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Treating the Poisoned Patient Barbara M. Kirrane, M.D., and Robert S. Hoffman, M.D. Dr. Kirrane is an Assistant Professor, Section of Emergency Medicine, Department of Surgery, Yale University School of Medicine, and Dr. Hoffman is Associate Professor of Emergency Medicine and Medicine, NYU School of Medicine, and Director, New York City Poison Control Center. What happens when a patient shows up at the emergency room exhibiting signs and symptoms of poisoning? The attending physician in the ER may not immediately know what type of toxin the patient was exposed to. Exposure to toxic compounds –what we tend to call poisoning – may be due to a variety of agents: pharmaceutical drugs, illegal drugs, or even environmental toxins. Poisoning may occur for many different reasons: intentional harm (suicide), deliberate misuse (recreational drug abuse), accidental use (such as ingestions by small children exploring their environment), or by a prescribed dose that causes a toxic reaction. Poison Control Centers estimate approximately two million exposures to toxins per year1; this may be an underestimate of actual exposures, since not all are reported to officials. Some antidotes exist for certain drugs, but if the patient’s symptoms are not clear-cut, it is often necessary, and quite possible, to treat the patient with basic supportive care such as IV fluids or vasopressors. Given how relatively common poisoning is, it is useful to know the established guidelines for treatment that the doctor may follow in order to arrive at the best possible outcome. Some of these are described below. First Steps Looking for Clues Electrocardiogams (ECG or EKG) are performed on all patients who exhibit exposure to toxic compounds, as they may be good indicators of the type of toxin involved. For example, a specific change in the pattern of the ECG can indicate the presence of tricyclic antidepressants. Doctors can then treat the patient accordingly and do a repeat ECG to monitor the patient’s progress and recovery. 2 Low Blood Pressure and Poisoning Decontaminating the Digestive Tract Pumping the Stomach Administering Activated Charcoal Whole Bowel Irrigation Though the three methods of gastrointestinal decontamination mentioned above have sometimes not been shown to be of significant benefit in clinical studies, it is important to realize just how difficult studying these mechanisms is. For example, there are some animal and human volunteer studies out there, but these usually involve very small doses of a toxic substance – doses which may not reflect the situation of the real-life poisoned patient. Furthermore, the actual poisoned patient may ingest more than one toxic substance, each of which might have a different method of action on the body. But each of the three GI decontamination methods has specific benefits and ER doctors will use each one under different circumstances, depending on the specific situation of the patient he or she is treating at the moment. What’s the Toxic Substance? Testing for Drugs in the SystemBlood Serum Test Approximately 1 in 500 patients who go to the ER for intentionally ingesting toxic substances (in attempts to do self-harm) will also have potentially toxic acetaminophen levels, even though they do not report that acetaminophen has been ingested. This is difficult for doctors in the ER because a patient can have toxic levels of acetaminophen in the body while having no or non-specific symptoms. If treated early enough, the prognosis is excellent. Doctors may also request blood serum tests if he or she feels there is a likelihood that certain other drugs are involved; these include salicylates (found in aspirin and other pain medications), lithium (a mineral used to treat bipolar disorder), and methanol. Urine Screen There are also some real limitations to urine drug screens. For one thing, they are not comprehensive, only testing for a small range of certain chemicals, so negative screens don’t exclude all possible drug exposures. Also, positive screens can result long after symptoms from the drug have passed. Therefore the presence of the drug in the urine may not actually be responsible for the current condition. This unfortunate effect is one that may often mislead doctors to attribute a patient’s symptoms to a specific drug, when actually a different (and non-drug-related) diagnosis should be made. For example, a patient’s altered mental state might be attributed to a drug when in fact, it is actually related to an underlying meningitis. However, drug screening is still beneficial in cases of suspected malicious poisoning or to confirm the presence of certain substances in suspected child abuse or neglect. 