Toxicology in Emergency Medicine

Ehab Aki; Mohammed Abdurabu; Mohamed Elgassim

doi:10.5772/intechopen.1010983

Abstract

Toxicology is a critical component of emergency medicine, requiring rapid assessment and management to prevent morbidity and mortality. This chapter provides a structured approach to poisoned patients, beginning with initial stabilization using airway, breathing, and circulation (ABCs) and a focused history, including the AMPLE mnemonic (Allergies, Medications, Past medical history, Last meal, Events leading to presentation). A key focus is on toxidromes—distinctive clinical syndromes that offer diagnostic clues for poisoning—including cholinergic, anticholinergic, opioid, sympathomimetic, and serotonin syndromes, along with their characteristic signs and treatment strategies. The discussion then shifts to common toxic substances encountered in the emergency department, such as pharmaceuticals (acetaminophen, salicylates, and opioids), illicit drugs (cocaine and amphetamines), environmental toxins (carbon monoxide, pesticides, and heavy metals), and household poisons (ethylene glycol and methanol). For each, toxicokinetic, clinical presentation, diagnostic evaluation, and evidence-based management—including antidotes and supportive care—are addressed. Additionally, the chapter explores decontamination strategies (activated charcoal and whole bowel irrigation), enhanced elimination techniques (hemodialysis and urinary alkalinization), and risk assessment tools to guide disposition decisions. Special considerations for pediatric and geriatric populations, who may present with unique toxicologic challenges, are also discussed. By integrating a systematic clinical approach with key toxicology principles, this chapter equips emergency physicians with the knowledge necessary to recognize, diagnose, and effectively manage toxicologic emergencies, ultimately improving patient outcomes.

Keywords

toxicology
emergency medicine
poisoning
toxidromes
overdose
decontamination
antidotes
toxicokinetic
supportive care
critical care toxicology

Author Information

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Ehab Aki *
- Hamad Medical Corporation, Doha, Qatar
Mohammed Abdurabu
- Hamad Medical Corporation, Doha, Qatar
Mohamed Elgassim
- Hamad Medical Corporation, Doha, Qatar

*Address all correspondence to: akiehab2004@gmail.com

1. Introduction

Poisoning is a significant global public health issue. According to data from the World Health Organization in 2012, nearly 190,000 people died from poisoning worldwide, and in 2008, the number of deaths from poisoning surpassed those from motor vehicle accidents. Additionally, the poisoning death rate nearly tripled globally. There has also been an increase in the number of patients presenting to emergency departments due to both intentional and accidental overdoses. These statistics highlight the importance of Toxicology in emergency medicine [1, 2].

The management of intoxicated patients requires a specific approach due to the complexities involved in diagnosing and treating overdoses. This chapter focuses on the general strategies for handling intoxicated patients, with an emphasis on initial management. It also explores how a patient’s history and physical exams can help doctors identify the drugs involved and provides an overview of the mechanisms of action, physical signs, and treatments for the most common toxic substances, including those associated with high mortality and morbidity rates.

2. A general approach to toxicological cases in emergency medicine

The management of poisoned patients in the emergency department involves resuscitation, obtaining a history, conducting a physical examination, and implementing appropriate treatment strategies.

2.1 Resuscitation

The primary considerations for a poisoned patient arriving at the emergency department include securing the airway, ensuring adequate respiration and maintaining circulatory stability. Mechanical ventilation and intubation may be necessary if ventilation is inadequate, intubation with mechanical ventilation may be necessary. Hypotension should be initially treated with an IV fluid bolus (10–20 mL/kg). If the hypotension does not respond to fluids, administering a specific antidote may be necessary. In cases of suspected opioid overdose (e.g., low Glasgow Coma Scale (GCS), respiratory depression, and pinpoint pupils), naloxone (0.1–2.0 mg IV) should be administered. Additionally, blood sugar should be checked, and hypoglycaemia should be treated with a 50% dextrose solution (50 mL) [3].

2.2 History

History is crucial and should be gathered from the patient whenever possible. If the patient is comatose or unable to provide information, collateral details can be obtained from family members, friends, or medical records. This should include any history of psychiatric disorders, previous suicide attempts, drug abuse, or ongoing medication use. The history should also cover factors such as the time and route of exposure, the amount of substance involved, whether the exposure was intentional or accidental, and the availability of drugs at home. Additionally, it is important to check for signs like missing tablets, empty pill bottles, or other relevant materials found near the patient, as well as whether any family members have chronic conditions such as hypertension or diabetes [4].

2.3 Physical examination

A physical examination of a poisoned patient is crucial in identifying the substance involved and any associated toxidromes. The exam should begin with assessing the patient’s general appearance and mental status, noting any signs of confusion or agitation. The skin should be checked for cyanosis, flushing, or signs of intravenous drug use, such as track marks. Eye examination is important to assess pupil size, reactivity, and the presence of symptoms like excessive tearing or involuntary eye movements (nystagmus). The presence of any unusual odors, such as garlic, bitter almonds, glue, or alcohol, can offer clues about specific toxins. The oropharynx should be checked for signs of hypersalivation or dryness, while the chest examination includes listening for breath sounds, assessing for bronchorrhea, and wheezing, and assessing heart rate and rhythm. Abdominal examination should include bowel sounds, tenderness, or rigidity, while extremities should be checked for tremors or muscle fasciculations. Finally, inspecting the patient’s clothing for any medications or illegal drugs may provide further insight into the cause of poisoning. This thorough examination is key to guiding diagnosis and treatment [3].

2.4 Toxidromes

Mofenson and Greensher introduced the term “toxidrome” in 1970. Toxidromes refer to a set of abnormal physical findings and vital signs that typically occur in response to a particular class of drugs or substances. The most common toxidromes include cholinergic, anticholinergic, sympathomimetic, opioid, and serotonin syndrome [4, 5].

2.4.1 Cholinergic

Individuals with cholinergic toxidrome usually present with “wet” symptoms, which can be easily recalled using the mnemonics “SLUDGE + 3 Killer B’s” or “DUMBELLS.” These mnemonics summarize the common clinical signs, with “SLUDGE” representing salivation, lacrimation (tearing), urination, defecation, gastrointestinal cramping, and emesis (vomiting), along with the “Killer B’s” which include bronchorrhea (excessive mucus), bradycardia (slow heart rate), and bronchospasm (narrowing of the airways). The “DUMBELLS” mnemonic stands for diarrhea, urination, miosis (small pupils), bradycardia, emesis, lacrimation, lethargy, and salivation. The most common causes of cholinergic toxidrome are organophosphate pesticides, carbamates, certain mushrooms, and sarin (a chemical warfare agent) [4].

