Dermatology

At the end of the unit, the student
will have acquired knowledge on the
following:
• Management of a burn injury p 968
• Types
– Thermal
– Chemical
– Electrical
– Smoke and inhalation
– Radiation
• Classification 968, PCCM p 15
– Extent
– Depth
• Partial thickness
• Full thickness
• Location
• Risk factors
• Pathophysiology
• Localised manifestations
• Assessment and common findings
– First degree
– Second degree
– Third and fourth degree
•
• Rehabilitation p 978
• Management (T&E Periods)
– Immediate care in hospital
– Outcomes box 50.1
• General Nursing care plan for a
burn injury p 974
– Disfigurement
– Immobility
– Hypovolaemia
– Tissue perfusion
– Infection
– Malnutrition
• Principles of wound care
– Wound care
– Debridement
• Complications of burns
• Therapeutic positioning for
prevention of contractures
5/8/2018 Compiled by C Settley 2

The skin
 Skin is made up of three layers.
 The epidermis, the outermost layer of skin,
provides a waterproof barrier and creates our skin
tone.
 The dermis, beneath the epidermis, contains
tough connective tissue, hair follicles, and sweat
glands.
 The deeper subcutaneous tissue (hypodermis) is
made of fat and connective tissue.

The skin layers
 The skin is the largest organ of the body, with a
total area of about 20 square feet.
 The skin protects us from microbes and the
elements, helps regulate body temperature, and
permits the sensations of touch, heat, and cold.
 The skin’s color is created by special cells called
melanocytes, which produce the pigment
melanin. Melanocytes are located in the
epidermis.

The skin layers

The skin layers
 The epidermis
 The epidermis is the top layer of your skin.
 It’s the only layer that is visible to the eyes.
 The epidermis is thicker than you might expect and has
five sublayers (thick skin) or four layers (thin skin).
 Your epidermis is constantly shedding dead skin cells
from the top layer and replacing them with new
healthy cells that grow in lower layers.
 It is also home to your pores, which allow oil and sweat
to escape.

The skin layers
 The epidermis
 In order from the deepest layer of the epidermis to the
most superficial, these layers (strata) are the:
 Stratum basale.
 Stratum spinosum.
 Stratum granulosum.
 Stratum lucidum.
 Stratum corneum.

The epidermis layers

The epidermis:
Stratum Basale
• The stratum basale is the deepest epidermal layer and
attaches the epidermis to the basal lamina, below
which lie the layers of the dermis.
• The cells in the stratum basale bond to the dermis via
intertwining collagen fibers, referred to as the
basement membrane.
• A finger-like projection, or fold, known as the dermal
papilla.
• Dermal papilla is found in the superficial portion of the
dermis and increases the strength of the connection
between the epidermis and dermis; the greater the
folding, the stronger the connections made.

The epidermis:
Stratum Basale
• The stratum basale is a single layer of cells
primarily made of basal cells.
• A basal cell is a cuboidal-shaped stem cell that is
a precursor of the keratinocytes of the epidermis.
• All of the keratinocytes are produced from this
single layer of cells, which are constantly going
through mitosis to produce new cells.
• As new cells are formed, the existing cells are
pushed superficially away from the stratum
basale. Two other cell types are found dispersed
among the basal cells in the stratum basale.

The epidermis:
Stratum Basale
• The first is a Merkel cell, which functions as a receptor and
is responsible for stimulating sensory nerves that the brain
perceives as touch. These cells are especially abundant on
the surfaces of the hands and feet.
• The second is a melanocyte, a cell that produces the
pigment melanin. Melanin gives hair and skin its color, and
also helps protect the living cells of the epidermis from
ultraviolet (UV) radiation damage.
• In a growing fetus, fingerprints form where the cells of the
stratum basale meet the papillae of the underlying dermal
layer (papillary layer), resulting in the formation of the
ridges on your fingers that you recognize as fingerprints.

