The Effect of TECAR Therapy and Extracorporeal Shock Wave Therapy Combined With Complex Decongestive Therapy in the Treatment of Bilateral Lower-Limb Secondary Lymphedema in Severely Obese Patients: A Randomized Controlled Trial
Phase: NA
Conditions: Lymphedema, Obesity & Overweight
Sponsor: Applied Science Private University

The Effect of TECAR Therapy, Extracorporeal Shock Wave Therapy and Complete Decongestive 
Therapy in the Treatment of Bilateral Lower-Limb Secondary Lymphedema in Severely Obese Patients: 
A Prospective Randomized Controlled Study 
Abstract 
Background: Lymphedema associated with severe obesity is a progressive condition characterized by bilateral 
lower-limb swelling, functional impairment and reduced quality of life. Complex Decongestive Therapy (CDT) 
remains the standard treatment, but its effectiveness in obesity-related lymphedema is limited. Adjunctive 
therapies such as Transfer Energy Capacitive and Resistive therapy (TECAR) and Extracorporeal Shock Wave 
Therapy (ESWT) may enhance outcomes by targeting distinct pathophysiological mechanisms. 
Objective: To compare the effectiveness of CDT alone versus CDT combined with TECAR or ESWT in reducing 
limb circumference, improving quality of life, alleviating pain and decreasing tissue stiffness in severely obese 
patients with bilateral lower-limb lymphedema. 
Methods: In this prospective randomized controlled trial, 45 female patients (BMI ≥40 kg/m²) with bilateral 
lower-limb lymphedema were allocated to CDT alone, CDT+TECAR, or CDT+ESWT groups (n=15 each). All 
groups received standardized CDT protocols for 4 weeks. TECAR was applied five times weekly, while ESWT 
was delivered three times weekly. Outcomes included limb circumference, Lymphedema Quality of Life 
Questionnaire (LYMQOL), pain intensity (VAS), and tissue stiffness (tonometry), assessed at baseline, 4 weeks, 
and 8 weeks. Data were analyzed using two-way mixed ANOVA (Group × Time) with Greenhouse-Geisser 
correction, followed by Bonferroni-adjusted post-hoc comparisons. Effect sizes (partial eta squared and Cohen's 
d) and 95% confidence intervals were reported. 
Results: A significant Group × Time interaction was observed for all outcomes (p < 0.001). For left ankle 
circumference, the mean reduction from baseline to 4 weeks was −2.82 cm (95% CI: −2.88, −2.76) in CDT, −3.92 
cm (95% CI: −3.99, −3.85) in CDT+TECAR, and −4.51 cm (95% CI: −4.60, −4.43) in CDT+ESWT (interaction 
ηp² = 0.957). Between-group effect sizes at 4 weeks were large (Cohen's d: CDT vs CDT+ESWT = 1.83; CDT 

vs CDT+TECAR = 1.37). VAS pain reduction was significantly greater in CDT+ESWT versus CDT (mean 
difference = 0.83, 95% CI: 0.66–1.01, d = 3.54). Overall LYMQOL improvement favored CDT+ESWT over 
CDT (d = 7.29). Benefits were sustained at 8 weeks, though modest deterioration was observed. No serious 
adverse events occurred. 
Conclusion: Both TECAR and ESWT significantly enhance CDT outcomes in severely obese patients with 
bilateral lower-limb lymphedema. ESWT demonstrated the most pronounced benefits with large effect sizes, 
suggesting its potential as a preferred adjunctive therapy. These findings support integrating adjunctive modalities 
into standard CDT protocols to optimize outcomes in this challenging patient population. 
Trial Registration: [Reg. No. SREC.PT.SUE (19) 1025]; date of registration: 25/10/2025. 
Keywords: Secondary lymphedema; Severe obesity; Complex decongestive therapy; Extracorporeal shock wave 
therapy; Transfer energy capacitive and resistive therapy 
 
 

Background 
 
Lymphedema is a chronic, progressive condition characterized by protein-rich fluid accumulation, limb swelling, 
functional impairment, and reduced quality of life [1]. While cancer-related lymphedema has been extensively 
studied, obesity-associated lymphedema remains underrecognized despite its rising prevalence. Severe obesity 
both predisposes to lymphatic dysfunction and worsens treatment outcomes once lymphedema develops [2,3]. 
Prevalence increases sharply with body mass index, affecting around 6% of individuals with BMI <50 kg/m² and 
nearly 90% of those with BMI ≥60 kg/m² [4]. Unlike the typically unilateral presentation of cancer-related 
lymphedema, obesity-related disease is usually bilateral, creating distinct therapeutic challenges [5]. 
Complex decongestive therapy (CDT) is the gold standard treatment across etiologies [6]. This multimodal 
approach, including manual lymphatic drainage, compression bandaging, exercise and skin care, has proven 
efficacy but limited effectiveness in obesity-related lymphedema. Obese patients often show reduced response, 
with some reverting to baseline volumes within one year [7,8]. Pathophysiological features such as chronic 
inflammation, tissue fibrosis, and adipose deposition further compromise CDT outcomes [9]. 
Adjunctive therapies have therefore gained attention. Transfer energy capacitive and resistive therapy (TECAR) 
delivers radiofrequency energy to generate endogenous tissue heating, promoting vasodilation, microcirculation, 
and potentially lymphatic drainage [10]. Preliminary studies suggest TECAR achieves faster volume reduction 
than manual drainage, though controlled trials remain scarce [11]. Extracorporeal shock wave therapy (ESWT), 
widely used in musculoskeletal disorders, stimulates lymphangiogenesis via VEGF-C/VEGFR-3 upregulation 
and reduces fibrosis through collagen modulation [12–16]. Clinical studies in breast cancer-related lymphedema 
report sustained volume reduction and tissue softening, but evidence in obesity-related lower-limb disease is 
limited. 
Obesity-related lymphedema is increasingly recognized as a separate clinical condition in which excessive body 
weight contributes to a gradual decline in lymphatic system function. Evidence from clinical assessment and 

imaging studies indicates a reduction in lymphatic drainage capacity that correlates with rising body mass index. 
The disorder typically manifests with bilateral involvement of the lower extremities and is often difficult to 
manage, especially in individuals with advanced obesity [17]. 
Lymphedema is a long-standing, progressive disorder characterized not only by fluid retention but also by 
irreversible structural alterations within the affected tissues. Ongoing impairment of lymphatic function promotes 
chronic inflammation, increased fat accumulation, and fibrotic changes leading to reduced tissue elasticity and 
diminished response to conventional decongestive treatment. These pathological changes tend to be more severe 
in late-stage disease and in cases associated with obesity [18]. 
However, most studies focus on upper-limb cancer-related lymphedema; comparative effectiveness data are 
lacking, and objective assessment of tissue quality has been underexplored. Therefore, this trial was designed to 
address these gaps by comparing CDT alone with CDT combined with TECAR or ESWT in severely obese 
patients with bilateral lower-limb lymphedema. Both adjunctive therapies were expected to enhance outcomes 
beyond standard complex decongestive therapy, with primary emphasis on limb circumference reduction and 
secondary outcomes including quality of life, pain intensity, and tissue stiffness. The results are anticipated to 
contribute to clinical decision-making and to advance understanding of optimal therapeutic strategies for patients 
with obesity-related bilateral lower-limb lymphedema. 
 
