|
SUMMARY
 TOC
In November of 1997, Mr. Alan R. Yurko was
accused of, and arrested for, killing his
son, the two-and-a-half month old baby Alan
Ream Yurko, by vigorous shaking of the head.
Mr. Yurko was convicted by a jury in 1999
and sentenced to spend his life + 10 years
in prison. Mr. Yurko and his wife, Francine
requested that I evaluate their case to find
the factual cause(s) that led to baby Alan’s
cardiac arrest and death in November of 1997.
I evaluated their case by reviewing the baby’s
medical records, H & E stained tissue
sections of Alan’s organs obtained at
the time of autopsy, the autopsy report, Francine’s
medical record during her pregnancy with Alan,
the trial document and testimonies of expert
witnesses, and related published medical literature.
I used differential diagnosis to evaluate
the contribution of causes and the synergistic
actions among these causes that led to the
cardiac arrest, apnea, subdural bleeding,
and death in this case.
I
present my review and analysis of Francine’s health problems during
her pregnancy with Alan in Section I of this report. Section II contains
a detailed description of baby Alan’s health problems from the time
of birth on September 16, 1997 to the day of his cardiac arrest on November
24, 1997, and my analysis. In Section III, I describe the clinical events
during Alan’s five days in Princeton and Florida hospitals, and my
analysis of these events. My detailed review and analysis of the medical
examiner’s autopsy report and his court testimony are presented in
Section IV. My review of the testimonies of the other state witnesses
and the defense witness is described in Section V. Section VI contains
my conclusions
and recommendations.
Baby
Alan was born five weeks premature on September 16, 1997 by induced labor
because his mother, Francine, suffered from oligohydramnios. Francine
also suffered from multiple chronic illnesses during her pregnancy that
included gestational diabetes, anemia, loss of appetite, spastic colon,
urinary tract and vaginal bacterial infections, and hemorrhoids. She gained
only two pounds during her entire pregnancy (I). The baby spent the first
week of his life in the hospital because he suffered from respiratory
distress syndrome, jaundice, hypoxia, hypoglycemia, and bacterial infections
(II). At day three following his birth, Alan’s serum bilirubin level
was l7.4 mg/dL, which is capable of causing encephalopathy.
Review
of the medical literature revealed that gestational diabetes, oligohydramnios,
and jaundice have tremendous negative impact on the prenatal, natal, and
postnatal developments. These conditions caused increases in mortality
rate, congenital anomalies, growth retardation, skeleton deformities,
rate of premature labor, respiratory distress syndrome, hypoxia, hypoglycemia,
encephalopathy, and rate of infections in the newborn (II-A).
Baby
Alan was released from the hospital one week following his birth, with
jaundice and respiratory system problems. He continued to have symptoms
of chest congestion and difficulty in breathing following discharge from
the hospital. He gained only 0.5 lb in his first twenty-four days of life.
However, his growth was improved during his second month of life. He gained
2.7 pounds.
On
November 11, 1997, at two months of age, Alan was given six vaccines (DTaP,
Hib, OPV and Hepatitis B) and sent home without monitoring or medical
supervision. The baby developed a high-pitched cry, his skin became warm
to touch, and there was an increasing lethargy with a falling-off feeding
pattern at about l0 or 11 days, following the vaccine injections. His
mother had been told in the doctor’s office that these symptoms might
result following these vaccinations. This led her not to worry about her
baby’s symptoms and not to call his doctor. On November 24th, at
13 days post vaccination, the baby had a cardiac arrest and apnea episode,
and his father took him to the emergency room at Princeton Hospital in
Orlando Florida (II-B).
Serious
adverse reactions, such as apnea, cardiorespiratory problems, and oxygen
desaturations that require medical intervention, are commonly associated
with vaccination of preterm infants. Preterm babies who were vaccinated
at 70 days of age or less, similar to baby Alan, developed the most serious
adverse reactions to vaccines. The authors of many well-documented studies
concluded that the risk and benefit of vaccination in preterm infants
should be evaluated prior to administering vaccines (II-C). They also
emphasized that preterm infants who received vaccines should be monitored.
Adverse reactions to vaccines that were administered to baby Alan are
not limited to preterm infants. They have also been reported in full term
infants. For example, in the USA, reports to the Vaccine Adverse Event
Reporting System (VAERS), concerning infant immunization against pertussis
between January 1, 1995 and June 30, 1998 revealed 285 cases of death
and 971 cases of nonfatal serious illnesses (II-C).
On
November 24th, baby Alan was admitted to Princeton Hospital with cardiac
arrest and apnea; he was then resuscitated. The first examination revealed
that he was flaccid, his corneas were somewhat cloudy, and he had gastric
ulcer. There was no injury caused by trauma found on his head or his body,
except for a small reddish linear bruise under the right eye. His four-year-old
sister caused this minor injury accidentally when she was handing a baby
bottle to her father. The baby’s first blood test revealed that he
suffered from metabolic and respiratory acidosis (PH of 7.18), diabetes
(blood glucose level of 337 mg/dL and Anion gap level of 22 mEq/L), anemia,
elevated serum liver enzymes and LDH. He also had elevated white blood
cell count (20,900/µL) and platelet count (571,000/µL). The
baby was treated with high therapeutic doses of three antibiotics—
rocephin, gentamicin, and Claforan (cefotaxime sodium)—to fight the
bacterial infections, given IV fluids and dopamine, and then transferred
to Florida Hospital at about 2:00 PM on November 24th.