The epidermis:
Stratum Spinosum
• As the name suggests, the stratum spinosum is
spiny in appearance due to the protruding cell
processes that join the cells via a structure called
a desmosome.
• The desmosomes interlock with each other and
strengthen the bond between the cells.
• It is interesting to note that the “spiny” nature of
this layer is an artifact of the staining process.
• Unstained epidermis samples do not exhibit this
characteristic appearance.

The epidermis:
Stratum Spinosum
• The stratum spinosum is composed of eight to
10 layers of keratinocytes, formed as a result
of cell division in the stratum basale.
• Interspersed among the keratinocytes of this
layer is a type of dendritic cell called the
Langerhans cell, which functions as a
macrophage by engulfing bacteria, foreign
particles, and damaged cells that occur in this
layer.

The epidermis:
Stratum Spinosum
• The keratinocytes in the stratum spinosum
begin the synthesis of keratin and release a
water-repelling glycolipid that helps prevent
water loss from the body, making the skin
relatively waterproof.
• As new keratinocytes are produced atop the
stratum basale, the keratinocytes of the
stratum spinosum are pushed into the stratum
granulosum.

The epidermis:
Stratum Granulosum
• The stratum granulosum has a grainy appearance due to
further changes to the keratinocytes as they are pushed
from the stratum spinosum. The cells (three to five layers
deep) become flatter, their cell membranes thicken, and
they generate large amounts of the proteins keratin, which
is fibrous, and keratohyalin, which accumulates as lamellar
granules within the cells.
• These two proteins make up the bulk of the keratinocyte
mass in the stratum granulosum and give the layer its
grainy appearance. The nuclei and other cell organelles
disintegrate as the cells die, leaving behind the keratin,
keratohyalin, and cell membranes that will form the
stratum lucidum, the stratum corneum, and the accessory
structures of hair and nails.

The epidermis:
Stratum Lucidum
• The stratum lucidum is a smooth, seemingly
translucent layer of the epidermis located just above
the stratum granulosum and below the stratum
corneum. This thin layer of cells is found only in the
thick skin of the palms, soles, and digits. The
keratinocytes that compose the stratum lucidum are
dead and flattened.
• These cells are densely packed with eleiden, a clear
protein rich in lipids, derived from keratohyalin, which
gives these cells their transparent (i.e., lucid)
appearance and provides a barrier to water.

The epidermis:
Stratum Corneum
• The stratum corneum is the most superficial layer of the epidermis
and is the layer exposed to the outside environment.
• The increased keratinization (also called cornification) of the cells in
this layer gives it its name. There are usually 15 to 30 layers of cells
in the stratum corneum. This dry, dead layer helps prevent the
penetration of microbes and the dehydration of underlying tissues,
and provides a mechanical protection against abrasion for the more
delicate, underlying layers. Cells in this layer are shed periodically
and are replaced by cells pushed up from the stratum granulosum
(or stratum lucidum in the case of the palms and soles of feet). The
entire layer is replaced during a period of about 4 weeks. Cosmetic
procedures, such as microdermabrasion, help remove some of the
dry, upper layer and aim to keep the skin looking “fresh” and
healthy.

The epidermis
There are conditions that start in the epidermis layer of your skin. These
conditions can be caused by allergies, irritations, genetics, bacteria, or
autoimmune reactions. Some of them are:
• seborrheic dermatitis
(dandruff)
• atopic dermatitis
(eczema)
• plaque psoriasis
• skin fragility syndrome
• boils
• acne
• melanoma (skin cancer)
• keratosis (harmless skin
growths)
• epidermoid cysts
• pressure ulcers
(bedsores)
• nevus (birthmark, mole,
or “port wine stain”)

The skin layers
 The dermis
 The dermis is thicker than the epidermis and contains
all sweat and oil glands, hair follicles, connective
tissues, nerve endings, and lymph vessels.
 While the epidermis covers your body in a visible layer,
the dermis is the layer of skin that really enables the
function of pathogen protection that your body needs.
 Since the dermis contains collagen and elastin, it also
helps support the structure of skin that we see.
 Consists of two components of the dermis—the
papillary layer and the reticular layer.

