Journal of Plastic, Reconstructive & Aesthetic Surgery 84 (2023) 302–312

Review

Lipedema: What we don’t know

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⁎
R.F.D van la Parra , C. Deconinck, G. Pirson, M. Servaes,
Ph. Fosseprez

Department of Plastic, Reconstructive, and Aesthetic Surgery, CHU UCL Namur, Université Catholique de
Louvain, Belgium

Received 21 December 2022; Accepted 14 May 2023

KEYWORDS Summary Background: Lipedema is a loose connective tissue disease characterized by a

Lipedema; disproportionate accumulation of adipose tissue in the limbs of women. Despite its incidence of
Adipose tissue; 10–20%, lipedema is often underdiagnosed and misdiagnosed.
Lymphatic drainage; Objectives: This review aims to outline current, available evidence regarding this enigmatic
Diagnostic imaging; syndrome and gives a synopsis of the subjects that are still unknown.
Liposuction Materials and methods: PubMed and Embase searches were conducted to identify relevant
articles on lipedema pathophysiology, clinical presentation, diagnosis, and treatment.
Results: Lipedema can be considered a disease of the adipocytes or a circulatory disorder of
the lymphatics. The relationship between lymphatics and adipose tissue remains controversial.
The clinical distinction between lipedema, lymphedema, phlebolymphedema, and lipolym­
phedema can be difficult. Diagnoses often coexist, further complicating the diagnosis of lipe­
dema, which is currently made on clinical grounds alone. The value of diagnostic imaging
studies is unclear. Liposuction appears to be an effective treatment and significantly improves
symptoms.
Conclusion: Diagnosing lipedema remains a challenge due to its heterogeneous presentation,
co-existing diseases, and lack of objective diagnostic imaging. Further directions for research
include the effect of excess skin resection surgery on lymphatic drainage.
© 2023 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by
Elsevier Ltd. All rights reserved.

⁎
Correspondence to: Chirurgie Plastique, Reconstructrice et Esthétique, CHU UCL Namur, Site St Elisabeth, Place Louise Godin 15, 5000
Namur, Belgium.
E-mail address: [email protected] (R.F.D. van la Parra).

https://doi.org/10.1016/j.bjps.2023.05.056
1748-6815/© 2023 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved.
 Journal of Plastic, Reconstructive & Aesthetic Surgery 84 (2023) 302–312

Contents

. Objective . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 303
. Method . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 303
. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304
. Genetic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304
. Hormonal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304
. Loose connective tissue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304
. Vascular lymphatic. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304
. Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304
. Clinical presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304
. Comorbidities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 306
. Differential diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 306
. Imaging. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
. Ultrasound . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
. Lymphoscintigraphy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
. MR imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
. MR lymphangiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
. Dual-energy X-ray absorptiometry (DXA) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 309
. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 309
. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 309
. Funding. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 310
. Ethical approval . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 310
. Declaration of Competing Interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 310
. References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 310

