This article was published in an Elsevier journal.

The attached copy

is furnished to the author for non-commercial research and
education use, including for instruction at the authors institution,
sharing with colleagues and providing to institution administration.
Other uses, including reproduction and distribution, or selling or
licensing copies, or posting to personal, institutional or third party
websites are prohibited.
In most cases authors are permitted to post their version of the
article (e.g. in Word or Tex form) to their personal website or
institutional repository. Authors requiring further information
regarding Elseviers archiving and manuscript policies are
encouraged to visit:

http://www.elsevier.com/copyright
 Author's personal copy

Phys Med Rehabil Clin N Am

18 (2007) 925948

Rehabilitation Methods for the Burn

Injured Individual
M. Catherine Spires, MD*,
Brian M. Kelly, DO, Percival H. Pangilinan, Jr, MD
Department of Physical Medicine and Rehabilitation, University of Michigan
Health System, 325 E. Eisenhower, Suite 100,
Ann Arbor, MI 48108, USA

Burn injury is not a new problem. Since ancient times, humans have
known the tragedy of severe burn injuries. Hippocrates described treatments
for burn injury in his early works [1]. During the rst century of Rome, Cor-
nelius Celsus described a technique for surgical excision of burn scar [2].
The economic and human cost of burn injuries is enormous. Excluding
the tragedy of September 11, 2001, on average more than 3900 persons
die from re each year. An additional 750 persons die from motor vehicle
and airplane crashes, contact with electricity, chemicals, or other causes of
burn. In 2005, more individuals died secondary to re than all natural disas-
ters combined. The direct cost of burn injuries is staggering, exceeding more
than $10 billion in the year 2005 alone [3]. Residential res account for most
burn injuries. Cooking res account for 47% of residential res, and heating
res account for 19% [3,4]. The incidence of res involving persons over age
65 is increasing as the population of the United States ages [4].
Age impacts survival, with mortality highest in very young and very old
persons. Thirty-ve percent of burn injuries occur in children. Burns are also
the primary cause of accidental death in children younger than age 2 and the
second cause of death for children younger than age 4. The most common
type of childhood burn is a scald injury, which accounts for 72% of pediat-
ric burns [5]. Most (85%) pediatric burns occur in residential settings.
Nationally, approximately 20% of pediatric burn injures are nonaccidental
burns and result from abuse or neglect. It is critical for clinicians to dier-
entiate between burn injuries caused by child abuse and those caused by ac-
cidental injuries [6].

* Corresponding author.
E-mail address: mcspires@umich.edu (M.C. Spires).

1047-9651/07/$ - see front matter 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.pmr.2007.07.002 pmr.theclinics.com
 Author's personal copy

926 SPIRES et al

Approximately 50,000 persons (4%) who sustain a burn injury each year
require hospitalization, and approximately 95% survive a burn injury [7]. In
individuals who have equivalent sizes of burn, the presence of an inhalation
injury reduces survival rate 30% to 50% [6,8]. Most victims of re die of in-
halation injury, not burns [9].

The integument
As the largest organ of the body, the skin provides a mechanical barrier
that protects internal organs. The skin also provides an immunologic
defense, supports uid homeostasis, and assists with thermoregulation.
Skin is a complex organ composed of two major layersdthe epidermis and
dermisdand a network of collagen, elastic bers, blood vessels, and nerve
endings. The biomechanical properties of skin allow for normal body mo-
tion. Skin demonstrates a complex response to mechanical loading. It elon-
gates with low loads; however, once the limit of extensibility is reached, the
tissue tears. This limit is called the yield point. The skin also demonstrates
preconditioning. After several repetitive applications of a low load, it demon-
strates a variable relationship between stress and strain. After several repeti-
tions, the stress-strain relationship stabilizes, which means that the initial
rapid elongation with stretch slows and the tissues become stier.

Medical care
Burn injury causes necrosis and damage of tissue secondary to exposure to
an external agent. It can result from thermal, electrical, frostbite, chemical, or
radiation exposure. Response to injury involves a series of complex physiologic
events. In addition to local tissue responses, systemic responses involve the car-
diovascular, pulmonary, metabolic, endocrinologic, and immunologic systems.
Most burn injuries (O90%) are thermal in nature [5]; the rest are secondary
to other causes, including chemical, electrical, and radiation burns. In addi-
tion to managing the airway, breathing, and circulation, initial management
includes removing the source of the burn injury and determining causes, the
size/extent, and the body location of the injury. Thermal injury ceases once
the source is removed, but chemical reactions continue until the oending
agent is neutralized or the chemical reaction with the tissues is complete.
The presence of an inhalation injury or other coexisting injuries must be deter-
mined because these comorbidities impact medical and surgical management.
Serious burns require care by burn care specialists at a burn center that
has multispecialty and multidisciplinary sta who are experienced in manag-
ing burn injuries. The criteria established by the American Burn Association
for transfer of patients who have burn injuries to a burn center include
burns that cover more than 10% of the total body surface area (TBSA),
electrical injuries, chemical burns, and injuries to specialized body regions,
such as the face and genitalia.
 Author's personal copy

BURN REHABILITATION 927

Classication of burns
The severity of a burn is determined by the age of the injured individual,
the extent and depth of burn injury, and the presence or absence of associ-
ated injuries.

Burn depth
The extent to which the epidermis and dermis are injured determines the
depth of injury. Describing a burn injury as supercial or partial or full
thickness is increasingly preferred over the traditional classication of
rst-, second-, third-, and fourth-degree burns. Partial- and full-thickness
burns impact uid homeostasis, thermoregulation, and the bodys defense
against infection. Loss of tissue integrity and disruption of normal microcir-
culation allow uid loss and microbial invasion.
First-degree burn or supercial burn is limited to the epidermis. The skin
is erythematous and tender. No blistering occurs. These injuries heal within
a few days and are not associated with scarring. The damaged epithelium
usually exfoliates in 5 to 10 days. Second-degree burns can be classied as
supercial, partial-thickness, or deep partial-thickness injuries. These in-
juries involve the entire epidermis and varying depth of injury to dermis. Su-
percial partial-thickness burns are limited to the upper third of the dermis.
Microvascular damage and increased capillary permeability occur, causing
blistering. These wounds are painful because sensory nerve endings are ex-
posed. They typically heal in 7 to 14 days.
In deep partial-thickness burns, the epidermis and dermis are injured and
only the skin appendages, such as sebaceous gland and hair follicles, are
spared. The wound is red and blanches with pressure. Typically these
wounds are less painful because most nerve endings are destroyed. A mar-
ginal residual blood supply exists. A few epithelial cells survive in the hair
follicles and other skin appendages. Repopulation by epithelial cells is
slow. Regeneration with eventual wound closure can take weeks and months
depending on the wound size. Wounds that heal in this manner demonstrate
a poor cosmetic and functional outcome. Skin grafts are used to expedite
wound closure and healing. Early closure prevents complications such as
infection and leads to better cosmetic and functional outcomes [10].
In full-thickness burns, the entire dermis and epidermis are lost. The
wound bed is avascular, the texture is dry and leathery, and the wound is
insensitive to pain. These burns have a white, brown, or tan waxy appear-
ance and may appear charred. The skin does not blanch or rell because
the blood vessels are thrombosed or destroyed (Figs. 1 and 2). Distinguish-
ing a full-thickness burn from a deep partial-thickness injury is often
dicult, particularly during the rst 3 to 5 days. When the depth of the
wound is in question, the wound is treated as a full-thickness injury. Infec-
tion or inadequate circulation can convert a partial-thickness injury to
a full-thickness wound. Re-epithelialization does not occur because no
 Author's personal copy

928 SPIRES et al

Fig. 1. Burn injuries typically are a mix of partial- and full-thickness injury. This gure is an
example of the typical mix of deep partial-thickness and full-thickness burns of the chest and arm.

epithelial cells remain. These wounds require skin grafting unless the wound
is small. Thick, dense scarring results. Fourth-degree burns extend to deep
structures such as muscle, tendon, and bone. This type of burn is a severe
injury that may require amputation or extensive deep debridement.

