Download Burn lecture postg 2008









TABLE. Immersion time to produce fullthickness burns
Time
Temperature (°F)
1 second
158
2 seconds
150
10 seconds
140
30 seconds
130
1 minute
127
10 minutes
120
Causes


Scalds72 %
Fires flame
– 85% of burn mortality


Chemical
Electrical
high tension >1000V
Low tension
<1000V
Pathophysiology



Cell damage and death causes
vasoactive mediator release: Histamine,
thromboxane, cytokine
Increasing capillary permeability causes
edema, third spacing and dehydration
Possible obstruction to circulation
(compartment syndrome) and/or
airway

First degree Red, erythematous Very sensitive to touch Very
painful .Usually moist No blisters Surface markedly and widely
blanches to light pressure
Second degree Erythematous or whitish with a fibrinous exudate
Wound base is sensitive to touch Painful Commonly have blisters
Surface may blanch to pressure
Third degree Surface may be: White and pliable Black, charred,
and leathery Pale and mistaken for normal skin Bright red from
hemoglobin fixed in the subdermis Generally anesthetic or
hypoesthetic Subdermal vessels do not blanchNo blisters .Hair easily
pulled from its follicle
Fourth degree Involves deep tissues including fascia, muscle,
bone, and tendons
Zones of BURN
 ZONE
1:
Zone 2:
Zone 3:
Coaggulation
Ischemia
Errythemia
Burn extent

The overall extent of the burn injury is best
estimated by recording the affected areas on a
burn diagram and estimating the percentage of
the body surface area using the 'rules of nines'
in the adult or using the Lund–Browder chart in
children. Special consideration is necessary in
children, in whom the head forms a much
greater percentage and the lower extremities a
lower percentage of the total body surface area
than in adults.
Management

–
–
–
–
–
–
–
Airway
Any respiratory complications consider PICU
Most swelling occurs in first 24 hours to 3 days
Oxygen for all burn patients
Clinical signs to watch for:

Hoarseness, stridor, cough, and visible redness of pharynx

Overt respiratory distress or hypoxia
Consider early intubation for thermal injury to airway, face and neck,
inhalation injury and central nervous system (CNS) dysfunction
For intubation use Vecuronium (no Succinylcholine due to possible
high K+)
Children burnt in confined spaces may suffer carbon monoxide
poisoning

Loss of consciousness, confusion or disorientation are likely signs

Give high concentration oxygen even if SaO2 is high (Carbon
monoxide will bind with the hemoglobin causing a false SaO2
reading)

Consider carboxyhemoglobulin level

Consider hyperbaric oxygen


Fluid resuscitation and maintenance
–
Two large bore IV’s (might need to be sutured),start with forearm
veins ,intraosseous catheter may be needed in children.
–
Bolus with normal saline (NS) or lactated ringers (LR) to restore
perfusion
 Blood pressure might be high due to high systemic vascular
resistance (SVR) but perfusion poor
 LR most often used because it has physiologic concentrations
of Na+, K+, CL- & HCO3–
Albumin in the first 12 to 24 hours may leak into the interstitium
and can worsen tissue edema
–
Goal is to normalize vital signs and maintain end organ perfusion
thus improving capillary refill and urine output
–
First degree burns: use normal maintenance formula (tissue and
fluid losses are minor)
–
Second and Third degree burns use Parkland Formula:
 LR 4cc/Kg x % burned over 24hrs plus maintenance
 Give half of the volume in 8 hours
– Important: clock starts when burned occurred
Give second half in 16 hours
Resuscitation


Rations
% X wt.
(RL) or ( NS )
X 3 12 hr .
X 2 12 hr.
X 1 12 hr .
D2 Maintanance + Ev. Water loss
(or colloid ÷ 2 )


Baxter
D2
4 ml X wt. X %
1/2 8 hr.
( RL )
1/2 16 hr .
D5 w Maintain U.O.P. 1 ml / kg/hr
Other
Brooke :colliod 0.5ml Xkg X%
crystaliod 1.5ml Xkg X %
+ 5%D 2000ml/m2
Modefied Brooke crystaliod 2ml Xkg X %
Evans :colliod 1ml Xkg X%
crystaliod 1ml Xkg X%
Monafo :250meq Na
150meq lactate
100meq Cl
titer to UOP





