CHAPTER 40

Approach to Poisoning
Mohan Punja and Robert J. Hoffman

c INTRODUCTION c HISTORY 409

409

c LABORATORY AND DIAGNOSTIC ASSAYS c DECONTAMINATION, PREVENTING DRUG ABSORPTION, AND ENHANCED ELIMINATION 414

411

c PHYSICAL EXAMINATION

409

c INTRODUCTION
Patients with poison exposure and toxicity may present with a spectrum of various clinical signs, symptoms, and problems. Most of these are very straightforward and easily anticipated, but others may be unpredictable or associated with exposure to unidentied substances that hinder the clinician from knowing what to expect. There are, however, general principles that may be employed as a framework on which approach to most poisonings may be based. These are employed when managing adverse effects from poisoning by known or unidentied substances. Less than 5% of poisonings require use of specic antidotes; thorough general supportive care is the most important approach in caring for most poisoned patients.1 The initial principles of management of poisoned patients generally follow the protocol used for the management of urgent and emergent problems. There are some slight differences if the airway, breathing, circulation approach is used, with some specic amendments relevant to poison exposures and toxicity. Airway, breathing, circulation, disability, dextrose, exposure, ECG comprise the general A, B, C, D, D, E, E mantra of poison management. This may differ from other emergency department (ED) management in that disability and exposure, necessary for patients with trauma, are not essential in most poisoned patients, but can reveal some valuable diagnostic information.

ing a poisoned patient, a good approach is to identify the reason of exposure (i.e., intentional, unintentional, misadventure), the type of substance involved (i.e., prescription, over-the-counter, herbal, illicit drug), the formulation (i.e., immediate vs. sustained release), the dose of the substance, the amount of substance involved, the route of exposure (i.e., ingestion, inhalation, intravenous, dermal), the time of exposure (hours since exposure, acute vs. chronic), any potential coingestion, and the severity of exposure. Obtaining a medical history from the poisoned patient may be difcult, and, therefore, other people such as family members, friends, prehospital personnel, the patients physician or therapist, or previous medical records may provide crucial information to aid in management. Thorough medical knowledge of all ailments, medical history, medication history, and other medications or substances the patient had access to often provides useful information. After initial assessment, stabilization, and physical exam, further management may include (1) decontamination, (2) prevention of absorption, (3) administration of antidote, and (4) enhanced elimination of the toxic substance.

c PHYSICAL EXAMINATION
Examination of patients with poison exposure and toxicity is often more focused than a general physical examination, with particular attention to areas that are expected to yield useful information (Table 40-1). Assessment of vital signs, neurologic status, pupils, skin, bowel, and bladder permits the recognition of a toxidrome. A toxidrome, or toxicologic syndrome, is a constellation of signs and symptoms that herald toxicity

c HISTORY
Critical to proper management of poisoning is recognition that poison exposure occurred. When evaluat-

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c TABLE 40-1. COMMON FINDINGS IN POISONING

