CASE: Two years after emergency cesarean, you are served
M.K., age 29 years, presents at term and in labor to the state-of-the-art hospital where you practice. During labor, transient slowing of the fetal heart rate (FHR) is detected, and you perform an urgent cesarean section, with successful delivery of the infant. Cord blood shows no evidence of acidosis, and the Apgar score is 8 at 1 minute and 9 at 5 minutes.
Two years later, after the child is diagnosed with ataxic cerebral palsy (CP), the parents file a $10 million lawsuit that names you as defendant.
Could you have done something to avoid litigation?
Absolutely! But the best preventive strategy has nothing to do with the science of medicine.
Because of the near certainty of being sued—usually, without merit—over the course of one’s career, an ObGyn has little choice but to practice defensive medicine. Until true tort reform is passed, we believe that physicians should rely on contract law to avoid lawsuits such as the one described above. The best defense begins at the patient’s first appointment, when she should be asked to sign a basic agreement. This article describes how such a strategy can greatly bolster your case should a lawsuit eventually be filed.
Avoiding the “death knell”
Until recently, a diagnosis of CP coupled with a lawsuit sounded the proverbial death knell for an obstetrician. The high stakes, long statute of limitations, and availability of “experts” willing to testify about standard-of-care violations all but guaranteed an early settlement. No obstetrician could risk presenting his or her case to a jury likely to be sympathetic to the plaintiff. The settlement of such cases was usually substantial—in the high 6 or low 7 figures—and the physician’s name was subsequently entered into the National Practitioner Data Bank. These settlements fueled high professional liability premiums, which remain extreme across the country.
Causes of CP are now more clearly understood
In 2003, the American College of Obstetricians and Gynecologists (ACOG) and the American Academy of Pediatrics published a report, “Neonatal encephalopathy and cerebral palsy: Defining the pathogenesis and pathophysiology” (NEACP),1 that challenged a number of long-held assumptions—among them the belief that electronic FHR monitoring can highlight fetal distress in time to prevent intrapartum fetal asphyxia and lower the number of cases of CP. (For the findings of this report, see “Tracing the origin of a case of CP.”) Sadly, electronic fetal monitoring has had no impact on the rate of CP, despite a dramatic increase in cesarean deliveries. A study by Nelson et al2 found that nonreassuring FHR patterns had a 99% false-positive rate for predicting CP.
The overall conclusion of the NEACP report: Most cases of CP are not the result of intrapartum events.
“Neonatal encephalopathy and cerebral palsy: Defining the pathogenesis and pathophysiology” (NEACP),1 the report published jointly by the American College of Obstetricians and Gynecologists and the American Academy of Pediatrics, was created to educate patients, physicians, and the public about the causes of cerebral palsy (CP) and provide a deeper understanding of what used to be called “birth asphyxia.”
The report also set out to identify cases in which intrapartum events can be implicated in the development of CP, with the aim of preventing them. According to the NEACP report, CP can be attributed to an intrapartum event when 4 “essential criteria” are present:
- evidence of metabolic acidosis in fetal umbilical cord arterial blood obtained at delivery (pH
- early onset of severe or moderate neonatal encephalopathy in infants born at or beyond 34 weeks’ gestation
- cerebral palsy of the spastic quadriplegia or dyskinetic type
- exclusion of other identifiable causes, such as trauma, coagulopathy, infection, or genetic disorders
In addition, 5 other nonessential or nonspecific criteria may have a bearing on the timing of events leading to CP:
- a sentinel (signal) hypoxic event occurring immediately before or during labor
- a sudden and sustained fetal bradycardia or the absence of FHR variability in the presence of persistent, late, or variable decelerations, usually after a hypoxic sentinel event when the pattern was previously normal
- an Apgar score of 0 to 3 beyond 5 minutes
- onset of multisystem involvement within 72 hours of birth
- early imaging study showing evidence of acute nonfocal cerebral abnormality.
According to these criteria, fewer than 30% of CP cases are caused by a lack of oxygen to the fetus during labor and delivery. Most cases apparently are caused by events that disrupt normal brain development before labor.
Given these criteria, it is critical to obtain cord blood gases and perform early imaging of the newborn brain to help define the cause of encephalopathy in a newborn. Also crucial is a thorough investigation of other potential causes, especially in view of the relative rarity of intrapartum events capable of causing this devastating condition.