COMPROMISED BABY
CAUSATION

Diffuse damage to the developing fetal and young child’s brain, up to about 2 years of age, may result in cerebral palsy, mental retardation and epilepsy, in a variety of combinations and with a range of severity. Such consequences may result from inborn metabolic errors, moderate to severe traumatic brain injury and meningitis.

By consensus with the American Academy of Pediatrics (AAP), the American College of Obstetricians and Gynecologists (ACOG) criteria¹ require that all the following be present for diagnosis of birth asphyxia : umbilical artery pH <7.0, APGAR score <4 at 5 minutes, multi-organ failure, and evidence in the newborn period of hypoxic-ischemic encephalopathy (brain damage from diminished oxygen and/or blood supply), namely disturbance of consciousness, neurological abnormalities, or seizures.

However, most newborn encephalopathy is not caused by labour events ². and severe metabolic acidemia (birth asphyxia) is infrequently associated with subsequent injury ³, so brain damage identified following severe birth asphyxia may be partly or wholly caused by pre-existing abnormalities of the developing brain.

Even when cerebral palsy does follow severe birth asphyxia a direct causal relationship may not be present: both conditions may be the result of brain injury before the onset of labour ^{4, 5}. Thus, although asphyxia of a newborn infant may result from events during labour, and therefore be potentially preventable, it may also be the final common path of insults to the brain occuring before the onset of labour.

The majority of cerebral palsy is not attributable to intrapartum asphyxia ^{6, 7, 8}, or even to any recognisable events, intrauterine or postnatal ⁴. Further, two-thirds of cerebral palsy occurs in low risk patients ⁹. There are familial occurrences of cerebral palsy, in only some of which recognisable inherited errors of metabolism can be identified. Thus, even if largely unpreventable factors such as trauma and infection are included, less than 10% of cerebral palsy is attributable to labour events¹⁰.

Danish authors reviewed¹¹ 30 years of systematic studies of outcome for term (full time) infants born alive after presumed asphyxia during labour. Persistent neurological damage could be attributed in only 15%, three-quarters of whom were multiply-handicapped. The one-in-12 rate of developmental delay was no different from that of the normal population.

A recent study¹² of potentially asphyxiating events and cerebral palsy confirmed a causal relationship with cord tightly around the neck when 4 limbs were affected (quadriplegia) but not 2 limbs (diplegia, hemiplegia).

Furthermore, there is a widespread misconception about the strength of the causal relationship between birth asphyxia and brain damage. Clinicians involved with the delivery of infants overestimated tenfold the percentage of newborn infants with an APGAR score of 3 or less who will subsequently have abnormal neurological findings ¹³.

A central clinical and medicolegal problem is that methods of detecting intrapartum asphyxia, including Continuous Electronic Fetal Monitoring (EFM), are highly sensitive but not specific for this source of damage ¹⁴.

As with Pap smears, setting the sensitivity of the detection method so high that only a tiny percentage of occurrences are missed involves submitting a significant minority to unnecessary inconvenient, expensive and sometimes hazardous investigation and therapy. 
 
 

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