Question Of The Day #9

August 21, 2020August 20, 2020 ~ Joseph Ciano, USA ~ Leave a comment

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

Explanation

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

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❓Which of the following is the most appropriate next step in management for this patient’s condition? – ❓A detailed answer will be found in https://t.co/XvqTTNtHys on Friday 10 AM UK time.
— iem-student (@iem_student) August 20, 2020

References

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. https://www.wikem.org/wiki/Cocaine_toxicity

Cite this article as: Joseph Ciano, USA, "Question Of The Day #9," in International Emergency Medicine Education Project, August 21, 2020, https://iem-student.org/2020/08/21/question-of-the-day-9/, date accessed: March 26, 2023

Question Of The Day #8

August 14, 2020August 13, 2020 ~ Joseph Ciano, USA ~ Leave a comment

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

Explanation

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

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

Cite this article as: Joseph Ciano, USA, "Question Of The Day #8," in International Emergency Medicine Education Project, August 14, 2020, https://iem-student.org/2020/08/14/question-of-the-day-8/, date accessed: March 26, 2023

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

April 6, 2020March 26, 2020 ~ Mohammad Anzal Rehman, UAE ~ Leave a comment

Introduction

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.

Various mnemonics and visual aids serve to highlight a few classes of common toxic plants that are prominent for both their inclusion in the academic assessment as well as their prevalence in the community. This series will sequentially present a series of visual aids and mnemonics that highlight key features in the identification of well-known toxic plant species, designed to aid clinicians from various regions of the globe as well as hone the skills of aspiring toxicologists.

Picture the Scene

A 28-year-old male is brought to your Emergency Department (ED) via ambulance due to a reportedly altered mental status. His wife, who accompanied the paramedics, states that she found him lying unconscious in the grass near a basket he was using to collect berries during an outdoor picnic in the fields. He was arousable at the scene but has had a fluctuating level of consciousness up to arrival to the hospital.

Upon initial examination, the patient is observed to be irritable with irregular, shallow breathing. Vital signs revealed a Blood Pressure of 127/75 mmHg, Heart Rate of 140, Respiratory rate of 24, Temperature of 37.9 C, and spO2 96% on room air. His pupils were found to be equally reactive to light but were significantly dilated, and his mucus membranes were notably dry.

The patient’s wife, believing the cause for her husband’s condition to be ingestion of the berries from the field, approaches you and shows you pictures of the plants she had photographed near where her husband was found. (see below images)

Why we care about toxic plant identification

The intoxicated patient, while frequently encountered in the ED, poses a uniquely challenging puzzle for the average ED Physician. Beyond the routine resuscitative and supportive care, the doctor who receives a patient that has consumed an unknown substance is tasked with the burden of deducing what kind of substance was taken and the expected sequelae for the same.

Among the numerous causes of intoxication, ingested plant species are a particularly ambiguous class of toxic substances to identify because the vast majority of intoxicated patients consume them unknowingly with only vague descriptions for what they ate. Often, however, these plants are brought with the patient or are present on their person at the time of arrival.

Whereas a vast majority of cases that present to the Emergency Department may not exhibit similar tell-tale signs and symptoms, the patient in the case described above displayed clinical manifestations typical to an anticholinergic syndrome. Furthermore, the photographs provided by the patient’s wife confirmed the cause of his symptoms as toxic ingestion of berries from the plant species Atropa Belladonna.

Plants with anticholinergic toxicity

The two most important plant species that contribute to this class of toxicity are the Datura stramonium (Jimson weed, angel’s trumpet), and the Atropa Belladonna (Deadly nightshade). The seeds of D. Stramonium and the berry-like fruits and leaves of A. Belladonna contain scopolamine, hyoscyamine and atropine. Ingestion of these parts of the plant results in suppression of Acetylcholine in the body, manifesting as an antimuscarinic syndrome that is characterized by dry skin, altered mental status, flushing, decreased gastrointestinal motility, increased body temperature, tachycardia, pupillary dilation (mydriasis) and urinary retention.

