Calcium channel blocker toxicity: Difference between revisions

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**[[Hyperglycemia]] (due to insulin resistance)
**[[Hyperglycemia]] (due to insulin resistance)


==Work-Up==
==Differential Diagnosis==
#ECG
##PR prolongation (varying degrees of AV block)
###AV block occurs more commonly with verapamil
##Bradydysrhythmia
#Glucose
#Chemistry
##Serum calcium is often normal
 
==DDx==
#[[Beta-blocker toxicity|Beta blockers]]
#[[Beta-blocker toxicity|Beta blockers]]
##More likely to cause CNS changes
##More likely to cause CNS changes
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#Cholinergic agents
#Cholinergic agents
##SLUDGE
##SLUDGE
==Diagnosis==
#[[ECG]]
##PR prolongation (varying degrees of AV block)
###AV block occurs more commonly with verapamil
##Bradydysrhythmia
#Glucose
#Chemistry
##Serum calcium is often normal


== Treatment  ==
== Treatment  ==

Revision as of 01:30, 7 June 2015

Background

  • Hemodialysis is ineffective
  • Precipitous deterioration is common (esp w/ verapamil)
  • Nifedipine can kill a child with a single pill

2 Classes

Dihydropyridines

  • Nifedipine, Amlodipine, Nicardipine
    • Systemic vasodilation, mild effect on heart
  • Toxicity = Hypotension, reflex tachycardia
  • With higher doses of toxicity peripheral selectivity is lost
    • I.e. may see decreased inotrophy, bradycardia

Non-dihydropyridines (verapamil, diltiazem)

  • Stronger effect on heart, weak vasodilators
  • Toxicity = Bradycardia, decreased inotropy

Clinical Features

Differential Diagnosis

  1. Beta blockers
    1. More likely to cause CNS changes
    2. Hypoglycemia is more common
  2. Digoxin
    1. Nausea/vomiting is more common
  3. Clonidine
    1. Miosis, somnolence
  4. Cholinergic agents
    1. SLUDGE

Diagnosis

  1. ECG
    1. PR prolongation (varying degrees of AV block)
      1. AV block occurs more commonly with verapamil
    2. Bradydysrhythmia
  2. Glucose
  3. Chemistry
    1. Serum calcium is often normal

Treatment

  • Monotherapy only successful for trivial overdoses


The majority of literature on calcium channel blocker overdose management is low-quality evidence and high-dose insulin and extracorporeal life support have the best evidence and other therapies such as include calcium, dopamine, norepinephrine, and lipid emulsion therapy may be beneficial but are poorly studied[1]

Charcoal

  • 1g/kg (max 50g) x1
    • Consider if present w/in 1-2hr w/ delayed-release preparation

High-dose insulin and glucose

  1. Takes 30-60min for effect
  2. Glucose:
    1. Adult: 50mL of D50W
    2. Ped: 2.5mL/kg of D10
  3. Insulin bolus 1 unit/kg followed by 0.5units/kg/hr
    1. Titrate infusion until hypotension is corrected or max 2u/kg/hr
    2. Requires frequent glucose and K checks
  4. Potassium
    1. If <3 administer 20mEq IV

Calcium

Avoid if digoxin toxicity is possible

  1. Calcium gluconate 3g (30-60mL of 10% soln)
  2. Calcium chloride 1-3g IV bolus (10-20mL of 10% soln (requires large IV/central line)
    1. Preferred over calcium gluconate because it provides triple the amount of calcium on a weight-to-weight basis [2]
    2. Effects of calcium are transient
    3. Repeat dosing often required
      1. Alternatively, can be given as an infusion: 2-6g/hour

Vasopressors

  1. Norepinephrine is agent of choice

Glucagon

  1. 5mg IV bolus q10min x 2

Fluids

  • Initial 20cc/kg bolus especially if source of hypotension is undifferentiated and also possibly hypovolemic or due to Sepsis

Atropine

  1. Adult: 0.5-1mg IV q2-3min to max of 3g
  2. Ped: 0.02mg/kg (minimum is 0.1mg)

When standard treatment fails

  1. Intravenous lipid emulsion
    1. 1.5mL/kg of 20% lipid followed by 0.25mL/kg/minute
    2. Data show significant benefit in animals and case reports show promise in humans
    3. If used, report on http://www.lipidrescue.org to contribute to the database

Disposition

  • Admit all symptomatic pts
  • Admit all sustained-release ingestions
  • D/C if asymptomatic x 6-8hrs

See Also

References

  1. St-Onge M, et al. Treatment for calcium channel blocker poisoning: a systematic review. Clin Toxicol 2014 PDF
  2. Tintinalli's 7th Ed.