2 Minute Medicine Rewind Oct 27, 2025

Development of a Clinical Prediction Model for Anastomotic Leakage in Colorectal Surgery

1. An integrative machine learning predictive model based on individual base models can accurately predict the incidence of anastomotic leakage (AL) after colon resection.

Evidence Rating Level: 2 (Good)

AL after colorectal surgery is associated with higher reoperative rates, longer hospital stays, and increased morbidity and mortality. Although multiple risk factors correlate with the incidence of AL, it is difficult for surgeons to objectively predict this risk. This study sought to develop a machine learning meta-model that combines pre-existing models to improve the assessment of AL incidence. This retrospective prognostic study was conducted across 13 centres in Europe and North America in 9120 patients (mean [SD] age, 61.26 [15.71] years; 50.8% male). Four pre-existing machine learning algorithms (CatBoost, LightGBM, random forest, and bagging classifier) were trained with 34 preoperative AL risk factors. This yielded 144 meta-model combinations, with the most optimal configuration yielding an F1 score of 87% (95% CI, 78%-95%). The model was also evaluated on an external validation test set, achieving an F1 score of 70%. Compared to its individual models, the meta-model was significantly better at predicting AL risk than LightGBM (p=0.0009), random forest (p=0.0005), and bagging classifier (p=0.0035), but not CatBoost(p=0.1692). These findings suggest that machine learning may reduce bias and help risk-stratify patients based on the likelihood of requiring AL after colorectal surgery. However, prospective validation and larger studies assessing the clinical utility of these models are required before they are integrated into standard care.

 

Effect of Intensive Blood Pressure Lowering Treatment on Retinal Microvasculature: Secondary Analysis From ESPRIT

1. Intensive systolic blood pressure (SBP) management reduces hypertension-mediated retinal microvascular damage in populations with high cardiovascular risk.

Evidence Rating Level: 1 (Excellent)

Hypertension affects the retinal microvasculature by inducing a spectrum of structural and functional changes collectively termed hypertensive retinopathy. Antihypertensive treatment has been shown to slow the progression of hypertensive retinopathy. However, it is unclear if intensive treatment targeting SBP provides additional benefit compared with standard treatment targeting SBP. This multicentre, open-label, randomized controlled trial allocated 2,518 patients (mean age ± SD, 62.7 ± 6.4; 37.8% female) who were at least 50 years of age, had a SBP 130-180 mm Hg, and had an increased cardiovascular risk (defined as having established cardiovascular disease or at least 2 major cardiovascular risk factors) to either intensive treatment (SBP target <120 mm Hg) or standard treatment (SBP target <140 mm Hg) in a 1:1 ratio. Investigators adjusted participants’ antihypertensive medications based on pre-specified algorithms. After 3 years, patients in the intensive arm had significantly increased arteriolar calibre, as demonstrated by a higher arteriole-venule ratio (β = 0.16; 95% CI: 0.05-0.28; P = 0.005). This effect was consistently observed across subgroups. Intensive arm patients also showed significantly increased arteriolar complexity (β = 0.19; 95% CI: 0.08-0.30; P = 0.001) and arteriolar density (β = 0.17; 95% CI: 0.07-0.28; P = 0.002). This study suggests intensive blood pressure management reduces hypertension-mediated retinal microvasculature damage in populations with high cardiovascular risk. These findings contribute to emerging evidence that intensive blood pressure management may be beneficial compared to standard management in certain populations.

 

Adjunctive terlipressin versus placebo in the treatment of refractory septic shock: a randomized, placebo-controlled trial

1. Terlipressin in the treatment of refractory septic shock is significantly better than placebo at maintaining mean arterial pressure (MAP) but does not improve overall mortality.

Evidence Rating Level: 1 (Excellent)