The above constellation of symptoms is usually simplified by using the following phrases:

‘Mad as a Hatter’ – Delirium/Altered Mental Status
‘Hot as a Hare’ – Hyperthermia
‘Red as a Beet’ – Flushing
‘Bloated as a Toad’ – Decreased gut motility/Constipation
‘Blind as a Bat’ – Mydriatic pupils
‘Dry as a Bone’ – Dry skin/decreased sweat production

Management involves benzodiazepines for agitation, adequate hydration, and supportive care. Physostigmine is reserved for cases refractory to Benzodiazepines.

Plant Identification

A useful method of visual identification of the plant species outline above is as follows:

Black in green, Black on green Don’t trust their high, they inhibit Acetylcholine!

Mnemonic break-down

Black in green

Black-colored toxic seeds reside within green ‘spiky’ fruit of Datura stramonium (Jimson weed)
Black on green

Black-colored berry-like fruit (often mistaken for common blueberries) nestled on top of greenish petal-like structures and leaves of Atropa Belladonna (Deadly nightshade)
Don’t trust their high

These plant species are commonly ingested for recreational purposes due to reported hallucinogenic properties
They inhibit Acetylcholine

Both cause antimuscarinic syndrome: Dry skin, flushing, decreased GI motility, hallucinations, mydriasis, hyperthermia, tachycardia, urinary retention

Cite this article as: Mohammad Anzal Rehman, UAE, "Can I Eat This? – A Helpful Guide To Plant Toxicology – Anticholinergics," in International Emergency Medicine Education Project, April 6, 2020, https://iem-student.org/2020/04/06/anticholinergics/, date accessed: March 26, 2023

Reference

Lim, C.S., Aks, S.E. (2017), ‘Chapter 158 – Plants, Mushrooms and Herbal Medications’, Rosen’s emergency medicine 9th edition, Pg. 1957 – 1973

A Farmer’s Dilemma

July 19, 2019September 4, 2019 ~ Shaza Karrar, UAE ~ Leave a comment

Case Presentation

It was a rainy night preceding my morning shift as a year 3 EM resident at one of our training centers in Abu Dhabi. The paramedics barged in with an agitated patient, who was found soaking wet in a farm field.

According to brief history that we got from the paramedics, the patient works at a farm and his boss found him collapsed, cold to touch and confused in the early morning hours. Paramedics also reported a confused, hypothermic, and tachycardic patient. They brought him directly to the ED, with no accompanying friends or family.

As we proceeded to resuscitate the patient, we noted that his initial vital signs did confirm hypothermia of 32 Celsius measured rectally, tachycardia, hypertension, and normal O2 saturation. We hooked him to the monitor, removed his wet clothing, gained IV access, started him on warm IV fluids, and covered him with blankets and a warming Bair Hugger (a warming blanket system).

Physical Exam

The patient was confused, agitated and uttering incomprehensive words, with a GCS of 11 (E3 V3 M5). I proceeded to examine him looking for more clues of why he was laying semiconscious under the rain all night. Systematic physical examination revealed pinpoint pupils, frothing and excessive salivations. Furthermore, diffuse mild crackles were noted on chest auscultation, and he was tachycardic with a regular rate and rhythm. Remaining physical exam was unremarkable, and a complete neurological exam was challenging.

Differential Diagnosis and Workup

Thinking of a broad differential diagnosis of altered mental status, systematic consideration of all possible etiologies similar to our patient presentation was reviewed. We have considered metabolic derangements, head trauma, CNS causes such as seizures and post-ictal status, infectious causes such as pneumonia or meningitis, and toxicologic causes, such as alcohol withdrawal, or medications overdose.

You may find useful this mnemonic for altered mental status!

Further management plan included giving him benzodiazepines for the agitation and possible post-ictal status. We collected basic blood work and proceeded for a head CT to rule out traumatic or atraumatic intracranial pathologies. Blood workup was inclusive of an alcohol level, Aspirin, Acetaminophen level, and a urine toxicology screen.

As the patient returned from the CT, he apparently had passed the copious amount of loose stools, that smelled surprisingly like garlic that studded the ED with its smell.

The head CT was normal, and most of his blood workup came back unremarkable. But, he remained confused and agitated as the benzodiazepines were wearing off and despite all the warming measures. ECG showed only sinus tachycardia, and a chest X-Ray was unremarkable.

smells like garlic!

