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Ostermayer: Created page with "Toxic inhalation injury encompasses pulmonary and systemic damage from inhaling noxious gases, fumes, vapors, or smoke. It is the '''leading cause of death in fire-related injuries''' and accounts for over 125,000 ED visits annually from chemical inhalation alone in the United States.Boggust D. Diagnostics and therapeutics: inhalation injuries. ''Taming the SRU''. March 2025. The '''water solubility of the inhaled agent''' is the single most importa..."

2026-03-11T15:43:02Z

Created page with "Toxic inhalation injury encompasses pulmonary and systemic damage from inhaling noxious gases, fumes, vapors, or smoke. It is the '''leading cause of death in fire-related injuries''' and accounts for over 125,000 ED visits annually from chemical inhalation alone in the United States.<ref name="SRU">Boggust D. Diagnostics and therapeutics: inhalation injuries. ''Taming the SRU''. March 2025.</ref> The '''water solubility of the inhaled agent''' is the single most importa..."

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Toxic inhalation injury encompasses pulmonary and systemic damage from inhaling noxious gases, fumes, vapors, or smoke. It is the '''leading cause of death in fire-related injuries''' and accounts for over 125,000 ED visits annually from chemical inhalation alone in the United States.<ref name="SRU">Boggust D. Diagnostics and therapeutics: inhalation injuries. ''Taming the SRU''. March 2025.</ref> The '''water solubility of the inhaled agent''' is the single most important determinant of injury location and symptom timing — a concept critical for ED disposition decisions.<ref name="PMCAcute">Gorguner M, Akgun M. Acute inhalation injury. ''Eurasian J Med''. 2010;42(1):28-35.</ref> '''Delayed pulmonary edema''' occurring hours after exposure in an initially asymptomatic patient is the most dangerous pitfall.

==Background==
*'''Three zones of injury:'''<ref name="Medscape">Smoke Inhalation Injury. ''Medscape/eMedicine''. Updated 2024.</ref>
**'''Supraglottic (thermal/upper airway):''' Direct heat injury; steam carries 4000× the heat capacity of dry air; causes edema, erythema, and mucosal sloughing → progressive airway obstruction over 12–24 hours
**'''Tracheobronchial (chemical/lower airway):''' Chemical irritation from inhaled toxins → epithelial damage, bronchospasm, mucosal sloughing, cast formation, impaired mucociliary clearance
**'''Alveolar/parenchymal (systemic/gas exchange):''' Damage to alveolar-capillary membrane → noncardiogenic pulmonary edema, V/Q mismatch, [[ARDS]]; also systemic asphyxiant effects (CO, HCN)
*'''The water solubility principle''' — the most important clinical concept:<ref name="PMCAcute"/>

{| class="wikitable"
|-
! Solubility !! Injury Location !! Symptom Onset !! Key Agents !! Clinical Implication
|-
| '''High''' || Upper airway (nose, pharynx, larynx) || '''Immediate''' (seconds to minutes) — early warning drives patient to escape || Ammonia, hydrogen chloride, sulfur dioxide, hydrogen fluoride, acrolein || Upper airway obstruction; if asymptomatic after 6h observation → low risk of delayed injury
|-
| '''Intermediate''' || Upper AND lower airways || '''Minutes to hours''' — partial early warning || '''Chlorine''', isocyanates || Both upper airway symptoms AND potential for delayed lower airway injury/pulmonary edema
|-
| '''Low''' || Distal airways and alveoli || '''DELAYED''' (hours to 48h+) — '''little or no early warning''' || '''Phosgene''', nitrogen dioxide (NOx), ozone || '''The most dangerous group''' — patient may be asymptomatic at presentation then develop fulminant pulmonary edema hours later; requires prolonged observation
|}

