Intermittent Pneumatic Compression Enhances Formation of Edema Tissue Fluid Channels in Lymphedema of Lower Limbs.

BACKGROUND: In lymphedema, tissue fluid steadily accumulates in the subcutaneous space containing loose connective tissue. We documented previously that deformation of the structure of subcutaneous collagen bundles and fat by excess fluid leads to formation of "lakes" and interconnected channels with irregular shape. Since there is no force that could mobilize and propel stagnant fluid to the regions where lymphatics absorb and contract, this task should be taken over by external massage. The most effective in this respect seems to be the sequential intermittent pneumatic compression (IPC). AIM: The aim of the study was to observe whether IPC would enhance and accelerate formation of tissue fluid channels. METHODS: Together with the Biocompression Systems (Moonachie, NJ), we designed a high pressure intermittent compression device and used in it our therapy protocol for patients with obstructive lymphedema of lower limbs. The study was carried out on 18 patients with lymphedema stages II-IV. The IPC was applied daily for 1-2 hours. The follow up time was 24-36 months. Lymphoscintigraphy and immunohistopathology of tissue biopsies were used for evaluation of channel formation process. RESULTS: The forced fluid flow brought about increase of the area of fluid channels in the thigh and groin, with a decrease in the calf. Concomitantly, with decrease of channel area in the calf, there was a decrease of calf circumference. No new lymphatic collectors were observed. CONCLUSIONS: Compression of limb lymphedema tissues leads to formation of tissue channels as pathways for evacuation of edema fluid.

Tissue fluid pressure and flow during pneumatic compression in lymphedema of lower limbs.

BACKGROUND: Physiotherapy of edema in cases with obstructed main lymphatics of lower limbs requires knowledge of how high external pressures should be applied manually or set in compression devices in order to generate tissue pressures high enough to move tissue fluid to nonswollen regions and to measure its flow rate. METHODS: We measured tissue fluid pressure and flow in subcutaneous tissue of lymphedematous limbs stages II to IV at rest and during pneumatic compression under various pressures and inflation timing. An 8-chamber sequential compression device inflated to pressures 50-120 mmHg, for 50 sec each chamber, with no distal deflation, was used. Pressures were measured using a wick-in-needle and electronic manometer. Fluid flow was calculated from continuously recorded changes in limb circumference using strain gauge plethysmography. RESULTS: Before massage, in all stages of lymphedema, stagnant tissue fluid pressures in subcutaneous tissue ranged between -1 and +10 mmHg and did not differ from those measured in normal subjects. Pressures generated in tissue fluid by pneumatic compression reached 40-100 mmHg and were lower than those in inflated chambers. High pressure gradient through the skin was caused by its rigidity (fibrosis) and dissipation of applied compression force to proximal noncompressed limb regions. The calculated volumes of displaced tissue fluid ranged from 10 to 30 ml per compression cycle, to reach in some cases 100 ml in the groin region. CONCLUSIONS: Tissue fluid pressures generated by a pneumatic device were found lower than in the compression chambers. The obtained results point to the necessity of applying high pressures and longer compression times to generate effective tissue fluid pressures and to provide enough time for moving the stagnant fluid.

Topography of accumulation of stagnant lymph and tissue fluid in soft tissues of human lymphedematous lower limbs.

