The document provides a comprehensive overview of burn injuries including types, causes, and management protocols. It covers thermal, chemical, electrical, and frostbite injuries, outlining their pathophysiology, symptoms, and treatment strategies. Emphasis is placed on the importance of immediate care, fluid resuscitation, and monitoring for complications such as infection and shock.

1. Subject- general surgery
Presentor- DIYA SHARMA(3rd BDS)

3.  Burns is a type of coagulative necrosis caused by
heat, transferred from the source to the body.
 Frostbite which occurs in cold countries is also a
coagulative necrosis but it is caused by extreme
degrees of cold.
 Scald is a burn caused by moist heat (steam)
 Burns never occur at temperatures less than
44°C.

5.  History of burn.
 Pain, burning, anxious status, tachycardia,
tachypnoea, fluid loss.
 In severe degrees features of shock.
 Tolerable temperature to human skin is 40°C for
brief period.

8.  Occurs when skin or eyes come into
contact with an irritant such as acid/base.
 AKA caustic burns.
 They may cause reaction on skin or within
our body.
 These burns can affect internal organs if
chemicals are swallowed.
 Acids and bases cause most of chemical
burns.
 Burns caused by chemical can happen at
school,work,or any place where u can
handle chemical materials.

9.  car battery acid
 bleach
 ammonia
 denture cleaners
 teeth whitening products
 pool chlorination products
Acid burn occurs in skin, soft tissue, and GIT.
In GIT it is common in stomach due to either
nitric or sulphuric acid which may lead to
severe gastritis or pyloric stenosis.
Other acids are formic and hydrofluroic acid.

10. They can cause METABOLIC ACIDOSIS, RENAL
FAILURE, ARDS [ RESPIRATORY DISTRESS
SYNDROME], HAEMOLYSIS.
ACIDAEMIA should be corrected by giving
intravenous sodium bicarbonate.
Hydrofluoric acid that can produce corrosion
and dehydration chelates blood calcium
causing HYPOCALCAEMIA and ARRHYTTHMIAS.
Corrected with water irrrigation, application of
2.5% calcium gluconate gel at 15 min
interval.

11.  Local intradermal and intra arterial injection
of 10% calcium gluconate, continous cardiac
monitoring and intravenous calcium
gluconate or calcium chloride is needed.
 Either brush off compound or wash the area
with water.
 Neutralization with antidote should never be
done at initial phase of treatment as it
creates exothermic reaction which
aggravates tissue damage worsening the
burn.

12.  Late neutralization is done if required by
0.2% acetic acid in alkali burns and sodium
bicarbonate, calcium gluconate 10% gel,
topical ziphrin solution in acid burns.

13. If you swallow an alkaline chemical, it will
cause burns on the inside of your stomach.
This may produce different symptoms than a
chemical burn on your skin.
 In general, the common symptoms associated
with chemical burns include:
 blackened or dead skin, which is mainly seen in
chemical burns from acid
 irritation, redness, or burning in the affected
area
 numbness or pain in the affected area
 a loss of vision or changes in vision if chemicals
have come into contact with your eyes

14.  Some of the following symptoms may also
occur if you’ve swallowed a chemical:
 irregular heartbeat
 headache
 low blood pressure
 cardiac arrest or heart attack
 shortness of breath
 coughing
 seizures
 dizziness
 muscle twitches

15. Blistering caused by electrical burns

16.  It’s a high degree burn inducing tetany.
 Difficult for patient to leave the source that
might give rise to arrhythmia which is a
leading cause of death.
 Look for entry-exist burn.
 Patient may also have major internal organ
injuries, git, thoracic injuries.
 Often convulsions may develop.
 Gas gangrene is common after electric injury.

17.  Patient should always be admitted and
should be accessed by ECG, X ray, Ct scan .
 Fractures and dislocations are common in
electrical injures which is treated
accordingly.
 MAFENIDE ACETATE is better agent as it
penetrates well and is useful against
clostridial infection.
 MANNITOL is used to prevent myoglobin
induced renal failure.

18.  Wound excision, amputation, surgery for
internal organ injury, cardiac monitoring are
essential part of surgical management.

