Analysis of Causes That Led to Baby Alan Ream Yurko’s
Cardiac Arrest and Death in November of 1997

by Mohammed Ali Al-Bayati, PhD, DABT, DABVT
Toxicologist & Pathologist

Toxi-Health International
150 Bloom Dr. Dixon, CA 95620
Phone: (707) 678-4484
Fax: (707) 678-8505

TABLE OF CONTENTS || Free Yurko Home Page

List of Tables

Section I. Review of Francine Ream Yurko’s Medical Records During Her Pregnancy
With Alan Ream, and Analysis of Her Health Problems

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
A. Alan’s health problems during his first week of life
1. Gestational diabetes and associated health risk in fetus and infant
2. The impact of oligohydramnios on the infant’s health and development
3. The pathology of jaundice in infants

[Page 2]
B. Case history of baby Alan from one week of age to the time of his hospitalization
on November 24, 1997
C. Adverse reactions to vaccines in premature and healthy children

Section III. Review of Alan Ream Yurko’s Medical Records During His Hospitalization
on November 24 Through 29, 1997, and Analysis of His Health Problems

A. Clinical events and treatments at Princeton hospital

[Page 3]
B. Events and treatments at Florida Hospital
C. Analysis of hospital events and clinical data

[Page 4]
IV. Analysis of the Medical Examiner’s Autopsy Report and His Court Testimony
in the Case of Baby Alan

A. General appearance
B. Microscopic examination of the heart and liver function tests
C. Subdural hemorrhage, brain
D. Subdural hemorrhage, spinal cord
E. Bleeding inside the brain
F. Meningitis
G. Diffuse axonal injury
H. Retinal hemorrhage
I. Pneumonia and lungs hemorrhage
J. Rib fracture
K. Superficial bruise and contusions

[Page 5]
V. Review of Alan R.Yurko’s Jury Trial, Analysis of Expert Witnesses’ Testimonies
and the State’s Claim

A. Review of Dr. Ben Guedes’ testimony
B. Review of Dr. Matthew A. Seibel’s testimony
C. Review of Dr. Gary Steven Pearl’s testimony
D. Review of Dr. Douglas R. Shanklin’s testimony
E. Analysis of the State’s claim

Section VI. Conclusions and Recommendations

References [click]

List of Tables

Table 1. Blood analysis values for Francine (June-September 1997) [click]
Table 2. Results of the glucose tolerance tests performed during Francine’s pregnancy with Alan
Table 3. Alan’s serum bilirubin levels
Table 4. Baby Alan’s growth measurements [click]
Table 5. Composition of vaccines administered to baby Alan on November 11, 1997, per Physicians’ Desk Reference
Table 6. Medications given to baby Alan at Princeton Hospital on 11/24/97
Table 7. Medications given to baby Alan in Florida Hospital on November 24, 1997
Table 8. Baby Alan’s blood gases measurements [click]
Table 9. Coagulation parameters for Alan Ream Yurko 11/24-26/97 [click]
Table 10. Baby Alan’s blood pressure, heart rate, and temperature [click]
Table 11. Medications given to baby Alan in Florida Hospital from November 25-29, 1997 [click]
Table 12. Blood and serum analysis for Alan Ream Yurko, November 24-27/1997 (during his hospitalization) [click]
Table 13. Blood and serum analysis results for Alan Ream Yurko on 11/28/1997 [click]


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.


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[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.
[5] Yurko, Alan R. Hyperbilirubinemia and Kernicterus in the Case of Alan Yurko.
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[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.
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.


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