MAIN CONTENTS

List of Tables

PAGE 3 CONTENTS:

Section III (cont.) Review of Alan Ream Yurko’s Medical Records During His Hospitalization on November 24 Through 29, 1997, and Analysis of His Health Problems
B. Events and treatments at Florida Hospital
C. Analysis of hospital events and clinical data [click]

References [click]

III-B. Events and treatments at Florida Hospital
Baby Alan was transferred to Florida Hospital, Orlando and arrived at about 2:15 PM on November 24, 1997 [24]. His blood pressure and temperature were 40/20 and 98 F, respectively. He was placed on life support. Blood analysis at 2:40 PM revealed that his blood pH was 7.10, PCO2 of 60.5 mm Hg, PO2 of 151 mm Hg, and bicarbonate of 17.9 mEq/dL. The baby was treated with a long list of medications to treat dehydration, hypokalemia, metabolic and respiratory acidosis, infections, and fever. Also, he was given red blood cells and heparin. The list of medications given between 2:15-11:05 PM on November 24th is presented in Table 7. The blood pH rose from 7.10 at 2:40 PM to 7.67 (metabolic alkalosis) at 11:00 PM as a result of the bicarbonate treatment (Table 8). His temperature was 98 F at 2:20 PM and became 105.8 F at 6:00 PM. It dropped to 103 F at 8:00 PM due to the treatment with high therapeutic doses of antibiotics, Motrin, and Tylenol (Tables 7 and 8).

Furthermore, at 2:45 PM baby Alan was given heparin at a dose level of 2 cc per hour (500 IU/ml) by intravenous infusion. With the baby’s weight at 4.57 kg, the resulting effective heparin dose was 219 IU/kg per hour. The Physicians’ Desk Reference (PDR) recommends the following pediatric dosage schedule: initial dose of 50 units/kg IV drip, and maintenance dose of 100 units/ kg (IV drip) every four hours, or 25 units/kg per hour [17, p. 3306]. Heparin inhibits reactions that lead to the clotting of blood and the formation of fibrin clots both in vitro and in vivo. Heparin acts on multiple sites in the normal coagulation. Clotting time is prolonged by full therapeutic doses of heparin in most cases. Heparin also induces the formation of white clot due to the aggregation of platelets. At 3:15 PM, at about 30 minutes post-heparin infusion, blood analysis showed increased prothrombin time and fibrinogen split product level (Table 9).

The PDR states that bleeding can occur at virtually any site in patients receiving heparin. Fall in hematocrit, fall in blood pressure, or any other unexplained symptoms should lead to serious consideration of a potential hemorrhagic event. Heparin sodium should be used with extreme caution in disease states in which there is increased danger of hemorrhage. Baby Alan had hypotension (Table 10) and his hematocrit was very low (25.3%). The normal range for hematocrit is 36.5-52%.

A computerized tomography scan of the brain, taken at 7:50 PM (at about five hours following the start of heparin infusion) showed a right subdural hematoma, intraparenchymal hemorrhage in the right frontal region, and some mass affect in the right cerebral hemisphere. An ophthalmologist examined Alan’s eyes and found minimal right internal hemorrhages. At 4:21 PM, chest x-ray showed bilateral pulmonary infiltrates and healing fractures of the 6th rib. Dr. Scott Mahan stated that review of the bony structure revealed an old, healing fracture of left posterior rib #6 in the midclavicular line. The remaining bony structures revealed no significant abnormalities.

On November 25th, baby Alan was treated with a sedative, potassium, fluid, heparin, sodium bicarbonate, neuromuscular blocker, and antihistamine. The list of medications is presented in Table 11. This second sodium bicarbonate infusion was started at 8:00 AM as treatment for acidosis. However, the blood pH was 7.67 (highly alkaline) at 11:00 PM of the previous night, and it was 7.61 at 3:40 AM on November 25th. At this time, the baby was suffering from metabolic alkalosis, thus the treatment with bicarbonate was not justified. Metabolic alkalosis causes hypoxia by increasing the binding of oxygen with hemoglobin and preventing the release of oxygen to the tissues [7, 25, 26, 27].

