Changes in analgesic strategies for lobectomy from 2009 to 2018.

Objective: To evaluate trends in the use of epidural analgesia and nonopioid and opioid analgesics for patients undergoing lobectomy from 2009 to 2018. Methods: We queried the Premier database for adult patients undergoing open, video-assisted, and robotic-assisted lobectomy from 2009 to 2018. The outcome of interest was changes in the receipt of epidural analgesia and nonopioid and opioid analgesics as measured by charges on the day of surgery. We also evaluated postoperative daily opioid use. We used multivariable logistic and linear regression models to examine the association between the utilization of each analgesic modality and year. Results: We identified 86,308 patients undergoing lobectomy from 2009 to 2018 within the Premier database: 35,818 (41.5%) patients had open lobectomy, 35,951 (41.7%) patients had video-assisted lobectomy, and 14,539 (16.8%) patients had robotic-assisted lobectomy. For all 3 surgical cohorts, epidural analgesia use decreased, and nonopioid analgesics use increased over time, except for intravenous nonsteroidal anti-inflammatory drugs. Use of patient-controlled analgesia decreased, while opioid consumption on the day of surgery increased and postoperative opioid consumption did not decrease over time. Conclusions: In this large sample of patients undergoing lobectomy, utilization of epidural analgesia declined and use of nonopioid analgesics increased. Despite these changes, opioid consumption on day of surgery increased, and there was no significant reduction in postoperative opioid consumption. Further research is warranted to examine the association of these changes with patient outcomes.

Report from a quality assurance program on patients undergoing the MILD procedure.

OBJECTIVES: To characterize trends in pain and functional outcomes and identify risk factors in patients with lumbar spinal stenosis (LSS) and neurogenic claudication undergoing the "Minimally Invasive Lumbar Decompression" (MILD) procedure. DESIGN: Retrospective observational cohort study. SETTING: Academic multidisciplinary pain center at Stony Brook Medicine. SUBJECTS: Patients undergoing the MILD procedure from October 2010 to November 2012. METHODS: De-identified perioperative, pain and function related data for 50 patients undergoing MILD were extracted from the Center for Pain Management's quality assessment database. Data included numerical rating scale (NRS), symptom severity and physical function (Zurich Claudication Questionnaire), functional status (Oswestry Disability Index [ODI]), pain interference scores (National Institutes of Health Patient-Reported Outcomes Measurement Information System [PROMIS]), and patients' self-reported low back and lower extremity pain distribution. RESULTS: No MILD patient incurred procedure-related complications. Average NRS scores decreased postoperatively and 64.3% of patients reported less pain at 3 months. Clinically meaningful functional ODI improvements of at least 20% from baseline were present in 25% of the patients at 6 months. Preliminary analysis of changes in PROMIS scores at 3 months revealed that pre-MILD "severe" lumbar canal stenosis may be associated with high risk of "no improvement." No such impact was observed for NRS or ODI outcomes. CONCLUSION: Overall, pain is reduced and functional status improved in LSS patients following the MILD procedure at 3 and 6 months. Given the small sample size, it is not yet possible to identify patient subgroups at risk for "no improvement." Continued follow-up of longer-term outcomes appears warranted to develop evidence-based patient selection criteria.

Case report: Perioperative pacemaker-mediated tachycardia in the patient with a dual chamber implantable cardioverter-defibrillator.

Patients with cardiac implantable electronic devices are at additional risk for arrhythmias while undergoing surgical procedures. In this case report, we present a patient with a dual chamber implantable cardioverter-defibrillator who developed intraoperative pacemaker-mediated tachycardia causing significant hemodynamic instability. Management of this arrhythmia can be particularly challenging, because standard application of a magnet does not affect the pacing functions of an implantable cardioverter-defibrillator. Awareness by the anesthesiologist and timely coordination with the cardiac electrophysiology team helped to optimize care for this patient.

Coordinate effects of human immunodeficiency virus type 1 protein Tat and cellular protein Puralpha on DNA replication initiated at the JC virus origin.

JC virus (JCV) causes progressive multifocal leukoencephalopathy, a demyelinating disease in brains of individuals with AIDS. Previous work has shown that the Tat protein, encoded by human immunodeficiency virus type 1 (HIV-1), can interact with cellular protein Puralpha to enhance both TAR-dependent HIV-1 transcription and JCV late gene transcription. Tat has been shown to activate JCV transcription through interaction with Puralpha, which binds to promoter sequence elements near the JCV origin of replication. DNA footprinting has shown that Puralpha and large T-antigen cooperatively interact at several binding sites in the origin and transcriptional control region. Overexpression of Puralpha inhibits replication initiated at the JCV origin by T-antigen. In transfected glial cells Tat reversed this inhibition and enhanced DNA replication. In an in vitro replication system maximal activation by Tat, more than sixfold the levels achieved with T-antigen alone, was achieved in the presence of Puralpha. Effects of mutant Tat proteins on both activation of replication and binding to Puralpha have revealed that Cys22 exerts a conformational effect that affects both activities. The origin of an archetypal strain of JCV was less susceptible to activation of replication by Tat relative to the rearranged Mad-1 strain. These results have revealed a previously undocumented role for Tat in DNA replication and have indicated a regulatory role for JCV origin auxiliary sequences in replication and activation by Tat.