# Markell Vanslembrouck v. Andrew Jay Halperin Md

> Michigan Court of Appeals · October 28, 2014

URL: https://www.frixlaw.com/law-library/cases/2746684

## Case

- **Court:** Michigan Court of Appeals
- **Decided:** October 28, 2014
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Cited by:** 0 later opinions in the Frix Law Library

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## Opinion text

STATE OF MICHIGAN

COURT OF APPEALS

MARKELL VANSLEMBROUCK, Minor, by and UNPUBLISHED
through ERIC BRAVERMAN, Conservator, October 28, 2014

Plaintiff-Appellee,
and

KIMBERLY A. VANSLEMBROUCK,

Plaintiff,

v No. 309680
Oakland Circuit Court
ANDREW JAY HALPERIN, M.D., and LC No. 2006-754585-NH
WILLIAM BEAUMONT HOSPITAL,

Defendant-Appellants.
and

MICHIGAN INSTITUTE OF GYNECOLOGY
AND OBSTETRICS, P.C.,

Defendant.

Before: GLEICHER, P.J., and BORRELLO and SERVITTO, JJ.

PER CURIAM.

This medical malpractice case arises from Markell VanSlembrouck’s 1995 birth at
defendant William Beaumont Hospital. Markell is now 18 years old. She cannot walk, talk, or
feed herself, and requires full-time care. After an 18-day trial, a jury attributed Markell’s
neurologic injuries to the circumstances surrounding her birth and assessed her damages at $144
million.

The trial evidence centered on the cause of Markell’s neurologic condition and the
scientific validity of plaintiffs’ causation theories. Fifteen expert witnesses debated these
questions over the course of the lengthy trial. In a nutshell, plaintiffs’ expert witnesses opined
that Markell’s traumatic birth caused her disabilities. Defendants’ experts countered that a
genetic abnormality called pontine cerebellar hypoplasia (PCH) fully accounts for Markell’s

-1-
current condition. Plaintiffs’ experts conceded that important components of Markell’s brain
never properly developed. But absent birth trauma, they contended, this abnormality would have
caused Markell only relatively insignificant neurological problems.

From start to finish, this case was a battle of experts espousing widely divergent views.
Ultimately the jury credited plaintiffs’ negligence and causation explanations. Although the trial
was far from perfect, we affirm.

I. FACTUAL OVERVIEW

The underlying record is long and complex, but presents only a handful of factual
disagreements. Because most of the appellate issues hinge on evidentiary questions, we describe
the medical facts in considerable detail. Although we recite the evidence in the light most
favorable to the prevailing parties, we have noted important factual conflicts.

There was no debate about one central fact: Markell’s birth was traumatic. She was an
exceptionally large newborn, weighing in at 10.5 pounds. At delivery, Markell was limp, blue,
and unresponsive. She did not breathe spontaneously. Her head, trunk, and upper extremities
appeared bruised. Her collarbone was fractured during an obstetrical maneuver made necessary
when her shoulders became stuck in the birth canal. Markell’s one-minute Apgar score was one;
a zero score would have been consistent with her death.

In the days following Markell’s delivery, brain imaging studies displayed the presence of
blood in several different cerebral locations. The studies also revealed a striking congenital
abnormality: a portion of Markell’s cerebellum was missing, as was part of a brain structure
called the pons.

Plaintiffs’ experts acknowledged these abnormalities, and conceded that they contributed
to Markell’s abnormal neurological presentation. But in their view, birth trauma markedly
worsened any deficits attributable to the absence of these brain components. Plaintiffs’ experts
posited that Pitocin-induced hyperstimulation of Kimberly VanSlembrouck’s uterus, combined
with Markell’s large size, compressed Markell’s head during the last hour of Kimberly’s labor.
According to their theory, head compression resulted in cerebral ischemia (lack of adequate
blood flow to the cerebrum), bleeding into the brain itself, and permanent brain damage
attributable to the trauma.

Defendants’ experts insisted that Kimberly’s obstetrical care met all applicable standards.
Further, they steadfastly maintained that Markell’s neurological problems stem solely from a
genetic abnormality called pontine cerebellar hypoplasia, type 2 (PCH-2). PCH-2 is a rare
disorder. The children afflicted with it lack substantial portions of the cerebellum and pons, as
does Markell. Two medical articles describing children afflicted with PCH-2 portray its victims
as neurologically similar to Markell. Defendants’ experts further contended that despite the
brain bleeding and the evident trauma to Markell’s head, the substance of her cerebral cortex
remain uninjured. The initial indicia of trauma, defendants’ experts claimed, faded quickly and
produced no permanent damage.

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The trial court conducted a four-day Daubert hearing1 to evaluate the scientific reliability
of plaintiffs’ causation theory. At its conclusion, the court found plaintiffs’ experts qualified and
their opinions reliable under MRE 703.

A month-long, bitterly contentious trial followed. The jury found in Markell’s favor and
awarded the damages her counsel had sought. Defendants’ many appellate challenges focus
largely on issues related to causation and damages. All merit considerable discussion, but none
persuade us that a new trial is required.

A. PRENATAL EVENTS

Kimberly VanSlembrouck obtained her prenatal care from defendant Andrew Jay
Halperin, M.D., an employee of defendant Michigan Institute of Gynecology and Obstetrics,
P.C. Kimberly gained approximately 70 pounds during her pregnancy. One week prior to
delivery, Kimberly weighed 328 pounds. This weight gain exceeded normal limits.

The medical witnesses agreed that excessive weight gain during pregnancy signals the
possible presence of gestational diabetes. Gestational diabetes often leads to large (macrosomic)
infants.2 Undisputed evidence established that macrosomia creates a risk of traumatic delivery or
the need for a cesarean section. Plaintiffs’ experts opined that Kimberly’s undiagnosed
gestational diabetes caused Markell’s excessive growth, and that if Markell’s size had been
accurately established prenatally, her delivery would have been accomplished by an elective
cesarean section.

The parties further agreed that the standard of obstetrical care includes screening
pregnant women for gestational diabetes. Because Kimberly’s initial glucose screening test was
abnormal, Dr. Halperin ordered a three-hour glucose tolerance test. The three-hour test entails
an analysis of blood samples obtained before and after the patient drinks a liquid containing
glucose. If two values are elevated, the patient has gestational diabetes.

One of Kimberly’s blood sample results was elevated; two others were one point below
the normal limit. Dr. Halperin viewed this as a negative glucose tolerance test and advised
Kimberly to watch her diet. Dr. Jeffrey Soffer, one of plaintiffs’ obstetrical experts, conceded
that Kimberly did not meet the “strict criteria” for gestational diabetes, but opined that she
should have been classified with the disorder based on the lab results and her weight gain.
According to Dr. Soffer, Dr. Halperin breached the standard of care by failing to maintain
suspicion of gestational diabetes throughout the pregnancy and by neglecting to carefully
monitor the baby’s growth with serial ultrasounds. Had serial ultrasounds been obtained, Dr.
Soffer testified, Dr. Halperin would have recognized that Markell was a large baby and that a
cesarean delivery was required.

1
Daubert v Merrell Dow Pharm, Inc, 509 US 579; 113 S Ct 2786; 125 L Ed 2d 469 (1993).
2
Macrosomia is defined as newborn weighing more than 4,000 grams, which is 8 pounds, 13
ounces.

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Kimberly’s due date was calculated as December 1, 1995. Early that morning (1:25
a.m.), she presented at Beaumont Hospital in early labor. A resident obtained a bedside
ultrasound at 1:40 a.m., and calculated the baby’s weight as 3,200 grams. This estimate proved
to be off by approximately 35%, as Markell actually weighed 4,797 grams (just over 10.5
pounds). Dr. Halperin admitted that the resident’s estimate constituted “a large error,” but
claimed it fell within a reasonable “margin of error,” because ultrasounds are not as accurate in
“heavier women.” Plaintiffs’ experts disagreed, asserting that the estimate was so far off that it
violated the standard of care.

Dr. Halperin admitted that if he had known that Markell weighed 4,795 grams, he would
have discussed a cesarean section with Kimberly and allowed her to choose her delivery method.
Dr. Soffer testified that he did not know of any woman who could safely deliver a baby of
Markell’s size as a first child. Dr. Brian Torok, a Beaumont resident who participated in
Kimberly’s obstetrical care, conceded that if he had known that the baby weighed 4,795 grams,
“I would not labor that patient.”

B. THE DELIVERY

At 10:15 a.m. on the day of Markell’s delivery, a resident attending Kimberly ordered
Pitocin to augment her contractions. Plaintiffs’ experts claimed that the Pitocin caused
hyperstimulation of Kimberly’s uterus. Hyperstimulation is defined as more than five uterine
contractions during a ten-minute period.3 When it occurs, the doctors concurred, blood flow to
the baby through the placenta may be compromised. Plaintiffs’ experts relied on the electronic
fetal monitor tracing to support their theory that Kimberly’s uterus had been hyperstimulated
with Pitocin. Defendants’ experts disagreed with plaintiffs’ interpretation of the fetal monitor
tracing.

Electronic fetal monitoring produces a graph of the fetal heart rate and the maternal
contraction pattern. The parties’ experts generally agreed that reduced blood flow to the fetus
slows the fetal heart rate, which appears on the tracing as a dip in the heart rate graph. The dips
visible on the tracing are called decelerations. A deceleration occurring during a contraction
(variable deceleration) or after a contraction (late deceleration) may potentially signal inadequate
fetal oxygenation.

Dr. Soffer testified that during the second stage of Kimberly’s labor (the “pushing”
stage), the fetal monitoring tracing demonstrated that Kimberly’s uterus was being
hyperstimulated by Pitocin, causing “tumultuous” contractions and “severe late decelerations and
multiple variable[]” decelerations. By using Pitocin, Dr. Soffer explained, “[t]hey pushed this
baby through a pelvis . . . too small for this baby to fit.” Dr. Soffer maintained that the repetitive
decelerations visible on the fetal monitor represented “red flags” of fetal distress, and by 3:00
p.m., Dr. Halperin should have initiated a cesarean section.

3
Some of the testifying witnesses used the term “tachysystole” to refer to abnormally strong and
rapid uterine contractions.

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Markell was delivered at 4:47 p.m., after Kimberly pushed for two-and-a-half hours.
Although Markell’s head delivered spontaneously, Dr. Halperin encountered difficulty delivering
her shoulders. Dr. Halperin performed a McRoberts maneuver, which involves repositioning the
mother’s legs to open her pelvis. In the process of delivering Markell’s shoulders, her collarbone
fractured. At birth, Markell was limp, blue, unresponsive to stimulation, not breathing, and had a

slow heart rate. Her one-minute Apgar score was one.4 Resuscitation brought her five-minute
score up to seven, and she was then transferred to the Special Care Nursery.

C. THE SPECIAL CARE NURSERY

According to Special Care Nursery notations, Markell bore visible evidence of a
traumatic transit through the birth canal. The medical record documents “scalp and facial
bruising and swelling” as well as bruising on her left arm, left nipple, and right forearm. Nursing
notes document additional bruising to Markell’s torso. The swelling of Markell’s head, known
as a cephalohematoma, was caused by blood collecting under the tissue covering her skull bone.

In the nursery, Markell developed noticeable tremors and respiratory distress. She was
unable to suck, lacked rooting and grasp reflexes, and required oxygen to maintain normal
oxygen saturation. Within 24 hours of her birth Markell developed seizure activity. The
physicians caring for her described her condition in the medical record as “perinatal depression.”

Markell remained hospitalized in Beaumont’s Special Care Nursery until December 18,
1995. Several laboratory and radiologic studies conducted during this time formed the predicates
for the experts’ causation opinions. We now introduce the studies.

1. The Umbilical Blood Gases

The experts concurred that one objective indicator that a newborn has been deprived of
oxygen during the birth process is a decreased pH level in the umbilical arterial blood. A fetus
systemically deprived of oxygen (such as might occur when the umbilical cord is clamped or
compressed) accumulates lactic acid in the blood, causing the pH to decrease. An umbilical
artery blood pH of 7.0 or less signifies the presence of metabolic acidosis. This finding is
universally recognized as consistent with fetal hypoxia (lack of oxygen) during delivery.

Shortly after her birth, physicians attending Markell ordered an umbilical arterial blood
gas study. According to the medical record, the arterial study was “cancelled.” Instead of

4
Apgar scores reflect the health of a newborn at one minute and five minutes after birth. The
one minute Apgar score measures how well the baby tolerated labor and delivery, while the five
minute score assesses the baby’s adaptation to her environment and the efficacy of resuscitation
efforts. Five criteria are assessed: heart rate, respiration, muscle tone, response to stimulation,
and color. Each criteria is scored as zero, one or two, with two representing optimal health. The
top score is a 10. Markell received a zero for every criteria except heart rate.

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analyzing arterial umbilical blood, the Beaumont lab tested venous umbilical blood. The lab
reported a pH of 7.29, which is within normal limits for venous blood.

