Intrahepatic vein for fetal blood sampling: one center's experience.

OBJECTIVE: The objective of the study was to examine 1 center's experience with fetal blood sampling via the fetal intrahepatic vein (IHV) and cordocentesis. STUDY DESIGN: Consecutive IHV and cordocentesis procedures between July 1987 and February 2006 were compared with respect to success rates, streaming at the sampling site, nonreassuring fetal heart rate (NRFHR), or need for urgent delivery post procedure. A subanalysis of cases with fetal thrombocytopenia was performed. Data were analyzed using Fisher's exact and Student t tests. RESULTS: Two hundred ten procedures (130 IHV samplings and 110 cordocenteses) were identified. Success rates were significantly higher with IHV sampling than with cordocentesis (84.6% vs 69.1%, P = .004). Streaming from the sampling site occurred after 0.79% of IHV procedures vs 30.8% of cordocenteses (P < .0001). There was no difference between IHV and cordocentesis in the incidence of NRFHR or need for immediate delivery. Twenty-five cases of fetal thrombocytopenia (20 sampled via IHV, 5 by cordocentesis) were identified. Streaming from the sampling site occurred in 0 of 20 IHV cases vs 2 of 5 cordocentesis cases (40%) (P = .03). CONCLUSION: IHV has a significantly lower rate of streaming from the sampling site, compared with cordocentesis. Our data suggest that IHV sampling conveys a particular advantage when fetal thrombocytopenia is suspected.

Large fetal sacrococcygeal teratomas: could early delivery improve outcome?

OBJECTIVE: To determine if gestational age (GA) at delivery or tumor size impacts outcome in neonates with very large sacrococcygeal teratomas (SCTs). METHODS: Retrospective chart review from 1990 to 2006 of live-born infants with very large SCTs, defined as diameters exceeding 10 cm. Data analyzed using the independent t test and Fisher's exact test, with p values <0.05 considered significant. RESULTS: Nine infants with very large SCTs were identified. Six of the 9 infants survived, 4 of whom had evidence of early hydrops. Mean GA of survivors was 32.2 +/- 3.7 versus 31.7 +/- 0.6 weeks in nonsurvivors (p = 0.85). Infants with the largest SCTs did not survive. CONCLUSION: Risks of preterm delivery must be weighed against complications from further enlargement of very large SCTs and against the risks of in utero intervention.

Intrapartum electronic fetal heart rate monitoring and the identification of metabolic acidosis and hypoxic-ischemic encephalopathy.

OBJECTIVE: The purpose of this study was to determine whether electronic fetal monitoring can identify fetuses with metabolic acidosis and hypoxic-ischemic encephalopathy. STUDY DESIGN: The cases were 107 nonanomalous chromosomally normal fetuses with an umbilical arterial pH < 7.0 and base excess < or = 12 mmol/L. Controls were the subsequent delivery that was matched by gestational age and mode of delivery. The last hour of electronic fetal monitoring before delivery was evaluated by 3 obstetricians who were blinded to outcome. RESULTS: Cases had a significant increase in late and prolonged decelerations/hour and late decelerations/contractions. Those fetuses with hypoxic-ischemic encephalopathy had significant increases in bradycardia, decreased variability, and nonreactivity but no difference in late or variable decelerations/hour. For the identification of hypoxic-ischemic encephalopathy, the sensitivity, specificity, and positive and negative predictive values were 15.4%, 98.9%, 66.7%, and 89.4%, respectively, for bradycardia; 53.8%, 79.8%, 26.9%, and 92.6%, respectively, for decreased variability; 92.3%, 61.7%, 2.7%, and 82.9%, respectively, for nonreactivity; and 7.7%, 98.9%, 50.0%, and 88.6%, respectively, for all 3 abnormalities combined. CONCLUSION: Fetal metabolic acidosis and hypoxic-ischemic encephalopathy are associated with significant increases in electronic fetal monitoring abnormalities, but their predictive ability to identify these conditions is low.

Can electronic fetal monitoring identify preterm neonates with cerebral white matter injury?