2.4.2 Anticholinergics

Anticholinergic toxidrome presents with “dry” symptoms, including delirium, tachycardia, dry and flushed skin, dilated pupils, clonus, elevated body temperature, reduced bowel sounds, and urinary retention. A helpful mnemonic to remember these signs is: “Hot as a Hare, Mad as a Hatter, Red as a Beet, Dry as a Bone, Blind as a Bat.” The most frequent causes of anticholinergic toxidrome are antihistamines, antiparkinsonian drugs, muscle relaxants, antipsychotics, antidepressants, amantadine, scopolamine, atropine, and certain plants, such as Jimson weed [4].

2.4.3 Sympathomimetics

This toxidrome is characterized by psychomotor agitation, CNS stimulation, elevated blood pressure, fast heartbeat, dilated pupils, increased body temperature, sweating, and, in severe cases, seizures. The most common causes of these symptoms are cocaine and amphetamines [4].

2.4.4 Opioids

The most typical clinical manifestations of opioid toxidrome are bradycardia, hypotension, hypothermia, coma, respiratory depression, and pinpoint pupils (meiosis). An overdose of propoxyphene may result in seizures. But tiny pupils are not always seen; sometimes, like when meperidine and propoxyphene are poisonous, the pupils could seem normal in size [4].

2.4.5 Serotonin syndrome

Patients with serotonin syndrome typically present with altered mental status, high blood pressure, and a rapid heart rate. They may also experience myoclonus, hyperreflexia, hyperthermia, and increased muscle rigidity. The most common causes are interactions or overdoses involving SSRIs [4].

2.5 Decontaminations

Decontaminating a poisoned patient involves both removing the toxin from the patient and preventing further exposure. This can be done through external methods, like washing the patient, or internal methods, such as gastrointestinal decontamination or enhancing toxin elimination.

2.5.1 Gross decontamination

The patient must be fully undressed and given a thorough wash with lots of water. The decontamination process needs to be carried out in a confined space with all garments taken off. Usually, gross decontamination is applied to exposure to chemicals, biological agents, or radiation.

2.5.2 Gastrointestinal decontamination

The gastrointestinal tract can be decontaminated using a variety of techniques, such as gastric lavage and emesis (induced vomiting). Historically, gastric lavage was widespread and ipecac syrup was used to induce vomiting. But these are now rarely recommended due to the lack of supporting evidence and potential risks. These methods may reduce toxin absorption but can also increase complications. Inducing vomiting and gastric lavage might be considered for conscious, alert patients who have ingested a toxic substance within an hour. However, they are contraindicated in cases where the patient has an unprotected airway, ingested corrosive substances or hydrocarbons, or is in an unstable condition, such as being hypotensive or having seizures [6].

2.5.3 Activated charcoal

Activated charcoal is made by superheating carbon materials to increase its surface area. It works by preventing the absorption of toxins in the stomach and intestines but is ineffective against metals, alcohols, corrosives, and lithium. If administered within an hour of intake, the greatest outcomes are obtained. Lack of intestinal motility, gastrointestinal perforation, consumption of caustic substances, and an unprotected airway are among the contraindications (however if the patient is intubated, it can be given via a nasogastric tube). Potential complications from using activated charcoal include aspiration, which can lead to pneumonitis, ARDS, and issues like small bowel obstruction [7].

2.5.4 Whole-bowel irrigation

Whole-bowel irrigation is a process that cleanses the entire gastrointestinal tract to reduce toxin absorption. This is done using a polyethylene glycol solution. It is indicated for substances with slow absorption, such as sustained-release medications, toxins poorly absorbed by activated charcoal (e.g., metals, lithium), and in body packers. Some side effects include vomiting, bloating, and rectal irritation. It is contraindicated in cases where there are absent bowel sounds or a perforation [8].

2.5.5 Enhanced elimination

By speeding up the body’s disposal of toxins, enhanced elimination helps lessen the intensity and length of poisoning symptoms. While not routinely used, it is considered in cases of severe toxicity, when there’s poor response to supportive care or antidotes, or when the body’s natural elimination processes are slow. Methods for enhanced elimination include multiple-dose activated charcoal (MDAC), which is helpful in cases such as carbamazepine, phenobarbital, and disopyramide toxicity. Urinary alkalinization is effective for poisoning with salicylates or phenobarbital. Additionally, extracorporeal methods like hemodialysis, hemofiltration, plasmapheresis, and exchange transfusion can be used for substances such as lithium, carbamazepine, theophylline, salicylates, and toxic alcohols like ethylene glycol and methanol [4].

2.6 Antidotes

A drug known as the antidote can stop further poisoning from some toxins. The table below shows the most common antidote used in the emergency department (see Table 1) [4].

Toxin	Antidote
Acetaminophen	N-Acetylcysteine 150 mg/kg dextrose IV over 15–60 min then 50 mg/kg NAC IV over 4 hrs. Then 100 mg /kg NAC IV over 16 hrs.
Cholinergic (organophosphates, carbamates)	Atropine 1-2 mg every 2–3 mins, until there is drying of secretions Pralidoxime (2-PAM) 70 mg/kg IV then infusion at 500 mg/hour
Anticholinesterases	Physostigmine 0.5–1 mg IV as a slow push over 5 minutes and repeat every 10 min
Benzodiazepines	Flumazenil 0.2 Mg repeated max dose 2 mg
β-Blockers	Glucagon 3–10 mg
Calcium channel blockers	Calcium gluconate 10% 10–30 mL IV
Cyanide	Vitamin B12 (Hydroxocobalamin) 70 ml/kg IV. Amyl nitrite Sodium thiosulfate Sodium nitrite (3% solution)
Digoxin	Digoxin Fab 5–10 vials
Isoniazid	Pyridoxine (vitamin B6) 70 mg/kg IV (maximum 5 gm).
Methanol, ethylene glycol	Ethanol: Loading 8 ml/kg of 10% ethanol then 1–2 ml/kg/hour of 10% ethanol Fomepizole: Loading: 15 mg/kg in 100 ml IV over 30 minutes then maintenance:10 mg/kg IV over 30 minutes every 12 hours for 48 hr.
Narcotics	Naloxone 0.1–0.4 mg, may repeated
Tricyclic antidepressants	Sodium bicarbonate: 1–2 mEq/kg IV bolus followed by 2 mEq/kg per h IV infusion
Iron	Desferrioxamine IV infusion dose of 15 mg/kg/hour
Methemoglobinemia	Methylene Blue 1–2 mg/kg (0.1–0.2 ml/kg of 1% solution) IV slowly over 5 minutes. In case of G6PD, Vitamin C (Ascorbic Acid) 300–1000 mg/day orally in divided doses.
local anesthesia	Intravenous lipid emulsion 1–1.5 ml/kg 20% IV bolus over 1 minute and Repeat bolus at 3–5 minutes Then infuse 0.25 ml/kg/minute

Table 1.

