Burns in Horses (Equis) | Vetlexicon
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Burns

ISSN 2398-2977


Introduction

  • Cause: contact with fire, hot solutions, chemicals, electrocution, or lightning strike.
  • Signs: coat scorching or covered in soot, skin lesions of variable extent and degree, blepharospasm and epiphora, coughing, dyspnea, weakness, signs of shock, collapse, death.
  • Diagnosis: history and physical examination. Additional laboratory data and diagnostic imaging.
  • Treatment: patient stabilization followed by appropriate wound management.
  • Prognosis: good to poor depending on extent and degree of lesions.

ℹ️Print off the factsheet on Burns to give to your clients.

Presenting signs

  • Coat scorching or covered in soot.
  • Varying degrees of skin injury from erythema to skin sloughing with or without involvement of underlying tissues.
  • Corneal damage: blepharospasm, epiphora.
  • Pulmonary involvement due to smoke inhalation Smoke inhalation with dyspnea Respiratory: dyspnea and coughing Coughing.
  • If the burns are severe and extensive:
    • Weakness.
    • Tachycardia.
    • Dehydration.
    • Shock.
    • Collapse.

Geographic incidence

  • Worldwide.

Cost considerations

  • Loss of animal.
  • Treatment.

Special risks

  • Animals with pulmonary involvement and/or severe/extensive burns will be a high anesthetic risk.

Pathogenesis

Etiology

  • Possibilities include:
    • Horse trapped within a burning barn/stable.
    • Road traffic accident.
    • Electrocution or lightning strike Lightning strike.
    • Contact with hot water or chemicals.

Pathophysiology

  • The extent of tissue damage depends upon temperature, duration of exposure, local wound environment, and blood supply.
  • Severe burns are followed by “burn shock” which resembles hypovolemic shock Hypovolemic shock: a dramatic increase in vascular permeability and release of various mediators (cytokines, prostaglandins, NO, vasoactive leukotrienes, serotonin, histamine and ROS.
  • Massive protein coagulation and cellular death.
  • Fluid, protein, and inflammatory cells accumulate in the wound followed by thrombosis, dermal ischemia and further tissue damage continuing for 24-48 h.
  • Circulating myocardial depressant factors cause a decrease in cardiac output that associated with the fluid and protein loss into the extravascular space leads to hypovolemia.
  • Decreased tissue perfusion and organ failure follow.
  • Electrolyte disturbances: hyperkalemia occurs in the acute phase, followed by potassium deficit in the following 3-5 days.
  • The metabolic rate is increased in proportion to the size of injury exceeding 1% of the body.
  • Injured animals are prone to secondary infection.

Timecourse

  • Tissue damage and related systemic effects can continue for up to 5 days.
  • Convalescence in severe cases may take up to 2 years.

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.
  • Leise B S (2018) Topical wound medications. Vet Clin Equine 34 (3), 485-498 PubMed.
  • Marsh P S (2007) Fire and smoke inhalation injury in horses. Vet Clin Equine 23 (1), 19-30 PubMed.
  • Hanson R R (2005) Management of burn injuries in the horse. Vet Clin Equine 21 (1), 105-123 PubMed.

Other sources of information

  • Hanson R R (2009) Burn Injuries. In: Equine Wound Management. 2nd edn. Eds: Stashak T S & Theoret C L.  John Wiley & Sons Inc, USA. pp 569-584.