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NUR202 Integumentary System (2)

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NUR202
PATHOPHYSIOLOGY &
PHARMACOLOGY II
DISORDER OF THE
INTEGUMENTARY SYSTEM
Rose Heung
OUTLINE
 Review of Anatomy & Physiology - Skin
 Clinical Manifestation of Skin Lesions
 Diagnosis of Skin Disorders
 Disorders of Integumentary System:
 Acne
 Dermatitis
 Psoriasis
 Skin Cancer
 Burn
(Marieb, Brady, & Mallatt, 2020)
 Treatment and Nursing Implications for Integumentary System Disorders
Slide prepared by Rose Heung
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REVIEW OF ANATOMY & PHYSIOLOGY: SKIN
 Also called: integumentum
 The integumentary system is an organ system that
includes the skin and its accessory structures, including the
nails, hair, and sweat glands.
 One of the largest organs in the body, covering
approximately 2 m2
 Constitutes ~ 1/6 (16%) of the total body weight
 Receives ~ 1/3 of the body’s circulating blood volume
 Thickness: 1 – > 5mm
 Made up of 3 layers:
(i) Epidermis
Dermis
(iii) Subcutaneous tissue (also called the superficial fascia
or hypodermis)
(ii)
(Source: https://www.mdskinlab.ca/5-step-guide-to-rejuvenate-all-skinlayers-from-deep-to-superficial/)
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Slide prepared by Rose Heung
EPIDERMIS
 Outermost layer of the skin
 Composed of stratified squamous epithelium
 Provides mechanical protection for the body
 When intact, prevents the entry of micro-
organisms
 Very thin: average thickness only 0.1 mm
(varies from 0.05 mm on the eyelids to 0.8±1.5 mm on the soles
and palms)
 Avascular: no veins and capillaries in this layer
 Receives nourishment from the capillaries in the
dermis
(Gao & Gurd, 2019)
 Made up of 4 or 5 cell layers, depending on the
type of skin
Slide prepared by Rose Heung
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EPIDERMIS
 It is rich in a tough protein called keratin
and contains 4 different cell types:
1. Keratinocytes
2. Melanocytes
3. Langerhans cells
4. Merkel cells
(Source: https://www.earthslab.com/physiology/cells-layers-epidermis/)
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Slide prepared by Rose Heung
EPIDERMIS
(Source: https://www-anatomy-tv.ezproxy.cihe.edu.hk/anatomytv/html5uihap_2018/#/product/integumentary/type/Topics/displayType/displaySlide/id/3/structureID/-1)
Non-hairy skin found in the palms of the hands and soles of the feet is thickest
because the epidermis contains an extra layer, the stratum lucidum
Slide prepared by Rose Heung
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EPIDERMIS:
(1) STRATUM BASALE/GERMINATIVUM/BASAL LAYER
 Deepest layer of the epidermis
 Composed of a single layer of basal cells.
 Contains keratinocytes, melanocytes, merkel cells
 Keratinocytes
• The predominant cells (85%) produced in this layer:
Keratinocytes undergo mitosis (division) and migrate
upwards through each layer until they are eventually
shed at the stratum corneum. This process is called
turn-over.
During this turn-over, keratinocytes change their
structures and physiological functions.
On average, one cycle of this turn-over process
takes around 28 days.
(Source:https://med.libretexts.org/Bookshelves/Anatomy_and_Physiology/Book%3A_Anatomy_and_Physiology_(
Boundless)/5%3A_Integumentary_System/5.1%3A_The_Skin/5.1B%3A_Structure_of_the_Skin%3A_Epidermis)
Slide prepared by Rose Heung
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EPIDERMIS:
(1) STRATUM BASALE/GERMINATIVUM/BASAL LAYER
 Keratinocytes
• produce keratin, a tough fibrous protein that provides
the epidermis its tough, protective barrier function
• Primary function:
1.
Provide physical and mechanical protection
Forming a tight barrier to prevent foreign substances
from entering the body. E.g. Pathogens & UV radiation
2.
Minimize heat and water loss
3.
Inflammatory response
(Source:http://www.histology.leeds.ac.uk/skin/epidermis_layers.php)
• Pathogens invading the upper layers of the epidermis can cause
keratinocytes to produce proinflammatory mediators which
attract monocytes, natural killer cells, T-lymphocytes,
and dendritic cells to the site of pathogen invasion
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Slide prepared by Rose Heung
EPIDERMIS:
(1) STRATUM BASALE/GERMINATIVUM/BASAL LAYER
 Melanocytes
• ~ 10% – 25% of the cells in the stratum basale are melanocytes
• Pigment-synthesizing cells producing the pigment, melanin, which are responsible for skin color
• There are 2 major forms of melanin:
1. Eumelanin
 Brown and black pigment
 Most abundant in humans
 Exposure to the sun’s ultraviolet rays increases the production causing tanning to occur
2.
Pheomelanin
 Yellow to red pigment
• Primary function:
 Protect the skin by absorbing and scattering harmful ultraviolet rays
 Skin pigmentation
 Albinism
• A genetic disorder in which there is lack of pigmentation in the skin, hair, and the iris of the eye
Slide prepared by Rose Heung
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EPIDERMIS:
(1) STRATUM BASALE/GERMINATIVUM/BASAL LAYER
 Merkel Cells
• present in very small numbers found in the stratum
basale
• Function:
• Closely associated with terminal filaments of
(Source: https://www.skincancer.org/skin-cancerinformation/merkel-cell-carcinoma/)
cutaneous nerves: serve as sensory touch receptors,
especially in areas of the body such as palms, soles
and genitalia
Slide prepared by Rose Heung
(Source: https://ncimedia.cancer.gov/pdq/media/images/579043.jpg)
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EPIDERMIS: (2) STRATUM SPINOSUM
 Spiny appearance where their cell borders interconnect
 4 – 5 layers thick
 This layer is formed as a result of the cell division in the stratum
basale.
