Case Presentation: A 25-year-old male with a past medical history of well-controlled Celiac disease presented to the hospital with fever and altered mental status after a wellness check was initiated by a family member. The patient was feeling unwell over the past week with fatigue, headache, sore throat, vomiting, and diarrhea. On presentation he was markedly encephalopathic with high fever and tachycardia. COVID-19 test was positive. His encephalopathy was initially suspected to be secondary to COVID-19. He developed hypoxia and was treated with remdesivir and dexamethasone. However, given his young age, overall healthy baseline, and vaccinated status, the severity of his presentation raised suspicion for an additional underlying process. A random cortisol level, drawn at 3 AM while severely ill and before receiving dexamethasone, was 2.3 ug/dL and concerning for adrenal insufficiency. Additionally, an EKG revealed a type 1 Brugada pattern, which was thought to be induced by fever in the setting of his acute COVID-19 infection. The patient’s clinical status improved with remdesivir, steroid treatment, and volume resuscitation. He was transitioned to a hydrocortisone taper while inpatient and was discharged on daily prednisone and fludrocortisone with outpatient Endocrinology follow-up. Additional lab work that resulted after his discharge revealed a positive 21-hydroxylase antibody, confirming the diagnosis of primary adrenal insufficiency. He was arranged for Cardiology follow-up with plan for loop recorder implantation to further assess for cardiac arrhythmias.
Discussion: This case demonstrates the importance of strong clinical curiosity and thorough diagnostic evaluation when a patient’s presentation does not fully align with a presumed diagnosis. Although this patient’s encephalopathy was initially attributed to COVID-19, the severity of symptoms in an overall healthy, vaccinated young male raised suspicion for additional underlying processes. He was ultimately found to have two potentially life-threatening illnesses, primary adrenal insufficiency and Brugada syndrome. It is important to consider adrenal insufficiency in patients with illness severity out of proportion to a presenting infection. Adrenal crisis can mimic severe sepsis with high fevers, encephalopathy, tachycardia and hypotension. The presence of existing autoimmune diseases, such as Celiac disease in this patient, can be a clue to the diagnosis. Brugada syndrome can be incidentally uncovered on EKG in the setting of provoking factors such as fever. It is imperative to recognize these EKG patterns and establish a diagnosis as patients are at risk for fatal arrhythmias. Interestingly, a prior case report described the uncovering of a type 1 Brugada pattern in a COVID-19 patient who did not have a fever, suggesting there may be a more direct relationship between COVID-19 and Brugada syndrome. As highlighted by this case, hospital medicine plays an essential role in managing the acute stabilization of patients, ensuring a thorough diagnostic evaluation, and coordinating appropriate interdisciplinary care.
Conclusions: In this case, COVID-19 infection unmasked adrenal insufficiency and Brugada syndrome, two previously undiagnosed and high-risk conditions. When the severity of a patient’s symptoms is unexpected for an established diagnosis, it is important to maintain high clinical suspicion and avoid attributing all features of a presentation to only that disease process.