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tox.digoxin-toxicity.core.v1PRODUCTION
tox.digoxin-toxicity.core.v1

Digoxin toxicity

toxicologyacutechronicadultgeriatric
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Canonical 12-phase frame with authored status for this dossier.

Current phase

Frame

Detailed

Establish cardiac-glycoside poisoning frame; separate ACUTE deliberate ingestion from CHRONIC accumulation; include plant/herbal glycosides not measured by digoxin assay (ACMT/EXTRIP; tox reviews 2024-2025)

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Glycoside frame set; acute vs chronic vs plant-glycoside pathway selected

Patient inputs (14)

Geriatric chronic toxicity is the dominant phenotype; age-related renal decline raises steady-state level

Acute (high level, hyperK, GI, any dysrhythmia) vs chronic (elderly, normal/mildly high level, visual, neuropsych) drive DigiFab dosing + K interpretation

Known amount enables acute vial formula; time since ingestion gates level timing (≥6 h post-dose for distribution)

Amiodarone, verapamil, quinidine, macrolides, spironolactone, dronedarone, propafenone raise digoxin level / precipitate chronic toxicity

Level interpretation drives DigiFab steady-state dosing; caveats: timing, chronic vs acute, free vs total post-Fab, DLIS, not for plant glycosides

HYPERKALEMIA is the key acute prognostic marker (K+ >5.0–5.5 → high pre-Fab-era mortality, Bismuth 1973); hypoK potentiates chronic toxicity

Renal impairment is the dominant chronic precipitant; guides ongoing dosing; hemodialysis ineffective for digoxin but used for refractory hyperK

HypoMg potentiates toxicity + causes refractory dysrhythmia; Mg is therapeutic for tachydysrhythmia

Pathognomonic dysrhythmias: bidirectional VT, atrial tach with block, accelerated junctional, regularized AF; bradydysrhythmia / high-grade AV block

Bradydysrhythmia (sinus brady, AV block, junctional) vs tachydysrhythmia split the dysrhythmia management arm

Hemodynamic instability is a stand-alone DigiFab indication independent of level

Steady-state DigiFab vial formula uses body-burden = level × weight; pediatric/elderly dosing

Plant/herbal glycosides (oleander, foxglove, bufadienolide) cross-react variably and are NOT measured by digoxin immunoassay — clinical/empiric DigiFab

Hypercalcemia potentiates glycoside effect; informs the IV-calcium-in-hyperK "stone heart" caution

* = hard-required. Engine cannot meaningfully run until these are filled.

Severity triggers (6)

6 need judgement
  • informationallife_threateningacute_hyperkalemia_K_over_5
    Acute glycoside ingestion with K+ >5.0–5.5 mEq/L (Bismuth 1973 — pre-Fab mortality ~0% if K+ <5.0, ~50% if 5.0–5.5, ~100% if >5.5)
    Trigger could not be auto-evaluated — needs clinician judgement.
  • informationallife_threateningbidirectional_vt_or_life_threatening_dysrhythmia
    Bidirectional VT, VT/VF, or other life-threatening glycoside dysrhythmia (ACMT)
    Trigger could not be auto-evaluated — needs clinician judgement.
  • informationallife_threateninghemodynamic_instability_any_level
    Hemodynamic instability / shock attributable to glycoside toxicity regardless of digoxin level (ACMT)
    Trigger could not be auto-evaluated — needs clinician judgement.
  • informationallife_threateningglycoside_cardiac_arrest
    Cardiac arrest in known/suspected cardiac glycoside (digoxin or plant) toxicity (ACMT)
    Trigger could not be auto-evaluated — needs clinician judgement.
  • informationalseverehigh_grade_av_block_or_symptomatic_bradycardia
    High-grade/complete AV block or symptomatic bradycardia / junctional escape with hypoperfusion (ACMT)
    Trigger could not be auto-evaluated — needs clinician judgement.
  • informationalseveremassive_acute_ingestion
    Massive acute ingestion: >10 mg adult / >0.1 mg/kg child, OR acute level >10 ng/mL, OR known cardiotoxic plant/herbal glycoside ingestion (ACMT)
    Trigger could not be auto-evaluated — needs clinician judgement.

