Điều Trị Bỏng Toàn Diện (Bản Expert Consult)

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548
then be advanced to allow for progression during the ever-
changing phases that the burned individual goes through,
in what may be in excess of a 2-year recovery period.
During follow-up visits, screening monitoring of the patient’s
progress regarding the above categories is performed and the
necessary changes are completed. This detailed knowledge
of the patient’s status will allow the burn team to coordinate
the care for the patient so that recommendations can be fol­
lowed through. Providing the patients with a checklist is a
valuable tool to enable patients to assume some control of
the rehabilitation process, enable them to track their progress
and encourage their continuation of the program. Many
patients and their caregivers are often overwhelmed by the
rehabilitation program. It takes an extraordinary amount of
time and energy to plan and participate in a home exercise/
instruction program. Continuous communication among
the patient, caregiver and the burn team will ease the patient’s
transition into recovery.
One way of helping patients with the exercise program is
to establish communication with a community-based exer­
cise center, such as a commercial or hospital-based facility.
Often, direct and constant communication between a burn
hospital’s rehabilitation department, exercise physiologists
and/or physician and as well as the community-based
•
Monitor the individual’s progress. Reassess fitness every
6 weeks. You may notice that you need to increase the
amount of time you exercise in order to continue
improving (if part of the original goals).
•
The exercise professional or individual should keep an
exercise diary or logbook to help chart progress.
•
If the patient loses motivation, try setting new goals or
try a new activity (or activities). Sometimes, bringing a
friend or family member into the program may help
in motivation. Incorporate variety into the exercise
routine.
•
Finally, work on conveying to the patient or client
that a fun and safe exercise program can result in
maintenance of lifelong physical, as well as
psychosocial, healthy habits (Fig. 47.31).
Patient/caregiver education
When patients are being discharged from the acute hospital
stay, it is vital that they leave with an individualized home
exercise program. Splinting and positioning, Activity of
Daily Living performance, scar control measures, and psy­
chosocial issues should also be addressed. This program can
Figure 47.31  Overall long-term burn rehabilitation should result in lifelong physical as well as psychosocial healthy habits and improvements in quality
of life.

Comprehensive rehabilitation of the burn patient
549
Borg G, Hassmen P, Langerstrom M. Perceived exertion related to
heart rate and blood lactate during arm and leg exercise. Eur J Appl
Physiol Occup Physiol. 1987;56(6):679-685.
Kisner C, Colby LA. Therapeutic exercise: foundations and techniques
(Therapeutic exercise: foundations & techniques. 5th ed). Philadelphia:
FA Davis; 2007.
Mackin EJ, Callahan AD, Skirven TM, et al, eds. Rehabilitation of the
hand and upper extremity. 5th ed. St Louis, MO: CV Mosby; 2002.
Noble BJ, Borg GA, Jacobs I, et al. A category-ration perceived exertion
scale: relationship to blood and muscle lactates and heart rate.
Med Sci Sports Exerc. 1983;15(6):523-528.
Randall L, Braddom MD. Physical medicine and rehabilitation. 4th ed.
Philadelphia: Saunders; 2007.
Roberts L, Alvarado MI, McElroy K, et al. Longitudinal hand grip and
pinch strength recovery in the child with burns. J Burn Care
Rehabil. 1993;14(1):99-101.
exercise facility (i.e. personal trainer), will maximize the
potential for adherence to and the efficacy of such ‘home’
exercise programs, by adding supervision and structure.
Summary
The rehabilitation of burn patients, although challenging,
can be rewarding to all involved in their care. Continuous
evaluation of interventions provided is needed to ensure
each patient’s maximum functional outcome. Experience,
education and research will produce therapeutic interven­
tions that will optimize each patient’s recovery. Ultimately,
the goal of the rehabilitation team is to provide the patient
with the means for a productive life.
Further reading
American College of Sports Medicine. ACSM’s guidelines for exercise
testing and prescription. 8th ed. Philadelphia: Lippincott Williams &
Wilkins; 2009.
 
Access the complete reference list online at

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549.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
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144. Borg G. Borg’s perceived exertion and pain scales. Champaign:
Human Kinetics; 1998.
145. Cucuzzo NA, Ferrando A, Herndon DN. The effects of exercise
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146. Roberts L, Alvarado MI, McElroy K, et al. Longitudinal hand grip
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147. Rowland TW. Aerobic exercise testing protocols. In: Rowland TW,
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148. Myers J, Bellin D. Ramp exercise protocols for clinical and
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149. Myers J, Buchanan N, Walsh D, et al. Comparison of the ramp
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1334-1342.
150. Borg G, Hassmen P, Langerstrom M. Perceived exertion related
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151. Borg GA. Perceived exertion. Exerc Sport Sci Rev. 1974;2:131-153.
152. American College of Sports Medicine Position Stand. The
recommended quantity and quality of exercise for developing
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flexibility in healthy adults. Med Sci Sports Exerc. 1998;30(6):
975-991.
153. Kokkonen J, Nelson AG, Cornwell A. Acute muscle stretching
inhibits maximal strength performance. Res Q Exerc Sport.
1998;69(4):411-415.
154. Behm DG, Button DC, Butt JC. Factors affecting force loss with
prolonged stretching. Can J Appl Physiol. 2000;(3):261-272.
155. Howley ET. Type of activity: resistance, aerobic and leisure versus
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33(6 Suppl):S364-S369; discussion S419–S420.
156. Foster C, Florhaug JA, Franklin J, et al. A new approach to
monitoring exercise training. J Strength Cond Res. 2001;15(1):
109-115.
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159. Cronan T, Hammond J, Ward CG. The value of isokinetic
exercise and testing in burn rehabilitation and determination of
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162. Carpinelli RN, Otto RM. Strength training. Single versus multiple
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©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00048-5
Musculoskeletal changes secondary
to thermal burns
E. Burke Evans
Information
Among trauma states the burn is alone in the tendency of
its wound, even as it heals, to create musculoskeletal deform­
ity. In addition, the protracted burn illness that accompanies
severe burns may result in other skeletal change. Box 48.1
presents a classification of musculoskeletal changes second­
ary to burns; from that, the most commonly occurring and
clinically significant alterations have been selected for
discussion.
Changes confined to bone
Osteoporosis
Osteoporosis is the most frequently occurring post-burn
change involving bone. Klein’s ongoing studies suggest that,
among persons with serious burns, reduction of bone mass
density is pervasive.2 Stated causes of osteoporosis in thermal
burns are bed confinement, immobilization, hyperemia,3
reflex vasomotor phenomena,4 and adrenocortical hyperac­
tivity.5 In Chapter 26 of this book, Klein reviews the effects
of burn injury on bone metabolism.2,6 In this section only
what is clinically apparent is discussed.
The more extensive the burn and the greater the number
of complications, the longer the patient may be bed-confined
and relatively immobile. The onset of osteoporosis is acceler­
ated and its intensity more marked in the burn illness that
features a hypermetabolic state. If a single extremity of an
otherwise normal person is immobilized for a long period
of time because of local trauma, as with a fracture, loss of
bone density can be easily seen in a plain radiograph. So
with burns isolated to the extremities, the bones of affected
extremities become osteoporotic; and, in persons with gen­
eralized burns, the bones of deeply burned extremities may
show more profound mineral loss than is observed in non-
burned extremities or in the axial skeleton (Fig. 48.1). Van
der Wiel et al.7 found in an X-ray absorptiometry study of
16 adults with fractures of one tibia that there was eventual
loss of bone mineral density in the contralateral femur and
in the lumbar spine, but to a lesser degree than in the
ipsilateral femur. These findings, although not strictly analo­
gous to those observed in burns, nevertheless point to the
occurrence of generalized osteoporosis in other trauma
states and the difference in loss of bone density relative to
local factors. In fractures or in burns, impaired mobility and
local hyperemia could account for this difference.
Another characteristic of the osteoporosis of burns that
seems to set it apart is its persistence, not just until restora­
tion of the anabolic state, but for months and years after the
burn has healed (Fig. 48.2). This phenomenon may be most
clearly observed in patients who have survived 90% burns,
but Klein records less than normal bone among even
moderately burned children as long as 17 months after
injury.2 Muscle atrophy and/or the failure or inability of the
person to return to the preburn level of physical activity
may account in part for this protracted state of reduced
bone mineralization.
There is no way to prevent osteoporosis in a patient whose
burn is of such severity as to require an extended period of
bed confinement. On the other hand, the advance of bone
atrophy can at least be favorably modified even among
patients with large burns if mobilization and active exercise
are initiated soon after the burn. The bones of the axial
skeleton, the pelvis, and the lower extremities are most effi­
ciently stressed by weight bearing. Thus, standing is a prior­
ity measure, and it is common practice now to walk patients
to tolerance prior to permanent wound cover. Muscle con­
traction alone may help forestall bone atrophy and bone is
better stressed if the contraction is resisted. Incrementally
increasing resistance during motion or at the termination
of an arc of motion or to muscle contraction in an extremity
that may not be moved can be supplied by anyone who
attends a responsive patient. Isometric muscle contraction
can be exacted from even extensively burned patients and
is important for bone stress, for maintaining muscle tone
and bulk, and for the patient’s continuing ready identifica­
tion of the affected extremity. Passive motion has no effect
on bone and thus does not figure in the prevention of
osteoporosis. Other preventive measures, e.g. closure of the
wound and maintenance of nutrition, are routine in critical
burn care. Treatment of established osteoporosis involves
the more aggressive employment of measures for preven­
tion. There are no long-term comparative studies, however,
that persuasively measure the effectiveness of exercise, diet,
medication, or modality in the treatment of osteoporosis in
any state.
CHAPTER 48 
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IN THIS CHAPTER
PowerPoint Presentation Online

Total Burn Care
48
552
will in time sequestrate, separating at a well-defined fissure
between dead and living bone. With minor or moderate
exposure, the bone will usually survive long enough for
bordering granulation tissue to cover it. For large defects, it
may be useful to drill closely spaced holes through the
exposed cortex so as to encourage buds of granulation tissue
to emerge from the still vascular medullary canal. Another
way to encourage granulation tissue formation over exposed
bone is with superficial decortication with an osteotome or
burr to expose the capillaries of the inner cortex. With these
practices, there is little risk for infecting the bone. It may
be that there is sufficient centripetal pressure to discourage
the invasion of organisms when the holes are fresh and that
the holes are rapidly sealed by blood clot and advancing
tissue. There are no reports of deep bone infection related
to cortex drilling.
With open fractures at the base of a major soft tissue burn
wound, bone infection is probably inevitable. Even so, the
infection tends to remain at the fracture site and not to
involve the rest of the bone, so that local debridement and
stabilization of the soft tissue wound are all that are required
for treatment. Dowling reported osteomyelitis of the tibia
related to an open bimalleolar fracture in an extensively
burned extremity.8 On the other hand, osteomyelitis devel­
oped in neither of the two open fractures reported separately
by Choctaw9 and Wang.10 We treated three patients in
whom open fractures of the femur complicated thigh
burns. Each case required aggressive and repeated debride­
ment. One fracture was treated in traction, while the
other two were treated with external fixators. In one of the
patients, who was admitted 8 months after acute burn, there
was established osteomyelitis of the femur in relation to
the exposed fracture. Osteomyelitis did not develop in
Osteomyelitis
In burns, bones can become infected by exposure of bone
by the burn; by an open fracture accompanying the burn; by
extension of infection from a septic joint; by introduction of
organisms along traction pins or internal fracture fixation
devices; or by blood-borne organisms of bacteremia. Con­
sidering the apparent great liability for seriously burned
patients to develop osteomyelitis, it is surprising that it does
not regularly occur. As it turns out, clinically significant
osteomyelitis in burned patients is rare. Antibiotics given for
the general state may prevent seeding of the bone or may
repress any small focus of bone infection.
The cortex of long bones is a good barrier to surface
organisms. Even exposure of cortex will have little adverse
effect if the blood supply of the bone remains intact. Pro­
longed exposure will kill the outer layer of the cortex, which
Box 48.1  Classification of musculoskeletal changes secondary
to burns
Alterations limited to bone
•
Osteoporosis
•
Periosteal new bone formation1
•
Irregular ossification1
•
Diaphyseal exostosis1
•
Acromutilation of fingers2
•
Pathological fracture
•
Osteomyelitis
•
Necrosis and tangential sequestration
Alterations involving pericapsular structures
•
Pericapsular calcification
•
Heterotopic para-articular ossification
•
Osteophyte formation
Alterations involving the joint proper
•
Dislocation
•
Chondrolysis3
•
Septic arthritis
•
Spontaneous dissolution4–6
•
Ankylosis
Alterations involving muscles and tendons
•
Desiccation of tendons7
•
Fibrosis of muscles8
Alterations secondary to soft tissue
•
Muscle and joint contractures
•
Malposition of joints
•
Scoliosis
Soft tissue injury
•
Compartment syndrome
•
Nerve injury
Abnormalities of growth
•
Acceleration and retardation
•
Destruction of growth plate.
Figure 48.1  (a) At 6 months after injury there is the coarsened
trabeculation of marked osteoporosis of bones of the left hand and forearm
of a 4-year-old male whose 70% full-thickness burn involved head, chest,
and both upper extremities. (b) A roentgenogram of the left tibia and fibula
obtained on the same date as that of the hand shows minimal atrophy.
A
B

Musculoskeletal changes secondary to thermal burns
553
•
excessive movement of the extremity leading to
loosening of the pin;
•
sealing of the pin sites.
For traction or suspension, pins may be inserted through
acutely burned skin, through eschar, through granulation
tissue, or later through ischemic burn scar, which may be
colonized with uncommon and antibiotic-resistant organ­
isms. No amount of local cleaning is likely to sterilize the
surface through which the pin must pass, yet it seems that
organisms in sufficient numbers to colonize are rarely intro­
duced in this manner.
either of the other patients; in the end, all three had sound
femurs.
When traction pins are directed through burned skin
for the treatment of fractures or for suspension of a
burned extremity, the factors favoring development of infec­
tion along the pin track and the formation of cigarette
sequestra are:
•
the introduction or migration of organisms from the
burn wound;
•
linear pressure of the traction pin;
•
prolonged traction;
Figure 48.2  (a) Advanced osteoporosis in the hands of a 14-year-old male 9 months after 100% TBSA burn. All growth plates are open. (b) At 24 months
after injury, osteoporosis persists and there is irregular closure of metacarpal and phalangeal growth plates. (c) At 8 months after injury, growth plates of
distal tibiae and fibulae remain open. (d) At 24 months after injury, distal growth plates of tibiae and fibulae are closed. Other major growth plates remain
open. Osteoporosis is unchanged.
A
B
C
D

Total Burn Care
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554
required was support of the extremity until the fracture
consolidated, usually in 4–6 weeks. Children were more
often affected than adults and the fractures usually com­
pressed one cortex, producing an angular deformity that
rapidly corrected with growth. Klein’s study2 strongly sug­
gests that fractures occur more frequently in burned children
than in a matched normal population even months after the
acute burn. Now, however, in acute burn management the
most frequently seen fractures are those occurring at the time
of, or in association with, the burn injury. Falls or violent
trauma account for many of the fractures, and the sites are
those common to the causes, bearing no relation to the burn
itself.
Although fractures complicate burn treatment and occa­
sionally delay mobilization of patients, their management
need not be complex. Fractures in extremities not burned
can be treated by manipulative reduction and cast immobi­
lization, by open reduction and fixation, with an external
fixator, or with skeletal traction (Fig. 48.4). Fractures in
extremities with first-degree or superficial second-degree
burns can be managed in the same way. Deep second-degree
and third-degree burns present a different problem only with
respect to the early bacterial colonization of third-degree
burns and the degradation of deep second-degree burns to
full-thickness burns that will, in turn, become colonized.
There is a precious window of time when fractures requiring
open reduction and internal fixation can be definitively
treated without increased risk for infecting the bone; however,
fracture reduction and stabilization are so important in the
functional management of a severely burned patient that the
risk for bone infection should be acknowledged and shoul­
dered at any post-burn stage. Skeletal traction can often be
the management choice, particularly in children and adoles­
cents, even if the treatment protocol requires that the patient
be moved from bed for tubbing, dressing change, or addi­
tional surgery. The disadvantages of skeletal traction are the
confinement to bed and the imposed relatively fixed posi­
tion of the affected extremity. External fixators have made it
possible to align and stabilize fractures in burned extremities
without open operation. There is the added functional
advantage of patient mobility. Brooker’s extensive favorable
experience supports this concept.14 With both skeletal trac­
tion and external fixation, there is an added risk for bone
infection because of the path from surface to bone provided
by the pins. This is a risk worth taking, and it is minimized
by scrupulous pin site care and by removal and replacement
of any loosening pin. Frye and Luterman recognized and
discussed the specific and continuous difficulties encoun­
tered in the management of fractures and burns.15
When casts are used for stabilization of fractures in burned
extremities, the wound is made inaccessible and there is an
abiding fear that the unattended wound will seriously
degrade or at best not improve. Such fear may be well
founded; however, Wang10 showed that a bivalved circular
cast could be used effectively for an open comminuted frac­
ture of a proximal tibia with overlying deep burns, and
Choctaw9 reported successful use of a cast for immobiliza­
tion of an open comminuted fracture after immediate post-
burn grafting of the affected extremity. Common sense
should dictate which fractures can be treated with circular
or bivalved casts or with splints. If a reduced or moderately
displaced but aligned fracture is so stable as to require
Local low-grade infections usually resolve when pins are
removed if the pin sites are vigorously curetted of granula­
tion tissue. In one case in which a four-pin custom external
fixator was used in the treatment of an open infection of the
elbow, there resulted diffuse osteomyelitis of the humerus
and radius. The infection was controlled with antibiotics and
without surgery after the pins were removed. This case was
included in Barret’s report of skeletal pinning in 41 severely
burned children.11 In experience with the Ilizarov system for
correction of skeletal deformity in burns, one patient devel­
oped a pin track infection of such severity as to require
removal of the pin, curettage, and intravenous antibiotics for
control of methicillin-resistant Staphylococcus.12
Hematogenous osteomyelitis and that due to spread from
an infected joint are rare. There is no report of the occurrence
of either entity in association with burns. Were bone infec­
tion of this sort to be recognized, effective treatment would
depend upon the identification of the offending organisms
for organism-specific antibiotic regimens.
Fractures
Pathological fractures were at one time common in burn
management because of the practice of delayed excision of
eschar and of keeping patients in bed until wounds were
completely covered. During that time, fractures occurred
because of bone collapse when patients first stood or walked
or when stiff joints were manipulated (Fig. 48.3).13 The bones
most commonly affected were the femur at its distal meta­
physis and the tibia at its proximal one. The only treatment
Figure 48.3  Pathological fracture of the osteoporotic femur of a 9-year-old
girl sustained on the first day she stood after 5 weeks of confinement for
40% TBSA burn.