The significance of the venous blood gas result was hotly contested throughout the trial.
Plaintiffs maintained that the unexplained cancellation of the arterial blood study signaled a
“cover up.” Defendants contended that the arterial blood study was cancelled because the
laboratory received an insufficient quantity of arterial blood. Plaintiffs argued that the venous
sample was useless as an indicator of Markell’s perinatal asphyxia, as venous umbilical blood
derives from the mother and does not reflect the pH of the baby’s blood. During cross-
examination, Dr. Halperin agreed with plaintiffs’ position, stating: “the venous pH is the
mom’s.” Defendants’ experts took varying positions. Some asserted that the venous umbilical
blood was a mixture of the mother and the baby’s blood, while others claimed it was solely the
baby’s blood.5 The defense experts generally opined that the venous pH correlated well with
arterial pH, and that a venous pH of 7.29 indicated that Markell had not sustained any perinatal
asphyxia.6

2. The Cranial Ultrasound

An ultrasound of Markell’s head obtained the day after her birth revealed “no definite
evidence of hemorrhage,” according to the Beaumont radiologist who interpreted it. The
radiologist also noted: “The ventricular systems appear normal.” Plaintiffs’ radiology expert, Dr.
Barry Pressman, reviewed the same ultrasound films, and disagreed. Pressman testified that the
ventricles were “actually almost invisible” demonstrating “a swollen brain.” He elaborated:
“The whole brain is -- the cerebrum is swollen.” According to Dr. Pressman, brain swelling is
consistent with an ischemic injury (injury caused by lack of blood flow) that occurred before and
during delivery.

3. The CT Scan

A CT scan was performed on December 4. A Beaumont radiologist interpreted the study
in relevant part as follows:

5
We note that in an unpublished decision involving Dr. Ronald Gabriel, whose causation theory
is also at issue here, this Court stated in a footnote: “A venous sample [from the umbilical cord]
measures maternal blood gases and an arterial sample measures fetal oxygenation.” Dukes v
Harper-Hutzel Hosp, unpublished opinion per curiam of the Court of Appeals, issued January
30, 2007 (Docket No. 255824), unpub op at 3 n 3.
6
The dispute regarding the significance of a normal umbilical venous sample relates to one of
the issues presented on appeal, whether the trial court denied defendants a fair trial by excluding
from evidence criteria promulgated by the American College of Obstetricians and Gynecologists
(ACOG) and the American Academy of Pediatrics for diagnosing an acute intrapartum hypoxic
event.

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There is a small amount of hyperdensity within the occipital horns of both
lateral ventricles. This is consistent with a small amount of intraventricular
hemorrhage. There is also a small amount of hyperdensity in the interhemispheric
fissure which may represent a small area of hemorrhage.

***

There is hypoplasia of both cerebellar hemispheres as well as the vermis
inferiorly with a correspondently enlarged surrounding CSF space believed to
represent a megacisterna magna.

The experts for both sides agreed that this CT scan revealed two important findings: (1) the
presence of blood in Markell’s ventricles (the cerebrospinal fluid-filled chambers of the brain)
and subdurally (beneath the dura, the covering of the brain), and (2) the partial absence
(“hypoplasia”) of the cerebellum. Cerebellar functions include coordinating voluntary muscle
movement and modulating balance and equilibrium. The experts agreed that the abnormality of
Markell’s cerebellum is congenital, and not due to birth trauma. Dr. Pressman distinguished the
congenital disorder from the effects of birth trauma as follows:

So, we have a congenital hypoplasia or incomplete growth of the
cerebellum. However, that has nothing to do with the fact that the brain is
swollen and was traumatized and/or had inadequate blood supply or oxygen.
They are totally separate conditions.

Defendants’ neuroradiology expert, Dr. Douglas Quint, opined that only a tiny amount of
blood (“[m]aybe a 15th of an ounce”) remained in Markell’s ventricle by the time the CT scan
was obtained, and an equally small amount was present in her subdural space. According to Dr.
Quint, one-half of normal, asymptomatic babies have small brain bleeds following vaginal
delivery. He estimated that 30% of Markell’s cerebellum was missing, and 20% of her pons.
Dr. Quint testified that he observed none of the established indicia of hypoxic ischemia when he
reviewed Markell’s CT scan.

D. THE MEDICAL RECORDS

Plaintiffs employed several medical record discrepancies to buttress their negligence
claims. During the trial, plaintiffs alleged that the resident who performed Kimberly’s
ultrasound mixed up Markell’s estimated fetal weight with that of a different infant, baby boy
Vergeldt. Vergeldt was a patient of Dr. William Floyd. Dr. Halperin covered for Dr. Floyd
during the morning that both women labored. A resident obtained an ultrasound of the Vergeldt
baby several hours after Kimberly’s ultrasound had been completed. The resident estimated the
Vergeldt fetal weight as 3,210 grams. Vergeldt’s baby actually weighed 3,185 grams. However,
a handwritten notation of the Vergeldt baby’s weight reveals an obvious change. At some point,
someone changed the 3 to a 4 by overwriting the 3:

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A weight of 4,210 grams (9.28 pounds) corresponds more accurately to Markell’s delivery
weight. Defendants admitted that someone had changed the record but produced no further
explanation.

Dr. Halperin conceded a second mix-up regarding the Vergeldt and VanSlembrouck
babies. Five days after Markell’s birth, Dr. Halperin dictated an “operative report, delivery
summary” describing the delivery in some detail. The summary states, “an internal scalp lead
and intrauterine pressure catheter were placed. There were variable decelerations down to 90. A
scalp pH was done which was normal at 7.25.” Dr. Halperin admitted that the statements
regarding the variable decelerations down to 90 and the scalp pH referred to the Vergeldt baby,
and not to Markell. This dictation error occurred, Dr. Halperin claimed, because he had
confused Mrs. Vergeldt’s labor with Kimberly’s.

The medical record of Markell’s stay in the Special Care Nursery does not include a
discharge summary. Plaintiffs alleged that hospital rules required a discharge summary.
Throughout the trial, plaintiffs’ counsel argued that its absence evidenced an additional cover-up.

E. THE 2010 GENETIC TESTING

After four years of litigation, defendants moved the trial court to order that Markell
undergo genetic testing.7 The trial court granted the motion. In November 2010,
PreventionGenetics, a laboratory located in Marshfield, Wisconsin, reported that Markell had a
genetic disorder: PCH-2 as well as subtype 4.8 The lab report states in relevant part:
“Pontocerebellar hypoplasias subtype 2 . . . and subtype 4 . . . are subsets of neurodegenerative
disorders, characterized by small cerebellum and brainstem, variable neocortical atrophy, and

7
Genetic testing performed early in Markell’s life revealed no specific abnormalities.
8
Defendants’ genetics expert admitted that most children with PCH-4 die before age four, so “by
inference it’s thought that she’s a so-called type two.”

-8-
impaired cognitive and motor development . . . .” The admissibility of the PreventionGenetics
report supplies another contested issue on appeal.

II. PERTINENT PROCEDURAL BACKGROUND

Kimberly filed suit on Markell’s behalf in May 2006. In August 2006, the circuit court
granted defendants’ motion for summary disposition, ruling that the statute of limitations barred
plaintiffs’ claim. This Court reversed in Vanslembrouck v Halperin, 277 Mich App 558; 747
NW2d 311 (2008), and the Supreme Court granted defendants’ application for leave to appeal.
VanSlembrouck v Halperin, 481 Mich 918; 750 NW2d 591 (2008). In its order granting leave,
the Supreme Court directed the parties to address whether “the plaintiffs are entitled to the
benefit of the tolling provision in MCL 600.5856(c) where the plaintiffs provided a notice of
intent prior to the minor reaching 10 years of age but filed their complaint after the minor had
reached 10 years of age,” and “whether MCL 600.5851(7) provides a period of limitation.” Id.

Following oral argument the Supreme Court vacated its order granting leave, explaining
“we are no longer persuaded that the question presented should be reviewed by this Court.”
VanSlembrouck v Halperin, 483 Mich 965; 763 NW2d 919 (2009).

Thereafter, the parties brought numerous interlocutory issues to this Court’s attention,
including an application from the circuit court’s order denying defendants’ motion to strike as
scientifically unreliable the testimony of plaintiffs’ causation experts: Ronald Gabriel, M.D.,
Yitzchak Frank, M.D., and Carolyn Crawford, M.D. This Court issued the following order:

In lieu of granting leave to appeal, pursuant to MCR 7.205(D)(2), the
Court orders the case remanded to the Oakland Circuit Court for a pre-trial
evidentiary hearing regarding the bases for plaintiffs’ causation experts’ opinions,
whether those opinions are based on data viewed as legitimate in the context of
their area of medical expertise, and whether the opinions based on that data were
reached through reliable principles and methodology. MRE 702; Gilbert v
DaimlerChrysler Corp, 470 Mich 749, 782-783; 685 NW2d 391 (2004). The
circuit court shall perform a searching inquiry as to these factors as required by
MRE 702 and Gilbert and make specific findings regarding those factors on the
record or in a written opinion. [VanSlembrouck v Halperin, unpublished opinion
of the Court of Appeals, entered July 12, 2011 (Docket No. 303548).]

Defendants predicate error on the trial court’s ruling following the Daubert hearing.
According to defendants, the trial court abused its discretion in finding the causation theory
espoused by plaintiffs’ experts scientifically valid, and committed legal error by failing to apply
the reliability factors set forth in MCL 600.2955. We turn to a discussion of that hearing and our
analysis of defendants’ Daubert-related arguments.

III. THE DAUBERT HEARING

A. THE EVIDENCE

Four expert witnesses testified for plaintiffs at the Daubert hearing: Dr. Carolyn
Crawford, a neonatologist, Drs. Yitzchak Frank and Ronald Gabriel, pediatric neurologists, and

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Dr. Barry Schifrin, a specialist in maternal-fetal medicine.9 Plaintiffs submitted dozens of
medical articles, Markell’s voluminous medical records, the deposition testimony of Dr.
Pressman, and the depositions of several treating physicians. Defendants presented the
testimony of Dr. Mary Bedard, a neonatologist, and Dr. Yoram Sorokin, a maternal-fetal
medicine specialist. Defendants also produced volumes of medical articles for the trial court’s
review, including the ACOG criteria for hypoxic-ischemic encephalopathy.

Dr. Crawford testified that physical trauma to an infant’s brain during the birth process
can cause bleeding in the brain, and that this fact “has been known for years.” The trauma
occurs when “you have obstruction to the passage of the head[.]” In such cases, the head “can
act like a battering ram against the boney pelvis,” resulting in “traumatic brain lesions”
manifested by brain bleeds. “[T]he process that caused those bleeds,” Dr. Crawford asserted, “is
what causes the Cerebral Palsy.”

Markell’s forehead was noticeably bruised, Dr. Crawford claimed, “[b]ecause that’s
where [she] got stuck.” According to Dr. Crawford, a “mis-fit” between the infant’s head and
the mother’s pelvis can lead to trauma.10 Dr. Crawford emphasized that conceptually, it has been
established “ever since babies have been born” that if a baby’s brain is traumatized during birth,
permanent damage may result. In her opinion, Markell’s brain injury was attributable to “[l]ack
of oxygen and lack of blood flow.” She elaborated: “This baby was banged through the pelvis
for a long period of time. The uterus was stimulated to contract excessively” by Pitocin.
“[W]here you have so frequent contractions that you don’t provide oxygenated blood to the
baby’s brain . . . [y]ou cause increased pressure, the blood can’t profuse the brain.”

Defense counsel challenged Dr. Crawford’s testimony based on its lack of congruence
with criteria published in 2003 by the ACOG Task Force on Neonatal Encephalopathy and
Cerebral Palsy. See American College of Obstetricians & Gynecologists, Neonatal
Encephalopathy & Cerebral Palsy (American Academy of Pediatrics, 2003). The ACOG report
declares that to define an acute event during labor and delivery as sufficient to cause cerebral
palsy, four “essential criteria” must be met:

1. Evidence of a metabolic acidosis in fetal umbilical cord arterial
blood obtained at delivery (pH (accessed October 2,
2014).

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probably secondary to disturbances of placental or cerebral blood flow.)
[Volpe, Neurology of the Newborn at 813 (italics in original, bold added).]

In a 1952 article, the author specifically identifies “trauma due to cephalopelvic
disproportion” as a cause of cerebral palsy, elaborating:

Most of the traumatic causes of brain injury at birth may be considered as
physiologic. Just being born is a difficult hurdle to pass. In the birth process, the
baby uses its head for a battering ram propelled by strong uterine contractions.
When the child’s head is large and the pelvis small, the natural safeguards which
allow the skull to conform to the shape of the birth canal may be insufficient to
protect the brain from injury. [Deaver, Etiological Factors in Cerebral Palsy, 28
The Bulletin: NY Acad Med 532, 536 (1952).]

At least two articles supported Dr. Gabriel’s opinion that excessive uterine activity
lowers the amount of oxygenated blood perfusing the fetal brain. In 2007, the American Journal
of Obstetrics and Gynecology, a peer-reviewed journal, published a study evaluating “how UA
[uterine activity] affects fetal outcome.” The researchers analyzed 1,433 electronic fetal monitor
tracings, and compared them with the newborn infants’ umbilical artery pH. Bakker et al,
Elevated Uterine Activity Increases the Risk of Fetal Acidosis at Birth, 196 Am J Obstetrics &
Gynecology 313.el (2007). The study reported that “[i]ncreased uterine activity during the first
and second stage of labor is associated with an increased incidence of lower pH values in the
umbilical artery.” Id. at 313.e3.

