Background: The manual lymphatic drainage in lymphedema has proved to be successful; however, this method cannot be applied to millions of patients around the world. The only solution is to offer inexpensive, easily accessible mechanical devices for pneumatic compression (IPC). These devices should be designed on parameters of edema fluid hydromechanics. Recent data point to high pressures and long time of compression. Aim: To validate the effects of 3 years daily high pressure, long inflation time IPC therapy in terms of decrease of limb circumference/volume, tissue elasticity, histological changes, and incidental complications. Methods: A group of 18 patients with unilateral leg lymphedema stage II to IV was treated for a period of 3 years using an 8-chamber sleeve, sequential inflation of chambers to 100-120 mmHg for 50 sec (total 400 sec). Limb circumference and tissue tonicity were measured at monthly intervals. Correlation between decrease in calf and thigh circumference and increase in elasticity was done. Results: The treatment revealed durable permanent decrease of limb circumference and increased elasticity of tissues. The improvement was most expressed in the calf above the ankle and mid-calf. No complications as thigh ring or chronic genital edema were observed. There was no direct correlation between the decrease in limb circumference and increase in elasticity, most likely due to different mass of fibrous tissue. Conclusions: IPC takes over the permanently missing function of the obliterated lymphatics by squeezing edema tissue fluid to the regions with normal lymphatic drainage. The limb circumference is decreased or at least does not further increase, elasticity of tissue is increased and maintained. No complications in limb tissues were observed. The long-term, high pressure IPC, long inflation timed therapy can be safely be recommended to patients with lower limb lymphedema.
Objective Rheumatoid arthritis (RA) is characterized by inflammatory reactions in joints and adjacent tissues unaccompanied by clinically evident changes in lymphatics and lymph nodes draining the inflamed areas. The explanation for this phenomenon, which contrasts with infectious processes in joints and soft tissues that evoke major changes in the lymphatic system, is unclear. To determine which inflammatory factors produced in the joints of RA patients are transported in lymph to lymph nodes, we measured levels of immunoglobulins, cytokines, and chemokines in prenodal lymph from the foot joints of RA patients and quantified their rate of transport to regional lymph nodes. Methods Lymph was collected from the cannulated lymphatics draining the foot joints, tendons, fascia, and skin of 20 RA patients. Lymph flow rate and concentrations of proteins and immunoglobulins were measured. Cytokine and chemokine levels were quantified by enzyme‐linked immunosorbent assays. Results were compared with those obtained in 20 control subjects. Results In the cannulated vessel, the mean ± SEM lymph flow rate in RA patients was almost 2‐fold that in control subjects (22.6 ± 3.2 ml/24 hours versus 13.2 ± 1.1 ml/24 hours; P < 0.01). Lymph concentrations of total protein, IgG, and IgM were 1.80 ± 0.14 gm/dl, 384 ± 45 mg/dl, and 32.0 ± 1.5 mg/dl, respectively, in RA patients and 1.66 ± 0.14 gm/dl, 238 ± 32 mg/dl, and 15.0 ± 1.3 mg/dl, respectively, in control subjects. The corresponding lymph:serum (L:S) ratios were 0.21 ± 0.02, 0.22 ± 0.02, and 0.15 ± 0.02, respectively, in RA patients and 0.22 ± 0.02, 0.19 ± 0.02, and 0.11 ± 0.02, respectively, in control subjects. The L:S ratios of <1 and the absence of significant differences between groups suggested a lack of local production of immunoglobulins. In RA patients, lymph concentrations (in pg/ml) were as follows: interleukin‐1β (IL‐1β) 14.8 ± 3.9, IL‐6 511 ± 143, tumor necrosis factor α (TNFα) 9.9 ± 1.1, IL‐1 receptor antagonist (IL‐1Ra) 4,274 ± 737, IL‐10 13.3 ± 4.4, IL‐8 846 ± 174, IL‐15 6.2 ± 0.9, granulocyte–macrophage colony‐stimulating factor (GM‐CSF) 2.30 ± 0.15, vascular endothelial growth factor (VEGF) 80.4 ± 8.6, and macrophage inflammatory protein 1α (MIP‐1α) 171 ± 34. In control subjects, these values were as follows: IL‐1β 1.50 ± 0.25, IL‐6 79.0 ± 14.6, TNFα 4.4 ± 1.1, IL‐1Ra 208 ± 52, IL‐10 0.0, IL‐8 216 ± 83, IL‐15 5.00 ± 0.45, GM‐CSF 0.40 ± 0.05, VEGF 42.0 ± 2.4, and MIP‐1α 3.4 ± 1.7 (P < 0.05 versus RA patients for all except IL‐15). The L:S ratio was >1 in all RA patient samples for IL‐1β, IL‐6, IL‐1Ra, IL‐8, GM‐CSF, IL‐10, IL‐15, TNFα, and MIP‐1α, indicating local production of cytokines. Great variability in lymph cytokine concentrations, presumably reflecting differences in the intensity of local inflammation, was not reflected in serum cytokine concentrations. Intravenously infused methylprednisolone decreased lymph cytokine levels to normal within 12 hours. In contrast, their concentrations in serum showed little or no change. Conclusion High lymph c...
Pneumatic compression of tissues with lymph stasis is, aside from the manual massage, a commonly used therapeutic modality in limb lymphedema. A number of pneumatic devices have been constructed. There is lack of reports of comparative studies determining inflation pressure levels, inflation/deflation cycle times, and total pumping times. Aim: We tried to answer the question how high compression pressure and how long compression timing should be applied to the limb soft tissues to reach tissue fluid (TF) head pressure above 30 mmHg, necessary to initiate proximal flow. Methods: TF pressures were measured subcutaneously during intermittent pneumatic compression in the lymphedematous limbs stage II to IV. Pressures of 50, 80, and 120 mmHg and timing 5, 20, and 50 sec were applied. Results: a) the TF head pressures were lower than those in inflated chambers, b) inflation time of 5 and 20 sec was not long enough to generate TF head pressures above 30 mmHg, even if the compression pressures were as high as 120 mmHg, c) the 50 sec timing allowed to reach head pressures above 30 mmHg; however, they remained always lower than in the compression chamber, d) TF head pressures differed at various levels of the limb depending on the soft tissue mass, e) deflation of the inflated whole sleeve for 5 and 20 sec was followed by high end pressures, whereas that of 50 sec brought about pressure drop to 0, facilitating refilling with TF of the distal parts of the massaged limb. Conclusions: Our observations point to the necessity of applying high pressures and compression times over 50 sec, to generate effective TF pressures and provide enough time for creating TF flow. Short inflation times generate TF pressures as in one-chamber devices that preclude its effectiveness compared to the multi-chamber devices.
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