Base Deficit Levels Research Articles

Clinical value of a single postnatal lactate measurement after intrapartum asphyxia

Our aim was to compare the respective values of base deficit and lactate in birth asphyxia. Base deficit and lactate levels were measured from radial artery blood samples taken at 30 min of life in 115 term newborns suspected as having been asphyxiated during labour. Both base deficit and lactate levels were compared between patients who further developed moderate or severe encephalopathy and those who experienced no or only mild encephalopathy. Receiver operating characteristics curves and clinical values of both indicators were computed. The correlation between base deficit and lactate was significant (r2 = 0.51, p < 0.0001). Both indicators were significantly associated with neonatal outcome. Lactacidaemia lower than 5 mmol/l and/or base deficit level lower than 10 mEq/l were not followed by neurological complications. Plasma lactate concentration greater than 9 mmol/l was associated with moderate or severe encephalopathy with a sensitivity of 84% and a specificity of 67%. Base deficit and lactate had similar clinical values. Base deficit and lactate measurements in arterial blood at 30 min of life are equally valuable in assessing the severity of birth asphyxia.

Base deficit level indicating major injury is increased with ethanol

Analyses were performed to determine whether ethanol increases base deficit, independent of major injury, in blunt trauma patients from two Level I trauma centers. In 2140 Baltimore patients, base deficit was significantly higher in ethanol-positive patients (blood level ≥0.01%), independent of blood pressure (BP), Injury Severity Score (ISS), and blood loss. In 139 Youngstown, Ohio, patients, base deficit was significantly higher in ethanol-positive patients, independent of ISS and RBC units given. In 1796 awake Baltimore patients, major injury was defined as an ISS > 10, presence of blood loss, or need for RBC transfusion. A base deficit ≤−4.1 for ethanol-positive and ≤−1.1 for ethanol-negative patients had higher rates of major injury (odds ratio 3.2 and 2.1, respectively) and abdominal trauma (odds ratio 3.6 and 3.2, respectively). In blunt trauma patients, base deficit is increased with ethanol, independent of major injury. A base deficit of ≤−4.1 for ethanol-positive and ≤−1.1 for ethanol-negative awake patients may be an early warning for occult injury and suggest the need for an abdominal computed tomography (CT) scan or ultrasound.

Utilization of Fetal Heart Rate Acceleration Following Vibroacoustic Stimulation in Labor to Predict Fetal Acidemia and Base Deficit Levels

The absence of a fetal response to vibroacoustic stimulation (VAS) performed during labor may be an indicator of fetal acidemia. A lack of fetal heart rate (FHR) acceleration following VAS has been correlated with fetal scalp blood pH 7 mEq/L but was more sensitive to detect levels >10 mEq/L. All patients with pH 10 mEq/L. This stud...

Early Predictors of Postinjury Multiple Organ Failure

To find a predictive model for postinjury multiple organ failure (MOF). A 3-year cohort study ending December 1992 (first year: retrospective; last 2 years: prospective). Denver General Hospital (Colo) is a regional level I trauma center. Consecutive trauma patients with an Injury Severity Score (ISS) greater than 15, with an age greater than 16 years, and who survived longer than 24 hours. Stepwise logistic regression analysis was performed in all patients (n = 394), in the subgroup of patients with 0 to 12 hours, plus 12 to 24 hours base deficit (BD) results (n = 220), and in a second subgroup of patients with BD plus lactate results at 0 to 12 hours and 12 to 24 hours (n = 106). Postinjury MOF. The following variables were identified as independent predictors of MOF in the analysis of all patients: age more than 55 years, ISS greater than or equal to 25, and more than 6 U of red blood cells in the first 12 hours after admission (U RBC/12 hours). In the subgroup with BD results, the same analysis identified age greater than 55 years, greater than 6 U RBC/12 hours, and BD greater than 8 mEq/L (0 to 12 hours), while in the last subgroup analysis including BD and lactate results, greater than 6 U RBC/12 hours, BD greater than 8 mEq/L (0 to 12 hours), and lactate greater than 2.5 mmol/L (12 to 24 hours) were independently associated with MOF. Age greater than 55 years, ISS greater than or equal to 25, and greater than 6 U RBC/12 hours are early independent predictors of MOF. Subgroup analyses indicate that BD and lactate levels may add substantial predictive value. Moreover, these results emphasize the predominant role of the initial insult in the pathogenesis of postinjury MOF.

