Cyanide toxicity: Difference between revisions

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(VBG hyperoxemia)
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==Work-Up==
==Work-Up==
#Lactate
#Lactate
#VBG and ABG (narrowing of the venous-arterial PO2 gradient)
#VBG and ABG (narrowing of the venous-arterial PO2 gradient, causes venous hyperoxemia -- as does CO poisoning)
#Co-oximetry
#Co-oximetry
#Chemistry (anion gap acidosis)
#Chemistry (anion gap acidosis)

Revision as of 19:06, 25 May 2014

Background

  • Sources
    • Burning of nitrogen-containing polymers (plastics, wool, silk)
    • Prolonged use of nitroprusside
    • Pits of peaches, pears, apricots, crab apples
  • Pathophysiology
    • Binds to cytochrome oxidase in mitochondria; leads to cessation of electron transport
      • Causes switch from aerobic to anaerobic metabolism despite adequate O2

Clinical Features

Acute Intoxication

  • Affected by dose, route, formulation and exposure pattern
    • Inhaled toxins more rapid than ingested
      • Inhalation exposure may cause syncope and death after only a few breaths
  • Early signs
    • CNS stimulation (Headache, anxiety, confusion)
    • Tachycardia, palpitations and hypertension
    • Tachypnea
    • Cherry-red color (rarely seen)
  • Late signs
    • Nausea, Vomiting
    • Bradycardia, hypotension, arrhythmias, asystole
    • Coma, Seizures (rare), Mydiriasis
    • bradypnea and pulmonary edema (non-cardiogenic), apnea
    • Renal Failure
    • Hepatic Necrosis
    • Cyanosis
    • Rhabdo, bright red venules seen on fundoscopy

Chronic

  • Retrobulbar Optic Atropy (proposed)
    • Heavy smokers
  • Ataxic peripheral neuropathy
  • Konzo
    • Spactic upper motor neuron paraparesis seen in chronic ingestion of inadequately cooked casava

Diagnosis

  1. Smell of bitter almonds (only 60-80% of population can detect this)
  2. Severe unexplained metabolic acidosis (lactic)
  3. PO2 of venous blood similar to arterial blood
  4. normal SpO2
  5. Cherry-red skin color is uncommon

Work-Up

  1. Lactate
  2. VBG and ABG (narrowing of the venous-arterial PO2 gradient, causes venous hyperoxemia -- as does CO poisoning)
  3. Co-oximetry
  4. Chemistry (anion gap acidosis)

Treatment

  1. Supportive care
    1. O2 100% NRB
    2. IVF and vasopressors for hypotension
    3. Bicarb for acidemia (enchances of effect of nitrite and thiosulfate)
  2. Antidote

Cyanokit (Hydroxocobalamin)[1][2]

1st line therapy

Mechanism of action

Directly binds CN forming cyanocobalamin which is readily excreted in the urine

Administration

  1. Give 70mg/kg IV over 15min (5g is standard adult dose); may repeat 5g once as needed
  2. Also give 25% Na thiosulfate 1.65ml/kg IV (12.5g max dose) over 10min; may repeat at 1/2 original dose if needed

Adverse Effects

  1. May cause temporary reddish discoloration of skin, plasma, urine, mucous membranes
  2. Interferes with colorimetric tests -- Pulse ox, Hemoglobin, Carboyxhemoglobin, methemeglobin, oxyhemoglobin, Serum Cr, AST/ALT, bilirubin, magnesium for 2-3 days[3]
OBTAIN Co-ox and labs prior to Hydroxocobalamin administration


Cyanide Antidote Package

  1. 2nd line therapy - use if Cyanokit unavailable[4]
  2. Consider using only Na thiosulfate (no nitrites) in cases where concern for CO poisoning since nitrate administration will severely decrease oxygen carrying capacity

Mechanism of action

  1. Nitrites: form metHb which binds CN more avidly than cytochrome oxidase
    1. Thiosulfate: donates its sulfur group to CN to form thiocyanate (less toxic than CN)

Warnings

  1. Nitrites are relatively contraindicated in pts w/ concomitant CO toxicity
  2. Induction of metHb further exacerbates O2 delivery
  3. Avoid nitrites in presence of severe hypotension if diagnosis is unclear

Administration

Amyl nitrite
  1. Inhaled by pt (only use if unavailable to obtain IV)
  2. Hold under pt's nose for 30s of each minute, for 3 minutes
Sodium nitrite
  1. 10 mg/kg IV over 5min (use instead of amyl nitrite if IV is available)
  2. Lack of measurable MetHb levels after administration confirms CN presence
  3. Monitor MetHb and keep level <30%
Pediatric dosing is based on Hemoblogin (see Peds dosing below)
25% Sodium thiosulfate
  1. 1.65ml/kg IV (12.5g max dose) over 10min
  2. may repeat at 1/2 original dose if needed


Sodium Nitrite (Peds Dosing)

  • Max dose should not exceed 10mL
  • Do not give faster than 5mL/min (to avoid hypotension)
  1. Hb 7 g/dL, dose is 0.19 mL/kg of 3% sodium nitrite
  2. Hb 8 g/dL, dose is 0.22 mL/kg of 3% sodium nitrite
  3. Hb 9 g/dL, dose is 0.25 mL/kg of 3% sodium nitrite
  4. Hb 10 g/dL, dose is 0.27 mL/kg of 3% sodium nitrite
  5. Hb 11 g/dL, dose is 0.30 mL/kg of 3% sodium nitrite
  6. Hb 12 g/dL, dose is 0.33 mL/kg of 3% sodium nitrite
  7. Hb 13 g/dL, dose is 0.36 mL/kg of 3% sodium nitrite
  8. Hb 14 g/dL, dose is 0.39 mL/kg of 3% sodium nitrite

Disposition

  1. Admit all pts for obs

See Also

Source

  1. ↑ Borron SW, Baud FJ, Mégarbane B, Bismuth C. Hydroxocobalamin for severe acute cyanide poisoning by ingestion or inhalation. Am J Emerg Med. Jun 2007;25(5):551-8.
  2. ↑ Bebarta VS, Tanen DA, Lairet J, Dixon PS, Valtier S, Bush A. Hydroxocobalamin and sodium thiosulfate versus sodium nitrite and sodium thiosulfate in the treatment of acute cyanide toxicity in a swine (Sus scrofa) model. Ann Emerg Med. 2010;55(4):345-51.
  3. ↑ Lee J, Mukai D, Kreuter K, et al. Potential interference by hydroxocobalamin on co-oximetry hemoglobin measurements during cyanide and smoke inhalation treatments. Ann Emerg Med. 2007;49(6):802-805.
  4. ↑ Hall AH, Saiers J, Baud F. Which cyanide antidote?. Crit Rev Toxicol. 2009;39(7):541-52.
  • Anseeuw K. et al. Cyanide poisoning by fire smoke inhalation: a European expert consensus. Eur J Emerg Med. Feb 2013;20(1):2-9
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