Smoke Inhalation Injury - Surgery

Smoke Inhalation Injury
Trent Wray, MD
Trauma Conference
9/8/11

• Mel Otten
• Chris Droege
Thanks!

Objectives
• Clinical Course of Inhalation Injury
• Complications of Inhalation Injury
• Treatment of Inhalation Injury

Non‐Objectives
• Detailed lecture on CO or Cyanide
• Burn resuscitation
• Burn management
• Detailed airway management

House Fire
• 45 y/o male found at neighbor’s after house fire

House Fire
• 45 y/o male found at neighbor’s after house fire
• Per EMS:
– Covered c ice/wrapped in blanket by neighbor.
– c/o SOB, coughing.
– Soot around mouth.
– Does not remember event.
– GCS 10 (3E, 2V, 5M)

House Fire
• On Arrival:
– Confused, groaning, GCS 10 (3E, 2V, 5M).
– 96.0 R 128 161/100, 12
– Gen:
• No signs of trauma, numerous burns.
• Soot noted on clothes, around mouth and face
• Extending his neck (trying to control own airway)
• No audible stridor
• Labored breathing
• Accessory muscle use noted

House Fire
• On Arrival:
– HEENT:
• Partial‐Thickness facial burns – rubbery edema of eyes
• Scalp burns extending toward neck
• Obese neck, diminished neck extension
• Very erythematous OP with soot noted in oropharynx
– Chest/Abdomen:
• No signs of trauma
• Diminished breath sounds at bases
• Very coarse breath sounds bilaterally
• Partial and full thickness burns to chest, abdomen, and back
• Obese Abdomen

House Fire
• On Arrival:
– Extremities:
• Circumferential FT and PT burns to BLUE’s and BLLE’s.
– Neuro:
• GCS as above
• CN II –XII grossly intact
• Moves all extremities
– Overall:
• Burns to 46% TBSA
• Concern for inhalation injury

ED Course
• SaO2 92% on NRM, Soot in edematous airway,
diminished GCS Intubate.

ED Course
• Soot‐filled, edematous airway.
• Chords too edematous to get 8.0 tube
through
• Repeat attempt with bougie + 6.5 tube
successful.

• Initial Labs:
– CBC: WBC 27
– Renal Panel: AG 21
ED Course
– ABG: 7.16/46/64/16/‐13
– Lactate: 8.9

• Course:
ED Course
– Placed on ARDSNET Vent Settings
– Resuscitated using Parkland Formula
• 4 X Kg X % TBSA Burned
– Hydroxycobalamin given
– Bronchoscopy Performed:

Hospital Course
• HD 1:
– Bronch: edema and soot noted in distal bronchi
– Chest Tube (suspected PTx)
• HD 3:
– Trach; NJT Placement
• HD 5:
– Gets PNA
• HD 12:
– Excision of BLUE eschars + grafting
• HD 15:
– Excision of BL shoulder eschars + grafting
• HD 19:
– Trunk Eschars excised and grafted
• HD 26 & 27:
– Trunk and LE exchars excised and grafted
• Currently on HD 35:
– Trach + NJT continued.
– Now waking and following commands
– Ongoing grafting

• Epidemiology:
Inhalation Injury
– “Fire Deaths” in 2011: 3,500 (3,000 res/500 auto)
• U.S. Highest fire fatality rates in developed world.
– 75% occurred at scene or during transport
– Est 60‐80% deaths due to smoke inhalation
– Correlates with % TBSA Burned:
• < 5% TBSA = 10% Inhalation Injury
• > 85% TBSA = 80% Inhalation Injury
Sources:
1.) ABA Fact Sheet
2.) Muller et al 2001

• Epidemiology:
– Mortality:
• Burn Alone: 2%
Inhalation Injury
• Inhalation Injury Alone: 7%
• Both: 29%
Source: Marshall et al 1998

• What is Smoke?
Inhalation Injury
– Complete Combustion Rxn:
• CH 4 + 2 O 2 → CO 2 + 2 H 2 O + energy
– Incomplete Combustion Rxn (partial oxidation):
• CH4 + O2 CO + H2O + 3H
(insert misc product here)

• What is smoke?
Inhalation Injury
– Products of combustion
• Heat
• Gases
• Particles