Clinical and/or laboratory ndings in poisoning Agitation Anticholinergics,a ethanol and sedativehypnotic withdrawal, hypoglycemia, phencyclidine, sympathomimeticsb Alopecia Alkylating agents, radiation, selenium, strontium, thallium Ataxia Benzodiazepines, carbamazepine, carbon monoxide, ethanol, hypoglycemia, lithium, mercury, phenytoin, nitrous oxide Blindness or decreased Caustics (direct), cocaine, cisplatin, mercury, methanol, quinine, thallium visual acuity Blue skin Amiodarone, FD&C #1 dye, methemoglobin, silver, sulfhemoglobin Constipation Anticholinergics,a botulism, lead, opioids, thallium (severe) Tinnitus, deafness Aminoglycosides, cisplatin, heavy metals, loop diuretics, quinine, salicylates Diaphoresis Amphetamines, cholinergics,c ethanol and sedativehypnotic withdrawal, hypoglycemia, opioid withdrawal, salicylates, serotonin syndrome, sympathomimeticsb Diarrhea Arsenic and other metals/metalloids, boric acid (blue-green), botanical irritants, cathartics, cholinergics,c colchicine, iron, lithium, opioid withdrawal, radiation Dysesthesias, paresthesias Acrylamide, arsenic, ciguatera, cocaine, colchicine, n-hexane, thallium Gum discoloration Arsenic, bismuth, hypervitaminosis A, lead, mercury Hallucinations Anticholinergics,a dopamine agonists, ergot alkaloids, ethanol, ethanol and sedativehypnotic withdrawal, LSD, phencyclidine, sympathomimetics,b tryptamines (e.g., AMT) Headache Carbon monoxide, hypoglycemia, monoamine oxidase inhibitor/food interaction (hypertensive crisis), nitrites, serotonin syndrome Metabolic acidosis Cyanide, ethylene glycol, ketoacidosis (diabetic, starvation, alcoholic), iron, isoniazid, lactic (elevated anion gap) acidosis, metformin, methanol, paraldehyde, phenformin, protease inhibitors, salicylates, toluene, uremia Miosis Cholinergics,c clonidine, opioids, phencyclidine, phenothiazines Mydriasis Anticholinergics,a botulism, methanol, opioid withdrawal, sympathomimeticsb Nystagums Barbiturates, carbamazepine, carbon monoxide, ethanol, lithium, monoamine oxidase inhibitors, phencyclidine, phenytoin, quinine Purpura Anticoagulant rodenticides, clopidogrel, corticosteroids, heparin, pit viper venom, quinine, salicylates, warfarin Radiopaque ingestions Arsenic, body packer, chloral hydrate, enteric-coated tablets, halogenated hydrocarbons, metals (e.g., iron, lead) Red skin Anticholinergics,a boric acid, disulram interaction, hydroxocobalamin, scombroid, vancomycin Rhabdomyolysis Carbon monoxide, doxylamine, HMG CoA reductase inhibitors, sympathomimetics,b Tricholoma mushrooms Salivation Arsenic, caustics, cholinergics,c ketamine, mercury, phencylidine, strychnine Seizures Bupropion, carbon monoxide, cyclic antidepressants, ethanol and sedativehypnotic withdrawal, Gyromitra mushrooms, hypoglycemia, isoniaziad, theophylline Tremor Antipsychotics, arsenic, carbon monoxide, cholinergics,c ethanol, lithium, mercury, methyl bromide, sympathomimetics,b thyroid replacement Weakness Botulism, diuretics, magnesium, neuromuscular blockers, paralytic shellsh, steroids, toluene Yellow skin Acetaminophen (late), Amanita mushrooms, b-carotene, dinitrophenol, pyrrolizidine alkaloids
Reproduced with permission from Nelson LS, Lewin NA, Howland ME, Hoffman RS, Goldfrank LS, Flomenbaum NE. Goldfranks Toxicological Emergencies. 9th ed. New York: McGraw-Hill Companies Inc; 2010:40. Table 4-2. a Anticholinergics: for example, antihistamines, atropine, cyclic antidepressants, and scopolamine. b Sympathomimetics: for example, amphetamines, b-adrenergic agonists, cocaine, ephedrine, and methylxanthines. c Cholinergics: for example, muscarinic mushrooms, organic phosphorus compounds, and carbamates, including Alzheimers drugs and physostigmine, plocarpine, and other direct-acting cholinergics.

from a category of poisons. Recognition of the presence of a toxidrome is useful in managing patients with exposure to unidentied substances and is also useful after known exposure to a category of substances known to cause a specic toxidrome. Traditionally there are four described toxidromes: adrenergic/sympathomimetic, anticholinergic, cholinergic, and opioid. There is also a well-recognized pattern of clinical ndings associated with sedativehypnotic

substances. The classes of substances causing toxidromes include:

t

Adrenergic (sympathomimetic): sympathomimetic agents capable of a- and/or b-adrenergic agonism, for example, cocaine, amphetamines, theophylline, caffeine, pseudoephedrine, ephedrine, epinephrine, norepinephrine, and methylenedioxymethamphetamine (MDMA) (ecstasy).

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c TABLE 40-2. COMMON FINDINGS IN TOXIDROMES AND POISONINGS

Vital Signs Group Anticholinergics BP 2@ P R 6 T Mental Status Delirium Pupil Size Peristalisis Diaphoresis Other Dry mucous membranes, ush, urinary retention Salivation, lacrimation, urination, diarrhea, bronchorrhea, fasciculations, paralysis Hyporeexia, ataxia Hyporeexia Tremor, seizures Tremor, seizures

Cholinergics

2@

Normal to depressed

Ethanol or sedative hypnotics Opioids Sympathomimetics Withdrawal from ethanol or sedative hypnotics Withdrawal from opioids

2@ Depressed Depressed Agitated Agitated, disoriented, hallucinations Normal, anxious

2@

2 2

Vomiting, rhinorrhea, piloerection, diarrhea, yawning

, increase; , decrease; 6, variable; 2, change unlikely; BP, blood pressure; P, pulse; R, respirations; T, temperature. Reproduced with permission from Nelson LS, Lewin NA, Howland ME, Hoffman RS, Goldfrank LS, Flomenbaum NE. Goldfranks Toxicological Emergencies. 9th ed. New York: McGraw-Hill Companies Inc; 2010:40. Table 3-2.