Musculoskeletal changes secondary to thermal burns
555
the fracture ends was followed by treatment with skeletal
traction in one and by external fixation with the Ilizarov
system in the other. Both fractures healed without further
complication.
Fractures in burned patients heal quickly. There is no
recorded experience that suggests that healing is delayed by
the burn. Neither is there any record of failure of union.
Callus formation may be abundant.
Among severely burned patients, non-displaced or mini­
mally displaced fractures may not be detected until unusual
local pain in an affected extremity prompts radiographic
examination. A radiograph obtained for other reasons may
reveal a fracture as an incidental finding. These fractures
external support only for maintenance of alignment, then
cast or splint immobilization should be all that is needed. On
the other hand, if a fracture because of instability, requires
maintenance of reduction by three-point pressure or molding
of the cast material, it will be better treated by other means.
Dowling8 reported osteomyelitis resulting from open
bimalleolar fracture in an extremity with extensive deep
burns. In neither of the cases reported by Wang and Choctaw
did the bone become infected. There were also no infections
among Saffle’s 42 fractures, nine of which were treated by
open reduction and internal fixation.16 With two fractures of
the femur, each of which was exposed at the base of a deep
chronic burn, aggressive debridement of the wounds and
Figure 48.4  (a) This 15-year-old male sustained closed fractures of the right femur, left tibia
and left humerus at the time of a 46% TBSA burn involving mainly trunk and right lower
extremity. The femur and humerus fractures were treated in skeletal traction. Suspension of the
right lower extremity aided management of circumferential deep burns of that extremity. Lesser
burns of the left leg made it possible to treat the minimally displaced fracture of the left tibia in
a circular cast. All fractures consolidated in 6 weeks in satisfactory alignment. (b) Fracture of the
left humerus as it appeared at the time of admission to the hospital. (c) At 5 weeks after injury,
the fracture shows maturing callus. Traction was discontinued at 6 weeks.
A
B
C

Total Burn Care
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556
et al.19 have reported affected patients with total body surface
area burns of 8%, 14%, and 12%, respectively. In addition,
with the now-extensive experience with salvage of patients
with 80% or greater burns, it is clear that heterotopic bone
occurs no more frequently among these patients than in the
general burn population. Thus, the percentage of burn is not
a determining factor.
Location of burn
By no means has all of the reported heterotopic bone
occurred in joints with overlying burn. In their initial report,
Evans and Smith described heterotopic bone occurring a
distance from any third-degree burn involvement.29 John­
ston noted that in one of his three patients, the skin overly­
ing one affected joint was not even superficially burned.30 If
degradation of connective tissue milieu in burns is a total
body phenomenon, it follows that heterotopic bone forma­
tion need not be burn site dependent. Thus, the location of
the burn cannot alone be a determining factor.
Period of confinement
Evans and Smith expressed belief that length of bed confine­
ment was an important factor in the development of hetero­
topic bone.29 At the time of that report, patients with even
moderate burns might be kept in bed for several weeks. The
consequences of prolonged confinement were loss of active
range of joint motion and bone demineralization; it was
thought that each of these adverse changes might contribute
to the formation of heterotopic bone. Thus, any maloccur­
rence that necessitated longer confinement could be a factor
in the pathogenesis. Kolar implicated wound sepsis as an
independent factor, along with the length of confinement.26
Other investigators have not addressed the period of confine­
ment as specifically as Kolar, and there have been no com­
parative studies of groups of confined and non-confined
patients. Thus, it may never be determined whether the
current aggressive practice of early mobilization of patients
will have an effect on the incidence of heterotopic bone.
Osteoporosis
Only Schiele et al. have found a relation between hetero­
topic bone formation and osteoporosis.1 Among their group
of 70 adults with burns confined to the upper extremities,
11 of the 16 who developed heterotopic bone had radio­
graphically identifiable osteoporosis. In their series of
patients, there were 24 with osteoporosis. Thus, less than
one half of these developed heterotopic bone and there were
two in the group that developed heterotopic bone who did
not have osteoporosis. If the findings in that study are not
altogether persuasive, the matter is further confused by the
knowledge that the survivors of extensive total body surface
burns, who may develop profound osteoporosis, seem to
have no greater liability to the formation of heterotopic bone
than the general burn population.
Superimposed trauma
In one of the patients reported by Evans and Smith, the
elbow of the more often used and minimally burned right
upper extremity developed heterotopic bone, whereas the
are usually of no functional significance. Modest angular
deformity near a joint may be a problem in adults, although
not in children. On the other hand, undetected transphyseal
fractures in children can be a major functional threat.
Changes involving pericapsular structures
Heterotopic bone
Heterotopic bone formation is a rare but functionally impor­
tant complication of thermal burns. The incidence in a
general burn population is reported to be somewhere
between 1% and 3%.1,17–22 In select populations, the inci­
dence may be higher, as it will be if patients with periarticu­
lar calcification are included in the statistics. For example,
Tepperman et al. reported a 35.3% incidence among patients
referred to a tertiary care center for rehabilitation.23 Jackson
made the observation that the incidence of heterotopic bone
could be expected to be less in institutions that admit
patients with minor burns.24 Munster’s25 radiographic survey
of 88 adult and teenaged patients with 160 burned upper
extremities yielded a 16% incidence of pericapsular calcifica­
tion; the 23% incidence reported by Schiele et al.1 included
both heterotopic ossification and calcification. In the early
routine radiographic study reported by Evans,13 periarticular
calcification that did not progress to heterotopic bone was
excluded from the final calculation of an incidence of 2%.
The 3.3% incidence recorded by Kolar and Vrabec26 included
patients with pericapsular calcification. Even if heterotopic
bone occurs infrequently in thermal burns, it remains that
once it develops it often compromises joint motion and is
difficult to treat. In addition, its pathogenesis is still incom­
pletely understood; thus, protocols for prevention may in
fact miss the mark.
Pathogenesis
The metabolic changes occurring after thermal burn are
increased metabolic rate; protein catabolism; ureagenesis;
fat mobilization; glycogenolysis; gluconeogenesis; elevated
glucose flow; and eventual total body weight loss.27,28 There
is an accompanying suppression of the immune system that
favors wound infection, but at the same time favors survival
of skin allografts. Infection, failure of skin graft take, or any­
thing that delays closure of a burn wound will extend the
altered metabolic state. Although it might be assumed that
there occurs, along with the metabolic upheaval, an adverse
change in connective tissue milieu, the exact nature of such
a change is not known. It is also not known what the meta­
bolic changes have to do with the development of hetero­
topic bone, but it is apparent that the burn disease is
necessary to its formation. Other factors to be considered in
the genesis of heterotopic bone are percentage of burn, loca­
tion of burn, period of confinement, osteoporosis, super­
imposed trauma, and genetic predisposition.
Percentage of burn
Most reported cases of heterotopic bone have had a 20% or
greater total body surface area burn; however, heterotopic
bone has been found in patients with as little as 10% third-
degree burn.13 Peterson et al.,20 Munster et al.,25 and Elledge

Musculoskeletal changes secondary to thermal burns
557
and the more vigorous the remobilization, the greater was
the response. Muscle necrosis was a prominent histological
finding.41
Superimposed trauma is implicated in the development of
heterotopic bone in head-injured patients or those with
post-traumatic or infectious transverse myelitis.42–44 In these
patients, it is assumed that tissue media are altered by injury
to the central nervous system. The secondary injury, as in
burns, is periarticular. In post-traumatic myositis ossificans,
the development of heterotopic bone depends upon persist­
ence of the muscle lesion and local necrosis and, thus, at
least by inference, upon repeated insults to the affected
muscle.
The development of heterotopic bone in burns has been
associated with the agitation of patients and their resistance
to physical therapy.29,45 Two affected adults and one affected
child in a 10-year study resisted physical therapy program­
ming.39 One adult refused to move and the other was
extremely apprehensive. The child was likewise apprehensive
and refused to cooperate with the therapist. The develop­
ment in all three of posterior heterotopic bone in both
elbows could have been ascribed both to the difficulty
encountered in mobilizing the elbows and to the continual
pressure on the elbows in bed.
Genetic predisposition
It is difficult to explain the low incidence of heterotopic
bone among great numbers of patients similarly burned
except on the basis of some, as yet unidentified, inherited
factor. It is known that persons with proliferative non-
inflammatory arthritis of the hip are more likely to develop
heterotopic bone after total hip replacement than persons
who have hips replaced for other reasons. In this instance,
the predisposing inherited abnormality is identifiable.
Although heterotopic bone formation may occur more regu­
larly among spinal cord-injured and head-injured patients
than among burned ones, by no means do all persons with
head and spinal cord injuries develop heterotopic bone. The
total burn experience at The University of Texas Medical
Branch has yielded only two similarly affected siblings. Twin
brothers who had 19% and 20% total body surface burns
and who were mobile throughout much of their treatment
and recovery period developed near-identical heterotopic
bone of both elbows.46 There is, however, no scientific proof
that genetic predisposition has anything to do with the
formation of heterotopic bone in burns. Nor is there any
literature to support the idea that a person who develops
heterotopic bone when burned will be liable to develop it if
he or she sustains head or spinal cord injury. Vrbicky,47 in a
comprehensive review of post-burn heterotopic bone forma­
tion, suggests that a key for the genetic predisposition may
be in the human leukocyte antigen (HLA), reporting that an
HLA B27 survey showed a 7% HLA distribution in the
normal population compared with 70% in a population
with heterotopic bone.
Characteristics and behavior
Heterotopic bone associated with burns has been reported
to occur about all major joints. The joints most commonly
affected are elbow, shoulder, and hip, in that order of
elbow of the less used but more seriously burned left upper
extremity did not.29 In the same patient, the right hip spon­
taneously dislocated. After reduction, that hip developed
extensive heterotopic bone in the planes of the rectus femoris
and iliopsoas. The opposite hip developed only a small,
inoffensive spicule of heterotopic bone anteriorly at the joint
line. Experience with this one patient reinforced the authors’
belief that there occurs with burns a general compromise of
connective tissue that renders it particularly susceptible to
superimposed trauma and that it is this liability to injury
that accounts for the appearance of heterotopic bone at sites
of repeated stretching of soft tissue, as at the minimally
burned elbow or at sites of recognized abrupt excessive
stretching as with the dislocated hip. According to all reports,
the elbow is the most common site of heterotopic bone
formation in adults and children.19,20,26,31–38 Perhaps it is the
regular use of this joint that accounts for that orientation.
Jackson has pointed out that the elbows are subjected to
pressure posteriorly and medially when they are used for
leverage or are simply in contact with the bed.24 He suggests
with this observation that external pressure is a factor in the
orientation of heterotopic bone to the elbow. There may be
other factors that favor the elbow. Commonly, the elbow is
splinted in extension to prevent flexion contracture. If flexion
range is lost, passive stretch and encouragement of active
flexion are part of the rehabilitation effort. The posterior
structures most affected by this effort are those attached to
the olecranon. Heterotopic bone often develops medially in
line with and deep to the medial fibers of the triceps. If a
flexion contracture develops, the heterotopic bone is com­
monly in the line of brachialis or biceps attachments to
coronoid process and biceps tubercle. And if there is loss of
pronation and supination range, stretching may cause het­
erotopic bone to form in line with the proximal radioulnar
ligaments and interosseous membrane. There is an implica­
tion here that both the quality and timing of post-burn
exercise may be important. Gentle passive and active motion
should cause less tissue disruption than abrupt passive or
active or even chronically repeated motion, and the effect of
any mobilization effort must vary with the relative stiffness
of the joint and the intrinsic resistance of soft tissue. The
longer a joint is limited in its motion, the stiffer it will
become and the greater will be the soft tissue damage with
any forced manipulation.
The concept of superimposed trauma as a cause of hetero­
topic bone is supported by the experimental work of Evans39
and of Michelsson and Rauschning.40 Evans found that all
burned and non-burned rabbits given a single necrotizing
injection in one quadriceps muscle readily healed the lesions,
whereas rabbits burned or non-burned that were given a
second same-site injection 7 days after the first uniformly
developed well-defined and histologically identifiable het­
erotopic bone. In this experiment, it was clear that in sus­
ceptible animals it was not the burn that made the difference
but the chronicity of the wound. Michelsson and Rauschning
determined that forceful or regular active remobilization of
rabbit knees that had been immobilized for 1–5 weeks
resulted in the development of heterotopic calcification and
ossification in the muscles that were stretched. The response
was more consistent in the quadriceps of the knees immo­
bilized in extension than in the hamstrings of those immo­
bilized in flexion. The longer the period of immobilization

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558
frequency. The early manifestations are joint swelling and
tenderness not unlike any acute inflammatory process. The
patient may call attention to the process by a reluctance to
move the affected joint. Onset may be as early as 1 month
and as late as 3 months or more after the burn, but it is more
likely to be associated with the acute recovery phase of treat­
ment than later. Crawford et al. reported that the clinical
diagnosis was made in advance of radiographic changes in
9 of his 12 patients.31 Tepperman et al.23 and Peterson et al.20
found that bone scans could help make a diagnosis before
there were radiographic changes. The earliest radiographic
alteration is local periarticular increase in soft tissue density.
There follows diffuse, stippled calcification in the same dis­
tribution in or about the capsule of the joint. It is at this
point that the process may reverse itself, perhaps because of
the improved state of the patient. Owing to this change in
course, there may be patients whose periarticular calcifica­
tion is not detected. If the calcification persists, it may be
assumed that bone will develop by either the intramembra­
nous or the enchondral route or both, as it does in animal
models.
The flecks of calcification appear radiographically to lie
within the capsule, whereas heterotopic bone not only may
involve capsular structures but also may extend into the
planes of muscles and tendons. At each major joint there is
a more or less characteristic distribution of heterotopic bone,
which is similar to that associated with patients with head
and spinal cord injury. At the elbow, posteriorly disposed
bone extends from the olecranon to the medial epicondylar
ridge of the humerus in line with the medial border of the
triceps muscle (Fig. 48.5a,b). At the joint, it may extend
medially to bridge the ulnar groove.48,49 The medial, rather
than lateral, orientation of the heterotopic bone may be
related to the medial position of the olecranon and the
greater tension on soft tissue on that side, and, as Jackson
points out, the contact area of the elbow is consistently
medial.24 Heterotopic bone on the anterior surface of the
elbow develops in the planes of the brachialis and biceps
muscles extending from humerus to coronoid process or
biceps tubercle. Occasionally, a bridge of heterotopic bone
develops between the radius and ulna just distal to the joint.
More rarely, bone has been found to fill the olecranon fossa
and even to ensheath the entire joint. At the shoulder, bone
has been found to extend from the acromion to the humerus
in the line of the rotator muscles or deep to the deltoid (Fig.
48.5c), to lie anteriorly in the plane of the pectoralis major,
and, more deeply, to parallel the subscapularis. Hoffer et al.50
reported that heterotopic bone at the shoulder lay anteriorly
in the plane of the capsule. At the hip, heterotopic bone may
extend from pelvis to femur in the planes of rectus or iliop­
soas anteriorly or in the plane of the gluteal muscles laterally.
Jackson has reported heterotopic bone in the plane of the
quadratus femoris.24 Like the shoulder, the hip may be
ensheathed anteriorly with heterotopic bone that appears to
originate in the capsule.
When heterotopic bone bridges a joint, it becomes part of
the skeleton and may, if loaded, increase in dimension as a
fully developed ossicle with mature cortex and medullary
cavity. If the bone does not bridge a joint, it will, in children,
gradually disappear when the burn wound has healed and
the child is healthy. In recovering adults, non-bridging bone
will, in time, diminish in size, but it may not disappear. The
same tendency for heterotopic bone to regress after resolu­
tion of disease was noted by Lorber, who reported on two
patients with paraplegia secondary to tuberculosis in whom
deposits of heterotopic bone diminished in size, after return
of motor function.42 Bottu and Van Noyen51 reported a
similar experience with a patient who had transient viral
meningoencephalitis, and Jacobs reported almost complete
resorption of large bilateral deposits of heterotopic bone
in a patient who recovered from paralytic measles encepha­
lomyelitis.43 Serum concentrations of calcium, phosphorus,
and alkaline phosphatase have been reported by most
authors to be normal or, at best, insignificantly higher
in burned patients who have developed heterotopic
bone.17,25,29,52,53 In addition, there is no convincing evidence
that calcium intake affects heterotopic bone formation one
way or the other. Evans and Smith’s limited routine studies
of affected and unaffected patients led the authors to believe
that the values of serum calcium, phosphorus, and alkaline
phosphatase were so consistently normal as to make further
investigation unnecessary.29 One interesting observation was
that of Koepke, whose early, but incomplete, studies sug­
gested that those patients who were susceptible had eleva­
tion of serum alkaline phosphatase before development of
heterotopic bone, but not afterwards.18
Prevention and treatment
The incidence of heterotopic bone in burns is so low as to
make it impractical to administer indomethacin or other
non-steroidal anti-inflammatory drugs (NSAIDs) that are
currently used for patients at risk for development of het­
erotopic bone after major hip surgery. Rather, the thrust in
prevention should be toward reducing the period of bed
confinement and the duration of the post-burn hypermeta­
bolic state. The now-prevailing practice of early wound exci­
sion and grafting may, in fact, address both of these
problems as nearly as it is possible to do so. As noted above,
even patients with extensive total body surface burns
may now be out of bed and walking within the first post-
burn week.
If certain patients are predisposed to the development of
heterotopic bone, the quality and timing of joint mobiliza­
tion for those patients may be critical. Stretching edematous
pericapsular structures in the early post-burn period may
very well be hazardous if additional tissue damage is the
result; however, maintenance of joint motion and muscle
function is part of the early excision and grafting program,
and it is certain that the longer joint motion is restricted the
more likely it is that pericapsular structures will be damaged
by stretching. We like to think that secondary injury to soft
tissue can be avoided by controlled and assisted active range
of motion and terminal resistance.
When a patient is reluctant to move a joint previously
moved with relative ease, and certainly when there is evi­
dence of unusual swelling about the joint, radiographs
should be obtained to determine if there is pericapsular
calcification or ossification. Once heterotopic bone or calci­
fication is recognized, joint exercise should be restricted to
gentle passive and assisted active motion only. Crawford
et al.31 observed that ossification progressed to complete
ankylosis in all patients who persisted in moving an
affected joint beyond the pain-free range. They concluded

