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					VIRGINIA:                                                           08/29/2001

IN RE: TREVOR ELLINGTON                       Opinion by Colville
       Infant complainant                     Deputy Commissioner

                      VWC File No. B-00-24

Larry A. Pochucha, Esquire
5206 Markel Road, Suite 200
P.O. Box 11787
Richmond, VA 23230
For Deobrah, Robert and Trevor Ellington

Michael J. Miller, Esquire
809 Cameron Street
Alexandria, VA 22314
Co-counsel for Deborah, Robert and Trevor Ellington

Wirt P. Marks, IV, Esquire
W. Scott Johnson, Esquire
700 East Main Street
Suite 1015
P.O. Box 1474
Richmond, VA 23218-1474
Counsels for Duncan C. MacIvor, M.D.

Scott J. Fitzgerald, Esquire
Assistant Attorney General
900 East Main Street
Richmond, VA 23219
For the Virginia Birth-Related Neurological
Injury Compensation Program.

        Hearing before Chief Deputy Commissioner Colville in Richmond, Virginia, on March 30,

                                   PROCEDURAL HISTORY

        On May 5, 2000 Trevor Ellington, by his next friend and mother, Deborah Ellington, filed a

Motion for Judgment against Duncan C. MacIvor, M.D. in the Circuit Court of the City of
                                                                            VWC File No. B-00-24

Richmond. The case was assigned the number LL-888-3. Subsequently, Dr. MacIvor, by counsel,

moved to refer this matter to the Virginia Workers‟ Compensation Commission [Commission] for

the determination of whether the action satisfied the requirements of the Virginia Birth Related

Neurological Injury Compensation Act pursuant to Section 8.01-273.1, Code of Virginia. This

motion was granted and on September 26, 2000 the Circuit Court judge transferred the case and

stayed proceedings at the Circuit Court pending disposition by the Commission.

                                      PRESENT PROCEEDINGS

        On November 15, 2000 counsel for Dr. MacIvor filed an original and five copies of the

medical records in the case and in his letter set forth a summary of events and requested that the

Commission determine that Trevor Ellington [infant] sustained a brain injury that constituted a

birth-related neurological injury as defined by Section 38.2-5001, Code of Virginia.


        In its Response filed by the Birth-Related Neurological Injury Compensation Program

[Program] on December 15, 2000 the Program admitted that Dr. MacIvor was a participating

physician at the time of the infant‟s October 13, 1998 birth and that St. Mary‟s Hospital was a

participating hospital at the time of the infant‟s birth.


        The Program denied that the infant is permanently motorically disabled and

developmentally disabled and denied that the infant suffered a birth-related neurological injury as

defined by Section 38.2-5001, Code of Virginia. It sought to have the Commission determine that

the Program has rebutted the presumption that the infant complainant meets the definition.

                                                                             VWC File No. B-00-24

However, in his April 27, 2001 memorandum, counsel for the Program admitted that the infant was

sufficiently impaired to qualify for inclusion in the Program.


        By letter dated April 10, 2001 counsel for the Program related that he had an opportunity to

review the transcripts of depositions of Dr. Donald Taylor and Dr. Kathryn Kerkering taken prior to

the Circuit Court transfer of the case. He had no objection to their consideration. Thus, all medical

records and doctor‟s depositions obtained in conjunction with the pending Circuit Court case are

made a part of this record along with the medical records and expert testimony offered before and at

the pending hearing.

        Pursuant to leave granted at the hearing Dr. MacIvor‟s memorandum, filed by counsel on

April 16, 2001 is made a part of this record as is the memorandum of Trevor Ellington, filed by

counsel on April 27, 2001 and the memorandum of the Program, filed by counsel on April 27,

2001. At the time of the hearing the parties discussed the possibility of a further reply within three

to four days. Counsel for Dr. MacIvor filed a reply on May 3, 2001 which was made a part of this

record. The record was closed at that time.

                                 SUMMARY OF THE EVIDENCE

        The medical records in this case are voluminous and will not be repeated in detail except

where the information is significant to the experts who have expressed opinions in this case or

significant in evaluating their opinions.

        Mrs. Ellington was thirty-two years old of age at the time that the infant was born on

October 13, 1998. She had two prior pregnancies. The first pregnancy resulted in the delivery of a

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five pound nine ounce baby at 38 weeks gestation and the second pregnancy resulted in the delivery

of a five pound one ounce baby at 35 weeks following a spontaneous rupture of membrane. There

is no indication of any neurological or developmental difficulties in either child.

