BURN and its related anaesthesia complication

1. 1
Burns Injury-Critical care in severe burn
injury
Dr.zikrullah mallick

2. Definition of Burn
• Damage to body tissues caused by heat, chemicals,
electricity, sunlight, or radiation.
• Scalds from hot liquids & steam, building fires &,
flammable liquids & gases are the most common
causes.

3. The global burden
• Burn injuries are among the most devastating of all
injuries and a major global public health crisis.
• Burns are the 4th most common type of trauma
worldwide, following traffic accidents, falls, and
interpersonal violence.
[The Global Burden of Disease: World Health Organization, Geneva 2008]
• Approximately 90% of burns occur in low to middle
income countries, regions that generally lack the
necessary infrastructure to reduce the incidence
and severity of burns.
[Peck M, Pressman MA. The correlation between burn mortality rates from fire and
flame and economic status of countries. Burns 2013; 39:1054]
3

4. 4
• The WHO latest figures says nearly 1.95 lakh deaths
every year are caused by burns. Women in the south-
east Asian region have the highest rate of burns,
accounting for 27% of global burn deaths and nearly
70% of fatalities in the region.
• Burns are the 11th leading cause of death of children
aged between 1-9 years and are also the 5th most
common cause of non-fatal childhood injuries.

5. 5
"Non-fatal burn injuries are a leading cause of
morbidity even though burns are preventable. Burns
are a global public health problem accounting for an
estimated 195, 000 deaths annually. In many high-
income countries, burn death rates have been
decreasing, and the rate of child deaths from burns
is currently over 7 times higher in low and middle-
income countries than in high-income countries.“
- World Health Organization's (WHO)

6. Anatomy of The Skin
• Skin is the largest, most important organ
• 16% of total body weight
• 1.73 sq meter – surface area
Functions of the Skin
• Protection
• Sensation
• Temperature regulation
• Insulation from trauma
• Appearance
6

7. Anatomy of The Skin
• Layers
– Epidermis
– Dermis
– Subcutaneous
– Underlying Structures
• Fascia
• Nerves
• Tendons
• Ligaments
• Muscles
• Organs
7

8. Thermal Injuries / Burns
• Tissue destruction caused by application of heat in any
form to the external or internal surface of the body.
Causes of Burn Injuries
Fire burn – flash/flame
Scald burn - liquids or steam,
Contact burn - hot solid materials
Chemical burn - noxious chemicals /corrosives
Electrical burn - electrical current, lightning
Radiation burn - X ray, UV rays, laser, Radioactive materials
8

9. Burn Classification
• 1st degree - localized to the epidermis
• 2nd degree (Superficial) - epidermis, superficial dermis
• 2nd degree (deep) - epidermis and deep dermis
• 3rd degree - epidermis, dermis, subcutaneous fat
• 4th degree - epidermis, dermis, subcutaneous fat,
underlying muscle, bone or organ
9

10. Superficial (1st degree)
• Least destructive
• Painful, erythematous,
blanch to the touch.
• Sunburn or a minor scald
from a kitchen accident.
• Do not result in scarring.
10

11. Partial-thickness (2nd degree)
• Epidermis destroyed
• Involvement of varying
depth of dermis.
• Two types: superficial
and deep.
• distinction is based on
the depth of injury into
this structure
11

12. 12
Superficial dermal burns:
• Erythematous, painful, blanch to touch, blister.
• Spontaneously re-epithelialize in 7 to 14 days.
• After healing, slight skin discoloration.
Deep dermal burns:
• Painful, do not blanch to touch, pale.
• Heal in 14 to 35 days by re-epithelialization.
• Severe scarring as a result of the loss of dermis.

13. Full-thickness (3rd degree)
• Epidermis and dermis
• ESCHAR - Painless, hard,
leathery dead skin that
is black, white, or cherry
red.
• Compartment syndrome
• Chest restriction
• Patient will need grafting
13

14. Deep Full-thickness (4th degree)
14
• Extend beyond skin into underlying fascia and
tissues
• Muscle, bone and tendon damage with exposure
to surface
• Blackened and depressed, little or no sensation
• Early excision and grafting beneficial.