Markell’s umbilical artery pH was not measured. However, the study also includes the
following pertinent conclusion: “Excessive UA [uterine activity], by means of hyperstimulation
and tachysystole, shortens the relaxation time. This results in higher levels of cerebral
deoxygenated hemoglobin, lower levels of oxygenated hemoglobin, and decreased intracerebral
saturation.” Id. at 313.e5. The article continues: “A contraction rate of more than 4 per 10
minutes is considered ominous, leading to insufficient time for placental perfusion and iatrogenic
fetal distress.” Id.16 A second study of 10 fetuses, also published in a peer-reviewed journal,
reached a more easily understood conclusion: “These data provide evidence of a direct relation
between the frequency of uterine contractions and changes in human fetal cerebral oxygen
saturation, and they indicate a critical contraction interval below which cerebral saturation is
likely to fall.” Peebles et al, Relation Between Frequency of Uterine Contractions & Human
Fetal Cerebral Oxygen Saturation Studied During Labour by Near Infrared Spectroscopy, 101
Brit J Obstet & Gynaecology 44, 47 (1994). These articles generally validate that cephalopelvic
disproportion and difficult, traumatic delivery can cause fetal distress, compression of the fetal
skull, brain bleeds, and neurologic injury, satisfying MCL 600.2955(b) and (g).17

16
Dr. Schifrin testified that in his view, Kimberly’s “uterine activity . . . after the administration
of [Pitocin] . . . is simply excessive.” Dr. Crawford testified that Kimberly had “tachsystole.”
17
Subsection (g) requires an assessment of whether “the opinion or methodology is relied upon
by experts outside the context of litigation.” Defendants have not contended otherwise. As

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Plaintiffs’ experts’ testimony does not satisfy one § 2955 factor: “(c) The existence and
maintenance of generally accepted standards governing the application and interpretation of a
methodology or technique and whether the opinion and its basis are consistent with those
standards.” The ACOG standards reflect a general consensus in the medical community
regarding the criteria necessary to demonstrate hypoxic ischemic injury. However, the ACOG
standards include as an essential requirement an umbilical arterial blood gas demonstrating a pH
of less than 7.0. An umbilical arterial blood gas was not obtained here. Given this discrepancy,
Judge Nichols did not abuse his discretion by finding the ACOG criteria inapplicable to his
reliability analysis.

The remaining factors focus on whether the expert’s testimony is “generally accepted”
among other experts in the field, and whether other experts would reach similar conclusions:

(e) The degree to which the opinion and its basis are generally
accepted within the relevant expert community. As used in this subdivision,
“relevant expert community” means individuals who are knowledgeable in the
field of study and are gainfully employed applying that knowledge on the free
market.

(f) Whether the basis for the opinion is reliable and whether experts in
that field would rely on the same basis to reach the type of opinion being
proffered.

Both sides’ experts repeatedly opined that their causation views were generally accepted in the
medical community, and that the opposing views were not.18 And all testifying experts were
“gainfully employed” in the practice of their medical specialties rather than simply “experts for
hire.” Judge Nichols ruled that plaintiffs’ experts’ opinions “are based on legitimate data within
their field of expertise, that they are reliable and that they were reliably applied in this case.”
Accordingly, he applied these two criteria while claiming not to have done so, the evidence
supported his conclusion, and we discern no abuse of discretion.

Judge Nichols observed in his written opinion, the views expressed by all medical experts in this
case derive from “principles and methods from . . . their training and clinical experiences[.]”
Unlike in Daubert, the medical literature relied upon by the experts was, with the exception of
one or two articles, written by physicians other than the testifying experts. See Daubert v
Merrell Dow Pharm, Inc, 43 F3d 1311, 1314 (CA 9, 1995) (Daubert II) (“[A]part from the small
but determined group of scientists testifying on behalf of the Bendectin plaintiffs in this and
many other cases, there doesn’t appear to be a single scientist who has concluded that Bendectin
causes limb reduction defects.”).
18
Although defendants’ experts claimed that plaintiffs’ causation theories had been debunked or
were no longer accepted as scientifically valid, defendants produced no literature supporting this
argument. Given that plaintiffs’ literature submissions corresponded to their causation theory,
Judge Nichols did not abuse his discretion in finding the data “legitimate.”

-25-
Although we have rejected defendants’ claim that Judge Nichols’s purported failure to
apply MCL 600.2955 mandates reversal, we reiterate that application of this statute is mandatory
in every case involving death or personal injury in which scientific opinions are expressed.
Judge Nichols’s opinion that the statute lacks applicability in medical malpractice cases is simply
wrong.

2. Scientific Reliability Under MRE 702

MRE 702 requires that an expert’s testimony (1) rest on sufficient facts, (2) qualify as the
product of “reliable principles and methods,” and (3) reflect that the expert reliably applied the
principles and methods to the case facts. As a gatekeeper, Judge Nichols was required to
scrutinize plaintiffs’ scientific evidence to determine whether the “principles and methods”
employed by the experts were reliably applied to the facts of the case.

Defendants assert that plaintiffs’ experts’ testimonies do not fulfill the MRE 702
requirements because the experts failed to address the existence of Markell’s genetic disorder.
This omission, defendants argue, rendered plaintiffs’ experts’ opinions unreliable. Specifically,
defendants insist that plaintiffs’ experts’ failure to acknowledge the impact of Markell’s PCH
diagnosis “in and of itself renders unreliable the ipse dixit of Plaintiff[s’] causation experts’
opinions.”

We initially observe that during the Daubert hearing, defense counsel repeatedly
questioned plaintiffs’ experts about the PreventionGenetics report. Plaintiffs’ experts
persistently disagreed that the PCH diagnosis had any significant bearing on Markell’s
neurologic condition. For example, Dr. Crawford testified that Markell’s brain swelling was not
caused by a genetic defect, characterizing PCH as an “incidental finding” that had nothing to do
with the ischemia. Dr. Gabriel disputed that the partial absence of Markell’s cerebellum and
pons caused her cerebral palsy. Although Dr. Gabriel maintained that Markell’s neurological
presentation at birth was inconsistent with PCH, he conceded that the abnormality plays some
part in her disabilities:

Q. Doctor, is it your opinion that the [PCH] in this case did not affect
this child?

A. No, my opinion is that had Markell not gone through this terrible
labor and delivery she would be essentially near normal or normal. She would
probably not be an Olympic athlete or concert pianist or architect, but she would
be able to function more or less like an ordinary human being based upon what I
know about the condition of [PCH].

Thus, we find no merit in defendants’ contention that plaintiffs’ simply ignored relevant
evidence of an alternative causation mechanism.

Nor are we persuaded that the trial court abused its discretion by rejecting defendants’
argument that only PCH reliably explains Markell’s neurologic deficits. Trial courts must
carefully evaluate whether adequate data supports an expert’s opinion and whether the opinion
qualifies as reliable in the relevant expert community. Part of this process involves consideration
of alternate scientific explanations for a given result. The Committee Notes to FRE 702 provide
-26-
that a court may consider “[w]hether the expert has adequately accounted for obvious alternative
explanations.” FRE 702 (2000) Committee Note.

However, this does not mean that a trial court is empowered to decide which of two
competing and adequately supported scientific theories should prevail. “Although [Daubert]
places the judge in the role of gatekeeper for expert testimony, the key to the gate is not the
ultimate correctness of the expert’s conclusions.” Schultz v Akzo Nobel Paints, LLC, 721 F3d
426, 431 (CA 7, 2013). “In evaluating proffered expert testimony, the trial court is ‘a
gatekeeper, not a fact finder.’” City of Pomona v SQM North America Corp, 750 F3d 1036,
1043 (CA 9, 2014) (citation omitted). The Supreme Court emphasized in Daubert that trial
courts should focus “on principles and methodology, not on the conclusions they generate.”
Daubert, 509 US at 595. “Vigorous cross-examination, presentation of contrary evidence, and
careful instruction on the burden of proof are the traditional and appropriate means of attacking
shaky but admissible evidence.” Id. at 596.

To be sure, expert testimony may be excluded when there is “too great an analytical gap
between the data and the opinion proffered.” General Electric Co v Joiner, 522 US 136, 142;
118 S Ct 512; 139 L Ed 2d 508 (1997). The Supreme Court explained in Joiner that “[t]rained
experts commonly extrapolate from existing data. But nothing in either Daubert or the Federal
Rules of Evidence requires a district court to admit opinion evidence that is connected to existing
data only by the ipse dixit of the expert.” Id. at 146. The “data” referred to by the Court in
Joiner consisted of four epidemiological studies involving baby mice, which the plaintiff
claimed as support for linking his small cell lung cancer with occupational exposure to PCBs.
The district court found that the mice studies did not support the plaintiff’s expert’s conclusion:

The infant mice in the studies had had massive doses of PCB’s injected directly
into their peritoneums or stomachs. Joiner was an adult human being whose
alleged exposure to PCB’s was far less than the exposure in the animal studies.
The PCB’s were injected into the mice in a highly concentrated form. The fluid
with which Joiner had come into contact generally had a much smaller PCB
concentration of between 0-to-500 parts per million. The cancer that these mice
developed was alveologenic adenomas; Joiner had developed small-cell
carcinomas. No study demonstrated that adult mice developed cancer after being
exposed to PCB’s. One of the experts admitted that no study had demonstrated
that PCB’s lead to cancer in any other species. [Id. at 144.]

As the Court of Appeals for the Third Circuit subsequently explained, “[G]iven the tenuous link
in Joiner between plaintiff’s exposure to PCBs and the onset of his cancer a number of years
later, the lack of studies linking PCBs to cancer in humans left only ‘the ipse dixit of the expert’
to support his conclusion.” Heller v Shaw Indus, Inc, 167 F3d 146, 155 (CA 3, 1999). Thus,
Joiner instructs that trial courts must close the evidentiary gate when an expert’s conclusions
lack any genuine relationship to the science alleged to support them.

Here, science and fact supported both sides’ causation views. That Markell’s birth
involved head compression resulting in brain bleeding was not contested. Objective record facts
supporting birth trauma included her Apgar score of one, her lack of muscle tone and normal
newborn reflexes, her rapidly-emerging seizure disorder, and the blood detected in her brain.

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The medical literature discussed above links traumatic birth and neurologic injury. On the other
hand, genetic evidence indisputably demonstrated PCH. According to two articles supplied to
the trial court by the defense, children with PCH display near absence of cognitive and voluntary
motor development and progressive microcephaly. Markell’s condition fits that description.
Faced with this conflict among the experts, the trial court did not abuse its discretion by deciding
to admit both theories, finding both supported by peer-reviewed literature and credible expert
opinion, thereby qualifying as reliable.

3. This Court’s Prior Gabriel Opinions

Defendants’ final argument regarding the reliability of plaintiffs’ experts’ opinions rests
on this Court’s prior unpublished opinions upholding the exclusion of Dr. Gabriel’s causation
testimony in other medical malpractice cases. In nine different opinions, panels of this Court
have held Dr. Gabriel’s causation testimony inadmissible. Unpublished opinions of this Court
lack precedential value. MCR 7.215(C)(1). Moreover, our review of this Court’s previous
Gabriel jurisprudence reveals marked dissimilarities with this case. None of the prior cases
involved a baby with obvious head trauma and a one-minute Apgar score of one. Several of the
other Gabriel cases involved entirely different alleged mechanisms of injury, including neonatal
ischemic stroke and chorioamnionitis.19 Most importantly, Daubert and Craig instruct that a
trial court’s admissibility decision must flow from the record created during the reliability
hearing. Thus, cases presenting different facts and different scientific records may yield
different rulings. Just as this Court’s rejection of Dr. Gabriel’s testimony in other cases would
not have authorized Judge Nichols to entirely forego a Daubert hearing, the prior cases do not
permit us to deem incredible as a matter of law Dr. Gabriel’s testimony here. Moreover, in this
case, Dr. Gabriel was not the sole proponent of plaintiffs’ causation theory. Even were we to
exclude his testimony, Drs. Crawford, Schifrin and Frank attested to the same mechanical trauma
theory.

Nor does our Supreme Court’s opinion involving Dr. Gabriel, Craig, 471 Mich 67, alter
our analysis. Like this case, Craig involved the use of Pitocin during labor. Craig, 471 Mich at

19
We note that in one case, Mock v Hackley Hosp, unpublished opinion per curiam of the Court
of Appeals, issued November 20, 2008 (Docket No. 280269), this Court cited testimony from the
defendants’ experts which tends to support plaintiffs’ causation theory here:
Defendants never contested that, according to the medical literature submitted by
plaintiff and the testimony of their experts, certain compressive forces on the fetal
brain, such as those exerted by the use of forceps and those arising in cases of
cephalopelvic disproportion, may cause brain damage resulting in cerebral palsy.
[Id. at 2 (emphasis added).]

In Mock, this Court found that “none of the articles relied upon by Gabriel as supporting his
theory and none of the defense experts stated that abnormal uterine pressures, alone, can be
considered analogous to circumstances known to cause brain damage leading to cerebral palsy,
such as cephalopelvic disproportion and the use of forceps[.]” Id. at 6.

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72. According to the plaintiff’s obstetrical expert witness, the baby developed a slow heart rate
due to excessively long, intense contractions. Id. at 73. One expert described that the baby’s
“umbilical cord became compressed because of these contractions, thereby decreasing the
amount of blood flowing to plaintiff.” Id. At birth, the plaintiff’s Apgar scores were 8 and 9,
“well within the typical range,” although the plaintiff contended that other evidence supported
that the child had sustained head trauma. Id. at 73-74. Dr. Gabriel testified at deposition that
“hyperstimulation of the uterus” due to Pitocin caused the fetal head to pound against his
mother’s pelvic anatomy, producing permanent brain damage. Id. at 81 (quotation marks
omitted). The defendants moved for a Davis-Frye hearing, this state’s predecessor to a Daubert
hearing.20 In response,

plaintiff’s attorney produced several articles and authorities that were meant to
demonstrate a link between the use of Pitocin and the type of injury sustained by
plaintiff. But while some of these articles described a correlation between the use
of Pitocin and generalized brain injury, none of these authorities supported the
theory of causation actually put forth by Dr. Gabriel. That is, none supported a
causal connection between Pitocin and brain injury incurred through repeated
pounding of the fetal head against maternal anatomy. [Id.]

