01Approach to the Critical Patient/attcp56

Immediate airway threats

›Airway emergency triggers

›Stridor or progressive hoarseness

›Early intubation before edema progresses

›Delayed intubation leads to failed airway scenario

›Drooling or inability to manage secretions

›Impending complete obstruction

›Call anesthesia and ENT concurrently

›Supraglottic edema on visualization

›Video laryngoscopy preferred

›Surgical airway backup on standby

›Facial or oropharyngeal burns with fluid resuscitation underway

›Edema worsens over first 12-24 hours

›Low threshold for early prophylactic intubation

Systemic toxicity priorities

›Carbon monoxide poisoning recognition

›SpO2 unreliable — falsely normal with COHb elevation

›Co-oximetry required for accurate COHb measurement

›Pulse oximetry reads COHb as oxyhemoglobin

›COHb >30-40% — severe exposure threshold

›Cardiac ischemia risk at this level

›Unconsciousness possible

›100% O2 via non-rebreather mask immediately

›Reduces COHb half-life from 3-4 hours to under 1 hour

›Cyanide poisoning recognition

›Enclosed-space fire with nitrogen-containing materials

›Plastics, wool, silk, synthetic materials release HCN

›Thermal degradation releases cyanide gas

02History/hx59

Exposure context

›Scene characteristics

›Enclosed vs. open-space exposure

›Enclosed space is the single most important risk factor

›Concentrates toxic gases and depletes oxygen

›Duration of exposure

›Prolonged duration worsens systemic toxicity

›Bystander or EMS estimate critical

›Materials burning

›Plastics, vinyl, wool, silk — higher cyanide yield

›Nitrogen-containing compounds release HCN

›Wood and natural materials produce CO predominantly

›Prehospital events

›Loss of consciousness at scene

›High suspicion for significant CO or cyanide exposure

›Seizures associated with severe toxicity

›Prehospital O2 administered

›COHb drops rapidly with O2 therapy before ED arrival

›Normal COHb on arrival may mask severe exposure

›CPR or cardiac arrest at scene

›Strong indication for empirical cyanide antidote

Symptom characterization

›Airway and respiratory symptoms

›Cough

›Productive of carbonaceous sputum

›Hemoptysis in severe mucosal injury

›Hoarseness

›Indicator of supraglottic thermal injury

03Physical Exam/exam64

Airway examination

›Oropharyngeal findings

›Facial and perioral burns

›Indicator of direct thermal injury

›Predict progressive airway edema

›Singed nasal vibrissae

›Marker of intense heat exposure

›Associated with supraglottic injury

›Soot in nares or oropharynx

›Indicator of smoke inhalation confirmed

›Carbonaceous deposits on mucosa

›Oropharyngeal erythema or edema

›Early sign of impending obstruction

›Progressive with fluid resuscitation

›Voice and airway quality

›Hoarseness

›Supraglottic edema or mucosal injury

›Worsening is an emergency

›Stridor (inspiratory)

