Journal of the Dermatology Nurses' Association:
Dysplastic Nevi and the Risk of Melanoma: Current Evaluation and Management
Rubin, Krista M.
Krista M. Rubin, MS, RN, FNP-BC, Melanoma Disease Center, Massachusetts General Hospital, Boston, Massachusetts.
Disclosures: Speakers Bureau for Schering-Plough and Novartis Oncology. Advisory Board for Schering-Plough.
The author thanks Donald P. Lawrence, MD, for his review of this article.
Correspondence concerning this article should be addressed to Krista M. Rubin, MS, RN, FNP-BC, Massachusetts General Hospital, Boston, Massachusetts 02114. E-mail: email@example.com
Dysplastic or atypical nevi are premalignant proliferations of melanocytes and are both a risk factor and a precursor for the development of melanoma. The ultimate goal of managing patients with dysplastic nevi is the prevention or early detection of malignant melanoma, thereby reducing the incidence of metastatic melanoma. Although metastatic melanoma is relatively uncommon, it is one of the most lethal malignancies and is the cause of more years of lost life than is any cancer except leukemia. Melanocytic lesions are among the most common neoplasms in humans; however, the distinction between benign and malignant lesions is often quite difficult even for the most experienced dermatologist. Primary and secondary prevention strategies should be implemented with populations at large and more specifically in patients with risk factors such as dysplastic nevi that put them at risk for the development of melanoma. Close clinical surveillance of such patients is essential to detect and treat melanoma in its earliest stages when it is most curable. Data support that melanomas detected by clinicians are diagnosed earlier than the lesions recognized by patients themselves. Therefore, recognizing populations at risk, identifying both clinical and histomorphologic features of risky lesions, and recognizing features of melanoma are a cornerstone of early detection.
Malignant melanoma is the most serious form of skin cancer. Its incidence is rising and reaching epidemic proportions. Melanoma is a cancer of pigment-producing cells in the skin known as melanocytes. These tumors occur primarily in the skin but may also arise in other pigmented tissues including the eyes, gastrointestinal tract, rectum, and vagina (National Cancer Institute, 2009). The incidence rate of melanoma continues to rise faster in men than that of any other cancer, and in women, more rapidly than that of any other cancer except lung cancer (Houghton et al., 2006) and now represents the fifth in incidence among men and seventh among women and is the most common cancer among women aged 20-29 years (Tsao, Atkins, & Sober, 2004). It is increasing by 4% per year in every segment of our society. In the 1930s, the lifetime risk of developing a melanoma in the United States was 1 in 1,500. According to the American Cancer Society (ACS) (2009), the estimated risk is now 1 in 50 for Whites, with an estimated 62,480 new cases of melanoma diagnosed in 2008 and 8,420 deaths.
Efforts to reduce the risk of cutaneous melanoma have focused on identifying and screening persons at high risk and on promoting sun protection (Tsao et al., 2004). The presence of benign nevi and the presence of atypical nevi are both risk factors and can both be precursors for melanoma. In general, the higher the nevus count, the higher the risk (Seykora & Elder, 1996; Williams & Sagebiel, 1994). It is essential that those individuals having multiple nevi, particularly multiple atypical nevi, be identified and followed closely, with the goal being to detect and diagnose melanomas early while in a curable stage.
The ability to detect high-risk lesions and even melanomas can be extremely difficult. Full skin examinations including scalp and mucous membranes are critical for persons at risk. Clinical recognition of cutaneous melanomas and discrimination from surrounding clinically atypical moles can be challenging (Tsao et al., 2004). It is essential that providers recognize the common clinical features that distinguish atypical moles from typical moles In addition to clinical examination, dermatology practitioners may implement tools as an adjunct to examination (Table 1). These may include photography, computerized mole mapping systems, and use of a dermoscope. Specialty clinics, known as pigmented lesion clinics, have also been developed as a way to manage persons at risk and provide access to specialty care, including these tools of management.
Melanoma affects persons of all ages, and causes more years of lost life than any other cancer except leukemia (High, 2008). It is estimated that more than 62,000 men and women will be diagnosed with melanoma in 2008, with over 8,400 deaths, and an estimated lifetime risk was predicted to be 1 in 50 (ACS, 2009). Although deadly in its later stages, melanoma has an excellent prognosis if diagnosed early. Fortunately, most melanoma cases, approximately 82% to 85%, are diagnosed with localized disease, and the 5-year survival rate for this group is greater than 90% (Balch et al., 2001). Approximately 10%-13% of patients will present with regional disease (American Joint Committee on Cancer [AJCC] Stage III), and a minority of patients (2%-5%) will present with distant metastatic disease (AJCC Stage IV). The 5-year survival rates for this population are dismal: up to 15.3% in selected populations but typically far less than that (Balch et al., 2001). Treatment options for melanoma are based on the stage of disease at presentation.
