Hydrogen sulfide toxicity: Difference between revisions
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Hydrogen sulfide (H₂S) is an extremely toxic, colorless, flammable gas that inhibits mitochondrial cytochrome C oxidase — a mechanism nearly identical to [[Cyanide poisoning|cyanide]]. It is the '''most common cause of fatal toxic gas exposure''' in the workplace.<ref name="Tintinalli">Tintinalli et al. Hydrogen Sulfide. In: Tintinalli et al. Emergency Medicine A Comprehensive Study Guide. New York, NY: McGraw Hill. 2011. 1320.</ref> The classic toxidrome is | ==Background== | ||
*Hydrogen sulfide (H₂S) is an extremely toxic, colorless, flammable gas that inhibits mitochondrial cytochrome C oxidase — a mechanism nearly identical to [[Cyanide poisoning|cyanide]]. | |||
*It is the '''most common cause of fatal toxic gas exposure''' in the workplace.<ref name="Tintinalli">Tintinalli et al. | |||
*Hydrogen Sulfide. | |||
*In: Tintinalli et al. | |||
*Emergency Medicine A Comprehensive Study Guide. | |||
*New York, NY: McGraw Hill. 2011. 1320.</ref> | |||
*The classic toxidrome is knockdown (rapid loss of consciousness), pulmonary edema, conjunctivitis, and olfactory paralysis.<ref name="StatPearls">Hydrogen Sulfide Toxicity. ''StatPearls''. 2024. | |||
*PMID: 32119270</ref> | |||
===General information=== | ===General information=== | ||
*Colorless, highly flammable, heavier-than-air gas | *Colorless, highly flammable, heavier-than-air gas | ||
* | *"Rotten egg" odor at low concentrations (detectable at ~0.5 ppb)<ref name="ATSDR">Hydrogen Sulfide Medical Management Guidelines. Agency for Toxic Substances and Disease Registry (ATSDR). CDC.</ref> | ||
* | *WARNING: Odor is NOT a reliable safety indicator — olfactory nerve fatigue occurs at ≥100 ppm (within 2-15 minutes), causing complete loss of smell at the very concentrations that are dangerous<ref name="StatPearls"/> | ||
*Heavier than air → accumulates in '''enclosed, low-lying, and poorly ventilated spaces''' (sewers, manure pits, tanks) | *Heavier than air → accumulates in '''enclosed, low-lying, and poorly ventilated spaces''' (sewers, manure pits, tanks) | ||
*Encountered in: | *Encountered in: | ||
** | **Oil and gas industry (primary chemical hazard of natural gas production) | ||
**Sewers, wastewater treatment | **Sewers, wastewater treatment | ||
**Manure pits, animal confinement facilities | **Manure pits, animal confinement facilities | ||
| Line 15: | Line 23: | ||
**Mining, smelting | **Mining, smelting | ||
**Hot springs, volcanic areas | **Hot springs, volcanic areas | ||
* | *Suicide method ("detergent suicide"'''):''' mixing acidic household cleaners (toilet bowl cleaner) with sulfur-containing products (bath salts, lime sulfur pesticide) to generate H₂S in an enclosed space — increasing in prevalence<ref name="Tintinalli"/> | ||
*Most fatalities occur in '''confined spaces'''; rescuers entering without SCBA frequently become secondary victims<ref name="ATSDR"/> | *Most fatalities occur in '''confined spaces'''; rescuers entering without SCBA frequently become secondary victims<ref name="ATSDR"/> | ||
*Children are at higher risk at the same ambient concentration due to higher minute volume:weight ratios and shorter stature (gas settles near the ground)<ref name="ATSDR"/> | *Children are at higher risk at the same ambient concentration due to higher minute volume:weight ratios and shorter stature (gas settles near the ground)<ref name="ATSDR"/> | ||
| Line 45: | Line 53: | ||
===Mechanism of toxicity=== | ===Mechanism of toxicity=== | ||
*Rapidly absorbed through the lungs | *Rapidly absorbed through the lungs | ||
