Principles and Practice of Burn Care

386
Principles and Practice of Burn Care
prevention of contractures. The deeper the wounds more
frequent are the surgeries and more in number too.
For larger deep wounds surgical removal of devitalized
tissue by tangential excision and skin grafting of the resultant
wound is the main stay of management. Some authors
believe that one should wait until eschar separates to
maximize tissue preservation before one goes for grafting.
Tissue preservation in this area is important as specialized
tissue of this area is difficult to reconstruct. In the perineum
graft should preferably be meshed in order to accommodate
the irregular contour but expansion is not really required.
Perioperative management of the graft is very important.
The grafts require well vascularized bed with bacteriological
balance. The graft requires stabilization with sutures, staples
or fibrin glue. Post-operative shearing has to be prevented
where a nylon mesh over the graft is helpful. Use of air
ripple beds, nursing in prone position, minimization of fecal
soiling decreases wound infection and graft loss. It has
been observed that flame burns require more surgical
intervention than scalds as the former are deeper. In one
study, only 20% of scalds were classified as second degree
deep or third degree while in contrast 66% of flame burns
were of the same category.
When testes are involved, the burns are obviously full
thickness as these are protected by skin, dartos, tunica
vaginalis as well as cremasteric reflex. In such cases the
thin penile skin usually does not survive. Early surgical
intervention by excision followed by resurfacing with skin
grafts is beneficial. Decompression of penis by escharotomy
should be done for full thickness burns of the phallus when
vascular compromise is suspected. Excision and grafting is
done as soon as possible but efforts should be made to
spare the dartos which has a rich venous network. If this
can be preserved the problems of distal swelling, wound
contraction and subsequent contracture can be eliminated.
The laxity of penile skin enables about one fourth of the
circumference to be excised and primarily closed. This can
be a useful method when burns affect only the dorsum of
the penis. Unmeshed grafts are preferable for better aesthetic
appearance. Circumcision discarding non-burned penile skin
is forbidden as it might be required for later reconstruction.
Acute circumcision is indicated only for full thickness burns
of the prepuce. When testes are exposed, they can be
sutured together for stability and covered with partial
thickness skin graft. Intrinsic contractures of penis, scrotum
or vulva are rare but extrinsic contracture or webbing across
the perineum and groin are more common.
Prevention of Contractures
To prevent contractures, lower limbs should be in abducted
position during wound healing period with a spreading bar
or wedge splinting. Active and passive exercises for hip
joints, pressure garments with special inserts are also
important in the prevention of contractures.
MANAGEMENT OF PERINEAL BURN
CONTRACTURES/RECONSTRUCTION8-11
Gottlieb and Saunders3 have classified burn scar deformities
of perineum into quantitative and qualitative types.
Fig. 28.6A: Electrical contact burns in perineum showing necrosed
penis and scrotum with suprapubic cystostomy
Fig. 28.6B: Same patient with total loss of penis and both testes

Burns of Perineum and External Genitalia
387
Quantitative are those in which there is loss of skin surface
and/or functional tissues, for example, most contractures.
Qualitative scars are those which have altered skin texture,
hypo/hyperpigmentation and changes in pliability. Although
quantitative contractures are more disabling functionally,
the reconstruction of qualitative ones is more difficult, a
challenge that should not be neglected as it can lead to
problems of sexuality. Perineal burn contractures have also
been described as scar bands between the medial thighs
crossing the area between genitalia and anus or a band
extending from proximal medial thigh to perineum (Figs
28.7A to 28.8).
Fig. 28.7A: Post burn scarring of suprapubic area extending to root
of penis causing dorsal contracture of penis
Fig. 28.7B: Same patient in lateral view showing the dorsal contracture
of penis. Patient had difficulty during micturition as the stream of urine
was directed horizontally. Patient required a dorsal release at the root
of penis
Fig. 28.8: Showing a child with post burn contracture of perineum
In spite of early surgical intervention and early
mobilization perineal contractures occur in a small
percentage of patients. These numbers are higher in places
where education levels are low and patient follow up is
poor. Small contractures can usually be treated with Z plasty
or its variants. Scar excision and primary closure, local
rotation and transposition flaps are other methods of dealing
with small contractures. Larger contractures need to be
released and grafted (Figs 28.9A and B). Grafting of both
thighs leaving the intervening portion intact as advocated in
double release or bipedicled release for elbow and popliteal
fossa can be done. If lower abdomen is spared, this skin
can be brought down to avoid skin grafting in the suprapubic
area. It is a good method but is rarely applicable as in most
cases of burns of genitalia and perineum which require
surgery, the lower abdomen is also burnt. When the
undesirable scar is not extensive and the adjacent skin is
normal and adequate, tissue expansion is an option. It allows
one to get qualitatively normal skin without any donor site
deformity. However, expanders in the perineal area are
fraught with dangers. High incidence of infection and
exposure is seen. Patients find it very cumbersome to sit,
move around and perform their normal daily activities with
the bulges of the expanders. However, when the expanders
are successful they produce the best results. Alternatively
full thickness skin donor sites are expanded and used for
better cosmetic results.
Postoperative rehabilitation includes massage, stretching
and leg abduction exercises, maintenance of abducted
position with spreading bar splint and regular usage of
pressure garments for three to six months. Postoperative
rehabilitation did not appear to influence recurrence which
has been reported to be as high as 20%.

388
Principles and Practice of Burn Care
Indications for surgery are decreased range of motion
and leg abduction. The ideal time for contracture release is
after the scar has matured fully. This can take from six
months to two years. An exception to this rule is when
patient needs relief from a severe functional disability.
Intrinsic contracture of penis results from injury and
secondary scarring of dartos, Bucks fascia, tunica or
corpora. Small scars limited to dartos or Bucks fascia can
be treated with incision or excision. More severe deficiency
needs excision followed by reconstruction with dermal graft
and covered by Byar’s or any other local flap. If there is
scarring of urethral meatus dilatation may be enough for
mild cases, Z-plasty and other interdigitating flaps are
reserved for more severe cases.
Total reconstruction of penis was started with tube
pedicle flaps which gave way to the axial pattern flaps,
muscle flaps which have now been replaced by state of art
neuro-sensory fasciocutaneous free flaps. The best results
have been obtained by the neurosensory radial forearm flap
which can offer both erogenous and protective sensation
with prosthesis for erectile function. Other methods which
have been used include bilateral gracilis muscle flap and
rectus abdominis muscle flap. The girth provided by the
flap should be adequate to contain both the neourethra and
the prosthesis. Subtotal penile loss is treated the same way
adding the flap to the preserved portion of corpora and
urethra.
Vulvar injuries are rare but when they occur they might
lead to webbing which compromises normal sexual activity
and cause difficulty in micturition. If adjacent tissues are
healthy and pliable, Z-plasty, local transposition flaps or
V-Y advancement flaps can be done. Basically flaps from
normal tissue are used to break up the scar contracture
line. If surrounding skin is scarred, the contractures have
to be released and split skin grafted.
Extensive burns involving buttocks can sometimes result
in perianal stenosis or hooding which can impede fecal
evacuation. These patients, on closer examination, may
reveal entrapped unburned tissue. This can be released by
incising the burnt tissue from perineal body to coccyx
through the stenotic orifice and everting the unburned tissue
away from the anus. Lateral excisions of bands of burnt
skin allow recreation of gluteal folds.
Repeated discussions concerning realistic expectation
regarding appearance, sexual function and reconstructive
options is important. This should be started early in the
acute phase and continued throughout the treatment period
till reconstruction is complete. Discussions regarding nature
of deformity, surgical improvement, various available options
and realistic expectations of both the patient and surgeon
are critical.
SUMMARY
•
Burns involving perineum and genitalia only are rare.
They are usually seen in patients who have sustained
large percentage of burns more than 40%.
•
Superficial burns are treated conservatively while deeper
wounds need excision and resurfacing. Full thickness
burns need reconstructive procedures.
Fig. 28.9A: Severe post thermal burn contracture of perineum and
groin causing the penis to bury beneath the contracted skin
Fig. 28.9B: Same patient showing released contracture followed by
skin grafting

Burns of Perineum and External Genitalia
389
•
Urinary diversion with catheter is usually required but
fecal diversion is not done.
•
Perineal contractures are a rare complication.
•
Indications for surgery include decreased leg abduction
as well as urinary and bowel complications.
•
Surgery for perineal contractures usually requires simple
methods like local flaps and skin grafts and complicated
procedures are reserved for reconstruction of genitalia.
•
Local flaps are superior to skin grafts which should be
used only when local tissues are unavailable.
•
Aggressive rehabilitative techniques help preventing
recurrences.
REFERENCES
1. Michielsen D, Van Hee R, Neetens C, C.Lafaire and R.Peeters.;
Burns to the Genitalia and the Perineum; Journal of Urology
1998;159:418-19.
2. Angel C, Shu T, French D, Orihueta E, Lukefahr J, Herndon DN;
Genital and Perineal Burns in Children: 10 Years of Experience At
A Major Burn Center; Journal of Pediatric Surgery 2002;37(1):99-
103.
3. Gottlieb LJ, Saunders JN. Perineal burns In Burns Reconstruction
by Bruce M. Achauer, Thieme medical publishers Inc., New York,
1991;Chapter 13:165-82.
4. Nakazawa H, Ito H, Morioka K, Kikuchi Y, Honda T, Isago T; The
Use of Temporary Diverting Colostomy to Manage Elderly
Individuals With Extensive Perineal Burns; Burns 2002;28:
595-99.
5. D Michielsen, R Van Hee C, Neetens C.Lafaire, R.Peeters. Burns to
the Genitals and the Perineum In Children ; British Journal of
Urology 1996;78:940-41.
6. Abdel-Razek. Isolated Chemical Burns to the Genitalia; Annals of
Burns and Fire Disaster Vol xix n-3 Sept 2006.
7. EM Weiler-Mithoff, ME Hassall, DAR Burd. Burns of the Female
Genitalia and Perineum; Burns 1996;22:390-95.
8. Gaurav Bandi, Richard A Santucci; The Journal of Trauma, Injury,
Infection and Critical Care 2004;56:1368-69.
9. Gregory P Pisarski, David G Greenhalgh, Glenn D Warden. The
Management of Perineal Contractures In Children with Burns;
Journal of Burn Care and Rehabilitation 1994;15(3):256-59.
10. Sawhney CP. Management of Burn Contractures of the Perineum
Plast. Reconstr. Surg 1983;841-2.
11. Chr. H. Bangma, ABM van der Molen, H.Boxma. Burns to the
perineum and genitalia: management, results and function of the
thermally injured perineum in a five year review; European Journal
Plastic Surgery 1995;18:111-14.

390
Principles and Practice of Burn Care
Pediatric Burns
29
Harish Chellani, Sugandha Arya
Chapter
INTRODUCTION
In the pediatric age group, as is true for adults, a burn
injury is the second most important cause of trauma-related
deaths ranking after motor vehicular accidents only. Besides
causing death, a large number of children survive burns
only to have lifelong disfigurement, loss of function and
physical deformity leading to psychological sequelae. A burn
injury not only leaves the scars on the skin but also on the
mind of the child.
Burnt children account for almost 15 percent of all burn
patients admitted to a large burn center. The management
of a burn patient is complex and requires a multidisciplinary
approach. When the patient happens to be a child, the
challenges are further magnified and a competent and unified
approach to patient care becomes mandatory.
MODE OF INJURY
Most of the burns in children occur in the child’s own house.
The age of the child and his environment suggest subgroups
of children at risk for burn injury.1 The infants and toddlers
less than 2 years of age are frequently burnt. An important
factor leading to burns even in neonates is overcrowding in
a small house, where a small area in the room serves as
kitchen (with floor level cooking). The victim is looked
after by his/her siblings, who are themselves no more than
5-6 years old when the mother is away at work to earn.
Infants and small children are also the only victims when
clusters of ‘jhuggis’ (huts) catch fire and they are either
sleeping alone or unable to rescue themselves (Figs 29.1A
and B).
Fig. 29.1A: A 3-month-old infant with 35% full thickness burns sustained
accidentally in a ‘jhuggi’ fire when child was left unattended by mother
Fig. 29.1B: 2 weeks post burn picture of same patient showing eschar
separating and wounds starting to granulate from underneath

Pediatric Burns
391
Moreover, children out of curiosity actively search and
manipulate their physical environment. Scald burns are the
commonest type of thermal injury in children. They usually
suffer scalds by pulling down or knocking hot liquids on to
themselves. Immersion scalds can occur when a child steps
into a tub of hot water or stumbles onto a container of hot
milk or cooked food (Figs 29.2 and 29.3). Children also
feel a temptation to experiment with match boxes. Fireworks
during Diwali and other festivals is a major cause of burns
in children. In winter season, it is a common practice for
adults in our country to collect wooden sticks and old worn-
out automobile tyres and ignite them to keep warm. Children
often imitate adults and get burnt by this practice.
Electrical burns in children are generally caused by
domestic voltage electric current which is 220-250 volts in
India. Typically, a child bites an electric cord sustaining a
disfiguring third degree burn of the lips2 (Fig. 29.4). He
may introduce a finger or an object such as a metallic hair
pin into an electric socket and suffer an electrical injury.
Chemical burns may be caused by strong acids and alkalis
used for cleaning household toilets and drain and quite
commonly stored carelessly.
Majority of burn injuries in children are accidental.
Perineal scalds (Fig. 29.5) and acid burns are very common
in children. A very small percentage of pediatric burns are
due to homicide and child abuse in India, although they are
frequently reported from developed countries (Fig. 29.6).
Fig. 29.2: A 1½ year-old child with 20% scalds due to child
stumbling into a container of hot milk
Fig. 29.3: Another child with 20% superficial dermal scalds due to
hot water bucket falling on him
Fig. 29.4: Post burn microstomia following electric burn sustained
by a 4-year-old child while chewing on an electric cord
Fig. 29.5: Perineal scalds because of spilling of hot tea from a cup
lying on the table, when child pulled down the tablecloth

392
Principles and Practice of Burn Care
PATHOPHYSIOLOGY
A child is not merely a small adult. Children react differently
from adults to a thermal trauma, both in their local reaction
and systemic response. Therefore, in children, especially
those less than 2 years old, there are certain special
physiologic considerations which have to be kept in mind
while managing burns. One of the most important feature
of infants is their larger surface area relative to weight when
compared with older children and adults. The evaporative
water losses and hence the heat loss is greater for children
compared to adults because of their larger surface area.
The temperature regulatory mechanism in children is also
different in different age groups. For infants less than 6
months of age, the body temperature is usually regulated
by non-shivering thermogenic response wherein the stores
of brown fat are catabolized under the influence of
norepinephrine. Since this process utilizes large amounts of
oxygen, prolonged hypothermia can lead to excess lactate
production leading to acidosis. After 6 months of age,
children are able to shiver but body heat is still lost as their
surface area per unit body weight is larger than that of
adults. To reduce this loss external sources to preserve body
temperature are required. Therefore, infants and children
with burns have to be treated in cubicles where the ambient
temperature can be kept high so as to reduce the radiant
and evaporative heat loss from the body to the environment.
The physical immaturity and smaller size of infants
compared to adults result in significant structural and
functional differences in cardiovascular system and
maintenance of fluid balance. These differences affect the
response of infant and child to hypovolemia and in turn,
affect the management of fluid resuscitation following burns.
Infants, in particular, rely heavily on their heart rate to increase
their cardiac output and rates as high as 220 beats per minute
are seen in hypovolemic infants following burns. This
compensatory mechanism is easily exhausted making
infants more vulnerable to burn shock.
The infants also have less mature renal function as
compared to adults. The glomerular filtration rate and renal
blood flow of an infant is lower than that in adults. In fact
the glomerular filtration rate in infants reaches adult levels
only after approximately 9 to 12 months of age because of
delayed maturation of glomerular and tubular function.
During this time, the infant has approximately half the
osmolar concentrating capacity of the adult and water load
is handled inefficiently. During the first several weeks of
life the infant is likely to retain a large portion of water load
administered as part of burn resuscitation. This may apply
to a slightly lesser degree to other substances such as
sodium. All these differences are accentuated by the stress
of burn injury. The syndrome of inappropriate anti-diuretic
hormone secretion (SIADH) is associated with many acute
illnesses including burns. The elevated ADH levels result in
conservation of water and high sodium excretion causing
hyponatremia and water overload. The fluid overload in
children can also precipitate convulsions due to dilutional
hyponatremia.
It is important to know that normal heart rates of children
are higher than that of adults (Table 29.1).This helps in
meeting the substantially higher metabolic requirements of
an infant. The blood pressure is also on the lower side in
infants and children and it increases with age because of
corresponding increase in the systemic vascular resistance.
Fig. 29.6: Case of child abuse with full thickness burn both feet
(soles) after his feet were forcefully dipped into hot water
Table 29.1: Normal heart rate and Blood pressure in children
Age group
Heart rate
Blood pressure
(per minute)
(systolic/diastolic)
Newborn
140
65/45 mm Hg
1 year
110
75/50 mm Hg
3 years
100
90/60 mm Hg
8 years
90
95/65 mm Hg
10 years
80
100/70 mm Hg
FIRST AID
First aid is carried out by parents, other relatives or any
other person present at the site of accident, most commonly
the house of the child or neighbor. The public must be made
aware of how to prevent burn injuries in children and what
measures should be taken in case the unfortunate event
takes place. Media, especially television, has a great role to
play where the invited burn specialists teach the public
about it.

