You Have A New Patient!
A 32-year-old male who works as a farmer was brought to the Emergency Department by ambulance following a seizure episode. The patient has no known medical history and does not regularly take medications. According to his co-worker, he had been experiencing nausea and difficulty breathing throughout the day after engaging in crop fertilization work. The paramedic reported finding the patient lying on the ground in a confused state, with drooling and having vomited twice in the ambulance.
Initial vital signs upon assessment revealed a pulse rate of 52 beats per minute, blood pressure of 100/60 mmHg, respiratory rate of 40 breaths per minute, oxygen saturation of 89% on room air, and a temperature of 37°C. The patient’s Glasgow Coma Scale score was 9 out of 15. Upon arrival at the Emergency Department, the patient experienced another seizure episode. Primary assessment revealed excessive secretions in the airway, bilateral chest crepitations upon auscultation, and bowel and bladder incontinence. The patient also presented with pinpoint pupils bilaterally and diaphoretic skin. A quick check of glucose levels showed 110 mg/dL (6.1 mmol/L).
What Do You Need To Know?
Epidemiology
Organophosphates (OP) and carbamates, highly toxic classes of insecticides, were initially developed in the mid-1800s but saw extensive use as nerve agent weapons after World War II. Presently, they find predominant application in agricultural and indoor pest control, placing individuals such as pesticide applicators, manufacturing workers, and farm workers at significant risk of exposure. It is estimated that over 3 million people worldwide experience organophosphate exposure annually, resulting in approximately 300,000 deaths [1]. Examples of organophosphate pesticides include acephate, diazinon, parathion, ethoprophos, malathion…etc.
Importance
While unintentional exposure to organophosphates is not commonly encountered in emergency departments, pesticide poisoning remains a significant contributor to suicides, accounting for one-third of global suicide attempts [2]. The mortality rate associated with organophosphate poisoning rises with increasing lag time from the absorption of the compound [3]. Therefore, prompt recognition and timely management are imperative to prevent death from organophosphate poisoning.
Pathophysiology
Organophosphates
Organophosphates are through various routes, including dermal, respiratory, gastrointestinal, and parenteral pathways. It works through the inhibition of acetylcholinesterase, an enzyme responsible for the breakdown of acetylcholine. This inhibition leads to an excessive accumulation of acetylcholine at the postsynaptic cleft, resulting in overstimulation of cholinergic pathways and subsequent cholinergic toxicity (Figure 1).
Cholinergic overstimulation affects two key sites within the peripheral nervous system: the muscarinic and nicotinic receptors (Figure 2).
Muscarinic receptors are located in tear glands, sweat glands, bronchial secretion glands, and the sinoatrial and atrioventricular nodes of the heart. Stimulation of these muscarinic receptors leads to increased body secretions and cardiorespiratory depression, which will be further discussed in the history section.
Nicotinic receptors, on the other hand, are found at the neuromuscular junctions and adrenal glands. Excessive stimulation of nicotinic receptors can result in a spectrum of manifestations, including muscular fasciculations, profound muscular weakness, and, ultimately, flaccid paralysis due to depolarizing block. Stimulation of nicotinic receptors in the adrenal glands contributes to hypertension, sweating, tachycardia, and increased white blood cells with a left shift [4]. However, as acute intoxication progresses, the effects of muscarinic receptor stimulation predominate, leading to a subsiding of hypertension and tachycardia.
Central nervous system: Due to lipid solubility, organophosphates can cross the blood-brain barrier, leading to central nervous system effects such as confusion, seizures, and coma.
The binding process between organophosphates and acetylcholinesterase occurs in two distinct stages. The first stage is reversible, wherein the antidote can regenerate the acetylcholinesterase enzyme, restoring its normal function. The second stage, known as the “Aging” stage, represents a distinctive characteristic of organophosphate toxicity. During this stage, an irreversible bond is formed between the organophosphate and the enzyme. As a result, the enzyme becomes resistant to reactivation by the antidote.
Carbamates
Carbamates possess a distinct structural composition compared to organophosphates, yet they share a similar mechanism of toxicity. However, carbamates cause trainset cholinesterase inhibition with a duration of toxicity that is typically less than 24 hours. Furthermore, they exhibit poor lipid solubility and demonstrate a reduced ability to traverse the blood-brain barrier compared to organophosphates. As a result, the clinical course of carbamate toxicity tends to be more benign than organophosphate toxicity.
