NCLEX: SKIN DISORDERS

Skin disorders NCLEX: Nursing diagnoses

Skin Disorders NCLEX focuses on the caring for patients with skin disorders, you’ll find that several nursing diagnoses are applicable to many situations. These nursing diagnoses appear here, along with appropriate nursing interventions and rationales.

Skin disorders NCLEX: Impaired skin integrity

Related to illness, Impaired skin integrity can be associated with infection, immobility, excessive moisture, trauma, advanced age, and impaired blood flow.

Expected outcomes
• Patient verbalizes and demonstrates an understanding of all procedures and skin care regimens to prevent further tissue breakdown.
• Patient verbalizes feelings about his skin condition.

Nursing interventions and rationales
• Inspect the patient’s skin daily and document findings, particularly noting any change in status. Early detection prevents or minimizes skin breakdown.
• Perform the prescribed treatment regimen for the patient’s skin condition; monitor progress. Report favorable and adverse responses to treatment so the current regimen can be maintained or modified as needed.

Hygiene help

• Assist the patient with general hygiene and comfort measures as needed to promote comfort and a general sense of well-being.
• Promote mobility, and establish a pressure ulcer prevention routine if indicated.
• Apply a bed cradle to protect lesions from bed covers.
• Encourage the patient to express his feelings about his skin condition. This helps to allay anxiety and develop coping skills.
• Discuss precipitating factors if known. If the patient has a skin allergy to food, explain dietary restrictions to help reduce the occurrence and severity of skin reactions.
• Teach the patient about his skin care regimen to ensure compliance.

Skin disorders NCLEX: Risk for infection

Related to impaired skin integrity, Risk for infection may also apply to any condition that impairs the skin’s ability to guard against invasion by microorganisms.

Expected outcomes
• Patient remains free from additional infections.
• Patient maintains normal temperature and laboratory values.

Nursing interventions and rationales
• Minimize the patient’s risk of infection through proper hand washing and by using standard precautions when providing direct care.

Fever fears

• Take the patient’s temperature at least every 4 hours. Report elevations immediately. Sustained postoperative fever may signal the onset of pulmonary complications, wound infection or dehiscence (premature splitting open of the wound layers), or urinary tract infection.
• Monitor white blood cell (WBC) count as ordered. Report elevations or depressions. An elevated WBC count indicates infection.
• Inspect skin lesions for erythema, warmth, or purulent drainage to detect secondary infection.
• Culture urine, respiratory secretions, wound drainage, or blood according to your facility’s policy and the practitioner’s orders. This procedure identifies pathogens and guides antibiotic therapy.
• Instruct the patient to wash his hands before and after meals and after using the bathroom, bedpan, or urinal.
• Ensure adequate nutritional intake. Offer high-protein supplements, unless contraindicated, to aid healing, stabilize weight, and improve muscle tone and mass.
• Teach the patient about good hand-washing technique, factors that increase his infection risk, and signs and symptoms of infection. Doing this helps him participate in care and modify his lifestyle to maintain optimal health.

Skin disorders: Common skin disorders

This section covers common skin disorders and includes information on their causes, assessment findings, diagnostic tests, treatment, nursing interventions, patient teaching, and evaluation criteria.

Skin disorders NCLEX: Cellulitis

Focus Topic: Skin disorders

A diffuse inflammation of the dermis and subcutaneous tissue, cellulitis commonly appears around a skin break—usually a fresh wound or small puncture site. With timely treatment, prognosis is usually good.

What causes it
Cellulitis usually results from an infection by group A beta-hemolytic streptococci or Staphylococcus aureus. It may also stem from infection by other organisms.

Pathophysiology
A break in skin integrity almost always precedes infection. As the offending organism invades the compromised area, it overwhelms the defensive cells (such as neutrophils, eosinophils, basophils, and mast cells) that usually contain and localize the inflammation. As cellulitis progresses, the organism invades tissue around the initial wound site.

What to look for
Signs and symptoms of cellulitis include:
• a tender, warm, erythematous, swollen area, which is usually well demarcated
• a warm, red, tender streak following the course of a lymphatic vessel
• fever and chills.

What tests tell you
• Although diagnosis usually can be made from the clinical presentation, the doctor may order a Gram stain and culture of skin tissue.
• If the patient is acutely ill, blood cultures may be taken.

