Algorithmic approach to lymphedema surgery: a narrative review

Introduction

Background

Lymphedema represents a chronic and progressive disorder that significantly impairs quality of life and functional capacity in affected patients (1-5). It encompasses a heterogeneous group of conditions, including primary lymphatic dysplasia and secondary forms resulting from oncologic treatments, among which breast cancer-related lymphedema (BCRL) is the most prevalent and clinically significant entity. The growing population of cancer survivors has led to an increasing incidence of secondary lymphedema, particularly following axillary lymph node dissection and radiotherapy, making its management a major concern in contemporary breast surgery practice (6-8).

Rationale and knowledge gap

Despite advances in conservative management and the emergence of microsurgical techniques over the past two decades, therapeutic decision-making remains challenging due to the heterogeneous nature of the disease and the limited integration of pathophysiological, clinical and imaging data into standardized treatment algorithms (1-5). Selecting the appropriate surgical intervention requires a comprehensive understanding of lymphatic pathophysiology, accurate phenotypic characterization and a comprehensive diagnostic work-up (9,10).

Objective

This review aims to synthesize current knowledge on the pathophysiology and classification of lymphedema and to present a structured diagnostic workup that forms the foundation of an algorithmic approach to surgical management. Compared with previously published reviews, this manuscript provides a clinically oriented, phenotype-driven framework that integrates pathophysiology, clinical staging, functional imaging, and tissue composition to support surgical decision-making, with particular relevance to BCRL. Both primary and secondary forms of lymphedema are addressed, with emphasis on the integration of clinical staging, functional imaging and tissue composition analysis to guide individualized treatment selection while highlighting specific considerations related to breast cancer-associated lymphedema. We present this article in accordance with the Narrative Review reporting checklist (available at https://abs.amegroups.com/article/view/10.21037/abs-2026-0014/rc).

Methods

A narrative review methodology was used to synthesize current evidence on lymphedema pathophysiology, classification, imaging assessment, and surgical management. The review focused on integrating clinical staging systems, functional imaging findings, tissue composition analysis, and their role in guiding surgical decision-making in primary and secondary lymphedema, with particular emphasis on BCRL.

A structured literature search was performed in PubMed for English-language studies published up to March 2, 2026. The search combined MeSH terms and free-text keywords related to lymphedema, lymphatic surgery, lymphaticovenous anastomosis, vascularized lymph node transfer, suction-assisted lipectomy, and lymphatic imaging. Additional relevant studies were identified through manual screening of reference lists of included publications (Table 1).

Given the narrative nature of this review, no formal quality assessment or standardized risk-of-bias evaluation was performed.

Pathophysiology and classification of lymphedema

Lymphedema is characterized as a chronic, self-perpetuating failure of lymphatic transport rather than a static mechanical obstruction. The International Society of Lymphology (ISL) defines peripheral lymphedema as an external manifestation of lymphatic system insufficiency in which the capacity of lymphatic transport falls below that required to clear interstitial fluid and macromolecules, thereby leading to progressive tissue changes. The persistent accumulation of protein-rich interstitial fluid has been shown to induce chronic inflammation, accompanied by proliferation of parenchymal and stromal cells and excessive deposition of extracellular matrix and adipose tissue (1). These conditions explains its variable clinical trajectory and heterogeneous response to treatment.

Primary versus secondary lymphedema: distinct etiologies, convergent pathways

Lymphedema can be classified as primary or secondary based on etiology. Primary lymphedema results from congenital or developmental abnormalities of the lymphatic system and encompasses a spectrum of malformations including hypoplasia, aplasia and valvular incompetence (2,5,9,10). Traditionally, primary lymphedema has been subdivided into three clinical categories according to age of onset: congenital lymphedema (onset ≤2 years), like Milroy disease; lymphedema praecox (onset 2–35 years), like Meige disease; and lymphedema tarda (onset >35 years) (10). Large clinical series have demonstrated that primary lymphedema frequently involves the lower extremities, may present unilaterally or affect multiple segments and can be associated with recognized genetic syndromes. Because the underlying defect is structural and often diffuse, primary lymphedema is generally less responsive to conservative therapy than secondary forms, and a substantial proportion of patients ultimately require surgical intervention (3,10).

Secondary lymphedema, in contrast, is more common and arises in previously normal lymphatic systems that have been subjected to overload or injury. Globally, the vast majority of lymphedema cases are secondary in origin, predominantly attributable to filarial infection in low- and middle-income countries and to cancer treatment-related lymphatic damage in high-income settings (8). The ISL consensus document highlights several common triggers of secondary lymphedema, including radical lymph node dissection, radiotherapy, trauma and repeated episodes of lymphangitis with subsequent lymphangiosclerosis (1).

Despite their distinct etiologies, primary and secondary lymphedema have been shown to converge on a common final pathway characterized by chronic lymphatic insufficiency, sustained inflammation and progressive fibro-adipose tissue remodeling (1,3,10).

Classification systems and clinical staging

The ISL staging system remains the most widely adopted clinical framework for lymphedema and breaks down severity based on physical examination findings and tissue consistency (1). Stage 0, also referred to as latency, describes impaired lymphatic transport in the absence of visible swelling. Stage I corresponds to early pitting edema that reduces with limb elevation. Stage II is characterized by persistent swelling that is often non-pitting and accompanied by developing tissue fibrosis. Stage III, also known as lymphostatic elephantiasis, is marked by pronounced volume increase, skin thickening, trophic changes and deep skin folds (1). The ISL consensus explicitly notes that these stages describe the external condition of the limb and do not fully capture the underlying pathophysiology, nor do they reflect nuances such as adipose tissue hypertrophy or findings from functional imaging studies (1).

Several complementary classification systems have been proposed to address these limitations. The Cheng lymphedema grading system integrates limb volume discrepancy with clinical features to guide the selection between physiological reconstruction and debulking procedures (3,11). The Campisi classification system, which integrates lymphoscintigraphic findings with clinical presentation, remains particularly influential in microsurgical centers and serves as a valuable tool for selecting candidates for surgical intervention (12). In a recent scoping review published in 2025, Sheikh-Oleslami and colleagues identified a total of 33 distinct clinical scoring systems for lymphedema, including ten designed for the lower extremity, six for the upper extremity, two for both upper and lower extremitnine, nine for head and neck lymphedema and six general assessment scales (4). Although these systems commonly incorporate parameters such as limb volume, skin changes, functional impairment and pain, no single gold standard has been established, and the marked heterogeneity across systems complicates both comparison and standardization of outcomes (4).

