Dealing
with ACOG 163 and the
Importance of Neuroimaging
Presented by
E. Drew Britcher, Esq.
Britcher, Leone & Roth
LLC
For any
Plaintiff’s attorney prosecuting birth injury cases dealing with the
publications of the American College of Obstetricians and Gynecologists
(ACOG) is essential. ACOG’s publications can either become a great
resource for proving the standard of care or they can be the death of
your case.
The most common
publication that a plaintiff’s attorney in a medical malpractice case
must deal with is ACOG Technical Bulletin 163, first published in 1992.
ACOG Technical Bulletin 163 claims to set forth the criteria for
determining whether a fetus allegedly suffered asphyxia during the
delivery process resulting in brain damage. The criteria set forth in
ACOG Technical Bulletin 163, were later incorporated into ACOG Committee
Opinion 137, published in 1994, and ACOG Committee Opinion 197,
published in 1998. These publications set forth four criteria that ACOG
claims must be established before a "plausible link" can be made between
a defendant’s negligence resulting in perinatal asphyxia and neurologic
injury can be proven. These are:
-
Profound metabolic or mixed
acidemia found in the infant’s umbilical cord arterial blood,
exhibited by a pH of less than 7.00;
-
APGAR scores of a newborn child
persistently from 0-3 for more than five minutes;
-
Subsequent medical documentation
of neonatal neurological sequelae, illustrated by seizures,
hypotonia or coma; and
-
Dysfunction exhibited in any or
all of the newborn child’s cardiovascular, gastrointestinal,
hematologic, pulmonary or renal systems.
While most plaintiff’s
attorneys agree that ACOG 163, and the other publications have been to
help obstetricians defend medical malpractice lawsuits, juries can still
be swayed by such an important sounding group having codified these
standards. Thus, plaintiff’s attorney’s must look at the variety of
available attacks on ACOG 163 and alternative means of proving
causation.
There are
several articles or publications that should be known by any Plaintiff’s
attorney seeking to deal with the ACOG 163 criteria . These include, but
are not limited to Dr. Goodlin’s article published in the American
Journal of Obstetrics and Gynecology in June of 1995 entitiled, “Do
concept’s of Causes of Prevention of Cerebral Palsy Require Revision”,
Dr. Korst’s articles published in Prenatal Neonatal Medicine in 1997 and
in the Journal of Maternal Fetal Medicine in a 1997, the latter being
entitled, “Acute Fetal Asphyxia and Permanent Brain Injury, a
Retrospective Analysis of Current Indicators”, the International
Cerebral Palsy Task Force statement published in the British Medical
Journal in 1999 entitled “A Template for defining a Causal Relation
Between Acute Intrapartum Events and Cerebral Palsy: International
Consensus Statement”, Dr. Volpe’s textbook, “Neurology of the Newborn”
4th Edition, published in 2001, “The Continuing Value of the Apgar Score
for the Assessment of Newborn Infants”, published in the New England
Journal of Medicine in 2001 and the Report of the Quality Standards
Subcommittee of the American Academy of Neurology and the Practice
Committee of the Child Neurology Society, published as a Practice
Parameter: Neuroimaging of the Neonate in June 2002.
The Goodlin
article was one of the first peer-reviewed publications to call in to
question the criteria established by ACOG 163. Dr. Goodlin reviewed four
cases of intrapartum fetal insults with subsequent cerebral palsy, all
of which were considered to demonstrate the link between the two, but
all of which lacked the necessary criteria under ACOG 163 to qualify.
His ultimate conclusion was that exceptions to the criteria exist and
that despite the appeal to obstetricians to apply these criteria as hard
and fast rules, a revisiting of the criteria was needed. As noted in his
article, one can question whether the purpose of the criteria was to be
too limiting, as “when they are applied, few cases of cerebral palsy
appear to be due to perinatal asphyxia.”
