ABSTRACT
BACKGROUND: Postoperative delirium remains prevalent despite extensive research through randomised trials aimed at reducing its incidence. Understanding trial characteristics associated with interventions' effectiveness facilitates data interpretation. METHODS: Trial characteristics were extracted from eligible trials identified through two systematic literature searches. Multivariable meta-regression was used to investigate trial characteristics associated with effectiveness estimated using odds ratios. Meta-analysis was used to investigate pooled effectiveness. RESULTS: We identified 201 eligible trials. Compared with China, trials from the USA/Canada (ratio of odds ratio, 1.89; 95% confidence interval, 1.45-2.45) and Europe/Australia/New Zealand (1.67; 1.29-2.18) had an 89% and 67% higher odds ratio, respectively, suggesting reduced effectiveness. The effectiveness was enhanced when the incidence of postoperative delirium increased (0.85; 0.79-0.92, per 10% increase). Trials with concerns related to deviations from intended interventions reported increased effectiveness compared with those at low risk (0.69; 0.53-0.90). Compared with usual care, certain interventions appeared to have reduced the incidence of postoperative delirium in low-risk trials with low-to-moderate certainty of evidence. However, these findings should be considered inconclusive because of challenges in grouping heterogeneous interventions, the limited number of eligible trials, the prevalence of small-scale studies, and potential publication bias. CONCLUSIONS: The effectiveness of postoperative delirium trials varied based on the region of trial origin, the incidence of delirium, and the risk of bias. The limitations caution against drawing definitive conclusions from different bodies of evidence. These findings highlight the imperative need to improve the quality of research on a global scale. SYSTEMATIC REVIEW PROTOCOL: PROSPERO (CRD42023413984).
Subject(s)
Postoperative Complications , Randomized Controlled Trials as Topic , Humans , Postoperative Complications/epidemiology , Postoperative Complications/prevention & control , Delirium/prevention & control , Delirium/epidemiology , Emergence Delirium/prevention & control , Emergence Delirium/epidemiologyABSTRACT
BACKGROUND: To analyze the incidence of early acute kidney injury (AKI) and perioperative factors following hip and knee joint replacement. METHODS: A total of 6281 patients from the department of orthopedics from January 2016 to July 2018 were enrolled, and 1490 patients undergoing hip and knee arthroplasty met the inclusion criteria. The preoperative, intraoperative and postoperative parameters were recorded. The retrospective cohort study was carried out to analyze predictors for AKI and postoperative creatinine elevation following hip and knee joint replacement. RESULTS: Eighty patients (5.4%) met AKI criteria. Age, American Society of Anesthesiologists (ASA) physical status and preoperative diabetes were identified as independent predictors for postoperative AKI in patients undergoing hip and knee arthroplasty (p < 0.05). Age, male, preoperative diabetes, hypertension, and preoperative creatinine were identified as independent predictors for postoperative creatinine elevation (p < 0.05). Patients with AKI were more likely to enter the ICU than non-AKI patients (25% vs 5.6%, p < 0.05). Compared with non-AKI patients, the total hospital stay (16 [11-22] vs 13 [10-16] days) and postoperative hospital stay (11 [8-14] vs 8 [7-11] days) for AKI patients were significantly prolonged (p < 0.05). CONCLUSION: The study shows age, male, preoperative diabetes, hypertension, and preoperative creatinine were independent predictors for postoperative creatinine elevation. In addition, age, ASA physical status and preoperative diabetes are independent predictors for postoperative AKI in patients undergoing hip and knee joint replacement. Postoperative AKI seems to increase ICU admission and significantly prolonged hospital stay.
Subject(s)
Acute Kidney Injury/epidemiology , Arthroplasty, Replacement, Hip , Arthroplasty, Replacement, Knee , Creatinine/blood , Adult , Age Factors , Aged , Aged, 80 and over , Arthroplasty, Replacement, Hip/adverse effects , Arthroplasty, Replacement, Knee/adverse effects , Critical Care , Diabetes Mellitus/epidemiology , Female , Humans , Hypertension/epidemiology , Incidence , Length of Stay , Male , Middle Aged , Postoperative Complications/epidemiology , Preoperative Period , Retrospective Studies , Risk Factors , Sex Factors , VasoplegiaABSTRACT
BACKGROUND: The management of neuropathic pain (NP) is challenging despite it being the recent focus of extensive research. A number of clinical practice guidelines (CPGs) for the management of NP have been published worldwide over the past 2 decades. This study aimed to assess the quality of these CPGs. METHODS: We performed a systematic review of published CPGs for the management of NP. Three reviewers independently assessed the quality of the CPGs using the Appraisal of Guidelines Research and Evaluation II (AGREE-II) instrument, and recommendations of CPGs were also appraised. RESULTS: A total of 16 CPGs were included. Thirteen CPGs were developed using an evidence-based approach, and the remaining CPGs were produced by consensus panels. None of CPGs obtained a score greater than 50% in all six AGREE II instrument domains mainly owing to poor performance in the "Applicability" domain. The highest score of the CPGs was achieved in "Clarity and Presentation" domain, followed by "Scope and Purpose" and "Editorial Independence" domains, and the lowest scores were found the in "Applicability" domain. The majority of the CPG recommendations on the management of patients with NP were relatively consistent, especially regarding the recommendation of stepwise treatment with medication. CONCLUSIONS: Greater efforts are needed not only to improve the quality of development and presentation of the CPGs, but also to provide more efficacy evidence for the management of patients with NP.
