You are on page 1of 5


Low-level exposures to 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. Complications include the following:

Acute respiratory distress syndrome

Acute myocardial infarction
Delayed neuropsychiatric sequelae

Occurrence of long-term neurologic sequelae from hydrogen sulfide exposure is

unknown but appears to be linked to longer sub-lethal exposures. Paradoxically,
high-concentration exposures of hydrogen sulfide may have no long-term effects.
The presence of hydrogen sulfide 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.
Similarly, continuous exposure to low concentrations of hydrogen sulfide result in
olfactory fatigue/paralysis and loss of the ability to smell or detect the gas even if it
is still present in the environment.

Exposures can be subdivided into low-, high-, and very high-level categories. Lowlevel 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. Other toxic effects are
headaches, asthenia, and bronchitis.

High-level exposures of hydrogen sulfide result in more neurologic and pulmonary

symptoms, as follows:

Cough, Dyspnea
Vertigo, Confusion
Nausea and vomiting
Possible loss of consciousness


Very high concentrations lead to the following manifestations:

Myocardial infarction
Sudden loss of consciousness ("knockdown")
Cardiopulmonary arrest

Low-level exposure of hydrogen sulfide most often affects the mucous membranes
and may show:

Conjunctivitis (even at levels of only 4 ppm)

Green-gray line on gingiva

High-level exposure of hydrogen sulfide may manifest as follows:

Acute lung injury (patients may present with acute respiratory distress syndrome

Perform a secondary survey to rule out traumatic injuries. Historically, these have
been found in about 10% of victims.

Arterial blood gas (ABG)
testing usually reveals a marked uncompensated metabolic 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. Hydrogen sulfide toxicity may be associated with
carboxyhemoglobin or methemoglobinemia, depending on the source of the
hydrogen sulfide and co-exposure to other toxic gases.

An electrocardiogram may reveal ischemia or infarction patterns.

Chest radiographic findings initially may be normal, but up to 20% of patients

present with clinical evidence of acute lung injury. Acute respiratory distress
syndrome (ARDS) is viewed as a complication of hydrogen sulfide poisoning.
Computed tomography or magnetic resonance imaging scans of the head may also
be initially normal, with abnormal findings (eg, basal ganglia lesions) delayed.

Blood levels of sulfide (which is an unstable metabolite) and thiosulfate may be

elevated in cases of significant exposure, but these assays are rarely available,
especially on short notice.

With significant acute exposure, respiratory paralysis may terminate ongoing

exposure and decrease the amount of hydrogen sulfide absorbed and blood levels
may be surprisingly low.

Measurement of sulfide and thiosulfate levels is more appropriate for the evaluation
of low-level chronic exposures.

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 (self-contained breathing apparatus [SCBA]) to avoid serious

exposure. Protected rescue personnel can measure the environmental concentration
of hydrogen sulfide, providing an initial clue to the diagnosis.

In severe cases, intubation may be necessary for ventilatory support and airway
protection. Establish intravenous (IV) 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.

In the emergency department, 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 arterial blood gas and serum lactate values is

Based on the similarities in cyanide and hydrogen sulfide toxicity, induced

methemoglobinemia may be used in hydrogen sulfide toxicity. Methemoglobin acts
as a scavenger, and it has a stronger affinity to hydrogen sulfide than to
cytochrome oxidase. Administer 10 mL of 3% sodium nitrite IV over 2-4 minutes
(adult dose). Obtain a methemoglobin level 30 minutes after administration of

Patients who have suffered significant exposure (ie, anything other than chronic
low-level exposure with mucous membrane irritation) should be admitted to the
intensive care unit. Patients who are unresponsive to intravenous nitrites or who
have persistent or delayed neurologic sequelae should be considered for hyperbaric
oxygen therapy (HBO). Anecdotal reports indicate a salutary effect. All patients
should be discussed with the local poison center and/or a medical toxicologist.

Antidotal treatment of hydrogen sulfide (H2 S) poisoning is based on the creation of

methemoglobinemia. Symptomatic treatment includes the use of bronchodilators
for patients with bronchospasm.
Substances that can cause methemoglobinemia include the following:
Copper sulfate

Organic compounds Sodium chlorite, [34] ammonium carbonate (smelling

salts), and 2,4-dinitrophenol (weight loss agent)
Recreational drugs Phenylamine (psychoactive stimulant), cocaine, and volatile
Antimalarials Primaquine, chloroquine, and sitamaquine
Antineoplastic agents Cyclophosphamide, ifosfamide, flutamide
and 3-aminopyridine-2-carboxaldehyde thiosemicarbazone
Analgesics and antipyretics Acetaminophen, acetanilide, phenacetin, and
Herbicides and insecticides Paraquat (dipyridylium), indoxacarb, and aluminum
Methylene blue (high dose or in G6PD-deficient patients [46])
Indigo carmine
Antibiotics Sulfonamides, nitrofurans, and para-amino salicylic acid
Industrial/household agents Aniline dyes, nitrobenzene, naphthalene (moth
balls), aminophenol, and nitro ethane (nail polish remover)