The Issue At issue is whether Aiymani Arlynne Emmanuelli Alicea, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Preliminary findings Vanessa M. Alicea is the natural mother and guardian of Aiymani Arlynne Emmanuelli Alicea, a minor. Aiymani was born a live infant on July 20, 2002, at Orange Park Medical Center, a hospital located in Orange Park, Florida, and her birth weight exceeded 2,500 grams. The physician providing obstetrical services at Aiymani's birth was R. Roland Powers, 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 . . . caused by oxygen deprivation . . . 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."1 § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. Here, the parties have stipulated, and the proof is otherwise compelling, that Aiymani is permanently and substantially mentally and physically impaired. What remains to resolve is whether Aiymani's impairments resulted from an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period," as required for coverage under the Plan. Aiymani's birth and immediate postnatal course At or about 6:30 a.m., July 20, 2002, Ms. Alicea, with an estimated delivery date of July 15, 2002, and the fetus at 40 5/7 weeks' gestation, was admitted to Orange Park Medical Center, for induction of labor. At the time, it was noted that during her prenatal care (on June 18, 2002), Ms. Alicea had tested positive for Group B Streptococcus (GBS) in the vagina, and had been provided antibiotic treatment. Otherwise, her prenatal course was without apparent complication. Upon admission, Ms. Alicea's membranes were intact; blood pressure was noted as 117/76; mild contractions were documented, at a frequency of 3-6 minutes, with a duration of 50-60 seconds; vaginal examination revealed the cervix at 1 centimeter dilation, 70 percent effacement, and the fetus at -2 station; and fetal monitoring revealed a reassuring fetal heart rate, with a baseline in the 140-beat per minute range. An IV was started at 7:20 a.m., antibiotics (Ampicillin) were started at 8:19 a.m., and Pitocin induction was started at 8:40 a.m. Ms. Alicea's labor slowly progressed, and at 11:12 a.m., her membranes spontaneously ruptured, with a small amount of clear fluid noted. At the time, vaginal examination revealed the cervix at 3 centimeters dilation, 80 percent effacement, and the fetus at -1 station. Mild contractions continued to be documented, at a frequency of 2-6 minutes, with a duration of 50-60 seconds. However, beginning at 11:40 a.m., her contractions were noted as moderate, at a frequency of 2-4 minutes, with a duration of 60 seconds, and fetal monitoring continued to reveal a reassuring fetal heart rate, with a baseline in the 130 to 140-beat per minute range. Nevertheless, an occasional decrease in long-term variability was noted, as well as "subtle" late decelerations. At 1:21 p.m., an epidural anesthesia was started; moderate contractions continued, at a frequency of 1.5-5 minutes, with a duration of 50-60 seconds; and by 3:41 p.m., vaginal examination revealed the cervix at 4 centimeters, 80 percent effacement, and the fetus at -2 station. In the interim, at 2:02 p.m., postepidural hypotension was noted, and addressed intravenously with ephedrine (at 2:02 p.m., 2:18 p.m., and 2:24 p.m.). Fetal monitoring continued to appear reassuring, with a baseline in the 130 to 140/140 to 150-beat per minute range. However, occasional decreases in long-term variability were noted, and addressed with position change, oxygen by mask, and IV bolus. Ms. Alicea's labor continued, with moderate contractions, and at 4:08 p.m., vaginal examination revealed the cervix at 5 centimeters, 80 percent effacement, and the fetus at -1 to -2 station. At the time, while fetal monitoring was otherwise reassuring (with a baseline of 140-150 beats per minute, and short and long-term variability present), variable decelerations were documented. Amnioinfusion, to relieve umbilical cord compression, was started at 4:26 p.m., but variable decelerations persisted; by 5:53 p.m., long-term variability had decreased; by 6:08 p.m., accelerations were no longer documented; and at 6:40 p.m., variable late decelerations were noted. In the interim, maternal blood pressure had fallen, fetal heart rate baseline had risen to 150-beats per minute, and at 6:14 p.m., vaginal examination revealed an arrest of active labor (with the cervix at 5 centimeters, 90 percent effacement, and the fetus at -2 station), and at 6:40 p.m., fetal heart rate was noted as "150's - 170's" beats per minute. At the time, Pitocin was discontinued, and intervention included position change, oxygen by mask, and IV bolus. According to the labor and delivery records, at 6:44 p.m., Dr. Powers was called to come to labor and delivery, and notified of fetal tachycardia, decreased long-term variability, late decelerations and low maternal blood pressure (hypotension). On his orders, Ms. Alicea was given an IV bolus, terbutaline, and ephedrine, and Ms. Alicea was taken to the operating room for stat cesarean section, secondary to arrest of active labor and nonreassuring fetal rhythm. Notably, at 6:57 p.m., a portable external fetal monitor was attached, and at 7:00 p.m., revealed a fetal heart rate as "110's - 120's," beats per minute, with accelerations up to "140's for 50 seconds." Ms. Alicea was noted in the operating room at 7:05 p.m., surgery started at 7:15 p.m., and Aiymani was delivered by cesarean section at 7:20 p.m., with Apgar scores of 8 and 9, or 7 and 9, depending on which records are consulted, at one and five minutes respectively.2 Aiymani's delivery was described in Dr. Powers' Operative Report, as follows: . . . the fetal vertex [was] delivered with a vacuum extractor. The oropharynx and nasopharynx were bulb suctioned after nuchal cord x1 was reduced. (This was a loose nuchal cord.) The infant was placed out of the field where it was continued to be bulb suctioned with clear fluid noted. Cord was doubly clamped and cut. The infant was handed to the nurse practitioner for further care and treatment. Cord blood and cord pH obtained . . . . According to the medical records, resuscitation efforts included blowby oxygen, as well as bulb and deep suctioning, and cord pH (arterial) was reported as 7.089, and below the reference range of 7.1 to 7.4. Following delivery, Aiymani was transferred to the newborn nursery, where she was admitted at 7:30 p.m., and remained until she was discharged with her mother at 8:00 p.m., July 22, 2002. Initial examination on admission to the nursery was grossly normal, and her subsequent newborn course was uncomplicated and without evidence of neurologic compromise. Aiymani's subsequent development Following discharge from Orange Park Medical Center, Aiymani's development was without apparent complication until November 20, 2002, when, at 4 months of age, Ms. Alicea voiced concerns to Aiymani's pediatrician (Daya Patel, M.D.) that Aiymani was not holding her head up and was not bearing weight on her legs.3 Dr. Patel diagnosed generalized hypotonia and motor developmental delay, and referred Aiymani for physical therapy. However, no diagnostic workup was undertaken at this point. On February 20, 2003, Aiymani was admitted to Wolfson Children's Hospital on referral from her pediatrician for difficulty breathing. The Admission Admitting Note concluded: IMPRESSION: Respiratory infection with mild wheezing. Severe generalized hypotonia of prenatal onset. Her wheezing seems to not require much in the way of treatment. Since she is on day 3, even if this is an RSV infection she seems to be handling it reasonably well. On the other hand, given her weakness and hypotonia, she will have to be watched more carefully. As far as the hypotonia, it is severe and early onset without detectable reflexes, the most likely cause would be spinal muscular atrophy Type I. Other possibilities would be severe cerebral palsy, myotonic dystrophy, hypothyroidism, congenital syndrome such as Prader-Willi or major CNS malformations. Primary muscle disease is possible as well as diseases of neuromuscular junction. We will involve Neurology early in this admission in order to be efficient in finding the diagnosis. We will do some basic labs and check the neonatal screening for thyroid problems. Other consultations will be obtained as suggested by Neurology. As proposed, neurology was involved early in the admission when Daniel Shanks, M.D., of Nemours Children's Clinic, was called for consultation. Dr. Shanks evaluated Aiymani on February 21, 2003, and reported the results of his consultation, as follows: REASON FOR CONSULTATION: Evaluation of hypotnoia Mother reports that the decrease in overall movement pattern may date back to the third trimester, when she was poorly active in utero. They have been particularly concerned over the last 2 to 3 months with poor head control, poor movement patterns, and very prominent hypotonia. Her mother does report that perhaps she is a little more active over the last couple of months. She has been in physical therapy through Nemours in Orange park. No diagnostic workup has been undertaken to this point. She cannot roll. She can left her legs against gravity to a limited degree. She has had good p.o. feeding. She has had no significant respiratory events other than the present URI symptoms, for which she is admitted. She has not been critically ill or hospitalized. She is the 7 pound 4 ounce product of a term infancy [sic], that was generally unremarkable, other than the decreased movements. She was discharged by 2 days of age, and has had no significant hospitalizations, surgeries, or serious injuries. * * * FAMILY HISTORY: There is no history of neurologic, neurodevelopmental or neuromuscular abnormalities, and specifically no history of infants with severe hypotonia. REVIEW OF SYSTEMS: Generally unremarkable, other than her low tone and movement patterns. She is alert, interactive. There are no constitutional, HEENT, cardiac, respiratory, GI, GU, musculoskeletal, hematologic, endocrinologic, or immunologic concerns. * * * On physical examination, height 67 cm; weight 8.15 kg; head circumference 42.5 cm (50th percentile); weight for height is approximately 90th percentile. Generally, she is a well appearing, alert, socially interactive infant. She lays in a very hypotonic frog-leg posture. Anterior fontanelle is 1 x 2 cm and flat. Cranium appears normal. Neck is supple. There are no chest deformities. Abdomen is benign. Extremities have full range of motion, no deformities or asymmetries, and in fact range of motion is mildly exaggerated due to the hypotonia. Back is without midline lesions, and no significant neurocutaneous lesions are noted. NEUROLOGIC EXAM: She is visually attentive and socially interactive. Cranial nerves: Pupils equal, round and reactive to light. Red reflexes are intact bilaterally. Extraocular movements are full and conjugate. Facial muscle movements are symmetric. She responds to auditory stimulation. There are no overt oral motor abnormalities and no fasciculations are noted in the tongue. Motor exam shows profound hypotonia and apparent weakness. She has very minimal anti-gravity movement. She has little movement when trying to pull her extremity away from a noxious stimulus. She is areflexic. Sensory exam appears grossly intact, and there are no adventitial movements. She has essentially no head control and negative support reflex. She is hypotonic both truncally and peripherally. She has limited mobility, in that she can do very little anti-gravity, and has no ability to get from one point to another. IMPRESSION: Likely profound hypotonia due to neuromuscular disease and anterior horn cell disease would be statistically the most likely. One cannot exclude other neuromuscular processes, however. I think it would be reasonable to send SMN DNA test to Athena, as well as to obtain baseline CPK and a nerve conduction study. Further evaluations can be based on these. If they are unrevealing, then proceeding to muscle biopsy and other metabolic work-up will be considered. An MR Brain scan of February 21, 2003, concluded: FINDINGS: Midline structures of corpus callosum, pituitary gland and cerebellar vermis are within normal limits. Mega cisterna magna is present. There is no mass effect or midline shift. The ventricles have a slightly undulating contour, particularly involving the bodies of the lateral ventricles. The periventricular white matter volume is decreased. Because of the patient's age of 7 months, bright signal is seen on the T2-weighted images in the periventricular and subcortical white matter, but this is expected for the degree of myelination at this age. It is difficult, therefore, to evaluate for true signal abnormality or normal lack of myelination at this age. The decreased white matter volume may represent periventricular leukomalacia. Imaging followup when the patient is 2 years of age or older is suggested to evaluate for periventricular white matter signal abnormality. Mildly prominent extra-axial CSF spaces adjacent to the frontal and parietal lobes bilaterally is a normal finding for the patient's age . . . . IMPRESSION: Abnormal contour of the bodies of the lateral ventricles with decrease in volume of periventricular white matter as discussed above. Finding may be secondary to periventricular leukomalacia, although presence of signal abnormality in the periventricular white matter is difficult to assess at this age due to normal bright signal in the periventricular white matter from lack of myelination. Imaging followup is recommended when the patient is 2 years of age to determine presence of abnormal periventricular white matter signal.[4] Mega cisterna magna. No other structional anomalies are identified. The myelination pattern of the white matter is compatible with the patient's age of 7 months. A motor and sensory nerve conduction study of February 25, 2003, was reported normal for Aiymani's age, with "[n]o evidence of neuropathy at the sites tested." Aiymani was seen at Nemours Children's Clinic for follow-up by Dr. Shanks on March 18, 2003. At the time, Dr. Shanks noted the following: PE: . . . GENERAL APPEARANCE: alert, healthy, not in distress. HEAD: atraumatic, normorcephalic. NECK: supple with full range of motion. EXTREMITIES: no asymmetries or deformities. NEUROLOGICAL EXAM: On neurological exam, . . . muscle tone was severely decreased in extremities and trunk. There is little antigravity movement and I suspect diminished strength. Deep tendon reflexes were absent bilaterally. Sensation was normal to light touch. IMPRESSION: Congenital hypotonia which is significant and appears associated with weakness. Neuromuscular hypotonia which most likely represents anterior horn cell disease. Unfortunately, the critical test is not paid by Medicaid. Athena (the only lab available for the test) is to be in touch with the family to see if arrangements can be made. Alternatively, we may have to proceed with muscle biopsy as another potentially confirmatory test. I will see her back when this is settled. She should continue with PT and oral feeding competence will need to be monitored. Aiymani continued to be followed at Nemours Children's Clinic by neurology (Dr. Shanks, and following his retirement, Dr. David Hammond), genetics (Dr. Pamela Arn), and multiple Nemours sub-specialists. However, despite multiple studies, no etiology or unifying diagnosis for Aiymani's severe hypotonia and developmental delay was identified, and at no time did her treating physicians postulate that a likely cause for Aiymani's neurologic impairments was a brain injury (hypoxic or otherwise) suffered during the course of birth. The parties' experts Apart from the medical records related to Aiymani's birth and subsequent development, salient portions of which have been addressed supra, the parties offered the opinions of three physicians to address the likely etiology of Aiymani's neurologic impairment. These physicians' statements were brief, and in written format. (Petitioner's Exhibit 1; Respondent's Exhibits 12-16). Offered on behalf of Petitioner was the statement of Dr. James O'Leary, a physician board-certified in obstetrics and gynecology, and maternal-fetal medicine. Dr. O'Leary wrote: I have evaluated the medical care rendered to Vanessa Alicea and her 7 pound, 4 ounce daughter. At this time, I am prepared to provide you with my opinions concerning the relationship of that care to the adverse outcome. These opinions are based on the standard care applicable at the time the events in this case occurred, namely 2002 and they are expressed in terms of a reasonable degree of medical certainty. It is my opinion that the permanent neurologic damage sustained by her daughter, Aiymani, which left her brain damaged, occurred during the course of labor, on July 20, 2002, because of the delay in proper treatment of postepidural hypotension and fetal distress which complicated her labor. In addition, Dr. Powers should have performed an emergency cesarean section much sooner. The prenatal care was within accepted standards of care. The ultrasound examinations have excluded any possible intrauterine causes of brain damage. The labor progress was not normal. The rate of dilation was abnormal. There was also an arrest of dilation at 5 cm/minus two station at 6:14 p.m. based upon SVE documentation. Review of the fetal monitoring tracings reveals evidence of late decelerations and an increasing baseline heart rate, variable decelerations and a decrease in the number of accelerations. The standard of care required that the persistent hypotensive episode be rapidly treated and the Pitocin stopped. The failure to do this led to worsening of the fetal heart rate abnormalities, and the ultimate ischemic brain damage from persistent utero-placental insufficiency. Had the physician and nurse midwife properly treated the hypotension and stopped the Pitocin, the fetal distress would have resolved and Aiymani's neurological injuries would not have occurred. In contrast, Dr. Donald Willis, also an expert in obstetrics and maternal-fetal medicine, whose observations were offered on behalf of Respondent, wrote: I have reviewed the medical records for the above named individual. The mother was a 20 year old admitted for induction of labor due to post dates. Cesarean delivery was done for a non-reassuring fetal heart rate pattern and failure to progress. Amniotic fluid was clear. The birth weight was 3,290 grams. The newborn was not depressed. Apgar scores were 8/9. The baby was described as "term, pink, alert, strong cry." The newborn hospital course was uncomplicated and the baby was discharged home with the mother at 48 hours. There was no apparent Obstetrical incident that led to this child's injury. Stated otherwise, Dr. Willis concluded: As such; it is my opinion that there was not 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 as required by Section 766.302(2), Florida Statutes, for a claim to qualify for compensation under Sections 766.301 through 766.316, Florida Statutes. Finally, Dr. Michael Duchowny, a physician board- certified in neurology with special competence in child neurology, and associated with Miami Children's Hospital, offered observations on behalf of Respondent. Notably, Dr. Duchowny examined Aiymani on January 14, 2004, and on October 19, 2005, and based on the results of his examinations and review of the medical records, was of the opinion that Aiymani suffered a substantial mental and physical impairment. However, similar to Aiymani's treating physicians at Nemours Children's Clinic, Dr. Duchowny was of the opinion that Aiymani's neurologic impairments were most likely developmentally based, and not birth-related. Dr. Duchowny concluded: . . . medical records provide [] no support for believing that Aiymani's neurologic impairments resulted from either oxygen deprivation or mechanical injury at the time of birth. [Moreover,] I believe that Aiymani most likely has ataxic cerebral palsy which was acquired prenatally and therefore do not believe that she is compensable under the NICA statute. The likely etiology of Aiymani's neurologic impairments Given the record, it must be resolved that the cause of Aiymani's neurologic impairments, while yet unidentified, was most likely developmentally based, as opposed to birth-related. In so concluding, it is noted that the medical records reveal that Aiymani was not depressed at birth and her immediate postnatal course was uneventful. Moreover, among the physicians who have examined or treated Aiymani, and were well qualified to address the cause of her impairments, there appears to be no disagreement that the likely cause of her impairments was developmentally based, and not birth-related. Consequently, Dr. O'Leary's opinion regarding causation is rejected, as unlikely. Moreover, given the studies that have been done to identify the cause of Aiymani's impairments, as well as the conclusion that the cause of her impairments was most likely developmentally based, Dr. O'Leary's observation that "[t]he [prenatal] ultrasound examinations have excluded any possible intrauterine cause of brain damage" is less than persuasive.
