Management of civilian gunshot wound (GSW) fractures is controversial, with limited data on infection risk and controversy regarding treatment. While lower-energy GSWs are considered lower risk than other open fractures, complication rates remain high. This study aimed to identify risk factors for infection in operatively treated ballistic fractures.

After institutional review board approval, we identified 2136 GSW-related fractures from 01/01/2012 to 12/31/2021 at our level one trauma center. After excluding articular, hand, foot, injuries through viscera and pre-existing infections, 110 patients with 125 long bone fractures were retrospectively reviewed. The primary outcome was infection requiring reoperation. Statistical analysis included Mann-Whitney U, T-tests, Pearson's Chi-square, ROC analysis, and Youden's index.

Sixteen patients (14.5 %) developed infections requiring reoperation. The cohort had a mean age of 30 years, 90 % male, BMI 27.7 ± 7.2 kg/m², Charlson comorbidity index <1, and 37 % smokers. Increased infection risk was associated with admission glucose (p < 0.001) and length of stay (p < 0.001). Admission glucose >156 mg/dL increased odds of infection sixfold (OR 6.1, 95 % CI 2.0-19.0), while a hospital stay >10 days increased odds of infection twentyfold (OR 21.1, 95 % CI 5.3-82.7). Transfusion (p = 0.004), abdominal (p = 0.007), and chest trauma (p = 0.010) also correlated with infection risk. No significant associations were found with nicotine use, Charlson comorbidity index, or BMI.

Operatively treated long bone injuries had a 14.5 % infection rate. Elevated admission glucose and prolonged hospital stay significantly increased infection risk, particularly in polytrauma patients. Identifying high-risk patients, promoting early mobilization, and ensuring glycemic control may help reduce infections. Further research is needed to develop targeted prevention strategies.

3 (Retrospective Comparative Study).

Acute methanol poisoning signifies a global health issue. This study was designed to explore the role of the leukocyte glucose index (LGI) in predicting clinical outcomes; in-hospital mortality and visual impairment, and length of hospital stay, in acute methanol toxicity and to evaluate the association between LGI and all initial patient characteristics.

This was a retrospective analysis that involved 82 acutely methanol-intoxicated patients, starting from January 2021 to December 2023. Patients were categorized by on-admission LGI tertiles into low, intermediate, and high groups.

Approximately 27 % (22 out of 82) of patients died during hospitalization, with most of them belonging to the high LGI group. No significant differences existed in the proportions of patients with total vision loss, or the length of hospital stay. The majority of the undesirable findings were apparent in patients in either the intermediate or high LGI groups. LGI can distinguish exceptionally between survivors and non-survivors with an area under the curve of 0.808. However, LGI does not have any discriminatory power in predicting adverse visual outcomes.

LGI can serve as a valuable tool in predicting early in-hospital mortality in acute methanol poisoning.

Overfeeding, currently defined as providing excessive energy and nutrients beyond metabolic requirements, is a common yet often overlooked issue in the intensive care unit (ICU) setting. Understanding the factors contributing to overfeeding and implementing strategies to prevent it is essential for optimizing patient care in the ICU. Several factors contribute to overfeeding in the ICU, including inaccurate estimation of energy requirements, formulaic feeding protocols, and failure to adjust nutritional support based on individual patient needs. Prolonged overfeeding can lead to insulin resistance and hepatic dysfunction, exacerbating glycemic control, increasing the risk of infectious complications, and worsening clinical outcomes. Clinically, overfeeding has been linked to delayed weaning from mechanical ventilation, prolonged ICU stay, and increased mortality rates. Regular review and adjustment of feeding protocols, incorporating advances in enteral and parenteral nutrition strategies, are essential for improving patient outcomes. Clinicians must be proficient in interpreting metabolic data, understanding the principles of energy balance, and implementing appropriate feeding algorithms. Interdisciplinary collaboration among critical care teams, including dieticians, physicians, and nurses, is crucial for ensuring consistent and effective nutritional management. Overfeeding remains a significant concern in the ICU after discharge as well, implying further complications for patient safety and integrity. By understanding the causes, consequences, and strategies for the prevention of overfeeding, healthcare providers can optimize nutrition therapy and mitigate the risk of metabolic complications. Through ongoing education, interdisciplinary collaboration, and evidence-based practice, the ICU community can strive to deliver personalized and precise nutritional support to critically ill patients.

Red cell distribution width (RDW) and glycated hemoglobin index (HGI) is considered an important tool for assessing the prognosis of sepsis patients, closely related to the risk of mortality associated with sepsis. This study investigates the association between the HGI combined with RDW and the risk of in-hospital mortality in patients with sepsis. We analyzed data from 13,726 sepsis patients who were admitted to the intensive care unit (ICU) for more than 24 h, sourced from the American Medical Information Mart for Intensive Care (MIMIC-IV) database. Kaplan-Meier survival curves and multivariable Cox regression analyses were employed to assess the impact of various variables on patient outcomes, stratified by quartiles of HGI and RDW. Additionally, restricted cubic spline (RCS) analysis was utilized to explore how changes in HGI and RDW might influence the studied outcomes. The results indicated that the highest quartile (Q4) of the combined metrics significantly increased in-hospital mortality compared to the lowest quartile (Q1) (p < 0.0001). Multivariable Cox regression analysis revealed that patients in Q4 faced the highest risk of in-hospital mortality (hazard ratio: 1.22, 95% confidence interval: [1.10-1.36], p < 0.001). RCS analysis demonstrated a nonlinear relationship between HGI-RDW and the risk of adverse outcomes. Further analysis identified significantly elevated risks in patients over 65 years old, those who were widowed, those receiving macrolide antibiotics, and those with congestive heart failure or severe liver disease. In conclusion, elevated levels of the combined HGI and RDW metrics are independent risk factors for adverse outcomes in critically ill patients with sepsis, associated with increased mortality.

Acute pancreatitis (AP) is an inflammatory reaction of the pancreas. When the disease is severe, it is often accompanied by destruction of the pancreatic islets, resulting in dysfunction of the endocrine system of the pancreas. Stress hyperglycemia is a transient increase in glucose during a critical illness, and its possible mechanism is related to abnormal glucose metabolism and insulin resistance due to the increased release of counterregulatory hormones and cytokines, such as glucagon, cortisol, and catecholamines. Numerous studies have shown that stress hyperglycemia is strongly associated with morbidity, mortality, and increased risk of post-acute pancreatitis diabetes in AP patients. Therefore, stress hyperglycemia may be a significant independent risk factor for poor clinical outcomes and prognosis in patients with AP. This article reviews the clinical features, risk factors, and mechanisms of action of stress hyperglycemia in AP and its influence on adverse clinical outcomes and the prognosis of inpatients with AP. For AP patients with stress hyperglycemia, it is necessary to comprehensively consider their blood glucose levels, daily habits, and complications to develop an appropriate treatment plan for hyperglycemia. Limited evidence indicates that in the case of acute hyperglycemia in critically ill patients, especially during the first 3 days of hospitalization, insulin therapy should not be undertaken if the blood glucose level does not exceed 10 mmol/L. However, some important questions related to clinical practice remain to be answered. More clinical trials and studies are needed in the future to provide a sufficient basis for clinical practice.

