Relation Between Multiplication of Venous Carbon Dioxide Partial Pressure (PvCO2) and the Ratio of Gas Flow to Pump Flow (Ve/Q) with Hyperlactatemia During Cardiopulmonary Bypass.

BACKGROUND: The incidence of hyperlactatemia due to hypoperfusion during cardiopulmonary bypass (CPB) increases morbidity. Carbon dioxide production during CPB is one of the lactate production markers, in addition to other markers such as delivery oxygen (DO2), oxygen consumption (VO2), mixed vein oxygen saturation (SvO2), and oxygen extraction ratio (O2ER). METHOD: This observational analytic study was conducted on 40 adult cardiac surgery patients using a CPB machine. Initial lactate is taken when entering CPB and final lactate is examined 15 min after coming off bypass. The values of DO2, VO2, SvO2, VCO2, respiratory quotient (RQ), DO2/VCO2, PvCO2 × Ve/Q were calculated from the results of blood and venous gas analysis 1 h after entering CPB in the nadir of core temperature and lowest pump flow. RESULT: The multivariate test showed that the value of PvCO2 × Ve/Q was more effective than other oxygenation and carbon dioxide parameters in predicting an increase in the percentage of lactate. Each increase of 1 mmHg PvCO2 ×× Ve/Q can predict a final lactate increase of 29% from the initial lactate. The high PvCO2 × Ve/Q value is also the strongest correlation factor for the incidence of hyperlactatemia after CPB (final lactate >3 mmol/L). The cutoff value of this marker is >19.3 mmHg, which has a sensitivity of 100% and a specificity of 55.6% with a strong correlation value. CONCLUSION: The PvCO2 × Ve/Q value proved to be one of the significant markers in predicting hyperlactatemia during cardiac surgery using CPB.

Comparison of 4% Albumin and Ringer's Acetate on Hemodynamics in On-pump Cardiac Surgery: An Exploratory Analysis of a Randomized Clinical Trial.

OBJECTIVES: Compare hemodynamics between 4% albumin and Ringer's acetate. DESIGN: Exploratory analysis of the double-blind randomized ALBumin In Cardiac Surgery trial. SETTING: Single-center study in Helsinki University Hospital. PARTICIPANTS: We included 1,386 on-pump cardiac surgical patients. INTERVENTION: We used 4% albumin or Ringer's acetate administration for cardiopulmonary bypass priming, volume replacement intraoperatively and 24 hours postoperatively. MEASUREMENTS AND MAIN RESULTS: Hypotension (time-weighted average mean arterial pressure of <65 mmHg) and hyperlactatemia (time-weighted average blood lactate of >2 mmol/L) incidences were compared between trial groups in the operating room (OR), and early (0-6 hours) and late (6-24 hours) postoperatively. Associations of hypotension and hyperlactatemia with the ALBumin In Cardiac Surgery primary outcome (≥1 major adverse event [MAE]) were studied. In these time intervals, hypotension occurred in 118, 48, and 17 patients, and hyperlactatemia in 313, 131, and 83 patients. Hypotension and hyperlactatemia associated with MAE occurrence. Hypotension did not differ between the groups (albumin vs Ringer's: OR, 8.8% vs 8.5%; early postoperatively, 2.7% vs 4.2%; late postoperatively, 1.2% vs 1.3%; all p > 0.05). In the albumin group, hyperlactatemia was less frequent late postoperatively (2.9% vs 9.1%; p < 0.001), but not earlier (OR, 22.4% vs 23.6%; early postoperatively, 7.9% vs 11.0%; both p > 0.025 after Bonferroni-Holm correction). CONCLUSIONS: In on-pump cardiac surgery, hypotension and hyperlactatemia are associated with the occurrence of ≥1 MAE. Compared with Ringer's acetate, albumin did not decrease hypotension and decreased hyperlactatemia only late postoperatively. Albumin's modest hemodynamic effect is concordant with the finding of no difference in MAEs between albumin and Ringer's acetate in the ALBumin In Cardiac Surgery trial.

Lactate as an early prognostic indicator in yellow phosphorus rodenticide-induced acute hepatic failure: a retrospective observational study in a tertiary care hospital.

