Rosen & Barkin's 5-Minute Emergency Medicine Consult (185 page)

• Remove source of CN.
  
• Prevent others from becoming contaminated.
  
• Remove and bag all contaminated clothing and wash affected areas copiously with soap and water if a liquid exposure. If vapor contamination, removal of the patient from the CN environment may be all that is necessary.
  

• ABCs:
  
  • Administer 100% oxygen:
    
    • Even in presence of normal PaO
      ₂
      
    • Acts synergistically with antidotes
      
• Gastric decontamination for oral ingestions if within 1 hr:
  
  • Perform gastric lavage and administer activated charcoal (AC) if ingestion of solid CN or CN-containing products and no contraindications.
    
  • Do not induce emesis.
    
• Dermal exposure: Standard decontamination
  

• Hydroxocobalamin (B
  _12a
  ) Cyanokit®:
  
  • Administer if manifesting significant CN toxicity with persistent high anion gap metabolic acidosis and hyperlactatemia, with any syncope, seizures dysrhythmias, and hypotension.
    
  • Administration often instituted empirically; CN levels not immediately available
    
  • Binds to CN:
    
    • Forms nontoxic cyanocobalamin (B
      ₁₂
      ); renally excreted
      
  • Advantages:
    
    • No MH induction
      
    • Does not cause hypotension
      
    • Intracellular distribution
      
  • Limitations:
    
    • Cost
      
  • Incompatible in the same IV line with:
    
    • Diazepam
      
    • Dobutamine
      
    • Dopamine
      
    • Fentanyl
      
    • Nitroglycerin
      
    • Pentobarbital
      
    • Propofol
      
    • Sodium thiosulfate
      
    • Sodium nitrite
      
    • Ascorbic acid
      
    • Blood products
      
  • Side effects of hydroxocobalamin:
    
    • HTN
      
    • Red skin and all secretions
      
    • Interference of colorimetric assays of AST, ALT, total bilirubin, creatinine, Mg, iron
      
• CN antidote kit:
  
  • Administer if manifesting significant CN toxicity with persistent high anion gap metabolic acidosis, hyperlactatemia with any syncope, seizures dysrhythmias, and hypotension.
    
  • Administration often instituted empirically; CN levels not immediately available
    
  • Contents: Amyl nitrite pearls, sodium nitrite, and sodium thiosulfate
    
  • Nitrite action:
    
    • Induce a CN-scavenging MH by oxidizing hemoglobin (Fe
      ²⁺
      to Fe
      ³⁺
      ), which attracts extracellular CN away from the mitochondria-forming CN-MH, which is less toxic.
      
    • Do not administer empirically or prophylactically.
      
  • Sodium thiosulfate action:
    
    • Substrate for the enzyme rhodanese
      
    • Combines with CN to form a less toxic T-CN
      
• Hyperbaric oxygen therapy:
  
  • Can be used to treat CN exposures
    
  • Maximizes tissue oxygenation despite toxic MH level
    

AC: 1 g/kg PO

Hydroxocobalamin (B
_12a
):

• 70 mg/kg IV, max. 5 g
  
• The kit contains either two 2.5 grams/bottle or one 5 gram/bottle. The starting dose is 5 grams.
  
• Reconstitute the powder by gently rolling the bottle after filling with 100 mL of 0.9% NS.
  
• Infuse each 2.5 gram bottle over 7.5 minutes, or one 5 gram bottle over 15 minutes. The 5 gram dose can be repeated.
  

Consider adjunctive use of sodium thiosulfate

• CN antidote kit: Amyl nitrite, sodium nitrite, and sodium thiosulfate:
  
• Amyl nitrite pearls:
  
  • Crush 1 or 2 ampules in gauze and hold close to nose, in lip of face mask, or within Ambu bag.
    
  • Inhale for 30 sec–1 min until IV access obtained.
    
• Sodium nitrite (NaNO
  ₂
  ): 10 mL (300 mg) (peds: 0.15–0.33 mL/kg) IV as 3% solution over 5–20 min:
  
  • May repeat once at half dose within 30–60 min
    
  • Keep MH level <30%.
    
  • Dilute; infuse slowly if hypotensive.
    
• Sodium thiosulfate: 50 mL: 12.5 g (peds: 0.95–1.65 mL/kg) IV over 10–15 min of 25% solution:
  
  • 1/2 initial dose may be given after 30–60 min.
    

• Hydroxocobalamin is class C.
  
