Evidence Of Perinatal Asphyxia Research Articles

Differences in standardized neonatal encephalopathy exam criteria may impact therapeutic hypothermia eligibility.

Therapeutic hypothermia (TH) is routinely provided to those with moderate or severe neonatal encephalopathy (NE). Subtle differences exist in the standardized exams used to define NE severity. We aimed to assess if an infant's TH eligibility status differed if they were evaluated using either the NICHD/Neonatal Research Network's (NICHD-NRN) or TOBY/British Association of Perinatal Medicine's (TOBY-BAPM) neurological exam. Encephalopathic infants ≥36 weeks with evidence of perinatal asphyxia and complete documentation of the neurological exam <6 h of age were included. TH eligibility using the NICHD-NRN and TOBY-BAPM criteria was determined based upon the documented exams. Ninety-one encephalopathic infants were included. Despite good agreement between the two exams (κ = 0.715, p < 0.001), TH eligibility differed between them (p < 0.001). A total of 47 infants were deemed eligible by at least one method-46 using NICHD-NRN and 35 using TOBY-BAPM. Of the 12 infants eligible per NICHD-NRN, but ineligible per TOBY-BAPM, two developed electrographic seizures and seven demonstrated hypoxic-ischemic cerebral injury. Both the NICHD-NRN and TOBY-BAPM exams are evidence-based. Despite this, there is a significant difference in the number of infants eligible for TH depending on which exam is used. The NICHD-NRN exam identifies a greater proportion as eligible. There are subtle differences in the NICHD-NRN and TOBY-BAPM's encephalopathy exams used to determine eligibility for TH. This results in a significant difference in the proportion of infants determined to be eligible for TH depending on which encephalopathy exam is used. The NICHD-NRN encephalopathy exam identifies more infants as being eligible for TH than the TOBY-BAPM encephalopathy exam. This may result in different rates of cooling depending on which evidence-based neurological exam for evaluation of encephalopathy a center uses.

Neonatal Encephalopathy: Beyond Hypoxic-Ischemic Encephalopathy

Neonatal encephalopathy is a clinical syndrome of neurologic dysfunction that encompasses a broad spectrum of symptoms and severity, from mild irritability and feeding difficulties to coma and seizures. It is vital for providers to understand that the term "neonatal encephalopathy" is simply a description of the neonate's neurologic status that is agnostic to the underlying etiology. Unfortunately, hypoxic-ischemic encephalopathy (HIE) has become common vernacular to describe any neonate with encephalopathy, but this can be misleading. The term should not be used unless there is evidence of perinatal asphyxia as the primary cause of encephalopathy. HIE is a common cause of neonatal encephalopathy; the differential diagnosis also includes conditions with infectious, vascular, epileptic, genetic/congenital, metabolic, and toxic causes. Because neonatal encephalopathy is estimated to affect 2 to 6 per 1,000 term births, of which HIE accounts for approximately 1.5 per 1,000 term births, (1)(2)(3)(4)(5)(6) neonatologists and child neurologists should familiarize themselves with the evaluation, diagnosis, and treatment of the diverse causes of neonatal encephalopathy. This review begins by discussing HIE, but also helps practitioners extend the differential to consider the broad array of other causes of neonatal encephalopathy, emphasizing the epidemiology, neurologic presentations, diagnostics, imaging findings, and therapeutic strategies for each potential category.

Maternal risk factors for adverse outcome in asphyxiated newborns treated with hypothermia: parity and labor duration matter

Introduction Perinatal asphyxia remains a frequent cause of neonatal mortality and long-term neurodevelopmental sequelae, despite the introduction of therapeutic hypothermia. Specific maternal characteristics may predispose asphyxiated newborns treated with hypothermia to worse outcome. Objective To investigate the possible association between specific maternal factors and adverse outcome in asphyxiated newborns treated with hypothermia. Methods We conducted a retrospective review of our database of 215 asphyxiated newborns treated with hypothermia from 2008 to 2015. We collected maternal characteristics including parity and labor duration, and we defined adverse outcome as death and/or brain injury. We compared the maternal characteristics between the asphyxiated newborns who developed adverse outcome and those who did not. Results Asphyxiated newborns born to nulliparous mothers had a significantly higher risk of adverse outcome (61%), compared to asphyxiated newborns born from primiparous (19%) and multiparous (20%) mothers (p = .002). Labor duration was longer in nulliparous mothers (p = .04). Among mothers who delivered vaginally, labor duration was significantly longer in newborns developing adverse outcome (p = .04). In multivariable analysis, parity was confirmed as an independent predictor of adverse outcome in all newborns, but labor duration showed a borderline non-significant association with adverse outcome (p = .051) only in newborns born vaginally. Labor duration beyond 12 h of life was associated with maximal sensitivity and specificity in detecting asphyxiated newborns at an increased risk of adverse outcome despite hypothermia treatment (AUC 0.62, p = .044). Conclusions Newborns with evidence of perinatal asphyxia, born to nulliparous mothers, and especially to those in whom the duration of labor has been prolonged, might be at higher risk of death or brain injury despite the use of therapeutic hypothermia.