INTRODUCTION: Acute hepatic failure due to yellow phosphorus rodenticide ingestion is often lethal. This study aimed to analyze demographic characteristics and prognostic indicators, focusing on hyperlactataemia as a potential early indicator of mortality in patients poisoned with yellow phosphorus rodenticide. MATERIALS AND METHODS: This was a retrospective study of 96 patients poisoned with a yellow phosphorus-containing rodenticide (Ratol paste, which contains 3% yellow phosphorus). We examined demographic details, clinical symptoms, and biochemical markers to identify prognostic indicators. RESULTS: Demographics were similar among survivors and non-survivors. Mortality (36.5%) correlated with a higher ingested dose and treatment delays, with a mean (±SD) of 5.26 ± 2.2 survival days among those who died. Symptoms, including gastrointestinal and neurological features, typically appeared 48 h after ingestion. Non-survivors developed increased aminotransferase activities (74.3%), prolonged prothrombin time (65.7%), and hyperbilirubinaemia (65.7%) during hospitalization, significantly more commonly compared to survivors (P < 0.0001). Hyperlactataemia (lactate concentration >2 mmol/L) was present in 97.1% of non-survivors, with increased serial lactate concentrations observed in 88.6%. The median (interquartile range) admission lactate concentration among non-survivors was 4.6 mmol/L (3.36-7.53 mmol/L), and their peak median (interquartile range) lactate concentration was 6.1 mmol/L (8.74-10.6 mmol/L). In non-survivors, an increased lactate concentration preceded increased aminotransferase activities and prolonged prothrombin time. Logistic regression and receiver operating characteristic curve analysis confirmed that a 24 h lactate concentration ≥2.67 mmol/L predicted death with 94.3% sensitivity and 91.8% specificity. DISCUSSION: The majority of patients who ingest yellow phosphorus remain asymptomatic initially and typically present to hospital following the onset of gastrointestinal symptoms, usually a day later. As progression to death occurs within a week of yellow phosphorus ingestion in most cases, determining prognosis as early as possible enables swift referral to a liver transplant centre. Based on our study, a 24 h lactate concentration ≥2.67 mmol/L appears to be an early prognostic indicator of death. In another study, a lactate concentration >5.8 mmol/L was found to be a poor prognostic indicator. CONCLUSIONS: Hyperlactataemia on admission and increased serial lactate concentrations appear to be early poor prognostic signs in patients with yellow phosphorus-induced liver failure.

Severe hyperlactatemia in the emergency department: clinical characteristics, etiology and mortality.

BACKGROUND: Severe hyperlactatemia (lactate level ≥ 10 mmol/L) is associated with high mortality rates in critically ill patients. However, there is limited data on emergency department (ED) patients. We aimed to investigate the clinical characteristics, etiology and outcomes of patients with severe hyperlactatemia in the ED setting. METHODS: A retrospective cohort study was conducted at a tertiary care hospital in Thailand. We included adult patients with a venous lactate sample taken in the ED within one hour. We excluded patients after out-of-hospital cardiac arrest, transferred to/from another hospital or those with missing clinical data. Mortality rates were evaluated among patients with increasing degrees of lactate elevation and among patients with severe hyperlactatemia, stratified by causative etiology. RESULTS: We analyzed venous lactate levels in 40,047 patients, with 26,680 included in the analysis. Among these, 1.7% had severe hyperlactatemia (lactate ≥ 10 mmol/L), 10.5% moderate (4-9.99 mmol/L), 28.8% mild (2-3.99 mmol/L), and 59.0% normal levels (< 2 mmol/L). Severe hyperlactatemia was associated with high mortality rates of 29%, 37%, and 38% at 7, 28, and 60 days respectively, significant ICU admissions and mechanical ventilation rates. Patients with severe hyperlactatemia were stratified into high (> 50% mortality), moderate (21-50%), and low (< 20%) 28-day mortality risk groups. High-risk conditions included non-septic shock, traumatic injuries/burns, and neurological issues, with mortality rates of 51.1%, 61.8%, and 57.1%, respectively. In the moderate risk group, namely infection without shock showed a high prevalence, with a mortality rate of 36%. In the low-risk group, seizures and fainting were associated with lower mortality, exhibiting mortality rates of 0%. CONCLUSIONS: Severe hyperlactatemia is associated with higher rates of ICU admission and mortality compared to other degrees of lactate elevation in a general ED population. However, mortality rates can vary considerably, depending on the underlying etiology associated with different primary diagnoses.

Preadmission metformin use increased the incidence of hyperlactatemia at admission and 30-day in-hospital mortality among T2D patients with heart disease at high risk of hypoxia.

