Chapter 41 Integumentary System PDF

Structure, Function, and Disorders of the Integument Chapter 41 Learning Objectives 1. Describe the pathogenesis, manifestations, and outcomes of altered integumentary function. 2. Describe the pathophysiology of pressure ulcers, including the risk factors associated with their...

Structure, Function, and Disorders of the Integument Chapter 41 Learning Objectives 1. Describe the pathogenesis, manifestations, and outcomes of altered integumentary function. 2. Describe the pathophysiology of pressure ulcers, including the risk factors associated with their development. 3. Describe the depth and extent of injury for first-, second-, and third-degree burns. For each condition; know the “quick & dirty”, including risk factors, clinical manifestations & presentation, treatment and education. Structure & Function of the Skin - The skin is the largest organ of the body - Primary function is protection from the environment by serving as a barrier against microorganisms, UV radiation, loss of body fluids, and the stress of mechanical forces - Layers of the skin include: - EPIDERMIS: superficial or outer layer - DERMIS: deeper layer - HYPODERMIS or SUBCUTANEOUS LAYER: lowest-lying layer of connective tissue; this is where you will find macrophages, fat cells, nerves, blood vessels and hair follicle roots Pressure Ulcers An open sore resulting from unrelieved pressure, shearing forces, friction, and moisture. Usually develop over bony prominences, but can also occur in soft tissues (ex. pressure from nasal cannulas) If pressure is relieved, redness will occur but there will be no lasting tissue damage; if the pressure is not relieved, there will be platelet aggregation & disturb blood flow causing necrosis of the surrounding tissues Shearing and friction are mechanical forces moving parallel to the skin (ex. a patient sliding down the bed, using their elbow to boost themselves) Moisture from incontinence or sweating can increase the fragility of the skin Risk Factors of Pressure Ulcers External Factors Disease & Tissue Factors - Prolonged pressure - Impaired perfusion; ischemia - Immobilization - Fecal or urinary incontinence; prolonged - Infrequent position changes (sitting in a exposure to moisture wheelchair or lying in bed) - Malnutrition - Dehydration - Prolonged moisture exposure - Previous history of pressure ulcers - Pain - Thin skin associated with aging or prolonged - Sedation use of steroids - Friction and shearing forces - Lack of communication & education regarding pressure ulcer care Staging of Pressure Ulcers STAGE 1: Nonblanchable erythema (redness) of intact skin; warm to touch STAGE 2: Partial-thickness skin loss involving epidermis or dermis; open sore STAGE 3: Full-thickness skin loss involving damage or loss of subcutaneous tissue; crater-like appearance STAGE 4: Full-thickness skin loss with exposure of muscle, bone, or supporting structures UNSTAGEABLE: obscured full-thickness skin and tissue loss with base of ulcer covered by slough or eschar or both in wound bed DEEP TISSUE PRESSURE INJURY: intact or non-intact skin with localized area of persistent nonblanchable deep red discolouration; blood filled blisters may be present **next few slides have graphic photos** Stage 1 Note the redness; if you were to put pressure with your finger the area does not blanche (turn white) Treatment for this stage includes early recognition and then more frequent positioning, elimination of excess moisture, and ensuring adequate nutrition, oxygenation & fluid balance is maintained. Stage 2 Note that the wound is still vascular and pink. Treatment for this stage includes cleansing the wound bed with saline, patting dry with sterile gauze, and covering the wound with a flat, moisture-retaining dressing that cannot wrinkle. Successful healing requires continued relief of pressure, and dressing changes. Stage 3 Fat & granulation tissue may be visible “Crater-like” The white on the top photo is known as “slough” Treatment includes cleansing the would, involving a wound care nurse if available for further instructions of the best way to care for the wound bed. Successful healing requires continued relief of pressure, and dressing changes.  Stage 4 Exposure of muscle & supporting structures. Usually seen in people with paralysis (they cannot feel the pain/pressure) Treatment includes wound dressings as ordered by wound care nurse, potential debridement of dead tissue, negative pressure wound therapy (NPWT) by a VAC dressing, and pain management Successful healing requires continued relief of pressure, and dressing changes. Unstageable Base of ulcer is covered by slough or eschar. In this photo, the wound is completely covered by eschar (dead skin) Treatment includes debridement (surgical removal) of the wound before applying dressings which promote wound healing Deep Pressure Injury Prevention of Pressure Ulcers 1. Frequent skin assessment 2. Repositioning 3. Pressure reduction, removal, and distribution (use of specialty beds, off loading boots) a. Offloading boots “float” the heel off the bed 4. Elimination of moisture 5. Adequate nutrition, oxygenation, and