Nursing Care of Patients with Skin Disorders Chapter 54 Nursing Care of Patients with Skin Disorders

Pressure Ulcers Pathophysiology Etiology Pressure Against Skin Tissue Anoxia Etiology Pressure Friction Shear

Risk Factors Immobility Impaired Circulation Impaired Sensory Perception Elderly Very Thin or Obese

Prevention Assess Daily Cleanse and Dry Daily and PRN Lubricate Daily Clean Incontinence Promptly Use Moisture Barrier PRN Do Not Massage Reddened Areas Shift every Weight every 15 min

Prevention (cont’d) Turn/Reposition at Least every 2 hr Keep Heels Off Bed Pad/Protect Bony Prominences Use Pressure-Reducing Mattress Use Lift Sheet to Move Provide Nutrition and Hydration

Braden Scale Page 1306 Sensory Perception Moisture Activity Mobility Nutrition Friction and Shear

Signs and Symptoms Pain Open Ulcerated Area Color Tip Black: Necroses Yellow: Infection Red: Healing

Diagnosis Physical Examination Culture and Sensitivity Blood Supply Studies Wound Biopsy

Therapeutic Interventions Remove All Pressure Debride Mechanical- Scissors and forceps are used to selectively remove non-viable tissue, wet to dry dressings, and whirlpool bath Enzymatic- topical debriding agent, agents selectively digest necrotic tissue. Autolytic- synthetic dressing over the wound , eschar is self digested via the action of the enzymes that are present in the fluid environment of the wound Surgical – Removal of devitalized tissue Cleanse 4 – 15 PSI- Irrigation system- shower head, 30ml syringe

Dressings Types Moist Environment Caution with Tape Hydrogel Polyurethane Film Hydrocolloid Wafer Biological Alginate Gauze Moist Environment Caution with Tape

Negative Pressure Wound Therapy

Stages Deep Tissue Injury I – Skin Intact, Red, Does Not Blanch II – Partial Thickness Skin Loss III – Full Thickness Skin Loss, May Have Eschar IV – Damage to Muscle, Bone, or Support Structures Unstageable

Stages (cont’d)

Nursing Diagnoses Page 1312 Impaired Skin Integrity Risk for Infection Pain

Disorders of the Skin

Pruritus Etiology and risk factors Triggered by touch, temperature changes, emotional stress, and chemical, mechanical, and electrical stimuli Prominent symptom of psoriasis, dermatitis, eczema, insect bites

Pruritus Medical treatment Stress management and avoidance of known irritants, sudden temperature changes, and alcohol, tea, and coffee Lubricants in the bathwater and emollients applied after bathing also may help Medications include corticosteroids, antihistamines, and local anesthetics

Pruritus Assessment Collect data about symptoms that may help determine the cause The history of the current illness is important because pruritus may be just one symptom of a condition that requires attention

Pruritus Interventions Lubricants/emollients; adding oils to bathwater Advise to avoid bathing in very hot water Administer medications or instruct patient in their use Inspect skin daily to determine effects of treatment Explain possible causes of pruritus and encourage the patient to avoid them

Atopic Dermatitis (Eczema) Pathophysiology Acute stage: red, oozing, crusty rash and intense pruritus Subacute stage: redness, excoriations, and scaling plaques or pustules. Fine scales may give skin a silvery appearance Chronic stage: the skin becomes dry, thickened, scaly, and brownish gray

Types of Dermatitis Contact Irritant Allergic Atopic Seborrheic

Signs and Symptoms Rash, Itching Lesions Scales Crusts Fissures Macules Papules Pustules

Atopic Dermatitis (Eczema) Etiology and risk factors Personal or family history of asthma, hay fever, eczema, or food allergies People with atopic dermatitis have an immune dysfunction, but it is not known whether that dysfunction is a cause or an effect of the disorder

Complications Infection Sepsis

Atopic Dermatitis (Eczema) Medical diagnosis Health history and physical examination Skin biopsy, serum immunoglobulin E levels, and cultures; allergy tests

Therapeutic Interventions Antihistamines Analgesics Antipruritics Steroids Colloidal Oatmeal Baths Wet Dressings

