The Issue At issue in this proceeding is whether Joiner Abelove, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary matters John Abelove and Kathryn Abelove are the parents and natural guardians of Joiner Abelove (Joiner), a minor. Joiner was born a live infant on January 29, 1992, at Cape Canaveral Hospital, a hospital located in Cocoa Beach, Florida, and his birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Joiner was Fred Turner, 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. Abelove's antepartum course and Joiner's birth Mrs. Abelove's antepartum course was without apparent complication; however, by late January 1992, the fetus was noted to be large for gestational age and her obstetrician/gynecologist proposed to induce labor. Mrs. Abelove presented to Cape Canaveral Hospital for a Prostin/Pitocin induction of labor at or about 8:30 a.m., January 28, 1992, and was immediately placed on a fetal monitor. Fetal heart rate (FHR) was reassuring, with a baseline of 148 to 154 beats per minute and good variability.1 Mrs. Abelove received her first Prostin gel, as the first step in the induction of labor, shortly after admission, her second at or about 12:30 p.m., and continued with Prostin until about 7:00 a.m., January 29, 1992, when mild contractions were noted. Membranes were artificially ruptured at 7:25 a.m., revealing clear fluid, and onset of labor was confirmed at 7:30 a.m. At 9:25 a.m., Pitocin was started, and Mrs. Abelove's labor slowly progressed until 7:15 p.m., when she began to push. Until that time, the fetal heart rate tracing was unremarkable or, stated differently, revealed a reassuring fetal heart rate, with normal/average long and short term variability. When Mrs. Abelove began to push, variable decelerations were noted to the 120s for 10 to 20 seconds, with a return to the FHR baseline of 150 to 160 beats per minute. Several other decelerations of a similar nature were noted prior to delivery, but not in sufficient number or intensity to reflect fetal compromise or injury. At 9:18 p.m., January 29, 1992, Joiner, the product of a spontaneous vaginal delivery, was born. Nuchal cord X 3 was noted; however, cord blood pH was 7.36 (normal). Joiner was Deelee suctioned to clear mucus, stimulated and administered oxygen by bag and mask; however, he "did not come around to stimulation [as expected]" and was transported to the neonatal intensive care unit for further management. Joiner was assigned Apgars of 5, 5, and 7, at one, five, and ten minutes, respectively. The Apgar scores assigned to Joiner 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, reflex irritability, 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 Joiner's Apgar score totalled 5, with heart rate being graded at 2; respiratory effort, muscle tone and reflex irritability being graded at 1 each; and color being graded at 0. At five minutes Joiner's Apgar score was unchanged. At ten minutes, his Apgar score totalled 7, with heart rate, muscle tone and reflex irritability being graded at 2 each, respiratory effort being graded at 1, and color being graded at 0. Joiner was admitted to the nursery at 9:25 p.m., and administered whiffs of oxygen. At the time, Joiner was noted to be flaccid (decreased tone); evidence general cyanosis; and exhibit flaring, grunting, and retracting (evidence of respiratory distress). Moist lungs, bilaterally, were also observed. Otherwise, Joiner's newborn infant exam was grossly normal. At 9:28 p.m., Joiner was placed in a oxyhood at 30 percent oxygen, and then increased to 50 percent. By 9:30 p.m., Joiner's oxygen saturation was noted at 100 percent, and his color improving (now pale pink). At or about 9:40 p.m., Joiner was examined by a Dr. Radu and lab work and a chest x-ray were ordered. At 10:00 p.m., following the results of the lab work, Dr. Radu lowered the oxygen to 30 percent. Joiner's oxygen saturation was noted at 98 percent, and he was described as pink with occasional retracting. Chest x-ray noted no acute cardiopulmonary disease, and he was diagnosed with respiratory distress syndrome of the newborn, which proved to be transitory. Course of treatment was continued oxygenation via oxyhood. At 10:30 p.m., Joiner continued to exhibit occasional flaring, grunting, and retracting; however, his color remained pink and he was observed to be active. By 11:30 p.m., Joiner's respirations were described as easy or unlabored, and his color continued pink. His condition remained stable through the night and at 8:20 a.m., January 31, 1992, oxygen was discontinued. At 11:20 a.m., cardiac and oxygen saturation monitors were also discontinued, and Joiner was transferred to the central nursery. There, he was bathed and placed under a warmer. At 12:45 p.m., the warmer was discontinued and Joiner was delivered to Mrs. Abelove where he was noted to latch on and nurse well. At 3:10 p.m., Joiner, in apparent good health, was discharged with his mother from the hospital. Joiner's subsequent development and medical care Joiner was followed at The Pediatric Group, by Dr. Thomas Fisk, for regular routine well-baby care following his discharge from the hospital, and his early infancy was apparently unremarkable; however, some mild delays in gross motor skills were observed at some point during his first year of life. At 13 months, Dr. Fisk saw Joiner for a physical examination, and his mother and grandmother expressed concern over his developmental progress, primarily his expressive language. Regarding these concerns, Dr. Fisk also noted: [His grandmother and mother] did report, however, at that time that he had some new found skills, was verbalizing a lot more, and we decided to watch him over the next few months and see him back at 15 months. Review of the record revealed that he had no vocalization at 9 months, so he had made some progress. At 13 months he was not walking and the only problem that I noticed was what appeared to be some trunkal hypotonia. Joiner was next seen by Dr. Fisk at 16 1/2 months and he observed that Joiner was still suffering from a delay in receptive language and gross motor development. Specifically, Dr. Fisk observed: . . . In receptive language, he does not seem to follow commands or simple instructions very well and he presently says only "mama" and "dada", "no", and has a rather unusual flow of speech. He does not have normal jargon and vocalizations are more grunting and non-fluid in nature. From a gross motor standpoint, is still cruising, but has not begun independent walking. Observation of his gait reveals what appears to be some generalized hypotonia but fairly good strength. Movements involving the upper and lower extremities, however, are also not very fluid and are awkward, however, I cannot put my finger on what seems to be wrong otherwise more specifically. Dr. Fisk's conclusion was generalized developmental delay, and he referred Joiner to Dr. Frank Lopez, a member of the Society of Developmental and Behavioral Pediatrics, to direct the developmental evaluation; however, Joiner was apparently not evaluated by Dr. Lopez until May 29, 1997, as discussed infra. Joiner had a computer tomogram (CT) of the brain on July 23, 1993, which was normal. More specifically, the report noted: No masses are detected. There are no intracranial calcifications. The ventricles are normal. No abnormal fluid collections are seen. At the request of Dr. Fisk, Joiner was seen by Dr. Michael Pollack, a pediatric neurologist on January 17, 1995. Dr. Pollack's report of that examination reads, in pertinent part, as follows: NEUROLOGICAL EXAMINATION: During the initial portion of the office visit, the patient makes minimal eye contact with the examiner. Subsequently he displays more social interaction both with the examiner and with his parents. He engages in mildly mischievous behavior and appears amused. He is not able to stack rings in order after demonstration and does not assemble a Gesell Form Board after demonstration. He does not point to body parts on request. He produces no intelligible words during the office visit and makes minimal attempt to communicate by gesture. He scribbles but does not attempt to copy a figure. Joiner is quite active and enjoys scattering rings about the room but displays no interest in representational play and very little interest in interactive play with the examiner. He does not vocalize abundantly. He does turn to voice. Pupils are equal and reactive to light. Limited view of the ocular fundi shows no abnormalities. There is a full range of conjugate, horizontal eye movement without nystagumus. No facial weakness or significant asymmetry are present. Gag reflex is preserved. Gait is normal. He is not able to cooperate for testing of strength or coordination but functional testing suggests normal strength in all limbs. Tendon reflexes are symmetrically ++ and plantar responses flexor. IMPRESSION: At a chronological age of almost 3 years, Jointer appears to be functioning below the 2 year level. He has facial features which raise the possibility of cerebral gigantism (Soto's syndrome), but these are relatively non-specific and it is noted that his facial features are similar to those of his father. In addition, multiple members of both families are tall as noted above. Although his most conspicuous delay is in the language sphere, other areas of cognitive development also appear to be affected. He has a number of features which fall in the autistic spectrum but does display the ability to interact socially as described above. He has had a variety of diagnostic studies, all of which have been normal. RECOMMENDATIONS: 1. Genetics consultation was suggested. 