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Introduction to burns
Presented by: Naina Joshi
MPT 1st Year
contents
Definition
Structure of skin
Pathophysiology of burns
Classification of burns
Complication of burns
Fluid resuscitation
definition
 A burn is an injury to skin caused by biological, chemical,
electrical and physical agents with local and systemic
repercussions.
(Burns: Definition, Classification, Pathophysiology and Initial Approach. Garcia-
Espinoza et al., Gen Med (Los Angeles) 2017, 5:5)
Structure of skin
Pathological response
 Zone of coagulation—This occurs at the point of maximum
damage. In this zone there is irreversible tissue loss due to
coagulation of the constituent proteins.
 Zone of stasis—The surrounding zone of stasis is
characterised by decreased tissue perfusion. The tissue in
this zone is potentially salvageable. The main aim of burns
resuscitation is to increase tissue perfusion here and prevent
any damage becoming irreversible.
 Zone of hyperaemia—In this outermost zone tissue
perfusion is increased. The tissue here will invariably
recover unless there is severe sepsis or prolonged
hypoperfusion
Systemic responses
Renal response
 During the acute phase of burn injury, renal blood flow and
glomerular filtration rate (GFR), decrease.
 If untreated, the resulting oliguria may progress to acute renal
failure.
 Two different forms of acute renal failure have been described
in burned patients, differing in terms of their time of onset.
 The first occurs during the first few days after the injury and is
related to hypovolemia with low cardiac output.
 Elevated levels of stress hormones like catecholamines,
angiotensin, aldosterone and vasopressin have been reported
to be implicated in the pathogenesis of this form of ARF.
Gastrointestinal response
 adynamic ileus
 gastric dilatation
 delay in gastric emptying
 gastrointestinal hemorrhage
 ↑ gastric secretions
 ↑ ulcer incidence
 ↓ intestinal & colonic motility
 ↓ mesenteric blood flow
 ↓ nutrient absorption
 hepatic injury
Respiratory response
 hypoxemia
 pulmonary hypertension
 ↑ airway resistance
 ↓ pulmonary compliance
classification
 Burns may be distinguished and classified by their
mechanism or cause, the degree or depth of the burn, the
area of body surface that is burned, the region or part of the
body affected, as well as the extent.
Classification by mechanism or cause
• Causally, burns may be classified as thermal or inhalational.
• Thermal burns involve the skin and may present as: –
 scalds – caused by hot liquid or steam;
 contact burns – caused by hot solids or items such as hot
pressing irons and cooking utensils, as well as lighted
cigarettes
 flame burns – caused by flames or incandescent fires, such
as those started by lighted cigarettes, candles, lamps or
stoves
 chemical burns – caused by exposure to reactive chemical
substances such as strong acids or alkalis.
 electrical burns – caused by an electrical current passing from
an electric outlet, cord or appliance through the body
 Inhalational burns are the result of breathing in superheated
gases, steam, hot liquids or noxious products of incomplete
combustion. They cause thermal or chemical injury to the
airways and lungs and accompany a skin burn in
approximately 20% to 35% of cases. Inhalational burns are
the most common cause of death among people suffering fire-
related burn.
Classification : differential diagnosis
Epidermal: As the name implies, causes cell damage only
to epidermis.
• The classic sunburn or to brief contact with hot substances,
liquids or flash flames (scalds) is the best example.
• Clinically, the skin appears red or erythematous.
• No blisters, dry surface, tender.
• Minimal edema, spontaneous healing, no scars.
Superficial partial thickness: Damage occurs through the
epidermis and into the papillary layer of the dermis.
• Bright pink or red, inflamed dermis; erythematous with blanching
and brisk capillary refill.
• Intact blisters, glistening surface when blisters removed, sensitive
to change in temperature.
• Moderate edema, spontaneous healing, minimal scarring,
discoloration.
Deep partial thickness: It involves destruction of the
epidermis and the papillary dermis with damage down into the
reticular dermal layer.
 Mixed red, waxy white, blanching with slow capillary refill
 Broken blisters, wet surface, sensitive to pressure but
insensitive to light touch or soft pinprick.
 Marked edema, slow healing, excessive scarring.
Full thickness: All of the epidermal and dermal layers
are destroyed completely. In addition, the subcutaneous fat
layer may be damaged to some extent.
 White (ischemic), fawn, balck, red (haemoglobin fixation),
no blanching, poor distal circulation.
 Parchment like, leathery, rigid, dry, body hairs pull out
easily.
 Area depressed, heals with skin grafting, scarring.