Foley placement
–
Normal urine output > 1cc/kg
–
Teenagers > 30cc/hr
–
If urine output is low – increase fluids
Pain control
–
IV use of morphine, fentanyl or ketamine
–
IM route not well absorbed
Wound control
–
Clean with sterile normal saline or sterile water and cover with
non-adherent dressing
Asses neurovascular status of circumferential burns
–
Chest, limbs, fingers/toes
Keep patient warm
–
Cover with warm blankets
–
No ice packs- hypothermia causes more tissue injury





Chest X-ray
I-Stat on transport
Electrolytes, BUN, Creatinine
–
Low K+ needs to be supplemented
–
In compartment syndrome or excessive tissue burn:
Rhabdomyolysis (skeletal muscle decompostion) can occur
causing a high K+, Phosphorus and CPK; low Ph and Ca+
are common

NaHCo3 1meq/kg will reduce the Serum K+ and damage
to kidneys
 CaCl 10mg/kg will stabilize cardiac cell membrane and
lower phosphorus
Tetanus booster should be given if tetanus is incomplete or if >
5 years have elapsed since last given
Transport to a Burn Center (UCSD












Burn centers referral criteria
Second and third degree burns >10% body surface area (BSA) in patients <10
or >50 years old.
Second and third degree burns >20% BSA in other groups.
Second and third degree burns with serious threat of functional or cosmetic
impairment that involve face, hands, feet, genitalia, perineum, and major
joints.
Third-degree burns >five% BSA in any age group.
Electrical burns, including lightening injury.
Chemical burns with serious threat of functional or cosmetic impairment.
Inhalation injury with burn injury.
Circumferential burns with burn injury.
Burn injury in patients with pre-existing medical disorders that could complicate
management, prolong recovery, or affect mortality.
Any burn patient with concomitant trauma (for example fractures) in which the
burn injury poses the greatest risk of morbidity or morality. However , if the
trauma poses the greater immediate risk, the patient may be treated in a
trauma center initially until stable, before being transferred to a burn center.
Physician judgement will be necessary in such situations, and should be in
concert with the regional medical control plan and triage protocols.
Hospital without qualified personnel or equipment for the care of children
should Thermal injury suggested fluid resuscitation (modified Parkland formula
Inhalation injury

Pulmonary problems are a major source of
morbidity and mortality in the burn patient. To
help clarify this process, the burn injury can be
divided into the following phases. 1) The
Resuscitation Phase, 2) The Early Post
Resuscitation Phase and the 3) Inflammation,
Infection or Hypermetabolic Phase. The
pulmonary problems specific to each phase will
be discussed
I) Resuscitation Phase (0-48
hrs)

Smoke Inhalation Injury Complex
Pulmonary insufficiency caused by the inhalation of heat and smoke is
the major cause of mortality in the fire-injured person, accounting for
more than 50% of fire-related deaths. The magnitude of the problem
has been much better appreciated in recent years. The use of many
new synthetics in home furnishings and clothing have resulted in a
much more complex form of injury, due to the extremely toxic
combustion products of these advances in technology. A closed space
fire can result in a severe hypoxic insult as well as lung damage from
the inhalation of the toxic fumes. The exposure time, the
concentration of fumes, the elements release, and the degree of
concomitant body burn are critical variables. These factors cause a
very complex injury with morbidity and mortality risks, especially
when combined with a body burn. Improved knowledge of the
pathophysiology combined with an aggressive treatment plan has
made it possible to improve the outcome.

a) Carbon Monoxide Toxicity
b) Upper Airway Injury from Smoke
Exposure
c) Chemical Burn to Upper and Lower
Airways
d) Restrictive Chest Wall Burn
II) Post-Resuscitation Period (2-6 days)
This period is often the calm before the storm of
the hypermetabolic catabolic state. However,
during this period a number of major pulmonary
problems can occur, especially the progression of
a severe inhalation injury to respiratory
dysfunction. The most common disorders are
described below.

