Case of the Month #2, Answer 8/5/14

Sodium channel blockers! Vaughan-Williams Class Ia or 1c anti-arrhythmics such as: cocaine, diphenhydramine, TCA’s, amantadine, carbamazepine, flecainaide, encainide, procainamide, quinidine, quinine, propoxyphene, mesoridazine and thioridazine. Feel free to look up electropotentials and the different classes of anti-arrhythmics.

Cocaine…a little but the dry skin sounds more anticholinergic than sympathomimetic, TCA’s… a little, but would probably be sicker, with hypotension due to alpha blockade. Diphenhydramine YES!!!.

Antagonist of H1 receptors, antagonist of muscarinic receptors and antagonist of sodium channels. Commonly presents as anti-cholinergic toxidrome.

 

Sodium! Typically in the form of a sodium bicarbonate push, which acts NOT through the bicarbonate, but through the sodium, which, in larger concentrations, is able to overwhelm the sodium channel inhibitor. Per the case reports referenced below, peds dose of sodium bicarb is 1meq/kg. In the case reports, after giving the bicarb, the patient’s ECG can change to a narrow qrs with…a terminal R in AVR. What’s that?

Through a currently unknown mechanism, the sodium channel blockers block the right bundle better than the left leading to delayed right ventricle depolarization. This is reflected in right axis deviation including an R in AVR >3mm or an R/S ratio of >0.7

Can start sodium bicarbonate infusion and titrate to normalization of the qrs interval. This time, the sodium bicarb works through the bicarb as drug inhibitors bind to the Na channel blocker less well in higher pH’s. Otherwise, supportive care – benzos for seizures and, if those unsuccessful, propofol and intubation. Rarely, rhabdo occurs. Probably get labs including cbc/cmp, Tylenol/Aspirin levels, maybe dig level. 20 ml/kg bolus of NS followed by supportive care and admission. May need US to monitor for urinary retention, or place Foley catheter, which is both diagnostic and therapeutic for urinary retention.

Physiostigmine can be used for anti-cholinergic toxicity including diphenhydramine, but is CONTRA-INDICATED in patients with wide QRS, bradycardia, history of asthma or pulmonary disease

1. great review of ASA toxicity. You are correct that you must induce respiratory alkylosis on intubating them and you should avoid intubating them unless absolutely necessary. Any drop in pH in ASA overdose leads to increased ASA in the brain (bad). Here, I gave you an incomplete VBG, making it hard to tell if there was a metabolic or respiratory acidosis or a mixed picture. Her respiratory rate is 15, which would argue against the metabolic acidosis with the respiratory alkylosis found in ASA toxicity and ASA would theoretically not cause a prolonged qrs. I definitely had dig on the differential here (review of dig toxicity here)for her and metformin toxicity was great to include as well.

2. As for iron toxicity – also a possibility. It typically presents with vomiting/diarrhea/nausea/abdominal pain initially. They CAN develop lethargy after the initial GI stage. Then they proceed to shock and liver failure. Iron toxicity can be diagnosed with an iron level >300mcg from 2-6 hours after ingestion. Typically, abdominal xray is done to look for iron tablets, but does not rule out ingestion if negative. The abd x-ray can also be used to locate the tablets and help determine which GI decontamination should be used. After reading Goldfrank’s, you can also check out a good iron toxicity review here.