BURNS

• Thermal injury can be defined as traumatic injury caused by a

temperature increase beyond a threshold able to cause tissue
damage
Etiology of Burns

Thermal Burns
■ Flame - damage from superheated, oxidized air
■ Scald - damage from contact with hot liquids
■ Contact - damage from contact with hot or coldsolid materials
Chemicals Burns- contact with noxious chemicals
Electricity Burns- conduction of electrical current through tissue
Cold Burns- Frosbite
Radiation
Sunburns
 FIRST AID
THERMAL BURNS : STOP the burning process ELECTRICAL BURNS:-turns off
Apply running water for 10-20mins . Ice should never mains/switch off source (power point)
be used RESCUE from electrical shock-:
Examine for associated trauma
respiratory failure due to tetanic effect,
Assess the extend of burns for superficial burns
conservative management and deep burns excisional CPR to be given
surgery Examine for associated injuries
Prevent contamination-: non adherent dressing Cervical spine protection
Relief of pain:-choice of analgesic and route of
administration depends on the severity

CHEMICAL BURNS :-Irrigation with copious amount of water as

residual chemical will continue the burning sensation
For chemical eye injuries :-Continuos irrigation untill opthalmoloic
review ALWAYS ENSURE that unaffected eye is uppermost when
irrigation to avaoid contamination
ACID :- Irrigation (from the contaminated area to the floor to avoid
run off injury) with water fir upto 1 hour
ALKALI:-irrigation with water upto 2 hours
 PATHOPHYSIOLOGY OF BURNS
PATHOPHYSIOLOGY OF BURN WOUND
 PATHOPHYSIOLOGY OF SYSTEMIC CHANGES
Heat causes coagulation necrosis of skin and subcutaneoustissue

Release of vasoactive peptides

Altered capillary permeability

loss of fluid → Severe hypovolaemia

cardiac→ Decreased myocardial function

Decreased renal blood → Oliguria flow (Renal failure)

Altered pulmonary resistance causing pulmonary edema

Infection

Systemic inflammatory response syndrome (SIRS)

Multiorgan dysfunction syndrome (MODS

 SYSTEMIC CHANGES
• CARDIAC CHANGES:-Decreased cardiac output

• PULMONARY CHANGES :-Altered ventilation-perfusion ratio

Pulmonary oedema due to burn injury, fluid overload ARDS-
Aspiration Septicaemia.

• GASTROINTESTINEAL :- Acute gastric dilatation which occurs in 2-4

days.
• Paralytic ileus
• Curling's ulcer
• Acute acalculous cholecystitis
• Acutepancreatitis
• Abdominal Compartment syndrome
METABOLIC CHANGES:- Hypermetabolic rate (BMR)
.Negative nitrogen balance.
Electrolyte imbalance.
Deficiencies of vitamins and essential elements.
Metabolic acidosis due to hypoxia and lactic
acid.

IMMUNOLOGICAL -: Loss of protective barrier.

Increased risk of infection.
Suppression of humoral and cell-mediated immune
response
 PATHOPHYSIOLOGY OF BURNS SHOCK
COMPENSATED STAGE
the sympathetic reflexes (baroreceptor reflexes) and other factors
(formation of angiotensin ,vasopressin) compensate to prevent
further deterioration of shock

PROGRESSIVE STAGE -
Intravascular volume depletion due to massive edema
Myocardial depression – Circulating humoral factors eg TNF ,
decreased coronary bloodflow
Cellular changes – decrease in cell transmembrane potential
leading to generalised cellular swelling
• DECOMPENSATED STAGE
Two types of circulatory shock are encountered during burns
management

• HYPOVOLEMIC SHOCK
Vascular permeability

Edema intravascular volume

Blood volume hemocrit

viscosity
PERIPHERAL RESISTANCE

SHOCK
SEPTIC SHOCK
Presents as :- Increased or decreased temperature
Hypotension
tachycardia
oliguria
hyperventilation/
clouding of consciousness
Extremities turns pink(warm state)
 CLASSIFICATION OF BURNS
• SUPERFICIAL/ FIRST DEGREE BURNS