At
Florida Hospital, the baby’s temperature rose to 105.8 F, and his
blood glucose reached 397 mg/dL on November 24th. The treatment with three
types of antibiotics reduced his temperature, blood glucose level, and
serum enzymes. On November 26th, his serum glucose level dropped to a
normal level of 95 mg/dL (76% reduction); the LDH, alkaline phosphate,
and SGPT levels dropped by 70%, 47%, and 19%, respectively; and the white
blood cell count by 35%. These data clearly indicate that the baby had
liver, pancreas, and maybe heart bacterial infections, and that his infections
were resolved because of the treatment with antibiotics. The baby also
suffered from hypotension, dysrhythmia, dehydration and weight loss (lost
1.05 lb in five days). The baby was given IV fluid, plasmanate and red
blood cells, heparin, potassium, dopamine, and antidiuretic hormones.
Furthermore,
the baby was treated with excessive amount of sodium bicarbonate on November
24th. The blood pH increased from 7.10 to 7.67, and this treatment caused
metabolic alkalosis, hypoxia, hypokalemia, and cerebral edema. At high
blood pH, the release of oxygen from hemoglobin to the tissues is reduced
significantly. In addition, the baby was also given heparin at 2:45 PM
at high dose level of 219 IU/kg per hour. At 3:15 PM, blood analysis showed
elevated prothrombin time and fibrinogen split product level. Heparin
given to patients suffering from anemia, hypotension, and unexplained
symptoms similar to baby Alan’s has caused serious hemorrhagic events.
A computerized tomography scan of the brain taken at 7:50 PM showed a
subdural hematoma on the right side of the brain, and intraparenchymal
hemorrhage. Based on the hourly heparin dose (219 IU/kg per hour), the
estimated total dose infused in five hours was 1095 IU/kg, which is about
8.8 times the recommended maintenance dose for infants of 125 IU/kg per
five hours.
Unfortunately,
the baby was treated again with excessive doses of sodium bicarbonate
and heparin (219 IU/kg per hour) on November 25th, despite his problems
with metabolic alkalosis (pH 7.61) and bleeding in the brain. This treatment
caused metabolic alkalosis, hypoxia, hypokalemia, cerebral edema, and
bleeding. His serum potassium level dropped from 4.9 mEq/L to 2.3 mEq/L.
Also, baby Alan suffered from disseminated intravascular coagulation (DIC)
as a result of his treatment with heparin. The platelet count prior to
the administration of heparin on November 24, 1997 was 571,000/µL
of blood, and dropped to 397,000/µL (30% reduction) on November
25th. Heparin increases the tendency of the platelets to aggregate and
form a clot. Also, blood analysis performed at about 30 minutes post-heparin
infusion, shows increased fibrinogen split product level (160 µg/mL)
and prothrombin time (11.6 seconds). These values are 1600% and 115% of
normal, respectively. These values returned to normal on November 26th
following the cessation of the treatment with heparin.
On
the 24th of November, chest x-ray showed bilateral pulmonary infiltrates
and healing fracture of the 6th rib. My review of the medical literature
revealed that rib fractures have been reported to occur during labor,
and that these fractures were missed during the initial examination of
the baby. In addition, the mechanism of rib fractures during labor was
explained in the medical literature (IV-J). It has also been stated that
the specific clinical manifestations of ribs fractures are often absent,
making diagnosis difficult.
Baby
Alan was pronounced (brain) dead on November 27th, 1997—about 75
hours after the initial hospital admission. On November 29, Dr. Shashi
B. Gore, the Chief Medical Examiner of District Nine, Orlando, Florida,
performed an autopsy whose main objective was to establish the cause(s)
of death (prior to autopsy, the baby’s heart, liver, pancreas, and
a portion of the intestine were taken by Translife for organ transplant).
Dr. Gore concluded that baby Alan died of bleeding in the brain resulting
from vigorous shaking of the baby by his father, Alan Yurko.
My
review of Dr. Gore’s autopsy report indicates that it lacks the accuracy
and the expected minimum scientific detail to make it reliable and useful
for revealing the cause of death. For example, Gore described the histology
of the heart in his autopsy report, but the heart was donated prior to
autopsy. Therefore, he did not have the chance to examine it. He did not
present a description of the microscopic appearance of the meninges and
the presence of axonal injury in the brain and spinal cord. There is no
description of his x-ray findings on the rib fractures. In addition, Gore’s
measurement of 22 cm for the head circumference was obviously wrong. It
was 37.5 cm at eighteen days prior to the autopsy (Table
4).
Furthermore,
Gore’s description of the bleeding in the subdural spaces of the
brain and spinal cord indicates that the bleeding occurred in at least
three stages during a 2-5-day period, and it does not support his claim
that bleeding occurred within a few minutes or a few seconds. Also, the
presence of hemorrhage in the lungs, brain, and spinal cord, and the presence
of cerebral edema does not support his claim that the bleeding was caused
by vigorous shaking of the head, but shows that it was caused by metabolic
and cardiovascular problems.