Extent of the burn injury

The extent of the injury is determined by the TBSA involved. The Rule of
Nines is a commonly used as an estimate of injury in adults (Box 1) [11]. The
surface area of the palm of the hand is approximately 1% of the patients
body surface area and can be used as a quick estimate.
For children, the Rule of Nines is not an accurate measure because
a childs body proportions are not the same as an adults. For instance,
a childs head is proportionately larger than an adults and an infants
legs are proportionately smaller (approximately 13%). The Lund and Brow-
der chart is more accurate and provides some correction for developmental
dierences (Fig. 3) [12]. When calculating the TBSA of a burn injury, only
partial- and full-thickness areas of injury are included. Supercial wounds
are not calculated in TBSA percent determination.
 Author's personal copy

BURN REHABILITATION 929

Fig. 2. Typical pattern of a scald burn. Note the uneven depth and irregularity of the burn.

Medical and surgical care

The long-term goal of burn wound care is to restore skin integrity, func-
tion, and appearance. Immediate goals are to prevent infection, decrease
pain, prepare wounds for grafting if needed, prevent contracture, prevent
and suppress scarring, while maintaining strength and function.

Burn wound care

Wound debridement, the process of removing devitalized tissue and creat-
ing a viable base for wound healing and grafting, is typically required. Eschar
is a coagulum of necrotic tissue composed of denatured collagen, elastin, and
protein. Eschar and devitalized tissue are excellent media for bacterial growth
and must be removed. There are several techniques of debridement. Mechan-
ical debridement includes such things as wet-to-dry dressing and

Box 1. Rule of Nines

Head and neck, 9%
Each upper extremity, 9%
Each lower extremity, 18%
Anterior trunk, 18%
Posterior trunk, 18%
Perineum, 1%
 Author's personal copy

930 SPIRES et al

Fig. 3. (A) Rule of Nines. (B) Lund-Browder chart for children. (From The Merck manual
of medical informationsecond home edition. In: Beers MH, editor. Whitehouse Station (NJ):
Merck & Co., Inc. Copyright 2003 by Merck & Co., Inc. p. 1651. Available at: http://www.
merck.com/mmhe/sec24/ch289/ch289a.html?qtburn%20victim&altsh#sec24-ch289-ch289a-7.
Accessed September 4, 2007; with permission.)

hydrotherapy via water immersion or spraying. Enzymatic debridement uses

commercially available topical enzymes, such as sutilains, to induce proteoly-
sis, brinolysis, and collagenolysis. These agents may result in local pain and
cellulitis in some individuals. Their use is limited to small areas requiring de-
bridement. Surgical debridement procedures include sequential and fascial de-
bridement. Sequential or tangential wound debridement removes thin slices of
tissue until a viable tissue bed is identied. Fascial debridement involves sur-
gical removal of tissue down to fascia. Although a viable wound is virtually
ensured, a signicant soft tissue defect occurs.
Deep skin burns are inelastic. In the case of a circumferential wound of
the leg, the burned skin does not expand to allow for increasing edema.
In circumferential burns, a tourniquet-like phenomenon can occur and
create a tissue compartment with pressure that reaches 40 mm Hg or higher.
In this situation, surgical decompression of these compartments must be
urgently done or necrosis of the underlying tissues occurs. Escharotomy is
a surgical intervention performed to relieve the tourniquet eect of devital-
ized nonextensible burn tissue. This procedure is critical to limb salvage in
full-thickness circumferential injuries of the arms or legs. Incisions are
 Author's personal copy

BURN REHABILITATION 931

made medially and laterally throughout the length of the extremity involved.
It is performed with the arms supinated (Fig. 4). If this procedure is not suc-
cessful, fasciotomy is performed.

Wound dressings and skin grafts

Biologic dressings are biologic tissues used for wound closure. These
dressings provide for early wound coverage, reduce pain, decrease infection,
and limit evaporative uid loss. Cadaveric tissue and human fetal mem-
branes are termed homografts. Porcine grafts, which are heterografts or
xenografts, are also used. In addition to the goals mentioned, these tempo-
rary grafts are used as test grafts to determine if a wound will accept an
autograft. Often a patients immune system rejects these grafts. Typically
these grafts are changed after several days. Synthetic wound dressings
include polyvinylchloride and polyurethanes and other plastic membranes
that are water and gas permeable. These temporary dressings are used until
the wound has healed or autografting is possible. Bilaminate analogs, com-
posed of thin sheets of silastic and epidermal/dermal analogs, are available.
Biobrane and Integra are probably the two most commonly used analogs.
Autografting is the surgical transfer of skin from one body site of the patient
to another. Autografts are applied once the wound bed is free of devitalized
tissue and is not infected. A wound biopsy with a bacterial count of less than
106 is needed for the wound to accept a skin graft [13].
Split-thickness grafts, which are grafts of partial-thickness skin, are
applied in sheets or meshed. Meshed autografts undergo a process of creat-
ing small, staggered parallel slits in the sheet of skin. Meshing expands the
size of the graft from 1.5 times its original area to several times its normal
surface area. One disadvantage is that the greater the degree the graft is
meshed and expanded, the poorer the cosmetic outcome. The epithelializa-
tion of the interstices creates a mesh pattern that persists after the wound is
healed. Sheet grafts are more cosmetic because no interstices are cut into the

Fig. 4. Example of an escharotomy performed to improve chest expansion.

 Author's personal copy

932 SPIRES et al

graft. Sheet grafts are typically used for cosmetically important areas, such
as the face and hands. Full-thickness skin grafts are used for small areas or
critical areas, such as the palms of the hands, and are used in reconstructive
procedures. These grafts, as the term implies, involve removing the entire
skin thickness from one area and moving it to another [14]. Cultured epider-
mal autographs are sheets of cultured keratinocytes that show some promise
but are currently under development and are not commonly used [14].

Rehabilitation
The ultimate goal of rehabilitation after a burn injury is to assist an
individual in achieving optimal function and independence. This is a multi-
stage process that requires monthsdeven yearsdof treatment and patient
commitment. The goals of the acute period of burn rehabilitation are to pro-
mote wound healing and scar suppression, reduce pain, and prevent compli-
cations. Patient goals are individualized by burn location, depth of injury,
percent of body surface injured, associated injuries and complications. An
individuals age, previous functional level, and health also play a signicant
role in determining a rehabilitation plan.