 Composed of the keratinocytes in this layer which are referred to
as prickle cells
 The cells become differentiated as they migrate toward the
surface of the epidermis
(Essenfeld, 2014)
 Primary Function:
• Contains Langerhans
cell
• Immunologic cells responsible for recognizing foreign
antigens harmful to the body
• can engulf bacteria, foreign particles, and damaged cells that
occur in this layer
Slide prepared by Rose Heung
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EPIDERMIS:
(3) STRATUM GRANULOSUM & (4) STRATUM LUCIDUM
Stratum Granulosum
 Also known as the granular layer
 2 – 3 layers thick
 Keratinocytes migrating from the
underlying stratum spinosum become
known as granular cells in this layer
 The cells in this layer contains glycolipids
Stratum Lucidum
 A thin, transparent layer present in
the thick skin only - the palms of
the hands and soles of the feet
 Made up of flattened, dead
keratinocytes
that get secreted to the surface of the cells
and function as a glue, keeping the cells
stuck together
 A lipid layer is formed to prevent water
loss across the epidermis
Slide prepared by Rose Heung
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EPIDERMIS: (5) STRATUM CORNEUM
 Also called: Horny layer; Outermost layer
 The thickest: making up 75% of the epidermis’s total thickness which are
surrounded by intercellular lipids
 Consists of 20-30 sheets of dead keratinized cells:
• Horny cells/Corneocytes
• The keratinocytes harden in a process called keratinization :
• The cytoplasm fills with strands of tough, fibrous, waterproof keratin proteins.
• Many layers of tough, tightly packed dead cells accumulate in the stratum
corneum. These dead cells are eventually shed.
 These cells are shed from the skin (desquamation) continuously. These cells are
the dandruff shed from the scalp and the flakes that come off dry skin. The
complete process from formation to desquamation takes approximately 28 days in
young adults:
• They remain on the surface of the skin for about 2 weeks before they are
sloughed off
• This constant shedding of the cells ensures that the deeper layers of the
epithelium are covered by a protective and replaceable layer of dead, durable
cells
Slide prepared by Rose Heung
(Source:https://www.nursingtimes.net/clinicalarchive/dermatology/skin-1-the-structure-and-functionsof-the-skin-25-11-2019/)
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EPIDERMIS: (5) STRATUM CORNEUM
 Within this layer, the dead keratinocytes secrete defensins which are part of our first
immune defense
 This layer prevents excessive dehydration of the skin tissue and usually contains 10%-
15% of the mass of water in the epidermis:
• Principal constituent is ceramide: plays a crucial role in water retention
 Horny cells contain special chemical compounds called natural moisturizing factor
(NMF) which can attract and hold water
 Primary function:
• Form a barrier to protect underlying tissue from infection, dehydration, chemicals
and mechanical stress
Slide prepared by Rose Heung
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SUBCUTANEOUS TISSUE
 Also called Hypodermis/Superficial fascia
 3rd layer of skin
 Consists of areolar and adipose (predominate) connective
tissues along with some skin appendages e.g. the hair
follicles, sensory neurons, and blood vessels
 Primary Function:
• Anchoring: Helps the skin adhere to underlying
structures (mostly to muscles)
• Protection: The fat stored in the subcutaneous layer
provides protection to the internal structures
• Insulation: Fat is a poor conductor of heat so helps
prevent heat loss from the body
Slide prepared by Rose Heung
(Gao & Guard, 2019)
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DERMIS
 2nd Layer: Connective tissue layer that separates the epidermis from the subcutaneous fat layer
 The main components of the dermis are collagen and elastin fibers
 Compared to the epidermis, there are much fewer cells and much more fibers in the dermis
 Richly supplied with blood cells, nerve fibers, and lymphatic vessels
 Most of the hair follicles, sebaceous glands, and sweat glands are located in the dermis
 Consists of 2 layers:
1.
Papillary dermis:
• Upper layer, thinner; 20% of the thickness of the dermis
• Contains capillaries and receptors for pain and touch
2.