Alan
R.Yurko’s jury trial took place February 22 to 24, 1999 in the state
of Florida. The prosecutor provided four major witnesses testifying for
the state, and two of these were called for repeat appearances before
the jury, following that of the defense witness. Against these witnesses
the defense provided a single witness. The state witnesses were: 1) Dr.
Shashi B. Gore, the medical examiner; 2) Dr. Gary Pearl, a consultant
neuropathologist (testified twice); 3) Dr. Ben Guedes, the treating physician;
and 4) Dr. Matthew A. Seibel, a general pediatrician (testified twice).
The defense witness was Dr. Douglas Radford Shanklin, a pathologist.
Three
state witnesses (Gore, Guedes, and Seibel) said that baby Alan died as
result of Shaken Baby Syndrome. However, none of them provided medical
evidence to prove their case, and their testimonies were based only on
a theory. The fourth state witness, Dr. Pearl reported that the injuries
in the brain and spinal cord were acute injuries and did not start at
birth or shortly after birth. He did not say that these injuries were
caused by Shaken Baby Syndrome. None of the state witnesses reviewed the
baby’s prenatal record, his birth record, his doctor’s charts
during his two months of weekly visits, or adverse reactions to vaccines
and medications given to the baby. Also, they did not interview his parents
to get the case history. Furthermore, none of these witnesses presented
evidence in court to show the presence of axonal injury in the brain (IV,
V).
In
addition, Gore presented statements in court that are not supported by
his autopsy findings. He stated in court that the cerebrospinal fluid
(CSF) was mixed with blood, but in his report, he described that the CSF
was clear. He also stated in court and in his report that the heart was
donated prior to his examination, but he described the histology of the
heart in his report. Furthermore, Gore stated that the baby did not suffer
from meningitis, but his autopsy report and the clinical evidence described
in the baby’s chart, as well as the pathology evidence presented
by Dr. Pearl, Dr. Shanklin, indicate that the baby suffered from meningitis.
I also examined the H & E section of the meninges and observed evidence
of acute meningitis. The lesions and symptoms described by the pathologists,
autopsy report, and the baby’s chart that indicate the presence of
acute meningitis include swollen blood vessels, congestion, infiltration
of meningial tissue with inflammatory cells, brain edema, high white blood
cell count, and elevated body temperature of 105.8 F. Also, Gore overlooked
the influence of the treatment with antibiotics on the severity of the
lesions in the meninges.
Gore
presented the minor retinal bleeding in the right eye as evidence that
baby Alan died as a result of “Shaken Baby Syndrome,” but he
did not investigate the factual causes that led to retinal bleeding, such
as diabetes, infections, and hypoxia. Furthermore, Gore did not provide
x-ray findings to prove that Alan had fractures of ribs # 5, 7, and 10.
Also, he did not search the medical literature to find out if rib fractures
occurred during labor. However, he showed in court two photographs of
minor contusions in the temporal areas of the head that had occurred in
the hospital at about one day prior to autopsy, and had no relation to
the cause of death in this case. I believe that he did it to influence
the thinking of the jury that physical force was used.
The
second state witness, Dr. Guedes (the treating physician) did not reveal
to the court the following important events that show the baby died of
natural causes:
1. he treated the baby with three types of antibiotics to fight
bacterial infections and the baby responded very well to this treatment;
2. he treated the baby with excessive doses of sodium bicarbonate
and heparin that caused bleeding, metabolic alkalosis, hypoxia, and edema;
3. the baby had high blood glucose levels and suffered from diabetes
and complications of diabetes, such as dehydration, gastric ulcer, infections,
cerebral edema, hypokalemia, loss of weight, and cardiac dysrhythmia.
Dr.
Guedes and Florida Hospital contacted the Orange County Sheriff’s
Office and the Child Protective Office on November 24, 1997, and filed
a report of child abuse based on the assumption that baby Alan was injured
as a result of abuse by his father. Mr. Yurko was arrested on November
26, 1997, while his son was still alive in Florida Hospital. Dr. Guedes
assumed that Mr. Yurko was guilty of child abuse, but his own examination
of baby Alan revealed no injuries caused by trauma except a minor bruise
under the right eye. In fact, he treated the baby with excessive doses
of sodium bicarbonate and heparin that caused hypoxia and bleeding. Heparin
should not be given to an individual suffering from anemia, hypotension,
bleeding, and tissue inflammations similar to baby Alan’s.
I
believe that the medical practice and actions of Dr. Guedes do not protect
an ill child from bleeding in the brain and other tissues. No parent is
safe from being accused of killing his or her child by shaking. I believe
that Dr. Guedes’ work should be re-evaluated. It might stop these
horrible tragedies from happening to people!
The
defense witness, Dr. Shanklin, made very important contributions to this
case. He stated that baby Alan’s kidneys were not fully developed.
His finding might explain the mother’s problem with oligohydramnios
(II-A2). He also stated that the baby suffered from pneumonia and meningitis
of the brain and spinal cord. His findings might explain the susceptibility
of these organs to bleeding caused by treatment with heparin and sodium
bicarbonate. I also examined the H & E tissue sections of the brain,
spinal cord, and lungs, and I observed evidence of acute meningitis in
the brain, fresh bleeding in the subdural spaces of the brain and spinal
cord, bleeding in the brain and lung, and interstitial pneumonia. The
inflammation in these regions affected the integrity of the blood vessels,
and this would have predisposed them to leak fluid and blood when the
child was treated with excessive doses of heparin and sodium bicarbonate.
