Can I Eat This? – A Helpful Guide To Plant Toxicology

Not only is identification of toxic plants from their gross appearance a commonly tested topic in Emergency Medicine Board Exams, it is a necessary skill for doctors operating in institutions where an established Toxicology division does not exist or where the opinion of a specialist in the field is not immediately available.

This is the third part in a series of blog posts dedicated to providing you with original mnemonics and visual aids that serve to highlight a few classes of common toxic plants prominent for both their inclusion in academic assessment as well as their prevalence in the community. These memory tools will attempt to highlight key features in the identification of well-known toxic plant species and are designed to aid clinicians from various regions of the globe as well as hone the skills of aspiring toxicologists.

Picture the Scene

A 67-year-old man, known to have dementia secondary to Alzheimer’s disease, was brought to the Emergency Department with complaints of abdominal pain and 3 episodes of vomiting after being found by his grandson consuming some roots and leaves from a ‘berry-looking plant’ he had found in a local garden. Following the vomiting, the patient was lethargic, diaphoretic and had an ataxic gait, which prompted the family to bring him to the ED.

Upon arrival to the ED, patient looks tired and restless. Vital signs reveal the following:

BP 78/43                   HR 50                           RR 12                           Temp 37.7 C

You start IV fluids, obtain a Point-of-Care venous blood gas and order an ECG and laboratory investigations for the patient. The BP improves slightly up to 80/50, and the venous blood gas shows no significant acid/base disturbance, Sodium of 137 mEq/L, Potassium of 3.7 mEq/L, Hgb of 12.6 g/dL and Lactate 1.4. All other parameters seem to also fall within normal limits. The ECG, however, revealed a widened QRS. As you bring the rhythm strip to your Attending Physician, you hear the patient’s cardiac monitor beep and notice similar, but wider QRS intervals at a faster rate on the screen. You recognize the rhythm as Ventricular Tachycardia.

Recognizing the patient to be in shock with a persistently low blood pressure and a cardiac rhythm of ventricular tachycardia, you decide to perform synchronized electrical cardioversion. After delivery of shock, the patient’s rhythm converts to sinus rhythm. Your Attending Physician arrives with some additional family members who brought with them the berries the patient had reportedly ingested (Figure 1).

Figure 1- Photograph of the berry-like fruit ingested by the patient, identified later as a species of yew

Overview of Taxus Yew Toxicity

The poisonous nature of the Yew (Taxus spp.) has been attributed to taxine alkaloids present in all parts of the plant except the scarlet ‘berry’. The mechanism of toxicity from taxine alkaloids centers on their ability to antagonize sodium as well as calcium channels, primarily acting on cardiac myocytes. [1,2]

While most ingestions are accidental, with non-significant complaints reported, serious fatal outcomes can often be encountered when large amounts of the plant are consumed, usually with suicidal intent. [3]

Typical symptoms post-ingestion range from gastrointestinal complaints such as nausea and abdominal pain, but can easily progress to neurologic complaints of paresthesias and ataxias, along with the dreaded cardiovascular manifestations of bradycardia, conduction delays, wide-complex ventricular dysrhythmias that can cause rapid and fatal instability.

Unfortunately, no specific antidote exists to counter the effect of taxine alkaloids. Ventricular dysrhythmias causing instability are preferably controlled through cardioversion as per ACLS guidelines, though this admittedly treats the effect rather than the cause. [4] Anti-arrhythmic agents have not been shown to have a significant impact on management. Some limited reports show no benefit from hemodialysis,[5] but some promise of Extracorporeal life support with Membrane Oxygenation (ECMO)[6,7] in treating Yew berry poisoning, making management largely reactionary rather than targeted.

Identifying Plants with Sodium Channel Actions

Yew berry (Taxine alkaloid) poisonings can be grouped with other toxic plant species solely due to their common mechanism of action on the sodium channel. Three major plant types that are often encountered in literature are highlighted below:[8]

  1. Aconitum spp., commonly referred to by names such as monkshood, wolfsbane and helmet flower: Contain aconitine and other similar alkaloids that prevent inactivation of voltage-gated sodium channels in cardiac and CNS cells, producing both neurological (paresthesias, weakness, seizures) and cardiovascular (hypotension, bradycardia) effects.
  2. Taxine spp., commonly referred to as Yew plants: Contain taxine alkaloids as highlighted above, with actions of sodium and calcium channel blockade, producing effects primarily on the cardiovascular system, with chances of severe ventricular dysrhythmias and cardiac arrest.
  3. Rhododendron spp., commonly referred to as death camas, azalea and mountain laurel: Contain grayanotoxins that can be concentrated in honey (‘mad honey’), with actions propagated by binding to sodium channels, resulting in sustained depolarization and an increased vagal tone. This results in cardiovascular effects as with the other plants above (bradydysrhythmias, hypotension) as well as symptoms of diaphoresis, hypersalivation and dizziness/syncope.

Plant Identification

As you may notice, all of the above species have two things in common: they all act on the sodium channel and they all can manifest as hypotension and bradydysrhythmia.

Visual identification of these plants can then be made easier by correlating their appearance with the cartoon image below.

References and Further Reading

  1. Wilson, C. R., Sauer, J., & Hooser, S. B. (2001). Taxines: a review of the mechanism and toxicity of yew (Taxus spp.) alkaloids. Toxicon : official journal of the International Society on Toxinology, 39(2-3), 175–185.
  2. Jones, R., Jones, J., Causer, J., Ewins, D., Goenka, N., & Joseph, F. (2011). Yew tree poisoning: a near-fatal lesson from history. Clinical medicine (London, England), 11(2), 173–175.
  3. Labossiere, A. W., & Thompson, D. F. (2018). Clinical Toxicology of Yew Poisoning. The Annals of pharmacotherapy, 52(6), 591–599.
  4. Nelson LS, Shih RD, Balick MJ. Handbook of Poisonous and Injurious Plants. 2nd ed. New York, NY: Springer/New York Botanical Garden; 2007:288-290
  5. Dahlqvist M, Venzin R, König S, et al. Haemodialysis in Taxus baccata poisoning: a case report. QJM. 2012;105(4):359-361.
  6. Panzeri C, Bacis G, Ferri F, et al. Extracorporeal life support in severe Taxus baccata poisoning. Clin Toxicol. 2010;48(5):463-465.
  7. Soumagne N, Chauvet S, Chatellier D, Robert R, Charrière JM, Menu P. Treatment of yew leaf intoxication with extracorporeal circulation. Am J Emerg Med. 2011;29(3):354.e5-6.
  8. Lim, C.S., Aks, S.E. (2017), ‘Chapter 158 – Plants, Mushrooms and Herbal Medications’, Rosen’s emergency medicine 9th edition, Pg. 1957 – 1973
Cite this article as: Mohammad Anzal Rehman, UAE, "Can I Eat This? – A Helpful Guide To Plant Toxicology," in International Emergency Medicine Education Project, August 30, 2021,, date accessed: September 24, 2021

Question Of The Day #47

question of the day

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient presents to the Emergency Department with altered mental status.  This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.


The initial approach to all Emergency Department patients, especially those with abnormal vital signs, should include a primary survey (“ABCs”, or Airway, Breathing, Circulation).  This patient is breathing independently but at a significantly reduced rate and is hypoxic.  Hypoxia should prompt the administration of supplemental oxygen to the patient and reassessment of the SpO2.  The patient’s reduced respiratory rate, lethargy, and bilateral miosis (constricted pupils) should strongly hint at the possibility of opioid overdose.  Although the patient is lethargic and hypoxic, establishing a definitive airway (endotracheal intubation) should be avoided until after the antidote to opioid overdose is administered.  Naloxone is a mu-opioid receptor antagonist and functions as the antidote to opioid overdose.