Lipedema is a loose connective tissue (LCT) disease char­ lipedema) and vice versa, which further complicates its
acterized by the disproportionate accumulation of fibrotic diagnosis and treatment.8
subcutaneous adipose tissue and extracellular fluid in the The heterogeneous presentation and anatomy of the
limbs of women due to microvascular inflammation.1 There condition and the lack of a diagnostic imaging exam that is
is bilateral symmetric enlargement of the subcutaneous easy to perform and interpret complicate its diagnosis.
adipose tissue in the limbs, sparing the hands, feet, and There are gaps in our knowledge regarding lipedema
trunk. It is found almost exclusively in women and is most management due to a lack of assessment for the impact of
often isolated to the lower extremities. variable elements of the lipedema phenotype, such as
There is a disproportionate increase in leg circumference obesity, venous disease, lymphatic insufficiency, and skin
in relation to a slender torso that cannot be reversed by laxity, which each have an impact on patient outcomes.9
physical exercise or diet.2,3 Polygenic susceptibility combined with hormonal, micro­
Allen and Hines first described this disease in 1940 as a vascular, and lymphatic disorders and loose connective tissue
clinical syndrome, characterized by the combination of may be partly responsible for its development.10 However,
subcutaneous deposition of fat in the buttocks and lower consistent information on lipedema pathophysiology is still
extremities and the accumulation of fluid in the legs.4 lacking, and an etiological treatment is not yet available.
The reported incidence from specialized edema clinics
varies between 10% and 20%.5,6 The prevalence in the
general population has been estimated to be as high as 39% Objective
in the German lipedema-3 trial.7 Despite this high pre­
valence, lipedema is often underdiagnosed and mis­
This review aims to outline current evidence regarding this
diagnosed with other similarly presenting diseases.
enigmatic syndrome and gives a synopsis on the subjects
Lipedema, lymphedema, lipolymphedema, veno-lipolym­
that are still unknown. Thereby guiding further directions
phedema/ phlebedema, lipohypertrophy, gynecoid obesity,
for research and treatment.
and Dercum’s disease are all part of a spectrum of pathol­
ogies that are not well defined. There are multiple factors,
which are likely interconnected, that influence this spec­
trum of diseases. Diagnoses also often coexist, further Method
complicating the diagnosis of lipedema.
Progression of lipedema could lead to venous disease A systematic literature search in PubMed and Embase with
(veno-lipedema) and lymphatic abnormalities (lympho- no date restriction was conducted in April 2023 using the

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 R.F.D. van la Parra, C. Deconinck, G. Pirson et al.

following search terms: ‘’lipedema’’ AND (‘’pathophysiology’’ retention leads to a vicious cycle that further aggravates
OR ‘’symptoms’’ OR ‘’diagnosis’’ OR ‘’therapy’’). adipocyte growth.
All articles published in English, German, French, or Lymphatic malfunction plays a role in lipedema, as de­
Spanish describing lipedema etiopathogenesis, clinical monstrated by the biomarker Platelet factor 4 (PF4/
presentation, imaging, and treatment were included in this CXCL4).24 Whether those lymphatic alterations are the
review. Reference lists in all relevant publications were cause or consequence of the disease or are secondary to the
examined and used to identify additional articles for in­ related obesity features is not yet known.
clusion. Using this search strategy, 488 articles were iden­
tified, of which 79 articles were included in this review.