A. Continued Upper Airway Injury
B. Decreased Chest Wall Compliance
C. Tracheobronchitis from inhalation
injury
d) Pulmonary Edema (High Pressure )
III. Pulmonary problems in the
inflammation-infection phase (7
days to wound closure)

A) Nosocomial pneumonia
B) Hypermetabolism Induced
Respiratory Dysfunction (Power
Failure)
C) Adult Respiratory Distress Syndrome
(Low Pressure Pulmonary Edema)
Adult Respiratory Distress
Syndrome

The lung damage is the result of a systemic
process initiated by burn tissue, infection or
inflammation rather than a direct lung injury.
Phase One on the first, or initial phase dyspnea
and tachypnea
Phase Two Hypoxemia is now evident,
along with continuing dyspnea.
Phase Three acute respiratory failure
Phase Four progressive pulmonary fibrosis and
recurrent pneumonias

Treatment
Mortality rate of ARDS caused by burn inflammation
and infection is extremely high. The major reason for the
lethal nature of the process is that resolution will not
occur until the initiating process is removed: the wound
especially in the large burn, cannot be readily excised
and closed at this stage of the post burn process. The
most important early treatment is prevention, i.e., early
removal of as much of the potential source of the
systemic inflammatory response as is feasible.
A variety of new low pressure ventilation systems are
available for management, which appear to be effective.
Escharotomies and
fasciotomies

Edema may develop underneath
circumferential burns of extremities and
compromise the arterial circulation to the
more distal aspects. Early after the injury,
the adequacy of the peripheral circulation
can usually be assessed by palpation of
the peripheral pulses, but these pulses
frequently become impossible to identify
as edema develops under a
circumferential eschar

Increased compartment pressures can completely
obstruct arterial inflow, leading to distal ischemia,
necrosis, and gangrene. Signs and symptoms of
peripheral ischemia can be difficult to identify in
patients with large burns, who are often
intubated, receiving narcotics, and have
peripheral edema due to administration of
resuscitation fluid. The classic signs and
symptoms of peripheral ischemia (pain,
paraesthesias, pallor, pulselessness, and
paralysis) may therefore be masked, and Doppler
ultrasonography is the only reliable method for its
early detection. When vascular compromise
occurs, escharotomies (incisions made through
burned epidermis and dermis) are necessary to
restore both arterial and venous circulation
Nutritional support

Protein should be infused at a rate of 1.5 to 2.5 g/kg per
day, depending on the size of injury and the presence of
sepsis. This rate will maintain a positive nitrogen balance
in adults and in children, but neither the exact protein
requirements nor the optimal mixture of amino acids
required by seriously injured patients are known.
Unfortunately, studies of nitrogen balance do not
produce the exact information necessary to determine
the quantity and composition of the proteins required.
Until rates of synthesis of muscle protein, collagen
components of host defense, and other proteins can be
accurately measured in vivo, this protein-replacement
rate remains only an estimate.

Calculating the caloric equivalent received
by a seriously burned patient given
glucose at 5 mg/kg per minute and
protein at 2.5 g/kg per day shows that
their caloric requirement (calculated as
basal metabolic rate × 2) is not achieved.
Fats are therefore given to meet the
remaining caloric requirement, via either
the enteral or parenteral routes
Wound care and infections

Infection of the burn wound is a major cause of
complications and death in burn patients: the best
approach to the problem is the prevention of wound
infection. Infection is most likely to affect a large, open
wound containing necrotic tissue; susceptibility is
increased by the lowered host resistance that results
from serious trauma, and this is more important than the
virulence of most infecting bacteria in determining the
seriousness of the infection. Decreased host resistance
must be corrected or prevented. Necrotic tissue must be
removed and wounds properly closed. Secondary
derangements in physiology and metabolism leading to
caloric and protein starvation must be corrected. Crosscontamination of wounds must be prevented, and
antibiotic treatment to prevent invasive infections should
be administered only at times of increased
 The
goals for therapy are to
 1. Delay colonization of the wound.
 2. Keep the wound bacterial density
lower than would otherwise occur
3. Keep the wound flora more
homogeneous and less diverse than
without therapy


