DESCRIPTION

• Hydrogen sulfide (H₂S, hydrosulfuric acid) is a colorless gas with a characteristic "rotten eggs" odor.
• H₂S is heavier than air and is found naturally in caves, volcanoes, sulfur springs, natural gas, and swamps.
• Synonyms of H₂S include sewer gas, sour gas, and knock-down gas.

FORMS AND USES

• H₂S is a by-product of the decomposition of organic materials (sewage).
• Industrial sources include petroleum distillation/refining, paper production, heavy water production, leather finishing and manufacturing, and rubber vulcanizing processes.

TOXIC DOSE

H₂S is a "one-whiff" knock-down chemical; a few breaths of high concentration gas may be fatal immediately.

PATHOPHYSIOLOGY

• Toxic effects following exposure are typically severe, with coma and death occurring rapidly.
• H₂S inhibits cytochrome oxidase a₃, which results in interruption of oxidative phosphorylation and thereby of adenosine triphosphate production; this interruption forces a shift to anaerobic glycolysis, which results in rapid lactate accumulation and profound metabolic acidosis.

EPIDEMIOLOGY

• H₂S poisoning is an infrequent but important cause of sudden death in the workplace.
• Exposure results in multiple victims because rescuers attempt to retrieve the initial victim only to succumb to the gas themselves.
• Children may be at increased risk for exposure because of their tendency to explore potentially hazardous enclosed areas.

CAUSES

H₂S poisonings are usually the result of accidental occupational exposure during cleaning or servicing of septic tanks.

PREGNANCY AND LACTATION

Severe maternal poisoning with hypoxia may produce fetal hypoxia and distress.

WORKPLACE STANDARDS

• ACGIH. TLV TWA is 10 ppm; STEL is 15 ppm.
• OSHA. PEL TWA is 10 ppm; PEL STEL is 15 ppm.
• NIOSH. IDLH is 300 ppm.

Section Outline:

• DESCRIPTION
• FORMS AND USES
• TOXIC DOSE
• PATHOPHYSIOLOGY
• EPIDEMIOLOGY
• CAUSES
• PREGNANCY AND LACTATION
• WORKPLACE STANDARDS

DIFFERENTIAL DIAGNOSIS

• Other toxic agents that cause sudden knock-down effects include cyanide gas, very high concentrations of carbon monoxide, or asphyxiant gases.
• Nontoxic causes of sudden knock-down effects include pulmonary embolus, ventricular dysrhythmia, and catastrophic intracranial event, among others.

SIGNS AND SYMPTOMS

Most fatalities occur at the scene. If the patient rapidly recovers consciousness, recovery is usually complete if cerebral anoxic injury has not already occurred.

Vital Signs

Bradycardia or tachycardia and tachypnea may be followed quickly by respiratory arrest, hypotension, and coma.

HEENT

• Exposure results in intense mucous membrane irritation, including corneal abrasions (gas eye) and corneal ulceration.
• The characteristic odor serves as an olfactory warning for gas; the ability to smell the gas, however, is lost at higher concentrations because of paralysis of the olfactory nerve.
• Mydriasis may occur as a preterminal event.

Skin

Diaphoresis may occur.

Pulmonary

Cough and respiratory distress may be followed quickly by respiratory arrest.

Cardiovascular

Tachycardia or bradycardia may precede rapid onset of cardiovascular collapse and cardiac arrest.

Gastrointestinal

Nausea and vomiting are common.

Musculoskeletal

• Profound weakness with loss of reflexes may occur.
• Trauma secondary to a "quick knock-down" effect is common.

Neurologic

• Acute exposure. Headache and confusion may rapidly progress to seizures and coma; loss of consciousness may be transient if exposure is brief.
• Repeated exposure. Patients who experience repeated sublethal exposures are at risk for the development of cognitive function abnormalities, personality changes, and anosmia.

PROCEDURES AND LABORATORY TESTS

Essential Tests

• Arterial blood gases should be obtained to evaluate oxygenation and ventilation deficits caused by H₂S, a coingestant, aspiration pneumonia, or pulmonary edema.
• Serum electrolytes, BUN, creatinine, glucose, and lactate studies are warranted for patients with altered mental status.

Recommended Tests

• ECG, CT, lumbar puncture, blood, and cerebrospinal fluid cultures should be ordered as needed to evaluate altered mental status.
• Carboxyhemoglobin or methemoglobin level should be determined if coexposure may have occurred.
• Blood cyanide level should be considered to exclude cyanide exposure.
• A chest radiograph should be obtained for patients presenting after significant exposure or patients who remain symptomatic in the emergency department after minor exposure.

Not Recommended Tests

A sulfhemoglobin level is not useful, because acute H₂S exposure is not expected to produce sulfhemoglobin.

Section Outline:

• DIFFERENTIAL DIAGNOSIS
• SIGNS AND SYMPTOMS
  • Vital Signs
  • HEENT
  • Skin
  • Pulmonary
  • Cardiovascular
  • Gastrointestinal
  • Musculoskeletal
  • Neurologic
• PROCEDURES AND LABORATORY TESTS
  • Essential Tests
  • Recommended Tests
  • Not Recommended Tests

• Treatment should focus on airway management and oxygen administration.
• The dose and time of exposure for all substances involved should be determined.

