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==========================================Related Terms: Nonne-Milroy lymphedema, Milroy's Disease, Primary congenital hereditary lymphedema, hereditary lymphedema I, Nonne-Milroy-Meige disease, hereditary tropholymphoedema syndrome; idiopathic hereditary lymphedema, lymphoedema; lymphedema, early onset type; trophoedema hereditarium (chronicum extremitatum inferiorum); tropholymphoedema, elephantiasis congenita hereditaria, familial hereditary oedema
See also: Lymphedema
Disorder Subdivisions - Lymphedema
Hereditary Lymphedema, Type I
Congenital Hereditary Lymphedema
Hereditary Lymphedema, Type II
Familial Lymphedema Praecox
Hereditary Lymphedema Tarda
Milroy's Syndrome is an old term used to describe hereditary congenital
lymphedema. It is a congenital familial primary lymphedema which
results from vertical
autosomal inheritance of a single gene. The gene has been identified
as VEGFR3. The condition usually presents itself at birth with the
one or even both legs.
If the condition is unilateral (single leg), the other leg may continue in the latency stage for years before expressing itself. The same is indicated for arm lymphedema.
It is the rarest of the inherited lymphedema, accounting for approximately 2% of hereditary lymphedemas.
Hereditary lymphedema was first described by Nonne in 1891, however in 1892 Dr. William F. Milroy described a missionary who had returned from work in India who had swollen legs his entire life. His mother likewise was afflicted with the same condition. Milroy had also, previously studied the 250 year history of a family and had been able to identify 22 persons with this condition through 6 generations. He was also able to pinpoint when the condition entered the family through a marriage in 1768.
Basic diagnosis can be made by the fact that swelling (generally of the legs) presents at birth and there is a family history of similar swelling. Currently the most precise diagnosis can be made by a lymphoscintigraphy test. In this test a radioactive substance is injected into the limb and is traced on a computer screen. Through this method the exact location of the lymphatic blockages can be identified.
The cause of Milroy's Syndrome is a break in the VEGFR3 gene.
The usual complications involved with the condition include fibrosis of the limb tissues, cellulitis (and or lymphangitis and erysipelas infections). Other complications made include involvement of the genitalia, pain, skin conditions and in very rare situations lymphangiosarcoma, inflammation and various defects, including distichiasis, extradural cysts, vertebral anomalies, cerebrovascular malformations, yellow nails.
Decongestive therapy is the most widely accepted form of treatment. There is no cure for Milroy's but the condition can be managed by early diagnosis and treatment. Other treatments involved will focus on the complications such as infections, pain and associated skin problems.
Other therapies used may include compression pump therapy and surgical procedures.
Long term prognosis is excellent is the condition is identified early and treatment begins so after the diagnosis is made.
Stages of Milroy's Syndrome (Lymphedema)
Lymphatic transport capacity is reduced
No visible/palpable edema
Subjective complaints are possible
Accumulation of protein rich edema fluid
Reduces with elevation (no fibrosis)
(Spontaneously Irreversible Lymphedema)
Accumulation of protein rich edema fluid
Pitting becomes progressively more difficult
Connective tissue proliferation (fibrosis)
Accumulation of protein rich edema fluid
Fibrosis and sclerosis (severe induration)
Skin changes (papillomas, hyperkeratosis, etc.)
Fibrosis in Milroy's Syndrome
Long standing lymphedema causes a condition known as fibrosis.
As the fluid
continually collects in a limb, it becomes hard and dense. With each
lymphedema there is also a change in the tissue texture of a limb.
With stage one the tissue is still much like normal tissue, its just satiated with fluid. As the swelling continues and as he fluid changes to that protein-rich fluid referred to a lymphorrea, you enter into stage two. In this stage, the tissue become very similar to a grape (best image I can think of). Already it is becoming much more difficult for antibiotics to reach bacteria and it becomes less response to the decongestive therapy.
At stage three, the tissue become similar to one of those old synthetic kitchen sponges, the ones that become rock hard when they are dry.