Pediatric Burns
393
1. The burned area is cooled immediately with tap water
(preferably running water) to bring the burning skin to
normal body temperature. Very cold water or ice should
not be used as this can lead to hypothermia.
2. Rings, bracelet or watches, etc. should be removed from
the affected area as they may cause tightness or
constriction, when edema occurs.
3. After cooling, remove the clothing from the burnt area.
However, do not try to pull out clothing that is stuck to
the skin. This may cause more harm.
4. A cold compress such as a towel soaked in cold water
may be soothing over the burnt area. This can be applied
after the initial cooling.
5. Before going to hospital, cover the burned area with a
clean sheet to prevent contamination and hypothermia.
6. Paracetamol or ibuprofen syrup may be given to decrease
pain.
7. No topical agent should be applied to the burnt area lest
the evaluation of depth of burns become difficult.
MANAGEMENT
Before definitive wound care commences, a protocol for
rapid assessment of the injury and resuscitative measures
to be taken is formulated.
Assessment of Burn Injury
Treatment priorities begin with the basics; Airway, Breathing
and Circulation. To make a plan for further management,
the burn injury should be assessed for:
•
Percentage of total body surface area involved
•
Depth of burn injury
•
Location of the burns
•
Any associated injuries
Estimation of Burn Size
1. Lund and Browder’s Chart: The percentage of body
surface area involved can be readily assessed by standard
Lund and Browder chart3 (Table 29.2) which is an
accurate technique for assessing percentage of burn
surface area in children.
In children, the head is proportionately a larger
contributor to total body surface area (TBSA), while
the lower limbs contribute less as compared to adults
(Table 29.2). The head and neck comprises 19% of
total surface area in an infant. With each year the surface
area decreases by 1% till at 10 years of age it is similar
to that of an adult. Similarly, each lower limb constitutes
13% of surface area of body in an infant and it increases
by 0.5% per year till 10 years of age when it almost
matches that of an adult (18%).4
Another simple formula that can correct for
differences in body surface area in children is, to subtract
child’s age in years from 12 and the resulting number is
added to the figure for adult head and neck or subtracted
from the figure for both lower limbs.
Example: At 8 years the head and neck constitutes 9 +
(12 – 8) = 13% of total body surface area.
Table 29.2: Lund and Browder’s chart showing changes in body surface area (%) with age
Area
Birth to1
1 to 4
5 to 9
10 to 14
15 years
Adult
year
years
years
years
Head
19
17
13
11
9
7
Neck
2
2
2
2
2
2
Anterior trunk
13
13
13
13
13
13
Posterior trunk
13
13
13
13
13
13
Right buttock
2.5
2.5
2.5
2.5
2.5
2.5
Left buttock
2.5
2.5
2.5
2.5
2.5
2.5
Genitalia
1
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
2.5
2.5
2.5
2.5
2.5
Right thigh
5.5
6.5
8
8.5
9
9.5
Left thigh
5.5
6.5
8
8.5
9
9.5
Right leg
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:
100
100
100
100
100
100

394
Principles and Practice of Burn Care
At 8 years both lower limbs constitutes 36 – (12 – 8) =
32% of total body surface area i.e. 16% for each lower
limb.
2. Wallace’s Rule of ‘nine’: In children over 12 years,
burn wounds can be estimated by this formula which is
also used in adults.5
According to this,
•
Head and neck – 9% TBSA (9 × 1)
•
Each upper limb – 9% TBSA (9 × 2)
•
Anterior trunk– 18% TBSA (9 × 2)
•
Posterior trunk – 18% TBSA (9 × 2)
•
Each lower limb– 18% TBSA (9 × 2 × 2)
•
Perineum and external genitalia – 1% TBSA.
•
Total = 100%
3. Rule of ‘five’: Lynch and Blocker developed a formula
for estimating the extent of burns in children.6 It works
very well in infants where head and neck, anterior and
posterior aspects of trunk are 20% each and each limb
constitutes 10%. For older children, this is slightly
modified. The head, posterior trunk and lower limbs are
15% each, anterior trunk is 20% and each upper limb is
10%.
4. Rule of Palm or Hand: For all age groups, palmar
surface of one’s hand represents his/her 1% TBSA. This
is useful for assessing scattered burnt areas. Only
second-degree burns or greater should be included in
the TBSA burnt for burns management.
Estimation of Burn Depth (Figs 29.7 to 29.10)
The burn depth estimation is discussed in detail elsewhere
in this volume. During infancy, the epidermis is loosely
connected to the dermis. As a result, blisters form more
readily in burns in infants. The stratum corneum layer of
epidermis is thinner in children so that scalds cause deeper
burns in children compared to adults. The amount of sebum
and sweat production in infant’s skin is also less than that
in older children and adults. Due to all these reasons, a
child’s skin is susceptible to greater damage by heat and
chemicals even if exposure is for short duration.
Many burn wounds which initially appear superficial
may eventually turn out to be deeper and may require skin
grafting. A scald injury which looks bright red and is taken
as a superficial burn in an adult may actually turn out to be
full thickness burn in young children.
A severe burn is one that covers greater than 15% of
the body surface area or involves the face or perineum.
Second degree and third degree burns of the hands or feet,
as well as circumferential burns of the extremities are also
classified as severe. Inhalation injuries resulting in
bronchospasm and impaired pulmonary function must be
considered as severe burns.
Fig. 29.7: Accidental superficial dermal burns of face in an infant
Fig. 29.8: Full thickness burns of hand and distal forearm of a child
Fig. 29.9: Superficial dermal or superficial second degree scalds of
face of an infant

Pediatric Burns
395
Indications for Admission to Hospital
The indications to admit a child to a burn care facility are:7
1. Extent of the burn – Children with more than 10% burns.
2. Areas involved – Involvement of face, neck, both hands,
both feet or perineum.
3. Types of burn – Children with electrical or chemical
burns, third degree burns of greater than 5%.
4. Associated injuries – If burns are associated with soft
tissue trauma or head injury, fractures etc.
5. Inhalation burns.
6. Social problems – If there is suspected child abuse or
neglect, self-inflicted burns, poor guardianship at home
regarding wound care or psychological problems
present, ambulatory management may not desirable.
Initial Management
Although most children are victims of scalds, the initial
management must give first priority to airway. If a child is
involved in a fire in closed space or “Jhuggi” (hut) fire,
inhalational injury should be strongly suspected.The upper
airway is susceptible to burn injury, whereas the subglottic
space appears protected. Facial burns, singed nasal hairs or
eyebrows and acute inflammation of the oropharynx suggest
inhalation injury. Smoke inhalation may be associated with
carbon monoxide toxicity; 100% humidified oxygen should
be given if hypoxia or inhalation injury is suspected. A
carboxyhemoglobin assessment should be performed for
any suspected inhalation exposure (a house or closed space
fire or a burn victim who requires CPR). Hoarseness on
vocalization is also consistent with supraglottic injury. Some
children with inhalation injuries require intubation or
tracheostomy and mechanical ventilation (Figs 29.11A
and B).
Fluid Management
Adequate fluid resuscitation in the first 24 hours post burn
is of utmost importance. Many fluid resuscitation regimes
have been advocated over the last 50 years. Pruitt et al8
recommended 3 ml/kg/% burn surface area as resuscitation
formula for thermally injured children. Baxter reported 4
ml/kg/% BSA for fluid calculation9 while Warden et al10
recommended a mean fluid requirement of 5.8 ml/kg/%
BSA for children.
Compared to adults, children require fluid resuscitation
for burns as small as 10-20 % BSA because of their limited
physiological reserve. Various studies have demonstrated that
children with burns less than 30% area require less fluid/kg
/% burn than those with more than 30% burns.11,12
Fig. 29.10: Another infant with deep dermal or deep second
degree burns of face
Fig. 29.11A: Patient intubated for mechanical ventilation even though
child sustained only 10% scald with hot tea following which parents
poured bucket full of water on his face and child aspirated hot tea and
water both leading to aspiration pneumonitis
Fig. 29.11B: Another child with 10% facial burns with smoke
inhalation injury requiring tracheostomy for ventilation

396
Principles and Practice of Burn Care
There are many popularly used formulae for intravenous
fluid therapy. Though all the formulae are quantitative and
mathematical to a certain extent, clinical judgment is very
essential while deciding the quantity and quality of fluid
given to children. No single formula can be adhered to strictly
in the management of a burnt child. The most important
fact underlying this decision is not to overload the vascular
system and at the same time not to under-resuscitate the
child. In Parkland / Baxter formula, the total fluid requirement
is estimated on the basis of extent of burn and weight (in
kg) of patient only, without any additional daily maintenance
fluid. The fluid calculated as per these formulae in infants
especially with smaller burns may not suffice as it may not
even meet the total daily requirement. For example, in a 10
kg child with 20 % burns the daily fluid requirement is
1000 ml. However, the amount of resuscitation fluid
calculated for the same using Parkland formula (4 × 20 ×
10) comes to only 800 ml in first 24 hours. This results in
gross under-resuscitation of the patient. Therefore, the daily
maintenance fluid has to be added to these formulae in the
form of dextrose saline. This is given as N/2 saline with 2.5
% dextrose or N/4 saline with 3.75 % dextrose according
to the age of the child (For less than 2 months of age N/5 or
N/6; 2 months to 5 years, N/4 and for 5-12 years, N/3 or
N/2). The addition of dextrose decreases the incidence of
hypoglycemia in infants in the first 24 hours.
On the other hand, in extensive burns in children,
Parkland/Baxter formula is again unsatisfactory as the
amount of fluid calculated is very high. There is no restriction
to the percentage of burn area to be included. For example,
a 10 kg child with 80% burns would be predicted to require
10 × 80 × 4 = 3200 ml fluid in first 24 hours although the
daily fluid requirement for the same patient is only 1000 ml.
This large amount of ringer lactate, if given to the child,
can result in fluid overload and resultant hyponatremia can
precipitate convulsions in children. Therefore, a formula
with a ceiling of 50% TBSA is essential along with addition
of daily fluid requirement. For this purpose modified
Brooke’s formula satisfies all the requirements and is
followed in our burn unit as well.
According to modified Brooke’s formula, the first 24
hours requirement is calculated as follows:
2 ml × Wt in kg × % BSA burnt + Daily maintenance
The fluid of choice is crystalloid, namely ringer lactate.
Daily maintenance fluid is given in the form of N/2 dextrose
saline (0.45% NS with 2.5% dextrose) or N/4 dextrose
saline (0.23% NS with 3.75% dextrose) and is calculated
as per the weight of the child (Table 29.3).
Half of this fluid is given in first 8 hours and second half
in next 16 hours. In the second 24 hours, the formula
recommended for use is 1ml/kg/percent BSA burnt of ringer
lactate + Daily maintenance (same as above).
The decision to use colloids or crystalloids is
controversial. The rationale for giving crystalloids in the
form of ringer lactate and avoiding colloids in the first 24
hours is that following burns it is the plasma which is lost
from the intravascular compartment into extravascular space
because of increased capillary permeability. Since ringer
lactate is equivalent to plasma without proteins, it restores
the intravascular pressure without adding to the loss of
proteins into extravascular space. Colloids on the other hand,
add to the loss of high molecular proteins from vascular
compartment to extravascular space till such time that the
capillary permeability is increased, usually between 18 to
24 hours. By 48 hours post burn, even though the
permeability is restored to normal, the leaked out proteins
with their water content cannot be reabsorbed back into
the circulation easily. This increases the chances of
pulmonary edema and peripheral edema persisting for a very
long time with deleterious effects on the glomerular filtration,
coagulation and cardiac function.13,14 In studies by Baxter,
it has been shown that colloids probably do not exert any
measurable expansion of plasma over and above that exerted
by ringer lactate till second post burn day.9
Martin et al compared patients receiving only colloid
based fluids in first 24 hours and those receiving a
combination of colloids and crystalloids and reported that
the only colloid regime used much less fluid during
resuscitation with much reduced rates of ARDS,
hypoalbuminemia and sodium disturbances but more
peripheral and pulmonary edema and renal impairment.15
So, the general consensus is that in first 24 hours,
only if the fluid requirement is very high as in
extensive pediatric burns, colloids can be added to
crystalloids in the regime. In massive burns if only large
volumes of crystalloids are given, the intravascular volume
is expanded but the plasma oncotic pressures is not restored
as they are devoid of proteins. On the other hand, the plasma
oncotic pressure is restored faster with colloids because
Table 29.3: Daily maintenance therapy in children
Weight of child
Daily maintenance fluid (ml/kg /day)
0-10 kg
100 ml/kg
10-20 kg
1000 ml + 50 ml/kg for every 1 kg above 10 kg
More than 20 kg
1500 ml + 20 ml/kg for every 1 kg above 20 kg

Pediatric Burns
397
they contain high molecular weight molecules. Crystalloids
in large amounts dilute the remaining proteins further in the
intravascular space thus decreasing the oncotic pressure as
well. As a certain level of oncotic pressure is essential to
maintain glomerular filtration (GF), any further decrease in
this pressure will affect the GF and thus decrease the urine
output, which should be actually increasing. This gives a
false impression that fluid resuscitation is inadequate and
by fault more crystalloids may be infused to increase urine
output, resulting in volume overload without improving the
oncotic pressure. In such circumstances, infusion of
colloids is required to improve plasma oncotic pressure and
increase GF.
In the second 24 hours post burn, many centers prefer
to add colloids to their fluid regime.15, 16 In our unit we use
only crystalloids. Colloids are added only if the plasma
oncotic pressure is very low, indicated by low urine
output, despite adequate fluid replacement by
crystalloids in first 24 hours. Our belief is that the capillary
permeability is restored to normal only by 48 hours and
giving colloids prior to this stage will increase the peripheral
tissue edema and pulmonary edema which will persist for a
longer time as these high molecular weight proteins are not
reabsorbed back. Colloids are given in the form of 5%
albumin or plasma in a volume of 0.3-0.5 ml/kg/ % BSA
burnt.
Since the routine formulae are exclusively weight-based
and in children there is no linear relationship between weight
and surface area, there are problems of under and over
resuscitation in pediatric age group. To overcome this,
studies have shown the benefits of using Galveston formula
based on body surface area (BSA) calculated from the height
and weight of the child from standard nomograms.17,18
According to this formula, the amount of fluid administered
in first 24 hours is calculated as 5000 ml/m2 BSA burn +
2000 ml/ m2 BSA, with half the volume given in first 8
hours and second half in next 16 hours. This has not yet
been standardized and is not being used worldwide.
Monitoring of Fluid Resuscitation
The best way to monitor the adequacy of fluid resuscitation
is by measuring pulmonary capillary wedge pressure. Since
this is not routinely practicable in a clinical setting, hourly
urine output measurement is the most practical and easily
done to know the adequacy of resuscitation. The physiologic
goal is maintaining urine output of at least 1ml/kg body
weight/hour. During first 48 hours, adequate urine output
is considered as follows (Table 29.4).
The child’s pulse, respiratory rate and blood pressure
are also monitored closely. A close watch is maintained on
serum electrolyte levels because rapid fluid and electrolyte
shifts in burnt children can result in cerebral edema and
convulsions. Another parameter which has to be monitored
for assessing adequacy of fluid resuscitation is the hematocrit
which varies in children according to age. Both the
hemoglobin and hematocrit are high at birth and then
decrease in a few days. At one year, hematocrit is 35 %
which gradually increases to 40% at 12 years. The fluid
infusion is regulated to maintain hematocrit values between
35 and 40%.
From third day onwards, as the child is gradually started
on oral feeds, intravenous fluids are gradually reduced and
omitted. Once the capillary permeability is restored, urinary
volumes far exceed the total of oral and intravenous intake
due to return of fluid from the extracellular compartment
into the intravascular compartment.
Children with partial thickness burns that cover less
than 15% of the body surface may be given oral fluids in
the form of milk or other clear liquids, but carbonated
beverages should be avoided as they may contribute to
gastric dilatation and vomiting. Under most circumstances,
children with burn injuries in excess of 15% of BSA should
have a secure intravenous catheter placed, either
percutaneously or via a cut down. Unburned sites should
be used for catheter placement, whenever possible.
Adjunctive Management
•
Nasogastric tube – To prevent acute gastric dilatation,
vomiting or aspiration, a nasogastric tube is inserted
and the stomach is emptied. This is recommended for
all children with burns of 20% or more of body surface
area.
•
Urinary catheter – It is routinely inserted in all children
with > 20% burns to monitor hourly urine output.
•
H2 receptor antagonists – Children with burns
requiring admission should be given H2 receptor
antagonists (e.g. Ranitidine) and antacids for prophylaxis
against gastroduodenal erosions and ulcerations (Curling
ulcers).
Table 29.4: Required urine output according to age
Age of Child
Urine Output
0-2 years
10-20 ml/hour
2-5 years
20-30 ml/hour
Above 5 years
30-50 ml/ hour

