I.
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.
Complications specific to electrical injury include:
• 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 Epidermal Burn
renal dysfunction from prolonged chemical exposure). An epidermal burn, as the name implies, causes cell
Ultraviolet and Ionizing Radiation Burns damage only to the epidermis (Fig. 24.2). This depth
A nonblistering sunburn is a first-degree burn from of burns correlates to practice pattern 7B, Impaired
the overexposure of the skin to UV radiation. More Integumentary Integrity Associated with Superficial
severe burns can also occur due to UV exposure and Skin Involvement, in the Guide to Physical Therapist
would . Ionizing radiation burns with or without Practice. The classic “sunburn” is the best example of
thermal injury occur when electromagnetic or an epidermal burn. Clinically, the skin appears red or
particulate radiation energy is transferred to body erythematous.The erythema is a result of epidermal
tissues, resulting in the formation of chemical free damage and dermal irritation, but there is no injury to
radicals.2Ionizing radiation burns usually occur in the dermal tissue. There is diffusion of inflammatory
laboratory or industrial settings, but can also be seen mediators from sites of epidermal damage and
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
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
wound’s 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 infection can convert a deep partial-thickness burn
Integrity Associated with Partial-Thickness Skin into a deeper injury. The development of
Involvement and Scar Formation, in the Guide to hypertrophic and keloid scars is a frequent
Physical Therapist Practice.21 Most of the nerve consequence of a deep partial-thickness burn.
endings, hair follicles, and sweat ducts will be injured
because most of the dermis is destroyed. Full-Thickness Burn
Deep partial-thickness burns appear as a In a full-thickness burn (Fig. 24.5) all of the
mixed red or waxy white color. The deeper the injury, epidermal and dermal layers are destroyed
the more white it will appear. Capillary refill will be completely. In addition, the subcutaneous fat layer
sluggish after the application of pressure on the may be damaged to some extent. This burn depth is
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 consistent with practice pattern 7D, Impaired
wound to demarcate (between normal and damaged Integumentary Integrity Associated with Full-
tissue) during the first few days is necessary. Thickness Skin Involvement and Scar Formation, in
Demarcation becomes evident after several days as the Guide to Physical Therapist Practice.
the dead tissue begins to slough. Hair follicles that A full-thickness burn is characterized by a
penetrate into the deeper dermal regions below the hard, parchment-like eschar covering the area. Eschar
burn level remain viable. Preservation of hair follicles is devitalized tissue consisting of desiccated coagulum
and new hair growth will indicate a deep of plasma and necrotic cells. Eschar feels dry,
partialthickness burn rather than a full-thickness leathery, and rigid. The color of eschar can vary from
injury, and there is a corresponding greater potential black to deep red to white; the latter indicates total
for spontaneous healing. Particularly important ischemia of the area. Frequently, thrombosis of
factors that determine which epidermal structures superficial blood vessels is apparent and no blanching
survive and which die include the thickness of the skin of the tissue is observed. The deep red color of the
in a particular location and/or the distance of the area tissue results from hemoglobin fixation liberated from
from the source of heat. destroyed red blood cells.
Deep partial-thickness burns that are allowed Hair follicles are completely destroyed, so
to heal spontaneously will have a thin epithelium and body hairs pull out easily. All nerve endings in the
may lack the usual number of sebaceous glands to dermal tissue are destroyed so the wound will be
keep the skin lubricated. New tissue usually appears insensate (without feeling); however, a patient still
dry and scaly, is itchy, and is easily abraded. Creams may experience a significant amount of pain because
are necessary to artificially lubricate the new surface. adjacent areas of partial-thickness burn usually
Sensation and the number of active sweat ducts will surround a full-thickness injury.
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
 A major problem that arises from deep burns Subdermal Burn
is the damage to the peripheral vascular system.
Because large amounts of fluid leak into the
interstitial space beneath unyielding eschar, the
pressure in the extravascular space increases,
potentially constricting the deep circulation to the
point of occlusion (see later discussion of
cardiovascular complications in the section titled
Complications of Burn Injury). Because eschar does
not have the elastic quality of normal skin, edema
that forms in an area of a circumferential burn can
cause compression of the underlying vasculature. If
this compression is not relieved, it may lead to
eventual occlusion with possible necrosis of tissue
distal to the site of injury. To maintain vascular flow,
an escharotomy may be necessary. An escharotomy is
a midline lateral incision of the eschar the length of an An additional category of burn, the subdermal burn,
involves complete destruction of all tissue from the
epidermis down to and through the subcutaneous
tissue (Fig. 24.7). This depth of injury correlates with
practice pattern 7E, Impaired Integumentary Integrity
Associated with Skin Involvement Extending into
Fascia, Muscle, or Bone and Scar Formation, in the
Guide to Physical Therapist Practice.21 Muscle and
bone are subject to necrosis when burned. This type
of burn occurs with prolonged contact with a heat
source and routinely occurs as a result of contact with
electricity. Extensive surgical and therapeutic
management is necessary to return a patient to some
degreeof function.