fluid balance Skin Assessment- Describing Skin Lesions When describing a skin lesion, it is important to note the following features: - Size - Type (see on following slide & review pg 1025 in textbook) - Shape & symmetry - Colour & pigmentation - Surface area covered - Distribution over body surface (contained to one area or spread out?) Primary Lesions & Secondary Lesions Primary Lesions: basic reaction patterns of skin with a Secondary Lesions: develop during the evolutionary process of definite morphology skin disease or are created by infection - Macule - Scale - Patch - Papule - Lichenification - Plaque - Keloid - Wheal (urticaria; hives) - Scar - Nodule - Excoriation - Tumor - Fissure - Vesicle (chicken pox, shingles) - Bulla - Erosion - Pustule (acne, scabies) - Ulcer - Cyst - Atrophy - Telangiectasia - Scar Keloids & Hypertrophic Scars Keloids: are rounded, firm, elevated scars with irregular clawlike margins that extend beyond the original site of injury (left) Hypertrophic Scars: are elevated scars but do not extend beyond the border of injury (right) Both are caused by abnormal wound healing with excessive fibroblast activity and collagen formation Inflammatory Disorders of the Skin- Dermatitis (Eczema) Eczema and dermatitis (used interchangeably) are the most common inflammatory disorders of the skin Characterized by - Pruritus (itchiness) - Lesions with indistinct borders - Epidermal change (when chronic, the skin becomes thickened, leathery, and hyperpigmented from recurrent irritation and scratching) Types of Dermatitis - Allergic contact: hypersensitivity when allergen comes in contact with the skin (redness, swelling, pruritus & vesicular lesions) - Irritant contact: similar to allergic contact - Atopic: common with a history of hay fever or asthma - Statis: occurs in the legs as a result of venous stasis and edema (erythema, pruritus, scaling, petechiae, hyperpigmentation, ulcers) - Seborrheic: chronic inflammation of the skin involving the scalp, eyebrows, eyelids, axilla, chest and back (scaly, white or yellowish plaques) - Cradle cap in infants Papulosquamous Disorders Psoriasis - Chronic, relapsing, proliferative, inflammatory skin disorder - Caused by by complex interactions between macrophages, fibroblasts, dendritic cells, natural killer cells, T-helper, and regulatory T cells - Both the dermis and the epidermis thicken because of cellular hyperproliferation; the turnover time for shedding the epidermis decreases to 3-4 days from the normal of 14-20 days - Psoriasis can occur in other diseases as comorbidities (such as irritable bowel disease, rheumatoid arthritis, and Crohn's) Psoriasis Papulosquamous Disorders Acne rosacea - Inflammation of the skin that develops in adulthood - Lesions are associated with chronic, inappropriate vasodilation resulting in flushing and sensitivity to the sun Papulosquamous Disorders Lupus Erythematosus Systemic, inflammatory, autoimmune disease with cutaneous manifestations Discoid lupus erythematosus - Restricted to the skin - Photosensitivity - Butterfly pattern over the nose and cheeks - Related to genetic and environmental factors and an altered immune response - Lesions persist for months and then resolve spontaneously or atrophy Bacterial Infections - Folliculitis: fection of hair follicle - Furuncles: Inflammation of hair follicles “boils” - Carbuncles: Collection of infected hair follicles; abscesses may develop - Cellulitis: Infection of the dermis and subcutaneous tissue - Erysipelas: Acute superficial infection of the upper dermis - Impetigo: Superficial lesion of the skin caused by coagulase-positive Staphylococcus or beta-hemolytic streptococci Cellulitis Infection of the dermis and subcutaneous tissue that can occur as an extension of a skin wound, as an ulcer, or from furuncles or carbuncles--usually seen in the lower extremities S/S: area is warm, erythematous, swollen, and painful (can usually draw a line around the border of the infection) Treatment includes antibiotics, and pain management **Must be differentiated from necrotizing fasciitis, which is a rare rapidly spreading infection caused by Streptococcus pyogenes. Known as “flesh eating disease” - Treatment for necrotizing fasciitis includes antibiotics and often surgical debridement Cellulitis (Left) vs. Necrotizing Fasciitis (Right) Viral Infections- Herpes Simplex Virus (HSV) Transmitted by contact with infected saliva HSV-1: Associated with oral infections or infection of the cornea or mouth (cold sores); appear as a rash or clusters of inflamed and painful vesicles HSV-2: Genital infections, “genital herpes” Viral Infections- Herpes zoster (Shingles) & varicella (Chicken Pox) - Primary infection of the varicella zoster virus (chicken pox), can lead to a later activated virus which causes herpes zoster (shingles) - Initial symptoms of shingles include pain and paresthesia localized to the affected dermatome (one specific area innervated by a single spinal nerve), followed by vesicular eruptions along that dermatome - Treatment includes compresses, calamine lotion, antiviral medications, and analgesics - The varicella vaccine