C50-39 A Case of Refractory Shock Following Viral Upper Respiratory Infection

Abstract Introduction Fulminant myocarditis is a rare but catastrophic complication of common viral infections. At an advanced stage, it may present as cardiogenic shock resistant to every lifesaving effort. Case Description A previously healthy 34-year-old man presented to an outside hospital several days after being diagnosed with an upper respiratory infection. At presentation, he complained of worsening shortness of breath, and was hypothermic, tachypneic, and hypoxic. He was placed on bilevel positive airway pressure before experiencing cardiac arrest. Return of spontaneous circulation was achieved, and he was transferred via air ambulance to the medical intensive care unit (MICU). In the MICU, vital signs were temperature 37.9 °C, heart rate 127 bpm, respiratory rate 41/min, and mean arterial pressure (MAP) 51 mmHg despite norepinephrine, vasopressin, epinephrine, and phenylephrine infusions. Physical exam demonstrated cold extremities and diffuse cutaneous mottling. Laboratory data included hemoglobin 14.3 g/dL, white blood cell count 11800/mm3, absolute neutrophil count 6700/mm3 with 25% metamyelocytes, bicarbonate 13 mEq/L, anion gap 39, creatinine 5.62 mg/dL, aspartate aminotransferase 2303 U/L, lactate 20.8 mmol/L, pro-brain natriuretic peptide 53519 pg/mL, and procalcitonin 100.00 ng/mL. Computed tomography (CT) pulmonary angiogram was negative for pulmonary emboli but showed bilateral pleural effusions with adjacent atelectasis. Abdominal contrast CT showed a small caliber aorta and a flattened inferior vena cava (fig. 1). Electrocardiogram showed nonspecific T wave abnormalities. Despite escalation of care with broad-spectrum antibiotics, corticosteroids, bicarbonate, methylene blue, and continuous renal replacement therapy, the patient’s MAP continued to drop. In consultation with his family, it was decided not to attempt further resuscitation if he arrested again, and he subsequently expired. An infectious workup pending at the time of death, including blood and sputum cultures, was negative. At autopsy, it was discovered the patient died of fulminant myocarditis caused by human parvovirus B19. Discussion Although relatively rare, fulminant myocarditis is implicated in about 10 percent of sudden deaths in young, healthy patients. The vast majority of parvovirus-associated fulminant myocarditis cases are in infants and children, but cases have been described in adults. Patients often present with acute decompensated heart failure and thus show signs of both pulmonary vascular congestion and systemic hypoperfusion. Advanced therapeutic options—including extracorporeal membrane oxygenation and left ventricular assist devices—are increasingly utilized to promote survival through the acute phase of fulminant myocarditis. Early and correct identification of cardiogenic shock in these patients is critical to aid treatment planning. This abstract is funded by: None