Received: 2 March 2018 Accepted: 19 May 2018

DOI: 10.1111/iwj.12949

ORIGINAL ARTICLE

Lipoedema is not lymphoedema: A review of current literature

Eran Shavit1 | Uwe Wollina2 | Afsaneh Alavi1

1
Division of Dermatology, Department of
Medicine, Women’s College Hospital, University Lipoedema is a rare painful disorder of the adipose tissue. It essentially affects
of Toronto, Toronto, Ontario, Canada females and is often misdiagnosed as lymphoedema or obesity. It is globally mis-
2
Department of Dermatology and Allergology, diagnosed or underdiagnosed, and the literature is lacking appropriate guidance to
Academic Teaching Hospital Dresden-
assist clinicians towards this diagnosis. However, the need to recognise this disor-
Friedrichstadt, Dresden, Germany
der as a unique entity has important implications to establish proper treatment and,
Correspondence
Eran Shavit, MD, Division of Dermatology, therefore, its tremendous effect on patients. Early diagnosis and treatment can turn
Department of Medicine, Women's College these patients’ lives upside down. The aim of this review is to focus on the clinical
Hospital, University of Toronto, Toronto, Ontario, guidance, differential diagnosis, and management strategies. In addition, other
Canada.
Email: [email protected]
aspects of lipoedema, including epidemiology and pathogenesis, are also being dis-
cussed here. Lipoedema is distinct from obesity and distinct from lymphoedema,
although it might progress to involve the venous and lymphatic system (venolipe-
dema or lympholipedema or both). Late diagnosis can leave the patient debilitated.
Management of lipoedema includes weight loss, control of oedema, complex
decongestive physiotherapy, liposuction, and laser-assisted lipolysis. However;
there are increasing reports on tumescent liposuction as the preferred surgical
option with long-lasting results. The role of more randomised controlled studies to
further explore the management of this clinical entity remains promising.

KEYWORDS

lipoedema, lymphoedema, lympholipedema (in German lipo-lymphedema),

tumescent liposuction

1 | INTRODUCTION lymphoedema. The former has a possible inheritance of

X-linked dominant or autosomal dominant pattern with
Lipoedema is thought to be an uncommon disorder of adi- sex limitation.1 It is bilaterally symmetrically distributed,
pose tissue. It is a symmetrical, disproportional distribu- and it is associated with pain, oedema, and easy bruising.
tion of fat deposited in the lower limbs and/or upper It commonly affects females after puberty but may also
limbs featuring frequent ecchymosis because of even develop at other periods of hormonal change, such as
minor traumatic injuries. The pathophysiology of this pregnancy or menopause.1–3 It has a significant physical
group of disease with disproportional fatty distribution and psychological effect on its patients. The diagnosis of
lipodystrophies, such as multiple symmetric lipomatosis, lipoedema is quite frequently missed because of unfamil-
Dercum’s disease (DD), and lipoedema, is not clearly iarity of clinicians with this condition and, perhaps, the
elucidated. over-diagnosis of lymphoedema or, sometimes, obesity
Lipoedema almost exclusively affects women, and it instead.4,5 Lymphoedema is more commonly asymmetric
is commonly misdiagnosed as lymphoedema (Figures 1 (Figure 2), without associated pain or bruising. However,
and 2). The phonetic sound of both diagnoses is quite sim- lipoedema is a chronic progressive disease, and advanced
ilar, which might even add to the misconception and com- cases may deteriorate to involve either the lymphatic sys-
mon error between the two. However, lipoedema is a tem (lympholipedema) or the venous system (venolipe-
distinct entity with some differences in comparison with dema) (Figure 2), or both, which will add to the confusion

Int Wound J. 2018;15:921–928. wileyonlinelibrary.com/journal/iwj © 2018 Medicalhelplines.com Inc and John Wiley & Sons Ltd 921
922 SHAVIT ET AL.

