2. OVERVIEW
Part I
Historical perspective
Statistics
Classification of Burns
Pathophysiology
Evaluation
Part II
Management
Pre-hospital Care
Resuscitation & Nutritional support
Burn wound care
Complications
Rehabilitation
2
3. Definition
Injuries that result from direct contact or exposure to any physical, thermal,
chemical, electrical, or radiation source are termed as Burns.
3
5. Historical Perspective
First direct evidence of treatment for burns
- Cave paintings of Neanderthal man
1500 BC : Egyptian Smith Papyrus – Resin
& Honey
Ambroise Pare ( AD 1510 – 1590) :
Technique of early excision of burn wounds
5
7. Historical Perspective
19th century : Dupuytren’s
classification based on depth
1842 : Curling : Gastric &
Duodenal Ulceration
Thomas Blizard CurlingBaron Guillaume Dupuytren
7
8. Historical Perspective
1947 : Texas city disaster
Truman G. Blocker Jr:
Multidisciplinary team
approach of Burns.
First Burn Institute for
children in Galveston
8
11. Problem Statement : Global
An estimated 265000 deaths every year are caused by burns.
One of leading causes of disability-adjusted life-years (DALYs) lost in low- and
middle-income countries.
In 2004, nearly 11 million people worldwide were burned severely enough to
require medical attention.
WHO Apr 14
11
12. Problem Statement: US
Burn Injuries Receiving Medical Treatment : 486,000
Fire/Smoke Inhalation Deaths : 3,275
Hospitalizations Related to Burn Injury : 40,000
Survival Rate : 96.8%
American Burn Association, 2016
12
13. Problem Statement : India
70 lakh burn injury cases annually
Over 10,00,000 people are moderately or severely burnt every year
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 4/5 are women & children.
As many as 80% of cases admitted are a result of accidents at home (kitchen-
related incidents)
13
16. Thermal Injuries
Most common
Types : Dry & wet
Contact
Direct contact with hot object (i.e. pan or iron)
Anything that sticks to skin (i.e. tar, grease or
foods)
16
17. Thermal Injuries
Flame
Direct contact with flame (dry heat)
structural fires / clothing catching on fire
Scalding
Direct contact with hot liquid / vapours (moist
heat)
Cooking, bathing or car radiator overheating
Single most common injury in the paediatric pt
17
18. Electrical Burns
Usually follows accidental contact with exposed object conducting electricity
Electrically powered devices
Electrical wiring
Power transmission lines
Can also result from Lightning
Damage depends on intensity of current
18
19. Electrical Burns
Severity depends upon:
what tissue current passes through (Low voltage/ High voltage)
width or extent of the current pathway
AC or DC
duration of current contact
Tissues with the lowest resistance eg. nerves, blood vessels & muscles
Heat generation during passage of the current injures the tissues
Skin has a relatively high resistance, hence is mostly spared
19
20. Electrical Burns
Low-tension injuries(<1000 V)
Low energy burns Minimal damage to subcutaneous tissue
Entry & Exit points – fingers small deep burns
AC Tetany within muscles, cardiac arrest due to interference with
normal cardiac pacing
20
21. Electrical Burns
High-tension injuries(>1000V)
Flash/ Flame / Current
Earthed high tension lines Arc
over the patient Flash burn
Heating of the surrounding air
Explosion Flame burn
Direct contact patient acts as
conduction rod huge subcutaneous
damage
21
22. Electrical Burns
Lightning
HIGH VOLTAGE!!!
