Thermal burns,pathophysiology,changes,management By: Dr.ONKAR S KULKARNI M.CH PLASTIC SURGERY SKIMS, SRINAGAR.

1. THERMAL BURNS
By-Dr.Onkar.S.Kulkarni
Moderator: Dr.Peerzada Umar Farooq Baba
Dept. of Plastic & Reconstructive Surgery
SKIMS, SRINAGAR.

2.  Burn injury is a coagulative necrosis of tissue caused by
thermal energy.

3. • 2/3 male
• 2/3 white
• 2/3 drunk
• 2/3 have flammable liquid
• 2/3 reduction in death due to smoke detectors
• 23 mean age

4. • 66 % of all burns - at home,
• The MCCs are flame and scald burns.
• *Alcohol *
• Scald burns MC in children < 5 years
• Child abuse.
• The survival rate for all burns is 94.6%,
• But for at-risk populations, in communities lacking medical, lega
and public health resources, survival can be nearly impossible.

5. HISTORY
• Paulus Aeginata : herbs with vinegar/ Pigeon’s dung mixed with
• Fabrigus Hildanicus in his book De- Combustionibus first des
classification
• Parre distinguished between 2nd and 3rd degree burn
• Richard Wiseman 1676 : Splintage in burns

6. • Edward Kentish 1796: Pressure dressings to relief pain
• Earle 1799: Means to reduce effect of burn ..Ice usage
• Wallace 1949 open dressing for face
• Lister 1875 boric+ carbolic acid for dressing
• Baxter 1964
• Bradford Cannon : Skin grafting as main treatment line

7. Classification of Burn
• Thermal - Scald
- Flame
- Flash
- Contact
• Cold burn
• Inhalational burn
• Electric - Low tension
- High tension
- Lightning.
• Chemical : alkali and acid
• Radiation
• Frictional

8. Adult skin 1.5 to 2.0 m2
Newborn 0.2 to 0.3 m2
Epidermis plus dermis 1 to 2 mm.

9. Epidermis
- no blood vessels
-Nutrition source :- the underlying dermis.
-waste disposal via diffusion
There are“zones”:
Stratum malpighii (aka. Spindle / nucleated viable cells – basal
- spinous
- granular
Stratum corneum ( non-nucleated non-viable cells – lucidum
corneum

10. Stratum basalis – dividing stem cells & anchoring cells
Stratum spinosum –“prickle layer” ,
adhesions on cell surface looks like
spines (tonofibrils)
Stratum granulosum –contains basophilic granules of
keratohyalin
Stratum lucidum – only in glaborous skin in palms
and soles
Stratum corneum – “horny layer”, layer of keratinized,
non-nucleated cells. desquamating dead
superficial layer

11. The papillary dermis- loose connective tissue
-capillaries, elastic fibers,
-collagen (mainly type III)
The reticular dermis - dense connective tissue larger Vessels,
-elastic fibers,
-collagen fibers arranged in layers
-parallel to the surface (mainly type I)
-dermal cells, nerve endings

12. Effect of burn injury depends upon following variables :
• Type of burn
• Temperature
• Duration of exposure
• Type of Tissue .

13. Evaluation of extent of burn surface:
• Superficial burns are not included in the calculation.
• Only partial or full thickness burns are included.
1. Lund and Browder chart
2. Palm method
3. Rule of 9
4. Berkow’s percentages chart
• Partial-thickness burns - diagonal lines
full-thickness burns - completely filled in.

14. Palm method : Don’t confuse !
Rossiter ND et al study
• The area of the palm alone is
0.5 percent TBSA in males
0.4 percent TBSA in females
• Whereas the area of the palm +palmar surface of the 5 digits
0.8 percent BSA in males
0.7 percent BSA in females
Therefore, if a hand alone is used to assess
the size of a burn, the percent BSA is overestimated.
Rossiter ND et al. How big is a hand? Burns. 1996 May;22(3):230-1.

