Hyperkalemia in Digoxin Toxicity

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This topic was brought to our attention today by Dr. Glassman.
5 Facts about Digoxin: 
1) It is a cardiac glycoside that increases inotropy and automaticity
2) Treats tachyarrhythmias and CHF
3) Mechanism of action: inhibits the Na/K ATPase pump
4) Renally cleared (look out for pts with new renal failure on digoxin)
5) It's one of those tricky drugs with a narrow therapeutic index!
Net effect: increased intracellular Na+ and Ca2+ levels; increased extracellular K+ levels
Dig Tox by Systems: 
GI: nausea, vomiting, diarrhea, abd pain
Cardiovascular: palpitations, syncope, dyspnea
CNS: confusion/delirium, dizziness, altered color perception
Metabolic: hyperkalemia (early sign!)
Time Course of Toxicity: 
GI effects seen @ 2-4 hr
Life-threatening cardiovascular complications @ 8-12 hr
Peak serum levels @ 6 hr
More on the Cardiac Effects...
Digoxin can cause a multitude of dysrhythmias!
- Frequent PVCs (most common) including ventricular bigeminy and trigeminy
- Sinus bradycardia
- Slow atrial fibrillation
- Any degree of AV block (due to increased vagal effects at the AV node)
- SVT (due to the enhanced automaticity) with SLOW ventricular response (again due to increased vagal effects at the AV node)
- VT
Confused? Yet this makes some sense. If you've watched any lectures by Amal Mattu, he calls hyperkalemia the Syphilis of EKGs, referring to its status as the "Great Imitator" of many diverse pathologies. Gross, right? And what does digoxin cause? Hyperkalemia!
Some Possible EKG Findings in Dig Tox: 

This unique "scooped" or "swooping" depression of the ST segment memorably resembles the shape of Salvador Dali's mustache.

Paroxysmal atrial tachycardia with 2nd degree AV block AND frequenct PVCs

Atrial flutter with a slow ventricular rate due to AV nodal blockade by digoxin

Treatment: 

You'll find that digoxin-induced arrhythmias are usually refractory to standard therapies.

Ex: bradycardia resistant to atropine and pacing

The solution? Digibind (digoxin Fab fragments)! There are dosing formulas (ask your pharmacist for help!) but if in doubt, start with 5 vials for stable acute toxicity and 10 vials for unstable acute toxicity (ex: accidental ingestion by a child). For chronic toxicity, start with 2 vials empirically and titrate up.

References:

Life In the Fast Lane

UpToDate

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Hanging Injuries

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I'll start off the month with a POTD inspired by a case from the other day… 36 yo M bib NYPD after he was found passed out in a jail cell after being arraigned with a ligature mark around his neck…He wound up being ok and was transferred out for inpatient psych but lets talk hanging injuries…

CLASSIFICATION:

EVALUATION:

  • ABCs but of course!! Low threshold to intubate for airway protection as they can crash without warning!!
  • Look for pain to larynx, cough, stridor, muffled voice, resp distress, AMS, petechiae, abrasions/lacerations/contusions to neck and hard/soft signs of vascular injury
  • High risk of ARDS and cerebral edema so judicious fluids- don’t go flooding them!
  • Altered? Tube and treat for increased ICP
  • High risk of arrhythmias

IMAGING: CT brain (cerrebal hypoxia), CT c-spine (mc= c2 spondylolithesis) and consider CTA head/neck for vascular injury!

DISPO:

  • ALL should be admitted for 24hr obs as high risk for delayed airway and pulmonary complications

Sources:

Life in the Fast Lane. http://lifeinthefastlane.com/trauma-tribulation-016/

EM-Docs

Medscape, UpToDate

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Tetanus

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- Is a potentially lethal condition characterised by muscular rigidity and spasms, caused by the tetanospasmin toxin produced by Clostridium tetani

Types:

  • cephalic
  • local
  • generalised
  • neonatal (50% of tetanus deaths worldwide)

Tetanospasmin

  • taken up by motor nerves or haematogenous spread to CNS
  • preferentially prevents discharge from GABA inhibitory interneurons in spinal cord and brainstem -> unrestricted motor nerve activity and autonomic instability

Clinical features:

Clinical triad of rigidity, muscle spasms and, autonomic dysfunction

  • contaminated wound or umbilical stump in neonates
  • incubation period: 3-14d = time to first symptom
  • rigidity (persists > 2 weeks) — trismus, dysphagia, increased tone in trunk muscles – greater on side of injury initially
  • spasms (reduce after 2 weeks) — spontaneous or provoked by physical or emotional stimuli, laryngospasm, risus sardonicus, opisthotonos (severe spasm in which the back arches and the head bends back and heels flex toward the back)

  • autonomic disturbance (onset after spasms, lasts 1-2 weeks) — tachycardia and hypertension may alternate with bradycardia and hypotension, dysrhythmia, cardiac arrest — salivation, bronchial secretions — gastric stasis, ileus, diarrhoea
  • respiratory compromise — chest wall rigidity — laryngospasm — aspiration — retained secretions

Td Prophylaxis:

  • Past vaccination unknown or <3 total
    • Clean wound → Td
    • Dirty wound → Td & TIG
  • Past vaccination 3 or more total
    • Clean wound → Td Q10yrs
    • Dirty wound → Td Q5yrs

Management:

A – intubate because management requires large doses of sedatives to control muscle spasm and to overcome laryngospasm B – at risk of aspiration and have copious bronchial secretions requiring frequent suctioning, often ventilated for 2-3 weeks until spasms subside C – autonomic dysfunction requires monitoring in a critical care environment D – benzodiazepines in large doses (up to 100mg/h diazepam)

Specific Therapy:

  • metronidazole (first choice); penicillin is used throughout most of the world but is a GABA antagonist
  • anti-tetanus immunoglobulin: 100-300IU/kg of human Ig IM
  • benzodiazepines; adjuncts include barbiturates, propofol, chlorpromazine
  • Mg to 2-4mmol/L as useful in spasm treatment and limits autonomic instability
  • consider dantrolene (unproven)
  • clean and debride wounds (source control)
  • immunize (infection does not confer immunity) – Q10 yearly

Prognosis:

Mortality >50% if untreated (usually due to respiratory failure)

Sources: Life in the fastlane, WikiEM

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