Complications specific to electrical injury
include:
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.
Cardiovascular: Cardiac arrest
(ventricular fibrillation for electric current
or systole for lightning), arrhythmia (usually
sinus tachycardia or nonspecific
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
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.
Superficial Partial-Thickness Burn
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 gelatin-
like 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 partial-
thickness 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 re-
epithelialization. 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) ischemia of the area. Frequently,
during the first few days is necessary. thrombosis of superficial blood vessels is
Demarcation becomes evident after several apparent and no blanching of the tissue is
days as the dead tissue begins to slough. observed. The deep red color of the tissue
Hair follicles that penetrate into the deeper results from hemoglobin fixation liberated
dermal regions below the burn level remain from destroyed red blood cells.
viable. Preservation of hair follicles and Hair follicles are completely
new hair growth will indicate a deep destroyed, so body hairs pull out easily. All
partialthickness burn rather than a full- nerve endings in the dermal tissue are
thickness injury, and there is a destroyed so the wound will be insensate
corresponding greater potential for (without feeling); however, a patient still
spontaneous healing. Particularly important may experience a significant amount of
factors that determine which epidermal pain because adjacent areas of partial-
structures survive and which die include thickness burn usually surround a full-
the thickness of the skin in a particular thickness injury.
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 partial-
thickness 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
 A major problem that arises from grafting will be necessary. Grafting is
deep burns is the damage to the peripheral discussed in detail in the section titled
vascular system. Because large amounts of Surgical Management of the Burn Wound.
fluid leak into the interstitial space beneath
unyielding eschar, the pressure in the Subdermal Burn
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

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
may be necessary. An escharotomy is a a heat source and routinely occurs as a
midline lateral incision of the eschar the result of contact with electricity. Extensive
length of an extremity or chest wall. Figure surgical and therapeutic management is
24.6 shows an escharotomy and the result necessary to return a patient to some
of pressure that forces the incision to gape. degreeof function.
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 full-
thickness 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 re-
epithelialization of the wound. All epithelial
cells have been destroyed, and skin
 II. EPIDEMIOLOGY
approximately 90% of all burn deaths
worldwide occurring in low- and middle-
income 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

ANATOMY, PHYSIOLOGY, KINESIOLOGY Langerhans cells, macrophages, and
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
Biological Barriers
DNA
Langerhans cells in epidermis present
antigens to lymphocytes
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 Thin epidermis and lacks stratum lucidum
may be absorbed from the intestines or Lacks dermal papillae
may be produced Has more sebaceous glands
by the skin when the skin is exposed to Fewer sweat glands, sensory receptors
ultraviolet light (particularly sunlight).It is than thick skin
converted to Thick - up to 6 mm thick on palms of
its active form by the body in 2 steps, hands and soles of feet
occurring first in the liver and completed in Hairless
the kidneys. In Covers palms of hands and soles of feet
its active form, vitamin D acts as a Thick epidermis and a distinct stratum
hormone to regulate calcium absorption lucidum
from the intestine Epidermal ridges are present due to well
and to regulate levels of calcium and developed, numerous dermal papillae.
phosphate in the bones. Vitamin D Lacks sebaceous glands, has more sweat
deficiency causes glands
Rickets Sense receptors are also more densely
When the body is deficient in vitamin D, it packed.
is unable to properly regulate calcium and Layers of the Skin
phosphate
levels. If the blood levels of these minerals Epidermis
becomes low, the other body hormones Types of Cells
may Keratinocytes
stimulate release of calcium and phosphate 90 % of epidermal cells are keratinized
from the bones to the bloodstream. contains keratin (fibrous protein)
Chemical conversion of many substances protects and waterproofs the skin
Blood Reservoir preferential shunting of Melanocytes
blood as needed 8% of the epidermal cells
Types of Membranes - thin sheet-like produces melanin
structures that protect parts of the body contributes to skin color and absorbs UV
Serous Membranes light
Line body cavities that have no opening Langerhans cells
to the outside Arise from red bone marrow and
Secrete a watery fluid called serous fluid migrate to the epidermis
that lubricates surfaces. Constitute small portion of epidermal cells
Mucous Membranes Participate in immune responses
Line cavities and tubes that open to the Easily damaged by UV light
outside Merkel cells
Synovial Membranes Least numerous of the epidermal cells
Form the inner lining of joint cavities Found in the deepest layer of the
Secrete a thick fluid called synovial fluid epidermis
Cutaneous Membrane also known as Along with tactile discs, they function in
skin sensation of touch
Characteristics of Skin Layers of epidermis
The integument covers the entire body
and is the largest organ ~ 2 meters and Stratum corneum
heaviest organ 25-30 layers of dead flat keratinocytes
16% of body mass of the body. Shed continuously and replaced by cells
Composed of the epidermis and dermis from the
Pliable, yet durable deeper strata
Thickness: 1.5 to 6.0 mm Serves as a water, microbe, injury barrier
Types of Skin
Thin - 1-2 mm on most of the body and 0.5 Stratum lucidum
mm in eyelids Present only in thick skin
Hairy 3-5 layers of clear, flat, dead
Covers all parts of the body except palms keratinocytes
of hands and soles of feet 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 to
coagulation of constituent proteins.

