Continuous transcutaneous PO2 monitoring in vital distress of children.
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Biomedical subjects
Publications and source records attributed to F Beaufils.
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The clearance of endogenous creatinine in 20 burned patients, measured between the fourth and the 35th post-burn day, was a mean (+/- S.D.) of 172.1 p 48.4 ml per minute per 1.73 m2; in eight normal subjects the mean value was 125.4 g- 10.4 (P less than 0.02). Thirteen patients had values more than 2 S.D. above the normal mean. We confirmed this rise in glomerular filtration rate by measuring inulin or iothalamate clearance in nine patients. The pharmacokinetics of tobramycin were studied in 11 of the 20 patients and in eight normal subjects receiving continuous intravenous infusions of the drug. An inverse correlation was found between plasma half-life of the drug and creatinine clearance (r = 0.68, P less than 0.01). Increased creatinine clearances and shortened half-life of tobramycin occurred mainly in younger patients. Glomerular filtration rates in burned patients may rise to very high values and can be validly measured by creatinine clearance. The plasma half-lives of drugs with predominantly urinary excretion may decrease in patients with burns.
Surgical exploration of a 7-week-old infant with a diagnosis of 'pulmonary artery sling' (left pulmonary artery arising from the right) revealed the true nature of the abnormality to be persistence of the ductus arteriosus which connected the right pulmonary artery to the aortic isthmus. This malformation has not been described previously. It has the same symptomatology as 'pulmonary artery sling' and it may be treated by surgical ligation and division. We suggest the term 'ductus arteriosus sling' to describe this rare congenital anomaly.
The effect of antibiotic therapy on the intestinal flora was studied qualitatively and quantitatively in 41 infants. The results have been compared with 27 normal children of the same age and background. Antibiotics were responsible for the suppression of sensitive strains and for their replacement by resistant organisms but above all to a rapid multiplication of the intestinal flora. Colistin and pristinamycin caused these changes when given orally. Ampicillin when given both orally and parenterally but Colistin and the aminoglycosides when given parenterally did not have any effect. Fourteen cases of secondary septicaemia due to resistant organisms were observed but other factors were also important, namely the young age of the patients and intestinal problems (stasis and diarrhoea).
In some children severe hyperthermia may be the result of fever that causes cellular damage. This can be seen histologically as cell necrosis. When hyperthermia occurs with collapse or with neurological symptoms it should lead to a search for other lesions (renal, hepatic and/or coagulation disorders). Treatment of these conditions may, in some cases, lead to improvement. Simple prophylactic measures and close supervision of febrile children should prevent this serious syndrome.
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Coagulation and fibrinolysis studies were performed on 64 newborns; 16 premature infants with hyaline membrane disease (HMD), 17 newborns with other forms of respiratory distress syndrome (RDS) (8 of them were premature), 31 healthy newborns (11 of them were premature). All the babies were studied once in the first 48 hours of life. There was no significant difference between sick and healthy babies for 5 parameters; platelet count, factor VIII, fibrinogen, fibrin(ogen) degradation products, euglobulin lysis time. Factor II, VII and X were low in all infants, and premature infants had significantly lower levels compared to full term newborns. Factor V, plasminogen, alpha 2 macroglobulin (alpha 2M) and antithrombin III (AT III) levels were significantly lower in sick infants. Except for AT III, these deficiencies were not related to prematurity. No significant difference was found between HMD and other RDS. Of the 33 sick infants, 5 developed laboratory findings consistent with disseminated intravascular coagulation (DIC). The results indicate that the coagulation and fibrinolytic abnormalities reported are not specific to HMD.
In one year eighteen children were admitted to an intensive care unit with severe viral pneumonia. Four groups were identified by the appearance of the chest X-ray. Bronchiolitis was seen in eight patients, alveolitis in four, interstitial pneumonia in two and combined bronchiolitis and alveolitis in four. Three of the four children with alveolitis died and six of the twelve with bronchiolitis, alone or with alveolitis, had residual bronchial obstruction.
The problems associated with the ventilation of children who have congenital heart disease with left to righ shunts and pulmonary hypertension are more likely to be acquired than due to the congenital malformation. Haemodynamic, angiographic, bronchoscopic and bronchographic studies demonstrated that ventilation problems arose because of compression of the bronchus by the pulmonary artery. The bronchial compression should be treated by surgery to the heart defect without removing the lung. The intervention should be early to obtain maximum benefit and to avoid irreversible damage to the bronchus.
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Four cases of hereditary fructose intolerance with an early onset are reported. The features of acute liver failure in the neonatal period include a haemorrhagic syndrome, collapse, neurological features, hypoglycaemia, disturbed bleeding and clotting studies and abnormal liver function tests. Investigations into the aetiology include a search for bacterial or viral infection but particularly for a metabolic cause: especially for hereditary fructose intolerance which may be difficult to distinguish from tyrosinosis. Finally, methods of treatment are discussed: continuous glucose infusion, exchange transfusion, assisted ventilation, and dietary measures beginning with protein exclusion. The importance of careful observation is stressed (particularly sequential studies of bloodclotting factors).
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The discovery of a fructose-1,6-diphosphatase deficiency in two sisters leads to the discussion of the various loading tests which are required for the diagnosis. The diagnosis may be discussed clinically with type I glycogenosis, and biologically with hereditary fructose intolerance. The specific characteristics of these disorders are analyzed as well as the problem of fructose induced hypoglucosemia. The failure of the treatment with folic acid in one of the cases leads to emphasize the suppression of prolonged fast in order to avoid acute accidents.