Burn injury

SMF BEDAH RS AHMAD YANI METRO

AULIA AGRISTIKA
DIKA YUNISA
TEGAR DWI PRAKOSO
TIARA CHINTIA

Burns exert a catastrophic influence on people in

terms of human life, suffering, disability, and
financial loss. More than an estimated 2 million
people in the United States experience burn injuries,
most of which are minor and cared for primarily in
the ED. In 1991, burn injuries resulted in 5053
deaths. Approximately 1.4 million persons in the
United States sustain burn each year; an estimated
54,000 to 180,000 are hospitalized. Work-related
burns account for 20-25% of all serious burns.

Burn injuries result from a variety of causes. Scald burns are the most common

cause of burn injury in the civilian population. The depth of scald burn is
related to the temperature of the liquid, the duration of exposure to
the liquid (Table 17.1), and the viscosity of the liquid (there is usually
prolonged contact with more viscous liquids). Scald burns will typically heal
without the need for skin grafting. Grease burns, however, tend to result in
deeper dermal burns and will occasionally require surgical management.
Flame burns, the next most common cause of burn injury, typically result
from house fires, campfires, and the burning of leaves or trash. If the patients
clothing catches fire, burns are usually full thickness. Flash burns also are quite
common and typically result from ignition of propane or gasoline. Flash
burns typically injure exposed skin (most commonly face and extremities) and
usually result in partial-thickness burns. Contact burns occur from contact
with woodstoves, hot metals, plastics, or coals. Contact burns are usually deep
but limited in extent. In addition, burn injury can result from electrical and
chemical agents.

 Burn Depth

Burned patients' survival is related to the following factors: burn size/depth, age,
presence of inhalation injury, and patient comorbidity. Depth of burn injury is usually
classified according to degrees.
First-degree burns
In first-degree burns, minor epithelial damage of the epidermis exists. Redness,
tenderness, and pain are the hallmarks of this injury. Blistering does not occur, and 2point discrimination remains intact. Healing takes place after several days without
scarring. Because the epidermal barrier remains intact, metabolic response and risk of
infection are minimal. Most common causes of first-degree burns are flash burns and
sunburns.
Second-degree burns
Superficial partial-thickness and deep partial-thickness burns are the 2 types of
second-degree burns. In these burn injuries, some portion of the skin appendages
remains viable, allowing epithelial repair of the burn wound without skin grafting.
Superficial partial-thickness burn involves the epidermis and superficial (papillary)
dermis, often resulting in thin-walled, fluid-filled blisters. These burns appear pink,
moist, and soft and are exquisitely tender when touched by a gloved hand. They heal in
approximately 2-3 weeks, usually without scarring, by outgrowth of epithelial buds
from the viable pilosebaceous units and sweat glands residing in the papillary and
reticular dermis.

Deep partial-thickness burns extend into the reticular dermis. Skin color is
usually a mixture of red and blanched white, and capillary refill is slow.
Blisters are thick-walled and commonly ruptured. Two-point discrimination
may be diminished, but pressure and pinprick applied to the burned skin
can be felt. Superficial partial-thickness burns usually re-epithelialize 7-10
days after injury. Risk of hypertrophic scarring is very small. For deep
partial-thickness burns, tissue may undergo spontaneous epithelialization
from the few viable epithelial appendages at this deepest layer of dermis
and heal within 3-6 weeks (if no infection arises).
Because these burns have less capacity for re-epithelializing, a greater
potential for hypertrophic scar formation exists. In deep partial-thickness
burns, treatment with topical antimicrobial dressings is necessary to
prevent infection as the burn wound heals. Contraction across joints, with
resulting limitation in range of motion, is a common sequela. Splash scalds
often cause second-degree burns

Third-degree burns

Third-degree burns are full-thickness burns that destroy both

epidermis and dermis. The capillary network of the dermis is
completely destroyed. Burned skin has a white or leathery appearance
with underlying clotted vessels and is anesthetic. Unless a third-degree
burn is small enough to heal by contraction (< 1 cm), skin grafting
always is necessary to resurface the injured area. Immersion scalds,
flame burns, and chemical and high-voltage electrical injuries cause
third-degree burns.
Fourth-degree burns
Fourth-degree burns cause full-thickness destruction of the skin and
subcutaneous tissue, with involvement of the underlying fascia, muscle,
bone, or other structures. These injuries require extensive debridement
and complex reconstruction of specialized tissues and invariably result
in prolonged disability. Fourth-degree burns result from prolonged
exposure to the usual causes of third-degree burns.

 Burn size

The "rule of nines" is a practical technique for estimating the extent of TBSA involved
in a burn injury. This approach divides the major anatomic areas of the body into
percentages of TBSA. For the adult, it allots 9% of the TBSA to the head and neck and
to each upper extremity, 18% each to the anterior and posterior portions of the trunk,
18% to each lower extremity, and 1% to the perineum and genitalia. The patient's palm
area represents approximately 1% of TBSA and can be helpful in calculating scattered
areas of involvement.
In estimating the extent of burn injury, the extent of involvement of each anatomic
area (eg, an arm or leg) must be calculated separately, and the total is derived from the
simple addition of the burned anatomic sites. A small difference between TBSA of the
adult and infant reflects the size of the infant's head (18%), which is proportionally
larger than that of the adult, and the lower extremities (14%), which are proportionally
smaller than those of the adult. Lund-Brower charts with age-appropriate diagrams
can be used to better estimate the area of burn injury in children. Remember that firstdegree burns are not included in the calculation of burn size.
A study by Swords et al suggested that in children transferred from a referring
institution to a burn center, the referring institution often overestimates the patients
burned TBSA, leading to overresuscitation. The investigators found that the average
burned TBSA estimated by referring institutions was 15.5%, compared with an average
of 9.5% at the burn center in the study to which pediatric patients were sent. In
addition, overestimation of burned TBSA of at least 5% was found to be associated with
overresuscitation by at least 10 mL/kg.[17]