Outcome and Feasibility after 7 Years of Therapeutic Hypothermia in Southern Brazil.

This study aimed to describe the experience with a protocol of therapeutic hypothermia (TH) in southern Brazil. Newborns with gestational age > 35 weeks with evidence of perinatal asphyxia plus moderate or severe encephalopathy were recruited between March 2011 and November 2017. Whole-body hypothermia for 72 hours, starting within the first 6 hours of life was used. Survivors underwent magnetic resonance imaging (MRI) and electroencephalogram (EEG). The primary outcome was death during hospitalization and neurodevelopment assessed using the Bayley Scales of Infant Development III (BSID III) at 12 months of age. A total of 72 newborns were treated (41 with moderate encephalopathy and 31 with severe encephalopathy), of whom 16 died. MRI was performed in 56 patients, and 24 presented some alterations. Fifty-three patients had an EEG: 11 normal, 20 mildly altered, 12 moderately altered, and 10 severely altered. Forty patients were evaluated through BSID III: 45% presented with some delay in neurodevelopment, 8 (20%) had motor retardation, 15 (37.5%) had language delay, and 13 (32.5%) had a delay in cognitive development. Mortality and adverse events were similar to those described in large randomized controlled trials. TH is a safe and an effective method of neurologic protection in asphyxiated newborns in a developing country when performed adequately.

Therapeutic hypothermia for neonatal hypoxic-ischemic encephalopathy: magnetic resonance imaging findings and neurological outcomes in a Brazilian cohort

Objective: To determine the neurodevelopment outcomes after therapeutic hypothermia for neonatal hypoxic-ischemic encephalopathy (HIE) and identify the neonatal magnetic resonance imaging (MRI) findings associated with neurological outcome in a middle-income country.Study design: All infants born after 35 completed weeks’ gestation with signs of moderate to severe encephalopathy and evidence of perinatal asphyxia before 6 hours of life were submitted to whole-body hypothermia and were imaged at 18 ± 8.4 days of life (range 7–33 days) after birth. Surviving infants had the neurodevelopment outcome assessed at 12 to 18 months of age by trained professional masked to MRI findings.Results: Forty-eight infants included, MRI scans were obtained from 34 infants; 14 (29.1%) patients died during hospitalization before MRI was performed. Nine (64.3%) of 14 patients were classified as severe encephalopathy presented Posterior Limb Internal Capsule (PLIC) sign at the MRI, 10 (71.4%) thalamus and basal ganglia (TBG) lesion, 9 (64.3%) white matter (WM) lesion, and 7 (50.0%) cortical lesion. Severe encephalopathy was associated with the motor delay at 12–18 months by Bayley III, Alberta Infant Motor Scale (AIMS), and Gross Motor Function Classification System (GMFCS) scores (p = .020, p = .048, p = .033, respectively), but not for the cognitive (p = .167) or language skills (p = .309). Lower BSID-III motor, cognitive, and language composite scores were associated with PLIC sign (p = .047; p = .006 and p = .003, respectively). TBG lesion (p = .051) and cortical lesion (p = .030) were associated with lower language composite score. Motor delay by AIMS and the presence of PLIC sign, TBG lesion, WM lesion, and Cortical lesion on MRI were observed (p < .001; p = .002; p = .001 and p = .027, respectively); as well as higher GMFCS score were associated with the presence of PLIC sign, TBG lesion, WM lesion, and Cortical lesion on MRI (p < .001; p = .001; p = .001, and p = .011, respectively).Conclusions: Brain MRI in neonates with HIE after therapeutic hypothermia is a valuable tool for diagnosis of encephalopathy cerebral abnormalities and is an early predictor of outcome in infants treated with whole body hypothermia for HIE in the Brazilian experience.

