BURNS

Linda Mariam Joseph

114
Burn

■ Burn is defined as a wound caused by exogenous agent leading to coagulative necrosis

of the tissue.
Types of burns

■ • Thermal injury –
- Scald-spillage of hot liquids
- Flame burns
- Flash burns due to exposure of natural gas, alcohol, combustible liquids
- Contact burns-contact with hot metals/objects/materials
■ Non thermal injuries
• Electrical injury
• Chemical burns-acid/alkali
• Cold injury-frost bite
• Ionising radiation • Sun burns
Classification of burns
■ Depending on the Percentage of Burns (Burn Severity Classification)
•Mild (Minor):
- Partial thickness burns <15% in adult or <10% in children.
-Full thickness burns less than 2%. Can be treated on outpatient basis.
•Moderate:
-Second degree of 15- 25% burns (10-20% in children). Third degree between 2-10% burns.
-Burns which are not involving eyes, ears, face, hand, feet, perineum.
-Electrical Burns- Inhalation Injury -Chemical Burns
•Major (severe):
-Second degree burns more than 25% in adults, in children more than 20%.
-All third degree burns of 10% or more.
-Burns involving eyes, ears, feet, hands, perineum.
-All inhalation and electrical burns.
-Burns with fractures or major mechanical trauma.
. Depending on thickness of skin involved
a. First degree-. Here the epidermis looks red and painful, no blisters, heals rapidly in 5-
7 days by epithelialisation without scarring. It shows capillary filling.
b. Second degree: The affected area is mottled, red, painful, with blisters, heals by
epithelialisation in 14-21 days. Superficial second degree burn heals, causing
pigmentation. Deep second degree burn heals by causing scarring, and pigmentation.
Sensation is present but no blanching.
c. Third degree: The affected area is charred, parchment like, painless and insensitive,
with thrombosis of superficial vessels. It requires grafting. Charred, denatured ,
insensitive, contracted full thickness burn is called as eschar. These wound must heal
by re-epithelialisation from wound edge.
d. Fourth degree: Involves the underlying tissues- muscles, bones.
Depending on thickness of skin involved
a.Partial thickness burns: It is either first or second degree burn which is red and painful,
often with blisters.
b. Full thickness burns: It is third degree burns which is charred, insensitive, deep involving
all layers of the skin
 PATHOPHYSIOLOGY OF BURN
INJURY
Most common organ affected is the skin.
Airway injuries occur when the face and neck are burned.
Respiratory system injuries usually occur if a person is trapped in a burning vehicle, house, car
or aeroplane and is forced to inhale the hot and poisonous gases
Warning signs of burns to the respiratory system
■ Burns around the face and neck
■ A history of being trapped in a burning room
■ Change in voice
■ Stridor
INJURY TO THE AIRWAY AND
LUNGS
■ Physical burn injury to the airway above the larynx
■ Physical burn injury to the airway below the larynx
■ Metabolic poisoning
■ Inhalationl injury
■ Mechanical block on rib movement
Inflammation and circulatory changes

■ Burned skin activates a web of inflammatory cascades.

■ The release of neuropeptides and the activation of complement are initiated by the
stimulation of pain fibres and the alteration of proteins by heat.
■ The activation of Hageman factor initiates a number of protease-driven cascades,
altering the arachidonic acid, thrombin and kallikrein pathways.
■ At a cellular level, complement causes the degranulation of mast cells and coats the
proteins altered by the burn. This attracts neutrophils, which also degranulate, with
the release of large quantities of free radicals and proteases. These can, in turn, cause
further damage to the tissue.
■ Mast cells also release primary cytokines such as tumour necrosis factor alpha (TNF-
a). These act as chemotactic agents to inflammatory cells and cause the subsequent
release of many secondary cytokines.
■ These inflammatory factors alter the permeability of blood vessels such that
intravascular fluid escapes. The increase in permeability is such that large protein
molecules can also now escape with ease. The damaged collagen and these
extravasated proteins increase the oncotic pressure within the burned tissue, further
increasing the flow of water from the intravascular to the extravascular space
■ Burn size 10-15% TBSA – circulatory shock
■ 25% of TBSA - Fluid loss from remote vessels
The shock reaction after burns
■ Burns produce an inflammatory reaction
■ This leads to vastly increased vascular permeability
■ Water, solutes and proteins move from the intra- to the extravascular space
■ The volume of fluid lost is directly proportional to the area of the burn
■ Above 15 per cent of surface area, the loss of fluid produces shock
Other life threatening events with major
burns
■ The immune system and infection
■ Changes to intestine
■ Danger to peripheral circulation
Assessment of the burn wound

■ Assessing the area of a burn

•The patient’s whole hand is 1 per cent TBSA, and is a useful guide in small burns
• The Lund and Browder chart is useful in larger burns
•The rule of nines is adequate for a first approximation only
Assessing depth of a burn
Immediate care of the burn patient

