United Lincolnshire Hospitals NHS Trust

A 24-hour urine collection is central to the metabolic evaluation and prevention of nephrolithiasis. Despite its widespread use, methodological inconsistencies in data reporting and analysis limit the reliability, reproducibility, and clinical utility of findings. We aim to review and evaluate how 24-hour urine parameters are reported, analyzed, and interpreted in nephrolithiasis research. We conducted a methodological review of 264 studies involving 450,624 patients with nephrolithiasis. Data extraction covered urine collection protocols, parameter reporting, units used, statistical methods, and missing data handling. Retrospective cohort studies comprised 42.8% of included articles; cross-sectional and prospective cohort studies made up 25.0% and 19.3%, respectively. Only 6.8% (18/264) of studies reported power calculations, and 40.9% (108/264) provided reference ranges. Calcium was the most frequently reported parameter (93.9%), followed by citrate (87.5%), oxalate (86.7%), and uric acid (84.1%). Supersaturation indices were reported in 44.3% of studies. Reporting formats varied: continuous units were used in 94.7% for supersaturation, 91.7% for calcium/creatinine ratio, and 77.9% for calcium. Most common units were mg/day (e.g., calcium: 78.9%) and mmol/day (e.g., sodium: 56.9%). Regarding statistical analysis, 72.3% of studies used t-tests or Mann-Whitney U tests, 39.4% used chi-square tests, and only 21.6% used multivariate regression. Missing data were handled by complete case analysis in 71.2% of studies, while 27.7% did not report their approach. There is significant variability in how 24-hour urine data are reported and analyzed across nephrolithiasis studies. This inconsistency undermines evidence synthesis, limits external validation, and obstructs the integration of advanced tools like artificial intelligence. We recommend creating a standardized reporting checklist to improve the rigor, reproducibility, and clinical relevance of future research.

Abstract Surgical intervention for benign prostatic hyperplasia (BPH) can lead to postoperative stress urinary incontinence. Pelvic floor muscle exercises (PFME) are proposed as a non‐invasive strategy to mitigate symptoms, but their efficacy and optimal timing remain unclear. A systematic review of six studies (five randomized controlled trials and one prospective cohort) was conducted, evaluating PFME in men undergoing BPH surgery. Three studies investigated preoperative PFME, and three evaluated postoperative interventions. Outcomes included incontinence rates, lower urinary tract symptoms (LUTS), pelvic floor muscle strength, and quality of life. Evidence for preoperative PFME was mixed; one trial ( n = 70) demonstrated significantly reduced incontinence at 3 months (3% vs. 26%; p = 0.01), while another ( n = 49) found improved muscle endurance without clinical benefits. In contrast, postoperative PFME showed more consistent improvements. One randomized controlled trial (RCT) ( n = 61) reported significantly better LUTS at 12 weeks (IPSS: 3.32 vs. 6.33; p < 0.001) and better quality of life. Another ( n = 58) noted fewer incontinent episodes at 1–3 weeks ( p < 0.01). However, a large multicenter randomized controlled trial ( n = 442 TURP patients) found no long‐term benefit in incontinence rates at 12 months (65% vs. 62%). In conclusion, PFME may enhance the postoperative recovery of continence and LUTS, particularly when initiated early and performed consistently. Preoperative PFME shows promise but requires further validation. Heterogeneity in study designs highlights the need for standardized, large‐scale trials to define optimal PFME protocols for this population.

Endometriotic cyst infection is rare and typically associated with invasive pelvic procedures or pelvic inflammatory disease. We present a case of a 34-year-old nulligravida female with no recent surgical or gynaecological interventions, who developed acute abdominal pain due to a ruptured endometriotic cyst infected with Salmonella enterica serovar Typhi. This case underscores the potential for hematogenous spread of infection and the importance of considering infected endometriomas in the differential diagnosis of acute abdomen.

Background and aimsRectal prolapse and rectocele are socially and psychologically debilitating conditions. While laparoscopic rectopexy has improved outcomes over open surgery, it faces limitations in pelvic access, mesh positioning, and suturing. Robotic-assisted rectopexy may overcome these challenges through enhanced visualisation and manoeuvrability. This study presents a single-centre experience of robotic rectopexy.MethodsA retrospective review was conducted at Stepping Hill Hospital, Stockport, UK, from 2019-2024. Data collected included operative time, intra- and postoperative complications, analgesia requirement and length of stay.ResultsTwenty-one patients underwent robotic rectopexy. The mean operative time was three hours and 18 minutes. No conversions or intraoperative complications were observed. All patients were managed with simple analgesia. Fifteen (71.4%) were discharged on post-operative day (POD) 1, four patients on POD 2 and two patients were discharged later (POD >3). The mean hospital stay was 1.6 days. Two patients had small postoperative collections managed conservatively. One recurrence was observed on follow-up.ConclusionsRobotic rectopexy is a safe and effective technique for rectal prolapse, demonstrating minimal complications and short hospital stays. Further research is warranted to assess long-term outcomes.

Boerhaave syndrome is a rare but potentially fatal condition characterized by spontaneous transmural rupture of the esophagus, most often triggered by a sudden rise in intraluminal pressure against a closed glottis following forceful retching. Its clinical presentation can mimic other life‑threatening thoracic emergencies such as myocardial infarction, pulmonary embolism, or aortic dissection. A 50-year-old man presented to the Emergency Department with sudden onset of severe central chest pain radiating to the left side associated with shortness of breath, following multiple episodes of forceful vomiting. On examination, he was hemodynamically stable. Chest and soft-tissue neck radiographs demonstrated surgical emphysema, and a contrast-enhanced CT scan of the chest confirmed esophageal rupture with extraluminal air and food residue. The patient was managed with intravenous fluids, broad-spectrum antibiotics, and urgent cardiothoracic referral for definitive management. This case highlights the importance of maintaining a high index of suspicion for Boerhaave syndrome in patients presenting with chest pain following episodes of forceful vomiting, as early recognition and prompt intervention are vital to reduce morbidity and mortality.