21.  Flat burn- ghee, oil boiling,deep burn
 Flame burn- ordinary burn due to heat like
pus, clotting,bombs.

22.  Occurs after major fire burns.
 Its due to- inhalation of heat and noxious
gases and incomplete products of
combustion.
 At site of fire, oxygen concentration is less
than 2% which can cause death in 45 sec due
to hypoxia. Inhaled carbon monoxide binds
with Hb immediately to form
carboxyhaemoglobin causing SEVERE ANOXIA
and DEATH.

23.  Carbon monoxide has 240 times more affinity
for Hb than oxygen. Carboxyhaemoglobin in
blood more than 10% is dangerous, morethan
60% life threatening.
 Symptoms of carbon monoxide intoxication-
 HEADACHE
 DISORIENTATION
 VISUAL CHANGES
 FATIGUE
 VOMITING
 HALLUCINATIONS
 SHOCK & CARDIAC ARREST

24.  Laryngeal edema and laryngospasm
 Bronchial edema and bronchiospasm
 C/F: low oxygen saturation, charring of
mouth, oropharynx with facial burns, carbon
sputum, change in voice, singed facial and
nasal hair, decreased level of consciousness
with stridor/dyspnea. Acute pulmonary
insufficiency with upper airway obstruction.
After 3-5 days ARDS and hypoxia develops.
Bronchopneumonia with septicemia occurs
after 5 days.

25.  Frostbite occurs when the skin is exposed to
extreme or prolonged cold.
 The skin freezes, as do tissues beneath the
surface of the skin.
 In extreme cases, muscle, nerves, and blood
vessels may also freeze.
 Frostbite is most common in your
extremities, such as your fingers, toes, ears,
and nose.

26.  Frostnip is the first stage of frostbite. It’s
very mild and doesn’t damage your skin.
 When you have frostnip, your skin will turn
red and feel cold to the touch.
 If you stay in the cold, it may begin to feel
numb or have a prickling sensation.

28.  During this stage of frostbite, your skin will
begin to turn from a reddish color to a paler
color. In some cases, it may appear blue.

29.  Deep frostbite is the most severe stage of
frostbite and affects both your skin and the
tissues that lie below.
 If you’re experiencing deep frostbite, the
skin of the area may have a blue or splotchy
look to it. It may feel numb to sensations
such as cold or pain. Muscles close to the
affected area may not work properly. Blood-
filled blisters may also develop in people
with deep frostbite.

32.  Transient non keratotic white appearance of
mucosa like superficial pseudomembrane of
coagulated tissue with inflammatory
exduate.
 Saliva protects oral mucosa. Chronic mild
burns cause keratotic white lesions.
 Moderate burns- localized mucositis
 Severe burns, coagulate tissue with diffuse
white lesions leaving raw and painful
surface.

33.  2 types-thermal and chemical
 Thermal-hot and cold
1. Hot oral cavity burns-
Cause-hot food/beverages. Pain for short
duration. Site- anterior one third of tongue
and palate. Whitish appearance(coagulative
necrosis of superficial tissue).
Signs- frank ulceration and stripping of
mucosa.
Red area is tender, blanch on pressure and
bleed on touching, desquamated epithelium.

34.  Management- analgesics, topical application
of hydrocarbon in embolient base.
 PIZZA BURN- central palate, whitish
grey/ulcerated lesions in middle one third of
hard palate.
2. Cold oral cavity burn- common in children,
on tongue and lips, causing swelling and
redness. Long contact of icecream,frozen
items,cold metal and epithelium becomes
dry and rough.

35.  Chemical – due to causative agents causing
coagulative necrosis and inflammation of
epithelium.
Causes- aspirin,toothache drops, ethyl
alcohol, vitamin C tablets.
These are suicidal/accidental.
C/F- irregular appearance with white
pseudomembrane, painful. Gentle lateral
pressure causes white material to slide away,
exposing painful central ulceration, sloughing
of oral mucosa.

36. D/D- candidiasis
Management- palliative care with topical
application of anaesthestic or bland coating
suspension. Lesions heal quickly.

38.  Although the exact mechanism of the
postburn microvascular changes and
hypovolaemia leading to low cardiac output
and poor tissue perfusion has not been
determined, the following mechanisms have
been proposed:
1.Increased capillary permeability leading to fluid
and protein leakage from the intravascular
space.
2.Decreased plasma oncotic pressure due to
hypoproteinaemia resulting from loss of protein
from the intravascular space.