Subdermal: It involves complete destruction of all tissues
from epidermis down to and through the subcutaneous tissue.
 Muscles and bones are subject to necrosis when burned.
 Tissue defects, heals with skin grafts or flaps, scarring.
Classification according to extent
COMPLICATIONS OF BURN INJURY
 Depending on the extent of burn injury, the depth of the burn,
and the type of burn, there may be secondary systemic
complications.
Infection: Some virulent strains of Pseudomonas
aeruginosa and Staphylococcus aureus are resistant to
antibiotics and have been responsible for epidemic infections
in burn centers.
 Microbial invasion from the burn wounds to other healthy
tissue can create sepsis.
 Systemic antibiotics are used to treat both burn and infection.
Pulmonary Complications
 Any patient who has been burned in a closed space should
be suspected of having an inhalation injury.
 Signs of an inhalation injury include facial burns, singed nasal
hairs, harsh cough, hoarseness, abnormal breath sounds,
respiratory distress, and carbonaceous sputum and/or
hypoxemia.
 The primary complications associated with this injury are
carbon monoxide poisoning, tracheal damage, upper airway
obstruction, pulmonary edema, and pneumonia. Lung
damage from inhaling noxious gases and smoke may be
lethal.
Metabolic Complications
 Thermal injury causes a great metabolic and catabolic
challenge to the body.
 Metabolic rates may increase up to 50% in a 25% TBSA burn
and much more as the burn size increases.
 As a result of the increased metabolic activity, there will be an
increase of 1.8°F to 2.6°F (1°C to 2°C) in core temperature.
 It is recommended that room temperature be kept at 86°F
(30°C), which will significantly reduce the metabolic rate
Haemodynamic changes result from a shift in fluid to
interstitium which subsequently reduces the plasma
& intravascular fluid volume in a patient with burn.
Fluid shift occur as a result of local and temporary
systemic changes in capillary dynamics.
This shift of fluid to the interstitium can result in
significant edema.
 With these fluid shifts, there will be a tremendous initial
decrease in cardiac output, which may reach as low as 15%
of normal within the first hour after injury.
 Fluid replacement therapy is utilized initially to manage the
loss of circulatory fluid.
 Hematological changes also occur after a severe burn injury.
These changes include alterations in platelet concentration
and function, clotting factors, and white blood cell
components; red blood cell dysfunction; and decreases in
hemoglobin and hematocrit
Fluid resuscitation
 The principle of fluid resuscitation is that the intravascular
volume must be maintained following a burn, in order to
provide sufficient circulation to perfuse not only the essential
visceral organs such as the brain, kidneys and gut, but also
the peripheral tissues, especially the damaged skin.
 The resuscitation volume is relatively constant in proportion to
the area of the body burned and, therefore, there are
formulae that calculate the approximate volume of fluid
needed for the resuscitation of a patient of a given body
weight with a given percentage of the body burned
 These regimes follow the fluid loss, which is at its maximum in
the first 8 hours and slows, such that, by 24–36 hours, the
patient can be maintained on his or her normal daily
requirements.
 There are three types of fluid used. The most common is
Ringer’s lactate or Hartmann’s solution; some centres use
human albumin solution or fresh-frozen plasma; and some
centres use hypertonic saline.
Parkland Formula
 Adults: 2-4 ml RL x Kg body weight x % burn
 Children: 3-4 ml RL x Kg body weight x % burn
RL = Ringer’s Lactate solution
Half this volume is given in the first 8 hours and the second half
is given in the subsequent 16 hours
Monitoring of resuscitation
 The key to monitoring of resuscitation is urine output.
 Urine output should be between 0.5 and 1.0 mL/kg body
weight per hour.
 If the urine output is below this, the infusion rate should be
increased by 50%.
 If the urine output is inadequate and the patient is showing
signs of hypoperfusion (restlessness with tachycardia, cool
peripheries and a high haematocrit), then a bolus of 10 mL/kg
body weight should be given
references
 Physical rehabilitation Susanb.o’Sullivan
 Systemic Responses to Burn Injury Bar›fl ÇAKIR, Berrak Ç.