Administration of 1000mL of 0.9% NaCl (Choice A) is unlikely to fix the patient’s clinical condition.  The patient needs naloxone to improve respiratory status.  25g of IV dextrose (Choice B) would be helpful if this patient’s altered mental status was from hypoglycemia.  A normal glucose level is provided in the question stem.  100mg of IV thiamine (Choice D) may be helpful in the case of Wernicke-Korsakoff Syndrome, a state of thiamine deficiency often associated with malnutrition and alcohol abuse.  Wernicke-Korsakoff Syndrome presents with vision disturbances, ataxia, and confusion.  Typically, this syndrome does not present with severe lethargy or depressed mental status as is seen in this patient.

The best next step in management is 1mg of IV naloxone (Choice C).  If given appropriately, naloxone can prevent the need for intubation.  Naloxone has a very short onset to action (~1min).  If suspicion for opioid overdose is high and there is an inadequate respiratory response after a single naloxone dose, repeat doses of naloxone are appropriate.  Naloxone can be administered in repeat boluses every 3-minutes to a total dose of 10mg IV.  Patients who respond appropriately to naloxone should be observed for recurrent respiratory depression as naloxone is cleared.  Need for repeat doses of naloxone indicates the need for a continuous naloxone infusion and hospital admission.  The typical infusion dose is 2/3 the “wake-up” dose given over 1 hour as a continuous infusion.  For example, if the patient responded to 1mg IV initially, the continuous infusion dose would be 0.6mg/hour of IV naloxone.

Correct Answer: C


Cite this article as: Joseph Ciano, USA, "Question Of The Day #47," in International Emergency Medicine Education Project, July 23, 2021,, date accessed: September 24, 2021

Red lips, black teeth, and Betel nut toxicity

Red lips, black teeth, and Betel nut toxicity

Arecoline toxicity is rarely seen in the Emergency Department [1]; however, doctors and emergency workers should be aware of this plant and the intoxication it causes. The alkaloids associated with this intoxication are reported in multiple regions of the world. It is important to emphasize how arecoline is the fourth most consumed psychoactive substance after nicotine, ethanol, and caffeine.

What is the “Betel nut”?

The tropical Betel palm (Areca catechu) produces the Betel nut (it is not a fruit but the seed of this plant). The Betel nut contains piperidine alkaloids which have substantial psychostimulating effects. Among these alkaloids, arecoline isprimarily responsible for the muscarinic, nicotinic, and psychostimulating effects of Betel nut consumption. Other alkaloids are arecaine, arecolidine, isoguvacin, and guvacine.

Coloured areca nuts [Areca catechu] in the market. Bago, Burma [Myanmar] It is this red color that determines the color of the spits of the people who consume the “paan” (from: LBM1948 – Wikipedia – CC BY-SA 4.0)

What is the “Betel leaf”?

It is the leaf of a tropical liana belonging to the Piperaceae family. It contains phenolic aromatic compounds, such as cavibetol and cavitol, and in some plants, also a third compound called caditene. Also, it, like the paper of a candy, contain chopped Betel nut mixed with lime (calcium hydroxide, which has a preservative action) and other substances typical of the community that produces it (e.g., tobacco, tamarind, or cardamom)

How is Betel nut consumed?

The Betel nut is thinly cut, combined with lime (to extract the alkaloids), and wrapped in a Piper beetle leaf, giving it its aroma and increasing salivation. It is consumed through chewing, which is usually not accompanied by swallowing, instead being spat out.

Photograph of an areca nut vendor on the island of Hainan, China. (from: Rolfmueller – Wikicommons – CC BY-SA 3.0)

Where is Betel nut chewed?

About 200 million people around the world consume Betel nuts. Primarily produced in Southeast Asia (Myanmar, Thailand, Laos, Cambodia, and Taiwan), it is consumed in Southern China (Yunnan, Xingtan, Hainan Island), Ceylon, Micronesia (Saipan, Guam, Palau, Mariana Islands), Papua, New Guinea, the Indian subcontinent (India, Pakistan, Bangladesh), and the Philippines.

New consumption territories are Melanesia, New Zealand, Australia, and immigrants living in Europe and North America [2].

Why is Betel nut consumed?

The consumption of Betel nut is voluptuous, and the reasons given by consumers are many. In general, it is consumed to “stay awake” and therefore “work harder” and the sensation of heat and energy during chewing. The reasons also include supposed medical and health reasons, such as “strengthening the teeth”, “helping digestion”, and “freshening the breath”. The cultural aspect of its consumption should not be underestimated in Buddhist culture and during some marriage ceremonies in Maharashtra. Betel leaf and Areca nut consumption are common. At the same time, in many countries, it is convivial to consume Betel at the end of the meal.

What is arecoline?

It is a potent agonist of muscarinic and nicotinic receptors [3]. In addition, the calcium hydroxide in the product causes the arecoline to be hydrolyzed into arecaidine, which is a potent inhibitor of Gaba uptake. The result is a strong excitation of the nervous system due to the release of catecholamines (adrenaline and noradrenaline). Pregnant women who chewBetel nuts can transfer the active ingredients via the placenta to the fetus [4].

What are the symptoms of acute Arecoline intoxication?

It is a rare event [5].

The psychological acute arecoline intoxication symptoms are:

  • increased heart rate/palpitations
  • increased systemic pressure
  • increased temperature
  • increased sweating
  • increased salivation
  • nausea, vomiting

In some cases, it can lead to coma, respiratory failure, myocardial infarction.Therefore it is recommended that the patient be monitored closely and treated for cholinergic, neurological, cardiovascular, and gastrointestinal manifestations.

The psychological acute arecoline intoxication symptoms are [6]:

  • well-being
  • euphoria
  • increased alertness
  • increased ability to support hard work
  • feeling of heat

From the EEG point of view, we have widespread cortical desynchronization. So, in case of high consumption, psychosis can arise [7].

Woman with red gingivas chewing paan in Don Det in Laos. Paan is a preparation combining betel leaf with areca nut and tobacco. It is chewed for its stimulant and psychoactive effects. (from: Basile Morin, Wikipedia, CC BY-SA 4.0)

What symptoms does chronic arecoline intoxication give?

Chewing Betel nut leads to discoloration of normal dental enamel, similar to that observed in those who chew tobacco (often Tabac and Betel nut are chewed together). The saliva in the chewing of this nut becomes red and with a markedly alkaline pH. The mucous membranes, gums, and teeth take on this color. Consumption is associated with the development of necrotizing ulcerative gingivitis (ANUG), which is a bacterial infection of the periodontal tissue that can also cause systemic symptoms, such as lymphadenopathy and malaise.

What are the risks of chronic exposure to arecoline?

Betel consumers have an increased risk of cancer of the oropharynx, liver, and uterus [8] . Chronic consumption leads to evident stains on the dental enamel (black tartar) and marked red salivation for the release of tannins. Also, its consumption is predisposing for the development of oropharyngeal carcinoma as nitrogenous compounds deriving from the alkaloids are released. About 60% of oro-pharyngeal cancers occur in areas where people chewed Betel nut.


[1] Deng JF, Ger J, Tsai WJ, Kao WF, Yang CC. Acute toxicities of betel nut: rare but probably overlooked events. J Toxicol Clin Toxicol. 2001;39(4):355-60. doi: 10.1081/clt-100105155. PMID: 11527229.

[2] Nelson BS, Heischober B. Betel nut: a common drug used by naturalized citizens from India, Far East Asia, and the South Pacific Islands. Ann Emerg Med. 1999 Aug;34(2):238-43. doi: 10.1016/s0196-0644(99)70239-8. PMID: 10424931.

GHB/GBL overdose in Recreational Settings

GHB/GBL overdose in Recreational Settings

GHB and GBL are two drugs of abuse frequently used as stimulants at parties for various reasons. Acute intoxication quickly leads to coma, respiratory depression, cardiac arrest and death.

One of the usage of these agents is for psychoactive substances in sexual contexts. With respect to jargon, we speak of Party and Play (PNP). Psychoactive substances are taken both recreational purposes and because they reduce self-control and inhibitions, they act as a sexual enhancer. In some cases, gamma hydroxybutyrate/gamma butyrolactone (GHB/GBL) mixed with alcoholic drinks facilitate criminal actions, such as robbery or non-consensual sexual acts (date rape drugs).Use of these drug is not very common in the general population and can be ascribed to distinct user groups[1].