* | *Inhibits mitochondrial cytochrome C oxidase (complex IV) by binding to the ferric (Fe³⁺) moiety → blocks aerobic metabolism → cellular asphyxia<ref name="StatPearls"/> | ||
**Identical mechanism to [[Cyanide poisoning|cyanide]] | **Identical mechanism to [[Cyanide poisoning|cyanide]] | ||
**Tissues with high oxygen demand (brain, heart) are most sensitive | **Tissues with high oxygen demand (brain, heart) are most sensitive | ||
| Line 51: | Line 59: | ||
*Causes '''hyperpolarization of potassium-mediated neuronal channels''' → CNS depression<ref name="Tintinalli"/> | *Causes '''hyperpolarization of potassium-mediated neuronal channels''' → CNS depression<ref name="Tintinalli"/> | ||
*Potentiates neuronal inhibitory mechanisms; alters brain neurotransmitter content | *Potentiates neuronal inhibitory mechanisms; alters brain neurotransmitter content | ||
* | *Direct mucosal irritant → conjunctivitis, pulmonary edema | ||
*At very high concentrations, stimulates carotid/aortic chemosensors → initial hyperpnea, then central respiratory arrest | *At very high concentrations, stimulates carotid/aortic chemosensors → initial hyperpnea, then central respiratory arrest | ||
| Line 73: | Line 81: | ||
*Bronchospasm, wheezing | *Bronchospasm, wheezing | ||
*Rales, rhonchi | *Rales, rhonchi | ||
* | *Pulmonary edema — may be immediate or '''delayed up to 72 hours'''<ref name="ATSDR"/> | ||
*[[ARDS]] | *[[ARDS]] | ||
*Central respiratory arrest at high concentrations | *Central respiratory arrest at high concentrations | ||
| Line 85: | Line 93: | ||
===Central nervous system=== | ===Central nervous system=== | ||
*Headache, dizziness, weakness (early) | *Headache, dizziness, weakness (early) | ||
* | *"Knockdown" — sudden loss of consciousness within 1-2 breaths at ≥500 ppm; may be followed by apparent rapid recovery, but can leave lasting neurologic injury<ref name="StatPearls"/> | ||
*Disequilibrium, ataxia | *Disequilibrium, ataxia | ||
*Intention tremor, muscle rigidity | *Intention tremor, muscle rigidity | ||
| Line 110: | Line 118: | ||
===Gastrointestinal=== | ===Gastrointestinal=== | ||
* | *Green-gray line on gingiva (characteristic but not always present) | ||
*Nausea, vomiting, diarrhea | *Nausea, vomiting, diarrhea | ||
| Line 116: | Line 124: | ||
*Cyanosis (from respiratory failure, not methemoglobinemia in most cases) | *Cyanosis (from respiratory failure, not methemoglobinemia in most cases) | ||
*Metabolic acidosis with elevated lactate | *Metabolic acidosis with elevated lactate | ||
* | *Gray-green discoloration of skin/blood on autopsy (sulfhemoglobin formation — a postmortem finding) | ||
==Differential diagnosis== | ==Differential diagnosis== | ||
| Line 130: | Line 138: | ||
==Evaluation== | ==Evaluation== | ||
* | *No single rapid bedside test exists to confirm H₂S exposure<ref name="StatPearls"/> | ||
* | *Diagnosis is clinical: exposure history (confined space, rotten egg odor, industrial setting, detergent suicide setup) + compatible symptoms | ||
===Labs=== | ===Labs=== | ||
* | *ABG/VBG: metabolic acidosis with elevated lactate + '''normal or elevated PaO₂/SaO₂''' (cellular asphyxiant — oxygen delivery is adequate but cells cannot use it) | ||
**Classic finding: lactic acidosis with normal oxygen saturation (unless concurrent pulmonary edema reduces oxygenation) | **Classic finding: lactic acidosis with normal oxygen saturation (unless concurrent pulmonary edema reduces oxygenation) | ||
* | *Serum lactate: elevated (reflects impaired oxidative phosphorylation) | ||
* | *BMP: electrolytes, renal function | ||
* | *CBC: leukopenia, neutropenia reported | ||
* | *Hepatic function panel (hepatic injury reported in severe cases) | ||
