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I.DAVID THANKA EDISON
2 nd Yr MS PG
DEFINITION
Burns are wounds produced by various kinds
of agents that cause cutaneous injury and
destruction of underlying tissue.
TYPES OF BURNS
 Thermal injury
– Scald—spillage of hot liquids
– Flame burns
– Flash burns due to exposure of natural gas, alcohol,
combustible liquids
– Contact burns—contact with hot
metals/objects/materials
 Electrical injury
 Chemical burns—acid/alkali
 Cold injury—frost bite
 Ionising radiation
 Sun burns
Classification of Burns
I. Depending on thickness of skin
involved
a. First degree:
 Epidermis is red
and painful,
 No blisters,
 Heals rapidly in 5-7
days
 By epithelialization
without scarring.
b. Second degree:
 Mottled, red, painful,
with blisters,
 Heals in 14-21 days.
 Superficial burn heals,
causing pigmentation.
 Deep burn heals,
causing scarring, and
pigmentation.
 Third degree:
 Charred, painless and
insensitive,
 Thrombosis of superficial
vessels.
 It requires grafting.
 Eschar
Charred, denatured,
insensitive,contracted full
thickness burn.
 These wound must heal by re-
epithelialisation from wound
edge.
 d. Fourth degree:
Involves the underlying tissues—muscles, bones.
II. Depending on thickness of skin
involved
 a. Partial thickness burns:
It is either first or
second degree burn which is
red and painful, often with
blisters.
 b. Full thickness burns:
It is third degree
burns which is charred,
insensitive, deep involving
all layers of the skin.
Depending on the Percentage
of Burns
Mild (Minor):
 Partial thickness burns < 15% in adult or <10%
in children.
 Full thickness burns less than 2%.
 Can be treated on outpatient basis.
Moderate:
 Second degree of 15-25% burns (10-20% in
children).
 Third degree between 2-10% burns.
 Burns which are not involving eyes, ears, face,
hand, feet,perineum.
Major (severe):
 Second degree burns more than 25% in adults,
in children more than 20%.
 All third degree burns of 10% or more.
 Burns involving eyes, ears, feet, hands,
perineum.
 All inhalation and electrical burns.
 Burns with fractures or major mechanical
trauma.
Jackson`s thermal wound theory
 Zone of coagulation
Centre area of wound ,where
all tissuses are damaged
 Zone of stasis
Surrounds the coagulation
area some tissues are damaged
 Zone of hyperaemia
Unburned area surrounds
the stasis but it is red due to
inflammation
ASSESMENT OF BURNS
Wallace`s rules of nine
It is used for early assesment
The Lund and Browder chart
 Better method for
assessing the burns
wound.
 Here each part of
the body is individually
assessed
Rule of palm
 Patient’s entire hand
area is 1%.
 Clean piece of
paper is cut to the
size of hand and
through that
percentage of burns is
assessed.
CLINICAL FEATURES
 History of burn.
 Pain, burning, anxious status, tachycardia,
tachypnoea.
 In severe degrees features of shock.
Tolerable temperature to human skin is 40°C for
brief period.
PATHOPHYSIOLOGY
Pathophysiology
Heat causes coagulation necrosis of skin and subcutaneous
tissue
↓
Release of vasoactive peptides
↓
Altered capillary permeability
↓
Loss of fluid → Severe hypovolaemia
↓
Decreased cardiac → Decreased myocardial
output function
↓
Decreased renal blood → Oliguria
flow (Renal failure)
Altered pulmonary resistance causing
pulmonary edema
↓
Infection
↓
Systemic inflammatory response syndrome (SIRS)
↓
Multiorgan dysfunction syndrome (MODS).
Massive edema
Injury to basement membrane
Altered pressure gradient
Edema
Renal
Diminished blood flow and cardiac output leads to
decreased renal blood flow and GFR
Toxins released from the wound along with sepsis
causes acute tubular necrosis.
 Myoglobin released from muscles (in case of
electric injury or often from eschar) is most injurious
to kidneys.
Earlier resuscitation decreases renal failure and
improves assosciated mortality
LUNGS
 Altered ventilation-perfusion ratio.
 Pulmonary oedema due to burn injury, fluid
overload,
 ARDS.
 Aspiration.
 Septicaemia.
GIT
burnsmucosal atrophy
decreased absorption & increased
intestinal permeability
increased bacterial translocation
septicemia
GIT
Acute gastric dilatation which occurs in 2-4 days.
 Paralytic ileus.
 Curling’s ulcer.
 Acute acalculous cholecystitis, acute
pancreatitis
 Abdominal Compartment syndrome
IMMUNE SYSTEM
Decreased function of T and B
lymphocytes and macrophages 
increased infection rate
Metabolic
 Hypermetabolic rate (BMR).
 Negative nitrogen balance.
 Electrolyte imbalance.
 Deficiencies of vitamins and essential
elements.
 Metabolic acidosis due to hypoxia and lactic
acid.