Pathogenesis
Etiology
The pathophysiology of lipedema is poorly understood;
The etiology of lipedema is multifactorial and is influenced nevertheless, it is described as lymphatic compromise in its
by genetic, hormonal, loose connective tissue, and vascular initial stages and as frank lymphatic damage in the final
lymphatic factors. stage of lipolymphedema.
One possible mechanism leading to the development of
lipedema may involve one of increased adipogenesis.8,25,26
Genetic Previous studies on lymphedema have demonstrated en­
hanced adipocyte growth in the setting of excess lymphatic
A positive family history of similar "large legs" in female fluid, thereby regulating lipid accumulation.27,28
members is reported in 15–73% of patients.11–15 In a survey The mechanism of lipedema might be a continuing de­
among lipedema patients, the relatives who were most terioration in which the growing adipocytes keep slowing
often affected were grandmothers (35.4%) and mothers the lymphatic drainage, while it is still unclear whether the
(29.7%), followed by aunts (23.0%), sisters (14.8%), and primary factor is the growing adipocyte or an intrinsic
cousins (11.5%).14 A genetic predisposition is thus assumed. problem in the interstitial space or microlymphatic
Analyses of familial clusters suggest an autosomal dominant pathway.
inheritance pattern with incomplete penetrance.12,16 Moreover, in other conditions with comparable or even
more enlarged fat deposits, such as lipohypertrophy or
Hormonal adiposis, there is no reduction of the lymphatic flow.
Hypoxia, brought about by adipocyte hypertrophy,
Lipedema may manifest or aggravate at times of hormonal leading to endothelial dysfunction, plays a significant role in
changes, such as pregnancy or menopause, suggesting an lipedema and is a major inducer of angiogenesis.29 There is
estrogen-related etiology.13,15,17–19 A polygenically medi­ an increased capillary permeability due to microangiopathy
ated change in the distribution pattern of alpha- and beta- and a diminished venoarterial reflex.10,30 The venoarterial
estrogen receptors (ER) in the white fatty tissue of affected reflex protects the capillary bed from locally elevated hy­
body areas (ER-α expression ↓, ER-β expression ↑) has been drostatic pressure by constriction of the arterioles.31 Fluid
suggested.20 The effect of contraceptives on the evolution extravasation may be enhanced when this reflex is im­
of lipedema is unclear. paired.
The tissue edema can initially be compensated for by
increased lymph drainage.32–34 As the disorder progresses,
Loose connective tissue the amount of fluid produced exceeds the transport capa­
city of the lymphatic system, and the pressure of the fat
Lipedema tissue has an enlarged extracellular matrix where tissue itself causes obstruction of the lymphatic vessels and
proteoglycans reside, which bind sodium and water.21 Water secondary lymphedema35 with a reduced lymphatic flow as
may thus collect in fat tissue by swelling of the fat cells observed in lymphoscintigraphy of the lower ex­
and/ or collecting interstitial fluid, thereby producing tremity.22,36,37 The stasis of extravasation of proteins
edema of the fat cells and/or interstitium, a feature that causes first inflammation followed by fibrosis, leading to
has been demonstrated in the histopathology of biopsies pathological changes in lymphatic capillaries typical in li­
and liposuction aspirate of lipedema patients.5,6,19,22 Adi­ pedema.38
pocytes are thus a major source of lymph production.23 The term “lipolymphedema” is used to describe the
combined pathology during these stages.
Vascular lymphatic

Lymphatic fluid accumulation in the interstitium stimulates

adipocyte growth, which causes hypoxia by compression of Clinical presentation
capillaries. Hypoxia results in adipocyte cell death and the
recruitment of macrophages, which generates inflammation Lipedema is a clinical diagnosis made on the basis of clinical
thereby stimulating fibrosis. Hypoxia also induces micro­ examination findings.
angiopathy with an increase in capillary permeability re­ In 1951 Wold et al.13 proposed diagnostic criteria for li­
sulting in fluid extravasation leading to edema. This fluid pedema, which include the following (Figure 1):

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 Journal of Plastic, Reconstructive & Aesthetic Surgery 84 (2023) 302–312

(a) occurrence almost exclusively in women; (b) bilateral

and symmetrical nature with minimal involvement of
the feet; (c) minimal pitting edema; (d) pain, tender­
ness, and easy bruising; and (e) persistent swelling of
lower extremities despite elevation or weight loss.

Based on distribution, five types of lipedema have been

described (Figure 2).10,11,41
In type I, lipedema fat tissue accumulates around the
hips and buttocks (saddle bag phenomena); in type II, ac­
cumulation involves the area from hips to knees; and in type
III, a hip to ankle phenotype is observed. Approximately 30%
of affected women have an additional involvement of arms
(type IV), while it is rare to find fat dominating the calf
Figure 1 Criteria for lipedema diagnosis. region only (type V).
Reprinted with permission from Buso et al.39 The final, pub­ The types are determined by the segments of the lower
lished version of this article is available at https://www.kar­ body affected by abnormal adipose deposits rather than
ger.com/?doi= 10.1159/000527138. Allen and Hines’ description of generalized lower-body in­
volvement of the buttock, thighs, and lower legs.4 These

Figure 2 Lipedema types.

Reprinted with permission from Amato et al.40. The final, published version of this article is available at. https://journal­
s.sagepub.com/doi/10.1177/02683555211002340.

305
 R.F.D. van la Parra, C. Deconinck, G. Pirson et al.

thighs and inner aspects of the knees/ overhanging

masses of tissue (Figure 4).
• Stage IV: lipolymphedema.

