STATE OF FLORIDA

DIVISION OF ADMINISTRATIVE HEARINGS

EVAN BALASH and TRACY BALASH, as )

parents and natural guardians of ) ADAM JOSEPH BALASH, a minor, )

)

Petitioners, )

)

vs. ) Case No. 96-5183N

) FLORIDA BIRTH-RELATED NEUROLOGICAL ) INJURY COMPENSATION ASSOCIATION, )

)

Respondent. )

)

FINAL ORDER

Pursuant to notice, the Division of Administrative Hearings, by its duly designated Administrative Law Judge, William J. Kendrick, held a formal hearing in the above-styled case on March 17, 1998, in West Palm Beach, Florida.

APPEARANCES

For Petitioners: Patrick C. Massa, Esquire

Crystal Tree Office Centre

1201 U.S. Highway One, Suite 400 North Palm Beach, Florida 33408

For Respondent: W. Douglas Moody, Jr., Esquire

Graham & Moody, P.A.

101 North Gadsden Street Tallahassee, Florida 32301

STATEMENT OF THE ISSUE

At issue in this proceeding is whether Adam Joseph Balash, a minor, suffered an injury for which compensation should be

awarded under the Florida Birth-Related Neurological Injury

Compensation Plan.

PRELIMINARY STATEMENT

On November 5, 1996, Evan Balash and Tracy Balash, as parents and natural guardians of Adam Joseph Balash (Adam), a minor, filed a petition (claim) with the Division of Administrative Hearings (hereinafter referred to as "DOAH") for compensation under the Florida Birth-Related Neurological Injury Compensation Plan (hereinafter referred to as the "Plan").

DOAH served the Florida Birth-Related Neurological Injury Compensation Association (hereinafter referred to as "NICA") with a copy of the claim on November 6, 1996. NICA reviewed the claim, and on February 13, 1997, gave notice that it had "determined that such claim is not a 'birth-related neurological injury' within the meaning of Section 766.302(2), Florida Statutes," and requested that "an order [be entered] setting a hearing in this cause on the issue of the compensability of this claim." Following a number of continuances, such a hearing was ultimately held on March 17, 1998.

At hearing, the parties stipulated to the factual matters set forth in paragraphs 1 and 2 of the findings of fact, and further stipulated that Adam was permanently and substantially, mentally and physically impaired. Petitioners called

Barry Chandler, M.D., as a witness, and Petitioners' Exhibits

1 through 7 were received into evidence.1 Respondent called Lance Wyble, M.D., as a witness, and Respondent's Exhibits

1 and 2 were received into evidence.2

The transcript of the hearing was filed May 19, 1998, and the parties were accorded 30 days from that date to file proposed final orders. Consequently, the parties waived the requirement that a final order be rendered within 30 days after the transcript has been filed. Rule 60Q-2.031, Florida Administrative Code. The parties elected to file such proposals, and they have been duly considered.

FINDINGS OF FACT

Preliminary matters

1. Evan Balash and Terry Balash are the parents and natural guardians of Adam Joseph Balash (Adam), a minor. Adam was born a live infant on November 5, 1991, at Palms West Hospital, a hospital located in Palm Beach County, Florida, and his birth weight was in excess of 2500 grams.

2. The physicians providing obstetrical services during the birth of Adam were Robert Chaitin, M.D., and Ronald Ackerman, M.D., who were, at all times material hereto, participating physicians in the Florida Birth-Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes.

   Mrs. Balash's antepartum course and Adam's birth

3. Mrs. Balash's antepartum course was without apparent complication until November 5, 1991, when, with the fetus at

   37 weeks gestation (estimated date of confinement November 20, 1991), she presented to her obstetrician/gynecologist. At the time, examination was reassuring with fetal movement and a fetal heart rate of 136 beats per minute; however, Mrs. Balash reported decreased fetal movement over the last few days. Consequently, she was referred to Palms West Hospital for a non- stress test (NST).

