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Biomedical subjects

A Bourrillon

Publications and source records attributed to A Bourrillon.

89 records · Page 5Linked to original sources
PubMed1981

[The child's intestinal ecosystem: effect of colistin (author's transl)].

A differential quantitative study of the fecal flora was used to appreciated the intestinal bacterial flora of 41 hospitalized children, with no infection and receiving no antibiotic treatment. Thus, it was possible to establish the bacterial normal profile of intestinal of hospitalized child. Because of the stability of the fecal flora in those controls, it was possible to study the effect of colistin on the intestinal ecosystem, in 21 children. Colistin per os, with intestinal nutrition and colistin IM in combination with gentamicin IM did not have any quantitative or qualitative effect on fecal flora. Colistin per os, with exclusive parenteral nutrition caused by disappearance of sensitive strains and their replacement by resistant organisms; this was followed by secondary septicaemia. This fact being a very high infectious risk, it leads us to abstain from administering colistin per os, when the intestine does not receive any food.

Administration, Oral↗
PubMed1978

[Antibiotic therapy, intestinal microbial pullulation and risk of infection in children].

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).

Age Factors↗
PubMed1978

[Severe hyperthermia in children].

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.

Blood Coagulation Disorders↗
PubMed1977

[Severe viral pneumonia. A radiological classification with prognostic value].

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.

Adenoviridae Infections↗
PubMed1977

[An explanation of ventilation problems in congenital heart disease with left to right shunt].

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.

Bronchi↗
PubMed1976

[Hereditary fructose intolerance with early onset].

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).

Alanine Transaminase↗