BURNS

A burn is a tissue injury from thermal (heat or

cold) application, or from the absorption of
physical energy or chemical contact
 PATHOPHYSIOLOGY
 The burn injury can be one of the most serious
and devastating forms of trauma
 Destruction of the skin by heat results in
severe local and systemic physiological
alterations
 Burns can also damage the airway and lungs
 Tissue damage
 Direct cell rupture or cell necrosis.
 At the periphery the cells may be viable, but injured.
 Collagen is denatured and damage to the peripheral
microcirculation occurs.
 The capillaries are either thrombosed where the
damage is severe or in less damaged areas there is
increased capillary permeability such that the tissues
become oedematous
 Warning signs of burns to the
respiratory system

 Burns around the face and neck

 A history of being trapped in a burning room
 Physical burn injury to the airway above the larynx
 Once burned, the linings of these structure will start
to swell
 Oedema may completely block the airway
 This is manifest early on by stridor, hoarse­ness,
cough and respiratory obstruction.
Physical burn injury to the airway below the larynx
 Steam has a large latent heat of evaporation and can
cause thermal damage to the lower airway
 The respiratory epithelium rapidly swells and
detaches from the bronchial tree
 METABOLIC POISONING
 Systemic absorption of carbon monoxide and
hydrogen cyanide from burning plastics causes
poisoning.
 Patient presents with altered consciousness
 Carbon monoxide displaces oxygen from
haemoglobin to form carboxyhaemoglobin, reducing
the oxygen-carrying capacity of the blood.
 Levels of carboxyhaemoglobin >10% are dangerous
and needs treatment
 Hydrogen cyanide causes metabolic acidosis by
interfering with mitochondrial respiration
 INHALATION INJURY
 Caused by minute particles within thick
smoke, which, because of their small size, are
not filtered by upper airway, but are carried
down to the lung parenchyma
 Chemical pneumonitis- edema and decreases
gaseous exchange
 Mechanical block on the rib
movement

 Burned skin is thick and stiff

 Physically sTop the ribs movements if there is
large full thickness burn across the chest
 Inflammation and circulatory
changes

 More severely damaged tissue may develop a

more prolonged inflammatory response.
 Macrophages produce inflammatory mediators
or cytokines (e.g. transforming growth factor)
and phagocytose necrotic cells.
 Activation of Hageman factor-arachidonic cid,
thrombin and kallikrein pathways
 Compliment causes degranulation of mast
cells and coats the proteins altered by the
burns
 Neutrophils attract by them and degranulate
with release of free redicals and proteases
 These inflammatory factors alter the
permeability of blood vessels
 The damaged collagen and extravasated
proteins increase the oncotic pressure within
the burned tissue
 Net flow of water, solutes and proteins from
the intravascular to the extravascular space
 This flow occurs over the first 36 hrs
 Burn size over 10-15% of total body surface
area can cause circulatory shock
 THE IMMUNE SYSTEM
 Cell-mediated immunity is significantly reduced in
large burns, leaving them more susceptible to
bacterial and fungal infection
Potential sources of infection
 Burn wound
 Lungs
 Central venous lines
 Tracheostomies
 Urinary catheter
 Changes to the intestine
 Inflammtory stimulus and shock-microvascular
damage and ischaemia to the gut mucosa
 Reduced gut motility and absorption
 Translucatio of gut bacteria
 Curling’s ulcer
 Gut mucosal swelling, gastric stasis and peritoneal
oedema can cause abdominal compartyment
syndrome
Danger to peripheral circulation