The Issue At issue is whether Monifa Olamina, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts Dashea Jackson and Ifagbemi Olamina are the natural parents and guardians of Monifa Olamina, a minor. Monifa was born a live infant on July 31, 2002, at Putnam Community Medical Center, a hospital located in Palatka, Florida, and her birth weight exceeded 2,500 grams. The physician providing obstetrical services at Monifa's birth was Michael Akhiyat, 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. Monifa's birth and immediate newborn course At or about 2:30 a.m., July 31, 2002, Mrs. Jackson, with an estimated delivery date of August 12, 2002, and the fetus at 38 weeks' gestation, was admitted to Putnam Community Medical Center, with complaints of contractions since 10:20 p.m., July 30, 2002. At the time, strong, regular contractions (at a frequency of 1-2 minutes) were noted; the membranes were intact; vaginal examination revealed the cervix at 9 centimeters dilation, 100 percent effacement, and the fetus at 0 station; and fetal monitoring was reassuring for fetal well-being, with fetal heart rate in the 110s, with variability present. At 2:50 a.m., fetal heart rate continued in the 110s, with long term variability and accelerations present; at 2:53 a.m., Mrs. Jackson's membranes were artificially ruptured, with clear fluid noted; and soon thereafter an ISE (internal scalp electrode) was applied, IVF (intravenous fluid) bolus was started, and 02 (oxygen) per mask was given. At 3:00 a.m., variable decelerations were noted, with pushing; at 3:05 a.m., complete cervical dilation was documented; and at 3:09 a.m., Monifa was delivered, with vacuum assistance. Upon delivery, Monifa was bulb-suctioned, given blow-by oxygen, and accorded tactile stimulation. Apgar scores were noted as 5 and 8, at one and five minutes, respectively.3 Following stabilization, Monifa was transferred to the newborn nursery, where she was received at 3:17 a.m., and where she remained until discharged with her mother on August 1, 2002. In the interim, Monifa's new born course was normal, except for a sacral dimple and evidence of segmentation abnormalities, noted August 1, 2002. Given those issues, an appointment was made at Shands Children's Hospital at the University of Florida (Shands) for August 5, 2002, for an ultrasound of back and x-ray of spine (lumbar and sacral), and on discharge instructions were given to follow-up with the appointment. As instructed, Mrs. Jackson presented with Monifa at Shands on October 5, 2002. Ultrasound Lumbar and Sacral, noted the following findings and impression: FINDINGS: Clinical History: Ultrasound examination of the lower spine was done in this patient with a sacral dimple and the history of segmentation anomalies. There are no prior studies for comparison. Discussion: The spinal cord ends at about L2, a normal level. There is no evidence of tethering or a lipoma in the cord or nerve roots. There is no focal meningocele. IMPRESSION: Examination of the lower spine is normal. Monifa's subsequent development On August 19, 2002, Monifa was admitted to Shands on referral from her primary care doctor (Dr. Marcie Howard) for failure to thrive. At the time, the history of her illness was noted as follows: . . . The patient has had difficulty breast feeding and has been losing weight, although she has had a reasonable number of wet diapers and appears to try to take the breast, it is difficult to estimate how much she is getting. Her mother does indicate she tries to feed her about every two hours and that she latches on, but only for about 15 or 20 minutes and then does seem to have some difficulty staying on task. She often falls asleep. There is no spitting up, vomiting, diarrhea or emesis. Her weights have been six pounds at birth, four pounds eleven ounces on day six, four pounds eight ounces on day sixteen and four pounds fourteen ounces on day 19. That was measured at the scale in Dr. Howard's office. Her mother has tried to give her formula and been unsuccessful. She otherwise seems to [be] fine to her mother . . . . Monifa was discharged from Shands on August 28, 2002. At the time, her Discharge Summary described Monifa's hospital course, as follows: The patient was admitted to evaluate for poor feeding and the decrease in body weight . . . . OT, PT, Lactation and Nutrition consults were involved, and the patient was evaluated poor sucking coordination. Patient was once NPO, then NG tube inserted to feed formula . . . . BMP, thyroid, ammonia, urine organic acid/serum amino acid were sent originally, and all showed normal and urine organic acid/serum amino acid, which are still pending. Brain MRI was done with normal findings . . . . Patient's body weight was increased from 2,212 gm on admission to 2,762 gm today. We also sent HIV antibody which showed a negative, and a chromosome karyotype type which is still pending. Sara Plager was consulted to evaluate for swallow study, and at this point, she did not feel it was necessary to have one. Because of her cardiac murmur, we took chest x-ray and the EKG to discharge home, which both showed within normal limits. We also consulted with Developmental Evaluation Intervention to setup to see Monifa after discharge home. Patient noted DC home with NG tube feeding . . . and they will follow-up with primary care provider. Monifa was fed via NG tube for approximately 6 months,4 and then transitioned to a bottle. Of note, following discharge from Shands, Monifa did not require re-hospitalization. On May 21, 2004, Monifa was seen at the Pediatric Neurology Clinic, Shands Children's Hospital, for developmental delay. Dr. Paul R. Carney, a pediatric neurologist, reported the results of his evaluation, as follows: Monifa is a 1-9/12 year-old African-American female seen at today's Pediatric Neurology Clinic for her developmental delay. She is accompanied to clinic by her mom who provides the history. Her mom states that presently at 21 months of age the baby can scoot and the baby may sit in a tripod fashion for approximately two minutes. The baby is unable to get herself into a sitting position. She currently says "Dada" and will point. Other than that she is not crawling, is not making gains towards pulling herself up or moving towards walking. She has been in therapy. Mom reports that the child has undergone an EEG in October 2003. It was abnormal with slowing and disorganization, nonspecific cortical neuro dysfunction. * * * Review of systems: Mom describes her as basically being healthy. Developmental history has been her marked area of concern in which she only rolled over at 7 months and has just now started to tripod with some assistance. * * * On exam the baby has a height of 79.0 cm, weight of 9.1 kg, head circumference of 44 cm which is less than the 5th percentile. . . . On general exam HEENT reveals a closed anterior fontanel, microcephalic child with marked [a]symmetrical face. . . . Baby is noted to have multiple Mongolian spots on back. It is unclear if baby has cafe au lait spots. . . . Specifically on nerve exam, one of the most striking features about this child is her asymmetrical face. She has decreased movement of her right upper face as well as her lower face. She is noted to have drooling from her face on the right, widened palpebral fissure. The pupils are equal, round, and reactive to light. She does demonstrate full extraocular movements. Tongue is noted to be midline. Motor exam is most noticeable for marked hypotonia. Baby has significant head lag, given her age of 21 months of age. The baby, though, is noted to have positive brisk reflexes in lower extremities and upper extremities as well. Sensory is grossly intact. Cerebellar reveals no tremor when reaching out for objects. Impression: The patient is presenting most likely with a central nervous system disorder. Given the presence of brisk reflexes and her low tone, we have concern that she may have had an intrauterine stroke that was not apparent on the first MRI that was done when she was a few weeks of age. A stroke-like finding on MRIs could certainly explain her asymmetrical face and may indicate that there was some type of distress which has been a cause for her developmental delay. Plan: At this time we will repeat an MRI. We will send labs for a CMP, urine organic acid, and plasma amino acids. We will follow her back in clinic following these studies to further review [with] the mom. . . . The brain MRI was done July 9, 2004, and noted the following findings and impressions: Findings: Current study demonstrates striking cerebellar and pontine atrophy. There is a suggestion that the spinal cord is on the lower limits of size as well. In retrospect, the previous MR demonstrated a somewhat small cerebellum and cerebrum. These changes were not striking enough at that time to call abnormal. However, finding is more pronounced when compared to the current exam. No hydrocephalus, focal lesion, or intra-axial or extra-axial fluid collections are seen. IMPRESSION: Striking cerebellar and pontine atrophy. Differential diagnosis would include pontocerebellar atrophy syndrome, pontocerebellar hypoplasia, and spinocerebellar atrophy syndrome. Apparently, Monifa moved with her family to Jacksonville following her MRI, and returned to Gainesville in early 2006. Then, on March 30, 2006, on the recommendation of her pediatrician, she was again seen at the Pediatric Neurology Clinic for evaluation. The results of that evaluation noted: . . . Today, mom reports that the patient has been slowly progressing and gaining milestones. At 3 years 8 months old she now talks both single words and phrases. She converses with her 2-year-old sister and repeats what her sister says. She cannot walk independently, however, she can walk with difficulty if someone supports her either by the hands and arms or by the trunk. She is able to feed herself. She has been sitting by herself since she was a little over 1 year of age. She was getting some therapy services until she turned 3, but then the services terminated. She was not enrolled for any school this year and therefore received no therapy from the school system. * * * OBJECTIVE: PHYSICAL EXAM: Today her height is 91.3 cm. Her head circumference is 48 cm, and her weight is 12.65 kg. . . . Monifa is awake and tracks with her eyes. She seems interested in her surroundings. She holds on to her mom for balance, standing beside mom's chair and holding onto mom's leg. She bends forward at the hips most of the time. HEENT reveals an asymmetrical face, which appears to be perhaps somewhat weak on the right. She also has a slightly disconjugate gaze. She is hypotonic both centrally and peripherally. She has brisk reflexes throughout and appears to have an up-going toe on the right and down-going toe on the left. She is able to grasp onto a sticker that has been given to her, but does not spontaneously grasp when the examiner tries to hand her a pen. She ambulates with extreme difficulty occasionally taking a step which is very ataxic, and she has extremely poor balance and would fall immediately if she was not supported. She can sit on the exam table by herself, but is noted to hold one hand down on the table for support. ASSESSMENT: This is a 3-year 8-month-old child with history of developmental delay, hypotonia, and ataxia. Past MRI has shown cerebellar and pontine atrophy. She is gaining in milestones and is not declining. Because she continues to gain milestones, at this time, we do not think that she has spinal cerebellar atrophy, but most likely cerebral palsy. PLAN: We have discussed this with mom and told her that this is likely cerebral palsy which is caused by in the birth injury.[5] We are going to repeat her MRI to see if there has been any progression in her atrophy. We are going to sign her up for Children's Medical Services because the patient needs aggressive PT, OT, and Speech Therapy. We are going to have her come back to our clinic in three months. The brain MRI was done May 5, 2006, noted the following findings and impression: Findings: The previous examination demonstrates striking cerebellar and pontine atrophy consistent with possible pontocerebellar atrophy syndrome, pontocerebellar hypoplasia, and spinocerebellar atrophy syndrome. Today's examination demonstrates the same findings. There is apparent flattening of the clivus consistent with likely platybasia. There has been overall progression of cerebellar atrophy and malformation of the pons. There has been interval development of an area of increased signal intensity seen on FLAIR and T2 imaging within the left frontal lobe. This is uncertain etiology and may represent a focal area of gliosis. Otherwise, the brain density is appropriate for a young child. There is minimal retained interstitial water in the cerebral white matter. Myelination is appropriate for age with evidence of myelination in corticospinal tracts, visual pathways and corpus callosum. There is no hydrocephalus. IMPRESSION: Overall progression of cerebellar atrophy and pontine malformation with interval development of an area of increased signal intensity in the left frontal lobe of uncertain etiology. This may represent a focal area of gliosis. See above. On August 3, 2006, Monifa was seen at the Pediatric Neurology Clinic in follow-up for cerebellar atrophy. The results of that evaluation noted: . . . Monifa has been evaluated for speech and language [May 9, 2006]. It is noted that she is approximately one and a half to two years behind in her language development. She remains delayed in her motor skills as well. She still is unable to walk. She has very poor balance but can hold onto a chair and move around the chair without assistance. She definitely cannot ambulate independently. Her mom reports the patient is speaking in two to three word phrases but not in sentences. She does try to mimic her sister. The patient has been signed up for Children's Medical Services, however, mom is still waiting for a nurse to be assigned to her case so she can start getting PT, OT and speech therapy. Overall, Mom does not feel as though Monifa has changed significantly since we saw her on March 30th. She continues to be concerned because the patient is unable to walk. Today, her weight is 12.7 kg. . . . and her head circumference is 47.7 cm. Monifa is sitting in her stroller chair. Her face is asymmetrical, appearing to be weak on the right side. She has very little verbal output but when she does speak, she is dysarthic.