Anesthesia and analgesia最新文献

Background: The impact of pain intensity on the progression trajectories of cardiometabolic multimorbidity (CMM) is not well understood. We attempted to dissect the relationship of short-term pain (STP) and chronic pain intensity with the temporal progression of CMM.

Methods: We conducted a prospective cohort study based on the UK Biobank participants. Incident cases of cardiometabolic diseases (CMDs) were identified based on self-reported information and multiple health-related records in the UK Biobank. CMM was defined as the occurrence of at least 2 CMDs, including heart failure (HF), ischemic heart disease (IHD), stroke, and type 2 diabetes (T2D). The pain intensity was categorized into 5 levels based on pain duration and the number of sites involved, including chronic widespread pain (CWSP), chronic multilocation pain (CMLP), chronic single-location pain (CSLP), STP, and free-of-pain (FOP). Multistate models were used to assess the impact of pain intensity on the CMM trajectories from enrollment to initial cardiometabolic disease (ICMD), subsequently to CMM, and ultimately to death.

Results: A total of 429,145 participants were included. Over the course of a 12.8-year median follow-up, 13.1% (56,137/429,145) developed ICMD, 19.6% (10,979/56,137) further progressed to CMM, and a total of 5.3% (22,775/429,145) died. Compared with FOP, CMLP (hazard ratio [HR], 1.11; 95% confidence interval [CI], 1.06-1.17) and CWSP (HR, 1.26; 95% CI, 1.13-1.42) elevated the risk of transitioning from ICMD to CMM. STP (HR, 0.89; 95% CI, 0.82-0.96), CSLP (HR, 0.88; 95% CI, 0.82-0.95), and CMLP (HR, 0.87; 95% CI, 0.81-0.93) lowered the risk of transition from ICMD to mortality, and STP also reduced the risk of transition from enrollment to mortality (HR, 0.94; 95% CI, 0.89-0.98). The results of disease-specific transitions revealed that the influence of pain intensity varied across transitional stages. Specifically, CMLP and CWSP heightened the risk of conversion from T2D or IHD to CMM, whereas only CWSP substantially elevated the transition risk from HF to CMM.

Conclusions: Our results highlighted reductions in chronic pain may mitigate both the onset and progression of CMM, potentially having an important impact on future revisions of cardiometabolic and pain-related guidelines.

Background: Norepinephrine has recently been suggested to be as effective as phenylephrine for the prevention of hypotension after spinal anesthesia for cesarean delivery. Moreover, compared to phenylephrine, norepinephrine may be superior in maintaining heart rate (HR) and consequently, cardiac output (CO). A recent study demonstrated that norepinephrine given as a single intravenous bolus is approximately 13 times more potent than phenylephrine. However, it is uncertain whether this finding can be applied when these vasopressors are administered as infusions. Therefore, the optimum infusion rate of norepinephrine remains unknown. We aimed to determine the median effective dose (ED50; defined as the rate of vasopressor infusion required to prevent spinal hypotension in 50% of subjects) of both drugs needed to maintain maternal systolic blood pressure within 20% of the baseline after spinal anesthesia for cesarean delivery and to derive the relative potency ratio.

Methods: Sixty healthy patients undergoing elective cesarean delivery with standardized spinal anesthesia were randomized into 2 groups. The first patient in group 1 received phenylephrine 1200 µg in normal saline 0.9% w/v 60 mL at 60 mL/h infusion rate (20 µg.min-1). The first patient in group 2 received norepinephrine 96 µg in normal saline 0.9% w/v 60 mL at 60 mL/h infusion rate (1.6 µg.min-1). Using up-down sequential allocation technique, the vasopressor dose for every subsequent patient was determined by the response in the previous patient. If effective, the next patient received a dose reduced by 150 µg of phenylephrine (2.5 µg.min-1) or 12 µg (0.2 µg.min-1) of norepinephrine. If ineffective, the dose for the next patient was increased by the same amount. The ED50s were determined according to the Dixon-Massey formula. Stroke volume (SV), HR, and CO were also measured.