2. MRI scan of the head was also ordered since cerebral anomalies which are not evident on CT scan are sometimes demonstrated by MRI. The patient was referred to FDLRS and also to a speech/language pathologist. It is likely that he will benefit from medication to improve attention span and to reduce his high activity level, but, if the situation permits, it would be preferable to defer such medication for 1 or 2 years. His parents will call for the result of the MRI scan and the patient will return to the office for re-examination in one year. The results of the MRI scan and chromosome study were normal. Whether Joiner ever returned for re-examination by Dr. Pollack is not of record. Joiner continued to be followed by Dr. Fisk, who had resolved that Joiner suffered from pervasive developmental disorder. On Joiner's visit of June 4, 1996, at approximately 4 1/2 years of age, Dr. Fisk observed: . . . He attends Parton Elementary Pre-K program for children with developmental problems. Father indicates that he has made good progress especially with his expressive language over this last year, but he continues to be remarkably delayed. Expressive language skills are really at the 2-year level, and his visual attending is rated at the one-year level. He has very few skills above the 2-year level. He is extremely aggressive at school, very easily over stimulated, flaps his hands, stimulates himself, as is often seen in children with autism. He has much improvement when on his Ritalin with fair control over these particular symptoms, but the aggressive issue continues to be a major problem for the parents. Now that he is getting bigger, they literally can not go out of the house with him without getting into an aggressive situation. I have discussed in the past with these parents the need for him being involved with a specialist to manage his pervasive developmental delay. Insurance restrictions have preempted their attempts to do this, and they have been unwilling to see Dr. Frank Lopez here in town. I discussed his progress over the last year today in the office with the father. The last note of record by Dr. Fisk, relates to an office visit of February 27, 1997.2 At that time, Dr. Fisk observed: Patient well-known to me with pervasive developmental disorder. Joiner currently is in a developmental preschool situation and takes Ritalin. . . . Parents have noted a significant decrease in his aggressive tendencies and they have been helped out significantly by their present behavioral therapist who has gone to the school, come to their home, and tried to work a behavior program out for Joiner. He is much less aggressive, more cooperative in the classroom, settles down and does at least attend and participate, at least significantly more than he used to. He still has significant language problems, repeats a few words back when spoken to him, but is really still not putting words together in sentences; has significant communication difficulties. Has been feeling well over the time frame of the last several months. Mom was very reluctant originally to consider using Ritalin, but she has come to grips now with the fact that he seems to be doing well on it. They have not gotten involved with child psychiatrist, but have significant educational intervention ongoing. He does see OT and speech therapy as well. Been feeling well recently. Parents relate no medical problems. Uncooperative 5-year-old male who is tall for age, tends to cling to his dad in the office. He will ambulate, however, and cooperated with most of the exam until he had to lay down on the table. Even considering this, he was much better today than he has been in the past. . . . Chest is clear. Cardiovascular: normal. ABD: soft, nontender w/o organomegaly. GU: normal circumcised male. Testes descended. Back and extremities exam: essentially normal with normal gait. He has mild clinodactyly bilaterally. DTRs 2+ and symmetrical. Motor strength and tone equal and symmetrical as well. Hemoglobin today: 14.3. UA could not be obtained secondary to lack of cooperation - parents will be bringing that back. He could not cooperate with hearing or vision screen, but dad says he is scheduled to have his hearing retested next week. Joiner was seen by Dr. Frank Lopez on May 29, 1997. He observed, as follows: Joiner has been referred into this office by courtesy of Dr. Fisk. Joiner is here accompanied by his parents who serve as primary historians and report that he has been seen and had a work-up done by Dr. Colin Condron and Dr. Michael Pollack in the past. Their concerns are that they would like more information regarding Joiner's problems and "a more accurate diagnosis and supportive treatment plan." He has been diagnosed as Developmental Delay and Autistic Spectrum presentation. Mom and Dad are very concerned, not as much with the diagnostic category, but rather with how best to place and guide him. He is presently staffed into EMH at Partin Elementary and will be changing schools, going into TMH classroom due to his not keeping up. The Autistic Program has been considered, but the parents have not decided on its merits yet. Following consideration of Joiner's developmental history, family history, and physical examination, Dr. Lopez's impression was: Autism; Hypotonia; Dyspraxia. Given the proof, it cannot be subject to serious debate that Joiner suffers a serious neurologic impairment. What remains to resolve is the genesis of his impairment or, more pertinent to these proceedings, whether the proof supports the conclusion that his condition resulted from 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 by Section 766.302(2), Florida Statutes, for coverage to be afforded by the Plan.3 With regard to such issue, Petitioners contend that Joiner suffered an injury to his brain caused by oxygen deprivation (an hypoxic event) during the course of resuscitation, and that such injury was the cause of Joiner's neurologic impairment. In contrast, Respondent contends the proof is not consistent with hypoxic ischemic injury occurring during or immediately following child birth, but is consistent with a pervasive developmental disorder or autism.4 Respondent's view of the proof has merit. The genesis of Joiner's neurologic impairment To address the genesis of Joiner's neurologic impairment, the parties offered selected medical records relating to Mrs. Abelove's antepartum and intrapartum course, as well as for Joiner'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 as to the likely cause of Joiner's disorder. The physician selected by Petitioners was Danuta Deeb, M.D., board certified in pediatrics. The physicians offered by Respondent were Edward Lance Wyble, M.D., board certified in pediatrics and neonatology, and Michael Duchowny, M.D., board certified in pediatric neurology, pediatrics, and clinical neurophysiology. The medical records and other documentary proof, as well as the testimony of the physicians offered by the parties have been carefully considered. So scrutinized, 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, Joiner's neurologic impairment was associated with an injury to the brain caused by oxygen deprivation occurring during the course of labor, delivery, or resuscitation in the immediate post-delivery period. Rather, the proof demonstrates, convincingly, that Joiner's presentation is consistent with a pervasive developmental disorder, a disorder within the spectrum of childhood autism, which resulted from an anomaly in brain development, as opposed to a hypoxic ischemic injury during the birth process.5 In so concluding, it is observed that Joiner'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 during the course of labor and delivery does not support the conclusion that Joiner suffered an acute intrapartum event that led to hypoxic or ischemic injury.6 Further militating against the conclusion that Joiner's anomaly was caused by oxygen deprivation pre-delivery or new-onset hypoxia post-delivery, are the numerous inconsistencies between Joiner's presentation and development, and the clinical findings one would expect had he suffered hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, during that period. Notably, Joiner's Apgar scores were 5, 5, and 7 at one, five, and ten minutes. Apgars of 5 do not represent a threatening situation to the brain, but provide a reflection of the infant's status where, as here, the infant is going through a 10-minute to 15-minute change process after birth. Importantly, the Apgar did not stay at 5, but progressed to 7 by ten minutes and the infant was essentially normal when examined by the pediatrician at 9:40 p.m. Clearly, the infant was improving over that period, which compels the conclusion that there was no ongoing insult.7 Had Joiner suffered an injury to his brain during or immediately following birth, there are a number of clinical findings one would reasonably expect to observe. An infant who has suffered a neurologic injury should demonstrate a 6-hour to 12-hour period of decreased tone, followed by evidence of hyperactivity and irritability. Moreover, in cases of substantial neurologic injury, the infant should generally evidence seizure activity within 8 to 24 hours. Beyond the first 24-hour period, the infant should demonstrate moderate to significant decreased tone, depending on the magnitude of the injury, and within the first 48-hour period the injured infant should evidence resistance to feeding. Here, Joiner's decreased tone was resolved by 9:40 p.m., there was no evidence of hyperactivity and irritability, and no evidence of seizure activity. Moreover, at approximately 15 hours of life, Joiner was shown to latch on and breast-feed well. It is further observed that, while he suffered respiratory distress, Joiner did not suffer respiratory arrest or failure, and did not require intubation or mechanical ventilation. Rather, his respiratory effort was adequate to ventilate and, as confirmed by pulse oximeter, he was adequately oxygenated. Also inconsistent with brain injury during or immediately following birth, there was no evidence of other system dysfunction, such as the heart or kidney8; no evidence of brain swelling within 24 hours of birth9; Joiner's lab studies were normal, including cord pH; and follow-up blood-gas studies did not reflect acidosis of substance. In sum, there was no clinical evidence in the newborn period that Joiner's neurologic presentation was abnormal or, stated differently, that he had suffered or was suffering a neurologic injury. Finally, it is observed that Joiner's presentation is consistent with pervasive developmental disorder, a disorder within the spectrum of childhood autism, a serious neurologic disorder in which affected children display abnormalities in socialization, behavior, language and, occasionally, stereotyped motor movements. Such disorder is developmental in origin (an anomaly in brain development), acquired prenatally, and is not associated with events that might occur during labor, delivery, or resuscitation. Given the proof, it cannot be concluded that, more likely than not, Joiner's 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, Joiner'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, or immediately thereafter, without evidencing a single clinical symptom of such damage. Conversely, the existence of a prenatally acquired (predating labor and delivery) brain disorder (developmentally based) would be consistent with Joiner's presentation at birth and subsequent development.