The fat-fluid continuum and surgical implications

As said earlier, modern research has emphasized that lymphedema progresses along a fat-fluid continuum. In the early stages of disease, interstitial fluid accumulation predominates, whereas chronic stages are characterized by progressive adipose deposition and fibrosis. The ISL consensus document underscores that the deposition of extracellular matrix and adipose tissue begins early in the disease process and accumulates progressively over time (1).

This pathophysiological evolution provides a rationale for the differential response to treatment: early-stage disease, characterized by predominant lymphatic dysfunction and fluid accumulation, as typically observed in limbs with fluid-predominant morphology corresponding to ISL Stage I or early Stage II, tends to respond favorably to physiological procedures—such as lymphaticovenous anastomosis (LVA) and vascularized lymph node transfer (VLNT)—that aim to restore or bypass lymphatic flow and have been shown to achieve substantial volume reduction and symptomatic relief (3,11,13,14). In contrast, advanced-stage disease, marked by fibro-adipose transformation and increased tissue deposition, is typically associated with adipose-predominant morphology as seen in late ISL Stage II or Stage III lymphedema, in which the lymphatic network is often sclerosed or functionally absent. In these limbs, physiological bypass procedures alone rarely achieve meaningful volume reversal, and debulking interventions—particularly suction-assisted lipectomy (SAL) or other excisional techniques—become necessary to address the accumulated fibro-adipose burden and resulting tissue hypertrophy (3,11).

Diagnostic workup: the foundation of an algorithmic approach

Clinical assessment

An algorithmic approach to lymphedema management begins with a structured clinical assessment that integrates detailed history, physical examination and patient-reported outcome measures. The history should systematically document the onset and temporal evolution of limb swelling, any relation to prior surgery, radiotherapy or infection, the laterality and anatomical distribution of involvement (including single limb, multiple limbs, or genital and truncal extension), the frequency of cellulitis episodes, prior use of conservative therapies and their effectiveness, and the functional and psychosocial impact of the disease (9,10,15).

On physical examination, key elements include standardized limb circumference measurements to quantify inter-limb volume discrepancy, systematic assessment of whether edema is pitting or non-pitting, and detailed evaluation of skin changes (9,10,15). Pitting edema that improves with limb elevation is typical of earlier, fluid-predominant stages of lymphedema, whereas non-pitting, woody edema indicates advanced fibro-adipose tissue remodeling and is associated with reduced responsiveness to purely physiological surgical procedures (1,9,11). Characteristic skin changes, including peau d’orange appearance, hyperkeratosis and papillomatosis, have been shown to correlate with ISL Stage II–III disease and adipose-predominant phenotypes (1,2,10,15). A positive Stemmer sign—thickening of the skin at the base of the second toe or finger—provides additional diagnostic support, particularly in lower extremity lymphedema (2,9,10).

Lymphedema has been consistently associated with substantial deterioration in both quality of life and functional capacity, driven by chronic pain, activity limitation, recurrent infections, psychological distress, and altered body image perception. In this context, systematic assessment using validated patient-reported outcome measures is essential to capture the multidimensional impact of the disease. Many of the scoring systems identified in the review by Sheikh-Oleslami et al. include validated domains for pain, functional impairment and psychological distress (4,13,14).

Imaging modalities

Imaging has become central to lymphedema surgery, informing patient selection, preoperative mapping, and postoperative surveillance. In advanced, long-standing disease, diagnosis is usually clinical, whereas early or subtle forms often require adjunct imaging to document lymphatic dysfunction and abnormal fluid distribution. Preoperative multimodal imaging—using indocyanine green (ICG) lymphography, MR lymphography, ultra-high-frequency ultrasound, and lymphoscintigraphy—reduces the need for extensive dissection and refines surgical planning by combining functional and structural information (5,16,17).

ICG lymphography has become a cornerstone of preoperative evaluation, enabling real-time visualization of superficial lymphatic channels and their drainage territories (1). It is a widely used modality in lymphatic imaging owing to its simplicity, sensitivity, and high-resolution, real-time visualization of superficial lymphatic channels in the near-infrared range. It is now routinely employed as a diagnostic tool for staging lymphedema and refining treatment planning. In surgical practice, ICG plays a central role in planning LVA, where ICG-enhanced lymphatic collectors are typically selected as functional targets, is used postoperatively to assess anastomotic patency, and, in VLNT, assists in evaluating recipient vessels, flap perfusion, and performing reverse lymphatic mapping to reduce donor-site lymphedema risk (16,17). The ISL consensus document notes the increasing use to identify functional lymphatic vessels suitable for bypass procedures and to monitor disease progression and response to treatment (1).

In the absence of lymphatic obstruction, ICG lymphography typically demonstrates smooth, linear enhancement of superficial lymphatic channels extending from the injection site toward the regional nodal basin. In secondary lymphedema, proximal outflow obstruction increases intralymphatic pressure, leading to vessel dilatation and characteristic dermal backflow patterns that reflect progressive lymphatic failure (17). Yamamoto et al. described a stepwise spectrum of abnormalities, from focal retrograde filling of superficial precollectors (“splash”) to more punctate vertical reflux (“stardust”) and, ultimately, diffuse capillary staining of the skin (“diffuse”) (18). This pattern-based staging helps standardize disease severity and informs surgical decision-making. Linear enhancement indicates functional collecting vessels and represents the ideal scenario for LVA, while a splash pattern reflects early dysfunction that can still be compatible with effective bypass. In contrast, a stardust pattern suggests more advanced, partial obstruction with uncertain benefit from LVA, and a diffuse pattern of severe dermal backflow generally favors volume-reductive or reconstructive strategies such as VLNT or SAL (17).

Importantly, several studies have demonstrated that ICG-based functional staging correlates only weakly with traditional ISL clinical staging, meaning that some patients with advanced clinical stage may still retain functional collectors amenable to surgical intervention (14).

Magnetic resonance lymphangiography is a valuable adjunct in lymphedema assessment, as it provides high spatial and temporal resolution with three-dimensional mapping of the entire limb, while simultaneously visualizing lymphatic channels, lymph nodes, and the relative fluid versus fat composition of the tissues. It can demonstrate the presence, number, course, and depth of enhancing lymphatic channels, including those located more than 2 cm beneath the skin surface, and also depict secondary changes in adjacent soft tissues, thereby refining both staging and etiologic evaluation (1,16,17). In the surgical setting, MR lymphography supports preoperative planning for LVA by allowing projection of lymphatic channels and nearby veins onto the skin using fixed anatomical landmarks and, by distinguishing fat-predominant from fluid-predominant limbs and identifying absent channels, helps stratify patients between reductive procedures and physiologic options such as bypass or VLNT (16,17). Despite these advantages in anatomical accuracy and fluid-fat characterization, the technique remains costly, time-consuming, and dependent on specialized radiologic expertise (17).

