Vitamin B1 Deficiency Identified from Incidental Detection of Hyperlactatemia: A Case Report.

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.

Risk Factors and Consequences of Late-Onset Hyperlactatemia After Cardiac Surgery With Cardiopulmonary Bypass: A Single-Center Retrospective Study.

OBJECTIVE: Mechanisms and consequences of late-onset hyperlactatemia after cardiac surgery remain unclear. The aim of this study was to identify risk factors and outcomes of late hyperlactatemia, defined as a lactate value ≥3 mmol/L developing in the intensive care unit (ICU) after not being elevated on admission after cardiac surgery with cardiopulmonary bypass. DESIGN: A retrospective analysis of prospectively collected data. SETTING: A single-center University Hospital. PARTICIPANTS: Patients who underwent elective cardiac surgery with cardiopulmonary bypass in 2019 and who had normal lactatemia at ICU admission. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Patients were divided in 2 groups according to their lactatemia on postoperative day 1 (14.0 ± 3.0 hours after ICU admission): normal lactatemia (control group) and late hyperlactatemia (HL group). Risk factors for late hyperlactatemia were identified using a multivariate analysis, and postoperative outcomes were compared using a composite criterion of severe outcomes. Of the 432 included patients, 37 (8.5%) presented with late hyperlactatemia. Risk factors independently associated with hyperlactatemia were afternoon surgery (odds ratio [OR] 4.24, 95% CI 2.00-9.35), a bleeding >300 mL within the 6 hours after surgery (H6) (OR 3.77, 95% CI 1.71-8.30), and H6 fluid loading >250 mL (OR 2.64, 95% CI 1.22-5.55). Patients with hyperlactatemia presented more frequently with major postoperative complications, including acute kidney injury, and received more frequent red-cell transfusion. CONCLUSION: The strongest risk factors associated with late-onset hyperlactatemia in the authors' population were afternoon surgery and H6 bleeding >300 mL. Poor postoperative outcomes were more frequent in patients with late hyperlactatemia, even in the absence of early hyperlactatemia or severe obvious condition.

Hyperlactatemia and other perioperative metabolic disturbances in neuroanesthesia.

PURPOSE OF REVIEW: The concept of 'brain-body cross-talking' has gained growing interest in the last years. The understanding of the metabolic disturbances (e.g., hypernatraemia/hyponatraemia and hyperlactatemia) in neurosurgical patients has improved during the last years. RECENT FINDINGS: The impact of elevated lactate without acidosis in neurosurgical patients remains controversial. The pathophysiology of inappropriate secretion of antidiuretic hormone (SIADH) has become clearer, whereas the diagnosis of cerebral salt wasting should be used more carefully. SUMMARY: These findings will contribute to a better understanding of the pathophysiology involved and enable better prevention and therapy where possible in clinical practice.

Hyperlactacidemia as a risk factor for intensive care unit-acquired weakness in critically ill adult patients.

INTRODUCTION/AIMS: Intensive care unit-acquired weakness (ICUAW) is a severe neuromuscular complication of critical illness. Serum lactate is a useful biomarker in critically ill patients. The relationship between serum lactate level and ICUAW remains controversial. This study evaluated whether hyperlactacidemia (lactate level >2 mmol/L) was an independent risk factor for ICUAW in critically ill adult patients. METHODS: An observational cohort study was performed in a general multidisciplinary intensive care unit (ICU). Sixty-eight consecutive adult critically ill patients without preexisting neuromuscular disease or a poor pre-ICU functional status whose length of ICU stay was 7 or more days were evaluated. Patients were screened daily for signs of awakening. Muscle strength assessment using the Medical Research Council score was performed on the first day a patient was considered awake. Patients with clinical muscle weakness were considered to have ICUAW. RESULTS: Among the 68 patients who achieved a satisfactory state of consciousness, the diagnosis of ICUAW was made in 30 patients (44.1%). After multivariate analysis, hyperlactacidemia (P = .02), Acute Physiology and Chronic Health Evaluation II score (P = .04), duration of mechanical ventilation (P = .02), and the use of norepinephrine (P = .04) were found to be significantly associated with the development of ICUAW in critically ill patients. DISCUSSION: This study shows a number of risk factors to be significantly associated with the development of ICUAW in critically ill adults. These factors should be considered when building early prediction models or designing prevention strategies for ICUAW in future studies.