15. 15

16. 16

17. 17

18. 18

19. Jackson’s Theory of Thermal Wounds
• 3-D model showing burn depth and TBSA burned
19

20. 20
Zone of Coagulation
• Inner area nearest the burn
• The necrotic area of a burn where cells have been disrupted
• Ruptured cell memb. clotted blood and thrombosed vessels
Zone of Stasis
• area immediately surrounding the necrotic zone.
• moderate degree of insult with decreased tissue perfusion
• Potentially salvable; susceptible to additional injury
Zone of Hyperemia
• Peripheral area of burn
• vasodilation from inflammation surrounding the burn wound.
• Area of least cellular injury & increased blood flow
• Viable tissue from which the healing process begins.

21. American Burn Association (ABA)
Major Burn - >25% of TBSA
• Functionally significant involvement of hands, face, feet,
or perineum.
• Electrical or inhalation injury
Moderate Burn – 15% to 25% of TBSA
• No complications of involvement of hands, face, feet, or
perineum
• No electrical or inhalation injury
Minor Burn - <15% of TBSA
• No involvement of hands, face, feet, or perineum
• No electrical or inhalation injury
21

22. Rule of Nines
22

23. Infant Rule of nines
• 18 Head
• 9 Each upper limb
• 18 Front trunk
• 18 Back trunk
• 13.5 Each lower limb
• 1 perineum
ADULT Rule of Nines
• 9 Head
• 9 Each upper limb
• 18 Front trunk
• 18 Back trunk
• 18 Each lower limb
• 1 perineum
23

24. Palm Rule
• Area of the open hand (including the palm and
extended fingers) of the patient to be approximately 1%
of TBSA.
• An alternate system for approximating the extent of the
burn.
• An accurate assessment of size can be made by using
the patient's palmar hand surface, including the digits,
• This method is helpful when evaluating splash burns
and other burns of mixed distribution as well as smaller
burns.
24

25. Lund and Browder Chart
• Children have much larger
heads and smaller thighs in
proportion to total body
size than do adults.
• child's body proportions
do not fully reach adult
percentages until
adolescence
• More complicated and
time consuming method to
estimate BSA burned.
• BUT MORE ACCURATE!!
25

26. Laser Doppler Flowmeter
• Currently, burn depth is most accurately assessed by
the judgment of experienced practitioners. Accurate
depth determination is critical because wounds that
will heal with local treatment are treated differently
from those requiring operative intervention.
• Several recent reports claim superiority of this
method over clinical judgment in the determination
of wounds requiring skin grafting for timely healing
26

27. Laser Doppler Flowmeter
• The sensor is placed on
the skin in question,
which returns a value of
perfusion units.
• A value of 0 is necrotic,
whereas values of 80
indicate viable skin.
27

28. PATHOPHYSIOLOGY
OF
BURN INJURY
28

29. • Burn are caused by a transfer of energy from a heat source
to the body.
• Tissue destruction results from coagulation, protein
denaturation, or ionization of cellular content.
• Disruption of the skin can lead to increased fluid loss,
infection, hypothermia, scarring, compromised immunity,
and changes in function, appearance and body image.
• The depth of the injury depends on the temp of the
burning agent and the duration of contact with the agent
• For example in the case of scald burns in adults, 15
seconds of contact with hot tap water at 56 degree C may
result in a burn that destroys both the epidermis and the
dermis, causing a full thickness (third degree) injury.
29

30. Inflammatory Response to Burn
Prostaglandins, Catecholamines, Bradykinin, Vasoactive
amines, Leukotrienes, and activated Complement,
Histamine, Serotonin, Thromboxane A2
• Vasoconstriction and Vasodilation,
• Increased capillary permeability, and
• Edema
• Mesenteric vasoconstriction and decreased blood flow
to the gut that compromise gut mucosal integrity and
immune function.
30

31. Burn Shock
• Combination of hypovolaemic, and distributive shock,
refractory to i.v. resuscitation.
• Causes are:
• ↑ extracellular fluid
• ↓ Intravascular volume
• ↓ plasma volume
• Characterized by specific hemodynamic changes:
• ↑ systemic vascular resistance, and
• ↓ pulmonary artery occlusion pressures,
• ↓ cardiac output .
• ↓ contractility
31