Despite a trend toward earlier detection, patients with thick primary melanomas, labeled T4 in the tumor-node-metastasis tumor staging system, and those with pathologic or clinical evidence of regional nodal metastasis have a high risk of recurrence after definitive surgical treatment and continue to have a poor prognosis. Recurrence rates in these high-risk patient populations range from 40% to 90% (Sabel & Sondak, 2004), and the 5-year survival rates range from 10% to 60%, depending on factors such as nodal tumor burden (Houghton et al., 2006).
Stage IV (distant metastases) melanoma is associated with a poor prognosis, and median survival is 6-12 months, with <5% of patients alive at 5 years (Tsao et al., 2004). No curative or standard therapy exists for this stage of disease. Historically, melanoma has been resistant to treatment, and to date, there are no randomized controlled trials that have shown a survival advantage with the use of any specific drug or combination of drugs (Tsao et al., 2004). As such, efforts to detect melanoma at the earliest curable stage have been the focus of management of these high-risk patients.
POPULATIONS AT RISK
Certain populations have been identified as being at higher risk than the average person for the development of melanoma. They include persons with lighter complexions, an inability to tan, blonde or red hair and blue eyes, and with multiple nevi, particularly atypical nevi. Immunosuppression, sun sensitivity, and exposure to ultraviolet radiation are additional risk factors (Miller & Mihm, 2006). Patients with multiple nevi have a relative risk of 5-12 of developing melanoma, and those with multiple atypical nevi have a relative risk of 7-27 (Risser, Pressley, Veledar, Washington, & Chen, 2007). Patients at the greatest risk for developing melanoma include those with a strong family history of melanoma and multiple clinically atypical moles (Tsao et al., 2004). An interesting finding was that, although some moles are precursors to melanoma, dysplastic nevi are considered to be cutaneous markers, which identify persons who are at an increased risk for developing melanoma compared with the general population (Rigel et al., 1989; Tsao et al., 2004). Multiple studies have demonstrated that the presence of moles, either typical or atypical or in large numbers, is found much more frequently in patients with melanoma compared with control subjects (Schneider, Moore, & Sagebiel, 1994). Another higher risk population includes patients with a personal history of melanoma, with the greatest risk period being the 2 years after diagnosis (Tsao et al., 2004).
There is no question that the greatest environmental risk factor for the development of melanoma is sun exposure; however, genetics also influence this risk. In the past decade, progress has been made toward understanding the genes that contribute to inherited susceptibility for melanoma in some patients (Tsao & Haluska, 2007). There are multiple genes that can lead to a higher predisposition to melanoma. Polymorphisms in the melanocortin-1 receptor-1 gene lead to the synthesis of alternate types of melanin, resulting in red hair and an increased susceptibility to melanoma. Cyclin-dependent kinase inhibitor A (CDKN2A), also known as p16, is a gene located on chromosome 9 that controls growth and death of cells. Germline mutations in this gene, although uncommon, have been identified in approximately 20% of melanoma-prone families that have been studied to date. Pancreatic cancer occurs excessively in melanoma families with germline mutations in CDKN2A. It is reported that persons with a CDKN2A alteration have (a) a >50% chance of developing melanoma during their lifetime, (b) an increased risk of developing more than one primary melanoma, and (c) typically are diagnosed at a younger age. In addition, persons with mutations in CDKN2A have been shown to have an increased risk for the development of pancreatic cancer (Goldstein & Tucker, 2001; Tsao & Haluska, 2007) and increased risk for developing breast cancer (Niendorf & Tsao, 2006). Although only a small proportion of people with melanoma or with family histories of melanoma have hereditary alterations in CDKN2A, understanding these increased risks is critical in the management of this population.
The recommendation to obtain genetic testing is controversial. Some agencies, such as The Melanoma Genetics Consortium, argue that clinical CDKN2A genetic testing is premature because of the uncertainties regarding penetrance of these mutations and questions about the efficacy of melanoma prevention and risk-reduction strategies, whereas others support the available clinical testing (Fowler, Wolfe, Chesney, & Schwartzberg, 2006). Often, genetic testing is done within the confines of clinical research so that results may be examined. For providers caring for patients with melanoma who may have undergone genetic testing, it is important to recognize that negative CDKN2A test results in families without known mutations would not disprove hereditary melanoma because certain mutations may be undetectable with current molecular methodologies or because mutations might be present in other melanoma suppressor genes (Fowler et al., 2006). Positive results may be used to educate the patients and assess risk. For example, it is crucial for patients to learn about:
1. risk factors;
2. subsequent recommendations for continued dermatologic surveillance;
3. screenings for pancreatic cancer, possibly involving computed tomography imaging and a consultation with a gastroenterologist; and
4. regular breast self-examination and clinical breast examination along with imaging in female siblings.