What Is the Utility of Measuring Lactate Levels in Patients with Sepsis and Septic Shock?

Elevations in blood lactate concentrations have been studied in sepsis and other disease states for decades and are well known to be associated with increased mortality. Many studies have also demonstrated the prognostic accuracy of serial lactate levels, and some have suggested that lactate clearance may be a useful therapeutic target for resuscitation. Lactate measurements have therefore gained an increasingly prominent role in sepsis definitions, screening protocols, management guidelines, and quality measures over the past two decades. The heavy emphasis on lactate monitoring, however, has also generated controversy and concerns. Lactate is not specific to infection and its frequent use for sepsis screening and diagnosis may therefore trigger unnecessary broad-spectrum antibiotic use in some patients. Because hyperlactatemia does not always reflect fluid-responsive hypoperfusion, titrating resuscitation to lactate clearance can also lead to unnecessary fluid and volume overload. More broadly, there is a lack of high-quality evidence demonstrating that initial and serial lactate monitoring leads to better patient-centered outcomes. Indeed, a recent randomized controlled trial comparing resuscitation strategies based on lactate clearance versus normalizing capillary refill time showed no benefit and potential harm with lactate-guided therapy. In this article, we review the basic pathobiology of lactate metabolism and delineate why the traditional paradigm that hyperlactatemia reflects tissue hypoxia is overly simplistic and incomplete. We then review the evidence behind the diagnostic, prognostic, and therapeutic uses of lactate monitoring and place this in the context of evolving sepsis diagnosis and management guidelines.

Predictors of Increased Lactate in Neonatal Cardiac Surgery: The Impact of Cardiopulmonary Bypass.

OBJECTIVE: Hyperlactatemia develops intraoperatively during cardiac surgery and is associated with postoperative mortality. This study aimed to determine the factors that lead to an increase in lactate during cardiopulmonary bypass (CPB) in neonates undergoing cardiac surgery. DESIGN: Retrospective study from July 2015 to December 2018. SETTING: Academic tertiary children's hospital. PARTICIPANTS: The study comprised 376 neonates. INTERVENTIONS: No interventions were performed. MEASUREMENTS AND MAIN RESULTS: Lactate measurements at prebypass, upon initiation of CPB and before coming off CPB, last in the operating room, and first in the cardiac intensive care unit were collected. The changes in lactate levels were compared using the nonparametric Wilcoxon signed rank test for paired data. Univariate and multivariate median regression models of the change during CPB were determined. The cohort characteristics were male (60%), median age 5 days (range 1-30), and weight 3.2 kg (range 1.5-4.7). Most patients had a STAT score of 4 (45%) or 5 (23%). Significant increases in lactate were observed from pre-CPB to start of CPB (p < 0.001) and from start to end of CPB (p < 0.001). In the multivariate regression analysis, duration of circulatory arrest (coefficient = 1.216; 95% confidence interval [CI] 0.754-1.678; p < 0.001), duration of mean arterial pressure < 25 mmHg (coefficient = 0.423; 95% CI 0.196-to- 0.651; p < 0.001), and duration of mean arterial pressure between 35 and 39 mmHg (coefficient = -0.246; 95% CI -0.397 to -0.095; p = 0.001) were identified as significant independent predictors of the lactate change per 30- minutes duration. CONCLUSION: These results emphasized the importance of blood pressure management during CPB and the importance of the duration of circulatory arrest.

Prognostic relevance of pre- and postoperative plasma l-lactate measurements in calves with acute abdominal emergencies.

