key: cord-0034993-0cczzn21
authors: Varon, Joseph; Acosta, Pilar
title: Gastrointestinal Disorders
date: 2009-10-05
journal: Handbook of Critical and Intensive Care Medicine
DOI: 10.1007/978-0-387-92851-7_6
sha: bbc9847149ce3c2d2ed9ff967cf1113e29a34400
doc_id: 34993
cord_uid: 0cczzn21

A.Classification 1.Upper gastrointestinal (GI) bleeding is above the ligament of Treitz.2.Lower GI bleeding is below the ligament of Treitz.

c. Other Signs of Hypovolemia: Altered mental status, low urine output. d. Associated Findings: Petechiae, jaundice, hepatomegaly, and splenomegaly. e. Rectum: Look for hemorrhoids, fissures, etc. Examine stools for blood even if the patient has an upper GI source. 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 at the time of the procedure ≥0.5 mL/min 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 

a. Endoscopy therapy with sclerosing agents, or laser coagulation, or heater probe. b. Surgical intervention is indicated in cases of (1). Visible vascular pedicle on endoscopy (2). Transfusion of 6 U blood in 24 h (3). Arterial spurting 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. Definition. Acute mesenteric ischemia (AMI) is an acute reduction in blood flow to the intestine leading to inadequate perfusion. AMI may be a reflection of generalized poor perfusion, or it may result from local pathology. urgent laparotomy for possible resection. Heparin and broad-spectrum antibiotic are indicated before surgery. Most patients will undergo a "second-look" 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. Definition 1. Acute Fulminant Hepatic Failure Acute fulminant hepatic failure (FHF) is defined as acute liver failure associated with the development of hepatic encephalopathy within 8 weeks of the onset of symptoms attributable to hepatocellular dysfunction. This definition 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: a. History of preexisting liver disease 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 efficacious 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 Chapter 9, "Neurologic Disorders"). In recent years, emphasis on the use of therapeutic hypothermia for these patients seems encouraging. 5. Some clinical and experimental evidence shows that the benzodiazepine antagonist flumazenil (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)

3. Laboratory Evaluation a. Complete Blood Count (CBC): Shows marked leukocytosis. Thrombocytopenia may be present in those cases complicated by disseminated intravascular coagulation (DIC). b. Amylase: Elevated initially, but may decrease after 2-3 days if necrosis of the pancreas is widespread. False-positive results may occur in perforation of the esophagus, stomach, intestine, gynecologic disorders, renal failure, severe burns, diabetic ketoacidosis (DKA), salivary gland disorders, and macroamylasemia. c. Lipase: Hyperlipasemia persists longer than hyperamylasemia. However, if necrosis of the pancreas is widespread, these values may be normal. d. Serum calcium is usually low. When levels are <8 mg/dL, the prognosis is poor. e. Other electrolyte imbalances as well as hyperglycemia are usually present. f. Metabolic acidosis may be present. 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 "cut-off" 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 significant complications (i.e., abscess, phlegmon, pseudoaneurysms). (3). 5-6 criteria, 40% mortality (4). 7-8 criteria, 100% mortality 2. Intensive care management and prompt surgical consultation have lowered the mortality of acute pancreatitis.

A. Intestinal Transit. The normal 24-h intestinal fluid and electrolyte transport is depicted in Table 6 .8. Normal stool osmolality is <290 mOsm/L. If the SOG >100, it indicates an osmotic diarrhea. C. Liver Facts. The Child's classification for portal hypertension is commonly used in critically ill patients and is depicted in Table 6 .9.

Sedation and analgesia: Patients may require substantial amounts of analgesia, usually with meperidine (Demerol)

Adequate parenteral nutrition (see Chapter 10

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 fluid collections, CT-guided fine-needle aspiration is then indicated (for Gram's stain and cultures)

If the suspected diagnosis is pancreatic abscess, broad-spectrum antibiotics should be started and an emergent surgical consultation obtained

Prognosis 1. In assessing the severity of the disease and prognosis, several classifications have been used. The most commonly utilized is the Ranson's criteria (initially developed for patients with alcoholic pancreatitis): a. Three or more of the following criteria must be met: (1)

Lactic dehydrogenase (LDH) >350 IU/L

AST (serum glutamate pyruvate transaminase [SGPT]) >250 IU/L)

Serum urea nitrogen (BUN) rise >5 mg/dL (3). Partial pressure of O 2 in arterial blood (PaO 2 ) <60 torr (mmHg) (4). Calcium <8 mg/dL (5)

A. Definition. Acute pancreatitis is an inflammatory 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