burns

1. Burns

2. • A burn is an injury to the skin or other organic tissue primarily caused
by heat or due to radiation, radioactivity, electricity, friction or
contact with chemicals.

3. • 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 so far.

4. Types of burns
• Thermal burns
• Scald—spillage of hot liquids
• Flame burns
• Contact burns—contact with hot metals/objects/materials
• Electrical burns
• ™
Chemical burns—acid/alkali
• ™
™
Ionising radiation
• ™
Sun burns

5. Classification of Burns
• Burn wounds are commonly classified as
• Superficial (first-degree),
• partial-thickness (second-degree),
• full-thickness (third-degree),
• fourth-degree burns, which affect underlying soft tissue
• Fifth-degree burns (through muscle to bone) and
• sixth degree burns (charring bone)
• Depending on thickness of skin involved
• 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.

6. • 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, causing scarring, and pigmentation.
Sensation is present but no blanching.

7. • 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.

8. • Fourth degree: Involves the underlying tissues—muscles, bones.
• Clinically, first-degree burns are painful but do not blister,
• second-degree burns have dermal involvement and are extremely
painful with weeping and blisters,
• and third-degree burns are leathery, painless, and nonblanching.

9. 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.

10. 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

11. Mechanisms of injury
• Thermal injuries
• Scalds—About 70% of burns in children are caused by
scalds.
• They also often occur in elderly people.
• The common mechanisms are spilling hot drinks or liquids or
being exposed to hot bathing water.
• Scalds tend to cause superficial to superficial dermal burns

12. Thermal injuries
• Flame—Flame burns comprise 50% of adult burns. They are often
associated with inhalational injury and other concomitant trauma.
Flame burns tend to be deep dermal or full thickness.
• Contact—the burn result from direct contact, the object touched must
either be extremely hot or the contact was abnormally long. These
types of burns are commonly seen in people with epilepsy or those
who misuse alcohol or drugs. Contact burns tend to be deep dermal
or full thickness.

13. 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.

14. • 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.

15. 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.

16. Burn center referral criteria
• . Partial thickness burns >10% TBSA
• . Burns that involve the face, hands, feet, genitalia, perineum, or major joints
• . Full thickness burns in any age group
• . Burns caused by electric current including lightning
• . Chemical burns
• . Inhalation injury
• . Burn injury in patients with preexisting medical disorders that could complicate management,
prolong recovery, or affect mortality
• . Burned children in a hospital without qualified personnel or equipment for the care of children
• . Burn injury in a patient who will require special social, emotional, or rehabilitative intervention

17. 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

18. • 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 is trapped
in a burning vehicle, house, car or aeroplane and is forced to
inhale the hot and poisonous gases.

19. 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, much like a full
thickness burn, and will need
excision and grafting.

20. • 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.

21. • 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.
• These three zones of a burn are three
dimensional, and loss of tissue in the zone of
stasis will lead to the wound deepening as well
as widening.

22. 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.

23. 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.

24. 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

25. • 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.

26. 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

27. 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.

28. 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

29. 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.

30. 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.

31. 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.

32. 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

33. 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.

34. 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.

35. 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. Immunological changes
• Non-specific down regulation
of the immune response
occurs, affecting both cell
mediated and humoral
pathways.

37. 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
present.

38. 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.