Plastic surgery

PART IX

TRUNK AND LOWER EXTREMITY

CHAPTER 97  LYMPHEDEMA: DIAGNOSIS AND TREATMENT

STEVEN M. LEVINE, DAVID W. CHANG, AND BABAK J. MEHRARA

INTRODUCTION

Lymphedema is the accumulation of protein-rich interstitial fluid in tissues and occurs when the transport capacity of the lymphatic system is exceeded (Figure 97.1). Lymphedema can occur secondary to congenital abnormalities of the lymphatic system (primary lymphedema) or as a result of an acquired condition in which lymphatic channels are injured or obstructed (secondary lymphedema). In Western countries, lymphedema occurs most commonly as a complication of cancer treatment after lymph node excision with breast cancer patients making up the largest number of patients in the United States. As many as 50% of patients who undergo axillary lymph node dissection, and 4% to 7% of patients who undergo sentinel lymph node biopsy, will develop lymphedema.1 Lymphedema is also a common complication of the treatment of other malignancies. A recent meta-analysis of 7,790 patients reported a 16% risk of lymphedema in patients treated for a variety of tumors, including sarcoma (30%), melanoma (16%), gynecological (20%), and genitourinary (10%) malignancies.2 Overall, it is estimated that 3 to 5 million Americans suffer from lymphedema and as many as 25 to 50,000 new cases are diagnosed annually. Severe lymphedema is associated with recurrent infections, disfigurement, pain, secondary malignancies, and decreased quality of life, in addition to the financial burden on the health care system.

FIGURE 97.1. Patient with severe lymphedema of the right arm.

Development of effective treatment strategies for lymphedema has been hampered by the fact that the etiology of this disorder remains largely unknown. Although recent studies have delineated the molecular mechanisms that regulate lymphatic repair and regeneration, it is still not clear why lymphadenectomy or lymphatic injury results in lymphedema in some patients and not in others. Similarly, we cannot accurately predict the disease course for individual patients, their response to various treatment strategies, or the effectiveness of preventative options. As a result, treatment for lymphedema is palliative with a goal of preventing disease progression and symptomatic relief.

TYPES OF LYMPHEDEMA

Lymphedema that arises from a developmental abnormality of the lymphatic system is termed primary lymphedema. These disorders can be present at birth, or more commonly develop later in life manifesting as unilateral or bilateral limb edema. Congenital lymphedema is clinically evident at birth and accounts for 10% to 25% of all primary lymphedemas. As with most forms of primary lymphedema, females are affected twice as often as males and the lower extremity is involved three times more commonly than the upper extremity.

A subset of congenital lymphedema patients demonstrates a familial, sex-linked pattern of inheritance (termed Milroy’s disease) and accounts for approximately 2% of patients with congenital lymphedema. Milroy described this hereditary disorder in 1892 when he traced a single patient’s lymphedema through six generations. The disease is characterized histologically by hypoplastic lymphatic channels and variable degrees of dermal and collecting lymphatic agenesis. Recent studies have demonstrated that Milroy’s disease is caused by loss of function mutations in the vascular endothelial growth factor-3 receptor, a key regulator of lymphatic development and regeneration.

Lymphedema praecox is the most common form of primary lymphedema accounting for 65% to 80% of all cases. Patients with lymphedema praecox usually present with unilateral (70%) limb edema beginning after birth and before 35 years of age as a result of lymphatics that are reduced in caliber and number. Presentation at puberty is the most common age and females are affected four times as frequently as males.

Lymphedema tarda is a primary form of lymphedema that manifests clinically after the age of 35 years and accounts for a relatively small number of cases of primary lymphedema (10%). Lymphedema tarda most commonly affects the lower extremity and occurs more commonly in women. The diagnosis is made by exclusion of other forms of lymphedema or causes of limb swelling and often occurs with a familial pattern. Loss of function mutations of the FOXC2 gene have been reported in some patients, and histological examination usually demonstrates hyperplastic, tortuous lymphatics of increased caliber and number and incompetent or absent lymphatic valves.