A circumferential full-thickness burns to a

limb acts as a tourniquet as the limb swells
 Mechanisms of injury

Scalds
 Burn by Hot water
 Major determinant of the severity of injury is
the duration of contact.
 Common areas involved are the face, neck and
upper trunk or limbs
Fat burns
Cooking fat or oil has a much higher
temperature (1800C) than boiling water and
hot fat cools slowly on the skin surface. Spills
therefore cause deep burns
 FLAME BURNS
Aetiology
 House fires, clothing fires, spills of petrol on
the skin, butane gas fires. They often occur in
confined spaces and may be associated with
inhalation injury
 If clothing ignites there is a pro­longed flame
contact with the skin.
 Generally, deep burns will result
 Electrical burns
 Passage of electric current through the tissues causes
heating that results in cellular damage
 Bone is a poor conductor of electrical current,
whereas blood vessels, nerves and muscles are good
conductors. Bone can therefore become very hot and
cause secondary damage to tissues near to the bone.
 Low voltage (<1000 V) such as from a domestic
supply (240 V, 50 Hz) causes significant contact
wounds and may induce cardiac arrest, but no deep
tissue damage
 High­voltage burns (>1000 V) cause damage
by two mechanisms:
 flash and current transmission.
 The flash from an arc may cause a cutaneous
burn and ignite clothing, but will not result in
deep damage.
 High-voltage current transmission will result
in cutaneous entrance and exit wounds and
deep damage.
 COLD INJURY
 Industrial accidents due to spills of liquid nitrogen or
similar substances.
 The injuries cause acute cellular damage with the
possibility of either a partial-thickness or full-
thickness burn.
 Freezing injuries, however, seem to be less damaging
to the connective tissue matrix than heat injuries.
 Frostbite combined tissue damage from freezing,
together with vasospasm
 FRICTION BURNS
 Combination of heat and abrasion
 A superficial open wound that may progress to
full-thickness skin loss.
 Friction burns may be associated with
degloving injuries where the damage is judged
to be deep.
 IONISING RADIATION
 X-irradiation may lead to tissue necrosis
 The tissue necrosis may not develop
immediately
 Of greater significance is the long-term
cumulative effect of ionising radiation in the
induction of skin cancers and other tumours.
 CHEMICAL BURNS
 Tissue damage depends on the strength and quantity
of the agent and the duration of contact.
 Chemicals cause local coagulation of proteins and
necrosis, and some also have systemic effects (e.g.
liver and kidney damage with tannic, formic and
picric acids)
 The most important initial treatment is dilution with
running water.
 INDICATION OF ADMISSION
 Smaller burns may be managed satisfactorily
on an outpatient basis with arrangements for
further dressing either at a hospital follow-up
clinic or by the general practitioner.
 Patients with major burns should ideally be
treated in a specialised burns unit. Indications
for referral include:
 Burns of special areas (face, hands, feet,
perineum, genitalia)
 Full-thickness burns >5 per cent body surface
area
 Circumferential limb or chest burns
 Electrical burns
 Chemical burns
 Burns in children or the elderly
 Where nonaccidental injury is suspected in the
case of a child
 Associated medical conditions or pregnancy
 Associated other trauma.
 IMMEDIATE CARE OF BURN
PATIENT

PREHOSPITAL
CARE
 Stop the burning
process
 Check for other injuries
 Cool the burn surface
Immediate cooling of the part is beneficial and
should continue for 20 minutes
This provide analgesia and delayed
microvascular damage
The ideal temperature of cooling water is 15 0C
 Give oxygen
Especially those involved in a fire in an
enclosed space
 Elevate
Sitting a patient up with burned airway
Elevtion of burned limb
 Hospital care
The priorities in the management of a major burn
 A Airway control
 B Breathing & ventilation
 C Circulation
 D Disability-neurological status
 E Exposure
 F Fluid resuscitation
Initial management of burned airway
 Early elective intubation is safest
 Delay can make intubation very difficult due to
swelling
 So the key management is recognition of potentially
burned airway by
A history of being trapped in the presence of smoke
or hot gases
Burns on the palate or nasal mucosa, or loss of all of
the hairs in the nose
Deep burns around the mouth and neck
 BREATHING
 Inhalation injury
Clinical features
 Progressive increase in respiratory effort & rate
 Rising pulse
 Anxiety
 Confusion
 Decreasing oxygen saturation
 Symptoms can take 24 hrs to 5 days to develop
 Treatment
 Physiotherapy
 Nebulisers
 Warm humidified oxygen
 Patient’s progress should be monitored using
respiratory rate and ABG
 If deterioration occurs then continous or
intermittant positive pressure with mask
 Endotracheal intubation
 Metabolic pioisoning
 Fire within an enclosed space and altered
consciousness are important clues
 Measurement of blood gases
 Carboxyhaemoglobin levels >10%- high
inspired oxygen for 24 hrs
Mechanical block to breathing
 escharotomy
 Major determinants of outcome of a
burn

 Percentage surface area involved

 Depth of burn
 Presence of inhalation injury
 Assessment of the Burn Area
 Burn size needs to be formally assessed in a
controlled environment
 The patient’s whole hand is 1% TBSA, and is a usual
guide in small burns
 Rule of nine for large burns
Each upper limb is 9% TBSA
Each lower limb is 18% TBSA
Torso is 18% TBSA each side
Head & neck 9% TBSA
Assessment of Burn Depth
 Good history of the injury
 The temperature of the burning agent
 The duration of the contact
 Burning material
Clinical examination
Superficial partial thickness burn
 Not deeper than papillary dermis
 Blisters and loss of epidermis
 Underlying dermis is pink and moist
 Capillary filling
 Pinprick sensation is normal
 Healing without residual scarring in 2 weeks
Deep partial thickness burn
 Damage to reticular dermis

 Epidermis is lost

 Less moist exposed dermis

 No blenching

 Sensation reduced

 Healing with hypertrophic scarring in 3 or

more weeks
 Full thickness burn
 Whole dermis destroyed
 Hard leathery feel
 No capillary return
 Thrombosed vessels seen under the skin
 Complete anesthesia
 Fluid resuscitation
 IV resuscitation for child if TBSA > 10%
IV resuscitation for child if TBSA > 10%
 IV resuscitation for adult if TBSA > 15%
 Oral rehydration with salt & water
 Resuscitation volume in adults
Parkland formula
3-4 ml/kg body weight/% burn/in the first 24
hours
 Half of this vol. in first 8 hrs and second half in
subsequent 16 hrs
 Type of fluids- Ringer’s lactate or Hartman’s
solution, Human albumin solution or FFP or
Normal Saline
 In children
 100 ml/kg for 24 hrs for the first 10 kg
 50 ml/kg for the next 10 kg
 20 ml/kg for 24 hrs for each kg over 20 kg
body weight
 Type of fluid- Dextrose saline
 Monitoring of Resuscitation
 Urine output-0.5 to 1.0 ml/kg of body weight/hr
 If less urine output- increase infusion rate by 50%
 If more urine output (>2)- decrease the infusion rate
 Measurement of acid-base balance
 Haematocrit measurement
 Central venous pressure measurement
 Treating the Burn Wound

