Provision of postintubation sedation and analgesia is critical in emergency management of mechanically ventilated patients. Pain and sedation should be monitored using a validated scoring system, and medications titrated to a target sedation level, which should usually be light. Usually, fentanyl is the first-line analgesic and propofol is the first-line sedative. Dexmedetomidine and ketamine may be helpful in select populations, but further research is needed to define their role in the emergency department. Benzodiazepines should generally be avoided. Physicians should plan for postintubation sedation and analgesia in advance and consider using succinylcholine for intubation to avoid awareness with paralysis.

Glioblastoma multiforme (GBM) is the most prevalent and aggressive primary brain tumor, with a median survival of approximately 15 months despite current multimodal therapies. Recent clinical observations have suggested that the intravenous anesthetic propofol may be used to examine whether anesthetic agents can affect glioblastoma behavior. Several retrospective studies reported that, in surgical settings, propofol-based total intravenous anesthesia (TIVA) is associated with reduced operative time, faster recovery, lower intraoperative blood loss, and decreased postoperative complications such as seizures and cerebral edema, benefits particularly evident in patients with low Karnofsky Performance Scores. However, current clinical evidence remains limited, and the reported effects on survival and recurrence are still inconsistent. Preclinical studies showed that propofol's antitumor potential is mediated through modulation of the PI3K/AKT-Wnt-miRNA axis, reduction of oxidative stress, regulation of immune checkpoint molecules, and restoration of temozolomide sensitivity in resistant cells. However, some reports indicate that propofol may also induce stem-like features via GABA-A receptor activation, underscoring its complex and context-dependent nature. This narrative review summarizes the current molecular and clinical evidence about propofol in GBM. Available laboratory and retrospective clinical studies indicate possible antitumor effects, but the present evidence does not support definitive clinical conclusions. Large prospective and multicenter studies are still needed to clarify the clinical role of propofol in patients with GBM.

This study aimed to investigate whether propofol-remifentanil anesthesia offers superior perioperative outcomes compared to propofol-fentanyl in pancreatic cancer surgery patients, with a focus on its effects on apoptotic molecules, plasma CXCL10/CXCL13 levels, and postoperative recovery. A total of 150 pancreatic cancer patients were divided into 2 cohorts receiving either propofol-fentanyl (control group, n=75) or propofol-remifentanil (study group, n=75) anesthesia. We measured perioperative hemodynamics (cardiac index [CI], mean arterial pressure [MAP], heart rate [HR]), T-cell subsets, postoperative recovery indices (eye-opening time, extubation time, spontaneous respiration recovery time), sedation and analgesia levels (via Ramsay sedation score [RSS] and visual analog scale [VAS]), plasma CXCL10/CXCL13 levels, and apoptosis-related proteins (Survivin, Bax, Caspase-4, Bcl-2) using enzyme-linked immunosorbent assays (ELISAs). Adverse reactions were also recorded. The study group exhibited significant advantages in hemodynamic stability and immune preservation. Despite similar baseline cardiovascular parameters, the remifentanil group maintained better CI, MAP, and HR stability during and after surgery. Flow cytometry analysis revealed better preservation of T-cell immunity (CD4+, CD3+, CD4+/CD8+ T cells) at 24 hours post-surgery. The intervention group also demonstrated accelerated postoperative recovery with significantly reduced emergence times (eye-opening, extubation, spontaneous respiration). Notably, the study group had more favorable inflammatory profiles (lower CXCL10/CXCL13 levels) and enhanced apoptotic responses (modulated Bax, Caspase-4, Survivin, and Bcl-2 expression). Clinical outcomes were superior in the study group, with significantly fewer adverse events (2 vs. 9 patients). Propofol-remifentanil anesthesia provides effective sedation and analgesia in pancreatic cancer surgery, modulates key biological pathways related to apoptosis and inflammation, and improves postoperative recovery. These findings suggest that the choice of anesthesia regimen may have significant implications for perioperative outcomes and potentially long-term prognosis in pancreatic cancer patients. Future research should further explore the underlying mechanisms and long-term clinical benefits of this anesthesia strategy.

Postoperative gastrointestinal dysfunction (POGD) remains an important barrier to recovery after abdominal and non-abdominal surgery. This critical narrative review evaluates whether dexmedetomidine improves postoperative gastrointestinal recovery through an independent direct prokinetic action or predominantly through opioid-sparing and other indirect recovery pathways. Positive trials and meta-analyses report earlier flatus, defecation, or oral intake in selected settings, but most also permit simultaneous reductions in opioid exposure, pain, postoperative nausea and vomiting (PONV), inflammatory biomarkers, or sympathetic stress. These co-occurring effects limit causal attribution. We therefore propose a context-dependent dual-pathway model in which an opioid-sparing indirect pathway and a biologically plausible non-opioid pathway contribute with weights that vary according to baseline opioid burden, enhanced recovery after surgery (ERAS) maturity, dose, timing, and inflammatory phenotype. The available evidence is most consistent with, but does not prove, an opioid-sparing-dominant explanation; independent enteric effects remain clinically unisolated. Counter-evidence from healthy volunteers, isolated intestine, and sepsis models also argues against a universal prokinetic property. Clinically, dexmedetomidine should be positioned as a context-dependent multimodal adjunct rather than a stand-alone prokinetic therapy. Opioid-standardized trials with validated gastrointestinal endpoints and prespecified mediation analyses are needed to distinguish the two pathways.