basic burn injuries

1. Burn
Injuries
1
ANKIT KUMAR
ROLL NO. - 15

2. BURNS
Wounds caused by exposure to:
1. Excessive heat
2. Chemicals
3. Fire/steam
4. Radiation
5. Electricity
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3. 3
 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
Types of burns

4. 4
Scald Burn

5. Electrical burns
Chemical burns—acid/alkali
Cold injury—frost bite
Ionising radiation
Sun burns
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6. BURN WOUND ASSESSMENT
 Done according to depth of injury and
extent of body surface area involved
 Burn wounds differentiated depending
on the level of dermis and
subcutaneous tissue involved
1. superficial (first-degree)
2. deep (second-degree)
3. full thickness (third and fourth
degree)
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7. SUPERFICIAL BURNS
(FIRST DEGREE)
 Epidermal tissue only affected
 Erythema, blanching on pressure, mild
swelling
no vesicles or blister initially
 Not serious unless large areas involved
 eg. sunburn
 Heals in 5-7 days without any scar
formation 7
On the basis of
thickness of skin involved

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9. Partial Thickness (SECOND
DEGREE)
 Involves the epidermis and deep layer of
the dermis
 Affected area is mottled, red, painful
with blisters
 Heals in 14-21days
 2 types-
• Superficial-heals with pigmentation
• Deep –heals with scarring and
pigmentation
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12. FULL THICKNESS (THIRD &
FOURTH DEGREE)
 Destruction of all skin layers
 Requires immediate hospitalization
 Charred,parchment-like,painless with
superficial vessel thrombosis
 Requires grafting
 Charred,denatured,insensitive,contracted
full thickness burn is known as eschar
 Exposure to flames, electricity or
chemicals can cause 3rd degree burns
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Mild (Minor):
• Partial thickness burns < 15% in adult or
<10% in children.
• Full thickness burns less than 2%.
• Can be treated on outpatient basis.
Depending on the Percentage of
Burns

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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.

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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

19. Calculation of Burned Body
Surface Area
Calculation of Burned Body
Surface Area
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20. TOTAL BODY SURFACE AREA
(TBSA)
 Superficial burns are not involved in
the calculation
 Lund and Browder Chart is the most
accurate because it adjusts for age
 Wallace’s Rule of nines divides the
body – adequate for initial
assessment for adult burns
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21. Lund Browder Chart used for determining
BSA
21
Evans, 18.1, 2007)

22. WALLACE’S RULE OF NINES
 Head & Neck = 9%
 Each upper extremity (Arms) = 9%
 Each lower extremity (Legs) = 18%
 Anterior trunk= 18%
 Posterior trunk = 18%
 Genitalia (perineum) = 1%
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24. PATHPHYSIOLOGY
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Heat causes coagulation necrosis of skin and subcutaneous
tissue
↓
Release of vasoactive peptides
↓
Altered capillary permeability
↓
Loss of fluid → Severe hypovolaemia
↓
Decreased cardiac → Decreased myocardial
output function
↓
Decreased renal blood →Oliguria flow (Renal failure)
Altered pulmonary resistance causing pulmonary oedema
↓
Infection
↓
Systemic inflammatory response syndrome (SIRS)
↓
Multi-organ dysfunction syndrome (MODS).

