COLLEGE OF PHYSICAL AND RESPIRATORY THERAPY

S.Y. 2016-2017

This written report on

MEDICAL BACKGROUND: BURNS

Is submitted to the

COLLEGE OF PHYSICAL THERAPY AND RESPIRATORY THERAPY

In partial fulfillment to the requirements on the subject
SEMINAR I

SUBMITTED TO:
Mr. Bernardo Tayaban Jr., PTRP, MDA
Maverick Kaypee A. Colet, PTRP

SUBMITTED BY:
JOANNA EDEN GURTIZA

Novemeber 14, 2016

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

renal dysfunction from prolonged chemical exposure).
Ultraviolet and Ionizing Radiation Burns
A nonblistering sunburn is a first-degree burn from
the overexposure of the skin to UV radiation. More
severe burns can also occur due to UV exposure and
would . Ionizing radiation burns with or without
thermal injury occur when electromagnetic or
particulate radiation energy is transferred to body
tissues, resulting in the formation of chemical free
radicals.2Ionizing radiation burns usually occur in
laboratory or industrial settings, but can also be seen
in the medical setting following radiation treatment,
most often for cancer. The severity of the ionizing
radiation burn depends on the dose, the dose rate,
and the tissue sensitivity of exposed cells.
Often referred to as acute radiation syndrome,
complications of ionizing radiation burns include
Gastrointestinal: Cramps, nausea, vomiting,
diarrhea, and bowel ischemia
Hematologic: Pancytopenia (decreased number of
red blood cells, white blood cells, and platelets),
granulocytopenia (decreased number of granular
leukocytes), thrombocytopenia (decreased number of
platelets), and hemorrhage
Vascular: Endothelium destruction
classification of burn

Epidermal Burn
An epidermal burn, as the name implies, causes cell
damage only to the epidermis (Fig. 24.2). This depth
of burns correlates to practice pattern 7B, Impaired
Integumentary Integrity Associated with Superficial
Skin Involvement, in the Guide to Physical Therapist
Practice. The classic sunburn is the best example of
an epidermal burn. Clinically, the skin appears red or
erythematous.The erythema is a result of epidermal
damage and dermal irritation, but there is no injury to
the dermal tissue. There is diffusion of inflammatory
mediators from sites of epidermal damage and

release of vasoactive substances from mast cells. The

surface of an epidermal burn is dry. Blisters will be
absent, but slight edema may be apparent. After an
epidermal burn, there is usually a delay in the
development of pain, at which point the area
becomes tender to the touch. Following epidermal
damage, the injured epidermal layers will peel off or
desquamate in 3 to 4 days. Epidermal healing is
spontaneous; that is, the skin will heal by itself, and
no scar tissue will form.
Superficial Partial-Thickness Burn

With a superficial partial-thickness burn (Fig 24.3)

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

blanch, which means if pressure is exerted against the

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

Deep Partial-Thickness Burn

A deep partial-thickness burn (Fig. 24.4)
involves destruction of the epidermis and papillary
dermis with damage down into the reticular dermal
layer. As this burn nears the deepest dermis it begins
to resemble a full-thickness burn, and the depth best

matches practice pattern 7C, Impaired Integumentary

Integrity Associated with Partial-Thickness Skin
Involvement and Scar Formation, in the Guide to
Physical Therapist Practice.21 Most of the nerve
endings, hair follicles, and sweat ducts will be injured
because most of the dermis is destroyed.
Deep partial-thickness burns appear as a
mixed red or waxy white color. The deeper the injury,
the more white it will appear. Capillary refill will be
sluggish after the application of pressure on the
wound. The surface usually is wet from broken
blisters and alteration of the dermal vascular
network, which leaks plasma fluid. Marked edema is a
hallmark sign of this burn depth. There is a large
amount of evaporative water loss (15 to 20 times
normal) because of tissue and vascular destruction.
An area of deep partial-thickness burn has diminished
sensation to light touch or sharp/dull discrimination
but retains the sense of deep pressure due to the
location of the Pacinian corpuscle deep in the
reticular dermis. Healing occurs through scar
formation and re-epithelialization. By definition, the
dermis is only partially destroyed; therefore, some
viable epidermal cells may remain within the surviving
epidermal appendages and serve as a source for new
skin growth.
The depth of a deep partial-thickness injury is
sometimes difficult to determine, so allowing the
wound to demarcate (between normal and damaged
tissue) during the first few days is necessary.
Demarcation becomes evident after several days as
the dead tissue begins to slough. Hair follicles that
penetrate into the deeper dermal regions below the
burn level remain viable. Preservation of hair follicles
and new hair growth will indicate a deep
partialthickness burn rather than a full-thickness
injury, and there is a corresponding greater potential
for spontaneous healing. Particularly important
factors that determine which epidermal structures
survive and which die include the thickness of the skin
in a particular location and/or the distance of the area
from the source of heat.
Deep partial-thickness burns that are allowed
to heal spontaneously will have a thin epithelium and
may lack the usual number of sebaceous glands to
keep the skin lubricated. New tissue usually appears
dry and scaly, is itchy, and is easily abraded. Creams
are necessary to artificially lubricate the new surface.
Sensation and the number of active sweat ducts will
be diminished.
A deep partial-thickness burn generally will
heal in 3 to 5 weeks if it does not become infected. It
is critical to keep the wound free of infection, because

infection can convert a deep partial-thickness burn

into a deeper injury. The development of
hypertrophic and keloid scars is a frequent
consequence of a deep partial-thickness burn.
Full-Thickness Burn
In a full-thickness burn (Fig. 24.5) all of the
epidermal and dermal layers are destroyed
completely. In addition, the subcutaneous fat layer
may be damaged to some extent. This burn depth is

