Burns -BLS-MUKESH SUNDARARAJAN

1. BURNS

2. Definition
• Burns are a result of the effects of thermal
injury on the skin and other tissues
• Human skin can tolerate temperatures up to
42-440 C (107-1110 F) but above these, the
higher the temperature the more severe the
tissue destruction
• Below 450 C (1130 F), resulting changes are
reversible but >450 C, protein damage
exceeds the capacity of the cell to repair

3. Classification According to Depth
• First-degree Burns (mild): epidermis
Pain, erythema & slight swelling, no blisters

 Tissue damage usually minimal, no scarring
 Pain resolves in 48-72 hours
• Superficial Second-degree Burns: entire epidermis &
variable dermis
Vesicles and blisters characteristic
Extremely painful due to exposed nerve endings


 Heal in 7-14 days if without infection
• Midlevel to Deep Second-degree Burns:
Few dermal appendages left

 There are some fluid & metabolic effects
• Full-thickness or Third-Degree: entire epidermis and
dermis, no residual epidermis


Painless, extensive fluid & metabolic deficits
Heal only by wound contraction, if small, or if big,
by skin grafting or coverage by a skin flap

4. Burn Photos
Mild Burn
2nd degree Burn 1 hr
2nd degree Burn 1 day
2nd degree Burn 2 days

5. Classification According to Extent
• Mild: 10%
• Moderate:
10-30%
• Severe: > 30%
• Hospitalization
for > 10% of
body surface area
Infant Rule of Nines
(for quick assessment of
total body surface area
affected by burns)
Anatomic
structure
Surface
area
Head 18%
Anterior Torso 18%
Posterior Torso 18%
Each Leg 14%
Each Arm 9%
Perineum 1%

6. Kinds of Burns
• Scald Burn: most frequent in home injuries; hot
water, liquids and foods are most common causes;
above 65o C, cell death
• Flame Burn: due to gasoline, kerosene, liquified
petroleum gas (LPG) or burning houses
• Chemical Burn: common in industries and
laboratories but may also occur at home; acid is
more common than alkali
• Electrical Burn: worse than the other types; with
entrance and exit wounds; may stop the heart and
depress the respiratory center; may cause
thrombosis and cataracts
• Radiation Burn: from X-ray, radioactive radiation
and nuclear bomb explosions

7. Burn Photos
Scald Burns Flame Burns

8. Burn Photos
Chemical (Acid) Burns
Radiation (Flash) Burns

9. Burn Photos
Electrical Burns
Entrance Wounds
Entrance wound of electrical
burns from an overheated tool
Severe swelling
peaks 24-72 hrs after
Electrical Burns
Exit Wounds
Electrical burns mummified
1st 2 fingers later removed

10. Physiological Response
• Typically, biphasic response
• The initial period of hypofunction manifests as: (a)
Hypotension, (b) Low cardiac output, (c) Metabolic acidosis,
(d) Ileus, (e) Hypoventilation, (f) Hyperglycemia, (g) Low
oxygen consumption and (h) Inability to thermoregulate
• This ebb phase occurs usually in the first 24 hours and
responds to fluid resuscitation
• The flow phase, resuscitation, follows and is characterized by
gradual increases in (a) Cardiac output, (b) Heart rate, (c)
Oxygen consumption and (d) Supranormal increases of
temperature
• This hypermetabolic hyperdynamic response peaks in 10-14
days after the injury after which condition slowly recedes to
normal as the burn wounds heal naturally or surgically closed
by applying skin grafting

11. Pathologic Features
• Zone of coagulation (necrosis): Superficial area of
coagulation necrosis and cell death on exposure to
temperatures >450 (primary injury)
• Zone of stasis (vascular thrombosis): Local capillary
circulation is sluggish, depending on the adequacy of the
resuscitation, can either remain viable or proceed to cell
death (secondary injury)
• Zone of hyperemia (increased capillary permeability)

