European journal of pediatrics
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Two children, aged 3 1/2 and 5 1/2 years, are described. Both developed pulmonary oedema (PE) following a short episode of choking on a sweet and an orange, respectively. On admission diagnosis was made by chest X-ray. ⋯ Both children recovered spontaneously and chest X-rays showed a return to normal within 24 h. The mechanism of PE production is discussed. It is suggested that oedema formation occurs during the obstruction and that it is due to hypoxia and the severe negative pleural pressure resulting from attempts to inspire against the obstructed airway. both hypoxia and severe negative pleural pressure cause an increase in pulmonary capillary pressure and transduration of fluid across the capillary membrane.
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The locked in syndrome seldom occurs in children, is rarely due to trauma and only in exceptional cases has a favourable outcome. The case reported below is unusual in all these respects, and its evolution might be an example of successful axonal regeneration in the central nervous system.
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This prospective study comprises 40 infants with severe hypernatremic dehydration due to gastroenteritis. During the first 24h, natremia was closely monitored and infusion rates were adjusted so as to keep the rate of fall in natremia below 0.5 mEq/l/h. This could be achieved by giving a 70 mEq/l Na solution at the rate of 120 ml/kg/24 h. Rehydration was uneventful in all cases, and no convulsions were observed.
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We described the clinical and biochemical findings in a 32 day-old boy with the Dubin-Johnson syndrome. Only two other patients diagnosed as having the Dubin-Johnson syndrome during neonatal period have been reported in the literature. The ratio of urinary coproporphyrin isomer I of our patient was 97% and that of his parents were carrier level, confirming that increased urinary excretion of coproporphyrin isomer I is of diagnostic value in neonates with the Dubin-Johnson syndrome.