[6] She is hypotonic throughout. She has moderately brisk reflexes throughout. She has an upgoing toe on the right and a tight heel cord on the left. When stood up, the patient cannot stand without assistance. She has to be firmly supported. She does take a few steps, which are very ataxic. Assessment: This is a 4-year-old child with progressing cerebellar atrophy. Today, we are going to send her to the lab for repeat serum amino acids and urine organic acids. We are also sending a comprehensive spinal genetics-testing screen to Athena Laboratories for cerebellar atrophy. We are going to get a lactate, a pyruvate and ammonia level. We are going to request a Genetics consult to request their assistance in trying to determine the etiology of this patient's symptoms. . . . Today we have discussed the patient's most recent MRI scan with mom. As of this time, we are not sure whether or not she has spinocerebellar atrophy syndrome or whether she may have some metabolic disorder. Mom has asked if these conditions are progressive and she has been told that they are, however, at this point in time, the patient does not have a definitive diagnosis . . . . Insofar as the record reveals, Monifa has not been seen at the Pediatric Neurology Clinic since her visit of August 3, 2006. However, she was seen for a genetics consult by Charles Williams, M.D., at the Division of Genetics, Department of Pediatrics, Shands Children's Hospital, on February 13, 2007. The results of that consultation noted: The evaluation thus far has resulted in a normal peripheral blood karyotype, normal blood ammonia, essentially normal paravate, and lactate levels and she has had an [A]thena cerebellar ataxia mutation panel which was reported as normal. As well, she has had normal plasma amino acid studies. * * * She has been moving forward developmentally and the mother thinks that her mental age is somewhere between three and four years of age. There is no history of any progressive ataxia or loss of gross motor milestones. * * * On physical examination, Monifa was an interactive little girl who established eye contact and had obvious facial asymmetry with the left hypoplastic mandible and maxilla . . . She was able to smile with a reasonably symmetric facial expression. Her eating has been reported by the mother as fairly well now although she did have some difficulties with swallowing in the first year or two of life. The extremities show no abnormalities. The chest exam normal, abdominal exam negative. A skin exam was free of any birthmark abnormalities. We were able to review her two MRIs as well as her initial CT scan which was done at about two months [sic] of age with our neuroradiologists, and when we looked at all of these, it seemed evident that there was pontine atrophy and cerebellar atrophy present since the first CT scan was performed at age 2 months [sic] and the findings are consistent with actually nonprogressive, pons/brain stem atrophy problem. It is most reminiscent of some type of intrauterine disruption that would cause focal abnormalities in this area. Impression: Our thought at this time is that Monifa does not have any type of neuro- degenerative ponto cerebellar problem. We think that her facial abnormalities in combination with the brain stem findings on the various brain images points to some type of disruption problem . . . that occurred prenatally. However, it is somewhat noteworthy in that she does not show any obvious features of Moebius sequence in terms of her facial examination and although she has marked facial hypoplasia on the left, when we reviewed the literature regarding hemifacial microsomias, we found no association with pontocerebellar atrophic problems. Nevertheless, in view of her good moving forward clinical history, I think that is most likely that her brain abnormality represents some type of acquired in utero disruption process. For the time being, I do not recommend any additional genetic studies and I do appreciate an opportunity providing consultation. Coverage under the Plan 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. The etiology and significance of Monifa's impairments Insofar as the medical records reveal, among the physicians who have treated Monifa, and who were particularly qualified to address the etiology and significance of her impairments, none concluded that Monifa's impairments most likely resulted from a brain or spinal cord injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery or resuscitation in the immediate postdelivery period in the hospital, or that Monifa was permanently and substantially mentally and physically impaired. Indeed, to date her physicians have not identified a unifying etiology for her impairments, but are looking to etiologies other than those associated with Monifa's birth, as a likely cause for her difficulties. Apart from the medical records, Petitioners offered no medical evidence to demonstrate the likely cause or significance of Monifa's neurologic impairments. Consequently, the proof failed to support the conclusion that Monifa suffered a "birth- related neurological injury," as required for coverage under the Plan. See, e.g., Sunshine Plumbing v. Benecke, 558 So. 2d 162, 165 (Fla. 1st DCA 1990)("[T]he claimant bears the burden of proving a causal connection between the employment and the injury."); Vero Beach Care Center v. Ricks, 476 So. 2d 262, 264 (Fla. 1st DCA 1985)("There being no medical evidence of causation, claimant here has not met her burden of proving that her medical condition was causally related to her industrial accident."); Handy v. Golden Gem Growers, Inc., 454 So. 2d 69 (Fla. 1st DCA 1984)("For conditions not readily observable or discoverable without medical examination, proof of causation requires medical testimony based on reasonable medical probability that the injury . . . is causally connected to the employment."); Ackley v. General Parcel Service, 646 So. 2d 242, 245 (Fla. 1st DCA 1994)("[D]etermining . . . cause of a non- observable medical condition, such as psychiatric illness, is essentially a medical question," requiring expert medical evidence.); Broadfoot v. Albert Hugo Association, Inc., 478 So. 2d 863, 865 (Fla. 1st DCA 1985)("[L]ay testimony cannot be used to establish causal relationship within reasonable medical probability as to conditions and symptoms that are not readily observable.").7
The Issue Whether Eman Mustafa, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan). If so, whether the hospital and the participating physician gave the patient notice, as contemplated by Section 766.316, Florida Statutes, or whether any failure to give notice was excused because the patient had an "emergency medical condition," as defined by Section 395.002(9)(b), Florida Statutes, or the giving of notice was not practicable.
Findings Of Fact Stipulated facts Shiren Mustafa and Nehad Mustafa are the natural parents and guardians of Eman Mustafa, a minor. Eman was born a live infant on February 22, 2002, at University Community Hospital, a hospital located in Tampa, Florida, and her birth weight exceeded 2,500 grams. The physician providing obstetrical services at Eman's birth was Caryn L. Bray, 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. Eman's birth and immediate postnatal course At or about 8:00 p.m., February 21, 2002, Mrs. Mustafa, with an estimated delivery date of February 15, 2002, and the fetus at 40 6/7 weeks' gestation, was admitted to University Community Hospital, for induction of labor, and proposed vaginal birth, after prior cesarean section (VBAC). At the time, Mrs. Mustafa's membranes were intact; irregular contractions were noted; vaginal examination revealed the cervix closed, effacement at 60-70 percent, and the fetus at station -2; and fetal monitoring revealed a reassuring fetal heart rate, with a baseline in the 130-beat per minute range. At 9:00 p.m., Cervidil was placed to soften the cervix overnight, and by 7:15 a.m., February 22, 2002, vaginal examination revealed the cervix at 1-2 centimeters dilation, effacement at 90 percent, and the fetus at station -1. Cervidil was removed; at 7:40 a.m., the membranes spontaneously ruptured, with clear fluid noted; and Pitocin was started to augment labor. Fetal monitoring contained to reveal a reassuring fetal heart rate. Mrs. Mustafa's labor rapidly progressed and by 8:30 a.m., vaginal examination revealed the cervix at 5 centimeters,3 effacement complete and the fetus at station 0, and by 9:30 a.m., vaginal examination revealed complete dilation and effacement, and the fetus at station +2. Late decelerations were also noted at 9:30 a.m., but fetal heart rate was otherwise reassuring. Dr. Bray was paged at 9:32 a.m., and returned the page at 9:39 a.m. At the time, Dr. Bray was notified of Mrs. Mustafa's status and requested that the patient start pushing. However, due to the low station of the fetus, staff requested Dr. Bray's presence for pushing, and Dr. Bray stated she would be bedside in approximately 10 minutes. Thereafter, at 9:58 a.m., further decels were noted, and Pitocin was stopped. At 9:59 a.m., Dr. Bray was noted at bedside, oxygen was applied, fluid bolus started, and fetal heart rate decels to 60 beats per minute were documented. Thereafter, at 10:03 a.m., Mrs. Mustafa was pushing, complaining of pain when abdomen palpated, and fetal heart rate in the 50-beat per minute range was noted. Then, at 10:07 a.m., fetal heart rate in the 50s was noted, with brief accelerations to the 110-beat per minute range, and Dr. Bray requested a Kiwi vacuum. At 10:09 a.m., Kiwi vacuum-assisted delivery, with patient pushing, proved unsuccessful, and fetal heart rate was noted in the 110-beat per minute range, with deceleration back to the 60-beat per minute range. At 10:11 a.m., Dr. Bray requested fundal pressure, with patient pushing, but again Kiwi vacuum-assisted delivery was unsuccessful, despite three attempts. Medela vacuum was called for and at 10:17 a.m., two attempts at delivery with the Medela vacuum and fundal pressure proved unsuccessful. Then, at 10:19 a.m., with fetal heart rate remaining in the 60-beat per minute range, a stat cesarean section was called for non-reassuring fetal heart rate and suspected uterine rupture. At 10:22 a.m., Mrs. Mustafa was taken to the operating room, where she was admitted at 10:25 a.m.; surgery started at 10:30 a.m., at which time uterine rupture was confirmed; and Eman was delivered at 10:32 a.m., with Apgar scores of 1, 3, and 6, at one, five, and ten minutes respectively.4 According to the medical records, Eman required resuscitation at birth, with tracheal intubation, IPPV, and cardiac massage, and was then transferred to the neonatal intensive care unit (NICA), where she developed spontaneous respirations, and within two to three hours was weaned from the ventilator. Eman's subsequent newborn course was without incident or evidence of residual effects of birth trauma, and she was discharged with her mother on February 25, 2002. Eman's Discharge Summary included the following observations: PHYSICAL EXAMINATION: A term female infant, weight 3329 grams, length 51 cm, and hip circumference 32 cm. Temperature 97.3, heart rate 158, respiratory rate 62, blood pressure 51/48. HEENT: Normocephalic. Eyes examined at discharge: Pupils were reactive and the red reflex seen. No nasal flaring. Neck supple. Lungs: No retractions. Good air entry. Heart regular rate and rhythm. No murmur. Abdomen soft, no masses, three-vessel cord. Genitalia: Female. Extremities: Moving all limbs, hips stable. No rashes. Neurological: Good tone. INITIAL IMPRESSION: Term female infant. Perinatal depression. Maternal uterine rupture. Respiratory distress. At once (STAT) cesarean section. INITIAL TREATMENT: NICU admission. Pulse oximetry monitoring. Conventional mechanical ventilation. Nothing by mouth. Intravenous fluids. Sepsis workup. Antibiotics. Chest x-ray. PROGRESS: Respiratory: The infant was extubated and weaned to room air within approximately two to three hours of admission. Initial chest x-ray was not significant. Rule out sepsis: The infant was treated with antibiotics; namely, ampicillin and gentamicin for 48 hours. These were discontinued when the cultures remained negative. Fluids and electrolytes: On admission, the infant was given early intravenous fluids, approximately 24 to 48 hours enteral feeds were begun and increased progressively. At the present time the infant is breastfeeding only. She is voiding well, passing stools. Neurological: The infant has good tone and good reflexes, no clonus, and appears to be neurologically normal. SUMMARY: This is a term female infant who was delivered after having maternal uterine rupture. The infant did require neonatal resuscitation but recovered very quickly. At the present time the infant is doing well and feeding well. FINAL DIAGNOSIS: Term female infant. Cesarean section. Perinatal depression. Rule out sepsis. Respiratory distress. Eman's subsequent development Eman's early development was apparently without significant concern until approximately 19 months of age, when she was referred by her pediatrician (Issaam Albanna, M.D.) to Jose Ferreira, M.D., a physician board-certified in neurophysiology and neurology with special qualification in child neurology, for evaluation concerning "some gait disturbance with falling and some coordination problems." Pertinent to this case, Dr. Ferreira reported the results of his initial evaluation of October 6, 2003, as follows: I had the pleasure of seeing Eman for initial evaluation today accompanied by her mother and aunt. The main concern is some gait disturbance with falling and some coordination problems. They report that she started walking somewhat late at 14-15 months and was doing better initially and then seems to be falling more frequently recently and will walk on her toes at times. There is also some deficits with the coordination where she seems to be "clumsy" at times, hands "clinched" frequently and her muscles "give out" on her apparently more frequently then expected for age. She has been developing speech with about 5 words at this point. She tends to drool frequently She is potty training currently as she starts to talk with 5-6 words vocabulary . . . . PAST MEDICAL HISTORY: She was born at full term pregnancy. Birth weight was 7 lb 8 ounces. There was some traumatic delivery as she describes it with uterine rupture and labor requiring a stat cesarean section. She went home with her mother. There was no other problems noted initially. * * * GENERAL PHYSICAL EXAMINATION: HC: 45 cm (5th percentile) WT: 23 lb HR: 90 and regular. HEENT: Unremarkable. Normocephalic. . . . The extremities have full range of motion with no edema, deformities or joint tenderness. The midline back shows no midline defects and no point tenderness to percussion. The skin shows no neurocutaneous findings of significance and there was no dysmorphic features. NEUROLOGICAL EXAMINATION: Shows she was alert. She was initially showing significant stranger anxiety and then was more comfortable with the examiner as the interview took place. She was able to follow some simple commands from her mother. She did not say any words during the examination. The cranial nerve examination revealed full extraocular movements and visual fields full to confrontation. The pupils were equal and reactive. The funduscopic exam showed bilateral red reflex. The face is symmetric and the tongue midline with no fasciculations. There was some degree of drooling noted. Her motor exam shows she had no focal weakness. There is no significant increased resistance to pass of motion other than possibly the right upper extremities. She tended to maintain her hands fisted with some cortical thumbs at times specially when she walked. The gait shows she was somewhat stooped forward to a mild degree but otherwise wide based appropriate for age. She tended to fall occasionally. There was no asymmetry of the use of her extremities otherwise except that she tended to hold the right arm more flexed and the right hand more frequently closed and pronated. The deep tendon reflexes showed 2+. There is no sustained ankle clonus. The plantar responses were extensor bilaterally. Gait and coordination showed there was no tremors and no ataxia [failure of musculature coordination]5 of significance other than the tendency to fall which was somewhat limited coordination. The plantar responses were extensor bilaterally. IMPRESSION: 1. Gait disturbance associated with a mild degree of incoordination with her age with some mild upper motor neuron dysfunction signs as described above in the neurological examination. * * * RECOMMENDATIONS: She will have an MRI of the brain without contrast. She will have a metabolic screening including serum amino acids, ammonia levels, thyroid functions studies, total carnitine levels, ammonia and lactate and CPK levels. She will be seen for follow up here in approximately one and a half to two months or earlier if there is any acute changes. Physical and occupational therapy may be recommended at this point . . . . (Petitioners' Exhibit 2). Eman was reevaluated by Dr. Ferreira on December 15, 2003, and he reported the results of that visit, as follows: I had the pleasure of seeing Eman for follow up today accompanied by her parents. As you know, she has a history of difficulties with her gait and some developmental delay and coordination difficulties. She had an MRI of the brain, which was normal with the exception of some sinusitis. She also had a metabolic screen and had elevated T4[,] and T3 and TSH was normal. She continues having difficulties with her gait and coordination. She has had some drooling at times. Her speech has been somewhat delayed and she has approximately 10-15 word vocabulary but difficult to understand and does not show any signs to suggest regression. She has been sleeping and eating well. * * * HEENT: Unremarkable. . . . The extremities had full range of motion and no edema. NEUROLOGICAL EXAMINATION: She was alert and friendly. She was cooperative. Cranial nerve exam revealed full extraocular movements and visual fields grossly full to confrontation. The pupils are equal and reactive. The funduscopic exam shows bilateral red reflex. The face is symmetric and the tongue was midline with no fasciculations. The motor exams shows she had some difficulties with fine motor coordination. She did not have a good pincer grasp and she tended