minutes necessitating propofol and midazolam infusions. Her admission systolic blood pressures were in the 280s, and MRI brain revealed bilateral parieto-occipital T2/FLAIR hyperintensities consistent with PRES. Despite adequate control of hypertension following admission, patient remained encephalopathic and continuous electroencephalography (EEG) demonstrated nonconvulsive status epilepticus (NCSE). The patient's NCSE continued despite use of maintenance antiepileptics (fosphenytoin, lacosamide, levetiracetam) and high-dose infusions of midazolam and propofol. Ketamine infusion was started to maximize NMDA receptor blocking properties, and burstsuppression pattern on EEG was easily achieved with bolus infusions followed by continuous infusion. Addition of brivaracetam was used to replace levetiracetam and allowed patient to remain seizure-free when IV anesthetics were weaned off. Patient required prolonged hospitalization with gastrostomy tube placement and tracheostomy, which was later decannulated prior to patient's discharge to home with family.

High index of suspicion is necessary to identify patients in NCSE with prolonged encephalopathy that have PRES. Early use of ketamine along with a benzodiazepine may result in rapid achievement of burstsuppression to treat SE. Brivaracetam may be a useful agent to treat RSE.

Diagnosis of Diabetes Insipidus(DI) includes polyuria, hypernatremia and low urine specific gravity. We present two patients, receiving hyperosmolar therapy for intracranial hypertension (IHT), in whom using low urine specific gravity to diagnose DI lead to delayed treatment.

This is a retrospective case series. Criteria used to diagnose DI at our institution include polyuria, sodium <300mOsm/kg and urine to plasma osmolality ratio <2.

Case 1: 23-year-old male with subdural hematoma, IHT on hyperosmolar therapy, developed polyuria. Sodium rose from 141 to 172mEq/L. Urine specific gravity was 1.020 excluding DI. Eventually, sodium rose to 184mEQ/L. Specific gravity remained 1.009 but urine osmolality was 162mOsm/kg and urine/plasma osmolality ratio was 0.42, consistent with DI. Vasopressin was initiated, however the patient had already developed lactic acidosis and renal failure due to hypovolemia. Case 2: 49-year-old female with intracerebral hemorrhage and IHT on hyperosmolar therapy, developed polyuria. Sodium rose to 176mEq/L, specific gravity remained >1.005 but urine osmolality was 187mOsm/kg and urine/plasma osmolality ratio was 0.49 consistent with DI. Vasopressin was initiated.

Hyperosmolar therapy increases urine osmoles and raises urine specific gravity. This interferes with diagnosis of DI which requires low urine specific gravity. While specific gravity measures the weight of particles, osmolality measures particles independent of their weight and thus accurately measures urine tonicity in the presence of heavy particles like mannitol. Moreover, urine/plasma osmolality ratio is able to demonstrate relative hyposmolarity of urine when compared to serum assisting with diagnosis of DI even when urine specific gravity is elevated. We conclude that urine specific gravity does not reliably detect DI in patients receiving hyperosmolar therapy. Urine osmolality and urine/plasma osmolality ratio may detect DI earlier and prevent dehydration and kidney injury. These findings should be validated prospectively.

Endovascular intervention in the treatment of CVT(cerebral venous thrombosis) is an alternative strategy when cases deteriorate despite best medical management or develop refractory intracranialhypertension. We present a patient with CVT due to heparin-induced thrombocytopenia(HIT), with intraparenchymal hemorrhage(IPH) and refractory intracranial-hypertension, who was managed with systemic anticoagulation, continuous intra-sinus infusion of rTPA and Mechanical Thrombectomy(MT) resulting in excellent outcome.

Case Report: A 50-year-old woman with left parafalcine meningioma s/p cyberknife was started on subcutaneous heparin for radiation necrosis 5 days prior to admission. She presented to the hospital with new onset headaches and nausea. CT head showed increased edema with mid-line shift around the meningioma, for which steroids were started. Within 2 days her headaches worsened and repeat imaging demonstrated right temporal IPH. Emergent hematoma evacuation was performed. MRI brain showed right cerebellar infarct and MRA head showed extensive cavernous sinus thromboses, from right internal jugular vein and into sigmoid and transverse venous sinuses. She tested positive for HIT and was switched to Argatroban drip. Patient however continued to deteriorate due to refractory intracranial-hypertension. Intra-cavernous rTPA injection and MT was done but the thrombosis was noted to recur on repeat angiogram 24hrs later. An intra-sinus catheter was left in place for continuous infusion of rTPA at 1 mg/hr. for 12hrs was done while Argatroban drip was continued. The patient's intracranial pressure returned to normal. Repeat venogram showed resolution of CVT.

Patient tolerated the therapies well, without any further hemorrhagic complications. Modified Rankin score at 6 month follow-up was 1.

This case features successful aggressive endovascular interventions including in-situ rTPA infusion, MT and concomitant systemic anticoagulation for CVT due to HIT, complicated by intracranial hemorrhage and refractory intracranial hypertension. The paucity of high quality evidence related to safety, efficacy and modality of endovascular treatment lead to making therapeutic decision on individual basis.

Acute brain injury may be followed by encephalopathy marked by electroencephalographic features along the ictal-interictal continuum (IIC). The use of perfusion imaging to co-localize radiographic features of known malignant EEG patterns may add an important context to guide treatment escalation or de-escalation. This is only the second report in which widely available CT or MR perfusion techniques were favored for this application over more cumbersome metabolic imaging such as PET.

Retrospective analysis was performed on records for patients admitted to a Neurosciences ICU, exhibiting encephalopathy, with EEG features on the IIC, who underwent perfusion imaging. Studies included CT perfusion, MR perfusion, arterial spin labeling, or SPECT. These studies were obtained for unrelated purposes. Escalation or de-escalation of anti-convulsant and sedative medication, hospital course, and patient outcomes were extracted. Perfusion imaging data was juxtaposed with EEG patterns along the IIC, and patient outcomes are described in narrative form.

Seven cases were identified. Four cases occurred in the context of intraparenchymal hemorrhage, of which one was secondary to meningioma resection. Two cases occurred after treatment for subdural hematoma, and one case was related to ischemic stroke. Anti-convulsant and sedative management was escalated or de-escalated relative to the presence or absence of radiographic co-localization of hyperperfusion in all but one case.

Emerging data indicates that some IIC EEG patterns may merit aggressive treatment. Metabolic signatures of secondary brain injury as measured by cerebro-oximetry or microdialysis have associated these patterns with unfavorable outcomes. We report case studies in which information gleaned from basic perfusion imaging may suffice to distinguish between benign IIC patterns and those that should be regarded as near-ictal. The cases hint at novel ways to conceptualize treatment of encephalopathy following acute brain injury and suggest a dimensional shift in thinking towards electroperfusive status epilepticus.

SUDEP has classically been a diagnosis of exclusion. Recent studies have shown, however, that similar genes -and even genes within the same family -are associated with SUDEP and Brugada. This suggests that perhaps the cardiac irritability of Brugada Syndrome exists on a spectrum with epileptic sudden death.

A 25 yo man with a history of presumed seizure disorder presented as a transfer from another hospital after being found to have anoxic brain injury following cardiac arrest. He had been shopping with his wife when he was thought to have one of his typical seizures. He was non-responsive for about 20 minutes. On arrival EMS found him pulseless. CPR was started en route and continued for 30 minutes in the ED where he was defibrillated three times before achieving ROSC. He completed the therapeutic hypothermia protocol. Cardiac catheterization was clean. EEG showed diffuse slowing with no epileptiform discharges. Imaging showed diffuse anoxic brain injury. After nearly two weeks without clinical improvement he was made comfort care. .

Of note, previous seizure workup failed to identify epileptiform activity. He was given an AED prescription which he never filled. Further chart review showed that he had previously presented to the ED after a "seizure" episode which lasted 45 minutes. His neuroexam was non-focal. CT head was negative. Review of his EKG at that time showed type 1 Brugada Syndrome pattern with an elevated Jpoint and T-wave inversions in V1 and V2. His sudden cardiac arrest is most likely a result of symptomatic Brugada

Symptomatic Brugada is important to identify early since deaths such as the one discussed above may be prevented by an implanted defibrillator. This case highlights the need for heightened awareness and more effective testing for Brugada in the setting of seizure or pseudoseizure.

Patients with cerebral air embolism (CAE) often exhibit more severe symptoms than those typically associated with the number of air emboli and size of infarcts on brain images. However, this discrepancy between symptoms and imaging findings has not been sufficiently explained.

We report a case of CAE in which disruption of the blood-brain barrier (BBB) and perfusion defects were identified via brain magnetic resonance imaging (MRI).

A 79-year old man with a lung mass was admitted to our hospital. Percutaneous needle aspiration of the mass was performed in the left lower lobe of the lung. The patient developed sudden confusion and irritability after the procedure. During neurological examination, he could follow only simple commands and exhibited symptoms of left-sided weakness and neglect (Medical Research Council grade 2). Noncontrast computed tomography (CT) of the brain revealed a few small air emboli in the right frontal subcortical area. Multimodal MRI of the brain was performed 50 minutes after the onset of symptoms. T2-weighted gradient-echo imaging revealed only a few small air emboli in the right frontal area, and diffusion-weighted imaging findings were unremarkable. In contrast, time-to-peak imaging revealed widely distributed perfusion defects in the right hemisphere, while contrast-enhanced T1-weighted imaging revealed prominent leptomeningeal enhancement, suggestive of BBB disruption in the right hemisphere. Magnetic resonance angiography revealed no steno-occlusive lesions. The patient was treated with 100% oxygen via a high-flow nasal cannula. His weakness subsided the next day, although his confusion persisted for 18 days. Follow-up MRI performed five days after the onset of symptoms revealed resolution of the abnormal findings.

