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

Describe the Pathophysiology of

Burns

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Burns & Plastic Surgery

Introduction

? 66% of burn injuries occur at home

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? 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

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Causes
? Flame
? Scald
? Contact

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? Chemical
? Electricity

Classification ..
Depth of Burn

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

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form blisters.

? Sunburns fit this category of superficial,

epidermal injury.

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? Within 3?4 days, the dead epidermis sloughs

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

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? Extend into the papil ary dermis and characteristical y

form blisters.

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? Appearance is pink, wet and hypersensitive to touch.

? Painful as uncovering the wound al ows currents of air

to pass over it.

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? These wounds blanch with pressure as the blood flow

to the dermis is increased due to vasodilation.

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

without risk of scarring and therefore do not require

operation.

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3rd degree (Deep Dermal Burns)

? Extend into the reticular dermis and general y wil take

3 or more weeks to heal.

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? They also blister, but the wound surface appears

mottled pink and white

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? The patient complains of discomfort and pressure

rather than pain.

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

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slowly

? Partial-thickness burns that are predicted not to heal

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

? Ful -thickness burns involve the entire dermis and

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extend into subcutaneous tissue.

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

depressed when compared to adjoining normal skin.

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? These wounds are insensitive to light touch and

pinprick.

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

they may have a mottled appearance

? Must be excised and grafted early

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Local Changes in Burn Injury- Jacksons

Zones

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Zone of Stasis

? Can survive or go on to coagulative necrosis. The

zone of stasis is

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? associated with vascular damage and vessel

leakage.

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? Thromboxane A2, and Bradykinin a potent

vasoconstrictor, is present in high

? Local endothelial interactions with neutrophils

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mediate some of the local inflammatory

responses associated with the zone of stasis.

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? studies demonstrate that blockage of

leukocyte adherence with anti-CD18 or anti-

intercellular adhesion molecules &

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monoclonal antibodies improve tissue

perfusion and tissue survival in animal models.
Zone of Hyperemia

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? Contains viable tissue
? No risk of necrosis
? Characterized by vasodilation due to effect

from zone of stasis

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Systemic Changes in Severe

burns(>40%)
Hypermetabolic Response

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Phase 1 of Post Burn Metabolic

phenomenon(Ebb Phase)
? Lasts 48 hours

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? Decrease in Cardiac Output/O2 Consumption

? Causes hyperglycemia

Phase 2 ( Flow phase)

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? 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

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? 10-50 fold increase in corticosteroid and

catacholamine levels

? Results in Protein breakdown in muscles

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? Amino Acids ( Alanine ) from protein breakdown

recruited for gluconeogenesis

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? Fat breakdown in liver leads to glycerol formation

which is used for gluconeogenesis

? End product of anaerobic respiration in the burn

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wound (lactate) sent for gluconeogenesis

? Glucose is delivered to peripheral tissue but

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glucose oxidation does not occur

? This in turn raises insulin levels

? Overal effect is loss of lean body mass

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10% loss- decreased immune function

20% loss- chronic infections

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30% loss- pneumonia & pressure ulcers

40% loss- Can lead to death

? Severe burns cause upto 25% loss

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? Increased cotisol also causes transport of

calcium and magnesium from long bones

? Decreased bone mineral density and content

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leading to susceptibility to fractures

Immune Dysfunction

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? Depressed function of Macrophages,

Neutrophils, T cells and B cells

? Even though G-CSF levels actually increase

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after severe burn but bone marrow G-CSF

receptor expression is decreased, which may

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in part account for the immunodeficiency seen

in burns

? Release of negative regulators of myeloid

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growth decrease Macrophage production
? Neutrophil counts increase after severe burn

but they are dysfunctional

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? Altered diapedesis, chemotaxis and

phagocytosis due to loss of CD11b/CD18

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? Decreased Respiratory burst due to deficiency

of p47-phox activity

? Poor motility sue to impaired actin mechanics

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? 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