SECONDARY LYMPHEDEMA

Secondary lymphedema is the acquired dysfunction of otherwise normal lymphatics. Traumatic lymphedema occurs as a consequence of scarring or injury following trauma, cancer treatment, burn injury, or radiation exposure and is the most common cause of lymphedema in the United States. Traumatic lymphedema can also occur after extensive skin resection performed for a variety of conditions including massive weight loss. Infectious lymphedema is caused by invasion of the lymphatic vessels with a foreign organism. This is usually the filarial worm, Wuchereria bancrofti, but can also be other microorganisms such as Mycobacterium tuberculosisTreponema pallidum, or other organisms including streptococci and fungi. With between 140 and 250 million cases worldwide, filariasis remains the most common cause of lymphedema outside of the developed world. Inflammation resulting from invasion of the lymphatic system by microorganisms leads to progressive fibrosis and lymphatic dysfunction resulting in lymphedema of massive proportions.

Infiltration and obstruction of the lymphatic system with malignant cells can result in malignant lymphedema. This condition should be considered in the differential diagnosis of patients who present with lymphedema without an obvious cause. Post-venous thrombosis lymphedema can occur after ligation or thrombosis of a major extremity vein and is thought to occur as a result of increased venous pressure diminishing lymphatic return.

DIAGNOSIS OF LYMPHEDEMA

The diagnosis of lymphedema is usually made by clinical history and physical examination (Figure 97.2).3 Patients typically present with complaints of limb swelling; tightness in the skin; functional complaints such as heaviness, fatigue, and difficulty moving a joint; and a history of recurrent infections. Limb circumference or volume measurements can be performed to confirm limb swelling. A difference in limb measurement of greater than 2 cm or a 200 ml increase in volume when compared with the unaffected limb is generally considered clinically significant lymphedema. Most patients will also have a history of traumatic injury to the lymphatic system since secondary lymphedema is the most common form of lymphedema in the United States. Obesity, infections, and a history of radiation therapy increase the risk of lymphedema significantly after surgery. Patients with primary lymphedema may have a family history; however, sporadic forms of primary lymphedema also occur. In these situations, the diagnosis of primary lymphedema is a diagnosis of exclusion.

Rarely, patients with long-standing lymphedema will present with lymphangiosarcoma, an aggressive tumor with a 5-year survival of less than 10% (Figure 97.3). This complication was first reported by Stuart and Treves in 1948 in patients with postmastectomy lymphedema and is also referred to as Stuart-Treves syndrome. Patients present with red or purple nodules in the diseased tissues and are most commonly treated with amputation. Despite aggressive surgical management, however, the average survival after diagnosis is only 19 months.

The differential diagnosis of lymphedema includes deep vein thrombosis, congestive heart failure, malignancy, and infection. In some cases, additional tests may be required to diagnose lymphedema. Lymphoscintigraphy is performed by the injection of radiolabeled colloid into the region of interest and then its transport is followed using a gamma counter. Although lymphoscintigraphy is helpful in the diagnosis of lymphedema, the interpretation of these studies is not standardized making it difficult to compare findings between studies. The use of the lymphatic transport index has been suggested to standardize these findings but has not been widely accepted. Lymphoscintigraphy is differentiated from contrast lymphography, which involves the injection of radio-opaque dye directly into peripheral lymph vessels with radiological assessment of lymphatic flow. This test has largely been abandoned, however, due to technical difficulties and also because the contrast dye can injure the remaining lymphatic vessels resulting in worsening of lymphedema.