*'''Smoke inhalation''' is a '''mixed exposure''' — contains thermal injury + highly soluble irritants (HCl, SO₂, acrolein, ammonia) + systemic asphyxiants ([[carbon monoxide]], [[hydrogen cyanide]])<ref name="EMPract">Otterness K, et al. Emergency department management of smoke inhalation injury in adults. ''Emerg Med Pract''. 2018;20(3):1-24.</ref>
*Burning plastics, rubber, and synthetic materials produce phosgene, HCN, isocyanates, and acrolein — far more toxic than burning wood alone<ref name="SRU"/>
*'''Household chemical mixtures:''' Bleach (hypochlorite) + ammonia → chloramine gas; bleach + acid → chlorine gas — common accidental exposures<ref name="PMCAcute"/>
*'''Key specific agents:'''
**'''Phosgene (COCl₂):''' Odor of freshly mown hay; used in chemical synthesis (isocyanates, pesticides); produced when chlorinated hydrocarbons are heated/welded; WW1 chemical weapon (80% of chemical warfare deaths); '''latent period 30 min to 48 hours''' before fulminant pulmonary edema; no antidote<ref name="ATSDR">Phosgene: Medical Management Guidelines. Agency for Toxic Substances and Disease Registry (ATSDR).</ref>
**'''Nitrogen dioxide (NO₂):''' Silo filler's disease (silage generates NOx in first 10 days); also welding, electroplating, ice resurfacing (Zamboni) machines; '''triphasic illness''' — (1) initial mild irritation, (2) delayed chemical pneumonitis/pulmonary edema at 24–72h, (3) [[bronchiolitis obliterans]] at 2–6 weeks<ref name="NO2">Nitrogen Dioxide Toxicity. ''StatPearls''. NCBI Bookshelf. Updated July 2023.</ref>
**'''Chlorine (Cl₂):''' Pool chemicals, water treatment, industrial; intermediate solubility → both upper and lower airway injury; noncardiogenic pulmonary edema in severe exposures<ref name="PMCAcute"/>
**'''Ammonia (NH₃):''' Highly soluble → immediate upper airway burns; forms ammonium hydroxide (alkali) on mucous membranes → liquefactive necrosis; massive exposure can cause laryngospasm and pulmonary edema<ref name="Ammonia">Ammonia: Emergency Department/Hospital Management. CHEMM/HHS.</ref>
**'''Hydrogen sulfide (H₂S):''' "Knockdown gas"; rotten egg odor (olfactory fatigue at high concentrations — cannot smell it); mitochondrial toxin (inhibits cytochrome oxidase like cyanide); may cause sudden collapse and death<ref name="PMCAcute"/>
*'''Metal fume fever:''' Zinc oxide fume inhalation (welding galvanized steel); self-limited flu-like illness 4–12 hours after exposure; not true toxic injury but frequently presents to ED<ref name="Medscape"/>
*'''Reactive airways dysfunction syndrome (RADS):''' New-onset persistent asthma-like syndrome following single high-dose irritant inhalation exposure; may be permanent<ref name="PMCAcute"/>
*'''Long-term sequelae:''' [[Bronchiolitis obliterans]], bronchiectasis, RADS, pulmonary fibrosis, tracheal/bronchial stenosis<ref name="PMCAcute"/>

==Clinical Features==
'''Upper airway (thermal/highly soluble agents):'''
*Facial burns, singed eyebrows/nasal hairs, soot in nares or oropharynx
*Hoarseness, stridor, dysphonia
*Oropharyngeal erythema, edema, blistering
*Drooling, dysphagia
*'''Airway obstruction may be progressive''' — can worsen dramatically over 12–24 hours as edema develops; a patient with mild hoarseness on arrival may have complete obstruction hours later<ref name="OAEM">Tanizaki S. Assessing inhalation injury in the emergency room. ''Open Access Emerg Med''. 2015;7:31-37.</ref>

'''Lower airway (chemical irritants):'''
*Cough (initially dry, may become productive with soot-stained or blood-tinged sputum)
*Bronchospasm/wheezing
*Dyspnea, tachypnea
*Chest tightness
*Hypoxemia

'''Alveolar/parenchymal:'''
*Progressive hypoxemia
*Noncardiogenic pulmonary edema (frothy sputum, bilateral crackles)
*[[ARDS]]
*'''May be DELAYED hours to days''' — particularly with phosgene and nitrogen dioxide<ref name="ATSDR"/>

'''Systemic asphyxiant effects (smoke inhalation):'''
*'''[[Carbon monoxide poisoning]]:''' Headache, confusion, nausea, cherry-red skin (unreliable), syncope, [[seizures]], coma, cardiac ischemia; CO-oximetry required (standard pulse oximetry is falsely normal)
*'''[[Cyanide toxicity]]:''' Altered mental status, lactic acidosis, cardiovascular collapse; suspect in all enclosed-space fire victims with persistent lactic acidosis despite O₂ therapy