to keep her hands mostly in a pronated position and somewhat flexed at the elbow and especially when she walked. Her muscle tone was minimally increased in all extremities. Deep tendon reflexes were 2+/2+. The plantar responses were extensor bilaterally. Her gait was minimally spastic with a slightly wide base. She tended to walk somewhat stood forward to a mild degree. When she was sitting she also had some mild degree of truncal ataxia. IMPRESSION: History of developmental disorder with mild speech and language delay as well as some drooling. Mild degree of spasticity with gait disturbance. There is history of sinusitis. RECOMMENDATIONS: As her MRI did not show any intracranial pathology an EEG will be done to evaluate for any encephalopathic changes. She was referred to occupational, speech and physical therapy. The thyroid function (T4 was mildly elevated) will be repeated. She will be seen for follow up here in three to four months or earlier if there is any acute changes . . . . (Petitioners' Exhibit 2). Eman was last evaluated by Dr. Ferreira on February 11, 2004, and he reported the results of that visit, as follows: I had the pleasure of seeing Eman for follow up today accompanied by her parents for a history of gait disturbance with some developmental delay and coordination difficulties. She had an EEG done today which showed a mild abnormality with the right occipital rhythm being slightly lower voltage than the left. The EEG was otherwise normal. She is now in physical, occupational and speech therapy. This just started so it is difficult to say whether or not improvement has been noted. Her parents feel however that she has improved. She is learning new words and her parents feel that she is steadily showing improvement. She is falling still but is moving around better than she has previously. They also feel her drooling has improved. She is eating and sleeping well and they have no new concerns today. * * * HEENT: Unremarkable. . . . Extremities had full range of motion. NEUROLOGICAL EXAMINATION: She is awake and alert. She is very cooperative and friendly. She was speaking at times and was smiling. Cranial nerve and motor exams were unchanged from the last evaluation. Her pincer grasp was still not as good as expected for her age and she tended to keep her hands pronated when walking. Her muscle tone was still mildly increased. Deep tendon reflexes were 2+ and she was walking with a slightly wide based gait for age. She was sitting without assistance for short periods of time today but continued with a mild degree of truncal ataxia. RECOMMENDATIONS: The thyroid panel will be repeated as it was requested at the last visit but unable to be completed.[6] She will continue in the therapies . . . . (Petitioners' Exhibit 2). According to Dr. Ferreira, as of the last time he saw Eman (February 11, 2004) she was still showing some neurologic deficits, which he described as a mild degree of spasticity (increased muscle tone), with gait disturbance; mild upper motor dysfunction, with a less than age-appropriate pincer grasp and tendency to pronate her hands when walking; and a mild speech and language delay. (See Dr. Ferreira's reports of December 15, 2003, and February 11, 2004, supra, and Petitioners' Exhibit 2, pages 15-21, 28-32, and 42). As for permanency, Dr. Ferreira declined (given the limited contact he had with Eman) to offer an opinion regarding the significance of any dysfunction that might persist. Moreover, Dr. Ferreira, who was not familiar with Eman's birth records or those medical records that predated his evaluation of October 6, 2003, offered no opinion, within a reasonable degree of medical certainty, as to the likely etiology of Eman's neurologic defects (i.e., whether they resulted from brain injury caused by oxygen deprivation or mechanical injury occurring during labor delivery or resuscitation, or another etiology) or whether Eman suffered any mental impairment. Subsequent neurologic evaluations On February 23, 2005, Eman was, at NICA's request, evaluated by Michael Duchowny, M.D., a pediatric neurologist associated with Miami Children's Hospital. Dr. Duchowny reported the results of his evaluation, as follows: PRE-AND PERINATAL HISTORY: Eman was born in Tampa at University Hospital after a full term gestation. Her birth weight was 7 pounds 9 ounces, and she remained in the nursery for three days. Eman walked at eighteen months and said single words at two years. She is just beginning toilet training. She is fully immunized and has no known allergies. She has never undergone surgery and has not been hospitalized after birth. PHYSICAL EXAMINATION reveals an alert, well- developed and well-nourished, cooperative 3- year-old girl. Eman weighs 36 pounds and is 45 inches tall. The skin is warm and moist. There are no neurocutaneous stigmata . . . The spine is straight. The head circumference measures 45.8 centimeters, which is below the 3rd percentile for age. There are no cranial or facial anomalies or asymmetries. The neck is supple without masses, thyromegaly or adenopathy. The cardiovascular examination is unremarkable, and the lung fields are clear. There is no palpable abdominal organomegaly. Peripheral pulses are 2+ and symmetric. Eman's NEUROLOGIC EXAMINATION reveals her to be socially interactive and cooperative. She has a good attention span and is quite inquisitive. She smiles frequently. She is able to understand commands and completes them very clearly. She is quite interactive playing games. She knows body parts. She is behaviorally intact. Cranial nerve examinations reveal full visual fields to confrontation testing. The pupils are 3mm and briskly reactive to direct and consensually presented light. There are full and conjugate extraocular movements. Funduscopic examination is unremarkable with well-defined optic disc margins. There are no significant facial asymmetries. The tongue movements are poorly coordinated. Drooling is noted intermittently. Motor examination reveals static hypotonia with a mild increase in tone in all extremities. There are no contractures and there is full range of motion in all joints. The gait is complex with the left heel being slightly elevated with a mild degree of circumduction at the hips and internal rotation at the ankles. Deep tendon reflexes are 1+ in the upper extremities, 3+ at the knees, and 1+ at the ankles. Plantar responses are downgoing. Sensory examination is intact to withdrawal of all extremities to stimulation. Neurovascular examination reveals no cervical, cranial or ocular bruits and no temperature or pulse asymmetries. (Petitioners' Exhibit 3). Based on his neurologic evaluation and review of the medical records, Dr. Duchowny was of the opinion that Eman's impairments were most likely developmentally based (the product of atypical brain development), as opposed to birth trauma (brain injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery or resuscitation). In so concluding, Dr. Duchowny noted that following delivery, Eman's hospital course was inconsistent with traumatic brain damage (there being an absence of significant prolonged respiratory depression, an absence of systemic organ involvement, and an absence of seizure activity), and her MRI scan of November 13, 2003, was normal. Dr. Duchowny also noted that Eman's presentation on February 23, 2005, with a pattern of immature muscle control and expressive language delay, was typical of children with developmental disabilities, as opposed to disabilities associated with birth trauma. Finally, Dr. Duchowny was of the opinion that Eman's expressive language delay was mild to moderate, and her motor disability was moderate, as opposed to substantial, and that her condition was likely to improve with time. (Petitioners' Exhibit 4; Respondent's Exhibit 1). Subsequently, on March 11, 2005, Eman was, at University Community Hospital's request, evaluated by S. Parrish Winesett, M.D. a physician board-certified in pediatrics and neurology with special qualification in child neurology. Dr. Winesett reported the results of his evaluation, as follows: PHYSICAL EXAMINATION: General: Shows a young lady who is alert, who is quite interactive. She smiles easily. She has no obvious dysmorphic features. She has normally placed eyes, ears, nose, philtrum and mouth. Her mental status is that she said single words during my exam. I did not really hear her say sentences. She was rather quiet for the most part. She seemed to follow directions well. Cranial nerve exam showed her pupils were equal and responsive to light. She seemed to have full visual fields. Her extraocular eye movements were intact. Range of motion in all directions was full. Face was symmetrical with good facial movements in both the upper and lower face. Tongue was midline without any fasiculations. Palate raised symmetrically. She shrugged her shoulders will. Motor exam seemed to show that she was strong in all four extremities. I could not get her to fully resist me and give her full effort in trying to resist me, but she did seem to be fairly strong in what resistance I could elicit. She does not seem to have any obvious atrophy of the muscles. She seemed to have normal tone and bulk. In particular, I did not detect any asymmetry of tone nor did I detect any hypertonia. Reflexes in the upper extremities were normal in the biceps, brachial radialis and triceps. In the lower extremities, she did not have any pathologic increase in reflexes, but her patella and ankle reflexes were brisk. Her motor coordination showed that in reaching with both hands, she seemed to be somewhat jerky and has a very slow approach in reaching for my tape measure. She did not seem to be particularly adept at pushing the buttons and pulling the tape as I would expect a child of three to be. She seemed to be very slow. Finger tapping also seemed to be slow and somewhat labored. She did not diminish her amplitude as she tapped. Sensation was not extensively tested, but she did seem to acknowledge being touched in all four extremities in a normal fashion. Her gait was clearly abnormal. Her hands while sitting never showed any adduction of the thumbs within the palms. When she walked, she immediately assumed a posture in which she pulled her arms close to her side, bent her elbows and brought her thumbs within her palm. This was seen each time she started to walk. She did not circumduct her legs but instead seemed to drag her lower extremities and have an almost slapping motion of her feet as she pulled her legs forward. She did not particularly scissor while she was walking. She did not space out her gait while she was walking. * * * Review of the medical records provided to me of both the child, as well as the mother . . . showed the following. The child was born on February 22, 2002 as the product of a 41 week pregnancy. There was an attempted vaginal birth after previous C-section. At approximately 10:02, the fetal heart rate was noticed to be decelerating. The obstetrician was called at that time. The child had heart deceleration during this period that was noted in the nurses notes to be down in the 50's and noted in the physician's notes to be in the 70's. The child was then taken to the operating room where the child was born at approximately 10:32. The child, at that time, was handed over to the neonatal resuscitation team who started resuscitation effort and gave the child Apgar scores of 1, 3 and 6 at 1, 5 and 10 minutes. The patient had been intubated by the 3rd Apgar score. The child was taken back to the NICU where at 10:45, a blood gas was performed which showed a pH of 7.31, a PC02 of 22 and a base excess of -18. The child recovered quite quickly and was extubated in approximately two hours. Review of the operating notes showed that there was reported 200 to 300 cc of blood in the uterus and that there was a uterine rupture noted by the physicians at the operation. The child was discharged from the NICU on February 25, 2002 with the neurological exam reported to be normal. The child has subsequently been seen by Dr. Jose Ferriera for the same complaints that they presented to me with. He has done an MRI which was read as normal by the Tampa Children's Hospital radiologist. Thyroid function tests were ordered and showed a mild elevation of T4. . . . A speech therapy evaluation including the Rossetti Infant Toddler Language Scale showed that she scored at the 15 month range at the age of 23 months for her speech skills. There was apparently some splintering of the scoring but mostly within the 15 to 18 month range. An auditory comprehension subtest, she scores at 23 months which is normal. She is also noted to have some oral motor speech difficulties. Physical and occupational therapy evaluations were reviewed but not as significantly to the data. IMPRESSION: Eman is a young lady who is presenting with predominantly problems in gait disturbance, as well as speech problems. Many of her speech problems could be related to problems in the coordination of her speech. There is a mild increase in reflexes in the lower extremities; however, it does not appear to be a significant degree of hypertonia. Overall, this child appears to have predominant problems with dyscoordination. This is not a typical presentation for a neonatal hypoxic ischemic encephalopathy syndrome. In addition, the fact that the child recovered so quickly and was extubated within two hours and was discharged within two days makes it highly unlikely that the hypoxia suffered at birth is the cause of the neurologic syndrome. (Petitioners' Exhibit 3). Based on his neurologic evaluation and review of the medical records, Dr. Winesett was of the opinion that, while of unknown etiology, it was unlikely Eman's neurologic problems were related to birth trauma. Dr. Winesett also described Eman's motor difficulties as moderate, as opposed to substantial, and offered no opinion regarding her cognitive function. (Petitioner's Exhibit 3, pages 18, 19, 22-26, and 36). 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 . . . 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."7 § 766.302(2), Fla. Stat. See also §§ 766.309(1) and 766.31(1), Fla. Stat. The etiology and significance of Eman's impairments Here, among the physicians who have examined Eman, and who were particularly qualified to address the etiology and significance of her impairments, none concluded that Eman's impairments most likely resulted from brain injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitating in the immediate postdelivery period in the hospital, or that Eman was permanently and substantially mentally and physically impaired. See, e.g., Wausau Insurance Company v. Tillman, 765 So. 2d 123, 124 (Fla. 1st DCA 2000)("Because of the medical conditions which the claimant alleged had resulted from the workplace incident were not readily observable, he was obliged to present expert medical evidence establishing that causal connection."); Ackley v. General Parcel Service, 646 So. 2d 242 (Fla. 1st DCA 1995)(determining cause of psychiatric illness is essentially a medical question, requiring expert medical evidence); Thomas v. Salvation Army, 562 So. 2d 746, 749 (Fla. 1st DCA 1990)("In evaluating medical evidence, a judge of compensation claims may not reject uncontroverted medical testimony without a reasonable explanation."). Therefore, the proof fails to support the conclusion that Eman suffered a "birth-related neurological injury," as required for coverage under the Plan. The notice provisions of the Plan Given that Eman did not suffer an injury compensable under the Plan, it is unnecessary to address whether the healthcare providers complied with the notice provisions of the Plan. See, e.g., Galen of Florida, Inc. v. Braniff, 696 So. 2d 308, 309 (Fla. 1997)("[A]s a condition precedent to invoking the Florida Birth-Related Neurological Injury Compensation Plan as a patient's exclusive remedy, healthcare providers must, when practicable, give their obstetrical patients notice of their participation in the plan a reasonable time prior to delivery."); O'Leary v. Florida Birth-Related Neurological Injury Compensation Association, 757 So. 2d 624, 627 (Fla. 5th DCA 2000)("We recognize that lack of proper notice does not affect a claimant's ability to obtain compensation from the Plan. However, a healthprovider who disputes a plaintiff's assertion of inadequate notice is raising the issue of whether a claim can only be compensated under the plan.").