Lymphedema diagnosis and quantification can also be performed with a variety of noninvasive methods, including perometry, tissue tonometry, bioimpedance spectroscopy, and radiologic imaging techniques. Perometry is a method to calculate limb volumes and relies on the use of infrared scanning technology to estimate limb cross-sectional diameters at multiple intervals. Bioimpedance measures the rate of electrical current transmission through tissues and can estimate fluid content in a lymphedematous limb when compared with the normal limb. This technique is particularly helpful in early stage lymphedema. Finally, both magnetic resonance imaging (MRI) and computerized axial tomography (CT) can be used to assess lymphedema. On both MRI and CT scan, lymphedema appears as a subcutaneous honeycomb pattern. Finally, ultrasound can be used to evaluate lymphedema by correlating the thickness of the subcutaneous tissue with the progression of lymphedema and fibrosis.

STAGING OF LYMPHEDEMA

Lymphedema can be classified based on its clinical features, changes in limb volumes, or changes in limb circumference. Several classification schemes exist, though no single system has gained universal acceptance. The International Society of Lymphology stages lymphedema based on changes in the tissues.4 Stage 0 (latent lymphedema) is defined as impaired fluid transport without evidence of swelling or edema. Stage I is the early accumulation of protein-rich interstitial fluid, resulting in measurable swelling with pitting of the skin that decreases after compression garment treatment. Stage II is characterized by limb swelling (non-pitting) that does not decrease with compression due to fibrofatty tissue deposition. Stage III (lymphostatic elephantiasis) demonstrates severe swelling, fibrosis, adiposity, and skin changes (hyperkeratosis and acanthosis). Campisi et al. have proposed a similar staging scheme with stage I defined as initial or irregular edema, stage II as persistent lymphedema, stage III as persistent lymphedema with lymphangitis, stage IV as fibrolymphedema (“column” limb); and stage V as elephantiasis.5

FIGURE 97.2. Diagnosis of lymphedema. MRI, magnetic resonance imaging; CT, computed tomography; USG, ultrasonography.

FIGURE 97.3. Patient with lymphangiosarcoma of the right arm after long-standing lymphedema secondary to mastectomy and axillary lymph node dissection.

Lymphedema can also be classified based on changes in limb circumference when compared with preoperative measures or in comparison to the unaffected limb. Increases of less than 2 cm are considered mild lymphedema, 2 to 4 cm moderate lymphedema, and greater than 4 cm severe lymphedema. Though easy to conceptualize, this classification system has two major flaws: the inter-examiner variability of measurements and the relative nature of the grading scheme (i.e., a 2 cm increase in a thin patient is more noticeable than a 2 cm increase in an obese patient). Furthermore, circumference measurements may vary significantly due to the use of compression garments or changes in patient activity.

NONSURGICAL TREATMENT OF LYMPHEDEMA

Complex Decongestive Therapy

Complex decongestive therapy (CDT) is the mainstay of lymphedema management and aims to decrease the amount of fluid in lymphedematous tissues.6,7 CDT is comprised of multiple therapies and is usually divided into two phases. Phase 1 is an intensive treatment regimen typically performed once or twice daily for 4 to 6 weeks. Patients are treated with manual lymphatic drainage (MLD), skin care, compression wraps with short-stretch bandages, and light exercises. MLD is a form of soft tissue massage performed with light strokes in a directional manner to increase lymphatic fluid flow away from damaged lymphatics. In phase 2, MLD use is decreased and patients are primarily treated with compressive garments and skin care administered indefinitely since lymphedema is a chronic disease. Some patients are given additional phase 1 treatments if there is evidence of relapse or progression of disease. In addition, some centers prescribe intermittent pneumatic compression (IPC) in this phase.

CDT is effective in most patients; however, this therapy is time intensive, is expensive, and requires a high level of sophistication on the part of the patient and caregiver. Certified lymphedema therapists are sometimes difficult to find, and the costs of long-term care are not always covered by health insurance policies. These difficulties contribute to relatively high rates of patient noncompliance.

Compression Therapy

Compression therapy includes a wide range of treatments, including multilayer bandaging, self-adherent wraps, and custom-made pressure garments. The goal of these treatments is to restore hydrostatic pressure in the limb and improve lymph flow. It is important to note that wraps are performed with low-stretch bandages rather than high-stretch bandages (e.g., Ace bandage). This difference is important since short-stretch bandages maintain a constant pressure at rest but exert an increased pressure with exercise. In contrast, high-stretch bandages may exert high pressures at rest thereby causing circulatory compromise.