is safe and effective in both adults and children Viral Infections- Warts Benign lesions caused by the human papillomavirus (HPV) - Common in children - Usually on fingers - Plantar warts- usually on pressure points on bottom of feet Treatment includes cryotherapy or topical salicylic acid Venereal Warts (genital warts) - Highly contagious & sexually transmitted Fungal Infections Fungi causing superficial skin lesions are called dermatophytes Fungal disorders are called mycoses; mycoses caused by dermatophytes are termed tinea - Tinea capitis (scalp) - Tinea manus (hand) - Tinea pedis (athlete’s foot) - Tinea corporis (ringworm) Tinea pedis - Tinea cruris (groin, jock itch) - Tinea unguium (nails) or onychomycosis Vascular Disorders- Urticaria (Hives) Circumscribed area of raised erythema and edema of the superficial dermis Associated with type I hypersensitivity reactions to allergens - Histamine release causes endothelial cells of the skin to contract Causes leakage of fluid from the vessels…. Which would result in ______ Most lesions resolve spontaneously within 24 hours, but new lesions may appear Treatment: avoidance of allergen, antihistamines, corticosteroids Vascular Disorders- Scleroderma Localized or systemic Causes thickening (sclerosis) of the skin; Skin is hard, hypopigmented, taut, shiny, and tightly connected to the underlying tissue Associated with several antibodies Progression to body organs may occur Benign Tumours (benign = not harmful) Most benign tumours of the skin are associated with aging Seborrheic keratosis- Benign proliferation of cutaneous basal cells; can be removed by cryotherapy or laser therapy Keratoacanthoma- Benign, self-limiting tumour of squamous cell differentiation from hair follicles; biopsies are usually done to rule out squamous cell carcinoma (type of skin cancer), as they have a similar presentation Actinic keratosis- Premalignant lesion composed of aberrant proliferations of epidermal keratinocytes; removal of tumour done to test for squamous cell carcinoma & site should continue to be evaluated Nevi (moles or birthmarks)- Benign pigmented or nonpigmented lesions; multiple and changing moles require regular evaluation Skin Cancer Basal cell carcinoma (BCC) & squamous cell carcinoma (SCC) are the most prevalent forms of cancer Malignant melanoma is the most serious and most common cause of death from skin cancer Causes include Chronic exposure to UV radiation Genetic mutations Preventative measures include Protection from the sun and avoidance of tanning beds (particularly in childhood) Vitamin D (more research needed) People with darkly pigmented skin have more melanin, which is a protective factor against sun exposure; less likely to develop these malignant tumours BCC & SCC (nonmelanoma skin cancers) Basal Cell Carcinoma (BCC) Squamous Cell Carcinoma (SCC) - Most common cancer in the world - Tumour of the epidermis - Numerous subtypes (superficial, nodular, - Second most common human cancer pigmented) - Premalignant lesions include actinic keratosis - Grows slowly, often ulcerates, develop crusts, - Rarely invade surrounding tissue and is firm to the touch - Most common cause of lip cancer - Metastasis (spread to other parts of the body) - Lower lip is rare, as the tumours do not invade blood or - Usually older, white men, with history of lymph vessels immunosuppression, pipe smoking & chronic alcoholism Cutaneous Melanoma (1/2) - Malignant tumour of the skin originating from melanocytes (the cells that make the pigment melanin) - Most serious skin cancer - Risk factors - Personal or familial history - UV radiation exposure (including tanning bed use before age 30) - Immunosuppression - Fair skin with repeated sunburns, fair hair, freckles - Younger females, or older males - Geographical location (UV index) Cutaneous Melanoma (2/2) - Suspicious nevi should be evaluated and removed (ABCDE evaluation) - Asymmetry, Border irregularity, Colour variation, Diameter larger than 6mm, Elevation or Evolving - Treatment - No evidence of metastatic disease = surgical removal & lymph node biopsy - If there is metastatic disease = radiation therapy, chemotherapy, and immunotherapy Early detection is critical to decrease mortality from metastatic disease Kaposi Sarcoma (KS) - Vascular malignancy associated with immunodeficiency - Associated with human herpesvirus-8 (HHV-8), AIDS, and transplant recipients taking immunosuppressive medications - Pruritic, painful, purplish-brown lesions - Diagnosed by skin biopsy, chest x-ray to see lesions in the lungs - Treatment includes surgical removal of lesions, radiotherapy, and cytotoxic medications Burns May be a result of thermal sources (thermal contact, scalds or radiation) or non-thermal sources (chemical, electrical or radioactive) In addition to cutaneous injury (skin), burns can be associated with smoke inhalation and other traumatic injuries Often a need for ventilatory support with inhalation injuries Wound depth; 1st degree, 2nd degree, 3rd degree, 4th degree Total body surface area (TBSA) estimation; rule of 9’s Effect of fluid and water losses in large surface area burns Different body