Poisonings

Author Credentials

Written By: Al’ai Alvarez, MD, Stanford University

Edited By: Greg Tudor, MD, University of Illinois College of Medicine-Peoria,  Christopher Fowler DO, University of Arkansas for Medical Sciences

Last Update: September 2019

Case Study

A 19-year-old college student is brought into the emergency department via ambulance after her friends found her confused and she appears intoxicated. Her friend tells you that the patient was in a fight with her girlfriend and that she was really upset. She is uncertain about her medications but thinks that she takes something for her “mood”. She did not find any open pill bottles. Her vital signs are:

BP = 110/80, P = 140, RR = 38, T = 98.7F, O2 sat = 98% on room air.

Objectives

Upon completion of this self-study module, you should be able to:

  • List the key elements of history and physical exam in an overdose patient.
  • Explain the uses and limits of laboratory testing in the setting of an overdose.
  • Recall the types of decontamination used in poisonings and specific contraindications for their use.
  • Recognize the classic toxidromes including anticholinergic, sympathomimetic, cholinergic, and opioid poisoning.

Introduction

In 2017, 2.12 million poison exposures to humans were called in to 55 US poison control centers, though the true incidence is unknown due to under diagnosis and underreporting.1

Patients who have been poisoned may present with a wide array of symptoms or complaints. Some may be completely asymptomatic but state they have taken an overdose. Some may have altered mental status. Some may be unstable or apneic. Additionally, poisoned patients may present in stable condition and rapidly deteriorate.

Initial Actions

As you’re walking toward her bed, what actions should you take upon arriving?

  • Assess the primary survey
  • Place the patient in a monitor
  • Order basic laboratory tests and EKG
  • Order a safety companion/sitter and/or standard suicide precautions

Primary Survey

As with all patients, the initial survey begins with the ABC’s. If the patient is unstable, then the history and physical must be performed while simultaneously performing resuscitation. It is important to get collateral history if available from family, friends, EMS personnel. 

Depending on the ingestions, a poisoned patient may present obtunded. An unresponsive patient has lost their airway reflexes and is at risk for airway obstruction as well as aspiration. Faced with an unresponsive patient with a history of overdose, a quick run-through of a few reversible possibilities while preparing to control the patient’s airway is crucial. These reversible causes have come to be known as the “coma cocktail.” In this setting, the following should be considered: 

  • Hypoxia: Place on 100% O2 non-rebreather (also useful prior to intubation)
  • Hypoglycemia: obtain a point of care fingerstick blood glucose
  • Opioids: administer Naloxone 0.4 to 2mg IV to reverse opiates. Patients with difficult IV access who has some means to breath may benefit from nebulized naloxone. 

With an unresponsive patient, if these measures do not reverse the patient’s profound compromised mental status, proceed with intubation to control the airway.  

Once the airway is secured, attention may turn to breathing. Many toxins can affect the respiratory status and cause a variety of symptoms including frank respiratory failure, hypoxia, flash pulmonary edema, or bronchospasm. These should all be treated with standard therapies and in some cases specific antidotes.

Circulation can be compromised as well. A multitude of toxins can affect hemodynamics including heart rate and blood pressure, presenting with either hypertension or hypotension. Many medications can also affect cardiac rhythm and intervals leading dysrhythmias. Each of these symptoms can give a clue to what toxin has been ingested. Many agents cause tachycardia, beta blockers, calcium channel blockers, digoxin and clonidine can cause bradycardia; drugs such as tricyclic antidepressants (TCAs) can cause QRS widening, and many cause QT prolongation leading to lethal arrhythmia. 

Use Glasgow Coma Score (GCS) or Alert Verbal painful unresponsive (AVPU) scale for a quick assessment of level of consciousness and neurologic disability: (A=alert, V=responds to verbal stimuli, P=responds to painful stimuli, U=unresponsive).

If the patient is completely asymptomatic, there is time to obtain a more detailed history and perform a physical exam.

In all cases, there are essential elements that are important to elicit from the history.

