Complications specific to electrical injury

include:

Cardiovascular:
Cardiac
arrest
(ventricular fibrillation for electric current
or systole for lightning), arrhythmia (usually
sinus tachycardia or nonspecific

DEFINITION OF TERMS
Types of Burns
Thermal Burns
Thermal burns are the result of conduction
or convection, as
in contact with a hot object, liquid,
chemical, flame, or
steam. In order of frequency, the common
types of thermal
burns are scalds, flame burns, flash burns,
and contact burns
Electrical Burns
An electrical burn is caused by exposure to
a low- or highvoltage current and results in
varied degrees of visible cutaneous tissue
destruction at the contact points, as well as
less visible but massive damage of
subcutaneous tissue, muscle, nerve, and
bone. Tissue necrosis of these deeper
structures occurs from the high heat
intensity of the current and the electrical
disruption of cell membranes. Tissue
damage occurs along the path of the
current, with smaller distal areas of the
body damaged most severely. This pattern
of tissue damage accounts for the high
incidence of amputation associated with
electrical injury. The severity of an
electrical burn depends primarily on the
duration of contact with the source, the
voltage of the source, the type and
pathway current, and the amperage and
resistance through the body tissues.
Electrical burns are characterized by deep
entrance and exit wounds and arc wounds.
The entrance wound is usually an obvious
necrotic and depressed area, whereas the
exit wound varies in presentation. The exit
wound can be a single wound or multiple
wounds located where the patient was
grounded during injury. An arc wound is
caused by the passage of current directly
between joints in close opposition. For
example, if the elbow is fully flexed and an
electrical current passes through the arm,
burns may be located at the volar aspect of
the wrist, antecubital space, and axilla.

ST segment changes) secondary to

alterations in electrical conductivity of the
heart, myocardial contusion or infarction, or
heart wall or papillary muscle rupture.
As a result of the high risk of fatal
arrhythmias
in
this
population,
the
American
Burn
Association
(ABA)
recommends an electrocardiogram (ECG)
be performed on all patients who sustain
electrical injuries, and those with a
documented loss of consciousness or
presence of arrhythmia following injury
should
be
admitted
for
telemetry
monitoring.18 Neurologic: Headache,
seizure, brief loss of consciousness or
coma, peripheral nerve injury (resulting
from ischemia), spinal cord paralysis (from
demyelination),
herniated
nucleus
pulposus, or decreased attention and
concentration.
Orthopedic: Dislocations or fractures
secondary
to
sustained
muscular
contraction or from a fall during the
electrical injury.
Other: Visceral perforation or necrosis,
cataracts, tympanic membrane rupture,
anxiety, depression, or posttraumatic stress
disorder.
Lightning
Lightning, considered a form of very high
electrical current, causes injury via four
mechanisms:
1. Direct strike, in which the person is the
grounding site
2. Flash discharge, in which an object
deviates the course of the lightning current
before striking the person
3. Ground current, in which lightning strikes
the ground and a person within the
grounding area creates a pathway for the
current
4. Shock wave, in which lightning travels
outside the person and static electricity
vaporizes moisture in the skin
Chemical Burns

Chemical burns can be the result of

reduction,
oxidation,
corrosion,
or
desecration of body tissue with or without
an associated thermal injury.The severity of
the burn depends on the type and
concentration of the chemical, duration of
contact, and mechanism of action. Unlike
thermal burns, chemical burns significantly
alter systemic tissue pH and metabolism.
These
changes
can
cause
serious
pulmonary complications (e.g., airway
obstruction from bronchospasm, edema, or
epithelial
sloughing)
and
metabolic
complications (e.g., liver necrosis or renal
dysfunction from prolonged chemical
exposure).
Ultraviolet and Ionizing Radiation
Burns
A nonblistering sunburn is a first-degree
burn from the overexposure of the skin to
UV radiation. More severe burns can also
occur due to UV exposure and would .
Ionizing radiation burns with or without
thermal injury occur when electromagnetic
or
particulate
radiation
energy
is
transferred to body tissues, resulting in the
formation
of
chemical
free
radicals.2Ionizing radiation burns usually
occur in laboratory or industrial settings,
but can also be seen in the medical setting
following radiation treatment, most often
for cancer. The severity of the ionizing
radiation burn depends on the dose, the
dose rate, and the tissue sensitivity of
exposed cells.
Often referred to as acute radiation
syndrome,
complications
of
ionizing
radiation burns include

Gastrointestinal:
Cramps,
nausea,
vomiting, diarrhea, and bowel ischemia
Hematologic: Pancytopenia (decreased
number of red blood cells, white blood
cells, and platelets), granulocytopenia
(decreased number of granular leukocytes),
thrombocytopenia (decreased number of
platelets), and hemorrhage
Vascular: Endothelium destruction

classification of burn
Superficial Partial-Thickness Burn

Epidermal Burn
An epidermal burn, as the name implies,
causes cell damage only to the epidermis
(Fig. 24.2). This depth of burns correlates to
practice
pattern
7B,
Impaired
Integumentary Integrity Associated with
Superficial Skin Involvement, in the Guide
to Physical Therapist Practice. The classic
sunburn is the best example of an
epidermal burn. Clinically, the skin appears
red or erythematous.The erythema is a
result of epidermal damage and dermal
irritation, but there is no injury to the
dermal tissue. There is diffusion of
inflammatory mediators from sites of
epidermal
damage
and
release
of
vasoactive substances from mast cells. The
surface of an epidermal burn is dry. Blisters
will be absent, but slight edema may be
apparent. After an epidermal burn, there is
usually a delay in the development of pain,
at which point the area becomes tender to
the touch. Following epidermal damage,
the injured epidermal layers will peel off or
desquamate in 3 to 4 days. Epidermal
healing is spontaneous; that is, the skin will
heal by itself, and no scar tissue will form.

With a superficial partial-thickness burn (Fig

24.3) damage occurs through the epidermis
and into the papillary layer of the dermis.
The
epidermal
layer
is
destroyed
completely, but the papillary dermal layer
sustains only mild to moderate damage.
This depth of burn corresponds to practice
pattern
7C,
Impaired
Integumentary
Integrity Associated with Partial-Thickness
Skin Involvement and Scar Formation, in
the Guide to Physical Therapist Practice.
The most common sign of a superficial
partial-thickness burn is the presence of
intact blisters over the area that has been
injured.
Although the internal environment of
a blister is considered sterile, it has been
shown that blister fluid contains substances
that increase the inflammatory response
and retard the healing process, and it is
recommended that blisters be evacuated.
Healing will occur more rapidly if the
damaged skin is removed and an
appropriate topical agent and wound
dressing applied. Once blisters have been
removed, the surface appearance of the
burn area will be moist. The wound will be

bright red because the dermis is inflamed.

The wound will blanch, which means if
pressure is exerted against the tissue with
a finger, a white spot appears as a result of
displacement of blood in the capillaries
under pressure. On release of pressure, the
white area will demonstrate brisk capillary
refill. Edema can be moderate.
This type of burn is extremely painful
secondary to irritation of the nerve endings
contained in the dermis. When the wound
is open, the patient will be highly sensitive
to temperature changes, exposure to air,
and light touch. In addition to pain, fever
may be present if areas become infected.
Some topical antimicrobial creams
will cause the wound to develop a gelatinlike film that eventually will peel off, similar
to the desquamation that occurs with
sunburn. This exudate is a coagulum of the
topical antibiotic used to prevent infection
and serum that seeps from the wound as a
result of the insult to capillary integrity.
Superficial partial-thickness burns
heal without surgical intervention, by
means of epithelial cell production and
migration from the wounds periphery and
surviving skin appendages. Coverage by
new epithelium resumes the barrier
function of the skin, and complete healing
should occur in 7 to 10 days. There may be
some residual skin color change owing to
destruction of melanocytes, but scarring is
minimal.
Deep Partial-Thickness Burn

A deep partial-thickness burn (Fig.

24.4) involves destruction of the epidermis
and papillary dermis with damage down

into the reticular dermal layer. As this burn

nears the deepest dermis it begins to
resemble a full-thickness burn, and the
depth best matches practice pattern 7C,
Impaired
Integumentary
Integrity
Associated with Partial-Thickness Skin
Involvement and Scar Formation, in the
Guide to Physical Therapist Practice.21
Most of the nerve endings, hair follicles,
and sweat ducts will be injured because
most of the dermis is destroyed.
Deep partial-thickness burns appear
as a mixed red or waxy white color. The
deeper the injury, the more white it will
appear. Capillary refill will be sluggish after
the application of pressure on the wound.

The surface usually is wet from broken

blisters and alteration of the dermal
vascular network, which leaks plasma fluid.
Marked edema is a hallmark sign of this
burn depth. There is a large amount of
evaporative water loss (15 to 20 times
normal) because of tissue and vascular
destruction. An area of deep partialthickness burn has diminished sensation to
light touch or sharp/dull discrimination but
retains the sense of deep pressure due to
the location of the Pacinian corpuscle deep
in the reticular dermis. Healing occurs
through
scar
formation
and
reepithelialization. By definition, the dermis is
only partially destroyed; therefore, some
viable epidermal cells may remain within
the surviving epidermal appendages and
serve as a source for new skin growth.
The depth of a deep partial-thickness
injury is sometimes difficult to determine,
so allowing the wound to demarcate

(between normal and damaged tissue)

during the first few days is necessary.
Demarcation becomes evident after several
days as the dead tissue begins to slough.
Hair follicles that penetrate into the deeper
dermal regions below the burn level remain
viable. Preservation of hair follicles and
new hair growth will indicate a deep
partialthickness burn rather than a fullthickness
injury,
and
there
is
a
corresponding
greater
potential
for
spontaneous healing. Particularly important
factors that determine which epidermal
structures survive and which die include
the thickness of the skin in a particular
location and/or the distance of the area
from the source of heat.
Deep partial-thickness burns that are
allowed to heal spontaneously will have a
thin epithelium and may lack the usual
number of sebaceous glands to keep the
skin lubricated. New tissue usually appears
dry and scaly, is itchy, and is easily
abraded.
Creams
are
necessary
to
artificially lubricate the new surface.
Sensation and the number of active sweat
ducts will be diminished.
A deep partial-thickness burn
generally will heal in 3 to 5 weeks if it does
not become infected. It is critical to keep
the wound free of infection, because
infection can convert a deep partialthickness burn into a deeper injury. The
development of hypertrophic and keloid
scars is a frequent consequence of a deep
partial-thickness burn.
Full-Thickness Burn
In a full-thickness burn (Fig. 24.5) all
of the epidermal and dermal layers are
destroyed completely. In addition, the
subcutaneous fat layer may be damaged to
some extent. This burn depth is consistent
with
practice
pattern
7D,
Impaired
Integumentary Integrity Associated with
Full- Thickness Skin Involvement and Scar
Formation, in the Guide to Physical
Therapist Practice.
A
full-thickness
burn
is
characterized by a hard, parchment-like
eschar covering the area. Eschar is
devitalized tissue consisting of desiccated
coagulum of plasma and necrotic cells.
Eschar feels dry, leathery, and rigid. The
color of eschar can vary from black to deep
red to white; the latter indicates total

ischemia
of
the
area.
Frequently,
thrombosis of superficial blood vessels is
apparent and no blanching of the tissue is
observed. The deep red color of the tissue
results from hemoglobin fixation liberated
from destroyed red blood cells.
Hair follicles are completely
destroyed, so body hairs pull out easily. All
nerve endings in the dermal tissue are
destroyed so the wound will be insensate
(without feeling); however, a patient still
may experience a significant amount of
pain because adjacent areas of partialthickness burn usually surround a fullthickness injury.

