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BURNS OVERVIEW
Function of Skin
1. Protection From chemicals, micro-organisms, and minor trauma
2. Barrier Against water loss
3. Sensation Mediates touch, position, pressure, temperature, and pain
4. Immunological defence - Using Langerhans’ cells and local cytokine networks
5. Vitamin D synthesis Occurs in response to sun exposure
6. Ultraviolet protection with melanocytes
7. Aesthetics
.
 When the skin is burned, these functions are lost.
 The loss of the stratum corneum allows the invasion of micro-organisms, and the
Langerhans’ cells, which mediate local immune response, are also gone.
 In severely burned patients, the systemic immune response is suppressed, which renders
the patient highly susceptible to serious infections.
 Thus, topical antimicrobial dressings are essential in controlling wound surface pathogens.
 The loss of the epidermal barrier causes increased fluid losses until the wound is
completely reepithelialized, not just during the initial resuscitation period.
 Deep thermal injuries that destroy the dermis and subcutaneous tissue often heal with
significant wound contractures and impaired mobility, especially across joint surfaces.
 Main function of dermis is to support the epidermis
 Problems with major burns
Immediate
1. shock
2. inhalation injury
3. limb compartment syndrome
Early
1.
2.
3.
4.
5.
fluid shifts
systemic inflammatory response
infection
nutrition/metabolic
end organ complications
Late
1.
2.
3.
4.
joint contractures
scars – hypertrophic, keloid
squamous cell carcinoma
aesthetics
EPIDEMIOLOGY
U.S.A. - 2 million thermal injuries / year
- 130,000 admitted
- 10 - 12,000 die anually
Spend 1.0 - 1.5 days in hospital per percent tissue burnt
Only 1/6 total treatment
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4 high risk groups - young (<2 years)
- old ( >65 years)
- unlucky (21% are innocent bystanders of fire)
- careless (75% burns)
Most burns are scalds
50% of burns are in children - most are scalds in kitchen or bathroom
Most adult scalds - car radiators
Heating unit failure most common cause house fires
Clothing - when ignites 6x full thickness burns & 4x mortality
Cigarettes common cause of fatal fires
Mortality related to
1. total body surface area (TBSA) burn.
2. percent of full thickness burn
3. Age
4. presence of an inhalation injury
5. Comorbidities
Reduction in Burn Mortality due to:
1.
2.
3.
4.
5.
6.
early excision and skin grafting;
improved ICU care
early nutrition
ventilation
antibiotics (probably minor if any)
the “team approach”
Classification of burns
Depth Classification
Classification of Burns Based on Depth
Characteristics
Classification Cause
Appearance
Superficial
burn
Dry and red;
Painful
blanches with
pressure
Ultraviolet
light, very
short flash
(flame
exposure)
Superficial
Scald (spill or
partialsplash), short
thickness burn flash
Sensation
Healing
time
3 to 6
days
Blisters; moist, Painful to
7 to 20
red and
air and
days
weeping;
temperature
blanches with
pressure
2
Scarring
None
Unusual;
potential
pigmentary
changes
Deep partial- Scald (spill),
thickness burn flame, oil,
grease
Blisters (easily
unroofed); wet
or waxy dry;
variable color
(patchy to
cheesy white
to red); does
not blanch
with pressure
Full-thickness Scald
Waxy white to
burn
(immersion), leathery gray
flame, steam, to charred and
oil, grease,
black; dry and
chemical,
inelastic; does
high-voltage not blanch
electricity
with pressure
Perceptive More
of pressure than 21
only
days
Deep
pressure
only
Severe
(hypertrophic)
risk of
contracture
Never (if Very severe
the burn risk of
affects
contracture
more
than 2
percent
of the
total
surface
area of
the body)
 Partial thickness burn may be superficial or deep.
 Superficial PTB retains all intact skin appendages and heals well. Blistering wounds that
blanch with pressure are characteristic of superficial partial-thickness burns. These wounds
are also typically moist and weeping.
 deep PTB have minimal viable skin appendages and heals slowly and with significant
scarring. Typified by easily unroofed blisters that have a waxy appearance and do not
blanch with pressure.
Etiological classification
1. Thermal
2. Chemical
i. Oxidizing agents
 White phosphorus
ii. Acids
 Hydrofluoric acid
 Phenol
iii. Alkali
 Cement burns
 Anhydrous ammonia
iv. Skin preparation agents
 Providone iodine - usually occur in dependent parts of the body, such as the
buttocks or under a tourniquet, where the agent has not been allowed to dry.
Irritation and long-term pressure both appear to play roles in the pathogenesis of
these injuries.