Secondary Survey

Focused History

In all cases, these are some of the highest yield questions to ask:

  • What was ingested?
  • How much was ingested?
  • When was the ingestion and over how long?
  • Why? (accidental or intentional)?

To answer these questions, the physician should obtain information from all reliable sources; the patient, family, friends and EMS. Pill bottles can be of great help if available, understanding that reliable and accurate information may be difficult to obtain. The patient may purposely try to mislead the physician, or the patient may accidentally mislabel the agent ingested. For instance, some patients with call any over-the-counter pain reliever by a single name regardless of actual name and drug class. When the circumstances of the overdose are not clear, intentional overdose should be suspected and suicide precautions instituted until more information is available.

Focused Physical Exam

On the physical exam, there are a number of things to pay close attention to in addition to the standard exam:

  • Vital Signs 
  • Mental status (is the patient agitated, confused, somnolent?)
  • Pupils (fully dilated or pinpoint?)
  • Skin color (Pale? Flushed?)
  • Track marks (evidence of skin popping?)
  • Presence of sweat (dry or diaphoretic? The toxicologic handshake refers to checking a patient’s armpit for degree or lack of sweat)
  • Bladder size (Use point of care ultrasonography to assess for urinary retention. A full bladder may explain the patient’s level of agitation)

Some poisonings cause tachycardia (sympathomimetics, anticholinergics), bradycardia, apnea, hypotension, etc. Some toxins also cause mydriasis or miosis, flushed skin, sweating, diaphoresis, or lack of sweat when expected. All of these signs offer clues to the diagnosis.

Case Study Cont’d

Though she initially appeared intoxicated, she deteriorates during her observation period in the ED. You find her in the hallway unresponsive to painful stimuli. You immediately proceeded to control her airway, confirm tube placement, and re-examine her. Her pupils are 5mm and reactive. Her skin is not flushed. She is tachycardic with regular beats, and the rest of her exam is relatively unremarkable. There are no signs of trauma.

Toxidromes

While looking for clues to aide in the diagnosis, there are a few classic “doorway diagnoses” where “toxidromes” are easily recognizable. These classic presentations are called Toxidromes (see below). Each will be presented with a small case vignette to show how these patients might present. Remember that patients my ingest several medications which may mask or blunt the toxidrome.

Anticholinergic

A young college student is brought in by his friends after being found confused at a party. His friends tell you that he was just dumped by his girlfriend. His vital signs are as follows: HR 122, RR rate 18, BP 120/80, Temp 100.8F, O2 Sat 98% on room air. He is mumbling and picking at his clothes. On exam, his pupils are 8mm and his skin is flushed, although he is not sweating. He has suprapubic fullness and a bedside US demonstrates that his bladder is full.

This is the classic anticholinergic syndrome. These medications are going to block acetylcholine at both central and peripheral synapses and inhibit parasympathetic nervous system function. A convenient way to remember is:

  • Mad as a hatter (Altered mental status)
  • Blind as a bat (mydriasis/dilated pupils)
  • Hot as a hare (or hell or Hades)
  • Red as a beat
  • Dry as a bone

Patients with an anticholinergic toxidrome may present with some or all of these findings. Possible toxins with anticholinergic properties include the following:

  • Tri-cyclic Antidepressants (TCA)- imipramine, amitriptyline, nortriptyline
  • Antihistamines- fexofenadine, diphenhydramine, dimenhydrinate, loratadine, chlorpheniramine
  • Overactive bladder medication- oxybutynin, tolterodine, trospium

Treatment:  is mostly supportive. Please see specific therapies for TCA ingestions. Also keep in mind that anticholinergic medications can be used recreationally as drugs of abuse and may present as non self-harm induced ingestions.

Cholinergic

A migrant worker is found wandering on a deserted road. She is confused, sweating and wheezing. You notice that she has been incontinent. Her vitals are as follows: HR 36, RR rate 24, BP 100/68, Temp 98F, O2 Sat 96% on room air.