398
Principles and Practice of Burn Care
•
Tetanus prophylaxis – Tetanus toxoid is administered
for prophylaxis against tetanus along standard
recommended lines. With the great emphasis by the
Government of India in immunizing children against
many diseases in the first year of life, tetanus being one
of them, many children may be already immunized at
the time of burn. In children not properly immunized,
passive protection is also provided with 250 units of
tetanus immunoglobulin.
•
Analgesia and sedation – Pain relief and sedation must
be preceded by correction of hypovolemia and hypoxia
as they are the cause of restlessness in a burnt patient.
Morphine (0.05-0.1 mg/kg IV every 2-4 hours),
pethidine/pentazocine and promethazine combination in
appropriate doses are used intravenously (slowly) on
‘as and when required’ basis. After the initial shock
period is over, they may be given intramuscularly. For
children with minor burns being treated on outpatient
basis, Paracetamol (10-15 mg/kg every 6 hours) alone
or its combination with ibuprofen, nimesulide can be
used.
•
Blood transfusion – These are not required in the first
48 hours unless the child is anemic. It may be required
later to maintain hematocrit between 35 and 40% and a
hemoglobin level of more than 10 g/dl (Fig. 29.12).
Systemic Antibiotics
Burn wounds provide large, warm, moist and protein-rich
medium for growth of microorganisms from endogenous
and exogenous sources. Children with burns are also more
susceptible to infection because of depressed immune
system. Consequently sepsis is the leading cause of death
from burns. Routine use of prophylactic systemic antibiotics,
however, is not recommended as it leads to rapid emergence
of resistant strains. For protection against beta hemolytic
streptococcal infections especially in children, it was earlier
recommended that crystalline penicillin should be used
prophylactically for first 5 days following burns. However,
with changing wound flora and with emergence of new
strains even this practice has been discontinued at many
centers. Prophylactic penicillin therapy is indicated during
the phase of autogenous skin grafting since streptococcal
infection is likely to occur at that time.
Routine bacteriological monitoring of the burn wound
is carried out with surface swab cultures. Burn wound
biopsies have been used to provide a quantitative estimation
of the bacteria in the wound and infection is diagnosed when
more than 105 bacteria are present per gram of tissue or
there is invasion of subjacent healthy tissue. Local signs of
burn wound sepsis include development of black or purple
necrotic areas in the wound and hemorrhage in the sub-
eschar fat. Bacteria generally isolated in the burn wounds
are Pseudomonas, Klebsiella, Staph. aureus, Streptococcus
faecalis, Proteus and E.coli.
Whereas no clinical sign is diagnostic of septicemia, it
is clinically suspected with a change in condition of the
wound, presence of fever or hypothermia, altered sensorium,
tachycardia, tachypnea, abdominal distension, diarrhea and
oliguria. Although infection is accompanied by fever and
leukocytosis, sepsis in burnt children may manifest with
hypothermia and leucopenia.
For burn sepsis, systemic antibiotics are the mainstay
of treatment (Figs 29.13 and 29.14). If the culture and
sensitivity reports are available the appropriate antibiotic
treatment is directed towards the identified bacteria.
Otherwise, antibiotics are started in broad spectrum
combinations (e.g. cephalosporin and aminoglycosides)
empirically, pending culture reports. Antibiotics are started
at the first sign of sepsis, in maximal therapeutic doses and
stopped only after seven days or so.19
Nutrition
Nutrition plays an integral part in the treatment of a pediatric
burn patient. Adequate energy and protein intake is required
to meet the increased metabolic demands of the
hypermetabolic state of the burn injury as well as normal
growth and development. Prompt initiation of nutritional
Fig. 29.12: Infant with 20% post burn raw area with severe anemia.
Wounds show unhealthy pale granulation tissue. Requires building up
with blood transfusion and nutrition till wounds are prepared for grafting

Pediatric Burns
399
support is crucial and is associated with reduction in cost
of hospitalization.
Enteral route is preferred for nutritional support and is
generally available. Oral feeding is instituted by third post
burn day and by the fifth day it is increased to meet the
predicted caloric requirements. If the child is unable to take
orally, a nasogastric tube may be placed, through which
freshly prepared feeds, at body temperature, can be given
as drip. The feeds should have 1 kcal/ml and a low
osmolarity (300-700 mOsm/l) or else they lead to osmotic
diarrhea. Parenteral alimentation or supplements are
necessary if the child is having vomiting, diarrhea or
malabsorption. Parenteral alimentation is done with 10-20%
dextrose solution with emulsified fats and amino acid
solutions.
The daily caloric requirements in children can be
estimated by the following formulae:
1. Curreri’s formula:20 60 kcal/kg body weight + 35 kcal/
percent burn
2. Carjaval’s formula:21 2200 kcal/m2 of burnt area + 1800
kcal/m2 BSA
Along with calories, an adequate amount of protein is
given which is important to improve resistance and survival.
One of the formulas suggested for estimating protein
requirements in a burnt patient is 3 gm/kg + 1 g for every
one percent of BSA burnt. No more than 4 gm/kg protein
should be provided. Fats are concentrated source of energy
but excessive intake of fat has been associated with many
complications. 5-15% of non-protein calories should be
provided as fats and rest as carbohydrates. Dietary
supplements of vitamins and trace elements including zinc,
copper, chromium and molybdenum are also important for
wound healing and given orally or in intravenous fluids.
Management of the Burn Wound
Burn wounds in children are best treated by dressings as
the child will be able to move around and play more easily
after he is out of the resuscitation phase. Perineal burns are
a difficult area to treat in children. For this paraffin gauze
dressing with topical antimicrobial cream can be applied
directly on the nappy and the nappy can be changed as
frequently as required.
Microorganisms proliferate rapidly in burn wounds,
especially in those severe enough to impair immune function.
Topical antimicrobials have an important role to play. They
delay the interval between injury and colonization and
maintain low levels of the wound flora. Three agents have
proven efficacy for major burns viz., 1% silver sulfadiazine
cream, 0.5% silver nitrate solution and11.1% mafenide
acetate cream. Silver sulfadiazine 22 is most widely used.
Leucopenia is common during first week of treatment due
to marrow toxicity but usually resolves spontaneously.
Shallow burns are treated with daily dressings and local
wound care until epithelialization occurs. They can also be
treated by covering the denuded wound with skin allograft
or xenograft or synthetic membranes available commercially.
Collagen dressings have been found to be very helpful in
superficial burns as they decrease pain and evaporative
Fig. 29.13: A 2-year-old child with burn wound sepsis
due to Pseudomonas
Fig. 29.14: Child with typical gram-negative sepsis

400
Principles and Practice of Burn Care
losses, seal the wound from the environment, makes the
child more comfortable and encourages early healing (Figs
29.15A to 29.16C).
In case of full thickness circumferential burns or
electrical burns where the distal vascularity is getting
compromised, fasciotomy incisions should be given to
improve circulation to the distal parts of the extremities
(Figs 29.17A to C).
Children with deep dermal burns are particularly benefitted
by early excision and grafting as it reduces morbidity, allows
early recovery, reduces length of hospital stay, number of
dressings and thus lessens the psychological trauma at such
a young age. Blood should be kept ready in sufficient
amounts for transfusion during surgery as children tolerate
only small blood losses. A study on blood loss during excision
in pediatric burn patients has shown loss of 2% of
circulating blood volume for each 1% area excised and
grafted.23 Another important fact to be kept in mind during
excision in pediatric age group is that the dermis is very
thin. A true tangential excision leaving behind viable dermis
can be difficult at times and may actually turn out to be
excision till subcutaneous fat leading to marked cosmetic
deformities later on. This is also to be remembered while
procuring graft from the donor sites especially if the donor
site has to be reused.
Fig. 29.15A: Child with extensive superficial dermal burns with wet
collagen dressing
Fig. 29.15B: Same patient with healed areas in 10 days
Fig. 29.16A: Superficial dermal burns of hand in forearm in an infant
Fig. 29.16B: Same patient dressed with dry
collagen (Skin Temp®)
Fig. 29.16C: Healed area after 10 days

Pediatric Burns
401
In case of extensive deep burns in which patient cannot
be taken up for early excision and grafting, the patient is
treated by conservative management in the form of regular
dressings till the eschar separates and the wound starts
granulating (Figs 29.18A to 29.19C). In case there is
deficiency of donor areas because of extensive wounds or
in chronic neglected cases where the patient is cachexic
and not a favorable candidate for auto-grafting, the raw
areas can be covered with homograft till such time that the
area can be covered by autograft in stages. Homograft taken
from mother is preferred over other family members (Figs
29.20A to C). The best way is to apply alternate sheets of
Fig. 29.17A: Escharotomy incision in full thickness circumferential
burn in whole of the arm of an infant compromising distal circulation
Fig. 29.17B: Circulation improved following lateral escharotomy
incision
Fig. 29.17C: Medial escharotomy incision in same patient
Fig. 29.18A: Split skin graft applied over post burn raw area over
scalp in a 5-year-old child
Fig. 29.18B: Completely healed scalp

402
Principles and Practice of Burn Care
Fig. 29.19A: A 7-year-old girl with extensive post burn raw area
after separation of eschar
Fig. 29.19B: Same patient’s wounds grafted as soon as granulation
tissue was healthy
Fig. 29.19C: Healed areas after one month
Fig. 29.20A: Homograft being removed after 7 days of application in a
2-year-old child with 50% burns with 25% raw area (mother of the
child was the donor)
Fig. 29.20B: Autograft applied after removing homograft
Fig. 29.20C: Same child with completely healed areas after 2 months

Pediatric Burns
403
autograft and homograft. In such cases it is found that as
the autograft starts spreading by epithelialization from the
margins, the homograft starts separating automatically. But
more commonly, it becomes necessary to excise the
homograft before 2 weeks and replace them with autografts.
This intervening 2-3 week period allows exceptionally good
anabolic recovery of the child, improving not only the
condition of the wounds but also the general condition of
the patient.
Because of the paucity of epidermal appendages, the
healing by epithelialization in case of deep dermal burns is
much less in young children as compared to the older
children and adults and usually they heal by migration of
epithelium from the edges and contracture formation. In
children less than 1 year of age, the usual tendency is to
keep the limbs in an attitude of flexion so that at times the
wounds heal by formation of flexion contractures. All these
contractures should be prevented.
COMPLICATIONS
The most common complications of burns are burn wound
infections and pneumonia which are leading causes of death
in burnt children. Gastrointestinal complications are also
common and include gastric ulceration (stress ulcer–Curling
ulcer), pancreatitis, enterocolitis and superior mesenteric
artery syndrome. Adequate fluid resuscitation is most
effective means of prevention. Large surface area burns
may cause hemolysis and muscle necrosis and lead to
hemoglobinuria and myoglobinuria. Most often ignored are
psychological sequelae because of disfigurement and loss
of function.
PROGNOSIS
A large number of factors affect the prognosis in a burned
child. Mortality in pediatric burns is affected by three main
risk factors: inhalational injury, burn size more than 30%
and age less than 4 years.15 The presence of inhalational
injury doubles the mortality rate. Management of extensive
burns is extremely expensive and often prolonged. The poor
socio-economic status is certainly a contributing factor in
increasing the morbidity and mortality.
PREVENTION
Majority of burns in children can be prevented if adults
become more careful and do not leave the children
unattended. We should teach children about being careful
of hot liquids, fire and electricity from a very young age
(perhaps 2 years onwards). Since immersion scalds are
very common while giving a bath to the child especially in
winter, it is important for parents to ensure not to leave hot
water bucket unattended and mix hot water into cold water
while preparing for a child’s bath and not vice versa.
Firecrackers should be burst only under supervision of
adults. The electrical sockets should be at a higher level and
out of reach of small children. Strong acids and alkalis should
be stored in houses at a place not accessible to children.
Schools, television and other media can help in spreading
awareness in the community. In India, there are no laws
and regulations and strict enforcement of laws to prevent
burns in childhood resulting in a very high incidence of
burns. In developed countries like UK, there are a number
of Acts, like ‘The Children and Young Persons Act,1914’,
‘Heating Appliances Act,1971’, Night Dresses for Children’s
Act,1962. etc. to safeguard against burns in children.
SUMMARY
Burns in children leave lifelong scars which are enormous
stressors for both the child and his parents as they affect
their development not only physically but mentally as well.
Burn management in pediatric age group can be a great
challenge because physiologically, the skin and organ
systems are immature and cannot tolerate stress like an
adult and therefore, they respond differently to thermal injury.
Emotionally, children are again immature and incapable of
handling pain and disfigurement associated with burn. The
burn wound management and the surgical approach to
pediatric patients, therefore, varies according to depth and
extent of burns. Both the child’s family and the treating
doctor have an important role to play in the eventual outcome
of the child who comes out successfully from the physical
trauma of burns.
REFERENCES
1. Libber SM, Slayton DJ. Childhood burns reconsidered: The child,
the family and the burn injury. J Trauma 1985;24:245-52.
2. Leake JE, Curtin JW. Electrical burns of the mouth in children.
Clin Plast Surg 1984;11:669-83.
3. Lund CC, Browder NC. The estimation of area of burns Surg Gynecol
Obstet 1944;79:352-58.
4. Conway H. Management of burns in children. Am J Surg,
1964;107:537-43.
5. Knaysi GA, Crikelair GF, Cosman B. The rule of Nines: Its history
and accuracy. Plast Reconstr Surg 1968;41: 560-63.
6. Lynch JB, Blocker V. The rule of five in estimation of extent of
burn. In: Converse JM (Ed). Reconstructive plastic surgery. 1st
edn. Philadelphia WB Saunders Co. 1964; New York, 208.
7. Wachtel TL. Crit Care Clin 1985;1(1):3-26.

404
Principles and Practice of Burn Care
8. Pruitt BA, Jr. Advances in fluid therapy and the early care of the burn
patient. World J. Surg, 1978;2:139-50,
9. Baxter CR. Problems and complications of burn shock resuscitation.
Surg. Clin. North Am, 1978;58:1313-22.
10. Merrell SW, Saffle JR, Warden GD et al. Fluid resuscitation in
thermally injured children. Am. J. Surg 1986;152: 664-69.
11. O’Neill JA Jr. Fluid resuscitation in the burned child. A reappraisal.
J. Paed. Surg 1982;17:604-07.
12. Graves TA, Cioffi WG, McManus WF, Mason AD, Pruitt BA. Fluid
resuscitation of infants and children with massive thermal injury. J.
Trauma, 1988;28(12):1656-59.
13. Bissoni RS, Holtgrave DR, Lawler F, Marley DS. Colloids versus
crystalloids in fluid resuscitation: an analysis of randomized
controlled trials. J. Family Practice 1991;32(4);387-90.
14. Gore DC, Dalton JM, Gehr TW. Colloid infusion reduces glomerular
filtration in resuscitated burn victims. J. Trauma: Injury Infect Crit
Care 1996;40(3):356-60.
15. Cocks AJ, O’ Connell A, Martin H. Crystalloids, Colloids and kids:
a review of pediatric burns in intensive care. Burns 1998;24:
717-24.
16. Sheridan RL, Schnitzer JJ. Management of the high risk pediatric
burn patient. J Pediatric Surgery 2001;36(8): 1308-12.
17. Nguyen TT, Gilpin DA, Meyer NA, Herndon DN. Current treatment
of burned patients. Ann Surg 1996;223(1): 14-25.
18. Carvajal HF. A physiologic approach to fluid therapy in severely
burned children. Surg. Gynaecol. Obstet 1980;150:379-84.
19. Brown AP, Khan K, Sinclair S. Bacterial toxicosis toxic shock
syndrome as a contributor to mortality in children with burn injuries.
Burns 2003;29:733-38.
20. Curreri PW, Luterman A. Nutritional support of the burned patient.
Surg Clin North Am 1978; 58:1151-56.
21. Hildreth M, Carjaval HF. Caloric requirements in burned children: A
simple formula to estimate daily caloric requirements. J Burn Care
Rehabil 1982;3:78-80.
22. Manafo WW, Freedman B. Topical therapy for burns. Surg Clin
North Am 1987;67:133-45.
23. Housinger TA, Lang D and Warden GD. A prospective study of
blood loss with excisional therapy in pediatric burn patients. J
Trauma 1993;34:139-41.
24. Cason JS. Treatment of Burns Chapman and Hall, London, 1981;
4-5.