How it’s treated
Preventing widespread skin destruction requires I.V. or oral antibiotic therapy depending on the severity of the infection. If gangrene occurs, the patient must undergo surgical debridement and incision and drainage of surrounding tissue.

What to do
• Monitor the patient’s vital signs (especially temperature) every 4 hours.
• Assess the patient every 4 hours for an increase in the size of the affected area or worsening of pain.
• Administer an antibiotic, an analgesic, and warm compresses, as ordered.
• Evaluate the patient. He should show signs of resolution of erythema, pain, and warmth and improved skin integrity.

skin disorders nclex

Skin disorders NCLEX: Cutaneous ulcers

Focus Topic: Skin disorders NCLEX

Cutaneous ulcers are localized areas of cellular necrosis that arise from areas of poor tissue oxygenation. The ulcers may be superficial or deep (originating in underlying tissue). Ulcers that arise from deep tissues typically go undetected until they penetrate the skin.

What causes them
The three most common cutaneous ulcers include pressure ulcers, caused by pressure; arterial ulcers, which result from chronic arterial insufficiency that stems from peripheral arterial disease; and venous ulcers, the result of venous insufficiency. Less common causes of cutaneous ulcers include infection, lymphedema, vasculitis, malignancy, adverse medication reactions, and ulcerating skin diseases such as pyoderma gangrenosum.

A roll call of risk factors

Conditions that increase the risk of developing pressure ulcers include:
• altered mobility
• inadequate nutrition (leading to weight loss with reduction of subcutaneous tissue and muscle bulk)
• breakdown in skin or subcutaneous tissue (from edema or incontinence).
Other predisposing factors for pressure ulcers are infection, trauma, pathologic conditions, and obesity.
Conditions that increase the risk of developing arterial ulcers include:
• damage to arteries from atherosclerosis, hypertension, diabetes, smoking, trauma, or irradiation
• inflammatory vasculitis disorders, such as thromboangiitis obliterans, polyarteritis nodosa, and hypersensitivity arteritis
• vasospastic disorders such as Raynaud’s phenomenon
• congenital anomalies of the arterial system such as coarctation of the aorta.
Several conditions increase the risk of developing venous ulcers:
• In inherited or acquired venous valve disorders, valves are absent or don’t work properly. Incompetent venous valves allow blood to leak backwards through the valve cusps instead of moving towards the heart.
• In deep vein thrombosis, clots obstruct the veins and damage the venous valves. Such obstructions can lead to postphlebitic syndrome, characterized by chronic edema and ulcers that don’t heal well.

• Conditions such as edema from heart failure, abdominal surgery, obesity, and lymphedema can cause vein compression and impair venous outflow.

Pathophysiology
Pressure ulcers are caused by pressure that interrupts normal circulatory function. Intensity and duration of the pressure determine ulcer severity. Pressure exerted over an area for a moderate length of time (1 to 2 hours) produces tissue ischemia and increased capillary pressure, leading to edema, inflammation, cellular necrosis, and ulceration.

The fallout from faulty flow

In arterial ulcers, damage to the artery walls can lead to blockages, aneurysms, and microvascular changes. Impaired blood flow decreases the oxygen delivered to the tissue, which results in necrosis and ulcers.
In venous ulcers, blood flow towards the heart is impaired, causing high pressures within the veins. This venous hypertension causes local tissue inflammation, resulting in skin changes, tissue anoxia, necrosis, and ulcers.

What to look for
Pressure ulcers commonly develop over bony prominences. Early features of superficial lesions include shiny, erythematous changes over the compressed area, caused by localized vasodilation when pressure is relieved, and superficial erythema progressing to small blisters or erosions. As the lesion progresses, it may develop ulceration and necrosis.

Gauging the stage

On admission, every patient with pressure ulcers should receive a complete skin assessment, including pressure ulcer staging and an assessment for the risk of developing new pressure ulcers. Such assessments should be ongoing, at regular intervals and any time the patient’s condition changes, according to the facility’s policy. Early detection of skin changes associated with pressure ulcer development plays a key role in preventing pressure ulcers.

Arterial ulcers often occur in areas of increased focal pressure, such as the tips of the toes, metatarsal heads, and lateral malleolus. These ulcers are commonly dry and can cause signs and symptoms of ischemia in the affected limb, such as limb pain, pallor, decreased pulses, coolness, nail changes, and hair loss.