Reid, Ly-Anh, Jordan L. Rees, Miranda Kimber, Marina James, Graeme M. Purdy, Megan Smorschok, Lauren E. Maier, Normand G. Boulé, Trevor A. Day, Margie H. Davenport, and Craig D. Steinback. Blood glucose during high altitude trekking in young healthy adults. High Alt Med Biol. 26:30-36, 2025. Introduction: High altitude trekking is becoming more popular and accessible to an increased number of people. Simultaneously, there is a worldwide rise in the prevalence of metabolic diseases. The purpose of this study was to examine the impact of a gradual trekking ascent to high altitude on continuous glucose monitoring outcomes including fasting, mean 24-hour, postprandial, and post-75 g modified oral glucose tolerance test. This study also investigated the relationship between physical activity intensity, high altitude, and glucose concentrations. Methods: Individuals (n = 9) from Alberta, Canada participated in a 2-week trek in the Khumbu Valley in Nepal, ascending by foot from 2,860 m to 5,300 m (∼65 km) over 10 days. A standardized 75 g oral glucose load was given to participants at four different altitudes (1,130 m, 3,440 m, 3,820 m, 5,160 m). Physical activity (Actigraph accelerometry) and interstitial glucose (iPro2, Medtronic) were measured continuously during the trek. Results: Fasting and mean 24-hour glucose concentrations were not different between altitudes. However, 2-hour post dinner glucose and 2-hour post lunch glucose, AUC concentrations were different between altitudes. The relationship between physical activity intensity and glucose was not influenced by increasing altitudes. Conclusion: Our findings suggest that glucose regulation is largely preserved at high altitude; however, inconsistency in our postprandial glucose concentrations at altitude warrants further investigation.

Background/Objectives: Groove pancreatitis (GP) is an uncommon pancreatic condition implying a challenging differential diagnosis. This study aims to comprehensively evaluate the main risk factors, clinical presentation, imaging and endoscopic characteristics of patients with GP, providing insights into an effective diagnostic approach and therapeutic strategies. Methods: A retrospective analysis was conducted on patients diagnosed with GP, with demographic and clinical data collected. The diagnostic route was followed by an upper endoscopy and was finally confirmed by cross-sectional imaging. In patients with high malignancy suspicion or with an uncertain diagnosis, a pancreatic endoscopic ultrasound (EUS) was further performed. According to imaging features, we divided patients into two categories: with and without tumor-like appearance. Results: Altogether, 23 patients were included, 11 in the tumor-like category, and 12 in the non-tumor-like group; 95.6% were men, 78.2% alcohol consumers, and 73.9% smokers. In both groups, the main symptom was abdominal pain, followed by nausea and vomiting. The most frequent finding at upper endoscopy was edematous duodenal mucosa (16 patients, 80%), followed by mucosal hyperemia (8 patients, 40%). The main finding at cross-sectional imaging was duodenal wall thickening (14 patients, 60.9%), followed by pancreatic head enlargement and duodenal wall cysts (both seen in 12 patients, 52.2%). The EUS predominantly showed duodenal wall thickening (13 patients, 68.4%), and intramural and paraduodenal cysts (10 patients, 52.6%). Conclusions: GP predominantly affects men with a history of chronic alcohol and tobacco use. Its primary diagnostic challenge lies in distinguishing it from pancreatic carcinoma, with an accurate diagnostic workup being crucial in clinical practice.

Postoperative stress hyperglycemia is reported to be associated with increased postoperative complications (PCs) following various surgical procedures. However, most reports of postoperative hyperglycemia are based on conventional, point blood glucose measurements. We sought to clarify trends in post-gastrectomy glucose levels using continuous glucose monitoring (CGM) and investigate the relationship between postoperative hyperglycemia and stress-related factors such as PCs and the degree of surgical invasiveness.

The subjects of this prospective study were 40 patients who underwent gastrectomy between November, 2022 and September, 2023. We recorded their glucose levels by CGM immediately after surgery until discharge (up to 2 weeks postoperatively).

There was no increase in glucose levels caused by open gastrectomy, a strong inflammatory response, or PCs. Hyperglycemia, defined as the percentage of time that the glucose level was > 140 mg/dL, was associated only with the preoperative HbA1c value (P = 0.039). Patients with an HbA1c ≥ 6% had a significantly longer duration of hyper- and hypo-glycemia and greater glycemic variability than those with an HbA1c < 6% (glucose level < 70 mg/dL, P = 0.027; > 140 mg/dL, P = 0.001, coefficient of variation P = 0.024).

No association was observed between stress hyperglycemia during the acute phase following gastrectomy and PCs. Only patients with an elevated HbA1c had high rates of hypo- and hyper-glycemia and large glycemic variability, despite perioperative glucose management.

To investigate the association between admission glucose and HbA1c values and inflammatory plasma proteins in hospitalized patients with acute ST-elevation myocardial infarction (STEMI).

This analysis was based on 345 STEMI patients recorded by the population-based Myocardial Infarction Registry Augsburg between 2009 and 2013. Using the OLINK inflammatory panel, a total of 92 protein biomarkers were measured in arterial blood samples, which were obtained within the scope of cardiac catheterization immediately after admission. The associations between admission glucose and HbA1c levels and the 92 protein markers were investigated using multivariable linear regression models.

Admission glucose showed significantly positive associations with the inflammatory markers IL-10, IL-8, IL-6, FGF-21, IL-7, ST1A1, MCP-1, 4E-BP1, SIRT2, STAMBP and IL-18R1 after Bonferroni adjustment. HbA1c values were only significantly associated with IL-18R1. In stratified analyses, admission glucose was not significantly associated with any plasma protein in the diabetes subgroup, while there were several protein markers that showed significantly positive associations with admission glucose in STEMI patients without known diabetes, namely IL-10, CCL20, IL-8, MCP-1 and IL-6.

Admission glucose in patients hospitalized due to an acute STEMI seems to be related to an inflammatory and immune-related response, expressed by an increase in inflammation-related plasma proteins in particular in non-diabetic patients with stress hyperglycemia. The present results may open new avenues for the development of biomarkers suitable as potential diagnostic or prognostic clinical markers.

During stressful conditions, the human body synthesizes catecholamine neurotransmitters such as dopamine and adrenaline, and cortisol. The monitoring of these three molecules levels is crucial for stress management and holds significant medical applications. Here we developed an analytical device that incorporates a biomimetic (tongue-mimic) associated with an optical physico-chemical transducer, able to detect simultaneously cortisol, dopamine and adrenaline in human saliva without pre-treatments, using an array sensor based on fluorescent chemical receptors (BODIPY, Rhodamine, and Naphthylamides) able to interact by non-covalent interaction with cortisol, adrenaline and dopamine, leading to a change of the emission. Calibration, recovery and selectivity have been performed to validate the device. In particular, the linear responses of the array to concentration range of 1 pM-1 mM of the three analytes were demonstrated by PLS analysis, as well as the high selectivity by PLS-DA analysis performed with artificial saliva samples. Analyses in real human saliva samples, compared to the validated analytical methods, demonstrated that our prototype represents the first point-of-care device able to quantify these three analytes in human saliva with one single analysis in a wider concentration range respect to the other standard methods.

The current literature suggests hyperglycemia can predict poor outcomes in patients with primary intracerebral hemorrhage (ICH). Chronic hyperglycemia is seen in patients with pre-existing diabetes (DM); however, acute hyperglycemia in non-diabetic patients is defined as stress-induced hyperglycemia (SIH). This study explored the influence of hyperglycemia on outcomes of primary ICH patients both in the presence and absence of pre-existing DM.

Data regarding admission glucose, pre-existing DM, inpatient mortality, and modified Rankin Scale (mRS) scores at discharge were available for 636 patients admitted to Stony Brook Hospital from January 2011 to December 2022 with a primary diagnosis of ICH. Regression models were used to compare outcomes between patients with admission hyperglycemia and/or pre-existing DM to a control group of normoglycemic and non-diabetic ICH patients.

