Pathophysiology
Summary
Intestinal ischemia and necrosis result from inadequate perfusion to the bowel, most frequently affecting the small arteries near the luminal surface of the villi and mucosa. Early stages of ischemia lead to a neutrophilic infiltrate and sloughing off of villi, with intestinal crypts becoming involved as ischemia progresses. Inflammation-induced edema can obstruct venous drainage and further exacerbate the ischemia. Two key arteries in this context are the superior mesenteric artery (SMA), which supplies the small intestines and proximal large bowel, and the inferior mesenteric artery (IMA), serving the distal large bowel.
Acute mesenteric ischemia can be caused by either an occlusion of a major blood vessel or a non-occlusive pathology. Occlusive etiologies most commonly occur in the small bowel, often due to occlusion of the SMA. Occlusion of the SMA or IMA can be triggered by emboli (e.g atrial fibrillation) or atherosclerotic plaque rupture. Clinical manifestations include severe abdominal pain, nausea, vomiting, and loss of bowel sounds. Complications such as bowel infarction, perforation, and sepsis may ensue.
Non-occlusive acute mesenteric ischemia usually occurs in the colon and is caused by hypoperfusion of intestinal vessels, which can occur in cases of hypovolemia, septic shock, and cardiogenic shock. Acute colonic ischemia often occurs in watershed areas near the splenic flexure (anastomoses b/w SMA & IMA) and distal sigmoid colon (anastomoses b/w IMA and rectal arteries).
Chronic mesenteric ischemia occurs secondary to generalized atherosclerotic disease and manifests as ‘intestinal angina’ with postprandial abdominal pain, aversion to eating, and weight loss. Finally, angiodysplasia, commonly found in the colon, presents with recurrent, painless hematochezia and is sometimes associated with aortic valve stenosis.
Lesson Outline
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FAQs
Intestinal ischemia occurs due to inadequate perfusion of the bowel due to occlusive and non-occlusive etiologies. The primary occlusive cause is acute mesenteric artery occlusion, most commonly seen in the superior mesenteric artery (SMA) and often from an embolus or a thrombus formed from ruptured atherosclerotic plaques. Non-occlusive acute mesenteric ischemia occurs due to hypoperfusion of intestinal vessels. Acute mesenteric ischemia mainly affects the small bowel, while acute colonic ischemia is more common in the large bowel. Conditions like atrial fibrillation and various forms of shock can also precipitate acute mesenteric ischemia.
Ischemia initially affects the small vessels near the luminal surface of the villi in the bowel, leading to their sloughing. This triggers edema in the bowel wall, which increases pressure and obstructs venous drainage, exacerbating the ischemia. Initially, the crypts of the bowel are spared, but become involved as ischemia progresses. The end result is intestinal necrosis, patchy mucosal hemorrhage, and a neutrophilic infiltrate as a response to inflammation.
Acute mesenteric ischemia often presents with severe abdominal pain that is out of proportion to physical exam findings. Additional symptoms include nausea, vomiting, and a loss of bowel sounds due to ileus. If not promptly treated, the condition can lead to complications such as bowel infarction, perforation, and sepsis.
Chronic mesenteric ischemia is a long-term condition primarily caused by atherosclerosis leading to narrowing of the mesenteric arteries. It manifests as ‘intestinal angina,’ characterized by postprandial abdominal pain, aversion to eating, and subsequent weight loss. Unlike acute mesenteric ischemia, which has a rapid onset, chronic mesenteric ischemia follows a more gradual course and is more prevalent in obese older females with generalized atherosclerotic disease.
Angiodysplasia is a condition characterized by malformed blood vessels in the gastrointestinal tract, which are often thin-walled, dilated, and tortuous. It predominantly occurs in the colon, particularly in the cecum. Clinically, it can lead to recurrent, painless hematochezia. Angiodysplasia is also associated with aortic valve stenosis, which may exacerbate the bleeding.
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