Retrospective analysis of ingestions of iron containing products in the united states: are there differences between chewable vitamins and adult preparations?

Iron is the one of the leading causes of pediatric poisoning deaths in the United States. Most cases of serious iron overdose reported in the medical literature have resulted from adult formulations of iron. To begin evaluating the possibility that differences in toxicity exist between iron preparations, we performed a retrospective evaluation of all exposures to pediatric and adult iron products reported to the American Association of Poison Control Centers' (AAPCC) Toxic Exposure Surveillance System (TESS) from 1983 to 1998. We attempted to determine the incidence of fatal iron poisoning for each group. A total of 195,780 ingestions of children's vitamins containing iron were reported to the TESS between 1983 and 1998 with no resulting fatalities. During the same twelve-year study period, 147,079 exposures to adult forms of iron were reported with 60 fatalities (p < 0.0001). A prospective study is required to assess whether differences may exist in the toxicity of these two iron preparations.

Refining the level for anticipated hepatotoxicity in acetaminophen poisoning.

Treatment of an acetaminophen overdose with N-acetyl cysteine usually is based on the position of the 4-h acetaminophen (APAP) level on the Rumack-Matthew nomogram; however, there is disagreement on the level at which clinically relevant hepatotoxicity occurs. A retrospective review of all acute adult formulation APAP exposures reported to our poison center between 1986 and 1993 was performed and cases corresponding to the "possible risk or toxicity" range on the nomogram were identified. Our current poison center protocol for APAP poisoning does not recommend treatment with N-acetylcysteine (NAC) in low-risk patients if the 4-h serum APAP level or the extrapolated equivalent falls within the possible toxicity range on the nomogram. Seventeen cases met the inclusion criteria for the study and received no NAC; six additional patients met inclusion criteria but received one or two doses of NAC before therapy was discontinued. No patients in either group demonstrated clinical evidence of hepatotoxicity. This pilot study suggests that patients with no risk factors and APAP levels in the "possible risk" range may not require NAC therapy.

Hypermagnesemia following an acute ingestion of Epsom salt in a patient with normal renal function.

CASE REPORT: Hypermagnesemia is a rare condition that commonly follows excessive therapeutic administration of magnesium sulfate to treat eclampsia of pregnancy. Signs and symptoms of this condition include extreme muscle weakness, loss of deep tendon reflexes, mental status depression, and cardiac dysrhythmias. Clinically significant hypermagnesemia following oral or rectal administration of magnesium containing products in patients with normal renal function is rare. We report a case of hypermagnesemia following massive Epsom salt ingestion that resulted in extreme musculoskeletal weakness and altered mentation.

Iron overdose and detection of gastrointestinal bleeding with the hemoccult and gastroccult assays.

STUDY OBJECTIVE: To determine the ability of the Hemoccult and Gastroccult tests (SmithKline Diagnostics) to detect blood in vitro in whole-bowel irrigation (WBI) solution. INTERVENTIONS: One tablet of ferrous gluconate 324 mg, ferrous sulfate 325 mg, or ascorbic acid 500 mg; or one Materna prenatal vitamin tablet (Lederle Laboratories) was dissolved in 30 mL of Colyte. Colyte alone and each test solution were tested with Hemoccult and Gastroccult slides, then retested at pH values of 3 and 8. Fresh solutions were then spiked with blood and tested with Gastroccult slides. Materna and ascorbic acid solutions were spiked with blood, then tested with Hemoccult slides. RESULTS: Positive results were difficult to detect on Gastroccult slides. Hemoccult slides were falsely positive for solutions containing only iron and falsely negative for blood-spiked samples containing ascorbic acid. CONCLUSION: Both the Hemoccult and Gastroccult tests may be unreliable in detecting GI bleeding in cases of iron overdose treated with WBI.

Ciguatera fish poisoning. A southern California epidemic.

Ciguatera fish poisoning results from the bioconcentration of a variety of toxins produced by marine dinoflagellates. Signs and symptoms vary widely, but it usually presents as gastrointestinal and neurologic complaints beginning shortly after the ingestion of fish containing the toxins. Symptoms may persist for months and sometimes even years. Although cases have been reported throughout the United States, epidemics are most common along tropical and subtropical coasts and usually involve the ingestion of large carnivorous fish. We review the literature and report the first epidemic of 25 cases of ciguatera fish poisoning presenting to area hospitals in Southern California that were successfully tracked by the Department of Health Services and isolated to fish caught off the coast of Baja California, Mexico.

Cholinergic toxicity resulting from ocular instillation of echothiophate iodide eye drops.

A patient developed a severe cholinergic syndrome from the use of echothiophate iodide ophthalmic drops, presented with profound muscle weakness and was initially given the diagnosis of myasthenia gravis. Red blood cell and serum cholinesterase levels were severely depressed and symptoms resolved spontaneously following discontinuation of the eye drops.

