H2S POISONING

Overview Background
Hydrogen sulfide (H2 S) is a colorless gas that has strong odor of rotten eggs. H2 S poisoning is a rarity, mainly observed in industrial settings. Emergency physicians must be aware of the presentation and management of H2 S poisoning because rapid identification and treatment is essential for recovery.

Pathophysiology
Significant H2 S poisoning usually occurs by inhalation. Local irritant effects, along with arrest of cellular respiration, may follow. H2 S forms a complex bond to the ferric moiety causing inhibition of mitochondrial cytochrome oxidase (iron-containing protein), thereby arresting aerobic metabolism in an effect similar to cyanide toxicity. Very high lipid solubility allows it to penetrate easily through biologic membranes. As a cellular poison, H2 S affects all organs, particularly the CNS and pulmonary system. The spectrum of illness depends on the concentration and duration of exposure, with high concentrations (>700 ppm or >975 mg/m3) causing sudden death possibly due to hydrogen sulfide effect on the brainstem respiratory center.

Epidemiology
It is very important to realize that 25% of fatalities usually involve rescuers, professionals, or bystanders.[2]

Mortality/Morbidity
Low-level exposures of hydrogen sulfide usually produce local eye and mucous membrane irritation, while high-level exposures rapidly produce fatal systemic toxicity. Exposures of 700-800 ppm or greater can cause loss of consciousness and cardiopulmonary arrest.

Causes
H2 S most often is encountered as a byproduct of the petroleum, viscose rayon, rubber, and mining industries. Organic decomposition of sulfur compounds in sewers, barns, liquid manure pits, ships' holds, and sulfur springs also produces H2 S. The petroleum industry is responsible for most cases of H2 S toxicity in North America. In nature, hydrogen sulfide can be found in caves, sulfur springs, underground deposits of natural gas, or as result of volcanic eruptions. Hydrogen sulfide has recently been implicated in suicides in Japan.[

CLINICAL PRESENTATION History

The presence of H2 S usually is apparent because of the characteristic rotten egg smell. However, concentrations above 150 ppm may overwhelm the olfactory nerve so that the victim may have no warning of exposure. Exposures can be subdivided into low-, high-, and very highlevel categories. Low-level exposure often is more chronic in nature and usually is seen in industrial settings. Chronic low-level exposure of hydrogen sulfide results primarily in irritation to mucous membranes and the respiratory system. Patients exposed to continuous low-level concentrations or after acute exposure to the very high concentrations of hydrogen sulfide can lose their ability to smell/detect the gas even though it is still present in the environment (olfactory fatigue/paralysis). Headaches Asthenia Bronchitis High-level exposures of hydrogen sulfide result in more neurologic and pulmonary symptoms. Cough Dyspnea Vertigo Confusion Nausea and vomiting Possible loss of consciousness Hemoptysis Very high concentrations lead to cardiorespiratory arrest because of brainstem toxicity. Myocardial infarction Sudden loss of consciousness ("knockdown") Seizure Cardiopulmonary arrest

Physical
Low-level exposure of hydrogen sulfide most often affects the mucous membranes and may show the following few physical signs: Conjunctivitis (even at levels of only 4 ppm) Pharyngitis Green-gray line on gingiva Wheezing High-level exposure of hydrogen sulfide may elicit the following signs: Bradycardia Tremulousness Agitation Cyanosis Acute lung injury (may present with acute respiratory distress syndrome[ARDS])

Laboratory Studies
Arterial blood gas (ABG) usually reveals a marked uncompensatedmetabolic acidosis. Acidosis is associated with an elevation in serum lactate level. Oxygen tension (pO2) and calculated oxygen saturation are within the reference range unless the patient has concomitant pulmonary edema. As with other hemoglobinopathies, however, measured oxygen saturation often is low and indicates a saturation gap. Venous blood gas may indicate abnormally high oxygen tension (because of decreased oxygen utilization) resulting in a decrease in the PO2 gradient between arterial and venous blood. H2 S toxicity may be associated with carboxyhemoglobin ormethemoglobinemia, depending on the source of H2 S and coexposure

Imaging Studies
Chest radiography: Chest radiographic findings initially may be normal, but up to 20% of patients present with evidence of acute lung injury. ARDS is viewed as a complication in H2 S poisoning. CT scan or MRI of the head: Often only delayed findings, such as basal ganglia lesions, are found.

Other Tests
ECG may reveal ischemia or infarction patterns. Sulfide (unstable metabolite) and thiosulfate blood levels rarely are available (especially on short notice) and may be elevated in cases of significant exposure. However, with significant acute exposure due to respiratory paralysis, the amount of actually absorbed hydrogen sulfide can be lower in comparison to low-level chronic exposure. Measurement of sulfide and thiosulfate levels are more appropriate for the evaluation of low-level chronic exposures.

TREATMENT PLAN Prehospital Care

Initial treatment of hydrogen sulfide exposure requires immediate removal of the victim from the contaminated area into a ventilated/fresh-air environment. Prehospital care providers should take hazardous materials precautions with respirator devices (SCBA) to avoid serious exposure. In severe cases, intubation may be necessary for ventilatory support and airway protection. Gain intravenous access or initiate other initial supportive care as necessary. Search the patient's pockets for discolored copper coins, which can be an early diagnostic clue. Protected rescue personnel can measure environmental concentration of hydrogen sulfide providing initial clue to the diagnosis.

Emergency Department Care

High-flow (100%) oxygen is the mainstay of therapy for hydrogen sulfide poisoning. Supportive therapy includes aggressive ventilation and possible use of positive pressure ventilation for the patients with evidence of acute lung injury. IV fluids and vasopressors should be administered to hypotensive patients. Correction of acidosis based on ABG and serum lactate values is indicated. Based on the similarities in cyanide and hydrogen sulfide toxicity, induced methemoglobinemia may be used for the treatment of hydrogen sulfide toxicity. Methemoglobin acts as a scavenger, and it is more attractive to hydrogen sulfide than cytochrome oxidase. Administer 10 mL of 3% sodium nitrite intravenously over 2-4 minutes (adult dose). Obtain methemoglobin level 30 minutes after administration of antidote. Patients with persistent neurologic findings should be considered for hyperbaric oxygen therapy (HBO). Anecdotal reports indicate a salutary effect.

Consultations
Consultation with the local hyperbaric chamber facility may be necessary for patients who are unresponsive to nitrites

MEDICATIONS Medication Summary

Treatment of hydrogen sulfide (H2 S) poisoning is based on the creation of methemoglobinemia.

Nitrites
Class Summary
Nitrite administration leads to formation of methemoglobinemia. H2 S has a much greater affinity for methemoglobin than for cellular cytochromes, leading to lower metabolic toxicity.

Sodium nitrite
Initial DOC in hydrogen sulfide poisoning.

Bronchodilators
Class Summary
These agents are effective in reversing acute bronchospasm of allergic or irritant origin through combined alpha-adrenergic and beta-adrenergic agonist action. An additional option in the management of persistent bronchospasm involves anticholinergics. These agents block action of acetylcholine at parasympathetic sites in bronchial smooth muscle, causing bronchodilation.

Albuterol (Ventolin, Proventil)

Beta agonist useful in treatment of bronchospasm refractory to epinephrine. Relaxes bronchial smooth muscle by acting on beta2 receptors with little effect on heart rate.