Anticholinergic: substances that block cholinergic receptors, for example, atropine, scopolamine, antihistamines, phenothiazines, cyclic antidepressants, and cyclobenzaprine. Cholinergic: substances that afflict cholinergic receptors, for example, organophosphate pesticides and nerve agents, physostigmine, rivastigmine, and nicotine. Opioid: substances that afflict opioid receptors, for example, heroin, morphine, hydromorphone, methadone, diphenoxylate, clonidine, and tramadol. Sedativehypnotic: substances that increase GABA activity, for example, benzodiazepines, barbiturates, alcohols, GHB, and zolpidem.

to assay for hundreds of substances capable of causing toxicity, the most frequently indicated investigations are familiar to the ED and critical care physicians and are readily available in any setting where emergency and critical care are delivered.

ELECTROCARDIOGRAM
Electrocardiograms are indicated in patients with exposure to substances capable of inducing dysrhythmia, exposure to unidentied substances, and exposures with intent of self-harm. Most often, ECGs obtained in the ED setting for nonpoisoned patients are for the purpose of detecting ischemic changes. For patients with poison exposures and toxicity, evaluation for changes in cardiac conduction, conduction intervals, and dysrhythmia is of greatest interest. Ischemia is certainly of interest if present, but this is not the primary focus of ECG evaluation in patients with poison exposure and toxicity. The triad of pseudo right bundle branch block consisting of R wave in AVR, S wave in lead I, and S wave in AVL, are highly sensitive indicators of sodium channel blockade resulting from tricyclic antidepressant exposure.2 If these ndings are present, prolongation of QRS duration to 100 and 150 milliseconds is predictive of seizure and ventricular dysrhythmia, respectively.3,4

It is important to note that patients presenting with potential toxicity may have mixed clinical picture and may not entirely fall under a specic toxidrome. This is particularly true for patients presenting with polydrug overdoses, or in cases in which an ingested drug has been adulterated with another toxidrome-causing substance (Table 40-2).

c LABORATORY AND

DIAGNOSTIC ASSAYS
The investigations and assays most useful in management of poisoned patients are commonplace in emergency medicine and critical care. Although it is possible

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Dysrhythmias may result from toxins too numerous to list. Characteristic changes with ventricular bradydysrhythmia are seen with digoxin and other cardiac glycoside toxicity. Nonspecic ST changes throughout all leads and, occasionally bradycardia accompany lithium toxicity. Poison-induced dysrhythmias may require very different management from the same dysrhythmia that occurs due to other means. In such cases, use of the standard management will be ineffective, and occasionally use of the standard management algorithm will increase morbidity and mortality. Some of these managements are described by the American Heart Association.5 Patients with poison-induced cardiac dysrhythmias should be managed by clinicians familiar with and preferably experienced with these clinical scenarios. (See also the chapter The Critically Ill Poisoned Patient.)

LABORATORYROUTINELY INDICATED ASSAYS

Serum glucose measurement and serum electrolyte analysis are the two most indicated lab assays in the management of poisoned patients. These tests allow detection of hypoglycemia, which may result from a variety of poisons, including both agents known to cause hypoglycemia and substances that may cause hyperglycemia and a subsequent hypoglycemic response. Any patient with altered mental status, including depressed or altered sensorium, coma, or agitation, should have immediate bedside assessment of the blood glucose level. This assay provides a result that is immediately interpretable, meaningful to the treating clinicians, and allows an anticipated, appropriate response with administration of dextrose or glucagon. Serum chemistry assessment allows detection of anion gap metabolic acidosis, alterations of sodium, potassium, and serum bicarbonate, and alterations of the other measured substances. The anion gap is calculated by the following formula: [Na1] 2 [Cl2 1 HCO32], and the normal value is generally accepted to be between 6 and 14 mEq/L.6 Discovery of an anion gap in the poisoned patient should prompt investigation of the cause if unknown. Such causes may be exogenous or endogenous etiologies as represented by the MUDPILES mnemonic: methanol, uremia, diabetic ketoacidosis, paraldehyde/phenformin, iron/inhalants (carbon monoxide, cyanide, and hydrogen sulde), isoniazid/ibuprofen, lactic acidosis, ethylene glycol/ ethanol ketoacidosis, and salicylates/solvents (benzene, toluene)/sympathomimetics/starvation ketoacidosis. Measurement of the serum osmolar gap is occasionally useful in the patient with suspected toxic alcohol ingestion, but has many limitations. The measured serum osmolarity is compared with the calculated serum osmolarity to derive the gap that represents other osmotically

