Question Of The Day #80

question of the day
753 - bradycardia
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 generalized weakness and dizziness after accidently ingesting extra diltiazem tablets 1.5 hours prior to arrival.  The exam shows bradycardia, hypotension, an elevated glucose level, and a patient without altered mental status.  The EKG shows sinus bradycardia without any conduction blocks.

This patient’s clinical presentation is likely due to diltiazem overdose.  Diltiazem is a calcium channel blocker. Calcium channel blocker medications are categorized as the dihydropyridines (nifedipine, amlodipine, nicardipine) and the non-dihydropyridines (verapamil, diltiazem).  The dihydropyridines (DHPs) cause systemic vasodilation, hypotension, and often a reflex tachycardia in overdose.  The non-DHPs act more directly on the heart with less peripheral effects and cause hypotension and bradycardia.  Calcium channel blocker overdose can mimic beta blocker overdose as both medication classes have similar effects on the body. 

The initial management of any patient who has ingested a potentially dangerous medication is the “ABCs”, also known as the primary survey.  This includes assessment and management of the airway (i.e., intubation for somnolence and aspiration risk), breathing (i.e., supplemental oxygen for hypoxia), and circulation (i.e., IV fluids, vasopressors for hypotension).  Decontamination is another consideration depending on the agent the patient has been exposed to.  An EKG should be ordered early in all toxic ingestions to evaluate for signs of cardiac toxicity, such as a prolonged QT interval or prolonged QRS interval.  Checking for other dangerous coingestants, like serum levels of salicylates and paracetamol (APAP) should be routinely done.  Specific toxic effects seen in calcium channel blocker and beta blocker overdose are outlined in the chart below.

IV Glucagon (Choice A) is useful as an adjunctive treatment in both calcium channel blocker and beta blocker overdose.  However, glucagon often causes vomiting and is not a first-line agent.  IV fluids, atropine, vasopressors, and activated charcoal should be attempted before glucagon.  Antiemetics should be considered prior to IV Glucagon administration given its side effect of nausea and vomiting.  Transvenous pacing (Choice C) and IV Calcium gluconate (Choice D) are also considered second-line treatments to try when the patient is not responding to IV fluids, atropine, or vasopressors.  The best next step in this case is to administer IV Fluids (Choice B). 

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #80," in International Emergency Medicine Education Project, March 11, 2022, https://iem-student.org/2022/03/11/question-of-the-day-80/, date accessed: October 6, 2022

Question Of The Day #79

question of the day
Which of the following is the most appropriate next step in management?

This patient arrives to the Emergency department with altered mental status and hypotension after ingestion of multiple pills at home.  On exam, she is hypotensive, tachycardic, confused, and has dilated pupils with dry skin.  The patient has most likely ingested amitriptyline tablets given the history provided in the question.  Amitriptyline is a tricyclic antidepressant medication.  Despite the clear history, it is very important to check levels for possible other coingestants, like paracetamol (APAP) and salicylates.

Tricyclic antidepressants (TCAs) impact many different receptors in the body, so the clinical presentation of a patient with TCA overdose can vary considerably.  Important features to remember are cardiovascular toxicity with a widened QRS and hypotension, as well as an anticholinergic toxidrome.  A 12-lead EKG should be ordered early in any case of possible overdose, and an EKG in TCA overdose is a crucial step in evaluation.  Supportive care and IV sodium bicarbonate are the mainstays of treatment for TCA overdose.  See the table below for details regarding the clinical features and treatment of these patients. 

Toxic effects of Tricyclic Antidepressant (TCA) overdose

Clinical Features

Treatment

Na-channel blockade

Cardiac arrythmias,

Wide QRS (>100msec), Prominent R wave in AvR (>3mm)

IV Sodium Bicarbonate100mEq (1-2mEq/kg),

 

Titrate to QRS <100 and/or improved hypotension

Alpha-1 adrenergic receptor blockade

Hypotension

IVF, vasopressors

Serotonin reuptake blockade

Seizures

Benzodiazepines

Muscarinic- Ach receptor blockade (Anticholinergic)

Anticholinergic toxidrome– altered mental status, delirium, hyperthermia, tachycardia, hypertension, dilated pupils, dry skin

Benzodiazepines, supportive care.

 

Avoid Physostigmine.

