Excisional Procedures: Liposuction

Adipose Tissue Hypertrophy

Various possible explanations exist for the hypertrophy of adipose tissue seen in lymphedema. There is a physiologic imbalance of blood flow and lymphatic drainage, resulting in the impaired clearance of lipids and their uptake by macrophages. There is increasing support for the view that the fat cell is an endocrine organ and a cytokine-activated cell, and chronic inflammation may play a role in the alterations seen in the disease process. Also, previous research has highlighted the relationship between slow lymph flow and adiposity, as well as that between structural changes in the lymphatic system and adiposity. Other supported findings for adipose tissue hypertrophy include the following:

• The findings of increased adipose tissue in intestinal segments in patients with inflammatory bowel disease (Crohn disease), known as “fat wrapping,” have clearly shown that inflammation plays an important role.

• Consecutive analyses of the content of the aspirate removed under bloodless conditions using a tourniquet showed a high content of adipose tissue (mean, 90%).

• In Graves ophthalmopathy with exophthalmos, adipocyte-related immediate early genes are overexpressed and cysteine-rich, angiogenic inducer 61 may play a role in both orbital inflammation and adipogenesis.

• Tonometry can distinguish if a lymphedematous arm is harder or softer than the normal one. Patients with a harder arm compared with the healthy one have excess adipose tissue.

• An investigation with volume-rendering computed tomography in 11 patients also showed a significant preoperative increase in adipose tissue of 81% in the swollen arm, followed by a normalization at 3 months paralleling the complete reduction of the excess volume.

• Analyses with dual-energy X-ray absorptiometry in 18 women with postmastectomy arm lymphedema showed a significant increase in adipose tissue in the non-pitting swollen arm before surgery. Postoperative analyses showed normalization at 3 months. This effect was seen also at 12 months. These results paralleled the complete reduction of the excess volume.

• A functional inactivation of a single allele of the homeobox gene prospero-related homeobox (Prox)1 led to adult-onset obesity due to abnormal lymph leakage from mispatterned and ruptured lymphatic vessels.

• Parathyroid hormone–like hormone can inhibit adipogenesis and is downregulated both in active and chronic ophthalmopathy, indicating the possibility of an increased risk of adipogenesis.

• Adipogenesis in response to lymphatic fluid stasis is associated with a marked mononuclear cell inflammatory response.

• Lymphatic fluid stasis potently upregulates the expression of fat differentiation markers both spatially and temporally.

• The underlying pathophysiology of lymphedema drives adipose-derived stem cells toward adipogenic differentiation.

• Recent findings have shown that adipose tissue is also increased in the muscles of the lymphedematous arm.

Clinicians often believe that the swelling of a lymphedematous extremity is purely due to the accumulation of lymph fluid, which can be removed by the use of noninvasive conservative regimens, such as CDT and CCT. These therapies work well when the excess swelling consists of accumulated lymph but do not work when the excess volume is dominated by adipose tissue and related fibrosis. Conservative treatment and microsurgical procedures using lymphovenous shunts, lymph vessel transplantation, and vascularized lymph node transfer do not remove adipose tissue.