What are the psychoactive substances most used in these parties?

The most frequent psychoactive substances used these parties are usually five:

  • GHB (gamma hydroxybutyrate)
  • GBL (gamma-butyrolactone)
  • Cathinones (Mephedrone, methylenedioxypyrovalerone [MDPV], methylone)
  • Methamphetamine
  • Ketamine

However, concomitant use of other abuse drugs [2], such as cocaine, ethanol, benzodiazepines, cannabinoids, and methamphetamines, can lead to the more significant severity of poisoning caused by GHB/GLB.

What are the effects of GHB?

GHB is a drug used in liquid or powder form. In liquid form, it is a clear, salty, and odorless. GHB is gamma aminobutyric acid (GABA) sodium salt, a molecule present in many body tissues; it is linked to GABA neurotransmitters, which are inhibitory to the neurons to which it binds. It activates its receptors (GHB receptors) and also activates GABA-B receptors [3]. Binding of GHB o to the latter group of receptors leads to a release of dopamine in the brain and causes the depression of the central nervous system (CNS), which can lead to decreased consciousness or unconsciousness, especially when ingested together with other depressants, such as alcohol.

From a pharmacological point of view, GHB has a narrow therapeutic range. At low doses (20–30 mg/kg), it produces a euphoric effect. Higher doses (> 50 mg/kg) provoke a sedative–hypnotic effect, which can further induce coma, bradycardia, and hypoventilation. Absorption into the body is relatively fast (5–15 min.) With a relatively short half-life, the peak of plasma concentrations occurs after 20 to 45 min. The clinical symptoms and the duration of the symptoms are dose-dependent so that it is almost not present in the body after 4 to 6 hours.

Structural formula of GBL
Structural formula of the chemical compound gamma-hydroxybutyrate (from Wikipedia – Neurotiker – Public Domain)
Metabolic pathway of GBL and GHB.
Metabolic pathway of 1,4-butanediol, GBL and GHB. (from Wikipedia-Anypodetos – Public Domain)

What are the effects of GBL?

GBL is a liquid product of the chemical industry. GBL differs from GHB because it has a chemical smell and acid taste, but after ingestion, our body converts GBL to GHB. Compared to GHB, we have seen how GBL has faster absorption, a longer-lasting effect, and higher plasma concentrations. These characteristics indicate quicker absorption and explain how GBL intake rapidly evolves toward an overdose characterized by coma, respiratory depression, cardiac arrest, and death. The pharmacodynamics of GBL are even faster than those of GBH.

2D structure of GBL (from Wikipedia-Harbin – Public Domain)

What are the symptoms of GHB / GBL overdose?

Symptoms of GHB / GBL overdose include several features:

  • Unconsciousness (GCS 3–7)
  • Reduced consciousness (narcolepsy, cataplexy)
  • Psycho-motor agitation
  • Cardio-circulatory problems (bradycardia, hypotension)
  • Respiratory depression
  • Seizures

How to diagnose GHB/GBL overdose?

The diagnosis of acute GBL and GHB intoxication is clinical. The symptoms include two main forms of depression:

  • CNS depression
  • Respiratory depression

GHB/GBL blood or urine tests are not always available in all hospital settings, while diagnostic confirmation through chromatography or mass spectrometry takes several days. Obtaining a patient’s medical history is difficult, if not impossible, due to his/her altered mental state or coma onset. However, the discovery of bottles and participation in a rave/nightclub event can help recreate the events and form the clinical picture.

What to do in front of a patient with a GBL/GHB overdose?

Treatment of the patient suffering from a GBL/GBH overdose is primarily supportive. The patient should be monitored via pulse oximetry, cardiorespiratory monitoring, capnography, and temperature monitoring.

The patient’s airway should be protected and the patient should be managed conservatively (if possible). Ways to treat the airways are highly debated and are currently left to the treating physician’s discretion.  Intubation [4] should be avoided in the patient which he used only GHB as the half-life of this drug is extremely short, and the patient could awaken in 2 to 3 hours. On the other hand, if poly-intoxication is present, the patient is in critical condition, or there is a real risk of aspiration pneumonia, intubation should be performed. It should also be remembered that GBL is a highly inflammatory molecule for the upper respiratory tract tissues.

Atropine or catecholamines if the perfusion is not adequate should be used, but this event is rare in these patients.Moreover, the onset of the withdrawal symptoms [5] such as anxiety, insomnia, tremors, tachycardia, agitation, delirium, and hallucinations should be monitored and treated with benzodiazepines and muscle relaxants [6].

What are the other risks?

Patients who inject drugs via the intravenous route should be informed of the risk of contracting infectious diseases [7], such as human immunodeficiency virus, hepatitis C and B viruses (HIV, HCV, and HBV, respectively). Those on retroviral therapy should be notified that these agents decrease the effectiveness of antiretroviral drugs [8].

The patient should be informed that taking GBL/GHB with other drugs can lead to severe and potentially fatal conditions. It should be remembered that GHB and cocaine mixed with alcohol react by forming toxic metabolites, such as cocaethylene, or that GHB and opioids can lead to coma and death.

The patient who is dependent on GHB should be informed about the onset of withdrawal symptoms, which is of rapid onset and progression and can often be fatal as hallucinatory, delusional, upon sudden drug cessation. Epileptic seizures can occur and can endanger a patient’s life. Planning for reductions in GHB/GBL use before stopping altogether can reduce withdrawal symptoms and make them less severe. If a person is  a regular user of one or more of these drugs, a doctor should be consulted before discontinuing use as sudden withdrawal can be life-threatening. Also, withdrawal symptoms can last up to 15 days.

Useful links

References and Further Reading

  1. Tomkins A, Ahmad S, Cannon L, Higgins SP, Kliner M, Kolyva A, Ward C, Vivancos R. Prevalence of recreational drug use reported by men who have sex with men attending sexual health clinics in Manchester, UK. Int J STD AIDS. 2018 Mar;29(4):350-356. doi: 10.1177/0956462417725638. Epub 2017 Aug 23. PMID: 28835196.
  2. Madah-Amiri, D., Myrmel, L. & Brattebø, G. Intoxication with GHB/GBL: characteristics and trends from ambulance-attended overdoses. Scand J Trauma Resusc Emerg Med 25, 98 (2017).
  3. Le JK, Richards JR. Gamma-Hydroxybutyrate Toxicity. [Updated 2020 Oct 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
  4. P Dietze, D Horyniak, P Agius, V Munir, de Villiers Smit, J Johnston, C L Fry, L Degenhardt. Effect of intubation for gamma-hydroxybutyric acid overdose on emergency department length of stay and hospital admission Acad Emerg Med2014 Nov;21(11):1226-31
  5. Wojtowicz JM, Yarema MC, Wax PM. Withdrawal from gamma-hydroxybutyrate, 1,4-butanediol and gamma-butyrolactone: a case report and systematic review. CJEM 2008; 10:69–74
  6. Cappetta M, Murnion BP. Inpatient management of gamma-hydroxybutyrate withdrawal. Australas Psychiatry. 2019 Jun;27(3):284-287. doi: 10.1177/1039856218822748. Epub 2019 Jan 17. PMID: 30652947.
  7. Sewell, Janey et al. Poly drug use, chemsex drug use, and associations with sexual risk behaviour in HIV-negative men who have sex with men attending sexual health clinics. International Journal of Drug Policy 43, 33–43, 2017
  8. Pufall, EL et al. Sexualized drug use (‘chemsex’) and high-risk sexual behaviours in HIV-positive men who have sex with men, HIV medicine 19.4, pp. 261–270, 2018
Cite this article as: Francesco Adami, Italy, "GHB/GBL overdose in Recreational Settings," in International Emergency Medicine Education Project, April 12, 2021,, date accessed: September 24, 2021

Organophosphate poisoning

Organophosphate poisoning


  • Organophosphate compounds can be commonly found in insecticides and are associated with systemic illness.
  • Mortality is higher in developing countries where organophosphate pesticides are more commonly available.
  • Organophosphorus poisoning can result from occupational, accidental, or intentional exposure.
  • Its use as a suicidal agent is frequent.
  • The primary cause of death in acute organophosphate poisoning is bradyasystolic arrest from respiratory failure.


