STATE OF FLORIDA

DIVISION OF ADMINISTRATIVE HEARINGS

PAUL LAPIDUS and LORI BETH LAPIDUS, )

as parents and natural guardians of ) SUSAN LAPIDUS, a minor, )

)

Petitioners, )

)

vs. ) Case No. 98-4881N

) 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 September 1, 1999, in West Palm Beach, Florida.

APPEARANCES

For Petitioner: Brian J. Cooke, Esquire

David I. Spector, Esquire Arnstein & Lehr

515 North Flagler Drive, Suite 600 West Palm Beach, Florida 33401

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

Graham, Moody & Sox, P.A.

101 North Gadsden Street Tallahassee, Florida 32301

STATEMENT OF THE ISSUE

At issue in this proceeding is whether Susan Lapidus, a minor, suffered an injury for which compensation should be

awarded under the Florida Birth-Related Neurological Injury Compensation Plan.

PRELIMINARY STATEMENT

On November 3, 1998, Paul Lapidus and Lori Beth Lapidus, as parents and natural guardians of Susan Lapidus, 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 4, 1998. NICA reviewed the claim, and on January 29, 1999, 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 September 1, 1999.

At hearing, the parties stipulated to the factual matters set forth in paragraphs 1 and 2 of the Findings of Fact.

Petitioners presented the testimony of Lori Beth Lapidus; Seth J. Herbst, M.D.; Jaime Baquero, M.D.; Debra Saad; and Theodore Wasserman, Ph.D. Petitioners' Exhibits 1 through 11 were received into evidence. Respondent called Charles Kalstone,

M.D., as a witness, and Respondent's Exhibits 1 through 5 were received into evidence.

A transcript of the hearing was filed October 5, 1999, and the parties were accorded until October 15, 1999, to file proposed final orders. The parties elected to file such proposals, and they have been duly considered.

FINDINGS OF FACT

Preliminary matters

1. Paul Lapidus and Lori Beth Lapidus are the parents and natural guardians of Susan Lapidus (Susan), a minor. Susan was born a live infant on November 5, 1993, at Good Samaritan Medical Center, a hospital located in West Palm Beach, Florida, and her birth weight was in excess of 2500 grams.

2. The physician providing obstetrical services during the birth of Susan was Ronald Koch, M.D., who was at all times material hereto, a participating physician in the Florida Birth- Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes.

   Mrs. Lapidus' antepartum course and Susan's birth

   
   

3. At or about 1:00 p.m., November 4, 1993, Mrs. Lapidus was admitted to Good Samaritan Medical Center for an oxytocin challenge test (a contraction stress test), with suspected intrauterine growth retardation (IUGR), to assess fetal well- being. At the time, the fetus was at 39 weeks gestation, with an estimated date of delivery of November 17, 1993, and

   Mrs. Lapidus' antepartum course had not been without complication or risk.

4. Regarding those risk factors, the proof demonstrates that at the time of Susan's conception Mrs. Lapidus (date of birth November 1, 1955) was 37 years of age, with a history of five previous pregnancies. Of those pregnancies, four were aborted (one "therapeutic" in 1979, and the balance "spontaneous" in January 1985, October 1985, and 1990) and one was carried to term and produced a normal, healthy boy (Michael, date of birth, October 21, 1988). Further complicating her pregnancy, the proof demonstrated that (to the extent conceded by Mrs. Lapidus), she smoked approximately 10 cigarettes per day and drank white wine daily (1 glass with dinner) throughout her pregnancy. 1/

5. Because of her age and other risk factors, Mrs. Lapidus underwent a number of tests during the course of her pregnancy, including an amniocentesis and multiple sonograms which revealed (within the limits of testing accuracy) no apparent cause for concern. Finally, during the month preceding her admission to Good Samaritan Medical Center, Mrs. Lapidus underwent non-stress testing, and ultimately contraction stress testing by oxytocin challenge test (OCT), to assess fetal well-being. 2/ The non- stress tests and oxytocin challenge tests that were administered to Mrs. Lapidus prior to November 4, 1993, were apparently reassuring for fetal well-being and placental integrity.

