Tissue Integrity

What are the skin layers and what does each contain?

Epidermis: outer barrier, renewing surface barrier

Dermis: vessels, nerves, follicles, glands, collagen, sensation, and nourishment

Subcutaneous: fat, insulation, cushioning

What is a characteristic of the stratum corneum?

made up of keratinized cell that make the skin waterproof

Primary intention

clean wound edges that are brought together

Secondary intention

Open wound; tissue fills in from bottom with granulation; more tissue loss and scarring.

Tertiary intention

Wound left open initially, then closed after contamination/infection risk is reduced, delyed closure

Hemostasis

occurs minutes to hours and fibrin plug forms and provides scaffold for healing

Inflammatory phase

occurs from day 1-4 and WBCs (neutrophils, and macrophages) remove dead tissue and debris

Proliferative phase

Occurs day 3-21 days and fibroblasts make collagen; new vessels and granulation tissue form; epithelialization and contraction.

Remodeling phase

Occurs weeks to months and collagen reorganizes and strengthens; scar forms

What is one distinction with the remodeling phase?

tissue gains strength but never returns to 100% original strength

What are some examples of local barriers to healing?

contamination, dead tissue, and inadequate blood flow

What are some examples of systemic barriers to healing?

nutrition, heart disease, and periphreal vascular disease

What are some examples of complications to healing?

gain green, amputation, infection leading to sepsis

Protein deficiency

decreased collagen and impaired immune function

Vitamin C deficiency

impaired collagen synthesis = weakened connective tissue

Zinc deficiency

impaired cell division and decreased epithelialization (wound closure)

Iron deficiency

anemia and reduced hemoglobin can decrease oxygen delivery to healing tissues

Vitamin A deficiency

impaired epithelial cell growth

Inadequate calories

body lacks energy for cellular repair and new tissue formation

What medications can delay healing?

corticosteroids and antineoplastic drugs

What metabolic status can delay healing?

diabetes —> neuropathy and impaired perfusion

Actue wounds

sudden onset from a known cause that heals within a time frame

Chronic Wounds

gradual onset, often related to underlying conditions and do not progress through the normal healing process and persist for weeks to months

Hypoxia

decreased oxygen profusion in a wound

reduced blood flow delivers less oxygen to the tissue

Decreased Perfusion and Oxygen

Insufficient oxygen causes cellular injury and death impairs immune cell function, and decreases fibroblast activity and collagen production

Tissue Hypoxia - cellular changes

Ongoing hypoxia leads to tissue necrosis and creates an environment that increases the risk of wound infection and can not get better through normal healing

Tissue Necrosis and Increased Infection Risk

Without adequate oxygen and perfusion, the wound cannot progress through the normal healing stages and becomes a chronic, nonhealing wound

Impaired Healing

What happens if wounds become heavily contaminated?

the inflammatory phase can become extended

What happens with the Complement activation and the stages of healing?

the inflammatory phase can become extended

What is the greatest risk for a pressure injury?

immobilization

What are the central causes of pressure injuries?

sustained pressure, moisture, friction, shear, and reduced tissue tolerance

Pathophysiology of Pressure injury Stage 1

Skin is intact with localized redness that does not blanch

Pathophysiology of Pressure injury Stage 2

Partial-thickness skin loss; epidermis and part of dermis; no adipose exposed.

Assessment of Pressure injury Stage 2

Partial-thickness skin loss

Pathophysiology of Pressure injury Stage 3

Full-thickness skin loss that extends into subcutaneous tissue

Assessment of Pressure injury Stage 3

Full-thickness skin loss and the wound extends into subcutaneous tissue

Pathophysiology of Pressure injury Stage 4

Full-thickness tissue loss with exposed or directly palpable fascia, muscle, tendon, cartilage, or bone.

Pathophysiology of Unstageable pressure injury

Full-thickness loss, but slough/eschar obscures the depth.

Pathophysiology of Deep tissue pressure injury

Pressure/shear damage beneath skin; may precede surface breakdown.

Assessment of Deep tissue pressure injury

Persistent deep red, maroon, or purple discoloration; blood-filled blister; pain/temperature change.

What is the treatment for pressure injuries?

surgical debridement, autolytic debridement, skin grafting, topical and systemic antibiotics, film dressing, and iodine dressing

How does a skin infection develop?

an entry point/skin break, bacteria enters the skin, local infection on the skin, and spreads to deeper tissue, a potential systemic spread (sepsis)

Pathophysiology of Device-related / mucosal pressure injury

Device pressure can injure skin; mucosal injury cannot be staged.

Pathophysiology of Cellulitis

Bacterial infection into dermis/subcutaneous tissue causing a diffuse of inflammation

Assessment of Cellulitis

Warm, red, swollen, tender area; often spreading; fever may occur.

Nursing care for Cellulitis

Mark borders, monitor spread/systemic signs; elevate affected area; complete prescribed antibiotics.

Pathophysiology of MRSA

Bacteria that causes infection in different parts of the body that is more difficult to treat because of drug resistance

Where is MRSA harbored at?

Harbored or colonized at the nose

Pathophysiology of Impetigo

Superficial bacterial infection of epidermis that is highly contagious

Assessment of Impetigo

Honey-colored crusts; commonly around nose/mouth; contagious.

Pathophysiology of Ecthyma

Deeper infection extending into dermis; often follows impetigo.

Assessment of Ecthyma

Ulcer with thick crust and punched-out appearance; may scar.