Age and burn size

A direct but inverse relationship exists between age and survival for any
burn size. While the mortality of a 40% TBSA burn in a 20-year-old
patient is approximately 8%, the mortality of this same injury in someone
older than 70 years is 94%. The higher mortality of older patients with
burn injuries is attributed to their preexisting medical conditions,
including cardiac, pulmonary, renal, and hepatic dysfunction. Similarly,
children younger than 1 year survive large burns at a reduced rate.
When possible, make an attempt to further subdivide TBSA into partialthickness and full-thickness percentages to facilitate patient
categorization and subsequent management. Depth of burn injury can be
evaluated by numerous techniques, including burn wound biopsy, vital
dyes, ultrasound studies, fluorescein fluorometry, thermography, light
reflectance, MRI, and laser Doppler flowmetry. Most of these techniques
are not used in standard practice, but laser Doppler and light reflectance
show promise in measuring depth of burn injury.

Patient categorization

Severity of burn injury depends on (1) extent, depth, and location of burn injury;
(2) age of patient; (3) etiologic agents involved; (4) presence of inhalation injury;
and (5) coexisting injuries or preexisting illnesses. The American Burn Association
has used these parameters to establish guidelines for the classification of burn
severity.[18] This classification creates 3 categories of burn injury (major, moderate,
minor) and defines the optimal setting for the management of each.
Major burn injury
Major burn injury is defined as partial-thickness burns involving more than 25%
of TBSA in adults or 20% of TBSA in children younger than 10 years or adults
older than 50 years; full-thickness burns involving more than 10% of TBSA; burns
involving the face, eyes, ears, hands, feet, or perineum that may result in
functional or cosmetic impairment; burns caused by caustic chemical agents; highvoltage electrical injury; burns complicated by inhalation injury or major trauma;
or burns sustained by high-risk patients (those with underlying debilitating
diseases). These injuries are best managed in a specialized burn center staffed by a
team of professionals with expertise in the care of burn patients, including both
acute care and rehabilitation.

Moderate burn injury

Moderate burn injury includes partial-thickness burns of 15-25% of TBSA

in adults or 10-20% of TBSA in children or older adults, and full-thickness
burns involving 2-10% of TBSA that do not present serious threat of
functional or cosmetic impairment of the eyes, ears, face, hands, feet, or
perineum. This category excludes high-voltage electrical injury, all burns
complicated by inhalation injury or other trauma, and burns sustained by
high-risk patients. Patients with moderate burn injuries should be
hospitalized for their initial care but not necessarily at a burn center.
Minor burn injury
Minor burn injury includes burns involving less than 15% of TBSA in
adults or 10% of TBSA in children or older persons, and full-thickness
burns involving less than 2% of TBSA that do not present a serious threat
of functional or cosmetic risk to eyes, ears, face, hands, feet, or perineum.
These burns usually can be managed safely in the outpatient setting

Determination of Burn Extent

The extent and depth of burn wounds are established shortly following

admission. There are several techniques used to calculate the total body surface
area (TBSA) burned. When calculating TBSA, only include those areas of
partial- and full-thickness dermal injury. Superficial burns involving the
epidermis only are not included in the calculation. The rule of nines (Fig.
17.1) is the best-known method of estimating burn extent. However, it is
important to note that the proportions of infants and children are different
from those of adults. The heads of children tend to be proportionately greater
than 9% TBSA, and the lower extremities tend to be proportionately less than
18%. In addition, it is important to explain to the inexperienced person that the
percentage assigned to a body part represents a total area, so that a portion of
an arm burn is only a portion of 9%.
A second technique of estimating TBSA uses the patients hand. The

patients hand represents approximately 1% TBSA and total burn size can be
estimated by determining how much of the patients (not the examiners)
hand area is burned. Lund and Browder charts are a more accurate
method of assessing burn extent. They provide an age-based diagram to
assist in more precisely calculating the burn size (Fig. 17.2).

 Deep partial-thickness burns involve the entirety of the epidermis and extend into

the reticular portion of the dermis. These burns are typically dry and mottled pink
and white in appearance and have variable sensation. If protected from infection,
deep partial-thickness burns will heal within 3 to 8 weeks, depending on the number
of viable adnexal structures in the burn wound. However, they will typicall heal with
contraction, scarring, and possible contractures. Therefore, if it appears that the
wound will not be completely re-epithelialized in 3 weeks, operative excision and
grafting is recommended.
Full-thickness burns involve the epidermis and the entirety of the dermis. These

wounds are brown-black, leathery, and insensate (Fig. 17.4). Occasionally, fullthickness burn wounds have a cherry-red color from fixed carboxyhemoglobin in
the wound. These wounds can be differentiated from more superficial burns because they
are usually insensate and do not blanch. Full-thickness burns are best treated by
excision and grafting, unless they are quite small (size of a quarter).