32. Fluid/Electrolyte Changes
Fluid Shift
• ↑ capillary hydrostatic pressure and ↑ capillary permeability
• Leak of plasma from intravascular into interstitial space.
Fluid remobilization
• Capillary leak ceases and fluid shifts back into the circulation
• Restores fluid balance and renal perfusion
• Increased urine formation & diuresis
Electrolyte derangements:
• Initially tissue destruction - Hyperkalemia
• Later, Renal wasting & Gastric losses - Hypokalemia
• ↑ extracellular volume - Hyponatremia
32

33. Metabolic Response to Burn
Hypermetabolism
• Resting energy expenditure (REE) after burn injury
increases as much as 100%.
• Increase in oxygen consumption because of increased
production of catecholamines, cortisol, and glucagon.
• Increased heat loss from the burn wound secondary to
increased blood flow and increased beta-adrenergic
stimulation are probably primary factors.
• REE helps in assessing the nutritional status.
33

34. Glucose Metabolism
• ↑ Gluconeogenesis
• ↑ glycogenolysis
• ↑ basal rate of glucose production
• Hyperglycemia complicates the acute management,
related to poor outcomes, specifically increased risk of
infection & decreased graft take.
• Exogenous insulin administration to achieve euglycemia
has been shown to decrease donor site healing time and
decrease length of stay.
34

35. Lipid Metabolism
• Lipolysis occurs at a rate more than the requirements
for fatty acids as an energy source in burn patients
resulting in ↑ FFA.
• The majority of released fatty acids are not oxidized,
rather re-esterified into triglycerides, resulting in fat
accumulation in the liver and hepatic steatosis.
• Beta-blockade using propranolol appears helpful in
manipulating peripheral lipolysis and in preventing
hepatic steatosis.
35

36. Protein Metabolism
• Muscle protein breakdown is ↑ and is excreted in the
urine as urea. This results in an ↑ efflux of amino acids
from the skeletal muscle and hypoproteinemia.
• Wound healing & immunologic activity require
enhanced protein synthesis.
• Protein intake 1 g/kg/day has been recommended for all
burn patients, and for patients with normal renal
function, the intake is 2 g/kg/day.
36

37. Neuroendocrine Response
• Catecholamines ↑ & Glucagon ↑ and appear to be the
major endocrine mediators of the hypermetabolic
response in burn patients.
• Burn injuries abolish the normal diurnal variation in
glucocorticoid secretion, producing persistent
hypercortisolemia.
• growth hormone (GH) ↓
• T3 ↓ & T4 ↓ and reverse T3 ↑
37

38. Systemic Changes
• Cardiac: ↓ CO, ↓ BP
• Pulmonary: FRC ↓ lung & chest wall compliance ↓
• Renal: RBF ↓ GFR ↓
• Gastrointestinal: ↓ or absent motility, Curling’s ulcer
• Immune System:
• ↓ production of immunoglobulin
• ↓ opsonic activity
• ↓ bactericidal activity
• Impairment in host defense causes the burned patient
to become especially prone to infection.
38

39. MANAGEMENT
OF
BURN INJURIES
39

40. At the Site
• Remove to safe area, if possible
• Stop the burning process
• Extinguish fire
• Remove clothing and jewellery
• Cut around areas where clothing is stuck to skin
40

41. Emergency Care
• The initial management of a severely burnt patient
is similar to that of any trauma patient.
• Primary and secondary survey should follow ATLS
principles.
• Do not get distracted by the burn
• Burn injury must not distract from this sequential
assessment, otherwise serious associated injuries
may be missed.
41

42. Initial care based on ATLS Guidelines
• Many of the components are being assessed
simultaneously, which is essential for immediately
identifying life-threatening situations and its
management.
• If initial interaction reveals that the patient is alert,
talking, oriented, and moving all extremities…
• Patient has an adequate airway
• Is breathing adequately
• Oxygen is being circulated to the brain, and
• There is no major neurologic injury.
42

43. Airway Control
• Early tracheal intubation should be considered in the
presence of any of the following features:
• Stridor,
• Hypoxaemia or Hypercapnia,
• GCS ≤ 8
• Facial burns
• Inhalational injury / CO poisoning
• Upper airway / oropharyngeal oedema
• Full-thickness neck burns and
• Chest wall restriction
43