Ultrasound is able to visualize lymphatic flow in deeper tissue layers that are beyond the penetration of ICG lymphography, including regions where superficial collectors are embedded in deep fat and obscured by increased tissue thickness or severe dermal backflow or can be useful in patients with iodine allergy. In limb lymphedema, three characteristic ultrasonographic features are typically observed: increased skin thickness, increased subcutaneous tissue thickness, and increased subcutaneous echogenicity. Ultra-high frequency ultrasound additionally enables detailed preoperative assessment of lymphatic vessels by depicting both the extent of dilatation and the severity of wall thickening, thereby helping to select optimal targets for lymphovenous bypass (16,17). Ultrasound is also increasingly used to highlight tissue alterations (1). It offers a simple, non-invasive, and cost-effective approach for detecting adipose tissue remodeling in the limbs of patients with secondary lymphedema and is suitable even in low-budget, resource-limited settings where only conventional ultrasonography is available. This method may be key for assessing adipose hypertrophy, fibrotic septa, and overall tissue quality, while enabling clinicians to monitor subtle subcutaneous changes and initiate early preventive interventions before progression to fibrosis (19,20). It can therefore complement other imaging modalities to guide planning of SAL.

Despite these advantages, its wider implementation is currently limited by operator dependence and the restricted availability of dedicated ultra-high frequency probes (17).

Ultra-high frequency ultrasound (UHFUS) (30–100 MHz) provides submillimeter resolution (30–50 µm) of superficial dermal lymphatics <0.7 mm, identifying functional “champagne flow” patterns often obscured by ICG dermal backflow. By mapping deep or obscured collectors, UHFUS expands lymphovenous bypass indications to advanced disease, offering radiation-free intraoperative guidance despite limited <2 cm tissue penetration (21).

Lymphoscintigraphy remains a robust and well-established method for global functional assessment of the lymphatic system. It utilizes tracers and serial gamma-camera imaging to document lymphatic transport dynamics whereby lymphatic drainage can be mapped along the channels to the corresponding lymph node basin (5,17,22). Typical abnormalities observed in lymphedema include dermal backflow, delayed or absent tracer transport, cross-over drainage to contralateral lymphatic pathways, and delayed or absent visualization of regional lymph nodes (5,22). The ISL consensus highlights the particular value of lymphoscintigraphy for generating reproducible, preclinical diagnostic images in newborns and children. Lymphoscintigraphy is also widely employed in breast and melanoma surgery to localize sentinel lymph nodes after intradermal tracer injection (17).

Surgical phenotype stratification

By integrating clinical staging, functional imaging findings and tissue composition analysis, patients can be stratified into three distinct surgical phenotypes that guide optimal therapeutic intervention (1,3,4,11).

Phenotype 1 (fluid-predominant early disease) typically corresponds to ISL Stage I disease (1). Patients in this category present with pitting edema, minimal skin changes, linear or splash patterns on ICG lymphography, and imaging findings dominated by fluid accumulation with limited adipose tissue thickening (1,3,7,11,17). These patients are considered prime candidates for physiological reconstruction procedures, particularly in the setting of secondary lymphedema and in selected cases of primary lymphedema (3,11,14,23).

Phenotype 2 (intermediate mixed morphology) is generally observed in ISL Stage II disease (1). Patients exhibit partial loss of pitting edema, early signs of tissue fibrosis, stardust patterns on ICG lymphography with evidence of dermal backflow but residual functional collectors, and a mixed fluid–fat composition on MRI (1,4,11,17). These patients may benefit from hybrid surgical approaches that combine physiological reconstruction with debulking procedures, often in conjunction with ongoing complex decongestive therapy (CDT) (3,7,14).

Phenotype 3 (adipose-predominant chronic disease) corresponds to late ISL Stage II or Stage III disease (1). It is characterized by marked fibrosis, pronounced skin changes, non-pitting woody consistency of the limb, diffuse dermal backflow on ICG lymphography, and imaging evidence of substantial subcutaneous fat accumulation and fibrosis (1,4,11,17). In this phenotype, physiological procedures alone rarely provide sufficient volume reduction; excisional or suction-based debulking techniques become the mainstay of treatment for achieving meaningful volume reduction, with physiological procedures potentially added on a selective basis to improve residual lymphatic function (3,7,11).

Surgical options: mechanisms, indications, and outcomes

LVA

LVA is a supermicrosurgical, minimally invasive procedure in which functioning lymphatic collectors or subdermal lymphatic channels located upstream of an obstruction are connected to nearby venules to bypass the blockage and restore lymphatic drainage. LVA requires precise knowledge of the anatomy and location of both lymphatic vessels and veins, and often uses a collateral branch of the main vein whose valvular competence is carefully checked to ensure effective outflow. By creating an intima-to-intima coaptation between the lymphatic vessel and the venule, this technique diverts excess lymphatic fluid into the venous circulation, promoting the drainage of fluid trapped in lymphedematous tissues while reducing the risk of thrombosis at the anastomotic site (11,24-27).

This procedure is minimally invasive and associated with rapid recovery, as it requires only small 1–3 cm incisions limited to the affected limb. It is typically performed under local anesthesia, allowing same-day discharge or a brief overnight stay in most cases. These features make it a suitable and safe option even for high-risk patients (11,24).

However, this procedure is most effective when performed in carefully selected, optimal candidates.

Ideal candidates for lymphovenous anastomosis are patients with early or intermediate stage lymphedema, in whom at least a portion of the lymphatic collectors remains functional and the disease is predominantly fluid-dominant rather than fibrofatty (7,11,24,26).

LVA is most extensively documented in the context of secondary lymphedema, with a primary focus on BCRL, which constitutes the most frequently reported clinical cohort in the literature. In this patient population, robust evidence supports LVA as a cornerstone physiologic intervention for early-stage disease, consistently demonstrating significant improvements in limb volume, symptom burden, and the frequency of cellulitis episodes (13,26,28). In contrast, results in primary lymphedema are more variable due to congenital lymphatic dysfunction and reduced availability of functional collectors (3,10).

In this context, ICG lymphangiography has refined candidate selection by confirming the presence of patent, functioning lymphatics and has shown that, although surgery was traditionally reserved for early ISL stages, selected patients with higher ISL stages but favorable ICG patterns or high lymphatic flow velocities may still be appropriate candidates for LVA. As a result, preoperative ICG mapping has become essential to identify suitable target vessels and to prioritize patients with a fluid-dominant phenotype (7,14,24,26).