Determination of burn depth is usually easy for superficial

and very deep wounds. However, determining the depth of
deep dermal burns and their healing potential can be more
challenging. It often takes several days to determine which
wounds will heal within 3 weeks and which would be
better managed with excision and grafting. A variety
of techniques have been described for precise
determination of burn depth, including fluorescein dyes,
ultrasound, laser Doppler, and magnetic resonance
imaging. However, none of these methods have proved to
be more reliable than the judgment of an experienced burn
surgeon.

Fluid Resuscitation
Percent TBSA
All patients with a major burn injury must be subjected to fluid resuscitation that is
influenced by the percent TBSA as well as the presence of inhalation injury. Patients
with burn wounds smaller than 20% TBSA can be treated with a combination of oral
and IV fluid. For larger burns, the Parkland formula and its variations have become
the standard method for resuscitating the burned patient.
Moderate burn victims should have at least one large-bore intravenous line placed
through unburned skin, and severe burn victims should have at least 2 lines initiated.
If necessary, venous catheters may be placed through burned skin or via venous
cutdown using the saphenous vein at the groin or ankle. When a burn patient requires
considerable fluid resuscitation or has evidence of cardiopulmonary disease, a central
venous line is indicated. Patients with massive burns or respiratory injury and elderly
patients with severe burns or cardiac disease should be monitored with a Swan-Ganz
catheter to avoid fluid overload or inadequate replacement of volume.
Microvascular injury caused by a burn leads to increased vascular permeability with
edema formation that results in ongoing plasma volume loss. Maximal edema
formation occurs at 8-12 hours after burn injury for small burns, and 24-48 hours for
large burns. The purpose of fluid resuscitation is to restore effective plasma volume,
avoid microvascular ischemia, and maintain vital organ function. The amount of fluid
required varies with the patient's age, body weight, and extent of burned TBSA.

Crystalloid
The Parkland formula, as described by Baxter, is still the most commonly
used method for estimation of fluid requirements (Table 17.4). The formula (4
cc weight in kilograms %TBSA) provides an estimate of fluid required for 24
hours. The fluid administered should be lactated Ringer (LR) solution. LR is
relatively hypotonic and contains sodium, potassium, calcium chloride, and
lactate. Sodium chloride is not used because of the risk of inducing a
hyperchloremic acidosis. Half the calculated fluid resuscitation should be
administered over the first 8 hours, and the second half administered over the
next 16 hours. Children who weigh less than 15 kg should also receive a
maintenance IV rate with dextrose-containing solution because young children
do not have adequate glycogen stores.
It is important to remember that the formula provides merely an estimate of fluid
requirements. Fluid should be titrated to achieve a urine output of 30 cc/hr in
adults and 1 cc/kg/per hour in children. A Foley catheter should be used to
accurately track urine output. If urine output is inadequate, the fluid rate should
be increased; conversely if the urine output is greater than 30 cc/hr, the fluid rate
should be decreased. Fluid boluses should only be used to treat hypotension, and
should not be used to improve urine output. Patients with deeper, fullthickness burns
and patients with inhalation injury tend to require higher volumes of resuscitation.

Ideally, weigh the patient on a scale. In the absence of this measurement, obtain an

estimate of the patient's weight from the patient, a relative, or the patient's driver's
license. Carefully map the burned areas over the entire body, including the back, to
estimate fluid requirements during the first 48 hours after injury. Typically, burns
greater than 20% of TBSA require intravenous fluid resuscitation because the
accompanying GI ileus precludes sufficient oral intake.
Different formulas for fluid resuscitation
Several different formulas for fluid resuscitation have been recommended, although all uniformly
emphasize that adequate resuscitation is evidenced by a normal urinary output (1 mL/lb/h in
children younger than 2 years, 0.5 mL/lb/h in older children, at least 30-40 mL/h in adults), a
normal sensorium, and stable vital signs.
A recent survey of burn units in the United States and Canada demonstrated that 78% of the
centers used the Parkland formula to estimate resuscitation volume and that lactated Ringer
solution was the most popular type of fluid.[19] In marked contrast, the last United Kingdom survey
revealed that most burn units used human albumin solution and the Muir and Barclay formula to
estimate resuscitation volumes.[20] Following the publication of the findings of the Cochrane
Injuries Group Albumin Reviewers, much discussion has ensued regarding the use of human
albumin solution in patients who are critically ill.[21] In 2007, Baker et al reported that resuscitation
of patients with thermal injuries in burn units in the United Kingdom and Ireland is fairly
consistent with a shift to crystalloid resuscitation rather than the use of human albumin solution.
[22]

 The Parkland formula for fluid resuscitation of burn

patients is used as follows: lactated Ringer solution (4

mL/kg/% TBSA burned) is administered intravenously in
the first 24 hours, one half given in the first 8 hours, and
the other half administered over the next 16 hours.
Calculate fluid loss from the time of injury, and take into
account the fluid administered by prehospital personnel for
fluid replacement.

Strict adherence to a formula for fluid resuscitation does not

guarantee successful fluid therapy. If the patient does not appear to

be responding to resuscitation or signs of impending cardiac failure
are present (eg, progressive central venous pressure elevation,
pulmonary congestion, increasing edema with decreased urinary
output), insertion of a Swan-Ganz catheter for measurement of
pulmonary artery pressure and cardiac output is advisable.
During resuscitation, the most common error is overhydration,
which increases the risk of acute respiratory distress syndrome
developing 3-5 days postburn. In burn patients with concomitant
large TBSA burns and inhalation injury, the Parkland formula may
result in unnecessarily large fluid loads. To avoid overhydration,
resuscitate patients with inhalation injuries with substantially less
than formula predictions, with acceptance of a urinary output in the
range of 0.3-0.5 mL/kg/h.