 

Methods 
Study Design and Participants 
This prospective randomized controlled trial was conducted between 25 October 2025 and 6 February 2026 at 
Modawah Physical Therapy Center, Beni Suef, Egypt. The study protocol received approval from the institutional 
ethics committee, and all participants provided written informed consent prior to enrollment. The trial was 
registered at Al Salam University, Faculty of Physical Therapy, Scientific Research Ethics Committee under the 
identification number No: SREC.PT.SUE (19)1025. The study is reported according to the Consolidated 
Standards of Reporting Trials (CONSORT) guidelines, and the CONSORT flow diagram is presented in Figure 
5. 
Female patients aged 18–75 years with bilateral lower limb lymphedema secondary to severe obesity (BMI ≥40 
kg/m²) were eligible for inclusion. Lymphedema diagnosis required clinical assessment by an experienced 
lymphedema specialist and confirmation of bilateral limb swelling with pitting or non-pitting edema extending 
above the ankle. Additional inclusion criteria included lymphedema duration of at least 3 months and the ability 
to attend treatment sessions five times weekly for 4 weeks, plus follow-up assessments. 
Exclusion criteria encompassed secondary lymphedema due to other causes (malignancy, radiation, surgery, 
infection), primary lymphedema, acute deep vein thrombosis or history of recurrent thrombosis, active infection 
or cellulitis, peripheral arterial disease with ankle-brachial index below 0.8, uncontrolled cardiac failure or renal 
insufficiency, pregnancy or lactation, and contraindications to ESWT or TECAR therapy including pacemaker or 
other implanted electronic devices. Patients receiving concurrent lymphedema treatment or those who had 
received intensive treatment within the preceding 3 months were excluded to avoid confounding effects. 
Sample size was estimated a priori based on a between-group comparison using one-way ANOVA to detect a 
clinically meaningful difference of 1.5 cm in limb circumference reduction between groups (SD 1.2 cm, α=0.05, 
power=80%), yielding a minimum of 13 participants per group. Allowing for 15% attrition, 15 participants per 
group were recruited (total n = 45). Although the primary analysis employed a two-way mixed ANOVA, the 

sample size calculation based on between-group differences represents a conservative approach, as repeated-
measures designs typically provide greater statistical power than between-group comparisons alone due to the 
reduction in error variance achieved by accounting for within-subject correlations. 
Randomization and Blinding 
Eligible participants were randomly allocated to one of three treatment groups in a 1:1:1 ratio: CDT alone, CDT 
combined with TECAR, or CDT combined with ESWT. Randomization was performed using computer-
generated random numbers with block randomization to ensure balanced group allocation. Allocation 
concealment was maintained through sequentially numbered sealed opaque envelopes prepared by an investigator 
not involved in participant recruitment or assessment. 
Due to the nature of the interventions, therapists delivering treatment could not be blinded to group allocation. 
However, outcome assessors performing circumference measurements, tonometry, and administering 
questionnaires were blinded to treatment assignment. Participants were instructed not to discuss their treatment 
with assessors. Statistical analyses were performed by an investigator blinded to group allocation until completion 
of primary analyses. 
Interventions 
All three groups received identical complex decongestive therapy protocols following International Society of 
Lymphology consensus guidelines [1]. CDT was delivered five sessions per week for 4 weeks (a total of 20 
sessions), with each session lasting approximately 60 minutes. The treatment protocol included: skin care 
education and examination for signs of infection or skin breakdown; manual lymphatic drainage performed by 
certified lymphedema therapists using gentle, rhythmic circular movements to stimulate lymphatic flow, 
beginning proximally and progressing distally; multilayer compression bandaging using short-stretch bandages 
applied from toes to upper thigh bilaterally, worn continuously between sessions and removed only for bathing 
and subsequent treatment sessions; supervised therapeutic exercises performed while wearing compression 

bandages, including ankle pumps, knee flexion-extension, hip movements, and walking to promote muscle pump 
function; and patient education regarding self-care, risk reduction, and home exercise programs. 
The CDT+TECAR group received identical CDT protocols plus TECAR therapy delivered using a capacitive-
resistive device operating at 448 kHz frequency. TECAR was applied bilaterally to both lower limbs for 20 
minutes per limb (40 minutes total per session) immediately prior to manual lymphatic drainage. Treatment was 
delivered in capacitive mode for superficial tissues and resistive mode for deeper structures, with the applicator 
moved continuously in circular motions progressing from proximal to distal. Energy output was adjusted to 
produce gentle warmth without discomfort, maintained at comfortable thermal levels throughout treatment. 
TECAR sessions were delivered five times weekly, concurrent with CDT sessions throughout the 4-week 
intervention period. 
The CDT+ESWT group received identical CDT protocols plus extracorporeal shock wave therapy delivered using 
a radial ESWT device. Treatment was applied bilaterally to both lower limbs, targeting areas of maximum tissue 
firmness and edema. Each limb received 2000 shocks at 0.10–0.15 mJ/mm² energy density and 8–10 Hz 
frequency, distributed across ankle, calf, and thigh regions. ESWT was delivered three times weekly (sessions 1, 
3, and 5 of each week) for the 4-week intervention period, immediately prior to CDT. Treatment areas included 
medial and lateral aspects of the ankle, anterior and posterior calf, and anterior and posterior thigh bilaterally. 
Following completion of the 4-week intensive phase, all participants received standardized education regarding 
self-care and were fitted for custom compression garments to maintain treatment gains. Participants were 
instructed to wear compression stockings daily and perform self-manual lymphatic drainage. Compression 
bandaging was discontinued after the intensive phase. 
Outcome Measures 
All outcome assessments were performed at three time points: baseline (T0, prior to treatment initiation), 4 weeks 
(T1, immediately following completion of the 4-week intensive phase), and 8 weeks (T2, four weeks after 
cessation of intensive treatment). 

Primary Outcome: The primary outcome was the change in limb circumference measured at standardized 
anatomical landmarks bilaterally. Measurements were obtained with participants in the supine position after 10 
minutes of rest, using a flexible non-stretch tape measure. Circumferences were recorded at the following sites 
on both lower limbs: ankle (10 cm proximal to lateral malleolus), calf (widest circumference of gastrocnemius), 
knee (at mid-patella), mid-thigh (20 cm proximal to superior pole of patella), and upper-thigh (10 cm distal to 
inguinal crease). All measurements were performed by the same trained assessor, blinded to treatment allocation, 
with the average of two measurements recorded for each site. The assessor underwent reliability training, 
achieving an intraclass correlation coefficient ≥0.95 for all measurement sites. 
Secondary Outcomes: Lymphedema-specific quality of life was assessed using the Lymphedema Quality of Life 
Questionnaire (LYMQOL) for the lower limb [19]. This validated instrument comprises 28 items across four 
domains: Function, Appearance, Symptoms, and Mood, plus an overall quality of life item. Each item is scored 
on a 4-point scale (1 = not at all to 4 = a lot), with domain scores calculated by summing items and dividing by 
the number of questions answered. Higher scores indicate poorer quality of life. For analysis, scores were 
converted to a 1–10 scale, where lower values represent a better quality of life. The LYMQOL has demonstrated 
good internal consistency and test–retest reliability for lower limb lymphedema [20]. 
Pain intensity was measured using a 10 cm Visual Analog Scale anchored at 0 (no pain) and 10 (worst imaginable 
pain). Participants marked their current lower limb pain level on the horizontal line, with distance from zero 
measured in centimeters to generate the pain score. 
Tissue stiffness was quantified using tonometry at four sites bilaterally: left calf, right calf, left thigh, and right 
thigh. Tonometry was performed using a validated tissue tonometer device with standardized weight application. 
Measurements were taken at the point of maximum tissue firmness within each region, identified through 
palpation. The tonometer was applied perpendicular to the skin surface, and three measurements were obtained 
at each site with the median value recorded. Higher tonometry values indicate greater tissue stiffness. All 
tonometry measurements were performed by the same blinded assessor who underwent standardized training. 

Adverse events were systematically recorded throughout the study period, with participants specifically queried 
about skin reactions, pain, discomfort, or any other symptoms at each treatment session and assessment visit. 
Statistical Analysis 
Data were analyzed using SPSS version 25 statistical software. Descriptive statistics included means and standard 
deviations for continuous variables and frequencies with percentages for categorical variables. Baseline 
characteristics were compared across the three groups using one-way analysis of variance (ANOVA) for 
continuous variables and chi-square tests for categorical variables. 
The primary analysis employed a two-way mixed-design ANOVA (Group × Time) to evaluate treatment effects. 
The between-subjects factor was treatment group (CDT, CDT+TECAR, CDT+ESWT) and the within-subjects 
factor was time (baseline T0, 4 weeks T1, 8 weeks T2). This approach appropriately accounts for the repeated-
measures structure, correlated observations, and enables direct testing of the Group × Time interaction effect, 
which indicates whether treatment groups differ in their trajectories of change over time. 
Assumption testing included the Shapiro-Wilk test for normality of residuals, Levene's test for homogeneity of 
variances, and assessment of sphericity using the Greenhouse-Geisser epsilon. Where the sphericity assumption 
was violated (ε < 0.75), Greenhouse-Geisser corrected degrees of freedom and p-values were reported. Normality 
was confirmed for 97.2% of all group-by-time distributions (Shapiro-Wilk p > 0.05). 
Significant Group × Time interactions were followed by Bonferroni-adjusted post-hoc pairwise comparisons 
between treatment groups at each time point using independent-samples t-tests. Three pairwise comparisons were 
conducted at each time point: CDT versus CDT+TECAR (p1), CDT versus CDT+ESWT (p2), and CDT+TECAR 
versus CDT+ESWT (p3). 
Effect sizes were reported as partial eta squared (ηp²) for mixed ANOVA effects, interpreted as small (0.01), 
medium (0.06), and large (≥0.14), and as Cohen's d for between-group pairwise comparisons, interpreted as small 
(0.2), medium (0.5), and large (≥0.8). The 95% confidence intervals (CIs) were calculated for group means and 
mean differences between groups. Statistical significance was set at p < 0.05 for all analyses. All analyses 

followed intention-to-treat principles, with all randomized participants included in the analysis groups to which 
they were assigned. 
 