 Alcohol-based skin cleansers such as chlorhexidine gluconate 0.5% in 70%
methanol
3. Electrical
i. High voltage (>1000V)
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ii. Low voltage (<1000V)
4. Frostbite
5. Exfoliating disorders
i. Stevens-Johnson syndrome
ii. Toxic epidermal necrolysis (TEN)
Determination of burn depth & extent
1. Rule of Nines
2. Lund & Browner chart (Berkow’s method)
3. Rule of palm
a. palm of the person who is burned (not fingers or wrist area) is about 1% of the body
Rule of Nines
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5
Lund and Browder Chart for Estimating Area of Burns
Birth
10 to
to1 1 to 4 5 to 9 14
15
Area
year years years years years Adult 2nd* 3rd* TBSA
19
17
13
11
9
7
Head
Neck
2
2
2
2
2
2
Anterior
trunk
13
13
13
13
13
13
Posterior 13
trunk
2.5
Right
buttock
2.5
Left
buttock
Genitalia 1
13
13
13
13
13
2.5
2.5
2.5
2.5
2.5
2.5
2.5
2.5
2.5
2.5
1
1
1
1
1
Right
upper
arm
4
4
4
4
4
4
Left
upper
arm
4
4
4
4
4
4
Right
lower
arm
3
3
3
3
3
3
Left
lower
arm
3
3
3
3
3
3
Right
hand
2.5
2.5
2.5
2.5
2.5
2.5
Left hand 2.5
5.5
Right
thigh
2.5
2.5
2.5
2.5
2.5
6.5
8
8.5
9
9.5
Left thigh 5.5
Right leg 5
6.5
8
8.5
9
9.5
5
5.5
6
6.5
7
Left leg
5
5
5.5
6
6.5
7
Right
foot
3.5
3.5
3.5
3.5
3.5
3.5
Left foot 3.5
3.5
3.5
3.5
3.5
3.5
Total:
*--Second-degree burns are now more often designated as superficial partial-thickness or
deep partial-thickness burns, and third-degree burns are designated as full-thickness burns.
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Trials
 Rule of Nine's takes a shorter time to complete
 Rule of Nine's technique often overestimates the burn size
 Lund and Browder chart more reproducible; best in children
 Revisions of burn-depth estimations are often necessary in the first 24 to 72 hours and may
be required through the first two or three weeks
 laser Doppler flowmetry and laser Doppler perfusion scanner may be useful adjuncts to
clinical evaluation of burn depth but as yet
 Early bronchoscopy is the most accurate investigation for airways involvement- helpful in
confirming the diagnosis and determining airway management
Burn triage
Criteria for admission
1. 2o & 3o burns > 20% TBSA (adult) or 10% (<10yo and >50yo)
2. 3o burns > 5% in any age group
3. 2o & 3o burns posing a serious threat of functional or cosmetic impairment
4. face, hands, feet, genitalia, perineum, around major joints
5. Electrical burns including lightning
6. Chemical burns posing a serious threat of functional or cosmetic impairment
7. Inhalational burn
8. Burns associate with major trauma
9. NAI in children
History
1. type of agent
2. time
3. enclosure
Physical Examination
1. depth & extent (age + %)
2. evidence of airway burn
a. fire in enclosed burn
b. facial burn
c. singed hair
d. soot
e. stridor
f. CO>15% or COHb>15%
3. circumferential burns
Management
Airway - ? intubation
Breathing - ? inhalation, 100%O2
Circulation - monitor PR, BP, UO, mentation
Dressings & drugs - Pharmacologic vs biologic
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Escharotomy / fasciotomy ?
Fluid resuscitation - Crystalloid vs colloid vs hypertonic solution; blood
Gastric - nutrition & bleed (Curling ulcer)
Hand
Infection - bronchopneumonia; antibiotics
Psychological support
Rehabilitation - pre & post-op
Surgery & scars - early & late
Fluid Resuscitation
 Hypovolemic due to
1. Fluid losses
o Evaporation
o Third space losses
 Endothelial damage, increased permeability
 Starlings forces - heat-induced denaturing of collagen fibers in the
interstitium, causing a physical expansion of the potential third
space with a transient -20 to -30 mm Hg negative-pressure
gradient favoring extravasation of fluid
o Intracellular oedema
 Na ATPase pump failure
 Intracellular protein denaturation
2. reduced pump function (Ebb phase)
 During the first hours following thermal injury there are considerable changes in the
microcirculation of burn wounds.
 Early factors are histamine, serotonin, prostaglandins, platelet products, complement
components, and members of the kinin family. This process occurs in burned tissues and,
to lesser extent, in unburned tissues. The margination of neutrophils, macrophages, and
lymphocytes into these areas is associated with the release of a rich milieu of these
mediators, which affect both local and systemic capillary permeability.
 There is a loss of endothelial integrity with a massive flow of electrolytes and proteins to
the extravascular space, trapping a large volume of intravascular fluids. This is the main
cause of the hypovolaemic shock observed in the first 24 h. After approximately 12 h the
endothelial gaps created by vasoactive mediators are resolved, causing slow inflow of
fluids to the intravascular space.
 For this reason colloid therapy in the first hours of resuscitation aggravates burn
wound oedema.
 nearly one half of infused crystalloid volume is lost to the interstitium during early
resuscitation
 Hypovolamic shock will develop if the burns involve > 15–20% of the body surface
area
 Promptly addressed adult burns of <15-20% TBSA without inhalation injury are
usually not enough to initiate the systemic inflammatory response, and these patients
can be rehydrated successfully primarily via the oral route with modest IV fluid
supplementation.
