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 At issue in this proceeding is whether Respondent's proposal to accept the subject claim for compensation under the Florida Birth-Related Neurological Injury Compensation Plan should be approved and, if so, the amount and manner of payment (lump sum or periodic) of the parental award and the appropriate apportionment of the award between the parents.
Findings Of Fact The claim for compensation Petitioner, Crystal Waddell, and Intervenor, William Davis, are the natural parents of Chelsey Davis (Chelsey), a minor. Chelsey was born a live infant on August 23, 1997, at University Medical Center, a hospital located in Jacksonville, Florida, and her birth weight was in excess of 2500 grams. Ms. Waddell and Mr. Davis are not now, nor have they ever been, husband and wife. The physician providing obstetrical services during the birth of Chelsey was Edward Illions, M.D., who was, at all times material hereto, a participating physician in the Florida Birth- Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Here, the parties agree that Chelsey suffered a "birth- related neurological injury" as defined by Section 766.302(2), Florida Statutes, in that she suffered an injury to the brain caused by oxygen deprivation in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital, which rendered her permanently and substantially, mentally and physically impaired. The medical records filed with DOAH on June 15, 1998, as well as the report of neurological evaluation by Michael S. Duchowny, M.D., filed with DOAH on September 28, 1998, are consistent with the parties' agreement. Consequently, it is accepted that Chelsey suffered a "birth- related neurological injury," as defined by Section 766.302(2), Florida Statutes. Given the compensability of the claim, NICA agreed as follows: 8. The Association agrees to pay $100,000.00 as follows: Ms. Crystal Waddell has requested that $6,000.00 be paid to Ms. Cheryl Chieves as reimbursement for funds which she has loaned Ms. Waddell. The Association has no objection to this payment. The Association and Ms. Waddell also request that the Administrative Law Judge schedule a hearing as soon as feasible to determine the entitlement of the mother and/or father, if any, to the parental award. The Association will pay all benefits, past and future, as authorized by Section 766.31, Florida Statutes. . . . The Association agrees that $3,753.25, which includes fees and expenses incurred in the representation of the Claimant in this case, will be paid to Merrill C. Tunsil, Esquire, the attorney for the claimant. (Stipulation filed December 22, 1998.) Consequently, at the commencement of hearing, the parties stipulated that the only issues which remained for resolution were the apportionment of the $100,000.00 award between the parents, and whether such award should be made in lump sum or by periodic payment. (Transcript, page 8.) Background Chelsey's mother, Crystal Waddell (Ms. Waddell), was born May 30, 1979, and was 18 years of age when Chelsey was born.3 Chelsey, born August 23, 1997, was the product of Ms. Waddell's first pregnancy. According to the proof, Ms. Waddell's formal education ceased following her completion of the 11th grade. Thereafter, she was employed by Arby's and, subsequently, by McDonald's in the years preceding Chelsey's birth. Following Chelsey's birth, Ms. Waddell, with the assistance of her mother, dedicated herself to Chelsey's care; however, recently, Ms. Waddell resumed her formal education, with the aim of completing her high school education. Chelsey's father, William Davis (Mr. Davis), was born March 31, 1980, and was 17 years of age when Chelsey was born. At the time, Chelsey was the second child Mr. Davis had fathered without the benefit of marriage. According to the proof, Mr. Davis abandoned his formal education during the 8th grade and, since that time, has been periodically employed in various unskilled positions. Such employment has included a term at McDonald's (where he and Ms. Waddell met); a period of approximately 6 weeks at John Rigsby Painting Company, Raleigh, North Carolina, at and shortly after Chelsey's birth; a term at Top Choice Poultry, following Chelsey's birth and his return to Jacksonville, Florida; and, most recently (since approximately September 1998), employment by Bill Williams Heating and Air Conditioning, where he nets approximately $180.00 each week. As of the date of hearing, Mr. Davis announced that he had recently (that week) started a program designed to achieve his GED and, if successful, hoped to begin an apprenticeship program with his current employer. The nature of Mr. Davis' current employment or the apprenticeship program is not of record. Approximately one year preceding Chelsey's birth, Ms. Waddell and Mr. Davis met while employed at a McDonald's restaurant in Jacksonville, Florida. Apparently, their relationship blossomed and, based on a perceived foundation of love and devotion, they designed to have a child and Chelsey was conceived. While Ms. Waddell and Mr. Davis may have initially felt a sense of purpose or closeness, their relationship proved to be tempestuous. Moreover, while they initially professed commitment and sought parenthood, the couple was never capable of sustaining themselves, much less an infant. Indeed, throughout the course of their relationship, and to this date, Ms. Waddell has continued to reside with her mother, Cheryl Chieves (Ms. Chieves). As Ms. Waddell's delivery date neared, Mr. Davis, who was apparently unemployed at the time, elected to go to Raleigh, North Carolina. According to Mr. Davis, the reason for the trip was two-fold. One reason was to visit his son (the issue of a previous relationship). The other reason was "I had a job waiting there to get some money up, you know." (Transcript, page 131.) As for the duration of the trip, the record reflects that Mr. Davis remained in Raleigh for 3 months, returning at the end of November 1997 when Chelsey was 3 months old. As for the promised job, the proof reflects that Mr. Davis was employed by John Rigsby Painting Company for the first 6 weeks of his stay in Raleigh, but was otherwise unemployed. At or about 10:54 p.m., August 22, 1997, Ms. Waddell was admitted to University Medical Center in labor, and at 12:30 a.m., August 23, 1997, her membranes spontaneously ruptures, with clear fluid noted. Ms. Waddell's labor and delivery was noted in her discharge summary as follows: The patient was admitted to Labor and Delivery . . . with a term intrauterine pregnancy and spontaneous rupture of membranes. The patient's cervix at the time of admission was 6, complete, -3 and vertex presentation. The patient had a protracted, active phase, and was started on Pitocin augmentation. At 7 centimeters, the patient had an intrauterine pressure catheter which showed an adequate contraction pattern x one hour. Her fetal heart tracing showed some subtle decelerations . . . . Later on that day, the patient developed a temperature to 101.2 degrees and she was diagnosed with chorioamnionitis and started on clindamycin and gentamicin. The patient was allergic to penicillin. She continued to make no progress with her cervical examination. A scalp pH was performed [at 6:50 p.m.] and came back 7.29 which showed reassurance. The patient was continued with Pitocin augmentation. A repeat scalp pH [performed at 11:10 p.m.] was 7.05 and [at 11:20 p.m. was] 6.86 [consistent with metabolic acidosis], so the patient was taken to the operating room for a stat cesarean section [and the infant was delivered at 11:36 p.m.]. . . . Apgars were 3 at one minute, 5 at five minutes and 6 at 10 minutes. Findings at the time of surgery showed a live born baby with a terminal meconium. Postoperatively, the baby was taken to the Neonatal Intensive Care Unit. . . . Ms. Waddell was discharged August 30, 1997, and Chelsey was ultimately discharged to the care of her mother on September 12, 1997. Chelsey's course was noted in her discharge summary as follows: HISTORY OF PRESENT ILLNESS: This 3075 gram female infant was born by cesarean section at 38 weeks gestation for decreased fetal heart rate and a scalp pH of 6.8. . . . Rupture of membranes was approximately 18 hours prior to delivery. There was a history of maternal fever and the mother received Clindamycin and Gentamicin. The amniotic fluid was meconium stained and 0.5 cc of thick meconium stained fluid was suctioned from below the cords. Apgars were 3 at one minute, 5 at five minutes and 6 at ten minutes, after receiving positive pressure ventilation and then blow- by oxygen. The infant was transported to the neonatal intensive care unit. PHYSICAL EXAMINATION: Neurological examination showed decreased tone with symmetrical movement and no focal neurological deficits. ADMISSION LABORATORY DATA: The infant is A+ and Coomb's positive. Arterial blood gas on 100% blow-by oxygen revealed a pH of 7.08, pC02 of 18, p02 of 479 and a base excess of -23. ADMISSION DIAGNOSES: Term female. Respiratory depression. Metabolic acidosis. ABO incapability. Sepsis surveillance. HOSPITAL COURSE AND PROBLEM LIST: * * * Respiratory: Initially she had metabolic acidosis and received sodium bicarbonate. A chest x-ray was consistent with retained fetal lung fluid and she was placed on nasal cannula. Initially she had tachypnea which slowly resolved. The nasal cannula was discontinued on day three and she had no further respiratory distress and required no further oxygen. This problem is considered resolved. * * * Central Nervous System: On August 24, 1997 she developed seizure activity at less than 12 hours of age. She was placed on Phenobarbital. An electroencephalogram (EEG) showed "status", although clinically no seizures were noted after the initial episode of seizure activity. . . . Neurology was consulted and she was seen by Dr. Shanks whose impression was acute encephalopathy and recurrent electrographic seizures from multiple-foci despite Phenobarbital therapy. . . . [P]henobarbital was given until maximal serum levels were achieved. She was then started on Dilantin. A head ultrasound on August 25, 1997 was normal. A CT scan on August 26, 1997 showed extensive cerebral low attenuation suggesting anoxic injury. Phenobarbital and Dilantin levels were followed closely and doses were adjusted appropriately. Follow up electroencephalogram (EEG) on September 2, 1997 showed no electrographic seizures and marked suppression except for bursts of excessive sharp waves. The Dilantin was discontinued. No change in the neurological status was noted. Plan: Discharge home on Phenobarbital 12 mg.b.i.d. and follow up Phenobarbital level two weeks after discharge. . . . * * * Discharge Physical Examination: . . . Neurological examination shows symmetrical decreased tone, otherwise no gross neurological deficits were noted. DISCHARGE DIAGNOSES: Term female, 38 weeks gestation. Neonatal asphyxia, resolved. Neonatal seizures ABO incompatibility with hemolysis. Metabolic acidosis, resolved. Anemia. Hyponatremia, resolved. Hypoxic ischemic encephalopathy. . . . Since her discharge, Chelsey has been cared for by Ms. Waddell and her mother (Ms. Chieves), initially in an apartment leased by Ms. Chieves and more recently in a single family residence purchased by Ms. Chieves. Ms. Waddell and Ms. Chieves have jointly shared the responsibility for Chelsey's care and, apart from Aid For Dependent Children (AFDC), which Ms. Waddell started to receive at or about three months after Chelsey's birth, and Medicaid assistance, all financial support for the family has been provided by Ms. Chieves.4 More recently, Ms. Chieves has added her daughter and Chelsey as dependents to her health insurance coverage, which she enjoys as an employee of the State of Florida. The attendant responsibilities and sacrifices inherently associated with Chelsey's daily care may be gleaned from Dr. Michael Duchowny's report of neurological evaluation of August 18, 1998, as follows: HISTORY ACCORDING TO CHELSEY'S FAMILY: Chelsey is an almost 1 year old female who "has cerebral palsy and is legally blind". Ms. Waddell began by explaining that Chelsey has severe motor delay and has essentially made no progress past the newborn level. Chelsey is unable to roll over or sit on her own and requires almost constant feeding. She had an indwelling gastrostomy for the first few months of life, but is now able to mouth and swallow on her own. Still, Chelsey's oromotor problems limit her caloric intake. She is quite small for her age and now weighs only 15 pounds, 14 ounces with a length of 27 inches. Ms. Waddell feels that Chelsey's motor problems effect [sic] all extremities. Chelsey is also "legally blind". By that, her mother indicated that Chelsey is unable to understand what she sees and therefore has little visual information. She can respond to her mother's voice and apparently is hyper alert. She sleeps through the night. Chelsey also suffers from recurrent seizures. These apparently are a marked problem and Chelsey has between 10 and 20 brief tonic seizures per day. Her head and eyes tend to be deviated to the right side with stiffening of the upper extremities. She takes phenobarbital 8 cc b.i.d. and is under the care of Dr. Daniel Shanks in Jacksonville. Chelsey receives physical therapy on a once weekly basis and speech therapy twice weekly. Occupational therapy is administered on one occasion every 2 weeks. . . . * * * NEUROLOGIC EXAMINATION reveals an infant who lies supine with fixed postures in a right tonic neck response. Chelsey demonstrates a startle myoclonus. She has intermittent tongue thrusting movements. There is no drooling. The head is deviated to the right side, but can be passively rotated to the left. There is no central gaze fixation. Chelsey does have brief limited conjugate following. The funduscopic examination is unremarkable. Motor examination reveals increased tone in all extremities indicative of a spastic hemiparesis. The tonic neck response is obligate and can be obtained in both directions through passive movement of the head. There is a positive jaw jerk, sucking and snouting responses. The limbs are small with diminished muscle bulk. Fisting of the thumbs is noted bilaterally. There is evidence of guided reaching. The deep tendon reflexes are brisk at 3+ in all extremities with crossed adductor responses. There are florid bilateral Babinski responses with the large toes being held in passive Babinski attitudes. Sustained ankle and knee clonus are easily elicited. The jaw jerk and facial jerks are both hyperactive. The spine shows a slight curvature convex to the right. The neurovascular examination is unremarkable. In SUMMARY, Chelsey's neurologic examination reveals evidence of severe motor and cognitive delay. Chelsey is showing little progress past the newborn period and her microcephaly suggests that there has been little brain growth since birth. At the same time, Chelsey manifests cortical blindness and startle myoclonus. Chelsey additionally has medically resistant seizures of probable left frontal lobe origin. . . . As heretofore noted, Mr. Davis did not return to Jacksonville, or visit his daughter, until Chelsey was 3 months of age. Thereafter, apart from the first week he was in town and resided with Ms. Waddell and Ms. Chieves, Mr. Davis has lived apart from his daughter and Ms. Waddell, and his participation in his daughter's care, as well as any contribution to his daughter's support, has been de minimus.5 Mr. Davis' interest in Chelsey was stated by him at hearing to be as follows: Q. . . . You're not telling this Court that you want custody of this baby and that you're capable of taking care of it; are you? A. No, sir. I just want it where I can see her when I want to and I ain't got to go through so much trouble, you know, just to see her. Apportionment and manner of payment (lump sum or periodic payment) of the parental award As the primary caretaker for Chelsey, the demands placed on Ms. Waddell as the custodial parent, are, and will continue to be onerous. Clearly, without the support of her mother, the demands placed on Ms. Waddell for Chelsey's care would have left her little or no time for other activities or pursuits, and those demands greatly exceed, and will continue to exceed, those assumed by the parent of an infant not so impaired. In contrast, Mr. Davis has accepted none of the responsibilities (financial or otherwise) associated with Chelsey's care, and has evidenced no sincere inclination to do so. Under the circumstances, it is apparent that, as between them, the loss suffered by Ms. Waddell as a consequence of Chelsey's injury has been grossly disproportionate to that suffered by Mr. Davis, and that such disparity warrants a similar distinction, as between them, in the apportionment of the parental award. As for the method of payment, lump sum or periodic, it should not be subject to serious debate that Ms. Waddell and Mr. Davis have evidenced poor judgment in the past, and that, given their positions in life and young ages, they cannot be relied upon to make sound decisions in the immediate future. Consequently, except for the lump sums hereafter awarded, it is resolved that, absent further order, the bulk of the parental award should be paid periodically to the custodial parent. Given the foregoing considerations, as well as the legal principles discussed infra, it is resolved that of an award of $100,000, Ms. Waddell and Mr. Davis are each eligible to receive $2,500 in lump sum, and that the balance of $95,000 be paid to the custodial parent, retroactive to August 23, 1997, at the rate of $500 per month. Ms. Waddell, as the current and past custodial parent, shall receive the retroactive payment in lump sum and, absent a change in the custodial arrangement, the sum of $500 each month thereafter absent further order or until the principle is exhausted.