active substances. The formula is: Osmcalc 5 2[Na1] 1 (BUN/2.8) 1 (glucose/18) 1 (ethanol/4.6). Methanol, ethylene glycol, and numerous other drugs, chemicals, and disease states may contribute to this gap. There is a wide, poorly dened range of normal osmolar gap, usually ranging from 25 to 115 mOsm/kg.7,8 Given that the patients baseline osmolar gap is rarely known, it is difcult to reliably determine if an unmeasured osmotically active substance is present. Thus, the change in this gap as the toxic alcohol is metabolized, in conjunction with the anion gap and any laboratory levels of alcohols, is more important; a normal osmolar gap does not rule out exposure to a toxic alcohol. Additional laboratory assays that are commonly useful include serum acetaminophen level, salicylate level, ethanol level, and blood gas analysis. Serum acetaminophen assays are indicated for any patient with potentially toxic exposure to acetaminophen and any patient with exposure with intent of self-harm, regardless of whether acetaminophen exposure is reported,9 and may be useful in patients with elevation of hepatic transaminases after exposure to unidentied substances. Serum salicylate levels may aid in detection of undisclosed salicylate exposure. Salicylate toxicity may be identied by clinical ndings,10 but these may be obscured by polydrug exposure, other medical ailments, or lack of clinician exposure to salicylate-poisoned patients.11 We advocate routine use of serum salicylate screening in patients with unidentied exposures or exposures with intent of self-harm. Serum ethanol levels may provide insight into causality of depressed mental status. Although wide variability in patient tolerance to ethanol makes interpretation of serum ethanol level and correlation with degree of depression of consciousness less than fully accurate,12 this assay is a staple of ED assessment of patients with depressed consciousness. Readers are advised to interpret serum ethanol level with caution. Overlooking other emergent causes of depressed or altered mental status, such as intracranial hemorrhage, encephalitis, or sepsis, by inappropriately attributing the mental state to ethanol exposure is a very common error in emergency medicine. This error routinely results in morbidity and mortality, and is a common cause for legal cases brought against treating physicians. The presence of a serum ethanol level capable of causing intoxication should not cause the clinician to discontinue investigating potential emergent causes of altered or depressed mental status. Blood gas analysis is useful for a variety of reasons, including to elucidate the type and degree of acidosis or alkalosis, detect dyshemoglobinemias through carboxyhemoglobin or methemoglobin level, and determine oxygen extraction and utilization in poisonings that may result in blockade of oxidative phosphorylation, such as by cyanide. In nearly all cases, with the

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most common exception of cardiac arrest, venous blood gas sampling has been shown to be nearly equivalent to arterial sampling. The simplest correction or correlation of pH between venous and arterial blood gas samples is performed by adding 0.03 to the venous pH to obtain the arterial pH.13,14 In most cases venous blood gas sampling is adequate,13,14 and arterial blood sampling should only be performed when necessary. An exception to this general rule is evaluation for cyanide or other disruptors of oxidative phosphorylation, in which comparison of simultaneously obtained arterial and venous blood gas samples is used to assess oxygen extraction across the capillary and tissue bed. Serum creatine phosphokinase may be obtained when a patient exhibits signs of altered temperature regulation and muscle tone such as in the serotonin and neuroleptic malignant syndromes or the sympathomimetic toxidrome. Additionally, many common drugs have the potential to cause rhabdomyolysis, the most well known of which are statins, steroids, theophylline, and doxylamine. Any condition that has the potential to cause trauma or prolonged immobilization, such as the abuse of rapid-onset sedatives, may damage muscle, thereby releasing potentially dangerous amounts of potassium and creatine phosphokinase.

