Outcome after intrapartum hypoxic ischaemia at term

Summary

We consider the range of childhood disabilities that have been attributed to perinatal hypoxic ischaemia at term and review the strength of evidence for each. The strongest evidence is for a causal link between acute profound hypoxic ischaemia and dyskinetic tetraplegic cerebral palsy (CP). Hemiplegic CP is not usually due to a perinatal hypoxic ischaemic insult at term; an important cause is focal cerebral infarction or ‘stroke’. Characteristically, diplegic CP is seen in ex-preterm children with periventricular leukomalacia. Ataxic CP is unlikely to be due to perinatal asphyxia. Recent careful follow-up studies have shown that childhood survivors of perinatal hypoxic ischaemia are at risk for cognitive deficits even in the absence of functional motor disorders. There is no evidence that, in isolation, either attention deficit hyperactivity disorder or autism is caused by hypoxic ischaemia. As effective neuroprotective therapies are introduced, notably cooling, it is possible that the prevalence of CP may be reduced.

Introduction

Most neonatologists need no reminder of the words of the late Peter Hope (1951–2001) ‘It is no longer a matter for conjecture whether asphyxia and cerebral damage are causally related, or merely occur in the same antenatally imperfect individual. Ultrasonography, and many other objective tests of cerebral structure and function, allow us to follow the time course of evolving neuronal damage in the postnatal period following severe asphyxia’.¹

Neonatal physicians the world over are all too familiar with the sequence of events that begins with an acute fetal circulatory collapse, is followed by the birth of a virtually stillborn and acidotic baby who requires extensive resuscitation, continues with a baby who develops an evolving encephalopathy with an abnormal electroencephalogram (EEG) and neuroimaging, and ends with the discharge of an infant who has still not recovered normal neurological function and who develops athetoid cerebral palsy (CP). Whilst lawyers argue about the precise contribution of minutes, there is no real debate about the generality of cause and effect in this clinical scenario. The level of certainty that hypoxic ischaemia is the cause has been increased by the demonstration of a specific, reproducible pattern of damage to the thalami and putamina of the lentiform nuclei which is present in many of these cases.

But what if the outcome is not tetraplegic CP of the dyskinetic or spastic kind, or the magnetic resonance imaging (MRI) findings are not those of damage to the vulnerable structures of the deep grey matter or the parasagittal cortex? Whilst the ‘international consensus’ opinion, and the American Academy of Obstetricians, state dogmatically that only spastic quadriplegic or athetoid CP can be caused by intrapartum hypoxic ischaemia (Table 1),2, 3 many parents and clinicians find it difficult to ignore a clear history of intrapartum hypoxic ischaemia of potentially damaging severity as a possible causative factor when their child is later found to have hemiplegic CP, severe learning difficulties, visual problems, or neuropsychiatric disorders. The natural desire to find an explanation for a child's problems results in consideration of even a vague history of ‘birth asphyxia’ as a potential cause for clumsiness or autism. The casual, imprecise and unthinking use of the term ‘birth asphyxia’ in notes, laboratory requests and letters has led to lawsuits that are based on little else.

Most neonatologists and paediatric neurologists no longer believe that the adverse outcome of intrapartum hypoxic ischaemia at term is confined to the motor system, or that the damage cannot affect cognitive function without very significant involvement of the motor pathways. In this review we consider the range of childhood disabilities that have been attributed to intrapartum hypoxic ischaemia at term and review the evidence for each.