Joint care and protection

Proper positioning of the body is fundamental to preventing the develop-
ment of contractures. This also prevents compression neuropathies and de-
cubitus ulcers. The primary underlying principle of positioning is to keep
tissues in an elongated state, which can be dicult because an injured indi-
vidual typically assumes a position of comfort (ie, exion and adduction).
Extension and abduction are usually the most appropriate positions, but
positioning must be individualized in accord with each persons specic
injuries. Joints with deep partial-thickness or full-thickness burns overlying
them are at high risk for developing contracture and must be kept in an
elongated state (Fig. 5).
Splints are used to prevent joint contractures, maintain proper position-
ing, protect skin grafts, and prevent or assist motion. Splints should be user
friendly for the patient, nursing sta, and other caregivers. Poorly applied
splints can cause nerve injury, loss of skin grafts, and worsening of a burn
wound and cause new wounds. An eective splint avoids pressure over
bony prominences and is compatible with wound dressings and topical med-
ications. Splints fabricated of re-moldable materials can be modied as a pa-
tients needs change. Factors to consider when prescribing a splint include
the area of the body injured, extent and type of injury, the functional
goal, and the ability of the patient to participate.
If normal range of motion (ROM) of a joint is maintained, a splint is
typically not indicated. Exposed tendons require splinting in a slack
 Author's personal copy

BURN REHABILITATION 933

Fig. 5. Anticontracture position of burn patient. (From Helm PA, Kevorkian CG, Lushbaugh M,
et al. Burn injury: rehabilitation management in 1982. Arch Phys Med Rehabil 1982;63:8;
with permission.)

position. If a joint is exposed, a splint is indicated to provide protection.

Joints that have not sustained an overlying or direct injury typically do
not require splinting. Splinting or a positioning device may be needed in
some additional situations, such as preventing ankle contractures during
prolonged bed rest. During the acute period, many types of splints can be
prescribed. Upper and lower extremity splints include knee extension splints
to prevent knee exion contracture and posterior foot drop splints to main-
tain neutral ankle dorsiexion. In the case of axillary burns, a splint that
holds the upper extremity at 90 abduction to the side, often called an air-
plane splint, is used to prevent shoulder adduction contracture. Custom
splints can be designed for virtually all parts of the body. Commercially
available designs, which may reduce costs, are also available but often
need modications to t appropriately.

Exercise
Establishing a therapeutic exercise plan requires an understanding of the
location, depth, and TBSA of an individuals burn injury. Pre-existing med-
ical problems, such as coronary artery disease, impact the exercise prescrip-
tion for an individual patient. The strength and endurance of burn patients
also are compromised because of bed rest. Loss of strength in an inactive
muscle is approximately 3% per day and 22% by 1 week [15,16]. The
 Author's personal copy

934 SPIRES et al

goal of exercise is to maintain normal ROM, strength, and endurance. If

a patient is alert and able to participate, a program of active and active-
assisted exercise is appropriate. For obtunded or critically ill patients, passive
ROM exercises that emphasize the end of ROM are prescribed. In the event
that full ROM is not maintained, a program of stretching is prescribed.
ROM can be performed with a patient under anesthesia. It is often
a good choice for pediatric cases and for patients who cannot tolerate the
pain of ROM. Anesthesia allows accurate determination of ROM without
inducing pain. Eective stretching requires a slow sustained stretch. Stretch-
ing skin is not equivalent to stretching muscle, in which active contraction
and relaxation of the tissue is under patient control. Skin, a tissue without
active contractile elements, requires sustained mechanical stretch to facili-
tate alignment lengthening of the underlying collagen and other bers.
Skin demonstrates preconditioning, that is, initially it shows increasing
elongation at repetitive low loads but then the change in length plateaus.
Once this stage of preconditioning is reached, a prolonged stretch is applied
to maximize the stretch. In short, the joint is repeatedly moved slowly to its
end range several times before applying a prolonged stretch. When pro-
longed stretch is performed, the stretch is maintained until the tissue
blanches. Blanching is a clinical sign that capillary blood ow is impeded
and the tissues yield point is approaching [17].
Strengthening exercise begins as soon as a patient can tolerate it.
Strengthening programs include a wide range of programs, including pro-
gressive resistive exercise. Fatigue and loss of endurance are major issues
as a patient recovers. It is important to include endurance training and mon-
itor cardiopulmonary response.
Immediately after autografting, active and passive exercises are not per-
formed on the limb. Depending on the type of graft, condition of the graft
wound, and the judgment of the surgeon, no exercise or ROM is performed
for approximately 3 days for mesh grafts and 5 days for sheet grafts. Splints
are used to protect the graft and maintain tissue length. Heterografts,
synthetic dressings, escharotomies, and surgical debridements are not con-
traindications to exercise.

Ambulation
Walking is an important activity. Ambulating patients have fewer lower
extremity contractures, endurance problems, and venous thromboses. Early
ambulation maintains independence, balance, lower extremity ROM, and
function and decreases the risk of deep venous thrombosis. Once a patients
condition allows, ambulation should begin. Although the expertise of a phys-
ical therapist may be needed initially for many patients to resume
ambulation, nurses and family can be taught to assist and encourage
patients to ambulate. Physical therapy sessions should not be the only time
a patient ambulates.
 Author's personal copy

BURN REHABILITATION 935

Autografts to the lower extremities are a contraindication to ambulating

until stable circulation to the graft sites is established. Typically, depending
on the surgeon and the condition of the graft, the patient may not be
permitted to put lower extremities in a dependent position for 5 to 7 days
after grafting. Once a patient is cleared by the surgeon to resume lower
extremity weight bearing, a program of dangling the lower extremities is
initiated as a preambulation exercise. Dangling also helps to determine if
the graft tolerates the dependent position. Elastic wraps or other forms of
compression are used to avoid venous pooling, which can lead to graft
sloughing. The graft is evaluated before and after dangling. Initially, the
limb is dangled for 5 minutes and the duration is progressively increased.
If the graft tolerates dependency, walking with ace wraps or other support
is begun. Ambulation time is increased daily if no untoward eects on the
graft occur. Gait deviations are common. There are multiple causes, includ-
ing abnormalities caused by the location of the injury, pain, focal or gener-
alized weakness, contractures, impaired sensation, and central nervous
system causes. Although some gait deviations resolve as wounds heal,
some persist if not addressed early.
Scoliosis and kyphosis may occur because of asymmetrical burn injuries
of the trunk, pelvis, and shoulder regions. This type of injury can result in
abnormal posture. Aggressive exercise and positioning are critical to prevent
these abnormalities, which is especially important during the growing years
of childhood. Gait devices are used to protect, reduce pain, or assist with
weight bearing of injured lower extremities. These devices also can prevent
or correct abnormal posture or gait caused by burns of the chest, back, or
other areas that cause the patient to stand or move abnormally.
Finally, during periods when a patient cannot ambulate, wheelchairs pro-
vide mobility and can be adapted to patients needs, including using elevating
leg rests and attaching splints and other position devices to the chair.