Additionally, Dr. Shanklin described old neurological injuries to the
brain and spinal cord. I believe that the high levels of bilirubin observed
in the first week following birth caused these injuries.
During
Mr. Yurko’s jury trial, the prosecutor, Ms. Wilkinson presented only
one theory—that baby Alan died of “Shaken Baby Syndrome”
(SBS), and that Alan Yurko, his father, did it. My review of the medical
evidence and the trial transcript revealed that the state did not prove
that the injuries were caused by trauma, or that Mr. Yurko abused his
child. However, the prosecutor still achieved her goal of getting Alan
Yurko convicted of a horrible crime he didn’t commit. He received
a life sentence + 10 years. I believe that the prosecutor used questionable
practices that violated Mr. Yurko’s right to a fair trial. In Section
V of this report is a list of the prosecutor’s unfair tactics, with
evidence that the state did not prove its case. For example; the prosecutor
did not investigate other causes, such as adverse reactions to medications
and vaccines. Also, she allowed Dr. Gore to present as evidence two photographs
of minor contusions in the temporal areas of the head that occurred in
the hospital at about one day prior to autopsy. The medical examiner’s
main objective should have been finding the causes of injuries and death,
not prejudicing his findings by showing irrelevant photos that would influence
a jury.
As
a result of problems with our current medical system—the policy of
vaccinating premature babies (the treatment given to baby Alan in the
hospital) and the bias of the testimony of state witnesses in evaluating
evidence, as exemplified in this case— Alan Yurko and his family
suffered two tragedies. The first tragedy was the loss of baby Alan because
of the adverse reactions to vaccines and the treatment using excessive
doses of heparin and sodium bicarbonate given at the hospital. The Yurkos’
second tragedy was the conviction of Mr. Yurko of a horrible crime he
did not commit. He was convicted because the state’s four expert
witnesses did not take the time to review the evidence or the related
published literature. They did not take the time to sort out the facts,
and their testimonies were based on theories, not on medical evidence.
The prosecutor contributed to the problem by focusing on only one theory.
I
believe that the state of Florida has a responsibility to review the evidence
presented in this report and to free Mr. Yurko from prison as soon as
possible. The state and the medical system should be focused on finding
the facts—the causes of the injury and death of children in cases
such as this—and preventing these problems from happening again.
Accusing innocent parents of abusing and killing their children based
on unsupported theory, as it happened in the case of baby Alan, will not
prevent the death of another child by vaccines and wrong medications.
But it certainly puts innocent people in prison and causes their families
unimaginable suffering. It also costs the taxpayers huge sums of money
to pay for trials and legal fees. I spent more than 250 hours working
on the Yurko case to find the factual causes of death in this case and
to write a detailed report. I hope that the state of Florida, the medical
system, and our society will take advantage of this opportunity to see
the real problems facing premature babies who are receiving vaccines,
and, hopefully, take action to put an end to such tragedies.
In
addition, I believe that the state of Florida
and the doctors who caused the Yurko’s
tragedy should compensate Mr. Yurko and his
family for the loss of their child, their
suffering, and the expenses paid. Also, the
state should investigate the involvement of
the state witnesses who testified in this
case, and the prosecutor, with similar cases.
The medical evidence described in this report
shows that axonal injury, subdural bleeding,
and retinal bleeding can be caused by a variety
of causes, and these lesions are not necessarily
signs of injuries caused by trauma, as the
state witnesses and the prosecutor claimed.
Section
I. Review
of Francine Ream Yurko’s Medical Records
During Her Pregnancy With Alan Ream, and Analysis
of Her Health Problems
TOC
||
List
of Tables
Francine
Ream Yurko is a white female. She was 27 years old when her son, Alan
Ream Yurko was born five weeks premature on September 16, 1997. Alan is
her second child. The review of her medical records revealed that she
suffered from multiple chronic illnesses during her pregnancy with Alan.
She suffered from chronic spastic colon, loss of appetite, dehydration,
gestational diabetes, anemia, chronic urinary infection, vaginal infection
with group B Streptococcus, hemorrhoids, and oligohydramnios [1-5]. Her
weight was 130 lb at the start of her pregnancy in January of 1997, dropped
to 120 lb, and then returned to 130 lb on July 19, 1997. At the time of
delivery on September 16, 1997, her weight was 132 lb, so that she had
gained only 2 lb during her entire pregnancy. The currently recommended
weight gain for pregnancy is 25 to 30 lb.
The
results of Francine’s blood analysis and her glucose tolerance tests
performed during her pregnancy with Alan are presented in Table
1 and Table 2. These data indicate that she suffered from chronic
anemia and gestational diabetes. Her red blood cell count, hemoglobin
levels, and the hematocrit were low, and she had high blood and urine
glucose levels. The elevated fasting blood glucose levels and the abnormal
results of the glucose tolerance tests indicate that her gestational diabetes
was serious. The glucose levels in urine of both tests were high. The
date of urine and blood analysis indicates that Francine’s problem
with diabetes probably started at least three months prior to delivery.
Furthermore,
the high white blood cell counts and the results of urine culture show
that Francine was also suffering from chronic bacterial infections. A
urine culture test for bacteria was performed on June 25, 1997 and August
13, 1997. It revealed that she had urinary tract Escherichia coli (E.
coli) infection. E. coli was identified in both tests at growth levels
of 100,000 colony per mL of urine. She was treated with antibiotics.
