22.1 Esophageal, Gastric & Bowel Emergencies: Perforation, Obstruction, Ogilvie Syndrome & Colonic Ischemia

Esophageal Emergencies

Perforation and Rupture

• Presentation: severe chest, epigastric, or back pain, subcutaneous emphysema, odynophagia, fever, and rapid progression to septic shock from mediastinitis. The Mackler triad (vomiting, chest pain, subcutaneous emphysema) is often incomplete. A left pleural effusion with high amylase and low pH is suggestive.
• Imaging: CT of the chest with water-soluble oral contrast is the test of choice, showing extraluminal air and contrast, mediastinal fluid, and effusions. Avoid barium first, because it causes mediastinal inflammation, though it is more sensitive for small leaks.
• Management:
  1. Nil by mouth, large-bore intravenous access, resuscitation.
  2. Broad-spectrum antibiotics plus antifungal coverage (oral flora and Candida).
  3. Drainage of the mediastinum and pleural space.
  4. Definitive control: primary surgical repair with buttressing for early, large thoracic perforations; endoscopic stenting or clipping with drainage for contained leaks, iatrogenic injuries, and poor surgical candidates; esophageal diversion or resection for destroyed tissue.
  5. Nutrition by jejunal feeding or parenteral support.
• Caustic ingestion: assess the airway first; do not induce vomiting, do not neutralize, and do not place a blind nasogastric tube. Early endoscopy grades injury; steroids are not recommended, and strictures develop later.
• Variceal bleeding, food impaction, and Mallory-Weiss tears are covered in the gastrointestinal bleeding section.

Gastric Emergencies

• Perforated peptic ulcer: sudden severe epigastric pain with peritonitis; free air on upright chest radiograph or CT. Resuscitate, give antibiotics, and arrange surgical repair (often an omental patch); treat Helicobacter pylori afterward.
• Gastric outlet obstruction: vomiting with hypokalemic, hypochloremic metabolic alkalosis and paradoxical aciduria. Decompress, replace sodium chloride and potassium, and treat the cause (ulcer disease or malignancy).
• Gastric volvulus: organoaxial rotation, typically with a paraesophageal hernia. The Borchardt triad is severe epigastric pain, retching without vomiting, and inability to pass a nasogastric tube. It can strangulate and perforate: obtain urgent CT and surgical consultation, and attempt careful endoscopic or operative reduction.
• Stress-related mucosal bleeding: prophylaxis with a proton pump inhibitor is indicated for ventilated patients and those with coagulopathy; the REVISE trial showed less clinically important upper gastrointestinal bleeding with pantoprazole without a mortality difference.
• Gastroparesis in critical illness: manage with prokinetics (metoclopramide, erythromycin) and post-pyloric feeding.

Small and Large Bowel Obstruction

• Management of uncomplicated adhesive small bowel obstruction: nasogastric decompression, fluid and electrolyte repletion, and serial examination. Water-soluble contrast (gastrografin) is both diagnostic and therapeutic; contrast reaching the colon within 24 hours predicts resolution.
• Signs demanding surgery: peritonitis, a closed-loop or strangulated obstruction, pneumatosis, portal venous gas, free air, or failure to resolve. A rising lactate, fever, and localized tenderness in a patient who was improving indicate ischemia.
• Sigmoid volvulus: a "coffee bean" loop; endoscopic detorsion with rectal tube placement is first-line, followed by elective sigmoidectomy because recurrence is common. Peritonitis or gangrene requires immediate surgery.
• Cecal volvulus: usually operative (right colectomy), because endoscopic reduction fails more often.
• Malignant obstruction: a self-expanding metal stent can decompress as a bridge to surgery or as palliation.

Acute Colonic Pseudo-Obstruction (Ogilvie Syndrome)

• Setting: critically ill, postoperative (especially orthopedic, cardiac, and obstetric), neurologic injury, electrolyte disturbance, and opioids and anticholinergics.
• Presentation: massive abdominal distension with little pain, usually with passage of some flatus, and imaging that shows colonic dilation without a mechanical transition point.
• Risk: cecal diameter above about 10 to 12 cm, or distension lasting beyond about 6 days, raises the risk of ischemia and perforation.
• Stepwise management:
  1. Conservative measures for 24 to 48 hours: nil by mouth, nasogastric decompression, a rectal tube, correction of potassium, magnesium, and calcium, stopping opioids and anticholinergics, treating infection, and mobilizing and repositioning the patient.
  2. Neostigmine 2 mg IV over 3 to 5 minutes if conservative measures fail and there is no contraindication. Most patients respond within minutes with a dramatic passage of flatus and stool.
     • Requires continuous cardiac monitoring with atropine at the bedside, because bradycardia is common.
     • Contraindications: mechanical obstruction, suspected ischemia or perforation, significant bradycardia, active bronchospasm, pregnancy, and severe kidney failure (relative).
     • Oral or subcutaneous regimens and polyethylene glycol afterward reduce recurrence.
  3. Colonoscopic decompression with tube placement for failure of or contraindication to neostigmine.
  4. Surgery (cecostomy or colectomy) for perforation, ischemia, or refractory distension.
• Methylnaltrexone is an option when opioids are the dominant driver.

Toxic Megacolon

• Causes: C. difficile colitis, inflammatory bowel disease (ulcerative colitis more than Crohn disease), other infectious colitis (Salmonella, Shigella, Campylobacter, CMV in immunocompromised patients), and ischemic colitis.
• Definition: radiographic colonic dilation above 6 cm (transverse colon) plus systemic toxicity: fever, tachycardia, leukocytosis or leukopenia, anemia, and one of dehydration, altered mental status, electrolyte disturbance, or hypotension.
• Management:
  • Bowel rest, nasogastric decompression, aggressive fluid and electrolyte repletion, and transfusion as needed.
  • Stop antimotility agents, opioids, and anticholinergics.
  • Treat the cause: intravenous corticosteroids for inflammatory bowel disease (with infliximab or cyclosporine as rescue), or maximal C. difficile therapy.
  • Broad-spectrum antibiotics for suspected perforation or bacteremia.
  • Serial examinations and radiographs, often every 12 to 24 hours; avoid colonoscopy, which risks perforation.
  • Colectomy if there is no improvement within 48 to 72 hours of maximal medical therapy, or immediately for perforation, uncontrolled bleeding, or clinical deterioration. Perforation raises mortality several-fold, so operating before it occurs is the goal.

Colonic Ischemia

• Distinct from acute mesenteric ischemia: colonic ischemia is usually a nonocclusive, mucosal and submucosal injury in watershed areas (the splenic flexure and rectosigmoid), in older patients after hypotension, cardiac surgery, aortic repair, dialysis, or vasopressor use, and sometimes with vasoconstrictors such as cocaine.
• Presentation: crampy left-sided abdominal pain followed by bloody diarrhea, usually with less pain than the degree of concern raised by mesenteric ischemia.
• Diagnosis: CT with contrast shows segmental wall thickening; colonoscopy confirms mucosal changes and a sharply demarcated segment, with biopsy.
• Management: most cases resolve with supportive care: fluids, bowel rest, optimizing perfusion, stopping vasoconstrictors, and antibiotics for moderate or severe disease. Surgery is needed for gangrene, perforation, fulminant colitis, or a persistent protein-losing colopathy or stricture.
• After aortic surgery, bloody diarrhea with acidosis should prompt immediate sigmoidoscopy to evaluate for left colon ischemia from a sacrificed inferior mesenteric artery.