       Dr. Duncan C. MacIvor attended Mrs. Ellington during the pregnancy at issue. His records

are handwritten and are not altogether readable. According to his October 22, 1998 discharge

summary, there was no evidence of a significant viral illness during Mrs. Ellington‟s pregnancy

except for a possible episode of diarrhea that took place in early October. Her due date was

calculated to be November 3, 1998 from an earlier ultrasound. He wrote that two visits prior to

delivery, the “baby had seemed appropriate for gestational age and the amniotic fluid volume was

adequate.” Mrs. Ellington reportedly called his office reporting some brown discharge but without

contractions. She also reportedly indicated that there was fetal movement. Then the following day

she returned to the office. At that time he noted a reduced amniotic fluid volume without evidence

of a rupture of the membrane. He thought that the placenta did not look “overly mature.” He

decided to obtain a consultation by Dr. Fay Redwine, a perinatologist.

       However, Dr. Daniel G. Jenkins, a practicing obstetrician in Williamsburg who was

retained by the Program to review the medical records, noted in his December 5, 2000 report that

the fetus was small during the scans that took place at 12, 20, 24, 29, 30, 24 4/7, 35 3/7 and 37

weeks with a sonographic worksheet noted for only two of the scans, the first at 20 weeks and the

second at the 34 3/7 weeks. According to Dr. Jenkins, fetal size was small by almost two weeks

and femur length was off 3 weeks as of the 20 week scan. As of October 2, 1998 the abdominal

circumference was smaller by three weeks and the femur length smaller by 6 weeks as of October 2,

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1998. Worksheets were not available for the other visits but he reported that “asymmetric growth

retardation was clearly evident. A firm diagnosis of the IUGR was made by Dr. MacIvor at 37

weeks when referral was made.”

        According to Dr. Redwine‟s October 13, 1998 consultation, she conducted a complete OB

ultrasound, biophysical profile and doppler echocardiography for an intrauterine growth retardation.

She found that the amniotic fluid volume was normal but that the gestation age summary reflected

that the infant was at 30 weeks 5 days whereas he was actually at 37 weeks, which reflected an

intrauterine growth retardation. As reflected in the fetal surveillance, “[t]he fetal biophysical profile

scored 2/8 with –2 for breathing, -2 for movement, and –2 for tone. Doppler Evaluation: S/D ratio

7/67. There is reverse diastolic flow. This is nonreassuring fetal surveillance.” She recommended

continuous monitoring and delivery with a suspicion of a pleural effusion.

        In his October 13, 1998 admission report at St. Mary‟s Hospital, Dr. MacIvor then wrote

that the “pregnancy has been marked by decelerating fetal growth and when she had reached 37

weeks gestation and was noted to have oligohydramnios on office ultrasound as well as significant

intrauterine growth retardation, consultation was obtained from Dr. Fay Redwine who concurred

with these diagnoses and actually recommended immediate delivery.”

        Mrs. Ellington was sent to the labor room of the hospital. According to Dr. MacIvor‟s

discharge summary, upon her arrival in the labor room Mrs. Ellington was placed on the monitor.

He went on to write “[a]bout 10 minutes later, she had her first known spontaneous contraction,

which was accompanied by severe decelerations, and preparations were made for immediate C-

section.” The primary cesarean section was reportedly conducted for a diagnosed intrauterine

                                                                           VWC File No. B-00-24

growth retardation with oligohydramnios and nonreassuring fetal heart rate tracing.

       According to Dr. Jenkins‟ report, when she was placed on a monitor, the tracing was

nonreactive until ten minutes but there was a contraction. This was reportedly “followed by a 6-

minute deceleration to a 70 beat-per-minute heart rate. This was followed by a lesser deceleration.”

He wrote that the infant was delivered with meconium staining but not below the cords and

weighed 4 pounds, one ounce at 37 weeks. Apgars were 2 at one minute, 7 at five minutes and 8 at

ten minutes.

       The infant was intubated and responded to resuscitation. An initial pH was reportedly not

performed at birth but at one half an hour was 7.15. The infant was transferred to special care

nursery and was shortly thereafter in mild respiratory distress. Dr. Devin B. Al-Mateen initiated

neonatal treatment effective October 15, 1998. Dr. Al-Mateen ordered an October 19, 1998 head

ultrasound to rule out bleeding. This was interpreted by Dr. Douglas Cook as showing Grade 1

right subependymal hemorrhage. When the infant experienced seizures then Dr. Alan Taylor, a

pediatric neurologist, was brought in for a consultation effective October 20, 1998. In neurological

terms he found seizure activity, a depressive mental state and also a relatively small head

circumference. He ordered an October 22, 1998 head CT scan which was read by Dr. Jamette

Worthington as showing Grade II intracranial hemorrhage. During his stay in the hospital, Dr.

Kathryn W. Kerkering, a neonatologist, evaluated the infant on the weekend of October 31 and on

November 1, 998 as she was on call for Dr. Al-Mateen.

