Severe fetal acidemia and subsequent neonatal encephalopathy in the larger premature infant

doi:10.1016/j.pediatrneurol.2004.06.016

Pediatric Neurology

Volume 32, Issue 1, January 2005, Pages 25-29

https://doi.org/10.1016/j.pediatrneurol.2004.06.016 Get rights and content

The contribution of intrapartum hypoxia-ischemia to neonatal encephalopathy in the larger preterm infant remains poorly defined. Such infants could become potential candidates for neuroprotective strategies. The objective of this study was to determine in preterm infants of gestation 31 to 36 weeks, with severe fetal acidemia (i.e., cord arterial pH < 7.00) the incidence of moderate to severe neonatal encephalopathy as well as the perinatal characteristics that may facilitate early identification. The data of 61 preterm infants of mean birth weight 1998 gm and mean gestation of 33.6 weeks were retrieved. Short-term abnormal neurologic outcome measures included evidence of encephalopathy with or without seizures or neuroimaging abnormalities. Eight (13%) of 61 infants developed an abnormal neonatal neurologic outcome. More infants with abnormal vs normal outcome had 1-minute Apgar of 0, i.e., 4/8 vs 3/53, 5-minute Apgar score ≤5 (7/8 vs 17/53), required chest compressions (5/8 vs 6/53), cord pH (6.75 vs 6.90), and base deficit 20 vs 18 (P < 0.05). By multivariate analysis, only gestation was associated with abnormal outcome (P = 0.0003). We conclude that the larger depressed preterm infant is at increased risk for moderate to severe encephalopathy. Such infants could also be considered potential candidates for neuroprotective strategies.

Introduction

The contribution of intrapartum hypoxia-ischemia to neonatal encephalopathy has focused on the near term and term infant, i.e., >36 weeks gestation [1], [2], [3]. In this patient group, infants at highest risk for subsequent brain injury have been identified by a constellation of findings including severe fetal acidemia, neonatal depression, and the need for delivery room resuscitation when coupled with an abnormal early neurologic examination or abnormal-amplitude electroencephalographic recording [3], [4]. Infants with these combined findings have become candidates for neuroprotective strategies. The contribution of intrapartum hypoxia-ischemia to neonatal encephalopathy in the larger preterm infant, i.e., of 31 to 36 weeks gestation, remains poorly defined. This group would seem to be an important one to identify because such infants could also become potential candidates for neuroprotective strategies. We hypothesized that the larger preterm acidemic infant of gestation 31 to 36 weeks delivered depressed and requiring delivery room resuscitation as compared with the acidemic infant without respiratory depression would be at increased risk for neonatal brain injury, and that this risk would increase as a function of decreasing gestation. The objectives of this retrospective study were to determine in the larger preterm infant of estimated gestation 31 to 36 weeks, and delivered in the presence of severe fetal acidemia, the incidence of moderate to severe neonatal encephalopathy and the perinatal characteristics that may facilitate early identification of such infants.

Section snippets

Methods

In this retrospective cohort study, the data of 62 preterm infants of estimated gestation 31 to 36 weeks, and admitted to the neonatal intensive care unit at Parkland Hospital between January 1993 and December 2002 with an umbilical arterial pH < 7.00 were retrieved from a neonatal database and a resuscitation registry as previously described [1], [2], [3]. One infant with trisomy 18 was excluded from the analysis. The 62 infants represented 1% of 5533 infants of gestation 31 to 36 weeks who

Results

During the 10 years of review, 61 preterm infants of birth weight 1998 ± 505 gm and gestation 33.6 ± 1.6 weeks were admitted to the neonatal intensive care unit with a cord umbilical arterial pH < 7.00. Perinatal complications included abruption placentae (n = 34 [55.7%]) (two of these cases evolved after a motor vehicle accident); fetal heart rate abnormalities (n = 12; 19.7%); pregnancy-induced hypertension (n = 4; 6.6%); miscellaneous causes (n = 7; 11.4%), e.g., diabetes, nuchal cord (n =