In both human and veterinary medicine, l-lactate is a well-established prognostic biomarker of disease severity and mortality and has also attracted increasing attention in bovine medicine due to the availability and validation of cheap and portable l-lactate analyzers. The aim of the present study was to evaluate the prognostic accuracy of plasma L-lactate measurements in calves with acute abdominal emergencies before and during the initial therapeutic period after surgical intervention. A prospective observational study was carried out involving 83 hospitalized calves up to an age of 7 mo, which required surgical intervention for reasons of an acute abdominal emergency such as gastrointestinal ileus or peritonitis. Plasma l-lactate (L-LAC) concentrations were determined immediately before initiation of surgery and 6, 12, 24, 48, and 72 h later. The outcome of calves was evaluated 3 mo after discharge by a phone call to the farmer, and a positive outcome was defined if the calf was still alive and the owner was satisfied with the animal's postsurgical progress. A total of 29% of calves were discharged from the hospital and the proportion of calves with a positive outcome after the 3-mo period was 24%. At all sampling times during the first 48 h after initiation of surgical intervention, calves with a negative outcome had significantly higher L-LAC than calves with a positive outcome. A binary logistic regression analysis indicated that the odds for a negative outcome during the 3-mo observation period increased by a factor of 1.23 [95% confidence interval (CI): 1.04-1.44] for every mmol/L increase of L-LAC before initiation of surgical intervention, but by a factor of 5.29 (95% CI: 1.69-16.6) and 5.92 (95% CI: 1.29-27.3) at 12 and 24 h, respectively. The largest area under the receiver operating characteristic curve for L-LAC was observed at 12 h (0.91; 95% CI: 0.83-0.99), and a cut-point of 2.75 mmol/L was identified that had a sensitivity and specificity for predicting a negative outcome of 68 and 100%, respectively. In conclusion, persistent hyper-l-lactatemia during the early postoperative period is a more reliable indicator for a negative outcome in calves with acute surgical abdominal emergencies than hyper-l-lactatemia before initiation of surgical intervention. Postoperative measurements of L-LAC are therefore a clinically useful tool to identify patients with an increased risk for a negative outcome at an early stage after surgical intervention was carried out.

Agreement between arterial and peripheral venous lactate levels in the ED: A systematic review.

BACKGROUND: In the Emergency Department, lactate measurement is a useful tool to risk-stratify critically ill patients. However, it is unclear whether arterial or peripheral venous lactate levels can be used interchangeably for this purpose. In this systematic review, we provide an overview of studies investigating the agreement between arterial and peripheral venous lactate levels in the Emergency Department. METHODS: PubMed, Embase, the Cochrane Central Register of Controlled Trials/Wiley, Web of Science/Clarivate Analytics, and references of selected articles were assessed for all studies comparing arterial and peripheral venous lactate levels in adult patients in the emergency department. Two reviewers independently screened all potentially relevant titles and abstracts for eligibility using a standardized data-worksheet. RESULTS: Nine studies were included. Peripheral venous lactate levels tend to be higher than arterial lactate levels with mean differences ranging from 0.18 mmol/l to 1.06 mmol/l. Importantly, poorer agreement occurs in hyperlactatemia. At a cut-of level of 1.6 mmol/l, peripheral venous lactate can rule out arterial hyperlactatemia with a sensitivity between 94% and 100%. At a cut off value of 2 mmol/l, sensitivities of 97% and 100% were found. CONCLUSION: Agreement between arterial and peripheral venous lactate is poor in hyperlactatemia, making peripheral venous lactate an unreliable parameter to use interchangeably in the ED. In clinical practice, peripheral venous lactate can be used as a screening tool to rule out arterial hyperlactatemia at a cut-off value of 2 mmol/l. However, hyperlactatemia should be confirmed using arterial sampling in case of a peripheral venous lactate level > 2 mmol/l.

Practical Use of Lactate Levels in the Intensive Care.

Hyperlactatemia is a strong predictor of mortality in diverse populations of critically ill patients. In this article, we will give an overview of how lactate is used in the intensive care unit. We describe the use of lactate as a predictor of outcome, as a marker to initiate therapy and to monitor adequacy of initiated treatments.