OBJECTIVE: Although preterm delivery occurs in only 10% of all births, these infants are at high risk for cerebral white matter injury and constitute a third of all cerebral palsy cases. Our objective was to estimate if electronic monitoring can identify preterm fetuses diagnosed with brain injury during the neonatal period. METHODS: In this case-control study, 150 consecutive neonates with ultrasonography-diagnosed cerebral white matter injury were matched by gestational age within 7 days to 150 controls with normal head ultrasonograms. Tracings were retrieved for 125 cases (83%) and 121 controls (81%) and reviewed by 3 perinatologists blinded to outcome. Vaginal (64 cases, 72 controls) and cesarean deliveries (61 cases, 49 controls) were analyzed separately. RESULTS: There was no difference in baseline heart rate, tachycardia, bradycardia, short-term variability, accelerations, reactivity, number or types of decelerations, or bradycardic episodes between cases and controls in either the vaginal or cesarean delivery groups. For the 6 neonates with metabolic acidosis severe enough to increase the risk for long-term neurologic morbidity, there was a significant increase in baseline amplitude range less than 5 beats per minute; however, its positive predictive value in predicting severe metabolic acidosis was only 7.7%. Increasing late decelerations were associated with decreasing umbilical arterial pH and base excess, but were not significantly different in the acidosis and control groups (1.0 +/- 1.8, 0.55 +/- 1.23 late decelerations per hour, P = .39). CONCLUSION: Although decreased short-term variability and increased late decelerations are associated with decreasing umbilical arterial pH and base excess, electronic fetal monitoring is unable to identify preterm neonates with cerebral white matter injury.

Cord gas analysis, decision-to-delivery interval, and the 30-minute rule for emergency cesareans.

OBJECTIVE: Our primary objective was to examine the relationship between umbilical arterial gas analysis and decision-to-delivery interval for emergency cesareans performed for nonreassuring fetal status to determine if this would validate the 30-minute rule. STUDY DESIGN: For this retrospective cohort study, all cesarean deliveries performed for nonreassuring fetal status from September 2001 to January 2003 were reviewed. A synopsis of clinical information that would have been available to the clinician at the time of delivery and the last hour of the electronic fetal heart rate tracing prior to delivery were reviewed by three different maternal-fetal medicine specialists masked to outcome, who classified each delivery as either emergent (delivery as soon as possible) or urgent (willing to wait up to 30 minutes for delivery) since immediacy of the fetal condition is the key factor affecting the type of anesthesia used. RESULTS: Of 145 cesareans performed for nonreassuring fetal status during this period, 117 patients met criteria for entry, of which 34 were classified as emergent and 83 as urgent. Kappa correlation was 0.35, showing only fair/moderate agreement between reviewers. In the emergent group, general anesthesia was more common (35.3%, 10.8%, p=0.003), and the decision-to-delivery interval was 14 minutes shorter (23.0+/-15.3, 36.7+/-14.9 minutes, p<0.001). Linear regression showed a statistically significant relationship between increasing decision-to-delivery interval and umbilical arterial pH (r=0.22, p=0.02) and base excess (r=0.33, p<0.001) showing that delivery proceeded sooner for most of those with the worst cord gases, with a gradual improvement over time. For the 13 (11%) neonates with cord gases placing them at increased risk for long-term neurologic sequelae, the decision-to-delivery interval was 24.7+/-14.6 minutes (range 6 to 50 minutes), and 3/13 (23%) were classified as urgent rather than emergent. CONCLUSION: Electronic fetal monitoring shows considerable variation in interpretation among maternal-fetal medicine specialists and is not a sensitive predictor of the fetus developing metabolic acidosis. There is no deterioration in cord gas results after 30 minutes, and most neonates delivered emergently or urgently for nonreassuring fetal status even when born after 30 minutes have normal cord gases. The 30-minute rule is a compromise that reflects the time it takes the fetus to develop severe metabolic acidosis, our imprecision in its identification, and its rarity in the presence of nonreassuring fetal monitoring.

Phimosis as a cause of the prune belly syndrome: comparison to a more common pattern of proximal penile urethra obstruction.

The pathogenesis of the prune belly syndrome (PBS) remains controversial, but two theories predominate. The first theory supports an obstructive phenomenon early in gestation leading to irreversible damage to the genitourinary tract and abdominal wall. The second theory suggests mesodermal injury between the 6th and 10th weeks of gestation as the primary abnormality. This paper reports of two fetuses with the PBS phenotype that were examined postmortem at our institution. Thorough examination of the lower urinary tract allowed demonstration of anatomic obstruction of the urethra in both cases. One case illustrated a relatively common pattern of proximal penile urethral obstruction, a flap-like obstruction between the prostatic and penile urethra. The other case provided what we believe to be the first description of PBS caused by severe phimosis.