The most common antidotes in the emergency department [4].

3. Common toxic substances encountered in the emergency department

3.1 Acetaminophen poisoning

Since its clinical introduction in 1950, acetaminophen has become one of the most widely used over-the-counter medications for analgesia and antipyresis. However, in the US, it is also the main cause of acute liver failure [9, 10].

3.1.1 Mechanism of action

Acetaminophen is processed in the liver, where it is converted into nontoxic metabolites through glucuronidation (40–67%) and sulfation (20–46%). A hazardous byproduct known as NAPQI is only little formed at regular dosages, which is safely detoxified by conjugation with glutathione (GSH). Glutathione is an important molecule that helps neutralize harmful substances, like NAPQI, through a reaction that requires NADPH. In the case of an overdose, however, the liver’s usual processes are overwhelmed, and the pathways that normally handle acetaminophen are saturated. As a result, glutathione is depleted, and NAPQI builds up, causing it to bind to cellular proteins and ultimately leading to liver cell damage and death [11].

3.1.2 Clinical features

In the early stages of acetaminophen toxicity, symptoms are often nonspecific or may not appear at all. The condition progresses through four stages: In Stage I (the first 24 hours), patients may experience nausea, vomiting, fatigue, loss of appetite, or be asymptomatic, with blood tests revealing hypokalaemia and metabolic acidosis. In Stage II (Days 2–3), symptoms worsen, with nausea, vomiting, right upper abdominal pain, and significant liver damage indicated by elevated liver enzymes (AST and ALT). Stage III (Days 3–4) is the peak of liver damage, where patients may develop coma, encephalopathy, coagulopathy, kidney failure, jaundice, ARDS, sepsis, and cerebral edema. Finally, in Stage IV (Days 7–8), patients either begin to recover or progress to multi-organ failure and potential death [12, 13].

3.1.3 Treatment

After stabilizing the patient’s airway, breathing, and circulation, the next step is to consider gastrointestinal decontamination, typically with activated charcoal. The primary treatment for acetaminophen overdose is N-acetylcysteine (NAC). NAC helps replenish glutathione levels and can directly neutralize NAPQI, the toxic metabolite of acetaminophen. If administered within 8 hours of ingestion, NAC is highly effective at preventing liver damage. Although NAC is less effective after 8 hours, it still provides benefits, even in severe cases of liver failure. NAC should only be given to patients at risk of liver damage. The Rumack-Matthew nomogram is used to assess the risk of liver toxicity based on the acetaminophen level and the time since ingestion, typically within 24 hours. When the nomogram is not applicable—such as when the time of ingestion is unknown or when more than 24 hours have passed—NAC should be administered right away. If liver enzymes (AST, ALT) return to normal and acetaminophen levels are undetectable, NAC treatment can be stopped. Otherwise, NAC should continue.

It is advised to take 140 mg/kg orally first, then 70 mg/kg every 4 hours for 17 doses, or 150 mg/kg intravenously as a loading dose, followed by 50 mg/kg over 4 hours and 100 mg/kg over 16 hours (Figure 1) [14, 15, 16].

Figure 1.
Rumack-Matthew nomogram [14, 15, 16].

3.2 Cyclic antidepressants (CA) poisoning

Cyclic antidepressants were once commonly prescribed for depression, but their use has significantly decreased due to the availability of safer alternatives. In fact, in 2013, cyclic antidepressants were the most frequent type of antidepressant involved in overdose-related deaths [17, 18].

3.2.1 Mechanism of action

Cyclic antidepressants (CA) have several pharmacological effects. One of their key actions is their antihistamine effects, where they block postsynaptic histamine receptors, leading to sedation, a reduced level of consciousness, and potentially coma. They also have antimuscarinic effects, which can be divided into central and peripheral effects. In the central nervous system, blocking acetylcholine receptors can result in agitation, delirium, confusion, hallucinations, slurred speech, ataxia, and even coma. On the peripheral level, blocking acetylcholine receptors causes symptoms such as dilated pupils, tachycardia, hyperthermia, high blood pressure, dry skin, ileus, urinary retention, increased muscle tone, and tremors. Additionally, cyclic antidepressants inhibit α-adrenergic receptors, which can lead to sedation, orthostatic hypotension, tachycardia, and pupillary constriction, although the antimuscarinic effects typically counteract the pupillary dilation. The inhibition of amine reuptake can cause mydriasis (pupil dilation), sweating, tachycardia, early hypertension, myoclonus, and hyperreflexia. Furthermore, cyclic antidepressants block sodium channels, which slow conduction velocity, prolong repolarization, and depress myocardial contractility, potentially leading to heart blocks, bradycardia, and widening of the QRS complex. Finally, potassium channel blockade can result in QT interval prolongation and, in rare cases, Torsade de pointes [19].

3.2.2 Clinical features

Cyclic antidepressant toxicity symptoms can range from moderate antimuscarinic effects to severe cardiac toxicity, and they usually manifest within 2 hours of administration. The symptoms include excessive reflexes (hyperreflexia), muscular jerks (myoclonus), ataxia, slurred speech, lethargy, disorientation, and a fast heartbeat (sinus tachycardia). Symptoms of severe poisoning often appear 6 hours after intake and include ventricular tachycardia, low blood pressure, respiratory depression, unconsciousness, delays in cardiac conduction, and convulsions [20, 21].

ECG changes in cyclic antidepressant poisoning [22]:

Sinus tachycardia.
Right axis deviation of the terminal 40 milliseconds with positive terminal R wave in lead aVR and a negative S wave in lead I
QRS prolongation (if the QRS complex is longer than 100 ms, the risk of seizures rises).
QT and PR prolongation
Brugada pattern is seen 10–15% (Figure 2)

Figure 2.
ECG changes in TCA toxicity [22].