Inhalation Injury
• What is smoke?
– Gases:
• CN/HCN
• CO
• Other Nitrates
– Particles:
• Water Soluble:
– SO2, HCl, NH3, Propenal (Acrolein)
• Non‐Water Soluble:
– NO, NO2, N2O, Polyvinylchloride (PVC)

Inhalation Injury
• Mechanisms of Smoke Inhalation Injury:
– Thermal Damage
– Asphyxiation
– Pulmonary Irritation

Inhalation Injury
• Direct Thermal Injury (heated gases):
– Usually upper airway:
• Inhaled air doesn’t conduct heat well
• Glottic reflex
• Why laryngoscopy is usually recommended before
bronchoscopy
– Unless it’s steam/liquid:
• Heat carrying capacity ~ 4,000 X air
• May cause pan‐airway damage edema
• May perform bronchoscopy prior to laryngoscopy

• Asphyxia:
Inhalation Injury
– Low environmental FIO2
– CN
– CO
– Methemglobinemia

• Asphyxia:
Inhalation Injury
– Low environmental FIO2:
• O2 consumed in combustion reactions (see above)
• Pull them out and place on 100% O2

• Asphyxia:
– Cyanide (HCN, CN):
Inhalation Injury
• Present in nearly all structure fires
– Wool, Rubber, PVC, Paper, foods
– Colorless, Almond odor
• Present in up to 35% of all fire victims
• In one plane fire, 90% had CN toxicity (20% had CO)
Source: Walsh DW, Eckstein M (2004)

Inhalation Injury
• Asphyxia:
– Cyanide (HCN, CN):
• 20X more toxic than CO
• Binds to Fe2+ Cyanohemoglobin:
– Hypoxia
• Binds to Fe3+ on Cytochrome a3 disrupts ETC
– Shift toward Anaerobic Metabolism and uncoupling:
» Cannot use O2 Venous blood turns bright red
» Lactic Acidosis
» H+ production Decreased HCO3‐
• Particularly affects CV and Brain (Basal Ganglia)

Inhalation Injury
• Asphyxia:
– Cyanide (HCN, CN):
• Metabolized by Rhodanese enzyme Kidney
– Thiosulfate is sulfur donor
• Bound by Vitamin B12 (Hydroxycobolamin)
• S&S:
– “Sick and Cherry Red”
– Most patients who are sick after a house fire
• Treatment:
– Hydroxycobalamin 5 g IV (Cyanokit)
– 25% Sodium Thiosulfate 1.65 cc/kg IV
– NO EMPIRIC NITRITES
Source: Barron et al (2007); Morocco (2005)

• Asphyxia:
– CO:
Inhalation Injury
• Responsible for most fire deaths
• Leading cause of poisoning worldwide
• Carbon + incomplete O2 combustion rxn
• Binds to Hb with 200X greater affinity
• Also binds myoglobin, cytochrome a3
• Lipid Peroxidation Neuron demyelination
Source: Kao LW et al (2006)

• Asphyxia:
– CO:
Inhalation Injury
Source: Demling (2008)

• Asphyxia:
– CO:
• Removal:
Inhalation Injury
– t1/2 300 min on RA.
– t1/2 90 min on 15L NRM
• Consider HBO
– Primarily decreases neurological sequelae
– Particularly useful in pts with MI, Pregnant Women, Children
– May be limited by injuries
Source: Weaver et al (2002)

• Asphyxia:
– Methemglobinemia:
• Due to:
Inhalation Injury
– low O2 environment
– Nitrite inhalation
– Fairly rare
– Treat with Methylene Blue (1‐2 mg/kg IV over 5 min)
» Causes cyanosis
» Watch for rebound methemoglobinemia
Source: Howland, Goldfrank (2006)

• Pulmonary Irritation:
Inhalation Injury
– Airway Edema + Bronchoconstriction:
• Particle stimulation of neuropeptides
• Increase of transudate exudate
• Racemic Epi, Bronchodilators
– Damage to/Sloughing of endothelium:
– Increased necrotic tissue + trapping of mucociliary clearance
– May not be evident until after a 24‐48 hr “Honeymoon”
– May Lead to Delayed PNA, ALI/ARDS

