Heart rate variability monitoring in the detection of central nervous system complications in children with enterovirus infection.

PURPOSE: Previous studies suggest the possibility of autonomic dysfunction in patients with complicated hand, foot, and mouth disease (HFMD) and herpangina. Heart rate variability (HRV), an index for autonomic nervous system, may be useful to detect disease progression. MATERIALS AND METHODS: From 2001 to 2002, 66 patients (1-9 years old) were enrolled prospectively in either a control (20 patients) or disease (46 patients with HFMD or herpangina) group. The disease group was subdivided into stage I (fever only), stage II (with complications of encephalomyelitis), and stage III (with complications of encephalomyelitis as well as tachycardia, hyperglycemia, tachypnea, and hypertension or hypotension) groups. Data from electrocardiograms were transformed for HRV. RESULTS: The HRV parameters generally decreased and the low frequency (LF)/high frequency ratio (HF) increased in the disease groups. Patients in disease group stage II had significantly lower parameters of HRV (triangular index, total power, LF power, and HF power) and higher LF/HF ratio than those in disease group stage I. With this trend, patients with stage III disease had extremely low HRV parameters. The inferred criteria of HRV (standard deviation of normal-to-normal interval <17 milliseconds and HF power <24 milliseconds(2)) to define stage III patients (sensitivity, 100%; specificity, 71.4%) were also useful to predict disease progression. CONCLUSIONS: The HRV markedly decreased, most likely because of autonomic dysfunction, in patients with HFMD and herpangina when complicated with central nervous system involvement and cardiopulmonary failure and may be useful parameters to monitor disease progression.

Cardiopulmonary manifestations of fulminant enterovirus 71 infection.

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.