In the late 1970s and early 1980s, a series of research studies were published in several leading medical journals. These studies concluded that a constellation of neurologic symptoms discovered in term infants including alterations in consciousness, poor reflexes and muscle tone with depressed respiratory function were attributable to intrapartum events. These abnormal findings were typically documented within the first week of life and were preceded by perinatal asphyxia. This syndrome came to be known as “hypoxic-ischemic encephalopathy.” Studies published at that time also concluded that cerebral palsy, which is a chronic neuro-muscular disability characterized by abnormal control of movement or posture appearing in early life, was attributable to events occurring during labor and delivery. These findings suggested physician negligence during the intrapartum period and resulted in a flood of litigation nationally against obstetricians, anesthesiologists and other healthcare personnel. Claims typically involved allegations of:

a. Failure to diagnose signs of intrauterine fetal distress evidenced by monitor strips;
b. Failure to perform timely C-Section deliveries;
c. Failure to deliver infants in a timely fashion; and,
d. Failure to properly and appropriately respond to persistent fetal heart rate decelerations.

Claims usually alleged that the aforementioned failures resulted in hypoxic irreversible brain injuries, including cerebral palsy, neonatal encephalopathy and seizure disorder or death. Verdicts in these brain injured infant cases frequently reach into the tens of millions of dollars. These verdicts are often said to result in skyrocketing insurance premiums for healthcare providers. They are sited in support of efforts at Tort Reform legislation.

Typically, expert medical testimony establishing the following was sufficient to make a prima facie case of medical negligence; (1) existence of me conium in the amniotic fluid, (which is suggestive of fetal distress) (2) non-reassuring heart rate patterns, (3) low Apgar scores, and (4) neonatal encephalopathy. Taken together these four were often thought to be sufficient evidence of birth asphyxia, which was assumed to result in hypoxic-ischemic neonatal encephalopathy.

A study published in January 2003 by the American College of Obstetrics and Gynecology (ACOG), has concluded that the majority of these newborn brain injury cases are not the result of events occurring during the intrapartum period. The article goes on to conclude that most instances of neonatal encephalopathy and cerebral palsy are attributable to events occurring before labor began and not the result of physician negligence. Expert commentators including Garry D. V. Hankins, M.D., the chair of the ACOG Task Force has said that “for years, adverse neurological outcomes of pregnancy, including cerebral palsy and neonatal encephalopathy have been assumed to be the effect of events occurring during childbirth.” ACOG president, Charles B. Hammond, M.D. in a recent article was quoted as saying that in the face of a bad outcome, many faulted the obstetricians. Dr. Hammond went on to state that less than 10% of the cases of neurological impairments in newborns are the result of events occurring in labor and of these events the majority are not preventable. The ACOG study concluded that factors historically used to define perinatal asphyxia such as meconium stained amniotic fluid and Apgar scores are nonspecific to the disease process leading to neurologic damage. The report quoted studies by Nelson and Associates which showed that the use of non-reassuring fetal heart rate patterns to predict subsequent cerebral palsy had a 99% false positive rate. The study found that spastic quadriplegia associated with movement disorders is the only type of cerebral palsy associated with an acute interruption of blood flow. Purely dyskinetic or ataxic cerebral palsy especially associated with learning problems, commonly has a genetic origin and is not caused by intrapartum or peripartum asphyxia. The study concludes that absent these findings, cerebral palsy, epilepsy, mental retardation, nor attention deficit disorder can be attributed to birth asphyxia. The study further concluded that using markers such as meconium in the amniotic fluid, five-minute Apgar scores and fetal acidemia were poorly associated with adverse neurological outcomes.

Research has concluded that a serious event has to occur for a neurologically intact fetus to sustain a neurologically damaging acute result. These identifiable insults can take the form of a uterine rupture, umbilical cord prolapse, placental abruption or cardiopulmonary arrest. Any of these events can result in morbidity or mortality. As a result, ACOG has issued new criteria to define an acute intrapartum event as sufficient to cause cerebral palsy.

In light of these published studies, it would behoove both risk managers and defense counsel to reevaluate brain damaged baby cases filed prior to 2003. Consultant opinions should be reassessed. For new and pending cases, defense counsel should take steps to retain experts who are familiar with the new body of medical literature that gave rise to these emerging standards and challenge plaintiffs’ experts accordingly.