Several relevant outcomes have been demonstrated following lymphaticovenous procedures. These procedures have been shown to reduce limb heaviness and swelling, with consistent decreases in excess limb volume and circumference and parallel improvements in functional status and symptom burden. These changes are accompanied by better lymphedema-specific quality-of-life scores, including physical, functional, and psychosocial domains (7,11,25,27,29).

An additional key benefit is a marked reduction in cellulitis episodes, with several cohorts reporting a drop from more than one infection per year before surgery to almost none afterward, which has important implications for morbidity and healthcare use. Overall, the magnitude and durability of these effects appear greatest when surgery is performed in earlier, fluid-dominant stages of disease, before extensive fibrofatty remodeling has occurred (7,25,27).

Importantly, a significant proportion of published LVA outcome studies are derived from BCRL cohorts, which may partly explain the more favorable and consistent results reported in the literature compared with other etiologies. This highlights the need to interpret outcomes according to underlying etiology rather than pooling all lymphedema subtypes (13,26,30).

This technique, although effective in carefully selected patients, nonetheless carries several important limitations. Lymphovenous anastomosis fundamentally depends on the presence of functional lymphatic vessels, whose pumping capacity progressively declines with increasing disease severity. In advanced lymphedema, chronic elevation of interstitial pressure, recurrent infections, and irreversible loss of contractile smooth muscle often lead to sclerotic, nonfunctional lymphatics, making late-stage, fibrotic limbs a relative contraindication for LVA and limiting its long-term efficacy. Moreover, even when technically feasible, suitable lymphatic targets can be difficult to identify, and there is a risk of lymphatic collapse or failure of inflow at the anastomotic site, so that alternative physiologic options such as VLNT may be more appropriate in severe cases (6,27,28).

VLNT

VLNT involves microvascular transfer of a flap containing functional lymph nodes to the affected limb, where the viable nodes remain vascularized and active, secrete lymphangiogenic growth factors such as VEGF-C, and thereby drive gradual reconstruction of collateral lymphatic pathways and neo-lymphatico-venous shunts that divert lymph into the venous system via pressure gradients (3,14,31,32). While simultaneous modulating the local immune microenvironment and contributing to a reduction in infection susceptibility (32).

VLNT is principally indicated in advanced-stage lymphedema with severe lymphatic failure, in which conservative therapy and standard physiologic procedures no longer achieve satisfactory control. In this setting, the vascularized transfer of tissue containing multiple functional lymph nodes offers a truly restorative strategy, aiming not only to reduce limb volume but also to re-establish lymphatic drainage pathways within a structurally compromised extremity. Recurrent cellulitis further strengthens the indication for VLNT: although LVA remains appropriate when residual targetable collectors are present, patients lacking suitable channels—particularly those with repeated infections—are better served by VLNT, which has demonstrated superior outcomes in infection-prone lymphedema. Finally, preoperative lymphatic imaging is critical for selecting patients who lack suitable collectors for LVA. The presence of segmental dermal backflow with few or absent functional vessels supports the choice of VLNT and guides orthotopic versus heterotopic flap placement, while absence of usable channels on ICG lymphography often prompts the use of a gastroepiploic lymph node flap (7,24,31-34).

BCRL also represents a major indication for VLNT in patients with advanced disease who have failed conservative therapy or are no longer candidates for LVA. In this context, VLNT has been particularly studied in secondary lymphedema following oncologic lymphadenectomy, where recurrent infections and lymphatic obliteration are common (13,31,33,34).

Flap selection for VLNT is guided by balancing lymphatic efficacy, donor-site safety, and aesthetic considerations. The most commonly used donor sites include the groin, supraclavicular, submental, and gastroepiploic regions.

Groin-based VLNT uses the superficial inguinal basin, which drains the lower abdomen and allows preservation of lower-limb lymphatics when meticulously dissected and is most often based on the superficial circumflex iliac artery, with the superficial inferior epigastric or a small medial femoral branch as alternatives. It offers a well-concealed scar, abundant soft tissue, and reliable anatomy, but carries a risk of donor-site lymphedema, mitigated by careful preoperative mapping and refined microvascular techniques to optimize inflow and outflow (6,31,32).

Supraclavicular VLNT offers a small, well-concealed scar and a relatively low risk of iatrogenic lymphedema but provides limited soft tissue and fewer nodes. Its use is technically demanding due to variable vascular and lymphatic anatomy, requiring meticulous dissection to secure venous outflow, protect the thoracic duct and phrenic nerve, and prevent lymphatic leakage (6,31,32).

Submental VLNT uses a cervical lymph node basin that does not drain the limbs, conferring a very low risk of iatrogenic extremity lymphedema and making it attractive for lower-limb disease. Its drawbacks include a relatively conspicuous submandibular scar and the risk of marginal mandibular nerve injury, so nerve-sparing, microscope-assisted dissection and detailed knowledge of the variable vascular anatomy are essential to achieve the reported volume reductions and quality-of-life gains (6,31,32).

The gastroepiploic VLNT harvests nodes along the right gastroepiploic vessels, avoiding limb lymphatic basins and providing a small flap suitable for distal inset with discreet laparoscopic scars. It achieves meaningful limb-volume reduction with generally low donor-site morbidity, though intraperitoneal complications such as ileus, pedicle injury, or pancreatitis remain possible and require careful dissection (6,32).

The mechanisms underlying VLNT remain incompletely defined but likely involve three complementary processes. First, a “pump” function facilitates lymphatic drainage through newly formed lymphaticovenous shunts within the transferred nodes, driven by arterial-venous pressure gradients. Second, lymphangiogenesis, stimulated by VEGF-C secretion from viable lymphatic tissue, promotes the formation of collateral vessels reconnecting the graft to local lymphatic channels, thereby restoring continuity. Finally, VLNT exerts a local immunomodulatory effect, as reconnected lymphatic channels allow antigen presentation to transplanted nodes, reducing recurrent cellulitis and improving immune surveillance. Together, these mechanisms support the physiological and clinical efficacy of VLNT in re-establishing lymphatic function and alleviating lymphedema (14,24,31-34).