12. Burn Pathophysiology: Edema
• Injured tissue  Increased permeability of entire
vascular tree  loss of water, electrolytes and
proteins from the vascular compartment  severe
hemoconcentration
• Protein leakage  resultant hypoproteinemia,
increased osmotic pressure in the interstitial space
• Decreased cell membrane potential cause inward
shift of Na+ and H2O  cellular swelling
• In the injured skin, effect maximal 30 min after the
burn but capillary integrity not restored until 8-12
hours after, usually resolved by 3-5 days
• In non-injured tissues, only mild and transient
leaks even for burns >40% BSA

13. Burn Pathophysiology: Cardiac
• Cardiac output decreases due to:
1) Decreased preload induced by fluid shifts
2) Increased systemic vascular resistance caused
by both hypovolemia and systemic
catecholamine release
3) A myocardial depressant factor has been
described that impairs cardiac function
• Cardiac output normal within 12-18 hours, with
successful resuscitation
• After 24 hours, it may increase up to 2 ½
times the normal and remain elevated until
several months after the burn is closed

14. Burn Pathophysiology: Blood
• The red-cell mass decreases due to direct losses
• Immediate, 1-2 hours after, and delayed, 2-7 days
postburn, hemolysis occurs due to damaged cells
and increased fragility
• Anemia within 4-7 days is common and expected,
typically, will persist until wound healing occur;
depressed erythropoietin levels documented
• Early mild thrombocytopenia (sequestration)
followed by thrombocytosis (2-4x normal) and
elevated fibrinogen, factor V and factor VIII levels
commonly by end of the 1st week
• A “normal” platelet or fibrinogen level may be an
early sign of disseminated intravascular coagulation
• Persistent thrombocytopenia is associated with poor
prognosis -- suspect sepsis

15. Burn Pathophysiology: Metabolic
• Severe catabolism with breakdown of muscle
protein for gluconeogenesis as acute response
• Prostaglandins and cytokines implicated in
increased core temperature of 1-20 C and in
initiating acceleration of nitrogen catabolism
• Plasma levels of catecholamines, glucagon and
cortisol all increase, maximal in patients with
50-60% TBSAB, while insulin and thyroid hormone
levels decrease
• Hypermetabolic response may approach 200% of
BMR remaining elevated for months after burn
closed
• Early enteral feeding associated with lessening of
the hypermetabolic response

16. Burn Pathophysiology: Renal
• Renal blood flow and GFR decrease soon after
due to hypovolemia, decreased cardiac output,
and elevated systemic vascular  oliguria and
antidiuresis develops during 1st 12-24 hours
• Followed by a usually modest diuresis as the
capillary leaks seal, plasma volume normalizes,
and cardiac output increases after successful
resuscitation and coinciding with onset of the
postburn hypermetabolic state, and
hyperdynamic circulation

17. Burn Pathophysiology: Immunologic
• Mechanical barrier to infection is impaired because
of skin destruction
• Immunoglobulin levels decreased as part of general
leak and leukocyte chemotaxis, phagocytosis, and
cytotoxic activity impaired
• The reticuloendothelial system's depressed
bacterial clearance is due to decreases in opsonic
function
• These changes, together with a non-perfused,
bacterially-colonized eschar overlying a wound full
of proteinaceous fluid, put the patient in a
significant risk for infection

18. First Aid Measures in Burns
 Extinguish flames by rolling in the ground, cover
child with blanket, coat or carpet
 After determining airway is patent, remove



smoldering clothes and constricting accessories
during edema phase in the 1st 24-72 hours after
Brush off remaining chemical if powdered or solid
then wash or irrigate abundantly with water
Cover burn wounds with clean, dry sheet and
apply cold (not iced) wet compresses to small
injuries; significant burns (>15-20% BSA)
decreases body temperature which
contraindicates use of cold compress dressings
If burn caused by hot tar, mineral oil to remove it

19. Outpatient Management
• For 1st and 2nd degree burns less
than 10% BSA
• Blisters should be left intact and
dressed with silver sulfadiazine
cream
• Dressings should be changed daily
washing with lukewarm water to
remove any cream left

21. Recommendations for Hospitalization
1. Total burns >10% BSA or >2% full
thickness, halved for <2 or >40 yr
2. Hands, face, feet or genitalia involved
3. Evidence or suspicion of inhalation injury
4. Associated injuries present
5. Suspicion that burn inflicted
6. Burn is infected
7. Burn circumferential
8. History of prior medical illness
9. Patient is comatose
10.Patient or family unable to cope with
situation

