skin and wound issues in patients with parkinson’s … and wound issues in patients with...

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skin and wound Issues in Patients with Parkinson’s disease: an overview of Common disordersJanice M. Beitz, PhD, RN, CS, CNOR, CWOCN, CRNP

abstractParkinson’s Disease is a chronic neurodegenerative disorder that is expected to increase in coming decades as the American population continues to age. Although the motor dysfunction (bradykinesia, tremor, rigidity) of Parkinson’s Disease is well described in the literature, the nonmotor dysfunction related to autonomic system changes is not as com-monly addressed. Ironically, nonmotor changes, such as seborrhea, sialorrhea, hyperhidrosis, and sensory denervation occur earlier in the disease process and exert a profound effect on patients’ quality of life. The depletion of dopamine, a critically important neurotransmitter, is the critical pathology of Parkinson’s disease. Therapies targeting this abnormality and the effect of insufficient dopamine itself can affect the integumentary system and potentially wound healing. The pur-pose of this review is to describe changes in the autonomic nervous system due to Parkinson’s Disease with a focused overview of common skin and wound care issues that may affect wound care clinician practice. Implications for nurses and other clinicians caring for Parkinson’s Disease patients include surveillance for melanoma and other skin cancers, skin protection against excessive moisture or the effects of insufficient moisture, monitoring of wound healing progress, and interventions to prevent or ameliorate complications of immobility.

Keywords: Parkinson’s Disease, autonomic dysfunction, melanoma, hyperhidrosis, sialorrhea

Index: Ostomy Wound Management 2013;59(6):26–36

Potential Conflicts of Interest: none disclosed

Dr. Beitz is a Professor of Nursing, School of Nursing-Camden, Rutgers University, Camden, NJ. Please address correspondence to: Janice M. Beitz, PhD, RN, CS, CNOR, CWOCN, CRNP, 4 Coventry Court, Cherry Hill, NJ 08002; email: [email protected].

Parkinson’s Disease is a progressive neurodegenerative disease that affects approximately 1% of people over the

age of 60 years. In the United States, it is estimated that one million persons currently live with Parkinson’s Disease, with about 60,000 new cases diagnosed yearly.1,2 With the aging of the American population, the incidence and prevalence of Parkinson’s Disease are expected to rise.

Parkinson’s Disease hallmark is the loss of dopaminer-gic neurons of the substantia nigra. A pathological cellular hallmark is the presence of the Lewy Body, which is found without exception in Parkinson’s Disease. These intracellular inclusion bodies and the loss of dopamine characterize the critical pathophysiology of the disorder.3,4

Parkinson’s Disease is the most common neurodegen-erative movement disorder but is now widely recognized as a complex nonmotor multifocal disease as well.5,6 In addition to the classic cardinal features of tremor at rest, postural instabil-ity, rigidity, and akinesia, and possibly some cognitive impair-ment,7 Parkinson’s Disease also is characterized by a number of

autonomic dysfunction issues.8,9 What may not be as well rec-ognized in the non-neurology community is the effect of Par-kinson’s disease on the skin and its appendages (hair, nails).10

The purpose of this review is to describe changes in the autonomic nervous system due to Parkinson’s Disease with a focused overview of common skin and wound care issues that may affect wound care clinician practice.

BackgroundNonmotor symptoms intrinsic to Parkinson’s Disease oc-

cur earlier than motor symptoms and can affect quality of life substantially. Autonomic physiology changes in Parkin-son’s Disease underlie several nonmotor symptoms including orthostatic dizziness, gastrointestinal slowing, erectile dys-function, and swallowing problems.11,12 As autonomic func-tion deteriorates, patients can develop constipation, urinary urgency, frequency, nocturia, and urinary incontinence. It is often these nonmotor features that present the greatest man-agement challenge.12,13 What is lacking in Parkinson’s Disease

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sKIn and wound Issues and ParKInson’s dIsease

is drug therapy that is disease-modifying, such as has occurred in rheumatoid arthritis therapy.3,14,15 As the disease progresses, both motor and nonmotor symptoms worsen. In addition, no good predictive tests or symptom screens are yet available in the pre-symptomatic interval of Parkinson’s Disease.15

The autonomic changes of Parkinson’s Disease are mani-fested in many signs/symptoms that can affect the skin and its appendages such as the hair. These include sialorrhea (ex-cessive salivation), seborrhea, hyperhidrosis (excessive sweat-ing), sensory dysfunction/denervation of the skin, and sym-pathetic changes.10,16-20 Although exact occurrence of these autonomic changes is difficult to obtain, multiple authors describe them as “common” or “frequent” in Parkinson’s Dis-ease.19,21,22 A comparative descriptive design study10 analyzed 70 Parkinson’s patients and 22 control subjects; hyperhidro-sis was noted in 36 Parkinson’s Disease patients, and 18.6% of Parkinson’s Disease patients had seborrhea.

