Lymphedema Treatments
There are many types of lymphedema treatments available and all have different levels of effectiveness but when combined together they provide excellent results in reducing swelling, healing the lymphatic system and returning the body to good health.
As lymphoedema and the lymphatic system are not well understood or researched but the medical industry, recommendations of treatments are not always appropriate or effective. The treatment of choice by lymphedema specialists is Complete Decongestive Therapy (CDT) which consists of 4 different treatments combined together to provide
CDT involves manual lymphatic drainage (MLD), compression bandaging, therapeutic exercises and skin care. This combination can be very affective and provides good results.
MLD is a massaging technique which consists of gentle massaging of the lymphatic system to help stimulate and encourage lymph flow.
Compression Bandaging is self descriptive. Bandages are tightly applied to the swollen limb which helps to push lymph and fluid out of the area and back into circulation. This is a very simple action of basically squeezing a swollen limb to force fluid out of it but it is affective and can greatly reduce swellings.
Skin care is essential with lymphedema to avoid serious infection. As the limb swells circulation is diminished which restricts the flow of nutrients and blood to the area and a buildup of toxic waste occurs. Most often than not when suffering from this condition, the skin dry’s and becomes very scaly. This can become a problem if the skin cracks, opening a pathway for bacteria to enter the body and because the environment which the bacteria is entering is unhealthy and conducive to bacteria growth, it can quickly become infected and in serious cases, amputation is required.
Complete Decongestive Therapy is very effective in managing lymphoedema but there are is still much more that can be done in treating this condition, all of which can be found in the complete guide to treating lymphedema “Discover How to heal your Lymphatic System and Reduce swelling caused by Lymphedema”.
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Lymphedema: An Overview
Lymphedema, sometimes spelt as ‘lymphoedema’, is a health condition caused due to the accumulation of fluids in the body, mainly in the soft tissues of the arms and legs. Buildup of fluid or lymph is a painful condition that is usually caused due to the surgical removal of the lymph nodes. Patients who have undergone surgery or radiation therapy for breast cancer, prostrate cancer or malignant melanoma are at a higher risk of suffering from it. Chronic infection, especially in the legs may be a cause for lymphadema.
The lymphatic system of the body is responsible for the transportation of nutrients through our body and getting rid of the harmful materials. Damage to the lymphatic system of the body causes Lymphedema; it can either be primary or secondary. Children born with primary lymphoedema may show signs of the condition in their teens or even in adulthood. In such cases, the patient has a small number of vessels that cannot adequately transport the fluids in the body, causing the limbs to swell. Secondary or acquired lymph edema is more common and is the result of a trauma to the lymphatic system.
Prevention is better than cure, as the saying goes. Hence, doctors take adequate steps to prevent the onset of lymphedema in high-risk patients who have undergone radiation or surgery. If a person has had an attack of lymphedema, there is every chance for it to recur, so he has to take precautions to see that it does not happen again. The illness can be caused due to blot clots, burns, deep vein thrombosis as well as parasitic infections. Use of certain medicines may also trigger an attack.
Compression bandages, special compressive stockings and sleeves greatly help in controlling lymph edema. Some patients indulge in an exercise regime that keeps the affected limbs in good condition, thus stimulating circulation. Trained therapists use the concept of decongestive therapy that involves stimulating the flow of the fluids in the body with a massage. This appears to be the most favored course of treatment for the medical condition and patients can even do it themselves by learning the technique from a skilled therapist. Other forms of treatment include mechanical pumps that can be used to stimulate drainage of the pooled fluids and surgery.
Skin care is greatly important for those suffering from lymphadema. Swelling of the tissues can cause cracked and dry skin which is easily bruised and prone to infection. It is essential for such patients to maintain a good skincare regime which includes regular moisturizing and cleansing. Skin creams or oils help to keep the skin soft and lubricated. Persons who have a history of lymphoedema need to take life-long care to avoid injuries to the affected limb and must be constantly monitored for early signs of a recurrence by the doctors. They may also indicate the fact on medical bracelets so that medical personnel can take the necessary precautions in an emergency situation.
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Lymphedema Research
Over the years, very little effort had been made to conduct lymphedema research in order to understand the condition or possibly find a cure for the disease. However, more recently, with some increased funding, the pace of research has improved considerably. There has been progress in the understanding of the lymphatic system’s linkage to the other systems of the body as well as to other diseases. It has now been found that the lymphatic system plays a major role in all the body processes and is essentially connected to a number of other diseases as well.
Research on the topic of lymphedema has been focused on perceiving how lymphedema may affect the overall health of the patient. Studies try to understand how the lymph system grows and what procedures should be designed to improve the condition. Research is also being conducted to find new treatments to restore the lymphatic system to a healthy state. Numerous organizations around the world are involved in lymphedema research and they are being successful with new discoveries and new lines of treatment.
Studies on the genes which are important to the development of the lymphatic system are being performed with good results. In August 2009, researchers from the University of Kentucky have identified a new molecule that blocks the growth of lymphatics but not the growth of blood vessels. Similarly, lymphedema research is being done in the area of skin diseases that are a result of chronic lymphedema. Researchers are constantly working towards finding new methods for treatment of lymphedema or preventing the disease.
Until recently, it has been believed that women who have undergone mastectomy or surgery to treat breast cancer should not exercise or lift heavy objects. However, a recent study challenges this belief by showing that weight lifting might actually benefit breast cancer patients having lymphedema. The report states that breast cancer survivors may benefit from a controlled weight-lifting program combined with the use of compression garments and a monitoring of the arm and hand swelling. Supervision of the exercise routine by fitness professionals is recommended and women with lymphedema are required to wear a fitting compression garment during the exercise session.
Researchers in many countries like UK, America, Poland, Italy, Australia and Europe have been trying to find the cause of lymphedema. Over the past four years, research has lead to the finding of two genes believed to be responsible for this medical condition. Although lymphedema is being studied in Korea and China, these nations have not publicized their findings. Ongoing lymphedema research may help find a better course of treatment, or even possibly a cure for lymphedema, which is not available till today.
Even though currently there is no cure for lymphedema, there are many treatments which help in reducing swelling, avoiding infection and cleaning the lymphatic system and all of which can be found in “Discover how to Heal Your Lymphatic System and Reduce Swelling Caused by Lymphedema”.
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Lymphoedema Arm Exercises as a Form of Treatment
Lymphoedema arm is more often a side effect of breast cancer surgery; a condition that involves swelling in the arm, or, a feeling of tightness in the hand on the side of the body that has undergone the surgery. Although the problem is not life-threatening, it may be a life-long companion for breast cancer survivors. The scientific definition of lymphedema arm is the abnormal accumulation of lymphatic fluids in the soft tissues of the arm causing edema (swelling).
