Rosen & Barkin's 5-Minute Emergency Medicine Consult (214 page)

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Authors: Jeffrey J. Schaider,Adam Z. Barkin,Roger M. Barkin,Philip Shayne,Richard E. Wolfe,Stephen R. Hayden,Peter Rosen

Tags: #Medical, #Emergency Medicine

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
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History
  • Accidental adult or pediatric overdose of a known amount
  • Intentional acute overdose in a patient not taking digoxin chronically
  • Intentional acute or chronic overdose in a patient taking digoxin chronically
  • Unintentional chronic ingestion of digoxin in which renal clearance decreases or the dose chronically increases
  • Unintentional toxicity from recent antibiotic use (esp. macrolides) that alter GI flora, primarily by decreasing
    Eubacterium lentum
    , increasing absorption
Physical-Exam
  • Altered mental status
  • Bradycardia
  • Tachycardia
  • Irregular rhythm
  • Hypotension
ESSENTIAL WORKUP
  • ECG:
    • For dysrhythmia
  • Digoxin level:
    • Normal range: 0.5–2 ng/mL
    • Distribution after oral intake not complete until 6 hr; therefore, >6-hr level is most accurate steady state concentration.
    • False elevations possible with spironolactone use, pregnancy, hyperbilirubinemia, chronic renal failure, liver failure, CHF
    • May be falsely elevated after digoxin-specific Fab fragments given
DIAGNOSIS TESTS & NTERPRETATION
Lab
  • Electrolytes, BUN, creatinine, glucose:
    • Hypokalemia contributes to digitalis toxicity.
    • Hyperkalemia seen in acute toxicity and correlates with acute digitalis mortality better than digoxin serum levels.
    • Follow K
      +
      serially
  • Calcium, magnesium
ALERT

Serum digoxin concentration (SDC) should not be obtained after digoxin-specific antibody Fab fragments have been administered because it will be inaccurate.

DIFFERENTIAL DIAGNOSIS
  • Overdoses:
    • Calcium channel blockers
    • β-Blockers
    • Quinidine, procainamide
    • Clonidine
    • Organophosphates
    • Antidysrhythmics
    • Other antihypertensives
  • Primary cardiac dysrhythmias
  • Acute gastroenteritis
TREATMENT
PRE HOSPITAL
  • Establish IV access
  • Continuous cardiac monitoring
  • Apply pads for potential cardioversion
ALERT
  • If cardioversion is necessary for tachydysrhythmias, use low levels (50 J)
  • May precipitate refractory tachydysrhythmias
INITIAL STABILIZATION/THERAPY

ABCs:

  • IV, oxygen, monitor:
    • IV fluid bolus if hypovolemic
  • Administer naloxone, thiamine, dextrose for altered mental status.
ED TREATMENT/PROCEDURES
  • Cardiac arrest resuscitation:
    • Defibrillate for ventricular fibrillation, pulseless VT.
    • Standard advanced cardiac life support (ACLS) protocol
    • Administer digoxin-specific antibody Fab fragments (Digibind), up to 5–20 vials IV push (IVP).
    • MgSO
      4
      , 2 g IVP
    • Continue resuscitation for 30 min after digoxin-specific antibody Fab fragments.
  • General measures:
    • Activated charcoal if acute ingestion
    • Replenish magnesium.
    • Treat hyperkalemia with insulin, dextrose, bicarbonate, sodium polystyrene sulfonate.
      • Calcium can probably be used to treat hyperkalemia, but because other safer alternatives exist it is not recommended, unless life-saving membrane stabilization is needed secondary to hyperkalemia, in the unstable patient.
      • If the patient has hyperkalemia from digoxin toxicity treatment with digoxin-specific Fab fragments are indicated 1st in the hemodynamically stable patient.