Prognostic Value of Hyperlactatemia and Lactate Clearance After Mitral Valve Surgery.

OBJECTIVES: Blood lactate is frequently used to guide management in critically ill patients. In patients undergoing mitral valve surgery, an elevated lactate level is frequently observed; however, overall mortality is low. The authors hypothesized that hyperlactemia is not a useful predictor of poor outcomes in this patient population. The main aim of this study was to explore how blood lactate level and lactate clearance are associated with 30-day mortality and major adverse events in patients undergoing mitral valve surgery. DESIGN: This was a retrospective database review. Logistic regression analysis was performed to assess the associations of perioperative factors with blood lactate in the intensive care unit (ICU). SETTING: Tertiary-care teaching hospital. PARTICIPANTS: The study comprised 917 patients undergoing mitral valve surgery. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The majority of patients (71.8%) had elevated blood lactate ≥2 mmol/L on ICU admission; however, within 24 hours, 85.1% of all patients had normal lactate values. Overall 30-day mortality was 2.29% (n = 21). The combination of lactate ≥7 mmol/L on ICU admission and a persistent elevated blood lactate level 24 hours after ICU admission provides an excellent prediction of 30-day mortality (C statistic = 0.85). However, even a significantly elevated lactate level on ICU admission was well-tolerated in the majority of patients as long as lactate values normalized within 24 hours. Male sex, longer cardiopulmonary bypass time, blood transfusion in the ICU, and an elevated blood lactate level on ICU admission and 12 hours after ICU admission all were independent risk factors of clearance failure. CONCLUSIONS: An elevated blood lactate level is common after mitral valve surgery and is well-tolerated in the majority of patients. Adding lactate clearance improved the predictive value of the blood lactate level.

Continuous Monitoring of Lactate Using Intravascular Microdialysis in High-Risk Cardiac Surgery: A Prospective Observational Study.

OBJECTIVE: To assess the accuracy and applicability of a novel system, not requiring calibration, for continuous lactate monitoring with intravascular microdialysis in high-risk cardiac surgery. DESIGN: Single-center prospective observational study. SETTING: City Hospital #1 of Arkhangelsk, Russian Federation. PARTICIPANTS: Twenty-one adult patients undergoing elective complex repair or replacement of two or more valves or combined valve and coronary artery cardiac surgery. INTERVENTIONS: After induction of anesthesia, in all patients a dedicated triple-lumen catheter functioning as a regular central venous catheter with integrated microdialysis function was inserted via the right jugular vein for continuous lactate monitoring using the intravascular microdialysis system. MEASUREMENTS AND MAIN RESULTS: Lactate values displayed by the microdialysis system were compared with the reference arterial blood gas (ABG) values. In total, 432 paired microdialysis-ABG lactate samples were obtained. After surgery, the concentration of lactate increased significantly, peaking at 8 hours (p<0.05). The lactate clearance within 8 hours after peak concentration was 50% (39%-63%). There was a significant correlation between Lactatecont and Lactatecont (rho = 0.92, p<0.0001). Bland-Altman analysis showed a bias (mean difference)±limits of agreement (±1.96 SD) of 0.09±1.1 mmol/L. In patients with postoperative complications, peak lactate concentration was significantly higher compared with those without complications: 6.75 (4.43-7.75) mmol/L, versus 4.20 (3.95-4.87) mmol/L (p = 0.002). CONCLUSIONS: Lactate concentration increased significantly after high-risk cardiac surgery. The intravascular microdialysis technique for lactate measurement provided acceptable accuracy and can be used for continuous blood lactate monitoring in cardiac surgery.

Hyperlactemia Predicts Surgical Mortality in Patients Presenting With Acute Stanford Type-A Aortic Dissection.