Short-term prognostic value of serum cardiac troponin I levels in neonates with perinatal asphyxia

Background Neonatal hypoxic–ischemic encephalopathy (HIE) is a neonatal brain injury caused by perinatal asphyxia and is a major cause of neonatal morbidity and mortality. Cardiac dysfunction forms a part of the clinical spectrum of multiorgan dysfunction in asphyxiated newborns. The more cardiac dysfunction the patients have, the more severe encephalopathy they would suffer. Cardiac troponin I (cTnI) is one of neonatal HIE-related biomarkers that can aid the diagnosis of perinatal asphyxia and anticipate the severity of associated myocardial dysfunction. Aim The current study was designed to assess the serum cTnI concentration and to evaluate its short-term prognostic value in newborns with HIE. Patients and methods The present study is a prospective observational study conducted on 100 full-term newborn infants in the period from May 2016 to May 2017. Enrolled newborns were divided into two groups: the case group (50 full-term newborn infants with evidence of perinatal asphyxia) and the control group (50 full-term newborn infants without evidence of perinatal asphyxia). Quantitative estimation of serum cTnI concentrations was done in all enrolled newborns within 12 h of birth using direct chemiluminometric technology performed on ADVIA Centaur Immunoassay System (TnI-Ultra). Serum levels of creatine kinase-MB (CK-MB) were also measured to assess its sensitivity and specificity as a marker of perinatal asphyxia. Additionally, echocardiography was done to exclude structural heart diseases. Left ventricular fractional shortening (LVFS) was also measured to assess cardiac involvement. Results Serum concentrations of cTnI were statistically significantly higher among the case group when compared with the control group. Additionally, serum levels of cTnI were found to increase with increasing severity of HIE. Serum levels of CK-MB were also statistically higher among the case group. However, pairwise statistical comparison of serum CK-MB concentrations in different stages of HIE revealed no statistical significant difference. No statistical significant difference was found between the two studied groups regarding LVFS. Moreover, LVFS did not differ significantly between the different stages of HIE. Among the different markers of myocardial dysfunction assessed in the current study, cTnI was found to be the most sensitive and specific predictor of poor short-term outcome in newborns with perinatal asphyxia. When comparing serum concentrations of cTnI and CK-MB in both surviving and nonsurviving newborns in the asphyxia group, it was found that serum concentrations of cTnI were statistically significantly lower in the group of survivors. In contrast, there was no statistical significant difference regarding serum concentrations of CK-MB between surviving and nonsurviving asphyxiated newborns. Conclusion Serum concentrations of cTnI were elevated in asphyxiated newborns with respect to healthy infants and increase with increasing severity of HIE. cTnI can also be used as an excellent early predictor of mortality in newborns with perinatal asphyxia.

English

Neonatal care in India is advancing at an impressive phase at the level of the community as well as in tertiary care units. Concept of of newborn has given way to intact survival of the high risk newborn emphasizing detection of neurological subnormalities at the earliest. Neurosonography, which is now ubiquitously available, is an ideal tool for the primary screening of the neonatal brain. Despite its wide availability in the hospitals, the penetration of cranial ultrasonography in Indian NICU's is still very little. OBJECTIVE: This study was undertaken to assess the importance of cranial ultrasound as an investigatory modality for high risk neonates and to find out the morphology of various cerebral lesions and correlate clinically. METHODS: This observational clinical study was conducted at Kempegowda Institute of Medical Sciences Hospital and Research Centre, Bangalore between January 2013 and January 2014. 100 high risk neonates admitted to our NICU were included in the study. Detailed history and clinical examination with appropriate investigations were done. These neonates were subjected to neurosonography on selected days as per protocol and morphology of various findings was recorded. Clinical correlation with CUS findings and follow up was done. RESULTS: Incidence of CUS abnormalities in high risk neonates is 24% in the present study. 11% of these had evidence of intracranial bleed, 7% hyperechogenic thalami, 2% definite HIE, and 4% had cerebral edema. Of the 24% of neonates with abnormal findings on CUS 23.5% had no evidence of perinatal asphyxia, 28.6% had severe, 30% had moderate 33.3% had mild perinatal asphyxia as per Apgar scoring. Two neonates on regular follow up CUS had developed cystic encephalomalacia with hydrocephalus. CONCLUSION: This study highlights the convenience and diagnostic efficiency of cranial ultrasound in high risk neonates in NICU. It also emphasizes its use as a screening modality for preterms and birth asphyxia neonates influencing their neurodevelopmental outcome. CUS is critical as an investigatory modality in NICU

Neonatal encephalopathic cerebral injury in South India assessed by perinatal magnetic resonance biomarkers and early childhood neurodevelopmental outcome.