* | *Troponin, CK — myocardial and skeletal muscle injury | ||
* | *Methemoglobin level — obtained if nitrite therapy administered (target <30%) | ||
* | *Whole blood sulfide: >0.05 mg/L is abnormal; must be obtained '''within 2 hours''' of exposure and analyzed immediately; not available in most hospitals and will not affect acute management<ref name="StatPearls"/> | ||
* | *Urine thiosulfate: reflects H₂S exposure in acute setting; useful for workplace monitoring but rarely available acutely | ||
===Imaging=== | ===Imaging=== | ||
* | *Chest radiograph: pulmonary edema (may be delayed 24-72 hours) | ||
* | *CT head: consider if persistent altered mental status; basal ganglia necrosis has been reported after severe exposure | ||
===Other=== | ===Other=== | ||
* | *ECG: ST-T changes, QTc prolongation, dysrhythmias | ||
* | *Discolored copper coins found on the patient may turn dark/black (copper sulfide formation) — can serve as a supportive diagnostic clue<ref name="Tintinalli"/> | ||
==Management== | ==Management== | ||
===Immediate=== | ===Immediate=== | ||
* | *Remove from exposure — ensure scene safety; do '''not''' enter confined space without SCBA | ||
* | *100% high-flow oxygen via NRB mask — cornerstone of treatment | ||
**Competes with H₂S for cytochrome oxidase binding | **Competes with H₂S for cytochrome oxidase binding | ||
**Administer to all patients regardless of SpO₂ | **Administer to all patients regardless of SpO₂ | ||
| Line 165: | Line 173: | ||
====Hydroxocobalamin (preferred)==== | ====Hydroxocobalamin (preferred)==== | ||
* | *[[Hydroxocobalamin]] (Cyanokit): 5 g IV over 15 minutes; second dose may be given PRN<ref name="Haouzi2015">Haouzi P et al. High-dose hydroxocobalamin administered after H₂S exposure counteracts sulfide-poisoning-induced cardiac depression in sheep. ''Clin Toxicol (Phila)''. 2015;53(1):28-36.</ref> | ||
* | *Mechanism: binds sulfide directly, forming sulfhydroxocobalamin | ||
*Animal models demonstrate prevention of PEA cardiac arrest when given early<ref name="Haouzi2015"/> | *Animal models demonstrate prevention of PEA cardiac arrest when given early<ref name="Haouzi2015"/> | ||
*Emerging as the '''preferred antidote''' over nitrites due to safer side-effect profile (does not induce methemoglobinemia) and efficacy against both H₂S and cyanide | *Emerging as the '''preferred antidote''' over nitrites due to safer side-effect profile (does not induce methemoglobinemia) and efficacy against both H₂S and cyanide | ||
* | *[[Cobinamide]] (vitamin B₁₂ analog) shows promise in animal studies as a potentially superior antidote with greater sulfide-binding capacity<ref name="Jiang2016">Jiang J et al. Hydrogen Sulfide — Mechanisms of Toxicity and Development of an Antidote. ''Sci Rep''. 2016;6:20831.</ref><ref name="Brenner2014">Brenner M et al. The vitamin B₁₂ analog cobinamide is an effective hydrogen sulfide antidote in a lethal rabbit model. ''Clin Toxicol (Phila)''. 2014;52(5):490-497.</ref> | ||
====Nitrite therapy (alternative)==== | ====Nitrite therapy (alternative)==== | ||
*May use the '''nitrite component''' of the cyanide antidote kit — do '''NOT''' give the thiosulfate portion (thiosulfate is the product of H₂S detoxification and does not help)<ref name="Goldfrank">Goldfrank et al. Hydrogen Sulfide Poisoning. In: Goldfrank et al. Goldfrank's Toxicologic Emergencies. New York, NY: McGraw Hill. 2002. 1504-1507.</ref> | *May use the '''nitrite component''' of the cyanide antidote kit — do '''NOT''' give the thiosulfate portion (thiosulfate is the product of H₂S detoxification and does not help)<ref name="Goldfrank">Goldfrank et al. Hydrogen Sulfide Poisoning. In: Goldfrank et al. Goldfrank's Toxicologic Emergencies. New York, NY: McGraw Hill. 2002. 1504-1507.</ref> | ||