Thus, results of testing may be used in the primary prevention or at least possibly earlier detection of other cancers. Genetic counseling posttesting could be implemented in risk determination and would be a conduit to alter patient's understanding of risk, as well as a means to alter behaviors which could further reduce risk of development of a secondary malignancy. However, providers must also anticipate that there may be patients who do not wish to know their status and for whom positive results may increase anxiety or negative results may contribute to a false sense of security. Therefore, posttest genetic counseling must be considered a necessity.
Kasparian, Meiser, Butow, Job, and Mann (2006) explored the psychological consequence of genetic testing for mutations among individuals at increased risk for developing melanoma. Results revealed that, in response to being identified as a mutation carrier, most participants calmly accepted their increased risk, either increasing precaution adoption or maintaining already-vigilant behavioral practices, perceiving such information as important and valuable. Results further revealed that those identified as noncarriers felt relieved but expected to maintain current precautional health practices and to still perceive themselves at some risk of developing melanoma.
HOW TO RECOGNIZE BENIGN VERSUS ATYPICAL LESIONS
Benign Versus Atypical (Dysplastic) Nevi
The terms mole and nevi are synonymous. Nevi are composed of melanocytes that have lost their dendritic processes and typically proliferate clonally to form nests of cells (Armstrong, Liu, & Mihm, 2007). The average person has approximately 40 nevi. They can be present at birth or acquired from childhood through early adulthood. Nevi can vary in size, number, and color: from pink, to tan, to brown, to flesh colored. There are three types of nevi: congenital (present at birth or appearing within 1 year of birth), acquired or common nevi (regular), and atypical (dysplastic) nevi (unusual, abnormal). Common nevi typically originate as small, round, uniformly brown to brown-black spots (termed junctional nevi). They often arise in childhood and progress to elevated lesions (or compound nevi) during adolescence and young adulthood.
The term dysplastic nevi was first described in the late 1970s as part of the familial melanoma syndrome (Kang, Barnhill, Mihm, Fitzpatrick, & Sober, 1994). This was a familial form of melanoma that was described in which dysplastic nevi were sensitive phenotypic markers of increased melanoma risk and were identified in two index families. The initials of these families were B and K, and all of the family members had unusual moles and a strong history of melanoma. Thus, the term BK mole syndrome evolved. In 1980, it was renamed dysplastic nevus syndrome (and also called the familial atypical mole and melanoma syndrome, abbreviated FAM-M, coined by the National Institutes of Health in their consensus statement (Diagnosis and Treatment of Early Melanoma, 1992). This syndrome was defined by three characteristics: (a) occurrence of melanoma in one or more first- or second-degree relatives; (b) large number of moles, often >50, some of which are atypical and often variable in size; and (c) moles that demonstrate certain distinct histologic features (Diagnosis and treatment of early melanoma, 1992). Affected family members have a lifetime melanoma risk of developing melanoma that approaches 100%. For this reason, it is essential to identify these patients and follow them closely, and teaching self-skin examination is critical to the early detection of melanoma.
The term atypical mole was officially selected by the National Institutes of Health in 1992 to describe what were formerly termed dysplastic nevi (Diagnosis and treatment of early melanoma, 1992). Even the decision to call a lesion atypical is often subjective, and there is lack of consensus on criteria for diagnosis of atypical lesions. Atypical is thought to be a clinical description, and dysplastic implies histologic description or diagnosis, but the terms are often used interchangeably. Atypical moles may have irregular and/or poorly demarcated and indistinct borders and a textured surface; shapes vary and include oval, round, and asymmetric. Even for the most experienced dermatologist, atypical nevi can be extremely challenging.
Clinical presentations of atypical nevi will vary in descriptive characteristics, but all atypical nevi have common features both clinically and histologically. They share some or all of the features associated with melanoma. The ABCD mnemonic was developed as an aid for identifying biologically early, curable lesions. Some have also added the letter "e" to the mnemonic, for elevation or evolving (Halpern, Marghoob, & Sober, 2009); others also include enlargement.