Injury may result from
Direct Strike
Side Flash
Severe injuries often result
22
26. Chemical Burns
Usually associated with industrial exposure
Accidental mishandling of household cleaners
Degree of tissue damage determined by
- Chemical nature of the agent
- Concentration of the agent
- Duration of skin contact
26
27. Chemical Burns
Acids
Immediate coagulation necrosis creating an eschar; self-limiting
Bases (Alkali)
Liquefactive necrosis with continued penetration into deeper tissue resulting
in extensive injury
Eg. Lime, potassium hydroxide, cement
27
29. Radiation Exposure
Waves or particles of energy that are emitted from radioactive sources
Alpha radiation
Large, travel a short distance, minimal penetrating ability
Can harm internal organs if inhaled, ingested or absorbed
Beta radiation
Small, more energy, more penetrating ability
Usually enter through damaged skin, ingestion or inhalation
29
30. Radiation Exposure
Gamma radiation & X-rays
Most dangerous penetrating radiation
May produce localized skin burns & extensive internal damage
30
31. Classification
Based on Depth
I Degree - Epidermis
II Degree - Epidermis+ Dermis
III Degree - Epidermis+ Dermis +
Subcutaneous tissue
IV Degree - Above + Muscles/bone
31
32. Classification
Degree
of Burn
1st Degree 2nd Degree
Partial Thickness
2nd Degree
Deep Burns
3rd Degree 4th Degree
Involvement Epidermis Epidermis + Dermis E+ D E+D+Subcut tissue E+D+S+muscles,
tendons & bone
Appearance
Symptoms &
Signs
Pain ++ Pain ++++ Painful -less severe Painless,insensitive,
Severe Edema
No Edema
Healing 3-5 days ,
spontaneous
No Scarring
2 weeks, min
scarring, minimal
discolouration
2-6 weeks
Hypertrophic
scarring / formation
of contractures
No spontaneous
healing
No spontaneous
healing
32
35. Pathophysiology : Local Effects
Zone of coagulation
Necrotic area with cellular disruption
Irreversible tissue damage
Zone of stasis
Moderate insult with decreased tissue
perfusion
Can survive or go on to coagulative
necrosis depending on wound
environment
36
JACKSON’s burn zones
36. Pathophysiology : Local Effects
Zone of hyperemia
Viable tissue, not at risk for
further necrosis
37
38. Pathophysiology : Local Effects
Edema in non-burned tissue
Loss of capillary endothelial integrity
Reduced transmembrane potentials of skeletal muscle at the site of
injury as well as away from the site of damage [-90mv -70 to -80mv]
Increase in intracellular Na & water leading to edema
39
50. Pathophysiology : Systemic Effects
Immune system
Global depression in immune function
Diminished production of macrophages
Increased neutrophil count (dysfunctional) followed by decrease after 48-
72 hrs
Impaired cytotoxic T cell activity
Increase risk of infections
Depressed Th function
51
51. Pathophysiology : Systemic Effects
Hypermetabolic response
Phase I [ebb]
First 48 hrs
Decrease in
cardiac output
urine output
O2 consumption
BMR
Impaired glucose tolerance with hyperglycemia
52
52. Pathophysiology : Systemic Effects
Hypermetabolic response
Metabolic variables gradually increase within first five days post injury to reach a plateau
Phase II [flow]
Increase in metabolic rate
Urine cortisol
Serum catecholamines
Basal energy expenditure
Serum cytokines
Hyperdynamic state – increase in cardiac output
Insulin resistance
Persists for upto 3 years
53
55. Pathophysiology : Systemic Effects
Carbon Monoxide
Most frequent cause of death in smoke induced inhalational injury
Pathology : 0.1% of CO 50% Carboxy Hb
Hb affinity of CO 200-250 times that of O2
Mechanism: Competitive inhibition of Cyt P450
Free radical formation
(Xanthine dehydrogenase Xanthine Oxidase)
56
57. Pathophysiology
Hydrogen cyanide
Fires involving N2 containing
compounds
Mechanism :
Inhibition of cellular oxygenation
with resultant tissue anoxia
Reversible inhibition of Cyt oxidase
(Fe 3+) by CN
58
58. Pathophysiology : Oropharynx
Heat
Denaturation of proteins
Complement Activation
Histamine release
Formation of Xanthine Oxidase
Converts Uric acid to urea
Release of O2 free radicals
Edema formation
Release of Eicosanoids
Attract PMNs to the site
(Amplify effects)
Massive Edema
59
59. Pathophysiology : Tracheo-bronchial areas
Chemical Injury to airway
Seperation of ciliated epi-cells from
BM
Increased Circulation to lung &
bronchial circulation
Edema formation
Diffuse transudate in early changes
Bronchoconstriction Fibrin casts
Obstruction of smaller airways
Culture media for infections
Pneumonia , Sepsis & Death
60
66. Palm Method
Size of Patient’s palm 1% of TBSA
Irregular wounds with scattered distribution.