BACKGROUND: Surprisingly, despite the high prevalence of metformin use in type 2 diabetes (T2D) patients with heart disease, limited safety data is available regarding metformin use in patients with acute and critical heart disease. METHODS: In this single-center retrospective study, patients admitted to the cardiology department for heart failure (HF) or acute coronary syndrome (ACS) between December 2013 and December 2021 and who underwent arterial blood gas analysis at admission with an estimated glomerular clearance rate of ≥45 ml/min/1.73 m2 were identified. The incidences of hyperlactatemia, acidosis, and 30-day in-hospital mortality were compared between preadmission metformin users and nonusers. RESULTS: Of 526 admissions, 193/193 metformin users/nonusers were selected in a propensity score-matched model. Metformin users had greater lactate levels (2.55 ± 2.07 mmol/l vs. 2.00 ± 1.80 mmol/l P < 0.01), a greater incidence of hyperlactatemia [odds ratio (OR) = 2.55; 95% confidence interval (CI), 1.63-3.98; P < 0.01] and acidosis (OR = 1.78; 95% CI, 1.00-3.16; P < 0.05) at admission and a greater incidence of in-hospital mortality (OR = 3.83; 95% CI, 1.05-13.94; P < 0.05), especially those with HF/acute myocardial infarction, elderly age, or without preadmission insulin use. CONCLUSIONS: Our results suggest that, compared to metformin nonusers, preadmission use of metformin may be associated with a greater incidence of hyperlactatemia and acidosis at admission and greater 30-day in-hospital mortality among T2D patients with HF or ACS at high risk of hypoxia, particularly those without preadmission insulin use. The safety of metformin in this population needs to be confirmed in prospective controlled trials.

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.

Intestinal injury in paracetamol overdose (ATOM-8).

BACKGROUND AND AIM: Paracetamol, a widely used medication, is known for its delayed hepatotoxicity in cases of overdose. However, the potential for intestinal toxicity resulting from very high paracetamol concentrations during absorption is not well explored. This study aims to investigate the presence of intestinal toxicity and its correlation with observations in early and late paracetamol toxicity. METHODS: Serial samples of 30 patients with acute paracetamol overdose (> 10 g or 200 mg/kg) were prospectively tested. Markers of enterocyte damage, including plasma intestinal fatty acid binding protein (IFABP) and selected gut-related microRNAs (miR-21, miR-122, miR-194, and miR-215), were analyzed. Sub-analysis was performed on patients presenting with hyperlactatemia defined as a lactate greater than 2 mmol/L within 12 h post ingestion. RESULTS: In paracetamol overdose patients, median plasma IFABP was significantly elevated compared with healthy controls (720 µg/L [interquartile range, IQR, 533-1644] vs 270 µg/L [IQR 153-558], P < 0.001). Four patients had early hyperlactatemia and had significantly higher median plasma IFABP compared with those without early hyperlactatemia (3028 µg/L [IQR 1399-3556] vs 574 µg/L [IQR 526-943], P = 0.007). Furthermore, two microRNAs (miR-122 and miR-215) were downregulated in early hyperlactatemia (P = 0.019 and P = 0.006, respectively). Plasma IFABP concentrations correlated with paracetamol concentration (Spearman's r = 0.55) and lactate (r = 0.60). CONCLUSIONS: Paracetamol overdose causes concentration-related intestinal toxicity, and this is a possible explanation for the early hyperlactatemia syndrome. Intestinal toxicity has potential impacts on pharmacokinetics of other agents ingested and on the evolution of hepatotoxicity. Further studies are required to explore the mechanisms and prognostic implications of intestinal toxicity.

Could lactate clearance be a marker of mortality in pediatric intensive care unit?