* | *Mechanism: nitrites induce methemoglobinemia; methemoglobin (Fe³⁺) has high affinity for sulfide → converts it to the less toxic sulfmethemoglobin | ||
* | *[[Amyl nitrite]] inhaled (pearls crushed and inhaled) — may be used as a bridge | ||
* | *[[Sodium nitrite]] (3% NaNO₂): 10 mL (300 mg) IV over 2-4 minutes in adults; pediatric dose 0.33 mL/kg (max 10 mL) | ||
* | *Obtain methemoglobin level 30 minutes after dose — desired level <30% | ||
*Caution: nitrite-induced methemoglobinemia can worsen oxygen-carrying capacity in already hypoxic patients; not first-line if hydroxocobalamin is available | *Caution: nitrite-induced methemoglobinemia can worsen oxygen-carrying capacity in already hypoxic patients; not first-line if hydroxocobalamin is available | ||
===Supportive care=== | ===Supportive care=== | ||
* | *Aggressive IV fluid resuscitation | ||
* | *Bronchospasm: inhaled beta-2 agonists (albuterol), consider racemic epinephrine for stridor in children | ||
* | *Seizures: [[Benzodiazepines|benzodiazepines]] first-line | ||
* | *Pulmonary edema: positive-pressure ventilation (CPAP/BiPAP or mechanical ventilation); diuretics generally not effective for noncardiogenic pulmonary edema | ||
* | *Metabolic acidosis: treat with oxygen and supportive care; IV sodium bicarbonate if severe | ||
* | *Cardiac arrest: standard ACLS protocols; prolonged resuscitation may be warranted (potentially reversible etiology) | ||
* | *Hyperbaric oxygen therapy: has been used; no proven benefit; consider on a case-by-case basis for severe neurologic injury<ref name="Goldfrank"/> | ||
===Things to avoid=== | ===Things to avoid=== | ||
| Line 193: | Line 201: | ||
==Disposition== | ==Disposition== | ||
* | *Asymptomatic patients with possible low-level exposure: observe for '''minimum 4-6 hours'''; if asymptomatic with normal labs and CXR, may discharge with return precautions for delayed pulmonary edema (up to 72 hours)<ref name="ATSDR"/> | ||
* | *Any symptomatic patient or significant exposure: admit, likely to ICU | ||
**Continuous cardiac and pulse oximetry monitoring | **Continuous cardiac and pulse oximetry monitoring | ||
**Serial ABGs, lactate, CXR | **Serial ABGs, lactate, CXR | ||
**Watch for '''delayed pulmonary edema''' (may develop up to 72 hours after exposure)<ref name="ATSDR"/> | **Watch for '''delayed pulmonary edema''' (may develop up to 72 hours after exposure)<ref name="ATSDR"/> | ||
* | *"Knockdown" patients (even with apparent rapid recovery): admit for observation — high risk for persistent or delayed neurologic sequelae<ref name="StatPearls"/> | ||
* | *Outpatient follow-up: | ||
**Neuropsychiatric evaluation — cognitive impairment, amnesia, personality changes, and peripheral neuropathy may develop or persist weeks to months after exposure | **Neuropsychiatric evaluation — cognitive impairment, amnesia, personality changes, and peripheral neuropathy may develop or persist weeks to months after exposure | ||
**Pulmonary function testing if respiratory symptoms persist | **Pulmonary function testing if respiratory symptoms persist | ||
**Ophthalmologic evaluation for corneal injury | **Ophthalmologic evaluation for corneal injury | ||
* | *Toxicology consultation for all significant exposures | ||
*Contact [[Poison control]] (1-800-222-1222 in the US) for all cases | *Contact [[Poison control]] (1-800-222-1222 in the US) for all cases | ||
Revision as of 15:48, 19 March 2026
Background
- Hydrogen sulfide (H₂S) is an extremely toxic, colorless, flammable gas that inhibits mitochondrial cytochrome C oxidase — a mechanism nearly identical to cyanide.
