Hydrogen sulfide poisoningMANAGEMENT

TOXICOLOGIC PRESENTATIONS · 12 SECTIONS

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604 items

☷ Legend

01Approach to the Critical Patient/attcp61

Scene safety and rescuer protection

›Hydrogen sulfide is a knockdown gas that incapacitates and kills rescuers who enter without air-supplied protection

›Do not permit entry to the exposure space without a self-contained breathing apparatus and a tended lifeline

›Confined-space and multi-victim scenes: assume a second collapsed person is a would-be rescuer, not an independent case

›Air-purifying cartridge respirators do not protect against hydrogen sulfide at incapacitating concentrations

›Olfactory paralysis occurs within minutes above roughly 100 to 150 ppm, so absence of a rotten-egg odour does not mean the air is safe

›Continuous atmospheric monitoring with a calibrated multi-gas meter; the gas is denser than air and pools in pits, tanks, sewers, and ship holds

›Remove the patient to fresh air before any assessment or treatment

›Every intervention that can be delayed is delayed until the patient is out of the hot zone

›Chemical-suicide presentation (acid plus a sulfur source in a car or small room): treat as a hazardous-materials scene, ventilate before entry, look for notes and containers

›Decontamination

›The gas does not persist on skin, but saturated clothing and hair can off-gas in an enclosed ambulance or resuscitation room

›Remove and bag clothing and ventilate the transport vehicle and the resuscitation bay

›Irrigate exposed eyes with isotonic crystalloid or sterile water en route

›Pre-notify the receiving facility of a possible toxic-gas exposure and possible multiple casualties so staff don protective equipment and open the decontamination area

Immediate priorities

›Treat as histotoxic cellular asphyxiation until proven otherwise

›The lethal mechanism is inhibition of mitochondrial cytochrome c oxidase, identical in effect to cyanide

›Expect a high lactate with a narrow arterial-to-venous oxygen difference and a normal or high venous oxygen saturation

›Apply high-flow oxygen immediately at the highest available fraction

›Non-rebreather mask at 15 l/min, or bag-valve-mask with reservoir if hypoventilating

›Oxygen accelerates endogenous sulfide oxidation and is the single most important intervention after removal from source

›Attach continuous cardiac monitoring, pulse oximetry, and waveform capnography, and obtain a 12-lead ECG

›Obtain point-of-care glucose, venous or arterial blood gas with lactate, and co-oximetry in every obtunded patient

›Identify the small subgroup who may benefit from the sodium nitrite antidote: severe poisoning (coma, seizure, haemodynamic instability, cardiac arrest) presenting within minutes of exposure

›Anticipate delayed non-cardiogenic pulmonary edema even when the initial chest examination and radiograph are normal

›Involve the regional poison centre early

Airway and ventilation control

›Indications for intubation

›Coma or inability to protect the airway

›Apnea or agonal respiration from brainstem depression

›Refractory hypoxaemia or progressive non-cardiogenic pulmonary edema

›Seizures not rapidly terminated

›Induction agent choice in the shock-prone poisoned patient

›Ketamine 1.5 mg/kg IV (range 1 to 2 mg/kg), which preserves respiratory drive and vascular tone

›Reduce to 0.5 to 1 mg/kg IV if peri-arrest or profoundly hypotensive

›Etomidate 0.3 mg/kg IV is an acceptable haemodynamically neutral alternative

›Avoid propofol for induction while hypotensive; if used for maintenance, start 5 mcg/kg/min and keep below 40 mcg/kg/min with vasopressor support

›Neuromuscular blockade

›Rocuronium 1.2 mg/kg IV is preferred when potassium is unknown or rhabdomyolysis is suspected after collapse or seizure

›Succinylcholine 1.5 mg/kg IV is acceptable within the first hour when there is no hyperkalaemia risk

›Post-intubation ventilation

›Lung-protective settings: tidal volume 6 ml/kg predicted body weight, plateau pressure below 30 cmH2O

›Titrate PEEP upward for non-cardiogenic pulmonary edema

›Target SpO2 94 to 98 percent once oxygenation permits and do not deliberately run hyperoxia after the first hour

›Chronic obstructive pulmonary disease or chronic hypercapnia: target SpO2 88 to 92 percent

›Pregnancy: keep SpO2 at or above 95 percent and PaO2 above 70 mmHg for fetal oxygen delivery

›Suspected co-existing carbon monoxide poisoning or smoke inhalation: keep FiO2 at 1.0 regardless of SpO2 until carboxyhaemoglobin is known

Antidote and refractory shock

›Sodium nitrite is the only specific antidote with a plausible early benefit

›Adult 300 mg IV (10 ml of a 3 percent / 30 mg/ml solution) over 5 to 10 minutes

›Slow or pause the infusion for systolic pressure below 90 mmHg

›Have norepinephrine drawn up first, because nitrite is a venodilator and will lower the blood pressure

›Paediatric 6 mg/kg IV (0.2 ml/kg of 3 percent solution), maximum 300 mg, adjusted down for anaemia

›Verify against current pediatric guideline before use

›Do not give a second dose empirically; sulfide is cleared within minutes and later dosing adds methaemoglobin without benefit

›Refractory hypotension

›Balanced crystalloid 10 to 20 ml/kg IV, reassessed with lung ultrasound to avoid worsening pulmonary edema

›Norepinephrine infusion starting 0.05 mcg/kg/min IV, titrated every 2 to 5 minutes to a mean arterial pressure of 65 mmHg