consistent with practice pattern 7D, Impaired

Integumentary Integrity Associated with FullThickness Skin Involvement and Scar Formation, in
the Guide to Physical Therapist Practice.
A full-thickness burn is characterized by a
hard, parchment-like eschar covering the area. Eschar
is devitalized tissue consisting of desiccated coagulum
of plasma and necrotic cells. Eschar feels dry,
leathery, and rigid. The color of eschar can vary from
black to deep red to white; the latter indicates total
ischemia of the area. Frequently, thrombosis of
superficial blood vessels is apparent and no blanching
of the tissue is observed. The deep red color of the
tissue results from hemoglobin fixation liberated from
destroyed red blood cells.
Hair follicles are completely destroyed, so
body hairs pull out easily. All nerve endings in the
dermal tissue are destroyed so the wound will be
insensate (without feeling); however, a patient still
may experience a significant amount of pain because
adjacent areas of partial-thickness burn usually
surround a full-thickness injury.

A major problem that arises from deep burns

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

extremity or chest wall. Figure 24.6 shows an

escharotomy and the result of pressure that forces
the incision to gape. Following an escharotomy,
pulses are frequently examined to monitor
restoration of circulation. If the escharotomy is
successful, there will be an immediate improvement
in the peripheral blood flow, demonstrated by normal
pulses distal to the wound and by return of normal
temperature and capillary refill of the distal
extremity.
Although at times it may be difficult to
differentiate a deep-partial from a full-thickness burn
in the early postburn period, the differences will
become evident after several days. With a fullthickness burn, there are no sites available for reepithelialization of the wound. All epithelial cells have
been destroyed, and skin grafting will be necessary.
Grafting is discussed in detail in the section titled
Surgical Management of the Burn Wound.

Subdermal Burn

An additional category of burn, the subdermal burn,

involves complete destruction of all tissue from the
epidermis down to and through the subcutaneous
tissue (Fig. 24.7). This depth of injury correlates with
practice pattern 7E, Impaired Integumentary Integrity
Associated with Skin Involvement Extending into
Fascia, Muscle, or Bone and Scar Formation, in the
Guide to Physical Therapist Practice.21 Muscle and
bone are subject to necrosis when burned. This type
of burn occurs with prolonged contact with a heat
source and routinely occurs as a result of contact with
electricity. Extensive surgical and therapeutic
management is necessary to return a patient to some
degreeof function.
Allograft (or homograft): skin used for temporary
coverage of a burn wound;the skin is taken from the
same species(usually cadaver skin).
Autograft: skin taken from an unburned area of a
patoent, which is then transplanted to cover a wound
Blanch: a white spot seen in the skin when pressure is
applied. This is an indication of the presence of viable
capillary beds; and the blanched area will become
pink when pressure is released if capillary bed is
perfused.
Closed technique: the wound care technique of
covering a wound from the outside environment with
an appropriate dressing.
Contact inhibition: inhibition of the migration of
epithelial cells when they are in contact with other
epithelial cells on all sides.
Debribement: the removal of escar and or any loose
tissues from burn wound.
Sharp debridement: use of sterile scissors and forceps
to remove eschar.
Dermal healing: the process whereby the dermis is
repaired via scar formation.

Dermatome: device used to harvest then slices of skin

for skin grafting.
Dermis: deep layer of skin that contais bloodvessels,
lymphatics, nerve endings, collagen, and elastin, and
that encloses the sweat glands, sebaceous glands, and
hair folicles.
Desquamation: peeling of the outer layers of the
epidermis.
Donor site: site from which a skin graft is taken.
Electrical burn: injury sustained from the passage of
electric current through the tissues of the body.
Epidermis: the outer most layer of the skin, which
provides the body with a barrier to the environment.
Epithelial healing: the process of regeneration of the
epidermis through epithelial cell migration,
proliferation, and differentiation.
Epithelial islands: surviving tissue from which new
epithelial cell growth will originate.
Eschar: the dead, necrotic tissue from a burn wound.
Eschartomy: midlateral incision of the burned eschar
used to relived pressure in an extremity or on the
trunk.
Fibroblast: a connective tissue cell that forms the
fibrous tissues in the body.
Full thickness burn: burn involving the entire dermis.
Full thickness skin graft: graft containig epidermis
and full dermal thickness.
Heterotopic oddification: abnormal bone growth in
soft tissues.
Hypertrophy: increase in size or bulk.
Inhalation injury: injury sustained by the lungs due to
breathing hot and or toxic gases. Usually occurs when
individual is burned in a closed space.
Keloid scrar: raised scar that extends beyond the
boundaries of the original burn wound.
Mesh graft: proces whereby the donor skin is placed
through a device that increases the surface area of
the graft.
Open technique: absence of dressings: often used
after skin grafting to the face
Partial thicness burn: burns involving the epidermis
and parrt of the dermis. Subcategories are superficial
partial thickness and deep partial thickness burns,
depending on the amount of dermis involved.
Primary excision: surgical removal of eschar.
Rule of nines: estimation used to dtermis the amount
of total body surface area that has been burned. It
divides the body into segments that are
approximately 9 percent of the total.
Sheet graft: autograft that is aplied in a single sheet
without alteration. May be split-thickness or full
thciness in depth.

