Forensic Analysis of Umbilical and Newborn Blood Gas Values for Infants at Risk of Cerebral Palsy
Abstract
:1. Introduction
2. Methods
- Base deficit changes in labor: Previous reports have described the normal BD values prior to labor, changes with stages of labor and fetal heart rate decelerations, as well as normal blood gas values following a vaginal delivery [15,16]. Briefly, the normal fetal arterial BD averages 2 mmol/L prior to labor. The latent phase of labor has minimal change in fetal umbilical artery BD under normal conditions, though BD increases ~1 mmol/L every three-hours of the active phase and ~1 mmol/L per hour of active pushing in the second stage. Early decelerations do not increase fetal umbilical artery BD, though variable decelerations (dependent upon degree and duration) and late decelerations increase BD in a predictive manner [15,16,17,18,19,20,21] The duration of fetal bradycardia (50–70 bpm) corresponds to an increased BD by 1 mmol/L for every 2 minutes. The normal umbilical BDblood values following vaginal delivery approximate 5–6 mmol/L for umbilical artery and 4–5 mmol/L for umbilical vein [22,23].
- Clearance of acid in utero: Fetal acid clearance in utero is primarily across the placenta [24,25], as fetal renal blood flow is markedly reduced compared to postnatal values, and fetal renal acid clearance is immature [26]. As measured in animal models, placental clearance of metabolic acidosis occurs at a rate of ~0.1 mmol/L per minute during periods of normalized fetal blood flow and oxygenation [17,20,21]. Placental acid clearance may be limited under conditions of reduced placental function [19] or pathologies (i.e., placental abruption).
- BD changes during the neonatal period: Under conditions of normal newborn transition or rapid resuscitation, newborns do not increase the level of acidosis from delivery values once spontaneous heart rate exceeds 100 bpm. If born with significant metabolic acidosis, newborns minimally clear acid during the first one to two hours of life due to the early life impairment of hepatic and renal metabolism and clearance mechanisms as well as inhibition by acidosis [27,28]. Ultimately, the ‘’clearance’’ of systemic lactic acidosis depends on the initial peak level and the return and maintenance of spontaneous circulation and appropriate oxygenation. As neonatal cardiac compression produces less than 50% of normal cardiac output [29], newborns experience increasing acidosis during cardiac resuscitation until spontaneous heart rate exceeds 100 bpm. Similarly, severe newborn anemia, hypotension or septic shock will increase neonatal BD.
- Use of BD extracellular fluid (ECF): Blood gas analyzers measure pH, pCO2 and pO2, though bicarbonate values and BD are calculated. Most commercial blood gas analyzers report values as BD, though the calculation is performed for BDblood. However, BDblood values are significantly increased by elevated levels of pCO2 that commonly occur in fetal umbilical artery samples and may be dramatically elevated in cases of end-labor bradycardia. Thus, whereas BDblood values may be appropriate for most children and adults, recent reports have emphasized that BDECF [13,30] should be used rather than BDblood, as BDECF corrects for the altered pCO2 values. With the increasing recognition of BDECF, many of the commercial blood gas analyzers now include this measurement. Alternatively, formulas for the calculation of BDECF from measured pH and pCO2 are readily available. In this manuscript, the radiometer (Radiometer Medical, Brønshøj, Denmark) formula was utilized for all BDECF calculations [31,32].
- Comparison of umbilical artery and vein BD values: Under normal conditions, the (commonly reported) umbilical arterial BDblood is ~1 mmol/L greater than umbilical vein values [23,33], primarily due to the higher umbilical vein pCO2. BDECF values in the artery and vein are commonly similar as metabolic lactic acid is cleared slowly across the placenta. Under conditions of complete umbilical cord occlusion or placental separation from the uterine wall (complete placental abruption), there is no significant flow from the umbilical artery through the placenta to the umbilical vein. Consequently, umbilical venous values at birth represent fetal values at the time of the occurrence of complete cord occlusion or placental separation, while umbilical artery values represent the newborn at the time of birth [15], though the arterial level of acidosis may be impacted by prior occurrences of fetal ischemia or hypoxia. Fetal arterial BD increases by ~0.5 mmHg per minute of complete cord occlusion [20]. Thus, in conditions of complete cord occlusion umbilical venous blood can be completely normal, representing the state of the placenta prior to the sentinel event, though the fetus suffers from severe hypoxia-ischemia [34]. The difference between artery and vein values may be utilized to time the occurrence of cord occlusion or placental separation. Similarly, under conditions of complete umbilical cord occlusion, fetal umbilical artery pCO2 initially increases by ~7 mmHg per minute due to absent placental CO2 clearance [35].