›Upper airway obstruction >75% luminal narrowing

›Immediate intubation trigger

Pulmonary and cardiovascular exam

›Lung auscultation

›Wheezing

›Chemical bronchospasm from toxic gas injury

›May be diffuse bilaterally

›Crackles and rhonchi

›Early parenchymal injury or secretions

04Differential Diagnosis/ddx44

Life-threatening conditions

›Systemic toxidromes

›Carbon monoxide poisoning

›ICD-10 T58

›COHb co-oximetry confirms; SpO2 unreliable

›Cyanide poisoning

›ICD-10 T65.0

›Lactate >10 mmol/L is key differentiating clue

›Combined CO and cyanide co-poisoning

›Enclosed-space fires frequently involve both

›Hydroxocobalamin does not impair O2 carrying capacity

›Airway emergencies

›Supraglottic thermal airway injury

›ICD-10 T27.0

›Direct heat causes edema and mucosal sloughing

›Acute epiglottitis

›Isolated supraglottic edema without smoke exposure

›Fever, drooling, tripod positioning

›Anaphylaxis

›Airway edema and bronchospasm without clear exposure history

›Urticaria and hypotension may differentiate

›Foreign body aspiration

›Focal wheeze rather than diffuse

›No toxic exposure history

Pulmonary conditions

›Parenchymal and lower airway

›Chemical tracheobronchitis

›ICD-10 J68.0

05Laboratory Tests/lt53

Toxicology and co-oximetry

›Carboxyhemoglobin measurement

›Co-oximetry is only accurate method

›Venous or arterial sample acceptable

›Standard pulse oximetry falsely reads COHb as oxyhemoglobin

›COHb 10-20%: headache and nausea

›Mild-moderate exposure level

›Treatment with 100% O2

›COHb 20-30%: weakness and cognitive impairment

›Moderate exposure level

›Close monitoring for progression

›COHb >30-40%: severe exposure

›Cardiac ischemia and unconsciousness risk

›Consider HBO2 candidacy

›Lactate

›Elevated >2 mmol/L indicates tissue hypoxia

›CO-mediated cellular hypoxia

›Cyanide-mediated mitochondrial uncoupling

›Lactate >10 mmol/L strongly associated with cyanide toxicity

›Empirical hydroxocobalamin treatment threshold

›Lactate is the key cyanide surrogate in ED setting

›Cyanide levels

›Not available in real-time in most emergency departments

›Treatment is empirical based on clinical features

›Whole blood cyanide sent for retrospective confirmation

Arterial blood gas and metabolic labs

›Arterial blood gas

›PaO2/FiO2 ratio

06Diagnostic Tests/dt91

Scoring Systems

›Bronchoscopic grading of inhalation injury

›Grade 0: no injury

›Normal mucosa and secretions

›No intervention needed

›Grade 1: mild injury

›Minor erythema, edema, soot, secretions

›Limited to supraglottis and glottis

›Grade 2: moderate injury

›Moderate edema, blistering, mucosal sloughing

›Tracheobronchial involvement

›Grade 3: severe injury

›Extensive mucosal necrosis and cast formation

›High risk of ARDS and death

›Grade 4: massive injury

›Airway obstruction from cast and sloughing

›Associated with very high mortality

›Higher bronchoscopic grade associated with worse clinical outcomes

›ARDS incidence increases with grade

›Mortality increases with grade in systematic review (Burns 2025)

›Abbreviated Burn Severity Index (ABSI)

›Incorporates inhalation injury, TBSA, age, sex, burn depth

›Score 2-3: expected mortality <10%

›Score 8-9: expected mortality 50-70%

›Score >=11: expected mortality >90%

›Inhalation injury adds 1 point to ABSI score

›Independent predictor of mortality

›Doubles mortality when combined with cutaneous burns

›Revised Baux Score

›Age + TBSA% + 17 if inhalation injury

›Score >140 associated with >90% mortality

›Inhalation injury adds fixed 17-point penalty

›Used for burn center prognostication

MRI

›Brain MRI for CO-related neurologic injury

›Indications

›Persistent neurologic deficits after normalization of COHb

›Delayed neuropsychiatric syndrome

›Loss of consciousness with prolonged exposure

›Findings

›Bilateral globus pallidus lesions (T2 hyperintensity)

