Lymphedema, or lymphatic edema, refers to increased volume of body segments due to localized or extensive lymphatic system disturbances that cause decreased lymph transport, without regard to the primary cause. Characteristically, chronic lymph stasis promotes both fluid accumulation and tissue changes. Defective uptake of large molecules retains water within the interstitial space and, over time, lymph stasis leads to progressive tissue changes, characterized by abnormal growth of subcutaneous tissue and intercellular matrix, and increased skin thickness. It is noteworthy that, beyond tissue fluid control, lymphatics play other important roles in tissue homeostasis, which makes lymphedema unique and far more complex than edema caused by other vascular or systemic factors.
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
This is a preview of subscription content, log in to check access.
International Society of Lymphology. The diagnosis and treatment of peripheral lymphedema. Lymphology. 2009;42:51-60.Google Scholar
Olszewski WL, Engeset A, Romaniuk A, Grzelak I, Ziolkowska A. Immune cells in peripheral lymph and skin of patients with obstructive lymphedema. Lymphology. 1990;23:23-33.PubMedGoogle Scholar
Ruocco V, Brunetti G, Puca RV, Ruocco E. The immunocompromised district: a unifying concept for lymphoedematous, herpes-infected and otherwise damaged sites. J Eur Acad Dermatol Venereol. 2009;23:1364-1373.PubMedCrossRefGoogle Scholar
Tassenoy A, Vermeiren K, van der Veen P, et al. Demonstration of tissue alterations by ultrasonography, magnetic resonance imaging and spectroscopy, and histology in breast cancer patients without lymphedema after axillary node dissection. Lymphology. 2006;39:118-126.PubMedGoogle Scholar
Brorson H, Ohlin K, Olsson G, Karlsson MK. Breast cancer-related chronic arm lymphedema is associated with excess adipose and muscle tissue. Lymphat Res Biol. 2009;7:3-10.PubMedCrossRefGoogle Scholar
Browse NL, Stewart G. Lymphoedema: pathophysiology and classification. J Cardiovasc Surg (Torino). 1985;26:91-106.Google Scholar
Lee BB, Andrade M, Piller N, et al. Consensus on primary lymphedema. Int Angiol. 2010;29(5):454-470.PubMedGoogle Scholar
Földi E, Földi M. Lymphostatic diseases. In: Földi E, Földi M, Kübik S, eds. Textbook of Lymphology. Munich: Urban & Fischer; 2003:231-319.Google Scholar
Pannier F, Hoffmann B, Stang A, Jöckel KH, Rabe E. Prevalence of Stemmer’s sign in the general population. Results from the Bonn Vein Study. Phlebologie. 2007;36:289-292.Google Scholar
Andrade M, Nishinari K, Puech-Leão P. Intertrigo in patients with lower limb lymphedema. Clinical and laboratory correlation. Rev Hosp Clin Fac Med Sao Paulo. 1998;53:3-5.PubMedGoogle Scholar
Andrade M, Lederman A, Puech-Leão P. Lymphangiosarcoma in primary lymphedema of the lower limbs. Lymphology. 2002;35(suppl):737-744.Google Scholar
Holberg CJ, Erickson RP, Bernas MJ, et al. Segregation analyses and a genome-wide linkage search confirm genetic heterogeneity and suggest oligogenic inheritance in some Milroy congenital primary lymphedema families. Am J Med Genet. 2001;98:303-312.PubMedCrossRefGoogle Scholar
Kriederman BM, Myloyde TL, Witte MH, et al. FOXC2 haploinsufficient mice are a model for human autosomal dominant lymphedema-distichiasis syndrome. Hum Mol Genet. 2003;12:1179-1185.PubMedCrossRefGoogle Scholar