15. Lund & Browder chart of percentage of burn

16. By Berkow formula for adult :
• Face 7%
• Neck 2%
• Anterior and posterior trunk 13% each
• Each gluteal region 2.5%
• Genitalia 1%
• Upper limb 9.5% each [4+3+2.5]
• Lower limb 20% each [9.5+7+3.5]

17. Depth of burn assessment:
CLINICAL METHOD
• Superficial first degree burn :
• Only epidermis
• Red, extremely painful,
• Heal in 3-5 days
• Eg: Sunburns.

21. Superficial Second Degree :
• Epidermis and Papillary dermis layer
• Typically pink, moist, painful, blisters, blanches.
• Healing time – short , 2 weeks.
• No aesthetic sequellae.
• Can result in alteration of pigmentation.
• Eg: Water scald burns

22. At incidence
2 weeks
Healed but
nonpigmented
3 months normal

23. Deep Second Degree burn :
• Epidermis and dermis.
• Dry, mottled pink or white with variable sensation.
• Blanching of the skin – Negative
• Pinprick pain +ve
• Healing in 2–3 weeks.
• Deep dermis is exposed, a permanent scar will remain.

25. Third degree burns :-
• Involves the subdermal structures.
• Brown-black, leathery, insensate, don’t blanch.
• Lesion has a white color , is hard.
A black eschar after carbonization
• May lead to compromise of vascular supply.
• Watch out for ischemic changes.
• Needs surgical management. Best treated by excision and
grafting

27. Fourth degree burn :
• Involves beyond subcutaneous tissue
• Involves underlying muscles, bone, or organ

29. Other techniques for determination of burn depth :
• Flouroscein dye study
• Ultrasound
• Laser doppler
• MRI
But none of these methods have proven to be more reliable
than the judgement of an Experienced Burn management
Surgeon

30. Multisensor laser Doppler
flowmeter study
Red and Pink areas mark
superficial burn

31. Noncontact scanning technique
Color-coded perfusion map corresponds to varying burn depth.
Accuracy up to 99% PPV 98.4%
The latest, most accurate, most advanced modality of diagnosing burn depth
LASER DOPPLER PERFUSION MONITORING.
Can distinguish between burns that will and that wont heal in 3 weeks.

32. Increases in validity if adjunct tests added
• Sequential scans
• Heat provocation scan
• Digital imaging, High frequency USG 20-200 Hz
• Advantage -
noncontact technique.
No tissue trauma, infection.
painless for patient
• Disadvantage -
optic based
heterogeneity & tissue curvature
topical substances & infection affect depth.

33. THERMOGRAPHY
• Studied by Still-et-al
• Principle: deeper wounds have less temperature than superficial
• Accuracy 90%
• Ideal within 3 days of burn.
• Limitations :
heat loss in sorrounding
accuracy compromised in granulating wounds

34. VITAL DYES
• Injection of flourescent dyes f/b Illumination 360-400 nm UV light
• Nonfluorescent dyes like Evans Blue, Patent Blue V and Bromophenol
blue
• Disadvantage: not accurate
limitation in renal dysfunction
capillary leak initially limits use.

35. INDOCYANINE GREEN VIDEO ANGIOGRAPHY
• IV f/b Still images / Videography
• Correlates dermal vessels status with local perfusion
• Hepatic clearance. Benign course
• Limitation:
Topical ointments, Dressings , blood interferes.
 Haslik-et-al study: Above substances decrease absorption measurements
Overestimate depth of burn
 So remove all topical dressings atleast 10 minutes prior to study

36. BIOPSY
• Microscopic examination of vessels, collagen, viability
• MICROVASCULAR DAMAGE: PARTIAL THICKNESS
• COLLAGEN DENATURATION: FULL THICKNESS
Disadvantage: Sampling error
Structural damage may not correlate with functional loss
Invasive
Multiple biopsies may be required
risk of infection
Subjective interpretation

37. Methods Under research
• Reflection optical multispectral imaging
• Optical coherence tomography
• Polarization sensitive Optical coherence tomography :
Reduction in collagen birefringence
• Fibre optic confocal imaging :
Illumination of tissue with blue light frequency
AUTOFLUOROSCENCE
DIRECTLY PROPORTIONAL TO DEPTH OF BURN

38. Pathophysiology of burn injury:-
• Temp : 40° to 44° C (104° to 111.2° F)
- Enzymes malfunction
- Proteins denature
- Cellular pumps fail.
• > 44° C (111.2° F) the damage occurs faster than the
cell’s repair mechanism can function.

