Ernest Graham

Graded classification of fetal heart rate tracings: association with neonatal metabolic acidosis and neurologic morbidity.

OBJECTIVEnThe objective of the study was to measure the performance of a 5-tier, color-coded graded classification of electronic fetal monitoring (EFM).nnnSTUDY DESIGNnWe used specialized software to analyze and categorize 7416 hours of EFM from term pregnancies. We measured how often and for how long each of the color-coded levels appeared in 3 groups of babies: (A) 60 babies with neonatal encephalopathy (NE) and umbilical artery base deficit (BD) levels were greater than 12 mmol/L; (I) 280 babies without NE but with BD greater than 12 mmol/L; and (N) 2132 babies with normal gases.nnnRESULTSnThe frequency and duration of EFM abnormalities considered more severe in the classification method were highest in group A and lowest in group N. Detecting an equivalent percentage of cases with adverse outcomes required only minutes spent with marked EFM abnormalities compared with much longer periods with lesser abnormalities.nnnCONCLUSIONnBoth degree and duration of tracing abnormality are related to outcome. We present empirical data quantifying that relationship in a systematic fashion.

Glial fibrillary acidic protein as a biomarker for periventricular white matter injury.

OBJECTIVEnPeriventricular white matter injury (PWMI), a precursor of cerebral palsy, traditionally is not diagnosed until 6 weeks of life by head ultrasound scanning. We sought to determine whether early neonatal glial fibrillary acidic protein (GFAP) levels could identify PWMI in low birthweight (<2500 g) infants.nnnSTUDY DESIGNnEach case with PWMI on head ultrasound scanning at 6 weeks of life from April 2009 to April 2011 was matched by gestational age and mode of delivery to 2 subsequent neonates with a normal head ultrasound scan. GFAP was measured in cord blood at birth, at neonatal intensive care unit admission, and on days 1-4 of life.nnnRESULTSnDuring this 2-year period, 21 cases with PWMI with gestational age 27.4 ± 3.3 weeks were compared with 42 control infants. The incidence of cesarean delivery was 61.9% in both groups. GFAP was not significantly different in cord blood or at neonatal intensive care unit admission but was significantly elevated on day 1 (median, 5-95%; 0, 0-0.98 ng/mL cases; 0, 0-0.06 ng/mL control infants; Pxa0= .03), day 2 (0, 0-1.21 ng/mL; 0, 0-0.05 ng/mL, respectively; Pxa0= .02), day 3 (0.05, 0-0.33 ng/mL; 0, 0-0.04 ng/mL, respectively; Pxa0= .004), and day 4 (0.02, 0-1.03 ng/mL; 0, 0-0.05 ng/mL, respectively; P < .001). The odds of the development of PWMI significantly increased with increasing levels of GFAP from day 1-4 of life when adjustment was made for preeclampsia, antenatal steroid administration, and neonatal chronic lung disease.nnnCONCLUSIONnThe ability to predict PWMI with a blood test for GFAP shortly after birth opens the possibility for rapid identification of infants for early intervention and provides a benchmark for the qualification of new therapies to improve neurodevelopmental outcomes.

Congenital Giant Cervical Teratoma: Pre- and Postnatal Imaging

Pre- and postnatal imaging findings are presented in a fetus/neonate with congenital cervical teratoma (CCT). Prenatal fetal MRI proved to be essential in the exact localization and characterization of the CCT while excluding potentially life-threatening prenatal complications. The provided information improved outcome by guiding decisions concerning delivery and postnatal care.

Pre- and postnatal imaging of a congenital hepatoblastoma.

Prenatal ultrasound, magnetic resonance imaging and matching postnatal computer tomography imaging findings are presented in a neonate with histologically proven congenital hepatoblastoma. Familiarity with the prenatal imaging findings of a hepatoblastoma are essential to make a reliable, specific diagnosis facilitating decision-making about the pre-, peri- and postnatal management.

Detection of neurologic injury using vascular reactivity monitoring and glial fibrillary acidic protein

New noninvasive methods for monitoring cerebrovascular pressure reactivity coupled with a blood-based assay for brain-specific injury in preterm infants could allow early diagnosis of brain injury and set the stage for improved timing and effectiveness of interventions. Using an adaptation of near-infrared spectroscopy, we report a case of a very low birth weight infant undergoing hemoglobin volume index monitoring as a measure of cerebrovascular pressure reactivity. During the monitoring period, this infant demonstrated significant disturbances in cerebrovascular pressure reactivity that coincided with elevation of serum glial fibrillary acidic protein and new findings of brain injury on head ultrasound. This case report demonstrates the potential of emerging noninvasive monitoring methods to assist in both detection and therapeutic management to improve neurologic outcomes of the very low birth weight neonate.

Preterm Birth: An Overview of Risk Factors and Obstetrical Management.

