Current Concepts in Lymphedema Management

Advances in Skin & Wound Care, May 2004 by Sieggreen, Mary Y, Kline, Ronald A

PURPOSE

To provide physicians and nurses with an overview of the pathophysiology, assessment and diagnosis, and treatment of lymphedema.

TARGET AUDIENCE

This continuing education activity is intended for physicians and nurses with an interest in managing patients with lymphedema.

OBJECTIVES

After reading the article and taking the test, the participant will be able to:

1. Describe the pathophysiology of lymphedema and the difference between transient and chronic lymphedema.

2. Describe the assessment and diagnosis of lymphedema.

3. Identify treatment options and teaching considerations for patients with lymphedema.

ADV SKIN WOUND CARE 2004;17:174-80

Lymphedema-the accumulation of lymph in the interstitial spaces, principally in the subcutaneous fatty tissues-is caused by a defect in the lymphatic system. It is marked by an abnormal collection of excess tissue proteins, edema, chronic inflammation, and fibrosis.1 Understanding why it develops requires a familiarity with the lymphatic system, 1 of the 3 vascular systems in the body.

PATHOPHYSIOLOGY OF LYMPHEDEMA

The lymphatic system consists of superficial or primary lymphatic vessels that form a complex dermal network of capillary-like channels that drain into larger, secondary lymphatic vessels located in the subdermal space. These primary and secondary lymphatic vessels parallel the superficial veins and drain into a third, deeper layer of lymphatic vessels located in the subcutaneous fat adjacent to the fascia. A muscular wall and numerous valves aid active, unidirectional lymphatic flow in secondary and subcutaneous lymphatic vessels. Primary lymphatic vessels lack a significant muscular wall and do not have valves. An intramuscular system of lymphatic vessels that parallels the deep arteries and drains the muscular compartment, joints, and synovium also exists.

Although there is evidence that the superficial and deep lymphatic systems communicate near lymph nodes, they probably function independently, except in abnormal states.2 Lymph drains from the lower limbs into the lumbar lymphatic trunk, which joins the intestinal lymphatic trunk and cisterna chyli to form the thoracic duct that empties into the left subclavian vein. The lymphatic vessels of the left arm drain into the left subclavian lymphatic trunk, then into the left subclavian vein. Right arm lymph channels drain into the right subclavian lymphatic trunk, then into the right subclavian vein.

One function of the lymphatic system is to return excess fluid and protein from interstitial spaces to the blood vascular system. Because lymphatic vessels often lack a basement membrane, they can reabsorb molecules too large for venous uptake. Mechanisms of clinical edema include increased arteriovenous capillary filtration and reduced interstitial fluid absorption. Causes of increased capillary filtration include increased hydrostatic pressure in capillaries, decreased tissue pressure, and increased membrane permeability. Reduced interstitial fluid resorption can be caused by decreased plasma oncotic pressure, increased oncotic pressure of tissue fluid, and lymphatic obstruction.

Lymphedema is categorized as cither primary or secondary. Primary lymphcdcma is caused by congenital absence or abnormalities of lymphatic tissue and is relatively rare. Secondary lymphedema is generally caused by obstruction or interruption of the lymphatic system, which usually occurs at proximal limb segments (ie, lymph nodes) due to infection, ligation, malignancy, or scar tissue.1 The pelvic and inguinal nodes in the lower extremities and the axillary nodes ot the upper extremities are the primary sites of obstruction.

TRANSIENT VS. CHRONIC LYMPHEDEMA

Lymphedema can be transient or chronic. Transient lymphedema is a temporary condition that lasts less than 6 months and is associated with pitting edema with tactile pressure and lack of brawny skin changes.1 The following factors may place the patient at increased risk for transient lymphedema with an acute onset:

* surgical drains with extravasation of protein into the site of the surgical procedure.

* inflammation following injury, radiation, or infection leading to increased capillary permeability.

* immobility of the extremity or extremities that results in decreased external compression by the musculature

* proximal venous occlusion by thrombosis or phlebitis

* reversal of equilibrium at the capillary bed resulting in accumulation of third-space fluid.

Chronic lymphedema is more difficult to reverse because of its pathophysiology. A cycle is started, in which the limb's deficient lymphatic system cannot compensate for the increased demand for fluid drainage. This condition may occur subsequent to any of the following:

* tumor recurrence or progression in the nodal area

* infection and/or injury of lymphatic vessels

* immobility

* radiation injury to lymphatic structures

* surgery

* unsuccessful management of early lymphedema

* venous obstruction due to thrombosis.

Early in the course of developing lymphedema, the patient experiences soft, pitting edema that may be easily improved by limb elevation, gentle exercise, and elastic support. Continual and progressive lymphostasis, however, causes dilation of the lymph vessels and backflow of fluid to the tissue beds. Collagen proteins accumulate, further increasing colloid osmotic tissue pressure, leading to enhanced fluid flow from the vascular capillaries into the interstitial space. The stasis of fluid and protein stimulates inflammation and macrophage activity as the body attempts to degrade the excess proteins. Pibrosis of the interstitial connective tissue by fibrinogen and fibroblasts causes the development of the brawny, stiff, nonpitting lymphedema that no longer responds to elevation, gentle exercise, or elastic compression garments. Chronic lymphedema gradually becomes nonpitting.