Musculoskeletal changes secondary to thermal burns
559
Figure 48.5  (a) At 3 months after 94% TBSA burn of a 16-year-old male –
resistance to motion, local swelling, and pain of both elbows prompted
obtaining roentgenograms, each of which showed spotty linear soft-tissue
calcification and ossification along the distal humerus and between the radius
and ulna at the level of the biceps tubercle. (b) At 6 months after burn, elbow
flexion and extension were reduced to 10° on the left and to less than 5° on
the right. Bridges of immature heterotopic bone extended from the medial
epicondylar ridges to the olecranon. Forearm rotation was 0% because
of interosseous bridges of heterotopic bone at the level of the bicipital
tuberosities. Prognosis for restoring functional range of motion in the elbows is
poor. (c) At 6 months post-burn, glenohumeral motion on the right was limited
to a few degrees by heterotopic bone underlying the deltoid. At the same time,
a lesser deposit of heterotopic bone at the left hip did not limit motion.
A
B
C

Total Burn Care
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560
one plane, removal of the offending bone will usually restore
functional motion and recurrence of the bridge is unlikely.
When a joint is bridged in more than one plane, recurrence
is more likely and the chance for restoration of functional
range of motion is correspondingly diminished. When the
local inflammatory process has caused intra-articular syno­
vial proliferation and cartilage destruction, the joint is most
likely destined for ankylosis. Removal of the heterotopic
bone about a joint so affected may allow more functional
positioning of the joint, but it is not likely to arrest the
process. On the other hand, extra-articular arthrodesis by a
bridge of heterotopic bone may preserve the joint. This is
particularly the case at the elbow when there is only one
posterior bridge of bone from olecranon to medial epi­
condylar ridge of the humerus. In this situation, the ole­
cranon is fixed in the trochlea, but the radiocapitellar and
radioulnar joints remain functional. In Evans’s experience
with removal of single bridges at the elbow, joint cartilage
was found to be healthy as long as 5 years after ankylosis.
Preservation of pronation and supination was credited with
maintaining the synovial bath to provide nutrition for the
humeroulnar cartilage. Indeed, when pronation and supina­
tion additionally are blocked by bridging bone, cartilage
degradation is certain. Evans’s further experience with long-
term survival of glenohumeral cartilage after ankylosis by
bridging bone from acromion to humerus is not as easily
explained.
that active range of motion exercises and stretching were
contraindicated if heterotopic bone or calcification was sus­
pected, but that active range of motion could be safely
resumed within pain-free range once the diagnosis had been
confirmed. In the series of Peterson et al.,20 patients sus­
pected of having heterotopic bone had active range of
motion exercises only. Ten regained functional range of
motion and eight developed ankylosis.
Surgical excision of heterotopic bone is indicated when
joint motion is lost or significantly compromised by bridg­
ing bone or exostoses. Evans has suggested that surgery be
postponed until the burn wound has healed, scars are soft
and associated with no inflammatory response, the patient
is healthy, and the offensive bone is radiographically mature,
i.e. well-defined and not increasing in dimension (Fig.
48.6).13 This position makes sense considering the behavior
of heterotopic bone: i.e. proliferation while there are open
burn wounds or active scars and regression with wound
healing and scar softening. For removal of heterotopic bone,
surgical exposures should be planned with extensible inci­
sions so as to facilitate total excision. When there is a bridge
of bone, each end of the bridge should be slightly excavated.
When there is attachment at only one end, the cartilaginous
or fibrous extension should be removed along with the bone.
Capsular sheets of bone should be removed completely. If
bridging heterotopic bone is incompletely excised, the bridge
is likely to recur. When a joint is bridged by bone in only
Figure 48.6  (a) A mature sheet of heterotopic bone extends from humerus to olecranon, obliterating the olecranon fossa 11 months after 53% TBSA burn
in a 13-year-old female. Elbow flexion and extension range was less than 10%. Pronation and supination were near normal range. (b,c) At 3 months after
excision of heterotopic bone, the patient had attained 90° of elbow motion and a continuing increase to functional (hand to mouth) range was predicted.
Now the patient can extend the elbow and can flex it to 90°.
A
B
C

Musculoskeletal changes secondary to thermal burns
561
The joints most liable to structural compromise due to
exposure by the burn and loss of soft tissue support are knee,
elbow, proximal interphalangeal joints of the hand, and
metacarpophalangeal joints. These hinge joints have in
common a subcutaneous dorsal surface, accounting for their
ready exposure.
The elbow, for its trochlear architecture, is more intrinsi­
cally stable than the other joints in this group. It requires
loss of collateral support to render it easily displaceable. The
knee, on the other hand, is immediately in danger of sub­
luxation if there is loss of continuity of its central slip, the
patellar tendon, even if the retinacula remain intact. In this
circumstance, gravity alone will displace the tibia posteriorly
in relation to the femur if the patient is recumbent. The
hamstring muscles contribute to the displacement force
regardless of the position of the extremity. Loss of collateral
ligaments compounds the problem, but loss of collateral
ligament stability in the presence of an intact patellar tendon
and functioning quadriceps constitutes far less a threat than
loss of patellar tendon. For the lower extremity, persistent
posterior translation of the tibia beneath the femur with
inefficient quadriceps function is potentially a functional
disaster.
For both the elbow and the knee, the protecting position
is extension. These two joints are rarely at risk for articular
displacement from contracture alone and, if there is no liga­
ment or tendon loss, extension resting splints will give ade­
quate positional support. When there is soft tissue disruption,
splinting may not adequately protect either joint. An exter­
nal fixator with two-pin, four-cortex fixation above and
below the joint will provide stability and will permit access
to the wound. For the elbow, it allows fine adjustment to the
normal carrying angle as well. If the knee is accurately reduc­
ible at the time of application of the fixator, there is a good
possibility that the reduction can be maintained. If the tibia
cannot be brought forward completely by manual manipula­
tion, it may be necessary to suspend the tibia through a
transverse pin at the level of the tibial tubercle. For static
vertical traction, the extremity must be elevated from the
bed. For dynamic traction, enough weight must be used to
accomplish the same elevation. If the tibia can be brought
forward by this means, an external fixator will hold the
reduction. For the knee to remain stable with the tibia
forward, the patellar tendon must be reattached and quad­
riceps integrity reestablished; otherwise, when the fixator is
removed, the tibia will once again begin an incremental
posterior shift toward its own point of stability. No amount
of external splinting or bracing is likely to prevent that shift.
The proximal interphalangeal joints of the hands are more
frequently exposed by burn than any others. If the central
extensor slip remains intact, there is less risk for subluxation
of the joint. Even if there is loss of continuity of the central
slip but preservation of the lateral bands, subluxation is
easily prevented if the joint is maintained in extension while
soft tissue cover is being achieved. It is with loss of the
support of lateral bands and collateral ligaments that the
joints become liable to dislocation. With the metacar­
pophalangeal joints, the tendency to displacement or sub­
luxation may be greater because these joints are functionally
multiplanar, while the interphalangeal joints are uniplanar.
Fortunately, metacarpophalangeal joints are less often
exposed than the interphalangeal ones.
Reported experience with excision of heterotopic bone in
burns has not been uniformly favorable. Dias,53 Hoffer
et al.,50 and Peterson et al.20 reported restoration of func­
tional range of motion in most of their patients with timely
excision of heterotopic bone. Gaur et al.32 reported good
functional return in seven burned children with nine affected
elbows. Ring and Jupiter33 reported good results in a varied
population, and Chung et al.34 and Tsionos et al.36 have
reported good results with early excision a mean of 9 months
after the burn. Other surgeons have reported less satisfactory
results.22 In our own experience, results have varied, as antici­
pated, with severity of affliction. We have learned that if
heterotopic bone recurs after excision, it is worthwhile to
excise again if the joint affected remains structurally identifi­
able. For the most part, however, attempts to improve joint
function with second operations have failed. We believe that
ultimate failure can be predicted at the time of initial surgery;
we are convinced that the single most important factor in
successful initial excision is in timing surgery to coincide
with the patient’s return to good health.
Changes involving the joints
Dislocation
Luxations and subluxations of joints in burned patients may
occur as a result of direct destruction by the burn of liga­
ments and capsules, loss of articular cartilage due to infec­
tion, faulty positioning, and eventually scar contracture. In
all phases of management, but particularly in the acute
phase, positioning is of prime importance in the prevention
of joint deformity. The preferred positions, listed in Table
48.1, serve as a guide for the prevention of dislocation of
joints and of malposition secondary to scar contracture.
Table 48.1  Preferred positions for major joints
Joint
Preferred position
Neck
Midline in neutral or slight extension
Shoulders
Scapulothoracic retraction and depression 85°
of glenohumeral elevation with 20–25° of
horizontal flexion
Elbows
Extension
Wrists
Slight extension
Metacarpophalangeal
joints 2–5
80–90° of flexion
Fingers
Proximal and distal interphalangeal extension
Thumbs
Carpometacarpal flexion and abduction,
metacarpophalangeal flexion 5–10°,
interphalangeal extension
Spine
Extension with no lateral deviation
Hips
Extension and slight external rotation in 15°
of symmetric abduction
Knees
Extension
Ankles
Neutral
Feet
Neutral

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562
patient is positioned this way, whether supine or prone, the
forearms will be pronated and the arms will be in sufficient
internal rotation to favor seating of the head of the humerus
in the glenoid.
The hip will tend to subluxate posteriorly if the thigh is
persistently allowed to remain flexed, adducted, and inter­
nally rotated during the acute burn phase. For the most part,
however, the protecting position of extension to neutral or
180 degrees and 15–20 degrees of symmetric abduction is
easy to attain and maintain and is, in fact, the most desirable
position for wound management.
Infection of a joint may result in its subluxation or disloca­
tion. Hip displacement because of apparent spontaneous
dissolution has been described by Evans and Smith.29 Eszter
and Istvan56 and Cristallo and Dell’Orto57 reported similar
cases. In none of these cases, however, could it be deter­
mined that the joint destruction was due to infection.
Septic arthritis
A joint exposed by a burn or by removal of burn eschar is
presumed to be infected. The joints most frequently exposed
are the knee, the elbow, the proximal interphalangeal joints
of the hand, and the metacarpophalangeal joints, all on the
subcutaneous dorsal surfaces. The wrist and ankle are less
often affected and other joints rarely. Treatment requires
stable positioning of the joint for maximum reduction of
wound size so as to facilitate soft tissue closure or grafting
and to allow aggressive daily lavage. The position for all of
the joints listed except the ankle is extension. The ankle is
positioned in neutral. External fixation, intramedullary
pinning, or skeletal traction may be required to secure the
position. To maintain ankle position it is sometimes appro­
priate to insert a large vertical Steinmann pin through the
calcaneus and talus into the tibia. The position should be
maintained until the exposed joint is covered with epithelial­
ized granulation tissue or skin graft. Exposed adjacent bone
can be shaved or drilled, as previously described, to encour­
age surface granulation. Drilling is particularly useful at the
elbow where the olecranon is regularly exposed. Often,
however, granulation tissue will quickly extend the wound
margins and effectively close the wound so as to allow split-
thickness skin grafting. If the burn is isolated to the joint or
if the extremity is not otherwise seriously burned, a local
muscle, skin or compound flap may be used to close the
joint. Free vascularized flaps are useful and should always
be considered if it is anticipated that nerve graft or tendon
graft or transfer at the site will be required in the future.
Incremental remobilization of the joint may proceed when
wound closure is sound. Culture of material from an exposed
joint will likely yield a variety of organisms consistent with
those of the general burn wound, thus requiring broad-
spectrum antibiotic management.
The incidence of hematogenous septic arthritis is obscured
by its frequent association with severe burns and because
there are rarely separable clinical signs such as local heat and
swelling, elevation of temperature, and elevation of sedi­
mentation rate. Local tenderness and greater than usual pain
with motion may focus attention on the affected joint. Aspi­
ration of the joint will confirm a diagnosis. A radiograph is
helpful, but in the early phases of infection will show only
local cellulitis as increased periarticular soft tissue density. If
The protecting position for the proximal interphalangeal
joints is full extension. If only the central slip is lost, the
position may be held with an external splint. In states of
greater instability it may be necessary to use intramedullary
transarticular Kirschner wires to hold the position. The wires,
although reasonably efficient, do not control rotation, and
they carry with them a risk for post-treatment joint stiffness.
In small children it is impossible to introduce the Kirschner
wires through the distal phalanx; thus, it is better, with the
proximal phalanx flexed to 90 degrees, to place the wire
through the corresponding metacarpal head into the proxi­
mal and middle phalanges. Short-term transfixation does
not harm the joint, and metacarpophalangeal flexion is the
favored position for functional restoration. Pin traction
through the distal phalanges in a skeletally stabilized metal
splint is another method for maintaining extension of
threatened digital joints.54,55 It has the advantages of patient
comfort and mobility, secure positioning of hand and upper
extremity, easy maintenance of elevation, and easy access for
dressings, for additional surgery, and for exercise of lesser
affected joints. The system likewise makes it possible to keep
digits separated, thus facilitating local care. Traction should
not be used if collateral ligaments are not intact. By whatever
means attained, the corrected position must be maintained
until the joint is covered with graft. Protection should con­
tinue with a standard splint or brace until the joint is sound.
The two joints most likely to dislocate because of faulty
positioning are the shoulder and the hip. These two ball and
socket, multiplanar joints sacrifice stability in favor of mobil­
ity. This is particularly true of the shoulder, where the shallow
glenoid contains at any one time only one third of the head
of the humerus. In burns, the head of the humerus may
begin to subluxate forward if, during prone positioning for
management of back and buttock wounds, the arms are
maintained in full abduction in the coronal plane. In this
position the arms are in at least 15–20 degrees of extension
from the more secure neutral position in line with the scapu­
lae and the humeral heads are forced forward against the
anterior capsule. Even when the patient is supine, full abduc­
tion and extension of the arms should be avoided. For short-
term management, particularly when the patient gets out of
bed each day, this position probably does not threaten the
joint. But if the patient is to be bed confined and the position
unrelieved for days or weeks, the head of the humerus may
begin to subluxate forward. In the extreme situation, the
head of the humerus will dislocate to a medial subcoracoid
position. In patients with deep burns extending from chin
to axillae to chest, the common posture of elevation and
protraction of the scapulae may be associated with upward
subluxation of the humeral heads.
The head of the humerus is most secure in the glenoid
fossa when the arm is adducted to neutral and internally
rotated, a position that is incompatible with wound manage­
ment of burns of the trunk, neck, and upper extremities. The
protecting position that accommodates the need for abduc­
tion for axillary burns is elevation of the arms in line with
the scapulae. The arm is then approximately 20 degrees
forward of the coronal plane or in 20 degrees of horizontal
flexion. When the patient is prone, the protecting position
can be gained only if the chest is supported on a chest width
mattress, folded blankets or towels, or a foam rubber pad,
any of which will allow the arms to drop forward. When the

