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 Ernest Hall, Jr., a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Initial observations As observed in the preliminary statement, neither petitioners nor anyone on their behalf appeared at hearing, and no proof was offered to support their claim. Ordinarily, such failing would be dispositive of the case; however, notwithstanding petitioners' failure of proof, respondent elected to offer into evidence the medical records filed with DOAH on May 15, 1996, which included records relating to Ernest Hall, Jr.'s (Ernest's) birth and subsequent development, as well as the opinions of Charles Kalstone, M.D., a board certified obstetrician, and Michael Duchowny, M.D., a board certified pediatric neurologist, to affirmatively resolve the issue as to whether Ernest had suffered a "birth-related neurological injury," within the meaning of Section 766.302(2), Florida Statutes. Ernest's birth and development Ernest was delivered vaginally at 2:17 a.m., June 1, 1991, at Shands Hospital, the University of Florida, Gainesville, Florida. His Apgars were normal at birth (9 at one minute and 9 at five minutes) and arterial pH from the umbilical cord was normal at 7.19. Earnest's newborn course was characterized by anemia, transient thrombcytopenia, and prenatally acquired cytomegalovirus. Where, as here, the cytomegalovirus (CMV) was acquired prenatally, it has the potential to cause brain damage in the fetus, as well as hearing impairment, chorioretinitis (inflammation of the eye) and other central nervous system abnormalities. Consequently, Ernest was placed on a ten day regimen of Ampicillin and Gentamicin. A head CT taken on June 5, 1991, revealed periventricular calcification and probably parenchymal calcification consistent with a prenatal infection such as CMV. Notably, following insult, it would require several weeks for such calcifications to occur. Due to the high risk factor associated with CMV, Ernest's auditory brain stem response was evaluated on June 7, 1991. At the time, his response was noted to be within normal limits; however, follow-up was recommended in six months since he was at risk for hearing loss due to CMV. Ernest was discharged to his parents care on June 10, 1991. On February 28, 1994, Ernest was re-evaluated, and those results indicated a severe sensorineural hearing loss in the sound field. On June 19, 1996, Ernest was examined by Michael Duchowny, M.D., a pediatric neurologist associated with Miami Children's Hospital. Dr. Duchowny's neurologic examination revealed evidence of marked hearing impairment with both expressive and receptive language delay, a left ptosis (drooping of the upper eyelid) and exotropia (a deviation of the visual axis of one eye away from that of the other) with chorioretinitis (inflammation of the choroid and retina). In Dr. Duchowny's opinion, which is credited, such findings were consistent with early CMV exposure, and placed Ernest at risk for significant cognitive delay, accentuated by his hearing impairment. Ernest's motor abilities were, however, noted to be age appropriate. As for the cause of Ernest's neurological injury, it must be concluded that the proof fails to demonstrate that it resulted from a brain or spinal cord injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation. Rather, the proof demonstrates, more likely than not, that Ernest's neurologic impairments derive from a congenital CMV infection, which predated his birth by several weeks.
Findings Of Fact Eleanor was born on August 28, 2017, at Lower Keys Medical Center in Key West, Florida. Eleanor was a single gestation weighing over 2,500 grams at birth. Respondent retained Donald Willis, M.D., an obstetrician specializing in maternal-fetal medicine, to review the medical records of Eleanor and her mother, Laura Ann Ontiveros, and opine as to whether there was an injury to her brain or spinal cord that occurred in the course of labor, delivery, or resuscitation in the immediate postdelivery period due to oxygen deprivation or mechanical injury. In his report, dated September 9, 2018, Dr. Willis set forth the following: The mother was admitted to the hospital at 37 weeks gestational age in labor. A fetal heart rate (FHR) monitor tracing during labor was reviewed and showed no fetal distress. Delivery was by Cesarean section for arrest of dilation. Birth weight was 2,857 grams. Amniotic fluid was clear. The baby was not depressed at birth. Apgar scores were 8/9. No resuscitation