Hyperbilirubinemia and Kernicterus
in the Case of Alan Ream Yurko

By Alan R. Yurko

Alan Joseph Ream Yurko was born prematurely at 35 weeks gestation on September l6th, l997. Labor was induced due to oligohydramnios, (severe amniotic fluid deficiency), diagnosed by the delivery physician, Dr. King. There were multiple maternal complications during the pregnancy including an E.coli urinary tract infection, gestational diabetes, vaginal infection with group B Streptococcus, and continual sickness resulting inadequate nutrition and a net weight gain of 2 pounds during the pregnancy. Neonatal complications included severe hypoglycemia, respiratory distress syndrome with severe hypoxia (documented by arterial blood gas studies), dehydration, acidosis, and hyperbilirubinemia. As another predisposing factor, my wife had a long history of "spastic colon" problems and had been warned not to become pregnant, as her colon problem would make her vulnerable to toxemia of pregnancy. Laboratory findings during the neonatal hospitalization, which included 3 days spent in neonatal intensive care unit, included a high count of nucleated red blood cells (a marker for neonatal hypoxia) and other blood cell abnormalities including polychromatophilia, poikilocytosis, and macrocytosis. Alan's gestation, birth, neonatal period and infancy were met with many problems. A chart of laboratory values at birth and death are provided here as an addendum. This report is meant to review the role of hyperbilirubinemia and kernicterus in the case of Alan Yurko and to add to the considerable research done by several experts in the case to date.

The term, hyperbilirubinemia, denotes an excess of bilirubin, a condition which is potentially neurotoxic. Kernicterus is a neurologic syndrome resulting from deposition of unconjugated bilirubin in the brain. It can occur at much lower levels of serum bilirubin in sick or premature infants than in healthy, full-term babies. While the toxic level for healthy infants is listed at or above 25 mgs/dL in current pediatric texts, levels as low or lower than l0 mgs/dL can cause brain damage in a sick or premature infant.. Other predisposing factors to kernicterus include acidosis, lowered albumin levels, hypoxia, free fatty acids (lipids), salicylates (aspirin), antibiotics, and pitocin (used in Alan's mother to induce labor). The mortality rate can exceed 50%. Early symptoms include lethargy, poor feeding, vomiting, and neurological depression, and a high-pitched cry.

Even in normal newborns, serum bilirubin levels temporarily rise due to immaturity of the liver enzyme systems, including those which conjugate and excrete bilirubin, and to a lack of intestinal bacteria which aid in the processing of bilirubin. Serum albumin deficiency, when present, can contribute to the problem. If this is true in healthy newborns, it is far more so in immature and compromised infants.

Recently articles have appeared in the media reviewing the topics of hyperbilirubinemia and kernicterus, which have cited an increasing incidence of jaundice-related brain damage. These articles have expressed concern that doctors in many instances appear to be desensitized to these conditions and release the babies from hospitals without proper testing or follow-up. Others add that medical schools have lost their zeal in instructing doctors in the care of hyperbilirubinemia due to its apparent virtual abolishment in infant mortality statistics. Clinically observable jaundice or serum bilirubin levels exceeding 5 mg/dL within the first 24 hours of life is indicative of a pathological cause of hyperbilirubinemia. In premature infants this level can be much lower. In the instant case, initial serum bilirubin is 4.3 mg/dL. Alan was premature, acidotic, and hypoxic, which would indicate a lowered ceiling in the aforementioned level of 5 mg/dL. Alan's bilirubin levels sharply increased to extremely critical levels in the first week of life, and despite photo-treatments, remained that way as shown below:

Date: 9/17 9/17 9/18 9/19 9/19 9/20 9/21 9/22 9/23
Time: 0620 1800 0540 2215 0515 0430 0545 0630 0455
Level: 4.3 6.5H 8.0H 12.8H 17.4H 14.6H 14.8H 12.6H 13.2 mgs/dL

These levels were not given proper context in the role of hyperbilirubinemia in Alan's death. Alan was discharged with dangerously high bilirubin levels and without any prescribed treatment or follow-ups. Pediatric records show that he was extremely jaundiced for approximately 30 days until the pediatrician instructed us to expose Alan to short periods of sunlight as photo-therapy, which did seemingly clear the jaundice. However, the jaundice was manifest the entire neonatal period and beyond. This causes one to ponder the brain damage which may have occurred in a severely compromised infant as a result of prolonged elevation of bilirubin, which remained critically high and was actually rising when the baby was discharged from the hospital. A discussion of bilirubin metabolism is warranted to understand this in depth.