Skin substitutes; tissues engineeres in a laboratory

which are used to restore the essential funtions of the
skin, provide a barrier to the environment, and
control evaporative water loss.
Split-thickness sin graft: graft containing epidermis
and only the superficial layers of the dermis.
Subdermal burn: burn involving only the epidermial
layer.
Wound contraction: movement of the wound
margins toward the center of the defect. Thought to
be caused by the active movement of the fibroblat in
the wound bed.
Xenograft or heterograft: skin used as a temporary
wound cover; which is harvested from another
species of animal, usually a pic.
z-plasty: procedure used to surgically lengthen a burn
scar contracture to allow for greater ROM.
Zone of coagulation: cells are irreversible damage.
And skin death occurs.
Zone of hyperemia: site of minimal cell damage.
Tissue should recover within several days.
Zone of stasis: site of injured cells that may die
without specialized treatment

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 skins physical characteristics such as the
keratinized cells and
waterproofing properties of the glycolipids.
Keratin helps waterproof the skin and protects from
abrasions and bacteria
Glycolipids prevent diffusion of water and watersoluble 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
Langerhans cells and macrophages present in the
skin helps activate the bodys immune system.
DNA structure the electrons in DNA absorb UV
radiation and converts it to heat
Temperature regulation
Production of copious amounts of sweat to dissipate
heat
When body temperature rises and is hotter than the
external environment the
blood vessels in the dermal area dilates and sweat
glands are stimulated into activity.
Evaporation of the sweat from skins surface helps
dissipate heat from the body.
Constriction of dermal blood vessels to retain heat
When it is cold outside, the dermal blood vessels
constrict and pull the blood away
from the skin and keeps it close to the body core to
protect crucial internal organs.
Cutaneous Sensations
- cutaneous sensory receptors (see - nervous system)
Meissners corpuscles: light touch
Merkel discs: light touch
Pascinian receptors lies in deeper
dermis/hypodermis & detect deep pressure contacts
Hair root plexus: sensations from movement of
hairs
Hair follicle receptors movement across the
surface of the skin
Bare nerve endings: painful stimuli (chemicals, heat,
cold)
Excretion/Absorption
Elimination of nitrogen-containing wastes
(ammonia, urea, uric acid), sodium chloride, and
water. It regulates water loss
Metabolic Functions
Synthesis of Vitamin D increases calcium
absorption in the body
Vitamin D is a fat-soluble vitamin that may be
absorbed from the intestines or may be produced
by the skin when the skin is exposed to ultraviolet
light (particularly sunlight).It is converted to
its active form by the body in 2 steps, occurring first in
the liver and completed in the kidneys. In
its active form, vitamin D acts as a hormone to
regulate calcium absorption from the intestine
and to regulate levels of calcium and phosphate in the
bones. Vitamin D deficiency causes
Rickets

 When the body is deficient in vitamin D, it is unable

to properly regulate calcium and phosphate
levels. If the blood levels of these minerals becomes
low, the other body hormones may
stimulate release of calcium and phosphate from the
bones to the bloodstream.
Chemical conversion of many substances
Blood Reservoir preferential shunting of blood as
needed
Types of Membranes - thin sheet-like structures that
protect parts of the body
Serous Membranes
Line body cavities that have no opening to the
outside
Secrete a watery fluid called serous fluid that
lubricates surfaces.
Mucous Membranes
Line cavities and tubes that open to the outside
Synovial Membranes
Form the inner lining of joint cavities
Secrete a thick fluid called synovial fluid
Cutaneous Membrane also known as skin
Characteristics of Skin
The integument covers the entire body and is the
largest organ ~ 2 meters and heaviest organ
16% of body mass of the body.
Composed of the epidermis and dermis
Pliable, yet durable
Thickness: 1.5 to 6.0 mm
Types of Skin
Thin - 1-2 mm on most of the body and 0.5 mm in
eyelids
Hairy
Covers all parts of the body except palms of hands
and soles of feet
Thin epidermis and lacks stratum lucidum
Lacks dermal papillae
Has more sebaceous glands
Fewer sweat glands, sensory receptors than thick
skin
Thick - up to 6 mm thick on palms of hands and soles
of feet
Hairless
Covers palms of hands and soles of feet
Thick epidermis and a distinct stratum
lucidum
Epidermal ridges are present due to well developed,
numerous dermal papillae.
Lacks sebaceous glands, has more sweat glands
Sense receptors are also more densely packed.
Layers of the Skin
Epidermis

Types of Cells
Keratinocytes
90 % of epidermal cells are keratinized
contains keratin (fibrous protein)
protects and waterproofs the skin
Melanocytes
8% of the epidermal cells
produces melanin
contributes to skin color and absorbs UV
light
Langerhans cells
Arise from red bone marrow and
migrate to the epidermis
Constitute small portion of epidermal cells
Participate in immune responses
Easily damaged by UV light
Merkel cells
Least numerous of the epidermal cells
Found in the deepest layer of the epidermis
Along with tactile discs, they function in
sensation of touch
Layers of epidermis
Stratum corneum
25-30 layers of dead flat keratinocytes
Shed continuously and replaced by cells from the
deeper strata
Serves as a water, microbe, injury barrier
Stratum lucidum
Present only in thick skin
3-5 layers of clear, flat, dead keratinocytes
Dense packed intermediate filaments
Thick plasma membranes
Stratum granulosum
Located above the stratum spinsosum
3-5 layers of flattened keratinocytes undergoing
apoptosis
Organelles begin to disintegrate becomes nonliving
cells
Marks the transition between deeper
metabolically active strata and the dead cells of the
superficial strata.
Contains lamellar granules
Secretes lipid-rich secretion that acts as a water
sealant
Stratum spinosum
Located above the stratum basale
8-10 layers of keratinocytes
Some cells retain their ability for cell division
Cells have spinelike projections (bundles of