Escharotomy
 For circumferential full thickness burns to the
limbs
 For circumferential full thickness burns to the
chest
Incise the whole length of full thickness burn
 Clean the wound
 Antibacterial dressing
Full thickness burns and obvious deep
dermal wounds
 1% silver sulphadiazine cream
 0.5% silver nitrate solution
 Mafenide acetete cream
 Serum nitrate
 Superficial partial thickness wounds and
mixed depth wounds
 Dressing should be easy to apply, non painful,
simple to manage and locally available
 The simplest method of treating a superficial
wound is by exposure used in hot climates,
and for small burns on the face
 Or cover the wound with permeable dressing
 Or vaseline imperginated gauze
 Or fenestrated silicone sheet
 Hydrocolloid dressing- In mixed depth
wounds
High protease levels promote debridement
Moist environment is good for epithelialisation
Borderline depth wounds
 Cleansing under general anesthesia

 Silver sulphadiazine cream for 2-3 days

 It can be changed to a dressing that is more

efficient at promoting healing after this period

 ANALGESIA
 Small superficial burns-oral analgesia
paracetamol or NSAID’s
 Large burns- IV opiates
 NUTRITION
 Adult with >15% TBSA burn and children
>10% has an increased nutritional requirement
 Nasogastric feeding for patients having burns
over 20% TBSA
 Feeding should start within 6 hrs
 Catabolic phase- can be revert by rapid
excision of burn and stable coverage of wound
 Keep the patient warm- reduces energy
requirement
Monitoring & control of infection
 Burn patients are immunocompromosed
 Sterile precautions must be vigorous
 Bacteriological surveillance of the wound,
catheter tips and sputum
 A rise or fall in TLC, thrombocytosis,
increased catabolism are warnings of infection
 Antibiotics should be started if there is
suspicion of infection
 PHYSIOTHERAPY

Elevation, splintage and exercise reduce

swelling and improve final outcome
 Surgery for the Acute Burn Wound

 Any deep partial thickness and full thickness

burns, except those which are < 4cm 2 need
surgery
 Two alternative policies for deep burns
Spontaneous desloughing and apply split-
skin grafts at 3 weeks.
 Slow healing and greater scarring
 Early excision of the burn is carried out with the
application of skin cover, usually a skin graft, but
where indicated a flap followed by mobilisation and
rehabilitation
 Rapid healing and early restoration of function, and
minimises the risk of adverse scarring.
 Early tangential excision of skin grafting is a
technique used for deep dermal burns, usually
performed within 48 hours.
 Localised burns can usually be excised and closed in
a single episode.
 Delayed Recostruction and Scar
Management
 Acute contractures around the eyes
 Any contracture causing significant loss of
range of movements of a joint
Should be treated first
 Z-plasty for single band
 Transposition flap for wider bands of scarring
 Full thickness grafts and free flaps for larger or
difficult area
 Hypertrophy is treated with pressure garments
 Pharmacological management of itch
NON-THERMAL BURN INJURY

 Electrical injuries
Low voltage
High voltage
 Dividing line is 1000 V
 LOW TENSION INJURIES
Low voltage (<1000 V) such as from a
domestic supply (240 V, 50 Hz) causes
 Significant contact wounds, underlying tendon
and nerve damage but little damage in between
 Cardiac arrest due to interfering with the
normal cardiac pacing but no significant
myocardial damage
 No deep tissue damage
 HIGH TENSION INJURY
 Sources of damage
Flash (external burn)
Current (internal burn)
 Damage to the subcutaneous tissues and
muscles
 Entry & exit wounds, huge amount of
subcutaneous damage
 Damage to underlying muscles
Compartment syndrome
Myoglobinuria & renal dysfunction
 Resuscitation should include maintenance
Of high urine output (2ml/kg/hr)
 Acidosis- bolus of bicarbonate
 Myocardial damage-direct muscle damage
Raised cardiac enzymes, heat failure
 Severe injury to limb- amputation
 CHEMICAL INJURIES
 Damage due to
Physical destruction to skin
Poisoning by systemic absorption
Management
 Copious lavage with water (except phosphorus
& elemental sodium)
 Identify chemical and its concentration
IONISING RADIATION INJURY
 Localised radiation damage
Conservative management
Ulcer-excision and coverage with vascularized
tissue
 Whole body radiation
if lethal dose -acute desquamation of skin
Non lethal radiation-symptoms related to gut mucosa
and immune system dysfunction