Umbilical cord pH, blood gases, and lactate at birth: normal values, interpretation, and clinical utility.

Normal birth is a eustress reaction, a beneficial hedonic stress with extremely high catecholamines that protects us from intrauterine hypoxia and assists in the rapid shift to extrauterine life. Occasionally the cellular O2 requirement becomes critical and an O2 deficit in blood (hypoxemia) may evolve to a tissue deficit (hypoxia) and finally a risk of organ damage (asphyxia). An increase in H+ concentration is reflected in a decrease in pH, which together with increased base deficit is a proxy for the level of fetal O2 deficit. Base deficit (or its negative value, base excess) was introduced to reflect the metabolic component of a low pH and to distinguish from the respiratory cause of a low pH, which is a high CO2 concentration. Base deficit is a theoretical estimate and not a measured parameter, calculated by the blood gas analyzer from values of pH, the partial pressure of CO2, and hemoglobin. Different brands of analyzers use different calculation equations, and base deficit values can thus differ by multiples. This could influence the diagnosis of metabolic acidosis, which is commonly defined as a pH <7.00 combined with a base deficit ≥12.0 mmol/L in umbilical cord arterial blood. Base deficit can be calculated as base deficit in blood (or actual base deficit) or base deficit in extracellular fluid (or standard base deficit). The extracellular fluid compartment represents the blood volume diluted with the interstitial fluid. Base deficit in extracellular fluid is advocated for fetal blood because a high partial pressure of CO2 (hypercapnia) is common in newborns without concomitant hypoxia, and hypercapnia has a strong influence on the pH value, then termed respiratory acidosis. An increase in partial pressure of CO2 causes less increase in base deficit in extracellular fluid than in base deficit in blood, thus base deficit in extracellular fluid better represents the metabolic component of acidosis. The different types of base deficit for defining metabolic acidosis in cord blood have unfortunately not been noticed by many obstetrical experts and organizations. In addition to an increase in H+ concentration, the lactate production is accelerated during hypoxia and anaerobic metabolism. There is no global consensus on definitions of normal cord blood gases and lactate, and different cutoff values for abnormality are used. At a pH <7.20, 7% to 9% of newborns are deemed academic; at <7.10, 1% to 3%; and at <7.00, 0.26% to 1.3%. From numerous studies of different eras and sizes, it can firmly be concluded that in the cord artery, the statistically defined lower pH limit (mean -2 standard deviations) is 7.10. Given that the pH for optimal enzyme activity differs between different cell types and organs, it seems difficult to establish a general biologically critical pH limit. The blood gases and lactate in cord blood change with the progression of pregnancy toward a mixed metabolic and respiratory acidemia because of increased metabolism and CO2 production in the growing fetus. Gestational age-adjusted normal reference values have accordingly been published for pH and lactate, and they associate with Apgar score slightly better than stationary cutoffs, but they are not widely used in clinical practice. On the basis of good-quality data, it is reasonable to set a cord artery lactate cutoff (mean +2 standard deviations) at 10 mmol/L at 39 to 40 weeks' gestation. For base deficit, it is not possible to establish statistically defined reference values because base deficit is calculated with different equations, and there is no consensus on which to use. Arterial cord blood represents the fetus better than venous blood, and samples from both vessels are needed to validate the arterial origin. A venoarterial pH gradient of <0.02 is commonly used to differentiate arterial from venous samples. Reference values for pH in cord venous blood have been determined, but venous blood comes from the placenta after clearance of a surplus of arterial CO2, and base deficit in venous blood then overestimates the metabolic component of fetal acidosis. The ambition to increase neonatal hemoglobin and iron depots by delaying cord clamping after birth results in falsely acidic blood gas and lactate values if the blood sampling is also delayed. Within seconds after birth, sour metabolites accumulated in peripheral tissues and organs will flood into the central circulation and further to the cord arteries when the newborn starts to breathe, move, and cry. This influence of "hidden acidosis" can be avoided by needle puncture of unclamped cord vessels and blood collection immediately after birth. Because of a continuing anaerobic glycolysis in the collected blood, it should be analyzed within 5 minutes to not result in a falsely high lactate value. If the syringe is placed in ice slurry, the time limit is 20 minutes. For pH, it is reasonable to wait no longer than 15 minutes if not in ice. Routine analyses of cord blood gases enable perinatal audits to gain the wisdom of hindsight, to maintain quality assurance at a maternity unit over years by following the rate of neonatal acidosis, to compare results between hospitals on regional or national bases, and to obtain an objective outcome measure in clinical research. Given that the intrapartum cardiotocogram is an uncertain proxy for fetal hypoxia, and there is no strong correlation between pathologic cardiotocograms and fetal acidosis, a cord artery pH may help rather than hurt a staff person subjected to a malpractice suit based on undesirable cardiotocogram patterns. Contrary to common beliefs and assumptions, up to 90% of cases of cerebral palsy do not originate from intrapartum events. Future research will elucidate whether cell injury markers with point-of-care analysis will become valuable in improving the dating of perinatal injuries and differentiating hypoxic from nonhypoxic injuries.