Musculoskeletal changes secondary to thermal burns
563
offensive terminal exostoses develop. The overgrowing bone
can be shortened and the exostoses removed.
It is important in the early management of upper extremity
amputations in infants and young children to supply tem­
porary prosthetic extensions. This provides functional orien­
tation to a prosthesis, maintains muscle bulk and tone, and
encourages continuing bimanual activity at normal extrem­
ity length until a prosthesis with appropriate terminal device
can be applied. Children quickly acquire prehension and
transfer skills if they have an opposable stump and they may
reject prostheses if they are not applied early. It is equally
important to restore bipedal function as soon as possible. If
delay of healing or ulceration of a lower extremity stump
prevents early prosthetic fitting, an ischial weight-bearing
device that suspends the stump will permit the child to walk
in advance of prosthetic fitting. Inflatable plastic air bags
provide both even pressure and accurate fit for weight-
bearing in container sockets. Early prosthetic fitting is desir­
able in teenagers and adults as well, but is not as critical as
it is in children. As in non-burned persons, an upper extrem­
ity prosthesis may be rejected at any age if the opposite
extremity is fully functional.60
Alterations in growth
In 1959, Evans and Smith reported that a patient who was
24 years of age when burned had a subsequent 1 12 inch
increase in height. It was suggested that one explanation for
this growth spurt might be local change in hemodynamics
with stasis, passive hyperemia, and chronic inflammation.
We have not since documented height changes in burned
adults, but we have observed children whose growth after
burn has seemed to be retarded. If growth plates remain
open, it is difficult to explain overall growth retardation
except on an endocrine or humoral basis. It is easy, however,
to explain extremity length differences on the basis of pre­
mature closure of growth plates due to direct involvement
of the bone or to severity of overlying burn. Frantz reported
lower limb length discrepancy in four patients with foot and
ankle burns.61 Growth plates closed prematurely in only two
of the cases. Jackson described two patients with digital and
lower extremity deformity, respectively, due to partial closure
of growth plates.24 In Ritsilä et al’s case, contracture alone
was apparently the cause of growth retardation in an upper
extremity.62 It seems reasonable, although hard to prove, that
growth in a severely burned extremity would be retarded
because of functional impairment. One patient, a 3-year-old
boy with 80% total body surface burn and sufficiently deep
burns of the right upper extremity to require mid-humerus
amputation, demonstrated, 4 years after the burn, failure of
development of the right shoulder girdle. The factors operant
in this case could be premature closure of the growth plates
of scapula and clavicle, restrictive scar, and disuse atrophy.
There is yet another confusing aspect of premature closure
of growth plates in that within an extremity with total full-
thickness burn, only a few of the growth plates will close
prematurely. The explanation for this capricious selectivity is
at best obscure. Evans and Calhoun recorded an example of
spotty closure of growth plates in a 14-year-old male with
90% total body surface burn.12 There was complete closure
of distal tibial and fibular epiphyses 1 year after burn together
a patient has been receiving broad-spectrum antibiotics,
material aspirated from the affected joint may not grow an
organism in culture. Clearly, without organism identification
and sensitivity determinations, specific antibiotic therapy
cannot be initiated.
We have been of the opinion that debridement and exte­
riorization of the joint and regular vigorous lavage are as
important as antibiotics in the treatment of closed infected
joints.
We believe now that arthroscopic debridement and closed
irrigation should be considered as an alternative method of
management whether or not skin over the affected joint is
burned. Rarely in burns, a joint may become infected from
adjacent metaphyseal osteomyelitis. In this situation joint
preservation is the treatment priority, and measures are the
same as for septic arthritis of strictly hematogenous origin.46
In children, most infected joints can be salvaged. Adult joints
are less resilient. Persistent joint infection will destroy carti­
lage and lead to ankylosis.58,59 All chronically infected joints
are liable to dislocation because of surface destruction and
capsular laxity.
Amputations
In thermal burns, major amputations are most often per­
formed because of non-viability of the extremity or because
a surviving extremity is rendered useless by scar, deformity,
or insensitivity. Occasionally, in an extensive burn, a severely
burned extremity that might be salvaged in part is sacrificed
to reduce the extent of the burn or as a lifesaving measure.
In thermal burns, the level of extremity amputation is deter­
mined by the viability of muscles and tendons. The more
distal the site the better, and it is important to retain joints
even if motion will be restricted. For example, if a forearm
or leg must be sacrificed, the elbow or knee should be spared
if the more proximal muscles controlling that joint are
intact, if the bone bleeds, and if there is the possibility that
the remaining tissue of the stump has sufficient blood supply
to produce granulations for grafting. Aside from affording a
better functional prospect, sparing the joint will provide the
surgeon opportunity at a later time to choose an appropriate
revision level if the joint does not function. The patient will
at that time be healthier and stump closure will be routine.
Jackson suggests that it may be technically feasible to cover
even non-viable bone with a free flap in order to maintain
extremity length.24
In electrical burns, the level of amputation is most often
determined by muscle viability. Stump care is the same as
with thermal injury.
Prostheses can be easily fitted over stumps covered with
split-thickness grafts. Ridges of hypertrophic scar will break
down if there is friction within the socket of the prosthesis,
but scar often softens and flattens with the constant, even
pressure of a well-fitted socket; prostheses fitted early over
grafted stumps may prevent scar thickening. Breakdown may
occur at points where the graft is adherent to bone. This
problem may require surgical freeing of the adherent graft
and reshaping of the bone. Minor hip and knee flexion con­
tractures complicate the fitting and function of a prosthesis;
thus, every effort should be made to maintain full extension
of these joints. Late revisions of amputations in children are
required when the bone overgrows in length and when

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564
Further reading
Chen HC, Yang JY, Chuang SS, et al. Heterotopic ossification in burns:
our experience and literature reviews. Burns. 2009;35:857-862.
The most recent comprehensive review of the subject of heterotopic bone.
Evans EB. Heterotopic bone formation in thermal burns. Clin Orthop
Relat Res. 1991;263:94-101.
A detailed discussion of heterotopic bone and a comprehensive cover of the
subject.
Evans EB, Larson DL, Abston S, et al. Prevention and correction
of deformity after severe burns. Surg Clin North Am. 1970;50:
1361-1375.
Descriptions of burn-related deformity and management, with the important
inclusion of the concepts of Barbara Willis.
Johnston JT. Atypical myositis ossificans. J Bone Joint Surg Am.
1957;39:189-193.
The earliest description of burns related to heterotopic bone.
Klein GL, Herndon DN, Langman CB, et al. Long-term reduction
in bone mass after severe burn injury in children. J Pediatr.
1995;126:252-256.
A comprehensive discussion of causes and persistence of mineral loss.
Michelsson JE, Rauschning W. Pathogenesis of experimental
heterotopic bone formation following temporary forcible
exercising of immobilized limbs. Clin Orthop Rel Res.
1983;176:265-272.
With an introduction of the concept of superimposed trauma in burns.
Youel L, Evans E, Heare TC, et al. Skeletal suspension in the
management of severe burns in children. A sixteen-year experience.
J Bone Joint Surg Am. 1986;68:1375-1379.
Traction system in the management of wound burns.
with closure of all digital epiphyses in the feet and of several
digital epiphyses in the hands. Other major epiphyses were
spared (Fig. 48.2).
In early experience, abnormal growth plate closure was
observed in a 6-year-old girl with 50% third-degree burn that
did not involve legs or ankles.63 Rapidly destructive septic
arthritis of one ankle resulted in closure of the adjacent tibial
growth plate.
Only occasionally can growth changes be anticipated
because of obvious affection of the bone. More often the
changes are subtle. It seems clear, thus, that among seriously
burned children, regular height and extremity length meas­
urements must be part of ongoing post-burn assessment
until it is determined that the extremities and trunk are
developing symmetrically and on schedule. Extremity and
trunk alignment must likewise be part of the assessment as
subtle angular deformity can occur because of partial closure
of a growth plate. Jackson’s report addresses this problem.24
So-called growth arrest lines seen in the radiographs of
non-burned children, who have serious illness or major
trauma other than burns, are commonly observed in burned
children. In burns, as in other conditions, these transverse
markers of relatively increased mineralization represent
normal recovery from an insult to enchondral bone forma­
tion due to serious stress. They are of no clinical or func­
tional significance. They are more related to total burn than
to involvement of select burned extremities as all major long
bones are affected. There is no evidence that growth arrest
lines per se have any effect on growth.
 
Access the complete reference list online at

Musculoskeletal changes secondary to thermal burns
564.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
References
1. Schiele HP, Hubbard RB, Bruck HM. Radiographic changes in
burns of the upper extremity. Diagn Radiol. 1972;104:13-17.
2. Klein GL, Herndon DN, Langman CB, et al. Long-term reduction
in bone mass after severe burn injury in children. J Pediatr.
1995;126:252-256.
3. Owens N. Osteoporosis following burns. Br J Plast Surg.
1949;1:245-256.
4. Colson P, Stagnara P, Houot H. [Osteoporosis in burns of the
extremities.] Lyon Chir. 1953;48:950-956.
5. Artz CP, Reiss E. The treatment of burns. 1st ed. Philadelphia:
WB Saunders; 1957.
6. Klein GL, Herndon DN, Rutan TC, et al. Bone disease in burn
patients. J Bone Miner Res. 1993;8:337-345.
7. Van der Wiel HE, Lips P, Nauta J, et al. Loss of bone in the
proximal part of the femur following unstable fractures of the leg.
J Bone Joint Surg Am. 1994;76:230-236.
8. Dowling JA, Omer E, Moncrief JA. Treatment of fractures in burn
patients. J Trauma. 1968;8:465-474.
9. Choctaw WT, Zawacki BE, Dorr L. Primary excision and grafting
of burns located over an open fracture. Arch Surg. 1979;114:
1141-1142.
10. Wang XW, Zhang ZN, Nie QD, et al. The successful treatment
of a patient with extensive deep burns and an open comminuted
fracture of a lower extremity. Burns Incl Therm Inj. 1984;10:
339-343.
11. Barret JP, Desai MH, Herndon DN. Osteomyelitis in burn patients
requiring skeletal fixation. Burns. 2000;26:487-489.
12. Evans EB, Calhoun JH. Musculoskeletal changes complicating
burns. In: Epps Jr CH, ed. Complications in orthopaedic surgery.
Philadelphia: JB Lippincott; 1994:1239-1278.
13. Evans EB. Orthopaedic measures in the treatment of severe burns.
J Bone Joint Surg Am. 1966;48:643-669.
14. Brooker Jr AF. The use of external fixation in the treatment of
burn patients with fractures. In: Brooker Jr AF, Edwards CC, eds.
External fixation: the current state of the art. Proceedings of the 6th
International Conference on Hoffmann External Fixation. Baltimore:
Williams & Wilkins; 1979.
15. Frye KE, Luterman A. Burns and fractures. Orthop Nurs.
1999;18:30-35.
16. Saffle JR, Schnelby A, Hoffmann A, et al. The management
of fractures in thermally injured patients. J Trauma. 1983;
23:902-910.
17. Boyd Jr BM, Roberts WM, Miller GR. Periarticular ossification
following burns. South Med J. 1959;52:1048-1051.
18. Koepke GD. Personal communication, 1964.
19. Elledge ES, Smith AA, McManus WF, et al. Heterotopic bone
formation in burned patients. J Trauma. 1988;28:684-687.
20. Peterson SL, Mani MM, Crawford CM, et al. Post-burn heterotopic
ossification: insights for management decision making. J Trauma.
1989;29:365-369.
21. Chen HC, Yang JY, Chuang SS, et al. Heterotopic ossification in
burns: our experience and literature reviews. Burns. 2009;35:
857-862.
22. Hunt JL, Arnoldo BD, Kowalske K, et al. Heterotopic ossification
revisited: a 21-year surgical experience. J Burn Care Res.
2006;27:535-540.
23. Tepperman PS, Hilbert L, Peters WJ, et al. Heterotopic ossification
in burns. J Burn Care Rehabil. 1984;5:283.
24. Jackson D, Mac G. Destructive burns: some orthopaedic
complications. Burns. 1979;7:105-122.
25. Munster AM, Bruck HM, Johns LA, et al. Heterotopic calcification
following burns: a prospective study. J Trauma. 1972;12:
1071-1074.
26. Kolar J, Vrabec R. Periarticular soft-tissue changes as a
late consequence of burns. J Bone Joint Surg Am. 1959;41:103-111.
27. Heggers JP, Heggers R, Robson MC. Biochemical abnormalities in
the thermally injured. J Am Med Technol. 1981;43:333.
28. Herndon D. Mediators of metabolism. J Trauma. 1981;12:701.
29. Evans EB, Smith JR. Bone and joint changes following burns: a
roentgenographic study; preliminary reports. J Bone Joint Surg Am.
1959;41:785-799.
30. Johnston JT. Atypical myositis ossificans. J Bone Joint Surg Am.
1957;39:189-193.
31. Crawford CM, Varghese G, Mani MM, et al. Heterotopic
ossification: are range of motion exercises contraindicated? J Burn
Care Rehabil. 1986;7:323-327.
32. Gaur A, Sinclair M, Caruso E, et al. Heterotopic ossification
around the elbow following burns in children: results after
excision. J Bone Joint Surg Am. 2003;85:1538-1543.
33. Ring D, Jupiter JB. Operative release of complete ankylosis of the
elbow due to heterotopic bone in patients without severe injury
of the central nervous system. J Bone Joint Surg Am. 2003;85:
849-857.
34. Chung D, Hatfield S, Dougherty ME, et al. Heterotopic ossification
of the elbow in burn patients: results after early surgical treatment.
Proceedings of the 38th Annual Meeting of the American Burn
Association. Las Vegas, NV: American Burn Association;
2006:4–7April.
35. Djurickovic S, Meek RN, Snelling CF, et al. Range of motion and
complications after post-burn heterotopic bone excision about
the elbow. J Trauma. 1996;41(5):825-830.
36. Tsionos I, Leclercq C, Rochet JM. Heterotopic ossification of the
elbow in patients with burns. Results after early excision. J Bone
Joint Surg Br. 2004;86:396-403.
37. Holguin PH, Rico AA, Garcia JP, et al. Elbow achylosis due to
post-burn heterotopic ossification. J Burn Care Rehabil.
1996;17:150-154.
38. Vorenkamp SE, Nelson RL. Ulnar nerve entrapment due to
heterotopic bone formation after a severe burn. J Hand Surg Am.
1987;12:378-380.
39. Evans EB. Heterotopic bone formation in thermal burns. Clin
Orthop Relat Res. 1991;263:94-101.
40. Michelsson JE, Rauschning W. Pathogenesis of experimental
heterotopic bone formation following temporary forcible
exercising of immobilized limbs. Clin Orthop Rel Res.
1983;176:265-272.
41. Klein MB, Logsetty S, Costa B, et al. Extended time to wound
closure is associated with increased risk of heterotopic ossification
of the elbow. J Burn Care Res. 2007;28:447-450.
42. Lorber J. Ectopic ossification in tuberculous meningitis. Arch Dis
Child. 1953;28:98-103.
43. Jacobs P. Reversible ectopic soft tissue ossification following
measles encephalomyelitis. Arch Dis Child. 1962;37:90-92.
44. Garland DE, Blum CE, Waters RL. Periarticular heterotopic
ossification in head-injured adults. Incidence and location. J Bone
Joint Surg Am. 1980;62:1143-1146.
45. VanLaeken N, Snelling CT, Meek RN, et al. Heterotopic bone
formation in the patient with burn injuries. A retrospective
assessment of contributing factors and methods of investigation.
J Burn Care Rehabil. 1989;10:331-335.
46. Evans EB. Musculoskeletal changes complicating burns. In: Epps
Jr CH, ed. Complications in orthopaedic surgery. Philadelphia:
JB Lippincott; 1978:1133-1158.
47. Vrbicky B. Post-burn heterotopic joint ossifications. Annals of
Burns and Fire Disasters. 1991;4:161-164.
48. Cope R. Heterotopic ossification. South Med J. 1990;83:
1058-1064.
49. Peters WJ. Heterotopic ossification: can early surgery be
performed, with a positive bone scan? J Burn Care Rehabil.
1990;11:318-321.
50. Hoffer M, Brody G, Ferlic F. Excision of heterotopic ossification
about elbows in patients with thermal injury. J Trauma.
1978;18:667-670.