39. Proteins denature, cell necrosis progresses, and proteins
alter and coagulate.
• ZONE OF COAGULATION
• The first of three zones.
• The cell death is complete.
• Area nearest to the heat source.

40.  ZONE OF STASIS
•
• cells are viable
circulation is impaired
ischemia results.
• If untreated thrombosis and vasoconstriction Necrosis.
 ZONE OF HYPEREMIA.
• Minimal cellular injury
• Predominant vasodilation.
• These cells usually recover.

42. Zones of burn injury

44. Physiological response to burn injury
• Direct damage to the vessels.
• Increased capillary permeability to protein.
• Marked increase in interstitial space compliance
Implication : third space loss.

45. Heat alters proteins activates complement
 Histamine release
 Increased vessel permeability
 Thrombosis due to activation of the coagulation
systems
 Release of serotonin (vasoconstriction),
 Bradykinin (increased permeability).

46. Membrane phospholipids are altered or destroyed
Arachidonic acid cascade activation
Leukotrienes- increase in permeability and neutrophil
recruitment
• Thromboxane A2 –vasoconstriction
• Prostacyclin - vasodilator
• Prostaglandins PGD2 and PGE2- vasodilation
PGF2 alpha - vasoconstriction.

47. Thromboxane A2
in the plasma and wounds of burned .
- vasoconstriction and platelet aggregation
- expansion of the zone of stasis.
- mesenteric vasoconstriction
- decreased gut blood flow
-compromised gut mucosal integrity
-decreased gut immune function.

48. • Serotonin
• Edema formation.
• Pulmonary vascular resistance
• Aggravates the vasoconstrictive effects of various
vasoactive amines.
• Serotonin blockade - Improves cardiac index
- Pulmonary artery pressure
- Oxygen consumption

49. Hypermetabolism:
• Burn injury of greater than
 20% TBSA in adults
 40% in infants.
• Increased protein catabolism, increased gluconeogenesis,
and insulin resistance are seen.
• Feedback loops maybe reset hypothalamus is
stimulated Glucagon, cortisol, catecholamines
• Causative factors : ????? Still under research

50.  Factors under study for implication
• Interleukins 1 & 6
• Platelet-activating factor
• Tumor necrosis factor
• Endotoxin
• Nitric oxide
• Neutrophil adherence complexes
• Reactive oxygen species
• Coagulation as well as complement cascades

51. • Phases of Hypermetabolism
• The first phase occurs within the first 48 hours of injury
and has classically been called the ebb phase.
• Decreases in cardiac output
• Oxygen consumption reduced
• Metabolic rate reduced
• Impaired glucose tolerance
• Hyperglycemic state

52. • Metabolic variables gradually increase within the first 5 days
after injury to a plateau phase
This is k/a the flow phase
• hyperdynamic circulation
• the hypermetabolic state.
• Insulin release increases
• Persisted for up to 3 years after the initial burn injury.

53. PARAMETER LEVEL IN EARLY PHASE LATE LEVEL
CYTOKINE Immediately rise normal in 1 month
Acute phase proteins Rises after 5-7 days
IGF, IGFBP-3 Drop immediately 10 fold Decreased till 6 months
Osteocalcin,
Parathyroid
Drop immediately 10 fold Decreased till 6 months
Sex hormones immediate peak drop around 3 weeks
GH Drop around 3 weeks

54. The resting metabolic rate
140% At admission
130% Once the wounds are fully healed
120% 6 months
110% 12 months after burn injury.

56. • Protein degradation up to nearly 1 year after severe burn injury
• Daily nitrogen loss of 20 to 25 g/m2 of
burned skin.
• Lethal cachexia in less than 1 month.