The majority of patients experience their first symptoms

mostly during puberty up to the beginning of the third
decade.10 The reported delay between lipedema onset and
the correct diagnosis varies between 10 and 15 years.10,15,44
Hypermobile joints are present in 50% of women with
lipedema consistent with a connective tissue disease, such
as hypermobile Ehlers–Danlos syndrome.45 Reduced elasti­
city of the skin46 and aorta47 in women with lipedema
confirm lipedema as a connective tissue disease.48

Comorbidities

The prevalence of obesity (37.6%15), hypothyroidism

(27–36%14,15,48), migraine (23%15), and depression
(23–25.5%14,15) is often increased in lipedema. To what ex­
Figure 3 Lipedema stages.
tent there is a causal connection between lipedema and
Reprinted with permission from Buso et al.39 The final, pub­
these disorders or whether they are just an epiphenomenon
lished version of this article is available at https://www.kar­
of obesity remains unclear.14 Interestingly, patients with
ger.com/?doi= 10.1159/000527138.
lipedema display a less severe cardiovascular profile in
contrast to obesity.45
regional classifications are developed mainly for ther­
apeutic follow-up purposes and have no pathophysiological
basis. Differential diagnosis
Lipedema can be classified in four clinical stages based
on morphological appearance (Figure 3).5,20,42,43 Lipedema is often regarded as an extension of simple obe­
sity or erroneously diagnosed as one of the non-systemic
• Stage I: Thickening and softening of the subcutis with causes of enlarged lower extremities, e.g., lymphedema or
small nodules; skin is smooth. mixed lymphovenous disease. Confusion often exists con­
• Stage II: Thickening and softening of the subcutis with cerning the differential diagnosis, which includes17:
larger nodules due to increased fibrous tissue; skin tex­ Lipohypertrophy (similar disproportion, symmetric, but
ture is uneven (‘mattress phenomenon’). no edema and no pain),
• Stage III: Thickening and hardening of the subcutis with Herpetz et al. described lipohypertrophy as increased
large nodules, disfiguring lobules of fat on the inner symmetrical subcutaneous fat deposits, mostly on the legs

Figure 4 A 34-year-old patient with type 3, stage 3 lipedema. A, frontal; B, dorsal; and C, side views.

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 Journal of Plastic, Reconstructive & Aesthetic Surgery 84 (2023) 302–312