Cholinergic poisonings are caused by substances that stimulate, enhance or mimic acetylcholine. This is going to lead to an enhanced activation of the parasympathetic nervous system. A quick way to remember this is the classic mnemonic SLUDGE:

  • Salivation
  • Lacrimation
  • Urination
  • Diaphoresis and defecation
  • Gastrointestinal upset
  • Excessive bradycardia or tachycardia (muscarinic or nicotinic)

Another mnemonic is DUMBELLS:

  • Diarrhea
  • Urination
  • Miosis/Muscle weakness
  • Bronchorrhea
  • Bradycardia
  • Emesis
  • Lacrimation
  • Salivation/Sweating

Sources of cholinergic poisoning include organophosphate poisoning (pesticides) and nerve agents

Treatment: Atropine, pralidoxime, decontaminate. The administration of atropine should continue until improvement in the symptoms of bronchospasm and bronchorrhea, with an initial dose of 2 to 5 mg and repeated every 5 minutes to maintain improvement in symptoms. Additional doses are likely going to be required.  For more information on this topic please see the NCBI resource at this link: https://www.ncbi.nlm.nih.gov/books/NBK539783/

Sympathomimetic

A young college student is brought in by EMS after becoming combative at a concert. He is very agitated and altered and requires restraints. His vitals are as follows: HR 138, RR 24, BP 154/92, Temp 101.2, O2 Sat 98% on room air. Physical Exam reveals mydriasis, flushed skin, sweating and agitation.

Sympathomimetic poisonings are commonplace to the Emergency Department and the adept physician will have experience in managing these patients. As the name implies this toxidromes is going to present with increased sympathetic nervous system stimulation. The classic sympathomimetic syndrome is a fight or flight response:

  • Tachycardia
  • Hypertension
  • Mydriasis
  • Diaphoresis
  • Hyperthermia
  • Agitation

Sources include nonprescription sympathomimetic agents include the over-the-counter cold agents (containing ephedrine), street drugs (e.g., cocaine, amphetamines, methamphetamine), dietary supplements (ephedra), and illicit designer drugs (e.g., 3,4-methylenedioxy methamphetamine (MDMA, “ecstasy”)

Treatment: sedation, hydration, and treatment of complications such as rhabdomyolysis and hyperthermia. Often supportive treatment alone is necessary for mild ingestions.

Opioid

Friends bring in a young high school student who is apneic and unresponsive. They tell you they were just partying a little and their friend collapsed. Her vitals are as follows: HR 128, RR 4, BP 100/70, Temp 98F and O2 Sat 82% on room air.

Classic signs:

  • Apnea
  • Hypoxia
  • Unresponsiveness
  • Flash pulmonary edema (rare)

Treatment: These patients are usually apneic and may appear to require intubation. Timely administration of naloxone(Narcan) can reverse the apnea and obviate the need for intubation.

A word on naloxone. Naloxone has a relatively short half life. The naloxone may wear off before the offending opiate has been metabolized, depending on the type (e.g. methadone or extended release formulations). In shorter acting opioids (ie: fentanyl, heroin) additional doses may not be required. In longer acting formulations, re-dosing of naloxone may be required if symptoms return. Patients should have a reasonable period of observation to ensure that a recurrence of symptoms will not occur after discharge. Remember that naloxone is direct opioid receptor antagonist and it will precipitate acute withdrawal for chronic opioid use patients.  These patients can become agitated and combative. Judicious administration of dosages that will reverse the respiratory depression and not precipitation full withdrawal is preferred

Diagnostic Testing

Toxicology is one of the last areas of medicine where a keen mind and good diagnostic skills are still imperative without the benefit of advanced testing and technology to provide answers. Nonetheless, there are still important tests to perform:

  • EKG: may show changes in QRS or QT intervals, elevated terminal R wave or the last 40 msec in lead aVR, dysrhythmias, or other findings that can help diagnose the toxin and help with treatment.
  • Toxicology screen: is mandatory, but often of limited value in the acute setting. It is institution dependent. It is often not quantitative and usually only tests for a few toxins. Common drugs tested include: amphetamines, barbiturates, benzodiazepines, methadone, cocaine, opiates, phencyclidine (PCP), cannabis or tetrahydrocannabinol (THC). 
  • Ethanol levels: may provide clues on the patient’s mental status. It is important to highlight that ethanol levels and toxicology screen should be taken with a grain of salt. Vigilance to other causes of alterations in mental status must be pursued especially in the setting of poisoning. 
  • Acetaminophen and salicylate levels: One of the most important substances to screen are acetaminophen levels. Unlike other toxic ingestions, acute acetaminophen overdose can initially present without symptoms and can be easily missed if not tested.
  • Electrolytes: Many toxins will produce abnormalities in electrolytes 
  • Drug Levels (specific to medication): availability of these tests may vary depending on practice location.
  • Other levels that provide surrogate markers for toxicity depending on the situation, ie: ammonia levels in valproic acid toxicity, lactic acidosis in setting of volatile ingestions and metformin overdose

Another key portion of evaluating metabolic derangements is the presence of Anion Gap Metabolic Acidosis. There are several causes of an anion gap metabolic acidosis, and many of them involve poisonings. The mnemonic CAT-MUDPILES is a helpful list of differential diagnosis for high anion gap metabolic acidosis.

  • Carbon monoxide/Cyanide
  • Aminoglycosides
  • Theophylline/Toluene (glue sniffing)
  • Methanol
  • Uremia
  • DKA or AKA
  • Paraldehyde
  • Iron, Isoniazid
  • Lactate (many causes including carbon monoxide, cyanide, metformin, etc)
  • Ethylene Glycol
  • Salicylates

So How Do I Make the Diagnosis

With suspected overdoses in the emergency department, there are rarely perfect tests to provide absolute answers. The “toxicology screen” is often not quantitative and usually only tests for a few specific toxins and metabolites that may be common to a variety of substances. Also, some lasts in the urine after a week and may not be a reliable source of true cause of toxidrome. Always obtain an acetaminophen level and other levels as well depending specific drug levels as dictated by history. There are certain poisonings where the presence of an anion gap metabolic acidosis is key to helping diagnose the cause (see CAT-MUDPILES above).

Focus on key elements of history – if possible obtain what agent was ingested, when this occurred, and how much was ingested and over how long. Management changes for example when an entire bottle of acetaminophen is ingested in one sitting vs. over the course of the day. 

Look for clues in the physical exam – look at vital sign derangements, pupil size, skin color and moisture, and overall mental status.

Always check for pregnancy test in women of child bearing age. 

Use accessory data for collateral information. Though it may not reveal the answer, use the toxicology screen as well as electrolytes to aide in the diagnostic workup.

Be vigilant.

If the patient is asymptomatic for 4 – 6 hours and the work up is negative, they may not have taken a toxic level of ingestion. If the patient has findings, the provider must use all available information gathered to arrive at the most likely diagnosis and disposition the patient appropriately.

Case Study Cont’d

She does not appear to have a clear toxidrome.

Her EKG shows a sinus tachycardia with normal intervals.

You send a full set of labs including an ABG, CBC, complete metabolic panel, and a tox screen including ethanol level, acetaminophen level and salicylate. You also remembered to check her pregnancy status. 

Treatment

As with all patients, treatment begins with the ABC’s. The treatment of poisoned patients in particular also includes removing them from the toxin and decontaminating them when possible. Depending upon the substance that you are treating, it is important to remember external decontamination (particularly in organophosphate poisoning) as there can be residual materials on the skin.