Reticular dermis:
• Deeper layer, thicker; 80% of the thickness of the dermis
• Contains blood vessels, sweat and sebaceous glands, deep pressure receptors, and dense bundles of
collagen fibers
Slide prepared by Rose Heung
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SKIN APPENDAGES
 Sebaceous glands
 Sweat glands
 Ceruminous glands
 Hair
 Nails
 Sensory receptors
(Lewis, Dirksen, Heitkemper & Bucher, 2017)
Slide prepared by Rose Heung
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SKIN GLANDS
 There are three types of glands found in the skin
Slide prepared by Rose Heung
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SEBACEOUS GLANDS
 Occur over the entire body except the palms,
soles and sides of the feet
 Part of the pilosebaceous unit: Sebaceous
glands often open into the hair follicle rather
than directly onto the skin surface, and the
entire complex is known as the pilosebaceous
unit
 Secrete sebum: a mixture of lipids, including
triglycerides, cholesterol, and wax
 Production and secretion of sebum is under the
control of genetic and hormonal influences
(especially androgens)
 Sebaceous glands are relatively inactive during
childhood but are activated in both sexes during
puberty, when the production of androgens
begins to rise
Function of Sebum:
• Softens and lubricates the skin and hair:
preventing hair from becoming brittle, keeps
the epidermis from cracking
• Prevents undue evaporation of moisture from
the stratum corneum during cold weather
• Helps conserve body heat
• Protect body from infection by killing bacteria
Clinical Application:
• Whitehead on skin surface: when
a sebaceous gland becomes
blocked by sebum
• Blackhead: Darkens if the
material oxidizes and dries
• Pimple: blocked sebaceous glands
are likely to be infected by bacteria
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Slide prepared by Rose Heung
SWEAT GLANDS (SUDORIFEROUS GLANDS)
2 Types: Eccrine sweat gland & Apocrine sweat gland
Eccrine sweat gland
 Originate in the dermis
 Located over the entire body surface except the
lips and part of the external genitalia
 Most abundant on the palms, soles, and forehead
 The duct to the skin rise through the epidermis to
open in a pore at the surface is to cool the body by
evaporation
 Sweat, the secretion of the eccrine glands is
composed mostly of water (99%), combined with
sodium, ammonia, urea and other waste
 Production of sweat is regulated by sympathetic
nervous system and serves to maintain normal
body temperature and may occur in response to
emotions e.g. fear, stress (“cold sweat”)
Slide prepared by Rose Heung
Apocrine sweat gland

Located in the axillary, breast areolae, umbilical
and anogenital areas, external auditory canals and
eyelids
 The secretions are similar but contain fatty acids and
proteins that becomes odoriferous when altered by
skin surface bacteria
 These glands are enlarge and become active at puberty
because of reproductive hormones
Ceruminous glands
 Located in the skin of the external ear
 Modified apocrine sweat glands
 Secrete yellow-brown, waxy cerumen that
provides a sticky trap for foreign materials
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HAIR
 Originates from hair follicles in the dermis
 Entire hair structure consists of the hair follicle, sebaceous
gland, hair muscle (arrector pili), and, in some instances, the
apocrine gland
 Exposed part is known as shaft, consists mainly of dead cells
 A vascular network at the site of the follicular bulb nourishes




and maintains the hair follicle
Distributed all over the body, except the lips, nipples, parts of
the external genitals, the palms and soles
Various factors influences hair growth, such as nutrition,
hormones
Serves as protective functions:
Eyebrows & eyelashes: protect the eyes
• Hair in nose: helps keep foreign materials out of the upper
respiratory tract
• Hair on the head protects the scalp from heat loss and
sunlight
Slide prepared by Rose Heung
(Norris, 2020)
Clinical Application
Chemotherapy drugs used to
treat cancer target the most
rapidly dividing cells in the
body → destroy many hair
stem cells and cause hair loss
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NAILS
• Modified scalelike epidermal structure
• Consist mainly of dead cells
• Each nail has a distal free edge, a nail plate (the visible
•
•
•
•
•
(Brewer, 2016)
attached part), and a root (the proximal part embedded in the
skin)
At the root and the proximal end of the nail body, the bed
thickens to form the nail matrix, the actively growing part of
the nail
Lunule: (“little moon”) the white crescent under the nail’s
proximal region
Nail folds: Skin folds overlapped on the sides of the nail
The proximal nail fold is thickened and is called the
eponychium or cuticle
Nails form a protective coating over the dorsum of each digit on
the fingers and toes
Clinical Application
Ingrown toenail
 a nail whose growth pushes it painfully into the lateral nail fold
 Usually due to pressure of an ill-fitting shoe → nail grows crookely
Slide prepared by Rose Heung
(Marieb, Brady, & Mallatt, 2020)
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SKIN COLOUR
• Skin colour is the result of varying levels of pigmentation
• Varies among individuals and among people of different races
• Areas of the skin that exposed to the sun and environment may have a slightly
different colour from areas that are usually covered with clothing
 Exposure to sun causes a build-up of melanin and a darkening/ tanning of the skin in
people with light skin
• More abundant in the skins of individuals of Asian ancestry and together with
melanin, accounts for golden skin tone
• The epidermis in White skin has very little melanin and is almost transparent
Slide prepared by Rose Heung
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GENERAL FUNCTIONS OF THE SKIN
PROTECTION
 Skin cushions and insulates the deeper body organs and protects the body from injury
 The epidermis is waterproof: prevent unnecessary water loss across body surface
 Keratin : The layers of keratinized stratified squamous epithelium form a physical barrier against
pathogens, and protect deeper tissue against abrasion and heat
 Sweat: Sweat is secreted onto the skin regularly. It is relatively acidic and salty which help inhibit
microbial growth
 Defensins: Epithelial cells produce cationic proteins called defensins which have antimicrobial
properties and help prevent the colonization of the skin
 Langerhans cells: Epidermal Langerhans cells alert the body to pathogens while dermal macrophages
engulf viruses and bacteria
 Glycolipids: Glycolipids and the oily secretions of the sebaceous glands prevent both the absorption of
water into the skin, and excessive evaporation of water from the skin