 Objectives:
1.
Restore and maintain tissue perfusion
2.
Prevent organ ischemia and failure
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3.
Preserve heat-injured, but still viable, tissues (stop progression of stasis zone)
 Traditional method
o 1st 24 hours – crystalloid
 Parklands formula (Charles Baxter, MD, at Parkland Hospital at
Southwestern University Medical Center, Dallas)
 formula was devised after experiments by Baxter and Shires on
rhesus monkeys using Ringer's lactate in 1968
 4ml x kg weight x % TBSA
 First 50% given over 8 hours, next 50% over 16 hours
 Given in addition to maintenance in children
 Maintenance in children (0.45% saline and 2.5%Dextrose)
o 100ml/kg for 1st 10 kgs
o 50ml/kg for 2nd 10kgs
o 20ml/kg thereafter
o Second 24 hours - 5% albumin solution
 0.1 mL/kg/% burn infused over a period of 2 to 3 hours
 Burns < 30% TBSA do not require colloid infusion.
 Albumin is the plasma protein that most contributes to intravascular
oncotic pressure. When administered intravenously as a 5% solution
from pooled plasma product, approximately half the volume remains
intravascularly, as opposed to 20-30% of crystalloid solutions.
Alternatively, some centers prefer using fresh frozen plasma over using
albumin because of the theoretic advantage of replacing the whole
range of plasma proteins that are lost rather than just the albumin
fraction.
 Given at earliest 8 hours post burn - some studies have demonstrated
harmful effects secondary to increased pulmonary edema and some
evidence of renal dysfunction as manifested by a decreased glomerular
filtration rate.
 Review by H Cleland (ANZ J Surg Feb 06)
o Most studies show that fluid over the amount predicted by Parklands formula
is given - 'fluid creep'
o fluid creep phenomenon is more evident in the first 8 h.
 Patients with inhalation injuries require volumes as much as 30-40% higher (close to
5.7 mL/kg per percentage) than predicted by the Parkland formula for adequate
resuscitation. Delays in initiating resuscitation promptly have also been shown to increase
fluid requirements by as much as 30%, presumably by permitting the occurrence of an
increased inflammatory cascade.
 presence of an escharotomy or fasciotomy can substantially increase free water loss from
the wound, and this must be replaced. Patients with electrical burns, often associated with
large and underappreciated tissue insult, likewise require large-volume fluid resuscitations.
 Other strategies in the early post burn (<8hours)
1.
Hypertonic saline resuscitation (600mOsm/L)
o allows less fluid to be delivered for adequate resuscitation.
o Theory is that it avoids hyponatremia, hemoconcentration, and significant
weight gain associated with administration of isotonic solutions
o intracellular depletion of water that results is a debated concern, but it appears
to be well tolerated
o Jury is still out
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2.
3.






o Close monitoring of serum sodium levels is mandatory, and serum sodium
levels should not be allowed to increase to greater than 160mmols
Dextran
o solution of polymerized, high molecular weight glucose chains with almost
twice the oncotic pressure of albumin.
o An increase in microcirculatory flow is also produced by reducing erythrocyte
aggregation.
o Proponents of dextran point to the reduction of edema in nonburned tissues as
justification for its use. The edema-reducing properties are maintained for as
long as the infusion is continued, but upon withdrawal and subsequent
metabolism of the glucose, rapid loss of fluid occurs back into the interstitium
if the capillary leak is still present.
High dose ascorbic acid infusion
o minimize oxidant-mediated contributions to the inflammatory cascade.
o Theory is that it reduces resuscitation fluid volume requirements, and edema
generation
Patients who potentially benefit the most from lower-volume resuscitations aided by the
above are those with larger burns (>40%), those with preexisting heart disease, geriatric
patients, and those with burns with associated inhalation injuries
Monitor adequacy of resuscitation
a. urine output – aim adult 0.5ml/kg/hr; child 1ml/kg/hr
i. unreliable if having forced diuresis ie mannitol or
ii. glycosuria – may cause hypovolemia secondary to osmotic diuresis. Check the urine
for glucose and treat hyperglycemia with IV insulin as needed.
b. art.line
c. CVP
Sheridan pointed out that after 18–24 h, capillary integrity generally returns if
resuscitation has been successful. At this point, fluid requirements abruptly decrease,
and it is important to decrease fluid administration appropriately at this point.
Overadministering fluids at this time is associated with potential morbidity and mortality.
RBC loss in first 24 hours may be 0.5 to 1.0% for each 1% full thickness burn.
Only transfuse in first 24 hours if antecedent anaemia or associated injuries because of
increased viscosity. Transfuse on day 3 if Hct<40.
Burn wound anemia – until wounds are closed, burn patient RBC demonstrates reduced
survival (half life = 40 vs 120 days).
