Toxidromes (2024)

by Phalguni Sai Preethi Asapu & Thiagarajan Jaiganesh

You have a new patient!

A 24-year-old male university student was brought into the Resuscitation area of the Emergency department via ambulance after his friends found him collapsed and confused on the floor at a party. His friends tell you that this is not the first time and has happened to him in the past. He has had a history of recreational drug usage in the past. No further history is known. On arrival, you notice that the patient is confused, moves to localized pain, and opens their eyes to speech with GCS 12/15. His vitals T = 36.8. C, BP = 82/74 mmHg, HR = 52 bpm, RR = 8 bpm, O2% saturation = 90% on room air. On a quick examination, you notice that the patient has needle marks like train track appearances. His pupils are pinpoint.

What do you need to know?

Importance

Toxidrome, a term coined by Mofenson and Greensher in 1970, refers to a clinical fingerprint that comprises a specific set of characteristic signs and symptoms. These symptoms arise from neurochemical and autonomic processes triggered by exposure to a particular class of toxins [1]. For physicians, recognizing these toxidromes is crucial for saving lives, as they serve as a valuable tool for the prompt detection and management of toxic exposures. Additionally, this recognition aids in differentiating between toxins that may present similarly.

In this chapter, we will discuss the five major toxidromes: Cholinergic, Anticholinergic, Sympathomimetic, Sedative-Hypnotics, and Opioids. However, a detailed examination of each toxidrome is beyond the scope of this chapter.

Epidemiology

A major cause of morbidity and mortality worldwide is both accidental and intentional poisoning from illicit substances. The second most common presentation involves pediatric patients under 6 years of age with accidental poisoning [2].

The American Association of Poison Control Centers reported over two million human exposure calls in 2018. The rates of poisoning cases presented to the emergency department appear to be increasing annually worldwide, with the majority being adults with intentional overdoses [2].

Studies have shown that the most common classes of drugs involved are analgesics, antidepressants, and opioids [3]. Additionally, accidental poisoning from pharmaceuticals, envenomation, and environmental and occupational exposure from either agricultural or industrial agents are also sources of potential toxicity.

Pathophysiology

Cholinergic Toxicity

This particular toxidrome includes nicotinic toxicity, carbachol methacholine bethanechol or pilocarpine overdose, pyridostigmine toxicity, etc., results from inhibition or binding of acetylcholinesterase causes increased levels of acetylcholine in the synaptic clefts leading to an overstimulation of the parasympathetic portion of the autonomic nervous system which maintains the rest and digest functions. The typical presentation of these types of patients includes fluids coming out of every orifice [4,5].

Anticholinergic Toxicity

Anticholinergic toxidrome is frequently encountered because many pharmaceuticals have antimuscarinic properties with drugs such as diphenhydramine, tricyclic antidepressants, doxylamine, and scopolamine. It inhibits the muscarinic cholinergic neurotransmission, therefore blocking the acetylcholine from binding to the receptors, causing an alteration in the normal homeostatic balance between the sympathetic and parasympathetic arms of the autonomic nervous system. This allows the sympathetic side to function unopposed and generates a state of relative sympathomimetics. Therefore, this toxidrome is very similar to sympathomimetic toxicity [4,5].

Sympathomimetic Toxicity

This Toxidrome is defined by increased catecholamines such as epinephrine, norepinephrine, and dopamine, reducing the catecholamine reuptake in the preganglionic synapse. Simply a sympathomimetic excess leading to a fight or flight reaction. This class includes cocaine, amphetamines, phencyclidine hydrochloride (PCP), and lysergic acid diethylamide (LSD) [4,5].

Sedative Hypnotic Toxicity

This toxidrome is frequently encountered in the ED as it includes ethanol intoxication, hence presenting with sedation, and occurs on a spectrum depending on the particular substance, route, and potency. The pathophysiology typically involves an increase in GABA (gamma-aminobutyric acid) neurotransmission in the case of CNS Depressants and enhanced effects of GABA at GABA-A receptor in the case of benzodiazepines [4,5].

Opioid Toxicity

This toxidrome is similar to sedative/hypnotic toxidrome as it also involves sedation and depressed respiratory drive. Opioids stimulate three receptors Mu, Kappa, and Sigma. Receptors are found all over the central and peripheral nervous system producing effects analgesia by inhibiting the nociceptive information to the brain. Increasing the dopamine from the mesolimbic pathway causes euphoria and causing noradrenergic effects in the locus coeruleus producing anxiolysis [4,5].