Early Abnormalities in Gas Exchange in Infants with Congenital Diaphragmatic Hernia.

OBJECTIVE: To determine how blood gas exchange is altered during the transition in the first hour of life in infants with congenital diaphragmatic hernia (CDH). STUDY DESIGN: This was a prospective observational cohort study evaluating arterial blood gas (ABG) samples and ventilator support in 34 infants with CDH in the first hour of life. Infants were stratified into mild, moderate, and severe CDH. The first ABG was compared with the umbilical cord ABGs and response to intervention evaluated on subsequent ABGs among infants with different CDH severities. RESULTS: Infants were intubated at a median of 120 seconds (range 50-240 seconds) and ABGs obtained at a median of 6 minutes (IQR 4, 8 minutes), 16 minutes (IQR 13.5, 22.5 minutes), and 60 minutes (IQR 56, 64 minutes). Compared with the cord ABG, first ABG mean partial pressure of carbon dioxide (PaCO2) increased from 49.8 mm Hg to 82.1 mm Hg, mean base deficit decreased from -2.2 to -7.3, and mean pH from 7.298 to 7.060. With ventilator adjustments, second mean PaCO2 decreased to 76.7 mm Hg and third mean PaCO2 48.5 mm Hg. When stratified, with all CDH severities PaCO2 increased abruptly, remained elevated in moderate and severe CDH, and improved in all severities by 60 minutes after delivery. CONCLUSIONS: Gas exchange is markedly altered in the first hour of life in infants with CDH with abrupt onset of acidemia and a mixed respiratory and metabolic acidosis. Early implementation of adequate cardiopulmonary support may contribute to more timely stabilization of gas exchange.

Umbilical artery carbon dioxide decreases the risk for hypoxic-ischaemic encephalopathy.

AIM: An accurate biomarker for metabolic acidosis at birth is needed. Our aims were to investigate the link between umbilical artery pCO2 and the risk for hypoxic-ischaemic encephalopathy (HIE) and to compare false-negative screen results in newborn infants with HIE using three umbilical artery blood gas biomarkers. METHODS: From a cohort of newborn infants ≥35 weeks born in Ottawa, Canada, between January 2007 and December 2016, we highlighted those with HIE or who died. We compared the umbilical artery pCO2 for matched pH >mean versus matched pH ≤mean. We compared false-negative rates for three umbilical artery biomarkers-pH <7.0, base deficit ≥16 mmol/L and neonatal eucapnic pH ≤7.14. RESULTS: This study included 51 286 newborn infants, 51% male and a mean gestational age of 38.9 ± 1.5 weeks. The rate for HIE or death with umbilical artery pCO2 for matched pH >mean was 22%, compared to 78% for matched pH ≤mean. In 60 HIE or deaths, the false-negative rate for umbilical artery neonatal eucapnic pH ≤7.14 was 8%; compared to 31% for pH <7.00 and 36% for base deficit ≥16 mmol/L. CONCLUSION: The rate of HIE or death is lower in newborn infants with higher pCO2 . Using neonatal eucapnic pH decreases the risk of missing newborn infants with HIE.

Threshold of metabolic acidosis associated with newborn cerebral palsy: medical legal implications.

Obstetricians and gynecologists belong to 1 of the medical specialties with the highest rate of litigation claims. Among birth injury cases, those cases with cerebral palsy outcomes account for litigation settlements or judgments often in the millions of dollars. In cases of potential perinatal asphyxia, a threshold level of metabolic acidosis (base deficit ≥12 mmol/L) is necessary to attribute neonatal encephalopathy to an intrapartum hypoxic event. With increasing duration or severity of a hypoxic stress resulting in metabolic acidosis, newborn infant umbilical artery base deficit increases. It may be alleged that, as base deficit levels increase beyond 12 mmol/L, there is an increased likelihood and severity of cerebral palsy. As a corollary, it may be claimed that an earlier delivery (by minutes) would reduce the base deficit and prevent or reduce the severity of cerebral palsy. This issue is of relevance to obstetricians as defendants, because retrospective "expert" analysis of cases may suggest that optimal management decisions would have resulted in an earlier delivery. In addressing the association of metabolic acidosis and cerebral palsy, base deficit should be measured as the extracellular component (base deficitextracellular fluid) rather than the commonly used base deficitblood. Studies suggest that, beyond the base deficit threshold of 12 mmol/L, the incidence and severity of cerebral palsy does not significantly increase (until ≥20 mmol/L), although the risk of neonatal death rises markedly. Thus, among most infants with hypoxia-associated neonatal encephalopathy, the occurrence of cerebral palsy is unlikely to be impacted by delivery time variation of few minutes, and this argument should not serve as the basis for medical legal claims.