extremity or chest wall. Figure 24.6 shows an

escharotomy and the result of pressure that forces
the incision to gape. Following an escharotomy,
pulses are frequently examined to monitor
restoration of circulation. If the escharotomy is
successful, there will be an immediate improvement
in the peripheral blood flow, demonstrated by normal
pulses distal to the wound and by return of normal
temperature and capillary refill of the distal
extremity.
Although at times it may be difficult to
differentiate a deep-partial from a 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 grafting will be necessary.
Grafting is discussed in detail in the section titled
Surgical Management of the Burn Wound.
 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
 III. ANATOMY, PHYSIOLOGY, KINESIOLOGY
Functions of the Integumentary System
• Protection against injury and infection
• Regulates body temperature
• Sensory perception
• Regulates water loss
• Chemical synthesis
Protection – covers and protects the entire body
against injury and infection
Physical barriers
- continuity of the skin and hardness of keratinzed
cells
• Due to the skin’s 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
• Langerhans’ cells, macrophages, and DNA
• Langerhans’ cells in epidermis present antigens to
lymphocytes
• Dermal macrophages (2nd line of defense) – attack
bacteria and viruses that have penetrated the
epidermis
• Langerhan’s cells and macrophages present in the
skin helps activate the body’s 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 skin’s 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)
• Meissner’s corpuscles: light touch
• Merkel discs: light touch
• Pascinian receptors – lies in deeper
dermis/hypodermis & detect deep pressure contacts
• Hair root plexus: sensations from movement of
hairs
• Hair follicle receptors – movement across the
surface of the skin
• Bare nerve endings: painful stimuli (chemicals, heat,
cold)
Excretion/Absorption
• Elimination of nitrogen-containing wastes
(ammonia, urea, uric acid), sodium chloride, and
water. It regulates water loss
Metabolic Functions
• Synthesis of Vitamin D – increases calcium
absorption in the body
• Vitamin D is a fat-soluble vitamin that may be
absorbed from the intestines or may be produced
by the skin when the skin is exposed to ultraviolet
light (particularly sunlight).It is converted to
its active form by the body in 2 steps, occurring first in
the liver and completed in the kidneys. In
its active form, vitamin D acts as a hormone to
regulate calcium absorption from the intestine
and to regulate levels of calcium and phosphate in the
bones. Vitamin D deficiency causes
Rickets
• When the body is deficient in vitamin D, it is unable
to properly regulate calcium and phosphate
levels. If the blood levels of these minerals becomes
low, the other body hormones may
stimulate release of calcium and phosphate from the
bones to the bloodstream.
• Chemical conversion of many substances
• Blood Reservoir – preferential shunting of blood as
needed
Types of Membranes - thin sheet-like structures that
protect parts of the body
Serous Membranes
• Line body cavities that have no opening to the
outside
• Secrete a watery fluid called serous fluid that
lubricates surfaces.
Mucous Membranes
• Line cavities and tubes that open to the outside
Synovial Membranes
• Form the inner lining of joint cavities
• Secrete a thick fluid called synovial fluid
Cutaneous Membrane – also known as skin
Characteristics of Skin
•The integument covers the entire body and is the
largest organ ~ 2 meters and heaviest organ
16% of body mass of the body.
•Composed of the epidermis and dermis
•Pliable, yet durable
•Thickness: 1.5 to 6.0 mm
Types of Skin
Thin - 1-2 mm on most of the body and 0.5 mm in
eyelids
•Hairy
•Covers all parts of the body except palms of hands
and soles of feet
•Thin epidermis and lacks stratum lucidum
•Lacks dermal papillae
•Has more sebaceous glands
•Fewer sweat glands, sensory receptors than thick
skin
Thick - up to 6 mm thick on palms of hands and soles
of feet
•Hairless
•Covers palms of hands and soles of feet
•Thick epidermis and a distinct stratum
lucidum
•Epidermal ridges are present due to well developed,
numerous dermal papillae.
•Lacks sebaceous glands, has more sweat glands
•Sense receptors are also more densely packed.
Layers of the Skin
Epidermis
Types of Cells
Keratinocytes
•90 % of epidermal cells are keratinized
•contains keratin (fibrous protein)
•protects and waterproofs the skin
Melanocytes
•8% of the epidermal cells
•produces melanin
•contributes to skin color and absorbs UV
light
Langerhans cells
•Arise from red bone marrow and
migrate to the epidermis
•Constitute small portion of epidermal cells
•Participate in immune responses
•Easily damaged by UV light
Merkel cells
•Least numerous of the epidermal cells
•Found in the deepest layer of the epidermis
•Along with tactile discs, they function in
sensation of touch
Layers of epidermis
Stratum corneum
• 25-30 layers of dead flat keratinocytes
•Shed continuously and replaced by cells from the
deeper strata
•Serves as a water, microbe, injury barrier
Stratum lucidum
•Present only in thick skin
•3-5 layers of clear, flat, dead keratinocytes
•Dense packed intermediate filaments
•Thick plasma membranes
Stratum granulosum
•Located above the stratum spinsosum
•3-5 layers of flattened keratinocytes undergoing
apoptosis
•Organelles begin to disintegrate becomes nonliving
cells
•Marks the transition between deeper
metabolically active strata and the dead cells of the
superficial strata.
•Contains lamellar granules
•Secretes lipid-rich secretion that acts as a water
sealant
Stratum spinosum
•Located above the stratum basale
•8-10 layers of keratinocytes
•Some cells retain their ability for cell division
•Cells have spinelike projections (bundles of
filaments of the cytoskeleton) tightly joins cells
to each other.
•Provides skin both strength and flexibility
Stratum basale
•Also referred to as stratum germinatum because this
is where new cells are formed
•Deepest layer of the epidermis
•Single row of cuboidal or columnar keratinocytes
Growth of epidermis
•Newly formed cells in the stratum basale undergo
keratinazation as they are pushed to the surface.
•They accumulate more keratin during the process
•Then they undergo apoptosis
•Eventually they slough off and are replaced
•The process takes about 4 weeks
•Rate of cell division in the stratum basale increases
during injury
Dermis
•Second deepest part of the skin
•Blood vessels, nerves, glands and hair follicles are
embedded here
•Composed mainly of connective tissues (collagen
and elastic fibers)
•Collagen fibers make up 70% of the dermis and give
structural toughness and strength. Elastin fibers are
loosely arranged in all directions and give elasticity to
the skin
•Has two layers – Papillary Layer and Epidermal layer.
Papillary layer
•Superficial portion of the dermis
•Consist of areolar connective tissue containing
elastic fiber
•Surface area is increased due to projections called
dermal papillae
which contains capillaries or tactile receptors
•Epidermal ridges conforms to the dermal papillae
Reticular layer
•Deeper portion of the dermis
•Consist of dense irregular connective tissue
containing collagen/elastic fibers
•Provides skin with strength and elasticity
•Contains hair follicles, nerves, sebaceous and
sudoriferous glands
Hypodermis
– (subcutaneous) Attaches the skin to underlying
organs and tissues
•Not part of the skin - lies below the dermis
•Contains connective tissue and adipose tissues
(subcutaneous fat) for insulation
•Infants and elderly have less of this than adults and
are therefore more sensitive to cold
Skin Appearances
•Epidermis appears translucent when there is little
melanin or carotene
•White skin appears pink to red depending on
amount and oxygen content of blood moving
in the capillaries of the dermis.
•Albinism is an inherited trait where a person can’t
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 - Addison’s 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 º F. They
are most stimulated when the surface of the skin is at
77 º F and are no longer stimulated when the surface
of the skin drops below 41 º 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 º F and are
most stimulated at 113 º F. Beyond 113 º 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 An in depth knowledge of pathophysiology of burns,
skin thru pores or into hair follicles and their effects both locally and systemically is
•Two main types of sweat glands necessary to ensure effective management of a
•Eccrine sweat glands patient with a burn injury.
o Secretes cooling sweat
o Secretes directly onto the skin Zones of Injury and Wound Conversion
o Began to function soon after birth The local effect involves three burn zones:
o Sweat is composed of 98 percent water and two (Hettiaratchy and Dziewulski 2004)
percent dissolved salts and nitrogenous wastes,
such as urea and uric acid Zone of Coagulation:
o Helps regulate body temperature/aids in waste the point of maximum damage
removal Irreversible tissue loss due to coagulation of
•Appocrine sweat glands constituent proteins.
o Stimulated during emotional stress/excitement
o Secretes into hair folicle Zone of Stasis:
o Begins to function at puberty Characterised by decreased tissue perfusion
o Slightly more viscous than eccrine secretions Potential to rescue the tissue in this zone
o Composed of the same components as eccrine Problems such as prolonged hypotension, infection
sweat or oedema can convert this area into one of complete
plus tissue loss
o lipids and proteins.
o Referred to as “cold sweat”. Zone of Hyperaemia:
Sebaceous - oil glands (sebace = grease) The tissue here will invariably recover unless there
•They are mostly connected to hair follicles. is severe sepsis or prolonged hypoperfusion.
•Sebaceous glands are embedded in the dermis over
most of the body. The depth of the wound develops over time: The burn
•Absent in the palms and soles. process peaks at approximately three days.
•Vary in size, shape and numbers in other areas of the Progression is 3D- zone of coagulation both increases
body. in depth and width (Ever et al 2010).
•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
 burning household furniture, leading to severe
inhalation injuries as well as burns.
IV. ETIOLOGY – Contact burns from contact with molten metal or
plastic are common in industry. An unconscious
patient may sustain burns from contact with a cooker
 Thermal burns, the most common type, or a hot radiator.
frequently result from: – Electrical burns due to electrical current from plugs,
•residential fires sockets and wiring. Deep structures can be involved at
•automobile accidents the current entry and exit sites on the body. The
•playing with matches patient’s cardiac status requires close monitoring.
•improper handling of firecrackers •Elsevier
•scalding accidents and kitchen accidents
(such as a child climbing on top of a stove or
grabbing a hot iron)
•parental abuse of (in children or elders)
•clothes that have caught on fire.
 Chemical burns result from contact, ingestion,
inhalation, or injection of acids, alkalis, or
vesicants.
 Electrical burns usually result from contact with
faulty electrical wiring or high-voltage power
lines. Sometimes young children chew electrical
cords.
•Friction or abrasion burns
occur when the skin rubs
harshly against a coarse
surface.
•Sunburn results from
excessive exposure to sunlight.

