Barbiturate Poisoning
The author would like to provide special thanks to the author of the prior edition, Matthew Valento.
CODES
ICD9
969.4 Poisoning by benzodiazepine-based tranquilizers
ICD10
- T42.4X1A Poisoning by benzodiazepines, accidental, init
- T42.4X2A Poisoning by benzodiazepines, intentional self-harm, init
- T42.4X4A Poisoning by benzodiazepines, undetermined, init encntr
BETA-BLOCKER POISONING
Christopher S. Lim
•
Steven E. Aks
BASICS
DESCRIPTION
Normal Physiology
- Cardiovascular: β
1
-receptors:
- ATP converted to cAMP by adenyl cyclase with stimulation of β-receptors.
- cAMP activates protein kinase, which phosphorylates proteins of the sarcoplasmic reticulum.
- Sarcoplasmic reticulum releases calcium.
- Excitation–contraction coupling occurs.
- Effects of β-blockers:
- Cardiovascular:
- Decreased excitation/contraction
- Membrane stabilizing activity
- Sodium channel blockade causes a prolongation of the QRS complex (with some agents).
- Prolongation of QTc interval leading to ventricular dysrhythmias (with some agents)
- Intrinsic sympathomimetic activity
- Partial agonist properties (with some agents)
- Neurologic:
- CNS effects with the lipophilic agents (propranolol, metoprolol, labetalol)
DIAGNOSIS
SIGNS AND SYMPTOMS
- Cardiovascular:
- Hypotension
- Bradycardia
- Cardiac conduction delays
- Heart block
- Heart failure
- Electrical mechanical dissociation
- Loss of β-selectivity in overdose settings
- Neurologic:
- Pulmonary:
- Bronchospasm
- Pulmonary edema
- Metabolic:
History
- Inquire about risk of medication error.
- Inquire about risk of suicidal ideation with intent.
- Inquire about possible exposure to medications with a pediatric patient.
Physical-Exam
- Hypotension
- Bradycardia
- Dysrhythmias
ESSENTIAL WORKUP
- With unknown ingestion: Suspect β-blocker poisoning with bradycardia/hypotension.
- ECG:
- Conduction delays
- 1st-, 2nd-, or 3rd-degree heart block
- Bradycardia
DIAGNOSIS TESTS & NTERPRETATION
Lab
- CBC
- Electrolytes, BUN, creatinine, glucose
- Toxicology screen if coingestants suspected
DIFFERENTIAL DIAGNOSIS
- Calcium-channel blocker toxicity
- Clonidine toxicity
- Digitalis toxicity
- Acute myocardial infarction with heart block
TREATMENT
PRE HOSPITAL
- Transport pills and pill bottles when overdose suspected.
INITIAL STABILIZATION/THERAPY
- ABCs:
- Airway protection as indicated by mental status
- Supplemental oxygen as needed
- 0.9% NS IV access
- Close hemodynamic monitoring
- Naloxone and thiamine if altered mental status
- Bedside glucose determination, treat hypoglycemia with D
50
W
- Treat prolonged seizures with benzodiazepines
ED TREATMENT/PROCEDURES
Goals
- Heart rate >60 beats per minute
- Systolic BP >90 mm Hg
- Adequate urine output
- Improving level of consciousness
GI Decontamination
- Syrup of ipecac: Contraindicated in the prehospital and ED setting.
- Consider lavage with Ewald tube if ingestion within 1 hr:
- Propranolol may cause esophageal spasm producing difficulty with passage and removal of gastric lavage tube.
- Activated charcoal helpful especially in the presence of coingestants.
Bradycardia/Hypotension
- Atropine:
- Initial agent
- Low success rate
- Glucagon:
- Initial drug of choice for β-blocker–induced hemodynamic instability
- Administer if atropine does not increase heart rate.
- Promotes cAMP production through a receptor site other than the β-receptor
- May cause nausea and vomiting
- Mix with NS or D
5
W
- IV fluids:
- Administer cautiously in the hypotensive patient
- Swan-Ganz catheter or central venous pressure (CVP) monitoring to help follow volume status
- Amrinone:
- Selective phosphodiesterase inhibitor
- Indirectly increases cAMP leading to increased inotropy
- Use in conjunction with glucagon to treat symptomatic sustained bradycardia.
- Vasopressor agents:
- Initiate when symptomatic hypotension/bradycardia persists after atropine/glucagon.
- Use invasive monitoring to help guide therapy.
- Utility may be limited owing to β-blockade:
- Higher doses may be required.
- Isoproterenol (nonselective β-agonist):
- Titrate for BP and heart rate.
- Epinephrine (potent α- and β-receptor agonist):
- BP increases as a result of direct myocardial stimulation, increase in heart rate, and vasoconstriction.
- Use if no BP response with isoproterenol
- High-dose dopamine
- Sodium bicarbonate:
- In theory, this is used if there is evidence of prolongation of QRS >100 ms owing to some of the β-blockers also causing sodium channel blockade leading to a prolonged QRS.
- Not routinely administered for all β-blocker toxicities
- Electrical pacing: When other treatment options have failed
Experimental Treatment Options
- Consult with local poison center
- High-dose insulin:
- Promotes more efficient myocardial metabolism
- Hypoglycemia commonly seen in β-blocker overdose, will require frequent monitoring of glucose concentration
- Perform in consultation with local poison center
- IV fat emulsion therapy (20% intralipid)
Enhanced Elimination
- Hemodialysis helpful with water-soluble β-blocking agents:
- IV fat emulsion (20% Intralipid):
- Potential treatment in the future
MEDICATION
- Activated charcoal: 1 g/kg PO
- Amrinone: Loading dose 0.75 mg/kg; maintenance drip 2–20 μg/kg/min; titrate for effect
- Atropine: 0.5 mg (peds: 0.02 mg/kg) IV; repeat 0.5–1 mg IV (peds: 0.04 mg/kg)
- Dopamine: 2–20 μg/kg/min IV
- Dextrose: D
50
W 1 ampule (50 mL or 25 g; peds: D
25
W 2–4 mL/kg) IV
- Epinephrine: 2 μg/min (peds: 0.01 mg/kg [0.1 mL/kg 1:10,000]); titrate to effect
- Glucagon: 3–5 mg IV over 1–2 min (peds: 0.03–0.1 mg/kg) bolus followed by 70 μg/kg/h infusion
- Insulin (regular insulin): 1 IU/kg bolus IV followed by 0.5–1 IU/kg/h titrated to clinical response (be sure to supplement with dextrose)
- Isoproterenol: 5 μg/min IV and titrate for heart rate effect
- Norepinephrine: Start 2–4 μg/min IV, titrate up to 1–2 μg/kg/min IV
- Sodium bicarbonate: 1 mEq/kg IVP
First Line
- IV fluids
- Glucagon
- Vasopressor agents
Second Line
- Sodium bicarbonate
- Hemodialysis
FOLLOW-UP