Intermittent Pneumatic Compression

The IPC device is a pneumatic cuff connected to a pump that simulates the natural pump effect of muscular contraction on the peripheral lymphatic system. IPC pumps typically cycle and have pressures in the range of 35 to 180 mm Hg applied either uniformly or sequentially. Although some studies have shown that IPC can be effective in patients with secondary lymphedema, particularly when combined with compression garments, there is currently no consensus on the use of these devices and costs of these devices are usually not covered by insurance plans.

Exercise

For many years, it was thought that patients with lymphedema or those at risk for developing lymphedema should refrain from vigorous exercise with the affected limb. This concept was based on the idea that exercise increased blood flow and hence lymphatic load. More recently, however, multiple prospective studies have demonstrated significant benefits in monitored exercise regimens.Although the exact mechanisms by which exercise improves lymphedema remain unknown, it is thought that activation of the muscular pump mechanism helps propel lymphatic fluid in the affected extremity. It is also possible that exercise improves lymphedema by promoting weight loss and maintenance of ideal body weight since these factors have also been shown to decrease the incidence and severity of lymphedema.

SURGICAL TREATMENT OF LYMPHEDEMA

Although the mainstay of lymphedema treatment is nonsurgical, a number of surgical options have been described. However, there is currently no consensus on patient selection, the type of procedure, timing of intervention, or postoperative management. In most cases, surgery is reserved for patients with significant symptoms and functional complaints who have failed conservative management. Some authors, however, describe their experience with patients who are simply dissatisfied with compression garments.

The surgical options available for lymphedema can be broadly divided into physiologic approaches and reductive techniques (Figure 97.4). Physiological treatments aim to restore lymphatic flow and include flap transposition, lymph node transfers, and lymphatic bypass procedures. Reductive techniques, such as surgical excision or liposuction, simply aim to treat the consequences of sustained lymphatic fluid stasis by removing the fibrofatty tissues that has been pathologically generated.

FIGURE 97.4. Surgical options for lymphedema.

PHYSIOLOGICAL METHODS

Flap Transfer

The first reported case of flap transposition for the treatment of lymphedema is credited to Gilles who described a two-stage tubed flap transfer from the arm to the abdomen and ultimately the affected groin. He reported improvement in the patients’ chronic lymphedema and hypothesized that the skin flap provided a path for lymphatic fluid to bypass the damaged inguinal region. Goldsmith used this same concept and reported his experience with the use of pedicled omentum flap transpositions in a series of 22 patients (13 with lower extremity and 9 with upper extremity). Nearly half of the patients experienced good results; however, due to the high rates of complications, including adhesions, abdominal wall hernias with incarcerated bowel, pulmonary embolus, and wound healing complications, the procedure failed to gain widespread acceptance. With the advent of modern pedicled and free flap procedures, several case series and case reports have been published detailing improvements in lymphedema of the lower/upper extremity, genitalia, and head and neck after flap transfer. Unfortunately, the unpredictable outcomes associated with these procedures have precluded their widespread clinical application.

Lymphatic Bypass

With the understanding that lymphedema was the result of lymphatic fluid stasis, in 1908 Harvey attempted to re-establish lymphatic flow by tunneling silk threads subcutaneously from the lymphedematous tissue into adjacent healthy tissue. Lexer later modified the procedure to use strips of fascia lata instead of silk thread while Walther used rubber tubes. Although seemingly reasonable from a pathologic standpoint, none of these procedures produced long-lasting results. In the 1960s, shortly after the introduction of microsurgery, Laine and Howard and Olsewski and Nielubowicz first reported on using microsurgical techniques to help restore absent or scarred lymph basins. Since then, a variety of procedures have been proposed to bypass obstructed lymphatics either by connecting obstructed lymphatics to normal lymphatics (lymphatic–lymphatic bypass) or by connecting lymphatics to a local or distant vein (lymphaticovenous bypass; Figure 97.5).