DYSRHYTHMIA MANAGEMENT

  • 1st choice: Digoxin-specific antibody Fab fragments (Digibind, DigiFab)
    • Indications:
      • SDC ≥15 ng/mL at any time or ≥10 ng/mL at steady state (6 hr)
      • Ingestion of >10 mg in adults or 0.2 mg/kg or 4 mg in children
      • Hyperkalemia >5–5.5 mEq/L
      • Hemodynamically unstable or life-threatening dysrhythmias
      • VT, ventricular fibrillation
      • Atrial tachycardia
      • Variable AV block
      • Bradycardia with no response to atropine
      • Hypotension
    • Onset: 20–30 min
    • Digoxin levels may increase, decrease, or stay in therapeutic range after therapy owing to Fab digoxin complexes and redistribution.
    • Renal clearance of drug–antibody complexes:
      • Too large to be removed by dialysis
    • 2nd dose if rebound toxicity
    • Complications:
      • Exacerbation of CHF
      • Hypokalemia
      • Atrial fibrillation with rapid ventricular response
  • If digoxin-specific antibody Fab fragments not immediately available initiate the following:
    • Lidocaine:
      • For ventricular dysrhythmias without AV block
      • Not harmful but not very effective
    • For bradydysrhythmias:
      • Atropine
    • Pacing for symptomatic bradydysrhythmia
    • MgSO
      4
      for ventricular dysrhythmias with torsades de pointes
    • Quinidine, procainamide contraindicated
  • Cardioversion is last resort for severe, life-threatening tachydysrhythmia:
    • Start at low energy 10–50 J, then increase to high levels if ineffective.
    • Safe if digoxin level <2 ng/mL
MEDICATION
  • Activated charcoal slurry:
    • 1 g/kg if within 1 hr
  • Digoxin-specific antibody Fab fragments:
    • 40-mg vial neutralizes 0.5 mg of digoxin.
    • If amount ingested known:
    • Number of vials needed to treat equals [amount ingested (mg)/0.5 (mg/vial)]
    • If steady serum level known:
      • Number of vials needed equals [SDC (ng/mL) × weight (kg)]/100
    • If neither amount ingested nor serum level known:
      • Acute toxicity: 5–10 vials adults or children
      • Chronic toxicity: 1--2 vials in adults or children
    • Bolus digoxin-specific antibody Fab fragments for cardiac arrest
    • Additional doses as needed
  • Standard treatment for hyperkalemia and bradycardia (calcium only if necessary)
Geriatric Considerations
  • Dosage is based on weight and serum concentration. There is no change in the setting of renal or hepatic dysfunction.
  • Recrudescence of toxicity has been reported in patients with concomitant renal failure. Redosing of digoxin-specific antibody Fab fragments should be used again when indicated.
Pediatric Considerations
  • Weight-based dosing for children is the same as it is for adults.
  • On some occasions, accidental dose ingested by a child is known and the number of vials is indicated by the amount of digoxin bound by each vial. See dosing.
Pregnancy Considerations

Digoxin-specific Fab fragments are pregnancy class C.

FOLLOW-UP
DISPOSITION
Admission Criteria
  • ICU:
    • Unstable cardiovascular status in acute or chronic toxicity
  • Telemetry:
    • Asymptomatic or mildly symptomatic dysrhythmia
    • High risk for developing toxicity
Discharge Criteria

Acute/chronic ingestion:

  • Digoxin level <2 ng/mL
  • Asymptomatic for 6 hr and no ECG abnormalities
FOLLOW-UP RECOMMENDATIONS

Psychiatric referral for stable patients who are suicidal

PEARLS AND PITFALLS

When it is known that the patient is on digoxin and presents with cardiovascular instability, and/or hyperkalemia, treatment should begin with the antidote: Digoxin-specific Fab fragments.

ADDITIONAL READING
  • Erickson CP, Olson KR. Case files of the medical toxicology fellowship of the California poison control system-San Francisco: calcium plus digoxin-more taboo than toxic?
    J Med Toxicol
    . 2008;4(1):33–39.
  • Levine M, Nikkanen H, Pallin DJ. The effects of intravenous calcium in patients with digoxin toxicity.
    J Emerg Med.
    2011;40(1):41–46.
CODES
ICD9

972.1 Poisoning by cardiotonic glycosides and drugs of similar action

ICD10
  • T46.0X1A Poisoning by cardi-stim glycos/drug simlar act, acc, init
  • T46.0X4A Poisoning by cardi-stim glycos/drug simlar act, undet, init
DIPLOPIA
Jonathan A. Edlow
BASICS
DESCRIPTION
  • Double vision
    • Simultaneous perception of 2 images
    • Can be oriented horizontally, vertically, or diagonally from one another.
  • Diplopia is usually due to abnormal movement of the extraocular muscles (EOMs), which are innervated by 3 cranial nerves (CNs):
    • CN 3 – superior, inferior, and medial rectus and inferior oblique muscles
    • CN 4 – superior oblique muscle
    • CN 6 – lateral rectus muscle
  • Brainstem lesions can damage CN nuclei or their connections (medial longitudinal fasciculus, MLF), causing an internuclear ophthalmoplegia (INO)
  • CN dysfunction
    • Compression as they traverse the subarachnoid space and venous sinuses
    • Inflammation
    • Elevation (or reduction) of CSF pressure can cause CN 6 palsy
  • Disease affecting the orbits and the bony skull can cause restriction of motion of one or both eyes or EOMs

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