Organophosphate compounds bind irreversibly to acetylcholinesterase inactivating the enzyme through the process of phosphorylation and acetylcholine at nerve synapses and neuromuscular junctions. Thus, it results in overstimulation of acetylcholine receptors.

Clinical presentation

Here are a few mnemonics for the Muscarinic Effects of Cholinesterase Inhibition: SLUDGE, DUMBELS, and Killer B’s (Figure 1 & 2).

Killer B's
  • Out of four distinct syndromes that can occur from organophosphate poisoning, the first two are clinically important in emergency setting 1. Acute poisoning, 2.intermediate syndrome, 3.chronic toxicity, and 4.organophosphate induced delayed neuropathy. Of these syndromes, the intermediate syndrome is the most feared one as it presents with paralysis of the neck’s flexor muscles, muscles innervated by the cranial nerves, proximal limb muscles, and respiratory muscles. It occurs up to 40% of poisonings within 1 to 5 days of initial symptoms.
  • Acute organophosphate poisoning can present with differing severities. Mild poisonings generally present with symptoms like lightheadedness, nausea, headache, dyspnea, lacrimation, rhinorrhea, salivation, and diaphoresis while moderate poisonings cause autonomic instability, confusion, vomiting, muscle spasms, bronchorrhea and bronchospasm. Coma, seizures, flaccid paralysis, urinary and fecal incontinence, and respiratory arrest may occur in the course of severe poisonings.
  • Diagnosis is based on history (people may bring bottles/substance itself) in the presence of a suggestive toxidrome. Cholinesterase assays and reference laboratory testing for specific compounds may confirm the diagnosis but take time and have limitations. Treatment should be started without delay based on the clinical findings.
  • Miosis (papillary constriction) and muscle fasciculation are the most reliable signs of organophosphate toxicity and help in diagnosis.


  • The first step of the treatment is decontamination. Healthcare workers must wear protective equipment to avoid secondary poisoning. The patient should be decontaminated with ample water and soap preferably before arriving in a hospital or once stable. Water should be disposed of as hazardous waste.
  • In addition to decontamination, treatment consists of airway control, intensive respiratory support, general supportive measures, prevention of absorption, and the administration of antidotes.
  • The patient should be monitored continuously and provided 100% oxygen. Gastric lavage and activated charcoal are not recommended.
  • A non-depolarizing agent should be used when the neuromuscular blockade is needed during intubation since succinylcholine is metabolized by plasma butyrylcholinesterase, and therefore, may prolong paralysis.
  • The specific agents are atropine and Atropine can be given repeatedly every 5 minutes until tracheobronchial secretions attenuate (1-3 mg IV in adults or 0.01-0.04 mg/kg IV in children – never <0.1 mg per dose). Then, a continuous infusion should be started to maintain the anticholinergic state (0.4-4 mg/h in adults).
  • Pralidoxime is the single most important treatment for the nicotinic effect of organophosphate poisoning and is life-saving for intermediate syndrome if used within 48 hours (First dose: 1-2 g in adults or 20-40 mg/kg – up to 1 g – in children, mixed with NS and infused over 5-10 min, continuous infusion: 500 mg/h in adults or 5-10 mg/kg/h in children)
  • Seizures can be treated with benzodiazepines.

Disposition and follow-up

  • Minimal exposures may require only decontamination and 6 to 8 hours of observation in the ED to detect delayed effects.
  • Admission to the intensive care unit is necessary for significant poisonings.
  • Most patients respond to pralidoxime therapy with an increase in acetylcholinesterase levels within 48 hours.
  • The endpoint of therapy is the absence of signs and symptoms after withholding pralidoxime therapy.
  • Death from organophosphate poisoning usually occurs in 24 hours in untreated patients, usually from respiratory failure secondary to paralysis of respiratory muscles, neurologic depression, or bronchorrhea.

References and Further Reading

  1. Burillo-Putze, G. & Xarau S. N. “Pesticides. Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, Meckler GD, Cline DM, editors. Tintinalli’s emergency medicine: a comprehensive study guide 8th ed.” (2016): 1318-25.
  2. Katz K. D. & Brooks D. E. “Organophosphate Toxicity Treatment & Management” Medscape, Dec 31, 2020, Accessed Feb 05, 2021.
Cite this article as: Temesgen Beyene, Ethiopia, "Organophosphate poisoning," in International Emergency Medicine Education Project, March 29, 2021,, date accessed: September 24, 2021

Snakebite: Two years and 200 cases later


We practice as independent doctors right after MBBS in Nepal. One of my professors used to say, “One day, you will sleep as a medical student and wake up as a doctor.” What that meant for me was, after I graduate from medical school, I’d pack my bags and head towards a rural village to “save lives.” Like any other life transitions, this one felt unchartered, unknown, and scary. I felt severely underprepared. As time passed by, I started appreciating my internship year. We have a year of internship after MBBS at the teaching hospital where we work as a junior doctor. At Beltar—my workplace, I’d remember how the patient with enteric fever was managed back home, brush up on the details with a quick read in UptoDate, and play doctor.

"One day, you will sleep as a medical student and wake up as a doctor." What that meant for me was, after I graduate from medical school, I'd pack my bags and head towards a rural village to "save lives." Like any other life transitions, this one felt unchartered, unknown, and scary. I felt severely underprepared.

The general structure of how I practiced medicine was; model what my professors used to do, read up on what is new/has changed, and treat patients. One day, some people carried a young child with droopy eyes, flappy tongue, and drowning in his saliva to the PHC. “He was bit by this snake!” The man with tearful eyes was holding on to a dead brown snake. Do you see a problem there? My go-to structure for practicing medicine crumbled. Underprepared would be an understatement. We were lucky that a team of trained armies helped set up the snake bite center in the PHC.

As some months passed by, I started feeling somewhat competent in managing snakebite cases. Any lesson you learn in medicine is a work in progress, but here are some I can recall:

The oversimplified version of snakebite treatment is–give antivenom and wait. In my experience, what we do while waiting, matters a lot. The neurotoxin that makes the patient paralyzed does not shut his brain down. He can listen and see, and we can use that to our advantage. Tell him what you are doing. Let him know what to expect. Talk to him. Open his eyes and make him see his loved ones are nearby. Make him believe that people are working hard to help him.

Amid scrutinized protocols, results of giant multi-center RCTs, and excellent well-formatted articles, it is easy to forget that what we do is taking care of a patient—the most basic of human skills. “LATERAL RECUMBENT!” I found myself shouting out of instinct. The patient was drowning in his saliva. My team tried hard to protect the patient’s airway as per protocol by extending his neck. But the patient was having a hard time breathing due to secretions. Sure we could not use the suction; unreliable electricity supply, broken suction machine, lack of funding, and whatnot, but we could still care. Use your mirror neurons; what would you want people to do if you were where the patient is?

Timely referral can be the difference between life and death. Understand the limitations of where you are working. Do you have a properly functioning suction? How reliable is your electricity? Do you have a ventilator? How far would you have to send the patient to get one? Manage your internal alarm accordingly. For us, the only respiratory support was a bag valve mask, and the transport to the nearest facility with a ventilator was at least 2 hours. Knowing that helps you be acceptably anxious and make informed decisions.

There is no substitution for empathetic yet informative communication with the patient and their loved ones. Clarify your assessment, plan, and signs that will prompt you to refer the patient. Talk to the anxious patient parties in a supportive tone but tell them that antivenom has ADRs, probably more than most drugs you use. When working in rural, especially in high-risk cases like snakebite, keeping the patient and their caretakers informed should be a priority.

Talk about ways to prevent snake bites. These beautiful creatures aren’t violent. Be interested in how the patient was bitten. After a while, you will start recognizing a pattern that you can use to educate the target population. Also, not everyone comes with the snake to the hospital. Have a poster of different types of snakes available. Identifying if the snake was venomous is one of the initial steps, after all. Print the local and national statistics about antivenom use and results and paste them in the waiting area. It will help patient parties calibrate their expectations accordingly.