The skin layers

The skin layers
 The hypodermis
 The hypodermis is a layer directly below the dermis and
serves to connect the skin to the underlying fibrous
tissue of the bones and muscles.
 It is not strictly a part of the skin, although the border
between the hypodermis and dermis can be difficult to
distinguish.
 The hypodermis consists of well-vascularized, loose,
areolar connective tissue and adipose tissue, which
functions as a mode of fat storage and provides
insulation and cushioning for the integument.

The skin layers

Lipid Storage
• The hypodermis is home to most of the fat
that concerns people when they are trying to
keep their weight under control.
• Adipose tissue present in the hypodermis
consists of fat-storing cells called adipocytes.
• This stored fat can serve as an energy reserve,
insulate the body to prevent heat loss, and act
as a cushion to protect underlying structures
from trauma.

Lipid Storage
• Where the fat is deposited and accumulates within the
hypodermis depends on hormones (testosterone,
estrogen, insulin, glucagon, leptin, and others), as well
as genetic factors.
• Fat distribution changes as our bodies mature and age.
Men tend to accumulate fat in different areas (neck,
arms, lower back, and abdomen) than do women
(breasts, hips, thighs, and buttocks).
• The body mass index (BMI) is often used as a measure
of fat, although this measure is, in fact, derived from a
mathematical formula that compares body weight
(mass) to height.

Pigmentation
• The color of skin is influenced by a number of
pigments, including melanin, carotene, and
hemoglobin.
• Recall that melanin is produced by cells called
melanocytes, which are found scattered
throughout the stratum basale of the epidermis.
• The melanin is transferred into the keratinocytes
via a cellular vesicle called a melanosome

Pigmentation
The relative coloration of the skin depends of the amount of
melanin produced by melanocytes in the stratum basale and
taken up by keratinocytes.

• Too much sun exposure can eventually lead to
wrinkling due to the destruction of the cellular
structure of the skin, and in severe cases, can
cause sufficient DNA damage to result in skin
cancer.
• When there is an irregular accumulation of
melanocytes in the skin, freckles appear.
• Moles are larger masses of melanocytes, and
although most are benign, they should be
monitored for changes that might indicate the
presence of cancer

Moles range from benign accumulations of melanocytes to
melanomas. These structures populate the landscape of our
skin. (credit: the National Cancer Institute)

Albinism & Vitilgo
• Albinism is a genetic disorder that affects (completely or partially) the coloring of
skin, hair, and eyes.
• The defect is primarily due to the inability of melanocytes to produce melanin.
• Individuals with albinism tend to appear white or very pale due to the lack of
melanin in their skin and hair.
• Recall that melanin helps protect the skin from the harmful effects of UV radiation.
• Individuals with albinism tend to need more protection from UV radiation, as they
are more prone to sunburns and skin cancer.
• They also tend to be more sensitive to light and have vision problems due to the
lack of pigmentation on the retinal wall.
• Treatment of this disorder usually involves addressing the symptoms, such as
limiting UV light exposure to the skin and eyes.
• In vitiligo, the melanocytes in certain areas lose their ability to produce melanin,
possibly due to an autoimmune reaction. This leads to a loss of color in patches.