The Issue Whether Madison McCorkle, III, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan). Whether the notice provisions of the Plan were satisfied by the participating physician.
Findings Of Fact Preliminary Findings Petitioner, Rebekah Leah Scarfone, now Rebekah Scarfone Jackson, is the mother and natural guardian of Madison McCorkle, III, a minor. Madison was born a live infant on June 2, 1999, at Morton Plant Hospital, a hospital located in Pinellas County, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Madison's birth was Stanley E. Rosewater, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan. Madison's Birth At or about 1:15 a.m., June 2, 1999, Ms. Scarfone (with an estimated date of delivery of June 3, 1999, and the fetus at term) presented to Morton Plant Hospital, in labor. At the time, Ms. Scarfone's membranes were noted as intact, and vaginal examination revealed the cervix at three centimeters dilation, effacement at 90 percent, and the fetus at -1 station. Contractions were noted at a frequency of four minutes, with a duration of 70-80 seconds, and fetal monitoring revealed a reassuring fetal heart rate, with a baseline of 125-130 beats per minute. From 1:15 a.m. until 3:48 p.m., when she was first evaluated by Dr. Rosewater, Ms. Scarfone's labor progress was slow, but steady, and fetal monitoring continued to reveal a reassuring fetal heart rate. At 3:48 p.m., Dr. Rosewater's vaginal examination revealed the cervix at nine centimeters, effacement at 100 percent, and the fetus at 0 station. Thereafter, commencing at or about 4:35 p.m., and continuing until 6:00 p.m., when the fetal heart rate was noted at 50-60 beats per minute and Ms. Scarfone was moved to the operating room for a stat forceps delivery, a pattern of deceleration in fetal heart rate developed. Following admission to the operating room, at 6:13 p.m., the fetal heart rate was noted in the 160 beat per minute range, anesthesia was started at 6:15 p.m., forceps were applied by Dr. Rosewater at or about 6:25 p.m., and Madison was delivered at 6:29 p.m. According to the delivery notes, the cord was observed around the baby's shoulder during delivery, and reduced, and following delivery the baby was bulb suctioned on the perineum and taken to a warmer for resuscitation by the neonatology team. At delivery, Madison was depressed (limp, without spontaneous respiration), and required positive pressure ventilation for about one minute before spontaneous respiration was achieved. Apgar scores were recorded as 2, 7, and 7, at one, five and ten minutes, respectively.2 Following delivery, Madison was transferred to the neonatal intensive care unit (NICU) and at or about 10:15 a.m., June 3, 1999, with evidence of seizure activity, he was transported to All Children's Hospital for further management. On discharge from All Children's Hospital on July 1, 1999, Madison's Neonatal Discharge Summary described his history as follows: Discharge Diagnoses: Term Male Infant Perinatal Depression Hypoxic Ischemic Encephalopathy Seizures Right Optic nerve Hypoplasia and Left Macular Edema Acute Tubular Necrosis Evolving Encephalomalacia Right Submandibular Fat Necrosis * * * HISTORY: Baby Boy Scarfone was born by a forceps delivery with a vertex presentation to a 20 year old G1P0 mother. Apgars were 2,7, and 7 and 1, 5, and 10 minutes respectively. Birth weight was 3210 gms and estimated gestational age was term. Maternal history was significant for: blood type A+, HBS Ag-, RPR nonreactive, and Group B strep negative. During labor there were deep variable decelerations. The mother took prenatal vitamins and received Pitocin. This was a forceps delivery and the cord was noted to be around the body. Delivery room resuscitation included whiffs of oxygen and positive pressure ventilation via mask. Care at the referring hospital included intubation and ventilation, peripheral IV fluids, umbilical arterial catheter placement, Dopamine, normal saline boluses x 3, and sodium bicarbonate were given. Cranial ultrasound was performed.[3] Blood cultures were drawn and Ampicillin and Gentamicin initiated. The infant was noted to have 4 episodes of seizure activity and was started on Phenobarbital. The infant was transferred to All Children's Hospital for perinatal depression and seizures. RESPIRATORY: The infant was admitted on room air. The initial chest x-ray showed clear lung fields. The infant developed stridor, with feedings, at 21 days of life. A Pulmonology consult was obtained. An OPMS study was recommended. No evidence of aspiration or suck, [s]wallow, incoordination was noted. The pulmonologist did not feel a bronchoscopy was needed at this time. The infant had a sleep study performed with pH probe at 21 days of life. There were numerous central apneas and transient desaturations. There was no evidence of reflux. The infant was also studied in a car seat which showed intermittent central apnea, mixed apnea, and a few obstructive apneas and desaturations. The infant will be discharged home with an apnea monitor. He will also receive oxygen and when traveling will be placed in a car bed. He will have Pulmonology follow up 2 weeks after hospital discharge. CARDIOVASCULAR: The infant had hypotension due to perinatal depression at newborn day of age and required treatment with volume expansion and Dopamine for 4 days. * * * INFECTION: Blood cultures were obtained at the referring hospital. The infant was started on Ampicillin and Gentamicin. Gentamicin was discontinued due to increased creatinine level. Ampicillin was continued for a total of 3 days. * * * CENTRAL NERVOUS SYSTEM: The infant was admitted with a diagnosis of seizures which were treated with Phenobarbital, Dilantin, and Ativan. The infant was evaluated by Neurology. A CT scan at 1 day of age for perinatal depression revealed bra[i]n edema in the left parietal/occipital region. A MRI, at 5 days, revealed probably left cerebellar intraparenchymal subacute hemorrhage, abnormal signal in the left hemisphere and basal ganglia probably representing infarction. The infant was evaluated by Ophthalmology on 6/4/99 for retinal (macular) edema and right optic nerve hypoplasia. [H]e will be followed by Ophthalmology. A repeat CT scan, at 19 days of life, revealed evolving encephalomalacia. A follow up EEG at 22 days of age was within normal limits. At the time of hospital discharge the infant is receiving Phenobarbital with the last level 14.4. He will be followed by Neurology and have a follow up Phenobarbital level in one week. Due to the history of perinatal depression the infant will require developmental follow up, occupational therapy, and physical therapy intervention. . . . Discharge planning included follow-up with his pediatrician at Mother and Child Care (Dr. K. Adnan); Ophthalmology (Dr. J. Bruce Hess); Neurology (Pediatric Neurology Associates, P.A.); occupational therapy/physical therapy (Morton Plant Hospital - Barrett Center, Outpatient Rehabilitative Services); and the Early Intervention Program. Madison's Subsequent Development Madison received a physical therapy evaluation at the Barrett Center on July 13, 1999, and an occupational therapy evaluation on August 10, 1999, to assess his need for rehabilitative services. Assessment on physical therapy evaluation was, as follows: Musculoskeletal Status Madison presents normal to mild high tone. Range of motion marked by tightness in hip and knee flexion; range of motion of feet within normal limits for his age, but Madison has a tendency to maintain feet dorsiflexed. Madison has increased flexion recoil of lower extremities during range of motion testing and when placed in various positions. Recommendation was "[s]tart Physical Therapy services once a week; re-evaluation in six months." Assessment on occupational therapy evaluation was, as follows: Madison had normal tone in his upper extremities. He had the age appropriate grasp reflex. Passive and active range of motion of the upper extremities was within normal limits. Under the circumstances, occupational therapy was not recommended, but follow-up screening in three months to monitor progress was suggested. Thereafter, by February 8, 2000, Madison was also receiving occupational therapy. Madison had his first evaluation under the Early Intervention Program on August 2, 1999. The results of that evaluation were reported, as follows: Neurological Dubowitz is done with the patient in quiet alert state. Although he cries to aversive stimuli, he consoles readily with holding and a nipple. Movement and tone reveals symmetric arm and leg recoil. Flexion responses are initial in upper and lower extremities. There is some increase in tone in the lower extremities. Although head lags behind the body when brought from supine to sitting, in supported sitting he attempts to bring head upright from both anterior and posterior positions. In prone, he rolls head to the side and brings hand to shoulder level. No abnormal movements are noted. Reflexes indicate symmetric Moro response. Walking reflex is present. Palmar grasp is maintained. Suck is regular with good stripping. Neurobehavior includes conjugate eye movements, turning toward a rattle, and following a bright object horizontally and vertically. * * * Dubowitz Neonatal Neurological Examination is suspicious due to increased tone in the lower extremities. * * * EARLY INTERVENTION PROGRAM PLAN: * * * Recommend continuing with physical therapy on weekly basis. Madison was re-evaluated under the Early Intervention Program on May 12, 2000. According to standardized testing, Madison's cognitive skills were considered at risk for delay for his chronological age of 11 months 10 days; however, communication screening indicated his receptive and expressive language skills were age-appropriate. Neurological examination revealed that tone was mildly low, movements symmetrical. Recommendation was to follow-up in six months to monitor Madison's growth and development. Madison's next evaluation under the Early Intervention Program was on November 10, 2000, at age 17 months 8 days. At the time, assessment was "[c]ognitive skills are delayed at a 13 month age level"; [m]otor skills are within normal limits at a 16 month age level"; and "[c]ommunication skills are in an at risk category with both receptive and expressive language at a 14 month level." Based on such evaluation, a homebound teacher was recommended one hour per week to work on cognitive and communication skills, and physical or occupational therapy were no longer deemed developmentally necessary. Nevertheless, according to the records of Pediatric Neurology Associates, discussed infra, physical and occupational therapy continued. Subsequently, in early 2001, Madison was also accorded speech therapy. Madison's initial evaluation at Pediatric Neurology Associates, was on August 2, 1999. The results of that evaluation were noted, as follows: This 2 month old was seen for a hospital follow-up for experiencing difficulties at birth. He has suffered perinatal depression and then neonatal seizures. There have been no seizures since hospitalization. * * * PHYSICAL EXAMINATION: The patient is a well- developed, well-nourished 2 month old white male. Head circumference is 38.5 centimeters, which is at the 50th percentile. There are no skin rashes noted. Anterior fontanel is soft and flat. Head and facies are symmetric without dysmorphic features. He does track objects. The pupils are equal, round, and respond to light, and constrict, bilaterally, to light. The conjunctivae are pink. The funduscopic examination demonstrates a positive red reflex. Tongue and palate are symmetric. There is upper respiratory congestion. Neck is supple without lymphadenopathy. Chest is clear to auscultation, bilaterally. Heart demonstrates regular rate and rhythm with normal S1 and S2. Spine is straight without masses, lesions, or dimples. Abdomen is soft and round without hepatosplenomegaly or tenderness. Full range of motion noted. There are no motor asymmetries identified. Tone is within normal limits. Deep tendon reflexes are +2. Response to plantar stimulation is withdrawal, bilaterally. LABORATORIES: EEG, performed 06/04/99, is abnormal because of excessive sharp transients in the left posterior and central vertex region. EEG, performed 06/22/99, is normal. CT of the brain, 06/21/99, demonstrates peripheral foci of abnormal low density within the left parietal occipital region. High left parietal convexity and possibly more anteriorly within the left parietal lobe, as above. These regions likely represent evolving and encephalomalacia, possibly secondary to infarction, infection, or other brain insult. MRI of the brain, 06/07/99, demonstrates probably left cerebellar intraparenchymal early subacute hemorrhage. Abnormal signal in the left hemisphere, especially parietal occipital and in the basal ganglia (especially right thalamus) probably represents infarction. Phenobarbital level, 06/14/99, is 19.2 (15 to 40). IMPRESSION: Hypoxic ischemic encephalopathy. Seizures, which are currently under control. Perinatal depression. Right optic nerve hypoplasia. PLAN: Will obtain Dr. Hess' ophthalmologic report.[4] Will begin weaning Phenobarbital . . . . Madison was also seen at Pediatric Neurology Associates (or Children's Medical Services Clinic) on November 12, 1999, February 8, 2000, November 27, 2001, and June 26, 2002. Initially, Ms. Scarfone reported no evidence of seizure activity, abnormal movements, or altered consciousness; however, on November 27, 2001, she reported a paroxysmal episode ("a spasm or seizure") had occurred, about two weeks previous. A CT of the brain on November 30, 2001, demonstrated: Small focal area of decreased attenuation in the high left parietal area peripherally. This probably represents a small area of encephalomalacia. No definite additional areas of abnormal attenuation are identified. Specifically, the fairly prominent area of low attenuation seen in the left posterior parietal area on the previous study of 06/21/99 is no longer seen. No new abnormalities are appreciated. Subsequently, on June 26, 2002, Ms. Scarfone reported paroxysmal episodes, at one episode per month for the previous four to five months. At the time, the "Plan" included "[f]ollow- up in C[hildren's] M[edical] S[ervices] within the next two to four months," "[i]n the meantime, obtain a CT of the brain, noncontrast and repeat the EEG," and "[i]f episodes should continue, may consider an empirical trial of anticonvulsant therapy." On October 3, 2002, Madison had a prolonged seizure. At the time, the head CT scan was negative; however, EEG of October 4, 2002, was abnormal, and Madison was placed on maintenance Dilantin, which, given allergic reaction, was changed to Depakene and then to Keppra. Madison's follow-up visit at Pediatric Neurology Associates on December 18, 2002, was reported, as follows: This 3 year old returns for a follow-up for history of hospitalization for seizure exacerbation. His mother reports his seizures usually start with waking up out of his sleep with coughing and then vomiting. He will stare and then go into tonic-clonic activity. The last event was one to two weeks ago. DEVELOPMENT: He is in multimodal therapies at school for a history of developmental delay. PAST MEDICAL HISTORY: He has a history of anoxic encephalopathy and seizures. PHYSICAL EXAMINATION: The patient is a 3 year old, male weighing 43 pounds (19.5 kilograms). Height 39-3/4 inches. Blood pressure is 86/44. Heart rate is 108. There are no skin rashes noted. * * * The extraocular movements are full and intact without nystagmus noted. The pupils are equal, round, and respond to light, and constrict bilaterally to light. Convergence is positive. Conjunctivae are pink. The funduscopic exam demonstrates discs of normal color and sharp margins with no hemorrhage or exudates. He is slightly impulsive during the exam. The neck is supple without lymphadenopathy. The heart demonstrates regular rate and rhythm with normal S1 and S2. Full range of motion. Tone is slightly low. Reflexes are +2. Gait is without ataxia. * * * IMPRESSION: Seizure reoccurrence. PLAN: 1. Continue with Keppra . . . . 3. Follow-up will be in the CMS Clinic with Dr. Casadonte . . . Dr. Casadonte reported the results of his follow-up of April 18, 2003, as follows: Madison McCorkel [sic] presents to the CMS clinic. He's a child with seizures secondary to anoxic encephalopathy experienced at birth. He's on Keppra . . . . Mom reports he's had only one event in two months. The events are stereotypically where he awakens from his sleep. He coughs and stares. They last several minutes and then he's sleepy afterwards. He is three years 10 months . . . . He's alert. Pupils are equal and reactive. His face is symmetric. He moves his extremities equally. He attends Fuguitt Elementary through the FDLRS program. The plan is to continue Keppra . . . . Notably, Madison's medical records fail to support a conclusion that he is substantially mentally or physically impaired, much less permanently impaired, and none of his treating physicians has expressed such an opinion. It is also worthy of note that, while Respondent presented the testimony of Dr. Michael Duchowny, discussed infra, to address the issues, neither Petitioner nor Intervenors, although they had the burden to prove Madison suffered a birth-related neurological injury, offered any expert testimony to establish that Madison's current deficits resulted from a brain injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation, or that Madison was permanently and substantially mentally and physically impaired. Dr. Duchowny, a physician board certified in pediatrics, neurology with special competence in child neurology, and clinical neurophysiology, examined Madison, at NICA's request, on September 11, 2002, and reported the results of his evaluation, as follows: Madison's NEUROLOGIC EXAMINATION reveals him to be overactive, inattentive, and impulsive. He maintains poor eye contact and it is difficult to keep him on track for the evaluation. He is quite defensive and, for example, fends off attempts to have his fundi looked at in detail. There are marked imitative gestures and repetitive movements. He tends to wave goodbye throughout the evaluation in a semi-repetitive fashion. The speech sounds are poorly articulated for lingual, labial, and guttural consonance and it is very difficult to understand his speech output. He tends to speak in one or two words. He could identify some body parts but not others and was not able to articulate colors in any specific fashion. It was difficult to keep his attention span on track. The cranial nerve examination reveals full visual fields to direct confrontation testing. He blinks to threat in both directions and reacts to sound in all planes. The pupils are 3mm and briskly reactive to direct and consensually presented light. I could not get a full fundoscopic evaluation. The tongue and palate move well. The uvula is midline. Motor examination reveals symmetric strength and bulk. His tone is slightly diminished throughout and his movements are uncoordinated. He postures his