Decontamination Methods:

  • Activated Charcoal
  • Whole Bowel Irrigation
  • Gastric Lavage (rare)

Activated Charcoal: Charcoal is given orally to absorb toxins that are present in the GI tract. It is most efficacious if given within the first hour post ingestion but may still work beyond that point. Consult with your local toxicologist for guidance. Toxins bind to the charcoal and are excreted without being digested. Charcoal does not bind metals (such as iron), alcohols or hydrocarbons. It should be avoided in patients with somnolence as they run the risk of aspiration. Co-administration of antiemetics is recommended

Whole bowel irrigation: This involves the administration of an osmotically balanced polyethylene glycol electrolyte solution (like Go Lytely) to flush the bowel to prevent the absorption of ingested toxins. It is used in cases where charcoal is not effective, with certain sustained release products, and in cases of street drug packet ingestions (body packers).

Gastric lavage: This is rarely used and carries significant risks with questionable benefit. In some cases, however, such as recently ingest lethal doses or an intubated overdose following a known recent ingestion, the benefits may outweigh the risks and warrant consideration. Lavage involves the application of a very large bore (36 – 40 French) orogastric tube and then flushing the stomach with aliquots of water ideally to obtain pill fragments.

Note: Many years ago, there was an agent called Ipecac that was universally promoted as a decontamination method. This agent should no longer be used. It is not effective in removing toxin and has side effects that can cause lethargy further delaying the administration or reduce the effectiveness of other more useful decontamination methods and treatments.

Disposition

Many patients with potential ingestions may be observed for four to six hours and then dispositioned home or psychiatric treatment facility if clinically asymptomatic provided the ingestion is not an extended release agent. Your local toxicology center provides an invaluable resource. 

Other Specific Poisonings

Acetaminophen

Acetaminophen (APAP) overdose is one of the most common and also one of the most dangerous poisonings in the US. Acetaminophen is available in many formulations. Although an acute overdose usually causes symptoms, patients may present asymptomatic even after a lethal ingestion. Therefore, it is imperative that an acetaminophen level is checked on ALL overdose patients as treatment easily available and is lifesaving. There are four main stages of an acute APAP overdose. Typical symptoms usually involve nausea, vomiting in the first two stages. The lethal dose of APAP is 150mg/kg. In an acute overdose, APAP is metabolized to NAPQI which combines with glutathione and is excreted. When the majority of the glutathione is used, NAPQI causes hepatic toxicity. The toxic level of acetaminophen can be measured on the Rumack nomogram and the toxic plasma level at four hours is 150. In addition to decontamination with repeated doses of activated charcoal, the antidote N-acetylcysteine (NAC/Mucomyst) should be administered if indicated by the nomogram. Note that the Rumack nomogram is for acute ingestion. Ingestions over hours or unclear point of ingestion makes the Rumack nomogram not as helpful. Concomitant screening of liver function tests therefore may aid in your decision for initiating and finishing the NAC treatment. 

Aspirin/Salicylates

Unlike the Rumack nomogram of acetaminophen, the Done nomogram associated with aspirin ingestion is typically not used to determine toxicity and treatment. Patients with an acute overdose of aspirin are usually quite ill-appearing, have tachypnea secondary to the degree of acidosis, vomiting, confused, and sometimes febrile. The toxic effects are complex and involve an uncoupling of oxidative phosphorylation. This causes a profound high anion gap metabolic acidosis. The general approach to aspirin overdose is the management of the airway, gastric decontamination, the administration of sodium bicarbonate, and hemodialysis.

Tricyclic Antidepressants (TCA) 

TCAs have historically been some of the most dangerous agents ingested in an overdose situation. In addition to their anticholinergic properties, TCAs cause a direct alpha-adrenergic blockade, inhibition of norepinephrine and serotonin reuptake, and blockade of fast sodium channels in myocardial cells. This can lead to tachycardia, prolongation of the QRS complex, dysrhythmias (including Torsades de Pointe), and cardiovascular collapse. They also cause protracted seizures. 

Disposition of TCA overdose includes close monitoring for a period of at least six to eight hours in the asymptomatic patient. In altered patients with potential TCA overdose and are tachycardic and shows signs of widening of the QRS (note, over 100 and not 120 msec), administration of sodium bicarbonate provides not only a diagnostic but also therapeutic intervention. Check the QRS immediately after pushing sodium bicarbonate, and you should see the narrowing of the QRS complex. The height of the terminal R on aVR, however, will not be affected, and is present in patients taking therapeutic doses of TCA. It can also be a normal variant. Seizures may be treated with benzodiazepines but may be intractable until administration of sodium bicarbonate. Newer recommendations for lipid emulsion therapy exist in the treatment of severe toxicity.