system responses to burn injury Cardiovascular & systemic Cellular Metabolic Immunological Burn Wound Depth First Degree - Epidermis only, local pain and erythema - Ex. sunburn Second Degree - Superficial partial thickness (epidermis and some dermis; blisters) - Deep partial thickness (epidermis and dermis; waxy appearance) Third Degree - Full thickness (epidermis, dermis, and underlying subcutaneous tissue; dry leathery appearance) Fourth Degree - Full-thickness and deeper tissue (epidermis, dermis, and underlying subcutaneous tissue, tendons, muscle, and bone; require skin grafting) Total Body Surface Area (TBSA) Estimation - Rule of 9’s: estimates of the percentage of the total body surface (in multiples of 9) - 18% for each leg (9% front, 9% back) - 9% for each arm (4.5% front, 4.5% back) - 18% for front torso - 18% for back torso - 9% for the head (4.5% front, 4.5% back) - 1% for the genitalia *severity though*  Fluid & Water Losses >20% TBSA considered to be a major burn injury - Associated with massive evaporative water losses and fluctuations of large amounts of fluid, electrolytes, and plasma proteins into the body tissues - Manifested as generalized edema, circulatory hypovolemia & hypotension - Burn shock: a condition consisting of hypovolemic cardiovascular component & a cellular component - Hypovolemia is due to the fact that fluids shift into the interstitial space form the circulating blood volume - Decreased cardiac contractility and decreased blood volume; blood is shunted away from the liver, kidney, and gut - Intravenous fluid resuscitation is critical to restore circulating blood volume (Lactated RIngers); needs to be carefully monitored to ensure we don't cause fluid overload - Cellular metabolism is disrupted; along with cell membrane permeability and electrolyte allostasis Cardiovascular & Systemic Response to Major Burn Injury Hallmark of burn shock is decreased cardiac contractility and decreased cardiac output with inadequate capillary perfusion - Fluid and protein movement out of the vascular compartment results in an elevated hematocrit and white blood cell count and hypoproteinemia - Irreversible shock and death if not treated immediately - Total evaporative losses must be replaced to prevent volume deficit and shock Cellular Response to Major Burn Injury - Transmembrane potential disruption - Impairs the sodium–potassium pump - Increased intracellular sodium and water - Decreased potassium Metabolic Response to Major Burn Injury - “Flow phase” - Systemic hypermetabolic response beginning 24 hours after burn injury - Can persist for up to 2 years following a burn - Inflammatory response with local activation and recruitment of inflammatory cells at the site of injury - Hypermetabolism increases the thermoregulatory set point and core and skin temperatures Immunological Response to Major Burn Injury - Immediate, prolonged, and severe - End result is immunosuppression - Altered white blood cells - Impaired phagocytosis - Abnormal cellular and humoral immunity - Potentially fatal wound sepsis Evaluation & Treatments of Burns - Complex, prolonged recovery and complications with major burns - Goal is wound debridement and closure in a manner that promotes survival - Scar formation with contractures is often a consequence of healing in deep partial-thickness and third-degree burns - Elements of survival of major burn - Provision of adequate fluids and nutrition - Meticulous management of wounds with early surgical excision and grafting - Aggressive treatment of infection or sepsis - Promotion of thermoregulation - Pain management, nutritional therapy, reconstructive therapy Cold Injury Skin injury caused by exposure to extreme cold; usually affects fingers, toes, ears, nose, and cheeks - Frostnip: Cold exposure without tissue freezing, reversible, skin pallor and numbness - Chilblain: Violaceous skin colour with plaques or nodules, pain, and pruritus and without ice crystal formation - Frostbite: Occurs when tissues freeze slowly with ice crystal formation, numbness and no sensation of pain until thawing; then severe pain, classified by depth of injury - Flash freeze: Rapid cooling with intracellular ice crystals associated with contact with cold metals or volatile liquids Frozen skin becomes white or yellowish and is waxy in texture. There is numbness and no sensation, until thawed. When thawed, there is redness, edema, and burning pain Treatment of frostbite: cover affected areas with other body surfaces and warm clothing; do not rub or massage! Pain management is important. Debridement or amputation may be needed. Disorders of the Hair Alopecia: Loss of hair from the head or body Androgenic alopecia: Localized hair loss occurring in about 80% of men Female-pattern alopecia: Progressive thinning and loss of hair over the central part of the scalp, no loss of hair along the frontal hairline Alopecia areata: Autoimmune T-cell-mediated inflammatory disease against hair follicles that results in hair loss Hirsutism: Abnormal growth and distribution of hair on the face, body, and pubic area in a male pattern that occurs in women in androgen-sensitive areas