was required. Newborn physical exam states “Healthy Term Newborn.” The baby failed the newborn hearing test in one ear. Newborn hospital course was otherwise uncomplicated and the baby was discharged home on DOL 2. Hearing evaluation after hospital discharge identified hearing loss in one ear. Records also indicate the child had Torticollis and limited mobility. MRI at 7 months of age identified a small Arachnoid cyst, slightly increased extra axial fluid and a simple pineal cyst. There were mention of findings suggestive of hypoxic ischemic encephalopathy (HIE). In summary, pregnancy was essentially uncomplicated. Cesarean section was done during labor for Arrest of Dilation. The baby was not depressed at birth with Apgar scores of 8/9. No resuscitation was required. The baby was discharged home on DOL 2. MRI at 7 months of age did not describe findings consistent with HIE. There was no apparent obstetrical event that resulted in oxygen deprivation or mechanical trauma during labor, delivery or in the immediate post-delivery period. Respondent’s Motion also relies upon Dr. Willis’s January 14, 2019, affidavit, wherein he affirms, to a reasonable degree of medical probability, the above-quoted findings and opinions from the report. Respondent also retained Michael S. Duchowny, M.D., a pediatric neurologist, to review the medical records of Eleanor and her mother, conduct an Independent Medical Examination (IME) of Eleanor, and opine as to whether Eleanor suffers from a permanent and substantial mental and physical impairment as a result of a birth-related neurological injury, as that term is defined in Section 766.302(2), Florida Statutes. Dr. Duchowny reviewed the medical records, obtained historical information from Eleanor’s mother, and performed an IME on November 28, 2018. Respondent’s Motion also relies upon the attached affidavit from Dr. Duchowny, dated January 14, 2019. In his affidavit, Dr. Duchowny testifies, as follows: It is my opinion that: In summary, Eleanor’s examination reveals neurological findings consistent with a diagnosis of ataxic hypotonic cerebral palsy associated with sensorineural and conductive hearing losses. Eleanor has preserved social awareness. It is premature to adequately assess cognitive functioning although her speech output is obviously delayed. She evidences dysmorphism characterized by epicanthal folds and a saddle nasal bridge. A review of the medical records does not disclose any significant risk factors during labor or delivery. Eleanor’s Apgar scores were 8 and 9 at 1 and 5 minutes, and her post-natal course in the newborn nursery was unremarkable. MR imaging performed on April 26, 2018 revealed benign cysts of the right anterior temporal and pineal regions. Based on today’s evaluation and record review, I believe that Eleanor’s neurological disabilities were acquired prior to birth and did not result from either oxygen deprivation or mechanical injury in the course of labor or delivery. In his affidavit, Dr. Duchowny testifies that his opinions are to a reasonable degree of medical probability. A review of the file, including Petitioner’s Response, reveals that no contrary evidence was presented to dispute the findings and opinions of Drs. Willis and Duchowny. Their opinions are credited.1/
The Issue At issue is whether Elizabeth Ann Adams, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact April D. Adams and Jeffrey Floyd Adams are the natural parents of Elizabeth Ann Adams, a minor. Elizabeth was born a live infant on September 17, 2004, at St. Luke's Hospital, a licensed hospital located in Jacksonville, Florida, and her birth weight exceeded 2,500 grams. Obstetrical services were delivered at Elizabeth's birth by Michelle McLanahan, 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. Sufficient notice of participation in the Florida Birth-Related Neurological Injury Compensation Plan on the part of Michelle McLanahan, M.D., and St. Luke's Hospital was provided to April D. Adams. 