The trial court denied the defendant’s motion for an evidentiary hearing, and the jury returned a
large verdict for the plaintiff. Id. at 75.

The Supreme Court held that the trial court had abused its discretion by failing to conduct
a Davis-Frye hearing, and that the plaintiff failed to demonstrate that Dr. Gabriel’s causation
theory “was rooted in ‘recognized’ scientific or technical principles.” Id. at 82-83. The “causal
sequence” described by Dr. Gabriel, the Supreme Court explained, should have been rejected:

Plaintiff failed to introduce a single authority that truly supported Dr.
Gabriel’s theory in response to defendant’s motion. Instead, plaintiff repeatedly
stressed that medical literature amply supported the proposition that Pitocin could
cause brain damage—a proposition defendant did not contest-and supplied the
court with literature to that effect. But this literature had little to do with Dr.
Gabriel’s causal theory and therefore did not counter the proposition that his
expert opinion was based on novel science. [Id. at 83].

The Supreme Court rested this aspect of its opinion in Craig on several facts unique to
that case. “For one thing,” the Supreme Court observed, “Dr. Gabriel was unable to cite a single
study supporting his traumatic injury theory during a voir dire conducted at trial.” Id. at 84.
Instead, Dr. Gabriel pointed only to “studies . . . in animals” involving an excessive
administration of Pitocin. Id. “Second,” the Court explained,

20
See People v Davis, 343 Mich 348; 72 NW2d 269 (1955); Frye v United States, 54 App DC
46; 293 F 1013 (1923).

-29-
Dr. Gabriel’s theory lacked evidentiary support. Dr. Gabriel was unable to
identify the specific part of Ms. Craig’s anatomy with which, according to his
theory, plaintiff’s head repeatedly collided during labor. Indeed, Dr. Gabriel
pointedly refused to identify this anatomical structure on a chart, contending that
such testimony was beyond his expertise. This failure to root his causal theory in
anything but his own hypothetical depiction of female anatomy indicates that Dr.
Gabriel’s testimony may have been too speculative under MRE 702 to assist the
trier of fact. [Id.]

Dr. Gabriel also failed to offer testimony that his theory of vascular trauma could cause
cerebral palsy or the “asymmetrical development shown in plaintiff’s MRI.” Id. at 84-85.
“[G]iven the yawning gap between Dr. Gabriel’s testimony and the conclusions plaintiff hoped
the jury would draw from it,” the Court concluded, this evidence would not have assisted the
trier of fact and should have been excluded. Id. at 85.

Unlike in Craig, the peer-reviewed literature in this case supports that head compression
can cause brain injury. Here, plaintiffs’ experts had no difficulty explaining the head
compression mechanism: Dr. Crawford even insisted that a certain bruising pattern on Markell’s
head corresponded to where her head had been “banged” through the pelvis. The articles
submitted to Judge Nichols involved human babies and directly corresponded to plaintiffs’
experts’ testimony. Thus, the evidence presented during the Daubert hearing responded to and
overcame the evidentiary infirmities described in Craig.

Just as one court’s acceptance of Gabriel’s methodology and conclusions would not bind
another court to embrace Gabriel’s testimony without performing a “searching inquiry,” our
Supreme Court’s rejection of Gabriel’s causation opinions in a different case, expressed in a
different record, does not control the outcome here. In summary, we hold that Judge Nichols did
not abuse his discretion by allowing the jury to consider Dr. Gabriel’s causation theory.

IV. PROXIMATE CAUSE AT THE TRIAL

Defendants next contend that the trial evidence insufficiently supported plaintiffs’
causation theory. According to defendants, Markell’s genetic disorder accounts for the totality
of her neurologic disabilities, and plaintiffs’ expert witnesses failed to support that a cesarean
section “is capable of repairing genetic damage that inevitably causes profound retardation.”
Judge Nichols erred, defendants assert, by failing to enter a judgment notwithstanding the verdict
in favor of defendants regarding proximate cause.

A. THE TRIAL EVIDENCE

Defendants premise their proximate cause argument on a central piece of the evidence:
the PreventionGenetics report stating that Markell suffers from PCH-2. This genetic defect,
defendants contend, constitutes the sole cause of Markell’s neurologic problems. According to
defendants, plaintiffs “were unable to reconcile their opinions with the PCH evidence.”

Contrary to defendants’ argument, plaintiffs’ causation experts recognized that Markell
has a genetic condition that resulted in the malformation of her cerebellum. They rejected that
this genetic condition caused Markell’s cerebral palsy and her mental retardation. Accordingly,
-30-
plaintiffs created a fact question regarding whether birth trauma or PCH-2 caused Markell’s
neurological deficits.

Defendants’ proximate cause argument posits that Markell’s neurologic condition was
attributable only to PCH-2. Dr. Aubrey Milunsky served as the primary proponent of this
defense at the trial. Dr. Milunsky, a professor of pediatrics, human genetics, obstetrics and
gynecology and pathology at Boston University, testified that “Markell has a very well defined
genetic disorder. It’s called [PCH]. Well recognized, well characterized and diagnosed with
great precision by molecular or DNA diagnosis. It is really dramatically straightforward.”
Markell’s small cerebellum, he explained, “was the first flag that this is a child that was born
with an abnormality.” The genetic testing performed by PreventionGenetics cemented the
clinical diagnosis.

Dr. Milunsky reviewed the PreventionGenetics report with the jury, explaining that the
results revealed PCH types 2 and 4. In Dr. Milunsky’s view, the test is 99.9% accurate. “[T]he
molecular diagnosis made in this case,” he opined, “is indisputable and absolute.” Dr. Milunsky
maintained that Markell’s clinical findings of microcephaly, spasticity, seizures, mental
retardation, difficulty swallowing and the inability to control her movements “are just highly
typical of what’s been described before” as PCH-2. The infirmities caused by PCH-2 explain
why Markell spent 18 days in the Special Care Nursery. And according to Dr. Milunsky,
Markell’s life expectancy “is severely limited.”

Dr. Milunsky rejected that Markell suffered any injury related to the circumstances
surrounding her birth:

Q. Doctor, are you able to exclude trauma to the brain as a cause of
the current neurologic condition?

A. There’s absolutely no good reason to think trauma had anything
whatsoever to do with this genetic condition.

On cross-examination, Dr. Milunsky conceded, “a child can be injured by being battered against
the wall of the pelvis.” On redirect examination, he stated: “There may be similar features that
may appear [with perinatal depression] following lack of oxygen or . . . [b]ecause of a genetic
condition.” He further agreed that unlike most children with PCH-2, Markell’s head
circumference percentile initially increased instead of decreasing, and she has lived longer than
the majority of children studied. Although Dr. Milunsky maintained that the disease is
relentlessly progressive, he admitted that Markell does not appear to be getting worse; he noted,
however, that at age 15 she weighed only 50 pounds.

Another defense expert, University of Michigan neuroradiologist Douglas Quint, M.D.,
testified that a CT scan taken when Markell was five months old demonstrated a “dragon fly
pattern” in the area of her cerebellum, which is classic and diagnostic for PCH. The imaging
studies did not reveal any evidence of brain abnormalities consistent with hypoxic ischemic
encephalopathy, Dr. Quint maintained. Dr. Quint admitted that this is the only case of PCH that
he has ever seen.

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Defendants’ pediatric neurology expert, Dr. Steven Leber, also testified that the imaging
studies were inconsistent with hypoxic ischemic injury. The “dragon fly appearance” of
Markell’s cerebellum, Dr. Leber expressed, correlates with PCH-2, and the PreventionGenetics
report “very much” supported this diagnosis. Dr. Leber nevertheless conceded, “all of
[Markell’s] clinical symptoms can be seen in children who have hypoxic ischemic injury:”

Q. . . . All of the things that she showed when she was born you
testified under oath that they’re seen in children who have the injury that our
experts have testified she has, right?

A. That’s correct.

As he had done with Dr. Milunsky, plaintiffs’ counsel established on cross-examination
that although PCH-2 is a progressive neurological disorder (meaning that the condition of those
who have it progressively worsens), Markell seemed to have experienced periods of
improvement and gains in development. Markell can sit up and roll over, unlike many children
with PCH-2. Dr. Leber conceded that cerebral palsy, the diagnosis reached by Markell’s treating
physicians, is a nonprogressive disorder. Dr. Leber further acknowledged that his diagnosis is
“[t]otally inconsistent with what her treating doctors and her medical course since birth show.”

Plaintiffs’ experts did not dispute that Markell has PCH. Whether PCH-2 or birth trauma
caused Markell’s spastic quadriparesis and mental retardation, however, separated plaintiffs’
experts’ causation opinions from those of the defense witnesses.

Dr. Soffer testified that regardless of the genetic findings, the malpractice surrounding
Markell’s birth harmed her: “The point is no matter what the condition of this baby was
genetically the circumstances of events that happened during this labor made whatever condition
this baby may have had at birth far, far worse than it would have been otherwise.” Plaintiffs’
primary proximate cause witness, Dr. Gabriel, set forth his causation opinion as follows:

The reason for Markell’s present condition is because of two factors that occurred
towards the end of labor and delivery. The first factor is there was considerable
mechanical pressure, abnormal mechanical pressure on the unfused skull plates. . .
. You put pressure on those skull plates and you put pressure on the brain and that
can distort the vessels, stretch the vessels, and tear the vessels, and that’s what
caused the bleeding in Markell’s brain.

***

The second phenomenon or mechanism is the reduction in blood flow to
the brain. We know that happened independent of the mechanical trauma but
with it because when Markell was one minute of age she was essentially dead
with a very low heart rate. The Apgar was one and you have essentially a dead
baby with an Apgar of one. The one indicates that the heart rate was present but it
was abnormally low. So, we know that there was not enough blood getting to the
brain during that period of time.

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In Dr. Gabriel’s view, Markell’s injuries could have been avoided had a cesarean section been
performed “before she went through the last 30, 60, 90 minutes of labor and delivery.”

Dr. Gabriel testified that the cerebellum constitutes “a very small part of the brain,” and
claimed that “[m]ost” of Markell’s cerebellum is present. “What’s missing is probably anywhere
from 10 to 20--25 percent is not there because of underdevelopment.” He disagreed with the
opinion of defendants’ experts’ that Markell’s pons was congenitally absent: “She has both a
pons and a small bump as you’ll see on the MRI.” And in his view, the cerebellar abnormality
does not contribute to Markell’s condition:

Q. Does anything about the cerebellum or the smallness of her brain
stem have anything to do with the condition that we see Markell in today?

A. No. On examination she has no abnormal cerebellar findings.

***

Q: Let’s -- Doctor by the way, is she like the way she is now because she
has some genetic disease they just discovered?

A: No. Apart from the undergrowth of the cerebellum, no. The vast bulk
of her condition is due to the mechanisms that I just mentioned.

Dr. Gabriel admitted that the cerebellar abnormality qualified as a genetic defect. He
claimed to have read two research studies regarding PCH-2, but disagreed that they applied to
Markell, expressing that the studies included no information regarding the “past history” of the
children studied to determine whether other conditions, such as “meningitis, head trauma, birth
trauma” or “toxic drugs,” could account for their conditions. Dr. Gabriel further distinguished
Markell’s condition from that of the neurologically devastated children described in the
published studies regarding PCH-2 as follows:

She is able to reach and grasp and can transfer from hand to hand. She is
interactive with her family. She makes eye contact especially with the right eye.
She smiles. She enjoys music. She’s actually a vibrant youngster, severely
impaired, but she has a very vibrant ability to interact with her family. You see
she’s enjoying that. It’s the kind of tactile stimulation that makes her feel good
and she responds. And, you can see how she has such good head control which is
important in terms of her life expectancy.

Dr. Gabriel emphasized that the majority of the children described in the PCH articles die within
a few years of their birth. Nor did Dr. Gabriel discern the “classic dragonfly pattern” when he
reviewed Markell’s imaging studies.

Dr. Crawford, too, testified that Markell’s injuries would have been prevented by a
cesarean section. She rejected that the data in the PCH-2 studies applied to Markell because the
children in the studies had microcephaly at birth, while Markell had a normal head size and her
head actually grew normally for a short time.

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Thus, the battle lines were drawn. Defendants contend that the irrefutable PCH-2
evidence is simply irreconcilable with plaintiffs’ explanation for Markell’s disabilities, and that
plaintiffs’ failure to exclude PCH from the causation equation “with a fair amount of certainty”
mandated JNOV.