1. A for asymmetry,
2. B for border irregularity,
3. C for color variation,
4. D for diameter greater than 6 mm, and
5. E for elevation, evolving, and enlarging.
Atypical moles are often asymmetrical; have irregular, fuzzy borders; and have color variegation of hue and depth and tend to be larger than 6 mm, although there is no lower size limit. They are sometimes raised above the skin surface and often can have a combination of features. Atypical moles usually appear after age 6 to 12 months and before age 20 years at any site, even those typically protected from the sun. The chest and back are often most heavily involved, and there may be a single atypical mole or hundreds in the same individual (Cyr, 2008). Although most melanomas exhibit a sufficient array of clinical features to justify biopsy, melanoma may occasionally mimic a variety of benign lesions including common melanocytic nevi, seborrheic keratosis, and pyogenic granuloma, to name a few (Argenziano et al., 2007).
Barnhill and Roush (1991) attempted to quantify certain clinical features of atypical nevi with histologic assessment. They reported that, of the gross morphologic features, nevus size was correlated most strongly with histologically confirmed dysplastic nevi. The presence of irregular borders, in addition to other features, was also associated significantly with histologic features.
HISTORY AND EXAMINATION
Following patients with known increased risk for developing melanoma is challenging. The degree of risk can be estimated even before a provider enters the room. Consideration should be given to the patient's risk based on factors other than the examination. Questions to consider include the following:
1. Is there a personal history of melanoma?
2. If so, how long ago and what stage?
3. Is there a family history of melanoma?
4. If so, is it a first- or second-degree relative or a distant relative?
5. Does the patient have a history of previous clinically atypical mole excisions?
6. If so, what was the degree of atypia?
In addition, consider why the patient is presenting: Is it because of a specific complaint such as a changing mole, or for a routine examination? Reliability and compliance of the patient also need to be considered. These factors alone should provide the practitioner with enough information to determine a threshold for biopsy. For patients deemed high risk by the factors listed previously, even before conducting an examination, one would expect a very low threshold for biopsy. A history of severely dysplastic nevi has the most significant impact on provider biopsy behavior, resulting in lower threshold for biopsy suggestive of lesions (Risser et al., 2007). After entering the room, medical and family history should be updated to reassess risk factors. A thorough history is critical for patients with any risk for melanoma, including reviewing overall health and review of symptoms. Asking if there are any new or changing moles, or any that have itched or bled, or any skin concern is important to ask each and every patient, and this should be documented. Furthermore, it is essential to factor the patient's suspicion regarding a lesion into the decision to biopsy a lesion or not. If a patient is losing sleep or extraordinarily anxious about a specific mole, even if the practitioner examination is less worrisome, this should be considered. For any patient, it is critical to note the patient's report of change. The patient's report of change should trump all clinical evaluation. However, there are patients who are incredibly anxious, who want every single mole removed, and are hyperaware of even the slightest change. These patients present a dilemma. The nurses and physicians often feel that these patients are waiting "for the other shoe to drop" if they have had a previous melanoma.
In some patients, all of their nevi are atypical, and it is extremely challenging to differentiate which lesions warrant biopsy. For some patients, the likelihood of identifying dysplastic nevi is almost 100%; there are patients in whom all prior biopsies have demonstrated a certain degree of atypia. For those patients, biopsy or excision of all lesions is not feasible. So what is the best management for these patients? The "gestalt" of a lesion, or the intuition of the provider, should also be considered. There are certain clinical features of nevi that dermatology nurses must be familiar with, but before the examination is performed, the risk profile of the patient should be determined.
Proper physical examination is crucial for patients at risk for melanoma. A thorough skin examination should be conducted and patients should be fully undressed, including undergarments. Total body skin examination has been the standard of care for performing routine skin cancer screening for patients at high risk for developing melanoma (Risser et al., 2007). This includes scalp (use of a hair dryer may be necessary to see all areas) and mucous membranes. In addition to physical examination, management of patients with multiple atypical nevi may include the use of the tools in Table 1. The role of dermoscopy (also called epiluminescence microscopy or ELM) can be an excellent diagnostic tool and has been shown to be efficient in enhancing the correct detection of melanoma. It can aid in determining whether or not a lesion requires biopsy. It has been used as a second-level diagnostic procedure for clinically suggestive lesions, thereby decreasing the number of unnecessary biopsies of benign lesions (Argenziano et al., 2007). However, despite all the "tools" that aid in the determination of the malignant potential of a lesion, if there is any doubt about whether a lesion really does warrant biopsy, it should be biopsied ("if in doubt, cut it out"). High (2008) reported that the misdiagnosis of skin cancer is a substantial source of medical malpractice litigation and emphasizes that melanoma ranks second only to breast cancer as the most common source of pathology-related ("missed") diagnoses, and a false-negative diagnosis of melanoma was the single most common cause for a malpractice claim.