67
67. OVERVIEW
Part I
Historical perspective
Statistics
Classification of Burns
Pathophysiology
Evaluation
Part II
Pre-hospital Care
Resuscitation & Nutritional support
Burn wound care
Complications
Rehabilitation
68
69. PHASES OF TPT
Phase 1: Treatment at the scene and tpt to initial care facility
Phase 2: Assessment and stabilization at initial care facility and tpt to
burn ICU.
70. PRE HOSPITAL MANAGEMENT
Rescuer to avoid injuring himself
Remove patient from source of injury
Stop burn process
Burning clothing; jewelry, watches, belts to be removed
Pour ample water on burnt area (not ice/ ice packs – skin injury &
hypothermia)
71. PRE HOSPITAL MANAGEMENT
Chemical burns:
Remove saturated clothing
Brush skin if agent is powder
Irrigation with copious amount water to be started and continued in
hospital
Electrical burns:
Turn off the current
Use non-conductor item to separate from source
72. PRE HOSPITAL MANAGEMENT
PRIMARY ASSESSMENT
A – B – C – Cervical spine immobilization
Respiratory tract:
Edema of upper airway sets in very fast
Upper airway obstruction
100% humidified O2 if no obvious resp distress
73. PRE HOSPITAL MANAGEMENT
PRIMARY ASSESSMENT
ET intubation + assisted ventilation with 100% O2 if:
Overt signs and symptoms of airway obstruction (Progressive hoarseness)
Suspected inhalational injury (smoke/ carbon monoxide intoxication)
Unconscious patient/ rapidly deteriorating patient
Acute respiratory distress
Burns of face & neck
Extensive Burns (> 40% TBSA)
74. PRE HOSPITAL MANAGEMENT
PRIMARY ASSESSMENT
Pulse rate better monitor than BP
Spinal immobilization:
Explosion/ deceleration injury
Cervical collar (Philadelphia collar)
75. PRE HOSPITAL MANAGEMENT
Ice/ice cold water causes numbness, intense vasoconstriction, hypothermia
causing further damage.
Do not break blisters.
Do not apply lotions, powders, grease, ghee, gentian violet, calamine lotion,
toothpastes, butter and other sticky agents over the burn wound.
Prevent contamination: Wrap burn part in clean dry sheet /cloth.
Assess for life threatening injuries.
76. PRE HOSPITAL MANAGEMENT
NO I/M or S/C inj (Capillary leakage results in unpredictable absorption)
I/V morphine to allay anxiety
Pain relief and reassurance
Withhold oral intake
77. PRE HOSPITAL MANAGEMENT
Co-morbid conditions/ pre-existing illness
Initiate rapid transfer to hospital
Secure and protect the airway
Cervical spine immobilization; if necessary
78. PRE HOSPITAL MANAGEMENT
SECONDARY ASSESSMENT
Performed only if no immediate life threatening injury/ hazard present
Thorough head to toe evaluation
Medical history, medication, allergies, mechanism of injury
Start IV line (not reqd in hospital <60 min away)
79. PRE HOSPITAL MANAGEMENT
SECONDARY ASSESSMENT
RL infusion:
≥ 14 yrs – 500mL/hr
6-14 yrs – 250mL/hr
≤ 5yrs – 125mL/hr
Apply clean dressing/ sheet to protect area and minimize heat loss
IV Tramadol to relieve pain
No topical antimicrobial
80. HOSPITAL MANAGEMENT
INITIAL CARE FACILITY
C – A – B
Establish adequate airway
ET intubation – impending airway edema (post initiation of IV therapy)
Maintain cervical spine immobilization
81. INITIAL CARE FACILITY
History
Mechanism of injury
Time of injury
Surroundings (closed space/ chemicals)
Physical examination
Head to toe assessment
Careful neurological examination (cerebral anoxia)
Corneal fluorescent examination in facial burns
Labs: CBC, electrolytes, BUN
Pulmonary assessment: ABG, CXR, carboxyhemoglobin
82. INITIAL CARE FACILITY
Pulse in extremities: manual/ doppler
Loss of distal circulation
Pallor/coolness/absent pulse/loss capillary refill/decreased oxygen
saturation
Pain on passive extension
Deep pain at rest
Absent pulse: emergency escharotomy to release constrictive, unyielding
eschar
83. ESCHAROTOMY
Deep 2nd & 3rd degree circumferential burns
Chest: To allow respiratory movement
Limb: To restore circulation in limb with excess swelling under rigid eschar
Bedside, IV sedation, cautery
Midaxial incision into eschar, Across joints
Caution at elbow, wrist, fibular head, medial ankle, neck
Not in SC tissue Exposes SC fat
84.
