Abstracts

Patterns of brain injury seen in neonates presenting with a postnatal collapse

Presented at the Neonatal Society 2005 Autumn Meeting.

Foran A1, Rutherford M2, Cowan F1

1 Department of Paediatrics, Imperial College London, Hammersmith Hospital, London, UK
2 Robert Steiner MR Unit, Imaging Sciences Department, Imperial College London, London, UK

Purpose of study: There is little information regarding aetiology and outcome in apparently well newborns found collapsed in the early postnatal period. We present our perinatal data, brain imaging findings and outcome in term neonates, who collapse within hours of birth in whom no infective or metabolic cause is found.

Subjects/methods: Term infants considered well at birth who have an acute postnatal collapse (< 60 hours) that required extensive resuscitation were included in this study. Images were all done as part of clinical investigation with parental permission and ethical approval from the Hammersmith Hospital Ethics Committee for the MR studies. Cases were selected from all term inborn infants with these symptoms (5) and regional referral (5) in the last 12 years.

Data collected: Family and pregnancy histories. Labour onset and progress, evidence of fetal distress, analgesia, acute events, type of delivery. Infant gestational age (GA), sex, birth weight (BW), head circumference (HC), Apgar score, cord pH; time of collapse, relation to feeding, pH post resuscitation, cerebral function monitor/EEG findings, results of septic, metabolic and post mortem findings; neurodevelopmental follow-up. All but one infant had a brain MRI within 14 days from delivery.

Results: Ten infants fulfilled the entry criteria; all were Caucasian, 6 male, one twin; mean maternal age was 31.7 years (27-38); 8 were primipara; one had a hemiplegia from age 16; 5 infants were born by spontaneous vaginal delivery (1 breech, 1 OP, 2 water births), 4 with forceps and 1 by emergency section. One had meconium stained liquor. Mean Apgar scores were 7 (3-9) and 9 (8-10) at 1 and 5 minutes. Cord pH was 7.18-7.21 (n=3). Three infants only required 5 inflation breaths after delivery. Mean GA was 38 weeks (36-41); mean BW 3.04kg (1.9-4.0); mean HC 34.7cm (32-37.7) Mean age of collapse was 8.5 hours (10 min–55 hrs). All infants needed extensive resuscitation and seven developed seizures within 12 hours of their collapse. Mean pH and BE post-collapse were 6.83 (6.4-7.2) and –21.7g/dL (11.3-29.6). No infant had X-ray signs of aspiration or a blood glucose <2.5mmol/L. None had evidence of an antenatally established insult, a metabolic disorder or sepsis. Seven infants had severely abnormal basal ganglia and thalami typical of acute severe hypoxia-ischaemia with acute brain stem injury; five of these also had injury to white matter and four to the cortex. They all had severe encephalopathy, a severely abnormal CFM/EEG and all died. When available, post-mortem data confirmed the pattern of injury. Three infants had neuroimaging without persisting abnormalities; all had symptoms of persistent pulmonary hypertension (PPHN) and normal background CFM. All had normal neurodevelopmental outcomes (1-6 years).

Discussion: In this study infants who collapse postnatally divide into two groups: (1) those with severe acute damage to the central grey matter/brainstem consistent with severe hypoxia-ischaemia; only one of these infants had a normal delivery, all but one collapsed in their mother’s arms in relation to breast-feeding and all died. (2) those with normal imaging and background CFM who have a PPHN-like illness (two were water births); their collapse seemed unrelated to feeding; they had a normal outcome. There were no antenatal problems identified in either group and no clear evidence of intrapartum asphyxia. Why this pattern of damage occurs remains unexplained.

References
1. Badawi N, et al. BMJ 1998: 1549-53
2. Cowan F et al. Lancet 2003; 361: 736-42.

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