44. • Delay in performing the intubation can result in total
obstruction of the upper airway.
• In presence of facial burns and when the fasting status of
the patient is unknown, RSI should be performed.
• Succinylcholine is safe in the first 24 h after a burn. After
this time, its use is contraindicated due to the risk of
hyperkalaemia leading to cardiac arrest, thought to be due
to release of potassium from extrajunctional acetylcholine
receptors. This can persist up to 1 year post-burn.
• The intubation can be done by simple laryngoscopy,
intubation stylet, FOB or LMA-Fastrach(ILMA).
44

45. 45
• In patient with 3rd to 4th degree burns of the neck,
laryngoscopy may be impossible because of the rigidity
of the cervical tissue, an incision in neck can facilitate
laryngoscopy.
• Use of modern technique which involve less extension
like lightwand, airtraq or FOB.
• Extensive or circumferential 3rd to 4th degree burns to
the chest wall can cause severe restriction and may
require immediate escharotomy of the anterior chest
wall.

46. Tube fixation
• The fixation of the ET is a challenge in the burned
patient.
• Secure the tube safely without additional injury to the
tissue of the face and is flexible enough to adjust to
edema formation.
• Adhesive tape are not effective in the burn patient
because they do not adhere adequately. Usually, a soft
sling ribbon is used. It is tied at the back of the head (not
the neck).
• Suturing the tube to the gums, wiring the tube around a
tooth.
46

47. Inhalational Injury
• Any pulmonary insult associated with a burn injury
Three types:
• Heat injury to the airways
• Inhalation of toxic product of combustion like CO
• Chemical burn with deposition of carbon particles in
the lower airways.
• Leading cause of death from fires.
• Higher mortality than burn patients without
inhalation injury.
47

48. 48

49. Warning Signs of Airway Burn
Suspect airway burn if:
• Enclosed space
• Stridor, hoarseness, or cough
• Burns to face, lips, mouth, pharynx, or nasal mucosa
• Soot in sputum, nose, or mouth
• Dyspnoea, ↓ level of consciousness, or confusion
• Low O2 saturation on pulse oximetry
• Increased CO2( > 2%)
49

50. CO Poisoning
• When carboxy Hb >15% in blood.
• Causes tissue hypoxia due to:
• Binds to Hb 200-300 times more readily than O2 in
alveoli
• Rate of dissociation of CO Hb slow.
• Creates a left shift of O2 - Hb dissociation curve
• Impairs O2 unloading at tissue level.
• Signs and Symptoms:
• Headache, nausea/vomiting, dyspnea/tachypnea
• Cherry red appearance of mucous membranes
• Persistent metabolic acidosis with adequate volume
resuscitation. 50

51. Treatment
• The clinical manifestations are often delayed but are
usually apparent by 24 hours.
• There is no specific treatment for airway burns other
than ensuring adequate oxygenation and minimising
iatrogenic lung insult.
• Prophylactic corticosteroids or antibiotics have no role
in treatment.
• All patients suspected of having CO Poisoning should
be given 100% O2 .
51

52. 52
• The half life of CO-Hb breathing room air is 90 minutes,
whereas, when breathing 90 to 100% oxygen is 30
minutes, i.e., the concentration of carboxyhemoglobin is
reduced by approximately 50% every 30 minutes if an
oxygen concentration of 90 to 100% is used.
• Hyperbaric oxygen produces more rapid displacement
and is useful in cases of prolonged exposure.
• ET intubation and use of 100% oxygen with mechanical
ventilation is indicated for those patients with
impaired neurologic function and a high
carboxyhemoglobin.

53. Breathing
• Breathing, chest movement, and tracheal position
should be assessed clinically.
• All burn patients should receive 100% O2 through a
non-rebreathing mask on presentation.
• Oxygen administration is required for all major burns
until carbon monoxide toxicity has been ruled out.
• The oxygen saturation is most readily assessed by the
use of a pulse oximeter, as the clinical determination of
adequate oxygenation is virtually impossible by any
other noninvasive means.
• Artificial ventilation if required.
• If in doubt intubate!!
53

54. Circulation
• Two large-bore IV catheters are inserted into the peripheral veins,
Traditional sites for i.v. access may be unavailable and unusual
peripheral venous sites or central venous access may be required.
• Intravenous fluid if :
• >15 - 20% burn in adults
• >10% burn in children
• Age >65yrs or <2yrs
• Ringers lactate solution preferred.
• Pulse rate and character, color and temperature of the skin, and
mental status are rapidly evaluated to assess perfusion.
• BP is determined at the onset of resuscitation and then every 5 to
10 minutes until the patient's vital signs have stabilized.
54