in the diagnosis. While progressing to either lympholipe-

dema or to venolipedema, complication such as recurrent Key Messages
infections and ulceration might persist. • lipoedema is a rare painful disorder of the fatty tissue that
Obesity is another common misdiagnosis, but in obesity, affects women after puberty and is often misdiagnosed or
the distribution of fat is symmetrical with the involvement of underdiagnosed
the central body and common involvement of arms. Even • lipoedema is a distinct entity that must be differentiated from
though patients with lipoedema commonly have a high body obesity and lymphedema, although it may progress to involve
mass index (BMI), because of localised distribution, dieting and the venous and lymphatic systems, which increases the diffi-
exercises have limited success for weight loss. Oddly, the culty of its diagnosis
English literature is sparse regarding the pathogenesis, epidemi- • the diagnosis of lipoedema is clinical, and it is essential to rec-
ology, diagnosis, and management strategies for this disorder,6 ognise this unique entity in order to establish proper treatment
although the number of textbooks and publications dealing with • the literature is lacking an appropriate guidance towards this
lipoedema is extensive in the German literature.7 The need to diagnosis; therefore, we have provided in this article an algo-
recognise this disorder as a unique entity is universal and has rithm to guide clinicians to diagnose lipoedema
important implications as late diagnosis can delay proper treat- • the management of lipoedema includes conservative and sur-
ment and lead to true debilitation of these patients. The aim of gical approaches; in case the former fails and the latter is
this review is to increase the awareness of lipoedema as a dis- required, tumescent liposuction is marked as the preferred
tinct entity and to provide clues for the diagnosis; therefore, we option with long-lasting results
have emphasised the clinical guidance and differential diagnosis
for clinicians as well as revised the knowledge about epidemiol-
ogy, pathogenesis, and management strategies for lipoedema.
excluded as a result of being in another language (2 in
French and 2 in Serbian), and 14 did not pertain directly to
2 | MET HO D OL OG Y the topic of lipoedema, which led to a total of 94 articles.

We have conducted a database search of PubMed and

EMBASE for published articles on the subject of lipoedema. 3 | E PI DE M I OL OG Y A ND PA TH O GE NES IS
Using the keywords “lipedema” and lipoedema”, all studies
and review from 1995 to October 2017 were included. We The aetiology of lipoedema is unknown. The disorder was
have included papers published in the English and German originally described by Allen and colleagues in 1940 as
languages. Our search has demonstrated 112 reports; 4 were “large legs due to the subcutaneous deposition of fat in the

FIGURE 1 Stages of lipoedema. (From left to right) stages I-II-III

SHAVIT ET AL. 923

FIGURE 2 Differential diagnosis: (from left to right) unilateral lymphedema (notice the asymmetry), venolipoedema-notice the “ankle pad” sign is
prominent (also secondary changes of lipodermatosclerosis), acute lipodermatosclerosis and chronic lipodermatosclerosis (right picture)-notice the sharp
margination and sparing of the feet

buttocks and lower extremities and the accumulation of fluid the interstitial space demonstrates numerous capillary ves-
in the legs”.8 Based on a study of 330 family members, a sels. The infiltration surrounding the capillaries includes
possible autosomal-dominant inheritance with incomplete macrophages, fibroblasts, and mast cells and increased
penetrance was suspected; however, the exact genes fibrosis with disease progression.15
involved in lipoedema have not been identified. The Microangiopathy is one of the earliest changes in lipoe-
VEGFR-3 heterozygote-inactivating missense mutation and dematous tissue that could be related to endothelial barrier
mutation of PIT-1 gene have been reported. function. Adipocyte hyperproliferation because of hypoxia
Lipoedema is encountered exclusively in female may lead to adipocyte necrosis, production of inflammatory
patients, during or following puberty, during the second to cytokines, and macrophage infiltration.
the third decades of life. However, there have been reports Immunohistochemical analyses of lipoedematous tis-
of onset after pregnancy or even menopause.8 Although sue demonstrated necrotising adipocytes surrounded by
exclusive to females, there have been 8 case reports of infiltrating CD68+ macrophages, which is a feature com-
lip0edema in males in the context of pronounced hormonal monly seen in obese adipose tissue. Furthermore, there
imbalance.1,9 was a proliferation of adipose-derived stem cells, progen-
Oestrogen has a direct effect on white fat through its oes- itor cells, and stromal cells (Ki67+ CD34+ cells). Such
trogen receptors, but the exact change in oestrogen receptors findings suggest that the possible mechanism leading to
in lipoedematous tissue and the exact role of oestrogen is not the development of lipoedema may involve increased
clear. Most patients with lipoedema have a high BMI, which adipogenesis, leading to hypoxia, further adipocyte
can be either because they are overweight or obese; how- necrosis, and macrophage recruitment.5,15–17 However,
ever, many of these patients have a normal appearance above in a recent study, proteins from adipose tissue of lipoe-
their waist, accounting for a disfigurement between their dema patients were harvested and did not indicate
lower and upper extremities, and this might falsely elevate tyrosine-phosphorylated proteins in lipoedema tissue and
their BMI levels. controls. These results suggest the absence of activated
A positive family history suggesting lipoedema is linked growth factor receptors in the pathways of adipogenesis of
to a genetic component has been described in up to 60% of the lipoedema patient.18 Another interesting finding was
cases.1,10,11 The overall prevalence of lipoedema in the gen- that stromal vascular fraction cells (CD90+, CD146+)
eral population is uncertain, and it has been reported to be as were significantly enhanced in lipoedematous adipose tis-
low as 0.1%; however, some studies conducted on outpa- sue compared with normal adipose tissue. On the other
tient's clinics estimate the prevalence to be 7% to 10%.11 hand, the adipogenic differentiation potential of these cells
Whereas studies conducted on hospitalised patients demon- was significantly reduced when compared with healthy
strated prevalence percentages between 8% and 18%.10–13 In controls.19
a trial in southern Germany, the prevalence was 10% among Functional lymphoscintigraphy, which study the lym-
adult women.14 Despite the wide range of prevalence docu- phatic system, have been conducted comparing patients with
mented in various studies, we still believe that lipoedema is lipoedema, normal subjects, and patients with lymphoedema.
an uncommon disease. In the early stages of the disease, increased lymph flow
The histopathology of lipoedema is not pathogno- (high-volume insufficiency) has been reported, along with
monic and cannot serve as a diagnostic tool. With a decreased lymphatic flow with pathological lymph node
greater amount of fat cells and occasional hypertrophy, uptake at later stages,20,21 whereas some cases showed no
924 SHAVIT ET AL.

