The elderly patient who presents with lower gastrointestinal (GI) bleeding is not an uncommon presentation in primary care. The first priority should always be assessment of the hemodynamic status, followed by resuscitation as necessary; fortunately, this patient's vital parameters appear to be quite stable. Determination of the likely underlying etiology should be next; in this regard, note that the blood was fresh, and well mixed with the fecal matter, favoring a colonic pathology. A malignancy of the colon is an important consideration here, given his age and history; other key possibilities include infectious colitis and ischemic colitis. Note that while diverticulosis (as opposed to acute diverticulitis) can also give rise to lower GI bleeding, this is typically painless, with few or no associated abdominal signs. Furthermore, inflammatory bowel disease is unlikely to present for the first time at this age. Colonoscopy is a good next step; this reveals a large, necrotic-appearing mass occupying the descending colon; biopsies subsequently reveal features suggestive of mucosal infarction, showing this to be ischemic colitis. Note that barium enemas have largely been superseded by colonoscopy, and are best avoided in the acute setting, given the risk of perforation; neither can diagnostic laparoscopy be reasonably justified here. Mesenteric angiography has no role in the evaluation and management of ischemic colitis, because by the time of symptom onset, colonic blood flow has usually returned to normal. Key elements of his management include resting the bowel, and empirical broad-spectrum antibiotic therapy to minimize bacterial translocation and sepsis. In the acute setting, surgery is only indicated if there is fulminant colitis, peritonitis, or massive bleeding. Systemic corticosteroid therapy is contraindicated in these patients, as this may potentiate the ischemic damage, and predispose to colonic perforation.
Ischemic colitis is the most common form of ischemic injury involving the gastrointestinal tract, accounting from 1 in 1000 hospitalizations; over 90% of cases occur in patients over 60 years of age. Similar to the other forms of bowel ischemia, the initial insult is a reduction in the blood supply; this can be due to nonocclusive injury (i.e. due to a drop in the systemic perfusion pressure), or following arterial or venous occlusion. Note that the colon is more predisposed to (nonocclusive) ischemic injury than the remainder of the bowel, because of the relatively poorer network of collaterals between the superior and inferior mesenteric arteries (which provide the primary blood supply to the colon). The collateral circulation is particularly weak in the area of the splenic flexure; this is called the 'watershed area', and explains the relatively higher incidence of the disease in the left colon. Advanced age is a well known risk factor for ischemic colitis; one reason might be because of increased vascular resistance secondary to age-related tortuosity (thus predisposing the colon to ischemia following relatively smaller decreases in the systemic blood pressure). In addition, comorbid illnesses often encountered in the elderly (including hypertension and chronic kidney disease requiring hemodialysis) further predispose this age group towards ischemic injury; certain medications used in the management of these conditions (such as antihypertensives, digoxin, diuretics and NSAIDs) may also contribute. Ischemic colitis can present with a spectrum of severity ranging from mild transient disease, to fulminant pancolitis; in patients with the latter, the presence of peritonitis and hemodynamic instability may suggest the diagnosis. Mild to moderate disease typically assumes a nonspecific clinical picture; these patients may manifest symptoms such as abdominal pain, diarrhea, or the passage of stools mixed with blood; note that the last of these usually occurs within 24 hours of the onset of abdominal pain. Laboratory investigations are not diagnostic by themselves, but may provide supportive evidence; markers of tissue damage, such as lactate, creatine phosphokinase (CPK), amylase and alkaline phosphatase may be elevated. Electrolyte and acid-base disturbances (particularly metabolic acidosis) may be seen in patients with severe disease. Imaging studies are also not diagnostic, and are mainly of use in excluding other differentials. Plain abdominal radiographs may show bowel dilatation or air-fluid levels; in about 20% of patients, they may demonstrate thumbprinting from mural thickening, and rarely, pneumatosis coli, indicating advanced disease. In addition to the above, CT imaging may reveal further indirect evidence of ischemic colitis, such as mural thickening or ascites. Ultrasonography may also provide information regarding the colonic wall, and when combined with doppler studies, demonstrates a high degree of specificity for detection of ischemic changes in the colonic wall; however, the sensitivity is low. Note that barium, water-soluble, or air contrast enemas have been mostly superseded by colonoscopy; if performed, they may show thumbprinting, mucosal edema, eccentric mural deformity, sacculation or strictures. In addition, angiography of colonic vessels is only indicated if mesenteric ischemia needs to be excluded. Colonoscopy is the current gold standard for the diagnosis of ischemic colitis; in late disease, this may reveal highly specific features such as green or black mucosa (indicating transmural infarction), or the 'single-stripe sign' (a single longitudinal ulcerated or inflamed colon strip). In early disease, the mucosa may appear pale and edematous, with interspersed areas of hyperemia; later ulceration, pseudopolyps, pseudomembranes, and bleeding into the mucosa may be observed. Note that these features are less specific to ischemic colitis. It is important to appreciate that mucosal hemorrhages dissipate within approximately 48 hours; thus in patients in whom ischemic colitis is suspected, colonoscopy is recommended within this time period. Histology of an ischemic lesion typically demonstrates distorted crypts, mucosal and submucosal hemorrhages, inflammatory infiltration in the lamina propria, granulation tissue formation, intravascular platelet thrombi and necrosis, and ghost cells; the last of these is pathognomonic for ischemia. Note that endoscopic procedures are not without complications; bowel distension secondary to air insufflation may further diminish blood flow; furthermore, severe ischemia renders the colonic wall weak and prone to perforation with ungentle endoscopy. The management of ischemic colitis primarily depends on the severity of the disease. Patients with only mucosal ischemia respond well to a conservative approach; this should include bowel rest, intravenous fluids, optimization of cardiac function and oxygenation, and withholding of medications which might worsen bowel ischemia (for example, NSAIDS). Note also that bowel ischemia increases gut permeability and the potential for bacterial translocation; broad spectrum antibiotic therapy may reduce the incidence of infection and sepsis. Surgical intervention and resection of the diseased segment is warranted if bowel wall necrosis is present, or in the case of chronic colitis; unfortunately, the operative mortality of patients with severe ischemic colitis is as high as 60%. A minority of patients who recover may go on to develop strictures due to subclinical ischemia. Therefore, follow up endoscopy is important to ascertain that complete mucosal recovery has occurred. Certain patients may develop a form of chronic colitis due to persistent low grade ischemia; this may manifest as persistent diarrhea, rectal bleeding and weight loss. However, the majority of patients with less severe disease improve within days, and recover completely within 1 to 2 weeks.