55. Disability: neurologic status
• This should consist of determining the GCS score and
examining the pupils for size, symmetry, and reaction to
light.
• The GCS is the sum of scores for three areas of
assessment, including (a) eye opening, (b) verbal
response, and (c) best motor response.
• Pupillary size, symmetry, and reaction to light are
important diagnostic tools that aid in determining if
there is a lateralizing brain injury.
55

56. Exposure and Estimation
• Expose and ensure all jewellery and watches are removed
from burnt limbs.
• Burn patients become hypothermic easily, so should be
covered and warmed as soon as possible.
• The patient should be examined (including the back - log
roll if appropriate) to get an accurate estimate of the burn
area and to check for any concomitant injuries.
• A standard Lund–Browder chart is used for a quick
assessment of BSA burnt.
• If this is not available, the ‘Rule of Nines’ is fairly accurate
in adult patients.
56

57. Intensive Care Burn Units
• Severely burned patients are cared in specialized
intensive wards which have semi-sterile laminar flow
boxes, their own operating rooms, and special
bathrooms for patients.
• Intensive care therapy is a basis for further plastic
surgery therapy and plays an important role for the
survival of the patient.
• Controlled fluid and electrolyte management with
continuous monitoring of various laboratory parameters
are the basis of intensive care and decreases the risk of
common complications.
57

58. Intensive Care Management
• Fluid resuscitation and electrolyte management
• Airway burn/Inhalational injury
• Mechanical ventilation
• Nutrition & Metabolism
• Prevention of Infection
• Prevention of multiorgan failure
• Compartment syndrome, Hypothermia, DVT
• Bed sores
• Other supportive measures
58

59. ABA Burn Center Referral Criteria
• Burns >10% TBSA in patients <10 or >50 years of age
• Burns >20% TBSA in other age groups
• Full-thickness burns >5% TBSA in any age group
• Burns involving the face, hands, feet, genitalia, perineum, or
major joints.
• Electrical burns/Chemical burns/Inhalation injury
• Burn injury in patients with preexisting medical disorders.
• Burn with concomitant trauma (e.g., fractures) in which the
burn poses the greatest risk of morbidity or mortality.
• Burn injury in children admitted to a hospital without
qualified personnel or equipment for pediatric care.
59

60. Fluid Management
• TBSA <20% is associated with minimal fluid shifts and can
generally be resuscitated with oral hydration, except in cases of
facial, hand and genital burns, as well as burns in children and the
elderly.
• TBSA >20% is associated with massive fluid shifts, which result in
burn oedema and burn shock.
OBJECTIVES:
• HR < 110/minute
• Normal sensorium (awake, alert, oriented)
• Urine output – 0.5 ml/kg/hr (adult); 0.5-1 ml/kg/hr (paed)
• Resuscitation formulae provide estimates,
• Adjust to individual patient responses.
60

61. Choice of Fluid
• Isotonic crystalloids, hypertonic solutions and colloids have
been used for this purpose, but every solution has its
advantages and disadvantages.
• Plasma proteins generate the inward oncotic force that
counteracts the outward intravascular hydrostatic force.
Without protein, intravascular volume could not be
maintained.
• The sodium shift into the cell results in cellular oedema and
hypo-osmolar intravascular fluid volume. Rapid infusion of
hypertonic sodium solutions has proven to increase the
plasma osmolality and limit cellular oedema.
61

62. • Normal saline should be avoided, as the large volumes
required for resuscitation invariably lead to
hyperchloremic metabolic acidosis
• None of them is ideal, and none is superior to any of the
others. Combination of fluids can be used to achieve the
desired goal of end-organ perfusion.
• Crystalloid, in particular LR is the most extensively
used resuscitation fluid.
62

63. Fluid Resuscitation Formula
• Parkland formula
• Brooke formula
• Modified Brooke formula
• Evan’s formula
• Monafo formula
Formulas developed for children
• Shriner’s cincinnati
• Galveston
63

