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 weekswithout 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 pressurerather 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 asthey 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 potentvasoconstrictor, 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 ofleukocyte 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 andcatacholamine 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 formationwhich 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 ulcers40% loss- Can lead to death
? Severe burns cause upto 25% loss
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? Increased cotisol also causes transport ofcalcium 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 seenin 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 deficiencyof 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 mostlyantibody 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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EquationMediators involved in edema
formation
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? Mast cells in the burned skin release histaminein 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 permeabilityProstaglandin 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 resuscitationimproves 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 `fluidcreep'
? Complications of fluid creep are
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Eye injuries due to elevated orbital pressuresPulmonary 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 tenseabdomen combined + ventilation aberrations
due to elevated pulmonary inspiratory
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pressures
OR
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oliguria despite aggressive fluid resuscitationMyocardial 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 areRaised 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 dysfunctionGI 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 smallintestine
? 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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permeabilityLungs
? 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 occursRenal Dysfunction
? Local and Systemic cytokine release causes
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decreased renal blood flow which causes AcuteKidney 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 AcuteKidney 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 changethat it should be applied within 48 hours of
burn injury
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? Even though creatinine is not the idealbiochemical 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