Our findings suggest that disruption of BBB and perfusion defects may develop in patients with CAE. Extensive impairments of the BBB and perfusion may explain the mismatch between severe neurological symptoms and small air emboli/infarcts.

Co-existence of cerebral salt wasting and diabetes insipidus is an extremely rare entity that has only been described in 2 adult case series and a paediatric series. Due to the complex nature of diagnosing this entity, mistreatment may ensue and lead to high morbidity and mortality rates.

We report a case of a patient who was admitted to the neurosurgical intensive care unit after sustaining a subarachnoid haemorrhage secondary to a ruptured anterior communicating artery aneurysm.

A 67-year old lady presented with sudden onset of severe headache and nausea. GCS was 12 (E3V4M5) with no focal neurological deficits. She underwent endovascular coiling and embolisation of the aneurysm under general anaesthesia and had a left external ventricular drain inserted. In the immediate postoperative period, she was found to be polyuric, with the initial workup suggestive of diabetes insipidus. Desmopressin was administered with initial good effect. However, her polyuria recurred and persisted despite Desmopressin. The repeat workup revealed the presence of concomitant cerebral saltwasting. She was then treated with fludrocortisone and sodium chloride supplementation. Careful monitoring of her serum sodium levels and overall fluid balance allowed close titration of the Desmopressin, fludrocortisone and sodium chloride supplementation. She was eventually weaned off treatment and discharged well with normal sodium levels and with no neurological deficits.

This case highlights the difficulty encountered in managing concomitant cerebral salt wasting and diabetes insipidus in critically ill neurosurgical patients and the need to for a high index of clinical suspicion, early intervention and close monitoring.

Levetiracetam is a commonly used antiepileptic drug (AED) used to treat epilepsy. This agent was approved by the FDA in 1999, is available in oral and intravenous formulations, and offers advantageous pharmacokinetics, minimal drug interactions, and a favorable side effect profile. The purpose of this case report is to describe a case of severe, asymptomatic rhabdomyolysis exacerbated by levetiracetam administration.

The medical record was reviewed and data was collected to describe a case with a pertinent review of the literature.

A 43-year-old African-American male with a history of hypertension presented to the emergency department following a tonic-clonic seizure. Baseline labs were drawn and revealed a CK level of 1,226 IU/L, negative urine myoglobin and normal renal function. Levetiracetam therapy was initiated and no further seizures were noted. The patient's CK continued to trend up throughout his stay despite aggressive fluid resuscitation with a positive myoglobin on hospital day 2. The CK reached a peak of 41,463 IU/L on hospital day 4. After a literature review and evaluation of his medication list, six casereports were identified linking elevated CK and rhabdomyolysis to levetiracetam administration. At that time levetiracetam was discontinued and the CK rapidly declined to 6,426 IU/L on hospital day 6. The patient never had muscle pain or kidney injury and was discharged on hospital day 6.

This case-report describes rhabdomyolysis associated with levetiracetam administration with a Naranjo Probability Scale score of 6 indicating a probable adverse drug reaction. The adverse effects of generalized pain and neck pain are described in the package insert with an incidence of 2-8%; however, it is not reported that CK levels were monitored. Due to the frequent use of this AED and given the rare yet serious adverse effect of rhabdomyolysis, CK levels should be monitored upon initiation.

Acute Toxic Leukoencephalopathy (ATL) is a potentially reversible disturbance to white matter caused by exposure to toxins.

We report the first case of a patient with ATL in the setting of a fentanyl overdose and reviewed the literature.

A 28 year-old man with a history of opiate abuse was found unconscious, last seen well nine hours prior.

He was known to have purchased 10mg of fentanyl that day. He was intubated and briefly required blood pressure support. He was initially hypoglycemic and suffered fulminant liver damage, acute kidney injury, rhabdomyolysis, and stunned myocardium. Comprehensive toxicology screen was positive for cannabis and fentanyl. MRI of the brain showed pronounced bilateral restricted diffusion in the high frontoparietal subcortical white matter with radiographic stability five days later. He remained intubated and neurologic exam poor with fluctuating brainstem reflexes and posturing despite improvement in end-organ function. ATL has been reported in a 19-month-old girl and an 85-year-old man with exposure to transdermal fentanyl, both of whom had favorable outcomes (2,3). One case has been reported following oral oxycodone ingestion (11). Of 27 cases of ATL secondary to inhaled heroin, 48% were fatal (5). Preferential white matter injury has been seen in cases of hypoxic ischemic encephalopathy (HIE) (7,10). It was initially thought to be secondary to Wallerian degeneration following grey matter damage, but post-mortem pathology has shown direct insult to axons (6). ATL has been reported in one case of hypoglycemic coma (8) and one case of uremia (9). It has never been reported in isolated hepatic encephalopathy, secondary to seizure, or with cannabis use alone.

Based on our review of the literature, the most likely causes of this patient's ATL are fentanyl or HIE. Fentanyl should remain on the differential as a previously unreported cause of ATL.

Autonomic dysregulation is a common complication of acute spinal cord injury (SCI). Subsequent hypotension may worsen central nervous system injury as well as neurologic and mortality outcomes. To help mitigate this occurrence, consensus guidelines recommend maintaining patients' mean arterial pressure (MAP) >85 mmHg within the first seven days based on evidence from limited clinical trials. Limited data exists describing the use of midodrine, an alpha-1 agonist and the previously only available enteral vasopressor, for blood pressure (BP) augmentation in this setting. The use of midodrine is limited by cardiovascular side effects such as bradycardia. Droxidopa, a novel enteral precursor of norepinephrine that works independently of the central nervous system, may serve a role in sustaining MAP in acute SCI.

We describe a novel case of droxidopa use in a 64-year old male who sustained a spinal cord contusion secondary to severe stenosis at the fourth cervical vertebrae following a ten-foot fall. Droxidopa was used to facilitate vasopressor wean in the setting of neurogenic shock as a complication of acute spinal cord injury. To sustain adequate CNS perfusion (MAP goal >65-85 mmHg) and facilitate patient transfer to a lower level of care, droxidopa 100 mg three times daily was initiated after five days of continuous infusion of intravenous norepinephrine. Daily assessments of hemodynamic parameters were performed, including blood pressure, heart rate, MAP, and an electrocardiogram.

Successful wean of norepinephrine was achieved within 24 hours of droxidopa initiation, with an average MAP sustained above 65 mmHg. The patient was transferred to a lower level of care within 72 hours of droxidopa initiation. No cardiovascular side effects were observed.

Droxidopa was well tolerated and facilitated transition from norepinephrine infusion to an enteral option. Droxidopa may be a viable option in stable neurocritical care patients who require vasopressors to sustain adequate CNS perfusion.

Traumatic brain injury is acute and sometimes rapidly aggravated during or after surgical treatment. Imaging study is most important and Computed Tomography (CT) is the golden standard in TBI. However the patient should be transfer to CT room or relatively high cost mobile CT scanner may be used. Ultrasound is not expensive and also does not produce radiation exposure. We studied the effectiveness and advantages of intra-operative ultrasound examination in traumatic brain injury patients

Intra-operative ultrasound was used after decompression of injured brain from June 2016 to April 2017. The Ultrasound device was the Affiniti 50 (Philips Ultrasound Inc, USA) and 2.5 Mhz transducer was used. The transducer was covered by thin transparent sterilized vinyl with ultrasonic gel with aseptic manner. To protect brain injury by the ultrasonic probe, a saline soaked gauze was applied on the cerebral cortex. The axial images were captured and then stored in PACS system promptly. Ultrasound images were compared to postoperative CT scan.

There were 13 male and 2 female patients were examined by ultrasound during there surgery. Ipsilateral hemisphere, especially cortical layer was slightly distorted to identification. Brain stem area was visible in most cases. Contralateral hemisphere was seen in unilateral craniotomy and craniectomy cases. In bilateral craniectomy cases, both hemispheres were observed well. Parenchymal hemorrhage was also identified and confirmed for removal using ultrasound. In severe brain swelling cases, arachnoid space was seen increased echogenicity. Ultrasound image was compared to postoperative CT scan.

Intra-operative ultrasound is effective in real time inspection of brain during surgery and may helpful detect opposite or parenchymal hemorrhage before closure and leaving operation room.

To describe a rare case of a varicella zoster virus (VZV) meningitis with progressive multiple cranial nerve deficits in the absence of cutaneous zoster rash.

A young woman with idiopathic thrombocytopenic pupura on steroids presents with horizontal diplopia in the setting of seven days of intractable headache. She had no meningeal signs, fever, leukocytosis or cutaneous rash. Within three days into hospitalization, she developed bilateral CN VI, CN III, right CN V and right CN VII palsies in a progressive fashion.

CSF analysis revealed cell count of 1,146/mm3, a protein of 202 mg/dL and glucose 8 mg/dL. Cytology, tuberculosis, bacterial and fungal cultures, ACE and HIV testing were negative. VZV-DNA was detected in CSF in high titers VZV Quant: 3.9million. Contrasted brain MRI revealed mild diffuse leptomeningeal enhancement in the basilar region. She recovered almost all cranial nerve function within 10 days of treatment with acyclovir and high dose steroids.

A diagnosis of polyneuritis cranialis with zoster sine herpete (ZSH) was made given PCR positive VZV-DNA in CSF. VZV reactivation with a wide array of neurological deficits can present without rash making diagnosis challenging. ZSH should be in the differential for acute cranial nerve deficits as prompt treatment with acyclovir can lead to rapid recovery.