detect natural opioids but not synthetic opioids, such as methadone, fentanyl, propoxyphene, tramadol, etc. Many commonly abused drugs, such as ketamine and GHB, are not detected by any routine laboratory screening. Many medications known to cause false-positive drug of abuse screening exist. Screening for cocaine is the most accurate of the commonly used drug of abuse screening tests, but the tested metabolite benzoylecgonine typically is detectible in urine for 23 days after a single exposure.18 Failure to understand the limitations of drug of abuse screening leads uninformed clinicians to obtain this test, and often to misinterpret the results. Malicious exposures, exposures in children incapable of volitionally using drugs, and other circumstances for which forensic evidence of drug abuse exposure would be useful should be obtained in consultation with physicians with forensic experience and law enforcement ofcials.

IMAGING
Occasionally, imaging may be useful in evaluation. Some radiodense materials, such as lead, heavy metals, enteric-coated tablets, and ingested packages containing drugs such as cocaine or heroin, may be identied by plain radiography. In some circumstances, abdominal x-ray may reveal radiopaque materials, such as hydrocarbons, that may cause a characteristic double bubble sign in the stomach. Two heavy metals particularly amenable to detection by plain lms are nonchewable iron tablets and ingested lead containing foreign bodies. The sensitivity of plain x-ray to identify ingested drug packages is very high, and classic ndings may include visualization of staples used to hold packs closed, rosettelike nding of air trapped in knots where packets are tied, and the double condom sign in which air is seen trapped between layers of latex (Figures 40-1 and 40-2).19 Computerized tomography (CT) may also be indicated to identify ingested substances such as ingested drug packages or radiodense materials. In the case of rupture of ingested packages, CT scanning should be performed after surgery to document complete gastrointestinal tract clearance.19 Imaging is useful to evaluate for the consequences of poisoning; examples are chest radiograph that may identify pneumonitis associated with hydrocarbon or other aspiration, abdominal radiograph showing bowel obstruction or perforation, or CT that may provide information about the extent and severity of injury from caustic ingestion. Endoscopy may provide direct imaging of the airway or GI tract and may be particularly useful in patients with caustic exposures to aid in diagnosis, discharge,

LABORATORYQUANTITATIVE ASSAYS
Generally, on exposure to a substance for which a serum concentration, or level, may be obtained, such information may potentially be highly useful for management and/or prognosis. Occasionally these are critical to select a specic management, especially hemodialysis, other method of enhanced elimination, or antidote administration.

LABORATORYDRUG OF ABUSE SCREENING

Laboratory screening for drugs of abuse, commonly amphetamines, cannabinoids (marijuana), cocaine, PCP, and opioids, is the toxicology lab screening that is least useful, most overutilized, and most misunderstood and misinterpreted toxicologic lab assay.1517 Other than for forensic purposes, lab assay for drugs of abuse is not routinely indicated for patients with exposure to drugs or abuse or for patients with unidentied exposures. As these screenings are only qualitative, they conrm only that exposure to the substance in question that occurred within the previous days or week, depending on the substance. Many such assays are not complete for the respective drug category. A screening assay specic for amphetamine might not detect methamphetamine or MDMA (ecstasy), which are much more widely abused than amphetamine. A typical opioid screening will

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Figure 40-1. Iron tablet overdose. The identication of the large amount of radiopaque tablets corroborates the diagnosis in a patient with a suspected iron overdose. (Image contributed by the Toxicology Fellowship of the New York City Poison Center.)

and prognosis. We recommend endoscopy with all intentional caustic ingestions and most nonalkali exposures. In children, stridor, or the combination of drooling and vomiting, should prompt endoscopy.20 When indicated, endoscopy should be performed within 812 hours and no later than 24 hours.

Figure 40-2. A patient in police custody was

c DECONTAMINATION,

brought to the emergency department for allegedly ingesting drug packets. The patient admitted swallowing several plastic bags that were stapled closed. (Image contributed by the Toxicology Fellowship of the New York City Poison Center.)