Burns during Pregnancy
405
Burns during Pregnancy
30
Shailesh Ranade
Chapter
INTRODUCTION
Burns during pregnancy presents a unique medical problem.
Both mother and fetus are at great risk of fluid loss,
hypoxemia and sepsis. Most of the textbooks on obstetrics
do not deal with burns in pregnancy nor is the topic
considered in depth in books devoted to the treatment of
burns. In India and other countries, where burns present as
a socio-medical problem, the incidence of burns in pregnancy
is far more than that in the Western world.
INCIDENCE
The literature on burns during pregnancy is quite limited.
However, the incidence calculated by the various authors in
relation to the total number of female burn patients of
reproductive age, does not appear to be low. The incidence
in early pregnancy was unknown in past due to the absence
of routine pregnancy testing on admission. Easy availability
of pregnancy determination tests has increased the reporting
of burns in pregnancy.
The highest incidence of burns during pregnancy has
been reported from India. It has ranged from 7% as
calculated by Akhtar 1 to 13.3% reported by Jain 2 and 15%
reported by Prasanna.3 Taylor4 calculated an incidence of
7% while Amy5 (1985) reported the incidence as 6.7%.
Similar incidences have been reported by Gang 6 from
Kuwait (7.8%) and Srivastava 7 (7.9%). Benmeir 8 from
Israel reported an incidence of 0.6%.
ETIOLOGY
The aetiology of burns in pregnancy does not vary from
the general etiology of burns as a whole. A special mention
is, however, required for burns in pregnancy in countries
like India, where dowry and familial disputes in a joint family
are common causes of suicidal and homicidal burns. These
are wrongly reported as accidental burns due to false history
given by the victim. Most of these patients are very severely
burned and often have a very high maternal and fetal
mortality.
PATHOPHYSIOLOGY OF BURNS IN
PREGNANCY (FLOW CHART 30.1)
A pregnant burned patient presents following additional
pathophysiological changes.9,10
1. Pregnant patients have a lower FRC (Functional Residual
Capacity) and are less able to compensate for hypoxia.
Moreover, exposure to burns often puts the mother at
risk for carbon monoxide inhalation. The fetus is
especially susceptible to carbon monoxide poisoning
because fetal hemoglobin has a higher affinity for carbon
monoxide than maternal hemoglobin does. Thus, carbon
monoxide can easily lead to fetal hypoxia.
2. Effect of Burns on Uterine Activity: The onset of labor
in a premature delivery shortly after a serious burn was
in the past thought to be triggered by the endocrine
function, especially by secretion of adrenocortical
hormones related to stress. Later observations confirmed
that minor burns had no effect on the course of pregnancy,
while bums of at least 35% TBSA were capable of
provoking early labor and the loss of the fetus following
intrauterine death within a week of the burns.
Both spontaneous miscarriage and premature delivery
were subsequently thought to be related to the synthesis

406
Principles and Practice of Burn Care
and release of prostaglandins (responsible for early uterine
contractions) from the skin in the burned area. Later,
however, the correct importance was attributed both to
maternal shock, which determines a considerable reduction
in the uterine blood flow and causes fetal hypoxia and to
pleuropulmonary complications, especially in cases of
inhalation injuries with grave reduction of maternal pO2 and
consequently fetal hypoxia. The fetus may be able to tolerate
the early phases of maternal sepsis but is notably affected
in the advanced phases, when the mother is decompensated
and her cardiovascular system collapses. Thus, hypotension
and acute respiratory insufficiency with septicemia can lead
to complications in the fetus, even some time after the burn
(Flow chart 30.1)
As the maternal intravascular space is in a state of
equilibrium with the amniotic liquid, the reduction of this
liquid during serious hypovolemia can cause the intrauterine
death of the fetus. The onset of spontaneous uterine
contractions is also favored by the release from bacteria
and the placenta of an enzyme, phospholipase A, which is
necessary for the conversion of arachidonic acid into
prostaglandin. It has recently been shown that there is a
considerable reduction in plasma levels of 17β-estradiol in
pregnant burned women who had either an abortion
or a still birth in the first week post burn (Figs 30.1
and 30.2).
MANAGEMENT OF BURNS AND ITS INFLUENCE
ON THE COURSE OF PREGNANCY AND
THE FETUS
Medical Treatment
Resuscitation treatment in the burned pregnant woman is
no different from that in the non-pregnant burned woman.
The prevention of hypovolemic shock by adequate early
fluid resuscitation, therefore, requires that the uterine blood
flow should be able to maintain fetus tissue pO2 levels within
the normal range. It has been recommended that a quantity
of fluid should be administered that is sufficient to maintain
the mother’s blood pressure within the normal range and
maintain urine output to 0.5-1.0 ml/kg body weight/hour.
The maintenance of arterial pressure levels at normal values
is essential at all stages of the burn disease. Diuretics and
antihypertensive drugs should, therefore, be avoided,
whenever possible. Episodes of hypotension should also be
avoided in the event of surgical operations. It is
recommended that surgery should be performed with
intraoperative maintenance of a minimum of 1 ml/kg body
weight/hour of urine volume and 100% oxygen saturation.
Since extensive surface burns are frequently associated
with an increased rate of arterial shunting and hypoxia, it
becomes necessary to administer oxygen. A pregnant
patient’s oxygenation can often be improved by nursing her
in a semi-sitting position. Maternal pO2 values of less than
60 mm of Hg during the pleuropulmonary complications
Flow chart 30.1: Pathophysiological changes in pregnant patient following major burns, affecting the foetus (Courtesy: Rayburn, 1984)

Burns during Pregnancy
407
that are often secondary to inhalation have been considered
critical. It has, therefore, been recommended that ventilatory
support should be initiated as soon as possible. This is all
the more necessary because inhaled carbon monoxide can
also cross the placental barrier to compete for binding sites
on fetal hemoglobin, provoking fetal cardiac edema and also
affect cardiac development. The newer inventions in
respiratory supportive care, like BIPAP (Biphasic Positive
Airway Pressure) and CPAP (Continuous Positive Airway
Pressure) ventilators have added a non-invasive method of
ventilation as an option to standard ventilators. In cases of
bronchopneumonia, it is necessary to use antibiotic
treatment, if possible, by selecting drugs that the fetus can
tolerate.
Wound Care
The local treatment of burns in pregnant women is not
simple, because of the limitations imposed by the state of
pregnancy.
•
Sulfa drugs (silver sulfadiazine) are suspected of potential
teratogenous activity if administered before the 14th
week of pregnancy and of retarding growth, determining
low birth weight if subsequently administered. Sulfa
drugs administered at the term of pregnancy are
responsible for kernicterus.
•
Povidone-iodine is widely used for burns cleansing. It
must, however, be avoided during pregnancy since large
amounts of iodine can be absorbed through the burn
wound. Use of povidone-iodine is inadvisable in burns
exceeding 20% total body surface area (TBSA) because
the iodine passing through the placenta can be absorbed
in sufficient quantities to affect thyroid functions and
cause metabolic acidosis.
It is, thus, clear that the state of pregnancy
considerably reduces use of the commonest protocols
for the topical treatment of burns.
•
Salicylates exert an anti-prostaglandin action and may,
therefore, have a protective effect on pregnancy. For
the same reason they should not be used in the final
period of pregnancy because they prolong gestation and
delay spontaneous delivery. There is little evidence
regarding the possibility that salicylates have a
teratogenous effect, although the birth weight of babies
born to women subjected to chronic administration of
salicylates has been reported to be below average. An
increase in perinatal mortality has also been reported.
These results have not, however, been confirmed in other
studies.
•
Chloramphenicol, either in powder form or as an
ointment, is among the drugs to be avoided throughout
pregnancy since it is teratogenic if administered during
the first period of pregnancy and responsible for neonatal
pathology if used during the final period (Grey
syndrome).
•
Gentamicin (ointment form) is an aminoglycoside
capable of passing through the placenta after absorption
Fig. 30.1: Patient with 90% thermal burn and 7 months pregnancy
aborted on the third day post burn spontaneously. Aborted fetus seen
within intact membranes
Fig. 30.2: Patient with 60% thermal burns and full term pregnancy
was induced within 48 hours to deliver a normal live baby as seen in
the picture

408
Principles and Practice of Burn Care
through burned area. If used after the 14th week of
pregnancy, it can cause lesions in the 8th pair of cranial
nerves, with vestibular and acoustic damage. The full-
term fetus has been found to present antibiotic
concentrations analogous to those of the mother. In
addition aminoglycosides are responsible for
nephrotoxicity.
•
Rifamycin (for local application) is absolutely avoided
during the last period of pregnancy because its
interference with bilirubin metabolism can cause indirect
hyperbilirubinemia with risk of kernicterus.
•
Even the local use of antibiotics that are normally
administered systemically presents considerable
difficulties.
The only antibiotics that can be considered safe in
pregnancy are the penicillins and cephalosporins, while
vancomycin, one of the most frequently used and most
active antistaphylococcal drugs, is considered to be
potentially teratogenic and ciprofloxacin may possibly
damage articular cartilages in undeveloped organisms.
Other commonly used antibiotics (Imipenem,
teicoplanin) should be avoided in the absence of adequate
information about their safety during pregnancy unless they
are absolutely necessary and their advantages outweigh any
possible risk.
Tetracyclines are not widely used in burns but it should
not be forgotten that they are contra-indicated during
pregnancy because of their varying effects on fetal growth,
bones, teeth and the immune system.
With regard to surgical procedures performed under
anesthesia, it is important to avoid the use of ketamine,
which increases the excitability of the myometrium because
it is capable of triggering effective contractions. When the
pregnancy is near term and delivery is imminent, ketamine
may cause respiratory depression in the neonate.
It is preferable to keep the operative procedures as short
as possible. During the period of anesthesia, it is important
to maintain the oxygen saturation and blood pressure within
normal limits throughout the procedure.
Surgical Treatment
In view of the difficulties related to local medical treatment,
early surgical treatment assumes vital importance. This is
because early surgery facilitates healing of the wounds and
thus improves prognosis of both mother and neonate. Early
burn wound cover also minimizes septic complications and
the need to administer antibiotics; in addition, it reduces the
necessity of analgesic drugs.
The treatment for full thickness burns comprises early
tangential excision and split-thickness skin-grafting 3-7 days
post burn (but not more than 15-20% TBSA at one operation).
The invention of biological skin substitutes has dramatically
improved the management of II° burns. Processed animal
collagen sheets (Commercially available as Apocoll and
Kollagen), Integra, Biobrane help in covering even very large
burn wounds preventing the fluid loss, reducing pain,
chances of wound infection and obviating the need of regular
dressings.
Wounds over the abdomen and breast have to be treated
first. Good early healing of the abdominal wound favors:
•
Pain-free stretching of the abdominal skin during the
developing pregnancy to term
•
Abdominal obstetric supervision of the growing fetus
•
Performance of cesarean section if required
Early surgery of the breast wound prevents infection
and sloughing of nipples and permits subsequent
breastfeeding.
Obstetric Management of the Pregnant Woman
with Burns (Table 30.1)
If it is known that a burned female is pregnant, it is important
to establish as precisely as possible the exact stage of
pregnancy at the time of the burn accident. This must be
based upon the menstrual history and fetal ultrasound
examination. The gestational period is in fact one of the
factors determining obstetric procedures (no intervention,
protection of pregnancy by tocolytic treatment, induction
and/or acceleration of labor). Other factors such as the
severity of the burn and fetal viability must be confirmed
immediately. Ultrasound examination helps in anatomical
measurements such as biparietal diameter, to determine the
age of fetus, biophysical measurements such as fetal muscle
tone, limb motion and breathing patterns to know the
condition of fetus. In addition placental morphology,
placental blood flow and amniotic fluid volume may be
visualized in order to assess fetal health.
With regard to the stage of gestation, fetuses delivered
before 24 weeks generally do not survive, while those
delivered after 32 weeks do well with modern neonatal
intensive care if born without hypoxia or birth trauma. The
most difficult to manage are fetuses between 24 and 32
weeks’ of gestational age, where ex utero survival is
difficult to predict. In such cases, therefore, when preterm
labor occurs, tocolytic procedures are initiated.

Burns during Pregnancy
409
In women with advanced state of pregnancy (2nd and
3rd trimester) with more than 50% TBSA burns, it had an
unfavorable effect unless delivery was immediate, as the
burn created an unfavurable environment for the fetus. In
burns less than 40% TBSA, pregnancy and its continuation
had no effect on prognosis in the mother and every attempt
had to be made to interrupt inception of labor if the fetus is
too immature to survive.
Regarding the manner of delivery (vaginal route, cesarean
section), spontaneous vaginal delivery is generally preferred,
although obstetric considerations affect the choice of route
and the timing of the delivery. Serial fetal sonography and
fetal heart rate monitoring identifies fetal stress at an early
stage and may permit timely intervention, preventing
intrauterine death. In a critically burned woman with a living
and near-term pregnancy, fetal salvage by cesarian section
appears justifiable.
When there are obstetric indications for a cesarean
section, this can be performed even when the lower
abdominal wall is part of the burned area.
Thus, pregnant burned patient, especially when severely
burned, is a big challenge for a Burn Surgeon. A
comprehensive team effort involving a Plastic Surgeon,
Intensivist, Obstetrician, Neonatologist, Anesthesiologist,
Chest Physician and well trained nursing staff with other
supportive departments can help in saving two lives at
a time.
REFERENCES
1. Akhtar MA, Mulawkar PM, Kulkarni HR. Burns in pregnancy:
Effect on maternal and fetal outcomes. Bums, 1994;20:351-5.
2. Jain ML, Garg AK: Burns with pregnancy - a review of 25 cases.
Burns, 1993;19:166-7.
3. Prasanna M, Singh K. Early burn wound excision in major bums
with pregnancy: A preliminary report. Bums, 1996;22:234-7.
4. Taylor JW, Plunkett GD, McManus WF, Pruitt BA Thermal injury
during pregnancy. Obstet. Gynec 1976;47:434-8.
5. Amy BW, McManus WF, Goodwin CW, Mason A, Pruitt BA Thermal
injury in the pregnant patient. Surg. Gynec. Obst 1985;161:
209-12.
6. Gang RK, Bajee J, Tahboub M. Management of thermal injury in
pregnancy: An analysis of 16 patients. Burns 1992;18:317-20.
7. Srivastava S, Bang RL. Bums during pregnancy. Burns, 1998;14:
228-32.
8. Benmeir P, Sagi A, Greber B, Bibi C, Hauben D, Rosenberg L, Ben-
Yaqar Y, Mather D. Burns during pregnancy: Our experience. Burns
1988;14:233-6.
9. Rayburn W, Smith B, Feller I, Varner M, Cruikshank D. Major bums
during pregnancy: Effect on fetal well-being. Obstet. Gynecol
1984;63:392-5.
10. Napoli B, D’Arpa N, Masellis M, Graziano R Burns in Pregnancy,
Annals of Burns and Fire Disasters - vol. XIII – no. 1 - March
2000.
Table 30.1: Obstetric management in burned patients 6
Total % burn
Age of Gestation
Management
< 30 % TBSA
First trimester
No obstetric interference
Second trimester
No obstetric interference
Third trimester, less than 36 weeks
Conservative approach and monitoring of heart rate
Third trimester, more than 36 weeks
Induce labor/Cesarian section
30-50% TBSA
First trimester
Fetal monitoring by ultrasound 3-4 weeks
Second trimester
Fetal monitoring every 3-4 weeks. Tocolytic therapy
Third trimester, less than 36 weeks
Careful fetal monitoring
Third trimester, more than 36 weeks
Deliver fetus within 48 hours
50-70% TBSA
First trimester
Terminate pregnancy
Secotd trimester
Terminate pregnancy
Third trimester, if baby is viable
Induce labor/cesarian section within 24 hours.
Third trimester, intrauterine death
No active intervention up to 4 weeks/monitoring of
hemocoagulation factors
> 70% TBSA
First trimester
No treatment
Second trimester
No treatment
Third trimester
Cesarian section as an emergency procedure at the earliest

Multiple Organ Dysfunction Syndrome in Burns
411

(Trang không có chữ)

Multiple Organ Dysfunction
Syndrome in Burns
31
Anil Chadha, Indu Chadha, Amitabh Singh
Chapter
INTRODUCTION
“The body falling part, mind failing, spirits weakened and
the will lacking – all heralding grave tiding” conveys the
sense of hopelessness Multiple Organ Dysfunction
Syndrome reflects.1 MODS or Multiple Organ Dysfunction
Syndrome is the major cause of mortality in extensive
burns.2,3 It has been known for more than three decades
but an assured defense against it is yet to be convincingly
established. As has been understood since long, the
management of major burns is mainly an exercise in
combating the systemic inflammation precipitated by the
burn trauma. The inflammatory reaction of the body is the
physiological basis for recovery from such a trauma. It is
the self perpetuated excessive host defense that proves
counter-productive in some patients and leads to a state,
wherein there is dysfunction and eventual failure of one or
more organs, called MODS. The ability to prevent/treat
MODS is the defining point in the management of critical
burns. This chapter attempts to explain the meaning of
MODS and its significance in context to burns. The essence
of the reactions to the biochemical mediators of inflammation
has been mentioned without mentioning the details of each
one in the cascade in order to relate to this complex process
with burns in an undiluted manner.
As a prelude to the recognized entity of MODS, Tilney
et al (1973) reported the failure of multiple organs in the
postoperative period of ruptured aortic aneurysm.4
Interestingly, a similar clinical picture was seen in diverse
conditions like pancreatitis, peritonitis, bowel perforation,
prolonged shock following valve replacement and major
burns by Baue in 1975.5 It was termed ‘Sequential System
Failure’. In 1977, Eiseman, Beart and Norton named it
‘Multiple Organ Failure’.6 Fry and his colleagues in 1980
noticed that gram-negative sepsis was a common event that
preceded MOF due to the diverse causes.7 The
lipopolysaccharide (LPS) was identified as the responsible
bacterial endotoxin and from 1980 to 1985, empirical
treatment of infection with antibiotics was the mainstay of
therapy in multiple organ failure.7, 8 It was later realized that
not all patients of MODS were due to infection and those
dying of MODS did not always have culture proven
infection.7 Search for a common mechanism to the diverse
etiologies of MODS is still elusive and the molecular basis
for specific organ failure remains to be fully uncovered.
The clinical entity of MODS has come into being with
the prolonged survival of the critically ill patients due to the
advances in critical care in the last three decades.9 Earlier
these patients with multiple failing organs would surely have
died. Research in this field has improved the understanding
about the course of events and it has prompted promising
therapeutic interventions. Before understanding the
pathological basis of MODS, a brief overview of the course
of events in MODS would help us understand the condition
in a better context.
Since 1800s it has been known that a burn injury is an
inflammatory reaction.10 It is typically a defense reaction
for the benefit of the body. It remains localized as long as
the area of burns is small and the inflammatory state abates
with the healing of the wound. In instances where the area
of burns is large (> 20% TBSA), the body responds with
an inflammatory reaction of a larger magnitude. This state
is mainly homeostatic and immunological in the immediate