Medical History

Although intuitive, history is always the key for identifying the etiologies of poisoning; therefore, focused history is paramount. Often, patients are unable and unreliable to provide history due to their clinical state of being obtunded, confused, uncooperative, or even following intentional ingestion. Hence, history must be procured from paramedics, family members, friends, primary care physicians, medical records, and pharmacists as they can offer an in-site that must be correlated with signs and symptoms, physical examination, and laboratory values [6].

The elements that should be focused on during history taking include the type of substance consumed, timing and quantity of ingestion as the management can vary depending on the timing of presentation to the emergency department, intent, whether it was suicidal or homicidal, to be able to obtain all the medications found at the site since multiple drugs can be ingested at once and if there are any forms of chemical exposure or obtaining a product safety protocol.

Physical Examination

Physical examination of poisoned patients provides invaluable clues regarding the agent involved; namely, vital signs, mental status examination, and pupillary size are useful elements. It is also important to examine the skin and mucus membrane with attention to discoloration, moisture levels, track marks, and ulcerations.

A full neurological examination focusing on motor examination should be performed. The Image below highlights the features each patient presents with toxidromes [6,7]:

Alternative Diagnoses

There is a frequent encounter in which the patient presents with some level of delirium. Excluding pathological causes of altered mental status is important, such as acidosis, encephalopathy, electrolyte abnormalities, infection, uremia, trauma, insulin-related seizures/stroke, and psychosis. Identifying reversible causes, such as hypoglycemia and nutritional deficiencies, is vital. Having broad differentials, including toxicological and non-toxicological causes, is crucial for the management of the patient and helps avoid premature conclusions.

Acing Diagnostic Testing

Diagnostic testing in toxicology is guided by clinical findings and suspected toxins in a patient. The following basic tests can be performed in the ED, depending on the presentation.

Electrocardiogram (ECG)

Provides diagnostic and prognostic information; hence, it should be performed on all patients on arrival.
Keeping an eye out for QT prolongation and widening of QRS interval aids in diagnosis as sodium channel blockers (tricyclic antidepressants, cocaine, carbamazepine) and potassium efflux (most antipsychotics and sotalol), respectively [8].

Toxicology Screens [9-11]

It helps to aid diagnosis, although its use can be limited since drugs such as LSD, mushroom, and mescaline are not part of the panel.
Urine toxicology screens are superior to blood toxicology screens as they are more reliable and have a longer period for positive detection, 24-72 hrs. We need to understand that urine toxicology panel is a qualitative measure, not a quantitative test, and false negatives can occur. Hence, it should not delay therapy.
General toxicology panel coverage:
- Amphetamines
- Cocaine
- Ecstasy
- Methamphetamines
- Opiates
- Phencyclidine
- Marijuana
- Benzodiazepines
- Barbiturates
- Methadone
- Tricyclic antidepressants
- Oxycodone

Serum Acetaminophen and Salicylate levels

Serum acetaminophen and salicylate levels should be measured routinely in all patients with suspected drug overdose or substance abuse, as these are among the most commonly implicated substances in acute poisoning cases [12].

Basic Laboratory Testing

Symptomatic patients and those with an unknown/unreliable history should undergo a complete blood count, urinalysis, serum electrolytes, blood urea nitrogen, creatinine, and glucose as a minimum to rule out any pathological cause before a toxic cause.
In severely ill patients, serum ketones, renal function tests, liver function tests, creatinine kinase, ionized magnesium, and calcium should be measured.
If there is suspicion of toxic alcohol ingestion, then additional tests, such as serum osmolality, can be performed [10].

Arterial and Venous Blood Gas Analysis

Blood gas analysis, both arterial and venous, plays a vital role in the evaluation and management of patients presenting with toxidromes. These analyses provide critical insights into acid-base balance, oxygenation, ventilation, and the metabolic status of the patient, all of which can be profoundly affected by various toxic agents.

Routine Pregnancy Tests

Routine pregnancy testing is recommended for all women of childbearing age presenting with suspected poisoning [10], as pregnancy can significantly influence both the clinical presentation and management of toxic exposures.

