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      Is Open Access

      Management of the critically poisoned patient

      review-article

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          Abstract

          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.

          Methods

          An unsystematic review of the medical literature was performed and articles pertaining to human poisoning were obtained. The literature selected was based on the preference and clinical expertise of authors.

          Discussion

          If a poisoning is recognized early and appropriate testing and supportive care is initiated rapidly, the majority of patient outcomes will be good. Judicious use of antidotes should be practiced and clinicians should clearly understand the indications and contraindications of antidotes prior to administration.

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          Most cited references60

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          Acetylcysteine for acetaminophen poisoning.

          K Heard (2008)
          Article 0 comments Cited 108 times – based on 0 reviews     Review now
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            Toxic alcohol ingestions: clinical features, diagnosis, and management.

            Ira Kurtz, Jeffrey A. Kraut (2007)
            Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early.
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              Serotonin toxicity: a practical approach to diagnosis and treatment.

              N Buckley, R. Whyte, Geoffrey Isbister (2007)
              Excess serotonin in the central nervous system leads to a condition commonly referred to as the serotonin syndrome, but better described as a spectrum of toxicity - serotonin toxicity. Serotonin toxicity is characterised by neuromuscular excitation (clonus, hyperreflexia, myoclonus, rigidity), autonomic stimulation (hyperthermia, tachycardia, diaphoresis, tremor, flushing) and changed mental state (anxiety, agitation, confusion). Serotonin toxicity can be: mild (serotonergic features that may or may not concern the patient); moderate (toxicity which causes significant distress and deserves treatment, but is not life-threatening); or severe (a medical emergency characterised by rapid onset of severe hyperthermia, muscle rigidity and multiple organ failure). Diagnosis of serotonin toxicity is often made on the basis of the presence of at least three of Sternbach's 10 clinical features. However, these features have very low specificity. The Hunter Serotonin Toxicity Criteria use a smaller, more specific set of clinical features for diagnosis, including clonus, which has been found to be more specific to serotonin toxicity. There are several drug mechanisms that cause excess serotonin, but severe serotonin toxicity only occurs with combinations of drugs acting at different sites, most commonly including a monoamine oxidase inhibitor and a serotonin reuptake inhibitor. Less severe toxicity occurs with other combinations, overdoses and even single-drug therapy in susceptible individuals. Treatment should focus on cessation of the serotonergic medication and supportive care. Some antiserotonergic agents have been used in clinical practice, but the preferred agent, dose and indications are not well defined.
              Article 0 comments Cited 29 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Scand J Trauma Resusc Emerg Med
                Title: Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine
                Publisher: BioMed Central
                ISSN (Electronic): 1757-7241
                Publication date Collection: 2009
                Publication date (Electronic): 29 June 2009
                Volume: 17
                Page: 29
                Affiliations
                [1 ]Division of Medical Toxicology, Department of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, Virginia, USA
                [2 ]Division of Medical Toxicology, Department of Pediatrics, University of Virginia School of Medicine, Charlottesville, Virginia, USA
                Article
                Publisher ID: 1757-7241-17-29
                DOI: 10.1186/1757-7241-17-29
                PMC ID: 2720377
                PubMed ID: 19563673
                SO-VID: 0c21ecff-1982-4bbc-b958-c0c7de3dafe8
                Copyright © Copyright © 2009 Boyle et al; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 28 March 2009
                Date accepted : 29 June 2009
                Categories
                Subject: Review

                ScienceOpen disciplines: Emergency medicine & Trauma
                Data availability:
                ScienceOpen disciplines: Emergency medicine & Trauma

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