Albinism & Vitilgo

Review Questions
• 1. The papillary layer of the dermis is most closely associated
with which layer of the epidermis?
A. stratum spinosum
B. stratum corneum
C. stratum granulosum
D. stratum basale
• 2. Langerhans cells are commonly found in the ________.
A. stratum spinosum
B. stratum corneum
C. stratum granulosum
D. stratum basale

Review Questions
• 3. The papillary and reticular layers of the dermis are
composed mainly of ________.
A.melanocytes
B.keratinocytes
C.connective tissue
D.adipose tissue
• 4. Collagen lends ________ to the skin.
A.elasticity
B.structure
C.color
D.UV protection

Review Questions
• 5. Which of the following is not a function
of the hypodermis?
A.protects underlying organs
B.helps maintain body temperature
C.source of blood vessels in the epidermis
D.a site to long-term energy storage

Critical Thinking Questions
1. What determines the color of skin, and
what is the process that darkens skin when
it is exposed to UV light?
2. Cells of the epidermis derive from stem
cells of the stratum basale. Describe how
the cells change as they become integrated
into the different layers of the epidermis.

Solutions
• D
• A
• C
• B
• C

Solutions
• The pigment melanin, produced by melanocytes, is primarily responsible
for skin color. Melanin comes in different shades of brown and black.
Individuals with darker skin have darker, more abundant melanin, whereas
fair-skinned individuals have a lighter shade of skin and less melanin.
Exposure to UV irradiation stimulates the melanocytes to produce and
secrete more melanin.
• As the cells move into the stratum spinosum, they begin the synthesis of
keratin and extend cell processes, desmosomes, which link the cells. As
the stratum basale continues to produce new cells, the keratinocytes of
the stratum spinosum are pushed into the stratum granulosum. The cells
become flatter, their cell membranes thicken, and they generate large
amounts of the proteins keratin and keratohyalin. The nuclei and other cell
organelles disintegrate as the cells die, leaving behind the keratin,
keratohyalin, and cell membranes that form the stratum lucidum and the
stratum corneum. The keratinocytes in these layers are mostly dead and
flattened. Cells in the stratum corneum are periodically shed.

Burn injuries
 A burn results when the skin is damaged by
intense heat, radiation, electricity, or
chemicals.
 The damage results in the death of skin cells,
which can lead to a massive loss of fluid.
Dehydration, electrolyte imbalance, and renal
and circulatory failure follow, which can be
fatal.

Burn injuries
 Dehydration, electrolyte imbalance, and renal
and circulatory failure follow, which can be fatal.
 Burn patients are treated with intravenous fluids
to offset dehydration, as well as intravenous
nutrients that enable the body to repair tissues
and replace lost proteins.
 Another serious threat to the lives of burn
patients is infection. Burned skin is extremely
susceptible to bacteria and other pathogens, due
to the loss of protection by intact layers of skin.

Burn injuries: Types- pg. 968
 Thermal burns
 A thermal burn is a type of burn resulting from
making contact with heated objects, such as
boiling water, steam, hot cooking oil, fire, and hot
objects.
 Scalds are the most common type of thermal burn
suffered by children, but for adults thermal burns
are most commonly caused by fire.

 Chemical burns
 A chemical burn is irritation and destruction of
human tissue caused by exposure to a chemical,
usually by direct contact with the chemical or its
fumes.
 Chemical burns can occur in the home, at work or
school, or as a result of accident or assault.

 Electrical burns

Severe electrical burn
 Electrical burns

 Smoke and inhalation
 As a result of inhaling hot air, smoke or chemicals.
 Redness of the mucosa and oedema of the
airways may occur.
 Rapid assessment and intervention is important.

 Beware that patients may appear
asymptomatic on arrival but may
develop significant signs and
symptoms as long as 36 hours
after exposure, especially in fires,
which produce small particles
with low water solubility.
 Be aware of pertinent historical
risk factors when treating patients
with potential smoke inhalation
injury.

 Smoke and inhalation: mild edema and congestion of the
bronchus (A), without carbon soot being identified (B).

 Smoke and inhalation: The trachea was classified as grade
G2 with severe edema and congestion of the bronchus (A).
Carbon soot deposition and the formation of
pseudomembrane was also demonstrated (B).