At 8:00 AM, the baby was also given heparin by infusion similar to the dose given on November 24th (described above—219 IU/kg per hour). This treatment was not justified at all, because heparin at high therapeutic dosage should not be given to any patient suffering from bleeding and hypotension [17]. Baby Alan had a bleeding gastric ulcer, subdural hemorrhage, bleeding in the brain, and hypotension. The platelet count prior to the administration of heparin on November 24th was 571,000/µL of blood, dropping to 397,000/µL (30% reduction) at 5:45 AM on November 25, 1997 (at about 15 hours following the start of the first heparin infusion). Heparin increases the tendency of platelets to aggregate and form a clot. Blood analysis values of November 24th through November 27th are presented in Table 12.

In the first twenty-four hours after admission, the baby received 525.8 mL of fluid by IV; 10 mL by nasogastric tube (NG); 60 mL red blood cells; and 130 mL plasmanate. His total intake was 725.8 mL. However, his 24-hour output was 786 mL (756 mL urine and 30 mL from NG). The net output was 60.2 mL.

The baby was given a sedative, red blood cells, and plasmanate from November 26th through 28th. He was also given antidiuretic hormone on November 28th (Table 11). The results of the blood analysis are presented in Table 12 and Table 13. On November 26th, his serum glucose dropped to a normal level of 95 mg/dL from 397 mg/dL (76% reduction) on November 24, 1997. Also, on November 26th, the LDH, alkaline phosphate, and SGPT levels dropped by 70%, 47%, and 19% respectively from their levels on November 24. On 11/26/97, the total white blood cell count was reduced by 35% from the level on November 24th. This clearly indicates that the baby had liver and pancreas bacterial infections, and his infections were resolved because of the treatment with antibiotics (Table 6 and Table 7).

The baby was declared brain dead on November 27, 1997, at about 75 hours following the hospital admission. Autopsy was performed on November 29, 1997. Prior to autopsy, his heart, liver, pancreas, and a portion of his intestine were taken by Translife for transplantation.

III-C. Analysis of hospital events and clinical data
Francine stated that her baby Alan developed a high-pitched cry, and his skin became warm to touch at about 10 or 11 days following receiving his six vaccines listed in Table 5. Also, she observed the baby in a state of increasing lethargy with a declining feeding pattern [4, 16]. On the morning of November 24, the father was alone at home with the baby and his 4-year old sister. The father observed that, in rapid succession, the baby began wheezing, then spit up, then stopped breathing. While attempting mouth-to-mouth breathing, and going (daughter in tow) to a neighbor's house to borrow a car, the father rushed the baby to the Princeton Hospital of Orlando, where the baby was eventually resuscitated. Alan also stated that he did not shake his baby.

My review of the medical records of baby Alan obtained from Princeton and Florida hospitals and described above [III] confirmed Francine and Alan Yurko’s stories. Baby Alan’s blood analysis results of November 24, 1997 (Table 8, Table 12) revealed that he was suffering from diabetes mellitus and complications of diabetes such as cardiac arrest, apnea, hypokalemia, metabolic and respiratory acidosis, and infections.

Baby Alan’s serum glucose levels at 12:09 and 3:15 PM were 337 and 397 mg/dL, respectively. Normal serum glucose rage is 70-110 mg/dL. His blood pH was 7.18 at 12:09 PM and dropped to 7.1 at 2:40 PM (Table 8). His serum potassium level was 4.9 mEq/L at 12:09 PM and dropped to 2.3 mEq/L at 5:45 AM on 11/25/97 following treatment with excessive amount of sodium bicarbonate (blood pH was 7.6-7.7). His hypokalemia was severe. He was treated with potassium solutions by IV infusion several times on November 24th-25th (Table 7, Table 11). Also, he had elevated white blood cell count (20, 900/µL), elevated LDH (1148% of normal), alkaline phosphatase (202% of normal), and SGOT (414% of normal). His anion gap was 22 mEq/L.