85. ESCHAROTOMY
Elevate limbs above level of heart
Monitor pulses for 48 hrs
Chemical escharotomy if pulses +nt but feeble.
Useful in hand burns.
Enzyme – collagenase
Complications : bleeding, infection
Antimicrobial prophylaxis must to prevent sepsis
86. INDICATIONS FOR ADMISSION
>15% burns in adults
10% burns in children
Airway and inhalation injury.
Significant burn involving face, hands, feet and perineum.
Extremes of age.
Suspected non-accidental burns.
Burns that require early surgery (deep partial thickness / full thickness)
Patients deficient of nursing care by attendants at home
Severe electric and acid burns that is likely to have serious sequelae
87. RECEPTION
• Resuscitation –ensure ABC
• Large gauge I.V catheter
• Central line Insertion
• Venesection
• Foleys catheter and NG tube placement
• Quick assessment of extent
• Tetanus prophylaxis (the only IM administered inj)
• Weigh the patient
88. Respiratory Care
Assess airway, respiration & breath sounds
Removal of pulmonary secretions
O2 Humidification
Chest physiotherapy, deep breathing & coughing
Frequent position changes and suction
Pharmacologic Considerations:
Bronchodilators and mucolytics
Circumferential chest burns can impair ventilation
Escharotomy may be required
89. Cardiovascular Care
Increase capillary permeability
“Capillary Leakage Syndrome”
Fluid shift intravascular to interstitial space blistering and massive
edema
Excessive insensible loss via burn wound 3-5 lit/d !!
Finally hypovolemia untreated BURNS’ SHOCK
90. Severity of Burn Injuries
Treatment of burns as per severity of injury
Severity is determined by:
Depth of burns
TBSA involved
Site - face, hands, feet, face or perineum
Age
Associated injuries
N Engl J Med 1996;335:1581 J Trauma 1994;36;59
94. Parkland Formula
Fluid of Choice
Lactated Ringer’s (RL)
NS can produce hyperchloremic acidosis
4 ml x % of burn x weight (Kg) in 24 hours
First ½ of total volume given in the first 8 hours
Remaining ½ of total volume given over following 16 hours
NEXT 24 HRS
Total volume ½ of first day
Colloids ( 0.5 ml / kg / % )
5 % glucose to make up the rest
95. Parkland Formula
Maximum applicable TBSA – 50%
Fully dilated capillaries
Maximum capillary permeability
No further mounting of inflammatory response
96. Adult Fluid Resuscitation
Evan’s formula:
Requirement for first 24 hrs
Colloids : 1ml/kg/% burn
Saline : 1ml/kg/% burn
D5 : 2000ml
Requirement for second 24 hrs
½ of first 24 hrs
97. Adult Fluid Resuscitation
Brooke formula
Requirement for first 24 hrs
Colloids : 0.5ml / kg /% burn
RL : 1.5ml / kg / %burn
D5 : 2000ml in adults
Requirement for second 24 hrs
½ of first 24hrs
98. Pediatric age group
Carvajal Formula
5000cc x m2 x % BSA initial + 2000cc x m2 maint /d
Change to 5%D+RL with albumin after 6 hrs
Urine output 1-2 cc/ kg/h
99.