Venous ulcers most commonly occur just above the medial ankle and are typically superficial and moist. The skin may appear brawny and brown from fibrotic changes, and the patient may have chronic edema and varicosities.

skin disorders nclex

What tests tell you
Wound culture and sensitivity testing of ulcer exudate identify infecting organisms and help determine whether an antibiotic is needed.

How they’re treated
Treatment is similar for many types of cutaneous ulcers. Treatment begins by addressing any underlying disease process and maximizing blood flow to improve tissue oxygenation. Open lesions are cleaned with normal saline solution. Dressings, if needed, should be porous and taped lightly to healthy skin. Composite dressings (such as Coverderm and Tegaderm) are appropriate for wounds with minimal to heavy drainage, necrotic tissue, or healthy granulation tissue. Debridement of necrotic tissue may be necessary to promote healing.

What to do
• Clean the skin with warm water and a mild cleaning agent; then apply moisturizer if indicated. Raise the head of the bed to 30 degrees to prevent shearing pressure. Protect the wound from further trauma.
• Turn and reposition the patient every 1 to 2 hours unless contraindicated. For at-risk patients, use a pressure-relieving mattress.
• Ensure adequate dietary intake of protein and calories.
• Use pressure-reduction devices and control excess moisture.
• Evaluate the wound-healing process. With successful treatment, the ulcer should reepithelialize. The patient and caregivers should take adequate measures to prevent recurrence of cutaneous ulcers.

skin disorders nclex

Herpes zoster

Also called shingles, herpes zoster is an acute unilateral and segmental inflammation of certain nerve roots. Usually appearing in adults over age 40, herpes zoster causes localized vesicular skin lesions confined to a dermatome (an area of the skin innervated by sensory fibers from a single spinal nerve).

No gain from this pain

Severe neuralgic pain occurs in peripheral areas fed by the nerves arising in the inflamed ganglia.

What causes it
Herpes zoster results from the varicella-zoster virus, a herpesvirus that also causes chickenpox. Roughly 20% of people who have had chickenpox eventually get herpes zoster. It isn’t known what causes the virus to reactivate in healthy people. Perhaps a temporary weakness in immunity allows it to multiply and travel along nerve fibers toward the skin.

Pathophysiology
Herpes zoster erupts when the varicella-zoster virus reactivates after dormancy in the cerebral ganglia (extra-medullary ganglia of the cranial nerves) or the ganglia of posterior nerve roots. The virus may multiply as it reactivates, and antibodies remaining from the initial infection may try to neutralize it.

Neutralizing neurons

If antibodies don’t effectively neutralize the virus, it continues to multiply in the ganglia, destroys neurons, and spreads down the sensory nerves to the skin.

What to look for
Onset of herpes zoster is characterized by fever and malaise. Within 2 to 4 days, severe deep pain, pruritus, and paresthesia (burning, itching, prickling, or tingling sensations) or hyperesthesia (increased sensitivity to touch) develop—usually on the trunk and occasionally on the arms and legs. Pain may be continuous or intermittent.

Unilateral attack

Small, red, nodular skin lesions then usually erupt over the painful areas and spread unilaterally around the thorax or vertically over the arms or legs. They quickly become vesicles, or blisters, filled with clear fluid or pus. About 10 days after they appear, the vesicles dry and form scabs.

What tests tell you
• The dermatomic distribution of lesions is usually sufficient to confirm the diagnosis.
• A Tzanck test of vesicular fluid and infected tissue shows eosinophilic intranuclear inclusions and varicella virus.

• In unusual cases, a Tzanck smear, biopsy, and viral culture may be needed to confirm the diagnosis.

How it’s treated
Relief of itching and neuralgic pain may require calamine lotion or another topical antipruritic and pain medication. If bacteria have infected ruptured vesicles, treatment includes a systemic antibiotic.

Potent potions

Trigeminal zoster with corneal involvement calls for instillation of an antiviral agent. To help the patient cope with the intractable pain of postherpetic neuralgia, the doctor may order analgesics, a systemic corticosteroid to reduce inflammation, or a tranquilizer, sedative, or tricyclic antidepressant with a phenothiazine. Acyclovir or another antiviral is used to stop progression of the skin rash and prevent visceral complications.

An ounce of prevention

A vaccine called Zostavax can help prevent herpes zoster in those age 60 and up. However, Zostavax won’t cure herpes zoster once it occurs, and patients who have already had herpes zoster shouldn’t receive the vaccine.

