A 48-year-old woman presented to the ED with significant periumbilical abdominal pain and left lower extremity pain, which she rated an “8” on a scale of 1 to 10. She stated that the pain worsened with movement and change in position. The claudication in the patient’s left lower extremity began a few weeks prior to presentation, at which time she had received medical attention, including ankle brachial index testing that showed an abnormal value in the left lower extremity. The patient noted that when the abdominal pain began, the pain in her leg became more frequent and of higher intensity, with intermittent numbness. She reported some nausea, paresthesia, and sensory changes to the left lower extremity; however, she denied diarrhea, headache, fever, back pain, urinary symptoms, chest pain, and shortness of breath.
Regarding social history, the patient admitted to smoking half a pack of cigarettes a day and drinking alcohol socially. She denied any significant family history of disease. The patient’s own medical history included colon cancer, claudication, and multiple abdominal surgeries. The patient had been diagnosed with stage II colon cancer 4 years earlier, for which she had undergone a colon resection.
During the physical examination, the patient was diaphoretic, uncomfortable, and in severe distress. Her vital signs were: blood pressure, 146/77 mm Hg; respiratory rate, 18 breaths/minute; heart rate, 129 beats/minute; and temperature within normal limits. Oxygen saturation was 94% on room air.
The abdominal examination revealed a distended abdomen that was severely tender to palpation, with rigidity, guarding, and rebound tenderness. Examination of the lower extremities revealed an absent palpable dorsalis pedis pulse to the left lower extremity, but dorsalis pedis pulse and posterior tibial pulse in the left lower extremity were appreciated by Doppler. The right lower extremity had palpable 2+ dorsalis pedis and posterior tibial pulses.
The patient was immediately started on fentanyl and intravenous (IV) fluids; she was also given IV ondansetron and promethazine for nausea. Her pain was refractory to treatment, and required multiple doses of hydromorphone. Laboratory evaluation revealed leukocytosis with a white blood cell (WBC) count of 15.1 thou/cmm.
Computed tomography angiography (CTA) with runoff was ordered to evaluate lower extremity vasculature and perfusion, as well as abdominal vasculature and intra-abdominal organ pathology. The CTA revealed 99% stenosis in the left iliac artery; multiple areas of stenosis within the abdominal vasculature, including the superior mesenteric artery (SMA) and inferior mesenteric artery (IMA); and a small ventral hernia slightly left of the umbilicus but without evidence of obstruction. The patient remained stable while in the ED, and an emergent vascular surgery consultation was ordered. She was transferred to surgical services.
Mesenteric ischemia is a condition in which the intestine does not receive adequate blood supply, resulting in inflammation and injury. Cases of the disease may be acute or chronic. Acute mesenteric ischemia (AMI) may be occlusive or nonocclusive. Occlusive AMI is most commonly caused by embolic or thrombotic occlusion of one or more mesenteric arteries. Nonocclusive AMI (NMI) is most commonly due to primary splanchnic vasoconstriction.1 It can also be seen in patients on high-dose vasopressor agents. Chronic mesenteric ischemia indicates continuous intestinal hypoperfusion that is often associated with meals and referred to as postprandial or intestinal angina.
Mesenteric ischemia is associated with poor outcomes, having a mortality rate ranging from 40% to 70%.2 It is imperative that diagnosis and treatment commence rapidly to avoid potentially catastrophic complications such as transmural bowel infarction. Although visceral ischemia is rare, occurring in only 2 to 3 per 100,000, the high mortality rate makes prompt and accurate diagnosis essential to decreasing morbidity and mortality.3
Symptoms and Signs
The classical presentation of mesenteric ischemia is sudden onset of abdominal pain out of proportion to physical examination findings; however, peritoneal signs are also not uncommon later in the disease process. The most common presenting symptoms are abdominal pain, nausea, and diarrhea. Laboratory findings associated with mesenteric ischemia include leukocytosis, metabolic acidosis, elevated lactate, and an elevated D-dimer.2
Early recognition is crucial given the significant risk of bowel necrosis. Signs of peritonitis are frequently present late in the disease course; signs such as nausea, vomiting, and constipation are more frequent. Patients may also have complications such as ileus, gastrointestinal bleeding, and pancreatitis, which may mask the diagnosis of AMI.4
Prompt diagnosis and treatment are paramount. Acute AMI should especially be considered in patients who are over age 60 years, have a history of atrial fibrillation, claudication, hypercoagulable states or a previous history of atherosclerotic disease, myocardial infarction, and a history of postprandial abdominal pain and weight loss.