In breast cancer surgery, it is sometimes necessary to remove the lymph nodes. As there is an obstruction or alteration of the pathway for draining the fluids into the bloodstream, the lymphatic fluid gets accumulated in the arm area causing a swelling. Lymphoedema arm symptoms can be present in the whole arm or localized only in the wrist area, the hand, the area below the elbow and occasionally above the elbow region. Lymphedema may be present in the breast area too, if the fluids get blocked there. Although there is no way to find out if you are a candidate for lymphoedema arm condition after cancer treatment, you can always take precautions to reduce the chance of developing it.
New research being done on lymphedema challenges the old belief that exercise can worsen the condition. In the past, doctors would advise cancer patients not to lift with the arm, no exercising, no shoulder bags and no pressure cuffs on the affected arm. Recent research conducted by the University Of Pennsylvania School Of Medicine shows that gentle weight lifting exercises are good for controlling lymphedema after breast cancer surgery. However, it is recommended that the women should start a slowly progressive exercise program under the supervision of a certified fitness professional. They must learn the proper technique of performing these exercises and must always wear a compression garment during the exercise sessions.
Pole walking is another simpler form of exercise that gives the whole body a workout. Simple arm exercises like this will give your lymphoedema arm flexibility, muscle strength and also improve the circulation of lymphatic fluids. However, before embarking on any kind of exercise program, consult your doctor and therapist to chart out a course of action. If swelling is present in the arm, you must consult a massage therapist to take care of the problem. Wearing a compression sleeve can also control the swelling in the affected arm.
To prevent the development of lymphoedema arm condition it is best to avoid any injury or irritation to the arm. Wearing sunscreen to prevent sunburn and insect repellent to prevent insect bites are some general precautions you can take. Protecting the hands with gloves while doing housework, gardening or handling detergents helps to avoid nicks, cuts and scrapes. Skin care should include a regular cleaning and moisturizing routine. Consulting your doctor at the first signs of infection and starting treatment immediately can reduce the risk of further complications with arm lymphedema.
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Causes and Treatment for Lymphedema Leg Condition
One of the causes of a lymphedema leg is primary lymphedema, which is a hereditary condition due to the genetic make up of the individual. Usually there is a malformation of the lymphatic system at birth which results in the pooling of fluids in the lower extremities, causing a swelling. There is a family history of leg lymphedema in such cases as well.
Secondary lymphedema leg is caused due to trauma to the lymphatic system, generally after surgical removal of the lymphatic vessels, lymph nodes, radiation therapy for cancer in the abdominal region, the groin or the pelvic area. Lymphedema of the upper extremities is common with breast cancer while lymphedema of the leg is seen in cases with cancer treatment of the prostrate, lung, liver and abdominal cancers. The swelling caused by lymphedema can also be a result of fluid production in the abdomen which spreads to the legs.
Treatment for lymphedema must begin as soon as signs of the disease are seen. The most apparent sign is, of course, the swelling that may appear like a small bump with pain in the area. Other signs include heavy ankles or a small swelling on the inner knee area or sometimes even a pooling of fluid behind the knee. As soon as you notice any of these symptoms, visit your doctor. It is advisable to start treating lymphedema before it gets out of hand and becomes impossible to reverse. In the initial stage, simple methods of treatment help to get the swelling down. Daily use of well fitted elastic stockings is a must and you may keep your feet elevated as much as possible. At night, the lymphedema leg should be wrapped with elastic wraps and kept elevated to promote the lymphatic flow.
To keep the lymphedema in check, you can do simple leg exercises like leg kicks, pumping the feet up and down or going up and down on the toes while standing. Walking regularly and following an exercise routine can help in reducing the swelling and controlling lymphedema. As with any lymphedema symptoms, make sure to maintain good skin hygiene. It is essential to wash the legs with regular soap, rinse the legs thoroughly and dry the area between the toes to avoid infections. If you do get an infection or have an ingrown toe nail, ensure that you treat it immediately.
People suffering from lymphedema of the legs should wear closed shoes with padded socks to protect the feet from injury. The feet should be kept clean and dry and extreme care should be taken while cutting the toe nails. Patients should avoid using tight clothes and undergarments or socks with tight elastic bands. Constricting the limb may increase the pressure in the blood vessels leading to fluid retention and swelling. During air travel, it is desirable to wear compression stockings so as not to aggravate the lymphedema leg. Although, till date, there is no cure for lymphedema, with certain precautionary measures, it is possible to reduce the risk of developing the condition or at least delaying its onset.
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LYMPHATIC RESEARCH AND BIOLOGY
Volume 6, Number 3-4, 2008
© Mary Ann Liebert, Inc.
DOI: 10.1089/lrb.2008.1008
The Lymphatic System in Health and Disease
Leah N. Cueni, M.Sc., and Michael Detmar, M.D.
Abstract
The lymphatic vascular system has an important role in the regulation of tissue pressure, immune surveillance
and the absorption of dietary fat in the intestine. There is growing evidence that the lymphatic system also con-
tributes to a number of diseases, such as lymphedema, cancer metastasis and different inflammatory disorders.
The discovery of various molecular markers allowing the distinction of blood and lymphatic vessels, together
with the availability of a increasing number of in vitro and in vivo models to study various aspects of lymphatic
biology, has enabled tremendous progress in research into the development and function of the lymphatic sys-
tem. This review discusses recent advances in our understanding of the embryonic development of the lym-
phatic vasculature, the molecular mechanisms mediating lymphangiogenesis in the adult, the role of lym-
phangiogenesis in chronic inflammation and lymphatic cancer metastasis, and the emerging importance of the
lymphatic vasculature as a therapeutic target.
109
Introduction
SINCE ITS INITIAL description back in the seventeenth cen-
tury,1 the lymphatic system has probably never received
as much scientific attention as during the last decade. Being
the second vascular system found in higher vertebrates in
addition to the blood vasculature, it has several vital func-
tions including the regulation of tissue pressure, immune
surveillance and the absorption of dietary fat in the intes-
tine. Interest in basic lymphatic research was boosted by the
growing evidence that the lymphatic system also contributes
to a number of diseases, such as lymphedema, cancer me-
tastasis and different inflammatory disorders. The discovery
of various molecular markers allowing the distinction of
blood and lymphatic vessels, together with the availability
of a increasing number of in vitro and in vivo models to study
various aspects of lymphatic biology, has enabled tremen-
dous progress in our understanding of the development and
function of the lymphatic system.
