Burn Wounds: Pathophysiology and Classification
BURns
Gulshan Kumar
MVSc, PhD
•
Burns are complex inflammatory or gangrenous lesions due
to exposure of live tissue to dry or moist heat, chemicals
and electricity.
•
Scalds are burns caused by hot liquids or steam
•
Superficial (involving epidermis) First degree
Superficial (involving epidermis) First degree
•
Partial thickness (involving dermis)
Partial thickness (involving dermis)
•
Superficial dermal (Second degree) blood vessels and nociceptors
Superficial dermal (Second degree) blood vessels and nociceptors
•
Deep dermal (Third degree) Pressure receptors
Deep dermal (Third degree) Pressure receptors
•
Full thickness: (Fourth degree) subcutis, fascia, muscle, even bone,
Full thickness: (Fourth degree) subcutis, fascia, muscle, even bone,
eschar
eschar
formation
formation
Classification
Classification
•
Exposure to 44°C for 5 minutes can result full thickness burns
Exposure to 44°C for 5 minutes can result full thickness burns
•
Exposure to 70°C for about a second can result full thickness burns
Exposure to 70°C for about a second can result full thickness burns
•
Injury will occur when the heat energy is applied at a rate that
Injury will occur when the heat energy is applied at a rate that
exceeds the tissue’s ability to absorb and dissipate it
exceeds the tissue’s ability to absorb and dissipate it
•
A transition area separates the completely damaged tissue from the
A transition area separates the completely damaged tissue from the
un-injured healthy tissue.
un-injured healthy tissue.
•
Heat results in denaturation of the cellular proteins and coagulation
Heat results in denaturation of the cellular proteins and coagulation
of blood vessels.
of blood vessels.
Pathophysiology of burn wounds
Pathophysiology of burn wounds
•
Adjacent to the injured tissue, is the zone of stasis i.e. reduced blood
Adjacent to the injured tissue, is the zone of stasis i.e. reduced blood
flow, intravascular sludging and potentially reversible tissue damage.
flow, intravascular sludging and potentially reversible tissue damage.
•
If the insult continues-> irreversible damage may occur.
If the insult continues-> irreversible damage may occur.
•
In this stasis zone, some vessels are completely thrombosed.
In this stasis zone, some vessels are completely thrombosed.
•
Others may be patent but with endothelial cell damage.
Others may be patent but with endothelial cell damage.
•
Massive inflammatory reaction in response to the tissue injury results
Massive inflammatory reaction in response to the tissue injury results
massive dilatation of vessels, increased permeability and
massive dilatation of vessels, increased permeability and
extravasation of protein rich fluid into the extravascular spaces.
extravasation of protein rich fluid into the extravascular spaces.
Pathophysiology of burn wounds
Pathophysiology of burn wounds
•
Massive oedema, the pressure of which may compress blood vessels
Massive oedema, the pressure of which may compress blood vessels
hampering the microcirculation, tissue anoxia and necrosis.
hampering the microcirculation, tissue anoxia and necrosis.
•
Since the circulating fluid has been shifted to extravascular fluid the
Since the circulating fluid has been shifted to extravascular fluid the
animal is in shock.
animal is in shock.
•
Severe hypoproteinaemia. Hence further oedema which aggravates
Severe hypoproteinaemia. Hence further oedema which aggravates
the hypoproteinaemia
the hypoproteinaemia
Pathophysiology of burn wounds
Pathophysiology of burn wounds
•
Carbon monoxide poisoning.
Carbon monoxide poisoning.
•
If inflicted by flames, there may be accompanying inhalation
If inflicted by flames, there may be accompanying inhalation
injuries………
injuries………
•
Inhalation of hot gases and smoke..
Inhalation of hot gases and smoke..
