Vancouver IM LMR

Didactic slides from today’s noon report are found here. We reviewed a case of cardiac glycoside (digitalis) toxicity due to unintentional consumption of foxglove (Digitalis purpurea – native to Europe but well established in coastal BC as well)

Key takeaways:

1. Always involve Poison Control for suspected poisonings.
2. Remember the basic approach to poisoned patients – ABCDE (ABC + decontamination + elimination) and the physical exam components to identify toxidromes (vitals, pupils, tone, reflexes/tremor/clonus, skin moisture).
   • For your interest, IBCC has an excellent summary of approach to the poisoned patient
3. Main points of digoxin toxicity:
   • Identification: Exposure to cardiac glycosides, fatigue, n/v, anorexia, +/- neuro symptoms +/- visual symptoms (blurring/hazy vision, green-yellow tinted vision called xanthopsia, halos). Chronic toxicity can be more subtle eg elderly person on digoxin for AFib rate control develops an AKI and has onset of new neuro symptoms.
   • Important cardiac manifestations are arrhythmias (eg PVC, VT, VF, AFib, digitalis effect) and bradycardia (2/2 increased vagal tone).
   • Digoxin levels can be supportive but do not correlate well with toxicity. Levels over 2 lend more support to toxicity.
   • Risk factors for toxicity include advanced age, renal impairment, electrolyte abn (eg hypokalemia, hypomagnesemia)
   • Treatment is supportive in the absence of life-threatening complications
     • Activated charcoal if early presentation (guided by Poison Control)
     • Can temporize bradycardia with atropine if patient unstable.
   • Definitive treatment is with Digifab (specific Ab against digitalis), indicated for life-threatening toxicity including unstable bradycardia unresponsive to atropine, other life-threatening rhythms, very high digoxin levels, K > 5.5 (poor prognostic feature – 100% mortality without Digifab)
4. Digoxin and potassium
   • Digoxin blocks the Na-K-ATPase -> high extracellular K -> hyperkalemia in acute toxicity
   • In chronic toxicity, renal excretion of potassium leads to hypokalemia
   • Digoxin binds specifically to the K+ site of the Na-K-ATPase, thus someone with baseline hypokalemia before exposure is at higher risk for worse toxicity as the binding sites for digoxin are wide open in the absence of normal K levels.
   • Old pre-Digifab case series from the 1970s showed 100% survival with K < 5 and 100% mortality with K > 5.5. Potassium is a very important prognostic marker and K > 5.5 is an indication to give Digifab.