outstretched hands in a very marked fashion and there is marked decomposition of rapid alternating movement sequences. He has distal career from movements as well. There is no focal weakness or atrophy. The deep tendon reflexes are 1+ bilaterally. His gait and station are stable. There is pesplanus bilaterally. He did not fall while walking. The spine is straight without dysraphism. There is withdrawal of all extremities to provocation. Neurovascular examination discloses no cervical, cranial or ocular bruits, and there are no temperature or pulse asymmetries. IN SUMMARY, Madison's neurologic examination is significant for developmental delays in multiple areas. He is clearly delayed in terms of his expressive and receptive language skills, and has a speech articulation defect. He also has a short attention span, high activity level, and an impulsive behavioral style. Marked dyspraxia is also noted. Apart from these developmental findings, there are no focal or lateralizing features to suggest structural brain damage and I believe that Madison most likely has a pervasive developmental disorder and is at risk for falling within the autistic spectrum in the future. . . . I have not as yet had an opportunity to review Madison's medical records and will issue a final report once the review process is complete. Following review of the medical records, Dr. Duchowny concluded: A review of the medical records suggests that the pregnancy with Madison was complicated by a probable vira[l] infection, as evidenced by the placental pathology, ophthalmology findings, elevated liver function tests, and neuro-imaging findings. The findings on Madison's neurologic examination are most consistent with the developmental syndrome of pervasive developmental disorder, and I strongly suspect that Madison will ultimately be diagnosed with childhood autism. Given these findings, I do not believe that Madison suffers from a substantial motor or mental impairment, or that h[is] problems were acquired in the course of labor, deliver, or the immediate post partum period. Stated otherwise, while Dr. Duchowny acknowledged that Madison's birth was stressful, and resulted in a number of problems that had to be managed post-delivery, he was of the opinion that the deficits Madison currently exhibits are "developmentally based, meaning that they have to do with abnormalities during the formation of the brain as opposed to consequences of hypoxia, ischemia or trauma." (Respondent's Exhibit 3, at page 30.) As for Dr. Duchowny's opinion that Madison does not suffer from a substantial motor or mental impairment, it is worthy of note that, although they had the opportunity to do so during the course of his deposition, the parties did not challenge or otherwise question his opinion. Finally, pertinent to a current assessment of Madison's neurologic presentation is the deposition testimony of Ms. Scarfone, taken July 21, 2003. (Hospital Exhibit 2.) At the time, Ms. Scarfone offered the following observations: Q Is Madison currently enrolled in any school or educational program? A Yes. Q Where? A Fuguitt elementary in the FDLRS Program. Q What is the FDLRS Program? A It's for kids that have developmental problems, autistic children, for kids that are developmentally delayed. Q Is that a year-round program? A Yes. He was in pre-K, and he's going to be in pre-K again. Q Has he been diagnosed as suffering from autism? A No. Q What kind of developmental delays does he have? A Speech. He's four. They say that he's at age three. So I guess that would be developmental altogether. Q What other developmental delays does he have other than speech? A He's not like other kids. I mean, he's behind. I don't know what - what it would be called. I mean, he's four years old, and he acts as if he's three. I mean, healthwise, I mean, his vision is bad in his left eye, and he has seizures. Q Describe the seizures for me. A Before he was not placed on the medicine, he would wake up from a nap, and he would have convulsions. Since he's been placed on the medicine, he will just wake up with the gagging effect, and he'll just stare off. And he'll last maybe like a minute or two, and then he'll - it will go away, and he'll just want to go to sleep. Q How often does he have these seizures? A Since he's been on the medicine, he usually has maybe one to every three months. Q Does he have any problem with swallowing? A No. Q Does he have any motor problems? A Motor skills? Q Yes, ma'am. A I was told that he did, yes. Q By whom were you told? A I don't recall. Plenty of people have told me, but it was a certain program that I used to take him to. I was told by his occupational therapist that he had, and I don't remember what it was called. Q Is he currently enrolled in any programs designed to assist him with any motor problems? A No. Q What kind of motor problems has he had in the past? A He was delayed when he was young. He, like, wasn't sitting up when he should. They had to - I had to take him to therapy to set him up because his - when he was born, his legs were bowed up. I had to take him to therapy to stretch his legs. He was late sitting up and crawling, walking, stuff like that. Q Does he currently have any motor deficits? A No. Q He is able to walk, run, jump? A Yes. Q Skip? A Yes. Q As far as you're concerned, whatever motor problems he's had in the past with his legs have resolved? A Yes. Q Does he have any motor problems with his hands or arms? A No. * * * Q Fuguitt Elementary is a public school? A Yes. Q And he's going to be repeating the pre-K program? A Yes. Q Is he in school today? A No. He starts back when school starts back. Q Has he been off for the summer? A Yes. Q What has he been doing? A Stays home with me. Q And his brother? A Yes. A And his two stepsisters? A Yes. . . . Q Okay, Has he had any sort of therapy this summer? A Yes, he takes speech therapy in FDLRS. Q So even though school is not ongoing, that particular program provides some sort of summer therapy? A Oh, I'm sorry, no, not for the summer. No, he hasn't done anything in that. Q He hasn't had any kind of therapy since school let out in May? A No. Q Other than that which he receives at school, is he receiving any sort of therapy? A No. * * * Q Has anyone suggested to you now that he is in school, that he needs anything in addition to that which the school is providing? A No. I did sign - well, I did sign a paper for his school for vision. They wanted to see if he qualifies for vision class or vision therapy. Q You said it's the one eye that's bad, the left - A The left eye. * * * Q . . . Other than the problem with his left eye and the problems he has with respect to speech, are there any other objective problems that you, as his mother, have observed? A He's very active, very hyper. Q Has he been treated for that hyperactivity? A No. 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 post- delivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired."5 Section 766.302(2).6 See also Section 766.309. Here, given the proof, it must be resolved that Madison suffers neither a substantial mental impairment nor a substantial physical impairment, much less a permanent and substantial mental and physical impairment required for coverage under the Plan. Moreover, given Dr. Duchowny's observations, and the paucity of proof to the contrary, it cannot be resolved, as suggested by Intervenors, that the cause of Madison's deficits resulted from a brain injury caused by oxygen deprivation or mechanical injury that occurred during labor, delivery, or resuscitation, as opposed to a developmental abnormality, that preceded the onset of labor. See 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."); 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.") The Notice Provisions of the Plan Pertinent to this case, at the time of Madison's birth, Section 766.316, Florida Statutes (1998), 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 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. The hospital or the participating physician may elect to have the patient sign a form acknowledging receipt of the notice form. Signature of the patient acknowledging receipt of the notice form raises a rebuttable presumption that the notice requirements of this section have been met. Notice need not be given to a patient when the patient has an emergency medical condition as defined in s. [395.002(9)(b)][7] or when notice is not practicable. Here, there being no proof to support a contrary conclusion, Dr. Rosewater presumably did not provide Ms. Scarfone notice. See Balino v. Department of Health and Rehabilitative Services, 348 So. 2d 349, 350 (Fla. 1st DCA 1977)("[T]he burden of proof, apart from statute, is on the party asserting the affirmative issue before an administrative tribunal.") However, at the time, he was not required to do so. Notably, Section 766.316, Florida Statutes (1998), describes those circumstances under which notice need not be given, as follows: . . . Notice need not be given to a patient when the patient has an emergency medical condition as defined in [s. 395.002(9)(b)] or when notice is not practicable. Pertinent to this case, Section 395.002(9)(b), defines "emergency medical condition" to mean: (b) With respect to a pregnant woman: * * * 3. That there is evidence of the onset and persistence of uterine contractions or rupture of the membranes. Here, on presentation to Morton Plant Hospital, there was clear evidence of the onset and persistence of uterine contractions. Consequently, Dr. Rosewater was not required to provide Ms. Scarfone with notice.
The Issue Whether Jael Sutton, a minor, qualifies for benefits under Florida's Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Petitioner, Senboya Sutton, is the natural parent of Jael Sutton (Jael). At all times material, Senboya Sutton was an obstetric patient of Intervenor, Mark Davis, M.D., who was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by section 766.302(7). Dr. Davis provided obstetrical services "in the course of labor, delivery and resuscitation in the immediate postdelivery period in a hospital," as related to this case. Jael was born on November 28, 2006. At birth, Jael weighed in excess of 2,500 grams. Jael was a single gestation. Jael was born live at St. Joseph's. St. Joseph's is a licensed hospital located in Tampa, Florida. The parties stipulated that all notice requirements of the statute have been met and that the notice requirement of section 766.316, is not at issue herein.2 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." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat.3 Herein, it is undisputed that Jael is "permanently and substantially mentally and physically impaired." Also, as described more fully hereafter, all the testifying experts concur that Jael's underlying brain damage did not result from a mechanical injury, but did result from sepsis and/or meningitis. However, it remains for determination whether or not Jael's brain injury and permanent and substantial mental and physical impairment occurred in the course of "labor, delivery, or resuscitation in the immediate postdelivery period," hereafter referred to as "the statutory period."4 The following terms were defined within this record: "Hypoxia" means "not enough oxygen." "Cerebral ischemia" means "not enough blood is getting to the brain." "Perfusion," for purposes of the instant case, means "to pass blood through the brain to ensure adequate oxygen." For her pregnancy with Jael, Ms. Sutton was first seen by Dr. Davis on August 17, 2006. Her delivery date was estimated as January 25, 2007. On November 17, 2006, a vaginal culture was taken of Ms. Sutton. On November 25, 2006, it was reported as "positive" for Group B streptococcus (Group B-strep), a genus of bacteria that causes life-threatening infections in newborn infants.5 Dr. Chalhub testified that intrauterine infections are the leading cause of cerebral palsy in term infants. Jael was not a term infant, but cerebral palsy is one of the conditions with which he has been diagnosed. On November 27, 2006, at approximately noon,6 Ms. Sutton presented to St. Joseph's. She complained of a single episode of leaking fluid at 1:02 p.m. Hospital records characterized this as the onset of labor, despite Ms. Sutton's denial of contractions. The plan of treatment was to rule out spontaneous rupture of the membranes. A nitrazine test was performed to identify amniotic fluid outside the amniotic sac, and was negative. Dr. Davis was present and ordered a non- stress test. At 1:34 p.m., Ms. Sutton again complained of leaking fluid and mucus discharge was noted. At 1:58 p.m., Dr. Davis reviewed the fetal monitor strip and discharged Ms. Sutton. At approximately 5:50 p.m., on November 27, 2006, Ms. Sutton presented to UCH. Her membranes were noted as possibly ruptured, and she complained of small gushes of fluid since noon. Again, a nitrazine test was performed and was negative. A speculum vaginal examination was performed; fetal heart rate was monitored; and a non-stress test was performed. She was discharged home upon phone orders of the "on-call" physician and advised to follow up with her obstetrician. The next morning, before 10:00 a.m., Dr. Davis did an ultrasound in his office. The ultrasound showed what was believed to be decreased amniotic fluid; a 34-week, four day gestation; and ruptured membranes. Due to the Group B strep and the gestation in excess of 34 weeks, Dr. Davis initiated a plan of care to induce labor and perform a vaginal delivery. Later on November 28, 2006, Ms. Sutton was admitted to St. Joseph's. Examination by speculum showed positive nitrazine and a copious amount of fluid in the vaginal vault, which, in hindsight after Jael's birth, Dr. Davis recorded as "probably a high leak to begin with." A fern test for nitrazine was positive. The cervix was 2-3 centimeters dilated. Labor steadily progressed. At 11:32 a.m., a nurse noted a non- reassuring fetal heart rate. At 11:47 a.m., Dr. Davis reviewed fetal heart rate tracings from his office. These were better, without decelerations. Ms. Sutton was placed in a left lateral position and continuous face mask oxygen was maintained. At 11:49 a.m., another sterile vaginal exam was performed. The amniotic fluid was noted to be clear and of normal quantity. At 11:54 a.m., due to a non-reassuring fetal heartbeat, Dr. Davis called for an immediate Caesarean section. Jael's fetal heart rate was 160, just prior to the C-section. A low transverse uterine incision was performed at 12:16 p.m., and Jael was delivered. Throughout the C-section, under general anesthesia, Ms. Sutton's oxygen saturation levels remained at 100. There is no record of trauma or of mechanical injury to Jael during labor or delivery. Indeed, the parties agree that there was no mechanical injury to Jael during labor or delivery. See infra. The delivery record does not show checks or fill-ins for the following, but the following is printed or typed in on the delivery room record form: "suction bulb, suction catheter, tactile stimulation, oxygen/PPV[7], intubated, neonatologist present." Apgar scores were taken at one and five minutes after Jael's birth.8 Jael's one minute Apgar score showed: Heart rate 2 > 100 Respiratory effort 0 none Muscle tone 1 some flexion Activity 0 none Color 0 blue/pale Total 3 Jael's five minute Apgar score showed: Heart rate 2 > 100 Respiratory effort 2 good cry Muscle tone 1 some flexion Activity 1 grimace Color 1 extremities blue Total 7 It is a point of contention among the parties as to whether Jael was intubated in the delivery room or in the Neonatal Intensive Care Unit (NICU). It is more likely that intubation and administration of nitrous oxide began after he was stabilized, as evidenced by the good Apgar score at five minutes after birth. The "good cry" recorded at five minutes of life (12:21 p.m.) suggests that Jael was breathing on his own at that point, had stabilized, and was not intubated before his admission to the NICU at 12:40 p.m. Jael's cord blood gas was collected at ten minutes after birth at 12:26 p.m. Its pH measured 7.206. A cord blood of 7.2 or higher suggests absence of metabolic acidosis. Metabolic acidosis is a sign of a pathological condition, not of a mechanical injury or of oxygen deprivation.9 At 12:32 p.m., Jael was transferred by isolette from the delivery/operating room to NICU due to "post C-section respiratory status." It would be fair to say that, at this point, if not sooner, Jael's care passed from the NICA participating physician, who provided obstetrical services to the mother, to other health care professionals in the NICU. At 12:40 p.m., on November 28, 2006, Jael was admitted to the NICU. The records show that ventilation support was given, and Jael was intubated. No physician associated with Jael's delivery or NICU care testified. However, Dr. Katz, a pediatric neurologist, opined without refutation that intubation at that stage might have been for ventilation, but could as easily have been to keep Jael's airway open because he was born prematurely. The reasons that were contemporaneously documented for Jael's admission to NICU were "premi, 34 weeks, R/O sepsis." This notation most probably means, "34 week gestational, premature infant; rule out sepsis." "'Sepsis' refers to the presence in the blood or other tissues of pathogenic microorganisms or their toxins; the condition associated with such presence."10 As described more fully hereafter, all testifying medical experts, regardless of specialty, agreed that in the NICU, Jael suffered from vascular inflammation, decreased blood pressure, and diminished perfusion caused by infection. Where they disagree is whether it was sepsis or meningitis which was ultimately responsible for Jael's diminished blood supply to the brain. "'Meningitis' is an inflammation of the meninges, usually by either a bacterium (bacterial meningitis) or a virus (viral meningitis)."11 Upon admission to the NICU at 12:40 p.m., Jael's oxygen saturation levels were at 93 per cent, and despite continuing very low blood pressures, his oxygen saturation levels remained in the 80's and 90's until 6:40 p.m., that evening. Jael was not assessed again after NICU admission until 1:20 p.m. At that time, a nurse noted that she was unable to obtain his blood pressure in either leg, although no reason was given. Dr. Katz testified that this could mean anything, up to and including an ill-fitting blood pressure cuff. Jael's bedside glucose (BSG) was recorded as 10, and 50cc of D10 bolus were ordered. At 1:44 p.m., on November 28, 2006, the BSG was recorded as 43 and another bolus was administered. At 1:58 p.m., November 28, 2006, a blood culture was drawn which was not reported back until the next day, but when it was reported back, the blood culture was read as positive for Group B strep. 