Lymphatic capillaries start blind-ended in the tissue,
where they take up lymph, a protein-rich exudate from blood
vessels. They are lined by a single layer of overlapping en-
dothelial cells and lack a continous basement membrane as
well as pericyte or smooth muscle cell coverage. Tissue fluid
likely enters these intitial lymphatic vessels in between dis-
continous button-like cell junctions.2 Via larger collecting
lymphatic vessels and ultimately the thoracic duct, it is re-
turned to the blood vasculature through the lymphatico-ve-
nous connections at the junction of the jugular and subcla-
vian veins. In the intestine, specialized lymphatic vessels, so-
called lacteals, take up dietary fat and fat-soluble vitamins
to transport them to the venous circulation. Unlike the blood
vascular system, the lymphatic system does not feature a cen-
tral pump, instead lymph is moved forward by skeletal mus-
cle action, respiratory movement and contraction of smooth
muscle in walls of collecting lymphatic vessels.
Besides the vessels, which are found in almost all tissues
except for avascular structures such as epidermis, hair, nails,
cartilage and cornea, and some vascularized organs includ-
ing the brain and the retina, the lymphatic system also com-
prises the lymphoid organs. These include lymph nodes, thy-
mus, tonsils, spleen and Peyer’s patches and are crucial for
the immune function of the lymphatic system. Immune cells
such as lymphocytes and antigen-presenting dendritic cells
are transported via lymphatic vessels from the skin and other
organs to regional lymph nodes, where specific immune re-
sponses are initiated.
Embryonic Development of the Lymphatic Vasculature
Two concepts for lymphatic development in the embryo
are controversially discussed up to date, both of which have
been proposed already at the beginning of the 20th century.
The ”centrifugal” model, presented in 1902 by Florence
Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland
Research from the authors’ laboratory is supported by National Institutes of Health grant CA69184, Swiss National Fund grant 3100A0-
108207, Austrian Science Foundation grant S9408-B11, Cancer League Zurich, Oncosuisse and Commission of the European Communities
grant LSHC-CT-2005-518178 (M.D.).
Sabin, proposes that primary lymph sacs arise from endo-
thelial cells budding off the veins during early embryonic
development. The peripheral lymphatic system is subse-
quently formed by endothelial sprouting from these lymph
sacs into the surrounding tissues and organs.3 The “cen-
tripetal” model, introduced by Huntington and McClure in
1908, alternatively suggests the existence of mesenchymal
precursor cells, so-called lymphangioblasts, from which the
lymph sacs originate independently of the veins.4
Support for Sabin’s centrifugal model was provided by
studies in Prox1 deficient mice.5, 6 Prox1 is a homolog of the
Drosophila homeobox transcription factor prospero 7 and acts
as a master regulator of lymphatic development. Induced by
a yet unknown signal, it becomes expressed in a subset of
endothelial cells on one side of the cardinal vein around
mouse embryonic day (E) 9.5–10.5 (Fig. 1). These lymphati-
cally “competent” cells subsequently become lymphatically
committed and specified, and eventually give rise to the lym-
phatic vasculature throughout the body. Prox1 null mice
completely lack a lymphatic vascular system, since the bud-
ding and sprouting of lymphatically specified endothelial
cells from the embryonic veins halts prematurely at around
E 11.5–12.0 6 (Table 1). Corroborating this evidence, the ve-
nous origin of the mammalian lymphatic vasculature has re-
cently been demonstrated by lineage-tracing experiments 8
and is further supported by studies in zebrafish, in which
lymphatic endothelial cells (LECs) of the thoracic duct arise
from primitive veins.9 In avians and Xenopus frogs, how-
ever, parts of the lymphatic system are derived from adja-
cent veins while others likely originate from local lymphan-
gioblasts, which provides support for the centripetal model
of lymphatic development.10–12 Whether and how lym-
phangioblasts might also contribute to embryonic lymphan-
giogenesis in mammals remains unknown. Evidence for the
existence of lymphangioblasts also in mammals comes from
murine embryoid bodies. In these three-dimensional, em-
CUENI AND DETMAR110
FIG. 1. Lymphatic vasculature development and growth. During early embryonic development, all endothelial cells of the
cardinal vein display lymphatic competence and express the lymphatic markers LYVE-1 and VEGFR-3. Induction of Prox1
expression in a subset of endothelial cells on one side of the vein marks commitment to the lymphatic lineage. Subsequent
budding and migration of these cells to form the primary lymph sacs depends on VEGF-C signals. Several genes are re-
quired for the sustained separation of the developing lymphatic and blood vasculature, while others become important for
the remodeling of the initial lymphatic network into capillaries and collecting vessels. During these processes, lymphatic
endothelial cells adopt the expression of additional lineage markers. The relevance of lymphangioblasts and circulating pro-
genitor cells for mammalian lymphatic development is unclear. Postnatally, lymphatic vessel growth is promoted by nu-
merous factors. AM, adrenomedullin; Ang, angiopoietin; Angptl, angiopoietin-like protein; E, mouse embryonic day; FGF,
fibroblast growth factor; GH, growth hormone; HGF, hepatocyte growth factor; IGF, insulin-like growth factor; Nrp2, neu-
ropilin-2; PDGF, platelet-derived growth factor; VEGF, vascular endothelial growth factor.
