[Continuous perfusion of insulin in the treatment of acidoketotic coma in children]. / La perfusion d'insuline en continue dans le traitement du coma acidocétosique de l'enfant.

Ketoacidosis is still a frequent complication as far as our diabetic patients are concerned. The insulin regimen during this acute diabetic ketoacidosis was, until October 1981, administered at the start, half intravenously and half intramuscularly, then discontinuously every four hours, subcutaneously, according to the rate of glucose and acetoacetate. Since then, a new method has been used for the treatment of diabetic ketoacidosis providing a continuous perfusion without pumps, of insulin, glucose and electrolytes. The authors describe their experience, using this technique on ten children admitted to hospital because of severe diabetic ketoacidosis. A certain number of parameters and the evolution were studied. The glycemia graph shows a more harmonious and regular normalisation, urinary ketosis disappears within 8 and 24 hours (with an average of 16,22 h). The next step that consists in administering mixed insulin is taken between the 16th and 48th hours (with an average of 25,42 h). Two hypoglycemia have been reported contrary to the statements of other authors. Furthermore, these parameters were compared to those of 10 children submitted to the classical regimen. The authors conclude that a continuous perfusion presents a better method with approximately similar results, and its use is much simpler both for the patient and for the staff.

[Budd-Chiari syndrome in children. Apropos of 7 cases]. / Le syndrome de Budd-Chiari chez l'enfant. A propos de 7 observations.

Seven cases of Budd-Chiari syndrome are reported in children. The mode of onset was fulminant in one case with rapidly lethal liver failure, acute in 5 cases with rapid appearance of hepatomegaly and ascites and insidious in one case, with isolated hepatomegaly. Hepatomegaly, which is a constant sign, was present in the 7 patients. Ascites and collateral venous circulation were present in 6, splenomegaly in 2 and moderate jaundice in one only. Liver function tests, deeply abnormal in the patient with fulminant liver failure, was only slightly abnormal in the 6 others. Diagnosis was corroborated by ultrasonography, cavography, hepatic veins angiography and liver biopsy in 6 patients and by post mortem examination in the 7th. Etiologic investigations did not allow finding the cause of Budd-Chiari syndrome. However, this series can be distinguished by associated total villous atrophy in 3 cases, psoriasis in one, hepatitis B in one, hepatitis A and intestinal giardiasis in one. Portasystemic shunts were performed in 3 patients. One died in the immediate postoperative period, the 2 others are presently in good health with a 5 and 6 1/2 year-follow-up. One patient died rapidly from fulminant liver failure. Another, untreated, died 16 years after the onset of the disease, from an unknown cause. Two patients are lost to follow-up.