Search

Objective: Neonatal cerebral white matter injury represents a major precursor for neurological impairment and cerebral palsy. Our objective was to identify risk factors associated with its development., Study Design: This retrospective case-control study of all births between 23 and 34 weeks gestation at a single university hospital between May 1994 and September 2001 identified 150 cases with white matter injury characterized by periventricular leukomalacia or ventricular dilatation from white matter atrophy that were chromosomally normal and did not have other congenital anomalies. Cases were matched to controls without brain injury by the next delivery within 7 days of their gestational age., Results: There were small differences between controls and cases in gestational age (27.5 +/- 2.7, 27.4 +/- 2.6 weeks, P = .01) and birth weight (1053 +/- 402, 966 +/- 285 g, P = .002) that were statistically but not clinically significant. There was no difference in the percentage of controls and cases delivered by cesarean (45%, 49%, P = .64). There were no differences between controls and cases in umbilical arterial pH (7.27 +/- 0.11, 7.25 +/- 0.15, P = .19), base excess (-2.1 +/- 2.7, -3.0 +/- 4.1 mmol/L, P = .28), pH less than 7.0 (2/122 [2%], 3/107 [3%], P = 1.0), or base excess less than -12 mmol/L (4/121 [3%], 6/106 [6%], P = .75). The cases had a significant increase in positive blood (19%, 29%, P = .036), cerebrospinal fluid (6%, 17%, P = .002), and tracheal (9%, 22%, P = .003) cultures during the neonatal period. Conditional logistic regression showed a significant association among multiple gestations ( P = .02), intraventricular hemorrhage ( P < .001), and positive tracheal cultures ( P = .02) with cerebral white matter injury., Conclusion: Culture-positive infection was associated with an increased risk of cerebral white matter injury in preterm neonates. Intrapartum hypoxia-ischemia as manifested by metabolic acidosis was rarely associated with white matter injury and was not different from the incidence in premature neonates without injury.

Objective: Our goal was to evaluate the impact of fetal compromise on the outcome of borderline viable babies., Study Design: All 142 babies born in our hospital from 1990 to 1995 with a gestational age of 23 to 25 weeks were included. Fetal compromise was considered present if one of the following was documented: a major anomaly, congenital sepsis, chronic intrauterine infection, intrauterine drug exposure, congenital anemia, severe growth restriction, fetal acidosis, or cardiorespiratory and neurologic depression in the delivery room., Results: The 43 babies who had at least one cause of fetal compromise had a lower birth weight (p < 0.001), but there were no other differences in demographics or complications of prematurity. The survival rate was significantly better for babies free of fetal compromise (75% vs 33%, p < 0.001), particularly for babies born at 23 weeks of gestation (75% vs 6%, p < 0.001). For surviving babies free of fetal compromise, the outcome at 23 weeks was comparable to that at 24 to 25 weeks for major causes of long-term neurologic morbidity., Conclusions: Like advancing gestational age and increasing birth weight, the absence of fetal compromise has a major beneficial impact on the outcome of borderline viable babies that might be important when decisions are made about the appropriate level of support.

Objective: Our purpose was to determine the threshold of metabolic acidosis at delivery associated with newborn complications., Study Design: This study was a matched case-control study of 174 term newborn infants. Three groups defined by umbilical artery base deficit at birth were 4 to 8 mmol/L, 8 to 12 mmol/L, and 12 to 16 mmol/L. Newborn complications during the 5 days after birth were documented. A composite complication score defined the magnitude of all complications in each neonate., Results: Moderate and severe newborn encephalopathy and respiratory complications and composite complication scores >3 were increased in the group with an umbilical artery base deficit of 12 to 16 mmol/L. Moderate or severe newborn complications occurred in 10% of newborns in the same group, whereas such complications occur in 40% of neonates with an umbilical artery base deficit >16 mmol/L at birth., Conclusion: The threshold of fetal metabolic acidosis at delivery when moderate or severe newborn complications may occur is in an umbilical artery base deficit of 12 mmol/L. Thereafter, increasing metabolic acidosis is associated with a progression of severity of newborn complications.

