The Role of Physician-Directed Duplex after Brachial Plexus Block in Arteriovenous Fistula Creation.

BACKGROUND: Best practice guidelines for dialysis access creation emphasize distal sites and autogenous tissue before more proximal sites and synthetic shunts. Pre-operative vein mapping is a useful modality to evaluate optimal access location; however, vein size is often underestimated secondary to patient hypovolemia, room temperature, and basal vascular tone. Supraclavicular brachial plexus blocks (BPB) are routinely performed to provide surgical anesthesia but also have known vasodilatory effects. Although many surgeons use both techniques, most do not repeat vein mapping after BPB to re-evaluate targets after block-mediated vasodilation. Therefore, we evaluated whether the role of physician-directed vein mapping after BPB resulted in more favorable access creations. METHODS: All patients who underwent primary ipsilateral access creation with physician-directed post-block duplex between 2017 and 2018 were evaluated. Vein mapping was reviewed for "theoretical access location" using the criterion of >2.5 mm vessels. Fistula preference was analogous to current indications with the following order of preference: wrist radiocephalic, forearm radiocephalic, brachiocephalic, brachiobasilic, and finally prosthetic graft. RESULTS: Forty-three patients met inclusion criteria. In total, physician-directed duplex after regional block resulted in the creation of higher preference accesses than predicted in 62.8% of patients. In 34.9% the access was at the predicted level and only 2.3% were at a lower preference. Furthermore, there were no differences in the maturation rates between accesses placed at higher preference locations than predicted compared to those at expected sites (74% vs. 79%, P = 0.38). The overall revision rate for higher preference access was 22.2% compared to 23.1% for equal/lower preference accesses. Of those accesses that failed, 83.3% of new accesses were created at the original theoretical location while 17.7% required placement of a lower preference access. CONCLUSIONS: Physician-directed ultrasound after BPB allows for identification of more preferential targets for access creation compared to pre-operative vein mapping. For access created at more preferential locations than pre-operatively predicted prior to BPB, there was no difference in maturation rates compared to those created at the theoretical vein mapping location.

Surgical Management of a Torn ACL and Bucket-Handle Meniscal Tear in the Pregnant Patient: A Case Report.

CASE: A 36-year-old, 7-month pregnant woman presented to the office with a locked knee and a displaced bucket-handle medial meniscus tear, in the setting of chronic anterior cruciate ligament (ACL) insufficiency. After thorough discussion with the patient and her husband, the obstetrician, and the anesthesiologist, the patient was treated with left knee ACL reconstruction and medial meniscus repair. CONCLUSION: With sufficient preoperative planning and coordinated multidisciplinary care among orthopaedic, anesthesiologist, and obstetric specialists, elective knee surgery can be performed safely in time-sensitive situations during pregnancy.

Acute morphine associated alterations in the subcellular location of the AMPA-GluR1 receptor subunit in dendrites of neurons in the mouse central nucleus of the amygdala: comparisons and contrasts with other glutamate receptor subunits.

Within the amygdala, AMPA receptors expressing the AMPA-GluR1 (GluR1) subunit play an important role in basal glutamate signaling as well as behaviors associated with exposure to drugs of abuse like opiates. Although the ultrastructural location of GluR1 is an important functional feature of this protein, the basal distribution of GluR1, as well as its sensitivity to acute morphine, has never been characterized in the mouse central nucleus of the amygdala (CeA). Electron microscopic immunocytochemistry employing visually distinct gold and peroxidase markers was used to explore the distribution of GluR1 and its relationship with the mu-opioid receptor (µOR) in the mouse CeA under basal conditions and after morphine. We also looked at the effect of morphine on other glutamate receptor subunits, including AMPA-GluR2 (GluR2) and NMDA-NR1 (NR1). In opiate naive animals, GluR1 and µOR were present in diverse populations of neuronal profiles, but mainly in somatodendritic structures that expressed exclusive labeling for either antigen, as well as those co-expressing both proteins. Compared to saline treated animals, mice given morphine showed significant differences in the subcellular location of GluR1 in dendrites without co-expression of µOR. Although GluR2 also showed similar changes in non-µOR expressing dendrites, contrasting effects were seen in GluR2 and µOR co-expressing profiles. These results provide the ultrastructural basis for basal interactions involving the modulation of GluR1 or µOR activity in the mouse CeA. Further, they indicate that the subcellular distribution of GluR1 is modified by acute opiates in a manner that compares, as well as contrasts, with GluR2.

Corticotropin-releasing factor in the mouse central nucleus of the amygdala: ultrastructural distribution in NMDA-NR1 receptor subunit expressing neurons as well as projection neurons to the bed nucleus of the stria terminalis.