Stress-induced cardiomyopathy or neurogenic stunned myocardium is a well-documented cardiac complication following aneurysmal subarachnoid hemorrhage (SAH). Onset is usually immediate, within hours after aneurysm rupture, and is characterized by left ventricular dysfunction with pulmonary edema and elevation in cardiac biomarkers. This can often be mistaken for an acute myocardial infarction or ischemia. The pathogenesis appears to be the result of elevated catecholamine levels following injury leading to myocardial contraction band necrosis and cardiac dysfunction. This syndrome occurs more commonly in patients with severe or "high-grade" SAH.

We review a case of delayed cardiac dysfunction coinciding with the onset of vasospasm.

A 52-year-old female presented with a H&H3, mF4 SAH. She appeared to have lost consciousness prior to arrival and was reporting worst headache of life. She had an EVD placed upon arrival with opening pressure at 27. She underwent endovascular coiling of a ruptured aneurysm of her anterior communicating artery aneurysm. Initial echocardiogram demonstrated normal wall motion with EF of 63%, and minimal troponin I elevation at 0.04 ng/mL. On post-bleed day 10 the patient became more somnolent and developed chest pain with an ECG demonstrating ST-elevation in all anterolateral leads concerning for ACS. She was taken for cardiac catheterization where she had non-obstructive vessels with no vasospasm seen. Her EF was reported at 25-35% with apical ballooning present. Her repeat echocardiogram also demonstrated a new apical akinesis with EF 45%, and troponin peaked to 16 ng/mL. Her TCDs at the time were suggestive of vasospasm with bilateral LR >3, but no focal deficit present.

It appears that regardless of timeline, stress-induced cardiomyopathy or neurogenic stunned myocardium occurs after sympathetic or catecholamine surge and may occur after the onset of vasospasm in patients with aneurysmal SAH.

The rapid neurological assessment of critically ill patients with neurologic disease is paramount when determining a course of action. Neuromuscular blockade is often used during critical care transport and in the emergency department. Unfortunately, this can delay examination and assessment leading to unnecessary testing and procedures. Historically, neuromuscular blockade reversal was accomplished using a combination of neostigmine and glycopyrrolate. However, this can lead to incomplete reversal and unwanted side effects from these medications. Sugammadex is a cyclodextran injectable compound that has been FDA approved in the United States since 2015 for rapid reversal of rocuronium induced neuromuscular blockade. Sugammadex works by forming a complex with rocuronium and rendering it unable to bind to nicotinic cholinergic receptors at the neuromuscular junction. Sugammadex can reverse neuromuscular blockade without the unwanted side effects of cholinesterase inhibitors.

This is a case report of the successful use of sugammadex to reverse the effects of neuromuscular blockade in an intracerebral hemorrhage patient.

A 77 year old male with a history of atrial fibrillation and a supratherapeutic INR presented via aeromedical ambulance with a 63 mL left frontal intracerebral hermorrhage causing a 10mm midline shift. He received a 100 mg bolus of rocuronium prior to arrival and had a GCS of 3 upon presenting to the Neurosciences ICU. A train-of-four revealed 0/4 twitches. He was given 4 mg/kg of sugammadex with a return of 4/4 twitches within 30 seconds. A more accurate neurological examination was then obtained demonstrating that his brainstem reflexes were intact, he could open his eyes spontaneously and reacted purposefully to painful stimulation. This allowed a non-operative course to be taken.

Sugammadex can reliably and quickly reverse neuromuscular blockade allowing for the immediate assessment of the neurocritical care patient. It is a useful tool with minimal side effects.

Piperacillin-tazobactam is commonly deployed as empiric antibiotic therapy. Piperacillin-induced hematologic laboratory test abnormalities were rare in pre-marketing studies, and whether these alterations are of clinical significance has been studied little. Aberrations in platelet function have not been implicated.

In the present case, we discuss a patient presenting with hypertensive intracerebral hemorrhage (ICH) who sustained two additional hemorrhages in distinct locations after routine removal of intracranial monitors and an external ventricular drain (EVD). These significant bleeding events occurred exclusively during piperacillin-tazobactam therapy and were correlated with new abnormalities in the patient's platelet function assay (PFA) results.

A 55-year old Vietnamese male with hypertension presented for treatment of a left basal ganglia ICH. Epinephrine/collagen and adenosine diphosphate/collagen PFAs at the time of EVD and quad-lumen bolt placement were normal, and imaging showed no hemorrhage after placement. Hospital course was complicated by aspiration pneumonia requiring empiric piperacillin-tazobactam administration. After removal of the quad-lumen bolt and EVD on separate days, both follow-up CT scans showed new hematomas in the devices' tracts, with significant intraventricular hemorrhage. Repeat PFAs were abnormally prolonged, representing a distinct change from baseline. A trend toward normalization of PFAs was observed after discontinuation of piperacillin-tazobactam with progression toward baseline thereafter.

The present case is unique in that the significant bleeding that occurred was attributable to objectively confirmed platelet dysfunction rather than thrombocytopenia. Other possible innate causes of bleeding were less likely as the patient demonstrated normal platelet count, von Willebrand multimers, platelet morphology, and clotting factors. This is the first reported case of intracranial (periprocedural) hemorrhage potentially related to piperacillin-tazobactam; further research into this drug's impact upon qualitative platelet function is needed.

The life-saving potential of extracorporeal membrane oxygenation (ECMO) has been well recognized since the 1960s. Modern advancements of research and technology have allowed ECMO to be accepted as a dependable intervention for patients with severe pulmonary or cardiac failure. However, with increased use, associated complications that detract from the benefit of ECMO are surfacing as well. This case report describes a case of diffuse intracerebral hemorrhage (ICH) after prolonged ECMO resulting in cerebral edema, mass effect, and eventual brain herniation.

The patient is a previously healthy 19 year old female who presented with fever, chills, and myalgia. When evaluated at urgent care, she was noted to be hypoxic and was sent to an outside hospital where her Monospot test was positive. Upon arrival, the patient was placed on venovenous ECMO (VV-ECMO) due to severe hypoxia. She was also in acute renal failure requiring continuous renal replacement therapy (CRRT). She had an episode of hypotension with bradycardia. Subsequently, her pupils were noted to be fixed and dilated. A stat CT head then showed diffuse bilateral hemorrhages at the graywhite junction as well as diffuse edema. Labs showed thrombocytopenia likely due to disseminated intravascular coagulation (DIC). Her exam was consistent with brain death.

It has been estimated that up to 90% of patients who were placed on ECMO as a last resort for respiratory failure have neurological complications including ICH. There is no stereotypical pattern of bleeding but diffuse hemorrhage has been seen, which is consistent with the pattern seen in our patient. Notably, those with ICH have significantly higher rates of mortality. Thrombocytopenia, DIC, and platelet dysfunction that develop as a result of ECMO are thought to play a role in the development of ICH.

To present a case report of syndrome of the trepheined (SoT) and paradoxical herniation without craniectomy. SoT is reported when a constellation of positional neurological symptoms arise following large craniectomy, resolving in a delayed fashion following cranioplasty. Paradoxical herniation may occur in extreme cases.The pathophysiology is incompletely understood however proposed mechanisms include compression of underlying brain by the flaccid skin flap due to the gradient between atmospheric and intracranial pressure exacerbated by upright pressure, changes in cerebral blood flow, and CSF fluid.

A middle aged woman with a history of mood changes eight months preceding admission presents with worsening left hemiplegia over one week. MRI revealed a 78 x 44 mm right frontal cystic mass. Hyperosmolar therapy and steroids were initiated for midline shift and brainstem compression. Her immediate post operative course after tumour excision was uncomplicated. On post-operative day two, she developed uncontrolled hypertension, worsening anisocoria, and decerebrate posturing requiring urgent intubation.

Head CT revealed uncal and subfalcine herniation despite a large resection cavity. An external ventricular drain was placed and removed due to lack of drainage. Within 12 hours of Trendelenburg positioning, she improved both clinically and radiographically. She did not undergo an intraoperative CSF reduction and no preadmission history (back pain, orthostatic headache, trauma) to support an occult CSF leak. She had a recurrence of symptoms on post-operative day eight which also resolved upon lying flat for 48 hours. She was ultimately discharged to acute rehab and tumor pathology returned as glioblastoma (WHO grade 4).

This novel case of SoT in the absence of craniectomy demonstrates the complex and poorly understood consequences of slow growing massive tumors, CSF dynamics and exertional force on static CNS structures. This case also illustrates the benefits of a collaborative, multidisciplinary approach to patient care in the NeuroICU.

To present a lesser known leukoencephalopathy that occurs when patients overdose on inhaled heroin vapor

'Chasing the dragon" is a method of inhaled heroin vapor that is different from smoking or snorting heroin. Heroin powder is placed on aluminum foil, which is heated by placing a flame underneath. The white powder turns into a reddish-brown gelatinous substance that releases a thick, white smoke, which resembles a dragon's tail. The fumes are "chased" or inhaled through a straw or small tube. Currently the US is facing a growing epidemic of heroin use making this leukoencephalopathy more pronounced.

A 34-year-old female with history of drug abuse presented to the emergency department with altered mental status. The boyfriend informed staff that she likely smoked heroin. On arrival, she was drowsy but easily arousable. Her brainstem reflexes were intact but she was grossly dysmetric. Urine drug screen was positive for opiates only. Initial CT of the brain demonstrated extensive loss of gray-white differentiation within the cerebellar hemispheres and bilateral lucency in the globus pallidus and developing hydrocephalus. Patient was placed in the neurointensive care unit to monitor and was managed medically with hypertonic therapy to combat her cerebral edema. An MRI was done which demonstrated a distinctive pattern of symmetrical white matter T2 hyperintensities in the cerebellum, hippocampus and internal capsule bilaterally characteristically known as "chasing the dragon" sign. The patient gradually improved with supportive treatment, but continued to have mild ataxia upon discharge.