Objective: Fewer than 50% of neonates with an umbilical arterial pH < 7.00 have neonatal complications. Our objective was to identify clinical predictive factors for adverse outcomes in this group of neonates., Study Design: In this case-control study both cases and controls had an umbilical arterial cord pH < 7.00. Cases were defined as those neonates who had seizures, grade 3 to 4 intraventricular hemorrhage, gastrointestinal dysfunction, respiratory distress syndrome requiring intubation, sepsis, or death. Controls had an umbilical arterial cord pH < 7.00 and no complications. A multivariable prediction model was created, with variables having an association with adverse outcome by bivariate analyses, attempting to predict which neonates in this umbilical arterial pH range are at greatest risk for adverse outcomes., Results: We identified 73 of 10,705 neonates born between July 1992 and October 1996 with an umbilical arterial cord pH < 7.00. Thirty-five neonates met our case definition, and the remaining 38 composed the control group. Cases had significantly lower arterial pH values and 1- and 5-minute Apgar scores, greater arterial base deficit values, and a higher incidence of abruptio placentae and maternal cocaine use. More cases were delivered before 34 weeks. There were three neonatal deaths, two cases of grade 3 or 4 intraventricular hemorrhage, five cases of gastrointestinal dysfunction, and four cases of neonatal seizures. In our predictive model for adverse neonatal outcome, an arterial base deficit > or = 16 mmol/L and a 5-minute Apgar score < 7 had a sensitivity and a specificity of 79% and 80.8%, respectively., Conclusion: Neonatal morbidity in neonates with an umbilical arterial cord pH < 7.00 can be predicted by a high arterial base deficit value and low 5-minute Apgar score.

Studies of fetal monkeys and lambs have demonstrated the association between a single prolonged episode of severe fetal hypoxia and the occurrence of neurologic abnormality. This case represents a single episode of fetal hypoxia with severe metabolic acidosis at delivery accounting for neurologic abnormality on postmortem examination that closely parallels the results of experimental studies.

Objective: Our purpose was to determine the significance of an umbilical artery pH < 7.00 in relation to neonatal morbidity and mortality., Study Design: Between 1986 and 1993 acid-base assessment of the umbilical artery was performed routinely in 10,699 deliveries. In a retrospective cohort study 84 nonanomalous neonates with an umbilical artery pH < 7.00 were individually matched with 84 neonates with an umbilical artery pH > 7.24. Matched variables included year of delivery, gender, parity, maternal age, delivery mode, fetal presentation, gestational age, and birth weight. Differences in morbidity between the two groups during the neonatal period (until 28 days after delivery) were investigated., Results: Neonates with an umbilical artery pH < 7.00 versus > 7.24 showed significant differences in the following: neonatal condition directly post partum; neurologic, respiratory, cardiovascular, and gastrointestinal complications; and neonatal intensive care unit admissions. No significance was found in renal dysfunction and mortality rate. The proportion of premature infants (< 37 weeks) was 17% in both groups. In the acidotic group a 1-minute Apgar score < or = 3 and a 5-minute Apgar score < 7 was predictive for neonatal complications., Conclusions: Severe intrapartum asphyxia, quantified by an umbilical artery pH < 7.00, poses a threat to the neonate's health.

Objective: We performed neurodevelopmental assessment in children born with an umbilical artery pH < 7., Study Design: All infants born with an umbilical artery pH < 7 from a 19-month period were retrieved from the obstetric database. Obstetric, neonatal, and pediatric records were reviewed. At an age of 1 to 3 years, children were visited at home for semi-structured questioning of the mother and a Denver Developmental Screening Test of the child., Results: During the study period 1614 umbilical artery pH measurements were entered in the database. Thirty (1.9%) were < 7. From this group 23 infants were admitted to the neonatal intensive care unit, and 8 of them required intubation. Twenty-eight children survived the neonatal period. Three children experienced an episode of mild hypertonia. One child had a mild motor developmental delay., Conclusion: Babies born with an umbilical artery pH < 7 are at greater risk to experience considerable short-term morbidity. Those who leave the neonatal intensive care unit without major problems have good outcomes, and pessimism in counseling their parents in unwarranted.

Objective: Our purpose was to determine the nature of the complications in preterm newborns after intrapartum fetal asphyxia with metabolic acidosis at delivery., Study Design: Thirty-seven preterm fetuses with metabolic acidosis were matched with 37 preterm fetuses with normal blood gas measurements at delivery. A complication score expressed the magnitude of newborn complications during the 10 days after delivery., Results: The mean complication score for the preterm newborns at 32 to 36 weeks in the asphyxia group, 9.6, was significantly greater than that for the control group, 3.1. Fetal asphyxia was associated with severe complications in all systems. The complication scores for the preterm newborns < 32 weeks in the asphyxia group were of the same order as the control group. This may be related in part to a short duration of the asphyxial insult. The Apgar score at 1 minute was a valuable predictor of newborn complications in both the asphyxia and control groups., Conclusions: Intrapartum fetal asphyxia with metabolic acidosis at delivery is an important factor in the occurrence of severe complications, particularly in the central nervous system, respiratory system, and kidney, of preterm newborns.

