PATOPHYSIOLOGY OF

BURN INJURY
 WHAT IS A BURN?

AN INJURY TO TISSUE FROM:

– EXPOSURE TO FLAMES OR HOT LIQUIDS
–CONTACT WITH HOT OBJECTS
– EXPOSURE TO CAUSTIC CHEMICALS OR
RADIATION
– CONTACT WITH AN ELECTRICAL CURRENT
 ETIOLOGY
• THERMAL/COMBUSTION
• SCALD BURNS (BOILING WATER AND OIL, TAR, ASPHALT)
• FLAME BURNS (FIRE)
• FLASH BURNS (GAS EXPLOTION, PROPANE, GASOLINE)
• CONTACT BURNS
• CHEMICAL
• ACIDS
• BASES/ALKALI
• ORGANIC COMPONENET (FENOL, CREOSOTE)
• ELECTRIC
• DIRECT CONTACT
• ARC INJURIES
• LIGHTNING INJURY

• RADIATION
• ALPHA, BETA, GAMMA WAVE (NUCLEAR WEAPON,
RADIOACTIVE SUBSTANCE, NUCLEAR REACTOR)
• X-RAY (RÖNTGEN)
• RADIO WAVE DAN MICROWAVE
 ANATOMY OF THE SKIN

• EPIDERMIS
• OUTER CELLS ARE DEAD
• ACT AS PROTECTION AND FORM WATER TIGHT SEAL
• DEPER LAYERS DIVIDE TO PRODUCE THE STRATUM CORNEUM AND ALSO
CONTAIN PIGMENT TO PROTECT AGAINST UV RADIATION

• DERMIS
• CONSISTS OF TOUGH, ELASTIC CONNECTIVE TISSUE WHICH CONTAINS
SPECIALIZED STRUCTURES
• DERMIS - SPECIALIZED STRUCTURES
• NERVE ENDINGS
• BLOOD VESSELS
• SWEAT GLANDS
• OIL GLANDS - KEEP SKIN WATERPROOF, USUALLY DISCHARGES AROUND
HAIR SHAFTS
• HAIR FOLLICLES - PRODUCE HAIR FROM HAIR ROOT OR PAPILLA
• EACH FOLLICLE HAS A SMALL MUSCLE (ARRECTUS PILLORUM) WHICH CAN
PULL THE HAIR UPRIGHT AND CAUSE GOOSE FLESH
SKIN FUNCTIONS
 BURN CLASSIFICATIONS

• FIRST DEGREE
• EPIDERMIS ONLY
• ERYTHEMATOUS
• TENDERNESS AND PAIN
• INCREASED WARMTH
• NO BLISTERING
• EXAMPLE - SUNBURN
• USUALLY HEAL IN ~ 7
DAYS WITHOUT
SCAR
• SECOND DEGREE
• EPIDERMIS + PART OF
DERMIS
• SUPERFICIAL (IIA)
• DEEP (IIB)

• BLISTERS
• EDEMATOUS AND RED
• VERY PAINFUL
• SCARING VARIABLE
• USUALLY HEAL IN 10-
14 DAYS (IIA) OR >1
MONTHS (IIB)
• THIRD DEGREE
• EPIDERMIS AND DERMIS ARE
DESTROYED WITH BURNING
INTO SQ FAT
• THICK, DRY APPEARANCE
• WAXY WHITE, LEATHERY
BROWN OR CHARRED
BLACK
• PAINLESS
• HEALS WITH SCAR
• MAY BE MINOR BLEEDING
CLASSIFICATION OF BURN DEPTH
BURN DEPTH CATEGORIES IN USA

GRABB SMITH’S PLASTIC SURGERY 6TH ED, 2007

 BODY SURFACE AREA ESTIMATION

• RULE OF NINES
• ADULT

• PALM RULE
 BODY SURFACE AREA ESTIMATION

• RULE OF NINES
• PEDS
• FOR EACH YR
OVER 1 YOA,
SUBTRACT 1%
FROM HEAD AND
ADD EQUALLY TO
LEGS

• PALM RULE
 BODY SURFACE AREA ESTIMATION
• LUND BROWDER CHARTS
• PROVIDE MORE PRECISE
ESTIMATION OF TOTAL BURN
SURFACE AREA
• SPECIFIC NUMBER FOR EACH
BODY PART BASED ON
INDIVIDUAL’S AGE
CRITICAL BURN CRITERIA
• 3RD DEGREE > 10% BSA
• 2ND DEGREE > 30% BSA → 20% PEDIATRIC
• BURNS WITH RESPIRATORY INJURY
• HANDS, FACE, FEET, OR GENITALIA
• BURNS COMPLICATED BY OTHER TRAUMA
• UNDERLYING HEALTH PROBLEMS
• ELECTRICAL AND DEEP CHEMICAL BURNS
MODERATE BURN CRITERIA
• 3RD DEGREE 2-10% BSA
• 2ND DEGREE 15-30% BSA → 10-20% PEDIATRIC
• EXCLUDING HANDS, FACE, FEET, OR GENITALIA
• WITHOUT COMPLICATING FACTORS