TABLE 1 Stages of lipoedema it is extremely rare.11 A characteristic feature of lipoedema

Stages Characteristics is pain; it is described as dull, heavy, and pressing. The pain
Stage 1 Smooth skin; soft homogenous increase in subcutaneous can be elicited by touch or pressure, or it can occur after
tissue, cool skin in certain areas because of functional standing or sitting for a protracted period, as well as at the
vascular imbalance
Stage 2 Irregular skin surface, nodular changes of the
end of the day.11,24 This tenderness makes high-compression
subcutaneous tissue therapy challenging, particularly in cases where lipoedema is
Stage 3 Tender subcutaneous nodules, pronounced increase in associated with the involvement of veins or lymphatics. The
circumference with loose skin/tissue, bulging protrusion
of fat mainly at inner thighs and knees
nosology of oedema is divided according to the substance or
fluid involved; while the oedema content of lymphoedema
consists of lymph fluid, in lipoedema, swelling a result of
significant changes.22 These contradicting studies suggest
the deposition of fatty tissue.
that, unlike lymphoedema, lipoedema may not be related to
lymphatic disturbance and may rather be a form of lipody-
strophy or lipomatosis. 5 | D I A G N O S I S A N D D I F F E R E N TI A L
DI A GN OS IS
4 | CLINICAL PRESENTATION
The diagnosis of lipoedema is clinical and mainly relies only
on history and physical examination. Even though lipoe-
Lipoedema starts almost imperceptibly after puberty; it per-
dema is commonly mistaken to be obesity and lymphoe-
sists over the lifetime and progresses gradually. There are
three stages to this disease as listed in Table 1. Stage III of dema, striking clinical features, sparing feet and hands,
lipoedema may develop after several decades without appro- filling of retromalleolar sulci with fat, and pressure sensitiv-
priate therapy and leads to impairment of gait and disability ity of the below-knee medial fat pad is helpful for diagnosis
of these patients.23 Therefore, it is crucial to establish early when clinicians are familiar with the disease.
and correct diagnosis. Considering the enlargement of lower extremities, the
The changes associated with lipoedema occur symmetri- first step towards the diagnosis is to determine whether this
cally on the legs and arms (gynoid distribution). The typical enlargement is unilateral or bilateral (see Figure 3). Lipoe-
presentation is of a woman with bilateral “stovepipe” dema is always bilateral and non-pitting, and other diagnoses
enlargement of the legs and without involvement of the feet that might cause bilateral lower limb with pitting oedema
with a sharp demarcation between normal and abnormal tis- include early lipodermatosclerosis, dependent oedema, limb
sue at the ankle, referred to as the “cuff sign.” This is often swelling because of internal (such as thyroid, heart, kidney)
combined with a symmetrical involvement of arms, particu- diseases, and oedema because of certain medications.25
larly the upper arms, with sparing of hands. Lipoedema may Lipoedema is almost always bilateral, whereas lymphoe-
be isolated to the arms without involvement of the legs, but dema may be unilateral or bilateral, but the involvement