TOPICAL WOUND AGENTS

Following admission to the burn center, the patients wounds should be

cleansed with soap and water. Loose tissue and blisters should be
debrided. Body and facial hair should be shaved if involved in the area of
a burn. Daily wound care should occur on a shower table with soap and
tap water, or if the burn wound is small, at the patients bedside
following a shower. The use of tanks for wound care is disfavored
because of the risks of cross-contamination.
Burn injury destroys the bodys layer of protection from the

environment, and dressings are needed to protect the body from

infection and minimize evaporative heat loss from the body. The
ideal dressing would be inexpensive, easy to use, require infrequent
changes, and be comfortable. Although a number of topical agents are
available for burn wound care, it is best to have a simple, well-reasoned
wound care plan.

 The choice of topical burn wound treatment is contingent on the depth of

burn injury and the goals of management. Superficial burn wounds (such
as sunburns) require soothing lotions such as aloe vera that expedite
epithelial repair. Partialthickness burn wounds need coverage with
agents that keep the wound moist and provide antimicrobial protection.
Deeper partial-thickness burn wounds should be covered with agents
that protect the eschar from microbial colonization. Once the eschar has
lifted, and the wound has begun to epithelialize, a dressing that
optimizes epithelialization (e.g., greasy gauze and antibiotic ointment)
should be used. Full-thickness burns should also be covered with a
topical agent that protects the burn wound from getting infected
until the time of burn excision.
It

is important to emphasize that prophylactic systemic

antibiotics have no role in the management of burn wounds. In
fact, the use of prophylactic antibiotics increases the risk of
opportunistic infection. Because burn eschar has no microcirculation
there is no mechanism for the local delivery of systemically administered
antibiotics. Consequently, topical agents need to provide broad-spectrum
antimicrobial coverage at the site of colonizationthe eschar.

In the early postburn period, the dominant colonizing organisms

are staphylococci and streptococcitypical skin flora. Over time,

however, the burn wound becomes colonized with gram-negative
organisms. Thus, topical antimicrobial agents used in early burn
care should have broad-spectrum coverage to minimize
colonization of the wound, but they need not be able to penetrate the
burn eschar deeply.
Silver sulfadiazine is the most commonly used topical antimicrobial

agent. Silver sulfadiazine has broad-spectrum antimicrobial coverage,

with excellent staphylococcus and streptococcus coverage. However,
silver sulfadiazine does not penetrate an eschar and is therefore
less useful in the management of an infected burn wound. Wounds
treated with silver sulfadiazine develop a yellowish-gray pseudoeschar
that can be easily cleansed during daily wound care. Traditionally, the
principal drawback of silver sulfadiazine was thought to be
leukopenia. However, it is not clear whether the leukopenia that occurs
results from silver sulfadiazine toxicity or from the margination of
leukocytes as part of the bodys systemic inflammatory response to the
burn injury.

Regardless, the leukopenia is typically self-limited and, therefore, the silver

sulfadiazine should not be discontinued. Patients with a documented sulfa allergy

may or may not have a reaction to the silver sulfadiazine. If there is concern about an
allergy, a small test patch of silver sulfadiazine can be applied. Typically, if there is an
allergy, the silver sulfadiazine will cause irritation rather than be soothing, as is usually
the case. In addition, a rash could signal a silver sulfadiazine allergy.
Mafenide is another commonly used antimicrobial agent. Mafenide is available as a

cream and, more recently, a 5% solution. Mafenide, like silver sulfadiazine, has a broad
antimicrobial spectrum, including gram-positive and gram-negative organisms. In
addition, mafenide readily penetrates burn eschar, making it an excellent agent for
treating burn wound infections. Mafenide is commonly used on the ears and the nose
because of its ability to protect against suppurative chondritis; however, silver
sulfadiazine appears to be equally effective in this setting. Because mafenide penetrates
eschar well, twice-daily administration is typically necessary. Mafenidesoaked gauze can
also be used as a dressing for skin grafts that have been placed over an infected or
heavily colonized wound bed. There are two well-recognized drawbacks of mafenide.
Mafenide is a potent carbonic anhydrase inhibitor that can cause a metabolic acidosis,
which can confound ventilator management. In addition, the application of mafenide
can be painful, which may limit its use in partial-thickness burnwounds.

Significant burn injury not only results in local tissue injury, but initiates a
systemwide response that can impact nearly every organ system. The release of
inflammatory mediators (including histamine, prostaglandins, and cytokines) can lead to
decreased cardiac output, increased vascular permeability, and alteration of cell
membrane potential. In fact, for many decades there was believed to be a myocardial
depressant factor that decreased the cardiac output in the first several days following
burn injury. This decrease in cardiac function is likely caused by any number of
cytokines. The purpose of fluid resuscitation is to provide adequate replacement for fluid lost
through the skin and fluid lost into the interstitium from the systemic capillary leak that occurs
as part of the bodys inflammatory response. Therefore, significant volumes of intravenous fluid
may be required to maintain adequate organ perfusion.
Multiple organ dysfunction syndrome (MODS) has been the difficulty in clinical treatment of
severe burns. In the 1990s the incidence rate of MODS was 28,1% in severe burns patients,
while the mortality rate was as high as 78-98% (Huang, et al; 1998) . MODS was caused by two
attacks: the fist was the early plasma leakage and the effective circulating blood volume
reduction, as resulted in the systemic hypoxic-ischemic damage; the second attack was the
invasion of consequent systemic inflamatorry response and sepsis on the organs (sheng, 2002).
With the enhanchment of the clinacal treatment of burn, the present point of view argues that
the key to prevention of MODS is againts the first attack, ie, to control the burn shock which
can effectively prevent or mitigate the second attack to reduce the incidence of MODS (Sheng,
2002).