This is the very real serious side affect of stage three lymphedema. This type of tissue increases potential of persistent and very hard to treat cellulitis or lymphangitis.
The denseness of the limb prohibits antibiotics from reaching the infecting bacterium and it is often able to survive in pockets of fibrotic tissue. These pockets act as a septic foci and after antibiotic treatment is completed, the infections will reappear.
Generally at this stage it is going to take IV antibiotics to deal with any infection because oral antibiotics just are not able to penetrate this mass of hard tissue.
Also, as the fibrosis intensifies you become more susceptible to deep venous thrombosis (DVT) and other circulatory problems. You may also start to experience neuropathy as the pressure of this tissue compresses nerves within the limb.
Decongestive Therapy and Milroy's Syndrome
Lymphatic Drainage (MLD): is a unique, therapeutic method of
movement of fluids in the tissues. The gentle, rhythmic, pumping,
movements follow the direction of lymph flow and produce rapid results.
assists the cutaneous lymphatics in picking up and removing not just
all the waste products, protein particles and debris from our system.
It also is
successful in breaking fibrosis and fibrotic areas of a lymphodemous
This treatment was created and developed Danish therapists Dr. Emil Vodder and his wife, Estrid, in the 1930's and was introduced in Paris in 1936. They are also credit with creating a specialty of medicine called Lymphology.
First brought to North America in 1982, the school is located in
Victoria, British Columbia, Canada. Before it was introduced the standard treatment course in North American was either a surgery called debulking or the use of compression machines wherein the limb was literally squeezed by pneumatic air pressure.
Comprehensive Decongestive Therapy (CDT) is used primarily in the treatment of lymphedema and venous insufficiency edema. It is a combination of MLD, bandaging exercises and skin care. CDT may also involve breathing exercises, compressive garments and dietary measures. A frequent indication for CDT is lymphedema caused by irradiation or surgery due to cancer. It can relieve edema, fibrosis and the accompanying pain and discomfort.
Also known as Complete Decongestive Physiotherapy (CDP), this treatment therapy was pioneered in the United States by Dr. Robert Lerner.
Cellulitis and Milroy's Syndrome
Cellulitis is one of the complications of
lymphedema. The patient may not be aware of the source of the etiology.
Sometimes it may be a cut, mosquito bite, open wound or other infection
The first sign is increased or different quality of PAIN involving the lymphedema limb. The patients often describe this as a "flu like symptom or an ache" involving the Lymphedema arm or leg. This is usually followed by sudden onset of ERYTHEMA(redness, red streaks or blotches) on the involved limb. The HYPERTHERMIA(lymphedema limb becomes warm, hot) will follow and the patient may experience the CHILLS and even HIGH FEVER.
The early intervention and treatment with antibiotics will resolve this condition (it usually takes a very minimum ten day course of antibiotics). Only a Medical Doctor will be able to prescribe the Antibiotics, thus a consultation with a Doctor is necessary. Severe Cellulitis may require Inter venous Antibiotic treatment and hospitalization. Again, elevation of the affected limb is important.
During that phase the patient should NOT massage the Lymphedema limb, bandage, apply the pump, wear tight elastic sleeve or exercise excessively. Avoid the blood pressure and blood to be drawn from the involved arm. Keep the limb elevated as much as possible while resting. Once the symptoms dissipate the treatment MLD/CDP should be initiated.
How do we prevent this infection? The patient should be careful with daily activities and take all precautions to protect the skin (wear gloves when gardening, cleaning with detergents, etc.. ).
an injury to skin occurs on the
Lymphedema limb it is necessary to clean the wound with alcohol or
peroxide and apply Neosporin/Polysporin antibiotic ointment. If the
progress seek the attention of a physician immediately.
It is so very important to avoid getting cellulitus as it further destroys the lymphatic system. Allowed to spread or continue it can become systemic and can lead to gangrene, amputation of the limb or even death.
