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  1. Esophagus
    1. Esophageal perforation may arise from increased intraluminal pressure at the anatomic sites of narrowing, as well as sites narrowed by a malignancy, foreign body, or physiologic dysfunction. More than half of esophageal perforations are iatrogenic and may follow upper endoscopy procedures, NG tube placement, balloon tamponade of bleeding varices, dilation of strictures, endotracheal tube placement, or transesophageal echocardiography. Abnormal anatomy such as a Zenker diverticulum may predispose the patient to this complication. Perforation can occur in the cervical, thoracic, or abdominal esophagus, leading to cervical abscess, mediastinitis, empyema, or peritonitis.
      1. Diagnosis: Patients may have pain, fever, subcutaneous crepitus, leukocytosis, pneumomediastinum, or a pleural effusion. A contrast swallow study, CT scan, or an esophagoscopy can confirm and localize esophageal perforations.
      2. Treatment is urgent and includes broad-spectrum antibiotics, drainage, and gastric acid suppression. Some patients may be candidates for primary repair at the time of drainage. Most patients will remain npo for a prolonged period and will require nutritional support via a feeding tube.
    2. Boerhaave syndrome refers to spontaneous esophageal perforation, which may have no obvious precipitant or may be related to retching/vomiting, blunt trauma, weightlifting, or childbirth. Predisposing factors include reflux esophagitis, esophageal infections, PUD, and alcoholism.
    3. Ingestion of foreign bodies and caustic substances can cause significant esophageal injury.
      1. Ingested foreign bodies, most commonly food boluses, can present with dysphagia, odynophagia, chest pain, or airway obstruction. Blunt objects less than 2 cm in size may traverse the GI tract uneventfully, whereas objects larger than 6 cm can obstruct within the duodenum if not in the esophagus. Most objects that do not pass spontaneously may be removed endoscopically—this should be done early to minimize the risk of perforation from pressure-induced necrosis of the esophageal wall.
      2. Acids (pH <2) and alkalis (pH >12) cause severe burns when ingested. Vomiting after the ingestion exposes the esophagus to the caustic substance a second time.
        1. Initial management includes a careful assessment of the airway. Intraoral burns, edema of the uvula, and inability to swallow saliva may suggest impending airway compromise. Assessment of the airway should be ongoing as the injury evolves. Patients may also require significant resuscitation because of the inflammation of the mediastinal tissues. Radiographs of the chest and abdomen are helpful to evaluate for perforation. There is no role for gastric lavage, induced emesis, or activated charcoal.
        2. Endoscopy early in the patient’s course is controversial but can be helpful to assess the degree of injury. Endoscopy is helpful in evaluating and managing esophageal strictures that develop later on as a complication of caustic ingestions.
  2. Stomach
    1. Stress ulceration is discussed in Section III.E.1.
    2. Risk factors for PUD include H. pylori infection, NSAIDs, and aspirin use. Patients can present with pain, upper GI bleeding, obstruction, or peritonitis from perforation.
      1. The diagnosis of active H. pylori infection can be made during endoscopy utilizing the biopsy specimen and include histology, culture, urease testing, and polymerase chain reaction (PCR).
      2. Treatment of H. pylori is indicated in most patients on the basis of its association with peptic ulcers, gastric carcinoma, and gastric lymphoma. First-line regimens consist of a PPI plus two antibiotics such as amoxicillin + clarithromycin (first-line therapy), amoxicillin + metronidazole (for macrolide allergy), or metronidazole + clarithromycin (for penicillin allergy).
      3. Complications of PUD include upper GI bleeding (Section III.E.1), perforation, and obstruction. Perforation requires an operation with either a laparoscopic or an open approach.
  3. Pancreas
    1. Acute pancreatitis
      1. Most common etiologies are alcohol and gallstones (70%-80% of cases). Other causes include biliary reflux, contrast reflux, hypercalcemia, hyperlipidemia, trauma, and others.
      2. The pathogenesis of acute pancreatitis is related to the release of activated pancreatic enzymes that autodigest the pancreatic parenchyma and cause inflammation, microvascular injury, and necrosis. Activated enzymes may also circulate to distant organs, causing activation of the complement and coagulation cascades, vasodilatation, and endothelial injury. Systemic consequences may include shock, acute lung injury and acute respiratory distress syndrome (ALI/ARDS), and acute renal failure.