B. STANDARD OF REVIEW

We review de novo a trial court’s decision on a motion for JNOV. Reed v Yackell, 473
Mich 520, 528; 703 NW2d 1 (2005). When faced with a JNOV motion, a court must “review the
evidence and all legitimate inferences in the light most favorable to the nonmoving party. Only
if the evidence so viewed fails to establish a claim as a matter of law, should the motion be
granted.” Wilkinson v Lee, 463 Mich 388, 391; 617 NW2d 305 (2000). Granting a JNOV is
contrary to our policy of giving all due deference to jury verdicts and should not be taken lightly.
“The trial court cannot substitute its judgment for that of the factfinder, and the jury’s verdict
should not be set aside if there is competent evidence to support it.” Ellsworth v Hotel Corp of
America, 236 Mich App 185, 194; 600 NW2d 129 (1999).

C. ANALYSIS

Plaintiffs’ evidence supported that defendants’ negligence constituted both the cause in
fact and a proximate cause of Markell’s injuries and damages. Plaintiffs admitted that Markell
tested positive for PCH-2. They disagreed that this genetic condition caused her neurological
picture. Plaintiffs’ causation evidence was neither speculative nor insufficient. It was for the
jury to sort out this disagreement.

The plaintiff in a medical malpractice case must prove that the defendant’s breach of the
applicable standard of care proximately caused the plaintiff’s injuries. Craig, 471 Mich at 86.
Proximate cause incorporates two separate elements: (1) cause in fact and (2) legal or proximate
cause. Skinner v Square D Co, 445 Mich 153, 162-163; 516 NW2d 475 (1994).

Cause in fact “generally requires showing that ‘but for’ the defendant’s actions, the
plaintiff’s injury would not have occurred.” Id. at 163. “[L]egal or ‘proximate cause’ normally
involves examining the foreseeability of consequences, and whether a defendant should be held
legally responsible for them.” Id. “To establish legal cause, the plaintiff must show that it was
foreseeable that the defendant’s conduct ‘may create a risk of harm to the victim, and . . . [that]
the result of that conduct and intervening causes were foreseeable.’” Weymers v Khera, 454
Mich 639, 648; 563 NW2d 647 (1997) (alterations in original), quoting Moning v Alfono, 400
Mich 425, 439; 254 NW2d 759 (1977). It is well established that more than one proximate cause
may contribute to an injury. O’Neal v St John Hosp & Med Ctr, 487 Mich 485, 497; 791 NW2d
853 (2010). Proximate cause is a question for the jury to decide unless reasonable minds could
not differ regarding the issue. Nichols v Dobler, 253 Mich App 530, 532; 655 NW2d 787
(2002).

Plaintiffs’ cause-in-fact proof rests on the testimony of both the obstetrical experts (Drs.
Schifrin and Soffer) and Dr. Gabriel. Both Drs. Schifrin and Soffer testified that the standard of
care required that Kimberly undergo a cesarean delivery, and that the inappropriate use of
Pitocin “pushed this baby through a pelvis that now we know is too small for this baby to fit.”

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Dr. Schifrin opined that the defendants could have prevented injury to Markell by stopping the
Pitocin, and if that did not work, by performing a cesarean section. Dr Gabriel testified that had
a cesarean section been performed, Markell would have avoided injury. Viewed in the light
most favorable to plaintiffs, this testimony established causation in fact.

A genuine issue of material fact also existed regarding proximate cause. Defendants’
reliance on Skinner is misplaced, as in Skinner “[t]here was no evidence to support the plaintiff’s
theory of causation,” Craig, 471 Mich at 88-89, while here plaintiffs’ evidence substantiated that
Markell sustained an ischemic injury to her brain.

At the time of his death, the decedent in Skinner had been operating an electric metal
“tumbling machine” of his own design and manufacture. Skinner, 445 Mich at 157. The
plaintiffs theorized that defendant Square D Company defectively designed a switch that the
decedent had incorporated in his tumbling machine such that the switch’s “large ‘phantom
zone’” sometimes inaccurately signaled that the switch was “off” while power actually continued
flowing to the machine. Id. at 158. Because no one witnessed the decedent’s accident, no direct
evidence linked the switch and the decedent’s electrocution. The plaintiffs’ case against Square
D was entirely circumstantial, predicated on a mere assumption that the Square D switch had
played a role in the decedent’s death. Id. at 163. Furthermore, some of the physical evidence
directly contradicted the hypothetical accident scenario proposed by the plaintiffs. Id. at 171-
172. Square D maintained that even assuming the presence of a defect in its switch, the
plaintiffs’ circumstantial proofs failed to demonstrate that the decedent “was misled by the
switch when he was fatally electrocuted.” Id. at 158. The Supreme Court agreed, concluding
that the record contained no direct or circumstantial evidence from which a reasonable jury could
infer the mechanism of the decedent’s electrocution or whether the switch contributed to the
accident. Id. at 174. The Court emphasized in Skinner that “[t]o be adequate, a plaintiff’s
circumstantial proof must facilitate reasonable inferences of causation, not mere speculation.”
Id. at 164.

In Craig, the Supreme Court contrasted the facts in Skinner with those of Mulholland v
DEC Int’l Corp, 432 Mich 395; 443 NW2d 340 (1989). The plaintiffs in Mulholland operated a
dairy farm. Id. at 398. After they installed a new milking system supplied by the defendants,
many cows developed mastitis. Id. at 399. An expert witness, Sidney Beale, observed the
plaintiffs’ milking operation and concluded that the “problems were related to the configuration
of the milking machinery.” Id. at 400. Beale recommended machinery changes which resulted
in decreased mastitis and increased milk production. Id. In the subsequent litigation, Beale
linked a milking machine defect with the cows’ mastitis. Id. at 409. The trial court granted a
directed verdict for defendants, and the Supreme Court reversed.

The Supreme Court held that Beale was qualified as an expert, and also that his testimony
rested on an adequate factual foundation:

Beale’s own perceptions at the Mulholland farm provided an ample basis
for the conclusion that a defective milking machine caused the mastitis in the
plaintiffs’ herd by making the cows more susceptible to infection. As we have
noted, Beale observed a complete milking of the Mulholland herd on his first visit

-35-
to the farm. He noticed that a number of the cows had sore teat ends and mastitis.
Beale also inspected the milking machinery in particular. [Id. at 413.]

Beale’s testimony “did not rule out every other potential cause of mastitits[.]” Craig, 471 Mich
at 89. “[H]is opinion was nevertheless admissible and sufficient to support a finding of
causation.” Id. at 90. The Mulholland Court explained:

It is, of course possible, as the defendants suggested throughout the trial,
that the true or more immediate cause of the mastitis was improper bedding,
unsanitary stalls, or even mud in the barnyard. Neither Beale’s own perceptions
nor those made known to him at or before trial would allow this expert to rule out
these possibilities. Nevertheless, we do not find the greater wisdom in a rule
which would require an evidentiary basis of this sort. To the extent that they are
credible, the absence of an evidentiary basis upon which an expert may rule out
other potential causes may reduce the credibility of the expert. To the extent that
other potential causes are substantiated by the evidence of record, they may also
support a verdict of comparative negligence. However, to require for each expert
an evidentiary basis sufficient to negate all of the possible causes which might be
asserted by opposing counsel would virtually eliminate expert testimony. We
require only expertise of experts, not omniscience. In our view, it is sufficient if
the expert has an evidentiary basis for his own conclusions. See, generally, 7
Wigmore, Evidence (Chadbourn rev.), § 1922, pp. 26-29.

Here, the expert provided an ample basis in his own perceptions for his
testimony as to the cause of mastitis in the Mulholland herd. We do not find a
lack of evidentiary basis to be an adequate alternative ground upon which to
uphold the ruling of the trial court. [Mulholland, 432 Mich at 413-414.]

Here, the jury was presented with two competing theories of causation: the mechanical
pressure/ischemia explanation, and defendants’ claim that PCH-2 doomed Markell to suffer the
neurologic abnormalities she exhibits. Plaintiffs’ theory rested on an evidentiary foundation:
Markell’s large size, the electronic fetal monitor evidence of hyperstimulation and decelerations,
the difficult delivery, Markell’s brain bleeds, her low Apgar score, her neurologic problems at
delivery, and the radiologic findings which, according to plaintiffs’ radiology expert, were
consistent with ischemic brain injury. In other words, plaintiffs presented evidence illustrating a
logical sequence of cause and effect. Unlike the plaintiffs in Skinner, who lacked any factual
support connecting the switch with the mechanism of the decedent’s death, plaintiffs here
marshaled evidence from the medical records from which a jury could reasonably conclude that
Markell sustained an ischemic injury to the brain. Even Dr. Milunsky admitted that “a child can
be injured by being battered against the wall of the pelvis,” and that the clinical presentation of
PCH-2 shares “similar features” with perinatal depression due to birth trauma. Thus, plaintiffs’
proximate cause analysis was plausible and nonspeculative.

Moreover, plaintiffs cast some doubt on the credibility of defendants’ experts’ conclusion
that PCH-2 completely explained Markell’s problems. Plaintiffs questioning highlighted that
Markell’s condition differed from that of the children described in the PCH-2 articles relied upon
by defendants’ experts. She had lived to an age almost unheard of in the articles, had some

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control of her motor functions, and her head initially grew at a normal rate rather than becoming
progressively smaller in comparison to her peers. In other words, plaintiffs’ experts stressed that
the defense had conflated the laboratory diagnosis of PCH-2 with an immutable clinical
presentation.

Given the potential weaknesses in Dr. Milunsky’s claim that PCH-2 fully explained
Markell’s condition, Dr. Milunsky’s causation theory was subject to disbelief by the jury. And
even absent facts that seemed to distinguish Markell from the PCH-2 children described by Dr.
Milunsky, the jury was entitled to reject defendants’ experts’ opinions. A jury may disregard
testimony that, in the words of Justice Cooley, “probably ought to have satisfied any one. . . .”
Woodin v Durfee, 46 Mich 424, 427; 9 NW 457 (1881). As the Supreme Court expressed in
Mulholland, requiring plaintiffs to negate all other possible causes of injury “would virtually
eliminate expert testimony.” Mulholland, 432 Mich at 414.

In summary, viewed in the light most favorable to plaintiffs, Drs. Gabriel, Crawford and
Soffer neither ignored nor discounted that Markell had a genetic disorder. Plaintiffs’ experts
disagreed that this abnormality proximately caused her profound neurological disabilities.
Because the record evidence supplied a basis for this disagreement, Judge Nichols did not err by
denying defendants’ motion for judgment notwithstanding the verdict.

V. EXCLUSION OF THE ACOG CRITERIA

Defendants argue that Judge Nichols denied them a fair trial and abused his discretion by
excluding from evidence the ACOG criteria, which defendants contend would have “destroyed”
plaintiffs’ argument that Markell’s PCH-related disabilities were aggravated by hypoxic
ischemic encephalopathy. According to defendants, the ACOG criteria represent an
“international consensus . . . based upon the best science available” of the clinical findings
required to define an acute event during labor and delivery as a cause of cerebral palsy. Absent
admission of evidence concerning the ACOG criteria, defendants complain, the jury was left
unaware that the published standards would exclude birth trauma as a potential cause of
Markell’s cerebral palsy.

A. AN INTRODUCTION TO THE ACOG CRITERIA

In 2003, the American College of Obstetricians and Gynecologists (ACOG) published the
report of its Task Force on Neonatal Encephalopathy and Cerebral Palsy (NECP). This 105-page
document was intended “to collate and review the best scientific data available on the topic and
to publish these findings.” ACOG at xvii. The report sets forth “clearly delineated objective
criteria to use when defining an acute intrapartum hypoxic event,” and explains that an
examination focused on four identified benchmarks must be conducted before a physician
concludes that events during labor and delivery caused a baby’s cerebral palsy:

These criteria should be examined before a label of birth asphyxia or hypoxic-
ischemic encephalopathy is written into the infant’s case notes and given to the
parents as a diagnosis. Accurately defining the relatively uncommon event of
intrapartum asphyxia, with its uncommon sequelae of neonatal encephalopathy
and cerebral palsy, will allow for better definitions of the possible nonhypoxic

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causes of encephalopathy and cerebral palsy. Criticism of the management of
labor should not be confused with cerebral palsy causation because the two often
may not be linked. [Id. at xi.]

The report sets forth four “essential” criteria, and five additional criteria that “collectively
suggest an intrapartum timing . . . but are nonspecific to asphyxia insults.” Id. at xviii, 74. As to
the nine total criteria, the report highlights the importance of blood gases:

The nine criteria endorsed by the ACOG Task Force in Chapter 8
emphasize that analysis of peripartum blood gases is essential to prove that
hypoxia was present around birth. For a causative link to be established, a severe
metabolic acidosis must occur in sequence with early neonatal encephalopathy
and a type of cerebral palsy that could have been caused by the hypoxia. Because
intrapartum compromise can be simply a reflection of antenatal fetal pathology,
known etiologies or strong associations with subsequent cerebral palsy should
help to exclude primary intrapartum hypoxia as the likely cause. [Id. at xii.]

Before delving into the nine criteria, the NECP report describes various fetal and
maternal conditions that may generate a risk of neonatal cerebral palsy, and reviews fetal heart
monitoring and its impact on preventing adverse outcomes. At the outset of Chapter 6, the report
notes that “[d]ozens of distinct genetic, metabolic, and anatomic factors may contribute to the
etiology of neonatal encephalopathy.” Id. at 63. Chapter 8 addresses the “criteria required to
define an acute intrapartum hypoxic event as sufficient to cause cerebral palsy.” Id. at 73. The
report provides:

Part 1.1 of the criteria presents four essential criteria that are necessary
before an intrapartum hypoxic event can be considered as a cause of cerebral
palsy. If any 1 of the 4 essential criteria is not met, this provides strong evidence
that intrapartum hypoxia was not the cause of cerebral palsy. [Id.]

