The majority of pediatric intensivists would obtain respiratory secretion cultures and Gram stains in the evaluation of an intubated child with fever and leukocytosis and initiate antibiotics guided by the results. The specificity of respiratory secretion cultures and Gram stains for the diagnosis of ventilator-associated pneumonia requires critical evaluation as this diagnosis is responsible for more than half of antibiotic use in the PICU.

BACKGROUND AND OBJECTIVES: Propofol facilitates deep sedation without requiring intubation and is often used by infusion to maintain sedation. Variability in ordering and preparation strategies resulted in significant propofol volumes wasted at the conclusion of procedures in our clinic. With drug shortages now common, we designed a quality improvement initiative to reduce our propofol waste. METHODS: Data collection during the preintervention phase reflected current practice trends. Two propofol dosing tables ($50 or ,50 kg) were designed to estimate the volume of propofol infusion required for sedations spanning 15 to 180 minutes. Nurses prepared propofol infusions as directed by these tables. The primary outcome measure was reduction in waste when the infusion was prepared by standardized strategy versus usual practice. Balancing measures included occurrences of insufficient infusion volume and premature awakenings from deep sedation. Waste volumes were plotted and displayed chronologically in statistical process control charts for the clinic and individual providers. RESULTS: A total of 155 patients received a propofol infusion to maintain deep sedation. The preintervention phase included 77 patients, and the intervention phase included 78 patients. Special cause variation was achieved in the intervention phase. Median (interquartile range) propofol waste volume per procedure declined from 45.6 mL (24.3-71 mL) to 14.3 mL (9.6-19.4 mL), representing a 68% waste reduction. CONCLUSIONS: Using an internally derived systematic approach to ordering and preparing a propofol infusion, we reduced variability, reduced propofol waste, and created cost savings for our organization. This approach is tailorable to other infusions and clinical settings.

A former 34-week-old female infant with Down syndrome underwent surgical correction of a congenital heart defect at 5 months of age. Her postoperative course was complicated by severe pulmonary hypertension and junctional ectopic tachycardia. Following treatment with amiodarone infusion, she developed laboratory indices of acute liver injury. At their peak, liver transaminase levels were 19 to 35 times greater than the upper limit of normal. Transaminitis was accompanied by coagulopathy, hyperammonemia, and high serum lactate and lipid levels. Hepatic laboratory abnormalities began to resolve within 48 hr of stopping amiodarone infusion. Heart rate control was achieved concurrently with discovery of laboratory test result abnormalities, and no further antiarrhythmic therapy was required. The intravenous formulation of amiodarone contains the diluent polysorbate 80, which may have hepatotoxic effects. Specifically, animal studies suggest that polysorbate 80 may destabilize cell membranes and predispose to fatty change within liver architecture. Polysorbate was implicated in infant fatalities from Eferol use in the 1980s. This case illustrates a possible adverse event by the Naranjo probability scale. Given the extent of clinically apparent hepatic injury, this patient was not rechallenged with amiodarone during the remainder of her hospitalization. With amiodarone now used as first-line pharmacologic therapy for critical tachyarrhythmia in this population, the number of children exposed to this drug should be expected to increase. Laboratory indices of liver function should be evaluated at initiation of amiodarone therapy, as well as frequently throughout duration of therapy. Consideration should be given to polysorbate-free formulation of intravenous amiodarone for use in the cohort with congenital cardiac disease.INDEX TERMS amiodarone, congenital heart disease, hepatotoxicity, junctional ectopic tachycardia, polysorbate 80

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