Furthermore,
she was diagnosed with a vaginal infection with group B Streptococcus
and treated with amoxicillin and ampicillin on September 15, 1997, at
one day prior to delivery. She was also treated with Anusol-HC ointment
for hemorrhoids; acetaminophen for pain and fever; propoxyphene napsylate
for pain; and ferrous sulfate for anemia. In addition, on September 15,
1997, her gynecologist performed an ultrasound prenatal exam and discovered
that she had oligohydramnios. She lost the amniotic fluid completely without
noticing. This suggests that she lost the fluid gradually over a period
of days or even weeks, and/or there was a serious reduction in the production
of the fluid.
The
discovery of oligohydramnios led to the decision by her doctor to induce
labor chemically on 9/15/97 at 35 weeks gestation. The labor was induced
by pitocin. She was also given pain medications (nalbuphrine, butorphanol,
and promethazine). Baby Alan was born on 9/16/1997 at 2:15 PM, five weeks
premature. Francine left the hospital on 9/17/97 at 4:35 PM without her
baby. Baby Alan stayed in the Intensive Care Unit because of his respiratory
distress syndrome and other health problems. A detailed description of
Alan’s health problems following birth is presented in Section II
below.
Section
II. Review
of Alan Ream Yurko’s Medical Records From the Time of Birth on September
16th, to November 24, 1997, and Analysis of His Health Problems
TOC
||
List
of Tables
II-A.
Alan’s health problems during the first week of life
Baby Alan was born five weeks premature on 9/16/1997 at 2:15 PM. His weight
was 5 lb and 9 ounces, and head circumference was 31.3 cm. Immediately following
birth, the baby had grunting respirations with sternal and rib retractions.
The mother observed a persistent grayish color to the baby. At approximately
2 hours after birth, a blood glucose test revealed that he had a glucose
level of 37 mg/dL, and his follow-up glucose level was 32 mg/dL.His blood
glucose levels were below the low normal value of glucose in infants of
45 mg/dL. The baby suffered from hypoglycemia. Furthermore, his arterial
blood gasses on room air revealed that he suffered from hypoxia and acidosis.
The PCO2 and PO2 levels were 42 and 43 mm Hg, respectively. Also, the baby
had a low serum creatinine level of 0.4 mg/dL, which is 80% of low normal
(normal range is 0.6-1.2 mg/dL). Creatinine is a marker of muscle development,
and a low value indicates that the baby had low muscle mass. The infant
was placed in an oxyhood with 50%O2 to treat his hypoxia. Also, he was treated
with ampicillin and gentamicin to fight bacterial infections.
The baby's 7-day hospital course was complicated by continuing respiratory
distress, and he spent three days in the intensive care unit. A chest
x-ray showed persistent pulmonary infiltrates. Furthermore, Alan had neonatal
jaundice as indicated by elevated serum bilirubin levels, with a maximum
bilirubin level of l7.4 mg/dL at 3 days of age. His serum bilirubin levels
are presented in Table
3.
These health problems are commonly reported in preterm infants. For example,
Sanchez et al. conducted a prospective surveillance of 97 (50 girls and
47 boys) preterm infants younger than 37 weeks of gestation. They found
that the majority (64%) of infants had hyaline membrane disease, and 41%
developed chronic lung disease (CLD). Also, ninety-three infants (96%)
had experienced apnea of prematurity. The maximum intervention for apnea
was theophylline therapy in 21 infants, nasal continuous positive airway
pressure (CPAP) in 23 infants, and mechanical ventilation in 45 infants.
In addition, forty-seven infants (48%) had an intraventricular hemorrhage.
A total of 33 episodes of sepsis occurred among 26 infants, and 3 of them
developed meningitis [6].
Gestational
diabetes, oligohydramnios, and jaundice usually have tremendous impact
on fetal and postnatal development. Below are brief descriptions of health
problems observed during pregnancy and in children associated with these
conditions.
(II-A)
1. Gestational diabetes and associated health risk in fetus and infant
Diabetic mothers have high blood glucose levels. Glucose crosses the placenta
and leads to excessive fetal insulin secretion. Infants of diabetic mothers
frequently are hypoglycemic at birth, as it happened in the case of baby
Alan. His blood glucose level was 32 mg/dL, which is below the low normal
value for newborn of 45 mg/dL. The pancreatic islets of these infants
are hyperplastic because the mother called on the insulin supply of the
fetus during gestation [7-10]. Furthermore, pregnancy in diabetics is
usually associated with a higher prenatal mortality (3 to 5 percent vs.
1 to 2 percent in nondiabetic women) and a higher incidence of congenital
anomalies (6 to 12 percent vs. 2 to 3 percent in nondiabetic) [7].
Also,
hyperinsulinemia has been linked to hypoxemia in the fetus. It leads to
an increase in oxygen consumption and a decrease in arterial oxygen content.
When such a fetus becomes hypoxic, the maternal hyperglycemia accentuates
the rise in lactate and the decline in pH in the fetus. There is also
increased erythropoietin-induced red blood cell production in response
to fetal hypoxia, resulting in polycythemia in the neonate [10, pg 283].