37. At 2:00 p.m. and 2:05 p.m., on November 28, 2006, boluses and antibiotics were ordered, but one or more antibiotics were not administered to Jael for the first time until considerably later. At 2:05 p.m., on November 28, 2006, orders were written for survanta and dopamine. Dr. Katz opined that Jael was in septic shock at this time. At 2:16 p.m. on November 28, 2006, Neonatologist Dr. Amaizu entered an NICU admission note that Jael was lethargic with decreased reactions to stimuli. Capillary reflex was > 2 sec. Jael had decreased tone and activity. Although perfusion was decreased, his skin was pink. The active diagnosis at that point was "hypoglycemia, prematurity, respiratory distress syndrome, R/O sepsis newborn." At 2:25 p.m., an NICU nursing assessment was done. Jael was described as withdrawn, flaccid, lethargic with absent reflexes (suck, rooting, moro, and grasp). Central cyanosis (blueness in the torso) was observed. At 3:07 p.m., dopamine was administered. On the following day, November 29, 2006, Terry Declue, M.D., performed an endocrinology consult on Jael, who was on nitrous oxide via an oscillatory ventilator. He noted hypoglycemia. Perfusion was noted as good with capillary refill one second. The chest appeared clear, and Jael moved spontaneously. Dr. Declue's diagnosis was: Severe metabolic acidosis Lactic acidosis Respiratory failure Gram positive cocci sepsis Pulmonary hypertension On December 1, 2006, three days post-birth, a cranial neuro-sonogram was performed. At that time, hospital Radiologists Steen Mandel, M.D., and John Rasmussen, M.D., read the sonogram as normal. On December 4, 2006, four days post-birth, Jael underwent a lumbar puncture. His cerebrospinal fluid showed a white blood count of 185, reference 0-5. The consulting neurologist diagnosed Strep Group B sepsis and meningitis. On December 10, 2006, a second cranial ultrasound was done. This second sonogram was read by Michael Shaw, M.D. He recorded that ventricular size and configuration was normal, with no evidence of germinal matrix or inter-ventricular bleed, but the ventricles appeared slightly (not significantly) more prominent than the prior December 1, 2006, study. On December 15, 2006, an MRI was performed and interpreted by radiologist Elaine Engleman, M.D. Her impression was: Extensive cystic encephalomalacia[12] involving both cerebral hemispheres throughout all vascular territories. There is slightly less extensive involvement in the posterior cerebral artery territories. There is preservation of parenchyma involving the basal ganglia, thalami and brainstem. Jael was discharged from St. Joseph's on January 5, 2007, with a diagnosis of: Prematurity at 34 weeks gestational age Respiratory distress syndrome Neonatal depression Severe metabolic acidosis Patent ductus arteriosis Cholestasis Lactic acidosis Respiratory failure Meningitis that was treated for three weeks and supraventricular tachycardia On August 1, 2007, another MRI was performed on Jael's brain and interpreted by Radiologist, James Hanner, M.D. His report opined: FINDINGS: There is extensive cystic encephalomalacia seen throughout in the frontal, temporal, and parieto-occipital lobes associated with significant ex vacuo enlargement of the occipital horns, bilaterally, left greater than right. There is some sparing of the medial frontal accident, hemorrhage, or extra-axial fluid collection is identified. The hindbrain structures are normal without developmental anomaly. There is wallerian degeneration of the cerebral peduncles bilaterally. IMPRESSION: Extensive supratentorial systic encephalomalacia associated with ex vacuo enlargement of the lateral ventricles and occipital horns, left greater than right. The volume loss has progressed when compared to the earlier examination. Despite some variant medical testimony, across all experts, to the effect that Jael was probably infected with Group B-strep from his mother before labor, during labor, or during delivery, Intervenors collectively submit that, ". . . Jael Sutton did not suffer from oxygen deprivation during labor or delivery . . ." (proposed finding of fact 54 of Intervenors' proposed final order). Due to this admission and the other parties' similar positions, it is not necessary for the undersigned to resolve when labor began; when "active" labor began; when the amniotic fluid began to leak; or even whether Jael's delivery by C-section undermines any medical opinions rendered herein in terms of acquisition of bacterial infection during Jael's passage through the birth canal. Therefore, the issue is further narrowed to whether or not Jael suffered from oxygen deprivation "occurring in the course of . . . resuscitation in the immediate postdelivery period . . . which render[ed] the infant permanently and substantially mentally and physically impaired." The parties presented medical experts in a variety of fields who offered their opinions, within reasonable medical probability, as to what happened to Jael and within which periods of time. All experts testified by deposition, but the undersigned has had the benefit of viewing DVDs of the depositions of Dr. Robert Zimmerman and Dr. Mary K. Edwards- Brown. Michael Duchowny, M.D., a Florida-licensed physician, is a professor of neurology at the University of Miami Leonard Miller School of Medicine; a clinical professor of neurology at Florida International University College of Medicine; and senior attending physician at Miami Children's Hospital. He is board- certified in pediatric neurology, with special competence in child neurology, clinical neurology, and clinical neuro- physiology. He performed a medical examination of Jael on February 17, 2010, and reviewed the mother's and the child's medical records, including the ultrasound study of December 1, 2006, and the MRI scans of December 15, 2006, and August 1, 2007. He did not read the December 10, 2006, ultrasound. Dr. Duchowny's testimony confirmed, without equivocation, that Jael is tragically and profoundly permanently and substantially mentally and physically impaired. It was his ultimate opinion that Jael did not suffer a birth-related neurological injury due either to mechanical injury or deprivation of oxygen supply or blood flow to the brain within the statutory period. He reached this conclusion because, in his expert opinion, no impairment occurred during the statutory period. Dr. Duchowny did not see, on the films he reviewed, any sign of damage during the statutory period. He diagnosed the cause of Jael's multiple problems as meningitis, and opined, in pertinent part, as follows: Q: . . . Do you have an opinion, within a reasonable degree of medical probability, whether or not he had an impairment that was acquired during labor, delivery or post- delivery? . . . A: If we're going to define it as impairment, I would say, no. Q: So what you're saying is that no damage was done, even if he had the infection, right? A: I am saying that, because I don't see any indication of damage at that time. Q: . . . You don't find him -- you don't find that he had a mechanical injury; is that right? A: That's correct. Q: And you don't find that there was deprivation of blood flow or oxygen, correct? A: That's correct. (Depo. 33-34). Dr. Duchowny testified concerning the meningitis diagnosis as follows: A. . . . Meningitis means -- it specifically refers to a bacterial infection of the membranes covering the brain. These are anatomically called the meninges, so that in its strictest sense, a meningitis is an infection and an inflammation of the membranes covering the brain, but, in point of fact, it spreads from the membranes usually directly to the brain itself, and that's where the problems come in. . . . * * * I don't believe that Jael's brain damage was due to either a mechanical injury or oxygen- -deprivation of oxygen supply or blood flow to the brain. I think that Jael's brain damage is primarily due to the effects of meningitis. * * * . . . the MRI findings are consistent with severe bacterial meningitis, in this case, Group B strep meningitis. The findings, also, to me, are supported by the fact that if one looks at the clinical course of Jael, there really is no specific hypoxic or ischemic event that would be in the records to explain the findings on neuroimaging and the neurologic outcome. . . . So although one can see findings on MRI that are consistent with hypoxic and ischemic damage, for example, cystic encephalomalacia, if one looks at the totality of the picture, meaning, put the clinical events together with the neuroimaging findings and the neurologic examination, I think that this pattern of evidence all supports the fact that Jael's neurologic damage is primarily due to bacterial meningitis. (Depo. 20-26). Michael Katz, M.D., is a pediatric neurologist, and board-certified in pediatrics, pediatric neurology, and neuro- developmental disabilities. He is based at Hackensack University Medical Center, New Jersey. He examined Jael on September 14, 2009, and testified on behalf of Petitioners by a November 19, 2010, deposition. He considered the "resuscitative period" in Jael's case to be "until the Apgar is normalized at five minutes when the Apgar was seven," and opined that the injury to Jael's brain did not take place in that period. He concluded that the cause of Jael's permanent and substantial mental and physical impairment was a "strep B meningitis." More specifically, Dr. Katz testified: Q: In your opinion within a reasonable degree of medical probability, was there any injury to Jael Sutton's brain caused by oxygen deprivation occurring during labor or delivery or resuscitation in the immediate postdelivery period? A: No. * * * Q: What significant history did you elicit that leads you to reach that diagnosis and opinion of causation? * * * A: . . . First is that Mom was group B strep positive. The second was that mom had premature ruptured membranes. . . . Jael had a clinical deterioration, essentially went into shock and required pressors and resuscitation. And the ultimate, and probably most important fact, is when he was finally clinically stable, we were able to do a lumbar puncture, and we drew out group B strep spinal bacteria in his spinal fluid, along with a diagnosis of group B strep meningitis. (Depo. 11-12). Robert Zimmerman, M.D., is a professor of radiology of the division of neurosurgery at Children's Hospital of Pennsylvania. He has been chief of pediatric neurology there since 1989. He is licensed to practice medicine in Pennsylvania, New Jersey, and Israel, and has been board- certified in diagnostic radiology and neuroradiology. In Dr. Zimmerman's opinion, after having read the two ultrasounds (December 1, 2006 and December 10, 2006) and the two MRIs (December 15, 2006 and August 1, 2007) performed on Jael, the first ultrasound was abnormal and clearly showed decreased oxygen (hypoxia) and decreased blood flow (ischemia), and the remaining studies showed advancing stages of brain injury (the brain turning to "swiss cheese") due to lack of oxygen and lack of blood flow. This was cystic encephalomalacia. He acknowledged that a hypoglycemic event could possibly have contributed to the situation, but he perceived no traumatic event and no mechanical injury. As to timing, Dr. Zimmerman indicated that the progression of the ischemia possibly started intrauterine, even before delivery, but the best he could place a point of injury was, "in and around the time that the kid was being delivered, the day of birth or a little earlier, or perhaps right after birth, but somewhere in that vicinity . . . . Sometime around the 28th." He believed that hypoxic ischemia caused the holes in Jael's brain, and that the condition first began to develop more than 1-6 days before the first ultrasound of December 1, 2006. He indicated that sepsis was probably the cause of the oxygen insufficiency and ruled out bacterial meningitis, but he ultimately conceded he would defer those decisions to a clinician, such as a pediatric neurologist. Dr. Zimmerman's opinion is diminished by his vascillations on placing the time of injury and his disclaimers, and by there being no indication he reviewed any medical information on Jael other than the four films. Mary K. Edwards-Brown M.D., is a neuro-radiologist with a subspecialty interest in pediatric neuroradiology. She is board-certified in radiology and in neuroradiology. She is also a full professor of radiology at Indiana University and practices at Riley Children's Hospital, Riley, Indiana. She also teaches medical professionals at many levels, including preparation for specialty boards. Dr. Edwards-Brown also reviewed the history and all four of Jael's films (December 1, 2006; December 10, 2006; December 15, 2006, and August 1, 2007). She, unlike Dr. Zimmerman, considered the first ultrasound to be normal. In the December 10, 2006, MRI, she found non-specific brain damage by tissue destruction. In the December 15, 2006, MRI, she, like Dr. Zimmerman, found massive brain damage and diffused cystic encephalomalacia, which she also considered non-specific. According to Dr. Edwards-Brown, the most common cause for this condition is that insufficient oxygen was getting to the brain, which can occur by not enough oxygen being present, by infection, or by trauma. Dr. Edwards-Brown ultimately opined that: . . . [Jael] was suffering from a profound meningitis, which caused the pattern of hypoxic-ischemic encephalitis -- encephalomalacia. And it was a mechanism of meningitis that induced hypoglycemia and brain injury that happened after this child was born. * * * Given that Jael was born with Apgars of 3 and 7, and a pH of 7.2, those are signs that -- most children who have those Apgars and that non-acidotic pH at birth generally do very well, and certainly don't have a pattern of injury as we've seen here. And given the fact that the ultrasound of December 1st looks normal to me it is my opinion that this injury occurred after the time of birth [November 28, 2006]. And most likely, the bulk of the injury occurred after December 1st, that first ultrasound that looks so very normal. Doctors Duchowny, Katz, and Edwards-Brown concurred, in varying terminology, that Jael's situation was a slow- evolving brain injury not consistent with a sentinel hypoxic insult occurring during resuscitation in the immediate postdelivery period. Dr. Zimmerman also could not point to any specific sentinel event. Elias Chalhub, M.D., testified by a deposition taken November 26, 2010. Dr. Chalhub is board-certified in pediatrics, psychiatry, and neurology, but he has not done research or published in over 20 years. Based on a records review, and without examining Jael, he testified that Jael's Group B strep sepsis occurred within an hour and a half of birth when the child was in the NICU in septic shock. He noted the records of Jael's pale, blue color (cyanosis) but also agreed that the baby had reasonably good Apgars and normal cord gas before transfer to the NICU. He stated Jael deteriorated rapidly after the good Apgars, which, in his opinion, is consistent with septic shock. However, Dr. Chalhub conceded that the baby was stable at five minutes after birth; that there was nothing in the nursing notes at 1:00 p.m., on December 28, 2006, that alerted to a problem; that there was no indication about an inability to get blood pressures before 1:20 p.m.; that thereafter, the baby became hypotensive, and that the first abnormal blood pressure reading was at 1:52 p.m., an hour and 36 minutes after birth. Dr. Chalhub opined that between birth at 12:16 p.m. and 2:00 p.m., on November 28, 2006, there was sepsis and decreased perfusion that resulted in Jael's injury. He was satisfied that the Group B-strep, which may have been acquired before labor or during birth, resulted in sepsis and that the brain injury occurred before the sepsis became meningitis, but conceded the meningitis, which came later, could have contributed to Jael's brain damage. He stated he did not believe that hypoglycemia, detected at 1:20 p.m., contributed to the brain damage. That said, Dr. Chalhub, in asserting compensability, also set the "immediate postdelivery period in a hospital" at an arbitrary "six hours from birth," without even relating the six hour period to acts of "resuscitation" or to the facts of this case. He claimed "six hours" would be what neonatologists would say constituted the "immediate post-resuscitative period," but he quoted no neonatal authority for the proposition. Clearly, his arbitrary concept is not the understanding of the greater medical community as evidenced by the other testifying physicians, nor is it the status of Florida law.13 Accordingly, I have discounted his opinion that the oxygen deprivation occurred during the statutory period. It might have been helpful to have heard testimony from a perfusionist or neonatologist, but herein radiologists' opinions have been compared with each other and neurologists' opinions have been compared with those of other neurologists. Dr. Chalhub's opinion is less persuasive than some other witnesses for the reasons related supra. The opinions of the physicians who actually examined Jael are more persuasive than those of physicians who only did a records review. Finally, the logic and reasoning of all experts have been compared and weighed and one common theme appears: whether characterized as "sepsis" or "meningitis," the Group B-strep resulted in a plethora of diagnoses, culminating in ultimate brain cell death. Within these parameters, and upon the credible evidence as a whole, it is found that more likely than not, Jael did not suffer brain injury due to oxygen deprivation that occurred during labor, delivery or resuscitation in the immediate postdelivery period in a hospital. Rather, it is more likely than not that Jael suffered brain damage after he was initially stabilized and after he was removed to the NICU due to his premature birth status. Based on the credible evidence as a whole, it appears that wherever and whenever Jael was intubated, he probably was not intubated until after the Apgars and after the immediate resuscitative period ended. Due to Jael's "good cry" immediately after delivery, the increasingly good Apgars, the good cord blood report, and the fact that there was no indication of oxygen deprivation to the brain at least until the first ultrasound of December 1, 2006, three days after delivery, the more compelling evidence supports a finding that Jael did not suffer from oxygen deprivation during labor or delivery and did not suffer injury to the brain during that period, either. As to his intubation in NICU, it is as likely that his airway was being protected by intubation as it is that he suffered any problem breathing or any oxygen deprivation before 2:00 p.m., on November 28, 2006, when he went into shock. Accordingly, the record fails to support a finding that there was an hypoxic or ischemic event during the statutory period (labor, delivery, or resuscitation in the immediate postdelivery period in a hospital). Alternatively, it is conceivable, but not proven, that Jael suffered oxygen deprivation at some unspecified point in time which occurred after 2:00 p.m., on December 28, 2006, and after he had arrived in NICU, which still is not within the statutory period. Since both the oxygen deprivation and the injury cannot be placed in the statutory period, Petitioners cannot prevail.