 

Results 
Participant Characteristics 
A total of 62 patients were assessed for eligibility, of whom 17 were excluded (9 did not meet inclusion criteria, 
5 declined to participate, and 3 were excluded for other reasons). The remaining 45 patients with bilateral lower 
limb lymphedema secondary to severe obesity were randomized between 25 October 2025 and 6 February 2026 
(Figure 5, CONSORT flow diagram). All participants completed the 4-week intervention period and attended the 
8-week follow-up assessment, with no dropouts or loss to follow-up. 
The baseline demographic and clinical characteristics of participants are summarized in Table 1. The three 
treatment groups were comparable at baseline with respect to age, gender, body mass index, height, and weight 
(p > 0.05 for all comparisons). Similarly, no significant differences were observed between groups in baseline 
circumference measurements, LYMQOL scores, VAS pain, or tissue stiffness at all measurement sites (p > 0.05 
for all comparisons). 
Primary Outcome: Limb Circumference Reduction 
Two-way mixed ANOVA revealed significant Group × Time interaction effects for all limb circumference 
measurements, indicating that treatment groups differed significantly in their patterns of change over time. For 
left ankle circumference, the interaction effect was F(4, 84) = 464.06, p < 0.001, ηp² = 0.957 (large effect). Similar 
large interaction effects were observed at all other anatomical sites, with ηp² values ranging from 0.949 (left mid-
thigh) to 0.989 (right calf) (Table 2). 
At 4 weeks post-treatment, the mean reductions in left ankle circumference from baseline were −2.82 cm (95% 
CI: −2.88, −2.76) in the CDT group, −3.92 cm (95% CI: −3.99, −3.85) in the CDT+TECAR group, and −4.51 cm 
(95% CI: −4.60, −4.43) in the CDT+ESWT group. Post-hoc pairwise comparisons confirmed that both the 
CDT+TECAR and CDT+ESWT groups achieved significantly greater circumference reductions compared to the 

CDT-only group at all anatomical points (p < 0.001). Between-group effect sizes were large: CDT versus 
CDT+TECAR, Cohen's d = 1.37; CDT versus CDT+ESWT, d = 1.83 for left ankle circumference at T1. 
Furthermore, the CDT+ESWT group demonstrated superior outcomes compared to the CDT+TECAR group at 
most measurement sites (p < 0.05), with moderate-to-large between-group effect sizes (d = 0.53 to 1.46 at T1). 
The improvements were sustained at the 8-week follow-up assessment, with the CDT+ESWT group continuing 
to show the greatest circumference reductions (Table 2, Figures 1 and 2). 
Clinical significance: While there is no universally established MCID for limb circumference in lymphedema, a 
reduction of ≥2 cm has been proposed as clinically meaningful based on prior literature. All three groups exceeded 
this threshold at all measurement sites, with the CDT+ESWT group achieving mean reductions of 3.4–11.7 cm 
depending on the anatomical site, substantially exceeding the proposed MCID. The magnitude of between-group 
differences (1.0–3.6 cm favoring CDT+ESWT over CDT alone) suggests these differences are not only 
statistically significant but also clinically relevant for functional improvement and compression garment fitting. 
Secondary Outcomes 
Quality of Life (LYMQOL): A significant Group × Time interaction was observed for all LYMQOL domains 
(p < 0.001 for all; Table 3, Figure 3). The interaction effect sizes were very large (ηp² = 0.991–0.998). At 4 weeks, 
the mean change in overall quality of life score was −1.8 ± 0.2 in CDT, −2.2 ± 0.2 in CDT+TECAR, and −2.5 ± 
0.2 in CDT+ESWT. The CDT+ESWT group achieved significantly greater improvements than both CDT (d = 
7.29, p < 0.001) and CDT+TECAR (d = 3.25, p < 0.05) across all domains. These improvements were sustained 
at 8 weeks with slight deterioration. The MCID for LYMQOL has been estimated at approximately 1.0 point; all 
groups exceeded this threshold, with CDT+ESWT achieving the largest clinically meaningful gains. 
Pain Intensity (VAS): The Group × Time interaction for VAS pain was significant (F(4, 84) = 7864.25, p < 
0.001, ηp² = 0.997). The mean reduction in VAS scores at 4 weeks was −2.5 ± 0.3 in CDT, −2.9 ± 0.3 in 
CDT+TECAR, and −3.3 ± 0.3 in CDT+ESWT. CDT+ESWT demonstrated significantly greater pain reduction 
compared to both CDT (mean difference = 0.83, 95% CI: 0.66–1.01, d = 3.54) and CDT+TECAR (mean 

difference = 0.45, 95% CI: 0.28–0.61, d = 2.05). The established MCID for VAS is approximately 1.3–2.0 cm on 
a 10-cm scale; all groups exceeded this clinically important threshold (Table 4, Figure 4). At 8-week follow-up, 
pain scores showed slight increases but remained significantly improved from baseline. 
Tissue Stiffness (Tonometry): Significant Group × Time interactions were observed for tissue stiffness at all 
measurement sites (p < 0.001; ηp² = 0.969–0.996; Table 4, Figure 4). The mean reduction in left calf tissue 
stiffness at 4 weeks was −4.5 ± 0.4 units in CDT, −5.9 ± 0.4 units in CDT+TECAR, and −6.9 ± 0.4 units in 
CDT+ESWT. CDT+ESWT achieved significantly greater reductions compared to CDT (d = 2.68, p < 0.001) and 
CDT+TECAR (d = 1.24, p < 0.01) at all sites. Improvements were sustained at 8 weeks with modest increases in 
stiffness. 
Adverse Events: No serious adverse events were reported in any treatment group. Minor adverse events included 
temporary skin redness (2 patients in CDT+TECAR, 1 in CDT+ESWT) and transient discomfort during sessions 
(3 in CDT, 2 in CDT+TECAR, 1 in CDT+ESWT). All adverse events resolved spontaneously without requiring 
treatment discontinuation. 
Discussion 
This randomized controlled trial demonstrated that both transfer energy capacitive and resistive therapy (TECAR) 
and extracorporeal shock wave therapy (ESWT) significantly enhanced the effectiveness of complex 
decongestive therapy (CDT) in severely obese patients with bilateral lower-limb lymphedema. All groups 
achieved significant reductions in limb circumference, pain intensity, tissue stiffness, and improvements in quality 
of life; however, the significant Group × Time interactions (ηp² = 0.949–0.998) confirmed that adjunctive 
therapies produced differentially superior outcomes compared to CDT alone, with ESWT showing the most 
pronounced benefits across all measured outcomes. 
According to international consensus guidelines, complex decongestive therapy remains the cornerstone of 
lymphedema management. However, its effectiveness may be limited in advanced stages of the disease and in 
patients with obesity. These challenges emphasize the need for adjunctive therapeutic modalities to enhance 

clinical outcomes and support long-term disease control [21]. The findings align with previous reports that CDT 
remains the cornerstone of lymphedema management across etiologies [6]. Nevertheless, limitations in obesity-
related lymphedema have been documented, including reduced responsiveness and recurrence of limb volume 
within one year [7,8]. The present results confirm that adjunctive modalities can overcome some of these 
limitations. 
TECAR therapy, through radiofrequency-induced vasodilation and improved microcirculation [10,11], facilitated 
greater reductions in limb circumference and tissue stiffness compared to CDT alone. The mechanism of TECAR 
involves delivery of radiofrequency energy at 448 kHz, which induces endogenous tissue heating through both 
capacitive (superficial) and resistive (deep tissue) modes. Capacitive mode generates heating predominantly in 
water-rich tissues such as muscles and the lymphatic vasculature, while resistive mode targets tissues with higher 
impedance including fibrotic tissue and adipose deposits. This dual-mode heating promotes vasodilation, 
increases local blood flow, enhances cellular metabolic activity, and may facilitate the reabsorption of interstitial 
fluid by improving both venous and lymphatic return. In the context of obesity-related lymphedema, where 
adipose tissue compression of lymphatic vessels contributes to impaired drainage, the deep tissue heating effects 
of TECAR may be particularly relevant in reducing perilymphatic tissue resistance. 
ESWT produced the largest improvements across all measured outcomes, consistent with prior evidence of its 
lymphangiogenic and anti-fibrotic effects [12–16]. The mechanistic advantage of ESWT in chronic lymphedema 
is likely multifactorial. At the molecular level, mechanical shockwaves upregulate vascular endothelial growth 
factor-C (VEGF-C) expression, which binds to VEGFR-3 receptors on lymphatic endothelial cells, stimulating 
lymphangiogenesis—the formation of new lymphatic vessels. This neolymphangiogenesis may partially restore 
lymphatic drainage capacity in regions where existing lymphatic channels have been damaged or compressed by 
excess adipose tissue. Additionally, ESWT modulates collagen turnover by upregulating matrix 
metalloproteinases (MMPs), particularly MMP-2 and MMP-9, which degrade excess extracellular matrix 
components, thereby reducing tissue fibrosis. This anti-fibrotic effect is particularly relevant in obesity-related 
lymphedema, where chronic inflammation mediated by adipokines (leptin, TNF-α, IL-6) perpetuates a cycle of 