414
Principles and Practice of Burn Care
setting with other processes following for the defense of
the body. A state of systemic inflammation sets in as a local
defense and homeostatic control (Fig. 31.1). Adequate
resuscitation at this stage potentially reverses the deranged
systemic changes due to the burn trauma. However, due to
large extent of burn trauma, the hypermetabolic state has
been seen to persist even in the absence of any complications
or infection and sometimes even after the burn wound has
healed.11 The biochemical mediators that are released due
to the inflammatory/immune response and the
neuroendocrine activity, act for the benefit of the host
defense and repair mechanism. The presence of necrotic
slough, uncovered wounds, donor site raw areas, inadequate
resuscitation, pathological fluid derangements,
hypoperfusion of gut mucosa, nosocomial infections, access
port infections, stress response, reperfusion injury, etc.
perpetuates this state of systemic inflammation. These small
but persistent stimuli along with the high risk of wound
contamination to invasive infection link up to generate a
momentum in the systemic inflammatory state, which gets
detached from the control of counter-inflammatory measures
and becomes uncontrolled and self perpetuating. The local
and homeostatic responses become systemic derangements
exacerbated not only by endothelial damage but also
ischemia/reperfusion injury.12
As a protective reaction, the inflammatory process
induces vasodilatation and increased capillary permeability
at the local site of burn injury. When these mediators come
into systemic circulation it results in systemic vasodilatation
and leakage of intravascular fluid into the third space resulting
in pulmonary edema, generalized edema and severe
hypotension. This nonspecific activation of a generalized
inflammatory response mainly from leukocytes,
macrophages and endothelial cells results in a sequence of
events that leads to intravascular microthrombi and the
inability to use the available oxygen, which marks the
progression of a patient from SIRS(Systemic Inflammatory
Response Syndrome) to MODS. MODS encompasses
failure of one or more organs, most commonly the lungs; it
deteriorates from its optimal function and may progress to
failure. Since it is a dynamic change rather than an ‘all or
none’ phenomenon, the term MSOF (Multi System Organ
Failure) has been replaced by MODS Multiple Organ
Dysfunction Syndrome).13
The already decreased circulation due to the fluid shift
is further compromised by the formation of microthrombi;
resulting in global tissue hypoxia. Hypoxia activates the
sympathetic nervous system causing the stress response,14
which in essence shunts more blood to the heart depriving
other organs of oxygen, mainly the kidneys and gut.
Hypoperfusion of the gut, besides facilitating bacterial
translocation, results in release of pro-inflammatory
mediators, which contributes to the mediator-induced acute
lung injury, bone marrow depression, myocardial
dysfunction, neutrophil activation, red blood cell injury and
endothelial cell activation and injury.15 Compromised renal
function, due to hypoperfusion, impairs its ability to remove
toxins from the body and makes their function as an acid-
base buffer system ineffective at a time when it is more
efficiently required. Generalized hypoxia leads to anaerobic
metabolism and consequent lactic acidosis. The increased
lactate levels further exacerbate MODS by altering the
intracellular ion pumps, mitochondrial functions and normal
carbohydrate metabolism. The adrenergic activity of the
stress response leads to retention of sodium and water,
hyperglycemia and insulin-resistance. The function of the
other acid-base buffer system of the body, the lungs, is
already compromised due to the mediator-induced injury as
the lungs are more susceptible. Interestingly, the usual
sequence of organ dysfunction in progression from SIRS
to MODS is lungs, gut, central nervous system, vasomotor,
cardiac, hematologic, liver and then renal.16,17 To further
compromise the functioning of the body, the fluid shifts to
the third space result in pulmonary edema and further
decreases oxygenation at a time when it is most required.
At this juncture the autonomic dysfunction due to MODS
disjoints the cardio-respiratory system.18
All these events occur almost in tandem with the clinical
progress of the burn wound and the burnt patient. As long
as the majority of the areas are timely excised and covered
after efficient ‘goal directed’ resuscitation in a patient, who
is low risk for progressing to MODS; the wound heals and
the patient recovers. On the contrary, a similar patient with
Fig. 31.1: Natural course of MODS

Multiple Organ Dysfunction Syndrome in Burns
415
all the risk factors would probably end up with a prolonged
inflammatory state with high likelihood of progressing to
MODS (Fig. 31.2) if due attention to its prevention is not
given. It is imperative to understand in treatment of organ
support and MODS that the unregulated host response rather
than the triggering factor has the main bearing on the
outcome. Further sections detail the pathogenesis along with
the predisposing risk factors and the methods to monitor
the patient so that any deterioration or progression towards
MODS could be detected at the earliest and corrective
intervention prompted. Hence, the importance of a dynamic
scoring system for MODS in burn trauma with high
sensitivity and specificity to diagnose the severity/
reversibility of organ dysfunction, day-to-day monitoring
and if possible, predict mortality.
becomes unregulated, it may lead to endothelial damage of
capillaries resulting in interstitial edema and organ
dysfunction.
CYTOKINES:25 Briefly cytokines have the following
functions (1) directing a T lymphocyte response; (2)
inducing enzyme production in distant sites (e.g.
endothelium: nitric oxide, liver: C reactive protein); (3)
altering cell surface adhesion molecules.
They are categorized as (a) growth factors (e.g.
Transforming growth factor β); (b) leukocyte chemotactic
chemokines (e.g. IL-8); (c) modulators of lymphocyte
function (e.g. IL-4) and (d) modulators of inflammatory
response (IL-6 as a pro-inflammatory mediator, IL-10 as
an anti-inflammatory mediator). Cytokines induce MODS
by (1) excessive production of free radicals (2) induction
of elastase or endopeptidases and (3) elevation of circulating
soluble peptides that activate apoptosis (programmed cell
death). TNF-α and IL-1 are considered the most essential
mediators responsible for MODS.26 They activate the
immunological activity and endothelial cells, inducing fever
and excessive hypermetabolism besides causing local tissue
destruction, microvascular injury and increase in
microvascular permeability leading to hemodynamic
insufficiency and a refractory shock state.27
TNFα28—An amino acid polypeptide released as an
inflammatory reaction from monocytes, pulmonary
macrophages, Kupffer cells and endothelial cells; it has a
pleiotropopic effect on the target cells. Notable deleterious
effects are induction of fever, SIRS, myocardial depression
and cardiovascular collapse, shock, elevated liver enzymes,
coagulopathy and carbohydrate, fat and protein metabolism
leading to cachexia.
Interleukin-129—They are expressed from monocytes, tissue
macrophages, neutrophils and B lymphocytes during the
inflammatory response. IL-1, present as IL-α and IL-β,
accelerates the T cell proliferation and induces mature and
immature granulocytes from the bone marrow. It also directly
stimulates neutrophils and is a strong inductor of
granulocyte/macrocyte colony stimulating factor (CSF) and
CSF-release. It causes fever, hemodynamic abnormalities,
anorexia, arthralgia and headache by stimulating local release
of prostaglandins from the anterior hypothalamus.
Interleukin-6 – IL-6 is a glycoprotein, produced by
lymphocytes, fibroblasts and monocytes. It activates B and
T lymphocytes, protein production in liver and coagulopathy.
IL-6 is an integral part of cytokine cascade in organ injury.
Fig. 31.2: Outcome of MODS
Unfortunately, the quantum of research in MODS is
mainly related to the non-burn population and hence a
consolidated protocol for each event is still in evolution.
The most promising therapy for MODS, even today, is its
prevention.19 MODS has a reported mortality of more than
50%20,21 which increases to 60 to 98% with the number of
organs failing and the duration they remain dysfunctional.22
Treatment protocols include organ support, alleviation of
the trigger factors and an attempt to counter the unwanted
effects of the mediators of inflammation, which have yet to
significantly improve the outcome in critical burns.
COMMON CHEMICAL MEDIATORS
A very brief outline of the common chemical mediators is
mentioned here for ease of understanding; it is not a complete
description.
Endotoxins:23,24 This is the lipopolysaccharide component
of the outer membrane of the gram-negative bacteria. It
stimulates the release of the biochemical mediators of
inflammation and triggers the complement cascade. When
this beneficial inflammatory response to the endotoxin

416
Principles and Practice of Burn Care
Interleukin-8 – It is protein cytokine produced by
mononuclear phagocytes, PMN leukocytes, endothelial cells,
epithelial cells and mesothelial cells in response to endotoxin,
IL-1 and TNF-α. IL-8 attracts and activates neutrophils to
the site of inflammation and is an angiogenic factor. It causes
transient neutropenia but no tissue neutrophilia, inflammation
or injury has been seen with IL-8.
Soluble receptor and receptor antagonists – sTNFR - Soluble
cytokine receptors produced by proteolytic cleavage of cell
surface have been reported for TNF-α, IL-6 and IL-1β.
sTNFR has ability to bind TNF-α and mediate the actions
of the cytokines. The bioactivity of TNF-α is based on the
equilibrium between free TNF-α and that bound to sTNFR.
The IL-1 receptor antagonist concentration is seen to
increase in infection; however it does not correlate with the
outcome.
Adhesion molecules—The diapedesis of neutrophils from
the intravascular space to the site of inflammation is effected
by loose tethering (Primary adhesion), which either may
flow away with the blood stream or develop into strong
binding (Secondary adhesion) to the endothelium; a
prerequisite for migration into the extravascular space. These
adhesion molecules are induced by cytokines like TNF-α
and IL-1.
Nitric oxide (NO)30—TNF-α and endotoxins can induce
calcium independent synthesis of NO. It causes vascular
smooth muscle relaxation and inhibition of platelet induced
thrombosis, myocardial depression, cytotoxic effects and
organ failure. Activated macrophages and kupffer cells are
said to produce NO in shock state.
Arachidonic acid metabolites – They are released from
leukocytes, macrophages and pulmonary endothelial cells
via the cyclo and lipo-oxygenase pathways. These
metabolites can modify the host response in septic shock.
Thromboxane induces potent vasoconstriction,
bronchoconstriction and platelet aggregation. Leucotrienes
are implicated in ARDS and they participate in pulmonary
vasoconstriction, bronchoconstriction, allergy, coronary
vasoconstriction and myocardial depression.
PAF – It is an active phospholipid synthesized normally in
the body. It is produced by cytokines, macrophages,
neutrophils, eosinophils, endothelial cells and platelets, kidney
glomerular cells and gastrointestinal epithelial cells. PAF is
a critical mediator in septic shock, ARDS, graft rejection
and MODS by causing increase in vascularity, permeability
and causes endothelial bed leak and platelet aggregation.
Pro-inflammatory effects of PAF cause neutrophil priming
and PMN endothelial adherence, which are responsible for
the distant organ injury.
The following text describes the etiopathology of MODS
in Burns, the scoring systems and the management. To help
understand multiple organ dysfunction syndrome in context
to burns it is imperative that one follows a standard definition
to label an organ as dysfunctional or a patient to be in SIRS,
etc. Hence, a brief summary of the definitions of organ
failure, SIRS (Systemic Inflammatory Response Syndrome),
MODS and sepsis is being mentioned.
ORGAN-SPECIFIC DEFINITIONS OF FAILURE39
If the patient had one or more of the following during a 24
hour period (regardless of the values), OSF existed on that
day
Cardiovascular failure (presence of one or more of the
following)
Heart rate ≤ 54/min
Mean arterial blood pressure ≤ 49 mm Hg
Occurrence of ventricular tachycardia and/or ventricular
fibrillation
Serum pH ≤ 7.24 with a PaCO2 of ≤ 49 mm Hg
Respiratory failure (presence of one or more of the
following):
Respiratory rate ≤ 5/min or ≥ 40/min
PaCO2 ≥ 50 mm Hg
AaDO2 ≥ 350 mm Hg (AaDO2 = 713 FIO2 – PaCO2 –
PaO2)
Dependent on ventilator on the fourth day of OSF, e.g.
not applicable for initial 72 hours of OSF
Renal failure (presence of one or more of the following):
Urine output ≤ 479 ml/24 hour or ≤ 159 ml/8 hour
Serum BUN ≥ 100 mg/dl
Serum creatinine ≥ 3.5 mg/dl
Hematologic failure (presence of one or more of the
following):
WBC ≤ 1000 mm3
Platelets ≤ 20,000/mm3
Hematocrit ≤ 20%
Neurological failure
Glasgow Coma Score ≤ 6 (in absence of sedation at
any one point in the day)
Sheridan17 simplified the definitions of organ failure in
his review, they are as follows:

Multiple Organ Dysfunction Syndrome in Burns
417
Organ system Definition
Lung
Ventilator dependence more than 72 hours
after injury or PaO2/FiO2 ratio ≤ 150
Gut
Ileus requiring cessation of tube feedings
Central Nervous Glasgow Coma Score ≤ 6 in the
System
absence of neuromuscular blockade or
significant sedation
Vasomotor
Requirement for alpha vasopressors to
maintain normal mean arterial pressure
Cardiac
The requirement for Inotropes or
chronotropes or a serum pH ≤ 7.24 with
serum PaCO2 ≤ 49
Hematologic
Platelet count ≤ 100,000 or WBC count ≤
3500 per ml.
Liver
Serum transaminases ≥ 1.5 of normal
maximum value or PT and PTT ≥ 1.5
control with bilirubin ≥ 5.0
Renal
Serum BUN ≥ 100 and creatinine ≥ 3.5 or
urine output ≤ 500 ml/day.
SIRS (SYSTEMIC INFLAMMATORY RESPONSE
SYNDROME)32
The American College of Chest Physicians (ACCP), Society
of Critical Care Medicine (SCCM), The European Society
of Intensive Care Medicine (ESICM), the American
Thoracic Society (ATS) and the Surgical Infection Society
(SIS) Diagnostic Criteria for SIRS 2001.
Diagnostic criteria for SIRS include two or more of the
following:
Body temperature > 38° C or 36° C
Tachycardia with Heart rate > 90 beats per minute
Tachypnea manifested by respiratory rate > 20 breaths
per minute or PaCO2 < 32 mm Hg
Leukocytosis or white blood cell count > 12,000 cells/
mm3 or < 4,000 cells/mm3 or significant immature
neutrophils (>10%)
In 2001, the AACP, SCCM, ATS and ESICM updated
the previous criteria to include the following:
Chills, decreased urine output, decreased skin perfusion,
hypoglycemia
Poor capillary refill, petechiae, decreased platelet count,
skin mottling
Unexplained changes in mental status
SEPSIS11
Sepsis is a change in the burn patient that triggers the concern
for infection, the trigger includes at least three of the
following: (it is age-dependent and adjustments are necessary
for children)
I. Temperature > 39° or < 36.5° C
II. Progressive tachycardia
A.
Adults > 110 bpm
B.
Children > 2 SD above age-specific norms (85%
age-adjusted maximum heart rate)
III. Progressive tachypnoea
A.
Adults > 25 bpm not ventilated
B.
Children > 2 SD above age-specific norms (85%
age-adjusted maximum respiratory rate)
IV. Thrombocytopenia (will not apply until 3 days after
initial resuscitation)
A.
Adults < 100,000/mcl
B.
Children < 2 SD below age-specific norms
V. Hyperglycemia (in the absence of pre-existing diabetes
mellitus)
A.
Untreated plasma glucose > 200 mg/dl or
equivalent mM/L
B.
Insulin resistance – examples include
i. > 7 units of insulin/hour intravenous drip
(adults)
ii. Significant resistance to insulin (>25% increase
in insulin requirements over 24 hours)
VI. Inability to continue enteral feedings > 24 hours
A.
Abdominal distention
B.
Enteral feeding intolerance (residual > 150 ml/
hour in children or two times feeding rate in adults)
C.
Uncontrollable diarrhea (> 2500 ml/day for adults
or > 400 ml/day in children)
In addition, it is required that a documented infection
is identified
A.
Culture positive infection
B.
Pathologic tissue source identified
C.
Clinical response to antimicrobials
MODS (MULTIPLE ORGAN DYSFUNCTION
SYNDROME)33
MODS is defined as (definition from ACCP and SCCM)
“Presence of altered organ function in an acutely ill person
such that homeostasis cannot be maintained without
intervention. Primary MODS is the direct result of a well-
defined insult in which organ dysfunction occurs early and
(can) be directly attributable to the insult itself. Secondary
MODS develops as a consequence of a host response and
is identified within the context of SIRS (systemic
inflammatory response syndrome).”