'''Other:'''
*Conjunctival irritation, chemical keratitis (especially ammonia, chlorine, H₂S)
*Dermal burns (ammonia, HF, phosgene in liquid form)
*GI symptoms: nausea, vomiting (especially H₂S, metal fume fever)
*'''Hydrogen sulfide:''' Sudden loss of consciousness ("knockdown"), seizures, apnea, cardiac arrest — may be the presenting event with no preceding symptoms at high concentrations

==Differential Diagnosis==
*[[Anaphylaxis]] (bronchospasm, hypotension without inhalation history)
*[[Asthma]] or [[COPD]] exacerbation
*[[Pneumonia]] or aspiration pneumonitis
*[[Pulmonary embolism]]
*[[Acute coronary syndrome]] (CO poisoning causes myocardial ischemia)
*Cardiogenic [[pulmonary edema]]
*[[Sepsis]] (delayed presentation of toxic inhalation can mimic sepsis)
*Aspiration of gastric contents
*Thermal airway burns without chemical component
*Panic attack/hyperventilation (diagnosis of exclusion in exposure setting)

==Evaluation==
===Workup===
'''History — critical questions:'''
*'''What''' was inhaled? (specific agent, if known; or type of fire/materials burning)
*'''Where?''' Enclosed space → much higher risk of CO and HCN; high-dose parenchymal injury
*Duration of exposure
*Loss of consciousness at scene? (suggests significant CO or HCN exposure)
*Use of respiratory protection?
*Pre-existing pulmonary disease ([[asthma]], [[COPD]])?
*Occupational context (welding, farming/silo, pool chemical mixing, industrial setting)

'''Physical exam — focused assessment:'''
*Complete upper airway exam: oropharynx for soot, erythema, edema, blistering
*Facial/nasal hair singeing
*Voice quality (hoarseness = laryngeal involvement)
*Lung auscultation: wheezing, crackles, stridor, decreased breath sounds
*Associated burn assessment (% TBSA, depth)
*Neurologic status (CO/HCN)

'''Laboratory:'''
*'''CO-oximetry''' (ABG or VBG with co-oximetry): '''Mandatory''' in all smoke inhalation; standard pulse oximetry does NOT detect carboxyhemoglobin (SpO₂ reads falsely normal)
*'''Lactate:''' Elevated lactate with high-flow O₂ → suspect '''cyanide toxicity''' (lactate >8 mmol/L is highly suggestive)<ref name="EMPract"/>
*ABG/VBG: PaO₂, PaCO₂, pH, A-a gradient
*CBC, BMP, troponin (CO causes myocardial injury)
*'''Methemoglobin level''' (co-oximetry) — if nitrate/nitrite exposure suspected
*'''Serum cyanide level:''' Takes too long to guide acute management — treat empirically based on clinical suspicion; do not wait for results
*Serum ethanol, toxicology screen (fire victims may have concomitant intoxication)

'''Imaging:'''
*'''Chest X-ray:''' Often '''initially normal''' — this does NOT rule out significant inhalation injury; delayed pulmonary edema may develop hours later<ref name="Medscape"/>
*Serial CXR at 6h, 12h, 24h for significant exposures
*CT chest: more sensitive; may show ground-glass opacities, peribronchial thickening; not routinely obtained acutely unless diagnosis uncertain
*CT face/neck if concern for deep thermal airway injury

'''Bronchoscopy''' (coordinate with pulmonology/ICU):
*Gold standard for assessing lower airway injury severity
*Findings: mucosal erythema, edema, soot deposits, ulceration, necrosis, carbonaceous material
*Helps guide intubation decisions and predict need for ventilatory support

'''Other:'''
*'''EKG:''' All smoke inhalation patients (CO → myocardial ischemia, dysrhythmias)
*Continuous pulse oximetry AND end-tidal CO₂ monitoring
*Peak flow or bedside spirometry (if bronchospasm assessment needed)

===Diagnosis===
*Primarily '''clinical''' — based on exposure history + compatible symptoms + physical findings<ref name="EMPract"/>
*No single diagnostic test confirms or excludes inhalation injury
*'''High index of suspicion required''' for low-solubility agents (phosgene, NOx) where patients may be initially asymptomatic
*CO-oximetry confirms CO exposure; elevated lactate with normal PaO₂ suggests HCN
*'''Normal initial CXR does NOT exclude significant injury''' — serial imaging is essential<ref name="Medscape"/>