• Burns can be caused by

excessive heat or cold, by
chemicals, ultraviolet light
or radiation.
• The most common causes of
burns requiring hospital
treatment are:
– Scalds from hot fluids or
steam are common in the
under fives and the elderly.
-Explosions, flash flame or
steam, bonfires, fireworks,
barbeques and the use of
flammable liquids such as
petrol. Flash burns tend to be
partial-thickness burns, but can
be deeper if the patient’s
clothes ignite.
– Flame burns occur when the
patient’s clothes, hair or skin
catch light. The effect of
damage from house or car fires
is exacerbated by the inhalation of toxic gases from
 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.
 VI. CLINICAL SIGNS AND SYMPTOMS/ PHYSICAL DISABILITIES/
IMPAIRMENTS
Decreased respiratory function
Signs and symptoms Breast entrapment
Signs and symptoms depend on the type of burn and Perineal banding
may include:
Axilla Type 1: either anterior or
localized pain and erythema, usually without blisters
posterior contracture
in the first 24 hours (first-degree burn)
Type 2: anterior and posterior
chills, headache, localized edema, and nausea and
contracture with sparing of dome
vomiting (more severe first-degree burn)
Type 3: anterior and posterior
thin-walled, fluid-filled blisters appearing within
contracture and axillary dome
minutes of the injury, with mild to moderate edema
Hands Metacarpophalangeal extension
and pain
deformities
(second-degree superficial partial-thickness burn)
Wrist extension deformities
white, waxy appearance to damaged area (second-
Proximal interphalangeal flexion
degree deep partial-thickness burn)
deformities
white, brown, or black leathery tissue and visible
Interdigital web contractures
thrombosed vessels due to destruction of skin
Clawing of fourth and fifth digits
elasticity (dorsum of
Thumb contractures (adduction,
hand most common site of thrombosed veins),
opposition, flexion, or extension)
without blisters (third-degree burn)
silver-colored, raised area, usually at the site of Arms and legs Antecubital banding and flexion
electrical contact (electrical burn) Posterior popliteal banding and
singed nasal hairs, mucosal burns, voice changes, flexion
coughing, wheezing, soot in mouth or nose, and Anterior hip banding and flexion
darkened Medial and lateral malleolar
sputum (with smoke inhalation and pulmonary scarring
damage). Foot and ankle Hyperextension of
•OkDoKeY metatarsophalangeal joints
Equinovarus
Cavus foot
Potential impairment Rocker bottom deformity

Body area Impairment

Face Facial disfigurement (contractures
of eyelids, nose, mouth, ears, and
adjacent facial skin)
Inability to close eyes
Loss of facial expression
Teeth malalignment
Drooling and inability to close lips
Lower lip eversion
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
Systemic Complications of Burn Injury membrane rupture, anxiety, depression, or post-
Body System Complications traumatic stress disorder
Respiratory Inhalation injury, restrictive
pulmonary pattern Chemical Burns
(which may OCCur with a burn
on the trunk), pulmonary complications (e. g. , airway obstruction
atelectasis, pneumonia, from bronchospasm, edema, or epithelial sloughing)
microthrombi, and adult and metabolic complications (e. g., liver necrosis or
respiratory distress syndrome renal dysfunction from prolonged chemical
Cardiovascular Hypovolemiaihypotension, exposure).
pulmonary hypertension,
subendocardial ischemia, Ultraviolet and Ionizing Radiation Burns
anemia, and disseminated
intravascular coagulopathy
GastroinrestinaV Stress ulceration, hemorrhage, • Gastrointestinal: Cramps, nausea, vomiting,
genitourinary ileus, ischemic co\iris, diarrhea, and bowel ischemia
cholesrasis, liver failure, and • Hematologic: Pancytopenia (decreased number of
urinary rract infection red blood cells, white blood cells, and platelets),
Renal Edema, hemorrhage, acute granulocytopenia (decreased number of granular
tubular necrosis, acure leukocytes), thrombocytopenia (decreased number
renal failure of platelets), and hemorrhage
•paz
•paz
Complications
Possible complications of burns include:
Electrical burns
loss of function (burns to face, hands, feet, and
Complications specific to electrical injury include the
genitalia)
following"s:
total occlusion of circulation in extremity (due to
• Cardiovascular: Cardiac arrest (ventricular
edema from circumferential burns)
fibrillation for electric current or asystolic for
airway obstruction (neck burns) or restricted
lightning), arrhythmia (usually sinus tachycardia or
respiratory expansion (chest burns)
nonspecific ST changes) secondary to alterations in
pulmonary injury (from smoke inhalation or
electrical conductivity of the heart, myocardial
pulmonary embolism)
contusion or infarction, or heart wall or papillary
adult respiratory distress syndrome (due to left-
muscle rupture
sided heart failure or myocardial infarction)
• Neurologic: Headache, seizure, brief loss of
greater damage than indicated by the surface burn
consciousness or coma, peripheral nerve injury
(electrical and chemical burns) or internal tissue
(resulting from ischemia), spinal cord paralysis (from
damage along
demyelination), herniated nucleus pulposus, or
the conduction pathway (electrical burns)
decreased attention and concentration
cardiac arrhythmias (due to electrical shock)
• Orthopedic: Dislocations or fractures secondary to
infected burn wound
sustained
stroke, heart attack, or pulmonary embolism (due to
muscular contraction or from a fall during the burn
formation of blood clots resulting from slower blood
injury
flow)
• Other: Visceral perforation or necrosis, cataracts,
tympanic

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

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

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

I. DIFFERENTIAL DIAGNOSIS CONDITIONS

 VIII. DIAGNOSTIC TOOLS/ PROCEDURES OR TEST
Physiotherapy Assessment of the Burn Patient
The physiotherapist must be aware of the
importance of an early and adequate assessment of
Burn patients for optimal functional and cosmetic
outcomes to minimise the impact of the trauma long
term. They must have a concise knowledge of the
assessment procedure through from Accident and
Emergency to the ward, onto the rehabilitation
setting and out in the community. The following
information is gathered through assessment, and a
treatment plan is formulated,
constantly reassessed and revised.
had a reduced level of consciousness – aggressive
respiratory treatment to commence immediately
(ANZBA 2007; British Burn Association 2005;
Eisenmann-Klein 2010)
Total Body Surface Area (TBSA)
o The rule of nine or the Lund and Brower chart are
used to assess the TBSA
o The Lund and Brower Charts are
considered to be more accurate than rule of nines,

(ANZBA 2007; Hettiaratchy and

Papini 2004)

Physiotherapy aims
1. Prevent respiratory complications
2. Control Oedema
3. Maintain Joint ROM
4. Maintain Strength
5. Prevent Excessive Scarring

Patients are at high risk due to:

1. Injury factors - Inhalation injury;
burn area - systemic
inflammatory reaction
syndrome involving the
lungs; depth of burn and
scarring
2. Patient factors - Reduced
ambulation and mobility;
increased bed rest;
increased
Pain; pre-existing co-
morbidities
3. Iatrogenic factors – Skin
reconstruction surgery; invasive monitoring and
procedures, management in critical care but both are commonly used.

Database/Subjective Assessment •Measure burn wound areas by mapping wound –

The following pieces of information should be
included in the physiotherapists’ database.
Presenting Complaint
Inhalation injury
There should be a high index of suspicion if the
patient was injured in an enclosed space and / or
1% TBSA ≅ patient’s 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 ANZBA 2007; British Burn Association 2005;
destruction as it alters for at least 48 hours post Hettiaratchy et al 2004
burn injury
o Jacksons’ burn wound model.
•It is rare that a burn will present with a single Past Medical/ Drug History
depth.
• Likely to change depending on the early Social History
management e.g. appropriate first aid and other
patient factors. (ANZBA 2007; British Burn ANZBA 2007; British Burn Association 2005;
Association 2005; Eisenmann-Klein 2010) 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
• 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 management—removal 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

 IX. MANAGEMENTS

Pharmacological Pain Management an analgesia.