Preterm birth is the leading cause of neonatal mortality and a major public health concern. Risk factors for preterm birth include a history of preterm birth, short cervix, infection, short interpregnancy interval, smoking, and African-American race. The use of progesterone therapy to treat mothers at risk for preterm delivery is becoming more widespread. Tocolytics may not prevent preterm birth but have a role in prolonging pregnancy for administration of medications to benefit the preterm infant. These include antenatal steroids and, if indicated, magnesium sulfate for neuroprotection and intravenous antibiotics for Group B Streptococcus prophylaxis.

Obstetric Factors Related to Perinatal Brain Injury

Labor and delivery are the culminating events of the maternal–fetal relationship. Although the outcome for mother and child is favorable in the majority of cases, events may occur during parturition that affect the future neurological status of the fetus. In this chapter, we will review the definitions, incidence, and pathophysiology of neonatal encephalopathy and cerebral palsy, examine the impact that labor and delivery have on the fetus, review the methods used to evaluate for fetal compromise during labor and neonatal markers that predict brain injury, and examine the potential interventions to reduce the risk of perinatal brain injury.

Magnesium in inflammation-associated fetal brain injury

Injury to the fetal and perinatal brain is one of the leading causes of lifetime neurodevelopmental morbidity and mortality in children and affects more than 6,000 children born in the United States each year [1, 2]. The neonatal brain is vulnerable due to its rapid rate of growth and development and immature immunological mechanisms [3]. While the etiology of injury differs across the developmental spectrum with regard to gestational age, infection and inflammation play an important role in brain injury, especially in the very preterm neonate [4]. We now know that the most prevalent mechanism responsible for preterm birth and especially preterm birth < 28 weeks is mediated by inflammation [5]. The neonates born in the setting of infection or inflammation are at significantly increased risk for adverse neurodevelopmental outcomes [6, 7]. Clinical and epidemiological studies demonstrate the association between maternal infection, neonatal brain damage, and increased levels of proinflammatory cytokines in the fetal brain, umbilical cord, and amniotic fluid [8, 9]. Two meta-analyses conclude that clinical chorioamnionitis is a risk factor for both cerebral palsy and cystic PVL [10, 11]. There is also suggestion that less conspicuous infection as evidenced by histological chorioamnionitis is associated with brain injury and cerebral palsy [11]. Up to 50 % of infants who survive very preterm birth will suffer cognitive, behavioral, attention, and socialization deficits [12, 13]. Basic science studies using animal models (rodents, rabbits, cats, and sheep) have induced PWMD by inducing inflammation and infectious insults [14, 15]. Recently, a meta-analysis of six randomized controlled trials of antenatal magnesium sulfate for the prevention of cerebral palsy and other neurological abnormalities has concluded that magnesium appears to be protective in neonates at risk for delivery less than 34 weeks. The basic science mechanisms for the neuroprophylaxis are not completely understood. This chapter will concentrate on best possible evidence for mechanisms by which magnesium sulfate appears to act as neuroprotectant in the premature brain at risk for preterm birth.

Contents Vol. 27, 2010

R. Achiron, Tel Hashomer N.S. Adzick, Philadelphia, Pa. L. Allan, London A.A. Baschat, Baltimore, Md. K.J. Blakemore, Baltimore, Md. T.-H. Bui, Stockholm F.A. Chervenak, New York, N.Y. T. Chiba, Tokyo Y. Chiba, Osaka W.H. Clewell, Phoenix, Ariz. F. Crispi, Barcelona J.E. De Lia, Milwaukee, Wisc. J.A. Deprest, Leuven G.C. Di Renzo, Perugia J.W. Dudenhausen, Berlin N.M. Fisk, Brisbane A.W. Flake, Philadelphia, Pa. W.D.A. Ford, North Adelaide U. Gembruch, Bonn P.D. Gluckman, Auckland M.R. Harrison, San Francisco, Calif. J.C. Hobbins, Denver, Colo. L.K. Hornberger, San Francisco, Calif. E.R.M. Jauniaux, London M.P. Johnson, Philadelphia, Pa. C. Jorgensen, Copenhagen J.-M. Jouannic, Paris H.H.H. Kanhai, Leiden A. Kurjak, Zagreb P.M. Kyle, London O. Lapaire, Basel S. Lipitz, Tel-Hashomer Y.M.D. Lo, Hong Kong S. Mancuso, Roma G. Mari, Detroit, Mich. M. Martinez-Ferro, Buenos Aires P. Miny, Basel K.J. Moise, Houston, Tex. K.H. Nicolaides, London L. Otaño, Buenos Aires Z. Papp, Budapest R. Quintero, Tampa, Fla. G. Ryan, Toronto J. Rychik, Philadelphia, Pa. G.R. Saade, Galveston, Tex. H. Sago, Tokyo W. Sepulveda, Santiago P. Stone, Auckland D.V. Surbek, Bern M. Tanemura, Nagoya S. Tercanli, Basel J.-L. Touraine, Lyon B.J. Trudinger, Westmead J.M.G. van Vugt, Amsterdam S.L. Warsof, Virginia Beach, Va. C.P. Weiner, Kansas City, Kans. R. Zimmermann, Zürich Clinical Advances and Basic Research