418
Principles and Practice of Burn Care
Etiopathology
The clinical response to major burns brings about a state of
systemic inflammation. The initial insult due to burns on
the soft tissues, the hemodynamic system and the presence
of devitalized skin brings about an inflammatory change
mediated by the biochemical mediators, which act both
locally and systemically in defense of the host. A delayed or
inadequate resuscitation predisposes the patient to MODS,
also called ‘Primary MODS’. During the course of major
burns, there is a state of generalized systemic inflammation
due to the presence of devitalized tissue, raw areas,
inhalational injuries, split thickness donor sites, translocation
of bacteria from the gut and release of inflammatory
mediators from the hypoperfused gut, etc. Chen et al 34
reported that subeschar tissue fluid induced SIRS in healthy
rats possibly due to production of excessive inflammatory
mediators. The biochemical mediator response to these
inflammatory stimuli has remote organ effects as well, beside
the homeostatic and local defense it serves. The body is
primed for any further assault. Inherent to the nature of
burn trauma, burn wound infection is very likely and so are
events like breakdown of the gut mucosal barrier, access
port infection, etc. These repeated seemingly insignificant
events in an environment of burn trauma induced systemic
inflammatory state tend to maintain the internal milieu in a
condition similar to SIRS. SIRS or Systemic Inflammatory
Response Syndrome is a state of systemic inflammation
due to varied reasons and is suspected when the body
temperature, heart rate, respiratory rate and the leukocyte
count are abnormal along with chills, decreased urine output,
decreased skin perfusion, hypoglycemia, poor capillary
refill, petechiae, skin mottling, decreased platelet count
and unexplained mental aberration. In essence it is a
reflection of the compromised state of the various organ
systems. In certain circumstances this perpetual state of
inflammation becomes uncontrolled and multiple organs
of the body get affected. When this mechanism
overwhelms the critical threshold, defective oxygenation
occurs.35 This results in remote dysfunction of one more
organ not primarily affected by the burn trauma, most
commonly the lungs. Multiple Organ Dysfunction Syndrome
(MODS) is said to have set in when multiple organs are
affected, the defining factor between SIRS and MODS being
the inability of the host to use the available oxygen to its
benefit in MODS. When this constant state of SIRS is
perpetuated by the repeated stimuli and the host fails to
activate the required counter-inflammatory measures, there
is progressive deterioration in organ function and ultimately
the death of the patient.14
Proposed by SCOR23,36 (Specialized Center of Research)
for MODS. Initial insult (1st hit) such as inadequate tissue
perfusion, inflammation or dead tissue provoke the
inflammatory system by “priming PMN” to a latter insult
(2nd hit). The second hit can be any trauma, infection,
stress or an episode of hypotension. Second hit is an altered
response to injury and probably due to the initial activation of
the first insult. This can be altered or delayed by inadequate
resuscitation and is usually followed by an altered physiology
like microcirculatory ischemia, deterioration of the gut
barrier and if this sustained alteration continues it leads to
sustained SIRS followed by MODS and death (Fig. 31.3).
Fig. 31.3: Two hit model of MODS
Major burns are more likely to be complicated by MODS,
which could set in at the beginning–Primary MODS or later
in the course of treatment–Secondary MODS. In the large
majority, the cause of death in critical burns is MODS.
Hence, it is important to understand the pathogenesis of
this condition and know the predisposing factors and
conditions. The syndrome of multiple organ dysfunction is
a systemic manifestation of the overwhelming inflammatory
response incited by the trauma of burns or its consequent
course of events. A list of major predisposing factors is
mentioned below. These inciting factors or predisposing
conditions may precipitate MODS on their own or act as
small stimulating factors, which add up to aggravate the
ongoing controlled inflammatory state to an unregulated one.
Predisposing Factors for MODS
Known risk factors for MODS in Burns are listed
comprehensively as follows:
Advanced age
Inadequate resuscitation

Multiple Organ Dysfunction Syndrome in Burns
419
Prolonged tissue hypoxia during resuscitation
Reperfusion injury following ischemia
Presence of devitalized/necrotic tissue
Chronic recurring infections/sepsis
Endotoxemia
Massive blood transfusion
Inhalational injury, aspiration, lung contusion
Renal insufficiency
Malnutrition
Diabetes, Cancer, Pancreatitis, Trauma, Immuno-
suppressant therapy, chronic alcoholism.
Pathogenesis25,37-39
The progression from SIRS to MODS has been extensively
researched as regards the biochemical events and abundant
facts have emerged. However, despite the abundance of
experimental and clinical evidence, a single common
underlying event or process as the reason for a patient to
progress to MODS is yet to be precisely defined. It is difficult
to state that MODS is a single pathological process with
different expressions or a set of different pathological
processes which have a set defined end result.37 In spite of
these limitations the different events leading to MODS need
to be understood to be able to manage this condition better.
The pathogenesis of MODS is being described as related to
the more accepted theories.
Uncontrolled Infection
Sepsis in burns is a major cause for MODS. With extensive
availability of necrotic tissue and compromised tissue
vascularity, burn wound infection is the most expected
source of sepsis. However, early wound excision and
coverage with better infection control measures in burns
have decreased the incidence of fatal sepsis and though the
course of recovery is punctuated by multiple infectious
episodes, autopsy studies do not show uncontrolled infection
of the wound at the time of death from MODS.17 Lungs
and the gastrointestinal tract are also considered very likely
sources for systemic sepsis. Sepsis from burn wound
infection is a major cause of sustenance of the state of
systemic inflammation and progression to MODS.
As such, though infection is a common association with
MODS, it is not always present and nosocomial infection
may be considered a manifestation of MODS rather than a
cause of it.40 Effective infection prophylaxis like SDD
(selective digestive tract decontamination) has reduced the
incidence of pneumonia, bacteremias, etc. but has not shown
a significant reduction in mortality.41-43
It is a common understanding that it is the presence of
uncontrolled infection that leads to MODS. However,
currently it is theorized that infection usually follows MODS
rather than preceding it. In fact, nosocomial infection is
being considered a manifestation of MODS rather than a
cause of it.40 Nosocomial infection is uncommon in patients
without organ dysfunction and its occurrence is directly
proportional to the severity of MODS.37 The causative
organisms are usually Candida, Coagulase negative
Staphylococci, Pseudomonas and Enterococci, which have
low intrinsic virulence.
Endotoxin from the microbes may also be a reason for
MODS and endotoxemia is more commonly seen than
culture proven infection,44,45 possibly due to absorption of
endotoxins from the gut or lungs. Some of the bacterial
products may have direct cytotoxicity on the basic cellular
processes like induction of apoptosis of neutrophils or
epithelial cells.
The unifying infectious etiology suggested gut as a
potential source of bacteria (host for 108 aerobes and 1011
anaerobes in the colon) or at least circulating products of
bacteria.25 Hypoperfusion results in damage to the mucosal
and immunological barriers, leading to translocation of
endogenous bacteria or their products into the systemic
circulation. This ‘second hit’ acts as a trigger for the
precipitation of secondary MODS and distant organ effects
especially to the lungs.46 The hypoperfused mucosa is a
source of inflammatory mediators as well.15,47,48
Quantification of intramucosal pH (tonometry) can be used
to stratify mortality risk.49 Interestingly attempts to improve
the gut perfusion have not changed the MODS outcome in
septic patients.45,50
Uncontrolled Systemic Inflammation
More than the cytopathic effects of the microbes it is the
uncontrolled inflammatory host response that is responsible
for the progression of SIRS to MODS. The notable organ
dysfunction remote from the site of injury or functio laesa
of systemic inflammation is the result of the unregulated
systemic inflammation, the severity of which is the
determinant of the outcome of MODS.51
It is the activation of circulating cells (leukocytes), the
endothelium, the liver and multiple mediator networks that
are normally held in balance by the anti-inflammatory
mediators.25 The chemotactic agents attract, the adhesion
molecules focus and the cytotoxic agents drive the

420
Principles and Practice of Burn Care
inflammatory process and MODS occurs when the host’s
inflammatory or anti-inflammatory response (or both) to
injury are excessive.52 The myriad of actions from this
panoply of chemical mediators push the patient either
towards an inflammatory state or oppose it. It is the
dysregulation of this balance that causes MODS.
The proinflammatory actions can be seen in the form of
(1) Up regulation of the expression of inducible nitric oxide
synthetase53 resulting in increased release of nitric oxide
and its resultant effects on microvascular resistance and
capillary flow. (2) Augmentation of neutrophil cytotoxic
mechanisms by inducing the release of oxygen radicals and
proteolytic enzymes.54,55 (3) Up regulation of endothelial
cell adhesion molecule expression56 (4) Activation of
endothelial procoagulant activity.57 (5) Inhibition of the
expression of thrombomodulin,58, 59 a critical factor in the
activation of protein C anticoagulant pathway.
The other school of thought suggests the dysregulated
inflammatory response in MODS to be due to a state of
immunodeficiency or immune paralysis rather than excessive
inflammation.60 Such impaired immunity is suggested by
(1) anergy to delayed hypersensitivity recall testing with
common antigens;61 (2) impaired de novo antibody synthesis
to tetanus toxoid;62 (3) reduced monocytes expression of
human leukocyte antigen-DR (HLA-DR);63 (4) increased
circulating levels of counter-inflammatory cytokines such
as IL-1064 and transforming growth factor β.65
Raised circulating levels of cytokines such as IL-6 and
TNF-α or markers of TNF-α released in response to the
inflammatory stimuli are concomitant with organ
dysfunction and high mortality.66-70 Serum concentrations
of these pleiotropopic mediators not corresponding directly
to the mortality in MODS have also been reported.71
However, epidemiologically, postoperative septic patients
that have a high TNF concentration have a higher mortality
and MODS than those with low TNF levels.70
Huang et al in a prospective study and previous studies71-79
reported that post burns induction of SIRS was due to the
chemical mediators, which were mainly injurious to the
endothelial cells. Early eschar excision decreased SIRS and
prevented organ dysfunction and MODS. As part of the
study they observed deformation of the endothelial cell when
it was exposed to the sera of patients undergoing staged
escharotomy compared to no deformation of the endothelial
cells when it was exposed to sera of postoperative patients
of early eschar excision.
Tissue Hypoxia
Cellular hypoxia seems to be a very plausible final common
pathway for organ failure due to the diverse etiologies.80-81
It is either due to reduced oxygen delivery or oxygen
utilization leading to the cellular physiologic derangements.
Adequate resuscitation restores the oxygen deficiency on
the whole but regional hypoxia to the tissues, especially to
the gastrointestinal tract82,83 or brain84 is known to occur.
Meaningful resuscitation, thus, aims to correct systemic
and regional tissue hypoxia as soon as possible. It has been
seen that survivors have a higher cardiac index, lower
systemic vascular resistance and higher oxygen consumption
than non-survivors.85 Cardiac index more than 4.5 L/min/
m2, oxygen delivery index greater than 600 ml/min/m2 and
oxygen consumption greater than 170 ml/min/m2 are
critical.86 Tissue hypoxia, global or regional, is reflected
biochemically as increased concentrations of lactate and
correlates with adverse prognosis.87,88 Methods to improve
oxygen delivery by transfusions89 or large doses of
dobutamine90,91 were thought to be very effective but recent
trials do not support it. In fact they may worsen the outcome
and increase the severity of organ failure. Derangements in
the intracellular utilization of oxygen in the presence of
adequate oxygen delivery are the likely reason of tissue
hypoxia or ‘cytopathic hypoxia’.92
Tissue ischemia due to hypoperfusion results in depletion
of energy stores and accumulation of tissue metabolites. In
this scenario, resumption of tissue perfusion is crucial.
However, reperfusion can result in more tissue damage
through O2 derived free radicals, O2, H2O2 and OH. Reactive
oxygen species (ROS) are formed immediately, lasting for
2 to 5 minutes. These can damage lipid membranes,
enzymes, nucleic acid and receptors eventually leading to
cell death. Degeneration of the nucleic acid by Xanthine
oxidase can generate O2 and H2O2 during the oxidation of
hypoxanthine and xanthine, logically the enzyme inhibitors
can be protective. The neutrophils are abundant in splanchnic
vessels and their recruitment occurs during ischemia and
reperfusion. Neutrophils contain NADPH which reduces
O2 to free O2 radicals and myeloperoxidase in neutrophils
forms HOCL from Cl and H2O2 ions. HOCL is 100 times
more reactive than H2O2 as an oxidizing agent and mediates
cell damage. The oxygen free radicals have the following
effects (1) alteration of the vascular permeability, (2) cell
lipid peroxidation altering function, (3) initiation and
perpetuation of local and systemic inflammation, (4)
disruption of interstitial matrix, (5) impairment of

Multiple Organ Dysfunction Syndrome in Burns
421
macrophage phagocytic ability, (6) alteration of cell DNA
and (7) initiation of arachidonic acid metabolism.
Dysregulated Apoptosis
Apoptosis or programmed cell death is a process by which
cells activate an endogenous program that leads to controlled
cell death and its transformation to membrane bound vesicles
that are cleared by macrophages without inciting an
inflammatory reaction.93 This is a basic step in the embryonic
development, immune maturation, aging, cell turnover at
epithelial surfaces and resolution of inflammation.
Dysregulated apoptosis or premature cell death is one of
the pathways for organ dysfunction in critical illness.
MODS –associated release of cytokines, interleukin-1,
interleukin-6, NF heat shock proteins, oxidants and
glucocorticoids alter the rate of tissue apoptosis.37,94 It has
been drawn in as a reason for liver, kidney and cardiac
disease.95-97 On the contrary, apoptosis may be necessary
for the resolution of inflammation. Hence, the timing of
apoptosis and the cells involved are the main determinants
of whether the apoptosis will be favorable or unfavorable
for the patient.37 Studies have suggested that mitochondrial
dysfunction resulting in the crucial cytopathic hypoxia or
apoptosis is a key factor in the severity and duration of
MODS.98 Methods to modulate the expression of apoptosis
are not available clinically and hence their role is unproven.37
Microvascular Coagulopathy
The expression of inflammation and that of coagulopathy
are regulated by mechanisms which are interlinked and
hence, it is likely that with the activation of inflammation
there could be concomitant alteration in microvascular
coagulation during states of systemic inflammation. Many
studies suggest a crucial role of inappropriate intravascular
coagulation as a final common pathway to organ
dysfunction. It is known that disseminated intravascular
coagulation is a powerful predictor of MODS and platelet
counts below 80,000/ml has a sensitivity of 83.3 % and a
specificity of 100 % for the prediction of MODS.37 A shift
towards the procoagulant state commonly occurs in the
critically ill37 and this shift usually precedes the development
of organ dysfunction99 and persists in those who go further
downstream and die.100
The process of coagulation can be stimulated by tissue
factor on endothelial cells and monocytes. Besides the
physiological stimulus, this process could be induced by
endotoxin,101 cell surface components of Bacteroides
fragilis,102 by inflammatory cytokines58,103 or by integrin
cross linking.105 The coagulation cascade culminates in
cleavage of fibrinogen to fibrin and fibrin deposition, which
besides the physiological role of hemostasis and localization
of micro-organisms, obstructs oxygen delivery and further
aggravates inflammatory injury by hypoxia or through signals
delivered to the thrombin receptor. A number of
proinflammatory gene products are released with the
activation of the thrombin receptor and it results in the release
of nitric oxide.105
The biological regulators of coagulation are Antithrombin
III, Tissue factor pathway inhibitor and Protein C; they
have different mechanisms to contain the process of
coagulation. Protein C is a serine protease that complexes
with protein S to inhibit factors Va and VIIIa,106 circulates
as an inactive precursor and is synthesized primarily in the
liver.107 It is activated by the binding of thrombin to
thrombomodulin on the endothelial surface. Protein C binds
to a specific receptor on endothelial cells, the endothelial
cell protein C receptor (ECPR), this increases the release of
protein C by thrombin-thrombomodulin complexes.108
Activated protein C (APC) interactions are predominantly
anti-inflammatory, conversely inflammation reduces APC
levels and activity.37 Further to these complex interactions,
apoptosis and coagulopathy are interlinked through the
expression of phosphatidylserine.
A change to a procoagulant state is usually seen in the
critically ill patients and the increase in procoagulant markers
(Table 31.1) precedes the development of organ
dysfunction99 and persists in those who develop MODS or
die.100 Protein C levels are found to be decreased in acute
renal failure109 and in patients with neutropenia.110
Logically, modulation of the mediators regulating
coagulation looks possible and since dysregulated
coagulation seems to be the crux for the development of
MODS, attempts have been made to target the coagulation
cascade and have shown increased survival in experimental
models.111-118 Convincing results from human trials showing
improvement in clinical results is awaited. A successful
intervention at this level has shown promising results in
clinical trials and hopefully would translate into effective
therapy.
It has been found that the autonomic nervous system
continuously communicates amongst all vital organs in the
normal functioning of the body and an autonomic
dysfunction can result in severe inflammation and SIRS,
which could progress to MODS.122