filaments of the cytoskeleton) tightly joins cells

to each other.
Provides skin both strength and flexibility
Stratum basale
Also referred to as stratum germinatum because this
is where new cells are formed
Deepest layer of the epidermis
Single row of cuboidal or columnar keratinocytes
Growth of epidermis
Newly formed cells in the stratum basale undergo
keratinazation as they are pushed to the surface.
They accumulate more keratin during the process
Then they undergo apoptosis
Eventually they slough off and are replaced
The process takes about 4 weeks
Rate of cell division in the stratum basale increases
during injury
Dermis
Second deepest part of the skin
Blood vessels, nerves, glands and hair follicles are
embedded here
Composed mainly of connective tissues (collagen
and elastic fibers)
Collagen fibers make up 70% of the dermis and give
structural toughness and strength. Elastin fibers are
loosely arranged in all directions and give elasticity to
the skin
Has two layers Papillary Layer and Epidermal layer.
Papillary layer
Superficial portion of the dermis
Consist of areolar connective tissue containing
elastic fiber
Surface area is increased due to projections called
dermal papillae
which contains capillaries or tactile receptors
Epidermal ridges conforms to the dermal papillae
Reticular layer
Deeper portion of the dermis
Consist of dense irregular connective tissue
containing collagen/elastic fibers
Provides skin with strength and elasticity
Contains hair follicles, nerves, sebaceous and
sudoriferous glands
Hypodermis
(subcutaneous) Attaches the skin to underlying
organs and tissues
Not part of the skin - lies below the dermis
Contains connective tissue and adipose tissues
(subcutaneous fat) for insulation

Infants and elderly have less of this than adults and

are therefore more sensitive to cold
Skin Appearances
Epidermis appears translucent when there is little
melanin or carotene
White skin appears pink to red depending on
amount and oxygen content of blood moving
in the capillaries of the dermis.
Albinism is an inherited trait where a person cant
produce melanin. The have melanocytes but are
unable to make tyrsinase (the enzyme which initiates
melanin production) so. melanin is missing in
their hair, eyes, and skin.
Skin color as diagnostic clues for medical conditions
o Cyanotic (cyan = blue) Ex: someone who has
stopped breathing and the skin appears bluish
o because the hemoglobin is depleted of oxyen
o Jaundice (jaund = yellow) - Buildup of bilirubin
(yellow pigment) in the blood gives a yellowish
appearance of eyes and skin indicating liver disease
Bilirubin is produced when red blood cells
get old and are broken down by the body. Normally it
is processed in the liver and then deposited
in the intestine so it can come out in the stool.
o Erythema (ery = red) - Engorgement of capillaries in
the dermis indicating skin injury,
infection, heat exposure, inflammation, allergies,
emotional state, hypertension
o Pallor - paleness, emotional state, anemia, low
blood pressure
o Bronzing - Addisons disease, adrenal cortex
o Bruising (hematoma)- escaped blood has
clottedhematomas , deficiency in Vitamin C or
hemophilia
o leathery skin - overexposure clumping of elastin
fibers depressed immune system
o can alter DNA to cause skin cancer
o photosensitivity - to antibiotics & antihistamines
Skin Color
genetic factors, environmental factors and volume
of blood
Skin Pigments - three pigments are responsible for
skin color- melanin, carotene, hemoglobin
Melanin
Located mostly in epidermis
Number of melanocytes are about the same in all
races
Difference in skin color is due to the amount of
pigment that melanocytes produce and disperse to
keratinocytes.
Freckles are caused by the accumulation of melanin
in patches

Liver spots are also caused by the accumulation of

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

Most of your touch receptors sit close to your skin's

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

3- 4 million glands in your body empties onto the

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

An in depth knowledge of pathophysiology of burns,

and their effects both locally and systemically is
necessary to ensure effective management of a
patient with a burn injury.
Zones of Injury and Wound Conversion
The local effect involves three burn
(Hettiaratchy and Dziewulski 2004)

zones:

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

IV. ETIOLOGY

Thermal burns, the most common type,

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

or car fires is exacerbated by the inhalation of toxic

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

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

VI. CLINICAL SIGNS AND SYMPTOMS/ PHYSICAL DISABILITIES/

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

Potential impairment
Body area

Impairment

Face

Facial disfigurement (contractures

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

Neck

Trunk

Decreased respiratory function

Breast entrapment
Perineal banding
Axilla

Hands

Arms and legs

Foot and ankle

Type 1: either anterior or

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

Systemic Complications of Burn Injury

Body System
Complications
Respiratory
Inhalation injury, restrictive
pulmonary pattern
(which may OCCur with a burn
on the trunk),
atelectasis,
pneumonia,
microthrombi, and adult
respiratory distress syndrome
Cardiovascular
Hypovolemiaihypotension,
pulmonary hypertension,
subendocardial
ischemia,
anemia, and disseminated
intravascular coagulopathy
GastroinrestinaV
Stress ulceration, hemorrhage,
genitourinary
ileus, ischemic co\iris,
cholesrasis, liver failure, and
urinary rract infection
Renal
Edema, hemorrhage, acute
tubular necrosis, acure
renal failure
paz