Furthermore, at the time of admission to Princeton Hospital, the baby had a gastric ulcer, and his corneas were cloudy. Chest x-rays taken on November 24th showed lung infiltrate, which is a sign of lung infection. The elevated white blood cell count (20, 900/µL) and temperature (105.8 F at 6:00 PM) are other signs of bacterial infection.

In metabolic acidosis resulting from diabetes, potassium usually leaves the intracellular environment because the intracellular proteins bind with hydrogen, which leads to cardiac arrest and paralysis of the respiratory muscles. At this stage, serum potassium levels are usually normal or elevated, but after treatment with bicarbonate and elevation of pH to normal or above normal, the potassium leaves the blood and goes back inside the cells. This leads to hypokalemia, as we observed in this case. At time of admission, baby Alan had no muscle tone, no intestinal movement, and his abdomen was distended. Harrison’s Principles of Internal Medicine states that in metabolic acidosis, initial serum potassium concentrations are normal to high, despite depletion of body stores, and potassium concentrations fall rapidly during therapy with sodium bicarbonate, predisposing the patient to cardiac arrhythmias and/or paralysis of the respiratory muscles [7, p. 2060].

Baby Alan had all the symptoms and complications of diabetes as described in the medical literature, such as metabolic acidosis, cardiac arrest (hyperkalemia), cardiac arrhythmias (due to hypokalemia), infections, fever, cerebral edema, and gastric ulcer [7, 8, 11]. In diabetic children, cerebral edema is a common cause of death, and more frequent than in adults. Baby Alan had cerebral edema, as stated in the autopsy report [28]. The medical examiner, Dr. Shashi B. Gore reported that “the brain appears very edematous, shiny and fluffy. Differentiation of the cortex and medulla appears poor and the ventricles are slightly reduced in size. Cerebral edema is confirmed.”

Dr. Ben Guedes also confirmed on November 24th at Princeton Hospital that the baby had a gastric ulcer. Dr. Guedes stated that the child developed bleeding from the gastrostomy tube due to stress ulcer. The child was treated with cimetidine (histamine H2-receptor antagonist) in the hospital for his ulcer (Table 11). The presence of gastric ulcer can explain the inability of the baby to take his food at home in the days prior to his cardiac arrest on November 24th. In Florida Hospital, the baby was given 10 mL of liquid by a nasogastric tube (NG) on November 24th through November 25th, and 30 mL came back through the NG tube, as described above (III A).

Furthermore, baby Alan had metabolic acidosis, as indicated by low blood pH (7.1), high blood PCO2 level (74 mm Hg), low blood bicarbonate level (17.9 mEq/L), and high anion gap (22 mEq/L). In diabetic patients, the metabolic acidosis and anion gap are almost totally accounted for by the elevated plasma levels of acetoacetate and beta-hydroxybutyrate, although other acids (e.g., lactate, free fatty acids, phosphates) contribute [7]. Baby Alan was treated with sodium bicarbonate to correct his blood acidosis. However, he was given excessive amount of bicarbonate. His blood pH was 7.1 at 2:40 PM on November 24, 1997 and rose to 7.67 at 11:00 PM (Table 8). In addition, he was again given bicarbonate by IV infusion at 8:00 AM on November 25th (Table 11), and his blood pH was 7.61 at 3:40 AM of the same day (Table 8).

Harrison’s Principles of Internal Medicine states that bicarbonate therapy may be indicated in severely acidotic patients (PH 7.0 or below), especially if hypotension is present (acidosis itself can cause vascular collapse). Bicarbonate is not used routinely in less acutely ill subjects, because rapid alkalinization may have detrimental effects on oxygen therapy (7, p. 2073). Alkalinization increases the avidity of hemoglobin to bind oxygen, impairing the release of oxygen in peripheral tissues. The hemoglobin-oxygen dissociation curve is normal in diabetic ketoacidosis because of opposing effects of acidosis and deficiency of red blood cell 2,3-bisphosphoglycerate (2,3-BPG). If acidosis is rapidly reversed, the deficiency of 2,3-BPG becomes manifest, increasing the avidity with which hemoglobin binds oxygen. If bicarbonate is given, the infusion should be stopped when the pH reaches 7.2 to minimize possible detrimental side effects and to prevent metabolic alkalosis as circulating ketones are metabolized to bicarbonate with reversal of ketoacidosis. The key parameters to follow are the pH and the calculated anion gap.