LYMPHATIC SYSTEM IN HEALTH AND DISEASE 111
TABLE 1. GENETIC MOUSE MODELS DISPLAYING LYMPHATIC PHENOTYPES
Genes Function Models Phenotype
Prox16,101 Transcription KO No lymphatic vasculature (), adult-onset
factor obesity, chylous ascites ()
VEGF-C16 Growth factor KO No lymphatic vasculature (), delayed lymphatic
vascular development, lymphatic hypoplasia and
lymphedema ()
VEGFR-319 Growth factor KO Cardiovascular failure, defective remodelling of
receptor vascular networks
VEGFR-392 Growth factor Chy mice Lymphedema, chylous ascites, hypoplastic
receptor (inactivating cutaneous lymphatic vessels
mutation)
LYVE-122,23 Hyaluronan KO None or only subtle defects: increased interstitial-
receptor lymphatic flow, atypical shape of vessel lumen
Syk/SLP-7624,25 Tyrosine kinase/ KO Abnormal blood-lymphatic connections, chylous
adaptor protein ascites, defect in hematopoietic
endothelial progenitors
Spred-1/Spred-226 Negative Double KO Lymphedema, dilated and blood filled
regulators of lymphatic vessels
ERK activation
Angptl427 Inhibitor of KO Postnatal lymphatic-venous partitioning
lipoprotein defect in the small intestine
lipase
Podoplanin37 Membrane KO Lymphedema, dilatation and mispatterning of
glycoprotein lymphatic vessels, diminished lymphatic transport
Foxc228,139 Transcription KO Lymphatic hyperplasia, retrograde lymph
factor flow (), abnormal patterning and pericyte
investment of lymphatic vessels, absence of
valves, lymphatic dysfunction ()
Foxc1/Foxc2140 Transcription Compound Defective lymphatic sprouting from veins
factors mutant during development (reduced VEGF-C
(Foxc1 ; expression)
Foxc2 )
Ephrin B232 Ligand of EphB Mutant Defective remodeling of lymphatic vascular
receptors lacking PDZ network, hyperplasia, lack of valves,
interaction chylothorax
site
Neuropilin-231 Growth factor KO Transient absence or severe reduction of small
receptor lymphatic vessels and capillaries during
development
Angiopoietin-229,30 Growth factor KO Chylous ascites and subcutaneous edema, abnormal
patterning of lymphatic vessels, abnormal
periendothelial cell coverage of lymphatic capillaries
Aspp1141 p53-binding KO Subcutaneous edema, disorganized and
protein non-functional lymphatic vasculature in embryo,
mispatterned collecting lymphatic vessels in adult
Andrenomedullin89 Vasoactive KO Interstitial lymphedema (KO), abnormal jugular
peptide lymphatic vessels (conditional KO in ECs)
Emilin-1142 ECM protein KO Hyperplastic, enlarged, irregularly patterned lymphatic
vessels, reduction of anchoring filaments,
lymphedema
Integrin 952 Adhesion receptor KO Chylothorax, lymphedema
VEGF-C63 Growth factor TG (K14) Hyperplastic lymphatic vessels
VEGF-D64 Growth factor TG (K14) Hyperplastic lymphatic vessels
VEGF-A72 Growth factor TG (K14) Enlarged lymphatic vessels
HGF80 Growth factor TG Increased number and enlargement of
lymphatic vessels
Angiopoietin-179 Growth factor TG (K14) Lymphatic vessel enlargement and sprouting
Net (Elk3)143 Transcription KO Chylothorax, dilated lymphatic vessels
factor
SOX18 Transcription Spontaneous Edema, chylous ascites, cardiovascular and
(ragged)95 factor missense hair follicle defects
mutations
Pi3kca144 Phosphoinositide Mutant unable Chylous ascites, reduction of lymphatic
3-kinase to interact capillaries
with Ras
(continued)
’
lectin-like receptor 2 (CLEC-2) on platelets,39,40 and is in-
volved in the cytoskeletal organization of endothelial and
other cells.37,41,42 Its exact molecular function, however, has
remained unknown up to date. Given the phenotype of the
Syk/SLP-76 knockout mice 24 together with the fact that
CLEC-2 signals via Syk and SLP-76 to aggregate platelets,43
one might speculate on a potential function of podoplanin
in preventing anastomoses between lymphatic and blood
vessels by thrombus formation.
Although the endothelial cells lining lymphatic vessels
originate from blood vascular endothelial cells and hence
these two cells types are genetically closely related, in the
course of development LECs increasingly acquire specific
expression of diverse genes, distinguishing them from BECs
and reflecting the distinct functions of the two vascular sys-
tems. In addition to the above mentioned markers Prox1,
VEGFR-3, LYVE-1 and podoplanin, these genes include for
instance the lymphatic-specific chemokine CCL2144 and neu-
ropilin-2,31 a co-receptor for several growth factors includ-
ing VEGF-C 45 and hepatocyte growth factor (HGF).46
Thanks to the possibility of isolating LECs and BECs from
human skin and propagating them in culture for several pas-
sages without loss of their lineage-specific differentia-
tion,34–36,47 the molecular differences between the two cell
types could be explored in great detail on the transcip-
tome34,36 as well as on the proteome level.48 In addition, re-
cent studies comparing freshly isolated and cultured LECs
have highlighted the considerable impact of the in vivo tis-
sue microenvironment on the trancriptional profiles of en-
dothelial cells.49,50
A crucial role in the lineage-specification of LECs versus
BECs must be assigned to Prox1. Its ectopic expression in
BECs induces the expression of lymphatic marker genes in
these cells,36,51 whereas the acquisition of lymphatic marker
expression by budding endothelial cells during embryonic
development is abolished in Prox1 null mice.5 Recently, in-
tegrin 9—which was shown to be involved in the develop-
ment of the lymphatic system 52 (Table 1) and to be a re-
ceptor for VEGF-C and -D53—and VEGFR-3 have been
identified as target genes of Prox1,54 contributing to LEC mi-
gration towards VEGF-C signals. Corroborative for this po-
tential novel role of Prox1 in cell migration, we recently
found that it promotes the invasiveness of kaposiform he-
mangioendothelioma.55
Lymphangiogenesis in the Adult
In adult organisms, lymphangiogenesis takes place only
in certain pathological conditions such as tissue repair, in-
flammation and tumor growth. At present, it is unclear
whether lymphatic vessel growth in these settings is exclu-
sively due to proliferation of local endothelial cells and
sprouting of pre-existing vessels, or whether it involves also
the incorporation of circulating endothelial progenitor cells
at sites of active lymphangiogenesis.
Putative lymphatic endothelial progenitor cells, co-ex-
pressing lymphatic endothelial and stem cell markers, have
been identified in human fetal liver and cord blood.56 Nev-
ertheless, experiments using sublethally irradiated mice
grafted with GFP-expressing bone marrow suggested that
bone marrow-derived endothelial progenitor cells do not
contribute to tumor- or VEGF-C-induced lymphangiogene-
sis, since no GFP-positive donor cells were observed in the
newly formed lymphatic vessels when growth of lymphatic
vasculature was induced by VEGF-C application or by tu-
mor implants in these mice.57 In contrast to this, bone mar-
row-derived cells were incorporated into growing lymphatic
vessels in the inflamed or fibroblast growth factor (FGF)-2
treated corneas of GFP chimeric mice,58,59 as well as during
inflammation-associated lymphangiogenesis in human renal
transplants.60 These cells have been suggested to be macro-
phages, which transdifferentiate into LECs,59,60 and their rel-
ative contribution to the new vessels appears to be minor.