•During the first 48 hours • Regular and repeated pain assessments are used to
monitor the effectiveness of analgesia.
• Decreased organ blood supply alters the clearance of Thus there is no standard treatment of burns patients,
drugs each requires individual assessment.
• The body then enters a hyper metabolic state, Opioids: the cornerstone of pain management in
o Associated with increased clearance of burns, and are available in a variety of potencies,
analgesia. methods of administration and duration of action.
•Variations in levels of acute phase plasma and total Opioids used to effectively manage background pain,
body water volume further impact upon effectiveness with well-timed and effective doses of opioids used
Positive Side Effects Examples of Opioids separately to manage
Effects procedural pain

Simple analgesics:
Pain relief Respiratory distress Morphine paracetamol can be used
in conjunction with
Increased Itch Oxycodone opioids, to give a
comfort synergistic effect
comparable to a higher
Morphine Nausea and vomiting Fentanyl: potent, rapid onset, opioid dose. Paracetamol
related to Opioid tolerance – requiring short acting opioid. Used for is an effective anti-
reduced Post- increasing doses procedural pain management. pyretic and has few
traumatic Opioid induced hyperalgesia Remifentaril: ultra-short acting contra-indications.
stress disorder (OIH) – increased sensitivity, opiate. NSAIDS: synergistic with
throughout the body following Alfentaril: short acting, used for opioids and can reduce
opioid exposure post-procedural analgesia. opioid dose and thus
Provide poor defence against reduce side-effects. Not
central sensitisation used in wide spread
Physical dependence – burns due to already
common in long term use 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
- Nausea and increased risk of
aspiration
- Impaired memory and
communication
- Postural hypotension, and fainting

Non- Pharmacological Pain Management


The following is a synthesis of information form the
following articles: Summer et al (2007), Richardson and
Mustard (2009), ANZBA (2007) and de Jong et al (2007)
Overall, the levels of evidence to support the use of
alternative therapies for pain relief are of poor quality.
However, no negative side effects were reported in the
literature reviews and these therapies are all used in
conjunction with pharmacological management to
optimize pain relief for the individual.
Psychological techniques:
beneficial for reducing anxiety and providing patients
with coping methods for pain levels and durations.
These include relaxation, distraction and cognitive
behavioural therapy (CBT). CBT is beneficial in the
management of complex pain problems and can
reduce fear and anxiety associated with activities or
environments.
Hypnosis:
a state of “increased suggestibility, attention and
relaxation”. In the burn patient hypnosis is used in the
management of procedural pain and anxiety. The use
of hypnosis clinically is increasing but its usefulness is
dependent on the individual’s hypnotic susceptibility,
high baseline pain and the skill of the practitioner. The
current best available evidence for management of
procedural pain was found for active hypnosis, rapid
induction analgesia and distraction relaxation.
Virtual Reality:
immersing the patient in a virtual world has shown
some effect on procedural pain control and is better
than hand-held gaming devices. However, the
equipment is costly and bulky and not always suitable
for paediatric intervention. A paediatric intervention,
using hand-held game devices which provide
augmented reality was trialled among 3-14 year olds.
This has shown significantly lower pain scores than
standard distraction and relaxation when undergoing
dressing changes (Mott et al 2008).
Sleep Normalisation:
disrupted sleep occurs in up to 50% of burn patients
and links have been established between poor sleep
quality and pain severity, as well as pain and prolonged
experiences of sleep disturbance. Normalisation of the
24hour day, with a bedtime routine, within the limits
of the hospital environment is aimed for to promote
sleep, with the use of analgesics and night sedation.
Music therapy:
this is thought to target pain via the gate control
theory. This suggests that music serves as a distraction
from noxious stimuli. Also, the anxiety related to the
rehabilitation of burns can increase the activation of
the sympathetic nervous system. Music uses all three
cognitive strategies employed in pain and anxiety
management (imagery – envisioning events that are
inconsistent with pain, self-statements and attention-
diversion devices to direct attention away from the
pain ad redirects it to another event) (Ferusson and
Voll 2004; Presner et al 2001). A systematic review of
music therapy among pregnant women, medical-
surgical patients and critical care patients showed
statistically significant reductions in pain scores. Of the
seventeen studies reviewed by Cole and LoBiondo-
Wood (2012), 13 studies demonstrated the positive
effects of music on pain. Other positive findings of the
studies included reduced anxiety, muscle tension,
blood pressure and heart rate. A burn specific study
included showed reduced pain levels during and after
the debridement, reduced anxiety and decreased
muscle tension during and after dressing changes.
The Cochrane Review of music as an adjunct to pain
relief concluded that “music and other non-
pharmacological therapies could have a synergistic
effect to produce clinically important
benefits on pain intensity or analgesic requirements”
and thus requires further study. This is based on the
studies indicating that music resulted in reduced pain
intensity and reduced opioid requirements. The
reported changes in both of these outcomes were
small however, and their clinical importance is unclear
(Cepeda et al 2006).
Paediatric Burn Pain
(Richardson and Mustard 2009)
•children 0-4 years represent approx. 20% all
hospitalised burn patients
•In preschool aged children the half-life of opioids
(morphine and alfentanyl) are 50% those in adults.
Higher dosage required.
• Risk of accidental overdose due to difficulties with
pain evaluation resulting in overestimation of child’s
pain
•Childs environment has huge effect on pain
perception. Parents’ presence and aid during dressing
change can have beneficial for procedural pain and
reducing anxiety.
Medical and surgical Management
Reconstruction Post Burn Injury
 suspected infection has been cleared. Deep partial and
The impact of reconstructive surgery post burn injury full thickness burns both require surgical intervention.
has a major impact on a patient. As an allied health Surgery normally takes place within the first 5 days
professional, we must work as part of an MDT in order post injury to prevent infection which could extend the
to ensure successful surgery while at the same time depth of the tissue loss (Glassey 2004).
ensuring long term health and
function. Timely burn wound
excision and skin grafting form the
cornerstone for acute burn surgical
management (Klein 2010).Surgery
for burned patients is not normally
indicated until 48 hours after injury,
when the depth of the burn has
been established. The only
exception is when necrotic tissue is
evident then early excision may be
required. A plastic surgeon must
reconstruct the injured body part in
a way that is extensible, sensate
and cosmetically acceptable
(Glassey 2004). In addition to this,
they must rebuild or replace
muscles, tendons, joints and nerves
to ensure they are appropriately intact.
Skin Grafts
Aims “A skin graft is the transportation of skin from one
1. Achieve would closure area of the body to another.”
(Glassey 2004)
2. Prevent infection
3. Re-establish the function and properties of an intact A graft is an area of skin that is separated from its own
skin blood supply and requires a highly vascular recipient
bed in order for it to be successful. Prior to grafting,
4. Reduce the effect of burn scars causing joint the process of wound debridement must take place.
contractures Wound debridement involves removing necrotic
tissue, foreign debris, and reducing the bacterial load
5. Reduce the extent of a cosmetically unacceptable
on the wound surface (Cardinal et al 2009).This is
scar
believed to encourage better healing. The following
are the methods available for grafting onto a debrided
(Glassey 2004; BBA Standard 6 2005)
wound to obtain closure:
•Autograft (‘split skin graft’) (own skin)
Choosing the Correct Method of Reconstruction
The simplest management involves • Allograft (donor skin)
conservative wound care and dressings, while the most
complex is free-flap reconstruction. When deciding on • Heterograft or xenografts (animal skin)
the most appropriate intervention, a surgeon must
• Cultured skin
consider the extent of the missing tissue and the
structures effected (Glassey 2004). Generally, a • Artificial skin
superficial partial thickness burn will heal with
conservative treatment (secondary intention) in 10 (Glassey 2004)
days to 3 weeks, unless infection occurs. Primary Meshed vs. Sheet Grafts
intention occurs if a wound is of such size that it can be
closed directly without producing undue tension at the Sheet grafts are those which are not altered once they
wound site. Delayed primary closure occurs once a have been taken from the donor site.
 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

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
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