6. As heretofore noted, Mrs. Lapidus was admitted to Good Samaritan Medical Center at 1:00 p.m., November 4, 1993, for an OCT, which extended until 3:55 p.m., when Pictocin was discontinued. During the test some decelerations were observed late in contractions (late decelerations), consistent with placental aging/diminishing function, and Dr. Koch resolved it would be prudent to admit Mrs. Lapidus for observation overnight and induction of labor in the morning.

7. Mrs. Lapidus was admitted to labor and delivery at about 5:30 p.m., November 4, 1993. External fetal monitoring revealed a fetal heart rate (FHR) of 120 to 130 beats per minute (normal), and mild, irregular uterine contractions (most likely symptomatic of the prior administration of Pictocin). At 5:50 p.m.

   Mrs. Lapidus was repositioned, and external fetal monitor was positive for accelerations and continued mild, irregular uterine contractions.

8. Assessment at 7:30 p.m. noted continued mild contractions, as well as "variable decelerations [at] intervals but not consistently [with each] contraction," however, beat-to- beat variability was noted to be present. Continued monitoring overnight revealed occasional variable decelerations, but continued beat-to-beat variability.

9. At 7:10 a.m., external fetal monitoring revealed a FHR of 110 to 120 beats per minute, with spontaneous accelerations. Pictocin was administered to induce labor, at 7:30 a.m.

   contractions commenced (labor began), and an FHR deceleration to

   
   

   90 to 110 beats per minute for 2 1/2 minutes was observed.

   
   

   Mrs. Lapidus was repositioned to her left side, intravenous fluids (IV) were increased, and FHR returned to a 110 to 120 beat per minute baseline. Beat-to-beat variability in fetal heart rate persisted, and at 8:20 a.m. the membranes were artificially ruptured with clear fluid noted.

10. At or about 9:00 a.m., a FHR deceleration with contraction was noted. Mrs. Lapidus was again repositioned, intravenous fluids increased and FHR accelerated to 150 beats per minute following the contraction. A late deceleration was again noted with the next contraction.

11. At 9:40 a.m., the nurses' notes reveal 3 late decelerations were observed, and Pictocin was discontinued; FHR continued at 130 to 140 beats per minute, with moderate beat-to- beat variability. Vaginal examination at 9:50 a.m. revealed the cervix to be 5 centimeters dilated, effacement at 80 percent, and the fetus at station -2. Contractions were noted as moderate in intensity, with 3 to 5 minute frequency, and a duration of 60 to

    70 seconds.

    
    

12. At or about 10:10 a.m., an epidural was placed and at 11:45 a.m., with no further decelerations having been observed, Pictocin was restarted.

13. At 11:50 a.m., Mrs. Lapidus' bladder was noted as distended and a foley was inserted to help her void.

    Contemporaneously, FHR was noted to decelerate to the 60 beat per minute range for 30 seconds. When Mrs. Lapidus was repositioned, FHR returned to the 140 beat per minute range, with accelerations. At 12:29 p.m., the fetal monitor again revealed a late deceleration with contraction; however, it also noted continued moderate beat-to-beat variability and spontaneous acceleration. At 12:50 p.m. another late deceleration was noted and Mrs. Lapidus was repositioned to her right side. FHR remained in the 130 beat per minute range, with moderate beat-to- beat variability.

14. Vaginal examination at 1:25 p.m. revealed dilatation and effacement to be complete and the fetus at station -1. FHR was noted in the 130 to 140 beat per minute range, with moderate beat-to-beat variability. At 1:40 p.m. Mrs. Lapidus began pushing, and at 1:50 p.m. Susan was delivered (6 hours and 20 minutes after labor commenced).

15. Susan had a weak cry and was dusky at birth, and was placed on a warmer, dried, and given oxygen via blow-by. Apgars of 7 and 8 were assigned at one and five minutes, respectively. Cord specimen was obtained, and, when subsequently analyzed, revealed that, at delivery, Susan presented with a normal pH

    of 7.318.