      3. Symptoms of acute pancreatitis include severe epigastric pain radiating to the back, nausea and vomiting, and fever.
      4. The diagnosis is established with a consistent history and physical examination and increased serum amylase or lipase levels. An abdominal CT scan demonstrating pancreatic inflammation, edema, or necrosis may be a useful adjunct (Figure 28.2).
      5. The prognosis for the majority of patients is good and they experience mild, self-limiting disease. Severe acute pancreatitis, defined as acute pancreatitis with organ dysfunction, develops in 10% to 20% of patients, necessitating admission to the ICU. Various tools have been developed to assess the severity of acute pancreatitis—the most commonly used is the Ranson criteria (Table 28.3).
      6. Clinical course
        1. The early phase is characterized by local inflammation, significant retroperitoneal fluid sequestration, and a systemic inflammatory response that can be robust and may lead to multiple organ system failure.
          1. Initial treatment is largely supportive. Aggressive fluid resuscitation and electrolyte repletion should be undertaken. NG tube decompression can be helpful to alleviate nausea but does not shorten the clinical course. Pain relief, supplemental oxygen, invasive monitoring, mechanical ventilation, and inotropic support may be necessary.
          2. Prophylactic antibiotics are not indicated in severe pancreatitis without overt signs of sepsis or positive culture or aspiration. Even in patients with a large amount of necrosis (≥30%), routine use of antibiotics has been associated with no improvement in outcomes.
          3. Nutrition should be provided. Several trials support the use of early enteral feeding via an NG or a nasojejunal tube within the first 48 hours. Total parenteral nutrition (TPN) should only be considered for patients who cannot tolerate adequate enteral nutrition.
          4. Patients with mild gallstone pancreatitis should undergo cholecystectomy during the index hospitalization to prevent recurrence. The type of intervention and timing for patients with severe gallstone pancreatitis must be individualized. Patients who are too sick to undergo cholecystectomy may be treated with endoscopic retrograde cholangiopancreatography (ERCP) and sphincterotomy.
        2. The later phase of severe acute pancreatitis is characterized by local complications and can carry on for weeks or months.
          1. Pancreatic necrosis ( Figure 28.2) should be suspected in patients who fail to improve or suffer clinical deterioration. Necrosis is not present in the first 2 to 3 days of symptoms. The extent of pancreatic necrosis correlates well with the amount of devascularized pancreas, as demonstrated by a contrast-enhanced CT scan. Superinfection of the necrosis may occur. New organ failure, new fever, or an increasing leukocytosis should prompt CT-guided aspiration of necrotic tissue. Gram stain and culture aid in establishing the diagnosis of infected pancreatic necrosis. Patients with infected pancreatic necrosis should be treated with antibiotics and drainage. There has been evidence to suggest that percutaneous treatment as a bridge to definitive drainage is an option, using a step-up approach. The use of transgastric endoscopic debridement, video-assisted retroperitoneal debridement, and sinus tract endoscopy are newer modalities that may be considered if debridement is needed. The morbidity is significantly less than that with a laparotomy.
          2. Pancreatic pseudocysts ( Figure 28.2) are encapsulated fluid collections, rich in pancreatic enzymes, which form 4 to 6 weeks after an episode of acute pancreatitis. Typically, they communicate with the pancreatic duct. Collections that are observed earlier are referred to as acute fluid collections and may spontaneously regress. Small, asymptomatic pseudocysts can be observed safely.
            1. Large (>6 cm) or symptomatic pseudocysts can be drained either endoscopically or surgically.
            2. Complications associated with pseudocysts include rupture into the peritoneal cavity (resulting in pancreatic ascites), rupture into the pleural space (resulting in pancreaticopleural fistula), erosion into an adjacent vessel (resulting in upper GI bleeding), compression of intra-abdominal structures, and infection (resulting in abscess formation).
