A previously healthy 20–year–old woman presented to the emergency room (ER) with several days of fevers, sore throat, myalgias, and a diffuse rash. The rash emerged as papules on the back of one hand, soon coalescing into plaques over much of her body, including palms and soles, but sparing mucous membranes. The patient used oral contraceptives and had been sexually monogamous with no history of STDs. She denied recent sick contacts, travel, outdoor activity, animal exposures, or diet changes. She was well–appearing but febrile (40.3°C) and tachycardic (HR 112) with an exam notable for an erythematous oropharynx, tonsillar exudates, and cervical lymphadenopathy. White blood cell (WBC) count was 14,300/mL. She was empirically treated with dexamethasone and penicillin (PCN) for possible streptococcal pharyngitis vs. secondary syphilis and sent home. She returned to the ER the next day with odynophagia and dyspnea; she also had persistent fever, tachycardia, worsening rash, and periorbital edema with scleral injection. WBC count was now 24,200/mL with neutrophilic predominance and no eosinophilia. Antihistamines and corticosteroids were given for a possible anaphylactoid reaction along with broad–spectrum antibiotics. She developed hypotension and pulmonary edema with severe hypoxia within 24 hours of admission, requiring maximal vasopressor and ventilator support. Transthoracic echocardiogram revealed severe mitral regurgitation and biventricular failure with an ejection fraction of 25%. Extracorporeal membrane oxygenation (ECMO) was emergently initiated and continued for six 6 days to aid cardiac recovery. Myocardial biopsy showed an eosinophilic infiltrate without viropathic changes consistent with a hypersensitivity reaction. Ultimately, an extensive infectious and autoimmune evaluation returned negative, and she regained complete cardiac function. After a 14–day hospitalization, she was discharged with a diagnosis of fulminant PCN–induced hypersensitivity myocarditis preceded by a presumptive viral syndrome. A full recovery was expected.
Myocarditis is an inflammatory cardiomyopathy that presents as chest pain, arrhythmia, congestive heart failure, or sudden cardiac death. Precipitants of myocarditis are typically assessed as being infectious (most commonly viral) or non–infectious (e.g., toxins, hypersensitivity reactions, autoimmune). The absence of peripheral eosinophilia made it challenging to distinguish between the initial viral prodrome or drug–induced hypersensitivity as the underlying etiology. The demonstration of eosinophils on myocardial biopsy was essential in implicating the latter. ECMO proved to be a critical bridging therapy. Patients who survive a fulminant presentation typically have a good prognosis.
Hospitalists should recognize fulminant myocarditis as a rare complication of recently administered drugs, including PCN. In patients with refractory cardiogenic shock, prompt ECMO use may be life–saving.