• Patient is systemically fit

for surgery

•Patient has no
coagulation abnormalities

• Sufficient donor sites

available

•Would clear of
towards producing the optimal skin substitute. As a •Tendon without paratenon
general rule, skin substitutes are classified as either
temporary or permanent and synthetic or biological. A •Cartilage without perichondrium
very clear and concise overview of the different skin (Glassey 2004)
substitutes available for burn injuries is provided in Categorisation of Skin Flaps
Halim et al (2010).
Based on three factors:
The Recipient Site 1. Vascularity
2. Anatomical composition
The graft should take within 5 days and will
provide a permanent covering of the injury. A graft 3. Method of relocation (Glassey 2004)
should always be placed over bleeding, healthy tissue
to ensure it is vascularised for survival (Glassey 2004). Vascularity
Post-operatively the graft site is dressed to ensure Flaps can be classified as either random
pressure is created over the graft to limit haematoma pattern flaps or axial flaps depending on their
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 (Glassey 2004)
Reasons for Graft Failure
• Inadequate blood supply to wound bed
• Graft movement
• Collection of fluid beneath graft (e.g. haematoma)
• Infection (e.g. streptococcus)
• 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 • Fasciocutaneous Flap- epidermis, dermis and both
avascular”. A skin graft does not have this ability superficial and deep fascia
(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 • Myocutaneous Flap-muscle belly with the overlying
which a skin flap will include:
•Bone without periosteum
vascularity. Random pattern flaps are not raised on any
particular major blood vessel, but instead are raised on
smaller branches of these blood vessels known as the
subdermal plexus. These flaps are limited in size to
ensure distal parts do not become ischemic (Glassey
2004). Examples of these flaps include Z-plasty, V-Y
advancement flap, rotation flap and transposition flap.
Axial flaps, on the other hand, are raised upon a
specific blood vessel which allows them to be lifted on
a narrow pedicle and ensures greater perfusion for
survival.
Flap anatomical Composition
Flaps are also classified depending on their
composition, i.e. which layers of the skin they contain.
The composition is often clear from the name of the
flap.
Skin Flap- epidermis, dermis and superficial fascia
• Muscle Flap-muscle belly without overlying
structures
skin
• Osseous Flap- bone
• Osseomyocutaneous Flap-bone, muscle, skin
• Composite Flap- Contains a no. Of different tissues •Rehabilitation requires a prolonged, dedicated and
such as skin, fascia, muscle and bone. (Glassey 2004) multidisciplinary effort to optimise patient outcomes,
as inpatients and outpatients.
Relocation of Flaps (Schneider et al 2012; Disseldorp et al 2007; Esselman,
The third way in which flaps are classified is by 2007)
their method of relocation. Flaps are defined as either The aims of the multidisciplinary rehabilitation of a
‘local’ or ‘distant’ depending on the distance between burn include:
the donor and recipient sites (Glassey 2004). • Prevention of additional/deeper injuries

• Rapid wound closure

•Local Flaps:
•Rotation or transpositional flaps are tissue • Preservation of active and passive ROM
that is lifted and manipulated to cover the local defect,
maintaining their connection with the body. Therefore, •Prevention of infection
they are never fully excised.
•Advancement flaps are those in which the •Prevention of loss of functional structures
tissue is moved directly forward to cover the defect, • Early functional rehabilitation (Kamolz et al
e.g. V-Y flaps used to cover finger-tip injuries 2009)
(Glassey 2004).
•Distant Flaps:
• Pedicled flaps are those which are
transferred to another area of the body but
the vascular attachment is always
maintained and so the distance it can travel
depends on the length of the pedicle.
•Free flaps are those in which the
tissue is completely separated from the
body and transferred to another area and
the vascular supply is re-established by
anastomising the blood vessels (Glassey 2004). The physiotherapist may only have a role in achieving
some of these goals.
Rehabilitation Post Burn Injury • Above all cause no harm.

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.
• Burn survivors often suffer from
o permanent scarring, reduced range of
motion, weakness, and impaired functional
capacity
o psychological and social problems, which but gentle manner (Procter 2010).
significantly affect their ability to resume their
normal activities post discharge
Early initiation of rehabilitation is essential to maximise
functional outcomes for the patient
• The pain and psychological distress of a burn
has a massive impact on compliance
o An empathetic, encouraging and
understanding approach is necessary
•The urgency and importance of beginning
early rehabilitation should be communicated in a clear
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

• Oedema increasing for up to 36 hours post injury *Modify according to burn area, patient pain and
medical status.*
• Hypermetabolic response, peaking at five days post
injury 1mmobilisation post skin reconstruction surgery

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

Immobilisation of the hand

Deformity Prevention
The most common deformity associated 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. • A serial static splint is a device with no moving parts
Position of Safe Immobilisation designed to be remoulded as a contracture improves.
The most common serial static splint you will come
across is a thermoplastic palmar splint moulded in the
The position of safe immobilisation of the burned hand
position of safe immobilisation.
is essentially the opposite of the above claw deformity
position. This position involves: 20-30 wrist extension,
•A static progressive splint is a device designed to
80-90 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 stretch contractures through the application of
released, there is an immediate decrease in the tissue
incrementally adjusted static force to promote
tension but a delay in the retractions of the tissue to a lengthening of contracted tissue (Smiths 2009). There
shorter length. These stress relaxation properties of are various types of static progressive splints available
visco elastic scar tissue means it can accommodate to depending on the area affected. One such static
stretching force overtime. Dynamic and static splinting
progressive splint is a finger flexion strap splint. This
provide this prolonged low stretching force.
type of splint is used in the treatment of MCP
extension contractures. The flexion straps serially
Categories of Splints stretch scar bands along the dorsum of hand and wrist
causing extension contracture. The stretching force is
•Static or Dynamic

• Supportive or Corrective

• Rigid or soft

• Dorsal or Volar

• Digit, hand or forearm based

localised to the MCP joints by applying the straps via a
wrist extension splint. This stabilises the wrist
providing static support below the MCP joint
(Kwan 2002).
Dynamic Splinting
A dynamic splint is one which aids in initiating and
performing movements by controlling the plane and
range of motion of the injured part. It applies a mobile
force in one direction while allowing active motion in
the opposite direction. This mobile force is usually
•Precaution must be taken to ensure that splints do
not product friction causing unnecessary trauma to the
soft tissues (Duncan et al 1989).
• Precaution must be taken to ensure that splints do
not produce excessive pressure. There is particular risk
of pressure injury to skin after burn injuries due to
potential skin anaesthesia
(Leong 1997).
Splinting should not be used in isolation
but as an adjunct to a treatment regime

Management of Oedema Elevation

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

• A Bradford
sling can be
used to facilitate
elevation. This
type of sling
facilitates both
elevation and
applied with rubber bands, elastics and springs (Smith protection of wound
2009). area while still
•Dynamic extension splints are most commonly used allowing movement.
in the treatment of palmar and / or finger burns (i.e. Its foam design also
flexion contractures). All the finger joints including the reduces the risk of
MCP, PIP and DIP joints are in full extension (Smith the development of
2009). pressure points or
friction (Glassey
•Dynamic flexion splints are used in the treatment of 2004).
dorsal hand burns. During wound healing and When a patient is
subsequent scar maturation, the skin on the dorsal admitted with
aspect of the hand can markedly contract limiting digit severe burns of a
flexion. A dynamic flexion splint in the sub-acute stage large TBSA they are
of dorsal hand burns can aid in the prevention of MCP at risk of systemic
joint extension contractures (Kwan 2002). inflammation.
Therefore, not only
Splinting Precautions must the affected
•Splints need to be cleaned regularly to prevent limb be placed in elevation,
colonization by microbes which may lead to wound
infection the following precautions should also be taken
•Elevation of the head: This aids chest clearance,
(Wright et al 1989; Faoagali et al 1994) reduces swelling of head, neck and upper airways. It is
important not place a pillow underneath the head in
•Unnecessary use of splinting may cause venous and
the case of anterior neck burns as there is a risk of
lymphatic stasis, which may result in an increase in
neck flexion contractures
oedema
• Elevate all limbs effected
(Palmada et al 1999)
• Feet should be kept at 90 •Scar contraction