The skin can be affected by Parkinson’s Disease therapy as well. Medication side effects, untoward effects, or drug de-livery methods can cause iatrogenic lesions. In addition, the long-term motor deterioration of Parkinson’s Disease can alter the skin. As the occurrence of immobility and nonself-repositioning (related to possible “off” periods) rises, the risk for development of pressure ulcers also rises (see Table 1).23,24

Pathophysiology of autonomic nervous system Changes in Parkinson’s disease

The autonomic nervous system can be divided into the central autonomic networks, sympathetic pathways,

parasympathetic pathways, and the enteric nervous sys-tem. Parkinson’s Disease pathology affects these struc-tures through a presynaptic protein called a-synuclein. Whenαa-synuclein aggregates in the neuronal structures of the autonomic system, evidence supports that this aggrega-tion is a precursor to nerve degeneration.11 The pathology of Parkinson’s Disease affects autonomic innervation to sev-eral organ systems, including the cardiovascular, urinary, and gastrointestinal systems, generating the previously described nonmotor symptoms.11

Skin alterations. What may be less recognized by wound clinicians and other non-neurological specialists are the altera-tions in skin regulatory mechanisms associated with Parkinson’s

Key Points• Parkinson’sDiseaseaffectstheskininsomemanner

across the trajectory of the disease. • Nonmotorautonomicchangesincludesialorrhea,

hyperhidrosis, and seborrhea associated with Parkin-son’s Disease, malignant skin lesions associated with the disease pathology and/or therapy, and skin and wound care issues.

• NursescanprovidequalitycaretoParkinson’sDiseasepatients by being cognizant of and vigilant for potential skin problems affecting this patient population.

ostomy wound management 2013;59(6):26–36

table 1. Parkinson’s disease terminology59-61

Akinesia Delay in initiating movement, inability to move, “freezing”

Amantadine A drug improving symptoms of Parkinson’s Disease by increasing dopamine; classified as an antiviral agent

Anticholinergic drugs Group of drugs decreasing action of chemical acetylcholine; these drugs help reduce rigidity, tremors, and drooling in Parkinson’s Disease

Apomorphine A form of morphine that can increase the amount of dopamine available in the brain; used as rescue therapy in cases of freezing or other worsening symptoms

Bradykinesia Slowness of movement

Dopamine agonists A class of drugs used to treat Parkinson’s Disease; these drugs copy the effect of the brain chemical dopamine and increase available dopamine

Dyskinesias Involuntary nontremor movements

Levodopa A drug containing a form of the brain chemical dopamine; used to treat Parkinson’s symptoms

Livedo reticularis Cutaneous finding presenting as a mottled network of erythematous to violaceous discolor-ation; usually a benign condition affecting lower extremities

MAO-B inhibitors Newer class of drugs used to treat Parkinson’s Disease; includes rasagiline and selegiline

“Off” periods Relatively poor overall function and mobility corresponding to the PD medication not working (eg, slowed thinking, fatigue, irritability, drenching sweats)

Postural instability The tendency to fall without explanation usually when pivoting

Rigidity Stiffness of the limbs and trunk

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Disease. Not only are eccrine sweat glands altered,20 but also the innervation to skin blood vessels and erector pilli muscles is de-creased. Research has supported that sensory deficit in Parkin-son’s Disease results from cutaneous denervation. Parkinson’s Disease patients have increased thresholds for cold, warm, cold and heat pain, mechanical pain, and touch.17 Two comparative descriptive studies25,26 examining Parkinson’s Disease patients versus controls support that this autonomic denervation occurs early in Parkinson’s Disease and is more prevalent than previ-ously thought. Skin biopsy and measurement of sympathetic skin response, respectively, showed more absent skin responses and innervation loss in Parkinson’s Disease patients.