Pediatric Burns resuscitation
 Several important differences
1. Venous access in small children may be a difficult issue
2. proportionally larger BSAs than adults (Lund-Browder charts useful)
3. IV fluid resuscitations are usually required for patients with smaller burns (in the range
of 10-20%)
4. fluid requirement relatively larger - Parkland formula with the addition of a
maintenance rate
5. urine output closer to 1 mL/kg/h being a more appropriate goal (if weight <50kg)
6. modest hepatic glycogen reserves, which can be exhausted quickly and sometimes
require the change from isotonic saline solution to dextrose 5% to prevent lifethreatening hypoglycemia
 Dangers of fluid overresuscitation include pulmonary oedema, the need for fasciotomy in
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uninjured limbs and the need for tracheostomy in patients with scald burns
 Traditional concerns that excessive crystalloid volumes precipitate cardiopulmonary
overload have been rejected in studies using the double-dye dilution principle to monitor
the water content of the lung. This may explain the findings of Herndon that fluid
accumulation in the lung may result from inadequate resuscitation and increased
lung capillary permeability rather than from infusion of excessive fluid volumes.
SALVAGING ZONE OF STASIS
 In the zone of stasis, damage is seen in the microcirculation and intracellular
environment
1. Microcirculation affected by
i. Direct vessel damage - vessel thromboses
ii. hypercoagulability of the vessels
iii. endothelial cell damage due to free oxygen radicals (from PMNs)

1.
2.
3.
4.
5.
2. intracellular protein denaturation, inhibition of protein synthesis and the
changes in cell membrane permeability are the causes for cellular damage due to
burn.
Strategies:
increasing the tolerance of the tissues to ischemia
increasing tissue perfusion
o VAC dressing
anti-thrombotic
o TPA IV infusion shown to reduce zone of stasis in rats (Burns 1998)
antioxidant medications
o ascorbic acid
increase thermo-resistance of cells (Burns Dec 2005)
o Glutathione increases the thermo-resistance of cells
o GSH depletion inhibits production of heat shock proteins indirectly via
nonspecific inhibition of protein synthesis.
o Esterified glutathione (GSH) is also a major component of intracellular
antioxidant defense mechanism neutralizing free oxygen radicals and
peroxidases
INHALATION INJURY
Incidence
 50-60% of burns deaths involve inhalation injury as a contributing factor.
 Airway injury occurs in up to one third of those with major burns,
 Inhalation injury greatly increases the incidence of respiratory failure and acute respiratory
distress syndrome.
Pathophysiology
 Inhalation injury is generally caused by
1. direct thermal burns - In most cases, thermal injury is confined to the upper
airways, because the trachea usually protects the distal lung from thermal loads.
2. inhalation of gases and particulate matter – Gasses may be
i. Irritant
a. Causes mucosal sloughing or bronchospasm
b. ammonia, hydrogen chloride, sulfur dioxide
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



ii. Asphyxiants - gases that physically displace oxygen from the environment.
a. Simple asphyxiants, such as nitrogen, carbon dioxide, and methane, produce
hypoxia by lowering the ambient oxygen tension
b. Chemical asphyxiants, such as carbon monoxide and hydrogen cyanide,
directly interfere with the delivery and utilization of oxygen.
Thermal injury leads to two phases.
1. The initial cellular and exudative phase is characterized by an influx of neutrophils,
elaboration of oxygen-free radicals, liberation of complement degradation products,
and production of inflammatory mediators.
2. The repair and proliferation phase is characterized by cellular hyperplasia, fibrosis,
and hyaline membrane formation.
Ventilation defects may be
1. Obstructive pattern
a. Circumferential burns in the cervical area cause extrinsic upper airway
occlusion from encircling eschars.
b. bronchospasm, upper airway narrowing from laryngeal edema, bronchorrhea,
ciliary dysfunction, and inspissation of desquamated cells.
c. Particulate obstruction - Particles measuring 5 to 30 micrometers commonly
settle in the nasopharynx, whereas smaller particles enter the trachea and
bronchi. Particles measuring less than 1 micrometer can reach the distal
alveolar ducts and sacs.
2. Restrictive pattern (reduced lung compliance)
a. Constituents of smoke can cause atelectasis by destroying lung surfactant,
increasing pulmonary vascular resistance, and contributing to edema.
Perfusion defects
1. carboxyhaemoglobin
The risk of pneumonia is increased in the presence of atelectasis, bronchorrhea,
impairment of mucociliary clearance, and ineffectual cough secondary to pain or
excessive sedation.
Diagnosis
1. history of burn in a closed space
2. burns to head and neck
3. dyspnoea, stridor, coughing
Investigations
1. laryngoscopy/bronchoscopy 95% accuracy
2. Xenon 133 ventilation-perfusion lung scan may reveal nonhomogeneous uptake and can
be an accurate means of detecting lower airway damage.
3. bronchoalveolar lavage, which typically reveals an increased number of
polymorphonuclear cells and alveolar macrophages
4. transbronchial biopsy, which can be used to diagnose bronchiolitis obliterans and
interstitial fibrosis
Treatment
 Intubation for airway burns
 Indications for intubation
o upper airway
 progressive stridor, hoarseness, dyspnoea, hypoxia
 supraglottic oedema can be very rapidly progressive
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o lower airway



infiltrates on CXR
respiratory failure
ARDS
 Carbon Monoxide
 CO has strong affinity for hemoglobin (about 230 to 270 times greater than that of
oxygen), shifting the oxygen-hemoglobin curve to the left.