Radiological Imaging

This is not of much value except in cases of radiopaque toxins, ingested drug packets, non-cardiogenic pulmonary edema, and acute respiratory syndrome due to exposure to certain toxins [10].

Risk Stratification

Risk stratification is essential in managing patients with toxidromes to prioritize care, allocate resources, and guide treatment decisions. It involves assessing the severity of the toxic exposure, identifying life-threatening symptoms, and evaluating patient-specific factors that may influence outcomes. Key considerations include the type and amount of toxin ingested, the time since exposure, and clinical manifestations such as altered mental status, hemodynamic instability, respiratory compromise, or significant acid-base disturbances. Laboratory findings, such as elevated lactate, anion gap metabolic acidosis, or co-oximetry results, provide additional insights into systemic effects of the toxin. Patient factors such as age, comorbidities, and pregnancy status further impact risk categorization. Stratifying patients into low, moderate, or high-risk categories ensures that those with critical conditions receive immediate interventions, such as airway support or antidotal therapy, while lower-risk patients can be managed with observation or symptomatic care. This systematic approach optimizes outcomes by tailoring interventions to the urgency and severity of each case.

Any patient with significant toxicity along with any of the following should be admitted to the ICU [13,14].

CNS depression, lethargy, coma.
Patients with agitation who require either chemical or physical restraints.
If PCO2 >45 mmHg, hypoxia or respiratory failure, endotracheal intubation.
If the patient’s systolic blood pressure is ≤80 mmHg.
Prolonged or recurring seizures.
On an ECG, if a second or third-degree AV block is present.
On an ECG, presence of non sinus cardiac rhythm.
Any significant acid-base disturbances, such as metabolic acidosis with pH ≤7.2.
Any significant metabolic abnormalities requiring either close monitoring or aggressive correction, such as symptomatic hypoglycemia following sulfonylurea or insulin overdose.
Patients with temperatures are at extremes, such as hyperthermia with T >104°F.
Patients who ingest “toxic time bombs” like Ingested drug packets, sustained-release preparations, and ingestion of quantitative level of the drug have unfavorable outcomes.
If the patient needs invasive hemodynamic monitoring such as pulmonary artery catheter, arterial line, or cardiac pacing.
If the patient requires whole bowel irrigation to enhance GI elimination of the toxin.
If the patient is in need of emergency hemodialysis, hemoperfusion, or hemofiltration.
If the patient requires an emergency antidote that requires close monitoring, such as crotalid antivenin, Digi bind, physostigmine, or naloxone drip.
If the patient experiences ischemic chest pain from toxins, namely cocaine and carbon monoxide.
If the patient is exposed to TCA or other drugs with QRS >120 msec or QTc >500 msec.

Management

Optimal management of a poisoned patient depends on various parameters, including the type of poisoning involved, presenting symptoms, severity, and the time elapsed between exposure and presentation. Resuscitation is a crucial initial step for any poisoned patient coming through the ED. Subsequently, a structured risk assessment should identify patients who would benefit from supportive care, decontamination, antidotes, and enhanced elimination techniques. Further assistance can be obtained from a medical toxicologist. The generalized initial evaluation for all poisoned patients in an ED setting includes the following approach.

Primary Survey [15,16]

A: Airway

Assess whether the airway is patent or obstructed.
If not patent: Perform immediate intubation using rapid sequence intubation with pre-oxygenation and neuromuscular blockade.
- Exception: In cases of suspected opioid overdose, administer naloxone to reverse respiratory depression while ensuring adequate oxygenation and ventilation.
Always rule out hypoglycemia as a potential cause before proceeding with intubation.

B: Breathing

Evaluate respiratory rate (RR), effort, chest expansion, presence of abnormal sounds, and oxygen saturation (SpO₂).
Administer high-flow oxygen to all critically ill patients with suspected overdoses, regardless of SpO₂ levels.

C: Circulation

Assess heart rate (HR), blood pressure (BP), central and peripheral pulses, capillary refill time (CRT), and temperature to evaluate circulatory status.

D: Disability (Neurological Status)

Examine Glasgow Coma Scale (GCS), pupil size, and blood glucose levels.
Once Airway, Breathing, and Circulation (ABC) are secured, focus on neurological stabilization.
The traditional “Coma Cocktail” (dextrose, oxygen, naloxone, thiamine) is no longer recommended as a blanket approach. Instead, each component should be administered selectively based on clinical indications [15].