• SKIN LAYER INVOLVED :-Epidermal injury

• TISSUE LESION :-Epithelial desquamation
• COLOR:- Pink , blanches with pressure
• APPEARANCE:- Dry , Mild edema
• SENSITIVITY:- Mild pain
• HEALING:-4-5 DAYS
• SCAR:- No
• TREATMENT:- Topical hydration
• SKIN LAYER INVOLVED :-Papillary dermal injury
• TISSUE LESION :-Blister
• COLOR:- Bright red ,blanches with pressure
• APPEARANCE:- Intensely wet, severe edema
• SENSITIVITY:- Moderate pain
• HEALING:- <21 days
• SCAR:- No ,pigmentary changes
• TREATMENT :- Dressings
• SKIN LAYER INVOLVED :-partial reticular dermal injury
• TISSUE LESION :- Blister , eschar
• COLOR:- Dark red,yellowish white with red specks, doesnot
blanches with pressure
• APPEARANCE:- Mildly wet, decreased elasticity, Mild edema
• SENSITIVITY:- hypoesthesia, painless hair removal, deep pressure
pain
• HEALING:- >21 days
• SCAR:- yes, hypertrophic & retracted scar
• TREATMENT:- Surgery recommended
• SKIN LAYER INVOLVED :-total recticular dermal injury
• TISSUE LESION :-Eschar
• COLOR:- Marble white,gray (carbonization), blanches with
pressure
• APPEARANCE:- Dry (leathery), non elastic, depressed,
thrombosed vessels
• SENSITIVITY:- Anaethesia , deep pressure (+/-)
• HEALING:- >21 days (possible chronic wound)
• SCAR:- Yes, hypertrophic & retracted scar, skin cancer(marjolin
ulcer)
• TREATMENT:- Surgery mandatory
 ASSESSMENT OF BURNS
• WALLACES RULE OF NINE
LUND AND BROWLERS CHART
 DEFINITIVEMANAGEMENT
1. Maintain airway, breathing, circulation (ABC).

2. Sedation and analgesia

3. Assessment of percentage, degree and type of burn and

accordingly fluid management

4. Chemoprophylaxis: tetanus toxoid antibiotics andlocal

antiseptics.

5. Ryle's tube insertion initially for aspiration and later for feeding.
 TREATMENT FOR BURNS
• PRIMARY SURVEY

• A –AIRWAY laryngeal edema

• B –BREATHING : Acute respiratory insufficiency
• C –CIRCULATION : Refractory shock\
• D –DISABILITY : Glassglow coma scale score <8

• SECONDARY SURVEY
• Its done on stable patient
4 QUESIONARIES :-WHEN (“hour 0” )
WHAT (Injurious agent)
HOW (Injury mechanisms of incident)
WHERE (Indoor or outdoor)
 FLUID RESUSCITATION
• FLUID RESUSCITATION IN FIRST 24 HOURS

• EVANS – Normal saline: 1 mL/kg/%TBSA burn

Colloid:-1 mL/kg/%TBSA burn
5%Dextrose in Water:-2,000 mL

• Brooke – Ringer Lactate: 1.5 mL/kg/%TBSA burn

Colloid:-0.5 mL/kg/%TBSA
5%Dextrose in Water: 2000mL

• Parkland –Ringer Lactate: 4 mL/kg/%TBSA burn

Colloid: No
5% Dextrose in Water: No
• Modified Brooke –Ringer Lactate: 2 mL/kg/%TBSA burn
Colloid: No
5% Dextrose in Water: No

• Modified Parkland –Ringer Lactate:- 4 mL/kg/%TBSA burn

Colloid:-No
5% Dextrose in Water:- No
MUIR CLAY
• FLUID RESUSCITATION IN NEXT 24 HOURS