A major problem that arises from

deep burns is the damage to the peripheral
vascular system. Because large amounts of
fluid leak into the interstitial space beneath
unyielding eschar, the pressure in the
extravascular space increases, potentially
constricting the deep circulation to the
point of occlusion (see later discussion of
cardiovascular complications in the section
titled Complications of Burn Injury).
Because eschar does not have the elastic
quality of normal skin, edema that forms in
an area of a circumferential burn can cause
compression of the underlying vasculature.
If this compression is not relieved, it may
lead to eventual occlusion with possible
necrosis of tissue distal to the site of injury.
To maintain vascular flow, an escharotomy

may be necessary. An escharotomy is a

midline lateral incision of the eschar the
length of an extremity or chest wall. Figure
24.6 shows an escharotomy and the result
of pressure that forces the incision to gape.
Following an escharotomy, pulses are
frequently examined to monitor restoration
of circulation. If the escharotomy is
successful, there will be an immediate
improvement in the peripheral blood flow,
demonstrated by normal pulses distal to
the wound and by return of normal
temperature and capillary refill of the distal
extremity.
Although at times it may be difficult
to differentiate a deep-partial from a fullthickness burn in the early postburn period,
the differences will become evident after
several days. With a full-thickness burn,
there are no sites available for reepithelialization of the wound. All epithelial
cells have been destroyed, and skin

grafting will be necessary. Grafting is

discussed in detail in the section titled
Surgical Management of the Burn Wound.
Subdermal Burn

An additional category of burn, the

subdermal
burn,
involves
complete
destruction of all tissue from the epidermis
down to and through the subcutaneous
tissue (Fig. 24.7). This depth of injury
correlates with practice pattern 7E,
Impaired
Integumentary
Integrity
Associated
with
Skin
Involvement
Extending into Fascia, Muscle, or Bone and
Scar Formation, in the Guide to Physical
Therapist Practice.21 Muscle and bone are
subject to necrosis when burned. This type
of burn occurs with prolonged contact with
a heat source and routinely occurs as a
result of contact with electricity. Extensive
surgical and therapeutic management is
necessary to return a patient to some
degreeof function.

II. EPIDEMIOLOGY

approximately 90% of all burn deaths

worldwide occurring in low- and middleincome countries.
Intentional burn injuries, rare in the United
States but seen most commonly in young
men, are more common in young women in
India and middle-aged men in Europe.
Unintentional burn injuries are also more
common in girls than boys, in low- to
middle-income countries.
Changing burn mortality in the future may
be focused on improved treatments for
inhalation injury and preventing burns in
the elderly and in low- to middle-income
countries.
braddom
It is estimated that 1.25 million people
experience burn injuries each year. Of
those, approximately 500,000 receive some
form of medical treatment and 40,000 are
hospitalized.
Burns predominantly affect young men
(mode age: 20 to 40; male: 70%).
Two thirds of burn injuries affect adults
and onethird affect children.
Most burns occur by fire/flame (43%) or
scald injuries (36%)
Other etiologies that comprise the
minority of burns include electrical,
contact, chemical, tar, radiation, and
grease injuries as well as skin diseases.
Approximately one third of burn injuries
are associated with concomitant alcohol or
drug use. A large majority of burn survivors
have less than or equal to a high-school
education (82%).
Most injuries (65%) are result of an
accident that is not work related.
A minority of burn injuries (17%) occur at
work. Approximately 5% of burn injuries
are the result of child abuse or adult
assault or abuse.
Among children less than 2 years old,
burn injuries represent the most common
cause of accidental death; most of these
deaths are a result of abuse.
Overall, the survival rate is approximately
95%.
The risk of death is increased for those at
the extremes of age, with inhalation injury
and with larger burns
delisa

Biological Barriers
Langerhans cells, macrophages, and
DNA
Langerhans cells in epidermis present
antigens to lymphocytes

ANATOMY, PHYSIOLOGY, KINESIOLOGY

Functions
of
the
Integumentary
System
Protection against injury and infection
Regulates body temperature
Sensory perception
Regulates water loss
Chemical synthesis
Protection covers and protects the
entire
body
against
injury
and
infection
Physical barriers
- continuity of the skin and hardness of
keratinzed cells
Due to the skins physical characteristics
such as the keratinized cells and
waterproofing properties of the glycolipids.
Keratin helps waterproof the skin and
protects from abrasions and bacteria
Glycolipids prevent diffusion of water and
water-soluble substances between cells
Continuity prevents bacterial invasion
Substances that are able to penetrate the
skin:
Lipid-soluble substances (i.e., oxygen,
carbon dioxide, steroids, and fat-soluble
vitamins)
Oleoresins of certain plants (ex. poison
ivy and poison oak)
Organic solvents (ex. acetone, dry
cleaning fluid, and paint thinner)
Salts of heavy metals (ex. lead, mercury,
and nickel)
Topical medications as motion sickness
patch
Penetration enhancers
Chemical barriers
- (skin secretion and melanin)
Skin secretions such as sebum, human
defensins (antimicrobial peptides), acid
mantle of the skin
retards bacteria growth and/or kills them
Melanin provides protection from UV
damage
Skin secretions (acid mantle)
Low pH and sebum slow bacterial growth
on skin surface
Human defensin natural antibiotic
Cathelicidins proteins that prevent Strep
A infection in wounded skin
Melanin chemical pigment that prevents
UV damage

Dermal macrophages (2nd line of

defense) attack bacteria and viruses that
have penetrated the
epidermis
Langerhans cells and macrophages
present in the skin helps activate the
bodys immune system.
DNA structure the electrons in DNA
absorb UV radiation and converts it to heat
Temperature regulation
Production of copious amounts of sweat
to dissipate heat
When body temperature rises and is
hotter than the external environment the
blood vessels in the dermal area dilates
and sweat glands are stimulated into
activity.
Evaporation of the sweat from skins
surface helps dissipate heat from the body.
Constriction of dermal blood vessels to
retain heat
When it is cold outside, the dermal blood
vessels constrict and pull the blood away
from the skin and keeps it close to the body
core to protect crucial internal organs.
Cutaneous Sensations
- cutaneous sensory receptors (see nervous system)
Meissners corpuscles: light touch
Merkel discs: light touch
Pascinian receptors lies in deeper
dermis/hypodermis & detect deep pressure
contacts
Hair root plexus: sensations from
movement of hairs
Hair follicle receptors movement across
the surface of the skin
Bare nerve endings: painful stimuli
(chemicals, heat, cold)
Excretion/Absorption
Elimination of nitrogen-containing wastes
(ammonia, urea, uric acid), sodium
chloride, and water. It regulates water loss
Metabolic Functions
Synthesis of Vitamin D increases
calcium absorption in the body

 Vitamin D is a fat-soluble vitamin that

may be absorbed from the intestines or
may be produced
by the skin when the skin is exposed to
ultraviolet light (particularly sunlight).It is
converted to
its active form by the body in 2 steps,
occurring first in the liver and completed in
the kidneys. In
its active form, vitamin D acts as a
hormone to regulate calcium absorption
from the intestine
and to regulate levels of calcium and
phosphate in the bones. Vitamin D
deficiency causes
Rickets
When the body is deficient in vitamin D, it
is unable to properly regulate calcium and
phosphate
levels. If the blood levels of these minerals
becomes low, the other body hormones
may
stimulate release of calcium and phosphate
from the bones to the bloodstream.
Chemical conversion of many substances
Blood Reservoir preferential shunting of
blood as needed
Types of Membranes - thin sheet-like
structures that protect parts of the body
Serous Membranes
Line body cavities that have no opening
to the outside
Secrete a watery fluid called serous fluid
that lubricates surfaces.
Mucous Membranes
Line cavities and tubes that open to the
outside
Synovial Membranes
Form the inner lining of joint cavities
Secrete a thick fluid called synovial fluid
Cutaneous Membrane also known as
skin
Characteristics of Skin
The integument covers the entire body
and is the largest organ ~ 2 meters and
heaviest organ
16% of body mass of the body.
Composed of the epidermis and dermis
Pliable, yet durable
Thickness: 1.5 to 6.0 mm
Types of Skin
Thin - 1-2 mm on most of the body and 0.5
mm in eyelids
Hairy
Covers all parts of the body except palms
of hands and soles of feet

Thin epidermis and lacks stratum lucidum

Lacks dermal papillae
Has more sebaceous glands
Fewer sweat glands, sensory receptors
than thick skin
Thick - up to 6 mm thick on palms of
hands and soles of feet
Hairless
Covers palms of hands and soles of feet
Thick epidermis and a distinct stratum
lucidum
Epidermal ridges are present due to well
developed, numerous dermal papillae.
Lacks sebaceous glands, has more sweat
glands
Sense receptors are also more densely
packed.
Layers of the Skin
Epidermis
Types of Cells
Keratinocytes
90 % of epidermal cells are keratinized
contains keratin (fibrous protein)
protects and waterproofs the skin
Melanocytes
8% of the epidermal cells
produces melanin
contributes to skin color and absorbs UV
light
Langerhans cells
Arise from red bone marrow and
migrate to the epidermis
Constitute small portion of epidermal cells
Participate in immune responses
Easily damaged by UV light
Merkel cells
Least numerous of the epidermal cells
Found in the deepest layer of the
epidermis
Along with tactile discs, they function in
sensation of touch
Layers of epidermis
Stratum corneum
25-30 layers of dead flat keratinocytes
Shed continuously and replaced by cells
from the
deeper strata
Serves as a water, microbe, injury barrier
Stratum lucidum
Present only in thick skin
3-5
layers
of
clear,
flat,
dead
keratinocytes
Dense packed intermediate filaments

Thick plasma membranes

Stratum granulosum
Located above the stratum spinsosum
3-5 layers of flattened keratinocytes
undergoing apoptosis
Organelles begin to disintegrate becomes
nonliving cells
Marks the transition between deeper
metabolically active strata and the dead
cells of the superficial strata.
Contains lamellar granules
Secretes lipid-rich secretion that acts as a
water
sealant
Stratum spinosum
Located above the stratum basale
8-10 layers of keratinocytes
Some cells retain their ability for cell
division
Cells have spinelike projections (bundles
of
filaments of the cytoskeleton) tightly joins
cells
to each other.
Provides skin both strength and flexibility
Stratum basale
Also referred to as stratum germinatum
because this is where new cells are formed
Deepest layer of the epidermis
Single row of cuboidal or columnar
keratinocytes
Growth of epidermis
Newly formed cells in the stratum basale
undergo keratinazation as they are pushed
to the surface.
They accumulate more keratin during the
process
Then they undergo apoptosis
Eventually they slough off and are
replaced
The process takes about 4 weeks
Rate of cell division in the stratum basale
increases during injury
Dermis
Second deepest part of the skin
Blood vessels, nerves, glands and hair
follicles are embedded here
Composed mainly of connective tissues
(collagen and elastic fibers)
Collagen fibers make up 70% of the
dermis and give structural toughness and
strength. Elastin fibers are loosely arranged

in all directions and give elasticity to the

skin
Has two layers Papillary Layer and
Epidermal layer.
Papillary layer
Superficial portion of the dermis
Consist of areolar connective tissue
containing elastic fiber
Surface area is increased due to
projections called dermal papillae
which contains capillaries or tactile
receptors
Epidermal ridges conforms to the dermal
papillae
Reticular layer
Deeper portion of the dermis
Consist of dense irregular connective
tissue containing collagen/elastic fibers
Provides skin with strength and elasticity
Contains hair follicles, nerves, sebaceous
and sudoriferous glands
Hypodermis
(subcutaneous) Attaches the skin to
underlying organs and tissues
Not part of the skin - lies below the dermis
Contains connective tissue and adipose
tissues (subcutaneous fat) for insulation
Infants and elderly have less of this than
adults and are therefore more sensitive to
cold
Skin Appearances
Epidermis appears translucent when there
is little melanin or carotene
White skin appears pink to red
depending on amount and oxygen content
of blood moving
in the capillaries of the dermis.
Albinism is an inherited trait where a
person cant produce melanin. The have
melanocytes but are
unable to make tyrsinase (the enzyme
which initiates melanin production) so.
melanin is missing in
their hair, eyes, and skin.
Skin color as diagnostic clues for medical
conditions
o Cyanotic (cyan = blue) Ex: someone
who has stopped breathing and the skin
appears bluish
o because the hemoglobin is depleted of
oxyen

o Jaundice (jaund = yellow) - Buildup of

bilirubin (yellow pigment) in the blood gives
a yellowish
appearance of eyes and skin indicating
liver disease Bilirubin is produced when red
blood cells
get old and are broken down by the body.
Normally it is processed in the liver and
then deposited
in the intestine so it can come out in the
stool.
o Erythema (ery = red) - Engorgement of
capillaries in the dermis indicating skin
injury,
infection, heat exposure, inflammation,
allergies, emotional state, hypertension
o Pallor - paleness, emotional state,
anemia, low blood pressure
o Bronzing - Addisons disease, adrenal
cortex
o Bruising (hematoma)- escaped blood
has clottedhematomas , deficiency in
Vitamin C or
hemophilia
o leathery skin - overexposure clumping
of elastin fibers depressed immune system
o can alter DNA to cause skin cancer
o photosensitivity - to antibiotics &
antihistamines
Skin Color
genetic factors, environmental factors
and volume of blood
Skin Pigments - three pigments are
responsible for skin color- melanin,
carotene, hemoglobin
Melanin
Located mostly in epidermis
Number of melanocytes are about the
same in all races
Difference in skin color is due to the
amount of pigment that melanocytes
produce and disperse to
keratinocytes.
Freckles are caused by the accumulation
of melanin in patches
Liver spots are also caused by the
accumulation of melanin
Melanocytes synthesize melanin from an
amino acid called tyrosine along with an
enzyme called tyrosinase. All this occurs in
the melanosome which is an
organelle in the melanocyte.
Two types of melanin: eumelanin which is
brownish black and pheomelanin which is
reddish yellow