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."3 § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. Here, Petitioners were of the view that Elizabeth suffered a subgaleal hemorrhage4 (a bleed) and resulting subgaleal hematoma5 (a collection of blood within the tissue) between the skull and scalp (outside the brain) resulting from the use of the vacuum extractor during delivery, and that the hemorrhage was substantial enough to result in hypovolemia, and ultimately hypoxic-ischemic brain injury.6 (Petitioners' Memorandum Regarding Final Order, pp. 5-7). In contrast, NICA was of the view that the record failed to support the conclusion that Elizabeth's brain injury was caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period and that, regardless of the etiology of her brain injury, Elizabeth was not permanently and substantially mentally and physically impaired. Intervenor expressed no position on the issue. Elizabeth's birth and immediate newborn course At or about 11:24 a.m., September 16, 2004, Mrs. Adams, with an estimated delivery date of September 20, 2004, the fetus at 39 3/7 weeks' gestation, and a history of mild pregnancy induced hypertension (PIH), was admitted to St. Luke's Hospital for induction of labor. There, initial physical examination revealed her membranes were intact, no vaginal bleeding, and external fetal monitoring revealed a reassuring fetal heart rate baseline of 150-160 beats per minute, average long term variability and no decelerations. At or about 12:40 p.m., an IV was started for hydration, and at 3:14 p.m., Mrs. Adams' membranes spontaneous ruptured, with clear fluid noted. At the time, vaginal examination revealed the cervix at 2 centimeters dilation, effacement at 70 percent, and the fetus at -3 station. In the interim, external fetal monitoring was reassuring for fetal well-being. Thereafter, Cytotec ("miso[prostol]") was placed vaginally to soften the cervix (for induction of labor). Mrs. Adams' progress continued to be monitored, and at 6:10 p.m., vaginal examination revealed the cervix unchanged. However, at 6:58 p.m., vaginal examination revealed some change, with the cervix at 3-4 centimeters, effacement at 70 percent, and the fetus at -3 station, and an intrauterine pressure catheter (IUPC) was placed to measure the force of contractions during labor. Fetal monitoring continued to be reassuring for fetal well-being, with a fetal heart rate baseline of 145-160 beats per minute, average long term variability, and no decelerations. At 8:16 p.m., Pitocin infusion (for labor induction) was started, and at 8:37 p.m., contractions were noted at 1-2 minutes, and vaginal examination revealed the cervix at 5 centimeters dilation, effacement at 70 percent, and the fetus at -1 station. Fetal monitoring continued to be reassuring, with a baseline in the 150s. Mrs. Adams' progress continued, albeit slowly, with a prolonged second stage of labor (the expulsion/pushing stage) lasting more than two and a half hours,7 and at 5:03 a.m., September 17, 2004, Elizabeth was delivered vaginally, with vacuum assistance (three attempts). Of note, approximately three hours before delivery, recurrent variable decelerations and a mild baseline tachycardia developed, and approximately eight minutes before delivery severe, repetitive variable decelerations developed which prompted the vacuum-assisted delivery. At delivery, Elizabeth was dried, stimulated, and bulb-suctioned, otherwise no resuscitation measures were required. Apgar scores were good (8 and 9, at one and five minutes).8 Physical examination at 5:10 a.m., revealed no abnormalities, with the exception of an elevated temperature (102.7, rectal) and skin color (acrocyanosis was noted).9 By 5:40 a.m., skin color was noted as pink. Elizabeth roomed-in at her mother's bedside, and was routinely monitored by hospital staff. Of note, Elizabeth's temperature remained elevated until 1:30 p.m., when it was documented at 98.1 (auxiliary). In the interim, at 11:58 a.m., with temperatures of 100.0 (auxiliary) and 100.7 (rectal), complete blood count (CBC) and blood cultures were drawn. The CBC results revealed an elevated white blood count. Under the circumstances, the attending physician (Dr. Schwartz) noted, at 4:34 p.m., "[w]ill repeat CBC in a.m. . . . [w]ill not st[art] ABX unless temps elevated again." Blood culture was subsequently reported as negative. It also may be noted, although not shown to be clinically significant, that Elizabeth's behavior was, starting at 6:10 a.m., periodically described as "irritable" and "fussy." (Exhibit 18, pp. 22-24). Otherwise, Elizabeth's newborn stay was without incident, with normal newborn examinations, breastfeeding well, and voiding and stooling appropriately, until 8:35 p.m., when the attending nurse made the following entry in the records: Assumed care of infant. Infant/Mom ID # checked/verified. Physical assessment done and noted. Infant noted to be jittery and irritable. Mom states that infant has not breastfed since 1700-1730. Temp