Although brain injury after neonatal encephalopathy has been characterised well in high-income countries, little is known about such injury in low- and middle-income countries. Such injury accounts for an estimated 1 million neonatal deaths per year. We used magnetic resonance (MR) biomarkers to characterise perinatal brain injury, and examined early childhood outcomes in South India.MethodsWe recruited consecutive term or near term infants with evidence of perinatal asphyxia and a Thompson encephalopathy score ≥6 within 6 h of birth, over 6 months. We performed conventional MR imaging, diffusion tensor MR imaging and thalamic proton MR spectroscopy within 3 weeks of birth. We computed group-wise differences in white matter fractional anisotropy (FA) using tract based spatial statistics. We allocated Sarnat encephalopathy stage aged 3 days, and evaluated neurodevelopmental outcomes aged 3½ years using Bayley III.ResultsOf the 54 neonates recruited, Sarnat staging was mild in 30 (56%); moderate in 15 (28%) and severe in 6 (11%), with no encephalopathy in 3 (6%). Six infants died. Of the 48 survivors, 44 had images available for analysis. In these infants, imaging indicated perinatal rather than established antenatal origins to injury. Abnormalities were frequently observed in white matter (n = 40, 91%) and cortex (n = 31, 70%) while only 12 (27%) had abnormal basal ganglia/thalami. Reduced white matter FA was associated with Sarnat stage, deep grey nuclear injury, and MR spectroscopy N-acetylaspartate/choline, but not early Thompson scores. Outcome data were obtained in 44 infants (81%) with 38 (79%) survivors examined aged 3½ years; of these, 16 (42%) had adverse neurodevelopmental outcomes.ConclusionsNo infants had evidence for established brain lesions, suggesting potentially treatable perinatal origins. White matter injury was more common than deep brain nuclei injury. Our results support the need for rigorous evaluation of the efficacy of rescue hypothermic neuroprotection in low- and middle-income countries.

Alteraciones clínicas y paraclínicas en recién nacidos con PH arterial de cordón umbilical menor o igual a 7,18 Hospital de San José diciembre 2009 a marzo 2012

La depresión neonatal moderada y la asfixia perinatal son poco frecuentes en nuestro medio (2% en la unidad neonatal). El pH arterial del cordón umbilical &lt;=7.00 implica mayor riesgo de compromiso multiorgánico, aunque no es claro el pronóstico entre 7.00 y 7.18. El objetivo es describir la frecuencia de alteraciones clínicas y paraclínicas en los neonatos con Apgar &lt;=6 al primer minuto, cuyos gases arteriales de cordón cursaron con pH .&lt;=7.18 en el período diciembre 2009 a marzo 2012 en el Hospital San José de Bogotá DC. Metodología: estudio descriptivo prospectivo relativo a la frecuencia de alteraciones por sistemas en los neonatos que cumplieron criterios de inclusión. También se registraron los fallecimientos. Resultados: se incluyeron 52 pacientes, 45 con pH entre 7,11 y 7,18. La alteración más frecuente fue hepática, la dishidrogenia láctica estuvo elevada (100 % ) en quienes se realizó la medición, dos casos desarrollaron ecefalopatía (pH 6,96 y 7,13), y no se registró enterocolitis necrosante en dos hubo compromiso renal (oliguria). Cinco fallecieron durante el estudio con pH &lt;= 7.00. Conclusiones: aaunque el pH &lt;= 7.00 se considera la mejor evidencia de asfixia perinatal y es predictor de morbimortalidad, los pacientes entre pH 7.00 y 7.18 requieren evaluación y vigilancia clínica porque presentan alteraciones multisistémicas de gravedad variable e incluso muerte.