Fair-skinned
people
have
more
pheomelanin and dark skinned people have
more eumelanin
Environmental Factors
UV light increases enzymatic activity in
the melanosomes and leads to increased
melanin production.
A tan is achieved because the amount of
melanin has increased as well as the
darkness of the melanin. (Eumelanin
provides protection from UV exposure while
pheomelanin
tends to break down with too much UV
exposure)
The melanin provides protection from the
UV radiation but prolonged exposure may
cause skin cancer.
Carotene (carot = carrot)
yellow-orange pigment
precursor for Vitamin A which is used to
make pigments needed for vision
found in stratum corneum and fatty areas
of dermis and hypodermis layer
Hemoglobin
Oxygen-carrying pigment in red blood cells
Skin Markings
- skin is marked by many lines, creases
and ridges
friction ridges: markings on fingertips
characteristic of primates
allow us to manipulate objects more easily
- fingerprints are friction ridge skin
impressions
flexion lines: on flexor surfaces of digits,
palms, wrists, elbows etc skin is tightly
bound to deep fascia
at these points
freckles: flat melanized patches vary
with heredity or exposure to sun
moles: elevated patch of melanized skin,
of the with hair mostly harmless, beauty
marks
Derivatives of skin - during embryonic
development thousands of small groups of
epidermal cells from
stratum basale push down into dermis to
form hair follicles and glands
Skin receptors:
Your skin and deeper tissues contain
millions of sensory receptors.
Most of your touch receptors sit close to
your skin's surface.
Light touch
Meissner's corpuscles are enclosed in

a capsule of connective tissue

They react to light touch and are
located in the skin of your palms,
soles, lips, eyelids, external genitals
and nipples
These areas of your body are
particularly sensitive
Heavy pressure
Paccinian corpuscules sense pressure
and vibration changes deep in your
skin.
Every square centimeter of your skin
contains around 14 pressure receptors
Pain
skin receptors register pain
pain receptors are the most numerous
each square centimeter of your skin
contains around 200 pain receptors
Temperature
Skin receptors register warmth and cold
Each square centimeter of your skin
contains 6 receptors for cold and 1 receptor
for warmth
Cold receptors
start to perceive cold sensations when the
surface of the skin drops below 95 F. They
are most stimulated when the surface of
the skin is at 77 F and are no longer
stimulated when the surface of the skin
drops below 41 F. This is why your feet or
hands start to go numb when they are
submerged in icy water for a long period of
time.
Hot receptors
start to perceive hot sensations when the
surface of the skin rises above 86 F and
are
most stimulated at 113 F. Beyond 113 F,
pain receptors take over to avoid damage
being done to the skin and underlying
tissues.
Thermoreceptors
are found all over the body, but cold
receptors are found in greater density than
heat
receptors most of the time our
environment is colder than our body
temperature
The
highest
concentration
of
thermoreceptors can be found in the face
and ears so your nose and ears
always get colder faster than the rest of
your body on a chilly winter day
Skin Glands

Sudoriferous - sweat glands (sudori =

sweat) (ferous = bearing)
3- 4 million glands in your body empties
onto the skin thru pores or into hair follicles
Two main types of sweat glands
Eccrine sweat glands
o Secretes cooling sweat
o Secretes directly onto the skin
o Began to function soon after birth
o Sweat is composed of 98 percent water
and two percent dissolved salts and
nitrogenous wastes,
such as urea and uric acid
o Helps regulate body temperature/aids in
waste removal
Appocrine sweat glands
o
Stimulated
during
emotional
stress/excitement
o Secretes into hair folicle
o Begins to function at puberty
o Slightly more viscous than eccrine
secretions
o Composed of the same components as
eccrine sweat
plus
o lipids and proteins.
o Referred to as cold sweat.
Sebaceous - oil glands (sebace = grease)
They are mostly connected to hair
follicles.
Sebaceous glands are embedded in the
dermis over most of the body.
Absent in the palms and soles.
Vary in size, shape and numbers in other
areas of the body.
Secrete an oily substance called sebum.
which lubricates the hair and skin
Mixture of fats, cholesterol, proteins,
inorganic salts, pheromones.
Coats surface of hair
Prevents excessive evaporation of water
from skin
Keeps skin soft and pliable
Inhibits growth of some bacteria.
Sebaceous gland activity increases with
puberty, due to the male and female
hormone activity
Accumulation of sebum in the ducts =
white pimples if the sebum darkens -black
heads form
Acne - inflammation of sebaceous gland
ducts
Ceruminous - modified sweat glands of
the external ear that produce ear wax (cer
= wax)

Open directly onto the surface of the

external auditory canal
(ear canal) or into ducts of sebaceous
glands.
Earwax is the combination of secretion of
ceruminous and sebaceous glands.
Earwax and the hair combine to provide a
sticky barrier against foreign items.
Physiology of Burns
An in depth knowledge of pathophysiology
of burns, and their effects both locally and
systemically is necessary to ensure
effective management of a patient with a
burn injury.
Zones
of
Injury
and
Wound
Conversion
The local effect involves three burn
zones: (Hettiaratchy and Dziewulski 2004)
Zone of Coagulation:
the point of maximum damage

Irreversible
tissue
loss
due
coagulation of constituent proteins.

to

Zone of Stasis:
Characterised by decreased tissue
perfusion
Potential to rescue the tissue in this zone

Problems
such
as
prolonged
hypotension, infection or oedema can
convert this area into one of complete
tissue loss
Zone of Hyperaemia:
The tissue here will invariably recover
unless there is severe sepsis or prolonged
hypoperfusion.
The depth of the wound develops over
time: The
burn
process
peaks
at
approximately three days. Progression is
3D- zone of coagulation both increases in
depth and width (Ever et al 2010).

IV. ETIOLOGY

Thermal burns, the most common type,

frequently result from:
residential fires
automobile accidents
playing with matches
improper handling of firecrackers
scalding accidents and kitchen
accidents (such as a child climbing
on top of a stove or grabbing a hot
iron)
parental abuse of (in children or
elders)
clothes that have caught on fire.
Chemical burns result from contact,
ingestion, inhalation, or injection of
acids, alkalis, or vesicants.
Electrical burns usually result from
contact with faulty electrical wiring or
high-voltage power lines. Sometimes
young children chew electrical cords.
Friction or abrasion
burns occur when the
skin rubs harshly against
a coarse surface.
Sunburn results from
excessive exposure to
sunlight.
Burns can be caused by
excessive heat or cold,
by chemicals, ultraviolet
light
or radiation.
The most common
causes of burns requiring
hospital treatment are:
Scalds from hot fluids or
steam are common in the
under fives and the
elderly.
-Explosions, flash flame
or
steam,
bonfires,
fireworks, barbeques and
the use of flammable
liquids such as petrol.
Flash burns tend to be
partial-thickness
burns,
but can be deeper if the
patients clothes ignite.

Flame burns occur when the patients

clothes, hair or skin catch light. The effect
of damage from house or car fires is
exacerbated by the inhalation of toxic
gases from burning household furniture,
leading to severe inhalation injuries as well
as burns.
Contact burns from contact with molten
metal or plastic are common in industry. An
unconscious patient may sustain burns
from contact with a cooker or a hot
radiator.
Electrical burns due to electrical current
from plugs, sockets and wiring. Deep
structures can be involved at the current
entry and exit sites on the body. The
patients cardiac status requires close
monitoring.
Elsevier

V. PATHOPHYSIOLOGY/MECHANISM OF INJURY/PATHOLOGY
Pathophysiology of Burns Skin and
body tissue destruction occurs from
the absorption of heat energy and
results in tissue coagulation. This
coagulation is depicted in zones
(Figure 12-2). The zone of coagulation,
located in the center of the burn, is the
area of greatest damage and contains
nonviable tissue referred to as eschar.
Although eschar covers the surface
and may appear to take the place of
skin, it does not have any of the
characteristics or functions of normal
skin. Instead, eschar is constrictive,
attracts microorganisms, houses toxins
that may circulate throughout the
body, and prevents progression
through the normal phases of
healing.3 The zone of stasis, which
surrounds the zone of coagulation,
contains marginally viable tissue
which can easily be further
damaged from processes such as
hypoperfusion, edema, or infection.
Proper wound care can minimize
this conversion and preserve the
integrity of the viable tissue in this
zone. The zone of hyperemia, the
outermost area, is the least
damaged and heals rapidly unless
additional tissue injury occurs.7-9
The depth of a burn can be
described as superficial, moderate
partial thickness, deep partial
thickness, or full thickness (Figure
12-3). Each type has its own
appearance, sensation, healing time, and
level of pain, as described in Table 12-2.
First-degree burns have no significant
structural damage and therefore no zone of
stasis
or
coagulation.
Differentiation
between moderate and deep seconddegree burns can be made based on the
presence of the zones of coagulation,
stasis, and hyperemia in the deeper burns
while moderate second-degree burns will
only have zones of stasis and hyperemia.
Third-degree burns contain a significant
and easily identifiable zone of coagulation
as well.

INICAL SIGNS AND SYMPTOMS/ PHYSICAL DISABILITIES/ IMPAIRME

Signs and symptoms

Signs and symptoms depend on the type
of burn and may include:
localized pain and erythema, usually
without blisters in the first 24 hours (firstdegree burn)
chills, headache, localized edema, and
nausea and vomiting (more severe firstdegree burn)
thin-walled, fluid-filled blisters appearing
within minutes of the injury, with mild to
moderate edema and pain
(second-degree
superficial
partialthickness burn)
white, waxy appearance to damaged area
(second-degree deep partial-thickness
burn)
white, brown, or black leathery tissue and
visible thrombosed vessels due to
destruction of skin elasticity (dorsum of
hand most common site of thrombosed
veins), without blisters (third-degree burn)
silver-colored, raised area, usually at the
site of electrical contact (electrical burn)
singed nasal hairs, mucosal burns, voice
changes, coughing, wheezing, soot in
mouth or nose, and darkened
sputum (with smoke inhalation and
pulmonary damage).
OkDoKeY
Potential impairment
Body area

Impairment

Face

Facial
disfigurement
(contractures of eyelids,
nose, mouth, ears, and
adjacent facial skin)
Inability to close eyes
Loss of facial expression
Teeth malalignment
Drooling and inability to
close lips
Lower lip eversion
Loss of normal cervical
spine range of motion
Limited visual fields
Difficulties with anesthesia,
due to decreased neck
range of motion
Protraction of shoulders
Kyphosis
Functional scoliosis
Decreased
respiratory

Neck

Trunk

function
Breast entrapment
Perineal banding
Axilla

Hands

Arms
legs

and

Foot
ankle

and

Type 1: either anterior or

posterior contracture
Type
2:
anterior
and
posterior contracture with
sparing of dome
Type
3:
anterior
and
posterior contracture and
axillary dome
Metacarpophalangeal
extension deformities
Wrist extension deformities
Proximal
interphalangeal
flexion deformities
Interdigital
web
contractures
Clawing of fourth and fifth
digits
Thumb
contractures
(adduction,
opposition,
flexion, or extension)
Antecubital banding and
flexion
Posterior popliteal banding
and flexion
Anterior hip banding and
flexion
Medial
and
lateral
malleolar scarring
Hyperextension
of
metatarsophalangeal joints
Equinovarus
Cavus foot
Rocker bottom deformity

