β-BLOCKER (βB) OVERDOSE
History
• Witnessed or reported overingestion of βB
• Children who have been at homes of older relatives taking prescribed medications
Findings
• Symptomatic bradycardia, hypotension, AMS, weakness, bronchospasm
• Lipid-soluble βB (propranolol) – sz; sotalol – ↑ QTc, torsades de pointes
• May have hypoglycemia, nausea, vomiting, hyperkalemia
Evaluation
• ECG shows bradycardia, AV or intraventricular block, asystole
• Check cardiac enzymes, chemistries; drug levels not available
Treatment
• Continuous Tele, 2 large-bore IVs, place transcutaneous pacer pads on pt
• Place a cordis in the R IJ or L subclavian vein if transvenous pacing indicated
• For symptomatic or refractory βB OD, administer
• Atropine 0.5–1 mg IV (ACLS protocol) for severe bradycardia and/or hypotension
• Glucagon 5–10 mg IV bolus followed by infusion of 1–5 mg/h if hypotensive
• Pressors if indicated (epinephrine), cardiac pacing prn
• Sodium bicarbonate 1–2 mEq/kg for wide-complex conduction defects
• Consider hyperinsulinemia–euglycemia therapy &/or IV lipid emulsion (benefit in animals & case reports)
• No role for activated charcoal or whole bowel irrigation unless massive recent OD
• HD only useful for βB w/ low volume of distribution (acebutolol, atenolol, nadolol, timolol, sotalol) if unresponsive to medical intervention, or if pressors/glucagon necessary to maintain BP
Disposition
• Admission to floor vs. ICU (if symptomatic)
• Clinically significant βB OD develop sxs w/i 6 h; if remain asymptomatic, can be discharged unless ingested sustained release formulation (24 h observation)
CALCIUM CHANNEL BLOCKER (CCB) OVERDOSE
History
• Witnessed or reported overingestion of CCB
• Children who have been at homes of older relatives taking prescribed medications
Findings
• Symptomatic bradycardia, hypotension, AMS, n/v, weakness
• Transient hyperglycemia; sz rare
Evaluation
• ECG shows bradycardia, ventricular escape rhythm, 2nd- or 3rd-degree AV block; usually nl QRS complex (vs. βB OD)
• Check cardiac enzymes, chemistry; drug levels not available
Treatment
• Continuous Tele, 2 large-bore IVs, place transcutaneous pacer pads on pt
• Place a cordis in the R IJ or L subclavian vein if transvenous pacing indicated
• Continue supportive therapy including volume resuscitation & pressors for hypotension & depressed inotropy
• For either symptomatic βB or CCB OD, administer
• Atropine 0.5–1 mg IV (ACLS protocol)
• Glucagon 5–10 mg IV bolus followed by infusion of 1–5 mg/h if hypotensive
• Calcium gluconate 3 g slow IV push or calcium chloride 1 g IV q5–10min prn
• Can reverse depression of cardiac contractility; no effect on sinus node depression or peripheral vasodilation; variable effect on AV node conduction
• Pressors if indicated (dopamine, norepinephrine, amrinone)
• For CCB OD, hyperinsulinemia–euglycemia therapy can provide fuel for enhanced myocardial contractility
• If glucose <200 mg/dL, give dextrose 0.25 g/kg D25 up to 1 amp D50
• If K+ <2.5 mEq/dL, administer 40 mEq IV; monitor and replete K+ prn
• Administer regular insulin 0.5–1 U/kg IV bolus, followed by infusion of 0.5–1 U/kg/h
• Start D10 ½ NS at 80% maintenance rate
• Recheck serum glucose q20min × 1 h, then qh; titrate insulin infusion to maintain glucose b/w 100 & 200
• Consider IV lipid emulsion (promising in animal studies & case reports), glucagon
• No role for activated charcoal or whole bowel irrigation unless massive recent OD of extended-release formulation; then use multidose charcoal
• HD not useful for CCB OD due to extensive protein binding
Disposition
• Admission to floor vs. ICU (if symptomatic)
• CCB should be monitored for 6 h or 24 h for sustained release formulations
DIGOXIN OVERDOSE
History
• Usually in pts on chronic digoxin, occasional acute intentional OD occurs
• Weakness, fatigue, palpitations, syncope, AMS, n/v, diarrhea, HA, paresthesias
• Yellow-green vision or other vision disturbances pathognomonic in chronic OD (not always present),
• Recent worsening renal fxn, dehydration, electrolyte abn, recent addition of new med
Findings
• GI sxs (common), generalized neuro sxs, visual Δ w/ few objective findings
• Hemodynamic instability related to dysrhythmias or acute CHF
Evaluation
• ECG may show a number of cardiac dysrhythmias (see table)
• Digoxin level, cardiac enzymes, chemistry (↑ K in acute OD, nl or ↓ K, ↓ Mg in chronic OD)
Treatment
• Continuous Tele, trend digoxin & serum K levels w/ ECG & clinical picture
• Correct electrolyte abnormalities
• Acute overdose
• ↑ K is bad prognostic sign; treat immediately w calcium, glucose/insulin & bicarb (the notion that calcium is contraindicated in digoxin overdose is based on very weak evidence from animal models)
• Magnesium, lidocaine antiarrhythmic until Digibind available
• Digoxin spec Ab (antidote) if level >6, K >5, high-deg AV block, ventricular arrhythmias, AMS, hemodynamic compromise
• Each vial of Digoxin spec Ab binds 0.5 mg of digoxin
• # of Digoxin spec Ab = (serum digoxin [ng/mL] × TBW [kg])/100
• For unknown amount/level, empirically treat w/ 10 vials, repeat once prn for acute ingestion, 6 vials for chronic ingestion
• Phenytoin & lidocaine safe to control tachydysrhythmias
• Activated charcoal (if recent ingestion), dialysis ineffective due to large Vd
• Chronic tox
• Stop digoxin
• Verify need for Digoxin spec Ab, check Cr, electrolytes
Disposition
• Admission to floor vs. ICU (if hemodynamic instability, refractory dysrhythmia)
• If asymptomatic, no cardiac dysrhythmias, nl K & dig level, can d/c after 6 h
Pearl
• Many drug interactions (BZD, βB, CCB, diuretics, succinylcholine, some abx)
