Smoke inhalation injury causes damage to the lungs and systemic toxicity. It occurs in 17% of burn patients and increases mortality up to 24%. Diagnosis is clinical with bronchoscopy and other tests. Treatment involves airway management, cardiovascular support, antibiotics, steroids, and treatments for carbon monoxide and cyanide poisoning. Complications include respiratory failure, infections, and long term lung damage. Prognosis depends on factors like burn severity and lung injury score. Close monitoring is needed due to the progressive nature of inhalation injury.

1. INHALATION INJURY
BY
DR. LAWAL GBENGA
SNR REGISTRAR, PLASTIC AND RECONSTRUCTIVE UNIT
DEPARTMENT OF SURGERY
NATIONAL HOSPITAL ABUJA
23TH APRIL 2019

2. OUTLINE
• INTRODUCTION
• EPIDERMIOLOGY
• RELEVANT ANATOMY
• AETIOPATHOGENESIS
• MANAGEMENT
• PROGNOSIS
• CONCLUSION

3. INTRODUCTION
• Inhalation injury causes a heterogeneous cascade of insults that increase
morbidity and mortality among the burn population.
• Manifests within the first 5 days after injury.
• Despite major advancements in burn care for the past several decades,
there remains a significant burden of disease attributable to inhalation
injury.
• Smoke inhalation injury can be defined as damage caused by breathing in
harmful gases, vapours, and particulate matter contained in smoke
• It can manifest as thermal injury, chemical injury, and as systemic toxicity,
or any combination of these.

4. EPIDERMIOLOGY
• In the U.S.A., more than 1 million burn injuries occur every year.
• Inhalation injury is present in 17% of patients with flame burns
• Increases the overall mortality rate of these patients up to 24%, compared with the
mortality of burn patients without inhalation injury which is (on average) 3%.
• Incidence increase in extremes of age, and in those with physical or cognitive abilities,or
under influence of drugs and alcohol
• 12% patient inhalation injury alone require intubation
• 62% patient burn + inhalation injury intubated
• The presence of smoke inhalation injury prolongs the length of hospital stay 2.5-fold
compared to those without smoke inhalation injury (24 days vs. 10 days)

5. RELEVANT ANATOMY

6. AETIOPATHOGENESIS
• Inhalation injury occurs following fire incidence in enclosed spaces or poorly
ventilated arena, and where the victim is trapped.
Components of smoke
• Unique to each fire depending on the materials present, the available oxygen
and the nature of the combustion.
• Upto 150 toxic compounds already identified;
major compounds include carbon dioxide, carbon monoxide, Aldehydes
(formaldehyde, acrolein), ammonia, hydrogen sulfide, sulfur dioxide,
hydrogen chloride, hydrogen fluoride, phosgene, nitrogen dioxide, organic
nitriles
Three mechanisms of injury:
- Heat
- Particulate matter deposition
- Asphyxiation and systemic toxicity

9. AETIOPATHOGENESIS
Summary,
• Cilia loss, respiratory epithelial sloughing
• Neutrophilic infiltration
• Atelectasis, occlusion by debris/edema
• Pseudomembranes / fibrin and mucous casts
• Bacterial colonization at 72 hrs

10. Systemic Effects
CO Poisoning
• Most common cause of poisoning death and most common cause of fire
related death; generated through incomplete combustion of carbon
containing products
• Tissue asphyxiants released during combustion include CO and hydrogen
cyanide
• CO is rapidly transported across the alveolar membrane and binds
preferentially to Hb, which can be directly measured by co-oximetry
• HgCO shifts the oxyhemoglobin dissociation curve to the left, impairing
unloading of oxygen at the tissues
• With prolonged exposure, CO saturates cells and binds to cytochrome
oxidase, uncoupling mitochondrial oxidative phosphorylation and
decreasing APT production, resulting in metabolic acidosis

11. Systemic Effect

12. Systemic Effects
Hydrogen Cyanide
• Hydrogen cyanide is a combustion product of natural and synthetic materials
• Colourless gas with a bitter almond odour which only 40% of the population
are able to detect
• 20 times more toxic than CO
• Cyanide is rapidly absorbed and distributed to tissues
• Within seconds, it impairs the electron transport chain and inhibits oxidative
metabolism, by binding to ferric ion in cytochrome a3 oxidase in mitochondria
with high affinity
• Poisoned tissue rapidly deletes itself of ATP, then ceases to function causing
coma, seizures, cardiovascular collapse, and severe metabolic acidosis
• Presence of CO and cyanide has a synergistic effect of asphyxia

13. MANAGEMENT
• POINT OF RESCUE – 100% oxygen
• PRIMARY SURVEY – quick assessment - need for
immediate intubation?, level of consciousness;
bare in mind presence of associated injuries
Clinical findings suggestive of inhalation injury:
• Facial burns (96%)
• Wheezing (47%)
• Carbonaceous sputum (39%)
• Rales (35%)
• Dyspnea (27%)
• Hoarsness (26%)
• Tachypnea (26%)
• Cough (26%)
• Cough and hypersecretion (26%)

14. Diagnosis
• Clinical judgement supercedes
• Bronchoscopy
– Fiberoptic Bronchoscopy (gold standard, 86% accuracy)
• Limitations of Fiberoptic Bronchoscopy
– Direct and Fiberoptic Laryngoscopy
• Pulmonary function testing
• Xenon133 lung scan