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51. Bottu Y, Van Noyen G. Un cas d’ossification reversible des tissus
mous chez une petite patiente paraplégique. Acta Paediatr Belg.
1963;17:223.
52. Proulx R, Dupuis M. [Para-articular ossifications and calcifications
following burns: review of the literature and presentation of 3
cases.] Union Med Can. 1972;101:282-293.
53. Dias DA. Heterotopic para-articular ossification of the elbow with
soft tissue contracture in burns. Burns. 1982;9:128-134.
54. Harnar T, Engrav L, Heimbach D, et al. Experience with skeletal
immobilization after excision and grafting of severely burned
hands. J Trauma. 1985;25:299-302.
55. Youel L, Evans E, Heare TC, et al. Skeletal suspension in the
management of severe burns in children. A sixteen-year
experience. J Bone Joint Surg Am. 1986;68:1375-1379.
56. Eszter V, Istvan S. Atipusos septicus arthritisek spontan luxatiok
egesi serulteken. Orv Hetil. 1972;113:48.
57. Cristallo V, Dell’Orto R. [Pathological dislocation of the hip due
to burns]. Arch Ortop. 1966;79:57-61.
58. Evans EB, Larson DL, Abston S, et al. Prevention and correction
of deformity after severe burns. Surg Clin North Am. 1970;50:
1361-1375.
59. Jackson D, Mac G. Burns into joints. Burns. 1976;2:90-106.
60. Malone JM, Fleming LL, Roberson J, et al. Immediate, early,
and late postsurgical management of upper-limb amputation.
J Rehabil Res Dev. 1984;21:33-41.
61. Frantz CH, Delgado S. Limb-length discrepancy after third-degree
burns about the foot and ankle. Report of four cases. J Bone Joint
Surg Am. 1966;48:443-450.
62. Ritsilä V, Sundell B, Alhopuro S. Severe growth retardation of the
upper extremity resulting from burn contracture and its full
recovery after release of the contracture. Br J Plast Surg.
1976;29:53-55.
63. Evans EB, Larson DL, Yates S. Preservation and restoration of
joint function in patients with severe burns. JAMA. 1968;204:
843-848.

Mitigation of burn-induced
hypermetabolic and catabolic
response during convalescence
Oscar E. Suman, David N. Herndon, Celeste C. Finnerty, Elisabet Borsheim
Background
Advances in burn management and critical-care have greatly
improved acute outcomes following severe burn injuries in
recent decades. This has led to an increased focus on meas­
ures to improve long-term outcomes by enhancing rehabili­
tation and reintegration of burn survivors back into fulfilling
and productive roles in society. Long-term debilitation fol­
lowing severe burns results from a combination of physical
and psychological factors, including persistent hyper­
metabolism and physiological derangements, severe skeletal
muscle wasting, deformity, scar contracture, pain and itch,
limb amputation, multiple operative interventions over the
course of years, and psychological and social factors related
to loss, disfigurement, identity, and bereavement. Burn team
scientists and clinicians have barely begun to gain knowl­
edge into what the long-term quality of life for these survi­
vors can be.1,2 Rehabilitative challenges for such children
are numerous, and the best methods of achieving good
outcomes in children with severe burns are still being
developed.3
Despite the similarities in treatment of pediatric and adult
burns, pediatric injuries present unique challenges, both at
the time of acute treatment and throughout rehabilitation.
Increased experience and new data, gathered in large part
from courageous young survivors, have allowed burn team
clinicians and scientists to identify many long-term prob­
lems associated with large burns. A major problem during
convalescence of the pediatric burn patient is the prolonged
hypermetabolic state associated with catabolism and growth
delay. Recent gene expression studies have demonstrated
that, of the thousands of genes which are altered by a severe
burn injury in peripheral blood leukocytes, the expression
of 21% of the genes are age-specific.4 Many of these genes
play important roles in mitochondrial and immune func­
tion. These studies demonstrated that there is a temporal
component of the response to burn injury as well, with
complete resolution of the genomic response to injury
taking up to (and in some cases beyond) 1 year. Although
the direct role that these genes play in mediating age-specific
manifestations of burn-induced sequelae, on-going studies
will improve our ability to personalize treatment in pediatric
and adult burn patients.
In response to a severe burn, afferent stimuli are activated
causing a hypothalamic thermoregulatory re-set to occur.
This results in increased heat production, a faster heart rate
and a greater cardiac output, in addition to an exaggerated
increase in resting energy expenditure.5 The control and
treatment of prolonged postburn hypermetabolism remain
an unsolved problem.6 Whereas the cause is still not well
understood, catecholamines are the major mediators.7
Catecholamine and cortisol levels can be elevated for
up to 1 year post-burn.8 With this elevation in stress
hormones, there is a long-lasting increase in resting energy
expenditure, glucose production and catabolism. The effect
of this hypermetabolic, hypercatabolic state is rapid muscle
breakdown.9
The self-catabolism, which is manifested as an increase in
protein degradation with a lesser increase in synthesis, per­
sists, despite state-of-the-art nutritional care.10 As a result, the
rate of protein degradation continues to exceed that of syn­
thesis. The protein catabolic response to injury leaves patients
debilitated for months and severely delays the rehabilitation
process. Protein is degraded to provide amino acids for
energy as well as building blocks for host defense protein
synthesis. Most of the required amino acids are taken from
active muscle which serves as a pool for amino acids. The
increase in amino acid loss from muscle causes muscle
wasting and loss of strength. Severe muscle wasting is closely
related to overall morbidity and mortality in the burned
patients.
Finally, associated with the prolonged hypermetabolic,
hypercatabolic state, there is also reduced bone formation,
resulting in severe osteopenia or osteoporosis11 as well as
linear growth retardation.12–14 This may partly be caused by
the continuous elevation in endogenous glucocorticoids that
decrease osteoblasts on the mineralization surface of bone,
blocking of osteoclastogenesis leading to low bone turnover
and bone loss, and a reduced synthesis of vitamin D from
skin from burned patients.15
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00049-7
CHAPTER 49 
Access the complete reference list online at

Total Burn Care
49
566
REE. However, this is due to the increased lean mass. Fur­
thermore, it should be noted that exercise training in burned
children does not further exacerbate REE.27
Exercise and younger children
Because of the difficulties with young children (i.e. under 7
years of age) using the exercise equipment or cooperating in
obtaining certain measures, the exercise studies described
above were conducted with children ages 7–18. However, as
exercise treatment has proven incredibly beneficial, we have
now begun a program using music and movement for young
children. Movements are chosen to increase strength, flexi­
bility, and endurance. Children enjoy this ‘play,’ and prelimi­
nary data indicate the program to be beneficial to overall
development and specifically to maintaining or improving
joint range of motion beyond standard of care (prescribed
occupational–physical therapy exercises).29
Exercise and adults
To our knowledge there is only one published prospective,
randomized study involving adults with severe burns and
exercise training. One of these studies investigated the
Mitigation of hypermetabolism
Propranolol
Herndon et al. proposed that beta-blockade would miti­
gate the catecholamine driven hypermetabolic response.16
Their initial study demonstrated that propranolol, given to
decrease severe burn-induced tachycardia, attenuates catabo­
lism of skeletal muscle, reduces resting energy expenditure,
and decreases hypermetabolism during the acute hospitali­
zation period in severely burned children.16 This mitigation
of the catabolic response is associated with alterations in
genes for key proteins, including dynein, heat shock protein
70, and myosin.17 Decreases in free fatty acid availability by
inhibition of peripheral lipolysis and reduction of hepatic
blood flow through the use of propranolol lead to the reduc­
tion of fatty infiltration of the liver.18,19 These studies of short
treatment regimens of beta-blockade (2–4 weeks) have been
extended up to 2 years. Preliminary analysis demonstrates
that reduction in cardiac work is the major benefit noted
6 months following the injury. Long-term improvements
in lean body mass, increased bone mineral content, and
decreased formation of hypertrophic scar persist as well,
indicating that extended treatment of severely burned chil­
dren with propranolol continues to improve patient recov­
ery. Studies to determine the impact of beta-blockade on
muscle strength, cardiopulmonary function, and growth
will elucidate whether propranolol in combination with
exercise can cause even greater improvements in post-burn
recovery.
Mitigation of catabolism
As mentioned previously, the catabolic response decreases
lean mass, muscle strength and cardiopulmonary function.
Appropriate levels of lean mass, muscle strength and
cardiopulmonary function are essential for normal daily
activities. Several treatment options for improving these
outcomes have been investigated at our institution.
Exercise
Resistance exercise has an established influence on muscle
strengthening and muscle protein synthesis. The beneficial
effects of resistance training have been well documented in
healthy adults, adolescents, and older children.20–24 Ferrando
et al. demonstrated in healthy adults that moderate resist­
ance exercise is capable of ameliorating the decreases in
skeletal muscle protein synthesis and strength that accom­
pany inactivity.25 The acute stimulatory effects of resistance
exercise may last up to 48 h.26
Most of our experience with exercise has been in children
and adolescents older than 7 years of age. In burns, resist­
ance exercise alone is also capable of inducing increases in
lean mass, muscle strength and aerobic capacity. Suman
et al. demonstrated in severely burned children and adoles­
cents that a 12-week exercise program of resistive and aerobic
exercise significantly improved lean mass, muscle strength
and aerobic capacity relative to standard of care treatment
(Fig. 49.1).27,28 We should note that a 12-week exercise
program of resistive and aerobic exercise does not reduce
Figure 49.1  (a,b) A structured and supervised program of resistance and
aerobic exercises has been shown to be beneficial in attenuating loss of
muscle mass and muscle function, as well as improving aerobic capacity in
burned victims.
A
B
C

Mitigation of burn-induced hypermetabolic and catabolic response during convalescence
567
for 9 months and either participated in a 12-week exercise
program or received standard of care treatment (daily physi­
cal and occupational therapy).34 In this study, the mean
percentage change in lean body mass after 12 weeks was
similar for the groups of participants receiving GH alone,
exercise alone, or the combination of both. On the other
hand, the mean percentage change in muscle strength was
significantly greater only in the groups receiving exercise,
independent of rhGH. Preliminary results using a higher
dose of rhGH (0.1 mg/kg per day) also yielded similar
results; lean mass increased by GH alone, exercise alone,
or the combination. However, similar to low-dose rhGH,
muscle strength was only increased via exercise. Similarly to
muscle strength, peak aerobic capacity was only improved
by exercise. It is presently unknown what are the effects of
higher doses of rhGH on muscle mass of severely burned
children.
A difficulty confronted in these studies using rhGH, is that
rhGH is administered via daily injections. Although these
injections are relatively painless (the investigators have first
given them to themselves to be sure of this), they present a
daily source of irritation and tension to parent and child.
Therefore, we searched for a less-intrusive means to improve
body composition.
Oxandrolone
Oxandrolone is an anabolic steroid that has been used in
catabolic situations such as hepatitis and AIDS patients and
can be administered orally, thus eliminating one source of
stress for children and families. In a randomized trial Przkora
et al. treated severely burned children with oxandrolone
(0.1 mg/kg twice daily per os) or placebo from hospital dis­
charge up to 12 months after trauma. They found a signifi­
cant improvement in body composition, including linear
growth, bone density, and lean mass. Muscle strength was
also significantly improved with oxandrolone. As with long-
term rhGH treatment, no adverse side-effects were observed
in the year following treatment. Beneficial effects on growth
were noted even 1 year after treatment.35
We have also recently studied the effects of oxandrolone
in conjunction with the exercise program.36 Oxandrolone in
combination with exercise increased lean mass significantly
more than either the drug or exercise treatment alone. Muscle
strength and functional improvement were significantly
improved with the combination of oxandrolone and exercise
as well as with exercise alone. A surprising, but welcome
finding was that oxandrolone alone improved muscle mass
and strength. Finally, aerobic capacity was significantly
improved with the combination of oxandrolone and exercise
as well as with exercise alone. We have planned future studies
that will introduce propranolol instead of rhGH or oxan­
drolone and will follow a similar design as described above.
Mitigation of growth delay
One can think of this physical state as the body running at
almost twice its normal rate even though the individual is
at rest. The patient requires enormous amounts of nutri­
tional intake to keep up with the energy expenditure. Even
with adequate caloric intake, individuals in this state lose
efficacy of a 12-week exercise program in producing
greater improvement in aerobic capacity in adults with
burns relative to the usual care. This randomized, control­
led, double-blinded trial had patients completing a 12-week,
36-session, aerobic treadmill exercise program. Some
patients were in the work-to-quota (WTQ) program, and
intensified their exercise according to preset quotas. Other
participants were in the work-to-tolerance (WTT) program
and exercised to their tolerance. Participants completed a
maximal stress test at baseline and at the 12 weeks to
measure physical fitness. The authors reported that the WTT
and the WTQ exercise groups both made significant
improvements in aerobic capacity from baseline to 12
weeks. However, the control (usual care) group did not.
WTT and WTQ participants demonstrated significantly
greater improvements in aerobic capacity in comparison to
the usual group patients. The WTT and WTQ groups did
not differ significantly from each other with regard to their
improvements in aerobic capacity. This very well designed
study demonstrated that the aerobic capacity of adult burn
can be improved with participation in a structured, 12-week
exercise program after injury.30
Anabolic agents
Growth hormone
Anabolic agents studied at our institution have included
recombinant human growth hormone (rhGH), and oxan­
drolone, a synthetic testosterone analogue. Both have
shown promising results, significantly improving growth
and muscle gain following severe burns in children.31
However, a multicentre trial of adult critical-care patients
reported increased mortality in patients treated with growth
hormone,32 and its use is presently therefore only considered
in children.
Przkora et al. studied the effects of administering 0.05 mg/
kg per day of rhGH to children from hospital discharge until
12 months after burn injury. The investigators showed that
growth and bone mass as well as lean mass were significantly
increased in patients receiving rhGH compared with the
placebo group. Furthermore, both lean mass and muscle
strength improved significantly in the treatment group. The
observed beneficial effects on body composition were associ­
ated with significant elevations in anabolic hormones such
as insulin-like growth factor-1 (IGF-1). Additionally, serum
cortisol, a catabolic hormone, was significantly lower with
rhGH treatment when compared with placebo. The enrolled
patients were followed for an additional year once rhGH use
was discontinued and the authors demonstrated a persisting
effect on growth and on bone mass in the rhGH group
during this period. No rebound phenomena on body com­
position or on hormone metabolism were noted during the
year following cessation of rhGH.33
Because of the positive results obtained with exercise inter­
vention alone and with rhGH alone, we rationalized that an
exercise program that included resistance exercise in combi­
nation with rhGH would provide for a synergistic effect on
skeletal muscle protein synthesis by addressing separate
stimulatory mechanisms for an extended period of time.
Suman et al. studied 44 severely burned children and ado­
lescents who received rhGH (0.05 mg/kg per day) or placebo

Total Burn Care
49
568
muscle mass and bone density. Conventional thinking has
been that this state should dissipate with full healing of the
burn wound. However, in clinical work, we observed that
the children fail to develop muscle, to grow, and to gain
weight for a period of time extending far beyond wound
healing.
We followed systematically 25 severely burned children for
1 year to ascertain the duration of the hypermetabolic–
catabolic state.37 Stable isotope methodology and body com­
position studies were performed during acute hospitalization,
at initial hospital discharge, and at 6, 9, and 12 months
post-burn. The resting energy expenditure of these children
peaked at 1-week post-injury with a metabolic rate of 180%
of normal and progressively declined with time. At the
12-month exit from the study, their resting energy expendi­
ture remained 15% above basal metabolic rate. Catabolism
persisted for at least 9 months, which was 7 months after
complete wound healing. As muscle catabolism and the
hypermetabolic response persists well into the rehabilitative
phase, strategies to counter these effects should similarly
extend during rehabilitation.
Knowledge of the duration and extensive harm resulting
from the catabolic effects of trauma has also led to efforts to
better delineate mechanisms of catabolism38 and to a vigi­
lant pursuit of early interventions that could attenuate the
effects of the hypermetabolic–catabolic response. Factors
affecting the convalescence of severely burned children are
shown in Figure 49.2. The effect of the hypermetabolic–
catabolic response 6 months after burn is displayed in Figure
49.3. Such long-lasting deleterious effects upon the recovery
of severely burned children demand that we develop strat­
egies to attenuate the hypermetabolic–catabolic response
during and after discharge from acute hospitalization. For
most of the issues evolving from massive burn, we are still
in the early stages of this process; we are still learning about
problems and devising methods of improving treatments.
Our progress in developing such strategies is the subject of
this chapter.
In 1990, Rutan and Herndon demonstrated a dampened
growth curve for both height and weight in male and
female pediatric patients who had sustained major thermal
injury.12 The growth velocities were delayed up to 3 years
after burn injury. Even after the return to normal growth
velocities, the burned patients lagged behind age- and sex-
matched peers.
Figure 49.2  Various burn-induced problems that afflict many severely
burned survivors (left side of balance). These problems can last up to
2 years. On the right side are strategies to attenuate these problems.
Catabolism
Osteoporosis
Stunted growth
Exercise
Oxandrolone
Growth hormone
Combination
Burns
Normal linear growth and weight gain in children
are dependent upon a number of factors. The prenatal
environment, adequate nutritional intake, and an emotion­
ally nurturing household environment are crucial. Long
hospitalizations alone have been known to produce pro­
found arrests in growth and development in children. The
management of massively burned children includes multi­
ple operations and prolonged hospitalization. In cases of
fascial excision, subcutaneous fat layers in the injured area
are also removed. Fat stores are further depleted in provid­
ing energy for the process of gluconeogenesis from existing
protein stores for dietary supply. All the reasons for the
growth delay following severe burns are not currently
known.
Growth hormone
Growth hormone (GH) levels have been shown to decrease
in severely burned adults,15 and it is likely that children
experience a similar decrease. In children, measured serum
growth hormone levels remain depressed during both the
acute phase following severe burns, and may remain so for
at least 2 years.31,39
Administration of an anabolic agent such as recombinant
human growth hormone (rhGH) during the acute treatment
of severely burned children has been demonstrated to be
extremely beneficial in promoting healing and normalizing
growth.40 Studies of GH demonstrate that it can be given
safely to severely burned children and that it accelerates
wound healing and reduce tissue wasting commonly seen in
the catabolic patients. Using rhGH in the acute treatment of
children with severe thermal injuries has been shown to
improve net muscle protein synthesis as well as to accelerate
wound healing and reduces length of hospital stay.41,42
Knowledge gained from such studies suggests improved
treatment approaches that can be evaluated. Improvement
in each of these areas could contribute to improved growth
and weight gain; therefore, administration of GH was per­
ceived as a probably advantageous tool in the management
of pediatric burn patients toward normal growth.
Treatment with low dose rhGH (0.05 mg/kg per day) has
previously been shown to improve growth, lean body mass,
and bone mineral content when given to children following
severe burns. This low dose treatment with rhGH, however,
did not appear to reduce elevated metabolic rates, reflected
in resting energy expenditure and cardiac output measure­
ments.33 Furthermore, while both lean mass and muscle
strength were significantly improved at 12 months, when
treatment was discontinued, these were not significantly dif­
ferent by two years post-burn compared to controls. Benefi­
cial effects of low-dose rhGH have also included a reduced
number of operative reconstructive procedures.
More recently, Branski et al.31 reported on the effects of
long-term rhGH treatment at three different dosing levels in
children with severe burns over 40% TBSA, as part of a
single-center randomized controlled trial at our unit. Patients
received 0.05, 0.1 or 0.2 mg/kg per day for 12 months after
injury and were followed up for 2 years, with analysis
reported for 195 patients (n = 101 treatment groups, n = 94
controls).
Low et al.43 tested the hypothesis that rhGH would amel­
iorate the growth delay by following, for 3 years, 49 children

