Calcium channel blocker toxicity: Difference between revisions
m (Rossdonaldson1 moved page Calcium Channel Blocker Toxicity to Calcium channel blocker toxicity) |
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== Treatment == | == Treatment == | ||
''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; other therapies such as include calcium, dopamine, norepinephrine, and lipid emulsion therapy may be beneficial but are poorly studied<ref>St-Onge M, et al. Treatment for calcium channel blocker poisoning: a systematic review. Clin Toxicol 2014 [http://informahealthcare.com/doi/pdf/10.3109/15563650.2014.965827 PDF]</ref> | |||
*Monotherapy only successful for trivial overdoses | *Monotherapy only successful for trivial overdoses | ||
===Charcoal=== | ===Charcoal=== | ||
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===Calcium=== | ===Calcium=== | ||
''Avoid if [[digoxin toxicity]] is possible'' | ''Avoid if [[digoxin toxicity]] is possible'' | ||
*Calcium gluconate 3g (30-60mL of 10% soln) | *[[Calcium gluconate]] 3g (30-60mL of 10% soln) | ||
*Calcium chloride 1-3g IV bolus (10-20mL of 10% soln (requires large IV/central line) | *[[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 <ref>Tintinalli's 7th Ed.</ref> | **Preferred over calcium gluconate because it provides triple the amount of calcium on a weight-to-weight basis <ref>Tintinalli's 7th Ed.</ref> | ||
**Effects of calcium are transient | **Effects of calcium are transient | ||
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***Alternatively, can be given as an infusion: 2-6g/hour | ***Alternatively, can be given as an infusion: 2-6g/hour | ||
===Vasopressors=== | ===[[Vasopressors]]=== | ||
*[[Norepinephrine]] is agent of choice | *[[Norepinephrine]] is agent of choice | ||
===Glucagon=== | ===[[Glucagon]]=== | ||
*5mg IV bolus q10min x 2 | *5mg IV bolus q10min x 2 | ||
===Fluids=== | ===Fluids=== | ||
*Initial 20cc/kg bolus especially if source of hypotension is undifferentiated and also possibly hypovolemic or due to [[Sepsis]] | *Initial 20cc/kg bolus especially if source of hypotension is undifferentiated and also possibly hypovolemic or due to [[Sepsis]] | ||
===Atropine=== | ===[[Atropine]]=== | ||
*Adult: 0.5-1mg IV q2-3min to max of 3g | *Adult: 0.5-1mg IV q2-3min to max of 3g | ||
*Ped: 0.02mg/kg (minimum is 0.1mg) | *Ped: 0.02mg/kg (minimum is 0.1mg) | ||
Revision as of 01:32, 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
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; other therapies such as include calcium, dopamine, norepinephrine, and lipid emulsion therapy may be beneficial but are poorly studied[1]
- Monotherapy only successful for trivial overdoses
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