It is very obvious that these vital treatment recommendations were not followed in baby Alan’s case, and that his treatment with excessive amount of bicarbonate led to severe hypoxia and cerebral edema [25-27]. Furthermore, baby Alan suffered from hypoxia as a result of his severe anemia, as shown by very low hemoglobin (7.8 g/dL), hematocrit (25.3%), and low RBC (2.61 x 10(6)/µL). His apnea, cardiac arrest, and hypotension also resulted in hypoxia and general ischemia of the brain.

Dehydration, polyurea, weight loss, and wasting are symptoms and complications of diabetes mellitus. In the first twenty-four hours, baby Alan received 525.8 mL of fluid by IV; 10 mL by nasogastric tube (NG); 60 mL red blood cells; and 130 mL plasmanate. His total intake was 725.8 mL. However, his twenty-four hour output was 786 mL (756 mL urine and 30 mL from NG). The net output was 60.2 mL. He was dehydrated in spite of receiving adequate amount of fluid by IV infusion (Tables 6, 7 and 11).

Moreover, the baby was treated with antidiuretic hormone (DDAVP) on November 28th to prevent dehydration (Table 13). DDAVP is a synthetic analog of the natural pituitary hormone 8-arginine vasopressin (ADH), an antidiuretic hormone affecting renal conservation. On November 24th, the baby’s weight was 10.05 pounds; on November 29th, his weight was 9.0 lb. He lost 1.05 lb (10% of his weight) in five days during his stay in the hospital despite treatment with relatively high volume of fluid IV and antidiuretic hormone. Also, his average serum creatinine value on November 24th was 0.45 mg/dL (75% of low normal value) and dropped to 0.2 mg/dL (33% of low normal) on November 27th (Table 12). Low creatinine is an indicator of low muscle mass and wasting disease.

The clinical data indicate that Alan’s diabetes resulted from bacterial infection of the pancreas, and may have been due to infections of other organs. It has been stated that the metabolic decompensation of diabetes is due to a relative or absolute deficiency of insulin and a relative or absolute excess of glucagons [7]. Stress hyperglycemia, usually associated with infections and other life-threatening illnesses, is due to release of glucagons and catecholamines [7, p. 2061]. Bacterial and mycotic infections complicate the life of the diabetic, in whom hyperglycemia is poorly controlled. Multiple abnormalities in the host response to microbial invasion have been described in such patients. Leukocyte functions are compromised and immune response is blunted [7].

Blood analysis performed on November 24th prior to Alan receiving treatment with antibiotics shows that his white blood cells were elevated (20,900/µL). Also, he had elevated serum glucose level of 337 mg/dL, LDH level of 2411 IU/L (1148% of normal), alkaline phosphatase level of 255 IU/L ( 202% of normal), and SGOT level of 207 IU/L (414% of normal). He also had elevated anion gap of 22 mEq/L (Table 12). The treatment with high therapeutic doses of three types of antibiotics on November 24th resulted in significant reduction in serum glucose, liver enzymes, and anion gap levels (Tables 6, 7, 12). On November 26th, the serum glucose level was 95 mg/dL (normal), with low values for the following: LDH, 733 IU/L (reduced by 70%); alkaline phosphatase, 135 IU/L (reduced by 47%); SGOT, 167 IU/L (reduced by 19%); and anion gap 11 mEq/L (50% reduction). (Table 12).

On November 24th, baby Alan was treated with three types of antibiotic IVs to fight bacterial infections (Table 6 and 7). These included: 20 mg gentamicin (recommended dose 7.5 mg/kg/day); 300 mg rocephin (recommended dose 50-75 mg/kg/day); and 222 mg Claforan (recommended dose 50-180 mg/kg/day). Gentamicin sulfate is a water-soluble antibiotic of the aminoglycoside group. Intravenous administration of gentamicin is used to treat patients with bacterial septicemia or those in shock. Gentamicin is indicated in the treatment of serious infections caused by susceptible strains of Pseudomonas aeruginosa, Proteus species, Escherichia coli, Klebsiella-Enrtrobacter-Serratia species, Citrobacter species, and Staphylococcus species [17, pg 2845].

