Acute poisoning in children is still a major public health problem, and represents a frequent cause of admission in emergency departments. We carried out an epidemiological study of poisonings leading to admission to a paediatric emergency care unit (PECU). We analysed data from 2988 children who were admitted to the PECU of Bordeaux, France with acute poisoning from 1989 through 1995. During the 7-year period, the poison exposure numbers decreased slightly from 490 to 382 (6% vs. 3% of total medical emergencies). This represented a mean annual incidence of 1.4 poison exposures per 1000 children younger than 18 years of age and living in Bordeaux and its surroundings. Characteristics of the study population, circumstances of poisoning and substances involved were similar to those previously described. Eighty per cent of children were younger than 5 years of age, presented with a benign course. Forty per cent were not treated and 75% were discharged home either immediately or within 24 hours of admission. Only 1.5% of cases, mainly adolescent girls who attempted suicide, were admitted to a paediatric intensive care unit. Overall mortality rate was 0.33/1000. In children, most cases of acute poisoning are accidental, benign, and mainly attributed to the ingestion of a non-toxic substance. This points to the need for better information of the population on availability of poison control centre calling facilities, in order to decrease the number of admissions to the PECU. Patients suspected of having ingested a potentially dangerous substance can be managed in short-stay observation units, thus avoiding unnecessarily prolonged hospitalization. Acute poisoning in children remains a frequent problem, highlighting the need to develop an education programme on primary prevention in our region.

Mitochondrial cytopathies are multisystemic disorders of extremely variable expression due to a deficiency in oxidative phosphorylation. Cases have recently been reported in which fatal liver failure with neonatal onset was the major clinical and biochemical syndrome. In this series we reviewed the liver histology of 10 such patients who died in the first weeks of life (from 3 days to 6 mo). In six cases the diagnosis was confirmed by study of the mitochondrial respiratory chain in the muscle, liver or both; in the other four, appropriate tests were not available for diagnosis but symptoms were identical and all other diagnoses were ruled out. In all 10 cases we noted significant steatosis, mostly microvesicular; widespread hepatocytic, canalicular and bile duct cholestasis with bile thrombi and cholangiolar proliferation; and different degrees of hepatosiderosis and glycogen depletion. Fibrosis took varying forms: perisinusoidal, periportal with the formation of septa, even precirrhosis. In the two cases of infants who died, one at 5 and one 6 mo, micronodular cirrhosis was also present. Mitochondria, either densely or loosely packed, were abnormal-pleiomorphic with few or no cristae and a granular fluffy matrix. Dense, large granules were seen in two cases. The association of neonatal liver failure and hyperlactacidemia should lead to immediate examination of the respiratory chain. The expression of this mitochondrial cytopathy can be lethal, associated with severe liver damage due to the deficiency in oxidative phosphorylation.

To evaluate the effects of congenital diaphragmatic hernia (CDH) and pulmonary hypoplasia on subsequent lung function and development, we performed lung 133Xe ventilation and 99mTc perfusion scintigraphies in a group of infants who had undergone surgical repair of a severe left CDH with respiratory distress within the first 6 h of life. The initial lung scans performed in 15 children, 2-3 months of age, demonstrated a decreased ventilation in 7. In 9 children there was a trapping of 133Xe at the left lung base. Perfusion to the hernia side was reduced in 8 of the children. We re-evaluated 11 of these 15 patients after 1-2 years. The ventilation to the left lung was still decreased in 3, but perfusion remained decreased in 9. After 5 years, ventilation to the hernia side was normal in 4 of the 5 patients studied, whereas pulmonary blood flow was abnormal in 4. These results show a progressive improvement of ventilation with a persisting reduction of perfusion to the lung of the hernia side, suggesting a primary vascular pulmonary hypoplasia in CDH.

Children born at ≤ 32 weeks of gestation remain at risk for impaired lung function at school age in particular when they did not receive surfactant. Restrictive or mixed lung defects are mainly associated with prior BPD.