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Lymphedema and Venous Stasis Pathophysiology and Treatment Lymphatic system physiology Retrieval of plasma proteins filtered out through capillary walls. Lymphangions carry the high protein fluid back to the main lymph system. Lymphangions have valves and smooth muscle. Low pressure system. Skeletal muscle action, blood vessel pulsations and gravity assist. Lymphatic system physiology Lymphatic fluid is transported back to the venous circulation via regional lymph nodes and the long thoracic duct. Lymphatics can regenerate but if pressures are too great valves become incompetent. Regenerated lymphatics are sensitive to scar formation. Lymphatic system physiology Lymphatic fluid contains fibrinogen and thrombin, not thromboplastin. Clots more slowly than blood. Thromboplastin is present in bacteria and cell fragments; clotting occurs with infection and inflammation. Larger proteins pass into the interstitium when inflammation is present. Lymphedema Pathophysiology Obstruction of lymphatics with fibrosis of regional lymph nodes. High protein fluid predisposes to infection and fibrosis. Clotting due to infection/inflammation Subdermal fluid accumulation (lowest pressures) Lymphedema Pathophysiology: Compensatory factors Lymphatic vessel repair/reanastomosis (vulnerable) Macrophage proteolytic activity Mechanical measures to stabilize/improve lymphatic outflow. Etiology of Lymphedema Primary. Related to inborn defects in the lymphatic system, may be evident at birth(lymphedema praecox), or manifest in the 2nd or 3rd decades (lymphedema tarda). Secondary. Acquired lymphedema due to cancer, infection (filariasis leading cause worldwide), radiation, surgery or trauma Postmastectomy lymphedema Incidence about 15-20% after axillary dissection Higher incidence in patients who have received radiation therapy than in those without this modality Other risk factors are obesity, local infection or delayed healing, dominant side Onset may be delayed, even years Stages of lymphedema (Foldi) Stage I. Reversible. Pitting and swelling that become temporarily reduced by limb elevation. Stage II. Spontaneously irreversible. Progressive hardening, decreased pitting quality Lymphedema stages, Cont’d Stage III. Lymphostatic elephantiasis. Massive increase in volume, cartilagelike hardening of dermal tissues, and papillomatous outgrowth. Measurement of Lymphedema Volumetric measures. Tracy classification (absolute volume); Stillwell classification (percent difference from normal limb). Based on post-mastectomy studies. Circumferential measures Tracy classification Insignificant (0-150cc > normal limb) Slight (150-400cc > normal limb) Moderate (400-750cc > normal limb) Severe (more than 750cc > normal limb) Stillwell classification Insignificant (0-10% > normal limb) Slight (11-20% > normal limb) Moderate (21-40% > normal limb) Marked (41-80% > normal limb) Severe (above 80% > normal limb) Differential Dx: Upper Limb Lymphedema versus venous thrombosis Benign versus malignant lymphedema Differential Dx: Lower Limb Lymphedema Venous thrombosis Venous stasis disease Postphlebitic syndrome Chronic venous insufficiency: Pathophysiology Chronic abnormally high venous system pressures lead to valve incompetence, dilated leg veins, interstitial edema, rupture of small subcutaneous vessels. Stasis pigmentation from hemosiderin deposition. End stage ulceration due to chronic fibrosis and atrophy Stages of Venous Insufficiency Stage I. Pain, heaviness, superficial varicosities, perimalleolar edema Stage II. Moderate-severe edema, pigmentation, pruritis, dermatitis, moderate varicosities Stage III. Severe edema. Marked pigmentation. Ulceration. Pain. Lymphedema appearance Involves dorsum hand/foot, typically spares MCP’s/MTP’s and distally +/- Pitting Cellulitis common Other skin changes uncommon Ulceration rare; oozing in severe cases Involves entire limb Venous insufficiency appearance Pitting, dependent edema Better response to limb elevation than lymphedema Distal limb most affected (especially distal tibial area) Skin changes, ulceration common Pain more common? Laboratory evaluation Duplex to exclude DVT Imaging and/or electrodiagnosis to screen for recurrent tumor as cause of new swelling. Lymphoscintigraphy Lymphangiography Optoelectronic volumetry Treatment Skin care Limb elevation Proximal decongestion Gradient compression Exercise Acute Lymphedema (sx < 2 wks) Education and Stabilization Infection? Skin care Pump down? Bandaging and/or compression garment Contracture reduction (shoulder exercise to open lymphatic channels) Exercise Subacute lymphedema(sx>2 wks); Establish regimen Above acute measures plus Decongestive lymphatic massage, manual lymphatic drainage Low stretch bandaging Static compression garment Chronic lymphedema (sx>4 wks); Maintain regimen Above measures plus Trial of pneumatic sequential compression device (gradient pressure) Pumpdown versus daily use Compliance / preference factors Compression garments Available as 30/20, 40/30, and 50/40 (distal greater than proximal pressure). Stock versus custom Use 30/20 for early, mild cases, or when ease of donning is a major factor. Use 40/30 most of the time ?? Role of 50/40. Pressure possibly too high for the delicate lymphatic system. Compression garments, cont’d Dual role of edema control and protection from trauma Standard sleeve (wrist to shoulder) or stocking (foot to thigh) for lymphedema Glove or gauntlet Zippered garments, or use of rubber glove for ease of donning Compression garments, misc Wearing schedule largely empiric, generally 6-23 hrs per day, according to severity of the edema Provide 2 garments, unless wearing schedule is limited/intermittent Non-limb options Financial barriers Pumping options Jobst (single versus multi-chamber) Lymphapress Wright linear compression Contraindications to pumping Absolute: active regional metastatic disease or infection; deep vein thrombosis Relative: anticoagulated state, congestive heart failure, arterial insufficiency, skin lesions, ? Active chemotherapy or radiation therapy Pump settings Some advocate not going above 80mm Hg Maximum distal pressure: mean of systolic and diastolic blood pressures Other devices Reed sleeve Legacy Circ Aid Decongestive massage therapies Proximal decongestion: clear adjacent trunk (“lymphotome”) before moving distally down the affected extremity Gradient compression: maintain reduction with exercise, garments, bandaging or pump Vodder, Foldi, Lerner, Casley-Smith, LeDuc Surgical therapies Physiological surgery. Microlymphatic- venous anastomosis. But limited experience in post-malignancy lymphedema, and recurrence rate is high Excisional surgery. Removal of excessive tissue, suction lipectomy Drug therapies Antibiotics for cellulitis or lymphangitis No data supporting long-term diuretics Benzopyrones? Used in Europe. Stimulates proteolysis by macrophages, and increases the number of macrophages. Associated issues Pain Contracture Peripheral nerve or plexus pathology Psychologic/coping Lymphangiosarcoma (rare but aggressively malignant) Procedures Venous stasis treatment Similar mechanical measures (elevation, garment, exercises, pumping). Distal limb tx may be sufficient. Topical steroids to target eczematous skin changes and pruritis. Vigilance re infection usually not as crucial Wound treatment (protective moist dressings). References DeLisa, Gans. Rehabilitation Medicine: Principles and Practice, 3rd ed. 1998. Grabois M. Breast Cancer: Postmastectomy Lymphedema. PM&R: State of the Art Reviews. Vol 8, #2, 1994, 267-277. Brennan MJ, DePompolo RW, Garden FH. Focused Review: Postmastectomy Lymphedema. Arch Phys Med Rehabil, Vol 77, 1996, S74-S80.
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