MINOR BURN CRITERIA

• 3RD DEGREE < 2% BSA
• 2ND DEGREE < 15% BSA→10% PEDIATRIC
• 1ST DEGREE < 20% BSA
 PATHOPHYSIOLOGY OF BURN INJURY

• SURFACE TEMPERATURES OF 44° C DO NOT PRODUCE BURNS UNLESS

EXPOSURE TIME > 6 HOURS
• AT TEMPERATURES BETWEEN 44° AND 51° C THE RATE OF EPIDERMAL
NECROSIS APPROXIMATELY DOUBLES WITH EACH DEGREE OF
TEMPERATURE INCREASE
• AT 70° C OR GREATER, THE EXPOSURE TIME REQUIRED TO CAUSE
TRANSEPIDERMAL NECROSIS IS LESS THAN 1 SECOND
• THE DEGREE OF TISSUE DESTRUCTION DEPENDS ON THE TEMPERATURE
AND DURATION OF EXPOSURE
• FACTORS THAT INFLUENCE THE BODY’S ABILITY TO RESIST BURN
INJURY INCLUDE:
a. THE WATER CONTENT OF THE SKIN TISSUE
b. THICKNESS AND PIGMENTATION OF THE SKIN
c. PRESENCE OR ABSENCE OF INSULATING SUBSTANCES (E.G., SKIN
OILS, HAIR)
d. PERIPHERAL CIRCULATION OF THE SKIN, WHICH AFFECTS DISSIPATION
OF HEAT
 BURN INJURY PHASE

1. ACUTE PHASE AKUT  FLUID AND ELECTROLITE

IMBALANCE, BECAUSE OF SYSTEMIC THERMAL INJURY AND
INADEQUATE OXYGEN PERFUSION
2. SUB ACUTE PHASE  TISSUE LOSS PROBLEM THAT CAUSE
INFLAMMATION REACTION, INCREASED SUSCEPTIBILITY TO
INFECTION, HYPERMETABOLISM AND WOUND HEALING PROCESS
3. LATE PHASE  HYPERTHROPIC SCAR PROBLEM AND
CONTRACTURE AS THE COMPLICATIONS
 BURN INJURY PHASE

EMERGENT PHASE
• RESPONSE TO PAIN  CATECHOLAMINE RELEASE
FLUID SHIFT PHASE
• MASSIVE SHIFT OF FLUID - INTRAVASCULAR  EXTRAVASCULAR
HYPERMETABOLIC PHASE
•  DEMAND FOR NUTRIENTS  REPAIR TISSUE DAMAGE
RESOLUTION PHASE
• SCAR TISSUE AND REMODELING OF TISSUE
 BURN INJURY RESPONSE

• LOCAL RESPONSE
• SYSTEMIC RESPONSE
 LOCAL RESPONSE

• BURN INJURY IMMEDIATELY DESTROYS CELLS, OR DISRUPTS THEIR

METABOLIC FUNCTIONS SO COMPLETELY THAT CELLULAR DEATH
ENSUES
• CELLULAR DAMAGE IS DISTRIBUTED OVER A SPECTRUM OF INJURY
a. SOME CELLS ARE DESTROYED INSTANTLY
b. OTHERS ARE IRREVERSIBLY INJURED
c. SOME CELLS MAY SURVIVE IF RAPID AND APPROPRIATE INTERVENTION
IS PROVIDED IN THE PREHOSPITAL SETTING
 JACKSON’S THERMAL WOUND THEORY