Systemic Complications of Burn Injury

Body System
Complications
Respiratory
Inhalation
injury,
restrictive
pulmonary
pattern
(which may OCCur with a
burn on the trunk),
atelectasis, pneumonia,
microthrombi, and adult
respiratory
distress
syndrome
Cardiovascular
Hypovolemiaihypotensio
n,
pulmonary
hypertension,
subendocardial ischemia,
anemia,
and
disseminated
intravascular
coagulopathy
Gastroinrestina
Stress
ulceration,
V
hemorrhage,
ileus,
genitourinary
ischemic co\iris,
cholesrasis, liver failure,
and
urinary
rract
infection
Renal
Edema,
hemorrhage,
acute tubular necrosis,
acure
renal failure
paz
Electrical burns
Complications specific to electrical injury
include the following"s:

Cardiovascular:
Cardiac
arrest
(ventricular fibrillation for electric current
or asystolic for lightning), arrhythmia
(usually sinus tachycardia or nonspecific
ST changes) secondary to alterations in
electrical conductivity of the heart,
myocardial contusion or infarction, or
heart wall or papillary muscle rupture
Neurologic: Headache, seizure, brief loss
of consciousness or coma, peripheral
nerve injury (resulting from ischemia),
spinal cord paralysis (from demyelination),
herniated nucleus pulposus, or decreased
attention and concentration
Orthopedic: Dislocations or fractures
secondary to sustained
muscular contraction or from a fall during
the burn injury

Other: Visceral perforation or necrosis,

cataracts, tympanic
membrane rupture, anxiety, depression,
or post-traumatic stress disorder
Chemical Burns
pulmonary complications (e. g. , airway
obstruction from bronchospasm, edema,
or epithelial sloughing) and metabolic
complications (e. g., liver necrosis or renal
dysfunction from prolonged chemical
exposure).
Ultraviolet and Ionizing Radiation Burns
Gastrointestinal: Cramps, nausea,
vomiting, diarrhea, and bowel ischemia
Hematologic: Pancytopenia (decreased
number of red blood cells, white blood
cells, and platelets), granulocytopenia
(decreased
number
of
granular
leukocytes), thrombocytopenia (decreased
number of platelets), and hemorrhage
paz
Complications
Possible complications of burns include:
loss of function (burns to face, hands,
feet, and genitalia)
total occlusion of circulation in extremity
(due to edema from circumferential burns)
airway obstruction (neck burns) or
restricted respiratory expansion (chest
burns)
pulmonary injury (from smoke inhalation
or pulmonary embolism)
adult respiratory distress syndrome (due
to left-sided heart failure or myocardial
infarction)
greater damage than indicated by the
surface burn (electrical and chemical
burns) or internal tissue damage along
the conduction pathway (electrical burns)
cardiac arrhythmias (due to electrical
shock)
infected burn wound
stroke, heart attack, or pulmonary
embolism (due to formation of blood clots
resulting from slower blood flow)

burn shock (due to fluid shifts out of the

vascular compartments, possibly leading
to kidney damage and renal
failure)
peptic ulcer disease (due to decreased
blood supply in the abdominal area)
disseminated intravascular coagulation
(more severe burn states)
added pain, depression, and financial
burden (due to psychological component
of disfigurement).
Vascular: Endothelium destruction
OkDoKeY
Deprh

Appearance

Su perficial (first- Pink to red

degree)-epidermis
With or without
injured
edema
Dry
appearance
without blisters
Blanches
Sensation intact
Skin intact when
rubbed
Moderate
partial- Pink ro mortied red
thickness (second
or red with edema
degree)-superficial Moist appearance
dermis injured
with blisters
Blanches with slow
capillary refill
Sensation intact
Deep
partial- Pink ro pale ivory
thickness (second
Dry
appearance
degree)-deep
with blisters
dermis injured with May blanch wirh
hair follicles and slow capillary refill
sweat glands
Decreased
intact
sensation
ro
pinprick
Hair
readily
removed
Full-thicknessWhite, red, brown,
entire
dermis or black (charred if
injured
fourth degree)
(third degree) or Dry
appearance
fat, muscle, and
without blanching
bone
injured May be blistered
(fourth degree)
Insensate
to
pinprick
Depressed wound
Source: Data from P Wiebelhaus, SL
1999;62:52-75.

Healing

Pain

3-5
days
by Tenderness to
epithelialization
tOuch or
Skin appears intact painful

5 days to 3 wks by
epithelialization
Pigmentation
changes
are likely

Very painful

3 wks to mas by
Very painful
granulation tissue
formation and
epithelialization
Scar
formation
likely

Not
able
regenerate

to No pain, perhaps
an ache

Hansen, Burns: handle with care. RN

Systemic effects
Once the burn covers more than 30% of
TBSA, the injury has a systemic effect due
to
Molecular structural alterations
o Release of toxic metabolites
o
Release
of
antigen
and
immunomodulatory agents
Histamine,
Serotonin,
Bradykinin,
Nitric oxide, etc.
Causes systemic shock, cardiovascular,
respiratory
and
renal
failure,
immunosuppression
and
hypermetabolism.
(Evers et al 2010)
Cardiovascular Changes
Myocardial depression
o Myocardial contractility decreased
Oedema formation
o Capillary permeability is increased
o leads to loss of intravascular proteins
and fluids to the interstitial compartment
Hypovolemia
o Secondary to oedema and rapid fluid
loss from surface of wound

Peripheral
and
splanchnic
vasoconstriction occurs
o May cause renal failure
These changes may lead to systemic
hypotension
and
end
organ
hypoperfusion.
(Evers et al, 2010)
Respiratory Changes
Inflammatory
mediators
cause
bronchoconstriction
and
pulmonary
oedema
severely burnt adults acute respiratory
distress syndrome (ARDS) can occur
Exacerbated in the case of inhalation
injury (Evers et al 2010)
Metabolic Changes
Hypermetabolism begins approximately
five days post burn
o Metabolic state is initially suppressed by
the effects of acute shock
o Can persist for up to two years post
injury
Inflammatory,
milieu cause

hormonal

and

cytokine

Increased body temperature

Increased
oxygen
and
glucose
consumption
Increased CO2 and minute ventilation
Increased heart rate for up to 2 years
post burn
(Jeschke et al 2007; Grisbrook et al 2012a;
Hurt et al 2000)
This hyper metabolic state leads to energy
substrate release from protein and fat
stores Protein catabolism
Loss of lean muscle mass and wasting
Potentially fatal if structure and function
of organs are compromised
(Jeschke et al 2007; Hurt et al 2000)
In adults with burns of 25% TBSA,
metabolic rate ranges from 118-210%
that of predicted values. At 40% TBSA, the
resting metabolic rate in a thermoneutral
environment is
o 180% at acute admission
o 150% at full healing
o 140% post 6 months
o 120% at 9 months
o 110% at 10 months
(Jeschke et al 2007; Herndon and Tomkins
2004)
Gastrointestinal Changes
Impaired gastrointestinal motility
Impaired digestion and absorption
Increased intragastric pH
Feeding difficulties exacerbate effects of
hyper metabolism (Evers et al 2010)
Immunological Changes
(Hettiaratchy and Dziewulski 2004)
Immune deficiency occurs despite the
activation of the immune system. High
risk of infection, particularly while wounds
are open.

VII.

DIFFERENTIAL DIAGNOSIS CONDITIONS

sulivan

DIFFERENTIAL DIAGNOSIS CONDITIONS

The following pieces of information should

be included in the physiotherapists
database.

DIAGNOSTIC TOOLS/ PROCEDURES OR TEST

Physiotherapy Assessment of the
Burn Patient
The physiotherapist must be aware of the
importance of an early and adequate
assessment of Burn patients for optimal
functional and cosmetic outcomes to
minimise the impact of the trauma long
term. They must have a concise
knowledge of the assessment procedure
through from Accident and Emergency to
the ward, onto the rehabilitation setting
and out in the community. The following
information
is
gathered
through assessment, and a
treatment
plan
is
formulated,
constantly
reassessed and revised.

Presenting Complaint
Inhalation injury
There should be a high index of suspicion
if the patient was injured in an enclosed
space and / or

had a reduced level of consciousness

aggressive
respiratory
treatment
to

(ANZBA 2007; Hettiaratchy

and Papini 2004)
Physiotherapy aims
1.
Prevent
respiratory
complications
2. Control Oedema
3. Maintain Joint ROM
4. Maintain Strength
5.
Prevent
Excessive
Scarring
Patients are at high risk due
to:
1. Injury factors - Inhalation injury; burn
area
systemic
inflammatory reaction
syndrome
involving
the lungs; depth of
burn and scarring
2. Patient factors Reduced
ambulation
and
mobility;
increased bed rest;
increased
Pain; pre-existing comorbidities
3. Iatrogenic factors
Skin reconstruction surgery; invasive
monitoring and procedures, management
in critical care
Database/Subjective Assessment

commence immediately

(ANZBA 2007; British Burn Association

2005; Eisenmann-Klein 2010)
Total Body Surface Area (TBSA)
o The rule of nine or the Lund and Brower
chart are used to assess the TBSA

o The Lund and Brower Charts are

considered to be more accurate than rule
of nines, but both are commonly used.
Measure burn wound areas by mapping
wound 1% TBSA patients hand (palm
and fingers included)
Note: when calculating burn size area,
oedema should not be included.
A burn of > 20 25% TBSA creates a
global or systemic inflammatory reaction
affecting all body organs and indicates a
significant risk for the respiratory system
Burn Type and Depth
It is important to monitor extent of
tissue destruction as it alters for at least
48 hours post burn injury
o Jacksons burn wound model.
It is rare that a burn will present with a
single depth.
Likely to change depending on the early
management e.g. appropriate first aid and
other patient factors. (ANZBA 2007;
British Burn Association 2005; EisenmannKlein 2010)
Burn Site and Impact
Develop awareness of the implication of
burn to special areas of the body. the
following require specialised treatment
o Hands
o Face
o Perineum
o Joints
This is in consideration of the complexity
of the post burn reconstruction and
potential
functional
impact
of
inappropriate management of these
important body areas.
History of Presenting Complaint
History of the incident with specific
attention paid to the mechanism of injury.
First aid was adequate first aid given? If not, suspect deeper burn injury
Falls was there any indication that the
patient fell? From what height? possible
head injury, sprains or fractures
Electrical injury voltage involved? Parts
of body in contact with earth? suspect
nerve and deep muscle injury with high
voltage current

Explosions falls, high velocity injuries,

possible tympanic membrane injury loss
of hearing and difficulty communicating
Passage to hospital and time to
admission
ANZBA 2007; British Burn Association
2005; Eisenmann-Klein 2010;
Medical and Surgical History
Any surgical or medical management
o Pain medication
o Debridement
o Escharectomy
o Flaps/grafts
o Any particular MDT instructions to
be followed
ANZBA 2007; British Burn Association
2005; Hettiaratchy et al 2004
Past Medical/ Drug History
Social History
ANZBA 2007; British Burn Association
2005; Eisenmann-Klein 2010
Basic ADL e.g., dressing, bathing, eating
and Instrumental ADL e.g., shopping,
driving, home maintenance
Past physical function e.g., mobility,
climbing stairs, reaching, lifting
Past physical fitness e.g., strength,
flexibility, endurance, balance
Social support and home Situation
Occupation
Particularly important for hand burns
Psychosocial/ Yellow Flags
Self-image
Coping style
Mental health
Emotional behaviour
ANZBA 2007; British Burn Association
2005; Hettiaratchy et al 2004
Considerations for the Assessment of
Hand Burns
The area of the hand that is injured has a
huge impact on recovery. A burn on the
hand can have detrimental effects for
ADLs and functioning. Dependant on the

area and depth of the burn, it may lead to

significant deformity.
Assessment
Evaluation and classification of the size
and depth of the burn of the hand
Post burn Hand Deformities
o First web adduction contractures
o Web space contractures
o Dorsal skin contractures
o Digital flexion contracture
o Boutonniere deformity
o Dorsal skin deficiency
o Digital loss secondary to ischemia
o
Median
and
ulnar
nerve
compression
o Syndrome