3.2.3 Treatment

Treatment for cyclic antidepressant toxicity begins with supportive care, which includes securing the airway and administering intravenous fluids if the patient is hypotensive. Gastrointestinal decontamination with activated charcoal should be done within an hour of ingestion. If hypotension does not improve with IV fluids, vasopressors should be added. If the patient shows signs of cardiac conduction issues, ventricular arrhythmias, or persistent hypotension despite fluids, blood alkalinization with sodium bicarbonate should be started to maintain a blood pH of 7.50–7.55. For seizures, benzodiazepines are the first-line treatment; if seizures are resistant, phenobarbital (10–15 mg/kg) can be used. Certain medications are contraindicated in cyclic antidepressant toxicity, including Class I antiarrhythmics (such as lidocaine, phenytoin, and flecainide), Class III antiarrhythmics (such as amiodarone and sotalol), beta-blockers, calcium channel blockers, physostigmine, and flumazenil [23, 24].

3.3 Salicylate (aspirin) poisoning

Aspirin is a commonly used over-the-counter medication, frequently prescribed as an analgesic and antiplatelet agent for cardiovascular and cerebrovascular diseases. Due to its widespread availability and use, both accidental and intentional overdoses are common [25].

3.3.1 Mechanism of action

Aspirin works by inhibiting cyclooxygenase, which decreases the production of prostaglandins, prostacyclin, and thromboxane. This leads to platelet dysfunction and damage to the gastric mucosa. Aspirin also triggers the medulla’s chemoreceptor trigger zone, which results in nausea and vomiting. Additionally, it triggers the medulla’s respiratory center, resulting in respiratory alkalosis and hyperventilation. Moreover, aspirin causes metabolic acidosis by inhibiting the Krebs cycle and uncoupling oxidative phosphorylation [26].

3.3.2 Clinical features

Salicylate toxicity is divided into acute and chronic toxicities:

3.3.3 Acute toxicity

Acute toxicity presents with gastrointestinal, central nervous system (CNS), and metabolic symptoms. In the early stages, patients often experience gastric irritation, nausea, and vomiting, which are more common in acute poisoning cases. As salicylate levels in the CNS rise, symptoms such as tinnitus (ringing in the ears), reduced hearing, dizziness, and rapid breathing (hyperventilation) may occur. If the poisoning progresses, CNS effects can worsen, leading to agitation, hallucinations, delirium, seizures, and drowsiness. The metabolic effects of salicylate toxicity include uncoupling oxidative phosphorylation, which results in an elevated body temperature (a sign of severe toxicity) and a large anion gap metabolic acidosis. Severe cases can lead to renal failure, acute lung injury, and platelet dysfunction.

3.3.4 Chronic toxicity

Chronic salicylate toxicity, on the other hand, develops over a longer period, typically when a person unintentionally ingests more of the drug than their body can eliminate. This form of poisoning is more common in older individuals. The symptoms initially resemble those of acute toxicity, but they develop more slowly and are less severe. In elderly patients, chronic poisoning can easily be mistaken for conditions like sepsis, ketoacidosis, delirium, dementia, congestive heart failure, or respiratory failure. Delays in diagnosing chronic toxicity can lead to increased morbidity and mortality.

3.3.5 Treatment

Initial management of salicylate toxicity focuses on stabilizing airway, breathing, and circulation. Intubation should generally be avoided, as it can worsen the toxicity, but if it is required, the patient should receive adequate minute ventilation. If the patient is volume-depleted or experiencing acidosis, intravenous fluids should be administered. For early ingestions, gastrointestinal decontamination with activated charcoal may be helpful. Whole bowel irrigation (WBI) is recommended in cases of large or sustained ingestions, or when the medication is in sustained-release or enteric-coated form. Severe salicylate toxicity can be treated by alkalinizing the serum with sodium bicarbonate, aiming for a serum pH of around 7.5. In some cases, hemodialysis may be necessary, especially if there is clinical deterioration, severe acid–base imbalance, altered mental status, acute lung injury, failure of alkalinization methods, or renal failure [27, 28, 29].

3.4 Opioids poisoning

Opioid abuse has become a major medical and social issue globally. Over the past decade, there has been a significant rise in the number of opioid overdoses and related deaths. Opioids are a group of substances derived from opium, known for their pain-relieving and sedative properties. Opium itself is extracted from the poppy plant [30].

3.4.1 Mechanism of action

Opioids work by acting on three primary receptors in the body: μ (mu), κ (kappa), and δ (delta). When opioids bind to these receptors, they cause several effects, including pinpoint pupils (miosis), slowed breathing (respiratory depression), suppression of coughing, feelings of euphoria, and reduced movement in the digestive system (decreased GI motility).

3.4.2 Clinical features

The classic signs of opioid intoxication include a depressed mental state, slow breathing (low respiratory rate), and pinpoint (constricted) pupils. Other symptoms can include reduced bowel sounds, low blood pressure when standing (orthostatic hypotension), urinary retention, and localized skin reactions like hives (urticaria). In some cases, the pupils may appear normal, which can occur with toxins like meperidine, diphenoxylate, or propoxyphene, or when opioids are taken alongside other substances like sympathomimetics or anticholinergics (Table 2) [31, 32].

Opioids agent	Specific clinical feature
Dextromethorphan	Serotonin toxicity; at high doses
Loperamide	QRS and QT prolongation; Wide-complex tachycardia
Meperidine	Seizure, normal pupils size Serotonin syndrome (in combination with other agents)
Methadone	Long acting. QT prolongation, Torsade de Pointes
Oxycodone	QT interval prolongation
Tramadol	Seizure
Heroin	Acute lung injury

Table 2.

Opioids with specific clinical features [31, 32].

3.4.3 Treatment

The first crucial steps in treating opioid overdose are securing the airway and ensuring proper oxygenation and ventilation, typically using a bag-valve mask. It is important to check the patient’s blood glucose levels as well. Then, administer naloxone at a dose of 0.4 mg IV. For non-opioid-dependent patients with mild respiratory depression, this dose is usually sufficient. However, for opioid-dependent individuals with minimal respiratory depression, administer a smaller dose of naloxone, such as 0.1 mg IV, as higher doses could trigger withdrawal symptoms. If the patient is experiencing apnea, near-apnea, or cyanosis, give naloxone 2 mg IV regardless of their drug use history, and repeat the dose every 3 minutes if necessary [31, 32, 33].