Elevations in Circulating sST2 Levels Are Associated With In-Hospital Mortality and Adverse Clinical Outcomes After Blunt Trauma.

BACKGROUND: Soluble suppression of tumorigenicity 2 (sST2), a decoy receptor for interleukin (IL)-33, has emerged as a novel biomarker in various disease processes. Recent studies have elucidated the role of the sST2/IL-33 complex in modulating the balance of Th1/Th2 immune responses after tissue stress. However, the role of sST2 as a biomarker after traumatic injury remains unclear. To address this, we evaluated serum sST2 correlations with mortality and in-hospital adverse outcomes as endpoints in blunt trauma patients. METHODS: We retrospectively analyzed clinical and biobank data of 493 blunt trauma victims 472 survivors (mean age: 48.4 ± 0.87; injury severity score [ISS]: 19.6 ± 0.48) and 19 nonsurvivors (mean age: 58.8 ± 4.5; ISS: 23.3 ± 2.1) admitted to the intensive care unit. Given the confounding impact of age on the inflammatory response, we derived a propensity-matched survivor subgroup (n = 19; mean age: 59 ± 3; ISS: 23.4 ± 2) using an IBM SPSS case-control matching algorithm. Serial blood samples were obtained from all patients (3 samples within the first 24 h and then once daily from day [D] 1 to D5 after injury). sST2 and twenty-nine inflammatory biomarkers were assayed using enzyme-linked immunosorbent assay and Luminex, respectively. Two-way analysis of variance on ranks was used to compare groups (P < 0.05). Spearman rank correlation was performed to determine the association of circulating sST2 levels with biomarker levels and in-hospital clinical outcomes. RESULTS: Circulating sST2 levels of the nonsurvivor cohort were statistically significantly elevated at 12 h after injury and remained elevated up to D5 when compared either to the overall 472 survivor cohort or a matched 19 survivor subcohort. Admission sST2 levels obtained from the first blood draw after injury in the survivor cohort correlated positively with admission base deficit (correlation coefficient [CC] = 0.1; P = 0.02), international normalized ratio (CC = 0.1, P = 0.03), ISS (CC = 0.1, P = 0.008), and the average Marshall multiple organ dysfunction score between D2 and D5 (CC = 0.1, P = 0.04). Correlations with ISS revealed a positive correlation of ISS with plasma sST2 levels across the mild ISS (CC = 0.47, P < 0.001), moderate ISS (CC = 0.58, P < 0.001), and severe ISS groups (CC = 0.63, P < 0.001). Analysis of biomarker correlations in the matched survivor group over the initial 24 h after injury showed that sST2 correlates strongly and positively with IL-4 (CC = 0.65, P = 0.002), IL-5 (CC = 0.57, P = 0.01), IL-21 (CC = 0.52, P = 0.02), IL-2 (CC = 0.51, P = 0.02), soluble IL-2 receptor-α (CC = 0.5, P = 0.02), IL-13 (CC = 0.49, P = 0.02), and IL-17A (CC = 0.48, P = 0.03). This was not seen in the matched nonsurvivor group. sST2/IL-33 ratios were significantly elevated in nonsurvivors and patients with severe injury based on ISS ≥ 25. CONCLUSIONS: Elevations in serum sST2 levels are associated with poor clinical trajectories and mortality after blunt trauma. High sST2 coupled with low IL-33 associates with severe injury, mortality, and worse clinical outcomes. These findings suggest that sST2 could serve as an early prognostic biomarker in trauma patients and that sustained elevations of sST2 could contribute to a detrimental suppression of IL-33 bioavailability in patients with high injury severity.

Critically ill neonates displayed stable vital parameters and reduced metabolic acidosis during neonatal emergency airborne transport in Sweden.