 The toxicity of CO is directly related to the percentage of haemoglobin it saturates
 Signs and Symptoms of Carbon Monoxide Intoxication
% CO in Hb
Symptoms
0–10
None
10–20
Headache, confusion
20–40
Disorientation, nausea, and visual changes
40–60
Hallucination, combativeness, coma, shock
>60
Mortality 50%
 If COHb>15%, intubation with 100% O2
 Half life of carboxyHb on room air is 4-5 hours
 On 100% oxygen, reduced to 45 minutes
 Hyperbaric oxygen therapy (2.5 atm) further decreases the half-life to 22 minutes
 Hydrogen cyanide
 enters the erythrocytes and interferes with the cytochrome oxidase a-a3 enzymes of
the mitochondrial electron transport chain
 inhibition of the aerobic glycolytic pathway shunts intracellular metabolism to the
alternative anaerobic pathway, resulting in an accumulation of acid by-products.
 must be suspected in burn patients with unexplained respiratory failure or
persistent anion gap metabolic acidosis.
 Treatment includes cessation of exposure, adequate ventilation and oxygenation, and
inactivation or elimination of absorbed hydrogen cyanide. Patients have been
successfully treated with agents that bind to hydrogen cyanide, such as
methemoglobin-forming agents, hydroxocobalamin, or dicobalt edetate, or with
exogenous sulfur donors, such as sodium thiosulfate
 New areas of interest in the early treatment of airway burns has focused on acute
mechanical clearance of mucus and fibrin clot in the bronchial tree and inhaled
bronchodilators to blunt narrowing of the airway in response to irritating elements in
smoke. Aerosolized treatments of heparin, TPA, acetylcystine, and terbutaline/steroid
combinations have all been recently reported.
WOUND MANAGEMENT
Outpatient management
 Suitable for small 2nd or 3rd degree burns
 Clean wounds, debride ruptured blisters & loose epidermis.
 Blisters left intact unless impede motion.
 Cover wound with sterile antibiotic dressing, bulky gauze, splint.
 Regular outpatient followup
 When treated with topical agents, intermediate and deep second degree burns may heal
without sepsis and full thickness injury becomes obvious. Wound then debrided.
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Quantitative biopsies taken - if < 105/g of tissue and no strep then appriopriate to graft.
Inpatient management
Escharotomies
 circumferentially burned extremity is at risk of becoming vascularly compromised
 During the first 24 to 48 hours postburn, continual evaluation of the status of peripheral
circulation is mandatory.
 development of an “intrinsic minus” hand is an indication for decompression of the deep
muscle compartment of the hand.
Topical antimicrobials
 SSD – may cause pancytopenia
 When a sulfa allergy complicates care, alternative agents include Polysporin, bacitracin,
and Bactroban. These agents are relatively inexpensive but have a tendency to induce
allergies.
 Mafenide acetate
o only agent that can penetrate an eschar - makes it ideal for treatment of undebrided,
infected wounds. It is also the treatment of choice for serious burns of the ears to
help prevent infectious chondritis.
o Painful and is a carbonic anhydrase inhibitor (may cause metabolic acidosis)
 Acticoat takes advantage of the proven antimicrobial properties of the silver ion by coating
the dressing material with a thin, soluble silver film. The dressing seems to maintain
antibacterial levels of silver ions in the wound for up to 5 days. The Acticoat dressing
reduces infection rates and has the additional benefit of decreased pain and expense
because daily dressings do not seem to be necessary.
 An alternate method of managing wounds is with an occlusive dressing. When superficial
second-degree burns are clean and less than 24 hours old, an occlusive dressing can be
applied. These products maintain a moist wound environment, which speeds healing and
de-creases the frequency and pain of daily wound care. There are several new types of
occlusive dressings commercially available
 Biobrane is a biosynthetic wound dressing constructed of a silicon film with a nylon fabric
partially imbedded in the film. The fabric presents to the wound bed a complex, threedimensional structure of trifilament threads to which collagen has been chemically bound.
Blood / sera clot in the nylon matrix, thereby firmly adher-ing the dressing to the wound
until epithelialization occurs. The dressing is carefully trimmed as it falls off on an
outpatient basis.
 Transcyte is produced by culturing human dermal fibroblasts onto a biosynthetic material
consisting of an ultrathin, semipermeable membrane bonded to nylon mesh. The nylon
mesh forms a three-dimensional scaffold for growth of the dermal tissue, and the
membrane forms a synthetic (nonimmunogenic) epidermis. As the fibroblasts proliferate in
the nylon mesh, they secrete structural proteins and growth factors, thereby generating a
three-dimensional human dermal matrix.
 In general, occlusive dressings are an excellent alternative for small, superficial, or
previously debrided wounds. In general, when a patient’s wounds are not healing at a rate
sufficient to expect closure within 3 weeks, operative intervention should be considered.
Excision and grafting
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 Indications for surgery
1. Major burns
2. Surgery is indicated for full-thickness injuries or when the wound is unlikely to heal
within 3 weeks.
