Case #26: Where there’s smoke…
Author: Michael Gottlieb, MD
Peer Reviewer: Christopher Lim, MD
A 24 year old male is brought in by ambulance after being found unconscious outside of a burning building. On arrival, he begins to wake up, but is still lethargic. He does not remember what happened and denies any past medical history. He has neither external burns nor stigmata of inhalational injury. His exam is significant for tachypnea and bradycardia, but is otherwise non-focal. While being examined, he intermittently complains of a headache.
Vitals: Temp: 99.2, HR: 56, RR: 16, BP: 92/60, O2 Sat: 98% on RA
An ABG with CO-oximetry was performed which showed a lactate of 10.4 and a carboxyhemoglobin concentration (COHb) of 0.6%. Per the paramedics, his field COHb was 0.8%.
What is the most likely etiology of this patient’s presentation?
The two most important considerations in any person exposed to a fire in an enclosed space are carbon monoxide and cyanide poisoning. With a normal COHb in the field and significantly elevated lactate, his story is very concerning for cyanide toxicity.
What other clinical symptoms might you expect to see with this patient?
Cyanide binds to and directly inhibits mitochondrial cytochrome oxidase, preventing aerobic metabolism. Thus, almost all of the side effects are secondary to
cellular hypoxia.
General: Anxiety, Diaphoresis, Bitter Almond Odor
Cardiovascular: Tachycardia, Bradycardia, Hyper/Hypotension, Arrhythmias, Asystole
Pulmonary: Dyspnea, Tachypnea, Apnea
GI: N/V
Neurologic: Headache, Drowsiness, Seizures, Coma, and Death
Metabolic: Lactic Acidosis (>8 mmol/L)
What is the initial treatment for this patient?
Assess the ABCs first and place the patient on 100% O2. There are two antidotes available for cyanide toxicity (see below).
1. Cyanide Antidote Kit™
–Amyl Nitrite pearls (crack vial and inhale until IV access is established)
-10 mL of 3% Sodium Nitrite (give 0.19-0.39 mL/kg (based upon Hgb level) IV over 5-10 mins)
-50 mL of 25% Sodium Thiosulfate (give IV after Sodium Nitrite is given)
–Mechanism of action: Nitrites convert Hgb to Met-Hgb, which binds CN more avidly, thereby removing it from the cytochrome oxidase enzyme. Sodium Thiosulfate then scavenges CN from Met-Hgb, forming Sodium Thiocyanate, which can be safely excreted by the kidneys.
-Given the risk of hypotension and Methemoglobinemia, the Cyanokit™ (below) is now preferred.
2. Cyanokit™ (Hydroxycobalamin)
-5 g Hydroxocobalamin given IV over 15 mins
–Mechanism of action: Scavenges CN, forming Vit B12 (Cyanocobalamin). A common side effect of this treatment is red discoloration of the skin and urine, which may last up to two weeks.
–Preferred method of treatment.
What further work-up is required?
Plasma Cyanide levels rarely return in time to affect clinical management, so they are not recommended. An ABG with CO-oximetry will show a normal COHb and significantly elevated Lactate (> 8 mmol/L) with acidemia supporting the diagnosis. An elevated venous oxygen saturation > 90%, resulting from impaired cellular oxygen utilization, is an additional clue to the diagnosis.
References:
Baud FJ, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med. 1991 Dec 19;325(25):1761-6.
Baud FJ, Borron SW, Mégarbane B, et al. Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning. Crit Care Med. 2002 Sep;30(9):2044-50.
Borron SW, Baud FJ. Acute cyanide poisoning: clinical spectrum, diagnosis, and treatment. Arh Hig Rada Toksikol. 1996 Sep;47(3):307-22.
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