Electrical burns
Complications specific to electrical injury include the
following"s:
Cardiovascular: Cardiac arrest (ventricular
fibrillation for electric current or asystolic for
lightning), arrhythmia (usually sinus tachycardia or
nonspecific ST changes) secondary to alterations in
electrical conductivity of the heart, myocardial
contusion or infarction, or heart wall or papillary
muscle rupture
Neurologic: Headache, seizure, brief loss of
consciousness or coma, peripheral nerve injury
(resulting from ischemia), spinal cord paralysis (from
demyelination), herniated nucleus pulposus, or
decreased attention and concentration
Orthopedic: Dislocations or fractures secondary to
sustained
muscular contraction or from a fall during the burn
injury
Other: Visceral perforation or necrosis, cataracts,
tympanic
burn shock (due to fluid shifts out of the vascular
compartments, possibly leading to kidney damage
and renal
failure)
peptic ulcer disease (due to decreased blood supply
in the abdominal area) disseminated intravascular
coagulation (more severe burn states)

membrane rupture, anxiety, depression, or posttraumatic stress disorder

Chemical Burns
pulmonary complications (e. g. , airway obstruction
from bronchospasm, edema, or epithelial sloughing)
and metabolic complications (e. g., liver necrosis or
renal dysfunction from prolonged chemical
exposure).
Ultraviolet and Ionizing Radiation Burns

Gastrointestinal: Cramps, nausea, vomiting,

diarrhea, and bowel ischemia
Hematologic: Pancytopenia (decreased number of
red blood cells, white blood cells, and platelets),
granulocytopenia (decreased number of granular
leukocytes), thrombocytopenia (decreased number
of platelets), and hemorrhage
paz
Complications
Possible complications of burns include:
loss of function (burns to face, hands, feet, and
genitalia)
total occlusion of circulation in extremity (due to
edema from circumferential burns)
airway obstruction (neck burns) or restricted
respiratory expansion (chest burns)
pulmonary injury (from smoke inhalation or
pulmonary embolism)
adult respiratory distress syndrome (due to leftsided heart failure or myocardial infarction)
greater damage than indicated by the surface burn
(electrical and chemical burns) or internal tissue
damage along
the conduction pathway (electrical burns)
cardiac arrhythmias (due to electrical shock)
infected burn wound
stroke, heart attack, or pulmonary embolism (due to
formation of blood clots resulting from slower blood
flow)

added pain, depression, and financial burden (due to

psychological component of disfigurement).
Vascular: Endothelium destruction
OkDoKeY

Deprh

Appearance

Healing

Pain

Su
perficial
(first- Pink to red
3-5
days
by Tenderness to
degree)-epidermis
With or without 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
comorbidities
3. Iatrogenic factors Skin
reconstruction surgery; invasive monitoring and
procedures, management in critical care
Database/Subjective Assessment
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

but both are commonly used.

Measure burn wound areas by mapping wound
1% TBSA patients hand (palm and fingers
included)
Note: when calculating burn size area, oedema
should not be included.
A burn of > 20 25% TBSA creates a global or
systemic inflammatory reaction affecting all body
organs and indicates a significant risk for the
respiratory system

Burn Type and Depth

It is important to monitor extent of tissue
destruction as it alters for at least 48 hours post
burn injury
o Jacksons burn wound model.
It is rare that a burn will present with a single
depth.
Likely to change depending on the early
management e.g. appropriate first aid and other
patient factors. (ANZBA 2007; British Burn
Association 2005; Eisenmann-Klein 2010)
Burn Site and Impact
Develop awareness of the implication of burn to
special areas of the body. the following require
specialised treatment
o Hands
o Face
o Perineum
o Joints
This is in consideration of the complexity of the post
burn reconstruction and potential functional impact
of inappropriate management of these important
body areas.
History of Presenting Complaint
History of the incident with specific attention paid
to the mechanism of injury.
First aid was adequate first aid given? - If not,
suspect deeper burn injury
Falls was there any indication that the patient
fell? From what height? possible head injury,
sprains or fractures
Electrical injury voltage involved? Parts of body in
contact with earth? suspect nerve and deep
muscle injury with high voltage current
Explosions falls, high velocity injuries, possible
tympanic membrane injury loss of hearing and
difficulty communicating
Passage to hospital and time to admission
ANZBA 2007; British Burn Association 2005;
Eisenmann-Klein 2010;
Medical and Surgical History
Any surgical or medical management
o Pain medication
o Debridement
o Escharectomy
o Flaps/grafts
o Any particular MDT instructions to be
followed

ANZBA 2007; British Burn Association 2005;

Hettiaratchy et al 2004

Past Medical/ Drug History

Social History
ANZBA 2007; British Burn Association 2005;
Eisenmann-Klein 2010
Basic ADL e.g., dressing, bathing, eating and
Instrumental ADL e.g., shopping, driving, home
maintenance
Past physical function e.g., mobility, climbing
stairs, reaching, lifting
Past physical fitness e.g., strength, flexibility,
endurance, balance
Social support and home Situation
Occupation
Particularly important for hand burns
Psychosocial/ Yellow Flags
Self-image
Coping style
Mental health
Emotional behaviour
ANZBA 2007; British Burn Association 2005;
Hettiaratchy et al 2004
Considerations for the Assessment of Hand Burns
The area of the hand that is injured has a huge
impact on recovery. A burn on the hand can have
detrimental effects for ADLs and functioning.
Dependant on the area and depth of the burn, it
may lead to significant deformity.
Assessment
Evaluation and classification of the size and depth
of the burn of the hand
Post burn Hand Deformities
o First web adduction contractures
o Web space contractures
o Dorsal skin contractures
o Digital flexion contracture
o Boutonniere deformity
o Dorsal skin deficiency
o Digital loss secondary to ischemia
o Median and ulnar nerve compression
o Syndrome

o Surgical managementremoval of eschar,

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

Pain Intensity Assessment

Observational behavioural pain assessment scales
should be used to
Measure pain in children aged 0 to 4 years e.g. The
FLACC scale
Faces pain rating scale can be used in children
aged 5 years and older. E.g. The Wong-Baker FACES
pain rating scale
VAS can be used in children aged 12 years and
older and adults.
Inhalation Assessment
Physical signs to observe:
Hoarse vocal quality
Singed facial / nasal hair
Oedema
Erythema (Superficial reddening of
the skin, usually in patches, as a
result of injury or irritation causing
dilatation of the blood capillaries)
Soot stained sputum

Stridor
Inspiratory and end expiratory
auscultation

crackles on

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 subacute 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.