Mitigation of burn-induced hypermetabolic and catabolic response during convalescence
569
and thus, can maintain normal growth without exogenous
hormone.
Summary
In this chapter, we have described various interventional
strategies used in counteracting the hypermetabolism, cata­
bolism and growth delay (in children) which is present after
severe burns. These burn-induced sequelae can continue for
many years, thus mitigation of these responses is of vital
importance. Methods used to mitigate some of these
responses include aerobic and resistive exercise, as well as
the use of anabolic agents, such as growth hormone and
oxandrolone. Beta-adrenergic blockade to reduce cardiac
work is a promising interventional strategy, but needs
further evaluation. Strategies to attenuate catabolism, hyper­
metabolism, and other burn-induced problems should
also result in improvements in the quality of life of the
in a prospective, randomized, masked study. A total of
26 children received 0.2 mg/kg GH during their acute
hospitalizations and 23 children received 0.9% saline as
placebo during the same time periods of acute hospitaliza­
tion. Children who were treated with GH during their acute
care maintained stature (height for age percentile and
height-velocity), whereas untreated children who were not
in a growth spurt at the time of burn remained delayed in
linear growth at the end of the study, 3 years post-injury.
Continuing with this study, Low et al. found that the dif­
ferences in height percentiles had nearly resolved at 5 years
post-burn.44 Short-term (average of 6 weeks) administration
of GH did not attenuate the hypermetabolic state; resting
energy expenditures remained elevated for both groups of
children during the time they were being treated acutely.
However, the administration of GH apparently made up for
a deficit that commonly occurs following severe burn injury.
Children burned during a growth spurt are thought to have
the advantage of higher levels of growth hormone available
Figure 49.3  (a–c) The ravaging effects of a
severe burn are illustrated in these photos. The
body is in a hypermetabolic and catabolic state.
This results in loss of muscle mass and bone
mass, and is worsened by prolonged inactivity. In
addition, there are physical limitations sometimes
caused by the loss of digits or extremities and of
burn scar contractures.
A
B
C

Total Burn Care
49
570
burn victims (Fig. 49.4). We advocate the use of both
physical and psychosocial rehabilitation strategies to
enhance their potential of a full and effective re-incorporation
into society.
Further reading
Branski LK, Herndon DN, Barrow RE, et al. Randomized controlled
trial to determine the efficacy of long-term growth hormone
treatment in severely burned children. Ann Surg. 2009;250(4):
514-523.
Herndon DN, Hart DW, Wolf SE, et al. Reversal of catabolism by
beta-blockade after severe burns. N Engl J Med. 2001;345(17):
1223-1229.
Kulp GA, Herndon DN, Lee JO, et al. Extent and magnitude of
catecholamine surge in pediatric burned patients. Shock.
2010;33(4):369-374.
Jeschke MG, Chinkes DL, Finnerty CC, et al. Pathophysiologic
response to severe burn injury. Ann Surg. 2008;248(3):387-401.
Przkora R, Jeschke MG, Barrow RE, et al. Metabolic and hormonal
changes of severely burned children receiving long-term
oxandrolone treatment. Ann Surg. 2005;242(3):384-391.
Figure 49.4  The ultimate objective of strategies to attenuate catabolism,
hypermetabolism, and other burn-induced problems should be to improve
the quality of life of burn victims. This may be accomplished by offering the
burn victims physical and psychosocial rehabilitation strategies to enhance
their potential of a full and effective re-incorporation into society.
 
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Mitigation of burn-induced hypermetabolic and catabolic response during convalescence
570.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
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adjustment to burn injury: social functioning, body image, and
health policy perspectives. Int Rev Psychiatry. 2009;21(6):539-548.
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psychologic rehabilitation outcomes for pediatric patients who
suffer 80% or more TBSA, 70% or more third degree burns.
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adjustments made by postburn injury patients: an integrative
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8. Kulp GA, Herndon DN, Lee JO, et al. Extent and magnitude of
catecholamine surge in pediatric burned patients. Shock.
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9. Sakurai Y, Aarsland A, Herndon DN, et al. Stimulation of muscle
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10. Jahoor F, Desai M, Herndon DN, et al. Dynamics of the protein
metabolic response to burn injury. Metabolism. 1988;37(4):
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11. Klein GL, Herndon DN, Goodman WG, et al. Histomorphometric
and biochemical characterization of bone following acute severe
burns in children. Bone. 1995;17(5):455-460.
12. Rutan RL, Herndon DN. Growth delay in postburn pediatric
patients. Arch Surg. 1990;125(3):392-395.
13. Klein GL, Herndon DN, Langman CB, et al. Long-term reduction
in bone mass after severe burn injury in children. J Pediatr.
1995;126(2):252-256.
14. Shea JE, Bowman BM, Miller SC. Alterations in skeletal and
mineral metabolism following thermal injuries. J Musculoskelet
Neuronal Interact. 2003;3(3):214-222.
15. Klein GL. The interaction between burn injury and vitamin D
metabolism and consequences for the patient. Curr Clin
Pharmacol. 2008;3(3):204-210.
16. Herndon DN, Hart DW, Wolf SE, et al. Reversal of catabolism
by beta-blockade after severe burns. N Engl J Med. 2001;345(17):
1223-1229.
17. Herndon DN, Dasu MR, Wolfe RR, et al. Gene expression profiles
and protein balance in skeletal muscle of burned children after
beta-adrenergic blockade. Am J Physiol Endocrinol Metab.
2003;285(4):E783-E789.
18. Morio B, Irtun O, Herndon DN, et al. Propranolol decreases
splanchnic triacylglycerol storage in burn patients receiving a
high-carbohydrate diet. Ann Surg. 2002;236(2):218-225.
19. Barrow RE, Wolfe RR, Dasu MR, et al. The use of beta-adrenergic
blockade in preventing trauma-induced hepatomegaly. Ann Surg.
2006;243(1):115-120.
20. Biolo G, Maggi SP, Williams BD, et al. Increased rates of muscle
protein turnover and amino acid transport after resistance exercise
in humans. Am J Physiol. 1995;268(3 Pt 1):E514-E520.
21. Chesley A, MacDougall JD, Tarnopolsky MA, et al. Changes in
human muscle protein synthesis after resistance exercise. J Appl
Physiol. 1992;73(4):1383-1388.
22. MacDougall JD, Gibala MJ, Tarnopolsky MA, et al. The
time course for elevated muscle protein synthesis following
heavy resistance exercise. Can J Appl Physiol. 1995;20(4):
480-486.
23. Blimkie CJ. Resistance training during pre- and early puberty:
efficacy, trainability, mechanisms, and persistence. Can J Sport Sci.
1992;17(4):264-279.
24. Ramsay JA, Blimkie CJ, Smith K, et al. Strength training effects in
prepubescent boys. Med Sci Sports Exerc. 1990;22(5):605-614.
25. Ferrando AA, Tipton KD, Bamman MM, et al. Resistance exercise
maintains skeletal muscle protein synthesis during bed rest. J Appl
Physiol. 1997;82(3):807-810.
26. Phillips SM, Tipton KD, Aarsland A, et al. Mixed muscle protein
synthesis and breakdown after resistance exercise in humans. Am
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27. Al-Mousawi AM, Williams FN, Mlcak RP, et al. Effects of exercise
training on resting energy expenditure and lean mass during
pediatric burn rehabilitation. J Burn Care Res. 2010;31(3):400-408.
28. Suman OE, Spies RJ, Celis MM, et al. Effects of a 12-wk resistance
exercise program on skeletal muscle strength in children with
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29. Neugebauer CT, Serghiou M, Herndon DN, et al. Effects of a
12-week rehabilitation program with music and exercise groups
on range of motion in young children with severe burns. J Burn
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30. de Lateur BJ, Magyar-Russell G, Bresnick MG, et al. Augmented
exercise in the treatment of deconditioning from major burn
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31. Branski LK, Herndon DN, Barrow RE, et al. Randomized
controlled trial to determine the efficacy of long-term growth
hormone treatment in severely burned children. Ann Surg.
2009;250:514-523.
32. Takala J, Ruokonen E, Webster NR, et al. Increased mortality
associated with growth hormone treatment in critically ill adults.
N Engl J Med. 1999;341(11):785-792.
33. Przkora R, Herndon DN, Suman OE, et al. Beneficial effects of
extended growth hormone treatment after hospital discharge in
pediatric burn patients. Ann Surg. 2006;243(6):796-801;
discussion 801–803.
34. Suman OE, Thomas SJ, Wilkins JP, et al. Effect of exogenous
growth hormone and exercise on lean mass and muscle function
in children with burns. J Appl Physiol. 2003;94(6):2273-2281.
35. Przkora R, Jeschke MG, Barrow RE, et al. Metabolic and hormonal
changes of severely burned children receiving long-term
oxandrolone treatment. Ann Surg. 2005;242(3):384-389,
discussion 390–391.
36. Przkora R, Herndon DN, Suman OE. The effects of oxandrolone
and exercise on muscle mass and function in children with severe
burns. Pediatrics. 2007;119(1):e109-e116.
37. Hart DW, Wolf SE, Mlcak R, et al. Persistence of muscle
catabolism after severe burn. Surgery. 2000;128(2):312-319.
38. Hart DW, Wolf SE, Chinkes DL, et al. Determinants of skeletal
muscle catabolism after severe burn. Ann Surg. 2000;232(4):
455-465.
39. Jeschke MG, Chinkes DL, Finnerty CC, et al. Pathophysiologic
response to severe burn injury. Ann Surg. 2008;248(3):387-401.
40. Ramirez RJ, Wolf SE, Herndon DN. Is there a role for growth
hormone in the clinical management of burn injuries? Growth
Horm IGF Res. 1998;8(Suppl B):99-105.
41. Gilpin DA, Barrow RE, Rutan RL, et al. Recombinant human
growth hormone accelerates wound healing in children with large
cutaneous burns. Ann Surg. 1994;220(1):19-24.
42. Herndon DN, Barrow RE, Kunkel KR, et al. Effects of recombinant
human growth hormone on donor-site healing in severely burned
children. Ann Surg. 1990;212(4):424-429; discussion 430–431.
43. Low JF, Herndon DN, Barrow RE. Effect of growth hormone on
growth delay in burned children: a 3-year follow-up study. Lancet.
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44. Aili Low JF, Barrow RE, Mittendorfer B, et al. The effect of
short-term growth hormone treatment on growth and energy
expenditure in burned children. Burns. 2001;27(5):447-452.

Reconstruction of burn deformities:
an overview
Lars Peter Kamolz, Ted Huang
The severity of burn injuries is usually assessed, if not by
patient survival, by the consequence of burn injuries, i.e.
scar hyperplasia/hypertrophy, scar contracture, and struc­
tural deformities due to loss of bodily components. Since
the bodily deformity is closely related to the magnitude of
injuries, restorative procedures are seldom indicated if the
depth of injury is superficial and the burned area limited
(Fig 50.1) but are required for deep burns (Fig 50.2).
The possibility of surviving burn injuries has changed dra­
matically over the past 30 years, attributable singularly to an
aggressive approach in surgical treatment of burn wounds,
i.e. early wound debridement and wound coverage.1–3 It is
ironic that the success attained in burn treatment has resulted
in a higher number of patients who will need to undergo
reconstruction because of an aggressive ‘life-saving’ surgical
treatment.
Formation of scar tissues at a wound site and contraction
of the scar tissues are the normal consequence of an injury.
Although the exact mechanisms accounting for the sequen­
tial changes in wound healing and scar formation remain
incompletely understood, wounds with infection and/or
those allowed to heal spontaneously, for instance, tend to
result in a thickened scar that is contracted circumferentially;
an observation suggestive that various fibrogenic cytokines
such as transforming growth factor β could play an impor­
tant role in the pathogenesis of otherwise clinically undesir­
able consequences.4,5
Thickened and contracted scar tissues, i.e. the changes that
are ‘normal’ and ‘expected’ consequence of the wound
healing processes, are microscopically composed of colla­
gens arranged in whorls and nodules. The changes may be
observed as early as 3–4 weeks following the injury and
they are cosmetically unsightly and functionally disturbing
(Fig. 50.3).
Reconstruction of burn deformities
General principles
Burn injuries are a traumatic illness resulting in aberrant
body physiologic processes caused by thermal destruction of
the skin. The altered physiologic processes will affect not
only the healing of the original burn wounds but also
healing processes of the secondary surgical procedures
aiming to restore the consequence of the original injuries.
The treatment, under an aberrant physiologic circumstance,
should aim to repair the burn wounds first. Attempts to
restore deformities should be delayed until recovery from the
initial phase of injury is complete.6
Early treatment of deformity
Of the consequences of burn injuries, hyperplasia and con­
tracture of resultant scars at wound sites and the contraction
of mobile bodily parts, i.e. eyelids, neck, axilla, elbow, hands-
fingers, groin, knee and ankle-foot, are two most common
problems that are in need of attention. The regimen of
applying pressure upon scar tissues and of immobilizing
joint structures has been advocated to minimize the
undesirable consequences of scarring and scar contracture
(Fig. 50.4).
Although the true efficacy of a non-surgical regimen to
control the deformities has not been established, the fre­
quency of secondary joint release among individuals who
‘endured’ the morbidities associated with proper joint
splinting for a period of no less than 6 months has been
noted.7,8 The use of pressure dressing, especially in the areas
such as upper and lower limbs, with proper splinting of the
hand and fingers is strongly recommended soon following
the injury. The regimen of non-surgical management of
burn deformity must include daily physiotherapy and
exercise to maintain joint mobility and to prevent muscle
wasting.
Assessment of burn deformities
Objective assessment of deformities by the patient is neither
physically nor psychologically possible soon after the acci­
dent. Restoration of physical changes resulting from the
injury, in addition to the need of obtaining relief of pain and
discomfort, are the primary concerns of the patient. Medical
assessment of physical problems caused by scarring and
scar contracture will require a detailed understanding of the
extent of original injury and the precise treatment approach
used to manage the burn wound. Formulating a realistic
plan to restore physical problems and to alleviate pain and
discomfort in the area of injury requires an in-depth analysis
of the physical deformities and psychological disturbance
sustained by the patient. Psychiatric, psychosocial, and
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00050-3
CHAPTER 50 
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Total Burn Care
50
572
physiotherapeutic care, in this sense, must be continued
while the surgical treatment plan is instituted.
Indication and timing of surgical intervention
For a surgeon, making a decision of ‘how’ to operate on a
patient with burn deformities is quite simple. In contrast,
deciding ‘when’ to operate on a patient with burn deformi­
ties can be difficult.
The basic principle of restoring bodily deformities that
impose functional difficulties before surgical efforts are
directed to restoring appearance should be followed. The
surgeon’s efforts should be concentrated upon restoring the
deformed bodily parts essential for physical functions. An
exposed skull or a calvarial defect, contracted eyelids, con­
stricted nares, contracted major joints, and a urethral and/or
anal stricture in individuals with severe perineal burns, are
the prime indications for early surgical intervention. In con­
trast, restoration of contour deformity can be delayed. In
fact, reconstruction of the nose and the ear, for instance,
should not be initiated until its growth pattern has reached
the growth peak; ear reconstruction may be initiated once
the child has reached 6–8 years of age, while nasal recon­
struction should be delayed until 16–18 years.
Although the exact scientific basis remains unclear, it has
been advocated that attempts at reconstructing burn deform­
ities should be delayed for at least 2 years post-burn injuries;
the time needed for scar maturation. During the interim, the
use of pressure garments and splinting is recommended to
‘facilitate’ scar maturation and to ‘minimize’ joint contrac­
ture. The true efficacy of pressure garments in ‘facilitating’
scar maturation remains undefined. Lack of a reliable
method to determine various stages of scar maturation
and personal difference in assessing scar appearance could
Figure 50.1  (a) An 8-year-old boy sustained flash flame burns of the face.
The depth of injury was judged to be superficial. (b) The wounds healed
spontaneously. The scar formed was judged to be minimal 5 years later.
A
B
Figure 50.2  (a) A 4-year-old boy sustained flame burns involving 75% of
his total body surface. (b) The injury was extensive; the wound required
staged debridement and skin grafting, resulting in extensive scarring.
A
B
Figure 50.3  (a) Scarring formed around the injured sites became apparent
within 3 weeks. (b) Thickening of the scar continued during the subsequent
5–6 months. Contraction of scars caused difficulty in the closing and
opening of the eyelids and mouth.
A
B
Figure 50.4  The use of splints over the mobile joints and pressure
garments is an essential component of patient management.