›Add vasopressin 0.03 units/min IV as a fixed-rate second agent

›Add epinephrine infusion 0.05 mcg/kg/min IV, titrated to 0.5 mcg/kg/min, if cardiac output remains low

›Cardiac arrest

›Standard advanced cardiac life support with high-quality compressions, 100 percent oxygen, and aggressive treatment of the metabolic acidosis

›Prolonged resuscitation is justified because sulfide is rapidly metabolised and good neurologic recovery is reported after long downtimes

›Early consideration of veno-arterial extracorporeal membrane oxygenation as a bridge where available

02History/hx46

Exposure characterisation

›Setting and source

›Confined space: sewer, manhole, sewage wet well, water or fuel tank, ship hold, mine, silo, pit

›Agricultural liquid-manure storage or agitation, which releases dissolved sulfide as a bolus

›Oil and gas ("sour" gas), petroleum refining, drilling-mud handling

›Pulp and paper, tanning, viscose rayon, asphalt, geothermal or volcanic areas

›Home sewer-gas intrusion through a dry drain trap

›Deliberate mixing of an acid with a sulfur-containing product (chemical suicide); look for containers and notes

›Exposure intensity and duration

›Time in the space and whether the patient collapsed (knockdown) or self-extricated

›Enclosed versus ventilated space, and whether others were affected

›Any atmospheric monitor reading or alarm at the scene

›Rotten-egg smell early then loss of smell suggests a rising, dangerous concentration

›Rescue and prehospital course

›Down time, bystander cardiopulmonary resuscitation, prehospital oxygen, airway interventions, naloxone given

›Response to removal from source, since rapid improvement is characteristic

›Co-exposures

›Combustion or fire (carbon monoxide and cyanide), other stored chemicals, simple asphyxiant gases

›Protective equipment worn and whether it was air-supplied

Symptom evolution and knockdown

›Central nervous system

›Sudden loss of consciousness at the scene, with or without rapid recovery

›Headache, dizziness, nausea, vomiting, confusion, unsteadiness

›Seizure

›Respiratory

›Cough, chest tightness, breathlessness, wheeze

›Breathlessness may begin hours after the exposure from delayed pulmonary edema

›Ocular and mucosal

03Physical Exam/exam44

Vital signs and general appearance

›Level of consciousness

›Document a Glasgow Coma Scale; a witnessed scene knockdown with recovery is still significant

›Agitation or confusion may precede or follow depressed consciousness

›Blood pressure and perfusion

›Hypotension and narrow pulse pressure in significant poisoning

›Cool, mottled skin and prolonged capillary refill

›Heart rate and rhythm

›Sinus tachycardia early; bradycardia and heart block are ominous

›Respiratory rate and pattern

›Count an actual rate: transient tachypnoea then hypoventilation or apnoea

›Adult normal 12 to 20 breaths per minute; chronic lung disease baseline may be 20 to 24

›Oxygen saturation

›May read normal despite lethal tissue hypoxia; a low value may reflect sulfhaemoglobin

›Do not use pulse oximetry to gauge severity or to withhold oxygen

›Temperature

›Usually normal; hyperthermia suggests seizure, sepsis, or an alternative diagnosis

›General inspection

›Rotten-egg odour on breath, clothing, or vomitus

›Greenish-grey skin and mucosal discolouration and blackened silver or copper jewellery are classic but insensitive

Respiratory and cardiovascular examination

›Airway and breathing

›Stridor or hoarseness from upper-airway irritation

›Crackles and frothy pink sputum of non-cardiogenic pulmonary edema, which may be absent initially and appear hours later

›Wheeze from reactive airway irritation

›Signs of aspiration after collapse

›Cardiovascular

›Ventricular ectopy and bradydysrhythmias on the monitor

04Differential Diagnosis/ddx27

Toxic gases and cellular asphyxiants

›Cyanide poisoning

›Same histotoxic picture: coma, seizures, shock, high lactate, narrow arterial-venous oxygen gap

›Consider with fire smoke, industrial nitriles, or ingestion; empiric hydroxocobalamin covers it

›Carbon monoxide poisoning

›Co-occurs in fires and poorly vented combustion; measure carboxyhaemoglobin

›Alters the risk-benefit of nitrite because methaemoglobin plus carboxyhaemoglobin critically lowers oxygen carriage

›Simple asphyxiants (methane, carbon dioxide, nitrogen, argon)

›Displace alveolar oxygen in a confined space; hypoxaemia without the histotoxic pattern and a lower lactate

›Irritant gases (ammonia, chlorine, nitrogen oxides, phosgene, sulfur dioxide)

›Airway injury and pulmonary edema predominate; abrupt central nervous system collapse is less typical

›Methaemoglobinaemia from another oxidant

›Cyanosis unresponsive to oxygen, chocolate-brown blood, saturation gap on co-oximetry

›Opioid or sedative-hypnotic overdose

›Respiratory depression and coma, miosis; response to naloxone 0.04 to 0.4 mg IV titrated to breathing

Non-toxicologic mimics of collapse and acidosis

›Primary cardiac event

›Acute myocardial infarction, malignant arrhythmia, or structural heart disease causing collapse

›Neurologic catastrophe

›Subarachnoid haemorrhage, ischaemic stroke, traumatic brain injury with focal signs or trauma history

›Seizure disorder or status epilepticus from another cause

›Metabolic and endocrine

›Hypoglycaemia, diabetic ketoacidosis, adrenal crisis

›Toxic-alcohol or salicylate poisoning with an osmolar gap, ketones, or a salicylate concentration

