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This study aims to investigate the association between lactate trajectories and the risk of acute kidney injury (AKI) and hospital mortality in patients with hyperlactatemia. We conducted a multicenter retrospective study using data from three independent cohorts. By the lactate levels during the first 48 h of ICU admission, patients were classified into distinct lactate trajectories using group-based trajectory modeling (GBTM) method. The primary outcomes were AKI incidence and hospital mortality. Logistic regression analysis assessed the association between lactate trajectories and clinical outcomes, with adjusting potential confounders. Patients were divided into three trajectories: mild hyperlactatemia with rapid recovery (Traj-1), severe hyperlactatemia with gradual recovery (Traj-2), and severe hyperlactatemia with persistence (Traj-3). Traj-3 was an independent risk factor of both hospital mortality (all  < 0.001) and AKI development (all  < 0.001). Notably, Traj-2 was also associated with increased risk of mortality and AKI development (all  < 0.05) using Traj-1 as reference, except for the result in the Tianjin Medical University General Hospital (TMUGH) cohort for mortality in adjusted model (  = 0.123). Our finding was still robust in subgroup and sensitivity analysis. In the combination cohort, both Traj-2 and Traj-3 were considered as independent risk factor for hospital mortality and AKI development (all  < 0.001). When compared with the Traj-3, Traj-2 was only significantly associated with the decreased risk of hospital mortality (OR 0.17, 95% CI 0.14-0.20,  < 0.001), but no with the likelihood of AKI development (OR 0.90, 95% CI 0.77-1.05,  = 0.172). Lactate trajectories provide valuable information for predicting AKI and mortality in critically ill patients.

Background Hyperlactatemia is common in intensive care unit (ICU) patients. The aim of our retrospective observational study was to analyse the impact of serum lactate on admission on mortality in patients with acute kidney injury (AKI) treated with renal replacement therapy (RRT). Methods During the study period of 4 years, 2939 patients were admitted to the ICU, 503 patients were diagnosed with AKI and 209 of them required RRT. After excluding patients on chronic dialysis and with known malignant disease, we retrospectively analysed 154 patients. Hyperlactatemia was defined as a serum lactate concentration above 4 mmol/L on admission to the ICU. Results The mean age of patients was 62.8 years, and 69.5% were men. The mean Charlson Comorbidity Index (CCI) on admission to the ICU was 3.7 and fifty-six (36.4%) patients had acute hyperlactatemia. All included patients had AKI stage 3 and were treated with RRT, 125 (81.2%) with continuous RRT and 29 (18.8%) with intermittent hemodialysis. The mean length of stay in the ICU was 15.7 ± 13 days and 118 (76.6%) patients died during the 60-day observation period. A Kaplan-Meier survival analysis showed that the survival rate was statistically significantly lower in the group of patients with hyperlactatemia (log-rank; p  = 0.032). The univariate Cox regression analysis showed that serum lactate on admission to the ICU significantly predict 60-day survival (HR 1.075; 95%CI 1.015–1.140; p  = 0.014). In the multivariate Cox regression analysis, which included age, gender, diabetes, hypertension, chronic kidney disease, estimated glomerular filtration rate, serum lactate, CCI and C-reactive protein, only age (HR 1.031; 95%CI 1.007–1.056; p  = 0.011) and serum lactate (HR 1.067; 95%CI 1.004–1.134; p  = 0.035) were independent predictors of mortality. Conclusion Our study underscores the independent association between hyperlactatemia of more than 4 mmol/L on admission to the ICU and increased 60-day mortality in patients with AKI treated with RRT. These findings, which have significant implications for the management and prognosis of critically ill patients with AKI, provide a new understanding of the role of serum lactate in patient outcomes. Trial registration Name of the registry: ClinicalTrials.gov; Trial registration number: NCT06565403; Date of registration, followed by the words 'Retrospectively registered': August, 19,2024; URL of trial registry record: https://clinicaltrials.gov/study/NCT06565403.