The hand
The hand is a highly specialized body part that not only allows ne and
gross motor function but also has great social importance in communication
and human interaction. Injuries to the hand require intense and specialized
attention. Hand splints are used to preserve function and prevent contrac-
ture. The resting hand splint positions the wrist in slight extension, 60 to
80 of metacarpophalangeal exion, full interphalangeal extension, and
thumb abduction. This position places the exors and extensor, tendons,
and ligaments under maximal stretch to avoid the soft tissue shortening
associated with contractures.
Hand edema leads to deformation, which makes edema control a major
priority. Edema is an interstitial protein-rich substance that forms a gel-like
consistency and impedes vascular clearance. Mechanical joint and soft tissue
motion is inhibited and contracture develops. Elevation of the hand and arm
 Author's personal copy

936 SPIRES et al

is accomplished using splints, casts, bedside troughs, or other devices used to

inhibit edema formation (Fig. 6). Web spacers can be placed between digits
to prevent uid collection and edema formation. Once the wounds of the
hand are closed, compression gloves are placed to control edema further.

Postacute rehabilitation
Once wound care is no longer the primary focus, the stage of intense re-
habilitation begins and is geared toward maximizing an individuals inde-
pendent functioning and optimizing quality of life.

Skin care
Damaged skin is sensitive to sun and chemicals. Once healed, the skin is
fragile and easily abraded. Patients should be taught to monitor skin for
breakdown or injury from splints pressure garments, clothing, and other ir-
ritants. Education also includes the use of sun blocking agents and appropri-
ate clothing to protect skin from sunburn or other injuries.
In the rst few months after injury, partial-thickness burns lack the natural
lubrication of sebaceous glands and the epidermal lipids. In full-thickness
burns, the skin appendages needed for lubrication are lost and do not regen-
erate. Consequently, areas of full-thickness burn lack natural lubricants.
Moisturizers such as cocoa butter must be applied to healed skin several times
a day. Prolonged submersion in water, especially hot water, and use of deter-
gents or perfumed soaps are to be avoided. Skin should be washed with mild
soap and warm water and dried, and moisturizer should be applied.

Fig. 6. (A) Split-thickness sheet graft. Web spacers are placed to preserve interdigital web
spaces. (B) Custom compression gloves are placed over web spacers to control edema and
scarring.
 Author's personal copy

BURN REHABILITATION 937

Pruritus
Many patients experience intense problematic itching after a burn. Clin-
ically it seems that the larger the burn the more likely pruritus is a problem.
Pruritus is treated with pressure garments and topical or oral antihista-
mines. Doxepin hydrochloride cream is also eective. Finally, some clini-
cians prescribe oral gabapentin and pregabalin, which have been reported
anecdotally as an eective treatment.
Scar suppression
Immediately after deep partial-thickness and full-thickness burns heal,
the appearance is acceptable. With the passing of approximately 1 to
3 months, however, hypertrophic scarring typically appears. These red,
raised, rigid scars create a wide range of cosmetic and functional problems.
The scarring may develop into heavy rope-like scars that are inexible and
limit joint motion or soft tissue motion. Histologically, hypertrophic scar-
ring is collagen arranged in random orientation with whorls and nodules
[17]. In nonhypertrophic scarring, collagen is parallel to the skin surface
similar to normal skin. Mechanical pressure facilitates the alignment of
the collagen bers in a more parallel, normal orientation [18].
Clinically, it is generally accepted that scars treated with pressure result in
better function and appearance. Custom-tted garments, elastic bandages,
or rigid clear face masks are applied over the areas of scarring (Fig. 7). It
is believed that 25 mm Hg is needed to improve the collagen orientation
and exceed capillary pressure. The pressure garments and devices are
worn at least 23 hours a day. Areas in which it is dicult to provide
pressure, such as the web space between ngers, require additional inserts
of silicone or moldable materials to ensure an intimate t. As a side note,
silicone seems to have intrinsic properties that aid in scar suppression [19].
Once the scar has matureddusually after 18 to 24 monthsdthe use of pres-
sure garments and devices is discontinued. Scars are considered mature
when they are soft and no longer indurated and red.

Fig. 7. (A) Custom-made breast shield. The shield provides compression over the burned chest
wall. (B) The breast shield is worn under the custom pressure garment to suppress scar
formation.
 Author's personal copy

938 SPIRES et al

Neuropathy after burn injury

Peripheral neuropathy is not uncommon after severe burn injury. Hen-
derson and colleagues [20] were among the rst to study postburn neurop-
athy. Using nerve conduction studies to evaluate 249 patients, their
studies reported electrodiagnostic evidence of peripheral polyneuropathy
in approximately 18% of patients during acute hospitalization. They re-
ported that 15% had continued evidence of polyneuropathy, including
weakness, numbness, tingling, and deafness after discharge, and the neuro-
logic decits were not directly related to the injured body region [20].
Helm and colleagues [21] found that a generalized peripheral neuropathy
was the most common neuromuscular abnormality and presented as distal
weakness in the upper and lower extremities. Their incidence of neuropathy
was similar (15%) to that of Henderson and Kowalske and colleagues [22].
Dagum and colleagues [23] found that 7.4% of patients with more than 40%
TBSA thermal burns developed multiple mononeuropathies. Helm reported
that the most common sites of neuropathy were the peroneal, ulnar, brachial
plexus, and median nerves. Helm and colleagues [21] suggested that poor
positioning in the bed and on the operating table and the presence of bulky
dressings over supercial nerves increase the risk of developing a
mononeuropathy.
The cause of the generalized peripheral neuropathy associated with a se-
vere burn is likely multifactorial. Although the cause is unclear, it may be
a variant of critical care neuropathy seen in other groups of critically ill
patients. Henderson and colleagues [20] speculated that metabolic factors re-
lated to pancreatic, renal, or hepatic dysfunction after burns were possible
contributors. Medications used during burn treatment, such as neuromuscu-
lar blocking agents, also may contribute to neuropathy development [20].
Dagum and colleagues [23] isolated a high molecular weight lipoprotein in
patients with more than 25% TBSA burns and hypothesized that this neu-
rotoxin may be a contributor. Margherita and colleagues [24] suggested
that thermal injuries may induce an inammatory cascade that results in
alterations of nerve function. Marquez and colleagues [25] theorized that
vascular occlusion of the vasa nervorum, direct thermal injury, or a dissem-
inated neurotoxin also may be possible mechanisms.
Animal studies that investigated the causes of peripheral neuropathy
after burns included the work of Higashimori and colleagues [26]. They
studied full-thickness burns in mice and found that functional and morpho-
logic decits were produced in peripheral axons at sites distant to the site of
burn injury. In another study, Higashimori and colleagues [27] found that
early wound excision in mice with full-thickness 20% TBSA burns reduced
nerve conduction decits, and they hypothesized that nitric oxide and tumor
necrosis factor may play a role.
Risk factors for development of neuropathy after burns include older age
and burns over more than 20% TBSA [20,22,28]. Marquez and colleagues
 Author's personal copy

BURN REHABILITATION 939

[25] found that the length of hospitalization also correlated with the number
of nerves aected after burn injury. Kowalske [22] likewise reported an as-
sociation between the number of days in the intensive care unit and days on
the ventilator. A history of alcohol abuse or premorbid neuropathy also in-
creases risk.