Lipedema diagnostic algorithm

Enlargement of lower
extremities

Unilateral Bilateral

Acute Chronic Acute Chronic

Erythema - Erythema + Erythema +

Pitting Non-pitting
Erythema - Pitting Non-pitting

US Lymphangitis Stemmer’s Erythema CHF Stemmer’s sign - Stemmer’s sign +

Pain mostly + Pruritus+ Varicose Stemmer’s sign CHF
on calf area+ Lymphadenitis veins+ + sign - + cirrhosis
+ cirrhosis CRF Erythema +
R/O Erythema - LMP
COS DVT VM* CRF acute Maln
CD CVI KTS Meds
R/O Cellulitis LMP LPD Upper & lower
RBC CVI Lower limb
Ankle pad +
body LPD
ankle pad-

RBC-Ruptured Baker’s cyst LP Obesity

COS-Compartment syndrome
CD- Contact dermatitis
CHF-congestive heart failure
CRF-Chronic renal failure
CVI- chronic venous insufficiency
DVT- deep vein thrombosis
Maln-Malnutrition
Meds- Medication
LP- Lipedema
LPD- Lipodermatosclerosis
LMP- Lymphedema
VM*- Vascular malformation include Parkes Weber syndrome and May-Turner syndrome
Stemmer’s sign= is the inability to pinch the fold of skin at the base of the second toe
US-Ultrasound
TD- Thyroid disease

FIGURE 3 Lipoedema diagnostic algorithm (and approach to enlargement of lower extremities)

SHAVIT ET AL. 925

TABLE 2 Differential diagnosis of common entities that cause lower limb swelling

Characteristics Lipoedema Lymphedema LPD Obesity Venous insufficiency Dercum’s disease Myxedema
Pathophysiology Genetic, Defects in Fibrinolytic Multifactorial CVI Genetic Thyroid
primary lymph vessels abnormalities abnormalities
Incompetent valves
Primary or CVI
Other
secondary
Disproportion Yes No No No Yes No
Age of onset Puberty Any age Adults mostly Any age Adults PML Any age
elderly
Gender Female Both genders Both genders Both genders Both genders Female More common
in female
Skin consistency Firm Soft Wooden hard Firm Depending on Firm Firm
the stage
Skin colour Normal Brown, Early-red Normal Depending on Normal Reddish-orange
warty, sclerotic the stage
Sometimes Late-brownish Sometimes
ecchymosis ecchymosis
Extent of Bilateral Unilateral or Shins Bilateral Unilateral or bilateral Bilateral legs, Bilateral shins
involvement bilateral most lower limbs arms, trunk
Mainly legs Unilateral or Mainly
commonly on
bilateral most central body
legs and arms
commonly
bilateral
Symmetry Symmetric May be May be Symmetric May be symmetric Symmetric Symmetric
asymmetric asymmetric
Clinical clues “Cuff sign” ankle Verruca Hard consistency, Central obesity Other signs of Painful lipomas Reddish-brown
pad fatty papillomatosis colour change, venous disease, plaques on both
Involvement of
retromalleolar pebbly stone other changes stasis dermatitis, shins “peau
arms and trunk
sulcus or lack skin positive of CVI may varicose veins d’orange look”
of Achilles stemmer signa be present
tendon definition
Involvement No Yes No No Yes Yes No
of feet
Response to No Yes Yes No Yes Yes No
compression
therapy
Common Anxiety/depression Venous disease CVI Metabolic CVI Mood disorder Thyroid disease
associations syndrome
Hypermobility Recurrent DVT Diabetes Other autoimmune
cellulitis diseases
Easy bruising Yes No No No No Yes No

Abbreviations: CVI, chronic venous insufficiency; DVT, deep venous thrombosis; LPD, lipodermatosclerosis; PML, postmenopausal.
a
A positive Stemmer sign is the inability to pinch the fold of skin at the base of the second toe or finger, indicating the presence of lymphoedema.

