Ischemic colitis

Ischemic colitis: It is colonic inflammation as a result of decreased blood supply to the bowel wall from occlusive (e.g.emboli) or non-occlusive (e.g. shock) causes, which can be transient, or in severe, persistent cases lead to gangrene of the colon. Risk factors include age>65 years, female gender, smoking, HT, DM, COPD, IHD, peripheral vascular disease, IBS, sickle cell disease, constipation, abdominal surgery, thrombophilia etc. Symptoms are often precipitated after a colonoscopy, enema, laxative use, heavy drinking, pancreatitis, shock and burns. It presents with acute abdominal pain, cramping, hematochezia, nausea, vomiting and abdominal distension. Peritoneal signs like rebound tenderness, guarding and rigidity along with fever, tachycardia and leukocytosis are seen in severe cases with transmural necrosis and perforation. Small vessel disease is more commonly associated with ischemic colitis than large vessel disease. Initially, ischemic changes are seen in the mucosa and submucosa, eventually extending deeper and causing full thickness gangrene in severe cases. Changes are more prominent along the antimesenteric border of the colon. Revascularization is sometimes associated with reperfusion injury to the colon. A high index of clinical suspicion is needed for diagnosing ischemic colitis as it has vague, transient features and often clinically mimics other inflammatory disorders. Imaging studies show thumbprinting sign (from mucosal edema), thickening of the bowel wall, pericolonic fat stranding and “target sign”. CT with contrast is the imaging modality of choice. Danger signs on imaging are pneumoperitoneum, pneumatosis intestinalis and pneumatosis coli (air in the mesenteric or portal vein). Colonoscopy is the gold standard in confirming the diagnosis and shows pale and edematous mucosa with ulcerations, hemorrhages and sometimes pseudomembrane formation. Gangrenous bowel will look grayish-black and will be immobile. Management depends on severity. Most cases can be treated with supportive therapy, bowel rest, parenteral nutrition, nasogastric tube and broad spectrum antibiotics. Deteriorating cases are treated with bowel resection surgery.

Ischaemic colitis in a 74-year-old male with vasculitis who presented with abdominal pain and bloody diarrhoea. (a, b) Contrast-enhanced CT scan reveals involvement of the sigmoid colon and splenic flexure (orange arrows) with marked wall thickening and pericolic streakiness (asterisk). Diagnosis was confirmed at colonoscopy and biopsy. The ischaemic process resolved

Paralytic or adynamic ileus: It is a motility disorder of the intestine resulting from failure of peristalsis, typically of all segments of the gastrointestinal tract including small and large intestines. It can be a result of surgery especially abdominal surgery, electrolyte imbalances like hypomagnesemia, acid-base disturbances, uremia, pancreatitis, vitamin deficiencies, hypothyroidism, trauma, DM, drugs like narcotics, anesthesia, mesenteric ischemia, intraperitoneal infection etc. It presents with abdominal distension, absent bowel sounds, nausea and vomitings. Pain is not prominent, unlike in true bowel obstruction. Abdominal CT scan with Gastrografin, barium enema and abdominal X ray are preferred investigations. Imaging shows dilated loops of small and large intestine with air-fluid levels. Some cases may have local paralytic ileus. Treatment is supportive with bowel rest, nasogastric tube decompression, correction of underlying disorders like acid-base imbalances, initiation of early enteral feeding may help as well as drugs like neostigmine, erythromycin, metoclopramide and lactulose. Spontaneous return of gastrointestinal motility is seen in 2-4 days.

Diverticulosis and diverticulitis of the colon: Diverticulosis is a common disorder of old age, characterized by the formation of multiple sac-like outpouchings or diverticula. Diverticulitis occurs when the diverticula are inflamed, and is a potentially lethal condition. Diverticula form at weak points in the colon wall, specifically where the vasa recta penetrate the colon wall. They are composed of herniating mucosa and submucosa. Abnormal elastin deposition and increased collagen cross-linking is seen in the colonic wall in patients with diverticulosis. Increased intraluminal pressure in the colon, potentiated by constipation and lack of fibre in diet, predisposes to diverticula formation. It is more common in the left colon.

Most patients with diverticulosis are asymptomatic, some patients may present with mild abdominal pain, alterations in bowel habits and blood in stools. Diagnosis is confirmed by colonoscopy which shows diverticula. Treatment is by increasing fibre in the diet, probiotics, being more active and supportive therapy for bleeding. Mesalazine and rifaximin may reduce symptoms. Surgery is needed if massive bleeding or problematic symptoms with increased risk of infection are present.

Diverticulitis results from micro or macro-perforations in the diverticula which may be caused by food particles or due to obstruction by fecaliths and resultant inflammation. It may be complicated by abscess formation, fistula, peritonitis and sepsis. Smoking and NSAIDS increase the risk of perforation in diverticulitis. Patients present with fever, abdominal pain typically in the left lower quadrant, tenderness, diarrhea or constipation, nausea, vomiting and leukocytosis. Colovesicular fistula may present with passing gas and feces in urine. Peritoneal signs may be present. Endoscopy is contraindicated as the inflamed bowel is prone to perforation. CT scan with contrast is the investigation of choice. Imaging shows thickening of the bowel wall, pericolic fluid, pericolic fat stranding and complications like fistula or abscess may be seen. Treatment is by bowel rest, intravenous fluids and broad spectrum antibiotics with anaerobic coverage (metronidazole or clindamycin). Surgery is needed for complications and in severe inflammation, bowel resection with colostomy and anastomosis is done when appropriate.