Noone-Milroy-Type Hereditary Lymphedema
Also known as Lymphedema I, this disorder presents as brawny edema usually of the lower extremity. The diagnosis is usually made at birth. Tissue swelling occurs distally or proximally in the involved limbs, and either hypoplasia or hyperplasia of the lymphatics has been found.
Prenatal diagnosis of
Milroy's primary congenital
Makhoul IR, Sujov P, Ghanem N, Bronshtein M.
Department of Neonatology, Rambam Medical Center, Bat-Galim, Haifa, Israel. Makhoul@rambam.health.gov.il
Milroy's primary congenital lymphedema (PCL) (hereditary lymphedema type I, Milroy disease) is present at birth, and mostly affects the dorsal aspects of feet. It is mostly a life-long condition but does not affect longevity. Complications are rare except for chronic discomfort and warmness of affected areas. PCL is an autosomal dominant disease with incomplete penetrance due to a mutation in the gene locus encoding for VEGFR3 with resultant dysgenesis of microlymphatic vessels. We report on two fetuses where ultrasonographic examination at 15 weeks of gestation showed significant edema of the dorsal aspects of both feet with no evidence of other major malformations. Whereas in one fetus the edema resolved completely, it persisted in the second fetus and proved after birth to be of lymphedematous nature. To the best of our knowledge, this is the first report of early prenatal diagnosis of primary congenital lymphedema via fetal ultrasonographic examination and of spontaneous resolution of lymphedema during fetal life. Copyright 2002 John Wiley & Sons, Ltd.
Lymphedema - Milroy's Disease
Excerpt from Milroy Disease
Milroy's Syndrome - Genetic Cause
lymphedema caused by a mutation that
inactivates VEGFR3 tyrosine kinase.
Irrthum A, Karkkainen MJ, Devriendt K, Alitalo K, Vikkula M.
Laboratory of Human Molecular Genetics, Christian de Duve Institute of Cellular Pathology and Universite catholique de Louvain, B-1200 Brussels, Belgium.
Hereditary lymphedema is a chronic swelling of limbs due to dysfunction of lymphatic vessels. An autosomal dominant, congenital form of the disease, also known as "Milroy disease," has been mapped to the telomeric part of chromosome 5q, in the region 5q34-q35. This region contains a good candidate gene for the disease, VEGFR3 (FLT4), that encodes a receptor tyrosine kinase specific for lymphatic vessels. To clarify the role of VEGFR3 in the etiology of the disease, we have analyzed a family with hereditary lymphedema. We show linkage of the disease with markers in 5q34-q35, including a VEGFR3 intragenic polymorphism, and we describe an A-->G transition that cosegregates with the disease, corresponding to a histidine-to-arginine substitution in the catalytic loop of the protein. In addition, we show, by in vitro expression, that this mutation inhibits the autophosphorylation of the receptor. Thus, defective VEGFR3 signaling seems to be the cause of congenital hereditary lymphedema linked to 5q34-q35.
arthritis and Milroy's disease.
Albornoz MA, Myers AR.
Division of Rheumatology and Immunologic Diseases, Temple University Health Sciences Center, Philadelphia, PA 19140.
Milroy's disease is a rare disorder characterized by multiple physical anomalies, the most prominent of which is lymphedema of one or both lower extremities. We describe, with a review of proposed pathogenetic mechanisms, a patient with Milroy's disease who, over a 13-year period, manifested at least 14 isolated episodes of septic arthritis of the left knee. Recurrent septic arthritis associated with Milroy's disease has not been reported previously.
LYMPHANGIOSARCOMA ON CONGENITAL LYMPHOEDEMA - Milroy's Syndrome
Key Words: Chronic Lymphoedema Lymphangiosarcoma, Milroy disease
31 years old white male complaining of congenital – familial form-
non previously treated lymphoedema
Milroy disease - was admitted with the aspect seen - Images
1,2,3 -. A biopsy
the presence of lymphangiosarcoma – Images 4,5,6 -.