Patients with SIH had higher inpatient mortality rates and worse mRS scores at discharge (p < 0.001). An association with higher mortality and worse mRS scores at discharge was also seen in patients with hyperglycemia secondary to DM, although the strength of this association was weaker when compared to patients with SIH.

Our findings suggest that SIH may play a greater role in predicting poor outcomes at discharge rather than a history of poorly controlled DM with chronic hyperglycemia. To develop a more thorough understanding of this topic, prospective studies evaluating the effect of changes in serum glucose during hospital stay on short and long-term outcomes is needed.

The Vannucci procedure is widely used to model cerebral hypoxic-ischemic (HI) injury in neonatal rodents. Identifying minimally invasive biomarkers linked to brain injury would improve stratification of pups to experimental treatments. We hypothesized that extreme blood glucose (BG) and β-hydroxybutyrate (bHB) levels immediately after HI will correlate with severity of brain injury in this model.

C57BL6 mice of both sexes underwent the Vannucci procedure with BG and bHB measured immediately after hypoxia. GFAP and α-fodrin were measured to assess injury severity at 4h, P11, P18 and P40. Open field (OF), Y-maze (YM), and Object-location task (OLT) were tested at P40.

Clinical seizures-like stereotypies during hypoxia were associated with lower post-hypoxia BG in HI-injured mice. Low BG after HI was related to higher GFAP expression, higher α-fodrin breakdown, lower residual regional volume, and worse working memory. BG was superior to bHB in ROC analysis with BG threshold of <111 mg/dL providing 100% specificity with 72% sensitivity for hippocampal HI-injury.

Post-hypoxic BG is a minimally invasive screening tool to identify pups with significant HI brain injury in the Vannucci model modified for mice improving our ability to stratify pups to experimental treatments to assess effectiveness.

End hypoxic-ischemic blood glucose levels are a reliable and inexpensive biomarker to detect hypoxic-ischemic brain injury in mice. Screening with blood glucose levels post-hypoxia allows appropriate stratification of those mouse pups most likely to be injured to experimental treatments improving validity and translatability of the results. These findings provide biological plausibility to the clinical observation that extreme blood glucose levels relate to worse outcomes after hypoxia-ischemia.

The Stress Hyperglycemia Ratio (SHR), a new biomarker calculated from glucose and HbA1c levels, has been linked to significant clinical outcomes in diabetes. This study investigates the potential of the SHR to predict End-Stage Renal Disease (ESRD) among patients with Diabetic Kidney Disease (DKD).

We included 316 participants from the West China Hospital T2DM-DKD cohort (January 2008-September 2020), divided into three SHR tertiles: T1 (SHR <0.7), T2 (SHR ≥0.7 to <0.94) and T3 (SHR ≥0.94). A second retrospective cohort of 625 DKD patients was recruited from Sichuan University Hospital (January 2019-May 2022), with similar inclusion criteria. SHR was analysed using Restricted Cubic Spline, Kaplan-Meier curves and Cox proportional hazards models. Key confounders such as eGFR, proteinuria, hypoalbuminemia and glucose-lowering medications were adjusted for in the analysis.

In Cohort 1 (median follow-up 42 months), 38.6% developed ESRD. Kaplan-Meier curves showed a higher incidence of ESRD in the lowest and highest SHR tertiles compared to the middle group (p < 0.01). Multivariate analysis confirmed that SHR <0.7 (HR 1.71, 95% CI: 1.01-2.90) and SHR ≥0.94 (HR 1.93, 95% CI: 1.16-3.20) were significantly associated with ESRD. In Cohort 2 (median follow-up 18.6 months), patients with SHR <0.7 and ≥0.94 had significantly higher risks of ≥30% eGFR decline or ESRD, with adjusted HRs of 2.18 (95% CI: 1.15-4.11) and 2.68 (95% CI: 1.38-5.23), respectively.

This study observed a U-shaped relationship between SHR and ESRD in patients with DKD. Both very high and very low SHR values correlate with increased risks, highlighting the critical importance of glucose management in chronic diabetes care.

Prior research has indicated that adopting strict glycemic control measures might elevate the risk of hypoglycemia and result in higher mortality rates among critically ill patients. However, there is a lack of studies investigating the incidence of hypoglycemia and its consequential outcomes in real-world clinical settings. This retrospective cohort study was conducted at Taichung Veterans General Hospital, utilizing critical care databases covering the period from 2015 to 2020. The objective was to examine the outcomes and identify risk factors associated with hypoglycemia in critically ill patients. Out of the total of 16,699 patients admitted to the intensive care units (ICUs), 2,115(12.7%) experienced at least one episode of hypoglycemia were included in the analysis. Critically ill patients who developed hypoglycemia had a significantly higher hospital mortality rate compared to those who did not experience hypoglycemia. (48.9% vs. 15.9%, p < 0.001). Moreover, patients with more severe hypoglycemia exhibited a higher mortality rate (moderate hypoglycemia: hazard ratio [HR] 1.477, 95% confidence interval [C.I.] 1.351-1.614, p < 0.001; severe hypoglycemia: HR 1.847, 95% C.I. 1.607-2.123, p < 0.001) compared to those without hypoglycemia. Additionally, patients with greater frequency of hypoglycemic episodes also showed a higher mortality rate (one episode HR 1.504, 95% C.I. 1.366-1.657, p < 0.001; multiple episodes HR 1.613, 95% C.I. 1.444-1.801, p < 0.001) compared to those without hypoglycemia. Patient who experienced spontaneous hypoglycemia (53.9% vs. 42.4%, p < 0.001) and those without a prior diagnosis of diabetes (60.2% vs. 37.0%, p < 0.001) had higher mortality rate. Hypoglycemia frequently occurs and serves as an independent risk factor for mortality among critically ill individuals, particularly in cases of severe and recurrent episodes. Patients experiencing spontaneous hypoglycemia, as well as those lacking a diabetes diagnosis, demonstrated elevated mortality rates.

This study aimed to explore the association between the stress hyperglycemia ratio (SHR) and short- and long-term outcomes in critically ill patients with sepsis.

This retrospective observational cohort study was conducted using the Medical Information Mart for Intensive Care-IV (MIMIC-IV v2.2) database. Patients were categorized into 4 SHR quartiles. The main focus was on in-hospital mortality and 1-year all-cause mortality as primary endpoints, while intensive care unit and hospital stays were considered as secondary outcomes. Regression and subgroup analyses were used to assess the correlation between SHR and the primary and secondary outcomes. Restricted cubic spline analysis was utilized to explore the nonlinear relationships between SHR and in-hospital and 1-year all-cause mortality.

This study included two groups of patients, comprising 7456 and 6564 individuals. The in-hospital and 1-year mortality was 11.96% and 17.96% in Cohort 1 and 2, respectively. SHR was associated with an elevated risk of in-hospital mortality (OR: 2.08, 95%CI 1.66-2.61) and 1-year mortality (HR: 1.70, 95% CI 1.42-2.04). Patients in SHR quartile 4 had a higher risk of in-hospital (OR: 1.86, 95% CI 1.51-2.30) and 1-year (HR: 1.44, 95% CI 1.23-1.69) mortality than those in quartile 2. Restricted cubic spline analysis showed a "J-shaped" relationship between SHR and all-cause mortality in both cohorts. The relationship between high SHR and mortality remained consistent across almost all predefined subgroups.

Our study suggests that high SHR is associated with increased in-hospital and 1-year mortality in critically ill sepsis patients. Further investigations are needed to validate these results.