E: Exposure and Environmental Control

Conduct a thorough external examination, assessing for temperature abnormalities, skin findings, injuries, trauma, or signs of transdermal medication patches and external contaminants.
Remove clothing, external contaminants, and concealed items such as drugs or weapons that might provide clues to the history of poisoning.
Manage temperature extremes:
- Severe Hyperthermia (> 40°C): Requires aggressive treatment with sedation, paralysis, and ice bath cooling [17].
- Severe Hypothermia (< 30°C): Requires rapid rewarming. For unconscious patients who achieve return of spontaneous circulation after cardiac arrest, consider therapeutic hypothermia [17].

Secondary Survey

SAMPLE history should be taken, including site, allergies, medications, past medical conditions, last meal, and event history, which have been discussed in this chapter’s history and physical examination section.
A complete neurological examination should be performed.

Management of Patients Depending on The Toxidrome

The general management of a patient after stabilization involves supportive care, which remains the cornerstone of management, decontamination, and specific antidotal therapy when indicated since they do not exist for every potential poisoning.

Anticholinergic Toxidrome Management [18]

Initial management should focus on evaluating and stabilizing cardiovascular and neurological toxicity. If a patient is agitated or having seizures, administer benzodiazepines (lorazepam or diazepam). On an ECG, if the QRS interval is prolonged >120 msec, depicting sodium channel blockade, then Sodium bicarbonate boluses of 50 mEq can be given in adults.

If a patient with anticholinergic toxicity comes to the Emergency department within 2 hours of ingestion and the patient is cooperative, then consider gastrointestinal tract decontamination with activated charcoal. The most common reason for emergency intervention is when the patient presents with delirium, then an antidote, Physostigmine, should be administered since it reversibly inhibits cholinesterase in both central and peripheral nervous systems, allowing acetylcholine accumulation and competition with the antimuscarinic blocking agent occupying the receptor. Its dosage is 0.5 mg – 1 mg IV over 15 minutes, with a maximum of up to 2 mg in the first hours. If more than 3 doses are required in a span of 6 hours, start IV infusion; 1-2 mg followed by 1mg/hr. Reassess after a 12-hour period. Caution: if QRS >100, Na blockade signs and narrow-angle glaucoma, then Physostigmine are contraindicated.

Disposition [19]

Discharge if the patient has minimal symptoms after 6 hours of observation in the ED.
If the patient has had large ingestions, then observe for up to 24-48 hours, even if asymptomatic.
Admission is required if physostigmine is administered since the half-life of physostigmine is often shorter than the ingested drug).
The patient can be discharged if he remains asymptomatic within 6 hours of the last antidote dose.

Cholinergic Toxidrome Management

The management of patients presenting with cholinergic toxicity is directed towards Decontamination, supportive care, and reversal of acetylcholine excess and toxin binding at receptor sites on cholinesterase molecules.

Decontamination includes using universal PPE (full-face air purifying cartilage mask, eye shield, chemical-resistant suites, boots, nitrile/ butyl rubber gloves) to protect the providers due to the contaminant’s dermal absorption. All clothing is removed by thoroughly flushing the skin with water. Activated charcoal or gastric lavage is of no use.

Stabilization and supportive care, Airway management remain crucial due to the high probability of respiratory failure followed by death. Intubation should be considered with either Rocuronium 1mg/kg or Vecuronium, non-depolarizing paralytic agents, since cholinesterases do not metabolize them. Succinylcholine, which is long used in an emergency setting, should be avoided at all times since it is metabolized by cholinesterase and prolongs the duration of effect around 4-6 hours in this particular setting [20].

