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: July 2, 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: July 2, 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: July 2, 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: July 2, 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: July 2, 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: July 2, 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: July 2, 2022

Question Of The Day #9

question of the day
qod9

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

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: July 2, 2022

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 

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.

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: July 2, 2022

Triads in Medicine – Rapid Review for Medical Students

triads in medicine

One of the most convenient ways of learning and remembering the main components of disease and identifying a medical condition on an exam are Triads, and medical students/interns/residents swear by them.

Be it a question during rounds, a multiple-choice exam question to be solved, or even in medical practice, the famous triads help physicians recall important characteristics and clinical features of a disease or treatment in an instant.

Since exam season is here, this could serve as a rapid review to recall the most common medical conditions.

While there are a vast number of triads/pentads available online, I have listed the most important (high-yy) ones that every student would be asked about at least once in the duration of their course.

1) Lethal Triad also known as The Trauma Triad of Death
Hypothermia + Coagulopathy + Metabolic Acidosis

2) Beck’s Triad of Cardiac Tamponade
Muffled heart sounds + Distended neck veins + Hypotension

3) Virchow’s Triad – Venous Thrombosis
Hypercoagulability + stasis + endothelial damage

4) Charcot’s Triad – Ascending Cholangitis
Fever with rigors + Right upper quadrant pain + Jaundice

5) Cushing’s Triad – Raised Intracranial Pressure
Bradycardia + Irregular respiration + Hypertension

6) Triad of Ruptured Abdominal Aortic Aneurysm
Severe Abdominal/Back Pain + Hypotension + Pulsatile Abdominal mass

7) Reactive Arthritis
Can’t See (Conjunctivitis) + Can’t Pee (Urethritis) + Can’t Climb a Tree (Arthritis)

8) Triad of Opioid Overdose
Pinpoint pupils + Respiratory Depression + CNS Depression

9) Hakims Triad – Normal Pressure Hydrocephalus
Gait Disturbance + Dementia + Urinary Incontinence

10) Horner’s Syndrome Triad
Ptosis + Miosis + Anydrosis

11) Mackler’s Triad – Oesophageal Perforation (Boerhaave Syndrome)
Vomiting + Lower Thoracic Pain + Subcutaneous Emphysema

12) Pheochromocytoma
Palpitations + Headache + Perspiration (Diaphoresis)

13) Leriche Syndrome
Buttock claudication + Impotence + Symmetrical Atrophy of bilateral lower extremities

14) Rigler’s Triad – Gallstone ileus
Gallstones + Pneumobilia + Small bowel obstruction

15) Whipple’s Triad – Insulinoma
Hypoglycemic attack + Low glucose + Resolving of the attack on glucose administration

16) Meniere’s Disease
Tinnitus + Vertigo + Hearing loss

17) Wernicke’s Encephalopathy- Thiamine Deficiency
Confusion + Ophthalmoplegia + Ataxia

18) Unhappy Triad – Knee Injury
Injury to Anterior Cruciate Ligament + Medial collateral ligament + Medial or Lateral Meniscus

19) Henoch Schonlein Purpura
Purpura + Abdominal pain + Joint pain

20) Meigs Syndrome
Benign ovarian tumor + pleural effusion + ascites

21) Felty’s Syndrome
Rheumatoid Arthritis + Splenomegaly + Neutropenia

22) Cauda Equina Syndrome
Low back pain + Bowel/Bladder Dysfunction + Saddle Anesthesia

23) Meningitis
Fever + Headache + Neck Stiffness

24) Wolf Parkinson White Syndrome
Delta Waves + Short PR Interval + Wide QRS Complex

25) Neurogenic Shock
Bradycardia + Hypotension + Hypothermia

Further Reading

Cite this article as: Sumaiya Hafiz, UAE, "Triads in Medicine – Rapid Review for Medical Students," in International Emergency Medicine Education Project, June 12, 2020, https://iem-student.org/2020/06/12/triads-in-medicine/, date accessed: July 2, 2022

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

A Helpful Guide To Plant Toxicology – Anticholinergics

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)

anticholinergic
anticholinergic

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!

jimson weed - Datura Stromonium
Jimson Weed - Datura Stromonium
Atropa Belladonna
Deadly nightshade - Atropa Belladonna
jimson weed - Datura Stromonium
Jimson Weed - Datura Stromonium
Atropa Belladonna
Deadly nightshade - Atropa Belladonna

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: July 2, 2022

Reference

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

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