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RISK_STRATIFICATIONoptionalDrives risk stratification
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Recommended regimen

Cardiac glycoside toxicity — DigiFab-first (antidote → hyperK → bradydysrhythmia → tachydysrhythmia → electrolyte correction)
axis: digoxin_toxicity_digifab_firststep 1 - Step 1 — Digoxin immune Fab (DigiFab) — definitive antidote
Selected step "Step 1 — Digoxin immune Fab (DigiFab) — definitive antidote" — Any life-threatening criterion: life-threatening dysrhythmia (bidirectional VT, VT/VF, high-grade AV block, symptomatic bradycardia), hemodynamic instability, K+ >5.0 in ACUTE ingestion, end-organ dysfunction, massive ingestion (>10 mg adult / >0.1 mg/kg child / acute level >10 ng/mL), or any plant/herbal glycoside with toxicity
  • digoxin immune Fab (ovine, DigiFab)
    first line
    antibody_antidote_fragment
    ACUTE known amount: vials = (mg ingested × 0.8) / 0.5, round up. STEADY-STATE level: vials = (serum digoxin ng/mL × weight kg) / 100. EMPIRIC: acute unknown / arrest 10–20 vials; chronic toxicity 3–6 vials (often 1–2 vials titrated in elderly chronic to avoid AF/HF rebound) • IV • infuse over 30 min (IV push if cardiac arrest); GIVE AND REASSESS — redose for recrudescent/incompletely reversed toxicity
    triggers: life_threatening_dysrhythmia, bidirectional_VT, hemodynamic_instability, acute_K_over_5, massive_ingestion, plant_or_herbal_glycoside_toxicity, end_organ_dysfunction
    ACMT/EXTRIP + Antman 1990 multicenter trial — DigiFab binds free digoxin (and cross-reacts with most plant cardenolides/bufadienolides) → renal clearance of inactive complex; reverses dysrhythmia + hyperK within 30–60 min. Plant glycosides cross-react variably so dose empirically/clinically (assay does NOT quantify them). Each vial (40 mg) binds ~0.5 mg digoxin. Watch for hypoK rebound + loss of rate control / HF in AF/HFrEF patients

ed playbook — drug actions (5)

  1. 1. digoxin immune Fab (DigiFab)
    Acute known: (mg × 0.8)/0.5 vials; steady-state: (level × wt)/100 vials; empiric arrest 10–20 vials; chronic 3–6 vials • IV • over 30 min (push if arrest); reassess + redose
    trigger: Life-threatening dysrhythmia, instability, acute K+ >5.0, massive ingestion, plant glycoside toxicity
    Definitive antidote — give and reassess (Antman 1990)
  2. 2. insulin + dextrose (hyperK bridge)
    10 U regular insulin IV + 25 g dextrose IV • IV • repeat per K+/glucose
    trigger: K+ >5.5 or ECG hyperK changes
    Bridge K+ shift while DigiFab acts; AVOID empiric IV calcium (ACMT)
  3. 3. atropine
    0.5–1 mg IV q3–5 min (max 3 mg) • IV • PRN
    trigger: Symptomatic bradycardia / high-grade AV block
    Temporizing bridge — DigiFab definitive (ACMT)
  4. 4. magnesium sulfate
    2 g IV over 5–10 min • IV • bolus ± infusion
    trigger: Ventricular tachydysrhythmia / hypoMg (slow if AV block)
    Suppresses triggered activity; caution with block (ACMT)
  5. 5. activated charcoal
    1 g/kg PO/NG; multi-dose for oleander • PO/NG • single ± multi-dose
    trigger: Early (1–2 h) awake protected airway
    Interrupts enterohepatic recirculation (ACMT)

Auto-drafted A&P note

ed

Subjective

- Possible entry pathways: Deliberate or accidental digoxin tablet/elixir overdose (acute) (ACMT/EXTRIP); Chronic digoxin + new renal impairment / interacting drug / electrolyte derangement (ACMT/EXTRIP); Elevated serum digoxin level (≥2.0 ng/mL) on routine or symptomatic draw (ACMT/EXTRIP).

Objective

- No vitals, labs, or imaging entered for this encounter.

Assessment

**Digoxin toxicity** (tox.digoxin-toxicity.core.v1).
Phenotype framing: Distinguish from β-blocker / CCB overdose (bradycardia + shock but NOT hyperK from glycoside mechanism), hyperkalemia of other cause, primary AV-nodal disease, sick sinus, MI, sepsis, plant-glycoside vs digoxin (assay caveats), endogenous DLIS (renal failure/neonate/pregnancy false-positive low level)
Scope: Establish cardiac-glycoside poisoning frame; separate ACUTE deliberate ingestion from CHRONIC accumulation; include plant/herbal glycosides not measured by digoxin assay (ACMT/EXTRIP; tox reviews 2024-2025)

No severity triggers fired against current inputs.