Overall, complications after VLNT appear relatively uncommon. Donor-site morbidity remains a key concern, particularly the risk of iatrogenic lymphedema. To mitigate this, reverse lymphatic mapping has been introduced to identify and preserve nodes that preferentially drain the donor limb during groin or lateral thoracic lymph node harvest, by combining radiotracer and ICG mapping to spare “hot” nodes from the flap (6,24,31,35). Despite their overall low incidence, VLNT procedures still entail classic microvascular risks, including venous congestion or thrombosis, the need for microsurgical revision, and occasional partial or total flap loss, reflecting the inherent complexity of free flap surgery (3,13,36). Minor complications are more frequent and typically mild, including seroma, hematoma, wound-healing disturbances, and occasional fat necrosis. Compared with LVA, VLNT also entails longer operative times and a more extended postoperative hospital stay (13,31,35).

SAL

SAL is a reductive surgical technique that removes the excess fibro-adipose tissue characteristic of long-standing lymphedema. As the disease progresses from a fluid-predominant to a fat- and fibroadipose-dominant state, SAL becomes particularly valuable for debulking pathological adipose tissue in fat-dominant or mixed fluid-fat disease (37).

This procedure achieves substantial, and often complete, volume reduction in non-pitting extremity lymphedema driven by excess adipose deposition and refractory to conservative therapy, in both primary and secondary forms, whereas evidence in lipedema remains more limited (1). In more advanced stages, SAL is mainly indicated in non-pitting, adipose-dominant, often long-standing limbs with a predominant solid fibro-adipose component and only mild fibrosis or limited trophic skin changes, particularly when previous physiologic procedures have failed to provide durable symptomatic relief despite adequate follow-up. Power-assisted techniques may further facilitate disruption of fibrotic tissue and are commonly performed under tourniquet control with tumescent infiltration to limit intraoperative blood loss (1,6,24,37).

Although most evidence for SAL originates from secondary lymphedema cohorts, particularly post-breast cancer surgery patients, the same principles apply to other forms of secondary and selected primary lymphedema with advanced fibroadipose remodeling (38,39). However, outcomes in primary lymphedema remain less well documented, reflecting its lower prevalence and heterogeneity (3).

SAL provides the most reliable and durable limb-volume reduction in late-stage, adipose-dominant lymphedema, achieving complete or near-complete normalization when combined with strict, continuous compression, with stability reported up to 5–7 years. Beyond debulking hypertrophied adipose tissue, sustained reductions in both adipose and lean compartments have been observed, without major complications or further deterioration of lymph transport capacity (37,38,40-42). SAL yields high percentage volume reductions in both upper and lower extremities, decreases cellulitis recurrence, and improves range of motion, mobility, and performance of activities of daily living, translating into better hygiene, aesthetic appearance, and overall quality of life (37-39). Patient-reported outcomes also show improvements in pain, heaviness, perceived swelling, self-consciousness, anxiety, and emotional well-being, while infection rates can drop to as low as 0.2–0.3 episodes per year in primary and secondary lymphedema (39).

Despite its substantial benefits in volume reduction and symptom control, SAL also carries important limitations. It has the major disadvantages of requiring sustained, often lifelong, high-pressure compression to prevent recurrence of swelling (24,37-39). Postoperatively, continuous compression is recommended, typically starting with multilayer bandaging and transitioning to custom-made garments delivering 50–80 mmHg, worn around the clock and refitted several times during the first year as limb volume decreases (39). Because SAL does not restore lymphatic function, long-term outcomes remain closely dependent on adherence to compression, which may be difficult due to cost, discomfort, and climatic factors (24,37,38).

Hybrid and sequential approaches

Hybrid strategies combining LVA and SAL are particularly suited to mixed lymphedema phenotypes, where residual functional collectors coexist with a prominent fibroadipose component. In these patients, single-stage procedures that pair liposuction with LVA have been shown to achieve meaningful and durable limb-volume reduction, decrease cellulitis or lymphangitis episodes, and may shorten the duration of postoperative compression therapy, especially in intermediate to advanced stages of disease (37,43,44).

VLNT combined with SAL offers a rational option for chronic, more advanced lymphedema, as excisional procedures alone debulk adipose and fibrotic tissue but do not correct lymphatic dysfunction, leaving a persistent risk of recurrence (24). In contrast, hybrid VLNT-liposuction strategies have shown consistent early limb-volume reduction, improved infection control, and potentially better maintenance of postoperative outcomes compared with either VLNT or liposuction alone, particularly in stage II–III disease (45,46).

Some centers adopt a staged strategy that exploits the different temporal effects of each procedure, performing LVA first to provide immediate decompression by diverting lymphatic fluid into the venous system, and reserving VLNT for a subsequent stage to achieve more durable, lymphangiogenesis-driven restoration of lymphatic function (47). This sequencing leverages the distinct temporal profiles and mechanisms of both procedures and has been associated with meaningful reductions in limb volume and improved quality of life in patients with secondary upper and lower extremity lymphedema (48).

Table 2 summarizes surgical options based on a phenotype-driven selection framework, detailing primary indications, disease phenotypes, mechanisms of action, and clinical outcomes for both stand-alone and hybrid procedures.

Conventional and preventive treatment

CDT remains the cornerstone of lymphedema management worldwide. This two-phase approach includes an intensive phase with manual lymphatic drainage (MLD), multilayer bandaging, skin care, and exercise, followed by maintenance with low-stretch garments (20–60 mmHg) and ongoing MLD as needed (1,15). MLD consists of gentle, proximal-to-distal massage of lymphedematous tissue, starting centrally and progressing peripherally, avoiding deep tissue manipulation to protect lymphatic structures (49).

Preventive surgical strategies complement conservative management. The LYMPHA technique (Lymphatic Microsurgical Preventive Healing Approach), typically performed during axillary lymph node dissection for breast cancer, anastomoses divided arm lymphatics to nearby axillary veins using supermicrosurgery, reducing lymphedema incidence from 30% to 4% at 18 months in the original prospective study. This intraoperative approach preserves arm lymphatic drainage without oncologic risk, as arm lymphatics remain distinct from breast drainage pathways (50).

Postoperative management

Postoperative management represents a critical determinant of surgical success in lymphedema surgery and should be considered an integral component of treatment rather than an adjunctive measure. Regardless of the procedure performed, patients require structured follow-up, coordinated physiotherapy, and gradual adaptation of compression therapy.

After LVA, many centers apply immediate postoperative compression to enhance lymphatic flow through anastomoses (51), while others delay 3–5 days to prevent collapse of fragile anastomoses. Limb elevation and gentle mobilization are encouraged. Compression garments are progressively reintroduced after the first postoperative week, typically starting with low-pressure garments and gradually returning to preoperative levels over 2–4 weeks. MLD may be resumed after wound healing, usually at 2 weeks.