OBJECTIVE: Inspired by the limited facility of the Penn classification, the authors aimed to determine a rapid and optimal preoperative assessment tool to predict surgical mortality after acute Stanford type-A aortic dissection (AAAD) repair. DESIGN: Patients who underwent an attempted surgical repair of AAAD were determined using a de-identified single institution database. The charts of 144 patients were reviewed retrospectively for preoperative demographics and surrogates for disease severity and malperfusion. Bivariate analysis was used to determine significant (p≤0.05) predictors of in-hospital and 1-year mortality, the primary endpoints. Receiver operating characteristic curve generation was used to define optimal cut-off values for continuous predictors. SETTING: Single center, level 1 trauma, university teaching hospital. PARTICIPANTS: The study included 144 cardiac surgical patients with acute type-A aortic dissection presenting for surgical correction. INTERVENTIONS: Surgical repair of aortic dissection with preoperative laboratory samples drawn before patient transfer to the operating room or immediately after arterial catheter placement intraoperatively. MEASUREMENTS AND MAIN RESULTS: The study cohort comprised 144 patients. In-hospital mortality was 9%, and the 1-year mortality rate was 17%. Variables that demonstrated a correlation with in-hospital mortality included an elevated serum lactic acid level (odds ratio [OR] 1.5 [1.3-1.9], p<0.001), a depressed ejection fraction (OR 0.91 [0.86-0.96], p = .001), effusion (OR 4.8 [1.02-22.5], p = 0.04), neurologic change (OR 5.3 [1.6-17.4], p = 0.006), severe aortic regurgitation (OR 8.2 [2.0-33.9], p = 0.006), and cardiopulmonary resuscitation (OR 6.8 [1.7-26.9], p = 0.01). Only an increased serum lactic acid level demonstrated a trend with 1-year mortality using univariate Cox regression (hazard ratio 1.1 [1.0-1.1], p = 0.006). Receiver operating characteristic analysis revealed optimal cut-off lactic acid levels of 6.0 mmol/L and 6.9 mmol/L for in-hospital and 1-year mortality, respectively. CONCLUSION: Lactic acidosis, ostensibly as a surrogate for systemic malperfusion, represents a novel, accurate, and easily obtainable preoperative predictor of short-term mortality after attempted AAAD repair. These data may improve identification of patients who would not benefit from surgery.

Hyperlactatemia and Cardiac Surgery.

The normal blood lactate level is 0-2 mmol/L, and a value above 3-5 mmol/L is variably used to define hyperlactatemia. In cardiac surgical patients, hyperlactatemia can arise from both hypoxic and non-hypoxic mechanisms. The major non-hypoxic mechanism is likely stress-induced accelerated aerobic metabolism, in which elevated lactate results from a mass effect on the lactate/pyruvate equilibrium. The lactate/pyruvate ratio is normal (<20) in this circumstance. Hyperlactatemia can also result from impaired global or regional oxygen delivery, in which case the lactate/pyruvate ratio is typically elevated (>20). Lactate is a strong anion that is virtually fully dissociated at physiological pH. As such, increased lactate concentration reduces the strong ion difference and exerts an acidifying effect on the blood. Hyperlactatemia in cardiac surgery patients has been categorized as either early or late onset. Early-onset hyperlactatemia is that which develops in the operating room or very early following intensive care unit (ICU) admission. Early-onset hyperlactatemia is strongly associated with adverse outcome and probably arises as a consequence of both hypoxic (e.g., microcirculatory shock) and non-hypoxic (accelerated aerobic metabolism) mechanisms. By contrast, late-onset hyperlactatemia is a benign, self-limiting condition that typically arises within 6-12 hours of ICU admission and spontaneously resolves within 24 hours. Late onset hyperlactatemia occurs in the absence of any evidence of global or regional tissue hypoxia. The mechanism of late onset hyperlactatemia is not understood. Hyperlactatemia is a common accompaniment to treatment with ß2-agonists such as epinephrine. Epinephrine-induced hyperlactatemia is thought to be due to accelerated aerobic metabolism and requires no specific intervention. Irrespective of the cause, the presence of hyperlactatemia should trigger a search for remedial causes of impaired tissue oxygenation, bearing in mind that normal-or even supranormal-indices of global oxygen delivery may exist despite regional tissue hypoperfusion.

