Nonocclusive Mesenteric Ischemia
ELIZABETH A. JACKSON and ROBERT D. BROOK
Presentation
An 85-year-old female with a significant past medical history for coronary artery disease, cardiomyopathy with a reduced left ventricular ejection fraction of 20%, and chronic renal insufficiency (stage III) is admitted to the intensive care unit for increasing weight gain and dyspnea thought to be due to an exacerbation of heart failure. Workup for acute coronary syndrome was negative including no elevation in biomarkers (i.e., troponins) and no change in her electrocardiogram. She was treated with intravenous (IV) Lasix for heart failure. In addition, her angiotensin-converting enzyme (ACE) inhibitor dosage was increased, and spironolactone was added. Her clinical heart failure improved over the initial 24 hours; however, on transfer from the intensive care unit to the floor, she developed a low-grade fever and nausea. Vital signs revealed hypotension with a blood pressure of 78/40 mm Hg. IV fluids were initiated cautiously due to concern of her cardiomyopathy and worsening heart failure. Cardiac medications including her beta-blocker, ACE inhibitor, and diuretics were held. Several hours later, she complained of severe abdominal pain and her nausea increased.
On examination, blood pressure was 80/48 mm Hg, heart rate was 105 beats per minute, respirations were 26 per minute, and oxygen saturation was 92% with 3 L/min by nasal cannula. The patient appeared to be in acute distress with rapid respirations and complaints of severe abdominal pain. Neck veins were flat, and lungs were clear to auscultation. Heart sounds were regular with no gallops or murmurs. The patient’s abdomen was painful to palpation diffusely with guarding but no rebound tenderness. Bowel sounds were absent. Stool was trace-positive for occult blood. Abdominal plain films and laboratories are ordered.
Test Reports
Abdominal plain films were ordered and read as normal without evidence of obstruction, ileus, mass, or lumen perforation. Laboratory studies included a complete blood cell (CBC) count notable for a mild leukocytosis (white blood cells [WBCs] = 11.9). Comprehensive metabolic panel was unchanged from the morning’s labs and was within normal limits with the exception of serum bicarbonate of 19 mEq/L. Urinalysis was normal. Blood and urine cultures were drawn.
Differential Diagnosis
The differential diagnosis for acute periumbilical abdominal pain, fever, hypotension, and leukocytosis is broad. Peritonitis: lumen perforation (e.g., ulcer), ruptured diverticuli, or infections bacterial or nonbacterial organisms. Gastrointestinal: pancreatitis, early small bowel obstruction, diverticulitis, early appendicitis, inflammatory bowel disease, gastroenteritis, or Clostridium difficile colitis. Vascular: aortic dissection, aortic aneurysm leakage, and acute mesenteric ischemia. The latter includes splanchnic arterial thrombosis (usually in the setting of underlying atherosclerotic disease), arterial embolus or dissection, small vessel disease and vasculitis, venous thrombosis, watershed ischemia colitis, and small nonocclusive mesenteric ischemia (NOMI).
Discussion
In a patient with sudden (even relative) hypotension followed by severe abdominal pain greater than physical examination findings, NOMI should be immediately considered, particularly with a prior history of diminished left ventricular function and systemic atherosclerosis. In some cases, abdominal pain may be absent. Additional symptoms include abdominal bloating and nausea with vomiting. Mental status changes can also occur. The rectal examination being positive for occult blood and the concomitant metabolic acidosis are all nonspecific findings but are suggestive of mesenteric ischemia as well. Risk factors for NOMI include heart failure, vascular disease (cardiac or peripheral atherosclerosis), chronic renal disease, aortic insufficiency, shock (septic or cardiogenic), cardiac arrhythmias, use of vasoconstrictive medications or cocaine, and dialysis. Hypotension and the use of digoxin increase the risk for NOMI by causing vasoconstriction of the splanchnic vessels. The use of diuretics may increase renal blood flow and further diminish mesenteric perfusion. Any concomitant infection, septicemia, and volume depletion will also further contribute to NOMI. Due to the high morbidity and mortality rates and emergent nature of this diagnosis, immediate testing should focus on excluding this diagnosis and differentiating between occlusive versus NOMI.
Diagnostic Tests
Abdominal computed tomography, magnetic resonance imaging, or ultrasonography cannot exclude NOMI. However, abdominal CT can demonstrate focal bowel wall thickening, or dilation. CT can also be used to exclude other causes of abdominal pain. Selective mesenteric angiography is the test of choice when mesenteric ischemia is suspected.
Mesenteric Angiography
An emergent mesenteric angiogram demonstrates NOMI. Four arteriographic criteria for NOMI have been presented: (1) narrowing at the origins of multiple superior mesenteric branches; (2) alternate arterial dilation and narrowing; (3) mesenteric arcade spasms; and (4) impaired perfusion of intramural vessels.
Discussion
Acute NOMI is caused by severe and diffuse superior mesenteric artery narrowing due to vasospasm that is triggered by malperfusion secondary to hypotension (heart failure), dehydration (aggressive diuresis with furosemide), and digoxin therapy.
Diagnosis and Recommendation
The diagnosis of acute NOMI is made. In contrast to acute occlusive mesenteric ischemic disease (e.g., emboli, thrombosis), surgery is not indicated for early NOMI without mucosal necrosis.
Approach
After angiography displays NOMI, IV fluid hydration and vasodilator therapy should immediately be initiated. Direct intra-arterial mesentery infusions of papaverine and prostaglandins have been used with success to relieve ischemia. Nitroglycerin can also be used. Vasospasm is known to persist even after correction or resolution of the inciting events. Correction of precipitating factors such as dehydration and/or hypotension and infection is recommended.
Surgical Approach
Control of NOMI with vasodilator therapy should be tried initially. Indications for initial or subsequent laparotomy are failure of intra-arterial vasodilators to restore splanchnic perfusion, an increase in serum markers suggesting bowel necrosis, peritonitis, and persistent symptoms of abdominal pain after 24 to 72 hours.
Case Conclusion
An initial 20-μg bolus of prostaglandin E1 was followed by an infusion of 2.5 to 5.0 μg/h. Symptoms of nausea with abdominal pain resolved within 24 hours. Lactate dehydrogenase enzymes and bicarbonate levels (acidosis) subsequently returned to normal. Repeat angiogram demonstrated a significant restoration of splanchnic perfusion (Fig. 1). IV glucagon may be used in this setting as a splanchnic vasodilator, though clinical experience is anecdotal.
