*emedicine.medscape.com is one of the best medical resources on the internet. I strongly recommend it.
All that follows is from the Toxic Megacolon.
Toxic megacolon is a life-threatening condition characterized by nonobstructive segmental or pancolonic dilatation of at least 6 cm with systemic toxicity.  It was recognized by Marshak and Lester in 1950.  Although inflammatory bowel disease (IBD) is a common reason for toxic megacolon, other etiologies including infections, inflammation, bowel ischemia, radiation, and certain medications can lead to the development of this condition. [3, 4, 5]
It is important to differentiate toxic megacolon from other conditions that present with megacolon without systemic toxicity such as Hirschsprung disease,  idiopathic megacolon/chronic constipation, chronic long-standing constipation of any etiology, and intestinal pseudo-obstruction (Ogilvie syndrome).  Patients with these conditions do not develop signs of systemic toxicity and, therefore, do not fall into the category of having toxic megacolon (see the image below). (See also Etiology, Presentation, and Workup.)
Inflammatory causes of toxic megacolon include the following:
Crohn colitis 
Infectious causes of toxic megacolon include the following:
Salmonella species 
Shigella species 
Campylobacter species 
Entamoeba histolytica: About 3% of patients with amoebic infections develop severe colitis and a small percentage of these will have toxic megacolon; use of loperamide in this setting increases the risk of developing toxic megacolon 
Invasive aspergillosis 
Other etiologies of toxic megacolon include the following:
Often, triggering or predisposing factors can be identified. Signs and symptoms of acute colitis may be present for as long as 1 week before dilatation develops. Although the risk of toxic megacolon increases with the severity of the colitis, rapid tapering or abrupt discontinuation of medications such as steroids, sulfasalazine, and 5-aminosalicylic acid may precipitate toxemia and dilatation.
Medications that negatively impact bowel motility are also implicated in the development of toxic megacolon. These include, but are not limited to, anticholinergics, antidepressants, loperamide, atropine,  and opioids. Procedures such as barium enema or colonoscopy may cause distention, impair blood supply, or exacerbate a microperforation and cause subsequent toxemia. 
A retrospective study by Tschudin-Sutter et al indicated that the incidence of toxic megacolon is higher in pediatric patients with community–associated, rather than healthcare facility–associated, C difficile infection.  The study involved 202 pediatric patients with C difficile infection, including 38 with community–associated infection, 144 with healthcare facility–associated infection, and 20 with an indeterminate source of infection. Compared with the healthcare facility–associated group, children with a community–associated infection had a higher rate not only of toxic megacolon but also of toxic shock and recurrence. (They were less likely, however, to have comorbidities than were children with healthcare facility–associated infection.) 
Toxic megacolon mortality is variable depending on the treatment modality. One study revealed that before 1976, there was a 27% mortality of toxic megacolon among patients treated medically and a 19% mortality in patients treated surgically.  In-hospital mortality for patients with toxic megacolon fell from 9.2% to 6.5%, according to an observational study for the period between 2010 and 2014.  Older age, hypertension, neurologic disorders, coagulopathy, anemia, chronic lung disease, heart failure, and renal failure were the main predictors of increased mortality. 
Colon perforation is associated with higher surgical mortality relative to undergoing surgery before colonic perforation. [34, 38] Similarly, postoperative mortality in patients with C difficile infection and toxicity is lower when they undergo surgery before the development of septic shock compared to septic patients who have surgery. 
Fecal microbiota transplantation has shown promise as a salvage therapy for critically ill patients with C difficile infection and toxic megacolon in whom maximum medical therapy failed and who are not a surgical candidates. 
Mortality in patients with inflammatory bowel disease (IBD) and toxic megacolon have fallen in the last 3 decades due to multiple factors, including early recognition of toxic megacolon, early escalation from steroid treatment to biologics such as infliximab or cyclosporine, improved care in the intensive care unit (ICU), earlier surgical intervention, and optimal postoperative care. 
Note that C difficile infection in patients with IBD are associated with higher rates of colectomy and longer hospital stays compared to IBD patients without C difficile infection. 
Patients with inflammatory bowel disease (IBD) are at a higher risk of developing toxic megacolon during the early stages of their disease; in some cases, it can be the first manifestation of the disease. [43, 44] Patients with Crohn colitis are more vulnerable than those with ulcerative colitis for developing toxic megacolon. 
Findings of ileus may indicate the severity of colitis in patients with C difficile infection. 
Patients with toxic megacolon typically have signs and symptoms of acute colitis that may be refractory to treatment. Common complaints include diarrhea, abdominal pain, rectal bleeding, tenesmus, vomiting, and fever. In a paper that studied the clinical presentation of pseudomembranous enterocolitis complicated with toxic megacolon, the presenting symptoms and signs included diarrhea (100%), malaise (91%), abdominal pain (82%), abdominal distention (82%), and abdominal tenderness (72%).  However, another study revealed that absence of diarrhea does not rule out the severity of the C difficile infections and the risk of developing toxic megacolon. 