›Sepsis and septic shock

›Fever, identifiable source, slower onset, warm peripheries

›Environmental

›Heat stroke, hypothermia, or electrical injury in a collapsed worker

05Laboratory Tests/lt36

Blood gas, lactate, and acid-base

›Venous or arterial blood gas

›High-anion-gap metabolic acidosis is expected in significant poisoning

›Bicarbonate reported in mmol/l; follow the base deficit as a resuscitation marker

›Lactate

›Elevated and tracks severity; a level above 10 mmol/l after a gas exposure supports cellular asphyxiant toxicity (sulfide or cyanide)

›Serial lactate every 1 to 2 hours to gauge response

›Oxygen extraction pattern

›Central or mixed venous oxygen saturation is high or "arterialised" from failure of tissue oxygen use

›The arterial-to-venous oxygen content difference is narrow

›PaO2 pitfall

›The arterial oxygen tension is often normal even in lethal poisoning; do not use it to exclude the diagnosis or to withhold oxygen

›Repeat gases during and after sodium nitrite therapy to track methaemoglobin and acid-base

Metabolic panel and end-organ markers

›Electrolytes in mmol/l

›Potassium falls with bicarbonate therapy and rises with rhabdomyolysis or acidaemic shifts

›Replace magnesium and potassium before and during antiarrhythmic therapy

›Renal function and creatine kinase for rhabdomyolysis after collapse or seizure

›Glucose

›Check early and treat hypoglycaemia, which independently causes collapse and seizure

›Troponin for myocardial injury and stress cardiomyopathy

›Liver enzymes and coagulation studies if shocked

›Serum osmolality with a calculated osmolar gap if toxic-alcohol co-ingestion is possible

›Beta-hydroxybutyrate or urine ketones to separate diabetic ketoacidosis

›Pregnancy test in people of reproductive age

›Paracetamol (acetaminophen) and salicylate concentrations when the exposure may be intentional

Co-oximetry and exposure confirmation

›Co-oximetry rather than calculated saturation

06Diagnostic Tests/dt57

Scoring Systems

›No hydrogen-sulfide-specific severity score is validated

›Base severity on mental status, haemodynamics, lactate, and oxygenation

›Reassess frequently because early recovery and delayed deterioration both occur

›Glasgow Coma Scale

›Quantify and trend; any scene loss of consciousness warrants admission regardless of current score

›Poisoning Severity Score (IPCS and EAPCCT)

›Standardised grading for documentation and poison-centre communication

›Organ-dysfunction scores in the ICU

›SOFA to track multi-organ dysfunction; qSOFA is not a diagnostic tool here

›Berlin criteria

›Grade acute respiratory distress syndrome by PaO2/FiO2 once pulmonary edema develops

›Physiologic surrogates of response

›Lactate clearance and base-deficit trend

ECG and cardiac monitoring

›12-lead ECG on arrival, repeated at 1 to 2 hours and with any change

›Sinus tachycardia is usual; sinus bradycardia and atrioventricular block occur in severe poisoning

›Nonspecific ST-T changes are common

›Distinguishing stress cardiomyopathy from plaque rupture

›ST elevation or a regional wall-motion abnormality may reflect takotsubo cardiomyopathy after the toxic stress

›Default to the acute coronary syndrome pathway when ischaemic features are present and the diagnosis is not established

›QT interval surveillance

›Baseline QTc and repeat during any therapy that shifts potassium, such as sodium bicarbonate

›Watch for U waves and QT prolongation as potassium falls; keep potassium above 4.0 mmol/l and magnesium above 1.0 mmol/l

›Continuous telemetry for at least 24 hours after any loss of consciousness, dysrhythmia, hypoxia, or ischaemic change

›Non-contrast CT head

›Indicated for coma, seizure, focal deficit, suspected trauma, or failure to improve after removal from source

›Early CT is often normal; delayed CT may show bilateral globus pallidus and putaminal low attenuation and diffuse white-matter change, mirroring carbon monoxide injury

›CT chest or CT pulmonary angiogram

›When the presentation could be pulmonary embolism, or to characterise acute respiratory distress syndrome and exclude aspiration or pneumothorax

›CT cervical spine if the patient fell from height or the mechanism is unknown

›Contrast CT of the abdomen only for a specific indication such as trauma or mesenteric ischaemia after prolonged hypotension

MRI

›MRI brain is the test of choice for delayed neuropsychiatric sequelae and outperforms CT for basal ganglia and white-matter injury

›Typical findings: symmetric globus pallidus and putamen signal change, subcortical and periventricular white-matter hyperintensity, sometimes cerebellar and cortical involvement

›Diffusion-weighted imaging detects acute cytotoxic injury within days

›Indications

›Persistent or evolving cognitive, movement, or gait disorder after the acute phase

›Prognostic counselling for the patient and family

›Not required in the emergency department for a patient recovering to baseline; arrange through outpatient neurology

›Preferred to CT in pregnancy when neuroimaging is needed, avoiding gadolinium unless essential

Ultrasound

›Lung ultrasound

›Diffuse bilateral B-lines indicate pulmonary edema; a spared-area pattern with pleural-line abnormality favours acute respiratory distress syndrome over cardiogenic edema

›Repeat during the observation window to detect delayed edema

›Focused cardiac ultrasound

›Apical ballooning with a hyperdynamic base suggests stress cardiomyopathy

›A hyperdynamic underfilled ventricle suggests distributive or hypovolaemic shock