Macrophages and other inflammatory cells may, however,
in addition play an indirect role in neovascularization
through the secretion of lymphangiogenic factors such as
VEGF-C or VEGF-D.61,62
VEGF-C and the structurally closely related VEGF-D are
the most important and best characterized lymphangiogenic
growth factors to date. When overexpressed in the skin of
mice, they induce hyperplasia of cutaneous lymphatic ves-
sels63,64 (Table 1)—in contrast to VEGF-C, VEGF-D does so
mainly postnatally rather than in the embryo.65 VEGF-C
moreover promotes the growth, migration and survival of
cultured human LECs.47 The principal receptor of VEGF-C
and -D is VEGFR-3; after proteolytic cleavage, however,
these growth factors can also bind VEGFR-2.66–69 While it
has been shown that exclusive activation of VEGFR-3 sig-
naling is sufficient to promote lymphangiogenesis,64 the con-
tribution of VEGFR-2 signals to lymphangiogenesis is less
clear. In this context, several studies have demonstrated the
lymphangiogenic potential of VEGF-A—which is a ligand of
VEGFR-2 but not VEGFR-3—in vitro 34 and in vivo. 70–73 Al-
though VEGF-A might act indirectly by attracting VEGF-C
and -D-producing inflammatory cells,61,62,74 at least part of
its effects on lymphatic vessels can be attributed to VEGFR-
2, since they can be abolished by antibodies specifically
blocking this receptor.71,72 A recent study, dissecting
VEGFR-3 independent mechanisms of lymphangiogenesis,
suggests that VEGFR-2 signals in lymphatic vessels promote
their enlargement but not the formation of new vessel
sprouts.75 In an adult model of lymphangiogenesis in re-
generating skin, both VEGFR-2 and VEGFR-3 were required
for LEC migration and proliferation, while signaling via ei-
ther of them alone appeared to be sufficient for the subse-
quent organization of LECs into functional capillaries.76 The
question about a possible temporal component of VEGFR-3
dependent versus independent lymphangiogenesis was re-
cently addressed by application of a soluble VEGFR-3-Ig fu-
sion protein in postnatal and adult mice to block signaling
through VEGFR-3. This study suggests that, postnatally,
VEGF-C/D signals via VEGFR-3 are only required for the
maintenance of small lymphatic vessels during the first few
weeks of life. Thereafter, lymphatic vessels regenerate in
spite of constant VEGFR-3 inhibition.65 In agreement with
these findings, blockade of VEGFR-3 in adult mice by means
of a neutralizing antibody specifically inhibits the growth of
new lymphatics, leaving the survival and function of pre-ex-
isting vessels unaffected.77 Altogether, this indicates that
other factors might become important for the growth and
maintenance of lymphatic vessels during adult life. Indeed,
a multitude of growth factors capable of promoting lym-
phangiogenesis have been identified up to date, including
angiopoietin (Ang)-1,78,79 hepatocyte growth factor (HGF),80,
LYMPHATIC SYSTEM IN HEALTH AND DISEASE 113
81 fibroblast growth factor (FGF)-2,82–84 insulin-like growth
factor (IGF) 1 and 2,85 and platelet derived growth factors
(PDGF).86 Some of these may act on lymphatic vessels indi-
rectly via the VEGF-C/VEGFR-3 signaling pathway or only
in certain pathological situations (reviewed in87).
Newly identified lymphangiogenic factors include the
growth hormone (GH),88 and the multifunctional peptide
adrenomedullin (AM), which signals via the calcitonin re-
ceptor-like receptor (calcrl) associated with the receptor ac-
tivity modifying protein (RAMP) 2. In addition to AM sig-
naling having a role in lymphatic development as revealed
by knockout mice for either AM itself or calcrl or RAMP2
(Table 1), adrenomedullin treatment promotes the prolifera-
tion of cultured human LECs.89
The Lymphatic System in Disease
Lymphedema
The principal physiological function of the lymphatic vas-
culature is to take up fluid, leaking out of blood capillaries
into interstitial spaces in the tissue, and to return it to the
blood circulation. Any failure to effectively do so results in
lymphedema, a chronic, disabling and disfiguring condition.
The accumulation of protein-rich fluid in the tissues causes
swelling of the extremities and is in most patients also asso-
ciated with inflammatory reactions, fibrosis, overgrowth of
adipose and connective tissue in the affected areas, and other
symptoms.
Based on its cause, lymphedema can be classified into pri-
mary (hereditary) and secondary (acquired) forms. Primary
lymphedema is rare and generally characterized by hyper-
or hypoplastic lymphatic vessels and/or insufficient func-
tion of lymphatic valves. A variety of distinct syndromes
have been described, for some of which the underlying ge-
netic defects could be identified. Milroy’s disease, a form of
congenital lymphedema with autosomal dominant inheri-
tance, can be ascribed to kinase-inactivating mutations in the
VEGFR-3 gene, found in several affected families,90,91 as well
as in Chy mice which have hypoplastic cutaneous lymphatic
vessels associated with lymphedema92 (Table 1). Another
hereditary form of lymphedema, with a later onset around
puberty, is lymphedema-distichiasis syndrome—so called
because, in addition to edema, patients often have double
rows of eyelashes (distichiasis). This disorder is caused by
dominant, inactivating mutations in the FOXC2 gene,93
which encodes a forkhead-related transcription factor re-
quired for the proper formation of lymphatic valves and the
regulation of appropriate pericyte recruitment to lymphatic
vessels28 (Table 1). Finally, mutations in the gene encoding
SOX18, a SRY-related transcription factor, have been de-
scribed to cause recessive and dominant forms of hypotri-
chosis-lymphedema-telangiectasia syndrome.94 SOX18 is
known to be important for blood vascular development, and
the phenotype of ragged mice, which have a spontaneous
missense mutation in the Sox18 gene, indicates that SOX18
is also involved in lymphatic development95 (Table 1). In the
majority of families with lymphedema, however, none of the
above mentioned mutations occurs, thus several more genes
relevant for lymphedema are still awaiting their discovery.
Secondary lymphedema develops upon obstruction of
lymphatic vessels, which—in industrialized countries—is
mostly the result of surgery or radiotherapy for breast can-
cer, whereas in tropical countries lymphatic filariasis, a mos-
quito-borne parasitic infection, is the most common cause of
lymphedema (reviewed in 96).
