Diabetic Ketoacidosis and Acute Pancreatitis in Covid-19 Setting

Abstract

Introduction: Respiratory, kidney and gastrointestinal are some of the systems affected by COVID-19. Although COVID-19 has been studied as a lung pathogen, endocrine system involvement has rarely been studied. In this case report, we present a case of diabetic ketoacidosis (DKA) and acute pancreatitis in the setting of COVID-19. Case Description: A 52-year-old female with a PMH of type 1 diabetes mellitus and hypothyroidism, presented to the ED with nausea, vomiting, fatigue and diffuse abdominal pain. She reports cosmetic surgery a few weeks prior and she started feeling these symptoms at the beginning of admission day of admission. On admission, WBC was 34.9, blood glucose was 496, lactic acid of 3.1. Arterial blood gas revealed pH of 6.96, PCO2 of 17 mEq/L, PO2 of 143, HCO3 of 5 and anion gap of 23. DKA protocol was initiated and was upgraded to ICU. She was found to be RT-PCR positive for SARS-CoV-2. She denied other symptoms, including melena, jaundice, hematochezia, hematemesis, cough, SOB or diarrhea. She also denied use of alcohol, tobacco or illicit drugs, prior hospitalizations, or family history of pancreatitis. The physical exam was significant for tenderness to palpation in epigastric region without guarding or rebound. Laboratory studies revealed lipase: > 4000U/L, AST: 64 U/L, ALT: 57 U/L, ALKPHOS: 152 U/L, and total bilirubin: 1.1 mg/dL. Serum triglycerides and calcium levels were within normal limits. CT abdomen showed a severe peripancreatic inflammation and edema, moderate non-organized fluid surrounds pancreas. An abdominal ultrasound showed no calcified gallstone or gallbladder wall thickening. The common bile duct was 3 mm, normal size. Over the course of 24 hours, anion gap was 7, pH was 7.28, blood glucose was 158. For sepsis, lactic acid was 0.7 after initiation of azithromycin. For acute pancreatitis, she was treated conservatively with intravenous fluids, bowel rest and analgesia. Patient denied any upper respiratory symptoms and did not require oxygen so steroids were not started for COVID PNA. Her symptoms improved and she was discharged home. Discussion: Here we report a case of a patient who presented with DKA, found to have severe acute pancreatitis as well as SARS-CoV2 PCR positive. Few case reports have reported an association of DKA and acute pancreatitis. Although the exact mechanism by which SARS-CoV-2 is evolving, it is thought to be mediated by the Angiotensin-Converting Enzyme-2 which is present in intestine, and on islet cells of the pancreas. This injury may be due to cytopathic effect of viral replication or indirectly caused by the inflammatory response induced by the virus. Further studies are needed to better understand the pathophysiology behind AP in the setting of COVID-19. Conclusion: This case highlights DKA and AP as a possible initiating presenting manifestation of COVID-19 infection