Electrical injury
Sae and colleagues reported that 6.1% of burns recorded in the Amer-
ican Burn Association patient registry were caused by electrical injury, a sim-
ilar rate seen in other studies [7,29,30]. Electrical injuries are divided into
high-voltage (O1000 V) and low-voltage (!1000 V) injuries [31]. Electrical
current causes unique injuries that may be progressive, delayed in onset, and
remote from the site of entry into or exit from the body. Solem and col-
leagues [32] stated that electrical injuries are largely the result of the conver-
sion of electrical energy into heat. As Solem and colleagues pointed out, the
susceptibility of individual tissues to current does not necessarily correlate
with the amount of heat generated by the current. Tissues of the central
nervous system, peripheral nervous system, cardiac system, and vasculature
seem to be particularly sensitive to electrical injury. Other mechanisms that
cause additional pathology after electrical injuries are poorly understood.
Patients with electrical injury are susceptible to neuropathy. Habernal
and colleagues [33] followed 25 patients with electrical burns for years after
their initial injuries, clinically and electrodiagnostically. They found that the
most common electrodiagnostic abnormality was multiple nerve conduction
abnormality (36%). Weakness was the most prominent clinical nding
(24%). Solem and colleagues [32] found that 13% of their population had
peripheral nerve injuries, including median nerve, peroneal nerve, ulnar
nerve, and brachial plexus neuropathy. All of the patients had evidence of
some permanent decit. Smith and colleagues [34] noted that peripheral
nerve injury seemed to be associated with third- and fourth-degree burns.
They cited three cases of low-voltage electrical injury that had no clinically
signicant cutaneous burns but demonstrated symptoms and ndings of pe-
ripheral nerve compression. Because Smith and colleagues found bilateral
decits on qualitative sensory testing in upper and lower extremities, they
proposed systemic electrical injury as a cause of the peripheral neuropa-
thy-like syndrome.
Lower motor neuron disease has been reported after electrical injury.
Jafari and colleagues [35] reported six cases. Although the pathology started
at the site of trauma, the individuals later developed symptoms of lower mo-
tor neuron disease. One individual developed a lower motor neuron syn-
drome, another presented with a spinal cord injury syndrome, and
another had amyotrophic lateral sclerosis. The remaining three developed
symptoms similar to amyotrophic lateral sclerosis. The onset of these
 Author's personal copy

940 SPIRES et al

abnormalities ranged from weeks to years after the initial injury. Multiple
examples of central nervous system injury have been reported. Arevalo
and colleagues [36] reported two cases of spinal cord injury after high-volt-
age electrical injury that presented with signs of acute transverse myelopathy
despite normal CT and MRI evaluation at the time of diagnosis. Similarly,
Kalita and colleagues [37] reported a case of a woman with a normal spinal
MRI who developed spastic paraparesis with loss of pin prick sensation be-
low T2 after a high-voltage injury. Ko and colleagues [38] followed 13 pa-
tients who developed delayed spinal cord injury and reported that the
level of paralysis related to the entry and exit sites of electric current.
Kanitkar and Roberts [39] proposed the following mechanisms of spinal
cord injury after electrical injury:
1. Thermal damage of the nerve is caused by the electrical current, and
leads to injurious heat production
2. Vascular damage causes thrombosis and hemorrhage
3. Direct mechanical trauma from fracture or dislocation results from
intense muscle spasm
4. Changes in proteins after passage of electrical current leads to secondary
vascular changes
The exact mechanisms are poorly understood, however.
Patients with electrical injury are vulnerable to cardiac complications.
Barrash and colleagues [40] documented that cardiac arrest was common
(57%) after high-voltage injury. Hussmann [29] reported that cardiac ar-
rhythmias were the most serious medical problem associated with low-volt-
age electrical injury. Arrhythmias occurred in 29% of high-voltage injuries.
Solem and colleagues [32] found that approximately 20% of patients who
received electrical burns experienced cardiac complications, with almost
half of those patients developing major cardiac arrhythmias.
Cognitive decits occur after electrical injury, but it is not well under-
stood how electrical injury aects the central nervous system. Pliskin and
colleagues [41] reported signicant neuropsychological sequelae after electri-
cal injury, including cognitive and emotional decits. They stated that
almost half of the patients questioned reported diculty with concentration,
slowed thinking, and decreased memory. Barrash and colleagues [42] studied
18 survivors of high-voltage electrical injury and found decits in verbal
learning and delayed recall spanning acute, short-term, and long-term pe-
riods after injury. Martin and colleagues [43] documented global neuropsy-
chological impairments in a case after electrical injury and subsequently
documented a progressive decline on follow-up evaluation. In another
case study, Martin reported a decline in global intellectual functioning
when comparing the results of testing at 6 months after electrically injury
with repeat studies 4 years later. Finally, Kalita and colleagues [37] reported
a case study in which a patient with memory loss after electrical injury had
a hyperintensity of T2-weighted MRI in the right putamen. Kalita and
 Author's personal copy

BURN REHABILITATION 941

colleagues [37] suggested that the lesions found in the putamen were consis-
tent with anoxic brain injury and attributed them to cardiorespiratory arrest
after the electrical injury.
Mood disorders after electrical injury also seem common. Pliskin and col-
leagues [41] reported emotional diculties, such as depression and anxiety,
in nearly half of the patients. Similarly, Janus and Barrash [40] documented
that 92% of patients who were followed after electrical injury showed cog-
nitive dysfunction and aective disorders, including anxiety, depression, ir-
ritability, and poor frustration tolerance. Sixty-two percent of the patients
had problems with physically aggressive outbursts that were not present
before injury [40]. Consequently, neuropsychological monitoring is needed
during short- and long-term follow-up after electrical injury.

Burns and amputations

Amputation after a severe burn injury is not uncommon. Limb loss
results from several factors and occurs most commonly after electrical
burns. Amputation that results from low-voltage electrical injuries
(!1000 V) generally results in minor amputations, such as the toes, wrist,
and ngers. High-voltage injuries are associated with major amputations
in 10% to 50% of patients [44,45]. In severely burned limbs, escharotomy
and fasciotomy are performed if there is ischemia or neurovascular compro-
mise of muscle compartments. Failure to adequately decompress the
aected limbs leads to neurovascular compromise and increased the risk
of amputation [46]. Patients who are transferred to a specialized burn center
more than 5 days after injury are more likely to require amputation. Sepsis
and extensive tissue death from inadequate decompression are cited as the
main reasons [4749].

When to amputate
Surgical decision making for amputation is based on the presence of non-
viable tissue, life-threatening sepsis, or a limb that is insensate and nonfunc-
tional [50,51]. Most burn patients who undergo amputation survive and
become successful prosthetic users [5254]. The decision to amputate usually
falls into two groups: immediate amputation and delayed amputation [48].
Immediate or early amputation occurs within 72 hours of admission and
is commonly associated with electrical burns. Tissue destruction is readily
apparent and the decision for amputation is obvious. In contrast, the depth
or severity of injury associated with thermal burns is dicult to determine
initially. The extent of damage is often only apparent after surgical debride-
ment. Patients with thermal burns who require early amputation have severe
and extensive injuries. Amputation from thermal burns typically occurs 2 to
4 weeks after injury and is usually a response to infection or devitalized
tissue [48,52].
 Author's personal copy

942 SPIRES et al

Quality of life is an important criterion in the decision-making process.