39. 3. Increased capillary hydrostatic pressure due to
vasoconstriction or partial blockage of vessels
with aggregate of cells and platelets.
4. Reduced clearance of fluid and protein from the
interstitial space by lymphatic ducts due to
blockage by platelet aggregates and fibrin
clots.
5. Intracellular fluid accumulation due to impaired
cell membrane function.
6. Increase in osmotic pressure in the burned tissue
leading to further fluid accumulation.

40. 7. Increased evaporative water loss
RENAL CHANGES-
• Maximum water reabsorption by release of ADH from
posterior pituitary, as a compensatory mechanism.
• Aldosterone is released to cause maximum sodium
reabsorption.
• Acute tubular necrosis (ATN) can occur due to toxins.
• Injury to kidney can occur due to myoglobin
8. Depressed myocardial function
• Chemical mediators released from the site of injury are
responsible for the development of typical inflammatory
response.
This results in rapid and dramatic oedema formation.
• The activated complement cascade system facilitates
liberation of various permeability factors such as
histamine, prostaglandins (PGF-1, PGF-2, PGF-2a) and
thromboxane.

41.  Macromolecular leakage into burned areas,
catabolism and reduced immunoglobulin
synthesis results in a decreased
concentration of all individual
immunoglobulin levels and triggering of
complement cascade.
 Cardiac dysfunction is due to:
 Hypovolaemia.
 Release of cardiac depressants.
 Hormonal causes like catecholamines, vasopressin,
angiotensins.

42.  Pulmonary changes are due to:
 Altered ventilation-perfusion ratio.
 Pulmonary oedema due to burn injury, fluid
overload, inhalation injury.
 ARDS.
 Aspiration.
 Septicaemia.
 GIT changes are due to:
 Acute gastric dilatation which occurs in 2–4 days.
 Paralytic ileus, Curling’s ulcer (due to decreased
mucosal defence; not due to increased HCl).
 Cholestasis and hepatic damage.
 Acute acalculous cholecystitis, acute pancreatitis can
occur.

43.  Bowel mucosal ischaemia causes poor
motility, reduced food digestion and
absorption with increased translocation of
bacteria causing peritoneal oedema,
septicaemia and abdominal compartment
syndrome.
 Metabolic Changes :
 Hypermetabolic rate (BMR).
 Negative nitrogen balance.
 Electrolyte imbalance.
 Deficiencies of vitamins and essential elements.
 Metabolic acidosis due to hypoxia and lactic acid.

44.  Shock due to hypovolaemia.
 Renal failure.
 Pulmonary oedema, respiratory infection,
adult respiratory distress syndrome (ARDS),
respiratory failure.
 Infection by Staphylococcus aureus, beta
haemolytic Streptococcus, Pseudomonas,
Klebsiella leads to bacteraecaemia.
 Fungal and viral infections of dangerous
types can also occur.

45.  GIT: Hypovolaemia, ischaemia of mucosa,
erosive gastritis—Curling’s ulcer (seen in
burns >35%).
 Fluid and electrolyte imbalance.
 Postburn immunosuppression predisposes to
severe opportunistic infection.
 Eschar formation and its problems like
defective circulation, ischaemia when it is
circumferential.
 Electrical injuries often cause fractures,
major internal organ injury, convulsions.

46.  Development of contracture is a late
problem.
 It leads to ectropion, microstomia, disability
of different joints, defective hand functions,
growth retardation causing shortening.
 Inhalation burn causes pulmonary oedema,
respiratory arrest, ARDS.
 Chemical injury causes severe GIT
disturbances like erosions, perforation,
stricture oesophagus (alkali), pyloric stenosis
(acid), mediastinal injury.

47.  Toxic shock syndrome: It is a life-threatening
exotoxin mediated disease caused by
Staphylococcus aureus. It is common in
children, presents with rashes, myalgia,
diarrhoea, vomiting, and multiorgan failure
with high mortality.

48.  Ebb: Low metabolism and temperature;
cardiac output decreased.
 Flow: Hypermetabolism, high cardiac
output, hyperglycaemia, increased heat
production.