Biopsies to Determine if Melanoma
When clinical examination reveals a suspicious lesion or if a patient reports change in a lesion and a biopsy is being considered, the appropriate biopsy type is critical. There are few, if any, contraindications for biopsy, and it is essential to know that more errors are made from failing to biopsy promptly than from performing unnecessary biopsies (Alguire & Mathes, 2005).
When determining the best technique for biopsy, consider the goals of the procedure. If the goal is to obtain a histologic diagnosis, simply sampling a piece of the lesion is reasonable, and this is easily performed via a shave or incisional biopsy. A shave biopsy is quick, does not require suturing, and can be either superficial or deep. Superficial shave biopsies are performed across or nearly parallel to the skin surface and extend into the epidermis only or epidermis and limited superficial dermis. This type of biopsy is indicated for dome-shaped intradermal nevi, fibromas, warts, as well as actinic or seborrheic keratosis and mainly includes just a portion of the epidermis. When both the epidermal and dermal layers are necessary for evaluating a lesion, then a deeper shave biopsy (a saucerization) can be performed, allowing for a greater amount of tissue. These biopsies are best when basal or squamous cell carcinomas are in the differential. This technique is best applied to lesions where suspicion for melanoma is low, if the lesion is in a cosmetically sensitive location, or when it is impractical to perform excisional biopsy (Sober & Haluska, 2001).
For pigmented lesions, or nonpigmented lesions that are suspicious, or for any lesions for which a diagnosis of melanoma is being considered, an excisional biopsy is recommended. Excisional biopsy is performed when the goal is complete removal of the entire lesion, such as when there is moderate to high suspicion for melanoma. This procedure includes removal of the entire lesion plus a 1- to 2-mm peripheral zone of clinically normal skin, and it should extend into the subcutaneous fat (Sober & Haluska, 2001). For example, for a 3-mm lesion, one would perform a 5-mm punch biopsy, allowing for complete removal plus a 1-mm margin. In addition to the biopsy technique, communication between the clinician and the dermatopathologist is essential. A detailed description of the lesion and documentation of the clinical impression are often necessary to reach the correct pathologic diagnosis.
WHAT DOES MELANOMA LOOK LIKE?
Pigmented lesions can be difficult to evaluate even for very experienced clinicians, particularly in patients with multiple nevi. When evaluating atypical nevi, it is essential to be mindful of the main goal for screening: to properly identify melanoma in its earliest stages when it is considered curable. It is standard practice to remove any pigmented or nonpigmented lesion that is suggestive of melanoma and to perform histologic examination (Argenziano et al., 2007; Scope et al., 2008). This is necessary to determine if the lesion is or is not a melanoma and that the proper recommendations for further treatment can be determined. The implications for missing a melanoma are far too great to forego biopsy of moderately or highly suspicious lesions. Yet, identifying such lesions accurately remains a challenge.
It is important to be cognizant that most melanomas arise de novo rather than from preexisting nevi (Fuller, Bowen, Tanner, Florell, & Grossman, 2007). Only approximately one third of melanomas follow the ABCDE rule of melanoma recognition, and many lesions determined to be melanoma were clinically innocuous. Argenziano et al. (2007) emphasized that, although most melanomas exhibit a sufficient array of clinical features to justify biopsy, melanoma may occasionally mimic a variety of benign lesions, including common melanocytic nevi, seborrheic keratoses, and pyogenic granuloma, to name a few. Furthermore, very early melanomas and nodular melanoma can sometimes be symmetric, well-demarcated, homogenously pigmented, and less than 5 mm in size (Puig et al., 2007). Amelanotic melanoma can mimic other skin lesions, particularly more benign lesions, and therefore should be considered in the differential diagnosis of nonpigmented lesions. Spitz nevi (a benign melanocytic lesion that histologically resembles melanoma) versus atypical Spitz can also be challenging, and the age of the patient must be considered when determining the differential diagnosis, as Spitz nevi are most common in children but can be seen in adults. Melanomas frequently display irregularities in shape, color, and border; however, these features are neither invariant nor specific (Tsao et al., 2004). Geller, Swetter, Brooks, Demierre, and Yaroch (2007) performed a study in Sweden with 54 patients which revealed that thin nodular melanomas appeared to be smaller in diameter than thick lesions; nodular melanomas were found more often to be symmetric, elevated, and uniform in color; pigmented superficial spreading melanomas were primarily black or brown; and color change among nevoid melanoma was uncommon.