==Management==
'''Airway — the #1 priority:'''
*'''Intubate early if any concern for progressive airway compromise''' — the window to secure the airway may be narrow; waiting for desaturation is too late<ref name="OAEM"/>
*'''Indications for intubation:'''<ref name="OAEM"/>
**Respiratory distress, stridor, hoarseness with progression
**Blistering or edema of oropharynx
**Deep facial or neck burns
**Hypoventilation, obtundation
**GCS ≤8
**Progressive hypoxemia despite high-flow O₂
*Use the '''largest ETT possible''' (6.5–8.0) — airway edema will worsen, and a large tube facilitates suctioning of casts and secretions
*Consider awake fiberoptic intubation if airway anatomy is distorted
*Avoid nasal intubation in facial burns (mucosal fragility)
*'''Cricothyrotomy''' if oral intubation fails

'''Oxygen:'''
*'''100% FiO₂ via non-rebreather''' for ALL smoke inhalation patients until CO is excluded<ref name="EMPract"/>
*CO half-life: room air ~320 min; 100% NRB ~60–90 min; hyperbaric O₂ ~20–30 min
*Continue high-flow O₂ until COHb <5% and symptoms resolve

'''Carbon monoxide:'''
*See [[carbon monoxide poisoning]] for full management
*Hyperbaric oxygen (HBO) indications remain controversial; consider for: loss of consciousness, neurologic symptoms, COHb >25%, pregnancy, myocardial ischemia, persistent symptoms despite NRB<ref name="Medscape"/>

'''Cyanide:'''
*See [[cyanide toxicity]] for full management
*'''Hydroxocobalamin (Cyanokit)''' 5g IV — preferred antidote; safe to give empirically in enclosed-space fire with altered mental status + lactic acidosis; does not affect CO-oximetry readings<ref name="EMPract"/>
*Sodium thiosulfate is an alternative but slower acting
*'''Do NOT use nitrite-based cyanide antidotes (amyl nitrite, sodium nitrite) in smoke inhalation''' — they induce methemoglobinemia, which is dangerous in patients with concurrent CO poisoning (both COHb and MetHb impair O₂ delivery)

'''Bronchospasm:'''
*Inhaled beta-agonists (albuterol) and ipratropium
*Severe: IV magnesium, epinephrine
*'''Nebulized sodium bicarbonate (NaHCO₃ 3.75%)''' has been used for chlorine and acid gas exposures — limited evidence but may help neutralize acid deposits in airways<ref name="PMCAcute"/>

'''Agent-specific management:'''

{| class="wikitable"
|-
! Agent !! Key Management Points !! Observation Time
|-
| '''Smoke (fire)''' || 100% O₂; CO-oximetry; hydroxocobalamin if HCN suspected; early intubation for airway edema; burn center transfer if burns present || 24h minimum if enclosed-space exposure
|-
| '''Chlorine''' || Beta-agonists; O₂; observation for delayed pulmonary edema; humidified O₂; NaHCO₃ nebs may help || '''≥6 hours''' if symptomatic; 24h if significant exposure
|-
| '''Ammonia''' || Copious irrigation of eyes/skin; bronchodilators; early intubation for laryngeal edema; fluids CAUTIOUSLY (pulmonary edema is noncardiogenic — patients may be hypovolemic); '''diuretics usually contraindicated'''<ref name="Ammonia"/> || '''6–12 hours''' minimum
|-
| '''Phosgene''' || '''NO ANTIDOTE'''; avoid exertion (increases pulmonary blood flow → accelerates edema); supportive care for pulmonary edema; lung-protective ventilation; '''diuretics contraindicated''' (noncardiogenic edema, patients are hypovolemic); respiratory distress within 4h of exposure = probable LD₅₀ dose<ref name="ATSDR"/> || '''24–48 hours''' minimum (up to 72h)
|-
| '''Nitrogen dioxide (silo filler's)''' || Supportive; corticosteroids may prevent delayed [[bronchiolitis obliterans]] (limited evidence); monitor for '''triphasic illness''' — initial symptoms, delayed pneumonitis (24–72h), then BO (2–6 weeks)<ref name="NO2"/> || '''24–48 hours'''; warn about delayed BO at 2–6 weeks
|-
| '''Hydrogen sulfide''' || Remove from exposure (rescuers need SCBA — '''do not enter without PPE'''); high-flow O₂; ''nitrite'' antidotes (sodium nitrite or amyl nitrite) MAY be used (unlike in CO+HCN coexposure); cardiac monitoring for arrhythmias; HBO may help || 24h if symptomatic; treat like CO + CN combined
|-
| '''Metal fume fever (zinc oxide)''' || Self-limited; NSAIDs, fluids, observation; resolves in 24–48h || Brief observation if mild; usually can discharge
|}

