Poisoning

Knowledge of the toxicologic nature of ingested substances provides a proper framework for general and specific therapies best suited to meet the needs of the patient. Monitoring and direct observation provided in the PICU can aid proper therapy for many intoxicants. Good supportive care coupled with specific pharmacotherapy will provide the best chance for a successful outcome.     

Paraquat Poisoning

Abstract

The successful supportive management of an acute strychnine ingestion is described; clinical and biochemical findings are reported. A gas chromatographic assay for serum strychnine has been applied to the analysis of 19 serial blood samples. Four hours post ingestion, the serum strychnine concentration was 1.6?mg/L. This declined with T of 10 hours over a period of 50 hours. First order kinetics are indicated. Management of strychnine poisoning in general is discussed in the light of this case and the limited knowledge of the pharmacokinetics of the alkaloid in man.     

Intravenous Amitraz Poisoning

Amitraz, a derivative of dimethylformamidine, is an acariside and insecticide used to control parasites in animals. Amitraz inhibits monoamine oxidase and prostaglandin synthesis and is an alpha-2 adrenergic agonist. Xylene, a mixture of o-, m-, and p-dimethylbenzene, is widely used in industry. A 22-year-old woman was poisoned by an intravenous injection of 5–6 mL of an amitraz formulation (amitraz 12.5% + xylene 57.5%). Clinical findings were coma (Glasgow coma score 3), respiratory depression, hypotension, bradycardia, hematuria, and edema and hyperemia at the injection site. Although her coma and other symptoms quickly resolved, as has been seen in oral and dermal amitraz poisoning, intoxication with higher doses occurring from intravenous injection may result in more serious problems.     

Perils of Poisoning

Most persons who are accidentally poisoned inhale a toxic gas. Carbon monoxide accounts for 95 percent of deaths from gases, but ammonia, chlorine, nitrous dioxide, smog and smoke also occasionally kill. Other agents that cause problems in industry and agriculture are corrosive chemicals, metallic solutions and cholinesterase-inhibiting insecticides.     

Essential Oil Poisoning

Abstract

Alpha-ketoglutaric acid and sodium thiosulfate antagonize the toxic effects of cyanide. The present study was performed to test whether a synergistic effect may occur. The alpha-ketoglutaric acid/sodium thiosulfate solutions were injected intraperitoneally into mice prior to exposure to hydrogen cyanide (HCN) in a dynamic inhalation chamber or preceding an intraperitoneal injection of sodium cyanide (NaCN). All lethal concentration (LCT) and lethal dose (LD) values were determined after a period of 24?h. Alpha-ketoglutaric acid alone provided no protection at 250?mg/kg when challenged with HCN. Sodium thiosulfate 500?mg/kg provided a 5% protection. However, when these doses of alpha-ketoglutaric acid and sodium thiosulfate were combined, protection was increased by 18%. Alpha-ketoglutaric acid (250?mg/kg) and sodium thiosulfate (1000?mg/kg) provided an additional 48% protection against a LCT₈₈ of HCN. A single dose of alpha-ketoglutaric acid (500?mg/kg) and sodium thiosulfate (1000?mg/kg) solutions afforded a 70% increase in survivability of the exposed animals. When mice were injected ip with 100?mg/kg of alpha-ketoglutaric acid 15 min prior to the injection of 5.5?mg/kg (LD₅₀) of NaCN, the lethality was reduced to an LD₃₀. Two hundred?mg/kg alpha-ketoglutaric acid, challenged with the same dose of NaCN, reduced the lethality to 23%. When mice were challenged with 6.0?mg/kg of NaCN (LD₇₀) pretreated with 100?mg/kg of alpha-ketoglutaric acid or 200?mg/kg of sodium thiosulfate, the LD was not altered in the former but reduced to an LD_1S in the latter. At higher doses of sodium thiosulfate (500?mg/kg), an LD₆₀ occurred at 13.6?mg/kg NaCN (2.5 x LD₅₀). Combinations of alpha-ketoglutaric acid and sodium thiosulfate proved to be very effective. Injections in which alpha-ketoglutaric acid and sodium thiosulfate (200 and 500?mg/kg, respectively) were given 15 min prior to NaCN challenges of 26.5?mg/kg (4.8 x LD₅₀) produced an average lethality of 78%. Greater doses of alpha-ketoglutaric acid and sodium thiosulfate were required to provide protection against the lethal effects of inhaled HCN than those of parenteral NaCN. Also, alpha-ketoglutaric acid and sodium thiosulfate are synergistic in their antidotal effects against both HCN and NaCN.