Nursing Diagnoses Impaired Skin Integrity Disturbed Body Image Deficient Knowledge

Seborrheic Dermatitis Pathophysiology Chronic inflammatory disease of the skin Affects scalp, eyebrows, eyelids, lips, ears, sternal area, axillae, umbilicus, groin, gluteal crease, and under the breasts Areas affected by this condition may have fine, powdery scales, thick crusts, or oily patches Scales may be white, yellowish, or reddish Pruritus is common

Seborrheic Dermatitis Etiology and risk factors The cause is unknown May be an inflammatory reaction to infection with the yeast Malassezia

Seborrheic Dermatitis Medical diagnosis Health history and physical examination Medical treatment Topical ketoconazole (Nizoral), sometimes with topical corticosteroids Shampoos that contain selenium sulfide (Selsun), ketoconazole, tar, zinc pyrithionate, salicylic acid, or resorcin

Seborrheic Dermatitis

Seborrheic Dermatitis Assessment Inspect and describe the affected areas Interventions Explain the condition and reinforce the physician’s instructions for treatment

Psoriasis Pathophysiology Etiology and risk factors Abnormal proliferation of skin cells Classic sign: bright red lesions that may be covered with silvery scales Etiology and risk factors Caused by rapid proliferation of epidermal cells Usually chronic with cycles of exacerbations and remissions. No cure.

Aggravating Factors Stress Strep Pharyngitis Hormone Changes Cold Weather Skin Trauma Some Drugs

Signs and Symptoms Papules, Plaques Silvery Scales Itching

Complications Infection, Fever, Chills Arthritis Nail Changes Lymphadenopathy

Psoriasis Assessment diagnosis Describe symptoms and treatments Inspect affected areas for lesions and scales Document joint pain or stiffness because the condition may cause arthritis diagnosis Ineffective Therapeutic Regimen Management Disturbed Body Image Social Isolation

Therapeutic Interventions Tub Baths Corticosteroids Salicylic Acid Keratolytics Vitamin D Creams Retinoids Coal Tar, Anthralin UV Light Chemotherapy Occlusive Dressings Fish Oil Supplements

Intertrigo Pathophysiology Etiology and risk factors Inflammation where two skin surfaces touch: axillae, abdominal skinfolds, and under the breasts The affected area is usually red and “weeping” with clear margins; may be surrounded by vesicles and pustules Etiology and risk factors Results from heat, friction, and moisture between touching surfaces

Intertrigo Medical diagnosis and treatment Based on site/appearance of inflamed skin If the skin not broken, wash with water twice daily; rinse and pat dry; soft gauze used to separate layer of tissue and absorb moisture For severe inflammation or fungal infection: topical corticosteroid or antifungal agent

Intertrigo Assessment Complaints of pain, irritation, or redness in body folds Inspect susceptible areas daily

Intertrigo Interventions Areas where skin surfaces are in contact must be kept clean and dry Apply topical medications as ordered Report increasing redness and tenderness, fever, and broken skin to the physician Encourage women with pendulous breasts to wear a soft, supportive bra If incontinence has contributed to perineal intertrigo, position patient with legs apart to allow moisture to evaporate

Intertrigo

Fungal Infections Pathophysiology/Etiology Direct Contact with Fungus Overgrowth with Antibiotic Therapy Grows in Warm Moist Environment

Fungal Infections Pathophysiology Tinea pedis (athlete’s foot) Tinea manus (hand) Tinea cruris (groin) Tinea capitis (scalp) Tinea corporis (body) Tinea barbae (beard) Candidiasis: affects skin, mouth, vagina, gastrointestinal tract, and lungs

Fungal Infections Etiology and risk factors Spread through direct contact or by inanimate objects Lesions may be scaly patches with raised borders Pruritus common symptom Medical diagnosis Confirmed by microscopic examination of skin scrapings Medical treatment Fungal: treated with antifungal powders and creams Oral candidiasis: treated with clotrimazole troches, nystatin mouthwash or lozenges, oral amphotericin B

Figure 50-8

Fungal Infections Assessment Interventions Conditions that might make a person susceptible to fungal infections Inspect the skin and mucous membranes for lesions Interventions Disturbed Body Image Altered Oral Mucous Membrane Risk for Injury