Early change of cardiac function after severe burn

In the early 1960s, Fozzard observed myocardial damage and cardiac

output decrease in the burn patient and further found that this kind of the
heart failure was not due to pre-injury heart disease or excessive fluid
infusion (Fozzard, 1961). Some sholars attributed the cardiac dysfuntion to
the vascular leakage of plasma into the injury area, causing decreased
venous return and -cardiac pre-load reduction (Evans, et al., 1952)
In 1984, Adams et al established a guinea pig burn model to study the
systolic and diastolic function changes of the left ventricle after the injury.
They found that when the burn injury axceeded 47% of the total body
surface area (TBSA), the ventricular compliance was reduced and the
cardiac isovolumic relaxation period extended, accompanied by significant
myocardial contractile dysfunction, based on which they viewed that
inherent myocardial damage led to the decrease of the adverse cardiac
filling and ejection fraction of the left ventricle (Adam, et al., 1984)

Cardiac dysfunction after severe burns has been confirmed in many experimental studies.

However, the myocardial systolic/diastolic dysfunction occurred in different time post-burn

in different spesies animals models including mice, rats, hamster, guinea pigs, rabbits, dog,
sheep.
Horton et al, studied time course of heart function of the rabbits and rats after burn by
dissecting the heart for in-vitro perfusion at each time point. The result showed a transient
decrease of the cardiac function after burn, which first appeared at 2 hours, decreased
continually within 24-30 hours and gradually recovered at 48-72 hours after burn injury.
This short-term decreased heart function may be less risk for the otherwise healthy young
adult with burn but, may be so risky for the young, the elderly and the immunocompromise
patients that they had to receive unafforadable fluid resuscitation. Recent studies also show
that the cardiac dysfunction aftre burn is an index for predicting the proneness to secondary
infection, ie, it is closely related with morbidity and mortality of MODS in severelly burned
patients and can predict the long-term infection complication.
Therefore, we can be sure that the cardiac dysfunction soon after severe burns was cause by
myocardial cell damage and myocardial systolic/diastolic dysfunction of the heart itself
rather than the burn shock, as is worthy of further study and exploration on these
endogenous mechanisme

Organ Perfusion at early stage following severe

burn
Severe burn induced a strong stress response and high

excitement of the symphatetic adrenal medula system.

The chatecolamines secreted by the symphatetic adrenal
medula system can adjust the heart excitement, the
peripheral vascular resistance and the capacitance vessels
so the blood supply to tissue and organ at the shock stage
becomes more aduquate and reasonable. However, the
anatomy, phisiology, and tolerance to ischemia and
compensatory ability differs in various organ. which lead,
to different blood supply of the main organs including
heart, brain, liver, kidney, and intestine after severe burn.

Heart

The traditional pathophysiological view was that under severe stress conditions,
especially reduction of the effective circulating blood volume, the body reduced the
blood supply of most abdominal organs and gave priority to ensuring the blood supply
of the heart, brain, and the other vital organs. However, a lot experiments conducted in
our laboratory confirmed no effective protection of myocardial blood supply after severe
burn. Moreover, the earlist time point for determination of the myocardial blood flow
was at 1 hour after injury, which was the same time that cardiac function to decline.
The myocardial blood flow was rapidly reduced 10 minute after burn, which may be
related to the contraction of the coronary caused by myocardial renin-angiotensin
system (RAS) that was activated immediately after burn. The subsequent rebound
increase of the blood perfusion may be due to accumulation of hypoxic metabolites that
offset or exceeded the vascular contraction effect of Ang II and finally caused
vasodilation.
In fact, under continuos increase of the Ang II, the compensatory mechanism of the
heart itself was difficult to maintain too long and turned into decompensation about 3
hours post-birn, with continual decrease of the myocardial blood flow. Thus, the
myocardial blood flow was reduced before cardiac dysfunction

Brain

Currently, there has seldom reported the cerebral blood flow perfusion at early
stage after severe burns. But the cerebral edema was often complicated clinically
after burns, the pathological factors for which was different from brain trauma or
brain damage simply caused by brain trauma or hypoxia. The complicated
cerebral edema after burns is due to destructed microcirculation and blood brain
barrier function as well as increased permeability resulted from a variety of factors
including ischemia and hypoxia, cell medium, endotoxin, electrolyte imbalance,
acidosis and uncontrolled inflamation, which ultimately caused diffuse tissue
edema. The vascular endothelial cell played key role in the pathogenesis of brain
edema after burn. On the one hand, the vascular endothelial cell had clear
morphological changes, even formation of cracks and endothelial cell loss leading
to the semi-permeable membrane barrier dysfunction and vascular permeability
increase. On the other hand, the vascular endothelial cells could release a variety
of media to further promote the microcirculation disorder, aggravate tissue
ischemia and hypoxia and promote development of the tissue edema.

