1990 annual report of the American Association of Poison Control Centers National Data Collection System.
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Biomedical subjects
Publications and source records attributed to T L Litovitz.
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Two cases of pediatric accidental ingestion of an acetonitrile-containing cosmetic are reported. One of the children, a 16-month-old boy, was found dead in bed the morning after ingesting the product. No therapy had been undertaken, as the product was mistakenly assumed to be an acetone-containing nail polish remover. The second child, a 2-year-old boy, experienced signs of severe cyanide poisoning, but survived with vigorous supportive care. Both children had blood cyanide levels in the potentially lethal range. The observed delayed onset of severe toxic reactions supports the proposed mechanism of acetonitrile conversion to inorganic cyanide via hepatic microsomal enzymes. Physicians and poison centers should be alerted to the existence of this highly toxic product, sold for removal of sculptured nails and likely to be confused with the less toxic acetone-containing nail polish removers. We urge regulatory agencies to reconsider the wisdom of marketing a cosmetic that poses such an extreme health hazard.
A retrospective chart review was conducted at two regional poison centers to determine the clinical outcome of boric acid ingestions and to assess the relationship between serum boric acid levels and clinical presentation. A total of 784 cases were studied; all but 2 were acute ingestions. No patients developed severe manifestations of toxicity, and 88.3% were entirely asymptomatic. The most common symptoms were vomiting, abdominal pain, and diarrhea. Lethargy, headache, lightheadedness, and atypical rash were seen less frequently. Boric acid levels were obtained in 51 patients and ranged from 0 to 340 micrograms/mL. Blood levels were 70 micrograms/mL or more in 7 patients; 4 remained asymptomatic, whereas the other 3 had nausea or vomiting. Dialysis was performed in 4 of these 7 patients, only 1 of whom had symptoms (vomiting). On the basis of data from 9 patients, the mean half-life of boric acid was determined to be 13.4 hours (range, 4.0 to 27.8). Hemodialysis in 3 patients significantly shortened the half-life compared with pre- and postdialysis half-lives. Our results suggest that acute boric acid ingestions produce minimal or no toxicity and that aggressive treatment is not necessary in most patients.
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A series of 78 cases of accidental levothyroxine ingestion in children (less than 12 years old) with treatment limited to ipecac-induced emesis and a single oral dose of activated charcoal is presented. No patient received any form of dialysis or hemoperfusion, propylthiouracil, cholestyramine, steroids, or serial doses of oral activated charcoal. Propranolol was used in one case despite the absence of clinical manifestations of toxicity. Only four children developed symptoms, limited to modest fever (38.3 degrees C), supraventricular tachycardia (120-176 beats/min), lethargy, irritability, vomiting, diarrhea, and abdominal pain. Peak T4RIA values in three patients were 32.8, 30.0, and 26.4 micrograms/dl, respectively, and two of these patients remained asymptomatic. Initial therapy for acute levothyroxine ingestions in children can be safely limited to routine gastrointestinal decontamination. Hospitalization or prophylactic treatment with propranolol, propylthiouracil, corticosteroids, cholestyramine, or extracorporeal detoxification are unnecessary in the early asymptomatic phase.
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The efficacy of ipecac syrup in the induction of emesis and safety of its administration was studied in 105 poison-exposed infants 6 through 11 months of age (study subjects) and compared prospectively with 302 poison-exposed infants and children 12 through 35 months of age who served as age controls. Of the 105 study subjects 101 (96.2%) vomited. The failure of ipecac to induce emesis in six patients (four of 105 study subjects two of 302 age control subjects) is comparable with ipecac failure rates reported elsewhere. The frequency of side effects caused by ipecac syrup did not differ between study and control subjects. There were no serious medical complications resulting from the administration of ipecac syrup. When not readily available at home, ipecac administration was delayed an additional 21.8 minutes if obtained from a pharmacy and 38.4 minutes if obtained from an emergency department. Because of the time delay and the increased health care cost, home rather than emergency department administration of ipecac should be advised. These data demonstrate that ipecac syrup effectively induces emesis and is safe for home administration to poisoned infants 6 to 11 months old.
Results of 125 battery ingestions in 114 separate episodes over an 11-month period are analyzed. The 125 batteries included 119 button batteries and six cylindrical cells. The location of batteries just prior to ingestion (loose or discarded [48.7%], in product [34.4%], in manufacturer's battery packaging [3.4%]) determined the need for consumer education of this potential hazard. The observation that hearing aid batteries were the most common type swallowed (33.9%), and that 14 batteries were ingested by hearing-impaired children after they removed the batteries from their own aids, further directs appropriate prevention efforts. All the larger cylindrical batteries and 89.9% of the button cells passed through the gastrointestinal tract spontaneously. Endoscopic retrieval was unsuccessful in 66.7% of cases attempted. Ipecac syrup, administered to 11 patients, uniformly failed to expel the battery. Transit time was within 48 hours for 68.8% of button cells, and 85.4% of the batteries were passed by 72 hours, with a range of 12 hours to 14 days. Once beyond the esophagus, arrested battery progression failed to correlate with adverse outcome. Symptoms developed in 11 patients but were only severe in the single case of esophageal lodgment. The vast majority of battery ingestions are benign and can be managed without endoscopic or surgical intervention.