A 74-year-old hypertensive male presents with a four-hour history of acute-onset severe diffuse abdominal pain. Two weeks prior he was hospitalized with a large anterior wall MI complicated by intermittent atrial fibrillation. Due to a history of frequent falls, he was not anticoagulated. Physical examination is remarkable for an uncomfortable individual with an irregularly irregular heart rhythm and a minimally tender abdomen without peritoneal signs. Laboratory assessment is remarkable for a leukocytosis of 14,000 and mild metabolic acidosis. Electrocardiography indicates atrial fibrillation with a rapid ventricular response between 120 and 140 beats/minute. CT scan of the abdomen illustrates a distended small bowel and a questionable filling defect within the superior mesenteric artery (SMA). Mesenteric arteriography displays a “mercury meniscus sign” within the SMA 4 cm from the aorta. A diagnosis of cardioembolic acute mesenteric ischemia is made and the patient is immediately taken to the operating suite.
Incidence: 3 to 5 per 100,000.
Sixth to seventh decade of life; more often women.
Etiology: thromboembolism 50%, thrombosis 20%, nonocclusive mesenteric ischemia (NOMI) 20%, others 10%.1
Clinical presentation depends on adequacy of visceral perfusion by the three mesenteric arteries: celiac artery (CA), superior mesenteric artery (SMA), and inferior mesenteric artery (IMA) (Figure 45-1). There are usually collateralizations among the mesenteric arteries that compensate for flow if there are stenoses or occlusions, hence the common adage; two of the three mesenteric arteries need to be involved before symptoms arise. However, single mesenteric artery occlusion can be symptomatic in the absence of adequate collateralization, such as in acute thromboembolism.
FIGURE 45-1
Normal mesenteric artery anatomy, their branches and natural collateralization. Celiac artery (CA), superior mesenteric artery (SMA), inferior mesenteric artery (IMA), common hepatic artery (CHA), splenic artery (SA), gastroduodenal artery (GDA), superior pancreaticoduodenal artery (SPDA), inferior pancreaticoduodenal artery (IPDA), left gastric artery (LGA), right gastric artery (RGA), right gastroepiploic artery (RGEP), left gastroepiploic artery (LGEP), jejunal arteries (JAs), middle colic artery (MCA), right colic artery (RCA), ileocolic artery (ICA), marginal artery of Drummond (MAD)—between left branch of MCA and ascending branch of left colic artery (LCA), sigmoidal artery (SgA), superior rectal artery (SRA).
Thromboembolism to the SMA is common due to its obtuse angle and path, diverging gently away from the aorta and its flow.
Embolus source: cardiac arrhythmias (atrial or ventricular), atherosclerotic aorta, proximal thoracic aneurysms. Proximal small intestines may be uninvolved if embolus occludes the SMA a few centimeters beyond its origin, sparing proximal jejunal branches. Transverse colon may be spared if occlusion is beyond the middle colic branch of the SMA.
Patients are generally older and usually women.
Evidence of atherosclerotic disease in other vascular beds (coronary, lower extremities) is usually present.
More than half have chronic mesenteric ischemia (CMI) symptoms (postprandial pain, food fear, weight loss).2 Thus, patients develop acute mesenteric ischemia (AMI) in the setting of CMI secondary to occlusive disease.
AMI can also be precipitated in the background of hemodynamic compromise during other cardiovascular events (acute myocardial infarction [MI], coronary artery bypass, sepsis, shock).
Vasospasm of the mesenteric arteries in the absence of critically stenotic lesions can be incited by digitalis, alpha-adrenergic agents, low-flow states (cardiac failure, shock, etc), and less commonly early enteral feeding after revascularization for CMI.
Diagnosis is angiographic, and features include narrowing at origins of SMA branches, “string of sausage” sign—alternate narrowing and dilations of SMA intestinal branches—mesenteric arcades spasm, and nonfilling of the intestinal intramural branches.3
NOMI has a high mortality rate as patients tend to have more severe underlying conditions and diagnosis is often delayed.
Other causes of AMI include mesenteric vein thrombosis (MVT), aortic dissections, Takayasu arteritis, fibromuscular dysplasia, and polyarteritis nodosa.
Superior mesenteric vein (SMV) thrombosis is associated with hypercoagulability, visceral malignancies (eg, pancreatic mass causing extrinsic compression of the SMV or portal vein), pancreatitis, and cirrhosis. Venous occlusion and hypertension lead to intestinal edema and infarction.
Aortic dissection intimal flaps can exclude, compress, or extend into the mesenteric arteries resulting in thrombosis (Figure 45-2A and B).
FIGURE 45-2B
Extension of type-B aortic dissection into superior mesenteric artery (SMA) (small white arrow), patent and perfused right renal artery (RRA), and malperfusion or ischemia to the left kidney (LK) without contrast enhancement, ischemia to the left colon (LC) with mural thickening. (Image courtesy of Henry Baele, MD.)
Acute-onset abdominal pain (90%); nausea, vomiting, diarrhea—30% to 40%, blood per rectum, 10% to 15%2
Abdominal pain out of proportion to examination, initially
Peritoneal signs (diffuse abdominal tenderness, guarding, rebound tenderness, abdominal rigidity, absent bowel sounds); if intestinal necrosis ensues, sepsis, and shock