ISSN 2398-2993      

Smoke inhalation

obovis
Contributor(s):

Ash Phipps

Lisa Whitfield


Introduction

  • Cause: smoke inhalation from a fire (commonly from a bush or grass fire but also a barn fire).
  • Signs: in the acute phase, upper respiratory signs predominate followed by lower respiratory signs in the medium to longer term.
  • Diagnosis: diagnosis is based upon history of exposure to a fire event and concurrent clinical signs observed.
  • Treatment: euthanasia of severely affected animals. Treatment includes oxygen therapy (+/- intubation or tracheostomy), analgesia, NSAID, diuretics, fluid therapy, plasma transfer, appropriate nutrition, and antimicrobial therapy based on culture and sensitivity.
  • Prognosis: the prognosis for mild cases with early treatment intervention is good. More severely affected patients that develop bronchopneumonia or have severe burns (exceeding 15% of total body surface area) have a guarded to poor prognosis.

Pathogenesis

Etiology

  • Smoke inhalation and thermal exposure from a fire event; commonly from a bush or grass fire or a barn fire.

Pathophysiology

  • Smoke inhalation injury is a result of a combination of thermal injury to airways, carbon monoxide poisoning, and chemical injury to the airways.

Thermal injury to the airways

  • The heat from the fire event causes direct injury to the upper airways which results in edema and obstruction.

Carbon monoxide poisoning

  • Carbon monoxide poisoning affects oxygen exchange at the level of the hemoglobin (Hb) molecule. Carbon monoxide (CO) has a far greater affinity for hemoglobin than does oxygen. Therefore, it effectively out-competes the oxygen molecules for the hemoglobin binding sites, resulting in the formation of carboxyhemoglobin and reduced oxygen carrying capacity of the hemoglobin molecules.
  • CO binding to Hb also changes the stability of the hemoglobin molecule (known as the R-state). This change increases the affinity for oxygen of other sites within the Hb tetramer, which further reduces the ability of the hemoglobin molecule to release and deliver oxygen to tissues.
  • In human and canine studies, neither the clinical severity nor the clinical improvement of CO-poisoned patients directly correlates with the blood COHb level or COHb clearance.
  • In addition to Hb, CO binds to other heme-containing proteins, including myoglobin in heart and skeletal muscle.
  • CO also affects mitochondria and results in decreased ATP production in tissues such as the brain and heart.
  • Neurological signs, such as ataxia can develop secondary to hypoxia.

Chemical injury to the airways

  • Inhalation of chemicals, especially combustion products (such as hydrochloric acid, hydrogen cyanide, aldehydes, and sulfuric acid) can cause a pulmonary ventilation/perfusion mismatch. This occurs through the direct chemical injury to the airways causing severe tracheobronchitis, edema of the epithelial mucosa, mucosal sloughing, bronchoconstriction, decreased mucociliary transport, and altered surfactant action.
  • Particulate matter (such as soot) that is inhaled can line the upper and lower respiratory tract.

Timecourse

  • The timecourse can be influenced by the duration of exposure and chemicals within the smoke inhaled:
    • Initially upper airways damage and bronchoconstriction occurs within 6 h of exposure.
    • Development of pulmonary edema in 12-72 h post-exposure.
    • Development of bronchopneumonia in 24 h to 3 weeks post-exposure.

Epidemiology

  • Large numbers of animals can be affected during a fire event, particularly bush fire, grass fire and farm building fires.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Eid B, Beggs D & Mansell P (2021) The impact of bushfire smoke on cattle - A review. Animals 11 (3), 848 PubMed.
  • Jayanthi N, Saahithya R, Balachandran C & Pazhanivel N (2018) Death due to smoke inhalation in a cow. Int J Sci Envir Tech 7 (3), 920-924 IJSET (pdf download).
  • Rose J J (2016) Carbon Monoxide Poisoning: Pathogenesis, Management and Future Directions of Therapy. Am J Resp Crit Care 195 (5), 596-606 PubMed.
  • Hanson R R (2005) Management of burn injuries in the horse. Vet Clin Equine Pract 21 (1), 105-123 PubMed.
  • Neathery M W & Miller W J (1975). Metabolism and toxicity of cadmium, mercury, and lead in animals: a review. J Dairy Sci 58 (12), 1767-1781 PubMed.

Other sources of information

  • Beaupied B L, Martinez H, Martenies S et al (2021) Cows as Canaries: The effects of Ambient Air Pollution Exposure on Milk Production and Somatic Cell Count in Dairy Cows. Environmental Research.192-197.
  • Burkitt-Creedon J (2019) Treating Environmental Lung Injuries: Drowning and Smoke Inhalation. Today’s Veterinary Practice. Website: todaysveterinarypractice.com.
  • Hegazy A M, Khalifa M I & Nasr S M (2019) Monitoring of Carcinogenic Environmental Pollutants in raw cows’ milk. Biomed Pharmacol J 12 (1), 435-442.
  • Malmo J (2015) Assessment of Cattle Burnt in Bushfires. In: Proc Australian Cattle Veterinarians and Australian Sheep Veterinarians (ACV/ASV) Annual Conference. Hobart, Australia. pp 202-205.
  • Haskell S R (2011) Ed Blackwell's Five-Minute Veterinary Consult: Ruminant. Wiley & Sons, USA. pp 164-167.
  • Parkinson T J, Vermunt J J & Malmo J (2010) Diseases of Cattle in Australasia: A Comprehensive Textbook. New Zealand Veterinary Association Foundation for Continuing Education. pp 1119-1120.
  • Fries F, McCollum T & Gill R (2009) Cattle Escaping Fire Death may have Secondary Injuries - AgriLife Extension Consult Veterinarian to Identify Other Problems. AgriLife Today. Texas A&M, USA. Website: agrilifetoday.tamu.edu.
  • Radostits O M, Gay C, Hinchcliff K W & Constable P D (2006) Eds General Systemic States: Bushfire (Grassfire) Injury (Thermal burns) in Veterinary Medicine: A Textbook of the Diseases of Cattle, Horses, Sheep, Pigs and Goats. Elsevier, USA. pp 1792-1793.

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