Outcome and cost at a children's hospital following resuscitation for out-of-hospital cardiopulmonary arrest.

OBJECTIVE: To determine the outcome and cost for children resuscitated following out-of-hospital cardiopulmonary arrest. DESIGN: Retrospective case series. SETTING: An organized prehospital emergency medical system within Birmingham, Ala, in a county with 150,493 children under the age of 15 years. PATIENTS: Sixty-three pediatric victims of out-of-hospital cardiopulmonary arrest of any cause presenting to the emergency department of a children's hospital. INTERVENTION: Standard resuscitative techniques were performed for all patients until resuscitative efforts were discontinued in the hospital emergency department or successful resuscitation was achieved. MAIN OUTCOME MEASURES: Successful resuscitation, survival to hospital discharge, neurological outcome, final disposition, and cost of hospital care. RESULTS: Of 63 children with out-of-hospital cardiopulmonary arrest treated in the emergency department of a children's hospital, 60 were pulseless and apneic on arrival, 18 (28.6%) were successfully resuscitated and admitted to the intensive care unit, and six (9.5%) were discharged from the hospital. Five of the survivors had severe neurological deficits and one appeared normal. On follow-up, two patients had died (1 month and 7 months after discharge), three were in a vegetative state, and one was normal. The normal patient had successful defibrillation prior to arrival at the emergency department. The average inpatient charge was $10,667 per patient for those who died and $100,000 for those discharged. CONCLUSIONS: Aggressive treatment does not lead to intact survival for victims of out-of-hospital cardiopulmonary arrest who present to the pediatric emergency department with a preterminal rhythm and absence of spontaneous circulation. Resuscitation efforts in the emergency department are commonly successful but lead to death or severe neurological sequelae at discharge with extremely high cost of care.

Asphyxiated neonates: prognosis and outcome.

The prognosis of perinatal asphyxia depends on the severity and duration of the insult, the gestational age and weight of the affected infant, and the association with other serious medical conditions. The mortality is high in the newborn period. Survivors may escape unscathed or face long-term handicaps including cerebral palsy, mental retardation, and epilepsy. It is often difficult in the nursery to make predictions about later quality of life for an individual infant. Counseling the family can be especially difficult. By looking at data from longitudinal studies linking newborn findings with later outcome, some patterns emerge that may make prognostication more accurate.

Phenobarbital and cerebral blood flow during hypertension in the newborn beagle.

Phenobarbital sodium has been used in anticonvulsant concentrations (15 to 40 micrograms/mL serum) in premature newborns in attempts to prevent periventricular and intraventricular hemorrhages. Although its clinical usefulness in this regard is controversial, phenobarbital treatment has been shown to reduce periventricular and intraventricular hemorrhages after hypertensive insult in newborn beagles. In this study cerebral blood flow values in steady state and during phenylephrine-induced hypertension with and without phenobarbital pretreatment were measured in newborn beagles. At anticonvulsant dosage, phenobarbital sodium decreased mean arterial blood pressure transiently during steady state and significantly reduced total cerebral blood flow during phenylephrine-induced hypertension without reducing mean arterial blood pressure. This phenobarbital sodium effect on cerebral blood flow was not as great in the presence of acidosis, and the initial hypotensive effect of phenobarbital sodium was sustained for a longer period of time during acidosis. Phenobarbital sodium may reduce the incidence of hemorrhages in the newborn brain by providing protection against isolated hemodynamic stresses characterized by acute increases in cerebral blood flow, with or without increased mean arterial blood pressure.

Reversible neuromuscular syndrome in malnourished children.

Six young children are reported who were malnourished, with hypotonia, weakness and absent stretch reflexes, both proximally and distally, but with normal sensory examinations. Motor and sensory nerve conduction velocities also were normal. Five had mildly abnormal electromyograms, with scattered fibrillations, positive sharp waves and increased insertional activity, both proximally and distally. After adequate nutrition in hospital, all the children's reflexes returned and strength improved. Weight for height was an important indicator: it was decreased when the muscle stretch reflexes were absent and increased when they returned. The neurological and electrodiagnostic findings imply that this is a reversible lower motor-neuron or muscle disorder.

Pseudohypoparathyroidism, parkinsonism syndrome, with no basal ganglia calcification.

A 20 year old woman with pseudohypoparathyroidism, Parkinsonism and no basal ganglia calcifications shown by computed tomography is reported. She has typical features of pseudohypoparathyroidism and biochemical evidence of end-organ resistance to parathyroid hormone. She is mentally retarded and has tremor, rigidity, bradykinesia, and stooped posture. The cause of Parkinsonism in pseudohypoparathyroidism is thought to be basal ganglia calcification. This patient must have another pathophysiology, perhaps directly related to a G protein defect, causing impaired neurotransmission.

Suppression of murine neuroblastoma growth in vivo by mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase.

3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase catalyzes the formation of mevalonate, an essential precursor for isoprenoid compounds in mammalian cells. Recent studies have shown that mevinolin, a competitive inhibitor of the reductase, inhibits cell proliferation and induces differentiation in cultured C1300 (Neuro-2A) murine neuroblastoma cells. We now report that mevinolin can inhibit neuroblastoma growth in vivo. The specific activity of HMG-CoA reductase in subcutaneous neuroblastomas increased more than 20-fold between the fifth and eighth days after tumor inoculation, and remained elevated for the remainder of the tumor lifetime in mice. The increase in reductase activity was correlated with a marked increase in tumor DNA content and exponential increase in tumor weight. Using an in vitro assay to monitor the ability of mouse serum to suppress sterol synthesis, we determined that mevinolin was inactivated or cleared from the circulation within 3-6 h after a single subcutaneous injection. However, by using subcutaneous osmotic pumps to deliver a constant infusion of mevinolin, we were able to maintain adequate blood levels of the drug for 7 d. Mevinolin (5 mg/kg per h) suppressed tumor growth (wet weight) significantly when treatment was carried out between day 1 and day 8 or between day 5 and day 12 after tumor inoculation. Histopathological examination of tumors from mevinolin-treated mice revealed few or no mitotic figures and marked cellular degeneration. Measurements of incorporation of (3H)acetate into neuroblastoma sterols and ubiquinones 24 h after implantation of osmotic pumps showed that mevinolin produced a marked inhibition of isoprenoid synthesis in the tumors in vivo. The data suggest that, in addition to their demonstrated utility as cholesterol-lowering drugs, competitive inhibitors of HMG-CoA reductase may have considerable potential as novel antineoplastic agents.