Another neurologic change in Parkinson’s Disease related to the skin is alteration in microRNAs (miRNAs). MiRNAs are small, endogenous, noncoding RNAs (ribonucleic acids) that regulate many protein-coding genes. MiRNAs play criti-cal roles in important physiologic processes such as the cell cycle, cell differentiation, and cell development, growth, and apoptosis. MiRNAs also play some role, although not fully clarified, in angiogenesis.27 MiRNAs are involved in skin mor-phogenesis, hair follicle morphogenesis, skin carcinogenesis, and autoimmune and inflammatory disease affecting the skin such as in systemic lupus erythematosis. It is known that cutaneous wound healing is incomplete without functional miRNAs. Altered expression of miRNAs has been identified in Parkinson’s Disease. Although more research is needed to elucidate the impact of this alteration on skin health and wound healing in Parkinson’s Disease,27 impaired wound healing may theoretically occur as the disease progresses.

skin and wound ChallengesSialorrhea. Hypersalivation is a common symptom of

Parkinson’s Disease. The exact pathomechanism of this in-creased salivation is not clear. Parkinson’s Disease patients may have difficulty swallowing, but the excessive salivation occurs in addition to this change.11,21 In some instances, pa-tients have good response to injection of botulinum toxin in the lingual, salivary, and parotid glands.28

From an integumentary system effects perspective, exces-sive salivation can irritate the skin around the mouth and up-per chest (if drooling occurs). Skin protectants may be neces-sary topically, but they must be types that are safe around the face and oral cavity. In other words, oil- or petrolatum-based products would not be recommended because the potential exists for lipoid pneumonia secondary to aspiration of lip-ids.29 Drug therapy usually is used to control the situation, in-cluding anticholinergic agents (to dry up secretions) or weak anticholinergic antidepressants, especially with concomitant depression. Belladonna compounds also can be used to de-crease saliva production.21

Hyperhidrosis. Hyperhidrosis, or excessive sweating, is a frequent nonmotor complaint of Parkinson’s Disease. The excessive sweating involves mainly the face, head, and trunk. Conversely, sweating decreases in the palms of the hands in

some Parkinson’s Disease patients. One study compared 13 Parkinson’s Disease patients with excessive sweating versus 37 Parkinson’s Disease patients with no hyperhidrosis and identified the difference in axial and palmar sudomotor skin response. The investigators suggest this axial hyperhidrosis could be a compensatory phenomenon for reduced sympa-thetic function in the extremities,22 but this is only a theory.

Hyperhidrosis can be caused by too-high or too-low doses of dopamine or dopamine promoting drugs. Off-period hy-perhidrosis can be treated with dopamine agonist (eg, L-Dopa) dosage increases. Beta-blockers (eg, propanolol) and injections with botulinum toxin also have been used.21 Drenching sweats, especially at night, can be notably troublesome.

Seborrhea. Chronic seborrhea is a common nonmotor symptom of Parkinson’s Disease. The outcome is greasy skin on the face that can be associated with erythema and scaly patches in skin creases. The hair also can be very oily with dandruff.21 The oiliness seems to be associated with periods when the disease is most active.30 When seborrheic dermatitis occurs around the eyes, flaky skin may involve the eyelashes and get into the eyes. Irritation of the face and eyes can be very troublesome to the patient.16

The condition has been acknowledged for decades. In 1977, Flint30 described the skin of the Parkinson’s Disease patient as “coarse and thickened” and the epidermis as shiny and glistening. She noted the oily limp appearance of the hair. The mechanism by which the seborrhea develops is not well understood but is likely the impact of altered dopamine state on glandular function. Whether seborrhea contributes to any impaired wound healing is unknown.

Malignant skin lesions. Convincing epidemiologic evi-dence31,32 suggests a negative association between Parkinson’s Disease and many cancers. Conversely, others support that melanoma and other nonskin cancers occur more often in Parkinson’s Disease.33,34 Inzelberg et al33 conducted a cross-sectional study in which 490 Jewish patients in a Parkinson’s Disease clinic were genotyped and then assessed for onco-logic history. Patients with Parkinson’s Disease with a specific genetic mutation had higher likelihood of nonskin cancers such as breast, prostate, stomach, and colon cancer.

