Toxic megacolon

Introduction Toxic megacolon, also known as toxic colonic dilatation, is a serious or fatal complication caused by a variety of causes, mostly caused by inflammatory bowel disease and infectious colitis, often with symptoms of systemic poisoning and whole colon or segment Clinical manifestations of sexual colon expansion. The disease is acute and rapid development. If it is not diagnosed and treated in time, the prognosis is dangerous and the mortality rate is high.

Cause

Toxic megacolon is more spontaneous in the early stage of fulminant colitis or occurs within 3 months of the first onset, but can also be induced by hypokalemia and improper medication or special examination. The incidence rate is not exact. It is reported that the incidence of toxic colitis complicated with toxic megacolon is 1.6%-18%, and Crohn's disease is 1.0%-7.8%. Less than 20 years old ulcerative colitis or Crohn The risk of developing toxic megacolon is about 1% to 5%.

Common causes are:

1 inflammatory bowel disease, such as ulcerative colitis, Crohn's disease;

2 infectious enteritis, bacterial (pseudomembranous colitis, salmonella infection, Shigella enteritis, Campylobacter enteritis, Yersinia enteritis), viral (cytomegalovirus enteritis, HIV infection) Enteritis) and parasitic (intracellular amebic enteritis, Cryptosporidium enteritis);

3 Others have Kaposi's sarcoma (multi-focal malignant neovascular proliferation), pseudomembranous colitis caused by methotrexate treatment, volvulus, ischemic enteritis, diverticulitis, colonic intestinal obstruction.

Toxic megacolon in patients with severe active colitis, mainly due to rapid progression and improper treatment, may also be due to gas injection and catheter manipulation errors during barium enema or fibrinoscopy. Potassium deficiency and anticholinergic, anti-diarrhea drugs or opioid anesthetic analgesics can reduce intestinal muscle tone and inhibit bowel movement, which can induce the disease. Because of severe inflammation, the nerve and muscle regulation mechanism controlling normal intestinal tract is destroyed. Intestinal pressure causes the lumen wall to expand beyond its normal mobility.

In addition, bacterial overgrowth and the resulting toxins further exacerbate intestinal dilatation and can lead to peritonitis. The toxicity of bacteria further spreads to the systemic circulatory system, leading to the development of symptoms of systemic poisoning. The white blood cells in the patient's blood are significantly elevated, and produce hypokalemia, hypomagnesemia, anemia, and hypoproteinemia.

The toxic megacolon affects the whole colon, and the segmental lesions are marked by transverse colon and spleen. In addition to the characteristics of ulceration and pathological changes, pathological changes mainly include severe inflammation and deep ulceration. Crypt abscesses and pseudopolyps, etc., due to rapid colon expansion, thinning of the intestinal wall, blood circulation disorders or intestinal wall abscess penetration, prone to intestinal perforation.

an examination

Related inspection

Abdominal vascular ultrasonography colonoscopy fiber colonoscopy sigmoidoscopy

Patients with inflammatory bowel disease have severe abdominal pain, and the number of stools suddenly increases to dozens of bloody watery stools. It is necessary to be alert to emergencies. If the abdominal X-ray film shows that the transverse colon cavity diameter is greater than 6 cm, it can be diagnosed. Some people think that abnormal intestinal gas accumulation is an early phenomenon of toxic megacolon, but Caprilli believes that persistent intestinal gas accumulation and severe metabolic alkalosis make patients with severe inflammatory bowel disease easily complicated by toxic giant colon. Body temperature > 38.6. C, heart rate > 120 times / minute, blood white blood cells increased significantly. anemia. At the same time accompanied by disturbance of consciousness, lower blood pressure, dehydration and electrolyte imbalance.

Therefore, the early diagnosis of this disease depends on clinical strict monitoring and abdominal X-ray film, as well as the understanding of this disease. When the medical history is unclear or the toxic megacolon is the first symptom, attention should be paid to the toxic giants caused by bacterial dysentery, amoebic dysentery, typhoid fever, cholera, pseudomembranous colitis, ischemic colitis, diverticulitis, etc. Colonic differentiation. The course of illness from inflammatory bowel disease to toxic megacolon is generally shorter, and Fazio reports that it is about 24% less than 3 months.

Toxic megacolon can also be the first symptom of inflammatory bowel disease, manifested as hyperthermia, tachycardia, decreased blood pressure, lethargy, and systemic failure; the abdomen rapidly expands, there is tenderness, the percussion is drum sound, and the bowel sounds are weak or disappear. And occasionally the lower gastrointestinal bleeding. Acute perforation is often indicated when tenderness, rebound tenderness, and muscle tension occur in the abdomen. Laboratory tests showed a significant increase in the total number of white blood cells and neutrophils, with the left shift of the nucleus and the appearance of poisoning particles. Often have anemia, low protein, hypokalemia and low calcium hypomagnesemia, dehydration and so on.