Effect of beta-adrenoceptor blockade on H+ and K+ flux in exercising humans.

The effect of beta-adrenoceptor blockade (beta B) on muscle release and uptake of H+ and K+ in humans during maximal exercise has been investigated. Eight volunteers cycled intermittently at power outputs corresponding to 100% of maximal O2 uptake. Prior to exercise either propranolol (beta B) or saline (control) was infused into the femoral vein. Arterial and femoral venous blood samples were drawn at rest, during exercise, and during 30-min recovery. Peak arterial blood values for K+, lactic acid (LA), and base deficit (BD) (mean +/- SE) were respectively 5.5 +/- 0.1, 9.5 +/- 0.6, and 11.7 +/- 0.9 mmol/l during beta B and 5.1 +/- 0.1, 8.3 +/- 0.6, and 10.3 +/- 1.0 for control (P less than 0.05). The release of K+ from the working leg did not differ between treatments during exercise, but K+ uptake during late recovery (5-30 min) was slightly lower during beta B. Thus the higher arterial K+ levels during exercise (beta B) cannot be attributed to greater release by active muscle but are likely due to decreased K+ uptake by noncontracting muscle. Arterial-femoral venous differences for LA and BD did not differ significantly between treatments. Additionally LA exchange across the leg was similar to H+ exchange (arterial-femoral venous differences for BD) under all conditions. During early recovery (1-5 min), regardless of experimental treatment, BD levels iin arterial blood were higher than LA (P less than 0.05). These elevated BD levels may be due to unequal removal rates between LA and H+ equivalents by nonexercised tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Continuous drip lumbar epidural anaesthesia with lidocaine for vaginal delivery. II. Influence on labour and foetal acid-base status.

Abstract. A total of 22 full term women with uncomplicated pregnancies were given continuous epidural analgesia using a 0.4 per cent lidocaine drip solution either without (series I), or with freshly added epi‐nephrine (series II). In both series a transient decrease in uterine activity occurred immediately after the induction of analgesia with 50 mg lidocaine. The spontaneous recovery time was 20‐30 minutes. In series II a more marked transitory depression of the uterine activity was recorded following a dose of 50 mg lidocaine with epinephrine, given immediately before commencing the drip infusion. Apart from these initial effects, caused by single doses, the normal progress of the first stage of labour was not significantly altered by the drip infusion. As in a previously studied series of patients, given intermittent epidural anaesthesia, a tendency to prolongation of the second stage was observed. Pathological foetal heart rate patterns were rare and never present as a consequence of maternal hypotension. Serial determination of foetal and maternal pH, Pco2, and BDecf could not demonstrate any adverse effect of the block on these variables. The influence of the duration of the second stage on foetal pH and base deficit levels were less pronounced than in a “normal” control series, suggesting better intrauterine foetal condition in the anaesthetized cases.

Observations on fetal heart rate and fetal biochemistry: I. Base deficit

One hundred thirty-nine fetuses were studied during labor by continuous FHR monitoring and uterine contraction recording. Five hundred and ninety-one fetal base deficit samples were obtained. The fetal base deficit values were correlated with the FHR patterns present during the 30 minutes immediately preceding the sampling time. Correlations were established between specific FHR patterns and fetal base deficit levels: (a) normal FHR and early deceleration had low fetal base deficit values; (b) mild and moderate variable deceleration and mild late deceleration were associated with an increase in fetal base deficit; (c) severe variable, moderate, and severe late deceleration patterns were associated with more pronounced increases in fetal base deficit.