PREVENTING DRUG ABSORPTION, AND ENHANCED ELIMINATION

Decontamination to prevent adverse effects of poison exposure has long been advocated as a poison management strategy. The concept that removing a poison from the body may avert illness is easily understood by laypersons and clinicians alike, and this strategy seems to make common sense. Despite this, repeated and rigorous testing of gastrointestinal decontamination methods has routinely failed to demonstrate any convincing benet. Gastrointestinal decontamination plays an increasingly small and marginal role in the management of poisoned patients. External decontamination of the skin and eyes continues to play a vital role in some poison management.

body or exposed area thoroughly washed. For ocular exposures, the eyes are irrigated with copious isotonic solution (such as normal saline or lactated Ringers) for at least 30 minutes or until a normal ocular pH is obtained. For full efcacy, a Morgan lens should be used in the affected eye, and ocular anesthetic such as tetracaine or proparacaine should be instilled prior to the procedure.21

GI DECONTAMINATION
Multiple methods of gastrointestinal decontamination are available to reduce the bioavailability of an ingested toxin. Most of these methods are outdated and provide little clinical benet; however, there may be scenarios appropriate for their use. Emesis induced by syrup of ipecac is not recommended for routine use,22 and we recommend against its use except in the specic scenario of the alert, conscious patient within an hour of a large ingestion of a potentially fatal toxin (not a corrosive substance or hydrocarbon) that is not adsorbed to activated charcoal (AC). Gastrointestinal lavage is the passage of largebore orogastric tube to administer liquid and aspirate a toxic substance in the stomach. Due to serious risks and

EXTERNAL AND OCULAR DECONTAMINATION

When a toxin is on a patients body, external decontamination should be performed to protect staff from becoming ill and to limit ongoing toxicity to the patient. This is best performed at a designated shower or mass casualty decontamination area near the entrance of the ED. The patient should be completely disrobed; jewelry, watch, etc., should be removed and the entire

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limited benet, there is no place for the routine use of lavage, but use in the critically ill patient with toxic ingestion, depressed mental status, and instability presenting within 1 hour of ingestion may be appropriate.23,24 Use of nasogastric lavage to aspirate liquid poisons does not carry the risk of orogastric lavage and has been demonstrated to reduce poison absorbed.23 Nasogastric aspiration of liquid poison may be performed in patients presenting after ingestion of liquid poison who are still anticipated to have poison remaining in the stomach. Whole bowel irrigation (WBI) is a method of emptying the gastrointestinal tract in order to limit further absorption of a toxin. This is typically done using a warmed polyethylene glycolelectrolyte solution (PEGES) at rates of 0.51L/h in the adults, which often requires the placement of a nasogastric or orogastric tube.25 WBI may be performed in select situations, for example, large and potentially fatal ingestions of substances not bound by charcoal such as iron or lead, sustained-release preparations, or in the body packing of illicit substances. It is contraindicated in bowel obstruction, perforation, gastrointestinal hemorrhage, hemodynamic instability, unstable airway, or potential for deterioration of the airway.25 Of all methods of gastrointestinal decontamination, AC has the most potential benet but is still not recommended for routine use in the poisoned patient.26

AC may be used at 1 g/kg up to 100 g, and is best performed within 1 hour of ingestion with limitations similar to WBI. It decreases the bioavailability of a wide variety of toxins but is not useful for the ingestions of alcohols, corrosives (acids/alkalis), magnesium, potassium, or metals such as iron and lithium. A majority of the adverse effects related to AC are from aspiration or direct administration of charcoal into the lungs.27 Clinicians may sedate and intubate a patient in order to administer WBI or AC, but in doing so must recognize that the risk for aspiration, though small, still exists.

ENHANCED ELIMINATION
Enhancing elimination of a toxin is indicated in patients who have decreased elimination of a drug (i.e., renal failure with ingestion of drug that is mainly eliminated in the urine) or in toxins that have a prolonged elimination half-life. Multidose AC may be used in the appropriately alert patient with potential severe toxic or fatal ingestions of carbamazepine, dapsone, phenobarbital, quinine, phenytoin and theophylline, or in cases of ingestion of long-acting or enteric formulations, and in bezoar formation.28 After the initial dose of AC, administer 0.250.5 g/kg Q 26 hours for up to 12 hours. Urine alkalinization is method of enhancing elimination of weakly acidic toxins by trapping them in an

c TABLE 40-3. SELECTED NORMAL AND TOXIC LAB VALUES FOR COMMON SUBSTANCES, AND POTENTIAL ACTIONS TO BE TAKEN

Substance Acetaminophen Caffeine Carboxyhemoglobin Cyanide Digoxin Ethylene glycol Iron Lead Lithium Methanol Methemoglobin Phenobarbital Phenytoin Salicylates Theophylline