and arms in women. The difference between lipohyper­ diseases, although a diagnostic imaging exam for lipedema
trophy and lipedema is the absence of edema and pain in is currently still lacking.
lipohypertrophy.29
Primary lymphedema (asymmetric, decreased lymphatic Ultrasound
flow, positive Kaposi–Stemmer skin fold sign, no pain, and
no bruising), In contrast to lymphedema, Stemmer’s sign
Ultrasonography represents a minimally invasive cost-ef­
(i.e., the inability to pinch a fold of skin at the base of the
fective tool that can be of great value to distinguish lym­
second toe due to thickening of the skin and subcutaneous
phedema from lipedema. Lymphedema presents with
tissues) is negative, and lipedema is always symmetrical.
increased dermal thickness and decreased echogenicity,
Lymphedema commonly responds to compression therapy,
while lipedema is characterized by an increased thickness
while lipedema responds poorly to compression therapy.
of the subcutaneous tissue.7,52,53 For the diagnosis of lipe­
The skin in patients with lymphedema is brown, warty, and
dema, Campos et al.40 proposed cut-off values of the sub­
sclerotic, while the skin in lipedema is commonly intact.
cutaneous tissue thickness of 11.7 mm for the pre-tibial
Phlebedema/ chronic venous disease (pathological vein
region, 17.9 mm for the anterior thigh, and 8.4 mm for the
function tests, pitting edema, improvement of symptoms
lateral side of the leg.40
and swelling with leg elevation, and, in advanced stages,
skin changes with typical brown coloration (dermite ocra),
white scars (atrophie blanche), and ulcers.10 Lymphoscintigraphy
Phlebedema is associated with chronic venous in­
competence, swelling of the lower leg, varicosities, and Lymphoscintigraphy can be useful in the differential diag­
induration.49 Lipedema and chronic venous disease often nosis of edema, allowing the exclusion of clear lymphatic
coexist; 25–50% of women with lipedema have concomitant dysfunction. Patients suffering from lipedema have an ab­
venous disease.13,48 Many symptoms of lipedema mimic normal lymphoscintigraphic pattern, with a slowing of the
venous symptoms, including the feeling of heaviness and lymphatic flow.22,37,38,54–56 More severe lipedema may be
swelling in the legs. associated with greater lymphatic transport abnormal­
Both diseases could exacerbate each other. Advancing ities.55 A frequent asymmetry between the lower ex­
age, female gender, and BMI compound an underlying re­ tremities is also noticed in the lymphoscintigraphic findings
lationship between lipedema and chronic venous disease.48 in contrast to the bilateral clinical presentation of the dis­
Obesity (increased volume on the trunk, increased ease.29 Depending on the pattern of the adipocyte tissue
weight, body mass index > 30 kg/m2, often no obvious dis­ expansion in each limb, different degrees of lymphatic
proportion, no edema, and no pain). transport abnormalities may be observed. Further study is
Dercum’s disease (increased volume, pain, but no needed to identify causative factors behind differences in
edema). disease expression between patients.55 Interestingly, Van de
Dercum’s disease (adiposis dolorosa) is a clinical condi­ Pas et al.38 found a symmetrical lymphatic function after
tion that partly overlaps with lipedema, as the two share liposuction.
cardinal features such as spontaneous or palpation-induced
pain and bruising. At its onset, Dercum’s disease is char­
MR imaging
acterized by multiple painful lipomas with possible pro­
gression into circumscribed or general diffuse fatty
Magnetic resonance imaging may have an important role in
deposition. It is usually accompanied by recurrent head­
differentiating lipedema from lymphedema and in evalu­
aches and depression, which are less frequently described
ating mixed forms of lipedema such as lipolymphedema and
in lipedema.10,50,51
lipophlebolymphedema.
Launois–Bensaude benign symmetric lipomatosis (in­
Lipedema is characterized by an increased layer of sub­
creased accumulation of fatty tissue with typical dis­
cutaneous fat without changes in signal intensity between
proportion, mostly localized in the neck (type I), shoulders
T-2 and T-1 weighted images, confirming that the tissue
and upper arms (type II), or pelvic region (type III), no pain,
does not contain excess fluid.49,57
no edema).2

MR lymphangiography

MR lymphangiography is an accurate minimally invasive

Imaging
imaging modality to delineate pathologically modified
lymphatic pathways in patients with lipedema and lipo-
In lipedema, the medical history and clinical examination
lymphedema.
do not always indicate the nature or extent of the under­
In the study of Lohrman et al.,35 clinically pure lipedema
lying abnormality (i.e., the anatomical extent, pathology,
was characterized by an increased layer of subcutaneous fat
and cause). Furthermore, the clinical distinction between
in the leg, with a maximum mean diameter of 4.4 cm at the
lipedema, lymphedema, phlebolymphedema, and lipolym­
level of the lower leg and 7.7 cm at the level of the upper
phedema can be difficult. Diagnoses often coexist, further
leg. Enlarged lymphatic vessels up to a diameter of 2 mm
complicating the diagnosis of lipedema, which is currently
were found, indicating a subclinical status of lympohos­
made on clinical grounds alone. Imaging can be useful to
tasis.35 Lymphatic vessels showed a beaded appearance
differentiate lipedema from other similarly presenting
(microlymphatic aneurysms of lymphatic capillaries).35,58,59