The Issue At issue in this proceeding is whether Respondent's proposal to accept the subject claim for compensation under the Florida Birth-Related Neurological Injury Compensation Plan should be approved and, if so, the amount and manner of payment (lump sum or periodic) of the parental award and the appropriate apportionment of the award between the parents.
Findings Of Fact The claim for compensation Petitioner, Crystal Waddell, and Intervenor, William Davis, are the natural parents of Chelsey Davis (Chelsey), a minor. Chelsey was born a live infant on August 23, 1997, at University Medical Center, a hospital located in Jacksonville, Florida, and her birth weight was in excess of 2500 grams. Ms. Waddell and Mr. Davis are not now, nor have they ever been, husband and wife. The physician providing obstetrical services during the birth of Chelsey was Edward Illions, 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. Here, the parties agree that Chelsey suffered a "birth- related neurological injury" as defined by Section 766.302(2), Florida Statutes, in that she suffered an injury to the brain caused by oxygen deprivation in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital, which rendered her permanently and substantially, mentally and physically impaired. The medical records filed with DOAH on June 15, 1998, as well as the report of neurological evaluation by Michael S. Duchowny, M.D., filed with DOAH on September 28, 1998, are consistent with the parties' agreement. Consequently, it is accepted that Chelsey suffered a "birth- related neurological injury," as defined by Section 766.302(2), Florida Statutes. Given the compensability of the claim, NICA agreed as follows: 8. The Association agrees to pay $100,000.00 as follows: Ms. Crystal Waddell has requested that $6,000.00 be paid to Ms. Cheryl Chieves as reimbursement for funds which she has loaned Ms. Waddell. The Association has no objection to this payment. The Association and Ms. Waddell also request that the Administrative Law Judge schedule a hearing as soon as feasible to determine the entitlement of the mother and/or father, if any, to the parental award. The Association will pay all benefits, past and future, as authorized by Section 766.31, Florida Statutes. . . . The Association agrees that $3,753.25, which includes fees and expenses incurred in the representation of the Claimant in this case, will be paid to Merrill C. Tunsil, Esquire, the attorney for the claimant. (Stipulation filed December 22, 1998.) Consequently, at the commencement of hearing, the parties stipulated that the only issues which remained for resolution were the apportionment of the $100,000.00 award between the parents, and whether such award should be made in lump sum or by periodic payment. (Transcript, page 8.) Background Chelsey's mother, Crystal Waddell (Ms. Waddell), was born May 30, 1979, and was 18 years of age when Chelsey was born.3 Chelsey, born August 23, 1997, was the product of Ms. Waddell's first pregnancy. According to the proof, Ms. Waddell's formal education ceased following her completion of the 11th grade. Thereafter, she was employed by Arby's and, subsequently, by McDonald's in the years preceding Chelsey's birth. Following Chelsey's birth, Ms. Waddell, with the assistance of her mother, dedicated herself to Chelsey's care; however, recently, Ms. Waddell resumed her formal education, with the aim of completing her high school education. Chelsey's father, William Davis (Mr. Davis), was born March 31, 1980, and was 17 years of age when Chelsey was born. At the time, Chelsey was the second child Mr. Davis had fathered without the benefit of marriage. According to the proof, Mr. Davis abandoned his formal education during the 8th grade and, since that time, has been periodically employed in various unskilled positions. Such employment has included a term at McDonald's (where he and Ms. Waddell met); a period of approximately 6 weeks at John Rigsby Painting Company, Raleigh, North Carolina, at and shortly after Chelsey's birth; a term at Top Choice Poultry, following Chelsey's birth and his return to Jacksonville, Florida; and, most recently (since approximately September 1998), employment by Bill Williams Heating and Air Conditioning, where he nets approximately $180.00 each week. As of the date of hearing, Mr. Davis announced that he had recently (that week) started a program designed to achieve his GED and, if successful, hoped to begin an apprenticeship program with his current employer. The nature of Mr. Davis' current employment or the apprenticeship program is not of record. Approximately one year preceding Chelsey's birth, Ms. Waddell and Mr. Davis met while employed at a McDonald's restaurant in Jacksonville, Florida. Apparently, their relationship blossomed and, based on a perceived foundation of love and devotion, they designed to have a child and Chelsey was conceived. While Ms. Waddell and Mr. Davis may have initially felt a sense of purpose or closeness, their relationship proved to be tempestuous. Moreover, while they initially professed commitment and sought parenthood, the couple was never capable of sustaining themselves, much less an infant. Indeed, throughout the course of their relationship, and to this date, Ms. Waddell has continued to reside with her mother, Cheryl Chieves (Ms. Chieves). As Ms. Waddell's delivery date neared, Mr. Davis, who was apparently unemployed at the time, elected to go to Raleigh, North Carolina. According to Mr. Davis, the reason for the trip was two-fold. One reason was to visit his son (the issue of a previous relationship). The other reason was "I had a job waiting there to get some money up, you know." (Transcript, page 131.) As for the duration of the trip, the record reflects that Mr. Davis remained in Raleigh for 3 months, returning at the end of November 1997 when Chelsey was 3 months old. As for the promised job, the proof reflects that Mr. Davis was employed by John Rigsby Painting Company for the first 6 weeks of his stay in Raleigh, but was otherwise unemployed. At or about 10:54 p.m., August 22, 1997, Ms. Waddell was admitted to University Medical Center in labor, and at 12:30 a.m., August 23, 1997, her membranes spontaneously ruptures, with clear fluid noted. Ms. Waddell's labor and delivery was noted in her discharge summary as follows: The patient was admitted to Labor and Delivery . . . with a term intrauterine pregnancy and spontaneous rupture of membranes. The patient's cervix at the time of admission was 6, complete, -3 and vertex presentation. The patient had a protracted, active phase, and was started on Pitocin augmentation. At 7 centimeters, the patient had an intrauterine pressure catheter which showed an adequate contraction pattern x one hour. Her fetal heart tracing showed some subtle decelerations . . . . Later on that day, the patient developed a temperature to 101.2 degrees and she was diagnosed with chorioamnionitis and started on clindamycin and gentamicin. The patient was allergic to penicillin. She continued to make no progress with her cervical examination. A scalp pH was performed [at 6:50 p.m.] and came back 7.29 which showed reassurance. The patient was continued with Pitocin augmentation. A repeat scalp pH [performed at 11:10 p.m.] was 7.05 and [at 11:20 p.m. was] 6.86 [consistent with metabolic acidosis], so the patient was taken to the operating room for a stat cesarean section [and the infant was delivered at 11:36 p.m.]. . . . Apgars were 3 at one minute, 5 at five minutes and 6 at 10 minutes. Findings at the time of surgery showed a live born baby with a terminal meconium. Postoperatively, the baby was taken to the Neonatal Intensive Care Unit. . . . Ms. Waddell was discharged August 30, 1997, and Chelsey was ultimately discharged to the care of her mother on September 12, 1997. Chelsey's course was noted in her discharge summary as follows: HISTORY OF PRESENT ILLNESS: This 3075 gram female infant was born by cesarean section at 38 weeks gestation for decreased fetal heart rate and a scalp pH of 6.8. . . . Rupture of membranes was approximately 18 hours prior to delivery. There was a history of maternal fever and the mother received Clindamycin and Gentamicin. The amniotic fluid was meconium stained and 0.5 cc of thick meconium stained fluid was suctioned from below the cords. Apgars were 3 at one minute, 5 at five minutes and 6 at ten minutes, after receiving positive pressure ventilation and then blow- by oxygen. The infant was transported to the neonatal intensive care unit. PHYSICAL EXAMINATION: Neurological examination showed decreased tone with symmetrical movement and no focal neurological deficits. ADMISSION LABORATORY DATA: The infant is A+ and Coomb's positive. Arterial blood gas on 100% blow-by oxygen revealed a pH of 7.08, pC02 of 18, p02 of 479 and a base excess of -23. ADMISSION DIAGNOSES: Term