In my last day as TR, I will end with a final “Name that Poisonous Beast!”. Farewell, to poisonous beasts everywhere! In this case, back in the garden.
Name this poisonous beast!
A)
And it’s amphibian colleague:
B)
- A) Foxglove (Digitalis purpurea)
- Entire plant (seeds, flowers, leaves) contains digitalis (cardiac glycoside); sometimes brewed as teas
- B) Cane Toad (Bufo marinus)
- Venom considered an aphrodisiac and a hallucinogen 2/2 bufotenin (serotonin analog); people engage in toad licking for this purpose
- Unfortunately for toad lickers, the venom also contains bufadienolide (cardiac glycoside)
- Cardiac Glycosides are also found in oleander, lily of the valley, squill, dogbane, and henbane
- Mechanism: reversibly inhibits the sodium-potassium-ATPase pump, increasing intracellular sodium and decreasing intracellular potassium
- Increased cardiocyte sodium increases intracellular calcium, ultimately leading to depolarization
- Cardiotoxicity: prolongs refractory period in AV node, shortens refractory period in atria and ventricles, decreases resting membrane potential (increased automaticity)
- Effects:
- CV: palpitations, chest pressure, sob, lightheadedness
- Multiple dysrhythmias (i.e. sinus bradycardia with block, sinus arrest, atrial tachycardia with block, junctional rhythms, ventricular tachycardia, bidirectional ventricular tachycardia, ventricular fibrillation); hypotension
- Refractory hyperkalemia (magnitude is predictive of outcome)
- GI: anorexia, n/v/d/abd pain
- Neurologic: weakness, AMS (disorientation, confusion, lethargy, hallucinations), headache, hypotonia, hyporeflexia, dysarthria, ataxia, horizontal nystagmus, seizures
- Visual: photophobia, blurred vision, scotomas, decreased visual acuity, color vision aberrations (i.e. yellow halos around lights)
- Renal: dysfunction more in chronic toxicity
- Complications: MI, CVA, ATN, death
- CV: palpitations, chest pressure, sob, lightheadedness
- Diagnosis: clinical
- Can send dig level; however, not all glycosides are measured by this assay and levels do not correlate with severity of illness (and also can not be used to calculate Digibind dose)
- Treatment: in addition to supportive care,
- Activated charcoal (ideally within 1 hour)
- Atropine for clinically significant bradycardia
- Essential treatment: Digoxin Fab fragment (Digibind)
- Although not as effective as in Digoxin toxicity (2/2 incomplete cross-reactivity), give if unstable arrhythmias, hyperkalemia, or evidence of end-organ dysfunction
- Action may take 30-60 minutes
- Cardiac arrest: give 10-20 vials, prolonged resuscitation may be warranted
- Hyperkalemia should be corrected by Digibind, other treatments do not reduce mortality and may lead to hypokalemia
- If no Digibind, can use phenytoin, lidocaine, and/or magnesium for dysrhythmias; pacing and cardioversion may be attempted but could cause rhythm degeneration
- AVOID: isoproterenol, quinidine, procainamide, calcium (possible “stone heart” – though latest studies show no harm)
- HD ineffective for toxin removal 2/2 large volume of distribution
- Mechanism: reversibly inhibits the sodium-potassium-ATPase pump, increasing intracellular sodium and decreasing intracellular potassium