15. Grades of Inhalation Injury

16. DIAGNOSIS
• Other Diagnostic Studies
– Blood Gas analysis
– Full blood count
– Pulse Oximetry
– Non-invasive Pulse CO-Oximetry
– Lactic Acid level
– Cyanide Testing
– Electrocardiogram
– Chest X-Ray
– Lavage M/C/S

17. TREATMENT
Principles (managed in a burn centre)
• Airway Management
• Cardiovascular Support
• Medical Adjuncts
• Treatment for Carbon Monoxide Poisoning
• Treatment for Cyanide Poisoning
• Monitoring

18. TREATMENT
AIRWAY MANAGEMENT
• Early intubation, and PEEP ventilation
• A regimen of aerosolized heparin to alternate
with 20% N-acetylcysteine 2-4 hourly
• Nebulized Salbutamol 2-4 hourly
• Chest physiotherapy and regular respiratory
toilet
CARDIOVASCULAR SUPPORT
• IVF regimen using Parkland formula – more fluid required clinical jugdement
essential
MEDICAL ADJUNCTS : Antibiotics and steroid used controversial

19. TREATMENT
CO TREATMENT
• CO is displaced from Hb by the administration of supplemental oxygen
• The half-life of HbCO in air is 4-6 hours and inversely related to PaO2
• Breathing 90-100% O2 at 1 atmosphere reduces the half-life to 60-90
min
• Breathing 100% O2 at 3 atmospheres reduces the half-life to 30 min
• HBO is more effective at removing CO from mitochondrial
cytochromes
• CO levels do not correlate with outcomes
• The HBO controversy

20. TREATMENT
HYDROGEN CYANIDE POISONING
• Cyanide is detoxified in the liver by sulfur transferase to thiocyanate, then
excreted by the kidney, regenerating methemoglobin from
cyanomethemoglobin
• Surrogate marker of toxicity is lactate > 10 mmol/L
• Goal of therapy is to reactivate the cytochrome oxidase system by providing
an alternative high affinity source of ferric ions for cyanide to bind
• IV Hydroxocobalamin – forms Cyanocobalamin, renally excreted
• Nitrites by inhalation (amyl nitrite) or IV infusion (sodium nitrite) – forms
cyanomethemoglobin
• IV sodium thiosulfate is then to convert cyanide to thiocyanate

21. TREATMENT
• Special Populations
– Pregnant Patients

22. COMPLICATIONS
• Acute respiratory distress syndrome and respiratory failure needing ventilator
support
• ventilator-associated complications such as barotrauma and pneumonia.
• Infectious complications such as tracheobronchitis, bronchiectasis, bronchiolitis
obliterans, and pneumonia can develop in 38%–60% of the victims, after 3–10
days of smoke inhalation injury, and are associated with a mortality of up to
60%.
• Hyper-reactive air way for up to 6 months after extubation.
• Damage to the larynx by inhaled toxins or prolonged intubation can cause
persistent hoarseness or dysphonia.
• The injury to epithelium of upper airway from initial injury - tracheoesophageal
fistula, tracheomalacia, late subglottic stenosis, or tracheobronchial polyps.
• Smoke inhalation injury leads to severe restrictive ventilatory dysfunction which
may persist for many months.

23. PROGNOSIS
• Abbreviated Burn Severity Index
• Lung injury score

24. PROGNOSIS

25. CONCLUSION
• Smoke inhalation injury portends increased morbidity and
mortality in fire-exposed patients..
• Fibreoptic Bronchoscopy is the standard diagnostic tool, but
Clinicians should maintain a high index of suspicion for
concomitant traumatic injuries.
• Diagnosis is mostly clinical, aided by bronchoscopy and other
supplementary tests.
• Treatment is largely supportive.
• Due to its progressive nature, many patients with smoke
inhalation injury warrant close monitoring for development of
airway compromise.

26. References
• Grab and Smith, 7th ed
• Clark et al. J Burn Care Rehabilitation, 1990; 11:121-134
• DiVincenti et al. Journal of Trauma, 1971; 11:109-117
• Endorf and Gamelli. Journal of Burn Care and Research. 2007; 28:80-83
• https://emedicine.medscape.com/article/771194-overview
• https://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=572
• https://www.jems.com/articles/print/volume-39/issue-10/features/treating-smoke-inhalation-and-
airway-bur.html
• DiVincenti et al. Journal of Trauma, 1971; 11:109-117
• https://www.thechildren.com/sites/default/files/PDFs/Trauma/inhalation-injury.pdf
• https://academic.oup.com/jbcr/article-abstract/37/1/1/4582069?redirectedFrom=fulltext
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5879861/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5959399/
• https://journals.lww.com/annalsplasticsurgery/Abstract/2018/03002/Inhalation_Injury_in_the_Bur
ned_Patient.5.aspx
• https://journals.lww.com/annalsplasticsurgery/Abstract/2018/03002/Carbon_Monoxide_and_Cyan
ide_Poisoning_in_the.6.aspx
• https://accessmedicine.mhmedical.com/content.aspx?bookid=1344&sectionid=81195361