• ZONE OF COAGULATION
1) THE CENTRAL AREA OF THE BURN THAT HAS SUSTAINED THE MOST INTENSE
CONTACT WITH THE THERMAL SOURCE
2) COAGULATION NECROSIS OF THE CELLS HAS OCCURRED
3) THE TISSUE IS NONVIABLE
• ZONE OF STASIS
1) SURROUNDS THE CRITICALLY INJURED AREA
2) CONSISTS OF POTENTIALLY VIABLE TISSUE
3) CELLS ARE ISCHEMIC BECAUSE OF CLOTTING AND VASOCONSTRICTION AND DIE
WITHIN 24 TO 48 HOURS IF NO SUPPORTIVE MEASURES
• ZONE OF HYPEREMIA
1) INCREASED BLOOD FLOW BECAUSE OF NORMAL INFLAMMATORY RESPONSE
2) TISSUES RECOVER IN 7 TO 10 DAYS IF INFECTION OR PROFOUND SHOCK DOES
NOT DEVELOP
JACKSON’S THERMAL WOUND
THEORY
ZONE OF INJURY
 LOCAL RESPONSE

• BURN WOUND → THE RELEASE OF CHEMICAL MEDIATORS SWELLING

• INCREASE IN CAPILLARY PERMEABILITY AND A FLUID SHIFT FROM THE
INTRAVASCULAR SPACE INTO THE INJURED TISSUES
• INJURY TO THE SODIUM PUMP ACCENTUATES THE INCREASED
PERMEABILITY→ SODIUM MOVES INTO INJURED CELLS → INCREASE IN
OSMOTIC PRESSURE THAT INCREASES THE INFLOW OF VASCULAR FLUID
INTO THE WOUND
 LOCAL RESPONSE

• NORMAL PROCESS OF EVAPORATIVE LOSS OF WATER INTO THE

ENVIRONMENT IS DRAMATICALLY ACCELERATED (5 TO 15X NORMAL
SKIN) THROUGH THE BURNED TISSUE
• IN A SMALL WOUND THESE PHYSIOLOGICAL ALTERATIONS PRODUCE
A CLASSIC INFLAMMATORY RESPONSE WITHOUT ANY MAJOR
SYSTEMIC EFFECTS
• IN A LARGE BSA BURN, LOCAL TISSUE RESPONSES CAN PRODUCE
MAJOR SYSTEMIC EFFECTS AND LIFE-THREATENING HYPOVOLEMIA
 SYSTEMIC RESPONSE

• CARDIOVASCULAR RESPONSE
• PULMONARY RESPONSE
• KIDNEY RESPONSE
• GASTROINTESTINAL RESPONSE
• IMMUNE RESPONSE
 CARDIOVASCULAR RESPONSE

• ACUTE (HYPOVOLEMIA PHASE)

• ↑ CAPILLARY PERMEABILITY → EKSTRAVATATION
• ↓ BLOOD FLOW
• ↓ CARDIAC OUTPUT
• ↑ PERIPHERAL VASCULAR RESISTANCE

• CAN CONTINUE UP TO 48 JAM

 CARDIOVASCULAR RESPONSE

• HYPERMETABOLIC PHASE (SUB ACUTE)

• ↑ BLOOD FLOW
• EDEMA
• CARDIAC ARRHYTMIAS
• MYOCARD INFARCTION
• MYOCARDIAL DYSFUNCTION / CARDIAC INSTABILITY
(↑ END–DIASTOLIC VOLUME DAN ↓ EJECTION FRACTION RIGHT VENTRICLE)
 PULMONARY RESPONSE

• LUNG INFLAMMATION & LIPID PEROXIDATION → EDEMA

• PULMONAL ARTERIAL HYPERTENSION
• BRONCHIAL OBSTRUCTION
• ↑ AIRWAY RESISTANCE
• ↓ PULMONARY COMPLIANCE
• HYPOXEMIA → ARDS
• WORSE IF ACCOMPANIED BY INHALATION INJURY
 RENAL RESPONSE

• ACUTE PHASE (HYPOVOLEMIA PHASE)

• ↓ RENAL BLOOD FLOW
• ↓ GFR

• SUB ACUTE PHASE (HYPERMETABOLIK PHASE)

• ↑ RENAL BLOOD FLOW
• ↑ GFR
• TUBULE FUNCTION IMPAIRMENT
• ACUTE KIDNEY FAILURE
 GASTROINTESTINAL RESPONSE

• ↑ GASTRIC SECRETIONS
• ↑ ULCER INCIDENCE
• ↓ INTESTINAL & COLONIC MOTILITY
• ↓ MESENTERIC BLOOD FLOW
• ↓ NUTRIENT ABSORPTION
 GASTROINTESTINAL RESPONSE