In the first of
the Korst articles a similar review of 16 se4verely neurologically
impaired term infants was undertaken. All of these had been subject to
an acute intrapartum event, such as uterine rupture or prolapsing of the
cord. Each had been diagnosed as suffering from hypoxic-ischemic
encephalopathy and had no other identified cause of their brain injury,
However, when the ACOG 163 criteria were applied only one of the 16 met
all 4 criteria, 4 met 3 of the criteria, 8 met 2 criteria and 3 met only
1 criteria. The following were the specific findings for each
criteria:
-
Five had a pH <7.00
-
Five had a 5 minute Apgar score
<3
-
13 had seizures within the first
24 hours
-
8 had no multiorgan dysfunction,
while 4 had 1 system dysfunction and 4 had more than 1.
In the second study they reported on
47 neonates of similar condition. Their findings were:
-
10 met all 4 criteria
-
14 met 3 criteria
-
14 met 2 criteria
-
8 met 1 criterion
-
1 met no criteria
Also they found:
-
the mean pH was 7.06, with only
38percent <7.00
-
26 had a five minute Apgar <3
-
87 percent experienced seizures
within the first 24 hours
-
70 percent had multi-organ
dysfunction
Their conclusion was
“Our retrospective study suggests that currently used indicators to
define permanent fetal brain injury are not valid.”
The International Consensus provides the
following criteria, differing from ACOG 163. It should be noted that the
American College of Obstetricians and Gynecologists are listed as
supporters of this statement:
Essential criteria
1. Evidence of a metabolic acidosis in intrapartum
fetal, umbilical cord or very early neonatal blood samples, pH<7 and
base deficit > -12 mmol/L
2. Early onset of severe of moderate
neonatal encephalopathy in infants > 34 weeks gestation
3. Cerebral Palsy is of the spastic
quadriplegic or dyskinetic type.
Criteria that
together suggest an intrapartum timing, but by themselves are non
specific.
4. A sentinel event occurring immediately before or
during labour
5. A sudden, rapid and sustained
deterioration of the fetal heart rate pattern usually following the
sentinel event where the pattern was previously normal.
6. Apgar scores of 0-6 for longer than
5 minutes
7. Early evidence of multi-system
involvement.
8. Early imaging evidence of acute
cerebral abnormality.
Dr. Volpe’s textbook (both the 3rd and 4th
Editions) carries a very useful Tables that can be used effectively to
undermine the 163 criteria. Table 9-3 in the 3rd Edition
shows that 34% of asphyxiated infants have no organ injury and the 4th
Edition in the same table has 22%.
The New England Journal article examines the history of the Apgar score
and discusses its proper purpose and it’s misuse for determining long term
neurological outcome. While finding that ‘the Apgar scoring system
remains as relevant for the prediction of neonatal survival today as it
was almost 50 years ago” the authors conclude with “ We cannot dispute
the contemporary viewpoint that the use of the Apgar score for the
prediction of long-term neurologic outcome is inappropriate. However,
the poor performance of the Apgar system as a predictor of neurologic
development, a purpose for which it was never intended…….” Clearly this
article provides a valuable argument in a case where the subjective
Apgar scores are inconsistent with the child’s condition at birth and
beyond.
The Quality Standards Subcommittee of the American Academy of Neurology
and the Practice Committee of the Child Neurology Society in the
Practice Parameter published in 2002 provide the following useful
information. Neuroimaging plays two important roles:
1) diagnosis of brain injury in the newborn at risk so that appropriate
medical management can be provided and 2) detection of those lesions
associated with long-term neurodevelopmental disability. Currently,
cranial ultrasonography (US), CT, and MRI are the most available means
for these tasks.
Clinical examination of the term infant with signs and symptoms of
neonatal encephalopathy is often unable to determine the severity or
extent of cerebral damage and frequently provides little information
regarding the etiology of the insult. Although numerous reports suggest
that hypoxic–ischemic encephalopathy (HIE) is a common cause of neonatal
encephalopathy, the differential diagnosis of this condition is
extensive, including a spectrum of abnormalities ranging from infectious
to metabolic abnormalities and congenital malformations. Even in those
infants with documented HIE, the clinical presentation may vary widely.
Of those neonates with moderate to severe HIE, almost one-quarter have
mental retardation, seizures, and CP, and promising intervention
strategies are now becoming available. Therefore, for diagnostic and
prognostic reasons, early assessment and diagnosis of infants with
neonatal encephalopathy is important.
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