Rocephin is a semisynthetic, broad-spectrum antibiotic. The bactericidal activity of rocephin results from inhibition of cell wall synthesis. It has a high degree of stability in the presence of beta-lactamases (both penicillinases and cephalosporinases) of gram-negative and gram-positive bacteria [17, p. 2694]. Rocephin is usually used to treat the following systemic infections: 1) bacterial septicemia caused by Staphylococcus aureus, Streptococcus pneumonia, Escherichia coli, Haemohilus influenza or Klebsiella pneumonia, 2) meningitis caused by Haemophilus influenzae, Neisseria meningitides or Streptococcus pneumonia, 3) lower respiratory infections caused by Streptoccocus pneumonia, Staphyloccus aureus, Haemophilus influenza, Staphylococcus parainfluenza, Klebsiella pneumonia, Escherichia coli, Enterobacter aerogenes, Proteus mirabilis or Serratia marcescens.

Claforan (cefotaxime sodium) is a semisynthetic, broad spectrum cephalosporin antibiotic. The antibacterial activity of cefotaxime results from inhibition of cell-wall synthesis, and it has in-vitro activity against a wide range of gram-positive and gram-negative organisms [17, p. 1318]. Cefotaxime is indicated for the treatment of serious infections caused by susceptible strains of the designated microorganisms in these diseases: 1) lower respiratory infections, including pneumonia caused by Streptococcus pneumonia, Streptococcus pyogenes, Staphylococcus aureus, Escherichia coli, Klebsiella species, Haemophilus influenzae, Haemophilus parainfluenzae, Proteus mirabilis, Serratia marcescens, Enterobacter species, indole positive Proteus and Pseudomonas species; 2) central nervous system infections, e.g., meningitis and ventriculitis caused by Streptococcus pneumonia, Klebsiella pneumonia, and Escherichia coli; 3) bacteremia/septicemia caused by Escherichia coli, Klebsiella species, Serratia marcescens, Staphylococcus aureus, and Streptococcus species (including S. pneumonia).

Furthermore, at 2:45 PM, baby Alan was given heparin at a dose level of 2 cc per hour of 50% heparin sodium (500 IU/ml) by intravenous infusion. Heparin is a heterogeneous group of straight-chain anionic mucopolysaccharides, called glycosaminoglycans, having anticoagulant properties [17]. It inhibits reactions that lead to the clotting of blood and the formation of fibrin clots both in vitro and in vivo, acting on multiple sites in the normal coagulation cascade. Clotting time is prolonged by full therapeutic doses of heparin in most cases. Each one mL of heparin sodium injection, USP contains 1,000 units heparin sodium and 10 mg benzyl alcohol as a preservative. With the baby’s weight at 4.57 kg, the resulting effective heparin dose was 219 IU/kg per hour. The Physicians’ Desk Reference (PDR) recommends 50 units/kg IV as initial dose for infants and children, and a maintenance dose of 100 unit/ kg (IV, drip) every four hours, or 25 unit/kg per hour [17, p. 3306].

A computerized tomography scan of the brain taken at 7:50 PM (at about five hours following the start of heparin infusion) showed a right subdural hematoma and intraparenchymal hemorrhage in the right frontal region of the cerebral hemisphere. Based on the dose of heparin infused to the baby (219 IU/kg per hour), the estimated total dose of heparin 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 [17].

Hemorrhage can occur at virtually any site in patients receiving heparin. Patients suffering from anemia, any unexplained symptoms, and/or having low blood pressure are at the greatest risk of having serious hemorrhagic events after receiving a therapeutic dose of heparin. Alan had hypotension, and his hematocrit was very low (25.3%). The normal range for hematocrit is 36.5-52%. In addition, the baby was treated with adenosine, a potent vasodilator in most vascular beds, and causes significant hypotension (Table 7 and Table 11).

