18.3.5 Diagnostic Procedures
Nonspecific laboratory testing includes a complete blood count, which shows a large number of leukocytes and an absence of other symptoms.
Plain radiographic studies show:
Mild, diffuse bowel dilatation
Bowel wall thickening (a radiographic finding of “thumbprinting”)
“Sawtoothing” caused by multiple superficial ulcerations
Advanced ischemia or colonic infarction is associated with:
Free air in the abdominal cavity
Air within the bowel wall
Air in the portal venous system
In contrast studies, barium must be used with caution because of the risk of perforation and subsequent severe barium peritonitis. The following are seen on contrast imaging:
Thickening of the bowel wall
Narrowing and spasm
Three endoscopic stages are recognized:
Acute: petechiae, pale mucosa, hyperemia, and necrosis
Subacute: ulceration and exudation
Chronic: stricture, decreased haustration, and mucosal granularity
Some surgeons suggest that laparoscopy, rather than colonoscopy, should be used for the diagnosis and treatment of fulminant ischemic colitis.
Computed Tomography and Ultrasonography
These procedures may show irregular thickening of the submucosa or narrowing of the lumen. Color Doppler ultrasound has been used to differentiate the bowel wall thickening seen in ischemic colitis from that seen in inflammatory bowel disease. MRI, however, is used more often to confirm the diagnosis.
Angiography is not routinely used in ischemic colitis.
It rarely shows significant vascular occlusions.
It is limited to clinical situations in which ischemic colitis involves the ascending colon, such as acute thrombosis or embolism of the superior mesenteric artery.
18.3.6 Differential Diagnosis
Colonic injury induced by nonsteroidal anti-inflammatory drug use
Carcinoma of the colon
Ischemic colitis accounts for only a small percentage of colonic disease seen in medical and surgical offices. Most patients with ischemic colitis do not have peritoneal signs, which results in frequent misdiagnosis and a large underestimation of its incidence.
Outpatient therapy is possible in patients with mild symptoms. Patients with abdominal pain and no evidence of peritonitis or systemic toxicity should be treated expectantly.
Conservative treatment includes intensive care and monitoring of vital signs.
Patients must have frequent abdominal examinations.
Intravenous hydration, bowel rest measures, and administration of wide-spectrum antibiotics that cover enteric flora are usually required.
The use of pharmaceutical agents other than antibiotics should be avoided, particularly vasoconstricting drugs.
The use of vasodilators such as glucagon and papaverine is controversial.
The use of anticoagulants has not gained wide acceptance.
The use of corticosteroids is contraindicated in patients with ischemic colitis because it can lead to silent colonic perforation.
Patients usually respond to conservative measures within a few days to 2 weeks.
Follow-up colonoscopy may be necessary to identify progression of the colonic injury or stricture formation.
Surgery is indicated in patients with peritonitis, transmural infarction or perforation of the colon, or bleeding from ulcerations.
Surgical intervention may also be necessary in patients with chronic, segmental colitis or formation of stricture after ischemic injury.
Before referring patients with stricture to surgery, forceful endoscopic balloon dilation can be attempted in those who are asymptomatic.
Surgical intervention usually involves resection of the ischemic segment of the colon and exteriorization of the remaining ends of the bowel.
Primary anastomosis and revascularization are contraindicated.
18.4 Infectious Colitis
Infectious colitis is one of the most common forms of colitis and is usually caused by bacterial, viral, and parasitic agents. It often occurs during childhood.
Bacterial: The most common bacterial agents responsible for infectious colitis are E. coli and species of Shigella, Salmonella, Campylobacter, and Yersinia.
Parasitic: Entamoeba histolytica is the most common cause of parasitic colitis worldwide.
E. coli–mediated colitis is characterized by diarrhea, abdominal cramps, and fever. It mostly affects children. A risk of hemolytic uremic syndrome and hemorrhagic colitis after infection with enterohemorrhagic E. coli strains is estimated to be present in 10–15 % of children.
Shigella infections range from asymptomatic ones to mild gastroenteritis to severe dysentery. Dysentery has a sudden onset and presents with high fever (39–40 °C), abdominal pains, and diarrhea. Stools are frequent (more than ten daily) and contain blood and mucus. Symptoms of central nervous system irritation can also be observed.
Salmonella infections usually occur during summer and autumn, most commonly in children. They are characterized by a sudden onset within 8–48 h after ingestion of contaminated food. Patients present with abdominal cramps, nausea, and fever. Stools are watery and sometimes contain blood.
Enteritis caused by Campylobacter is characterized by a sudden onset, fever (sometimes >40 °C), and abdominal pain, followed by diarrhea. Stools are watery and frequent (2–20 times daily), and usually contain blood.
Yersinia enterocolitica infection presents with an abrupt onset of watery diarrhea containing blood. Patients complain of severe abdominal pain, joint pain, and skin eruption. A febrile response occurs in older children.
Amoebiasis commonly manifests with bloody diarrhea, abdominal pain, and fever.
In cases of severe diarrhea and vomiting, one must take care of physical signs suggesting dehydration (e.g., dry mucous membranes, decreased skin turgor, orthostasis) and leading to dysregulation of the acid–base balance.
18.4.5 Diagnostic Procedures
Most infectious factors can be cultured from the stool using appropriate media. Gram and methylene blue staining of the stool is recommended. White blood cell counts can be elevated or normal. In many cases, no pathogen is identified, and diagnosis is established based on medical history and clinical symptoms. In typical infectious colitis, the lamina propria of the large intestine is infiltrated by polymorphonuclear leukocytes.