•
Oedema of oro-pharynx and larynx…leading to upper airway
Oedema of oro-pharynx and larynx…leading to upper airway
obstruction and
obstruction and
•
tracheal, bronchial and pulmonary oedema….pulmonary failure
tracheal, bronchial and pulmonary oedema….pulmonary failure
Pathophysiology of burn wounds
Pathophysiology of burn wounds
•
Hypovolaemia leads to increased haematocrit and increased viscosity,
Hypovolaemia leads to increased haematocrit and increased viscosity,
hence renal and hepatic damage.
hence renal and hepatic damage.
•
Low protein synthesis, low immunity,
Low protein synthesis, low immunity,
•
More chances of infection
More chances of infection
•
Decreased splanchnic perfusion leads to compromised intestinal
Decreased splanchnic perfusion leads to compromised intestinal
mucosal barrier function, allowing bacterial translocation and
mucosal barrier function, allowing bacterial translocation and
absorption of endotoxins…sometimes may lead to ulceration of
absorption of endotoxins…sometimes may lead to ulceration of
duodenum (curling ulcers)
duodenum (curling ulcers)
Pathophysiology of burn wounds
Pathophysiology of burn wounds
•
Massive scars when burn wounds heal
Massive scars when burn wounds heal
Pathophysiology of burn wounds
Pathophysiology of burn wounds
•
Extent of injury is usually reported as the %age of surface area
Extent of injury is usually reported as the %age of surface area
involved, which is:
involved, which is:
•
Surface area = 0.1 x weight²/³
Surface area = 0.1 x weight²/³
•
Modified rule of 9
Modified rule of 9
•
Each forelimb =9% (9 x 2=18%)
Each forelimb =9% (9 x 2=18%)
•
Each hind limb =18% (18 x 2 =36%)
Each hind limb =18% (18 x 2 =36%)
•
Head & neck = 9%
Head & neck = 9%
•
Thorax= Ventral 9%, Dorsal 9% (total= 18%)
Thorax= Ventral 9%, Dorsal 9% (total= 18%)
•
Abdomen= Ventral 9%, Dorsal 9% (total= 18%)
Abdomen= Ventral 9%, Dorsal 9% (total= 18%)
•
Groin, perineum, tail = 1%
Groin, perineum, tail = 1%
Assessment of burn wounds
Assessment of burn wounds
•
Immediate cooling of the burnt area (not freezing-ice packs may
Immediate cooling of the burnt area (not freezing-ice packs may
damage actually)
damage actually)
•
Remove the aetiologic agent,
Remove the aetiologic agent,
•
If aetiology is chemicals, irrigate with large volumes of clean
If aetiology is chemicals, irrigate with large volumes of clean
water
water
•
Prevent infection
Prevent infection
First Aid
First Aid
Initial care:
•
Morphine sulphate (10 mg total dose for dog and 60 mg total dose
for large animals) or
•
Methadone at the rate of 0.25 mg per kg body weight for pain. OR
•
OTHER NSAIDS
•
Emesis can be controlled by phenothiazine derivatives. Sedatives,
narcotics are contraindicated.
•
Prophylaxis against tetanus should be done with anti tetanus serum
or penicillin.
Management
Management
•
Respiratory involvement, if present, can be judged by burnt lips and
nose, deep red oral and pharyngeal mucosae and cough.
•
Immediate intubation or tracheostomy should be performed and the
lungs be oxygenated with 40-60% oxygen.
•
Intravenous line should be established immediately, preferably
canulation should be done (canula should not be left for more than 7
days).
Management
Management
Choice of fluids: In full thickness burns saline bicarbonate, Ringer’s
lactate, plasma or whole blood should be considered.
Rate and dose of infusion:
Plasma/blood (ml) = body wt. x % burns x 1 ml - for 24 hrs.
Ringer’s lactate (ml) = body wt. x % burns x 1 ml- for24 hrs.
5% dextrose saline = 20-30 ml/ kg body wt. as maintenance.
*Half of the fluid should be administered in first 8 hours and the remaining half over 16 hours.
Management
Management
•
Efforts should also be made for prevention of thrombosis and
consequent ischaemia (anticoagulants like heparin)
.
•
Release incisions may be required in case of constricting burns.