Up to date, no curative treatment for lymphedema exists,
and therapeutic measures are limited to manual lymph
drainage and compression bandaging. Based on its potent
lymphangiogenic effect, VEGF-C has been tested for its abil-
ity to improve lymphatic function in animal models of
lymphedema. In Chy mice, virus-mediated VEGF-C gene
therapy stimulated the growth of functional cutaneous lym-
phatic vessels,92 and surgically induced lymphedema in a
rabbit ear model could successfully be treated by injection
of recombinant VEGF-C protein.97 The unwanted growth
and leakiness of blood vessels, resulting from activation of
VEGFR-2 by VEGF-C, could be circumvented using a
VEGFR-3-specific mutant form of VEGF-C.98 While these
studies have demonstrated the reconstitution only of lym-
phatic capillaries, it has recently been shown that by adeno-
viral delivery of VEGF-C or -D also functional and mature
collecting lymphatic vessels can be regenerated and con-
nected to lymph node transplants within six months after
surgical removal of the axillary lymph nodes and all of the
associated collecting lymphatic vessels in adult mice.99
The lymphatic vasculature in lipid homeostasis
Given the role of lymphatic vessels in mediating the up-
take of lipids from the intestine, the accumulation of fat ob-
served in the edematous tissues of lymphedema patients, the
close anatomical association of lymph nodes with adipose
tissue, and the ability of lymph to promote the differentia-
tion of pre-adipocytes to mature adipocytes in vitro,100,101 one
might suspect a connection between lymphatic function and
lipid homeostasis. A recent study in adult Prox1 / mice—
which survive exclusively on the NMRI background and are
obese compared to their wild-type littermates—indeed sug-
gests a link between lymphatic dysfunction and adult-onset
obesity. In these mice, abnormal leakage of lymph mainly
from mesenteric lymphatic vessels appears to promote lipid
accumulation in adipocytes as well as adipogenic differenti-
ation.101
The role of lymphatic vessels in inflammation
Inflammation occurs as a response to tissue injury or in-
fection, in the context of autoimmune diseases and during
tumor growth. The biological role of lymphatic vessels in
the pathogenesis of inflammation is not fully clarified up
to date. On the one hand, they might drain inflammation-
associated edema and participate in the removal of im-
mune cells and inflammatory cytokines from the site of in-
fection—on the other hand, they are crucial for the
establishment of immune responses by serving as exit
routes for activated antigen-presenting cells from the site
of infection to regional lymph nodes. Increasing evidence
suggests that lymphatic vessels might actively participate
in the inflammatory process.
Lymphatic hyperplasia and/or enhanced lymphangio-
genesis was observed in human psoriatic skin lesions,72 in
the intestinal mucosa of ulcerative colitis patients,102 in the
joints of mice with inflammatory arthritis,103 as well as dur-
ing kidney transplant rejection104 and chronic airway in-
flammation in mice.74
CUENI AND DETMAR114
VEGF-A appears to have a crucial role in inflammation-
associated lymphangiogenesis. Its expression is increased in
human psoriatic skin,105 and mice overexpressing VEGF-A
in the epidermis display a prolonged inflammatory response
after induction of cutaneous delayed-type hypersensitivity
(DTH) reactions, which is associated with LEC proliferation
and lymphatic hyperplasia and can be inhibited by blockade
of VEGFR-1 and -2.72 In fact, lymphangiogenesis associated
with chronic DTH reactions in mice was recently found to
strongly depend on VEGF-A, as it could be prevented by
means of a VEGF-A neutralizing antibody.106 Interestingly,
in this study VEGF-A not only induced lymphangiogenesis
at the site of inflammation where it was produced, but also
in the draining lymph nodes. Enhanced lymph node lym-
phangiogenesis was also observed after immunization; in
this case, however, it appeared to be mediated by B cells pro-
ducing lymphangiogenic factors within the lymph node it-
self.107
VEGF-A-mediated inflammatory lymphangiogenesis
might at least partially be the result of the recruitment of
macrophages, supplying VEGF-C and –D.61,62 In addition,
macrophages were reported to physically contribute to lym-
phangiogenesis by incorporation into newly forming lym-
phatic vessels in the inflamed mouse cornea.59
Our recent studies of lymphangiogenesis in UVB-irradi-
ated mouse skin suggest that VEGF-A predominantly in-
duces leaky, nonfunctional lymphatic vessels. Upon UVB-ir-
radiation, an increase in VEGF-A expression goes along with
the development of hyperpermeable, functionally impaired
lymphatic vessels in the skin, and these vessel abnormalities
could be prevented by administration of a neutralizing
VEGF-A antibody.108 Overall, inflammation-associated lym-
phangiogenesis induced by VEGF-A appears to have a rather
aggravating effect on the inflammatory process.
VEGF-C-mediated lymphangiogenesis, however, might
have a more favorable role in inflammation. In inflamed tis-
sues, VEGF-C is secreted predominantly by immune cells
such as dendritic cells, macrophages and neutrophils, and its
expression is upregulated in response to proinflammatory
cytokines.74,109 High levels of VEGF-C were detected in
arthritic joint synovium of rheumatoid arthritis patients.110
In joints of mice with inflammatory arthritis, VEGF-C—se-
creted by TNF stimulated CD11b-positive cells—induced
lymphangiogenesis,103 and enhanced lymphatic drainage
appeared to have a beneficial effect on the resolution of in-
flammation in these mice.111,112 In agreement with these find-
ings, inhibition of VEGFR-3 signaling by soluble VEGFR-3-
Ig prevented lymphangiogenesis in a mouse model of
chronic airway inflammation, which in turn aggravated
bronchial edema.74 Blockade of VEGFR-3 also resulted in
prolonged inflammation and edema in response to UVB ir-
radiation.113 Thus, in contrast to VEGF-A, VEGF-C appears
to promote lymphatic flow and contribute to the resolution
of inflammation, suggesting that stimulation of lymphan-
giogenesis by VEGF-C may be beneficial for the treatment of
certain inflammatory conditions.
Nevertheless, there might be some critical aspects to con-
sider in this regard. In a mouse model of corneal inflamma-
tion, local blockade of VEGFR-3 signaling significantly sup-
pressed trafficking of VEGFR-3-expressing dendritic cells
from the cornea to the draining lymph nodes, which pre-
vented the induction of delayed-type hypersensitivity (DTH)
and the rejection of corneal transplants. This effect was de-
pendent on dendritic cell trafficking per se rather than on re-
duced function of lymphatic vessels, since it occured earlier
than a potential inhibition of lymphangiogenesis one might
expect from anti-VEGFR-3 treatment.114
In the context of kidney transplant rejection, however, the
lymphatic endothelium indeed appeared to actively foster
the inflammatory process—through secretion of the
chemokine CCL21 which attracts CCR7 positive immune
cells, thereby facilitating their transport to the lymph node
and the generation of adaptive immunity.104
Besides the well-characterized CCL21/CCR7 pathway
and the mannose receptor, which was reported some years
ago to be important for lymphocyte adhesion to lymphatic
endothelium,115 novel mechanisms of immune cell entry into
the afferent lymphatic vessels are currently being unraveled.