    
    

16. The Apgar scores assigned to Susan are a numeric expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory

    effort, muscle tone, reflex response, 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 Susan's Apgar score totalled 7, with heart rate, muscle tone and reflex response being graded at 2 each; respiratory effort being graded at 1; and color being graded at 0. At five minutes, Susan's Apgar score totalled 8 with heart rate, respiratory effort, muscle tone, and reflex response being graded at 2 each, and color being graded at 0. Such scores were normal, and consistent with the delivery of a healthy, vigorous infant.

17. Following delivery, Susan developed slight retractions and coarse respirations, as well as a temperature of 100.2, and was transferred to the neonatal intensive care unit (NICU) for further evaluation and treatment. There, physical examination revealed the following:

    HEAD: The head is normocephalic. The anterior fontanel is soft.

    ENT: There is no nasal flaring. The ears are well set. The nasal choanae are patent. Slight protruding tongue.

    THORAX: The chest is symmetric. There is [sic] subcostal retractions.

    LUNGS: There are coarse breast sounds. There is audible grunting present.

    HEART: There is a normal regular rhythm with no murmurs.

    ABDOMEN: The abdomen is non-distended.

    There is no organomegaly. The umbilical cord has three vessels.

    EXTREMITIES: The extremities are symmetric. The hips are normal, without any dislocation or subluxation. The pulses are equal bilaterally. Bilateral simian creases.

    SKIN: There is no cyanosis, and no rashes are present. There is good capillary refill.

    GENITALIA: There are no anomalies noted. CNS: The baby is active and alert. There is good muscular tone.

    Admitting diagnosis (impression) was as follows: 1.- Term 38 weeks appropriate for

    gestational age female.

    2.- Respiratory distress.

    3.- Perinatal sepsis suspected.

    
    

18. Susan remained in the hospital until November 13, 1993, when she was discharged in satisfactory condition to her parents' care. While in the hospital Susan evidenced the following problems:

    RESPIRATORY: The patient developed respiratory distress that required no oxygen, and that subsided rapidly. The results of the CXR [chest x-ray] showed no infiltrate, congestion, pneumothorax or other pathology. The heart size is within normal limits. She developed inspiratory stridor. This was considered to be related to a certain degree of laryngomalacia [flacidity of the epiglottis and aryepiglottic folds (a softening of the cartilage in the upper airway), as in congenital laryngral

    stridor]. 3/

    
    

    R/O SEPSIS: In view of the initial presentation, the possibility of sepsis was considered. The patient was placed on antibiotics, ampicillin and Claforan in appropriate doses. Results of the cultures were negative. The antibiotics were discontinued on 11/12/93.

    
    

    DYSMORPHIC FEATURES: In view of the dysmorphic features, and the possibility of this has been associated with chromosomes pending, a new chromosome studies was sent on 11/12/93 for extended banding. 4/ Also a renal ultrasound was done on 11/10/93 and the result was negative.

    Notably, Susan evidenced no neurologic problems or sequela during the course of her admission. Final diagnosis on discharge was as follows:

    1.- Term 38 weeks appropriate for gestational age female.

    2.- Transient respiratory distress. 3.- Dysmorphic facies.

    4.- Bilateral simian creases. 5.- Perinatal sepsis suspected.

    6.- Mild degree of laryngomalacia. 7.- Slow feeder.

    Susan's subsequent development

    
    

19. Susan's early infancy was apparently unremarkable until around 10 months of age when her parents became concerned that her development (mental and physical) appeared delayed. Consequently, they sought the advice of Susan's pediatrician and, over time, Susan was referred to, and examined by, a number of medical specialists to assess her condition and to identify its etiology.