No evidence of
metastatic disease was clinically evident. High AK amputation was
performed followed by prosthetic extremity replacement. No
treatment was done. Patient is free of the disease three years after
and no evidence recurrence has been noticed so far..
(1) may be primary or secondary to the presence of other disease and/or
consequences of surgery or trauma (2). Primary lymphoedema may be
Milroy´s disease – or may occur at any phase of life but it most
appears at puberty – Meig’s disease -. Secondary lymphoedema is
more often. The most prevalent worldwide cause of lymphoedema is
which is particularly common in south-east Asia and Africa. In Western
postsurgical lymphoedema of the extremity prevails. Complications of
limb lymphoedema include recurrent cellulitis and lymphangiosarcoma
tumors such squamous-cell carcinoma (3,4), b-cell lymphoma (5)
and angiosarcoma (6,7,8,9)
has been reported.
cases of long-lasting or congenital lymphoedema the finding of
violaceous nodules or papules, or apparent traumatic ecchymoses should
act as a
diagnostic beacon warning of dangers. A case is reported of a
lymphangiosarcoma developing in a patient with congenital hereditary
(Milroy's disease) in a familial form (10). Hereditary lymphoedemas
that are not
associated with other malformations usually affect the lower limbs and
inherited in an autosomal dominant fashion. These non-syndromic
lymphoedemas are categorized by their age of onset, being either
(Milroy disease) or having an onset in childhood or around puberty
disease) (11). Development of lymphangiosarcoma
post-mastectomy lymphoedema, has been
described in late-onset hereditary lymphoedema. There is a high
multiple primary tumors in association with lymphangiosarcoma in the
Lymphangiosarcoma is a rare, aggressive, vascular neoplasm arising in chronic congenital or acquired lymphedema. Although it is most frequently associated with post-mastectomy lymphedema (Stewart-Treves's syndrome), lymphangiosarcoma can exceptionally arise in congenital hereditary lymphedema (11)(Milroy's syndrome and Meige's syndrome) and non-hereditary lymphoedema (congenital, praecox or forme tarde lymphoedemas) (13).
risk of appearance of lymphangiosarcoma following mastectomy and
therapy has been recently analyzed. Between 1954 and 1983, 7620
treated for breast carcinoma at Institut Gustave Roussy (France) (14).
patients, 6919 were followed for at least 1 year. Out of these, 11
with sarcomas thought to be induced by irradiation, 2 of which were
Syndrome, and 9 of which were sarcomas within the irradiated fields.
histological slides were reviewed and a comparison with those of breast
was done. The sites of these sarcomas were: parietal wall, 1 case;
cartilage, 1 case; infraclavicular region, 1 case; supraclavicular
cases; internal third of the clavicle, 2 cases; axillary region 2
cases; and the
internal side of the upper arm (Stewart-Treves syndrome), 2 cases. The
age of these 11 patients at the diagnosis of sarcomas was 65.8 (49-83).
latent period was 9.5 years (4-24). Three patients underwent radical
and nine modified radical mastectomy. Only one patient received
The radiation doses received at the site of the sarcoma were 45 Gy/18
fr. for 10
cases and 90-100 Gy for 1 case (due to overlapping between two fields).
histology was as follows: malignant fibrous histiocytoma, 5 cases;
3 cases; lymphangiosarcoma, 2 cases; and osteochondrosarcoma, 1 case.