Similar to blood vascular endothelium, LECs can be acti-
vated by inflammatory cytokines to expose key leukocyte
adhesion receptors, such as intercellular adhesion molecule-
1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1),
and E-selectin, promoting leukocyte transmigration across
lymphatic endothelium.116 Conversely, LYVE-1, which was
suspected to have a role in hyaluronan-mediated leukocyte
adhesion to lymphatic endothelium, is internalized and de-
graded upon LEC stimulation by proinflammatory cyto-
kines.117 Finally, sphingosine 1-phosphate (S1P) present in
inflamed peripheral tissues was recently suggested to inhibit
T-cell entry into afferent lymphatics through the S1P recep-
tor 1 expressed on T-lymphocytes.118
The role of lymphatic vessels in cancer
Lymphatic vessels as routes for trafficking through the
body are exploited not only by immune cells but also by can-
cer cells. Metastasis to regional lymph nodes represents the
first step of tumor dissemination in many cancers and is an
important prognostic indicator for disease progression. A
number of studies in animal tumor models have established
the concept that tumors—rather than just accidentally in-
vading pre-existing lymphatic vessels in their vicinity—can
actively induce tumor-associated lymphangiogenesis by se-
creting appropriate growth factors such as VEGF-C,119–121
VEGF-D,122 or VEGF-A,70 which promotes their spread to
the draining (sentinel) lymph nodes and beyond. Tumor-de-
rived factors, which could partially also be contributed by
tumor-infiltrating macrophages,61 have moreover been
found to induce expansion of the lymphatic network in the
sentinel lymph nodes, even before the arrival of the meta-
static cancer cells, as if to create a favorable environment for
the future metastasis70,119,123 (Fig. 2). Once there, metastatic
tumor cells continue to induce lymphatic vessel growth
within sentinel lymph nodes, which results in increased
drainage of growth factors to and lymphatic expansion in
distant lymph nodes (Fig. 2). VEGF-C-induced lymph node
lymphanigogenesis promoted squamous cell carcinoma me-
tastasis to distant lymph nodes and the lung,119 indicating
that lymph node lymphangiogenesis contributes to tumor
metastasis beyond the sentinel node. Importantly, while the
correlation between VEGF-C or -D expression and tumor me-
tastasis was repeatedly confirmed also in human cancers (re-
viewed in 124) and the extent of tumor-associated lymphan-
giogenesis was established as a potent predictor of lymph
LYMPHATIC SYSTEM IN HEALTH AND DISEASE 115
node metastasis in human melanoma,125,126 a significant cor-
relation between sentinel lymph node lymphangiogenesis
and distant lymph node metastasis was recently found in
human breast cancer patients.127 Taken together, these find-
ings indicate that lymphangiogenesis at the site of the pri-
mary tumor as well as in the draining lymph node actively
contributes to metastatic cancer spread and its inhibition
might be of interest for preventing tumor metastasis.
To this aim, suppressing the effects of VEGF-C and -D by
blocking VEGFR-3 signaling appears to be most promising,
given their crucial importance for lymphatic vessel growth.
Indeed, reduction of tumor lymphangiogenesis and lymph
node metastasis has been achieved by means of neutralizing
antibodies against VEGFR-3 or its ligands,122,128 soluble
VEGFR-3-Ig fusion protein,129,130 or small interfering RNA
(siRNA)-mediated VEGF-C gene silencing.131 Confidence
that inhibition of the VEGF-C/-D/VEGFR-3 pathway could
be a safe anti-lymphangiogenic strategy was provided by the
recent finding that it does not affect normal lymphatic ves-
sels in adult mice.65 Meanwhile, increasing evidence points
towards a role for VEGFR-3 also in tumor angiogenesis.
While in normal adult tissues VEGFR-3 expression is re-
stricted mainly to the lymphatic endothelium, it becomes re-
expressed on angiogenic tumor blood vessels.132–134 More-
over, it has recently been shown that interfering with
VEGFR-3 function by means of a blocking antibody inhib-
ited tumor angiogenesis and thereby growth of tumor
xenografts in mice,135 which might represent an additional
beneficial effect of anti-VEGFR-3 therapy against cancer.
Because VEGF-C and -D can activate VEGFR-2 and VEGF-
A promotes tumor lymphangiogenesis and metastasis, also
blockade of VEGFR-2 results in moderate suppression of
lymphangiogenesis and lymphatic metastases—in addition
to inhibition of angiogenesis and tumor growth—and anti-
CUENI AND DETMAR116
FIG. 2. Tumor and lymph node lymphangiogenesis promotes cancer metastasis. Tumor-derived VEGF-A and/or VEGF-
C/-D induce lymphangiogenesis at the site of the primary tumor and within sentinel LNs, even before metastasis, possi-
bly preparing the LN for the arrival of metastatic tumor cells. Once in the sentinel LN, these cells maintain their lymph-
angiogenic activity, likely promoting further cancer spread to distant lymph nodes and organs. The lymphatic
endothelial-derived chemokine CCL21 attracts CCR7-expressing cancer cells towards the lymphatic vessels, facilitating their
entry into the lymphatic system. CCR7, CC-chemokine receptor 7; LN, lymph node; VEGF, vascular endothelial growth
factor.
Breast Cancer Survivors who Receive Lymphedema Education are More Likely to Have Fewer Symptoms
Patients who receive additional information about lymphedema report significantly fewer symptoms and practiced more risk-reducing behaviors, according to a recent study co-authored by Deborah Axelrod, MD, associate professor in the department of surgery at NYU Langone Medical Center and a member of the NYU Cancer Institute. Risk reducing behaviors include elevating the affected limb to promote fluid drainage, avoiding blood draws and injections to the affected limb and avoiding tight fitting clothing which can aggravate symptoms.
Lymphedema is a condition resulting in the abnormal and debilitating swelling of the extremities that can follow breast cancer surgery. Approximately 30% of the 2.4 million breast cancer survivors in the United States have developed lymphedema and all are at a lifetime risk. Physical symptoms include swelling, firmness, pain fatigue, numbness and impaired limb mobility, but also predisposes patients to fibrosis, cellulitis, infections and septicemia. Psychologically, survivors often feel stigmatized because of the swollen limb which often brings about anxiety, depression and disruption of interpersonal relationships.
