Cardiopulmonary manifestations of fulminant enterovirus 71 infection.

Jing Ming Wu, Jieh Neng Wang, Yu Chien Tsai, Ching Chuan Liu, Chao Ching Huang, Yung Jung Chen, Tsu Fuh Yeh

Research output: Contribution to journalArticle

57 Citations (Scopus)

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/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.

Original languageEnglish
JournalPediatrics
Volume109
Issue number2
Publication statusPublished - Feb 2002
Externally publishedYes

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Enterovirus Infections
Pulmonary Edema
Hemodynamics
Vascular Resistance
Lung
Pulmonary Artery
Brain Stem
Pressure
Central Venous Pressure
Hydrostatic Pressure
Central Venous Catheters
Myocarditis
Capillary Permeability
Tachycardia
Stroke Volume
Hypotension
Nervous System
Fever
Heart Rate
Magnetic Resonance Imaging

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Cite this

Wu, J. M., Wang, J. N., Tsai, Y. C., Liu, C. C., Huang, C. C., Chen, Y. J., & Yeh, T. F. (2002). Cardiopulmonary manifestations of fulminant enterovirus 71 infection. Pediatrics, 109(2).

Cardiopulmonary manifestations of fulminant enterovirus 71 infection. / Wu, Jing Ming; Wang, Jieh Neng; Tsai, Yu Chien; Liu, Ching Chuan; Huang, Chao Ching; Chen, Yung Jung; Yeh, Tsu Fuh.

In: Pediatrics, Vol. 109, No. 2, 02.2002.

Research output: Contribution to journalArticle

Wu, JM, Wang, JN, Tsai, YC, Liu, CC, Huang, CC, Chen, YJ & Yeh, TF 2002, 'Cardiopulmonary manifestations of fulminant enterovirus 71 infection.', Pediatrics, vol. 109, no. 2.
Wu JM, Wang JN, Tsai YC, Liu CC, Huang CC, Chen YJ et al. Cardiopulmonary manifestations of fulminant enterovirus 71 infection. Pediatrics. 2002 Feb;109(2).
Wu, Jing Ming ; Wang, Jieh Neng ; Tsai, Yu Chien ; Liu, Ching Chuan ; Huang, Chao Ching ; Chen, Yung Jung ; Yeh, Tsu Fuh. / Cardiopulmonary manifestations of fulminant enterovirus 71 infection. In: Pediatrics. 2002 ; Vol. 109, No. 2.
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AB - 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.

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