Abdominal X-ray films showed segmental or total colon expansion, with the most obvious transverse colon and spleen. Fazio reported that the diameter of the dilated colon was 5.0-16.0 cm with an average of 9.2 cm. In the early hours of toxic megacolon, the colonic zone of the lower edge of the transverse colon can be thickened and then disappeared. At the same time, large amounts of gas in the stomach and small intestine can be observed, which may be intracellular potassium deficiency, low calcium, low phosphorus, and hypomagnesemia. Metabolic alkalosis causes gastrointestinal weakness. If there is free gas in the abdominal cavity, intestinal perforation is confirmed.

Differential diagnosis

Differential diagnosis of toxic megacolon:

1. Huge colon: Hirschsprung's disease is a false name because megacolon changes are not congenital. Because there is no ganglion cells in the distal intestinal wall of the megacolon, it is in a state of stenosis, loss of peristalsis and defecation function, resulting in proximal colonic stagnation and accumulation of gas, while continued expansion, hypertrophy, and gradually formed a megacolon change. Have a genetic predisposition.

2, colonic swelling: ulcerative colitis (UC), referred to as ulceration, unexplained rectal or colonic inflammatory disease. Mainly involving the rectum, sigmoid colon and descending colon, pathological features of mucosal congestion, edema, multiple superficial ulcers, advanced intestinal wall thickening, intestinal stenosis and associated with polyps. Clinically, it is characterized by intractable diarrhea, mucus, bloody stool or pus and bloody stool, abdominal pain and urgency. It can be accompanied by parenteral manifestations such as fever, anemia, arthritis, skin lesions and liver disease. Very few acute onset, most of the onset is slow, the course of disease is longer, often recurrent, and the period of reversal is also called chronic non-specific ulcerative colitis. Abdominal pain, diarrhea, and bloody stools can occur early. Different degrees of abdominal pain are caused by colonic muscle spasm, colonic swelling and inflammation stimulating local sensory nerves. Abdominal distension is mostly confined to the left lower abdomen or lower abdomen, showing paroxysmal mild pain. Colic can be present when the lesion is severe.

Patients with inflammatory bowel disease have severe abdominal pain, and the number of stools suddenly increases to dozens of bloody watery stools. It is necessary to be alert to emergencies. If the abdominal X-ray film shows that the transverse colon cavity diameter is greater than 6 cm, it can be diagnosed. Some people think that abnormal intestinal gas accumulation is an early phenomenon of toxic megacolon, but Caprilli believes that persistent intestinal gas accumulation and severe metabolic alkalosis make patients with severe inflammatory bowel disease easily complicated by toxic giant colon. Body temperature > 38.6. C, heart rate > 120 times / minute, blood white blood cells increased significantly. anemia. At the same time accompanied by disturbance of consciousness, lower blood pressure, dehydration and electrolyte imbalance. Therefore, the early diagnosis of this disease depends on clinical strict monitoring and abdominal X-ray film, as well as the understanding of this disease.

When the medical history is unclear or the toxic megacolon is the first symptom, attention should be paid to the toxic giants caused by bacterial dysentery, amoebic dysentery, typhoid fever, cholera, pseudomembranous colitis, ischemic colitis, diverticulitis, etc. Colonic differentiation. The course of illness from inflammatory bowel disease to toxic megacolon is generally shorter, and Fazio reports that it is about 24% less than 3 months. Toxic megacolon can also be the first symptom of inflammatory bowel disease, manifested as hyperthermia, tachycardia, decreased blood pressure, lethargy, and systemic failure; the abdomen rapidly expands, there is tenderness, the percussion is drum sound, and the bowel sounds are weak or disappear. And occasionally the lower gastrointestinal bleeding. Acute perforation is often indicated when tenderness, rebound tenderness, and muscle tension occur in the abdomen. Laboratory tests showed a significant increase in the total number of white blood cells and neutrophils, with the left shift of the nucleus and the appearance of poisoning particles. Often have anemia, low protein, hypokalemia and low calcium hypomagnesemia, dehydration and so on.

Abdominal X-ray films showed segmental or total colon expansion, with the most obvious transverse colon and spleen. Fazio reported that the diameter of the dilated colon was 5.0-16.0 cm with an average of 9.2 cm. In the early hours of toxic megacolon, the colonic zone of the lower edge of the transverse colon can be thickened and then disappeared. At the same time, large amounts of gas in the stomach and small intestine can be observed, which may be intracellular potassium deficiency, low calcium, low phosphorus, and hypomagnesemia. Metabolic alkalosis causes gastrointestinal weakness. If there is free gas in the abdominal cavity, intestinal perforation is confirmed.

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