1. Burns can be classified based on depth and percentage of total body surface area affected. Deeper burns involving more surface area lead to worse outcomes. 2. Burns trigger a complex pathophysiological response involving fluid shifts, immune dysfunction, and metabolic alterations. Locally, burns cause tissue damage and fluid accumulation. Systemically, burns induce hypovolaemic shock, immune suppression increasing infection risk, and a hypermetabolic state. 3. Managing the pathophysiological effects of burns, especially fluid shifts and immune dysfunction, is important for treatment and recovery from burn injuries. Deeper and more extensive burns have more severe local and systemic pathophysiological consequences.

1. BURN: Pathophysiology

2. What is a burn?
• Cutaneous injury caused by heat, electricity,
chemicals, friction, or radiation.

3. Types of burns

6. Circumstances of injury

7. Where do burns occur

8. Depth of burn
• Determined by :
– Temperature
– Length of exposure to the specific heat source
producing the burn

9. • Even low temperature (<44C) results in tissue
death if exposure long enough.
• Between 44 & 51C the rate of cell destruction
doubles with each degree rise in temperature.
• >70C tissue destruction instantaneous

10. Immersion time to produce full thickness burns
Temperature (C) Time
65 <1 second
60 2 seconds
55 10 seconds
50 30 seconds
47.5 1 minute
45 10 minutes

11. Superficial burn (1st degree)
• Only the epidermis
• Red and tender
• Mild discomfort

12. First Degree Burn
Only involves the EPI-dermis

13. Superficial partial-thickness burn
(Superficial 2nd degree burn)
• Epidermis and part of the dermis
• Blistered, red, blanches with pressure
• Often seen with scalding injuries
• Sensitive to light touch or pinprick
• Heal time 1-3 weeks

14. Second Degree Burn

15. Deep partial-thickness
(Deep 2nd degree)
• Epidermis and most of the dermis
• Appears white or poor vascularized; may not
blister
• Less sensitive to light touch than superficial
form
• Extensive time to heal (3-4 weeks)

16. Deep partial– White is deeper than pink

17. Full-thickness (3rd degree)
• Epidermis, dermis and into subcutaneous
tissue
• Dry, leathery and insensate. Typically no
blistering
• Commonly seen when clothes are caught on
fire or skin is directly exposed to flame
• Extensive healing time

18. Third Degree Burn

19. Fourth degree
• Full-thickness extends to muscle or bone
• Commonly seen with high voltage electric
injury or severe thermal burns

20. Fourth Degree
Electrical burns go deep

21. Classification
• More than 20% TBSA – Major burn
• More than 40% TBSA – Severe Burns

24. 1. LOCAL EFFECTS
2. FLUID SHIFTS
3. IMMUNOLOGICAL RESPONSE
4. METABOLIC EFFECTS

25. LOCAL EFFECTS

26. Zones of a burn (Jackson):
• Zone of coagulation
• Zone of Stasis (middle zone)
– Stagnation of microvasculature flow:
• Early (0 to 4 hours)
• Delayed (4 to 24 hours)
• Zone of hypereamia (outermost zone)
– Epidermis: reversibly injured
– Dermis: microvasculature dilated.
– Minimal fluid loss

29. Causes of stasis:
1. Endothelial injury
2. Arteriolar (1-2 hours post burn) and venular (3-4
hours post burn) dilatation
3. RBC aggregation
4. WBC clumping (8-24 hours post burn)
5. Platelet thrombi formation
6. Increased blood viscosity (due to plasma loss and
haemoconcentration)
7. Thromboplastin release

30. Zone of stasis may progress with
• Inadequate resuscitation
• Infection
• Sepsis
• Wound dries out

31. Proinflammatory
phenomena known as
systemic inflammatory
response syndrome
• macrophage
• cytokines TNF-α
• interleukin-6 (IL-6)
• Bax, Bcl-xl, and caspase-3
• reactive oxygen species
(ROS), such as
• superoxide anion, hydroxyl
radical, hydrogen peroxide,
• reactive nitrogen species,
such as nitric oxide (NO)
and peroxynitrite
Anti-inflammatory/ counter
antiinflammatory response
syndrome
• T lymphocytes of helper Th-
2
• Cytokines IL-4/IL-10
• TGF

32. FLUID SHIFTS

33. 1. Locally at burn site:
- Due to oedema formation
- Loss to exterior
- Loss into blisters
2. In burns > 30% TBSA
- Oedema of non-burned tissue
3. Systemic fluid shifts due to effects of
hypovolaemic shock

34. LOCAL OEDEMA AT BURN SITE
1. Increased microvascular permeability
2. Venular obstruction (RBC, WBC, platelets).
3. Increased interstitial osmolality (Bostwick)
secondary to protein shifts.
4. Dilatation of precapillary resistance vessels

35. An increase in microvascular permeability is the
predominant mechanism- Biphasic
1. Immediate and transient phase-
– Histamine mediated
– Lasts 5-10 minutes
– Slight increase in permeability with little
contribution to oedema formation.