Alan was suffering from hypoxia and acidosis at birth. His arterial blood
gasses on room air were 42 mm Hg for the PCO2 and 43 mm Hg for the PO2.
Gestational
diabetes can also lead to fetal macrosomia (large body size), and increases
the risk for birth trauma [7-9]. Macrosomia usually results from the increase
of body fat and the stimulation of growth by insulin [9]. Baby Alan’s
birth weight was 5 lb and 9 ounces. However, his serum creatinine level
was 0.4 mg/dL, which is 80% of low normal (normal range is 0.6-1.2 mg/dL).
Creatinine is a marker of muscle development and low value indicates low
muscle mass.
Also,
infants of diabetic pregnancies can develop hyperbilirubinemia, and factors
implicated have included preterm birth and polycythemia with hemolysis.
Venous hematocrits of 65 to 70% have been observed in as many as 40% of
these infants. Renal vein thrombosis has also been reported to result
from polycythemia [9]. Baby Alan had neonatal jaundice, as indicated by
high levels of serum bilirubin reaching a maximum level of l7.4 mg/dL
at 3 days of age (Table
3).
Furthermore,
infants of diabetic mothers, as contrasted with those of nondiabetic mothers,
have almost a six-fold increased risk in developing respiratory distress
syndrome (RDS), even when all confounding variable are taken into account.
The incidence of RDS is also inversely proportional to the gestational
age. It is estimated to occur in about 15 to 20% of those born between
32 and 36 weeks. Immaturity of the fetal lung in preterm infants is the
basis of surfactant deficiency. The production of surfactant increases
gradually after the appearance of type II alveolar cells, but the largest
increase occurs after 35 weeks of gestation [11, p. 483]. It appears that
baby Alan had two risk factors for RDS: premature birth at 35 weeks and
a diabetic mother. These facts explain the severity of his RDS condition.
He spent three days in the intensive care unit immediately after birth,
and one week in the hospital as a result of this illness. Also, his respiratory
problem continued after leaving the hospital.
(II-A)
2. The impact of oligohydramnios on the infant’s health and development
On
September 15, 1997, Francine visited her gynecologist for a prenatal exam.
He performed an ultrasound exam and discovered that she was suffering
from oligohydramnios. She lost the amniotic fluid completely without noticing.
Her condition indicated that she had premature rupture of the membrane
and/or there was a serious fetal development problem that led to a reduction
in renal output. The discovery of oligohydramnios led to the decision
by her doctor to induce labor chemically on 9/15/97 at 35 weeks of gestation.
Labor was induced by pitocin.
Oligohydramnios
is thought to be a reflection of fetal compromise in most circumstances.
A decrease in placental perfusion results in decreased blood flow, and,
therefore, decreased oxygen delivery to the fetus. There is also decreased
renal perfusion by the preferential shunting of blood to the fetal brain.
Decreased renal perfusion results in decreased urine output, which leads
to a decreased amniotic fluid volume. Amniotic fluid production increases
from 120 ml per day at 20 weeks to 1200 ml per day at term [12].
Dr.
Douglas Shanklin, the defense expert witness (pathologist) examined the
H & E stained kidney section of baby Alan microscopically and found
that his kidneys were not fully developed. He concluded that the child
had a developmental problem [13]. Dr. Shanklin’s finding may explain
the mother’s problem with oligohydramnios. Alan’s kidneys were
underdeveloped, and that led to the reduction in urine output and the
volume of the amniotic fluid.
Oligohydramnios
is commonly associated with fetal growth retardation, increased risk of
preterm delivery, and admission to a neonatal intensive care unit. In
a study involving 7582 high-risk obstetric referral patients, the corrected
prenatal mortality (PNM) rate for patients with normal amniotic fluid
volume was 1.97 in 1000. In patients with oligohydramnios, the PNM rate
increased over 5-fold to 10.4 in 1000 [11, p. 141].
The
patient with oligohydramnios is three times more likely to deliver preterm
and 30 times more likely to be induced for fetal indications than those
with normal amniotic fluid volume [12, p. 354]. Birth weight less than
10th percentile for gestational age at delivery is also common in pregnancies
with oligohydramnios. Chauhan et al. did a MEDLINE search and reviewed
all studies published in English between 1987 and 1997 that correlated
antepartum or intrapartum amniotic fluid index with adverse peripartum
outcomes. They found that an antepartum or intrapartum amniotic fluid
index of </=5.0 cm is associated with a significantly increased risk
of cesarean delivery for fetal distress, and with a low Apgar score at
5 minutes. They also found a few reports linking amniotic fluid index
and neonatal acidosis
[14].
Also,
fetal deformities have been observed in conditions of chronic oligohydramnios.
It is generally associated with genitourinary tract anomalies that inhibit
urination (renal agenesis, polycystic kidneys, and urinary obstruction).
Prolonged oligohydramnios, particularly during the critical period of
fetal pulmonary development, can cause pulmonary hypoplasia. Positional
deformities (skeletal and facial abnormalities) are also common in chronic
oligohydramnios (12). Furthermore, the antepartum testing records of 779
women seen over a 12-month period were reviewed, and it has been found
that antepartum oligohydramnios is associated with an increased risk of
fetal heart rate abnormalities [15].