Corticotropin-releasing factor (CRF) and glutamate are critical signaling molecules in the central nucleus of the amygdala (CeA). Central amygdala CRF, acting via the CRF type 1 receptor (CRF-R1), plays an integral role in stress responses and emotional learning, processes that are generally known to involve functional NMDA-type glutamate receptors. There is also evidence that CRF expressing CeA projection neurons to the bed nucleus of the stria terminalis (BNST) play an important role in stress related behaviors. Despite the potentially significant interactions between CRF and NMDA receptors in the CeA, the synaptic organization of these systems is largely unknown. Using dual labeling high resolution immunocytochemical electron microscopy, it was found that individual somata and dendrites displayed immunoreactivity for CRF and the NMDA-NR1 (NR1) subunit in the mouse CeA. In addition, CRF-containing axon terminals contacted postsynaptic targets in the CeA, some of which also expressed NR1. Neuronal profiles expressing the CRF type 1 receptor (CRF-R1), identified by the expression of green fluorescent protein (GFP) in bacterial artificial chromosome (BAC) transgenic mice, also contained NR1, and GFP immunoreactive terminals formed synapses with NR1 containing dendrites. Although CRF and GFP were only occasionally co-expressed in individual somata and dendritic profiles, contacts between labeled axon terminals and dendrites were frequently observed. A combination of tract tracing and immunocytochemistry revealed that a population of CeA CRF neurons projected to the BNST. It was also found that CRF, or GFP expressing terminals directly contacted CeA-BNST projection neurons. These results indicate that the NMDA receptor is positioned for the postsynaptic regulation of CRF expressing CeA neurons and the modulation of signals conveyed by CRF inputs. Interactions between CRF and NMDA receptor mediated signaling in CeA neurons, including those projecting to the BNST, may provide the synaptic basis for integrating the experience of stress and relevant environmental stimuli with behaviors that may be of particular relevance to stress-related learning and the emergence of psychiatric disorders, including drug addiction.

The NMDA-NR1 receptor subunit and the mu-opioid receptor are expressed in somatodendritic compartments of central nucleus of the amygdala neurons projecting to the bed nucleus of the stria terminalis.

The pathway between the central nucleus of the amygdala (CeA) and the bed nucleus of the stria terminalis (BNST) is emerging as a critical mediator of stress-related affective processes. Evidence also indicates that exposure to drugs of abuse, like opioids, is associated with NMDA-type glutamate receptor-dependent plasticity in the CeA and BNST. However, there is little evidence that NMDA receptors are expressed in CeA neurons projecting to the BNST, or are required for opioid-induced BNST neural activation. Immunoelectron microscopy, tract tracing, and conditional gene deletion technology were used to investigate the synaptic organization of the NMDA receptor and the mu-opioid receptor (µOR) in the CeA-BNST pathway. By dual labeling electron microscopy, numerous CeA-BNST projection neurons expressed the NMDA-NR1 receptor subunit (NR1) or µOR. By triple labeling, it was also found that NR1 and µOR were co-expressed in some CeA-BNST projection neurons. Despite being colocalized in somato-dendritic compartments of CeA neurons, NR1 and µOR were rarely expressed in their axonal terminations in the BNST. Deleting the NR1 gene in CeA neurons resulted in a reduction of morphine-induced Fos protein labeling in the ventral BNST. In summary, NR1 and µOR are coexpressed in somatodendritic sites of CeA neurons, including those projecting to the BNST. In addition, expression of the NR1 gene in CeA neurons is required for morphine-induced BNST neural activation. Thus, postsynaptic NMDA receptors and µORs are positioned for the co-modulation of CeA projection neurons to the BNST, which may provide a synaptic substrate for stress-induced emotional processes critically involved in opioid addictive behaviors.

Ultrastructural relationship between the AMPA-GluR2 receptor subunit and the mu-opioid receptor in the mouse central nucleus of the amygdala.

Activation of GluR2-expressing non-calcium-permeable AMPA-type glutamate receptors in the central nucleus of the amygdala (CeA) may play an important role in integrating emotion and memory with goal-directed behaviors involved in opioid addiction. The location of non-calcium-permeable AMPA receptors within distinct neuronal compartments (i.e., soma, dendrite, or axon) is an important functional feature of these proteins; however, their ultrastructural location and subcellular relationship with mu-opioid receptors (µOR) in the CeA are unknown. Immunocytochemical electron microscopy was used to characterize the ultrastructural distribution of GluR2 and its association with µOR in the mouse CeA. A single-labeling analysis of GluR2 distribution employing immunoperoxidase or immunogold markers revealed that this protein was frequently affiliated with intracellular vesicular organelles, as well as the plasma membrane of CeA neuronal profiles. Among all GluR2-labeled neuronal structures, over 85% were dendrites or somata. Unlabeled axon terminals frequently formed asymmetric excitatory-type synaptic junctions with GluR2-labeled dendritic profiles. Dual-labeling immunocytochemical analysis showed that GluR2 and µOR were co-localized in neuronal compartments. Among all dual-labeled structures, approximately 80% were dendritic. Synaptic inputs to these dual-labeled dendrites were frequently from unlabeled axon terminals forming asymmetric excitatory-type synapses. The presence of GluR2 in dendritic profiles receiving asymmetric synapses suggests that activation of the non-calcium-permeable AMPA receptor plays a role in the postsynaptic modulation of excitatory signaling involving CeA neuronal circuits that coordinate sensory, affective, and behavioral processes involved in drug addiction. Given the critical role of non-calcium-permeable AMPA receptor function in neural and behavioral adaptability, their dendritic association with µOR in CeA dendrites provides a neuronal substrate for opioid-mediated plasticity.