survival following diagnosis of sarcoma was 2.4 years (4 months-9
patients are still alive: one with recurrence of her breast cancer, the
complete remission, with 7 and 3 years follow-up, respectively. All
patients died from their sarcomas. The cumulative incidence of sarcoma
irradiation of breast cancer was 0.2% (0.09-0.47) at 10 years. The
incidence ratio (SIR) of sarcoma (observed n# of cases (Obs)/expected
cases (Exp) computed from the Danish Cancer Registry for the same
1.81 (CI 0.91-3.23). This is significantly higher than one, with a p =
Tailed Exact Test). The mean annual excess (Obs-Exp)/100.000
risk during the same period/(100,000) was 9.92. This study suggests
patients treated by radiation for breast cancer have a risk of
sarcomas that is higher than the general population. However, the
adjuvant radiation therapy in the treatment of breast cancer exceeds
the risk of
second cancer; therefore, the potential of radiation-induced sarcomas
be a factor in the selection of treatment for patients with breast
Moreover, we emphasized the importance of regular clinical controls in all patients affected by chronic lymphoedema (15,16). In fact, although the prognosis of this neoplasm is very poor, a prompt diagnosis and a rapid, ablative surgery associated with radiation therapy can increase the possibility of survival of these patients (17,18). Chemotherapy with intraarterial mitoxantrone and placitaxel with ex vivo previous sensitivity test seems a current adequate complementary approach (19).
Primary congenital lymphedema (Milroy's)
Véronique Mirlesse MD*, Ronaldo Levy MD*, Geneviève Brodaty MD*, Pascale Sonigo MD**, Dominique Teillac MD***, Luc Gourand, MD*, Fernand Daffos MD* Fernando Heredia MD"
Service de médecine foetale, Institut de Puériculture et Périnatalogie,
** Service de radio-pédiatrie, Hopital Necker Enfants Malades, Paris
*** Service de dermatologie, Hopital Necker Enfants Malades, Paris
" Women"s Health Alliance, Nashville, Tennessee.
Synonyms: Hereditary lymphedema type I, Nonne-Milroy Lymphedema, early-onset lymphedema, primary congenital lymphedema.
Etiology: Autosomal dominant with incomplete penetrance. The gene mutation has been found near the most telomeric region of 5q35.32, There is also some evidence of 2 different sub-mutations or variants depending on the nucleotide substituted,,,,.
Pathogenesis:All the anomalies found are due to dysgenesis of lymphatic microvessels. These dysgenesis ranges from mild to severe and even to aplasia of both, the lymphatic capillaries and collectors,,.
Main features: Present in one or both legs at birth. Lymphedema of PCL persists throughout life but does not appear to affect longevity. As the patient matures, the overlying skin displays a slightly rosy hue, and the size of the edematous parts remains proportional to the remainder of the body. It can rarely present with genital edema, resembling sexual ambiguity.
Ultrasound appearance:This condition is suggested by the finding of an isolated edema of the dorsum of feet in the fetus, a normal karyotype and absence of other significant malformations.
These are images obtained during a 28-week routine ultrasound examination. Fetal weight was over the 97th centile.
limbs: Edema of the lower limbs,
specially the distal portions. Compare the width of legs and thighs.
Reported complications, although rare, have been reported:
Management: If other fetal anomalies are ruled out, and fetal karyotype is normal, parental counseling concerning etiology, management, and possible complications is advisable.