›White matter changes in delayed neurologic sequelae

›Cerebral edema in severe acute cases

›Timing

›Acute MRI may be normal early in course

›Delayed imaging at 4-6 weeks if symptoms persist

›Neck MRI for airway assessment

›Limited role in acute setting

›CT or bronchoscopy preferred for airway evaluation

›MRI rarely adds over CT in acute phase

›May be used for delayed laryngeal scarring assessment

CT

›Chest CT

›Indications

›Suspected lower airway and parenchymal injury

›Progressive deterioration with initially normal CXR

›Evaluation for pneumonia or ARDS development

›Findings

›Ground-glass opacities and bronchial wall thickening

›Peribronchial edema from chemical injury

›Diffuse airspace disease indicating pulmonary edema or ARDS

›Tree-in-bud pattern if mucosal plugging develops

›Prognostic value

›When combined with bronchoscopy, significantly improves prognostication

›More sensitive than CXR for distal airway disease

›Head CT

›Indications

›GCS <13 or focal neurologic deficits

›Concurrent trauma or fall injury

›When MRI not available for neurologic evaluation

›Findings

›Cerebral edema in severe CO poisoning

›Bilateral basal ganglia hypodensity (late finding)

›Traumatic injury if concurrent

Ultrasound

›Point-of-care lung ultrasound

›Indications

›Rapid assessment of bilateral parenchymal involvement

›Fluid status assessment during resuscitation

›Pleural effusion detection

›Findings

›B-lines: interstitial edema or early ARDS pattern

›Consolidation: airspace disease with air bronchograms

›Pleural sliding: pneumothorax exclusion

›Cardiac ultrasound

›CO-induced cardiomyopathy assessment

›Wall motion abnormality from ischemia

›Reduced ejection fraction in severe poisoning

›Fluid responsiveness

›IVC collapsibility index

›Guides fluid resuscitation in hemodynamically unstable patients

›Vascular access ultrasound

›Central venous access in burn patients

›Avoid burned skin for line insertion

›US-guided femoral or subclavian if peripheral access unavailable

07Disposition/dispo42

ICU and burn center admission

›ICU admission criteria

›Confirmed or suspected inhalation injury with respiratory symptoms

›Any stridor, hoarseness, or airway concern

›Worsening dyspnea or O2 requirement

›Intubated patients

›All require ICU-level monitoring

›Mechanical ventilation management

›COHb >25% or any neurologic symptoms

›Serial neurologic assessment

›COHb monitoring every 4-6 hours until trend established

›Suspected cyanide toxicity

›Post-hydroxocobalamin monitoring

›Metabolic response tracking

›Concurrent significant cutaneous burns >20% TBSA

›Fluid resuscitation titration

›Burn wound management

›Burn center transfer criteria

›Inhalation injury is an ABA burn center referral criterion

›Regardless of cutaneous burn size

›Early transfer preferred before intubation if airway stable

›Combined inhalation and cutaneous burns

›Any inhalation with >10% TBSA burns

›Burns to face, hands, feet, genitalia, perineum

›Contact receiving burn center before transfer for guidance

Observation and discharge

›Observation criteria

›Asymptomatic with minor exposure and normal COHb

08Treatment/t96

Oxygen therapy

›High-flow oxygen via non-rebreather mask

›All smoke inhalation patients regardless of SpO2 reading

›SpO2 unreliable with CO poisoning

›Continue until COHb <5%

›Reduces COHb half-life from 3-4 hours to under 1 hour

›100% FiO2 mandatory

›Sealed NRB mask at 15 L/min

›Class I recommendation for CO poisoning

›Hyperbaric oxygen therapy

›Indications

›Loss of consciousness during exposure

›COHb >25% with neurologic symptoms

›CO-related cardiac complications

›Pregnancy (lower threshold COHb >15-20%)

›Reduces risk of delayed neuropsychiatric syndrome

›Controversial evidence; consultation with toxicology advised

›Avoid if wheezing, airway debris, or significant cutaneous burns

›COHb half-life on HBO2 approximately 20-30 minutes

›Faster clearance than normobaric O2

Cyanide antidote

›Hydroxocobalamin (Cyanokit)

›First-line antidote for suspected cyanide poisoning

›Preferred over sodium nitrite/thiosulfate in smoke inhalation

›Does not reduce oxygen-carrying capacity (unlike nitrite)

›Dosing: 5 g IV in adults over 15 minutes

›May repeat 5 g IV if inadequate response

›Maximum 15 g total (three doses)