64. Parkland formula
Initial 24 hours:
• RL @ 4 ml/kg/% burn for adults
• RL @ 3 ml/kg/% burn for children.
• Half in first 8 hrs, remaining half in next 16 hrs
• no colloid in the initial 24 hours.
• Next 24 hours: Colloids given as 20–60% of calculated
plasma volume. No crystalloids.
• maintain a urinary output of 0.5–1 ml/kg/hour in
adults and 1 ml/kg/hour in children.
64

65. Brooke formula
• Initial 24 hours: RL @ 1.5 ml/kg/% burn plus colloids @
0.5 ml/kg/% burn plus 2000 ml free water with glucose
• Next 24 hours: RL @ 0.5 ml/kg/% burn, colloids @ 0.25
ml/kg/% burn and the same amount of glucose in water
as in the first 24 hours
Modified Brooke
• Initial 24 hours: No colloids. RL @ 2 ml/kg/% burn in
adults and 3 ml/kg/% burn in children
• Next 24 hours: Colloids @ 0.3–0.5 ml/kg/% burn and no
crystalloids are given.
65

66. Evans formula
• First 24 hours: Crystalloids 1 ml/kg/% burn plus colloids
at 1 ml/kg/% burn plus 2000 ml glucose in water
• Next 24 hours: Crystalloids at 0.5 ml/kg/% burn,
colloids at 0.5 ml/kg/% burn and the same amount of
glucose in water as in the first 24 hours.
Monafo formula
• Monafo recommends using a solution containing 250
mEq Na, 150 mEq lactate and 100 mEq Cl.
• The amount is adjusted according to the urine output.
66

67. Galveston
• Initial 24 hours: RL 5000 ml/m² burn area + 1500
ml/m² total area
• (1/2 of total volume over 8 hours, rest of the total
volume in 16 hours)
67

68. Nutrition and metabolism
• Burn injury is associated with a considerable
hypermetabolic response, mediated by the systemic
response to the burn and related to the extent of the
burn injury.
• Even small burns can be associated with hyperpyrexia
directly due to hypermetabolism.
• Close attention to nutritional needs is critical to prevent
protein breakdown, decrease infection, increase wound
healing and improve immune status.
68

69. • In view of the greatly increased nutritional
requirements, appropriate nutrition must be initiated
rapidly through enteral route.
• Enteral food supply should be targeted as early as
possible, in order to avoid regression of intestinal villi.
• The capillary leak, which is responsible for the massive
displacement of fluids, spontaneously ceases after 24
hours. Till then, intensive fluid therapy must be
continued, in order to counteract the decreased cardiac
output, the reduced perfusion of the kidney, the liver
and the intestine.
69

70. Routes
Oral
Enteral: Energy requirements are proportional to the
size of the burn and should be met by enteral
nutrition, and this should be established as soon as
possible after the burn injury.
i.e. duodenal / gastrostomy / jejunaostomy tube
Parenteral i.e. TPN and PPN
Total parenteral nutrition is associated with
immunosuppression, an increase in infective
complications, and reduced survival.
70

71. • High-protein & high-calorie diet
• Often requiring various supplements- vitamin A & C.
• Glutamine, arginine, and omega 3 fatty acid
supplementation may improve immunity and gut
function.
71

72. Management of the hypermetabolic response
• Reduce heat loss - environmental conditioning
• Excision and closure of burn wound
• Early enteral feeding
• Recognition and treatment of infection
72

73. Infection in Burns Patients
• After the initial resuscitation, up to 75% of mortality in
burns patients is related to infection.
• Infective pulmonary complications are now the
commonest types of infection seen in burns patients.
Several factors contribute to the high frequency and
severity of infection:
Destruction of the skin or mucosal surface barrier
Presence of necrotic tissue and serosanguinous exudate
provides a medium to support growth of microorganisms
Invasive monitoring provides portals for bacterial entry.
Impaired immune function allows microbial proliferation
73

74. Signs of Wound Infection
• Change in wound appearance:
a) Discoloration of surrounding skin
b) Offensive exudate
• Delayed healing
• Graft failure
• Conversion of partial thickness wound to full
thickness
74

75. Causative Agents
Bacteria
• Haemolytic streptococci— Streptococcus pyogenes.
• Staphylococci— MRSA
• Gram negative bacteria— Pseudomonas aeruginosa,
Acinetobacter, Proteus species.
Fungi
• Candida—Most common fungal isolate.
• Filamentous fungi— Aspergillus, Fusarium, and
phycomycetes
Viruses
• Herpes simplex—Characterised by vesicular lesions
75