may be dominant on one side. Lipoedema typically presents be caused by thyroid hormone imbalance such as pretibial myx-
in women bilaterally and symmetrically with a sharp demar- edema, a rare autoimmune manifestation of Graves’ disease.27
cation at the ankle, referred to as the “cuff sign” or “reverse Typically, bilateral, non-pitting, doughy oedema is a result of
shouldering” (see Figure 2). The skin is normal, particularly thickening and induration because of mucin deposition. The
in the early phases, and as mentioned before, the patients oedema has a unique clinical feature with more predominant on
may complain of “painful lower limbs.” anterior shin. A thyroid-stimulating hormone (TSH) level
Lipodermatosclerosis presents as bilateral swelling of the should be set in patients with lower-extremity non-pitting
shins associated with erythematous changes, and the skin is oedema without known cause. Medications are another cause of
indurated with “woody-like” consistency. In the acute set- lower limbs swelling, most commonly calcium channel
ting, acute lipodermatosclerosis will not demonstrate indura- blockers (such as Amlodipine), and other culprit drugs include
tion yet, instead demonstrating bilateral erythema, oedema, gabapentin, non-steroidal anti-inflammatory drugs (such as ibu-
and increased warmth on palpation; the clinical presentation profen), oral contraceptives, corticosteroids (prednisone), and
somewhat mimics cellulitis (Figure 2).26 thiazolidinediones (such as pioglitazone).28
Dependent pitting oedema can be multifactorial, and the Lymphoedema and chronic venous insufficiency can present
common causes include congestive heart disease, chronic renal with lower limb swelling that can either be unilateral or bilateral.
insufficiency, liver cirrhosis, and hypoalbuminemia. Many clues Lymphoedema is more commonly presented bilaterally, whereas
can be provided in the history and during bed side physical unilateral involvement could be related to primary lymphoe-
examination, for example, dyspnoea, jugular veins distention, dema, or the inguinal nodes are affected iatrogenically either
pleural effusion, and ascites. Bilateral non-pitting oedema can post-surgery (lymph node dissection because of various causes)
926 SHAVIT ET AL.

TABLE 3 Various treatments deployed

Length of follow up
Author Sample study Study type Treatment and recurrence Outcome
Dadras et al39 25 patients Longitudinal study Liposuction 16 and 37 mo Significant reductions in
questionnaire spontaneous pain, sensitivity
No recurrence reported
to pressure, feeling of tension,
bruising, cosmetic impairment,
and general impairment to
quality of life
Baumgartner et al43 85 patients Single-Centre Liposuction 4 and 8 y Improvement in spontaneous pain,
study. A mail sensitivity to pressure, oedema,
No recurrence reported
questionnaire—often bruising, and restriction of
in combination with movement persisted
clinical controls
Couto JA et al44 1 patient Retrospective Liposuction 8y Suction-assisted tissue removal
No recurrence reported
Leclère et al45 30 patients Satisfaction Laser-assisted 3 mo Homogeneous reduction of fatty
questionnaire lipolysis tissue with skin tightening and
overall satisfaction reported in
29 of 30 patients
Wollina et al41 24 patients Open trial comparing Laser-assisted 3 to 60 mo Short operation time and early
liposuction liposuction mobilisation, reduction of pain
No recurrence reported
(n = 12) with and improved mobility
complex decongestive
therapy (n = 12)
Schmeller et al40 164 patients Monocentric Tumescent 1 to 8 y Significant reduction of subcutaneous
standardised liposuction (mean 3 y and 4 mo) fatty tissue, improvement of shape,
questionnaire pain, sensitivity to pressure, oedema,
No recurrence reported
bruising, restriction of movement,
(19% reported to need
and cosmetic impairment
MLD and compression
as before)
Rapprich et al46 25 patients Case series Tumescent 6 mo Measurement of the volume of the
liposuction legs using visual analogue scales
No recurrence reported
(VAS, scale 0-10). Results: The
volume of the leg was reduced by
6.9 %. Pain was the predominant
outcome. For symptom, quality
of life as a measure of the
psychological strain was assessed
Peled et al47 1 patient Case report Suction-assisted 4y Successful treatment of the
lipectomy lipodystrophy and maintenance
No recurrence reported
of improved aesthetic results at
4-y postoperative follow up
Szolnoky et al48 38 patients Case-control Complex decongestive Not available Significant reduction of
(21 vs 17) physiotherapy petechiae and capillary
fragility in treatment group
Szolnoky et al35 24 patients Prospective, Complex decongestive Not available No significant reduction in lower
randomised trial physiotherapy with or extremity volume with IPC
without IPC

Abbreviation: IPC, intermittent pneumatic compression; MLD, manual lymphatic drainage.

or because of compromising the lymphatic system through recur- et al. 94 patients with DD, 120 patients with lipoedema, and
rent infections (recurrent cellulitis/erysipelas) or in developing 18 with both conditions were studied. Patients with lipoedema
countries because of filariasis. Stemmer sign, or the inability to had a significantly lower prevalence of type 2 diabetes and a
pinch the base of the second toe, is a unique characteristic symp- higher prevalence of hypermobility. The location of fat, high
tom for lymphoedema.29 In contrast to lipoedema, lymphoedema average daily pain, presence of lipomas, and comorbid painful
is not typically associated with easy bruising and tenderness; disorders help in the differentiation of DD from lipoedema.31
Table 2 provides the differential diagnosis of lipoedema.30,31 We have established an algorithmic approach to guide
DD is an uncommon painful lipodystrophy with clinicians towards the diagnosis of lipoedema. An algorithm
autosomal-dominant inheritance that mainly involves post- for the diagnosis of lipoedema is given in Figure 3.
menopausal females. DD can be further classified into nodu-
lar, diffuse, and mixed type. Both diffuse and mixed are in 6 | T RE AT M EN T
included in the differential diagnosis of lipoedema. Although
DD and lipoedema share several characteristics, patients with The goal of therapy is to improve symptoms and prevent
DD have more systemic involvement. In a study by Beltran secondary complications, particularly to reduce pain and
SHAVIT ET AL. 927