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).
 Flame burns occur when the patients
clothes, hair or skin catch light. The effect
of damage from house or car fires is
IV. ETIOLOGY exacerbated by the inhalation of toxic
gases from burning household furniture,
Thermal burns, the most common type, leading to severe inhalation injuries as well
frequently result from: as burns.
residential fires Contact burns from contact with molten
automobile accidents metal or plastic are common in industry. An
playing with matches unconscious patient may sustain burns
improper handling of firecrackers from contact with a cooker or a hot
scalding accidents and kitchen radiator.
accidents (such as a child climbing Electrical burns due to electrical current
on top of a stove or grabbing a hot from plugs, sockets and wiring. Deep
iron) structures can be involved at the current
parental abuse of (in children or entry and exit sites on the body. The
elders) patients cardiac status requires close
clothes that have caught on fire. monitoring.
Chemical burns result from contact, Elsevier
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.
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 second-
degree 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
 function
Signs and symptoms Breast entrapment
Signs and symptoms depend on the type Perineal banding
of burn and may include:
Axilla Type 1: either anterior or
localized pain and erythema, usually
posterior contracture
without blisters in the first 24 hours (first-
Type 2: anterior and
degree burn)
posterior contracture with
chills, headache, localized edema, and
sparing of dome
nausea and vomiting (more severe first-
Type 3: anterior and
degree burn)
posterior contracture and
thin-walled, fluid-filled blisters appearing
axillary dome
within minutes of the injury, with mild to
moderate edema and pain Hands Metacarpophalangeal
(second-degree superficial partial- extension deformities
thickness burn) Wrist extension deformities
white, waxy appearance to damaged area Proximal interphalangeal
(second-degree deep partial-thickness flexion deformities
burn) Interdigital web
white, brown, or black leathery tissue and contractures
visible thrombosed vessels due to Clawing of fourth and fifth
destruction of skin elasticity (dorsum of digits
hand most common site of thrombosed Thumb contractures
veins), without blisters (third-degree burn) (adduction, opposition,
silver-colored, raised area, usually at the flexion, or extension)
site of electrical contact (electrical burn) Arms and Antecubital banding and
singed nasal hairs, mucosal burns, voice legs flexion
changes, coughing, wheezing, soot in Posterior popliteal banding
mouth or nose, and darkened and flexion
sputum (with smoke inhalation and Anterior hip banding and
pulmonary damage). flexion
OkDoKeY Medial and lateral
malleolar scarring
Foot and Hyperextension of
Potential impairment ankle metatarsophalangeal joints
Equinovarus
Body area Impairment Cavus foot
Face Facial disfigurement Rocker bottom deformity
(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
Neck Loss of normal cervical
spine range of motion
Limited visual fields
Difficulties with anesthesia,
due to decreased neck
range of motion
Trunk Protraction of shoulders
Kyphosis
Functional scoliosis
Decreased respiratory
Systemic Complications of Burn Injury Other: Visceral perforation or necrosis,
Body System Complications cataracts, tympanic
Respiratory Inhalation injury, membrane rupture, anxiety, depression,
restrictive pulmonary or post-traumatic stress disorder
pattern
(which may OCCur with a Chemical Burns
burn on the trunk),
atelectasis, pneumonia, pulmonary complications (e. g. , airway
microthrombi, and adult obstruction from bronchospasm, edema,
respiratory distress or epithelial sloughing) and metabolic
syndrome complications (e. g., liver necrosis or renal
Cardiovascular Hypovolemiaihypotensio dysfunction from prolonged chemical
n, pulmonary exposure).
hypertension,
subendocardial ischemia, Ultraviolet and Ionizing Radiation Burns
anemia, and
disseminated
intravascular Gastrointestinal: Cramps, nausea,
coagulopathy vomiting, diarrhea, and bowel ischemia
Gastroinrestina Stress ulceration, Hematologic: Pancytopenia (decreased
V hemorrhage, ileus, number of red blood cells, white blood
genitourinary ischemic co\iris, cells, and platelets), granulocytopenia
cholesrasis, liver failure, (decreased number of granular
and urinary rract leukocytes), thrombocytopenia (decreased
infection number of platelets), and hemorrhage
Renal Edema, hemorrhage, paz
acute tubular necrosis,
acure Complications
renal failure Possible complications of burns include:
paz loss of function (burns to face, hands,
feet, and genitalia)
total occlusion of circulation in extremity
Electrical burns (due to edema from circumferential burns)
Complications specific to electrical injury airway obstruction (neck burns) or
include the following"s: restricted respiratory expansion (chest
Cardiovascular: Cardiac arrest burns)
(ventricular fibrillation for electric current pulmonary injury (from smoke inhalation
or asystolic for lightning), arrhythmia or pulmonary embolism)
(usually sinus tachycardia or nonspecific adult respiratory distress syndrome (due
ST changes) secondary to alterations in to left-sided heart failure or myocardial
electrical conductivity of the heart, infarction)
myocardial contusion or infarction, or greater damage than indicated by the
heart wall or papillary muscle rupture surface burn (electrical and chemical
Neurologic: Headache, seizure, brief loss burns) or internal tissue damage along
of consciousness or coma, peripheral the conduction pathway (electrical burns)
nerve injury (resulting from ischemia), cardiac arrhythmias (due to electrical
spinal cord paralysis (from demyelination), shock)
herniated nucleus pulposus, or decreased infected burn wound
attention and concentration stroke, heart attack, or pulmonary
Orthopedic: Dislocations or fractures embolism (due to formation of blood clots
secondary to sustained resulting from slower blood flow)
muscular contraction or from a fall during
the burn injury
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 Healing Pain