100. Assessment of Adequacy of
Fluid Resuscitation
Monitor
Urinary Output
Adult: > 1 ml/ kg/ hr
Daily Weight
Vital Signs
Heart rate and blood pressure
CVP
Level of Consciousness
Laboratory values
102. Nutritional Support
Burn wounds consume large amounts of energy:
Requires massive amounts of nutrition to promote wound healing
Monitoring Nutritional Status
Weekly albumin levels
Daily weight
EMR (Estimated metabolic requirement) (Curreri formula)
=25kcal x body weight (kg) + 40 kcal x % BSA
103. Routes of Nutritional Support
High-protein & high-calorie diet
Often requiring various supplements
Routes:
ORAL (BEST)
Enteral
Gut is the preferred alternative route
G-tube or J-tube (Head injury/ surgery/ unconscious)
Parenteral
TPN and PPN
Associated with an increased risk of infections
104. Nutritional Support
Formulas to Predict Caloric Needs in Severely Burned Children
Age group Maintenance needs Burn wound needs
Infants (0-12 mo) 2100 KCal/ %TBSA/ 24hr 1000 KCal/ %TBSA/ 24hr
Children (1-12 yr) 1800 KCal/ %TBSA/ 24hr 1300 KCal/ %TBSA/24 hr
Adolescents (12-18 yr) 1500 KCal/ %TBSA/ 24hr 1500 KCal/ %TBSA/ 24hr
106. Burn Wounds
Risk for Infection
Skin first line of defense
Necrotic tissue bacterial growth
Management
Burn wounds are frequently monitored for bacterial colonization
Wound swab cultures and invasive biopsies
107. Role of burn wound cultures
Early cultures positive/ high counts early contamination of the burn wound
Routine cultures aid in empiric antimicrobial coverage if the patient subsequently
becomes ill
Increasing colony counts change topical antimicrobial agents.
Colonization by virulent or resistant organisms predictor of impending invasive burn
wound infection.
Wound colony counts >106 high risk of infectious & graft failure.
108. Burn Wound Care
Hydrotherapy
Shower, bed baths or clear water spray
Maintain appropriate water and room temperature
Limit duration to 20-30 minutes
Don’t burst blisters, aspirate them!!!
Trim hair around wound; except eyebrows
Dry with towel; pat dry, don’t rub!
Clean unburned skin and hair
109. Burn Wound Care
Antimicrobial Agent
Silvadene (silver sulfadiazine)
Broad spectrum; the most common agent used
Painless & easy to use
Doesn’t penetrate eschar
Leaves black tattoos from silver ion
Sulfamylon (mafenide acetate)
Penetrates eschar
Painful for approximately 20 minutes after application
Metabolic acidosis
110. Burn Wound Care
Antimicrobial agent
Bacitracin/ Neomycin/ Polymyxin B
- not broad spectrum, painless, easy to apply
Nystatin(Mycostatin)
- antifungal
Mupirocin(Bactroban)
- anti staphylococcal
111. Burn Wound Care
Betadine
Drying effect makes debridement of the eschar easier
Acticoat (antimicrobial occlusive dressing)
A silver impregnated gauze that can be left in place for 5 days
Moist with sterile water only; remoisten every 3-4 hours
112. Soak silver dressings and gauze
in WATER (not saline).
Apply the
silver dressing.
Wrap with moist gauze.
Secure with mesh, gauze or tape.
114. Closed Dressing
Advantages
• Less wound desiccation
• Decreased heat loss
• Decreased cross
contamination
• Debriding effect
• More comfortable
• Disadvantages
• Time consuming
• Expensive
• Increase chances of
infection if not changed
frequently
115. Burn Wound Care
Cover with a Sterile Dressing
Most wounds covered with several layers of sterile gauze dressings.
Special Considerations:
Joint area lightly wrapped to allow mobility
Facial wounds may be left open to air
Circumferential burns: wrap distal to proximal
All fingers and toes should be wrapped separately
Splints over dressings
116. Burn Wound Care
Debridement of the wound
May be completed at the bedside or as a surgical procedure.
Types of Debridement:
Natural
Body & bacterial enzymes dissolve eschar; takes a long time
Mechanical
Sharp (scissors), Wet-to-Dry Dressings or Enzymatic Agents
Surgical
117. Why excise the burn?
Burn wound is a focus for sepsis
Burn stimulates inflammatory mediators
Deep burns cannot heal without grafts
Possible effect on future scar quality
118
Non full-thickness burns may heal
spontaneously
Superficial burns heal with acceptable
scars
Excised burn wound must be closed
Major burn surgery is hazardous
but
121. Early excision of burns
Tangential excision to
viable tissue on day 2-3
Janzekovic (1970)
Jackson & Stone (1972)
Current concept – within hours
Hardly any bleed
Upto 60% burns
122
123. TANGENTIAL BURN EXCISION
& EARLY SPLIT SKIN GRAFTING
124
Early wound closure; shorter hospital stay
No increase in morbidity
Significant ↓ in mortality
Reduced bacterial colonization
Tissue preservation
Maintenance of function
Less scaring
124. Early burn surgery
Superior outcomes where suitably equipped
mortality
length of hospital stay
morbidity during acute burn
scar quality
125
125. Desirable surgical management
Excision of all non-shallow burns as soon as practicable in as few stages as
possible
Closure of excised wounds with autograft, allograft or artificial material
Definitive wound closure
126
126. Surgical Management
Skin Grafting
Closure of burn wound
Spontaneous wound healing would take months for even a small full-thickness
burn
Eschar is removed as soon as possible to prevent infection
Wound needs to be covered to prevent infection, loss of heat, fluid and
electrolytes
Therefore, skin grafting is done for most full-thickness burns.
Can be permanent or temporary
127. Burn Wound Closure
Permanent Skin Grafts
Two types:
Autografts and Cultured Epithelial Autografts (CEA)
Autograft
Harvested from pt
Non-antigenic
Less expensive
Decreased risk of infection
Can utilize meshing to cover large area
Disadvantage : lack of sites and painful
128. Burn Wound Closure
Cultured Epithelial Autografts (CEA)
A small piece of pt’s skin is harvested and grown in a culture medium (PDGF
impregnated)
Takes 3 weeks to grow enough for the first graft
Very fragile; immobile for 10 days post grafting
Useful for limited donor sites
Disadvantage : very expensive; poor long term cosmetic results and skin
remains fragile for years
130. Burn Wound Closure
Temporary Skin Grafts
Why temporary ??
Available donor sites are used first, but in large burns not
enough donor sites.
While waiting for donor site to heal it can be reused as a temporary
covering.
132. Burn Wound Closure
Biosynthetic Temporary Skin Grafts
Homograft
Allograft
Live or cadaver human donors
Fairly expensive/ all the function of skin
Best infection control of all biologic coverings
Disadvantage :
Disease transmission (HBV & HIV)
Antigenic: body rejects in 2 weeks
Not always available
Storage problems
133. Biosynthetic Temporary Skin Grafts
Heterograft
Xenograft
Graft between 2 different species
Porcine most common
Fresh, frozen or freeze-dried (longer shelf life)
Amenable to meshing & antimicrobial impregnation
Antigenic: body rejects in 3-4 days
Fairly inexpensive
Disadvantage : Higher risk of infection
134. Biosynthetic Temporary Skin Grafts
Artificial Skins
Transcyte:
A collagen based dressing impregnated with newborn fibroblasts.
Integra:
A collagen based product that helps to form a “neodermis”
no anti-microbial property
Synthetic
Any non-biologic dressing that will help prevent fluid & heat loss
Biobrane, Xeroform, OpSite or Beta Glucan collagen matrix
135. Biobrane
Artificial dressing has elastic
property
Bilayer fabric
Inner layer - knitted nylon threads
coated with porcine collagen
Outer layer - rubberized silicone
Pervious to gases but not to liquids
and bacteria
Epithelialization takes place under
the dressing in
partial thickness wound in 1-2 wks
136. Donor Site: Wound Considerations
The donor site is often the most painful aspect for the post-operative pt
brand new wound !!
Variety of products are used for donor sites
Most are left in place for 24 hours and then left open to air
Donor sites usually heal in 3 wks
138. Burn Wound Infection
Focal/ multi focal/ generalized
More the area of infection ↑chances of septicemia
Common org- Strep, Staph & Pseudomonas
139. Monitoring Wound Infection
Definite diagnosis wound biopsy
More than 100,000 organisms is highly suggestive of burn wound infection
Concomitant positive blood culture is a reliable indicator
Children & burns > 30% TBSA are more likely to develop burn sepsis
140. Clinical Signs of Burn Wound Infection
2nd degree burn full-thickness necrosis
Focal dark-brown or black discoloration
Wound degeneration “neo-eschar” formation
Unexpectedly rapid eschar separation
Hemorrhagic discoloration of sub-eschar fat
Erythematous or violaceous edematous wound margin
Septic lesions in unburned tissue
Crusted serrations of wound margin
143. Sepsis in burn pt concern for infection.
Age-dependent definition with adjustments for children.
