2. Burns
• Burns is defined as a wound caused by exogenous
agent leading to coagulative necrosis of the tissue.
3. Causes of Burns
• Thermal Burns
• Dry heat Contact burn - contact with hot metals/objects/materials
• Flame burn
• Smoke and inhalational injury
• Moist heat- Scald burn
• Chemical Burns- acids & alkali
• Electrical burns- High & low voltage
• Ionizing Radiation
• Sun Burns
4. History
• The history of the burn injury should include:
• Whether accidental , suicidal or homicidal
• Date and time of burn injury.
• Mechanism of injury and length of contact time.
• Did the flame burn occur in an enclosed space?
• Adequacy of first aid given
5. Classification
• Depending on the Percentage of Burns:
• (a) Mild:
• Partial thickness burn less than 15% in adult or less than 10% in children or full thickness less
than 2%.
• (b) Moderate:
• Second degree 15-25% burns in adult or 10-20% in children or third degree 2-10% burns.
• (c) Major:
• Second degree >25% burns in adult or >20% burns in children or third degree >10% burns or
burns involving eyes, ears, feet, hand, perineum. All inhalational and electrical burns.
6. Classification 2. Depending onThickness of
Skin Involved:
• (a)First degree: injury localized to the epidermis.
• (b) Second Degree:
• i) Superficial second degree: injury to the epidermis and superficial papillary dermis.
• ii) Deep second degree: injury through the epidermis and deep upto reticular dermis.
• (c)Third degree: full-thickness injury through the epidermis and dermis into
subcutaneous fat.
• (d) Fourth degree: injury through the skin and subcutaneous fat into underlying
muscle or bone.
7. Clinical Features:
• First degree burns
• Here the epidermis looks red and painful, no blisters, heals rapidly in 5–7
days by epithelialisation without scarring. It shows capillary filling.
8. Clinical features Superficial 2nd Degree Burns :
• Intense pain
• White to red skin
• Blisters
• Involves epidermis & papillary layer of dermis
• Spares hair follicles, sweat glands
• Erythematous & blanch to touch
• Very painful/sensitive .
• No or minimal scarring.
• Spontaneously re-epithelialization from retained epidermal structures in 7-14
days
9. Clinical Features - Deep second degree
burns:
• Injury to deeper layers of dermis, i.e, reticular dermis.
• Appears pale & mottled.
• Do not blanch to touch.
• Capillary return sluggish or absent.
• Less painful, remain painful to pinprick.
• Takes 14 to 35 days to heal by re-epithelialization from hair follicles & sweat
gland,
• Contractures possible.
10. Clinical Features 3rd Degree Burn:
• Dry, leathery skin (white, dark brown, or charred). •
• Loss of sensation (little pain). •
• All dermal layers/tissue maybe involved.
• 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.
13. Initial Evaluation and Resuscitation
Primary survey:
• Initial evaluation of the burned patient should include airway
management, evaluation of other injuries, estimation of burn size,
and diagnosis of CO and cyanide poisoning.
• Evaluate the airway; this is an area of particular importance in burn
patients. Early recognition of impending airway compromise, followed
by prompt intubation, can be lifesaving.
• Obtain appropriate vascular access and place monitoring devices,
then complete a systematic trauma survey, including indicated
radiographs and laboratory studies.
14. Secondary survey
• Burn patients should then undergo a burn-specific secondary survey,
• which should include a
• determination of the mechanism of injury,
• an evaluation for the presence or absence of inhalation injury and carbon
monoxide intoxication,
• an examination for corneal burns,
• the consideration of the possibility of abuse, and a detailed assessment of the
burn wound
15. Pathophysiology of burns
• Understanding the pathophysiology of a burn injury is important
for effective management.
• Burn injuries result in both local and systemic responses.
• Different causes lead to different injury patterns, which require
different management.
• It is therefore important to understand how a burn was caused and
what kind of physiological response it will induce
16. Pathophysiology
• Burns cause damage in a number of different ways, but by far
the most common organ affected is the skin.