Histamine receptor (H1) blockade

Drowsiness, coma

Supportive care

IV Physostigmine (Choice A) can be used to treat an anticholinergic toxidrome along with supportive care and benzodiazepines.  This patient does appear to have an anticholinergic toxidrome, but there is a high suspicion for TCA overdose.  Physostigmine should be avoided in TCA overdose due to data indicating worse outcomes in TCA overdose patients who receive physostigmine.  IV Norepinephrine (Choice B) may eventually be required to manage this patient’s hypotension.  However, IV fluids and sodium bicarbonate to reverse the cardiac toxicity should be used first.  IV Metoprolol (Choice D) may help relieve the tachycardia, but it would worsen the patient’s hypotension and shock state.   The best next step is IV Sodium bicarbonate (Choice C), which is the treatment for TCA overdose.  Sodium bicarbonate prevents TCA binding to cardiac sodium channels, thereby stabilizing the heart and preventing cardiac dysrhythmias and death. Sodium bicarbonate is given as an infusion until the QRS interval shortens <100msec and the hypotension improves. 

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #79," in International Emergency Medicine Education Project, March 4, 2022, https://iem-student.org/2022/03/04/question-of-the-day-79/, date accessed: October 6, 2022

Question Of The Day #78

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

This patient presents to the Emergency department from a party with slurred speech and somnolence after drinking homemade alcohol.  On exam, his vital signs and glucose are normal, he is nonresponsive to pain, and he has a GCS of 3 (normal GCS is 15).  He is intubated due to his inability to protect his airway and risk for aspiration.  Intubation is an important first step in managing this patient.

Altered mental status has a broad differential diagnosis, including intracranial bleeding, stroke, post-ictal state, hypoglycemia, electrolyte abnormalities, other metabolic causes, infectious etiologies, toxicological causes, and many other conditions.  The immediate evaluation and treatment of this patient should focus on the ‘ABCs’, or any abnormality in the airway, breathing, and circulation.  Any rapidly correctable causes of altered mental status, like hypoxia, hypoglycemia, or hyperthermia, should be addressed appropriately at this stage (i.e., supplemental oxygen, intubation, IV dextrose, body cooling). 

Paracetamol (APAP) overdose (Choice A) is often accompanied with little to no symptoms in the first 24hours.  Later in the ingestion timeline, liver failure and its associated sequalae can occur if no antidote is given.  The symptoms exhibited by the patient do not correlate with APAP overdose.  Opioid overdose (Choice D) can cause severely depressed mental status as seen in this patient.  However, opioid overdose also has decreased respiratory rate, pinpoint pupils, and sometimes associated bradycardia or hypotension.  This patient has normal vital signs and normal pupil size.  This patient ingested some type of alcohol at the party, but it is unclear if it is ethanol or a toxic alcohol (i.e., methanol, ethylene glycol).  Both ethanol and methanol ingestion (Choice B) can cause similar exam findings of depressed mental status as in this patient.  Other features of toxic alcohol ingestion include vision changes (methanol), hemorrhagic gastritis (isopropyl alcohol), coma, seizures, and hyperventilation (respiratory compensation for severe acidosis).  Ethanol and many of the toxic alcohols will cause an increased anion gap metabolic acidosis with an increased osmolar gap.  Helpful tests to differentiate ethanol from a toxic alcohol are serum levels of ethanol and serum toxic alcohol levels (if available).  A somnolent, intoxicated-appearing patient with a negative ethanol level should raise suspicion for toxic alcohol poisoning.  Urine studies may also show oxalate crystals in ethylene glycol ingestion. 

Since ethanol is not a listed choice and laboratory studies are not provided, methanol ingestion (Choice B) is the most likely cause of this patient’s symptoms.  Fomepizole (Choice C) is an intravenous medication that inhibits the alcohol dehydrogenase enzyme.  Fomepizole is the antidote to toxic alcohols by slowing the production of dangerous toxic alcohol metabolites.  The correct answer is Choice B.

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #78," in International Emergency Medicine Education Project, February 25, 2022, https://iem-student.org/2022/02/25/question-of-the-day-78/, date accessed: October 6, 2022

Question Of The Day #77

question of the day

 

Test Value

Reference Range

pH

7.55

(7.35-7.45)

pCO2

20

(35-45)

pO2

84

(80-100)

HCO3

18

(22-26)

Which of the following is the most appropriate next step in management?