Hyperlactataemia and clinical severity of acute metformin overdose.

BACKGROUND: Although metformin-associated lactic acidosis is well described, there is less information on metformin overdose and whether it is of similar severity. AIMS: This study aims to describe the clinical features, laboratory investigations and outcome of acute metformin overdoses. METHODS: Retrospective case series of acute metformin overdoses (> 3 g) admitted to a toxicology unit over 20 years. Cases were identified from a prospective database and data extracted included demographics, dose, coingestants, clinical effects, investigations, treatment and outcomes. RESULTS: There were 36 acute metformin overdose cases. Median age 41 years old (15-68 years old); 25 were female. Median ingested dose was 10 g (interquartile range (IQR): 5-16.1 g; range: 3.5-50 g), with coingestants taken in 34 presentations. Gastrointestinal symptoms were present in 12/36, tachycardia in 10, bradycardia in three, hypotension in four and hypoglycaemia in eight. Hypotension and bradycardia were consistent with coingestants taken. Blood pH and lactate levels were available in 25/36. Median lowest pH was 7.35 (IQR: 7.28-7.38) and acidosis (pH < 7.35) occurred in 11/25. Median peak lactate was 3.9 mmol/L (IQR: 2.6-5.2 mmol/L). There was a statistical association between dose and lactate (r = 0.51; P = 0.01) and dose and pH (r = -0.70; P = 0.0001). Hyperlactataemia (lactate > 2 mmol/L) without acidosis occurred in 10/25, and hyperlactataemia with acidosis in 11/25; five had lactic acidosis. The median time to peak lactate in 10 presentations with peak lactate > 2 was 6 h (2-19 h). There were six intensive care unit admissions, one for lactic acidosis, and five related to coingestants. There were no deaths. CONCLUSION: Metformin overdose is characterised by hyperlactataemia and minor gastrointestinal effects, with a few large ingestions progressing to lactic acidosis. Coingestants are common and may dominate toxicity.

Effect of glucose-insulin-potassium on hyperlactataemia in patients undergoing valvular heart surgery: A randomised controlled study.

BACKGROUND: Hyperlactataemia represents oxygen imbalance in the tissues and its occurrence during cardiac surgery is associated with adverse outcomes. Glucose-insulin-potassium (GIK) infusion confers myocardial protection against ischaemia-reperfusion injury and has the potential to reduce lactate release while improving its clearance. OBJECTIVES: The objective of this study is to compare the effect of GIK on the incidence of hyperlactataemia in patients undergoing valvular heart surgery. DESIGN: A randomised controlled study. SETTING: Single university teaching hospital. PATIENTS: One hundred and six patients scheduled for elective valvular heart surgery with at least two of the known risk factors for hyperlactataemia. INTERVENTION: Patients were randomly allocated to receive either GIK solution (insulin 0.1 IU kg(-1) h(-1) and an infusion of 30% dextrose and 80 mmol l(-1) potassium at 0.5 ml kg(-1) h(-1)) or 0.9% saline (control) throughout surgery. MAIN OUTCOME MEASURES: The primary outcome was the incidence of hyperlactataemia (lactate ≥ 4 mmol l(-1)) during the operation and until 24 h after the operation. Secondary outcomes included haemodynamic parameters, use of vasopressor or inotropic drugs, and fluid balance until 24 h postoperatively. Postoperative morbidity endpoints were also assessed. RESULTS: The incidences of hyperlactataemia were similar in the groups (32/53 patients in each of the control and GIK groups, P > 0.999). There were no intergroup differences in haemodynamic parameters, use of vasopressor and inotropic drugs, or fluid balance. The incidences of postoperative morbidity endpoints were similar in both groups. CONCLUSION: Despite its theoretical advantage, GIK did not provide beneficial effects in terms of the incidence of hyperlactataemia or outcome in patients undergoing valvular heart surgery. TRIAL REGISTRATION: Clinicaltrials.gov identifier: NCT01825720.