Conservative
or
operative
treatment
o Surgical managementremoval
of eschar, transplantation of skin
grafts, flap
Early postoperative physical therapy
Functional rehabilitation
Secondary and tertiary corrections if
necessary
Objective Assessment
Inspection and Palpation
To assist with treatment planning,
pertinent data that can be gathered from
the direct observation of a patient or
palpation include the following:
Level of consciousness
Presence of agitation, pain, and stress
Location of the burn or graft, including
the proximity of the burn to a joint
Presence and location of dressings,
splints, or pressure garments
Presence of lines, tubes, or other
equipment
Presence and location of edema
Posture
Position of head, trunk, and extremities
Heart rate and blood pressure,
respiratory rate and pattern, and oxygen
saturation
Pain Intensity Assessment

Observational
behavioural
pain
assessment scales should be used to
Measure pain in children aged 0 to 4 years
e.g. The FLACC scale

Faces pain rating scale can be used in

children aged 5 years and older. E.g. The
Wong-Baker FACES pain rating scale
VAS can be used in children aged 12
years and older and adults.
Inhalation Assessment
Physical signs to observe:
Hoarse vocal quality
Singed facial / nasal hair
Oedema
Erythema (Superficial reddening of the
skin, usually in patches, as a result of
injury or irritation causing dilatation of the
blood capillaries)
Soot stained sputum
Stridor
Inspiratory and end expiratory crackles
on auscultation
Chest x-ray changes
(ANZBA
2007;
Association 2005)

British

Burn

Oedema Assessment
Overview
An acute burn injury creates inflammation
and swelling. After wound healing is
complete, scar tissue maturation and
contraction may lead to sub-acute and
chronic states of oedema formation. With
time, oedema fluid changes in its
composition and creates greater stiffness
and resistance to movement within the
tissues. This is particularly notable when
surgical reconstruction is required and if
the burn is circumferential around limbs or
other structures. See table 4 for clinical
stages of oedema.
(ANZBA 2007; British Burn Association
2005; Eisenmann-Klein 2010)
Mobility Assessment
The assessment and treatment of mobility
can be separated into two aspects - the
limbs & trunk, and general functional
mobility
(e.g.
transferring
and
ambulation). A physiotherapist must also

consider factors such as increased bed

rest, increased pain and pre-existing comorbidities.
(ANZBA 2007; Hettiaratchy et al 2004;
Settle 1986; Siemionow and EisenmannKlein 2010)
Limb and Trunk
Assessment of limbs and trunk should
include joint ROM and strength. Limiting
factors may include pain, muscle length,
trans-articular burns, scar contracture and
the individual specificity of the burn.
General Functional Mobility
Assessment of general mobility is twofold,
prevention
of
complications
associated with prolonged bed rest and
the
restoration
of
function
&
independence. All functional transfers,
gait, endurance and balance should be
assessed once the patient is medically
stable.
Factors to consideration when assessing
mobility:
Posture
Demands of vocational roles and
ADLs
Cardiovascular
mobilisation

response

to

Neurological status
Pain
Concomitant
bearing status

injuries/weight-

MANAGEMENTS

Pharmacological Pain Management

Regular and repeated pain assessments

are used to monitor the effectiveness of
During the first 48 hours
analgesia.
Decreased organ blood supply alters the Thus there is no standard treatment of
burns patients, each requires individual
clearance of drugs
assessment.
the
cornerstone
of
pain
The body then enters a hyper metabolic Opioids:
management
in
burns,
and
are
available
in
state,
a
variety
of
potencies,
methods
of
o Associated with increased clearance
administration and duration of action.
of analgesia.
used
to
effectively
manage
Variations in levels of acute phase plasma Opioids
background
pain,
Positive
Side Effects
Examples of Opioids
with well-timed and
Effects
effective doses of
opioids
used
Pain relief
Respiratory distress
Morphine
separately
to
manage procedural
Increased
Itch
Oxycodone
pain
comfort
Simple analgesics:
paracetamol can be
Morphine
Nausea and vomiting
Fentanyl: potent, rapid
used in conjunction
related
to Opioid
tolerance
onset, short acting opioid. with opioids, to give
reduced
requiring
increasing Used for procedural pain a synergistic effect
Postdoses
management.
comparable to a
traumatic
Opioid
induced Remifentaril: ultra-short higher opioid dose.
Paracetamol is an
stress
hyperalgesia
(OIH)
acting opiate.
disorder
increased
sensitivity, Alfentaril: short acting, effective anti-pyretic
and has few contrathroughout
the
body used for post-procedural
indications.
following opioid exposure analgesia.
NSAIDS: synergistic
Provide poor defence
with opioids and can
against
central
reduce opioid dose
and thus reduce
sensitisation
side-effects.
Not
Physical dependence
used
in
wide
spread
common in long term use
burns due to already
increased risk of
renal failure and peptic
ulceration.
There
is
potential
to
increase
bleeding in large burns
also, due to the antiplatelet effect.
Possible side effects
analgesics:
- Drowsiness

of

- Adverse reaction
and total body water volume further impact
upon effectiveness an analgesia.

- Nausea
aspiration

and

increased

risk

of

Impaired
communication

and standard distraction and relaxation when

undergoing dressing changes (Mott et al
2008).
- Postural hypotension, and fainting
Non-

memory

Pharmacological

Pain

Sleep Normalisation:
disrupted sleep occurs in up to 50% of burn
patients and links have been established
between poor sleep quality and pain
severity, as well as pain and prolonged
experiences
of
sleep
disturbance.
Normalisation of the 24hour day, with a
bedtime routine, within the limits of the
hospital environment is aimed for to
promote sleep, with the use of analgesics
and night sedation.

The following is a synthesis of information

form the following articles: Summer et al
(2007), Richardson and Mustard (2009),
ANZBA (2007) and de Jong et al (2007)
Overall, the levels of evidence to support
the use of alternative therapies for pain
relief are of poor quality. However, no
negative side effects were reported in the
literature reviews and these therapies are
all used in conjunction with pharmacological Music therapy:
management to optimize pain relief for the this is thought to target pain via the gate
control theory. This suggests that music
individual.
serves as a distraction from noxious stimuli.
Also,
the
anxiety
related
to
the
Psychological techniques:
rehabilitation
of
burns
can
increase
the
beneficial for reducing anxiety and
providing patients with coping methods for activation of the sympathetic nervous
pain levels and durations. These include system. Music uses all three cognitive
relaxation,
distraction
and
cognitive strategies employed in pain and anxiety
behavioural therapy (CBT). CBT is beneficial management (imagery envisioning events
in the management of complex pain that are inconsistent with pain, selfproblems and can reduce fear and anxiety statements and attention-diversion devices
to direct attention away from the pain ad
associated with activities or environments.
redirects it to another event) (Ferusson and
Voll 2004; Presner et al 2001). A systematic
Hypnosis:
review of music therapy among pregnant
a state of increased suggestibility,
women, medical-surgical patients and
attention and relaxation. In the burn
critical care patients showed statistically
patient hypnosis is used in the management
significant reductions in pain scores. Of the
of procedural pain and anxiety. The use of
seventeen studies reviewed by Cole and
hypnosis clinically is increasing but its
LoBiondo-Wood
(2012),
13
studies
usefulness is dependent on the individuals
demonstrated the positive effects of music
hypnotic susceptibility, high baseline pain
on pain. Other positive findings of the
and the skill of the practitioner. The current
studies included reduced anxiety, muscle
best available evidence for management of
tension, blood pressure and heart rate. A
procedural pain was found for active
burn specific study included showed
hypnosis, rapid induction analgesia and
reduced pain levels during and after the
distraction relaxation.
debridement,
reduced
anxiety
and
decreased muscle tension during and after
Virtual Reality:
dressing changes.
immersing the patient in a virtual world has The Cochrane Review of music as an adjunct
shown some effect on procedural pain to pain relief concluded that music and
control and is better than hand-held gaming other non-pharmacological therapies could
devices. However, the equipment is costly have a synergistic effect to produce
and bulky and not always suitable for clinically important
paediatric
intervention.
A
paediatric benefits on pain intensity or analgesic
intervention, using hand-held game devices requirements and thus requires further
which provide augmented reality was study. This is based on the studies indicating
trialled among 3-14 year olds. This has that music resulted in reduced pain intensity
shown significantly lower pain scores than and reduced opioid requirements. The

reported changes in both of these outcomes 5. Reduce the extent of a cosmetically

were small however, and their clinical unacceptable scar
importance is unclear (Cepeda et al 2006).
(Glassey 2004; BBA Standard 6 2005)
Paediatric Burn Pain
(Richardson and Mustard 2009)
Choosing the Correct Method of
children 0-4 years represent approx. 20% Reconstruction
all hospitalised burn patients
The simplest management involves
In preschool aged children the half-life of conservative wound care and dressings,
opioids (morphine and alfentanyl) are 50% while the most complex is free-flap
those in adults. Higher dosage required.
reconstruction. When deciding on the most
appropriate intervention, a surgeon must
Risk of accidental overdose due to consider the extent of the missing tissue
difficulties with pain evaluation resulting in and the structures effected (Glassey 2004).
overestimation of childs pain
Generally, a superficial partial thickness
Childs environment has huge effect on pain burn will heal with conservative treatment
perception. Parents presence and aid (secondary intention) in 10 days to 3 weeks,
during dressing change can have beneficial unless infection occurs. Primary intention
occurs if a wound is of such size that it can
for procedural pain and reducing anxiety.
be closed directly without producing undue
tension at the wound site. Delayed primary
Medical
and
surgical
closure occurs once a suspected infection
has been cleared. Deep partial and full
Reconstruction Post Burn Injury
thickness burns both require surgical
The impact of reconstructive surgery post intervention. Surgery normally takes place
burn injury has a major impact on a patient. within the first 5 days post injury to prevent
As an allied health professional, we must infection which could extend the depth of
work as part of an MDT in order to ensure the tissue loss (Glassey 2004).
successful surgery while at the same time
ensuring long term health and function.
Timely burn wound excision and skin
grafting form the cornerstone for acute burn
surgical management (Klein 2010).Surgery
for burned patients is not normally indicated
until 48 hours after injury, when the depth
of the burn has been established. The only
exception is when necrotic tissue is evident
then early excision may be required. A
plastic surgeon must reconstruct the injured
body part in a way that is extensible,
sensate
and
cosmetically
acceptable
(Glassey 2004). In addition to this, they
must rebuild or replace muscles, tendons,
joints and nerves to ensure they are
appropriately intact.
Aims
1. Achieve would closure
2. Prevent infection
3. Re-establish the function and properties
of an intact skin
4. Reduce the effect of burn scars causing
joint contractures

Skin Grafts
A skin graft is the transportation of skin
from one area of the body to another.
(Glassey 2004)

A graft is an area of
skin that is separated from its own blood
supply and requires a highly vascular
recipient bed in order for it to be successful.
Prior to grafting, the process of wound
debridement must take place. Wound
debridement involves removing necrotic
tissue, foreign debris, and reducing the
bacterial load on the wound surface
(Cardinal et al 2009).This is believed to
encourage better healing. The following are
the methods available for grafting onto a
debrided wound to obtain closure:
Autograft (split skin graft) (own
skin)
Allograft (donor skin)
Heterograft or xenografts (animal
skin)
Cultured skin
Artificial skin
(Glassey 2004)
Meshed vs. Sheet Grafts
Sheet grafts are those which are not altered
once they have been taken from the donor
site.