female. Respiratory depression. Metabolic acidosis. ABO incapability. Sepsis surveillance. HOSPITAL COURSE AND PROBLEM LIST: * * * Respiratory: Initially she had metabolic acidosis and received sodium bicarbonate. A chest x-ray was consistent with retained fetal lung fluid and she was placed on nasal cannula. Initially she had tachypnea which slowly resolved. The nasal cannula was discontinued on day three and she had no further respiratory distress and required no further oxygen. This problem is considered resolved. * * * Central Nervous System: On August 24, 1997 she developed seizure activity at less than 12 hours of age. She was placed on Phenobarbital. An electroencephalogram (EEG) showed "status", although clinically no seizures were noted after the initial episode of seizure activity. . . . Neurology was consulted and she was seen by Dr. Shanks whose impression was acute encephalopathy and recurrent electrographic seizures from multiple-foci despite Phenobarbital therapy. . . . [P]henobarbital was given until maximal serum levels were achieved. She was then started on Dilantin. A head ultrasound on August 25, 1997 was normal. A CT scan on August 26, 1997 showed extensive cerebral low attenuation suggesting anoxic injury. Phenobarbital and Dilantin levels were followed closely and doses were adjusted appropriately. Follow up electroencephalogram (EEG) on September 2, 1997 showed no electrographic seizures and marked suppression except for bursts of excessive sharp waves. The Dilantin was discontinued. No change in the neurological status was noted. Plan: Discharge home on Phenobarbital 12 mg.b.i.d. and follow up Phenobarbital level two weeks after discharge. . . . * * * Discharge Physical Examination: . . . Neurological examination shows symmetrical decreased tone, otherwise no gross neurological deficits were noted. DISCHARGE DIAGNOSES: Term female, 38 weeks gestation. Neonatal asphyxia, resolved. Neonatal seizures ABO incompatibility with hemolysis. Metabolic acidosis, resolved. Anemia. Hyponatremia, resolved. Hypoxic ischemic encephalopathy. . . . Since her discharge, Chelsey has been cared for by Ms. Waddell and her mother (Ms. Chieves), initially in an apartment leased by Ms. Chieves and more recently in a single family residence purchased by Ms. Chieves. Ms. Waddell and Ms. Chieves have jointly shared the responsibility for Chelsey's care and, apart from Aid For Dependent Children (AFDC), which Ms. Waddell started to receive at or about three months after Chelsey's birth, and Medicaid assistance, all financial support for the family has been provided by Ms. Chieves.4 More recently, Ms. Chieves has added her daughter and Chelsey as dependents to her health insurance coverage, which she enjoys as an employee of the State of Florida. The attendant responsibilities and sacrifices inherently associated with Chelsey's daily care may be gleaned from Dr. Michael Duchowny's report of neurological evaluation of August 18, 1998, as follows: HISTORY ACCORDING TO CHELSEY'S FAMILY: Chelsey is an almost 1 year old female who "has cerebral palsy and is legally blind". Ms. Waddell began by explaining that Chelsey has severe motor delay and has essentially made no progress past the newborn level. Chelsey is unable to roll over or sit on her own and requires almost constant feeding. She had an indwelling gastrostomy for the first few months of life, but is now able to mouth and swallow on her own. Still, Chelsey's oromotor problems limit her caloric intake. She is quite small for her age and now weighs only 15 pounds, 14 ounces with a length of 27 inches. Ms. Waddell feels that Chelsey's motor problems effect [sic] all extremities. Chelsey is also "legally blind". By that, her mother indicated that Chelsey is unable to understand what she sees and therefore has little visual information. She can respond to her mother's voice and apparently is hyper alert. She sleeps through the night. Chelsey also suffers from recurrent seizures. These apparently are a marked problem and Chelsey has between 10 and 20 brief tonic seizures per day. Her head and eyes tend to be deviated to the right side with stiffening of the upper extremities. She takes phenobarbital 8 cc b.i.d. and is under the care of Dr. Daniel Shanks in Jacksonville. Chelsey receives physical therapy on a once weekly basis and speech therapy twice weekly. Occupational therapy is administered on one occasion every 2 weeks. . . . * * * NEUROLOGIC EXAMINATION reveals an infant who lies supine with fixed postures in a right tonic neck response. Chelsey demonstrates a startle myoclonus. She has intermittent tongue thrusting movements. There is no drooling. The head is deviated to the right side, but can be passively rotated to the left. There is no central gaze fixation. Chelsey does have brief limited conjugate following. The funduscopic examination is unremarkable. Motor examination reveals increased tone in all extremities indicative of a spastic hemiparesis. The tonic neck response is obligate and can be obtained in both directions through passive movement of the head. There is a positive jaw jerk, sucking and snouting responses. The limbs are small with diminished muscle bulk. Fisting of the thumbs is noted bilaterally. There is evidence of guided reaching. The deep tendon reflexes are brisk at 3+ in all extremities with crossed adductor responses. There are florid bilateral Babinski responses with the large toes being held in passive Babinski attitudes. Sustained ankle and knee clonus are easily elicited. The jaw jerk and facial jerks are both hyperactive. The spine shows a slight curvature convex to the right. The neurovascular examination is unremarkable. In SUMMARY, Chelsey's neurologic examination reveals evidence of severe motor and cognitive delay. Chelsey is showing little progress past the newborn period and her microcephaly suggests that there has been little brain growth since birth. At the same time, Chelsey manifests cortical blindness and startle myoclonus. Chelsey additionally has medically resistant seizures of probable left frontal lobe origin. . . . As heretofore noted, Mr. Davis did not return to Jacksonville, or visit his daughter, until Chelsey was 3 months of age. Thereafter, apart from the first week he was in town and resided with Ms. Waddell and Ms. Chieves, Mr. Davis has lived apart from his daughter and Ms. Waddell, and his participation in his daughter's care, as well as any contribution to his daughter's support, has been de minimus.5 Mr. Davis' interest in Chelsey was stated by him at hearing to be as follows: Q. . . . You're not telling this Court that you want custody of this baby and that you're capable of taking care of it; are you? A. No, sir. I just want it where I can see her when I want to and I ain't got to go through so much trouble, you know, just to see her. Apportionment and manner of payment (lump sum or periodic payment) of the parental award As the primary caretaker for Chelsey, the demands placed on Ms. Waddell as the custodial parent, are, and will continue to be onerous. Clearly, without the support of her mother, the demands placed on Ms. Waddell for Chelsey's care would have left her little or no time for other activities or pursuits, and those demands greatly exceed, and will continue to exceed, those assumed by the parent of an infant not so impaired. In contrast, Mr. Davis has accepted none of the responsibilities (financial or otherwise) associated with Chelsey's care, and has evidenced no sincere inclination to do so. Under the circumstances, it is apparent that, as between them, the loss suffered by Ms. Waddell as a consequence of Chelsey's injury has been grossly disproportionate to that suffered by Mr. Davis, and that such disparity warrants a similar distinction, as between them, in the apportionment of the parental award. As for the method of payment, lump sum or periodic, it should not be subject to serious debate that Ms. Waddell and Mr. Davis have evidenced poor judgment in the past, and that, given their positions in life and young ages, they cannot be relied upon to make sound decisions in the immediate future. Consequently, except for the lump sums hereafter awarded, it is resolved that, absent further order, the bulk of the parental award should be paid periodically to the custodial parent. Given the foregoing considerations, as well as the legal principles discussed infra, it is resolved that of an award of $100,000, Ms. Waddell and Mr. Davis are each eligible to receive $2,500 in lump sum, and that the balance of $95,000 be paid to the custodial parent, retroactive to August 23, 1997, at the rate of $500 per month. Ms. Waddell, as the current and past custodial parent, shall receive the retroactive payment in lump sum and, absent a change in the custodial arrangement, the sum of $500 each month thereafter absent further order or until the principle is exhausted.