20. On June 5, 1995, Susan was evaluated by Amanda Naguiat, M.D., Assistant Professor of Clinical Neurology, University of Miami Children's Hospital Center. Dr. Naguiat's assessment was as follows:

    . . . Susan appears to have global development delay with relative strength in social interaction. Her exam is significant for diffuse hypotonia and probably some associated weakness, dysmorphic features and depressed deep tendon reflexes. Her yellowish discoloration is secondary to carotenemia. So far, I cannot put her in a definite syndrome, although phenotypically, the only thing that comes to mind here is some of the rhizomelic forms of

    chondrodysplasia, belonging to the group of peroxisomal disorders. There is a definite need to find etiology for all of these. As discussed with her parents, I would like for her to have an MRI of the brain to look for any malformations or any white matter anomalies that would guide us to further testing. I would like to have some initial metabolic testing, which would include serum quantitative amino acids, urine organic, acids, carnitine total and free levels, and thyroid function tests. I have referred her to Dr. Benke, who they will see this coming Saturday, on June 10, in his clinic up in West Palm Beach, to see if he can shed light on any type of syndrome in view of her dysmorphic features. I concur with the recommendations for her to have early intervention in the form of speech, occupational and physical therapy. As discussed with her parents, I do not believe that her condition will be 'outgrown' and if we do not find any etiology, I would assume that she will follow a static encephalopathy with improvement over time but with persistent impairments. If a cerebral cause for her problems are not found, she should have further investigation for neuromuscular disease, as I am concerned that there might be a concomitant peripheral nervous system problem in view of her hypotonia and weakness and depressed reflexes.

    I will arrange a followup with them as soon as all these tests are done.

    
    

21. On July 17, 1995, an MRI of the brain without contrast was performed and interpreted by Walter H. Forman, M.D. The MRI was considered normal and revealed no changes or anomalies one would associate with hypoxic injury. Specifically the MRI revealed that:

    The ventricles are normal in size and position. No masses or mass effects are identified. I don't see any areas of

    abnormal signal. The myeline maturation appears to be normal for age.

    
    

22. On October 7, 1995, Susan was seen by Paul Benke, M.D., Ph.D., Director, Clinical Genetics, University of Miami School of Medicine, for a second time in a follow-up visit. 5/ Dr. Benke reported the results of that visit as follows:

    I saw this 23 mo old girl with minor anomalies and developmental delay in genetic clinic in Palm Beach Gardens on this date in follow-up. She has made a lot of progress; she can now stand and is starting to talk, she has about 10 words and a sense of humor, and has made up a lot of ground. She has not been sick. The two chromosome studies (including amnio) were sent in to me, and were of sufficient quality that a routine repeat chromosome study would not be helpful. I asked the parents to bring in pictures, since they claimed that pictures of the father, taken as a child, were similar, and I thought there was small, not large resemblance. To my delight (and surprise) the family was quite right about this, and the father had a prominent forehead, low set ears, and slightly small chin as a child. He also had some speech delay, but is very normal now, and these features minimally evident.

    She has had a lot of OT, PT and speech therapy for the past 3 1/2 months, and the parents attribute a lot of her gains to that. But I think that they have done a lot as well, and have had a positive attitude about her development. She has not been sick, and has had no fever, seizures or other problems. Importantly, she had tracheomalacea, and high pitched breathing, and grew out of it by

    1 yr, and the father has a retarded brother.

    
    

    PHYSICAL FINDINGS: Interactive girl with lots of personality, mild dysmorphic features. She is very interactive today. HT: 29 in(?) WT: 22 1/2 lb. HC: 48 cm

    Head: prominent forehead Eyes: mongoloid

    slant IC: 3.5, IP: 6.0, IP: 9.5 (mild increase) Ears: +/-low set Nose: slight depressed nasal bridge Chin: small chin, high arched palate Chest: clear, no rales. Heart: [n]o murmur. Abdomen: neg, no masses, organomegaly Genitals: neg. Spine: no scoliosis.

    Extremities: small hands and feet, hypoplastic 5th toe nail. She is hyperextensible. She has fusiform fingers. Skin: negative

    Neurological: tone a little better. poor DTR. No localizing finding.

    
    

    Diagnosis: Multiple Minor Anomalies, Probable FG (Optiz Frias) Syndrome.

    Counseling: Deferred Pending testing. The Opitz Frias is a very variable disorder, compatible with normal intelligence, and mild-moderate effects on intelligence.