There are several general approaches that clinicians use to recognize melanoma. These include overall pattern recognition (e.g., instant recognition of an image); recognition based on analytical criteria such as the ABCDE's of melanoma or the 7-point checklist of dermoscopy (Argenziano et al., 1998); and differential recognition, also known as the "ugly duckling" concept, to demonstrate that nevi in the same individual tend to resemble one another and that melanoma often deviates from an individual's nevus pattern (Scope et al., 2008).
The definition and management of atypical nevi are a controversial issue. The vast majority of pigmented lesions are completely benign in nature and do not require intervention; however, some lesions do have features that fall in between a benign nevus and melanoma. This malignant transformation, or dysplasia, is ranked from mild to severe in degree. Although studies have shown that most atypical nevi will never progress to melanoma, the question of whether partially removed atypical nevi should be re-excised with clear margins to prevent their evolution into melanoma remains unanswered (Kmetz, Sanders, Fisher, Lang, & Maize, 2009). Most practitioners agree that excision of a lesion with a positive margin is required for lesions that demonstrate severe atypia. For lesions that demonstrate moderate atypia, the recommendations are less clear, and should be determined on a case-by-case basis. Some providers would recommend excision, while others would follow clinically. For lesions that demonstrate mild atypia, most would agree that even with an involved margin, excision is not necessary.
For management of biopsy-proven melanoma, either invasive or in situ, wide local excision is standard. The recommended surgical margin in the treatment of melanoma depends on tumor thickness and is based on the analysis of several large randomized clinical trials evaluating appropriate surgical margins (National Comprehensive Cancer Network, 2004), as seen in Table 2. For patients with in situ lesions, a 0.5-cm margin is recommended. For lesions 1.0 mm or less in thickness, a 1.0-cm margin is recommended. For lesions between 1.01 and 2.0 mm, a 1- to 2-cm margin is recommended, and for thicker lesions (1.0 mm or greater), a 2-cm margin is recommended. Margins may be modified to accommodate individual anatomic or cosmetic considerations.
There is no standard of care regarding how often to follow patients identified as being at risk for developing melanoma, and there is no consensus on recommendations for skin examinations. Despite the lack of consensus, it is clear that identification of persons at risk is certainly the cornerstone of early diagnosis. Recommendations on frequency of follow-up visits and exactly how to follow patients vary in the literature and thus are often based on the patient's risk. Factors to be considered when developing a plan for follow up must encompass overall risk and are included in Table 3. Physician preference, as well as patient preference, will also factor into decision making for follow-up. There are some patients who are extraordinarily anxious and require more frequent visits, although other patients do not wish to follow up more often than necessary.
In one pigmented lesion clinic, a large referral center located in an urban tertiary care hospital, patients with established risk factors for melanoma but without personal history of melanoma are typically followed at 3- to 6-month intervals, and the visits alternate between the nurse practitioner and the physician. Routine blood tests or radiological screenings are not advised due to the lack of data supporting a decrease in relapse rates or overall survival if obtained and the lack of cost-effectiveness. Patients with established risk factors for melanoma and a personal history of melanoma are followed at 3-month intervals in dermatology for the first 2 to 3 years from diagnosis (the greatest risk period for recurrence), typically for 5 years, and then are discharged to general dermatology practice for continued skin surveillance. Patients are always encouraged to continue a relationship with their local (or primary) dermatologist for routine dermatologic issues, in addition to aiding in routine skin surveillance. Patients with AJCC Stage IIB, IIC, III, and IV melanoma are typically followed both by medical oncology and dermatology.
Nurses are in key positions to identify populations at risk for the development of melanoma, to perform screening evaluations in the primary care setting, and to play a significant role in the education process of those at risk. For example, nurses in nursing homes are in positions to identify those high-risk men older than 65 years, a population with the greatest mortality from melanoma, and to refer them for screening if appropriate. School nurses and nurses in college or university student health services are in positions to identify students with a family history of melanoma by seeing that thorough health histories are taken and acting to facilitate proper referral. Health fairs are a means to increase awareness of skin cancer and prevention strategies, and nurses are often the drivers behind these activities. Educating not only patients and families but also colleagues and coworkers is a means to increase awareness. Teaching proper skin self-examination is a foundational role of not only dermatology nurses but also nurses at large, as most melanomas are found by patients themselves.