Lymphatic–lymphatic bypass is performed by transferring a soft tissue graft containing superficial lymphatics from the anterior thigh to the affected limb and connecting the collecting lymphatics of the graft to lymphatic channels in the lymphedematous region. The graft is then tunneled subcutaneously into a non-lymphedematous area, and the proximal lymphatic vessels in the graft are anastomosed to the local, healthy lymphatics. Alternatively, vein grafts can be harvested and several small, transected lymphatic vessels are inserted into the distal cut end of the vein. The vein graft is then tunneled into the neck or distal to the damaged groin lymphatics and anastomosed to local lymphatic channels.5

Connection of lymphatic vessels to regional veins forms the basis of lymphaticovenous procedures. These procedures were initially described as end-to-side anastomoses to large superficial veins (e.g., saphenous). However, some authors have criticized this approach as theorizing that the high pressures in the veins would impede lymphatic drainage. More recently, supermicrosurgical techniques have been used to connect collecting lymphatics in an end-to-end manner with subdermal veins to avoid this issue.

Lymph node transfers are performed by harvesting lymph nodes from an unaffected region (usually the superficial inguinal nodes) and transferring them either as grafts or as a free flap with microsurgical anastomoses of the artery and vein. The transplanted lymph nodes may be transferred to the site of the original lymph node resection or to nonanatomic areas such as the dorsum of the arm in upper extremity lymphedema. Although there have been anecdotal reports of success utilizing these procedures, the rationale for their success, particularly when lymph nodes are transferred to nonanatomic sites, is not entirely clear. Furthermore, engraftment of avascular lymph nodes with reconnection to the surrounding lymphatic networks has not been verified clinically and occurs at relatively low rates in animal models, casting further doubt on the effectiveness of these procedures. Finally, given that even relatively minor injury to the lymphatic system such as sentinel lymph node biopsy can result in lymphedema, it is possible that harvesting of lymph nodes for transfer may cause lymphedema in the donor extremity.

Although there is no general consensus for indications or timing of lymphatic bypass procedures, most authors agree that these interventions should be reserved for patients who have failed conservative management or suffer from recurrent cellulitis or lymphangitis. Bypass procedures are, in general, thought to be feasible even years after the onset of lymphedema so long as fibrosis and fat hypertrophy in the affected limb are not severe. Most authors consider patients with early stage lymphedema (Campisi stage I, II, or early stage III) as the ideal candidates and it is thought that patients with more advanced lymphedema are less likely to benefit from lymphatic bypass procedures. As a result, many authors consider extensive soft tissue fibrosis or fatty deposition as relative contraindications to lymphatic bypass procedures. Similarly, due to the potential for backflow into the lymphatic system, venous hypertension is also considered a contraindication to these procedures by most authors.

Several groups have reported the results of lymphatic bypass procedures; however, the reported outcomes have been highly variable with some groups describing excellent results and others reporting modest or no improvement in either objective measures or subjective measures of lymphedema symptoms (Table 97.1). A number of factors contribute to this variability. Perhaps, the most significant problem has been the retrospective nature of analysis and irregular or inadequate follow-up after surgery. In addition, there is considerable variability between studies in how lymphedema is assessed both objectively and subjectively and significant differences in criteria for patient selection, timing of intervention, identification of suitable lymphatic vessels, and the type of lymphatic bypass procedure that is performed. Objective analysis is particularly problematic with a variety of techniques used by different groups to estimate the excess volume in the affected limb before and after surgery. In addition, most studies have utilized just one measure (either limb volume or circumference, for example) and have not used complementary noninvasive techniques to assess lymphatic flow or changes in tissue pliability or fluid content. Perhaps most significantly, there is also wide ranging differences in the use of compression garments/physical therapy postoperatively that may alter limb volumes independently from surgical interventions. Subjective analysis has been particularly problematic with most studies utilizing non-validated, non-standardized questionnaires to evaluate patients. Finally, many studies have reported mixed series of patients with either upper or lower lymphedema or lymphedema resulting from various etiologies, including cancer surgery, trauma, congenital conditions, and filariasis. In fact, these weaknesses cast significant doubt on any conclusions demonstrating a benefit.