• EVANS – Normal saline: 0.5 mL/kg/%TBSA burn

Colloid:-0.5 mL/kg/%TBSA burn
5%Dextrose in Water:-2,000 mL

• Brooke – Ringer Lactate: 0.5 mL/kg/%TBSA burn

Colloid:-0.25 mL/kg/%TBSA
5%Dextrose in Water: 2000mL

• Parkland –Ringer Lactate: 4 mL/kg/%TBSA burn

Colloid: 20-60% of estimated plasma volume
5% Dextrose in Water: to maintain diuresis
➤ Half of the volume is given in first 8 hours, rest is given in next 16
hours.
• Modified Brooke –Ringer Lactate:- No
Colloid:- 0.3-0.5 mL/kg/%TBSA burn
5% Dextrose in Water:- to maintain diuresis

• Modified Parkland –Ringer Lactate:- No

Colloid:-0.3-1 mL albumin 5%/kg/%TBSA Burn/16 per hour
5% Dextrose in Water:- to maintain diuresis
 LOCAL MANAGEMENT
1) Open Method: Application of silver sulphadiazine without any
dressings commonly used in burns of face and neck. Mafenide
acetate & silver nitrate can be used

2) Closed Method: With dressings done to soothen and protect

wound, to reduce pain and as an absorbent

3) Tangential excision: Skin grafting can be done within 48 hours with

less than 25% burns . Its done in deep dermal and full thicklness
injury without extensive involvement of subcutaneous tissue

4) Fascial excision:- is done for full thickness burn of skin and

subcutaneous tissue of large areas if muscle involved can be
excised
 COMPLICATIONS OF BURNS
• Eschar: It is a charred, denatured, full thickness, deep burns with
contracted dermis.
• Escharotomy:
• Incise along medial and/or lateral surfaces.
• Avoid bony prominences.

Avoid tendons, nerves, major vessel

 COMPLICATIONS OF BURNS
• Contracture :- Disorganised over formation of compact collagen
(three times than normal) causes hypertrophic scar finally
leading to contracture

• .Classification of Contracture in Neck (BM Achauer)

1. Mild Inability to see ceiling

2. 2. Moderate: Flexion possible but not extension.
3. 3. Severe: Fully contracted in flexed position with pull on lower
lip.
4. 4. Extensive: Mentosternal adhesions.
• Complications of contracture:-
1. Ectropion
2. Disfigurement of face.
3. Microstomia.
4. Hypertrophic scar and keloid formation.
5. Marjolin's ulcer.

• Treatment:
1) Z- Plasty
2) Random cutaneous flap, microvascular free flap, faciocutaneous
flap.
3) Physiotherapy
.4) Pressure garments.
 CHEMICAL BURNS
• ACIDS :- Protein injury by hydrolysis
• Thermal injury is made with skin contact

• ALKALI :- Saponification of fat

Hygroscopic effect- dehydrates cells
Dissolves proteins by creation of alkaline proteinates
(hydroxideions)
• Treatment:-
Late neutralization with antidote done by 0.2% acetic acid in alkali
burns, sodium bicarbonate or calcium gluconate for acid burns.
 ELECTRICAL BURNS
• Greatest heat occurs at the points of resistance
i.e, at Entrance and Exit wounds.
Dry skin = Greater resistance , Wet Skin = Less resistance

• Longer the contact, the greater the potential of injury

• Smaller the point of contact, the more concentrated theenergy, the

greater the injury

• Treatment:-
• Assess Entrance & Exit wounds.
• Remove clothing, jewelry, and leather items.
• Treat any visible injuries.
 RADIATION BURNS
• Local burns causing ulceration need excision andvascularised flap
cover - usually with free flaps.
• Systemic overdose needs supportive treatment
• The damage is more difficult to define and slower to develop than
burns.
• Acute frost bite needs rapid rewarming , then observation.
• Delay surgery until demarcation is clearly
 COLD BURNS
• The damage is more difficult to define and slower to develop
than burns

• .• Acute frostbite needs rapid rewarming, then observation

• .• Delay surgery until demarcation is clear.