Predicting motor outcome and death in term hypoxic-ischemic encephalopathy

Central gray matter damage, the hallmark of term acute perinatal hypoxia-ischemia, frequently leads to severe cerebral palsy and sometimes death. The precision with which these outcomes can be determined from neonatal imaging has not been fully explored. We evaluated the accuracy of early brain MRI for predicting death, the presence and severity of motor impairment, and ability to walk at 2 years in term infants with hypoxic-ischemic encephalopathy (HIE) and basal ganglia-thalamic (BGT) lesions. From 1993 to 2007, 175 term infants with evidence of perinatal asphyxia, HIE, and BGT injury seen on early MRI scans were studied. BGT, white matter, posterior limb of the internal capsule (PLIC), and cortex and brainstem abnormality were classified by severity. Motor impairment was staged using the Gross Motor Function Classification System. The severity of BGT lesions was strongly associated with the severity of motor impairment (Spearman rank correlation 0.77; p < 0.001). The association between white matter, cortical, and brainstem injury and motor impairment was less strong and only BGT injury correlated significantly in a logistic regression model. The predictive accuracy of severe BGT lesions for severe motor impairment was 0.89 (95% confidence interval 0.83-0.96). Abnormal PLIC signal intensity predicted the inability to walk independently by 2 years (sensitivity 0.92, specificity 0.77, positive predictive value 0.88, negative predictive value 0.85). Brainstem injury was the only factor with an independent association with death. We have shown that in term newborns with HIE and BGT injury, early MRI can be used to predict death and specific motor outcomes.

170 Predicting Feeding Problems in Infants with Central Grey Matter Damage Following Hypoxic-Ischaemic Encephalopathy (HIE)

Background and aims: Feeding problems are common following HIE and are a huge burden for infants and families. We aimed to evaluate, in term newborns with HIE and basal ganglia/thalamic (BGT) lesions, the relation between feeding difficulties and early MRI findings.Methods: From 1993-2007, all term infants with evidence of perinatal asphyxia, HIE and BGT injury seen on MRI within 6 postnatal weeks were included. BGT, white matter, internal capsule, cortex and brainstem lesions were classified by severity. Cerebral palsy (CP) severity was determined from the Gross Motor Function Classification System (GMFCS).Results: 175 infants fulfilled the entry criteria. 49 died (23 neonatally, 26 in infancy). Feeding problems occurred in all who died, both early and late, and in 65% of survivors; 44% had difficulty with liquids, 48% with solids and 27% only tolerated pureed foods. 33% had a gastrostomy (median age 11 (range 3-48) months). All but 3 of the 82 children with feeding problems had CP, 91% GMFCS level IV/V. In a logistic regression model BGT/mesencephalic injury was associated with feeding problems (p< 0.001) and BGT/pons injury with gastrostomy (p< 0.001). The need for gastrostomy occurred in only 3.5% of infants with mild/moderate BGT + normal pons but in 90.6% of surviving infants with severe BGT+ pons injury.Conclusions: The occurrence and severity of feeding problems in neonates with HIE and BGT injury relates to the severity of the BGT/brainstem lesions. These findings enable planning of care and a better approach to nutrition in these children.

Incidencia y prevalencia de la encefalopatía hipoxico-isquémica en la primera década del siglo xxi

Aim To examine the incidence and the prevalence of neonatal hypoxic-ischemic encephalopathy (HIE) in a tertiary Spanish center over a 9-year period, before the implementation of a hypothermia program. Methods All infants ≥34 weeks gestation, born between 2000 and 2008 with evidence of perinatal asphyxia and neonatal encephalopathy were identified. HIE was classified as mild, moderate or severe. Joinpoint regression model was used to identify changes in the trends of HIE incidences. Results A total of 90,963 live infants were born in La Paz Hospital between 2000 and 2008, and 23.3% of them (21.228) were admitted to the Neonatal Unit. In addition, 200 infants were referred from other centers. A total of 110 infants had HIE, of which 90% were inborn. The overall incidence of HIE was 1.088 per 1,000 live births, and the incidence of clinically significant HIE (moderate and severe grades) was 0.49 per 1,000 live births. The incidence of HIE showed a linear downward trend throughout the study period (slope=−5.37; P<0.05). Fifty-two neonates had moderate or severe HIE, this represents a prevalence of 2.42 per 1,000 infants admitted to the Neonatal Unit and means that 5–6 infants a year would have been candidates for therapeutic hypothermia. Conclusions Neonatal HIE, and in particular significant HIE, is an infrequent condition. The low prevalence of HIE requires that these infants are referred to regional centers with sufficient experience in the use of therapeutic hypothermia, and in the management of all the medical problems associated with HIE.