 Melanin: Melanin absorbs ultraviolet (UV) radiation to protect deeper tissue from damage
 Normal flora: Some non-pathogenic micro-organisms grow on the epidermal surface, which helps
prevent colonization by other pathogenic microbes
Slide prepared by Rose Heung
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GENERAL FUNCTIONS OF THE SKIN
THERMOREGULATION
 The skin’s rich capillary networks and sweat glands regulate heat loss from the body
thus helps to control body temperature
 Changes in core body temperature cause the hypothalamus to send nerve impulses to
the sweat glands, muscles and blood vessels (vasoconstriction or vasodilation) to
raise or lower the body temperature
 4 major principles govern thermoregulation by the skin:
(i) Evaporation (ii) Radiation; (iii) Conduction; (iv) Convection
(Source: https://www.abpischools.org.uk/topic/homeostasis-sugar/6/1)
Slide prepared by Rose Heung
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GENERAL FUNCTIONS OF THE SKIN
SENSATION
• Skin contains sensory nerve and specialized
receptors:
• provides sensory perception for
environmental stimuli including touch,
vibration, pressure, surface temperature
(heat and cold), and pain
(Source:https://www.slideshare.net/jamiehworkman/skin-27557308)
Slide prepared by Rose Heung
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GENERAL FUNCTIONS OF THE SKIN
Absorption
Excretion
 Skin (percutaneous, dermal) absorption:
 transport of chemicals via the skin into circulation
 Small quantities of metabolic waste
 for the delivery of drugs
 via patches or creams applied directly to the skin
 Example: Transdermal patch works well for small
lipid-soluble drug molecules to diffuse through the
epidermis to the blood vessels in the dermal layer
e.g. nitroglycerin and nicotine
(Brewer, 2016)
Slide prepared by Rose Heung
products can leave the body via the
skin
 via sweat glands - ammonia and
urea, which are waste products
resulting from the breakdown of
protein
 Carbon dioxide
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GENERAL FUNCTIONS OF THE SKIN
VITAMIN D SYNTHESIS
 Endogenous synthesis of vitamin D is essential to calcium and phosphorus
balance, occurs in the epidermis
 The epidermal cells use UV radiation to synthesize vitamin D
 When ultraviolet light penetrates the skin, it converts 7-dehydrocholesterol
into cholecalciferol → transported in the blood to the liver and kidneys →
further processing into calcitriol (a biologically active form of vitamin D)
Slide prepared by Rose Heung
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CLINICAL MANIFESTATION OF SKIN LESIONS
PRIMARY SKIN LESIONS
CYST (囊腫)
Encapsulated fluid-filled or semisolid
mass in the subcutaneous tissue or
dermis
Example: Sebaceous cyst, Cystic acne
PLAQUE (斑)
Elevated, firm, and rough lesion
with flat top surface > 1 cm in
diameter
Example: Vitiligo, Mongolian Spots
TELANGIECTASIA (血管擴張症)
Slide prepared by Rose Heung
Fine , irregularred lines produced by
capillary dilation;
Example: acne face, venous
hypertenesion (spider veins in legs),
or developmental abnormalities
(birthmarks)
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CLINICAL MANIFESTATION OF SKIN LESION
SECONDARY SKIN LESIONS
Resulted from thinned epidermis and/or dermis
LICHENIFICATION (苔癬化)
Rough, thickened epidermis
secondary to persistent rubbing,
itching, or skin irritation; often
involves flexor surface of extremity
EXAMPLE: Chronic dermatitisAMPLE:
KELOID (蟹形腫)
Irregular-shaped, elevated,
progressively enlarging scar; grows
beyond the boundaries of the wound;
caused by excessivecollagen formation
during healing
EXAMPLE: Keloid formed after surgery
EXCORIATION (抓痕)
Loss of the epidermis, linear, hollowedout, crusted
EXAMPLE: Abrasion or scratch, Scabies
EROSION (麋爛)
Loss of part of the epidermis; depressed,
moist, glistening; follows rupture of a
vesicle or bulla or chemical injury
EXAMPLE: Chemical injury
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Slide prepared by Rose Heung
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DIAGNOSTIC TESTS OF SKIN DISORDERS
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DIAGNOSTIC TESTS OF SKIN DISORDERS
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Slide prepared by Rose Heung
DISORDERS OF THE INTEGUMENTARY SYSTEM
Noninflammatory Acne
Acne
InflammatoryAcne
Contact dermatitis
Dermatitis
Atopic dermatitis
Psoriasis
Basal cell carcinoma
Skin Cancer
Squamous cell
carcinoma
Malignant Melanoma
Burn
Slide prepared by Rose Heung
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ACNE VULGARIS
(ACNE) 痤瘡 (青春痘)
• 8th most common skin disease
• Commonly occurs during adolescence
(ranging from 35% to ~100% of adolescents
having acne at some point)
(Heng & Chew, 2020)
Slide prepared by Rose Heung
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ACNE VULGARIS (ACNE)
Pathophysiology and Etiology
 Acne is a common skin disorder of the sebaceous glands and their hair follicles that usually occurs on
the face and upper parts of the chest and back
Etiology is multifocal:
• Exact cause is unknown
• Various factors may contribute to the development: e.g. hormonal changes, infection, diet, hereditary
tendency, stress, and external irritants such as strong soaps or cosmetics
• Most common cause is hormonal changes during puberty:
• Excessive sebum production: Due to stimulation of androgens
• Gradual obstruction of the pilosebaceous ducts with accumulated debris, ruptures the sebaceous glands,
which causes an inflammatory reaction that may lead to papules, pustules, nodules, and cysts,
abscess → Scar; hyperpigmentation
• Acne occurs when the ducts through which this sebum flows become plugged
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Slide prepared by Rose Heung
(Anatomical Chart Co. originator, 2010)
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DIAGNOSIS & TREATMENT OF ACNE
Diagnosis
• Based on (i) history (ii) location and appearance of lesions
• If presence of pustules → culture of the drainage
Treatment
• Aim: clear up existing lesions, prevent new lesions, and limit scar formation
1. Topical agents for mild to moderate acne
 Antibacterial agents, such as benzoyl peroxide gels (2%, 5% or 10%),
clindamycin, tetracycline, or erythromycin
2. Keratolytic agents
 Dry and peel the skin to open blocked follicles and release sebum
e.g. Tretinoin (Retin-A): acts locally to decrease the cohesiveness of epidermal cells
and increase epidermal cell turnover
• Benzoyl peroxide: common topical OTC medication for acne (1st line treatment)
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NURSING CONSIDERATION IN ADMINISTRATING BENZOYL PEROXIDE (OXY)
Pharmacologic Class: Keratinolytic
Therapeutic class: Antiacne drug
Action
• Keratolytic effect which helps dry out and shed the outer
layer of the epidermis.