Hyperglycemia is a serious condition and associated with an increased risk of complications and mortality in both critically ill and non-critically ill people. Improvement in the glycemic level reduces the length of hospital stay, systemic infections and short- and long-term mortality. The aim was to test the effectiveness of insulin degludec vs insulin glargine and regular insulin in controlling blood sugar in patients with critical hyperglycemia.

Using random control trial, the patients were randomly divided into three equal groups-group R, group G and group D. Each group included 30 patients. Group G was managed using regular insulin together with an insulin glargine. Group D was managed using regular insulin together with an insulin degludec. However, group R was managed using only regular insulin.

The incidence of hypoglycemia was statistically more significant in the group of regular insulin than in groups G and group D with a p-value 0.0069. There was no statistically significant difference between the three groups regarding the frequency of hypoglycemia.

Ultra-long-acting insulin can effectively control random blood sugar (RBS) with a decrease in the total dose of insulin used. It is recommended that using insulin degludec is a safe and effective alternative to regular insulin for glycemic control in critically ill patients.

El Sherif IM, Haggag AM, Abbas MH, Kamel WY. Insulin Degludec vs Insulin Glargine for Glycemic Control in Critical Illness Hyperglycemia. Indian J Crit Care Med 2025;29(1):52-58.

Bakground: The mortality rate from community-acquired pneumonia (CAP) or coronavirus disease 19 (COVID-19) is high, especially in hospitalized patients. This study aimed to assess the disturbances of glucose and lipid metabolism with in-hospital complications and short-term outcomes for patients with pneumonia with different etiologies. Methods: This observational study comprised 398 patients divided as follows: 155 with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonia, 129 participants with viral CAP, and 114 with bacterial pneumonia. Results: Fasting plasma glucose (FPG) at admission and glycemic variation during hospitalization was linked with acute kidney injury (AKI) in bacterial CAP. Compared with a value <110 mg/dL for FPG at admission, levels between 110 and 126 mg/dL are associated with mortality in both COVID-19 (OR = 3.462, 95% CI: 1.275-9.398, p = 0.015) and bacterial CAP participants (OR = 0.254; 95% CI: 0.069-0.935, p = 0.039), while a value ≥126 mg/dL was linked with mortality only in patients with SARS-CoV-2 (OR = 3.577, 95% CI: 1.166-10.976, p = 0.026). No relation between lipid biomarkers and complications or in-hospital outcomes was observed in all three participant groups. Conclusions: Patients with bacterial CAP are more prone to developing AKI due to increased FBG at admission and glycemic variations during hospitalization, while elevated FBG values at admission are associated with mortality in both COVID-19 and bacterial CAP.

The association between admission hyperglycemia and postoperative pneumonia is unclear in hip fracture patients. We investigated the relationship between admission hyperglycemia and postoperative pneumonia after hip fracture surgery. This retrospective study analyzed data from 1,267 geriatric patients admitted for hip fractures. Patients were categorized into normoglycemic (< 6.10 mmol/L) and hyperglycemic (≥ 6.10 mmol/L) groups based on admission blood glucose levels. Multivariable logistic regression and propensity score matching (PSM) were used to control for potential confounding variables and estimate adjusted odds ratios and 95% confidence intervals for postoperative pneumonia (POP). We also examined the dose-dependent link between admission blood glucose and the likelihood of developing POP. Further analyses evaluated whether admission hyperglycemia has differing impacts on POP outcomes among hip fracture patients without diabetes (NDM) versus those with diabetes (DM). Additionally, subgroup analyses were conducted to assess the influence of other factors on the relationship between admission blood glucose and POP occurrence. Patients with admission hyperglycemia had significantly higher rates of POP compared to normoglycemic patients, both before (13.2% vs. 4.8%) and after (10.1% vs. 5.8%) PSM. Admission hyperglycemia is an independent risk factor of POP (OR = 2.64, 95% CI: 1.42-4.92, p = 0.002). The association persisted after PSM(OR = 2.90, 95% CI: 1.35-3.86, p = 0.016). Additionally, higher blood glucose levels correlated with a greater likelihood of developing POP. A dose-response relationship was observed between blood glucose levels and the risk of POP. Non-diabetic group patients with hyperglycemia were at higher risk of POP than diabetic group patients with hyperglycemia. Finally, the relationship between hyperglycemia and increased POP risk is modulated and influenced by the ASA classification of the patient. Admission hyperglycemia is an independent risk factor for POP after hip fracture surgery in the elderly. There is a dose-response relationship between admission blood glucose and the occurrence of POP, which is more significant in non-diabetic patients than diabetic patients.

An intelligent insulin delivery system targeting intestinal absorption and glucose responsiveness can enhance the bioavailability through oral insulin therapy, offering promising diabetes treatment. In this paper, a glucose and pH dual-response polymer hydrogel using carboxymethyl agarose modified with 3-amino-phenylboronic acid and l-valine (CPL) was developed as an insulin delivery carrier, exhibiting excellent biocompatibility and effective insulin encapsulation. The insulin encapsulated in the hydrogel (Ins-CPL) was released in a controlled manner in response to the in vivo stimulation of blood glucose and pH levels with higher levels of intracellular uptake and utilization of insulin in the intestinal environment simultaneously. Notably, the Ins-CPL hydrogel effectively regulated blood sugar in diabetic rats over a long period by simulating endogenous insulin, responding to changes in plasma pH and glucose levels, and overcoming the intestinal epithelium barrier. This indicates a significant boost in oral insulin bioavailability and broadens its application prospects.

Gestational metabolic diseases adversely impact the health of pregnant persons and their offspring. Pregnant persons of color are impacted disproportionately by gestational metabolic disease, highlighting the need to identify additional risk factors contributing to racial-ethnic pregnancy-related health disparities. Trauma exposure and posttraumatic stress disorder (PTSD) are associated with increased risk for cardiometabolic disorders in nonpregnant persons, making them important factors to consider when identifying contributors to gestational metabolic morbidity and mortality health disparities. Here, we review current literature investigating trauma exposure and posttraumatic stress disorder as psychosocial risk factors for gestational metabolic disorders, inclusive of gestational diabetes, low birth weight and fetal growth restriction, gestational hypertension, and preeclampsia. We also discuss the physiological mechanisms by which trauma and PTSD may contribute to gestational metabolic disorders. Ultimately, understanding the biological underpinnings of how trauma and PTSD, which disproportionately impact people of color, influence risk for gestational metabolic dysfunction is critical to developing therapeutic interventions that reduce complications arising from gestational metabolic disease. KEY POINTS: · Gestational metabolic diseases disproportionately impact the health of pregnant persons of color.. · Trauma and PTSD are associated with increased risk for cardiometabolic disorders in nonpregnant per.. · Trauma and PTSD impact physiological cardiometabolic mechanisms implicated in gestational metabolic..

Stress-induced hyperglycemia (SIH) is associated with poor outcomes in cardiogenic shock (CS), and there have been inconsistent results among patients with or without diabetes mellitus (DM). The glycemic gap (GG) is derived by subtracting A1c-derived average glucose from blood glucose levels; it is a superior indicator of SIH. We aimed to explore the role of GG in the outcomes of patients with CS.

Data on patients diagnosed with CS were extracted from the MIMIC-IV v2.0 database to investigate the relationship between GG and 30-day mortality (Number of absolute GG subjects = 359; Number of relative GG subjects = 357). CS patients from the Second Affiliated Hospital of Wenzhou Medical University were enrolled to explore the correlation between GG and lactic acid (Number of absolute GG subjects = 252; Number of relative GG subjects = 251). Multivariate analysis, propensity score-matched (PSM) analysis, inverse probability treatment weighting (IPTW), and Pearson correlation analysis were applied.