       As reflected in his November 5, 1998 discharge summary, Dr. Al-Mateen diagnosed

respiratory problems after birth, transient neonatal thrombocytopenia, convulsions, transitory

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neonatal electrolyte disturbances, hypocalcemia & hypomagnesemia, secondary thrombocytopenia,

fetal growth retardation, unspecified and congenital chordee. The infant reportedly had undergone

continuous mechanical ventilation of at least 96 hours, insertion of endotracheal tube, spinal tap,

arterial catheterization, venous catheterization, transfusion of platelets and circumcision.

        The infant underwent a January 19, 2000 MRI of the brain ordered by Dr. Taylor. It was

interpreted by Dr. Janette Worthington as showing “[g]eneralized loss of whit matter volume and

abnormality of signal intensity throughout the existing deep whit matter of both cerebral

hemispheres most consistent with a blobal insult (hypoxic, ischemic, or inflammatory) which may

have been periatal.”

        Following the discharge the infant was followed by Dr. Kerkering until February 17, 2000

and was neurologically followed by Dr. Taylor. Dr. Taylor ordered a February 24, 1999 CT of the

head which was compared with that previously performed on October 22, 1998. The radiologist

wrote that there was a diffuse decrease in cerebral white matter with increased focal areas of

encephalomalacia. According to the radiologist, the pattern suggested a diffuse hypoxic/ischemic

injury although there was an admonition that the injury should be correlated clinically. A January

19, 2000 brain MRI ordered by Dr. Taylor revealed that the cerebral white matter volume was

severely diminished. The infant was ultimately diagnosed with cerebral palsy.

        In his December 5, 2000 report, Dr. Jenkins opined that the infant sustained an injury to the

brain caused by deprivation of oxygen which rendered the infant permanently motorically and

developmentally disabled and that he would be permanently in need of assistance in all activities of

daily living. In his August 25, 2000 deposition Dr. Taylor likewise opined that the infant would be

                                                                             VWC File No. B-00-24

permanently and severely disabled in all aspects of life and that he would never be able to provide

any care for himself. [Taylor dep. 47].

       The Commission has received numerous expert opinions concerning the cause of the

cerebral palsy. Doctors Al-Mateen, Kerkering and Taylor, all of whom treated the infant, the latter

two for a lengthier period of time, expressed their opinions in depositions. In addition, the

Commission has received a December 5, 2000 report from Dr. Jenkins who was retained by the

Program to evaluate the records and a March 26, 2001 report of Dr. William N.P. Herbert filed in

accordance with Section 38.2-5008(B), Code of Virginia. Lastly the Commission received live

testimony from Dr. Mathew Frank, who was retained by Dr. MacIvor to offer evidence and from

Dr. Victor Borden, who was retained by the parents to offer evidence.

       Dr. Al-Mateen, board certified for pediatrics, neonatal and perinatal medicine, treated the

infant only during the initial hospitalization following the birth starting on October 15, 1998. He

offered testimony in two depositions with the first on September 5, 2000 in conjunction with the

malpractice suit and the second, on March 9, 2001 in conjunction with the present action.

       At the time of his September 5, 2000 deposition, he was basically asked about the treatment

rendered during the initial hospitilization. He observed that at birth the infant was cynaolic without

respiratory effort with delivery through meconium stained fluid. The lack of respiratory effort was

not deemed unusual within the first minute because there are some babies that have trouble making

the transition. The infant was immediately intubated and suctioned with no meconiuim below the

cords. [Al-Mateen dep. #1, 16]. The Apgars reflected that the infant stabilized and this would

again have simply reflected a delayed transition. [Al-Mateen dep. #1, 17]. The O2 saturation was

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low but this would have been otherwise thought to have a problem with transition. [Al-Mateen

dep. #1, 17-18]. Overall the findings from October 13, 1998 showed mild respiratory distress

which was not frightening to something worse to happen. [Al-Mateen dep. #1, 20]. He observed

that the blood gas showed respiratory acidosis with a Ph of 7.15 showing a baby with a build up of

acid with the CO2 of 62 meaning that the source of the acid was respiratory. As a result, the

implication was that the source of the acidosis was pulmonary rather than metabolic. [Al-Mateen

dep. #1, 21]. In addition, the infant had asymmetrical growth retardation which in the infant‟s case

was a head size at a different percentile than the rest of the baby. This would imply that there was

some in utero placental insufficiency that led the body to try to spare the head as with low oxygen

or low nutrition the fetus will give preferential blood flow to the brain. [Al-Mateen dep. #1, 24-25].