AIM: This study evaluated the medical quality of acute airborne transports carried out by a neonatal emergency transport service in a Swedish healthcare region from 2012 to 2015. METHODS: The transport charts and patient records of all infants transported to the regional centre were reviewed for transport indications and vital parameters and outcomes. RESULTS: We identified 187 acute airborne transports and the main indications for referral were therapeutic hypothermia after perinatal asphyxia, extremely preterm birth and respiratory failure. There were 37 deaths, but none of these occurred during transport and none of the deaths that occurred within 24 hours after transport were found to be related to the transport per se. No differences were found in vital parameters or ventilator settings before and after transport, except for an improvement in blood pH (7.22 ± 0.13 versus 7.27 ± 0.13, mean ± SD, p < 0.01), due to a decrease in base deficit (-8.0 ± 6.8 versus -5.4 ± 6.3 mmol, p < 0.001), while the partial pressure of carbon dioxide remained unchanged. CONCLUSION: During air transport, critically ill neonates displayed stable vital parameters and reduced metabolic acidosis. No transport-related mortality was found, but the high number of extremely preterm infants transported indicates the potential for improving in-utero transport.

Correlation of Lactic Acid and Base Deficit Values Obtained From Arterial and Peripheral Venous Samples in a Pediatric Population During Intraoperative Care.

Lactic acid and base deficit (BD) values are frequently monitored in the intensive care unit and operating room setting to evaluate oxygenation, ventilation, cardiac output, and peripheral perfusion. Although generally obtained from an arterial cannula, such access may not always be available. The current study prospectively investigates the correlation of arterial and peripheral venous values of BD and lactic acid. The study cohort included 48 patients. Arterial BD values ranged from -8 to 4 mEq/L and peripheral venous BD values ranged from -8 to 4 mEq/L. Arterial lactic acid values ranged from 0.36 to 2.45 µmol/L and peripheral venous lactic acid values ranged from 0.38 to 4 µmol/L. The arterial BD (-0.4 ± 2.2 mEq/L) was not significantly different from the peripheral venous BD (-0.6 ± 2.2 mEq/L). The arterial lactic acid (1.0 ± 0.5 µmol/L) was not significantly different from the peripheral venous lactic acid (1.1 ± 0.6 µmol/L). Pearson correlation coefficients demonstrated a very high correlation between arterial and peripheral venous BD ( r = .88, P < .001) and between arterial and peripheral venous lactic acid ( r = .67, P < .001). Bland-Altman plots of both pairs of measures showed that the majority of observations fell within the 95% limits of agreement. Least-squares regression indicated that a 1-unit increase in arterial BD corresponded to a 0.9-unit increase in peripheral venous BD (95% confidence interval [CI]: 0.7-1.0; P < .001) and a 1-unit increase in arterial lactic acid corresponded to a 0.9-unit increase in peripheral venous lactic acid (95% CI: 0.6-1.2; P < .001). These data demonstrate that there is a clinically useful correlation between arterial and peripheral venous lactic acid and BD values.

A Clinical Study on the Initial Assessment of Arterial Lactate and Base Deficit as Predictors of Outcome in Trauma Patients.

BACKGROUND: Trauma is a leading cause of mortality in India. Outcomes can be improved by early recognition of hemorrhagic shock and expedited management. At present, we rely on traditional vital signs, which are not sensitive measures. Point of care biochemical markers have been emerging as prognostic markers in trauma, but have not been studied in Indian setting. AIMS: This study aims to study the association between arterial lactate and base deficit (BD) at emergency department (ED) admission and 24 h outcome in trauma patients at risk of hemodynamic compromise. MATERIALS AND METHODS: This was a prospective observational study on 100 trauma patients at risk of hemodynamic compromise in tertiary care center ED. Arterial blood gas analysis at admission and 24 h outcomes were noted and statistically analyzed. RESULTS: Arterial lactate ≥4 mmol/L (sensitivity 100% and specificity 85.9%), BD ≥12 mEq/L (sensitivity 87.5% and specificity 82.6%) had more sensitivity than vital signs for predicting 24 h mortality. Higher lactate and BD were associated with increased blood transfusion requirement. Best cutoff values for predicting transfusion were lactate ≥2.9 mmol/L (sensitivity 65.2% and specificity 90.7%), BD ≥8 mEq/L (sensitivity 78.3% and specificity 75.9%). BD-based classification was comparable to ATLS classification in predicting mortality and determining transfusion requirements. Patients with higher arterial lactate and BD were found to have higher 24 h Intensive Care Unit (ICU) admission. CONCLUSION: Emergency admission arterial lactate and Base Deficit are useful predictors of mortality, need for blood transfusion and ICU admission at 24 h. It can be used to triage, identify shock early, assess transfusion requirement, and prognosticate trauma patients.

The effect of pH versus base deficit on organ failure in trauma patients.