Antidote therapy is a definitive treatment aimed at reducing the effects and levels of acetylcholine at various receptor sites. Atropine is one of them, and it acts as a competitive inhibitor of acetylcholine at the muscarinic sites. The dosage includes 0.6 – 1 mg atropine can be given. If severely poisoned, then administer 3mg. If there is no response with the first dose, double the dose after 5 minutes until clinical improvement is observed. Sometimes, it may require prolonged administration, which can be done via infusion. The initial loading doses should be followed by an infusion using 20% per hour of the total bolus dose. Note that the endpoint of atropinization includes drying of respiratory secretions, respiratory effort, and normalizing respiratory rate. The second part includes regenerating the acetylcholinesterase function by using an oxime that binds to the organophosphate-cholinesterase complex, leading to a conformational change that allows cholinesterase to function normally. This can be used if there is respiratory depression or failure, seizures, fasciculations, hemodynamic instability, dysthymias, or large amounts of repeated doses of atropine to completely control the signs and symptoms of this type of poisoning. Commonly used agents are Pralidoxime chloride 1-2 g over 30 minutes followed by a continuous infusion at 0.5 to 1 g/hour for several days. Alternatively, Obidoxime can be given in a loading dose of 4 mg/kg over 20 minutes, followed by an infusion of 0.5 mg/kg/hour. It is usually given as 250 mg loading dose in adults followed by 750 mg every 24 hours [20].

Disposition

If the patient is asymptomatic and has had minimal exposure for at least 12 hours after the ingestion, then the patient can safely be discharged.
If there is any evidence of self-harm, consult psychiatry.

Sympathomimetic Toxidrome Management

Patients with this type of toxicity should first undergo stabilization and supportive care, which includes loading the patient with IV fluids to avoid renal failure secondary to rhabdomyolysis. For decontamination, 50 g of activated charcoal can be used if the patient has ingested the toxin within an hour and their airway is protected. Moreover, Benzodiazepines are the key to managing sympathomimetic toxicities as they provide the cleanest pharmacological approach in treating agitated patients because they act by facilitating the binding of the inhibitory neurotransmitter GABA at various GABA receptors throughout central nervous system, such as 10-20 mg oral or IV diazepam or 1-2 mg lorazepam. If the patient remains agitated and has no respiratory depression, then proceed with further boluses via IV. If Oral or IV are unavailable, consider giving via IM 1-2 mg lorazepam or 5-10 mg Midazolam and repeat as necessary.

Another medication is haloperidol (5-10 mg intramuscular), which blocks the postsynaptic dopamine 2 receptors in the mesolimbic system of the brain. It can be used in agitated patients who are unresponsive to two or more doses of benzodiazepines. Ketamine, an N-methyl-D-aspartate receptor antagonist that induces a dissociative state, is used in the setting of uncontrollable agitation in sympathomimetic toxicity [21, 22].

Disposition

Discharge is no symptoms once symptoms resolve after 6 hours of observation.

Opioid Toxidrome Management

Physicians should prioritize stabilizing the airway, oxygenation, and ventilation. Most opioids are extended-release preparation that decreases gastric motility. Activated charcoal can be used, although discouraged due to lack of sufficient evidence to support its use in opioid poisoning. The key management is the use of Naloxone, a competitive opioid antagonist, therefore reversing opioid intoxication effects. Its use is indicated when a patient experiences significant respiratory or central nervous system effects. In general, starting with lower doses and subsequently increasing the doses as needed to alleviate symptoms is an optimal choice. Doses range from 0.04 – 15mg intravenously; starting dose of 0.04 mg is recommended, followed by titration of the subsequent dosages. It can be given via IV, IM, or SC but is ineffective when given orally due to first-pass metabolism [23].

Disposition

If the patient is on long-acting opioids, then admit to an observation unit.
Consider discharge after 6 hours of observation if the patients are asymptomatic.
Asymptomatic body packers should be admitted until the packets are passed or retrieved.

Sedative/Hypnotic Toxidrome Management

Benzodiazepine Toxicity

Initially, patients need to be stabilized, which includes endotracheal intubation with close respiratory and end-tidal carbon dioxide monitoring when obligated, and should not be delayed by the administration of an antidote. Administer activated charcoal (50 g) only if the patient arrives at the emergency department within one hour of ingestion and the patient’s airway is protected. An antidote that can be administered in these cases is Flumazenil, a nonspecific competitive antagonist at the benzodiazepine receptor site, which reverses benzodiazepine sedation after overdose, procedural sedation, and general anesthesia. It is to be noted that Flumazenil reverses the central nervous system depressant effects more than respiratory depression. Flumazenil is not recommended for routine use in the emergency department [23, 24]. It can precipitate acute withdrawal who are chronically dependent on benzodiazepine, leading to status epilepticus. The decision should be based on balancing risk and benefits and the reliability of the user. The dosage includes 0.2 mg IV over 30 seconds. A second dose of 0.2 mg followed by 0.2 mg at a minute interval to a total of 1 mg [25].