Objective: The neuropathologic mechanisms of the ovine fetal brain in response to several hours of sustained hypoxemia with variable degrees of metabolic acidemia was investigated in both the preterm and near-term ovine fetus., Study Design: Three groups of fetuses were studied in each of the near-term and midgestation groups: a hypoxic group, a control group, and an uninstrumented control group. Histopathologic studies were performed after a 40-hour recovery period after experimentation., Results: Pathologic findings consisted of predominately white matter damage with some adjacent cortical necrosis but no selective neuronal injury. In the near-term group the hypoxia group fetuses demonstrated significantly higher white matter injury scores than did control group fetuses (p < 0.05). Periventricular white matter injury was the predominant pattern seen in the midgestation group., Conclusions: In spite of normalization of biophysical and biochemical parameters after hypoxemia both midgestation and near-term fetuses sustained pathologic changes. Presence or extent of injury did not correlate with the degree of hypoxemia or metabolic acidosis achieved.

Objectives: Our purpose was to determine the newborn complications after respiratory or metabolic acidosis at delivery and to demonstrate the characteristics of an asphyxial insult predictive of these complications., Study Design: Fifty-nine term fetuses with metabolic acidosis were matched with 59 fetuses with normal blood gas measures at delivery. Fifty-one fetuses with respiratory acidosis were also examined. A complication score expressed the magnitude of newborn complications during the 10 days after delivery., Results: Newborn complications were not increased after respiratory acidosis. Newborn complications after metabolic acidosis increase in frequency and severity with the increasing severity and duration of the metabolic acidosis. Thirty-two of the 59 newborns in the metabolic acidosis group had a high complication score. The index values predictive of high scores were the duration of the metabolic acidosis and the Apgar score at 1 minute., Conclusions: Intrapartum fetal asphyxia with a severe metabolic acidosis accounts for complications in all newborn systems. The probability of a high complication score increases from 14% with favorable index values to 85% with unfavorable index values.

The degree of umbilical arterial acidemia associated with immediate newborn morbidity has not been determined. Therefore we compared 358 term infants with umbilical artery acidemia (pH less than 7.20) with 358 term, nonacidotic matched control infants, to evaluate immediate neonatal complications in both groups. Nonacidotic was defined as an umbilical artery pH greater than or equal to 7.20. Complications included seizures, persistent hypotonia, and/or signs of end-organ damage such as renal or cardiac dysfunction. None of the 693 newborns with an umbilical artery pH greater than or equal to 7.00 had such complications. Two of 23 infants with an umbilical artery pH less than 7.00 had sequelae related to intrapartum asphyxia. In these two infants the umbilical artery pH was less than 7.00, the 1-minute and 5-minute Apgar scores were less than or equal to 3 and the acidemia was metabolic in nature.

One hundred twenty preterm newborns less than 34 weeks' gestational age have been studied prospectively to determine the frequency of fetal and newborn metabolic acidosis and to examine the relationship of metabolic acidosis to periventricular leukomalacia as demonstrated by serial newborn ultrasonographic examinations. Fetal metabolic acidosis, based on an umbilical artery buffer base less than 34 mmol/L at delivery, occurred in three cases (2%), one of which had evidence of periventricular leukomalacia. Newborn metabolic acidosis that is based on a buffer base less than 34 mmol/L during the 4 days after delivery occurred in 12 cases (10%), five of which had evidence of periventricular leukomalacia. There is a significant relationship between the degree and duration of newborn metabolic acidosis and the occurrence of periventricular leukomalacia. This study indicates that systemic metabolic acidosis is an important pathophysiologic marker of periventricular leukomalacia. Intrapartum fetal asphyxia with metabolic acidosis, although an infrequent occurrence in the preterm newborn, may account for a few cases of periventricular leukomalacia, while the more common newborn metabolic acidosis, when of sufficient degree and duration, carries a high risk of periventricular leukomalacia.

The clinical characteristics of 124 pregnancies complicated by intrapartum fetal asphyxia have been reviewed. The evidence of fetal asphyxia tends to appear earlier in patients with maternal medical and obstetric complications than in those with labor complications. Evidence of clinical fetal distress was present in 36 per cent and was not related to the severity of the asphyxia. Low Apgar scores occurred in 40 per cent of infants with moderate asphyxia and in 80 per cent of infants with severe asphyxia at delivery. In the newborn infants, clinical evidence of cerebral abnormality was observed in 3 per cent, and evidence of the respiratory distress syndrome was seen in 3 per cent of the study group.