We present a case of leukoencephalopathy that was generally rare to see, but now that heroin use is now at a 20 year high within the US, this phenomenon may become more prominent. Heroin inhalation leukoencephalopathy should be suspected in all patients with a history of chasing the dragon when they present with neurological abnormalities.

The use of intra-venous (IV) thrombolysis for the treatment of acute ischemic stroke is now the standard of care. This is typically followed by endovascular thrombectomy if patient is eligible does not improve . We present a rare acute ischemic posterior circulation stroke that had progression of the stroke despite receiving both intra-venous thrombolysis and endovascular thrombectomy.

Case Report: A 38 years old African-American gentleman with past history of obesity, sleep apnea and prostatic hyperplasia, presented with acute onset left hemiparesis, with limb ataxia, who then progressed to altered sensorium in the Emergency Room needing endotracheal intubation. His initial NIHSS was 10. He was given IV thrombolysis, with subsequent vascular imaging that showed a top of the basilar clot, that was removed via endovascular intervention. A sister and one of the aunts reported a history of 'clots' when asked about family history. Despite initial improvement, the patient deteriorated clinically after about 14 hours from symptom onset, and was found to have extension of stroke into the brainstem, with simultaneous acute loss of brainstem reflexes . The patient was started on palliative withdrawal of care by the family about 2 days from the initial onset of symptoms. His thrombophilia work-up revealed later that he was homozygous for Methylenetetrahydrofolate reductase (MTHFR) gene mutation, 677C >T.

This case with a poor outcome due to extension of the ischemic stroke despite receiving the standard of care therapy, highlights the need for considering the use of anticoagulation within 24 hours postthrombolysis and thrombectomy in cases with underlying thrombophilia. The current guidelines do not support this aggressive approach. There is a dire need for randomized controlled trial about such cases to provide evidence based care to avoid a repetition of a similar poor outcome.

Barbiturate therapy has shown benefit in reducing intracranial pressure (ICP) in patients who are refractory to other treatment modalities. However, severe adverse drug effects can accompany barbiturate use when used at the high doses required for ICP management, such as hypotension, hepatic/renal dysfunction, and infection, among other deleterious consequences. Dyskalemia has been reported infrequently in the literature with most of the cases involving patients on thiopental. There remains little guidance for management of this adverse effect. We present a case of severe dyskalemia induced by high-dose pentobarbital therapy and experience with management of this rare but life threatening effect.

The patient was a 26-year-old male with traumatic brain injury and subdural hematomas complicated by refractory ICP elevations. After hyperosmolar therapy, sedation, and CSF drainage failed to control ICP, and he was deemed to not be a candidate for surgical decompression, high-dose pentobarbital was started. After initiation of pentobarbital, his initial potassium of 4.0 mmol/L decreased to a nadir of 1.9 mmol/L over the next 24 hours despite aggressive repletion with a total of 600 mEq of oral and intravenous potassium chloride. Upon down-titration and discontinuation of pentobarbital, the serum potassium rapidly rebounded to 8.3 mmol/L with ST-segment elevations on EKG. Pentobarbital was restarted in an attempt to stabilize escalating ICPs and elevated serum potassium. Subsequently a slow taper was utilized to mitigate dyskalemia during barbiturate discontinuation.

Dyskalemia associated with high-dose barbiturate therapy presents a significant dilemma to practitioners as both severe hypo-and hyperkalemia can be life threatening. Published literature provides little guidance on how to safely manage patients who experience this adverse effect. Patients receiving barbiturate therapy should have frequent potassium monitoring especially in the initiation and discontinuation phases. Potassium repletion should be approached with caution, especially preceding discontinuation of barbiturate therapy.

Diffuse astrocytoma (formerly known as 'Gliomatosis cerebri') may present with seizures or symptomatic raised intra-cranial pressure. This is typically followed by a few months of relatively stable phase (with treatment) and then possible subsequent development of Glioblastoma multiforme. We present a rare case of a previously healthy Caucasian lady who had new onset seizures, that showed glioblastoma multiforme already present on a background of diffuse astrocytoma.

Case report: A 65 years old Caucasian lady with no significant past medical history was admitted with new onset focal seizures with secondary generalization, needing intubation and Propofol for airway protection. Brain imaging showed left frontal ring-enhancing mass, with a smaller satellite lesion in the left insular cortex, on a background of diffuse infiltrative lesion involving left fronto-temporal lobe and a smaller area of right parafalcine frontal lobe. Biopsy of the left frontal mass revealed it to be Glioblastoma multiforme. This is a rare situation when a previously healthy patient presents with new onset seizures and already has Glioblastoma multiforme on a background of diffuse astrocytoma (or 'Gliomatosis cerebri'). Her post operative imaging revealed disease progression with increase in the size of the left insular cortical lesion. She was discharged home with plan for radiotherapy and chemotherapy.

Diffuse astrocytoma with Glioblastoma multiforme within can remain asymptomatic till late in the disease course.

Diffuse astrocytoma (or 'Gliomatosis cerebri') is a rare disease and even more rare is to have this remain asymptomatic till the development of Glioblastoma multiforme within. This particular case highlights the need for vigilance about such a possibility, as this aggressive brain tumor carries a grave prognosis, especially when it develops on background of a diffuse astrocytoma.

Subdural hygromas (SDG) are cerebral spinal fluid collections in the subdural space that may occur following trauma. Decompressive craniotomy may increase the risk for acute SDG or other forms of external hydrocephalus along the surgical plane. While these are traditionally benign and resolve spontaneously, they may in rare cases cause clinical deterioration. We report three cases.

Cases 1 and 2 were alcoholic men aged 54 and 69, respectively, who suffered severe traumatic brain injury (TBI) following falls while intoxicated. They had early clinical deterioration prompting emergent hemicraniectomy for left-sided SDH with midline shift (MLS). Case 1 clinically worsened on postoperative day (POD) 6 with posturing, decreased pupillary responses, and new-onset seizures. New bilateral, extensive subdural hygromas were noted, enlarging over serial CT scans up to 1-cm with progressive mass effect. Uncal herniation and downward brainstem displacement occurred by POD8 despite external ventricular drainage. Case 2 deteriorated on POD4 with fluctuating exam and newonset seizures. Imaging revealed new subgaleal fluid collection measuring 1.8-cm and a contralateral SDG. On POD8, hemicraniectomy was performed for new MLS from enlarging fluid and hemorrhage in extradural component. Both died shortly after withdrawal-of-care. Case 3 was a 68 year-old man with dural arteriovenous fistula who presented with spontaneous left-sided SDH and underwent left hemicraniectomy. On POD3, he had new-onset seizures and new bilateral SDG measuring 1.5-cm on the left and 0.5-cm on the right without mass effect. Two days later; the right SDG grew to 2.8-cm causing significant mass effect. He recovered after burr-hole evacuation and temporary subdural drain placement.

SDG following SDH evacuation can have a malignant course, causing clinical deterioration without prompt recognition and CSF diversion. All patients had large volume SDH and two were alcoholic; larger prospective cohorts are required to identify risk factors. Seizures may be an early clinical sign.

Moyamoya disease is an intracranial vasculopathy that results in stenosis of bilateral internal carotid arteries with subsequent development of extensive collateralization. The diagnostic criteria for moyamoya disease are well established and generally accepted, yet reaching the diagnosis can be challenging in some cases. Herein, we present an unusual case of progressive cerebral vasospasm triggered by pituitary apoplexy that led to a delay in the underlying diagnosis of moyamoya disease.

Case report.

A 53-year-old female with hyperlipidemia presented to the emergency department with a bifrontal headache, right-sided weakness, and dysarthria. CT angiogram showed extensive multifocal narrowing of the bilateral supraclinoid ICAs, proximal ACA/MCAs, and posterior circulation. MRI brain revealed a left insular stroke as well as a sellar mass with a central hemorrhagic component. MR perfusion demonstrated decreased perfusion in the right hemisphere. Lumbar puncture and extensive vasculitic workup was unremarkable. Endocrine studies were notable for elevated prolactin with low FSH and LH levels. Despite protracted blood pressure augmentation strategies, the patient continued to experience progressive infarcts in the left MCA/ACA territory. Repeat CT angiogram showed progression of vasculopathy, and transcranial Doppler studies demonstrated worsening vasospasm of the right MCA and left PCA arteries. The patient received corticosteroids given concern for apoplexy, and was maintained on aspirin and verapamil. Given the aggressive nature of her vasculopathy, the patient underwent conventional angiography two weeks later, which revealed bilateral Suzuki grade III moyamoya. Following this diagnosis, she received bilateral STA-MCA bypass surgeries.

It is important to revisit the differential diagnosis of cerebral vasospasm when the clinical course does not conform to expectations. This case highlights moyamoya as the causative agent in progressive vasculopathy likely masqueraded by pituitary apoplexy and concomitant vasospasm. Moyamoya is an important diagnosis to consider in patients with a fulminant vasculopathy refractory to traditional treatment of vasospasm.

Visualization of intracranial structures by ultrasound in adults is limited by the presence of skull, though ultrasound imaging can occur through temporal windows. Point of care ultrasound allows assessment of midline shift, brainstem, and ventricles. Doppler allows visualization of cerebral perfusion patterns.

Patients with a hemicraniectomy have better temporal windows available since a portion of their skull has been removed. In such patients, ultrasound can provide a non-invasive method to serially assess midline shift, intracranial hematomas, and focal ischemia at the bedside.

We present images of a cranial ultrasound that shows remarkable anatomical details that correlate well with computed tomography (CT) head.

