Cardiac Toxicity from Intentional Ingestion of Pong-Pong Seeds (Cerbera Odollam).

BACKGROUND: A variety of plants contain cardiac glycosides. This has resulted in many of them being used to commit suicide. In southeast Asia, Cerebera odollam (pong-pong or suicide tree) is frequently used for suicidal ingestion. Seeds, or kernels, of this plant can cause hyperkalemia, heart block, and death due to the effects of its cardiac glycosides. CASE REPORT: We describe six cases of pong-pong seed ingestion reported to US poison centers. The most common symptoms were vomiting and bradycardia. Three patients survived and three died. All patients who died had heart block, serum digoxin levels > 1.0 ng/mL, and were treated with anti-digoxin immune FAB. Anti-digoxin immune FAB may be ineffective in a large pong-pong seed ingestion. Patients ingesting pong-pong seeds who develop a potassium level > 8.0 meq/L or have a digoxin level > 1.0 ng/mL may be at a higher risk for death. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: The apparent ease of acquiring C. odollam seeds on the Internet makes knowledge of it important, as it can be used as a means to commit suicide. The apparent failure of digoxin immune FAB to treat toxicity from pong-pong is important, as other lifesaving techniques, such as extracorporeal membrane oxygenation, might be needed in severely toxic patients.

Plant poisoning.

Each year over 100,000 exposures to toxic plants are reported to poison centers throughout the United States. Most of these exposures are of minimal toxicity largely because of the fact that they involve pediatric ingestions, which are of low quantity. The more serious poisonings usually involve adults who have either mistaken a plant as edible or have deliberately ingested the plant to derive perceived medicinal or toxic properties. The plants within this manuscript have been chosen because they have been documented to cause fatalities or account for emergency medicine visits. In this discussion, plants are grouped by their toxins rather than on the basis of their taxonomy.

Brown recluse spider envenomation.

Brown recluse spider bite is a common diagnosis in almost every state in America. In fact, cases have been reported in areas where the spider has never been seen. A review of medical literature reveals that most current concepts regarding brown recluse spider envenomation are based on supposition. In this article, we attempt to review critically our present understanding of brown recluse bites with a focus on the published evidence.

Hepatotoxicity associated with herbal products.

A significant number of herbal products have been associated with hepatotoxicity. Attribution of liver injury to a specific herbal pro-duct may be difficult. There are few clinical or laboratory manifestations that specifically suggest that liver injury is the result of aspecific herbal. Compounding this difficulty is that the patient may have liver disease from another cause, may be consuming other potentially hepatotoxic products, or may be using a contaminated herbal product. The most important clue often is the temporal relationship between initiation of the herbal product and the appearance of liver injury; of equal importance is the resolution of the injury following withdrawal of the herbal product.

Criminal poisoning: medical murderers.

It is impossible to determine the true incidence of homicides that occur within health care facilities. Over the years there have been numerous documented examples of health care providers preying on helpless patients. For several reasons, the health care system has been inadequate in its response. This article reviews some of those cases, the hospitals' responses, and the outcome of investigations,to reveal the common factors that can identify the warning signs of these tragic events.

Drug-induced q-T prolongation.

Drug therapy may induce Q-T prolongation by alteration of potassium ion currents in cardiac cells, resulting in abnormal repolarization. Q-T prolongation, whether congenital or acquired, has been associated with the development of the malignant dysrhythmia Torsade de Pointes (TdP), which may result in sudden death. Re-cent regulatory actions and drug withdrawals due to Q-T prolongation or TdP have focused attention on this issue. Although our understanding of the pathophysiology continues to evolve, both patient and medication factors contribute to the individual risk of drug-induced Q-T prolongation or TdP. The clinician should be aware of these issues when prescribing new drugs and should weigh the risks and benefits carefully when prescribing drugs known to prolong the Q-T interval.

Toxicity and drug interactions associated with herbal products: ephedra and St. John's Wort.

Health care providers are being increasingly confronted with the use of herbal medications by their patients. It is imperative that patients be questioned regarding herbal preparation use and that health care providers become familiar with these agents. Research into the active components and mechanisms of action of various herbals is ongoing [350]. Long-range studies need to be performed to follow patients for efficacy or toxicity in chronic use [351,352]. Adverse reactions to herbal remedies should be reported to the FDA MedWatch at http://www.fda.gov/medwatch. As withany therapeutic agent, risk of use must always be weighed against potential benefits.

Historical neurotoxins: what we have learned from toxins of the past about diseases of the present.