• It also suppresses sebum production and exhibits
antibacterial effects
Indication
• Acne
Adverse effect
Dry skin, erythema, peeling of skin and burning sensation,
pruritus, irritation, swelling face
Contraindication:
• Hypersensitivity
• Patients with asthma
• Drug-drug: salicylic acid
Nursing Implication
• Avoid unnecessary sun exposure, use sunscreens and wear protective clothing when outdoor
• Monitor adverse effects, e.g. local irritation, e.g. burning, blistering, scaling, swelling, the
frequency of application should be reduced or suspended
• Educate the patient in monitoring the adverse effect, e.g. redness or severe skin irritation, and
inform health care staff whenever necessary
Slide prepared by Rose Heung
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NURSING CONSIDERATION IN ADMINISTRATING TRETINOIN (ACTA)
Pharmacologic Class: Retinoid
Therapeutic class: Antiacne drug
Action
• A natural derivative of vitamin A
• Acne symptoms take 4-8 weeks to improve and
maximum therapeutic benefit may take 5-6 months
Indication
• Topical use: The early treatment and control of
mild to moderate acne vulgaris
• Oral use: Acute promyelocytic leukaemia
Adverse effect
• Topical use: Redness, scaling, erythema, crusting,
and peeling of the skin
• Oral use: Headache, dizziness, skin/ mucous
membrane dryness
Contraindication:
• Topical use: Patients who are allergic to fish
(the product contains fish proteins)
• Pregnancy
• Oral use: Not suitable for patients who have
hepatic disease, leukopenia or neutropenia
Nursing Implication
• Oral tablet should be taken with food
• Oral drug may cause dizziness or severe headache, do not drive or operate machinery
• Avoid administering over-the- counter medications and using skin products that cause excessive drying of the
skin during therapy
• Avoid excessive exposure to sunlight and UV light, use sunscreens and wear protective clothing when outdoor
• Educate the patient in monitoring the adverse effect, e.g. redness or severe skin peeling, and inform health care
staff whenever necessary
Slide prepared by Rose Heung
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DERMATITIS
 Also known as eczema
 a group of inflammatory skin condition.
 Various types: atopic dermatitis (AD) , contact dermatitis, dyshidrotic eczema,
nummular eczema, seborrheic dermatitis, and stasis dermatitis.
 Very common skin condition worldwide:
 over 31 million Americans have some form of eczema.
 Affect all age group:
can begin during early childhood (in babies between two-to-six months of
age), adolescence, or adulthood and it can range from mild to severe.
Prevalence of adult AD ranged from 2.1% to 4.9% across countries.
Slide prepared by Rose Heung
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DERMATITIS
(Lawton & Gill, 2009)
• An inflammation of the skin characterized by pruritus, erythema, lesions
• Can be acute or chronic
刺激性接觸性皮膚炎 (ICD)
(Lawton & Gill, 2009)
過敏性接觸性皮膚炎 (ACD)
接觸性皮膚炎
Slide prepared by Rose Heung
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(Lawton & Gill, 2009)
Diagnosis of
ICD/ACD
- Comprehensive
history taking
- Clinical presentation
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prepared
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Heung
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Rose
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- Patch testing
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Atopic comorbidities of
asthma, allergic rhinitis,
& food allergies
are well recognized in
patients with AD
etiology
Slide prepared by Rose Heung
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Slide prepared by Rose Heung
(EAAI, 2020)
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TREATMENT OF ATOPIC DERMATITIS
• Avoidance of allergens and irritants, e.g. detergents or wool,
extreme temperature changes, and other precipitating factors
• Prevent excessive dryness of the skin: maintaining adequate
fluid intake and humidifying air
• Topical corticosteroid ointment: ↓ inflammation
• Systemic antihistamines
• Cetirizine or Loratadine (Non-sedative)
• Diphenhydramine (sedative)
 Adequate moisturizing of the skin: use of moisturizers or
emollients (e.g. Cetaphil® cream) with warm baths or showers
to repair the skin barrier.
• Wet-wrap therapy: a wet dressing is applied over emollients
in combination with topical antiseptics or topical
corticosteroids
(Norris, 2020)
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Slide prepared by Rose Heung
NURSING CONSIDERATION IN ADMINISTRATING DIPHENHYDRAMINE (BENADRYL)
Pharmacologic Class:
Antihistamines (1st generation)/
H1 receptor antagonist
Therapeutic class: Anti-allergic
Action
Block the actions of histamine at the H1 receptor to
relieve the allergy symptoms
Indication
• Allergy conditions
Adverse effect
• Chest tightness
• Dizziness, drowsiness
• Fatigue
• Headache
• Irritability
• Dry mouth
• tachycardia
Contraindication:
• Hypersensitivity
• Benign prostatic hypertrophy
• Narrow-angle
glaucoma
• GI obstruction
• Should be used cautiously in patients with
asthma or hyperthyroidism
Nursing Implication
• May cause significant drowsiness, educate patient avoid to perform tasks requiring mental alertness or
physical coordination (e.g. driving or operating heavy machinery)
• Monitor the therapeutic and adverse effect
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NURSING CONSIDERATION IN ADMINISTRATING CETIRIZINE (ZYRTEC)
Pharmacologic Class: Antihistamines (1st generation) Therapeutic class: Antiacne drug
Action
Block the actions of histamine at the H1 receptor to
relieve the allergy symptoms
Indication
• Allergy conditions
Adverse effect
• Insomnia
• fatigue,
• dizziness,
• Headache
• dry mouth
• Abdominal pain
• coughing
Contraindication:
• Special precaution to epileptic patient and
patients at risk of convulsion
• Hepatic and renal impairment
• Pregnancy and
lactation
Nursing Implication
• May impair ability to perform tasks requiring mental alertness or physical coordination (e.g. driving
or operating heavy machinery)
• Monitor the therapeutic and adverse effects
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PSORIASIS
 Psora : means “itching” (originate from Greek word)
 A chronic, autoimmune, inflammatory disease of the
skin
 Epidermal cells are produced at a rate 6-9 times faster
than normal
 is a global health challenge, affecting over 125 million
people worldwide.