This review highlights recent studies that refute the following hypothesis on the genesis of cerebral palsy: The risk factors that cause death are also risk factors for brain damage resulting in cerebral palsy, if they occur at lower intensity, less frequently, or for a shorter duration. Untested, unproved, and invalid theories that emerged in the 1950s stimulated the assembly of much data that are at odds with the notion that the pathways of causation for cerebral palsy and perinatal mortality are identical.

The pulmonary course and respiratory management of 65 asphyxiated infants with at least one arterial pH less than or equal to 7.00 within the first 2 hours of life was determined. Asphyxia in the preterm and term infants in the absence of respiratory distress syndrome or meconium aspiration syndrome was associated with a transient respiratory insufficiency requiring assisted ventilation which markedly improved in the first 24 hours of life. In contrast, infants with asphyxia complicated by respiratory distress syndrome or meconium aspiration syndrome developed profound lung disease including pulmonary hemorrhage and persistence of the fetal circulation. The course of their illness was significantly worse than control infants without asphyxia. Ineffective neonatal resuscitation allowing for the development of meconium aspiration syndrome and persistent respiratory acidosis contributed to the severity of illness in more than 50% of the infants. Central nervous system pathologic conditions were present in asphyxiated infants with and without severe pulmonary disease. We conclude that severe asphyxia in the absence of underlying lung disease results in a predictable postasphyxial transient respiratory insufficiency, with marked improvement in the first 24 hours of life.

One hundred nineteen very low-birth weight infants were studied to see whether intrapartum fetal distress with or without acidosis correlated with the development of intraventricular and subependymal hemorrhage. Of 112 infants studied prospectively, 24% (27/112) had intraventricular/subependymal hemorrhage documented by real-time ultrasound studies shortly after birth; only 4.4 (5/112) had severe hemorrhage (grade 3/4). Ominous fetal heart rate patterns occurred in 50% of monitored infants with severe intraventricular/subependymal hemorrhage compared to 8% of matched controls (p less than 0.01). Reassuring fetal heart rate patterns were more predominant in infants without intraventricular/subependymal hemorrhage (p less than 0.05). Neonatal depression and the need for assisted ventilation beyond the immediate delivery period were more frequent in infants who developed intraventricular/subependymal hemorrhage. Antepartum and intrapartum complications, fetal presentation, cesarean section, duration of labor, hyaline membrane disease, and volume expansion appeared to play no role in the incidence of intraventricular/subependymal hemorrhage. Preliminary data presented here suggest that intrapartum fetal distress and acidosis may be significant factors in predicting which very low-birth weight infant will develop intraventricular/subependymal hemorrhage. The condition of the infant at birth may be more significant with respect to the extent of intraventricular/subependymal hemorrhage than a variety of obstetric variables. Aggressive management of appropriately selected patients and judicious resuscitation of the very low-birth weight infant may keep the incidence of severe intraventricular/subependymal hemorrhage at a minimum, thereby optimizing neurological outcome for this high-risk group.

In this study we examined the relationship between fetal metabolism, cardiovascular function, brain function, and eventual neuropathological outcome in the last third of gestation in the chronic fetal lamb preparation under a variety of environmental conditions. We concluded that the progressive hypoxia and metabolic acidosis secondary to acute placental insufficiency result in cerebral damage and functional deficit. Growth retardation and its attendant chronic hypoxemia, secondary to chronic placental insufficiency, do not have these results. However, intermittent interference with the umbilical circulation is associated with both functional and structural evidence of cerebral damage without systemic metabolic abnormality. The experimental, physiologic, and clinical implications of these observations are discussed.

Sixty children with biochemical evidence of intrapartum fetal hypoxia were studied to define the factors which distinguish the children with deficits from those without deficits of motor and cognitive development. Follow-up assessment included growth measures, neurological examination, Bayley Scales of Infant Development, and a modified Uzgiris and Hunt Scale. Eight children (13%) had a major deficit and 10 children (16%) had a minor deficit at 1 year. Children with deficits had an episode of hypoxia that was more severe and prolonged and, subsequent to delivery, a greater incidence of severe respiratory complications, apnea, and newborn encephalopathy. No other significant risk factors were identified. It is concluded that an episode of hypoxia less than one hour may occur without subsequent deficits. However, an episode of hypoxia in excess of 1 hour resulting in a metabolic acidosis of the order of 25 mEq/L will be followed by motor and cognitive deficits in approximately 50% of children.