OUTCOME :
• ADYNAMIC ILEUS
• GASTRIC DILATATION
• DELAY IN GASTRIC EMPTYING
• GASTOINTESTINAL HEMORRHAGE
• BACTERIAL TRANSLOCATION
• HEPATIC INJURY
IMMUNE RESPONSE
SYSTEMIC RESPONSE TO BURN INJURY
 POTENTIAL COMPLICATIONS

• FLUID AND ELECTROLYTE LOSS  HYPOVOLEMIA

• HYPOTHERMIA, INFECTION, ACIDOSIS
•  CATECHOLAMINE RELEASE, VASOCONSTRICTION
• RENAL OR HEPATIC FAILURE
• FORMATION OF ESCHAR
• COMPLICATIONS OF CIRCUMFERENTIAL BURN
 CHEMICAL BURNS

• ALKALIS
• HYDROXIDES, CARBONATES AND CAUSTIC SODAS OF SODIUM,
AMMONIUM, LITHIUM, BARIUM & CALCIUM
• OVEN & DRAIN CLEANERS, FERTILIZERS, INDUSTRIAL CLEANERS
• ACIDS
• HCL, OXALIC, MURIATIC & SULFURIC ACIDS
• COMMON IN HOUSEHOLD & SWIMMING POOL CLEANERS
• ORGANIC COMPOUNDS
• PHENOLS, CREOSOTE, PETROLEUM PRODUCTS
• CONTACT CHEMICAL BURNS & SYSTEMIC EFFECTS
 CHEMICAL BURNS
• FACTORS THAT DETERMINE SEVERITY:
• AGENT
• CONCENTRATION
• VOLUME
• DURATION OF CONTACT (DELAY IN TREATMENT)
• ALKALINE BURNS CAUSE MORE SEVERE INJURY THAN ACID BURNS
BECAUSE ALKALINE AGENTS CAUSE A LIQUEFACTION NECROSIS THAT
ALLOWS THE ALKALI TO PENETRATE DEEPER, EXTENDING THE AREA OF
INJURY
 PATHOPHYSIOLOGY OF
CHEMICAL BURNS

• ALKALI BURNS MECHANISM:

1. SAPONIFICATION OF FAT CAUSES LOSS OF THE INSULATION OF HEAT
FORMED IN THE CHEMICAL REACTION WITH TISSUE
2. MASSIVE EXTRACTION OF WATER FROM CELLS CAUSES DAMAGE BECAUSE
OF THE HYGROSCOPIC NATURE OF ALKALI
3. ALKALIS DISSOLVE AND UNITE WITH THE PROTEINS OF TISSUES TO FORM
ALKALINE PROTEINATES, WHICH ARE SOLUBLE AND CONTAIN HYDROXIDE
IONS

• ACIDS INDUCE PROTEIN BREAKDOWN BY HYDROLYSIS, WHICH RESULTS

IN A HARD ESCHAR
 ELECTRICAL BURN INJURY

• OCCURS WHEN ELECTRICITY IS CONVERTED TO HEAT AS IT TRAVELS THROUGH

TISSUE→NECROSIS AND COAGULATION
• USUALLY FOLLOWS ACCIDENTAL CONTACT WITH EXPOSED OBJECT CONDUCTING
ELECTRICITY (EG. ELECTRICAL DEVICES & WIRING) AND FROM LIGHTNING

• ELECTRICAL FOLLOWS SHORTEST PATH TO GROUND

• HIGHER VOLTAGE MAY RESULT IN MORE OBVIOUS EXTERNAL BURNS→ TRIVIAL
LOOKING
• CURRENT KILLS, VOLTAGE SIMPLY DETERMINES WHETHER CURRENT CAN ENTER THE
BODY (OHM’S LAW: I=V/R)
 ELECTRICAL BURN INJURY

• SEVERITY DEPENDS ON:

• AMPERAGE AND VOLTAGE (HIGH VOLTAGE > 1000 VOLTS)
• TISSUE RESISTANCE
• BONE > FAT > SKIN > MUSCLE > BLOOD > NERVE
• WIDTH OR EXTENT OF THE CURRENT PATHWAY
• TYPE OF CURRENT: AC OR DC
• DURATION OF CONTACT
• CURRENT PATHWAY
• LOW-VOLTAGE → LEAST RESISTANCE
• HIGH-VOLTAGE → SHORTEST PATHWAY
• CURRENT FLOW (ENTRANCE → EXIT)
 ELECTRICAL BURN INJURY