 Reduced perfusion and hypoxic-ischemic injury of the liver, kidney

and intestine
Catecholamines in the blood at early stage after burns was increased
tens even hundreds times more than that in the normal time. The
small blood vessels in the abdominal organs and kidney had rich
sympathetic excitement and catecholamine increase, the
microvascular contraction of these organs significantly increased
precapillary resistance and sharply decreased the microcirculation
perfusion. While the B-adrenergic reseptor stimulation opened the
arterial-venous anastomosis, which resulted in increase od the
microcirculation non-nutritive blood flow, decrease of the nutritional
blood flow and severe tissue ischemia and hypoxia in addition, a
great deal of Ang II produced by the activated circulation system
RAS was also involved in the vasocontriction.

 The blood flow changes differed significantly in different organs, ie, the

blood flow was reduced the most significantly in the kidney, followed by the
intestine and the liver the least. Judging from recovery, the liver restored the
blood flow better 24 hours after burn, while the kidney and intestinal
ischemia were still under serious conditions especially the intestines, which
may be due to so called covert compensated ie, the blood supply was
difficult to recover even quite a long time after adequate systemic blood
supply. Liver blood supply has it own peculiarities, the portal vein and
hepatic artery converged in to the hepatic capillary network and
subsequently returned to heat via the hepatic vein. Under the resting state
20% of the cardiac output entered into liver, of which 1/3 passed by the
hepatic artery and 2/3 by the portal vein. Liver cells are extremely sensitive
to the ischemia and hypoxia, easy inducing the liver cell damage. The central
lobular hepatocytes received less blood flow than the peripheral cells of the
lobule and it suffered the earliest and the most serious damage. Visceral
injury was closely related to the circulatory state especially the microcirculation after burn. After the ischemic phase, the substrate concentration
of the intracelullar xanthine oxidase was increased, which prompted the
substrate transforming to the xanthine oxidase via proteolysis or histamine.
During the course of reperfusion, a large number of free radicals were
produced with the improvement of hypoxia and finally induced injury.

that ALT was increased at 1 hour and reached the peak at 12 hours
after burn and that AST began to increased at 6 hours and continued
to 48 hours after burn. The increase of blood AST and ALT was the
inevitable result of serious liver parenchyma damage, indicating tha
burns can cause liver damage and progressive agravation in a
relatively short period of time.
In the normal adult, kidney is body organ with the largest blood flow,
with 1000-1250ml/min, accounting for 20-25% of cardiac output. The
renal damage at burn shock stage is primarily due to sharp decline of
the blood volume, reduction of the cardiac output and decrease of the
renal blood flow. The heart failure induced by severe burns would
directly result in of effective circulating blood volume decrease, the
sympathetic excitement and redistribution of systemic blood, which
affected the renal blood flow most with reduction of glomerular blood
flow and filtration 30-50% or less of the normal when the below 60
mmHg.

The nerve-humoral regulation early after burn induced redistribution of the

blood and the gastrointestinal hypoperfusion lasted for the longest. 80% and
60%. A 10% decrease of systemic blood volume may lead to 40% decrease of
the whole gastrointestinal tract blood flow. The vascular loop of the
intestinal vili was with an extremely bent ring structure, which contributed
to a short circuit exchange of the central villus arterioles with the venulues
and capillaries. Under shock and low perfusion state, the short circuit
exchange increased to further reduce the oxygen supply of the villus top. The
intestinal tissue had high metabolic rate and demanded great deal of the
oxygen , indicating that the intestinal tissue was sensitive to ischemia and
hypoxia and easy to be the damaged, with slow recovery. Under stress state,
the mucosal partial pressure of oxygen was decreased but the lactid acid
levels significantly increased, the latter of which, during the ischemiareperfusion process, released large amounts of the oxygen free radicals that
were the initiating factor for inflammatory mediators and cytokines cascade.

The burn resulted in up-regulation of variety of proteins regulating the

stress response, reduction of sel-repair ability of the intestinal mucosa
by free radical damage, energy metabolism disorder of the intestines,
increase of cell apoptosis.
Cytoskeletal damage of the intestinal lymph node cells destructed the
intestinal immune barrier. Which may cause damage to the intestinal
bacterial translocation and even endotoxemia. The intestinal
ischemia-reperfusion injury caused waterfall-like cascade of
inflammatory mediators by the way of p38/mitogen activated protein
kinase, as made the intestine as the source of systemic inflammatory
response syndrome (SIRS). The uncontrolled development of SIRS
would inevitable lead to MODS or multiple organ failure (MOF), so
hassoun et al consided the intestines was the initiating organ for posttraumatic MOF.

Effect of cardiac dysfunction on hepatic, renal, and

intestinal blood flow

The heart is power organ of the circulatory system. It
was found that the liver, kidney and intestinal blood
flow was significantly increased accordingly with the
cardiac function improvement and decreased with
further suppression of the cardiac function. The result
indicated that immediate early cardiac dysfunction
may be an important initiating factor for secondary
ischemia and hypoxia damage of multiple organs after
severe burn.

Mechanism for cardiac damage/ heart function depression at

early post burn stage
Undoubtedly, myocardial cell damage is the immediate cause heart function
depression in the early burn period. In the 1990s, serum troponin (cTnI) was
proposed as highly specific and sensitive indicator in detecting cardiomyocyte injury,
randomly examined the level of serum cTnI was negative in the patients with less
than 10% TBSA burns, while it continually rose in patients with morw than 20%
TBSA burns within 12 hours post-burn. It provided solid evidance for post-burn
myocardial damage. Other parameters of myocardial damage like myosin light chain
1 (CMLC1) and tropinin T (cTnT) also increased evidently after burn. Pathological
observation found cloudy sweeling of the myocardial cells, interstitial vascular
dilatation , congestion, edema, hemorrhage and inflammatory cell infiltration at 3
hours post-burn in scalded rats with 30% TBSA 3 rd degree burns. At 12 hours postburn, an irregular arrangement of cardiac muscle fibers (in the wavy-pattern) and
sarcoplasm condensation were observed, all these facts implied that cardiac damage
already existed in early severe burns, accompanied by decreased heart function.
Since the evidence of burn toxin presented. Baxter and his colleagues attempted to
seek myocardial depressant factor (MDF) in the plasma of burn and patients. They
infused the plasma of burn patients into the free hearts of normal guinea pigs and
proved that such plasma was myocardial depressant.