What to do
• Promote patient comfort.
• Administer medications as ordered.
• If lesions are severe and widespread, apply a wet dressing. If vesicles rupture, apply a cold compress as ordered.
• Watch an immunosuppressed patient closely for signs and symptoms of dissemination (such as generalized lesions) and central nervous system infection (such as headache, weakness, fever, and stiff neck).
• Evaluate the patient. With successful treatment, he should show resolution of all skin lesions, although extensive lesions may produce scars. Determine whether he has postherpetic neuralgia.

skin disorders nclex

Skin disorders NCLEX: Psoriasis

Focus Topic: Skin disorders NCLEX

A chronic disorder, psoriasis is a noncontagious inflammatory skin disease marked by reddish papules (solid elevations) and plaques covered with silvery scales. The condition takes a recurrent course, with remissions and exacerbations. Psoriatic lesions vary widely in severity and distribution. The disorder occurs in about 1% of the North American population, with usual onset between ages 25 and 30.

What causes it
The tendency to develop psoriasis may be genetically determined. Researchers have found a significantly higher-than-normal incidence of human leukocyte antigen (HLA) in patients with psoriasis, suggesting a possible autoimmune deficiency.

Pathophysiology
Psoriatic skin cells have a shortened maturation time as they migrate from the basal membrane to the surface or stratum corneum.

Plaque attack

As a result, the stratum corneum develops thick, scaly plaques (the chief sign of psoriasis).

What to look for
Small, erythematous papules usually are the initial sign of psoriasis.
These lesions enlarge or merge to form red, elevated plaques with
silver scales. Most commonly, they’re symmetrical and seen on the
scalp, face, chest, elbows, knees, back, buttocks, and genitalia.
Other features of psoriasis include pruritus, nail pitting, and
joint stiffness (psoriatic arthritis).

What tests tell you
• Skin biopsy helps rule out other disorders.
• The serum uric acid level may be elevated.
• In early-onset familial psoriasis, tests typically show the presence of the HLA known as Cw6, B13, and Bw57.

How it’s treated
Interventions for psoriasis vary because no permanent cure exists. All treatments are merely palliative. Lukewarm baths and application of occlusive ointment bases (petroleum jelly or preparations containing urea) or salicylic acid preparations may soften and remove psoriatic scales. Steroid creams are the mainstay of therapy.

A sunny suggestion

To slow rapid cell proliferation, the practitioner may recommend exposure to ultraviolet light (wavelength B [UVB] or natural sunlight) to the point of minimal redness.

Advice on anthralin

Anthralin, combined with a paste mixture, may be used for well-defined plaques. However, this drug must not be applied to unaffected areas because it may cause inflammation. Anthralin irritates and stains the skin. It also stains clothing and household items such as the bathtub.

Tar? Sounds bizarre

For a patient with severe chronic psoriasis, the Goeckerman treatment—which combines tar application and UVB treatments— may help achieve remission and clear the skin. The Ingram technique, a variation of the Goeckerman treatment, uses anthralin instead of tar. Psoralen plus ultraviolet A (PUVA) therapy combines methoxsalen (a psoralen derivative) with exposure to ultraviolet A light. Methotrexate may help severe, refractory psoriasis.

Oatmeal, emollients, and aspirin

Low-dosage antihistamines, oatmeal baths, emollients (perhaps with phenol and menthol), and open wet dressings may relieve pruritus. Aspirin and local heat alleviate the pain of psoriatic arthritis; severe cases may require NSAIDs such as indomethacin. For scalp psoriasis, therapy usually consists of a tar shampoo, followed by application of a steroid lotion while the hair is still wet. Severe disease may require systemic treatment with drugs such as methotrexate (Trexall), cyclosporine (Gengraf), etanercept (Enbrel), or infliximab (Remicade).

Not much for nails

No effective treatment exists for psoriasis of the nails. However, the nails usually improve as skin lesions improve.

What to do
• Monitor for adverse reactions to therapy. The patient may develop allergic reactions to anthralin, atrophy and acne from steroids, and burning, itching, nausea, and skin cancer from PUVA. Metho trexate may cause liver or bone marrow toxicity.
• Evaluate the patient. With successful treatment, skin eruptions should be under control; he should be able to demonstrate proper skin care. Note whether he keeps follow-up appointments required to monitor for adverse reactions to therapy.

skin disorders nclex

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