Medical History
Obtaining a detailed history from a patient with suspected organophosphate poisoning might be challenging based on the initial presenting state of the patient. In unconscious patients, collateral history from patient relatives, friends, or emergency responders should be obtained if feasible.
The following are key elements of history that should be obtained:
Route of Exposure
Occupation: Commonly encountered individuals include farm workers or those involved in pesticide manufacturing, who are at the highest risk of exposure to organophosphates through inhalation. Organophosphate molecules readily vaporize, making inhalation an easily accessible route of exposure. Other potential routes of exposure include direct dermal or ocular contact with pesticides. Therefore, it is also important to ask about the use of personal protective measures during work.
Suicidal history: A history of suicidal ideation or previous suicide attempts may provide a clue of intentional ingestion.
Household pesticides: Accidental ingestion, however, is more commonly seen in children and often involves pesticide exposure within the storage areas.
Time to Exposure
Time of exposure significantly influences the clinical manifestations of toxicity. Symptoms can manifest within minutes to hours after exposure. However, manifesting intermediate and delayed neurological complications may take several days to weeks. Therefore, knowing the onset of symptoms aids in determining the potential reversibility of symptoms and the effectiveness of treatment interventions.
Acute Toxicity
Local Toxicity: In the early stages of local toxicity, patients may exhibit a range of seemingly vague symptoms. Inhalational exposure can lead to mucous membrane irritation and chest tightness. Direct skin exposure may cause local skin irritation, sweating, and muscle fasciculations. Ingestion of organophosphorus insecticides and their solvents can irritate the gastrointestinal tract, resulting in burning sensations in the mouth and throat, gastric cramping, vomiting, and diarrhea.
Systemic Toxicity: As systemic cholinergic toxicity develops, patients present with symptoms affecting the central and peripheral nervous systems. Central nervous system manifestations include headache, vertigo, seizures, confusion, and coma. Peripheral nervous system symptoms can be categorized into nicotinic and muscarinic manifestations. The days of the week acronym “MTWThF” is used to recall nicotinic manifestations (Figure 3). Muscarinic manifestations of cholinergic toxicity are represented by the mnemonic “DUMBELS” (Figure 4).
Intermediate Toxicity
Intermediate neurologic symptoms typically occur 24 to 96 hours after exposure [5]. Symptoms include proximal muscle weakness, cranial nerve abnormalities, and respiratory insufficiency. It can last for days or weeks and require ventilatory support.
Delayed Toxicity
Delayed polyneuropathy is rare. It starts 2-3 weeks after exposure and is a mixed type of sensory and motor neuropathy. The lower limbs are predominantly affected, manifesting as stocking-glove paraesthesia, cramping, and flaccid paralysis that progresses from the lower to the upper extremities.
Chronic Toxicity
Because it is lipid soluble, organophosphate can deposit in the adipose tissues at cumulative doses, resulting in chronic neurotoxicity and neuropsychiatric deficits, including confusion, memory impairment, psychosis, and Parkinson ‘s-like syndrome [1].
Medications
Inquire about the recent administration or use of acetylcholinesterase inhibitor medications, such as felbamate, which is used in severe epilepsy; physostigmine and rivastigmine, which are used to treat mild to moderate dementia in Alzheimer’s disease; ophthalmic agents such as echothiopate, sulforaphane, and neostigmine, which are used in myasthenia gravis; and neostigmine, which is used in myasthenia gravis.
Physical Examination
It is important to perform a head-to-toe examination aimed at identifying systemic signs of cholinergic effects, keeping in mind that patients may present with signs of muscarinic or nicotinic predominance or a mixed clinical picture.
Vital signs
Clinical assessment should start with a full set of vital signs, including heart rate, respiratory rate, oxygen saturation, blood pressure, and temperature.
General Appearance
Alertness: The level of consciousness should be assessed, prioritizing immediate attention to unconscious or unstable patients using the ABCDE approach (Airway, Breathing, Circulation, Disability, and Exposure), as discussed in detail in the management section.
Irritability: Look for restlessness, agitation, or confusion, which indicates central neurotoxicity.
Smell: Some organophosphates have distinctive odors resembling garlic or petroleum, which can be detected upon approaching the patient.