• Neutral position of hips Aims

• Care must be taken to reduce the risk of pressure • Optimise scar appearance
sores. •Limit effects of scar contraction/prolonged
(Procter 2010) positioning on range of motion and function
Coban
Coban wrap can be used to decrease hand oedema. •Address effects of prolonged bed rest
The main advantage of Coban wrap is that it does not
stick to underlying tissue, making it suitable for use in Common modalities
the acute stages of burns (Lowell 2003). There is •Mobilisation- both mobility and specific joint
currently limited quantity of evidence to support the mobilisation
use of Coban wrap in the treatment of Oedema. In
2003 Lowell et al carried out a case study involving a • Scar management adjuncts
subject with dorsal hand burns. o Pressure garments, silicone, massage
• Continuation of oedema/ positioning management
where necessary
Oedema Glove/Digi Sleeve
These are hand specific oedema management
Mobilisation
products. There is currently no specific evidence
The advantages of general mobilisation for a burns
available to support the efficacy of oedema gloves or
patient to counteract the effects of prolonged bed rest
digi sleeves in the reduction of oedema. However it is
are no different to that of a surgical or medical patient.
common practice in Irish hospital to provide these
Burns patients should be mobilised as early as possible
products to patients with excessive hand and finger
to avoid deconditioning and possible respiratory
oedema. Their use is based on the principle of
complications associated with prolonged bed rest
compression to reduce oedema which is heavily
(Esselman 2007).
supported by evidence (Latham and Radomski 2008).
As outlined in the above introduction, due to the
Role of the Physiotherapist in the Rehabilitation of
ethical issues surrounding withdrawal or modification
the Sub Acute Burn Patient
of treatment the evidence surround the optimal
duration, frequency and methods of physiotherapy
Beyond the acute stage of immobilisation, inpatient
interventions in the treatment of burn patients is
and outpatient rehabilitation typically consists of a
unclear. Despite this lack of clarify surrounding these
variety of interventions including pressure garment
issues it is clear that both active and passive
therapy, silicone therapy, scar massage, range of
mobilisation plays a key role throughout the stages of
motion and mobilisation techniques, strengthening,
burn recovery. Below is a summary of the
functional and gait retraining, and balance and fine
recommendations from the currently literature on
motor retraining ( Schneider et al, 2012). Interventions
passive and active mobilisation of burns.
should be tailored according to a full patient
assessment.
Active ROM
As it would be unethical to withhold treatment,
•Depending on the need for immobilisation gentle
physiotherapy intervention as a whole is not well
active ROM exercises is the preferred treatment during
investigated.
the acute stage of injury as it is the most effective
Schneider et al (2012) found a significant
means of reducing oedema by means of active muscle
improvement in contractures; balance and hand
function with inpatient rehabilitation, through a contraction (Glassey 2004). If this is not possible due to
longitudinal observational study of eleven people. sedation, surgical intervention etc. then positioning
However, in the following section, we will attempt to the patient is the next best alternative (see
immobilisation and position).
display the evidence for commonly used modalities.
The patient
Passive ROM
• Primary closure of wound
•Passive ROM exercises in the acute stage are
•Scar remodelling contraindicated as applying passive stretching forces
may result in future damage to the burned structures
(Boscheinen-Morrin 2004). Applying these passive •Observe the patient carrying out the AROM and
manoeuvres in the acute stage will result in increased PROM exercises prior to beginning treatment. Also
oedema, haemorrhage and fibrosis of the burned observe the patient taking on/off splints.
tissues (Cooper 2007).
•Always monitor for post exercise pain and wound
•The biomechanical principle of creep when passive breakdown.
stretching. A slow sustained stretch is more tolerable
for patient and more effective for producing •Avoid blanching for long period as you may
lengthening (Kwan 2002). compromise vascularity.

•Passive joint mobilisations can begin during the scar •The patient may present with a reduced capacity for
maturation phase once the scar tissue has adequate exercise secondary to increased metabolic rate, altered
tensile strength to tolerate friction caused by thermoregulation and increased nutritional demands.
mobilisation techniques •Postural hypotension may be present due to
(Boscheinen-Morrin and Connolly 2001). prolonged bed rest and low haemoglobin.
(ANZBA 2007)
Frequency, Duration Recommendations
•Physiotherapy intervention should be twice daily with Scar Management
patients prescribed frequent active exercises in Abnormal scarring is the most common complication
between sessions. of burn injuries, with the estimated prevalence of >
•For the sedated patient gentle passive range of 70% of those who suffer burn injuries (Anzarut et al,
motion exercises should be done 3 times a day once 2009). Not only do hypertrophic scars cause
indicated (Boscheinen-Morrin and Connolly 2001). psychosocial difficulties through their cosmetic
appearance, they may also be painful, pruritic, and
• Dependent on the severity of the burn active and they may limit range of motion where they occur on or
very gentle passive range of motion exercises for the near a joint (Morien et al 2009; Polotto 2011).
hand and fingers are begun from day one of injury. Hypertrophic scars require a continuum of dedicated
and specialised treatment from the acute stage to
Contraindications many years post treatment
• Active or Passive range of motion exercises should (Procter, 2010, ANZBA 2007).
not be carried out if there is suspected damage to
extensor tendons (common occurrence with deep The following is an examination of the evidence and
dermal and full thickness burns). Flexion of the PIP recommendations for use in the most common of
joints should be avoided at all costs to prevent these, including silicone gel, pressure garment therapy,
extensor tendon rupture. The hand should be splinted and massage. The positioning and mobilisation advice
in the position of safe immobilisation or alternatively a above is all applicable, and should be continued in the
volar PIP extension splint until surgical intervention management of hypertrophic scars where necessary.
(Boscheinen-Morrin and Connolly 2001) is discussed.
Scar Outcome Measures
• Range of motion exercises are also contraindicated 1. Vancouver Burn Scar Scale (VBSS/VSS)
post skin grafting as a period of 3-5 days
immobilisation is required to enable graft healing 2. Patient and Observer Scar Assessment Scale (POSAS)
(Boscheinen-Morrin and Connolly 2001).
Vancouver Burn Scar Scale (VBSS/VSS)
Practical factors to consider when mobilising Use: Most familiar burn scar assessment. Measures:
• Be aware of dressing clinic/daily dressing changes. pigmentation, pliability, thickness and vascularisation
Mobilisation should coincide with this as it is important (Fearmonti et al 2010).
to monitor the wound during AROM frequently. Reliability: Not enough evidence to make it a ‘gold
standard’ OCM. Moderate to high overall inter rater
•Timing of pain relief. This should be timed reliability. Test- Retest and intra – rater reliability has
appropriately to ensure maximal benefit during not been assessed for burn scars to date
treatment sessions. (Durani et al 2009).
Validity: When compared with POSAS scale, validity 2) Increase in temperature: A rise in temperature
was evident increases collagenase activity thus increased scar
(Durani et al 2009) breakdown.
Sensitivity: Most Scar OCM rely on categorical/ordinal
data with few levels which provides limited sensitivity 3) Polarized Electric Fields: The negative charge within
and can only identify considerable differences between silicone causes polarization of the scar tissue, resulting
scars in involution of the scar.
(Fearmonti et al 2010).
4) Presence of silicone oil: The presence of silicone has
Patient and Observer Scar Assessment Scale (POSAS) been detected in the stratum corneum of skin exposed
to silicone. However other researchers suggest
Use: Measures pigmentation, vascularity, thickness,
occlusive products without silicone show similar
relief, pliability and surface area. Also includes
results.
assessment of patient pain, itching, colour, stiffness,
thickness and relief. The only scale to measure 5) Oxygen tension: After silicone treatment the
subjective aspects of pain and pruritus (severe itching) hydrated stratum corneum is more permeable to
(Fearmonti et al 2010). oxygen and thus oxygen tension in the epidermis and
Reliability: Good internal consistency and reliability upper dermis rises. Increased oxygen tension will
(Durani et al 2009) inhibit the ‘‘hypoxia signal’’ from this tissue. Hypoxia is
Validity: Good concurrent validity a stimulus to angiogenesis and tissue growth in wound
(Durani et al 2009) healing, as a consequence removing the hypoxia stops
Sensitivity: Like the VBSS/VSS above, limited sensitivity new tissue growth. This theory has been
due to categorical/ordinal data contraindicated by other researchers.
(Fearmonti et al 2010)
Further studies are required to validate the reliability 6) Mast cells: It is suggested that silicone results in an
and validity of these scales as they are considered to increase of mast cells in the cellular matrix of the scar
be very subjective measures with subsequent accelerated remodelling of the tissue.
(Durani et al 2009). 7) Static electricity: Static electricity on silicone may
Scar scales like the Vancouver Burn Scar Scale influence the alignment of collagen deposition
(VBSS/VSS) and the Patient and Observer Scar (negative static electric field generated by friction
Assessment Scale (POSAS) are cost effective and can between silicone gel/sheets and the skin could cause
be easily transferred within a clinical setting. To collagen realignment and result in the involution of
optimise the scar scales, photographic evidence of the scars.
scar at timed intervals is of great value also to the (Bloemen et al 2009; Momeni et al 2009)
clinician
(Brusselaers et al 2010) Pressure Garment Therapy (PGT)
Silicone
Though the effectiveness of PGT has never been
proven, it is a common treatment modality for
Silicone Overview reducing oedema and managing hypertrophic scars
The use of silicone gel or sheeting to prevent and treat (Procter, 2010).
hypertrophic scarring is still relatively new. It began in Aims
1981 with treatment of burn scars o Reduce scarring by hastening maturation
(O’Brien & Pandit 2008). o Pressure decreases blood flow
The physiological effects of silicone in the treatment
of scarring remain unclear. Below is a summary of the o Local hypoxia of hypervascular scars
current hypotheses surrounding the physiological
effects of silicone. This summary has been adapted o Reduction in collagen deposition
from the most recently published literature on this o Therefore
topic. o Decreases scar thickness
1) Hydration Effect: Hydration can be caused by the o Decreases scar redness
occlusion of the underlying skin. It decreases capillary
activity and collagen production, through inhibition of o Decreases swelling
the proliferation of fibroblasts
o Reduces itch
 o Protects new skin/grafts Garments should be worn for up to one year, or until
scar maturation
o Maintains contours (Anzarut et al 2009; Engrav et al 2010 and Bloeman et
(Procter 2010) al 2009).
Possible complications/ confounding factors for use
The exact physiological effects of how pressure of PGT
positively influences the maturation of hypertrophic
•Lack of a scientific evidence to established optimum
scars remain unclear.
pressure
Below is a summary of the current hypotheses
surrounding the physiological effects of pressure •Non-Compliance ( due to comfort, movement,
garments. This summary has been adapted from the appearance)
most recently published literature on
•Heat and perspiration