They ruled out an infection but were not really able to rule out a chronic intrauterine hypoxia. [Al-

Mateen dep. #1 30]. He explained that the meconium stained fluid means that the infant expelled

meconium in response to some stress which becomes a problem when the stress continues and that

the infant starts taking in deep breaths in utero and sucks in the mecomium. [Al-Mateen dep. #1,

32]. As a rule of thumb he noted that the longer the stressful event, the longer it takes to

resuscitate. In the infant‟s case, the fact that the first Apgar was two showed that something was

going on at one minute but was eight at ten minutes, which is normal. Thus within ten minutes the

infant looked like there was a normal transition from the intrauterine to extrauterine life. [Al-

Mateen dep. #1, 38]. They performed a workup to try to find an etiology of his difficulties but that

the problem with asphyxia is that you are not to really able find it unless it is right away, such as an

abruption of the placenta, a knot in the cord or a mother‟s infection. [At-Mateen dep. #1, 43-44].

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His working impression at the time before the seizures was that there was a chronic intrauterine

infection or intrauterine hypoxia with some acute event around the time of delivery that made some

of the transient laboratory findings. [Al-Mateen dep. #1, 54]. The seizures would not be a

diagnosis by themselves, but rather, would be sign of a problem and would be consistent with an

asphyxial event or an abnormal brain which occurred with a cerebritis that would be consistent with

a viral infection. [Al-Mateen dep. #1, 55]. Overall at the time, everything seemed to fit a perinatal

asphyxia except for the blood gas at the beginning and that the infant responded to resuscitation

quickly. [Al-Mateen dep. #1, 56, 73-74]. At the time of the discharge summary after which time

he did not see the infant, his conclusion was that the seizures and the neurological problems were

secondary to multi organ system involvement of the initial asphysxial event around the time of

delivery. [Al-Mateen dep. #1, 77-78].

       At the time of the second deposition, Dr. Al-Mateen was specifically asked about his

opinions concerning causation. He started out his deposition by expressing that he did not hold an

opinion to a reasonable degree of medical certainty concerning the causes of the infant‟s

neurological conditions or his growth retardation, although the latter could not be attributed to

anything around the time of the delivery. [Al-Mateen dep. #2, 8-9]. He felt that the pH was

acidotic at 7.15 along with the CO2 were consistent with a baby who had an asphyxial event or had

a deprivation of oxygen just before or around the time of delivery rather than a chronic occurrence

or one of several hours duration. [Al-Mateen dep. #2, 9, 12-13]. He again stated that at the time of

the hospital discharge he would have felt pretty certain that other than the growth retardation, the

infant‟s condition would be attributed to the events around the time of delivery. [Al-Mateen dep.

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#2, 16-17]. Overall, the infant has two separate and distinct problems: 1) growth retardation; and

2) neurological problems, the latter of which he attributed to the acute events during this treatment.

However, he acknowledged that the delivery event is not based on any particular event occurring

around delivery, but rather, is based on the pH and the blood gases pieced together. [Al-Mateen

dep. #2, 36]. He estimated that the asphysia occurred sometime within one to two hours before the

delivery as opposed to something going on for months. [Al-Mateen dep. #2, 38]. In particular, the

blood gases of 7.15 and CO2 of 62 are consistent with an acute event around the time of delivery

because it was largely a pure respiratory acidosis without a metabolic component. [Al-Mateen dep.

#2, 40]. Moreover, the fetal heart rate decelerations would point to an acute asphyxial event around

the time of delivery and the fact that the infant was cyanotic at the time of birth would pretty much

indicate a lack of oxygen. {Al-Mateen dep. #2, 42-43]. He did not find any other causes for the

neurological problems other than his conclusion that there was an asphyxial event at the time of the

birth. [Al-Mateen dep. #2, 44].

       In the second part of his deposition, Dr. Al-Mateen expressed that he could not state with

reasonable degree of medical certainty that the neurological problems were related to those events.

However, he then went on to say that his conclusions in the discharge summary were more likely

than not true and were more than 50-50. [Al-Mateen dep. #2, 47-48]. Thus his overall opinion was

that the infant‟s neurological conditions were attributed to something that happened at the time of

delivery. [Al-Mateen dep. #2, 52]. This is because if the infant was having the acute event for

more than an hour then he would have expected the pH to be much lower, the CO2 much higher,

the bicarb much lower and the base deciti would be an increased. [Al-Mateen dep. #2, 53].

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However, he cannot rule out a chronic intrauterine hypoxia contributing to the delivery problems.

[Al-Mateen dep. #2, 57]. Overall, putting everything together, more than likely, the infant had a

chronic intrauterine distress which culminated in fetal distress which led to the passage of

meconium and that fortunately the infant got out but still had seizures that went along with an acute

problem but with the underlying etiology linked to the chronic intrauterine insufficiency. [Al-

Mateen dep. #2 58-59]. Thus, there was a chronic event that was going on that led to an acute event

that led to hypoxic events at delivery. [Al-Mateen dep. #2, 59]. His opinions were expressed as

more than 50% likely rather than reasonable degree of medical certainty as he understood the terms.

[Al-Mateen dep. #2, 68].