Following VLNT, postoperative management differs because lymphangiogenesis and lymphatic reconnection require time to develop. Patients typically continue compression therapy initially, but progressive reduction can be considered over several months depending on clinical evolution. Physiotherapy is reintroduced cautiously to avoid excessive pressure over the transferred nodes. Improvement is generally gradual and may continue for 12–24 months (7,22).

After SAL, strict lifelong compression therapy is mandatory to maintain volume reduction. Unlike physiologic procedures, SAL does not restore lymphatic drainage; therefore, postoperative management focuses on maintaining mechanical control of interstitial fluid accumulation. Early ambulation is encouraged, and compression garments are worn continuously during the first postoperative months, followed by daytime use long term.

Long-term follow-up includes monitoring limb volume, infection episodes, and patient-reported outcomes. Multidisciplinary management involving surgeons, physiotherapists, and specialized nurses significantly improves stability of results and patient adherence (24,52-54).

Based on these considerations, a decision tree summarizing the proposed therapeutic algorithm is presented in Figure 1.

Figure 1 Algorithmic flow chart for surgical decision-making in lymphedema. CDT, complex decongestive therapy; ICG, indocyanine green; LVA, lymphovenous anastomosis; QoL, quality of life; SAL, suction-assisted lipectomy; VLNT, vascularized lymph node transfer.

Outcomes and comparison of surgical strategies

The effectiveness of lymphedema surgery varies according to disease stage, lymphatic function, and tissue composition. When interpreting surgical outcomes, it is essential to distinguish between lymphedema etiologies. BCRL, the most extensively studied subgroup, consistently demonstrates favorable outcomes after physiologic procedures due to its acquired nature and preserved proximal lymphatic architecture. In contrast, primary lymphedema often present more diffuse lymphatic abnormalities, leading to more heterogeneous surgical responses (3,7,33). Physiologic procedures such as LVA typically provide rapid symptomatic improvement, particularly in early disease. Patients often report decreased limb heaviness and fewer cellulitis episodes even when volume reduction is modest. However, in advanced fibrotic disease, outcomes are less predictable because lymphatic collectors may be absent or nonfunctional (9,11,14,24,28).

VLNT demonstrates greater benefit in moderate and advanced lymphedema, particularly in patients with recurrent infections. Improvement is slower compared with LVA but may be more durable. The mechanism is believed to involve lymphangiogenesis, restoration of lymphatic continuity, and local immunomodulatory effects. Some patients experience progressive reduction of compression requirements over time (13,31,32,34).

SAL provides the most consistent limb volume reduction in adipose-dominant disease. However, it does not restore lymphatic function and therefore requires lifelong compression. For this reason, SAL is best considered a volume-reduction procedure rather than a physiologic reconstruction. In selected cases, combining SAL with VLNT may improve long-term maintenance by addressing both tissue hypertrophy and lymphatic dysfunction (37,39,45,46).

Long-term outcomes require cautious interpretation. LVA patency appears variable over time, with studies reporting 56.5% anastomoses still patent at 1 year but limited data beyond this timeframe (30). For VLNT, preclinical studies demonstrate lymphangiogenesis with dense lymphatic networks forming around engrafted nodes, confirmed by ICG lymphography and histology showing vessel regeneration (55). SAL achieves reliable volume reduction but requires lifelong compression when used without physiologic procedures (39).

Overall, the choice of procedure should not rely solely on clinical stage but on identification of the dominant disease component. Fluid-predominant disease favors LVA, mixed disease may benefit from combined approaches, and adipose-predominant disease requires reductive surgery (54,56).

Limitations of current evidence

Interpretation of the lymphedema surgery literature remains challenging due to heterogeneity in study design and outcome reporting. Most available studies are retrospective and involve relatively small patient cohorts. Randomized controlled trials are rare, and standardized outcome measures are lacking.

Short-term vs. long-term success varies significantly across procedures. LVA achieves early volume reduction that remains stable long-term when initial patency is established, though late occlusion remains possible (57). VLNT neolymphangiogenesis requires prolonged maturation with uncertain long-term durability (55). SAL volume reduction depends on lifelong compression adherence (39).

Combined surgical-conventional approaches represent the current standard, as isolated surgery fails to address lymphedema’s multifactorial pathophysiology. CDT remains essential for maintenance across all techniques, emphasizing multidisciplinary management over surgery alone (1).

In addition, measurement methods vary widely among studies, including circumferential measurements, volumetric analysis, imaging findings, and patient-reported outcomes. The absence of uniform reporting standards makes comparison between techniques difficult and limits the ability to establish evidence-based guidelines.

Another limitation concerns imaging interpretation. Although ICG lymphography has become widely used, classification systems and decision thresholds are not universally standardized, leading to variability in surgical indication between centers.

Future research should focus on prospective multicenter studies, standardized outcome reporting, and long-term follow-up to better define indications and optimize patient selection (58).

Conclusions

This review synthesizes current evidence on lymphedema pathophysiology, diagnostic workup, and surgical management, proposing a structured algorithmic approach that integrates clinical phenotyping, functional imaging (ICG lymphography, MR lymphangiography, ultrasound, lymphoscintigraphy), and tissue composition analysis to guide individualized therapy. Early fluid-predominant phenotypes (ISL Stage I–early II) benefit most from physiologic procedures like LVA and VLNT, achieving rapid volume reduction, symptom relief, and decreased cellulitis rates through restoration of lymphatic drainage. Advanced adipose-dominant disease (late Stage II–III) requires reductive interventions such as SAL for durable debulking of fibro-adipose tissue, necessitating lifelong compression. Hybrid and sequential strategies combining physiologic reconstruction with reductive techniques optimize outcomes in mixed phenotypes, particularly when guided by preoperative imaging to identify functional lymphatics. Multidisciplinary postoperative care—encompassing compression therapy, MLD, and long-term monitoring—ensures result stability and enhances quality-of-life gains. By shifting from stage-based to phenotype-driven decision-making, this framework improves patient selection, treatment reproducibility, and long-term functional recovery in both primary and secondary lymphedema.

Acknowledgments

None.

Footnote

Provenance and Peer Review: This article was commissioned by the Guest Editor (Ayush Kapila) for the series “Innovations in Breast Surgery” published in Annals of Breast Surgery. The article has undergone external peer review.

