Inhalation Injury

Arek Wiktor M.D.

Burn Fellow
University of Colorado Hospital
 Outline
 Background
 Smoke
 Pathophysiology
 Diagnosis
 Treatment
 Specific Lethal Compounds

http://spanishlakefd.com/firealarms/
 Learning Objectives
 Describe the pathophysiology of inhalation
injury
 How is inhalation injury diagnosed?
 What adjunctive measures are used to treat
inhalation injury?
 What is the treatment for carbon monoxide and
cyanide poisoning?
A Sunday afternoon stroll thru the fire…

http://www.aeromedix.com/product-exec/parent_id/1/category_id/12/product_id/1074/nm/Safe_Escape_Smoke_Hood
 Epidemiology

 15-30% of burn admissions have inhalation

injury
 Independent predictor of mortality, ↑ by 20%
 Increases pneumonia risk
 Leading diagnosis of those hospitalized and
treated on 9/11, World Trade Center attack
 Anatomic Classification

 Upper airway
 Lower airway

 Systemic toxicity

http://www.monroecc.edu/depts/pstc/backup/parasan4.htm
 SMOKE
 Variable, changes with time burning
 Toxic gases and low ambient oxygen
 Ingredients:
Aldehydes (formaldehyde, acrolein), ammonia,
hydrogen sulfide, sulfur dioxide, hydrogen chloride,
hydrogen fluoride, phosgene, nitrogen dioxide, organic
nitriles
 Particulate matter

Prien et al. Burns 1988; 14:451-460

 Pathophysiology
 Cilia loss, respiratory epithelial sloughing
 Neutrophilic infiltration
 Atelectasis, occlusion by debris/edema
 Pseudomembranes
 Bacterial colonization at 72 hrs

Hubbard et al. J Trauma 1991; 31:1477-1486

Bartley et al. Drug Design, Development and
Therapy. 2008; 2: 9–16.
 Secondary Lung Injury
 Unilateral smoke inhalation damages
contralateral lung
 Immune response, increased permeability
 Oxygen-derived free radicals
 NO mediated damage (chemotactic factor neuts)
 Eiscosanoids (TXA2→TXB2)
 Reduced phagocytosis in macrophages
 Systemic Effects

 Larger fluid resuscitation (2→5cc/kg/%)

 Additive effect to burns
 12% pts inhalation injury alone require
intubation*
 62% pts burn + inhalation injury intubated*

Clark et al. J Burn Care Rehabilitation, 1990; 11:121-134

Miller et al. Journal of Burn Care Research. 2009; 30(2) 249-256
 Diagnosis
 Clinical findings:
 Facial burns (96%)
 Wheezing (47%)
 Carbonaceous sputum (39%)
 Rales (35%)
 Dyspnea (27%)
 Hoarsness (26%)
 Tachypnea (26%)
 Cough (26%)
 Cough and hypersecretion (26%)

DiVincenti et al. Journal of Trauma, 1971; 11:109-117

 NO ONE FINDING IS
SUFFICIENTLY SENSITIVE
OR SPECIFIC!

Must use clinical judgment!

 Tools for Diagnosis

 Bronchoscopy
 Pulmonary function testing
 Xenon133 lung scan
Grades of Inhalation Injury

Endorf and Gamelli. Journal of Burn Care and Research. 2007; 28:80-83
 Treatments
 Airway Control
 Chest physiotherapy
 Suctioning
 Therapeutic bronchoscopy
 Ventilatory strategies
 Pharmacologic adjuncts
 Treatment
Control the Airway!!!
 ≥ 40% burn
 Transport

http://www.burnsurgery.com/Betaweb/Modules/initial/bsinitialsec2.htm
 Ventilator Strategies
 Airway pressure release ventilation (APRV)
 Intrapulmonary percussive ventilation (IPV)
 High-frequency percussive ventilation (HFPV)
 High frequency oscillatory ventilation (HFOV)
 Single center, prospective randomized trial 2006-2009
 387 pts screened
 31 pts HFPV, 31 pts LTV (ARDSnet)

Chung et al. CCM; 2010: 38(10) 1970-1977

 Results
 No significant difference in mortality or ventilator free
days
 Significant difference in “Rescue Therapy”
 Results
 No significant difference in mortality or ventilator free
days
 Significant difference in “Rescue Therapy”
P/F ratio vs Ventilator Mode

Chung et al. CCM; 2010: 38(10) 1970-1977

 Study Conclusions
 Study stopped for safety concerns in LTV group
 Gas exchange goals met in all HFPV pts, and
not in 1/3 of LTV pts
 Trend for less barotrauma, less VAP, less
sedation
“Strict application of LTV may be suboptimal
in the burn population”
Pharmacologic Intervention

Bartley et al. Drug Design, Development and Therapy. 2008; 2: 9–16.

Pharmacologic Intervention

Bartley et al. Drug Design, Development and Therapy. 2008; 2: 9–16.