1) Hydration effect: decreased scar hydration results in •Swelling of extremities caused by inhibited venous
mast cell stabilization and a subsequent decrease in return
neurovascularisation and extracellular matrix
production. However this hypothesis is in contrast with • Skin breakdown
a mechanism of action of silicone, in which an increase •Web space discomfort
of mast cells causes scar maturation.
• Inconvenience
2) Blood flow: a decrease in blood flow causes
excessive hypoxia resulting in fibroblast degeneration •Personal hygiene difficulties possibility of infection
and decreased levels of chondroitin-4-sulfate, with a
subsequent increase in collagen degradation. •Allergies to material
(MacIntyre & Baird 2006; Glassey 2004)
3) Prostaglandin E2 release: Induction of prostaglandin Massage
E2 release, which can block fibroblast proliferation as
well as collagen production Five principles of scar massage:
(MacIntyre & Baird 2006) 1. Prevent adherence

Recommendations for practice and safety 2. Reduce redness

considerations
3. Reduce elevation of scar tissue
Pressure: 15 mmHg has been noted as the minimum to
elicit change, and pressures of above 40 mmHg have 4. Relieve pruritus
been found to cause complications. Both Anzarut et al
5. Moisturise (Glassey 2004)
(2009) and Engrav et al (2010) used pressures of
between 15 and 25 mmHg.
Scar Massage Techniques
Time: It is recommended that garments are worn for
up to 23 hours a day, with removal for cleaning of the •Retrograde massage to aid venous return, increase
wound and garment, and moisturisation of the wound. lymphatic drainage, mobilise fluid

• Effleurage to increase circulation

(Procter 2010; Anzarut et al 2009 and Bloeman et al
2009).
Duration: garments can
be worn as soon as
wound closure has been
obtained, and the scar is
stable enough to
tolerate pressure. Post
grafting, 10-14 days
wait is recommended,
at the discretion of the
surgeon
(Bloeman et al 2009).
• Static pressure to reduce pockets of swelling (Procter 2010).

•Finger and thumb kneading to mobilise the scar and Aerobic and Resistance Training Post Burn
surrounding tissue

• Skin rolling to restore mobility to tissue interfaces Rationale for Aerobic and Resistance Training
• Low cardiorespiratory endurance has been found to
• Wringing the scar to stretch and promote be a concern for all
collagenous remodelling
(Willis et al 2011)
• Frictions to loosen adhesions
•Aerobic capacity as measured by VO2 peak and time
(Holey and Cook 2003) to fatigue has been found to be lower in adults and
children of >15% TBSA at one year post burn,
Recommendations for practice and safety compared to age matched healthy controls
considerations.
(Willis et al 2011; McEntine et al 2006)
Insufficient consistency in literature with regards to
protocols on frequency or duration of treatment. •Muscular strength and lean body mass has been
Suggestions for practice include found to be significantly less in patients suffering from
(Shin and Bordeaux, 2012, Morien et al, 2008) burns of >30% TBSA, particularly in exercises requiring
• Clean hands essential a high velocity (Disseldorp et al 2007; Ebid et al 2012).
The systemic effects caused by large surface area
• Use non irritating lubricant, free of any known
burns means that weakness may be global, not just
sensitisers.
local to the site of the injury
• Modify practice according to patient stage of healing,
(Grisbrook et al 2012b)
sensitivity and pain levels.
•Reduced lean body mass, endurance and strength has
Contraindications: been associated with limited standing/walking
Shin and Bordeaux 2012 tolerance, reduced upper limb function and lower
• Compromised integrity of epidermis health related QOL and ability to participate in
activities
• Acute infection
(Grisbrook et al 2012b).
• Bleeding
•This has been found to persist beyond discharge from
• Wound dehiscence, hospital despite routine physiotherapy and
• Graft failure occupational therapy in hospital (Disseldorp et al
2007). Though protein metabolism begins to normalise
• Intolerable discomfort 9-12 months post burn, patients are still found

•Hypersensitivity to emollient •All found a decrease of up to 20% in lean muscle mass

compared to age matched controls
The Role of the Physiotherapist in the Rehabilitation
of the Chronic Burn Patient. •Adults with a TBSA >30% suffered a significant
The patient decrease in torque, work and power in the quadriceps
•Healing process may continue for up to two years, as muscles compared to age matched controls.
scar tissue remodels and matures (De Lauter et al 2007)
Exercise and Hypermetabolism
•May require functional retraining and integration
back into the community and activities. Though exercise requires an increase in energy
expenditure and metabolism for a short period of time
It is important to note that though scar management is no adverse effects have been found with regard to
initiated in the sub-acute phase, it may need to be exacerbating hypermetabolism or protein catabolism.
continued long term, as many patients suffer from
continuing limitation to range of motion
o All studies investigating the effects of exercise on • None showed significant intolerance for heat as
lean body mass found it to increase, particularly with measured by heart rate and core temperature,
resistance training measured rectally
( Grisbrook et al 2012b; Suman and Herndon 2007; • No significant difference in whole body sweat rate
Suman et al 2001; Przkora et al 2007)
• Overcompensation by healthy skin in the burned
o Suman et al, 2001, found an increase of 15% in patients.
resting energy expenditure in children with burns of
>40% TBSA who were not treated with resistance and •Suggested physical history was a factor in
aerobic exercise, while the REE of those who determining patients’ ability to thermoregulate.
participated in the intervention remained stable. Therefore adaptations may occur through training.
o Suggested that exercise may have sympathetic
nervous system attenuating effects However, studies involving heat loads of 40 degrees
have found a significant inability to maintain adequate
•A balance of resistance and aerobic exercise may thermoregulation. Due to the small study numbers of
cause a decrease in SNS activity, decreasing catabolic the above, and the controversy surrounding the
effects. efficacy of measuring core temperature accurately, it is
o Exercise is required to integrate dietary amino acids advised that patients are closely monitored initially
into lean muscle mass (Herndon and Tomkins 2004) during aerobic exercise for signs of heat intolerance.