(II-A)
3. The pathology of jaundice in infants
Baby Alan suffered from neonatal jaundice. His serum bilirubin levels
were l7.4 and 13.2 mg/dL at 3 and 7 days of age, respectively (Table
3).
In the full-term newborn, physiologic jaundice is characterized by a progressive
rise in serum unconjugated bilirubin concentration from approximately
2 mg/dL in cord blood to a mean peak of 5 to 6 mg/dL between 60 and 72
hours of age in white infants. This is followed by a rapid decline to
approximately 2 mg/dL by the fifth day of life. During the period from
the fifth to tenth day of life in white infants, serum bilirubin concentrations
decline slowly, reaching the normal adult value of less than 1.3 mg/dL.
However, in premature neonates, physiologic jaundice is more severe than
in the full-term neonates, with mean peak concentrations reaching 10 to
12 mg/dL by the fifth day of life. This delay in reaching normal concentration
of less than 1.3 mg/dL as compared with the full-term neonates reflects
the delay primarily in maturation of hepatic glucuronyl transferase activity
in the premature neonate [12].
Bilirubin
is one of the products of heme catabolism. It is a weak acid and not water
soluble or readily excreted at pH 7.40 without conjugation with glucuronic
acid in the liver. It can penetrate the blood brain barrier and cause
neurological problems. Hyperbilirubinemia is capable of producing a spectrum
of neurological dysfunction in the newborn, ranging from transient mild
encephalopathy to permanent sever neurological impairment secondary to
neuronal necrosis (12, p. 1324). A mean peak unconjugated bilirubin concentrations
of 10 to 12 mg/dL may cause bilirubin encephalopathy in certain high-risk,
low-birth-weight neonates [12, p. 1317]. Brain stem auditory evoked response
(BAER) studies showed significant prolongation of latencies of waves III,
IV-V, and interpeak I-III and I-V in neonates with moderate unconjugated
hyperbilirubinemia (10 to 20 mg/dL) compared with those of similar gestational
and postnatal ages without hyperbilirubinemia. This suggests interference
with brain stem conduction.
Furthermore,
approximately half of all infants with kernicterus observed at autopsy
also have extraneural lesions of bilirubin toxicity. These include necrosis
of renal tubular cells, intestinal cells, and pancreatic cells in association
with intracellular crystals of bilirubin. The term kernicterus has been
traditionally used to describe the pathology of bilirubin toxicity within
the brain (necrosis followed by gliosis).
Bilirubin
usually binds with serum albumin, and this complex does not cross the
brain barrier. The bilirubin-binding capacity of albumin is decreased
in sick premature and full-term human neonates. In addition, serum albumin
is lower in these patients. Ampicillin and other antibiotics can displace
bilirubin from albumin and make it free, which enhances the CNS toxicity
of bilirubin. Hypoxemia also increases CNS permeability to bilirubin.
Baby Alan had moderate bilirubin levels of l7.4 and 13.2 mg/dL at 3 and
7 days of age, respectively. However, his treatment with antibiotics (ampicillin
and gentamicin) that bind with albumin might have increased the toxicity
of bilirubin by increasing the level of unbound bilirubin [12]. He also
suffered from hypoxia, which also increases bilirubin toxicity.
Dr.
Douglas Shanklin, the defense expert witness (pathologist), examined the
H & E stained sections of the brain and spinal cord in Alan’s
case and found evidence of neurological damage in both brain and spinal
cord that occurred at about 10-12 weeks prior to the baby’s death.
He found evidence of nerve cells necrosis and axonal injury in the brain
and spinal cord. He also reported the replacement of nerve tissue by hundreds
of small blood vessels. Furthermore, he observed an old infarction and
deposition of calcium in the spinal cord [13]. I believe that bilirubin
caused these old lesions in the brain and spinal cord in this case.
TOC
Continue
to Page 2
References
[1]
Medical records of Francine Ream (1997). Florida Hospital, Orlando Florida.
[2] Medical records of Francine Ream (1997). Birthing Cottage of
Winter Park,
Inc., 434 Grove Avenue, Winter Park, Florida.
[3] Medical records of Francine Ream (1997). Fairview Hospital,
Cleveland Ohio.
[4] Buttram, HE, M.D. and Yazbak, E., M.D. Shaken Baby Syndrome
or Vaccine-Induced Encephalomyelitis? The Story of Baby Alan.
[http://www.freeyurko.bizland.com/storyofbabyalan.html]
[5] Yurko, Alan R. Hyperbilirubinemia and Kernicterus in the
Case of Alan Yurko.
[http://www.freeyurko.bizland.com/kernic.html]
[6] Sanchez PJ, Laptook AR, Fisher L, Sumner J, Risser RC, Perlman
JM. Apnea after immunization of preterm infants. J Pediatr 1997;
130(5):746-51.
[7] Harrison’s Principles of Internal Medicine. 14th
edition. Editors: Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin
JB, Kasper DL, Hauser SL, Longo DL. McGraw-Hill, New York, 1998.
[8] Pathology, Second Edition. Editors: Rubin, E and Farber,
JL. J. B. Lippincott Company, Philadelphia, 1994.
[9] Williams Obstetrics, 21st Edition, 2001. Editors: Cunningham
FG, Gant NF, Leveno KJ, Gilstrap LC, Hauth JC, Wenstrom KD. McGraw-Hill,
New York.
