Case Presentation: An 18 year old Caucasian male with no known medical history presented with a chief complaint of sharp epigastric pain radiating to the back for two days after meals, associated with multiple episodes of non-bloody emesis and high grade fevers. Patient denied any history of alcohol use and did not have any known history of autoimmune diseases. He admitted to COVID-19 exposure several days prior to the onset of his symptoms without experiencing any respiratory symptoms. He received his COVID-19 vaccine earlier in the year. Patient was febrile with Tmax 101.2 F and blood pressure was noted to be 171/96. Labs showed WBC 11.1, lipase of 149, calcium 8.8, and triglyceride 130. CT abdomen pelvis showed acute pancreatitis with a developing phlegmon and possible necrosis, and no evidence of gallstones. Ultrasound of the gallbladder provided no evidence of cholelithiasis. Patient was treated with aggressive fluid resuscitation, bowel rest, antibiotics, and pain management. To uncover patient’s etiology of acute pancreatitis, further lab testing was completed, which showed negative IgG4 levels and EBV titers. Patient was stabilized and discharged with a 2 week antibiotic course. Pt was readmitted about a month later due to recurrent pain and MRI abdomen showed pancreatic tail pseudocyst formation without evidence of necrosis. Patient was managed conservatively and has recovered well.
Discussion: Acute pancreatitis is a common cause of hospitalization in the United States. It is caused by an inflammation of the pancreas, leading to acinar cell injury and zymogen secretion impairment. It can further be complicated by a pseudocyst, an abscess, or necrosis. The two most common instigators are gallstones and alcohol. However, viral infections have been identified as a cause in 10% of all cases. Since the start of the pandemic, COVID-19 is now emerging as a potential cause as well. Although COVID-19 typically presents with pulmonary manifestations, some extra-pulmonary manifestations, such as pancreatitis, hepatitis, and ATN, have been described. COVID-19 induced AKI has been seen in 25% to 29% of cases. 14% to 53% of COVID induced transaminitis has also been noted. It has been researched that COVID 19 uses ACE2 as an entry receptor, which is expressed in multiple tissues. Proposed pathophysiology of acute pancreatitis is endothelial damage and entry of virus via a protein expressed on the pancreas. In order to diagnose COVID-19 induced pancreatitis, all other etiologies must be ruled out. Although further data is needed to establish the correlation of covid 19 and acute pancreatitis especially in vaccinated patients, the increase in prevalence across the globe cannot be overlooked.
Conclusions: SARS-CoV-2 is now increasingly leading to extra-pulmonary manifestations, such as acute pancreatitis and hepatitis. Although research in the exact mechanism is still not well understood, the increase in number of cases of covid 19 related acute pancreatitis must be recognized and clinicians must be more vigilant.
