RESUMO
PURPOSE OF REVIEW: The purpose of this review is to summarize the recent literature regarding regional anesthesia (RA) techniques and outcomes for total hip arthroplasty (THA) in the face of changing surgical techniques and perioperative considerations. RECENT FINDINGS: Based on large meta-analyses, peripheral nerve blocks are indicated for THA. Each block has its own risks and benefits and data for outcomes for particular techniques are limited. New surgical techniques, improved use of multimodal analgesia, and improved ultrasound guided regional anesthetics lead to better pain control for patients undergoing THA with less associated risks. Block selection continues to be influenced by provider comfort, surgical approach, patient anatomy, and postoperative goals. Head-to-head studies of particular nerve blocks are warranted.
RESUMO
The incidence of hip fractures has continued to increase as life expectancy increases. Hip fracture is one of the leading causes of increased morbidity and mortality in the geriatric population. Early surgical treatment (<48 h) is often recommended to reduce morbidity/mortality. In addition, adequate pain management is crucial to optimize functional recovery and early mobilization. Pain management often consists of multimodal therapy which includes non-opioids, opioids, and regional anesthesia techniques. In this review, we describe the anatomical innervation of the hip joint and summarize the commonly used peripheral nerve blocks to provide pain relief for hip fractures. We also outline literature evidence that shows each block's efficacy in providing adequate pain relief. The recent discovery of a nerve block that may provide adequate sensory blockade of the posterior capsule of the hip is also described. Finally, we report a surgeon's perspective on nerve blocks for hip fractures.
RESUMO
In melanoma, therapies with inhibitors to oncogenic BRAFV600E are highly effective but responses are often short-lived due to the emergence of drug-resistant tumor subpopulations. We describe here a mechanism of acquired drug resistance through the tumor microenvironment, which is mediated by human tumor-associated B cells. Human melanoma cells constitutively produce the growth factor FGF-2, which activates tumor-infiltrating B cells to produce the growth factor IGF-1. B-cell-derived IGF-1 is critical for resistance of melanomas to BRAF and MEK inhibitors due to emergence of heterogeneous subpopulations and activation of FGFR-3. Consistently, resistance of melanomas to BRAF and/or MEK inhibitors is associated with increased CD20 and IGF-1 transcript levels in tumors and IGF-1 expression in tumor-associated B cells. Furthermore, first clinical data from a pilot trial in therapy-resistant metastatic melanoma patients show anti-tumor activity through B-cell depletion by anti-CD20 antibody. Our findings establish a mechanism of acquired therapy resistance through tumor-associated B cells with important clinical implications.Resistance to BRAFV600E inhibitors often occurs in melanoma patients. Here, the authors describe a potential mechanism of acquired drug resistance mediated by tumor-associated B cells-derived IGF-1.