fibrosis, adipose deposition, and further lymphatic impairment. ESWT also stimulates nitric oxide production, 
promoting vasodilation and improving microvascular perfusion in affected tissues [22,23]. The combination of 
these mechanisms—lymphangiogenesis, fibrosis reduction, and improved microcirculation—provides a 
comprehensive biological rationale for ESWT's superior performance compared to both CDT alone and 
CDT+TECAR in this trial. 
In the specific pathophysiological context of obesity-related lymphedema, excessive adipose tissue exerts 
mechanical compression on lymphatic vessels and impairs their contractile function. Adipose-derived 
inflammatory mediators further damage lymphatic endothelium and promote subendothelial fibrosis. The finding 
that both adjunctive therapies improved tissue stiffness, as measured by tonometry, suggests that targeting the 
fibrotic component of obesity-related lymphedema may be essential for optimizing treatment outcomes. The 
larger effect sizes observed for ESWT across tissue stiffness measurements support the hypothesis that its anti-
fibrotic properties confer a distinct therapeutic advantage in this population. It should be noted, however, that 
some of the Cohen’s d values reported in this study are notably large, which may be partially attributable to the 
small within-group variability observed across several outcome measures and the relatively small sample size (n 
= 15 per group). Accordingly, the mean differences and their 95% confidence intervals should be considered the 
more clinically interpretable measures of treatment effect, while the d values should be interpreted with 
appropriate caution. 
Importantly, this study extends existing literature by focusing on obesity-related bilateral lower-limb 
lymphedema, a population underrepresented in prior trials that predominantly examined breast cancer-related 
upper-limb disease [14,15]. The demonstration of efficacy in severely obese patients with large effect sizes 
(Cohen's d > 0.8 for all CDT vs CDT+ESWT comparisons) addresses a critical gap and highlights the potential 
of ESWT and TECAR as adjuncts in this challenging clinical context. 
Clinical implications include the integration of ESWT into CDT protocols, particularly for patients with advanced 
fibrosis, where its anti-fibrotic properties may yield sustained benefit. TECAR remains a valuable option, 

especially where rapid volume reduction is desired. Both modalities were well tolerated, with only minor, 
transient adverse events reported, underscoring their safety in this population. 
Limitations 
Several limitations warrant consideration and should be acknowledged for methodological transparency. First, 
the sample size was modest (n = 15 per group), and although powered for the primary outcome of circumference 
reduction, larger multicenter studies are needed to confirm generalizability and detect smaller between-group 
differences with greater precision. Second, the follow-up period was limited to 8 weeks (4 weeks post-
intervention), preventing assessment of long-term durability of treatment effects; given that obesity-related 
lymphedema is a chronic progressive condition, studies with 6–12 month follow-up are essential to determine 
whether the observed benefits are maintained. Third, the study population comprised only female patients, 
restricting extrapolation to males with obesity-related lymphedema. 
Fourth, the absence of a sham control group for TECAR and ESWT means that specific treatment effects cannot 
be fully separated from non-specific effects such as therapist attention and patient expectation. Fifth, therapists 
delivering the interventions were not blinded to treatment allocation, which may introduce performance bias, 
although outcome assessors remained blinded. Sixth, no objective imaging modalities such as lymphoscintigraphy 
or indocyanine green lymphography were employed to assess lymphatic function directly; the reliance on 
circumference measurements and tonometry, while clinically relevant, does not capture the underlying lymphatic 
structural and functional changes. Seventh, tissue fibrosis was assessed indirectly via tonometry rather than by 
elastography or histological analysis, limiting the depth of conclusions regarding fibrosis remodeling. Eighth, this 
was a single-center study, which may limit the generalizability of findings to other clinical settings and 
populations. Ninth, the trial was registered through an institutional ethics committee registry rather than an 
international public registry (e.g., ClinicalTrials.gov), and retrospective registration on a public platform is 
currently underway; this may be considered a limitation regarding registration transparency. 

Future research should evaluate longer-term outcomes, include male participants, incorporate sham control arms, 
and explore combined or sequential use of TECAR and ESWT. Objective imaging modalities such as 
lymphoscintigraphy, indocyanine green lymphography, or shear wave elastography could provide deeper insights 
into tissue remodeling, lymphatic function, and fibrosis resolution. Dose-response studies to optimize ESWT 
parameters in this population are also warranted. 
Conclusion 
Adjunctive TECAR and ESWT significantly improved outcomes beyond CDT alone in severely obese patients 
with bilateral lower-limb lymphedema, with large effect sizes across all measured outcomes. ESWT demonstrated 
the greatest benefits, consistent with its lymphangiogenic and anti-fibrotic mechanisms. The significant Group × 
Time interactions and clinically meaningful differences support the incorporation of adjunctive therapies, 
particularly ESWT, into standard CDT protocols to optimize management of obesity-related lymphedema. Larger 
multicenter trials with longer follow-up and objective imaging are needed to confirm durability and broaden 
applicability. 
 
 

Ethics Approval 
The study was conducted in accordance with the Declaration of Helsinki, and the protocol was approved by the 
Scientific Research Ethics Committee, Al Salam University. All participants provided written informed consent 
before enrollment. The trial was registered at Al Salam University under the identification number No: 
SREC.PT.SUE (19)1025, on 25.10.2025. 
Informed Consent 
Written informed consent was obtained from all participants before the start of the study. 
Consent for Publication 
All authors have reviewed the final version of the manuscript and agree to its submission. We confirm that the 
work is original, has neither been published elsewhere nor under consideration for publication in any other journal. 
Availability of Data 
The datasets used during the current study are available from the corresponding author on reasonable request. 
Competing Interests 
The authors declare no competing interests. 
Funding 
The research was funded by the Applied Science Private University, Amman, Jordan, Grant number: DRGS/2025-
13. 
Authors' Contributions 
Mostafa A Abdelhameed, Mohamed I. Mabrouk, Rama Alrawajfeh, Aseel Aburub, and Sami Elmahgoub 
contributed to the study design, data collection, data analysis, methodology development, literature review, and 
drafting of the manuscript. Shymaa M. Ali and Pongrác Ács contributed to methodology development, literature 

review, and statistical analysis, and provided critical revisions to the manuscript. Bence Cselik contributed to the 
study design and methodology, supervised the study, guided the conceptual framework, and provided important 
feedback throughout the research process. All authors read and approved the final version of the manuscript. 
Acknowledgements 
The authors would like to acknowledge the financial support provided for this research by the Applied Science 
Private University. We also acknowledge the assistance of the Rehabilitation Department and Physical Medicine 
Unit at Modawah Physical Therapy and Rehabilitation Center, which helped with the study for access to facilities. 
Trial Registration Transparency Statement 
This trial was registered with the Scientific Research Ethics Committee (SREC) at Al Salam University, Faculty 
of Physical Therapy, under the identification number SREC.PT.SUE (19)1025, on 25 October 2025. Ethical 
approval and registration were obtained prior to the commencement of data collection. The authors acknowledge 
that this registration was conducted through an institutional ethics committee registry rather than an international 
public clinical trial registry (e.g., ClinicalTrials.gov, ISRCTN). To enhance transparency and public accessibility, 
the trial is being retrospectively registered on ClinicalTrials.gov, and the full protocol and registration details will 
be made publicly available upon completion of this process. 
List of Abbreviations 
CDT: Complex Decongestive Therapy; ESWT: Extracorporeal Shock Wave Therapy; TECAR: Transfer Energy 
Capacitive and Resistive Therapy; LYMQOL: Lymphedema Quality of Life Questionnaire; VAS: Visual 
Analogue Scale; BMI: Body Mass Index; RCT: Randomized Controlled Trial; VEGF-C: Vascular Endothelial 
Growth Factor C; VEGFR-3: Vascular Endothelial Growth Factor Receptor 3; MMP: Matrix Metalloproteinase; 
MCID: Minimal Clinically Important Difference; CI: Confidence Interval; ANOVA: Analysis of Variance; 
CONSORT: Consolidated Standards of Reporting Trials. 
 