We repeat the four “essential” criteria here:

1. Evidence of a metabolic acidosis in fetal umbilical cord arterial blood
obtained at delivery (pH <7 and base deficit ≥12 mmol/L)

2. Early onset of severe or moderate neonatal encephalopathy in infants
born at 34 or more weeks of gestation

3. Cerebral palsy of the spastic quadriplegic or dyskinetic type

4. Exclusion of other identifiable etiologies, such as trauma, coagulation
disorders, infectious conditions, or genetic disorders. [Id. at xviii, 74.]

The report examines each criterion in some detail. As to the metabolic acidosis
requirement, the report makes no mention of substituting a venous umbilical blood gas result for
an arterial pH. See id. at 74. Regarding the fourth criterion, the report instructs:

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A large proportion of cerebral palsy cases are associated with maternal
and antenatal factors, such as preterm birth, intrauterine growth restriction,
intrauterine infection, maternal or fetal coagulation disorders, multiple pregnancy,
antepartum hemorrhage, breech presentation, and chromosomal or congenital
abnormalities . . . . These causes must be considered and excluded before
concluding intrapartum hypoxia is the cause of cerebral palsy. [Id. at 75.]

B. PROCEDURAL BACKGROUND

Plaintiffs filed a motion in limine seeking to prevent defendants from referencing the
ACOG criteria during the trial, arguing initially that exclusion was an appropriate sanction for
Beaumont’s failure to obtain an umbilical arterial blood gas or to report the results of an arterial
blood gas in Markell’s medical record. Plaintiffs also urged that the criteria did not apply to the
facts of this case. The trial court issued a lengthy opinion and order granting plaintiffs’ in-limine
motion, identifying two evidentiary bases for its ruling. First, the trial court ruled that because
plaintiffs’ causation theory involved ischemia due to trauma and not simply hypoxia, the ACOG
criteria could not be reliably applied to the facts of the case:

Under MRE 702, the Court must say the principles and methods are
reliable and reliably applied. Here the Court cannot say that Defendants are
reliably applying their four criteria to establish a sufficient hypoxic-ischemic
event causing cerebral palsy because Defendants are unilaterally and deliberately,
it appears to this Court, distorting Plaintiff[s’] theory in saying that it must be an
hypoxic–ischemic event. Plaintiff[s’] theory is a combination of trauma and
ischemia leading to minor Plaintiff’s injuries and damages. This is very
significant, because the Court held, as a matter of fact and law on September 7,
2011, that cerebral palsy can occur in the face of a multiple of factors -- not just
those in ACOG, especially here where Plaintiff[s are] not arguing hypoxia alone.

Next, the trial court found that the unavailability of an arterial blood gas result rendered
scientifically unreliable any attempted application of the criteria:

In addition, and most significantly here, the Court cannot find Defendants’
defense theory was reliably employed because the Court cannot conclude that
Defendants’ witnesses correctly applied the medical facts to the criteria. The
Court cannot find as a fact that arterial blood was tested (and thus used) and
that there was no trauma. [ACOG at] 74 left column (“must meet all four”).
The Court finds conclusively that Defendants’ own witnesses say there was
no arterial blood gas tested and there was trauma. Defendants fail to
establish, from the medical testimony, records and reports admitted at the
hearings, all of which define this case from a medical perspective, that two of
its four mandated criteria apply. [Bold in original].

The court continued:

For these reasons, the Court cannot conclude that Defendants’ attempt to
use this theory in order to discredit Plaintiff[s’] case is reliable or reliably applied.

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The court holds that the Defendants have failed, in particular, to carry their
burden by a preponderance of the evidence under MRE 702 that the defense
theory has been reliably applied.

The trial court then turned to a discussion of MRE 403, and found that the probative
value of the criteria was “significantly outweighed” by the prejudicial effect:

Employing the weighing process of MRE 403, the probative value of
Defendants’ defense stating Plaintiff[s] cannot prove an hypoxic-ischemic event
based upon ACOG’s four criteria is significantly outweighed by its prejudicial
effect, confusion of the issues, misleading the jury, and considerations of undue
delay and waste of time, where, as here, it misstates Plaintiff[s’] theory of the case
and has been erroneously applied in methodology. It is undisputable that the
criteria required by ACOG has not been established in this case. Specifically as
to the first and fourth criteria, no arterial blood was tested and birth trauma exists.
To allow testimony on Defendant[s’] theory here will unnecessarily confuse and
mislead the jury and be a waste of time since the criteria has not established and
has even been conceded as existing as to birth trauma by Defendant[s’] own
witnesses. The probative value of the evidence is clearly substantially
outweighed by the potential of prejudicial effect to Plaintiff[s].

The trial court concluded:

Finally, the Court agrees in theory that the ACOG hypoxic-ischemic event
defense could be critical to Defendants. But to allow it in view of its MRE 702
deficiencies as to reliability and its MRE 403 effects would be clearly
inappropriate and an invitation to error on appeal which this Court is trying to
avoid.

C. ANALYSIS

We review Judge Nichols’s evidentiary rulings for an abuse of discretion. People v
Bragg, 296 Mich App 433, 445; 824 NW2d 170 (2012). “A trial court abuses its discretion when
its ruling falls outside the range of principled outcomes.” Id.

Judge Nichols perceived that the ACOG criteria lacked applicability to the facts of this
case for two reasons: no arterial blood sample was obtained, and neither trauma nor genetics
could be ruled out as causative of Markell’s injuries. He further concluded that admission of the
criteria would confuse the jury. Although we partially disagree with Judge Nichols’s reasoning,
his decision falls within the range of principled outcomes, and we find no error meriting reversal.

Defendants sought to use the ACOG criteria to prove that an intrapartum hypoxic event
could not have caused Markell’s cerebral palsy because (1) the umbilical blood test results did
not demonstrate metabolic acidosis, and (2) a genetic disorder had not been excluded as a cause

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of her neurological infirmities.21 By its plain terms, however, the NECP report mandates that
physicians assessing whether perinatal events caused cerebral palsy take into account an arterial
umbilical blood gas result. Defendants presented no evidence that the ACOG criteria may be
reliably applied when only a venous umbilical blood sample is available. None of the defense
experts claimed that the ACOG guidelines treated arterial and venous samples as interchangeable
or that umbilical venous blood accurately reflects fetal acid-base status at the time of delivery.
And given that an arterial umbilical blood gas is one of the touchstones of the ACOG rubric, we
cannot fault Judge Nichols’s conclusion that application of the ACOG standards would neither
qualify as reliable nor as grounded in the case facts. Thus, Judge Nichols acted within his
discretion in excluding opinion testimony premised on the ACOG criteria under MRE 703. Nor
do we find that Judge Nichols abused his discretion in finding admission of the criteria confusing
under MRE 403.

We do take issue with one aspect of Judge Nichols’s reasoning. The NECP report
additionally posits that before a physician concludes that an intrapartum hypoxic event caused
cerebral palsy, both traumatic and genetic causes of cerebral palsy must be ruled out. In other
words, the report instructs physicians that when either trauma or genetic abnormalities are
present, intrapartum hypoxia cannot be considered to have caused a child’s neurologic injuries.
Plaintiffs contended (and Judge Nichols agreed) that because (1) their experts premised their
causation theories on ischemia rather than hypoxia, and (2) trauma cannot be ruled out as
causative, the criteria lack applicability. We reject this logic. The term “trauma” is not
specifically defined in the ACOG document. However, it is used along with other terms
(“coagulation disorders, infectious conditions, or genetic disorders”) describing maternal
conditions or conditions unrelated to the birth process. The “trauma” alleged by plaintiffs
occurred intrapartum and, according to plaintiffs, resulted in ischemia. The claimed ischemia, in
turn, disrupted the supply of oxygen to involved brain tissue. Accordingly, had an arterial
umbilical blood gas been obtained, the ACOG criteria would have been fully applicable.

Despite partially premising his ruling on a specious ground, Judge Nichols accurately
assessed that expert testimony premised on the ACOG criteria would not “‘serve to give the trier
of fact a better understanding of the evidence or to assist in determining a fact in issue.’” Craig,
471 Mich at 79, quoting People v Beckley, 434 Mich 691, 711; 456 NW2d 391 (1990) (opinion
of BRICKLEY, J.). In other words, the ACOG criteria would not fulfill the relevancy requirement
incorporated within MRE 702. “[E]ven proposed expert testimony that is offered by a qualified
expert and based on reliable scientific data and methods may be properly excluded if it is not
relevant to the facts of the case[.]” People v Kowalski, 492 Mich 106, 122; 821 NW2d 14
(2012). Thus we find no fault with Judge Nichols’s ruling that without the data necessary to
perform the ACOG assessment, the criteria were inadmissible under MRE 403.

21
Markell’s condition fulfilled the remaining two criteria: she experienced an early onset of
severe or moderate neonatal encephalopathy, and had been diagnosed with cerebral palsy of the
quadriplegic or dyskinetic type.

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In summary, because exclusion of the ACOG was a reasonable and principled outcome
given that the criteria could not reliably be applied to Markell, the trial court’s decision did not
amount to an abuse of discretion.

VI. EXCLUSION OF THE PREVENTIONGENETICS REPORT

Defendants next assert that the trial court erred by refusing to allow them to place in
evidence the PreventionGenetics report. According to defendants, the PreventionGenetics report
constituted the “core of Defendants’ proximate cause defense” because it confirmed with 99.9%
certainty that Markell carries the gene defect that causes PCH-2. Although Judge Nichols ruled
that the PreventionGenetics report satisfied the conditions precedent to admission as an exhibit,
defendants claim that he inexplicably reversed this ruling during the trial, disallowed the report’s
use, and proceeded to denigrate the importance of the report in the jury’s presence.

Plaintiffs’ response to this argument is simple: the report was placed in evidence, went to
the jury, and defendants’ argument lacks any factual foundation. At oral argument, we explored
with counsel a question we thought quite basic: did the report go to the jury, or did it not? Not
surprisingly, the parties vehemently disagreed.

Thus, we are in a difficult position, as the foundation for defendants’ evidentiary
argument—that a key piece of evidence was improperly kept from the jury—may or may not be
accurate. Based on our study of the record, we have concluded that the evidence probably was
given to the jury, and that even if the report itself did not make it to the jury room, its substance
was well-presented throughout the trial. The path to our decision has required us to dig deeply
into the trial court record. We begin with a detailed review of the facts from which we have
drawn our conclusions.

A. PROCEDURAL BACKGROUND

Pursuant to the trial court’s order, in November 2010, two test tubes of Markell’s blood
were drawn at the Detroit Medical Center for further genetic testing.22 The blood eventually
made its way to the PreventionGenetics laboratory in Wisconsin, where a gene sequencing test
proved positive for PCH-2. Plaintiffs moved in limine to exclude the PreventionGenetics report
based on alleged failures of defendants to (1) establish the chain of custody of the blood, and (2)
“authenticate” the test results. Plaintiffs asserted that authentication could be accomplished only
“from the testimony of every witness that handled the unsealed and non-tamper proof blood,
from the time it was allegedly drawn from Markell . . . at DMC Children’s Hospital by a
phlebotomist named Nicole Fuller in Detroit, Michigan, to then allegedly being sent to Spokane,
Washington, to Salt Lake City, Utah, and/or to Marshfield, Wisconsin.”

22
All genetic testing previously performed at Beaumont had proven negative for an identifiable
genetic disorder. When one of defendants’ experts suggested testing Markell for the genetic
defect giving rising to PCH-2, the trial court ordered additional testing.

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At a hearing held on September 7, 2011, plaintiffs’ counsel, Geoffrey Fieger, attempted
to withdraw his motion to preclude the PreventionGenetics report, but the trial court expressed
concern regarding “the nature of [the] evidence. Whether an item is what it purports to be.
Authentication.” Joseph Babiarz, one of defendants’ attorneys, explained that the blood was
obtained at the DMC, both tubes were sent to Signature Genomics, a laboratory in Washington.
Signature Genomics took “a couple of drops of the blood out of one of the tubes” and sent the
rest to ARUP “to do a microarray,” which was “normal.”23

While those blood tests were in progress, Mr. Babiarz learned from one of his experts
that only two labs in the United States could test for the specific gene defect suspected by
defendants’ experts. PreventionGenetics was one of them. Mr. Babiarz averred that Signature
Genomics transferred the blood to PreventionGenetics, where it tested positive for TSEN54, the
genetic defect consistent with PCH-2.

Following this recitation, Mr. Fieger complained that the PreventionGenetics testing “has
never been subjected to any testing” and was not peer reviewed. The trial court inquired, “Why
aren’t you moving to have it struck for reliability?” Mr. Fieger responded: “Because I think I
want to do it at trial, but I don’t want to take any more time.” After more discussion on the
record, the trial court stated, “both the questions regarding chain and reliability were withdrawn
but reserved.”

The parties reconvened on September 19, 2011. Judge Nichols introduced that day’s
hearing by explaining that the court would consider the chain of custody of the blood used for
the PreventionGenetics testing, and would “examine the reliability of the genetics testing that
was done . . . both in terms of the test and in terms of its application.” The court invited
defendants “to make a record regarding chain of custody.”

