Laboratory Evaluation
The most common laboratory abnormalities in AMI are hemoconcentration, leukocytosis, elevated lactic acid, metabolic acidosis, and a high anion gap. Elevated amylase and creatinine phosphokinase are also frequently observed but are not specific for AMI. Hyperphosphatemia and hyperkalemia are frequently late signs and are associated with bowel infarction. Findings on plain abdominal radiographs are nonspecific and should not be utilized in the workups. Barium enemas also have no place in diagnosis, as this may reduce perfusion to the bowel wall and cause perforation.5 Leukocytosis and high lactate levels appear to be present in the majority of patients, though these are not specific for acute mesenteric ischemia.4
Imaging Studies
In the past, catheter-based angiography was considered the gold standard for diagnosis. However, the more readily available CTA is emerging as the primary imaging modality to diagnose mesenteric ischemia.3 Both CT and contrast angiography play a major role in the diagnosis. In addition to mesenteric ischemia, CT also allows for identification of nonvascular causes of abdominal pain. Contrast angiography has an important role in early diagnosis and is helpful in treatment planning as well as operative interventions.4
While CTA is the most frequently used technique in suspected AMI, contrast-enhanced three-dimensional magnetic resonance angiography (MRA) is also widely used. However, the inferior mesenteric artery and other splanchnic vessel periphery are currently better assessed with CTA due to the higher special and temporal resolution of the former. Both CTA and MRA are excellent screening techniques for AMI due to various causes.6
Duplex Doppler sonography has also been suggested as a screening tool in patients with suspected mesenteric ischemia, but this modality has multiple limitations, including failure to obtain adequate Doppler signal due to bowel gas or vessel wall calcification. Since significant disease is often common in the SMA and the celiac arteries of asymptomatic elderly patients, this modality should be considered when examining patients with suspected mesenteric ischemia.7
Treatment
Endovascular intervention or catheter-directed vasodilator therapy can be started immediately postangiography. The role of endovascular therapy in AMI is controversial. In NMI, a catheter-directed vasodilator infusion continues to be the treatment of choice in patients without peritonitis. Catheter-directed thrombolysis and percutaneous angioplasty have also been investigated in the treatment of AMI.4
The goal of surgical care is the removal of necrotic and nonsalvageable bowel and the prevention of further infarction. Stenting of the affected arteries may be utilized. An exploratory laparotomy remains the gold standard for assessment of bowel viability. Multiorgan failure poses a great risk in patients with AMI and mortality remains high.4 The most preferred surgical revascularization technique in embolic AMI remains the balloon catheter thromboembolectomy—with or without patch angioplasty of the superior mesenteric artery.
Prevention therapy should be utilized aggressively for AMI; patients with atrial fibrillation should be started on anticoagulants. Elective and timely revascularization may be undertaken in patients with chronic claudication and AMI secondary to atherosclerotic disease. In addition, patients should be advised not to smoke.4
Upon diagnosis of AMI, aggressive IV fluid resuscitation with crystalloids should be administered starting with volumes as high as 100 mL/kg to correct any metabolic derangements. A broad-spectrum antibiotic should also be started as early as possible. If no contraindications to anticoagulation exist, therapeutic IV heparin sodium should be administered to maintain an activated partial thromboplastin time at twice the normal value.5 The patient in this case was started on IV heparin and broad-spectrum antibiotics. In an optimized hemodynamic status, attempts to reduce acute vasospasm in AMI can be made with an IV glucagon infusion, starting at 1 mcg/kg/minute. The presence of peritoneal signs indicates bowel infarction and mandates an emergency laparotomy.5 As noted in the patient’s history, she was not on any anticoagulants on presentation and was a smoker.
Conclusion
The causes of abdominal pain range from benign to life threatening; therefore, it is imperative for clinicians to obtain a thorough history and physical examination of patients presenting with abdominal pain, and to consider a vascular etiology in the differential diagnosis. This case is unique in that the patient had multiple areas of stenosis within the abdomen, including the SMA and IMA, and either an acute or chronic occlusion, and claudication of her left lower extremity.
Dr Orlik is a resident, department of emergency medicine, Akron General Medical Center, Ohio. Mr Bosman is an undergraduate research fellow, department of emergency medicine, Akron General Medical Center, Ohio. Dr Simon is the emergency medicine research director, department of emergency medicine, Akron General Medical Center, Northeast Ohio Medical University.