Su perficial (first- Pink to red 3-5 days by Tenderness to

degree)-epidermis With or without epithelialization tOuch or
injured edema Skin appears intact painful
Dry appearance
without blisters
Blanches
Sensation intact
Skin intact when
rubbed
Moderate partial- Pink ro mortied red 5 days to 3 wks by Very painful
thickness (second or red with edema epithelialization
degree)-superficial Moist appearance Pigmentation
dermis injured with blisters changes
Blanches with slow are likely
capillary refill
Sensation intact
Deep partial- Pink ro pale ivory 3 wks to mas by Very painful
thickness (second Dry appearance granulation tissue
degree)-deep with blisters formation and
dermis injured with May blanch wirh epithelialization
hair follicles and slow capillary refill Scar formation
sweat glands Decreased likely
intact sensation ro
pinprick
Hair readily
removed
Full-thickness- White, red, brown, Not able to No pain, perhaps
entire dermis or black (charred if regenerate an ache
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 Hansen, Burns: handle with care. RN
1999;62:52-75.
Systemic effects Increased body temperature
Increased oxygen and glucose
Once the burn covers more than 30% of consumption
TBSA, the injury has a systemic effect due Increased CO2 and minute ventilation
to Increased heart rate for up to 2 years
Molecular structural alterations post burn
o Release of toxic metabolites
o Release of antigen and (Jeschke et al 2007; Grisbrook et al 2012a;
immunomodulatory agents Hurt et al 2000)
Histamine, Serotonin, Bradykinin, This hyper metabolic state leads to energy
Nitric oxide, etc. substrate release from protein and fat
stores Protein catabolism
Causes systemic shock, cardiovascular, Loss of lean muscle mass and wasting
respiratory and renal failure, Potentially fatal if structure and function
immunosuppression and of organs are compromised
hypermetabolism. (Jeschke et al 2007; Hurt et al 2000)
(Evers et al 2010)
In adults with burns of 25% TBSA,
Cardiovascular Changes metabolic rate ranges from 118-210%
Myocardial depression that of predicted values. At 40% TBSA, the
o Myocardial contractility decreased resting metabolic rate in a thermoneutral
Oedema formation environment is
o Capillary permeability is increased o 180% at acute admission
o leads to loss of intravascular proteins o 150% at full healing
and fluids to the interstitial compartment o 140% post 6 months
Hypovolemia o 120% at 9 months
o Secondary to oedema and rapid fluid o 110% at 10 months
loss from surface of wound (Jeschke et al 2007; Herndon and Tomkins
Peripheral and splanchnic 2004)
vasoconstriction occurs
o May cause renal failure Gastrointestinal Changes
Impaired gastrointestinal motility
These changes may lead to systemic Impaired digestion and absorption
hypotension and end organ Increased intragastric pH
hypoperfusion. Feeding difficulties exacerbate effects of
(Evers et al, 2010) hyper metabolism (Evers et al 2010)