       In her September 11, 2000 deposition, Dr. Kerkering, a specialist in pediatrics and neonatal

medicine who initially treated the claimant on October 31 and November 1, 1998 on an on-call

weekend and who later treated the infant from March 19, 1999 until February 17, 2000 reviewed

her course of treatment. She explained that the infant‟s CT Scan at St. Mary‟s Hospital showed a

diffuse decrease in the cerebral white matter volume with a focal encephalmoacia that is a pattern

which is consistent with hypoxic ischemic injury. [Kerkering dep. 26]. She could not precisely

explain why he had the problem but she speculated at the time that it was probably due to an

decreased blood flow to the brain in utero. She reached this conclusion because of the diffuseness

of the brain injury and also due to the fact that it was described as hypoxic ischemic which mean

that at some point there was inadequate circulation to the brain and inadequate oxygenation.

[Kerkering dep. 29]. She did not feel that Apgar scores of 2, 7 and 8 were consistent with asphyxia

at birth although there was some “issue” that occurred at birth which required intervention but these

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scores would suggest that he recovered quite quickly. She noted that children who recover that fast

are usually recovering from an acute event at birth which is quickly reversible. [Kerkering dep. 29,

31]. She could not conclusively state when the damage occurred and whether thee was any damage

caused by the event at the time of delivery. [Kerkering dep. 31]. However, she felt that it was more

likely than not that the infant‟s condition was the result of something in utero or genetics as

opposed to something at birth. [Kerkering dep. 62].

       In his August 25, 2000 deposition, Dr. David Alan Taylor identified that he exclusively

practices in pediatric neurology. He verified that he initially evaluated the infant on October 20,

1998. In neurological terms the infant then had seizure activity, a depressed mental state and had a

relatively small head circumference. With reference to the then CT scan, he stated that at that point

in time he had offered the opinion that the overall course was the most consistent with a subacute

and relatively prolonged hypoxic-ischemic encephalopathy that went back to prior to birth. [Taylor

dep. 13]. Two pages later he indicated that the clinical course was most consistent with a prolonged

injury to the brain or an early injury to the brain by which he meant a problem that began prior to

birth but he did not specifically rule out an infection based on his notes and recollection. [Taylor

dep. 15]. He explained that the primary basis for that conclusion were the multiple problems that

the infant had that clearly existed prior to the onset of labor and birth. By way of examples he

referenced that the infant was small for his gestational age, that there was excessive amniotic fluid,

that the infant had developmental abnormalities of the body that including the hypospadias and that

the infant was below the 10th percentile in the size of his head all of which would suggest a more

long-term process. [Taylor dep. 16]. Looking back in time he thought that as of October 23, 1998

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he would most likely have considered labor and delivery but felt that a longer term process was

most likely the cause. [Taylor dep. 16]. According to Dr. Taylor, he continued to treat the infant

and in over a two year period of treatment he did not recall a point in time that his conclusion

changed. He again expressed the belief that the hypoxic-ischemic injury could have been an

important if not the main part of the injury with an infection in utero possibly having been ruled in

or out as he had no recollection about the latter. [Taylor dep. 25-26]. He recalled that on March 31,

1999 Mrs. Ellington called and asked him about the age of the brain injury. [Taylor dep. 26-27].

His answer was that the information they had did not give a definite timing for the injury.

However, he has consistently said both to the Ellingtons and to others that he felt that the injury

went back prior to birth. [Taylor 29]. Thus when he replied to her on April 1, 1999 it would be

quite consistent for him to have said this to her. [Taylor dep. 29]. With reference to the February

24, 1999 CT scan, he expressed that the physician who had read it concluded that it would be

consistent with a hypoxic-ischemic injury and he personally had no reason to think otherwise.

[Taylor dep. 24]. He reached no other conclusion. [Taylor dep. 34].

       In his December 5, 2000 report, Dr. Jenkins outlined the sequence of events leading up to

the delivery and beyond. He noted that in the delivery room, the infant responded to resuscitation

promptly which he felt indicated mild acute asphyxia. He then went on to note the following

sequence of events and opinions:

       He then deteriorated and was on a ventilator for two days and then three days of CPAP,
       which connotes more problems than acute respiratory embarrassment at term. Initial pH
       was not performed at the birth, but a half an hour later was 7.15, placental pathology had a
       microscopic diagnosis which was noted as being withheld. Seizures began and were
       treated. Labs showed rapidly diminishing platelets to 100,000 and then less, with a plaural

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       effusion, and allo-immune thrombocytopentia was suspected. Glucose level was initially 25
       and then normalized. Trevor had negative CMV and other bacterial cultures. He had a
       decreased T4 and an elevated TSH. His chest x-ray showed lungs that were read as ground
       glass in appearance on 10/13, but had cleared by 10/22. Scan of the cranium showed a
       grade I hemorrhage, and head CT showed a grade II intramural hemorrhage. The baby was
       found to have microcephaly, hypospadias, and an echocardiogram showed pulmonary
       hypertension with thickened right ventricle, again connoting a chronic problem in utero
       prior to delivery. Trevor also later developed spastic CP, GERD, cataracts, and has failed to
       grow or develop normally.