“I believe that anyone undergoing breast cancer surgery – whether it is a sentinel node biopsy alone or more extensive axillary surgery — should be informed about the risks of lymphedema,” says Dr. Axelrod. “Until now, we had little evidence of the effectiveness of the behaviors to recognize and reduce symptoms.”
Co-author Mei R. Fu, RN, PhD, ACNS-BC assistant professor in the College of Nursing at New York University says this is the first study to show that education can reduce risk of lymphedema. “Nurses can play a leadership role in educating patients about lymphedema and can play a role in improving the quality of life in cancer survivors,” says Fu.
“It is important to identify the early warning signs and symptoms of the condition, as well as determine what interventions to take,” added Dr. Axelrod. “We also enroll patients into ongoing behavior and risk modification trials and work with physical therapists to ensure symptom reduction.”
About NYU Cancer Institute
The NYU Cancer Institute is an NCI-designated cancer center. Its mission is to discover the origins of human cancer and to use that knowledge to eradicate the personal and societal burden of cancer in our community, the nation and the world. The center and its multidisciplinary team of experts provide access to the latest treatment options and clinical trials along with a variety of programs in cancer prevention, screening, diagnostics, genetic counseling and supportive services. For additional information, please visit: www.nyuci.org.
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Lymphedema Secondary – An Acquired Health Condition
Lymphedema is a health condition which is caused due to abnormal accumulation of fluids in the body as a result of a dysfunction in the lymphatic system. Primary lymphedema is the result of the genetic makeup of the individual while lymphedema secondary is acquired due to trauma, injury or removal of the lymph vessels and lymph nodes. Typically, persons who have been treated for cancer with chemotherapy, radiation or by removal of the lymph nodes are prone to the lymphedema secondary condition.
Secondary lymphedema is caused by chronic infection and involves the lower portion of the body. The legs are usually affected in this case. In America, the highest number of patients suffering from lymphedema are those who have undergone breast cancer surgery involving the removal of lymph nodes. About 40% of such patients may experience some degree of secondary lymph edema in the upper region of the body, i.e. the arms and hands. World over, two hundred and fifty million cases of lymphedema are in existence. The most widespread cause of secondary lymphedema in the tropical regions is filariasis, which is a parasitic infection caused by mosquitoes.
Occasionally, lymphedema may be caused due to certain medications that promote deep vein thrombosis or blood clots in the legs. Sometimes the onset of secondary lymphadema in cancer survivors is triggered during an airplane flight, probably due to a sudden drop in cabin pressure. Precautions against this eventuality can be taken by breast cancer patients by wearing compressive garments like a sleeve and gauntlet.
Lymphedema usually results in a swelling in the affected body part causing discomfort. The condition may progress to a stage where there is grave disability and disfigurement. Lymphadema may worsen in case the person suffers from a skin infection. Although there is no cure for it till today, the condition can be managed or controlled with a combination therapy of manual lymph drainage, massage, compressive garments, bandaging and exercise. Skin care is also important for patients with severe secondary lymphedema.
Persons who have had a surgery involving cancer treatment or any other surgery involving the removal of the lymphatic vessels must be alert to the signs of secondary lymphoedema. Symptoms could be severe fatigue, fluid retention in a particular area of the body, especially the limbs, swelling or discoloration of the skin. Swellings may occur due to a traumatic event like a cut, bruise or an injury. Other signs a person may notice is a feeling of heaviness of the limb or rings and bracelets suddenly becoming tight.
Lymphoedema is generally categorized by its severity. Mild edema is reversible with early detection, correct diagnosis and treatment. In the advanced stages, the affected limbs balloon to a gigantic size due to complete blockage of the lymph channels, causing severe discomfort and disfigurement to the patient. Hence, it is advisable not to ignore any signs of secondary lymphoedema, but to consult the doctor at the very first opportunity. Beginning a treatment in the early stages ensures better success in managing lymphedema.
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Using Lymphedema Products for Treatment
Treatment of lymphedema involves manual lymph drainage, use of compression garments, bandaging and skin care. Lymphedema can be effectively managed with treatment that makes use of several lymphedema products which include compression garments, bandages, footwear, foams and padding, accessories like hooks and fasteners, donning aids, pneumatic pumps, compression devices, etc. Massage and bandaging is the first step of treatment, followed by the constant use of compression garments and meticulous skin care.
In order to maintain the edema reduction after decongestive therapy, the patient is required to wear elastic compression garments at all times. You can have a custom-made compression garment or purchase one over the counter. These are to be worn each day and replaced at regular intervals. Lymphedema garments for the upper extremities include compression arm sleeves, bras, gloves and gauntlets. Knee-high and thigh-high stockings, compression pantyhose and compression devices for the legs are also available. However, before purchasing the product, you must consult your physician to find out which garment is right for your condition.
Bandaging or wrapping the affected body part is essential so that lymphedema is reduced. Compression bandaging provides a resistance on the skin and the muscles underneath. This resistance helps the tissues to re-absorb the fluid and prevents fluid retention in the limb. Usually short stretch bandages give a better result as they produce the tension required to enhance the pumping action for the lymph vessels. During daily activity and exercise, bandaging is a must to encourage the lymphatic flow and soften the swelling. There are various categories of bandages and they come in the form of tubular stockinettes, finger and toe bandages, tapes and adhesive bandages. The patient can choose to use whatever is suitable.
Another lymphedema product that plays a major role in the treatment of the condition is the lymphedema pump. The Sequential Gradient Pump and the FlexiTouch Pump are the two types of pumps used for complete decongestive therapy. The lymphedema pump can either be purchased or rented from a surgical supply store. Those who do not have access to a therapist can make use of the lymphedema pump for their treatment. It is crucial for lymphedema patients to maintain a meticulous skin care routine. Various gels, creams, ointments and lotions are available for cleansing and moisturizing the skin.
For those suffering from lymphedema, compression therapy and a life-long follow up on the treatment is essential. New lymphedema products are coming in the market and therapists are using them to take care of problem areas of tissue fibrosis and swelling. For instance, a special tape known as the Elastic Therapeutic tape is being used to soften the edemas. Donning and doffing aids, special footwear and accessories like bandage rollers try to make life a bit easier for lymphedema patients. Due to the convenience of online shopping, it is now possible to procure lymphedema products quite easily. Many online stores have trained therapists who can assist you with the selection of a suitable lymphedema product that you might need.
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