Prophylactic antibiotics may be useful against the high
incidence of bacteremia that occurs during and after
excision of colonized burn eschar. Treatment should
begin immediately before the operation and last through
the immediate postoperative period, until normal
cardiovascular hemodynamics are restored (usually
within 24 h) and other normal physiologic signs return.
The perioperative antibiotic given should be chosen on
the results of previous cultures from the burn wound and
the sensitivities of the organisms. If these are
unavailable, general antimicrobial coverage for both
Gram-positive cocci and Gram-negative rods is
recommended. Intravenous antibiotics should be
directed toward the commonly encountered
Staphylococcus aureus, Pseudomonas aeruginosa, E.
coli, Enterobacter, Klebsiella, Acinetobacter, and Proteus
spp. Serum concentrations of both vancomycin and
aminoglycoside should be measured when these
antibiotics are used perioperatively but continued for
more than 48 to 72 h.

The risk of death for a burn patient without a significant
inhalation injury is highest from systemic sepsis. There
are many dose-related factors that make the burn patient
highly susceptible to the development of invasive sepsis.
First is the burn wound itself, representing a major
compromise in the body’s defense mechanism. The burn
wound, in addition to being locally susceptible to
infection, is associated with dose-related
immunosuppression of the specific and nonspecific
immune systems. Further, because these patients are
often critically ill, they are subjected to a variety of
invasive devices that bypass normal defense mechanisms;
these devices include endotracheal tubes, bladder
catheters, and arterial or venous intravascular catheters.
Depending on other associated injuries, devices such as
chest tubes, intracranial pressure monitors, and
pulmonary artery catheters may be present for extended
periods.

Though the burn wound, especially when
covered with necrotic eschar, is a common site
of primary infection in the septic burn patient,
other sites are common, including the upper and
lower respiratory tracts, the urinary tract, and,
less frequently, infections from osteomyelitis or
suppurative phlebitis. By far the most common
sites of primary infection in burn patients are the
blood stream, the burn wound,

Silver sulfadiazine
Broad antibacterial action
AD Fair penetration of eschar, Painless
DIS.Occasional sulfonamide sensitivity
(rash) Safety in pregnancy
unknown Occasional leucopenia, which is
reversible

Mafenide
Excellent antibacterial action
AD.Good eschar penetration
DIS. Very painful(10%) sulfonamide
sensitivity rash Common carbonic
anhydrase inhibition leading to metabolic
acidosis

Silver nitrate
Universal antibacterial action
AD.Effective for donor sites, newly-grafted
areas, and burn wounds
DIS.Poor penetration of eschar(0.5%)
Leaches sodium and chloride, causing
hyponatremia, or hypochloremic
alkalosis Stains all it touches
Wound debridements and
dressing changes
Classical burn wound care has been performed in a
Hubbard tank or some other immersion facility. This
creates for the patient, a warm, pleasant, antigravity
environment, where range of motion can be performed
comfortably by physical and occupational therapists.
Concern regarding potential cross-contamination has led
many burn centers to shower patients on a cart rather than
immerse them, especially patients with large, deep burn
wounds. This procedure is somewhat more uncomfortable
for the patient and must be done more quickly. There is a
greater tendency towards hypothermia, even with a high
ambient temperature in the tub room. There are
advantages, however, in terms of infection control. Even
intubated patients can be debrided and cleansed very
adequately in this fashion.

Critically ill patients are still debrided and dressed
in their beds, though this is done less frequently
with increased use of the shower cart. We still
use tubbing for smaller wounds and in preparing
patients to take care of their wounds after
discharge. Initially, dressings must be bulky in
the presence of eschar to absorb the substantial
exudate created. Post-grafting, after the graft is
revascularized, a properly applied dressing will
protect the fragile grafts until they gain strength.
However, if dressings are too bulky, they may
decrease range of motion.
Recognition&management of sepsis

