Mohammed Ali Al-Bayati, PhD, DABT, DABVT
Toxicologist & Pathologist
150 Bloom Dr. Dixon, CA 95620
Phone: (707) 678-4484
Fax: (707) 678-8505
Yurko Home Page
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
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.
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).
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
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).
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).
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.
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.
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
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.
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.
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.
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
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.
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,
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.
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.
second state witness, Dr. Guedes (the treating physician) did not reveal
to the court the following important events that show the baby died of
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.
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!
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.
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 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.
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.
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.
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.
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.
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
Alan’s health problems during the first week of life
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