Calcium channel blocker toxicity

Revision as of 03:36, 27 February 2015 by Hkm91450 (talk | contribs) (elaboration)

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

Diagnosis

  • Cardiovascular
    • Hypotension (any CCB overdose)
    • Bradycardia (usually only seen with verapamil/dilt)
    • AV/sinus block
    • CHF
  • Pulmonary
    • Respiratory depression
    • Pulmonary edema
  • GI
    • Nausea/vomiting
  • Neurologic
    • Lethargy, confusion, coma
  • Metabolic
    • Hyperglycemia (due to insulin resistance)

Work-Up

  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

DDx

  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

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 1g (10-20mL of 10% soln (requires large IV/central line)

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)
  1. Intravenous lipid emulsion (when standard treatment fails)
    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

Source

  1. St-Onge M, et al. Treatment for calcium channel blocker poisoning: a systematic review. Clin Toxicol 2014 PDF