57. • GLUCOSE AND INSULIN
• increase after burn injury
• Postreceptor insulin resistance
• Glucose delivery to peripheral tissues 3 times
•
• Glucose oxidation restricted.
• Glycolytic-gluconeogenetic cycling 250%
• Insulin resistance - first week after burn injury
and persists - after discharge up to 3 years.

58. LOSS OF LEAN BODY MASS RESULT
10% immune dysfunction.
20% decreased wound healing.
30% increased risk for pneumonia
and pressure sores.
40% risk of death.

59. CARDIOVASULAR CHANGES
• plasma volume peripheral vascular resistance
• Cardiac output REDUCES initially because
- blood volume
- blood viscosity
- cardiac contractility.
• Ventricular dysfunction- Circulating Myocardial Depressant Factor
present in lymphatic fluid
• 3 to 4 days after the burn injury, cardiac output is more than
1.5 times

60. Effects on the Renal System
-Oliguria
-Acute tubular necrosis and pre-renal failure
Patients in whom renal failure develops in the postburn period,
• 88% mortality rate for severely burned adults
• 56% mortality rate for severely burned children

61. HEMATOLOGICAL CHANGES
• Coagulopathy due to depletion of coagulating factors
• Thrombocytopenia
• Breakdown of the blood-brain barrier brain lipids
Are exposed to the plasma activates the coagulation cascade
• Platelet <50000 is common. No treatment needed
• Severely burned - risk for thrombotic and embolic events
• Likely related to immobilization.
• Erythropoeisis suppressed, Fragile RBC, decreased t1/2.

62. Effects on the gastrointestinal system
• Mucosal atrophy,
• Increased intestinal permeability.
• Atrophy of the small bowel mucosa occurs within 12 hours of injury
• Reduced uptake of glucose and amino acids
• Decreased absorption of fatty acids,
• Reduction in brush border lipase activity.
peak in the first several hours after burn injury and
Return to normal at 48 to 72 hours.

63. • Vesiculation of microvilli
• Disruption of the terminal web actin filaments.
These findings were most pronounced 18 hours after injury,

64. • Intestinal permeability to macromolecules, which are normally
repelled by an intact mucosal barrier, increases.
• Gut permeability increases even further when burn wounds
become infected.
• Transmigration of gut flora.

65. A study using fluorescent dextran showed that
• Larger molecules appeared to cross the mucosa between the
cells,
• The smaller molecules traversed the mucosa through the
epithelial cells, by pinocytosis and vesiculation.
• Mucosal permeability also paralleled increases in gut
epithelial apoptosis.

66. HEPATOBILIARY CHANGES
• Liver size by 2.5 times by 2 weeks after burn injury and
At discharge by 2 times of normal.
• by 4.5 times in triglyceride–fatty acid cycling.
• HEPATIC DYSFUNCTION
• Acalculous cholecystitis,

67. Immunity changes
• Macrophage production
• Reasons:
- Elaboration of negative regulators of myeloid growth.
- Presence of endotoxin
• G-CSF levels after severe burn.
• However, bone marrow G-CSF receptor expression is
• Neutrophil count
• Neutrophils that are present are dysfunctional in terms of diapedesis,
chemotaxis, and Phagocytosis.

68. Reasons :-
- CD11b/CD18 expression after inflammatory stimuli
- respiratory burst activity
- p47phox activity
-impaired actin mechanics related to neutrophil motile responses.
After 48 to 72 hours, neutrophil counts

69. • T-helper cell function is depressed
• Polarization from the interleukin-2 and interferon-γ
cytokine-based T-helper 1 (Th1) response toward the Th2 response.
• Th2 response Interleukin-4 , Interleukin-10.
• Increase in the risk of infection, particularly from fungi and
viruses.
• Early burn wound excision improves cytotoxic T-cell activity.
I

70. Management:
• View the patient as any trauma patient.
• The associated trauma
• History-Taking
• Mechanism of injury
• The method of escape from the fire

71.  PROPER LEGAL FORMALITIES.
Source removal & Universal precautions
PRIMARY SURVEY- ABCDE
• Airway
Endotracheal intubation is the most definitive way to
secure the airway.
C-spine precautions are essential.
• Breathing
• Circulation
• Disability
• Exposure