 Airway Obstructive Casts
 Mucus secretions
 Denuded airway epithelial cells
 Inflammatory cells
 Fibrin
 -Solidifies airway content
 Several studies shown reduction in size of casts
with fibrinolytic agents (tPA)
 Casts

Enkhbaatar et al., 2007

Theory Behind Inhaled Heparin
 Animals with Burn + ARDS have decreased
levels of antithrombin in plasma and BAL
specimens
 Heparin potentiates antithrombin by 2000x
 Prevention of fibrin deposition in lungs
 Heparin inhibits antihrombin’s anti-
inflammatory effect - ? systemic rhAT ?
 Shriners Protocol
Since 1990 (560+ patients treated)

Mlcak RP et al. Burns, 2007;33:2-13

 Evidence (Pro)
 Desai et al. 1998
 Pediatric burns (90 pts total)
 1985-1989 (43) vs 1990-1994 (47pts)
 ↓ reintubation, atelectasis, and mortality
 Miller et al. 2009
 30 patients over 5 years, retrospective review
 Tx 10,000 units heparin, 20% NA, 0.5 ml AS q4 hrs
 Survival benefit, improved LIS scores, compliance
 Number needed to treat 2.73
 Evidence (Con)
 Holt et al. 2008
 Retrospective review 1999-2005, 150 pts total
 Burn size, LOS, time on vent, mortality SAME
 Only 68% pts had bronchoscopy,
 Attending discretion which treatment to use
TOXIC GASES
 Carbon Monoxide (CO)

 CO from incomplete combustion

 CO + Hb → COHb (affinity 200-250x)
 LEFT shift of oxy-Hb curve (Haldane effect)
 CO binding to intracellular cytochromes and
metalloproteins (myoglobin)
 “Two compartment” pharmacokinetics
 Animal experiment 64% COHb transfusion
 CO Toxicity Symptoms

 “Cherry-red lips, cyanosis, retinal hemorrhage”-

rare
 CNS and Cardiovascular
 ↑ RR, ↑HR, dysrhythmias, MI, ↓BP, coma, seizures
 Delayed neuropsychiatric syndrome (3-240d)
 Cognitive/personality changes/parkinsonianism
 Spontaneous resolution
Signs and Symptoms

Weaver LK. N Engl J Med 2009;360:1217-25.

 CO Toxicity Diagnosis
 Pulse oximetry false COHb Symptoms
HIGH SpO2 %
 Need cooximetry direct 0-5 Normal

measurement of 15-20 Headache, confusion,

fatigue
COHb
 Older ABG analyzers (estimate 20-40 Hallucination, vision
off dissolved PO2) Δ’s
40-60 Combative, coma
 MRI – lesions globus
pallidus/basal 60 + Cardiopulmonary
ganglia/deep white arrest
matter
 CO Toxicity Diagnosis
 Pulse oximetry false COHb Symptoms
HIGH SpO2 %
 Need cooximetry direct 0-5 Normal

measurement of 15-20 Headache, confusion,

fatigue
COHb
 Older ABG analyzers (estimate 20-40 Hallucination, vision
off dissolved PO2) Δ’s
40-60 Combative, coma
 MRI – lesions globus
pallidus/basal 60 + Cardiopulmonary
ganglia/deep white arrest
matter
 CO Toxicity Treatment
 OXYGEN
 Half-life COHb (min)

RA 100% 100% O2
1ATM O2 2.5 ATM
Male 240 47 22

Female 168 33 15

 Carbogen – normobaric, normocapnic, hyperventilation (4.5-

4.8% CO2)
 Hyperbaric oxygen???
 Cyanide (CN)
 Combustion of synthetics (plastics, foam, varnish,
paints, wool, silk)
 Binds to cytochrome c oxidase – dose dependent
 Uncouple mitochondria
 Aerobic → anaerobic = Lactic acid
 Half-life 1-3 hours
 CN Toxicity Symptoms
 Dyspnea
 Tachypnea
 Vomiting
 Bradycardia
 Hypotension
 Giddiness/Coma/Siezures
 Death
* The smell of bitter almonds on the breath suggests exposure
(cannot be detected by 60% of the population)
 CN Toxicity Diagnosis
 No rapid assay
 High lactate (>10mmol/L) (s/s, 87%/94%)

 Metabolic acidosis

 Elevated mixed venous saturation (<10% a-v)

difference
 High index of suspicion

** Also get: COHb and Methemoglobin levels

 CN Treatment

Cyanokit (Hydroxocobalamin)
 70mg/kg dose (5g vials)
 Combines with cyanide to from cyanocobalamin (Vit B12)

 Red membranes/urine

 Hypertension, Anaphylaxis

 5% increase COHb, interfere with HD

LFTs/Cr/Fe levels
 Cyanide Antidote Kit (CAK)
Amyl nitrite pearls, sodium nitrite, and sodium thiosulfate

 Amyl nitrate and sodium nitrate induce methemoglobin

 Methemoglobin+cyanide→releases cyanide from CC
 Sodium thiosulfate enhances cyandide→thiocynate→renal
excretion
 Avoid nitrate portion in pts with inhalation injury
(COHb >10%)
 Vasodilation and hypotension
 Acquired Methemolgobinemia
 NO2, NO, benzene gases → oxidation of iron
 Fe2+ → Fe3+
 Shift curve to LEFT
 Blood “Chocolate brown color”
 Normal PaO2, pulse ox >85%
 Tx: Methylene blue (1-2 mg/kg Q 30-60min)
 Final Thoughts
 Inhalation injury is bad
 Support the airway
 Frequent bronchoscopy and monitoring
 Different ventilatory strategies
 Adjunctive measures need further investigation
The Toilet Snorkel

http://www.icbe.org/2006/01/18/the-toilet-snorkel/
Thank You!
 Learning Objectives
 Describe the pathophysiology of inhalation
injury
 How is inhalation injury diagnosed?
 What adjunctive measures are used to treat
inhalation injury?
 What is the treatment for carbon monoxide and
cyanide poisoning?