• However, burns can also damage the airway and lungs, with
life-threatening consequences.
• Airway injuries occur when the face and neck are burned.
• Respiratory system injuries usually occur if a person gets
trapped in a burning vehicle, house, car or aeroplane and is
forced to inhale the hot and poisonous gases.
17. PATHOPHYSIOLOGY
• Local Changes:
• Thermal injury causes coagulative necrosis of epidermis and underlying
tissue, with depth of injury dependent on temperature to which skin is
exposed
18. Local response
• The three zones of a burn were
described by Jackson in 1947
• Zone of coagulation—This occurs
at the point of maximum damage.
In this zone there is irreversible
tissue loss due to coagulation of
the constituent proteins.
• It is the most severely burned portion
and is typically in the center of the
wound. The affected tissue is
coagulated and sometimes frankly
necrotic, and will need excision and
grafting.
19. • Zone of stasis—The surrounding
zone of stasis is characterised by
decreased tissue perfusion.
• The tissue in this zone is
potentially salvageable.
• The main aim of burns
resuscitation is to increase tissue
perfusion and prevent any
damage becoming irreversible.
• Additional insults—such as
prolonged hypotension, infection,
or oedema—can convert this zone
into an area of complete tissue
loss.
20. • Zone of hyperaemia—In this
outermost zone tissue
perfusion is increased
• The tissue here will invariably
recover unless there is severe
sepsis or prolonged
hypoperfusion.
21. Systemic response
• The release of cytokines and other inflammatory mediators at
the site of injury has a systemic effect once the burn reaches
30% of total body surface area.
22. INFLAMMATION AND CIRCULATORY
CHANGES
• The cause of circulatory changes following a burn are more
complex.
• The changes occur because 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.
23. INFLAMMATION AND CIRCULATORY
CHANGES
• 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-α).
• 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 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
24. • The overall effect of these changes is to produce a net flow of water,
solutes and proteins from the intravascular to the extravascular
space.
• This flow occurs over the first 36 hours after the injury, but does not
include red blood cells.
• In a small burn, this reaction is small and localised but, as the burn
size approaches 10–15% of total body surface area (TBSA), the loss
of intravascular fluid can cause a level of circulatory shock.
• Furthermore, once the area increases to 25% of TBSA, the
inflammatory reaction causes fluid loss in vessels remote from the
burn injury.
• This is why such importance is attached to measuring the TBSA
involved in any burn.
25. 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% of surface area, the loss of fluid produces shock
26. Cardiovascular changes
• Capillary permeability is increased, leading to loss of
intravascular proteins and fluids into the interstitial
compartment.
• Peripheral and splanchnic vasoconstriction occurs.
• Myocardial contractility is decreased, possibly due to release of
tumour necrosis factor .
• These changes, coupled with fluid loss from the burn wound,
result in systemic hypotension and end organ hypoperfusion.
27. Respiratory changes
• Inflammatory mediators cause
bronchoconstriction, and in
severe burns adult respiratory
distress syndrome can occur.
• 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
28. Physical burn injury to the airway
above the larynx
• The hot gases can physically burn the nose, mouth, tongue,
palate and larynx.
• Once burned, the linings of these structures will start to swell.
• After a few hours, they may start to interfere with the larynx and
may completely block the airway if action is not taken to secure
an airway.
29. Physical burn injury to the airway
below the larynx
• This is a rare injury as the heat exchange mechanisms in the
supraglottic airway are usually able safely to absorb the heat
from hot air.
• However, steam has a large latent heat of evaporation and can
cause thermal damage to the lower airway.
• In such injuries, the respiratory epithelium rapidly swells and
detaches from the bronchial tree.
• This creates casts, which can block the main upper airway.
30. Inhalational injury
• Inhalational injury is caused by the minute particles within thick
smoke, which, because of their small size, are not filtered by the
upper airway, but are carried down to the lung parenchyma.