Sambol et al found that pre-burn mesentric lymph duct ligation could greatly improve the
impaired cardiac contractile function, which suggested the existance of myocardial
depressant factors in burned animals . All these research implied that burn injuries
indeed stimulated the activation and release of certain protein factors which had a
negative regulatory or damaging role on cardiac muscles.
Tumor necrosing factor (TNF) serum level were initially believed to be associated with
the progression of infection. Some researchers also thought that the increased of TNF-
in post-burn plasma could be used as a measurement of the bodys immune response,
which indicated increased risk of secondary sepsis and death. Subsequent researced
asseyed the post-burn TNF-, IL6 and other factors and suggested that taking multiple
factors into consideration, rather than a single inflammatory factor TNF- could better
predict the onset of sepsis. Role of TNF- in postburn myocardial dysfunction and
found enhanced synthesis of TNF- by myocardial cells with a more than 40% TBSA
burns. The Anti- TNF- strategy could prevent myocardial contractile dysfunction and
elevate cardiac output. Subtantial evidence has proved TNF- to be one the initial
mediators in the waterfall-like inlammatory cascade response. In the animal models,
intravenous injection of recombinated TNF- could induce myocardial depression.

TNf- was a significant initiation factor in the postburn uncontrolled inflammatory

cascade, as well as an important inflammatory factor in myocardial damage, playing an
important role in MODS after severe burn.
In the case of severe burn, tissue ischemia and hypoxic metabolism still continues under
large-volume fluid resucitation. When ischemia is improved in the tissue, re-exposure to
molecular oxygen will generate a large number of oxygen free radicals, leading to tissue
damage. Metabolism of xanthine oxidase (XO) is the major source oxygen free radicals
produced after burns. Allopurinol is a competitive antagonist of XO. Allopurinolpretreatment can prevent oxyradical-induced myocardial damage and cardiac function
depression in rats. The rise of myocardial lactic acid levels after burns suggest the
exitance of hypoxic metabolism. Rapid large-volume fluid replacement will remove
lactic acid accumulation and improve the myocardial creatine phosphorylation level.
The addition of allopurinol to the replacement fluid will remove depolarization in
cardiac cell membrane and enchance myocardial contractile function.
Neutrophils release a large number of oxygen free radicals explosively and sstrengthen the
effect of xanthine oxidase, causing damage to tissue and organs. In addition, burns also
destroy the bodys antioxidant defense mechanism, so that the tissue are more
vulnerable to oxygen free radicals. The role of oxygen free radicals in postburn organ
damage and dysfunction.

Multiple cellular and molecular signal transduction pathways have been verified to
cause myocardial damage and mechanical dysfunction. The p38/MAPK pathway,
for instance, regulates the synthesis and secretion of cytokines and plays a
significant role in many heart disease like myocardial hypertrophy,
ischemia/reperfusion injury, and myocardial cell apoptosis. P38/MAPK activity
was evidently elevated in cases of over 40% TBSA burns.
Additionally, through F-actin cytoskeleton rearrangement and phosphorilation of Lcaldesmon, p38/MAPK conducted an important role in endothelial barrier
dysfunction induced by burn serum.
The rho-kinase pathway has been proved by other researches to perform a critical
role in the recontruction of cardiac muscle fibers after burn injuries. The
activation and up-regulation of -1 adrenergic pathway led to activation of
RhoA/Rho-kinase. Evidance showed that the myocardial Rho-kinase expression
was considerably enhanced at 1 hour, 2 hours, and 8 hours post-burn, and
engaged in regulating the synthesis and release of inflammatory factors like TNF, IL-1 and IL-6 by myocardial cells in rats ith over 40% TBSA burns.

Protein kinase C (PKC) was also by some research to engage in regulating myocardial
inflammatory reaction and cardiac dysfunction. It has been confirmed that PKC pathway
involved in the regulation of myocardial cytokine synthesis. The inhibitor of PKC, either
calphostin or chelerythine, could significantly reduce inflammatory cytokines secretion bt
myocardial cells and improve the damaged myocardial contractile function.
The transcription factor NF-KB, downstream of the PKC/ p38/ MAPK/ JNK/ Rho-kinase
pathway, regulates a variety of genes of inflammatory cytokines, such as TNF- and IL-1,
which are detrimental to cardiac function. The level of myocardial NF- KB, according to
carlson et als finding, continuosly increased from 1 hour to 24 hours post-burn. The NF- KB
activation started earlier than secretion of TNF- and IL-1 by myocardial cells, which was
again earlier than occurrence of heart function impairment.
These fact imply that activation of NF-KB was upstream of signal transduction pathway, which
perform a critical in the pathological progression of burn-induced myocardial damage and
cardiac dysfunction. Although the mechanism of myocardial damage and cardiac function
depression in the early post-burn period has been explored and analyzed from various
perpective in multiple researches, it cannot be accurately explained only from a single
aspect. The exact mechanism of myocardial damage may be the combined effect of multiple
factors, or perhaps there are more convincing causes, which await our further investigation.