Respiratory Changes Immunological Changes

Inflammatory mediators cause (Hettiaratchy and Dziewulski 2004)
bronchoconstriction and pulmonary Immune deficiency occurs despite the
oedema activation of the immune system. High
severely burnt adults acute respiratory risk of infection, particularly while wounds
distress syndrome (ARDS) can occur are open.
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, hormonal and cytokine

milieu cause
VII. DIFFERENTIAL DIAGNOSIS CONDITIONS
sulivan
DIFFERENTIAL DIAGNOSIS CONDITIONS
 The following pieces of information should
be included in the physiotherapists
DIAGNOSTIC TOOLS/ PROCEDURES OR TEST
database.
Physiotherapy Assessment of the
Burn Patient Presenting Complaint
The physiotherapist must be aware of the Inhalation injury
importance of an early and adequate There should be a high index of suspicion
assessment of Burn patients for optimal if the patient was injured in an enclosed
functional and cosmetic outcomes to space and / or
minimise the impact of the trauma long
term. They must have a concise
knowledge of the assessment procedure
through from Accident and Emergency to had a reduced level of consciousness
the ward, onto the rehabilitation setting aggressive respiratory treatment to
and out in the community. The following
information is gathered
through assessment, and a
treatment plan is
formulated, constantly
reassessed and revised.

(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 commence immediately
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 co-
morbidities
3. Iatrogenic factors
Skin reconstruction surgery; invasive
monitoring and procedures, management (ANZBA 2007; British Burn Association
in critical care 2005; Eisenmann-Klein 2010)

Database/Subjective Assessment 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; Eisenmann-
Klein 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; British Burn
Association 2005)
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 co-
morbidities.

(ANZBA 2007; Hettiaratchy et al 2004;

Settle 1986; Siemionow and Eisenmann-
Klein 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 two-
fold, 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 response to
mobilisation
Neurological status
Pain
Concomitant injuries/weight-
bearing status
 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 body then enters a hyper metabolic Opioids: the cornerstone of pain
state, management in burns, and are available in
o Associated with increased clearance a variety of potencies, methods of
of analgesia. administration and duration of action.
Variations in levels of acute phase plasma Opioids used to effectively manage
Positive Side Effects Examples of Opioids background pain,
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
Post- doses management. comparable to a
traumatic Opioid induced Remifentaril: ultra-short higher opioid dose.
stress hyperalgesia (OIH) acting opiate. Paracetamol is an
disorder increased sensitivity, Alfentaril: short acting, effective anti-pyretic
and has few contra-
throughout 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
sensitisation and thus reduce
Physical dependence side-effects. Not
common in long term use used in wide spread
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 anti-
platelet effect.

