key: cord-0037543-fpvhjuof authors: Varon, Joseph title: Gastrointestinal Disorders date: 2016-06-03 journal: Handbook of Critical and Intensive Care Medicine DOI: 10.1007/978-3-319-31605-5_6 sha: dbd56a723dcd7c0cd523fe24bffa300b1d0cca5a doc_id: 37543 cord_uid: fpvhjuof This chapter reviews extensively gastrointestinal bleeding that require intensive care unit admission. Its management, including with assessment of the airway, breathing, and circulation (ABCs), is emphasized as well as the use of proton pump inhibitors and H(2)-receptor blockers to prevent further hemorrhage. Acute mesenteric ischemia (AMI), an acute reduction in blood flow to the intestine leading to inadequate perfusion, is reviewed. Acute pancreatitis, an inflammatory process of the pancreas, having alcoholism, gallstones, hyperlipidemia, trauma, and infections as the most common etiologies, is also reviewed. B. Etiology. The most common causes of acute GI bleeding requiring admission to the intensive care unit (ICU) are depicted in Table 6 .1 . The most common sources of GI bleeding in the ICU are gastroduodenal stress ulcerations. C. Diagnostic Evaluation 1. History Although the history and physical assessment in a critically ill patient with acute GI bleeding may be limited by the patient's clinical condition, the following are points that need to be investigated: The precise cause of acute GI bleeding is unlikely to be evident from physical examination alone (except in chronic liver disease, Osler-Rendu-Weber syndrome, or hemorrhoids). 3. A nasogastric (NG) tube should be placed in all patients with acute GI bleeding. The major advantages and disadvantages of NG tubes are shown in Table 6 .2 . All patients admitted to the ICU with GI bleeding should undergo the laboratory tests depicted in Table 6 .3 . All patients should undergo chest radiograph and abdominal X-rays. These may show evidence of perforation or obstruction and may indicate ischemic changes. Contrast studies have a low diagnostic yield and may be hazardous for the critically ill patient. They may also interfere with other diagnostic studies (i.e., endoscopy, angiography). Special tests may be required in the evaluation of acute GI bleeding. These include: (a) Selective angiography may be used as a diagnostic as well as therapeutic tool (e.g., embolization). A bleeding rate ≥0.5 mL/min at the time of the procedure is needed for diagnosis. (b) Radionuclide scans are sensitive in detecting lesions with lower bleeding rates. 6. Endoscopy is indicated in the vast majority of patients requiring ICU admission for GI bleeding. (a) Upper endoscopy is indicated when blood is obtained from the NG tube or when frank hematemesis is present. (b) Flexible sigmoidoscopy should be performed initially if lower GI bleeding is suspected. If this is not diagnostic, colonoscopy should be considered. (c) Special endoscopic procedures may be required (i.e., wireless video capsule endoscopy, push enteroscopy, double balloon enteroscopy). D. Initial ICU Management 1. As in any critically ill patient, the management of acute GI bleeding starts with assessment of the airway, breathing, and circulation (ABCs). A low threshold for endotracheal intubation is recommended in the event of clouding of consciousness or overt shock, to prevent aspiration. 2. Insert at least two large-bore (16-gauge) IV catheters. 3. Infuse blood, plasma expanders, and/or normal saline to maintain a mean arterial pressure ≥65 mmHg. 4. Some authors still recommend NG placement in all patients with GI bleeding and lavage of the stomach until the return is clear. This practice is considered useful only in settings where emergency endoscopy is not available. 3. Active Lower GI Bleeding (a) If a lesion is reachable with sigmoidoscopy or colonoscopy, local therapy may be attempted (e.g., laser coagulation). (b) Arterial embolization is indicated if the above fails. (c) All patients with active lower GI bleeding should receive surgical consultation in case an emergent intervention is needed. A. Defi nition. Acute mesenteric ischemia (AMI) is an acute reduction in blood fl ow to the intestine leading to inadequate perfusion. AMI may be a refl ection of generalized poor perfusion, or it may result from local pathology. B. Epidemiology. The incidence of AMI has increased over the past few decades. The rising incidence may be attributable to advances in medical technology and to new therapies extending the life of critically ill patients who are prone to develop AMI (e.g., elderly). The mortality in AMI is between 55 % and 100 %. 3. Patients with suspected embolic or thrombotic occlusion should undergo urgent laparotomy for possible resection. Heparin and broad-spectrum antibiotic are indicated before surgery. Most patients will undergo a "secondlook" operation within 24 h of the initial laparotomy. 4. In those cases with nonocclusive AMI, intra-arterial infusions of vasodilators (e.g., papaverine 30-60 mg/h) are advocated by some. A. Defi nition 1. Acute Fulminant Hepatic Failure Acute fulminant hepatic failure (FHF) is defi ned as acute liver failure associated with the development of hepatic encephalopathy within 8 weeks of the onset of symptoms attributable to hepatocellular dysfunction. This defi nition assumes that there is no preexisting liver disease. Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome precipitated by abnormal liver function. This syndrome is a feature of acute and/ or chronic hepatocellular failure. Common causes of FHF and HE are depicted in Table 6 .5 . C. Diagnostic Evaluation 1. History A detailed history should be obtained from family members. The following points need to be investigated: Table 6 .6 .) All patients with HE and/or FHF should undergo the following tests: (a) Chest X-ray, abdominal X-rays. (b) Blood glucose may reveal hypoglycemia. The development of renal failure with FHF carries a poor prognosis. (a) In most instances, the renal failure is related to "prerenal" causes. (b) The hepatorenal syndrome is a diagnosis of exclusion. It is associated with a normal urine sediment, a urinary sodium concentration of <20 mmol/L, and resolution if liver function improves. Thrombocytopenia, diminished clotting factors with episodes of severe bleeding Susceptibility to infection is increased in patients with FHF. Hypoglycemia, metabolic acidosis, hypokalemia, hyponatremia E. Management 1. Supportive Therapy (a) As in any critically ill patient, the management of AMI starts with assessment of the ABCs. (b) The usual indications for endotracheal intubation and assisted mechanical ventilation apply to these patients. 2. The use of corticosteroids for patients with FHF has not been proven to improve survival and, indeed, may worsen the clinical picture. 3. Some authors suggest avoiding parenteral nutrition, as protein and amino acids may worsen the clinical picture. However, new total parenteral nutrition solutions with "branched-chain" amino acids are probably effi cacious and help maintain a positive nitrogen balance. 4. The management of FHF-associated cerebral edema is no different from that for non-hepatic-related causes (see Chap. 9 , "Neurologic Disorders"). In recent years, emphasis on the use of therapeutic hypothermia for these patients seems encouraging. Some clinical and experimental evidence shows that the benzodiazepine antagonist fl umazenil (Romazicon) may have some role in improving the signs and symptoms of HE. 6. Investigational data have shown some improvement in the hemodynamics of patients with FHF treated with n-acetylcysteine. 7. Liver transplantation may be an alternative form of therapy (in a few specialized transplant centers) for some patients with no known contraindication to the procedure. 8. Liver "dialysis": A few specialized centers are currently exploring this form of therapy. 9. Agents aimed at stimulating ammonia metabolism have also been tried (e.g., ornithine-aspartate, sodium benzoate). (g) C-reactive protein: Usually elevated. (h) Urinalysis may reveal proteinuria, casts (25 % of the cases), and glycosuria. Every patient with suspected acute pancreatitis should get a chest X-ray (to rule out free air under the diaphragm, evidence of pleural effusions, etc.) and an abdominal X-ray (signs of intestinal obstruction, ileus, gallstones, the so-called sentinel loop of pancreatitis, or the colon "cutoff" sign, etc.). In addition, when the diagnosis remains in doubt, especially in the more severely ill, the following can be obtained: (a) Ultrasonography (US) is the modality of choice in patients with edematous pancreatitis or suspected biliary pancreatitis and to follow up phlegmon or abscesses. Unfortunately, US cannot be accurately performed in obese patients and in those with moderate-to-severe ileus. (b) CT is the most useful tool in assessing the retroperitoneum. Its use in acute pancreatitis is mainly to follow up on signifi cant complications (i.e., abscess, phlegmon, pseudoaneurysms). Balthazar CT scoring system was the fi rst and is still in use. This scoring system includes fi ve grades: grade A (normal), grade B (pancreas enlargement), grade C (infl ammation of the pancreas and surrounding tissue), grade D (single peripancreatic fl uid accumulation), and grade E (two or more peripancreatic fl uid accumulation and/or air accumulation). Grade D and E have a mortality of 14 % and morbidity of 54 % (Table 6.7 ) . Therefore, contrast CT and necrosis classifi cation, found by Balthazar, were used simultaneously (CT Severity Index): grade 1 (<30 %), grade 2 (30-50 %), and grade 3 (>50 % necrosis) ( Necrosis of one-half of pancreas (50 %) 4 Necrosis of more than one-half of pancreas 6 (>50 %) Many clinicians use the following agents in acute pancreatitis; however, clinical studies have not supported the routine use of these agents Calcitonin (300 IU/24 h) Somatostatin (250-μg IV bolus, then 250 μg/h as IV drip) Glucagon (d) Of interest is the use of intramuscular (IM) clonidine (not yet available in the United States) for patients hemodynamically stable with acute pancreatitis. Preliminary data show encouraging results Sedation and analgesia: Patients may require substantial amounts of analgesia, usually with meperidine (Demerol) Adequate parenteral nutrition (see Chap Correct hypocalcemia only if there is clinical evidence of tetany The most common complications of acute pancreatitis are depicted in Table 6 Those patients who demonstrate fever >39 °C with a white blood cell count >20,000/mm 3 should be evaluated for the presence of a pancreatic abscess (with the use of CT). If there are any fl uid collections, CT-guided fi ne-needle aspiration is then indicated (for Gram's stain and cultures) Intravascular fluid depletion (a) Prerenal azotemia (b) Shock A. Defi nition. Acute pancreatitis is an infl ammatory process of the pancreas with a wide range of clinical severity ranging from self-limited to a lethal disease, complicated by multiple organ system failure (10 % of cases A. Intestinal Transit . The normal 24-h intestinal fl uid and electrolyte transport are depicted in Table 6 .10 .B. Stool Formulas . As part of the diagnostic workup of patients with diarrhea, stool osmolal gap (SOG) is usually calculated utilizing the following formula:SOG stool osmolality stool Na stool K = -´+ + + ( ) 2 Normal stool osmolality is <290 mOsm/L. If the SOG >100, it indicates an osmotic diarrhea.C. Liver Facts . The Child ' s classifi cation for portal hypertension is commonly used in critically ill patients and is depicted in Table 6 .11 .