The trigger includes at least three of the following:
I. Temperature >39° or <36.5°C
II. Progressive tachycardia
Adults >110 bpm
Children >2 SD above age-specific norms (85% age-adjusted max
heart rate)
Burn Sepsis
144. III. Progressive tachypnea
Adults >25 /min not ventilated
Minute ventilation >12 L/min ventilated
Children >2 SD above age-specific norms
(85% age- adjusted max respiratory rate)
IV. Thrombocytopenia (only 3 days after initial resuscitation)
Adults <100 000/mcl
Children <2 SD below age-specific norms
Burn Sepsis
145. V. Hyperglycemia (in the absence of pre-existing diabetes mellitus)
Untreated plasma glucose >200 mg/dL or equivalent mM/L
Insulin resistance – examples include
>7 units of insulin/h intravenous drip (adults)
Resistance to insulin (>25% increase in insulin requirements over 24 hours)
VI. Inability to continue enteral feedings >24 hours
Abdominal distension
Enteral feeding intolerance (residual >150 mL/h in children or 2× feeding rate in adults)
Uncontrollable diarrhoea (>2500 mL/d for adults or >400 mL/d in children)
Burn Sepsis
150. Begins day one and may last several years
Nursing care
Meticulous asepsis continues to be important
Major areas of focus:
Support for adequate wound healing
Prevention of hypertrophic scarring & contractures
Psychosocial Support
Patient and family
Promotion of maximal functional independence
Rehabilitation
151. Hypertrophic Scar Formation
Excessive scar formation, which rises above the skin
Management: Pressure Garments
Elasticized garments that are custom fitted
Maintains constant pressure on the wound
Result: smoother skin & minimized scar appearance
Pt Considerations:
Must be worn 2-3 hours a day
Up to 1-2 years
Jobst garments, foam sponge, foam tape, silicon gel sheet
152. Contracture Formation
Shrinkage and shortening of burned tissue
Results in disfigurement
Especially if burn injury involves joints
Management is application of opposing force:
Splints, proper positioning, mobilisation
Must begin at day one
Multidisciplinary approach is essential
153. Psychosocial Considerations
Alterations in Body Image
Loss of Self-Esteem
Returning to community, work or school
Sexuality
Supports Services
Psychologist, social work & vocational counselors
Local or national burn injury support orgs
Psy Considerations
Encourage pt & family to express feelings
Assist in developing positive coping strategies
155. RAs (grafts)
Liposomal gene transfer Branski L, Pereira CT, Herndon DN, Jeschke MG. Gene therapy in
wound healing: Present Status and Future Directions. Gene Therapy, 2006 Aug 24
cationic cholesterol-containing liposomal constructs
(best so far)
Naked DNA application,
Viral transfection,
High-pressure injection
Liposomal delivery
156. RAs (grafts)
ARTIFICIAL SKIN SUBSTRATES
Dermal matrices with epidermal components Boyce ST, Kagan RJ, Yakuboff KP, Meyer
NA, Rieman MT, Greenhalgh DG, Warden GD. Cultured skin substitutes reduce donor skin
harvesting for closure of excised, full-thickness burns. Ann surg, 2002 Feb; 235(2):269-279
Amniotic wound coverage devices . Branski LK, Herndon DN, Masters OE, Celis M,
Norbury WB, Jeschke MG. Amnion in the treatment of pediatric partial-thickness facial
burns. Burns, 2007 Oct 4.
Dermal component matrices Schulz JT 3rd, Tompkins RG, Burke JF. Artificial skin. Ann
Rev Med, 2000; 51:231-244
157. CONCLUSION
Early, aggressive, controlled fluids
Monitor urine output as a guide to resuscitation
Prevent extension of injury
Maintain high suspicion for inhalation injury & low thresh hold for intubation
Always rule out co-incident trauma
Frequent reassessment of extremities
Seek out & treat CO poisoning
Liberal use of analgesia
Prevent hypothermia
Provide for increased metabolic demands
158. BURNS !!!
B Breathing
U Urinary output
R Rule of Nines & Resuscitation with fluid
N Nutrition
S Shock & Silvadene
159. References
Total Burn Care; David N Herndon 4th Ed
Bailey And Love's Short Practice of Surgery 26th Ed 2013
Schwartz’s Principles of Surgery, 10th Ed
Sabiston Textbook of Surgery 19th ed 2012
160