    Affected patients frequently have tracheomalacea or feeding problems, frontal prominence, low set ears, hypertelorism and other findings. Recent research suggests a microdeletion of chromosome #22, determinable by Florescence-in-situ-hybridization (FISH) testing. She has greatly improved, and is functioning at a 12-14 month level today.

    Recommendations: 1) Fish Testing of chromosome #22. We should be able to have blood sent off to the researchers who do this testing. 2. Get pictures of Paul's retarded brother. 3. See in clinic after

    testing. . . .

23. A second genetics evaluation of Susan was conducted on January 21, 1998, by Parul Jayakar, M.D., a clinical geneticist associated with the Genetics Center of South Florida. Dr. Jayaker's report of that examination reads as follows:

    Susan Lapidus came to our office accompanied by her parents, Lori and Paul Lapidus, for a genetics evaluation because she has speech and developmental delay. The patient was born by NSVD at term to a 37 year old gravida 8 para 1061 (2 TAb, 4 SAb) woman. An amniocentesis done because of advanced

    maternal age was normal, 46,XX. The patient's mother states that she was put on progesterone during her pregnancy because of her history of multiple miscarriages. She also smoked approximately 10 cigarettes per day and drank white wine daily throughout her pregnancy. The patient remained in the NICU for 1 week after delivery because she had a strep infection. The patient has not had any major hospitalizations or illnesses. An MRI of the brain was normal at approximately

    2 1/2 years of age. Her vision and hearing have both been evaluated and are reportedly normal.

    
    

    * * *

    
    

    Physical Examination: Height of 39 inches (90%), weight 31 lb. (25%), head

    circumference 48.5 cm (5%).

    
    

    Patient was awake, alert and active, pupils equal and reactive to light, no ectropien, with temporal receding hairline, good hair growth, prominent glabella, slight hypertelorism, flat long philtrum, thin upper lip (? familial), slightly high arched palate, broad nasal root. Chest - no heart murmur; abdomen - soft, no hepatosplenomegaly; genitalia female.

    Extremities - right single palmar crease, slightly hypoplastic toenails.

    Neurologically - vocabulary limited to monosyllables, no obvious cranial nerve palsies.

    Impression: 4 year old with

    
    

    1. Speech and developmental delay

    2. Minor dysmorphic features

    
    

    Susan, in the past, has been seen by

    Dr. Benke who contemplated the diagnosis of Optiz syndrome. At the moment I do not feel that she meets the clinical criteria for Opitz syndrome and the chromosomes done revealed a 46,XX, normal female karyotype and the FISH for chromosome 22 microdeletion was normal. 6/ She was seen also, in June of 1995, by Dr. Naguiat at that time the Mom

    reports that a significant workup was done including MRI of the brain and hearing test which were all normal (verbal report, I do not have these reports in hand). As Mom tells me, an ophthalmology evaluation was also done which was also normal.

    
    

    She has been receiving OT, PT and speech therapy since 17 months of age but lately her speech therapy has been discontinued in her recent school. I feel she is in great need of speech therapy to be able to increase her vocabulary for day to day life.

    
    

    Based on her clinical features I do not feel that she has characteristics of any particular syndrome, the only things which come to mind is the hypoplastic toenails, the long philtrum and the thin upper lip which may be reminiscent of ? Fetal Alcohol Effects (Mom had 1 glass of white wine with dinner every day). I do not think this amount of alcohol intake would cause full blown Fetal Alcohol Syndrome. Certainly some of her facial characteristics also appears to be familial. Therefore, I feel that right now I am unable to label her in any definite syndrome. 7/ As explained to the family, she clinically does not seems to have a progressive neural degenerative condition since she has not have [sic] regression of milestones and seems to be doing much better.

    The dispute regarding compensability

    
    

24. Here, there is no dispute that Susan suffers neurologic dysfunction, mental and physical. What is at issue is whether that dysfunction may reasonably be described as permanent and substantial and, more fundamentally, whether the cause (etiology) of such dysfunction is, more likely than not, attributable to "an injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as required for coverage to

    be afforded under the Plan. Section 766.302(2), Florida Statutes.