The Issue At issue in this proceeding is whether Jacqueline LaPoint, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary matters Catherine LaPoint is the mother and natural guardian of Jacqueline LaPoint (Jacqueline), a minor. Jacqueline was born a live infant on July 2, 1994, at Holy Cross Hospital, a hospital located in Fort Lauderdale, Florida, and her birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Jacqueline was Marsh McEachrane, 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. LaPoint's antepartum course and Jacqueline's birth At or about 1:00 a.m., July 2, 1994, Mrs. LaPoint's membranes spontaneously ruptured (while she was at home), with clear fluid noted, and contractions commenced approximately one to two hours later. At the time her estimated date of delivery had been noted as July 24, 1994, and, apart from the borderline prematurity of the fetus at the time labor commenced, her antepartum course was without apparent complication; however, Mrs. LaPoint did present with a number of risk factors, including a history of chronic smoking; obesity3 (a risk factor of gestational diabetes4); four previous cesarean sections (representing a risk of uterine compromise or rupture); and a large for gestational age fetus. Given the previous uterine surgery, Mrs. LaPoint had been scheduled for a repeat cesarean section. At or about 4:45 a.m., Mrs. LaPoint presented to Holy Cross Hospital in active labor. On presentation, contractions were noted as moderate (with a frequency of 3 to 4 minutes and a duration of 40 to 60 seconds), and vaginal examination revealed the cervix to be at 5 to 6 centimeters, effacement at 80 to 90 percent, and the fetus at station -3. External fetal monitor revealed a normal fetal heart tone (FHT) baseline of 150 to 160 beats per minute. Given her history of previous cesarean sections (uterine surgery) and her presentation of active labor, Mrs. LaPoint was admitted at or about 4:49 a.m. for a repeat cesarean section. FHT was monitored by external fetal monitor from admission until 5:26 a.m., when it was disconnected and Mrs. LaPoint was transported to the operating room (OR). During that period, FHT baseline remained consistent at 150 to 160 beats per minute, except for one episode of variable/late deceleration to the 90-beat per minute range at about 3:00 a.m., but with good beat-to-beat variability and recovery to baseline was noted. One other variable deceleration was noted shortly thereafter to the 120-beat per minute range with spontaneous recovery to baseline. Notably, while the tape reveals some diminished long term variability with contractions, it does not reveal a pattern of persistent deceleration. Mrs. LaPoint was transported to the OR at 5:26 a.m., at which time FHT was noted as 150 beats per minute, and contractions were noted as moderate (with a frequency of 2 minutes and a duration of 40 to 60 seconds). Anesthesia was noted to commence at 5:50 a.m., the operation started at 6:08 a.m., and Jacqueline was delivered at 6:14 a.m. Cord specimen was obtained, and when subsequently analyzed revealed that, at delivery, Jacqueline presented with a pH of 7.085, PCO2 of 90.3, PO2 of 19.2, HCO3 of 27, and a Base Excess (BE) of -6. During delivery amniotic fluid was noted to be thin merconium stained, and oropharyngeal suctioning was done before the shoulders were delivered. Jacqueline was noted as limp (hypotonic) and apnic at birth, and intermittent positive pressure ventilation was given by bag and mask for about one minute. Laryngoscopy revealed cords were clear. Apgars of 4 and 8 were assigned at one and five minutes, respectively. The Apgar scores assigned to Jacqueline 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 irritability, and skin 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 Jacqueline's Apgar score totalled 4, with heart rate being graded at 2; respiratory effort and color being graded at 1 each; and muscle tone and reflex irritability being graded at 0. At five minutes, Jacqueline's Apgar score totalled 8, with heart rate, respiratory effort, and reflex irritability being graded at 2 each, and muscle tone and color being graded at 1 each. While the one minute Apgar was low,5 the five minute Apgar was quite normal or, stated otherwise, not predictive of neurologic complications.6 Following stabilization, Jacqueline continued to evidence respiratory difficulty and, at or about 6:30 a.m., she was admitted to the neonatal intensive care unit (NICU) for further evaluation and management. Initial assessment on admission evidenced an unusual neurologic and respiratory presentation. Neurologically, Jacqueline was noted as lethargic, floppy, and jittery. As for her respiratory presentation, although her breathing rate was regular, she evidenced rales, grunting, flaring, and moderate retractions. Dextrostix (a reagent strip designed for determination of blood-glucose levels with the use of fingertip venous blood) on admission was low, at 26, and immediate glucose testing was ordered and also reported as critically low at 24. Diagnosis was respiratory distress syndrome (RDS) and possible hypoglycemia (an abnormally diminished concentration of glucose in the blood). Respiratory support (for RDS) and intravenous (IV) glucose (for hypoglycemia) were ordered. For respiratory support, Jacqueline was initially placed in an Oxyhood (on an infant warmer bed) with 96 percent oxygen; however, when she continued to require a high oxygen concentration to maintain her gases and saturation levels within normal limits she was intubated (at or about 8:15 a.m.) and ventilator support was provided. Thereafter, her oxygenation was maintained within normal limits without difficulty.7 While Jacqueline's RDS was successfully managed, without apparent harm (by oxygen deprivation or otherwise) to the infant, her hypoglycemia proved refractory or, stated differently, recalcitrant or not responsive to treatment. Indeed it was not until the afternoon of July 4, 1994, that her condition started to resolve, and then only after progressively intensive intervention.8 Here, Jacqueline may reasonably be described as an infant of a diabetic mother9 (IDM)--a hyperglycemic mother--who, consequently, presented with hyperinsulinism, resulting in hypoglycemia.10 Such presentation is clearly demonstrated by elevated readings of insulin in Jacqueline's blood (of 24.7 at 7:00 p.m. on July 3, 1994),11 as well as the severe hypoglycemia she developed subsequent to delivery. Jacqueline was noted as "jittery" throughout the course of treatment; however, the most pronounced period of physiological abnormality was noted at or about 8:00 a.m., July 4, 1994. At that time, an apnic episode was noted during assessment, and tone was flaccid, color pale, and lips dusky. Jacqueline was accorded tactile stimulation without response, and manual breaths were given from the ventilator for approximately 30 seconds before a response was noted. Jacqueline was noted as jittery and diaphoretic (evidencing profuse perspiration). Other apnic episodes, with similar observations, were noted and addressed at 8:15 a.m., 8:18 a.m., and 8:30 a.m. Neurologic consult was called, and an EEG was recommended to rule out seizures, and an ultrasound to rule out possible intraventricular hemorrhage. The EEG was read as normal and the head ultrasound was read as within normal limits, as follows: "No evidence of intraventricular or subpendymal hemorrhage. The ventricles appear normal in size, left slightly larger than right." Jacqueline was started on a course of antibiotics to address the possible presence of sepsis. At or about 4:00 p.m., July 4, 1994, Jacqueline's urinary output was noted to be diminished. Her output continued as diminished and at or about 5:40 p.m., given such development, as well as her continued complex metabolic problems, her treating physician ordered Jacqueline transferred to the Level III Neonatal ICU at Broward General Medical Center for continued evaluation and management. Final diagnosis on discharge was, as follows: Prematurity. Large for gestational age. Respiratory distress syndrome. Hyperglycemia. Hypocalcemia. Hypomagnesemia. Rule out hypoparathyroidism. Seizure disorder. Ventriculoseptal hypertrophy. Jacqueline was discharged from Holy Cross Hospital at or about 8:30 p.m., July 4, 1994, and transported to Broward General Medical Center, where she was admitted at or about 9:18 p.m. in stable condition. There, Jacqueline's condition progressively improved and on July 11, 1994, she was discharged in her mother's care. Jacqueline's course at Broward General