Sepsis-associated hyperlactatemia.

There is overwhelming evidence that sepsis and septic shock are associated with hyperlactatemia (sepsis-associated hyperlactatemia (SAHL)). SAHL is a strong independent predictor of mortality and its presence and progression are widely appreciated by clinicians to define a very high-risk population. Until recently, the dominant paradigm has been that SAHL is a marker of tissue hypoxia. Accordingly, SAHL has been interpreted to indicate the presence of an 'oxygen debt' or 'hypoperfusion', which leads to increased lactate generation via anaerobic glycolysis. In light of such interpretation of the meaning of SAHL, maneuvers to increase oxygen delivery have been proposed as its treatment. Moreover, lactate levels have been proposed as a method to evaluate the adequacy of resuscitation and the nature of the response to the initial treatment for sepsis. However, a large body of evidence has accumulated that strongly challenges such notions. Much evidence now supports the view that SAHL is not due only to tissue hypoxia or anaerobic glycolysis. Experimental and human studies all consistently support the view that SAHL is more logically explained by increased aerobic glycolysis secondary to activation of the stress response (adrenergic stimulation). More importantly, new evidence suggests that SAHL may actually serve to facilitate bioenergetic efficiency through an increase in lactate oxidation. In this sense, the characteristics of lactate production best fit the notion of an adaptive survival response that grows in intensity as disease severity increases. Clinicians need to be aware of these developments in our understanding of SAHL in order to approach patient management according to biological principles and to interpret lactate concentrations during sepsis resuscitation according to current best knowledge.

Successful Anesthetic Management of an Adult Patient With Glycogen Storage Disease Type 1 During Liver Transplant: A Case Report.

Glycogen storage disease type 1 is a congenital abnormality of metabolism caused by the deficiency of the glucose-6-phosphatase enzyme, essential in glucose homeostasis. Patients with this disease are at high risk of developing hypoglycemia, hyperlipidemia, lactic acidemia, growth retardation, neutropenia, inflammatory bowel disease, and many other severe complications, such as hepatic adenomas converting into hepatocellular carcinomas. To prevent these complications, a liver transplant is the ultimate method of treatment. We present the successful anesthesia management for a 21-year-old man who had gross hepatomegaly, severe hypoglycemia, and hyperlactatemia and who received a liver transplant from his mother, which is a substantial challenge for anesthesiologists. Anesthesiologists should know the underlying pathophysiological condition and perform a comprehensive preoperative evaluation to determine the correct anesthesia plan in patients with glycogen storage disease type 1 who will undergo an orthotopic liver transplant due to multiple system disorders. Successful perioperative management of patients with glycogen storage disease type 1 relies on effective communication and collaboration between specialists through a multidisciplinary team approach.

Even mild hyperlactatemia is associated with increased mortality in critically ill patients.

INTRODUCTION: The clinical significance of elevation of lactate levels within the reference range is not well studied. The objective of this study was to determine the best cutoff threshold for serum lactate within the reference range (0.01 to 2.00 mM) that best discriminated between survivors and nonsurvivors of critical illness and to examine the association between relative hyperlactatemia (lactate above the identified threshold) and mortality. METHODS: This was a retrospective cohort study of adult patients admitted to the medical-surgical intensive care unit (ICU) of a tertiary care academic center. Youden index was calculated to identify the best lactate cutoff threshold that discriminated between survivors and nonsurvivors. Patients with lactate above the identified threshold were defined as having relative hyperlactatemia. Multivariate logistic regression, adjusting for baseline variables, was performed to determine the relationship between the above two ranges of lactate levels and mortality. In addition, a test of interaction was performed to assess the effect of selected subgroups on the association between relative hyperlactatemia and hospital mortality. RESULTS: During the study period, 2,157 patients were included in the study with mean lactate of 1.3 ± 0.4 mM, age of 55.1 ± 20.3 years, and acute physiology and chronic health evaluation (APACHE) II score of 22.1 ± 8.2. Vasopressors were required in 42.4%. Lactate of 1.35 mM was found to be the best cutoff threshold for the whole cohort. Relative hyperlactatemia was associated with increased hospital mortality (adjusted odds ratio (aOR), 1.60, 95% confidence interval (CI) 1.29 to 1.98), and ICU mortality (aOR, 1.66; 95% CI, 1.26 to 2.17) compared with a lactate level of 0.01 to 1.35 mM. This association was consistent among all examined subgroups. CONCLUSIONS: Relative hyperlactatemia (lactate of 1.36 to 2.00 mM) within the first 24 hours of ICU admission is an independent predictor of hospital and ICU mortality in critically ill patients.