Possible side effects of

analgesics:
- Drowsiness
- Adverse reaction
and total body water volume further impact - Nausea and increased risk of
upon effectiveness an analgesia. aspiration
 - Impaired memory and standard distraction and relaxation when
communication undergoing dressing changes (Mott et al
2008).
- Postural hypotension, and fainting
Sleep Normalisation:
Non- Pharmacological Pain disrupted sleep occurs in up to 50% of burn
patients and links have been established
The following is a synthesis of information between poor sleep quality and pain
form the following articles: Summer et al severity, as well as pain and prolonged
(2007), Richardson and Mustard (2009), experiences of sleep disturbance.
ANZBA (2007) and de Jong et al (2007) Normalisation of the 24hour day, with a
Overall, the levels of evidence to support bedtime routine, within the limits of the
the use of alternative therapies for pain hospital environment is aimed for to
relief are of poor quality. However, no promote sleep, with the use of analgesics
negative side effects were reported in the and night sedation.
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
individual. control theory. This suggests that music
serves as a distraction from noxious stimuli.
Psychological techniques: Also, the anxiety related to the
beneficial for reducing anxiety and rehabilitation of burns can increase the
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, self-
problems and can reduce fear and anxiety statements and attention-diversion devices
associated with activities or environments. to direct attention away from the pain ad
redirects it to another event) (Ferusson and
Hypnosis: Voll 2004; Presner et al 2001). A systematic
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
for procedural pain and reducing anxiety. occurs if a wound is of such size that it can
be closed directly without producing undue
tension at the wound site. Delayed primary
Medical and surgical closure occurs once a suspected infection
Reconstruction Post Burn Injury has been cleared. Deep partial and full
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. Skin Grafts
Timely burn wound excision and skin A skin graft is the transportation of skin
grafting form the cornerstone for acute burn from one area of the body to another.
surgical management (Klein 2010).Surgery (Glassey 2004)
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
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 and remodelling raised upon a specific blood vessel which
(Glassey 2004) 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) Skin Flap- epidermis, dermis and

The grafts properties (e.g. vascularity of
donor site) (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
Tendon without paratenon
Cartilage without perichondrium
(Glassey 2004)
Categorisation of Skin Flaps
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)
Relocation of Flaps
The third way in which flaps are
classified is by their method of relocation.
Flaps are defined as either local or distant
depending on the distance between the
donor and recipient sites (Glassey 2004).

Based on three factors: Local Flaps:

1. Vascularity Rotation or transpositional flaps are
tissue that is lifted and manipulated to
2. Anatomical composition cover the local defect, maintaining their
connection with the body. Therefore, they
3. Method of relocation (Glassey 2004)
are never fully excised.
Advancement flaps are those in
Vascularity
which the tissue is moved directly forward
Flaps can be classified as either to cover the defect, e.g. V-Y flaps used to
random pattern flaps or axial flaps cover finger-tip injuries
depending on their vascularity. Random (Glassey 2004).
pattern flaps are not raised on any Distant Flaps:
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
 Pedicled flaps are those which are Early initiation of rehabilitation is essential
transferred to another area of the body but to maximise functional outcomes for the
the vascular attachment is always patient
maintained and so the distance it can travel The pain and psychological distress
depends on the length of the pedicle. of a burn has a massive impact on
Free flaps are those in which the compliance
tissue is completely separated from the o An empathetic, encouraging
body and transferred to another area and and understanding approach is
the vascular supply is re-
established by anastomising the
blood vessels (Glassey 2004).

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 of loss of functional
structures
Early functional rehabilitation
(Kamolz et al 2009)