BACKGROUND: Hyperlactatemia is a common finding in critically ill patients and has significant prognostic implications. However, a single lactate measurement has not been correlated to mortality consistently. In this study, we aimed to correlate the clinical efficacy of lactate clearance for the prediction of mortality in pediatric intensive care unit patients. METHODS: This retrospective observational study was performed in the pediatric intensive care unit in patients with lactate level >3 mmol/lt. Initial, 6th h, and 24th h lactate levels were recorded and lactate clearance was calculated using these values (lactate level at admission - level 6 h later × 100/lactate level at admission). RESULTS: A total of 172 patients were included in the study. Forty-four out of 172 patients died. Median (IQR) lactate (mmol/L) at admission was low in those who survived in comparison to nonsurvivors 4.4 (3.1) vs. 5.75 (7.7) (p = 0.002). Clearance at 6th h was significantly lower in those who died (11.7%) than those who survived (36.7) (p = 0.001). 6th h lactate clearance level <20.7% predicted mortality with a sensitivity of 63.6% and specificity of 69.5% along with a positive predictive value of 41.8 and a negative predictive value of 84.8 (p = 0.004). Both lactate levels and lactate clearance values were significantly predictive factors for mortality (p < 0.05). Only a positive moderate correlation was found between the percentage of PRISM-IV % and 6th h lactate level. DISCUSSION: The present study revealed that lactate clearance is a simple and rapid risk-stratification tool holding to be a potential biomarker of managing the treatment efficacy of children in the pediatric intensive care unit.

Risk factors and in-hospital mortality of postoperative hyperlactatemia in patients after acute type A aortic dissection surgery.

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 χ2 = 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 risk factors of intraoperative hyperlactatemia in patients undergoing laparoscopic colorectal surgery.

AIM: The aim of this study is to determine the incidence of intraoperative hyperlactatemia and its risk factors in patients undergoing laparoscopic colorectal surgery. MATERIAL AND METHODS: We retrospectively enrolled 75 patients who underwent laparoscopic resection for colorectal cancer. Initial lactate levels were determined from blood gas analysis before the incision. The end lactate values were recorded after the termination of the pneumoperitoneum. Hyperlactatemia defined as lactate levels between 2 mmol/L and 5 mmol/L without evidence of acidosis. The patients were divided into two groups as normolactatemia and hyperlactatemia according to lactate values at the end of the surgery. RESULTS: Of the 75 patients, 45 (60.0%) had higher lactate levels than normal at the end of the surgery. The median age of the study population was 62 (24-84) years. Forty (53.3%) of the patients were male. Most of the patients in the study had colon cancer origin [56 cases (74.7%)]. Univariate logistic regression analysis for a possible independent risk factor in terms of hyperlactatemia showed that Charlson comorbidity index (CCI) ≥ 3, body mass index (BMI) ≥ 30 kg/m2, the operative time, and the tumor size were significant (p < 0.05). Multivariate analysis found that only BMI ≥ 30 kg/m2 and the operative time were significant (p = 0.004, and p < 0.001, respectively). CONCLUSION: According to our work, obesity (BMI ≥ 30 kg/m2) and the operative time in laparoscopic colorectal surgery were independent risk factors for intraoperative hyperlactatemia at the end of the operation. Therefore, clinicians should be vigilant about the inevitable consequences of surgery by making appropriate preparation. KEY WORDS: Colorectal cancer, Lactate, Hyperlactatemia, Laparoscopy.

Hyperlactatemia associated with diabetic ketoacidosis in pediatric intensive care unit.

BACKGROUND: Children with diabetic ketoacidosis often have elevated lactate. In this study, we investigated the clinical variables associated with hyperlactatemia in children with diabetic ketoacidosis. METHODS: We designed a single-center retrospective descriptive study of children with diabetic ketoacidosis in a pediatric intensive care unit. RESULTS: Of the 107 patients with diabetic ketoacidosis included in the analysis, 61 developed hyperlactatemia. Multivariate logistic regression analysis showed that heart rate (p = 0.003),diastolic blood pressure (p = 0.001) and stage of severity (p = 0.042) were independently associated with the development of hyperlactatemia in diabetic ketoacidosis. We found that lactate level was not significantly associated with length of hospital stay (p = 0.115) or the length of time to diabetic ketoacidosis resolution (p = 0.143). CONCLUSIONS: Children with diabetic ketoacidosis presenting with severer stage, elevated heart rate and higher diastolic blood pressure may be prone to hyperlactatemia. Hyperlactatemia was not associated with length of time to DKA resolution and length of hospital stay.

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.

Significance of lactate clearance in septic shock patients with high bilirubin levels.