Raising the decontamination level for thyroid hormone ingestions.

Ninety-two pediatric cases (age < or = 6 years) of acute thyroid hormone ingestions that were reported over a 20-month period to one American Association of Poison Control Centers (AAPCC)-certified regional poison center were reviewed to determine whether significant toxicity in pediatric patients is associated with acute ingestions of < or = 5 mg levothyroxine (T4) equivalent of thyroid hormone and the highest-tolerated milligram-per-kilogram dose. Parameters evaluated included patient weight, amount ingested, drug preparation, treatment type, outcome, management site, and relevant comments. Eight patients had mild symptoms requiring no specific medical intervention and there was no correlation between the amount ingested and symptoms observed. The maximum T4 dose ingested without gastrointestinal decontamination was 0.13 mg/kg (2 mg). A literature review was also conducted. Only one case of moderate toxicity with a dose of less than 5 mg T4 equivalent was found in the literature review. Significant toxicity is not expected with ingestions of less than or equal to 5 mg T4 equivalent of thyroid hormone.

Sunlight and the plant: a toxic combination: severe phytophotodermatitis from Cneoridium dumosum.

A severe case of phytophotodermatitis occurred in a patient who had spent several hours walking through an area densely populated with Cneoridium dumosum. This patient's co-worker experienced a similar reaction after undergoing patch testing of an area of skin and exposing it to sunlight. Voluntary patch testing by one of the authors produced a reaction consistent with the other two cases. Approximately twenty other cases were described by a U.S. Fish and Wildlife Service ranger in students who came into contact with the plant during a field trip with him to Baja California, Mexico. Cneoridium dumosum is a common native bush that grows in the chaparral vegetation zone of southern California and Baja California, Mexico. In a search of Poisindex, Medline, Agris International, and Agricola databases, no previous reports of toxic exposures were found.

Severe cyanide poisoning from the ingestion of an acetonitrile-containing cosmetic.

A 39-year-old woman ingested 59 mL of Super Nail Nail Off (American International Industries, Hollywood, CA) (containing 99% acetonitrile) in a suicide attempt. Following a latent period of approximately 12 hours, the patient developed cyanide poisoning with severe metabolic acidosis, seizures, and shallow respirations. She responded to the administration of sodium nitrite and sodium thiosulfate, although the administration of nitrite produced bradycardia and hypotension. She developed several relapses over the course of her hospitalization and each time responded to sodium thiosulfate administration. The patient developed hypernatremia from the sodium load given to her; hemodialysis and charcoal hemoperfusion were initiated to correct the hypernatremia and to attempt to remove cyanide, thiocyanate, and acetonitrile. On the fifth hospital day, the patient was fully recovered and was discharged.

Characterization of the enzymatic lesion in inherited phosphofructokinase deficiency in the dog: an animal analogue of human glycogen storage disease type VII.

Mammalian phosphofructokinase (PFK; ATP:D-fructose-6-phosphate 1-phosphotransferase, EC 2.7.1.11) exists in multimolecular forms, which result from random tetramerization of three distinct subunits, M (muscle-type), L (liver-type), and P (platelet-type), each under a separate genetic control. Human muscle and liver contain homotetramers M4 and L4, respectively, whereas erythrocytes contain a mixture of M4, M3L, M2L2, ML3, and L4 isozymes. Homozygous deficiency of the M subunit in man results in glycogen storage disease (GSD) type VII, which is characterized by exertional muscle weakness and compensated hemolysis; the residual erythrocyte PFK consists of isolated L4 isozyme. Recently, PFK deficiency associated with isolated hemolytic anemia has been identified among English springer spaniel dogs. We investigated the genetic control of the dog PFK system and the nature of the enzymatic defect in two PFK-deficient animals, using chromatographic and immunological techniques. Our studies indicate the existence of a trilocus isozyme system for the dog, as is the case with other mammals. Muscle PFK consists of M4 isozyme, whereas the predominant species of liver and platelet consists, respectively, of the L4 and P4 isozyme; erythrocyte PFK consists of a three- or four-membered set composed of M and P subunits. PFK deficiency in the dogs was found to result from a total and universal lack of the M subunit, as is the case in man. However, the probands consistently exhibited L4 isozyme in their muscle; P4, L4, and hybrids thereof in their erythrocytes; and an increase in the L-containing isozymes in their platelets, indicating a generalized anomalous presence of the L subunit. The apparent absence of muscle disease in these animals is most likely accounted for by both the well-known high oxidative potential of the canine muscle in general and the presence of liver PFK in the M-deficient muscle in particular. In contrast, presence of hemolysis despite residual P4 and hybrids of P and L in the erythrocytes may be inferred to result in severe glycolytic handicap under existing intraerythrocytic conditions.