Therapeutic Interventions Keep Skin Clean and Dry Topical Antifungals Oral Antifungals Corticosteroids Teach to Avoid Spread

Acne Pathophysiology Etiology and risk factors Medical diagnosis Affects the hair follicles and sebaceous glands Comedones (whiteheads, blackheads), pustules, cysts Often develop on the face, neck, and upper trunk Etiology and risk factors Androgenic hormones cause increased sebum production; bacteria proliferate, causing sebaceous follicles to become blocked and inflamed Medical diagnosis Health history and physical examination findings

Acne Medical treatment Topical medications: antibiotics, keratolytics such as benzoyl peroxide, topical vitamin A preparations Oral antibiotics given over several months Nonpharmacologic treatment: comedo extraction or cryotherapy Dermabrasion to reduce scarring

Acne Assessment Interventions Document any treatments being used Inspect skin to determine extent and severity Interventions Disturbed Body Image Ineffective Therapeutic Regimen Management

Herpes Simplex Etiology and risk factors Medical diagnosis Viral infection begins with itching and burning and progresses to vesicles that rupture and form crusts Nose, lips, cheeks, ears, genitalia most often affected Oral lesions called cold sores or fever blisters Infections on the face and upper body usually caused by HSV-1; genital infections by HSV-2 Medical diagnosis Laboratory studies of exudate from a lesion and blood studies to detect specific antibodies

Figure 50-9

Herpes Simplex Pathophysiology Viral Infection HSV1 – Above Waist HSV2 – Below Waist

Herpes Simplex (cont’d) Primary Infection Direct Contact Respiratory Droplet Fluid Exposure Lies Dormant Recurs with Stress

Herpes Zoster Etiology and risk factors Commonly called shingles Varicella-zoster virus; also causes chickenpox Symptoms: pain, itching, and heightened sensitivity along a nerve pathway, followed by the formation of vesicles in the area When the skin is affected, crusts form Older adults especially susceptible to complications Immunosuppressed at greater risk for herpes zoster infections; may have serious systemic complications

Figure 50-10

Signs and Symptoms Prodromal Phase Vesicles and Pustules Burning, Tingling Vesicles and Pustules Burning, Itching, Pain Contagious Until Scabs Form

Herpes Zoster Assessment Conditions or treatments that might cause the patient to have a reduced immune response Distribution and appearance of the lesions Interventions Impaired Skin Integrity Acute Pain Ineffective Coping

Therapeutic Interventions Antiviral Agents (Acyclovir/Zovirax) Topical Oral Antibiotics for Secondary Infection Avoid Triggers of Recurrence

Herpes Zoster (Shingles) Pathophysiology Acute Inflammation/Infection Painful Vesicules Follows Nerve Distribution Usually One-sided

Etiology Reactivation of Varicella Zoster Virus (Chickenpox Virus) Occurs with Reduced Immune Function Elderly AIDS Immunosuppressed

Prevention Avoidance of Infected Persons Varicella Vaccine (Varivax) Zostavax

Signs and Symptoms Vesicles, Plaques Irritation Itching Fever Malaise Pain

Complications Postherpetic Neuralgia Persistent Dermatomal Pain Hyperesthesia Opthalmic Herpes Zoster Sepsis

Diagnosis History and Physical Culture

Therapeutic Interventions Acyclovir IV, Oral, Topical Analgesics Anticonvulsants/Antidepressants Antihistamines Corticosteroids Antibiotics for Secondary Bacterial Infection

Cellulitis Pathophysiology Etiology Inflammation of Skin/Connective Tissue Infection Staphylococcus/MRSA Streptococcus Etiology Open Wound/Trauma May be Unknown

Signs and Symptoms Warmth Redness Edema Pain, Tenderness Fever Lymphadenopathy

Diagnosis Culture and Sensitivity Blood Cultures

MRSA

Therapeutic Interventions Antibiotics Topical Systemic Debridement

Acne Vulgaris Increased Sebum Production Obstruction of Pilosebaceous Ducts

Acne Vulgaris (cont’d) Signs and Symptoms Comedones Open Closed Therapeutic Interventions Benzoyl Peroxide Vitamin A Acid Antibiotics Estrogen Therapy