Absolute GG was associated with 30-day all-cause mortality in CS patients (HRadjusted: 1.779 95% CI: 1.137-2.783; HRPSM: 1.954 95% CI: 1.186-3.220; HRIPTW: 1.634 95% CI: 1.213-2.202). The higher the absolute GG level, the higher the lactic acid level (βadjusted: 1.448 95% CI: 0.474-2.423). A similar trend existed in relative GG (HRadjusted: 1.562 95% CI: 1.003-2.432; HRPSM: 1.790 95% CI: 1.127-2.845; HRIPTW: 1.740 95% CI: 1.287-2.352; βadjusted:1.294 95% CI: 0.369-2.219). Subgroup analysis showed that the relationship existed irrespective of DM. The area under the curve of GG combined with the Glasgow Coma Scale (GCS) for 30-day all-cause mortality was higher than that of GCS (absolute GG: 0.689 vs. 0.637; relative GG: 0.688 vs. 0.633). GG was positively related to the triglyceride-glucose index. Kaplan-Meier curves revealed that groups of higher GG with DM had the worst outcomes. The outcomes differed among races and GG levels (all P < 0.05).

Among patients with CS, absolute and relative GGs were associated with increased 30-day all-cause mortality, regardless of DM. The relationship was stable after multivariate Cox regression analysis, PSM, and IPTW analysis. Furthermore, they reflect the severity of CS to some extent. Hyperlactatemia and insulin resistance may underlie the relationship between stress-induced hyperglycemia and poor outcomes in CS patients. They both improve the predictive efficacy of the GCS.

Stress-induced hyperglycemia (SIH) and malnutrition are common in trauma patients and are linked to worse outcomes. This study examined the influence of nutritional status, determined by the Geriatric Nutritional Risk Index (GNRI), on the incidence of SIH in trauma patients.

A retrospective analysis was conducted on adult trauma patients admitted to a Level I trauma center from 1 January 2009 to December 31, 2021. Patients were categorized into four groups: SIH, diabetic hyperglycemia (DH), diabetic normoglycemia (DN), and non-diabetic normoglycemia (NDN). Nutritional status was assessed using GNRI: high risk (GNRI < 82), moderate risk (82 ≤ GNRI < 92), low risk (92 ≤ GNRI ≤ 98), and no risk (GNRI > 98). Incidence of SIH and outcomes were analyzed across GNRI groups.

SIH was associated with higher mortality across all GNRI groups compared to NDN, with the highest rate (45.7%) in the high-risk group. Mortality decreased as GNRI increased in all glucose groups. NDN patients had the lowest mortality rates across GNRI groups. There was no correlation between GNRI and SIH incidence (p = 0.259).

SIH significantly influenced mortality across all nutritional status groups, with the highest impact in malnourished patients. Although malnutrition did not affect SIH incidence, both SIH and poor nutritional status independently contributed to worse trauma outcomes. Targeted management of hyperglycemia and nutritional deficiencies is crucial for improving survival.

Everyone knows that an infection can make you feel sick. Although we perceive infection-induced changes in metabolism as a pathology, they are a part of a carefully regulated process that depends on tissue-specific interactions between the immune system and organs involved in the regulation of systemic homeostasis. Immune-mediated changes in homeostatic parameters lead to altered production and uptake of nutrients in circulation, which modifies the metabolic rate of key organs. This is what we experience as being sick. The purpose of sickness metabolism is to generate a metabolic environment in which the body is optimally able to fight infection while denying vital nutrients for the replication of pathogens. Sickness metabolism depends on tissue-specific immune cells, which mediate responses tailored to the nature and magnitude of the threat. As an infection increases in severity, so do the number and type of immune cells involved and the level to which organs are affected, which dictates the degree to which we feel sick. Interestingly, many alterations associated with metabolic disease appear to overlap with immune-mediated changes observed following infection. Targeting processes involving tissue-specific interactions between activated immune cells and metabolic organs therefore holds great potential for treating both people with severe infection and those with metabolic disease. In this review, we will discuss how the immune system communicates in situ with organs involved in the regulation of homeostasis and how this communication is impacted by infection.

The objective of this work is to develop a highly miniaturized, low-power, biosensing platform for continuous glucose monitoring (CGM). This platform is based on an application-specific integrated circuit (ASIC) chip that interfaces with an amperometric glucose-sensing element. To reduce both size and power requirements, this custom ASIC chip was implemented using 65-nm complementary metal oxide semiconductor (CMOS) technology node. Interfacing this chip to a frequency-counting microprocessor with storage capabilities, a miniaturized transcutaneous CGM system can be constructed for small laboratory animals, with long battery life.

A 0.45 mm × 1.12 mm custom ASIC chip was first designed and implemented using the Taiwan Semiconductor Manufacturing Company (TSMC) 65-nm CMOS technology node. This ASIC chip was then interfaced with a multi-layer amperometric glucose-sensing element and a frequency-counting microprocessor with storage capabilities. Variation in glucose levels generates a linear increase in frequency response of this ASIC chip. In vivo experiments were conducted in healthy Sprague Dawley rats.

This highly miniaturized, 65-nm custom ASIC chip has an overall power consumption of circa 36 µW. In vitro testing shows that this ASIC chip produces a linear (R2 = 99.5) frequency response to varying glucose levels (from 2 to 25 mM), with a sensitivity of 1278 Hz/mM. In vivo testing in unrestrained healthy rats demonstrated long-term CGM (six days/per charge) with rapid glucose response to glycemic variations induced by isoflurane anesthesia and tail vein injection.

The miniature footprint of the biosensor platform, together with its low-power consumption, renders this CMOS ASIC chip a versatile platform for a variety of highly miniaturized devices, intended to improve the quality of life of patients with type 1 and type 2 diabetes.

There have been many developments in diabetes technology in recent years, with continuous glucose monitoring (CGM), insulin pump therapy (CSII) and automated insulin delivery (AID) becoming progressively accepted in outpatient diabetes care. However, the use of such advanced diabetes technology in the inpatient setting is still limited for several reasons, including logistical challenges and staff training needs. On the other hand, hospital settings with altered diet and stress-induced hyperglycemia often pose challenges to tight glycemic control using conventional treatment tools. Integrating smarter glucose monitoring and insulin delivery devices into the increasingly technical hospital environment could reduce diabetes-related morbidity and mortality. This narrative review describes the most recent literature on the use of diabetes technology in the hospital and suggests avenues for further research.

Advanced diabetes technology has the potential to improve glycemic control in hospitalized people with and without diabetes, and could add particular value in certain conditions, such as nutrition therapy or perioperative management. Taken together, CGM allows for more accurate and patient-friendly follow-up and ad hoc titration of therapy. AID may also provide benefits, including improved glycemic control and reduced nursing workload. Before advanced diabetes technology can be used on a large scale in the hospital, further research is needed on efficacy, accuracy and safety, while implementation factors such as cost and staff training must also be overcome.

Postoperative urinary tract infections (UTIs) worsen the prognosis of elderly patients with hip fractures. This study aimed to assess the predictive ability of blood-based biomarkers, specifically the glucose-albumin ratio (GAR), in predicting postoperative UTIs.

A retrospective observational study of 1,231 patients from a Level I trauma center was conducted. We evaluated the prognostic and predictive value of 15 biomarkers, including the glucose-albumin ratio, in elderly patients with hip fractures. The primary outcome measure was the incidence of postoperative UTIs.