This patient presents to the Emergency department for altered mental status, nausea, and tinnitus (ear ringing).  Her exam shows a confused female with tachypnea, tachycardia, borderline fever, wet skin, and normal pupil size.  Altered mental status has a broad differential diagnosis, including intracranial bleeding, stroke, post-ictal state, hypoglycemia, electrolyte abnormalities, other metabolic causes, infectious etiologies, toxicological causes, and many other conditions.  The immediate evaluation and treatment of this patient should focus on the ‘ABCs’, or an abnormality in the airway, breathing, and circulation.  Any rapidly correctable causes of altered mental status, like hypoxia, hypoglycemia, hyperthermia, should be addressed appropriately at this stage (i.e., supplemental oxygen, IV dextrose, body cooling).

This patient’s exam mimics many aspects of a sympathomimetic toxidrome, however, having the awareness that oil of wintergreen is a potent salicylate will lead to the diagnosis.  This patient has salicylate poisoning.  Salicylates are present in many over the counter pain medications, including aspirin, oil of wintergreen (methyl salicylate), and Pepto-Bismol (bismuth subsalicylate).   An acute overdose of salicylates may present as tachycardia, hypertension, and hyperthermia, similar to a sympathomimetic toxidrome.  Other features include tinnitus, altered mental status, seizures, and coma. 

The patient’s ABG shows a respiratory alkalosis (elevated pH, low pCO2) mixed with a metabolic acidosis (low HCO3).  Salicylic acid disrupts the body’s ability to process energy at the cellular level by acting as an ‘uncoupler’ of the oxidative phosphorylation process.  Salicylates directly stimulate the respiratory centers in the brainstem, triggering hyperventilation and increased lactic and pyruvic acid.  Hyperventilation causes the initial respiratory alkalosis, and the elevated lactic and pyruvic acid later causes an increased anion gap metabolic acidosis or a mixed metabolic acidosis and respiratory alkalosis.   

The treatment of salicylate overdose is prompt IV NaHCO3 infusion (Choice D) to alkalinize the urine and blood.  This assists in the more rapid clearance of salicylates.  Hemodialysis can be considered if salicylate levels are over 80-100mg/dL, or if there is persistent altered mental status, acidosis, or organ failure despite starting the NaHCO3 infusion.  PO Activated charcoal (Choice A) is helpful in binding certain toxins and preventing their absorption through the GI tract.  Charcoal is most beneficial when it is used early after drug ingestion.  This patient was exposed to salicylates by a topical route, so PO charcoal would not be helpful.  IM Glucagon (Choice B) is helpful in hypoglycemia and betablocker overdose.  This patient is not hypoglycemic and was not exposed to betablockers.  IV Atropine (Choice C) is helpful in patients with a cholinergic toxidrome (i.e., organophosphates, nerve gases), but would not be helpful in this patient.  Atropine would likely worsen the patient’s tachycardia.  The best next step would be IV NaHCO3 infusion (Choice D).

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #77," in International Emergency Medicine Education Project, February 18, 2022, https://iem-student.org/2022/02/18/question-of-the-day-77/, date accessed: October 6, 2022

Question Of The Day #76

question of the day

Which of the following is the most appropriate next step in management?

This patient arrives to the Emergency department 10 hours after ingesting 11grams of paracetamol (APAP).  She has mild symptoms of nausea and upper abdominal discomfort and has normal vital signs. 

Paracetamol, also known as acetaminophen or APAP, is a commonly used pain medication safe for use in childhood, pregnancy, and breastfeeding.  Paracetamol is an ingredient present in many over the counter pain, headache, and cold medications.   Toxic paracetamol doses are acute ingestions over 150mg/kg, or about 10grams in adults.  Toxic paracetamol doses for children are 150mg/kg.  Multiple ingestions of paracetamol over 24 or 48 hours can also cause toxicity.  Ingestions of 10grams over 24hours or 6 grams/day over 48hours can also cause toxicity in adults.  Symptoms of acute poisoning can be absent or mild in the first 24 hours as seen in this patient.  After 24 hours, AST, ALT, bilirubin, and INR levels begin to increase, and over 72 hours post-ingestion, hepatic failure ensues.  5 days after an acute ingestion is when multi-organ failure occurs or hepatotoxicity resolves (less common).  Toxicity of APAP is thought to be caused by a toxic metabolite produced during APAP breakdown in the liver known.  This toxin is known as NAPQI.

APAP overdose can be fatal without treatment with the antidote commonly known as NAC, or N-acetylcysteine.  NAC is a free radical scavenger and prevents the damage caused by NAPQI.  If serum APAP testing is available, APAP levels drawn 4 hours after the time of an acute ingestion are used to determine if NAC is warranted.  APAP levels over 150mcg/mL at 4hours are the threshold for starting NAC.  This is based on use of the Rumack-Mathew Nomogram for APAP (see below).