A visual poster of common snakes found in Nepal placed at the entrance of Snakebite Treatment Center.

Summer and rainy seasons are when the unfortunate encounters between humans and snakes happen. It is easy to forget the snakebite management protocol, equipment necessary, what workarounds were used to help us, and what drugs we have in stock. A small refresher session can go a long way in boosting your team’s confidence in treating snakebites.

Snakebite Management Protocol posted in treatment center.
Logistics arranged for snakebite management.
Cite this article as: Carmina Shrestha, Nepal, "Snakebite: Two years and 200 cases later," in International Emergency Medicine Education Project, February 1, 2021,, date accessed: September 24, 2021

Recent blog posts by Carmina Shrestha

The toxic honey that destroyed several armies

The toxic honey that destroyed several armies

Ingestion of “mad honey” causes severe hypotension and bradycardia. Let us learn about the intoxication given by the grayanotoxin family.

In Italian, there is a literary expression known as: “losing the Trebizond,” which means losing control, feeling confused and disoriented. Trebizond was an important port on the southern coast of the Black Sea, where the maritime lighthouse was strategically located for sailors, especially the Venetians, whose colonial rule extended from the coasts of western Greece to the straits of the Dardanelles and the Bosporus. In the province of this seaside town, a type of honey produced disorientation, confusion, and fainting. We then explored why it is called “mad honey.”

Panoramic view of the city of Trabzon and its port on the Black Sea (from Wikipedia – Nezih Durmazlar – Flickr: Panoromik Trabzon – CC BY-SA 2.0)

What is meant when we talk about “mad honey?

“Mad honey” is toxic, and is from the nectar of various species of rhododendron, in particular Rhodendrum ponticum and Rhododendrum luteum. These plants are largely found in Turkey (in the Black Sea area near the city of Trebizond), but are also in Japan, Nepal (especially in the area where the Gurung people live), and Brazil. This honey, made by local bees, is called “mad,” because it contains several toxins of the grayanotoxin family (GTX). GTXs belong to liposoluble diterpenoids [1]; similar to veratridine, aconitine, and batrachotoxin, they are known for poisoning and killing livestock.

Rhododednrum luteum (from Wikipedia – Chrumps – CC BY 3.)
Rhododendron ponticum (from Wikipedia – Ragnhild&Neil Crawford – CC BY-SA 2.0)

Why did this honey undermine two armies?

In 401 BC, the Greek general Xenophon described one of the first intoxications with this honey, which affected over 10,000 men of his army:

“For the most part, there was nothing which they found strange; but there were numerous swarms of bees in the neighbourhood, and soldiers who ate it went out of their heads,suffering from vomiting and diarrhea: not one of them could stand up, but those who had eaten a little were like very drunk people, while those who had eaten a lot seemed like crazy, or in some cases, dying men.”

(Anabasis 4.8.20)

In 67 BC, another case of intoxication was described by the Roman general, Pompey the Great. His retreating troops were the protagonists of the first bioweapon case in history. Their adversary, King Mithridates, deliberately placed combs of mad honey in the path of the advancing Romans, staging a strategic withdrawal. The Roman troops were so weakened (from intoxication), that they were defeated by Mithridates’ army. In 946 AD, Queen Olga of Kiev massacred over 5,000 Drevians, who rushed to her husband’s funeral using mad honey as poison; in 1489 AC, about 10,000 Tatar soldiers were killed after drinking too many flasks of mead, who were purposely abandoned by the Russian soldiers. In the past, however, the mad honey was also used as a drug. Aristotle [2], Dioscorides [3], and Pliny the Elder [4] had described the therapeutic properties of this honey

The statue of Xenophon is located near the Greek Parliament. (from Wikipedia – Wienwiki / Walter Maderbacher – CC BY-SA 3.0)

Is mad honey still used today?

“Mad honey” is still sold today in an unprocessed form in rural markets, under the Turkish name “DELI BAL.” In fact, studies and clinical cases on GTX intoxication come from the Trabzon province (more widely, from Turkey [5] where the honey is used not only as a food, but in folk medicine as a sexual stimulant [6], antihypertensive [7], and hypoglycemic drug. Other uses of this honey in folk medicine were to treat peptic ulcer, abdominal pain, indigestion, flu, and arthritis.

How long does it take from ingestion to onset of symptoms?

On average, symptoms appear about one to two hours after ingestion. The average quantity for symptoms is varied (people report from 1 to 5 tablespoons, so it is estimated as 5 to 180 g). Given that the diffusion of grayanotoxins is not uniform in honey, we should think of this data as not highly predictive [8]: we note that the severity of symptoms also depends on other factors, such as the quantity of toxin ingested, the body’s sensitivity to it, and when the honey was produced.

What are the most common symptoms of intoxication with mad honey?

The symptoms would usually be:

  • nausea and vomiting
  • profuse sweating
  • blurred vision
  • hypersalivation
  • prostration
  • bradycardia
  • severe hypotension
  • syncope

For a more complete history for reaching the diagnosis of mad honey intoxication, it was helpful to ask a patient if he traveled to areas where it existed if he has ingested it, the reason for that (for pharmacological purposes, this question helps us understand if a patient is suffering from certain diseases, such as hypertension or diabetes), and where this mad honey was bought.

Are there any electrocardiographic changes?

Electrocardiographic changes such as sinus bradycardia and atrioventricular blocks [9] of varying degrees (I-III) are frequently found. It would appear that the GTXs act by dysregulating the voltage-dependent sodium channels in the nervous system, which are activated in a permanent state of depolarization [10]. Continued activation of these cells causes bradycardia, respiratory depression, hypotension, and loss of consciousness [11].

Voltage-gated sodium channel with group II receptor site domains highlighted in red. (from Wikipedia -Cthuljew – CC BY-SA 3.0)
The patient’s initial electrocardiography (ECG) findings upon arrival to the emergency department consistent with third-degree atrioventricular block. This finding prompted consultation of the cardiology service for treatment guidance and is a common manifestation of grayanotoxin ingestion. (from JACC: CASE REPORTS – – CC BY-NC-ND 4.0)

What therapeutic approach should be adopted?

  • Monitor vital and cardiac parameters.
  • Support therapy with intravenous crystalloid fluid (normal saline solution).
  • Use atropine sulfate at a moderate dose from 0.5 to 2 mg intravenously to resolve marked hypotension and respiratory depression.
  • Vasopressors or pacemakers if/when the rhythm is not restored.

We should consider achieving a normal heart rate and normal blood pressure values as therapeutic goals. Once these goals are achieved, the patient should be kept for a short period of observation in the emergency department – and if no other problems arise, he can be safely discharged [12, 13]. Furthermore, I would like to emphasize that grayanotoxin metabolism and excretion take place within 24 hours, and thus the symptoms last no more than a day.

What is the take-home message?

In patients with bradycardia and hypotension of unexplained origin, this type of intoxication should be considered especially in middle-aged males who have probably taken mad honey as a sexual stimulant.


References and Further Reading

[1] Jansen SA, Kleerekooper I, Hofman ZLM et al (2012) Grayanotoxin Poisoning: ‘Mad Honey Disease’ and Beyond. Cardiovasc Toxicol 12:208–215.

[2] Aristotle (1936) De mirabilius auscultationibus. Aristotle Minor Works on Marvelous Things Heard. Loeb, Cambridge, p. 245.

[3] Dioscorides (2000) De materia medica. Ibidis Press, Johannesburg, p. 226.

[4] Mayer A (1995) Mad honey. Archaeology 46(6):32–40.

[5] Sibel Silici A, Timucin A (2015) Mad honey intoxication: A systematic review on the 1199 cases. Food Chem Toxicol 86:282-290.

