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