The potential for successful prosthetic use, ambulation, and activities of
daily living must be considered in the decision to amputate. Ideally, the
patient and family are included in the decision to amputate a severely
injured limb [15]. A well performed amputation results in a limb with pres-
ervation of the proper bone length, adequate soft tissue coverage, appropri-
ate bone beveling, and sharp nerve transection. However, at times, the
specics of the injury may not allow for adequate muscle, fascia, or skin
to preserve ideal bone length and provide full-thickness skin coverage of
the residual limb [53]. Although less desirable, the burn surgeon may nd
it necessary to use split-thickness skin grafts to achieve closure [55]. Free tis-
sue transfers may help prevent amputation [56,57]. Recent advances in
bioengineered materials for wound coverage, the development of vacuum-
assisted closure, and advances in secondary grafting have allowed some
patients to avoid amputation [5860].

Skin grafts
Does greater residual limb length outweigh the disadvantage of the
grafted residual limb? It depends. Split-thickness skin grafts are prone to
breakdown and may require revision if problems persist [15,53,61]. Intermit-
tent breakdown of the skin graft usually presents within the rst year of
prosthetic use. The split-thickness graft shrinks over time and may pull nor-
mal thickness tissue over the previously injured area, increasing the amount
of normal thickness skin covering the residual limb (Fig. 8) [55]. Breakdown
of the split-thickness skin graft usually occurs within 1 month of initial pros-
thetic tting. Grafts applied directly over bone frequently require revision
[55]. Children seem more tolerant of split-thickness skin grafts, particularly
if they are less than 25% of total surface area. A total surface area of 26% to
50% is more prone to skin breakdown, which complicates prosthetic usage
[55].

Fig. 8. Transtibial amputation with meshed split-thickness grafts for closure.

 Author's personal copy

BURN REHABILITATION 943

Rehabilitation and preprosthetic management

Residual limb contractures result from postoperative soft tissue retrac-
tion, hypertrophic scarring, and muscle tightness from inactivity [15].
ROM and strengthening exercises of all joints and musculature proximal
to the amputation site are indicated to maximize the likelihood of successful
prosthetic use. Education in residual limb shaping and edema control pre-
and post-amputation improves outcomes. Edema control can be managed
by using elastic bandage wraps, o-the-shelf stump shrinkers, or cus-
tom-made elastic cotton stump shrinkers. Massage also helps prevent skin
adherence and prevents further problems of pain and skin breakdown at
a later phase in prosthetic restoration.
Adjustment
Psychological issues pertaining to burns and amputation need monitoring
[53,62]. Pain, depression, activity avoidance because of physical limitations
and social anxiety secondary to disgurement are medical and psychological
issues associated with burns [6365]. Literature shows that young amputees
seem to have more diculty with adjustment and depression than older am-
putees [53,62]. Adjustment often improves with successful use of a prosthesis.
Some authors propose that improvement occurs because the prosthesis pro-
vides a visual replacement of the absent limb and increases function
[45,62,66]. Burn patients often report intermittent use of their prosthesis
[52,54,66]. The decision to discard or not routinely use a prosthesis does
not necessarily indicate a psychological maladjustment to the amputation
or burn [53].
Prosthetic tting
The majority of burn patients who have an amputation experience suc-
cessful prosthetic restoration and rehabilitation. Minor delays may be un-
avoidable because of full- or split-thickness skin grafts and their location.
Modern prosthetic materials and techniques allow less-than-optimal resid-
ual limbs to succeed with prosthetic restoration and rehabilitation.
Fitting with an initial provisional prosthesis may be delayed as tissues
and grafts heal and mature [61]. The delay ranges from 6 to 14 weeks for
the upper extremity and 10 to 26 weeks for the lower extremity. The timing
of tting depends on healing and the mechanical tolerance of the residual
limb. In the case of lower limb loss, the use of a thigh corset or ischial
weight-bearing socket allows earlier ambulation without full weight bearing
[56]. Dynamic sockets fabricated with rigid frames and soft, exible liners
coupled with 6- to 9-mm silicone gel liners allow more intimate socket t
for irregularly contoured limbs. The silicone gel liners allow skin protection
and close adherence to the stump. The liner also oers decreased friction be-
tween the stump surface and prosthetic socket [67]. Optimal suspension,
prosthetic comfort, and skin protection enhance prosthetic usage [6770].
 Author's personal copy

944 SPIRES et al

Complications and outcomes

Complications that prevent successful prosthetic use include skin fragility,
skin breakdown, painful scars, bone spurs, joint contractures, muscle weak-
ness, and heterotopic ossication. Individuals with full-thickness burns of
the upper extremity and persons with 20% or more TBSA are predisposed
to heterotopic ossication [7173]. The elbow is the most common site of het-
erotopic ossication in the burn population; the second most common site is
the shoulder in adults and the hip in children [74]. Heterotopic ossication in-
terferes with joint mobility, prosthetic tting, and comfort [75]. Wounds on
other parts of the body can interfere with successful prosthetic use as well [54].
Phantom pain may be problematic, but successful prosthesis use is asso-
ciated with decreased phantom limb pain [76]. Individuals with electrical
injuries are more likely to report phantom limb pain than persons with ther-
mal injuries [77]. Clinicians should take a careful history to dierentiate
phantom pain from phantom sensations. Phantom sensations are not pain-
ful and do not require treatment.
Upper extremity prosthetic use ranges from 13% to 50% in burn survi-
vors [54]. In general, most (71.3%) upper extremity amputees report di-
culty using their prosthesis. Individuals who have burn injuries have
additional diculties, such as pain or contractures, that impact successful
use [78]. Lower extremity prosthetic use is reported at 39.6% to 67% for
transtibial and 32.1% to 50% for transfemoral amputees [54,79]. Patients
who were not successful prosthetic users identied pain and skin breakdown
as major barriers to use [48,52,54].
Most burn amputees return to work [48,54,80]. Only 5.3% of patients in-
jured by high-voltage trauma are able to return to their previous occupation
[48]. Most amputees return to gainful employment, but only a few return to
the same position [48]. Many individuals seek alternate positions and re-
quire assistive devices at home and work [81].

Work and school

Finally, individuals who have experienced a serious burn face the chal-
lenge of reintegrating into their family, community, and vocational setting.
Work or school issues depend on an individuals age, subsequent impair-
ments, and the location and extent of injury. Loss of hand function, reduced
ne motor function, impaired sensation, impaired coordination, heat and
cold intolerance, pruritus, skin fragility, and limb loss are all factors to be
weighed when return to work, school, or vocational rehabilitation is consid-
ered. Adjustment to a burn injury and the resulting problems require ongo-
ing evaluation. Many burn injuries occur at work, and an individual may
nd it dicult to return to the place of injury.
Once an individual leaves the hospital or inpatient rehabilitation unit,
recovery is not complete. Ongoing scar suppression therapy continues as
 Author's personal copy

BURN REHABILITATION 945

does increasing emphasis on endurance, strength, and maintenance of

ROM. Psychological adjustment, reintegration into the community, and
return to work and school require ongoing periodic evaluation to ensure
success.

