Case Presentation:

A 65–year–old Black woman with PMH of hypertension presented with 1 hour history of an acute onset of nausea, vomiting, epigastric discomfort, diaphoresis and dizziness. She denied any significant chest pain or shortness of breath. Denied any back pains. She vomited about four times before coming to ED. On exam, her BP was 70/24 with heart rate of 117. She was afebrile with sO2 92% on room air. She was alert, diaphoretic with cool skin. Her cardiac and respiratory exam was benign. She had mild epigastric tenderness with no peritoneal signs. No focal neurological deficits. A stat EKG done showed significant ST elevation in inferior leads. STEMI protocol was initiated and patient was life flighted to our hospital. She was given 3 liters of IV bolus fluids and aspirin on the way. She underwent emergent cardiac catheterization which revealed only trivial coronary artery disease without any need for intervention. She was transferred to Cardiac ICU and labs showed WBC of 23,000; Hb 12 gm/dl, Troponin <0.01 and lipase of 5600 with alkaline phosphatase of 246 and AST/ALT of 236/186. CT scan of abdomen done next day showed necrotizing pancreatitis of 50–70% of gland with minimal fluid collections, dilated thick walled gallbladder with stones suggestive of acute cholecystitis. The patient was treated with maintenance IV fluids and antibiotics were started after CT findings. The patient did not improve with these interventions, had a PEA arrest and had anoxic brain injury and eventually expired.


This case highlights the fact that ST elevations in inferior leads can have an abdominal etiology. Transient electrocardiographic changes in patients with acute cholecystitis, pancreatitis, and pneumonia have been reported in the past. These changes usually are in the form of T–wave inversion, ST–segment depression, and rarely ST–segment elevation in the absence of coronary artery disease. With advances in cardiology and emphasis on door–to–balloon time, this patient actually had a coronary angiogram done before his lab results came back showing elevated lipase to suspect pancreatitis. Also, it is easier and faster to get a CT scan of abdomen in ED then to get lipase results back and many patients get CT scans on presentation when the pancreatitis changes might not have developed yet. Ideally CT scan should be done in 48––72 hours after symptom onset to assess the severity of the pancreatitis unless another acute pathology is suspected.


It is important for hospitalists to be aware of this uncommon presentation of acute pancreatitis as ST elevation in inferior leads. This would prompt checking lipase levels in these patients and also resuscitate for pancreatitis while acute MI is being ruled out. Fortunately, thrombolytics have fallen out of favor now but administration of thrombolytic therapy in such patients where primary coronary intervention is still not available might end up with fatal consequences.

Figure 1Necrotizing severe pancreatitis.