›Inferior vena cava calibre and collapsibility to guide cautious fluid therapy without provoking pulmonary edema

›Integrated (RUSH) scan in the peri-arrest or undifferentiated-shock patient to exclude tamponade, tension pneumothorax, and large pulmonary embolism

›Point-of-care ocular ultrasound is not used for chemical eye injury; use slit-lamp examination

Chest radiography and ocular imaging

›Portable chest radiograph

›On arrival for any respiratory symptom, hypoxia, or altered mental status, repeated at 6 hours and with deterioration

›Findings: bilateral alveolar and interstitial infiltrates without cardiomegaly or vascular redistribution

›A normal early film does not exclude delayed edema

›Repeat after intubation to confirm tube position and exclude aspiration or pneumothorax

›Slit-lamp examination with fluorescein for every patient with ocular symptoms

›Map epithelial defects, check for stromal haze and anterior-chamber reaction, and measure intraocular pressure

›Evert the lids and sweep the fornices for particulate matter

›Photograph or diagram corneal findings for follow-up comparison

›Formal visual acuity in each eye before discharge

07Disposition/dispo32

Observation and discharge

›Minimum observation before discharge

›Asymptomatic or only mild eye or throat irritation, with normal vital signs and mental status: observe at least 6 hours from the end of exposure

›Normal lung examination, room-air SpO2 at the patient's baseline, and a normal repeat chest radiograph

›Normal or near-normal lactate with no persistent metabolic acidosis

›Safe for discharge only when all of the above hold and the patient has a reliable adult at home and a means to return

›Provide written return precautions emphasising that pulmonary edema can appear up to 72 hours after exposure

›Arrange occupational-medicine or primary-care follow-up within 24 to 48 hours, and ophthalmology within 24 to 48 hours for any corneal defect

›Do not discharge a worker back to the same environment until the source is controlled and monitoring confirms a safe atmosphere

›Any intentional exposure: psychiatric evaluation and clearance before discharge; most such patients are admitted

Admission and ICU criteria

›Admit to a monitored bed

›Any loss of consciousness or seizure at the scene, even if now normal, for delayed pulmonary edema and neurologic sequelae

›Any respiratory symptom, hypoxia, abnormal chest radiograph, or chest pain

›Persistent metabolic acidosis or lactate above 2 mmol/l

›Syncope, dysrhythmia, or ECG ischaemia

›Admit to the ICU

›Intubation, non-cardiogenic pulmonary edema, or an escalating oxygen requirement

›Shock or any vasopressor requirement

›Coma, status epilepticus, or post-cardiac-arrest care

›pH below 7.2, or receiving sodium nitrite with haemodynamic instability

›Telemetry for at least 24 hours for every admitted patient

Transfer and consultation

›Consult the regional poison centre for every case

›Transfer after stabilisation to a centre with hyperbaric oxygen, medical toxicology, and extracorporeal life support when

›Coma or persistent neurologic deficit, or cardiovascular instability, that might benefit from hyperbaric oxygen

›Concomitant carbon monoxide poisoning meeting hyperbaric criteria

›Refractory cardiogenic shock or arrest that is an extracorporeal membrane oxygenation candidate

08Treatment/t142

Oxygen and airway management

›High-flow oxygen for every symptomatic patient

›100 percent by non-rebreather at 15 l/min, continued until asymptomatic with a normal lactate

›Oxygen speeds endogenous sulfide oxidation and is the primary treatment

›Do not wait for a measured fall in SpO2; pulse oximetry is unreliable in this poisoning

›Support ventilation

›Bag-valve-mask with an oxygen reservoir for hypoventilation or apnea

›Intubate for coma, apnea, refractory hypoxaemia, progressive pulmonary edema, or uncontrolled seizures

›Lung-protective ventilation

›Tidal volume 6 ml/kg predicted body weight, plateau pressure below 30 cmH2O

›Titrate PEEP upward for oxygenation in permeability pulmonary edema

›Oxygen targets once stable

›SpO2 94 to 98 percent for most patients

›SpO2 88 to 92 percent in chronic hypercapnic respiratory disease

›SpO2 at or above 95 percent, PaO2 above 70 mmHg, in pregnancy

›Maintain FiO2 1.0 until carboxyhaemoglobin is known when carbon monoxide co-exposure is possible

›Wean FiO2 once the acidosis clears to limit hyperoxic lung injury

Sodium nitrite antidote

›Indication

›Severe poisoning (coma, seizure, haemodynamic instability, cardiac arrest) presenting within minutes of exposure

›Benefit is unproven in humans and biologically implausible once the patient has been away from source for more than a few minutes, but it is reasonable in early severe poisoning

›Do not give for isolated mucosal irritation, mild headache, or a fully recovered brief knockdown

›Adult dose

›Sodium nitrite 300 mg IV (10 ml of 3 percent / 30 mg/ml solution) over 5 to 10 minutes

›Continuous blood-pressure monitoring; slow or hold for systolic below 90 mmHg

›Start norepinephrine before or alongside the infusion because nitrite causes venodilation and hypotension

›Target methaemoglobin below 30 percent; check co-oximetry at 30 minutes and 2 hours

›Do not repeat empirically

›Amyl nitrite as a bridge only

›Crush a 0.3 ml pearl into gauze held at the mouth or endotracheal tube, inhaled 15 to 30 seconds each minute until intravenous access

›Paediatric dose

›Sodium nitrite 6 mg/kg IV (0.2 ml/kg of 3 percent solution), maximum 300 mg, reduced for anaemia and dosed to measured haemoglobin

