Accidental isopropanol ingestion in children.

OBJECTIVE: To describe the clinical course and determine the minimal observation period required following isopropanol ingestion in children. METHODS: The emergency department records of children less than 6 years of age with isopropanol ingestion who presented between June 1992 and December 1998 were identified. Demographics, type, and amount of ingested substance, and time of ingestion were recorded. Symptoms, time of onset, and the results of physical examination and laboratory tests were collected. Group 1 included patients who did not have isopropanol level assayed, and group 2 members had isopropanol level assayed. RESULTS: Ninety-one cases of isopropanol ingestion were identified. Clinical evidence of toxicity was noted in 26 (29%) patients. Symptoms included spontaneous emesis in (24/26), ataxia (5/26), altered mental status (3/26), and apnea (1/26). Toxic isopropanol levels were noted in three patients; all had altered mental status. Clinical evidence of toxicity developed between 0.5 and 2 hours post-ingestion. Patients who ingested more than 1 ounce of isopropanol were more likely to become symptomatic (RR 4.26, 95% CI = 1.61-11.2). CONCLUSIONS: An observation period of 2 hours post-ingestion can be used to rule out clinical toxicity in pediatric patients with suspected isopropanol ingestion. Patients with a history of ingesting more than 1 ounce are likely to develop adverse clinical effects. The development of altered mental status is the most useful clinical predictor of a toxic blood isopropanol level.

Accidental pediatric ingestion, hospital charges and failure to utilize a poison control center.

PROBLEM: Telephone contact with a poison control center may determine that accidental poison ingestion may not pose a risk of developing adverse clinical effect. Over 50% of reported human poisonings occur in children less than 6 years old. Yet most of these accidental childhood ingestions do not produce clinical toxicity. Such nontoxic ingestions can be managed by telephone rather than treated in a health care facility. This study evaluated the clinical effects produced, and the cost of emergency department care, versus obtaining telephone advice from a poison control center, following accidental poison ingestion in children age 6 and under. METHODS: 1 year review of all cases of accidental ingestion in children 6 years and under evaluated in a pediatric emergency department. Utilizing the hospital's poison control center criteria, cases were grouped as nontoxic (no risk of adverse effect) or toxic (significant risk for adverse effect). Groups were compared for demographics, clinical effect, dispositions, charges. RESULTS: 467 cases were seen; 141 met nontoxic criteria. Toxicity was not related to race or gender. Children age 2 and less accounted for the majority of cases (p = .003) [table: see text] Estimated poison control center costs are less than $25 per telephone call. CONCLUSION: Significant charges are billed to health care payers when an emergency department is utilized as the primary means of evaluating children with nontoxic ingestions. Utilization of a poison control center as the initial means of intervention following an accidental pediatric ingestion results in significant savings in health care expenditures.

Upper airway compromise in acute chlorpromazine ingestion.

A 16-year-old boy developed symptoms of acute upper airway compromise after chlorpromazine ingestion. The patient took six 100-mg Thorazine tablets "to help him sleep". Laryngeal-pharyngeal dystonia is a life-threatening form of dystonic reaction that is dose-dependent. In children, acute upper airway compromise should raise the suspicion of exposure to phenothiazines.

Pediatric carbamazepine intoxication.

STUDY OBJECTIVE: To describe the clinical effects of carbamazepine ingestion in a pediatric population. DESIGN: Case series of prospectively evaluated patients and a historical retrospective group. PARTICIPANTS: All patients younger than 18 years who presented to an urban emergency department with history of carbamazepine ingestion and positive laboratory confirmation. INTERVENTIONS: Patient demographics, findings on physical examination, serum carbamazepine levels, analysis of 12-lead ECGs, and time and doses of activated charcoal were recorded. RESULTS: Seventy-seven patients were enrolled, of whom 17 were evaluated prospectively. Serum carbamazepine levels were greater than 12 micrograms/mL (50 mumol/L) in 61 patients. In those 61 patients, mean peak serum level was significantly higher in patients with dystonic reactions (P = .009), coma (P = .002), and apnea (P = .008) than in patients without these symptoms. There was no significant difference in mean peak serum levels between patients with and without seizures. Serum carbamazepine half-life was significantly shorter (P = .022) in patients who received multiple doses of activated charcoal (8.2 +/- 1.6 hours) than in those who received a single dose (12.1 +/- hours). CONCLUSION: Pediatric patients with suspected carbamazepine ingestion are at higher risk for dystonic reactions, coma, and apnea if the peak serum carbamazepine level exceeds 28 micrograms/mL (117 mumol/L). The development of seizures is not related to peak serum level. Multiple doses of activated charcoal can significantly shorten serum carbamazepine half-life.