36. 2. Delayed prolonged phase
• Begins + 2 hours post burn, lasts + 8 hours.
• Due to:
– (1) Direct heat injury and destruction of
vasculature.
– (2) Mediators
• Arachidonic acid metabolites
• Free oxygen radical
• kinins, serotonin, etc.

37. • Worsens oxygen delivery to the tissues.
• Peaks + 6 hours post burn (later in large
burns).
• Starts resolving after about 24 hours. Resolves
by end of first week.
• Magnitude depends on depth and extent of
burn.
• Full thickness burns may result in less oedema
due to coagulation of vessels.

40. • PMN - microvascular occlusion both
systemically and locally
• Endothelial cells and PMN release:
– PMN-derived proteases
– Toxic oxygen radicals
– Hydrogen peroxide and hydroxyl radicals.
• Peroxidation of lipids in cell membranes and
resultant cell lysis and thrombosis

42. • Collagen denaturation - ground substance
destruction results in increased negativity of
colloid osmotic pressure of interstitial fluid

43. NON BURNED TISSUE
• > 25% TBSA- Generalised oedema of all body
tissues
• Arturson: General increase in capillary
permeability.
• Demling: Hypoproteinaemia is the main
cause. Effect of burns is increased flow to
CNS, heart, liver and adrenals and diminished
flow to skin, muscle, gut and kidneys

44. SYSTEMIC EFFECTS - HYPOVOLAEMIC
SHOCK
Effects of shock:
1. Cellular Hypoxia, therefore:
– 1. Failure of Na-K ATPase pump - cellular swelling
- cell death.
– 2. Anaerobic metabolism - lactic acidosis
– 3. Mitochondrial calcium depletion - myocardial
depression
– 4. Cellular damage - cytokine release

45. 2. Compensatory Mechanisms:
I. Collapse, hyperventilation
II. Microcirculatory changes (resorption of
fluid from interstitial & intracellular
spaces)
III. Neurohumoral changes
IV. Splanchnic vasoconstriction
• Hepato-renal dysfunction
• Ileus, gut ischaemia and translocation

46. 3. Decompensation, if overwhelming shock
I. Cellular failure (Na-K pump, mitochondria,
lysozomal and cellular lysis)
II. Microcirculatory failure (massive fluid leak from
vasculature)
III. Organ failure - MOF

47. IMMUNOLOGICAL RESPONSE TO
BURNS

48. • Suppression of host defence mechanisms
• Infection: primary or major cause of death in
75%
1. INTEGUMENT
2. NON SPECIFIC IMMUNITY (Early acute
inflammatory response)
3. HUMORAL IMMUNITY
4. CELL MEDIATED IMMUNITY

49. INTEGUMENT
EARLY –
• Skin damage results in loss of protection against
microbial invasion.
• Inhalational burns destroy respiratory tract
mucosa.
• Intestinal mucosa is affected by splanchnic
vasoconstriction
• Increased systemic bacterial and endotoxin load
LATE –
• Coagulated skin and eschar form an ideal growth
media for micro-organisms

50. NON SPECIFIC IMMUNITY Early acute
inflammatory response
Mediator release:
* Vasoactive amines (Histamine and Serotonin)
* Arachidonic Acid Metabolites (PG's, PGI2, TxA2,
LT's)
* TNF
* Interleukins (1, 2, 6)
* Interferons (gamma)
* Colony stimulating factors
* Free oxygen radicals

51. • Diminished neutrophil function (chemotaxis,
opsonisation, phagocytosis, killing).
• Diminished macrophage function
• Activation and consumption of C' factors.
• Depletion of fibronectin.
• Circulatory immunosuppressive factors:
(autoantibodies, immune complexes, toxins, α
globulins)

53. HUMORAL IMMUNITY
Immunoglobulins are depleted due to:
• Decreased synthesis
• Capillary leakage
• Increased catabolism
• Haemodilution

54. IgG
• - Most affected. The most important opsonic
Ab for both G-ve and G+ve bacteria.
• - Level of depletion can be correlated
prognostically with septic complications.
IgM
• - Because of its size, is least affected

55. CELL MEDIATED IMMUNITY
Depressed by burns:
1. - Blast transformation and lymphocyte
proliferation is impaired.
2. - Decreased T-helper : T-suppressor cell ratio.
3. - Diminished activity of T-helper and T-killer
cells.

