Calcium channel blocker toxicity: Difference between revisions
| Line 51: | Line 51: | ||
*Monotherapy only successful for trivial overdoses | *Monotherapy only successful for trivial overdoses | ||
===[[Charcoal]] | ===GI decontamination=== | ||
*1g/kg (max 50g) x1 | *[[Charcoal]] | ||
**1g/kg (max 50g) x1 | |||
**Consider if present within 1-2hr with delayed-release preparation | **Consider if present within 1-2hr with delayed-release preparation | ||
*Consider [[whole bowel irrigation]] if sustained or extended-release, esp if the drug is verapamil or diltiazem | |||
===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]]=== | ||
*[[ | *Adult: 0.5-1mg IV q2-3min to max of 3g | ||
*Ped: 0.02mg/kg (minimum is 0.1mg) | |||
*Administer to anyone with symptomatic [[bradycardia]] | |||
===Calcium=== | ===Calcium=== | ||
| Line 69: | Line 73: | ||
**If effect in BP is seen can give as a drip at 10-50mg/kg/hr | **If effect in BP is seen can give as a drip at 10-50mg/kg/hr | ||
**can safely push serum Calcium levels to 15-18 or even low 20s if patient tolerates (double normal) | **can safely push serum Calcium levels to 15-18 or even low 20s if patient tolerates (double normal) | ||
===[[Glucagon]]=== | |||
*5mg IV bolus q10min x 2 | |||
*will often cause severe nausea/vomiting, give Zofran prior | |||
===[[Vasopressors]]=== | |||
*[[Norepinephrine]] is agent of choice | |||
** Start at 2mcg/min, uptitrate rapidly, goal MAP 65mmHg | |||
===[[High dose insulin therapy| High-dose insulin and glucose]]=== | ===[[High dose insulin therapy| High-dose insulin and glucose]]=== | ||
| Line 81: | Line 93: | ||
*Potassium | *Potassium | ||
**If <3 administer 20mEq IV | **If <3 administer 20mEq IV | ||
===[[Intralipid|Intravenous lipid emulsion]]=== | ===[[Intralipid|Intravenous lipid emulsion]]=== | ||
Revision as of 19:40, 6 May 2017
Background
- Hemodialysis is ineffective
- Precipitous deterioration is common (esp with 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 (inhibits insulin release from pancreatic islet cells)
- Helps to differentiate from Beta-Blocker Toxicity
- Hyperglycemia (inhibits insulin release from pancreatic islet cells)
Differential Diagnosis
Symptomatic bradycardia
- Cardiac
- Inferior MI (involving RCA)
- Sick sinus syndrome
- Neurocardiogenic/reflex-mediated
- Increased ICP
- Vasovagal reflex
- Hypersensitive carotid sinus syndrome
- Intra-abdominal hemorrhage (i.e. ruptured ectopic)
- Metabolic/endocrine/environmental
- Hyperkalemia
- Hypothermia (Osborn waves on ECG)
- Hypothyroidism
- Hypoglycemia (neonates)
- Toxicologic
- Infectious/Postinfectious
- Other
Evaluation
- ECG
- PR prolongation (varying degrees of AV block)
- AV block occurs more commonly with verapamil
- Bradydysrhythmia
- PR prolongation (varying degrees of AV block)
- Glucose
- hyperglycemia, may help distinguish beta blocker toxicity
- Chemistry
- Serum calcium is often normal
Management
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
GI decontamination
- Charcoal
- 1g/kg (max 50g) x1
- Consider if present within 1-2hr with delayed-release preparation
- Consider whole bowel irrigation if sustained or extended-release, esp if the drug is verapamil or diltiazem
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)
- Administer to anyone with symptomatic bradycardia
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]
- Give Calcium 1g Q5min to titrate to BP effect
- If effect in BP is seen can give as a drip at 10-50mg/kg/hr
- can safely push serum Calcium levels to 15-18 or even low 20s if patient tolerates (double normal)
Glucagon
- 5mg IV bolus q10min x 2
- will often cause severe nausea/vomiting, give Zofran prior
Vasopressors
- Norepinephrine is agent of choice
- Start at 2mcg/min, uptitrate rapidly, goal MAP 65mmHg
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 given with 1amp of D50
- Titrate infusion until hypotension is corrected or max 2u/kg/hr
- Titrate dextrose drip to avoid hypoglycemia
- initial glucose checks q15 minutes until blood sugar stability established
- Potassium
- If <3 administer 20mEq IV
Intravenous lipid emulsion
- 1.5mL/kg bolus of 20% lipid followed by 0.25mL/kg/minute
Disposition
- Admit all symptomatic patients
- Admit all sustained-release ingestions
- Discharge if asymptomatic x 6-8hrs
See Also
Video
{{#widget:YouTube|id=twKMOXaH2dE}}