Meshed grafts are those which are passed

through a machine that places fenestrations
(small holes) in the graft. Meshed grafts
have advantages over sheet grafts of 1)

allowing the leakage of serum and blood

which prevents haematomas and seromas
and 2) they can be expanded to cover a
larger surface area.
(Klein 2010)
Criteria to be met Pre- Grafting
Diagnosis of DEEP tissue loss
Patient is systemically fit for surgery
Patient has no coagulation abnormalities
Sufficient donor sites available
Would clear of streptococcus
(Glassey 2004)
The Donor Site
The thigh is the
most common donor
site for split thickness
skin grafts (STSG). A
split thickness graft
involves a portion of
the thickness of the dermis while a full
thickness skin graft (FTSG) involves the
entire thickness of the
dermis (Klein 2010). The most common site
for full thickness skin grafts is the groin.
Cosmetic areas such as the face should be
avoided for graft donation.
The donor site should just be left with
a superficial or a superficial partial thickness
wound which will heal in 10-14 days and
may be reused if necessary. Often, the
donor site can be more painful than the
recipient due to exposure of nerve endings
(Glassey 2004).
Skin Substitutes
Skin Substitutes are defined as a
heterogeneous group of wound cover
materials that aid in wound closure and
replace the functions of the skin either
temporarily or permanently
(Halim et al 2010)
Conventionally, STSG and FTSG have
been found to be the best option for burn
wound coverage (Halim et al 2010).
However, in cases of extensive burn injury,
the supply of autografts is limited by
additional wound or scarring at donor sites.
For this reason, skin substitutes will be
required. Skin substitutes require higher
cost, expertise and experience than

autografts. However, they also offer

numerous advantages in the form of rapid
wound
coverage
requiring
a
less
vascularised wound bed, an increase in the
dermal component of a healed wound,
reduced inhibitory factors of wound healing,
reduced
inflammatory
response
and
reduced scarring (Halim et al 2010).
Currently, there are various skin
substitutes on the market but scientists and
engineers are working towards producing
the optimal skin substitute. As a general
rule, skin substitutes are classified as either
temporary or permanent

and synthetic or
biological. A very

clear

and

concise

overview of the different skin substitutes

available for burn injuries is provided in
Halim et al (2010).
The Recipient Site
The graft should take within 5 days
and will provide a permanent covering of
the injury. A graft should always be placed
over bleeding, healthy tissue to ensure it is
vascularised for survival (Glassey 2004).
Post-operatively the graft site is dressed to
ensure pressure is created over the graft to
limit haematoma formation. The body part
is immobilised in an anti- deformity position
at first in order to prevent shearing forces
that could disrupt the graft (Edgar and
Brereton 2004). Some very mobile body
parts, such as the hand, may require
splinting to ensure joint immobility.
Process of Graft Take
Serum Inhibition (24-48hrs): fibrin layer
formation and diffusion of fluid from the
wound bed
Inoscultation (day 3): capillary budding
from the wound bed up into the base of the
graft

Capillary
in-growth
(Glassey 2004)

and

remodelling raised upon a specific blood vessel which

allows them to be lifted on a narrow pedicle
and ensures greater perfusion for survival.

Reasons for Graft Failure

Inadequate blood supply to wound bed

Flap anatomical Composition

Flaps are also classified depending on
Graft movement
their composition, i.e. which layers of the
Collection of fluid beneath graft (e.g. skin they contain. The composition is often
clear from the name of the flap.
haematoma)
Infection (e.g. streptococcus)
The grafts properties (e.g. vascularity of
donor site) (Glassey 2004)

Skin Flap- epidermis, dermis and

superficial fascia
Fasciocutaneous Flap- epidermis, dermis
and both superficial and deep fascia
Muscle Flap-muscle belly without overlying
structures
Myocutaneous Flap-muscle belly with the
overlying skin
Osseous Flap- bone
Osseomyocutaneous Flap-bone, muscle,
skin
Composite Flap- Contains a no. Of
different tissues such as skin, fascia, muscle
and bone. (Glassey 2004)

Skin Flaps
The difference between a skin graft and a
skin flap is that a skin flap contains its
own vasculature and therefore can be used
to take over a wound bed that is avascular.
A skin graft does not have this ability
(Glassey 2004). When speaking about grafts
and flaps in the research, skin flaps is often
incorporated into the term skin grafts.
Tissues which a skin graft will not take over
include and which a skin flap will include:
Bone without periosteum
Relocation of Flaps
The third way in which flaps are
Tendon without paratenon
classified is by their method of relocation.
Flaps are defined as either local or distant
Cartilage without perichondrium
depending on the distance between the
(Glassey 2004)
donor and recipient sites (Glassey 2004).
Categorisation of Skin Flaps
Based on three factors:
1. Vascularity
2. Anatomical composition
3. Method of relocation (Glassey 2004)
Vascularity
Flaps can be classified as either
random pattern flaps or axial flaps
depending on their vascularity. Random
pattern flaps are not raised on any
particular major blood vessel, but instead
are raised on smaller branches of
these blood vessels known as the
subdermal plexus. These flaps
are limited in size to ensure distal
parts do not become ischemic
(Glassey 2004). Examples of
these flaps include Z-plasty, V-Y
advancement flap, rotation flap
and transposition flap. Axial
flaps, on the other hand, are

Local Flaps:
Rotation or transpositional flaps are
tissue that is lifted and manipulated to
cover the local defect, maintaining their
connection with the body. Therefore, they
are never fully excised.
Advancement flaps are those in
which the tissue is moved directly forward
to cover the defect, e.g. V-Y flaps used to
cover finger-tip injuries
(Glassey 2004).
Distant Flaps:

 Pedicled flaps are those which are

transferred to another area of the body but
the
vascular
attachment
is
always
maintained and so the distance it can travel
depends on the length of the pedicle.
Free flaps are those in which the
tissue is completely separated from the
body and transferred to another area and
the
vascular
supply
is
reestablished by anastomising the
blood vessels (Glassey 2004).

Early initiation of rehabilitation is essential

to maximise functional outcomes for the
patient
The pain and psychological distress
of a burn has a massive impact on
compliance
o An empathetic, encouraging
and
understanding
approach
is

Rehabilitation Post Burn Injury

Significant improvements in the
medical and surgical management
of burns has occurred in the last
century. Increased survival rates
mean that focus is turning to
achieving optimal functional outcomes.
necessary
Burn survivors often suffer from
The urgency and importance of
o permanent scarring, reduced range beginning early rehabilitation should be
of motion, weakness, and impaired communicated in a clear but gentle manner
functional capacity
(Procter 2010).
o psychological and social problems,
which significantly affect their ability
to resume their normal activities post
discharge
Rehabilitation
requires
a
prolonged,
dedicated and multidisciplinary effort to
optimise patient outcomes, as inpatients
and outpatients.
(Schneider et al 2012; Disseldorp et al 2007;
Esselman, 2007)
The
aims
of
the
multidisciplinary
rehabilitation of a burn include:
Prevention of additional/deeper
injuries
Rapid wound closure
Preservation of active and passive
ROM
Prevention of infection
Prevention
structures

of

loss

Early functional
(Kamolz et al 2009)

of

functional

rehabilitation

The physiotherapist may only have a role in

achieving some of these goals.
Above all cause no harm.

Role of the Physiotherapist

in the Rehabilitation of the
Acute Burn Pa For the
purpose
of
clarity,
the
following section has been
divided into acute, sub acute
and
chronic
rehabilitation.
However, rehabilitation is a
continuum, and significant
crossover may occur. All of the
following concepts apply to
burns on any part of the body,
with specialised treatment
addressed for the hand where
necessary.
Depending on the size and the
severity of the injury this
stage may last from a few
days to a few months (Procter
2010)
Patient
Acute phase of inflammation
Pain

1mmobilisation
post
skin
reconstruction
surgery
Oedema increasing for up to 36 hours post
injury
Stopping movement and function of the
Hypermetabolic response, peaking at five body parts involved should be enforced
after skin reconstruction for a burn has
days post injury
taken place. When a body part must be
Early synthesis and remodelling of collagen immobilised, it should be splinted or
positioned in an anti-deformity position for
Aims
the minimum length of time possible
Reduce risk of complications
(Edgar and Brereton 2004; ANZBA 2007)
o Reduce oedema, particularly where
it poses a risk for
The following is a table drawn up using
impinging
on
peripheral current literature on the recommended
circulation or airways
immobilisation times for the various skin
grafts:
Predisposition to contractures
The times frames for mobilisation post Prevent deformities/loss of range
surgery outlined in this booklet are merely a
guide taken from an analysis of current
Protect/promote healing
literature and are NOT a replacement for the
specific time frames directed by the
Common treatment techniques
operating surgeon or consultant (ANZBA
Immobilisation
2007).
o Bed rest
For a physiotherapist the most important
o Splinting
concepts to grasp are:
Positioning
What is the minimum timeframe of
Immobilisation
immobilisation post-surgery
What structures MUST be immobilised
Rationale for Immobilisation
Special considerations for movement,
function and ambulation dependent on
Positioning in the Acute Stage
*Modify according to burn area, patient
pain and medical status.*

 Rigid or soft
Donor sites and the structures repaired or
excised during surgery.

Dorsal or Volar

Immobilisation of the hand

Digit, hand or forearm based

(Boscheinen-Morrin 2004)

Deformity Prevention
Static Splinting
The most common deformity associated A serial static splint is a device with no
with burns is the claw deformity. It
involves extension of the MCP joints,
flexion of the PIP joints, adduction of the
thumb and flexion of the wrist (Kamolz
2009). This position is also referred to as
the intrinsic minus position.
Position of Safe Immobilisation
The position of safe immobilisation of the
burned hand is essentially the opposite of
the above claw deformity position. This
position involves: 20-30 wrist extension, 8090 degrees flexion MCP joints, full extension
PIP and DIP joints and palmar abduction of
the thumb
(Boscheinen-Morrin 2004).
Splinting
Physiological rationale for splinting (Kwan
2002)
Scar tissue is visco-elastic. It will elongate
steadily within a certain range. When this
stretching force is released, there is an
immediate decrease in the tissue tension
but a delay in the retractions of the tissue to
a shorter length. These stress relaxation
properties of visco elastic scar tissue means
it can accommodate to stretching force
overtime. Dynamic and static splinting
provide this prolonged low stretching force.
Categories of Splints
Static or Dynamic
Supportive or Corrective

moving parts designed to be remoulded as a

contracture improves. The most common
serial static splint you will come across is a
thermoplastic palmar splint moulded in the
position of safe immobilisation.

A static progressive splint is a device

designed
to
stretch
contractures
through
the
application
of
incrementally adjusted static force to
promote lengthening of contracted
tissue (Smiths 2009). There are various
types of static progressive splints
available depending on the area
affected. One such static progressive splint
is a finger flexion strap splint. This type of
splint is used in the treatment of MCP
extension contractures. The flexion straps
serially stretch scar bands along the dorsum
of hand and wrist causing extension
contracture. The stretching force is localised
to the MCP joints by applying the straps via
a wrist extension splint. This stabilises the
wrist providing static support below the MCP
joint
(Kwan 2002).
Dynamic Splinting
A dynamic splint is one which aids in
initiating and performing movements by
controlling the plane and range of motion of
the injured part. It applies a mobile force in
one direction while allowing active motion in

Splinting Precautions

Splints need to be cleaned regularly to

prevent colonization by microbes which may
lead to wound infection
(Wright et al 1989; Faoagali et al 1994)
Unnecessary use of splinting may cause
venous and lymphatic stasis, which may
result in an increase in oedema
(Palmada et al 1999)
Precaution must be taken to ensure that
splints do not product friction causing
unnecessary trauma to the soft tissues
(Duncan et al 1989).
Precaution must be taken to ensure that
splints do not produce excessive pressure.
There is particular risk of pressure injury to
skin after burn injuries due to
potential skin anaesthesia
(Leong 1997).
Splinting should not be used in
isolation but as an adjunct to a
treatment regime

the opposite direction. This mobile force is

usually applied with rubber bands, elastics
and springs (Smith 2009).
Dynamic extension splints are most
commonly used in the treatment of palmar
and / or finger burns (i.e. flexion
contractures). All the finger joints including
the MCP, PIP and DIP joints are in full
extension (Smith 2009).
Dynamic flexion splints are used in the
treatment of dorsal hand burns. During
wound healing and subsequent scar
maturation, the skin on the dorsal aspect of
the hand can markedly contract limiting
digit flexion. A dynamic flexion splint in the
sub-acute stage of dorsal hand burns can
aid in the prevention of MCP joint extension
contractures (Kwan 2002).