Lactate clearance is affected by hepatic function. However, it is unclear whether the association between hepatic dysfunction and lactate clearance can act as a prognostic marker of clinical outcomes in patients with septic shock. We aimed to evaluate the association between lactate clearance and mortality in two cohorts of septic shock patient who had hepatic dysfunction based on their total serum bilirubin levels (TBIL). Lactate clearance at 24 h after the onset of septic shock was analyzed using two cohorts, sub-categorized into two groups based on TBIL: < 2 mg/dL and ≥ 2 mg/dL. In the derivation cohort, lactate clearance was lower in non-survivors than in survivors with TBIL ≥ 2 mg/dL, while there was no significant difference in lactate clearance between non-survivors and survivors with TBIL < 2 mg/dL. Multivariate logistic regression analysis revealed that increased lactate clearance was significantly associated with decreased 28-day mortality in the TBIL ≥ 2 mg/dL group (10% lactate clearance, adjusted odds ratio [OR]: 0.88, 95% confidence interval (CI): 0.80-0.97, P = 0.0075), Creatinine level ≥ 2 mg/dL group (adjusted OR: 0.88, 95% CI: 0.81-0.95, P = 0.00069) and APACHE II score ≥ 35 group (adjusted OR: 0.93, 95% CI: 0.87-0.98, P = 0.013). In the validation cohort, lactate clearance was lower in non-survivors than in survivors with TBIL ≥ 2 mg/dL, while no significant difference in lactate clearance was observed between non-survivors and survivors with TBIL < 2 mg/dL. Increased lactate clearance was significantly associated with decreased 28-day mortality in the TBIL ≥ 2 mg/dL group (10% lactate clearance, adjusted OR: 0.89, 95% CI: 0.83-0.96, P = 0.0038) and the association was just about significant in APACHE II score ≥ 35 group (adjusted OR: 0.86, 95% CI: 0.74-1.00, P = 0.051). In conclusion, increased lactate clearance in septic shock patients with hepatic dysfunction (TBIL ≥ 2 mg/dL) or high severity (APACHE II score ≥ 35) was associated with decreased 28-day mortality.

Semiquantitative acid-base analysis in dogs with typical hypoadrenocorticism.

OBJECTIVE: To describe the semiquantitative acid-base status of dogs with untreated naturally occurring typical hypoadrenocorticism and to compare this to the status determined by traditional acid-base analysis. DESIGN: Retrospective study. SETTING: University teaching hospital. ANIMALS: Thirty-three dogs with newly diagnosed typical hypoadrenocorticism between 2000 and 2017. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Dogs were included if they had newly diagnosed hypoadrenocorticism, post-ACTH stimulation serum cortisol concentration <2 µg/dL, and blood collected within 6 hours of presentation for acid-base, electrolyte, and serum biochemical assays. Dogs were excluded if the Na+ :K+ ratio was ≥28 or the dog had received a mineralocorticoid-containing corticosteroid medication within the preceding month. Traditional acid-base analysis identified normal acid-base status in 1 dog, simple respiratory acid-base abnormalities in 2 of 33 dogs, and simple metabolic acidosis in 14 of 33 dogs. A mixed disorder was most common, noted in 16 of 33 dogs. The semiquantitative approach identified metabolic abnormalities in all cases. All dogs had ≥1 acidifying process, and 29 of 33 had both acidifying and alkalinizing processes. Acidosis attributable to excess free water was present in all dogs, and an acidifying phosphate effect was present in 27 of 33. Hyperlactatemia contributed to the acidosis in 8 of 33 dogs, with a median (range) lactate concentration of 1.5 mmol/L (13.5 mg/dL) (0.3-4.2 mmol/L [2.7-37.8 mg/dL]). CONCLUSIONS: Dogs with untreated Addison's disease have complex acid-base derangements. The semiquantitative approach to acid-base analysis provides greater insight into the underlying mechanisms of metabolic acid-base abnormalities in these dogs, particularly because lactic acidosis appears to be a minor influence in most cases.

The effect of adding lactic acid to canine whole blood on platelet aggregation as measured by impedance aggregometry.

BACKGROUND: Acidemia in sick dogs often results from the accumulation of lactic acid. The resulting decrease in blood pH can have many physiologic effects, including alteration of platelet function. OBJECTIVES: We aimed to evaluate the effect of hyperlactatemia and subsequent acidemia on platelet aggregation in canine blood using impedance aggregometry. METHODS: Platelet aggregation was measured in blood from 27 healthy dogs using the Multiplate analyzer at baseline and after in vitro addition of two different volumes of lactic acid to adjust the pH. The area under the curve (AUC), reported by the Multiplate analyzer, was used to assess the extent of platelet aggregation in each sample. A linear mixed effects model was used to test for the association between platelet aggregation and pH. The association of baseline platelet aggregation with HCTs, platelet counts, and WBC counts was assessed using Pearson's correlations. RESULTS: Acidemia was associated with a significant decrease in platelet aggregation. No significant correlations were detected between platelet aggregation and HCT, platelet count, or WBC count. Platelet aggregation measured using the Multiplate analyzer showed substantial individual variation. CONCLUSIONS: Worsening acidemia due to the addition of lactic acid caused a mild but significant decrease in platelet aggregation in canine blood. The clinical significance of this change is uncertain but could be important when combined with other abnormalities of hemostasis associated with illness.