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://abs.amegroups.com/article/view/10.21037/abs-2026-0014/rc

Peer Review File: Available at https://abs.amegroups.com/article/view/10.21037/abs-2026-0014/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://abs.amegroups.com/article/view/10.21037/abs-2026-0014/coif). The series “Innovations in Breast Surgery” was commissioned by the editorial office without any funding or sponsorship. The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. The diagnosis and treatment of peripheral lymphedema: 2020 Consensus Document of the International Society of Lymphology. Lymphology 2020;53:3-19.
2. Rockson SG. Update on the biology and treatment of lymphedema. Curr Treat Options Cardiovasc Med 2012;14:184-92. [Crossref] [PubMed]
3. Gaxiola-García MA, Escandón JM, Manrique OJ, et al. Surgical Treatment for Primary Lymphedema: A Systematic Review of the Literature. Arch Plast Surg 2024;51:212-33. [Crossref] [PubMed]
4. Sheikh-Oleslami S, Baharmand I, Khorrami A, et al. A review of the heterogeneity of clinical lymphoedema scoring systems. J Lymphoedema 2025;20:74-83.
5. Szuba A, Rockson SG. Lymphedema: classification, diagnosis and therapy. Vasc Med 1998;3:145-56. [Crossref] [PubMed]
6. Ciudad P, Escandón JM, Manrique OJ, et al. Lessons Learnt from an 11-year Experience with Lymphatic Surgery and a Systematic Review of Reported Complications: Technical Considerations to Reduce Morbidity. Arch Plast Surg 2022;49:227-39. [Crossref] [PubMed]
7. Yesantharao PS, Nguyen DH. Lymphedema surgery in breast cancer patients: a systematic review of preoperative evaluation and surgical planning. Ann Breast Surg 2024;8:28.
8. Rockson SG, Rivera KK. Estimating the population burden of lymphedema. Ann N Y Acad Sci 2008;1131:147-54. [Crossref] [PubMed]
9. Greene AK, Goss JA. Diagnosis and Staging of Lymphedema. Semin Plast Surg 2018;32:12-6. [Crossref] [PubMed]
10. Connell FC, Gordon K, Brice G, et al. The classification and diagnostic algorithm for primary lymphatic dysplasia: an update from 2010 to include molecular findings. Clin Genet 2013;84:303-14. [Crossref] [PubMed]
11. Forte AJ, Khan N, Huayllani MT, et al. Lymphaticovenous Anastomosis for Lower Extremity Lymphedema: A Systematic Review. Indian J Plast Surg 2020;53:17-24. [Crossref] [PubMed]
12. Campisi C, Campisi C, Accogli S, et al. Lymphedema staging and surgical indications in geriatric age. BMC Geriatr 2010;10:A50.
13. Kappos EA, Fabi A, Halbeisen FS, et al. Vascularized lymph node transfer (VLNT) versus lymphaticovenous anastomosis (LVA) for chronic breast cancer-related lymphedema (BCRL): a retrospective cohort study of effectiveness over time. Breast Cancer Res Treat 2025;210:319-27. [Crossref] [PubMed]
14. Hahn BA, Kleeven A, Richir MC, et al. Objectifying Clinical Outcomes After Lymphaticovenous Anastomosis and Vascularized Lymph Node Transfer in the Treatment of Extremity Lymphedema: A Systematic Review and Meta-Analysis. Microsurgery 2025;45:e70050. [Crossref] [PubMed]
15. Keast DH, Despatis M, Allen JO, Brassard A. Chronic oedema/lymphoedema: under-recognised and under-treated. Int Wound J 2015;12:328-33. [Crossref] [PubMed]
16. Du X, Liu C. Application of imaging in lymphedema surgical therapies. Gland Surg 2020;9:582-8. [Crossref] [PubMed]
17. Kondra K, Stanton E, Salibian AA, Patel KM. Imaging in lymphedema management: a narrative review of preoperative assessment & surgical planning. Ann Breast Surg 2024;8:5.
18. Yamamoto T, Narushima M, Yoshimatsu H, et al. Indocyanine green velocity: lymph transportation capacity deterioration with progression of lymphedema. Ann Plast Surg 2013;71:591-4. [Crossref] [PubMed]
19. Suehiro K, Morikage N, Murakami M, et al. Subcutaneous tissue ultrasonography in legs with dependent edema and secondary lymphedema. Ann Vasc Dis 2014;7:21-7. [Crossref] [PubMed]
20. Piyaman P, Sitthinamsuwan P, Apichonbancha S, et al. Assessing subcutaneous changes in lymphedema by subcutaneous tissue ultrasonography and pathological association. Sci Rep 2025;15:15516. [Crossref] [PubMed]
21. Cho MJ, Chratian S, Visconti G, et al. Ultra high-frequency ultrasound in lymphatic surgery: the next frontier. Expert Rev Med Devices 2024;21:995-8. [Crossref] [PubMed]
22. Unno N, Nishiyama M, Suzuki M, et al. Quantitative lymph imaging for assessment of lymph function using indocyanine green fluorescence lymphography. Eur J Vasc Endovasc Surg 2008;36:230-6. [Crossref] [PubMed]
23. Koshima I, Narushima M, Yamamoto Y, et al. Recent advancement on surgical treatments for lymphedema. Ann Vasc Dis 2012;5:409-15. [Crossref] [PubMed]
24. de Sire A, Losco L, Lippi L, et al. Surgical Treatment and Rehabilitation Strategies for Upper and Lower Extremity Lymphedema: A Comprehensive Review. Medicina (Kaunas) 2022;58:954. [Crossref] [PubMed]
25. Campisi C, Bellini C, Campisi C, et al. Microsurgery for lymphedema: clinical research and long-term results. Microsurgery 2010;30:256-60. [Crossref] [PubMed]
26. Zapata-Ospina A, Lopera-Muñetón C, Betancur-Bedoya SP, et al. Effectiveness of Lymphovenular Anastomosis and Complex Decongestive Therapy for the Treatment of Lymphedema in Patients with Breast Cancer: A Systematic Review. Lymphat Res Biol 2024;22:232-40. [Crossref] [PubMed]
27. Huang A, Chang DW. Lymphovenous bypass. Ann Breast Surg 2024;8:6.
28. Verhey EM, Kandi LA, Lee YS, et al. Outcomes of Lymphovenous Anastomosis for Lower Extremity Lymphedema: A Systematic Review. Plast Reconstr Surg Glob Open 2022;10:e4529. [Crossref] [PubMed]