Association of prematurity and neonatal infection with neurologic morbidity in very low birth weight infants.

OBJECTIVE: To identify risk factors predictive of neurologic morbidity in very low birth weight (VLBW) infants. METHODS: This is a case-control study of all infants weighing 1500 g or less admitted to a single tertiary neonatal intensive care unit between April 1999 and December 2001. The case group were those neonates with neurologic morbidity including intraventricular hemorrhage, seizures, hydrocephalus, and periventricular leukomalacia. The control group were those without neurologic morbidity. Wilcoxon rank-sum, Fisher exact test, chi(2), and univariate and stepwise multiple logistic regression were performed, with P < 0.05 considered significant. RESULTS: Of 213 VLBW infants, 77 had neurologic morbidity: 61 had intraventricular hemorrhage, eight had seizures, 13 had hydrocephalus, and nine had periventricular leukomalacia. Several infants had more than one morbidity. Gestational age (odds ratio [OR] 0.95; 95% confidence interval [CI] 0.94, 0.96; P <.005), birth weight (OR 0.62; 95% CI 0.49, 0.79; P <.005), and neonatal infection (OR 1.36; 95% CI 1.17, 1.58; P <.005) were highly associated with neurologic morbidity. There was no difference in mean umbilical arterial cord pH (7.25 +/- 0.15, 7.28 +/- 0.09, P =.45) or base excess (-3.8 +/- 4.8 mEq/L, -2.3 +/- 3.0, P =.10). Only three of 52 infants (5.8%) in the case group had an umbilical arterial pH of less than 7. CONCLUSION: Prematurity and neonatal infection were the dominant factors associated with neurologic morbidity in VLBW infants. Intrapartum acidosis occurred in less than 6% of those with neurologic morbidity.

An amniotic fluid index < or =5 cm within 7 days of delivery in the third trimester is not associated with decreasing umbilical arterial pH and base excess.

OBJECTIVE: To determine if an amniotic fluid index (AFI) < or =5.0 cm within 7 days of delivery in the third trimester is associated with decreasing umbilical arterial pH and base excess. STUDY DESIGN: Cases for this retrospective cohort study were all pregnancies > or =26 weeks with intact membranes and an AFI < or =5.0 cm within 7 days of delivery between 11/99 and 7/02. Multiple gestations, aneuploid, and anomalous fetuses were excluded. Controls with an AFI >5.0 cm within 7 days of delivery were matched to each case within 1 week by gestational age. For a control group with a mean+/-SD umbilical arterial pH of 7.26+/-0.07 and alpha=0.05, a sample size of 100 would have a power of 99% to detect a difference with a study group whose mean was 7.20. Data were compared using paired Student's t-test, Mann-Whitney, Fisher's exact, chi(2) and risk ratios with 95% confidence intervals. RESULTS: In all, 131 neonates with an AFI < or =5.0 cm were matched to 131 controls with an AFI >5 cm. There was no difference in gestational age (37.6+/-3.0, 37.7+/-3.0 weeks) or birth weight (2897+/-810, 2762+/-788 g). There was no difference in umbilical artery pH (7.25+/-0.07, 7.26+/-0.07) or base excess (-3.32+/-2.59, -2.83+/-2.45 mmol/l), even in small for gestational age (SGA) infants in both groups. There was no difference in the number of SGA neonates, 5-minute Apgar <7, respiratory distress syndrome, necrotizing enterocolitis, or neurologic morbidity. Linear regression showed no correlation between AFI and either umbilical arterial pH (r=-0.00047, SE=0.001, p=0.63) or base excess (r=-0.029, SE=0.037, p=0.428). CONCLUSION: An AFI < or =5.0 cm measured within 7 days of delivery in the third trimester is not associated with decreasing umbilical arterial pH and base excess.

Neonatal nucleated red blood cells and the prediction of cerebral white matter injury in preterm infants.