Results: The ED50 was 12.7 µg.min-1 (95% CI, 10.5-14.9) for phenylephrine and 1.01 µg.min-1 (95% CI, 0.84-1.18) for norepinephrine, giving a potency ratio of 12.6 (95% CI, 9.92-15.9). HR, SV, and CO did not differ between the groups.

Conclusions: Norepinephrine is more potent than phenylephrine by a factor of approximately 13 when administered as infusion for equivalent maternal blood pressure control. Based on these findings, we recommend a variable rate prophylactic infusion of norepinephrine to be initiated at 1.9 to 3.8 µg.min-1 for the management of hypotension during cesarean delivery under spinal anesthesia.

Background: The clinical significance and incidence of phosphate abnormalities in cardiac surgery have not been investigated extensively. We hypothesize that phosphate abnormalities are associated with a longer time to tracheal extubation.

Methods: This was a single-center, retrospective cohort study in patients who underwent nontransplant cardiac surgery with cardiopulmonary bypass between August 2009 and December 2020. Serum phosphate levels were measured within 6 hours of arrival to the intensive care unit (ICU). Select clinical outcomes were extracted from an intramural database: time to tracheal extubation, hospital length of stay, and in-hospital mortality. The lactate level within 6 hours of arrival to the ICU was extracted as well.

Results: A total of 2659 patients were included. There were 502 (18.9%) patients who were found to be hypophosphatemic (phosphate <2.5 mg/dL), 1905 (71.6%) had normal phosphate levels (phosphate 2.5-4.5 mg/dL), and 252 (9.5%) were hyperphosphatemic (phosphate >4.5 mg/dL). Hyperphosphatemia was associated with 26% longer time to tracheal extubation (incident rate ratio, 1.26, 95% confidence interval [CI], 10%, 44%, P = .001), 37% longer hospital length of stay (acceleration factor = 0.63, 95% CI, -43% to -30%); P < .001), and increased in-hospital mortality (odds ratio, 4.0; 95% CI, 2.3-7.1; P < .001) when compared to patients with normal phosphate levels. These associations were not found for hypophosphatemia.

Conclusions: Hyperphosphatemia in the immediate postoperative period after cardiac surgery is associated with adverse clinical outcomes. Future studies will need to investigate if actively correcting the phosphate level has an impact on clinical outcomes.

After an induction dose of rocuronium, sugammadex in a dose of 16 mg.kg-1 has been shown to provide early reversal of the neuromuscular blockade. However, the use of sugammadex to rescue a "cannot intubate, cannot ventilate" (CICV) scenario remains controversial. The aim of this systematic review was to discuss case reports describing the use of sugammadex as a rescue reversal in CICV scenarios and analyze the influencing factors potentially shaping the outcome of such reversal. The study has been registered on International Prospective Register of Systematic Reviews (PROSPERO) (CRD42024514255). We conducted a systematic review of the literature using PubMed, Medline, and Embase. Records were included if they were case reports or case series published in peer-reviewed journals, describing the administration of sugammadex as a rescue reversal in CICV scenarios, and including clinical outcomes and details of the management. Sources were last searched on November 30, 2023. The articles selected were initially screened based on their titles and abstracts, and then complete articles were examined to determine their eligibility and compliance with the inclusion criteria. Two independent authors evaluated the quality of the individual studies using the Joanna Briggs Institute Critical Appraisal Checklist for Case Reports. Eight articles were included in our review. In all patients, CICV scenarios were declared minutes following induction. In 6/8 cases (75%), adequate spontaneous ventilation was restored after the administration of sugammadex. In the remaining 2 cases, sugammadex administration resulted in an obstructed pattern of breathing, and surgical airway was the successful rescue technique. There was wide variability in the sugammadex dose with a median (range) of 14 (5-16) mg.kg-1 and median timing (range) from rocuronium administration of 6 (2-10) minutes. This case-report-based review is susceptible to reporting bias and may not encompass all pertinent data and adverse events. Also, cases with both favorable and unfavorable outcomes may have not been published, and the heterogeneity of cases limits the ability to draw definitive conclusions. In summary, although these case reports suggest that sugammadex might be helpful in CICV scenarios, further research is needed to confirm its effectiveness. However, due to the rare occurrence of CICV events, gathering sufficient data for conclusive evidence may be challenging.