Melanoma, a cancerous tumor of melanin-producing cells in the skin, occurs more frequently than should be expected in Parkinson’s Disease patients. No identified biologic mech-anism is available; some but not all sources suggest levodopa may increase the risk of melanoma.6

The nature of the Parkinson’s Disease-skin cancer (mela-noma) relationship is complex. Some reviews35 suggest skin cancer rates are higher in Parkinson’s Disease patients due to the disease process itself, while others suggest that dopamine therapy in its many forms is the critical factor.35,36 This focus is not a new area of study. The possible association between levodopa use and the development of malignant melanoma has been described since the 1970s.35 It is hypothesized that a genetic profile contributes to both melanoma development

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and the substantia nigra pathology of Parkinson’s Disease. A literature review35 suggests the increased incidence of mela-nomas in patients with Parkinson’s Disease, both before and after diagnosis, supports the pathophysiological rather than the pharmacological contribution. However, both Parkinson’s Disease and malignant melanoma incidence increase with age. In the 2 x 2 factorial, randomized, double-blind, placebo-con-trolled multicenter clinical DATATOP trial, Constantinescu et al37 followed 800 Parkinson’s Disease patients for 6 years. They found a higher-than-expected incidence (1.4%) of malignant melanoma compared to a healthy population. No causal rela-tionship between L-Dopa therapy and melanoma was noted. Age was an important factor for both Parkinson’s Disease and melanoma. “Consequently, it is expected that over 100 Ameri-cans every year will be coincidentally affected by both Parkin-son’s Disease and malignant melanoma without a causal rela-tionship between the two diseases.”37

Ferreira et al38 analyzed the frequency of neoplastic and precancerous skin lesions in Parkinson’s Disease patients. Us-ing a Parkinson’s Disease group and a matched control group (150 and 146 patients, respectively), they found Parkinson’s Disease patients had an increased risk of nonmelanoma skin cancer. They supported screening of the skin more frequently in Parkinson’s Disease patients, because a higher prevalence of preneoplastic and neoplastic skin lesions was observed in Parkinson’s Disease patients versus age-matched controls. The researchers hypothesized that nonmelanoma skin can-cer’s higher risk in Parkinson’s Disease patients may be due to increased sensitivity to the sun’s role in skin cancer genesis

among Parkinson’s Disease patients. Larger population stud-ies are needed.

Schwid et al36 studied skin cancer incidence in Parkinson’s Disease patients treated with a new agent (CEP-1347) de-signed to slow cell death of neuronal cells. Their multicenter study of 806 patients with early Parkinson’s Disease found that non-melanoma skin cancers were the most common type, but they did not occur at an excessive rate due to the drug. The incidence of melanomas was 20.9 times that pre-dicted in the general population. This increased rate was seen in patients who had never received dopaminergic therapy. The researchers proposed that Parkinson’s Disease itself in-creases melanoma risk unrelated to dopaminergic therapy.

drug therapy and Parkinson’s disease: Iatrogenesis

Levodopa and malignant melanoma. Levodopa, the ma-jor drug used in Parkinson’s Disease therapy, has been impli-cated in the development of malignant melanoma (see Table 2). Despite the previously described research findings, com-mon drug guides for clinicians continue to warn against us-ing levodopa in patients with suspicious skin lesions or a his-tory of melanoma. The concept developed because of “shared biochemical pathways between synthesis of both dopamine and melanin.”39 Levodopa is an important substance in the formation of melanin.

In 2003, Fiala et al39 performed a systematic review of the literature and reviewed case studies from their home insti-tution on the association between levodopa use in Parkin-son’s Disease and melanoma. They found that in a total of 54 patient cases, the occurrence of both Parkinson’s Disease and melanoma was coincidental rather than causal. Vigilance about the issue is warranted, because the controversy exists and the warning about melanoma and dopaminergic therapy persists in drug references. For example, Lehne28 states le-vodopa can “activate malignant melanoma and consequently should be avoided in patients with undiagnosed skin lesions.”

Apomorphine and skin necrosis. Apomorphine is a do-pamine agonist that is prescribed for treatment of acute, in-termittent off episodes associated with Parkinson’s Disease. Considered “rescue” therapy for off periods, apomorphine is given by injection or infusion.

Although generally benign, apomorphine can be associ-ated with skin damage. Ganesalingam and Bain40 described a case study of a 57-year-old man receiving apomorphine infusion subcutaneously who developed necrotic skin ul-cers despite the fact that he had received the drug for 4 years without problem. His necrotic ulcers resolved 1 month after stopping apomorphine.