422
Principles and Practice of Burn Care
The number of theories (Table 31.2) explaining the basis
of MODS betrays the fact that its nuances are still not fully
understood, especially the mechanism of multiple organ
failure. However, collectively many of the observations have
been explained through these theories, which form the basis
of the interventions that have shown promising results in
both the experimental and clinical setup.
Scoring
Though the understanding of this recently uncovered
condition, MODS, is not crisp and clear but the management
of this critical illness demands an accurate and detailed day
to day assessment. Since the key to win the battle against
MODS is its prevention, it is imperative that any downstream
events in the course of treatment are detected early, when it
is likely to be controlled before it becomes autonomous. A
number of clinical measurement systems have been tried
for the evaluation and monitoring of MODS in critical care
patients. The basic clinical need for a monitoring system is
to be able to document the course of events, the status of
the organs involved, whether the damage is reversible or
not and hopefully predict the outcome with a scope for
gradation of the dysfunction regarding its severity rather
than just a dichotomous data.
For easy clinical assessment and reproduction of data,
the parameters and the conditions need to be defined. A
number of definitions and parameters are mentioned as a
yardstick for a standard monitoring of the patient. Most of
these conditions have been defined on the basis of research
on non-burn critically ill subjects; hence some of the
definitions do not appear logical for patients of burns
progressing from SIRS to MODS and death. For instance
SIRS or the state of systemic inflammation is normally
present in large burns due to the hypermetabolic state. The
baseline temperature is reset to 38.5°C, tachycardia and
tachypnea persist for months in patients with extensive burns
and continuous exposure leads to leucocytosis. Hence, the
usual criteria for SIRS are normally present and confounding
if they were to be taken as markers for a deteriorating
condition.
The recommendations of the American Burn Association
Consensus Conference to define Sepsis and Infection in
Burns in January 200711 are very pertinent in this matter.
They are as follows:
Table 31.1: Coagulation abnormalities in trauma and sepsis
Increased
Decreased
Procoagulant activity/Tissue factor
Platelets
Fibrinogen
Antithrombin III
Thrombin-antithrombin
Protein C antigen
Fibrinopeptide A
Protein C inhibitor
Prothrombin fragment 1 + 2
Protein S
Plasmin alpha-2-antitrypsin complexes
Factor VII
D-dimers
Factor XII
Thrombomodulin
tPA activity
tPA antigen
Plasminogen activator inhibitor-1
von Willebrand factor
von Willebrand factor propeptide
Platelet thrombospondin
Table 31.2: Conceptual models of MODS and the therapeutic aim37
Pathologic process
Manifestation
Therapeutic implications
Uncontrolled infection
Persistent infection, nosocomial-ICU acquired
Aggressive use of antibiotics and source
infection, endotoxemia
control measures
Systemic inflammation
Cytokinemia (particularly IL-6, IL-8, TNF),
Neutralization of specific cytokines (IL-1,
leukocytosis, increased capillary permeability
TNF, PAF) or of activational pathways
Immune paralysis
Nosocomial infection, increased anti-inflammatory
Granulocyte Colony Stimulating factor,
cytokine (IL-10) levels, decreased HLA-DR expression
Interferon
Tissue hypoxia
Increased lactate
Augmentation of DO2
Microvascular
Increased procoagulant activity, decreased anticoagulant
Augmentation of anticoagulant mechanisms
coagulopathy and
activity, increased von Willebrand factor, soluble
(APC, TFPI, Antithrombin)
endothelial activation
thrombomodulin, increased capillary permeability
Dysregulated apoptosis
Increased epithelial and lymphoid apoptosis,
Caspase inhibition
decreased neutrophil apoptosis
Gut-liver axis
Increased infection with gut organisms,
Selective digestive tract decontamination,
endotoxemia, Kupffer cell activation
enteral feeding
APC- activated protein C, IL-interleukin, PAF - platelet activating factor, TFPI – tissue factor pathway inhibitor, TNF – tumor necrosis factor

Multiple Organ Dysfunction Syndrome in Burns
423
SYSTEMIC INFLAMMATORY RESPONSE
SYNDROME (SIRS)
SIRS should not be applied to burns. Though patients of
moderate to major burns have not been evaluated
systematically, they normally exhibit tachypnea and
tachycardia with raised body temperature. Since no studies
of the epidemiology and time-course manifestations of SIRS
in burns have been done, it is less meaningful to prognosticate
the course of burns with the criteria for SIRS. Normally,
persistence of SIRS for more than three days after trauma
was associated with increased risk of MODS and death.
However, burn trauma is different in having persistence of
signs of SIRS even after the acute inflammation has subsided
and its persistence does not necessarily suggest any clinical
complication or sepsis. And no study has demonstrated that
at a certain point in the course of burns the SIRS criteria
becomes significant. Moreover, the course of burns can be
fairly well estimated by the surface area of burns, age of
the patient and co-morbidities while SIRS or its related
scoring systems like APACHE II, etc. fail to gauge the
severity of the situation. It has been suggested that increasing
the temperature component of SIRS to 38.3 would increase
its specificity.120 Besides having been developed for adults,
SIRS is not helpful for clinical trials.
The ongoing inflammation could be defined by the
presence of base deficit and/or lactic acidosis and it correlates
with the severity of injury and mortality in burn and trauma
patients.121-123 It remains to be seen whether the absolute
values or their persistence over time is more important.
Other biochemical markers of significance are C reactive
protein,124 procalcitonin,125 tumor necrosis factor-alpha,126
interleukin-6, etc.127-130 They, however, do not appear to
correlate adequately with the prognosis in burn patients.131
Once again these changes in clinical parameters may be
normally present in a burnt patient without any overt
infection. Hence, the definition of burn sepsis must
differentiate changes in the patient’s status due to microbial
infection from changes due to burns itself or its associated
complications like inhalation injury. Due to the hypermetabolic
state the baseline temperature is reset to 38.5°C in patients
with large burns. Hence, fevers are not considered a sign
of sepsis unless they reach at least 39°C. Chronic wound
exposure due to open burns or split thickness donor sites
induces leucocytosis on its own and hence, an unreliable
sign of infection. However, thrombocytopenia after 3 days
of resuscitation is a valuable sign of sepsis.
The MODS scoring systems can be classified using
general physiological critical care scores (Acute
Physiological and Chronic Health Evaluation – APACHE,
Simplified Acquired Physiological Score – SAPS, Mortality
Probability Model – MPM132 or specific organ dysfunction
scores (Multiple Organ Dysfunction Score – MODS, Sepsis
Organ Failure Assessment – SOFA (Table 31.4), Logistic
Organ Dysfunction System – LODS). The inference from
scoring systems could be dichotomous, suggesting an organ
failure to be present or not133 and some provide information
regarding the severity (graded)134-136 of organ dysfunction
in which a deterioration creates a higher score. The different
scoring systems may use different criteria or different organs
or be different in assessment in the point of time during the
course of the disease. The American Burn Association
consensus conference in January 200711 made the following
recommendations regarding scoring systems for MODS in
burns.
•
The committee decided to use the Marshall MODS
Scoring System (as modified by Cook) till a better system
was found (Table 31.3).
•
The ACCP/SCCM consensus criteria for sepsis should
not be used, especially during the initial period of volume
resuscitation.
•
Organ dysfunction/failure should not be assessed until
the acute resuscitation period is over (approximately day
3 post burn). Since major burns require large fluid
Table 31.3: Modified Marshall MODS Scoring System 137
Organ System
0
1
2
3
4
Cardiovascular (heart rate, inotropes, lactate)
≤120
120-140
>140
Inotropes
Lactate >5
Respiratory, PO2/FIO2
>300
226-300
151-225
76-150
≤75
Renal (creatinine, μmol/L)
≤100
101-200
201-350
351-500
>500
Central nervous system (Glasgow Coma Score)
15
13-14
10-12
7-9
≤6
Hepatic (total bilirubin, μmol/L)
≤ 20
21-60
61-120
121-240
>240
Hematologic (platelet count × 103)
>120
81-120
51-80
21-50
≤20
Six domains of the MODS. The original MODS cardiovascular component was defined by the heart rate X right atrial pressure/mean arterial pressure.
The modified cardiovascular component of MODS is defined as follows: 0, heart rate <120 beats per minute (bpm); 1, heart rate 120-140 bpm;2, heart
rate >140 bpm; 3, need for inotropes more than dopamine >3 μg/kg/min; 4, serum lactate >5 mmol/L. The scores can range between 0 and 24.

424
Principles and Practice of Burn Care
transfusions during resuscitation there is a massive fluid
shift in the vascular and extravascular space with
significant reversible changes in the levels of important
parameters like leukocyte and platelet count, which
reflect a temporary decrease due to the dilution effect.
•
Organ dysfunction scores should preferably reflect the
severity of organ failure rather than just the presence or
absence of it (Table 31.5). It would conceptually be an
advantage to start therapeutic action early in response
to a scoring system that would reveal deterioration in
organ functions rather than simply presence or absence
of failure. The scoring systems that grade the organ
dysfunction are the Marshall’s MODS scoring system,
Cook’s modification of the Marshall MODS scoring
system, SOFA (Sepsis – related organ failure
assessment), the Brussels score and LODS (Logistic
organ dysfunction system). These are specific organ
scoring systems in contrast to the scoring systems using
the general physiological critical care scores like APACHE
(Acute Physiological and Chronic Health Evaluation),
Simplified Acquired Physiological Score (SAPS),
Mortality Probability Model (MPM), etc.134-136 Amongst
SOFA and the modified version of Marshall’s MODS
scoring system, the later has been used in burn
Table 31.4: Sequential Organ Failure Assessment (SOFA) score133
Organ failure/Variable
Score 0
Score 1
Score 2
Score 3
Score 4
Respiratory
≥ 400
< 400
< 300
< 200 on MV
< 100 on MV
PaO2/FiO2, mmHg
Hematology
≥ 150
< 150
< 100
< 50
< 20
Platelets, 109/L
Liver
< 1.2
1.2-1.9
2.0-5.9
6.0-11.9
> 12.0
Bilirubin, mg/dL
Cardiovascular
Mean arterial blood pressure, mmHg
≥ 70
< 70
Dopamine, µg/kg/min
≤ 5
> 5
> 15
Dobutamine, µg/kg/min
any dose
Epinephrine, µg/kg/min
≤ 0.1
≤ 0.1
Norepinephrine, μg/kg/min
≤ 0.1
≤ 0.1
Central Nervous System
15
13-14
10-12
6-9
< 6
Glasgow Coma Scale
Renal
Creatinine, mg/dL
< 1.2
1.2-1.9
2.0-3.4
3.5-4.9
≥ 5.0
Urine output, mL/day
≥ 500
< 500
< 200
Table 31.5: Parameters and scores used in assessing organ dysfunction25,134-136
Parameter
SOFA
Score
MODS
Score
LODS
Score
Respiratory
PaO2/FiO2 and
0 to 4
PaO2/FiO2
0 to 4
PaO2/FiO2
0-3
ventilation
Ventilation and CPAP
Coagulation
Platelet number
0 to 4
Platelet number
0 to 4
Platelet, white blood
0-3
Cell number
Hepatic
Bilirubin
0 to 4
Bilirubin
0 to 4
Bilirubin,
0-3
Prothrombin time
Cardiovascular
Blood pressure and
0 to 4
Heart rate, Central
0 to 4
Heart rate and
0-3
vasopressor use
venous pressure,
blood pressure
blood pressure
Central
Glasgow Coma Scale
0 to 4
Glasgow Coma Scale
0 to 4
Glasgow Coma Scale
0-3
Nervous
System
Renal
Creatinine Urine
0 to 4
Creatinine Urine
0 to 4
Creatinine Urine
0-3
output
output
output
Aggregate score Add worst daily scores
0 to 24
Add worst daily scores
0 to 24
Add worst daily scores
0-22

Multiple Organ Dysfunction Syndrome in Burns
425
patients138,139 and the parameters are easily obtained
clinically. The neurological assessment is subjective in
both the MODS and SOFA scoring systems and may
affect the overall accuracy.
The modified Marshall MODS scoring system and SOFA
scoring system are useful for a pre-emptive diagnosis of
organ dysfunction during the management of critical burn
patients. A daily worst score is useful to detect any
deterioration and is likely to improve the outcome by
facilitating an early therapeutic intervention.
MANAGEMENT OF MODS
The management of MODS in burns encompasses a few
salient principles, prevention of MODS being the ultimate
goal because once a certain stage of systemic inflammation
is reached, set protocols of management fail to make a
significant effect, treatment becomes empirical and
prognosis poor. The spectrum of activity of the numerous
pleiotropopic inflammatory mediators affects almost every
system of the body with proinflammatory and anti-
inflammatory actions closely enmeshed; making the choice
of the time and mode of therapeutic intervention at the
molecular level very difficult and risky. Hence, despite the
advancements in experimental and clinical research, the basis
of treatment of MODS remains primarily its prevention and
alleviation of inflammatory stimuli and organ support when
the scoring parameters suggest progression towards organ
dysfunction. A brief outline about management strategy is
discussed.
The management of MODS in burns aims at
1. Prevention
2. Identification of risk factors
3. Control inflammatory stimuli
4. Balance oxygen supply and demand
5. Nutrition
6. Specific organ support
7. Specific therapeutic interventions
Prevention
The prevention of multi-organ failure is likely to be more
effective than its treatment – Baue.19 Besides adequate timely
resuscitation of burns and treatment of other attendant
injuries and co-morbidities, a proactive approach for timely
detection and management of any event that would
potentially stimulate the inflammatory state would likely
contain the SIRS from progressing to MODS. It is important
to understand that all the preventive actions need to be early
in the course of any event as it unlikely to have a significant
impact once it becomes autonomous.37 For example,
prevention of infection in critical illness may reduce the
morbidity and mortality43 but once the proinflammatory
cascade is activated their perpetuation may not require the
presence of infectious stimuli. Hence, the late treatment of
infection may not ameliorate its effects and prevent the
clinical deterioration of the patient. The neutralization of the
proinflammatory mediator release in patients with sepsis
has not shown a significant improvement in outcome.44 On
the contrary, coagulopathy develops late in the cascade of
the inflammatory response and therapeutic intervention
against it appears more achievable.37
Some of the accepted therapeutic options that aid in
prevention of the inflammatory state from progressing to
MODS are:
1. Adequate timely fluid resuscitation and early homeostatic
normalcy.
2. Early burn wound excision and coverage – besides
decreasing chances of sepsis and inflammation, it also
decreases release of inflammatory mediators.
3. Preservation of gut mucosal barrier by maintaining adequate
perfusion and enteral feeding.
4. Efficient management of inhalational injuries.
5. Management of the pre-existing co-morbid conditions
like diabetes, cardiac disease, etc.
6. Maintaining homeostasis and peripheral oxygen delivery.
High degree of suspicion for infection of the burn wound
and port access sites is required as typical physical signs
may not be well distinguished in this state of systemic
inflammation. Hence it is important to look for the risk factors.
Identification of Risk Factors
Besides the above known threats for instigation of MODS,
any other vulnerable inciting factors should be contained. It
is important to be constantly vigilant with the “two hit
theory” of MODS7 in context, where the onset of secondary
MODS is more likely even by small adverse stimuli as the
immune system is already primed by the initial insult on the
inflammatory system. Though each small inciting stimulus
on its own would not precipitate MODS but a constant flux
of multiple such events may tip the course of major burns
towards MODS and eventual death in a large majority.
Patients of burns are prone to unusual and often occult
infections.140 The important risk factors are infection at the
port access sites (intravenous access, urinary catheters,
central lines etc). The standard protocols for infection

426
Principles and Practice of Burn Care
control have a very important role. Suppurative
thrombophlebitis and endocarditis are known to occur
without localizing signs.38 Ventilator associated respiratory
infection and pneumonia is a known hazard of assisted
ventilation and suppurative sinusitis in those with
nasotracheal intubation.141 Burn patients are more susceptible
to pneumonia142,143 because of (1) relative immuno-
suppression (2) dysfunctional ciliary movement in
inhalational injuries leading to impaired secretory clearance
(3) pulmonary inflammatory activation with acute lung injury
(4) increased leakage of nutrient rich plasma into the lung
parenchyma (5) ventilator associated injury due to aggressive
ventilation because of decreased lung and chest wall
compliance. Acalculous cholecystitis may present with
generalized sepsis without any localizing signs.38 All these
unusual complications of burns are managed as per the
specific requirement and protocol.
Control of Inflammatory Stimuli
Early excision of devitalized tissue and coverage of raw
areas as far as possible is the key to prevention of infection
in burns and the ensuing inflammatory state. The uncovered
wound and the devitalized tissue are also a source of stimulus
for release of the biochemical mediators of inflammation,
such as interleukin-6, interleukin-8, tumor necrosis factor,
etc. These mediators besides causing a hypermetabolic and
inflammatory state, can have remote organ effects, for
instance interleukin-8 from the wound gets upregulated in
the lungs and is responsible for pulmonary dysfunction.38
Even split thickness donor sites invoke an inflammatory
response. On the other hand, complete wound closure
without donor sites decreases oxygen consumption and the
inflammatory response from the wound. Huang et al144
reported early eschar excision to be effective in preventing
and treating early post burn organ dysfunction and MODS,
mainly by alleviating SIRS and endothelial cell injury.
Wound sepsis has been a major cause of the persistent
inflammatory state and MODS. It is however, decreasing
in incidence due to early wound coverage and these days
death from infection is more commonly due to pneumonia
than due to wound sepsis.38 Burn patients who are at risk
of MODS should be closely monitored for any signs of
infection and treatment promptly instituted. Standard
infection control protocols need to be strictly followed to
curb any stimulation of the inflammatory state. Though the
institution of anti-inflammatory therapy with ibuprofen145
or corticosteroids seemed to be an attractive option but
have not been found to be useful in SIRS or MODS.146,147
On the contrary, the immunosuppressive effect of steroids
predisposes to complications.146,148,149 Experimental studies
indicate that granulocyte/macrophage colony stimulating
factors may enhance the compromised immune system and
be useful.150 It has been found useful for chronic
neutropenia and in bone marrow transplantation.
Theoretically, MODS therapy directed against
inflammation are:25 (1) cell adhesion retardation; (2)
inflammatory mediator reduction (translation/transcription
inhibition)(3) neutralizing (polyclonal or monoclonal)
antibodies directed at cytokine/vasoactive/coagulation/
complement mediators; (4) cytokine/vasoactive/coagulation/
complement mediator receptor inhibitors; (5) anti-
inflammatory protein induction (preconditioning, substrates,
products, or genes); and (6) anti-oxidants and anti-
proteases.151 The newer developments entail measurement
of specific elements152 in the inflammatory cascade and
countering the abnormally increased ones with cloned
proteins and antibodies (monoclonal and polyclonal).153
Thus, it envisioned to continuously titrate and adjust anti-
inflammatory therapy in response to specific biochemical
changes in the inflammatory cascade.154,155
Balancing Oxygen Supply and Demand
Cellular hypoxia, due to either decreased supply (impeded
extraction of oxygen as in sepsis) or increased demand
changes the ATP generation in the cells from the aerobic to
the anaerobic pathway. It results in a rise in intracellular
hydrogen ion and calcium with a decrease in function of
the sodium calcium pump.38 It is also responsible for the
release of oxygen free radicals. When all these persist due
to persistent low oxygen tension, the membrane
phospholipids maybe degraded and result in cellular
dysfunction. Clinical data suggests that inadequate oxygen
delivery is associated with MODS.38
Knowing the amount of oxygen being consumed by
the patient is more valuable than oxygen saturation and
cardiac output. It helps optimize the oxygen supply, reverse
any oxygen debt and makes it easier to understand which
interventions help decrease oxygen demand. It is the basis
of maintaining a balance of oxygen supply and demand.
Survival rates have been shown to improve where supra-
normal values of cardiac index, oxygen delivery and
consumption were reached.85,156
Normally the (VO2) consumption is dependent on (DO2)
up to a certain point called critical point. Beyond this point