57. 4. Suppressor cells proliferate maximally at
about 7 to 14 days post injury, coinciding
with the appearance of septic complications.
5. Impaired response to antigens
6. Prolonged allograft survival
7. Diminished resistance to tumours

58. OTHER FACTORS AFFECTING
IMMUNITY
1. Extremes of age
2. Concomittant disease (eg. Diabetes)
3. Poor nutritional status
4. Drugs (Antibiotics, topical agents, steroids)
5. Blood transfusions
6. Surgery

59. METABOLIC ALTERATIONS

60. Cuthbertson (1930) - Biphasic metabolic
response to injury:
1. EBB PHASE (Hypofunction/hypometabolic
state)
• CVS Decreased intravascular volume
(hypovolumia), Low cardiac output
• Pulm hypoventilation
• Renal Oliguria
• CNS Agitation
• Endocrine Catabolism, decreased O2 consumption
• GIT Ileus
• Skin Poor tissue perfusion

61. 2. FLOW PHASE: (Hyperfunction)
Hypermetabolic phase following successful resuscitation
from ebb phase (after 24-72 hours)
• CVS Hyperdynamic, Increased cardiac output
• Pulm Hyperventilation
• Renal Diuresis
• CNS Depression
• Endocrine Anabolism, Increased oxygen consumption
• GIT Hypermotility
• Skin Hyperemia

62. • Persists until remodelling is complete- Many
months.
• Increase BMR/Energy expenditure (2-3X
increase in 60% TBSA burn)
• Increased nitrogen losses (via normal channels
and from burn directly)

63. • Mediated by the hypothalamic-pituitary axis
which receives
– Neuronal (pain, fear, anxiety, hypoxia,
hypotension) signals
– humoral (prostoglandins, interleukins, C',
endotoxins) signals.
• Volume, chemo, osmo and baro receptors act
on the hypothalamus resulting in a
neurohumoral response

64. Neuro-humoral cascade
- Adrenergic outflow
- Anti-insulin hormones:
- ACTH and Catecholamines
- Glucagon
- Growth Hormone
- Insulin (Diminished levels initially)
(Hours or days post burn, insulin levels rise)
(Insulin resistance occurs)
- Renal hormones:
- ADH
- Renin/Angiotensin
- Aldosterone
- Other hormonal mediators:
- TSH
- Endorphins
- Interleukins

65. 1. GLUCOSE METABOLISM
1. Increased glycolysis
2. Increased gluconeogenesis
3. Hyperglycaemia due to insulin resistance
4. Increased utilization and oxidation of glucose
5. Increased futile cycles (Cori and glucose-alanine
cycles)

66. 2. FAT METABOLISM
1. Increased lipolysis
2. Increased cycling (TG FFA + Glycerol)
- Increasingly recognised role of fats in
immunological function:
* Prostinoid substrates
* Lipoproteins
* Cell membranes
- Dietary fat supplementation is important

67. 3. PROTEIN METABOLISM
• Massive proteolysis and muscle catabolism
occur leading to a negative N balance.
• Urinary nitrogen losses: 30 gm per day in the
fasting severely burned patient.
• Exudative wound protein losses: 150 gm per day.
• Average 70 kg male has: 4500 gm of skeletal
muscle protein and 8500 gm of visceral, plasma
and bone protein. Loss of > 40% of body protein
is fatal

68. • Protein is also mobilised from other tissues
(eg, gut, leading to translocation), which is
used for:
– Gluconeogenesis
– Acute phase proteins
– Components of immune system: cells, Ig, clotting
factors, etc.
– Wound repair.

69. 1. Weakness, myopathy, wasting
2. Impaired mobilisation
3. Impaired respiratory function
4. Impaired immunity
5. Poor wound healing

78. Conclusion
The aim of the body's metabolic response to a
severe burn is
• to provide an effective physiological response
to fluid depletion, shifts and hypovolaemia;
• to mount a protective immunological barrier
to micro-organism invasion and infection and
• to mobilise the body's substrate resources so
as to allow effective wound healing and a
return to health

79. References
• Total Burn Care; David N Herndon. 3rd edn
• Burns: Pathophysiology of Systemic
Complications and Current Management;
Colton B. Nielson, Nicholas C. Duethman,
James M. Howard. American Burn Association
• ABC of burns: Pathophysiology and types of
burns; Shehan Hettiaratchy, Peter Dziewulski