Difference between revisions of "Low Temperature Damage"

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(Created page with "*Prolonged cold can cause ice crystal formation and vascular injury resultic in damage to tissue due to increased intracellular salt concentration *Slow chilling can cause vasoco...")
 
 
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*Prolonged cold can cause ice crystal formation and vascular injury resultic in damage to tissue due to increased intracellular salt concentration
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*Slow chilling can cause vasoconstriction, cellular damage -> secondary vasodilation and increased permeability -> oedema
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Also known as: '''''Frostbite'''''
*Severe and persistent cold causes vasoconstriction, increase in blood viscosity and tissue anoxia
 
*Lesions may occur in wet or hypoglycaemic neonates or animals recently moved from warm to cold environment
 
*Areas affected are extremities
 
*Lesions consist of [[Necrosis - Pathology#Gangrene|gangrene]] and necrotic tissue
 
  
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==Introduction==
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Frostbite refers to '''damage or injury to the skin and body tissues''' resulting from their freezing following exposure to '''excessive cold'''.
  
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Severe frostbite is a grave physiological condition with potentially '''life-threatening consequences'''.
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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 very susceptible to frostbite.
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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.
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Cold injury most commonly affects '''ears, tail, teats, scrotum and distal extremities''' (feet and lower limbs).
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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.
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==Pathophysiology==
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The four phases describing the mechanism of cellular injury are:
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:Phase I (pre-freeze phase): congestion and leakage of fluid from the vascular compartment due to arterial constriction and venous dilation.
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:Phase II (freeze-thaw phase): extracellular '''ice crystal formation''' causes cell membrane rupture and cellular dehydration.
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:Phase III (vascular stasis phase): more severe arterial spasm and venous dilation leading to '''tissue hypoxia'''
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:Phase IV (ischemia phase): tissue damage due to prolonged tissue hypoxia
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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.
 +
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Direct cellular destruction, release of catecholamines and tissue anoxia have potentially significant secondary effects in severe frostbite cases, resulting in '''damage to other organs'''.
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==Clinical Signs==
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'''Mild frostbite''' causes blanching of tissue and reduced sensation followed by painful erythema, scaling and alopecia.
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'''Severe frostbite''' results in necrosis, '''dry [[Necrosis - Pathology#Gangrene|gangrene]]''' and sloughing of the affected parts.
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'''Death''' from low core body temperature can result if not treated before vital organs are affected.
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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.
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'''Vesicles and blisters''' can develop on the affected area.
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==Diagnosis==
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This is based on the history and the appearance of the skin and tissue on the affected area.
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'''Differential diagnoses''' include: traumatic injury, tissue damage from ergot toxicosis in mammals.
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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.
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 +
==Treatment==
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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.
 +
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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'''.
 +
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'''Trauma and self-mutilation''' is prevented if possible, but bandaging of the areas is not recommended.
 +
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Conservative treatment is indicated until there is clear demarcation of viable and non-viable tissue, unless infection develops. Dry gangrene and sloughing then follow.
 +
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'''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.
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{{Learning
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|flashcards = [[Avian Medicine Q&A 22]]
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}}
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==References==
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Slatter, D. (2002) '''Textbook of small animal surgery''' ''Elsevier Health Sciences''
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Haskell, S. (2008) '''Blackwell's five minute veterinary consult: ruminant''' ''John Wiley and Sons''
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Radiostits, O. (2000) '''Veterinary clinical examination and diagnosis''' ''Elsevier Health Sciences''
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{{review}}
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{{OpenPages}}
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[[Category:Expert Review]]
 
[[Category:Integumentary System - Physical Damage]]
 
[[Category:Integumentary System - Physical Damage]]

Latest revision as of 20:20, 11 July 2012


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 very 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.

Pathophysiology

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 in mammals.

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 then follow.

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.


Low Temperature Damage Learning Resources
FlashcardsFlashcards logo.png
Flashcards
Test your knowledge using flashcard type questions
Avian Medicine Q&A 22


References

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




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