Heparin sodium should be used with extreme caution in disease states where there is increased danger of hemorrhage. In addition to serious bleeding, heparin has been found to induce the formation of white clot due to the aggregation of platelets and to reduce the platelet count due to consumption. At 3:15 PM, at about 30 minutes post-heparin infusion, blood analysis showed increases in fibrinogen split product (160 µg/mL) and prothrombin time (11.6 seconds), which are 1600 % and 115% of normal respectively. Platelet count prior to the administration of heparin on November 24th was 571,000/µL of blood, and dropped to 397,000/µL (30% reduction) at 5:45 AM on November 25, 1997 (at about 15 hours following the start of the first heparin infusion). Blood analysis values of November 24th through November 27th are presented in Table 12.

Alan was given heparin again at 8:00 AM on November 25th by IV infusion at a dose similar to that of November 24th, described above (219 IU/kg per hour). This treatment was not justified at all, because heparin at high therapeutic dosage should not be given to any patient suffering from bleeding, hypotension, and anemia [17]. Baby Alan had bleeding gastric ulcer, subdural hemorrhage, bleeding in the brain, and hypotension. One day later, on November 26th, the fibrinogen split product value and prothrombin time returned to normal. This indicates that the elevation of these values were associated with the heparin treatment.

Furthermore, the baby was suffering from metabolic alkalosis as a result of his treatment with excessive amounts of sodium bicarbonate, and this condition causes hypoxia, as described above. His blood pH and bicarbonate levels at 3:40 AM on November 25th were 7.61 and 30.4 mEq/L, respectively (Table 8). He was also given bicarbonate by IV infusion at 8:00 AM on November 25th at the time of his treatment with heparin (Table 11).

An ophthalmologist examined the baby’s eyes and observed minimal bleeding in the retina of the right eye. Many risk factors existed in Alan’s case that usually lead to retinal bleeding. These include: 1) diabetes—retinal hemorrhage, including hemorrhage in the inner retinal areas and superficial nerve fiber layer, and preretinal hemorrhage, is commonly described in patients suffering from diabetes [7], 2) hypoxia as a result of severe anemia, apnea, hypotension, metabolic and respiratory acidosis, and metabolic alkalosis from the excessive use of bicarbonate, 3) probable corneal infection, as indicated at the time of hospital admission on November 24th (his corneas were cloudy).

The treating physician, Dr. Ben Guedes examined Alan on November 24th and found no signs of injuries except a small reddish linear bruise under the right eye. Dr. Guedes stated that the tympanic membranes were clear—no hemotympanum—and the mouth was free of injury externally. Moreover, examination of the thorax, both anterior and posterior, and examination of the extremities did not reveal any bruise or other injury. In addition, Dr. Scott Mahan reviewed the chest x-ray taken on November 24th and found no significant abnormalities in the bony structure except for an old healing fracture of left posterior rib #6 in the midclavicular line.

In conclusion, baby Alan’s many health complications resulted from being diabetic and from the treatment received in the hospital on November 24-25/1997. These complications included: hyperglycemia; metabolic acidosis and respiratory acidosis; dehydration; weight loss; cardiac arrest; apnea; metabolic alkalosis; hypokalemia; cardiac dysrhythmias; subdural hemorrhage and bleeding in the brain (a result of excessive treatment with heparin, hypotension, and severe hypoxia); systemic infections; retinal hemorrhage and corneal edema; liver damage (elevated liver enzymes, heart damage (LDH was very high); and anemia.

The Medical Examiner, Dr. Shashi Gore, and other physicians who testified in court that baby Alan died as a result of “Shaken Baby Syndrome” overlooked the clinical data described in this report and based their conclusions on a theory only. My review of the autopsy report and the testimonies of the state expert witnesses revealed that these witnesses did not take the time to review all relevant data. My review and analysis of the autopsy report and testimonies of witnesses are presented in the next two sections of this report (IV, V).

TOC

Continue to PAGE 4

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 4