Relationship between peripheral ischemic microvascular reserve, persistent hyperlactatemia, and its temporal dynamics in sepsis: a post hoc study.

OBJECTIVE: To measure the prognostic value of peripheral ischemic microvascular reserve in the context of persistent sepsis-induced hyperlactatemia and measure its influence on the temporal dynamics of lactate and the strength of association between these variables. METHODS: This post hoc analysis of the peripheral perfusion index/postocclusive reactive hyperemia trial, an observational cohort study that enrolled patients with sepsis who persisted with lactate levels ≥ 2mmol/L after fluid resuscitation (with or without shock). Peripheral ischemic microvascular reserve was evaluated using the association of the peripheral perfusion index and postocclusive reactive hyperemia techniques. The cutoff point of ∆ peripheral perfusion index peak values (%) defined the groups with low (≤ 62%) and high peripheral ischemic microvascular reserve (> 62%). RESULTS: A total of 108 consecutive patients with persistent sepsis-induced hyperlactatemia were studied. The high peripheral ischemic microvascular reserve group showed higher 28-day mortality than the low peripheral ischemic microvascular reserve group (p < 0.01). The temporal dynamics of lactate within the first 48 hours showed a rapid decrease in lactate levels in the low peripheral ischemic microvascular reserve group (p < 0.01). However, this result was not reproduced in the linear mixed effects model. A weak correlation between peripheral ischemic microvascular reserve (%) and lactate level (mmol/L) was observed within the first 24 hours (r = 0.23; p < 0.05). CONCLUSION: The prognostic value of high peripheral ischemic microvascular reserve was confirmed in the context of persistent sepsis-induced hyperlactatemia. Although there was a weak positive correlation between peripheral ischemic microvascular reserve value and lactate level within the first 24 hours of sepsis diagnosis, the low peripheral ischemic microvascular reserve group appeared to have a faster decrease in lactate over the 48 hours of follow-up.

Hyperlactatemia and altered lactate kinetics are associated with excess mortality in sepsis : A multicenter retrospective observational study.

Severe hyperlactatemia (>10mmol/L) or impaired lactate metabolism are known to correlate with increased mortality. The maximum lactate concentration on day 1 of 10,724 septic patients from the eICU Collaborative Research Database was analyzed and patients were divided into three groups based on maximum lactate in the first 24 h (<5mmol/l; ≥5mmol/l & <10mmol/l; ≥10mmol/l). In addition, delta lactate was calculated using the following formula: (maximum lactate day 1 minus maximum lactate day 2) divided by maximum lactate day 1. A multilevel regression analysis was performed, with hospital mortality serving as the primary study end point. Significant differences in hospital mortality were found in patients with hyperlactatemia (lactate ≥10mmol/l: 79%, ≥5mmol/l & <10mmol/l: 43%, <5mmol/l, 13%; p<0.001). The sensitivity of severe hyperlactatemia (≥10mmol/l) for hospital mortality was 17%, the specificity was 99%. In patients with negative delta lactate in the first 24 h, hospital mortality was excessive (92%). In conclusion, mortality in patients with severe hyperlactatemia is very high, especially if it persists for more than 24 h. Severe hyperlactatemia, together with clinical parameters, could therefore provide a basis for setting treatment limits.