Case Presentation: This is a 21 year old man with prior polysubstance use who presented with worsening pleuritic chest pain, subjective fever, diffuse abdominal pain, and diarrhea for three days. He reported testing positive for COVID-19 17 days prior to admission, but for 14 days thereafter had only mild symptoms of non-productive cough and malaise. On initial examination, he was noted to be febrile, tachycardic, and tachypneic. He reported excruciating substernal chest pain and had rebound abdominal tenderness to palpation. Labs were notable for elevated white blood cell count of 14.99, aspartate aminotransferase (62), and alanine transaminase (75). Erythrocyte sedimentation rate (38) and C-reactive protein (22.73) were also markedly elevated, as was D-dimer (966), and troponin (0.3). EKG showed sinus tachycardia. Chest radiograph was unremarkable. CT angiogram was negative for pulmonary embolus. CT of abdomen and pelvis demonstrated multiple prominent mesenteric lymph nodes, poor visualization of distal appendix, and right colonic thickening. On admission, COVID-19 test was negative and SARS-CoV-2 antibody was positive. Notably, repeat COVID-19 test on hospital day (HD) 2 was again positive.The patient decompensated within hours of admission, developing hypotension requiring vasopressor support, and was transferred to the ICU. Echocardiogram revealed reduced left ventricular systolic function of 35-40%. The patient was treated initially with broad spectrum antibiotics, but after noting cardiogenic shock and new onset cardiomyopathy, he was also started on Solumedrol and IVIG for concern of Multi-system Inflammatory Syndrome (MIS) with likely myocarditis. He was also given Remdesevir for possible persistent COVID-19 infection. He was weaned off of vasopressors and reported improvement in symptoms by HD 2. Repeat echocardiogram showed improvement in ejection fraction to 57% on HD 6. He was discharged in stable condition on HD 8 with plans to follow up with cardiology.
Discussion: Multi-system Inflammatory Syndrome, or MIS, has been observed in pediatric patients. (1) Patients typically present two to four weeks after acute COVID-19 infection, with elevated serum inflammatory, coagulative, and cardiac markers. Cardiogenic shock with abnormal echocardiogram is quite common. (2) Recently, case reports of MIS in adults have come to light. A key distinguishing factor between MIS and a generalized hyper-inflammatory response to severe COVID-19 is that patients with MIS, such as our patient, do not have prominent respiratory symptoms nor imaging (CT, chest radiograph) consistent with pulmonary infectious process. (3) Autopsy evidence of patients with COVID-19 infection has demonstrated presence of SARS-CoV-2 virus in myocardial tissues. (4) However, an official diagnosis of myocarditis requires confirmatory endomyocardial biopsy, and data at this time is quite limited. (5) Myocarditis is a suspected complication of SARS-CoV-2, especially from MIS as in our patient, but the exact mechanism of cardiac injury remains to be determined.
Conclusions: MIS has been increasingly reported in adults with recent COVID-19 infection, and causes severe cardiac dysfunction. Although myocarditis is the likely complication in these patients, more robust endomyocardial biopsy data is required to make an official diagnosis as well as determine the exact mechanisms of cardiac injury. Early recognition of MIS as a separate entity from severe COVID-19 infection is imperative to prevent morbidity and mortality.