ACMT Toxicology Visual Pearls: Discolored Skin and Urine

Posted by Hannah Malashock, MD on

A patient is brought to the Emergency Department by EMS (Emergency Medical Services) from a house fire. The patient’s skin and urine are discolored as shown. What is the most likely cause of the discoloration?

  1. Acute liver failure
  2. An antidote administered by prehospital provider
  3. Carbon monoxide poisoning
  4. Massive hemolysis


Answer: 2- An antidote administered by prehospital provider

Hydroxocobalamin

Hydroxocobalamin often used by pre-hospital personnel for suspected cyanide poisoning, is intensely red, and is well known to turn sweat, tears, skin, and urine a dark red color.1

In the setting of a house fire, cyanide may be liberated by burning of wool, silk, or polyurethane and causes poisoning by inhalation.2,3 Cyanide toxicity may also arise after exposure to substances such as acetonitrile used in artificial nail remover, sodium nitroprusside, cassava root, and apricot pits. Cyanide binds to cytochrome a3 and inhibits aerobic metabolism. Patients with cyanide poisoning may exhibit hypotension, coma, seizures, and apnea.

Laboratory findings are characterized by:4

  1. Anion gap metabolic acidosis
  2. Precipitous rise in lactic acid

The treatment includes administration of either Nithiodote© (sodium nitrite and sodium thiosulfate, Hope Pharmaceuticals) or Cyanokit© (hydroxocobalamin, Meridian Medical Technologies).

Cyanide Poisoning: Bedside Pearls

Decision to Treat

  • A high level of clinical suspicion (such as smoke inhalation, concerning chemical exposure) and recognition of associated risk factors (coma, hypotension, lactemia) are imperative in making the diagnosis of cyanide toxicity.
  • The initial treatment consists of supportive care including oxygen, fluid resuscitation, and intubation, if necessary.

Choice of Antidote

  • Nithiodote 5
    • Contains sodium nitrite and sodium thiosulfate
    • Sodium nitrite
      • May cause vasodilation and hypotension
      • Forms methemoglobin which binds cyanide
      • Methemoglobinemia decreases oxygen carrying capacity, which may be unsafe in smoke inhalation patients with possible concurrent carbon monoxide exposure
    • Sodium thiosulfate
      • Augments cyanide excretion
      • Can be used in conjunction with hydroxocobalamin
      • Has mild adverse effects including nausea, emesis, headache
  • Cyanokit 6
    • Contains hydroxocobalamin, a form of Vitamin B12
    • Binds to cyanide and is excreted as cyanocobalamin
    • Generally well tolerated
    • Preferred for smoke exposure patients who will not tolerate methemoglobinemia
    • Discolors bodily fluids and may alter results of laboratory tests due to spectral effects
    • Adverse effects are generally mild may include transient hypertension, headache, and bradycardia.

Dosing of Hydroxocobalamin for Cyanide Toxicity (Adults)6

  • Initial dose: 5 grams administered as an IV infusion over 15 minutes
    • Has been infused faster in cardiac arrest or severe shock7
  • Second dose: 5 grams administered over 15 minutes to two hours, if needed, depending on severity of toxicity or persistence of symptoms

This post was peer-reviewed by Dr. Vikhyat Bebarta, Dr. Bryan Judge, and Dr. Louise Kao.

References

1.
Thompson J, Marrs T. Hydroxocobalamin in cyanide poisoning. Clin Toxicol (Phila). 2012;50(10):875-885. [PubMed]
2.
Baud F, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med. 1991;325(25):1761-1766. [PubMed]
3.
MacLennan L, Moiemen N. Management of cyanide toxicity in patients with burns. Burns. 2015;41(1):18-24. [PubMed]
4.
Hall A, Rumack B. Clinical toxicology of cyanide. Ann Emerg Med. 1986;15(9):1067-1074. [PubMed]
5.
Nithiodote (R). [Prescribing Information]. Scottsdale, AZ:Hope Pharmaceuticals; 2011:0.
6.
Cyanokit (R). [Package Insert]. Columbia, MD: Meridian Medical Technologies; 2011:0.
7.
Bebarta V, Pitotti R, Dixon P, et al. Hydroxocobalamin and epinephrine both improve survival in a swine model of cyanide-induced cardiac arrest. Ann Emerg Med. 2012;60(4):415-422. [PubMed]

Author information

Hannah Malashock, MD

Medical Toxicology Fellow
Department of Medical Toxicology
University of Arizona College of Medicine- Phoenix

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