Toxic Alcohols

While any alcohol consumed in great quantities can be dangerous, there are three major alcohols that are considered “toxic”. These “toxic” alcohols include isopropanol, methanol, and ethylene glycol. Isopropyl alcohol is found in many solvents, mouthwashes, and rubbing alcohols. Methanol is found in windshield wiper fluid. Ethylene Glycol is typically found in antifreeze. Patients who have ingested any of these agents may appear to be intoxicated or even comatose. It is important to obtain a metabolic panel on these patients. Isopropanol will NOT cause significant metabolic acidosis, while methanol and ethylene glycol both cause a profound high anion gap metabolic acidosis. Additional diagnostic measures include the application of a wood’s lamp to the urine of a patient with an ethylene glycol ingestion. Since the source is antifreeze, sometimes the urine in the setting will fluoresce. The urine can also be examined for the presence of calcium oxalate crystals. Osmolal gap will help clue in other volatile ingestions. 

Isopropanol is usually not life threatening and can be managed with supportive care. In rare instances hemodialysis may be required. Methanol and ethylene glycol, on the other hand, are more lethal and should be aggressively treated as soon as suspected. Methanol is metabolized to formaldehyde, and ethylene glycol is broken down into oxalate. All alcohols are metabolized by alcohol dehydrogenase (ADH). Therefore, the initial treatment for methanol and ethylene glycol involves the blockade of ADH. This can be accomplished by either simple ethanol or fomepizole. In addition, removal of the toxin may be necessary by hemodialysis. Sodium bicarbonate and glucose may also be necessary. For chronic ethanol drinkers, consider high dose thiamine as this may be the cause of their elevated lactic acidosis. 

Pearl and Pitfalls

  • Vigilance is key when evaluating patients with suspected poisoning. 
  • Awareness of different toxidromes may help determine the diagnosis. 
  • Patients may initially present with benign or no symptoms and can deteriorate fast. Directed history and physical exams are crucial. Observation is one of the main interventions we are able to provide in the ED. 
  • EKG, confirmation of pregnancy status, and evaluation for suicidality and harm is a must. 
  • Common ingestions in the ED should be ruled out—acetaminophen and salicylates—as we have antidotes for them, and they pose high mortality and/or morbidity. 
  • Beware of half-life of ingestions and antidotes; naloxone wears off sooner than heroin. 
  • Target treatment to underlying cause. 
  • Have a low threshold to involve the poison control centers for resources and surveillance. 

Case Study Resolution

Her EKG shows Sinus Tachycardia with normal intervals.

Her labs return with an ABG as follows:

pH = 7.1, pCO2 = 25, pAO2 = 400.

Her electrolyte panel and tox screen show:

  • Na = 138, K = 5.8, Cl = 100, HCO3 = 9
  • Acetaminophen = 0.0, Salicylates = 0.0
  • Ethanol = 186, TCAs = negative

What did she take and how would you treat it?

On more detailed examination, you note some evidence of lingual trauma, and also notice that the patient has soiled herself. One possibility is that the patient had an unwitnessed seizure, which explains the electrolyte derangements and abrupt change in mental status. Once the patient was intubated, you repeat the lab including the basic metabolic panel. The repeat laboratory results have normalized. You also obtained a head CT, which is unremarkable. You admitted the patient to the ICU, and a few hours later, while still boarding in the ED, the patient starts to wake up. The patient eventually is extubated. She admits to have been mixing vodka with several bottles of energy drinks17. She is treated conservatively and eventually improved clinically. She complains of suicidality and a psychiatric consultation is requested. Eventually the patient is admitted to psychiatry. 