Mr. Babiarz summarized affidavits and depositions filed with the court attesting to the
chain of custody. Kelly Sartor, Supervisor of DMC University Labs, testified and averred that
when Markell’s blood was drawn at the DMC on November 19, 2010, the phlebotomist placed
handwritten labels stating Markell’s name and birth date on two tubes of blood. Joyce Simmons,
a DMC employee, brought the two tubes of blood to Sartor. Sartor packaged the two tubes in a
sealed bag and placed them in a “secure fridge.” Sartor filled out a Signature Genomics request
for genetic testing, and on November 22, 2010, packed the blood and the request in a container
labeled with a Federal Express tag and placed the package in a FedEx drop-off bin at the DMC.

Dr. Bessem Bejjani, the chief medical officer for Signature Genomics in Spokane,
Washington, averred that Signature Genomics received intact the FedEx package sent by Sartor.
DNA was extracted and the blood was maintained under refrigeration at Signature Genomics.
On December 10, 2010, Mr. Babiarz instructed Signature Genomics to send the blood to
PreventionGenetics. Dr. Marwan Tayeh, a clinical molecular geneticist at PreventionGenetics,
received the FedEx package from Signature Genomics on December 14, 2010. It contained one
tube of blood labeled with Markell’s name and birth date. Mr. Babiarz asserted that the

23
“ARUP” refers to a lab in Utah. The microarray study it performed is inconsequential.

-43-
affidavits and deposition testimony substantiating these facts sufficed to satisfy any chain of
custody concerns.

Mr. Fieger complained that defendants had failed to produce every person who had
touched the blood during its travels, and pointed out that one of the tests done at Signature
Genomics reported that the blood contained male chromosomes. Judge Nichols then ruled,
“[E]very item that plaintiff raises in this regard goes not to admissibility but to weight. Plaintiff
must let the jury decide that. The Court’s opinions on whether or not and what the jury will do
with it is irrelevant.” Judge Nichols continued: “At this point, the matter goes forward and the,
the chain of custody has been reasonably satisfied as far as this Court is concerned and it is now
incumbent [upon] the parties to address the question of weight which they will do during the
trial.” Although this ruling seems relatively straightforward, it disintegrated into many pieces at
the trial.

The court then turned its attention to whether the gene sequencing test qualified as
reliable. Mr. Fieger asserted that he intended to challenge both the “scientific reliability” of the
test and “the scientific basis of the conclusions” offered in the report, which he characterized as
“if you have these genes you have this disease.” Judge Nichols advised Mr. Babiarz:

You need to satisfy the Court by a preponderance of the evidence that . . .
the tests done here is [sic] not novel and invented by Marwan Tayeh, number one
. . . . And number two, that the tests for genetic sequence allows the argument to
the jury that there is a diagnostic human disease here that you can argue.

The court then took telephone testimony from Dr. Tayeh, who testified that the gene sequencing
study he performed was the “gold standard method” and had been in existence “for a long time.”
He asserted that DNA sequencing is reliable and has been subjected to peer-review testing. Dr.
Tayeh further claimed that “[w]hat we found is consistent with the diagnosis” of PCH. During
deposition testimony later read to the jury, Dr. Tayeh displayed a test tube with three labels, each
bearing Markell’s name, and stated that the blood used to conduct the genetic testing came from
that tube. PreventionGenetics also kept a log listing the names of every person who had received
and handled the blood.

On September 20, 2011, the parties again gathered in Judge Nichols’s courtroom to argue
about the trial exhibits. During the arguments, Judge Nichols and Mr. Babiarz engaged in the
following exchange regarding plaintiffs’ chain of custody challenge to the admissibility of the
PreventionGenetics report:

Mr. Babiarz: Your Honor, since the Court has already ruled that the
chain of custody is not relevant what’s the --

The Court: Hold on, hold on --

Mr. Fieger: No.

The Court: -- Mr. Babiarz, I don’t like you misstating things I say.

Mr. Babiarz: I’m sorry if I did, your Honor.

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The Court: And I don’t like it if Mr. Fieger does too, but I seem to hear
it more from you. And you misstate what I say.

Mr. Babiarz: Okay, maybe I did, your Honor.

The Court: I didn’t say they weren’t relevant.

Mr. Babiarz: Well yesterday, your Honor, you ruled that the chain of
custody that he had failed to meet his burden attacking our chain of custody. That
was my understanding of your ruling.

The Court: I, I said that -- I’m saying his arguments go to an argument
to be made before the jury. Can they -- can they trust this chain or not. It’s not
me that can make that decision, that’s what I’m saying.

At the end of that day, Judge Nichols issued a four-page opinion and order titled:
“Opinion and Order Denying Plaintiff’s Objections to Defendants’ Genetic Testing.” In his
opinion and order, Judge Nichols addressed only “the Court’s findings on the reliability of that
testing.” After summarizing the PreventionGenetics report and Dr. Tayeh’s testimony, Judge
Nichols concluded in relevant part:

Having considered the arguments, the testimony of Tayeh, and referenced
publications, the Court finds that the genetic testing methodology is reliable
within the scientific community and is sufficiently based on discoveries of
mutations that identify a genetic defect consistent with [PCH]. While Plaintiff
argues no article exists establishing that a genetic defect in TSEN54 causes
[PCH], the very title of Budde states just that -- mutations cause cerebellar
hypoplasia. Moreover, while the articles use adjectives like “associated”,
“corresponds” and “is responsible for most patients with [PCH-2]”, Tayeh
testified that more probable [sic] than not, and based on the gene being reported
several times with patients having [PCH], the genetic defect is the cause of
Plaintiff’s [PCH].

To conclude, the Court finds the genetic testing and application in this
case reliable under MRE 702 and existing law.

During the presentation of plaintiffs’ proofs at trial, defendants frequently referenced the
PreventionGenetics report. Dr. Soffer admitted that Markell tested positive for PCH-2. Dr.
Gabriel acknowledged that PreventionGenetics “confirmed by DNA testing” that Markell has
PCH. Kimberly VanSlembrouck, too, was questioned regarding her knowledge of the genetic
testing results.

Although defendants freely referenced the report when cross-examining plaintiffs’
witnesses, confusion regarding the report’s admissibility surfaced during Mr. Babiarz’s
examination of the first defense witness, Yoram Sorokin, M.D., on the tenth day of the trial.
Despite the trial court’s rulings that (1) the report was scientifically reliable and admissible under
MRE 702, and (2) whether the chain of custody had been satisfied would be for the jury, Mr.
Fieger objected when Mr. Babiarz attempted to question Dr. Sorokin about it:

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Q. Doctor, have you seen the report from PreventionGenetics?

A. Yes.

Q. Would that support your conclusion?

Mr. Fieger: Objection. That’s not in evidence.

The Court: Sustained.

Mr. Babiarz: Your Honor, it’s been admitted as an exhibit I thought.

Mr. Fieger: It has not. There’s --

The Court: Sustained.

Mr. Fieger: Thank you.

The Court: The ruling necessarily been as to its admission or not, [sic]
the ruling is as to his ability to do -- testify to that topic matter.

BY MR. BABIARZ:

Q. Doctor, if this child has been found to have a genetic disease
would that assist your, your -- confirm your belief that labor and delivery did not
cause her harm?

A. It will not change . . . my opinion.

Q. Would it support your opinion?

A. Yes.

At the close of Dr. Sorokin’s testimony and after the jury had been excused for the day,
Mr. Fieger raised the chain of custody with the trial court:

Mr. Fieger: Okay. I foresee a problem, your Honor, arising tomorrow.
I want to alert the Court, I don’t know if you want to deal with it now or
tomorrow morning? But Doctor Milunsky is a geneticist and there has been no
chain of custody evidence here.

And your order is quite clear and you can’t start putting in this evidence
without having a chain of custody, he just doesn’t get it miraculously in.

The parties then embarked on a lengthy discussion (19 pages of transcript) regarding the chain of
custody issue.

Mr. Fieger argued that Judge Nichols’s original order for the genetic testing required that
the DMC accomplish the testing. According to Mr. Fieger, Mr. Babiarz “ignored your order and

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started sending blood all over the world. And so tests got conducted in Washington, in Salt Lake
City, in Washington again and then in Wisconsin.” Mr. Fieger continued: “[W]e probably
[would] not have a chain of custody problem if your order had been followed. But instead now
and you’ve ordered that I’m entitled to contest the chain of custody.”

Mr. Babiarz responded in relevant part:

Your Honor, we had a hearing a couple weeks ago on the chain of custody
and you, you took testimony from Doctor Tayeh and some deposition testimony
and affidavits were brought to your attention which clearly established a clear
chain of custody.

You found that the chain of custody he be allowed to attack it, it went to
weight not admissibility, that was the Court’s finding. He can attack the chain all
he wants, but we’ll establish without any doubt that there’s a good secure chain of
custody pursuant to Michigan law.

***

. . . [Y]ou made a ruling that you found the chain of custody to be
sufficient under Michigan law. It went to weight not admissibility and Mr. Fieger
could attack it.

So here’s what we’re left with. You found that the, the admissibility of
the document was in. It was admissible but the weight of it was in question and
you found it was reliable.

So, therefore, under Michigan law under 901 it meets all the criteria for
inclusion as an exhibit.

Judge Nichols seemed to have difficulty recalling his ruling, and indicated: “I speak
through a written order.” Mr. Babiarz offered to “bring in an order that conforms with what you
said from the bench[.]” Judge Nichols stated, “Well I’m not going to sign it tomorrow morning
in view of this objection.” After further argument, the court stated that in making its prior ruling,
“I did not say that it was authenticated.” The court continued, “[B]ut if a witness sits up here and
testifies that, that it was marked and you know they’re reasonably satisfied that it is what came
from DMC then they’re going to satisfy it. You can argue all you want to the jury.”

Mr. Fieger continued to argue that no chain of custody could be established. Mr. Babiarz
pointed out that Dr. Milunsky was scheduled to testify the next day, and that was the only day
that he could appear. And defendants could not establish the chain of custody prior to Dr.
Milunsky’s testimony, Mr. Babiarz asserted. The Court ruled, “I mean it’s conditional
admissibility. . . . [I]t’s not a burden that’s impossible to overcome, but there’s got to be some
reasonable satisfaction that this DMC sample is the one that ended up where it ended up.” The
issue closed for the day with Judge Nichols’s admonition:

Okay, so we’re not done yet. So we’re going to proceed tomorrow and do
remind me, I’ll tell the jurors this is conditional admissibility depending upon

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whether or not chain of custody has been established, but which is also a question
they’re going to answer to their satisfaction.

The next morning, the parties again took up the chain of custody issue. The judge stated:
“But you know it’s not -- folks, we’re elevating this thing to way out of proportion. Chain, chain
of custody is simply the jurors[’] satisfaction that the blood sample started at DMC. It’s a blood
sample in Wisconsin.” Mr. Fieger requested that the court instruct the jury that the
PreventionGenetics report was “not in evidence yet.” The Court evidently agreed, stating
“[Y]ou’ve not asked for a formal admission of the sample into evidence and it’s not in
evidence.”24 Mr. Babiarz then moved for the introduction of “the PreventionGenetics exhibit.”
Mr. Fieger objected, asserting: “He wants to put it in without having to put in the chain of
custody.” The following colloquy ensued:

Mr. Babiarz: Your Honor, you ruled that the chain of custody had been
satisfied and the cases we cited in a civil case you don’t have to bring in every
person that handled it. In the cases we cited --

The Court: I agree.

Mr. Babiarz: -- say you can establish chain of custody by direct, indirect
and circumstantial evidence.

The Court: You know what--you know whether I do it or not I’m still
going to let the jurors know that they’ll need to be reasonably satisfied because
it’s their question, not the Court’s. Okay?

Mr. Babiarz: Fair enough, Your Honor.

The Court: So I’m going to let them know one way or another. Again,
we’re making . . . a mountain out of a mole hill.

During Dr. Milunsky’s testimony, defendants displayed the PreventionGenetics report to
the jury. Mr. Fieger asked for an instruction. The court complied:

Ladies and gentlemen, let me--let me bring this to your attention. Facts or
data upon which an expert bases his opinion normally must be in evidence. The
Court can in its discretion allow . . . proposed testimony with a condition that the
evidence will be admitted later.

Previously at a hearing that you need not be concerned with I made the
decision to allow it for that hearing. That, however, is not binding on you in

24
Here and elsewhere in the record, the Judge seemed confused about whether defendants
intended or needed to introduce the actual blood “sample,” or the report of the testing.

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terms of whether you believe it is what defendant says it is, that is the blood
sample of Markell.

In other words, I’m admitting this testimony conditionally based on this
sample here, but it’s up to at least six of you to decide it is the blood sample of
plaintiff Markell, okay. Got that?

When testimony concluded on October 6, Mr. Babiarz’s co-counsel again brought up the
chain of custody issue:

Ms. Andreou: Actually I have -- tomorrow, your Honor, we have Doctor
Quinn[t] but what I would like to give Mr. Fieger a heads up on is that as it relates
to chain of custody if there’s still a question in the Court’s mind we do have the
deposition of --

The Court: Okay. What do you mean if there’s a question in the Court’s
mind?

Ms. Andreou: Well if we need further evidence on that.

The Court: Folks, I’m not the one you have to convince.

Ms. Andreou: Okay.

The Court: You have six people here that will need to decide. I’ll say it
one more time and I’m not going to say it again, that the sample blood from DMC
was what ended up in Wisconsin. Okay.

Now if Mr. Fieger wants to keep poking holes at it and poking holes at it
then you know maybe you go through the chain, you show it. I can’t tell you how
to practice. [Emphasis added].

