Accidental poisoning in New Zealand

Objective: To examine mortality and morbidity associated with accidental poisoning in New Zealand for the period of 1993–97, and make comparisons with international trends. Methods: Poison Centre call data, and mortality and public hospital discharge data from the New Zealand Health Information Service were examined. Mortality and hospitalization rates were calculated. Statistical trends were examined using Poisson regression. Results: Poison Centre calls regarding household agents and therapeutics were most frequent. Accidental poisoning with analgesics, antipyretics and antirheumatics (18%) was a common cause of hospitalization. Children under 5 years had the highest hospitalization rates, but were less at risk of death by accidental poisoning than other age groups. Common causes of death from accidental poisoning included utility gas/carbon monoxide (16%), psychotropic agents (16%), and analgesics, etc. (15%). Mortality rates varied between 0.54 and 0.72/100 000 population. Conclusion: Mortality rates in New Zealand are lower than in many countries, but hospitalization rates are higher. Possible explanations and prevention implications are discussed.     

Accidental poisoning after ingestion of "aphrodisiac" berries: diagnosis by analytical toxicology

Background

A large number of plants, seeds, and berries have been used for medicinal, psychotropic, or aphrodisiac purposes for a thousand years. Mandragora officinarum belongs to the family of Solanaceae and is traditionally known as an aphrodisiac and is closely associated with witchcraft.

Objectives

In this study we report a case of an accidental poisoning after ingestion of some “aphrodisiac” berries and the contribution of the toxicological analysis in the case investigation.

Case Report

A 35-year-old man was admitted to the hospital with clinical signs and symptoms of an anticholinergic syndrome. The diagnosis of the poisoning was made by the toxicological analysis of the patient’s urine. The cause of the poisoning was revealed by his girlfriend’s disclosure that the patient had intentionally consumed some “aphrodisiac” berries to enhance his sexual performance. Subsequently, berries similar to the ones consumed were sent to the laboratory. The analysis of the urine and the berries revealed the presence of hyoscyamine and scopolamine; the berries were identified as Mandragora officinarum berries. Decontamination and symptomatic treatment were proven effective for the control of this poisoning. The patient recovered completely after hospitalization for 4 days.

Conclusion

This case report indicates the importance of analytical toxicology in diagnosis of intoxications after the consumption of unknown plants or plant products and presents the clinical aspects of Mandragora intoxication.     

Heavy metal poisoning: clinical presentations and pathophysiology

Humans have had a long and tumultuous relationship with heavy metals. Their ubiquitous nature and our reliance on them for manufacturing have resulted at times in exposures sufficient to cause systemic toxicity. Their easy acquisition and potent toxicity have also made them popular choices for criminal poisonings. This article examines the clinical manifestation and pathophysiology of poisoning from lead, mercury, arsenic, and thallium.     

Accidental oral poisoning caused by RDX (cyclonite): a report of 5 cases

The explosive RDX (hexogen, cyclonite) is usually used for the production of C-4 explosive. The rare occurrence of accidental and intentional RDX intoxications has been reported during manufacturing process or in wartime. In this article, the authors report 5 cases of accidental oral RDX poisoning. On admission, observed signs and symptoms included repetitive generalized tonic-clonic convulsions, postictal coma, lethargy, confusion, hyperreflexia, postictal amnesia, nausea, vomiting, abdominal tenderness, sinusal tachycardia, dysrhythmia with frequent ventricular premature beats, generalized muscle spasms, and myoclonus. Leukocytosis, mild anemia, methemoglobinemia, elevated levels of blood glucose, serum aspartate transaminase, alanine transaminase, lactic dehydrogenase, creatine phosphokinase, amilase, hypokalemia, metabolic acidosis, proteinuria, glucosuria, and myoglobinuria were also noted. Plasma RDX concentrations were 268 to 969 ng/mL at 3 hours of ingestion. For management, supportive and symptomatic measures were taken. Whole-bowel irrigation might have been an effective therapeutic procedure due to probable slow gastrointestinal absorption of RDX. Three patients who developed severe metabolic acidosis underwent urgent hemodialysis. All patients were discharged 7 to 21 days after admission without any sequelae. Plasma RDX levels were strongly correlated with the clinical and laboratory manifestations. The available toxicological data on this rare accidental poisoning are reviewed in light of the literature.     

A neonate with metabolic acidosis: Intentional ethylene glycol poisoning

We present a rare case of the intentional poisoning of a neonate. An 8-day old child presented to an academic pediatric emergency department (ED) with respiratory distress and decreased intake. In the ED the patient was stabilized, and workup uncovered an anion gap metabolic acidosis. Blood, urine, and CSF cultures were negative at 48 h and a metabolic screen revealed elevated glycine. Calcium oxalate crystals were later found in the urinalysis, raising concern for ethylene glycol poisoning. The patient's father admitted to mixing antifreeze with the child's formula. The workup of an ill or distressed neonate should be methodical, ruling out sepsis, inborn errors of metabolism, cardiac disease, trauma, and less common etiologies such as intestinal catastrophes, renal or hepatic disease, neurologic disease, drug withdrawal, non-accidental trauma, formula mixing errors, and poisoning.     

Accidental hypothermia and active rewarming: the metabolic and inflammatory changes observed above and below 32 degrees C

Objectives: In accidental hypothermia the underlying physiological mechanisms responsible for poor outcome during rewarming through 32°C remain obscure, although possible associations include changes in acid-base balance, divalent cations, and inflammatory markers. This study investigated the metabolic and inflammatory changes that occur during the rewarming of hypothermic patients.

Methods: Eight patients, four men and four women, age 45 to 85 years, admitted with core temperatures <35°C were included in the study. Patients were rewarmed with dry warm blankets and fluid replaced by crystalloid at 40°C. Bloods for pH, ionised calcium (Ca²⁺) and magnesium (Mg²⁺), parathyroid hormone (PTH), interleukin 1 (IL1), interleukin 6 (IL6), tissue necrosis factor α (TNFα), were collected at presentation, during rewarming, and at 24 hours.

Results: Four patients were admitted with mild (32°–35°C) and four with moderate (28°–32°C) hypothermia. Rewarming to 32°C had no significant effect on the presenting acidosis (p=0.1740), although above 32°C pH increased with temperature (p<0.0001). There was a negative correlation between pH and both Ca²⁺ (p=0.0005) and Mg²⁺ (p=0.0488) below 32°C; above this temperature the relation was significant only for Ca²⁺ (p=0.0494). PTH and Ca²⁺ correlated positively (p=0.0041) and negatively (p=0.0039) below and above 32°C respectively. There was no relation between IL1 or TNFα with Ca²⁺ during rewarming, but IL6 and Ca²⁺ correlated positively (p=0.0039) and negatively (p=0.0018) when presentation temperature was below and above 32°C respectively.

Conclusions: During rewarming pH remains unchanged until patient temperature approaches 32°C. Ca²⁺ and Mg²⁺ decline is associated with the pH increase above 32°C. Poor outcome is associated with presentation temperature (<32°C), non-physiological correlation between IL6-PTH-Ca²⁺, and age (≥84 years).