Managing patients at high risk for melanoma is challenging, particularly as there is no uniform standard of care for this population as a whole. As such, the approach must be individualized, and the patient's preferences and goals must be considered. Providing holistic care to these patients including psychosocial intervention (especially managing anxiety) is a key role for nurses in addition to guiding patients through the decision process and ensuring that they understand their disease, treatment options, and goals of care. Educating patients about their diagnosis and disease-related signs and symptoms may help empower patients to recognize and report such problems promptly, therefore allowing more timely management.
Five-year survival rates for melanoma now exceed 90% in the United States, Australia, and Sweden for early-stage disease. Because skin is readily accessible to direct visual inspection, screening of high-risk persons is strongly recommended (Tsao et al., 2004), and early detection is key to reducing disease-related mortality. Early detection is also cost-effective. The estimated total direct cost associated with the treatment of melanoma in 2004 was $291 million. Of that total, office visits account for $101 million; hospital outpatient treatment accounts for $76 million; prescription drugs account for $78 million; hospital inpatient treatment accounts for $35 million; and emergency room treatment accounts for $1 million (Bickers et al., 2006). In general, 5% of the total costs involve the care of patients with Stages I and II disease, and 95% of the cost are directed to the small minority of patients with advanced disease. Patients presenting with multiple nevi or atypical nevi pose a challenge to the practitioner as there is no uniform standard for the evaluation and management of this population. Risk assessment, accurate history, clinical examination, and the level of patient concern must all be taken into account in managing these patients, and there should be a low threshold for biopsy of moderately or highly suspicious lesions. New or changing moles clearly warrant full evaluation. New technologies are being utilized as adjuncts to clinical examination but cannot substitute for evaluation by an experienced clinician. Early detection efforts (secondary prevention) are likely to result in a reduction in mortality from melanoma, and interventions will be most successful if they target those at greatest risk of disease, including patients with dysplastic nevi (Geller et al., 2007). Nurses are in key positions to encourage screening and early detection in these high-risk populations and assist in assessment, treatment, and follow-up.
Alguire, P., & Mathes, B. (2005). Skin biopsy technique. UpToDate
. Retrieved August 29, 2009, from http://www.uptodate.com
American Cancer Society. (2009). Overview: Melanoma
. Retrieved April 15, 2009, from http://www.cancer.org
Argenziano, G., Fabbrocini, G., Carli, P., De Giorgi, V., Sammarco, E., & Delfino, M. (1998). Epiluminescence microscopy for the diagnosis of doubtful melanocytic skin lesions: comparison of the ABCD rule of dermatoscopy and a new 7-point checklist based on pattern analysis. Archives of Dermatology, 134, 1563-1570.
Argenziano, G., Zalaudek, I., Ferrara, G., Johr, R., Langford, D., Puig, S., et al. (2007). Dermoscopy features of melanoma incognito: Indications for biopsy. Journal of the American Academy of Dermatology, 56(3), 508-513.
Armstrong, A., Liu, V., & Mihm, M. (2007). Pathologic characteristics of melanoma. UpToDate
. Retrieved October 17, 2007, from http://www.uptodate.com
Balch, C., Buzaid, A., Soong, S., Atkins, M., Cascinelli, N., Coit, D., et al. (2001). Final version of the American Joint Committee on Cancer staging system for cutaneous melanoma. Journal of Clinical Oncology, 19(16), 3635-3648.
Barnhill, R., & Roush, G. (1991). Correlation of clinical and histopathologic features in clinically atypical melanocytic nevi. Cancer, 67(12), 3157-3164.
Bickers, D., Lim, H., Margolis, D., Weinstock, M., Goodman, C., Faulkner, E., et al. (2006). The burden of skin diseases: 2004 a joint project of the American Academy of Dermatology Association and the Society for Investigative Dermatology. Journal of the American Academy of Dermatology, 55(3), 490-500.
Cyr, P. (2008). Atypical moles. American Family Physician, 78(6), 735-740.
Diagnosis and treatment of early melanoma. NIH Consensus Development Conference. January 27, 1992. (1992). Consensus Statement, 10(1), 1-25.
Fowler, E., Wolfe, K., Chesney, M. C., & Schwartzberg, L. (2006). Genetic testing for hereditary melanoma: Controversial, standard or care, or somewhere between the two? Community Oncology, 3(3), 158-161.
Fuller, S., Bowen, G., Tanner, B., Florell, S., & Grossman, D. (2007). Digital dermoscopic monitoring of atypical nevi in patients at risk for melanoma. Dermatologic Surgery, 33(10), 1198-1206.