›Pediatric: 70 mg/kg IV

›Indications for empirical use

›Cardiac arrest at scene

›GCS <10

›Lactate >10 mmol/L

›COHb >10% with enclosed-space nitrogen-containing fire

›AHA 2023 and 2025 guidelines support empirical use in cardiac arrest from smoke inhalation

›Sodium nitrite — avoid in smoke inhalation

›Induces methemoglobin

›Further reduces O2 carrying capacity when COHb already elevated

›Risk of profound tissue hypoxia

›Only use if isolated cyanide without CO poisoning

Bronchospasm and airway management

›Nebulized beta-2 agonist

›Albuterol (salbutamol) 2.5-5 mg nebulized

›For bronchospasm from chemical mucosal injury

›Repeat every 20 minutes for three doses then every 4 hours

›Continuous nebulization if severe bronchospasm

›Add ipratropium bromide 0.5 mg nebulized for refractory bronchospasm

›Combine with albuterol in first hour

›Repeat every 4-6 hours

›Nebulized racemic epinephrine

›For severe mucosal edema

›0.5 mL of 2.25% solution in 3 mL NS

›Monitor for rebound edema

›Alpha-1 mediated vasoconstriction reduces mucosal edema

›Nebulized heparin and N-acetylcysteine

›Heparin 5,000-10,000 IU alternating with NAC 20% 3 mL every 2-4 hours

›Aimed at prevention of fibrin cast formation

›Reduces obstructive cast shedding

›Limited evidence from case reports and small series

›Reserve for intubated patients with evidence of cast formation

Airway management protocols

›Rapid sequence intubation

›Indications

›Progressive airway edema with stridor or hoarseness

›Inability to protect airway

›GCS <8 from CO or cyanide toxicity

›Anticipated fluid resuscitation worsening edema

›Video laryngoscopy preferred

›Edematous airway makes direct laryngoscopy hazardous

›Smaller endotracheal tube may be needed

›Surgical airway backup ready before induction

›Difficult airway cart at bedside

›Cricothyrotomy kit immediately available

›Contraindicated therapies

›Prophylactic antibiotics — not recommended

›Do not reduce pneumonia or mortality in inhalation injury

›May promote resistant organisms

›Empirical corticosteroids — contraindicated

›Associated with increased mortality and pneumonia in burn patients

›Class III (harm) in burn-related inhalation injury

Mechanical ventilation

›Lung-protective ventilation strategy

›Tidal volume 6 mL/kg ideal body weight

›Reduces ventilator-induced lung injury

›Class I recommendation from ARDS network evidence

›Plateau pressure limit <30 cmH2O

›Higher pressures increase barotrauma risk

›Permissive hypercapnia acceptable if pH >7.20

›PEEP titration

›Adequate PEEP to prevent atelectasis

›Avoid excessive PEEP increasing airway pressures

›High-frequency percussive ventilation (HFPV)