FIGURE 97.5. Schematic of physiologic procedures for lymphedema. A. Lympholymphatic bypass utilizing lymphatic vessels and soft tissues harvested from the anterior thigh. B. Lympholymphatic bypass utilizing saphenous vein as conduit. C. Lymph node transfer. D.Lymphovenous bypass.

Chang8 reported his early experience in using lymphaticovenular bypass in 20 patients with upper extremity lymphedema related to the treatment of breast cancer. Nineteen patients (95%) reported that their symptoms improved after surgery, and 13 patients had quantitative improvement. The mean reduction in volume differential was 29%, 36%, 39%, and 35% at 1, 3, 6, and 12 months, respectively.

One recent advance in the lymphovenous bypass operation has been the use of fluorescence lymphography to image the lymphatic system during lymphovenous shunt operations and to diagnose the severity of lymphedema.9 Fluorescence lymphography allows surgeons to locate a functional lymphatic vessel for the lymphovenous shunt before making a skin incision. This technique allows for the prompt identification of the functional lymphatic vessels, and thus has the potential to significantly improve the outcomes of lymphovenous bypass operations (Figure 97.6).

While the benefits of lymphatic bypass procedures are unverified, complication rates of these procedures appear low.5,8,10,11 These complications are usually minor (wound healing, lymphatic fistula, and cellulitis) and improve spontaneously. Further, extended antibiotic use decreases postoperative cellulitis. Interestingly, despite the fact that lymphedema is a chronic, progressive disease, very few studies have reported worsening of lymphedema symptoms after surgery.

FIGURE 97.6. A. Indocyanine green fluorescent lymphography of the normal upper limb with photos of the limb (color). Arrows indicate injection sites of indocyanine green. B. Fluorescent lymphography of the dorsal (left) and volar (right) sides of a lymphedematous upper limb. Injection sites of indocyanine green (black arrows) identified collecting lymphatic vessels (white arrows). (Reprinted with permission from Suami H, Chang DW, Yamada K, et al. Use of indocyanine green fluorescent lymphography for evaluating dynamic lymphatic status. Plast Reconstr Surg. 2011;127:74e-76e.)

Recent reports have utilized immediate lymphatic bypass procedures as a means of preventing lymphedema following axillary lymph node dissection.12 Using a prospective randomized clinical trial, one study found that lymphovenous bypass procedures performed at the time of lymphadenectomy significantly decreased the incidence of lymphedema (4.3% vs. 30.4%) 18 months after surgery. In addition, the authors found that patients treated with bypass procedures had increased lymphatic transport capacity as assessed by lymphoscintigraphy. These results should be interpreted with caution since the trial included relatively few patients and the authors defined lymphedema as an increase in volume of 100 cc. This volume is controversial since it is considered to be within the standard error of volume measurements. As a result, most previous studies have considered volume changes of more than 200 cc consistent with lymphedema. In addition, many patients in a study probably received the benefits of limb elevation, compression therapy, and other noninvasive measures.