Hendrickson RG, McKeown NJ. Acetaminophen. In: Nelson LS, Howland M, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS. eds. Goldfrank’s Toxicologic Emergencies, 11e. McGraw Hill; 2019.

Since this patient’s acute ingestion is above the known 10gram toxic dose, it is reasonable to start N-acetylcysteine therapy (Choice B) without first knowing the exact serum APAP level.  PO Activated charcoal (Choice A) can be used after oral ingestions to help bind some toxic substances and prevent their absorption through the GI system.  The majority of APAP is absorbed 2-4 hours after ingestion, so charcoal would not be helpful in this case where the ingestion was 10 hours ago.  Liver transplantation (Choice C) may ultimately be required for this patient depending on the liver function tests and how the patient responds over the coming days.  However, the best next step is NAC treatment to prevent liver failure and death.  IV Sodium bicarbonate (Choice D) is used in salicylate and tricyclic antidepressant overdose, but it has no role in APAP overdose.  The best next step is IV N-Acetylcysteine (Choice B).   

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #76," in International Emergency Medicine Education Project, February 11, 2022, https://iem-student.org/2022/02/11/question-of-the-day-76/, date accessed: October 6, 2022

Question Of The Day #75

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

This patient presents to the Emergency Department with altered mental status after ingestion of an unknown agent as part of a suicide attempt.  Her exam demonstrates hypertension, tachycardia, elevated temperature, disorientation, dilated pupils, and dry and hot skin.  Altered mental status has a broad differential diagnosis, including intracranial bleeding, stroke, post-ictal state, hypoglycemia, electrolyte abnormalities, other metabolic causes, infectious etiologies, toxicological causes, and many other conditions.  This patient’s history and exam support the presence of a toxidrome.  See the chart below for a review of the most common toxidromes (toxic syndromes). 

*Treatment of all toxic ingestions should include general supportive care and management of the airway, breathing, and circulation of the patient. Examples include administration of supplemental oxygen in hypoxia, IV fluids in hypotension, cooling measures in hyperthermia, etc.
**Flumazenil is the antidote for benzodiazepine overdose, but it is rarely used clinically as it can trigger benzodiazepine-refractory seizures.

 

Paracetamol (Choice A) is often accompanied with little to no symptoms in the first 24hours.  Later in the ingestion timeline, liver failure and its associated sequalae can occur if no antidote is given.  The symptoms exhibited by the patient do not correlate with APAP overdose.  Dextroamphetamine (Choice B) is a sympathomimetic agent that could be responsible for many of the patient’s symptoms, like elevated heart rate, hypertension, agitation, and dilated pupils.  However, dextroamphetamine should cause diaphoretic skin, not the dry skin that the patient has.  Ethanol (Choice C) may be a co-ingested agent in this scenario that could lead to agitation and confusion, but ethanol alone should not cause fever.  Diphenhydramine (Choice D) is an antihistamine agent, but it also has anticholinergic properties, especially when taken in excess.  This patient has all the signs of an anticholinergic toxidrome.  The presence or absence of dry skin can help differentiate a sympathomimetic toxidrome from an anticholinergic toxidrome.  Diphenhydramine (Choice D) is the most likely agent responsible for this patient’s symptoms.  Correct Answer: D

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #75," in International Emergency Medicine Education Project, February 4, 2022, https://iem-student.org/2022/02/04/question-of-the-day-75/, date accessed: October 6, 2022

Question Of The Day #74

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, difficulty breathing, vomiting, and hypersalivation after an unknown ingestion.  His exam shows an ill patient with constricted pupils (miosis), wet skin (diaphoresis), bradycardia, and tachypnea.  Altered mental status has a broad differential diagnosis, including intracranial bleeding, stroke, post-ictal state, hypoglycemia, electrolyte abnormalities, other metabolic causes, infectious etiologies, toxicological causes, and many other conditions.  This patient’s constellation of signs and symptoms support the presence of a cholinergic toxidrome due to organophosphate poisoning.  See the chart below for a review of the most common toxidromes (toxic syndromes). 

*Treatment of all toxic ingestions should include general supportive care and management of the airway, breathing, and circulation of the patient. Examples include administration of supplemental oxygen in hypoxia, IV fluids in hypotension, cooling measures in hyperthermia, etc.
**Flumazenil is the antidote for benzodiazepine overdose, but it is rarely used clinically as it can trigger benzodiazepine-refractory seizures.

