Transcript Inhalation Injury - University of Colorado Denver

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 antiinflammatory 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
HIGH SpO2
Need cooximetry direct
measurement of
COHb


Older ABG analyzers (estimate
off dissolved PO2)
MRI – lesions globus
pallidus/basal
ganglia/deep white
matter
COHb Symptoms
%
0-5
Normal
15-20
Headache, confusion,
fatigue
20-40
Hallucination, vision
Δ’s
40-60
Combative, coma
60 +
Cardiopulmonary
arrest
CO Toxicity Diagnosis


Pulse oximetry false
HIGH SpO2
Need cooximetry direct
measurement of
COHb


Older ABG analyzers (estimate
off dissolved PO2)
MRI – lesions globus
pallidus/basal
ganglia/deep white
matter
COHb Symptoms
%
0-5
Normal
15-20
Headache, confusion,
fatigue
20-40
Hallucination, vision
Δ’s
40-60
Combative, coma
60 +
Cardiopulmonary
arrest
CO Toxicity Treatment

OXYGEN

Half-life COHb (min)


RA
1ATM
100%
O2
100% O2
2.5 ATM
Male
240
47
22
Female
168
33
15
Carbogen – normobaric, normocapnic, hyperventilation (4.54.8% 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?