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

Oedema increasing for up to 36 hours post
injury
Hypermetabolic response, peaking at five body parts involved should be enforced
days post injury
Early synthesis and remodelling of collagen immobilised, it should be splinted or
Aims
Reduce risk of complications
o Reduce oedema, particularly where
it poses a risk for
impinging on peripheral current literature on the recommended
circulation or airways
Predisposition to contractures
Prevent deformities/loss of range
Protect/promote healing
Common treatment techniques
Immobilisation
o Bed rest
o Splinting
Positioning
Immobilisation
Rationale for Immobilisation
Positioning in the Acute Stage
*Modify according to burn area, patient
pain and medical status.*
reconstruction surgery
Stopping movement and function of the
after skin reconstruction for a burn has
taken place. When a body part must be
positioned in an anti-deformity position for
the minimum length of time possible
(Edgar and Brereton 2004; ANZBA 2007)
The following is a table drawn up using
immobilisation times for the various skin
grafts:
The times frames for mobilisation post-
surgery outlined in this booklet are merely a
guide taken from an analysis of current
literature and are NOT a replacement for the
specific time frames directed by the
operating surgeon or consultant (ANZBA
2007).
For a physiotherapist the most important
concepts to grasp are:
What is the minimum timeframe of
immobilisation post-surgery
What structures MUST be immobilised
Special considerations for movement,
function and ambulation dependent on
 Rigid or soft
Donor sites and the structures repaired or
excised during surgery. Dorsal or Volar
Digit, hand or forearm based
Immobilisation of the hand (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
moving parts designed to be remoulded as a
The position of safe immobilisation of the contracture improves. The most common
burned hand is essentially the opposite of serial static splint you will come across is a
the above claw deformity position. This thermoplastic palmar splint moulded in the
position involves: 20-30 wrist extension, 80- position of safe immobilisation.
90 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
A static progressive splint is a device Splinting Precautions
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 Splints need to be cleaned regularly to
is a finger flexion strap splint. This type of prevent colonization by microbes which may
splint is used in the treatment of MCP lead to wound infection
extension contractures. The flexion straps
serially stretch scar bands along the dorsum (Wright et al 1989; Faoagali et al 1994)
of hand and wrist causing extension
Unnecessary use of splinting may cause
contracture. The stretching force is localised
venous and lymphatic stasis, which may
to the MCP joints by applying the straps via
result in an increase in oedema
a wrist extension splint. This stabilises the
wrist providing static support below the MCP (Palmada et al 1999)
joint
(Kwan 2002). Precaution must be taken to ensure that
Dynamic Splinting splints do not product friction causing
A dynamic splint is one which aids in unnecessary trauma to the soft tissues
initiating and performing movements by (Duncan et al 1989).
controlling the plane and range of motion of
Precaution must be taken to ensure that
the injured part. It applies a mobile force in
splints do not produce excessive pressure.
one direction while allowing active motion in
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

Management of Oedema
the opposite direction. This mobile force is Elevation
usually applied with rubber bands, elastics Elevation of the hand above heart level is
and springs (Smith 2009). the most simple and effective ways to
Dynamic extension splints are most prevent and decrease oedema (Kamolz
commonly used in the treatment of palmar 2009).
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).
 A 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
Feet should be kept at 90 evidence (Latham and Radomski 2008).