 In Hong Kong, ~ 0.3% of the population, i.e. more
than 20,000 people, are living with this disease.
(Source: https://www.healthymatters.com.hk/complete-guide-psoriasis-hong-kong-causes-symptoms-treatment/)
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(Hubert & VanMeter, 2018)
psoriatic arthropathy
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Psychological support for the patient and the family
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NURSING CONSIDERATION IN ADMINISTRATING TOPICAL CORTICOSTEROIDS :
(1) FLUOCINOLONE ACETONIDE (SYNALAR) (2) HYDROCORTISONE (CORTIZONE, HYCORT) Available form: Creams, Lotions, solutions
Pharmacologic Class: Topical Corticosteroids
Therapeutic class: Anti-dermatitis
Action
Local anti-inflammatory action, immunosuppressant and
antimitotic actions
Indication
Control the inflammation and itching of dermatitis
Adverse effect
• Prolonged administration causes epidermal thinning,
irritation, redness, hypopigmentation
• May cause adrenal insufficiency, mood changes,
serum imbalances and loss of bone mass if systemic
absorption occur
Contraindication:
• Primary infections (bacterial, viral, fungal)
• Ulcers
• Neonates
• Hypersensitivity
Nursing Implication
• Treatment should be limited to 2 to 3 weeks of therapy
• Systemic absorption is rare if the drug is administered appropriate, the patient should stop if systemic effect
presents, such as mood changes, oedema, and attend medical consultation immediately
• Monitor adverse and therapeutic effect
• Educate the patient in monitoring the adverse effect, e.g. skin irritation, skin infection, and inform health care
staff whenever necessary
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57
CLASSIFICATION OF TOPICAL SKIN PREPARATIONS
9 principal categories according to their action:
1
Antipruritics
Relieve itching
2
Corticosteroids
Treat dermatological disorders associated with
allergic reactions
3
Emollients and protectants Soothe skin irritation
4
Keratolytic agents
Loosen epithelial scales
5
Enzymatic agents
Promote the removal of necrotic or fibrous tissue
6
Scabicides and
pediculicides
Treat scabies or lice
7
Local anti-infectives
Prevent and treat fungal, bacterial, and viral
infections
8
Burn medications
Prevent or treat infections
9
Anti-acne medications
Treat acne
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ANTI-PRURITICS
 Antipruritics: used to relieve discomfort from dermatitis associated with allergic reactions.
They relieve itching by the use of products, singly or in combination, containing:
Local anesthetics (e.g., the “-caines,” such as benzocaine)
Drying agents (e.g., calamine)
Anti-inflammatory agents (e.g., corticosteroids) applied locally or given orally for
systemic effect. Use should be avoided in patients with pruritus without inflammation.
Topical agents are preferred because of fewer adverse effects.
Antihistamines administered orally for systemic effect (antihistamines applied topically can
cause hypersensitivity reactions – use only a few days).
 Side Effects of antipruritics include:
• Skin irritation, rash, stinging and a burning sensation
• Allergic reactions: Seizures and heart rhythm problems with topical anesthetics when used
on broken skin or in large amounts
• Sedation from antihistamines orally or paradoxical agitation in children
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ADMINISTRATION GUIDE FOR TOPICAL SKIN MEDICATION
 Clean area thoroughly before application
 Rub in gently until the medication vanishes
 Use caution if patient have allergies
 Avoid contact of the medication with eyes or mucous membranes
 Avoid contact with surrounding tissues
 Avoid covering the area with dressing unless directed by the physician
 Avoid prolonged use (not longer than one week) unless directed by the physician
 Discontinue and seek medical aid: if condition worsens or irritation develops
 Trim fingernails (in children and elderly) to reduce the possibility of infection from scratching
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SKIN CANCER
Basal Cell Carcinoma
3 main types
1.
Squamous cell carcinoma (SCC)
2.
Basal cell carcinoma (BCC)
3.
Malignant melanoma
Non-melanoma
 The main difference between melanomas and other
Squamous Cell Carcinoma
skin cancers: melanoma can metastasize to distant
body sites e.g lungs, liver or brain.