3. After this time period, the risk of hypertrophic scar and contracture formation
increase and outweigh the morbidity and costs of surgery.
4. When the depth of injury is indeterminate, a close observation of wound healing for
7 to 10 days before initiating surgical intervention is reasonable. However, in areas
harbouring a deep and dense cross-section of dermal appendages, such as the face,
scalp, and ears, an observational period of up to 3 weeks is reasonable until the
healing potential of the wound has a chance to declare itself.
 Burnt skin is toxic and if left on the patient is largely responsible for systemic
inflammatory response syndrome, immunosupression and progression to multiorgan
failure syndrome.
 It is now clear that much of the morbidity and mortality from major burns is due to
alterations in immune function.
1. significant reduction in the T-cell helper/suppressor ratio after burns, probably due
to an increase in the T-cell suppressor subpopulation
2. significant elevation of the helper/suppressor ratio produced by anti-inflammatory
agents such as cimetidine, ibuprofen, indomethacin and cyclophosphamide and by
the topical application of cerium nitrate;
 Burn toxin responsible for this immunosuppression was isolated in 1975 and has
subsequently been identified as a high molecular weight (3,000,000 Da) lipid protein
complex (LPC) formed by heat-induced polymerisation of six skin polypeptides.
 LPC is a potent inhibitor of IL-2-dependent cell growth, thus it appears that at least part of
the immunosuppressive action of LPC is by interference in T-cell activation.
 Strategies
1. Delayed excision (>1 week)
o Traditionally, patients with major burns have been treated with dressings and
topical antimicrobial agents until the eschar separates.
o The granulating wound would then be covered with split thickness skin graft, a
process which could take 3–5 weeks. Patients with severe burns treated in this
manner are more likely to die from sepsis due to the massive release of
inflammatory mediators from the burn wounds.
o Cerium Nitrate (Flammacerium)
 an excellent topical treatment for most cutaneous burns not undergoing
immediate excision and closure.
 Useful in situations where expensive skin substitutes not available or coexistent morbidities that make it undesirable for early operation under general
anaesthesia
 Mechanisms of action
1. renders the eschar firm and impermeable, often described as leather-like in
appearance with a greenish yellow discolouration.
2. shown experimentally to bind the LPC and its precursors and denature the
toxic components
3. mildly bacteriostatic – best against pseudomonas, little additional
antibacterial effect from Cerium in combination with silver sulphadiazine
4. Modulates calcium dependent systems
5. There appears to be inhibition of granulation and contraction of full
thickness wounds beneath the Cerium eschar, which acts as a biological
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dressing.
 no prospective randomised trial has yet confirmed improvements in mortality
from burn injury after treatment with cerium
 Marketed as a micronised 1% silver sulphadiazine in a hydrophilic cream base
with 2.2% Cerium nitrate
2. Early excision (3-7 days)
o paradigm shift with introduction of tangential excision of burns by Janzekovic in
1970
o This technique involved removal of necrotic burnt tissue while preserving as much
of the underlying viable tissue as possible.
o The wounds are then covered immediately with split thickness skin graft - only
caveat to this practice is that a wound must not be excised unless it can be
immediately closed.
o When performed early, excision and immediate wound closure has been shown to
improve survival, decrease length of hospital stay in burn patients, especially
children
o rationale for early excision of burns is that it
1. decreases release of inflammatory mediators
2. reduces bacterial colonization of wounds.
3. removes LPC toxin
4. This, in turn, attenuates the systemic inflammatory response syndrome
(SIRS) hence reducing the occurrence of metabolic derangements, sepsis and
multi-organ failure
o opponents of early excision from the early days of early excision were mainly
concerned with the massive blood loss seen after early excision. Other reasons
cited against early excision include difficulty of assessing depth of burn in the
early period and the need to use cadaveric skin for coverage after early excision
o Early trials by Burke et al., Alexander et al. and Tompkins et al have shown
excellent mortality statistics in children treated by early excision.With early
excision, it is now unusual for a child to succumb to burn injury of any size even
when it is associated with inhalational injury. Other factors like better nutrition
and control of sepsis play a less important role. The evidence for adults, on the
other hand, is less conclusive.
o Meta-analysis by Song (Burns 2006) showed that the reduction in mortality with
early excision was not statistically significant compared to traditional treatment of
burns. The reduction in mortality with early excision was only significant in
patients without inhalational injury. A possible explanation could be that the
mortality in patients with inhalational injury is usually high hence it did not make
a difference whether their burns were excised early. A statistically significant
increase in blood loss was seen in patients who had their burns excised early when
compared to the traditional group. Length of hospital stay was significantly shorter
in patients who had early excision. This is not surprising as patients who have
their burns excised early tend to have their wounds covered earlier and hence have
a shorter stay in hospital.
o In terms of cosmesis, Engrav et al. showed that burn scar hypertrophy was less
prevalent in the excision group but there were more surface irregularities in this
group due to the use of meshed skin grafts. They also concluded that the function
of joints was more dependent of the quality of physiotherapy rather than the
modality of treatment.