 

References 
1. Executive Committee of the International Society of Lymphology. The diagnosis and treatment of peripheral 
lymphedema: 2020 consensus document of the International Society of Lymphology. Lymphology. 2020;53(1):3-
19. 
2. Greene AK, Grant FD, Slavin SA. Lower-extremity lymphedema and elevated body-mass index. N Engl J 
Med. 2012;366(22):2136-2137. 
3. Duyur Çakıt B, Pervane Vural S, Genç H. Complex decongestive therapy in breast cancer-related lymphedema: 
does obesity affect the outcome negatively? Lymphat Res Biol. 2019;17(1):45-50. 
4. Greene AK, Sudduth CL. Obesity-induced lymphedema. Cold Spring Harb Perspect Med. 2022;12(6):a041176. 
5. Greene AK, Grant FD, Maclellan RA. Obesity-induced lymphedema: clinical and lymphoscintigraphic 
features. Plast Reconstr Surg Glob Open. 2015;3(6):e426. 
6. Lasinski BB, McKillip Thrift K, Squire D, et al. A systematic review of the evidence for complete decongestive 
therapy in the treatment of lymphedema from 2004 to 2011. PM R. 2012;4(8):580-601. 
7. Yaman A, Borman P, Karakuzu Güngör Ö, et al. The impact of obesity on the outcomes of complex 
decongestive therapy among patients with breast cancer-related lymphedema. Turk J Phys Med Rehabil. 
2025;71(1):64-73. 
8. Borman P, Yaman A, Yasrebi S, İnanlı AP, Arıkan Dönmez A. Combined complete decongestive therapy 
reduces volume and improves quality of life and functional status in patients with breast cancer-related 
lymphedema. Clin Breast Cancer. 2022;22(3):e270-e277. 
9. Mehrara BJ, Greene AK. Lymphedema and obesity: is there a link? Plast Reconstr Surg. 2014;134(1):154e-
160e. 

10. Hernandez-Bule ML, Toledano Macías E, Martínez Pascual MA, et al. Does the application of Tecar therapy 
affect temperature and perfusion of skin and muscle microcirculation? A pilot feasibility study on healthy 
subjects. J Clin Med. 2019;8(10):1645. 
11. Cau N, Cimolin V, Aspesi V, et al. Preliminary evidence of effectiveness of TECAR in lymphedema. 
Lymphology. 2019;52(1):35-43. 
12. Kubo M, Li TS, Kamota T, et al. Extracorporeal shock wave therapy ameliorates secondary lymphedema by 
promoting lymphangiogenesis. J Vasc Surg. 2010;52(2):429-434. 
13. Serizawa F, Ito K, Matsubara M, et al. Extracorporeal shock wave therapy induces therapeutic 
lymphangiogenesis in a rat model of secondary lymphoedema. Eur J Vasc Endovasc Surg. 2011;42(2):254-260. 
14. Lee JH, Kim SB, Lee KW, Ha WW. Long-term effects of extracorporeal shock wave therapy on breast cancer-
related lymphedema. J Clin Med. 2022;11(22):6747. 
15. Tsai YL, I TJ, Chuang YC, Cheng YY, Lee YC. Extracorporeal shock wave therapy combined with complex 
decongestive therapy in patients with breast cancer-related lymphedema: a systematic review and meta-analysis. 
J Clin Med. 2021;10(24):5970. 
16. Lee KW, Kim SB, Lee JH, Kim YS. Effects of extracorporeal shockwave therapy on improvements in 
lymphedema, quality of life, and fibrous tissue in breast cancer-related lymphedema. Ann Rehabil Med. 
2020;44(5):386-392. 
17. Greene AK, Grant FD, Slavin SA. Obesity-induced lymphedema: clinical and lymphoscintigraphic features. 
Plast Reconstr Surg. 2015;135(6):1715-1719. 
18. Rockson SG. Lymphedema. N Engl J Med. 2018;379(20):1937-1944. 
19. Keeley V, Crooks S, Locke J, Veigas D, Riches K, Hilliam R. A quality of life measure for limb lymphoedema 
(LYMQOL). J Lymphoedema. 2010;5(1):26-37. 
20. Nuwayhid R, Mardian Y, Ure C, et al. Translation, cross-cultural adaptation and validation of the LYMQOL 
in German-speaking patients with lymphedema of the lower limbs. Healthcare (Basel). 2024;12(3):409. 

21. International Society of Lymphology. The diagnosis and treatment of peripheral lymphedema: 2016 consensus 
document. Lymphology. 2016;49(4):170-184. 
22. Wang CJ, Wu RW, Yang YJ. Treatment of diabetic foot ulcers: a comparative study of extracorporeal shock 
wave therapy and hyperbaric oxygen therapy. Diabetes Res Clin Pract. 2011;92(2):187-193. 
23. Mabrouk MI, Badr NM, Taha MM, El-Shiwi AM, Abdelaal AM, Ali SM, Abd El-Hamed A. Effect of 
extracorporeal shock wave therapy on skin blood perfusion in patients with diabetic foot: a randomized controlled 
trial. Int J Adv Res. 2015;3(3):144-154. 
 
 

Tables  
Table 1: Baseline Demographic and Clinical Characteristics of Participants 
Variable 
CDT (n=15) 
CDT+TECAR (n=15) 
CDT+ESWT (n=15) 
p-
value 
Demographics 
Age (years) 
57.1 ± 3.8 [55.0, 59.1] 
56.8 ± 3.0 [55.1, 58.5] 
57.2 ± 2.7 [55.7, 58.7] 
0.941 
BMI (kg/m²) 
44.3 ± 1.8 [43.3, 45.3] 
44.1 ± 1.5 [43.3, 45.0] 
44.4 ± 1.4 [43.6, 45.1] 
0.937 
Height (cm) 
159.6 ± 2.1 [158.4, 
160.8] 
159.5 ± 1.7 [158.6, 
160.4] 
159.7 ± 1.5 [158.9, 
160.6] 
0.928 
Weight (kg) 
112.9 ± 7.7 [108.7, 
117.2] 
112.4 ± 6.2 [109.0, 
115.8] 
113.2 ± 5.8 [110.0, 
116.4] 
0.947 
Gender (Female), n 
(%) 
15 (100%) 
15 (100%) 
15 (100%) 
— 
Baseline Circumference — Left Limb (cm) 
Ankle 
28.2 ± 1.1 [27.6, 28.8] 
28.1 ± 0.9 [27.6, 28.6] 
28.2 ± 0.9 [27.7, 28.7] 
0.883 
Calf 
45.4 ± 1.9 [44.4, 46.5] 
45.4 ± 1.5 [44.5, 46.2] 
45.7 ± 1.5 [44.8, 46.5] 
0.875 
Knee 
52.1 ± 2.1 [50.9, 53.2] 
52.0 ± 1.7 [51.1, 53.0] 
52.3 ± 1.6 [51.4, 53.3] 
0.881 
Mid-thigh 
68.4 ± 2.4 [67.1, 69.7] 
68.2 ± 1.9 [67.1, 69.2] 
68.5 ± 1.9 [67.5, 69.6] 
0.898 
Upper-thigh 
72.6 ± 2.5 [71.2, 74.0] 
72.5 ± 2.0 [71.4, 73.6] 
72.8 ± 2.0 [71.7, 74.0] 
0.892 
Baseline Circumference — Right Limb (cm) 
Ankle 
28.2 ± 0.6 [27.9, 28.5] 
28.3 ± 0.6 [28.0, 28.7] 
28.3 ± 0.5 [28.0, 28.6] 
0.779 
Calf 
45.6 ± 0.9 [45.2, 46.1] 
45.9 ± 0.8 [45.5, 46.4] 
45.9 ± 0.7 [45.5, 46.3] 
0.554 
Knee 
52.6 ± 1.0 [52.1, 53.2] 
53.0 ± 1.0 [52.4, 53.6] 
52.9 ± 0.9 [52.4, 53.4] 
0.619 