Discussion

These data describe the neonatal neurologic consequences in the larger preterm infant of gestation 31 to 36 weeks delivered in the presence of severe fetal acidemia. An abnormal neurologic outcome was observed in 13% of the infants and was almost exclusively confined to the larger preterm infant. Indeed the risk for abnormal outcome increased by approximately three and a half fold for each week increase in gestation. The absence of any activity at birth, i.e., a 1-minute Apgar score of 0, a

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Citation Excerpt :
There is little data on HIE in the preterm population. Salhab and Perlman report a low incidence of fetal acidaemia (1.1/1000, 31–36 weeks GA infants) with only 8 of the 61 infants described as encephalopathic, all with abnormal outcomes [80]. Chalak et al. [81] identified 9 of 1305 (0.7%) infants of 33–35 weeks GA, three with poor outcome.
Neonatal brain imaging undoubtedly can provide the most accurate information from which to determine whether cerebral palsy is likely to affect an individual infant born preterm. The sensitivity and specificity of that information is different between cranial ultrasound and MRI, depending on what approaches and sequences are used and the timing of the examinations. In this chapter we highlight the changing incidence of different patterns of brain injury in the preterm newborn and present a comparison of cranial ultrasound and MRI for predicting cerebral palsy in preterm infants affected by the commoner intracranial pathologies.
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The preterm newborn is at significant risk of neural injury and impaired neurodevelopment. Infants with mild or no evidence of injury may also be at risk of altered brain development, with evidence impaired cell maturation. The underlying causes are multifactorial and include exposure of both the fetus and newborn to hypoxia-ischemia, inflammation (chorioamnionitis) and infection, adverse maternal lifestyle choices (smoking, drug and alcohol use, diet) and obesity, as well as the significant demand that adaptation to post-natal life places on immature organs. Further, many fetuses and infants may have combinations of these events, and repeated (multi-hit) events that may induce tolerance to injury or sensitize to greater injury. Currently there are no treatments to prevent preterm injury or impaired neurodevelopment. However, inflammation is a common pathway for many of these insults, and clinical and experimental evidence demonstrates that acute and chronic inflammation is associated with impaired brain development. This review examines our current knowledge about the relationship between inflammation and preterm brain development, and the potential for stem cell therapy to provide neuroprotection and neurorepair through reducing inflammation and release of trophic factors, which promote cell maturation and repair.
Safety and Short-Term Outcomes of Therapeutic Hypothermia in Preterm Neonates 34-35 Weeks Gestational Age with Hypoxic-Ischemic Encephalopathy
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To evaluate the safety and short-term outcomes of preterm neonates born at 34-35 weeks gestation with hypoxic-ischemic encephalopathy (HIE) treated with therapeutic hypothermia.
Medical records of preterm neonates born at 34-35 weeks gestational age with HIE treated with therapeutic hypothermia were retrospectively reviewed. Short-term safety outcomes and the presence, severity (mild, moderate, severe), and patterns of brain injury on magnetic resonance imaging were reviewed using a standard scoring system, and compared with a cohort of term neonates with HIE treated with therapeutic hypothermia.
Thirty-one preterm and 32 term neonates were identified. Therapeutic hypothermia-associated complications were seen in 90% of preterm infants and 81.3% of term infants (P = .30). In the preterm infants, hyperglycemia (58.1% vs31.3%, P = .03) and rewarming before completion of therapeutic hypothermia (19.4% vs 0.0%, P = .009) were more likely compared with term infants. All deaths occurred in the preterm group (12.9% vs 0%, P = .04). Neuroimaging showed the presence of injury in 80.6% of preterm infants and 59.4% of term infants (P = .07), with no differences in injury severity. Injury to the white matter was more prevalent in preterm infants compared with term infants (66.7% vs 25.0%, P = .001).
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: Salhab WA, Perlman JM. Severe fetal acidemia and subsequent neonatal encephalopathy in the larger premature infant

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Original articlesSevere fetal acidemia and subsequent neonatal encephalopathy in the larger premature infant

Introduction

Section snippets

Methods

Results

Discussion

Pediatr Neurol

J Pediatr

Am J Obstet Gynecol

Am J Obstet Gynecol

Am J Obstet Gynecol

Cardiopulmonary resuscitationAssociated clinical features

Arch Pediatr Adolesc Med

Original articles
Severe fetal acidemia and subsequent neonatal encephalopathy in the larger premature infant