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Enterovirus (Nonpoliovirus)...

PEDIATRICS Vol. 109 No. 2 February 2002, pp. e26

ELECTRONIC ARTICLE

Cardiopulmonary Manifestations of Fulminant Enterovirus 71 Infection

Jing-Ming Wu, MD*, Jieh-Neng Wang, MD{ddagger}, Yu-Chien Tsai, MD*, Ching-Chuan Liu, MD, MPH*, Chao-Ching Huang, MD*, Yung-Jung Chen, MD, PhD* and Tsu-Fuh Yeh, MD, PhD*

* Department of Pediatrics, National Cheng Kung University Hospital, Tainan, Taiwan
{ddagger} Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan

--> 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/M2 (normal: 30–60 mL/M2), 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.

Key Words: enterovirus 71 • pulmonary edema • pathogenesis • hemodynamics • hand-foot-mouth disease

Abbreviations: EV71, enterovirus 71 • PE, pulmonary edema • PH,pulmonary hemorrhage • CNS, central nervous system • CK, creatine kinase • PAP, pulmonary artery pressure • PAOP, pulmonary artery occlusion pressure • CI, cardiac index • MRI, magnetic resonance imaging

Received for publication Aug 27, 2001; Accepted Sep 24, 2001.




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