We report an uncommon presentation of necrotizing autoimmune myopathy (NAM) associated with anti-HMGCR antibodies in a middle-aged woman who lacked typical risk factors, including statin use, malignancy, or connective tissue disease. The patient presented with muscle weakness, markedly elevated creatine kinase levels, and muscle biopsy findings consistent with necrosis. Diagnosis of NAM was confirmed through the detection of anti-HMGCR antibodies. Despite the initiation of corticosteroid therapy, the condition progressed rapidly, highlighting the aggressive nature of this form of autoimmune myositis. This case underscores the importance of considering NAM in the differential diagnosis of idiopathic myopathy, even in the absence of common predisposing factors, and emphasizes the need for early detection and individualized treatment strategies.

Abstract Background Systemic inflammation is a hallmark of acute myocardial infarction (AMI) with residual inflammatory risk a key player in reoccurring cardiovascular events. Use of sodium-glucose cotransporter-2 inhibitors (SGLT2i) in patients with type-2 diabetes mellitus (T2DM) and AMI improves cardiovascular outcomes, yet the mechanism of action is unknown. Purpose We posit that Empagliflozin (EMPA) provides anti-inflammatory protection via suppression of the nod-like receptor protein-3 (NLRP3) inflammasome in monocyte-derived macrophages (MDMs), and that this protection is greater in early (Arm A: prescribed EMPA during AMI admission at T0, T30, T90 and T180days) versus delayed therapy (Arm B: EMPA prescribed 90days post-discharge with sampling at T90, T120 and T180days), plus appropriate controls (T0-T90). Methods Patients presenting with T2DM-AMI, eligible but not already taking an SGLT2i were recruited and randomised to Arm A (n=28) or B (n=27). Blood CD14+ monocytes were isolated and differentiated into MDMs. An inflammasome assay measured Caspase-1 activity (direct inflammasome activation) in lipopolysaccharide (0.1ug/mL) + ATP (2mM) stimulated MDMs. Quantitative RT-PCR and Lumit immunoassays measured IL1β, IL6, and TNFα gene expression/secretion. Results IL1β expression (NLRP3 priming) decreased in MDMs isolated from patients in Arm A given EMPA at T0, at all subsequent timepoints from 2.13±0.53 (T0) to 0.64±0.37 (T30; P<0.05), 0.89±0.20 (T90; P<0.05) and 0.66±0.14 (T180; P<0.05). No change in IL1β expression was observed in Arm B both without EMPA (T0-90) or when EMPA was delayed (T90-180). Caspase-1 activity decreased with EMPA in Arm A from 8677±1550 to 4751±591.7 (T0-90; P<0.05) and 3772±450.2 RLu; (T0-180; P<0.01) whilst no significant reduction in caspase-1 activity was recorded in MDMs from Arm B. Although early therapy failed to alter TNFα levels (T0-T180), EMPA prevented the early increase in TNFα gene expression in Arm B MDMs (No EMPA) at T0-T30 (0.537±0.104 to 1.148±0.236 P<0.01). EMPA also reduced TNFα release when taken immediately prior to discharge (from 5240±1201 to 2409±363.6pg/mL; P<0.05; T0-90) compared to Arm B patients without EMPA (T0-90;) or with delayed therapy (T90-180). Lastly, early initiation of EMPA reduced IL6 secretion from 2248± 609.5 (T0) to 883.3±180.4 (T30; P<0.05) and 735.2±0.5pg/mL (T180; P<0.05). In the absence of EMPA, IL6 release increased from 571.9±96.57 (T0) to 1279±243.3 (T30; P<0.05) and 1617±396pg/mL (T90; P<0.05). Levels were restored with EMPA (from 1617±396 to 661.9±82.95pg/mL; P<0.05; T90-180). Conclusion UK NICE guidelines do not stipulate if SGLT2i’s should be prescribed during admission with AMI prior to discharge, or 90days post-discharge. This study suggests that anti-inflammatory protection of EMPA on MDMs from people with T2DM who have had an AMI is greatest following early therapy, timing of which may reduce residual inflammatory risk and improve clinical outcomes.

Traumatic brain injury (TBI) is a leading cause of mortality worldwide. It is caused by blunt force, explosive blasts, sudden head acceleration or deceleration, or penetrating trauma to the skull. TBI can be classified according to GCS into mild (GCS 13-15), moderate (GCS 9-12), and severe (GCS 3-8). Symptoms of TBI vary from mild symptoms to neurodegenerative diseases. Neuroimaging is the most utilized diagnostic tool in cases of TBI. However, its complex pathophysiology mechanisms make it difficult to diagnose TBI early. Biomarkers of TBI, such as glial cell injury biomarkers, axonal injury biomarkers, and inflammation biomarkers, are emerging as diagnostic and prognostic tools in TBI. However, the diagnostic and prognostic values of biomarkers showed mixed results. The aim of this review is to discuss the role of biomarkers in the early diagnosis of TBI in adults and children. Pathophysiology of TBI includes disruption of blood-brain barrier (BBB), inflammatory response, mitochondrial dysfunction, and oxidative stress. Various biomarkers have been reported as potential diagnostic biomarkers for TBI, including neuron-specific enolase (NSE), S100B, neurofilament proteins (NFs), and tau proteins. Identifying the role of biomarkers in the diagnosis of TBI in children is challenging due to age-dependent baselines, sampling limitations, and funding gaps. Future research should focus more on investigating kinetics of TBI biomarkers before their application in clinical settings.