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It is the clinical term to refer to acute toxic colitis with dilation of the colon.
The dilation can be total or segmental.
A more contemporary term for toxic megacolon is toxic colitis because patients can develop toxicity without megacolon.
The distinctive signs of toxic megacolon (toxic colitis), a potentially lethal condition, are nonobstructive colonic dilation more significant than 6 cm and symptoms of systemic toxicity.
The researchers Jalan and Cols described the diagnostic criteria, which are the following:
- Radiographic evidence of colon dilation – The classic finding is more than 6 cm in the transverse colon.
- Any of 3 of the following – Fever (> 101.5 ° F), tachycardia (> 120 beats / min), leukocytosis (> 10.5 x 10 3 / μL), or anemia.
- Any of the following – Dehydration, altered mental state, electrolyte abnormality, or hypotension.
Pathophysiology
Although the pathophysiology of megacolon / toxic colitis is not proven, several factors can contribute to its development and precipitation. In cases of uncomplicated colitis, the inflammatory response is limited to the mucosa.
The microscopic mark is the inflammation that extends beyond the mucosa in the smooth muscle and the serosa layers.
The extent of dilation seems to be correlated with the depth of inflammation and ulceration.
While the inflammatory response typical of ulcerative colitis is limited to the mucosa, the toxic megacolon is characterized by severe inflammation that extends into the smooth muscle layer, paralyzing the colon’s smooth muscle and leading to dilation.
The Mourelle studies showed significantly higher amounts of inducible nitric oxide synthetase in the muscular propria of patients with toxic megacolon, particularly in the more dilated colon segments.
It is believed that nitric oxide inflammation and synthetase positively regulate local levels of nitric oxide, which inhibits the smooth muscle of the colon and causes dilation.
As inflammation progresses to the smooth muscle layers of the colon, nitric oxide and local inflammatory modulators appear to be involved in the pathogenesis.
In toxic megacolon, neutrophils also invade the muscle layer and directly damage muscle cells by releasing proteolytic enzymes, cytokines, and leukotrienes.
Systemic uptake of cytokines and other inflammatory mediators produces fever, tachycardia, hypotension, and other signs of systemic toxicity.
Nitric oxide is generated by inflammatory cells such as neutrophils and macrophages in the inflamed parts of the colon, inhibiting smooth muscle tone and leading to dilation of the colon.
The involvement of the myenteric plexus is not consistent and probably does not contribute to colon dilation. Hypokalemia and other electrolyte disorders probably do not contribute to dilation in most patients.
Epidemiology
The incidence of toxic megacolon (toxic colitis), cited in the literature, depends on the etiology. It is estimated that the risk of toxic megacolon in ulcerative colitis is 1-2.5%.
In a series of 1236 patients admitted to a hospital over 19 years, toxic megacolon was present in 6% of patients, precisely 10% of admissions for ulcerative colitis, and 2.3% of admissions of Crohn’s disease.
Toxic megacolon has been reported in approximately 5% of severe attacks of ulcerative colitis. In pseudomembranous colitis, toxic megacolon occurs in 0.4-3% of patients.
This number is expected to increase in proportion to the increasing prevalence of pseudomembranous colitis, which is believed to be due to the increased use of broad-spectrum antibiotics.
Demographic data related to race, sex, and age
In the United States, Jews are more prone to ulcerative colitis than people who are not Jewish. In Israel, the Ashkenazi Jewish people have a higher incidence of ulcerative colitis than the Sephardic Jewish people. There are no data on race and incidence.
As for ulcerative colitis, most studies show that both sexes are affected equally.
Young adults (20-40 years) are mainly affected by ulcerative colitis, but this disease can occur at any age.
There is no preference concerning this condition, which seems to exist for any particular age group.
All ages can be affected. It has been reported that the average duration of the disease is 3-5 years.
Forecast
Some studies have shown that the prognosis is poor with the medical management of toxic megacolon (toxic colitis).
A study by Grant and Dozois followed the clinical course and the outcome in 38 patients with toxic megacolon who were treated with non-operative success.
Thirty-two patients had ulcerative colitis, and 6 had Crohn’s disease, with a complete follow-up of 3 to 22 years (average, 13 years). Eleven of the 38 patients (29%) suffered a second episode of acute fulminating colitis or recurrent toxic megacolon.
In short, 18 patients (47%) underwent colon resection, which was performed urgently in 15 patients.
The survival forecast of toxic megacolon should be excellent without perforation. Mortality rates of toxic megacolon have improved substantially in recent decades, from 20% in 1976 to 4-5%.
The decrease results from previous recognition, intensive medical management, early surgical consultation, and improved surgical technique and postoperative care.
If perforation occurs, the mortality rate is approximately 20%.
In the case of ulcerative colitis, a proctocolectomy cures the patients of the disease.
In the case of Crohn’s disease, proctocolectomy does not necessarily cure the patient because Crohn’s disease can occur in any part of the gastrointestinal tract.