 

Cholinergic toxidromes can be caused by organophosphate or carbamate pesticides, as well as nerve gas agents (i.e., sarin gas).  These agents cause poisoning by increasing the amount of acetylcholine at the neuromuscular junction, causing stimulation at muscarinic and nicotinic acetylcholine receptors.  This causes a dramatic increase in bodily secretions with increased respiratory secretions and airway compromise as the most common cause of death in this population.  The cholinergic toxidrome can be remembered with the mnemonic “DUMBBELLS” (diarrhea/diaphoresis, urination, miosis, bradycardia, bronchorrhea, emesis, lacrimation, low BP, salivation). 

The first step in treating any patient who has the potential cause to harm or expose staff members to the poisoning agent is patient decontamination (Choice C).  This patient should be undressed and adequately decontaminated by staff members who are wearing personal protective equipment (PPE).  Once the patient is decontaminated, the airway should be established with endotracheal tube placement (Choice A) and IV atropine (Choice B) should be given to reverse the toxidrome.  Atropine can be started at 2-4mg IV and repeated every 5-10 minutes until respiratory secretions are cleared.  Pralidoxime (Choice D) should also be given as soon as possible to prevent irreversible changes (“aging”) to the acetylcholinesterase at the neuromuscular junction.  This timeframe varies from minutes to hours after exposure, depending on the agent. All choices provided in this question are important actions to take, but patient decontamination (Choice C) is the most important initial next step. Correct Answer: C

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #74," in International Emergency Medicine Education Project, January 28, 2022, https://iem-student.org/2022/01/28/question-of-the-day-74/, date accessed: October 6, 2022

Question Of The Day #73

question of the day

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

This patient presents to the Emergency Department with a depressed mental status and normal sized pupils after an unknown toxic ingestion.  Many different agents can act as Central Nervous System depressants and cause this clinical presentation.  Some examples include ethanol, toxic alcohols (methanol, ethylene glycol, isopropyl alcohol), benzodiazepines, barbiturates, opioids, and muscle relaxants. 

Of the choices listed, Heroin (Choice A) and Alprazolam (Choice B) are the most likely.  Heroin is an opioid, and Alprazolam is a benzodiazepine (a sedative-hypnotic agent).  The clinical presentation caused by overdoses of opioids versus sedative-hypnotic agents overlaps in many areas, but the pupillary exam can help the most in differentiating the type of ingestion.  Opioids will can constricted, pinpoint pupils, while benzodiazepines should not cause change in pupillary size.  See the chart below for a review of the most common toxidromes (toxic syndromes). 

*Treatment of all toxic ingestions should include general supportive care and management of the airway, breathing, and circulation of the patient. Examples include administration of supplemental oxygen in hypoxia, IV fluids in hypotension, cooling measures in hyperthermia, etc.
**Flumazenil is the antidote for benzodiazepine overdose, but it is rarely used clinically as it can trigger benzodiazepine-refractory seizures.

Cocaine (Choice C) is a sympathomimetic with a CNS excitatory effect, not a CNS depressant effect as in this patient.  A large ingestion of paracetamol (Choice D) is often accompanied with little to no symptoms in the first 24hours.  Later in the ingestion timeline, liver failure and its associated sequalae can occur if no antidote is given.  Correct Answer: B

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #73," in International Emergency Medicine Education Project, January 21, 2022, https://iem-student.org/2022/01/21/question-of-the-day-73/, date accessed: October 6, 2022

Question Of The Day #72

question of the day

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

This patient presents to the Emergency Department with severe agitation and altered mental status.  His exam demonstrates hypertension, tachycardia, elevated temperature, restlessness, dilated pupils, and wet diaphoretic skin.  Altered mental status has a broad differential diagnosis, including intracranial bleeding, stroke, post-ictal state, hypoglycemia, electrolyte abnormalities, other metabolic causes, infectious etiologies, toxicological causes, and many other conditions.  This patient’s history and exam support the presence of a toxidrome.  See the chart below for a review of the most common toxidromes (toxic syndromes). 

*Treatment of all toxic ingestions should include general supportive care and management of the airway, breathing, and circulation of the patient. Examples include administration of supplemental oxygen in hypoxia, IV fluids in hypotension, cooling measures in hyperthermia, etc.
**Flumazenil is the antidote for benzodiazepine overdose, but it is rarely used clinically as it can trigger benzodiazepine-refractory seizures.