Subject(s)
Neuralgia/diagnosis , Neuralgia/therapy , Pain Management/standards , Practice Guidelines as Topic/standards , Analgesics, Opioid/therapeutic use , Anticonvulsants/therapeutic use , Cannabinoids/therapeutic use , Humans , Pain Management/methodsABSTRACT
The present study was aimed to explore the expressions of transforming growth factor-ß1 (TGF-ß1) and Snail1 in renal tissues of diabetic rats, and their role in tubular epithelial-mesenchymal transition (TEMT). Induced diabetic rats were randomly divided into 2-, 4-, 8-, 12-, 16-, 20-, 24-week and 16wA, 20wA, 24wA groups. The rats in 16wA, 20wA and 24wA groups were treated with insulin to control blood glucose to the normal level from the 13th week. The age-matched rats were set as controls. Blood glucose, 24-hour urine protein, serum creatinine (Scr), kidney index of rats were measured. PAS staining was used to observe the renal pathological changes. Immunohistochemical staining and (or) Western blot were employed to determine the expressions of TGF-ß1, Snail1, E-cadherin, α-smooth muscle actin (α-SMA) and fibronectin (FN) proteins. The expressions of Snail1 and E-cadherin mRNAs in renal cortex were examined by RT-PCR. Blood glucose, 24-hour urine protein, Scr and kidney index increased remarkably in diabetic rats as compared with those in the control groups (P<0.05, P<0.01) and insulin-treated rats (P<0.01). TGF-ß1 and Snail1 protein expressions could not be detected by immunohistochemical staining in the normal renal tissues, however, the strongly positive staining was observed in diabetic rat renal tubules. A time-dependent loss of TGF-ß1 and Snail1 expressions was detected in the kidney of insulin-treated rats. In diabetic rats tubular α-SMA positive staining was seen at the 16th week. E-cadherin expression was lost in diabetic rats. The expressions of TGF-ß1, Snail1 proteins and Snail1 mRNA were significantly up-regulated in diabetic rats, while down-regulated in insulin-treated rats (P<0.01). The expressions of E-cadherin protein and mRNA in the cortex were contrary to the expressions of TGF-ß1 and Snail1. Therefore, TGF-ß1 and Snail1 are possibly involved in the pathogenesis of TEMT in diabetic nephropathy rats.
Subject(s)
Epithelial-Mesenchymal Transition , Kidney Tubules/metabolism , Transcription Factors/metabolism , Transforming Growth Factor beta1/metabolism , Animals , Diabetes Mellitus, Experimental/metabolism , Diabetic Nephropathies/metabolism , Down-Regulation , Kidney/pathology , Rats , Snail Family Transcription FactorsABSTRACT
The aim of the present study was to investigate the role of p38 MAPK in the renal tubular epithelial-mesenchymal transition (TEMT) induced by high glucose. In in vivo study, the rats were randomly divided into control (C), diabetes mellitus (DM) and insulin-treated DM groups. Immunohistochemical staining and Western blot were employed to determine the expression of p38 MAPK and p-p38 MAPK protein in renal cortex of rats. In in vitro study, primary renal tubular epithelial cells (PTECs) were cultured with normal glucose (5.5 mmol/L), high glucose (20 mmol/L D-glucose), high osmolality (20 mmol/L D-mannitol) and SB202190 (a p38 MAPK inhibitor) plus high glucose respectively for 72 h. The expressions of p38 MAPK, p-p38 MAPK, Snail1, transforming growth factor-beta1 (TGF-beta1), alpha-smooth muscle actin (alpha-SMA) and E-cadherin protein and mRNA were detected by immunocytochemical staining, Western blot and RT-PCR. The p38 MAPK and p-p38 MAPK were specifically upregulated by high glucose in both in vivo and in vitro studies. The p38 MAPK activation was abolished by insulin controlling hyperglycemia to normal level in DM rats and inhibited dramatically by SB202190 in high glucose-cultured PTECs. The protein and mRNA of alpha-SMA were markedly increased in PTECs cultured with high glucose and were 12-fold and 8-fold respectively over that in the normal glucose, which were significantly suppressed by SB202190. SB202190 down-regulated the high glucose-induced Snail1 protein expression in PETCs, and restored partly the depression of E-cadherin protein and mRNA. These results suggest that p38 MAPK mediates high glucose-induced TEMT via transcription factor Snail1.