A newly designed SIPC device for management of lymphoedema.

WARNING TO ALL LYMPHEDEMA PATIENTS

This abstract is a prime example of just how bad information can be that is presented even through PubMed.

Lymphology 101 clearly shows that high pressure pneumatic devices can cause serious damage to the good lymphatics, making lymphedema even worse.

Read this for education, but please, please, please, what ever you do never ever ever set the compression level on high if you use a pneumatic device.

A newly designed SIPC device for management of lymphoedema.

PubMed

Pat

Lymphangiogenesis: A Potential New Therapy for Lymphedema?

Lymphangiogenesis: A Potential New Therapy for Lymphedema?

2012 Jan

Cooke JP.

Source

Stanford Cardiovascular Institute, Stanford, CA.

Abstract

At the level of the capillaries, the systemic circulation loses about 2-4 liters of fluid and about 100g of protein into the interstitium daily. This ultrafiltrate of the systemic capillaries is returned to the circulatory system by the lymphatics. The lymphatic vasculature is highly specialized to perform this service, beginning with the blind-ended lymphatic capillaries. These vessels are highly permeable to protein, fluid and even cells, due to fenestrations in their basement membrane, and discontinuous button-like junctions rather than tight intercellular junctions as observed in the systemic capillaries(1). The lymphatic capillaries merge into collectors and larger lymphatic conduits that are invested with vascular smooth muscle (capable of contracting and propelling lymph forward) and valves for unidirectional flow. These conduits merge at lymph nodes, delivering antigens to the immune cells and serving as an early warning system of pathogen invasion. The lymph nodes drain into conduits that ultimately merge into the thoracic duct which empties into the left subclavian vein.

American Heart Association

The Lymphatics and Inflammation

The primary valves in the initial lymphatics during inflammation.

"More substantiation on the involvment of lymphedema and the body's inflammatory response system."

Lymphat Res Biol. 2007

Lynch PM, Delano FA, Schmid-Schönbein GW. Department of Bioengineering, University of California San Diego, La Jolla, California 92093-0412, USA. g...@bioeng.ucsd.edu

BACKGROUND: The primary valve system in the initial lymphatics prevents fluid transport from the initial lymphatics back into the interstitium. The authors hypothesize that since the primary valves are made up of an extraordinarily thin endothelium, they are readily compromised by mechanical or biochemical inflammatory stimuli. Thus, the opening dimension of the primary valves and their ability to prevent reflux into the interstitium during inflammation were investigated.

METHODS AND RESULTS: Acute inflammation was generated in the intact rat spinotrapezius muscle by suffusion of f-Met-Leu-Phe and platelet-activating factor. Once inflamed, the effective opening dimensions of the primary valves and the transport back out of the initial lymphatics were determined by examining the transport of fluorescent tracers from the interstitium to the lymphatics. Quantum dots and fluorescently labeled albumin readily enter initial lymphatics from the interstitium. The maximum diameter of microspheres that enter the initial lymphatics is between 0.5 microm and 0.8 microm in both control and inflamed tissue. While under control conditions no quantum dots escaped from initial lymphatics back into the interstitium, during inflammation there was extensive escape of quantum dots.

CONCLUSIONS: These results suggest that, in acute inflammation, the function of the endothelial barriers in the initial lymphatics may be compromised. A failure of the primary lymphatic valves has two consequences. First, fluid clearance from the tissue is less efficient, which causes the level of edema to increase. Second, the leaking initial lymphatics allow inflammatory mediators to accumulate in the tissue, therefore enhancing interstitial and lymphatic inflammatory reactions.

Article

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Inflammation, lymphatic function, and dendritic cell migration.

Lymphat Res Biol. 2006

Angeli V, Randolph GJ. Department of Gene and Cell Medicine, Mount Sinai School of Medicine, New York, New York, USA. micva@nus.edu.sg

The lymphatic system is not only essential for maintenance of normal fluid balance, but also for proper immunologic function by providing an extensive network of vessels, important for cell trafficking and antigen delivery, as well as an exclusive environment, the lymph node (LN), where antigen-presenting cells (APCs) and lymphocytes can encounter and interact. Among APCs, dendritic cells (DCs) have a remarkable capacity to traffic from peripheral tissues to the draining LN, which is critical for execution of their functions.

To reach the LN, DCs must migrate towards and enter lymphatic vessels. Here, the authors review what is known about the factors that drive this process. They touch particularly on the topic of how DC migration is affected by inflammation and discuss this in the context of lymphatic function.

Traditionally, inflammatory mediators are regarded to support DC migration to LNs because they induce molecules on DCs known to guide them to lymphatics. The authors recently showed that inflammatory signals present in a strong vaccine adjuvant induce swelling in LNs accompanied by lymphangiogenesis in the draining LN and radius of peripheral tissue. These increased lymphatics, at least for several days, lead to a more robust migration of DCs.

However, the density of lymphatic vessels can become overly extended and/or their function impaired as observed during lymphedema and various chronic inflammatory reactions. Diseases characterized by chronic inflammation often present with impaired DC migration and adaptive immunity. Gaining a better understanding of how lymphatic vessel function may impact adaptive immunity by, for example, altering DC migration will benefit clinical research aiming to manipulate immune responses and manage chronic inflammatory diseases.

Article

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Inflammatory manifestations of experimental lymphatic insufficiency.

PLoS Med. 2006 Jul

Tabibiazar R, Cheung L, Han J, Swanson J, Beilhack A, An A, Dadras SS, Rockson N, Joshi S, Wagner R, Rockson SG. Stanford Center for Lymphatic and Venous Disorders, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, United States of America.

BACKGROUND: Sustained lymph stagnation engenders a pathological response that is complex and not well characterized. Tissue inflammation in lymphedema may reflect either an active or passive consequence of impaired immune traffic.

METHODS AND FINDINGS: We studied an experimental model of acute post-surgical lymphedema in the tails of female hairless, immunocompetent SKH-1 mice. We performed in vivo imaging of impaired immune traffic in experimental, murine acquired lymphatic insufficiency. We demonstrated impaired mobilization of immunocompetent cells from the lymphedematous region. These findings correlated with histopathological alterations and large-scale transcriptional profiling results. We found intense inflammatory changes in the dermis and the subdermis. The molecular pattern in the RNA extracted from the whole tissue was dominated by the upregulation of genes related to acute inflammation, immune response, complement activation, wound healing, fibrosis, and oxidative stress response.

CONCLUSIONS: We have characterized a mouse model of acute, acquired lymphedema using in vivo functional imaging and histopathological correlation. The model closely simulates the volume response, histopathology, and lymphoscintigraphic characteristics of human acquired lymphedema, and the response is accompanied by an increase in the number and size of microlymphatic structures in the lymphedematous cutaneous tissues. Molecular characterization through clustering of genes with known functions provides insights into processes and signaling pathways that compose the acute tissue response to lymph stagnation. Further study of genes identified through this effort will continue to elucidate the molecular mechanisms and lead to potential therapeutic strategies for lymphatic vascular insufficiency.

Article