AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Lymphedema is a notoriously debilitating progressive condition with no known cure. The unfortunate patient faces a lifelong struggle of medical, and sometimes surgical, treatment fraught with potentially lethal complications.

The underlying problem is lymphatic dysfunction, resulting in an abnormal accumulation of interstitial fluid containing high molecular weight proteins. This condition underscores the tremendous importance of a normally functioning lymphatic system, which returns proteins, lipids, and accompanying water from the interstitium to the venous circulation near the subclavian vein–internal jugular vein junction, bilaterally.

Frequency

• In the United States, the highest incidence of lymphedema is observed following breast cancer surgery, particularly among those who undergo radiation therapy following axillary lymphadenectomy. Among this population, 10-40% develop some degree of ipsilateral upper extremity lymphedema.
• Worldwide, 140-250 million cases of lymphedema are estimated to exist, with filariasis being the most common cause.

Etiology

Lymphedema may be classified as primary or secondary, based on underlying etiology. However, this classification usually has little significance in determining treatment modality.

• Primary lymphedema represents a developmental abnormality of the lymphatic system.
• • Primary lymphedema has been further subdivided into 3 forms, including congenital lymphedema, lymphedema praecox, and lymphedema tarda, depending on age at presentation. These conditions are most often sporadic, with no family history, and involve the lower extremity almost exclusively.
  • All 3 forms of primary lymphedema likely originate from a developmental abnormality that is present, but not always clinically evident, at birth. Some cases may become evident later in life when a triggering event or worsening of the condition causes the lymphatic transport capacity to exceed the volume of interstitial fluid formation, causing the patient to be unable to maintain normal lymphatic flow.
  • Congenital lymphedema represents all forms that are clinically evident at birth and accounts for 10-25% of all primary lymphedema cases. Females are affected twice as often as males, and the lower extremity is involved 3 times more frequently than the upper extremity. Two thirds of patients have bilateral lymphedema, and this form may improve spontaneously with increasing age.
  • • A subset of patients with congenital lymphedema has a familial sex-linked pattern of inheritance, which is termed Milroy disease. It accounts for 2% of primary lymphedema cases.
    • The histology of the lymphatic channels often demonstrates an anaplastic pattern without subcutaneous lymphatic trunks but with normal dermal plexus.
  • Lymphedema praecox is the most common form of primary lymphedema. By definition, it becomes clinically evident after birth and before age 35 years. This condition accounts for 65-80% of all primary lymphedema cases and most often arises during puberty. Females are affected 4 times as often as males. About 70% of cases are unilateral, with the left lower extremity being involved more often than the right. Histologically, these patients are likely to demonstrate a hypoplastic pattern, with the lymphatics reduced in caliber and number.
  • Lymphedema tarda, also known as Meige disease, does not become clinically evident until age 35 years or older. As the rarest form of primary lymphedema, it accounts for only 10% of cases. Histologically, patients are likely to demonstrate a hyperplastic pattern, with tortuous lymphatics increased in caliber and number. They often display absent or incompetent valves.
• Secondary lymphedema represents an acquired dysfunction of otherwise normal lymphatics.
• • Secondary lymphedema has an identifiable cause that destroys or renders inadequate the otherwise normal lymphatics.
  • In the United States, it commonly results from damage or removal of regional lymph nodes through surgery, radiation, infection, or tumor invasion or compression.
  • Worldwide, the most common cause is filariasis, the direct infestation of lymph nodes by the parasite Wuchereria bancrofti.
  • Other causes include vein stripping, peripheral vascular surgery, lipectomy, burns, burn scar excision, and insect bites.

Pathophysiology

The normal function of the lymphatics is to return proteins, lipids, and water from the interstitium to the intravascular space; 40-50% of serum proteins are transported by this route each day. High hydrostatic pressures in arterial capillaries force proteinaceous fluid into the interstitium, resulting in increased interstitial oncotic pressure that draws in additional water.

Interstitial fluid normally contributes to the nourishment of tissues. About 90% of the fluid returns to the circulation via entry into venous capillaries. The remaining 10% is composed of high molecular weight proteins and their oncotically associated water, which are too large to readily pass through venous capillary walls. This leads to flow into the lymphatic capillaries where pressures are typically subatmospheric and can accommodate the large size of the proteins and their accompanying water. The proteins then travel as lymph through numerous filtering lymph nodes on their way to join the venous circulation.