YE⁄EN Department of Physiology, Faculty of Medicine,
Marmara University, istanbul – Turkey Turk J Med Sci 34
(2004) 215-226
 Burns: Definition, Classification, Pathophysiology and Initial
Approach Garcia-Espinoza et al., Gen Med (Los Angeles)
2017, 5:5
 Bailey and love
 Burn clinical practise and guideline Developed by Texas EMS
Trauma & Acute Care Foundation Trauma Division

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Introduction to burns

  • 1. Introduction to burns Presented by: Naina Joshi MPT 1st Year
  • 2. contents Definition Structure of skin Pathophysiology of burns Classification of burns Complication of burns Fluid resuscitation
  • 3. definition  A burn is an injury to skin caused by biological, chemical, electrical and physical agents with local and systemic repercussions. (Burns: Definition, Classification, Pathophysiology and Initial Approach. Garcia- Espinoza et al., Gen Med (Los Angeles) 2017, 5:5)
  • 5.
  • 6. Pathological response  Zone of coagulation—This occurs at the point of maximum damage. In this zone there is irreversible tissue loss due to coagulation of the constituent proteins.  Zone of stasis—The surrounding zone of stasis is characterised by decreased tissue perfusion. The tissue in this zone is potentially salvageable. The main aim of burns resuscitation is to increase tissue perfusion here and prevent any damage becoming irreversible.
  • 7.  Zone of hyperaemia—In this outermost zone tissue perfusion is increased. The tissue here will invariably recover unless there is severe sepsis or prolonged hypoperfusion
  • 8.
  • 9.
  • 11.
  • 12. Renal response  During the acute phase of burn injury, renal blood flow and glomerular filtration rate (GFR), decrease.  If untreated, the resulting oliguria may progress to acute renal failure.  Two different forms of acute renal failure have been described in burned patients, differing in terms of their time of onset.  The first occurs during the first few days after the injury and is related to hypovolemia with low cardiac output.  Elevated levels of stress hormones like catecholamines, angiotensin, aldosterone and vasopressin have been reported to be implicated in the pathogenesis of this form of ARF.
  • 13. Gastrointestinal response  adynamic ileus  gastric dilatation  delay in gastric emptying  gastrointestinal hemorrhage  ↑ gastric secretions  ↑ ulcer incidence  ↓ intestinal & colonic motility  ↓ mesenteric blood flow  ↓ nutrient absorption  hepatic injury
  • 14. Respiratory response  hypoxemia  pulmonary hypertension  ↑ airway resistance  ↓ pulmonary compliance
  • 15. classification  Burns may be distinguished and classified by their mechanism or cause, the degree or depth of the burn, the area of body surface that is burned, the region or part of the body affected, as well as the extent.
  • 16. Classification by mechanism or cause • Causally, burns may be classified as thermal or inhalational. • Thermal burns involve the skin and may present as: –  scalds – caused by hot liquid or steam;  contact burns – caused by hot solids or items such as hot pressing irons and cooking utensils, as well as lighted cigarettes  flame burns – caused by flames or incandescent fires, such as those started by lighted cigarettes, candles, lamps or stoves  chemical burns – caused by exposure to reactive chemical substances such as strong acids or alkalis.
  • 17.  electrical burns – caused by an electrical current passing from an electric outlet, cord or appliance through the body  Inhalational burns are the result of breathing in superheated gases, steam, hot liquids or noxious products of incomplete combustion. They cause thermal or chemical injury to the airways and lungs and accompany a skin burn in approximately 20% to 35% of cases. Inhalational burns are the most common cause of death among people suffering fire- related burn.
  • 18.
  • 19. Classification : differential diagnosis Epidermal: As the name implies, causes cell damage only to epidermis. • The classic sunburn or to brief contact with hot substances, liquids or flash flames (scalds) is the best example. • Clinically, the skin appears red or erythematous. • No blisters, dry surface, tender. • Minimal edema, spontaneous healing, no scars.
  • 20. Superficial partial thickness: Damage occurs through the epidermis and into the papillary layer of the dermis. • Bright pink or red, inflamed dermis; erythematous with blanching and brisk capillary refill. • Intact blisters, glistening surface when blisters removed, sensitive to change in temperature. • Moderate edema, spontaneous healing, minimal scarring, discoloration.
  • 21. Deep partial thickness: It involves destruction of the epidermis and the papillary dermis with damage down into the reticular dermal layer.  Mixed red, waxy white, blanching with slow capillary refill  Broken blisters, wet surface, sensitive to pressure but insensitive to light touch or soft pinprick.  Marked edema, slow healing, excessive scarring.
  • 22. Full thickness: All of the epidermal and dermal layers are destroyed completely. In addition, the subcutaneous fat layer may be damaged to some extent.  White (ischemic), fawn, balck, red (haemoglobin fixation), no blanching, poor distal circulation.  Parchment like, leathery, rigid, dry, body hairs pull out easily.  Area depressed, heals with skin grafting, scarring.