stable now at 98.8. Infant noted to settle after wrapping. Placed in mother's arms. Mom will breastfeed infant shortly. Will eval infant's next feeding. Thereafter, at 8:42 p.m., the attending nurse made the following entry: Called into room by parents. States that infant shreiked then arched her back and turned purple. Upon enter room infant's color noted to be dusky with purple lips. Left eye noted to be turned in and rt eye gazed. Unwrapped and body noted to be modled but no shaking present at this time. Infant taken to nicu for immediate evaluation. Elizabeth's subsequent care was summarized in her Discharge Summary, as follows: . . . Nursing brought the infant to this Special Care Nursery and it was felt that the infant was having seizure activity. At this point a complete septic workup was performed. The infant was placed on IV antibiotics and further cultures including spinal fluid were sent. The workup was initially benign; however, a CT scan [on September 18, 2004] was within normal limits except that J. Norman Patton, M.D., Division of Cardiovascular Diseases, Internal Medicine, could not completely rule out some mild evidence of inflammatory response in the brain . . . . The CT scan of September 18, 2004, was done to rule out a bleed as the cause of Elizabeth's seizures, and was read as follows: CT head without and with contrast. Iodinated contrast was given per protocol. Nonionic contrast was utilized. Small subgaleal hematoma in the biparietal locations. The intracranial contents appear unremarkable. Specifically, there is no evidence for parenchymal/extra-axial hemorrhage, nor pathologic enhancement. The ventricle volume is within normal limits, and without midline shift. A subgaleal hematoma or hemorrhage is a bleeding between the skull and the skin on the outside of the skull (scalp), and not within the brain. (Exhibit 18, pp. 15, 16, and 18). The Discharge Summary continued, and documented Elizabeth's care as follows: At this point acyclovir was also added to the antibiotic regimen. The CSF PCR was negative, but surface cultures revealed positive HSV [herpes simplex virus] in the rectal swab, although negative in the oropharynx. For this reason the infant was continued on acyclovir for a total of 21 days. After negative cultures the ampicillin and gentamicin were discontinued. The infant also required mild oxygen in this period and was placed on 1.5 liters 30-40%. Over the next several days this was able to be discontinued. Dr. Gamma, Pediatric Neurology, was involved in the patient's case and consulted on a regular basis. EEG was consistent with seizure activity. The infant was on phenobarbital and later secondary to continued occasional seizures, was started on Cerebyx. The goal was to get this infant's phenobarbital level to between 20 and 30; however, the infant metabolized the phenobarbital very well and despite increasing the dose, the phenobarbital level remained in the 19-20 range. Eventually the Cerebyx was discontinued and the infant is discharged home only on phenobarbital. The infant initially was fed fairly slowly, but by the end of admission was eating well and gaining weight steadily. The infant was ready for discharge on 10/09/04 following 21 days of acyclovir and at this point the infant had a phenobarbital level of 19.3 and a weight of 3940 grams or 8 pounds 11 ounces. The parents have been very involved with the infant, visited often, and have demonstrated good care for this baby. The infant's workup also includes urine for amino acids, which was within normal limits. Liver function tests were within normal limits. Screening CBCs were within normal limits. Ammonia was normal at 36. Urine organic acids were within normal limits . . . . An MRI performed on September 22, 2004, revealed: . . . restricted diffusion in the left occipital lobe, both parietal and frontal lobes, worse on the left, consistent with cytotoxic edema as seen in infarction, secondary to ischemic and or sequelae of severe meningoencephalitis The ventricle volume is within normal limits, and without midline shift. A head ultrasound performed on September 30, 2004, was normal and reported, as follows: Using the anterior fontanelle as an acoustic window, routine coronal and sagittal images were obtained. No evidence for intracranial or germinal matrix hemorrhage. Ventricles are not dilated and appear normal in shape and position. No obvious parenchymal abnormality. Elizabeth was discharged on October 9, 2004. Physical examination on discharge