72. • Remove Burning clothing
• Rings, watches, jewellery, and belts
retain heat and tourniquet-like effect.
• Room temperature water can be poured
• Dry sheets for dressing and no damp dressings
• Intramuscular or subcutaneous narcotic injections for pain should
never be used

73. • A study in New Zealand showed that initial burn first aid treatment was
inadequate in 60% of patients interviewed.
• After proper initial care, Transport of patient to tertiary care is important
• Helicopter transport when the distance between the accident and the
Hospital is 30 to 150 miles.
• For distances of more than 150 miles, transport by fixed-wing aircraft is
most appropriate.

74. ABA REFERRAL CRITERIA

75. • Partial thickness burn >10%
• Burn involving face, hand, feet,genitalia, major joints
• 3rd degree burn any age
• Electric, chemical burn or inhalational injury
• Burn with concomitant life threatening trauma
• Burnt child without caretaker
• If requires social, emotional or rehabilitative intervention

76. Secondary Survey
Airway:-
• Is the face involved?
• Are blackened or charred areas present?
• Is carbonaceous sputum noted?
• Is soot present in the oropharynx?
• Is the patient able to clear his or her secretions?

77. Breathing :
• Is the patient moving a sufficient amount of
air?
•
• Is the patient voice hoarse?
• Is stridor present?
• Bronchoscopy to document airway damage
and swelling secondary to heat or toxins

78. • Edema at the oropharynx, causes upper airway obstruction
• Intubation will protect the airway against delayed
compromise
• An escharotomy should be considered if the burns on the
chest are full thickness
• If the wounds are partial-thickness burns, a chemical
escharotomy with a proteolytic agent, such as Santyl, may
be needed.

79. Circulation :
• Pressure and signs of perfusion are monitored
(warm knee caps, warm toes, and adequate urine output).
Diuretic or mobilization phase
• Usually occurs on the 4th to 6th day, but may extend
for longer periods.
• The microvascular system and the cell membranes recover
from the thermal insult and resorption of the fluid from the
extravascular space begins.
• Search for areas of hemorrhage and penetrating injuries

80. Disability
• Palpation includes areas over bones
• Complete head to toe examination for other injuries .
Exposure :
• Evaluate the patient and estimate the body surface area
involved.
• Evaluate for any decompressive procedure if to be done.

81. Rescucitation
Superficial veins = thrombosed in full-thickness injuries
and therefore are not suitable for cannulation.
• The initial 24-hour fluid replacement with lactated
Ringer’s solution
• Parkland formula
• Use urine output as an indicator of the adequacy of fluid
resuscitation.
• Acceptable urine output is usually 0.5 to 1ml/kg/hr.

82. • If the urine output is below this, the infusion rate should
be increased by 50%.
• If the urine output is inadequate + signs of hypoperfusion
a bolus of 10 mL/kg body weight should be given.
• During first 24-48 hrs ,if urine output is less +other para-
meters are normal –
-Raised ADH and Aldosterone
-Reduced renal blood flow.
• Output in excess of 2 mL/kg body weight per hour
should signal a decrease in the rate of infusion.

83. • After the first 24 hours, the maintenance fluid
• The rate is calculated for 24 hours as
• First 10 kg 100 ml/kg
• Second 10 kg 50 ml/kg
• Every kilogram
above 20 kg 20 ml/kg

84. For example, the rate for a 70 kg patient is calculated as
follows:
[100 * 10 (for the first 10 kg)] +
[50 * 10 (for the second 10 kg)] +
[20 * 50 (for the 50 kilograms not yet covered)]:
i.e 1000 ml + 500 ml + 1000 ml = 2500 ml/24 hr.

85. Adjuvant administration of high-dose ascorbic acid
(66 mg/kg/hr) during the first 24 hours after thermal injury
significantly reduces
• resuscitation fluid volume requirements by 30%
• wound edema
• severity of respiratory dysfunction
Reduction of Resuscitation Fluid Volumes in Severely Burned Patients Using Ascorbic
Acid Administration Arch Surg. 2000;135:326-331.