Summary
The eld of burn rehabilitation requires multispecialty evaluation, diag-
nosis, and management. Physiatrists are in a unique position to facilitate
optimal recovery and function across all spheres of human function and
lifespan.

References
[1] Fraser PM. Ptolemaic Alexandria. Oxford (UK): Clarendon Press; 1937.
[2] Mettler CC. History of medicine. Philadelphia: Blakiston; 1947.
[3] Karter MJ. Fire loss in the U.S. during 2005: full report. Quincy (MA): National Fire
Protection Association, Fire Analysis and Research Division; 2006. p. 5, 7.
[4] Hall JR. Characteristics of home re victims. Quincy (MA): National Fire Protection Asso-
ciation, Fire Analysis and Research Division; 2005. p. 127, 23.
[5] American Burn Association. National burn repository, 2002 report. Chicago: American
Burn Association; 2002. p. 23, 28.
[6] Sheridan RL. Burns. Crit Care Med 2002;30(Suppl 11):S50014.
[7] Centers for Disease Control and Prevention. Mass casualties: burns: Centers for Disease
Control and Prevention, Department of Health and Human Services: emergency prepared-
ness and response. 2006.
[8] Sae JR, Davis B, Williams P. Recent outcomes in the treatment of burn injury in the United
States: a report from the American Burn Association patient registry. J Burn Care Rehabil
1995;16(3 Pt 1):21932 [discussion: 2889].
[9] Hall JR. Burns, toxic gases, and other hazards associated with res: deaths and injuries in re
and non-re situations. Quincy (MA): National Fire Protection Association, Fire Analysis
and Research Division; 2001.
[10] Yarbrough DR. Improving survival in the burned patient. J S C Med Assoc 1990;86(6):
3479.
[11] Spires MC. Rehabilitation of patients with burns. In: Braddom RL, editor. Physical medi-
cine and rehabilitation. 2nd edition. Philadelphia: WB Saunders; 2000. p. 1325.
[12] Helm PA, Kevorkian CG, Lushbaugh M, et al. Burn injury: rehabilitation management in
1982. Arch Phys Med Rehabil 1982;63:616.
[13] Garner WL, Magee W. Acute burn injury. Clin Plast Surg 2005;32(2):18793.
[14] Wood FM, Kolybaba ML, Allen P. The use of cultured epithelial autograph in the treatment
of major burn injuries: a critical review of the literature. Burns 2006;32(4):395401.
[15] Ward RS, Hayes LC, Schnebly WA, et al. Rehabilitation of burned patients with concom-
itant limb amputation: case reports. Burns 1990;16:297301.
[16] Millington PF, Wilkinson R. Skin. Cambridge (MA): Cambridge University Press; 1983.
p. 83112, 17292.
[17] Jensen LL, Parshley PH. Postburn scar contractures: histology and eects of pressure treat-
ment. J Burn Care Rehabil 1984;5:11923.
[18] Kischer CW, Shetlar MR, Shetlar CL. Alteration of hypertrophic scars induced by mechan-
ical pressure. Arch Dermatol 1975;111:604.
[19] Van den Kerckhove E, Stappaerts K, Boeckx W, et al. Silicones in the rehabilitation of burns:
a review and overview. Burns 2001;27(3):20514.
 Author's personal copy

946 SPIRES et al

[20] Henderson B, Koepke GH, Feller I. Peripheral polyneuropathy among patients with burns.
Arch Phys Med Rehabil 1971;52(4):14951.
[21] Helm PA, Pandian G, Heck E. Neuromuscular problems in the burn patient: cause and pre-
vention. Arch Phys Med Rehabil 1985;66(7):4513.
[22] Kowalske K, Holavanahalli R, Helm P. Neuropathy after burn injury. J Burn Care Rehabil
2001;22(5):3537 [discussion: 352].
[23] Dagum AB, Peters WJ, Neligan PC, et al. Severe multiple mononeuropathy in patients with
major thermal burns. J Burn Care Rehabil 1993;14(4):4405.
[24] Margherita AJ, Robinson LR, Heimbach DM, et al. Burn-associated peripheral polyneur-
opathy: a search for causative factors. Am J Phys Med Rehabil 1995;74(1):2832.
[25] Marquez S, Turley JJ, Peters WJ. Neuropathy in burn patients. Brain 1993;116(Pt 2):47183.
[26] Higashimori H, Whetzel TP, Mahmood T, et al. Peripheral axon caliber and conduction
velocity are decreased after burn injury in mice. Muscle Nerve 2005;31(5):61020.
[27] Higashimori H, Carlsen RC, Whetzel TP. Early excision of a full-thickness burn prevents
peripheral nerve conduction decits in mice. Plast Reconstr Surg 2006;117(1):15264.
[28] Khedr EM, Khedr T, el-Oteify MA, et al. Peripheral neuropathy in burn patients. Burns
1997;23(78):57983.
[29] Hussmann J, Kucan JO, Russell RC, et al. Electrical injuries: morbidity, outcome and treat-
ment rationale. Burns 1995;21(7):5305.
[30] Garcia-Sanchez V, Gomez Morell P. Electric burns: high- and low-tension injuries. Burns
1999;25(4):35760.
[31] Blue GE. Electrical burns. Int J Surg 1926;39:1169.
[32] Solem L, Fischer RP, Strate RG. The natural history of electrical injury. J Trauma 1977;
17(7):48792.
[33] Haberal MA, Gurer S, Akman N, et al. Persistent peripheral nerve pathologies in patients
with electric burns. J Burn Care Rehabil 1996;17(2):1479.
[34] Smith MA, Muehlberger T, Dellon AL. Peripheral nerve compression associated with low-
voltage electrical injury without associated signicant cutaneous burn. Plast Reconstr Surg
2002;109(1):13744.
[35] Jafari H, Couratier P, Camu W. Motor neuron disease after electric injury. J Neurol Neuro-
surg Psychiatry 2001;71(2):2657.
[36] Arevalo JM, Lorente JA, Balseiro-Gomez J. Spinal cord injury after electrical trauma
treated in a burn unit. Burns 1999;25(5):44952.
[37] Kalita J, Jose M, Misra UK. Myelopathy and amnesia following accidental electrical injury.
Spinal Cord 2002;40(5):2535.
[38] Ko SH, Chun W, Kim HC. Delayed spinal cord injury following electrical burns: a 7-year
experience. Burns 2004;30(7):6915.
[39] Kanitkar S, Roberts AH. Paraplegia in an electrical burn: a case report. Burns Incl Therm Inj
1988;14(1):4950.
[40] Janus TJ, Barrash J. Neurologic and neurobehavioral eects of electric and lightning
injuries. J Burn Care Rehabil 1996;17(5):40915.
[41] Pliskin NH, Capelli-Schellpfeer M, Law RT, et al. Neuropsychological symptom presenta-
tion after electrical injury. J Trauma 1998;44(4):70915.
[42] Barrash J, Kealey GP, Janus TJ. Neurobehavioral sequelae of high voltage electrical injuries:
comparison with traumatic brain injury. Appl Neuropsychol 1996;3(2):7581.
[43] Martin TA, Salvatore NF, Johnstone B. Cognitive decline over time following electrical
injury. Brain Inj 2003;17(9):81723.
[44] Ferreiro I, Melendez J, Regalado J, et al. Factors inuencing the sequelae of high tension
electrical injuries. Burns 1998;24(7):64953.
[45] Esselman PC, Thombs BD, Magyar-Russell GP, et al. Burn rehabilitation: state of the
science. Am J Phys Med Rehabil 2006;85(4):383413.
[46] Mann R, Gibran N, Engrav L, et al. Is immediate decompression of high voltage electrical
injuries to the upper extremity always necessary? J Trauma 1996;40(4):5847.
 Author's personal copy