The nadir hematocrit (HCT) on cardiopulmonary bypass (CPB) is a recognized independent risk factor for major morbidity and mortality in cardiac surgery. The main interpretation is that low levels of HCT on CPB result in a poor oxygen delivery and dysoxia of end organs. Hyperlactatemia (HL) is a marker of dysoxic metabolism, and is associated with bad outcomes in cardiac surgery. This study explores the relationship between nadir HCT on CPB and early postoperative HL. Retrospective study on 3,851 consecutive patients. Nadir HCT on CPB and other potential confounders were explored for association with blood lactate levels at the arrival in the Intensive Care Unit (ICU), and with the presence of moderate (2.1 - 6.0 mMol/L) or severe (> 6.0 mMol/L) HL. Nadir HCT on CPB demonstrated a significant negative association with blood lactate levels at the arrival in the ICU. After adjustment for the other confounders, the nadir HCT on CPB remained independently associated with moderate (odds ratio 0.96, 95% confidence interval 0.94-0.99) and severe HL (odds ratio 0.91, 95% confidence interval 0.86-0.97). Moderate and severe HL were significantly associated with increased morbidity and mortality. Hemodilution on CPB is an independent determinant of HL. This association, more evident for severe HL, strengthens the hypothesis that a poor oxygen delivery on CPB with consequent organ ischemia is the mechanism leading to hemodilution-associated bad outcomes.

Background Polymyxin B hemadsorption (PMX-HA) reduces blood endotoxin levels, but characteristics of patients with sepsis likely to benefit from PMX-HA are not well known. We sought to identify patient subgroups likely to benefit from PMX-HA. Methods We retrospectively identified 1911 patients with sepsis from a retrospective observational study in Japan (the JSEPTIC-DIC study) and 286 patients with endotoxemic septic shock from a randomized controlled trial in North America that restricted patients to those with high endotoxin activity (the EUPHRATES trial). We applied the machine learning-based causal forest model to the JSEPTIC-DIC cohort to investigate heterogeneity in treatment effects of PMX-HA on 28-day survival after adjusting for potential confounders and ascertain the best criteria for PMX-HA use. The derived criteria for targeted therapy by PMX-HA were validated using the EUPHRATES trial cohort. Results The causal forest model revealed heterogeneity in treatment effects of PMX-HA. Since patients having higher treatment effects were more likely to have severe coagulopathy and hyperlactatemia, we identified the potential treatment targets of PMX-HA as patients with PT-INR > 1.4 or lactate > 3 mmol/L. In the EUPHRATES trial cohort, PMX-HA use on the targeted subpopulation (75% of all patients) was significantly associated with higher 28-day survival (PMX-HA vs. control, 68% vs. 52%; treatment effect of PMX-HA, + 16% [95% CI + 2.2% to + 30%], p  = 0.02). Conclusions Abnormal coagulation and hyperlactatemia in septic patients with high endotoxin activity appear to be helpful to identify patients who may benefit most from PMX-HA. Our findings will inform enrollment criteria for future interventional trials targeting patients with coagulopathy and hyperlactatemia.

Background Hyperlactatemia may be caused by increased production due to tissue hypoxia or non-hypoxia. The aim of this study was first to identify risk factors for postoperative hyperlactatemia (POHL) after Stanford type A acute aortic dissection surgery (AADS) and construct a predictive model, and second to evaluate the impact of POHL on prognosis. Methods This retrospective study involved patients undergoing AADS from January 2016 to December 2019 in Wuhan Union Hospital. Multivariate logistic regression analysis was performed to identify independent risk factors for POHL. A nomogram predicting POHL was established based on these factors and was validated in the original dataset. The receiver operating characteristic curve was drawn to assess the ability of postoperative lactate levels to predict the in-hospital mortality. Results A total of 188 patients developed POHL after AADS (38.6%). Male gender, surgery history, red blood cell transfusion and cardiopulmonary bypass time were identified as independent predictors. The C-index of the prediction model for POHL was 0.72, indicating reasonable discrimination. The model was well calibrated by visual inspection and goodness-of-fit test (Hosmer–Lemeshow χ 2  = 10.25, P  = 0.25). Decision and clinical impact curves of the model showed good clinical utility. The overall in-hospital mortality rate was 10.1%. Postoperative lactate levels showed a moderate predictive power for postoperative in-hospital mortality (C-index: 0.72). Conclusion We developed and validated a prediction model for POHL in patients undergoing AADS, which may have clinical utility in personal risk evaluation and preventive interventions. The POHL could be a good predictor for in-hospital mortality.