›Alternative under investigation in inhalation injury

›May improve secretion clearance

›Available in specialized burn centers

›Not universally available

›Bronchoscopy for intubated patients

›Serial bronchoscopy for cast removal and airway toilet

›Therapeutic and diagnostic

›Clears obstructing casts and necrotic debris

›Guides grading of injury severity

09Special Populations/sp70

Pregnancy

›Physiologic considerations

›Fetal hemoglobin binds CO 2.5-3x more avidly than maternal hemoglobin

›Fetal COHb levels substantially higher than maternal

›Fetal toxicity occurs at maternal COHb levels tolerated by mother

›Fetal hypoxia risk

›Even mild maternal CO exposure can cause fetal distress

›CO-induced placental insufficiency

›Lower threshold for aggressive treatment and HBO2

›Treatment modifications

›HBO2 strongly considered for any smoke inhalation in pregnancy

›Threshold COHb >15-20% vs. >25% in non-pregnant

›Fetal indication may override relative contraindications

›Maternal exposure duration doubles fetal risk

›Hydroxocobalamin for suspected cyanide

›Animal data suggests fetal safety

›Benefits outweigh risks in life-threatening cyanide poisoning

›Sodium nitrite contraindicated in pregnancy

›Continuous fetal monitoring after ED stabilization

›Electronic fetal monitoring for viable gestations

›Obstetric consultation emergently

›Maternal airway management

›Early intubation at lower threshold

›Reduced functional residual capacity in third trimester

›Desaturation occurs more rapidly

›Left lateral positioning to avoid aortocaval compression

Geriatric

›Physiologic vulnerability

10Background/b70

Epidemiology

›Incidence and mortality

›Approximately 15% of burn patients have concomitant inhalation injury

›20-30% of severe burns are associated with inhalation injury

›Inhalation injury independent predictor of mortality

›Mortality impact

›Inhalation injury doubles mortality when combined with cutaneous burns

›Isolated inhalation injury (without cutaneous burns) has lower mortality

›Combined injury mortality substantially higher than either alone

›Epidemiologic context

›Fire-related deaths — leading cause of home injury death in US

›Majority of fire deaths from smoke inhalation not direct thermal injury

›Enclosed-space fires (residential) highest risk

›Extremes of age have worse outcomes

›Children and elderly disproportionately affected

›Pre-existing cardiopulmonary disease worsens prognosis

›Coding

›ICD-10 T59.91 — toxic effects of other gases, fumes, and vapors

›T58 for CO specifically

›T65.0 for cyanide

›T27.0 for corrosion of larynx and trachea

Pathophysiology

›Three-component insult model

›Supraglottic thermal injury

›Heat damages upper airway mucosa

›Water vapor in steam carries heat deeper

›Dry smoke heat largely filtered at nasopharynx

›Edema peaks over 12-24 hours worsened by fluid resuscitation

›Tracheobronchial chemical injury

›Toxic gases (acrolein, HCl, HCN, aldehydes) cause mucosal necrosis

›Disruption of mucociliary clearance

›Surfactant inactivation

›Progressive cast formation from fibrin, mucus, and necrotic debris

›Systemic toxicity (CO and cyanide)

›CO binds hemoglobin with 240x greater affinity than O2

›CO impairs mitochondrial cytochrome oxidase (cellular level)

›Cyanide blocks cytochrome c oxidase — histotoxic anoxia

›Both impair tissue O2 utilization independently of PaO2

›Downstream injury mechanisms

›Inflammatory cascade from airway injury

›Neutrophil recruitment and cytokine release

›Progression to ARDS in 24-72 hours in severe cases

›Reactive oxygen species generation

›Xanthine oxidase activation from ischemia-reperfusion

›Nitric oxide radical formation from inducible NOS

›Airway cast formation

›Fibrin, mucus, sloughed epithelium

›Obstructs bronchioles causing atelectasis and air trapping

Therapeutic Considerations

›Evidence base summary

›100% O2 via NRB mask

›Universally recommended; Class I evidence

›Reduces COHb half-life from 3-4 hours to <1 hour

›Hydroxocobalamin for cyanide

›AHA 2023 Focused Update (Lavonas et al.) — supported for cardiac arrest from poisoning

›Preferred over sodium nitrite in smoke inhalation due to no methemoglobin effect

›AHA 2025 CPR Guidelines affirm role in smoke inhalation cardiac arrest

›Nebulized heparin/NAC regimen

›Limited evidence; case reports and small series only

›May reduce cast formation and mechanical ventilation duration

›Burns evidence mixed; not universally recommended

›Therapeutic controversies

›Hyperbaric oxygen

›Randomized evidence mixed; Cochrane review inconclusive

›Strong indication for pregnancy, severe neurologic symptoms, cardiac ischemia

›Practical limitation — most centers lack 24-hour HBO2 access

›Early vs. delayed intubation

›Sheridan (NEJM 2016): inhalation injury does not mandate intubation

›Airway patency not threatened and <20% TBSA burns: supportive care acceptable

›Head-of-bed elevation and humidified air for non-intubated patients

›Inhaled nitric oxide

›Under investigation for reducing pulmonary hypertension in ARDS from inhalation injury

