Addressing Pain and Inflammation in Veno-Lymphatic Disorders Through Compression Therapy

Chronic venous disease (CVD)

Venous stasis, causing local hypoxia and abnormal (lower) shear stress (the frictional force generated by the blood flow in the veins) leads to the release of inflammatory mediators from endothelial cells. These inflammatory mediators are theorized to sensitize and activate venous nociceptors, causing the characteristic pain of CVD (2, 3, 4). CVD patients without risk for neuropathy from other causes, had a decreased function in nerve fibers (2). This could be additional evidence for the negative effects of CVD on nerve fibers.

Lymphedema (LE)

Both experimental and clinical studies spanning several decades have implicated inflammation as a critical component in the physiopathology of lymphedema (5). Chronic interstitial fluid stasis promotes activation of chronic inflammatory pathways, adipose deposition and further decrease lymphatic function, thereby activating a feed-forward mechanism leading to tissue hypoxia and disease progression (6).

Although pain is not as frequently associated with LE like with lipedema, more recent studies have shown, that there is a signifi-cant association between LE, pain, and the level of distress experienced by patients (7).
Newer findings further suggest that one component of LE pain may be related to the increased fluid accumulation and/or associated inflammatory responses (8).

Lipedema (LiE)

The etiology of pain in lipedema is unclear, though histology findings of inflammation and hypoxia may be contributing elements (9). Recent findings, that identify a chronic low-grade state of inflammation and tissue hypoxia as the most plausible explanations for the pain in LiE patients, support this hypothesis (10).

Fat cells are only able to expand with increased vascular growth. The vessels’ inability to keep pace with the expanding adipose tissue may lead to the observed tissue hypoxia. The hypoxic conditions in the LiE tissue further lead to an increased expression of hypoxia-inducible factors (HIF1a), inducing inflammation of the adipose tissue. Recently it has come to understand that chronic pain can also be (co-)triggered by stress or even personal conditions. This is another interesting aspect regarding a possi-ble explanation for the etiology of pain (10).

Chronic venous disease (CVD)

Medical compression leads to an increase of shear stress in the microcirculation and to a release of anti-inflammatory mediators from the endothelial cells (11, 12). It also enhances venous emptying, reduces pain and edema (4), and can, by decreasing ambulatory venous hypertension in the area, counteract the chronic inflammation in the tissues and finally aid healing processes. In addition to other effects, compression therapy also acts on trophic changes by releasing anti-inflammatory mediators, minimizing areas of interstitial fibrosis 13. The pressure differential (increase in interstitial fluid pressure) induced by the compression therapy reduces capillary filtration, increases

Lymphedema (LE)

In addition to other effects, compression therapy also acts on trophic changes by releasing anti-inflammatory mediators, minimizing areas of interstitial fibrosis (13).

The pressure differential (increase in interstitial fluid pressure) induced by the compression therapy reduces capillary filtration, increases the microcirculation blood flow and facilitates interstitial fluid movement and lymph drainage, thereby reducing limb volume (14).

The anti-fibrotic and anti-inflammatory effects of the compression therapy might thereby contribute to counteract the progression of lymphatic dysfunction and to lower LE related pain.

Lipedema (LiE)

In the light of recent findings explaining the etiology of pain and inflammation in LiE patients in more details, it can be imagined that the basis for prescribing compression therapy might not be the edema reduction anymore, but rather the reduction of pain by the frequently demonstrated anti-inflammatory effects of compression therapy on the subcutaneous tissue (10).

Although the use of medical compression brings only a small reduction in tissue volume (5 – 10 %) in various studies, it does lessen tenderness (pain on pressure) and feelings of tightness in the limbs (15). Studies demonstrate that medical compression wearing results in a significant reduction in oxidative stress, a finding that also points to improved microcirculation in the subcutaneous tissues (10).