Throughout history, humans have fallen victim to a variety of neurotoxins, with exposures coming in the form of tainted products, industrial pollution, drugs of abuse, and even the bread and water that sustain them. Despite this long and tumultuous history, neurotoxic outbreaks still occur with regular frequency. Although many difficulties currently exist in linking many of today's unexplained neurologic disorders to toxins, the past suggests a prominent role for neurotoxins in diseases (such as amyotrophic lateral sclerosis and PD), unexplained peripheral neuropathies, neurodevelopmental disorders, and many psychiatric disturbances.

What is the rate of adverse events after oral N-acetylcysteine administered by the intravenous route to patients with suspected acetaminophen poisoning?

STUDY OBJECTIVE: We conduct a study to determine the rate of adverse events (anaphylactoid and cardiorespiratory) associated with the use of oral N-acetylcysteine by the intravenous route for the treatment of suspected acetaminophen poisoning and to examine specific variables that may be associated with adverse events. METHODS: We conducted a retrospective medical record review with explicit criteria. All patients who received oral N-acetylcysteine by the intravenous route from September 1995 to September 2001 were included. Patients were identified by cross-matching 3 databases. Adverse events were divided into categories of cutaneous, systemic, or life threatening. Five reviewers abstracted charts by using a standardized data collection form. Interrater reliability was calculated by using 24 medical records abstracted by all 5 reviewers. RESULTS: There were 7 adverse events identified in 187 patients (3.7%; 95% confidence interval 1.0% to 6.5%). Six adverse events were cutaneous and responded rapidly to antihistamines. One adverse event was life threatening but not clearly related to N-acetylcysteine. A high rate of antihistamine exposure (53%) was identified before the administration of N-acetylcysteine. Interrater agreement was higher than 95%. CONCLUSION: Intravenous administration of an oral solution of N-acetylcysteine is associated with a low rate of adverse events and should be considered for selected patients with suspected acetaminophen poisoning.

Dimercaptosuccinic acid and Prussian Blue in the treatment of acute thallium poisoning in rats.

INTRODUCTION: Despite being banned as a pesticide, thallium still results in human and animal poisonings. Current recommended treatments include the use of the chemical Prussian Blue. Limitations in its availability may result in Prussian Blue not being obtainable in the thallium-poisoned patient. The chelator 2,3-Dimercaptosuccinic acid (DMSA) is currently FDA-approved for use in childhood lead poisoning and has been reported to be beneficial in treating other heavy metal poisonings. The objective of this study was to determine the efficacy of DMSA as a treatment for thallium poisoning by studying mortality and whole-brain concentrations in thallium poisoned rats. MATERIAL AND METHODS: Rats were gavaged with 30 mg/kg of thallium. After 24 hours they were randomized to DMSA (n = 20) 50 mg/kg twice daily for 5 days, Prussian Blue (n = 20) 50 mg/kg twice daily for 5 days, or control (n = 30). Animals were monitored twice daily for weight loss and mortality. Animals losing greater than 20% of their starting weight were euthanized and counted as a mortality. All surviving rats at 120 hours had their brains harvested and digested and underwent subsequent thallium analysis. RESULTS: The rate of survival in DMSA-treated animals compared to control was 45% vs. 21%, p = 0.07. Mean whole-brain thallium concentrations between DMSA and control rats were 3.4 vs. 3.0 microg/g, p = 0.06. Prussian Blue-treated rats had significantly improved survival (70% vs. 21%, p < 0.01) and lower whole-brain thallium concentrations (1.6 vs. 3.0 microg/g, p < 0.01 tissue) compared to controls. CONCLUSION: DMSA failed to reduce brain thallium concentrations in rats poisoned with thallium and had an indeterminate effect on mortality while Prussian Blue significantly reduces both brain thallium concentrations and mortality.

Thallium and arsenic poisoning in a small midwestern town.

Thallium and arsenic have been used as a means of criminal poisoning. Although both manifest characteristically with peripheral neuropathies, thallium is associated with alopecia and arsenic with gastrointestinal symptoms. We describe the symptoms, physical findings, diagnostic test results, and outcomes in a group of men poisoned with thallium and arsenic. Seven patients had evidence of elevated thallium levels, and 2 patients had elevated arsenic and thallium levels. The most commonly reported symptoms included myalgias, arthralgias, paresthesias, and dysesthesias. Five patients developed alopecia. All patients with symptoms and peripheral neuropathies had characteristic blackening of their hair roots. Initially treated with dimercaptosuccinic acid, patients were switched to multiple-dose activated charcoal after testing revealed thallium poisoning. By 6 months, all patients' symptoms and peripheral neuropathies improved, but 5 patients had ongoing psychiatric problems. Thallium remains a means of criminal poisoning and should be considered in any patient with a rapidly progressing peripheral neuropathy with or without alopecia.