Medical Center is reasonably stated in her discharge summary as follows: Admission diagnoses: 36 week white female Large for gestational age Grandmultiparity Respiratory distress R/O RDS I, RDS II, Pneumonia R/O Sepsis R/O Meconium aspiration syndrome R/O Congenital heart disease R/O Pulmonary hypertension R/O Seizures R/O Hyperparathyroid R/O Hypoglycemia, hypocalcemia Transfer from Holy Cross CLINICAL PROBLEMS: Respiratory: RDS I Persistent pulmonary hypertension was diagnosed. The highest delivered FI02 was 0.46, with time spent in increased oxygen = 3 days (total). The infant was intubated and on intermittent mandatory ventilation for approximately 3 days (at BGMC). Cardiac: A cardiac consultation was performed on 7/5/94 by Dr. Miller to reassess previous consult of 7/2/94 at Holy Cross. Echocardiogram revealed hypertrophied left ventricular septum and left posterior wall, turbulance of the left ventricular outflow tract, a PDA with bidirectional shunting and increased pulmonary reistance. Dr. Millers impression as that of RDS with evidence of pulmonary hypertension and hypertrophic cardiomyopathy. Metabolic: Hypoglycemia - treated with IV glucose. Hyponatremia. IV sodium was given. Hypocalcemia. There was treatment with IV calcium. Endocrine: A consultation was performed by Dr. Motkin- Kalia on 7/5/94. Findings were most likely consistent with IDM although there was no maternal history of diabetes/gestational diabetes. Infection: A septic workup was performed on 7/2/94 at Holy Cross Hospital. There was antibiotic treatment with Ampicillin and Gentamicin for 10 days (total) due to clinical evidence of sepsis. Neurologic: Dr. Epstein was consulted on 7/5/94 due to report of seizure at Holy Cross Hospital. Most probable etiology [of seizures] was felt to be hypocalcemia. There was no further seizure activity, infant was treated with phenobarbital X 1 dose after the seizure noted on 7/4/94 An EEG was performed on 7/5/94. It was reported as within normal limits. * * * Final Discharge Diagnoses: 36 week white female Large for gestational age RDS I PFC Hypoglycemia Hyponatremia Hypocalcemia Seizure Clinical sepsis Probable IDM Condition on discharge - Recovered. Jacqueline's subsequent development Jacqueline's early infancy was apparently unremarkable until around the age of 5 to 6 months when she was noted to have visual inattention. Around the same time she was also noted to have intermittent deviation of the head downwards without any associated symptoms. On May 5, 1995, Jacqueline was evaluated by Jaime L. Baquero, M.D., a pediatric neurologist. His neurologic evaluation revealed the following: PHYSICAL EXAM: . . . she indeed appeared visually inattentive . . . [and] did have intermittent downward head deviation which was not fixed and was not associated with any other signs or symptoms. There were no overt dysmorphic features or evidence of neurocutaneous signs. The appendicular muscle tone was felt to be normal, although her axial tone diminished. No other abnormalities were noted on examination. IN SUMMARY, based on clinical history and examination, it does appear that Jacqueline is experiencing significant visual impairment which at this point in my view is very difficult to distinguish whether this is a congenital blindness or delayed visual maturation. The possibility of optic nerve hypoplasia should be entertained being that the mother has possible maternal gestational diabetes, and in addition manifestations of hypoglycemia and hypocalcemia were seen in the neonatal period with seizures accompanying this metabolic deficit. It is known that there is a higher incidence of septal optic dysplasia associated with infants born to diabetic mothers. This sometimes is accompanied by hypopituitarism, therefore, I would recommend obtaining an MRI of the brain to R/O that possibility. In addition, I would like to obtain an EEG because of the concern with this startle and jerking which is seen more often in the morning. In addition, I would like to obtain a Visual Evoked Response to evaluate the integrity of the visual pathways, although if her visual deficits would be cortical, it could still be within normal limits. At some point she would deserve an endocrinologic evaluation to R/O the presence or absence of hypopituitarism. Obviously, being that her APGARS were somewhat low and that she was ventilated, the optic atrophy associated with hypoxic ischemia encephalopathy is still a possibility. I discussed all these different diagnoses with Mrs. LaPointe and we will sit down in a follow-up visit to discuss these issues after the tests have been obtained. Consistent with Dr. Baquero's suggestion, Jacqueline was admitted to Broward General Medical Center on June 6, 1995. The Visual Evoke Response test was normal, "suggesting normal conduction of the pathway between the retina and the occipital lobes bilaterally." The electroencephalogram (EEG) was read as abnormal "due to the presence of intermittent polymorphic slowing noted primarily in the left posterior quadrant but with a field extending sometimes to the right posterior quadrant with admixed spike discharges. These findings are indicative of a regional disturbance of cerebral function that is potentially epiteptogenic maximally noted in the left posterior quadrant."12 On June 14, 1995, Jacqueline was referred to Broward General Medical Center for evaluation of "daily episodes of upper extremity rapid 'jerks'" (possible new onset seizure activity). No seizures were noted on the 24-hour video EEG and on June 15, 1995, Jacqueline was discharged. On June 20, 1995, an MRI of the brain was finally obtained. That MRI revealed the following: FINDINGS CONSISTENT WITH PERIVENTRICULAR LEUKOMALACIA. DELAYED MYELINATION SEEN THROUGHOUT THE CEREBRAL CORTEX AS DESCRIBED ABOVE. THERE ARE NO MRI FINDINGS SEEN TO SUGGEST SEPTAL OPTIC DYSPLASIA. The dispute regarding compensability Here, there is no dispute that Jacqueline suffered an injury to her brain which has resulted in permanent and substantial mental and physical impairment. Indeed, the record reflects, without contradiction, that Jacqueline presents with severe spastic diplegia, is wheelchair dependent for all community mobility, and suffers cortical blindness. What is subject to dispute is the cause and timing (genesis) of Jacqueline's brain injury or, pertinent to these proceedings, whether the proof demonstrates, more likely than not, that her neurologic impairment resulted from an "injury to the brain . . . caused by oxygen deprivation or mechanical injury, occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as opposed to some other genesis. With regard to such issue, Petitioner is of the view that, while there is no dispute that Jacqueline suffered (post- delivery) a significant brain injury caused by severe hypoglycemia, Jacqueline also suffered pre-natal or immediate post-natal oxygen deprivation which caused, or operating in concert with her subsequent hypoglycemia caused, her brain injury. (Petitioner's Proposed Final Order, at page 18.) In contrast, Respondent is of the view that the proof is not consistent with brain injury caused by oxygen deprivation occurring during or immediately following birth and must, therefore, be attributable to Jacqueline's hypoglycemia. Respondent's view of the proof has merit. The genesis of Jacqueline's injury To address the genesis of Jacqueline's brain injury, the parties offered selected records relating to Mrs. LaPoint's antepartum and intrapartum course, as well as for Jacqueline's birth and subsequent development.13 Portions of those records have been addressed supra, and further salient portions will be addressed infra. The parties also offered the opinions of six physicians to address the likely cause of Jacqueline's injury. The physicians offered by Petitioner were Marsh McEachrane, M.D., a board certified obstetrician and gynecologist; Michael Tidwell, M.D., a board certified orthopedist; Lalit Shah, M.D., a board certified neonatologist; and Jaime Baquero, M.D., a pediatric neurologist, board certified in pediatrics and board eligible in neurology. The physicians offered by Respondent were Charles Kalstone, M.D., a board certified obstetrician and gynecologist; and Edward Lance Wyble, M.D., a board certified neonatologist. 