There are several issues in determining the causes of cerebral palsy. According to a book written by the American College of Obstetricians and Gynecologists (in conjunction with the American Academy of Pediatrics), combining clinical signs with investigation, hypoxia during labor may be more reliably determined. With 4 million live births each year in the United States, that translates into 8-9,000 new cases of cerebral palsy (Neurology of the Newborn by Joseph Volpe).

The British Medical Journal states, “24% of a population based series of children with moderate or severe spastic quadriplegia were thought possibly or very likely to have been affected by intrapartum events.” Here are some questions they provide that are pertinent to assessing the preventability of cerebral palsy during labor.

  • Were there risk factors?
  • Was there a sentinel hypoxic event?
  • Was there an intervention available proved to reduce the rate of cerebral palsy?
  • Have the criteria for defining an acute intrapartum hypoxic event been met?
  • Could the signs of fetal compromise reasonably have been detected?
  • Was there an avoidable major delay in expediting delivery?
  • Would quicker delivery of the baby have compromised the mother’s health or life?
  • Would an earlier delivery, if practical, have prevented or ameliorated the outcome?

Any significant deviations from normal clinical responses can be considered critical to the development of cerebral palsy. The British Medical Journal also states the actual length of time and degree of hypoxia required to produce cerebral palsy in a previously healthy human fetus is not known. Many special physiological mechanisms protect the fetus from acute hypoxia, allowing it to survive intact for longer period- minutes to perhaps hours-than an adult with similar blood gas concentrations.

Clinical signs to look for that could contribute to cerebral palsy:

  1. Evidence of metabolic acidosis in fetal umbilical cord arterial blood obtained at delivery
  2. Early onset of severe or moderate neonatal encephalopathy in infants
  3. Exclusion of other identifiable etiologies, such as trauma, coagulation disorders, infectious conditions or genetic disorders.

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