bubble_chart Overview

Toxic megacolon is one of the severe complications of inflammatory bowel disease, most commonly occurring in patients with pan-colonic ulcers. It is primarily seen in fulminant and severe cases. The clinical features include severe toxic symptoms, segmental or total colonic dilation, significant abdominal distension, with the most pronounced dilation typically in the transverse colon. The prevalence of toxic megacolon complicating inflammatory bowel disease ranges from 1.6% to 13%. According to reports by Binden et al., the mortality rate with medical treatment is 30%, rising to 80% in cases without surgical intervention for perforation. The surgical mortality rate is 21.6%, with perforated cases having a mortality rate of 51.2% and non-perforated cases 8.7%.

bubble_chart Etiology

The occurrence of toxic megacolon in patients with severe active colitis is primarily due to rapid disease progression and inappropriate treatment, but may also result from barium enemas or errors in air insufflation and catheter manipulation during fiberoptic colonoscopy. Hypokalemia, anticholinergic drugs, anti-diarrheal medications, or opioid analgesics can reduce intestinal muscle tone and inhibit bowel movements, potentially triggering the condition. Severe inflammation disrupts the neural and muscular regulatory mechanisms that control normal intestinal function, allowing intraluminal pressure to expand the intestinal wall beyond its normal range of motion. Additionally, bacterial overgrowth and the toxins they produce further exacerbate intestinal dilation and may lead to peritonitis. The bacterial toxins spread further into the systemic circulation, causing systemic toxic symptoms. Patients exhibit significantly elevated white blood cell counts, along with hypokalemia, hypomagnesemia, anemia, and hypoalbuminemia.

bubble_chart Clinical Manifestations

The progression from inflammatory bowel disease to toxic megacolon is generally short, with Fazio reporting that approximately 24% of cases occur within less than 3 months. Toxic megacolon can also be the initial symptom of inflammatory bowel disease, presenting with high fever, tachycardia, hypotension, drowsiness, and systemic exhaustion; rapid abdominal distension with tenderness, tympany on percussion, weakened or absent borborygmi, and occasional massive lower gastrointestinal bleeding. The presence of abdominal tenderness, rebound tenderness, and muscle rigidity often indicates acute perforation. Laboratory tests reveal a significant increase in total white blood cell count and neutrophils, with a left shift and the appearance of toxic granules. Anemia, hypoalbuminemia, hypokalemia, hypocalcemia, hypomagnesemia, and dehydration are commonly observed.

Abdominal X-ray plain films show segmental or total colonic dilation, most pronounced in the transverse colon and splenic flexure. Fazio reported that the diameter of the dilated colon ranges from 5.0 to 16.0 cm, with an average of 9.2 cm. In the early stages of toxic megacolon, thickening of the taenia coli along the lower edge of the transverse colon may be observed within a few hours, followed by its disappearance. Concurrently, significant gas accumulation in the stomach and small intestine may be noted, likely due to gastrointestinal paralysis caused by intracellular potassium deficiency, hypocalcemia, hypophosphatemia, hypomagnesemia, and metabolic alkalosis. The presence of free air in the peritoneal cavity confirms intestinal perforation.

bubble_chart Diagnosis

Inflammatory bowel disease patients experiencing severe abdominal pain and a sudden increase in bowel movements to dozens of bloody, watery stools should be alert to the emergence of an emergency. If an abdominal X-ray shows a transverse colon lumen diameter exceeding 6 cm, a diagnosis can be made. Some believe that abnormal gas accumulation in the small intestine is an early sign of toxic megacolon, but Caprilli suggests that persistent small intestine gas accumulation and severe metabolic alkalosis make patients with severe inflammatory bowel disease more prone to developing toxic megacolon. Symptoms include a body temperature >38.6°C, heart rate >120 beats per minute, significantly elevated white blood cell count, anemia, accompanied by impaired consciousness, decreased blood pressure, dehydration, and electrolyte imbalances. Therefore, early diagnosis of this condition relies on close clinical monitoring, abdominal X-rays, and awareness of the disease. When the medical history is unclear or toxic megacolon presents as the initial symptom,

bubble_chart Treatment Measures

1. Internal management: Immediate fasting, high-dose steroids plus antibiotics, continuous gastrointestinal decompression, or rectal tube for gas drainage. According to Preston's report, changing the patient's position to redistribute and concentrate gas in the colon, followed by suction with a long rectal tube, can achieve effective decompression. Avoid any medications that may induce or exacerbate toxic megacolon, such as opium derivatives, anticholinergics, and antidiarrheals.
2. Drip enema: Our hospital has achieved significant results in treating toxic megacolon with drip enema, successfully rescuing several severe cases of ulcerative colitis. The patient lies supine with the hips elevated, and the end of an infusion tube is connected to a catheter inserted into the anus. The drip rate should be adjusted to avoid the urge to defecate, effectively alleviating severe tenesmus. The enema is administered continuously after bowel movements. This method controls symptoms much faster than others. The enema solution primarily contains 5-aminosalicylic acid, steroids, metronidazole, lidocaine, and 654-2, with adjustments made after symptom control. Intravenous fluids are administered to correct typical edema, electrolyte imbalances, and acid-base disturbances, with particular emphasis on potassium, calcium, and magnesium supplementation. Albumin preparations are given to address hypoalbuminemia, and fresh whole blood transfusions may also be administered. Toxic megacolon often carries risks of bacterial infection and intestinal perforation, making antibiotic therapy essential. Third- or fourth-generation cephalosporins (20 mg/kg every 8 hours) can be administered intravenously; for renal failure, carbenicillin (20 g/day) may be used in divided doses. Bolton reported two cases involving Clostridium difficile infection, where combined metronidazole and quinolone therapy improved colonic dilation. Early and high-dose corticosteroids (e.g., prednisolone 100–200 mg or dexamethasone 40–80 mg/day in divided IV doses) can alleviate toxic symptoms. ACTH (25–50 U/day IV) may also be used. Some authors suggest that endoscopic decompression and intraluminal drug delivery allow higher steroid doses while resting the bowel and promoting nitrogen balance. Rectal administration of dexamethasone (40 mg twice daily) or hydrocortisone sodium succinate (200 mg twice daily) is another option. Institutions with resources may opt for high-calorie intravenous nutrition to improve the patient's baseline condition and prepare for surgery.
3. If the condition shows no improvement after 2–3 days of aggressive medical management, or if intestinal perforation, massive bleeding, or progressive colonic dilation occurs, immediate surgical intervention is required. Timely surgery significantly reduces mortality. A review of 94 surgical cases from four international institutions reported an average time from diagnosis to surgery of 1.9 days, with a mortality rate of 4.8%, significantly lower than Binder's report. The preferred surgical approach is total colectomy with ileostomy, often preserving the distal rectum for potential future anastomosis.

bubble_chart Differentiation

Attention should be paid to differentiate toxic megacolon caused by bacterial dysentery, amoebic dysentery, cold-damage disease, cholera, pseudomembranous colitis, ischemic colitis, diverticulitis, etc.

Toxic megacolon involves the entire colon and may present as segmental lesions, most notably in the transverse colon and splenic flexure. In addition to the characteristic pathological features of ulcerative colitis and Crohn's disease, the main manifestations include grade III inflammation, deep ulcers, crypt abscesses, and pseudopolyps. Due to rapid colonic dilation, thinning of the intestinal wall, circulatory disturbances, or penetration of intestinal wall abscesses, intestinal perforation is prone to occur.