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 support (or allow a conclusion to be drawn with any sense of confidence) that, more likely than not, Jacqueline's brain injury was caused by oxygen deprivation occurring during the course of labor, delivery, or resuscitation in the immediate post-delivery period. Rather, the proof demonstrates, more likely than not, that Jacqueline's brain injury was directly related to the severe and intractable hypoglycemia she suffered following delivery and that it was not associated with any event which may have occurred during the course of labor, delivery, or resuscitation in the immediate post-delivery period.14 In so concluding, it is observed that Jacqueline'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 during the course of labor and delivery does not support the conclusion that Jacqueline suffered an acute intrapartum event that led to hypoxic or ischemic injury. Notably, there were only two variable decelerations (one to 90 beats per minute and the other to 120 beats per minute), but with good beat-to-beat variability and spontaneous recovery to baseline, and no persistent or pattern of persistent decelerations. Under such circumstances, the monitoring tape was reassuring and it is unlikely, based on such tape, that fetal oxygenation was adversely affected during labor and delivery.15 Further militating against the conclusion that Jacqueline's brain injury was caused (in whole or part) by oxygen deprivation pre-delivery, or new-onset hypoxia post-delivery, is the lack of trauma associated with Mrs. LaPoint's labor and delivery (labor was short, approximately 5 hours, and delivery was by cesarean section), and the numerous inconsistencies between Jacqueline's presentation and development, and the clinical findings one would expect had she suffered hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, during that period.16 Notably, Jacqueline's Apgar scores were 4 at one minute and 8 at five minutes. While an Apgar of 4 at one minute is less than average or not normal, it is but a reflection of the infant's status where, as here, the infant is going through the change process after birth. Importantly, the Apgar did not remain depressed, as it would have had she suffered an acute intrapartum event, but progressed to 8 (a very normal Apgar score) by five minutes. Clearly, the infant was improving over that period, which also compels the conclusion that there was no new or ongoing insult. Also inconsistent with brain injury during or immediately following birth, there was no evidence of metabolic acidosis on the cord blood sample and, consequently, no evidence to support an ongoing hypoxic process during the course of labor. Moreover, had Jacqueline suffered an injury to her brain during or immediately following birth, there are a number of other clinical findings one would reasonably expect to observe that were absent in her case. For example, an infant who suffered a hypoxic ischemic injury during such period would not only present with initial depression (more severe than Jacqueline evidenced), but would continue to demonstrate severe depression at one, five, and ten minutes. Additionally, in cases of substantial neurologic injury, the infant should generally evidence seizure activity within 8 to 24 hours. Finally, inconsistent with brain injury during or immediately following birth, there was no evidence (within 5 or 6 hours of delivery) of other or multi- organ system dysfunction, including kidney dysfunction. Evidence of such dysfunction would be reflected in decreased urine out-put and on biochemical analysis of blood with elevated serum creatinine levels. No such dysfunction was present in the hours immediately following Jacqueline's birth. Contrasted with the paucity of compelling evidence of perinatal asphyxia as the cause for Jacqueline's brain injury, the medical records and other persuasive proof clearly demonstrate the presence of severe and untractable hypoglycemia and support the conclusion that Jacqueline's brain injury was caused, post-delivery, by the presence of such metablic derangement. Supportive of such conclusion, it is observed that contemporaneously with the observed on-set of hypoglycemia (at or about 6:30 a.m., following admission to the neonatal ICU), Jacqueline was observed to be jittery, lethargic, and floppy, clinical symptoms typically associated with hypoglycemia. Such presentation persisted as Jacqueline's hypoglycemia proved severe and intractable, and at or about 8:00 a.m., July 4, 1994, Jacqueline was noted to undergo an apnic episode, and her tone was flaccid, color pale, and lips dusky. Such events are clinical evidence of the on-set of seizure activity which, given its timing, is compelling proof of brain injury associated with hypoglycemia and not any event associated with labor or delivery, which occurred over 48-hours previously. Further supporting the timing and cause of Jacqueline's insult, is evidence of kidney dysfunction (diminished urine output) at or about 4:00 p.m., July 4, 1994. Given the proof, it cannot be concluded that, more likely than not, Jacqueline's brain injury, and resultant neurologic impairment, was caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Notably, Jacqueline's presentation and neonatal course were not consistent with an acutely acquired neurologic injury, and it is improbable that she could have experienced an acute injury during labor and delivery, or immediately thereafter, without evidencing clinical symptoms of such damage. Conversely, a brain injury, resulting from hypoglycemia acquired post-delivery, would be consistent with Jacqueline's presentation at birth and subsequent development.
Findings Of Fact By stipulation filed November 8, 1995, petitioners and respondent stipulated as follows: That pursuant to Chapter 766.301 - 766.316, Florida Statutes, a claim was filed on behalf of the above-styled infant against the Florida Birth-Related Neurological Injury Compensation Association (the Association) by Susan Petty Rogers and Calyvin Rogers (the petitioners) for benefits under Chapter 766.301 - 766.316, F.S. That a timely filed claim for benefits complying with the requirements of F.S. 766.305 was filed by Petitioners and a timely denial was filed on behalf of the Association. That the Division of Administrative Hearings has jurisdiction of the parties and the subject matter of this claim That the parties agree the medical records of Chelsea Rogers reveal that she suffers form an injury to the right brachial plexus. A brachial plexus injury is not, however, a brain or spinal cord injury. Chelsea has also been diagnosed by T. Wayne Conger, Ph.D., a neuropsychologist, as having a cognitive disorder which may be related to her birth. The cognitive disorder is not, however, a brain injury " which renders the infant permanently and substantially mentally and physically impaired." Therefore, Chelsea does not fit within the strict definition of claims covered by the Florida Birth-Related Neurological Injury Compensation Association under Section 766.302.(2), Florida Statutes. That the infant, Chelsea Rogers was born at Tallahassee Memorial Hospital on April 5, 1990, and that the said hospital was a licensed Florida hospital. The participating physician who was present at the birth and delivered obstetrical services was A. J. Brickler, M.D. That the infant, Chelsea Rogers, weighed 4,510 grams which is in excess of 2,500 grams. WHEREFORE, based upon the above stipulated set of facts, it is respectfully requested that the Division of Administrative Hearings approve the stipulations as being consistent with the evidence in this cause and enter an order denying the claim against the Association on the basis that Chelsea Rogers did not suffer a birth-related neurological injury as defined by Section 766.302(2), Florida Statutes. The medical records and other documentation of record in this case reveal, consistent with the parties' stipulation, that Chelsea Rogers suffered a right brachial plexus injury at birth. A brachial plexus injury is not, however, a brain or spinal cord injury and such injury did not render her substantially physically impaired. Moreover, while Chelsea Rogers may have a cognitive disorder, she is not substantially mentally impaired.
Recommendation Based on the foregoing Findings of Fact and Conclusions of Law, it is ORDERED that the petition for compensation filed by Susan Petty Rogers and Calyvin Rogers, as parents and natural guardians of Chelsea Rogers, a minor, be and the same is hereby denied with prejudice. DONE AND ORDERED this 14th day of November 1995 in Tallahassee, Leon County, Florida. ___________________________________ WILLIAM J. KENDRICK Hearing Officer Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-1550 (904) 488-9675 Filed with the Clerk of the Division of Administrative Hearings this 14th day of November 1995.