›Not standard of care; specialized center use only

11Patient Discharge Instructions/pdi34

copy discharge instructions

›What happened to you

›You were exposed to smoke, which contains carbon monoxide and other toxic gases

›Carbon monoxide can linger in your blood for hours after leaving the fire

›Symptoms may develop or worsen over the next 24-48 hours

›Your lungs and airway may be irritated even if you feel better now

›Swelling and injury can develop slowly after smoke exposure

›A follow-up appointment within 24-48 hours is required

›Return to emergency immediately if you develop

›Worsening shortness of breath or difficulty breathing

›Any new or worsening stridor (high-pitched breathing sound)

›Coughing up blood

›Chest pain or irregular heartbeat

›Feeling faint or losing consciousness

›Severe persistent headache not relieved by pain medication

›Voice changes, increasing hoarseness, or difficulty swallowing

›Throat tightness

›Drooling or inability to handle secretions

›Confusion, memory problems, or personality changes

›These can be delayed symptoms of carbon monoxide poisoning

›May develop days to weeks after exposure

›Worsening cough or fever

›Lung infection can develop in the days after smoke inhalation

›Activity and home care instructions

›Rest and avoid strenuous activity for 24-48 hours

›Do not exercise until cleared by follow-up physician

›Avoid smoke and air pollutants

›Do not use a gas stove, fireplace, or gas heater until inspected

12References/r30

Guidelines and key sources

›Sheridan RL. Fire-Related Inhalation Injury. N Engl J Med. 2016

›Foundational review on management algorithm and indications for intubation

›Outlines three-component injury model

›Greenhalgh DG. Management of Burns. N Engl J Med. 2019

›Comprehensive review including inhalation injury epidemiology

›Mortality data and burn center criteria

›Enkhbaatar P, Pruitt BA, Suman O et al. Pathophysiology, Research Challenges, and Clinical Management of Smoke Inhalation Injury. Lancet. 2016

›Pathophysiology of chemical tracheobronchitis and cast formation

›Evidence for nebulized heparin/NAC regimen

›Lavonas EJ et al. 2023 AHA Focused Update: Management of Cardiac Arrest or Life-Threatening Toxicity from Poisoning. Circulation. 2023

›Hydroxocobalamin as preferred cyanide antidote in smoke inhalation

›Avoidance of sodium nitrite in combined CO/cyanide poisoning

›Cao D et al. Part 10: Adult and Pediatric Special Circumstances. 2025 AHA CPR Guidelines. Circulation. 2025

›Updated guidance for smoke inhalation cardiac arrest

›Affirms empirical hydroxocobalamin use

›Deutsch CJ, Tan A, Smailes S, Dziewulski P. Diagnosis and Management of Inhalation Injury: An Evidence Based Approach. Burns. 2018

›Systematic review of nebulized therapies and airway management

›Evidence levels for treatment interventions

›Amarasekera NN et al. Evaluating Bronchoscopic Severity of Burns-Related Smoke Inhalation Injury and Clinical Outcomes. Burns. 2025

›Systematic review and meta-analysis of bronchoscopic grading

›Higher grade associated with increased ARDS and mortality

›Culnan DM et al. Carbon Monoxide and Cyanide Poisoning in the Burned Pregnant Patient. Ann Plast Surg. 2018

›Pregnancy-specific HBO2 indications

›Fetal hemoglobin CO binding avidity data

›Foncerrada G, Culnan DM et al. Inhalation Injury in the Burned Patient. Ann Plast Surg. 2018

›Pathophysiology of airway injury and cast formation

›Role of bronchoscopy in diagnosis and management

Evidence & Review

Evidence & Review