The glucose to albumin ratio transformed into GAR was superior to any other biomarker in predicting postoperative UTIs in elderly hip fracture patients (AUC = 0.756, p < 0.001). Elevated GAR (using the best cut-off value of 0.18) was independently associated with postoperative UTIs (OR 3.20, 95% CI 2.23-4.58). Further analysis dividing GAR levels into four groups according to quartiles showed that compared to patients with GAR levels of Q1 (< 0.14), GAR levels of Q2 (0.14-0.17; OR 2.11, 95% CI 1.07-4.15), Q3 (0.17-0.21; OR 3.36, 95% CI 1.74-6.52) and Q4 (> 0.21; OR 7.55, 95% CI 3.84-14.83) patients had significantly higher odds of UTIs.

GAR holds potential as a novel biomarker for predicting postoperative UTIs in elderly patients with hip fractures.

There is limited evidence evaluating the impact of insulin treatment strategies on glucose variability in critically ill patients without preexisting diabetes.

Compare basal plus insulin (BPI) and sliding scale insulin (SSI) impact on glycemic control outcomes in critically ill patients without preexisting diabetes experiencing hyperglycemia.

This multicenter, retrospective review analyzed critically ill patients with hyperglycemia who received either BPI or SSI. Patients with a hemoglobin A1C >6.5% during the admission of interest or in the previous 3 months, or a diagnosis of diabetes at the time of discharge were excluded. The primary outcome was glucose variability during the intensive care unit (ICU) admission. Secondary outcomes included hypoglycemia frequency, frequency of goal glucose levels, mortality, and length of stay.

The analysis included 228 patients (39 in BPI, 189 in SSI). Average glucose variability was higher in the BPI group compared with the SSI group (85.8 mg/dL ± 33.1 vs 70.2 mg/dL ± 30.7; P = 0.009), which remained when controlling for baseline confounding (-12.1 [5.6], 95% CI -23.2 to -0.99; P = 0.033). Hypoglycemia incidence was similar between groups. BPI patients had a lower incidence of glucose values within goal range than SSI patients (P = 0.046). There was no difference in length of stay or hospital mortality.

The use of SSI compared with a BPI regimen may result in reduced glycemic variability in critically ill patients without preexisting diabetes. Future prospective studies, with a larger sample size, are warranted to confirm our exploratory findings and characterize clinically significant benefits.

The circadian timing system coordinates daily cycles in physiological functions, including glucose metabolism and insulin sensitivity. Here, the aim was to characterise the 24-h variation in glucose levels in critically ill patients during continuous enteral nutrition after controlling for potential sources of bias.

Time-stamped clinical data from adult patients who stayed in the Intensive Care Unit (ICU) for at least 4 days and received enteral nutrition were extracted from the Medical Information Mart for Intensive Care (MIMIC)-IV database. Linear mixed-effects and XGBoost modelling were used to determine the effect of time of day on blood glucose values.

In total, 207,647 glucose measurements collected during enteral nutrition were available from 6,929 ICU patients (3,948 males and 2,981 females). Using linear mixed-effects modelling, time of day had a significant effect on blood glucose levels (p < 0.001), with a peak of 9.6 [9.5-9.6; estimated marginal means, 95% CI] mmol/L at 10:00 in the morning and a trough of 8.6 [8.5-8.6] mmol/L at 02:00 at night. A similar impact of time of day on glucose levels was found with the XGBoost regression model.

These results revealed marked 24-h variation in glucose levels in ICU patients even during continuous enteral nutrition. This 24-h pattern persists after adjustment for potential sources of bias, suggesting it may be the result of endogenous biological rhythmicity.

This work was supported by a VENI grant from the Netherlands Organisation for Health Research and Development (ZonMw), an institutional project grant, and by the Dutch Research Council (NWO).

Background and Objectives: The risk of developing glycemic dysregulation up to overt diabetes mellitus (DM) after an episode of acute pancreatitis (AP) is increasingly being analyzed. We aimed to assess the changes in serum glucose levels associated with the first episode of AP, as well as the impact of dysglycemia on outcomes such as the severity of inflammation, the length of hospitalization, mortality, and the persistence of hyperglycemia at follow-up. Materials and Methods: All patients experiencing their first episode of AP, who presented to the Emergency Room (ER) between 1 January 2020 and 31 December 2023, were retrospectively included. On-admission serum glucose and peak serum glucose during hospitalization were the biological markers used to assess glucose metabolism impairment, and they were correlated with outcomes of AP. Results: Our study included 240 patients, 46.67% (112 patients) having a biliary etiology for an AP flare. Patients with COVID-19-associated AP exhibited the highest on-admission and peak serum glucose levels (244.25 mg/dL and 305.5 mg/dL, respectively). A longer hospital stay was noted in patients with peak serum glucose levels of ≥100 mg/dL (9.49 days) compared to normoglycemic patients (6.53 days). Both on-admission and peak glucose levels were associated with elevated CRP levels during hospitalization. A total of 83.78% of patients who received antibiotics exhibited on-admission hyperglycemia, and 72.07% had peak serum glucose levels of ≥100 mg/dL. The presence of hyperglycemia at follow-up was associated with both on-admission and peak serum glucose levels of ≥100 mg/dL, as well as with a longer stay, higher CRP levels, and antibiotic use during index admission. Conclusions: On-admission hyperglycemia predicts a higher inflammatory response in patients at the first episode of AP, while the presence of hyperglycemia during hospitalization is associated with imaging and biological severity and longer hospitalizations, indicating a more severe disease course. Both on-admission and peak in-hospital hyperglycemia were identified as risk factors for sustained hyperglycemia at follow-up.

Type 2 Diabetes Mellitus (T2DM) presents a significant healthcare challenge, with considerable economic ramifications. While blood glucose management and long-term metabolic target setting for home care and outpatient treatment follow established procedures, the approach for short-term targets during hospitalization varies due to a lack of clinical consensus. Our study aims to elucidate the impact of pre-hospitalization and intra-hospitalization glycemic indexes on in-hospital survival rates in individuals with T2DM, addressing this notable gap in the current literature.

In this pilot study involving 120 hospitalized diabetic patients, we used advanced machine learning and classical statistical methods to identify variables for predicting hospitalization outcomes. We first developed a 30-day mortality risk classifier leveraging AdaBoost-FAS, a state-of-the-art ensemble machine learning method for tabular data. We then analyzed the feature relevance to identify the key predictive variables among the glycemic and routine clinical variables the model bases its predictions on. Next, we conducted detailed statistical analyses to shed light on the relationship between such variables and mortality risk. Finally, based on such analyses, we introduced a novel index, the ratio of intra-hospital glycemic variability to pre-hospitalization glycemic mean, to better characterize and stratify the diabetic population.

Our findings underscore the importance of personalized approaches to glycemic management during hospitalization. The introduced index, alongside advanced predictive modeling, provides valuable insights for optimizing patient care. In particular, together with in-hospital glycemic variability, it is able to discriminate between patients with higher and lower mortality rates, highlighting the importance of tightly controlling not only pre-hospital but also in-hospital glycemic levels.

Despite the pilot nature and modest sample size, this study marks the beginning of exploration into personalized glycemic control for hospitalized patients with T2DM. Pre-hospital blood glucose levels and related variables derived from it can serve as biomarkers for all-cause mortality during hospitalization.

Despite advancements in pediatric burn care, the profound hypermetabolic response associated with severe burns remains a multifaceted challenge throughout the continuum of care. Understanding the various physiologic disturbances that constitute hypermetabolism is crucial for a thorough evaluation and for implementing appropriate surgical and nonsurgical interventions. In this article, we describe the pathophysiology and treatment of hypermetabolism in pediatric burn patients with a focus on reducing resting energy requirements, minimizing infection, and optimizing nutrition for patients undergoing frequent surgical intervention.