• They stick to the moist lining, causing an intense reaction in the
alveoli.
• This chemical pneumonitis causes oedema within the alveolar
sacs and decreasing gaseous exchange over the ensuing 24
hours, and often gives rise to a bacterial pneumonia.
31. Dangers of smoke, hot gas or steam
inhalation
• Inhaled hot gases can cause supraglottic airway burns and
laryngeal oedema
• Inhaled steam can cause subglottic burns and loss of
respiratory epithelium
• Inhaled smoke particles can cause chemical alveolitis and
respiratory failure
• Inhaled poisons, such as carbon monoxide, can cause
metabolic poisoning
• Full-thickness burns to the chest can cause mechanical
blockage to rib movement
32. Mechanical block on rib movement
• Burned skin is very thick and stiff, and this can physically stop
the ribs moving if there is a large full-thickness burn across the
chest
33. Metabolic changes
• The basal metabolic rate increases up to three times its original
rate.
• This, coupled with splanchnic hypoperfusion, necessitates
early and aggressive enteral feeding to decrease catabolism
and maintain gut integrity.
34. Metabolic poisoning
• There are many poisonous gases that can be given off in a fire, the most
common being carbon monoxide, that is often produced by fires in enclosed
spaces.
• This is the usual cause of a person being found with altered consciousness at the
scene of a fire.
• Carbon monoxide binds to haemoglobin with an affinity 240 times greater than
that of oxygen and therefore blocks the transport of oxygen.
• Levels of carboxyhaemoglobin in the bloodstream can be measured.
• Concentrations above 10% are dangerous and need treatment with pure oxygen
for more than 24 hours.
• Death occurs with concentrations around 60%.
• Another metabolic toxin produced in house fires is hydrogen cyanide, which
causes a metabolic acidosis by interfering with mitochondrial respiration.
36. The immune system and infection
• Cell-mediated immunity is significantly reduced in large burns,
leaving them more susceptible to bacterial and fungal
infections.
• There are many potential sources of infection, especially from
the burn wound and from the lung if this is injured, but also from
any central venous lines, tracheostomies or urinary catheters.
37. Changes to the intestine
• The inflammatory stimulus and shock can cause microvascular
damage and ischaemia to the gut mucosa.
• This reduces gut motility and can prevent the absorption of food.
• Failure of enteral feeding in a patient with a large burn is a life-
threatening complication.
• This process also increases the translocation of gut bacteria, which
can become an important source of infection in large burns.
• Gut mucosal swelling, gastric stasis and peritoneal oedema can also
cause abdominal compartment syndrome, which splints the
diaphragm and increases the airway pressures needed for
respiration.
38. Systemic changes
• Cardiac: Decreased cardiac output.
• Pulmonary: Respiratory insufficiency as a secondary process. Can progress to
respiratory failure.
• Gastrointestinal: Decreased or absent GI motility. 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 immuneresponses.
39. Electrical burns
• Electrical injuries are caused by electrocution. An electric current will
travel through the body from one point to another, creating “entry”
and “exit” points. The tissue between these two points can be
damaged by the current.
• High voltage injuries can be further divided into “true” high tension
injuries, caused by high voltage current passing through the body, and
“flash” injuries, caused by tangential exposure to a high voltage
current arc where no current actually flows through the body.
40. • A particular concern after an
electrical injury is the need for
cardiac monitoring.
• If the patient’s electrocardiogram
on admission is normal and there is
no history of loss of consciousness,
then cardiac monitoring is not
required.
• If there are electrocardiographic
abnormalities or a loss of
consciousness, 24 hours of
monitoring is advised.
41. Chemical injuries
• Chemical injuries usually occur as a result of industrial accidents but
may occur with household chemical products.
• These burns tend to be deep,
• The corrosive agent continues to cause coagulative necrosis until
completely removed.
• Alkalis tend to penetrate deeper and cause worse burns than acids.
• Cement is a common cause of alkali burns.