- Umbilical artery and vein blood gas values: On occasion, samples of umbilical artery and vein blood are obtained from the same vessel, or samples are mislabeled. Normal fetal umbilical arterial and venous O2 and CO2 values [34], in conjunction with pH and BD values, can be used to assess if the values are consistent with the identified vessel. Similarly, if blood samples are exposed to an air bubble, umbilical pO2 values will increase and pCO2 values decrease due to atmospheric concentrations.
- Additional criteria for timing hypoxic ischemic injury: In addition to umbilical cord and newborn BD and blood gas values, Apgar scores, nucleated red blood cell count (nRBC), newborn platelet count and evidence of cerebral injury and edema may provide insight into timing. Briefly, as detailed in Neonatal Encephalopathy and Neurologic Outcome, Second Edition, a 5-min Apgar score of 7–10 is classified as reassuring, a score of 4–6 as moderately abnormal, and a score of 0–3 as low in the term infant and late-preterm infant [36]. Thus, 5-min Apgar scores of 7 or more are generally inconsistent with a sentinel hypoxic-ischemic event during labor. Whereas the normal nRBC count in a term infant is 0–4 nRBC/100 white blood cells [37], pre-existing hypoxic injury may produce nRBC counts of ≥26/100 white blood cells [38]. Acute hypoxic-ischemic injury typically results in an increase in nRBC counts, though to values below this level. Erythropoietin mediated stimulation requires ~ 24 h to increase newborn nRBC [39]. Thus, the relatively acute increase in nRBC following a sentinel obstetric event (e.g., uterine rupture) likely reflects release from fetal/newborn hematopoietic stores [40]. Nonspecific increases in nRBC counts may occur as a result of maternal smoking; anemia; hemolysis; and maternal diabetes [41]. Coagulopathy may be a consequence of asphyxia-induced hepatic dysfunction, as the international normalized ratio (INR) of asphyxiated infants may increase significantly on day 1 and 2 of life [42]. Newborn thrombocytopenia (<100,000) generally requires 24 h from a hypoxic injury to be manifest, while cerebral edema, sometimes evident by slit ventricles, generally does not present on an ultrasound or MRI (magnetic resonance imaging) until 18 to 24 h following an insult and generally abates by 5–6 days. Whereas deep gray matter (thalami, basal ganglia) injury is associated with an acute, profound hypoxic injury, cortical watershed regions have been associated with partial, prolonged hypoxic injury in term fetuses [43]. In addition to sites of injury, specific MRI sequences (T1, T2, diffusion weighted images, Flair and spectroscopy) [44] can differentiate myelination, ischemia, cytotoxic edema and other patterns of injury and can aid in timing. Early brain MRI showing ex vacuo brain changes suggests a more chronic timing in injury. Thus, an early brain MRI within the first one to two days of life may be valuable in the timing of an injury if it demonstrates a pattern of edema which would precede labor and delivery.
3. Case Studies
4. Discussion
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Ross, M.G. Forensic Analysis of Umbilical and Newborn Blood Gas Values for Infants at Risk of Cerebral Palsy. J. Clin. Med. 2021, 10, 1676. https://doi.org/10.3390/jcm10081676
Ross MG. Forensic Analysis of Umbilical and Newborn Blood Gas Values for Infants at Risk of Cerebral Palsy. Journal of Clinical Medicine. 2021; 10(8):1676. https://doi.org/10.3390/jcm10081676
Chicago/Turabian StyleRoss, Michael G. 2021. "Forensic Analysis of Umbilical and Newborn Blood Gas Values for Infants at Risk of Cerebral Palsy" Journal of Clinical Medicine 10, no. 8: 1676. https://doi.org/10.3390/jcm10081676
APA StyleRoss, M. G. (2021). Forensic Analysis of Umbilical and Newborn Blood Gas Values for Infants at Risk of Cerebral Palsy. Journal of Clinical Medicine, 10(8), 1676. https://doi.org/10.3390/jcm10081676