Therapeutic or Normal Level 1030 g/mL 110 g/mL 02% Up to 10% in smokers ,1 g/mL 0.82.0 ng/mL 0 mg/dL 80180 g/dL ,10 g/dL 0.61.2 mEq/L 0 mg/dL ,1% 1540 mg/L 1020 mg/L 1530 mg/dL 515 g/mL

Toxic or Actionable Level .150 g/mL or if toxic on RumackMatthew nomogram .25 g/mL chronic .90 g/mL acute .15% (dependent on pt symptoms/pregnancy) .2.0 ng/L .25 mg/dL .500 g/dL .25 g/dL .2.5 mEq/L chronic .4.0 mEq/L acute .25 mg/dL .1520% .100 g/mL .30 mg/L .30 mg/dL chronic .60 mg/dL acute .25 g/mL chronic .90 g/mL acute

Action N-Acetylcysteine Multiple dose activated charcoal Dialysis Oxygen 1 hyperbaric oxygen chamber Cyanide antidote kit DigiFab Fomepizole and/or dialysis Deferoxamine Deferoxamine, calcium EDTA, dimercaprol, or succimer Hemodialysis Fomepizole and/or hemodialysis Methylene blue Hemoperfusion Exchange transfusion in infants Multidose activated charcoal Urine alkalinization Hemodialysis Multidose activated charcoal Hemoperfusion/dialysis

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TOXICOLOGIC CONDITIONS 2. Liebelt EL, Francis PD, Woolf AD. ECG lead aVR versus QRS interval in predicting seizures and arrhythmias in acute tricyclic antidepressant toxicity. Ann Emerg Med. 1995;26(2):19. 3. Liebelt EL, Ulrich A, Francis PD, et al. Serial electrocardiogram changes in acute tricyclic antidepressant overdoses. Crit Care Med. 1997;25(10):1721. 4. Boehnert M, Lovejoy FH. Value of the QRS duration versus the serum drug level in predicted seizures and ventricular arrhythmias after acute OD of TCAs. N Engl J Med. 1985;313:474. 5. American Heart Association. 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 10.2: toxicology in ECC. Circulation. 2005;112:IV-126. 6. Ishihara K, Szerlip HM. Anion gap acidosis. Semin Nephrol. 1998;18(1):83. 7. Glasser L, Sternglanz PD, Combie J, et al. Serum osmolality and its applicability to drug overdose. Am J Clin Pathol. 1973;60(5):695. 8. Hoffman RS, Smilkstein MJ, Howland MA, et al. Osmol gaps revisited: normal values and limitations. J Toxicol Clin Toxicol. 193;31(1):81. 9. Sporer KA, Khayam-Bashi H. Acetaminophen and salicylate serum levels in patients with suicidal ingestion or altered mental status. Am J Emerg Med. 1996; 14(5):443. 10. Mongan E, Kelly P, Nies K, et al. Tinnitus as an indication of therapeutic serum salicylate levels. JAMA. 1973;226(2):142. 11. McGuigan MA. A two-year review of salicylate deaths in Ontario. Arch Intern Med. 1987;147(3):510. 12. Sullivan JB, Hauptman M, Bronstein AC. Lack of observable intoxication in humans with high plasma alcohol concentrations. J Forensic Sci. 1987;32(6):1660. 13. Barker SJ, Curry J, Redford D. Measurement of carboxyhemoglobin and methemoglobin by pulse oximetry: a human volunteer study. Anesthesiology. 2006;105:892. 14. Kelly AM, McAlpine R, Kyle E. Venous pH can safely replace arterial pH in the initial evaluation of patients in the emergency department. Emerg Med J. 2001;18:340. 15. Kellermann AL, Fihn SD, LoGerfo JP, et al. Impact of drug screening in suspected overdose. Ann Emerg Med. 1987;16:1206. 16. Mahoney JD, Gross PL, Stern TA, et al. Quantitative serum toxic screening in the management of suspected drug overdose. Am J Emerg Med. 1990;8:16. 17. Brett A. Toxicologic analysis in patients with drug overdose. Arch Intern Med. 1988;148:2077. 18. Perrone J, De Roos F, Jayaraman S, et al. Drug screening versus history in detection of substance use in ED psychiatric patients. Am J Emerg Med. 2001;19:49. 19. Traub SJ, Hoffman RS, Nelson LS. Body packing the internal concealment of illicit drugs. N Engl J Med. 2003;349:2519. 20. Crain EF, Gershel JC, Mezey AP. Caustic ingestions: symptoms as predictors of esophageal injury. Am J Dis Child. 1984;138(9):863. 21. Kuckelkorn R, Schrage N, Keller G, et al. Emergency treatment of chemical and thermal eye burns. Acta Ophthalmol Scand. 2002;80(1):4.

