Inhalation Injury - University of Colorado Denver

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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

Xenon 133 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 SpO

2

Need cooximetry direct measurement of

COHb

Older ABG analyzers (estimate off dissolved PO

2

)

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 SpO

2

Need cooximetry direct measurement of

COHb

Older ABG analyzers (estimate off dissolved PO

2

)

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

Male 240

Female 168

100%

O

2

47

100% O

2

2.5 ATM

22

33 15

Carbogen – normobaric, normocapnic, hyperventilation (4.5-

4.8% CO

2

)

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

Fe 2+ → Fe 3+

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?

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