REDUCTIVE METHODS

Direct Excision

Since the late 19th century, a number of surgical procedures have been described for debulking of lymphedematous tissues (Figure 97.7). Although occasionally used in cases of severe lymphedema, direct excision procedures are largely of historical significance. In the early 20th century, Diffenbach, Mikulicz, and others were among the first surgeons to describe their results with surgical excisions of lymphedematous skin and subcutaneous tissue. They achieved temporary improvements, though they were unclear whether this was a result of their operation or the postoperative bed rest and extremity elevation. Other surgeons attempted to bypass damaged lymphatics by creating lymphatic bridges between the superficial and deep systems. Some of these attempts were clearly misguided such as the procedures proposed by Lanz in which pedicled strips of fascia lata were buried into underlying trephined bone. In 1912, Kondoleon popularized a simpler procedure in which he used a large strip of fascia lata in the diseased leg as a free graft to form a connection between the skin and the underlying muscle. This was based on the theory that this connection would lead to the formation of new venous and lymphatic channels thereby bypassing obstructed dermal lymphatics. Around the same time period, Sir Richard Charles described the treatment of lower extremity lymphedema with circumferential skin and subcutaneous tissue excision to the level of the deep fascia and resurfacing with skin grafts harvested from the discarded tissue. In 1927, Sistrunk and later Thompson modified this approach for the treatment of upper extremity lymphedema in breast cancer survivors by excising an elliptical area of skin and soft tissues in the medial aspect of the arm and directly closing the resulting defect. They also attempted to form new lymphatic connections between the superficial and deep systems by burying dermal flaps connecting the skin with the underlying fascia.

FIGURE 97.7. Schematic of excisional procedures for lymphedema. A. Charles procedure. B. Sistrunk operation.

The Charles procedure and similar debulking treatments are still used in extreme cases of extremity lymphedema, and a number of authors have contributed case series with varying lengths and follow-up and varying reports of success (Table 97.2). A variety of modifications, including the use of split-thickness or full-thickness grafts, allograft, and negative pressure wound therapy, have been described. However, these procedures are acknowledged to be invasive and may result in significant morbidity, including pain, wound healing complications, infections, and lymph fistulas. In fact, severe wound healing complications in some cases have resulted in worsening of lymphedema and limb amputation.

Liposuction

Since the popularization of liposuction for cosmetic procedures, a number of surgeons have evaluated the use of this technique for the treatment of upper and lower extremity lymphedema. Although there is no general consensus regarding indications for this technique, most surgeons reserve liposuction for the treatment of non-pitting upper extremity lymphedema that has failed conservative management for at least 3 months with volume differences of at least 600 cc when compared with the unaffected limb, absence of active cancer or metastasis, and no clotting abnormalities or circulatory compromise. In addition, some groups consider subjective complaints such as heaviness, pain, and functional impairments and recurrent infections as indications for treatment. Some authors advocate liposuction as a first-line therapy for lymphedema,13 while others reserve it as second-line treatment when microsurgical treatment is not an option or has failed.14

The efficacy of liposuction has been most intensely studied in patients with breast cancer–related upper extremity lymphedema. Prospective studies of this patient population have reported overall favorable and long-lasting results with significant reductions in limb volumes (on average, half of the preoperative value) after circumferential liposuction and continuous use of postoperative compression garments. Improvements have been noted even as long as 4 years postoperatively. Several studies have also reported decreased rates of cellulitis in the affected limb after liposuction. In addition, although subjective analysis of lymphedema symptoms was not performed in a systematic manner, the majority of patients reported symptomatic relief.

It is important to note that liposuction is not a cure for lymphedema but rather a treatment designed to address the effects of chronic lymphatic insufficiency. This concept is highlighted by the fact that continued use of postoperative garments and conservative therapy is critical for the maintenance of volume reductions after upper extremity liposuction. Without these measures, fluid and fatty tissue re-accumulation occurs rapidly with only modest improvements in limb measurements 1 year after surgery. Because of this, most groups that utilize liposuction as a treatment for lymphedema follow patients closely postoperatively and adjust garments routinely to maintain a tight fit.

The scientific evidence supporting the use of liposuction for lower extremity lymphedema is less clear as most reports have been either case studies or small series. In fact, the initial reports of lower extremity liposuction were distinctly disappointing demonstrating very minor improvements in limb volume if liposuction was used as the only treatment modality. More recent studies have reported better outcomes with modern liposuction devices and tumescent techniques. In addition, the use of intraoperative tourniquets has been helpful in decreasing blood loss associated with these procedures.

