Low Temperature Damage
Also known as: Frostbite
Introduction
Frostbite refers to damage or injury to the skin and body tissues resulting from their freezing following exposure to excessive cold.
Severe frostbite is a grave physiological condition with potentially life-threatening consequences.
All species are susceptible, but neonates are at greatest risk due to thin skin and lack of subcutaneous fat stores. Avian species endogenous to warm climates but kept in temperate areas are most susceptible to frostbite.
Frostbite may be primary or secondary to an underlying disease which compromises the animal's resistance to cold. For instance sick calves may suffer from the condition despite adequate housing and nutrition.
Cold injury most commonly affects ears, tail, teats, scrotum and distal extremities (feet and lower limbs).
Tissue damage is substantially increased if thawing is followed by refreezing (freeze-thaw-freeze-thaw syndrome). Tissue previously damaged by freezing is more susceptible to injury on subsequent exposure to cold temperatures.
Pathphysiology
The four phases describing the mechanism of cellular injury are:
- Phase I (pre-freeze phase): congestion and leakage of fluid from the vascular compartment due to arterial constriction and venous dilation.
- Phase II (freeze-thaw phase): extracellular ice crystal formation causes cell membrane rupture and cellular dehydration.
- Phase III (vascular stasis phase): more severe arterial spasm and venous dilation leading to tissue hypoxia
- Phase IV (ischemia phase): tissue damage due to prolonged tissue hypoxia
Additional injury occurs during rewarming. Damaged mast cells release histamine which leads to capillary hyperpermeability and interstitial oedema. Subcutaneous haemorrhages can also occur and the skin develops vesicles.
Direct cellular destruction, release of catecholamines and tissue anoxia have potentially significant secondary effects in severe frostbite cases, resulting in damage to other organs.
Clinical signs
Mild frostbite causes blanching of tissue and reduced sensation followed by painful erythema, scaling and alopecia.
Severe frostbite results in necrosis, dry gangrene and sloughing of the affected parts.
Death from low core body temperature can result if not treated before vital organs are affected.
A line of demarcation between viable and non-viable tissue usually appears within 3 days of rewarming affected areas and becomes more distinct within 7 days.
Vesicles and blisters can develop on the affected area.
Diagnosis
This is based on the history and the appearance of the skin and tissue on the affected area.
Differential diagnoses include: traumatic injury, tissue damage from ergot toxicosis.
To avoid frostbite, long-legged birds reduce peripheral circulation to their limbs, which can result in skin lesions such as cracking and low-grade bacterial infections.
Treatment
Initial treatment involves rapid rewarming of the affected area in a water bath at a temperature of between 39°c and 42°c. Rewarming is continued until circulation is adequate.
The affected areas will become oedemateous and erythematous and rapid rewarming may be painful, but results in less cellular and tissue damage than slow rewarming.
Trauma and self-mutilation is prevented if possible, but bandaging of the areas is not recommended.
Conservative treatment is indicated until there is clear demarcation of viable and non-viable tissue, unless infection develops.
Dry gangrene and sloughing develop.
Systemic anti-inflammatories and topical agents such as aloe vera creams have been found to reduce the amount of tissue loss and the length of hospitalisation in small animals.
References
| Low Temperature Damage Learning Resources | |
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 Test your knowledge using flashcard type questions |
Avian Medicine Q&A 22 |
Slatter, D. (2002) Textbook of small animal surgery Elsevier Health Sciences
Haskell, S. (2008) Blackwell's five minute veterinary consult: ruminant John Wiley and Sons
Radiostits, O. (2000) Veterinary clinical examination and diagnosis Elsevier Health Sciences