decrease the bulk of fat deposition. Conservative treatment removed during multiple sessions. This leads to significant
should be employed to control associated oedema, and reductions of subcutaneous fat tissues. However, studies
options include: combined decongestive therapy, manual comparing the outcome of each technique do not favour one
lymphatic drainage, compression garments or bandages, and of the procedures considering the efficacy and safety for the
mobilisation.32 patient, although laser-assisted liposuction provides better
Compression therapy is a challenge in these patients tissue tightening.41,42
because of lower leg tenderness. In a study from the United Other available options in the literature include laser sur-
Kingdom, the two main reasons for non-adherence in these gery and lipectomy (see Table 3 for other therapeutic
patients included discomfort and difficulty in putting on the options). Lipectomy, however, bears the risk of relapse and
compression garments.33 The effectiveness of compression
always produces long scars. Lipectomy should be reserved
therapy is also minimal, but it is beneficial for the associ-
to the juxtarticular lipoedema of the knee. The procedure is
ated oedema in these patients through the reduction in
indispensable in advanced cases of fibrotic tissue conver-
interstitial fluid. The better outcome is associated with the
sion.49 Liposuction in lipoedema does not aim to remove
introduction of compression therapy to these patients at the
giant amounts of adipose tissue but improve quality of life
early stage of the disease.34–36 A good support measure can
and significantly reduce pain. If there is concomitant morbid
include manual lymphatic drainage and intermittent pneu-
matic compression if the pneumatic compression has at obesity, this should be treated first.
least 6 to 12 chambers.34 Diet has very limited effect in In conclusion, healthy life style, weight control, oedema
lipoedema patients on the surplus weight accumulated in reduction, and other supportive therapies are recommended
the lower extremities that would eliminate the obvious dis- in the management of patients with lipoedema. However,
proportion between the relatively thin upper half of the tumescent liposuction is the treatment of choice in case of
body and the large lower extremities. This may contribute progression despite consequent conservative therapy.
to some frustration, reduction in self-esteem, and mental
health consideration.2,37 The role of diet is much more rele- Conflict of interest
vant in the case of combined obesity. Surgical options are
used to permanently reduce the amount of subcutaneous No conflict of interest was declared.
fatty tissue from the affected areas. Liposuction can be per-
formed under tumescent local anaesthesia. Presently, lipo- OR CID
suction under tumescent local anaesthesia has become an Eran Shavit https://orcid.org/0000-0003-2397-6316
established and low-risk surgical procedure; in fact, the
largest study to date has demonstrated tumescent liposuc-
tion to be the most effective option.38,39 This procedure is REFERENCES
associated with a pronounced improvement in pain, tender- 1. Child AH, Gordon KD, Sharpe P, et al. Lipedema: an inherited condition.
Am J Med Genet A. 2010;152A:970-976.
ness to pressure, oedema ,and easy bruising.39 In a study
2. Fife CE, Maus EA, Carter MJ. Lipedema: a frequently misdiagnosed and
by Baumgartner et al., 85 patients with lipoedema had misunderstood fatty deposition syndrome. Adv Skin Wound Care. 2010;23:
bilateral leg liposuction and made comparisons between 81-92.
baseline and the 4- and 8-year follow-up periods in terms 3. Okhovat JP, Alavi A. Lipedema: a review of the literature. Int J Low Extrem
Wounds. 2015;14(3):262-267.
of pain, oedema, bruising, restriction of movement, cos- 4. Fonder MA, Loveless JW, Lazarus GS. Lipedema, a frequently unrecog-
metic impairment, quality of life, overall impairment, and nized problem. J Am Acad Dermatol. 2007;57(2 suppl):S1-S3.
the necessity of decongestive therapy. The result of the 5. Godoy Mde F, Buzato E, Brigidio PA, Pereira de Godoy JM. Is lymphosta-
study confirmed the role of liposuction as the main stay of sis an aggravant of lipedema? Case Rep Dermatol. 2012;4:222-226.
6. Schmeller W, Meier-Vollrath I. Lipedema and liposuction. In: Weissleder H,
treatment for this challenging condition and preservation of Schuchhardt C, eds. Lymphedema. Diagnosis and Therapy. 4th ed. Essen,
the long-term effect of the procedure in any stage of the Germany: Vivavital; 2008:294, 473-323, 89.
disease. Early recognition of these cases and appropriate 7. Schmeller W, Meier-Vollrath I. Tumescent liposuction: a new and successful
intervention will decrease the burden of this disease for therapy for lipedema. J Cutan Med Surg. 2006;10:7-10.
8. Allen EVN, Hines EA. Lipedema of the legs: a syndrome characterized by
patients and health care professionals.40 fat legs and orthostatic edema. Proc Staff Meet Mayo Clin. 1940;15:
Liposuction can be performed either manually or laser- 184-187.
assisted. Due to numerous advantages, liposuction prefera- 9. Chen SG, Hsu SD, Chen TM, Wang HJ. Painful fat syndrome in a male
patient. Br J Plas Surg. 2004;57:282-286.
bly performed under tumescent local anesthesia, using the
10. Langendoen SI, Habbema L, Nijsten TE, Neumann HA. Lipoedema: from
wet technique with blunt cannulas. Supportive techniques in clinical presentation to therapy. A review of the literature. Br J Dermatol.
the form of vibration-assisted or water jet-assisted liposuc- 2009;161:980-986.
tion can be used in this context. In tumescent liposuction, 11. Reich-Schupke S, Schmeller W, Brauer WJ, et al. S1 guidelines: Lipedema.
J Dtsch Dermatol Ges. 2017;15(7):758-767.
large amounts of a mixture of saline, lidocaine, adrenaline,
12. Herpertz U. Lipedema. Z Lymphol. 1995;19(1):1-11.
and sodium bicarbonate are injected in to the tissue, and with 13. Lulay G. Lymphologische Akutklinik. Lymphol Forsch Praxis. 2010;14:
a blunt micro cannula, up to 10 to 20 L of liquid fat can be 90-95.
928 SHAVIT ET AL.