Tracheobronchomalacia refers to an abnormally excessive collapse of the trachea and/or bronchi during exhalation. In the pediatric population, tracheobronchomalacia is increasingly recognized as a cause of morbidity and mortality. Historically, options for medical management and surgical intervention were limited, and patient outcomes were poor. Over the last decade, select US pediatric institutions have devoted significant resources to the establishment of dedicated surgery and anesthesia teams and the development of novel techniques for the successful identification, assessment, and surgical correction of tracheobronchomalacia in a highly complex subset of the pediatric population. The close communication, collaboration, and evolution of anesthesia techniques to meet the unique requirements of new surgical procedures have greatly improved patient safety and optimized outcomes. More than 800 cases have been performed across 2 US pediatric institutions using these techniques. This article reviews the posterior tracheopexy procedure, a newer but increasingly common surgery designed to address tracheobronchomalacia, and provides an overview of related anesthesia considerations and unique challenges. In addition, this article describes novel anesthesia techniques developed specifically to facilitate optimal diagnosis of tracheobronchomalacia and intraoperative management of posterior tracheopexy and similar airway surgeries. These include methods to safely enable 3-phase rigid dynamic bronchoscopy for accurate tracheobronchomalacia diagnosis, recurrent laryngeal nerve monitoring during cervical and thoracic surgical dissection, continuous intraoperative bronchoscopy to enable real-time images during airway reconstruction, and intraoperative assessment of airway repair adequacy to ensure successful correction of tracheobronchomalacia.

It is almost 2 decades since it was first hypothesized that anesthesia technique might modulate cancer biology and thus potentially influence patients' long-term outcomes after cancer surgery. Since then, research efforts have been directed towards elucidating the potential pharmacological and physiological basis for the effects of anesthetic and perioperative interventions on cancer cell biology. In this review, we summarize current laboratory and clinical data. Taken together, preclinical studies suggest some biologic plausibility that cancer cell function could be influenced. However, available clinical evidence suggests a neutral effect. Observational studies examining cancer outcomes after surgery of curative intent for many cancer types under a variety of anesthetic techniques have reported conflicting results, but warranting prospective randomized clinical trials (RCTs). Given the large patient numbers and long follow-up times required for adequate power, relatively few such RCTs have been completed to date. With the sole exception of peritumoral lidocaine infiltration in breast cancer surgery, these RCTs have indicated a neutral effect of anesthetic technique on long-term oncologic outcomes. Therefore, unless there are significant new findings from a few ongoing trials, future investigation of how perioperative agents interact with tumor genes that influence metastatic potential may be justified. In addition, building multidisciplinary collaboration to optimize perioperative care of cancer patients will be important.

Background: Anesthetics like propofol increase electroencephalography (EEG) power in delta frequencies (0.1-4 Hz), with a decrease of power in bandwidths >30 Hz. Propofol is nonselective for gamma amino butyric acid type A receptor subtypes (GABAAR) as it enhances all 3 GABAAR subtypes (slow, fast, and tonic). Our newly developed anesthetic class selectively targets GABAAR-slow synapses to depress brain responsiveness. We hypothesized that a selective GABAAR-slow agonist, KSEB 01-S2, would produce a different EEG signature compared to the broad-spectrum GABAAR agonist (propofol), and tested this using rat EEG recordings.