 Acute respiratory distress usually responds very well
to aggressive initial management.
 Normal laboratory values and imaging studies,
coupled with clinical improvement, can give the
health care provider a false sense of security.
 The patient then may be discharged, only to
deteriorate as delayed pulmonary edema ensues.
 Any patient with significant exposure to toxic smokes
should be observed for 24-48 hours and imaged with
serial chest radiographs.

 Provide intravenous (IV) access, cardiac monitoring,
and supplemental oxygen in the setting of hypoxia.
 A small subset of patients manifests bronchospasm
and may benefit from the use of bronchodilators,
although this is not well documented.
 This is especially true of patients with underlying
chronic obstructive pulmonary disease (COPD) or
asthma.

Smoke and inhalation injury:
Types- pg. 969
 Carbon monoxide poisoning
 Carbon monoxide (CO) is a colorless, odorless gas
produced by incomplete combustion of
carbonaceous material.
 Clinical presentation in patients with CO poisoning
ranges from headache and dizziness to coma and
death.
 Examples: Propane-fueled forklifts, Gas-powered concrete saws,
Inhaling spray paint, Indoor tractor pulls, Swimming behind a
motorboat.

The throat

Types- pg. 969
 Inhalation injury above the glottis
 Inhalation of hot air, smoke or steam.
 Pharynx and larynx may be involved
 Present with redness, blistering, swelling, causing
mechanical obstruction
 Life threatening
 Rapid assessment is critical

Types- pg. 969
 Inhalation injury above the glottis
 Clues of the nature of the injury involves:
 History of being burned in an enclosed area
 Clothing that is burned around the neck and chest
 Facial burns
 Singed eyebrows and nasal hair
 Hoarseness of the voice
 Painful swallowing
 Darkened oral and nasal membranes
 Black sputum

Types- pg. 969
 Inhalation injury below the glottis
 Usually due to chemicals
 Extent of tissue damage is related to the duration
of exposure
 ARDS

Types- pg. 969
 Radiation burns
 A radiation burn is damage to the skin or other
biological tissue as an effect of radiation.
 The radiation types of greatest concern are
thermal radiation, radio frequency energy,
ultraviolet light and ionizing radiation.
 The most common type of radiation burn is a
sunburn caused by UV radiation.

Types- pg. 970
 Radiation burns

Types- pg. 970
 Radiation burns
 Severity depends on: length of exposure, strength
of radiation, distance from the source & size of
body surface subjected to the source.
 Characterized by redness, blistering, wet or dry
desquamation or ulceration.
 Radiation syndrome: anorexia, nausea & vomiting
 Sunburn

Classification of burn injury- pg. 970
 ACCORDING TO:
 The extent of the body surface that has been
burnt
 Rule of nines

Classification of
burn injury- pg. 970
 ACCORDING TO:
 The depth of the burn:
 A first-degree burn is a superficial burn that affects
only the epidermis. Although the skin may be painful
and swollen, these burns typically heal on their own
within a few days. Mild sunburn fits into the category of
a first-degree burn.

Classification of
 ACCORDING TO:
 A second-degree burn (partial thickness burn) goes
deeper and affects both the epidermis and a portion of
the dermis.
 These burns result in swelling (oedema) and a painful
blistering of the skin. It is important to keep the burn
site clean and sterile to prevent infection.
 If this is done, the burn will heal within several weeks.

Classification of
 ACCORDING TO:
 A third-degree burn (full thickness burn) fully extends
into the epidermis and dermis, destroying the tissue
and affecting the nerve endings and sensory function.
These are serious burns that may appear white, red, or
black; they require medical attention and will heal
slowly without it.
 A fourth-degree burn is even more severe, affecting
the underlying muscle and bone. Oddly, third and
fourth-degree burns are usually not as painful because
the nerve endings themselves are damaged.

