RESUMO
IMPORTANCE: Peri-operative blood loss during joint replacement procedures is a modifiable risk factor that impacts wound complications, hospital stay and total costs. Tranexamic acid (TXA) is an anti-fibrinolytic that has been widely used in orthopedic surgery, but its efficacy in the setting of total ankle arthroplasty (TAA) has not been quantified to date. AIM: The purpose of this systematic review and meta-analysis was to evaluate the efficacy and safety of administering TXA in patients undergoing TAA. EVIDENCE REVIEW: The Medline, Embase and Cochrane library databases were systematically reviewed using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Five comparative studies examining blood loss following administration of TXA for patients undergoing TAA were included. The outcome measures of interest were blood loss, reduction in hemoglobin concentration, transfusion requirements, total complications and wound complications. FINDINGS: In total, 194 patients received TXA and 187 patients did not receive TXA while undergoing TAA. Based on the common-effects model for total blood loss for the TXA group versus control, the standardized mean difference (SMD) was -0.7832 (95% CI, -1.1544, -0.4120; P â< â0.0001), in favor of lower total blood loss for TXA. Based on the random-effects model for reduction in hemoglobin for the TXA group versus control, the SMD was -0.9548 (95% CI, -1.7850, -0.1246; P â= â0.0242) in favor of lower hemoglobin loss for TXA. Based on the random-effects model for total complications for the TXA group versus control, the risk ratio was 0.512 (95% CI, 0.1588, 1.6512; P â= â0.1876), in favor of lower total complications for TXA but this was not statistically significant. CONCLUSIONS: This current review demonstrated that administration of TXA led to a reduction in blood loss and hemoglobin loss without an increased risk of the development of venous thromboembolism in patients undergoing TAA. No difference was observed with respect to total complication rates between the TXA cohort and the control group. TXA appears to be an effective hemostatic agent in the setting of TAA, but further studies are necessary to identify the optimal timing, dosage and route of TXA during TAA. LEVEL OF EVIDENCE: III.
RESUMO
Colonoscopy and polypectomy remain the gold standard investigation for the detection and prevention of colorectal cancer. Halting the progression of colonic adenoma through adequate detection of pre-cancerous lesions interrupts the progression to carcinoma. The adenoma detection rate is a key performance indicator. Increasing adenoma detection rates are associated with reducing rates of interval colorectal cancer. Endoscopists with high baseline adenoma detection rate have a meticulous technique during colonoscopy withdrawal that improves their adenoma detection. This minireview article summarizes the evidence on the following simple operator techniques and their effects on the adenoma detection rate; minimum withdrawal times, dynamic patient position change and proximal colon retroflexion.
RESUMO
During systemic inflammation, indoleamine 2,3-dioxygenase 1 (IDO1) becomes expressed in endothelial cells where it uses hydrogen peroxide (H2O2) to oxidize L-tryptophan to the tricyclic hydroperoxide, cis-WOOH, that then relaxes arteries via oxidation of protein kinase G 1α. Here we show that arterial glutathione peroxidases and peroxiredoxins that rapidly eliminate H2O2, have little impact on relaxation of IDO1-expressing arteries, and that purified IDO1 forms cis-WOOH in the presence of peroxiredoxin 2. cis-WOOH oxidizes protein thiols in a selective and stereospecific manner. Compared with its epimer trans-WOOH and H2O2, cis-WOOH reacts slower with the major arterial forms of glutathione peroxidases and peroxiredoxins while it reacts more readily with its target, protein kinase G 1α. Our results indicate a paradigm of redox signaling by H2O2 via its enzymatic conversion to an amino acid-derived hydroperoxide that 'escapes' effective reductive inactivation to engage in selective oxidative activation of key target proteins.