4. Mrs. Balash presented to Palms West Hospital at or about 2:00 p.m. (1400 hours), November 5, 1991, and was placed on a fetal monitor for the NST at or about 2:04 p.m.3 Fetal heart rate (FHR) baseline was noted at 150 beats per minute and continued at that rate until about 2:25 p.m. when a period of bradycardia was shown to develop, down to approximately 90 beats per minute, and persist for approximately 5 minutes, with a return to baseline.4 Reassuringly, beat-to-beat variability and reactivity to Doppler were present, and no further episodes of bradycardia were noted during the course of Mrs. Balash's labor and delivery.5

5. Given the prolonged deceleration noted on the NST, Mrs. Balash was admitted to labor and delivery at 2:30 p.m. Vaginal examination revealed the cervix to be at 2-3 centimeters, effacement at 80 percent, and the fetus at station

   -2,6 with contractions at 1 to 2 minutes. Mrs. Balash complained of abdominal tenderness, and the abdomen palpated firm. No vaginal bleeding was noted. Dr. Chaitin was advised of Mrs.

   Balash's status, and intravenous (IV) fluids and lab work were ordered.

6. At 3:00 p.m. the FHRs were noted as 140s, without accelerations, and at 3:20 p.m. vaginal examination revealed no change or progress. Dr. Chaitin was updated.

7. At 3:34 p.m. Mrs. Balash was attended by Dr. Chaitin.

   
   

   His examination noted the fetus at station -3; however, dilation remained at 2 centimeters. The uterus was noted to be "rock hard without any relaxation," a presentation consistent with placental abruption. Consequently, Dr. Chaitin ruptured the membranes, yielding bright red amniotic fluid (further evidence of placental abruption).7 Internal fetal monitor was placed, revealing FHRs of 140s, with good variability and no decelerations.8 The fetus was noted to be in frank breech presentation.

8. Given the evidence of fetal stress and probable placental abruption, Dr. Chaitin opted for a stat (immediate) cesarean section.

9. Between 3:40 p.m. and 3:54 p.m., Mrs. Balash was prepared for surgery, anesthesia was started, and she was moved to the operating room. According to the labor and delivery

   summary, she was in the operating room at 3:55 p.m., the incision was made at 3:56 p.m., and Adam was delivered at 3:57 p.m., November 5, 1991.

10. Pertinent to this case, the operative report reads as follows:

    . . . The uterus was noted to be rock hard in all quadrants. A low transverse incision was made with a scalpel. The uterine incision was extended bilaterally. The fetal breech was noted to be in frank breech position and with care, the butt was delivered and both arms were reduced appropriately.

    
    

    The fetal head was then removed, the baby was well bulb suctioned, and started crying extremely vigorously. [Infant dried and provided whiffs of oxygen, but no resuscitation required.] Cord was clamped, and neonatology present and baby evaluation was normal. A 6 pound, 12 ounce, baby boy was born with Apgar's 8/9. The cord ph was obtained which was 7.322 [normal]. The placenta was actively delivering, and was found to be 40% abrupted and was sent to pathology for evaluation. . . .

    
    

11. The Apgar scores assigned to Adam are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, muscle tone, gag reflex, and color, with each category being assigned a score ranging from the lowest score of 0 through a maximum score of 2. As noted, at one minute Adam's Apgar score totalled 8, with heart rate, respiratory effort, muscle tone, and gag reflex being graded at 2 each, and color

    being graded at 0. At five minutes, his Apgar score totalled 9, with heart rate, respiratory effort, muscle tone, and gag reflex being graded at 2 each, and color being graded at 1. Such scores are grossly normal, as were Adam's newborn assessments, and he was admitted to the newborn nursery for routine care. (Petitioners' Exhibit 5, tabs 4 and 8).

12. At approximately one hour of life (5:00 p.m.), Adam was observed to have turned dusky. One hundred percent oxygen via mask was applied, and Adam's color improved. Heart rate and respiratory rate were noted as stable.

13. Adam was subsequently attended by Dr. Lerma Te, who noted nasal flaring, grunting, and retraction. Dr. Te's impression was "respiratory distress" and "rule out sepsis." Blood cultures were ordered, and intravenous Ampicillin and Claforan were started.

14. Adam developed increasing oxygen requirements and at or about 6:40 p.m. he was intubated and assisted ventilation was begun. X-rays revealed "homogenous bilateral extensive ground glass appearance of the air bronchograms." Impression was that "[t]his either represents transient respiratory distress syndrome in the newborn or hyaline membrane disease."9

15. Given Adam's needs, he was transported to Good Samaritan Hospital, where he was admitted to the neonatal intensive care unit (NICU) at or about 10:25 p.m. Notably,

    notwithstanding his respiratory problems, Adam's neurological status remained essentially normal throughout his hospital stay.