In a diseased state, the lymphatic transport capacity is reduced. This causes the normal volume of interstitial fluid formation to exceed the rate of lymphatic return, resulting in the stagnation of high molecular weight proteins in the interstitium. It usually occurs after flow has been reduced by 80% or more. The result, as compared to other forms of edema that have much lower concentrations of protein, is high-protein edema, or lymphedema, with protein concentrations of 1.0-5.5 g/mL. This high oncotic pressure in the interstitium favors the accumulation of additional water.

Accumulation of interstitial fluid leads to massive dilatation of the remaining outflow tracts and valvular incompetence that causes reversal of flow from subcutaneous tissues into the dermal plexus. The lymphatic walls undergo fibrosis, and fibrinoid thrombi accumulate within the lumen, obliterating much of the remaining lymph channels. Spontaneous lymphovenous shunts may form. Lymph nodes harden and shrink, losing their normal architecture.

In the interstitium, protein and fluid accumulation initiates a marked inflammatory reaction. Macrophage activity is increased, resulting in destruction of elastic fibers and production of fibrosclerotic tissue. Fibroblasts migrate into the interstitium and deposit collagen. The result of this inflammatory reaction is a change from the initial pitting edema to the brawny nonpitting edema characteristic of lymphedema. Consequently, local immunologic surveillance is suppressed, and chronic infections, as well as malignant degeneration to lymphangiosarcoma, may occur.

The overlying skin becomes thickened and displays the typical peau d'orange (orange skin) appearance of congested dermal lymphatics. The epidermis forms thick scaly deposits of keratinized debris and may display a warty verrucosis. Cracks and furrows often develop and accommodate debris and bacteria, leading to lymphorrhea, the leakage of lymph onto the surface of the skin.

Clinical

Patients present with varying degrees of severity, from mild swelling to severe disabling enlargement with potentially life-threatening complications. This disease is often first noticed by the patient as an asymmetry or increased circumference of an extremity. As swelling slowly progresses, patients may have difficulty fitting into clothing. Once well established, lymphedema may cause fatigue related to the size and weight of the extremity, embarrassment in public, and severe impairment of daily activities. Recurrent bacterial or fungal infections are also common.

The diagnosis is usually made with a thorough history and physical examination. Other causes of edema, such as edema secondary to congestive heart failure, renal insufficiency, hepatic insufficiency, or venous stasis disease, must be excluded. Malignancy must always be considered, particularly when patients report sudden onset, rapid progression, or associated pain. These symptoms may indicate direct tumor growth or metastatic disease in the regional lymph node basin.

INDICATIONS

Section 3 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Surgical treatment is palliative, not curative, and it does not obviate the need for continued medical therapy. Moreover, it is rarely indicated as the primary treatment modality. Rather, reserve surgical treatment for those who do not improve with conservative measures or in cases where the extremity is so large that it impairs daily activities and prevents successful conservative management.

RELEVANT ANATOMY

Section 4 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Before embarking on the treatment of lymphedema, a thorough knowledge of the relevant anatomy is essential. Blind-ended lymphatic capillaries arise within the interstitial spaces of the dermal papillae. These unvalved superficial dermal lymphatics drain into interconnected subdermal channels, which parallel the superficial venous system. These subsequently drain into the deeper, epifascial system of valved trunks lined with smooth muscle cells and located just above the deep fascia of the extremity. This system is responsible for the drainage of lymph from the skin and subcutaneous tissues. Valves provide for unidirectional flow towards regional lymph nodes and eventually the venous circulation in the neck. Flow is achieved by variations of tissue pressure through skeletal muscle contractions, pulsatile blood flow, and contractions of the spiral smooth muscle fibers surrounding larger lymphatic channels.

A deeper valved subfascial system of lymphatics is responsible for the drainage of lymph from the fascia, muscles, joints, ligaments, periosteum, and bone. This subfascial system parallels the deep venous system of the extremity. The epifascial and subfascial systems normally function independently, although valved connections do exist in the popliteal, inguinal, antecubital, and axillary regions where lymph nodes form interconnected chains. These connections probably do not function under normal conditions; however, in lymphedema, some reversed flow through perforators from the epifascial to the subfascial system may occur as a mechanism of decompression of the epifascial system. In lymphedema, the derangement is almost always exclusive to the epifascial lymphatic system, with the subfascial system being uninvolved. This is the basis for the surgical approaches to lymphedema, which focus on the epifascial system.