A 74 year-old male presented with right-sided weakness and confusion and was found to have a left parietal intraparenchymal hemorrhage with cerebral edema and left-to-right midline shift on CT head. Increase in cerebral edema and expansion of the hematoma caused clinical neurological decline necessitating a left-sided hemicraniectomy with clot evacuation. A cranial ultrasound was performed two days after surgery to assess for progression of cerebral edema and intracranial hemorrhage. A transtemporal approach in axial plane was used to visualize intracranial structures through the craniectomy window. Physiological structures like the falx cerebri, lateral ventricles, midbrain, mammillary bodies, choroid plexus, splenium of corpus callosum, thalami, and circle of Willis were visualized with incredible anatomical detail. Pathology such as intracranial hemorrhage, focal ischemic areas, vasogenic edema as well as encephalomalacia were identified with close correlation to the noncontrast head CT. The patient is currently recovering in the neurocritical care unit with supportive care.

Cranial ultrasound has potential applications in point of care assessment of intracranial pathology in neurocritical care patients. This application has promising use in directing therapy in patients who are otherwise unstable for transport or are unable to undergo neuroimaging secondary to positioning needed for management of cerebral edema.

Cerebral mucormycosis is a rare infection caused by fungi found in soil and decaying vegetation. The rhino-orbital-cerebral type is classically associated with AIDS, diabetes, malignancy and immunosuppression. We observed a series of young immunocompetent patients who presented with a fulminant form of isolated cerebral mucor associated with severe meningoencephalitis, parenchymal necrosis and symptomatic cerebral edema.

Six patients with histopathological diagnosis of CNS mucormycosis admitted to the University of Cincinnati Neurocritical Care Unit between 2008 and 2017 are presented.

Patient ages ranged from 22-45 (median 27). None had diabetes or HIV. Drug use (intravenous and intranasal) was confirmed in 4 patients. They presented with altered mental status (2) and focal neurologic deficits (4). Four patients presented with fever and leukocytosis. MRI revealed lesions in the basal ganglia (5) or cerebellum (1) which were characterized by T2 hyperintensities with patchy restriction and susceptibility signal. Contrast enhancement was present in 5 patients. Mass effect (6) and midline shift (4) were prominent. Mechanical ventilation was required in four patients. All but one patient received Amphotericin B. Three died from intractable intracranial pressure (ICP). One patient eventually gained functional independence, one still requires high level of care, and one was lost to follow-up. CSF analysis was negative for mucor in all cases.

Fulminant Cerebral mucormycosis should be considered in every young patient presenting with rapid onset meningo-encephalitis and necrotized cerebral lesions, especially if located in the basal ganglia. History of IVDU should raise further suspicion. These patients should be monitored in intensive care settings as they can rapidly develop malignant cerebral edema and increased ICP. Antifungal therapy should be initiated upon presentation as it has been shown to improve morbidity and mortality.

The incidence of acute ischemic stroke in the immediate post-partum period ranges between 4-18% and is considered a serious cause of morbidity and mortality. Pregnant or postpartum women are less likely to receive IV tissue plasminogen activator (tPA) primarily because of pregnancy, ongoing peripartum bleeding and/or recent delivery. The FDA classifies tPA as a category C drug and current recommendations consider pregnancy a relative contraindication for receiving tPA.

We present two cases of peripartum ischemic strokes with varying ischemic stroke time windows requiring aggressive revascularization therapy (endovascular and pharmacologic).

A 32Y G2P2 presented to an outside hospital 12 days post-partum with new onset of facial droop and left upper extremity weakness (NIHSS 6). Imaging showed right M1 cutoff and occlusion of several M2 branches. The patient was not a candidate for tPA given ongoing vaginal bleeding. The decision was made to proceed with mechanical thrombectomy when her exam worsened to NIHSS 12. The thrombectomy was successful with TICI 2C reperfusion. She was discharged home 4 days later with a NIHSS of zero. A 30Y G1P1 presented 4 days post-partum with new onset of left facial droop and slurred speech (NIHSS 2). Imaging showed right M1 cutoff with reconstitution, but with significant associated penumbra. Acute worsening of exam post tPA triggered a push for mechanical thrombectomy achieving a TICI 3 recanalization. Post procedure the patient's only symptom was decreased sensation in left fingertips. At 30-day follow up the patient had returned to her baseline with a NIHSS of zero.

Endovascular and pharmacologic revascularization therapy should be considered on an individual basis in the peripartum population. Current literature is limited to case reports /case series. Larger multicenter trials are warranted and anticipated in the near future.

While the optimal duration of burst suppression for status epilepticus (SE) has not been established, burst suppression poses significant morbidity that may be dependent on the amount of time spent in burst suppression. Herein, we report a case of SE that resolved after ultra-short burst suppression.

Case report.

A 74 year-old female was admitted to the neuro-intensive care unit after experiencing several brief tonic-clonic seizures characterized by right-sided shaking and left-sided head turn. Despite lorazepam and levetiracetam administration, the patient did not return to baseline and was transferred to our unit. On presentation, her workup revealed a leukocytosis and a glucose level > 300 mg/dL. Lumbar puncture showed a mild pleocytosis for which broad spectrum antibiotics were initiated. On initial examination, she was unresponsive and was not following commands. Electroencephalogram (EEG) demonstrated frequent sharp and slow discharges in the right posterior quadrant with generalization (~20 seizures/hour) with minimal improvement following levetiracetam and phenytoin administration. Given the refractory nature of seizures, the patient was intubated and treated with general anesthetics. Using Propofol, burst suppression was achieved (consisting of 1-2 s bursts with intermixed suppressions) and was continued for < 2 hours. Following weaning, the patient had no further evidence of seizures, and EEG showed lateralized periodic discharges in the right occipital lobe. MRI did not demonstrate an occipital focus, but did reveal cortical diffusion restriction in the bilateral posterior hemispheres. The patient was extubated the following morning, and was transferred to the neurology floor two days later.

This case provides evidence that in certain situations, relatively brief periods of burst suppression in SE can serve as a "reset switch", allowing for resolution of seizures while minimizing toxicities associated with prolonged burst suppression. Further studies to determine which patients may benefit from ultrashort burst suppression are warranted.

There are two systems of facial control, voluntary and emotional; these are independent up to the level of the facial nucleus. We described a case of a patient who presented with isolated emotional facial palsy after intracerebral hemorrhage (ICH).

Retrospective review of a case admitted to the Neurocritical Care Unit (NCCU) of the Johns Hopkins Hospital.

A 29 year-old woman with history of migraines who presented to the emergency room after a colleague noticed she was not moving the left lower side of her face when she smiled. Head CT showed a large right frontal ICH involving the medial frontal lobes and anterior thalami. On review of an old MRI done, an underlying developmental venous anomaly with an associated cavernoma was seen. Her exam was notable for a flattened emotional affect, no facial palsy when asked to activate on command, but a facial droop that occurred in the context of her smiling to jokes and other humor. Her NCCU course was complicated with significant brain edema requiring osmotherapy up to 3 weeks out from the initial insult with self-limited episodes of brain herniation characterized by extensor posturing, dilated pupils, hypertension, hyperventilation and tachycardia. These were initially dismissed as sympathetic storming vs seizures as she will come out of those to her baseline (awake with mild left sided weakness) many times without therapy. She eventually required a hemicraniectomy two weeks after presentation.

Conclusions solated emotional facial palsy can be the presenting sign after ICH when the hemorrhage involves the contralateral thalamus, of the striato-capsular region or the medial frontal lobes. In this case, transient ICP elevations were leading to dilated pupils, tachycardia and hypertension -highlighting that heart rate changes can be variable with elevated ICPs and that in young patients, brain herniation episodes can be self-resolved with hyperventilation.

18 yo female with no PMH developed fever, headache, and neck pain. She presented to outside hospital day 2 after CT head was negative, patient was discharged. Symptoms did not improve and she went to her PCP on day 4 and was instructed to go to the ED. She presented to OSH and underwent a LP that was indicative of viral meningitis with WBC 357 cells/mm3 and protein 215 mg/dL. Patient admitted and treated with Acyclovir. On day 6, she developed generalized body aches. On day 8, she was trying to stand with assistance and she became rigid. Parents report a total of 4 seizures and was intubated for airway protection. She underwent another LP on day 8 with an opening pressure of 55 cm H2O. CSF was sent for paraneoplastic panel. CSF analyses and blood cultures were negative. EVD placed for ICP pressures of 30-34 cm H2O. History obtained from mother and father who reported the patient had been hiking 2 weeks prior.

Results MRI brain showed meningeal enhancement scattered throughout the supratentorial and infratentorial brain and most compatible with inflammatory sequela of meningitis. Patient continued on keppra, high dose steroids, antibiotic, antiviral, antifungal therapy until cultures resulted. Additional treatments included IVIG therapy followed by plasmapheresis, and finally Rituximab. Continued workup with brain biopsy showed demyelinating process and possible necrotizing encephalitis. MRI four weeks after initial presentation showed white matter demyelination and deep gray nuclei lesions consistent with ADEM. FOUR score of 0 on admission improved to 11 (E3, M0, B4, R4) 5 weeks after patient presented from OSH. Diagnosis of ADEM vs MS variant made based on the above data.

Case provides information for the clinician diagnosing and treating ADEM. Potential for further studies with treatments described above and their effect on meaningful neurological outcomes.

Dengue is a flaviviruses transmitted via mosquitos and prevalent in South East Asia. Neurological complications are rare but can involve encephalitis, myelitis, neuromuscular dysfunction and neuroophthalmological problems. We describe an interesting case of dengue encephalomyelitis.