16. On November 20, 1991, Adam was discharged, in apparent good health, to his mother's care. His course at Good Samaritan Hospital noted no neurological problems, and is summarized on his discharge summary as follows:

    HISTORY:

    
    

    Mother is a 27 year old gravida 2, para 1, blood type 0 negative. Admitted at 37 weeks gestational age with abruptia placenta.

    Stat cesarean section was done and the baby was in breech position with Apgar score of eight and nine at one and five minutes respectively. Weight 2920 grams. The baby developed respiratory distress with increasing FI02 requirement. He was intubated and assisted ventilation started. Blood cultures were done. Intravenous Ampicillin and Claforan were started and the baby was transferred to Good Samaritan Hospital from Palm West.

    
    

    PHYSICAL EXAMINATION:

    
    

    Baby's weight 2920 grams, heart rate 156, respiratory rate 60, blood pressure 65/38. Premature 37 week male infant in respiratory distress. Head and Face: Anterior fontanelle flat. Oral cavity: No cleft plate noted. Chest: The baby is on assisted ventilation. Air entry heard both sides.

    Cardia: Heart sounds normal. Abdomen is soft. Umbilical cord has two vessels.

    Genitalia: Male. Extremities: No click at the hips. Central nervous system: Tone and reflexes equal on both sides.

    ASSESSMENT:

    
    

    1. Premature 37 weeks.

    2. Respiratory distress.

    3. Maternal complications, abruptia placenta.

    4. Cesarean section delivery.

    5. Suspected sepsis.

    6. Maternal history of herpes.

       
       

       HOSPITAL COURSE:

       
       

       Complete blood count, blood cultures x 7 were done. The baby continued on intravenous Ampicillin, endotracheal tube and cultures were sent for herpes.

       Umbilical catheter was inserted through the umbilicus about nine centimeters. He was started on Exosurf. The baby remained on assisted ventilation from 11/5 through 11/10/91 and was extubated on 11/10 and placed on Oxy-Hood. The baby was weaned from oxygen to room air by 11/18/91.

       
       

       The baby was also noted to be jaundiced and was started on photo therapy on 11/9/91 and was discontinued on 11/11/91 when the bilirubin declined.

       
       

       Echocardiogram done on 11/7/91 revealed moderate size patent ductus arteriosus and the baby was given Indocin and the patent ductus closed after the Indocin.

       
       

       The baby was on Ampicillin and Claforan for suspected sepsis and this was discontinued after a course of antibiotics of seven days. The baby was started on feedings on 11/18/91 and was advanced and IV's decreased. The baby tolerated adequate amounts of feedings and tolerated feeds well. The baby was discharged home at fifteen days of age when the baby weighed 6 lbs. 7.6 oz., was clinically stable and tolerating feedings well.

       DISCHARGE DIAGNOSIS:

       
       

       1. Premature 37 weeks male.

       2. Respiratory distress syndrome.

       3. Patent ductus arteriosus.

       4. Hyperbilirubinemia.

       5. Suspected sepsis.

       
       

       DISCHARGE PLAN:

       
       

       To be followed by Dr. Marineau in one week and Dr. Friedman for eye examination on 12/11/91. Brain stem auditory evoke potential examination to be done on 12/5/91 at Good Samaritan Hospital. Cranial ultrasound on 11/6 showed no evidence of [hydrocephalus or] intracranial bleeding.

       
       

       Adam's development

       
       

17. Adam's early infancy was apparently unremarkable, and no problems were observed until approximately eight to ten months of age. At that time, developmental delay became evident and the parents reported their concerns to Adam's pediatrician, who referred him for neurologic consult at the Palm Beach Neurological Group.10

18. Adam was examined by a Dr. Mate, at the Palm Beach Neurological Group, in 1992; however, those observations are not of record. What is of record are the observations of Luis

    Bello-Espinosa, M.D. (Dr. Bello), another neurologist associated with the Palm Beach Neurological Group, who first examined Adam in April 1994. Dr. Bello describes Adam's presentation as consistent with severe cerebral palsy (profound brain dysfunction), that is characterized by spastic quadriparesis (an

    abnormal motor development affecting all four extremities) and mental retardation. Here, there is no dispute that Adam's impairments, mental and physical, are permanent and substantial.