[10] Neonatal-Perinatal Medicine, Volume 1, Seventh edition,
2002. Editors: Fanaroff AA and Martin RJ. Mosby, St. Louis, Missouri.
[11] Pathologic Basis of Disease, Third edition, 1984. Editors:
Robbins SL, Cortran RS, and Kumar V. W. B. Saunders Company, Philadelphia,
USA.
[12] Neonatal-Perinatal Medicine, Volume 2, Seventh Edition,
2002. Editors: Fanaroff AA and Martin RJ. Mosby, St. Louis, Missouri.
[13] Jury Trial Document for the trial of Alan Yurko, February
22-24, 1999. Orlando, Florida.
[14] Chauhan SP, Sanderson M, Hendrix NW, Magann EF, Devoe LD.
Perinatal outcome and amniotic fluid index in the antepartum and intrapartum
periods: A meta-analysis. Am J Obstet Gynecol 1999 Dec;181(6):1473-8
[15] Voxman EG, Tran S, Wing DA. Low amniotic fluid index as a
predictor of adverse perinatal outcome. J Perinatol 2002 Jun;22(4):282-5.
[16] Doctors charts for Alan Ream Yurko, weekly exams for October
10, 1997 through November 11, 1997.
[17] Physicians’ Desk Reference, Edition 53, 1999.
Medical Economics Company, Inc, Montavale, NJ, USA.
[18] Sen S, Cloete Y, Hassan K, Buss P. Adverse events following
vaccination in premature infants. Acta Paediatr 2001; 90(8):916-20.
[19] Botham SJ, Isaacs D, Henderson-Smart DJ. Incidence of apnoea
and bradycardia in preterm infants following DTPw and Hib immunization:
a prospective study. J Paediatr Child Health 1997; 33(5):418-21
.
[20] Slack MH, Schapira D. Severe apnoeas following immunisation
in premature infants. Arch Dis Child Fetal Neonatal Ed. 1999; 81(1):F67-8.
[21] Botham SJ, Isaacs D. Incidence of apnoea and bradycardia in
preterm infants following triple antigen immunization. J Paediatr Child
Health 1994; 30(6):533-5.
[22] Braun MM, Mootrey GT, Salive ME, Chen RT, Ellenberg SS. Infant
immunization with acellular pertussis vaccines in the United States: assessment
of the first two years' data from the Vaccine Adverse Event Reporting
System (VAERS). Pediatrics 2000; 106(4):E51 [23] Medical records
of Alan Ream Yurko (1997). Princeton Hospital, Florida.
[24] Medical records of Alan Ream Yurko (1997). Florida Hospital,
Orlando, Florida.
[25] Spurgeon D. Study shows which children at greatest risk of
cerebral oedema in diabetic crisis. BMJ 2001; 322:258.
[26] Glaser N, Barnett P, McCaslin I, Nelson D, Trainor J, Louie
J, Kaufman F, Quayle K, Roaback M, Malley R, and Kuppermann N. Risk factors
for cerebral edema in children with diabetic ketoacidosis. N Engl J
Med 2001; 344:264-69.
[27] Bureau MA, Begin R, Berthiaume Y, Shapcott D, Khoury K, and
Gagnon N. Cerebral hypoxia from bicarbonate infusion in diabetic acidosis.
Journal of Pediatrics 1980; 96:968-73.
[28] Shashi B. Gore, MD, MPH, autopsy report for Alan Ream-Yurko
(sic), case # MEH-1064-97, 1997. Office of The Medical Examiner, District
Nine, 1401 Lucerne Terrace, Orlando, Florida 32806-2014.
[29] Dolinak D, Smith C, Graham DI. Hypoglycaemia is a cause of
axonal injury. Neuropathol Appl Neurobiol 2000; 26(5):448-53.
[30] Dolinak D, Smith C, Graham DI. Global hypoxia per se is an
unusual cause of axonal injury. Acta Neuropathol (Berl) 2000; 100(5):553-60.
[31] Kaur B, Rutty GN, Timperley WR. The possible role of hypoxia
in the formation of axonal bulbs. J Clin Pathol 1999; 52(3):203-9
[32] Oehmichen M, Meissner C, Schmidt V, Pedal I, Konig HG. Pontine
axonal injury after brain trauma and nontraumatic hypoxic-ischemic brain
damage. Int J Legal Med 1999; 112(4):261-7.
[33] Oehmichen M, Meissner C, Schmidt V, Pedal I, Konig HG, Saternus
KS. Axonal injury--a diagnostic tool in forensic neuropathology? A review.
Forensic Sci Int 1998; 95(1):67-83.
[34] Shannon P, Smith CR, Deck J, Ang LC, Ho M, Becker L. Axonal
injury and the neuropathology of Shaken Baby Syndrome. Acta Neuropathol
(Berl).
1998; 95(6):625-31.
[35] Hartmann RW Jr. Radiological case of the month. Rib fractures
produced by birth trauma. Arch Pediatr Adolesc Med 1997; 151(9):947-8.
[36] Rizzolo PJ, Coleman PR. Neonatal rib fracture: birth trauma
or child abuse? J Fam Pract 1989; 29(5):561-3.
[37] Cumming WA. Neonatal skeletal fractures. Birth trauma or child
abuse? J Can Assoc Radiol 1979; 30 (1):30-3.
TOC
Continue
to Page 2
|