Retrospective review of a case admitted to the Neurocritical Care Unit (NCCU) of the Johns Hopkins Hospital

A 54 year-old ship Filipino captain with no significant past medical history but an extensive exposure to heavy metals, travel throughout the Pacific, who presented with progressively worsening fevers, encephalopathy, urinary retention and tremors. He was transporting iron ore and other metals in a cargo ship from Russia through South-East Asia through to Bermuda. While passing through the Pacific, he began to experience malaise, myalgia, and fever. He was treated with Amoxicillin but became worse, developing urinary retention, periods of confusion, and word finding difficulties. He was initially hospitalized in Bermuda and then transferred to our hospital for further workup. Given his rapid deterioration, he was initially in the NCCU. His exam was notable for mild expressive aphasia, paratonias, right-sided weakness with hyper-reflexia, and a low amplitude tremor. His CSF was notable for lymphocytic pleocytosis, elevated protein, low glucose. MRI Brain showed flair hyper-intensities in the frontal lobes, and diffusion restrictions in the bilateral basal ganglia and thalami. MRI spine showed extensive flair hyper-intensity lesions. An extensive workup evaluated for heavy metal toxicities, autoimmune disorders and infectious workup. CSF analysis came back positive for Dengue IgG and IgM, leading to a diagnosis of acute Dengue fever and encephalomyelitis. With supportive care in the NCCU, he improved considerably over 2-3 weeks and was discharged home to the Philippines.

Dengue encephalomyelitis is a rare infection but should be considered in patients living in endemic areas. Treatment includes supportive care with fluid resuscitation, neurological monitoring and monitoring for hemorrhage.

Posterior Reversible Encephalopathy Syndrome (PRES) is known to cause altered mental status and leukoencephalopathy in the setting hypertensive emergency.

We present a novel case of severely asymmetric PRES due to a concurrent right transverse sinus dural arteriovenous fistula (dAVF).

A 53 year-old woman with hypertension, non-compliant on medication, had fatigue and 2 weeks of intermittent left sided weakness when she presented to an outside hospital for evaluation. Initially upon arrival her Glascow Coma Scale (GCS) was 14. Her mental status deteriorated over 6 hours, eventually requiring intubation. Her peak blood pressure was 269/147. Outside CT demonstrated scattered intracerebral hemorrhage (ICH) and she was transferred for higher level of care. On admission her GCS was 4. Review of her outside CT was remarkable for extreme right-sided white matter hypodensity, moderate left white matter hypodensity, and small scattered ICH. Workup including infectious, inflammatory, and neoplastic processes were excluded through serum, CSF studies, and MRI. Conventional angiogram demonstrated a right transverse sinus dAVF with reflux into cortical veins, which was subsequently embolized. Her white matter T2-weighted hyperintensities improved on follow-up MRI, and her GCS was 11 at the time of discharge.

Our case highlights the possibility of asymmetric PRES due to abnormal venous congestion due to the right-sided dAVF. Venous hypertension likely caused the patient's intermittent left sided symptoms in the weeks prior to admission. Few cases of unilateral or asymmetric PRES have been reported following induced hypertension for treatment of subarachnoid hemorrhage or in the setting of vascular malformation. To our knowledge, this is the only case of severely asymmetric PRES and preceding stroke like symptoms due to a dAVF.

The most common pathology associated with an intraluminal carotid thrombus is underlying atherosclerosis. In rare cases it may be associated to thrombocytosis. Currently there are no clear recommendations for the treatment of ischemic stroke associated with thrombocytosis. Our case describes the use of plateletpheresis for the acute management of thrombocytosis complicated by an internal carotid artery thrombus resulting in a right MCA stroke.

A 55-year-old female with past medical history of menorrhagia who presented complaining of left face, arm and leg weakness with associated shortness of breath. Upon arrival her NIHSS was 1 and the initial head CT was unremarkable. Laboratory results revealed a hemoglobin 8.2 mg/dL, hematocrit 30 mg/dL, and platelet count of 1014 x 103/mL. She was not a candidate for thrombolytic therapy due to the time window. Soon after admission she had acute worsening of symptoms with an NIHSS of 17. A CTA of the head and neck showed acute ischemic infarction involving the right MCA territory with non-occlusive intraluminal thrombus within the right carotid bulb. ASA 325 mg and heparin infusion were initiated promptly. After a thorough work-up for thrombocytosis, reactive thrombocytosis secondary to iron deficiency anemia was diagnosed. Plateletpheresis as well as oral ferrous sulfate were started. After one plateletpheresis cycle the platelet count stabilized at 400x103/mL. Complete thrombus resolution was confirmed on follow-up CTA on day 10 of admission without need for surgical revascularization.

The role for plateletpheresis is not well established in secondary thrombocytosis. In cases with extreme thrombocytosis immediate surgical thrombectomy may be contraindicated due to high risk of rethrombosis. Urgent cytoreduction with correction of the putative mechanism for thromboyctosis should be undertaken for optimal management.

Plateletpheresis is safe and efficient in reducing the platelet count to decrease the risk of clot progression or further clot formations which could worsen patient outcome.

Hyperpyrexia is an elevated core body temperature secondary to an elevated hypothalamic set temperature. Hyperthermia is an elevated core body temperature beyond the normal hypothalamic set temperature. Intracranial hypotension can present with a wide variety of symptoms ranging from orthostatic headache up to coma. It has never been reported to present with fever, namely hyperpyrexia.

A case report of a 55 year old female patient with a history of depression, diabetes mellitus, hypertension, and angiogram negative subarachnoid hemorrhage status post ventriculo-peritoneal (VP) shunt placement six years ago who was complaining of worsening headaches and slurred speech for the past three months but acutely decompensated one morning. She suddenly became confused and agitated but became obtunded. Initially, she was given Haldol. She was found to be febrile (rectal temperature of 104.8 F). She was given dantrolene and bromocriptine for suspected malignant neuroleptic syndrome with no effect. Creatine phospho-kinase was not elevated.

She underwent infectious work up which later came negative. Cooling measures like external cooling, peripheral IV cooling, Tylenol and NSAIDs were also not helpful. Fever responded to central Intravascular cooling but encephalopathy did not. Several expert attempts of LP and shunt tapping failed to obtain CSF. Brain imaging showed bilateral chronic symmetrical hygromas, diffuse pachy-meningeal thickening and enhancement, slit-like ventricles and slumping of the midbrain with closure of the mammillary pontine distance. Following shunt setting adjustment, the encephalopathy markedly improved and the fever did not recur after stopping the cooling measures and antimicrobials.

Intracranial hypotension might present with hyperpyrexia, likely secondary to hypothalamic dysfunction. In our case, hyperpyrexia was reversible as the intracranial hypotension was emergently treated. Nevertheless, spontaneous intracranial hypotension might be difficult to diagnose especially if it presented with non-classical symptoms like fever.

Complex emotions about critical illness can affect families in the ICU. Rightfully, we put focus on how they are impacted, but we also need to pay attention to how it can affect providers and our decision making.

A poignant case from my training was a 15-year-old girl struggling with lupus. She had now developed lupus cerebritis and had massive intracranial hemorrhages. Despite aggressive efforts to manage cerebral edema, she repeatedly herniated brain matter out of old craniotomy scars with incredible force. It was the most horrifying thing I've ever seen. Other organs were also failing, with four consulting services working to salvage them unsuccessfully, prompting numerous procedures. This went on for a month.

The therapies that we can offer have limits from a physiological standpoint which we must recognize and respect. We struggle with reconciling the interventions we feel compelled to implement versus what is realistic. I remembered the most valuable advice that I once received: "only do something to someone if it does The complexity of the neuro ICU is amplified by the nature of intracranial catastrophes and poor recovery (in contrast to pure medical illness). Providers cling to what is technically indicated while families cling to hope, but neither is enough and concurrently too much. We lose our autonomy to grieving families telling us to "do everything" losing sight of the bigger picture. We lose our autonomy to one another by pushing onwards, which can unintentionally push each other into the territory of doing more harm than good. something for them". All services began to share this view, thus slowly dialysis, steroids and immunosuppression stopped. Eventually, her heart stopped.

My experiences have reiterated a simple paradigm: to do no harm. Through this, I can empower myself to take control of each situation by first taking control of myself.

We report a case of an HIV positive patient who presented with Cryptococcus gattii meningitis who then developed acute respiratory distress syndrome (ARDS) secondary to Pneumocystis jirovecii pneumonia (PJP) that required ECMO support.

ARDS in immunocompromised HIV positive patients is associated with extremely high mortality. ECMO can improve oxygenation in patients without increasing alveolar pressure and therefore avoid mechanical lung damage with ventilation. We present a patient with newly diagnosed AIDS with Cryptococcus gattii meningitis and course complicated by PJP that progressed to severe acute respiratory distress syndrome (ARDS) for which veno-venous ECMO was initiated.

Patient is a 27year old male who presented to the emergency department with new onset seizures. Lumbar puncture in the ED overflowed the manometer and demonstrated WBC 62, RBC 610, protein 41, glucose 51, positive yeast gram stain positive for yeast with PCR and Ag positive. His cultures later grew out Cryptoccoccus gattii. He was admitted to the NSICU and we placed a lumbar drain and an intraparenchymal IPC monitor that demonstrated elevated ICPs to the 60-80mmH20 but improved with drainage. The day of admission he acutely desaturated and required emergent endotracheal intubation. Chest x-ray demonstrated bilateral infiltrates. BAL was positive for PJ. Five days following presentation and respiratory failure he was started on veno-venous ECMO. Two days following initiation of PJP treatment with Bactrim his chest x-rays and lung compliance began to improve. He remained on ECMO for a total of 10 days before decannulation. He underwent induction chemotherapy for four weeks for meningitis.

This case report demonstrates the use of ECMO in a complicated and critically ill patient with AIDs, PJP, and Cryptoccous gattii meningitis. To our knowledge, few cases of ARDS secondary to PJP are reported and none are reported with concurrent Cryptococcus gattii infection.