 In HK, skin cancer accounted for 3.6% of all new
cancer cases in 2017. In 2017, there were 1190 new
cases of skin cancer, with 1101 cases of nonmelanoma and 89 cases of melanoma. (CHP, 2020)
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Evolving
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63
BURN
• A global public health problem,
accounting for an estimated 180 000
deaths annually
• Non-fatal burn injuries are a leading
cause of morbidity
• Burns occur mainly in the home and
workplace
• Burns are preventable
(WHO, 2018)
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BURN - TYPES OF BURN
(I) Thermal Burn:
(1) Scalds: Steam and hot liquids
(2) Dry burn: Flames, hot surfaces & friction
(III) Electrical Burn:
(1) Electric cables
(2) Lightning
(II) Chemical Burn:
(1) Domestic chemicals (e.g. bleach,
potassium hydroxide)
(2) Industrial chemicals (e.g. gases,
acids, alkaline)
(IV) Radiation Burn:
(1) Sunburn (Ultraviolet light)
(2) X-rays
(3) Radioactive agents
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BURN CLASSIFICATION
 Tradition
Classification from
classification
• First
• Second
• Third
• Fourth degree
American Burn Association (ABA)
Zones of burn injury for different depths
• Superficial
• Partial-thickness:
• Superficial partial thickness
• Deep partial thickness
• Full-thickness
(https://doi.org/10.1093/burnst/tkaa047)
 Burns are classified by the depth of skin damage and the percentage of body
surface area involved
 Depth of the burn largely determines the healing potential and the need for
surgical grafting
 Traditional classification of burns as first, second, third, or fourth degree was
replaced by a system reflecting the need for surgical intervention
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BURN CLASSIFICATION
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(UpToDate, 2021)
67
1st Degree Burn
2nd Degree Burn
2nd Degree Burn
3rd Degree Burn
(Rebar et al., 2019)
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(UpToDate, 2021)
68
(1st degree burn)
(2nd degree burn)
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(2nd degree burn)
(3rd degree burn)
Full-thickness burn (4th degree burn)
(Source: https://en.wikipedia.org/wiki/Burn; UpToDate, 2021)
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EXTENT OF BURNS
 A thorough and accurate estimation of burn
size is essential to guide therapy
 Extent of burns: estimated and expressed as the
total percentage of body surface area (TBSA)
 Superficial (first-degree) burns
are not included in percentage TBSA burn
assessment
"Rule of Nines.“: commonly used methods of
assessing percentage TBSA in adults
(Hubert & VanMeter, 2018)
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EXTENT OF BURNS
 Lund-Browder chart
Lund and Browder diagrams for estimation
of total burned surface area (TBSA)
 Recommended method in infants and children:
 Rule of Nines: not use for infants and children
because their body section percentages differ from
those of adults
 The relative percentage of body surface area of infants
and children is affected by growth
 For example, an infant’s head accounts for about 17%
of the total body surface area compared with 7% for
an adult
 Palm method/Rule of palm
(Source: https://doi.org/10.1093/burnst/tkaa047)
 Provides a rough estimate:
 The surface area of a palm is equal to 0.5% to 1%
of his/her body surface area (BSA).
 Estimate the total burn size by holding a palm over
burns and adding up the areas
 May be more useful if the burn is irregular and/or
patchy
Slide prepared by Rose Heung
(Source: https://www.emnote.org/emnotes/burn-size-estimation)
71
PATHOPHYSIOLOGY & ETIOLOGY OF BURN INJURY


A burn injury result in tissue loss or damage
Injury to tissue can be resulted from traumatic injuries to the skin or other tissues primarily caused by
thermal (heat) or nonthermal (electrical, chemical, radiation, light, or friction) exposures
 Most common thermal burns: associated with flames, hot liquids, hot solid objects, and steam
 The severity of the burn depends on the cause of the burn, contact temperature, duration of the contact,
extent of the burn surface, and the thickness of the skin

Tissue damage can occur at various temperatures, usually between 40OC and 44OC

The burn wound has local and systemic effects, tissue damage is caused by enzyme malfunction and
denaturation of proteins

Prolonged exposure or higher temperatures can lead to cell necrosis

The areas extending outward from the central area of injury sustain various degrees of damage
and are identified by zones of injury

3 concentric zones are present in the burn injury:

Zone of coagulation
 Zone of stasis
 Zone of hyperaemia
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PATHOPHYSIOLOGY & ETIOLOGY OF BURN INJURY
 Immediately after injury, the burn wound can be divided into three zones:
1)
Zone of coagulation (with the most damage in the central portion)
2)
Zone of stasis/Zone of ischaemia (characterized by decreased perfusion that is
potentially salvageable)
3)
Zone of hyperaemia (the outermost region of the wound characterized by increased
inflammatory vasodilation)
 The degree of cellular injury varies depending on the zone of injury and spans the
spectrum from immediate cellular autophagy within the first 24 hours following
injury, delayed-onset apoptosis ~24–48 hours after the burn injury and the presence of
reversible oxidative stress.
 The natural healing of these wounds involves dynamic and overlapping phases that
include an inflammatory phase, which is initiated by neutrophils and monocytes
homing to the injury site via localized vasodilation.
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Hemodynamic
instability
Respiratory distress
SYSTEMIC
COMPLICATIONS OF
BURNS
Infection/Sepsis
Multiple organ
dysfunctions
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HEMODYNAMIC INSTABILITY
 Burn shock: a form of hypovolemic shock due to loss of vascular volume
• Begins almost immediately with injury to capillaries in the burned area and surrounding tissue
• No bleeding occurs with a burn injury (tissue and blood are coagulated or solidified by the heat).
Under the burn surface, an inflammatory response occurs.
• Where the burn area is large, the inflammatory response results in a massive shift of water,
protein, and electrolytes into the tissues  fluid excess or edema.
• Loss of water and protein from the blood   circulating blood volume,  blood pressure, and
hypovolemic shock,  hematocrit (percentage of red blood cells in a volume of blood) due to
hemoconcentration.
• Fluid imbalance: aggravated by the protein shift out of the capillaries and the resulting lower
osmotic pressure in the blood, making it difficult to maintain blood volume until the
inflammation subsides.
•  cardiac output  perfusion of vital organs
 Prolonged shock may cause kidney failure or damage to other organs.
 In severe shock, e.g. extensive full-thickness burns  acute renal failure
 Electrical injuries: can cause cardiac arrhythmias that require immediate attention
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RESPIRATORY DISTRESS
 Smoke inhalation and postburn lung injury is common in burn
 Inhalation of toxic or irritating fumes: significant amounts of smoke, carbon
monoxide, and other toxic fumes e.g. ammonia, sulfur dioxide, nitrous oxide
 Inhalation of flame, hot air, steam, or irritating chemicals: Thermal
injury/damage to the mucosal lining of the trachea and bronchi
 Clinical features of inhalation injury: wheezing, hoarseness, drooling, an
inability to handle secretions, hacking cough, and labored and shallow breathing
 Signs of mucosal injury and airway obstruction often are delayed for 24 to 48
hours after a burn
 Pneumonia: due to inflammation in the respiratory tract and immobility
Continually monitor the person for early signs of respiratory distress
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INFECTION/SEPSIS
MULTIPLE ORGAN DYSFUNCTION
 Sepsis may arise from the burn wound, pneumonia,
 Burn shock results in impaired perfusion
urinary tract infection, infection elsewhere in the
body, or the use of invasive procedures or monitoring
devices.