BURN REHABILITATION 947

[47] Brown RL, Greenhalgh DG, Kagan RJ, et al. The adequacy of limb escharotomies-fasciot-
omies after referral to a major burn center. J Trauma 1994;37(6):91620.
[48] Kennedy PJ, Young WM, Deva AK, et al. Burns and amputations: a 24-year experience.
J Burn Care Res 2006;27(2):1838.
[49] Yowler CJ, Mozingo DW, Ryan JB, et al. Factors contributing to delayed extremity ampu-
tation in burn patients. J Trauma 1998;45(3):5226.
[50] Yakubo KP, Kurtzman LC, Stern PJ. Acute management of thermal and electrical burns of
the upper extremity. Orthop Clin North Am 1992;23(1):1619.
[51] Winkley JH, Gaspard DJ, Smith LL. Amputation as a life-saving measure in the burn
patient. J Trauma 1965;5(6):78291.
[52] Viscardi PJ, Polk HC Jr. Outcome of amputations in patients with major burns. Burns 1995;
21(7):5269.
[53] Prasad JK, Bowden ML, McDonald K, et al. Rehabilitation of burned patients with bilateral
above-knee amputations. Burns 1990;16(4):297301.
[54] Ward RS, Hayes-Lundy C, Schnebly WA, et al. Prosthetic use in patients with burns and
associated limb amputations. J Burn Care Rehabil 1990;11(4):3614.
[55] Dedmond BT, Davids JR. Function of skin grafts in children following acquired amputation
of the lower extremity. J Bone Joint Surg 2005;87(5):10548.
[56] Acikel C, Peker F, Akmaz I, et al. Muscle transposition and skin grafting for salvage of
below-knee amputation level after bilateral lower extremity thermal injury. Burns 2001;
27(8):84952.
[57] De Lorenzi F, Van der Hulst R, Boeckx W. Free aps in burn reconstruction. Burns 2001;
27(6):60312.
[58] Greenberg JE, Falabella AF, Bello YM, et al. Tissue-engineered skin in the healing of wound
stumps from limb amputations secondary to purpura fulminans. Pediatr Dermatol 2003;
20(2):16972.
[59] Argenta LCMD, Morykwas MJPD, Marks MWMD, et al. Vacuum-assisted closure: state of
clinic art. Plast Reconstr Surg 2006;117(7S):127S42S.
[60] Bishara SA, Gunn SW, Shady NH. State of the art in burn treatment. World J Surg 2005;
29(2):13148.
[61] Wood MR, Hunter GA, Millstein SG. The value of stump split skin grafting following am-
putation for trauma in adult upper and lower limb amputees. Prosthet Orthot Int 1987;11(2):
714.
[62] Frank RG, Kashani JH, Kashani SR, et al. Psychological response to amputation as a func-
tion of age and time since amputation. Br J Psychiatry 1984;144:4937.
[63] Rumsey N, Clarke A, White P, et al. Altered body image: appearance-related concerns of
people with visible disgurement. J Adv Nurs 2004;48(5):44353.
[64] Rumsey N, Clarke A, White P. Exploring the psychosocial concerns of outpatients with
disguring conditions. J Wound Care 2003;12(7):24752.
[65] Rumsey N, Clarke A, Musa M. Altered body image: the psychosocial needs of patients.
Br J Community Nurs 2002;7(11):5636.
[66] Fleet J. The psychological eects of burn injuries. British Journal of Occupational Therapy
1992;55:198201.
[67] Baars EC, Geertzen JH. Literature review of the possible advantages of silicone liner socket
use in trans-tibial prostheses. Prosthet Orthot Int 2005;29(1):2737.
[68] Carroll K. Lower extremity socket design and suspension. Phys Med Rehabil Clin N Am
2006;17(1):3148.
[69] Datta D, Vaidya SK, Howitt J, et al. Outcome of tting an ICEROSS prosthesis: views of
trans-tibial amputees. Prosthet Orthot Int 1996;20(2):1115.
[70] Narita H, Yokogushi K, Shii S, et al. Suspension eect and dynamic evaluation of the total
surface bearing (TSB) trans-tibial prosthesis: a comparison with the patellar tendon bearing
(PTB) trans-tibial prosthesis. Prosthet Orthot Int 1997;21(3):1758.
[71] Hunt JL, Sato RM, Baxter CR. Acute electric injuries. Arch Surg 1980;115:4348.
 Author's personal copy

948 SPIRES et al

[72] Dudek NL, DeHaan MN, Marks MB. Bone overgrowth in the adult traumatic amputee. Am
J Phys Med Rehabil 2003;82(11):897900.
[73] Potter BK, Burns TC, Lacap AP, et al. Heterotopic ossication in the residual limbs of trau-
matic and combat-related amputees. J Am Acad Orthop Surg 2006;14(10):S1917.
[74] Evans EB. Orthopaedic measures in the treatment of severe burn. J Bone Joint Surg Am
1966;48:64369.
[75] Helm PA, Walker SC. New bone formation at amputation sites in electrically burn-injured
patients. Arch Phys Med Rehabil 1987;68(5 Pt 1):2846.
[76] Karl A, Birbaumer N, Lutzenberger W, et al. Reorganization of motor and somatosensory
cortex in upper extremity amputees with phantom limb pain. J Neurosci 2001;21(10):
360918.
[77] Thomas CR, Brazeal BA, Rosenberg L, et al. Phantom limb pain in pediatric burn survivors.
Burns 2003;29(2):13942.
[78] Dudkiewicz I, Gabrielov R, Seiv-Ner I, et al. Evaluation of prosthetic usage in upper limb
amputees. Disabil Rehabil 2004;26(1):603.
[79] Poljak-Guberina R, Zivkovic O, Muljacic A, et al. The amputees and quality of life. Coll
Antropol 2005;29(2):6039.
[80] Fletchall S, Hickerson WL. Early upper-extremity prosthetic t in patients with burns.
J Burn Care Rehabil 1991;12(3):2346.
[81] Chang JK. Assistive devices in the rehabilitation of patients with electrical burns: three case
reports. J Burn Care Rehabil 2001;22(1):906.