25. With regard to the issue of causation and timing, Petitioners are of the view that Susan's presentation is consistent with a brain injury caused by oxygen deprivation which occurred during the course of labor and delivery. In contrast, Respondent is of the view that the proof is not consistent with brain injury caused by oxygen deprivation during or immediately following birth and must, therefore, be attributable to some other etiology. Respondent's view of the proof has merit, and it is unnecessary to address whether Susan's neurologic dysfunction is permanent and substantial.

    The etiology (genesis) of Susan's neurologic dysfunction

    
    

26. To address the etiology of Susan's neurological dysfunction, the parties offered selected records relating to Mrs. Lapidus' antepartum and intrapartum course, as well as for Susan'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 three physicians, at hearing, to address the likely etiology of Susan's presentation. Those physicians were Seth J. Herbst, M.D., a board-certified obstetrician and gynecologist; Jaime Baquero, M.D., a pediatric neurologist, board-certified in pediatrics and board-eligible in neurology; and Charles Kalstone, M.D., a board-certified obstetrician and gynecologist. 8/

27. The medical records and other proof, including the testimony of the physicians offered by the parties, have been carefully considered. So considered, it must be concluded that the proof does not demonstrate (or allow a conclusion to be drawn with any sense of confidence) that, more likely than not, Susan's neurologic dysfunction is related to an "injury to the

    brain . . . caused by oxygen deprivation . . . [which] occurr[ed] in the course of labor, delivery, or resuscitation in the immediate post-delivery period."

28. In reaching such conclusion, it is observed that Susan's course pre-delivery and post-delivery was inconsistent with hypoxic or ischemic injury having occurred during the course of labor, delivery, or resuscitation. First, the evidence documenting fetal heart rate from admission through the period of labor and delivery does not support the conclusion that Susan suffered an acute intrapartum event that led to hypoxic or ischemic injury. Notably, while there were multiple late decelerations (which evidenced periods of diminished oxygenation or, stated differently, periods of transient hypoxia) the fetal monitoring tape also provided reassuring evidence of fetal wellbeing (by documenting good beat-to-beat variability, spontaneous accelerations, normal FHR baseline, and the absence of a progressive or persistent pattern of decelerations). Given such positive evidence of fetal reserve, it is unlikely that

    fetal oxygenation was significantly adversely affected during labor and delivery.

29. Further militating against the conclusion that Susan's impairments were caused by oxygen deprivation during labor or delivery are the numerous inconsistencies between Susan's presentation and development, and the clinical findings one would expect had she suffered hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, during that period. For example, Susan's Apgars were within the normal range; her breathing at birth was essentially stable; cord pH was normal; and she did not evidence neurologic problems in the neonatal course. Finally, the results of Susan's MRI were normal and inconsistent with an hypoxic ischemic brain injury.

30. Given the proof, it cannot be concluded that Susan's neurologic dysfunction resulted from a brain injury caused by oxygen deprivation or that it was related to an event which may have occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Notably, Susan's presentation and neonatal course were not consistent with an acutely acquired neurological injury caused by oxygen deprivation, and it is improbable that she could have experienced an acute event during labor and delivery, or immediately thereafter, without evidencing clinical symptoms of such damage. Conversely, Susan's presentation, and Mrs. Lapidus' prenatal

    history, suggest a genetic or congenital anomaly (or syndrome) as the more likely etiology for Susan's presentation.

    CONCLUSIONS OF LAW

    
    

31. 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.

32. 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.

33. 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.

34. 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.

35. 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.

36. 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.

37. 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.")

38. Here, the proof demonstrated that the attending physician who provided obstetrical services at birth was a "participating physician" 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. However, the record developed in this case failed to demonstrate that Susan suffered a "birth-related neurological injury," within the meaning of Section 766.302(2), Florida Statutes. As noted in the findings of fact, the proof failed to demonstrate, more likely than not, that Susan suffered an injury to the brain caused by oxygen deprivation during the course of labor, delivery, or resuscitation in the immediate post-delivery period. Rather, the proof demonstrated, more likely, that Susan's impairments must derive from some other etiology. Accordingly, the subject claim is not compensable under the Plan. Sections 766.302(2), 766.309(1), and 766.31(1), Florida Statutes.

