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 assi - PowerPoint PPT Presentation
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1. Lymphedemaand Venous Stasis Pathophysiology and Treatment
2. 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.
3. 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.
4. 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.
5. 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)
6. Lymphedema Pathophysiology:Compensatory factors Lymphatic vessel repair/reanastomosis (vulnerable)
Macrophage proteolytic activity
Mechanical measures to stabilize/improve lymphatic outflow.
7. 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
8. 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
9. 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
10. Lymphedema stages, Cont’d Stage III. Lymphostatic elephantiasis. Massive increase in volume, cartilagelike hardening of dermal tissues, and papillomatous outgrowth.
11. Measurement of Lymphedema Volumetric measures. Tracy classification (absolute volume); Stillwell classification (percent difference from normal limb). Based on post-mastectomy studies.
12. Tracy classification Insignificant (0-150cc > normal limb)
Slight (150-400cc > normal limb)
Moderate (400-750cc > normal limb)
Severe (more than 750cc > normal limb)
13. 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)
14. Differential Dx: Upper Limb Lymphedema versus venous thrombosis
Benign versus malignant lymphedema
15. Differential Dx: Lower Limb Lymphedema
Venous stasis disease
16. 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
17. 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.
18. Lymphedema appearance Involves dorsum hand/foot, typically spares MCP’s/MTP’s and distally
Other skin changes uncommon
Ulceration rare; oozing in severe cases
Involves entire limb
19. 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?
20. Laboratory evaluation Duplex to exclude DVT
Imaging and/or electrodiagnosis to screen for recurrent tumor as cause of new swelling.
21. Treatment Skin care
22. Acute Lymphedema (sx < 2 wks)Education and Stabilization Infection?
Bandaging and/or compression garment
Contracture reduction (shoulder exercise to open lymphatic channels)
23. Subacute lymphedema(sx>2 wks); Establish regimen Above acute measures plus
Decongestive lymphatic massage, manual lymphatic drainage
Low stretch bandaging
Static compression garment
24. 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
25. 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.
26. 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
27. 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
28. Pumping options Jobst (single versus multi-chamber)
Wright linear compression
29. 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
30. Pump settings Some advocate not going above 80mm Hg
Maximum distal pressure: mean of systolic and diastolic blood pressures
31. Other devices Reed sleeve
Circ Aid Legacy
32. 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
33. 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
34. 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.
35. Associated issues Pain
Peripheral nerve or plexus pathology
Lymphangiosarcoma (rare but aggressively malignant)
36. 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).
37. 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.