• DIRECT CONTACT
• HAND AND WRIST → ENTRANCE SITE; FOOT → EXIT SITE
• EXIT DAN ENTRANCE SITE → SEVERE BURN INJURY
• AREA BETWEEN THE WOUNDS THAT POSES THE GREATEST THREAT TO THE
PATIENT’S LIFE

• FLAME AND FLASH BURNS

• THE HEAT OF ELECTRIC CURRENT IGNITES A NEARBY COMBUSTIBLE SOURCE
• COMMON INJURY SITES INCLUDE THE FACE AND EYES (WELDER’S FLASH)
• NO ELECTRICAL CURRENT PASSES THROUGH THE BODY IN THIS TYPE OF BURN
• ARC INJURIES
• HIGH VOLTAGE ELECTRICAL BURN INJURY
• OCCUR WHEN A PERSON IS CLOSE ENOUGH TO A HIGH-VOLTAGE
SOURCE THAT THE CURRENT BETWEEN TWO CONTACT POINTS NEAR THE
SKIN OVERCOMES THE RESISTANCE IN THE AIR → PASSING THE CURRENT
FLOW THROUGH THE AIR TO THE BYSTANDER
• TEMPERATURE: 2000 - 4000°C
• CURRENT FLOW MAY JUMP 10 M
 ELECTRIC BURN PATHOPHYSIOLOGY

• ENTRANCE SITE :
• CHARACTERISTIC OF “BULL’S EYE” WOUND
• MAY APPEAR DRY, LEATHERY, CHARRED, OR DEPRESSED

• EXIT SITE :
• ULCERATED
• HAVE AN “EXPLODED” APPEARANCE WHERE AREAS OF TISSUE ARE MISSING
• CATHECOLAMINE RELEASE →HYPERTENSION, TACHICARDIA
• ELECTRICAL CURRENT CAUSE DYSRHYTHMIAS, VENTRICULAR FIBRILLATION
(VF), ASYSTOLE AND MYOCARDIUM DAMAGE
 ELECTRIC BURN PATHOPHYSIOLOGY

• NERVE → EXCELLENT CONDUCTOR

• CNS DAMAGE → SEIZURE – COMMA WITH OR WITHOUT FOCAL
NEUROLOGICAL FINDINGS
• PERIPHERAL NERVE → PERMANENT MOTORIC OR SENSORIC DAMAGE
• BRAIN STEM → RESPIRATORY ARREST – DEPRESSION
• BRAIN → EDEMA, HEMORRHAGE
• VASCULAR :
• VASCULAR NECROSIS → RUPTURED → IMMEDIATE OR DELAYED INTERNAL
BLEEDING
 ELECTRIC BURN PATHOPHYSIOLOGY

• ARTERY AND VEIN THROMBOSIS

• EMBOLISM AND DIC
• HAEMOLYSIS → HB ACCUMULATION ON KIDNEY TUBULE → ACUTE KIDNEY
FAILURE

• MUSCLE :
• RHABDOMYOLISIS → MYOGLOBIN → ACCUMULATION ON KIDNEY TUBULE →
ACUTE KIDNEY FAILURE
• EXTENSIVE MUSCLE SPASM → FRACTURE AND JOINT DISLOCATION
 RADIATION EXPOSURE

• WAVES OR PARTICLES OF ENERGY THAT ARE EMITTED FROM RADIOACTIVE

SOURCES
• ALPHA RADIATION
• LARGE, TRAVEL A SHORT DISTANCE, MINIMAL PENETRATING ABILITY
• CAN HARM INTERNAL ORGANS IF INHALED, INGESTED OR ABSORBED
• BETA RADIATION
• SMALL, MORE ENERGY, MORE PENETRATING ABILITY
• USUALLY ENTER THRU DAMAGED SKIN, INGESTION OR INHALATION
• GAMMA RADIATION & X-RAYS
• MOST DANGEROUS PENETRATING RADIATION
• MAY PRODUCE LOCALIZED SKIN BURNS AND EXTENSIVE INTERNAL DAMAGE
 RADIATION EXPOSURE
• RADIATION EXPOSURE MAY RESULT IN:
• EXTERNAL INJURY
• CONTAMINATION
• INCORPORATION INJURY
• COMBINED INJURIES OF ORGAN, TISSUE, CELL, DNA

• EFFECT OF INJURY DEPENDENT UPON:

• DURATION OF EXPOSURE
• DISTANCE FROM THE SOURCE
• SHIELDING