OBJECTIVE: To estimate whether neonates with cerebral white matter injury have significant elevations in nucleated red blood cell counts and to estimate their predictive ability in identifying injury. METHODS: This case-control study identified 176 infants born at 23-34 weeks of gestation between November 1994 and October 2004 at a single university hospital and with cerebral white matter injury characterized by periventricular leukomalacia (PVL) or ventriculomegaly due to white matter atrophy. A control was matched to each case using the subsequent delivery within 7 days of that gestational age without brain injury. RESULTS: The gestational age at birth was 27 weeks for both groups, but the cases had a significantly lower birth weight (mean +/- standard deviation: 958 +/- 306 g compared with 1,038 +/- 381 g, P = .001). There was no difference in cesarean delivery (48% cases compared with 44% controls, P = .59). The cases had a significant increase in nucleated red blood cells per 100 white blood cells (WBC) (median, 5th percentile and 95th percentile: 22, 3 and 374 cases compared with 14, 1 and 312 controls; P = .02). Markers of chronic hypoxia, such as intrauterine growth restriction and oligohydramnios, and markers of acute hypoxia, such as an umbilical arterial pH less than 7.0 or base excess less than -12 mM, were both associated with significantly elevated neonatal nucleated red blood cell counts. A neonatal nucleated red blood cell count of 18 per 100 WBCs had a sensitivity of 56.9%, specificity of 57.9%, positive predictive value of 57.9%, and negative predictive value of 56.9% in predicting the development of cerebral white matter injury in this matched case-control sample. CONCLUSION: Preterm neonates with cerebral white matter injury have significant increases in nucleated red blood cell counts. Both acute and chronic hypoxia-ischemia can increase these counts, which limits their usefulness in timing injury. The predictive value of nucleated red blood cell counts at birth in identifying injury is poor. LEVEL OF EVIDENCE: II-2.

Neonatal cerebral white matter injury in preterm infants is associated with culture positive infections and only rarely with metabolic acidosis.

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.

Are histopathologic chorioamnionitis and funisitis associated with metabolic acidosis in the preterm fetus?

OBJECTIVE: Perinatal infection increases the risk of neonatal neurologic injury. Our objective is to determine whether histologically confirmed chorioamnionitis and funisitis is associated with fetal metabolic acidosis. STUDY DESIGN: This is a retrospective cohort study of all infants 34 weeks or less born at a single tertiary hospital admitted to the neonatal intensive care unit (NICU) between April 1999 and September 2002. Maternal and neonatal records and placental pathology reports were reviewed. RESULTS: There were 392 infants at 23 to 34 weeks' gestational age admitted to the NICU during this period of whom 354 had placental pathology reported; 259 infants had umbilical cord gases available. These neonates were placed into 3 groups: group 1 (208 infants) had no signs of placental infection, group 2 (59 infants) had isolated chorioamnionitis, and group 3 (87 infants) had both chorioamnionitis and funisitis. The gestational age (30.2 +/- 2.8, 28.3 +/- 3.4, 27.8 +/- 2.8 weeks, P < .01) and birth weight (1358 +/- 520, 1242 +/- 547, 1103 +/- 381 g, P < .01) were significantly higher in group 1. There was an increase in neurologic morbidity in groups 2 and 3 (25.2%, 34.4%, 43.7%), which was not significant when corrected for gestational age. Groups 2 and 3 had a small but significant increase in umbilical arterial pH (7.25 +/- 0.10, 7.29 +/- 0.10, 7.30 +/- 0.08, P < .01) and base excess (-3.5 +/- 3.6, -2.2 +/- 3.6, -2.3 +/- 2.7 mmol/L, P = .02). When a single pathologist reviewed all placentas with any inflammation and staged them on the basis of the degree of the fetal inflammatory response, no relationship was found between the degree of fetal inflammation and umbilical arterial pH (stage 1, 7.27 +/- 0.09; stage 2, 7.30 +/- 0.09; stage 3, 7.30 +/- 0.08; P = .41) or base excess (stage 1, -2.82 +/- 3.47 mmol/L; stage 2, -1.95 +/- 3.17 mmol/L; stage 3, -2.23 +/- 3.07 mmol/L; P = .62). When stepwise multiple linear regression was performed, neither histologic chorioamnionitis nor histologic funisitis were associated with a change in umbilical cord pH or base excess. CONCLUSION: Intrauterine infection, as confirmed by histologic chorioamnionitis and funisitis, is not associated with fetal metabolic acidosis. Intrauterine infection may represent a nonhypoxic form of encephalopathy that produces neurologic morbidity by a mechanism independent of hypoxia-ischemia leading to metabolic acidosis.