[6] Demircan A, Keleş A, Bildik F, Aygencel G, Doğan NO, Gómez HF (2009) Mad honey sex: therapeutic misadventures from an ancient biological weapon. Ann Emerg Med 54(6):824-829. doi: 10.1016/j.annemergmed.2009.06.010

[7] Hanson JR (2016) From ‘mad honey’ to hypotensive agents, the grayanoid diterpenes. Sci Prog 99(3):327-334. doi: 10.3184/003685016X14720691270831

[8] Aygun A, Sahin A, Karaca Y, Turkmen S, Turedi S, Ahn SY, Kim S, Gunduz A (2017) Grayanotoxin levels in blood, urine and honey and their association with clinical status in patients with mad honey intoxication. Turk J Emerg Med 18(1):29-33. doi: 10.1016/j.tjem.2017.05.001

[9] Cagli KE, Tufekcioglu O, Sen N, Aras D, Topaloglu S, Basar N, Pehlivan S (2009). Atrioventricular block induced by mad-honey intoxication: confirmation of diagnosis by pollen analysis. Tex Heart Inst J 36(4):342-344.

[10] Gunduz A, Tatli O, Turedi S (2008). Mad honey poisoning from the past to the present. Turk J Emerg Med 8:46-49.

[11] Sana U, Tawfik AS, Shah F (2018) Mad honey: uses, intoxicating/poisoning effects, diagnosis, and treatment. RSC Adv 8:18635-18646.

[12] Gündüz A, Meriçé ES, Baydin A, Topbas M, Uzun H, Türedi S, Kalkan A (2009) Does mad honey poisoning require hospital admission? Am J Emerg Med 27:424-427.

[13] Yaylacı S, Ayyıldız O, Aydın E, Osken A, Karahalil F, Varım C, Demir MV, Genç AB, Sahinkus S, Can Y, Kocayigit İ, Bilir C (2015) Is there a difference in mad honey poisoning between geriatric and non-geriatric patient groups? Eur Rev Med Pharmacol Sci 19(23):4647-4653.

Cite this article as: Francesco Adami, Italy, "The toxic honey that destroyed several armies," in International Emergency Medicine Education Project, January 25, 2021,, date accessed: September 24, 2021

Local Anaesthetic Toxicity (LAST)

Local Anesthetic Toxicity (LAST)

Think about the number of times a month you use a local anaesthetic; maybe not every day, but I know there are a lot of emergency department shifts when I use a local anaesthetic. The uses and applications for local anaesthesia abound: wound care and laceration closure, pain control with painful procedures like a paracentesis or lumbar puncture, and targeted regional anaesthesia blocks after a broken hip. It is important to know and understand a bit more about this commonly used class of drug given how often we use them in emergency medicine, including the recommended dosing, signs of toxicity, and treatment of toxicity.

Local anaesthetics fall into two divisions, based on their chemical structure:

  • the Esters (have one i): procaine, cocaine, tetracaine, chloroprocaine, etc
  • the Amides (have two i’s): lidocaine, bupivacaine, mepivacaine, prilocaine, ropivacaine, etc


These drugs have their effect as sodium-channel blocking medications with variable durations of action. Interestingly, 1% diphenhydramine has also been used as a local anaesthetic since the 1930s, given its sodium channel blocking mechanism. Local anaesthetics can be administered with other drugs, namely epinephrine, to help increase the duration of action and minimize the spread of the anaesthetic from the site of injection.

Maximum Dose

The safe maximal dose for the local anaesthetics is based on patient weight and correlates to the risk of systemic toxicity. The maximally safe dose of two common local anaesthetics is detailed below, and as you can see, the use of epinephrine allows for an increased dose of local anaesthetic injection.

Max dose without Epi Max dose with Epi Duration of Action
4.5 mg/kg
7 mg/kg
0.5 - 1.5 hours
3 mg/kg
3 mg/kg
6-8 hours

Usage abd Absorbtion

Absorption into the bloodstream of a local anaesthetic can occur when the drug is injected directly into the bloodstream. Still, it can also occur in highly vascular areas or near neurovascular bundles in locations such as intracostal, epidural, and the brachial plexus. Local anaesthetic systemic toxicity (LAST) occurs when there are elevated circulating levels of local anaesthetic and occurs within minutes of injection. As you may know, lidocaine is used intravenously as an antiarrhythmic drug, and cocaine when used (or abused) systemically can cause numerous systemic effects and a sympathomimetic toxidrome. Bupivacaine is the most commonly discussed cause of LAST, and extra care should be taken when utilizing this for local anaesthesia.

Sign and Symptoms of LAST

Signs and symptoms of LAST predominate in the central nervous system and the cardiovascular system. CNS symptoms can include oral/perioral numbness, paresthesia, restlessness, tinnitus, fasciculations/tremors, seizures, decreased level of consciousness, and/or apnea. Cardiovascular symptoms can include: hypertension and tachycardia though more commonly vasodilation and hypotension, sinus bradycardia, AV blocs, conduction defects (notably: long PR and QRS), ventricular dysrhythmias, cardiovascular collapse, and/or cardiac arrest.

The differential diagnosis for LAST includes anaphylaxis (rare with amides), other sodium channel blockers (antihistamines, TCAs, cocaine, antimalarials), and anxiety. However, the timing nearly immediately following local anaesthetic administration should help one to hone in on the diagnosis.


If a patient develops LAST, ACLS protocols should be followed. Furthermore, lipid emulsion (Intralipid) is the treatment that will help bind the anaesthetic in the bloodstream. While this medication is not on the WHO essential medication list, in a patient with LAST, Intralipid should be administered if available. Dosing is a 1.5 mL/kg bolus (standard dose of 100mL for 70kg patient), followed by a 0.25-0.5 mL/kg/min infusion until the patient is hemodynamically stable (and for at least 10 minutes).

How To Decrease Risk of LAST

A few strategies to minimizing the risk of causing harm to your patients when using local anaesthetics: 
  • know the maximum dose your patient can receive
  • know the dose you’re giving by dose (milligrams) and how that correlates to drug volume (mg/mL)
  • aspirate prior to injection(s) to ensure you are not in a blood vessel
  • consider using point of care ultrasound to ensure needle location

References and Further Reading

Cite this article as: J. Austin Lee, USA, "Local Anaesthetic Toxicity (LAST)," in International Emergency Medicine Education Project, November 23, 2020,, date accessed: September 24, 2021

More Posts By Dr. Lee

Giant Hogweed Burns

Giant Hogweed…and the Lesions it Causes.

Summer is the time when outdoor work and leisure activities increase. It is also the season when plants like giant hogweed grow and bloom most. Direct contact with this beautiful umbrella plant, however, leads to serious skin lesions and skin burns[1] that often necessitates a visit to the emergency room.

Have you ever heard of the giant hogweed?

The giant hogweed is an extremely toxic exotic plant particularly present in the British popular culture. It is also mentioned in the 1971 studio album entitled “Nursery Cryme” by the English rock band Genesis where the eternal struggle between this exotic plant and the English authorities trying to eradicate it is (humorously) narrated. Historically this plant was rediscovered in 1895 by two Italian doctors: Emile Levier and Carlo Pietro Stefano Sommier, to which they gave the botanical name of Heracleum mantegazzanium, in honour of their friend and physician Paolo Mantegazza, the first popularizer of Darwin’s scientific theories in Italy.

How can you recognize giant hogweed?

Giant hogweed, also known as Heracleum mantegazzianum, is considered to be the largest and most beautiful umbrella plant in the world[2]; it can reach a height of over 3 meters[3]. It is recognizable due to the colour of its leaves, which are a bright light green colour tending towards yellow with deep lobes and segmentations. The trunk is very thick and robust, similar to that of artichoke, with dark red streaks and surrounded by spiky hairs. The diameter of the umbrella makes it the largest among the umbrella plants. 

The fruits have an ovoid appearance, and at the moment of flowering, their envelopes remain attached to the base of the umbrella and subsequently tend to wither. Giant hogweed blooms from early spring until late summer, especially in the vicinity of wetlands (streams or canal banks). These characteristics differentiate it from the garden angelica (Angelica archangelica) and the common hogweed (Heracleum sphondylium).

Who is most at risk of coming across giant hogweed?

Gardeners, trekkers, forest workers, and people who work outdoors in wooded or undergrowth areas where giant hogweed is present are most at risk of injury caused by giant hogweed.

How is giant hogweed sap toxic?

