EM@3AM: Toxic Megacolon

Author: Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 28-year-old male presents with abdominal pain, diarrhea, distension, and fever. He has no appetite. He has a history of ulcerative colitis. He has no prior surgeries.

Triage vital signs (VS): BP 97/58, HR 121, T 100.9 Oral, RR 24, SpO2 98% on RA.

Physical exam reveals a patient who appears systemically ill. His oral mucosa is dry, his heart is normal except for tachycardia, and his abdomen is diffusely tender.  His bowel sounds are decreased, but he has no peritoneal findings. KUB shows markedly dilated loops of bowel.

What’s the next step in your evaluation and treatment?

Answer: Toxic Megacolon

• Background: Defined as nonobstructive colonic dilation > 6 cm with systemic toxicity.
  • Diagnostic criteria:
    • Radiographic evidence of dilation (> 6 cm).
    • Three of the following: Fever (> 101.5 F), tachycardia > 120 bpm, leukocytosis (> 10.5), or anemia.
    • One of the following: Dehydration, altered mental status, electrolyte abnormalities, hypotension.
  • First thought to be a complication of ulcerative colitis. However, toxic megacolon may occur as a complication of any condition affecting the colon: inflammatory, infection, radiation, and pseudomembranous.
  • The most concerning complication of toxic megacolon is perforation, which may occur even without dilation.
• Pathophysiology:
  • Pathophysiology includes inflammation extending beyond the GI mucosa into the bowel smooth muscle and serosa. This paralyzes the smooth muscle and results in dilation. Nitric oxide production also results in dilation.
  • Neutrophil invasion of the muscle layer and cytokine release results in systemic toxicity (fever, hypotension, tachycardia).
• Etiologies:
  • Most commonly IBD (Ulcerative colitis more commonly than Crohn’s disease). Patients with UC have a lifetime risk of 1-2.5%.
  • Infection: Bacterial, viral, fungal. Pseudomembranous colitis is associated with the disease, with toxic megacolon occurring in 0.4-3% of cases.
  • Drugs: anti-motility agents such as opioids, anticholinergics, loperamide.
  • Ischemic colitis, collagenous colitis, chemotherapy, radiation, cancer, Kaposi’s sarcoma.
• History and Exam:
  • Patients typically present with diarrhea, abdominal pain, rectal bleeding, tenesmus, vomiting, fever. They may have a history of IBD or other risk factor, and direct questioning for presence of risk factors is necessary.
  • Inquire about travel, antibiotic use, chemotherapy/radiation, IBD, immunosuppression.
  • Patients often appear septic and toxic. Early resuscitation is advised during initial evaluation.
  • Abdomen may be distended, and bowel sounds are often decreased.
  • Evaluate for evidence of peritonitis.
  • If the patient is on immunomodulators (Steroids), then perforation may present subtly. Patients not on steroids more commonly present with rebound, guarding, and other peritoneal findings if perforation has occurred.
• Differential Diagnosis:
  • Intraabdominal pathology (appendicitis, cholecystitis, diverticulitis, colitis, small or large bowel obstruction).
• Evaluation:
  • Plain abdominal radiographs:
    • Colonic dilation > 6 cm diameter.
    • Loss of haustra; bowel wall edema may be present with “thumb-printing”.
    • Air-fluid levels.
    • Free air suggests perforation.
  • CT:
    • Recommended if stable to identify local or contained perforation.
    • Evaluate for inciting etiology.
  • Ultrasound:
    • Thin colonic walls.
    • Evidence of obstruction, but larger dilation (diameter > 6 cm).
  • Labs: CBC (elevated WBC, anemia), renal function/electrolytes (hypokalemia, hypomagnesemia), ESR/CRP (elevated), albumin (low), liver function, lipase, lactate.
  • Obtain blood cultures, stool cultures, and C. difficile testing.
• Management: Three goals include reducing distension, correcting fluid/electrolyte disturbances, and treating toxemia/precipitating factors.
  • IV fluid resuscitation, electrolyte repletion, and bowel rest.
  • IV corticosteroids (Hydrocortisone 100 mg IV) for inflammatory causes (IBD); may provide in other etiologies in association with GI/surgical consultation.
  • Antibiotics: Ampicillin plus metronidazole plus ciprofloxacin, OR impenem.
  • Surgical consultation.
  • If considering C. diff, utilize vancomycin
  • If known cause is CMV, use ganciclovir.
  • DO NOT use anti-motility agents.
  • Admit to surgical service.
  • Colectomy may be required for free perforation, hemorrhage, increasing toxicity, and worsening colonic dilation after medical treatment is attempted.
• Prognosis:
  • Excellent survival in absence of perforation. Mortality has decreased from 20% to 4-5% with early diagnosis and treatment.
  • Perforation is associated with 5-fold increase in mortality.

References:

1. Strong SA. Management of acute colitis and toxic megacolon.Clin Colon Rectal Surg. 2010 Dec. 23(4):274-84.
2. Marshak RH, Lester LJ. Megacolon a complication of ulcerative colitis.Gastroenterology. 1950 Dec. 16(4):768-72.
3. Jalan KN, Sircus W, Card WI, et al. An experience of ulcerative colitis. I. Toxic dilation in 55 cases.Gastroenterology. 1969 Jul. 57(1):68-82.
4. Autenrieth DM, Baumgart DC. Toxic megacolon.Inflamm Bowel Dis. 2012 Mar. 18(3):584-91.
5. Khasanov R, Schaible T, Wessel LM, Hagl CI. The surgical treatment of toxic megacolon in Hirschsprung disease.Pediatr Emerg Care. 2016 Nov. 32(11):785-8.
6. Sheth SG, LaMont JT. Toxic megacolon.Lancet. 1998 Feb 14. 351(9101):509-13.