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https://t.me/med1917
Chapter42
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Frostbite
Denition of frostbite 354
Pattern of injury 354
Predisposing factors 354
Clinical assessment 355
Classication 356
Pathophysiology 358
Imaging 360
Treatment 362
Long- term sequelae 366
Prevention 366
Further reading 366
References 366
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CHAPTER42 Frostbite
Definition offrostbite
Frostbite is the damage sustained by tissues when exposed to temperatures
below their freezing point (<0°C).
Pattern ofinjury
• The severity of injury is proportional to the temperature, duration of
exposure, and the depth of tissue involvement
• The spectrum of disease can vary signicantly with just a small area
of frostbite with minimal tissue loss, to the involvement of a whole
extremity requiring amputation
• Most commonly aected extremities include:ngers, toes, nose, ears,
cheeks, and genitalia
Predisposing factors
A variety of factors have been associated with the development of frostbite injury.
Extrinsic
• Prolonged exposure to cold
• Inadequate or constrictive clothing
• Extremes of age
• Military occupation
• Immobilization
• Homelessness
• Smoking
• Alcohol
• Drug abuse
• Psychiatric disease
• High altitude
• Moist/ wet skin
• Afro- Caribbean descent
Intrinsic
• Dehydration and hypovolaemia
• Systemic disease:diabetes, peripheral vascular disease, Raynaud’s
disease
• Drugs:vasoconstrictive drugs (eg. β blockers), sedatives, neuroleptics
• Peripheral neuropathy
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CLINICAL ASSESSMENT
Clinical assessment
History
The following factors are relevant from the history to assess the severity of
injury, treatment, and prognosis.
• Patient age
• Comorbidities
• Smoking status
• Drug history:medical and social
• Alcohol history
• Timing of injury
• Duration of exposure
• Temperature
• Presence of wind chill
• Periods of thawing
• Protective clothing worn
• Previous frostbite injury
Symptoms and signs
• Commonest symptoms initially are a cool extremity, sensory loss, and a
feeling of clumsiness
• Frozen tissue may appear mottled blue, violaceous, yellowish- white
or waxy
• Although the initial appearance of the injury may appear insignicant,
the demarcation of non- viable tissue and the true extent of injury may
take several weeks to determine
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CHAPTER42 Frostbite
Classification
The severity of frostbite has been divided into four grades (Table 42.1) depending on the appearance of the extremity.
Good prognostic indicators include
• Light coloured blisters
• Normal skin colour
• Retained sensation
• Presence of oedema
Poor prognostic factors include
• Haemorrhagic blisters (indicate damage to sub- dermal vascular plexus)
• Non- blanching cyanosis
• Lack of oedema
• Firm non- deforming tissues
Table42.1 Grading ofseverity offrostbite
Grade Clinical features
First degree Supercial, partial thickness injury
Second degree Full thickness skin freezing (dermal involvement)
Third degree Full thickness skin and subcutaneous freezing
Fourth degree Full thickness necrosis
White plaque with surrounding erythema
Oedema, hyperaemia
No blisters or necrosis
Erythema, substantial oedema
Vesicles with clear uid
Skin desquamation and formation of black eschar
Haemorrhagic blisters
Skin necrosis
Blue- grey discolouration
Involving skin, subcutaneous tissue, muscle, tendon and bone
Minimal oedema
Initially mottling, deep red or cyanotic
In late stages, dry, black and mummied
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CLASSIFICATION
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CHAPTER42 Frostbite
Pathophysiology
Local cold injury produces a series of progressive, overlapping changes that
are divided into
1. Pre- freeze phase
2. Freeze thaw phase
3. Vascular stasis phase
4. Late ischaemic phase
The injury associated with frostbite occurs by two mechanisms.
1. Direct cell damage and death from cold injury
2. Vascular changes leading to progressive tissue ischaemia
Cellular injury
• Cellular injury occurs through the formation of ice crystals
• When freezing is gradual, ice crystals initially form in the extracellular
space, increasing the extracellular osmotic pressure. This draws water
across the cell membrane leading to intracellular dehydration and
altered cell haemostasis due to electrolyte and pH imbalance
• With continued freezing, there is formation of intracellular ice crystals,
enzyme destruction, decreased DNA synthesis, and a localized vascular
response due to release of histamine from the injured cell
• In contrast, if the freezing is very rapid, intracellular ice crystals are
formed prior to extracellular crystals, leading to more severe cell
damage and death
Vascular changes
The triad of vasoconstriction, endothelial injury and thromboembolism contribute to the vascular insuciency and tissue ischaemia seen in frostbite.
• Freezing leads to vasoconstriction which leads to reduced blood ow
and exacerbates skin cooling to produce further vasoconstriction
• Cooling of vascular contents leads to loss of the vascular endothelial
integrity, which precipitates brin deposition, transcapillary plasma loss,
and oedema formation. Oedema formation is further exacerbated
by mast cell degranulation and histamine release from the damaged
endothelial cells
• Cooling and endothelial damage also results in increased blood
viscosity and vascular stasis with formation of microemboli that occlude
capillaries
Inammatory response
• The progressive changes and inammatory response observed in
frostbite injury is similar to that of a burn wound
• Freezing leads to the release of pro- inammatory mediators with
high levels of prostaglandin F2α (PGF2α) and thromboxaneA2 (TXA2)
detected in frostbite blisters. These factors have been implicated in
vasoconstriction, platelet aggregation, and leucocyte adhesion which
worsen the ischaemia
https://t.me/med1917
Freeze– thaw– refreeze cycles
• The ‘freeze– thaw– refreeze’ cycles are thought to produce the most
damage than the initial ice crystal formation in the tissues
• Refreezing after thawing produces intracellular ice crystal formation
with extensive cell destruction and further release of prothrombotic
and vasoconstrictive PGF2α and TXA2 which in turn cause progressive
thrombosis and ischaemia
PATHOPHYSIOLOGY
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CHAPTER42 Frostbite
Imaging
Imaging can help determine the severity and depth of injury. A variety
of modalities have been used including plain radiographs, laser Doppler
studies, digital plethysmography, infrared thermography, and MRI. Triple
phase bone scanning (technitium- 99) and MRI are the most useful adjuncts
to clinical practice.
• Plain radiographs can demonstrate soft- tissue swelling initially. With
time, tissue loss, bone demineralization, and periosteal inammation can
be evident
• Technetium scans can be useful in the rst few days after injury to
determine the extent of tissue necrosis to allow for early debridement
and coverage of bony structures. However, technetium scintigraphy fails
to show the condition of the surrounding tissues or demarcate the level
of soft- tissue ischaemia
• MRI is regarded as a more superior modality as it allows direct
visualization of the occluded vessels, images the adjacent tissues, and
clearly demarcates the ischaemic tissues, which can aid surgical planning
prior to debridement
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IMAGING
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