›Verify against current pediatric guideline before use

›Continuous blood-pressure and methaemoglobin monitoring; small children and anaemic patients tolerate excess methaemoglobin poorly

›Contraindications and cautions

›Concomitant carbon monoxide poisoning or significant smoke inhalation: added methaemoglobin plus carboxyhaemoglobin critically lowers oxygen carriage, so generally withhold unless exchange transfusion is available

›Pre-existing anaemia, methaemoglobinaemia, or haemodynamic instability

›Concurrent phosphodiesterase-5 inhibitor use, which causes severe hypotension

›Excess methaemoglobinaemia with clinical compromise

›Supportive care and exchange transfusion are preferred

›Methylene blue 1 mg/kg IV only as a last resort, because it can re-liberate bound sulfide

Hemodynamic support and dysrhythmia

›Fluid resuscitation

›Balanced crystalloid 10 to 20 ml/kg IV for hypotension, reassessed after each bolus with lung and inferior vena cava ultrasound

›Stop boluses and switch to vasopressors when B-lines increase or the ventricle is full

›Vasopressors and inotropes

›Norepinephrine first line, start 0.05 mcg/kg/min IV, titrate every 2 to 5 minutes to mean arterial pressure 65 mmHg

›Target 65 mmHg for most patients; individualise upward in longstanding hypertension

›Add vasopressin 0.03 units/min IV as a fixed-rate second agent

›Add epinephrine 0.05 mcg/kg/min IV, titrated to 0.5 mcg/kg/min, if cardiac output stays low

›Dobutamine 2.5 to 10 mcg/kg/min IV for cardiogenic shock from stress cardiomyopathy, with an arterial line

›Dysrhythmia management

›Correct acidosis, hypoxia, hypokalaemia, and hypomagnesaemia first

›Ventricular tachycardia or fibrillation: standard advanced cardiac life support; amiodarone 300 mg IV push in arrest, or 150 mg IV over 10 minutes with a pulse

›Torsades de pointes: magnesium sulfate 2 g IV over 15 minutes, keep potassium above 4.0 mmol/l and magnesium above 1.0 mmol/l

›Bradycardia with hypoperfusion: atropine 0.5 mg IV every 3 to 5 minutes to a maximum of 3 mg, then transcutaneous pacing and an adrenergic infusion

›Therapy-is-not-working troubleshooting

›Re-check that the patient is fully removed from source and that off-gassing clothing is not exposing the team

›Reconsider co-exposure to carbon monoxide, cyanide, or a simple asphyxiant, and occult trauma from the collapse

›Look for tension pneumothorax after positive-pressure ventilation, pericardial effusion, and unrecognised haemorrhage

›Confirm the sodium nitrite did not cause the deterioration through hypotension or methaemoglobinaemia

›Escalate to a hyperbaric oxygen or extracorporeal membrane oxygenation discussion

Hyperbaric oxygen and extracorporeal support

›Hyperbaric oxygen rationale and evidence

›Proposed to enhance sulfide oxidation, deliver haemoglobin-independent oxygen, and limit delayed basal ganglia and white-matter injury

›Evidence is limited to case reports; there is no randomised trial

›Reasonable indications after stabilisation and discussion with toxicology and the hyperbaric service

›Coma or depressed mental status not clearing with normobaric oxygen

›Persistent or evolving focal neurologic or cardiovascular dysfunction

›Concomitant carbon monoxide poisoning meeting its own hyperbaric criteria

›Practical points

›Schedules mirror carbon monoxide protocols (for example 2.5 to 3.0 atmospheres absolute); the hyperbaric physician sets the profile

›Risks include decompensation in a monoplace chamber, barotrauma, oxygen-toxicity seizures, and the hazard of moving an unstable patient

›Veno-arterial extracorporeal membrane oxygenation

›Consider as a bridge for refractory cardiogenic shock or refractory arrest with a witnessed brief downtime

›Rational because sulfide is metabolised within minutes, so short-term mechanical support can outlast the toxidrome

›Good neurologic recovery is reported after prolonged resuscitation supported by extracorporeal circulation

›Intra-aortic balloon pump has no specific role and does not address the cellular oxygen-utilisation defect

Non-cardiogenic pulmonary edema and bronchospasm

›Anticipation and monitoring

›Expect delayed onset 24 to 72 hours after exposure; repeat imaging and lung ultrasound through the observation window

›Escalating oxygen requirement is the earliest sign

›Oxygenation support

›Supplemental oxygen, then continuous positive airway pressure 5 to 10 cmH2O for hypoxaemia with an adequate mental status and no vomiting

›Intubation with lung-protective ventilation and PEEP titration for progressive hypoxaemia or fatigue

›What not to do

›Diuretics are not indicated; this is permeability edema, not volume overload

›Furosemide 20 to 40 mg IV only if there is coexisting cardiogenic congestion

›Routine corticosteroids are not supported for the chemical lung injury

›Bronchospasm

›Salbutamol (albuterol) 2.5 to 5 mg nebulised every 20 minutes as needed, then every 2 to 4 hours

›Ipratropium bromide 0.5 mg nebulised every 20 minutes for up to 3 doses

›Established acute respiratory distress syndrome

›Low tidal volume, conservative fluid strategy after resuscitation, prone positioning for PaO2/FiO2 below 150 mmHg

›Antibiotics only for a specific superimposed infection, not for the chemical pneumonitis