Introduction: Hypertension is a prevalent condition in the United States and leads to an increased risk of developing various comorbidities. However, the impact of new-onset hypertension after severe burns on patient outcomes is not known. We posit that hypertension onset after severe burn is associated with increased risk of developing comorbidities and mortality. Methods: Using the TriNetX database, burned patients diagnosed with essential hypertension after injury were compared with those who did not develop hypertension; neither had prior hypertension. Each cohort was grouped by sex, percent total body surface area (TBSA) burned, and age, then propensity matched for sex, race, ethnicity, and laboratory values. Outcomes assessed were acute kidney injury (AKI), hyperglycemia, heart failure, myocardial infarction (MI), and death. Results: Those diagnosed with hypertension after severe burn were 4.9 times more likely to develop AKI, 3.6 times for hyperglycemia, 5.3 times for heart failure, 4.7 times for acute MI, and 1.5 times for mortality. Sex analysis shows that men were at greater risk for AKI (1.5 times), heart failure (1.1 times), and death (1.4 times). Women were 1.3 times more likely to develop hyperglycemia. Percent TBSA burned grouping showed increased risk for all outcomes with increasing severity. Age grouping indicated an elevated risk of developing AKI, heart failure, acute MI, and death. Conclusion: New-onset hypertension diagnosis in severely burned patients is associated with acute kidney injury, heart failure, acute MI, and death. Overall, males, older patients, and those with a higher % TBSA burned are at a higher risk of developing these comorbidities.

The Chinese Society of Critical Care Medicine (CSCCM) has developed clinical practice guidelines for nutrition assessment and monitoring for patients in adult intensive care units (ICUs) in China. This guideline focuses on nutrition evaluation and metabolic monitoring to achieve optimal and personalized nutrition therapy for critically ill patients. This guideline was developed by experts in critical care medicine and evidence-based medicine methodology and was developed after a thorough review of the system and a summary of relevant trials or studies published from 2000 to July 2023. A total of 18 recommendations were formed and consensus was reached through discussions and reviews by expert groups in critical care medicine, parenteral and enteral nutrition, and surgery. The recommendations are based on currently available evidence and cover several key fields, including screening and assessment, evaluation and assessment of enteral feeding intolerance, metabolic and nutritional measurement and monitoring during nutrition therapy, and organ function evaluation related to nutrition supply. Each question was analyzed according to the Population, Intervention, Comparison, and Outcome (PICO) principle. In addition, interpretations were provided for four questions that did not reach a consensus but may have potential clinical and research value. The plan is to update this nutrition assessment and monitoring guideline using the international guideline update method within 3-5 years.

Stress hyperglycaemia occur often in critically injured patients. To gain new consideration about it, this review compile current as well as known immunological and biochemical findings about causes and emergence.

Glucose is the preferred energy substrate for fending immune cells, reparative tissue and the cardiovascular system following trauma. To fulfil these energy needs, the liver is metabolically reprogrammed to rebuild glucose from lactate and glucogenic amino acids (hepatic insulin resistance) at the expenses of muscles mass and - to a less extent - fat tissue (proteolysis, lipolysis, peripheral insulin resistance). This inevitably leads to stress hyperglycaemia, which is evolutionary preserved and seems to be an essential and beneficial survival response. It is initiated by damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs), intensified by immune cells itself and mainly ruled by tumour necrosis factor (TNF)α and catecholamines with lactate and hypoxia inducible factor (HIF)-1α as intracellular signals and lactate as an energy shuttle. Important biochemical mechanisms involved in this response are the Warburg effect as an efficient metabolic shortcut and the extended Cori cycle.

Stress hyperglycaemia is beneficial in an acute life-threatening situation, but further research is necessary, to prevent trauma patients from the detrimental effects of persisting hyperglycaemia.

The purpose of this study was to examine associations of serum phosphate levels with mortality, target organ damage and length of hospital stay in adults with infectious diseases hospitalized outside of the intensive care unit.

This nationwide retrospective cohort study comprised patients admitted with infections, to medical and surgical departments in eight tertiary hospitals during 2001-2020. The main exposure variable was the first serum phosphate levels at admission (up to 1 week). The analysis included multivariable logistic regression models and quantile regression.

Of 126,088 patients (49% males, mean age: 69.3 years), 24,809 (19.7%) had decreased phosphate levels, 92,730 (73.5%) normal phosphate levels, and 8,549 (6.8%) elevated phosphate levels on admission. Overall- and in-hospital mortality rates were highest among those with hyperphosphatemia (74.5 and 16.4%, respectively), followed by those with normophosphatemia (57.0 and 6.6%), and lastly the hypophosphatemia group (48.7 and 5.6%); p < 0.001 for all. After adjusting for confounders, the lowest predicted mortality rate was observed in the normophosphatemia group. In the multivariable model, hyperphosphatemia conferred a higher probability of target organ damage (OR [95% CI]: 2.43 [2.06-2.86]), while moderate hypophosphatemia conferred a lower probability (OR [95% CI]: 0.73 [0.65-0.82]), compared to normal phosphate levels and extreme hypophosphatemia showed a non-significant association (OR [95% CI]: 0.87 [0.57-1.28]). The associations were independent of renal failure. In a multivariable model, hyperphosphatemia was associated with a slight increase of 0.33 days in length of stay compared to normal phosphate levels.

A J-shaped relation was found between phosphate levels and prognosis in patients hospitalized with infectious diseases, regardless of their renal function.

This article tells the story of our long search for the answer to one question: Is stress hyperglycemia in critically ill patients adaptive or maladaptive? Our earlier work had suggested the lack of hepatic insulin effect and hyperglycemia as jointly predicting poor outcome. Therefore, we hypothesized that insulin infusion to reach normoglycemia, tight glucose control, improves outcome. In three randomized controlled trials (RCTs), we found morbidity and mortality benefit with tight glucose control. Moving from the bed to the bench, we attributed benefits to the prevention of glucose toxicity in cells taking up glucose in an insulin-independent, glucose concentration gradient-dependent manner, counteracted rather than synergized by insulin. Several subsequent RCTs did not confirm benefit, and the large Normoglycemia in Intensive Care Evaluation-Survival Using Glucose Algorithm Regulation, or "NICE-SUGAR," trial found increased mortality with tight glucose control associated with severe hypoglycemia. Our subsequent clinical and mechanistic research revealed that early use of parenteral nutrition, the context of our initial RCTs, had been a confounder. Early parenteral nutrition (early-PN) aggravated hyperglycemia, suppressed vital cell damage removal, and hampered recovery. Therefore, in our next and largest "TGC-fast" RCT, we retested our hypothesis, without the use of early-PN and with a computer algorithm for tight glucose control that avoided severe hypoglycemia. In this trial, tight glucose control prevented kidney and liver damage, though with much smaller effect sizes than in our initial RCTs without affecting mortality. Our quest ends with the strong recommendation to omit early-PN for patients in the ICU, as this reduces need of blood glucose control and allows cellular housekeeping systems to play evolutionary selected roles in the recovery process. Once again, less is more in critical care.

