Background: Breast cancer survivors are at increased risk for the development of breast cancer-related lymphedema (BCRL), a chronic, debilitating, and disfiguring condition that is progressive and requires lifelong self-management of symptoms.
Purpose
To investigate discrepancy patterns among anatomic and physiologic imaging and clinical feature of breast cancer related lymphedema and to identify factors influencing these rates.
Methods
Breast cancer patients were assessed by history, physical examination, lymphoscintigraphy and ultrasonography. Lymphoscintigraphy scan was started as dynamic viewing followed by static body imaging at 5 minute, 30 minute and 1 hour after injection. Uptake by axillary lymph nodes and the presence of dermal backflow on lymphoscintigraphy at 5 minute and 1 hour were evaluated. Subcutaneous ultrasound echogenicities were assessed on the medial side of the upper arm and forearm of both arms and graded by revised subcutaneous echogenicity grade (rSEG). Lymphedema was staged by reference to the guidelines of the International Society of Lymphology (ISL) consensus document based on the amount of swelling and the condition of the skin and tissues. The interlimb volume difference (ILD) was the volume of the ipsilateral arm minus the volume of the contralateral arm. The inter-limb impedance ratio was calculated on each side for the whole arm using a bioelectrical impedance analyzer (BIA).
Results: In total, 98 breast cancer patients participated in this study. Visualized axillary lymph or vessel were significantly correlated with ILD (β coefficiency =158.50, p =0.009) and ECF ratio (β coefficiency =-0.127, p =0.004). In patients with ISL stage 3 and whole arm lymphedema measured by ultrasonography, the correlation were significant among ILD, ECF ratio, presence of lymph node (LN) and dermal back flow and rSEG. However, there are six different discrepancy patterns among studies in patients with ISL stage 0 to 2; 1) euvolemic, localized tissue change, presence of LN, 2) euvolemic, localized tissue change, absence of LN, 3) hypervolemic, localized tissue change, presence of LN, 4) hypervolemic, localized tissue change, absence of LN, 5) euvolemic, general tissue change, presence of LN, 6) euvolemic, general tissue change, absence of LN (figure).
Conclusion: This study presents a descriptive review of the anatomical and physiologic imaging studies of the lymphatic system in breast cancer-related lymphedema and attempts to answer the questions of why some people develop lymphoedema after cancer and some do not, and what causes the variability in lymphoedema status. Interpretation of discrepancy patterns could predict the outcome of intensive treatment or risk of lymphedema progression.
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