       Follow up visits with Dr. Taylor notes that the diffuse decrease in cerebral white matter was
       compatible with hypoxic injury. Dr. Kerkering later felt that the diffuse damage was
       compatible with decreased blood flow to the brain in utero. Dr. Aal-Mateen of MCV, who
       was the perinataologist attending, was quoted in his deposition as feeding that chronic
       utero-placental insufficiency had occurred, and that he had ruled out sepsis but could not
       rule out a chronic viral infection or insult at an early gestation.

       My opinion is that the of the pediatricians involved in the case in that a long-term process
       had occurred. Referral should have been made at 34 weeks, if not earlier, when the number
       of ultrasounds performed at routine visits are considered. The 20-week femur length should
       and could have been followed up, and diagnosis could have possibly been made earlier,
       especially if there was fetal harm early in pregnancy. I do not feel that this would have
       changed the outcome of the pregnancy at all, but it would have made the obstetrician seem
       more astute and taken the onus off himself. Had this child had normal morphology at birth,
       a case could be made for birth trauma, but the patient really never labored, and this prevents
       inclusion in the Virginia Birth-Related Neurological Injury Compensation Act. . .

       In his March 26, 2001 report, Dr. Herbert, Professor and Chair of the Department of

Obstetrics and Gynecology at the University of Virginia, identified that his committee was

compromised of himself, Dr. James E. Ferguson and Dr. Giancarlo all of whom had completed a

fellowship in Maternal-Fetal Medicine and all of whom were certified by the American Board of

Obstetrics and Gynecology, both in general obstetrics and gynecology but also the subspecialty of

Maternal-Fetal Medicine. He related that they reviewed all of the pediatric and obstetric records

that were provided.

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       Thereupon, Dr. Herbert went on to express the following opinions on behalf of his panel:

       The clinical course of both the mother and the child were carefully noted. In thoughtfully
       reviewing this case, in light of the birth-related neurological injury compensation act, it is
       out opinion that criteria for „birth-related neurological injury‟ are not met by the evidence
       presented in this case. Chronic intrauterine hypoxia is strongly suggested by the Doppler
       assessment of the umbilical artery flow. A biophysical profile of 2/8 also suggests an
       abnormal intrauterine environment and is associated with a low pH at and soon after
       delivery. We feel that this child suffered an antepartum and, likely, chronic insult, rather
       than an acute event during the child birth process.

       The attention and care given Trevor by family and health care providers are impressive and
       out compassion goes out to all involved. Nonetheless, the circumstances surrounding this
       birth did not fulfill the criteria for birth-related neurological injury as noted above.

       Dr. Mathew Frank, a board certified pediatric neurologist, testified that in his opinion the

infant sustained a brain injury around the time of labor and delivery on the basis of the results of the

MRI, CT scan and the ultrasound studies performed with an ultra sound the most accurate. He

contended that the ultrasound did not reveal any evidence of a severe hypoxic-ischemic injury. In

particular, the hypoxic event would have occurred three to seven days prior to the ultra sound with

six to seven days probably “stretching it.” He contended that if the injury occurred prior to the date

of delivery then it would have shown on this test. He pointed to the events around the labor and

delivery as the cause. In particular, he pointed to the fact that Dr. MacIvor saw fetal movement the

day before delivery which would be incompatible with the later neurological damage, that the

growth retardation would place the infant at an increased risk, that Dr. Redwine‟s evaluation

showed a child already at greater risk immediately prior to delivery, that there was a severe fetal

heart rate deceleration at the hospital, that the infant had elevated liver enzymes, moderate

meconium present at delivery, that the infant required resuscitation and that growth retardation

                                                                            VWC File No. B-00-24

would place the infant at increased risk of brain injury at the time of labor and delivery. He

admitted that it is not unusual for a child to be not breathing at birth, that the Apgar scores show

that the acute distress was corrected and that the birth as a pretty normal cesarean section but the

baby was not. He admitted that the injury could have occurred prior to labor and delivery and even

earlier than Dr. Redwine‟s evaluation.

       Dr. Victor Borden, a board certified obstetrician, testified that the brain injury was the

product of a poor environment and occurred over a period of several weeks commencing with the

cessation of growth which began on September 18, 1998 and which had already taken place by Dr.