Overview of Bilirubin Metabolism:
Bilirubin is an insoluble waste product. To be excreted, it must be made water-soluble. This transformation in the body takes place in five steps: formation, plasma transport, liver uptake, conjugation, and biliary excretion.

l) Formation: 250 to 350 mgs of bilirubin forms daily in humans. 70-80% derives from breakdown of red blood cells (RBCs). The remaining 20 to 30% comes from heme proteins located mostly in the bone marrow and liver. As RBCs break down, hemoglobin (Hgb) is degraded to iron and the intermediate product, biliverdin, by an enzyme called heme-oxygenase. Then, another enzyme called biliverdin reductase converts biliverdin to bilirubin. These steps primarily occur in the reticuloendothelial (mononuclear phagocyte) system. Increased hemolysis is the primary and most significant cause of increased bilirubin levels. Infants have greater erythrocyte concentrations; thus increased hemolysis.

2) Plasma Transport: Bilirubin is not water soluble due to its internal hydrogen bonding. Unconjugated bilirubin (UCB) (or "early-labeled" or indirect-reacting bilirubin as it is alternately termed) is therefore transported in the plasma, where it binds to albumin. Since the albumin-bound bilirubin cannot pass through the renal glomerular membranes, it does not appear in the urine. However, the binding weakens under certain conditions such as acidosis or in premature infants with lower serum albumin. Also, sulfonamides and salicylates will compete for the binding sites.

CASE NOTE: Alan's laboratory values show only one report of indirect bilirubin (ll.5 mgs/dL on September 2l, l997). Whether this was given as a simple subtraction of direct bilirubin from total bilirubin, or whether it was detected in the urine is unclear.

3) Liver Uptake: Absorption or uptake of bilirubin is via active transport. It takes place rapidly and does not include the uptake of bound albumin. Beyond this the details are unclear and complicated, including complex intracellular binding proteins such as ligandin and Y protein.

4) Conjugation: Conjugated bilirubin (CBR)(also termed "late-labeled" or direct-reacting bilirubin) is processed in the liver when UBR is conjugated with glucuronic acid to form bilirubin diglucuronide, brought about by the enzyme glucuronyl transferase. This process renders the bilirubin water-soluble, enabling it to be excreted by the kidneys.

5) Biliary Excretion: CBR is secreted into the bile. Organic anions can affect this complicated process. Bacterial flora in the intestines deconjugate and reduce bilirubin to compounds called stercobilinogens. Most are excreted in the stool giving it its brown pigment. Small amounts do reach the urine as urobilinogen.

CASE NOTE: In the present case, virtually all of the risk factors were present for brain damage from kernicterus, as previously reviewed, including prematurity, hypoxia, acidosis, hypoglycemia, and ongoing respiratory distress. Severely affected infants show signs of anemia, as in the case under discussion. Neonatal hyperbilirubinemia would also have been increased as a result of hemolysis from hematomas, as well as brain hematomas, and the swallowing of blood from nose bleeds, which occurred during intubations during days in the neonatal intensive care unit. Oxytocin (pitocin) is also connected as a cause, as well as administration of salicylates and antibiotics following birth. Maternal predisposing complications included gestational diabetes, chronic urinary infection, and chronic sickness during pregnancy resulting in malnutrition and almost total failure in weight gain.