          3. Pseudoaneurysms occur most commonly in the splenic artery because of the proximity of this structure to the inflamed pancreas. Splenic artery pseudoaneurysms have a 75% bleeding rate and may rupture into a pseudocyst or intraperitoneally. Hemorrhage requires immediate intervention, either angiographically or surgically.
          4. Splenic vein thrombosis may occur and lead to the later development of portal hypertension. Patients may require splenectomy if variceal bleeding develops. Thrombosis of the mesenteric vessels leading to gut ischemia is rare.
  4. Biliary Tree
    1. Acute acalculous cholecystitis is an inflammatory disease of the gallbladder occurring in the absence of gallstones. Predisposing factors include critical illness, trauma, sepsis, burns, hypotension, TPN, atherosclerosis, and diabetes.
      1. The pathogenesis of acute acalculous cholecystitis (AAC) is multifactorial and appears to be related to chemical and ischemic injury of the gallbladder. Pathology specimens reveal an occluded or impaired gallbladder microcirculation, possibly due to inflammation or inappropriate activation of the coagulation cascade.
      2. Diagnosis requires a high index of suspicion because fever may be the only symptom. Other signs and symptoms can include right upper quadrant or epigastric pain, nausea/vomiting, and new intolerance of enteral feeding. Laboratory findings may be limited to leukocytosis and LFT abnormalities, which may already be present in the patient who is critically ill and in the ICU. Ultrasound and CT scans are used to confirm the diagnosis.
        1. Ultrasound can be performed at the bedside. Diagnostic findings include gallbladder wall thickness greater than 3.5 mm, gallbladder distension greater than 5 cm, sludge or gas in the gallbladder, pericholecystic fluid, mucosal sloughing, and intramural gas or edema. However, the sensitivity of ultrasound in diagnosing AAC may be as low as 30%.
        2. Computed tomography scan (Figure 28.3) may be helpful when the diagnosis is uncertain and other intra-abdominal pathology needs to be excluded.
        3. Hepatobiliary iminodiacetic acid scan is another option to establish the diagnosis. A nonfilling gallbladder confirms the diagnosis.
      3. Treatment involves antibiotics and cholecystectomy if the patient can tolerate an operation, or more commonly in the critically ill the placement of a percutaneous cholecystostomy tube for drainage. There are now also endoscopic options for the treatment of cholecystitis.
    2. Cholangitis is an infection of the biliary tract, often associated with septic shock and is described in Chapter 30.
  5. Spleen: Patients may be admitted to the ICU for management of a splenic laceration or rupture following blunt abdominal trauma. Other splenic pathology encountered in the ICU includes splenomegaly, infarction, or abscess. Splenic infarcts usually occur in patients with preexisting splenomegaly due to portal hypertension or hematologic disorders such as leukemia, sickle cell disease, polycythemia, or hypercoagulable states. Splenic abscess usually requires splenectomy or percutaneous drainage and can be due to direct extension of infection or hematogenous seeding. Thus, the possibility of endocarditis should be entertained in the setting of splenic abscess. Patients who undergo splenectomy should receive vaccination against Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitides and should be counseled about their immunocompromised state and the need for revaccination.
  6. Intestines
    1. Enteritis and colitis are common causes of abdominal pain and may affect variable portions of the small or large intestine. Their differential diagnosis is broad, including ischemic, infectious, and inflammatory pathologies.
    2. Ischemic enterocolitis refers to a spectrum of pathology wherein inflammation of and injury to the intestine result from inadequate blood supply.
      1. Acute mesenteric ischemia occurs as a result of arterial obstruction (embolic, thrombotic, or due to aortic dissection) or venous obstruction. Acute mesenteric ischemia (AMI) can also be nonocclusive and result from hypoperfusion, vasoconstriction, or vasospasm.
        1. AMI typically presents with severe abdominal pain out of proportion to physical examination findings. Other signs include sudden intolerance of enteral feeding, nausea, vomiting, fever, intestinal bleeding, abdominal distension, and altered mental status.
        2. Leukocytosis and metabolic acidosis are common early laboratory abnormalities, whereas elevated serum lactate and amylase are late findings.