Transdermal drug delivery skin reactions. Some anti-Parkinson drugs are available in transdermal patches. The benefit of this delivery system is substantial in that it can lower the pill burden of Parkinson’s Disease and help with compliance. In addition, transdermal delivery systems can

table 2. Parkinson’s disease medication therapy: commonly used agents62

Dopamine•Levodopa

o Carbidopa-levodopa (Parcopa)a

Dopamine agonists•Pramipexole(Mirapex)b

•Ropinirole(Requip)c

•Rotigotine(Neupro)d

•Apomorphine(Apokyn)e

•Bromocriptine(Parlodel)f

Catechol O-methyltrans-ferase (COMT) inhibitors•Tolcapone(Tasmar)g

•Entacapone(Comtan)H

Others•N-methyl-D-aspartate

receptor inhibitoro Amantadine

•AnticholinergicAgentso Benztropine (Cogentin)i

MAO-B inhibitors•Rasagiline(Azilect) j

•Selegiline(Eldepryl)k

a Jazz Pharmaceuticals, Philadelphia, PA; b Boehringer Ingelheim Phar-maceuticals, Ridgefield, CT; c GlaxoSmithKline, Philadelphia, PA; d UCB Pharma Inc. Atlanta, GA; e Vernalis Pharmaceuticals, Morristown, NJ; f Validus Pharmaceuticals, Parsippany, NJ; g Valeant Pharmaceuticals International, Bridgewater, NJ; h Novartis Pharmaceuticals, Philadelphia, PA; i Akorn, Inc. Lake Forest, IL; j Teva Neuroscience Inc, Petach Tikva, Israel; k Somerset Pharmaceuticals, Tampa, FL

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be used safely in elderly patients and avoid the well-known “first pass” phenomenon of oral agents.41 Schnitzler et al42 as-sessed compliance rates of transdermal once-daily rotigotine patch use in Germany. The majority of the 943 patients stud-ied were compliant with patch use regardless of their clinical state. The downside of use was skin reactions. Adverse skin reactions at the application site (3.7% frequency) led to early withdrawal in 34 patients. The skin reactions ranged from mild to moderate but were severe in one patient.

Skin sensitivity, especially in elders with sensitive and fragile skin, is the most frequent adverse side effect of trans-dermal delivery systems. A review41 suggests one approach to minimizing skin sensitivity reaction is varying the site of patch application. Both rotigotine and selegiline were avail-able in transdermal formulations. Watts et al43 conducted a multicenter, randomized, double-blind study of early Parkin-son’s Disease patients (N = 277) comparing rotigotine patch (n = 181) to placebo (n = 96). The results showed that mild to moderate application site reactions occurred in 44% of roti-gotine transdermal patch versus 12% of placebo recipients.43 Skin reactions were so bothersome, the rotigotine patch was

removed from the market.28 A recent drug safety evaluation of rotigotine patch was positive, and the transdermal form is still available in Europe.44 Transdermal selegiline is still avail-able but is used to treat major depressive disorder, and is not labeled for Parkinson’s Disease.28

Drug side effects: amantadine. Certain oral anti-parkinso-nian drugs are associated with dermatologic conditions. Aman-tadine, an antiviral drug that releases endogenous dopamine, is used more often in advanced Parkinson’s Disease to mitigate problematic dyskinesias. However, it also can cause skin changes.

Drug rashes can occur from amantadine. The lower ex-tremities may acquire a red and mottled edematous appear-ance called livedo reticularis (see Figure 1). Livedo reticularis is a reticulated (network) vascular pattern that appears as a lace-like purplish discoloration.45,46 The exact mechanism of amantadine-induced livedo reticularis is unclear. It is usually asymptomatic and can occur 1 month to 4 years after drug initiation. Most often, the lower extremities are affected, but the trunk and upper extremities can be altered as well. The change usually resolves when the drug is discontinued.16

skin/wound risks in Parkinson’s diseaseAs Parkinson’s Disease progresses, immobility and off peri-

ods may increase in severity. Difficulty in turning and moving in bed can exacerbate the challenges. The effects of pressure, shear, moisture, and friction on skin microcirculation have been known for decades. In 1994, Schubert and Heraud47 studied 30 elderly patients and the impact of pressure and shear on skin micro-circulation in the sacral area using a laser Doppler. Immobility, especially in the supine position, increased the risk for ischemic skin damage. Parkinson’s Disease immobility can play a great role in increasing risk for pressure ulcers. In addition, urinary/fecal incontinence challenges associated with more long-term Parkin-son’s Disease can combine with mobility alterations to increase risk for pressure ulcerations. The role of moisture-associated skin damage (MASD) and incontinence-associated dermatitis (IAD) in augmenting wound risk has been well documented.48-55

MASD in the form of urinary/fecal incontinence affects the normal protective strength of the skin. Once the incontinence be-comes IAD, substantive skin breakdown can occur in as little as 2 days.48 Although pressure ulcers need to be differentiated from IAD or MASD because treatments differ,49-51,53 both MASD/IAD increase the risk for pressure ulceration.