Origin and Timing of Brain Lesions in Term Infants With Neonatal Encephalopathy

It is not clear whether intrapartum asphyxia is an important factor in neonatal encephalopathy and seizures in term infants. Antenatal factors have been implicated, but there is no firm evidence that brain damage occurs in utero. This study examined the proposal that neonatal encephalopathy and early postnatal seizures, or both, are sequelae of early adverse antenatal events. Cerebral magnetic resonance imaging (MRI) or autopsy was carried out in 351 full-term infants having encephalopathy and/or seizures within 72 hours of birth. Infants with major congenital malformations or known chromosomal disorders were excluded. The 261 infants placed in group 1 had a diagnosis of neonatal encephalopathy, with or without seizures, as well as evidence of perinatal asphyxia. The 90 group 2 infants presented with seizures but failed to meet diagnostic criteria for encephalopathy. Cerebral MRI disclosed evidence of acutely evolving lesions not related to established injury or atrophy in 80% of group 1 infants. These lesions, which usually were bilateral, were consistent with a hypoxic-ischemic insult. In addition to white matter, abnormalities were found in the basal ganglia, thalamus, or cortex. Only 2 group 1 infants, fewer than 1% of the total, had evidence of established injury. Three of 21 autopsies showed, in addition to an acutely evolving lesion, very small foci of established gliosis in the periventricular white matter. Acute ischemic or hemorrhagic lesions were found in 69% of group 2 infants. Two infants (3%) had, in addition, changes of antenatal injury. Thirteen of the 28 remaining group 2 infants had MRI findings of a specific nonhyoxic-ischemic condition. The other 15 infants had normal scans. Seven of 10 infants with no specific diagnosis continued to have seizures. Antenatal risk factors that were significantly more frequent in infants having apparent antenatal lesion or disorders of genetic or neurometabolic origin included a family history of seizures or neurologic disorder, low birth weight, head circumference below the 10th percentile, and low maternal age. In this study, more than 90% of term infants with neonatal encephalopathy and/or early seizures had evidence of a perinatally acquired insult. Established brain injuries acquired before birth were quite infrequent. The findings do not rule out the change that antenatal (or genetic) factors could predispose some infants to perinatal brain injury.

Origin and timing of brain lesions in term infants with neonatal encephalopathy

The role of intrapartum asphyxia in neonatal encephalopathy and seizures in term infants is not clear, and antenatal factors are being implicated in the causal pathway for these disorders. However, there is no evidence that brain damage occurs before birth. We aimed to test the hypothesis that neonatal encephalopathy, early neonatal seizures, or both result from early antenatal insults. We used brain MRI or post-mortem examination in 351 fullterm infants with neonatal encephalopathy, early seizures, or both to distinguish between lesions acquired antenatally and those that developed in the intrapartum and early post-partum period. We excluded infants with major congenital malformations or obvious chromosomal disorders. Infants were divided into two groups: those with neonatal encephalopathy (with or without seizures), and evidence of perinatal asphyxia (group 1); and those without other evidence of encephalopathy, but who presented with seizures within 3 days of birth (group 2). Brain images showed evidence of an acute insult without established injury or atrophy in 197 (80%) of infants in group 1, MRI showed evidence of established injury in only 2 infants (<1%), although tiny foci of established white matter gliosis, in addition to acute injury, were seen in three of 21 on post-mortem examination. In group 2, acute focal damage was noted in 62 (69%) of infants. Two (3%) also had evidence of antenatal injury. Although our results cannot exclude the possibility that antenatal or genetic factors might predispose some infants to perinatal brain injury, our data strongly suggest that events in the immediate perinatal period are most important in neonatal brain injury.

Changes in risk factors for hypoxic-ischaemic seizures in term infants.

Term infants with seizures and evidence of perinatal asphyxia were prospectively identified in 1 city and 2 time periods: 1978-1981 and 1991. Infants with multiple congenital abnormalities, hypocalcaemia or infection were excluded. Although there was little change in the overall incidence of neonatal seizures between 1978-1981 (1.9 per 1,000) and 1991 (1.78 per 1,000, N.S.) there was a marked reduction in small for dates infants with seizures: 8 of 19 infants in 1978-1981 compared to none of 16 in 1991 (p < 0.005). In contrast, infants > or = 41 weeks continued to show a markedly increased risk for asphyxia (relative risk 4.48, 95% CI: 1.7-12.3). The mechanism of this improved outcome for small for gestational age infants is unknown, but speculatively may be due to improved obstetric monitoring techniques allowing early identification of compromised infants.