There are many dose-related factors that make the burn patient highly
susceptible to the development of invasive sepsis. First is the burn wound
itself, representing a major compromise in the body’s defense mechanism.
The burn wound, in addition to being locally susceptible to infection, is
associated with dose-related immunosuppression of the specific and
nonspecific immune systems. Further, because these patients are often
critically ill, they are subjected to a variety of invasive devices that bypass
normal defense mechanisms; these devices include endotracheal tubes,
bladder catheters, and arterial or venous intravascular catheters. Depending
on other associated injuries, devices such as chest tubes, intracranial
pressure monitors, and pulmonary artery catheters may be present for
extended periods. Though the burn wound, especially when covered with
necrotic eschar, is a common site of primary infection in the septic burn
patient, other sites are common, including the upper and lower respiratory
tracts, the urinary tract, and, less frequently, infections from osteomyelitis
or suppurative phlebitis. By far the most common sites of primary infection
in burn patients are the blood stream, the burn wound, the lower
respiratory tract, and the urinary tract.
Because of the immunocompromised state of
these patients as well as their intense and
long-lasting hypermetabolism, they do not
exhibit the usual clinical parameters of
infection found in other immunosuppressed
populations (e.g., organ allograft recipients).
Thus, the burn surgeon must be constantly
aware of the clinical status of the patient
and be alert for any subtle changes. These
are often the first indicators of incipient
sepsis.

The burn wound may change in appearance with
the development of sepsis. It may exhibit
softening of the eschar or surrounding cellulitis,
purulent material may begin to issue from the
wound, or once-healthy granulation tissue may
begin to deteriorate. Equally common, however,
is the absence of change in wound appearance.
Infection from the urinary or lower-respiratory
tract is infrequently accompanied by symptoms
in these ill patients. Thus, periodic culture
surveillance is advisable to monitor the flora in
these areas.


Careful serial clinical and laboratory monitoring of the
patient is the most sensitive method of diagnosing sepsis
before disastrous hemodynamic effects occur. We perform
twice weekly eschar biopsies for quantitative culture,
though their value is debatable. Wound colonization with
>100,000 organisms/gram tissue is an indication to
perform expedient eschar excision rather than to begin
antibiotics.
Clinically, any change in the patient’s general status
should lead to a high suspicion of sepsis. Possible changes
include unexplained hypotension, tachypnea, spiking
fevers above the patient’s daily baseline, tachycardia, new
onset of ileus, altered mental status, thrombocytopenia,
hyper- or hypoglycemia, hypoxia or hypothermia, and
decreased urine output or progressive leukocytosis with
“left shift,” including myelocytes and promyelocytes in the
peripheral smear. The development of hypothermia and
leukopenia are particularly ominous signs in the patient
who is clinically becoming septic and demand aggressive
intervention.
Pseudomonas aeruginosa and Staphylococcus aureus
are the dominant pathogens in burn centers. This is a
generalization only; it is more helpful for each burn
center to know and monitor its own resident flora.
Candida species are the most commonly isolated fungal
organisms recovered from burn patients; other fungal
infections are uncommon. Viral infections, particularly
with cytomegalovirus, are reported with increasing
frequency, though their clinical impact is undetermined.
There is little place for prophylactic antibiotic usage in burn
patients. Penicillin G used to be recommended for the first post
burn week to prevent group A beta-hemolytic Streptococcal burn
wound cellulitis. There is still arguably a place for this prophylaxis
if topical antibiotics are not used (e.g., with Biobrane), but several
studies suggest it is not necessary in addition to usual topical
antibiotic treatment.
Fungal infections are an uncommon but difficult problem. It is our
current practice to systemically treat burn patients with fungus found
in two sites (i.e., sputum, intravenous catheter tip, urine or wound).
This is most often Candida species and occurs two to three weeks
postburn. We have aggressively treated these patients with systemic
amphotericin B. This drug has a number of side effects. It has clearly
decreased morbidity and mortality from fungal infections. Delaying
treatment until fungemia occurs is associated with a high mortality
rate.
Other adjunctive measures may be necessary in the patient with lifethreatening infection. Adequate fluid must be given to maintain
intravascular volume and urine output. Invasive monitoring should be
added as the clinical situation demands. Often a change in topical
antibiotic or an increase in the frequency of wound care is added to
the management of the burn patient with invasive infection and a
large eschar burden. Certainly, if one topical agent has been used for
a long period, a change to another may be of benefit. In particular,
mafenide has a much greater ability to penetrate the burn wound
than other topical agents. It should be strongly considered in the
presence of invasive burn wound infection, keeping in mind its
When sepsis is suspected, support of the cardiopulmonary and GI
system should be of primary concern. Consideration should be given to
eschar debridement, depending on the character of the burn wound.
Empiric antibiotic therapy should be started after cultures are obtained.
Depending on the resident flora of a particular burn center, some
combination of agents to cover Staphylococcus aureus and gram
negative rods should be initiated. Aminoglycoside dosage requirements
are difficult to predict in burn patients; individualized therapy is
mandatory. Drug level monitoring is also advised for Vancomycin, which
is used increasingly for methicillin-resistant Staphylococcus aureus. It is
important to obtain culture results as soon as possible, including in vitro
sensitivities. These may not correlate with in vivo behavior. Antibiotic
therapy should then be targeted for the likely infecting organism(s). The
use of new antibiotics or untested combinations of antibiotics is
recommended only as part of an investigational study or with the
assistance of a physician fully versed in their usage and complications.
Order of excision
In the absence of significant inhalation injury, it is rare for burns to cause
significant infectious complications before the fifth through the tenth post
burn day. In the presence of a large burn, the highest priority is to diminish
the overall necrotic tissue load. Broad areas like the trunk and lower
extremities are given priority for excision. Lower priority is given burns on
the face and hands. They take more time to excise and cover with
autograft. Delayed excision of hands can result in very acceptable function
if accompanied by meticulous therapeutic assistance.
 In a major burn, the posterior trunk should be given high priority as the
first area to be excised. The patient is stable and will generally tolerate the
prone position better than later in his course. The posterior trunk and
buttocks are frequent sites of burn wound infection and are difficult to
inspect and keep well debrided; the flat, broad area lends itself well to
quick excision and grafting. Complete full-thickness burns of the back are
quite rare, due to the thickness of the skin. We therefore recommend
tangential excision for all but the most obvious full-thickness back burns
(for which excision to fascia is only rarely indicated).