**Thermoregulation ***Inhalation injury and pulmonary insufficiency

Human skin produces sweat to dissipate heat in
response to thermal stress (McEntine et al 2006). A Long term pulmonary function is compromised in some
proper sweat response requires functional integrity of patients post severe burn
the • Lasts several years
• Sweat glands
• Documented in both children and adults (Grisbrook
•Skin circulation et al 2012a)

• Neural control of the skin (McEntine et al 2006) •Caused by

o Smoke inhalation
Full thickness burns damage the dermal appendages
o Direct thermal damage to airways
including sweat glands. These are not replaced by
grafting. There is also a decreased density of sweat o Pulmonary oedema
glands in the donor site post grafting
(Esselman et al 2007). o Respiratory tract infection
However, McEntine et al 2006 found that in 15
children with an average of 55% TBSA there was o Complications from intubation
•No significant difference in core temperature, o Recurrent infection leading to chronic
measured tympanically, pre or post 20 minutes of inflammation
treadmill exercise at room temperature compared to Less likely to cause dysfunction in <30% TBSA,
age matched healthy controls. no injury over torso, and no inhalation injury
(Willis et al 2011)
•No significant difference in average skin temperature
Evidence for impact on aerobic and exercise capacity
between burned and healthy children.
conflicting (Grisbrook et al 2012a). However Willis et al
•Significantly increased skin temperature in healthy (2011) studied 8 males post > 15% TBSA burns at one
versus burned skin per child. year post injury, and found
• Significantly decreased FEV1, peak VO2 and time to
Austin et al, 2003 studied 3 adults with > 60% TBSA, 3 fatigue, in the burned patients
with between 30-40 TBSA and 2 unburned patients
• No significant decrease in SpO2 at baseline or peak
post 1 hr cycling at 35 degrees and 60% humidity
VO2- however, the SpO2 of burned patients took
significantly longer to stabilise at baseline post
exercise.
• No significant difference in participation levels in
physical activity, though burn survivors were more
likely to participate in work rather than leisure activity.
•Burns survivors were less likely to participate in normal guidelines may be adequate.
vigorous intensity exercise over 9 METs
•Therefore, decreased pulmonary function did not week. There have been no studies to investigate the
prevent them from participating
•The lower relative intensity of their exercise may have
caused their decreased aerobic capacity.
All of the above factors must be considered as both a
contributor to the patients’ loss of strength and
aerobic capacity, and a potential limiter of their ability
to participate in therapy. Careful monitoring and
modification of treatment according to individual
response is advised.
Resistance Training Summary and Recommendations
for Practice
Exercise prescription: Post two years, Grisbrook et al
(2012b) found that burned patients responded to
resistance exercise similarly to controls. Therefore,
•Frequency: All studies investigating the effects of
resistance training used a frequency of three times per
optimum frequency for resistance training in this
population. Suman et al (2001), suggested that a break
of more than 48 hrs must be given between bouts of
resistance training.
o Resistance exercise causes microtrauma to
muscles already in a compromised state.
o Resistance exercise in burned patients
stimulates protein synthesis as in unburned
subjects- However; a longer period of recovery
may be required for optimum results.

Aerobic Training Summary and Recommendations for •Type/ Intensity: Children: using free weights or
Practice resistive machines: 1 set of 50-60% of the patients 3
RM week 1, followed by a progression to 70-75% for
Exercise prescription: week 2-6 (4-10 repetitions), and 80-85% week 7-12, (8-
•Frequency: The majority of papers which investigated 12 repetitions) (Suman et al 2001; Suman and Herndon
an aerobic intervention used 3 times per week as their 2007).
frequency (De Lauteur et al 2007; Grisbrook et al •Isokinetic training: 10 reps at 150 degrees per
2012). These obtained significant improvements. second, using 1-5 sets for the 1st -5th session,6 sets for
However, Przkora et al (2007) used a frequency of 5 the 6th -24th session, and 10 sets from 25th to 36th
times per week with children. There have been no session, with three minute rests between sets. (Ebid et
studies investigating optimal frequency. al 2012).
•Intensity: All studies used between 65 and 85% •Mixed and functional strength training: Grisbrook et
predicted heart rate max, with one study using al (2012b) commenced on the biodex, targeting
interval training of 120 seconds 85% HRM and 120 specific muscle groups for the desired functional goal,
seconds of 65-70 HRM. All studies obtained positive and progressed to resistive machine and finally free
effect, with none directly comparing intensities to weight training using functional items. Intensity was
determine the optimum. De Lauteur et al (2007), 50-60% of 1 RM initially, for 10-15 reps, adjusting as 1
concluded that whether the patient gradually RM increased. While no studies have compared the
increased their intensity by working to a specific quota optimum type/intensity of exercise, this may be the
each week, or if they simply worked at their target optimum approach. Providing functional exercises may
heart rate for as long as they could tolerate, there was also increase motivation and compliance.
no significant difference in gains in aerobic capacity. •Time: All the studies used a protocol of 12 weeks.
•Type: All interventions used treadmill training, There were no studies comparing the efficacy of
whether walking or running. shorter or longer time frames, however, given that loss
•Time: All studies recommended the duration of of lean body mass is a possible cause of strength loss
treatment be 12 weeks, with the exception of Paratz et post burn, an exercise programme of longer than eight
al, 2012, who investigated a high intensity six week weeks is probably required to ensure hypertrophy and
programme. However, the specific results of this are optimum gains in the burn patient (Suman et al 2001)
unknown. Sessions were 20-40 minutes in length, with
the majority using 30 minutes (Grisbrook et al 2012; De Safety Considerations for Strength and Aerobic
Lauteur et al 2007; Przkora et al 2007) Training:
Initiating aerobic and strength training: pressure may be advisable, particularly on initiation of
•studies stipulated a minimum of six months to two exercise and when exercising with additional thermal
years post burn before initiation of programmes, stress. Manage the environment to minimise thermal
though many subjects were included who had been stress initially in particular.
burned many years before. These participants all
benefited from the interventions. •Particularly those at risk of reduced pulmonary
function post burn (i.e., >30% TBSA, injury to torso, or
•Suman and Herndon (2007) suggested that the time inhalation injury), monitor SpO2 and RPE during
frame of 6 months post burn was chosen based on exercise. Allow additional rest periods to allow SpO2 to
clinical experience because by this time paediatric return to normal levels post exercise, as this has been
patients with >40% TBSA burns were shown to be delayed.
o 95% healed
o ambulatory
o had had the opportunity to return home
•Therefore, more favourable psychological status
• There were no studies investigating early training
o With extensive burns, adequate healing of
wounds and medical stability required before
initiating aerobic/strength exercise

Other safety considerations:

• Though exercise has been shown to increase lean
body mass, liaison with doctors concerning anabolic
steroids and medication and with dieticians regarding
optimal nutrition is recommended in order to ensure
correct management of hypermetabolisim.

•Caution should be used with regard to impaired

thermoregulation. Monitoring of heart rate and blood
 REFERENCES
 Physical medicine and rehabilitation 3rd edition
 Braddom’s physical medicine & rehabilitation
5th edition
 Handbook of Pathophysiology (January 15,
2001): by Springhouse Corporation, With 13
Contributors, Springhouse By OkDoKeY
 Delisa’sphysical 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