Sialorrhea that persists as drooling can generate MASD. In ad-dition to drug therapy, topical protection such as nonalcohol skin sealants may help prevent breakdown and maceration. Oil-based ointments would not be recommended, because they could po-tentially be inhaled or aspirated into nearby airways.

Parkinson’s Disease patients’ excessive sweating also can gen-erate skin breakdown risk. A potential exists for intertriginous dermatitis, another form of MASD, particularly if hyperhidrosis occurs near or within skin folds. Drying agents such as powder or materials that wick moisture away from the skin fold (eg, InterDry, Coloplast Corp, Minneapolis, MN) may help with management.

Figure 1. Livedo reticularis. Photo courtesy of Herbert P. Goodheart, MD, Associate Clinical Professor, De-partment of Dermatology, Mount Sinai Medical School, New York, NY. Used with permission.

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Risk for fungal skin infection of the perineal and perirectal area increases when the Parkinson’s Disease patient is incontinent. Commonly, fungal infections of the perigenital area present as a moist, red, itchy rash with classic satellite lesions as the fungal infection spreads across the skin. Antifungal ointment topical therapy (eg, mycostatin ointment) may be needed to control the infection.28 In addition, dry-ing materials with topical silver can act to wick moisture away plus decrease skin microbial count (InterDry Ag; Coloplast Corp, Minneapolis, MN).

Periwound moisture also may affect the Parkinson’s Disease patient’s skin integ-rity. As stated previously, Parkinson’s Disease patients have altered autonomic nerve supply, especially as the disease progresses. Chronic wounds such as exudative ve-nous ulcers also could pose a special challenge due to MASD.56

Hospitalization and/or critical illness can increase skin and wound risk for the Parkinson’s Disease patient. In a recent retrospective correlational study of predic-tors of pressure ulcers in critical care, Cox57 examined 347 critical care patient risk factors for predicting pressure ulcer development. She found altered mobility, older age, length of stay, and cardiovascular disease were the most significant predictors. All may affect the Parkinson’s Disease patient.

Implications for Clinical Practice and educationNurses have great opportunity to influence the quality of Parkinson’s Disease

patient care by being cognizant of and vigilant for potential skin problems affect-ing this patient population. The physiologic, pathophysiologic, and disease therapy mechanisms that may affect skin integrity affect nursing care.

Results of a review by Pan et al6 support that the skin changes associated with Parkinson’s Disease, especially the risk of malignant melanoma and other nonmelanoma skin cancers, suggest that periodic dermatological surveillance is critical to good care whether in primary, specialist, or long-term care set-tings. Nurses and other clinicians should carefully inspect the skin of the entire body (including the feet because sun exposure may not be a critical factor in skin cancer pathogenesis).35 For melanoma, clinicians should look at identified lesions with the melanoma mnemonic ABCDE (asymmetry, irregular border, color variability, diameter >6 mm, enlarging and elevated). The appearance of both basal cell and squamous cell cancers should be noted as well. Suspicious skin lesions should be referred to dermatology.

Sialorrhea, seborrhea, and hyperhidrosis mechanisms should be understood and addressed. Skin protection around the mouth and upper chest may be needed. Commercial products are available for protection, and nurses should contact skin and wound specialists such as wound, ostomy, continence nurses for advice.

To help seborrheic skin and hair, both should be frequently washed. If derma-titis occurs, topical steroids or dandruff shampoos may be necessary. If dermatitis with flakiness develops around the eyes, the use of a dandruff shampoo pyrithione zinc (Head and Shoulders, Proctor & Gamble, Cincinnati, OH) or selenium sulfate (Selsun Blue, Sanofi-Aventis, Bridgwater, NJ), allowed to run over the face (with the eyes closed) may help.16,28 Interestingly, both seborrhea and seborrheic dermatitis improve with treatment of levodopa in Parkinson’s Disease.31

In addition to pharmacological (dopamine) therapy for hyperhidrosis, other approaches may help. The patient with hyperhidrosis can be taught to take luke-warm showers, wear lighter weight clothing in warm weather, drink extra fluids, use lightweight cotton sheets for bedding, and avoid saunas.18,19 Dry skin on the extremities and palms can benefit from moisturizing lotions.