Tangantial excision

Excision of full-thickness eschar may be assisted by
dressing the eschar with povidone-iodine foam 12 hours
prior to operation. This dehydrates the eschar and
makes it more physically amenable to tangential
excision. A variety of dermatomes (manual and
powered) may be used. Manual knives (e.g., Weck,
Goulian) are especially advantageous for small, irregular
surfaces, such as the hands and face, while a powered
dermatome can be used to remove quickly uniform
sheets of eschar from larger surfaces. Excision is
continued until punctate uniform brisk bleeding is seen.
If there is dermis left when this viable tissue level is
reached, it will be white and shiny. Gray, dull appearing
dermis is nonviable and will not support an immediatelyplaced skin graft. If the dermis is completely destroyed,
tangential excision should be continued into the
subcutaneous fat
Tangential excision can be performed under tourniquet
control. The cadaveric appearance of the tissues distal to
the inflated tourniquet makes differentiation of viable and
nonviable tissues difficult, but with experience this can be
appreciated. With concern about blood transfusions, this
technique is increasing in popularity. Tangential excisions
are bloody procedures, and adequate blood should be
available. We routinely type and cross-match six units of
packed red cells for major excisions of the trunk, four units
for each lower extremity and four units for each upper
extremity, including two units for hand excision alone (if
tourniquets are not used). Without a tourniquet, the best
method to limit blood loss is to work on only one area at a
time, completing that area before proceeding. Extremities
should be excised from distal to proximal so that hemostatic
compressive dressings applied after excision do not produce
a tourniquet effect.
Fascial excision