The Issue Whether Jordan Green, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan). If so, whether the notice provisions of the Plan were satisfied.
Findings Of Fact Preliminary findings Petitioners, Kizzy Bouler Green and Benny Green, are the parents and natural guardians of Jordan Green, a minor. Jordan was born a live infant on October 3, 1995, at Regency Medical Center, a division/campus of Winter Haven Hospital, in Winter Haven, Polk County, Florida, and his birth weight exceeded 2,500 grams. Among the physicians who provided obstetrical services at Jordan's birth was Vincent Gatto, M.D., who, at the time, was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Mrs. Green's antepartum course and Jordan's birth Mrs. Green's antepartum course was without apparent complication until approximately 12:37 p.m., October 3, 1995, when, with the fetus at term (40 weeks by last menstrual period) and an estimated date of delivery of October 1, 1995, she was involved in an automobile accident in Winter Haven, Florida. Emergency medical services (EMS) responded to the scene and, following arrival (at 12:53 p.m.) noted: P[atien]t denies any traumatic pain . . . . [Pt] states immediately following accident that H20 broke, felt no fetal movement . . . . Mrs. Green was "c-spined" (immobilized), an IV was established, and she was transported to Winter Haven Hospital, where she was admitted to the Emergency Department between 1:10 p.m., and 1:20 p.m. On admission, Mrs. Green reported that she was having contractions since the accident, about 3-4 minutes apart, and that she had not felt the baby move following the accident. Mrs. Green was examined by Charles Henrichs, M.D., the Emergency Department physician, between 1:10 p.m., and 1:20 p.m. Dr. Henrichs reported Mrs. Green's history and the results of her physical evaluation, as follows: HISTORY OF PRESENT ILLNESS: This 18-year-old white female primigravida was the unrestrained driver of a car which reportedly was struck by another vehicle in the front end at a significant rate of speed . . . . She indicates that she is having contractions of her uterus, that she thinks her water broke, and that she has not felt any fetal movement since the accident. PHYSICAL EXAMINATION: * * * GENERAL: She is alert and fully oriented and quite lucid. She is fully immobilized by EMS. Primary survey shows the airway to be patent, breathing to be equal and unlabored, circulation to be good with all extremities, warm and with good pulses and there to be no neuro deficits. HEENT: The head shows no visible or palpable signs of trauma. The immobilization was removed, and the neck was entirely nontender with full range of motion. Eyes PERRL/EOMI. Maxillofacial and dentition stable. LUNGS: Clear. CHEST: No chest wall tenderness. HEART: Regular rate and rhythm. MUSCULOSKELETAL: Lower spine, hips, pelvis nontender. ABDOMEN: The abdomen shows a gravid uterus. There are no tetanic contractions. I detect no fetal movements. Fetal heart tones were auscultated for by the nurse and by myself. I was briefly able to listen for fetal heart tones and heard none before my discussions [by telephone] with the obstetrician [at Regency Medical Center, Dr. Matt Koike] . . . . PELVIC: Exam shows a Nitrazine to be negative, vertex presentation, . . . [fingertip to] 1 cm dilated, no bleeding . . . . NEUROLOGIC: She has normal sensorium, motor, sensation and reflex findings. . . . The IV established by EMS is maintained, and she is maintained on oxygen. I have discussed the case with Dr. Koike who responded promptly, and he indicated that we should make arrangements for her transfer to the Regency but to obtain a limited abdominal sonogram for fetal heart activity. This was obtained on an emergent basis, and the fetal heart rate was between 80-90. Upon her return to the emergency department, her exam is essentially unchanged [with contractions 3-5 minutes apart, and no fetal movement]. She was maintained on oxygen and intravenous fluids and transferred to the awaiting ambulance for immediate transfer to the Regency . . . . PROVISIONAL DIAGNOSIS: 1) Abrasions. 2) Contusions. 3) Fetal distress in a term primigravida. Mrs. Green was transported to Regency Medical Center, where she was admitted at or about 2:10 p.m., and, following a sonogram which revealed a fetal heart rate (still bradycardiac at 80-90 beats per minute), she was wheeled directly to a surgical suite and an emergency cesarean section was performed. Dr. Koike described Mrs. Green's history and Jordan's delivery in his Operation Note, as follows: HISTORY: . . . An emergency vehicle brought the patient to the emergency service at Winter Haven Hospital and Dr. Charles Heinrichs, emergency physician, as well as the nursing staff could not hear a fetal heart or detect the fetal heart by Sonicate. Multiple trauma was evaluated and she was ruled out any central nervous system injury, including head injury. Dr. Koike was on call for OB/GYN backup and was called. He was told that there was a fetal demise term pregnancy patient present as a result of a car accident in the emergency service. Dr. Koike asked if there was a sonogram and the response was that a sonogram [had not been done]; however, it was available immediately. A sonogram was immediately performed and showed a severe bradycardia. Dr. Koike was told that there was an emergency vehicle available ready to take the patient over the Regency if need be. At that time, the decision had to be made if she should be operated at the main campus or the Regency Medical Center. However, at the Regency Medical Center there were at least five doctors available near the nursing station, as well as Dr. Kong [a neonatologist]. There was no surgery going on at that time at Regency, and an anesthesiologist was available, as well. It was decided it would be faster overall to bring the patient over and make sure the baby was alive and surgery to be done at Regency Medical Center. An ambulance brought the patient to Regency and the patient was wheeled directly to the recovery room where a sonogram was performed by Dr. Gatto and Dr. Koike, making sure there was still a fetal heart rate present. There was a fetal heart present, and the patient was wheeled directly to the surgical suite and surgery was performed. PREOPERATIVE DIAGNOSIS: Fetal distress, status car accident trauma; intrauterine pregnancy at term. POSTOPERATIVE DIAGNOSIS: Severe oligohydramnios with severe bradycardia, with ruptured membranes. OPERATION: Primary low segment transverse cesarean section delivery of baby boy, 8 pounds 13 ounces, Apgars of 1 at one minute, 4 at five minutes and 8 at 10 minutes at 2:29 p.m., on October 3, 1995. SURGEON: Matt J. Koike, M.D. ASSISTANT: Vincent Gatto, M.D. * * * OPERATIVE FINDINGS: Oligohydramnios. There was blood in the uterine cavity. PROCEDURE: . . . The patient was brought to the OR, an IV was already in. The patient was placed in the supine position, the abdomen was doused with Betadine solution and draped quickly for primary cesarean section. The Foley was already in place and draining clear urine. An incision was made 3 cm above the symphysis pubis with a Pfannenstiel incision to the skin, through the subcutaneous tissue and fascia. The peritoneum was entered longitudinally. Then the uterus was incised at low segment. As soon as the uterine cavity was entered, it was evidence there was blood in the uterine cavity. However, the baby's head was delivered and the nasopharynx suctioned out with DeLee suction and then the baby was delivered without any problem. The umbilical cord was clamped in two places and incised between. The baby was handed over to Dr. Kong for her care . . . . At delivery, Jordan was severely depressed (blue and limp, with no spontaneous respirations, and a heart rate of approximately 80 beats per minute), and was immediately intubated. Spontaneous respirations were noted at 2-3 minutes of life. Arterial cord blood gas revealed, following delivery, a pH of 6.65 and base excess of -31.4, consistent with severe acidosis and acute brain injury (caused by oxygen deprivation), most likely within 30 to 45 minutes of delivery. At or about 2:45 p.m., Jordan was transported to the neonatal intensive care unit (NICU) for further observation and management, and at 5:20 p.m., he was transferred to Tampa General Hospital, where he remained until discharged to his parents' care on October 21, 1995. While there, sequential CT head scans (on October 9, 1995, and October 18, 1995) revealed findings consistent with diffuse ischemic encephalopathy. Subsequent evaluations following discharge confirmed significant brain injury, with severe delay in all areas of development. 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 . . . caused by oxygen deprivation . . . 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." Section 766.302(2), Florida Statutes. See also Section 766.309(1)(a), Florida Statutes. Here, it is undisputed that Jordan suffered an injury to the brain caused by oxygen deprivation (secondary to placental abruption, precipitated by the automobile accident) which rendered him permanently and substantially mentally and physically impaired. What remains to resolve is whether the brain injury occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital. As to that issue, Petitioners are of the view that the injury occurred following the accident, but before delivery, and that Mrs. Green was not in labor during that time period. In contrast, while NICA and the Intervenors agree the injury followed the automobile accident, they are of the view that the proof supports the conclusion that Mrs. Green was in labor and, consequently, the injury occurred during labor, delivery, or resuscitation. Pertinent to this case, when the proof demonstrates that the infant suffered an injury to the brain caused by oxygen deprivation that rendered him permanently and substantially mentally and physically impaired, a rebuttable presumption arises that the injury is a "birth-related neurological injury," as defined by the Plan. Section 766.309(1)(a), Florida Statutes. Under the circumstances of this case, the presumption is that Jordan's injury occurred "in the course of labor, delivery or resuscitation in the immediate post-delivery period in a hospital." Consequently, the issue is whether there was credible evidence produced to support a contrary conclusion and, if so, whether absent the aid of such presumption the record demonstrates, more likely than not, that Jordan's injury occurred during labor, delivery, or resuscitation.1 Here, there was no credible or persuasive evidence produced to support a contrary conclusion.2 Indeed, the credible proof was consistent with the presumption.3 The notice provisions of the Plan While Petitioners have stipulated that the giving of notice by the hospital and the participating physician prior to delivery was not practicable, they contend the notice provisions of the Plan were not satisfied because post-delivery notice was not given in a timely manner. Pertinent to this case, at the time of Jordan's birth, Section 766.316, Florida Statutes, prescribed the notice requirement, as follows: Each hospital with a participating physician on its staff and each participating physician, other than residents, assistant residents, and interns deemed to be participating physicians under s. 766.314(4)(c), under the Florida Birth- Related Neurological Injury Compensation Plan shall provide notice to the obstetrical patients thereof as to the limited no-fault alternative for birth-related neurological injuries. Such notice shall be provided on forms furnished by the association and shall include a clear and concise explanation of a patient's rights and limitations under the plan. In Galen of Florida, Inc. v. Braniff, 696 So. 2d 308, 309 (Fla. 1997), the court resolved that the notice provision existent at the time of Jordan's birth required, "as a condition precedent to invoking the Florida Birth-Related Neurological Injury Compensation Plan as a patient's exclusive remedy, healthcare providers must, when practicable, give their obstetrical patients notice of their participation in the plan a reasonable time prior to delivery." Here, since the giving of notice was not practicable prior to delivery, the hospital and the participating physician were not required to give predelivery notice. As for Petitioners' contention (that the notice provisions of the Plan were not satisfied because post-delivery notice was not given in a timely manner), it must be resolved that, given "the purpose of the notice is to give an obstetrical patient an opportunity to make an informed choice between using a health care provider participating in the NICA plan or using a provider who is not a participant and thereby preserving her civil remedies," post-delivery notice is not required, as a condition precedent to invoking the Plan as a patient's exclusive remedy.4 Id. at 309. Turner v. Hubrich, 656 So. 2d 970, 971 (Fla. 5th DCA 1995)("The statute is silent as to when notice is to be given, but it would make little sense to allow the patients to be apprised of rights and limitations after the services leading to the alleged injuries have been performed.")
The Issue At issue is whether Dillon Campbell, a minor, is permanently and substantially physically impaired.