22. Hospital Management
1. General assessment and
cardiopulmonary stabilization
2. Resuscitation
3. Establishment of IV lines and blood
studies
4. Wound care and infection control
5. Pain relief and psychological support
6. Nutritional support
7. Physical Therapy/Occupational
Therapy

23. Airway compromise?
Respiratory distress?
Circulatory compromise?
Intubation, 100% O2
IV access, fluids Multiple trauma?
Yes No
Evaluate & treat
injuries Burns >15% or
complicated burns?
Yes
No
Burn care, tetanus prophylaxis,
analgesia
IV access;
fluid replacement
Circumferential full
thickness burns?
Escharotomy
Yes
Yes
No
No

24. Initial Procedures
• Fluid infusion must be started immediately
• NGT insertion to prevent gastric dilatation,
vomiting and aspiration
• Urinary catheter to measure urine output
• Weight important and has to be taken daily
• Local treatment delayed till respiratory
distress and shock controlled
• Hematocrit and bacterial cultures necessary

25. Fluid Resuscitation
• For most, Parkland formula a suitable starting
guide (4 ml Ringer’s Lactate/kg body weight/%
BSA burned), ½ to be given over 1st 8 hr from
time of onset while remaining over the next 16 hr
• During 2nd 24 hr, ½ of 1st day fluid requirement to
be infused as D5LR
• Oral supplementation may start 48 hr after as
homogenized milk or soy-based products given
by bolus or constant infusion via NGT
• Albumin 5% may be used to maintain serum
albumin levels at 2 g/dl
• Packed RBC recommended if hematocrit falls
below 24% (Hgb <8 g/dl)
• Sodium supplementation may be needed if burns
greater than 20% BSA

26. Inhalation Injury
• Three syndromes:
1. Early CO poisoning, airway obstruction &
pulmonary edema major concerns
2. ARDS usually at 24-48 hrs or much later
3. Pneumonia and pulmonary emboli as late
complications (days to weeks)
• Assessment:
1. Observation (swelling or carbonaceous material
in nasal passages
2. Laboratory determination of
carboxyhemoglobin and ABGs
• Treatment:
1. Maintain patent airway by early ET intubation,
adequate ventilation and oxygenation
2. Aggressive pulmonary toilet and chest
physiotherapy

27. Infection Control
• Tetanus prophylaxis: 250-500 IU TIG or 3000
units equine ATS ANST IM; Toxoid also
• Antibiotic of choice is one that will include
Pseudomonas in its spectrum; most frequent
pathogens in burns are Staphylococcus aureus,
Pseudomonas aeruginosa and the Klebsiella-
Enterobacter species
• Topical therapy:
 0.5% Silver nitrate dressing
 Mafenide acetate or Sulfacetamide acetate
cream
 Silver sulfadiazine cream
 Povidone-iodine ointment
 Gentamicin cream or ointment

28. Pain Relief and Adjustment
• Important to provide adequate
analgesia, anxiolytics and
psychological support to:
a) Reduce early metabolic stress
b) Decrease potential for
posttraumatic stress syndrome
c) Allow future stabilization and
rehabilitation
• Family support patient through
grieving process and help accept
long-term changes in appearance

29. Nutritional Support
• Shriners Burn Institute at Galveston,
Texas Guidelines for Caloric Intake
Infants
1000 kcal/m2 BSA burned +
2100 kcal/m2 total BSA
2-15 years
1300 kcal/m2 BSA burned +
1800 kcal/m2 total BSA
Adolescents
1500 kcal/m2 BSA burned +
1500 kcal/m2 total BSA

30. Complications of Burns
• Burn Shock
• Pulmonary complications due to
inhalation injury
• Acute Renal Failure
• Infections and Sepsis
• Curling’s ulcer in large burns over
30% usually after 9th day
• Extensive and disabling scarring
• Psychological trauma
• Cancer called Marjolin’s ulcer, may
take 21 years to develop

31. THANK YOU