Cardiopulmonary Manifestations of Fulminant Enterovirus 71 Infection

Abstract

ABSTRACT. Background. The pathogenesis of acute pulmonary edema and cardiac collapse after enterovirus 71 (EV71) infection are not completely understood.Objective. To determine the hemodynamic features and the mechanism of pulmonary edema (PE) after EV71 infection by direct intracardiac monitoring.Design. Prospective clinical and laboratory study at a tertiary medical center.Participants. Five consecutive infants, ages 2 to 13 months, with EV71 infection-proved by viral isolation in 4 and antibody in 1-with PE were enrolled. The clinical characteristics were systemically assessed. Hemodynamic profiles were determined every 4 hours by simultaneously implanted pulmonary arterial and central venous catheters during the acute stage.Results. Magnetic resonance imaging revealed that all 5 infants had brainstem lesions. All patients had tachycardia and hyperthermia. Transient systolic hypertension was noted in 1 patient, and 1 presented with hypotension. Pulmonary artery pressure in all 5 infants was normal or mildly elevated (26 -31 mm Hg), and central venous pressure ranged from 10 to 22 mm Hg. Pulmonary artery occlusion pressures were normal or slightly elevated (13-16 mm Hg). Systemic and pulmonary vascular resistances were transiently increased in only 1 patient. The stroke volume index decreased to 15.3 to 35.7 mL/M 2 (normal: 30 -60 mL/M 2 ), but because of the elevated heart rate, the cardiac index did not decrease. All hemodynamics normalized within days.Conclusion. Fulminant EV71 infection may lead to severe neurologic complications and acute PE. The acute PE and cardiopulmonary decompensation in EV71 infection are not directly caused by viral myocarditis. The mechanism of PE may be related to increased pulmonary vascular permeability caused by brainstem lesions and/or systemic inflammatory response instead of increased pulmonary capillary hydrostatic pressure. Pediatrics 2002;109(2). URL: http://www.pediatrics.org/ cgi/content/full/109/2/e26; enterovirus 71, pulmonary edema, pathogenesis, hemodynamics, hand-foot-mouth disease.

Enterovirus 71: epidemiology, pathogenesis and management

“…In this circumstance, PE is thought to occur secondarily to direct hydrostatic force as well as to increased permeability from endothelial injury [27]. Hemodynamic studies of patients with PE revealed normal cardiac function and normal pulmonary hydrostatic pressure [28]. Pathologic studies showed no myocardium necrosis and calcification [4,26].…”

Predictors of Unfavorable Outcomes in Enterovirus 71-Related Cardiopulmonary Failure in Children

“…8 suggested that the pathogenesis of heart failure and subsequent PE/PH is related to systemic inflammatory response syndrome rather than myocarditis. 9 The inotrope demand can be extraordinarily high during the hypotension period. Eight patients (five survived) had an IE higher than 45, an indication in some medical centers for use of extracorporeal membrane oxygenation (ECMO).…”

Virology, epidemiology, pathogenesis, and control of enterovirus 71

“…98 Severe systemic and pulmonary hypertension is not always seen in children with EV71-associated pulmonary oedema. [99][100][101] This disparity might arise because the changes in vascular pressures in neurogenic pulmonary oedema are only transient. 96 Some commentators have argued that cardiac dysfunction is a major contributor to the pulmonary oedema.…”