This is a retrospective case series reporting lactic acidosis in four pediatric patients with acute severe asthma treated with nebulized beta2-agonists in a pediatric intensive care unit of a tertiary care teaching facility. During treatment with beta2-agonists, these patients developed lactic acidosis with a peak concentration of 5.2 to 13 mmol/l. Lactic acidosis improved within 24 h after discontinuation or decrease in the dosage of beta2-agonists. We conclude that the intensive use of beta2-agonists for acute severe asthma in children may be the primary and significant cause of lactic acidosis.
An alcohol-naive 16-year-old male is presented with alcohol-induced atrial fibrillation. Past medical history, review of systems, and presentation were all otherwise benign. Atrial fibrillation occurred early in the intoxication at an alcohol level slightly higher than the legal limit for intoxication (153 mg/dL). His complete cardiac evaluation was otherwise normal. The atrial fibrillation was not treated aggressively and resolved as the alcohol level quickly fell to zero, consistent with his "nonalcoholic" metabolism. Complete follow-up found the adolescent with no evidence of cardiac or other disease.
The combined clinical and biochemical profile of diabetic ketoacidosis, hyperglycemic hyperosmolar non-ketotic syndrome, complicated by acute pancreatitis, in an 11-year-old with established insulin-dependent diabetes mellitus, is presented. The management requires diligent correction of dehydration and hyperglycemia, while monitoring neurological status and blood chemistry. It is imperative to monitor and avoid potentially fatal complications of the combined entity, namely, cerebral edema, thromboembolism, acute respiratory distress syndrome and rhabdomyolysis. Excluding acute pancreatitis in the face of persistent abdominal pain in this setting is emphasized.
Evaluate the usage of octreotide for the control of acute upper gastrointestinal bleeding in children with portal hypertension. A retrospective electronic database analysis of these children was performed over a period of five years. Setting was a tertiary pediatric intensive care. Case notes of 18 encounters in 13 children were reviewed. A loading dose (1.27 ? 0.76 ?g/kg) was administered in seven, with median starting dose of 1.44 ? 1.19 ?g/kg/h in all other episodes. The mean maximum dose was 1.68 ? 1.38 ?g/kg/h. Re-bleeding occurred in one third; hemostasis was eventually achieved in all. Octreotide infusion appears to be safe and effective in controlling pediatric upper gastrointestinal bleeding due to portal hypertension. We also recommend its use in community and rural hospital settings prior to transfer of such patients to a tertiary care center.
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