  • 23.
  • 24. Subdermal: It involves complete destruction of all tissues from epidermis down to and through the subcutaneous tissue.  Muscles and bones are subject to necrosis when burned.  Tissue defects, heals with skin grafts or flaps, scarring.
  • 25.
  • 26.
  • 28.
  • 29. COMPLICATIONS OF BURN INJURY  Depending on the extent of burn injury, the depth of the burn, and the type of burn, there may be secondary systemic complications. Infection: Some virulent strains of Pseudomonas aeruginosa and Staphylococcus aureus are resistant to antibiotics and have been responsible for epidemic infections in burn centers.  Microbial invasion from the burn wounds to other healthy tissue can create sepsis.  Systemic antibiotics are used to treat both burn and infection.
  • 30. Pulmonary Complications  Any patient who has been burned in a closed space should be suspected of having an inhalation injury.  Signs of an inhalation injury include facial burns, singed nasal hairs, harsh cough, hoarseness, abnormal breath sounds, respiratory distress, and carbonaceous sputum and/or hypoxemia.  The primary complications associated with this injury are carbon monoxide poisoning, tracheal damage, upper airway obstruction, pulmonary edema, and pneumonia. Lung damage from inhaling noxious gases and smoke may be lethal.
  • 31. Metabolic Complications  Thermal injury causes a great metabolic and catabolic challenge to the body.  Metabolic rates may increase up to 50% in a 25% TBSA burn and much more as the burn size increases.  As a result of the increased metabolic activity, there will be an increase of 1.8°F to 2.6°F (1°C to 2°C) in core temperature.  It is recommended that room temperature be kept at 86°F (30°C), which will significantly reduce the metabolic rate
  • 32. Haemodynamic changes result from a shift in fluid to interstitium which subsequently reduces the plasma & intravascular fluid volume in a patient with burn. Fluid shift occur as a result of local and temporary systemic changes in capillary dynamics. This shift of fluid to the interstitium can result in significant edema.
  • 33.  With these fluid shifts, there will be a tremendous initial decrease in cardiac output, which may reach as low as 15% of normal within the first hour after injury.  Fluid replacement therapy is utilized initially to manage the loss of circulatory fluid.  Hematological changes also occur after a severe burn injury. These changes include alterations in platelet concentration and function, clotting factors, and white blood cell components; red blood cell dysfunction; and decreases in hemoglobin and hematocrit
  • 34. Fluid resuscitation  The principle of fluid resuscitation is that the intravascular volume must be maintained following a burn, in order to provide sufficient circulation to perfuse not only the essential visceral organs such as the brain, kidneys and gut, but also the peripheral tissues, especially the damaged skin.  The resuscitation volume is relatively constant in proportion to the area of the body burned and, therefore, there are formulae that calculate the approximate volume of fluid needed for the resuscitation of a patient of a given body weight with a given percentage of the body burned
  • 35.  These regimes follow the fluid loss, which is at its maximum in the first 8 hours and slows, such that, by 24–36 hours, the patient can be maintained on his or her normal daily requirements.  There are three types of fluid used. The most common is Ringer’s lactate or Hartmann’s solution; some centres use human albumin solution or fresh-frozen plasma; and some centres use hypertonic saline.
  • 36. Parkland Formula  Adults: 2-4 ml RL x Kg body weight x % burn  Children: 3-4 ml RL x Kg body weight x % burn RL = Ringer’s Lactate solution Half this volume is given in the first 8 hours and the second half is given in the subsequent 16 hours
  • 37. Monitoring of resuscitation  The key to monitoring of resuscitation is urine output.  Urine output should be between 0.5 and 1.0 mL/kg body weight per hour.  If the urine output is below this, the infusion rate should be increased by 50%.  If the urine output is inadequate and the patient is showing signs of hypoperfusion (restlessness with tachycardia, cool peripheries and a high haematocrit), then a bolus of 10 mL/kg body weight should be given
  • 38. references  Physical rehabilitation Susanb.o’Sullivan  Systemic Responses to Burn Injury Bar›fl ÇAKIR, Berrak Ç. YE⁄EN Department of Physiology, Faculty of Medicine, Marmara University, istanbul – Turkey Turk J Med Sci 34 (2004) 215-226  Burns: Definition, Classification, Pathophysiology and Initial Approach Garcia-Espinoza et al., Gen Med (Los Angeles) 2017, 5:5  Bailey and love  Burn clinical practise and guideline Developed by Texas EMS Trauma & Acute Care Foundation Trauma Division