14. Marshall M, Schwahn-Schreiber C. Prävalenz des Lipödems bei berufstäti- 35. Szolnoky G, Borsos B, Barsony K, Balogh M, Kemeny L. Complete decon-
gen Frauen in Deutschland (Lipödem-3-Studie). Phlebologie. 2011;40: gestive physiotherapy with and without pneumatic compression for treat-
127-134. ment of lipedema: a pilot study. Lymphology. 2008;4:40-44.
15. Suga H, Araki J, Aoi N, Kato H, Higashino T, Yoshimura K. Adipose tissue 36. Szolnoky G, Varga E, Varga M, Tuczai M, Dósa-Rácz E, Kemény L.
remodeling in lipedema: adipocyte death and concurrent regeneration. Lymphedema treatment decreases pain intensity in lipedema. Lymphology.
J Cutan Pathol. 2009;36:1293-1298. 2011;44:178-182.
16. Földi M, Földi E, eds. Lehrbuch der Lymphologie: für Mediziner, Masseure 37. Reich-Schupke S, Altmeyer P, et al. Pilotstudie zur Kompressionsversor-
und Physiotherapeuten. Stuttgart, Gemany: Urban & Fischer; 2005:374-378. gung bei Patienten mit Lipödem. Lymphödem und Lipolymphödem Lymph-
17. de Godoy JM, Barufi S, Godoy Mde F. Lipedema: is aesthetic cellulite an Forsch. 2012;16:65-69.
aggravating factor for limb perimeter? J Cutan Aesthet Surg. 2013;6:167-168. 38. Hodson S, Eaton S. Lipoedema management: gaps in our knowledge. J Lym-
18. Schneble N, Wetzker R, Wollina U. Lipedema—lack of evidence for the involve- phoedema. 2013;8:30-34.
ment of tyrosine kinases. J Biol Regul Homeost Agents. 2016;30(1):161-163. 39. Dadras M, Mallinger PJ, Corterier CC, Theodosiadi S, Ghods M. Liposuc-
19. Priglinger E, Wurzer C, Steffenhagen C, et al. The adipose tissue-derived tion in the treatment of lipedema: a longitudinal study. Arch Plast Surg.
stromal vascular fraction cells from lipedema patients: are they different? 2017;44(4):324-331.
Cytotherapy. 2017 Jul;19(7):849-860. 40. Schmeller W, Hueppe M, Meier-Vollrath I. Tumescent liposuction in lipoe-
20. Bilancini S, Lucchi M, Tucci S, Eleuteri P. Functional lymphatic alterations dema yields good long-term results. Br J Dermatol. 2012;166:161-168.
in patients suffering from lipedema. Angiology. 1995;46:333-339. 41. Wollina U, Heinig B. Tumsescent microcannular (laser-assisted) liposuction
21. Boursier V, Pecking A, Vignes S. Comparative analysis of lymphoscintigra- in painful lipedema. Eur J Aesthet Med Dermatol. 2012;2(2):56-69.
phy between lipedema and lower limb lymphedema. J Mal Vasc. 2004;29: 42. Goldman A, Wollina U, de Mundstock EC. Evaluation of tissue tightening
257-261. by the subdermal Nd: YAG laser-assisted liposuction versus liposuction
22. Bräutigam P, Földi E, Schaiper I, Krause T, Vanscheidt W, Moser E. Analy- alone. J Cutan Aesthet Surg. 2011;4(2):122-128.
sis of lymphatic drainage in various forms of leg edema using two compart- 43. Baumgartner A, Hueppe M, Schmeller W. Long-term benefit of liposuction
ment lymphoscintigraphy. Lymphology. 1998;31:48-55. inpatients with lipoedema: a follow-up study after an average of 4 and
