Transient versus Chronic Lymphedema

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 risk for acute-onset, transient lymphedema:

Surgical drains with extravasation of protein into the surgical site.
Inflammation following injury, radiation, or infection leading to increased capillary permeability.
Immobility of the limb(s) that results in decreased external compression by the musculature.
Temporary absence of collateral lymphatics.
Proximal venous occlusion by thrombosis or phlebitis.

Reversal of equilibrium at the capillary bed that results in accumulation of third-space fluid.

Chronic lymphedema is the most difficult of all types of edema to reverse, due to the nature of its pathophysiology. A cycle is started, in which the deficient lymphatic system of the limb is incapable of compensating 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.

* * Editor's note:

(1) It is imperative to understand that any transient lymphedema can become chronic and permenant without proper intervention. Therefore, even if a physcian believes a patient has "transient" lymphedema, they should be referred to a certified lymphedema therapist for an evaluation and treatment.

(2) Chronic lymphedema can be hereditary and/or congenital. It is also associated with various conditions that involve lymphatic dysplaysia. This lymphedema is also referred to as primary.

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. Fibrosis 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.

Lymphedematous tissues have lower oxygen content, a greater distance between lymph vessels due to fluid accumulation and swelling, impaired lymphatic clearance, and depressed macrophage function, rendering patients at increased risk of infection and cellulitis. Since there is no other route for tissue protein transport, treatment for patients with advanced lymphedema with chronic fibrosis is more difficult than when treated earlier. Additionally, once these tissues are stretched, edema recurs more readily.

Generalized lymphedema may also occur subsequent to hypoalbuminemia with low plasma oncotic pressure due to the following:

Inadequate oral nutrition (secondary to anorexia, nausea, vomiting, depression, chemotherapy).
Decreased intestinal absorption of protein or abnormal protein synthesis/anabolism.

Protein loss due to leakage of blood, ascites, effusions, or surgical drains.

Contributing medical conditions leading to hypoalbuminemia (e.g., diabetes, kidney malfunction, hypertension, congestive heart failure, liver disease).

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