Findings Of Fact Fundamental findings Monique A. Campbell and Gregory P. Campbell are the parents and natural guardians of Dillon Campbell (also referred to as "Twin A" in the medical records), a minor. Dillon was born a live infant on November 18, 1996, at HCA Health Services of Florida, Inc., d/b/a Columbia Blake Medical Center (Blake Medical Center), a hospital located in Bradenton, Florida, and his birth weight exceeded 2500 grams. The physician providing obstetrical services during Dillon's birth was James S. Albin, 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. Women's Health Associates of Manatee, P.A., was at all times material hereto, Doctor Albin's professional association. Coverage under the Plan Pertinent to this case, coverage under the Plan is available when the claimant demonstrates, more likely than not, that the infant suffered 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 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, Petitioners and Respondent were of the opinion that it was unlikely that the proof would support the conclusion that Dillon was permanently and substantially physically impaired and suggested, given the Plan requirement that the infant suffer both substantial mental and physical impairment for coverage to be afforded by the Plan [Florida Birth-Related Neurological Injury Compensation Association v. Florida Division of Administrative Hearings, 686 So. 2d 1349 (Fla. 1997)], that Dillon's physical presentation be addressed initially, with the view that unnecessary expense might be avoided in resolving the claim. Given the circumstances, it was resolved to bifurcate the issue of physical impairment from the other issues that would also have to be resolved were coverage to be accepted (i.e., the cause and timing of Dillon's brain injury, as well as whether he was also rendered permanently and substantially mentally impaired.) In this case, the proof supports Petitioners' and Respondent's view of the record that Dillon's physical impairments are not substantial, and it is unnecessary to reconvene to take proof with regard to any other issue on the claim. Dillon's birth and subsequent development Dillon was born at 3:28 p.m., November 18, 1998, at Blake Medical Center, and by 6:25 p.m., on the orders of Alberto Soto, M.D., was transferred to Manatee Memorial Hospital for neonatal intensive care. Dillon's birth and subsequent care at Manatee Memorial Hospital were described by Dr. Soto in his discharge summary, as follows: SUMMARY OF NURSERY STAY: Dillon Campbell was a newborn infant born at Columbia Blake Hospital on November 18, 1996. I was called to Blake Hospital for an emergency cesarean section that was being performed on Monique Campbell. She had twin gestation and it was noted that twin A [Dillon] had a decrease in fetal heart rate and also developed a non- reassuring strip and because of that emergency cesarean section was being undertaken. In the operating room, a quick check by one of the nurses could not [detect] heart tones on twin A . . . . On extraction, [twin A] had no pulse and no respiratory effort. Full cardiopulmonary resuscitation was started with positive pressure ventilation and cardiac compressions. The baby was intubated through endotracheal tube and given Epinephrine through the endotracheal tube as well as per the resuscitation protocol. At first Epinephrine dose got the heart rate to about 80 beats per minute; a second dose was given and that got us to a normal count of above 100. This was achieved at about 2 minutes of age. At that point, there still was no respiratory effort. The first attempt of the baby to breathe were observed at about 6 minutes of age. These appeared to be more like gasping than true breaths. Normal easy respiration's were seen at about 11 minutes of age. As part of our resuscitation, Plasmanate was given intravenously because of low blood pressure and slow capillary refill. Blood sugar was checked by chem strip; this was also low so a bolus of D10W was given IV push; these boluses were given by an umbilical venous catheter which was placed as part of resuscitation measures. After those two things were given, an umbilical arterial catheter was placed also. [Apgars were 1 at one minute and 3 five minutes.] I had done an initial venous blood gas from the umbilical vein and this showed a pH of 6.95, a pC02 of 80. Because it was done so quickly from the umbilical vein, I am assuming that this would be the equivalent of a cord blood venous gas. The first arterial blood gas has pC02 of 7.06, after which we gave sodium bicarbonate. Once we settled him in the nursery, we repositioned the tubes both endotracheal, oral gastric, and umbilical artery catheters. The blood sugar dropped again so a second bolus was given. Intravenous fluids were raised and increased from 7 cc per hour to 15 cc per hour of 10 percent Dextrose. A second dose of sodium bicarbonate was given. We gradually had a rising pH. The second pH was 7.32 and the third pH was 7.43. I then went on to get more routine labs and started antibiotics. On visual inspection of the twins, I saw that this baby looked ruddy or plethoric and that the other twin had looked pale. This made us suspect a twin to twin transfusion. I also contacted the Neonatal Intensive Care Unit at Manatee Memorial Hospital for transfer. Part of our initial physical assessment on Dillon was that there was . . . generalized edema noticed mostly at the posterior and all other parts of the body were also puffy. The abdomen appeared distended which we felt was possibly due to ascites but x-rays did not show evidence of that. Overall, we did not see any stigmata of genetic abnormalities or birth defects. No overt seizure activity was noted at Blake Hospital although we did observe a degree of obtundation. The baby was transferred then to Manatee Memorial Hospital for Neonatal Intensive Care as the baby was still on the respirator, suspected cause was a twin to twin transfusion with possibility of hydrops non-immune type. Other than the blood gases, additional laboratory analysis findings at Blake had an liver enzymes that were abnormally high, ALT was 231, AST was 935, and LDH was 2281. This was right after birth. Another unusual finding was that the laboratory reported a creatine kinase isoenzyme that is very rare. They found a mitral chondral CK isoenzyme which has been reported only on a handful of babys throughout the world. It seems to be, according to my research, originated in either the liver or the heart and so far in the handful of babys that have been described with this macro C2 creatinine kinase there seems to be no long-term sequelae. The official report on the x-rays from Blake Hospital have pleural effusion on the right and possible ascites. At about 2015 hours over at the Neonatal Intensive Care Unit we noticed some suspicious tongue thrusting movements with tremors, we considered it a possibility that it might be seizure activity and treated it as such with Phenobarbital. It was a brief episode but we knew that this baby was at risk for seizures so we went ahead and started loading the baby with Phenobarb dose of 30 milligrams. X-rays had showed that the umbilical arterial line was low. I had come back shortly after midnight and replaced the umbilical lines now with good placements for high lines. I stayed with the baby further because of acuity at 0220 hours, we observed movements of arms and posturing of the legs; this was more typical of seizure activity and Lorazepam was given for this episode. Further dose was required at 0355 hours. Shortly thereafter, the baby[']s blood pressure started to come down at 0435 hours [and] we started Dopamine drip which was able to maintain a normal mean arterial blood pressure. I was at the baby[']s bedside on and off throughout the night up to about 0500 hours. The day after the admission, we had no[] tonic or clonic activity but still an occasional fasciculation of the tongue was seen; these kinds of autonomatism are very difficult to control. We were getting also brown, thick secretions from the endotracheal tube which were suspicious of either pulmonary hemorrhage or pulmonary edema. We continued to fine tune treatment for the seizure activity because shortly after 1600 hours, we saw another small episodes of what could [be] tonic activity of one of the arms. Tongue thrusting continued on and off. The nurses had mentioned what they called cogwheel motion of arms. The baby was now on Phenobarbital, Dilantin and p.r.n. Ativan. We continued trying to determine if there are any other causes of all this symptomatology. We did TORCH titers, chromosome analysis and electroencephalogram. The electroencephalogram to my eyes was abnormal and consistent with deep seizure activity. Initially on admission, the mother had told me that her brother was a "bleeder". Eventually, we were able to find the actual charts on him and found him to have had a subacute type of idiopathic thrombocytopenia; this should not be an issue for these infants. During the baby[']s second day of stay, I had the ophthalmologist examine him. He had seen retinal hemorrhages and suggested coagulation studies which were done; these were abnormal an we started the baby treating him as DIC, that included fresh frozen plasma, cryoprecipitate and intravenous gamma globulins. That day #2, we had two episodes of seizure activities that was treated with intravenous Ativan. By day #3, the respirator was down to minimal settings, the oxygen was 25 percent only and the mechanical respirations were only 15 breaths per minute. X-rays already did not show any pleural effusions although the monogram of the abdomen did still reveal small effusions present. Still on Dopamine drip, we occasionally had myoclonic movement of the arms and legs and occasional small episodes of seizure activity. The DIC was still being treated by twice a day cryoprecipitant plasma. Also one transfusion of platelets was required. On day three, we did not give any more platelets but he did get one transfusion of fresh frozen plasma and one of cryoprecipitant and with one infusion of intravenous gamma globulin. The baby was still on Dopamine drip for low blood pressure and by the early morning of day number four, we were able to start cutting back on the Dopamine dosage. We had during day #4, labile blood pressures, we had to adapt and adjust with the Dopamine drip going up and down according to the measurements that we were getting. Late that evening, about 2000 hours, he had another seizure activity with sucking motions and jerky movements also blinking of the eyes. The left leg was rigid and arms were also clonic. We adjusted Phenobarbital level because the level was 27. Platelet count that day was 78. On day #5, we had mild metabolic alkalosis with mild C02 retention. The cardiac echo was reported as normal. The generalized edema was slightly improved, had a 15 second episode of seizure activity. Platelets were found to be low so full DIC profile was repeated. Platelets were ordered and given transfusion. Also repeat doses of cryo and FFP added as well. On day 6, blood levels of Phenobarbital were at 22 and Dilantin was 26. After the transfusion, the platelet count was now 98,000 and held both the Phenobarb and the Dilantin. On days 6, 7, and 8, no seizure activity was reported. We tried him on continuous positive airway pressure on day #8, hence we tried to wean him off the ventilator. In the late evening, day 8, into day 9, we transfused with platelets again because platelet count had dropped to 36,000. On day 9, we tried him off the respirator and extubated him at 1350 hours, started on oxygen by hood. The electroencephalogram was repeated and still was abnormal. By the early morning hours of day 10, we were able to get him completely off oxygen. Still no overt seizure activities once we had held the medications. By day 11, we were able to see that he had lost peripheral edema, no apneas were noted and no seizures either. By day #12, nurses were commenting that he looked more awake and on my physical examination, the only other thing I noted was that there is still neuromuscular irritability as evidenced by increased and clonus beats although they were symmetric. Extensor tone still also was slightly increased. On day #12, I removed the umbilical lines and started oral feedings. On days 13 and 14, we had him on 1/2 strength Nutramigen feeds by tube. Platelets counts were on the lower range of normal at 53 and 55,000. No overt seizure activity was noted but occasionally the nurses would still comment on tremors and occasional mild irritability. On day 15, I switched him to 1/2 strength Enfamil feeds, platelet count was still 53, the number of clonus beats at the ankles was normal but the deep tendon reflexes were still brisk. Again, no asymmetries were noted, no dystonias were noted either. On day 16, the platelet count was 91,000 and beyond that it was always above 100,000. Gradually, he started to tolerate feeds better. On day #16, he nipple fed all his feeds. We advanced him to full strength feeds and got him into an open crib. We did a hearing screen which he failed on both ears. On December 7, which was day #19, I repeated the[] DIC profile one more time and this time everything was normal. The blood counts including white blood cells and platelet counts were normal. The chemistry panel done that included liver enzymes were also fully normal. The baby was then discharged at 1600 hours on December 7, 1996, to the parents, told to be followed in about a week with the pediatrician. DISCHARGE PHYSICAL EXAMINATION: Discharge weight 5 pounds and 5.3 ounces. . . DISCHARGE VITAL SIGNS: Temperature 98.7, pulse 136, respirations 36. GENERAL APPEARANCE: Strong and vigorous. HEAD, EYES, EARS, NOSE AND THROAT: Anterior fontanel is flat, sutures feel normal to palpation. Examination of the eye grounds have good red reflexes bilaterally. There is no sign of nasopharyngeal infections, both nares are patent. There is no cleft of lip or palate. No signs of any congenital abnormalities or genetic traits. NECK: Good range of motion. Clavicles intact to palpation without callus formation. No lymph nodes palpable. No masses, no goiter. CHEST: Breathing effortlessly in room air. HEART: No murmurs. LUNGS: All lung fields clear. ABDOMEN: No organomegaly, no abnormal masses. Belly is soft and not tender. GENITALIA: Normal newborn male. Both testes palpable. The meatus is well placed. ANUS: Patent and well placed. EXTREMITIES: No hip clicks. NEUROLOGICAL: Get the impression, the baby[']s muscle tone is normal now which was true since about day 16. The deep tendon reflexes are still slightly brisk but there is no other evidence of neuromuscular irritability; for example, clonus beats at ankles are normal in terms of numbers and they are symmetric. Cannot detect any asymmetries in muscle tone nor in any of the reflexes. I do have a good Moro reflex, good Perez, and Galant reflexes with again no asymmetries, good placing and stepping reflexes with no focal findings. DISCHARGE DIAGNOSIS: Full term twin born by cesarean section. Cardiorespiratory arrest at birth. Hypoglycemia. Non-immune hydrops. Hypocalcemia. Hypokalemia. Low Apgar scores. Neonatal seizures. Hypothrombocytopenia. Disseminated intravascular coagulation. Feeding problems of the newborn. Apnea. PLAN: Discharged to the parents as noted above with follow-up Dr. Alfredo A. Giangreco. COMMENT: Areas that need follow-up: We need to repeat the hearing screen as the baby[']s hearing screen at discharge failed both ears. Long-term follow-up purposes should also include neuro developmental evaluations preferably by a pediatric neurologist; this may or may not include repeat electroencephalograms. This of course to be left up to the judgment of the pediatric neurologist. Perhaps a repeat monogram of the brain is warranted since the healing stages of any incidence before birth and after birth may not be visible on sonography of the brain until 6 to 8 weeks of age.2 Following discharge, Dillon was followed by Alfredo Giangreco, M.D., or other pediatricians associated with his practice. The medical records related to Dillon's first visit on December 12, 1996, reflect an alert, active 3-week-old infant in no apparent distress, with good Moro-suck, and good muscle tone or, stated otherwise, no hypertonia. Dillon's subsequent visits at 1 month of age (December 26, 1996), 2 months of age (January 17, 1997), and 3 months of age (February 19, 1997) were likewise unremarkable except that his 3-month visit reflects a clinical observation that his head was microcephalic (an abnormal smallness of the head.) Apart from the microcephalia, Dillon's remaining visits were unremarkable until his visit at 7 months of age (June 18, 1997), when the doctor noted a spastic paresis of the left arm and hand, as well as both legs. At the time, the parents disclosed that they planned to move to Rhode Island in 4 days, and the doctor recommended a follow-up on such findings and reminded them of the importance of a hearing evaluation (the parents had failed to pursue following Dillon's discharge from Manatee Memorial Hospital.) Following the family's move to Rhode Island, Dillon came under the primary care of Roxanne Simmons, M.D., a board- certified pediatrician. On her initial examination of March 11, 1998, Dr. Simmons noted "symmetrical decreased strength throughout all four extremities," as well as expressive language delay with disarticulation. Given the "global issues," which included microcephalia, Dr. Simmons referred Dillon to Dr. Maria Younes, a pediatric neurologist and, given his speech delay, referred Dillon for a hearing assessment. Dillon was also referred to the Earl Intervention Program for assessment, and occupational and physical therapy, as needed, to address his speech, language, and/or oral-motor delays. Dr. Younes' evaluation of Dillon will be discussed infra. As for Dillon's hearing assessment, testing on April 2, 1998, revealed a "moderate (probably conductive) hearing loss." Following that test, Dillon had "tubes inserted [in his ears]" by Dr. Blat, on referral by Dr. Simmons, and further assessment on July 13, 1998, found his "hearing is developmentally adequate." Dillon also received occupational and physical therapy through