Background: Clinicians are often challenged to manage critically ill poison patients. The clinical effects encountered in poisoned patients are dependent on numerous variables, such as the dose, the length of exposure time, and the pre-existing health of the patient. The goal of this article is to introduce the basic concepts for evaluation of poisoned patients and review the appropriate management of such patients based on the currently available literature.

Objectives: Recent animal research and clinical case reports suggest benefit from high-dose insulin therapy (HDIT) for the treatment of calcium channel blocker (CCB) toxicity. One molecular signaling pathway, the phosphatidylinositol 3-kinase (PI3K) pathway, that contributes to CCB toxicity and the efficacy of HDIT, was examined for a role in this phenomenon.Methods: A differentiated 3T3-L1 adipocyte model system was utilized to characterize metabolic and molecular signaling events dysregulated in response to acute CCB toxicity. Glucose uptake assays were performed in the presence of representatives of three classes of CCB drugs, and the ability of HDIT to reverse observed inhibition was assessed. Western blot analyses were utilized to probe which insulindependent signaling pathway was inhibited by CCB toxicity.Results: Representative compounds from the dihydropyridine and phenylalkylamine classes of CCBs were more effective at inhibiting glucose uptake in differentiated 3T3-L1 adipocytes than a representative from the benzothiazepine class. Phosphorylation at serine 473 of the Akt protein (P-Akt), a protein representing a common pathway for insulin receptors (IR), insulinlike growth factor receptors (IGFR), and hybrid receptors formed by IR and IGFR subunits, was abolished in the presence of toxic doses of the phenylalkylamine CCB verapamil. Phosphorylation at serine 473 of Akt was rescued in the presence high concentrations of insulin.Conclusions: These data suggest that dysregulation of the insulin-dependent PI3K pathway is partially responsible for insulin resistance and the hyperglycemic state observed in response to acute CCB toxicity.ACADEMIC EMERGENCY MEDICINE 2008; 15:368-374 ª

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Food poisoning is encountered throughout the world. Many of the toxins responsible for specific food poisoning syndromes are no longer limited to isolated geographic locations. With increased travel and the ease of transporting food products, it is likely that a patient may present to any emergency department with the clinical effects of food poisoning. Recognizing specific food poisoning syndromes allows emergency health care providers not only to initiate appropriate treatment rapidly but also to notify health departments early and thereby prevent further poisoning cases. This article reviews several potential food-borne poisons and describes each agent's mechanism of toxicity, expected clinical presentation, and currently accepted treatment.