49.  Gluconeogenesis and glycogenolysis is increased.
 Lipolysis: It is increased and fatty acids are
released. They are re-esterified into
triglycerides resulting in fat accumulation in the
liver.
 Proteolysis: The result is increased production of
urea which is excreted in the urine. As a result
of this, there ii increased efflux of amino acids
from skeletal muscle poo including alanine and
glutamine.
 Significance: Burns patient requires more than 1
g/kg/day) proteins

50.  Glutamine can also be given
 Catecholamines are massively elevated in
bum injury.

51.  It is due to inhalation injury
 Direct injury from hot air/smoke
 Inflammatory response to burns
 Oedema from resuscitation fluids
 Suspect in patients with facial burns,
tachypnoea, and progressive hoarseness
 Oxygen, pulse oximetry
 Bronchoscopy, early endotracheal intubation

54.  Sepsis is identified by fever, lethargy,
leucocytosis, thrombocytopenia
 Focus may be at the burn site, catheter site,
cannula/CVP line site, or respiratory
infection.
 Low immunity, loss of proteins and
immunoglobulins, loss of barrier causes
sepsis.
 Opportunistic infection is also common.
 Associated conditions like diabetes, HIV
infection, old age, respiratory diseases
worsen the sepsis in burn injury.

55.  It may be local infection commonly by
staphylococcus aureus in early period,
pseudomonas, candida , aspergillus , herpes
simplex virus in partial thickness nasolabial
burns.
 It maybe suppurative thrombophlebitis also.
 Systemic infection like pneumonia,
bacteraemia, septicaemia can occur.
 Burns itself creates immunosuppression (cell-
mediated immunity).

56.  Any patient exposed to smoky fire should
receive 100% oxygen via a non-rebreathing
mask. If he is unconscious, endotracheal
intubation should be performed.
 Intravenous line and administration of
lactated Ringer solution at 1 L/h in adult.
 Transport the patient-warm and wrapped in a
clean sheet. Clothing and jewellery should
be removed because the swelling begins
immediately.
 Small bums can be managed by cool water.
Do not use ice-cold water.

57.  1. First aid: Cold water bath should be given
immediately.
 This takes away the heat, stabilises mast cell,
thus decreasing the release of histamine and
reduces oedema.
 2. Careful history-taking AMPLE: Allergy,
Medications ,Past medical history, Last
meal,Events regarding injury
 The time since sustaining the injury, the type of
heat source, location and circumstances of the
bum should be recorded.
 3. Hospitalisation and admission in a burns ward
with airconditioning facility.

58. 4. Assessment of depth of burn :
• Partial thickness burns: Here, superficial
layers of skin are destroyed.
Epidermis and variable portion of dermis are
involved.
Since the nerve endings are exposed, it causes
severe degree of pain.
• Full thickness burns: Involvement of full
thickness of dermis with epidermis.
Since, the nerves are destroyed, it is less
painful.

59. 5. Assessment of extent of burns in terms of
body surface area (BSA): It is calculated by a
Rule of 9 "Rule of Wallace"

61. 6. Temperature, pulse, respiration and blood
pressure are monitored and maintained within
nonnal limits.
7. An indwelling urinary catheter (Foley catheter)
is introduced, and strict intake and output chart
must be maintained.
8. A Ryle's tube is passed. A burn patient can
develop "acute stress ulcers" called acute peptic
ulcers or Curling ulcers.
Hence, to prevent bleeding, a cold stomach wash
is given through the Ryle's tube.
Antacids and H2 receptor blockers such as
Ranitidine 150 mg twice a day are also given.

62. 9. Replacement of fluid volume is done using
anyone of the following formulas:
a. Muir and Barclay formula
b. Parkland's formula
c. Modified Brooke formula
10. Broad-spectrum antibiotics are given
against gram +ve, gram -ve and anaerobic
organisms.
• To treat septic shock, higher antibiotics such
as cephalosporins have to be given

63. 1. Uncontrolled hypovolaemic shock
(refractory hypervolaemia).
2. Choking, suffocation due to respiratory
burns especially in burns of head and neck.
3. Septicaemic shock is the most common
cause of death.
4. Mnemonic: Look for 6 Ps- Pain, Pallor,
Pulselessness, Paraesthesia, Paralysis
Poikilothermia (in the affected part).
5. If these are present, it indicates
compartment syndrome.
6. It needs to be treated by escharotomy

64.  Depending on the Percentage of Burns (Burn
Severity Classification)
Mild (Minor):
 Partial thickness burns less than 15% in adults or less
than 10% in childrens
 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.

65. 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.