76. Treatment
• Use of topical antimicrobial agents are effective.
• Silver sulfadiazine, Silver nitrate and Mafenide are
most frequently used.
• Early closure of the burn wound by surgical techniques
then lessens the surface area available for further
microbial colonisation and subsequent infection.
• Prophylactic use of systemic antibiotics is controversial
and is not indicated, in patients with burns covering less
than 40% of TBSA.
76

77. Prevention of Multiorgan damage
Pulmonary complications
• Aggressive airway toilet is essential.
• Diluted heparin and acetyl cystine nebulisation may be
helpful.
• Early surgical debridement, enteral feeding, mobilisation
of the patient, and early extubation are desirable.
• Antibiotics should be reserved for established infections
and guided by regular microbiological surveillance.
77

78. Heart Failure
• Myocardial dysfunction is a potential consequence of
major burn injury, attributed to a circulating myocardial
depressant factor.
• Administration of an inotropic agent is preferable to
overloading a failing myocardium with large volumes of
fluid.
• However, the inotropic drug can produce vasoconstriction
in the burn wound, reducing the viability of critically
injured tissue.
• Inotropic drugs should not be used until adequate fluid
resuscitation has been ensured.
• Inotropic drugs that do not produce vasoconstriction (such
as dopexamine or dobutamine) will preserve wound
viability.
78

79. Renal Failure
• Early renal failure after burn injury is usually due to
delayed or inadequate fluid resuscitation or from
substantial muscle break down or haemolysis.
• Delayed renal failure is usually the consequence of sepsis
and is often associated with other organ failure.
• A reduced urine output, despite adequate fluid administration,
is usually the first sign of ARF.
• This will be followed by a rise in serum creatinine and urea
concentrations.
• Early renal support (CRRT) will control serum electrolytes
and accommodate the large volumes of nutritional
supplementation required in a major burn.
79

80. Cerebral Injury
• Hypoxic cerebral insults and closed head injuries are
not uncommon in burn injuries.
• Fluid administration for the burn injury will increase
cerebral oedema and intracranial pressure.
• Monitoring intracranial pressure may help in
minimising the adverse effects of trying to achieve
two contradictory treatment goals.
80

81. Compartment Syndromes
• A lifethreatening complication caused by high volume
resuscitation is abdominal compartment syndrome
(ACS).
• Defined as intra-abdominal pressure >20 mm Hg plus at
least one new organ dysfunction.
• ACS has been associated with renal impairment, gut
ischemia, and cardiac and pulmonary hypoperfusion.
• Clinical manifestations include tense abdomen,
decreased pulmonary compliance, hypercapnia, and
oliguria.
81

82. • Appropriate intravascular volume, appropriate body
positioning, pain management, sedation, nasogastric
decompression, muscle relaxants if required, and torso
escharotomy are all interventions to increase abdominal
wall compliance and decrease intra-abdominal
pressures.
Extremity compartment syndromes can also result from
extensive edema formation.
• Patients may require escharotomies, fasciotomies, or
both for the release of extremity compartment
syndrome.
82

83. • Hypothermia - Strategies to vigorously prevent
hypothermia include a warmed room, warmed inspired
air, warming blankets, and countercurrent heat
exchangers for infused fluids.
• Deep Venous Thrombosis - The incidence of DVT in burn
patients is estimated to be 1% to 23%
• Prevention of BED SORES - These patients may require a
prolong bed rest, so care should be taken concerning
development of BED SORES.
• Stress Ulcers - Patients with major burn injuries are at
risk so should receive routine prophylaxis beginning at
admission.
83

84. • Neutropenia - Transient leukopenia is common,
primarily due to a decreased neutrophil count. Maximal
WBC depression occurs several days after admission
with rebound to normal a few days later. Use of silver
sulfadiazine has been associated with this transient
leukopenia.
• Adrenal Insufficiency - Those with massive burns have
higher cortisol levels but may be resistant to serum
cortisol increases in response to stimulation. Absolute
adrenal insufficiency occurs in up to 36% of patients
with major burns .
84

