Abstract P1-01-15: Relationship amongst sentinel lymph node pressure, volume, and breast cancer tumor size
Authors: Krasnick BA , Arbabi CN , Nathanson DS , Chitale DA 
Published: August 2014

Abstract
Background:
Angiogenesis in growing breast cancers (BCs) leads to leaky vessels with resultant increased interstitial fluid volume, pressure, and enhanced lymphatic flow to axillary sentinel lymph nodes (SLNs). As the BC grows the intra-tumoral pressure increases. SLNs are often firm and enlarged because of reactive sinusoidal hyperplasia, growth of metastases, and stromal responses to cytokines and fluid flow. We hypothesized that intranodal pressure (INP) of the SLN would increase with increasing primary BC tumor and SLN size.
Methods:
Axillary SLNs were identified intra-operatively using standard blue dye and radioactive techniques. The stained lymph node was visually detected and confirmation was made with a gamma probe. Pressure in the SLN was measured in vivo using a noncoring needle and recording device in 278 patients. A zero mmHg reading was obtained in the air adjacent to the node, and the INP was recorded in the SLN. The axillary SLNs along with the primary BC were excised and examined using standard pathological techniques. The size of the primary tumor (maximum dimension in cm) was recorded for each patient, along with the SLN volume = (4/3)(π)(length x width x thickness), and compared to the INP. Spearman's correlation coefficients were used to look at relationships between variables. We looked for significant relationships between variables while controlling for SLN metastasis size using multiple regression modeling. Statistical significance was set at p≤0.05.
Results:
INP from tumor-containing SLNs was 21.39±12.83 mmHg (N = 62), and 9.25±6.33 mmHg (N = 216) for those with no SLN metastasis (p&lt;0.0001). SLN metastasis size increased significantly with increasing tumor size (p&lt;0.0001). Increasing INP significantly correlated with increasing SLN volume (p = 0.0030, R = 0.1776), tumor size (p&lt;0.0001, R = 0.2603), and SLN metastasis size (p&lt;0.0001, R = 0.4633). Increasing tumor size did not significantly correlate with SLN volume (p = 0.3510, R = -0.0561). Volume of the SLN did not significantly differ between nodes with and without metastases (p = 0.2462). When controlling for the SLN metastasis size, the relationship between increasing volume of the SLN and INP remained significant (p = 0.0309), while the relationship between increasing tumor size and INP was no longer significant (p = 0.0910).
Conclusion:
The INP of BC SLNs increased with increased tumor metastasis size and also with the volume of the SLN. Because the SLN volume did not differ when metastasis was present or not, and because the INP was elevated when there was metastasis present, it is likely that pre-metastatic angiogenesis and lymphangiogenesis, seen pathologically as sinusoidal hyperplasia, may not be enough to cause the interstitial fluid pressure to rise. Our data suggests that increased INP requires tumor cells in the SLN or mechanical factors due to tumor emboli to create conditions sufficient to increase the measurable pressure significantly. Proof of this postulate requires careful quantitative evaluation of other components in the metastatic SLN, such as stromal and lymphoid hyperplasia.
Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P1-01-15.