Redwine‟s October 13, 1998 evaluation that had shown the absence of breaking, movement and

tone. He expressed that movement can occur even with a neurological injury, that while meconium

fluid can be a sign of stress this can occur in a normal labor and here was no major significance,

that the 4 to 5 minute labor and delivery did not contribute to the brain injury and did not contain

any event and that the fetal heart deceleration did not contribute to the injury in any meaningful

way. He indicated that Dr. Redwine‟s evaluation revealed only one normal parameter and that was

the amniotic fluid volume which he stated was the last parameter to fail to register. With reference

to the fetal monitors that were set up, there was already a significant lack of variability which

indicated an already stressed fetus which had no reserve and that the deceleration which was noted

thirteen minutes later was not severe and one which a healthy fetus could have easily tolerated.

                                      ISSUE NUMBER ONE

       The initial issue before the Commission is whether Dr. MacIvor has failed to comply with

the procedural requirements of the Act and thus the petition should be dismissed.

     VWC File No. B-00-24

                                                                            VWC File No. B-00-24


        In their April 27, 2001 memorandum, counsel for the parents sought to have Dr. MacIvor‟s

petition dismissed on the basis that it failed to meet the requirements of Section 38.2-5006, Code of

Virginia in that he failed to provide information required by Section 38.2-5004. In particular, it

failed to provide: 1) “[d]ocumentation of expenses and services incurred to date, which indicates

whether such expenses and services have been paid for, and if so, by whom” [paragraph i]; and 2)

“[d]ocumentation of any applicable private or governmental source of services or reimbursement

relative to the alleged impairments” [paragraph j].

        However, this Commission agrees with counsel for Dr. MacIvor, that the applicable

statutory provision is Section 8.01-273.1, Code of Virginia which sets forth the procedure in those

cases wherein the court refers the cause of action to the Commission to determine whether it

satisfies the requirements of the Virginia Birth-Related Neurological Injury Compensation Act.

The moving party, in this case Dr. MacIvor, was to provide the Commission with an original and

five copies of specified medical records. These medical records and the pleadings are specifically

considered to constitute a petition.

        In this particular case the evidence unambiguously establishes that counsel for Dr. MacIvor

filed the necessary medical documents which with the pleadings also provided constitute a proper


                                       ISSUE NUMBER TWO

        The second and final issue before the Commission is whether the infant sustained a birth-

related neurological injury.

                                                                             VWC File No. B-00-24


       As defined in Section 65.2-5001, Code of Virginia, a “birth-related neurological injury”

constitutes an “…injury to the brain or spinal cord of an infant caused by the deprivation of oxygen

or mechanical injury occurring in the course of labor, delivery or resuscitation in the immediate

post-delivery period in a hospital which renders the infant permanently motorically disabled and (i)

developmentally disabled or (ii) for infants sufficiently developed to be cognitively evaluated,

cognitively disabled.”

       In determining whether an infant meets the statutory definition, the Commission is mindful

that “[a] rebuttable presumption shall arise that the injury alleged is a birth-related neurological

injury where it has been demonstrated to the satisfaction of the Virginia Workers‟ Compensation

Commission, that the infant has sustained a brain or spinal cord injury caused by oxygen

deprivation or mechanical injury, and that the infant was thereby rendered permanently motorically

disabled and (i) developmentally disabled or (ii) for infants sufficiently developed to be cognitively

evaluated, cognitively disabled.” That provision goes on to state that “[I]f either party disagrees

with such presumption, that party shall have the burden of proving that the injuries alleged are not

birth-related neurological injuries within the meaning of the chapter.”

       In this case it is abundantly clear that the infant sustained his devastating neurological

injuries as a result of a deprivation of oxygen and not because of any mechanical injury. As a

result, the infant is presumed to have sustained a birth-related neurological injury. It is also

abundantly clear that the infant‟s parents and the Program seek to have the Commission find that it

has no jurisdiction to award benefits.      Under such circumstances they have the burden of

                                                                            VWC File No. B-00-24

overcoming this presumption and to prove that the neurological injuries were not birth-related

neurological injuries. As set forth in the case of Program v. Young, 34 Va. App. 306, 312 541

S.E.2d 298, 301 (2001), the presumption would shift to the Program and the parents “…both the

burden of production and the burden of persuasion on the issue of causation.”

       As held by the majority in the Full Commission Opinion in In re: Jamie Michelle Wells,

Claim No. 90-2 (February 5, 1992), the statutory presumption has not been rebutted where the

medical evidence establishes that the injury caused by oxygen deprivation commenced prior to the

hospitalization but continued through the birthing process. Most recently, the Full Commission

found that the presumption was not rebutted when it determined that there was in fact oxygen

deprivation during labor and the child was not breathing when born. In re: William T. Young, Jr.,

Claim No. 98-9 (March 10, 2000). The Court of Appeals did not reverse this finding although in

her dissent Judge Annuniziata disputed that the evidenced had established that oxygen deprivation

during the statutory period of labor, delivery or resuscitation in fact caused the child‟s injury and

thus was of the opinion that the presumption had been rebutted.