the Early Intervention Program with good results, as noted infra. Dr. Simmons continued to provide primary care for Dillon, and saw him as recently as June 9, 2000. As of that date, Dr. Simmons noted that Dillon now evidenced good strength in his extremities and no gross motor deficits. As for his fine motor skills, Dr. Simmons offered no opinion, and deferred to others more appropriately suited to make such an assessment. Currently, according to Dr. Simmons, the issues now confronting Dillon are behavioral, as evidenced by his aggressive character (otherwise described as an attention deficit, hyperactivity disorder,) and continued delay in his expressive language with disarticulation. As for any relationship between Dillon's current presentation and any injury to or anomaly in brain development, Dr. Simmons deferred to Dr. Younes. (Dr. Albin's Exhibit 1, pages 30 and 31.) Dillon's neurologic assessments Dillon was first seen by Dr. Younes on June 2, 1998. At the time, Dr. Younes noted the mother's concerns regarding his speech and language delays, a perceived mild delay in fine motor skills, and a possible mild left hemiparesis (a muscular weakness or partial paralysis affecting the left side of the body); however, Dr. Younes' examination did not reveal any significant difference in his muscle tone or the strength in his extremities. Nonetheless, Dr. Younes noted a working diagnosis of left hemiparesis and developmental delay and, given Dillon's microcephaly, his mother's concerns, and Dillon's birth history, ordered an MRI of the head. The MRI examination occurred on June 26, 1998, and the results of that examination were reported as follows: Axial T2 and FLAIR images demonstrate confluent hyperintense white matter signal abnormality predominantly involving the periatrial white matter of the bilateral cerebral hemispheres. In addition, there is periventricular white matter signal abnormality involving the bilateral frontal periventricular white matter, left greater than right. The MR imaging appearance is most consistent with periventricular leukomalacia. No evidence of hydrocephalus. No evidence of intracranial hemorrhage, mass, or midline shift. Normal vascular flow voids are present. IMPRESSION: MRI EXAMINATION DEMONSTRATES EXTENSIVE WHITE MATTER HYPERINTENSE SIGNAL ABNORMALITY PREDOMINANTLY INVOLVING PERIVENTRICULAR WHITE MATTER BILATERALLY. GIVEN THE CLINICAL HISTORY OF PERINASAL [SIC] ASPHYXIA, THE PATTERN IS MOST CONSISTENT WITH PERIVENTRICULAR LEUKOMALACIA. As read, the MRI results are consistent with an abnormality in brain development associated with prematurity or a brain injury associated with hypoxic insult.3 Following receipt of the MRI results, Dillon was further evaluated by Dr. Younes on August 23, 1999, and April 3, 2000. Based on her multiple examinations, Dr. Younes offered the following observations with regard to the physical impairments Dillon manifests, which she perceives are related to his periventricular leukomalacia: Q. I would ask you, of course, as you respond to questions that I put to you about this child's condition and the way you found him on April 3, 2000, if you need to draw upon your knowledge of him gained from August 23rd of 1999, 6/2/98, or certainly any tests that you ordered or information that you received such as from the school psychologist, that kind of thing. A. Yes. He was now three years and a half. Because school takes over services at age 3 here in Rhode Island, he had had a complete evaluation from Lincoln School Department, and he was found to have delays in his speech and language, occupational therapy, the most concerning a low IQ. IQ is 67.4 * * * Q. With regard to the speech impairment that Dillon Campbell has, do you have an opinion as to whether there is an element of motor dysfunction or motor deficit that is either causing or contributing to the child's speech deficit? A. He does have articulation problems, but he also has basically both expressive and receptive language delays. Q. Is the child's speech -- is the child's speech deficit permanent and substantial? A. He will continue to improve. He will be getting speech and language therapy, so some of these things will improve with time. Also as he continues to develop, he will continue to improve. Eventually his output could be very good, but his receptive language may be impaired long term. Q. At the current time, however, clearly the speech impairment that he has is now substantial? A. Yes. Q. Are you able to say to a reasonable medical probability that his speech impairment will completely abate, completely go away, or will there always be some speech impairment? A. There will always be some speech impairment -- impediment. * * * Q. Are you able to at this point, based upon the information you have, give an opinion held to a reasonable medical probability with regard to whether this child for sure does have or doesn't have impairments of fine motor skills? A. He has impairment of fine motor skills. Q. Do you believe that the impairment that he has of fine motor skills are substantial? A. No. Q. Do you believe that the impairments that he has in fine motor skills, if they do not get better, will affect him in later life? A. No. * * * Q. How has the periventricular leukomalasia affected this child in terms of his physical being outside of the brain? * * * Q. Has it affected or contributed to his speech deficit? A. Yes. Q. In what way has the . . . periventricular leukomalasia affected this child's speech? A. Significantly. I think the periventricular leukomalasia will be most significant for this child in the areas of cognitive ability. He is mentally retarded and his speech and language. His fine motor and gross motor will be fine. Q. In terms of periventricular leukomalasia that this child suffers from, is that periventricular leukomalasia consistent with speech difficulties that are motor related, motor function related? * * * A. Speech and language requires a lot of different parts of the brain, the left hemisphere, and it has a lot of different components, and the motor component to the ability of articulating words, he has a problem in that area; but he also has a problem understanding language and also expressing himself. * * * Q. Are you able to give an opinion as to how much of the child's speech problem or speech impairment is related to motor deficiency versus cognitive deficiency? A. It's a combination of both, but the cognitive is probably a greater component. * * * Q. The articulation problem that Dillon has, you indicated I believe that there could be several causes to it; is that correct? A. Yes. Q. One could be a cognitive dysfunction? A. Yes. Q. And the other could be a motor dysfunction? Q. Yes. Q. If I understand correctly, when asked by Mr. Marchbank, you said more likely than not it was more cognitive than motor; isn't that true? * * * A. I said it is a component of both, that most likely the articulation may improve with time, but the cognitive part may persist. Q. At the present time, what if anything do you find to enable you to continue, if you do, with the diagnosis of left hemiparesis? A. Could you ask the question again? Q. Yes. What is it in his physical condition right now that you have determined by examination that Dillon still has a persistent left hemiparesis? A. I don't think that's significant. I think it's only been picked up by an occupational therapist, by the mother after a lot of observation of her child, but not something that you could pick up just by looking at him. Q. In fact, in your examination of him when you see him grossly, it would appear to you that he has no gross motor impairment; is that true? A. Exactly. Notably, Dr. Younes was not requested to address and offered no opinion as to the gravity of Dillon's behavior disorder (also referred to as attention deficit, hyperactivity disorder), or whether there was any causal relationship between such disorder and the periventricular leukomalacia he suffered. In addition to Dr. Younes' evaluation, Dillon's neurologoic status was also assessed by Michael Duchowny, M.D., a pediatric neurologist associated with Miami Children's Hospital. Dr. Duchowny's examination occurred on February 17, 2000, and he reported the results of his evaluation as follows: HISTORY ACCORDING TO MRS. CAMPBELL: Dillon is a 3 year old right handed boy who is one of monozygotic twins. The family resides in Lincoln, Rhode Island. Mrs. Campbell began by explaining that Dillon is a "very loving child" and that he has been "making progress and wants to learn". His major difficulty centers over speech delay. He can communicate in single words, but the words are poorly articulated. Dillon has been working in speech therapy at the Fairlawn Early Learning Center where he is in a secluded classroom. He receives speech therapy once a week, as well as occupational therapy on a weekly basis. Mrs. Campbell also indicated that Dillon "has sensory stuff". She feels that he does not listen and is very active. She went on to express that Dillon is extremely aggressive and will throw things, have temper tantrums and bite indiscriminately . . . . The teachers have not yet recommended medication for his behavior, but Mrs. Campbell feels that this is likely in the near term . . . . Dillon's coordination has been a problem, in that he has had trouble walking up stairs. These difficulties have apparently resolved. His vision is good and his hearing has been tested on multiple occasions because he has bilateral tubes . . . . FAMILY HISTORY: The father is 31; the mother is a 30 year old, gravida 3, pare 4, ABO. A 13 year old brother and 16 year old sister are healthy. There is a strong family history of mental illness. The father suffers from depression, anxiety and an obsessive/compulsive disorder for which he takes Paxil and Xanax. A maternal brother suffers from a bipolar disorder and has a spinal cord injury. He also has been diagnosed as having borderline schizophrenia. The mother's family background is from Portugal. There are no family members with neurodegenerative illnesses or spinocerebellar ataxia. There is no history of familial dementia. Dillon had a single febrile seizure, but was not . . . been treated with medication. PRE- AND PERINATAL HISTORY: Dillon was the product of a 38-week gestation at Blake Memorial Hospital. His delivery was by emergency caesarean section and he required immediate resuscitation. His birth weight was 5-pounds, 15-ounces and he remained in the nursery for 19 days. He had recurrent seizures which were treated with 3 anti- epileptic drugs including phenobarbital and Phenytoin. GROWTH AND DEVELOPMENTAL MILESTONES: Dillon did not sit up until 8 months. He stood at 11 months and walked at 18 months. Dillon began saying single words at 15 months. He is not yet toilet trained. Dillon is fully immunized, has no significant allergies and has never undergone surgery. PHYSICAL EXAMINATION reveals Dillon to be an alert, but extremely active well proportioned child. His weight is 26-pounds and height 34-inches. Dillon's head circumference measures 46.8 cm, which is below standard percentiles for age matched controls and approximates the 50th percentile for age 15 months. The hair is brown and of normal texture. There are no cranial or facial anomalies or asymmetries. The neck is supple without masses, thyromegaly or adenopathy. The cardiovascular, respiratory and abdominal examinations are normal. The spine is straight without dysraphic features. Dillon's NEUROLOGIC EXAMINATION was significant for a high activity level and short attention span. His behavior was virtually uncontrollable for much of the evaluation and he required coaxing and stimulation to keep his interest. Dillon spoke in single words periodically, but these were poorly articulated and it was difficult to understand their meaning. The tongue movements were reasonably well coordinated and he did not drool. Dillon could interact at a very basic level and certainly understood simple commands. Cranial nerve examination revealed full visual fields to direct confrontation testing and a brief, but normal ocular fundoscopic examination. The pupils were 3 mm and reacted briskly to direct and consensually presented light. The uvula was midline and there were no facial movement asymetries. Motor examination revealed symmetric strength and bulk. The tone was slightly diminished for age. His gait was stable with symmetric arm swing. Dillon could run and jump without difficulty. The deep tendon reflexes were 1 to 2+ bilaterally with flexor planter responses. The stance was appropriately narrowly based. Sensory examination was deferred. Neurovascular examination revealed no cervical, cranial or ocular bruits and no temperature or pulse asymmetries. Dillon could build a tower of 5 cubes using primarily his right hand. He had well developed pincer grasp bilaterally. Dillon knew simple body parts, but could not identify pictures of animals. In SUMMARY, Dillon's neurologic examination is significant for a short attention span, high activity level and marked expressive language delay with disarticulation. He additionally manifests microcephaly and has a history of neonatal seizures. Dillon presently is on no medications. I regard Dillon's motor abilities to be within the normal range and he therefore has no evidence of a significant motor impairment . . . . The conclusion regarding Dillon's physical presentation To address whether Dillon is permanently and substantially physically impaired, the parties offered selected records relating to Mrs. Campbell's antepartum and intrapartum course, as well as for Dillon's birth and subsequent development. The parties also offered the opinions of three physicians and Mrs. Campbell, by deposition, to address the character of his physical presentation. Those physicians were Doctors Simmons, Younes, and Duchowny. 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 that, more likely than not, Dillon is permanently and substantially physically impaired. To the contrary, the proof reveals that the physicians most knowledgeable in the area (Doctors Younes and Duchowny) share strikingly similar and consistent opinions regarding the nature of Dillon's presentation, and that he is not permanently and substantially physically impaired.5
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 Briana Gwendolyn Dabriel, 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 Edward Dabriel and Wendy Breedlove Dabriel are the parents and natural guardians of Briana Gwendolyn Dabriel (Briana), a minor. Briana was born a live infant on December 1, 1998, at Aventura Hospital and Medical Center, a hospital located in Aventura, Florida and her birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Briana was Mark Firestone, 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. 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, Briana's neurologic presentation is dispositive of the claim. Briana's neurologic status On February 7, 2000, following the filing of the claim for compensation, Briana was examined by Michael Duchowny, M.D., a board-certified pediatric neurologist. The results of Dr. Duchowny's examination were reported as follows: PHYSICAL EXAMINATION reveals an alert 14 month old black infant. The weight is 21- pounds. The skin is warm and moist. There is a healed surgical scar over the left lateral neck. There are no dysmorphic features and the spine is straight. The head circumference measures 46.4 cm (including dreadlocks). There are no cranial or facial anomalies or asymmetries. The anterior fontanelle is still open, but quite small. The neck is supple without masses, thyromegaly or adenopathy. The cardiovascular, respiratory and abdominal examinations are unremarkable. Peripheral pulses are 2+. NEUROLOGIC EXAMINATION is significant for normal cranial nerves and an appropriate mental status. She makes cooing and babbling sounds quite frequently and is very interactive socially. Briana does not drool. There is full extraocular movements and the pupillary light responses are intact to direct and consensually presented light. Brief fundoscopic examination is unremarkable. The pigmentation is dark brown bilaterally. There is a marked asymmetry of upper extremity function. The left upper extremities are smaller than the right for the fingers, hands, forearm and arm compartments. There is a decrease in muscle bulk and some hollowing in the left biceps and triceps regions. The thumb is fisted. The upper extremity is held in a position of internal rotation and flexion at the shoulder, with flexion at the elbow and wrist. The temperature is similar to the right. Gross sensation appeared to be intact, but was difficult to examination with any confidence. There is a marked reflect asymmetry being 2+ on the right biceps, but dropped on the left. The lower extremity reflexes are intact and there is no asymmetry of strength, bulk or tone. I did think that the left leg showed some eversion at the hip. Briana's gait is stable, but she tends to walk on tiptoes while running. Tests of cerebellar coordination, including heel-to-shin maneuvers were not tested. The neurovascular examination revealed no cervical, cranial or ocular bruits and no temperature or pulse asymmetries. In SUMMARY, Briana's neurologic examination is significant for a moderate to severe left Erb's palsy [consequent to a brachial plexus injury suffered at birth], status post surgical repair. The prognosis for further recovery seems guarded with the exception of functionality that may return in the course of neuroregeneration. In contrast, Briana's cognitive development appears to be proceeding at age level and her head is growing normally. A brachial plexus injury, such as that suffered by Briana during the course of her birth, is not, anatomically, a brain or spinal cord injury, and does not affect her mental status, which has been noted as essentially normal. Consequently, while Briana has been shown to have suffered a substantial and permanent injury (to her left brachial plexus) during the course of birth, it is Dr. Duchowny's opinion, which is credited, that such injury is not related to the brain or spinal cord and, moreover, that she has not been rendered permanently and substantially mentally and physically impaired.