Plan

Regimen axis: **Cardiac glycoside toxicity — DigiFab-first (antidote → hyperK → bradydysrhythmia → tachydysrhythmia → electrolyte correction)** — step "Step 1 — Digoxin immune Fab (DigiFab) — definitive antidote".
1. digoxin immune Fab (ovine, DigiFab) ACUTE known amount: vials = (mg ingested × 0.8) / 0.5, round up. STEADY-STATE level: vials = (serum digoxin ng/mL × weight kg) / 100. EMPIRIC: acute unknown / arrest 10–20 vials; chronic toxicity 3–6 vials (often 1–2 vials titrated in elderly chronic to avoid AF/HF rebound) IV infuse over 30 min (IV push if cardiac arrest); GIVE AND REASSESS — redose for recrudescent/incompletely reversed toxicity (antibody_antidote_fragment, first line) — ACMT/EXTRIP + Antman 1990 multicenter trial — DigiFab binds free digoxin (and cross-reacts with most plant cardenolides/bufadienolides) → renal clearance of inactive complex; reverses dysrhythmia + hyperK within 30–60 min. Plant glycosides cross-react variably so dose empirically/clinically (assay does NOT quantify them). Each vial (40 mg) binds ~0.5 mg digoxin. Watch for hypoK rebound + loss of rate control / HF in AF/HFrEF patients

Setting playbook (ed) — Recognize acute vs chronic glycoside toxicity, obtain level + K + ECG, give DigiFab for any life-threatening criterion, manage hyperK without empiric IV calcium, decontaminate if early (ACMT/EXTRIP)
2. digoxin immune Fab (DigiFab) Acute known: (mg × 0.8)/0.5 vials; steady-state: (level × wt)/100 vials; empiric arrest 10–20 vials; chronic 3–6 vials IV over 30 min (push if arrest); reassess + redose — Life-threatening dysrhythmia, instability, acute K+ >5.0, massive ingestion, plant glycoside toxicity (Definitive antidote — give and reassess (Antman 1990))
3. insulin + dextrose (hyperK bridge) 10 U regular insulin IV + 25 g dextrose IV IV repeat per K+/glucose — K+ >5.5 or ECG hyperK changes (Bridge K+ shift while DigiFab acts; AVOID empiric IV calcium (ACMT))
4. atropine 0.5–1 mg IV q3–5 min (max 3 mg) IV PRN — Symptomatic bradycardia / high-grade AV block (Temporizing bridge — DigiFab definitive (ACMT))
5. magnesium sulfate 2 g IV over 5–10 min IV bolus ± infusion — Ventricular tachydysrhythmia / hypoMg (slow if AV block) (Suppresses triggered activity; caution with block (ACMT))
6. activated charcoal 1 g/kg PO/NG; multi-dose for oleander PO/NG single ± multi-dose — Early (1–2 h) awake protected airway (Interrupts enterohepatic recirculation (ACMT))

Non-pharmacologic actions:
- Continuous cardiac monitor + defib pads on (cardiovert at lowest energy only, DigiFab first) (ACMT)
- IV access × 2; transcutaneous pacing pads as bradydysrhythmia bridge (ACMT)
- Hold all further digoxin + offending interacting drugs (ACMT)
- Do NOT dialyze for digoxin clearance — ineffective (large Vd) (EXTRIP 2016)
- Poison control / medical toxicology consult (ACMT)

AVOID / contraindication checks:
- Avoid empiric IV calcium for hyperkalemia in digoxin toxicity — classic "stone heart"/intractable VF caution; modern evidence is weaker but caution stands, prefer DigiFab + K shift (ACMT)
- Avoid class IA antiarrhythmics (quinidine, procainamide, disopyramide) — slow conduction + raise digoxin level, worsen toxicity (ACMT)
- Avoid amiodarone for glycoside dysrhythmia — raises digoxin level and slows AV conduction (ACMT)
- Hemodialysis does NOT remove digoxin (large Vd, tissue bound) — only for refractory hyperK in renal failure (EXTRIP 2016)
- Cardioversion/defibrillation in digoxin toxicity is proarrhythmic — use lowest energy, treat with DigiFab first when not in arrest (ACMT)
- Transvenous pacing is proarrhythmic in glycoside toxic myocardium — DigiFab preferred, lowest effective output (ACMT)
- Do not replete potassium during the hyperkalemic phase — only treat hypoK in chronic toxicity / post Fab rebound (ACMT)
- Isoproterenol/catecholamines may precipitate ventricular dysrhythmia in glycoside toxicity — avoid for bradycardia (ACMT)

Monitoring

Regimen monitoring:
- continuous telemetry until dysrhythmia-free off DigiFab effect (ACMT)
- serum K+ q1-2h after DigiFab — anticipate HYPOkalemia rebound (ACMT)
- serum Mg + Ca + renal function serially (ACMT)
- FREE digoxin level only post-Fab — total assay uninterpretable ~5-7 days (longer in renal failure) (ACMT)
- glucose q1h after insulin/dextrose for hyperK (ACMT)
- reassess dysrhythmia + hemodynamics 30-60 min post-DigiFab; redose if recrudescent (Antman 1990)
- rate/HF surveillance in AF/HFrEF patients after Fab (loss of rate control / decompensation) (ACMT)