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 Table 1 Studies assessing the effectiveness of liposuction for lipedema treatment.
Author N Age Mean BMI Lipedema Technique No. Mean amount of fat Mean Median FU Pain Cons
stage operations weight loss treatm po
Rapprich, 201033 25 38 NR NR TL 1–5 1909$ 6.9% VR 6 mo ↓↓↓ 16%
(mean 2.5)
Wollina, 201034 6 (LE+DD) 58 38 II, n = 2 TL 1–4 2808 ml NR 6–48 mo ↓ NR
III, n = 4
Schmeller, 2012&2 112 39 NR I, n = 35 TLA 1–7 9846 ml or 3077 ml per 4.3 kg 4 yrs ↓↓↓ 77%
II, n = 75, session
III, n = 2
Wollina, 201270 18 (LE + 47 35.3 I, n = 1 TL + LATL 1–4 TL 4200 ml 7.8 kg 18 mo ↓↓↓ N/A
1 DD) II, n = 6 LATL 2600 ml/session
III, n = 11
Baumgartner, 2016 85 40 NR I, n = 24 TLA NR NR NR 8 yrs 70%
&71 II, n = 61
Dadras, 201772 25 45 35.3 I, n = 1 TL 1–7, mean 3 9914 ml 16/37 mo ↓↓↓ N/A
II, n = 11

308
III, n = 13
Mü nch, 201773 141 37 26.6 NR WAL + sed NR 4200 ml 3.4 kg 36 mo ↓↓↓ 95%
Bauer, 201914 209 38 NR II, n = 209 TL 1–9, 10.1 L= average amount of NR 12 mo ↓↓↓ 49.3%
Average 3 total fat
Wollina and Heinig, 111 44 NR I, n = 7 TLA NR Median 4700 ml LC 2 yrs ↓↓↓ 84
201974 II, n = 50 -6 cm
III, n = 48
Ghods, 202015 106 41 31.6 I= 11 TL Median 3 6355 ml/operation 34 mo after 1st ↓↓↓
II= 61 17,887 ml throughout entire operation
R.F.D. van la Parra, C. Deconinck, G. Pirson et al.

III= 34 surg treatment

Witte, 202075 63 35 28.4 I (29%) WAL 1 (10%) 12,922 ml 5.6 kg 22 mo* ↓↓↓ 44%
II (71%) 2 (33%)
3 (38%)
4 (19%)
*mean; mo, months; $, amount of pure fat; VR, volume reduction; NR, not reported; TL, tumescent liposuction; TLA, tumescent local anesthesia; WAL, water-assisted liposuction; LATL,
laser-assisted tumescent liposuction; LE, lipedema; DE, Dercum’s disease; LC, limb circumference; FU, follow-up; sed, sedation; cons treatm, conservative treatment; po, postoperative; &,
indicates same study population but different follow-up times.
 Journal of Plastic, Reconstructive & Aesthetic Surgery 84 (2023) 302–312