Use of brain lactate levels to predict outcome after perinatal asphyxia

Perinatal asphyxia is an important cause of neurological disability, but early prediction of outcome can be difficult. We performed proton magnetic resonance spectroscopy (MRS) and global cerebral blood flow measurements by xenon-133 clearance in 16 infants with evidence of perinatal asphyxia. Cerebral blood flow was determined daily in the first 3 days after birth in seven cases. Proton MRS was performed in 11 infants within the first week (mean 3.7 days), the rest within the first month (mean 22.2 days), and all had a scan around 3 months of age. Four infants died neonatally, three showed neurological deficits and the rest seemed to be progressing normally at neurodevelopmental follow-up at 1 year of age. A significant correlation was found between initial brain lactate levels and severe outcome (p = 0.0003) just as between cerebral hyperperfusion (mean cerebral blood flow (CBF) 86 ml(100 g)-1 min-1), (p = 0.02) and outcome. The diagnostic and prognostic implications of early MRS and CBF are predictive of poor outcome in severely asphyxiated infants.

Neonatal dural sinus thrombosis

Dural sinus thrombosis in the newborn period has been infrequently documented and its clinical presentation remains obscure. Seventeen patients, all of whom were born at term with dural sinus thrombosis diagnosed in the neonatal period, were retrospectively identified and reviewed. Diagnosis was determined by unenhanced computed tomography which demonstrated a dense sagittal sinus with concomitant small ventricles. Two patients had ancillary studies (i.e., cerebral angiography and nuclear flow scan) which confirmed the diagnosis. Only 4 patients had evidence of perinatal asphyxia. Three patients were identified as having associated conditions known to predispose them to dural sinus thrombosis. None of the patients tested had an identifiable hypercoagulable state. Neonatal seizures were the initial presentation in 15 patients. Seizure onset predominantly occurred during the first week of life. Subsequent examinations were available in all 17 patients and ranged up to 6 years. Only 3 patients had seizures beyond the neonatal period. In 11 of 12 infants with no history of perinatal asphyxia, neurodevelopmental outcomes were normal. Two of 4 infants with perinatal asphyxia had neurologic sequelae. Dural sinus thrombosis represents an important and under-recognized cause of neonatal seizures in term infants. In the absence of perinatal asphyxia, normal neurodevelopmental outcome is likely and the risk of seizure recurrence is low.

Association of elective repeat cesarean delivery and persistent pulmonary hypertension of the newborn

Seventy-one cases of persistent pulmonary hypertension of the newborn have been reviewed in an attempt to identify possibly preventable causes. Three groups of infants were identified. The first group consisted of 36 infants with evidence of perinatal asphyxia. The second group was made up of 23 infants who exhibited a variety of associated factors including pneumonia, septic shock, and congenital diaphragmatic hernia. A third group included 12 infants delivered by elective repeat cesarean section. Infants in the third group did not have evidence of perinatal asphyxia, meconium aspiration, or infection. Chest roentgenograms revealed amniotic fluid aspiration in seven cases, retained lung fluid in three cases, and normal findings in two cases. All 12 infants in the third group developed respiratory distress which eventually progressed to respiratory failure and persistent pulmonary hypertension of the newborn. These data suggest that infants of elective repeat cesarean deliveries are at risk for developing persistent pulmonary hypertension of the newborn and constitute a group of patients with a potentially preventable course of events.

Neonatal Hyperammonemia

Goldberg et al1 described 12 infants with hyperammonemia in association with severe perinatal asphyxia, characterized by low Apgar scores and prolonged resuscitation, in premature, term, and postmature neonates. Ballard and colleagues2 reported five preterm infants with transient hyperammonemia and respiratory distress. We wish to summarize briefly the course of an infant who exhibited transient hyperammonemia without evidence of perinatal asphyxia or primary respiratory distress. This 2,520-gm female infant was the product of an uncomplicated pregnancy in a 21-year-old primigravida.

Neonatal heart rate reactivity following variable decelerations during labor

The instantaneous heart rate of 65 healthy neonates was continuously monitored during labor and the first 30 minutes of neonatal life. It was found that infants who had moderate or severe variable decelerations in utero had a significantly delayed neonatal heart rate (NHR) reactivity without any evidence of perinatal asphyxia. The NHR pattern of infants with and without variable decelerations is described and possible mechanisms which could explain the delayed NHR reactivity are discussed.