Skin changes related to drug therapy should be in the mind of the clinicians caring for the Parkinson’s Disease patient. Attention to the development of skin rashes, lesion patterns, and areas of irritation is necessary especially if apomorphine or amantadine are being used.

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Another noteworthy issue is the change in the protective na-ture of the integumentary system due to the disease. Research suggests that Parkinson’s patients’ skin has less sensitivity to heat, cold, and mechanical pain.20,25,26 Other sources suggest altered sensitivity to sunlight.38 Both require the nurse to educate pa-tients about these risks and good preventative self-care related to burns and cold exposure.

Jaul’s review52 notes that pressure ulcer prevention and treat-ment involves optimal treatment of irreversible medical con-ditions. Specifically, rigidity and immobility must be treated promptly with dopaminergic therapy as necessary. The implica-tions for prompt delivery of Parkinson’s medications are evident in that they may prevent or ameliorate the motor issues and off periods. Nursing staff and caregivers must understand this rela-tionship and make sure patients experiencing poor symptom control are promptly medicated.

Parkinson’s Disease also is associated with urinary tract dys-function, especially nocturia and urgency.58 Skin integrity can be at risk with urinary incontinence. Frequent assessment and use of continence aids may be necessary. Barrier ointments in the peri-genital area can protect against MASD and IAD.

Wound healing processes in long-term Parkinson’s Disease patients are an area for future research and nursing vigilance. Wounded Parkinson’s patients should be monitored closely for healing progress. A slow-to-heal wound may have other in-hibitory processes occurring because of the disease. Attention to known wound healing factors such as nutrition and topical therapy is warranted.

The effects of Parkinson’s Disease on the skin have been de-scribed in this article. But disease impact is also more profound. Leibson et al’s9 epidemiologic study of 197 Parkinson’s Disease pa-tients in Minnesota for 5 years before and 15 years after diagnosis supports that Parkinson’s Disease patients have greater mortality and morbidity than matched nonParkinson’s Disease patients over time. These disorders include other diseases of the circulatory system, veins, lymphatics, and digestive system. Nurses and other providers need to be attentive for comorbidity development.

ConclusionParkinson’s Disease affects the skin in some manner across

the trajectory of the disease. The nonmotor autonomic chang-es include sialorrhea, hyperhidrosis, and seborrhea associ-ated with Parkinson’s Disease, malignant skin lesions associ-ated with the disease pathology and/or therapy, and skin and wound care issues with nursing implications. Nurses and other health clinicians can promote optimal care by increasing their understanding of disease impact and the methods by which po-tential complications can be anticipated and prevented. n

acknowledgmentThis article was generated as a result of participation in the Vis-

iting Nurse Faculty Program of the Edmond J. Safra Foundation. The author offers special thanks to all who devised and imple-mented this wonderful activity for nurse educators.

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A28 WOUNDS® www.woundsresearch.com

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INDEX OF ADVERTISERS

Dermagraft®

Human Fibroblast-Derived Dermal Substitute Essential Prescribing Information Numbers in parentheses ( ) refer to sections in the Directions for Use of the product labeling.Device Description: Dermagraft is a cryopreserved human fibroblast-derived dermal substitute. (1)Intended Use/Indications: Dermagraft is indicated for use in the treatment of full-thickness diabetic foot ulcers greater than six weeks duration which extend through the dermis, but without tendon, muscle, joint capsule, or bone exposure. Dermagraft should be used in conjunction with standard wound care regimens and in patients that have adequate blood supply to the involved foot. (2)Contraindications:• Dermagraft is contraindicated for use in ulcers that have signs of clinical infection or in ulcers with sinus

tracts.• Dermagraft is contraindicated in patients with known hypersensitivity to bovine products, as it may contain