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.
Opioids: the cornerstone of pain management in
The body then enters a hyper metabolic state,
o Associated with increased clearance of burns, and are available in a variety of potencies,
methods of administration and duration of action.
analgesia.
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
separately to manage
Positive
Side Effects
Examples of Opioids
procedural pain
Effects
During the first 48 hours

Pain relief

Respiratory distress

Increased
comfort

Itch

Morphine
related
to
reduced Posttraumatic
stress disorder

Nausea and vomiting

Opioid tolerance requiring
increasing doses
Opioid induced hyperalgesia
(OIH) increased sensitivity,
throughout the body following
opioid exposure
Provide poor defence against
central sensitisation
Physical
dependence

common in long term use

Simple
analgesics:
paracetamol can be used
in conjunction with
Oxycodone
opioids, to give a
synergistic
effect
comparable to a higher
Fentanyl: potent, rapid onset, opioid dose. Paracetamol
short acting opioid. Used for is an effective antiprocedural pain management.
pyretic and has few
Remifentaril: ultra-short acting contra-indications.
opiate.
NSAIDS: synergistic with
Alfentaril: short acting, used for opioids and can reduce
post-procedural analgesia.
opioid dose and thus
reduce side-effects. Not
used in wide spread
burns due to already
increased risk of renal
failure
and
peptic
ulceration. There is potential to
increase bleeding in large burns
also, due to the anti-platelet
effect.
Morphine

Possible
side
analgesics:
- Drowsiness

effects

of

- Adverse reaction
- Nausea and increased risk of
aspiration
Impaired
memory
communication
- Postural hypotension, and fainting
Non- Pharmacological Pain Management

and

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 individuals 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 attentiondiversion 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, medicalsurgical patients and critical care patients showed
statistically significant reductions in pain scores. Of the
seventeen studies reviewed by Cole and LoBiondoWood (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 nonpharmacological 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 childs
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

The impact of reconstructive surgery post burn injury

has a major impact on a patient. As an allied health
professional, we must work as part of an MDT in order
to ensure successful surgery while at the same time
ensuring long term health and
function. Timely burn wound
excision and skin grafting form the
cornerstone for acute burn surgical
management (Klein 2010).Surgery
for burned patients is not normally
indicated until 48 hours after injury,
when the depth of the burn has
been
established.
The
only
exception is when necrotic tissue is
evident then early excision may be
required. A plastic surgeon must
reconstruct the injured body part in
a way that is extensible, sensate
and
cosmetically
acceptable
(Glassey 2004). In addition to this,
they must rebuild or replace
muscles, tendons, joints and nerves
to ensure they are appropriately intact.
Aims
1. Achieve would closure
2. Prevent infection

suspected infection has been cleared. Deep partial and

full thickness burns both require surgical intervention.
Surgery normally takes place within the first 5 days
post injury to prevent infection which could extend the
depth of the tissue loss (Glassey 2004).

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

3. Re-establish the function and properties of an intact A graft is an area of skin that is separated from its own
blood supply and requires a highly vascular recipient
skin
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
Heterograft or xenografts (animal skin)
complex is free-flap reconstruction. When deciding on
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

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 PreGrafting
Diagnosis of DEEP tissue
loss
Patient is systemically fit
for surgery
Patient
has
no
coagulation abnormalities
Sufficient donor sites
available
Would

clear

of

Skin Substitutes are defined as a heterogeneous

group of wound cover materials that aid in wound
closure and replace the functions of the skin either
temporarily or permanently
(Halim et al 2010)
Conventionally, STSG and FTSG have been
found to be the best option for burn wound coverage
(Halim et al 2010). However, in cases of extensive burn
injury, the supply of autografts is limited by additional
wound or scarring at donor sites. For this reason, skin
substitutes will be required. Skin substitutes require
higher cost, expertise and experience than autografts.
However, they also offer numerous advantages in the
form of rapid wound coverage requiring a less
vascularised wound bed, an increase in the dermal
component of a healed wound, reduced inhibitory
factors of wound healing, reduced inflammatory
response and reduced scarring (Halim et al 2010).
Currently, there are various skin substitutes on
the market but scientists and engineers are working

towards producing the optimal skin substitute. As a

Tendon without paratenon
general rule, skin substitutes are classified as either
Cartilage without perichondrium
temporary or permanent and synthetic or biological. A
(Glassey 2004)
very clear and concise overview of the different skin
Categorisation
of Skin Flaps
substitutes available for burn injuries is provided in
Halim et al (2010).
Based on three factors:
1. Vascularity
The Recipient Site
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)

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

The grafts properties (e.g. vascularity of donor site)
Flaps are also classified depending on their
(Glassey 2004)
composition, i.e. which layers of the skin they contain.
The composition is often clear from the name of the
Skin Flaps
flap.
The difference between a skin graft and a skin flap is
that a skin flap contains its own vasculature and
Skin Flap- epidermis, dermis and superficial fascia
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
Muscle Flap-muscle belly without overlying
in the research, skin flaps is often incorporated into
structures
the term skin grafts.
Tissues which a skin graft will not take over include and Myocutaneous Flap-muscle belly with the overlying
skin
which a skin flap will include:
Osseous Flap- bone
Bone without periosteum
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.
(Schneider et al 2012; Disseldorp et al 2007; Esselman,
Relocation of Flaps
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:
Prevention of additional/deeper injuries
the donor and recipient sites (Glassey 2004).
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,
Prevention of infection
maintaining their connection with the body. Therefore,
they are never fully excised.
Prevention of loss of functional structures
Advancement flaps are those in which the
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