39. 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 Paul Lapidus and Lori Beth Lapidus, as parents and natural guardians

of Susan Lapidus, a minor, be and the same is hereby denied with prejudice.

DONE AND ORDERED this 16th day of November, 1999, 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 www.doah.state.fl.us

Filed with the Clerk of the Division of Administrative Hearings this 16th day of November, 1999.

ENDNOTES

1/ Mrs. Lapidus is the sole source of information regarding her smoking and alcohol consumption during the course of her pregnancy, and it is unknown whether the stated (admitted) amounts reliably reflect the upper limits of her habit.

2/ The oxytocin challenge test (OCT), a contraction stress test, induces contractions (by the administration of Pictocin) and provides incite into fetal well-being and the integrity (aging) of the placental unit. Essentially, by inducing contractions, the physician may observe how the fetus will react (handle) labor, and resolve whether the fetus can survive its present environment through term or whether (because of placental aging insufficiency or otherwise) the fetus needs to be removed from that environment sooner.

3/ Congenital laryngeal stridor is a stridor (a harsh, high- pitched respiratory sound) and dyspnea (difficult or labored breathing) of the newborn due to an indrawing or infolding of a congenitally flabby epiglottis and aryepiglottic folds (laryngomalacia) during inspiration. Dorland's Illustrated Medical Dictionary, Twenty-Sixth Edition.

4/ The results of the November 11, 1993, chromosome study revealed a normal female karyotype.

5/ Susan was first seen by Dr. Benke on August 31, 1995. In his report to the referring physician regarding that visit, Dr. Benke stated:

We always worry a bit about a child with hypotonia and delay, but I was optimistic when I examined this child because of her personality and curiosity. Nevertheless, we have to proceed because she does have some minor physical changes, she is behind developmentally, and the family history of all the miscarriages and fetal deaths is striking. I had hoped to have the chromosome pictures to look at, the first and most likely cause for concern, and will work on this again by asking the mother to make sure this gets done. If the testing is really negative, we should do metabolic testing, even though the chance of finding a metabolic basis is small. Her physical features were not specific enough at this point to identify a syndrome, and I left this as an open question.

6/ Testing is not, however, conclusive, and does not identify all patients with the syndrome. See Petitioners' Exhibit 7 and Transcript, pages 145 and 146.

7/ A syndrome is a constellation of anomalies that are found in an individual which suggests either a neuro-metabolic or a genetic disorder as the cause of their illness or presentation.

8/ Dr. Herbst was an expert retained by and called to testify by Petitioners. Dr. Baquero was an expert retained by Respondent, but called to testify by Petitioners. Respondent also elicited testimony (on cross-examination) from Dr. Baquero. Dr. Kalstone was an expert retained and called to testify by Respondent.

Here, the medical records and other proof, including the testimony of the physicians offered by the parties, have been carefully considered. So considered, the analysis and opinions of Doctors Baquero and Kalstone as to the likely cause or timing of Susan's neurologic impairment were shown to rest on a logical premise, were grossly consistent with the record, and have been accepted as credible and persuasive.

COPIES FURNISHED:

(By certified mail)

Brian J. Cooke, Esquire David I. Spector, Esquire Arnstein & Lehr

515 North Flagler Drive, Suite 600 West Palm Beach, Florida 33401

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

101 North Gadsden Street Tallahassee, Florida 32301

Lynn Larson, Executive Director Florida Birth-Related Neurological

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

Ronald Koch, M.D.

2611 Poinsettia Avenue

West Palm Beach, Florida 33407

Good Samaritan Medical Center Legal Department

1309 North Flagler Drive

West Palm Beach, Florida 33402

Ms. Charlene Willoughby

Agency for Health Care Administration Consumer Services Unit

Post Office Box 14000 Tallahassee, Florida 32308

Daniel Y. 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: 98-004881N

Orders for Case No: 98-004881N