BACKGROUND: Base deficit (BD) calculations are affected by trauma-related changes in circulating concentrations of anions after injury. In contrast, pH is a direct measurement that corresponds to hypoperfusion. We hypothesized that changes in pH would more closely correspond to organ dysfunction compared with changes in BD. MATERIALS AND METHODS: BD and pH values were collected for the first 48 h after injury from a retrospective cohort of 74 multiply injured adult patients who were admitted to the surgical intensive care unit for a minimum of 1 wk. Mean and extreme (minimum pH and maximum BD) values of pH and BD were determined for day 1 (0-24 h) and for day 2 (24-48 h) after injury. Organ dysfunction was measured by averaging daily sequential organ failure assessment scores over the entire duration of intensive care unit admission. BD and pH values were compared with mean modified sequential organ failure assessment scores by univariate and multivariate linear regression. RESULTS: Organ dysfunction corresponded more closely with changes in pH compared with those in BD. Minimum pH and maximum BD showed better correspondence to organ dysfunction compared with mean values. Minimum pH values at 24-48 h had the highest univariate (r(2) = 0.43) correspondence to organ dysfunction. In contrast, mean BD values at 24-48 h showed no correspondence (r(2) = 0.07) to organ dysfunction. Multivariate analysis demonstrated that 24-48 h of minimum pH had the highest numerical effect on organ dysfunction. CONCLUSIONS: Correspondence between organ dysfunction and BD deteriorated in contrast to increasing correspondence between organ dysfunction and pH measured within 48 h after injury.

A comparison of initial lactate and initial base deficit as predictors of mortality after severe blunt trauma.

BACKGROUND: After injury, base deficit (BD) and lactate are common measures of shock. Lactate directly measures anaerobic byproducts, whereas BD is calculated and multifactorial. Although recent studies suggest superiority for lactate in predicting mortality, most were small or analyzed populations with heterogeneous injury severity. Our objective was to compare initial BD with lactate as predictors of inhospital mortality in a large cohort of blunt trauma patients all presenting with hemorrhagic shock. MATERIALS AND METHODS: The Glue Grant multicenter prospective cohort database was queried; demographic, injury, and physiologic parameters were compiled. Survivors, early deaths (≤24 h), and late deaths were compared. Profound shock (lactate ≥ 4 mmol/L) and severe traumatic brain injury subgroups were identified a priori. Chi-square, t-test, and analysis of variance were used as appropriate for analysis. Multivariable logistic regression and area under the receiver operating characteristic curve analysis assessed survival predictors. P < 0.05 was significant. RESULTS: A total of 1829 patients met inclusion; 289 (15.8%) died. Both BD and lactate were higher for nonsurvivors (P < 0.00001). After multivariable regression, both lactate (odds ratio [OR] 1.17; 95% confidence interval [CI]: 1.12-1.23; P < 0.00001) and BD (OR 1.04; 95% CI: 1.01-1.07; P < 0.005) predicted overall mortality. However, when excluding early deaths (n = 77), only lactate (OR 1.12 95% CI: 1.06-1.19; P < 0.0001) remained predictive but not BD (OR 1.00 95% CI: 0.97-1.04; P = 0.89). For the shock subgroup, (n = 915), results were similar with lactate, but not BD, predicting both early and late deaths. Findings also appear independent of traumatic brain injury severity. CONCLUSIONS: After severe blunt trauma, initial lactate better predicts inhospital mortality than initial BD. Initial BD does not predict mortality for patients who survive >24 h.

The significance of base deficit in acidemic term neonates.

OBJECTIVE: Much emphasis is placed on the metabolic component of umbilical cord acidemia at birth, with an importance attached to an arterial level of <7.00 accompanied by a base deficit of 12 mmol/L. We hypothesized that in acidemic neonates, the level of arterial base deficit provides no prognostic information beyond that provided by the level of arterial pH. STUDY DESIGN: This is a cohort study using a database of deliveries from a major teaching hospital, with additional information from neonatal records. A total of 8797 term, singleton, nonanomalous neonates were identified who had paired and validated cord blood gas analysis. Of these, 520 were acidemic (pH <7.1) and 84 were severely acidemic (pH <7.0). Outcomes examined were encephalopathy grade 2/3 and/or death, Apgar <7 at 5 minutes, neonatal unit admission, and composite outcomes of neurological and systemic involvement. Hierarchical logistic regressions were done using IBM SPSS Statistics 20.0 (Armonk, NY) to assess the predictive value of arterial pH and arterial base deficit. RESULTS: For each outcome the median pH and base deficit of those neonates affected by the adverse outcome was significantly lower than for those who were unaffected. Hierarchical logistic regressions showed that pH is a significant predictor of all adverse outcomes studied (P < .001 for all outcomes). When base deficit, and then the cross-product, are added to the model, neither add predictive value. CONCLUSION: In acidemic neonates, the metabolic component does not predict those at risk of adverse outcomes once pH is taken into account. The apparently worse outcomes with greater base deficit simply reflect a greater degree of acidemia. The prognostic significance attached to the base deficit among acidemic neonates is questionable.