19. In an effort to identify the etiology of Adam's dysfunction, he was referred to Paul J. Benke, M.D., for genetic consultation. The results of Dr. Benke's first consultation were reported on November 2, 1993, as follows:

    DIAGNOSTIC IMPRESSION: Chromosome Anomaly. GENETIC COUNSELING: The developmental delay, now performing at 11-12 months, is probably related to the chromosome anomaly. It could not be determined today whether the neonatal problems played a role. One cell strain, the 20 deletion with 2 normal 7 chromosomes, is probably derivative from the dominant strain with the apparently balanced translocation. This would mean that the translocated #7 broke and lost most of the translocated #20, or far more likely, the whole chromosome was lost, the normal #7 was duplicated, and the 2 #7 chromosomes are derived from 1 parent. Blood was taken today to see if 1 parent is a translocation carrier. A skin biopsy, with a presumably higher proportion of 20 p- cells, would be required to determined (sic) why the translocated 7 was lost.

    
    

    Dr. Benke recommended follow-up studies.

    
    

20. The results of Dr. Benke's follow-up studies were reported on October 1, 1994, as follows:

    This boy . . . [has] a mosaic chromosome abnormality . . . We did a skin biopsy months ago to determine the proportion of cells with a derivative chromosome 20, partial trisomy 7 and deletion 20. Most of the sample (29/30) cells had the balanced

    7:20 translocation, with the deriviative (sic) 20 in just 3 percent. This suggests also that the balanced translocation was probably the first genetic lesion.

    Compounding conclusions of etiology for slow development is that a new balanced translocation leads to slow development and birth defects 7-10 per cent of the time.

    Also, the derivative 20 chromosome could be responsible since the neurons with this anomaly may function poorly. Also, he had a delay in his C-section of more than one hour when there was a demonstrable disruption of the placenta, associated with attendant neonatal problems. It is tough to say which of the factors is most responsible, but I think that the balanced translocation is the least important. Interestingly, children with chromosome 20 deletion are not particularly dysmorphic, but are delayed, and have some findings similar to those found in Adam. . . .

    
    

21. In sum, Dr. Benke's conclusion was that Adam suffered a chromosonal abnormality known as a balanced translocation affecting approximately 3 percent of his cells. This genetic abnormality generally does not lead to any clinical problems; however, in 7 to 10 percent of the cases involving this type of translocation there may be genetic predisposition to decreased neurological development or birth (genetic) defect.

    The dispute regarding compensability

    
    

22. Here, it is not subject to serious debate that the cause of Adam's neurologic impairment is associated with brain dysfunction or anomaly.11 What is at issue is the cause and timing (genesis) of that anomaly (encephalopathy)12 or, more

    pertinent to these proceedings, whether the proof demonstrates, more likely than not, that Adam's neurologic impairment resulted from an "injury to the brain . . . caused by oxygen deprivation13

    . . . occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as opposed to some other genesis. Section 766.302(2), Florida Statutes.

23. With regard to such issue, Petitioners contend that Adam suffered an hypoxic event, consequent to the stresses of labor (placental abruption and uterine hypertonicity), which caused a microscopic brain injury, and that such injury was the cause of Adam's neurologic impairment. In contrast, Respondent contends the proof is not consistent with hypoxic ischemic injury occurring during the course of childbirth, and, therefore, Adam's disorder must be attributable to some other etiology. Respondent's view of the proof has merit.

    The genesis of Adam's brain anomaly

    
    

24. To address the genesis of Adam's brain anomaly, the parties offered selected medical records relating to

    Mrs. Balash's antepartum and intrapartum course, as well as for Adam's birth and subsequent development. Portions of those records have been addressed supra, and further salient portions will be addressed infra. The parties also offered the opinions of five physicians as to the likely cause of Adam's birth disorder. The physicians selected by Petitioners were Paul J.

    Benke, M.D., a board certified clinical and biochemical geneticist; Luis J. Bello, M.D., a board certified neurologist; and, Barry D. Chandler, M.D., a board certified neonatologist. The physicians offered by Respondent were Charles Kalstone, M.D., a board certified obstetrician and gynecologist; and Lance

    E. Wyble, M.D., a board certified neonatologist.

    
    

25. The medical records and other documentary proof, as well as the testimony of the physicians offered by the parties, have been scrutinized. So considered, it must be concluded that the proof does not allow a conclusion to be drawn with any sense of confidence, that, more likely than not, Adam's brain anomaly was associated with an injury caused by oxygen deprivation during labor, delivery, or resuscitation in the immediate post- delivery period, as opposed to some other etiology.14

26. In reaching the foregoing conclusion, neither the evidence of placental abruption nor fetal stress during labor has been overlooked. However, while the presence of such factors could lead one to assume a connection and attribute Adam's anomaly to hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, an examination of the clinical data and observations suggests that such would be a speculative and unlikely explanation for Adam's presentation.