'''General supportive care:'''
*IV access, cardiac monitoring, continuous pulse oximetry
*Lung-protective ventilation if intubated (6 mL/kg IBW; PEEP as needed)
*Aggressive pulmonary toilet — frequent suctioning for cast and secretion management
*'''Avoid fluid overload''' — pulmonary edema from inhalation injury is noncardiogenic (permeability-based); excessive fluids worsen it
*Steroids: '''Not routinely recommended''' for smoke inhalation (increase infection risk, impair wound healing); may be considered for refractory bronchospasm, nitrogen dioxide-induced BO, or patients on chronic steroids<ref name="Medscape"/>
*'''Decontamination:''' Skin/clothing decontamination if external chemical exposure; remove contaminated clothing; healthcare workers may be at risk from off-gassing — use appropriate PPE

==Disposition==
*'''Admit (ICU):'''
**Intubated patients or those with high risk of progressive airway compromise
**Significant smoke inhalation with enclosed-space exposure
**Abnormal CO-oximetry (COHb >15% symptomatic, >25% asymptomatic)
**Suspected cyanide toxicity
**Pulmonary edema or significant hypoxemia
**Phosgene or nitrogen dioxide exposure with any symptoms
**Hydrogen sulfide exposure with syncope or altered mental status
**Concurrent burns requiring burn center care
*'''Admit (observation):'''
**Symptomatic chlorine or ammonia exposure with improving symptoms — observe minimum 6h (some recommend 12–24h for ammonia)
**Any exposure to low-solubility agents (phosgene, NOx) — observe '''24–48 hours minimum''' even if asymptomatic at presentation<ref name="ATSDR"/>
**Moderate smoke inhalation without concurrent CO/HCN toxicity
*'''Discharge (with precautions):'''
**Asymptomatic patients with exposure to '''highly soluble''' agents only (ammonia, HCl, SO₂) who remain asymptomatic after '''6 hours''' of observation with normal exam and normal CXR<ref name="PMCAcute"/>
**Metal fume fever with mild symptoms and improving
**Minor smoke exposure in open/well-ventilated space with normal CO-oximetry and no symptoms
**'''Critical discharge instructions:'''
***Return '''immediately''' for any new dyspnea, cough, chest tightness, or breathing difficulty — '''delayed pulmonary edema may occur hours to days later'''
***Avoid exertion for 24–48 hours (especially after phosgene — exertion accelerates pulmonary edema)
***Follow up with PCP or pulmonology within 48–72 hours
***For nitrogen dioxide: warn about '''delayed bronchiolitis obliterans''' at 2–6 weeks — return for new cough, dyspnea, or wheezing
***Occupational health referral and OSHA reporting as appropriate
***Smoking cessation

==See Also==
*[[Carbon monoxide poisoning]]
*[[Cyanide toxicity]]
*[[Smoke inhalation]]
*[[Chlorine gas]]
*[[Hydrogen sulfide toxicity]]
*[[ARDS]]
*[[Burns]]
*[[Chemical burns]]
*[[Metal fume fever]]
*[[Methemoglobinemia]]

==External Links==
*[https://www.ncbi.nlm.nih.gov/books/NBK554539/ Nitrogen Dioxide Toxicity — StatPearls]
*[https://chemm.hhs.gov/phosgene_hospital_mmg.htm Phosgene: Medical Management — CHEMM/HHS]
*[https://chemm.hhs.gov/ammonia_hospital_mmg.htm Ammonia: Medical Management — CHEMM/HHS]
*[https://emedicine.medscape.com/article/771194-overview Smoke Inhalation Injury — Medscape]
*[https://pmc.ncbi.nlm.nih.gov/articles/PMC4261306/ Acute Inhalation Injury — PMC Review]
*[https://www.tamingthesru.com/blog/diagnostics-and-therapeutics-inhalation-injuries Inhalation Injuries — Taming the SRU]

==References==
<references/>

[[Category:Toxicology]]
[[Category:Pulmonary]]
[[Category:Environmental]]

Toxic inhalation - Revision history

Danbot: Strip excess bold

Danbot: Moved intro into Background as bullets; removed excessive bold from bullet lead-ins; added Toxic gas exposure DDX template; bold retained for critical items only