Fascial excision is another method of immediate excision: it is
reserved for limited indications. Fascial excision offers the following
advantages over tangential excision:
1. A viable bed for grafting is reliably provided.
2. Excision may be easily performed on extremities under
tourniquet control with decreased blood loss.
3. Less experience is required to obtain a good bed for grafting.
Fascial excision has a number of disadvantages. Excised fat does
not regenerate, and permanent cosmetic deformity, which can be
severe, is guaranteed—especially in obese patients. With
circumferential excision, there is a risk of distal edema and a 100%
risk of damage to superficial nerves and tendons. There is a greater
incidence of cutaneous denervation; loss of sensation may be
permanent. The fascia over joint surfaces such as the elbow, knee,
and ankle is relatively avascular, and eventual flap coverage may be
required in these areas.
Operative treatment
Improvements in resuscitation consistently
present the burn surgeon with patients who
are physiologically stable 48–72 hours
postburn. These patients carry a variable
load of dead tissue in immediate contact
with healthy (or injured but potentially
salvageable) tissue. Leaving this eschar in
situ and waiting for separation due to
autolysis to occur violates many surgical
principles of debridement developed in the
16th century by Paré
physiologically stable 48–72 hours
postburn. These patients carry a variable
load of dead tissue in immediate contact
with healthy (or injured but potentially
salvageable) tissue. Leaving this eschar in
situ and waiting for separation due to
autolysis to occur violates many surgical
principles of debridement developed in the
16th century by Paré

In 1970, a Yugoslavian plastic surgeon, Janzekovic,
published a short paper in the Journal of Trauma. Using
the knowledge that deep donor sites could be
overgrafted successfully with thinner autografts to
hasten their healing and improve their appearance, she
applied this technique to dermal burns by repeatedly
shaving layers of burned dermis until she reached a
viable-appearing bed. She covered this with an
immediate autograft. She reported that graft take was
excellent and provided a clean, closed wound. Most of
the burns she treated in this way were small, but, in her
opinion, the hospital stay-related pain and need for
reconstructive procedures decreased dramatically. She
reported that “esthetic disability” was also greatly
reduced.

Burke and associates in Boston also developed an active
program of early excision and grafting in the early 1970s.
Long-term results were much better in their aggressively
operated group of patients. Controversy still surrounded
the procedure in the late 1970s, however. Though there
was general agreement that small full-thickness burns
could be safely excised and grafted with good results, the
issue of deep dermal burns had not been resolved. A
prospective randomized study was performed at the
University of Washington. Results clearly showed that
early excision and grafting of indeterminate burns of
<20% TBSA was superior to spontaneous healing. It
decreased hospital stay and cost and decreased the need
for secondary reconstruction. These patients returned to
work twice as fast as the nonoperative group.

Burke and associates in Boston also developed an active
program of early excision and grafting in the early 1970s.
Long-term results were much better in their aggressively
operated group of patients. Controversy still surrounded
the procedure in the late 1970s, however. Though there
was general agreement that small full-thickness burns
could be safely excised and grafted with good results, the
issue of deep dermal burns had not been resolved. A
prospective randomized study was performed at the
University of Washington. Results clearly showed that
early excision and grafting of indeterminate burns of
<20% TBSA was superior to spontaneous healing. It
decreased hospital stay and cost and decreased the need
for secondary reconstruction. These patients returned to
work twice as fast as the nonoperative group.

Skeptics of this procedure have continued
to maintain that mortality is not improved
in large burns treated in this way. The
reasons for this are threefold. First, as yet
no ideal skin substitute has been
developed. This means that in large burns,
while the eschar can be excised in a timely
manner, permanent and reliable wound
closure still cannot be performed
simultaneously.

The second reason is that burns of >70%
TBSA or burns in the elderly are complex
injuries with multi-factorial deleterious
effects on multiple organ systems that
lead to morbidity or death. In this setting,
reduction of the bacteriologic load from
eschar excision may, in fact, not be
enough to decrease overall mortality.
Further, the number of patients with these
severe injuries is small.