Findings Of Fact Addyson Tilka was born on June 22, 2012, at Bayfront Medical Center, Inc., located in St. Petersburg, Florida. Addyson weighed in excess of 2,500 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Addyson. In an affidavit dated August 3, 2016, Dr. Willis opined as follows: In summary, the baby was delivered prematurely at 34 weeks due to premature rupture of the membranes. Apgar scores were 5/8. The baby had respiratory distress syndrome of prematurity. Oxygen and ventilation support was required for respiratory distress. Neurologic exam was appropriate for gestational age. The baby did not have seizures. No head imaging studies were done during the newborn hospital course. There was no apparent obstetrical event that resulted in loss of oxygen deprivation or mechanical trauma to the baby’s brain during labor, delivery or the immediate post delivery period. NICA retained Laufey Y. Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to examine Addyson and to review her medical records. Dr. Sigurdardottir examined Addyson on January 20, 2016. In an affidavit dated August 5, 2016, Dr. Sigurdardottir summarized her examination of Addyson and opined as follows: NEUROLOGICAL EXAM: Mental status: Addyson is a beautiful, interactive girl who speaks in full sentences with minor pronunciation difficulties. She has no autistic features and seems age appropriate in all aspects. Cranial nerves are intact. Pupils are equal and reactive to light. Visual fields are full. There is nystagmus, no amblyopia, no strabismus. Her facial expressions are symmetric. There is no hearing abnormality noted. Her motor exam reveals normal muscle tone, motor strength, symmetric reflexes are present. Balance and coordination seems grossly intact for age. ASSESSMENT AND PLAN: In summary, here we have a 3 year 6 month old girl who was born premature at 34 weeks and needed a neonatal intensive care unit (NICU) stay due to respiratory compromise. There are, however, no clear concerns of her development at this time. No suggestions of physical impairment. There is nothing on history or record review that suggests neurologic injury to the brain or spinal cord acquired due to oxygen deprivation or mechanical injury. Results as to question 1: The patient is found to have no substantial physical or mental impairment. Results as to question 2: there is no evidence of perinatal neurologic depression and no evidence of ischemic injury at birth or in the immediate postnatal period. Results as to question 3: We would expect full life expectancy as no noted abnormalities are found on exam. In light of the above-mentioned details, I do not recommend Addyson to be included in the Neurologic Injury Compensation Association program and will be happy to answer additional questions. All of my opinions are within a reasonable degree of medical probability. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Willis that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby's brain during labor, delivery or the immediate post- delivery period. Dr. Willis’ opinion is credited. There are no expert opinions filed that are contrary to Dr. Sigurdardottir’s opinion that Addyson does not have a substantial physical or mental impairment. Dr. Sigurdardottir’s opinion is credited.
The Issue At issue is whether Katelyn Kutzer, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts related to compensability Daniel M. Kutzer and Michelle D. Kutzer, are the natural parents of Katelyn Kutzer, a minor. Katelyn was born a live infant on November 15, 2002, at St. Vincent's Medical Center, a licensed hospital located in Jacksonville, Florida, and her birth weight exceeded 2,500 grams. Obstetrical services were delivered at Katelyn's birth by Annette Laubscher, M.D., and Karen D. Tammela, M.D., then known as Karen D. Bonar, M.D., who, at all times material hereto, were "participating physician[s]" in the Florida Birth- Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Katelyn's birth and immediate newborn course At or about 5:00 a.m., November 15, 2002, Mrs. Kutzer, with an estimated delivery date of December 4, 2002, and with fraternal twins (described as Twin A and Twin B in the medical records) at 37 2/7 weeks' gestation, presented to St. Vincent's Medical Center in active labor. There, the membranes were noted as intact; vaginal examination revealed the cervix at 5-6 centimeters dilation, effacement at 90 percent, and the fetus at -1 station; and external monitoring was reassuring for fetal well-being, with a fetal heart rate (FHR) baseline for Twin A (Kassandra) in the 120-130 beat per minute (bpm) range, and a FHR baseline for Twin B (Katelyn) in the 130 bpm range. Mrs. Kutzer was admitted to the maternity suites at or about 5:41 a.m., she progressed to complete dilation by 10:41 a.m., and at or about 11:00 a.m., the external fetal monitor was disconnected and she was moved to an operating room (OR) for delivery. Notably, during the course of Mrs. Kutzer's admission, and until it was disconnected at 11:00 a.m., fetal monitoring was reassuring for fetal well-being. At 11:05 a.m., Mrs. Kutzer was noted in the OR, with Dr. Bonar at bedside. At the time, FHR baseline for Twin A was documented as 125-135 bpm, and for Twin B it was documented in the 140s. (Exhibit 3, Labor Flow Record Twins, p. 14). Thereafter, fetal monitor strips are available for Twin A, but not Twin B, for the 10-minute period preceding Twin A's delivery (at 11:15 a.m.), which reveal a reassuring FHR in the 140-150 bpm range. (Exhibit 3, fetal monitor strips, panel numbers 28735-28737; Exhibit 27, pp. 24-27). However, the medical records document a reassuring FHR baseline for Twin B at 11:16 a.m. (one minute after Twin A's delivery) as 115-125 bpm, and at 11:20 a.m., as in the 130s. (Exhibit 3, Labor Flow Record Twins, p. 16). Twin A (Kassandra) was born by spontaneous vaginal delivery at 11:15 a.m. The cord was clamped and cut, and cord blood was collected; however, cord gases were not ordered. Fetal heart tones (FHTs) at delivery were 115-150 bpm; and resuscitation following delivery included bulb suction, mechanical suction, and blow-by oxygen. Apgar scores were normal (8 and 9, at one and five minutes, respectively),1 initial newborn assessment revealed no abnormalities; and Kassandra was transported to the newborn nursery. (Exhibit 3, Maternity Suites Delivery Record Twins, pp. 1 and 2; Exhibit 26, pp. 16 and 17). Following Kassandra's delivery, the medical records document a reassuring FHR for Twin B (Katelyn) at 11:16 a.m. (one minute after Kassandra's delivery), as 115-125 bpm, and at 11:20 a.m., as in the 130s. (Exhibit 3, Labor Flow Record Twins, p. 16). Thereafter, but before 11:23 a.m., when a stat cesarean section was called for delivery, the amniotic membranes were ruptured to assist in delivery, at which time the umbilical cord prolapsed.2 Dr. Bonar described the events in her Operative/Procedure Report, as follows: . . . Twin B was noted to remain cephalic by ultrasound. Artificial rupture of membranes was performed with fundal pressure. Cord prolapse was noted with face presentation and mentum anterior position. Subsequent to artificial rupture of membranes, physician was unable to auscultate fetal heart tones using the external monitor or to visualize them using the ultrasound; therefore, stat cesarean section [was called for delivery at 11:23 a.m., surgery started at 11:30 a.m., and Katelyn was delivered at 11:33 a.m.]. (Exhibit 3, Operative/Procedure Report, p. 1, and Labor Flow Record Twins, pp. 17 and 19; Exhibit 27, p. 9). The cord was clamped and cut, and cord blood was collected; however, cord gases were not ordered. FHTs at delivery were 60-155 bpm, and following delivery the baby was bulb-suctioned, but no further resuscitative efforts were required. Apgar scores were noted as normal (7 and 9, at one and five minutes, respectively)3 which, like the Apgar score of her sibling (Kassandra), was consistent with an infant with good reserves, who has tolerated labor and delivery well; initial newborn assessment noted no abnormalities; and Katelyn was transported to the newborn nursery. (Exhibit 3, Maternity Suites Delivery Record Twins, pp. 2-4; Exhibit 26, pp. 16 and 17). Dr. Schwartz, described in the medical records as the neonatal attending ("Ped/Neo MD"), attended Katelyn's delivery, and assigned her Apgar scores. (Exhibit 3, Maternity Suites Delivery Record Twins, pp. 3 and 5). Dr. Schwartz's progress notes, documented at 11:45 a.m., described his involvement and observations, as follows: Asked by Dr. Bonar to attend this stat C/S for the 2nd of twins b/c of face presentation & fetal HR bradycardia . . . Twin "A" delivered w/o problems. At delivery infant cried after sxn [suctioning]. Taken to warmer & dried, stim[ulated], bulb/deep sxn. Pinked up quickly w/o BB02 [without blow by oxygen]. Apgars 7, 9. To NBN [newborn nursery] pink & vigorous. (Exhibit 4, Progress Record). Following admission to the newborn nursery, Raoul Sanchez, M.D., a pediatrician associated with The Carithers Pediatric Group,4 examined Katelyn. Dr. Sanchez's examination noted no abnormalities except an occasional right hip click, which bore followup to see if it was associated with a hip dislocation. Routine care was ordered. (Exhibit 4, Newborn Physical Examination; Exhibit 26, pp. 21-25). Further newborn evaluations were performed by Doctors Thomas Connolly, Wendy Sapolsky, and Julie Baker, also pediatricians associated with The Carithers Pediatric Group, on November 16, 17, and 18, 2002, respectively. Dr. Connolly's progress note documents a normal newborn examination, with positive breast feeding, with formula supplement; positive urine output; lungs clear to auscultation bilaterally; cardiovascular, regular rate and rhythm; and no hip clicks. Plan was supportive care, and anticipated discharge when mom was ready to go. Dr. Sapolsky's progress note also documents a normal newborn examination, but with mild jaundice; nursing well; and routine care. Finally, Dr. Baker's progress note documents a normal newborn examination; feeding well; lungs clear; heart, regular rate and rhythm; and plan to discharge Katelyn home with her mom. Nurses' progress notes for November 15, 2002, through Katelyn's discharge with her mom and Kassandra on November 18, 2002, at day 4 of life, reveal a normal newborn course, without evidence of distress.5 (Exhibit 4, Progress Record, Newborn Admission and Transitional Care Record, and Nurses Progress Notes; Exhibit 26, pp. 25-27). Katelyn's subsequent development As Katelyn matured, her parents began to notice that she was substantially behind her sister (Kassandra) in reaching developmental milestones, including rolling over, sitting up, crawling, walking, and language. Reportedly, Katelyn did not crawl until after her first birthday, and first walked independently at 19 months of age. Weakness of the right lower extremity was suspected during the first year of life, and confirmed when she began to stand. Katelyn has received physical, occupational, speech, and Applied Behavioral Analyses (ABA) therapy, and has been fitted with an AFO for her right lower extremity. Given Katelyn's developmental delay, Katelyn was referred to Michael Pollack, M.D., by her pediatrician (Dr. Connolly). Dr. Pollack is a pediatric neurologist associated with Shands Children's Hospital at the University of Florida, and he evaluated Katelyn on September 6, 2006. Dr. Pollack described his evaluation, impression, and plan, as follows: SUBJECTIVE: Katelyne is an almost 4-year- old fraternal twin referred because of developmental delay. History is obtained from the patient's parents. Conception was via in vitro fertilization. The patient was twin B and was delivered by emergency cesarean section at term. Her co- twin was delivered vaginally. Katelyne remained in hospital for five days. Mother indicates that there were difficulties with temperature control, but the patient did not require intubation. There was no intracranial hemorrhage. Weakness of the right lower extremity was suspected during the first year of life. The patient did not crawl until after her first birthday and she first walked independently at 19 months of age. She currently wears an AFO over the right lower extremity and also uses a smaller foot orthosis on the left. She receives physical, occupational and speech therapy. Her language development has been delayed. She currently produces phrases of one to three words. Pronoun confusion has been noted. The patient rarely uses pronouns spontaneously. Echolalia[6], both immediate and delayed, are also reported. Eye contact has been minimal, but there has been recent improvement. Parents use a variety of techniques for behavioral management. These include time out and various positive reinforcement techniques. For example, they use M&Ms for short term rewards and have a variety of toys which the patient uses only at dinner in order to encourage her to participate in meals. She has longstanding difficulties settling at night and usually awakens at least once during the night. She has frequent temper outbursts and it is difficult for parents to take the patient to public places such as malls or restaurants. By coincidence, I stayed at the same hotel as the family on the night prior to the visit and was personally able to verify the patient's behavioral difficulties in the hotel breakfast room. * * * FAMILY HISTORY: Speech delay is present in the patient's twin sister, who is otherwise in good health.[7] The patient's 20-year-old half brother and 18-year-old half sister are in good health. PHYSICAL EXAMINATION: . . . The patient is a well-nourished, normally proportioned [almost 4]-year-old girl. There are no dysmorphic facial features. Examination of the eyes, nose and oropharynx is unremarkable. Neck is supple. Chest is clear. No significant cardiac murmurs are present. There is no hepatosplenomegaly [enlargement of the liver and spleen].[8] Spine is straight. The patient wears a right AFO and a small left foot orthosis as noted above. Neurological examination: The patient is active and distractible and shows little behavioral inhibition. At times she lies on the floor. However, her behavior is easily redirected during the office visit and she is generally cooperative. She does establish eye contact with the examiner, although it is often fleeting. She follows a variety of commands including commands which employ a variety of prepositions. She does demonstrate first and second person pronoun confusion. She identifies a variety of body parts, but does not identify a number of body parts which she would be expected to have mastered at 3 years 10 months of age. Her verbal productions are generally limited to two or three words. Her responses are often tangential []or unrelated to the examiner's questions and reflect limited language comprehension. Echolalia is not noted during the office visit. Pupils are equal and reactive to light. Ocular fundi are not adequately visualized. There is no disturbance of ocular motility. No facial weakness or significant asymmetry are present. Tongue protrudes in the midline. Her gait is characterized by circumduction of the right foot. She manipulates objects with either hand. Tendon reflexes are normally and symmetrically active. The right plantar response is extensor and the left is variable. IMPRESSION: Katelyne appears to have a nonprogressive encephalopathy. Her condition is probably of prenatal origin. There is an increased incidence of cerebrovascular disease in twin gestation. She has a monoparesis[9] of the right lower extremity. Her language development has been delayed and there are also difficulties with socialization and behavior. She does have a number of features which fall within the autistic spectrum. PLAN: An MRI of the head will be obtained under sedation/anesthesia at the discretion of the anesthesiologist. The patient was also referred to the clinic of Dr. Krestin Ridonovich for further evaluation of her language and socialization difficulties. A trial of low does Ritalin, which will be used on an occasional basis, will be carried out. Daily psychostimulant medication does not appear warranted at this time. The patient should receive special educational services through the public school system and it is likely that physical, occupational and a speech/language therapy will be available to her through the public school system, once placement has been completed. She will return to this clinic in two to three months. (Exhibit 18). Katelyn's MRI of the brain was done September 28, 2006, and was reported as negative (without evidence of brain injury). Findings were noted, as follows: There is, in general, normal brain density, normal gray and white matter differentiation, and normal brain formation. Ventricular size, and cisternal/sulcal patterns are appropriate for chronological age. There is no evidence of mass lesion, hydrocephalus, intra or extra axial fluid collection. There is opacification of the maxillary sinuses probably. Correlation should be made clinically for sinusitis. The diffusion imaging including both DWI and ADC mapping demonstrates no evidence of water restriction to suggest an acute ischemic event. (Exhibit 19). Katelyn saw Dr. Pollack on November 29, 2006, for follow-up. Dr. Pollack reported the results of that visit, as follows: Katelyne is a 4-year-old fraternal twin who was initially seen here 09/2006 because of developmental delay. Her history is reviewed in the previous report. . . . Mother indicates that my impression that the patient had autistic features was supported by recent psychological testing. Interestingly, the patient's MR scan of the head was normal. This suggests that the lesion responsible for the patient's right lower extremity monoparesis is small. In addition, a normal scan makes it unlikely that an ischemic event is responsible for the patient's atypical language and social development . . . . A prescription for low-dose Ritalin therapy to be used on an occasional basis was provided when the patient was seen here two months ago, but the medication has not yet been used. * * * Results of the MR scan were reviewed during today's visit. In view of the normal scan, it appears unlikely that the patient's autistic spectrum disorder has an ischemic etiology even though she is a twin and there is an increased incidence of cerebral ischemia in twin gestations. Studies for Rett syndrome will be initiated. The patient will also be referred to Genetics Clinic . . . . She will return to clinic in six months. (Exhibit 18). Katelyn was last seen by Dr. Pollack on April 11, 2007. The results of that visit were reported, as follows: Katelyne is a 4-year-old fraternal twin with an autistic spectrum disorder. Her history is viewed in the note of 11/29/2006 . . . . Psychological testing has supported my initial impression that autistic features were present in this patient. * * * The patient has been seen in Genetics Clinic. Mother indicates that Genetics' studies for Rett syndrome were negative