BURNS

 Burns is defined as a wound caused by exogenous agent

leading to coagulative necrosis of the tissue.
CAUSES
 Thermal Burns
 Dry heat
 Contact burn
 Flame burn

 Moistheat- Scald burn

 Smoke and inhalational injury

 Chemical Burns- acids & alkali

 Electrical burns- High & low voltage

 Cold Burns- frostbite

 Radiation
THERMAL BURNS

 Heat changes the molecular structure of tissue Causing

Denaturation of proteins
 Extent of burn damage depends on
 Temperature of agent
 Amount of heat
 Duration of contact

 The effects of the burns are influenced by the:

 Intensity of the energy
 duration of exposure
 type of tissue injured
PATHOPHYSIOLOGY OF BURNS
 Fluid Shift
 Period of inflammatory response
 Vessels adjacent to burn injury dilate → ↑ capillary hydrostatic
pressure and ↑ capillary permeability
 Continuous leak of plasma from intravascular space into interstitial
space
 Associated imbalances of fluids, electrolytes and acid-base occur
 Hemoconcentration– Lasts 24-36 hours
FLUID REMOBILIZATION
 Capillary leak ceases and fluid shifts back into the
circulation
 Restores fluid balance and renal perfusion
 Increased urine formation and diuresis
 Continued electrolyte imbalance
 Hyponatremia
 Hypokalemia

 Hemodilution
SYSTEMIC CHANGES
 Cardiac– Decreased cardiac output
 Pulmonary– Respiratory insufficiency as a secondary
process
 Canprogress to respiratory failure
 Aggressive pulmonary toilet and oxygenation

 Gastrointestinal
 Decreased or absent motility (may need NG tube)
 Curling’s ulcer formation
 Metabolic
 Hypermetabolic state
 Increased oxygen and calorie requirements
 Increase in core body temperature

 Immunologic
 Loss of protective barrier
 Increased risk of infection
 Suppression of humoral and cell-mediated immune responses
ACUTE PHASE
 Clinical shock
 External loss of plasma

 Loss of circulating red cells

 Burn edema
SUB ACUTE PHASE
 Diuresis
 Clinical Anemia

 Accelerated metabolic rate

 Nitrogen Disequilibrium

 Bone and joint changes

 Endocrine Disturbances

 Electrolyte and chemical imbalance

 Circulatory Derangements

 Loss of function of skin as an organ

BODY’S RESPONSE TO BURNS
 Emergent Phase (Stage 1)
 Painresponse
 Catecholamine release
 Tachycardia, Tachypnea, Mild Hypertension, MildAnxiety

 Fluid Shift Phase (Stage 2)

 Length 18-24 hours
 Begins after Emergent Phase
 Reaches peak in 6-8 hours
 Damaged cells initiate inflammatory response
 Increased blood flow to cells
 Shift of fluid from intravascular to extravascular space

 MASSIVE EDEMA
 Hypermetabolic Phase (Stage 3)
 Last for days to weeks
 Large increase in the body’s need for nutrients as it repairs
itself
 Resolution Phase (Stage 4)
 Scarformation
 General rehabilitation and progression to normal function
JACKSON’S THEORY OF THERMAL WOUNDS
 Jackson’s Theory of Thermal Wounds
 Zone of Coagulation
Area in a burn nearest the heat source that suffers
the most damage as evidenced by clotted blood
and thrombosed blood vessels
 Zone of Stasis
Area surrounding zone of coagulation
characterized by decreased blood flow
 Zone of Hyperemia
Peripheral area around burn that has an increased
blood flow
 Severity is determined by:
 depth of burn
 extend of burn calculated in percent of total body surface
(TBSA)
 location of burn
 patient risk factors
CLASSIFICATION OF BURNS
 First degree
 injury localized to the epidermis
 Superficial second degree
 injury to the epidermis and superficial papillary dermis
 Deep second degree
 injury through the epidermis and deep up to reticular dermis
 Third degree
 full-thicknessinjury through the epidermis and dermis into
subcutaneous fat
 Fourth degree
 injury through the skin and subcutaneous fat into underlying muscle
or bone