27. In so concluding, it is observed that Adam's course pre-delivery and post-delivery was inconsistent with hypoxic or

    ischemic injury having occurred during the course of birth. First, the evidence documenting fetal heart rate during the course of labor and delivery, particularly when compared with Adam's post-delivery presentation, does not support the conclusion that Adam suffered an acute intrapartum event that led to an hypoxic or ischemic injury. Notably, there was only one event of fetal heart rate deceleration and overall the monitoring tape was reassuring. Under such circumstances, it is unlikely that the partial abruption Mrs. Balash suffered adversely affected fetal oxygenation during labor and delivery.

28. Further militating against the conclusion that Adam's anomaly was caused by oxygen deprivation during the course of labor and delivery are the numerous inconsistencies between Adam's presentation and the clinical findings one would expect had he suffered hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, during that period. Notably, had such an event occurred, one would reasonably expect a severely depressed infant on delivery, with an absence of respiratory effort; a depressed cord pH; and the onset of seizure activity during the neonatal period. Here, Adam was alert and active on delivery, with good respiratory effort; his Apgars were normal, as were his newborn assessments; his cord pH was normal; and no seizure activity was noted in the neonatal period.

29. Also of note, within approximately 24 hours of birth, Adam was administered a cranial ultrasound, which proved negative for hemorrhage and edema. Edema is a clinically anticipated consequence of neurological injury, and is anticipated within 6 to 12 hours of the event. Subsequent brain studies (MRIs), at or about 11 and 18 months of age, were also read as normal or, stated differently, failed to reveal global or bilateral injury generally associated with hypoxic ischemic encephalopathy.

30. Finally, had Adam suffered an hypoxic ischemic event during birth, one would reasonably expect damage to multiple organ systems. Included would be the kidneys, bone marrow, the liver, and the heart. Here, Adam's creatine levels and urine output remained normal throughout the neonatal period, indicating that his kidneys were not subjected to an acute hypoxic event. Additionally, Adam evidenced no myocardial injury, and his bone marrow reflected no evidence of lymphocrytosis, which one would anticipate had there been an acute hypoxic event.15 Finally, Adam's first CBC (complete blood count) at Palms West Hospital indicated an extremely elevated level of nucleated red blood cells, which would be consistent with the presence of a chronic injury, as opposed to an acute insult.

31. Given the proof, it cannot be concluded that, more likely than not, Adam's brain disorder and resulting neurologic impairment was associated with a brain injury caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Notably, Adam's presentation at birth and his neonatal course were not consistent with an acutely acquired neurological injury, and it is improbable that he could have experienced an acute injury during labor and delivery without evidencing a single clinical symptom of such damage. Conversely, the existence of a prenatally acquired (predating labor and delivery) brain disorder (whether genetically or otherwise based) would be consistent with Adam's presentation at birth and during the neonatal period.

    CONCLUSIONS OF LAW

    
    

32. The Division of Administrative Hearings has jurisdiction over the parties to, and the subject matter of, these proceedings. Section 766.301, et seq., Florida Statutes.

33. The Florida Birth-Related Neurological Injury Compensation Plan (the "Plan") was established by the Legislature "for the purpose of providing compensation, irrespective of fault, for birth-related neurological injury claims" relating to births occurring on or after January 1, 1989. Section 766.303(1), Florida Statutes.

34. The injured "infant, his personal representative, parents, dependents, and next of kin" may seek compensation under the Plan by filing a claim for compensation with the Division of Administrative Hearings within five years of the infant's birth. Sections 766.302(3), 766.303(2), 766.305(1), and 766.313, Florida Statutes. The Florida Birth-Related Neurological Injury Compensation Association (NICA), which administers the Plan, has "45 days from the date of service of a complete claim . . . in which to file a response to the petition and to submit relevant written information relating to the issue of whether the injury is a birth-related neurological injury." Section 766.305(3), Florida Statutes.

35. If NICA determines that the injury alleged in a claim is a compensable birth-related neurological injury, it may award compensation to the claimant, provided that the award is approved by the administrative law judge to whom the claim has been assigned. Section 766.305(6), Florida Statutes. If, on the other hand, NICA disputes the claim, as it has in the instant case, the dispute must be resolved by the assigned administrative law judge in accordance with the provisions of Chapter 120, Florida Statutes. Sections 766.304, 766.307, 766.309, and 766.31, Florida Statutes.

