The influence of patient position on ultrasound examination of the sciatic nerve in the popliteal fossa: A cross-sectional study.

Introduction/Purpose: Ultrasound-guided popliteal fossa sciatic nerve (PFSN) blocks are performed with patients in the supine, lateral or prone position. No known studies compare the quality of images obtained from each approach. This study examines the quality of supine and prone PFSN ultrasound images. Methods: Thirty-eight adult volunteers were sorted into two groups. Five regional anaesthesiologists performed ultrasound examinations of the PFSN on volunteers in supine and prone positions. Popliteal fossa sciatic nerve image quality was analysed with grayscale techniques and peer evaluation. Popliteal fossa sciatic nerve depth, distance from the popliteal crease and time until optimal imaging were recorded. Results: The grayscale ratio of the PFSN vs. the background was 1.83 (supine) and 1.75 (prone) (P = 0.034). Similarly, the grayscale ratio of the PFSN vs. the immediately adjacent area was 1.65 (supine) and 1.55 (prone) (P = 0.004). Mean depth of the PFSN was 1.6 cm (supine) and 1.7 cm (prone) (P = 0.009). Average distance from the popliteal crease to the PFSN was 5.9 cm (supine) and 6.6 cm (prone) (P = 0.02). Mean time to acquire optimal imaging was 36 s (supine) and 47 s (prone) (P = 0.002). Observers preferred supine positioning 53.8%, prone positioning 22.5% and no preference 23.7% of the time. Observers with strong preferences preferred supine imaging in 70.9% of cases. Conclusions: Supine ultrasound examination offered quicker identification of the PFSN, in a more superficial location, closer to the popliteal crease and with enhanced contrast to surrounding tissue, correlating with observer preferences for supine positioning. These results may influence ultrasound-guided PFSN block success rates, especially in difficult-to-image patients.

Acoustic sensor versus electrocardiographically derived respiratory rate in unstable trauma patients.

Respiratory rate (RR) is important in many patient care settings; however, direct observation of RR is cumbersome and often inaccurate, and electrocardiogram-derived RR (RRECG) is unreliable. We asked how data derived from the first 15 min of RR recording after trauma center admission using a novel acoustic sensor (RRa) would compare to RRECG and to end-tidal carbon dioxide-based RR ([Formula: see text]) from intubated patients, the "gold standard" in predicting life-saving interventions in unstable trauma patients. In a convenience sample subset of trauma patients admitted to our Level 1 trauma center, enrolled in the ONPOINT study, and monitored with RRECG, some of whom also had [Formula: see text] data, we collected RRa using an adhesive sensor with an integrated acoustic transducer (Masimo RRa™). Using Bland-Altman analysis of area under the receiver operating characteristic (AUROC) curves, we compared the first 15 min of continuous RRa and RRECG to [Formula: see text] and assessed the performance of these three parameters compared to the Revised Trauma Score (RTS) in predicting blood transfusion 3, 6, and 12 h after admission. Of the 1200 patients enrolled in ONPOINT from December 2011 to May 2013, 1191 had RRECG data recorded in the first 15 min, 358 had acoustic monitoring, and 14 of the latter also had [Formula: see text]. The three groups did not differ demographically or in mechanism of injury. RRa showed less bias (0.8 vs. 6.9) and better agreement than RRECG when compared to [Formula: see text]. At [Formula: see text] 10-29 breaths per minute, RRa was more likely to be the same as [Formula: see text] and assign the same RTS. In predicting transfusion, features derived from RRa and RRECG gave AUROCs 0.59-0.66 but with true positive rate 0.70-0.89. RRa monitoring is a non-invasive option to glean valid RR data to assist clinical decision making and could contribute to prediction models in non-intubated unstable trauma patients.

The adaptor protein insulin receptor substrate 2 inhibits alternative macrophage activation and allergic lung inflammation.

Insulin receptor substrate 2 (IRS2) is an adaptor protein that becomes tyrosine-phosphorylated in response to the cytokines interleukin-4 (IL-4) and IL-13, which results in activation of the phosphoinositide 3-kinase (PI3K)-Akt pathway. IL-4 and IL-13 contribute to allergic lung inflammation. To examine the role of IRS2 in allergic disease, we evaluated the responses of IRS2-deficient (IRS2(-/-)) mice. Unexpectedly, loss of IRS2 resulted in a substantial increase in the expression of a subset of genes associated with the generation of alternatively activated macrophages (AAMs) in response to IL-4 or IL-13 in vitro. AAMs secrete factors that enhance allergic responses and promote airway remodeling. Moreover, compared to IRS2(+/+) mice, IRS2(+/-) and IRS2(-/-) mice developed enhanced pulmonary inflammation, accumulated eosinophils and AAMs, and exhibited airway and vascular remodeling upon allergen stimulation, responses that partially depended on macrophage-intrinsic IRS2 signaling. Both in unstimulated and IL-4-stimulated macrophages, lack of IRS2 enhanced phosphorylation of Akt and ribosomal S6 protein. Thus, we identified a critical inhibitory loop downstream of IRS2, demonstrating an unanticipated and previously unrecognized role for IRS2 in suppressing allergic lung inflammation and remodeling.

STAT6 controls the number of regulatory T cells in vivo, thereby regulating allergic lung inflammation.

STAT6 plays a central role in IL-4-mediated allergic responses. Several studies indicate that regulatory T cells (Tregs) can be modulated by IL-4 in vitro. We previously showed that STAT6(-/-) mice are highly resistant to allergic lung inflammation even when wild-type Th2 effectors were provided and that they have increased numbers of Tregs. However, the role of STAT6 in modulating Tregs in vivo during allergic lung inflammation has not been thoroughly investigated. To examine Treg and STAT6 interaction during allergic inflammation, STAT6(-/-), STAT6xRAG2(-/-), and RAG2(-/-) mice were subjected to OVA sensitization and challenge following adoptive transfer of OVA-specific, wild-type Th2 effectors with or without prior Treg depletion/inactivation, using anti-CD25 (PC61). As expected, STAT6(-/-) mice were highly resistant to airway inflammation and remodeling. In contrast, allergic lung inflammation was partially restored in STAT6(-/-) mice treated with PC61 to levels observed in STAT6xRAG2(-/-) mice. In some cases, STAT6xRAG2(-/-) mice were also given natural Tregs along with Th2 effectors. Adoptive transfer of natural Tregs caused a substantial reduction in bronchoalveolar lavage eosinophil composition and suppressed airway remodeling and T cell migration into the lung in STAT6xRAG2(-/-) mice to levels comparable to those in STAT6(-/-) mice. These results demonstrate the STAT6-dependent suppression of Tregs in vivo to promote allergic airway inflammation.

Regulation of the T helper cell type 2 (Th2)/T regulatory cell (Treg) balance by IL-4 and STAT6.

During the development of immune responses to pathogens, self-antigens, or environmental allergens, naive CD4(+) T cells differentiate into subsets of effector cells including Th1, Th2, and Th17 cells. The differentiation into these subsets is controlled by specific transcription factors. The activity of these effector cells is limited by nTregs and iTregs, whose differentiation and maintenance are dependent on the transcription factor Foxp3. The regulation of autoimmune diseases mediated by Th1 and Th17 cells by Tregs has been studied and reviewed extensively. However, much less has been presented about the interplay between Tregs and Th2 cells and their contribution to allergic disease. In this perspective, we discuss the regulation of Th2 cells by Tregs and vice versa, focusing on the interplay between the IL-4-activated STAT6/GATA3 pathway and Foxp3.