Neutral position of hips 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.
These are hand specific oedema Schneider et al (2012) found a
management products. There is currently no significant improvement in contractures;
specific evidence available to support the balance and hand function with inpatient
efficacy of oedema gloves or digi sleeves in rehabilitation, through a longitudinal
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
attempt to display the evidence for as it is the most effective means of reducing
commonly used modalities. oedema by means of active muscle
The patient contraction (Glassey 2004). If this is not
Primary closure of wound possible due to sedation, surgical
intervention etc. then positioning the
Scar remodelling patient is the next best alternative (see
immobilisation and position).
Scar contraction
Passive ROM
Aims
Optimise scar appearance Passive ROM exercises in the acute stage
are contraindicated as applying passive
Limit effects of scar contraction/prolonged stretching forces may result in future
positioning on range of motion and function damage to the burned structures
(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
Mobilisation during the scar maturation phase once the
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
of a surgical or medical patient. Burns (Boscheinen-Morrin and Connolly
patients should be mobilised as early as 2001).
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 (Boscheinen-
and 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
of burns. exercises should not be carried out if there
is suspected damage to extensor tendons
Active ROM (common occurrence with deep dermal and
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
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
during AROM frequently. Vancouver Burn Scar Scale (VBSS/VSS)
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).
Observe the patient carrying out the AROM Reliability: Not enough evidence to make it
and PROM exercises prior to beginning a gold standard OCM. Moderate to high
treatment. Also observe the patient taking overall inter rater reliability. Test- Retest and
on/off splints. intra rater reliability has not been
assessed for burn scars to date
Always monitor for post exercise pain and (Durani et al 2009).
wound breakdown. Validity: When compared with POSAS
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
(ANZBA 2007) Scale (POSAS)
Use: Measures pigmentation, vascularity,
Scar Management thickness, relief, pliability and surface area.
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)
2009). Not only do hypertrophic scars cause (Fearmonti et al 2010).
psychosocial difficulties through their Reliability: Good internal consistency and
cosmetic appearance, they may also be reliability
painful, pruritic, and they may limit range of (Durani et al 2009)
motion where they occur on or near a joint Validity: Good concurrent validity
(Morien et al 2009; Polotto 2011). (Durani et al 2009)
Hypertrophic scars require a continuum of Sensitivity: Like the VBSS/VSS above,
dedicated and specialised treatment from limited sensitivity due to categorical/ordinal
the acute stage to many years post data
treatment (Fearmonti et al 2010)
(Procter, 2010, ANZBA 2007).
Further studies are required to validate the Hypoxia is a stimulus to angiogenesis and
reliability and validity of these scales as tissue growth in wound healing, as a
they are considered to be very subjective consequence removing the hypoxia stops
measures new tissue growth. This theory has been
(Durani et al 2009). contraindicated by other researchers.
Scar scales like the Vancouver Burn Scar
Scale (VBSS/VSS) and the Patient and 6) Mast cells: It is suggested that silicone
Observer Scar Assessment Scale (POSAS) results in an increase of mast cells in the
are cost effective and can be easily cellular matrix of the scar with subsequent
transferred within a clinical setting. To accelerated remodelling of the tissue.
optimise the scar scales, photographic 7) Static electricity: Static electricity on
evidence of the scar at timed intervals is of silicone may influence the alignment of
great value also to the clinician collagen deposition (negative static electric
(Brusselaers et al 2010) field generated by friction between silicone
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
caused by the occlusion of the underlying o Local hypoxia of hypervascular
skin. It decreases capillary activity and scars
collagen production, through inhibition of
the proliferation of fibroblasts o Reduction in collagen deposition
o Therefore
2) Increase in temperature: A rise in o Decreases scar thickness
temperature increases collagenase activity
thus increased scar breakdown. o Decreases scar redness
o Decreases swelling
3) Polarized Electric Fields: The negative
charge within silicone causes polarization of o Reduces itch
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
occlusive products without silicone show pressure positively influences the
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 Lack of a scientific evidence to established
hydration results in mast cell stabilization optimum pressure
and a subsequent decrease in
neurovascularisation and extracellular Non-Compliance ( due to comfort,
matrix production. However this hypothesis movement, appearance)
is in contrast with a mechanism of action of Heat and perspiration
silicone, in which an increase of mast cells
causes scar maturation. 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
degradation. Inconvenience

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
Five principles of scar massage:
safety considerations
1. Prevent adherence
Pressure: 15 mmHg has been noted as
the minimum to elicit change, and pressures 2. Reduce redness
of above 40 mmHg have been found to
cause complications. Both Anzarut et al 3. Reduce elevation of scar tissue
(2009) and Engrav et al (2010) used 4. Relieve pruritus
pressures of between 15 and 25 mmHg.
Time: It is recommended that garments are 5. Moisturise (Glassey 2004)
worn for up to 23 hours a day, with
removal for cleaning of the wound and Scar Massage Techniques
garment, and moisturisation of the wound. Retrograde massage to aid venous return,
increase lymphatic drainage, mobilise fluid
(Procter 2010; Anzarut et al 2009 and
Bloeman et al 2009). Effleurage to increase circulation
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). Static pressure to reduce pockets of
Garments should be worn for up to one swelling
year, or until scar maturation
(Anzarut et al 2009; Engrav et al 2010 and Finger and thumb kneading to mobilise the
Bloeman et al 2009). scar and surrounding tissue
Possible complications/ confounding
factors for use of PGT
 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
Frictions to loosen adhesions Training
Low cardiorespiratory endurance has been
(Holey and Cook 2003) found to be a concern for all
(Willis et al 2011)
Recommendations for practice and
safety considerations. Aerobic capacity as measured by VO2 peak
Insufficient consistency in literature with and time to fatigue has been found to be
regards to protocols on frequency or lower in adults and children of >15% TBSA
duration of treatment. Suggestions for at one year post burn, compared to age
practice include matched healthy controls
(Shin and Bordeaux, 2012, Morien et al,
2008) (Willis et al 2011; McEntine et al 2006)
Clean hands essential
Muscular strength and lean body mass has
Use non irritating lubricant, free of any been found to be significantly less in
known sensitisers. patients suffering from burns of >30%
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
Graft failure and ability to participate in activities

Intolerable discomfort (Grisbrook et al 2012b).