3. Immediate excision (<24 hours)
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o Desai et al. showed in his review of 1662 paediatric burn patients that blood loss is
significantly reduced if burns are excised within 24 h of injury or more than 16
days after the injury when compared to those excised between 2 and 16 days after
injury. He attributed this to the high circulating levels of vasoactive mediators like
thromboxane A2 in the first 24 h. These mediators cause vasoconstriction and
hence reduce blood loss. The blood loss is also less if burns are excised after 16
days as it is a blunt debridement of a granulating bed rather than sharp removal of
adherent eschar as in the case of early excision.
o In Adelaide, tumescent technique is used together with immediate excision.
Rationale is reduction in sepsis and mortality. Blood loss said to be minimal
o Risk of overdebridement
 Eschar excision may be tangential or fascial
3. Fascial excision leads to less blood loss but is more deforming. Reserved for latge
areas of full thickness burns
 Biological dressings – required when there is insufficient autograft . Options include
allograft, amnion, porcine xenograft,"synthetic skin", cultured epithelial autografts
a) Decrease bacterial count
b) Decrease evaporative water and protein loss
c) Diminish pain
d) Prevent dessication
e) Protect wound
f) Test of suitability for autografting
INFECTIONS
 Infection is the leading cause of death in burn patients.
 During the past 10 years, the primary cause of death has shifted from invasive burn wound
infection to bronchopneumonia
 syndrome of decreased bowel mucosal integrity, capillary leak, and decreased mesenteric
blood flow, which can result in bacterial translocation into the portal circulation. These
bacteria and their by products can significantly alter hepatocyte function, spread
systemically to induce systemic sepsis, and act as a source of pathogens for infections of
the blood, lungs, wound, or bladder
 The prevention of these events involves
1. Adequate resuscitation ensures mesen teric blood flow.
2. Enteral nutrition in general and glutamine in particular have a tropic effect on the
enterocytes that preserve mucosal integrity.
 Topical antibiotics are used to decrease microbial growth and to prevent invasive
infection.
 Prophylactic systemic antibiotics do not have a role in the prevention of wound
sepsis.
 use of prophylactic antibiotics such as penicillin offers no protection against the
development of either cellulitis or burn wound sepsis, but does promote the selection of
antibiotic-resistant bacteria.
 Antibiotics are indicated when cellulitis exists in the surrounding unburned tissue.
 importance of environment in the spread of infection cannot be overemphasized.
McManus and associates report a profound decrease in gram negative bacteremia when
burn patients were moved from open wards to single-bed isolation environments where no
cross infection or colonization by endemic resistant bacteria occurred.
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 Burn wound sepsis is defined as >105 organisms per gram of tissue.
 Group D streptococci (Enterococcus sp) are important pathogens in the severely burned
patient. Secondary enterococcal bacteremia has been associated with 50% mortality. Once
blood cultures are positive, therapeutic intervention appears to have little effect on
mortality.
 Most partial-thickness burns less than 10 percent TBSA can be simply and safely cared for
with a once-daily antibiotic dressing.
IMMUNE RESPONSE
 Virtually every aspect of the immune system is disturbed by the burn injury.
 Humoral as well as cell-mediated immunity is impaired and manifests as depressed levels
of immunoglobulin, reduced activation of complement to form membraneattacking
complexes and diminished stimulation of lymphocyte proliferation and response.
 Therapeutic interventions to enhance the immune state are still experimental.
BURN METABOLISM AND NUTRITION
 Hypermetabolic response due to alteration of neural-humoral control.
 Patients with burns less than 40% TBSA do not have catabolism unless sepsis develops.
 Those with burns more than 40% TBSA always experience catabolism, which causes
metabolic derangements that persist for at least 1 year after the injury in most body
tissues.
 induce an inflammatory and cytokine response that results in a marked increase in
metabolic rate.
 Basal energy expenditure is increased up to two-fold above normal.
 The main principles for successful management of the post-burn hypermetabolic response
are :
1) Providing adequate nutritional support
2) Controlling the external environment by warming
3) Preventing burn sepsis
4) Achieving early wound closure
 Goal of nutritional support
o Provide adequate calories and protein to match the elevated metabolic needs and
nitrogen loses to prevent erosion of lean body mass
 Benefits of early enteral feeding
1. maintains gut mucosal integrity
2. stimulates greater insulin release (promotes anabolism)
3. reduces bacterial and fungi translocation
 Nutritional support is begun within 18 hours of admission through a Dobbhoff feeding
tube. Although gastric feedings are safe in most patients, placing the tip more distally
prevents the aspiration of food during anaesthesia and allows the patient to be fed
continuously, with-out holding feeds before and during repetitive debridement and grafting
sessions.
 Metoclopramide or erythromycin can be used to help propel the tip of the tube past the
pylorus.
 Feedings do not need to be interrupted by multiple operative procedures.
 Estimating nutritional needs
o Harris-Benedict equation – calculates Basal Energy Expenditure (kcal/day).
