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T L Litovitz

Publications and source records attributed to T L Litovitz.

At least 19 recordsLinked to original sources
PubMed1997

Characterization of fatal beta blocker ingestion: a review of the American Association of Poison Control Centers data from 1985 to 1995.

OBJECTIVE: To characterize beta blocker-related deaths. METHODS: This is a retrospective review of beta blocker-related exposure data and fatality case abstracts reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System during the 11 year period, 1985 to 1995. Historical and laboratory data were used to determine those fatalities which resulted primarily from beta blocker intoxication. RESULTS: Of 52,156 reported beta blocker exposures, 164 were fatal. In 38 cases, beta blockers were implicated as the primary cause of death. Propranolol was responsible for the greatest number of exposures (44%) and implicated as the cause of death in a disproportionately high percentage of fatalities (71%). Patients were generally young women; 63% were female and 92% were less than 50 years old. The dysrhythmias most often noted in fatal cases were bradycardia and asystole. Cardiopulmonary arrest did not develop until patients were in the care of health care personnel in 59% of cases. Though glucagon was initiated more often than any other intervention in fatal intoxications (83%), optimal dosing and maintenance infusions appear to have been underutilized. CONCLUSIONS: The predominance of fatalities associated with propranolol compared to other beta blockers reflects both its greater frequency of use over the time period studied and its greater toxicity. Since 59% developed. cardiac arrest after reaching health care personnel, further study should focus on identifying medical intervention that can reduce mortality in this group.

Administration, Oral↗
PubMed1996

Fatal accidental dibucaine poisoning in children.

Dibucaine is a potent amide anesthetic available in over-the-counter preparations. Compared with lidocaine, substantially lower doses of dibucaine may result in seizures, dysrhythmias, and death. We present three fatal cases of accidental dibucaine ingestion in children and discuss the toxicity, treatment, and prevention of such ingestions.

Administration, Oral↗
PubMed1996

State of the national's poison centers: 1995 American Association of Poison Control Centers Survey of US Poison Centers.

The American Association of Poison Control Centers (AAPCC) 1995 annual survey is summarized. A decline in the total number of poison centers was noted (from 104 in 1991 to 83 in 1995). The 83 US poison centers handled 2,431, 599 human exposure cases. Certified centers (44) served 63.1% of the US population, handled 72.5% of all poison exposures handled by poison centers nationally, and achieved higher utilization rates within their regions (10.9 vs 7.4 human exposure cases handled/1,000 population). Certified centers had superior staff credentials as measured, by passing the certification examinations for specialists in poison information or board certification for medical and managing directors. Funding for poison centers in 1995 to-total $74.6 million, although this funding level was recognized to be inadequate as only 63.1% of the population was served by certified centers and utilization of poison centers was not optimal. The annual cost of covering the entire US with adequate poison control services (meeting AAPCC certification standards and with utilization at a level of 15 human exposures per thousand population) is estimated at $120 million. Funding difficulties were prevalent. Thirty-five centers indicated that closure had been a real threat at least once in the previous 5 years. Analysis of cost per human exposure case by center volume demonstrated that economies of scale were achieved when a center handled at least 20,000 to 30,000 human exposure calls/year. Increasing human exposure volume beyond 30,000/year did not lead to a reduction in the average cost per human exposure case.

Cost-Benefit Analysis↗
PubMed1988

Pediatric cyanide intoxication and death from an acetonitrile-containing cosmetic.

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.

Acetonitriles↗
PubMed1988

Clinical manifestations of toxicity in a series of 784 boric acid ingestions.

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.

Adolescent↗