Comparison of Apgar scores and cord blood gas parameters in fetuses with isolated congenital heart disease and healthy controls.

OBJECTIVE: This retrospective study aimed to investigate how congenital heart disease (CHD) affects early neonatal outcomes by comparing Apgar scores and umbilical cord blood gas parameters between fetuses with structural cardiac anomalies and healthy controls. Additionally, within the CHD group, the study explored the relationship between these parameters and mortality within six months. METHODS: Data from 68 cases of prenatally diagnosed CHD were collected from electronic medical records, excluding cases with missing data or additional comorbidities. Only patients delivered by elective cesarean section, without any attempt at labor, were analyzed to avoid potential confounding factors. A control group of 147 healthy newborns was matched for delivery route, maternal age, and gestational week. Apgar scores at 1, 5, and 10 minutes, as well as umbilical cord blood pH, base deficit, and lactate levels, were recorded. RESULTS: Maternal age, gestational week at delivery, and birth weight were similar between the CHD and control groups. While Apgar score distribution was significantly lower at 1st, 5th, and 10th minutes in the CHD group, umbilical cord blood gas parameters did not show significant differences between groups. Within the CHD group, lower umbilical cord blood pH and larger base deficit were associated with mortality within six months. CONCLUSION: Newborns with CHD exhibit lower Apgar scores compared to healthy controls, suggesting potential early neonatal challenges. Furthermore, umbilical cord blood pH and base deficit may serve as predictors of mortality within six months in CHD cases. Prospective studies are warranted to validate these findings and integrate them into clinical practice, acknowledging the study's retrospective design and limitations.

Triage vital signs do not correlate with serum lactate or base deficit, and are less predictive of operative intervention in penetrating trauma patients: a prospective cohort study.

BACKGROUND: Triage vital signs are often used to help determine a trauma patient's haemodynamic status. Recent studies have demonstrated that these may not be very specific in determining major injury. The purpose of this study was to determine if there is any correlation between triage vital signs, base deficit (BD) and lactate, and to determine the odds of operative intervention in penetrating trauma patients. METHODS: A prospective observational cohort study was undertaken. Baseline vital signs, BD and lactate were recorded in all patients for whom the trauma team was activated. Pearson correlation and coefficient (ρ) were calculated. ORs were calculated. RESULTS: 75 patients were enrolled. Pearson correlations and coefficients calculated for lactate to systolic blood pressure were: -0.052 (ρ=0.0011, 95% CI -0.225 to 0.228); lactate and HR: 0.23 (ρ=0.0166, 95% CI -0.211 to 0.242); lactate and RR: 0.23 (ρ=0.054, 95% CI -0.174 to 0.277). BD to systolic blood pressure were: 0.003 (ρ=0.00001, 95% CI -0.229 to 0.224); BD and HR: -0.19 (ρ=0.038, 95% CI -0.399 to 0.038); BD and RR: -0.019 (ρ=0.0004, 95% CI -0.244 to 0.208). Odds of operative intervention were greater in patients with abnormally high lactate, OR 4.17 (95% CI 1.57 to 11), but not for BD, OR 2.53 (95% CI 0.99 to 6.45), or any of the vital signs. CONCLUSIONS: Triage vital signs have no correlation to lactate or BD levels in penetrating trauma patients. Odds of operative intervention are greater in patients with abnormally high serum lactate levels, but not in those with abnormal triage vital signs or BD.

Combination of Lactate and Base Deficit Levels at Admission to Predict Mortality in Blunt Trauma Patients.

INTRODUCTION: Elevated lactate levels are associated with increased mortality in both trauma and non-trauma patients. The relation between base deficit (BD) and mortality is less clear. Traumatologists debate the utility of elevated lactate (EL) versus BD in predicting mortality. We hypothesized that EL (2mmol/L to 5mmol/L) and BD (≤-2mmol/L) in combination could predict mortality in blunt trauma patients.  Methods: This is a retrospective analysis of the trauma registry from 2012 to 2021 at a level 1 trauma center. Blunt trauma patients with admission lactate and BD values were included in the analysis. Exclusion criteria were age <18, penetrating trauma, unknown mortality, and unknown lactate or BD. Logistics regression of the total 5153 charts showed 93% of the patients presented with lactate levels <5mmol/L, therefore patients with lactate >5mmol/L were excluded as outliers. The primary outcome was mortality. RESULTS: A total of 4794 patients (151 non-survivors) were included in the analysis. Non-survivors had higher rates of EL + BD (35.8% vs. 14.4%, p <0.001). When comparing survivors and non-survivors, EL + BD (OR 5.69), age >65 (5.17), injury severity score (ISS) >25 (8.87), Glasgow coma scale <8 (8.51), systolic blood pressure (SBP) <90 (4.2), and ICU admission (2.61) were significant predictors of mortality. Other than GCS <8 and ISS >25, EL + BD had the highest odds of predicting mortality. CONCLUSION: Elevated lactate + BD on admission in combination represents a 5.6-fold increase in mortality in blunt trauma patients and can be used to predict a patient's outcome on admission. This combination variable provides an additional early data point to identify patients at elevated risk of mortality at the moment of admission.