Mid-thigh 
68.7 ± 1.4 [68.0, 69.5] 
69.2 ± 1.3 [68.5, 70.0] 
69.1 ± 1.2 [68.4, 69.8] 
0.584 
Upper-thigh 
73.1 ± 1.5 [72.2, 73.9] 
73.6 ± 1.4 [72.8, 74.4] 
73.5 ± 1.3 [72.7, 74.2] 
0.555 
Baseline LYMQOL Scores (1–10) 
Function 
6.6 ± 0.3 [6.4, 6.8] 
6.7 ± 0.3 [6.6, 6.9] 
6.7 ± 0.3 [6.5, 6.8] 
0.598 
Appearance 
6.9 ± 0.2 [6.8, 7.0] 
6.8 ± 0.2 [6.7, 6.9] 
6.9 ± 0.2 [6.8, 7.0] 
0.587 
Symptoms 
6.3 ± 0.3 [6.1, 6.5] 
6.4 ± 0.3 [6.2, 6.5] 
6.3 ± 0.3 [6.2, 6.5] 
0.796 
Mood 
6.1 ± 0.2 [6.0, 6.2] 
6.1 ± 0.1 [6.0, 6.2] 
6.1 ± 0.2 [6.1, 6.2] 
0.648 
Overall QOL 
6.5 ± 0.1 [6.4, 6.6] 
6.5 ± 0.1 [6.5, 6.6] 
6.5 ± 0.1 [6.5, 6.6] 
0.720 
Baseline Pain and Tissue Stiffness 
VAS Pain (0-10) 
6.1 ± 0.3 [6.0, 6.2] 
6.2 ± 0.2 [6.1, 6.3] 
6.2 ± 0.2 [6.1, 6.3] 
0.395 
Stiffness Calf Left 
34.7 ± 1.4 [33.9, 35.5] 
34.5 ± 1.3 [33.7, 35.2] 
34.7 ± 1.3 [34.0, 35.5] 
0.833 
Stiffness Calf Right 
34.8 ± 0.5 [34.5, 35.0] 
34.8 ± 0.4 [34.5, 35.0] 
34.8 ± 0.4 [34.6, 35.0] 
0.990 
Stiffness Thigh Left 31.5 ± 1.3 [30.8, 32.2] 
31.4 ± 1.2 [30.7, 32.0] 
31.6 ± 1.2 [30.9, 32.3] 
0.869 
Stiffness Thigh 
Right 
31.6 ± 0.6 [31.3, 32.0] 
31.6 ± 0.6 [31.3, 31.9] 
31.6 ± 0.5 [31.4, 31.9] 
0.943 
Data presented as Mean ± SD [95% CI] or n (%). 
Statistical test: One-way ANOVA for continuous variables; Chi-square test for categorical variables. 
No significant between-group differences at baseline (p > 0.05 for all comparisons). 

Table 2: Primary Outcome — Limb Circumference Comparison Between Groups 
Variable 
Time CDT (n=15) 
CDT+TECAR 
(n=15) 
CDT+ESWT 
(n=15) 
p1 (d) 
p2 (d) 
p3 (d) 
Left Ankle 
T0 
28.2 ± 1.1 [27.6, 
28.8] 
28.1 ± 0.9 [27.6, 
28.6] 
28.2 ± 0.9 [27.7, 
28.7] 
— 
— 
— 
Left Ankle 
T1 
25.4 ± 1.0 [24.8, 
26.0] 
24.1 ± 0.8 [23.7, 
24.6] 
23.7 ± 0.8 [23.3, 
24.1] 
<0.001 
(1.37) 
<0.001 
(1.83) 
0.145 
(0.55) 
Left Ankle 
T2 
24.8 ± 1.0 [24.3, 
25.4] 
23.9 ± 0.8 [23.5, 
24.4] 
23.5 ± 0.8 [23.1, 
23.9] 
0.011 
(1.0) 
<0.001 
(1.47) 
0.145 
(0.55) 
Left Calf 
T0 
45.4 ± 1.9 [44.4, 
46.5] 
45.4 ± 1.5 [44.5, 
46.2] 
45.7 ± 1.5 [44.8, 
46.5] 
— 
— 
— 
Left Calf 
T1 
40.9 ± 1.7 [39.9, 
41.9] 
39.0 ± 1.3 [38.3, 
39.8] 
38.3 ± 1.2 [37.7, 
39.0] 
0.003 
(1.21) 
<0.001 
(1.69) 
0.156 
(0.53) 
Left Calf 
T2 
40.0 ± 1.7 [39.1, 
41.0] 
38.6 ± 1.3 [37.9, 
39.3] 
37.9 ± 1.2 [37.3, 
38.6] 
0.016 
(0.94) 
<0.001 
(1.39) 
0.178 
(0.5) 
Left Knee 
T0 
52.1 ± 2.1 [50.9, 
53.2] 
52.0 ± 1.7 [51.1, 
53.0] 
52.3 ± 1.6 [51.4, 
53.3] 
— 
— 
— 
Left Knee 
T1 
46.9 ± 1.9 [45.8, 
47.9] 
44.8 ± 1.4 [44.0, 
45.6] 
44.0 ± 1.4 [43.2, 
44.7] 
0.002 
(1.27) 
<0.001 
(1.77) 
0.128 
(0.57) 
Left Knee 
T2 
45.9 ± 1.8 [44.8, 
46.9] 
44.2 ± 1.4 [43.5, 
45.0] 
43.5 ± 1.4 [42.8, 
44.3] 
0.010 
(1.0) 
<0.001 
(1.43) 
0.183 
(0.5) 
Left Mid-
thigh 
T0 
68.4 ± 2.4 [67.1, 
69.7] 
68.2 ± 1.9 [67.1, 
69.2] 
68.5 ± 1.9 [67.5, 
69.6] 
— 
— 
— 

Left Mid-
thigh 
T1 
61.5 ± 2.1 [60.4, 
62.7] 
58.6 ± 1.6 [57.7, 
59.5] 
57.5 ± 1.5 [56.7, 
58.3] 
<0.001 
(1.54) 
<0.001 
(2.21) 
0.059 
(0.72) 
Left Mid-
thigh 
T2 
60.2 ± 2.1 [59.1, 
61.4] 
58.0 ± 1.6 [57.1, 
58.8] 
56.9 ± 1.5 [56.1, 
57.7] 
0.002 
(1.21) 
<0.001 
(1.82) 
0.072 
(0.68) 
Left Upper-
thigh 
T0 
72.6 ± 2.5 [71.2, 
74.0] 
72.5 ± 2.0 [71.4, 
73.6] 
72.8 ± 2.0 [71.7, 
74.0] 
— 
— 
— 
Left Upper-
thigh 
T1 
65.4 ± 2.3 [64.1, 
66.6] 
62.3 ± 1.7 [61.4, 
63.3] 
61.2 ± 1.7 [60.3, 
62.1] 
<0.001 
(1.53) 
<0.001 
(2.1) 
0.080 
(0.66) 
Left Upper-
thigh 
T2 
64.0 ± 2.2 [62.7, 
65.2] 
61.6 ± 1.7 [60.7, 
62.6] 
60.6 ± 1.7 [59.7, 
61.5] 
0.003 
(1.17) 
<0.001 
(1.71) 
0.097 
(0.63) 
Right Ankle 
T0 
28.2 ± 0.6 [27.9, 
28.5] 
28.3 ± 0.6 [28.0, 
28.7] 
28.3 ± 0.5 [28.0, 
28.6] 
— 
— 
— 
Right Ankle 
T1 
25.4 ± 0.5 [25.1, 
25.7] 
24.4 ± 0.5 [24.1, 
24.6] 
23.8 ± 0.4 [23.5, 
24.0] 
<0.001 
(2.07) 
<0.001 
(3.43) 
0.001 
(1.31) 
Right Ankle 
T2 
24.8 ± 0.5 [24.5, 
25.1] 
24.2 ± 0.5 [23.9, 
24.4] 
23.6 ± 0.4 [23.3, 
23.8] 
0.001 
(1.29) 
<0.001 
(2.64) 
0.001 
(1.31) 
Right Calf 
T0 
45.6 ± 0.9 [45.2, 
46.1] 
45.9 ± 0.8 [45.5, 
46.4] 
45.9 ± 0.7 [45.5, 
46.3] 
— 
— 
— 
Right Calf 
T1 
41.1 ± 0.8 [40.6, 
41.5] 
39.5 ± 0.7 [39.1, 
39.9] 
38.5 ± 0.6 [38.2, 
38.9] 
<0.001 
(2.1) 
<0.001 
(3.63) 
<0.001 
(1.46) 
Right Calf 
T2 
40.2 ± 0.8 [39.8, 
40.6] 
39.1 ± 0.7 [38.7, 
39.5] 
38.1 ± 0.6 [37.8, 
38.5] 
<0.001 
(1.52) 
<0.001 
(2.95) 
<0.001 
(1.4) 