References

  1. Gummin DD, Mowry JB, Spyker DA, Brooks DE, Osterthaler KM, Banner W. 2017 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 35th Annual Report. Clin Toxicol. 2018;56(12):1213-1415. doi:10.1080/15563650.2018.1533727
  2. Erickson TB, Thompson TM, Lu JJ. The approach to the patient with an unknown overdose. Emerg Med Clin North Am. 2007;25(2):249-281; abstract vii. doi:10.1016/j.emc.2007.02.004
  3. Toxidromes- ClinicalKey. https://www.clinicalkey.com/#!/content/playContent/1-s2.0-S0749070412000607?returnurl=null&referrer=null. Accessed November 13, 2019.
  4. Holstege CP, Borek HA. Toxidromes. Crit Care Clin. 2012;28(4):479-498. doi:10.1016/j.ccc.2012.07.008
  5. Broderick ED, Crosby B. Anticholinergic Toxicity. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2019. http://www.ncbi.nlm.nih.gov/books/NBK534798/. Accessed November 13, 2019.
  6. King AM, Aaron CK. Organophosphate and carbamate poisoning. Emerg Med Clin North Am. 2015;33(1):133-151. doi:10.1016/j.emc.2014.09.010
  7. King A, Dimovska M, Bisoski L. Sympathomimetic Toxidromes and Other Pharmacological Causes of Acute Hypertension. Curr Hypertens Rep. 2018;20(1):8. doi:10.1007/s11906-018-0807-9
  8. Parthvi R, Agrawal A, Khanijo S, Tsegaye A, Talwar A. Acute Opiate Overdose: An Update on Management Strategies in Emergency Department and Critical Care Unit. Am J Ther. 2019;26(3):e380-e387. doi:10.1097/MJT.0000000000000681
  9. Clarke SFJ, Dargan PI, Jones AL. Naloxone in opioid poisoning: walking the tightrope. Emerg Med J. 2005;22(9):612-616. doi:10.1136/emj.2003.009613
  10. Grunbaum AM, Rainey PM. Laboratory Principles. In: Nelson LS, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS, eds. Goldfrank’s Toxicologic Emergencies. 11th ed. New York, NY: McGraw-Hill Education; 2019. accessemergencymedicine.mhmedical.com/content.aspx?aid=1163007318. Accessed November 13, 2019.
  11. Procopio GL, Patel R, Gupta A. Clinical Pearls in Medical Toxicology: Updates Ranging From Decontamination to Elimination. J Pharm Pract. 2019;32(3):339-346. doi:10.1177/0897190019854565
  12. Höjer J, Troutman WG, Hoppu K, et al. Position paper update: ipecac syrup for gastrointestinal decontamination. Clin Toxicol Phila Pa. 2013;51(3):134-139. doi:10.3109/15563650.2013.770153
  13. Hendrickson RG, McKeown NJ. Acetaminophen. In: Nelson LS, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS, eds. Goldfrank’s Toxicologic Emergencies. 11th ed. New York, NY: McGraw-Hill Education; 2019. accessemergencymedicine.mhmedical.com/content.aspx?aid=1163010069. Accessed November 13, 2019.
  14. O’Malley GF. Emergency Department Management of the Salicylate-Poisoned Patient. Emerg Med Clin North Am. 2007;25(2):333-346. doi:10.1016/j.emc.2007.02.012
  15. 15. Kerr GW, McGuffie AC, Wilkie S. Tricyclic antidepressant overdose: a review. Emerg Med J. 2001;18(4):236-241. doi:10.1136/emj.18.4.236
  16. Ng PCY, Long BJ, Davis WT, Sessions DJ, Koyfman A. Toxic alcohol diagnosis and management: an emergency medicine review. Intern Emerg Med. 2018;13(3):375-383. doi:10.1007/s11739-018-1799-9
  17. Wolk BJ, Ganetsky M, Babu KM. Toxicity of energy drinks. Curr Opin Pediatr. 2012;24(2):243-251. doi:10.1097/MOP.0b013e3283506827