Pathophysiology of Necrotizing fasciitis “flesh eating disorder”

Rapid, destructive infection of soft tissue; toxins and ischemia cause tissue death.

Assessment of Necrotizing fasciitis

Severe pain out of proportion, rapid spread, edema, systemic toxicity; bullae/crepitus may occur.

Pathophysiology of Staphylococcal scalded skin syndrome

Staph toxin causes epidermal splitting; skin becomes fragile.

Assessment of Staphylococcal scalded skin syndrome

Diffuse tenderness/erythema, flaccid blisters, peeling; mucosa usually spared; often infants/children.

What is the Cutaneous candidiasis (yeast infection)

a fungal skin infection caused by an overgrowth that thrives in warm, moist, and creased areas of the body

Assessment of Mucocutaneous candidiasis

Oral white plaques; erythematous moist skin rash; may itch/burn.

HSV-1 / HSV-2

remain latent in sensory nerves and reactivate; spread by contact.

HSV-1

more commonly causes oral herpes ABOVE the waist

HSV-2

more commonly causes genital herpes and can also go to the anal area, BELOW the waist

What does HSV-1 and HSV-2 both have?

lifelong latency in sensory nerve ganglia, recurrent outbreaks, can spread without visible lesions present, can feel the outbreak before it occurs

Pathophysiology of Herpes zoster

someone gets chicken pox and it sets root on the ganglia and becomes latent —> from sensory ganglion causes nerve inflammation and travels down nerves then to skin

Signs and Symptoms of Herpes zoster

persistent nerve pain in the area that lasts for months to years, motor paralysis, limb weakness, numbness or tingling in the affected area, widespread of rash, secondary bacterial infection, can affect ear too

What helps/treats Herpes Zoster?

vaccine, cool compress, analgesic, glucocorticoids, and antiviral medications

Pathophysiology of Atopic dermatitis

Skin barrier dysfunction and immune inflammation; exagerated inflammatory response

Assessment of Atopic dermatitis

Intensely itchy, dry, inflamed patches; chronic relapsing; often flexural.

Pathophysiology of Psoriasis

Immune-mediated chronic inflammation accelerates keratinocyte growth; cells accumulate.

Assessment of Psoriasis

Well-demarcated erythematous plaques with silvery scale; often extensor surfaces; nail changes.

Pathophysiology of Lichen planus

Immune-mediated inflammation at skin/mucosa; interface damage.

Assessment of Lichen planus

Itchy, purple, polygonal, flat-topped papules; may have white lacy oral lesions.

Pathophysiology of Stevens-Johnson syndrome (SJS)

Severe drug-triggered or infection-associated immune reaction causing epidermal detachment; <10% body surface area.

Assessment of Stevens-Johnson syndrome (SJS)

Painful rash, blisters/skin sloughing, mucosal erosions, fever/prodrome.

Treatment of SJS

stopping all non-essential medications, fluid replacement, nutrition, wound and eye care, pain medications…

Pathophysiology of Toxic epidermal necrolysis (TEN)

Same severe epidermal necrolysis process as SJS but >30% body surface area detached so WORSE with widespread keratin death

Assessment of Toxic epidermal necrolysis (TEN)

Widespread painful skin detachment and mucosal involvement; high fluid/infection risk.

Pathophysiology of Basal cell carcinoma

Malignancy of basal cells, usually from UV exposure; grows slowly and rarely metastasizes.

Assessment of Basal cell carcinoma

Pearly papule, rolled border, telangiectasia, or nonhealing sore.

Pathophysiology of Squamous cell carcinoma

Malignancy of keratinocytes; UV exposure; more likely to invade/metastasize than BCC.

Assessment of Squamous cell carcinoma

Scaly/firm red nodule or nonhealing ulcer; may arise in sun-damaged skin.

Pathophysiology of Malignant melanoma

Malignant melanocytes; may spread rapidly.

Assessment of Malignant melanoma

ABCDE: asymmetry, border irregularity, color variation, diameter/evolving; changing lesion.

Pathophysiology of Thermal burns

Heat damages skin/tissue; severity depends on temperature, duration, and depth.

Brief exposure to intense heat from an explosion or sudden ignition

Flash burns

Touching hot surfaces, stoves, irons, or metal

Contact burns

Assessment of Thermal burns

Redness, blistering, or deep tissue destruction; assess extent/depth.

Pathophysiology of Chemical burns

Chemical causes ongoing tissue injury until removed/neutralized appropriately.

Assessment of Chemical burns

Pain, burns, tissue damage; may continue after contact.

Pathophysiology of Electrical burns

Current causes internal heat injury, muscle/nerve damage, arrhythmias; entry/exit wounds may be small.

Assessment of Electrical burns

Possible dysrhythmia, loss of consciousness, deep injury, rhabdomyolysis.

Pathophysiology of First-degree / superficial burn

Epidermis injured; dermis intact.

Assessment of First-degree / superficial burn

Red, dry, painful; blanches; no blisters.

Pathophysiology of Second-degree / superficial partial-thickness burn

Epidermis and upper dermis injured.

Assessment of Second-degree / superficial partial-thickness burn

Pink/red, moist, blisters, very painful, blanches.

Pathophysiology of Second-degree / deep partial-thickness burn

Deeper dermis injured; damage to deeper skin structures.

Assessment of Second-degree / deep partial-thickness burn

Pale/mottled, less moist, reduced blanching; sensation may be decreased; slower healing.

Pathophysiology of Third-degree / full-thickness burn

Entire epidermis and dermis destroyed; may extend into subcutaneous tissue.