Depth of burn injury- pg. 970

Classification of
 ACCORDING TO:
 The location of the burn
 Face and neck- respiratory problems
 Extremities, joints and eyes- functionality, neurologic
impairment
 Ears and nose- infection due to poor blood supply to
cartilage
 Buttocks and perineum- infection

Classification of
 ACCORDING TO:
 The patient risk factors
 Age
 Pre existing illnesses
 DM
 Malnourishment

Pathophysiology of
 Impairment of normal skin structure and function
 Protective barrier compromised
 Susceptible to infections
 Destruction of sweat glands and sebaceous
glands decreased functioning of sensory
receptors
 Which allow fluids and body temperatire to
escape

Pathophysiology of
 Pathophysiological changes of burn injuries can be localized or systemic
 Localised manifestations
 An inflammatory response occurs with the release of histamine, bradykinin
and serotonin
 These chemicals are responsible for vasodilatation of blood vessels
 Capillaries become more permeable and fluid shift occurs
 Oedema and blisters form
 Albumin in the exudate increases the extracellular oncotic pressure and more
fluid is retained, resulting in more oedema
 In deep, full thickness burns, the response is marked by necrotic tissue
formation
 A crust forms within 72 hours of the injury
 Eschar develops which restricts further fluid loss

Pathophysiology of
 Pathophysiological changes of burn injuries can be localized or
systemic
 Systemic manifestations
 Damage to the capillary system causes fluid and electrolyte shift from
the intravascular to the interstitial spaces, which causes oedema
 Increase in capillary permeability causes water, sodium and plasma
proteins, especially albumin to move into interstitial spaces and other
surrounding tissue
 Osmotic pressure decreases with progressive loss of protein from the
vascular space into interstitial spaces
 Fluid may shift to unusual spaces like blister formation

Pathophysiology of
 Pathophysiological changes of burn injuries can be
localized or systemic
 Plasma is reduced
 Resulting in a drop in the volume in the bloodstream
 Cardiac output is reduced and circulation to vital organs is
decreased
 Hypovolemic shock can occur
 Electrolyte imbalances (hyperkalemia, hyponatremia &
hypernatremia) may occur

Pathophysiology of
 Pathophysiological changes of burn injuries can be localized
or systemic
 BP drops and heart rate increases
 If untreated, the patient becomes restless, which is indicative of
hypoxia
 May lead to death
 Depleted volume of blood is further impaired by loss of RBC’s
 Thrombosis may occur
 Increased hematocrit due to haemo concentration

Assessment & common findings of
Partial thickness (superficial or
1st degree) burn
• Erythema (superficial
reddening of the skin, usually
in patches, as a result of injury
or irritation causing dilatation
of the blood capillaries)
• Pain
• Moderate to severe
tenderness
• Minimal oedema
• Blanching with pressure
Partial thickness (deep, 2nd
degree) burn
• Blister that increases in size
• Mottled, white, pink or
cherry skin colour
• Hypersensitive to touch or
air
• Moderate to sever pain
• Blanching with pressure
(when the skin becomes
white or pale in
appearance)

Assessment & common findings of
Full thickness (3rd and 4th degree) burns
• Dry leathery eschar
• Waxy white, dark brown, or charred appearance
• Strong burn odour
• Impaired sensation when touched
• Absence of pain with severe pain in surrounding tissue
• Lack of blanching with pain

Management- pg. 973
• Pre hospital care/first aid
– Extinguish flames
– Superficial wounds should be submerged in cold
water or covered with a sheet
– Do not remove clothing
– Do not apply ointments or oils
– Do not open blisters
– Call the ambulance and transfer to hospital

Management- pg. 973
• Immediate care in hospital
– 1st hour of treatment is crucial
– Cause must be determined + respiratory involvement
– Establish an IV line (Ringer’s Lactate at 2ml/ kg/ % burn)
– Keep patient warm, administer oxygen if blood gases show
problems with concentration
– Analgesics
– Anti anxiety drugs
– Vital signs
– Urinary output
– Monitor wounds (foul smell may indicate infection)
– Tetanus propholaxis

