A total of 42,203 live infants were born in Göteborg in 1985-1991, and 292 term infants had Apgar scores < 7 at 5 min. Infants with congenital malformations, infections and opioid-induced respiratory depression were excluded and thus 227 infants were included in the birth asphyxia group, which formed the basis of this retrospective study. Clinical signs of mild, moderate or severe hypoxic-ischemic encephalopathy (HIE) were present in 65 infants, and in another 10 infants, sedated and on controlled ventilation, HIE was assumed but grading was not possible. The incidences of Apgar scores < 7 at 5 min, birth asphyxia and birth asphyxia with HIE were 6.9, 5.4 and 1.8 per 1,000 live born infants: 95% of infants resuscitated with bag and mask ventilation only, did well, compared with 1 of 11 in whom resuscitation included adrenaline. Seizures occurred in 27 of 227 infants, beginning in 18 infants within 12 h of birth. Small-for-gestational-age (SGA) infants were overrepresented in the birth asphyxia group but not in the birth asphyxia-HIE group. All infants with severe HIE died or developed neurological damage. Half of the infants with moderate, and all of the infants with mild, HIE were reported to be normal at 18 months of age. A total of 0.3 per 1,000 live born infants died and 0.2 per 1,000 developed a neurological disability related to birth asphyxia. The disabilities were dyskinetic (4), tetraplegic (2), spastic diplegic (2), cerebral palsy and mild neuromotor dysfunction (1). The relatively low incidences of birth asphyxia and HIE were probably due to effective antenatal care.

In a 2-year (1990-92) prospective national investigation, comprising all stillborn and live-born ELBW infants with a birthweight of < or = 1000 g born at 23 completed weeks of gestation or more, we examined the incidence, neonatal mortality, major morbidity and infant survival in relation to level of care and place of residence. A total of 633 ELBW infants were live-born, i.e. 0.26% of all live-born infants, and 298 were stillborn. The average neonatal mortality was 37% and 91% at 23 weeks, 70% at 24 weeks, and 40% at 25 weeks of gestation. Of neonatal survivors, 8% had intraventricular haemorrhage grade 3, 10% retinopathy of prematurity of stage > or = 3, 2% necrotizing enterocolitis, and 28% were oxygen-dependent at a time corresponding to 36 weeks of gestation. In all, 77% were treated with mechanical ventilation, whereas 19% survived without, almost all of them being CPAP treated. Infant mortality among infants born at level III (tertiary centres) was 30%, at level IIa (with full perinatal service) 46% and at level IIb (with basic neonatal service) 55%. Only 1% was born at hospital level I. Regarding the relation to place of residence, the mortality rates among infants residing in the areas served by levels III, IIa and IIb hospitals were 36%, 45% and 41%, respectively. The referral system thus functioned well, but can be improved, and increased perinatal referral, at borderline perinatal viability, might provide a better quality of care and a better chance of survival.

Cerebral Function Monitor (CFM) recordings were performed on 10 term and 19 preterm healthy infants. Term infants were monitored once, while preterm infants were followed serially. Forty-six recordings were made on 7, 14, 16 and 9 occasions in the age groups 30-31, 32-33, 34-35 and 36-37 weeks. All infants were examined clinically at 18 months of age and found healthy. By drawing weighted lines derived from the lower and upper limits of the CFM traces, mean values of minimum and maximum cerebral activity were calculated for the different age groups. In the term infants different CFM traces were identified corresponding to quiet sleep and active sleep. In the preterm infants a similar cyclic variability of the CFM trace was noted. A gradual increase in the minimum cerebral activity was found with increasing gestational age, resulting in a gradual narrowing of the trace.

Asphyxiated (n = 27) and control infants (n = 25) were subjected to spinal taps. Amino acids were measured with liquid chromatography and the degree of hypoxic-ischemic encephalopathy was determined in each case. In asphyxiated infants, the concentrations of aspartate and glutamate were 286% and 387% (p < or = 0.01 and p < or = 0.05) of the control values, respectively. The cerebrospinal fluid aspartate levels were significantly (p < or = 0.05) higher in the group with severe (3.4 mumol/l) compared with the group with mild hypoxic-ischemic encephalopathy (1.0 mumol/l). Glutamate was also higher in the group with severe (12.3 mumol/l) than in the groups with mild (2.7 mumol/l) or moderate (3.2 mumol/l) hypoxic-ischemic encephalopathy (p < or = 0.05). High concentrations of excitatory amino acids were present in the CSF of asphyxiated infants which may exert excitotoxic effects.

Neuron specific enolase (NSE) in serum and cerebrospinal fluid (CSF) and glutamate in CSF were investigated in the immediate postasphyctic period in 22 term newborn infants. The cerebral function monitor (CFM) pattern was also assessed and hypoxic-ischaemic encephalopathy (HIE) was graded. NSE was significantly increased in the CSF of infants with HIE (median value 25'4 pug/l) compared with control infants (10.0 Rg/I). Infants with the highest concentrations died.NSE in CSF correlated with the degree of asphyxial damage. Glutamate and NSE in CSF did not correlate, presumably due to the different time factors of the release after the insult. NSE in CSF corresponded weli with the type of CFM pattern, which was also highly predictive of outcome. (Arch Dis Child 1995; 72: F39-F42)