Disposition

Asymptomatic patients, after 4 hours of ED observation, can be discharged.
If there is a deliberate overdose, consult psychiatry.

Barbiturates Overdose

Patients with barbiturate toxicity should initially be stabilized by maintaining the airway (Eg. mechanical ventilation), administering IV fluids and vasopressor to eliminate hypotension (Systolic blood pressure >90 mmHg), and adequate urine output, rewarming measures to annihilate hypothermia. There is no specific antidote for barbiturates overdose. Decontamination with 50 g of activated charcoal can be applied if the patient presents within one hour of ingestion and the airway is secured. Dialysis plays a role as enhanced elimination only in patients ingesting phenobarbital, and who are deteriorating despite aggressive supportive care because routine use of it has limited evidence since phenobarbital is a weak acid, alkalization of the urine increases the amount of drug present in ionized form, therefore, minimizing tubular reabsorption and increases drug clearance [25].

Disposition

Consider discharge if the patient shows improvement in the neurological status and vital signs over 6-8 hours.
If symptoms continue after 6 hours, admit the patient.

Special Patient Groups

There aren’t any significant differences in identifying and managing toxidromes in children, pregnant women, or the geriatric population except for the drug dosages. The clinical features remain the same, and the management involves following primary and secondary surveys followed by supportive care, decontamination, antidotes, and enhanced elimination techniques depending on the toxic syndrome involved.

Revisiting Your Patient

Let’s revisit the case discussed at the beginning of the chapter. A patient presents to the ED

collapse and confused on the floor at a party with a history of drug usage of GCS 12/15.

Vitals shows T = 36.8. C, BP = 82/74, HR = 52, RR = 8, O2 sat = 90 on room air. You notice needle track marks on the skin and pinpoint pupils during quick examination. Discussed below is how one should approach this case.

Connect the patient to the monitors and establish two IV access points, along with a 12-lead ECG, to look for abnormal rhythm patterns.
Maintain a clear airway with adequate ventilation since opioids cause respiratory depression.
Administer Naloxone immediately (Begin with small doses of 0.05 mg IV or 0.1 mg IM when the dependence is possible and ventilation can be maintained, then double the dose until respiratory depression is reversed) since the patient’s consciousness level is impaired. Consider referring the patient to the intensive care unit.
Expose the patient and look for transdermal medication patches or concealed drug packets.
Simultaneously with the resuscitative efforts, Obtain the necessary laboratory investigations, such as CBC, U&Es, glucose, LFTs, and CK, a toxic screen, APAP and salicylate levels, and ABG (metabolic acidosis).
Ensure adequate hydration to maintain a good urine output (0.5 mL/kg/hour) and perfusion.
Check for infection at injection sites and for clinical signs of endocarditis, pneumonia, and pulmonary edema.
Discuss testing for HIV and hepatitis in all patients using intravenous drugs.
The secondary survey obtains a thorough history with a neurological examination of the patient.

Authors

Phalguni Sai Preethi Asapu

Dr. Preethi Asapu, is currently a first-year emergency medicine resident at Tawam Hospital, Al Ain, UAE. She graduated with an MBBS from Ras Al Khaimah Medical and Health Sciences University in 2021 and completed her internship at NMC Royal Hospital, Abu Dhabi, UAE. Dr. Asapu is competent researcher with publications to her name. She has Keen interest in Emergency Medicine and Toxicology.

Thiagarajan Jaiganesh

Dr. Jaiganesh is a Chairman and Consultant in Adult and Pediatric Emergency Medicine and serves as an Adjunct Assistant Professor at UAE University. As the former Director of the Emergency Medicine Residency Program at Tawam Hospital in Al Ain, UAE, Dr. Jaiganesh is dedicated to training the next generation of emergency medicine professionals. With a strong academic and professional background, Dr. Jaiganesh has published numerous peer-reviewed articles on emergency medicine and contributes as a Section Editor and Chapter Author for notable medical texts, including the Oxford Handbook for Medical School. A sought-after speaker, Dr. Jaiganesh has been invited to present at numerous national and international conferences and serves as an instructor in various life support courses. Additionally, Dr. Jaiganesh is an expert in medico-legal and clinical negligence matters, providing valuable insights into complex legal and ethical cases in healthcare.

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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.