66. a. First degree: red, nonblistered skin
1. 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: blisters and some thickening of
the skin
1. The affected area is mottled, red, painful,
with blisters, heals by epithelialisation in 14–21
days. Superficial second degree burn heals,
causing pigmentation.
2. Deep second degree burn heals, causing
scarring, and pigmentation. Sensation is
present but no blanching.

67. c. Third degree: widespread thickness with a
white, leathery appearance
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.

68. d. Fourth degree: Involves the underlying
tissues—muscles, bones.

69.  First-degree burns cause minimal skin damage.
They are also called “superficial burns” because
they affect the outermost layer of skin. Signs of
a first-degree burn include:
 redness
 minor inflammation, or swelling
 pain
 dry, peeling skin occurs as the burn heals
 Since this burn affects the top layer of skin, the
signs and symptoms disappear once the skin cells
shed. First-degree burns usually heal within 7 to
10 days without scarring.

70.  First-degree burns are usually treated
with home care. Healing time may be
quicker the sooner you treat the burn.
Treatments for a first-degree burn include:
 Soaking the wound in cool water for five
minutes or longer
 Taking acetaminophen or ibuprofen for pain
relief
 Applying lidocaine (an anesthetic) with aloe
vera gel or cream to soothe the skin
 Using an antibiotic ointment and
loose gauze to protect the affected area

71.  Make sure you don’t use ice, as this may
make the damage worse.
 Never apply cotton balls to a burn because
the small fibers can stick to the injury and
increase the risk of infection.
 Also, avoid home remedies like butter and
eggs as these are not proven to be effective.

72.  Second-degree burns are more serious
because the damage extends beyond the top
layer of skin.
 This type burn causes the skin to blister and
become extremely red and sore.
 Some blisters pop open, giving the burn a
wet or weeping appearance.
 Over time, thick, soft, scab-like tissue
called fibrinous exudate may develop over
the wound.

73.  Due to the delicate nature of these wounds,
keeping the area clean and bandaging it
properly is required to prevent infection.
 This also helps the burn heal quicker.
 Some second-degree burns take longer than
three weeks to heal, but most heal within
two to three weeks without scarring, but
often with pigment changes to the skin.

74.  Treatments for a mild second-degree burn
generally include:
 Running the skin under cool water for 15
minutes or longer
 Taking over-the-counter pain medication
(acetaminophen or ibuprofen)
 Applying antibiotic cream to blisters

75.  Excluding fourth-degree burns, third-degree
burns are the most severe.
 They cause the most damage, extending
through every layer of skin.
 There is a misconception that third-degree
burns are the most painful.
 However, with this type of burn the damage
is so extensive that there may not be any
pain because of nerve damage.

76.  Depending on the cause, the symptoms third-
degree burns can exhibit include:
 waxy and white color
 char
 dark brown color
 raised and leathery texture
 blisters that do not develop

77. 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.

78. 1. Clean the wound with antiseptic agents such as
savlon, iodine.
2. Dressing-
Open method: Exposure line of management: If
facilities available are good, with a fumigated
ward, the wound can be left open to the
atmosphere after applying Silver Sulfadiazine
cream.
Closed method: Alternately, after applying silver
sulfadiazine, 1 % silver nitrate and mefenide
cotton rolls are applied, over which a bandage
is applied. This is called closed method.
Advantages of closed method are less pain, reduced
infection and sogging, and better medication

79. 3. Surgery: Tangential excision followed by
grafting is done after about 48-72 hours in
which the burn wound is excised tangentially
till fresh bleeding occurs.
This is followed by skin grafting. Skin is taken
from the remaining normal area, or can be
obtained from skin bank. A mesh expander
and cell culture may also be used.
4. Treatment of circumferential deep 2nd and
3rd degree burns.

80. 1. It prevents secondary infection and
septicaemia.
2. Decreases the hospital stay (2-5 weeks is
the usual time taken for eschar of III0 bum
to separate. This is reduced by tangential
excision).
3. Decrease of incidence of contractures and
hypertrophic scar.
4. Cost of the treatment is reduced.

81.  It depends upon several factors , the most
important being percentage of burns and
facilities of treatment.
 If untreated, postbums contractures can
occur.
 Factors affecting outcome-
 Extremes of age
 Depth of burns
 Inhalation of noxious fumes
 Cardiopulmonary disease

83.  Manipal manual of surgery- 4th edition
 SRB’s manual of surgery- 5th edition