Circumferential liposuction for lymphedema is a safe technique with few postoperative complications. Most procedures are performed in the outpatient setting and the majority of patients have no complications. Complications that do occur tend to be minor and usually resolve spontaneously. Temporary parasthesias and minor wound healing complications comprise the majority of these problems. Contrary to common belief, circumferential liposuction does not appear to disrupt lymphatic vessels or decrease the already impaired lymphatic transport capacity of the limb if performed in parallel to the long axis of the extremity.

CONCLUSIONS

Despite the advances in cancer treatment, lymphedema remains a significant and common complication, and treatment of lymphedema remains palliative in nature. Recent advances in surgical treatment of lymphedema have shown promise; however, additional studies are required in order to verify the benefit and define the patient population most likely to respond. A better understanding of the etiology of lymphedema is probably required for these goals.

References

1.  McLaughlin SA, Wright MJ, Morris KT, et al. Prevalence of lymphedema in women with breast cancer 5 years after sentinel lymph node biopsy or axillary dissection: objective measurements. J Clin Oncol. 2008;26:5213-5219.

2.  Cormier JN, Askew RL, Mungovan KS, et al. Lymphedema beyond breast cancer: a systematic review and meta-analysis of cancer-related secondary lymphedema. Cancer. 2010;116:5138-5149.

3.  Warren AG, Brorson H, Borud LJ, et al. Lymphedema: a comprehensive review. Ann Plast Surg. 2007;59:464-472.

4.  Bernas MJ, Witte CL, Witte MH. The diagnosis and treatment of peripheral lymphedema: draft revision of the 1995 Consensus Document of the International Society of Lymphology Executive Committee for discussion at the September 3-7, 2001, XVIII International Congress of Lymphology in Genoa, Italy. Lymphology. 2001;34:84-91.

5.  Campisi C, Davini D, Bellini C, et al. Lymphatic microsurgery for the treatment of lymphedema. Microsurgery. 2006;26: 65-69.

6.  Szuba A, Achalu R, Rockson SG. Decongestive lymphatic therapy for patients with breast carcinoma-associated lymphedema. A randomized, prospective study of a role for adjunctive intermittent pneumatic compression. Cancer. 2002;95:2260-2267.

7.  Szuba A, Cooke JP, Yousuf S, et al. Decongestive lymphatic therapy for patients with cancer-related or primary lymphedema. Am J Med. 2000;109: 296-300.

8.  Chang DW. Lymphaticovenular bypass for lymphedema management in breast cancer patients: a prospective study. Plast Reconstr Surg. 2010;126:752-758.

9.  Suami H, Chang DW, Yamada K, et al. Use of indocyanine green fluorescent lymphography for evaluating dynamic lymphatic status. Plast Reconstr Surg. 2011;127:74e-76e.

10.  Koshima I, Inagawa K, Urushibara K, et al. Supermicrosurgical lymphaticovenular anastomosis for the treatment of lymphedema in the upper extremities. J Reconstr Microsurg. 2000;16:437-442.

11.  O’Brien BM, Mellow CG, Khazanchi RK, et al. Long-term results after microlymphaticovenous anastomoses for the treatment of obstructive lymphedema. Plast Reconstr Surg. 1990;85:562-572.

12.  Boccardo FM, Casabona F, Friedman D, et al. Surgical prevention of arm lymphedema after breast cancer treatment. Ann Surg Oncol. 2011;18: 2500-2505.

13.  Brorson H, Svensson H. Liposuction combined with controlled compression therapy reduces arm lymphedema more effectively than controlled compression therapy alone. Plast Reconstr Surg. 1998;102:1058-1067; discussion 1068.

14.  O’Brien BM, Khazanchi RK, Kumar PA, et al. Liposuction in the treatment of lymphoedema; a preliminary report. Br J Plast Surg. 1989;42:530-533.