What do you think? What are the causes for this?

agents smells like garlic

phosphorus, tellurium, inorganic arsenicals and arsine gas, organophosphates, selenium, thallium, dimethyl sulfoxide

Learn More

The garlic smell did give us a lead though, we thought further of possible toxic agents that may give such a smell, along with a consistent similar clinical picture.

Case Management and Disposition

Collecting our clues once more, we had pinpoint pupils, frothing, salivation, wet lungs, vomiting and loose motions. Patient’s collective symptoms and signs indicated a Cholinergic Toxidrome, possibly due to Organophosphates ingestion.

The patient was already decontaminated with removal of all his clothes. All healthcare providers were equipped with personal protective equipment.

This was confirmed an hour later when his farm owner showed up with a Pesticides Bottle that he found near him in the early morning hours before calling an ambulance. Pesticide is shown in Figure. The content of the bottle is consistent with Organophosphates Toxicity, and hence his Cholinergic Toxidrome.

He was started on Atropine, and Pralidoxime, assessed and admitted to the ICU with arranged psychiatric consult to assess his suicidal ideations once he stabilizes.

Critical Thinking and Take-home Tips

What is Toxidrome?

A collection of symptoms and physical signs caused by a certain toxic agent.

What are the main Toxidromes I should be familiar with?

Cholinergic
Anticholinergic
Sedative/Hypnotic
Sympatholytic
Sympathomimetics

What is Cholinergic Toxidrome?

Cholinergic toxicity represents a cholinesterase inhibitor poisoning. It results from the accumulation of excessive levels of acetylcholine in synapses. Clinical picture resulting from the Acetylcholine build up depends on the type of receptors that it stimulates and where is it found in the body. It can stimulate the nicotinic and muscarinic receptors. The balance of these stimulations reflects such clinical presentations.

What are the clinical features of an Organophosphates toxicity? (1)

Think of the symptoms that can be caused depending on the type of receptors affected by the buildup of acetylcholine.

Muscarinic Receptors – SLUDGE(M)

Nicotinic Receptors (NMJ) – MTWThF

What are the common causes of mortality in such cases?

These are called the Killers B’s which consist of Bradycardia, Bronchorrhea and Bronchospasm.

How to Treat Cholinergic Toxicity?

Decontamination should always be considered first in all cases with possible hazardous exposure from the patient and his environment to all health care providers in contact with him. All caregivers should wear appropriate personal protective equipment’s and make sure to remove all clothing and possible objects with the suspected contaminant.

Supportive care is a cornerstone to all unstable patients, make sure that they are monitored, with proper IV access and supplemental oxygen as needed.

Furthermore, airway management is lifesaving in similar patients, as bronchorrhea is one of the killer B’s and can lead to high fatality.

Antidotes such as Atropine and Pralidoxime in Cholinergic toxicity are paramount, as they help reverse the etiology, and prevent further worsening of the toxicity.

Make sure that such patients are admitted under needed specialty care with proper observation and reassessment for the patient.

Consult a toxicologist if feasible in your center to provide you with further management details and interventions that can help your patients better.

Conclusion

Organophosphates can be found in pesticides, chemical weapons such as nerve gases, and few medications as well such as neostigmine or edrophonium. They are highly lipid soluble making them easily absorbed via breathing and skin contact as well. Encountering similar patients, it is quite important to always be systematic in your approach, resuscitate your patient first, and make sure to use your history taking as feasible and physical examination to collect all the clues needed to narrow down your differentials and find the most appropriate treatment needed for your patient.

References and Further Reading

Organophosphate toxicity on WikEM: https://www.wikem.org/wiki/Organophosphate_toxicity
Das RN, Parajuli S. Cypermethrin poisoning and anti-cholinergic medication- a case report. Internet J Med Update. 2006;1:42–4.
Aggarwal, Praveen et al. “Suicidal poisoning with cypermethrin: A clinical dilemma in the emergency department.” Journal of emergencies, trauma, and shock vol. 8,2 (2015): 123-5. doi:10.4103/0974-2700.145424
Lekei EE, Ngowi AV, London L. Farmers’ knowledge, practices and injuries associated with pesticide exposure in rural farming villages in Tanzania. BMC Public Health. 2014;14:389. Published 2014 Apr 23. doi:10.1186/1471-2458-14-389