Reconstruction of burn deformities: an overview
573
left attaching to the base. The conventional approach of
wedged scar excision will result in depression along the site
of scar excision, an iatrogenic consequence that could be
difficult to amend secondarily. In order to minimize vascular
supply interference along the wound edges, undermining of
scar edge should be kept minimal. Synthetic sutures are
preferred for wound closure (Fig. 50.5).
Skin grafting technique
Free skin graft without incorporating a dermal template
Covering an open wound with a piece of skin graft harvested
at an uneven thickness is the conventional approach of
wound closure. While the whole structure of the skin
removed as an intact unit, i.e. epidermis and dermis, is
defined as a full thickness skin graft, a piece of skin cut at a
thickness varying between 8/1000th of an inch (0.196 mm)
and 18/1000th of an inch (0.441 mm) is considered to be a
partial- or a split thickness skin graft. The thickness of a full
thickness skin graft is quite variable depending upon the
body site. A full thickness skin graft harvested from the back,
for instance, will be 16/1000th of an inch (4 mm) in thick­
ness, while one harvested from the upper eyelid will be
around 35/1000th of an inch (0.8 mm). The difference is
attributable to the difference in the thickness of the dermis.
While a power-driven dermatome is usually used to harvest
a partial- (split-) thickness skin graft, a free hand knife could
be used to cut a piece of full thickness skin graft. A paper
template may be made to determine the size of skin graft
needed to close a wound. The skin graft is laid onto the
wound, colloquially known as the ‘wound bed’, and is
anchored into place by suturing the graft to the wound edge-
to-edge at various sites. An apposition of the skin graft with
the ‘wound bed’ is essential to ensure an in-growth of vas­
cular network in the graft within 3–5 days for graft survival,
as any mechanical barriers, i.e. blood clot or pool of serous
or purulent fluid, will prevent vascularizing processes,
leading to graft loss. A gauze or cotton bolster tied over a
graft has been the traditional technique to anchor and to
prevent fluid accumulating underneath a graft even though
no objective evidence supports the efficacy of this maneuver.
A quilting technique instead of bolstering technique has
been found to be more effective in immobilizing a skin graft
and is associated with fewer morbidities (Fig. 50.6).
The basis for using a free skin graft of various thicknesses
to close all wounds is not entirely clear. It is, however, clear
that the use of a thin graft is more appropriate for closing
wounds with unstable vascular supplies, particularly if skin
graft donor sites are scarce. Although the exact reasons
remain undefined, the quality and the presence of dermis
could influence the extent of wound contraction. That is, the
extent of contraction noted in a ‘wound bed’ is more if a
piece of skin graft with minimal dermal inclusion, i.e. a thin
partial thickness skin graft, is used. By inference, the presence
of dermal structure in the ‘wound bed’ could affect wound
contracture.
Free skin graft with prior incorporation
of a dermal regenerative template
For the past several years, artificial dermal substitutes that
have been manufactured from alloplastic or xenographic
materials, e.g. Alloderm™, Integra™, etc. (the manufacturing
account for the controversy. Splinting a joint imbedded in
burned scars with an external device to maintain a proper
joint angulation, on the other hand, was found to be effec­
tive in reducing the need for re-operation to achieve joint
function. However, this was possible only if the patient
would wear the splint faithfully for a minimal period of 6
months. A physical exercise regimen to provide vigorous
movements of a burned joint was found to be effective in
reducing the need for surgical intervention.
The 2-year ‘moratorium’ on early burn reconstruction, in
some ways, is justifiable. Operating on an ‘immature’ scar
characterized by redness and induration is technically more
cumbersome; hemostatic control of the wound is difficult
and inelasticity and lack of tensile strength noted in scar
tissues render tissue manipulation more difficult. A high rate
of contracture noted in instances where a partial-thickness
skin graft is used for releasing a wound showing active
inflammatory processes may further support the advocacy of
two years of delay in initiating burn reconstruction.9
Our recent change in handling individuals who were in
need of reconstruction followed the finding that contracted
bodily parts can be effectively reconstructed in the first 2
years post-burn if skin flap, fasciocutaneous flap or muscu­
locutaneous flap techniques are used. Reconstruction is initi­
ated in individuals as early as 3–6 months following the
initial injury. The approach is well-suited for those encoun­
tering functional difficulties because of scarring and scar
contracture.10
The techniques of reconstruction
There are several techniques routinely used to reconstruct
bodily deformities common to burn injuries, i.e. unsightly
scar, scar contracture, and joint contracture. Principally, they
are: (1) excision of scars with primary closure technique; (2)
wound closure following scar excision with a piece of free
skin grafting technique with or without the use of dermal
template; (3) an adjacent skin flap technique; (4) an adja­
cent fasciocutaneous (FC) flap technique; (5) an adjacent
musculocutaneous (MC) flap technique, and (6) a distant
skin, fasciocutaneous (FC) flap, or musculocutaneous (MC)
flap via microsurgical technique.
Primary wound closure technique
Excision of an unsightly scar with layered closure of the
resultant wound is the simplest and the most direct approach
in burn reconstruction. The technique is also useful in
handling scars that are hyperesthenic and pruritic.
The margins of scar requiring excision are marked. It is
important to determine the amount of scar tissue that can
be removed, yet the resultant defect could be closed directly.
‘Pinching’ the edge of scar at three or four different sites
along the length of scar to determine the mobility of the
wound edges is the simplest yet most reliable method to
determine the amount of scar tissues that can be removed
safely. Leaving a rim of scar tissue is generally necessary
unless the size of scar is so small that removal and direct
closure of the resultant wound would not lead to contour
deformity. A circumferential incision is made in the line
marked and is carried through the full thickness of the scar
down to the subcutaneous fatty layer. While the outer layer
of the scarred tissue is excised, 4–5 mm of collagen layer is

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an open wound has been found to form a layer of
parenchymal structures resembling a dermis rendering
wound coverage with an autologous skin graft where an
immediate closure is not possible. The need for a staged
approach to graft a wound, however, is considered cumber­
some (Fig. 50.7).
Skin flap technique
The approach of using a segment of skin with its intrinsic
structural components attached to restore a destroyed and/
or absent bodily part follows the fundamental principle of
reconstructive surgery. The technique, however, will not only
cause skin scarring in the flap donor site but also a donor
site contour alteration that may be considered cosmetically
unsightly. Loss of a skin flap, more commonly encountered
in burn patients when the altered vascular supplies to the
skin are altered by injuries and surgical treatment, could
render this technique unsuitable, if not even undesirable.
Despite the drawbacks, the approach to restoring a damaged
bodily part with a piece of analogous-tissue is technically
sound and the procedure will provide an outcome to restore
bodily function and contour. The recent technical innova­
tion of incorporating a muscle and/or fascial layer in skin
flap design, especially in burned areas further expanded the
scope of burn reconstruction as more burned tissues could
be used for flap fabrication.
process was initially described by Yannis and Burke in
1980), are biosynthetic two-layered membranes composed
of a three dimensional porous matrix of fibers and of
cross-linked
bovine
tendon
and
glycosaminoglycan
(chondroitin-6-sulfate). The material when implanted over
Figure 50.6  A partial thickness skin graft was used to cover an open
wound resulted from releasing of a contracted lower lip.
Figure 50.5  (a) The scar formed in the left submental area was pruritic and unsightly. The extent of the excision was marked and the area was infiltrated
with 0.25% lidocaine containing 1 : 400 000 epinephrine to achieve hemostasis. (b) The epidermal layer was sharply excised leaving the dermal layer intact.
(c) The wound edges were closed primarily in layers using nylon sutures. (d) The extent and appearance of scarring noted before excision, 10 months
following the initial burns. (e) The appearance of the operative site five years following partial scar removal.
A
B
C
D
E

Reconstruction of burn deformities: an overview
575
Figure 50.7  (a) A 6-year-old girl bothered by recurrent infection caused by scar-imbedded inclusion cysts in the left flank area extending from the lower
axilla to the upper trochanteric region. (b) A piece of Integra™ was used to cover a wound of 25–30 cm × 10–15 cm. (c) The vascularized Integra™-covered
wound was covered with a partial thickness skin graft of 8/1000th of an inch in thickness 3 weeks later. (d) The appearance of the grafted area a year
following the operation. The scar was noted to be soft and pliable.
A
B
C
D
Figure 50.8  (a) A triangular skin mark made over the right nasolabial area to mark an axial skin flap fabricated for left lower eyelid ectropion reconstruction.
(b) The size of skin flap was equal to the size of the lower eyelid defect to cover an open wound that had a cartilage graft for tarsal replacement. (c) The
triangular flap was rotated cephalad and laterally to fill the left lower eyelid tissue defect. (d) The left lower eyelid ectropion consequential to the loss of
eyelid skin and the tarsus. (e) Appearance of the left lower eyelid 3 years following the reconstructive procedures.
A
B
C
D
E
The axial skin flap
The skin in many areas is nourished directly by known cuta­
neous arteries. A skin flap, regardless of its length-to-width
ratio requisite, may be fabricated if the vascular trees are
included in the flap pattern (Fig. 50.8).
The z-plasty technique
This technique, in short, is based upon the principle of
mobilizing a full segment of skin, with its vascular supplies
undisturbed, from an area adjacent to the site needing tissue
replacement. This is conventionally achieved by interposing
two skin flaps of an equilateral triangle, i.e. 60° that has a
common limb drawn along the scarred area. A scarred and
contracted area is released as the flaps are interposed in an
opposite direction. Any space defect due to skin and underly­
ing tissue movement is made up by mobilizing tissues from
an adjacent area (Fig. 50.9).
The modified z-plasty technique; alias 3 4 z-plasty technique
Two flaps are used, as in the conventional z-plasty tech­
nique, of a right angled triangle, i.e. one internal 90° angle
and the other with a ‘modified’ 45° angle; the angle for the
triangular flap has decreased from a conventional 60° to
45°, hence the 3 4 z-plasty technique. The limb of the 90°
triangle is made in the scarred area resulting from the tissue
loss. The second limb of the triangle is made perpendicular
to the first one. The angle formed by the second limb of
the right-angled triangle and the hypotenuse of the second
right-angled triangle is 45°. A triangular skin flap fabricated
in this manner is rotated to fill a tissue defect formed from
surgical releasing of the contracted scarred area. The proce­
dure, in this sense, is a variant of the conventional rotational/
interpositional skin flap technique by rotating the 45°
triangular skin flap singularly to make up the defect
(Fig. 50.10).
Despite its geometric advantage in flap design, fabricating
a skin flap or skin flaps for z-plastic reconstruction of burn
deformities is not infrequently plagued with skin necrosis.
Aberrant vascular supplies to the skin attributable to the
original injury and/or surgical treatment could be the factor
responsible for the problems. The use in recent years of a
skin flap designed to include muscle or fascia, has further
expanded the usefulness of conventional z-plasty and 34
z-plasty techniques in burn reconstruction.

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Figure 50.9  (a) Neck scar. (b) Two equilateral triangles were marked into a ‘z’ and incisions were made to free up two triangle skin flaps. (c) Two flaps were
interposed to achieve the release. (d) Before release, the patient, a 13-year-old boy, complained of tightness over the neck area caused by a tight scar band.
(e) The appearance of the neck 4 years following releasing procedures. The z-plasty procedure alleviated the neck tightness.
A
B
C
D
E
Figure 50.10  (a) A horizontal line was drawn along the site of tightness. A triangular skin marking was also drawn with its cathetus perpendicular to the line
of release. (b) The triangular flap was rotated cephalad and medialward to make up the wound defect resulted from release. (c) The flap donor site closure as
well as the inset of flap was achieved primarily.
A
B
C

Reconstruction of burn deformities: an overview
577
Musculocutaneous (MC) or fasciocutaneous
(FC) flap technique
Inclusion of not only the skin but also the subcutaneous
tissues and the fascia and the muscle is necessary to fabricate
a skin flap to reconstruct tissue defect in individuals with
deep burn injuries. That is, fabricating a flap in a burned area
is possible if the underlying muscle or the fascia is included
in the design.
Musculocutaneous z-plasty technique
While the skin pattern is identical to the conventional
z-plasty technique, the muscle underneath must be included
in the flap fabrication. Although physical characteristics of
Figure 50.11  (a) Two equilateral triangles were marked into a ‘z’. (b) Incisions were made to free up two triangle skin flaps that included the platysmal
musculatures underneath. (c) Two flaps were interposed to achieve the release. (d) Before release, the patient, a 9-year-old boy, complained of tightness over the
neck area caused by a tight scar band. (e) The appearance of neck 4 years following releasing procedures. The z-plasty procedure alleviated the neck tightness.
A
B
C
E
D
normal skin, i.e. the skin pliability and expandability, are
absent if scarred skin is included in the flap design, a ‘scarred-
skin’ MC or FC flap could be safely elevated and transferred
to close an open wound. In practice, the MC z-plasty
technique is useful in neck release and in the eyelid because
of the character of underlying muscle; i.e. the platysma and
orbicularis oculi muscles are thin, pliable and easily movable
(Fig. 50.11).
Fasciocutaneous z-plasty technique
This is a technical modification of the MC z-plasty tech­
nique, by including the muscular fascia only. Separation of
skin and its subcutaneous tissues from the underlying fascia

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Tissue expansion technique
An extreme stretching of the integument is quite commonly
observed in human bodies. The tissue expansion technique
follows the same principle, except it is carried out intention­
ally with an inflatable device, i.e. a tissue expander. Because
of excessively active scarring processes more frequently
observed in burn victims, especially during the period soon
following the accident, timing to initiate the procedure
could be difficult. Use may be limited because of pain and
discomfort associated with expansion (Fig. 50.14).
Free composite tissue transfer via
microsurgical technique
With the advent of microsurgical technique, transplanting a
composite tissue can be carried out with minimal morbidi­
ties. Opportunities for this regimen, however, may be limited
in burn care because of a paucity of donor materials. It is
ironic that burn patients with suitable donor sites seldom
require such elaborate treatment. Those who are in need
of microsurgical tissue transplantation are inevitably those
with no appropriate donor sites because of extensive tissue
destruction.
must be avoided in order not to impair the blood supply to
the flap. In practice, the technique is useful in reconstructing
contractural deformities around the knee and ankle areas.
3 4 Fasciocutaneous z-plasty technique
A 45° triangular FC flap that includes the fascial layer may
be fabricated anywhere in the body. The flap is elevated and
then turned 90° to cover a tissue defect resulting from releas­
ing a contracted wound. Although an unburned skin when
used to fabricate a triangular flap is more versatile, a scarred
skin with or without subcutaneous tissues may be used also
for flap fabrication. Suturing the fascia to the skin edge is a
useful maneuver to avoid accidental separation of the fascia
from the overlying skin, and impairing the vascular supplies
to the dermal structures (Fig. 50.12).
Paratenon cutaneous z-plasty and 3 4 paratenon cutaneous
z-plasty techniques
In instances where fabrication of a composite skin flap is
indicated in the distal section of the upper and lower extrem­
ities, i.e. wrist and ankle, the paratenon, a fascial extension
of the voluntary musculatures, should be included in the flap
design and fabrication (Fig. 50.13).
Figure 50.12  (a) A triangle skin marking was made with its cathetus drawn along the line of contracture and perpendicular to the inferior wound edge
resulting from the release. (b) Incisions were made along the skin marking for flap fabrication. (c) The triangle skin flap was elevated to include the fascial
layer to form a random fasciocutaneous flap. (d) The appearance of flap and the wound 10 days following the release and flap reconstruction.
A
B
C
D
Figure 50.13  (a) Two equilateral triangles were marked over the left heel cord, the area felt to be tight. (b) The skin flap was fabricated to include the fascial
layer underneath. (c) Two FC flaps were interposed to achieve the release. (d) The inset of two flaps completed. (e) The appearance of left heel cord before
release. (f) The appearance of left heel cord 4 years following release.
A
B
C
D
E
F