The effect of diabetes mellitus (DM) on the incidence of postoperative wound complications in patients with coronary artery bypass grafting (CABG) is still unclear. Thus, we performed a meta-analysis of CABG in DM patients to evaluate existing data from both prospective and historical cohorts. The objective of this trial was to assess the relevance and extent of the effect of diabetes on the outcome of previous CABG procedures. Data sources like Embase and Pubmed were found throughout the research, and the language was limited to English through manual search. The searches were performed up to August 2023. The data were extracted from the study of the inclusion/exclusion criteria, the features of the population, the statistical approach and the clinical results. A qualitative evaluation of the qualifying studies has been carried out. Out of the 1874 studies identified, 21 cohort studies were chosen for analysis. Meta-analyses were performed in 258 454 patients (71 351 diabetic and 187 103 non-diabetic). Twenty-one studies on deep sternal wound infections in CABG patients showed a lower rate of deep sternal wound infections in non-diabetes group compared with those with diabetes (OR, 2.13; 95% CI: 1.97, 2.31, p < 0.00001). And 16 studies of superficial wound infections in patients undergoing CABG were found to be associated with a lower rate of superficial injury (OR, 1.93; 95% CI: 1.53, 2.43, p < 0.00001) compared with those with diabetes; In five trials, perfusion time during CABG (MD, 2.31; 95% CI: -0.16, 4.79, p = 0.07) was observed, and there were no significant differences between diabetes and non-diabetes. Currently, there is a higher risk for CABG in diabetes than in non-diabetes patients with sternal infections and superficial injuries. Future randomized trials will concentrate on the treatment of such perioperatively related complications, which will lower the risk of postoperative wound infection in diabetes.

Syphilis, an infectious disease caused by the spirochete Treponema pallidum, represents a pervasive global epidemic. Secondary syphilis is typically marked by the emergence of highly contagious mucocutaneous manifestations, including non-pruritic rashes on the palms and soles of the feet, alopecia, mucous patches, and condyloma lata. Here, we report a rare case of a 30-year-old male with newly discovered type 2 diabetes mellitus who presented with severe odynophagia due to secondary syphilis, confirmed by both nontreponemal VDRL/RPR and treponemal TPHA tests. Following the administration of a single-dose intramuscular injection of benzathine penicillin G 2.4 million units, the symptoms gradually decreased, allowing the patient to regain his health.

Hypoglycemia has not been previously reported as a postoperative complication of mitral valve repair (MVR) in dogs; however, the authors have encountered cases of hypoglycemia after MVR. This study aimed to determine the incidence of hypoglycemia in dogs after MVR and investigate its causes. Blood glucose levels were measured at multiple timepoints in dogs undergoing MVR. Simultaneously, insulin and glucagon blood concentrations in dogs with hypoglycemia preoperatively and postoperatively were compared to verify the physiological responses to hypoglycemia. Furthermore, risk factors for hypoglycemia, using variables selected based on the characteristics of MVR and dogs undergoing MVR, were examined prospectively. The incidence of hypoglycemia after MVR was 14.2%, and plasma glucagon concentrations increased in these dogs (mean: 260 pg/mL and 644 pg/mL pre- and postoperatively, p < 0.001), whereas serum insulin concentrations decreased (median: 0.50 ng/mL and 0.29 ng/mL pre- and postoperatively, p = 0.002). Therefore, hyperinsulinemia or hypoglucagonemia is unlikely to be the cause of postoperative hypoglycemia. The identified risk factors for hypoglycemia included low body weight and asymptomatic myxomatous mitral valve disease. Monitoring blood glucose levels after MVR should be included in the standard hospitalization plan to prevent hypoglycemic emergencies in dogs.

Despite known risks of hyperglycemia on postoperative complications, the influence of intraoperative dexamethasone on blood glucose has yet to be evaluated within the diabetic limb salvage population. This study aimed to assess the effect of intraoperative dexamethasone on postoperative blood glucose in diabetic patients undergoing atraumatic major lower extremity amputations. A single-center retrospective review of diabetic patients undergoing below-knee amputation between January 2017 and December 2022 was performed. Blood glucose levels for the 5 days before and after amputation were recorded and compared with the primary endpoints of postoperative hyperglycemia (>200 mg/dL) and glucose variability (>200 mg/dL). Cohorts were divided by patients who did and did not receive intraoperative administration of dexamethasone. Three hundred eighty-one were screened for eligibility with 180 patients included. Of these, 50 patients received dexamethasone intraoperatively (38.5%). Average pre- and postoperative blood glucose, rate of pre- and postoperative hyperglycemia, perioperative glucose variability, and postoperative dehiscence and infection were comparable between cohorts. On multivariate analysis, intraoperative administration of dexamethasone was not associated with postoperative hyperglycemia (p = .104) or perioperative blood glucose variability > 200 mg/dL (p = .334). Perioperative blood glucose variability > 200 mg/dL was associated with higher odds of surgical site infection (SSI) (odds ratio 5.12, p = .003). Administration of intravenous dexamethasone to diabetic patients undergoing below-knee amputation is not associated with postoperative hyperglycemia or complications. This study confirms previous findings that high glucose is a predictor of SSI. Concerted effort by a multidisciplinary team to attain tight glycemic control is critical to optimizing healing.

Hyperglycemia is widespread in the world's population, increasing the risk of many diseases. This study aimed to explore the regulatory effect and mechanism of astragaloside IV (ASIV)-mediated endothelial progenitor cells (EPCs) exosomal LINC01963 in endothelial cells (HUVECs) impaired by high glucose.

Morphologies of exosomes were observed by light microscope and electron microscope. Immunofluorescence was used to identify EPCs and detect the expressions of caspase-1. LINC01963 was detected by quantitative reverse transcription PCR. NLRP3, ASC, and caspase-3 were detected by Western Blot. Nanoparticle tracking analysis was carried out to analyze the exosome diameter. High-throughput sequencing was applied to screen target lncRNAs. The proliferation of endothelial cells was measured by cell counting kit-8 assay. The apoptosis level of HUVECs was detected by flow cytometry and TdT-mediated dUTP Nick-End labeling. The levels of IL- 1β, IL-18, ROS, SOD, MDA, and LDH were measured by enzyme-linked immunosorbent assay.

ASIV could promote the secretion of the EPC exosome. LINC01963 was obtained by high-throughput sequencing. It was observed that high glucose could inhibit the proliferation, reduce the level of SOD, the expression of NLRP3, ASC, and caspase- 1, increase the levels of IL-1β, IL-18, ROS, MDA, and LDH, and promote apoptosis of HUVECs. Whereas LINC01963 could inhibit the apoptosis of HUVECs, the increase the expression of NLRP3, ASC, and caspase-1, and decrease the levels of IL-1β, IL-18, ROS, MDA, and LDH.

EPCs exosomal LINC01963 play an inhibitory role in high glucoseinduced pyroptosis and oxidative stress of HUVECs. This study provides new ideas and directions for treating hyperglycemia and researching exosomal lncRNAs.

This paper reports a sensor architecture for continuous monitoring of biomarkers directly in the blood, especially for ICU/CCU patients requiring critical care and rapid biomarker measurement. The sensor is based on a simple optical fiber that can be inserted through a catheter into the bloodstream, wherein gold nanoparticles are attached at its far distal end as a plasmonic material for highly sensitive opto-chemical sensing of target biomolecules (glucose in our application) via the excitation of surface plasmon polaritons. For specificity, the nanoparticles are functionalized with a specific receptor enzyme that enables the localized surface plasmon resonance (LSPR)-based targeted bio-sensing. Further, a micro dialysis probe is introduced in the proposed architecture, which facilitates continuous monitoring for an extended period without fouling the sensor surface with cells and blood debris present in whole blood, leading to prolonged enhanced sensitivity and limit of detection, relative to existing state-of-the-art continuous monitoring devices that can conduct direct measurements in blood. To establish this proof-of-concept, we tested the sensor device to monitor glucose in-vivo involving an animal model, where continuous monitoring was done directly in the circulation of living rats. The sensor's sensitivity to glucose was found to be 0.0354 a.u./mg.dl-1 with a detection limit of 50.89 mg/dl.