Seizures and post-arrest neuroprotection

›First-line benzodiazepine

›Lorazepam 4 mg IV, repeated once at 5 minutes

›Midazolam 10 mg IM (0.2 mg/kg, maximum 10 mg) when there is no intravenous access

›Paediatric: lorazepam 0.1 mg/kg IV (maximum 4 mg per dose) or midazolam 0.2 mg/kg IM (maximum 10 mg)

›Verify against current pediatric guideline before use

›Second-line agent if seizures persist

›Levetiracetam 60 mg/kg IV (maximum 4500 mg), or another guideline agent such as fosphenytoin or valproate

›Refractory status epilepticus

›Rapid-sequence intubation and a continuous infusion (midazolam or propofol with vasopressor cover) and continuous EEG

›Correct hypoglycaemia, hyponatraemia, hypocalcaemia, and hypomagnesaemia as contributors

›Post-cardiac-arrest care

›Targeted temperature management with a constant target between 32 and 37.5 degrees Celsius and active fever prevention, per current resuscitation guidance

›Maintain mean arterial pressure at or above 65 mmHg, SpO2 94 to 98 percent, and normocapnia

›Defer neuroprognostication at least 72 hours off sedation and use multimodal assessment

›Counsel that delayed extrapyramidal and cognitive syndromes can appear days to weeks later and need neurology referral

Ocular decontamination and corneal injury

›Immediate irrigation

›Copious isotonic crystalloid or sterile water for at least 15 to 30 minutes

›Check conjunctival pH and continue irrigation until it is neutral (7.0 to 7.4)

›Examination aids

›Topical proparacaine 0.5 percent, 1 to 2 drops, to permit examination and irrigation; never dispense for home use

›Slit-lamp examination with fluorescein; evert the lids and sweep the fornices

›Epithelial defect management

›Preservative-free lubricants every 1 to 2 hours

›Topical antibiotic: erythromycin 0.5 percent ointment four times daily, or a fluoroquinolone drop four times daily for contact-lens wearers

›Cyclopentolate 1 percent, 1 drop three times daily, for photophobia and ciliary spasm

›Oral analgesia; do not patch a contact-lens wearer or an infected-appearing eye

›Urgent ophthalmology referral for stromal haze, a large epithelial defect, limbal ischaemia, or raised intraocular pressure

›Recheck within 24 hours because alkaline-sulfide corneal injury can progress

Adjuncts, therapies to avoid, and interventions to modify

›Sodium bicarbonate

›Reserve for pH below 7.1 with haemodynamic compromise: 1 mmol/kg IV bolus, then reassess the gas

›Expect potassium and ionised calcium to fall and the QT to lengthen; replace potassium to keep it above 4.0 mmol/l

›It does not treat the toxidrome; oxygenation and perfusion do

›Sodium thiosulfate

›Adult 12.5 g IV is low-risk and may be given when cyanide cannot be excluded

›Limited rationale in pure sulfide poisoning because rhodanese is not the main clearance pathway

›Hydroxocobalamin

›5 g IV over 15 minutes is reasonable empirically when the toxic gas is unknown or cyanide co-exposure is likely, such as in a fire

›Not a proven sulfide antidote; it turns skin, urine, and many laboratory specimens red and can interfere with co-oximetry

›Methylene blue

›1 mg/kg IV is generally avoided because reversing the therapeutic methaemoglobinaemia can re-release bound sulfide

›Use only for life-threatening methaemoglobinaemia when exchange transfusion is unavailable

›Iatrogenic-harm checklist for routine emergency interventions

›Oxygen: always indicated; the only caveat is to wean from 100 percent once the acidosis resolves

›Intubation and sedation: use ketamine or etomidate; avoid propofol boluses while hypotensive; avoid succinylcholine if rhabdomyolysis or hyperkalaemia is suspected after collapse

›Fluid loading: give for hypotension but titrate to perfusion with ultrasound, since over-resuscitation worsens permeability pulmonary edema

›Vasopressors: needed early because the nitrite antidote causes vasodilation; norepinephrine first line

›Sodium nitrite: the main iatrogenic hazard through hypotension and methaemoglobinaemia; withhold with significant concurrent carbon monoxide poisoning or anaemia

›Anticoagulation and fibrinolysis: not indicated for the poisoning; the lactic acidosis and shock mimic pulmonary embolism and myocardial infarction, so reserve these for an independently confirmed diagnosis

›Analgesia: topical ocular anaesthetic for examination only; titrate systemic opioids carefully when mental status or respiratory drive is already depressed

›Mechanical circulatory support: veno-arterial extracorporeal membrane oxygenation is the appropriate rescue; intra-aortic balloon pump has no role

›Diuretics: not indicated for permeability edema

›Methylene blue: can worsen poisoning by liberating sulfide

09Special Populations/sp51

Pregnancy

›The fetus tolerates maternal hypoxia poorly, so aggressive maternal resuscitation is the best fetal therapy

›Positioning and oxygen

›Left lateral uterine displacement after about 20 weeks

›High-flow oxygen, keeping maternal SpO2 at or above 95 percent and PaO2 above 70 mmHg

›Fetal monitoring

›Continuous fetal heart-rate monitoring once the fetus is viable (from about 23 to 24 weeks) and the mother is stable

›Involve obstetrics early

›Sodium nitrite in pregnancy

›Limited human data; methaemoglobinaemia reduces oxygen delivery to the fetus and fetal haemoglobin is more susceptible to oxidation

›Reserve for life-threatening maternal poisoning where maternal benefit clearly outweighs fetal risk

›Same dose, 300 mg IV over 5 to 10 minutes, with close methaemoglobin monitoring and a target below 20 percent