3.5 Sympathomimetic (cocaine) poisoning

Cocaine is made from the leaves of the coca plant and is one of the most potent sympathomimetics. It was initially employed in medicine in 1884 as a local anesthetic for eye-related procedures. In the United States, using cocaine is one of the most common causes of acute drug-related ED visits.

3.5.1 Mechanism of action

Cocaine causes vasoconstriction in the cardiovascular system by stimulating alpha and adrenergic receptors by raising norepinephrine levels. It also prevents neuronal serotonin reuptake, which results in euphoria. Cocaine prolongs the QRS interval by blocking the sodium (Na+) channel [34, 35].

3.5.2 Clinical features

Cocaine poisoning can have vasoconstrictive and sympathomimetic effects on a number of systems, including the heart and central nervous system etc.).

Cardiovascular: High blood pressure and dysrhythmias, such as tachycardia, sinus tachycardia, SVT, and AF, are common in individuals with cocaine poisoning. Moreover, QT interval prolongation and a rightward shift of the terminal part of the QRS complex are examples of ECG abnormalities. Patients may have myocarditis, cardiomyopathy, aortic and coronary artery dissection, and acute coronary syndromes (cocaine-associated acute coronary syndrome).
CNS: A range of central nervous system symptoms, such as agitation, seizures, and coma, are seen in patients with cocaine poisoning.
Pulmonary: Patients who use crack cocaine are more likely to get asthma, barotrauma, pneumonitis, and pulmonary hemorrhage.
Gastrointestinal: Cocaine raises the risk of bleeding and ulcer perforation and can result in intestinal ischemia, ischemic colitis, and bowel necrosis.
Renal: Rhabdomyolysis can result from cocaine poisoning, which can cause abrupt renal failure [36, 37, 38].

3.5.3 Treatment

The first stages of therapy include securing the airway and ensuring proper breathing. Benzodiazepines are used to sedate CNS symptoms (such as agitation or seizures). Rapid cooling is necessary for a patient suffering from hyperthermia. Phentolamine or a sodium nitroprusside infusion can be used to treat severe hypertension that is not responding to sedation (avoid B-ac blockers). Acute coronary syndrome caused by cocaine poisoning is treated with nitroglycerin and aspirin, and calcium channel blockers may also be used. Serum alkalinization by sodium bicarbonate is used to treat wide-complex tachycardia with cocaine toxicity; ensure that the serum pH does not rise over 7.55. When a patient has significant cocaine toxicity and resistant wide-complex tachycardia or cardiovascular instability, an intravenous lipid emulsion may be utilized [38].

Body packing: swallowing smuggling packages or narcotic containers.
Body stuffing: ingesting less medication out to fear of being arrested

3.6 Digitalis glycoside toxicity

Cardiac glycosides have been used for heart failure treatment for centuries, with their presence in plants such as foxglove, lily of the valley, and oleander. Digoxin is still a commonly used digitalis derivative for the treatment of congestive heart failure and atrial fibrillation [38].

3.6.1 Mechanism of action

During cardiac repolarization, digoxin inhibits Na+/K + -ATPase, which raises intracellular sodium and lowers intracellular potassium. This leads to an increase in intracellular calcium concentration, producing a positive inotropic effect. Additionally, digoxin enhances automaticity and shortens repolarization intervals in the atria and ventricles [39].

3.6.2 Clinical features

Toxicity from digoxin can be classified as acute or chronic:

Acute toxicity: It typically results from accidental or intentional overdose and presents with nausea, vomiting, nonspecific abdominal pain, headache, and dizziness. Severe cases can progress to confusion, coma, bradyarrhythmias, atrioventricular (AV) block, supraventricular tachyarrhythmias, and hyperkalemia. A hallmark feature is xanthopsia, where patients perceive yellow-green halos around objects, though the most common visual disturbance is nonspecific color perception changes. Serum digoxin levels are significantly elevated [40, 41].
Chronic toxicity: It is more common in elderly patients and often results from drug interactions (e.g., with calcium channel blockers, amiodarone, beta-blockers, or diuretics) or impaired renal clearance. Unlike acute toxicity, chronic digoxin toxicity prominently features CNS symptoms such as weakness, fatigue, confusion, or delirium. Ventricular arrhythmias are frequently observed. Serum potassium levels can be normal or decreased, with only slight elevations in serum digoxin levels [40, 41, 42, 43].

3.6.3 Treatment

Supportive care is the cornerstone of management, including airway stabilization, ventilation support, and IV fluid resuscitation for hypotension. Activated charcoal is beneficial for early acute ingestion. Atropine is administered for symptomatic bradycardia. Digoxin-specific antibody fragments (digoxin-Fab) serve as an antidote in cases of life-threatening arrhythmias unresponsive to standard treatment or hyperkalemia exceeding 6 mEq/L. Digoxin-Fab dosage requirements are determined by total-body digoxin burden, which may be calculated from blood levels or the amount consumed [44]. Every digoxin-Fab vial neutralizes around 0.5 milligrams of digoxin. An empirical dosage of ten vials may be given if the amount consumed is unclear. Hyperkalemia is managed with insulin, dextrose, and sodium bicarbonate. The use of calcium salts remains controversial due to historical reports of increased ventricular arrhythmias and mortality [40, 41].

3.7 Beta-blocker toxicity

Beta-adrenergic antagonists, commonly known as beta-blockers, have been widely used for over three decades in the management of cardiovascular, neurological, and ophthalmologic conditions. However, beta-blocker overdose is associated with significant morbidity and mortality [17].

3.7.1 Mechanism of action

Beta receptors are categorized into three types based on their location and function: (see Table 3).

Beta-1 (B1): Found in the myocardium, kidneys, and eyes, these receptors enhance inotropy, chronotropy, and renin release. Beta-1 blockade results in reduced myocardial contractility, heart rate, and renin secretion.
Beta-2 (B2): Located in bronchial smooth muscle, skeletal muscle, the liver, and vasculature, these receptors promote bronchodilation, uterine relaxation, increased contraction force, and vasodilation. Beta-2 antagonism leads to bronchospasm, inhibition of glycogenolysis and gluconeogenesis, and minimal vasoconstriction.
Beta-3 (B3): Present in adipose tissue and skeletal muscle, these receptors stimulate lipolysis and thermogenesis. Beta-3 blockade results in the inhibition of these processes.