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
o psychological and social problems, which but gentle manner (Procter 2010).
significantly affect their ability to resume their
normal activities post discharge

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

1mmobilisation post skin reconstruction surgery
injury
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
Prevent deformities/loss of range
Protect/promote healing
Common treatment techniques
Immobilisation
o Bed rest
o Splinting
Positioning
Immobilisation
Rationale for Immobilisation
Positioning in the Acute Stage

The following is a table drawn up using current

literature on the recommended immobilisation times
for the various skin grafts:
The times frames for mobilisation post-surgery
outlined in this booklet are merely a guide taken from
an analysis of current literature and are NOT a
replacement for the specific time frames directed by
the operating surgeon or consultant (ANZBA 2007).
For a physiotherapist the most important concepts to
grasp are:
What is the minimum timeframe of immobilisation
post-surgery
What structures MUST be immobilised
Special considerations for movement, function and
ambulation dependent on

(Boscheinen-Morrin 2004)
Donor sites and the structures repaired or excised
Static Splinting
during surgery.
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
A serial static splint is a device with no moving parts
also referred to as the intrinsic minus position.
designed to be remoulded as a contracture improves.
Position of Safe Immobilisation
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
released, there is an immediate decrease in the tissue
tension but a delay in the retractions of the tissue to a
shorter length. These stress relaxation properties of
visco elastic scar tissue means it can accommodate to
stretching force overtime. Dynamic and static splinting
provide this prolonged low stretching force.
Categories of Splints
Static or Dynamic
Supportive or Corrective
Rigid or soft
Dorsal or Volar
Digit, hand or forearm based

stretch contractures through the application of

incrementally adjusted static force to promote
lengthening of contracted tissue (Smiths 2009). There
are various types of static progressive splints available
depending on the area affected. One such static
progressive splint is a finger flexion strap splint. This
type of splint is used in the treatment of MCP
extension contractures. The flexion straps serially
stretch scar bands along the dorsum of hand and wrist
causing extension contracture. The stretching force is

localised to the MCP joints by applying the straps via a

wrist extension splint. This stabilises the wrist
providing static support below the MCP joint
(Kwan 2002).
Dynamic Splinting
A dynamic splint is one which aids in initiating and
performing movements by controlling the plane and
range of motion of the injured part. It applies a mobile
force in one direction while allowing active motion in
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).

applied with rubber bands, elastics and springs (Smith

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

A Bradford
sling can be
used to facilitate
elevation. This
type of sling
facilitates both
elevation
and
protection of wound
area
while
still
allowing movement.
Its foam design also
reduces the risk of
the development of
pressure points or
friction
(Glassey
2004).
When a patient is
admitted
with
severe burns of a
large TBSA they are
at risk of systemic
inflammation.
Therefore, not only
must the affected
limb be placed in elevation,

Splinting Precautions
Splints need to be cleaned regularly to prevent
colonization by microbes which may lead to wound
the following precautions should also be taken
infection
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
o Pressure garments, silicone, massage
subject with dorsal hand burns.
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
compromise vascularity.
lengthening (Kwan 2002).
Passive joint mobilisations can begin during the scar
maturation phase once the scar tissue has adequate
tensile strength to tolerate friction caused by
mobilisation techniques
(Boscheinen-Morrin and Connolly 2001).

The patient may present with a reduced capacity for

exercise secondary to increased metabolic rate, altered
thermoregulation and increased nutritional demands.
Postural hypotension may be present due to
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
psychosocial difficulties through their cosmetic
indicated (Boscheinen-Morrin and Connolly 2001).
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).
Reliability: Not enough evidence to make it a gold
to monitor the wound during AROM frequently.
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

was evident
(Durani et al 2009)
Sensitivity: Most Scar OCM rely on categorical/ordinal
data with few levels which provides limited sensitivity
and can only identify considerable differences between
scars
(Fearmonti et al 2010).

2) Increase in temperature: A rise in temperature

increases collagenase activity thus increased scar
breakdown.

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

7) Static electricity: Static electricity on silicone may

influence the alignment of collagen deposition
(negative static electric field generated by friction
between silicone gel/sheets and the skin could cause
collagen realignment and result in the involution of
scars.
(Bloemen et al 2009; Momeni et al 2009)

3) Polarized Electric Fields: The negative charge within

silicone causes polarization of the scar tissue, resulting
in involution of the scar.

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
with subsequent accelerated remodelling of the tissue.
be very subjective measures

Pressure Garment Therapy (PGT)

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
(OBrien & Pandit 2008).
o Pressure decreases blood flow
The physiological effects of silicone in the treatment
o Local hypoxia of hypervascular scars
of scarring remain unclear. Below is a summary of the
current hypotheses surrounding the physiological
o Reduction in collagen deposition
effects of silicone. This summary has been adapted
o Therefore
from the most recently published literature on this
o Decreases scar thickness
topic.
1) Hydration Effect: Hydration can be caused by the
o Decreases scar redness
occlusion of the underlying skin. It decreases capillary
o Decreases swelling
activity and collagen production, through inhibition of
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
mast cell stabilization and a subsequent decrease in
neurovascularisation
and
extracellular
matrix
production. However this hypothesis is in contrast with
a mechanism of action of silicone, in which an increase
of mast cells causes scar maturation.

