(230) Stokes-Adams Syndrome! Atypical Presentation of Fulminant Myocarditis

Introduction: Fulminant myocarditis is an uncommon cause of cardiogenic shock that can lead to death. Patients typically presents with dyspnea, chest pain, and arrhythmias. Atypical presentations of this disease delay recognition and care in a condition associated with a high mortality rate of 50%.

Description: A 37-year-old male was admitted to the ICU for management of seizures. The patient had nausea, vomiting and a poor appetite. He then developed brief episodes of loss of consciousness concerning for seizures. He was intubated for airway protection. Shortly after, he went into ventricular fibrillation arrest and shocked twice with ROSC in 5 minutes. He became hypotensive requiring vasopressor support. Beside ECHO showed a depressed EF and global hypokinesis. Labs showed an elevated troponin of 9156 (ng/L), elevated lactic acid, creatinine and liver function tests and several electrolyte derangements: all consistent with shock and multiorgan failure. EKG showed an LBBB. Cardiology was consulted but concluded that the cardiac arrest and troponin leak was due to seizures and there was no indication for cardiac catheterization or mechanical circulatory support. The patient continued to worsen, requiring escalating doses of vasopressors and transcutaneous pacing for complete heart block. EEG monitoring demonstrated that the seizures were myoclonic jerks from cerebral hypoperfusion due to cardiac dysrhythmias. The loss of consciousness was due to the large drop in cardiac output: Stokes Adams syndrome. The patient was finally taken to Cath lab which revealed no obstructive coronary disease, elevated RA and PCWP pressures consistent with cardiogenic shock and EF of < 5%. The patient received an Impella and was placed on VA-ECMO. A RV biopsy revealed diffuse lymphocytic myocarditis. High dose steroids were started, and the patient made a full recovery and weaned off mechanical circulatory support in 2 weeks.

Discussion: This case highlights the importance of understanding the pathophysiology of fulminant myocarditis and the clinical progression to heart failure. This patient did not have the classic presentation but came in with seizure like episodes. These were not true seizures but a manifestation of end organ hypoperfusion due to cardiogenic shock from fulminant myocarditis.