Reconstruction of burn deformities: an overview
579
Figure 50.14  (a) The patient was a 4-year-old with scalp alopecia resulting from extensive burns involving the scalp and the face area. (b) No attempt was
made to reconstruct the scalp alopecia until she was 8 years of age. The tissue expander technique was used to expand the left side of scalp for wound
coverage. (c) The appearance of right temporal scalp following two scalp expansion-advancement procedures.
A
B
C
Comments
The regimen of burn treatment has changed drastically over
the past 50 years. The central focus of burn treatment was
moved from understanding the pathophysiology of burn
injuries and mastering patient resuscitation in the 1950s, to
learning how to cover a burn wound in the 1960s, even
though the principle of early debridement of burn wound
was clear to the physicians. Reconstructive efforts offered
to those who had survived the trauma were mostly
limited to restoration of lost physical functions. Cosmetic
recons­truction was simply seldom offered. The treatment
outcome, however, was in most instances suboptimal
because of excessive scarring and scar contracture, two con­
sequences which continue to limit the outcome of burn
reconstruction.
A more aggressive approach in managing burned wounds
came in the 1980s. Various pharmacological agents have
been used to control aberrant metabolic processes induced
by the trauma to control infectious consequences and safer
anesthetic agents have contributed substantially to the sur­
vival of burn victims. The regimen of an early debridement
and wound coverage initially with biological dressing and
later with autologous skin grafts, had further enhanced the
survival rate. It is, however, ironic that this improved survival
has caused an upsurge of patients in need of reconstruction.
That is to say that everyone who had survived burns would
be in need of reconstruction, functional or otherwise.
Unsightly hypertrophic scar, scar contracture affecting
particularly the joint structures, and destroyed body parts
are still the most common sequelae of burn injuries today.
Although the use of skin grafting and skin flaps have
remained the mainstay of burn reconstruction, the outcome
can still be suboptimal because of techniques that cannot
meet the therapeutic objectives to correct the three problems
listed.
The exact timing to initiate reconstruction of burn deform­
ities remains unsettled. Difficulty in obtaining suitable
tissues for replacement, morbidities associated with surgical
procedures that involve scar tissues that are active, and out­
comes that cannot be assured, could account for the contro­
versy. The predicament, on the other hand, could be due
to the techniques used. The use of flap techniques,
particularly the use of techniques such as 34 fasciocutaneous
z-plasty and/or 34 paratenon cutaneous z-plasty, enable us
to reconstruct contractural deformities that involve the major
joints as well as eyelid deformities as early as 4–6 months
following the injuries.
Questions concerning the ideal approach in managing
burn deformities remain unanswered. Although surgery has
been the mainstay of reconstructive approach for the past
half century, these problems perhaps, should be handled
completely non-surgically or with limited use of surgical
means. That is, reducing the inflammatory phase following
injury and controlling the level of various fibrogenic
cytokines could be useful in forming scar tissues considered
to be physiomechanically, sound yet cosmetically pleasant.
The science of tissue engineering could lead to the formation
of bodily parts that could be used to replace absent or
destroyed body components.
Summary
Reconstruction of bodily deformities due to burns is diffi­
cult, if not impossible. The difficulty is largely due to the lack

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Further reading
Brou J, Robson MC, McCauley RL. Inventory of potential
reconstructive needs in patients with burns. J Burn Care Rehabil.
1989;10:556-560.
Celis MM, Suman OE, Huang T, et al. Effect of a supervised exercise
and physiotherapy program on surgical intervention in children
with thermal injury. J Burn Care Rehabil. 2003;24:57.
Huang T, Larson DL, Lewis SR. Burned hands. Plast Reconstr Surg.
1975;56:21.
Larson DL, Abston S, Willis B, et al. Contracture and scar formation
in burn patients. Clin Plast Surg. 1974;1:653.
Robson MC, Barnett RA, Leitch IOW, et al. Prevention and treatment
of postburn scars and contracture. World J Surg. 1992;16:87-96.
of understanding of the pathomechanism of wound healing
and scar tissue formation. Furthermore, technical limitations
to replacing bodily parts further fuels the psychological frus­
trations for reconstructive surgeons.
The use of a musculocutaneous flap and/or fasciocutan­
eous flap, particularly as modified to follow the principles
of z-plasty or 34 z-plasty, has been found to be effective in
restoring functions lost because of scarring and scar contrac­
ture. Furthermore, it is conceivable that refinement in micro­
surgical tissue transfer techniques in conjunction with
advances that will be made in tissue engineering/body parts
formation, would render the task of reconstructing burn
deformities easy and simple.
 
Access the complete reference list online at

Reconstruction of burn deformities: an overview
580.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
References
1. Tomkins RG, Burke JF, Schoenfeld DA. Prompt eschar excision:
A treatment system contributing to reduced burn mortality.
Ann Surg. 1986;204:272-281.
2. Munster AM, Smith-Meek M, Sharkey P. The effect of early
surgical intervention in mortality and cost-effectiveness in burn
care. Burns. 1994;20:61-64.
3. Brigham PA, Mcloughlin E. Burn incidence and medical care in
the United States: estimates, trends, and date source. J Burn Care
Rehabil. 1996;17:95-107.
4. Larson DL, Abston S, Willis B, et al. Contracture and scar
formation in burn patients. Clin Plast Surg. 1974;1:653.
5. Scott PG, Ghahary A, Tredget EE. Molecular and cellular basis of
hypertrophic scarring. In: Herndon D, ed. Total burn care.
Philadelphia: WB Saunders; 2002.
6. Brou J, Robson MC, McCauley RL. Inventory of potential
reconstructive needs in patients with burns. J Burn Care Rehabil.
1989;10:556-560.
7. Huang T, Larson DL, Lewis SR. Burned hands. Plast Reconstr Surg.
1975;56:21.
8. Celis MM, Suman OE, Huang T, et al. Effect of a supervised
exercise and physiotherapy program on surgical intervention in
children with thermal injury. J Burn Care Rehabil. 2003;24:57.
9. Robson MC, Barnett RA, Leitch IOW, et al. Prevention and
treatment of postburn scars and contracture. World J Surg.
1992;16:87-96.
10. Huang T, Herndon D. The early burn reconstruction in burned
patients. Presented at the annual meeting, Texas Surgical Society,
San Antonio, Texas, April 1, 2005.

The use of skin grafts, skin flaps and
tissue expansion in burn deformity
reconstruction
Ted Huang, Manuel Dibildox
Introduction
Although the magnitude varies, scars formed around
injury sites and/or structural deformities are the common
sequelae of burn injuries. Secondary surgical treatment of
the consequences, whether it is for function or appearance
is usually necessary. Secondary reconstruction of bodily
deformities requires the use of autologous uninjured tissues
harvested as a free skin graft, a pedicled skin flap with or
without fascia and/or muscle layer attached, and a free com­
posite graft.
Skin grafts
The skin thickness varies depending upon the bodily loca­
tions; the eyelid skin, especially the upper eyelid, and the
skin located behind the ear is thin, while the scalp, trunk,
the palmar skin, and the sole of the foot are thick.1–3
A skin graft is classified into two types depending upon
the amount of skin structures included, i.e. a piece of skin
shaved to contain epidermis and various layers of dermis is
said to be a split- (partial-) thickness skin graft (STSG). The
graft can be harvested in different thicknesses; a thin graft is
6–8/1000th of an inch (0.15–0.20 mm) in thickness, while
a graft with a thickness of 16–18/1000th of an inch (0.40–
0.45 mm) is a thick split-thickness skin graft. A skin cut
to contain all components of the skin, i.e. epidermis and
dermis, is classified as a full-thickness skin graft (FTSG)
(Fig. 51.1).4,5
Skin flaps
A skin flap is a graft composed of all skin elements, i.e. epi­
dermis, dermis and subcutis that includes fatty tissues and
neurovascular structures. Depending upon the type, it may
include the fascial layer or the muscles underneath. The flaps
are classified into: (1) a random cutaneous flap; (2) an axial
(arterialized and/or neuroarterialized) skin flap; (3) a fascio­
cutaneous flap; (4) a musculocutaneous flap, and (5) a free
composite flap attached with neurovascular structures.
The techniques to fabricate various skin flaps
A random cutaneous flap
Design and fabrication of a random cutaneous flap could be
made anywhere in the body surface. The shape and the form
of a random skin flap can vary depending upon the treat­
ment plan; a flap is configured according to the outline of
the wound defect. A fabricated skin flap is advanced to com­
plete wound closure. The flap mobility, however, could be
restricted if the layer of underlying subcutaneous tissues is
thick or fibrous. The length and the width of a random cuta­
neous flap are determined according to the pattern of vascu­
lar supplies to the skin; the ratio of flap length and the width
is limited to 2 : 1. Necrosis of the skin at the end is common
for a long and narrow skin flap (Fig. 51.2).6–8
An axial or an arterialized skin flap
As shown, a nasolabial flap can be fabricated with a length
versus width ratio in excess of 2 : 1; this is a skin flap formed
along the side of nose. The Bakamjian flap, a deltopectoral
flap, basing its vascular supplies upon the branches of
intercostal vessels, has been used frequently to reconstruct
deformities that involve the lower face and the neck
(Fig. 51.2).9–12
Z-plasty
Surgical release of a tight band can be achieved by switching
right angularly two triangular skin flaps 60° with their
catheti formed in continuity along the axis of a tight scar, i.e.
the z-plasty technique.13–15 Although the technique is suited
for releasing a tight scar band across a joint surface, in prac­
tice a scarred area is seldom left with unburned skin on both
sides of a burn scar band. Consequently, the relief of contrac­
tion obtainable by means of classic z-plasty technique may
be limited.
Modified z-plasty alias 3 4 z-plasty
The flap configuration of z-plasty may be modified by chang­
ing the angle of two opposing triangles, i.e. from 60° to 90°
and 45°, respectively. The technique is also known as a
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00051-5
CHAPTER 51 
Access the complete reference list online at

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582
easily fabricated to make up an open wound that is long
(Fig. 51.4).
Flap techniques to reconstruct common
burn deformities
The eyelid deformities
Although the use of a skin graft has been advocated as the
method to reconstruct eyelid deformities, i.e. eyelid ectro­
pion and entropion, recurrence of contraction is quite
common. The use of a nasolabial skin flap is a preferred
technique to reconstruct ectropic or entropic deformities of
the lower eyelid. It provides the tissue bulk needed and the
means for a complex eyelid reconstruction that requires the
use of cartilage graft (Fig. 51.5).
rotational flap technique, a transpositional flap technique or
a banner flap technique, an asymmetrical z-plasty or a 34
z-plasty.
Switching or transferring the flaps, unlike a z-plasty tech­
nique, is limited to one, as the opposing 90° skin flap fab­
ricated by incising a contracted scar is unmovable. The
narrower flap is rotated 90° to make up an open wound
resulted from releasing maneuver (Fig. 51.3).
3 4 Fasciocutaneous z-plasty
The flap length versus width ratio of a random skin flap may
be increased from a standard 2 : 1 to 4 : 1 if not to 5 : 1, by
including the underlying fascial layer in the flap fabrication.
That is also to say that a long and narrow skin flap may be
Figure 51.1  (a.i) A piece of partial-thickness skin
graft, 14/1000th of an inch in thickness, with its
dermal layer shown. (a.ii) STSG with the epidermal
surface shown. (b.i) A segment of skin with its
subcutaneous tissues retained. (b.ii) A piece of
full-thickness skin graft (FTSG) is fabricated by
removing all the subdermal structures.
Ai
Aii
Bi
Bii

The use of skin grafts, skin flaps and tissue expansion in burn deformity reconstruction
583
Figure 51.2  (a) A segment of skin, oblong in shape, is dissected out in the area along the nasolabial
fold on the left. (b) The skin and its subcutaneous layer is separated at the level just above the muscle
to assure the inclusion of the vasculatures. (c) The flap with the skin left upon the subcutaneous
tissues, i.e. an island skin flap, is rotated laterally to cover an open wound located underneath the
ciliary border. (d) The wound edges are closed primarily.
A
B
C
D
Figure 51.3  (a–c) The technique of z-plasty may be modified by changing the flap angle from 60° to 90° for one and 30–45° for the other to achieve the
tight scar release.
A
B
C

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Figure 51.4  (a–c) The conventional technique of a modified z-plasty method of contractural release is modified by incorporating a segment of fascia
underneath to assure blood supplies.
A
B
C
Neck contracture
A 34 musculocutaneous (MC) z-plasty is a modified trans­
positional composite skin flap technique. A triangular skin
flap with its underlying musculature, i.e. platysma muscle
attached, is fabricated in the area adjacent to the opened
wound resulted from neck release. Cathetus of the triangular
skin flap is made perpendicular to the corner of the wound.
The flap, with its dimension fitting the wound defect, is
fabricated as an MC flap. The flap is rotated 90° to close the
wound defect (Fig. 51.6).
Axilla contracture
Although the exact reasons remain unclear, the axilla is the
joint among the large joints most commonly plagued with
contracture. Splinting has been advocated as the method to
manage the problem, but the efficacy of this treatment
modality remains undefined. Similarly, outcomes obtaina­
ble with the conventional approach of surgical release and
skin grafting are unpredictable.
A 34 fasciocutaneous (FC) z-plasty is a modified transpo­
sitional or interpositional composite skin flap technique.
The fascial layer is included in the flap fabrication. The flap
donor defect is closed primarily, or with the use of skin graft
(Fig. 51.7). Neither the use of splint nor physiotherapy are
prescribed following the surgery.
Elbow and wrist contracture
The indication and the technique are similar to the approach
used to attain release of axillary contracture. The patient is
encouraged to move the joints within 1–2 weeks following
the release.
Knee contracture
The contracture is noted to involve the popliteal area more
often than the patellar surface of the knee. As in other joints,
a modified transpositional skin flap technique is suited for
reconstructing the deformity. The technical details are similar
to those used in the axilla and elbow joint release.
Ankle contracture
Contractural deformities involving an ankle joint are quite
common among individuals sustaining extensive burn inju­
ries. Although reconstruction of ankle deformities is indi­
cated in instances where non-surgical maneuvers to control
the consequence are ineffective, closure of a surgical wound
in the ankle area can be difficult because of limited available
tissue suitable for wound repair. A composite skin flap that
includes the fascia/paratenon and the overlying skin struc­
tures fabricated from the area adjacent to the ankle, a 34 FC
z-plasty technique, has been used to cover the wound result­
ing from surgical release of the contraction (Fig. 51.8).
Splinting of the ankle by wearing a high-top shoe for a
period of 3–6 months following the procedure is strongly
recommended.
Tissue expansion
Bodily deformity reconstruction by means of a tissue
expander is based upon the principle of utilizing the excess
skin resulting from stretching of normal skin.16 A silicone
balloon is placed in a tissue pocket mostly above the muscle
layer, inflated to a designated volume via an injection port
placed in the adjacent area. An expanded skin is suited
for replacing a scarred skin as it retains the color and

The use of skin grafts, skin flaps and tissue expansion in burn deformity reconstruction
585
Figure 51.5  (a) Blepharophimosis resulted from the loss of the eyelids. (b–d) A nasolabial island skin flap was fabricated to reconstruct the lower eyelid
deformity. (e) The appearance of the left eyelid 4 years following reconstruction.
A
B
C
D
E

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Figure 51.6  (a–e) The muscle is incorporated in the fabrication of triangular
flaps used to release this neck contracture 6 months following the injury. The
muscle-skin flap donor site is closed primarily.
A
B
C
D
E

The use of skin grafts, skin flaps and tissue expansion in burn deformity reconstruction
587
A
B
C
D
Figure 51.7  (a–e) 34 MC z-plasty technique is utilized to achieve contractural release; contracture developed within 4–5 months following the injury.
(e) Denotes the appearance of leased right axilla 2 years later.
E
texture, and in some instances, the hair and sensation, of the
donor skin.
The use of a tissue expander in reconstructing
burn deformities
Indications for tissue expansion
The technique is considered useful for instances where a
deformity requires a large segment of uninjured skin to
restore structural deformities, provided that an ample
amount of unburned skin is available in the locale adjacent
to a proposed flap recipient site. The skin over the flap donor
site must be sufficiently pliable for expansion.
Contraindications for tissue expansion
Skin elasticity is often altered with burns because of scarring.
Loss of skin elasticity essentially renders the mechanical
stretching of scarred skin difficult, if not impossible. Although
the exact reasons remain unclear, scarred skin can be
broken easily with the force of traction resulting in wound

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Figure 51.8  (a–d) The 34 FC z-plasty technique is used to relieve tightness developed in the right
anterior ankle surface. (d) Denotes the appearance of the ankle area 3 years following the releasing
procedures. No recurrence of tightness was noted.
A
B
C
D
disruption and consequently, expander extrusion. The use of
the tissue expansion technique in an area with extensive
scarring is therefore, contraindicated, if not impractical.
Description of a tissue expander (TE)
placement technique
The subcutaneous layer is infiltrated with local anesthetics,
i.e. 0.25% lidocaine containing epinephrine in 1 : 400 000
concentration is used. A subcutaneous tissue pocket is surgi­
cally created with a size that will house an implant. Instilled
into the lumen is 30–40 cc of physiologic saline solution to
stretch out the implant. A second subcutaneous tissue pocket
is located adjacent to the incision site to house the accom­
panying injection port.
After care of TE
Balloon expansion should be delayed for 3–4 weeks. Once
the healing processes are complete, 30–45 cc of physiologic
saline solution is injected into the expander via an injection
port. The injection is repeated at a rate of once or twice a
week until the desired extent of skin stretching is attained.
TE in clinical use
The use of TE in scalp alopecia reconstruction
The method of scalp alopecia reconstruction centers upon
the principle of replacing scalp alopecic tissues; a hair-
bearing scalp flap mobilized from the area adjacent is
advanced directly or with rotation of the flap. It is important
to assess the density of hair follicles in the scalp planned
for expansion. The hair density may decrease with scalp
stretching and aesthetic appearance of a reconstructed scalp
deformity may be suboptimal.
The outcome of scalp alopecia reconstruction can be sat­
isfactory for a defect that is less than one-third of the total
scalp area. An acceptable outcome is attainable with two or
three procedures. In contrast, the outcome is judged to be