Full recovery from a potentially lethal dose of mercuric chloride.

INTRODUCTION: Mercuric chloride poisoning is rare yet potentially life-threatening. We report a case of poisoning with a potentially significant amount of mercuric chloride which responded to aggressive management. CASE REPORT: A 19-year-old female presented to the Emergency Department with nausea, abdominal discomfort, vomiting of blood-stained fluid, and diarrhea following suicidal ingestion of 2-4 g of mercuric chloride powder. An abdominal radiograph showed radio-opaque material within the gastric antrum and the patient's initial blood mercury concentration was 17.9 µmol/L (or 3.58 mg/L) at 3 h post-ingestion. Given the potential toxicity of inorganic mercury, the patient was admitted to the intensive care unit and chelation with dimercaprol was undertaken. Further clinical effects included mild hemodynamic instability, acidosis, hypokalemia, leukocytosis, and fever. The patient's symptoms began to improve 48 h after admission and resolved fully within a week. DISCUSSION: Mercuric chloride has an estimated human fatal dose of between 1 and 4 g. Despite a reported ingestion of a potentially lethal dose and a high blood concentration, this patient experienced mild to moderate poisoning only and she responded to early and appropriate intervention. Mercuric chloride can produce a range of toxic effects including corrosive injury, severe gastrointestinal disturbances, acute renal failure, circulatory collapse, and eventual death. Treatment includes close observation and aggressive supportive care along with chelation, preferably with 2,3-dimercapto-1-propane sulfonate or 2,3-meso-dimercaptosuccinic acid.

Ricin as a weapon of mass terror--separating fact from fiction.

In recent years there has been an increased concern regarding the potential use of chemical and biological weapons for mass urban terror. In particular, there are concerns that ricin could be employed as such an agent. This has been reinforced by recent high profile cases involving ricin, and its use during the cold war to assassinate a high profile communist dissident. Nevertheless, despite these events, does it deserve such a reputation? Ricin is clearly toxic, though its level of risk depends on the route of entry. By ingestion, the pathology of ricin is largely restricted to the gastrointestinal tract where it may cause mucosal injuries; with appropriate treatment, most patients will make a full recovery. As an agent of terror, it could be used to contaminate an urban water supply, with the intent of causing lethality in a large urban population. However, a substantial mass of pure ricin powder would be required. Such an exercise would be impossible to achieve covertly and would not guarantee success due to variables such as reticulation management, chlorination, mixing, bacterial degradation and ultra-violet light. By injection, ricin is lethal; however, while parenteral delivery is an ideal route for assassination, it is not realistic for an urban population. Dermal absorption of ricin has not been demonstrated. Ricin is also lethal by inhalation. Low doses can lead to progressive and diffuse pulmonary oedema with associated inflammation and necrosis of the alveolar pneumocytes. However, the risk of toxicity is dependent on the aerodynamic equivalent diameter (AED) of the ricin particles. The AED, which is an indicator of the aerodynamic behaviour of a particle, must be of sufficiently low micron size as to target the human alveoli and thereby cause major toxic effects. To target a large population would also necessitate a quantity of powder in excess of several metric tons. The technical and logistical skills required to formulate such a mass of powder to the required size is beyond the ability of terrorists who typically operate out of a kitchen in a small urban dwelling or in a small ill-equipped laboratory. Ricin as a toxin is deadly but as an agent of bioterror it is unsuitable and therefore does not deserve the press attention and subsequent public alarm that has been created.

Diethylene glycol poisoning.

INTRODUCTION: Diethylene glycol (DEG) is a clear, colorless, practically odorless, viscous, hygroscopic liquid with a sweetish taste. In addition to its use in a wide range of industrial products, it has also been involved in a number of prominent mass poisonings spanning back to 1937. Despite DEG's toxicity and associated epidemics of fatal poisonings, a comprehensive review has not been published. METHODS: A summary of the literature on DEG was compiled by systematically searching OVID MEDLINE and ISI Web of Science. Further information was obtained from book chapters, relevant news reports, and web material. AIM: The aim of this review is to summarize all main aspects of DEG poisoning including epidemiology, toxicokinetics, mechanisms of toxicity, clinical features, toxicity of DEG, diagnosis, and management. EPIDEMIOLOGY: Most of the documented cases of DEG poisoning have been epidemics (numbering over a dozen) where DEG was substituted in pharmaceutical preparations. More often, these epidemics have occurred in developing and impoverished nations where there is limited access to intensive medical care and quality control procedures are substandard. TOXICOKINETICS: Following ingestion, DEG is rapidly absorbed and distributed within the body, predominantly to regions that are well perfused. Metabolism occurs principally in the liver and both the parent and the metabolite, 2-hydroxyethoxyacetic acid (HEAA), are renally eliminated rapidly. MECHANISMS OF TOXICITY: Although the mechanism of toxicity is not clearly elucidated, research suggests that the DEG metabolite, HEAA, is the major contributor to renal and neurological toxicities. CLINICAL FEATURES: The clinical effects of DEG poisoning can be divided into three stages: The first phase consists of gastrointestinal symptoms with evidence of inebriation and developing metabolic acidosis. If poisoning is pronounced, patients can progress to a second phase with more severe metabolic acidosis and evidence of emerging renal injury, which, in the absence of appropriate supportive care, can lead to death. If patients are stabilized, they may then enter the final phase with various delayed neuropathies and other neurological effects, sometimes fatal. TOXICITY OF DEG: Doses of DEG necessary to cause human morbidity and mortality are not well established. They are based predominantly on reports following some epidemics of mass poisonings, which may underestimate toxicity. The mean estimated fatal dose in an adult has been defined as approximately 1 mL/kg of pure DEG. MANAGEMENT: Initial treatment consists of appropriate airway management and attention to acid-base abnormalities. Prompt use of fomepizole or ethanol is important in preventing the formation of the toxic metabolite HEAA; hemodialysis can also be critical, and assisted ventilation may be required. CONCLUSIONS: DEG ingestion can lead to serious complications that may prove fatal. Prognosis may be improved, however, with prompt supportive care and timely use of fomepizole or ethanol.