Release incisions may be required in case of constricting burns.
•
Antiseptic ointments like silver sulphadiazine (1% cream), furacillin
Antiseptic ointments like silver sulphadiazine (1% cream), furacillin
1:5000)…costly for animals
1:5000)…costly for animals
•
Carron oil…linseed/coconut oil + lime water topically
Carron oil…linseed/coconut oil + lime water topically
•
Non adherent dressings
Non adherent dressings
Management
Management
Supportive
•
Protein rich diet, enhance anabolism
Protein rich diet, enhance anabolism
•
Vit. A, B, C and Zn are advised
Vit. A, B, C and Zn are advised
•
If burns involve genitalia, catheterise.
If burns involve genitalia, catheterise.
Management
Management
•
Frost bite results due to exposure of extremities to extremely low
temperatures, e.g. in icy mud,
•
The damage thus caused is either to the supporting tissue or
primary circulation or both.
•
Extremities show oedema and bright red dyscolouration which is at
its maximum after 24 hours of thawing.
Frost bite
Frost bite
•
Ischaemia and mummification (dry gangrene) followed after 4-5
hours in cases of severe damage,
•
S
hrunken tissue hang with the body for 30-40 days following which
it may separate spontaneously.
•
Restoration towards normalcy after 72 hours is a favourable
prognostic sign.
•
Infection may cause moist gangrene to form.
Frost bite
Frost bite
Treatment
•
Rapid rewarming at 108°F is the most acceptable method because
following this endothelium of blood vessels remains attached to the
intima and starts proliferating after the third day.
•
Unless the infection is apparent no local treatment is indicated.
•
Amputation if indicated should be postponed till dry gangrene has
a clear-cut separation from the normal healthy tissue.
•
Local anaesthesia, blockade and parenteral analgesics and antibiotics
are indicated.
•
Infection may cause moist gangrene to form.
Frost bite
Frost bite
Burn injuries, such as burns and scalds, are complex inflammatory conditions caused by exposure to heat, chemicals, or electricity. This article delves into the pathophysiology of burn wounds, explaining how tissue damage occurs and the classification of burn depths based on layers of skin affected. It covers the effects of heat energy, vascular changes, inflammatory responses, and complications like oedema and carbon monoxide poisoning. Understanding these processes is crucial for effective management of burn injuries.
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Presentation Transcript
BURns Gulshan Kumar MVSc, PhD
Burns are complex inflammatory or gangrenous lesions due to exposure of live tissue to dry or moist heat, chemicals and electricity. Scalds are burns caused by hot liquids or steam
Classification Superficial (involving epidermis) First degree Partial thickness (involving dermis) Superficial dermal (Second degree) blood vessels and nociceptors Deep dermal (Third degree) Pressure receptors Full thickness: (Fourth degree) subcutis, fascia, muscle, even bone, eschar formation
Pathophysiology of burn wounds Exposure to 44 C for 5 minutes can result full thickness burns Exposure to 70 C for about a second can result full thickness burns Injury will occur when the heat energy is applied at a rate that exceeds the tissue s ability to absorb and dissipate it A transition area separates the completely damaged tissue from the un-injured healthy tissue. Heat results in denaturation of the cellular proteins and coagulation of blood vessels.
Pathophysiology of burn wounds Adjacent to the injured tissue, is the zone of stasis i.e. reduced blood flow, intravascular sludging and potentially reversible tissue damage. If the insult continues-> irreversible damage may occur. In this stasis zone, some vessels are completely thrombosed. Others may be patent but with endothelial cell damage. Massive inflammatory reaction in response to the tissue injury results massive dilatation of vessels, increased permeability and extravasation of protein rich fluid into the extravascular spaces.