A careful history may reveal recent travel, antibiotic use, chemotherapy, occupational exposure, or immunosuppression. Patients are usually very ill, and they can present with signs of fever, tachycardia, hypotension, and/or abdominal distention and tenderness.
The vital signs in a patient with toxic megacolon generally reveal tachycardia and fever. If the condition is severe, the patient may be hypotensive or tachypneic; patients may be obtunded.
As noted earlier, it is important to differentiate toxic megacolon from other conditions that present with colon dilatation without systemic toxicity (eg, Hirschsprung disease,  idiopathic megacolon/chronic constipation, chronic long-standing constipation of any etiology, and intestinal pseudo-obstruction [Ogilvie syndrome]).  Patients with these conditions do not develop signs of systemic toxicity and, therefore, do not fall into the category of having toxic megacolon.
In inflammatory colitides (ie, ulcerative colitis, Crohn colitis), physical findings may be minimal, because high-dose steroids are routinely administered; however, the abdomen may be distended, and the bowel sounds are usually hypoactive. Signs of perforation may also be masked by high-dose steroids.
Peritoneal signs may indicate perforation. They include the following:
In general, toxic megacolon should be suspected in patients presenting with abdominal pain with distention and acute-onset chronic diarrhea. The diagnosis is made based on the clinical picture of systemic toxicity along with evidence of colon dilatation more than 6 cm. 
The most common criteria used to diagnose toxic megacolon are the ones proposed by Jalan et al in 1969,  as follows:
Radiographic evidence of colonic dilatation: The classic finding is a more than 6-cm dilatation in the transverse colon
Any three of the following: Fever (>101.5°F [>38°C]), tachycardia (>120 beats/min), neutrophilic leukocytosis (>10.5 x 103/µL), or anemia
Any of the following: Dehydration, altered mental status, electrolyte abnormality, or hypotension
Plain abdominal radiographs are essential for the diagnosis and management of toxic megacolon. Repeated serial abdominal plain films are necessary to monitor the progress of the disease and the efficacy of treatment.
Radiographic findings include the following:
Air-fluid levels in the colon with an absent or abnormal haustral pattern
Deep mucosal ulcerations and possible pseudopolyp projections into the colon lumen
The presence of air in the small bowel on x-ray: Can be predictive of toxic megacolon 
Segmental parietal thinning: Pathognomic for toxic megacolon 
Comparison with old baseline films, if available, is helpful. Avoid barium enema studies in a patient who is severely toxic; the potential for perforation is considerable.
Ultrasonography of the intestines appears to be a potential diagnostic test for toxic megacolon.  In one study, investigators demonstrated similar findings in four cases, including the following:
Complete loss of haustra coli of the colon
Hypoechoic and thickened bowel walls with irregular internal margins in the sigmoid and descending colon
Marked dilatation of the transverse colon (>6 cm), a finding that correlated well with the plain radiograph of the abdomen
Hypoechoic and thin (< 2 mm) bowel walls without haustra coli in the dilated colon; in patients who underwent surgery, the postoperative pathohistologic findings of the bowel walls correlated with the ultrasonographic features observed before surgery
Slight dilatation of ileal bowel loops (diameter >18 mm) with increased intraluminal gas and fluid
Computed Tomography Scanning
Computed tomography (CT) scanning should be obtained in patients in whom the diagnosis of toxic megacolon is being considered. This imaging modality may identify a local or contained perforation.  If the diagnosis remains unclear or the cause of toxicity is thought to be an abscess, CT scanning may be helpful.
Imbriaco and Balthazar found that CT scanning was more accurate than plain radiography in detecting severe colitis.  CT scans may show diffuse colonic wall thickening, thickened haustra with alternating bands of high and low density (‘‘accordion sign’’), a multilayered appearance caused by different densities of edematous submucosa, or hyperemic mucosa (‘‘target sign”) and peri colic stranding. CT scanning was superior in showing the severity and length of colitis as well as the presence of dilatation. 
Endoscopy can provide a further advantage for evaluating the etiology of toxic megacolon such as identifying cytomegalovirus (CMV) or pseudomembranous colitis, especially when clinical suspicion exists despite negative stool studies for C difficile.
Endoscopy may take the form of flexible sigmoidoscopy or colonoscopy. However, if clinical concern for toxic megacolon exists, the examination should not progress beyond the sigmoid colon, if at all. The scope should be advanced only as far as necessary for diagnosis. Air insufflation should be minimal. Sigmoidoscopy can miss the diagnosis of CMV infection because the lesions can be localized in the cecum or ascending colon. 
According to some experts, colonoscopy is generally justified only if the patient has no or minimal inflammation of the sigmoid colon or rectum. Perforation is an obvious potential complication of this approach. 
Please see Toxic Megacolon Treatment & Management for details of treatment. Updated: Mar 16, 2021
Author: Fadi Alali, MD;