Sympathetic storming occurs during the acute care of patients following severe brain injury. Cannabinoid CB1 receptors (CB1R) mediate the effects of delta(9)-tetrahydrocannabinol (THC), the psychoactive component in marijuana. Expression of CB1R is widespread in the central nervous system and includes the hypothalamus, which is thought to mediate the hypothermic inducing effects of cannabinoids. Dronabinol is a synthetic analogue of THC

We present a novel therapeutic use of cannabinoids in a case of super-refractory sympathetic storming following coccidioidal meningitis and extensive bilateral subcortical stroke

A 26-year-old previously healthy man was transferred from an outside hospital for treatment of meningitis, vasculitis, and hydrocephalus requiring placement of a ventriculostomy. Workup subsequently revealed coccidioidal meningitis. During hospitalization the patient had severe vasospasm, elevated intracranial pressure, diabetes insipidus, cerebral salt wasting, and severe sympathetic storming. Intermittent storming episodes with high fever persisted for over 8 weeks despite treatment with bromocriptine, dantrolene, tylenol, ibuprofen, phenobarbital, and sinemet. Due to its mechanism of action, a trial of dronabinol 10mg divided twice daily was tried. The storming episodes ceased and within 6 hours the average temperature decreased by about 2.5 degree centigrade. Temperature over the next several days was better controlled with a substantial reduction in use of anti-pyretics, surface cooling measures, and other storming medications

Our case highlights a novel therapeutic use of cannabinoids in super-refractory sympathetic storming related to brain injury. Dronabinol may be an alternative pharmacotherapy with unique mechanism of action in difficult to control sympathetic storming

Patients with poor grade subarachnoid hemorrhage(SAH) commonly present with significant mental status changes that preclude reliance on neurologic exam for screening for neurologic deterioration. Jugular venous oximetry monitoring has been suggested for use in guidance of hyperventilation therapy, barbiturate coma, and vasospasm monitoring. No studies are found in literature validating its use in SAH. Milrinone has been using for the treatment of vasospasm in SAH in an established protocol in The Montreal Neurological Hospital. This study was performed using multiple methods of monitoring, but not jugular bulb oximetry. We report one case with high grade subarachnoid hemorrhage complicated by vasospasm treated with milrinone using jugular bulb monitoring for dose titration.

Methods 71 years old female presented with thunderclap headache and subsequently became comatose. Noncontrast head computer tomography showed posterior fossa subarachnoid blood. She was intubated, external ventricular drain (EVD) was placed and she was admitted to neurosurgical intensive care unit (NSICU). Angiogram showed left posterior inferior cerebellar artery aneurysm and was successfully coiled. Her hospital course was complicated by refractory symptomatic vasospasm. Angiogram showed basilar artery vasospasm treated with intra-arterial verapamil. Post procedure patient was not able to tolerate norepinephrine due to tachycardia and could not maintain hypertension on phenylephrine. Milrinone was then started. Jugular bulb catheter was place because the area at risk was not amenable to invasive multimodality monitoring. Oximetry was monitored and her milrinone rate was titrated to goal of venous oximetry in the range of 50-70%.

On day 20, angiogram showed no more evidence of vasospasm. Her exam was back to her prior poor baseline. Subsequently, she was discharged to long term care facility.

Our case demonstrates the benefit of using jugular venous oximetry monitoring guidance for milrinone dose titration. Further, it may be an effective tool is research studying treatments of cerebral vasospasm

Repetitive transcranial magnetic stimulation (rTMS) is increasingly used in treatment of various conditions including depression, chronic pain, and movement disorders. The use of rTMS for chronic management of medically refractory epilepsy has grown substantially in the last 15 years. However, little literature exists on use of rTMS for acute status epilepticus. The exact antiepileptic mechanism of rTMS remains unclear, but may be secondary to inhibition of cortical excitability. We report promising response to rTMS in a case of super-refractory focal status epilepticus.

The study is a case report. A daily dose of 1800 pulses of 1Hz rTMS was applied to the left occipital lobe. Treatment course was divided into 3 periods of 3-5 consecutive days each for a total of 13 days of treatment over 18 days.

A 63-year-old woman with recent hemiarthroplasty complicated by wound infection presented with acute unresponsiveness and right gaze deviation, evolving into fluctuating encephalopathy, word finding difficulty, and right hemineglect. EEG revealed persistent left posterior quadrant lateralized periodic discharges (LPDs), at times evolving into electrographic seizures, and positron emission tomography demonstrated a co-localized hypermetabolic focus. MRI revealed subtle bilateral occipital T2 hyperintensity without diffusion restriction, which later resolved; cerebrospinal fluid was noninflammatory. Seizures continued despite treatment with multiple AEDs, burst suppression, and empiric trial of high dose corticosteroids. The patient demonstrated abrupt electrographic and clinical improvement after rTMS initiation. Previously unseen brief periods of LPD resolution were observed within 30 minutes after first TMS session with further improvement in EEG background correlating with improvement in encephalopathy and clinical findings over subsequent days.

Given excellent safety profile, rTMS may be useful transitional therapy in management of some cases of status epilepticus. Durability of efficacy, patient selection, and optimal treatment schedules remain important unresolved questions. Further study is required.

Central Pontine Myelinolysis (CPM) occurs due to rapid osmotic shifts causing demyelination in white matter, typically due to rapid correction of hyponatremia mostly in setting of alcoholism, malnutrition, and/or liver/renal dysfunction. Sequelae may include cranial neuropathies, quadriparesis, seizures, and encephalopathy. No specific treatment exists; literature reports indicate favorable outcomes in only 50-67% of patients.

Our patient is a 50 year old male with hypertension, tobacco and alcohol abuse, admitted with severe aortic stenosis, complicated by alcohol withdrawal, pneumonia, and acute kidney injury. He was treated with benzodiazepines, broad spectrum antibiotics, and fluid resuscitation. On Hospital Day (HD) 10, he had to be intubated for airway protection due to acute confusion and quadriparesis. His blood work was notable for wide fluctuations in serum sodium, from 131 on admission to 155 on HD7 to 146 on HD10. Otherwise, laboratory evaluation was remarkable only for mildly elevated AST and serum creatinine. MRI brain 2 days after symptom onset (HD12) showed DWI and FLAIR hyperintensities around central pons bilaterally crossing midline. EEG showed severe generalized slowing. Diagnosis of CPM was made and intravenous immunoglobulin (IVIG) (0.4 g/kg/day for 5 days) was initiated within 4 days of symptom onset, on HD 14.

After initiation of IVIG, patient showed rapid improvement, first noted in the bilateral upper extremities. By HD 20 i.e., 6 days after initiation of IVIG, he was able to be successfully extubated; and he had regained 3-4/5 strength in all extremities. Neuropsychology testing at 1 month demonstrated intact cognition.

We describe a case of rapid clinical improvement in CPM following treatment with IVIG. In addition to ours, about 5 similar cases have been reported, in which beneficial outcomes were demonstrated following prompt initiation of IVIG. One proposed theory would be through reduction of myelinotoxic antibodies, thus promoting remyelination.

Few cases have reported central neuronal hyperventilation (CNH) secondary to infiltrative malignancy or autoimmune disease. The lesion is usually located at the pontine tegmentum and interrupts the fibers between the respiratory centers in the pons and those in the medulla.

We report a case of a 57 year old female with multiple comorbidities who was admitted to the neurocritical-care unit after intra-operative rupture of a 4mm distal basilar aneurysm while being electively coiled. An external ventricular drain (EVD) was placed due to early signs of ventriculomegaly.

The postoperative exam showed progressive encephalopathy, left > right hemiplegia progressive tachypnea (rate and depth) despite being on assisted mode ventilation leading to severe hypocapnia (12.8 mmHg) and compensatory renal acidosis (Bicarbonate = 8.5 mmol/L) to maintain normal PH. Attempt to sedate the patient led to severe metabolic acidosis. Intraventricular nicardipine was started and the patient ventilator settings were changed to Bi-level pressure control. Transcranial Doppler (TCD) showed markedly improved vasospasms. The patient respiratory rate and, to a lesser extent, the tidal volumes improved after several days. Sedation was weaned off successfully. EVD was successfully weaned off and removed.

TCD and CT angiogram showed severed basilar artery vasospasm while MRI done later showed bilateral tegmental midbrain ischemia.

One case has reported acute central neuronal hyperventilation following left thalamic bleed while another reported chronic neuronal hyperventilation that was attributed to old bilateral lacunar thalamic strokes by exclusion. Our case is the first to report central neuronal hyperventilation following aneurysmal subacrachnoid hemorrhage that got complicated by bilateral tegmental midbrain strokes. While respiratory centers are known to exist in the medulla and the pons, more recent articles have described networks that regulate breathing extending to the midbrain peri-acquiductal grey and possibly the thalami. Our unique case supports this hypothesis.

Serotonergic and atypical antipsychotic drugs are often used in the critically ill in the treatment of posttraumatic depression and anxiety disorders. Hyperactive delirium may mask serotonin syndrome, which carries high morbidity and mortality if left untreated.

We describe a case of serotonin syndrome in a critically ill patient in the setting of surgical and neurocritical intensive care unit.

A 56-year-old male with remote trauma presented with left upper abdominal pain. A CT-scan of abdomen showed left diaphragmatic hernia. He underwent left thoracotomy and repair of diaphragmatic hernia. His postoperative course was complicated by sepsis, ileus, and aspiration pneumonitis. He was started on sertraline and quetiapine for stress-induced anxiety disorder, depression and agitation. Despite increasing doses of sertraline, patient became agitated, tremulous, and confused. Physical examination included fever, tachycardia, hypertension, diaphoresis, dilated pupils, hyperactivity, and clonus. Initially considered to be due to hyperactive delirium, these manifestations did not improve with haloperidol. Neurocritical care was consulted. Due to presence of hyperactivity, fever and clonus, Serotonin syndrome was strongly suspected. Sertraline and quetiapine was discontinued and cyproheptadine added. Within 24-hours his symptoms improved and Cyproheptadine was tapered over 10 days.