and additional studies have been ordered. A trial of low-dose Ritalin was carried out a few months ago. Mother felt that 2.5 mg produced little apparent change while 5 mg was poorly tolerated when it was used in class. The patient does have frequent angry outbursts. Some of these are triggered by her inability to delay gratification. She is less likely to have spells when she is the center of attention. Mother also believes that some episodes are precipitated by anxiety. On examination today, Katelyne is noted to be well nourished and normally proportioned . . . . The patient is emotionally labile[10] during a portion of the office visit. She has a minor temper tantrum in which she lies down on the floor and thrashes when she does not immediately receive her request from mother. However, when the examiner's attention is directed to Katelyne, she is pleasant and cooperative and readily establishes eye contact. Her responses to questions are tangential and at times unrelated. Many of her responses are telegraphic. She is not able to engage in a free-flowing conversation. She correctly identifies colors, and she enumerates fingers. She follows multi-step commands. Cranial nerve examination is, again, normal. Functional testing suggests normal strength. Tendon reflexes are symmetrically 2+, and plantar responses are flexor. In summary, Katelyne appears to have a developmental language disorder which she shares with her fraternal twin who is less severely affected. Katelyne's socialization is also atypical, and she does appear to fall in the autistic spectrum. She has behavioral difficulties as described above. Mother is adept at managing the patient's behavior at home but explosive episodes do occur in the classroom. The patient is currently in a school program for the physically impaired, but it is likely that she will be transferred into an autistic program in the near future. Improvement in the patient's classroom behavior would facilitate optimal school placement. PLAN: I urged the mother to carry out a trial of Ritalin at a lower dose, 2.5 mg, in the classroom two or three days. It is noted that the previous trial of Ritalin, in the classroom, was with the 5 mg dose. If Ritalin is ineffective, a trial of low-dose BuSpar, 5 mg, will be carried out . . . . (Exhibit 18). Following the filing of the claim in the instant case on April 27, 2007, Katelyn was, at NICA'S request, evaluated by Paul Carney, M.D. Dr. Carney, like Dr. Pollack, is a pediatric neurologist associated with Shands Children's Hospital at the University of Florida, and he evaluated Katelyn, on June 28, 2007. Dr. Carney's description of Katelyn's medical history was similar to that of Dr. Pollack, and no useful purpose would be served to duplicate it here. The results of Dr. Carney's evaluation were described as follows: Today records were reviewed including all orthopedics records completed at Nemours, birth records from St. Vincent's Medical Center, previous therapist records and primary care records. On exam today, Katelyne weighed 20.4 kg, height is 108.0 cm, . . . head circumference 56.8 cm. Neurologically, Katelyne was awake and alert. She had increased activity and was hyperactive throughout the room and did require frequent redirection. She did have a lot of repetitive or echolalia speech but she would eventually engage the examiner and had to be redirected multiple times. Her pupils were equal, round and reactive to light with accommodation. Extraocular movements were intact. Her face was symmetric[,] tongue was midline and palate rose symmetrically. On motor exam, upper extremity strength was 5/5 throughout with good tone and bulk. Lower extremity exam revealed weakness of the right lower extremity 4/5. He gait was abnormal. She had a circumducted gait on the right. With her AFO off her ankle with [sic] pronate and upon running she actually could not run and would require assistance. She had increased tone of her right lower extremity and was hyper-reflexic right greater than left bilateral lower extremity. Cognitively, she was noted to have developmental delay for a child of her age, required frequent redirection of behavior Assessment specifically [as] it . . . relates to NICA. Answering the three questions required, we feel that she does suffer from a permanent and substantial mental impairment. She does have the disability that is quite obvious and likely to be lifelong and unlikely to resolve. She does have global developmental delay. The etiology of her disabilities is not clear as she does not have overt evidence of perinatal hypoxia ischemia or mechanical injury at the time of delivery. We would like to request the following studies specifically, cord gas results and blood glucose results done from the cord gas at the time of delivery that were not available for our review. Once this information is provided, we can complete our recommendations or would certainly be available via phone call to discuss her case further. Nonetheless, she will have global developmental delay, likely will not resolve and will require therapies for speech, language, physical and occupational therapies with a goal of trying to reach her maximum potential. If you have any questions or concerns, please give my office a call. (Exhibit 18). As heretofore noted, cord gases were not ordered. Consequently, the results were not available for Dr. Carney to review and, insofar as the record reveals, he expressed no further opinions and made no further recommendations. Of further note, neither Dr. Pollack nor Dr. Carney was called to testify, or offer further explanation for their conclusions. 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."11 § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. Here, it is undisputed that Katelyn is permanently and substantially mentally impaired. What must be resolved is whether the record supports the conclusion that, more likely than not, Katelyn is also permanently and substantially physically impaired and, if so, whether her impairments resulted from a brain injury caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in the hospital, as required for coverage under the Plan. As to these issues, Petitioners were of the view that Katelyn was also permanently and substantially physically impaired, and that her impairments were the result of a brain injury caused by oxygen deprivation she suffered at St. Vincent's Medical Center, likely secondary to a prolapsed cord, that occurred following rupture of the membranes between 11:20 a.m. (when a reassuring FHR was noted) and 11:23 a.m. (when the stat cesarean section was called), and 11:30 a.m., (when Katelyn was delivered). (Petitioners' Proposed Final Order, p. 7). In contrast, NICA was of the view that Katelyn was not permanently and substantially physically impaired, and that what impairments she may suffer are most likely developmentally based, as opposed to birth-related. The hospital adopted Petitioners' argument, and the physicians took no position on the issues. (Transcript, pp. 67 and 68). The likely etiology of Katelyn's neurologic impairments, and the significance of her physical impairment To address the etiology of Katelyn's neurologic impairments, the parties offered the testimony of three expert witnesses to support their respective positions. Offered by Petitioners was the testimony of Richard Boehme, M.D., and offered by Respondent was the testimony of Donald Willis, M.D., and Michael Duchowny, M.D. Doctors Boehme and Duchowny also spoke to the significance of Katelyn's physical impairment. Dr. Willis is a physician board-certified in obstetrics and gynecology, and maternal-fetal medicine. Based on his review of the medical records, Dr. Willis was of the opinion the records failed to support a conclusion that Katelyn suffered a brain injury caused by oxygen deprivation during labor, delivery, or immediately thereafter. Dr. Willis expressed the basis for his opinion, as follows: [DIRECT EXAMINATION] Q From that review, were you able to form an opinion as to whether or not Katelyn Kutzer suffered a birth-related neurological -- A Yes, it is my medical opinion from the review that this child did not suffer brain damage due to oxygen deprivation or mechanical injury during labor, delivery, or the immediate post-delivery period. * * * Q Can you please explain for us the foundation for your opinion in that regard, with respect to the records you reviewed? A Yes. . . . During labor, the fetal heart rate monitor strip really did not show any fetal distress. The first baby was born by vaginal birth and had normal Apgars of eight and nine. The B baby was born next and had a prolapse of the umbilical cord. Q Dr. Willis, let me interrupt you there for a just a second. When you refer to the B baby, are you referring to the petitioner in this case, Katelyn Kutzer? A Yes. Q Okay. A So when Katelyn was delivered, they did a rupture of the amniotic membranes to assist in her delivery. At that time, the umbilical cord prolapsed. They did an ultrasound and they tried to auscultate the fetal heart tones and could not detect heart tones with either of those methods and therefore they did an emergency cesarean section delivery. Amniotic fluid was clear when the membranes were ruptured. Birth weight was 2975 grams. The baby was not depressed at birth. Apgar scores were seven and nine. The baby required no resuscitation after birth. It went to the newborn nursery and the statement by the pediatric or neonatal staff said the baby went to the newborn nursery pink and vigorous. The baby had a normal newborn course and was discharged home with the mother on the third day of life. Now, if a baby suffers oxygen deprivation or mechanical injury to the brain significant enough to cause brain damage, those babies are usually depressed at birth and they usually have some type of multisystem failure after birth, which would include things such as respiratory distress, feeding difficulties, seizures within the first 72 hours of birth, abnormal neurologic findings on physical exam, those types of things. And for this child, I did not see anything that would suggest oxygen deprivation that had caused any brain injury. * * * Q Okay. You mentioned and the medical records indicate that there was a prolapsed cord during Katelyn's delivery. A Correct. * * * Q In your opinion, does the fact that there was a prolapse cord mean that Katelyn suffered oxygen deprivation that would have been significant enough to cause brain injury? A No. I think in this case, although the umbilical cord did prolapse, I do not think that it caused any oxygen deprivation to the child. Q. Would Katelyn's Apgar scores indicate how she tolerated or responded to the prolapse score [sic]? A. Yes. To some degree, yes. And the Apgar scores were good. Q And they were -- I think you indicated? A Seven and nine, I believe. Q And those are normal? A Those are normal. Low Apgar score's considered to be a score less than seven. * * * Q Okay. You mentioned earlier on describing or summarizing the -- of labor and delivery here, that at some point the physician or staff personnel was not able to obtain a fetal heart rate. What is the significance of that in the context of this case in your opinion? A I don't think it has any real significance, because the failure to either hear, auscultate, or to see fetal heart with ultrasound prior to birth can't be a true finding because, you know, if a baby had no heartbeat inside the uterus, then certainly they could not be born five or ten minutes later, however long it took to deliver the baby, and have heartbeat and normal Apgar scores without resuscitation. Q So it is your opinion that that -- notation that they were unable to -- fetal heartbeat or get a visual on a heartbeat is inconsistent with the actual clinical newborn -- that is described here? A That's right. And it's probably just a technical problem. It's probably not that there was not a heartbeat, it's probably simply that they just didn't see it or couldn't hear it because of the position of the baby or some technical problem, not because it wasn't there. * * * [CROSS-EXAMINATION] Q So going back to my original question, I guess, as far as Katelyn, B baby is concerned, the last monitor strip that we're sure we have ends at about 11:00 a.m.? A Correct. Q Which means that for approximately 33 minutes, we have no record [monitor strip] how Katelyn was doing, at least as it was represented on a fetal heart monitor? A Correct. Q Okay. So back to my question where I said that your sentence[12] where it says, fetal heart rate tracing during labor did not suggest fetal distress, I am suggesting was a more accurate statement that the fetal heart rate tracing during up to 11:00 a.m., did not suggest fetal distress; is that a fair statement? A I don't think it's a distinguishing feature that's necessary, because if a baby were to sustain oxygen deprivation severe enough to cause brain oxygen during the 30 minutes prior to birth, that baby would be born depressed and would have some abnormalities, would require resuscitation. So although I don't see the fetal heart rate monitor strip during that time, the outcome, the baby's condition at time of birth is not consistent with a hypoxic event during that period. * * * Q Okay. Now, tell me a little bit about a prolapsed cord. What is the effect of a prolapsed cord that is not immediately recognized -- A Well, when the umbilical prolapses, goes through the cervix and into the vagina, then it may cause no disruption in blood flow at all or it may result in varying degrees of disruption in the blood flow from the placenta to the baby. And of course the placenta is where the baby gets its oxygen exchanged. Q Is it fair to say that the prolapsed cord is an emergency situation that needs to be addressed immediately? A Yes. Q And the reason for that is because if the cord is compressed for too long, you will have oxygen deprivation and distress to the baby and/or -- A Yes, umbilical cord prolapse can cause oxygen deprivation if the umbilical cord is compressed. And two, I mean, once the umbilical cord prolapses, it's unlikely that you're going to have a vaginal birth at that point. Q Okay. And that's the reason why a cesarean section was called for in this case? A Correct. * * * Q Do you believe you have seen babies that have had fetal rates down in the 60 range for any period of time have not had some subsequent injury? * * * A Yes, yes. And in fact, I mean in this baby, if you look, I mean, there was this range of heart rate that was irregular and there were some low heartbeats probably prior to birth, but if you look at the one- minute Apgar score, which is just towards the bottom of that page, the baby had got two points for Apgar with one minute. So without resuscitation, the baby had a heart rate above 100 beats a minute at one minute of life, and that would just not be compatible with a baby that got oxygen deprivation a short period of time before, enough to result in brain injury. (Exhibit 27, pages 8-14, 26, 27, 30 and 31). Dr. Duchowny is a pediatric neurologist associated with Miami Children's Hospital, where he is a senior staff attending physician in neurology, as well as the director of the neurology training programs and the epilepsy programs, and holds an appointment as a clinical professor in neurology and pediatrics at the University of Miami Miller School of Medicine. Based on his review of the medical records, Dr. Duchowny was of the opinion that Katelyn's neurologic impairments were likely developmentally based, as opposed to birth-related, and that she was not permanently and substantially physically impaired. Dr. Duchowny expressed the basis for his opinions, as follows: Q . . . So you are saying, so I am understanding you completely clearly here, that in your opinion, she does not meet the NICA criteria for a severe and permanent injury in a NICA case condition? A Well, I should say I do not believe that she has a substantial physical impairment. The records indicate that she does have a substantial mental impairment, but I do not believe that Katelyn's mental impairment was acquired in the course of labor and delivery. * * * Q Okay. You do recognize, I guess, that Katelyn, and as you mentioned, she is developmentally delayed. You state[13] that from your review of the records, or at least the records documented that she was developmentally delayed, that she had limited social interaction, poor eye contact and preservative behaviors. She has [mild] hypertonia in the right lower limb. * * * Q Are you saying, Doctor, that none of that, in your opinion, constitutes a serious and permanent injury? A As I indicated previously, I don't believe there is any injury to the brain. I believe these are developmentally-based problems and are related to brain maturation, but are not a consequence of brain damage. Q Okay. Are you saying that problems that develop, and let's just say hypothetically during the first trimester, that result in a developmentally delayed child are not considered definitionally as brain injuries? A Yes. * * * Q Okay. How do you define that then, if it's not a brain injury or brain damage, what is it that causes a person, again, hypothetically, like this, to be profoundly disabled if something happens to them during the first trimester? A This is a developmentally-based brain disorder and the cause of most of these disorders is unknown. Q Okay. Are you saying that the brain in these people is normal? A No, I'm not. I'm saying that there is no brain injury. Q Okay. Even though that damage might be caused by some insult that occurred during the first trimester, for example, that is, again by definition, not considered to be a brain injury or brain damage? A No. Let's be clear. If there is an injury that occurred in the first trimester that resulted in structural brain damage, I would agree that individual has brain damage or a brain injury, but if there is no evidence of structural brain damage, I would disagree that the patient has brain damage or brain injury. I would regard the neurological problems as being developmentally based. Q Define that for me then, if you will. what is the definition of a developmentally- based injury? A It is a prenatal intrauterine acquired abnormality of brain maturation resulting in neurological problems. * * * Q Okay. You mention in your letter[14] that she would ultimately fit within the autism spectrum. Explain what you mean by that. A Autism is a developmental disability that arises from unknown intrauterine acquired factors and is primarily a disorder of social development, although there are a number of co-morbid features, and children with autism fall within a spectrum of severity between those that are severely impaired and those that function relatively well except for the social disability. Q Do patients that fall within the autism spectrum have orthopedic components to their problems? A It's not the part of autism, no. Q Being more specific again, you mention hypertonia in the right lower limb. Is that