Refractory Hyperlactatemia After a Septic Shock in a Patient With Carnitine Deficiency: A Case Report.

A 56-year-old woman with septic shock presented with persistent hyperlactatemia, despite an adequate clinical response to treatment. Carnitine deficiency was suspected, as the patient was malnourished and chronically taking valproic acid. No other plausible cause of hyperlactatemia was found. Carnitine supplementation resulted in rapid normalization of lactatemia.

Hyperlactatemia After Intracranial Tumor Surgery Does Not Affect 6-Month Survival: A Retrospective Case Series.

BACKGROUND: Patients undergoing neurosurgery frequently exhibit hyperlactatemia. The aim of this study was to identify factors associated with hyperlactatemia and assess how hyperlactatemia impacts survival and hospital length of stay after intracranial tumor surgery. MATERIALS AND METHODS: This retrospective cohort study included 496 adult patients that underwent surgery between January 1, 2014 and December 31, 2015. We evaluated patient characteristics, surgery characteristics, pH, lactate, and blood glucose from blood samples collected on admission to the high-dependency unit and the morning after surgery, and 6-month outcome data. RESULTS: Hyperlactatemia (>2.0 mmol/L) occurred in >50% of patients, but only 7.7% had acidosis. Postoperative hyperlactatemia was not correlated with 6-month survival (P=0.987), but was correlated with (median [interquartile range]) longer hospital stays (6 [4 to 8.5] d vs. 5 [4 to 8] d; P=0.006), longer surgery duration (4:53 [4:01 to 6:18] h:min vs. 4:28 [3:33 to 5:53] h:min; P=0.001), higher dexamethasone dose (16 [16 to 35] mg vs. 16 [16 to 20] mg; P<0.001), and higher blood glucose concentration (8.4 [7.5 to 9.6] mmol/L vs. 8.0 [7.1 to 8.9] mmol/L; P<0.001). Patients that received total intravenous anesthesia developed hyperlactatemia less frequently than those that received balanced anesthesia with inhalational agents (48.4% vs. 61.5%, P=0.008). Hyperlactatemia was not associated with increased postoperative neurological deficits or the need for rehabilitation therapy. CONCLUSIONS: Hyperlactatemia was common after intracranial tumor surgery. It did not influence 6-month outcomes but was associated with longer hospital length of stay. Several potential causative factors for hyperlactatemia were identified.

Hyperlactataemia with acute kidney injury following community assault: cause or effect?

BACKGROUND: Crush injury is a common presenting clinical problem in South African trauma patients, causing acute kidney injury (AKI). It has been theorised previously that the AKI was not due to an anaerobic phenomenon. A previous local study noted the presence of a mild hyperlactataemia among patients with crush syndrome, but the significance and causes of this was not fully explored. This study aimed to examine the incidence of hyperlactataemia in patients with crush syndrome presenting to a busy emergency department (ED) in rural South Africa. METHOD: The study was conducted at Edendale Hospital in KwaZulu-Natal province in South Africa from 1 June 2016 to 31 December 2017. All patients from the ED who had sustained a crush injury secondary to a mob assault were included in the study. Patients with GCS on arrival of < 13 or polytrauma were excluded from analysis. The primary outcome of interest was the presence of hyperlactataemia (> 2.0mmol/L) on presentation. The Kidney Disease Improving Global Outcomes (KDIGO) criteria were used to diagnose and stage AKI as a secondary outcome. RESULTS: A total of 84 patients were eligible for analysis. Sixty-nine (82%) patients presented with hyperlactataemia. The median serum lactate was 4.9mmol/L (IQR 2.3-7.2mmol/L). Fifteen (18%) patients were diagnosed with AKI on presentation according to serum creatinine. Ten patients were diagnosed as Stage 1, three were Stage 2 and two Stage 3 AKI respectively. There was no difference in the incidence of AKI in patients with or without hyperlactataemia (p = 0.428). Time from injury to presentation was a median 365 minutes (IQR 180-750 minutes). Six (7%) patients were admitted to high care unit and nine (11%) were admitted to the intensive care unit (ICU). No patients died within 48 hours of admission. Two patients received renal replacement therapy during the first 48 hours of admission to hospital. CONCLUSION: Hyperlactataemia is a common feature of patients presenting to the ED following crush syndrome secondary to beatings received during interpersonal violence. The origin of this hyperlactataemia is currently unknown. Further research needs to be conducted into the origin of the hyperlactataemia and its clinical significance. In this cohort, the utilisation of RRT was low but the incidence of AKI was high and developed rapidly following the injury. The utilisation of RRT also needs to be further studied in larger patient populations in South Africa to make local clinical recommendations for use.