36. In discharging this responsibility, the administrative law judge must make the following determination based upon the available evidence:

    1. Whether the injury claimed is a birth-related neurological injury. If the claimant has demonstrated, to the satisfaction of the administrative law

       judge, 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 and substantially mentally and physically impaired, a rebuttable presumption shall arise that the injury is a birth-related neurological injury as defined in s.

       766.303(2).

       
       

    2. Whether obstetrical services were delivered by a participating physician in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital; or by a certified nurse midwife in a teaching hospital supervised by a participating physician in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital.

    
    

    Section 766.309(1), Florida Statutes. An award may be sustained only if the administrative law judge concludes that the "infant has sustained a birth-related neurological injury and that obstetrical services were delivered by a participating physician at birth." Section 766.31(1), Florida Statutes.

37. Pertinent to this case, "birth-related neurological injury" is defined by Section 766.302(2), Florida Statutes, to mean:

    . . . injury to the brain or spinal cord of a live infant weighing at least 2,500 grams at birth caused by oxygen deprivation 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 and substantially mentally and physically impaired. This definition shall apply to live births only and shall not include disability or death caused by genetic or congenital abnormality.

    
    

38. As the claimants, the burden rests on Petitioners to demonstrate entitlement to compensation. Section 766.309(1)(a), Florida Statutes. See also Balino v. Department of Health and Rehabilitative Services, 348 So. 2d 349, 350 (Fla. 1st DCA

    1977), ("[T]he burden of proof, apart from statute, is on the party asserting the affirmative issue before an administrative tribunal.")

39. Here, it has been established that the attending physicians who provided obstetrical services during the birth of Adam were "participating physician[s]" as that term is defined by Section 766.302(7), Florida Statutes, and as that term is used in Sections 766.301 through 766.316, Florida Statutes. Moreover, the proof demonstrated that Adam suffered a brain anomaly that rendered him "permanently and substantially mentally and physically impaired." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. However, the proof failed to demonstrate, more likely than not, that Adam's impairments

    resulted from an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or the immediate post-delivery period." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Accordingly, the subject claim has not been shown to be compensable under the Plan. Sections 766.302(2), 766.309(1), and 766.31(1), Florida Statutes.

40. Where, as here, the administrative law judge determines that ". . . the injury alleged is not a birth-related neurological injury . . . he [is required to] enter an order [to such effect] and . . . cause a copy of such order to be sent immediately to the parties by registered or certified mail." Section 766.309(2), Florida Statutes. Such an order constitutes final agency action subject to appellate court review. Section 766.311(1), Florida Statutes.

CONCLUSION

Based on the foregoing Findings of Fact and Conclusions of Law, it is

ORDERED that the petition for compensation filed by

Evan Balash and Tracy Balash, as parents and natural guardians of Adam Joseph Balash, a minor, be and the same is hereby denied.

DONE AND ORDERED this 30th day of June, 1998, in Tallahassee, Leon County, Florida.

WILLIAM J. KENDRICK

Administrative Law Judge

Division of Administrative Hearings The DeSoto Building

1230 Apalachee Parkway

Tallahassee, Florida 32399-3060

(850) 488-9675 SUNCOM 278-9675

Fax Filing (850) 921-6847

Filed with the Clerk of the Division of Administrative Hearings this 30th day of June, 1998.

ENDNOTES

1/ Petitioners' Exhibit 1 was the curriculum vitae of Barry Chandler, M.D.; Exhibit 2 was the deposition of Luis Bello, M.D.; Exhibit 3 was the deposition of Paul Benke, M.D.; Exhibit 4 consisted of the labor and delivery records for Tracy Balash (Palms West Hospital); Exhibit 5 consisted of the infant's

(Adam Balash's) birth records (Palms West Hospital); Exhibit 6 consisted of the infant's records from Good Samaritan Hospital; and Exhibit 7 consisted of the fetal monitor strips from Palms West Hospital.

2/ Respondent's Exhibit 1 was the deposition of Charles Kalstone, M.D., which, with the parties agreement, was filed post-hearing and received into evidence. (The transcript incorrectly identifies the subject of the deposition as "Dr.