something specifically that falls within the autism spectrum? A No. Q What about the developmental delay itself, is that something that falls within autism? A Yes, very often. * * * Q So you are reaching a conclusion here that whatever we call the injuries, developmental delays, problems that Katelyn is experiencing, you are also of the opinion that none of those were caused during any event during birth? A That's correct. I do not believe that Katelyn's neurological disability is a result of factors that arose in the course of labor or delivery. Q And what is the basis of that opinion, specifically that it was not caused during the birthing process? A It's based on several factors: Firstly, a review of the records indicates that there were no features during labor and delivery, per se, which would be contributing. Number two, that the immediate postnatal course was inconsistent with either hypoxic ischemic brain damage or mechanical injury. Number three, that Katelyn's present neurological circumstances are inconsistent with perinatally acquired damage. And, fourthly, that the MRI scan of the brain confirms that there is no structural brain damage. * * * Q Okay. Now, you said, in the beginning you said there were no features about this birth that are contributing, contributing features to either a hypoxic or mechanical injury, I think that was your point number one? A Yes. Q Are you saying then that the documented fetal distress is not a feature that could be contributing to an injury in this case? A Yes. * * * Q Okay. Another factor in this case was a prolapsed cord. You are aware of that, I assume? A Yes. Q Okay, and a prolapsed cord can compromise blood supply to the body and brain of the child? A Hypothetically, yes. Q Are you saying that it is definitive in this case that the prolapsed cord did not do that? A Well, my prior statement was that I didn't see any evidence, and that includes the prolapsed cord, that Katelyn's neurological disability was acquired as a result of hypoxia, ischemia or mechanical injury in the course of labor and delivery. Q There was a time of at least 15 minutes and maybe longer than that when there was an inability to obtain or to record a heart rate from this child. Are you aware of that? A Yes. Q So there is no way to judge during that period of time where the child's heart rate was? A That's correct. Q And it is documented that once the ability to record or to monitor the heart rate of the child was restored, once that was restored, that heart rate was measured at the low end at about 60 beats. Are you aware of that? A Yes. Q Okay, and do you recognize that in a newborn child that a heart rate of 60 beats is well below normal and well into the range that would be considered dangerous? A Yes. Q But are you continuing to say that even knowing that, there is no likelihood in this case that that heart rate could have resulted in damage to this child? A Yes. Q And why is that? A There is no evidence of any brain damage in this child and none of the information in the records or the factors that I have enumerated suggest that it occurred. Q Okay. Now, you mentioned the immediate postnatal period was inconsistent. Are you referring there to the Apgar scores? A I'm referring to the fact that the Apgar scores were good, there was no need for intubation or mechanical intubation, the doctor saw no need to draw arterial blood gases and there is no evidence of multi- organ involvement caused by hypoxia or ischemia. In other words, there are no problems with the heart, the lungs, the liver or the kidneys. (Exhibit 28, pp. 9, 11-14, 16-21). Dr. Boehme is a neurologist practicing in Jacksonville Beach, Florida. Primarily, Dr. Boehme treats adults, although he occasionally treats pediatric patients. However, the ages of his pediatric patients, their numbers, or the nature of the care he provides is not of record.15 Based on his review of the medical records, Dr. Boehme was of the opinion that Katelyn was permanently and substantially mentally and physically impaired, "due to perinatal hypoxia at the time of delivery." (Exhibit 29, p. 18 and 19). Dr. Boehme expressed the basis for his opinions, as follows: Q What in your opinion was the event that occurred during delivery that caused that perinatal hypoxia? A It was the -- the time where she went into respiratory distress until the time that she was delivered via C-section. Q And it is your opinion based upon your review of the Shands medical records and the Nemours Children's records that Katelyn was in respiratory distress at some point in time prior to the time she was delivered? A That's why they did the cesarean section. Q What specifically occurred during the labor and delivery that in your opinion resulted in that respiratory distress? A Like what happened? Q Well, do you understand from your review of the medical records -- * * * A I think that she suffered an hypoxic event that led her to have -- the decision being made for a cesarean section. I'm not here to comment on standard-of-care issues by the physicians or the nursing staff. I think that the -- there was a prolapsed cord there for about 15 minutes. And the fact that even though a blood sample was obtained, that it was never evaluated -- at least to my knowledge, there's no record of it -- and prolapsed cords can certainly lead to hypoxic events. And we don't have any rhythm strips for the baby for approximately 30 minutes. So we have no way of knowing for sure what happened. But, obviously, the -- the decision was made to deliver via C-section, so -- emergently. So even though the Apgars are 7 and 9 -- and I've seen that before. You can have brain damage from hypoxic events with Apgars of 7 and 9. Q Okay. A So that's the basis of my opinion. Q Is it your opinion that the prolapsed cord that you talked about a moment ago resulted in the oxygen deprivation that was significant enough to cause a hypoxic ischemic injury to Katelyn's brain? A More likely than not. Q Okay. Is it your testimony that every time there's a prolapsed cord during delivery it results in oxygen deprivation significant enough to cause a hypoxic ischemic brain injury? A No. Q So you recognize and appreciate that a prolapsed cord in itself does not mean that there was going to be or is going to be oxygen deprivation significant enough to cause a brain injury? A There's no 100 percent certainty of prolapsed cord leading to hypoxic injuries, that is correct. Q A prolapsed cord may reduce blood flow to the baby but not necessarily cause a brain injury? A That is correct. It may not be enough. Q But in your opinion, in this case, you believe that the prolapsed cord caused an oxygen deprivation that was significant enough to cause an injury to Katelyn's brain? A That is correct. Q An hypoxic ischemic injury? A Yes, by definition. Q Do you agree that the best evidence of whether there was oxygen deprivation at the time of delivery that was significant enough to cause brain injury is the baby's clinical course during the immediate post-natal period? A No. It's the blood gases from the umbilical blood would be the best evidence. Q Or in a case -- in a case such as this case where we don't have cord blood gas results -- A Oh, then -- Q -- would you agree that the clinical course of the baby in the immediate post- delivery period would be that the best evidence as to whether or not that baby suffered an insult to the brain from oxygen deprivation that was significant enough to actually cause a brain injury? A That would be the best evidence initially, that is correct. (Exhibit 29, pp. 19-22). Notably, Dr. Boehme did not identify any sign, symptom, test result, or event during Katelyn's immediate newborn course that would support his opinion that Katelyn suffered a brain injury caused by oxygen deprivation, secondary to a prolapsed umbilical cord, during the course of labor and delivery. It is also notable that Dr. Boehme is not board-certified in any specialty, was not shown to have any special training or experience in pediatrics or pediatric neurology, and although he occasionally treats pediatric patients, was not shown to care for newborns. The medical records, as well as the testimony of the physicians and other witnesses, have been thoroughly reviewed. Having done so, it must be resolved that the record in this case compels the conclusion that, more likely than not, Katelyn is not substantially physically impaired, and that the cause of her neurologic impairments is most likely a developmental-based brain disorder, as opposed to a birth-related brain injury. In so concluding, Dr. Duchowny was shown to be the more qualified to address the significance of Katelyn's physical impairment, not Dr. Boehme, and Doctors Duchowny and Willis the more qualified to address the issue of etiology. Moreover, their testimony was candid, logical, and consistent with the record, whereas Dr. Boehme's was not. Indeed, Dr. Boehme's opinion appears grounded on little more than speculation, and not science.
The Issue Whether Kevin A. Hackerman, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Petitioners, Susan Hackerman and Steven Hackerman, are the parents and natural guardians of Kevin A. Hackerman, a minor. Kevin was born a live infant on September 25, 2000, at Halifax Hospital Medical Center, a hospital located in Daytona Beach, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Kevin's birth was Pamela Carbiener, 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.1 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." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. Here, indisputably, Kevin is permanently and substantially mentally and physically impaired. What remains to resolve is whether the proof supports the conclusion that, more likely than not, Kevin's neurologic impairment resulted from an "injury to the brain . . . caused by oxygen deprivation or mechanical injury, occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period," as required for coverage under the Plan. The cause and timing of Kevin's neurological impairment To address the cause and timing of Kevin's neurological impairment, Petitioners offered selected medical records related to Kevin's birth and subsequent development (Petitioners' Exhibit 1); the deposition of Michael Duchowny, M.D., a physician board-certified in pediatrics, neurology with special competence in child neurology, and clinical neurophysiology (Petitioners' Exhibit 2); the results of Dr. Duchowny's neurologic examination of Kevin, as well as Dr. Duchowny's conclusions following review of the medical records (Petitioners' Exhibits 3-5); the deposition of Rubin Lopez, M.D., a physician board-certified in pediatrics, who attended Kevin on September 26, 2000, at Halifax Hospital (Petitioners' Exhibit 6); the deposition of Pamela Carbiener, M.D., the delivering obstetrician (Petitioners' Exhibit 7); the deposition of Robert Hartmann, M.D., a physician board-certified in pediatrics, who practices pediatrics and neonatology, and who attended Kevin at Halifax Hospital (Petitioners' Exhibit 8); the deposition of Susan Newell, R.N., the nurse who attended Kevin following delivery (Petitioners' Exhibit 9); the deposition of Donald Willis, M.D., an obstetrician who reviewed the medical records (Petitioners' Exhibit 10); and the lay testimony of Susan Hackerman, Kevin's mother, and Beverley Giardina, Kevin's maternal grandmother. As for the event, and its timing, which caused Kevin's neurologic impairment, it was Dr. Duchowny's opinion, based on the results of his neurologic evaluation of Kevin on November 27, 2002, and review of the medical records, that, while of unknown etiology, Kevin's neurologic impairment was prenatal (developmental) in origin, having occurred prior to the onset of labor, and not associated with oxygen deprivation or mechanical injury, during labor, delivery, or resuscitation. Dr. Duchowny described the bases for his opinion, as follows: Q. . . . Could you tell me why [in your opinion Kevin does not qualify under the NICA statute]? A. I believe that Kevin's neurologic impairment was unlikely to be acquired in the course of labor, delivery or the immediate resuscitation period. He was born at 40 weeks gestation, but was small for his gestational age in that his birth weight was only five pounds-seven ounces. His head circumference was small at birth. It was 32 centimeters, indicating an inadequate development of the brain prior to birth and, additionally, he had Apgar scores which were three and eight, and the eight Apgar score at five minutes suggested he was doing reasonably well at the time of delivery. In fact, he was doing well enough that the doctors didn't need to intubate him and provide ventilatory support, elected not to draw blood gases and, in fact, felt that he was reasonably stable just after delivery. Kevin did experience some respiratory problems subsequently in that he developed left lower lobe pneumonia and a left tension pneumothorax but, in my opinion, these problems were treated adequately and he was not significantly hypoxic nor was there any evidence of damage to the brain as a consequence of these postnatal events. Furthermore, Kevin's MRI scan which was performed in May of 2001 demonstrated the possibility of a small degree of periventicular leukomalacia [PVL] but was otherwise within normal limits. In my opinion, this MRI finding is inconsistent with the severe nature of Kevin's neurologic impairment. Q. When you say that that MRI was . . . inconsistent, what do you mean by that, doctor? A. What I mean is that given Kevin's severe degree of impairment, had the cause been perinatal hypoxia, I would have expected to see many more abnormalities and more widespread involvement on the MRI scan, abnormalities such as diffuse brain atrophy, enlargement of the ventricles, possibly areas of abnormal signal. None of those were present. * * * Q. There is some notation in the records throughout this case of meconium staining. Can you please indicate whether nor not the meconium staining that is noted has any significance with regard to your medical opinion. A. Yes . . . . Meconium staining represents distress in utero and requires approximately 72 hours for this finding to take place. This finding, therefore, again, predates Kevin's neurological problems prior to the onset of labor and delivery. The opinions of Daniel Shanks, M.D., Kevin's consulting pediatric neurologist following discharge from Halifax Hospital, were consistent with those expressed by Dr. Duchowny. Pertinent to this case, Dr. Shanks evaluated Kevin on March 30, 2001, at 6 months of age, and concluded: IMPRESSION: Developmental delays likely global but worse in regard to his motor skills as compared to social skills. Language skills may be significantly delayed as well. He has microcephaly and has had this since birth. This suggests more likely a prenatal situation which could either be related to malformation, injury, chromosomal or metabolic abnormality, or alternate syndromic-type diagnosis. Often, no specific etiology can be established with certainty. My bias would be to pursue initial evaluations to include brain MRI Scan, high- resolution karyotype and lactate, and baseline ophthalmologic evaluation. It would seem reasonable also to undergo a baseline genetics evaluation to help guide additional need for metabolic work up or for review of any abnormalities on karyotype. Additional work up can be guided by the above. (Petitioners' Exhibit 1.) Following testing, Kevin was again evaluated by Dr. Shanks on June 15, 2001. Dr. Shanks reported the results of that testing and his evaluation as follows: . . . Kevin is seen today in the Pediatric Neurology Clinic for follow-up of evaluation for static encephalopathy and quadriplegic cerebral palsy. He underwent neuroimaging with brain MRI last month that demonstrated findings suspicious for PVL, however, somewhat difficult to well assess due to his age. He had chromosomes high resolution that were negative and a normal lactate. No specific etiology is apparent for his encephalopathy and he continues to evidence significant motor delays. Language delays are a little bit more difficult to assess. He is very visually alert and socially attentive. He has poor head control and low truncal tone and low base tone when relaxed. He has very limited mobility . . . . (Petitioners' Exhibit 1.) Following evaluation, Dr. Shanks, reported his impression, as follows: . . . Static encephalopathy likely from a prenatal process. No specific etiology has been established to this point. If he has a dysmyelinating or PVL type evolution, this would suggest a process that adversely affected CNS during third trimester. There is no evidence of tissue loss or an injury. As for Dr. Willis, the obstetrician who reviewed the medical records, it was his opinion that the birth records failed to support a conclusion that Kevin suffered a brain injury from oxygen deprivation or other trauma associated with his birth or resuscitation. Dr. Carbiener, the attending obstetrician, was also of the opinion that it was unlikely Kevin suffered an injury during labor and delivery, but declined to address the period following delivery, since she was attending the mother, not the child, at the time. Dr. Lopez, the pediatrician who examined Kevin at approximately 4 hours of age (12:38 a.m., July 26, 2000), offered no opinion regarding the etiology of Kevin's developmental delays, or whether he suffered oxygen deprivation or mechanical injury during labor and delivery.2 Dr. Hartmann, the attending neonataologist at Halifax Hospital, likewise ventured no opinion regarding the etiology of Kevin's developmental delays or whether he suffered oxygen deprivation during labor; however, based on the newborn resuscitation record, Dr. Hartmann was of the opinion that Kevin did not suffer any significant lack of oxygen from the time of delivery until positive pressure ventilator was initiated. Nurse Newell, who attended Kevin following delivery, voiced no opinion regarding the likelihood that Kevin suffered brain injury from oxygen deprivation or other trauma. Given the record, it must be concluded that the proof demonstrated, more likely than not, that Kevin's deficits were not occasioned by 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, but were occasioned by a developmental abnormality, that preceded the onset of labor. 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."); 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."). In so concluding, the testimony of Mrs. Hackerman and Mrs. Giardina has not been overlooked; however, while competent to demonstrate that Kevin was depressed at birth, and later developed respiratory distress, it was not competent proof to support any conclusion regarding the etiology of Kevin's developmental delays. See, e.g., Vero Beach Care Center v. Ricks, 476 So. 2d 262, 264 (Fla. 1st DCA 1985)("[L]ay testimony is legally insufficient to support a finding of causation where the medical condition involved is not readily observable.").
