Surviving acute hydrogen sulfide inhalation with circulatory arrest: a case report
Introduction
Hydrogen Sulfide (H2S) inhalation is often fatal, especially if the patient is in cardiac arrest (CA) on scene. Kamijo et al. found an overall mortality of 58%, and none of the 48 patients who were in CA on scene survived(1). H2S is classified as a “knock down” pulmonary irritant, causing rapid loss of consciousness. This colorless gas with an irritation odor of rotten eggs causes systemic toxicity by inhibition of mitochondrial respiration similar to cyanide(2).
Case
A 42 year old employee in a waste processing company was working alone in a confined space. Due to production system failure, a tank was opened too early, causing loss of consciousness. A colleague got him evacuated. After evacuation, employees started cardiac compressions during 3 minutes. An attached AED did not deliver a shock. H2S intoxication was immediately suspected given the production process and the smell of rotten eggs. Measurements showed a H2S release of >100ppm (which was the maximum measurable value of the device). At arrival of the Emergency Medical Service (EMS), return of spontaneous circulation was observed without need for defibrillation nor adrenaline. Since the victim breathed obstructively, he needed intubation followed by transfer to the emergency department (ED). During transport and stay at the ED, his vital signs were stable without need for fluids nor vasopressors. He could easily be ventilated. Blood analysis showed metabolic acidosis (pH 7.02/Bicarbonate 13.5mmol/L) with high lactate (150 mg/dL). Because the presence of cyanide in the gas mixture could not be excluded, we gave hydroxocobalamin (HyCo) 5 grams empirically. The lactate normalized four hours after the incident. The next day he was extubated without major problems besides confusion, which resolved after a few days.
Discussion
Supportive therapy is the cornerstone in case of H2S intoxication. The administration of sodium nitrite, thereby inducing methaemoglobinemia, is controversial. H2S has a greater affinity for methaemoglobin than for cellular cytochromes, leading to lower metabolic toxicity. It’s recommended by Goldfrank’s Toxicologic Emergencies(2), but not mentioned by Toxbase(3), on which the protocols of the Belgian poison center are based. We choose not to administer Sodium nitrite, since inducing methaemoglobinemia in a patient with cellular hypoxia (high lactate) seemed contradictory.
HyCo might have had a positive impact on outcome. In a rat and sheep model, a reduction in free H2S concentrations to almost zero after HyCo 70mg/kg injection was demonstrated(4), and in sheep experiments, CA was prevented if HyCo was infused within minutes of H2S intoxication(5). In a case report of fatal H2S intoxication, a reduction in sulfide concentrations of 0.22µg/ml to 0.11 µg/ml after administration of HyCo was shown(6).
Conclusion.
In case of H2S intoxication, decontamination (removing clothes, washing), personal protective equipment and supportive measures are the mainstay of therapy. Since HyCo is available in most EMS prehospital teams, the available evidence and the low toxicity of HyCo, we recommend early administration of HyCo in case of cardiorespiratory instability or neurologic symptoms, but further studies are needed.