       Applying all of the above to the record in this case, this Commission finds that the Program

and the parents have not rebutted the presumption that the infant sustained a birth-related

neurological injury. As is apparent from the summary, the infant suffered from growth retardation

which is a separate issue from the neurological injury sustained. It is equally apparent that when

Mrs. Ellington sought treatment from Dr. MacIvor on October 13, 1998 and was then referred to

Dr. Redwine that the infant was already suffering from hypoxia and was already at great risk. The

hypoxia continued through the time that she arrived at the hospital, was hooked up to the

                                                                              VWC File No. B-00-24

monitoring, commenced contractions and underwent an emergency cesarean section because of the

severe deceleration noted. The baby was not breathing upon birth and needed resuscitation. The

meconium represented a child at stress and the Apgars appear to reflect a recovery that was not

ultimately sustained given the devastating ultrasound and CT findings. From all of this and the

above caselaw, the Commission finds that the infant suffered oxygen deprivation both before and

during the applicable statutory period. Given the holding in Wells and more resent in Young this

Commission further finds that the burden was upon the Program and the petitioners needed to

establish that none of the injury occurred during the statutory period of labor, delivery and

resuscitation. It is not enough for experts to state that an injury occurred in utero. This has not been

accomplished here as only one physician, Dr. Borden upon questioning by the Commission at the

hearing, opined that labor and delivery did not contribute to the injury. Others, such as Doctors

Kerkering, Taylor and Jenkins and also the panel pointed to an intrauterine injury, but expressed no

opinion whether or not the injury continued. In the context of the presumption and also contrary

opinions by Dr. Al-Mateen and Dr. Frank, this is simply not enough. In making this determination,

this Commission is aware that Dr. Al-Mateen was unwilling to express an opinion using his own

definition about reasonable medical certainty. However, he plainly felt that there was such a birth

injury as a more likely event than not which constitutes sufficient certainty to be considered.

       This Commission is cognizant that at the Circuit Court and beyond the parties have

seemingly delineated positions in accord with an acute injury during labor, delivery and

resuscitation versus a chronic injury in utero. This is evident in the detailed and thoughtful

memorandum filed with the Commission after the hearing wherein the parties attempted to divide

                                                                             VWC File No. B-00-24

the doctors along these liens. As a result, Doctors Al-Mateen and Frank were seemingly aligned

against Doctors Kerkering, Taylor, Jenkins, Borden and the panel. This Commission does not

conclude that the injury sustained by this unfortunate child fits into such easy categories. The

evidence establishes that the child was already well on his way towards having an injury due to his

oxygen state when Mrs. Ellington entered Dr. Redwine‟s office and the specialist found that he was

not breathing. This lack of oxygen most certainly continued from that time until the delivery.

Given the state of Commission caselaw pertaining to the rebuttal of the presumption noted above, it

appears that the Full Commission and the Court of Appeals has taken the position and with such a

continuity of oxygen deprivation the party seeking to overcome the presumption must establish

something more than opinions that the injury was chronic versus an acute, as otherwise this

Commission would in fact agree with the Program and the parents. Certainly the injury appears to

have started prior to the time that Mrs. Ellington arrived at the hospital but the Commission simply

cannot find that the evidence preponderates in proving that the injury was complete at that time.

The presumption and the testimony of Doctors Al-Mateen and Frank would point to the contrary

and the circumstances would likewise point to a continuing loss of oxygen.

       For the above reasons the Commission shall advise the Circuit Court of the City of

Richmond that it has determined that the actions satisfies the requirements of the Virginia Birth-

Related Neurological Compensation Act and our award shall enter accordingly.

                                                                              VWC File No. B-00-24


       The Birth-Related Neurological Injury Compensation Fund shall be and is hereby directed

to pay Deborah Ellington all amounts expenses provided by Section 38.2-5009, Code of Virginia,

for the benefit of Trevor Ellington.

       Upon submission of itemized expenses the Commission will also an award of an

appropriate attorney‟s fee and costs to counsel for the parents and infant.

       This case is ordered removed from the hearing docket.


       You may appeal this decision by filing a request for review with the Commission within
twenty days from receipt of this Opinion.

cc:    Elinor J. Pyles, Executive Director
       Virginia Birth-Related Neurological
       Injury Compensation Program
       9100 Arboretum Parkway
       Suite 365
       Richmond, VA 23236

       Linda Wilhelm
       Health Facility Regulator
       3600 West Broad Street
       Suite 216
       Richmond, VA 23230

       William L. Harp, M.D.
       Board of Medicine
       6606 West Broad Street
       4th Floor
       Richmond, VA 23230

                               VWC File No. B-00-24

Duncan C. MacIvor, M.D.
5855 Bremo Road
Suite 206
Richmond, VA 23226

St. Mary‟s Hospital
5801 Bremo Road
Richmond, VA 23226