Swelling of extremities caused by inhibited venous

return
Skin breakdown
Web space discomfort

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
Allergies to material
subsequent increase in collagen degradation.
(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
considerations
Pressure: 15 mmHg has been noted as the minimum to
elicit change, and pressures of above 40 mmHg have
been found to cause complications. Both Anzarut et al
(2009) and Engrav et al (2010) used pressures of
between 15 and 25 mmHg.
Time: It is recommended that garments are worn for
up to 23 hours a day, with removal for cleaning of the
wound and garment, and moisturisation of the wound.
(Procter 2010; Anzarut et al 2009 and Bloeman et al
2009).
Duration: garments can
be worn as soon as
wound closure has been
obtained, and the scar is
stable
enough
to
tolerate pressure. Post
grafting, 10-14 days
wait is recommended,
at the discretion of the
surgeon
(Bloeman et al 2009).

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

 Static pressure to reduce pockets of swelling

(Procter 2010).

Finger and thumb kneading to mobilise the scar and Aerobic and Resistance Training Post Burn
surrounding tissue
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
to fatigue has been found to be lower in adults and
(Holey and Cook 2003)
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
occupational therapy in hospital (Disseldorp et al
Graft failure
2007). Though protein metabolism begins to normalise
9-12 months post burn, patients are still found
Intolerable discomfort
Skin rolling to restore mobility to tissue interfaces

Hypersensitivity to emollient
The Role of the Physiotherapist in the Rehabilitation
of the Chronic Burn Patient.
The patient
Healing process may continue for up to two years, as
scar tissue remodels and matures

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

compared to age matched controls
Adults with a TBSA >30% suffered a significant
decrease in torque, work and power in the quadriceps
muscles compared to age matched controls.
(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.
Therefore adaptations may occur through training.
participated in the intervention remained stable.
o Suggested that exercise may have sympathetic
However, studies involving heat loads of 40 degrees
nervous system attenuating effects
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
efficacy of measuring core temperature accurately, it is
effects.
o Exercise is required to integrate dietary amino acids advised that patients are closely monitored initially
during aerobic exercise for signs of heat intolerance.
into lean muscle mass (Herndon and Tomkins 2004)
**Thermoregulation
Human skin produces sweat to dissipate heat in
response to thermal stress (McEntine et al 2006). A
proper sweat response requires functional integrity of
the
Sweat glands
Skin circulation
Neural control of the skin (McEntine et al 2006)
Full thickness burns damage the dermal appendages
including sweat glands. These are not replaced by
grafting. There is also a decreased density of sweat
glands in the donor site post grafting
(Esselman et al 2007).
However, McEntine et al 2006 found that in 15
children with an average of 55% TBSA there was
No significant difference in core temperature,
measured tympanically, pre or post 20 minutes of
treadmill exercise at room temperature compared to
age matched healthy controls.

***Inhalation injury and pulmonary insufficiency

Long term pulmonary function is compromised in some
patients post severe burn
Lasts several years
Documented in both children and adults (Grisbrook
et al 2012a)
Caused by
o Smoke inhalation
o Direct thermal damage to airways
o Pulmonary oedema
o Respiratory tract infection
o Complications from intubation

o Recurrent infection leading to chronic

inflammation
Less likely to cause dysfunction in <30% TBSA,
no injury over torso, and no inhalation injury
(Willis et al 2011)
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
year post injury, and found
versus burned skin per child.
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

Resistance Training Summary and Recommendations
exercise.
for Practice
No significant difference in participation levels in
Exercise prescription: Post two years, Grisbrook et al
physical activity, though burn survivors were more
(2012b) found that burned patients responded to
likely to participate in work rather than leisure activity.
resistance exercise similarly to controls. Therefore,
Burns survivors were less likely to participate in normal guidelines may be adequate.
Frequency: All studies investigating the effects of
vigorous intensity exercise over 9 METs
resistance training used a frequency of three times per
Therefore, decreased pulmonary function did not week. There have been no studies to investigate the
prevent them from participating
optimum frequency for resistance training in this
population. Suman et al (2001), suggested that a break
The lower relative intensity of their exercise may have
of more than 48 hrs must be given between bouts of
caused their decreased aerobic capacity.
resistance training.
o Resistance exercise causes microtrauma to
All of the above factors must be considered as both a
muscles already in a compromised state.
contributor to the patients loss of strength and
aerobic capacity, and a potential limiter of their ability
o Resistance exercise in burned patients
to participate in therapy. Careful monitoring and
stimulates protein synthesis as in unburned
modification of treatment according to individual
subjects- However; a longer period of recovery
response is advised.
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
week 2-6 (4-10 repetitions), and 80-85% week 7-12, (8Exercise prescription:
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
al 2012).
studies investigating optimal frequency.
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.
Time: All the studies used a protocol of 12 weeks.
no significant difference in gains in aerobic capacity.
Type: All interventions used treadmill training, There were no studies comparing the efficacy of
shorter or longer time frames, however, given that loss
whether walking or running.
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
Training:
Lauteur et al 2007; Przkora et al 2007)

Initiating aerobic and strength training:

studies stipulated a minimum of six months to two
years post burn before initiation of programmes,
though many subjects were included who had been
burned many years before. These participants all
benefited from the interventions.

pressure may be advisable, particularly on initiation of

exercise and when exercising with additional thermal
stress. Manage the environment to minimise thermal
stress initially in particular.

Particularly those at risk of reduced pulmonary

function post burn (i.e., >30% TBSA, injury to torso, or
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

Braddoms physical medicine & rehabilitation
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Contributors, Springhouse By OkDoKeY
Delisasphysical medicine & rehabilitation 5th
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Physiotherapy in burns, plastic and
reconstructive surgery by hale