ISSN 2398-2993      

Burns

obovis
Contributor(s):

Ash Phipps

Lisa Whitfield


Introduction

  • Cause: thermal injury from a fire (commonly from a bush fire or grass fire or a barn fire).
  • Signs: varied from, mild erythema and superficial scabbing of the skin to severe extensive tissue damage, necrosis, and protein exudation. Affected animals can be divided into 4 categories to optimise management of cases.  
  • Diagnosis: based on clinical signs and history of exposure to a fire event.
  • Treatment: treatment varies based on clinical category and the burns degree classification.
  • Prognosis: varies depending on the severity of injuries.

Pathogenesis

Etiology

  • Thermal injury from a fire, commonly from a bush or grass fire or a barn fire).
  • Thermal injury associated with dehorning/disbudding Disbudding and dehorning.

Pathophysiology

  • Burns patients experience an array of pathophysiological effects.
  • Cardiovascular “burns” shock (hypovolemic shock):
    • The physiological effect of burns shock is due to diffuse increase in capillary permeability which occurs as a result of heat and the release of inflammatory mediators including histamine, cytokines, nitric oxide, prostaglandins, oxygen free radicals, leukotrienes, thromboxane and serotonin.
    • Initially, there is a reduction in cardiac output due to circulating levels of myocardial depressant factors.
  • Ischemic injury:
    • At the local level, there is extensive tissue damage from immense protein coagulation and cellular death.  The arteries and veins constrict, the capillary beds dilate and have increased permeability because of inflammatory mediators released by tissue destruction.
    • There is ischemic injury from vascular thrombosis which may continue for 24-48 hours post insult.
  • Fluid loss and hypoproteinemia:
    • There is an accumulation at the site of the insult, as well as loss from the body of the following components: inflammatory cells, fluid, and protein including albumin.
    • With fluid and protein accumulation/loss, protein concentrations can reach 3 g/dL in the extracellular space, which can shift the osmotic gradient and lead to edema in the tissues. This greatly contributes to the reduced circulatory blood volume.
  • Organ failure:
    • With a reduction on circulatory blood volume and cardiac output there is a concurrent increase in peripheral and pulmonary vascular resistance and reduced peripheral tissue perfusion which all can lead to diffuse organ failure.
  • Electrolyte imbalances:
    • Affected patients can experience electrolyte abnormalities, particularly hyperkalemia, as a results of fluid loss and cellular damage. Hypernatremia may occur as a result of the sodium retention. Sodium and potassium: overview
  • Anemia:
    • Anemia Anemia: overview can occur in patients with burns exceeding 30% of the total body surface area due to erythrocyte destruction, wound hemorrhage, and splenic sequestration of erythrocytes.
  • Thrombocytopenia:
    • Thrombocytopenia may result from platelet aggregation on damaged capillary endothelium and hemorrhage.
  • Immunosuppression and increased infection risk:
    • Affected patients experience immunosuppression through a combination of reduced serum immunoglobulin levels (especially at day 2 post-burns event) and impaired neutrophil function. This results in a patient that is prone to infection.
  • Increased metabolic demand:
    • The metabolic rate of burns patients is increased, particularly when burns >10% total surface body area is involved, due to a rise in core body temperature of 1-2°C/33.8-35.6°F. With a rise in body temperature, there is increased oxygen consumption, adipose breakdown, and protein catabolism and glucose use.

Timecourse

  • Acute exposure to a fire event.

Epidemiology

  • Large numbers of livestock can be affected with varying degrees of thermal injuries in a fire event, particularly bush and grass fire events. Particularly if the exposed animals have been unable to flee due to fences or confined in a building.  

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.
  • Hanson R R (2005) Management of burn injuries in the horse. Vet Clin Equine Pract 21 (1), 105-123 PubMed.

Other sources of information

  • Malmo J (2015) Assessment of Cattle Burnt in Bushfires. In: Proc Australian Cattle Veterinarians & 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
  • Radostits O M, Gay C, Hinchcliff K W & Constable P D (2006) Eds Chapter 4 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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