DIRECTING PATIENT COURSE

The health-care provider should call a poison control center when:

• Signs and symptoms are not consistent with H₂S poisoning.
• Drug interaction, or underlying disease presents an unusual problem.

The patient should be referred to a health-care facility when:

• Suspicion of H₂S exposure exists.
• Attempted suicide or homicide is possible.
• Respiratory arrest, altered mental status, hypotension, or other severe effects are present.
• Drug interaction or underlying disease presents an unusual problem.

Admission Considerations

Inpatient management for at least 24 hours is warranted for all patients with significant exposure to H₂S gas or persistent symptoms to observe and evaluate for delayed pulmonary edema or CNS symptoms.

DECONTAMINATION

Out of Hospital

The patient should be removed from the source of exposure, but rescuers should not attempt retrieval of the victim unless equipped with self-contained breathing apparatus.

In Hospital

H₂S toxicity does not result from dermal or ingestion exposure, so decontamination is unnecessary.

ANTIDOTES

• There is no proven antidote for H₂S poisoning.
• Cyanide antidote kit. Administration of only the sodium nitrite component of the kit in conjunction with supportive therapy within 15 to 20 minutes of exposure is supported by anecdotal reports (see SECTION III, Cyanide Antidote Package chapter). Because 85% of the sulfide is eliminated from the blood within minutes of exposure, however, this procedure is often of no benefit.

ADJUNCTIVE TREATMENT

• Hyperbaric oxygen has been described as effective in reversing CNS depression and acidosis in anecdotal reports and may be a reasonable intervention in serious cases.
• Hypotension is treated with isotonic fluid infusion, the Trendelenburg position, and vasopressor if needed; dopamine is preferred, and norepinephrine is used for refractory hypotension.
• There is no specific treatment for metabolic acidosis resulting from H₂S poisoning; the health-care provider should optimize hemodynamic parameters with intensive supportive care.

Section Outline:

• DIRECTING PATIENT COURSE
  • Admission Considerations
• DECONTAMINATION
  • Out of Hospital
  • In Hospital
• ANTIDOTES
• ADJUNCTIVE TREATMENT

PATIENT MONITORING

• Patients who have sustained significant exposure to H₂S gas should be observed for at least 24 hours with cardiac monitoring and attention primarily focused on the possible development of pulmonary edema.
• The health-care provider should be vigilant for sequelae of hypoxia.

EXPECTED COURSE AND PROGNOSIS

• Prognosis is directly related to the concentration of the exposure and, to a lesser extent, the length of time of the exposure.
• If the patient rapidly regains consciousness, recovery is usually complete, provided cerebral anoxic injury has not already occurred.
• Prolonged unconsciousness indicates a poor prognosis.

DISCHARGE CRITERIA/INSTRUCTIONS

• From the emergency department
  • Patients who have not sustained a significant H₂S exposure and who remain asymptomatic after a 4- to 6-hour observation period may be discharged.
  • Patients who have sustained a significant H₂S exposure or have local airway irritative effects should not be discharged.
• From the hospital. Patients may be discharged after sequelae of poisoning have resolved or remained stable for at least 24 hours.

PATIENT EDUCATION

• Patients should be aware of the risk of brain injury as a result of the cumulative effects of multiple knock-downs.
• Workers who come into contact with gases from sewage or other organic matter should avoid entering enclosed areas or areas with poor ventilation until quantitative air sampling can be performed to exclude the presence of H₂S gas or other toxic gases.
• Workers in high-risk industries need to be cognizant of the dangers of entering an enclosed area to retrieve a fallen comrade.

Section Outline:

• PATIENT MONITORING
• EXPECTED COURSE AND PROGNOSIS
• DISCHARGE CRITERIA/INSTRUCTIONS
• PATIENT EDUCATION

DIAGNOSIS

It is important to consider exposure to another toxic gas, such as methane, ammonia, chlorine, carbon monoxide, cyanide, or sulfur dioxide, as well as alternative causes for altered level of consciousness, including metabolic, infectious, and traumatic events.

TREATMENT

It is important to treat the victim for possible comorbid conditions such as traumatic injury to the spine or myocardial ischemia secondary to hypoxia.

Section Outline:

• DIAGNOSIS
• TREATMENT

Toxic effect of other gases, fumes, or vapors.

See Also: SECTION II, Hypotension chapter; SECTION III, Cyanide Antidote Package chapter; and SECTION IV, Cyanide chapter.

RECOMMENDED READING

Hoffman HE, Guidotti TL. Natural gases. In: Greenberg MI et al., eds. Occupational, industrial and environmental toxicology. St. Louis: Mosby, 1997:359-366.

Smith RP, Gosselin RE. Hydrogen sulfide poisoning. J Occup Med 1979;21:93-97.

Author: Gerald F. O'Malley

Reviewer: Richard C. Dart