Kernicterus is defined as brain damage due to the deposition of bilirubin in the basal ganglia and brain stem nuclei. Bilirubin itself cannot cross the blood-brain barrier because of its binding to albumin. However, lipid-soluble indirect bilirubin may cross the blood brain barrier and enter the brain by diffusion if the bilirubin-binding capacity of albumin and other plasma proteins is exceeded by the increase in free bilirubin levels. There was only one serum albumin determination during the neonatal hospitalization (3.8 gms/100ml on 9/22/97), which was in the lower range of normal. However, even this capacity was likely to have been exceeded when there were other substances competing with binding sites: 1)The mother's labor was induced by pitocin. 2) Perpetual acidosis during the newborn hospitalization resulted in an excess of hydrogen ions. 3) Salicylates (aspirin) as well as antibiotics were given to the infant, and 4) free fatty acids were administered by tube feedings for several days.

Discussion and Conclusions:
During the immediate newborn period of Alan Joe Ream Yurko, labored breathing was immediately apparent with marked rib and sternal retractions on inspiration. My wife and I noted a persistent dusky color of our baby. An Accu-Check approximately two hours after birth was 37; a follow-up blood glucose was 32. Arterial blood gasses during the same time period showed severe acidosis and hypoxia with a pH of 7.38, CO2 42, and pO2 of 43 (normal pO2: 85-105). Either one of these complications (hypoglycemia and hypoxia) may be sufficient to cause significant brain damage in the newborn, but when one adds the likelihood of brain damage from hyperbilirubinemia, as reviewed here, there is a high probability that significant brain damage took place surrounding birth and the neonatal period.

It is pertinent to point out that the defense witness, Dr. Douglas R. Shanklin, in his testimony during my trial, reviewed a pathological slide of the spinal cord in which he described extensive nerve degeneration as well as extensive "revascularization." From the presence of the revascularization, which was necessarily a slow process, Dr. Shanklin concluded that the brain damage must have taken place during the birth process or neonatal period, as supported by the findings presented here. It was especially remarkable since he had limited medical records for review at the time, as he commented on during his testimony.
During the testimonies of the state witnesses, in contrast, there is no mention at any point of any awareness of these newborn complications or on their bearing on the tragic course of subsequent events. One witness who reviewed the slides, in fact, denied seeing any evidence of hypoxia on the post-mortem slides. He could not and would not have made such a statement if he had carefully reviewed the medical records of the neonatal hospitalization. Another of the state witnesses was compelled to admit, under oath, that he had neither sought nor read the newborn hospital records. Each and every one of these, it would appear, never considered the possibility that there may have been causes other than shaken baby syndrome leading to my son's death.

As a final observation, our baby might have survived, damaged as he was, had it not been for the vaccines. As reviewed in more detail elsewhere (see "Story of Baby Alan"), it was almost certainly the 6 vaccines given at the 8th week of life which triggered the train of events leading my son's death and which were misinterpreted as shaken baby syndrome, with the onset of cerebral edema ll days post-vaccines, abrupt onset of apnea 3 days later, and the onset of a small area of subdural bleeding at time of the terminal hospital admission, as shown on a brain Ct scan. The bleeding in turn would have been due to increased blood vessel fragility, which has been shown to be a possible complication of the pertussis vaccine, and torsion on the blood vessels from the brain edema, the latter also a possible complication from pertussis vaccine, as well as findings indicative of meningitis (mononuclear infiltrates of the meninges), as described by the defense witness.

Finally, the fact that intravenous administration of heparin on both the first and second days of the terminal hospitalization may have contributed to an extension of the original relatively small hemorrhage into the two massive bilateral hemorrhages found at autopsy, possibly also aggravated by manipulations during the resuscitation process during the terminal hospital admission. Kernicterus along with several other serious complications, fulminated by childhood vaccines, and followed by premature heparinization and other iatrogenic factors killed my son. I did not.



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Florida Hospital; Medical records of Alan Joseph Ream-Yurko (1997).

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Newman TB & Maisels MJ, Evaluation and treatment of jaundice in the term-newborn: A kinder and gentler approach (l992).

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Taylor PM et al, Hyperbilirubinemia in infants of diabetic mothers, Biol Neonate,5:289 (l963).

State of Florida vs Alan R. Yurko; complete trial transcripts, depositions, and court records (1999).

USA TODAY, 26 October, 2000, "Jaundice-linked brain damage on the rise," by Julie Appleby.

Alan Yurko

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