26. VASCULAR CHANGES RESULTING
FROM BURN INJURIES
Circulatory disruption occurs at the burn
site immediately after a burn injury
Blood flow decreases or cease due to
occluded blood vessels
Damaged macrophages within the tissues
release chemicals that cause constriction
of vessel
Blood vessel thrombosis may occur causing
necrosis
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27. FLUID SHIFT
 Occurs after initial vasoconstriction
 Blood vessels dilate and leak fluid into the
interstitial space
 Known as third spacing or capillary leak
syndrome
 Causes decreased blood volume and blood
pressure
 Occurs within the first 12 hours after the
burn and can continue to up to 36 hours
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28. FLUID IMBALANCES
 Occur as a result of fluid shift and cell
damage
 Hypovolemia
 Metabolic acidosis
 Hyperkalemia
 Hyponatremia
 Hemoconcentration (elevated blood
osmolarity, hematocrit/hemoglobin)
due to dehydration
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29. FLUID REMOBILIZATION
 Occurs after 24 hours
 Capillary leak stops
 Diuretic stage where edema fluid
shifts from the interstitial spaces
into the vascular space
 Blood volume increases leading to
increased renal blood flow and
diuresis
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30. CURLING’S ULCER
 Acute ulcerative gastro duodenal disease
 Seen in >35% patients
 Occur within 24 hours after burn
 Due to reduced GI blood flow and mucosal
damage
 Treatment - with H2 blockers,
mucoprotectants, and early enteral nutrition
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31. Inhalational Injury
 It occurs after major fire burns.
 It is due to:
 Inhalation of heat.
 Noxious gases and incomplete products of
combustion.
 At the site of fi re, oxygen concentration is less
than 2% which can cause death in 45 seconds due
to hypoxia.
 Inhaled carbon monoxide binds with Hb
immediately to form carboxyhaemoglobin causing
severe anoxia and death.
 CO has got 240 times more affinity for
haemoglobin than oxygen. Carboxyhaemoglobin
in blood more than 10% is dangerous; more than
60% is life-threatening.
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32.  Symptoms of carbon monoxide intoxication—
headache, disorientation, visual changes,
fatigue, vomiting, hallucinations, shock and
cardiac arrest.
 Smoke contains hydrocyanide which causes
tissue hypoxia and profound acidosis.
 Laryngeal oedema and laryngospasm.
 Bronchial oedema and bronchospasm.
 Formation of bronchial cast is typical which is
due to oedema, lymph exudation, separation of
ciliated epithelial cells from basement
membrane. Inhaled gas causes supraglottic
airway burn, laryngeal oedema, loss of
respiratory epithelium, ARDS, CO poisoning,
mechanical restriction of chest wall movement.
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33. Clinical Features
 They have low oxygen saturation.
 Charring of mouth, oropharynx with facial
burns.
 Carbon sputum.
 Change in the voice, singed facial and nasal
hair.
 Decreased level of consciousness with stridor
or dyspnoea.
 Acute pulmonary insufficiency with asphyxia,
CO poisoning, upper airway obstruction. After
3 to 5 days, ARDS and hypoxia develops.
Bronchopneumonia with septicaemia occurs
after 5 days.
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34. Management
 Replacing the patient from the site earliest.
 Ventilator support for several weeks.
 Antibiotics.
 Bronchoscopy, at regular intervals to remove bronchial cast.
 Tracheostomy whenever required.
 Hyperbaric oxygen.
 IV heparin to reduce bronchial cast. Heparin nebulisation
(10,000 units in 3 ml saline 4th hourly) is also useful. N-
acetylcysteine nebulisation—20% in 3 ml saline 4th hourly,
bronchodilators like albuterol 2nd hourly is very useful.
Hypertonic saline inhalation induces the effective coughing to
remove casts. Racemic epinephrine is used to reduce mucosal
oedema.
 Steroids are not beneficial in inhalation burns.
 Monitoring the patient with arterial blood gas analysis
regularly.
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35. ELECTRICAL BURNS
 Types of Electrical Injury
Low tension injury: Less than 1000 volts.
High tension injury: More than 1000
volts—may be due to current itself causing intense
damage on the tissues up to 2000°C; flash injury
due to electrical arc up to 4000°C; flame injury by
catching of fi re to the clothing and body;
traumatic injury like fractures and internal organ
injuries.
 It is always a deep burn (always a major
burn).
 There is a wound of entry and wound of exit.35

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 Patient may also have major internal organ injuries.
GIT, thoracic injuries.
 Often convulsions can develop.
 Death may occur due to cardiac arrhythmias
(instant death due to ventricular fibrillation).
 Gas gangrene is common after electric injury.
 Release of myoglobin can cause renal tubular
damage and renal failure.
 Acidosis is common and so often bicarbonate
infusion is needed.

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 Patient should always be admitted and should be
assessed by ECG, cardiac monitor, U/S abdomen, chest
X-ray, sometimes even CT scan head, cardiac enzyme
analysis.
 Depending on the injury it is managed accordingly.
 Fractures and dislocations are common in electrical
injuries which is treated accordingly.
 Mafenide acetate is used as it penetrates well and it is
useful against clostridial infection.
 Mannitol is used to prevent myoglobin induced renal
failure.

38. Electrical Burn
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39. CHEMICAL BURNS
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In chemical burns, tissue destruction is
more and progressive.
It is always a deep burn.
Acid burn occurs in skin, soft tissues and
GIT. In GIT, it is common in stomach
either due to nitric acid or sulphuric acid
which may lead to severe gastritis or
pyloric stenosis.
Other acids are formic acid, hydrofluoric
acid. They cause metabolic acidosis, renal
failure, ARDS, haemolysis.
Acidaemia should be corrected by IV
sodium bicarbonate.

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Hydrofluoric acid is commonly used in
industrial areas.
• It is strongest inorganic acid that can
produce corrosion and dehydration.
• It chelates blood calcium causing
hypocalcaemia and arrhythmias.
• It is managed with water irrigation,
application of 2.5% calcium gluconate
gel at 15 minutes interval, local
intradermal and intra-arterial injection of
10% calcium gluconate.
• Continuous cardiac monitoring, IV
calcium gluconate or calcium chloride
administration is needed

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 Alkali burns occur in oral cavity and oesophagus which
leads to multiple oesophageal strictures.
• Sodium hydroxide, lime, potassium hydroxide and
bleach are common alkalis involved.
• They cause saponification of fat, fluid loss, release of
alkali proteinates and hydroxide ions which are toxic.
 External chemical burns are always deep and cause
extensive disfigurement with cosmetic problems.
• Initial treatment is dilution with water (Hydrotherapy).
• It is done using 15-20 litres of running tap water.
 Neutralisation with antidote should never be done at initial
phase of treatment as it creates exothermic reaction which
aggravates the tissue damage. Late neutralisation is done,
if required by 0.2% acetic acid in alkali burns, sodium
bicarbonate, calcium gluconate 10% gel, topical ziphrin
solution in acid burns.

42. Chemical Burn
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 Cold injuries are principally divided into two types:
• Acute cold injuries from industrial accidents
• 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.
Cold Injury

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