Presented at the Neonatal Society 2006 Spring Meeting.
Okereafor A1, Allsop J2, Counsell S2, Fitzpatrick J2, Azzopardi D1, Rutherford M2, Cowan F1
1 Department of Paediatrics, Imperial College, Hammersmith Hospital, London, UK
2 Department of Imaging Sciences, Imperial College, Hammersmith Hospital, London, UK
Background: Brain injury in term neonates following an acute hypoxic-ischaemic insult due to a sentinel event around the time of delivery typically damages the basal ganglia and thalami (BGT) (1). However antenatal and perinatal factors are implicated in the causal pathway for such sentinel events and it is possible that the pattern of brain injury seen might reflect different aetiologies.
Aims: 1) to evaluate the pattern of brain injury in encephalopathic term neonates exposed to a perinatal sentinel event, 2) to investigate whether these infants prior to the event were different from term infants considered normal after birth and, 3) to assess whether the clinical outcome was as expected for the pattern of injury found.
Methods: Brain injury was determined from neonatal MRI scans of 43 case infants, all born at or referred to the Hammersmith Hospital. Antenatal and perinatal data from these infants and 229 term-born neurologically normal low-risk infants were compared. Neurological and developmental outcome was documented. Ethical permission for the study was obtained from the Hammersmith Hospital REC and permission for scanning obtained from the parents.
Results: Lesions were seen in the BGT in 63% of case infants. Myelination of the posterior limb of the internal capsule (PLIC) was abnormal or absent in 96% of infants with BGT damage (2) [Fig 1]. Six infants with severe BGT lesions also had moderate or severe white matter (WM) damage. BGT damage was associated with severe neurodevelopmental impairment or death in 89% of infants.
Eleven infants did not develop BGT lesions. Most had scans considered normal. One had moderate WM change. Nine out of these 11 were neurologically normal at 3 years; one child, a twin, had a mild diplegia and the other a global developmental delay with a possible syndromic diagnosis. MRI showed no evidence of long-standing brain injury established prior to delivery in any infant.
The case infants were more likely to be acidotic at birth (p=0.027), have a pluriparous mother (p=0.003), maternal hypertension (p=0.03) and be of African descent (p=0.0065) than controls. Uterine rupture followed previous caesarean section (CS) in 8/11 cases and cord prolapse accompanied undiagnosed breech in 4/9 cases. All but one infant with severe BGT and WM lesions had had a severe placental abruption.
Conclusions: BGT lesions are the imaging signature for acute perinatal hypoxic-ischaemia in term encephalopathic infants born after a sentinel event. The study infants were not intrinsically different from our control population and appeared to have been developing normally until the acute event. Placental abruption was associated with severe BGT and WM lesions suggesting that the aetiology of placental abruption is more complex than for other sentinel events or the diagnosis is made less quickly giving rise to a more prolonged insult. Acute BGT lesions are the common pattern of damage after sentinel events and confirms the need for anticipating sentinel events: previous CS, undiagnosed breech, hypertension and being of African descent are risk factors; prompt detection of signs and symptoms in the mother and fetus and an expedited delivery are paramount for reducing serious brain damage following sentinel events.
References
1. Cowan FM et al. Lancet 2003; 361: 736-42
2. Rutherford M et al. Pediatrics 1998; 102: 323-8