The Issue At issue is whether Eli Joe Arellano, Jr., a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts Cathy Arellano and Eli Joe Arellano, Sr., are the natural parents of Eli Joe Arellano, Jr., a minor. Joe was born a live infant on February 17, 1999, at Fort Walton Beach Medical Center, a hospital located in Fort Walton Beach, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Joe's birth was Thomas H. Moraczowski, 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(1) and 766.31(1). In this case, Petitioners are of the view that Joe suffered a "birth-related neurological injury" because it is their "belief . . . [based on] the medical records and injuries sustained at birth [such as bruises on top of the head and face and broken collarbone] . . . Joe has sustained a spinal cord or brain injury resulting in Cerebral Palsy Hypotonia." (Pre- Hearing Stipulation, paragraph B1) In contrast, NICA is of the view that Joe did not suffer a "birth-related neurological injury" because his impairments were not occasioned by an "injury to the brain or spinal cord . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation" and, regardless of the etiology of Joe's impairments, he is not "permanently and substantially mentally and physically impaired." (Pre-Hearing Stipulation, paragraph B2). Here, Respondent's view is most consistent with the proof. Joe's birth and immediate postnatal course At or about 3:30 p.m., February 16, 1999, Mrs. Arellano, with an estimated delivery date of February 21, 1999, and the fetus at 39 2/7 weeks gestation, presented to Fort Walton Beach Medical Center, in labor. At the time, Mrs. Arellano's membranes were noted as intact, and vaginal examination revealed the cervix at 5-6 centimeters dilation, effacement at 75 percent, and the fetus at -3 station. Uterine contractions were described as moderate, at a frequency of 5-7 minutes, and fetal monitoring revealed a reassuring fetal heart rate, with a baseline in the 130-beat per minute range. Mrs. Arellano was admitted to labor and delivery at 4:15 p.m.; an IV was started at 5:18 p.m.; her membranes were artificially ruptured at 5:22 p.m., with clear fluid noted; and Petocin augmentation was started at 6:20 p.m. Thereafter, Mrs. Arellano's labor slowly progressed until 1:55 a.m., February 17, 1999, when complete cervical dilation was noted, and Joe was delivered vaginally at 2:01 a.m. Notably, fetal monitoring revealed a reassuring fetal heart rate throughout the course of labor, but, at 10 pounds 7 ounces, Joe was large for gestational age (LGA), and delivery was complicated by a shoulder dystocia, which was relieved by hyperflexion of the legs to the maternal abdomen, suprapubic pressure, and corkscrew rotation of the infant's posterior shoulder to the anterior plane. Nevertheless, although not diagnosed at the time, Joe suffered a fractured clavicle during delivery, which healed without apparent complication. At delivery, Joe was reported to be "healthy and vigorous," and did not require resuscitation. Cord blood pH was reported as normal (7.25), as were Joe's Apgar scores, which were noted as 9 and 9, at one and five minutes, respectively.1 Following delivery, Joe was transported to the regular newborn nursery, where he was received at 2:30 a.m. Newborn assessment noted "L[igh]t bruising to forehead/top of head" and "mild" molding, observations that were not shown to have any clinical significance in this case. Otherwise, Joe's newborn assessment was unremarkable, as was the remainder of his postnatal course, and he was discharged with his mother on February 19, 1999. Joe's subsequent development Following discharge from Fort Walton Beach Medical Center, Joe's early development was age appropriate; however, over time, his mother voiced a number of concerns about his development, and in December 2000 he was referred by his pediatrician to the Child Neurology Center of Northwest Florida for evaluation. There, Joe was initially seen for a neurology consultation by Tim S. Livingston, M.D., who reported the results of his January 4, 2001, evaluation, as follows: REASON FOR CONSULTATION: Hypotonia. PRESENT ILLNESS "Joe" is a 22-month-old, possibly left- handed young boy who presents with his family for evaluation of the above concerns. His mother indicates she has several concerns about his development. She is most concerned about his gait. She indicates that ever since he has been walking he has had a tendency to in-toe (right greater than left). This was not significantly disabling and did not significantly impair attainment of his milestones. However, over the last month she feels this has worsened and that he has more frequent falls. She does not notice any diurnal variation of this gait or any apparent dystonia. She also indicates that she has concerns about his speech. She indicates that he said his first words at 12 months and knows approximately 10 words at the present. However, she feels the words he does know are poorly articulated. He is able to point to some body parts and understands "yes" and "no." He does make good eye contact with family members and others and is variably affectionate. He does not have significant ritualistic behavior or any apparent stereotypes. She is also concerned about his fine motor and gross motor coordination. She indicates that he is able to throw a ball but remains incoordinated when he attempts to feed himself. He does not always know how to properly hold utensils. She denies any apparent . . . regression of milestones. PAST HISTORY Antenatal: He was born to his mother after a pregnancy complicated by weight loss and gestational diabetes. There is no apparent hypertension, infection, bleeding, drug use or alcohol use. Birth: He was felt to be born at term and weighed 10 pounds, 7 ounces. His mother reports he did not have any significant immediate perinatal difficulties. Neonatal: She indicates that he did not have significant jaundice, cyanotic episodes, respiratory distress, or other problems. However, she does indicate that since the newborn period he has had constipation. Development: Held head up at 2 months, sat alone at 4 months, walked at 13 months, fed himself at 1 year. The remainder of development as per History of Present Illness. Behavior: He has frequent episodes of crying. He is somewhat shy but is affectionate when he is familiar with people. She does indicate that he does not sleep well at all. * * * NEUROLOGICAL EXAMINATION General: Healthy, alert young boy in no apparent distress. Skull: Occipitofrontal circumference 50 centimeters (75th percentile). Normocephalic, without evidence of cranial trauma. Fontanel is closed. No boney abnormalities or bruits. Neck and Spine: Supple, full range of motion, no meningeal signs. Speech and Language: As per above. Mental Status: The child was awake, alert. He follows simple commands. He was not fully compliant with language or speech testing, though spontaneous language seemed age appropriate. * * * Motor: Tone - Spontaneous observation demonstrates hypotonic posture (i.e., exaggerated kyphosis, mild froglegging), also passive range of motion demonstrates reduced tone in a generalized distribution which is mildly greater in truncal musculature. Power - there is no asymmetry of movement. He moved all extremities appropriately and symmetrically. Coordination - He was able to hold a ball appropriately and throw it. There is no obvious incoordination. Cerebellar - No apparent ataxia with spontaneous reaching and hand movements or spontaneous movements of the lower extremities. Involuntary movements - no obvious tics, tremors, chorea, athetosis or other abnormal movements. Reflexes: His tendon reflexes were 0 to 1+ at biceps, triceps, radialis, knee jerks, and ankle jerks (reduced in a generalized distribution). Gait and Stance: Spontaneous observation of his gait demonstrated bilateral in-toeing (right greater than left). His gait was not abnormally wide-based or ataxic. Heel walking and toe walking was appropriate. He was not able to comply with tandem gait. Sensation: Intact to temperature, light touch and vibration throughout. * * * ASSESSMENT Generalized hypotonia. Abnormal gait (in-toeing). Possible developmental articulation difficulties. Based on the history, I suspect that "Joe" is suffering from mild developmental hypotonia which may be benign in nature. However, potential causes such as hypothyroidism and inborn errors of metabolism need to be considered. Furthermore, abnormalities of myelinization should be considered. I am not entirely convinced that his abnormal gait is directly related to his hypotonia. It is possible that he is suffering from tibial torsion or femoral anteversion. Regardless, I do not think his gait is significantly abnormal to warrant orthopedic evaluation. His parents do give a history of significant difficulty with articulation which was difficult to confirm at bedside testing. Regardless, his cognitive and receptive language skills appear to be normal, as do most of his other developmental milestones. It is possible that he has a mild developmental speech disorder. I have discussed the above in detail with his mother and she wishes to proceed as outlined below at my recommendation. PLAN Magnetic resonance imaging of the brain with sedation. Blood work for TSH, amino acids and ammonia. Urine amino and organic acids. Physical therapy, occupational therapy and speech therapy. Return in 1 month. Over the years, Joe has had multiple consults at the Child Neurology Center, initially with Dr. Livingston and then, beginning in 2003, with Dr. J.B. Renfroe. Those consults ultimately produced an assessment of static encephalopathy, developmental delay, and initially, cerebral palsy hypotonia and later, autism/pervasive developmental disorder (PDD).2 Over the years, Joe has also undergone multiple studies to identify the etiology of his neurologic deficits, without success. Such studies have included multiple blood and urine studies, including genetic and metabolic analyses, which have been unrevealing; an MRI of the brain on February 5, 2001, which was normal; an MRI of the cervical spine on March 28, 2002, which was normal; electroencephalograms (EEGs) on February 21, 2002, and October 30, 2003, which were normal; and a video EEG on June 11 and 12, 2002, which demonstrated an abnormal generalized slowing of background activity, consistent with encephalopathy, but nonspecific with regard to etiology, and no epileptiform abnormalities or seizure activity. On March 24, 2004, following the filing of the claim for compensation, Joe was examined by Michael S. Duchowny, M.D., a physician board-certified in pediatrics, neurology with special competence in child neurology, electroencephalography, and child neurophysiology. The results of that evaluation were reported, as follows: PHYSICAL EXAMINATION reveals an alert, reasonably cooperative, well developed and well nourished 5-year-old boy. Joe weighs 73 pounds and is 47 inches tall. The skin is warm and moist. There are no cutaneous stigmata. The neck is supple without masses, thyromegaly or adenopathy. There are no cranial or facial anomalies or asymmetries. The head circumference measures 53.1 cm, which is within standard percentiles. The cardiovascular, respiratory and abdominal examinations are unremarkable. There is bilateral pes planus. Peripheral pulses are 2+ and symmetric. NEUROLOGICAL EXAMINATION reveals a boy with a pleasant disposition, but poor eye contact and diminished social skills. Joe rarely speaks spontaneously. He is dysarthric for lingual and labial sounds. He does know his colors, body parts and pictures of animals. He does not drool. He understands simple commands, but his cooperation is limited. He is able to build a tower of tubes. MOTOR EXAMINATION reveals mild generalized hypotonia. Joe is able to use both hands, but prefers the right. He has well- developed pincer grasp and uses his hands bimanually. He exhibits intermittent hand waiving sterotype movements. There are no other adventitious movements and no focal weakness or atrophy. The deep tendon reflexes are 1+ and symmetric. Plantar responses are downgoing. The stance is reasonably based and he walks with symmetric arm swing. He has trouble doing tandem walk and tends to posture his upper extremities. Sensory examination is intact to withdrawal of all extremities to stimulation. Neurovascular examination reveals no cervical, cranial or ocular bruits and no temperature or pulse asymmetries. Joe can perform finger-to-nose and heel-to-shin movements at an age appropriate level. In SUMMARY, Joe's neurological examination, in detail, reveals evidence of immature social skills, poor eye contact, short attention span, mild generalized hypotonia and delayed speech and language development. He demonstrates no focal or lateralizing findings. Joe's neurologic findings fit best within the autistic spectrum. Findings from my evaluation together with a review of medical records . . . indicate that Joe does not suffer from a permanent or substantial mental or physical impairment and that his neurologic findings did not result from oxygen deprivation or mechanical injury at birth . . . . The etiology and significance of Joe's impairments To address the cause and timing of Joe's impairments, the parties offered, inter alia, medical records related to Mrs. Arellano's antepartum course; those associated with Joe's birth and subsequent development; and the opinions of Dr. Duchowny and Dr. Donald Willis, a physician board-certified in obstetrics and gynecology, as well as maternal-fetal medicine, regarding the likely etiology and significance of Joe's impairments. As for the etiology of Joe's impairments, it was Dr. Duchowny's opinion, based on the results of his neurologic evaluation of Joe on March 24, 2004, and review of the medical records, that, while of unknown etiology, Joe's impairments were most likely developmentally based, and not associated with oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation. In so concluding, Dr. Duchowny observed that contrary to the clinical evidence one would expect if Joe had suffered a severe hypoxic event or mechanical injury during labor or delivery, Joe's Apgar scores were normal, his cord blood gases were normal, his neonatal course was normal, his neuro-imaging studies were within normal limits, and his EEGs were normal. As for Dr. Willis, he, like Dr. Duchowny, was of the opinion that the medical records failed to reveal any evidence of neurologic injury having occurred during the course of labor, delivery, or the immediate postdelivery period. In so concluding, Dr. Willis observed that the fetal heart rate was reassuring throughout the course of labor; Joe was reported to be healthy and vigorous at birth, and did not require resuscitation; Joe's Apgar scores were normal, as were his cord blood gases; and Joe's newborn course and subsequent neuro-imaging studies were normal. Finally, the medical records, including the observations of the physicians who have treated Joe, while unrevealing as to etiology, also point to the likelihood of a developmental disorder, as opposed to birth trauma, as the likely cause of Joe's impairments. As for the significance of Joe's impairments, it was Dr. Duchowny's opinion, based on his neurologic evaluation of Joe and review of the medical records, that Joe does not suffer from a substantial mental or physical impairment. Notably, Dr. Duchowny's opinion was uncontroverted, grossly consistent with the record, and credible. Given the record, it must be resolved that Joe's impairments were, more likely than not, occasioned by a developmental abnormality, that preceded the onset of labor, and not by an injury to the brain or a spinal cord occurring in the course of labor, delivery, or resuscitation, and, regardless of the etiology of Joe's impairments, he is not permanently and substantially mentally or physically impaired. See, e.g., Wausau Insurance Company v. Tillman, 765 So. 2d 123, 124 (Fla. 1st DCA 2000)("Because the medical conditions which the claimant alleged had resulted from the workplace incident were not readily observable, he was obliged to present expert medical evidence establishing that causal connection."); Ackley v. General Parcel Service, 646 So. 2d 242 (Fla. 1st DCA 1995)(determining cause of psychiatric illness is essentially a medical question, requiring expert medical evidence); Thomas v. Salvation Army, 562 So. 2d 746, 749 (Fla. 1st DCA 1990)("In evaluating medical evidence a judge of compensation claims may not reject uncontroverted medical testimony without a reasonable explanation.")