29. Bowman C, Hircock C, Haykal S. A Prospective Study of the Impact of Lymphatic Venous Anastomosis as a Treatment for Lymphedema. Plast Reconstr Surg Glob Open 2025;13:e7088. [Crossref] [PubMed]
30. Winters H, Tielemans HJP, Verhulst AC, et al. The Long-term Patency of Lymphaticovenular Anastomosis in Breast Cancer-Related Lymphedema. Ann Plast Surg 2019;82:196-200. [Crossref] [PubMed]
31. Ozturk CN, Ozturk C, Glasgow M, et al. Free vascularized lymph node transfer for treatment of lymphedema: A systematic evidence based review. J Plast Reconstr Aesthet Surg 2016;69:1234-47. [Crossref] [PubMed]
32. Schaverien MV, Badash I, Patel KM, et al. Vascularized Lymph Node Transfer for Lymphedema. Semin Plast Surg 2018;32:28-35. [Crossref] [PubMed]
33. Moon KC, Kim HK, Lee TY, et al. Vascularized lymph node transfer for surgical treatments of upper versus lower extremity lymphedema. J Vasc Surg Venous Lymphat Disord 2022;10:170-8. [Crossref] [PubMed]
34. Ciudad P, Escandón JM, Duarte-Bateman D, et al. Surgical management of breast cancer-related lymphedema: a narrative review of contemporary practices. Ann Transl Med 2023;11:418. [Crossref] [PubMed]
35. Almeida A, Ofir H, Zeltzer AA. The lymphatic system—a surgeon’s point of view. Lymphatics 2023;1:220-36.
36. MacKenzie EL, Huang A, Cho MJ, et al. Physiologic lymphedema surgery: current treatments and future trends. Lymphatics 2025;3:35.
37. Zurbuchen EA, Yu N, Salibian AA. Modern approaches to lymphatic surgery: a narrative review. Transl Breast Cancer Res 2025;6:6. [Crossref] [PubMed]
38. Boyages J, Kastanias K, Koelmeyer LA, et al. Liposuction for Advanced Lymphedema: A Multidisciplinary Approach for Complete Reduction of Arm and Leg Swelling. Ann Surg Oncol 2015;22:S1263-70. [Crossref] [PubMed]
39. Forte AJ, Huayllani MT, Boczar D, et al. Lipoaspiration for the Treatment of Lower Limb Lymphedema: A Comprehensive Systematic Review. Cureus 2019;11:e5913. [Crossref] [PubMed]
40. Karlsson T, Hoffner M, Ohlin K, et al. Complete Reduction of Leg Lymphedema after Liposuction: A 5-Year Prospective Study in 67 Patients without Recurrence. Plast Reconstr Surg Glob Open 2023;11:e5429. [Crossref] [PubMed]
41. Karlsson T, Mackie H, Koelmeyer L, et al. Liposuction for Advanced Lymphedema in a Multidisciplinary Team Setting in Australia: 5-Year Follow-Up. Plast Reconstr Surg 2024;153:482-91. [Crossref] [PubMed]
42. Brorson H. Liposuction in arm lymphedema treatment. Scand J Surg 2003;92:287-95. [Crossref] [PubMed]
43. Gabriele G, Nigri A, Chisci G, et al. Combination of Supramicrosurgical Lymphatico-Venular Anastomosis (sLVA) and Lymph-Sparing Liposuction in Treating Cancer-Related Lymphedema: Rationale for a Regional One-Stage Approach. J Clin Med 2024;13:2872. [Crossref] [PubMed]
44. Ciudad P, Manrique OJ, Bustos SS, et al. Single-stage VASER-assisted liposuction and lymphatico-venous anastomoses for the treatment of extremity lymphedema: a case series and systematic review of the literature. Gland Surg 2020;9:545-57. [Crossref] [PubMed]
45. Forte AJ, Huayllani MT, Boczar D, et al. Lipoaspiration and Lymph Node Transfer for Treatment of Breast Cancer-related Lymphedema: A Systematic Review. Cureus 2019;11:e6096. [Crossref] [PubMed]
46. Wei M, Wang L, Wu X, et al. Synchronous supraclavicular vascularized lymph node transfer and liposuction for gynecological cancer-related lower extremity lymphedema: A clinical comparative analysis of three different procedures. J Vasc Surg Venous Lymphat Disord 2024;12:101905. [Crossref] [PubMed]
47. Park JK, Myung Y. Combination of lymphovenous anastomosis and lymph node transfer for breast cancer-related lymphedema. Plast Aesthet Res 2023;10:40.
48. Chang DW. Combined Approach to Surgical Treatment of Lymphedema. Lymphat Res Biol 2021;19:23-4. [Crossref] [PubMed]
49. Senger JB, Kadle RL, Skoracki RJ. Current Concepts in the Management of Primary Lymphedema. Medicina (Kaunas) 2023;59:894. [Crossref] [PubMed]
50. Boccardo FM, Casabona F, Friedman D, et al. Surgical prevention of arm lymphedema after breast cancer treatment. Ann Surg Oncol 2011;18:2500-5. [Crossref] [PubMed]
51. Chen WF, Bowen M, Ding J. Immediate limb compression following supermicrosurgical lymphaticovenular anastomosis – is it helpful or harmful? Int Microsurg J 2018;2:1.
52. Sacks J, Riley B, Doubblestein D, et al. Expert-consensus on lymphedema surgeries: candidacy, prehabilitation, and postoperative care. Med Oncol 2024;41:266. [Crossref] [PubMed]
53. Flores AM, Fu MR, Bock KJ, et al. Post-operative care for patients following surgical treatment of lymphedema. Med Oncol 2024;41:296. [Crossref] [PubMed]
54. Farid Y, Pozzi M, Bolletta A, et al. Effective Management Strategies for Primary Lymphedema of the Lower Extremities: Integrating Conservative and Surgical Therapies in Early and Late Stages. Microsurgery 2025;45:e70014. [Crossref] [PubMed]
55. Kim KM, Kim KY. Lymphangiogenesis after nonvascularized lymph node transplantation: Lymphangiographic findings in mice and minipigs. PLoS One 2023;18:e0295836. [Crossref] [PubMed]
56. Pozzi M, Seclì DD, Bolletta A, et al. Gastroepiploic Vascularized Lymph Node Transfer for Extremity Lymphedema: Tips and Insights from Extensive Clinical Experience. Medicina (Kaunas) 2025;61:503. [Crossref] [PubMed]
57. Lee KT, Park JW, Mun GH. Serial two-year follow-up after lymphaticovenular anastomosis for the treatment of lymphedema. Microsurgery 2017;37:763-70. [Crossref] [PubMed]
58. Meuli JN, Guiotto M, Elmers J, et al. Outcomes after microsurgical treatment of lymphedema: a systematic review and meta-analysis. Int J Surg 2023;109:1360-72. [Crossref] [PubMed]