25 26 27 28 Seizures Hyperthermia Neuroleptic malignant syndrome is potentially life-threating. It may cause hyperthermia, along with altered mental status and motor movement problems such as rigid muscles and tremors. The disorder typically occurs in response to a sudden drop in the level of the common neurotransmitter dopamine – this can happen either with the addition of medications that block the dopamine receptor or in the withdrawal of medications that mimic the actions of dopamine (which are used in the treatment of Parkinson’s disease). 31 32 Serotonin syndrome is another that may cause hyperthermia and occurs when there is too much serotonin stimulating specific varieties of serotonin receptors. This can happen in response to high levels of common antidepressants in the body, like monoamine oxidase inhibitors (MAOIs) or selective serotonin reuptake inhibitors (SSRIs), cocaine, MDMA (ecstasy), or even some antibiotics. Like neuroleptic malignant syndrome, there are multiple symptoms other than hyperthermia that can occur (e.g., muscle rigidity, tremors, altered mental status, to name a few), and it can therefore be tricky for the physician to diagnose. However, clonus – involuntary muscle contractions – is the primary means of identifying serotonin syndrome. 33 34 35 Whatever the root of the drug-induced hyperthermia, doctors will generally employ the same series of treatments: rapid cooling, hydration through an IV drip, and removal of the drug from the system. It may be necessary to sedate the patient in these cases, because muscle rigidity and general agitation can prevent effective cooling of the body temperature. Conclusion
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Multiple-dose activated charcoal for treatment of yellow oleander poisoning: a single-blind, randomized, placebo-controlled trial. The Lancet 2003;361:1935-1938 return 18. Davis GR, Santa Ana CA, Morawski SG. Development of a lavage solution associated with minimal water and electrolyte absorption or secretion. Gastroenterology 1980;78:991-995return 19. Tenebein M, Cohen S, Sitar DS. Whole bowel irrigation is a decontamination procedure after acute drug overdose. Archives of Internal Medicine 1987;147:905-907. return 20. Kirshenbaum LA, Mathews SC, Sitar DS, et al. Whole-bowel irrigation versus activated charcoal in sorbitol for the ingestion of modified-release pharmaceuticals. Clin Pharmacol Ther 1989;46:264-271return 21. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists Position Paper: whole bowel irrigation. Journal Toxicology Clinical Toxicology 2004;42:843-854 return 22. Traub SJ, Hoffman RS, Nelson LS. Body packing-The internal concealment of illicit drugs. New England Journal of Medicine 2003;349:2519-2526 return 23. Ashbourne JF, Olson KR, Khayam-Bashi H. Value of rapid screening for acetaminophen in all patients with intentional drug overdose. Annals of Emergency Medicine 1989;18:1035-1038 return 24. Smilkstein MJ, Knapp GL, Kulig KW and Rumack BH. Efficacy of oral n-acetylcysteine in the treatment of acetaminophen overdose. Analysis of the National Multicenter Study (1976-1985). New England Journal of Medicine 1988; 319:1557-1562 return 25. Brett AS. Implications of discordance between clinical impression and toxicology analysis in drug overdose. Archives of Internal Medicine 1988;148:437-41 return 26. Montague RE, Grace RF, Lewis JH, et al. Urine drug screens in overdose patients do not contribute to immediate clinical management. Theraputic Drug Monitoring 2001;23:47-50 return 27. Eisen JS, Sivilotti ML, Boyd DU, et al. Screening urine for drugs of abuse in the emergency department: do test results affect physicians’ patient care decisions? Canadian Journal of Emergency Medicine 2004;6:104-111 return 28. Belson MG, Simon HK, Sullivan K, et al. The utility of toxicologic analysis in children with suspected ingestions. Pediatric Emergency Care 1999;15:383-387 return 29. Callaham M, Schumaker H, Pentel P. Phenytoin prophylaxis of cardiotoxicity in experimental amitriptyline poisoning. Journal of Pharmacologic and Experimental Therapeutics 1988:245:216-220return 30. Hoffman A, Pinto E, Gilhar D. Effect of pretreatment with anticonvulsants on theophylline-induced seizures in the rat. J Crit Care 1993;8:198-202 return 31. Juurlink DN. Antipsychotics in Flomenbaum NE, Howland MAH, Goldfrank LR, Lewin NA, Hoffman RS, Nelson LS eds. Goldfrank’s Toxicologic Emergencies. 8th Edition. New York: McGraw Hill 2006:1039-1051 return 32. Strawn JR, Keck PE, Caroff SN. Neuroleptic Malignant Syndrome. American Journal of Psychiatry 2007:164:870-876 return 33. Gillman PD. The serotonin syndrome and its treatment. Journal of Psychopharmacology 1999;13:100-109 return 34. Darmani NA and Zhao E. Production of serotonin syndrome by 8-OH DPAT in Cryptitis parva. Physiology & Behavior 1998:65:327-331 return 35. Boyer EW and Shannon M. The serotonin syndrome. The New England Journal of Medicine 2005;352:1112-1120 return | |||||
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