Increased secretions: Additional suggestive features include diaphoresis, active emesis, and urinary incontinence.
Respiratory System
Look for signs of respiratory failure or distress. These should be assessed, including tachypnea, oxygen desaturation, cyanosis, increased work of breathing, poor respiratory effort, and fatigue. Auscultation of the chest may reveal wheezing due to bronchospasm or diffuse transmitted sounds and crepitations due to increased respiratory secretions and pulmonary edema, respectively [6].
Cardiovascular System
Check for tachyarrhythmia or bradyarrhythmia associated with inadequate peripheral perfusion. Ideally, these abnormalities should be identified early during the initial assessment of vital signs.
Nervous System
Carefully assess for cranial nerve palsies, muscle weakness, fasciculations, loss of deep tendon reflexes, and sensory deficits. In particular, check for signs of intermediate neurological syndrome.
Gastrointestinal System
Check for signs of excessive gastrointestinal motility, such as generalized abdominal tenderness on palpation or hyperactive bowel sounds on auscultation.
Integumentary System
Sweating, often accompanied by a distinctive odor, can be observed due to muscarinic activation of sweat glands. Excessive secretions, including salivation and tearing, may also be evident. Moist and pale mucous membranes reflect autonomic dysfunction and potential hypoperfusion.
Alternative Diagnoses
The differential diagnosis for poisoning related to acetylcholinesterase inhibitors is relatively narrow, including (1) cholinesterase inhibitors, (2) cholinomimetics, and (3) nicotine alkaloids [7].
Cholinesterase inhibitors: Non-insecticidal medications include pyridostigmine, physostigmine, neostigmine, and echothiopate.
Cholinomimetics: Mushroom toxicity, particularly the Aminata muscaria species, can be categorized as cholinomimetics. Clinical manifestations typically occur within 6-24 hours after ingestion and primarily present with gastrointestinal symptoms. Based on the history of ingestion, it can be relatively identifiable.
Nicotine and nicotine alkaloids: At high doses, these agents can activate muscarinic receptors, resembling or full clinical picture of organophosphate and carbamate toxicity.
Medical conditions: Other conditions include severe gastroenteritis, acute respiratory distress, thyrotoxicosis, sepsis, and neuromuscular disorders like Guillain-Barre, botulism, and amyotrophic lateral sclerosis. However, a thorough clinical evaluation and detailed history-taking can differentiate these medical conditions.
Acing Diagnostic Testing
Organophosphate poisoning is a clinical diagnosis. If there is no obvious history of exposure, a high index of suspicion should be maintained. If patients present with the characteristic toxidrome, empirical treatment with atropine is recommended. If symptoms improve, it strengthens the likelihood of organophosphate poisoning.
Bedside Tests
Electrocardiogram (ECG) and echocardiography should be obtained to evaluate for arrhythmias and myocardial infarction.
Laboratory Tests
Plasma and red blood cell (RBC) cholinesterase concentrations can help evaluate known or suspected exposures to organophosphates. However, these measurements are not readily available in real-time clinical settings. During acute toxicity, plasma cholinesterase levels tend to decrease first. However, in chronic toxicity, low-level exposure may cause plasma enzyme levels to appear normal while RBC cholinesterase levels remain decreased. This discrepancy arises from the longer recovery time needed for RBC cholinesterase, which can take up to 12 weeks to fully recover compared to 4 to 6 weeks for plasma cholinesterase.
Other tests: further laboratory studies should focus on assessing pulmonary, cardiovascular, renal function, and electrolyte balance. Obtaining blood gases is crucial as it allows for the measurement of acid-base status, considering that patients with acidosis have higher mortality rates.
Imaging
Brain computed tomography (CT) can aid in ruling out ischemic or hemorrhagic stroke and other structural brain abnormalities as a cause of the seizure and depressed mental state. Chest X-ray can help assess for the presence of pulmonary edema or aspiration pneumonia in a confused patient with vomiting and compromised respiration.
Risk Stratification
Organophosphate poisoning severity is directly correlated with the quantity, type, and duration of exposure. Mortality rates for organophosphate insecticides range from 2% to 25%. Among the insecticides associated with fatal outcomes, fenitrothion, dichlorvos, malathion, and trichlorfon are the most commonly implicated. Respiratory failure stands as the primary cause of death in these cases [1].
