title: Cardiopulmonary manifestations of fulminant enterovirus 71 infection.
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.
  
  
  METHODS
  Prospective clinical and laboratory study at a tertiary medical center.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Pediatrics, National Cheng Kung University Hospital, Tainan, Taiwan. jingming@mail.ncku.edu.tw
authors.forename: Jing-Ming
authors.initials: JM
authors.lastname: Wu
authors.forename: Jieh-Neng
authors.initials: JN
authors.lastname: Wang
authors.forename: Yu-Chien
authors.initials: YC
authors.lastname: Tsai
authors.forename: Ching-Chuan
authors.initials: CC
authors.lastname: Liu
authors.forename: Chao-Ching
authors.initials: CC
authors.lastname: Huang
authors.forename: Yung-Jung
authors.initials: YJ
authors.lastname: Chen
authors.forename: Tsu-Fuh
authors.initials: TF
authors.lastname: Yeh
mesh_terms: D001927:Brain Diseases / Q000503:physiopathology* / Q000821:virology; D001933:Brain Stem / Q000503:physiopathology* / Q000821:virology; D004770:Enterovirus / Q000145:classification* / Q000302:isolation & purification; D006232:Hand, Foot and Mouth Disease / Q000209:etiology / Q000503:physiopathology / Q000821:virology*; D006557:Herpangina / Q000209:etiology / Q000503:physiopathology / Q000821:virology*; D006801:Humans; D007223:Infant; D008297:Male; D011654:Pulmonary Edema / Q000209:etiology / Q000503:physiopathology / Q000821:virology*