Recognizing acute mesenteric ischemia

In this video, we'll take you through a systematic approach to diagnosing acute mesenteric ischemia, provide you with a key symptom that will immediately differentiate it from other abdominal pathologies, and explain when it's critical for you to consult with a surgeon.

Olutayo A. Sogunro, DO, FACS, FACOS
Olutayo A. Sogunro, DO, FACS, FACOS
6th Oct 2021 • 5m read

In this video, we'll take you through a systematic approach to diagnosing acute mesenteric ischemia, provide you with a key symptom that will immediately differentiate it from other abdominal pathologies, and explain when it's critical for you to consult with a surgeon.

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Video transcript

In this Medmastery lesson, we will discuss mesenteric ischemia. So what is mesenteric ischemia? Intestinal or mesenteric ischemia can affect the small or large intestine. It can be caused by any process that reduces intestinal blood flow. thrombo-embolic occlusion of the superior mesenteric artery is the most common cause of acute mesenteric ischemia.

The incidence of mesenteric ischemia is 8.6 per 100,000 per year. Acute mesenteric arterial occlusion account for 67 to 95% of cases of acute mesenteric ischemia. Mesenteric ischemia can be divided into occlusive disease and non-occlusive disease. In occlusive disease the major causes are classified as thrombotic disease, or embolic disease, and can be of an arterial or venous origin.

About 70% of superior mesenteric artery occlusion is caused by embolism and about 30% by thrombosis. Non occlusive mesenteric ischemia or NOMI develops when delivery of oxygen or nutrients to the bowel is insufficient for cellular metabolism, but there is not a complete occlusion of the blood flow. NOMI accounts for 5 to 15% of patients with acute mesenteric ischemia.

Thrombotic or embolic disease can compromise intraluminal small intestinal vessels and lead to decreased perfusion of the bowel wall. Prolonged ischemia leads to progressive vasoconstriction in the obstructed vascular bed, which increases its pressure and reduces collateral blood flow. This leads to ischemia and wall necrosis and can ultimately cause bowel perforation. Now let's talk about the risk factors for embolic disease.

The risk of embolism is increased in patients with cardiac arrhythmias and valvular disease, infective endocarditis, recent myocardial infarction, aortic atherosclerosis and aortic aneurysms. The risk of thrombotic occlusion is increased in patients with peripheral artery disease, advanced age, and low cardiac output seeds seen in heart failure and myocardial dysfunction.

Traumatic injury can also increase the risk for thrombotic disease. The history of these patients is very important. So what are the signs and symptoms of mesenteric ischemia? Patients with acute mesenteric ischemia will usually present with significant abdominal pain that is out of proportion to the physical exam. This is present in 1/3 to one half of patients.

Pain associated with arterial embolism of the superior mesenteric artery is typically sudden, severe, periumbilical and often accompanied by nausea and vomiting. Diarrhea can also be present, bloody diarrhea is less common, but can be a very particular sign for advanced ischemia from sloughing of the intestinal mucosa. Now let's discuss the workup.

On observation the patient can be ill-appearing, especially in disease complicated by advanced ischemia or perforation. The patient may also be laying very still and not want to move with pain out of proportion to the exam. They may have an alteration in their vital signs, most notably tachycardia, hypotension, and fever. On inspection, mild distension may be noted.

On palpation, the patient will have pain around the periumbilical region. As well ischemia progresses they may develop severe, diffuse abdominal pain on palpation and significant distension. Bowel sounds may become absent. In cases of major complications such as perforation, a patient may have a rigid abdomen and peritoneal signs. A digital rectal exam should be performed to identify gross or occult blood. Now let's discuss the labs.

Laboratory studies for mesenteric ischemia are nonspecific and normal laboratory values do not exclude acute mesenteric ischemia. A complete blood count with differential may show leukocytosis with left shift, which may indicate the presence of bowel complications. An elevated hematocrit consistent with hemo concentration and dehydration may also be identified.

A chemistry panel can also be obtained to look for metabolic acidosis. A useful clinical guidelines is that any patient with acute abdominal pain, and metabolic acidosis has intestinal ischemia until proven otherwise. A lactate can also be ordered, often it's elevated after the ischemic insult has progressed to severe or bowel necrosis. Lactate has a sensitivity for acute mesenteric ischemia of about 86%.

Elevated serum amylase levels have been observed in approximately one half of patients with intestinal ischemia. Plain x rays should be the initial imaging modality in a patient with peritonitis or suspected to have bowel perforation. Pneumoperitoneum, seen as air under the diaphragm is best seen on the upright chest X ray and usually indicates perforation of a hollow viscus such as small bowel.

If the plain X ray films do not have findings that indicate the need for immediate intervention, then we can proceed to use computed tomography angiography (CTA) of the abdomen. CTA is the ideal imaging modality for most patients with clinical features consistent with an intestinal ischemia. The CTA scan should be performed without oral contrast, which can obscure the mesenteric vessels, obscure bowel wall enhancement and can lead to a delay of the diagnosis.

On CT scan the celiac superior mesenteric and inferior mesenteric arteries can be visualized and thromboemboli can be identified. Stenosis or occlusion on mesenteric vessels can be seen. Venous thrombosis are identified as filling defects in those vessels. Now let's discuss treatment. The initial management includes gastrointestinal decompression via nasal gastric tube, while the patient is on bowel rest with nothing per mouth or NPO.

Then fluid resuscitation, hemodynamic monitoring and support and correction of electrolyte abnormalities such as potassium. The patient should have adequate pain control that is typically done via intravenous opioids. Anticoagulation should be started for patients with acute intestinal ischemia due to mesenteric, arterial or venous occlusion or non occlusive mesenteric ischemia.

Systemic anticoagulation should be administered to prevent thrombus formation and propagation. A contraindication to this would be active bleeding. Initiation of broad spectrum antibiotics is recommended for patients with acute mesenteric and colonic ischemia, presenting signs of infection or perforation.

When should you consult a surgeon? Bowel ischemia, necrosis or perforation need immediate surgery. Clinically, a patient with peritoneal signs and persistent alteration in vital signs such as fever, tachycardia and hypotension will require immediate operation. Surgery should not be delayed in patients suspected of having intestinal infarction, or perforation based upon clinical radiographic or laboratory parameters, regardless of etiology.

For patients with non occlusive mesenteric ischemia or NOMI, surgical exploration should be limited to patient with peritoneal signs and medical and non surgical management should be the goal. Surgery includes open exploratory laparotomy to evaluate and release adhesions, reduce and treat hernias, egg tumors and more. This can also be done laparoscopically. A diagnostic laparoscopy can help identify the exact location of the obstruction.

After the acute management of mesenteric ischemia, it is important to work up and try to determine the cause of the mesenteric ischemia. An echocardiogram will look for cardiac sources such as valvular disease, and endocarditis. And the carotid Doppler will look for atherosclerotic disease. Patients with acute intestinal ischemia should be systemically anticoagulated to prevent thrombus formation or propagation, provided there are no contraindications.