Management outcomes- pg. 973
• A patent airway
• Fluid replacement with ringers lactate as it contains the initial
resuscitation fluid
• Urinary output more than 30ml/hour
• Arterial blood gases within normal limits
• Peripheral pulses palpable
• BP above 100/70 mmHg
• Apical pulse slightly tachycardic
• Passing flatus
• Normal respiration
• Lungs clear
• Contractures (permanent shortening of a muscle or joint) prevented
• Patient feeling at ease

Management- pg. 976
• Drugs commonly used in the management of
a patient with burns
– Analgesics. USUALLY GIVEN INTRAVENOUSLY
– This is the fastest route
– Gastro intestinal function is slowed or impaired
due to paralytic ileus
– Intramuscular injections will not be adequately
absorbed

Nursing care plan- pg. 974
• Disfigurement
• Immobility
• Hypovolaemia
• Tissue perfusion
• Infection
• Malnutrition

Principles of wound care- pg. 977
• Done x3 per day
• Septic techniques
• Pain medication
• Continous monitoring to detect signs of infections
• Cleansing of wounds- water and normal saline,
debridement
• Eschar using sterile equipment
• Hydrotherapy done before dressings are done
• Anti microbial agents
• Soaking is done in a tub where anti microbial agents
may be added and should not exceed 30 minutes

Complications of burns- pg. 978
• Infection
• Fluid volume deficit and electrolyte imbalance
may lead to hypovolemic shock
• Respiratory insufficiency/ ARDS
• Renal compromised or complete renal failure
• Hepatic injury
• Psychological disturbances
• Scar formation
• Contractures

Contractures- pg. 978

Therapeutic positioning for the
prevention of contractures- pg. 978
• Neck
– No pillow
– Towel under the cervical spine
– Neck splint
– 90 degree abduction, neutral rotation
• Shoulder
– Elbow splint to help in maintaining position

• Axilla
– Abduction with 10-15 degrees forward flexion and external
rotation
– Support for the abducted arm with suspension from the IV
stand or bedside locker
– Axilla splint
• Hand
– Hand splint
– Flexion
– Hyperextension

• Elbow
– Extension
– Support for the extended arm or bedside table
– Elbow splint
• Hip
– Extension with neutral rotation
– Supine with lower extremities extended
– Prone position
– Trochanter roll

• Knee
– Extension
– Prone position
– Patient out of bed with lower extremities extended
– Knee splint
• Ankle
– Dorsiflexion
– Padded footboard with heels free of pressure
– Ankle splint

Rehabilitation after a
• Physiotherapy
• Occupational therapy
• Psychiatric therapy
• Self care
• Return to being productive
• Restoring function with regard to mobility
• Social and role functioning
• Emotional assistance
• Collaborative approach

 Mogotlane, S. Chauke, M. Matlakala, M, Mokoena , J. & Young, A. (eds). 2013.
Juta’s complete Textbook of Medical Surgical Nursing. Cape Town: Juta.
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653X%3Byear=2014%3Bvolume=22%3Bissue=1%3Bspage=22%3Bepage=32%3Baul
ast=Sarabahi.
 https://doi.org/10.1186/1746-1596-8-174© Bai et al.; licensee BioMed Central
Ltd. 2013Received: 23 September 2013Accepted: 9 October 2013Published: 21
October 2013
 https://openi.nlm.nih.gov/detailedresult.php?img=PMC4255836_umj0083-0158-
f5&req=4
 https://criticalcaremcqs.com/2011/05/30/burns/
 https://www.webmd.com/skin-problems-and-treatments/picture-of-the-skin#1
 http://faculty.collin.edu/mweis/Images/Histology/2401%20histology/Integumenta
ry%20Histo/integ%20histo%20labeled/histo_INTEG_SKIN_HYPODERMIS_labeled.p
ng

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