Geller, A., Swetter, S., Brooks, K., Demierre, M. F., Yaroch, A. (2007). Screening, early detection, and trends for melanoma: Current status (2000-2006) and future directions. Journal of the American Academy of Dermatology, 57(4), 555-572.
Goldstein, A., & Tucker, M. (2001). Genetic epidemiology of cutaneous melanoma: A global perspective. Archives of Dermatology, 137, 1493-1496.
Halpern, A., Marghoob, A., & Sober, A. (2009). Clinical characteristics of melanoma. In C. Blach, A. Houghton, A. Sober, S. Soong, M. Atkins, & J. Thompson (Eds.), Cutaneous Melanoma (5th ed., p. 162). St. Louis, MO: Quality Medical Publishing.
High, W. (2008). Malpractice in dermatopathology: Principles, risk mitigation, and opportunities for improved care for the histologic diagnosis of melanoma and pigmented lesions. Clinics in Laboratory Medicine, 28(2), 261-284.
Houghton, A., Coit, D., Daud, A., Dilawari, R., Dimaio, D., Gollob, J., et al. (2006). Melanoma. Journal of the National Comprehensive Cancer Network, 4(7), 666-684.
Kang, S., Barnhill, R., Mihm, M., Fitzpatrick, T., & Sober, A. (1994). Melanoma risk in individuals with clinically atypical nevi. Archives of Dermatology, 130, 999-1001.
Kasparian, N., Meiser, B., Butow, P., Job, R., & Mann, G. (2006). Better the devil you know? High-risk individuals' anticipated psychological responses to genetic testing for melanoma susceptibility. Journal of Genetic Counseling, 15(6), 433-447.
Kmetz, E., Sanders, H., Fisher, G., Lang, P., & Maize, J. (2009). The role of observation in the management of atypical nevi. Southern Medical Journal
. Retrieved April 14, 2009, from http://www.smajournalonline.com
Miller, A., & Mihm, M. (2006). Melanoma. New England Journal of Medicine, 355, 51-65.
National Cancer Institute. (2009). What you need to know about melanoma
. Retrieved April 15, 2009, from http://www.cancer.gov
National Comprehensive Cancer Network. (2004). Melanoma: Clinical practice guidelines in oncology. Journal of the National Comprehensive Cancer Network, 2(1), 46-60.
Niendorf, K., & Tsao, H. (2006). Cutaneous melanoma: Family screening and genetic testing. Dermatologic Therapy, 19, 1-8.
Puig, S., Argenziano, G., Zalaudek, I., Ferrara, G., Palou, J., Massi, D., et al. (2007). Melanomas that failed dermoscopic detection: A combined clinicodermoscopic approach for not missing melanoma. Dermatologic Surgery, 33(10), 1262-1273.
Rigel, D., Rivers, J., Kopf, A., Friedman, R., Vinokur, V., Heilman, E., et al. (1989). Dysplastic nevi. Markers for increased risk for melanoma. Cancer, 63, 386-389.
Risser, J., Pressley, Z., Veledar, E., Washington, C., & Chen, S. (2007). The impact of total body photography on biopsy rate in patients from a pigmented lesion clinic. Journal of the American Academy of Dermatology, 57, 428-434.
Sabel, M., & Sondak, V. (2004). Point: Interferon alfa for adjuvant therapy for melanoma patients. Journal of the National Comprehensive Cancer Network, 2(1), 61-68.
Schneider, J., Moore, D., & Sagebiel, R. (1994). Risk factors for melanoma incidence in prospective follow-up. The importance of atypical (dysplastic) nevi. Archives of Dermatology, 130, 1002-1007.
Scope, A., Dusza, S., Halpern, A., Rabinovitz, H., Braun, R., Zalaudek, I., et al. (2008). The "ugly duckling" sign: Agreement between observers. Archives of Dermatology, 144(1), 58-64.
Seykora, J., & Elder, D. (1996). Dysplastic nevi and other risk factors for melanoma. Seminars in Oncology, 23(6), 682-687.
Sober, A., & Haluska, F. (Eds.). (2001). Skin cancer. London: BC Decker.
Tsao, H., Atkins, M., & Sober, A. (2004). Management of cutaneous melanoma. New England Journal of Medicine, 351
, 998-1012. Retrieved April 18, 2005, from http://www.jejm.org
Tsao, H., & Haluska, F. (2007). Inherited susceptibility to melanoma. UpToDate.
Retrieved August 28, 2007, from http://www.uptodate.com
Williams, M., & Sagebiel, R. (1994). Melanoma risk factors and atypical moles. Western Journal of Medicine, 160(4), 343-350.
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