Background: Risk assessment plays an important role in surgical decision-making. To estimate complication risk, many surgeons rely on gestalt, a mental process that involves integrating a range of clinical information. Others utilize dedicated risk scoring tools, which offer more standardized assessments. The aims of this systematic review were to explore the current evidence on the predictive value of gestalt for adverse postoperative events and to compare gestalt prediction with various scoring tools. Methods: This systematic review was conducted following the PRISMA 2020 guidelines and the Cochrane Handbook for Systematic Reviews of Diagnostic Test Accuracy. MEDLINE, Embase, Scopus, ClinicalTrials.gov, ACM digital library, and IEEE Xplore databases were searched. Studies concerned with surgeon gestalt prediction of adverse postoperative outcomes were included. Risk of bias was assessed using the QUADAS-2 tool. Outcomes evaluated were gestalt and scoring tool predictive accuracies for mortality and morbidity. A narrative synthesis was conducted. Results: A total of 34 studies encompassing 33 657 patients were included. Surgeons had good discrimination when predicting mortality, but consistently overestimated risk. Scoring tools generally outperformed surgeons, but integrated tools incorporating both gestalt and scoring tool outputs performed best. There was some evidence that gestalt accuracy improved with surgeon experience. Surgeons may also be better at predicting complications for elective procedures compared with emergency procedures. Conclusion: Surgeon gestalt can be a valuable predictor of surgical outcomes both on its own and as a component of integrated risk scoring tools. Future studies should aim to elucidate what factors contribute to effective gestalt assessment.

Chronic hyperglycaemia impairs insulin secretion by disrupting beta‐cell metabolism and reducing expression of insulin. These changes are mediated by glucose metabolites downstream of glucokinase. We hypothesized that chronically enhancing glucokinase activity at low glucose would mimic the effects of glucotoxicity and, conversely, that reducing glucokinase activity would prevent the deleterious effects of chronic hyperglycaemia. Human islet microtissues or INS‐1 cells were cultured at low or high glucose for 2 weeks (islets) or 48 h (INS‐1 cells) in the presence or absence of either a glucokinase activator (MK‐0941 or dorzagliatin) or a glucokinase inhibitor (mannoheptulose). We measured changes in glucose‐stimulated insulin secretion, insulin content, glycogen content, gene expression, and oxygen consumption. Chronic glucokinase activation in low‐glucose‐cultured islet microtissues and INS‐1 cells downregulated insulin secretion and content, impaired mitochondrial metabolism, and altered metabolic gene expression, to the same extent as high‐glucose culture. Conversely, reduction of glucokinase activity in high‐glucose‐cultured islet microtissues by mannoheptulose prevented the changes produced by chronic hyperglycaemia. Moreover, the effects of chronic hyperglycaemia on insulin secretion and metabolic gene expression (but not insulin content) were largely reversed by subsequent inhibition of glucokinase. Chronic glucokinase activation in euglycaemia thus mimics the effects of chronic hyperglycaemia, whereas partial inhibition of glucokinase in hyperglycaemia restores normal beta‐cell function. This explains why, in the long term, glucokinase activators are ineffective at controlling glycaemia in type 2 diabetes, and demonstrates that normalizing glucokinase activity can prevent and reverse chronic glucose toxicity.