BACKGROUND: The knowledge of where does excess tissue fluid accumulate in obstructive lymphedema is indispensable for rational physical therapy. However, it has so far been limited to that obtained from lymphoscintigraphic, ultrasonographic, and MR images. None of these modalities provide composite pictures of dilated lymphatics and expanded tissue space in dermis, subcutis, and muscles. So far, only anatomical dissection and histological processing of biopsy material can visualize the tissue lymphatic network and the sites of accumulation of the excess of mobile tissue fluid. METHODS AND RESULTS: We visualized the "tissue fluid and lymph" space in skin and subcutaneous tissue of foot, calf, and thigh in various stages of lymphedema in specimens obtained during lymphatic microsurgical procedures or tissue debulking, using special staining techniques. The volume of accumulated fluid was calculated from the densitometric data of stained tissue sections. We found that lymph was present only in the subepidermal lymphatics, whereas the collecting trunks were obliterated in most cases. Mobile tissue fluid accumulated in the spontaneously formed spaces in the subcutaneous tissue, around small veins and above and underneath muscular fascia. Deformation of subcutaneous tissue by free fluid led to formation of interconnecting channels. The volume of subcutaneous free fluid ranged around 50% of total tissue volume and there were no significant differences in various stages of lymphedema. This could be explained by the presence of thick layers of subcutaneous fat tissue even in the most advanced stage of lymphedema. CONCLUSIONS: In lymphedema caused by obliteration of collecting trunks, lymph is present only in the subepidermal lymphatics, whereas the bulk of stagnant tissue fluid accumulates in the subcutaneous tissue and above and beneath muscular fascia. These findings should be useful for designing pneumatic devices for limb massage as well as for rational manual lymphatic drainage in terms of sites of massage and level of applied external pressures.

Memory response in allografting and bacterial infections in lymphoid and non-lymphoid tissues.

Allografting with immunosuppression is accompanied by chronic rejection and continuing response of the host to infections. Upon first encounter with allogeneic and bacterial antigens the naive T and B cells react within days. Simultaneously cohorts of memory cells are created characterized by rapid response to the second antigenic stimulus. A number of unanswered questions remains as to whether where are the memory cells located, do they persist in the region of the first encounter with antigens or are they mobilized from the bone marrow and spleen, do they react differently to allogeneic and bacterial antigens, are they sensitive to the immunosuppressive drugs? This review cumulates recent data on the subject. Scanty information points to the necessity of more intensive studies on memory cells to allogeneic, bacterial and self-antigens after transplantation in the environment saturated with immunosuppressive drugs.

The reaction of the regional lymph nodes on the skin bacterial and allogeneic antigens.

Transplantation of hands in humans has become an accepted therapeutic modality. A hand transplant is composed of various tissues of different degree of immunogenicity. In addition, skin contains own resident bacterial flora that may become virulent in the ischemic and rejecting graft. Discrimination between skin rejection and bacterial inflammation is difficult. The aim of our experimental study was to investigate the cellular reaction to skin bacteria and alloantigen in the regional lymph nodes draining skin and analyse the changes in cell phenotypes. The study was carried out on rats inoculated into hind-limb paw either with S. epidermidis or allogeneic peripheral blood mononuclear cells. An increase in lymph node weight and cell concentration was observed after bacterial infection. After stimulation with allogeneic cells, node mass increased significantly but its cell number rose much less. The percentage of lymph node W3/13 (leukocytes, T cells), W3/25 (CD4), OX8 (CD8), OX6 (class II), OX12 (B cells), EDI (CD14), CD31 (lymphocytes), OX7 (stem cells), and OX62 (migrating dendritic) cells did not change in both groups compared to controls. There was a significant rise of the CD54 (ICAM I) subset after bacterial infection and increase in percentage of OX8-cytotoxic and decrease of W3/25 (helper) subset after allogeneic stimulation. Lack of major differences between stimulated and control contralateral nodes may be explained by systemic reaction to the tested antigens affecting also nodes on the non-injected side. Comparison of the reaction of bacteria and alloantigen stimulated nodes revealed an increase in percentage of OX6, OX12, CD31, CD54, OX33 and OX62 after infection with S. epidermidis, whereas allostimulation brought about only rise in T (W3/13) cell population. Neither stimulation caused increase in expression of class II antigens on T cells. The obtained results demonstrate evident differences in type of response to bacteria and alloantigens. To what extent can bacterial stimulation enhance allogeneic reaction is now under study. Our data are helpful in understanding differences in the character and kinetics of reaction to both types of antigens and may taken into consideration when planning therapy in recipients of hand allografts, immunosuppressive drugs or antibiotics.