In addition to the aforementioned factors, the Glasgow Coma Scale (GCS) serves as a valuable prognostic tool. In a prospective study including patients acutely poisoned by either organophosphates (OPs) or carbamates, it was observed that an initial GCS score below 13 indicated poor prognosis [7].
Senanayake et al. (1993) introduced the Peradeniya Organophosphorus Poisoning (POP) scale as a valuable prognostic tool for assessing organophosphate (OP) poisoning (Table 1) [8]. This scale evaluates five frequently observed clinical manifestations, each rated on a 3-point scale ranging from 0 to 2. Upon initial presentation, the severity of poisoning is classified as mild (score 0-3), moderate (score 4-7), or severe (score 8-11) based on these assessments.
Parameter | Criteria | Score |
Pupil Size | >2 mm | 0 |
| <2 mm | 1 |
| Pinpoint | 2 |
Respiratory Rate | <20/min | 0 |
| >20/min | 1 |
| >60/min | 2 |
Heart Rate | >60/min | 0 |
| 41–60/min | 1 |
| <40/min | 2 |
Fasciculation | None | 0 |
| Present, generalized/continuous | 1 |
| Both generalized and continuous | 2 |
Level of Consciousness | Conscious and rational | 0 |
| Impaired response to verbal command | 1 |
| No response to verbal command | 2 |
Seizures | Absent | 0 |
| Present | 1 |
Scoring:
- 0–3: Mild poisoning
- 4–7: Moderate poisoning
- 8–11: Severe poisoning
In subsequent validation studies, the POP scale on admission was found to significantly correlate with critical outcomes such as the requirement for ventilator support, the total dose of atropine needed, duration of stay in the intensive care unit, the occurrence of complications, and mortality [9] [10].
Management
The management approach for organophosphate poisoning has around four primary objectives: (1) decontamination, (2) initial stabilization following the ABCDE approach, (3) counteracting the effect of acetylcholine, and (4) reversing the toxin’s binding to the cholinesterase.
Decontamination
Personal protective equipment (PPE): Healthcare providers should utilize PPE as the initial step in managing organophosphate poisoning due to the potential presence of residual toxic substances on the patients. Latex gloves do not offer sufficient protection against insecticides; thus, neoprene or nitrile gloves should instead be used [11].
Skin decontamination: Decontamination involves completely removing and properly disposing all clothing, as residual contamination can persist even after washing. Cleanse the patient’s skin with water, soap, or dry substances such as flour, sand, or bentonite.
GI decontamination: In cases of toxin ingestion, gastrointestinal decontamination procedures and the administration of activated charcoal do not provide significant advantages. This is attributed to the rapid absorption of anticholinergic agents and the occurrence of profuse vomiting and diarrhea early in the ingestion process.
Initial Stabilization
Secure a cardiac monitor, pulse oximeter, blood pressure cuff, and 2 large-bore peripheral vascular access points before initiating medical resuscitation to ensure the efficient administration of medications and fluids.
Airway: The priority is maintaining a clear airway. To prevent obstruction, continuous suctioning of secretions or vomitus should be performed. Early endotracheal intubation is recommended for patients with excessive respiratory secretions, bronchospasm, impaired mental status, or severe skeletal muscle weakness. However, succinylcholine should be avoided during intubation as it is metabolized by acetylcholinesterase, which can lead to prolonged paralysis of 4 to 6 hours.
Breathing: Maintain sufficient ventilation and oxygenation. Target peripheral oxygen saturation (SPO2) > 94%. This is crucial as respiratory failure and hypoxemia are the primary cause of mortality in cholinergic toxicity.
Circulation: Evaluate for the presence of life-threatening arrhythmias, particularly bradycardia. Among the detrimental effects of cholinergic toxicity, bradycardia, bronchospasm, and bronchorrhea are collectively referred to as the “killer Bs” [12]. Tachydysrhythmia, if present, typically resolves as the underlying cholinergic excess is appropriately managed. Therefore, it is not advisable to administer symptomatic treatment with beta-blockers.
Antidote
The definitive treatment for organophosphate poisoning is the intravenous administration of atropine and Pralidoxime.