 When serious infection develops,  risk of
microorganisms or toxins spreading throughout the
body
 septic shock
 Common microbes in burn injury infections:
of vital organs e.g. kidneys, GI tract,
nervous system and musculoskeletal
tissues.
 Sepsis may contribute to impaired organ
function after the initial resuscitation
period
Pseudomonas aeruginosa, Staphylococcus aureus,
Klebsiella, and Candida
 Burn wound sepsis  Antimicrobial drugs: usually
administered only after specific microorganisms from
the wound have been cultures and identified.
 Skin destruction:
 open to bacterial infection
 Loss of normal protective skin flora and a shift to
colonization by more pathogenic flora
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DIAGNOSTIC STUDIES
 Serum electrolytes, especially sodium (Na + ) and potassium (K + ): monitor
fluid and electrolyte shifts
 Chest x-ray, arterial blood gases (ABGs), and sputum: for inhalation injury
 Urine output and serum creatinine: to evaluate fluid replacement and detect
acute tubular necrosis and/or renal ischemia
 Complete blood count (CBC): to detect anemia and immunologic response to
injury
 White blood cell (WBC) count and wound cultures: if infection is suspected
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BURN
MANAGEMENT
Classified into 3 stages:
1. Emergent/Resuscitative
2. Acute
3. Rehabilitative
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CLINICAL MANIFESTATIONS/
EMERGENCY & LONG-TERM TREATMENT
1. EMERGENT/RESUSCITATIVE STAGE
 Hypovolemic shock: the greatest initial threat to a patient with a major burn
 Shivering: a result of heat loss or anxiety
 Paralytic ileus: if the burn area is large
 Full-thickness and deep partial-thickness burns are initially painless because nerve endings have been destroyed. Superficial to
moderate partial-thickness burns are very painful
 Blisters: common in partial-thickness burns
 Unconsciousness or altered mental status: the result of smoke inhalation or head trauma
 Complications: respiratory distress, dysrhythmias, venous thromboembolism, and acute tubular necrosis. The emergent
phase ends when fluid mobilization and diuresis begin
Management
 Rapid and thorough assessment and intervention
 Airway management and fluid therapy
 Pain medication
 Wound care
 Support to patient and family
 Nutritional support: Begin feeding patient by most appropriate route as soon as possible
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2. ACUTE STAGE
 Partial-thickness wounds form eschar. After eschar is removed, reepithelialization begins at wound margins and appears as red or pink
scar tissue. Wound closure and healing usually occur within 10 to 21 days. Separation of eschar from full-thickness wounds takes
longer, and these wounds require surgical debridement and skin grafting. Wound infection is a serious complication.
 Other possible complications: extreme disorientation and delirium, contractures, Curling's ulcer, hyperglycemia, and pneumonia.
Management
 Wound care: ongoing observation, assessment, cleansing, debridement, dressing, excision and grafting
 Pain management: the original injury, body movements, and application of grafts and other treatments contribute to pain. Analgesics
are required
 Physical and Occupational therapy
 Nutritional therapy:
 increased dietary intake of protein and carbohydrates is required due to :
 Hypermetabolism, considerable heat loss from the body, feeling chill and produce more body heat, protein continues to be lost in
exudate from the burn site until healing is complete; stress response contributes to an increase metabolic rate; anemia because many
erythrocytes are destroyed or damaged by the burn injury
 Respiratory therapy: continue to monitor respiratory status and assess oxygenation needs
 Psychosocial care: ongoing support, counseling
 Drug therapy: assess need for drugs (e.g. antibiotics); continue to monitor effectiveness and adjust dosage as needed
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SKIN GRAFT
ANTISCAR SUPPORT GARMENT
Scar tissue
• Occurs even with skin grafting and impairs function as well as appearance
• Hypertrophic scar tissue is common
• Long-term use of elasticized garments and splints may be necessary to control scarring
(Hubert & VanMeter, 2018)
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3. REHABILITATIVE STAGE
 Mature healing of burns occurs in about 12 months when suppleness has returned, and the color has
faded to a slightly lighter hue than the surrounding unburned tissue.
 New scar tissue shrinks, causing a contracture if not prevented with range-of-motion (ROM) exercises.
 The healing site, which is extremely sensitive to trauma, may itch.
 Complications: skin and joint contractures and hypertrophic scarring
Management
 Social service team support
 Education to patient and caregiver: wound care, actively participate in care
 Continue physical and occupational therapy routines: necessary to reduce the effects of scar tissue and
increase functional use of the area
 Assess risk for scarring: management includes surgery, physical and occupational therapy, splinting,
pressure garments
 Discuss possible reconstructive surgery
 Psychosocial support: Assist patients in adapting to a realistic, yet positive appraisal of the situation.
Stress what they can do instead of what they cannot do
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83
(LeMone, Burke, Bauldoff & Gubrud, 2015)
84
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of pathophysiology (Third ed.).
Arnold, G., Munden, Julie, & ProQuest , ebook provider. (2007). Pathophysiology (Lippincott manual of nursing practice series).
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Nicol, N.H. (2020). Step-wise treatment of atopic dermatitis: Basics and beyond. Pediatric
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