CONTRAINDICATIONS

Section 5 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Contraindications to intermittent pneumatic pump compression therapy include congestive heart failure, deep vein thrombosis, and active infection.

WORKUP

Section 6 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Imaging Studies

• Although infrequently required to establish the diagnosis, certain tests may be useful to confirm the diagnosis in complex cases, to determine residual lymphatic function, to establish treatment preferences, and to evaluate therapy.
• Lymphangiography was the criterion standard for evaluating the lymphatic system for many years.
• • This technique has been shown to cause an inflammatory reaction of the endothelium of the remaining lymphatic channels, leading to scarring, atrophy, and even luminal obliteration.
  • Lymphangiography has been replaced by less invasive techniques and should no longer be performed on patients with lymphedema.
• Lymphoscintigraphy has replaced lymphangiography.
• • It does not promote further damage to the delicate lymphatic channels.
  • This test can be used to define anatomy and patency, evaluate dynamics of flow and reversal of flow, and determine the severity of obstruction.
• Computed tomography (CT) scans and magnetic resonance imaging (MRI) have been advocated by some authors.
• • These tests can delineate nodal architecture at a greatly increased cost, but they have very few advantages over lymphoscintigraphy.
  • An indication for CT scan or MRI is suspicion of malignancy, for which these tests offer the most information.
• Doppler ultrasonography is also used by some to evaluate flow in the lymphatic and venous systems.
• • The presence of a deep vein thrombosis is in the differential diagnosis of unilateral extremity swelling, and it may also occur concomitantly with lymphedema.
  • This is a very cost-effective test in the appropriate clinical situation.

TREATMENT

Section 7 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Medical therapy

The goal of conservative therapy is to eliminate protein stagnation and to restore normal lymphatic circulation. Initiate therapy as early as possible before extensive irreversible fibrosclerotic changes occur in the interstitium. These techniques are often cumbersome, uncomfortable, inconvenient, and time-consuming. Strict compliance is essential, and treatment lasts throughout the lifetime of the individual. The majority of compliant patients can be treated successfully with conservative measures.

Meticulous hygiene is necessary to remove keratinaceous debris and bacteria. Cleanse the skin regularly and dry thoroughly. Regular inspection is necessary to identify any open wounds or developing cellulitis. Bland skin moisturizers applied conservatively may ameliorate cracking and furrowing. Even with excellent skin care, chronic cellulitis may occur. At the earliest signs of infection, institute topical or systemic antifungal or antimicrobial therapy to prevent the development of sepsis. Long-term prophylactic antimicrobial treatment with agents, such as penicillin, cephalexin, or erythromycin, may be required in 15-25% of patients experiencing recurrent lymphangitis or cellulitis. Although relatively uncommon in this country, filariasis is treated with diethylcarbamazine.

Encourage patients to lose weight, avoid even minor trauma, and avoid constrictive clothing that might have a tourniquet effect. Encourage elevation of the affected extremity whenever possible, particularly at night. For lower extremity lymphedema, this may be accomplished by elevating the foot of the bed to an appropriate level.

Patients should use compression garments continuously during the day. They may be removed at night when the extremity is elevated in bed, but they should be replaced promptly each morning. To encourage compliance, the elastic compression garments must fit appropriately. Garments should be custom fit when the extremity is decompressed, they should be comfortable, and they should not have a tourniquet effect. They should also have graduated compression, increasing from distal to proximal, on the affected extremity.

Intermittent pneumatic pump compression therapy may also be instituted on an outpatient basis or in the home. These manual lymphatic devices are most appropriate prior to fibrosclerotic evolution, and they assist in preventing fibrosclerotic evolution of the condition. These devices provide sequential active compression from distal to proximal, effectively milking the lymph from the extremity. In Europe, the best available nonsurgical therapy is manual lymphatic drainage according to the Vodder and/or Leduc techniques. Compression garments are essential between treatments. Contraindications to this therapy include congestive heart failure, deep vein thrombosis, and active infection. Similarly, other authors advocate manual massage of the affected extremity to recruit collateral vessels so that the accumulated lymph can be drained into neighboring regions with normally functioning lymphatics.

Diuretics have no role in the treatment of lymphedema.

Benzopyrenes, including flavonoids and coumarin, have become a useful adjuvant in other countries but are currently not available for clinical use in the United States. These drugs bind to accumulated interstitial proteins, inducing macrophage phagocytosis and proteolysis. The resulting protein fragments pass more readily into the venous capillaries and are removed by the vascular system.

