Calcium channel blocker toxicity: Difference between revisions
No edit summary |
|||
Line 31: | Line 31: | ||
**[[Hyperglycemia]] (due to insulin resistance) | **[[Hyperglycemia]] (due to insulin resistance) | ||
== | ==Differential Diagnosis== | ||
#[[Beta-blocker toxicity|Beta blockers]] | #[[Beta-blocker toxicity|Beta blockers]] | ||
##More likely to cause CNS changes | ##More likely to cause CNS changes | ||
Line 50: | Line 41: | ||
#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
- Cardiovascular
- Hypotension (any CCB overdose)
- Bradycardia (usually only seen with verapamil/diltiazem)
- AV/sinus block
- CHF
- Pulmonary
- Respiratory depression
- Pulmonary edema
- GI
- Neurologic
- Lethargy, confusion, coma
- Metabolic
- Hyperglycemia (due to insulin resistance)
Differential Diagnosis
- Beta blockers
- More likely to cause CNS changes
- Hypoglycemia is more common
- Digoxin
- Nausea/vomiting is more common
- Clonidine
- Miosis, somnolence
- Cholinergic agents
- SLUDGE
Diagnosis
- ECG
- PR prolongation (varying degrees of AV block)
- AV block occurs more commonly with verapamil
- Bradydysrhythmia
- PR prolongation (varying degrees of AV block)
- Glucose
- Chemistry
- 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
- Takes 30-60min for effect
- Glucose:
- Adult: 50mL of D50W
- Ped: 2.5mL/kg of D10
- Insulin bolus 1 unit/kg followed by 0.5units/kg/hr
- Titrate infusion until hypotension is corrected or max 2u/kg/hr
- Requires frequent glucose and K checks
- Potassium
- If <3 administer 20mEq IV
Calcium
Avoid if digoxin toxicity is possible
- Calcium gluconate 3g (30-60mL of 10% soln)
- Calcium chloride 1-3g IV bolus (10-20mL of 10% soln (requires large IV/central line)
- Preferred over calcium gluconate because it provides triple the amount of calcium on a weight-to-weight basis [2]
- Effects of calcium are transient
- Repeat dosing often required
- Alternatively, can be given as an infusion: 2-6g/hour
Vasopressors
- Norepinephrine is agent of choice
Glucagon
- 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
- Adult: 0.5-1mg IV q2-3min to max of 3g
- Ped: 0.02mg/kg (minimum is 0.1mg)
When standard treatment fails
- Intravenous lipid emulsion
- 1.5mL/kg of 20% lipid followed by 0.25mL/kg/minute
- Data show significant benefit in animals and case reports show promise in humans
- 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