Freon inhalational abuse presenting with ventricular fibrillation.

Inhalation of volatile halogenated hydrocarbons may produce life-threatening cardiac and neurological toxicity. A 15-year-old boy developed ventricular fibrillation immediately after intentional inhalation of a fluorinated hydrocarbon from an automobile air conditioner recharge unit. After the use of intravenous bretylium, a hemodynamically stable sinus tachycardia was restored. Aspiration pneumonitis and rhabdomyolysis complicated his hospital course before complete neurological recovery. The mechanism and treatment of cardiac arrhythmias after volatile fluorinated hydrocarbon inhalation are reviewed.

Survival following hydrofluoric acid ingestion.

Systemic toxicity after significant dermal exposure to hydrofluoric acid includes rapid development of hypocalcemia and hyperkalemia, leading to ventricular fibrillation. Similar dysrhythmias have occurred in patients after ingestion of sodium fluoride-containing compounds. Ingestion of hydrofluoric acid could induce similar cardiac toxicity; however, reported cases of hydrofluoric acid ingestion rarely have been described, and the rapid death of these patients has not allowed verification of this hypothesis. On two separate occasions, a 70-year-old woman ingested up to 2 oz of a 8% hydrofluoric acid-containing solution. Recurrent ventricular fibrillation with concurrent hypocalcemia and hypomagnesemia complicated her first episode, whereas a more aggressive administration of calcium and magnesium may have prevented dysrhythmias in the second episode. Survival from ventricular fibrillation after hydrofluoric acid ingestion has not been reported previously and suggests a role for aggressive empiric calcium and magnesium replacement.

Clinical characteristics of children with fever and transient neutropenia who experience serious bacterial infections.

A review of consecutive previously healthy children with fever and newly discovered neutropenia without underlying malignancy, evaluated during a three-year period, was performed. A total of 68 episodes occurred in 68 patients; blood culture was performed on each. Of 17 patients who appeared compromised (ill, irritable, toxic) on presentation, five (30%) had either bacteremia or bacterial meningitis. All five patients had clinical evidence of a fulminant disease process on examination. By contrast, all 51 patients who appeared to be well on presentation were culture-negative. Fever and new-onset neutropenia in children is a heterogeneous disorder with several outcomes. Any child with fever and newly discovered neutropenia who appears ill should be presumed to be at high risk for systemic bacterial infection and receive hospitalization for parenteral antibiotic therapy. By contrast, the previously healthy child older than two months of age with fever and new-onset neutropenia who appears to be well, and whose clinical evaluation does not indicate a serious underlying disease process, is at low risk for accompanying systemic bacterial infection; hospitalization with empiric antibiotic therapy pending culture results is not warranted for the majority of such children. Close outpatient monitoring with serial evaluation of the peripheral blood absolute neutrophil count to document bone marrow recovery is recommended for such cases.

Trends in mortality in children hospitalized with meningococcal infections, 1957 to 1987.

We reviewed charts of 261 children seen at Children's Hospital of Wisconsin from 1957 to 1987 with culture-proven meningococcemia or meningococcal meningitis, and we analyzed trends in mortality and disease severity for that interval. Overall case fatality was 10%, ranging from 9% in the period 1957 to 1963, to 16% in the period 1980 to 1987 (P = 0.15). The percent of patients admitted with severe disease increased from 14% to 38% (P = 0.001). When stratified by disease severity, case-fatality rates did not change with time. We conclude that technologic advances of the past 30 years had no measurable impact on mortality from meningococcal infection in our hospital and that crude case-fatality rates can be misleading if disease severity is not considered.