        3. Abdominal radiograph may show an ileus. CT scan may show a thickened bowel. Portal venous gas and pneumatosis intestinalis are late findings of intestinal ischemia and suggest infarction. CTA may reveal the site of arterial occlusion. Conventional angiography can also be used to establish the diagnosis and may be therapeutic. Duplex ultrasound can be used to assess proximal celiac and superior mesenteric artery (SMA) flow. However, overlying edematous bowel can make ultrasonography nondiagnostic.
        4. Treatment of AMI should be prompt and is aimed at restoring intestinal blood flow to avoid intestinal infarction. Patients should be given volume resuscitation, correction of hypotension, broad-spectrum antibiotics, and NG drainage. Systemic anticoagulation is appropriate after aortic dissection and is ruled out as a cause of mesenteric ischemia. Depending on the cause of ischemia, patients may require surgical or endovascular revascularization or observation. A second-look laparotomy may be necessary in 12 to 24 hours to reassess bowel viability.
          1. SMA emboli cause 50% of AMI. Emboli typically originate from the left atrium, left ventricle, and cardiac valves. The SMA is susceptible because of its anatomy (large caliber, nonacute angle off the aorta). Most emboli lodge in the SMA, just distal to the origin of the middle colic artery. Vasoconstriction of surrounding nonobstructed arteries further exacerbates intestinal hypoperfusion. Treatment involves aggressive resuscitation and anticoagulation. Laparotomy and embolectomy are performed before evaluating bowel viability.
          2. SMA thrombosis generally occurs acutely in patients with chronic mesenteric ischemia from atherosclerosis. Blunt trauma to the abdomen is also a risk factor, presumably from endothelial disruption. Surgical revascularization usually requires thrombectomy, a bypass graft, or an endovascular stent.
          3. Nonocclusive mesenteric ischemia results from mesenteric arterial vasospasm and accounts for 20% to 30% of AMI. Vasopressors, diuretics, cocaine, arrhythmia, and shock predispose patients to this condition. Therapy involves resuscitation, anticoagulation, administration of vasodilator agents, and discontinuation of the offending agent.
          4. Mesenteric venous thrombosis is a less common cause of intestinal ischemia. Risk factors include inherited or acquired hypercoagulable states, abdominal trauma, portal hypertension, pancreatitis, and splenectomy. Diagnosis is by CT scan. Treatment is with systemic anticoagulation (heparin followed by warfarin). Laparotomy is indicated only in cases of suspected bowel infarction.
      2. Ischemic colitis is a common form of mesenteric ischemia typically affecting the “watershed” areas (splenic flexure and rectosigmoid junction) of the colon. It is usually caused by underlying atherosclerotic disease in the setting of hypotension, although embolism, vasculitis, hypercoagulable states, vasospasm, and inferior mesenteric artery (IMA) ligation during aortic surgery are other causes.
        1. The diagnosis of ischemic colitis is suspected in patients with left-sided crampy abdominal pain, often associated with mild lower GI bleeding, diarrhea, abdominal distension, nausea, and vomiting. Other signs and symptoms include fever, leukocytosis, and abdominal tenderness to palpation. The diagnosis is confirmed by CT scan or by endoscopy.
        2. Most cases resolve within days to weeks with supportive care including bowel rest, fluid resuscitation, and broad-spectrum antibiotics. Fifteen percent of patients will develop transmural necrosis. Indications for colon resection include peritonitis, colonic perforation, and clinical deterioration despite adequate medical therapy. Long-term complications include chronic colitis and colonic strictures.
      3. Infectious enterocolitis is due to bowel inflammation caused by bacteria, viruses, or parasites. Common pathologies include diverticulitis, Clostridium difficile colitis (see subsequent text), cytomegalovirus enterocolitis (particularly in the immunosuppressed), and other infectious entities.
      4. Diverticulitis is a condition affecting one or more colonic or small bowel diverticula (outpouchings). It most commonly affects the sigmoid colon, although it may affect the entire colon and, rarely, the small bowel. Secondary infectious pathology is common and antibiotic therapy is warranted.
        1. The diagnosis of diverticulitis is suspected in patients with left lower quadrant abdominal pain, nausea, vomiting, fevers, and leukocytosis. CT scan is typically used to confirm diagnosis.
