RESUMO
During an outbreak of hand-foot-mouth disease caused by enterovirus 71 (EV-71) in 1997, 4 children presented with sudden cardiopulmonary collapse and minimal neurologic features. All children received cardiopulmonary resuscitation but died within a few hours of admission. Postmortem studies showed infection by EV-71 with extensive damage to the medulla and pons. We postulate an etiologic link between EV-71 and brainstem encephalomyelitis as the cause of pulmonary edema and death.
Assuntos
Encefalomielite/virologia , Infecções por Enterovirus , Pré-Escolar , Encefalomielite/patologia , Infecções por Enterovirus/patologia , Evolução Fatal , Feminino , Humanos , Lactente , Masculino , Bulbo/patologia , Edema Pulmonar/virologiaRESUMO
OBJECTIVES: Auto-inhalation of nitric oxide (NO) produced in the upper airways may have physiologic effects on lung function. For intubated patients, the upper airway source of NO is eliminated, but the hospital compressed air source from the environment is contaminated with varying levels of NO, creating an "occult" form of NO therapy. We examined the physiologic significance of occult inhaled NO in ventilator-dependent pediatric patients. We hypothesized that very low levels of NO contamination in inspired gas improve PaO2 in ventilator-dependent children. STUDY DESIGN: Inspired NO levels at the mouth were measured by chemiluminescence in 4 pediatric subjects with normal lungs and 3 with parenchymal lung disease. Subjects were sequentially ventilated with first standard hospital gas (H1), switched to pure nitrogen-oxygen at a similar FIO2 but with no NO contamination (A2), hospital gas again (H2), the nitrogen-oxygen (A2) to control for time and sequence, and finally the nitrogen-oxygen mixture with supplemental NO in an amount equal to the NO previously measured in hospital gas (A2 + NO). Inhaled NO levels and PaO2 were recorded 15 minutes into each of the 5 steps. Two patients were studied a second time, remote from their first examination. RESULTS: NO levels in inhaled hospital gas mixtures ranged from 13 to 79 ppb (mean H1 = 53.3 +/- 23.7 ppb, mean H2 = 53.2 +/- 20.7 ppb, mean A2 + NO = 45 +/- 15.3 ppb; P < .0001). Removing NO from ventilator gas decreased PaO2 in all subjects, whereas replacing NO in artificial gas restored PaO2 to baseline values (P < .0001). CONCLUSION: Concentrations of NO in hospital compressed air are variable and have physiologic effects. The long-term implications of these findings remain to be defined.