Pathophysiology of burn wounds Massive oedema, the pressure of which may compress blood vessels hampering the microcirculation, tissue anoxia and necrosis. Since the circulating fluid has been shifted to extravascular fluid the animal is in shock. Severe hypoproteinaemia. Hence further oedema which aggravates the hypoproteinaemia
Pathophysiology of burn wounds Carbon monoxide poisoning. If inflicted by flames, there may be accompanying inhalation injuries Inhalation of hot gases and smoke.. Oedema of oro-pharynx and larynx leading to upper airway obstruction and tracheal, bronchial and pulmonary oedema .pulmonary failure
Pathophysiology of burn wounds Hypovolaemia leads to increased haematocrit and increased viscosity, hence renal and hepatic damage. Low protein synthesis, low immunity, More chances of infection Decreased splanchnic perfusion leads to compromised intestinal mucosal barrier function, allowing bacterial translocation and absorption of endotoxins sometimes may lead to ulceration of duodenum (curling ulcers)
Pathophysiology of burn wounds Massive scars when burn wounds heal
Assessment of burn wounds Extent of injury is usually reported as the %age of surface area involved, which is: Surface area = 0.1 x weight / Modified rule of 9 Each forelimb =9% (9 x 2=18%) Each hind limb =18% (18 x 2 =36%) Head & neck = 9% Thorax= Ventral 9%, Dorsal 9% (total= 18%) Abdomen= Ventral 9%, Dorsal 9% (total= 18%) Groin, perineum, tail = 1%
First Aid Immediate cooling of the burnt area (not freezing-ice packs may damage actually) Remove the aetiologic agent, If aetiology is chemicals, irrigate with large volumes of clean water Prevent infection
Management Initial care: Morphine sulphate (10 mg total dose for dog and 60 mg total dose for large animals) or Methadone at the rate of 0.25 mg per kg body weight for pain. OR OTHER NSAIDS Emesis can be controlled by phenothiazine derivatives. Sedatives, narcotics are contraindicated. Prophylaxis against tetanus should be done with anti tetanus serum or penicillin.
Management Respiratory involvement, if present, can be judged by burnt lips and nose, deep red oral and pharyngeal mucosae and cough. Immediate intubation or tracheostomy should be performed and the lungs be oxygenated with 40-60% oxygen. Intravenous line should be established immediately, preferably canulation should be done (canula should not be left for more than 7 days).
Management Choice of fluids: In full thickness burns saline bicarbonate, Ringer s lactate, plasma or whole blood should be considered. Rate and dose of infusion: Plasma/blood (ml) = body wt. x % burns x 1 ml - for 24 hrs. Ringer s lactate (ml) = body wt. x % burns x 1 ml- for24 hrs. 5% dextrose saline = 20-30 ml/ kg body wt. as maintenance. *Half of the fluid should be administered in first 8 hours and the remaining half over 16 hours.
Management Efforts should also be made for prevention of thrombosis and consequent ischaemia (anticoagulants like heparin). Release incisions may be required in case of constricting burns. Antiseptic ointments like silver sulphadiazine (1% cream), furacillin 1:5000) costly for animals Carron oil linseed/coconut oil + lime water topically Non adherent dressings
Management Supportive Protein rich diet, enhance anabolism Vit. A, B, C and Zn are advised If burns involve genitalia, catheterise.
Frost bite Frost bite results due to exposure of extremities to extremely low temperatures, e.g. in icy mud, The damage thus caused is either to the supporting tissue or primary circulation or both. Extremities show oedema and bright red dyscolouration which is at its maximum after 24 hours of thawing.
Frost bite Ischaemia and mummification (dry gangrene) followed after 4-5 hours in cases of severe damage, Shrunken tissue hang with the body for 30-40 days following which it may separate spontaneously. Restoration towards normalcy after 72 hours is a favourable prognostic sign. Infection may cause moist gangrene to form.
Frost bite Treatment Rapid rewarming at 108 F is the most acceptable method because following this endothelium of blood vessels remains attached to the intima and starts proliferating after the third day. Unless the infection is apparent no local treatment is indicated. Amputation if indicated should be postponed till dry gangrene has a clear-cut separation from the normal healthy tissue. Local anaesthesia, blockade and parenteral analgesics and antibiotics are indicated. Infection may cause moist gangrene to form.