Atropine is the first-line treatment for cholinergic toxicity. It binds to muscarinic receptors, counteracting the cholinergic effects. In adults, the initial intravenous dose ranges from 2 to 5 mg, while in children, it is administered at a dose of 0.05 to 0.1 mg/kg via intravenous (IV), intramuscular (IM), or subcutaneous (SC) routes, gradually increasing until the adult dosage is achieved. Doses can be doubled every 3 to 5 minutes until “Atropinisation” is achieved, which includes clearing respiratory secretions, resolving bronchoconstriction, maintaining a systolic blood pressure of >80 mmHg, and achieving a heart rate of >80 beats per minute. Once the stabilizing dose is reached, atropine infusion is maintained at a rate of 10–20% of the total cumulative dose per hour.
Mydriasis and tachycardia may occur after atropine administration, but they are not endpoints of therapy and do not contraindicate continued use. However, atropine does not affect nicotinic receptors, limiting its ability to manage neuromuscular dysfunction associated with cholinergic toxicity. Therefore, Pralidoxime should be added to the treatment regimen, ideally within 1 to 2 hours of exposure, before “aging” occurs [13]. This drug has three advantageous effects: detoxifying unbound organophosphates, reactivating acetylcholinesterase, and possessing endogenous anticholinergic properties.
For adults, a bolus dose of at least 1 to 2 grams of pralidoxime should be administered over 30 minutes, with caution to prevent cardiac arrest. For children, the bolus dose is 20 to 50 mg/kg. Following this, a continuous infusion should be initiated, delivering 8 mg/kg/hr for adults and 10 to 20 mg/kg/hr for children. This infusion can continue several days if necessary.
Specific Dosage Summary
Atropine:
- Adult Dose: 2–5 mg IV/IM/SC every 5–30 minutes, with no maximum dose.
- Pediatric Dose: 0.05–0.1 mg/kg IV/IM/SC every 5–30 minutes, followed by infusion at 10–20% of the cumulative dose needed to achieve symptom control.
- Cautions/Comments:
- Tachycardia or mydriasis are not contraindications to continued use.
- Pregnancy Category: C.
Pralidoxime:
- Adult Dose: 1–2 grams IV/IM/SC, followed by an infusion of 8 mg/kg/hr.
- Pediatric Dose: 25–50 mg/kg IV/IM/SC, followed by an infusion of 10–20 mg/kg/hr.
- Frequency: Administered over 1 hour.
- Maximum Dose: 1 gram for pediatric doses; no maximum dose for adults.
- Cautions/Comments:
- Given over 30 minutes to avoid the risk of cardiac arrest.
- Should be administered within 1–2 hours of exposure.
- Pregnancy Category: C.
Supportive Management
Benzodiazepine: Should be administration for patients with low GCS, anxiety, or seizures should be managed with benzodiazepines.
Sodium bicarbonate: For patients with metabolic acidosis despite correction of hypoxia and fluid resuscitation, consider administering sodium bicarbonate. The initial adult dose is 50-100 mmol (1-2 mmol/kg for children), and it may be repeated as needed, guided by arterial blood gas monitoring, aiming for a normal pH.
Special Patient Groups
The principles of managing organophosphate toxicity remain consistent across all age groups, including pregnant patients. However, in individuals who have undergone cardiac transplantation, the use of atropine and other anticholinergic agents is not effective due to heart denervation. In such cases, bradycardia should be managed with sympathomimetic agents such as epinephrine. It is also important to use atropine cautiously in patients with predisposing factors for angle closure glaucoma, as it can precipitate this condition.
When To Admit This Patient
Patients who have had minimal exposure and have been free of symptoms for at least 12 hours can be safely discharged. However, it is crucial to admit and closely monitor individuals with severe symptoms, especially those experiencing acute respiratory compromise accompanied by low cholinesterase levels. Such patients often require admission to the intensive care unit (ICU). For patients who exhibit self-harm or suicidal ideation, psychiatric counseling and admission to a supervised setting with 1:1 observation and mental assessment are necessary.
Discharge instructions: Upon discharge, clear instructions should be provided to patients to avoid further exposure to insecticides and to remain vigilant for the recurrence of respiratory or neurological symptoms. These measures are necessary to promptly identify and manage intermediate syndrome and delayed neuropathy [14].