	Location	Action	Antagonism
B1	Myocardium Kidney Eye	Increases inotropy Increases chronotropy Stimulates renin release	Decreases inotropy Decreases chronotropy Inhibits renin release
B2	Bronchial smooth muscle Skeletal muscle Liver Vascular	Bronchodilation Relaxes uterus Increases force of contraction Stimulates glycogenolysis & gluconeogenesis Vasodilation	Causes bronchospasm Inhibits glycogenolysis and gluconeogenesis Minimal vasoconstriction
B3	Adipose tissue Skeletal muscle	Stimulates lipolysis Stimulates thermogenesis	Inhibits lipolysis Inhibits thermogenesis

Table 3.

Beta receptor: Locations and actions.

Beta-blockers are classified as either selective (targeting beta-1 receptors) or nonselective (affecting both beta-1 and beta-2 receptors). These drugs work by competitively inhibiting beta receptors, reducing intracellular cyclic adenosine monophosphate (cAMP) levels. Selective beta-1 blockade primarily impacts myocardial contractility, pacemaker automaticity, and AV node conduction, whereas nonselective beta-blockers have systemic effects, including bronchoconstriction and impaired gluconeogenesis. Lipophilic beta-blockers, such as propranolol, cross the blood–brain barrier rapidly, leading to neurological symptoms like seizures and delirium [45, 46].

3.7.2 Clinical manifestations

Beta-blocker toxicity primarily affects the cardiovascular system, resulting in bradycardia and hypotension. Bradycardia arises from sinus node suppression or conduction abnormalities. However, beta-blockers with partial agonist activity may initially present with hypertension and tachycardia. Some beta-blockers, such as sotalol, also block potassium channels, leading to QT interval prolongation and potential arrhythmias.

CNS and pulmonary involvement may include delirium, coma, seizures (more common with lipophilic beta-blockers like propranolol), bronchospasm, and hypoglycemia [46, 47].

3.7.3 Treatment

Management includes early GI decontamination with activated charcoal if the patient presents within 1 hour of ingestion. The primary focus of treatment is restoring perfusion to critical organs by increasing cardiac output. This can be achieved through:

Fluid resuscitation
Glucagon administration (3–10 mg IV) to enhance myocardial contractility
Vasopressors (e.g., epinephrine) for refractory hypotension
High-dose insulin-glucose therapy (1 unit/kg IV bolus of insulin)
Intravenous lipid emulsion therapy is considered in severe toxicity cases unresponsive to standard treatments. In cases refractory to pharmacological therapy, advanced interventions such as hemodialysis, hemoperfusion, cardiac pacing, or intra-aortic balloon pump placement may be required. Wide QRS-interval arrhythmias caused by sodium channel inhibition caused by beta-blockers are treated with sodium bicarbonate (2–3 mEq/kg IV over 1–2 minutes) [48, 49].

3.8 Calcium channel blocker toxicity

Many cardiovascular diseases, including hypertension, coronary artery disease, and arrhythmias, are treated with calcium channel blockers (CCBs). Due to their widespread prescription, toxicity from these drugs is common. CCBs are available in immediate-release and extended-release formulations [17].

3.8.1 Mechanism of action

CCBs are classified into two primary categories based on their predominant physiological effects:

Dihydropyridines (e.g., amlodipine, nifedipine): Primarily act on L-type calcium channels in vascular smooth muscle, leading to vasodilation and reflex tachycardia.
Non-dihydropyridines (e.g., verapamil, diltiazem): Preferentially block L-type calcium channels in the myocardium, reducing cardiac contractility and causing bradycardia.

In overdose, dihydropyridines primarily result in vasodilatory shock, whereas non-dihydropyridines can lead to significant myocardial depression and conduction abnormalities [50].

3.8.2 Clinical manifestations

The cardiovascular system is the primary target of CCB toxicity. Patients often present with hypotension, bradycardia, and, in the case of dihydropyridine toxicity, reflex tachycardia. Verapamil and diltiazem overdoses typically result in sinus bradycardia. Unlike beta-blockers, CCBs generally do not have a primary effect on the CNS or pulmonary system. CNS manifestations such as seizures, delirium, and coma are secondary to poor organ perfusion. Severe cases may develop cardiogenic pulmonary edema and acute lung injury [47].

3.8.3 Treatment

Initial management includes securing the airway and stabilizing ventilation and circulation. Decontamination with activated charcoal is effective if administered within 1 hour of ingestion, while whole-bowel irrigation is recommended for extended-release CCB ingestions.
IV fluid resuscitation for hypotension
Calcium chloride or calcium gluconate to counteract myocardial depression
Glucagon (3–10 mg IV) if initial measures fail
Vasopressors (e.g., norepinephrine) if unresponsive to fluids and calcium

For refractory cases, high-dose insulin-glucose therapy can improve cardiac contractility. If hypotension persists despite maximal medical therapy, lipid emulsion therapy may be considered. Circulatory support measures such as intra-aortic balloon pump placement may be used in severe cases [48, 49, 51].

3.9 Carbon monoxide poisoning

Carbon monoxide (CO) is a colorless, odorless, tasteless, and nonirritating gas. Common sources of exposure include automotive exhaust, fuel-powered heaters, wood or coal-burning stoves, structure fires, and gasoline-powered generators. The increasing use of wood stoves, space heaters, and charcoal indoors during the winter increases the risk of CO poisoning.

3.9.1 Mechanism of action

CO has a 200-fold higher affinity for hemoglobin than oxygen and diffuses quickly across the pulmonary capillary membrane. This binding forms carboxyhemoglobin, which impairs oxygen delivery to tissues and shifts the oxyhemoglobin dissociation curve to the left, reducing oxygen release at the tissue level [51].

3.9.2 Clinical features

Symptoms of CO poisoning vary based on exposure severity:

Mild to moderate: Headache, nausea, and dizziness
Severe: Confusion, seizures, and coma
Cardiovascular complications: Myocardial injury, life-threatening arrhythmias
Neurological sequelae: Delayed neuropsychiatric syndrome (DNS), which presents with cognitive impairments, movement disorders, and focal neurologic deficits

Standard pulse oximetry cannot distinguish carboxyhemoglobin from oxyhemoglobin, making it unreliable for diagnosis. Carboxyhemoglobin levels must be measured via arterial blood gas analysis [52, 53, 54, 55].

