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1862, William Little, an orthopedic surgeon, perpetuated
the concept that peripartum asphyxia and birth trauma
were two of the primary causes of cerebral palsy
(CP).1
Despite Sigmund Freud’s opposing view that
abnormal antenatal development was responsible,
for more than 100 years peripartum asphyxia has
been thought to be responsible for most cases of
cerebral palsy.2
To date, the cause of most cases of newborn brain
injury cannot be determined, and yet this age-old
belief continues to make obstetricians and anesthesiologists
vulnerable to litigation. Litigation for newborn
brain injury, particularly CP, is frequently based
on emotional suffering of the patient and family
rather than evidence of harm.3
We analyzed claims for newborn brain injury from
the ASA Closed Claims Project database, looking
at factors that possibly contributed to the neonatal
and liability outcome.
Claims for Newborn Brain Injury
The ASA Closed Claims Project database contains
standardized summary data on closed anesthesia malpractice
claims from 35 insurance companies throughout the
United States. Obstetric anesthesia claims make
up 12 percent (850) of the total 6,894 claims to
date, and of these, 18 percent involve newborn brain
injury. There has been a significant decrease in
the proportion of claims for newborn brain injury
from the 1980s (22 percent) to the 1990s (13 percent)
(p<0.05). From 1990 to 2000, the diagnosis of
CP was documented in 19 of the 48 newborn brain
injury claims (40 percent). Cesarean section was
the mode of delivery in 80 percent of newborn brain
injury claims, with 79 percent of these being urgent
or emergent.
Possible Causative Factors: Newborn Brain
Injury 1990-2000
Claims for newborn brain injury were reassessed
to evaluate the possible contribution of anesthesia
and obstetric care to the outcome. Claim narratives
also were reviewed for the mention of maternal,
fetal or delivery factors that might have contributed
to poor outcome. The most consistent factor was
a nonreassuring fetal heart tracing, which was documented
in more than 60 percent of newborn brain injury
claims [Figure 1]. In less than one-third of newborn
brain injury claims, we determined that anesthesia
care may have contributed to fetal outcome, while
maternal condition and poor communication were possibly
involved in 17 percent and 8 percent of claims,
respectively [Figure 1]. In half of the 12 claims
in which anesthesia may have contributed to fetal
outcome, some delay by anesthesia was alleged. Other
factors that occurred in fewer than 10 percent of
claims included fetal acidosis, meconium aspiration,
chorioamnionitis, fetal congenital problems, uterine
rupture, placental and umbilical cord problems,
breech and attempted vaginal birth after cesarean
section [Table 1].
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Payment
In 60 percent of claims for newborn brain injury in
the 1990s, the anesthesiologist was either dismissed
or dropped from the case or no payment was made. Payment
was more likely to be made by anesthesia in claims
in which we assessed that anesthesia may have contributed
to the neonatal outcome (71 percent paid), compared
to 13 percent paid when anesthesia did not contribute
(p<0.05). In the 1990s, 57 percent of newborn brain
injury claims resulted in payment by at least one
of the defendants, compared with 78 percent of maternal
death and brain injury claims and 29 percent of newborn
death claims. Median payment for newborn brain injury
was greater than $1 million, while median payment
for all obstetric anesthesia claims was only $153,000.
Discussion
Forty percent of newborn brain injury claims in the
1990s were diagnosed as CP. This may be an underestimate,
as CP is often not diagnosed until 3 to 4 years of
age. Most other claims did not document a specific
neurological diagnosis.
A nonreassuring fetal heart tracing was the most common
factor in newborn brain injury claims. Electronic
fetal heart monitoring (EFM) was introduced in the
late 1960s to help to detect fetal heart rate patterns
that might indicate hypoxia and has been associated
with a five-fold increase in the cesarean section
rate.4
It has not lived up to expectations, and although
multiple late decelerations of fetal heart rate and
decreased beat-to-beat variability have been associated
with an increased risk of CP, the false positive rate
of EFM abnormalities is very high at 99.8 percent.5
Over the last three decades, the incidence of CP in
developed countries has remained very stable at two
to three per 1,000 live births.4
Alleged anesthesia delay was cited in half of the
claims where anesthesia care may have contributed
to neonatal outcome. A decision-to-delivery interval
for emergency cesarean section within 30 minutes is
the international standard for fetal compromise.6,7
The evidence to support this standard is weak.8
One particular study showed that decision-to-delivery
intervals of more than 75 minutes are associated with
poorer maternal and baby outcomes.8
While this refutes the basis of many of the claims
we reviewed, it is recognized that some benchmark
is needed to maintain quality of care, and the 30-minute
decision-to-delivery interval is prudent but poorly
supported by evidence.
The etiology of CP is probably the most researched
area of neonatal brain injury. There are many risk
factors, including those in Figure 1 and Table 1,
but the current literature suggests that 70 percent
to 80 percent of cases are due to antenatal factors,
most of which are not preventable.2,9
Only 6 percent to 8 percent
were related to birth asphyxia.
The findings of this analysis show that anesthesia
care is often not in question, reflected by the proportion
of claims resulting in no payment. Payments, however,
when made, are generally larger than for other obstetric
anesthesia claims because of the length of chronic
care for a brain-damaged child.
The etiology of newborn brain injury, particularly
CP, has been the focus of much research, primarily
as a result of the financial impact of litigation
on both obstetricians and anesthesiologists. In 2003
an American College of Obstetricians and Gynecologists
task force introduced criteria, modified from a International
Cerebral Palsy Task Force consensus statement, to
help to define the causal relationship between acute
intrapartum events and cerebral palsy.1
Hopefully these new criteria will be positively reflected
in future malpractice claims against both obstetricians
and anesthesiologists.
References:
1. Hankins GD, Speer M. Defining the pathogenesis
and pathophysiology of neonatal encephalopathy and
cerebral palsy. Obstet Gynecol. 2003; 102:628-635.
2. Reddihough DS, Collins KJ. The epidemiology and
causes of cerebral palsy. Aust J Physiother.
2003; 49:7-12.
3. MacLennan A, Nelson KB, Hankins G, Speer M. Who
will deliver our grandchildren? Implications of
cerebral palsy litigation. JAMA. 2005;
294:1688-1690.
4. Clark SL, Hankins GD. Temporal and demographic
trends in cerebral palsy? Fact and fiction. Am
J Obstet Gynecol. 2003; 188:628-633.
5. Nelson KB, Dambrosia JM, Ting TY, Grether JK.
Uncertain value of electronic fetal monitoring in
predicting cerebral palsy. N Engl J Med.
1996; 334:613-618.
6. Royal College of Obstetricians and Gynaecologists.
The use of electronic fetal monitoring: The use
and interpretation of cardiotocography in intrapartum
fetal monitoring. RCOG. 2001:No. 8.
7. American Academy of Pediatrics, American College
of Obstetricians and Gynecologists. Intrapartum
and postpartum care care of women. Guidelines for
perinatal care. 2002:125-161.
8. Thomas J, Paranjothy S, James D. National cross
sectional survey to determine whether the decision
to delivery interval is critical in emergency caesarean
section. Brit Med J. 2004; 328:665-669.
9. Jacobsson B, Hagberg G. Antenatal risk factors
for cerebral palsy. Best Pract Res Clin Obstet
Gynaecol. 2004; 18:425-436.
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Joanna
M. Davies, M.B., B.S., F.R.C.A., is Assistant
Professor of Anesthesiology, University of Washington
School of Medicine, Seattle, Washington. |
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