The sap of giant hogweed contains different photoactive agents called furocoumarins, of which the most predominant is 5-MOP (5-methoxypsoralen). Injuries are caused when these photoactive agents are exposed to and activated by UV-A rays present in sunlight. This gives rise to a toxic process in which the furan ring of the photoactive agent is cross-linked with the pyrimidine bases of DNA in the patient’s skin, thus causing an increase in oxidative stress leading to cell membrane damage and subsequent inflammation and oedema. The culmination of these processes leads to the development of phytophotodermatitis (PPD)[4].

Similar to other plants capable of phototoxicity, skin damage is dependent on certain factors[5] such as:

  • The concentration of the phototoxic agent
    • During summer months, levels of phototoxic agents are higher. Moreover, they are more concentrated in fruit, present in intermediate levels in the leaves, and are minimally present in the stem.
  • The thickness of the skin
    • Damage is more extensive and deeper in the skin that is thinner.
  • Sun exposure
    • When sun exposure is prolonged, there is greater photoactivation and therefore greater damage.
  • Skin moisture
    • Sweat or dew that may be present on the skin can accelerate the toxicity process.

What are its symptoms?

Symptoms of giant hogweed exposure usually involve an erythematous lesion[6] accompanied by extremely intense pain. If not treated early, erythematous lesions evolve into burns[7] with the appearance of one or more liquid-filled vesicles. Generally, patients may have fatigue and slight tachycardia, but vital signs and laboratory test may be normal.

During the history and physical examination, staphylococcal infection, allergic dermatitis, purpura, impetigo, and fungal infection must be considered in the differential diagnosis.


Upon contact, the subject should immediately wash the red area abundantly, dry it, and cover it to avoid sun exposure. Other recommendations would include avoiding to take baths and showers and apply high protection sunscreen to the lesion.

If erythema appears, the use of sulfadiazine cream and analgesic anti-inflammatory drugs should be considered. Moreover, the use of ice to reduce inflammation can also be useful. In the event of an injury characterized by one or more blisters or loss of tissue, a conservative treatment[8] consisting of cleansing with antiseptic solution (i.e. Clorexidine) and bandaging with synthetic microporous membranes[9] have proven effective. In cases where the phototoxicity process has been prolonged enough to cause extensive and deep burns, skin grafting and surgical debridement are necessary.

Take-home message

In conclusion, the message for our patients who operate or live in areas where giant hogweed is present is to “look but absolutely don’t touch” this beautiful plant. Secondarily, it is also important to subsequently report its presence to public authorities; in fact, many countries or regions follow a specific eradication program for this plant which can prove dangerous for humans and animals.

Look but absolutely don't touch this beautiful plant.

References and Further Reading


[2] Heracleum mantegazzianum (giant hogweed) – Invasive Species Compendium –

[3] Derraik JG. Heracleum mantegazzianum and Toxicodendron succedaneum: plants of human health significance in New Zea-land and the National Pest Plant Accord. N Z Med J 2007;120: U2657.

[4] Marcos LA, Kahler R. Phytophotodermatitis. Int J Infect Dis 2015;9(July (38)):7–8.

[5] Pira E, Romano C, Sulotto F, et al. Heracleum mantegazzianum growth phases and furocoumarin content. Contact Derm 1989; 21:300e3.

[6] J Emerg Nurs. 2006 Jun;32(3):246-8. A 43-year-old woman with painful, vesicular lesions from giant hogweed photodermatitis. Langley DM(1), Criddle LM.

[7] Baker BG, Bedford J, Kanitkar S. Keeping pace with the media; Giant Hogweed burns – A case series and comprehensive review. Burns. 2017 Aug;43(5):933-938. DOI: 10.1016/j.burns.2016.10.018.

[8] Chan JC, Sullivan PJ, O’Sullivan MJ, Eadie PA. Full thickness burn caused by exposure to giant hogweed: delayed presentation, histological features and surgical management. J Plast Reconstr Aesthet Surg. 2011;64(1):128-130. doi:10.1016/j.bjps.2010.03.030

[9] Pfurtscheller K, Trop M. Phototoxic plant burns: report of a case and review of topical wound treatment in children. Pediatr Dermatol 2014;31:e156–9.

Cite this article as: Francesco Adami, Italy, "Giant Hogweed Burns," in International Emergency Medicine Education Project, August 31, 2020,, date accessed: September 24, 2021

Question Of The Day #9

question of the day

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient is suffering from sympathomimetic toxicity. Signs of a sympathomimetic toxidrome include agitation, psychosis, delirium, tachycardia, hypertension, diaphoresis, mydriatic (dilated) pupils, and decreased bowel sounds. The features of anticholinergic toxidromes overlap with many features of sympathomimetic toxidromes. A clinical finding that can be used to differentiate the two toxidromes is diaphoresis. Diaphoretic skin supports a sympathomimetic ingestion, while dry, warm skin supports anticholinergic ingestion. Examples of substances that can cause a sympathomimetic toxidrome ae cocaine, amphetamines, synthetic cannabinoids, ketamine, bath salts, and ecstasy (MDMA). The treatment for this toxidrome is mostly supportive care, such as benzodiazepines and cooling. Cocaine can cause coronary artery vasospasm along with sodium-channel blockade, which can predispose to cardiac arrhythmia. For this reason, a 12-lead EKG is important in any patient with possible cocaine toxicity. Sodium bicarbonate (Choice A) would be beneficial in salicylate toxicity, tricyclic antidepressant toxicity, or cocaine toxicity if the QRS was widened. The EKG for this patient has a normal QRS interval (<120msec). Physostigmine (Choice C) is an acetylcholinesterase inhibitor. This medication would likely worsen the patient’s tachycardia. Physostigmine is the antidote for anticholinergic toxicity. However, physostigmine should not be used in TCA overdose as it may increase the risk of cardiac arrhythmia. Naloxone (Choice D) is the antidote for opioid toxicity. Signs of opioid overdose include miotic (constricted) pupils, respiratory depression, and CNS depression. This patient does not possess these symptoms on exam. Diazepam (Choice B) is the best treatment. Correct Answer: B


Greene S. General Management of Poisoned Patients. “Chapter 176: General Management of Poisoned Patients”. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill.

Donaldson, R. (2019). Cocaine toxicity. WikEm.

Cite this article as: Joseph Ciano, USA, "Question Of The Day #9," in International Emergency Medicine Education Project, August 21, 2020,, date accessed: September 24, 2021

Question Of The Day #8

question of the day
qod 8 toxicology

Which of the following is the most likely cause of this patient’s condition?

This patient is suffering from an anticholinergic toxidrome. Symptoms of anticholinergic medication toxicity include altered mental status with agitation or delirium, tachycardia, hypertension, hyperthermia, mydriatic (dilated) pupils, hot and dry skin, decreased bowel sounds, and urinary retention. The sympathomimetic toxidrome is very similar to the anticholinergic toxidrome; however, patients with anticholinergic ingestions have dry skin while patients with sympathomimetic ingestions have diaphoretic skin. Some notable types of anticholinergics are atropine, antihistamines, Tricyclic antidepressants (TCAs), and Jimson weed. Amitriptyline (Choice A) is a TCA medication and can cause anticholinergic toxicity. When taken in high doses, a major adverse effect of TCAs is Na-channel blockade, resulting in QRS widening on EKG and cardiac arrhythmias. Therapy includes sodium bicarbonate and supportive care. This patient has a normal QRS interval on EKG, making this choice less likely. Cocaine (Choice B) is a sympathomimetic. Many features of the exam support sympathomimetic toxicity, but the presence of dry skin makes this choice less likely. Physostigmine (Choice C) is an acetylcholinesterase inhibitor which would have a cholinergic toxidrome if taken in excess. Features of this include bradycardia, bronchorrhea, bronchospasm, diarrhea, hypersalivation, sweating, and hyperactive bowel sounds. Treatment for cholinergic toxicity is atropine. Along with supportive care, physostigmine is the main treatment for anticholinergic toxicity. One exception is in TCA toxicity where physostigmine should be avoided. Diphenhydramine (Choice D) is an antihistamine with anticholinergic properties, and it is the most likely medication ingested in this case scenario. Correct Answer: D 


Greene S. General Management of Poisoned Patients. “Chapter 176: General Management of Poisoned Patients”. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill.