• Pulmonary Irritation:
Inhalation Injury
– Damage to/Sloughing of endothelium:
– Increased necrotic tissue + trapping of mucociliary clearance
– May not be evident until after a 24‐48 hr “Honeymoon”
– May Lead to Delayed PNA, ALI/ARDS
– Early (and repeat?) bronchoscopy recommended
Source: .
Marek et al (2007)

Inhalation Injury
• Pulmonary Irritation:
– Laryngoscopy to diagnose upper airway edema
• If present, consider intubating
– Bronchoscopy to diagnose lower airway edema
• Soot
• Mucosal Pallor
• Mucosal Ulceration
• Mucosal Erythema
*If any of the above present = + Bronchoscopy
‐Negative does not rule out inhalation injury

• Management:
– 100% O2
– Coximetry
Inhalation Injury
– CBC, Renal, ABG/VBG, Lactate
– Concern for cyanide Hydroxycobalamin
– Concern for CO
– Methemoglobinemia (> 30%) Methylene Blue

• Management:
Inhalation Injury
– Consider early intubation if:
• Any evidence of respiratory distress
• Deep burns to the face/neck
– If not, oropharyngeal exam:
• Erythema, hoarseness Laryngoscopic exam
– + edema INTUBATE Lung Protective Ventilation
• No erythema, no hoarseness, stable pulm exam
– follow closely (repeat exams)
Source: Plurad et al (2007)

• Management:
– Once Intubated:
• ARDSNET Proocol
Inhalation Injury
• Repeat Bronchoscopies?
• Watch fluid resuscitation.
• Vigilance for AKI/ARDS, PNA.
• No role for prophylactic antibiotics or corticosteroids
– Manage Burns
Source: Plurad et al (2007)

Inhalation Injury
• Most common cause of “Fire Deaths”
• Aggressive airway management
• Watch for physical and chemical asphyxia
– HCN, CO, MetHb
• Vigilance for rapidly worsening respiratory
status

Questions?

References
• Borron SW, Baud FJ, Barriot P, Imbert M, Bismuth C. Prospective study of hydroxocobalamin for acute cyanide poisoning in
smoke inhalation”. Ann Emerg Med. 2007;49(6):794
• Carr JA, Phillips BD, Bowling WM (2009). “The utility of bronchoscopy after inhalation injury complicated by pneumonia in
burn patients: results from the National Burn Repository.” J Burn Res Care. 2009 Nov‐Dec;30(6):967‐74.
• Demling, RH. “Smoke Inhalation Lung Injury: An Update”. Eplasty. 2008;8:e27
• Howland MA. Methylene blue. In: Goldfrank's Toxicologic Emergencies. 8 th ed. 2006:1746‐1748.
• Kao LW, Nanagas KA. Toxicity associated with carbon monoxide. Clin Lab Med. Mar 2006;26(1):99‐12
• . Marek K, Piotr W, Stanislaw S, et al. Fibreoptic bronchoscopy in routine clinical practice in confirming the diagnosis and
treatment of inhalation burns. Burns. 2007;33(5):554–560
• Marshall SW, Runyan CW, Bangdiwala SI, Linzer MA, Sacks JJ, Butts JD. “Fatal residential fires: who dies and who survives?”.
JAMA. May 27 1998;279(20):1633‐7
• Morocco AP. “Cyanides”. Crit Care Clin. 2005;21(4):691
• Muller MJ, Pegg SP, Rule MR. Determinants of death following burn injury. Br J Surg. Apr 2001;88(4):583‐7.
• Plurad D, Martin M, Green D, et al. The decreasing incidence of late posttraumatic acute respiratory distress syndrome: the
potential role of lung protective ventilation and conservative transfusion practice. J Trauma. 2007;63(1):1–7. discussion
• Sauer SW, Keim ME. “Hydroxocobalamin: improved public health readiness for cyanide disasters” . Ann Emerg Med.
2001;37(6):635.
• Walsh DW, Eckstein M.”Hydrogen Cyanide in Fire Smoke: an Underappreciated Threat.” Emerg Med Serv. 2004;33(10):160
• Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. Oct 3
2002;347(14):1057‐67