This is a tough one and congratulations to the thorough responders. This month’s winner – Dr. Nico Grundmann!
To start, TCA ingestion is the most common cause of Na-channel toxicity that we see in ECGs – but this patient was not taking TCA’s. She ingested more than 4 grams of the Flecainide she had been prescribed for her SVT.
Now, for a walk down memory lane. Remember your two best friends from medical school, Pharmacology and Biochemistry? Well, they’re back (sigh)…
Flecainide?!
Treatment for this toxidrome?
Sodium bicarbonate! Give if QRS > 100 msec or a ventricular arrhythmia. It narrows the QRS, improves systolic blood pressure, and decreases ventricular arrhythmias. Bicarb pushes act via a Na depended effect. It essentially competes for binding at the Na channel with the Na-Channel blocking drug. Bicarb drips act via a pH-dependent effect by converting the Na-channel blocker to its non-ionized form, which reduces its ability to bind to the Na-channel binding site. Some authors advocate a goal pH of 7.50-7.55 (can also hyperventilate if the patient is intubated).
Sodium bicarbonate can induce hypokalemia (likely by shifting potassium intracellularly), leading to prolonged QTc. Serum pH and potassium levels should be checked hourly until pH levels are within desired range. Replete potassium as needed.
If patients present within 2 hours of ingestion, one dose of activated charcoal may be given.
Supportive care such as airway management prn, cardiac monitoring, IV fluids and vasopressors prn.
Dispo: Patients with mild symptoms and no signs of conduction abnormalities (i.e QRS <100) after being observed for several hours may be admitted to a non-critical care setting with telemetry.
Treatment for this toxidrome if super-sick?
Intravenous fat emulsion can be used as an antidote for highly lipophilic drugs (i.e flecainide, propofol, etc.). There are 3 proposed mechanisms, the most popular being the lipid sink/sponge model where the drug is removed from its site of toxicity and deposited into areas with high lipid content (like Intralipid) where it is then excreted. Current indications for lipid emulsion include patients not responding to standard therapy (including sodium bicarbonate) and cardiac arrest. Consider it early! Up to three IV boluses can be given, followed by an infusion for up to one hour or until hemodynamic recovery.
Lidocaine is recommended in some textbooks but may not be a great choice as it can also block sodium channels and further widen the QRS in toxicity. Again, think Intralipid!
Dispo: Patients with AMS, conduction abnormalities, hypotension, or seizures should be admitted to MICU.
If only pharmacology and biochemistry were this cool in medical school…
By Dr. Yonatan Yohannes, Dr. Elizabeth Abram and supervised by Dr. Jennifer Martindale. Snazzy web-editing by Dr. Andy Grock
References:
Lewin, NA, Nelson, LS. Chapter 63: Antidysrhythmics. Goldfrank’s Toxicologic Emergencies. 9th edition. 2011.
Wax, PM. Antidotes in Depth (A5): Sodium Bicarbonate. Goldfrank’s Toxicologic Emergencies. 9th edition. 2011.
Bania, TC. Antidotes in Depth (A21): Intravenous Fat Emulsions. Goldfrank’s Toxicologic Emergencies. 9th edition. 2011.
Jang, DH, Hoffman, RS, Nelson, LS. A Case of Near-Fatal Flecainide Overdose in a Neonate Successfully Treated with Sodium Bicarbonate. J of Emerg Med. April 2013; 44(4): 781-783.
Life in the Fast Lane. http://lifeinthefastlane.com/ecg-library/basics/tca-overdose/.
Salhanick, SD. Tricyclic Antidepressant Poisoning. Up To Date 2014. http://www.uptodate.com.
eabram
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1 Comment
adam.aluisio · December 19, 2014 at 1:48 pm
If you need to know how to dose lipid therapy look here.
http://blog.clinicalmonster.com/2014/05/morning-report-522014/#respond
Also there is an approved protocol at UHB for using LRT in patients with instability from toxic overdoses.