Cite this article as: Joseph Ciano, USA, "Question Of The Day #8," in International Emergency Medicine Education Project, August 14, 2020,, date accessed: September 24, 2021

Can I Eat This? – A Helpful Guide To Plant Toxicology – Cardiac Glycosides


Not only is the identification of toxic plants from their gross appearance a commonly tested topic in Emergency Medicine Board Exams, but it is also a necessary skill for doctors operating in institutions where an established Toxicology division does not exist or where the opinion of a specialist in the field is not immediately available.

This is the second part in a series of blog posts dedicated to providing you with original mnemonics and visual aids that serve to highlight a few classes of common toxic plants prominent for both their inclusion in the academic assessment as well as their prevalence in the community. These memory tools will attempt to highlight key features in the identification of well-known toxic plant species and are designed to aid clinicians from various regions of the globe as well as hone the skills of aspiring toxicologists.

Picture the Scene

A 21-year-old female is brought to your Emergency Department via ambulance due to persistent vomiting, abdominal pain, and some dizziness. She is visibly distressed, clutching her stomach, and reports having vomited at least six times over the past 3 hours. Her brother reports that she had been feeling ill with reported abdominal cramping and diarrhea for the past two days. Earlier that day, she had been given some herbal soup to help with her abdominal cramps by her grandmother, who had prepared it using leaves and flowers from the backyard garden. Soon after drinking the soup, the patient was reported to have multiple episodes of vomiting and began to experience some occasional dizziness, prompting contact of Emergency Medical Services and transfer to the hospital.

Upon initial examination, the patient’s vital signs were significant for a heart rate of 50 beats/minute with a Blood Pressure of 135/76 and spO2 of 95% on room air. No fever, abnormal breathing patterns, or signs of poor perfusion were noted. An Electrocardiogram (ECG) was done and revealed bradycardia, with a first-degree AV block, but no other T wave, QT, ST, or QRS segment abnormalities.

A laboratory workup was initiated, and the patient was given IV Atropine for her bradycardia. A Venous Blood Gas (VBG) was remarkable for hyperkalemia of 6.8 mEq/L with no acid/base disturbance. Therefore, treatment for hyperkalemia was initiated with IV Dextrose and Insulin as per standard management. When bradycardia persisted, a second dose of IV Atropine was given. The patient’s heart rate improved, but the blood pressure was noted to drop down to 95/68. After that, IV fluids were initiated, and the possibility of toxic ingestion explored by asking the patient’s brother for details of the ingredients present in the herbal soup.

The brother contacted the family at home and provided a picture of the plant used, as shown in Figure 1. The in-house Medical Toxicologist was shown the image and confirmed that the patient was suffering from Cardiac Glycoside toxicity secondary to the ingestion of an Oleander plant species.

Figure 1- Photograph of the flower used to make herbal soup. The flower was correctly identified as part of the toxic Oleander species.

Overview of Cardiac Glycoside Toxicity

Cardiac glycosides and related cardenolides represent a group of compounds that exhibit their effects primarily through their action on the Sodium-Potassium (Na+/K+) ATPase pump in cardiac myocytes and other tissues.[1] Inhibition of this pump, as outlined in Figure 2, causes an increase in intracellular Sodium (Na+), with subsequent activation of the Sodium-Calcium (Na+/Ca2+) exchanger, resulting in accumulation of intracellular calcium (Ca2+).

The increased intracellular Ca2+, along with direct stimulation of vagal tone, produces inotropic effects on the heart, increases ventricular ectopy, causes bradycardia, and impaired conduction through the atrioventricular (AV) node. At the same time, the inhibition of the Na+/K+ ATPase pump can lead to hyperkalemia.[2]

Cardiac glycosides are found in a variety of naturally occurring plant and animal species. Acute poisoning often presents with gastrointestinal manifestations (such as nausea, vomiting, abdominal pain or diarrhea), generalized body weakness, and dizziness. However, toxicity can also cause hyperkalemia and cardiotoxicity, represented by bradycardia, heart blocks, and various other dysrhythmias. Death is usually a result of ventricular fibrillation or tachycardia.[3]

Management involves addressing specific symptoms of severe disease. Atropine can be used to increase heart rate and reverse the effects on vagal tone in patients presenting with bradycardia. Reversal of toxicity can be achieved using Anti‐digoxin Fab as with Digoxin overdoses. Hyperkalemia can be managed using a combination of Insulin and dextrose solution to shift potassium back into cells. Activated charcoal may be used for initial decontamination, with Multidose activated charcoal for enhanced elimination.[4]

IV Calcium Chloride or Carbonate use in hyperkalemia was traditionally discouraged in patients suffering from cardiac glycoside poisoning. This was due to concerns that the additional calcium load would result in sustained cardiac contraction, termed as ‘the stone heart.’ However, several studies have since proven that such a phenomenon is unlikely to manifest in patients treated with IV Calcium.[5]

calcium mechanism

Figure 2- Mechanism of action of cardiac glycosides/digitalis drugs

Identifying Plants with Cardiac Glycoside toxicity

The most prominent species of plants known to contain cardiac glycosides include the foxglove plants Digitalis purpurea and Digitalis lanata, Oleander species (e.g., Nerium oleander and Thevetia peruviana), and Lily of the Valley (Convallaria majalis).[6] These plant species are commonly found in numerous tropical and subtropical countries around the world. Unfortunately, toxicity from accidental or intentional ingestion of their toxic leaves, roots, stems, and seeds is not uncommon and has, in several cases, lead to fatal outcomes for patients.[7-11]

cardiac glycosides plant identification

References and Further Reading

  1. Lingrel J. B. (2010). The physiological significance of the cardiotonic steroid/ouabain-binding site of the Na,K-ATPase. Annual review of physiology, 72, 395–412.
  2. Benowitz, N. (2012). ‘Chapter 61- Digoxin and Other Cardiac Glycosides’ Poisoning & drug overdose. New York, N.Y.: McGraw Hill Medical.
  3. Kanji, S., & MacLean, R. D. (2012). Cardiac glycoside toxicity: more than 200 years and counting. Critical care clinics, 28(4), 527–535.
  4. Roberts, D. M., Gallapatthy, G., Dunuwille, A., & Chan, B. S. (2016). Pharmacological treatment of cardiac glycoside poisoning. British journal of clinical pharmacology, 81(3), 488–495.
  5. Levine, M., Nikkanen, H., & Pallin, D. J. (2011). The effects of intravenous calcium in patients with digoxin toxicity. The Journal of emergency medicine, 40(1), 41–46.
  6. Hollman A. (1985). Plants and cardiac glycosides. British heart journal, 54(3), 258–261.
  7. Bavunoğlu, I., Balta, M., & Türkmen, Z. (2016). Oleander Poisoning as an Example of Self-Medication Attempt. Balkan medical journal, 33(5), 559–562.
  8. S, Lokesh & Arunkumar.R,. (2013). A clinical study of 30 cases of Acute Yellow Oleander Poisoning. Journal of Current Trends in Clinical Medicine and Laboratory Biochemistry. 1. 29-31.
  9. Haynes, B. E., Bessen, H. A., & Wightman, W. D. (1985). Oleander tea: herbal draught of death. Annals of emergency medicine, 14(4), 350–353.
  10. Janssen, R. M., Berg, M., & Ovakim, D. H. (2016). Two cases of cardiac glycoside poisoning from accidental foxglove ingestion. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne, 188(10), 747–750.
  11. McVann, A., Havlik, I., Joubert, P. H., & Monteagudo, F. S. (1992). Cardiac glycoside poisoning involved in deaths from traditional medicines. South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde, 81(3), 139–141.
Cite this article as: Mohammad Anzal Rehman, UAE, "Can I Eat This? – A Helpful Guide To Plant Toxicology – Cardiac Glycosides," in International Emergency Medicine Education Project, July 17, 2020,, date accessed: September 24, 2021