Revisiting Your Patient
As the patient was actively seizing, he was promptly triaged to the resuscitation bay, connected to a cardiac monitor, pulse oximeter, and blood pressure monitor. The patient was positioned on the left recumbent position to prevent aspiration, oral secretions were suctioned, and oxygen support was provided through a non-rebreather mask. An intravenous administration of 4mg lorazepam was given to control the seizure activity.
Following the cessation of the seizure, a repeat set of vital signs revealed a heart rate of 50 beats per minute, blood pressure of 98/50 mmHg, oxygen saturation of 85%, and a respiratory rate of 10 breaths per minute. Considering the worsening level of consciousness, bradycardia, increased respiratory distress, and the patient’s occupational history on a farm, organophosphate toxicity was suspected, and the patient was prepared for endotracheal intubation to maintain a patent airway and provide adequate ventilation. A bolus of 1L of 9% sodium chloride solution was administered to manage hypotension. Atropine 5mg and pralidoxime 2g were given, followed by an infusion of atropine at a rate of 1mg/hr as definitive management for the suspected cholinergic toxicity. A post-intubation chest X-ray revealed proper endotracheal tube placement and bilateral haziness suggestive of acute respiratory distress syndrome. The electrocardiogram showed sinus bradycardia, which can be explained by the muscarinic effect of cholinergic toxicity. Initial arterial blood gas demonstrated mixed respiratory failure with a pH of 7.25, PCO2 of 56mmHg, PO2 of 60mmHg, and HCO3 of 28meq/L, attributed to pulmonary edema and decreased ventilation.
After the initial stabilization, the patient was fully exposed, and his wet clothes were appropriately disposed of. His diaphoretic skin, with a garlic odor, was cleansed with soap and water. Additional history was obtained from the co-worker, who indicated that the patient has no history of smoking, alcohol consumption, cardiac or pulmonary conditions, seizures, or previous suicidal attempts, which aids in ruling out acute coronary syndrome, pulmonary hypertension, or severe exacerbation of asthma.
Further investigations were initiated to evaluate other potential causes, including intracranial hemorrhage or lesions, sepsis, thyrotoxicosis, and electrolyte imbalances. Brain CT revealed no abnormalities or intracranial bleeding. The white blood cell count showed leucocytosis, while serum electrolyte levels were within the normal range. Procalcitonin levels were unremarkable, further undermining the possibility of sepsis.
Given the provisional diagnosis of organophosphate toxicity, the patient was admitted to the intensive care unit for close monitoring and further management.
Authors
Tasnim Ahmed
Emergency Medicine Residency graduate from Zayed Military Hospital, Abu Dhabi, UAE. Deputy Editor-in-Chief of the Emirates Society of Emergency Medicine (ESEM) newsletter. Senior Board Member and Website Manager of the Emirates Collaboration of Residents in Emergency Medicine (ECREM). Awarded Resident of the Year twice, at ESEM23 and Menatox23. Passionate about medical education, with a focus on blending art and technology into innovative teaching strategies.
Rauda Alnuaimi
Emergency Medicine Department
Zayed Miliraty Hospital, Abu Dhabi, UAE
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Reviewed and Edited By
Jonathan Liow
Jonathan conducts healthcare research in the Emergency Department at Tan Tock Seng Hospital. A graduate of the University at Buffalo with a BA in Psychology and Communication, he initially worked on breast cancer research studies at GIS A*STAR. His research interests focus on integrating AI into healthcare and adopting a multifaceted approach to patient care. In his free time, Jonathan enjoys photography, astronomy, and exploring nature as he seeks to understand our place in the universe. He is also passionate about sports, particularly badminton and football.
James Kwan
James Kwan is the Vice Chair of the Finance Committee for IFEM and a Senior Consultant in the Department of Emergency Medicine at Tan Tock Seng Hospital in Singapore. He holds academic appointments at the Lee Kong Chian School of Medicine, Nanyang Technological University, and the Yong Loo Lin School of Medicine, National University of Singapore. Before relocating to Singapore in 2016, James served as the Academic Head of Emergency Medicine and Lead in Assessment at Western Sydney University's School of Medicine in Australia. Passionate about medical education, he has spearheaded curriculum development for undergraduate and postgraduate programs at both national and international levels. His educational interests focus on assessment and entrustable professional activities, while his clinical expertise includes disaster medicine and trauma management.
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.