Umbilical Cord Blood Acid-Base Parameters and Lactate as Predictors of Subsequent Meconium Aspiration Syndrome in Neonates.

Meconium aspiration syndrome (MAS) in neonates born through meconium-stained amniotic fluid (MSAF) causes significant morbidity and mortality. Early recognition of at-risk neonates could help optimize treatment. The aim was to determine predictive characteristics of cord blood pH, base deficit and lactate with subsequent MAS. Receiver operating characteristic (ROC) curves with area under curve (AUC) were estimated. Among 231 MSAF complicated pregnancies, 25 (10.8%) had MAS. Mean cord pH was significantly lower in neonates with MAS compared to those without MAS (7.15 ± 0.11 vs. 7.26 ± 0.07; p < 0.001). Median lactate between the two groups [5.6 (7.5, 3.7) vs. 2.7 (4.5, 2.0)] and base deficit [-10.6 (-13.2, -4.2) vs. -3.7 (-6.3, -2.6)] also differed significantly (p = 0.01). ROC curve area for cord lactate, pH, and base deficit were 0.81, 0.79, and 0.75, respectively. The predictive cutoff values for pH, lactate, and base deficit were 7.20, 3.55 mmol/L, and -5.3 mmol/L, respectively.

The Association Between Serum Lactate Concentration, Base Deficit, and Mortality in Polytrauma Patients as a Prognostic Factor: An Observational Study.

Introduction In polytrauma patients, it is crucial to identify the severity of the injuries to ensure patient safety and survival. Polytrauma leads to hypotension and hypoperfusion, which results in an anaerobic metabolism with acidosis and a decrease in base excess. Thus, blood lactate levels above a certain threshold indicate the existence of global tissue hypoxia, which is a precursor to shock and multiple organ dysfunction syndrome (MODS). The serum lactate and base deficit (BD) levels are used in polytrauma patients as measures of damage severity and resuscitation endpoints and as a way to evaluate therapy efficacy and to predict outcomes. Thus, arterial blood gas analysis is of great value in assessing the status and prognosis of patients with polytrauma. There are few comparative studies on the predictive values of these markers in trauma patients. To determine which measure can more accurately predict the prognosis of polytrauma patients, the present study investigated the predictive values of mortality of these indicators for mortality within 48 hours of admission to the emergency room (ER) in patients with polytrauma. Methods This prospective study was designed for a single tertiary care center in northern India. We included 90 patients with polytrauma who were between the ages of 18 and 70 years, with the exception of pregnant women, who presented to the ER within six hours of injury with an injury severity score (ISS) >16, serum lactate level >2.0 mmol/L, and BD -4.0 mEq/L at the time of admission. If the patient's ISS was >16 at the time of ER presentation, arterial blood samples were drawn to determine the serum lactate and BD level at the time of admission and at 12, 24, and 48 hours intervals after ER admission. The primary outcome was the change in serum lactate and BD level in polytrauma. The secondary outcomes were an association of serum lactate and BD with mortality and the correlation between serum lactate with the BD and ISS with mortality of polytrauma patients. The timing of all outcome assessments was at 48 hours after each patient's ER admission. Results Lactate clearance from 0-12 hours (t = 2.28, p <0.05), 0-24 hours (t = 6.01, p <0.001), and 0-48 hours (t = 7.98, p <0.001) and a correction in BD from 0-24 (t = 2.68, p <0.01 ) and 0-48 hours (t = 5.46, p <0.001) were significantly higher in nonsurvivors as compared with survivors. In survivors and nonsurvivors, mean serum lactate levels (2.46 ± 1.46 versus 4.15 ± 2.99, t = 3.31, p <0.001, 95%Cl) and mean BD (-3.17 ± 2.58 versus -6.5 ± 4.91, t = 3.86, p <0.001, 95%CI) had a statistically significant difference. The serum lactate and BD levels at time of ER admission (r L0, BD0 = -0.765, p <0.01) and 48 hours after ER admission (r L48, BD 48 = -0.652, p <0.001) were highly negatively correlated. Conclusion In polytrauma patients, serum lactate and BD are simple, quick, and independent biochemical predictors of 48-hour mortality, and this single arterial blood test would thereby improve decision-making for resuscitation effectiveness. Prolonged lactate and BD normalization time were associated with higher mortality. Serum lactate and BD are negatively correlated. A higher ISS at admission was associated with a higher incidence of mortality in polytrauma patients.