Findings Of Fact Owen Light was born on November 26, 2013, at Florida Hospital Altamonte located in Altamonte Springs, Florida. Owen weighed 3,980 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Owen, to determine whether an injury occurred in a hospital due to oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Dr. Willis described his findings in pertinent part as follows in a medical report dated November 3, 2014: In summary, there was no obvious distress during labor or delivery. The newborn was not depressed. Apgar scores were 9/9. The initial exam in the nursery noted some decreased muscle tone, but no acute distress. The baby was apparently doing well until about 12-hours after birth, when seizure activity was noted. Imaging studies showed venous thrombosis in the dural sinus. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post-delivery period. The baby suffered brain injury, as indicated by the abnormal EEG and imaging studies of a venous thrombosis in the dural sinus. However, the brain injury does not appear to be related to either mechanical trauma or hypoxic injury during labor, delivery or the immediate post-delivery period. Dr. Willis reaffirmed his opinion in an affidavit dated January 20, 2015, that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post delivery period. NICA retained Laufey Y. Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to examine Owen and to review his medical records. Dr. Sigurdardottir examined Owen on July 22, 2015, and opined in pertinent part as follows in an affidavit dated August 3, 2015: The opinions expressed in my Report are accurate and my opinions are as follows: The patient is found to have a permanent substantial mental and physical impairment and is overall functioning at approximately a 7-9 month level at the biologic age of 19-20 months. He is noted to have hypotonia, delayed gross and fine motor skills, a past history of epilepsy, delayed visual maturation, although no periods of stagnation or developmental regression have been noted. There is little evidence from the records that we have reviewed to suggest a perinatal ischemic or mechanical injury as the cause for his delays. Prenatal care was complete and documentation during the vaginal delivery was continuous revealing only 2 brief periods of mild fetal heart rate deceleration. Upon delivery, there was no indication of an acute ischemic event with normal Apgar scores of 9 after 1 minute and 9 after 5 minutes. There is documentation from a consulting geneticist that mom described possible prenatal seizure- like events, although a clear description was not given. The patient certainly had an abnormal immature EEG and seizure activity that continued for a few weeks. MRI findings have not been consistent with a profound ischemic event, in fact been completely normal. At this time, it is more likely that Owen has delays in his gross and fine motor skills as well as delayed cognitive development due to a congenital disorder that seems non-progressive in nature. He seems to be receiving excellent care provided to him by his parents and caretakers. At this time, it is difficult to measure Owen’s global cognition but based on acquired skills he functions at a 7-8 month level at the age of 19 months. This would be considered a developmental quotient of 40-45. His life expectancy is not felt to be limited if he shows ongoing developmental progress. He is likely to need lifelong care. I therefore am not recommending Owen to be included into the NICA program. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Willis that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post- delivery period. Dr. Willis’ opinion is credited. There are no expert opinions filed that are contrary to Dr. Sigurdardottir’s opinion that although Owen has both a substantial mental and physical impairment, it is more likely that his neurological impairments are due to a congenital disorder and not due to either mechanical injury or oxygen deprivation during labor, delivery or the immediate post-delivery period. Dr. Sigurdardottir’s opinion is credited.
Findings Of Fact Alvaro Tadeo Iriarte Quiroga was born on May 31, 2007, at Jackson Memorial Hospital in Miami, Florida. Alvaro weighed 2,865 grams at birth. NICA retained Michael S. Duchowny, M.D., as its medical expert in pediatric neurology. Dr. Duchowny examined Alvaro and reviewed his medical records. Dr. Duchowny opined as follows: In summary, Alvaro's neurological examination reveals evidence of abnormal cranial configuration, speech dysarthria, short attention span, high activity level, inconsistent social visual regard, and limited social interaction. He manifests an expressive language delay. He also demonstrates fine motor incoordination. These findings are consistent with a diagnosis of pervasive developmental disorder (PDD) which does not constitute either a substantial mental or motor impairment. A review of Alvaro's medical records indicates that he was born at 37 weeks gestation at Jackson Memorial Hospital with a birth weight of 2,865 gm. Cord Blood gases reveled [sic] significant acidosis and he did not get oxygen for a prolonged period of time (23 minutes). He went on to evidence renal failure and liver dysfunction and had polcythemia and thrombocytopenia. A brain CT scan revealed partial craniosynostois of the anterior sagittal suture. Of note, Alvaro's MRI scan of the brain performed on June 7, 2007 showed no significant abnormalities. Despite his adverse perinatal circumstances, I do not believe that Alvaro's present neurological problems resulted from either mechanical injury or oxygen deprivation in the course of labor or delivery. Furthermore, he has neither a substantial mental nor motor impairment. For these reasons, I am not recommending Alvaro for compensation within the NICA program. A review of the file does not show any opinion contrary to Dr. Duchowny's opinions Alvaro did not suffer a neurological injury due to oxygen deprivation or mechanical injury during labor or delivery and that Alvaro does not have a substantial and permanent mental and physical impairment due to lack of oxygen or mechanical trauma are credited.
The Issue At issue in this proceeding is whether Halle Cohen Martinez, III, a minor, qualifies for coverage under the Florida Birth- Related Neurological Injury Compensation Plan.
Findings Of Fact Petitioners, Barbara Mary Martinez and Halle Martinez, Jr., are the natural parents and guardians of Halle Cohen Martinez, III, a minor. Halle was born a live infant on November 12, 2001, at Leesburg Regional Medical Center, a hospital located in Leesburg, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Halle's birth was Wendell Courtney, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth- Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury" defined as an "injury to the brain or spinal cord . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat. See also, §§ 766.309 and 766.31, Fla. Stat. To address the cause, timing, and significance of Halle's impairment, Petitioners offered selected medical records relating to Halle's birth and subsequent development, as well as the testimony of Mr. and Mrs. Martinez. In turn, Respondent offered the affidavits and the reports of Doctors Donald C. Willis and Paul R. Carney. The cause and significance of Halle's neurologic impairment At birth, Halle suffered a left brachial plexus injury, with resultant left arm brachial plexus palsy, and a left posterior dislocated shoulder, secondary to the birth brachial plexus palsy. Thereafter, at age 5 months, Halle underwent corrective surgery of the brachial plexus using sural nerve grafts, and at 8 months he underwent corrective surgery to improve the function of his left shoulder. The operations resulted in functional improvements; however, as of the date of hearing, Halle continued to suffer impairments of his left arm and hand, which are likely to be permanent, with notable atrophy within the left upper extremity. Apart from the physical impairment Halle exhibits in his left upper extremity, he is otherwise neurologically sound, without evidence of impairment in his right upper extremity or lower extremities; without evidence of cognitive delay; and without evidence of vision or hearing impairment. Accordingly, although Halle evidences a significant birth-related left brachial plexus injury, he is not, on balance, substantially physically impaired, and evidences no mental impairment. Therefore, for reasons appearing fully in the Conclusions of Law, the claim is not compensable, and it is unnecessary to address whether Halle's brachial plexus injury is, anatomically, an injury to the spinal cord.
The Issue At issue in this proceeding is whether Gordon Quinn Kowlessar, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Carmen L. Diaz and Andrew Kowlessar are the parents and natural guardians of Gordon Quinn Kowlessar (Gordon), a minor. Gordon was born a live infant on August 26, 1997, at Halifax Medical Center, a hospital located in Daytona Beach, Florida, and his birth weight was in excess of 2500 grams. The physicians providing obstetrical services during the birth of Gordon were Linda Hensley, M.D., assisted by Julia Harris, M.D., and they 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. Coverage under the Plan Pertinent to this case, coverage is afforded under the Plan when the claimant demonstrates, more likely than not, that the infant suffered an "injury to the brain or spinal cord . . . 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." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Here, the parties agree that Gordon suffered an injury to his brain caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post- delivery period which rendered him permanently and substantially physically impaired. Consequently, the sole issue to resolve is whether such injury likewise resulted in permanent and substantial mental impairment. As to that issue, Petitioners are of the opinion that Gordon's mental development is age appropriate, and Respondent is of the opinion that, at the present time, Gordon's mental status can not be adequately assessed. Gordon's neurologic condition On October 23, 1998, following the filing of the claim for compensation, Gordon was examined by Michael Duchowny, M.D., an expert in pediatric neurology. At the time, Dr. Duchowny was unable to reach an opinion regarding Gordon's mental status for two reasons. First, Gordon was quite young to perform such an assessment. Second, Gordon had a significant motor impairment which made, at his age, the assessment of mental status difficult. Consequently, Dr. Duchowny was unable to offer an opinion as to whether Gordon's brain injury also produced permanent and substantial mental impairment. The infant's mother, Carmen L. Diaz, based on her observations and experience, expressed the opinion that Gordon's mental status or function was normal or, stated differently, age appropriate. Such opinion was premised on Gordon's language development, as well as his reaction/interaction with others and his environment, which in Ms. Diaz's opinion failed to reveal any delay in development of his mental functions. Apart from the observations of Dr. Duchowny and Ms. Diaz, the parties also offered certain medical records pertaining to Gordon's birth and subsequent development (Petitioners' Exhibit 1); however, these records do not provide any meaningful assessment of Gordon's mental status. Indeed, consistent with Dr. Duchowny's observations, they reveal that due to Gordon's motor impairment, a meaningful assessment of his mental status, at the time, was difficult.