trace amounts of bovine proteins from the manufacturing medium and storage solution. (3)Warnings: None (4)Precautions:Caution: The product must remain frozen at -75°C ± 10°C continuously until ready for use.Caution: Do not use any topical agents, cytotoxic cleansing solutions, or medications (e.g., lotions, ointments, creams, or gels) on an ulcer being treated with Dermagraft as such preparations may cause reduced viability of Dermagraft.Caution: Do not reuse, refreeze, or sterilize the product or its container.Caution: Do not use the product if there is evidence of container damage or if the date and time stamped on the shipping box has expired.Caution: Dermagraft is packaged with a saline-based cryoprotectant that contains 10% DMSO (Dimethylsulfoxide) and bovine serum. Skin and eye contact with this packaging solution should be avoided.Caution: Dermagraft has not been studied in patients receiving greater than 8 device applications.Caution: Dermagraft has not been studied in patients with wounds that extend into the tendon, muscle, joint capsule, or bone. Dermagraft has not been studied in children under the age of 18 years, in pregnant women, in patients with ulcers over a Charcot deformity of the mid-foot, or in patients receiving corticosteroids or immunosuppressive or cytotoxic agents.Caution: To ensure the delivery of metabolically active, living cells to the patient’s wound, do not hold Dermagraft at room temperature for more than 30 minutes. After 30 minutes, the product should be discarded and a new piece thawed and prepared consistent with Preparation for Use instructions.Caution: The persistence of Dermagraft in the wound and the safety of this device in diabetic foot ulcer patients beyond six months has not been evaluated. Testing has not revealed a tumorigenic potential for cells contained in the device. However, the long-term response to these cells is unknown.Caution: Always thaw and rinse product according to the Preparation for Use instructions to ensure the delivery of metabolically active, living cells to the patient’s wound.Caution: Do not use Dermagraft after the expiration date indicated on the labeled unit carton. (5)Adverse Events: In clinical studies conducted to date, the overall incidence of reported adverse events was approximately the same for patients who received Dermagraft compared to those who received the Control treatment. (6)Maintaining Device Effectiveness: Dermagraft must be stored continuously at -75°C ± 10°C. Dermagraft must be thawed and rinsed according to the Preparation for Use instructions. After the initial

application of Dermagraft, subsequent sharp debridement of the ulcer should continue as necessary. Additional wound preparation should minimize disruption or removal of previously implanted Dermagraft. (13)Patient Counseling Information: After implantation of Dermagraft, patients should be instructed not to disturb the ulcer site for approximately 72 hours (three days). After this time period, the patient, or caregiver, should perform the first dressing change. The frequency of additional dressing changes should be determined by the treating physician. Patients should be given detailed instructions on proper wound care so they can manage dressing changes between visits. Compliance with off weight-bearing instructions should be emphasized. Patients should be advised that they are expected to return for follow-up treatments on a routine basis, until the ulcer heals or until they are discharged from treatment. Patients should be instructed to contact their physician, if at any time they experience pain or discomfort at the ulcer site or if they notice redness, swelling, or discharge around/from the ulcer. (8)How Supplied: Dermagraft is supplied frozen in a clear bag containing one piece of approximately 2 in x 3 in (5 cm x 7.5 cm) for a single-use application. The clear bag is enclosed in a foil pouch and labeled unit carton.Caution: Dermagraft is limited to single-use application. Do not reuse, refreeze, or sterilize the product or its container.Dermagraft is manufactured using sterile components and is grown under aseptic conditions. Prior to release for use, each lot of Dermagraft must pass USP Sterility (14-day), endotoxin, and mycoplasma tests. In addition, each lot meets release specifications for collagen content, DNA, and cell viability.

Dermagraft is packaged with a saline-based cryoprotectant. This solution is supplemented with 10% DMSO (Dimethylsulfoxide) and bovine serum to facilitate long-term frozen storage of the product. Refer to the step-wise thawing and rinsing procedures to ensure delivery of a metabolically active product to the wound bed. (9)Customer Assistance: For product orders, technical support, product questions, reimbursement information, or to report any adverse reactions or complications, please call the following number which is operative 24 hours a day:Shire Regenerative Medicine Customer Service(877) DERMAGRAFT or (877) 337-6247Caution: Federal (U.S.) law restricts this device to sale by or on the order of a physician (or properly licensed practitioner).Shire Regenerative Medicine, Inc.US PAT Nos.4,963,489; 5,266,480; 5,443,950©2012 Shire Regenerative Medicine, Inc.All Rights ReservedDERMAGRAFT is a registered trademark of Shire Regenerative Medicine, Inc.

11095 Torreyana RoadSan Diego, CA 92121-1104

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