The Issue At issue in this proceeding is whether Shalyn L. Hayman, 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 Shalyn L. Hayman (Shalyn) is the natural daughter of Rosalee Hayman and Basil Hayman. She was born a live infant on January 6, 1993, at St. Mary's Hospital, a hospital located in West Palm Beach, Palm Beach County, Florida, and her birth weight was in excess of 2,500 grams. The physician providing obstetrical services during the birth of Shalyn was John Pauly, M.D., who was, at all time material hereto, a participating physician in the Florida Birth- Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. The parties have stipulated and the proof demonstrates, that Shalyn is permanently and substantially mentally and physically impaired. What is at issue is the cause and timing of the event or events giving rise to such impairment or, stated differently and pertinent to these proceedings, whether Shalyn's impairment resulted from 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 the hospital." Section 766.302(2), Florida Statutes. Mrs. Hayman's antepartum course and Shalyn's delivery Mrs. Hayman's pregnancy was essentially uncomplicated, except for being post-term. In this regard, it is noted that Mrs. Hayman's due date was established as December 25, 1992, at forty weeks gestation, and that when delivered on January 6, 1993, Shalyn was almost two weeks overdue, a high risk situation. At or about 5:30 a.m., January 6, 1993, Mrs. Hayman presented to St. Mary's Hospital. At the time, Mrs. Hayman was experiencing mild, irregular contractions, and vaginal examination revealed the cervix to be at 1 to 2 centimeters, effacement at 50 percent, and the fetus at station -1. The membrane was noted to be intact, and monitoring revealed a fetal heart tone in the 130's, with poor variability and no observed reactivity. Given the circumstances, Mrs. Hayman was admitted to the labor and delivery area at or about 6:00 a.m. At or about 7:50 a.m., Mrs. Hayman's contractions were still noted as irregular; however, vaginal examination revealed her cervix was changing, and it was recorded at 2 centimeters, effacement at 80 percent, and the fetus at station -3. Fetal monitoring reflected a fetal heart tone in the 140's, but an abnormal pattern, with decreased variability, lack of acceleration, and persistent late decelerations. That heart rate and pattern persisted through delivery. Mrs. Hayman's labor continued to progress slowly, and at 9:20 a.m. vaginal examination revealed the cervix to be 3 centimeters, with effacement at 80 percent, and at 10:44 a.m. the cervix was noted to be 4 to 5 centimeters. At 10:55 a.m., labor was augmented with Pitocin, and thereafter progressed fairly normally. At 1:55 p.m., January 6, 1993, Shalyn was delivered vaginally. Upon delivery thick meconium stained fluid was noted, but none was present below the cords. Shalyn initially required intubation and bagging with 100 percent oxygen for a low heart rate and poor respiratory effort, but was extubated at approximately 10 to 15 minutes of age in the delivery room. Her Apgar scores were 4, 7 and 8 at one, five and ten minutes. 3/ Shalyn was noted to have the physical stigmata of Down's syndrome, which was later substantiated by chromosomal analysis, and was ultimately transferred to the neonatal intensive care unit (NICU) for further care and management. Following admission to the NICU, Shalyn failed to maintain appropriate respirations or oxygenation, and she was re- intubated and placed on ventilator support. Her hospital course was consistent with severe persistent pulmonary hypertension of the newborn, and she required extensive ventilator support. Cardiac disease was ruled out by echocardiogram. Shalyn's initial hematocrit was 57 with a platelet count of 43,000. The reason for this thrombocytopenia was unknown, although Down's syndrome or perinatal depression were considered as possibilities. On January 7, 1993, Shalyn developed symptomatic polycythemia and a partial exchange transfusion was done. The same day, Shalyn suffered cardiac arrest, which responded to epinephrine and Bicarb. On January 8, 1993, Shalyn was noted to have developed seizure activity, which was treated with Phenobarbital, Dilantin and intermittent lorazepam before the seizures were under control. An electroencephalogram demonstrated bilateral spiked discharges. In response to the seizure activity, a neonatal head ultrasound was taken on January 8, 1993, to rule out intraventricular hemorrhage. The ultrasound was entirely normal, with no evidence of hemorrhage into the ventricular system or the tissue immediately surrounding the ventricle. Shalyn was slowly weaned from ventilatory support and by January 11, 1993, was on an oxygen hood, and by January 14, 1993, was on room air. Physical examination on January 12, 1993, revealed Shalyn to be alert and active under the oxygen hood, her anterior and posterior fontanelle open and flat, not bulging, and neurologically to demonstrate good activity, but decreased tone. On January 15, 1993, Shalyn underwent a CT brain scan to rule out congenital malformation. That scan revealed the following: There is a large right sided intracerebral hematoma involving the occipital area with mild mass effect on the right lateral ventricle. There is a much smaller area of intracerebral hematoma anterior to the larger one in the high frontal parietal area and there is a tiny intracerebral hematoma in the high left frontal parietal region. There is also some hemorrhage in the body of the left lateral ventricle and the ventricular system shows mild dilatation but no midline shift. There is no extra-axial fluid collections. IMPRESSION: There are bilateral intracerebral hematomas but the primary and largest one is located in the right parietal occipital region and causing mild mass effect on the ventricular system. There is minimal hydrocephalus with no midline shift. There is some extension into the ventricular system with blood in the left lateral ventricle. A follow-up head ultrasound was administered on January 23, 1993. In contrast to the head ultrasound conducted on January 8, 1993, the January 23rd ultrasound clearly demonstrated "a dilated ventricle system with bilateral intraventricular hemorrhage with large right occipital parenchymal bleed, essentially unchanged from the previous CT scan" of January 15, 1993. On January 25, 1993, Shalyn underwent a second brain CT scan. The January 25th scan indicated the hemorrhage was now resolving and had decreased in size. In place of the resolving hemorrhage, a resultant encephalomalacia was diagnosed. Subsequent CT scans have confirmed bilateral damage in the form of porencephalic cystic areas in the right temporal parietal and occipital lobes. These areas are consistent with the resolution of an infarct and hemorrhage. The focal damage to Shalyn's brain, evident from the CT scans, is consistent with an injury caused by an intraventricular hemorrhage, but is not consistent with the global changes to the structures of the brain associated with asphyxia. Shalyn was discharged from St. Mary's on January 30, 1993, with evident neurologic impairment. Currently, Shalyn is microcephalic, cortically blind, and has increased tone and spasticity of all four limbs, with very limited motor development. In sum, neurological examination reveals a severe degree of both mental and motor impairment, that is permanent in nature. The cause and timing of Shalyn's injury In addressing the cause and timing of Shalyn's injury, it is first observed that Shalyn has been diagnosed with Trisomy 21, also known as Down's Syndrome. Down's Syndrome is a genetic condition, which often results in mental and physical impairment. In Shalyn's case, however, her neurological impairments are significantly different and more severe than one would normally expect in a child suffering only from Down's Syndrome. Consequently, it must be concluded that Down's Syndrome is not the cause of Shalyn's current impairments. Having rejected Down's Syndrome as the cause of Shalyn's injury, the only logical conclusion to be drawn from the proof is that the injury Shalyn suffered to her brain was occasioned by a large intracerebral hemorrhage, and not asphyxia. In so concluding, it is observed that the pattern of her brain damage is focal, as opposed to the global damage one would attribute to asphyxia. Moreover, the medical records do not evidence associated organ damage, which would normally be present if Shalyn had suffered acute hypoxia. Finally, while the delivery records clearly reflect an abnormal fetal heart rate from the onset of labor, no pattern developed that would reflect acute hypoxia or an asphyxial state during labor or delivery and, as heretofore noted, there was no objective evidence of brain damage consistent with asphyxia. Consequently, it is unlikely that Shalyn suffered a hypoxic episode during labor or delivery. Having resolved that the cause of Shalyn's brain injury, and the resultant permanent and substantial mental and physical impairment, was the intracerebral hemorrhage she suffered, it becomes necessary to address the timing and origin of that hemorrhage. As for the timing, the proof demonstrates that Shalyn's ultrasound of January 8, 1993, demonstrated a normal ventricular system and no evidence of hemorrhage; however, the CT brain scan of January 15, 1993, did reveal the presence of such hemorrhage. Therefore, based on the medical evidence of record, it is reasonable to conclude that Shalyn experienced the disabling intracerebral hemorrhage sometime between January 8, 1993, and January 15, 1993, or, stated differently, after labor, delivery and resuscitation in the immediate post-delivery period. As for the cause of the hemorrhage, the proof demonstrates that, shortly after birth, Shalyn developed polycythemia, and that polycythemia is associated with hemorrhages, including hemorrhagic stroke. 4/ Given the proof, the opinion of Michael Duchowny, M.D., a board certified pediatric neurologist associated with Miami Children's Hospital, that Shalyn's hemorrhage most likely was associated with her polycythemia and was not related to any event during the birth process, is credited.
The Issue Whether Hunter Lewis, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Petitioners, Angel Lewis and Jerry Lewis, are the parents and natural guardians of Hunter Lewis, a minor. Hunter was born a live infant on June 2, 2000, at Tallahassee Memorial Hospital, a hospital located in Tallahassee, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Hunter's birth was Arthur S. Clements, 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.1 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." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. The cause and timing, as well as the significance of Hunter's neurologic impairment To address the cause and timing of Hunter's neurologic impairment, as well as its significance, Petitioners offered selected medical records relating to Hunter's birth and subsequent development (Petitioners' Exhibit 1); the Verified Medical Opinion of Richard J. Inwood, M.D., a neonatologist (Petitioners' Exhibit 2); and the deposition of Donald C. Willis, M.D., an obstetrician (Petitioners' Exhibit 3). In turn, Respondent offered the deposition of Paul R. Carney, M.D., a pediatric neurologist (Respondent's Exhibit 1). As for the significance of Hunter's impairments, it was Dr. Carney's opinion, based on the results of his neurologic evaluation of November 21, 2002, that Hunter's assessment "indicates substantial cognitive and language impairment," but "very mild long tract neurological findings." Dr. Carney described Hunter's developmental delay as static, as opposed to progressive, and he ventured no opinion as to the cause or timing of Hunter's impairments. As for Dr. Inwood, he was of the opinion that: . . . Hunter Lewis [ ] was delivered by induced labor prior to 38 weeks and had immature lungs. Because of the immaturity of the lungs he suffered hypoxic insult and, to a reasonable degree of medical probability, sustained significant neurological injury. This injury would not have occurred had his delivery been delayed until he had demonstrated lung maturity. His problems are not congenital and did not occur during labor or delivery, but rather after delivery . . . . Notably, Dr. Inwood did not further address Hunter's neurologic injury or, stated otherwise, did not speak to whether in his opinion, Hunter suffered both cognitive and motor impairment and, if so, the significance of each. As for Dr. Willis, he was of the opinion that the medical records revealed no evidence of oxygen deprivation or other trauma associated with labor, delivery, or resuscitation immediately following Hunter's birth. Significantly, the medical records are consistent with the opinions of Doctors Inwood and Willis that the cause and timing of Hunter's impairment was not associated with labor, delivery, or resuscitation, and with the opinion of Dr. Carney that, while Hunter may demonstrate substantial cognitive delay, his motor impairment is mild. Given the record, it must be concluded that the proof demonstrated, more likely than not, that Hunter's impairments were not occasioned by 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 the hospital, and that he is not permanently and substantially physically impaired.