Dual-energy X-ray absorptiometry (DXA) Compared to more conventional liposuction the water-
assisted technique better respects the anatomical struc­
Dual-energy x-ray absorptiometry, measuring regional body tures without damaging them.3,68,69
composition, provides quantification and distribution in­ It is recommended that liposuction be performed in
formation about total and regional fat, lean, and bone multiple sessions since extensive amounts of adipose tissue
mass, thus representing a useful tool for diagnosis, staging, have to be removed.
and follow-up of lipedema patients.60 To date, all studies show clinical improvements for
Analysis by Dietzel et al.60 suggested that fat mass in the women with lipedema using tumescence or WAL techniques
legs adjusted for BMI was the best index for diagnosing li­ (Table 1).2,14,15,33,34,70–75
pedema, with a cut-off value of 0.46.60 Liposuction is effective in the treatment of lipedema and
However, BMI analysis may be misleading since it con­ significantly improves symptoms (pain, sensitivity to pres­
siders total weight without considering regional fat dis­ sure, tendency to swelling, and restriction of movement)
tribution, which is a hallmark of lipedema. Buso et al.39 and quality of life, with a lasting benefit, even after an 8-
therefore optimized diagnostic efficacy by dividing the year follow-up.71
amount of leg fat mass by total fat mass and presented this It also improves lymphatic symptoms, reducing the need
index with a cut-off value of 0.383. for conservative therapy,2,14,33,71,74–76 and it does not de­
These references may be particularly helpful for a dif­ crease lymphatic drainage as shown by lymphangioscinti­
ferential diagnosis in otherwise doubtful cases. graphy.38,77 However, conservative therapy must be
consistently continued even after surgery in order to avoid
or slow down the progression of the disease.
Lipedema reduction surgery may be less effective in
advanced stages of lipedema61,72,74 and in women with li­
Treatment pedema and severe obesity,2,71,76,78 although recent data
demonstrate a greater reduction of symptoms in more ad­
An etiological treatment for lipedema is currently still vanced cases.74,79
lacking. Treatment is focused on symptom reduction, Fat embolism after liposuction has been observed in up
functional limitation amelioration, and prevention of dis­ to 8.5% of patients undergoing liposuction. There are no
ease progression. data indicating a higher risk of fat embolism in liposuction
Therapeutic approaches also aim at impacting factors for lipedema compared to esthetic indication.74
negatively influencing lipedema progression, such as obe­ With increasing age, skin laxity after liposuction may occur.
sity, lymphedema, venous insufficiency, and decreased Skin laxity is also a serious problem after massive weight loss.
physical activity.10 Patients with advanced lipedema after liposuction usually
Treatment of lipedema is based on two pillars: con­ have a vertical tissue excess propagated by the looser ad­
servative decongestive treatment (CDT) and surgery. herence of skin and adipose layers of the medial thigh.
According to international guidelines, conservative treat­ Secondary surgical procedures to correct this skin laxity
ment should always be initiated.42,48,61–63 Manual lymph might become necessary but carry an increased risk of
drainage (MLD), compressive garments, and physical ex­ lymphatic vessels destruction. It is important to objectify
ercise should improve lipedema tissue by increasing lym­ the presence of lymphedema preoperatively to detect
phatic flux, which in turn increases the movement of subclinical lymphatic insufficiency that could decom­
glycosaminoglycans from the extracellular matrix into pensate after surgery. The vertical scars in post-bariatric
lymphatic vessels.48 These measures can offer some reconstructive surgery follow the anatomical course of the
symptom relief (less tenderness and tightness) and reduce lymphatics and are thus expected to be less problematic
capillary fragility, resulting in a reduction of petechiae and with regard to lymphatic drainage than transverse incisions.
hematoma formation following minor trauma.64 However, An imaging study to objectify the effect of excess skin re­
the long-term benefit is questionable and in the absence of section on the lymphatics could answer this hypothesis.
edema even doubtful since CDT has no effect on adipose A combination of lymphovenous anastomosis and debulking
tissue25,41 In addition, compression may not be tolerated by surgery might offer improvement in physiologic drainage of
lipedema patients because of pain. excessive lymphatic fluid and removal of excess adipose
If symptoms persist liposuction should be considered to tissue, respectively.55 Combining these techniques may re­
reduce the volume of adipose tissue in lipedema. It is the duce cellular and metabolic load on the lymphatic system
only treatment that slows progression of lipedema and while adding capacity to the system of lymphatic transport by
ideally would be performed before complications and dis­ bypassing the native routes of lymphatic flow and increasing
abilities from lipedema develop.48 However, several articles the drainage of the limb. Removal of lymphatic fluid may in
suggest that liposuction could induce lymphedema due to turn decrease adipogenesis, as lymphatic fluid has been shown
destruction of the lymphatic vessels, especially classic dry to upregulate adipose generation and differentiation.55
liposuction.65,66 Tumescence or water-jet-assisted liposuc­
tion (WAL) is therefore often recommended to spare the
lymphatic vessels. Cadaver studies have shown markedly
reduced injury to lymphatic structures when the tumescent Conclusion
technique was used and when the liposuction cannula is
oriented longitudinally instead of radially with regard to the Many questions remain to be answered regarding lipedema.
vessels.66,67 Its diagnosis remains a challenge due to its heterogeneous

309
 R.F.D. van la Parra, C. Deconinck, G. Pirson et al.

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