ABSTRACT
Case Report A 29-year-old male with a past medical history significant for severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection presented with epigastric pain, vomiting, fever, and inability to tolerate oral intake for 1 day. The patient was diagnosed with COVID-19 six weeks prior to presentation and four weeks later was diagnosed with idiopathic acute pancreatitis. He reported initial resolution of pain, however symptoms recurred for one day prior to this admission. The patient denied a history of alcohol use disorder. He is a lifetime nonsmoker. He does not take any medications. Vital signs were stable and he was afebrile. Labs on presentation were remarkable for elevated lipase of 1,527 and leukocytosis (23,000). The patient was still positive for COVID-19. However, he maintained oxygen saturation >95% on room air with no apparent distress. On physical examination, he had severe tenderness to palpation at the epigastrium and left upper and lower quadrants. Abdominal ultrasound had no evidence of gallstones. Triglyceride levels were within normal limits. CT abdomen showed necrotizing pancreatitis. MRCP showed evidence of acute pancreatitis with peripancreatic acute necrotic collection in the pancreatic head measuring up to 8.8 cm. Intrinsic T1 signal within the peripancreatic collection compatible with hemorrhagic pancreatitis. There was about 30% pancreatic parenchymal necrosis in the pancreatic head. A nonocclusive thrombus involving the main portal vein was also seen. Autoimmune workup was negative. In the setting of hemorrhagic pancreatitis, treatment with anticoagulation was deferred. The patient was treated with supportive measures, including intravenous fluids and adequate pain control with eventual advancement of his diet. He was started on empiric antibiotics and discharged for outpatient follow-up. SARS-CoV2 is known to cause many extrapulmonary effects, including transaminitis, myocarditis and pericarditis. There have been rare cases of SARS-CoV2-induced acute pancreatitis reported in the literature. The exact mechanism behind pancreatic injury in the setting of SARS-CoV2 infection remains unclear, but it is hypothesized that it may occur secondary to the presence of SARS-CoV2 receptors on the pancreas. The main receptor used by SARS-CoV2 is angiotensin- converting enzyme 2, which is also expressed in the GI tract. The most common causes of acute pancreatitis, including alcohol abuse, gallstones, medications and autoimmune causes were ruled out in our patient. In a patient with no particular risk factors, it is likely that SARS-CoV2 precipitated his first episode of acute pancreatitis. Moreover, it is well known that acute pancreatitis can commonly lead to necrotizing pancreatitis as the initial injury and inflammation from the first attack can cause the pancreatic tissue to necrotize and later become infected. This case highlights that SARS-CoV2 can be a possible etiology of acute pancreatitis and its local complications.