Prehospital care. Hospital care

•Ensure rescuer safety A, airway control
•Stop the burning process. B, breathing and ventilation
•Check for other injuries C, circulation
•Cool the burn wound. D, disability status
• Give oxygen E, exposure with environmental control
• Elevate. F, Fliud resuscitation
Fluid resuscitation
■ Parkland formula.
This calculates the fluid to be replaced in the first 24 hours by the following
formula: total percentage body surface area × weight (kg) × 4 = volume (mL).
Half this volume is given in the first 8 hours and the second half is given in the
subsequent 16 hours
■ . Crystalloid resuscitation
Ringer’s lactate
In children, maintenance fluid must also be given. This is normally dextrose–
saline given as follows:
• 100 mL/kg for 24 hours for the first 10 kg;
• 50 mL/kg for the next 10 kg;
• 20 mL/kg for 24 hours for each kilogram over 20 kg body weight
■ Collioid resuscitation
■ Human albumin solution
■ The most common colloid-based formula is the Muir and Barclay formula:
• 0.5 × percentage body surface area burnt × weight = one portion;
• periods of 4/4/4, 6/6 and 12 hours, respectively;
• one portion to be given in each period.
Monitoring of resuscitation

■ Urine output
■ 0.5-1 ml/kg body weight per hour
■ Below this, infusion rate should be increased by 50%
Escharotomy

■ It is charred, denatured, full thickness, deep burns with contracted dermis.

■ It is insensitive, with thrombosed superficial veins
■ Circumferential full-thickness burns to the limbs require emergency surgery .The
tourniquet effect of this injury is easily treated by incising the whole length of full-
thickness burns.
■ This should be done in the mid-axial line, avoiding major nerves .
■ One should remember that an escharotomy can cause a large amount of blood loss;
therefore, adequate blood should be available for transfusion if required
Escharotomy

■ Upper limb Mid-axial, anterior to the elbow medially to avoid the ulnar nerve
■ HandMidline in the digits. Release muscle compartments if tight. Best done in theatre
and with an experienced surgeon
■ Lower limb Mid-axial. Posterior to the ankle medially to avoid the saphenous vein
■ Chest Down the chest lateral to the nipples, across the chest below the clavicle and
across the chest at thelevel of the xiphesternum
Options for topical treatment of deep
burns
■ 1% silver sulphadiazine cream
■ 0.5% silver nitrate solution
■ Mafenide acetate cream
■ Serum nitrate, silver sulphadiazine and cerium nitrate
Additional aspects of treating the burned
patient
■ Analgesia
- acute – oral analgesia, paracetamol and nsaids ,Topical cooling,
Large burns-opiates (IM is contraindicated)
- Subacute - In patients with large burns, continuous analgesia is required, beginning
with infusions and continuing with oral tablets, such as slow-release morphine.
Powerful, short-acting analgesia should be administered before dressing changes.
Administration may require an anaesthetist, as in the case of general anaesthesia or
midazolam and ketamine, or less intensive supervision, as in the case of morphine and
nitrous oxide.
■ Nutrition in burns patients
•Burns patients need extra feeding
•A nasogastric tube should be used in all patients with burnsover 15 per cent of TBSA
• Removing the burn and achieving healing stops the catabolic drive
■ Infection control in burns patients
•Burns patients are immunocompromised
•They are susceptible to infection from many routes
•Sterile precautions must be rigorous
• Swabs should be taken regularly
•A rise in white blood cell count, thrombocytosis and increased catabolism are warnings of infection
■ Nusring care
■ Physiotherapy
■ Pyscological
Electrical burns

■ Low-voltage injuries cause small, localised, deep burns

■ They can cause cardiac arrest through pacing interruption without significant direct
myocardial damage
■ High-voltage injuries damage by flash (external burn) and conduction (internal burn)
■ Myocardium may be directly damaged without pacing interruption
■ Limbs may need fasciotomies or amputation
■ Look for and treat acidosis and myoglobinuria
Chemical injuries

■ Damage is from corrosion and poisoning

■ Copious lavage with water helps in most cases
■ Then identify the chemical and assess the risks of absorption
Ionising radiation injury

■ Local burns causing ulceration need excision and vascularised flap cover, usually with
free flaps
■ Systemic overdose needs supportive treatment
Cold injuries

acute cold injuries from industrial accidents and frostbite.

■ Exposure to liquid nitrogen and other such liquids will cause epidermal and dermal
destruction. The tissue is more resistant to cold injury than to heat injury, and the
inflammatory reaction is not as marked. The assessment of depth of injury is more
difficult, so it is rare to make the decision for surgery early.
■ Frostbite injuries affect the peripheries in cold climates. The initial treatment is with
rapid rewarming in a bath at 42°C. The cold injury produces delayed microvascular
damage similar to that of cardiac reperfusion injury. The level of damage is difficult to
assess, and surgery usually does not play a role in its management, which is
conservative, until there is absolute demarcation of the level of injury.
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