Methods: Male rats were studied after Institutional Animal Care and Use Committees (IACUC) approval from the US Army Medical Research Institute of Chemical Defense and the University of Michigan. Rats were anesthetized using isoflurane (3%-5% induction, 1%-3% maintenance) with oxygen at 0.5 to 1.0 L/min. Stainless steel screws were placed in the skull and used to record subcranial cortical EEG signals. After recovery, either propofol or KSEB 01-S2 was administered and effects on EEG signals were analyzed.

Results: As previously reported, propofol produced increased power in delta frequencies (0.1-4 Hz) compared to predrug recordings and produced a decrease in EEG power >30 Hz but no significant changes were seen within ±20 seconds of losing the righting reflex. By contrast, KSEB 01-S2 produced a significant increase in theta frequency percent power (median 14.7%, 16.2/13.8, 75/25 confidence interval; to 34.7%, 35/31.8; P < .015) and a significant decrease in low gamma frequency percent power (16.9%, 18.6/15.8; to 5.45%, 5.5/5.39; P < .015) for all rats at ± 20 seconds of loss of consciousness (LOC). Both anesthetics produced a flattening of chaotic attractor plots from nonlinear dynamic analyses, like that produced by volatile and dissociative anesthetics at LOC.

Conclusions: KSEB 01-S2 produced a markedly different EEG pattern, with a selective increase observed in the theta frequency range. KSEB 01-S2 also differs markedly in its activity at the GABAAR-slow receptor subtype, suggesting a possible mechanistic link between receptor subtype specificity and EEG frequency band signatures. Increased theta together with depressed gamma frequencies is interesting because GABAAR slow synapses have previously been suggested to underlie theta frequency oscillations, while fast synapses control gamma activity. These reciprocal effects support a previous model for theta and nested gamma oscillations based on inhibitory connections between GABAAR fast and slow interneurons. Although each anesthetic produced a unique EEG response, propofol and KSEB 01-S2 both increased slow wave activity and flattened chaotic attractor plots at the point of LOC.

Background: Neuromuscular blocking agents (NMBAs) play an integral role in modern anesthesia by facilitating endotracheal tube placement, assisting with mechanical ventilation, and creating optimal surgical conditions. However, NMBAs can have deleterious side effects. The purpose of this study was to retrospectively analyze acute complications of 2 pharmacodynamically similar but pharmacokinetically different NMBAs and their respective reversal agents.

Methods: The global research network database, TriNetX, was used to evaluate deidentified patient information from 63 health care organizations. Cohort A was defined as patients aged 18 to 80 years who had chronic kidney disease (CKD) and were administered rocuronium with sugammadex. Cohort B was defined as patients aged 18 to 80 years who had CKD and were administered cisatracurium with neostigmine. Cohorts were propensity matched for age at event, ethnicity, race, sex, and relevant confounding pathologies. All outcomes besides mortality were analyzed from the same day to 1 week after administration of the indexed drug. Mortality was analyzed from the same day to thirty days after administration of the indexed drug.

Results: A total of 95,740 patients with CKD-administered rocuronium with sugammadex were matched with 10,708 patients with CKD-administered cisatracurium with neostigmine. Patients administered rocuronium with sugammadex had a significantly higher associated risk of respiratory failure (risk ratios [RR], 1.98, confidence interval [CI], 1.71-2.29, P < .0001), acute respiratory distress (RR, 2.70, CI, 1.31-5.58, P = .0052), hypertensive crisis (RR, 1.85, CI, 1.37-2.49, P < .0001), heart failure (RR, 1.14, CI, 1.06-1.23, P = .0004), pleural effusion (RR, 1.30, CI, 1.14-1.49, P < .0001), and 30-day mortality (RR, 1.31, CI, 1.10-1.56, P = .0021).

Conclusions: From 2003 to 2023, patients who were administered rocuronium plus sugammadex were at a significantly higher risk for acute cardiovascular and pulmonary complications when compared to patients who were administered cisatracurium plus neostigmine.