Incidence and risk factors for hyperlactatemia in ED patients with acute metformin overdose.

INTRODUCTION: The goals of this study are to describe clinical characteristics and risk factors for metabolic acidosis with hyperlactatemia in emergency department (ED) patients with acute metformin overdose. METHODS: This was a secondary analysis of data from a retrospective observational cohort of adult ED patients presenting with acute drug overdose at two tertiary care hospitals over 5 years. The primary outcomes were: (1) hyperlactatemia, defined as a lactate concentration ≥ 2 mmol/L at any point during hospital admission and, (2) metformin associated lactic acidosis (MALA), defined as a lactate concentration ≥ 5 mmol/L and pH <7.35 at any point during hospital admission. RESULTS: We screened 3739 acute overdoses; 2872 met eligibility, 56 self-reported metformin overdose (57% female, mean age 55.8). Of these, 39 had measured lactate values. There was a high incidence of hyperlactatemia (56.4%); MALA was less frequent (17.9%). There were no deaths. Low serum bicarbonate was an independent clinical risk factor for hyperlactatemia (adjusted p < 0.05). Acetaminophen co-exposure was an independent clinical risk factor for MALA (OR 24.40, 95% CI 1.6-376.4). CONCLUSIONS: In ED patients with acute metformin overdose, initial hyperlactatemia is common but MALA is unusual. Acetaminophen co-exposure is a novel independent risk factor for the occurrence of MALA that deserves further investigation.

Vagus Nerve Stimulation Attenuates Multiple Organ Dysfunction in Resuscitated Porcine Progressive Sepsis.

OBJECTIVES: To investigate the potential benefits of vagus nerve stimulation in a clinically-relevant large animal model of progressive sepsis. DESIGN: Prospective, controlled, randomized trial. SETTING: University animal research laboratory. SUBJECTS: Twenty-five domestic pigs were divided into three groups: 1) sepsis group (eight pigs), 2) sepsis + vagus nerve stimulation group (nine pigs), and 3) control sham group (eight pigs). INTERVENTIONS: Sepsis was induced by cultivated autologous feces inoculation in anesthetized, mechanically ventilated, and surgically instrumented pigs and followed for 24 hours. Electrical stimulation of the cervical vagus nerve was initiated 6 hours after the induction of peritonitis and maintained throughout the experiment. MEASUREMENTS AND MAIN RESULTS: Measurements of hemodynamics, electrocardiography, biochemistry, blood gases, cytokines, and blood cells were collected at baseline (just before peritonitis induction) and at the end of the in vivo experiment (24 hr after peritonitis induction). Subsequent in vitro analyses addressed cardiac contractility and calcium handling in isolated tissues and myocytes and analyzed mitochondrial function by ultrasensitive oxygraphy. Vagus nerve stimulation partially or completely prevented the development of hyperlactatemia, hyperdynamic circulation, cellular myocardial depression, shift in sympathovagal balance toward sympathetic dominance, and cardiac mitochondrial dysfunction, and reduced the number of activated monocytes. Sequential Organ Failure Assessment scores and vasopressor requirements significantly decreased after vagus nerve stimulation. CONCLUSIONS: In a clinically-relevant large animal model of progressive sepsis, vagus nerve stimulation was associated with a number of beneficial effects that resulted in significantly attenuated multiple organ dysfunction and reduced vasopressor and fluid resuscitation requirements. This suggests that vagus nerve stimulation might provide a significant therapeutic potential that warrants further thorough investigation.