Chaitin"). Respondent's Exhibit 2 includes reports of Dr. Benke, as well as chromosome analysis requests and results.

3/ At hearing, there was some confusion as to which fetal monitor strips covered the NST of November 5, 1991. Here, by reading the physician's history and physical (Petitioners' Exhibit 4, tab 4) and the nurse's progress notes (Petitioner's Exhibit 4, tab 7), and comparing them with the fetal monitor strips (Petitioners' Exhibit 7), it is apparent that the fetal monitor strips numbered 17061 through 17065 relate to the NST of November 5, 1991, and strips numbered 17099 through 17109 relate

to the remainder of the admission on November 5, 1991. As for the other strips included in Petitioners' Exhibit 7, consisting of 5 pages numbered 27288 through 27292, they are apparently not related to the admission of November 5, 1991, but are most likely the results of a NST performed in October 1991. (Petitioners' Exhibit 4, tab 22 (prenatal flow records).)

4/ The period of bradycardia was associated with an episode of tetanic (continuous) contraction of the uterus. Petitioners' expert, Dr. Chandler, was of the opinion that this episode of bradycardia was also a reflection of diminished fetal reserve.

If such was the case, the fetal reaction would be consistent with fetal compromise prior to admission.

5/ A non-stress test involves the use of electronic fetal monitors to assess fetal well-being. If there is fetal activity, an acceleration or rise in fetal heart rate will be recorded.

Where there is an acceleration of more than fifteen beats per minute, occurring at least two times in ten minutes, the result is termed "reactive," and is reassuring for fetal well-being.

Where such accelerations are not present, the result is termed "non-reactive," and is not reassuring for fetal well-being or, stated differently, the fetus is considered high-risk. Here, the non-stress test was noted as non-reactive.

Generally, when the non-stress test is non-reactive, further testing is done to assess fetal well-being, such as a nipple stimulation contraction stress test. Here, there is no evidence that any further testing was done, and it may have been considered unnecessary given Mrs. Balash's admission to the hospital.

6/ Such presentation demonstrated progress from the results obtained on examination at her obstetrician's office and was consistent with the onset of labor.

7/ The fluid was also noted to be meconium stained, a common observation where, as here, the fetus presents in frank breech position.

8/ Dr. Chaitin's history (Petitioners' Exhibit 4, tab 4) states, following placement of the internal monitor, that "some areas of fetal tachycardia and also areas of decreased beat-to-beat variability" were noted. What Dr. Chaitin describes as fetal tachycardia may, however, best be described as accelerations (a

positive sign of fetal well-being). There is, however, some evidence on the strips, between 3:10 p.m. and 3:20 p.m., of decreased beat-to-beat variability.

9/ Respiratory distress syndrome is a condition of the newborn, usually premature, marked by difficult or labored breathing.

Causes include, pulmonary immaturity, infection, and hyaline membrane disease. Hyaline membrane disease was described in this case as a condition affecting newborns, usually premature, in which the pulmonary alveoli collapse after initial expansion by air, requiring assisted ventilation. Causes include a deficiency of pulmonary surfactant. Adam, at 37 weeks, was only slightly premature, and the presence of hyaline membrane disease would be unusual. Moreover, in slightly immature infants, like Adam, if surfactant insufficiency is the problem, responsive and appropriate breathing can be quickly reestablished by the administration of surfactant. Here, Adam was administered surfactant on numerous occasions, but did not respond as one would anticipate if a surfactant deficiency were the cause of his respiratory distress syndrome. Consequently, it is likely that Adam's respiratory problems had an etiology other than hyaline membrane disease. Such etiologies would include infection and congenital abnormality.

10/ The medical records of Adam's early infancy are not of record, and the foregoing conclusions are drawn from Petitioners' counsel's opening statement (Transcript, page 9), and Dr. Benke's November 2, 1993, report (Respondent's Exhibit 2). That no developmental delay was noted for eight to nine months is atypical of hypoxic ischemic encephalopathy suffered at birth and may be considered an admission against interest. Section 90.801(18), Florida Statutes. See also Am. Jur. 2d, Evidence, Section 820.

11/ Adam's presentation is consistent with a group of persisting motor disorders appearing in young children, commonly referred to as cerebral palsy, that are characterized by delayed or abnormal motor development, and often accompanied by mental retardation, seizures or ataxia. Such disorders may result from brain damage caused by birth trauma, such as that which may result from oxygen deprivation or mechanical injury during labor or delivery (the intrapartum period), or may be associated with an antenatal (prenatal) event or pathology of a similar nature, as well as genetic or developmental abnormality (testimony of record).