23. JJ S, D K. Water jet-assisted liposuction for patients with lipoedema: histo- 8 years. Br J Dermatol. 2016;174(5):1061-1067.
logic and immunohistologic analysis of the aspirates of 30 lipoedema 44. Couto JA, Maclellan RA, Greene AK. Management of vascular anomalies
patients. Aesth Plast Surg. 2009;33:153-162. and related conditions using suction-assisted tissue removal. Plast Reconstr
24. Schmeller W, Meier-Vollrath J. Schmerzen beim Lipödem. LympForsch. Surg. 2015;136(4):511e-514e.
2008;12:8-12. 45. Leclere FM, Moreno-Moraga J, Mordon S, et al. Laser assisted lipolysis for
25. Schellong SM, Wollina U, Unger L, Machetanz J, Stelzner C. [Leg swelling] ankle remodelling: a prospective study in 30 patients. Lasers Med Sci. 2014;
(German: Das geschwollene Bein). Internist (Berl). 2013;54(11):1294-1303. 29:131-136.
26. Hirschmann JV, Raugi GJ. Lower limb cellulitis and its mimics: part II. Conditions 46. Atiyeh B, Costagliola M, Illouz YG, Dibo S, Zgheib E, Rampillon F. Func-
that simulate lower limb cellulitis. J Am Acad Dermatol. 2012;67(2):177. tional and therapeutic indications of liposuction: personal experience and
27. Bartalena L, Fatourechi V. Extrathyroidal manifestations of Graves' disease: review of the literature. Ann Plast Surg. 2015;75(2):231-245.
a 2014 update. J Endocrinol Invest. 2014;37(8):691-700. 47. Peled AW, Slavin SA, Brorson H. Long-term outcome after surgical treat-
28. Ratchford EV, Evans NS. Approach to lower extremity edema. Curr Treat ment of lipedema. Ann Plast Surg. 2012;68(3):303-307.
Options Cardiovasc Med. 2017;19(3):16. 48. Szolnoky G, Nagy N, Kovacs RK, et al. Complex decongestive physiother-
29. Stemmer R. A clinical symptom for the early and differential diagnosis of apy decreases capillary fragility in lipedema. Lymphology. 2008;41:161-166.
lymphedema. Vasa. 1976;5:261-262. 49. Wollina U, Heinig B, Schönlebe J, et al. Debulking surgery for elephantiasis
30. Porter JM, Moneta GL. Reporting standards in venous disease: an update. nostras with large ectatic podoplanin-negative lymphatic vessels in patients
International consensus committee on chronic venous disease. J Vas Surg. with lipo-lymphedema. Eplasty. 2014;14:e11.
1995;21:635-645.
31. Beltran K, Herbst KL. Differentiating lipedema and Dercum's disease. Int J
Obes (Lond). 2017;41(2):240-245.
32. Heinig B, Wollina U. Komplexe Entstauungstherapie. Hautarzt. 2015;
How to cite this article: Shavit E, Wollina U,
66(11):810-818.
33. Alavi A, Sibbald RG, Phillips TJ, et al. What's new: management of venous Alavi A. Lipoedema is not lymphoedema: A review
leg ulcers: approach to leg ulcers. J Am Acad Dermatol. 2016;74(4):627-640. of current literature. Int Wound J. 2018;15:921–928.
34. Fetzer A. Specialist approaches to managing lipoedema. Br J Community https://doi.org/10.1111/iwj.12949
Nurs. 2016;21(Suppl):S30-S35.