3.9.3 Treatment

After airway stabilization, the primary treatment is 100% oxygen via a non-rebreather mask or mechanical ventilation if necessary. Oxygen therapy reduces the half-life of carboxyhemoglobin from approximately 250–320 minutes in room air to 90 minutes with 100% oxygen.

Hyperbaric oxygen (HBO) therapy is recommended in specific cases, including:

Pregnant patients with carboxyhemoglobin levels >15%
Nonpregnant patients with carboxyhemoglobin levels >25%
Evidence of acute myocardial ischemia
Severe metabolic acidosis [56].

3.10 Iron toxicity

Iron tablets are commonly found in households, particularly those with children and pregnant women. Their candy-like appearance, bright color, and sugar coating make them attractive to children, raising the risk of accidental ingestion [57].

3.10.1 Mechanism of action

Excessive iron exerts corrosive effects on the gastrointestinal tract and has cytotoxic actions, particularly in the liver, leading to hepatocellular necrosis. Additionally, iron has cardiotoxic effects, acting as a negative inotrope and inhibiting thrombin activity, resulting in coagulopathy. These effects contribute to metabolic acidosis [58].

3.10.2 Clinical features

Iron poisoning occurs in five stages:

Within 6 hours: Vomiting, hematemesis, diarrhea, abdominal pain, drowsiness, and irritability. Severe poisoning may cause coma, seizures, rapid breathing, and hypotension.
6–48 hours: Symptoms may improve during a latent phase, leading to misinterpretation as recovery.
12–48 hours: Shock, fever, bleeding, jaundice, liver failure, metabolic acidosis, and seizures can occur.
2–5 days: Liver failure, coagulopathy, hypoglycemia, and coma.
2–5 weeks: Gastrointestinal scarring may cause bowel obstruction [59, 60].

3.10.3 Treatment

Initial management includes stabilizing the airway, breathing, and circulation.
An abdominal X-ray may confirm the presence of iron tablets.
Whole bowel irrigation is recommended for patients with large ingestions, especially of sustained-release formulations.
Activated charcoal is ineffective in binding iron.
Asymptomatic patients require observation for 6 hours.
Serum iron levels <300–350 mcg/dL allow for safe discharge.
Chelation therapy with deferoxamine is indicated for:
Serum iron >350 mcg/dL with symptoms
Serum iron >500 mcg/dL regardless of symptoms
In severe cases with persistent metabolic acidosis or hemodynamic instability, deferoxamine therapy should not be delayed. Hemodialysis is ineffective in removing iron but may be considered in cases of acute renal failure to facilitate removal of the iron-deferoxamine complex [61, 62].

3.11 Toxic alcohol poisoning

Toxic alcohols, including methanol, ethylene glycol (EG), and isopropanol, are fewer common causes of poisoning but can result in severe morbidity and mortality if not promptly diagnosed and managed [63, 64].

3.11.1 Mechanism of action and clinical features

Methanol: It is found in windshield wiper fluid, paint removers, and deicing solutions. In the liver, methanol metabolized to formaldehyde and subsequently to formic acid, which inhibits mitochondrial cytochrome c, leading to lactic acidosis and optic nerve toxicity. Classic signs include severe anion gap metabolic acidosis, visual disturbances, and altered mental status. Pancreatitis may also occur.
Ethylene glycol: It is present in radiator antifreeze and metal cleaners. It is metabolized to glycolic and oxalic acid, leading to metabolic acidosis, hypocalcemia, and calcium oxalate crystal deposition in the kidneys, resulting in renal failure. Neurological symptoms include coma, seizures, and muscle spasms.
Isopropanol: It is found in solvents, disinfectants, and hand sanitizers. It is metabolized to acetone and typically does not cause metabolic acidosis. Clinical features include inebriation, cerebellar signs, and hemorrhagic gastritis [64, 65, 66, 67, 68, 69, 70].

3.11.2 Investigations

Osmolar gap >10 mOsm/kg suggests toxicity from ethylene glycol, methanol, or isopropanol.
High anion gap metabolic acidosis is seen in methanol and ethylene glycol poisoning.
Hypoglycemia may occur with isopropanol, whereas hyperglycemia and hypocalcemia can occur in methanol and ethylene glycol poisonings, respectively.
Urinary calcium oxalate crystals are indicative of ethylene glycol intoxication [71, 72].

3.11.3 Treatment

Early stabilization includes airway management, respiratory support, and correction of metabolic derangements.
Fomepizole: Inhibits alcohol dehydrogenase, preventing the formation of toxic metabolites from methanol and ethylene glycol.
Hemodialysis: Indicated in cases of severe metabolic acidosis, refractory hypotension, or end-organ damage.
Vitamin therapy: Folic or folinic acid for methanol poisoning to facilitate detoxification of formic acid. Pyridoxine and thiamine for ethylene glycol toxicity to promote metabolism to nontoxic metabolites [73, 74, 75, 76].

3.12 Organophosphate poisoning

Organophosphates (OPs) are widely used in insecticides for agricultural and domestic purposes and serve as the primary toxic agents in nerve gases like sarin. OP pesticide self-poisoning is a significant public health issue, particularly in rural regions of Asia [77].

3.12.1 Mechanism of action

The most severe cases of OP poisoning occur via ingestion, while dermal absorption and inhalation of sprays are less likely to result in critical toxicity. OPs exert their toxic effects by inhibiting acetylcholinesterase, leading to an excessive accumulation of acetylcholine at muscarinic, nicotinic, and central nervous system (CNS) receptors.

3.12.2 Clinical features

Patients present with a cholinergic crisis within 4 hours of exposure, which may include:

Muscarinic effects: Bronchospasm, pinpoint pupils, bradycardia, hypotension, excessive salivation, lacrimation, urination, diarrhea, vomiting, and profuse sweating.
Nicotinic effects: Muscle fasciculations, cramps, weakness, tachycardia, and hypertension.
CNS effects: Delirium, seizures, and coma.
Respiratory failure: The primary cause of mortality in severe OP poisoning due to bronchorrhea and respiratory muscle paralysis.