alkaline urine compartment. This is only recommended as rst line for the treatment of moderately severe salicylate poisoning and as second line in the ingestion of uoride, methotrexate, phenobarbital, 2,4-dichlorophenoxyacetic acid, and mecoprop.29 A urine pH of 8.0 can be achieved by an initial bolus one to two ampules of sodium bicarbonate followed by an infusion of two to three ampules in 1 L of D5W at 1.5 times maintenance with concurrent aggressive repletion of potassium. Hemodialysis and charcoal hemoperfusion are the most invasive and expensive methods of enhancing elimination of toxins and have the added advantage of improving acidbase and electrolyte imbalances. Salicylate, methanol, ethylene glycol, theophylline, caffeine, carbamazepine, lithium, and procainamide (refer to Table 40-3) are amenable to dialysis.

ANTIDOTES
Although most management of the poisoned patient is supportive care, the judicious use of an antidote is sometimes the only therapy capable to prevent morbidity or mortality. Examples of this are the administration or hydroxocobalamin or sodium thiosulfate for cyanide poisoning, oxygen for carbon monoxide toxicity, digoxin Fab, fomepizole and/or ethanol for toxic alcohol poisoning, or N-acetylcysteine for acetaminophen toxicity, and calcium for calcium channel blocker overdose. Critically ill patients who present with symptoms justifying reasonable suspicion for poison exposure can also be treated empirically. Examples of such include empirical use of naloxone in patients with respiratory depression and pinpoint pupils or use of pyridoxine for the child in status epilepticus whose household member is being treated for tuberculosis with isoniazid. Antivenom exists for the hematologic, neurologic, and cytotoxic effects of the two main categories of snakes in the United States (Elapidae and Crotalinae). There are other antivenoms for scorpions and spiders that are available in specic geographic areas of the United States where they are relevant. There are also antivenins for rare, nonindigenous exotic snakes that are imported and used in zoos and research facilities and occasionally used to treat envenomation from exotic animals illicitly imported and kept as pets. These exotic antivenins tend to be available at facilities that must be prepared for such envenomations, such as zoos or the hospitals that serve them.

REFERENCES
1. Bronstein AC, Spyker DA, Cantilena LR, et al. 2008 annual report of the American Association of Poison Centers National Poison Data System (NPDS): 26th annual report. J Clin Toxicol. 2009;47:911.

CHAPTER 40 22. American Academy of Clinical Toxicology, European Association of Poisons Centres and Clinical Toxicologists. Position paper: ipecac syrup. J Toxicol Clin Toxicol. 2004;42(2):133. 23. American Academy of Clinical Toxicology, European Association of Poisons Centres and Clinical Toxicologists. Position paper: gastric lavage. J Toxicol Clin Toxicol. 2004;42(7):993. 24. Kulig K, Bar-Or D, Cantril SV, et al. Management of acutely poisoned patients without gastric emptying. Ann Emerg Med. 1985;14(6):562. 25. American Academy of Clinical Toxicology, European Association of Poisons Centres and Clinical Toxicologists. Position paper: whole bowel irrigation. J Toxicol Clin Toxicol. 2004;42(6):843.

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26. American Academy of Clinical Toxicology, European Association of Poisons Centres and Clinical Toxicologists. Position paper: single dose activated charcoal. Clin Toxicol. 2005;43:61. 27. Sabga E, Dick A, Lertzman M, Tenenbein M. Direct administration of charcoal into the lung and pleural cavity. Ann Emerg Med. 1997;30:695. 28. American Academy of Clinical Toxicology, European Association of Poisons Centres and Clinical Toxicologists. Position paper and practice guidelines on the use of multi-dose activated charcoal in the treatment of acute poisoning. J Toxicol Clin Toxicol. 1999;37(6):731. 29. Proudfoot AT, Krenzelok EP, Vale JA. Position paper on urine alkalinization. J Clin Toxicol. 2004;42(1):1.

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