 Makhoul IR, Sujov P, Ghanem N, Bronshtein M. Prenatal diagnosis of Milroy"s primary congenital lymphedema. Prenat Diagn 2002 Sep;22(9):823-6
 Ferrell RE, Levinson KL, Esman JH, Kimak MA, Lawrence EC, Barmada MM, Finegold DN. Hereditary lymphedema: evidence for linkage and genetic heterogeneity. Hum Mol Genet 1998 Dec;7(13):2073-8
 Sarda P, Jalaguier J, Montoya F, Bonnet H. Hereditary congenital lymphedema with pseudosexual ambiguity.J Genet Hum 1988 Aug;36(4):353-60
 Dale RF.Primary lymphoedema when found with distichiasis is of the type defined as bilateral hyperplasia by lymphography. J Med Genet 1987 Mar;24(3):170-1
 Fang J, Dagenais SL, Erickson RP, Arlt MF, Glynn MW, Gorski JL, Seaver LH, Glover TW. Mutations in FOXC2 (MFH-1), a forkhead family transcription factor, are responsible for the hereditary lymphedema-distichiasis syndrome.Am J Hum Genet 2000 Dec;67(6):1382-8
 Herbert FA, Bowen PA. Hereditary late-onset lymphedema with pleural effusion and laryngeal edema. Arch Intern Med 1983 May;143(5):913-5
 Mucke J, Hoepffner W, Scheerschmidt G, Gornig H, Beyreiss K. Early onset lymphoedema, recessive form--a new form of genetic lymphoedema syndrome. Eur J Pediatr 1986 Aug;145(3):195-8
 Evans AL, Brice G, Sotirova V, Mortimer P, Beninson J, Burnand K, Rosbotham J, Child A, Sarfarazi M. Mapping of primary congenital lymphedema to the 5q35.3 region. Am J Hum Genet 1999 Feb;64(2):547-55
 Irrthum A, Karkkainen MJ, Devriendt K, Alitalo K, Vikkula M. Congenital hereditary lymphedema caused by a mutation that inactivates VEGFR3 tyrosine kinase. Am J Hum Genet 2000 Aug;67(2):295-301
 Karkkainen MJ, Ferrell RE, Lawrence EC, Kimak MA, Levinson KL, McTigue MA,Alitalo K, Finegold DN. Missense mutations interfere with VEGFR-3 signalling in primary lymphoedema.Nat Genet 2000 Jun;25(2):153-9
 Finegold DN, Kimak MA, Lawrence EC, Levinson KL, Cherniske EM, Pober BR, Dunlap JW, Ferrell RE. Truncating mutations in FOXC2 cause multiple lymphedema syndromes. Hum Mol Genet 2001 May 15;10(11):1185-9
 Holberg CJ, Erickson RP, Bernas MJ, Witte MH, Fultz KE, Andrade M, Witte CL. Segregation analyses and a genome-wide linkage search confirm genetic heterogeneity and suggest oligogenic inheritance in some Milroy congenitalprimary lymphedema families. Am J Med Genet 2001 Feb 1;98(4):303-12
 Jeltsch M, Kaipainen A, Joukov V, Meng X, Lakso M, Rauvala H, Swartz M, Fukumura D, Jain RK, Alitalo K. Hyperplasia of lymphatic vessels in VEGF-C transgenic mice. Science 1997 May 30;276(5317):1423-5
 Partsch H, Urbanek A, Wenzel-Hora B. The dermal lymphatics in lymphoedema visualized by indirect lymphography. Br J Dermatol 1984 Apr;110(4):431-8
 Bollinger A, Isenring G, Franzeck UK, Brunner U. Aplasia of superficial lymphatic capillaries in hereditary and connatal lymphedema (Milroy"s disease). Lymphology 1983 Mar;16(1):27-30
 Pfister G, Saesseli B, Hoffmann U, Geiger M, Bollinger A. Diameters of lymphatic capillaries in patients with different forms of primary lymphedema. Lymphology 1990 Sep;23(3):140-4
 Wheeler ES, Chan V, Wassman R, Rimoin DL, Lesavoy MA. Familial lymphedema praecox: Meige"s disease. Plast Reconstr Surg 1981 Mar;67(3):362-4
 Mehta SD, Robinson RJ, Bern SA. Pedal manifestations of Milroy"s disease. J Am Podiatr Med Assoc 1996 Aug;86(8):400-2
 Albornoz MA, Myers AR. Recurrent septic arthritis and Milroy"s disease. J Rheumatol 1988 Nov;15(11):1726-8
 Offori TW, Platt CC, Stephens M, Hopkinson GB. Angiosarcoma in congenital hereditary lymphoedema (Milroy"s disease)--diagnostic beacons and a review of the literature. Clin Exp Dermatol 1993 Mar;18(2):174-7
 Brostrom LA, Nilsonne U, Kronberg M, Soderberg G. Lymphangiosarcoma in chronic hereditary oedema (Milroy"s disease). Ann Chir Gynaecol 1989;78(4):320-3
Milroy's Disease Treatment and Management
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