• Amyl nitrite is class X.
  
• Sodium nitrite is unknown.
  
• Sodium thiosulfate is class C.
  

• ∼50 known or suspected CN victims aged 65 or older received hydroxocobalamin and it had similar safety and efficacy as younger patients.
  
• Hydroxocobalamin is renally excreted unchanged in the urine so renal impairment could prolong the elimination half-life.
  
• The safety and effectiveness of hydroxocobalamin is unknown in hepatic impairment.
  
• Sodium thiosulfate is metabolized in the liver and excreted by the kidney. Impairment in either organ may prolong elimination.
  
• The nitrites are short acting. Hepatic or renal impairment may prolong elimination.
  

The safety and effectiveness of hydroxocobalamin has not been established in children, but the 70 mg/kg dose has been used.

• Sodium nitrite has weight-based dosing for children.
  
• Sodium nitrite dosing can be based on serum hemoglobin when the clinical scenario does
  NOT
  require life-saving administration of the antidote before lab testing:
  

FOLLOW-UP

ICU admission of all symptomatic exposures

• Asymptomatic patients after at least 4 hr of observation
  
• Survival after 4 hr of acute exposure usually associated with complete recovery
  

Psychiatry referral for intentional overdose and suicidal patients

• In a patient with hypotension, high anion gap metabolic acidosis, hyperlactatemia, seizures, syncope, altered mental status consider CN in the differential diagnosis and treat presumptively.
  
• Use serum lactate as a surrogate marker for CN exposure.
  
• Victims of smoke inhalation may have combination of:
  
  • CN toxicity
    
  • MH
    
  • CO toxicity
    
  • If the COHgb concentration is extremely elevated, considered a concomitant CN exposure as well
    
  • To avoid further reduction in oxygen transport; initially treat with hydroxocobalamin or sodium thiosulfate, without sodium nitrite to avoid methemoglobinemia.
    

• Borron SW, Baud FJ, Barriot P, et al. Prospective study of hydroxycobalamin for acute cyanide poisoning in smoke inhalation.
  Ann Emerg Med
  . 2007;49(6):794–801.
  
• Fortin JL, Giocanti JP, Ruttimann M, et al. Prehospital administration of hydroxycobalamin for smoke inhalation-associated cyanide poisoning: 8 years of experience in the Paris fire brigade.
  Clin Toxicol
  . 2006;44:37–44.
  
• Handbook
  . 4th ed. Boca Raton, FL: Lexi-Comp; 2008:781–782, 830, 991, 1011.
  
• Leikin J, Paloucek F.
  Cyanide, nitrites, sodium thiosulfate, sodium nitrite, hydroxycobalamin
  . In: Leikin JB, Paloucek F, eds. Leikin and Paloucek’s Poisoning and Toxicology
  
• Thompson JP, Marrs TC. Hydroxocobalamin in cyanide poisoning.
  J Toxicol Clin Toxicol
  . 2012;50:875–885.
  

CODES

• 987.7 Toxic effect of hydrocyanic acid gas
  
• 989.0 Toxic effect of hydrocyanic acid and cyanides
  

BASICS

Abnormal bluish discoloration of the skin or mucous membranes

• Caused by abnormal elevations of deoxygenated hemoglobin or hemoglobin derivatives in the capillaries:
  
  • Deoxygenated hemoglobin >5 g/dL
    
  • Methemoglobin >1.5 g/dL
    
  • Sulfhemoglobin >0.5 g/dL
    
• The absolute amount of deoxygenated hemoglobin is the pigment that creates the bluish tint
  
  • The amount of oxyhemoglobin does not affect the blood’s color
    
  • Cyanosis is more common in patients with polycythemia and less common in patients with anemia.
    
• Cyanosis varies based on skin thickness or pigment
  
• Accumulation of deoxygenated hemoglobin may be systemic producing central cyanosis or localized producing peripheral cyanosis
  
  • Central cyanosis
    
    • Hypoxemia
      
    • Anatomic right to left shunts
      
    • Abnormal hemoglobin derivatives
      
  • Peripheral cyanosis
    
    • Tissue extracts more than normal amounts of O
      ₂
      from the blood
      
    • Hypoperfusion
      
    • Vasoconstriction to cold air or water
      
    • Arterial insufficiency
      
    • Venous insufficiency
      
    • Acrocyanosis: Painless, symmetrical, cyanosis in distal parts of body, the pathophysiologic cause of which is not known