›Hyperbaric oxygen is considered acceptable in pregnancy when indicated, drawing on carbon monoxide experience, and does not by itself harm the fetus

›Imaging: prefer ultrasound and non-contrast MRI; shield for an unavoidable CT and do not withhold a necessary head CT

›After viability, prepare for perimortem caesarean delivery within 4 minutes if the mother arrests and does not respond

›Acetaminophen 1000 mg by mouth every 6 hours as needed (maximum 3000 mg in 24 hours) is the preferred analgesic; avoid NSAIDs after 20 weeks

Geriatric

›Reduced cardiopulmonary reserve

›Hypoxia, hypotension, and methaemoglobinaemia are tolerated poorly; lower the threshold for admission and ICU care

›Confounded neurologic assessment

›Baseline cognitive impairment obscures the examination; obtain a collateral baseline and image sooner for persistent confusion

›Polypharmacy interactions

›Nitrates, antihypertensives, and phosphodiesterase-5 inhibitors amplify sodium-nitrite hypotension

›Dapsone, sulfonamides, nitrates, and topical anaesthetics add to the methaemoglobin burden

›Beta-blockers blunt the tachycardic response to shock and may worsen bradycardia

›Higher risk of aspiration during knockdown and of rib fracture and occult injury from the collapse

›Renal impairment affects clearance of co-administered drugs and tolerance of the acid load; dose-adjust and monitor

›Establish goals of care early when the poisoning is severe and pre-existing frailty is significant

10Background/b43

Epidemiology

›Hydrogen sulfide is the second most common cause of fatal toxic-gas inhalation in the workplace after carbon monoxide

›Approximately 8 to 15 occupational fatalities per year are recorded in the United States (Bureau of Labor Statistics Census of Fatal Occupational Injuries), with several times that number of hospitalised exposures

›Roughly a quarter of fatal incidents involve more than one victim, most often a co-worker or family member who collapses attempting a rescue

›Highest-risk industries

›Oil and gas extraction and "sour" gas operations

›Wastewater and sewage systems

›Agriculture, especially liquid-manure storage and agitation

›Pulp and paper, tanning, viscose rayon manufacture, mining, and geothermal work

›Non-occupational exposure

›Sewer gas in homes, decaying organic matter, volcanic and geothermal areas

›Intentional chemical-suicide mixtures of an acid with a sulfur-containing product

›A Japanese outbreak of chemical-suicide by hydrogen sulfide caused more than 1000 deaths in 2008, after which the method was reported in North America and Europe

›Case fatality among workers who suffer a knockdown is historically about 2 to 6 percent and is higher when collapse occurs deep in a confined space with delayed rescue

›Persistent neuropsychiatric sequelae are reported in a substantial minority of survivors of severe poisoning, including memory and concentration deficits, mood change, and movement disorders

Pathophysiology

›Physical properties

›Colourless gas, denser than air, soluble in water and lipid, with a rotten-egg odour only at low concentrations

›Also an endogenous gasotransmitter made by cystathionine beta-synthase, cystathionine gamma-lyase, and 3-mercaptopyruvate sulfurtransferase

›Primary toxic action

›Reversible binding to the ferric iron of mitochondrial cytochrome c oxidase (complex IV) halts oxidative phosphorylation, so cells cannot use delivered oxygen

›The result is anaerobic metabolism, a widening lactic acidosis, and failure first of the brain and myocardium

›Venous blood stays oxygenated and the arterial-to-venous oxygen difference narrows, the same picture as cyanide

›Additional actions

›Inhibition of carbonic anhydrase, monoamine oxidase, and Na/K-ATPase, and interaction with NMDA and GABA-A receptors, contributing to rapid central nervous system depression and seizures

›Brief carotid-body-mediated hyperpnoea then apnoea, with direct brainstem respiratory-centre depression producing the knockdown

›Mucosal and pulmonary injury

›Contact forms alkaline sulfides that cause liquefactive injury to the conjunctiva ("gas eye"), airway, and alveoli

›The result is tracheobronchitis and permeability pulmonary edema that may be delayed 24 to 72 hours

›Endogenous detoxification is rapid

›Mitochondrial sulfide:quinone oxidoreductase oxidises sulfide to thiosulfate and sulfate; methaemoglobin and oxidised glutathione also scavenge it

›This explains rapid recovery after early rescue and the vanishing target for a late antidote

›Delayed neurologic injury

›Symmetric basal ganglia (globus pallidus, putamen) and subcortical white-matter lesions from combined direct neurotoxicity and hypoxic-ischaemic injury, analogous to carbon monoxide

Therapeutic Considerations

›Removal from source plus 100 percent oxygen is the mainstay; at the biochemical level the poisoning is self-limited when oxygen delivery and perfusion are maintained

›Sodium nitrite mechanism and limits

›It induces methaemoglobin, which competes with cytochrome oxidase for sulfide to form sulfmethaemoglobin

›Animal models show benefit only when it is given within minutes of exposure

›Human evidence is limited to case reports, and benefit is implausible once the patient has been away from source for more than a few minutes

›It is still offered in early severe poisoning because hypotension and methaemoglobinaemia are manageable and the ceiling of alternatives is low

›Sodium thiosulfate, central to cyanide treatment through rhodanese, has little rationale here because rhodanese is not the main sulfide clearance pathway; it is low-risk and is given when cyanide cannot be excluded

›Hydroxocobalamin binds sulfide in vitro and is used empirically for an unknown asphyxiant gas or a likely cyanide co-exposure; it is not an established sulfide antidote