86. • During the fourth 8-hour period after a burn, salt-poor
albumin (SPA) is infused using the formula
0.1 * kilograms * %TBSA.
• The SPA is infused over 4 to 6 hours. This is given to
increase oncotic pressure.
• Add free water if the patient becomes hypernatremic.

87. The calculation for water evaporation is:
%TBSA + [25 * BSA in m2] = milliliters/hr
of evaporative water loss
• BSA is calculated as
[87 (Height in cm + Weight in kg) – 2600] / 10,000
= Surface in m2
• Evaluation of serum Na will give an indication
of adequate replacement.
• The optimal level of Na to be maintained is 135 to 137
mg/dl

89. • Hyponatraemia and water intoxication can be fatal.
• Give ORS
• Proteins should be given after the first 12 hours of burn.
The most common colloid-based formula is the Muir and
Barclay formula:
● 0.5 × percentage body surface area burnt × weight = one
portion;
● Periods of 4/4/4, 6/6 and 12 hours, respectively;
● One portion to be given in each period.

90. COLLOIDS
Dextran :
• Low molecular weight 4000
• British Dextran 150000
• Swedish Dextran 70000 or Dextran 70
Dextran 70 : allergic risk and interferes with blood typing.
Dextran 40 improves micro circulating flow by decreasing RBC
aggregation.

91. • It was concluded that
• colloid solutions should not be used in the first 24 hours until
capillary permeability returned closer to normal
• Parkland formula often underestimates the volume of
crystalloid received in the first 24 hours
• This phenomenon has been termed Fluid Creep.
• Causes: ????? under research
- More liberal use of opioid analgesia
-Positive pressure ventilation

92. New data suggestion about Parkland formula as
5.5-6.0 ml/kg per TBSA%
Cartotto RC et. al. How well does the Parkland formula estimate actual fluid
resuscitation volumes? Burn Care Rehabil. 2002 JulAug;23(4):258-65.
Mitra B et.al. Fluid resuscitation in major burns J Surg. 2006 Jan-Feb;76(1-2):35-8.

93. Patients with flame burns and inhalation injury have a mean fluid
requirement of
2 ml/kg/% burn above patients with flame burns without
inhalation injury for adequate resuscitation.
Dai NT et al. The comparison of early fluid therapy in extensive flame burns between inhalation and
noninhalation injuries. Burns 1998 Nov;24(7):671-5.

94. EARLY FLUID RESUSCITATION IMPROVES
OUTCOMES IN THE PEDIATRIC PATIENT
 Barrow-et-al study
• The incidence of sepsis, renal failure, death due to cardiac arrest, and
overall mortality is significantly higher in burned children receiving
fluid resuscitation that was delayed >2 hr.
• Fluid resuscitation, given within 2 hr of a thermal injury, may be
one of the most important steps in the prevention of multi-organ
failure and mortality.
Barrow RE et al. Early fluid resuscitation improves outcomes in
severely burned children. Resuscitation. 2000 Jul;45(2):91-6.

95.  In a study , Hagstrom M et al found that 47% were
under-resuscitated in emergency dept. before transferring to
Burn centre.
Hagstrom M et al. A review of emergency department fluid resuscitation of burn
patients transferred to a regional, verified burn center. Ann Plast Surg. 2003;51:173-6.

96. PAIN MANAGEMENT
• PCM
• Morphine 0.04mg/kg 4hrly
• Sedation
• Anxiolytics
• Pentazocine
• Tramadol

97. OTHER MEDICATIONS
• PPI
• Antibiotics for infected burns

98. Measures of tissue perfusion:-
• Urine output and vitals
• Hematocrit
• ABG
• Filling pressure by transoesophageal ultrasound
• Central line invasive monitoring
• JVP

99. Normal Output Volume (mL) in 70 kg man;
Urine 1500 ml
Insensible Losses 900 ml
Faeces 100 ml
Water from Oxidation 300 ml

100. Role of hypertonic saline in burns :
• Young patients with more than 50% burns with inhalational
injury to avoid massive oedema.
• Elderly with limited cardiac reserve.
• High risk of pulmonary oedema.
• Monitor urine output as output will be higher due to
natriuresis.
• Serum Na should be monitored regularly

101. Unresponsiveness to resuscitation:
• Underestimation of severity of injury
• Cardiac depression
• Vasoconstriction
• Other causes like sepsis.