Setting (ed) monitoring:
- Continuous telemetry; ECG q1h initially (ACMT)
- K+ q1-2h (rebound hypoK after DigiFab) (ACMT)
- Glucose q1h after insulin/dextrose (ACMT)
- Reassess dysrhythmia 30-60 min post-DigiFab (Antman 1990)

Follow-up plan: Reconcile/withhold or dose-adjust chronic digoxin (re-evaluate indication — narrow therapeutic index, deprescribe in HFrEF if alternatives); review interacting drugs + renal dosing; patient/caregiver education on toxicity signs (visual halos, GI, confusion); psychiatry follow-up if intentional; plant-source removal counseling (ACMT)
- Close-out criterion: Digoxin reconciled/deprescribed + interaction review + education + psych follow-up (if intentional) booked

Monitoring phase: Continuous telemetry; serial K+ (q1-2h after DigiFab — watch for HYPOkalemia rebound as glycoside-blocked Na/K-ATPase reactivates); recheck Mg/Ca/renal; FREE digoxin level only (total is uninterpretable post-Fab for ~5-7 days, longer if renal failure); reassess dysrhythmia resolution; redose DigiFab if recrudescent toxicity (ACMT)

Disposition

Current setting: ed — Recognize acute vs chronic glycoside toxicity, obtain level + K + ECG, give DigiFab for any life-threatening criterion, manage hyperK without empiric IV calcium, decontaminate if early (ACMT/EXTRIP)

Disposition criteria:
- ICU/monitored: any dysrhythmia, hyperK, DigiFab given, instability, intentional ingestion (ACMT)
- Observation: asymptomatic chronic, stable level, normal K+, normal ECG, no dysrhythmia (ACMT)
- Discharge only after toxicology clearance + digoxin reconciliation + psych eval if intentional (ACMT)

Escalation triggers (move to higher acuity):
- Refractory dysrhythmia or arrest → ICU + repeat empiric DigiFab + prolonged resuscitation (ACMT)
- K+ >5.5 in acute ingestion → DigiFab now + ICU (Bismuth 1973)
- Hemodynamic instability / shock → ICU + DigiFab + pacing bridge (ACMT)
- Refractory hyperK in renal failure → nephrology + hemodialysis for K+ only (EXTRIP 2016)

Earlier-Return Triggers

Return-precaution thresholds (watch for):
- [LIFE_THREATENING] Acute glycoside ingestion with K+ >5.0–5.5 mEq/L (Bismuth 1973 — pre-Fab mortality ~0% if K+ <5.0, ~50% if 5.0–5.5, ~100% if >5.5)
- [LIFE_THREATENING] Bidirectional VT, VT/VF, or other life-threatening glycoside dysrhythmia (ACMT)
- [LIFE_THREATENING] Hemodynamic instability / shock attributable to glycoside toxicity regardless of digoxin level (ACMT)

Citations

- 2024-2025 critical-care toxicology reviews; ACMT/EXTRIP digoxin position (Mowry/EXTRIP 2016); Antman 1990 multicenter digoxin-specific Fab trial; Bismuth 1973 hyperkalemia prognosis in acute digitalis poisoning [PMID:2178391](https://pubmed.ncbi.nlm.nih.gov/2178391/)
- Cited evidence (PMID 4685633) [PMID:4685633](https://pubmed.ncbi.nlm.nih.gov/4685633/)
- Cited evidence (PMID 27286369) [PMID:27286369](https://pubmed.ncbi.nlm.nih.gov/27286369/)
- Cited evidence (PMID 1985395) [PMID:1985395](https://pubmed.ncbi.nlm.nih.gov/1985395/)
- Cited evidence (PMID 6694694) [PMID:6694694](https://pubmed.ncbi.nlm.nih.gov/6694694/)

Last reconciled with current guidelines: 2026-05-16.
References
  • 2024-2025 critical-care toxicology reviews; ACMT/EXTRIP digoxin position (Mowry/EXTRIP 2016); Antman 1990 multicenter digoxin-specific Fab trial; Bismuth 1973 hyperkalemia prognosis in acute digitalis poisoning — PMID:2178391
  • Cited evidence (PMID 4685633) — PMID:4685633
  • Cited evidence (PMID 27286369) — PMID:27286369
  • Cited evidence (PMID 1985395) — PMID:1985395
  • Cited evidence (PMID 6694694) — PMID:6694694