        2. Uncomplicated disease can be managed conservatively with bowel rest and antibiotics. Complicated disease may include perforation, abscess formation, or frank peritonitis. Antibiotics and percutaneous drainage of abscesses are the mainstays of treatment in the absence of peritonitis.
      5. Inflammatory enterocolitis can be primary (inflammatory bowel disease, vasculitis) or secondary (chemotherapy, radiation therapy, graft-versus-host disease, and others). Two common forms of inflammatory bowel disease are ulcerative colitis and Crohn disease. Ulcerative colitis always involves the rectum and a variable amount of colon, whereas Crohn disease typically involves the distal ileum.
    3. Adynamic or paralytic ileus refers to an alteration in GI motility that leads to failure of intestinal contents to pass. Ileus can affect the entire GI tract or a localized segment. Ogilvie syndrome refers to isolated colonic ileus (pseudo-obstruction). This most often affects the more proximal colon up to the level of the splenic flexure.
      1. Ileus may be related to a number of predisposing factors. After an uncomplicated abdominal operation, small bowel motility generally returns within 24 hours. Gastric motility follows within 48 hours and colonic motility returns in 3 to 5 days. Early feeding decreases the incidence of ileus.
      2. Diagnosis is clinical and radiologic. Patients may present with nausea/vomiting, abdominal distension, intolerance of enteral feeding, and diffuse abdominal discomfort. Abdominal radiographs show distension of the affected part of the GI tract with intraluminal air throughout. Contrast studies are sometimes needed to exclude mechanical obstruction.
      3. Complications of ileus depend on the portion of the GI tract involved. A severe ileus can lead to increased intra-abdominal pressure and even abdominal compartment syndrome. Ileus can also lead to bacterial overgrowth and reflux of bowel contents into the stomach can predispose to aspiration. Fluid sequestration due to intestinal wall edema can compromise the gut’s microcirculation. Colonic dilation can lead to ischemia, necrosis, and perforation. Patients with a cecal diameter more than 12 cm or duration more than 6 days are at higher risk for perforation, although perforations have been reported with smaller cecal diameters. Patients with chronic colonic dilation may tolerate much larger diameters.
      4. Treatment begins with supportive care, which consists of fluid and electrolyte repletion and NG tube drainage. Potential causes of ileus should be reviewed and corrected (Table 28.4). If tolerated, fiber-containing enteral diets or minimal enteral nutrition can promote GI motility. Patients should be encouraged to ambulate. Medications such as metoclopramide, erythromycin, and neostigmine have been used with mixed results. Osmotic laxatives are contraindicated.
        1. Neostigmine (2-2.5 mg IV given over 3 minutes) can successfully treat Ogilvie syndrome (colonic pseudo-obstruction) in approximately 80% of cases. Close monitoring for bradycardia is required. Atropine should be readily available at the bedside, if needed, during the administration.
        2. If conservative measures fail or if perforation appears imminent, colonoscopic or operative decompression is indicated.
    4. Bowel obstruction presents with signs and symptoms similar to that of ileus. As with ileus, plain x-rays (Figure 28.1) and CT scan (Figure 28.4) can confirm the diagnosis. Unlike ileus, the diagnosis of bowel obstruction requires a mechanical blockage and there are usually decompressed loops of intestine more distal to the obstruction.
      1. Small bowel obstruction is most often due to adhesions. Other causes include abdominal wall and internal hernias, tumors, foreign bodies, and gallstones. Patients with partial small bowel obstruction (SBO) often respond to nonoperative management, which consists of fluid and electrolyte repletion and NG tube drainage. Fevers, leukocytosis, persistent pain, and tenderness on examination are indications to proceed with exploratory laparotomy. Complete SBO should be managed surgically because of the high risk of bowel ischemia, necrosis, and perforation.
      2. Large bowel obstruction is commonly due to malignancy and develops insidiously over time. Other causes include sigmoid or cecal volvulus (Figure 28.5), diverticular strictures, and fecal impaction. Treatment of large bowel obstruction (LBO) is usually operative. Complete LBO represents a surgical emergency in patients with a competent ileocecal valve because ischemia and perforation are imminent.