102. Blood transfusion and burns:
• Administration of blood in first 24 hrs leads to decreased
peripheral perfusion.
• Whole blood is avoided to prevent sequestration of albumin
and plasma proteins in extravascular space.
• In a patient with hematocrit less than 40 transfusion should
begin after 3 days .
• Fresh frozen plasma and packed cell volume have great role
in burns.

103. • All patients with burns should receive 0.5 mL of
tetanus toxoid.

104. • Baseline investigations
• The patient is wrapped with warm blankets to prevent
hypothermia.
• Dressings : minimize heat and water losses and barrier
function
• Debridement in the burn center should take place in a room
with warm ambient temperature (at least 28° C [82° F]).

105. Energy balance and nutrition
1] Curreri formula
Age 16–59 years: (25)W + (40)TBSA
Age 60+ years: (20)W + (65)TBSA
2] Sutherland formula
Children: 60 kcal/kg + 35 kcal/ % TBSA
Adults: 20 kcal/kg + 70 kcal/% TBSA
3] Protein needs :Greatest nitrogen losses between days 5 & 10
20% of kilocalories should be provided by proteins.
4] Davies formula
Children: 3 g/kg + 1 g%TBSA
Adults: 1 g/kg + 3 g%TBSA

106. Monitoring feeding regimes.
Daily
• Body weight
• Fluid balance
• Full blood count, urea and electrolytes
• Blood glucose
• Electrolyte content and volume of urine
• Urine and intestinal losses
• Temperature

107. Weekly (or more frequently if clinically indicated)
• Urine and plasma osmolality
• Calcium, magnesium, zinc and phosphate
• Plasma proteins including albumin
• Liver function tests including clotting factors
• Thiamine
• Acid–base status
• Triglycerides

108. Fortnightly
• Serum vitamin B12
• Folate
• Iron
• Lactate
• Trace elements (zinc, copper, manganese)

109. • The caloric requirement can be estimated as 40 to 50 kcal/kg
for severe stress.
• The basal energy expenditure is estimated to be 25 kcal/kg.
This is multiplied by the stress factor used [2.0 for high stress]
• Patients with severe stress, such as a burn injury,
require 2.2 to 3.2 g of protein/kg/day.

110. Concept of Positive nitrogen balance
• Target of positive balance : 2 to 4 g of nitrogen
(15 to 30 g of protein) per day.
• 1 gm of Biologically active nitrogen is obtained from
6.25 gm protein
• Grams of protein given/6.25 = Grams of nitrogen given
• Grams of nitrogen given – TNL =Nitrogen balance
• TNL = TOTAL NITROGEN LOSS
In Burns TNL is 2 + 24-hr UUN + Wound nitrogen loss

111. TBSA (%) Nitrogen/kg/day Wound Loss
<10 0.02 g nitrogen/kg/day wound loss
10-30 0.05 g nitrogen/kg/day wound loss
>30 0.12 g nitrogen/kg/day wound loss

112. • Daily weight measurement
• Bed in 20-degree semi-Fowler position
• Elevate extremities
• Foot cradle, splints
• Abduct shoulders
• Pressure sore precautions
• No pillow for a head/neck burn

113. Tests and monitoring
• Baseline investigations
• Tripple serology
• UPT [record with timing and test to be attatched along with]

114. expensiveMore effective
staphylococcal coverage;
Mupirocin (Bactroban)
Often combined with
mycostatin into Polymyco
Petroleum-based keeps
grafts moist
Polymyxin B
Gram-positive coverageBacitracin
Impairs wound healing in
high doses
Broad spectrumSodium hypochlorite
Limited penetrationBroad spectrumSilver nitrate [ACTICOAT]
Painful, carbonic anhydrase
inhibitor
PenetratesMafenide acetate
Lack of penetrationPainlessSilver sulfadiazine
DisadvantagesAdvantagesTopical agents