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phagocytosis and intracellular killing is

decreased

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? Increase in IL4 and IL 10 which is mostly

antibody based immunity

? Cytotoxic T lymphocyte activity also decreased

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? Administration of IL 10 antibodies and growth

factors decreases the effect of the polarization

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of immune response

Inflamation and Odema-Landis Starling

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Equation
Mediators involved in edema

formation

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? Mast cells in the burned skin release histamine

in large quantities immediately after injury,

which elicits a characteristic response in

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venules by increasing intercellular junction

space formation causing increased

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permeability

? Serotonin released from aggregated platlets

causes pulmonary vasoconstriction

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

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hypertension

? Angiotensin & Vasopressin responsible for

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systemic vasoconstriction and gut ischemia

? In the first 12 hours there is an abrupt

increase in the fluid levels in the burn tissue

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? After 24 hour there is a more gradual increase

in fluid content both in burned and non

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burned soft tissue

? This gradual 3rd space loss is eventually

responsible for burn shock

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? Prompt and adequate fluid resuscitation

improves outcome of the burn patient

? It is imperative to avoid Over ?resuscitation

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as well

? This trend of providing fluid in excess of the

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Parkland formula has been termed `fluid

creep'

? Complications of fluid creep are

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Eye injuries due to elevated orbital pressures
Pulmonary edema
Prolonged mechanical ventilation
Graft failure
Need for fasciotomy of uninjured extremities

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Abdominal Compartment Syndrome
? Intra-abdominal pressure (IAP) >30 cmH2O is

defined as intra-abdominal hypertension (IAH).

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? ACS is sustained IAH + clinically tense

abdomen combined + ventilation aberrations

due to elevated pulmonary inspiratory

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pressures

OR

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oliguria despite aggressive fluid resuscitation

Myocardial Dysfunction

? Myocardial contractility is depressed along

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with relaxation capacity leading to a stiff

myocardium

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

isolated)

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

cardiac Output may be increased upto 130-

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150% for a period of 2 years

? Adrenergic stimulation causes increased heart

rate as well as raised Systemic and Pulmonary

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vascular resistance

? Mortality occurs because of cardiac stress in a

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setting of myocardial dysfunction

GI System

? Apoptosis of epithelium of Small intestine

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mucosa

? Vesiculation of microvilli with breakdown of

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actin filaments in the microvilli of small

intestine

? Loss of brush border lipase activity ? loss of

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fatty acids

? Poor uptake of Glucose and amino acids from

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

causes bacterial and endotoxin translocation

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across the mucosa causing septicemia

? Inverse relation between blood flow and gut

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permeability

Lungs

? In large burns there is a pronounced increase

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in pulmonary vascular resistance (PVR)

? Both pre and post capilary vasoconstriction

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occurs which causes pulmonary odema

? Hypo-protenemia still remains the dominant

cause of pulmonary odema

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? In case of inhalational injury factors released

due to injury to bronchial tree and lung

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parenchyma occurs
Renal Dysfunction

? Local and Systemic cytokine release causes

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decreased renal blood flow which causes Acute

Kidney Injury

? Free Oxygen Radicles can cause direct tubular

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damage

? Other factor maybe myoglobinurea fol owing

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rhabdomyolysis ( Myoglobin> 1500-3000ng/ml)

? AKI may occur despite adequate fluid

resuscitation by Parkland Formula

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? Imperative to identify and diagnose Acute

Kidney Injury so that patient can be shifteds

for renal replacement therapy( Dialysis)

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? RIFLE and AKIN criteria developed to aid

diagnosis and plan therapy

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? AKIN is modification of RIFLE with only change

that it should be applied within 48 hours of

burn injury

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? Even though creatinine is not the ideal

biochemical marker of kidney dysfunction it

still remains the gold standard

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

shown promise as earlier detectors of changes

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in GFR

? In order to differentiate pre renal from renal

failure it is important to analyze the following

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indices


? Fractional excretion of urea is a more reliable

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indicator as it negates the effect of diuretic

use
Change in Membrane Potentials

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? Membrane potential in non burned distant

tissues such as skeletal muscles , nerves, Gi

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

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

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which may be responsible for tissue dysfunction

? This change is brought about increased sodium

conductance

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? The factor which leads to this has not yet been

identified but it has a complex and probably

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dynamic structure