Current guidelines for septic shock where hemodynamics are refractory to norepinephrine infusion recommend beginning vasopressin as it raises blood pressure through a non-adrenergic receptor pathway, minimizing the risk of excessive stimulation. However, there is limited data on the efficacy of adding terlipressin as a second vasopressor. Terlipressin is a vasopressin analog with a longer half-life and greater selectivity for V1 receptors compared to vasopressin. In this prospective, single-center, double-blind, randomized controlled trial, patients aged 18 years or older were included if they had a serum lactate > 2 mmol/L and required norepinephrine doses above 0.2 mcg/kg/min to maintain a MAP of at least 65 mmHg. 130 patients were randomized in a 1:1 ratio to receive up to a maximum of 0.025 mcg/kg/min of terlipressin or 0.9% sodium chloride solution to achieve a MAP above 65 mmHg. The primary outcome was successful septic shock hemodynamic stabilization within 6 hr, defined as maintaining a MAP of at least 65 mmHg with a total catecholamine requirement (norepinephrine dose + epinephrine dose + [dopamine dose]/100 + [dobutamine dose]/100) below 0.2 mcg/kg/min. This outcome occurred significantly more frequently in the terlipressin group compared to the control group (22.7% vs 9.4%; RR = 1.53, 95% CI = 1.09–2.14, P = 0.039); however, there was no significant difference at 24 and 74 hours. There was no significant difference in 28-day mortality (RR = 0.93, 95% CI = 0.66 − 1.31, P = 0.684) or adverse effects such as non-onset atrial fibrillation (RR = 1.05, 95% CI = 0.61 − 1.80, P = 0.848) or fatal arrhythmias (RR = 0.98, 95% CI = 0.43 − 2.23, P = 1.000). Patients with a SOFA score below 12 (adjusted odds ratio [aOR] = 33.33, 95% CI = 3.45–100.0, P = 0.003) and an initial serum lactate level below 4 mmol/L (aOR = 33.33, 95% CI = 3.12–100.0, P = 0.004) were independently associated with responsiveness to terlipressin. Although terlipressin in refractory septic shock may safely improve hemodynamics and reduce catecholamine use, it is unclear whether these benefits translate to overall mortality.

 

Code stroke of large vessel occlusion at triage improves candidate selection and workflow efficiency of endovascular thrombectomy

1. Incorporating acute ischemic stroke due to large vessel occlusion (LVO) screening using the Los Angeles Motor Scale (LAMS) is feasible and reduces time to computed tomography angiography (CTA) and time to endovascular thrombectomy (EVT).

Evidence Rating Level: 2 (Good)

Timely EVT for acute ischemic stroke caused by LVO is critical for patient outcomes. However, current Code Stroke protocols are not designed to identify patients with LVO, potentially delaying gold standard therapy. Conventional Code Stroke protocols recommend noncontrast CT head as initial imaging to rule out intracranial hemorrhage. However, the preferred imaging modality for LVO ischemic stroke is CTA with or without CT perfusion (CTP). This study implemented Code LVO, where patients were first triaged for LVO with LAMS. Patients with LAMS ≥ 4 underwent immediate CTA/CTP and early EVT team notification while patients with LAMS < 4 were managed with the conventional code stroke pathway. This single-center retrospective study included 1025 acute stroke patients presenting within 6 hours of onset. 808 patients (mean age ± SD, 68.0 ± 13.8; 60.4% male) were seen before Code LVO implementation and 217 patients (mean age ± SD, 68.0 ± 13.4; 64.1% male) were seen after. Code LVO patients significantly fewer patients receiving non-contrast CTA before CT (8.8% vs. 34.7%, P < 0.001), shorter door-to-CTA times (median [IQR] minutes: 19 [15–24] vs. 42 [27–61], P < 0.001), higher proportion of patients receiving EVT (24.4% vs. 11%, P < 0.001), and shorter door-to-puncture times compared to pre-Code LVO patients (median [IQR] minutes: 107.5 [97–117.25] vs. 140 [114.75–160.25], P < 0.001). Overall, incorporating LVO screening at triage is a quick and feasible strategy to expedite door-to-CTA and door-to-EVT times.

 

Gut inflammation is associated with structural spinal damage in axial spondyloarthritis – results from the observational SPARTAKUS cohort

1. Increased gut inflammation, as measured by fecal calprotectin, is significantly associated with greater structural spinal damage in axial spondyloarthritis.

Evidence Rating Level: 2 (Good)

A significant proportion of patients with axSpA have comorbid inflammatory bowel disease (IBD) or elevated inflammation, measured histologically and through fecal calprotectin. Prior studies have identified a link between the degree of inflammation and more active disease in axSpA. However, it is unknown whether gut inflammation is also associated with more structural spinal damage in axSpA. This cross-sectional analysis of the SPARTAKUS cohort analyzed 228 patients (mean age ± SD, 51.0 ± 13.0; 53% male) with well-established non-radiographic or radiographic axSpA. axSpA Patients were stratified by fecal calprotectin levels (< 50 mg/kg, 50-149 mg/kg, and ≥ 150 mg/kg). There was significantly higher structural spinal damage, measured with the modified Stoke ankylosing spondylitis spinal score (mSASSS) in the fecal calprotectin > 50 mg/kg group compared to the fecal calprotectin < 50 mg/kg group (OR 95% CI, 2.17 (1.24-3.80), p = 0.007). This relationship remained after removing IBD patients from analysis (OR 95% CI, 2.48 (1.36-4.53), p = 0.003). Overall, this study suggests the degree of gut inflammation is a good prognostic indicator of spinal radiographic progression in axSpA. However, prospective studies are required to elucidate causality.

Image: PD

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