- It is the most common cause of fatal toxic gas exposure in the workplace.[1]
- The classic toxidrome is knockdown (rapid loss of consciousness), pulmonary edema, conjunctivitis, and olfactory paralysis.[2]
General information
- Colorless, highly flammable, heavier-than-air gas
- "Rotten egg" odor at low concentrations (detectable at ~0.5 ppb)[3]
- WARNING: Odor is NOT a reliable safety indicator — olfactory nerve fatigue occurs at ≥100 ppm (within 2-15 minutes), causing complete loss of smell at the very concentrations that are dangerous[2]
- Heavier than air → accumulates in enclosed, low-lying, and poorly ventilated spaces (sewers, manure pits, tanks)
- Encountered in:
- Oil and gas industry (primary chemical hazard of natural gas production)
- Sewers, wastewater treatment
- Manure pits, animal confinement facilities
- Paper/pulp mills, tanneries
- Roofing/asphalt operations
- Mining, smelting
- Hot springs, volcanic areas
- Suicide method ("detergent suicide"): mixing acidic household cleaners (toilet bowl cleaner) with sulfur-containing products (bath salts, lime sulfur pesticide) to generate H₂S in an enclosed space — increasing in prevalence[1]
- Most fatalities occur in confined spaces; rescuers entering without SCBA frequently become secondary victims[3]
- Children are at higher risk at the same ambient concentration due to higher minute volume:weight ratios and shorter stature (gas settles near the ground)[3]
Concentration-dependent effects
| Concentration (ppm) | Effects |
|---|---|
| 0.01-0.03 | Rotten egg odor detectable |
| 2-5 | Nausea, headache, tearing with prolonged exposure |
| 10-20 | Eye irritation ("gas eye"), mild respiratory irritation |
| 50-100 | Conjunctivitis, respiratory tract irritation; olfactory fatigue begins at 100 ppm |
| 100-200 | Olfactory paralysis (loss of smell); cough, eye irritation, drowsiness; potentially fatal after 4-48 hours |
| 200-300 | Marked conjunctivitis, respiratory irritation after 1 hour; pulmonary edema risk |
| 500-700 | Staggering, collapse within 5 minutes; serious eye damage; fatal in 30-60 minutes |
| 700-1000 | Rapid "knockdown" — LOC within 1-2 breaths; respiratory paralysis; death within minutes |
| >1000 | Immediate collapse, cardiac arrest, death after single breath |
Mechanism of toxicity
- Rapidly absorbed through the lungs
- Inhibits mitochondrial cytochrome C oxidase (complex IV) by binding to the ferric (Fe³⁺) moiety → blocks aerobic metabolism → cellular asphyxia[2]
- Identical mechanism to cyanide
- Tissues with high oxygen demand (brain, heart) are most sensitive
- Causes lactate accumulation and metabolic acidosis from impaired oxidative phosphorylation
- Causes hyperpolarization of potassium-mediated neuronal channels → CNS depression[1]
- Potentiates neuronal inhibitory mechanisms; alters brain neurotransmitter content
- Direct mucosal irritant → conjunctivitis, pulmonary edema
- At very high concentrations, stimulates carotid/aortic chemosensors → initial hyperpnea, then central respiratory arrest
Healthcare worker safety
- Rescuers entering confined spaces without SCBA frequently become fatalities themselves[3]
- SCBA is mandatory for any responder entering the hot zone
- Chemical-protective clothing is generally NOT needed (H₂S is not significantly absorbed through skin)
- In detergent suicide scenarios:
- Approach with extreme caution; do not enter enclosed space (car, bathroom) without respiratory protection
- Look for warning signs posted by the patient
- Ventilate the space before entry
- Patients exposed only to H₂S gas do not generally require decontamination
- H₂S burns to produce sulfur dioxide (SO₂) — a secondary hazard if ignited
Clinical features
- The classic toxidrome: "knockdown + pulmonary edema + conjunctivitis + olfactory paralysis"[2]
Respiratory
- Dyspnea, cough, chest tightness
- Hemoptysis
- Bronchospasm, wheezing
- Rales, rhonchi
- Pulmonary edema — may be immediate or delayed up to 72 hours[3]
- ARDS
- Central respiratory arrest at high concentrations
Ophthalmic ("gas eye")
- Conjunctivitis (often the earliest sign at low concentrations)
- Corneal ulceration, corneal scarring
- Photophobia, tearing
- Blepharospasm
Central nervous system
- Headache, dizziness, weakness (early)