Multiple Organ Dysfunction Syndrome in Burns
427
VO2 will not increase no matter how much DO2 is increased.
The increasing slope becomes a plateau (Fig. 31.4). In septic
shock, hypoxia and MODS, this critical point increases and
in order to maintain the same VO2, supra normal levels of
DO2 have to be provided. The adequacy of VO2 can be
monitored by the fall in lactic acid level, increase in mixed
venous saturation (>75%) and improvement of gastric
mucosal pH (N=7.34) and tissue oximetry.
frequency oscillatory ventilation and high frequency
percussive ventilation.158 There is increased risk of ventilator
associated lung injury in burns due to the reduced pulmonary
compliance and chest wall rigidity, which may lead to
aggressive ventilatory management and high airway
pressures.157 If the oxygenation is still not adequate, then
attention should be paid to cardiac output and hematocrit to
optimize O2 delivery. Extra corporal membrane oxygenator
(ECMO), Intravenous oxygenator (IVO), surfactant therapy,
and partial liquid ventilation with perflourocarbon are the
ultimate salvage options.
Adjunctive therapies include inhaled nitric oxide for
hypoxic vasoconstriction thereby improving ventilation/
perfusion mismatch and tissue oxygenation.159,160
Aerosolized heparin and N-acetylcysteine have shown
promising results.161,162
Cardiovascular System
Adequate resuscitation for homeostatic stabilization with
end points being return of parameters to normalcy. Lactate
levels are an important means of ascertaining the adequacy
of tissue oxygenation. Myocardial function is depressed as
a part of global ischemia and circulatory myocardial
depressant substance. If this fails to reverse the hypotension
and tissue perfusion, inotropes and vasopressors may be
used. Dopamine 1-5μu/kg/min exerts β agonist dopaminergic
effects. Low dosage Dobutamine is preferred for
vasodilatation. It also increases O2 delivery. Noradrenaline,
ephedrine, phenyl ephedrine can be used to maintain the
blood pressure. In the initial phase Dopexamine dilates
splanchnic vessels when gut ischemia is suspected. The
supports should be weaned as soon as possible. Maintaining
hemoglobin concentrations at 7.0-9.0 g/dL may be superior
to maintaining it at 10.0 to 12.0 g/dL in critically ill patients
except those with acute myocardial infarction and unstable
angina.89 In fact, a recent study reported an increased
mortality in burn patients associated with blood
transfusions.163 In a trend to avoid blood transfusions,
recombinant human erythropoietin was tried but did not
show any significant improvement in post burn anemia.
However, the animal study showed improved healing of the
burn wound.
Hematological
DIC and thrombocytopenia is a common feature in sepsis
and MODS. As a part of therapy, Vitamin K and FFP are
helpful in providing clotting factors.22 PRP, platelet
Fig. 31.4: Elevated and altered oxygen requirement in MODS
Decreasing Oxygen Demand
Since the oxygen demand is more than the supply (e.g.
deficient peripheral oxygen extraction in sepsis) in MODS,
it is logical to increase the supply and decrease the demand
of oxygen for a favorable outcome. In fact interventions to
reduce the oxygen demand are equally valuable as increasing
oxygen supply. Fever, chills, tachycardia, tachypnea and
pain are some of the basic clinical conditions, which if
controlled could reduce the oxygen demand on an already
deficient system. Assisted ventilation, hypothermic devices,
pain medications, sedation, analgesics are elementary but
effective in reducing the oxygen demand.
Specific Organ Support
Respiratory
Maintenance of adequate airway patency by intubation and
supplementary O2 therapy may have to be done early. If the
patient is refractory, he/she should be put on mechanical
ventilation. Normally a tidal volume–10-15ml/kg, FiO2 -1/L
with PEEP of 3-5 cm of water is sufficient to avoid
pulmonary edema. To avoid O2 toxicity PEEP of 10-15 cm
of water with end inspiratory plateau pressure of 30-35 cm
are sufficient. Low tidal volume ventilation, allowing
permissive hypercapnia has shown to reduce ventilator
associated lung injury and significantly improves the
outcome.157 Alternative ventilatory strategies are high

428
Principles and Practice of Burn Care
concentrate and fresh blood should be used in anemia with
platelet counts < 50,000/mm3. 1-Deamino-8-arginine
vasopressin (DDAVP) in the dose of 0.3 mg/kg in 50 ml of
saline is used in platelet dysfunction due to uremia.
Renal and Hepatic
It is essential to avoid all nephrotoxic and hepatotoxic drugs.
Quick, adequate resuscitation can provide adequate perfusion
to these important organs for them to function normally.
Mannitol and frusemide may be needed to prevent
hepatorenal shutdown. Use of neomycin for decontamination
of gut and use of lactulose can avoid hepatic
encephalopathy. If renal functions are not improved, patient
may need dialysis.
Nutrition
Major burns are associated with a catabolic state with a
significant increase in calorie requirement, which if not
supplemented from outside, uses the available resources in
the body leading to muscle protein catabolism, immune
dysfunction, etc. The use of early enteral feeding may
attenuate this catabolic response after thermal injury.164
Calorie supplementation by enteral or parenteral (not
preferred) feeding has been known to reverse the muscle
catabolism. However, an aggressive high calorie feeding
has been found to be associated with increase in mortality.165
It is now recommended to provide adequate calorie intake
via the enteral route with avoidance of over feeding. A high
carbohydrate and high fat content in the diet may balance
the skeletal muscle protein.166 Understandably, an aggressive
monitoring and treatment of hyperglycemia is highly
recommended.167,168
Specific Therapeutic Interventions
Modulation of Hormonal and Endocrine
Response
Burn trauma is associated with a state of catabolism and
raised levels of catecholamines. Beta-adrenergic blockers
have been studied and have shown some encouraging
results.
The use of Beta-adrenergic receptor blockers in the
patients of burns have been found to blunt the effects of
catecholamines by attenuating hypermetabolism, decreasing
oxygen demand and resting energy expenditure and
decreasing heart rate and cardiac oxygen demand.169 It has
also shown decrease in catecholamine induced muscle
catabolism and lipolysis.170, 171 The catecholamine mediated
defect in lymphocyte activation is modified by the beta
blockade and hence, improves the immune response with
decreased infectious complications.172 Clinical studies have
shown its usefulness in both adults and the pediatric
population173-176 with decreased mortality and wound
infection rate and improved wound healing time. Further
clinical trials are needed to authenticate its usefulness.
Immunotherapy
Immune modulation may be of use in targeting the systemic
inflammatory response, infection, sepsis and immuno-
suppression.
Immunonutrition: Immune enhancing diets/agents have
been studied for patients with extensive burns, which have
a high risk of infection, sepsis and immunosuppression
leading to an increased risk of organ dysfunction.177 These
diets/agents contain arginine, glutamine, omega-3 fatty acids
and anti-oxidants such as ascorbic acid (Vitamin C) and α-
tocopherol (Vitamin E). A combination of these constituents
is tried and has been investigated. Glutamine has been shown
to have very favorable results. However, the trials and
multiple studies have agreed that indiscriminate use of the
combination formula is not beneficial and a selective
approach is proposed.178-182 Anti-oxidants such as ascorbic
acid (Vitamin C) and α-tocopherol (Vitamin E) have been
shown to reduce the morbidity and prevalence of organ
failure in the critically ill.183, 184
Recombinant Human Activated Protein C:177
Recombinant activated protein C (activated drotrecogin alfa)
is the first agent approved by the Food and Drug
Administration for the treatment of severe sepsis. The
Protein C Worldwide Evaluation in Severe Sepsis
(PROWESS) trial has shown a statistically significant relative
risk reduction of 28 day mortality.118 Other trials have also
shown a favorable result. However, there have not been
any published trials on burn patients. Based on the available
information, activated protein C can be considered for those
in severe sepsis, who lack the exclusion criteria. The
exclusion criteria includes within 12 hours of surgery,
pregnancy, recent cerebrovascular accident, intracranial
pathology, active bleeding or anticipated need for surgery
within a 96-hour period.
Topical immunomodulation:177 Burns induces local dermal
inflammatory response, which in the absence of inhalational
injury, is the source triggering the systemic inflammatory
response by the release of a vast spectrum of proinflammatory

Multiple Organ Dysfunction Syndrome in Burns
429
mediators. Experimentally it has been seen that control of
the dermal inflammation by topical application of p38-
mitogen-activated protein kinase inhibitor to the burn wound
abates the systemic inflammatory response and acute lung
injury.185 However, this has yet to be proved clinically.
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Guidelines for Nutritional
Management of the Burn Patient
32
Savita Arora
Chapter
INTRODUCTION
Aggressive nutritional support in severe burns is an essential
life saving therapy as important as control of infection and
early excision and skin grafting. Due to the presence of
acute phase responses in starving critically ill patients, a
number of pathophysiological alterations develop caused
by severe metabolic, hormonal, immunologic and circulatory
disturbances. They lead to extensive nitrogen loss,
malnutrition, markedly increased metabolic rate and
immunologic deficiency predisposing the burn patients to
frequent infections, poor wound healing, increased length
of hospitalization and increased mortality.
Driven by the series of inflammatory mediators,
catecholamines and hormones, the catabolic state leads to
increased nitrogen loss due to increased amino acid efflux
from the skeletal muscles, in order to accommodate
increased demand of amino acids for tissue repair, acute
phase protein production, cellular immunity and
gluconeogenesis. This leads to diminished lean body mass
which directly relates to outcome. Treatment of burn patient
is incomplete and often unsuccessful if proper nutritional
care is not provided. By way of nutritional management, it
is possible to modulate the inflammatory response, immune
status and promote burn wound healing.
Nutritional support requires high protein and high energy
diets to provide metabolic support during heightened
inflammatory state by giving sufficient calories and protein
to minimize further loss of lean body mass (LBM). A 40%
loss in body weight or a loss of one half to one third of
protein is associated with death, particularly if this is rapid,
as it may be in extensive burns.
Wound healing is limited when weight loss exceeds
>20% of the pre-burn values. 10% weight loss is acceptable.
Oral feeding is the preferred method of providing
nutrition to a patient with small burns. In extensive burns,
however, nutritional therapy requires careful decision-making
regarding the safe use of enteral and parenteral nutrition
and the aggressiveness of nutrient therapy.
The effects of increased dietary components such as
glutamine, arginine and omega-3 fatty acids and related
compounds have been evaluated in burn victims. The
components, when supplied in quantities two to seven times
of those in normal diets of healthy persons, appear to have
beneficial pharmacological effects on the pathophysiological
alterations associated with burns.
PHYSIOLOGIC AND METABOLIC RESPONSES
TO BURN INJURY
Effective nutritional therapy in burn patients involves an
understanding of the physiologic and metabolic alterations
that accompany traumatic injury. Nutritional practice in burn
injury requires a multifaceted approach aimed at providing
metabolic support, while accommodating surgical and
medical needs of the patients.
Metabolism after burn injury is mediated through
hypothalamic and pituitary axis. There are three phases:
•
Ebb Phase/Shock Phase
•
Flow Phase/Recovery Phase
•
Anabolic Phase
Nutritional care is adjusted to individual needs and is
given in three stages.

Guidelines for Nutritional Management of the Burn Patient
435
EBB or Shock Phase
This is usually brief and lasts up to 12-24 hours and occurs
immediately post burn. Blood pressure, cardiac output, body
temperature and oxygen consumption are all reduced. Loss
of skin cover in burn and increased capillary permeability
leads to loss of water and electrolytes, mainly sodium and
also proteins. As a result, body water shifts from
extracellular spaces in other parts of the body to the burn
site adding to the continuous loss of fluids and electrolytes.
Capillary fluid shift leads to hypotension, hemo-
concentration and reduced urine output. Intracellular water
is also drawn out to balance extracellular fluid losses leading
to cellular dehydration. Patients with extensive burns need
immediate fluid and electrolyte replacement during first 12-
24 hours. A balanced salt solution such as Ringer lactate
solution is given to correct hypovolemia and prevent
metabolic acidosis.
A colloidal solution such as albumin or plasma is not
effective at this stage as it passes into the extravascular
fluids due to the increased capillary permeability which
returns to normal only after the first day. During this initial
period, fulfilling the nutritional requirements of protein and
energy are not attempted as the entire focus is on rapid and
effective fluid and electrolyte therapy so as to prevent shock.
The goal is to maintain an adequate blood pressure,
hematocrit and urine output.
Flow Phase/Recovery Phase
Following the restoration of circulating blood volume, patient
enters the catabolic or flow phase after 48-72 hours, fluid
and electrolytes are reabsorbed into the general circulation
and excess fluid is excreted (Fig. 32.1). From 5th to 12th
day post burn, metabolism increases greatly and is
characterized by abnormal substrate utilization, increased
heat elimination and weight loss. The magnitude of post
burn hypermetabolism is proportional to the extent of the
injury. Metabolic rate may be accentuated by intervening
infection. Cardiac output and oxygen consumption is
increased with significant increase in blood flow to the burn
wound, which is necessary to provide adequate glucose
substrate as an energy source for wound healing. The wound
preferentially utilizes anerobic glycolytic pathways which
are inefficient for energy production.
Large open wounds, increased blood flow to the burn
wound and loss of cutaneous vasomotor reflexes for heat
retention account for major heat loss via evaporation. This
also leads to increased oxygen consumption. To prevent
lethal cooling, the core temperature of burn patient is
elevated. Wound evaporative losses are estimated by the
following formula:
Body Surface Area × (25 + % of burn) =
cubic cm of water loss/hour1
Being an energy consuming process, evaporation adds
to energy loss. For example, a patient losing 86 ml of water/
hour by evaporation needs 1200 kcal/day in addition to his/
her energy requirement. The increase in basal metabolic
rate (BMR) is brought about by increased secretion of
catecholamines which stimulate the production of glucagon
which promotes glycogenolysis and gluconeogenesis and
suppresses the insulin release. Protein catabolism
(proteolysis) occurs mainly in the skeletal muscles. Alamine
and glutamine released from the muscles are transported to
liver which disintegrates them into pyruvates and then in
turn into glucose (gluconeogenesis). Amino acids are wasted
as gluconeogenesis is exceeding the demand of cells.
Enhanced lipolysis to increased demand combined with
impaired fat oxidation results in futile recycling of free fatty
acids and triglycerides. There may be increased excretion
of nitrogen (20-25% of total nitrogen loss is from burn
wound exudates), potassium, phosphate, creatinine,
magnesium and zinc sulfate in urine. In addition, endogenic
anabolic activity decreases because of burns. Therefore, if
a patient is not getting proper nutrition, the visceral proteins
are wasted, the muscle volume declines and, as a result, the
body is incapable of adapting to the existing situation and
unable to economize the use of energy. With the onset of
wound healing, the metabolic rate and the production of
catecholamines return to normal levels and protein synthesis
follows as the insulin glucagon molar ratio reverses after
the wound is healed.
Anabolic Phase
During this period, the patient is well hydrated and the
reactions due to metabolic stress are under control. The
patient may still be hypermetabolic and has depleted reserves
of all nutrients. Rigorous nutritional support during this period
is essential to promote fast recovery and proper rehabilitation.
Proper nutritional care during this period can help in preparing
the patient physically for undergoing successful skin grafting.
Rate of utilization of nitrogen does not differ in flow or
anabolic phase but the obligatory nitrogen loss and the
requirements for nitrogen equilibrium decrease as the post
burn course progresses through convalescence.