        1. Sigmoid volvulus commonly presents in older males with diabetes and/or neuropsychiatric disorders. Primary management in the absence of peritonitis includes colonoscopic decompression and rectal tube placement, followed by elective sigmoidectomy.
        2. Cecal volvulus presents more commonly in younger females and is only corrected by surgical management.
    5. Diarrhea occurs when fluid intake into the gut lumen does not match fluid absorption from the GI tract.
      1. Under normal conditions, 9 to 10 L of fluid enters the bowel lumen each day from oral intake and intestinal secretions. The majority is absorbed in the small bowel, leaving the remaining 1 to 1.5 L to be absorbed in the proximal half of the colon, with approximately 100 mL lost daily in stool.
      2. Water is absorbed secondary to osmotic flow as well as active and passive transport of sodium. Changes in GI motility and epithelial mucosal integrity can drastically affect fluid absorption.
      3. Common etiologies of diarrhea in the patient who is critically ill include infections, enteral nutrition, medications, ischemic colitis, fecal impaction, intestinal fistula, pancreatic insufficiency, and hypoalbuminemia.
        1. Infectious diarrhea in the ICU setting is usually due to C. difficile infection in patients treated with antibiotics.
          1. Clinical presentation varies from asymptomatic leukocytosis to severe colitis and toxic megacolon.
          2. Because the sensitivity of the toxin assay for C. difficile is no greater than 90%, testing three separate stool samples is the standard for diagnosis if the clinical suspicion is there, unless PCR is available. PCR has a sensitivity nearing 100%. First-line treatment is with oral vancomycin, as described in Chapter 12.
          3. Indications for operative management, subtotal colectomy, are failure of medical therapy in the face of escalating cardiopulmonary support. The mortality approaches 80% for those who need a subtotal colectomy; however, earlier intervention seems to be associated with a mortality closer to 30%.
        2. Enteral nutrition causing diarrhea is a diagnosis of exclusion. Osmotic diarrhea is secondary to malabsorption of nutrients and usually stops with fasting. Malnutrition and hypoalbuminemia can also cause malabsorption.
          1. An osmolar gap in the stool of greater than 70 mOsm suggests an osmotic diarrhea. The osmolar gap is the difference between the measured stool osmolarity and the predicted osmolarity, which is 2 × ([Na+] + [K+]), based on serum electrolyte measurements.
          2. Treatment of enteral nutrition-related diarrhea involves slowing the rate of feeding, diluting the tube feeds, changing the formula, or temporarily stopping enteral nutrition. Enteral nutrition should be lactose free. In some patients, peptide-based, fiber-rich, or elemental diets with reduced fat and residue may be helpful.
        3. Fecal impaction can paradoxically lead to diarrhea as a result of decreased fecal tone, mucus secretion, and impaired anorectal sensation.
        4. An altered enterohepatic circulation, leading to increased bile acid in the colon, can induce net fluid secretion. This is seen in diseases of the ileum, fatty acid malabsorption, and altered bowel flora.
      4. Management of diarrhea consists of replacement of lost fluids and electrolytes and treatment of the underlying cause. After excluding infectious etiologies, diarrhea can be treated symptomatically with agents such as diphenoxylate with atropine (Lomotil 5 mg/dose, 4 doses/d, reduce dose once controlled), loperamide (Imodium 4-16 mg/d), bismuth subsalicylate (Pepto-Bismol 262 mg/dose up to 8 doses/d), and deodorized or camphorated opium tincture (0.3-1 mL/dose every 2-6 hours up to 6 mL/d).
    6. Constipation may affect up to 83% of patients in the ICU and has been associated with prolonged ICU length of stay, infectious complications, pulmonary complications, and increased mortality in some studies.
      1. The etiology of constipation in the ICU is incompletely understood. Proinflammatory mediators, poor perfusion, dehydration, immobilization, and medications (vasopressors and opiates) likely contribute to the problem.
      2. A bowel regimen should be initiated and titrated to avoid constipation and can include stool softeners (Colace), bulking agents (methylcellulose, psyllium), stimulants (castor oil, senna), lubricants (mineral oil), or osmotic agents (lactulose, magnesium).