Cardiopulmonary manifestations of fulminant enterovirus 71 infection

被引:62
作者
Wu, JM
Wang, JN
Tsai, YC
Liu, CC
Huang, CC
Chen, YJ
Yeh, TF
机构
[1] Natl Cheng Kung Univ Hosp, Dept Pediat, Tainan 704, Taiwan
[2] Natl Cheng Kung Univ, Coll Med, Inst Clin Med, Tainan 70101, Taiwan
关键词
enterovirus; 71; pulmonary edema; pathogenesis; hemodynamics; hand-foot-mouth disease;
D O I
10.1542/peds.109.2.e26
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
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.
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页数:5
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