Nursing Diagnoses: Skin Infections Risk for Spread of Infection Acute Pain

Pediculosis Pathophysiology/Etiology Infestation by Lice Transmission by Direct Contact

Types Pediculosis Capitis Pediculosis Corporis Pediculosis Pubis

Signs and Symptoms Itching Papular Rash Presence of Lice, Nits, and Excreta

Diagnosis History and Physical Test for STD if Pediculosis Pubis

Figure 50-12

Therapeutic Interventions Pediculosides Permethrin, Pyrethrin, Lindane Mechanical Removal Antipruritics Topical Corticosteroids

Patient Education Self Medication Removal of Nits Cleaning of Clothing and Objects Inspection of Family and Friends

Scabies Pathophysiology Etiology Sarcoptes Scabiei Mites Burrow into Skin Etiology Contact with Infected Clothing or Animals

Signs and Symptoms Itching Rash Burrows

Diagnosis Shaving of Lesion Microscopic Evaluation

Therapeutic Interventions Topical Scabicides Permethrin Crotamiton Antipruritics

Patient Education Self Medication Treat Family Members Wash Clothing and Linens Itching May Continue 2 Weeks Following Treatment

Pemphigus Pathophysiology/Etiology Triggers Autoimmune Disorder Bullae on Skin and Mucous Membranes Triggers Sun Some Drugs or Foods

Signs and Symptoms Bullae Pain Burning Itching Mucous Membranes Spread to Skin Rupture Raw Wounds Pain Burning Itching

Pemphigus

Diagnosis Positive Nikolsky’s Sign- Sloughing or blistering of normal skin, when minimal pressure is applied Biopsy- Biopsy of blister reveals acantholysis ( separating of the epidermal cells from each other)

Therapeutic Interventions Corticosteroids Cytotoxic Agents Antibiotics Analgesics Antipruritics Fluid Replacement High Protein, High Calorie Diet

Nursing Care Monitor Fluid Balance Monitor Diet Administer Wet Dressings or Baths Control Pain Maintain Oral Hygiene Provide Psychosocial Support

Malignant Skin Lesions Cancer Arising From Basal Cell Layer Basal Cell Carcinoma Epidermis Squamous Cell Carcinoma Menalocytes Malignant Melanoma

M Malignant Melanoma Basal Cell Carcinoma Figure 50-13D

Squamous cell carcinoma

Nonmelanoma Skin Cancer Basal cell carcinoma Painless, nodular lesions; pearly appearance Related to sun exposure Grow slowly and rarely metastasize Treated with surgical excision, Mohs’ micrographic excision, electrodesiccation and curettage, cryotherapy, radiation, or drugs that are applied topically or injected into the lesion

Nonmelanoma Skin Cancer Squamous cell carcinoma Scaly ulcers or raised lesions Develop on sun-exposed areas including the lips, and in the mouth Caused by overuse of tobacco and alcohol Grow rapidly and metastasize Treatment may include surgical excision, cryotherapy, and radiation therapy

Basal Cell Carcinoma

Squamous Cell Carcinoma

Melanoma Arises from pigment-producing cells in the skin Most serious form of skin cancer; fatal if it metastasizes Found anywhere on the body Irregular borders and uneven coloration; many are dark, but some are light. Begin as tan macule that enlarges Removed surgically; a wide area around a melanoma is usually excised Chemotherapy and immunotherapy also may be employed

Malignant Melanoma

Lentigo Maligna Melanoma Slow growing dark macula on exposed skin surfaces, especially on the face of elderly patients

Risk Factors Ultraviolet Rays Fair Skin Genetic Tendency X-Ray Therapy Chemicals Immunosuppressive Therapy

Prevention Limit Exposure to UV Rays Report Changes in Moles Use Sunscreen Wear Protective Clothing Report Changes in Moles

Diagnosis Examination Biopsy

Therapeutic Interventions Surgical Excision Chemotherapy Radiation Therapy

Dermatological Surgery Rhinoplasty- Nasal reconstruction Blepharoplasty- Eyelids Rhytidoplasty- Face lift Otoplasty- correction of ear