Toxicity may persist due to irreversible binding of OPs to cholinesterase enzymes, known as “aging.” This process stabilizes the enzyme-inhibitor complex, leading to prolonged symptoms. The “intermediate syndrome” occurs 24–96 hours post-exposure, characterized by cranial nerve involvement, proximal muscle weakness, and variable recovery over days to weeks [78].

3.12.3 Treatment

Medical management requires immediate decontamination, administration of antidotes, and supportive care. Healthcare providers must wear protective clothing to prevent secondary contamination.
Decontamination: Remove contaminated clothing and perform a thorough wash in a designated decontamination area.
Atropine: Acts as a muscarinic antagonist to counteract cholinergic effects. Doses are titrated to the resolution of bronchorrhea.
Oximes (Pralidoxime): Reactivates acetylcholinesterase by cleaving the phosphate bond if administered early, preventing aging of the enzyme.
Respiratory Support: Mechanical ventilation may be required in cases of respiratory failure.
Observation: Patients must be monitored for recurrent toxicity due to lipophilic OP redistribution [79, 80].

4. Conclusion

Managing poisoned patients in the emergency department poses unique challenges due to difficulties in obtaining an accurate history and identifying the specific toxic agent. A structured approach begins with resuscitation, stabilization of the airway, breathing, and circulation, and early decontamination when appropriate.

A thorough physical examination and recognition of toxidromes can aid in diagnosis. Most cases require laboratory tests, including complete blood count, electrolyte panels, kidney function assessments, and specific drug levels. Paracetamol levels should be obtained in all suspected overdose cases.

Symptomatic treatment remains the foundation of toxicology management, supplemented by antidotes in specific poisonings. Coordination with local poison control centers is crucial for up-to-date guidance and advanced interventions.

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[1] 1. Warner M, Chen LH, Makuc DM, et al. Drug Poisoning Deaths in the United States, 1980-2008. NCHS Data Brief, no. 81. Hyattsville, MD: National Center for Health Statistics; 2011

[2] 2. Liu Q, Zhou L, Zheng N, et al. Poisoning deaths in China: Type and prevalence detected at the Tongji forensic medical Center in Hubei. Forensic Science International. 2009;193:88

[3] 3. Erickson TB, Thompson TM, Lu JJ. The approach to the patient with an unknown overdose. Emergency Medicine Clinics of North America. 2007;25:249

[4] 4. Greene S et al. In: Tintinalli JE et al., editors. General Management of Poisoned Patients. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 8e ed. New York, NY: McGraw-Hill; 2016

[5] 5. Mofenson HC, Greensher J. The nontoxic ingestion. Paediatric Clinics of North America. 1970;17(3):583-590

[6] 6. Manoguerra AS, Cobaugh DJ. Guidelines for the Management of Poisoning Consensus Panel: Guideline on the use of ipecac syrup in the out-of-hospital management of ingested poisons. Clinical Toxicology (Philadelphia, Pa.). 2005;43:1

[7] 7. Adams BK, Mann MD, Aboo A, et al. Prolonged gastric emptying half-time and gastric hypomotility after drug overdose. The American Journal of Emergency Medicine. 2004;22:548

[8] 8. Position paper: Whole bowel irrigation. Journal of Toxicology. Clinical Toxicology. 2004;42:843

[9] 9. Bunchorntavakul C, Reddy KR. Acetaminophen-related hepatotoxicity. Clinics in Liver Disease. 2013;17:587

[10] 10. Watson WA, Litovitz TL, Klein-Schwartz W, et al. 2003 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. The American Journal of Emergency Medicine. 2004;22:335

[11] 11. Manyike PT, Kharasch ED, Kalhorn TF, Slattery JT. Contribution of CYP2E1 and CYP3A to acetaminophen reactive metabolite formation. Clinical Pharmacology and Therapeutics. 2000;67:275

[12] 12. Fontana RJ. Acute liver failure including acetaminophen overdose. The Medical Clinics of North America. 2008;92:761

[13] 13. Waring WS, Stephen AF, Malkowska AM, Robinson OD. Acute acetaminophen overdose is associated with dose-dependent hypokalaemia: A prospective study of 331 patients. Basic & Clinical Pharmacology & Toxicology. 2008;102:325

[14] 14. Bernal W et al. Blood lactate as an early predictor outcome in paracetamol-induced acute liver failure: A cohort study. Lancet. 2002;359:558-563

[15] 15. Harrison PM, Wendon JA, Gimson AES, et al. Improvement by acetylcysteine of hemodynamic and oxygen transfort in fulminant hepatic failure. The New England Journal of Medicine. 1991;324:1852-1857

[16] 16. Rumack-Matthew H. Acetaminophen poisoning and toxicity. Pediatrics. 1975;55:871

[17] 17. Mowry JB, Spyker DA, Cantilena LR, McMillan H, Ford M. Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 31th annual report. Clinical Toxicology (Philadelphia, Pa.). 2013;52(1032):2014

[18] 18. Furukawa TA, McGuire H, Barbui C. Meta-analysis of effects and side effects of low dosage tricyclic antidepressants in depression: Systematic review. BMJ. 2002;325:991

[19] 19. Fanoe S, Kristensen D, Fink-Jensena, et al. Risk of arrhythmia induced by psychotropic medications: A proposal for clinical management. European Heart Journal. 2014;35:1306

[20] 20. White N, Litovitz T, Clancy C. Suicidal antidepressant overdoses: A comparative analysis by antidepressant type. Journal of Medical Toxicology. 2008;4:238

[21] 21. Bateman DN. Tricyclic antidepressant poisoning, central nervous system effects and management. Toxicological Reviews. 2005;24:181

[22] 22. ECG Changes in TCA Toxicity; 2024. Available from: https://litfl.com/tricyclic-overdose-sodium-channel-blocker-toxicity/

[23] 23. Teece S, Hogg L. Towards evidence based emergency medicine: Best BETs from the Manchester Royal Infirmary. Glucagon in tricyclic overdose. Emergency Medicine Journal. 2003;20:264

[24] 24. Lo Vecchio F. Cyclic Antidepressants. In: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 8e ed. New York, NY: McGraw-Hill; 2016

[25] 25. Herres J, Ryan D, Salzman M. Delayed salicylate toxicity with undetectable initial levels after large-dose aspirin ingestion. The American Journal of Emergency Medicine. 2009;27:1173.e1

[26] 26. O'Malley GF. Emergency department management of the salicylate-poisoned patient. Emergency Medicine Clinics of North America. 2007;25:333

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