Several important points should be kept in mind.
First, small burns that will eventually heal should
be able to be excised with 0% operative
mortality. This implies that early excision
requires an experienced surgeon. Inadequate
excision and skin grafting will lead to skin graft
loss, adding the size of the donor site to the total
wound area. This may necessitate another
operation. Second, non-life-threatening burns in
patients with other medical problems should not
be excised until the associated problems are
under control so that the operation is associated
with no mortality and minimal morbidit
Complications



Pulmonary
Bronchogenic infections or pneumonia occur frequently, usually
accompany inhalation injury, and are commonly due to the
organism colonizing the burn wound. Prophylactic corticosteroid
therapy is detrimental, and preventive antibiotics are probably
ineffective after inhalation injury. Daily sputum cultures are
appropriate in the susceptible patient and dictate the choice of
antibiotic if pneumonia does occur. Attention to pulmonary therapy
and toilet is also indicated.
The adult respiratory distress syndrome occurs frequently in
thermally injured patients, but is particularly difficult to distinguish
from inhalation injury. In addition, cardiogenic pulmonary edema,
bronchopneumonia, and severe tracheobronchial infection need to
be excluded. The typical chest radiographic findings and pulmonary
gas-exchange abnormalities usually confirm the diagnosis in the
absence of significant inhalation injury and infectious processes.
Treatment is supportive, as in other critically ill patients with
associated organ failures. Pulmonary toilet is particularly important
in these patients.


Gastrointestinal and biliary
Curling first noted the association between
bleeding duodenal ulcers and burn injury in
1842. The incidence of diagnosed gastric or
duodenal ulceration in burn patients was about
10 per cent in 1970; however, ulcer-related
complications have markedly decreased in the
last decade, probably due to the advent of
continuous tube feedings and exacting control of
gastric pH. The pathophysiology of the initial
mucosal injury appears to be related to mucosal
hypoxia, which increases susceptibility to
damage by normal concentrations of gastric
acid. This hypoxia may be due to diminished
organ blood flow or submucosal arteriovenous
shunting

The other notable gastrointestinal complication
is impaired motility involving the gastrointestinal
tract and the biliary system. Acute gastric
dilation and intestinal paralytic ileus are
commonly seen; they are probably the result of
frequent anesthesia, sepsis, fluid overload, and
electrolyte imbalances. Delayed gastric emptying
and ileus frequently limit the success of enteral
alimentation. Acute acalculous cholecystitis is
common in these critically ill patients. It usually
manifests as sepsis, pain and mass in the right
upper quadrant, and abnormalities of liver
function. An ultrasonographic examination or
radionuclide scan usually supports the diagnosis.
Cholecystitis can often be treated by antibiotics
plus percutaneous cholecystostomy, or
laparoscopic or open cholecystectomy.


Renal
Acute renal failure may be secondary to hypoperfusion
and hypoxia occurring before plasma volume was
replaced in resuscitation. Failure may also be
exacerbated by precipitation of free hemoglobin from
damaged red blood cells or muscular myoglobin from
crush or electrical injuries; or it may be a result of
nephrotoxic drugs, particularly antimicrobial agents, that
are administered to these patients. These insults may
also be superimposed on pre-existing renal compromise.
Oliguric or nonoliguric acute tubular necrosis can result,
with the additive attendant clinical problems of acute
renal failure in combination with management of the
burn injury. Careful attention to intravascular volume will
minimize renal dysfunction.
Cardiovascular
 Congestive heart failure occurs either in
the acute phase of the burn injury or
during the mobilization of the peripheral
edema. Endocarditis may also complicate
burn sepsis and should be kept in mind as
an infrequent cause of infection. The use
of digitalis and antiarrhythmics may
become necessary in specific patients.
Rapid atrial fibrillation is a common
arrythmia in elderly patients during burn
resuscitation.

Neurologic
 Burn encephalopathy encompasses a wide
range of syndromes of cerebral
compromise whose causes include water
intoxication, acute hypertension, drug
narcosis, septicemia, hyperpyrexia,
electrolyte shifts, and dehydration.
Autopsy at the endstage of this
encephalopathic picture reveals cerebral
edema and uncal or cerebellar herniation

 Scaring
Hypertrophic scars
keloid scars
H.T.S.KELOIDS-
INTERMEDIATENORMAL-
ACTIVITY
0
3/12
6/12
1
2
ACTIVITY OF DIFFERENT TYPES
OF SCARS IN RELATION TO TIME