- "Knockdown" — sudden loss of consciousness within 1-2 breaths at ≥500 ppm; may be followed by apparent rapid recovery, but can leave lasting neurologic injury[2]
- Disequilibrium, ataxia
- Intention tremor, muscle rigidity
- Seizures
- Coma
Neuropsychiatric (may be delayed/persistent)
- Amnesia (particularly surrounding the event)
- Lack of insight, disorientation
- Delirium
- Cognitive impairment, dementia
- Depression, personality changes
- Peripheral neuropathy
- Persistent neurologic deficits may follow "knockdown" events even with apparent recovery[2]
Cardiovascular
- Chest pain
- Bradycardia
- Tachycardia (early sympathetic stimulation)
- Hypotension
- Myocardial injury (elevated troponin/CK reported)[4]
- ECG: T-wave changes, P-wave abnormalities, QTc prolongation
- Cardiac arrest (PEA, asystole)
Gastrointestinal
- Green-gray line on gingiva (characteristic but not always present)
- Nausea, vomiting, diarrhea
Other
- Cyanosis (from respiratory failure, not methemoglobinemia in most cases)
- Metabolic acidosis with elevated lactate
- Gray-green discoloration of skin/blood on autopsy (sulfhemoglobin formation — a postmortem finding)
Differential diagnosis
Toxic gas exposures
- Cyanide poisoning (virtually identical mechanism; distinguish by exposure context)
- Carbon monoxide poisoning
- Arsine gas exposure
- Phosphine poisoning (Aluminum phosphide poisoning, Zinc phosphide poisoning)
- Methane / simple asphyxiant exposure
- Chlorine gas exposure
- Sulfur dioxide exposure
Toxic gas exposure
- Carbon monoxide toxicity
- Chemical weapons
- Cyanide toxicity
- Dichloromethane toxicity
- Hydrocarbon toxicity
- Hydrogen sulfide toxicity
- Inhalant abuse
- Methane toxicity
- Smoke inhalation injury
- Ethylene dibromide toxicity
Evaluation
- No single rapid bedside test exists to confirm H₂S exposure[2]
- Diagnosis is clinical: exposure history (confined space, rotten egg odor, industrial setting, detergent suicide setup) + compatible symptoms
Labs
- ABG/VBG: metabolic acidosis with elevated lactate + normal or elevated PaO₂/SaO₂ (cellular asphyxiant — oxygen delivery is adequate but cells cannot use it)
- Classic finding: lactic acidosis with normal oxygen saturation (unless concurrent pulmonary edema reduces oxygenation)
- Serum lactate: elevated (reflects impaired oxidative phosphorylation)
- BMP: electrolytes, renal function
- CBC: leukopenia, neutropenia reported
- Hepatic function panel (hepatic injury reported in severe cases)
- Troponin, CK — myocardial and skeletal muscle injury
- Methemoglobin level — obtained if nitrite therapy administered (target <30%)
- Whole blood sulfide: >0.05 mg/L is abnormal; must be obtained within 2 hours of exposure and analyzed immediately; not available in most hospitals and will not affect acute management[2]
- Urine thiosulfate: reflects H₂S exposure in acute setting; useful for workplace monitoring but rarely available acutely
Imaging
- Chest radiograph: pulmonary edema (may be delayed 24-72 hours)
- CT head: consider if persistent altered mental status; basal ganglia necrosis has been reported after severe exposure
Other
- ECG: ST-T changes, QTc prolongation, dysrhythmias
- Discolored copper coins found on the patient may turn dark/black (copper sulfide formation) — can serve as a supportive diagnostic clue[1]
Management
Immediate
- Remove from exposure — ensure scene safety; do not enter confined space without SCBA
- 100% high-flow oxygen via NRB mask — cornerstone of treatment
- Competes with H₂S for cytochrome oxidase binding
- Administer to all patients regardless of SpO₂
- Airway management: intubate early for altered mental status, respiratory failure, or airway compromise
- IV access, continuous cardiac monitoring
Antidotal therapy
Hydroxocobalamin (preferred)
- Hydroxocobalamin (Cyanokit): 5 g IV over 15 minutes; second dose may be given PRN[5]
- Mechanism: binds sulfide directly, forming sulfhydroxocobalamin
- Animal models demonstrate prevention of PEA cardiac arrest when given early[5]
- Emerging as the preferred antidote over nitrites due to safer side-effect profile (does not induce methemoglobinemia) and efficacy against both H₂S and cyanide
- Cobinamide (vitamin B₁₂ analog) shows promise in animal studies as a potentially superior antidote with greater sulfide-binding capacity[6][7]
Nitrite therapy (alternative)