Hypersensitivity to emollient 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
Patient. protein metabolism begins to normalise 9-
The patient 12 months post burn, patients are still found
Healing process may continue for up to two
years, as scar tissue remodels and matures All found a decrease of up to 20% in lean
muscle mass compared to age matched
May require functional retraining and controls
integration back into the community and
activities. Adults with a TBSA >30% suffered a
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.
phase, it may need to be continued long (De Lauter et al 2007)
term, as many patients suffer from Exercise and Hypermetabolism
continuing limitation to range of motion
(Procter 2010).
Though exercise requires an increase in room temperature compared to age
energy expenditure and metabolism for a matched healthy controls.
short period of time no adverse effects have
been found with regard to exacerbating No significant difference in average skin
hypermetabolism or protein catabolism. temperature between burned and healthy
o All studies investigating the effects of children.
exercise on lean body mass found it to Significantly increased skin temperature in
increase, particularly with resistance healthy versus burned skin per child.
training
( 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
2006) Long term pulmonary function is
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
there was o Direct thermal damage to airways
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 There have been no studies investigating
optimal frequency.
o Recurrent infection leading to Intensity: All studies used between 65
chronic inflammation and 85% predicted heart rate max, with
Less likely to cause dysfunction in one study using interval training of 120
<30% TBSA, no injury over torso, and seconds 85% HRM and 120 seconds of 65-
no inhalation injury 70 HRM. All studies obtained positive effect,
(Willis et al 2011) with none directly comparing intensities to
Evidence for impact on aerobic and exercise determine the optimum. De Lauteur et al
capacity conflicting (Grisbrook et al 2012a). (2007), concluded that whether the patient
However Willis et al (2011) studied 8 males gradually increased their intensity by
post > 15% TBSA burns at one year post working to a specific quota each week, or if
injury, and found they simply worked at their target heart rate
Significantly decreased FEV1, peak VO2 for as long as they could tolerate, there was
and time to fatigue, in the burned patients no significant difference in gains in aerobic
No significant decrease in SpO2 at capacity.
baseline or peak VO2- however, the SpO2 of Type: All interventions used treadmill
burned patients took significantly longer to training, whether walking or running.
stabilise at baseline post exercise. Time: All studies recommended the
duration of treatment be 12 weeks, with
No significant difference in participation the exception of Paratz et al, 2012, who
levels in physical activity, though burn investigated a high intensity six week
survivors were more likely to participate in programme. However, the specific results of
work rather than leisure activity. this are unknown. Sessions were 20-40
minutes in length, with the majority using
Burns survivors were less likely to 30 minutes (Grisbrook et al 2012; De
participate in vigorous intensity exercise Lauteur et al 2007; Przkora et al 2007)
over 9 METs
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
aerobic capacity. similarly to controls. Therefore, normal
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),
individual response is advised. suggested that a break of more than 48 hrs
must be given between bouts of resistance
Aerobic Training Summary and training.
Recommendations for Practice o Resistance exercise causes
microtrauma to muscles already in a
Exercise prescription: compromised state.
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, Therefore, more favourable psychological
followed by a progression to 70-75% for status
week 2-6 (4-10 repetitions), and 80-85% There were no studies investigating early
week 7-12, (8-12 repetitions) (Suman et al training
2001; Suman and Herndon 2007). o With extensive burns, adequate
Isokinetic training: 10 reps at 150 healing of wounds and medical
degrees per second, using 1-5 sets for the stability required before initiating
1st -5th session,6 sets for the 6th -24th aerobic/strength exercise
session, and 10 sets from 25th to 36th
session, with three minute rests between Other safety considerations:
sets. (Ebid et al 2012). Though exercise has been shown to
Mixed and functional strength increase lean body mass, liaison with
training: Grisbrook et al (2012b) doctors concerning anabolic steroids and
commenced on the biodex, targeting medication and with dieticians regarding
specific muscle groups for the desired optimal nutrition is recommended in order
functional goal, and progressed to resistive to ensure correct management of
machine and finally free weight training hypermetabolisim.
using functional items. Intensity was 50-
60% 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
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