›Hyperbaric oxygen is proposed to accelerate sulfide oxidation, supply haemoglobin-independent oxygen, and limit delayed central nervous system injury, but is supported only by case reports

›Methylene blue is avoided because reversing the therapeutic methaemoglobinaemia can re-liberate bound sulfide

›Odour is not a severity gauge: olfactory fatigue and paralysis above roughly 100 to 150 ppm mean the most dangerous atmospheres are the least odorous, so exposure must be judged by monitoring and circumstances

11Patient Discharge Instructions/pdi31

copy discharge instructions

›Why you were seen

›You were exposed to hydrogen sulfide, a poisonous "rotten egg" gas found in sewers, manure pits, oil and gas work, and from mixing certain chemicals

›It can irritate the eyes and lungs and, at higher levels, cause sudden collapse

›Return to the emergency department immediately or call 911 if you develop

›Shortness of breath, cough, chest tightness, wheezing, or coughing up frothy or pink spit; lung swelling from this gas can start up to 3 days (72 hours) after the exposure

›Trouble breathing when lying flat, or waking from sleep short of breath

›Fainting, chest pain, a pounding heartbeat, or a fast or irregular pulse

›Confusion, a severe headache that does not ease with acetaminophen, trouble speaking or walking, weakness, or numbness

›A seizure

›Caring for your eyes

›If your eyes were affected, use the lubricating and antibiotic drops exactly as prescribed

›Do not wear contact lenses until an eye doctor says it is safe

›Return within 24 hours, or sooner, for worsening eye pain, light sensitivity, blurred vision, a gritty "something in my eye" feeling, or eye discharge

›Do not use numbing eye drops at home; they slow healing and can hide worsening injury

›Delayed brain and nerve effects

›Some people develop memory or concentration problems, mood changes, tremor, or difficulty walking days to weeks later

›If this happens, contact your doctor and ask for a referral to a neurologist

›Medicines

›For headache or eye discomfort you may take acetaminophen 1000 mg by mouth every 6 hours as needed, and no more than 3000 mg in 24 hours; take less or none if you have liver disease or drink alcohol daily

›Avoid ibuprofen and other anti-inflammatory painkillers if you are pregnant or have kidney disease unless your doctor approves

›Activity

›If you lost consciousness, felt dizzy, or had a seizure, do not drive or operate machinery for at least 24 hours and until your doctor clears you

›Rest today; you may return to normal activity as you feel able if you have no breathing or heart symptoms

›Follow-up

›See your family doctor or an occupational-medicine clinic within 1 to 2 days

›See an eye doctor within 24 to 48 hours if you had any eye injury

›Preventing another exposure

12References/r34

Toxicology references and guidelines

›ATSDR hydrogen sulfide guidance

›Agency for Toxic Substances and Disease Registry. Medical Management Guidelines for Hydrogen Sulfide; and Toxicological Profile for Hydrogen Sulfide and Carbonyl Sulfide, 2016 update

›NIOSH Pocket Guide

›National Institute for Occupational Safety and Health. Pocket Guide to Chemical Hazards, Hydrogen sulfide entry; Immediately Dangerous to Life or Health value 100 ppm

›OSHA hydrogen sulfide standard

›Occupational Safety and Health Administration. Hydrogen Sulfide Fact Sheet and permissible exposure limits

›Goldfrank's Toxicologic Emergencies

›Nelson LS, Howland MA, Lewin NA, et al., editors. Goldfrank's Toxicologic Emergencies, 11th edition, 2019; chapter on hydrogen sulfide and sulfur compounds

›Reiffenstein review

›Reiffenstein RJ, Hulbert WC, Roth SH. Toxicology of hydrogen sulfide. Annual Review of Pharmacology and Toxicology, 1992

›Guidotti review

›Guidotti TL. Hydrogen sulfide intoxication. Handbook of Clinical Neurology, volume 131, 2015

Antidote and hyperbaric evidence

›Methaemoglobin and sulfide binding

›Smith L, Kruszyna H, Smith RP. The effect of methemoglobin on the inhibition of cytochrome c oxidase by cyanide, sulfide or azide. Biochemical Pharmacology, 1977

›Sodium nitrite antidotal role

›Hall AH, Rumack BH. Hydrogen sulfide poisoning: an antidotal role for sodium nitrite? Veterinary and Human Toxicology, 1997

›Hyperbaric oxygen case report (1985)

›Smilkstein MJ, Bronstein AC, Pickett HM, Rumack BH. Hyperbaric oxygen therapy for severe hydrogen sulfide poisoning. Journal of Emergency Medicine, 1985

›Liquid-manure hydrogen sulfide toxicity

›Belley R, Bernard N, Côté M, et al. Hyperbaric oxygen therapy in the management of two cases of hydrogen sulfide toxicity from liquid manure. Canadian Journal of Emergency Medicine, 2005

›Hyperbaric oxygen with induced hypothermia

›Asif MJ, Exline MC. Utilization of hyperbaric oxygen therapy and induced hypothermia after hydrogen sulfide exposure. Respiratory Care, 2012

›Extracorporeal support in poisoning

›Extracorporeal Life Support Organization guidance and published case reports of veno-arterial extracorporeal membrane oxygenation for poison-induced refractory cardiovascular collapse

Critical care and airway references

›Low-tidal-volume ventilation

Evidence & Review

Reviewed by SymptomDx Medical Team · Last reviewed September 13, 2026

SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.