Right Knee 
T0 
52.6 ± 1.0 [52.1, 
53.2] 
53.0 ± 1.0 [52.4, 
53.6] 
52.9 ± 0.9 [52.4, 
53.4] 
— 
— 
— 
Right Knee 
T1 
47.4 ± 1.0 [46.8, 
47.9] 
45.6 ± 0.9 [45.1, 
46.1] 
44.4 ± 0.8 [44.0, 
44.9] 
<0.001 
(1.93) 
<0.001 
(3.37) 
<0.001 
(1.35) 
Right Knee 
T2 
46.4 ± 0.9 [45.8, 
46.9] 
45.0 ± 0.9 [44.5, 
45.5] 
44.0 ± 0.8 [43.6, 
44.5] 
<0.001 
(1.42) 
<0.001 
(2.68) 
0.003 
(1.21) 
Right Mid-
thigh 
T0 
68.7 ± 1.4 [68.0, 
69.5] 
69.2 ± 1.3 [68.5, 
70.0] 
69.1 ± 1.2 [68.4, 
69.8] 
— 
— 
— 
Right Mid-
thigh 
T1 
61.9 ± 1.3 [61.2, 
62.6] 
59.5 ± 1.2 [58.9, 
60.2] 
58.1 ± 1.0 [57.5, 
58.6] 
<0.001 
(1.92) 
<0.001 
(3.27) 
<0.001 
(1.35) 
Right Mid-
thigh 
T2 
60.5 ± 1.2 [59.9, 
61.2] 
58.9 ± 1.2 [58.3, 
59.6] 
57.5 ± 1.0 [57.0, 
58.1] 
0.001 
(1.34) 
<0.001 
(2.69) 
0.001 
(1.32) 
Right Upper-
thigh 
T0 
73.1 ± 1.5 [72.2, 
73.9] 
73.6 ± 1.4 [72.8, 
74.4] 
73.5 ± 1.3 [72.7, 
74.2] 
— 
— 
— 
Right Upper-
thigh 
T1 
65.8 ± 1.3 [65.0, 
66.5] 
63.3 ± 1.2 [62.6, 
64.0] 
61.7 ± 1.1 [61.1, 
62.3] 
<0.001 
(1.94) 
<0.001 
(3.35) 
<0.001 
(1.4) 
Right Upper-
thigh 
T2 
64.3 ± 1.3 [63.6, 
65.1] 
62.7 ± 1.2 [62.0, 
63.4] 
61.1 ± 1.1 [60.5, 
61.7] 
0.001 
(1.31) 
<0.001 
(2.69) 
<0.001 
(1.36) 
Data presented as Mean ± SD [95% CI]. 
Statistical test: Two-way mixed ANOVA (Group × Time) for overall effects; Bonferroni-adjusted 
independent t-tests for post-hoc pairwise comparisons. 
p1: CDT vs CDT+TECAR; p2: CDT vs CDT+ESWT; p3: CDT+TECAR vs CDT+ESWT. d = 
Cohen's d. 
All Group × Time interactions significant (p < 0.001). See Table 5 for full ANOVA results. 

Table 3: Secondary Outcome — LYMQOL Scores Comparison Between Groups 
Variable 
Time CDT (n=15) 
CDT+TECAR 
(n=15) 
CDT+ESWT 
(n=15) 
p1 (d) 
p2 (d) 
p3 (d) 
Function 
T0 
6.6 ± 0.3 [6.4, 6.8] 6.7 ± 0.3 [6.6, 6.9] 6.7 ± 0.3 [6.5, 6.8] — 
— 
— 
Function 
T1 
4.9 ± 0.3 [4.7, 5.1] 4.5 ± 0.3 [4.4, 4.7] 4.2 ± 0.3 [4.0, 4.3] 0.004 
(1.13) 
<0.001 
(2.39) 
0.002 
(1.22) 
Function 
T2 
5.1 ± 0.3 [4.9, 5.3] 4.6 ± 0.3 [4.5, 4.8] 4.3 ± 0.3 [4.1, 4.4] <0.001 
(1.44) 
<0.001 
(2.72) 
0.002 
(1.22) 
Appearance 
T0 
6.9 ± 0.2 [6.8, 7.0] 6.8 ± 0.2 [6.7, 6.9] 6.9 ± 0.2 [6.8, 7.0] — 
— 
— 
Appearance 
T1 
5.2 ± 0.2 [5.1, 5.3] 4.6 ± 0.2 [4.5, 4.7] 4.4 ± 0.2 [4.3, 4.5] <0.001 
(2.81) 
<0.001 
(4.35) 
0.001 
(1.3) 
Appearance 
T2 
5.4 ± 0.2 [5.3, 5.5] 4.7 ± 0.2 [4.6, 4.8] 4.5 ± 0.2 [4.4, 4.6] <0.001 
(3.3) 
<0.001 
(4.87) 
0.001 
(1.3) 
Symptoms 
T0 
6.3 ± 0.3 [6.1, 6.5] 6.4 ± 0.3 [6.2, 6.5] 6.3 ± 0.3 [6.2, 6.5] — 
— 
— 
Symptoms 
T1 
4.6 ± 0.3 [4.4, 4.8] 4.2 ± 0.4 [4.0, 4.4] 3.8 ± 0.3 [3.7, 4.0] 0.004 
(1.16) 
<0.001 
(2.38) 
0.006 
(1.09) 
Symptoms 
T2 
4.8 ± 0.3 [4.6, 5.0] 4.3 ± 0.4 [4.1, 4.5] 3.9 ± 0.3 [3.8, 4.1] <0.001 
(1.45) 
<0.001 
(2.69) 
0.006 
(1.09) 
Mood 
T0 
6.1 ± 0.2 [6.0, 6.2] 6.1 ± 0.1 [6.0, 6.2] 6.1 ± 0.2 [6.1, 6.2] — 
— 
— 
Mood 
T1 
4.4 ± 0.2 [4.3, 4.5] 3.9 ± 0.1 [3.8, 4.0] 3.6 ± 0.2 [3.6, 3.7] <0.001 
(3.11) 
<0.001 
(4.64) 
<0.001 
(1.91) 
Mood 
T2 
4.6 ± 0.2 [4.5, 4.7] 4.0 ± 0.1 [3.9, 4.1] 3.7 ± 0.2 [3.7, 3.8] <0.001 
(3.73) 
<0.001 
(5.24) 
<0.001 
(1.91) 

Overall QOL T0 
6.5 ± 0.1 [6.4, 6.6] 6.5 ± 0.1 [6.5, 6.6] 6.5 ± 0.1 [6.5, 6.6] — 
— 
— 
Overall QOL T1 
4.8 ± 0.1 [4.7, 4.9] 4.3 ± 0.1 [4.3, 4.4] 4.0 ± 0.1 [4.0, 4.1] <0.001 
(3.66) 
<0.001 
(7.29) 
<0.001 
(3.25) 
Overall QOL T2 
5.0 ± 0.1 [4.9, 5.1] 4.4 ± 0.1 [4.4, 4.5] 4.1 ± 0.1 [4.1, 4.2] <0.001 
(4.65) 
<0.001 
(8.24) 
<0.001 
(3.34) 
Data presented as Mean ± SD [95% CI]. LYMQOL scores range 1–10 (lower scores = better 
quality of life). 
Statistical test: Two-way mixed ANOVA (Group × Time) for overall effects; Bonferroni-adjusted 
independent t-tests for post-hoc pairwise comparisons. 
p1: CDT vs CDT+TECAR; p2: CDT vs CDT+ESWT; p3: CDT+TECAR vs CDT+ESWT. d = 
Cohen's d. 
 