 Males = 66.5 + (13.7 x Wt kg) + (5.0 x Ht cm) - (6.8 x Age)
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 Females = 655 + (9.6 x Wt kg) + (1.7 x Ht cm) - (4.7 x Age)
 Twice the formula is usually used
o Currreri formula
 BMR(25kcal/kg) + 40kcal per %BSA burn
o Indirect calorimetry is the most accurate method for determining resting energy
expenditure (REE) for hospitalized individuals. REE is slightly higher than BEE,
accounting for the energy expended by the body at rest while awake. REE is
calculated indirectly using measurements of oxygen consumption and CO2 production
according to the following formula:
 REE (kcal/day) = [3.9(VO2) + 1.1 (VCO2)] x 1.44
o Aim to measure 24 hour urine collection for nitrogen and 1-2 weekly indirect
calorimetry
In general, burn patients require 30kcal/kg/day
Ideal nonprotein calorie to nitrogen ratio should be between 100:1 – 150:1
Excessive glucose administration is detrimental to burn patients - excessive glucose is
converted to fat, while excessive carbon dioxide and water production may cause fluid
overload or inability to wean the patient from mechanical ventilation.
Modulating postburn hypermetabolism for the burned patient is of overwhelming
importance in both the immediate care stage and the rehabilitative stage. Postburn
hypermetabolism cannot be completely reversed but may be manipulated by
nonpharmacologic and pharmacologic means.
Early burn wound excision and complete wound closure, prevention of sepsis, the
maintenance of thermal neutrality for the patient by elevation of the ambient temperature,
and graded resistance exercises during convalescence are simple, highly effective primary
treatment goals.
Although the initial burn injury and sepsis-related complications principally determine the
extent of the metabolic response in burn victims, obligatory activity, background- and
procedural-related pain, and anxiety also greatly increase metabolic rates. Judicious
maximal narcotic support, appropriate sedation, and supportive psychotherapy are
mandatory if their effects are to be minimized.
Several anabolic and anticatabolic agents are available for use during immediate care and
rehabilitation. Exogenous, continuous low-dose insulin infusion, beta-blockade with
propranolol, and the use of the synthetic testosterone analogue oxandrolone are the most
cost-effective and least toxic therapies to date. These greatly assist therapeutic
minimization of the loss of lean body mass and linear growth delay and are effective in
burned patients with and without sepsis.
Recombinant human growth hormone has been shown to increase protein anabolism
and improve donor site healing
COMPLICATIONS
 With effective topical agents and more aggresive surgical excision, burn wound sepsis less
common. LD50 now > 70% TBSA.
 Infection leading cause of death in burns.
 Still major threat, but bronchopneumonia most common cause of death in burns.
Predisposed to by inhalation injury, tracheostomy, aspiration.
 Other causes are septic thrombophlebitis and bacterial endocarditis.
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 Pseudomonas aeruginosa used to be the main organism. Now replaced by other G-ve &
G+ve e.g. Enterococcus, MRS, Candida.
 Clinical signs of wound sepsis include :
1. Sudden colour change to black, dark brown, red-violet
2. Haemorrhage of sub-eschar fat
3. Conversion of partial to full thickness injury or sudden breakdown of healed second
degree burn to new eschar
4. Premature eschar separation
5. Appearance of purple or black eruptions in unburned skin
6. Sudden development of hypotension, ileus or hypothermia
 Treatment - excision of burn wound, change topical agent and give I.V. AB's
 Suppurative thrombophlebitis is curable if picked early. Prevention - no line > 72 hours.
If no signs must systematically open previously cannulated veins. Open dissection in
proximal direction until normal vein encountered and wound left open.
 Gastrointeestinal complications - Curling's ulcer, formerly incidence of 12% now
infrequent. Can document gastric lesions as early as 5 hours. Prevent with use of antacids
and H2 antagonists. SMA syndrdome
 Common orthopaedic problems include osteomyelitis, heterotopic calcification, nonunion.
REHABILITATION
 Team approach - reconstructive plastic surgeon, O.T., physio, psychiatrist/ologist, social
worker, vocational guidance.
 A rough indicator of an individual’s psychological rehabilitation after a burn injury is
reflected by employment status. Patients who re-turn to work after a burn injury have
higher self-esteem, less behavioural avoidance, and greater attention to goals.
 A 1995 study showed that the most significant predictors of return to work are hand
involvement, grafting, and size of burn
 A 1989 study showed that the most significant variables influencing return to work after
injury are the degree of burns, hand burns, age (those younger than 45 have a higher return
to work rate), and the type of work done before injury.
 The length of time a patient is off work, their burn size, and their pre injury employment is
the best predictors of eventual return to work status. On average, burn patients with a mean
TBSA of 5 percent returned to work within 1 month, patients with a mean TBSA of 10
percent re-turned to work within 1 to 6 months, patients with mean TBSA of 20 percent
returned to work within 6 months to a year, and patients with a mean TBSA of 35 percent
returned to work more than a year later.
 Interdisciplinary involvement, such as counselling, group therapy, and occupational and
physical therapy, is very important in maximizing a patient’s clinical outcome.
Interventions designed to aid adjustment, work hardening, and other rehabilitation services
and marital/family therapy are also important.
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