Lymphedema and Venous Stasis by BKKESqq0


   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
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
Lymphedema Pathophysiology:
Compensatory factors
 Lymphatic vessel repair/reanastomosis
 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
 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
 Stage II. Spontaneously irreversible.
  Progressive hardening, decreased pitting
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:
Chronic abnormally high venous system
  pressures lead to valve incompetence,
  dilated leg veins, interstitial edema, rupture
  of small subcutaneous vessels.
Stasis pigmentation from hemosiderin
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
 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
 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
 Lymphoscintigraphy
 Lymphangiography
 Optoelectronic volumetry
 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
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,
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
 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
   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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