Download MBBS Burns and Plastic Surgery PPT 1 Burn Pathophysiology Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Burns and Plastic Surgery PPT 1 Burn Pathophysiology Lecture Notes

Describe the Pathophysiology of


Burns & Plastic Surgery


? 66% of burn injuries occur at home
? Fatalities at extremes of age
? Flame and Scald most common cause
? Scald burn victims commonly< 5years
? Survival rate for all burns 94.6%
Burn Classification

? Flame
? Scald
? Contact
? Chemical
? Electricity

Classification ..
Depth of Burn

1st Degree
? Burns involving only the epidermis.
? Erythematous and very painful but do not

form blisters.

? Sunburns fit this category of superficial,

epidermal injury.

? Within 3?4 days, the dead epidermis sloughs

and is replaced by regenerating keratinocytes.
2nd degree (Superficial dermal burns)

? Extend into the papil ary dermis and characteristical y

form blisters.

? Appearance is pink, wet and hypersensitive to touch.

? Painful as uncovering the wound al ows currents of air

to pass over it.

? These wounds blanch with pressure as the blood flow

to the dermis is increased due to vasodilation.

? Superficial dermal burns usual y heal within 2?3 weeks

without risk of scarring and therefore do not require

3rd degree (Deep Dermal Burns)

? Extend into the reticular dermis and general y wil take

3 or more weeks to heal.

? They also blister, but the wound surface appears

mottled pink and white

? The patient complains of discomfort and pressure

rather than pain.

? When pressure is applied to the burn, capil aries refil


? Partial-thickness burns that are predicted not to heal

by 3 weeks should be excised and grafted.
4th Degree (Ful Thickness)

? Ful -thickness burns involve the entire dermis and

extend into subcutaneous tissue.

? Their appearance may be charred, leathery, firm, and

depressed when compared to adjoining normal skin.

? These wounds are insensitive to light touch and


? Non-charred ful -thickness burns can be deceptive as

they may have a mottled appearance

? Must be excised and grafted early

Local Changes in Burn Injury- Jacksons

Zone of Stasis

? Can survive or go on to coagulative necrosis. The

zone of stasis is

? associated with vascular damage and vessel


? Thromboxane A2, and Bradykinin a potent

vasoconstrictor, is present in high

? Local endothelial interactions with neutrophils

mediate some of the local inflammatory

responses associated with the zone of stasis.

? studies demonstrate that blockage of

leukocyte adherence with anti-CD18 or anti-

intercellular adhesion molecules &

monoclonal antibodies improve tissue

perfusion and tissue survival in animal models.
Zone of Hyperemia
? Contains viable tissue
? No risk of necrosis
? Characterized by vasodilation due to effect

from zone of stasis

Systemic Changes in Severe

Hypermetabolic Response

Phase 1 of Post Burn Metabolic

phenomenon(Ebb Phase)
? Lasts 48 hours
? Decrease in Cardiac Output/O2 Consumption

? Causes hyperglycemia

Phase 2 ( Flow phase)
? Begins after 48 hours
? Increase in metabolic rate and cardiac output
? Hyperglycemia in spite of raised insulin
? Reaches a plateau in about 5-7 days
? Persists upto 1-3 years
? 10-50 fold increase in corticosteroid and

catacholamine levels

? Results in Protein breakdown in muscles

? Amino Acids ( Alanine ) from protein breakdown

recruited for gluconeogenesis

? Fat breakdown in liver leads to glycerol formation

which is used for gluconeogenesis

? End product of anaerobic respiration in the burn

wound (lactate) sent for gluconeogenesis

? Glucose is delivered to peripheral tissue but

glucose oxidation does not occur

? This in turn raises insulin levels

? Overal effect is loss of lean body mass

10% loss- decreased immune function

20% loss- chronic infections

30% loss- pneumonia & pressure ulcers

40% loss- Can lead to death

? Severe burns cause upto 25% loss
? Increased cotisol also causes transport of

calcium and magnesium from long bones

? Decreased bone mineral density and content

leading to susceptibility to fractures

Immune Dysfunction

? Depressed function of Macrophages,

Neutrophils, T cells and B cells

? Even though G-CSF levels actually increase

after severe burn but bone marrow G-CSF

receptor expression is decreased, which may

in part account for the immunodeficiency seen

in burns

? Release of negative regulators of myeloid

growth decrease Macrophage production
? Neutrophil counts increase after severe burn

but they are dysfunctional

? Altered diapedesis, chemotaxis and

phagocytosis due to loss of CD11b/CD18

? Decreased Respiratory burst due to deficiency

of p47-phox activity

? Poor motility sue to impaired actin mechanics
? Counts begin to fall after 72 hours