SUMMARY OF PATHOPHYSIOLOGY
Infections
 Streptococci (Beta haemolytic—most common)
 Pseudomonas
 Staphylococci
 Other gram-negative organisms
 Candida albicans
Causes of death
Hypovolaemia (refractory and uncontrolled) and
shock
 Renal failure
 Pulmonary oedema and ARDS
 Septicaemia
 Multiorgan failure
 Acute airway block in head and neck burns
THANK YOU

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Pathophysiology of burns

  • 2. DEFINITION Burns are wounds produced by various kinds of agents that cause cutaneous injury and destruction of underlying tissue.
  • 3. TYPES OF BURNS  Thermal injury – Scald—spillage of hot liquids – Flame burns – Flash burns due to exposure of natural gas, alcohol, combustible liquids – Contact burns—contact with hot metals/objects/materials  Electrical injury  Chemical burns—acid/alkali  Cold injury—frost bite  Ionising radiation  Sun burns
  • 5. I. Depending on thickness of skin involved a. First degree:  Epidermis is red and painful,  No blisters,  Heals rapidly in 5-7 days  By epithelialization without scarring.
  • 6. b. Second degree:  Mottled, red, painful, with blisters,  Heals in 14-21 days.  Superficial burn heals, causing pigmentation.  Deep burn heals, causing scarring, and pigmentation.
  • 7.  Third degree:  Charred, painless and insensitive,  Thrombosis of superficial vessels.  It requires grafting.  Eschar Charred, denatured, insensitive,contracted full thickness burn.  These wound must heal by re- epithelialisation from wound edge.
  • 8.  d. Fourth degree: Involves the underlying tissues—muscles, bones.
  • 9. II. Depending on thickness of skin involved  a. Partial thickness burns: It is either first or second degree burn which is red and painful, often with blisters.  b. Full thickness burns: It is third degree burns which is charred, insensitive, deep involving all layers of the skin.
  • 10. Depending on the Percentage of Burns Mild (Minor):  Partial thickness burns < 15% in adult or <10% in children.  Full thickness burns less than 2%.  Can be treated on outpatient basis. Moderate:  Second degree of 15-25% burns (10-20% in children).  Third degree between 2-10% burns.  Burns which are not involving eyes, ears, face, hand, feet,perineum.
  • 11. Major (severe):  Second degree burns more than 25% in adults, in children more than 20%.  All third degree burns of 10% or more.  Burns involving eyes, ears, feet, hands, perineum.  All inhalation and electrical burns.  Burns with fractures or major mechanical trauma.
  • 12. Jackson`s thermal wound theory  Zone of coagulation Centre area of wound ,where all tissuses are damaged  Zone of stasis Surrounds the coagulation area some tissues are damaged  Zone of hyperaemia Unburned area surrounds the stasis but it is red due to inflammation
  • 14. Wallace`s rules of nine It is used for early assesment
  • 15. The Lund and Browder chart  Better method for assessing the burns wound.  Here each part of the body is individually assessed
  • 16. Rule of palm  Patient’s entire hand area is 1%.  Clean piece of paper is cut to the size of hand and through that percentage of burns is assessed.
  • 17. CLINICAL FEATURES  History of burn.  Pain, burning, anxious status, tachycardia, tachypnoea.  In severe degrees features of shock. Tolerable temperature to human skin is 40°C for brief period.
  • 19. Pathophysiology Heat causes coagulation necrosis of skin and subcutaneous tissue ↓ Release of vasoactive peptides ↓ Altered capillary permeability ↓ Loss of fluid → Severe hypovolaemia ↓
  • 20. Decreased cardiac → Decreased myocardial output function ↓ Decreased renal blood → Oliguria flow (Renal failure) Altered pulmonary resistance causing pulmonary edema ↓ Infection ↓ Systemic inflammatory response syndrome (SIRS) ↓ Multiorgan dysfunction syndrome (MODS).
  • 21. Massive edema Injury to basement membrane Altered pressure gradient Edema
  • 22. Renal Diminished blood flow and cardiac output leads to decreased renal blood flow and GFR Toxins released from the wound along with sepsis causes acute tubular necrosis.  Myoglobin released from muscles (in case of electric injury or often from eschar) is most injurious to kidneys. Earlier resuscitation decreases renal failure and improves assosciated mortality
  • 23. LUNGS  Altered ventilation-perfusion ratio.  Pulmonary oedema due to burn injury, fluid overload,  ARDS.  Aspiration.  Septicaemia.
  • 24. GIT burnsmucosal atrophy decreased absorption & increased intestinal permeability increased bacterial translocation septicemia
  • 25. GIT Acute gastric dilatation which occurs in 2-4 days.  Paralytic ileus.  Curling’s ulcer.  Acute acalculous cholecystitis, acute pancreatitis  Abdominal Compartment syndrome
  • 26. IMMUNE SYSTEM Decreased function of T and B lymphocytes and macrophages  increased infection rate
  • 27. Metabolic  Hypermetabolic rate (BMR).  Negative nitrogen balance.  Electrolyte imbalance.  Deficiencies of vitamins and essential elements.  Metabolic acidosis due to hypoxia and lactic acid.
  • 28.
  • 30. Infections  Streptococci (Beta haemolytic—most common)  Pseudomonas  Staphylococci  Other gram-negative organisms  Candida albicans
  • 31. Causes of death Hypovolaemia (refractory and uncontrolled) and shock  Renal failure  Pulmonary oedema and ARDS  Septicaemia  Multiorgan failure  Acute airway block in head and neck burns