 

This patient has a sympathomimetic toxidrome (Choice C), which can be caused from cocaine, MDMA (ecstasy), methamphetamine, and other drugs.  The anticholinergic toxidrome (Choice A) has many overlapping features with the sympathomimetic toxidrome, such as elevated blood pressure and heart rate, elevated temperature, agitation, and dilated pupils.  One feature that can be used to differentiate these toxidromes is the skin exam.  Sympathomimetic agents commonly cause wet diaphoretic skin, while anticholinergic agents cause dry skin.  The cholinergic toxidrome (Choice B) presents with increased secretions (wet skin, diarrhea, vomiting, hypersalivation, bronchorrhea, etc.). One cause of this toxidrome is exposure to organophosphates.  This patient is diaphoretic, but otherwise does not possess the other features of the cholinergic toxidrome.  The opioid toxidrome (Choice D) would present with somnolence, as opposed to the CNS excitation seen in this patient.  Correct Answer: C

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #72," in International Emergency Medicine Education Project, January 14, 2022, https://iem-student.org/2022/01/14/question-of-the-day-72/, date accessed: October 6, 2022

Question Of The Day #71

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

This patient arrives to the Emergency Department with lethargy, decreased respiratory rate, hypoxemia, pinpoint pupils, and a normal glucose level.  The initial evaluation and treatment of this patient should be focused on management of the patient’s airway, breathing, and circulation (ABCs, also known as the ‘primary survey’).  The airway should be repositioned to minimize obstructions to breathing, such as the tongue.  Vomitus in the airway can also be removed manually or via suction to prevent obstruction of the airway or aspiration.  Next, supplemental oxygen should be provided to treat the patient’s hypoxemia. 

Altered mental status has a broad differential diagnosis, including intracranial bleeding, stroke, post-ictal state, hypoglycemia, electrolyte abnormalities, other metabolic causes, infectious etiologies, toxicological causes, and many other conditions.  This patient’s history and exam support the presence of an opioid toxidrome.  See the chart below for a review of the most common toxidromes (toxic syndromes). 

toxidromes
*Treatment of all toxic ingestions should include general supportive care and management of the airway, breathing, and circulation of the patient. Examples include administration of supplemental oxygen in hypoxia, IV fluids in hypotension, cooling measures in hyperthermia, etc.
**Flumazenil is the antidote for benzodiazepine overdose, but it is rarely used clinically as it can trigger benzodiazepine-refractory seizures.

In addition to supportive treatments, like airway repositioning and supplemental oxygen, the antidote to opioid overdose should be promptly administered.  Naloxone (Choice C) is the antidote to opioid overdose.  Naloxone can be administered intravenously, intramuscularly, and intranasally.   Naloxone should be started at a dose of 0.04mg and can be administered every 2-3 minutes at incrementally higher doses to a maximum total dose of 10mg.  The goal of Naloxone administration is to achieve independent ventilations.  Administering a larger initial dose of 0.4mg or 1mg can precipitate acute opioid withdrawal in a chronic opioid user. 

IV Lorazepam (Choice A) is a benzodiazepine and would make the patient more sedated.  Benzodiazepines are helpful in patients with an active seizure, severe agitation, or anxiety.  Anticholinergic overdose (atropine, scopolamine) or sympathomimetic overdose (cocaine, methamphetamines, MDMA) are also responsive to benzodiazepines.  IV Atropine (Choice C) is an anticholinergic agent.  Atropine would worsen this patient’s borderline hypotension and mild bradycardia.  IV Dextrose (Choice D) would be a reasonable medication to give if the glucose was unknown.  The question stem provides a normal glucose level. Correct Answer: B

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #71," in International Emergency Medicine Education Project, January 7, 2022, https://iem-student.org/2022/01/07/question-of-the-day-71/, date accessed: October 6, 2022

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. https://doi.org/10.1016/s0041-0101(00)00146-x
  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. https://doi.org/10.7861/clinmedicine.11-2-173
  3. Labossiere, A. W., & Thompson, D. F. (2018). Clinical Toxicology of Yew Poisoning. The Annals of pharmacotherapy, 52(6), 591–599. https://doi.org/10.1177/1060028017754225
  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, https://iem-student.org/2021/08/30/can-i-eat-this-a-helpful-guide-to-plant-toxicology/, date accessed: October 6, 2022

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.

ALTERED MENTAL STATUS

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

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #47," in International Emergency Medicine Education Project, July 23, 2021, https://iem-student.org/2021/07/23/question-of-the-day-47/, date accessed: October 6, 2022