 

Table 4: Secondary Outcome — VAS Pain and Tissue Stiffness Comparison Between 
Groups 
Variable 
Time CDT (n=15) 
CDT+TECAR 
(n=15) 
CDT+ESWT 
(n=15) 
p1 (d) 
p2 (d) 
p3 (d) 
VAS Pain 
T0 
6.1 ± 0.3 [6.0, 6.2] 6.2 ± 0.2 [6.1, 6.3] 6.2 ± 0.2 [6.1, 6.3] — 
— 
— 
VAS Pain 
T1 
3.6 ± 0.3 [3.5, 3.7] 3.2 ± 0.2 [3.1, 3.3] 2.8 ± 0.2 [2.7, 2.9] <0.001 
(1.59) 
<0.001 
(3.54) 
<0.001 
(2.05) 
VAS Pain 
T2 
3.9 ± 0.3 [3.8, 4.0] 3.4 ± 0.2 [3.3, 3.5] 3.0 ± 0.2 [2.9, 3.1] <0.001 
(2.0) 
<0.001 
(3.96) 
<0.001 
(2.05) 
Stiffness Left 
Calf 
T0 
34.7 ± 1.4 [33.9, 
35.5] 
34.5 ± 1.3 [33.7, 
35.2] 
34.7 ± 1.3 [34.0, 
35.5] 
— 
— 
— 
Stiffness Left 
Calf 
T1 
30.2 ± 1.3 [29.5, 
30.9] 
28.5 ± 1.1 [27.8, 
29.1] 
27.1 ± 1.0 [26.5, 
27.7] 
<0.001 
(1.48) 
<0.001 
(2.68) 
0.002 
(1.24) 
Stiffness Left 
Calf 
T2 
30.7 ± 1.3 [30.0, 
31.4] 
28.8 ± 1.1 [28.1, 
29.4] 
27.4 ± 1.0 [26.8, 
28.0] 
<0.001 
(1.65) 
<0.001 
(2.85) 
0.002 
(1.24) 
Stiffness 
Right Calf 
T0 
34.8 ± 0.5 [34.5, 
35.0] 
34.8 ± 0.4 [34.5, 
35.0] 
34.8 ± 0.4 [34.6, 
35.0] 
— 
— 
— 
Stiffness 
Right Calf 
T1 
30.3 ± 0.4 [30.0, 
30.5] 
28.7 ± 0.3 [28.5, 
28.9] 
27.2 ± 0.3 [27.0, 
27.4] 
<0.001 
(4.09) 
<0.001 
(8.08) 
<0.001 
(4.49) 
Stiffness 
Right Calf 
T2 
30.8 ± 0.4 [30.5, 
31.0] 
29.0 ± 0.3 [28.8, 
29.2] 
27.5 ± 0.3 [27.3, 
27.7] 
<0.001 
(4.59) 
<0.001 
(8.6) 
<0.001 
(4.55) 
Stiffness Left 
Thigh 
T0 
31.5 ± 1.3 [30.8, 
32.2] 
31.4 ± 1.2 [30.7, 
32.0] 
31.6 ± 1.2 [30.9, 
32.3] 
— 
— 
— 

Stiffness Left 
Thigh 
T1 
27.4 ± 1.1 [26.8, 
28.1] 
25.9 ± 1.0 [25.4, 
26.5] 
24.7 ± 0.9 [24.2, 
25.2] 
<0.001 
(1.43) 
<0.001 
(2.64) 
0.001 
(1.29) 
Stiffness Left 
Thigh 
T2 
27.9 ± 1.1 [27.3, 
28.6] 
26.2 ± 1.0 [25.7, 
26.8] 
25.0 ± 0.9 [24.5, 
25.5] 
<0.001 
(1.62) 
<0.001 
(2.84) 
0.001 
(1.29) 
Stiffness 
Right Thigh 
T0 
31.6 ± 0.6 [31.3, 
32.0] 
31.6 ± 0.6 [31.3, 
31.9] 
31.6 ± 0.5 [31.4, 
31.9] 
— 
— 
— 
Stiffness 
Right Thigh 
T1 
27.5 ± 0.5 [27.3, 
27.8] 
26.1 ± 0.5 [25.8, 
26.3] 
24.7 ± 0.4 [24.5, 
24.9] 
<0.001 
(3.04) 
<0.001 
(6.54) 
<0.001 
(3.36) 
Stiffness 
Right Thigh 
T2 
28.0 ± 0.5 [27.8, 
28.3] 
26.4 ± 0.5 [26.1, 
26.6] 
25.0 ± 0.4 [24.8, 
25.2] 
<0.001 
(3.46) 
<0.001 
(7.0) 
<0.001 
(3.36) 
Data presented as Mean ± SD [95% CI]. VAS Pain: 0 = no pain, 10 = worst pain. Tissue 
stiffness measured by tonometry (higher values = greater stiffness). 
Statistical test: Two-way mixed ANOVA (Group × Time) for overall effects; Bonferroni-adjusted 
independent t-tests for post-hoc pairwise comparisons. 
p1: CDT vs CDT+TECAR; p2: CDT vs CDT+ESWT; p3: CDT+TECAR vs CDT+ESWT. d = 
Cohen's d. 
 
 

Table 5: Two-Way Mixed ANOVA Summary — Group, Time, and Group × Time 
Interaction Effects 
Variable 
Group 
F 
Group 
p 
Group 
ηp² 
Time F 
Time 
p 
Time 
ηp² 
G×T F 
G×T 
p 
G×T 
ηp² 
Left Ankle 
4.89 
0.012 
0.189 
34867.3 
<0.001 0.999 
464.06 
<0.001 0.957 
Left Calf 
3.8 
0.031 
0.153 
31330.72 <0.001 0.999 
442.92 
<0.001 0.955 
Left Knee 
4.16 
0.022 
0.165 
37801.64 <0.001 0.999 
522.79 
<0.001 0.961 
Left Mid-thigh 
6.67 
0.003 
0.241 
28142.22 <0.001 0.999 
393.92 
<0.001 0.949 
Left Upper-thigh 
6.16 
0.005 
0.227 
51351.44 <0.001 0.999 
700.58 
<0.001 0.971 
Right Ankle 
12.66 
<0.001 0.376 
99864.63 <0.001 1.0 
1339.66 <0.001 0.985 
Right Calf 
14.54 
<0.001 0.409 
140211.95 <0.001 1.0 
1936.93 <0.001 0.989 
Right Knee 
12.25 
<0.001 0.368 
130336.79 <0.001 1.0 
1786.39 <0.001 0.988 
Right Mid-thigh 
11.84 
<0.001 0.361 
98099.18 <0.001 1.0 
1353.53 <0.001 0.985 
Right Upper-thigh 
12.22 
<0.001 0.368 
121148.13 <0.001 1.0 
1683.22 <0.001 0.988 
Function 
9.7 
<0.001 0.316 
188568.84 <0.001 1.0 
2675.2 
<0.001 0.992 
Appearance 
36.58 
<0.001 0.635 
865741.0 <0.001 1.0 
12676.0 <0.001 0.998 
Symptoms 
9.58 
<0.001 0.313 
303009.35 <0.001 1.0 
4352.07 <0.001 0.995 
Mood 
44.69 
<0.001 0.68 
150530.8 <0.001 1.0 
2329.6 
<0.001 0.991 
Overall QOL 
98.08 
<0.001 0.824 
317898.37 <0.001 1.0 
4655.74 <0.001 0.996 
VAS Pain 
22.48 
<0.001 0.517 
823974.5 <0.001 1.0 
7864.25 <0.001 0.997 
Stiffness Left Calf 
11.66 
<0.001 0.357 
26586.52 <0.001 0.998 
663.57 
<0.001 0.969 
Stiffness Right Calf 
109.21 <0.001 0.839 
209224.15 <0.001 1.0 
5179.01 <0.001 0.996 

Stiffness Left Thigh 
11.21 
<0.001 0.348 
25660.92 <0.001 0.998 
648.23 
<0.001 0.969 
Stiffness Right Thigh 65.49 
<0.001 0.757 
144570.48 <0.001 1.0 
3630.7 
<0.001 0.994 
Statistical test: Two-way mixed-design ANOVA. Between-subjects factor: Treatment Group 
(CDT, CDT+TECAR, CDT+ESWT). Within-subjects factor: Time (Baseline, 4 weeks, 8 weeks). 
ηp² = partial eta squared (effect size): small ≥ 0.01, medium ≥ 0.06, large ≥ 0.14. 
G×T = Group × Time interaction. Greenhouse–Geisser correction applied where sphericity 
assumption was violated (ε < 0.75). 
Assumption testing: Normality confirmed for 97.2% of distributions (Shapiro–Wilk p > 0.05). 
Homogeneity of variances verified via Levene's test. 
 
 

 
Figures 
Figure 1: Limb Circumference (Ankle, Calf) Changes Over Time by Treatment Group. 
Error bars represent 95% confidence intervals. 
 
Figure 2: Thigh Circumference Changes Over Time by Treatment Group. Error bars 
represent 95% confidence intervals. 

 
 
 

Figure 3: LYMQOL Domain Scores Over Time by Treatment Group. Lower scores indicate 
better quality of life. Error bars represent 95% confidence intervals. 
 
Figure 4: VAS Pain and Tissue Stiffness Over Time by Treatment Group. Error bars 
represent 95% confidence intervals. 
 

Figure 5: CONSORT Flow Diagram of participant enrollment, allocation, follow-up, and 
analysis.