Management
of
Oedema
Elevation
Elevation of the hand above heart level is
the most simple and effective ways to
prevent and decrease oedema (Kamolz
2009).

these

Bradford sling can be used to facilitate

elevation. This type of sling facilitates both
elevation and protection of wound area
while still allowing movement. Its foam
design also reduces the risk of the
development of pressure points or friction
(Glassey 2004).
When a patient is admitted with severe
burns of a large TBSA they are at risk of
systemic inflammation. Therefore, not only
must the affected limb be placed in
elevation,
the following precautions should also be
taken
Elevation of the head: This aids chest
clearance, reduces swelling of head, neck
and upper airways. It is important not place
a pillow underneath the head in the case of
anterior neck burns as there is a risk of neck products to patients with excessive hand
flexion contractures
and finger oedema. Their use is based on
the principle of compression to reduce
Elevate all limbs effected
oedema which is heavily supported by
evidence (Latham and Radomski 2008).
Feet should be kept at 90
Role of the Physiotherapist in the
Rehabilitation of the Sub Acute Burn
Care must be taken to reduce the risk of Patient
pressure sores.
(Procter 2010)
Beyond the acute stage of immobilisation,
Coban
inpatient and outpatient rehabilitation
Coban wrap can be used to decrease hand typically
consists
of
a
variety
of
oedema. The main advantage of Coban interventions including pressure garment
wrap is that it does not stick to underlying therapy, silicone therapy, scar massage,
tissue, making it suitable for use in the range
of
motion
and
mobilisation
acute stages of burns (Lowell 2003). There techniques, strengthening, functional and
is currently limited quantity of evidence to gait retraining, and balance and fine motor
support the use of Coban wrap in the retraining ( Schneider et al, 2012).
treatment of Oedema. In 2003 Lowell et al Interventions should be tailored according to
carried out a case study involving a subject a full patient assessment.
with dorsal hand burns.
As it would be unethical to withhold
treatment, physiotherapy intervention as a
Oedema Glove/Digi Sleeve
whole is not well investigated.
Schneider et al (2012) found a
These
are
hand
specific
oedema
management products. There is currently no significant improvement in contractures;
specific evidence available to support the balance and hand function with inpatient
through
a
longitudinal
efficacy of oedema gloves or digi sleeves in rehabilitation,
the reduction of oedema. However it is observational study of eleven people.
common practice in Irish hospital to provide However, in the following section, we will
Neutral position of hips

attempt to display the

commonly used modalities.
The patient
Primary closure of wound
Scar remodelling
Scar contraction

evidence

for as it is the most effective means of reducing

oedema by means of active muscle
contraction (Glassey 2004). If this is not
possible
due
to
sedation,
surgical
intervention etc. then positioning the
patient is the next best alternative (see
immobilisation and position).

Passive ROM
Passive ROM exercises in the acute stage
are contraindicated as applying passive
Limit effects of scar contraction/prolonged stretching forces may result in future
to
the
burned
structures
positioning on range of motion and function damage
(Boscheinen-Morrin 2004). Applying these
Address effects of prolonged bed rest
passive manoeuvres in the acute stage will
result in increased oedema, haemorrhage
Common modalities
and fibrosis of the burned tissues (Cooper
Mobilisation- both mobility and specific 2007).
joint mobilisation
The biomechanical principle of creep when
Scar management adjuncts
passive stretching. A slow sustained stretch
o
Pressure
garments,
silicone, is more tolerable for patient and more
massage
effective for producing lengthening (Kwan
Continuation of oedema/ positioning 2002).
management where necessary
Passive joint mobilisations can begin
during the scar maturation phase once the
Mobilisation
The advantages of general mobilisation for a scar tissue has adequate tensile strength to
burns patient to counteract the effects of tolerate friction caused by mobilisation
prolonged bed rest are no different to that techniques
(Boscheinen-Morrin and Connolly
of a surgical or medical patient. Burns
2001).
patients should be mobilised as early as
possible to avoid deconditioning and
possible
respiratory
complications Frequency, Duration Recommendations
associated
with
prolonged
bed
rest Physiotherapy intervention should be twice
(Esselman 2007).
daily with patients prescribed frequent
active exercises in between sessions.
As outlined in the above introduction, due to
the ethical issues surrounding withdrawal or For the sedated patient gentle passive
modification of treatment the evidence range of motion exercises should be done 3
surround the optimal duration, frequency times a day once indicated (Boscheinenand methods of physiotherapy interventions Morrin and Connolly 2001).
in the treatment of burn patients is unclear.
Dependent on the severity of the burn
Despite this lack of clarify surrounding these
active and very gentle passive range of
issues it is clear that both active and
motion exercises for the hand and fingers
passive mobilisation plays a key role
are begun from day one of injury.
throughout the stages of burn recovery.
Below
is
a
summary
of
the
Contraindications
recommendations
from
the
currently
literature on passive and active mobilisation Active or Passive range of motion
exercises should not be carried out if there
of burns.
is suspected damage to extensor tendons
(common occurrence with deep dermal and
Active ROM
full thickness burns). Flexion of the PIP joints
Depending on the need for immobilisation
should be avoided at all costs to prevent
gentle active ROM exercises is the preferred
extensor tendon rupture. The hand should
treatment during the acute stage of injury
be splinted in the position of safe
Aims
Optimise scar appearance

immobilisation or alternatively a volar PIP

extension splint until surgical intervention The following is an examination of the
(Boscheinen-Morrin and Connolly 2001) is evidence and recommendations for use in
discussed.
the most common of these, including
silicone gel, pressure garment therapy, and
Range of motion exercises are also massage. The positioning and mobilisation
contraindicated post skin grafting as a advice above is all applicable, and should be
period of 3-5 days immobilisation is required continued
in
the
management
of
to enable graft healing (Boscheinen-Morrin hypertrophic scars where necessary.
and Connolly 2001).
Scar Outcome Measures
Practical factors to consider when 1. Vancouver Burn Scar Scale (VBSS/VSS)
mobilising
Be aware of dressing clinic/daily dressing 2. Patient and Observer Scar Assessment
changes. Mobilisation should coincide with Scale (POSAS)
this as it is important to monitor the wound
Vancouver Burn Scar Scale (VBSS/VSS)
during AROM frequently.
Use: Most familiar burn scar assessment.
Timing of pain relief. This should be timed Measures: pigmentation, pliability, thickness
appropriately to ensure maximal benefit and vascularisation
during treatment sessions.
(Fearmonti et al 2010).
Reliability:
Not
enough
evidence to make it
Observe the patient carrying out the AROM
a
gold
standard
OCM.
Moderate to high
and PROM exercises prior to beginning
overall
inter
rater
reliability.
Test- Retest and
treatment. Also observe the patient taking
intra

rater
reliability
has
not been
on/off splints.
assessed for burn scars to date
(Durani et al 2009).
Always monitor for post exercise pain and
Validity: When compared with POSAS
wound breakdown.
scale, validity was evident
Avoid blanching for long period as you may
(Durani et al 2009)
compromise vascularity.
Sensitivity: Most Scar OCM rely on
categorical/ordinal data with few levels
The patient may present with a reduced
which provides limited sensitivity and can
capacity for exercise secondary to increased
only
identify
considerable
differences
metabolic rate, altered thermoregulation
between scars
and increased nutritional demands.
(Fearmonti et al 2010).
Postural hypotension may be present due
to prolonged bed rest and low haemoglobin. Patient and Observer Scar Assessment
Scale (POSAS)
(ANZBA 2007)
Use: Measures pigmentation, vascularity,
thickness, relief, pliability and surface area.
Scar Management
Abnormal scarring is the most common Also includes assessment of patient pain,
complication of burn injuries, with the itching, colour, stiffness, thickness and
estimated prevalence of > 70% of those relief. The only scale to measure subjective
who suffer burn injuries (Anzarut et al, aspects of pain and pruritus (severe itching)
(Fearmonti et al 2010).
2009). Not only do hypertrophic scars cause
Reliability:
Good
internal
consistency and
psychosocial
difficulties
through
their
reliability
cosmetic appearance, they may also be
(Durani et al 2009)
painful, pruritic, and they may limit range of
Validity:
Good
concurrent
validity
motion where they occur on or near a joint
(Durani
et al 2009)
(Morien et al 2009; Polotto 2011).
Sensitivity:
Like
the
VBSS/VSS
above,
Hypertrophic scars require a continuum of
limited
sensitivity
due
to
categorical/ordinal
dedicated and specialised treatment from
the acute stage to many years post data
(Fearmonti et al 2010)
treatment
(Procter, 2010, ANZBA 2007).

Further studies are required to validate the

reliability and validity of these scales as
they are considered to be very subjective
measures
(Durani et al 2009).
Scar scales like the Vancouver Burn Scar
Scale (VBSS/VSS) and the Patient and
Observer Scar Assessment Scale (POSAS)
are cost effective and can be easily
transferred within a clinical setting. To
optimise the scar scales, photographic
evidence of the scar at timed intervals is of
great value also to the clinician
(Brusselaers et al 2010)
Silicone

Hypoxia is a stimulus to angiogenesis and

tissue growth in wound healing, as a
consequence removing the hypoxia stops
new tissue growth. This theory has been
contraindicated by other researchers.
6) Mast cells: It is suggested that silicone
results in an increase of mast cells in the
cellular matrix of the scar with subsequent
accelerated remodelling of the tissue.

7) Static electricity: Static electricity on

silicone may influence the alignment of
collagen deposition (negative static electric
field generated by friction between silicone
gel/sheets and the skin could cause collagen
realignment and result in the involution of
Silicone Overview
scars.
The use of silicone gel or sheeting to
(Bloemen et al 2009; Momeni et al 2009)
prevent and treat hypertrophic scarring is
still relatively new. It began in 1981 with Pressure Garment Therapy (PGT)
treatment of burn scars
Though the effectiveness of PGT has never
(OBrien & Pandit 2008). been proven, it is a common treatment
The physiological effects of silicone in the modality
for
reducing
oedema
and
treatment of scarring remain unclear. Below managing hypertrophic scars
is a summary of the current hypotheses
(Procter, 2010).
surrounding the physiological effects of Aims
silicone. This summary has been adapted
o Reduce scarring by hastening
from the most recently published literature
maturation
on this topic.
o Pressure decreases blood flow
1) Hydration Effect: Hydration can be
o Local hypoxia of hypervascular
caused by the occlusion of the underlying
scars
skin. It decreases capillary activity and
collagen production, through inhibition of
o Reduction in collagen deposition
the proliferation of fibroblasts
o Therefore
o Decreases scar thickness
2) Increase in temperature: A rise in
temperature increases collagenase activity
o Decreases scar redness
thus increased scar breakdown.
o Decreases swelling
3) Polarized Electric Fields: The negative
o Reduces itch
charge within silicone causes polarization of
the scar tissue, resulting in involution of the
o Protects new skin/grafts
scar.
o Maintains contours
4) Presence of silicone oil: The presence of
(Procter 2010)
silicone has been detected in the stratum
corneum of skin exposed to silicone.
However
other
researchers
suggest The exact physiological effects of how
positively
influences
the
occlusive products without silicone show pressure
maturation of hypertrophic scars remain
similar results.
unclear.
5) Oxygen tension: After silicone treatment Below is a summary of the current
the hydrated stratum corneum is more hypotheses surrounding the physiological
permeable to oxygen and thus oxygen effects of pressure garments. This summary
tension in the epidermis and upper dermis has been adapted from the most recently
rises. Increased oxygen tension will inhibit published literature on
the hypoxia signal from this tissue.

1)
Hydration
effect:
decreased
scar
hydration results in mast cell stabilization
and
a
subsequent
decrease
in
neurovascularisation
and
extracellular
matrix production. However this hypothesis
is in contrast with a mechanism of action of
silicone, in which an increase of mast cells
causes scar maturation.

Lack of a scientific evidence to established

optimum pressure
Non-Compliance
(
due
movement, appearance)

to

comfort,

Heat and perspiration

Swelling of extremities caused by inhibited
venous return

2) Blood flow: a decrease in blood flow

causes excessive hypoxia resulting in Skin breakdown
fibroblast degeneration and decreased
levels of chondroitin-4-sulfate, with a Web space discomfort
subsequent
increase
in
collagen
Inconvenience
degradation.