[...]the duration of exposure to surgery was the factor most highly associated with hyperlactatemia. (d) Despite a similar DO2, haemoglobin values were lower for patients experiencing hyperlactatemia, suggesting a role for insufficient microvascular O2 delivery. (e) Finally, hyperlactatemia was associated with tissue acidosis and higher values for the venoarterial pCO2gap/arteriovenous O2 content difference ratio and respiratory exchange ratio, suggesting microvascular hypoperfusion with tissue metabolic uncoupling [4]. [...]hyperlactatemia may not only be explained by low blood flow but also by time-dependent surgical trauma with disturbances of microvascular O2 delivery, metabolic acidosis, and low arterial haemoglobin content. Lactate < 3 mmol l−1 N = 366 Lactate ≥ 3 mmol l−1 N = 68 p-value Clinical parameters Temperature, °C 35.8 ± 0.8 35.9 ± 0.8 0.54 Heart rate, bpm 73 [64–85] 86 [73–95] <0.001 MAP, mmHg 75 [69–85] 72 [66–81] 0.10 PPV, % 8 [5–11] 9 [6–13] 0.06 Cardiac index, l min−1 m−2 2.7 [2.3–3.5] 2.8 [1.9–3.4] 0.23 Respiratory exchange ratio 0.82 [0.75–0.94] 0.98 [0.80–1.21] <0.001 Systemic parameters PaO2, mmHg 158 [120–197] 177 [129–197] 0.11 PvO2, mmHg 58 [46–63] 59 [51–73] <0.001 PaCO2, mmHg 40 [37–44] 41 [37–46] 0.39 PvCO2, mmHg 46 [42–50] 46 [42–51] 0.71 PCO2gap, mmHg 5.7 [3.8–7.8] 5.8 [3.3–8.2] 0.66 CaO2, ml 16.2 [14.6–17.6] 14.8 [12.6–16.6] <0.001 CvO2, ml 13.2 [11.5–14.6] 12.4 [10.0–15.1] 0.08 DavO2, ml 2.9 [1.8–3.8] 2.2 [1.4–3.5] 0.008 pCO2gap/DavO2, mmHg ml−1 2.0 [1.2–3.3] 2.3 [1.7–4.6] 0.02 SaO2, % 99 [98–99] 99 [98–99] 0.14 SvO2, % 83.1 [77.1–88.5] 86.0 [81.7–91.2] 0.002 DO2, ml min−1 m−2 480 [374–672] 461 [310–865] 0.95 VO2, ml min−1 m−2 88 [51–136] 76 [33–143] 0.28 Arterial lactate, mmol l−1 1.3 [1.0–1.8] 3.9 [3.4–5.7] <0.001 Arterial Haemoglobin, g dl−1 11.7 ± 1.8 10.5 ± 2.1 <0.001 Acid basic balance Arterial pH 7.35 [7.31–7.39] 7.26 [7.22–7.33] <0.001 Venous pH 7.32 [7.28–7.35] 7.24 [7.19–7.30] <0.001 Arterial bicarbonates, mmol l−1 23.1 ± 2.6 19.7 ± 4.0 <0.001 Arterial base excess, mmol l−1 −2.7 [−4.5– –1.1] −7.4 [−9.9– –4.4] <0.001 Table 1 Comparison of clinical and biological parameters in the overall population according to the presence of hyperlactatemia.

PurposeThe aim of this study was to examine the effects of intravenous (IV) fluid restriction on time to resolution of hyperlactatemia in septic shock. Hyperlactatemia in sepsis is associated with worse outcome. Sepsis guidelines suggest targeting lactate clearance to guide fluid therapy despite the complexity of hyperlactatemia and the potential harm of fluid overload.MethodsWe conducted a post hoc analysis of serial plasma lactate concentrations in a sub-cohort of 777 patients from the international multicenter clinical CLASSIC trial (restriction of intravenous fluids in intensive care unit (ICU) patients with septic shock). Adult ICU patients with septic shock had been randomized to restrictive (n = 385) or standard (n = 392) intravenous fluid therapy. The primary outcome, time to resolution of hyperlactatemia, was analyzed with a competing-risks regression model. Death and discharge were competing outcomes, and administrative censoring was imposed 72 h after randomization if hyperlactatemia persisted. The regression analysis was adjusted for the same stratification variables and covariates as in the original CLASSIC trial analysis.ResultsThe hazard ratios (HRs) for the cumulative probability of resolution of hyperlactatemia, in the restrictive vs the standard group, in the unadjusted analysis, with time split, were 0.94 (confidence interval (CI) 0.78–1.14) at day 1 and 1.21 (0.89–1.65) at day 2–3. The adjusted analyses were consistent with the unadjusted results.ConclusionIn this post hoc retrospective analysis of a multicenter randomized controlled trial (RCT), a restrictive intravenous fluid strategy did not seem to affect the time to resolution of hyperlactatemia in adult ICU patients with septic shock.

