PLE can occur at an early age and can also be triggered by trauma, surgery or other reasons. BCRL is a common SLE, usually confined to the affected upper limb or and thorax-back. The traditional view of BCRL pathophysiology is that removal of axillary nodes results in obstruction to the flow of lymph from the arm, leading to accumulation of protein-rich fluid in the interstitium: the‘stopcock’ hypothesis. But some women develop BCRL after sentinel node biopsy, whereas others do not after clearance surgery, which suggest that a simple ‘stopcock’ mechanism does not explain many clinical aspects, including the delayed onset and selective sparing of some regions, e.g, hand. BCRL is a result of interaction between several pathophysiological processes, and is not simply a ‘stopcock’ effect resulting from removal of axillary lymph nodes. Predisposition hypothesis has therefore attracted the attention of some researchers. Aldrich found the appearance of vessel abnormalities on unaffected arms with increasing time which indicated that BCRL might progress to affect the clinically “normal” arm and become a systemic, rather than local, malady. So care should be given to both arms after cancer treatment.In other two studies, rates of depot clearance after subcutaneous injection of radiolabeled protein in the hands and subsequent appearance in venous blood suggested lymphatic dysfunction in both affected and contralateral “normal” arms[4, 5]. Bains found that women with upper-limb BCRL had reduced lower-limb lymphatic function and a large proportion of women with breast cancer had abnormal lower-limb lymphatic function, irrespective of whether they had symptoms of upper-limb BCRL or not. Possible explanations could be a systemic effect of breast cancer or its treatment, or an unidentified association between breast cancer and lymphatic dysfunction. There is a constitutional ‘global’ lymphatic dysfunction in patients who develop BCRL.Furthermore, the risk factors of BCRL are multiple. A genetic predisposition for lymphatic dysfunction, other surgical or injury damage to lymphatics, body mass index, medications, and fitness level are all suspected systemic factors contributing to the development of lymphedema[7, 8].
In addition, WeiRen Pan found that the individualization of lymphatic system development varies greatly. The clinical symptoms and signs of lymphedema are related to the anatomical differences of individual lymphatic system.
The special point of this case was that radical mastectomy aggravated the original lymphedema of trunk and upper limb, but it only occurred in the opposite side of the operation. In addition to the above predisposing hypothesis and cancer treatment could trigger or aggravate systemic edema, the individual differences of lymphatic dysplasia and the resection or damage of lymphatic vessels and lymph nodes in the affected trunk and upper extremities after surgery should also be taken into account. And the lymph flow of the affected side might be past sagital watershed and be reversed toward the opposite side, thus leading to the progressive PLE of the unaffected trunk and upper limb. Bobbio had ever reported the similar situation, as showed in the following figure.
To summarize, PLE and SLE may be both results of the interaction of multiple factors. Tumor itself or cancer treatment may induce or aggravate SLE in susceptible patients. PLE can be induced or aggravated by trauma, surgery or other reasons besides the abnormal lymphatic development of individuals, and may be manifested differently according to the specific conditions of individual lymphatic abnormalities. Further studies need to determine whether systemic manifestation of lymphatic abnormalities in cancer-related lymphedema are indicative of progressive disease and their relationship with cancer treatment.