Subsequently, defendants read into the record the deposition testimonies of Sartor, Bejjani, and
Tayeh.

When questioning of defendants’ final witness concluded, the following colloquy ensued:

The Court: Does defendant have any other witnesses?

Mr. Babiarz: No, your Honor. But . . . before we rest we would like to
offer our exhibits and identify them for the jury if we may.

Mr. Fieger: They’ve already been--they’ve been accepted into
evidence, Judge, way before this trial started.

Mr. Babiarz: Okay, I won’t rattle them off then your Honor.

The Court: Okay. No other witnesses?

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Mr. Babiarz: Yeah, and . . . I just want to make clear we are offering the
PreventionGenetics report, your Honor, as an exhibit.

***

The Court: Mr. Fieger, do you have any rebuttal?

Mr. Fieger: No, your Honor.

The Court: Ladies and gentlemen, we’re ready for closing arguments
tomorrow morning. The game plan I think will be like this, we’ll start--they can
take a total together up to three hours. Not apiece, they’ll take an hour and a half
most, okay. It doesn’t mean they have to. I keep telling them that, but I keep
telling them that I’m going to tell you, remind you that what they say is not
evidence. They’re going to marshal the facts according to the way they see them
as it pertains to their clients, okay.

But the evidence comes from what you’ve heard here on the witness stand
and the exhibits that have been offered and received. So hold them to that test.

During closing argument, Mr. Babiarz referenced the chain of custody issue:

Let’s talk a little bit about the chain of custody. You heard -- and it’s a
little bit boring to have depositions read to you, but -- and Mr. Fieger said we
were boring the jury. Well, the reason we had to do that is because he was
questioning the chain of custody and those long and boring questions were the
ones being asked by his partner which he refused to read. But, let’s look at the
chain of custody. October second the Court orders a blood draw of Markell
Vanslembrouck [sic]. November 19th, 2010, blood drawn at DMC Nicole Fuller.
November 22nd, blood sent from DMC to Signature Genomics (ph). You heard
the deposition of Ms. Sartor (ph) with FedEx tracking number 796477091951.
November 23rd, blood received by Signature Genomics from DMC per the
deposition of Dr. Bejoini (ph), exact same tracking number. December 13th,
blood sent from Signature Genomics in Spokane to Prevention Genetics in
Wisconsin per the deposition of Dr. Bejoini [sic], FedEx tracking number
received, same tracking number -- or sent rather with this tracking number.
Received by Prevention Genetics from Signature Genomics per the deposition of
Dr. Tayeh (ph) with the exact same FedEx tracking number. And, then on
January 24th after they complete their testing what do they report? Molecular
genetics report by Prevention Genetics, [PCH], subtype two and four, TSEN-54
gene sequencing positive. There was never any break in the chain of custody.
And, we are obligated to read those depositions to you to link that up.

Again, if Mr. Fieger questioned the chain of custody, why didn’t he have
the blood tested. Why didn’t he have the parents tested? He didn’t do it.

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This excerpt tends to indicate that the report was, in fact, admitted in evidence.25

Nevertheless, defendants filed a motion for JNOV, contending that the trial court erred by
excluding the report. During oral argument regarding that motion, plaintiffs’ counsel (Mr.
Beam) and the trial court questioned Mr. Kamenec, representing defendants, regarding whether
he contended that the report had not actually gone to the jury. Mr. Kamenec responded, “I don’t
know if it went to the jury. It was never admitted.” Mr. Beam represented: “It went to the . . .
jury, Your Honor, as far . . . as I know. And if it didn’t go to the jury, that was . . . nobody’s
fault but defense counsel.” After more argument, the judge stated: “I have no doubt that it went
to the jury.”

B. ANALYSIS

Defendants premise their legal argument on their claim that Judge Nichols refused to
admit the PreventionGenetics report in evidence. Although the numerous and protracted
arguments regarding the report reflect some inconsistency and lack of clarity on Judge Nichols’s
part, he found that the jury was provided with the report and the record tends to support this
finding.

Plaintiffs’ “chain of custody” challenge to the report rested on a factually unsupported
allegation that the blood tested at PreventionGenetics was not Markell’s blood. Defendants
argued that any gaps in the chain of custody of Markell’s blood from the time it was drawn until
the time it allegedly arrived in Wisconsin went to the weight of the evidence, not its
admissibility. Assuming that plaintiffs’ chain of custody argument had any merit whatsoever,
defendants are correct. Moreover, the trial court agreed with defendants.

Plaintiffs’ chain of custody argument boiled down to an assertion that defendants never
properly authenticated the PreventionGenetics report. MRE 901 sets out the “requirement of
authentication or identification” and governs our analysis of this issue:

(a) General Provision. The requirement of authentication or
identification as a condition precedent to admissibility is satisfied by evidence
sufficient to support a finding that the matter in question is what its proponent
claims.

25
And even assuming that it was not, the issue was squarely placed before the jury throughout
the trial. Mr. Babiarz summarized during his closing argument:
To their credit though they all agree there’s a genetic defect of the brain
and they all agree it occurred in the first or second trimester of pregnancy, they
just won’t acknowledge what it is or what the significance of it [is]. They won’t
admit this child has [PCH] even though it’s been tested with DNA certainty.
[Emphasis added].

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(b) Illustrations. By way of illustration only, and not by way of
limitation, the following are examples of authentication or identification
conforming with the requirements of this rule:

(1) Testimony of Witness With Knowledge. Testimony that a matter is
what it is claimed to be. . . .

“Evidence sufficient to support a finding means evidence upon which a reasonable jury
could find by a preponderance of the evidence an item to be what the proponent claims it is.” 2
McCormick, Evidence (7th ed), § 212, p 6. The judge has a “limited screening role” in making
this determination. Id. “If a witness has personal knowledge and gives direct testimony on the
matter, this is sufficient.” Id. at 6-7.

Here, the question confronting Judge Nichols was whether PreventionGenetics tested
Markell’s blood or that of someone else. Dr. Tayeh testified that PreventionGenetics tested a
blood sample contained in a tube labeled with Markell’s name. That evidence sufficed to satisfy
MRE 901. Notably, plaintiffs identified no evidence supporting a gap in the chain of the blood’s
custody along the path it traveled to PreventionGenetics. Assuming for the sake of argument that
the side trip to Signature Genomics introduced some uncertainty regarding the integrity of the
blood sample, the trial court correctly allowed the jury to consider the significance of this detour.

“Once a proper foundation has been established, any deficiencies in the chain of custody
go to the weight afforded to the evidence, rather than its admissibility.” People v White, 208
Mich App 126, 133; 527 NW2d 34 (1994). Plaintiffs’ unsubstantiated claims that the chain of
custody had been broken did not preclude the report’s admission. Rather, plaintiffs’ fanciful
concern that somehow other blood was substituted for that of Markell affected only the weight of
the evidence. Id. And although Judge Nichols perhaps could have been more consistent, his
core ruling—that it was for the jury to decide whether to credit that the blood sampled was that
of Markell—remained unchanged.26 The record further indicates that on more than one

26
Moreover, we believe that the chain-of-custody argument was legally baseless, and that Judge
Nichols should have ended this controversy well before trial. Defendants sought to introduce the
PreventionGenetics report, not the blood sample itself. The report was clearly admissible under
MRE 803(6), which provides an exception to the hearsay rule for records of regularly conducted
activity:

A memorandum, report, record, or data compilation, in any form, of acts,
transactions, occurrences, events, conditions, opinions, or diagnoses made at or
near the time by, or from information transmitted by, a person with knowledge, if
kept in the course of a regularly conducted business activity, and if it was the
regular practice of that business activity to make the memorandum, report, record,
or data compilation, all as shown by the testimony of the custodian or other
qualified witness, unless the source of information or the method or
circumstances of preparation indicate lack of trustworthiness. The term
“business” as used in this paragraph includes business, institution, association,

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occasion, Judge Nichols stated that the report satisfied the standard for admissibility with the
caveat that plaintiffs remained at liberty to attack the chain of custody.

Nor do we perceive that Judge Nichols “denigrated” the report in the jury’s presence.
While we agree that Judge Nichols should have ruled more forcefully at the outset that the
physical document containing the report would be admitted, the jury was well aware of its
contents. We find no error regarding the PreventionGenetics report warranting reversal.

VI. THE ARGUMENT OF PLAINTIFFS’ COUNSEL

Defendants assert that Mr. Fieger’s misconduct “permeated this trial, and overshadowed
the legitimate defense argued to the jury.” According to defendants, Mr. Fieger employed his
“signature trial strategy” of accusing defendants and their witnesses of lying, conspiring,
covering up, and fabricating evidence. Mr. Fieger’s misconduct reached its zenith, defendants
insist, when he urged the jurors during closing argument “not to kill Markell.”

The following framework guides our evaluation of this argument:

When reviewing an appeal asserting improper conduct of an attorney, the
appellate court should first determine whether or not the claimed error was in fact
error and, if so, whether it was harmless. If the claimed error was not harmless,
the court must then ask if the error was properly preserved by objection and
request for instruction or motion for mistrial. If the error is so preserved, then
there is a right to appellate review; if not, the court must still make one further
inquiry. It must decide whether a new trial should nevertheless be ordered
because what occurred may have caused the result or played too large a part and
may have denied a party a fair trial. If the court cannot say that the result was not
affected, then a new trial may be granted. Tainted verdicts need not be allowed to

profession, occupation, and calling of every kind, whether or not conducted for
profit. [Emphasis added.]

No evidence supported that the “circumstances of preparation” of the report indicated a lack of
trustworthiness. Before trial, defendants established that the report was created and kept in the
regular course of business. This foundation sufficed for admission of the document. Not a shred
of evidence or shadow of reasonable inference supported that the blood tested did not come from
Markell. Accordingly, the report was admissible under MRE 803(6). See Merrow v Bofferding,
458 Mich 617, 626-627; 581 NW2d 696 (1998).

Although the issue has not been considered in Michigan, we are of the view that “chain
of custody” arguments such as the one advanced by plaintiffs apply only to physical evidence or
to “time-sensitive tests” taken when an event, arrest, or accident occurs, such that the result
“cannot be replicated outside that time frame.” Ex parte Dep’t of Health & Environmental
Control v Doe, 350 SC 243, 248-249; 565 SE2d 293 (2002). No chain of custody analysis was
warranted here, as retesting could have readily confirmed the accuracy of the PreventionGenetics
report, adding to its trustworthiness.

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stand simply because a lawyer or judge or both failed to protect the interests of
the prejudiced party by timely action. [Reetz v Kinsman Marine Transit Co, 416
Mich 97, 102-103; 330 NW2d 638 (1982).]

A lawyer’s comments will usually not be cause for reversal unless they indicate a
deliberate course of conduct aimed at preventing a fair and impartial trial or
where counsel’s remarks were such as to deflect the jury’s attention from the
issues involved and had a controlling influence on the verdict. [Ellsworth, 236
Mich App at 191-192.]

A. THE TRIAL

Before we describe the episodes of claimed misconduct, we offer the following overview.
The record in this case reflects that counsel for both sides argued with each other incessantly,
delayed the trial by making long-winded and legally meritless objections, interjected snide,
sarcastic remarks at every opportunity, and otherwise acted unprofessionally on a daily basis.
Neither came close to modeling acceptable courtroom behavior. Judge Nichols’s frustration with
the behavior of the lawyers emerged on several occasions. The following excerpts from just one
trial day (September 27) illustrate the combative atmosphere that permeated these proceedings:

Mr. Fieger: You told us earlier there were no abnormal. Here’s two
abnormal and then there’s a third one. A three hour glucose tolerance test was
done. It had one abnormal value, did you write that?

A. I did write that.

Q. Okay, now --

A. Well, like I explained the one hour -- the three hour with one abnormal
does not make a patient a diabetic.

Q. And, the other two were just one number below abnormal, weren’t
they?

A. It was normal test.

Q. Please it will be much easier. I’m just asking. The other two that
[you] say were normal was one number below abnormal, wasn’t it?

A. It was one below the upper limit of the normal.

Q. Right. So, if it had been one higher it would have been abnormal, the
other two right?

A. Yes.

Mr. Babiarz: Your Honor, objection. If wishes were horses, beggars
would ride. The test was normal.

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Mr. Fieger: What does this --

The Court: What is your objection? I would appreciate not little phrases
of Dickens of whoever is, but the, you know --

Mr. Babiarz: He’s arguing with the witness, that’s my objection.

The Court: Well, they went through different wording processes and, if
anything Mr. Fieger, it’s not necessary that you summarize his statement; likewise
with you.

***

Q. She was actually -- they used an ultrasound on her didn’t they on those
pre-hospital admissions?

A. I believe they did just to check the position of the baby.

Q. And, the other -- if you want to you can check the size of the baby
can’t you?

A. Yes.

Q. But, nobody did that apparently?

A. What happened --

Q. Yes or no, did anybody do that?

A. No.

Q. Okay. I didn’t ask for excuses, I’m just asking for facts.

Mr. Babiarz: Your Honor, that’s argumentative --

The Court: I agree. That will be struck from the record.

Mr. Babiarz: Move to strike.

The Court: I agree.

Mr. Fieger: We’ll get -- I’ll get -- I’m not trying to be argumentative with
you, I’m just trying to get you to answer my questions.

Mr. Babiarz: Could have fooled me, Your Honor, th

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/2746684. Public record. Not legal advice.