Introduction: Vitamin B1 deficiency poses a significant risk of impaired consciousness, with manifestations ranging from anorexia and fatigue to severe neurological and cardiovascular disturbances. Wernicke’s encephalopathy, a neurological disorder stemming from vitamin B1 deficiency, presents as the triad of ophthalmoplegia, altered mental state, and cerebellar ataxia. However, these symptoms are not consistently present, complicating the diagnosis. In addition, subclinical vitamin B1 deficiency can progress unnoticed until severe complications arise. Studies indicate a high rate of undiagnosed cases, emphasizing the need for early detection and intervention. Case presentation: We present the case of a 65-year-old man in whom hyperlactatemia was incidentally detected, leading to the diagnosis of vitamin B1 deficiency. The patient, presenting with vertigo and vomiting, had been eating boxed lunches bought from convenience stores following the death of his wife 3 years earlier. Vertigo gradually improved with rest, but the persistence of hyperlactatemia prompted further investigation, revealing low vitamin B1 levels and high pyruvate levels. Treatment with dietary adjustments and supplements significantly improved his symptoms. Discussion: In this case, hyperlactatemia was found in a vertigo patient, revealing asymptomatic vitamin B1 deficiency. Elevated lactate is often linked with conditions like sepsis but can also stem from overlooked factors such as low vitamin B1 levels due to poor diet habits like consuming fried foods. Conclusion: This case highlights the importance of considering vitamin B1 deficiency in patients with unexplained hyperlactatemia, even in high-income countries. Early detection can prevent progression to the severe complications associated with Wernicke’s encephalopathy. Proactive measurement of lactate levels in at-risk populations may facilitate early diagnosis and intervention, ultimately improving patient outcomes.

Background Linezolid-induced hyperlactatemia may be masked by metabolic alkalosis, creating diagnostic challenges. This case demonstrates how acid–base disturbances can delay toxicity recognition in geriatric patients. Case presentation An 82-year-old Han Chinese woman with carbapenem-resistant  Acinetobacter baumannii  pneumonia developed severe hyperlactatemia (peak 17 mmol/L) during linezolid therapy (600 mg every 12 hours for 14 days). Despite progressive lactate elevation (1.6 → 17 mmol/L), alkalotic pH (7.45–7.51) and normal anion gap (8–12 mmol/L) obscured the diagnosis. Interventions Serial monitoring included arterial blood gas analysis and serum lactate levels. Linezolid was discontinued upon recognition of hyperlactatemia. Continuous renal replacement therapy was initiated post-discontinuation. Outcomes A lactate/HCO 3 − ratio > 0.17 (day 20) preceded metabolic decompensation by 5 days. Renal replacement failed to correct lactate accumulation, suggesting irreversible mitochondrial damage. Conclusion pH-based monitoring inadequately detects linezolid toxicity in alkalotic patients. Lactate/HCO 3 − ratios (> 0.17) should be incorporated into geriatric antimicrobial protocols for early intervention.

To describe the incidence, causes and associated mortality of hyperlactatemia in critically ill patients and to evaluate the association between lactate clearance and in-hospital survival. Retrospective cohort study of patients with hyperlactatemia admitted to the ICU. Hyperlactatemia was defined as a blood lactate concentration ≥5mmol/L and high-grade hyperlactatemia a lactate level ≥10mmol/L. Lactate clearance was calculated as the percentage of decrease in lactate concentration from the peak value. Of 10,123 patients, 1373 (13.6%) had lactate concentration ≥5mmol/L, and 434(31.6%) of them had ≥10mmol/L. The most common causes of hyperlactatemia were sepsis/septic shock and post-cardiac surgery. An association was found between lactate concentration and in-hospital mortality (p<0.001). The area under the receiver-operating-characteristics (ROC) of lactate concentration and the optimal cut off to predict mortality were 0.72 (0.70–0.75) and 8.6mmol/L, respectively. ROC analysis for lactate clearance to predict in-hospital survival showed that the best area under the curve was obtained at 12h: 0.67 (95% confidence interval 0.59–0.75). Hyperlactatemia was common and associated with a high mortality in critically ill patients. Lactate clearance had limited utility for predicting in-hospital survival. •Hyperlactatemia was common and associated with a high mortality in critically ill patients.•It was possible to rescue patients at any lactate concentration.•Lactate clearance had limited clinical utility in our sample