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Lower Extremity Lymphedema in a Patient With Melanoma

Lower Extremity Lymphedema in a Patient With Melanoma

ABSTRACT: Surgical resection and lymph node dissection and assessment are essential to staging and treatment of melanoma, but can result in lower-extremity lymphedema that impairs patients’ mobility.

It is estimated that more than 62,000 men and women will be diagnosed with melanoma in 2008, with more than 8,400 deaths, and an estimated lifetime risk predicted to be 1 in 55.[1] Although deadly in its later stages, melanoma carries an excellent prognosis if it is diagnosed early. Fortunately, most melanoma cases (80%) are diagnosed at a localized stage; the 5-year survival rate for this group is 98.5%.

Unfortunately, a minority of patients have metastatic disease at diagnosis (3%), and 5-year survival rates for these patients are dismal, at 15.3%.[2] Treatment options for melanoma are based on the stage of disease at presentation. For patients with AJCC (American Joint Committee on Cancer) Stage I and II melanoma, sentinel lymph node (SLN) biopsy has become a standard staging procedure. SLN biopsy has emerged as a reliable technique for identifying micrometastatic disease in clinically negative regional lymph node basins.

SLN biopsy is based on a theory that lymphatic metastases follow an orderly progression through lymph channels from the primary tumor to a particular lymph node (“sentinel,” simply “guard” node) before spreading into other regional nodes.[3] Simply put, if the sentinel node does not contain evidence of metastatic melanoma, then the remainder of the lymph nodes in the basin are also highly likely free of disease, thus further dissection is spared. The status of the sentinel node evaluation has become the single most important predictive factor for recurrence and survival for melanoma patients[4,5] and should be considered for patients with melanomas ≥ 1 mm, or in patients with lesions < 1 mm if there are additional factors that should be considered, such as ulcerated lesions, Clark’s Level IV lesions (defined as invasion of the reticular dermis) or lesions with a high mitotic rate.

Traditionally, management of Stage II, or in some cases Stage I, cutaneous melanoma involved elective dissection of the draining nodal basin as a means to improve survival. However, improved survival has been difficult to demonstrate in randomized trials, and therapeutic gains have been questioned. Likely reasons include high morbidity associated with the procedure, a high complication rate, and the possibility of incorrectly identifying the proper draining nodal basin, and/or missing a second or aberrant nodal drainage basin.

Therefore, elective nodal dissection is no longer recommended; instead, completion (or therapeutic) nodal dissection is advised when a sentinel node has been identified; it is considered to be definitive treatment, with the goal of surgery being long-term survival. Prognosis for patients with cutaneous melanoma is dependent on the number of involved regional nodes and the thickness of the primary tumor.

Patients with pathologic or clinical evidence of regional nodal metastases as well as those with thick primary lesions (T4) have been demonstrated to be at high risk of disease recurrence.[6] Once palpable nodal disease develops, the ability to provide effective local/regional control and long-term survival is diminished.[7] Because local spread of melanoma commonly occurs in regional lymph nodes, sampling these nodes is necessary to assess the extent of disease and identify appropriate treatment, therefore sentinel lymph node assessment has become the procedure of choice for assessing status of the lymph nodes.

While surgical resection and lymph node assessment offers the most effective treatment for management and staging of melanoma, the long-term effects of LN resection can result in long-term consequences for the patient; for some, effects such as lymphedema can be disabling. Furthermore, SLN biopsy, though minimally invasive and regularly performed with little morbidity, also can be associated with lymphedema.[5]

PATHOPHYSIOLOGY OF LYMPHEDEMA
Lymph fluid comprises protein, water, fats, and cellular waste. It is transported through lymph vessels to lymph nodes and empties into blood vessels. These vessels are thin, allowing the large proteins to filter through easily.

In the case of an obstruction (from surgery, radiation, trauma, infection, tumor, etc), the large proteins filter through the vessels and invade the interstitial tissues, which causes an accumulation of highly concentrated, protein-filled fluid in an area distal to the blockage.[8] Surgery and infection cause scarring that can obstruct blood lymph flow and cause a proximal collection of fluid.

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