85. Other Supportive Measures
• Appropriate analgesia:
- Avoid IM injections!!!
- Intravenous:
Ketamine 0.5mg/kg
Morphine 0.2mg/kg every 5 mins
• All patients with burns > 10%
0.5ml Tetanus toxoid.
• Gastric decompression with NGT in all major burns.
• Antibiotic use is controversial.
• Neck, oral & joint splints can prevent deformities.
85

86. Key Points
• Fluid resuscitation must be based on frequent
reassessment. Formulas are only a guide.
• Pulse oximetry readings may be normal in carbon
monoxide toxicity
• Unnecessary intubation is preferable to systemic
hypoxia.
• Early enteral nutrition in major burns may improve
survival by increasing immune status and reducing risk of
infection.
• Antibiotics should be used wisely to limit emergence of
multiresistant organisms: close liaison with a clinical
microbiologist is crucial.
• Failure to respond to treatment should trigger an
escalation in the invasiveness of the monitoring
86

87. Deaths are only part of the problem, for every person
who dies as a result of their burns; many more are left
with lifelong disabilities and disfigurements. For some
this means living with the stigma and rejection that all
too often comes with disability and disfigurement.
[Krug E. A WHO plan for burn prevention and care,
Geneva, Switzerland, 2008]
87

88. Follow-up and Rehabilitation
• Rehabilitation measures should be implemented as soon as
possible.
• Early respiration training deepens inhalation and therefore
prevents pulmonary infections.
• Edema prophylaxis and therapy, scar care, compression
garments and the specific prophylaxis of scarred
contractures in critical locations (throat, face, hands, and
joints) are the fundamental pillars of multimodal
rehabilitation
• After completion of the intensive care period, the patients
are transferred to a follow-up ward where further wound
care, physiotherapy and psychiatric care help to maximize
the patient’s autonomy. . 88

89. • A burn injury is a frightening & potentially life-changing
event for patients and families. Because of this
loss/change in their lives, they can often face many
difficult emotions at varying stages after the injury.
• The impact of the burn can result in permanent
disability and disfigurement. In the long term, many
patients suffer from their changed appearance.
• Burns of the face and hands are felt as especially
disturbing, as they are continuously visible to other
people.
89

90. • Given the nature of burn injury and its treatment there are
many stressors that may trigger psychological problems,
particularly those associated with anxiety and depression
• Over 60% of all severely burned patients develop
psychological problems like PTSD, depression and sleep
disturbances.
• A multidisciplinary team of physiotherapists,
psychologists, nurses, and councillors are vital to aid
rehabilitation and reduce long-term impairment.
90

91. Indian Scenario
• According to WHO, in India, over 10 lakh people are
moderately or severely burnt every year.
• The MOHFW says India records 70 lakh burn injury
cases annually of which 1.4 lakh people die of burn
every year. Around 70% of all burn injuries occur in
most productive age group (15-35 years). Around four
out of five burnt cases are women and children. As
many as 80% of cases admitted are a result of accidents
at home (kitchen-related incidents).
[The Times of India. New Delhi. June 7, 2012]
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92. • Of all burn death cases, 80.8% were females, 82.4%
married ones, 71.9% belonged to the young age group
of 21-40 years and 75.0% came from the rural parts of
the district.
• In all female suicides, burns was the commonest
method adopted by over 60% females. Torture by in-
laws (32.1%) was the commonest reason for committing
suicide by burns in married women.
[Batra AK. Burn mortality: recent trends and sociocultural determinants in rural
India. Burns. 2003 May;29(3):270-5.]
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93. National Programme for Prevention of Burn Injuries
• The high incidence is attributed to illiteracy, poverty and
low level safety consciousness in the population.
• The situation becomes further grim due to the absence
of organized burn care at primary and secondary health
care level.
93

94. • The GOAL of National programme for prevention of
burn injuries (NPPBI) would be to ensure prevention
and capacity building of infrastructure and manpower at
all levels of health care delivery system in order to
reduce incidence, provide timely and adequate
treatment to burn patients to reduce mortality,
complications and provide effective rehabilitation to the
survivors.
94

95. The programme note says…
"Among all traumas, burn cases have highest
duration of hospital bed occupancy. Cost of
hospitalized burn injury case management is
extremely high which may cost enormous financial
burden to the country. The rehabilitation of the
individual may be a challenging and daunting task.“
National programme for prevention of burn injuries
(NPPBI)
95

96. THANK YOU
96