? Depressed T helper function
? Polarization from Th1 to Th2 immune response
? IL2 and IFN- responsible for initiation of

phagocytosis and intracellular killing is


? Increase in IL4 and IL 10 which is mostly

antibody based immunity

? Cytotoxic T lymphocyte activity also decreased

? Administration of IL 10 antibodies and growth

factors decreases the effect of the polarization

of immune response

Inflamation and Odema-Landis Starling

Mediators involved in edema


? Mast cells in the burned skin release histamine

in large quantities immediately after injury,

which elicits a characteristic response in

venules by increasing intercellular junction

space formation causing increased


? Serotonin released from aggregated platlets

causes pulmonary vasoconstriction
? Mediators causing Increased permeability
Prostaglandin E2 and I2
Free Oxygen Radicles
Thromboxane A2 & B2
? Leukotrines B4 and D4 cause pulmonary


? Angiotensin & Vasopressin responsible for

systemic vasoconstriction and gut ischemia

? In the first 12 hours there is an abrupt

increase in the fluid levels in the burn tissue

? After 24 hour there is a more gradual increase

in fluid content both in burned and non

burned soft tissue

? This gradual 3rd space loss is eventually

responsible for burn shock
? Prompt and adequate fluid resuscitation

improves outcome of the burn patient

? It is imperative to avoid Over ?resuscitation

as well

? This trend of providing fluid in excess of the

Parkland formula has been termed `fluid


? Complications of fluid creep are
Eye injuries due to elevated orbital pressures
Pulmonary edema
Prolonged mechanical ventilation
Graft failure
Need for fasciotomy of uninjured extremities
Abdominal Compartment Syndrome
? Intra-abdominal pressure (IAP) >30 cmH2O is

defined as intra-abdominal hypertension (IAH).

? ACS is sustained IAH + clinically tense

abdomen combined + ventilation aberrations

due to elevated pulmonary inspiratory



oliguria despite aggressive fluid resuscitation

Myocardial Dysfunction

? Myocardial contractility is depressed along

with relaxation capacity leading to a stiff


? Possible causes for this are
Raised Intracellular calcium levels
Circulating Myocardial depressant factor( not

Raised TNF alpha levels
? Even though contractility is depressed , the

cardiac Output may be increased upto 130-

150% for a period of 2 years

? Adrenergic stimulation causes increased heart

rate as well as raised Systemic and Pulmonary

vascular resistance

? Mortality occurs because of cardiac stress in a

setting of myocardial dysfunction

GI System

? Apoptosis of epithelium of Small intestine


? Vesiculation of microvilli with breakdown of

actin filaments in the microvilli of small


? Loss of brush border lipase activity ? loss of

fatty acids

? Poor uptake of Glucose and amino acids from

the lumen
? Increased gut permeability leading to fluid loss
? Vasoconstriction leading to ischemia which

causes bacterial and endotoxin translocation

across the mucosa causing septicemia

? Inverse relation between blood flow and gut



? In large burns there is a pronounced increase

in pulmonary vascular resistance (PVR)

? Both pre and post capilary vasoconstriction

occurs which causes pulmonary odema

? Hypo-protenemia still remains the dominant

cause of pulmonary odema

? In case of inhalational injury factors released

due to injury to bronchial tree and lung

parenchyma occurs
Renal Dysfunction

? Local and Systemic cytokine release causes

decreased renal blood flow which causes Acute

Kidney Injury

? Free Oxygen Radicles can cause direct tubular


? Other factor maybe myoglobinurea fol owing

rhabdomyolysis ( Myoglobin> 1500-3000ng/ml)

? AKI may occur despite adequate fluid

resuscitation by Parkland Formula
? Imperative to identify and diagnose Acute

Kidney Injury so that patient can be shifteds

for renal replacement therapy( Dialysis)

? RIFLE and AKIN criteria developed to aid

diagnosis and plan therapy

? AKIN is modification of RIFLE with only change

that it should be applied within 48 hours of

burn injury
? Even though creatinine is not the ideal

biochemical marker of kidney dysfunction it

still remains the gold standard

? New markers of AKI, such as cystatin-C, have

shown promise as earlier detectors of changes

in GFR

? In order to differentiate pre renal from renal

failure it is important to analyze the following


? Fractional excretion of urea is a more reliable

indicator as it negates the effect of diuretic

Change in Membrane Potentials

? Membrane potential in non burned distant

tissues such as skeletal muscles , nerves, Gi

tissues partial y depolarize ( from -90 to -70)

? Cel death can occur at resting potentials of -60
? This change causes action potential dampening

which may be responsible for tissue dysfunction

? This change is brought about increased sodium


? The factor which leads to this has not yet been

identified but it has a complex and probably

dynamic structure

This post was last modified on 07 April 2022