Serotonin syndrome, a potentially life-threatening syndrome, is manifested by triad of mental status changes, neuromuscular and autonomic hyperactivity. A multitude of drug combinations can result in Serotonin syndrome. Serotonin syndrome is a diagnosis of exclusion, based on history and neurological examination in a patient taking serotonergic drug. 5HT-2A receptors are most commonly incriminated along with high levels of norepinephrine.The keys to management include discontinuation of all serotonergic agents, supportive care, and cyproheptadine. Cyproheptadine, a potent 5HT-2A antagonist, is effective in ameliorating symptoms. A high suspicion for diagnosis is important for reducing morbidity and mortality associated with this neurologic syndrome in the critically ill.

Ruptured cerebral mycotic aneurysm as consequence of Infective Endocarditis (IE): A management

QEEG ADR in Poor Grade SAH: Is it Really Useful?

Recognize the Various Subtypes of Cerebral Amyloid Angiopathy Bilal Butt Baylor College of Medicine

24-hour Development of a Giant Infectious Intracranial Aneurysm: A Case Report Catherine Albin

Intra-operative Ultrasound in traumatic brain injury patients Namkyu You

Syndrome of the trepheined (SoT) and paradoxical herniation without craniectomy

Elysia James Spectrum Health Neurosciences -ICU Division

Stephen A. Trevick 1 , Andrew Naidech 2 , Leah Tatebe 

2672 patients were included. Median age was 54 years. 66% were female, 26% smokers, 54% hypertensive and 12% diabetic. 8% had a history of CAD or MI and 14% had hyperlipidemia. In the multivariable analysis, the odds ratio for unfavorable outcome, defined as mRS score of 3-6, was 5.7(95%C.I: 4.6-7.0) and 66.0(95%CI: 44.0-99.1) for the intermediate-grade(III) and high-grade(IV and V) HH groups respectively, when compared to the low-grade(I and II) HH group. Age, hypertension and diabetes were found to be negatively associated with mRS, while hyperlipidemia was positively associated. Gender, race, smoking and history of CAD/MI were not significantly related to mRS. A positive trend for better mRS outcome was observed across years (p=0.008). This trend was not related to HH grade on admission, (p=0.18 for interaction between HH grade and year).

HH scale on admission is associated with the mRS outcome upon discharge for patients with nontraumatic SAH. Models predicting the probability of a good mRS outcome could be created based on the HH grade on admission, age, hypertension, diabetes and hyperlipidemia status. The data suggest a trend toward improvement in medical and surgical care for this patient population across years.

Ciro 

Poor-grade subarachnoid hemorrhage (SAH) is associated with high mortality rates. Although death rates have decreased in the last three decades, the exact mechanisms of demise are still to be determined in this patient population.

A retrospective study of consecutive poor-grade SAH patients (World Federation of Neurosurgical Societies grades IV and V) aggressively treated in two academic high-volume centers, one in The Netherlands (AMC) and one in Canada (SMH). The primary outcome was in-hospital mortality. The main reasons of death were evaluated.

A total of 357 poor-grade SAH patients were admitted between 2009 and 2013, 178 to AMC and 179 to SMH. 152 (43%) patients died, and 85 (24%) of those patients died before having the culprit aneurysm treated. The median interval between hospital admission and death was three days (IQR 1-12).Withdrawal of life support was the main reason of death in both centers (total of 107 deaths -71%), cardiopulmonary causes, aneurysm rebleeding, refractory intracranial hypertension, and other extracranial causes), represented less than 15%. 

Extensive review of patients chart for all the data collection including literature search for similar cases if reported before.

Although rare, there are multiple case reports and series of NKH and clinical findings of Hemichorea-Hemiballism (HC-HB). There are few case reports of NKH with unilateral signal changes in the caudate and putamen. Our patient presented with acute right basal ganglia ICH. Despite the typical imaging findings of NKH, work-up and management of ICH took precedence over control of BG. MRI findings were different in our patient given presence of positive GRE and DWI/ADC in areas other than T1 hyperintensity, which is known to be associated with NKH. We hypothesize an association between Ischemia and hemosiderin deposition with Hyperglycemia. The selective vulnerability of unilateral involvement of basal ganglia and caudate is unclear and needs more research.

Identification of neuroimaging findings in NKH in absence of focal neurological deficits (HC-HB) is important, especially for a first responder. Early recognition can prevent ICU admission, provide efficient patient care and allocation of resources. Although most metabolic diseases affect basal ganglia bilaterally; NKH is associated with specific unilateral neuroimaging findings even in absence of movement disorders or focal neurological deficits. 

A 32 year old male with a history of seizure disorder due to mesial temporal lobe sclerosis, presented with altered mental status after a lamotrigine overdose. He had consumed 9.6 gm of the drug. He was awake and alert at presentation.

Urine toxicology was negative. Initial Creatine Kinase (CK) was 1478 IU/L and peaked at 5974 IU/L; his creatinine was 1.3 mg/dL. Lamotrigine level went from 14 mcg/ml to 38.6 mcg/ml after 18 hours. Four days after admission it was 31 mcg/ml. A head CT at admission was negative.

Despite initial alertness, he developed profound encephalopathy with agitation and rigidity, requiring heavy sedation, induced paralysis, and intubation. This in turn lead to hemodynamic instability, which along with persistently elevated lamotrigine levels, prompted initiation of Continuous Veno-Venous Hemodia-Filtration (CVVHDF) on hospital day 5. The lamotrigine level declined to 13.3 mcg/mL within 24 hours, the encephalopathy and rigidity resolved, and he was extubated.

To our knowledge, this is the first reported case of lamotrigine toxicity managed with CVVHDF. Overdoses up to 15 g have been reported and can even result in death. While cleared hepatically, the half-life of lamotrigine is approximately twice as long when patients have chronic renal failure. In a small series of 6 patients with renal failure, approximately 20% of lamotrigine was reported to be removed by hemodialysis. We applied this principal to our patient. Our experience suggests that augmenting drug clearance with dialysis may help reduce the time on mechanical ventilation, need for higher doses of sedatives, and improve time to discharge. CVVHDF should be considered a supplemental treatment option for lamotrigine toxicity. 

Traumatic brain injury (TBI) complicated by percutaneous coronary intervention (PCI) remains a significant clinical dilemma. Dual anti-platelet therapy (DAPT) is standard after PCI, but may contribute to progression of TBI. Novel antiplatelet drugs with ultra-short half-lives, such as the P2Y12-adenosine receptor antagonist, cangrelor, may provide added clinical flexibility in avoiding TBI-associated hematoma progression, particularly in the absence of reversibility options.

Case report.

We report a 53 year-old female who presented to the ED after a syncopal episode with a fall down a flight of stairs. An EKG was obtained demonstrating inferior wall STEMI. Signs of head trauma included facial and scalp contusions, and bloody otorrhea. Initial GCS was 14. A non-contrast head CT demonstrated tSAH and contusions of bilateral frontal lobes and left temporal lobe, and a non-displaced fracture of the left temporal bone. Neurosurgery, Interventional Cardiology and Critical Care were consulted. The patient developed signs of cardiogenic shock related to STEMI and was taken emergently to cath lab. Successful revascularization of proximal RCA occlusion was achieved. Heparin was given per protocol, and aspirin and cangrelor administered post-PCI. Cath lab was complicated by tonic-clonic seizures requiring intubation. Repeat head CT demonstrated blossoming of bifrontal contusions, trace subdural hematoma development and increased tSAH conspicuity. DAPT infusion was continued, and subsequent imaging was stable, allowing transition to ASA and clopidogrel. She survived with only minor disability.

Newer generation P2Y12 inhibitors can be administered intravenously with reliable platelet inhibition similar to older P2Y12 receptor inhibitors. With rapid reversibility upon discontinuation, their utilization should be considered any time PCI complicates TBI. 

Cerebral air embolism (CAE) is a rare but potentially fatal entity with high morbidity and mortality, commonly seen secondary to iatrogenic causes like neurosurgical procedures, Vascular surgeries, etc. as also deep sea diving. CAE after esophagogastroduodenoscopy (EGD) is extremely uncommon. We present a rare case of CAE post EGD resulting in diffuse cortical infarction.

An 80 year old man underwent an elective (EGD) for esophageal stricture with biopsy and balloon dilatation. Patient did not wake up after procedure. On initial exam, patient was comatose, Glasgow Coma Scale 4T with decerebrate posturing. Computed tomography (CT) revealed multiple foci of cerebral air embolism. CT Angiogram of the brain was negative. Diffusion Weighted Imaging and Apparent Diffusion Coefficient imaging sequences in magnetic resonance imaging (MRI) showed diffuse, global bi-hemispheric cortical infarction. CT chest showed pneumomediastinum.

Only 21 cases of CAE from EGD have been reported in literature prior to this case. 5 received Hyperbaric Oxygen therapy(HBO). 12 patients had a documented Patent Foramen Ovale (PFO) or some form of Arteriovenous (AV) shunt. Presence of AV shunts/ PFO, therapeutic endoscopic procedures providing vascular communication as well as providing pressure gradient are all factors facilitating air embolism associated with EGD. HBO therapy has been shown to improve outcomes in CAE patients, initiating therapy >6 hours after insult and early and significant ischemic changes seen on CT/ MRI prior to starting therapy were strong predictors of poor outcomes. Our patient did not have a documented Echocardiogram with a shunt study prior to the EGD.

CAE after EGD causing global cerebral bi-hemispheric ischemia as seen in our case is extremely rare. HBO has been shown to improve outcomes. Time to treatment > 6hours and early CT/ MRI changes suggest poor outcomes. Studies do not recommend benefit of screening for PFO or AV shunts prior to every EGD.