Surgical therapy

Surgical treatment is palliative, not curative, and it does not obviate the need for continued medical therapy. Moreover, it is rarely indicated as the primary treatment modality. Rather, reserve surgical treatment for those who do not improve with conservative measures or in cases where the extremity is so large that it impairs daily activities and prevents successful conservative management. The goals of surgical therapy are volume reduction to improve function, facilitation of conservative therapy, and prevention of complications. A myriad of surgical procedures have been advocated, reflecting a lack of clear superiority of one procedure over the others. In general, surgical procedures are classified as physiologic or excisional.

Physiologic procedures attempt to improve lymphatic drainage. Multiple techniques have been described, including omental transposition, buried dermal flaps, enteromesenteric bridging, lymphangioplasty, and microvascular lympholymphatic or lymphovenous anastomoses. None of these techniques has clearly documented favorable long-term results. Further evaluation is necessary. Moreover, many of these physiologic techniques also include an excisional component, making it difficult to distinguish between the two approaches.

Excisional techniques remove the affected tissues, thus reducing the lymphedema load. Some authors advocate suction-assisted removal of subcutaneous tissues, but this technique is difficult because of the extensive subcutaneous fibrosis that is present. Additionally, this approach does not reduce the skin envelope, and the lymphedema often rapidly recurs. Suction-assisted removal of subcutaneous tissue followed by excision of the excess skin envelope has no clear advantage over direct excisional techniques alone.

The Charles procedure is another quite radical excisional technique. This procedure involves the total excision of all skin and subcutaneous tissue from the affected extremity. The underlying fascia is then grafted, using the skin that has been excised. This technique is extreme and is reserved for only the most severe cases. Complications include ulceration, hyperkeratosis, keloid formation, hyperpigmentation, weeping dermatitis, and severe cosmetic deformity.

Staged excision has become the option of choice for many authors. This procedure involves removing only a portion of skin and subcutaneous tissue, followed by primary closure. After approximately 3 months, the procedure is repeated on a different area of the extremity. This procedure is safe, reliable, and demonstrates the most consistent improvement with the lowest incidence of complications.

Preoperative details

Prior to surgery, appropriate documentation is necessary to evaluate the outcome of treatment. This includes photographic documentation as well as extremity measurements. Ideally, these measurements are of limb volume by water displacement, although some rely on circumferential measurements alone. Obtain measurements and photographs at the same time of day each time, document both affected extremities and contralateral extremities, and preferably conduct documentation in the morning after extremity elevation in bed overnight.

Institute strict elevation and pneumatic compression, if available, 24-72 hours prior to surgery. This allows maximum excision to be performed. The extremity must also be free of infection at the time of surgery, and a single dose of preoperative intravenous antibiotic is administered.

Intraoperative details

• After the establishment of appropriate anesthesia, the operative field is sterilized and draped according to surgeon preference.
• A pneumatic tourniquet is placed at the root of the extremity and insufflated after the extremity has been exsanguinated.
• A longitudinal incision is made along the entire extremity, and skin flaps, 1.0-1.5 cm thick, are elevated.
• Subcutaneous tissue is then excised, taking care not to injure peripheral sensory nerves.
• Some authors also excise a strip of deep fascia, but this should not be performed around joints because it may cause instability.
• Once the subcutaneous excision is complete, redundant skin is resected. Often, a strip that is 5-10 cm wide may be removed.
• The wound is closed over suction drains.

Postoperative details

• Postoperatively, the extremity is immobilized in a splint and elevated while the patient is placed on strict bed rest.
• Antibiotics may be continued until drain removal, according to surgeon preference.
• Drains are typically removed at 5-7 days postoperatively, as dictated by a decrease in drain output.
• Sutures are removed at 10-14 days and replaced by Steri-Strips.
• Measure the patient for a new compression garment when the new dimensions of the extremity have stabilized.
• After approximately 10 days, the patient may gradually begin dependency on the extremity with compression bandages or an elastic garment in place.

Follow-up

• Once discharged from the hospital, the patient should be seen regularly in the outpatient clinic.
• Patients must wear compression garments for 4-6 weeks continuously, and dependency on the involved extremity may be gradually increased at the discretion of the treating physician.
• Once healed to physician satisfaction, the patient may return to a normal routine of elevation at night and compression garment therapy during the day.
• Follow-up visits should include documentation of circumferential measurement or water displacement of the affected and contralateral extremities as well as photographic documentation.
• When staging procedures, allow approximately 3 months between procedures to allow complete healing of the initial operative site.