Polytraumatized patient lower extremity nonunion development: Raw data.

In this article we report data collected to evaluate the pathomechanistic effect of acute anaerobic metabolism in the polytraumatized patient and its subsequent effect on fracture nonunion; see "Base Deficit ≥6 within 24 Hours of Injury is a Risk Factor for Fracture Nonunion in the Polytraumatized Patient" (Sardesai et al., 2021) [1]. Data was collected on patients age ≥16 with an Injury Severity Score (ISS) >16 that presented between 2013-2018 who sustained a fracture of the tibia or femur distal to the femoral neck. Patients presenting to our institution greater than 24 hours post-injury and those with less than three months follow-up were excluded. Medical charts were reviewed to collect patient demographic information and known nonunion risk-factors, including smoking, alcohol use, and diabetes. In addition, detailed injury characteristics to quantify injury magnitude including ISS, Glasgow Coma Scale (GCS) at admission, and ICU length of stay were recorded. ISS values were obtained from our institutional trauma database where they are entered by individuals trained in ISS calculations. Associated fracture-related features including fracture location, soft-tissue injury (open vs. closed fracture), vascular injury, and compartment syndrome were recorded. Finally, vital signs, base deficit (BD), and blood transfusions over 24 hours from admission were recorded. We routinely measure BD and less consistently measure serum lactate in trauma patients at the time of presentation or during resuscitation. BD values are automatically produced by our laboratory with any arterial blood gas order, and we recorded BD values from the medical record. Clinical notes and radiographs were reviewed to confirm fracture union versus nonunion and assess for deep infection at the fracture site. Patients were categorized as having a deep infection if they were treated operatively for the infection prior to fracture healing or classification as a nonunion. Nonunion was defined by failure of progressive healing on sequential radiographs and/or surgical treatment for nonunion repair at least six months post-injury.

Forensic Analysis of Umbilical and Newborn Blood Gas Values for Infants at Risk of Cerebral Palsy.

Cerebral palsy litigation cases account for the highest claims involving obstetricians/gynecologists, a specialty that ranks among the highest liability medical professions. Although epidemiologic studies indicate that only a small proportion of cerebral palsy (10-20%) is due to birth asphyxia, negligent obstetrical care is often alleged to be the etiologic factor, resulting in contentious medical-legal conflicts. Defense and plaintiff expert opinions regarding the etiology and timing of injury are often polarized, as there is a lack of established methodology for analysis. The objective results provided by umbilical cord and newborn acid/base and blood gas values and the established association with the incidence of cerebral palsy provide a basis for the forensic assessment of both the mechanism and timing of fetal neurologic injury. Using established physiologic and biochemical principles, a series of case examples demonstrates how an unbiased expert assessment can aid in both conflict resolution and opportunities for clinical education.

Base Deficit ≥ 6 within 24 h of Injury is a risk factor for fracture nonunion in the polytraumatized patient.

BACKGROUND: Polytrauma patients are at risk for fracture nonunion, but the reasons are poorly understood. Increased base deficit (BD) is associated with hypovolemic shock. Although shock delays bone healing in animal models, there have been no clinical studies evaluating the impact of BD on nonunion risk. MATERIALS AND METHODS: Patients age ≥ 16 with injury severity score > 16 that presented to an academic Level One trauma center with an operative femur or tibia fracture were reviewed. Clinical notes and radiographs were assessed to determine fracture healing status. Patient demographics, injury characteristics, BD, and number of packed red blood cell transfusions were recorded. Bivariate and multivariate analyses of multiple risk factors associated with nonunion were conducted to investigate the association of BD with nonunion. RESULTS: The union group was comprised of 243 fractures; there were 36 fractures in the nonunion group. The following predictors were associated with nonunion: smoking (p = 0.009), alcohol use (p < 0.001), open fracture (p < 0.001), and treatment for deep infection at fracture site (p = 0.016). Additionally, worst BD over 24 h ≥ 6 (p = 0.031) was significant for nonunion development. A multivariate logistic regression analysis revealed worst BD ≥6 over 24 h remained significantly associated with the development of nonunion (odds ratio 3.02, p = 0.011) when adjusting for other risk factors. CONCLUSIONS: A BD ≥ 6 within 24 h of admission was associated with a significantly increased risk of developing lower extremity fracture nonunion in polytrauma patients, even after adjusting for multiple other risk factors. Acute post-traumatic acidosis may have effects on long-term fracture healing.