What is the pathophysiology of lymphedema?

Updated: Mar 24, 2021
  • Author: Robert A Schwartz, MD, MPH; Chief Editor: William D James, MD  more...
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In a diseased state, the lymphatic transport capacity is reduced. Consequently, the normal volume of interstitial fluid formation exceeds the rate of lymphatic return, resulting in the stagnation of high-molecular-weight proteins in the interstitium. This usually occurs after flow has been reduced by 80% or more. The result, as compared with 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. [10]

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