COMPLICATIONS

Section 8 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Patients with chronic lymphedema for 10 years have a 10% risk of developing lymphangiosarcoma, the most dreaded complication of this disease. Patients with this tumor commonly present with a reddish purple discoloration or nodule that tends to form satellite lesions. It may be confused with Kaposi sarcoma or traumatic ecchymosis. This tumor is highly aggressive, requires radical amputation of the involved extremity, and has a very poor prognosis. The 5-year survival rate is less than 10%, and the average survival following diagnosis is 19 months. This malignant degeneration is most commonly observed in patients with postmastectomy lymphedema (Stewart-Treves syndrome), where incidence is estimated to be 0.5%.

Other complications of lymphedema include recurrent bouts of cellulitis and/or lymphangitis, deep venous thrombosis, severe functional impairment, cosmetic embarrassment, and necessary amputation. Complications following surgery are common and include partial wound separation, seroma, hematoma, skin necrosis, and exacerbation of foot or hand edema.

OUTCOME AND PROGNOSIS

Section 9 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

At present, no cure for lymphedema exists. Surgery is palliative at best, and it may be a part of the lifelong therapy patients must endure to manage this disease.

FUTURE AND CONTROVERSIES

Section 10 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

A myriad of surgical procedures have been advocated, reflecting a lack of clear superiority of one procedure over the others. Multiple physiological and excisional techniques have been described. None of the physiological techniques has clearly documented favorable long-term results; further evaluation is necessary. Moreover, many of the physiologic techniques also include an excisional component, making it difficult to distinguish between the two approaches.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Media file 1:  Lymphedema. The body quadrants of superficial lymph drainage.
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Media type:  Image

Media file 2:  Lymphedema. (1) Normal lymphatic flow in (a) deep systems and (b) superficial systems. Note the small collateral vessels interconnecting the 2 systems. (2) Lymphedema develops from obstruction, dilation of valves, valvular insufficiency, and subsequent reversal of lymphatic flow.
	View Full Size Image
Media type:  Image

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

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• Gerber LH. A review of measures of lymphedema. Cancer. Dec 15 1998;83(12 Suppl American):2803-4. [Medline].
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• Leitch AM, Meek AG, Smith RA, Boris M, Bourgeois P, Higgins S, et al. American Cancer Society Lymphedema Workshop. Workgroup I: Treatment of the axilla with surgery and radiation--preoperative and postoperative risk assessment. Cancer. Dec 15 1998;DA - 19990128(12 Suppl American):2877-9. [Medline].
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• Ottesen EA, Duke BO, Karam M, Behbehani K. Strategies and tools for the control/elimination of lymphatic filariasis. Bull World Health Organ. 1997;75(6):491-503. [Medline].
• Rajan TV, Gundlapalli AV. Lymphatic filariasis. Chem Immunol. 1997;66:125-58. [Medline].
• Rinehart-Ayres ME. Conservative approaches to lymphedema treatment. Cancer. Dec 15 1998;83(12 Suppl American):2828-32. [Medline].
• Rockson SG. Precipitating factors in lymphedema: myths and realities. Cancer. Dec 15 1998;83(12 Suppl American):2814-6. [Medline].
• Rockson SG, Miller LT, Senie R, Brennan MJ, Casley-Smith JR, Földi E, et al. American Cancer Society Lymphedema Workshop. Workgroup III: Diagnosis and management of lymphedema. Cancer. Dec 15 1998;DA - 19990128(12 Suppl American):2882-5. [Medline].
• Runowicz CD. Lymphedema: patient and provider education: current status and future trends. Cancer. Dec 15 1998;83(12 Suppl American):2874-6. [Medline].
• Shimony A, Tidhar D. Lymphedema: a comprehensive review. Ann Plast Surg. Feb 2008;60(2):228. [Medline].
• Thiadens SR. Current status of education and treatment resources for lymphedema. Cancer. Dec 15 1998;83(12 Suppl American):2864-8. [Medline].
• Walley DR, Augustine E, Saslow D, Bailey S, Jeffs E, Lasinski B, et al. American Cancer Society Lymphedema Workshop. Workgroup IV: Lymphedema treatment resources--professional education and availability of patient services. Cancer. Dec 15 1998;DA - 19990128(12 Suppl American):2886-7. [Medline].

Article Last Updated: Mar 18, 2008