Trends in Peripheral Nerve Block Usage in Mastectomy and Lumpectomy: Analysis of a National Database From 2010 to 2018.

BACKGROUND: Compared to general anesthesia, regional anesthesia confers several benefits including improved pain control and decreased postoperative opioid consumption. While the benefits of peripheral nerve blocks (PNB) have been well studied, there are little epidemiological data on PNB usage in mastectomy and lumpectomy procedures. The primary objective of our study was to assess national trends of the annual proportion of PNB use in breast surgery from 2010 to 2018. We also identified factors associated with PNB use for breast surgery. METHODS: We identified lumpectomy and mastectomy surgical cases with and without PNB between 2010 and 2018 using the Anesthesia Quality Institute National Anesthesia Clinical Outcomes Registry (AQI NACOR). We modeled the nonlinear association between year of procedure and PNB use with segmented mixed-effects logistic regression clustered on facility identifier. The association between PNB use and year of procedure, age, sex, American Society of Anesthesiologists physical status (ASA PS), facility type, facility region, weekday, and tissue expander use was also modeled using mixed-effects logistic regression. RESULTS: Of the 189,854 surgical cases from 2010 to 2018 that met criteria, 86.2% were lumpectomy cases and 13.8% were mastectomy cases. The proportion of lumpectomy cases with PNB was <0.1% in 2010 and increased each subsequent year to 1.9% in 2018 (trend P < .0001). The proportion of mastectomy cases with PNB was 0.5% in 2010 and 13% in 2018 (trend P < .0001). The year 2014 was the breakpoint selected for segmented regression. Before 2014, the odds of PNB among the mastectomy cases was not significantly different from year to year. After 2014, the odds of PNB increased by 2.24-fold each year (95% confidence interval [CI], 2.00-2.49; P < .001); interaction test for pre-2014 versus post-2014 was P < .001. Similar trends were seen in the lumpectomy cases, where after 2014, the odds of PNB increased by 2.03-fold (95% CI, 1.81-2.27; P < .001); interaction test for pre-2014 versus post-2014 was P < .001. In the mastectomy cohort, year of procedure ≥2014, female sex, facility region, and tissue expander use were associated with higher odds of PNB. For lumpectomy cases, year of procedure ≥2014 and facility region were associated with higher odds of PNB use. CONCLUSIONS: We found increased annual utilization of PNB for mastectomy and lumpectomy since 2010, although absolute prevalence is low. PNB use was associated with year of procedure for both lumpectomy and mastectomy, particularly post-2014.

Role of Kidneys in Sex Differences in Angiotensin II-Induced Hypertension.

The significance of kidneys in regulation of sodium and water balance and hemodynamics has been demonstrated both in patients and animal models. In the present study, we tested our hypothesis that kidneys play an essential role in control of sex differences in angiotensin II (Ang II)-dependent hypertension. Kidney transplantations (KTXs) were performed between male (M) and female (F) C57BL/6 mice (donor→recipient: F→F, M→M, F→M, and M→F). Radiotelemetry transmitters were implanted for measurement of mean arterial pressure during the infusion of Ang II (600 ng·kg-1·min-1). Gene expressions and inflammatory responses in the transplanted grafts were assessed. We found that same-sex-KTX mice still exhibited sex differences in Ang II-dependent hypertension (31.3±0.8 mm Hg in M→M versus 12.2±0.6 mm Hg in F→F), which were reduced between males and females when they received kidneys of the opposite sex (32.9±1 mm Hg in M→F versus 22.3±0.7 mm Hg in F→M). The sex differences in gene expressions, including AT1R (angiotensin II receptor, type 1), AT1R/AT2R, ET-1 (endothelin-1), ETA (endothelin receptor type A), NHE3 (sodium-hydrogen exchanger 3), α-ENaC (α-epithelial sodium channel), and γ-ENaC, were unaltered in same-sex KTXs and much lessened in cross-sex KTXs. In addition, the cross-sex KTXs exhibited more robust inflammatory responses reflected by higher expression of IL-6 (interleukin 6), TNFα (tumor necrosis factor α), and KC (keratinocyte-derived chemokine) than same-sex KTX. Our results indicate that kidneys play an essential role in sex differences of Ang II-dependent hypertension. KTX of male kidneys to females augmented the blood pressure response, whereas KTX of female kidneys to males attenuated the blood pressure response. The host's extrarenal systems modulate expressions of many genes and inflammatory response, which may also contribute to the sex differences in blood pressure regulation.

Enhanced hemodynamic responses to angiotensin II in diabetes are associated with increased expression and activity of AT1 receptors in the afferent arteriole.

The prevalence of hypertension is about twofold higher in diabetic than in nondiabetic subjects. Hypertension aggravates the progression of diabetic complications, especially diabetic nephropathy. However, the mechanisms for the development of hypertension in diabetes have not been elucidated. We hypothesized that enhanced constrictive responsiveness of renal afferent arterioles (Af-Art) to angiotensin II (ANG II) mediated by ANG II type 1 (AT1) receptors contributes to the development of hypertension in diabetes. In response to an acute bolus intravenous injection of ANG II, alloxan-induced diabetic mice exhibited a higher mean arterial pressure (MAP) (119.1 ± 3.8 vs. 106.2 ± 3.5 mmHg) and a lower renal blood flow (0.25 ± 0.07 vs. 0.52 ± 0.14 ml/min) compared with nondiabetic mice. In response to chronic ANG II infusion, the MAP measured with telemetry increased by 55.8 ± 6.5 mmHg in diabetic mice, but only by 32.3 ± 3.8 mmHg in nondiabetic mice. The mRNA level of AT1 receptor increased by ~10-fold in isolated Af-Art of diabetic mice compared with nondiabetic mice, whereas ANG II type 2 (AT2) receptor expression did not change. The ANG II dose-response curve of the Af-Art was significantly enhanced in diabetic mice. Moreover, the AT1 receptor antagonist, losartan, blocked the ANG II-induced vasoconstriction in both diabetic mice and nondiabetic mice. In conclusion, we found enhanced expression of the AT1 receptor and exaggerated response to ANG II of the Af-Art in diabetes, which may contribute to the increased prevalence of hypertension in diabetes.