See also Dorland's Illustrated Medical Dictionary, Twenty-eighth Edition (1994).

12/ "Encephalopathy" is a generic term used to describe "any degenerative disease ('any deviation from the normal structure') of the brain." Such change in brain structure may result from a number of factors, including injury occasioned by "hypoxia" and "ischemia." "Hypoxia" is considered a "reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood." Possible causes include a "reduction of the oxygen-carrying capacity of the blood as a result of a decrease in the total hemoglobin" (anemic hypoxia), and "insufficient oxygen reaching the blood" (hypoxic hypoxia). "Ischemia" is a deficiency of blood in a part, due to functional constriction or actual obstruction of the coronary arteries." Dorland's Illustrated Medical Dictionary, Twenty-sixth Edition (1985). The presence of either (hypoxia or ischemia) may result in the delivery of insufficient oxygen to a part of the brain, with resultant injury (encephalopathy).

13/ There is no suggestion that any injury Adam may have suffered was related to the "spinal cord" or that it was caused by "mechanical injury." Section 766.302(2), Florida Statutes.

14/ In reaching the foregoing conclusion, the testimony of Doctors Benke, Bello and Chandler have been found less than compelling. In this regard, it is observed that Dr. Benke was not well informed concerning Adam's presentation at birth and course at Good Samaritan Hospital, and did not offer any rational explanation as to how his opinions could be reconciled with Adam's presentation, which failed to reflect characteristic indicators of neurologic injury (brain damage) suffered during the course of birth. Doctors Bello and Chandler also failed to offer any rational explanation as to how their opinions could be reconciled with the absence of such indicators and, consequently, their opinions were less than compelling. In sum, the opinions of Doctors Benke, Bello and Chandler seem to be grounded on little more than speculation, rather than scientific or medical probability. Conversely, the analysis and opinions of Doctors Kalstone and Wyble rest on a logical premise, are grossly consistent with the record, and have been accepted as credible and persuasive.

15/ One of the markers of an acute hypoxic event is an abnormally high presence of lymphocytes in the blood usually exceeding levels of over 10,000 for 24 hours with a rapid diminution below 5,000. In Adam's case, the lymphocyte count never exceeded 5,000, well within normal limits.

COPIES FURNISHED:

Patrick C. Massa, Esquire Crystal Tree Office Centre

1201 U.S. Highway One, Suite 400 North Palm Beach, Florida 33408

Evan and Tracy Balash

4521 PGA Boulevard, Suite 210

Palm Beach Gardens, Florida 33418

W. Douglas Moody, Jr., Esquire Graham & Moody, P.A.

101 North Gadsden Street Tallahassee, Florida 32301

Lynn Dickinson, Executive Director Florida Birth-Related Neurological

Injury Compensation Association Post Office Box 14567 Tallahassee, Florida 32317-4567

Robert Chaitin, M.D.

3345 Burns Road, Suite 202

Palm Beach Gardens, Florida 33410

Ronald Ackerman, M.D.

603 Village Boulevard, Suite 201 West Palm Beach, Florida 33409

Palms West Hospital Legal Department Star Route 80

13001 Southern Boulevard

Loxahatchee, Florida 33470-1150

Ms. Charlene Willoughby

Agency for Health Care Administration Consumer Services Unit

Post Office Box 14000 Tallahassee, Florida 32308

Daniel Sumner, General Counsel Department of Insurance

The Capitol, Lower Level 26 Tallahassee, Florida 32399-0300

NOTICE OF RIGHT TO JUDICIAL REVIEW

A party who is adversely affected by this final order is entitled to judicial review pursuant to Sections 120.68 and 766.311, Florida Statutes. Review proceedings are governed by the Florida Rules of Appellate Procedure. Such proceedings are commenced by filing one copy of a Notice of Appeal with the Agency Clerk of the Division of Administrative Hearings and a second copy, accompanied by filing fees prescribed by law, with the appropriate District Court of Appeal. See Section 120.68(2), Florida Statutes, and Florida Birth-Related Neurological Injury Compensation Association v. Carreras, 598 So. 2d 299 (Fla. 1st DCA 1992). The Notice of Appeal must be filed within 30 days of rendition of the order to be reviewed.

Docket for Case No: 96-005183N

Orders for Case No: 96-005183N