- May use the nitrite component of the cyanide antidote kit — do NOT give the thiosulfate portion (thiosulfate is the product of H₂S detoxification and does not help)[8]
- Mechanism: nitrites induce methemoglobinemia; methemoglobin (Fe³⁺) has high affinity for sulfide → converts it to the less toxic sulfmethemoglobin
- Amyl nitrite inhaled (pearls crushed and inhaled) — may be used as a bridge
- Sodium nitrite (3% NaNO₂): 10 mL (300 mg) IV over 2-4 minutes in adults; pediatric dose 0.33 mL/kg (max 10 mL)
- Obtain methemoglobin level 30 minutes after dose — desired level <30%
- Caution: nitrite-induced methemoglobinemia can worsen oxygen-carrying capacity in already hypoxic patients; not first-line if hydroxocobalamin is available
Supportive care
- Aggressive IV fluid resuscitation
- Bronchospasm: inhaled beta-2 agonists (albuterol), consider racemic epinephrine for stridor in children
- Seizures: benzodiazepines first-line
- Pulmonary edema: positive-pressure ventilation (CPAP/BiPAP or mechanical ventilation); diuretics generally not effective for noncardiogenic pulmonary edema
- Metabolic acidosis: treat with oxygen and supportive care; IV sodium bicarbonate if severe
- Cardiac arrest: standard ACLS protocols; prolonged resuscitation may be warranted (potentially reversible etiology)
- Hyperbaric oxygen therapy: has been used; no proven benefit; consider on a case-by-case basis for severe neurologic injury[8]
Things to avoid
- Do NOT give thiosulfate (the third component of the traditional cyanide antidote kit) — thiosulfate is the end product of endogenous H₂S detoxification and provides no benefit
- Do NOT rely on odor as a gauge of ongoing exposure — olfactory nerve fatigue renders it unreliable at dangerous concentrations
Disposition
- Asymptomatic patients with possible low-level exposure: observe for minimum 4-6 hours; if asymptomatic with normal labs and CXR, may discharge with return precautions for delayed pulmonary edema (up to 72 hours)[3]
- Any symptomatic patient or significant exposure: admit, likely to ICU
- Continuous cardiac and pulse oximetry monitoring
- Serial ABGs, lactate, CXR
- Watch for delayed pulmonary edema (may develop up to 72 hours after exposure)[3]
- "Knockdown" patients (even with apparent rapid recovery): admit for observation — high risk for persistent or delayed neurologic sequelae[2]
- Outpatient follow-up:
- Neuropsychiatric evaluation — cognitive impairment, amnesia, personality changes, and peripheral neuropathy may develop or persist weeks to months after exposure
- Pulmonary function testing if respiratory symptoms persist
- Ophthalmologic evaluation for corneal injury
- Toxicology consultation for all significant exposures
- Contact Poison control (1-800-222-1222 in the US) for all cases
See Also
- Cyanide poisoning
- Carbon monoxide poisoning
- Arsine gas exposure
- Aluminum phosphide poisoning
- Zinc phosphide poisoning
- Methemoglobinemia
External Links
- ATSDR — Hydrogen Sulfide Medical Management Guidelines
- StatPearls — Hydrogen Sulfide Toxicity
- NIOSH — Hydrogen Sulfide IDLH Documentation
- OSHA — Hydrogen Sulfide Hazards
References
- ↑ 1.0 1.1 1.2 1.3 Tintinalli et al.
- Hydrogen Sulfide.
- In: Tintinalli et al.
- Emergency Medicine A Comprehensive Study Guide.
- New York, NY: McGraw Hill. 2011. 1320.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 Hydrogen Sulfide Toxicity. StatPearls. 2024.
- PMID: 32119270
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Hydrogen Sulfide Medical Management Guidelines. Agency for Toxic Substances and Disease Registry (ATSDR). CDC.
- ↑ Chou S, et al. Hydrogen sulfide exposure in an adult male. Ann Saudi Med. 2010;30(1):76-80. doi:10.4103/0256-4947.59379
- ↑ 5.0 5.1 Haouzi P et al. High-dose hydroxocobalamin administered after H₂S exposure counteracts sulfide-poisoning-induced cardiac depression in sheep. Clin Toxicol (Phila). 2015;53(1):28-36.
- ↑ Jiang J et al. Hydrogen Sulfide — Mechanisms of Toxicity and Development of an Antidote. Sci Rep. 2016;6:20831.
- ↑ Brenner M et al. The vitamin B₁₂ analog cobinamide is an effective hydrogen sulfide antidote in a lethal rabbit model. Clin Toxicol (Phila). 2014;52(5):490-497.
- ↑ 8.0 8.1 Goldfrank et al. Hydrogen Sulfide Poisoning. In: Goldfrank et al. Goldfrank's Toxicologic Emergencies. New York, NY: McGraw Hill. 2002. 1504-1507.