115. Dressings
• Open
• Emollient type
• Wet to dry type
• Chemical agents like eusol betadine
• Turmeric, banana leaves,honey
• Synthetic dressings
• Biological dressings
• CEA

116. • Available topical antibiotics can be divided into two classes:
SALVES AND SOAKS.
• Salves are generally applied directly to the wound
with cotton dressings placed over them,
• Soaks are generally poured into cotton dressings on the
wound.
There can be Synthetic coverings like Opsite, Integra, Transcyte
which provide barriers decreasing pain.
Integra has antimicrobial activity

117. INHALATIONAL INJURIES
• Approximately 80% of fire-related deaths result not from burns but
from inhalation of the toxic products of combustion.
• Inhalation injury has remained associated with an overall mortality rate
of 25% to 50% when patients require ventilator support for more than
1 week after injury
• Gamelli and co found grading system of inhalation injury (0 to 4)
derived from findings at initial bronchoscopy and based on
Abbreviated Injury Score criteria

118. If the patient has a pulmonary injury:
• Aminophyline (6.0 mg/kg IV load, then 0.5 mg/kg/hr IV)
• Ventolin (0.5 mg in 2 ml NS via nebulizer q4h )
• Heparin 4000 U (mix with Ventolin nebulizer in the 2 ml
NS)
will help to decrease pulmonary casts.
Consider bronchoscopic evaluation.
• Pain management
• Role of corticosteroids in facial burns.

119. • Smoke inhalation in combination with cutaneous
burns is fatal in 30% to 90% of patients
• >30% level of carbon monoxide - disorientation
>60% level, the mortality rises to more than 50%.
• Treatment with 100% oxygen for 40 minutes will decrease
a patient’s carbon monoxide level by half.
• Umbilical tape should be used and tied to the endotracheal
tube and around the back of the head.

120. • Decrease in inspiratory pressures with oscillatory breath
decreased barotrauma with sufficient oxygenation.
• The oscillatory breaths also provide internal chest physical
therapy.
• A circumferential chest burn can cause respiratory
embarrassment by restricting chest movement
• In contrast to the upper airway, the lower airways sustain
less injury from dry heat.
• The vocal cords close at 150° C (302° F) and tend to
serve as a protective measure.

121. Respiratory Quotient
Carbohydrates 1.0
Protein 0.8
Lipids 0.7
• In suspected inhalational injuries, increase of fats to 60%
of the daily requirement to lower the respiratory quotient
(CO2/O2) and decrease CO2 production is advisable.
• The patient may wean more easily from the ventilator.
• The patient should receive at least 1000 kcal/wk as fat to
prevent essential fatty acid deficiency

122. VENTILATOR SETTINGS AND PEEP
Preferred ventilator: VDR4 [Volumetric diffusive ventilator]
Initial settings
Oscillatory rate 600 breaths/min
PIP 30-35 cm H2O
2-sec inspiration
2-sec expiration
• Burn patients require increased respiratory rate and
decreased tidal volume, because contraction from the burn
limits chest expansion.
• ABG monitoring is essential in ventilated patients.

123. High-frequency ventilation decreased mortality to 29% from 41%
Clinical diagnosis of pneumonia includes two of the following:
• Chest radiograph revealing a new and persistent infiltrate,
• Consolidation or cavitation;
• Sepsis,
• A recent change in sputum
• Purulence in the sputum as well as quantitative culture
Clinical indications for Intubation
Criteria Value
• Pao2 <60 mm hg
• Paco2 >50 mm hg (acutely)
• Pao2/FIO2 ratio <200
• Respiratory or ventilatory failure impending
• Upper airway edema severe

124. • Plastics, which on burning can produce cyanide.
• Cyanide interferes with oxidative phosphorylation at the
cellular level and causes metabolic acidosis.
• Cyanide toxicity due to plastic burning if suspected doesn’t
need treatment in burn cases unless the pH<7.