Prevention and therapy strategies of the burn-related

myocardial damage/ cardiac dysfunction
For the damage of inflammatory mediators by the myocardial function after burn injury,
many studies have focused on limiting the adhesion and activation of the neutrophils. The
monoclonal antibody spesific for the intracellular adhesion molecule 1 and 2 (ICAM-1 and
ICAM-2), P, L, E-selectin has been proved to be with hemodynamic and myocardial
protection effect during the treatment of the burns.
The most widely recognized clinical prevention and therapy means is to curb the oxygen free
radicals damaging the organs, including clinical use a large dose of the anti-oxidants. After
burn injury, vitamin C and N-acetylcysteine can effectively improve the tissue energy load,
improve the level of vitamin C and E in the tissues, enchance the elastase activity, enhance
the microvascular function and inhibit production of the free radicals. The enhanced
antioxidant capacity is helpful or maintenance of the high-energy phospate level in the
tissues, improvement local micro-circulation and effective prevention of the burn edema.
Antioxidant therapy can protect the mitochondrial membrane integrity and thereby prevent
cardiac dysfunction after burns. The antioxidants therapy can protect the mitochondrial
membrane integrity and thereby prevent cardiac dysfunction after burns. The antioxidants
vitamin therapy could reduce the planned amount of resuscitation fluid with an adequate
cardiac output.

Ulinastatin (UTI) the refined protease inhibitors extracted from the

human urine, can not only inhibit the activities of many hydrolytic
enzymes including trypsin, phospholipase A2, hyaluronidase and
elastate, but also prevent MDF production and ameliorate the
circulatory state of shock. The experimental and clinical studies
have proved that UTI exerted a significant effect on prevention and
treatment of the myocardial damage, for it could regulated the
inflammatory response balance, remove the oxygen free radicals,
reduce the lipid peroxidation and inhibit the myocardial apoptosis.
For the patients with total burn area over 35% TBSA (of which 3 rd
degree burn over 20% TBSA), surgical removal of the entire eschar
early after burns can reduce SIRS and endothelial system damage
and hence effectively prevent the MODS.

conclusion
The cardiac local RAS which is activated immediately after severe burn causing
vasocontriction result in ischemic and hypoxic injury in myocardiums, which
contributes mostly and initially to the post-burn myocardial damage and heart
dysfunction. The uncontrolled cascade response of the inflammatory factors,
cytoskeleton and mitochondria destruction in cardiomyocytes, apoptosis and
necrosing following ischemia and hypoxia are directly responsible for thw post-burn
myocardial damage and cardiac dysfunction. And the cardiac pumping deficit with
reduced output offers insufficient blood flow to the organs such as liver, kidney, and
intestines, which induced and further aggravates the burn shock. In the
pathophysiological course of severe burns, the myocardial damage/ cardiac
dysfunction and the burn shock (microcirculation disturbance and inadequate tissue
and organ perfusion) are two crossed main lines, the vicious circulation of which may
lead the patients to MODS and even death. Can the originating factor for the
myocardial damage be effectively blocked, the survival rate of the patients with the
extensive burns will be greatly improved. Thus, it is worthy of looking forward to a
breakthrough in more in depth and effective endogenous protection mechanism of
the myocardial damage.

Definition

Staphylococcal toxic shock syndrome (TSS) is

History

Staphylococcal toxic shock syndrome (TSS) was first describe

Risk Factor
Tampon
Vaginal
Nasal
Subcutaneous
Cellulitis
Infected
Pneumonia
Viral
infections
tampons
colonization
burns
use.areabscesses
for
some
such
procedures
with
as
of varicella
the
toxin-producing
non-surgical
ofand
the ears,
influenza
focal
noseinfections
are
andsometimes
throat.
associated
responsible.
with TSS.

Kare M, Dang A. Staphylococcal Toxic Shock Syndrome vol. 56. Japi;2008.

Cont....

The Centers for Disease Control and Prevention in Atlanta, USA there we

Edwards V, Jones. Toxic shock syndrome:

causes in people with burn wounds. UK
Wounds;2006.

Clinical features
Malaise

Kare M, Dang A. Staphylococcal Toxic Shock Syndrome vol. 56. Japi;2008.

Classic criteria for clinical diagnosis of TSS

Fever above 38.9C
Hypotension or orthostatic dizziness
Diffuse or palmar erythroderma
Desquamation of hands and feet
Hyperaemia of conjunctivae and of the mucous membranes of the oropharynx or vagina
Multisystem dysfunction which must include at least four of the following:

Diarrhoea and vomiting

Alterations in consciousness
Impaired renal function
Impaired hepatic function
Thrombocytopenia
Elevated muscle creatinine phosphokinase
Cardiopulmonary dysfunction
Decreased serum calcium and phosphate

Edwards V, Jones. Toxic shock syndrome: causes in people with burn wounds. UK Wounds;2006.

Diagnostic test
Currently there is no diagnostic test for TSS. But we can use:

Differential diagnosis
Streptococcal TSS

Kare M, Dang A. Staphylococcal Toxic Shock Syndrome vol. 56. Japi;2008

Treatment

Treatment consists of immediate and aggressive management of hypovolemic sho

Kare M, Dang A. Staphylococcal Toxic Shock Syndrome vol. 56. Japi;2008

Cont...
Antibiotics

Edwards V, Jones. Toxic shock syndrome: causes in people with burn wounds.
UK Wounds;2006.