3) Prostaglandin E2 release: Induction of Personal hygiene difficulties possibility of

prostaglandin E2 release, which can block infection
fibroblast proliferation as well as collagen
Allergies to material
production
(MacIntyre & Baird 2006; Glassey 2004)
(MacIntyre & Baird 2006)
Massage
Recommendations for practice and
safety considerations
Pressure: 15 mmHg has been noted as
the minimum to elicit change, and pressures
of above 40 mmHg have been found to
cause complications. Both Anzarut et al
(2009) and Engrav et al (2010) used
pressures of between 15 and 25 mmHg.
Time: It is recommended that garments are
worn for up to 23 hours a day, with
removal for cleaning of the wound and
garment, and moisturisation of the wound.
(Procter 2010; Anzarut et al 2009 and
Bloeman et al 2009).
Duration: garments
can be worn as soon
as wound closure
has been obtained,
and the scar is
stable enough to
tolerate
pressure.
Post grafting, 10-14
days
wait
is
recommended,
at
the discretion of the
surgeon
(Bloeman et al 2009).
Garments should be worn for up to one
year, or until scar maturation
(Anzarut et al 2009; Engrav et al 2010 and
Bloeman et al 2009).
Possible complications/ confounding
factors for use of PGT

Five principles of scar massage:

1. Prevent adherence
2. Reduce redness
3. Reduce elevation of scar tissue
4. Relieve pruritus
5. Moisturise (Glassey 2004)
Scar Massage Techniques
Retrograde massage to aid venous return,
increase lymphatic drainage, mobilise fluid
Effleurage to increase circulation

Static pressure to reduce pockets of

swelling
Finger and thumb kneading to mobilise the
scar and surrounding tissue

 Skin rolling to restore mobility to tissue

interfaces
Aerobic and Resistance Training Post
Burn
Wringing the scar to stretch and promote
collagenous remodelling
Rationale for Aerobic and Resistance
Training
Low cardiorespiratory endurance has been
(Holey and Cook 2003) found to be a concern for all

Frictions to loosen adhesions

Recommendations for practice and

safety considerations.
Insufficient consistency in literature with
regards to protocols on frequency or
duration of treatment. Suggestions for
practice include
(Shin and Bordeaux, 2012, Morien et al,
2008)
Clean hands essential

(Willis et al 2011)
Aerobic capacity as measured by VO2 peak
and time to fatigue has been found to be
lower in adults and children of >15% TBSA
at one year post burn, compared to age
matched healthy controls
(Willis et al 2011; McEntine et al 2006)

Muscular strength and lean body mass has

Use non irritating lubricant, free of any been found to be significantly less in
patients suffering from burns of >30%
known sensitisers.
TBSA, particularly in exercises requiring a
Modify practice according to patient stage high velocity (Disseldorp et al 2007; Ebid et
of healing, sensitivity and pain levels.
al 2012). The systemic effects caused by
large surface area burns means that
Contraindications:
weakness may be global, not just local to
Shin and Bordeaux 2012 the site of the injury
Compromised integrity of epidermis
(Grisbrook et al 2012b)
Acute infection
Reduced lean body mass, endurance and
Bleeding
strength has been associated with limited
standing/walking tolerance, reduced upper
Wound dehiscence,
limb function and lower health related QOL
and ability to participate in activities
Graft failure
Intolerable discomfort

(Grisbrook et al 2012b).

This has been found to persist beyond

discharge from hospital despite routine
The Role of the Physiotherapist in the physiotherapy and occupational therapy in
Rehabilitation of the Chronic Burn hospital (Disseldorp et al 2007). Though
protein metabolism begins to normalise 9Patient.
12 months post burn, patients are still found
The patient
Hypersensitivity to emollient

Healing process may continue for up to two

All found a decrease of up to 20% in lean
years, as scar tissue remodels and matures
muscle mass compared to age matched
May require functional retraining and controls
integration back into the community and
Adults with a TBSA >30% suffered a
activities.
significant decrease in torque, work and
It is important to note that though scar power in the quadriceps muscles compared
management is initiated in the sub-acute to age matched controls.
(De Lauter et al 2007)
phase, it may need to be continued long
term, as many patients suffer from Exercise and Hypermetabolism
continuing limitation to range of motion
(Procter 2010).

Though exercise requires an increase in

energy expenditure and metabolism for a
short period of time no adverse effects have
been found with regard to exacerbating
hypermetabolism or protein catabolism.
o All studies investigating the effects of
exercise on lean body mass found it to
increase,
particularly
with
resistance
training

room temperature compared

matched healthy controls.

to

age

No significant difference in average skin

temperature between burned and healthy
children.
Significantly increased skin temperature in
healthy versus burned skin per child.

( Grisbrook et al 2012b; Suman and Austin et al, 2003 studied 3 adults with >
Herndon 2007; Suman et al 2001; Przkora et 60% TBSA, 3 with between 30-40 TBSA and
al 2007) 2 unburned patients post 1 hr cycling at 35
degrees and 60% humidity
o Suman et al, 2001, found an increase of None showed significant intolerance for
15% in resting energy expenditure in heat as measured by heart rate and core
children with burns of >40% TBSA who were temperature, measured rectally
not treated with resistance and aerobic
exercise, while the REE of those who No significant difference in whole body
participated in the intervention remained sweat rate
stable.
Overcompensation by healthy skin in the
o Suggested that exercise may have
burned patients.
sympathetic nervous system attenuating
effects
Suggested physical history was a factor in
determining
patients
ability
to
A balance of resistance and aerobic thermoregulate. Therefore adaptations may
exercise may cause a decrease in SNS occur through training.
activity, decreasing catabolic effects.
o Exercise is required to integrate dietary However, studies involving heat loads of 40
amino acids into lean muscle mass degrees have found a significant inability to
(Herndon and Tomkins 2004)
maintain adequate thermoregulation. Due to
the small study numbers of the above, and
**Thermoregulation
the controversy surrounding the efficacy of
Human skin produces sweat to dissipate measuring core temperature accurately, it is
heat in response to thermal stress (McEntine advised that patients are closely monitored
et al 2006). A proper sweat response initially during aerobic exercise for signs of
requires functional integrity of the
heat intolerance.
Sweat glands
***Inhalation injury and pulmonary
Skin circulation
insufficiency
Neural control of the skin (McEntine et al
Long
term
pulmonary
function
is
2006)
compromised in some patients post severe
Full thickness burns damage the dermal burn
appendages including sweat glands. These Lasts several years
are not replaced by grafting. There is also a
Documented in both children and adults
decreased density of sweat glands in the
(Grisbrook et al 2012a)
donor site post grafting
(Esselman et al 2007). Caused by
However, McEntine et al 2006 found that in
o Smoke inhalation
15 children with an average of 55% TBSA
o Direct thermal damage to airways
there was
No
significant
difference
in
core
o Pulmonary oedema
temperature, measured tympanically, pre or
post 20 minutes of treadmill exercise at
o Respiratory tract infection

o Complications from intubation

o Recurrent infection leading to
chronic inflammation
Less likely to cause dysfunction in
<30% TBSA, no injury over torso, and
no inhalation injury
(Willis et al 2011)
Evidence for impact on aerobic and exercise
capacity conflicting (Grisbrook et al 2012a).
However Willis et al (2011) studied 8 males
post > 15% TBSA burns at one year post
injury, and found
Significantly decreased FEV1, peak VO2
and time to fatigue, in the burned patients
No significant decrease in SpO2 at
baseline or peak VO2- however, the SpO2 of
burned patients took significantly longer to
stabilise at baseline post exercise.
No significant difference in participation
levels in physical activity, though burn
survivors were more likely to participate in
work rather than leisure activity.
Burns survivors were less likely to
participate in vigorous intensity exercise
over 9 METs

There have been no studies investigating

optimal frequency.
Intensity: All studies used between 65
and 85% predicted heart rate max, with
one study using interval training of 120
seconds 85% HRM and 120 seconds of 6570 HRM. All studies obtained positive effect,
with none directly comparing intensities to
determine the optimum. De Lauteur et al
(2007), concluded that whether the patient
gradually increased their intensity by
working to a specific quota each week, or if
they simply worked at their target heart rate
for as long as they could tolerate, there was
no significant difference in gains in aerobic
capacity.
Type: All interventions used treadmill
training, whether walking or running.
Time: All studies recommended the
duration of treatment be 12 weeks, with
the exception of Paratz et al, 2012, who
investigated a high intensity six week
programme. However, the specific results of
this are unknown. Sessions were 20-40
minutes in length, with the majority using
30 minutes (Grisbrook et al 2012; De
Lauteur et al 2007; Przkora et al 2007)

Resistance Training Summary and

Therefore, decreased pulmonary function
Recommendations for Practice
did not prevent them from participating
Exercise prescription: Post two years,
The lower relative intensity of their Grisbrook et al (2012b) found that burned
exercise may have caused their decreased patients responded to resistance exercise
similarly to controls. Therefore, normal
aerobic capacity.
guidelines may be adequate.
All of the above factors must be considered Frequency: All studies investigating the
as both a contributor to the patients loss of effects of resistance training used a
strength and aerobic capacity, and a frequency of three times per week. There
potential limiter of their ability to participate have been no studies to investigate the
in
therapy.
Careful
monitoring
and optimum frequency for resistance training in
modification of treatment according to this population. Suman et al (2001),
suggested that a break of more than 48 hrs
individual response is advised.
must be given between bouts of resistance
Aerobic
Training
Summary
and training.
o
Resistance
exercise
causes
Recommendations for Practice
microtrauma to muscles already in a
compromised state.
Exercise prescription:
Frequency: The majority of papers which
o Resistance exercise in burned
investigated an aerobic intervention used 3
patients stimulates protein synthesis
times per week as their frequency (De
as in unburned subjects- However; a
Lauteur et al 2007; Grisbrook et al 2012).
longer period of recovery may be
These obtained significant improvements.
required for optimum results.
However, Przkora et al (2007) used a
frequency of 5 times per week with children.
Type/ Intensity: Children: using free
weights or resistive machines: 1 set of

50-60% of the patients 3 RM week 1,

followed by a progression to 70-75% for
week 2-6 (4-10 repetitions), and 80-85%
week 7-12, (8-12 repetitions) (Suman et al
2001; Suman and Herndon 2007).
Isokinetic training: 10 reps at 150
degrees per second, using 1-5 sets for the
1st -5th session,6 sets for the 6th -24th
session, and 10 sets from 25th to 36th
session, with three minute rests between
sets. (Ebid et al 2012).
Mixed
and
functional
strength
training:
Grisbrook
et
al
(2012b)
commenced on the biodex, targeting
specific muscle groups for the desired
functional goal, and progressed to resistive
machine and finally free weight training
using functional items. Intensity was 5060% of 1 RM initially, for 10-15 reps,
adjusting as 1 RM increased. While no
studies have compared the optimum
type/intensity of exercise, this may be the
optimum approach. Providing functional
exercises may also increase motivation and
compliance.
Time: All the studies used a protocol of 12
weeks. There were no studies comparing
the efficacy of shorter or longer time
frames, however, given that loss of lean
body mass is a possible cause of strength
loss post burn, an exercise programme of
longer than eight weeks is probably required
to ensure hypertrophy and optimum gains in
the burn patient (Suman et al 2001)
Safety Considerations for Strength and
Aerobic Training:
Initiating aerobic and strength training:
studies stipulated a minimum of six
months to two years post burn before
initiation of programmes, though many
subjects were included who had been
burned
many
years
before.
These
participants
all
benefited
from
the
interventions.
Suman and Herndon (2007) suggested that
the time frame of 6 months post burn was
chosen based on clinical experience
because by this time paediatric patients
with >40% TBSA burns were
o 95% healed
o ambulatory
o had had the opportunity to return
home

Therefore, more favourable psychological

status
There were no studies investigating early
training
o With extensive burns, adequate
healing of wounds and medical
stability required before initiating
aerobic/strength exercise
Other safety considerations:
Though exercise has been shown to
increase lean body mass, liaison with
doctors concerning anabolic steroids and
medication and with dieticians regarding
optimal nutrition is recommended in order
to
ensure
correct
management
of
hypermetabolisim.

Caution should be used with regard to

impaired thermoregulation. Monitoring of

heart rate and blood pressure may be

advisable, particularly on initiation of
exercise and when exercising with additional
thermal stress. Manage the environment to
minimise
thermal
stress
initially
in
particular.
Particularly those at risk of reduced
pulmonary function post burn (i.e., >30%
TBSA, injury to torso, or inhalation injury),
monitor SpO2 and RPE during exercise.
Allow additional rest periods to allow SpO2
to return to normal levels post exercise, as
this has been shown to be delayed.

REFERENCES

Physical medicine and rehabilitation

3rd edition
Braddoms physical medicine &
rehabilitation 5th edition
Handbook of Pathophysiology
(January 15, 2001): by Springhouse

Corporation, With 13 Contributors,

Springhouse By OkDoKeY
Delisasphysical medicine &
rehabilitation 5th edition
Marieb human anatomy & physiology
9th editionz
Physical rehabilitation 5th edition by
sulivan
Acute care handbook for physical
therapist 4th edition by paz