was noted in her Discharge Summary, as follows: Physical exam on discharge revealed a discharge weight of 3940 grams, length of 53 cm, and head circumference of 35.5 cm. The infant was well-developed, well- nourished, alert, pink non-jaundiced female in no acute distress. HEENT was negative. Anterior fontanelle was soft and flat. Lungs were clear to auscultation in no distress. Heart - Regular rhythm without murmur. Abdomen - Soft, benign and nontender. GU - Normal female. Back - Normal extremities, negative Ortolani, negative bilaterally. Neurologic exam intact. Discharge medication was phenobarbital. Follow-up was recommended with pediatrics, neurology, Early Intervention Program at Shands, and Occupational Therapy and Physical Therapy at Nemours. Discharge Diagnoses were: HSV ENCEPHALITIS - SEPSIS. NEONATAL SEIZURES. TERM FEMALE NEWBORN. Of note, subsequent testing revealed that Elizabeth had not been exposed to the herpes simplex virus (HSV), and the positive HSV result was a false positive. Elizabeth's subsequent development Following Elizabeth's discharge from St. Luke's, she was evaluated by the Early Intervention Program (in October 2004) to resolve whether she qualified for services. At the time, it was felt Elizabeth did not qualify for the program, as her development was within normal limits (WNL) for her age. However, in March 2005, at age 6 months, Elizabeth was reevaluated and found eligible for occupational, speech, and physical therapy services due to motor and language delay. Those services were discontinued by October 2005, since Elizabeth's developmental growth appeared age appropriate. (Exhibit 7). Elizabeth was weaned off phenobarbital at age 15 months (about December 2005) and remained seizure-free until October 13, 2006, when a seizure was noted and she was ultimately transported (after treatment in a local emergency room) to Wolfson's Childrens Hospital (Wolfson's) in Jacksonville. There she was loaded with phenobarbital and Dilantin, the seizures stopped, and on October 15, 2006, she was discharged on maintenance dosage of phenobarbital. However, on October 16th, she had a second seizure and was readmitted to Wolfson's, and then on October 18, 2006, discharged on an increased dosage of phenobarbital. Thereafter, in December 2006, her medication was changed from phenobarbital to Trileptal. (Exhibit 9). Since that time, Elizabeth has experienced seizures on four occasions, three of which she was treated at Wolfson's (April 17-19, 2007; March 19-20, 2008; and July 10, 2008) and the last of which (March 1, 2009) she apparently was treated at home in North Carolina. (Exhibits 9 and 27). Apart from her seizure disorder, Elizabeth's health has been good, and developmentally she continued to make good progress, without the need for any therapies since they were discontinued in October 2005. Currently, Elizabeth attends a regular school program, and was shown to evidence very mild physical impairment and no mental impairment. (See, e.g., Exhibits 16, 17, and 19). Whether Elizabeth suffered a "birth-related Neurological injury" To address whether Elizabeth suffered a "birth-related neurological injury," the parties offered a Stipulated Record (Exhibits 1-28), that included the medical records associated with Mrs. Adam's antepartal course, the medical records associated with Elizabeth's birth and subsequent development, the deposition testimony of the delivering obstetrician (Dr. McLanahan), and the deposition testimony of Mr. and Mrs. Adams. The parties also offered the deposition testimony of Donald Willis, M.D., a physician board-certified in obstetrics and gynecology, and maternal-fetal medicine, and Michael Duchowny, M.D., a physician board-certified in pediatrics, neurology with special competence in child neurology, electroencephalography, and neurophysiology. Based on his evaluation of the medical records, it was Dr. Willis' opinion that Elizabeth did not suffer a brain injury caused by oxygen deprivation or mechanical injury during labor, delivery, or resuscitation in the immediate postdelivery period.10 In so concluding, Dr. Willis observed Elizabeth was not depressed at birth; her Agpar scores were normal (8 at one minute, and 9 at five minutes); she did not require any significant resuscitation (only stimulation and bulb- suctioning); and her newborn course was without incident until seizures were noted at 16 hours after birth. As for the subgaleal hemorrhage (the bleed between the skull and the scalp) Elizabeth was shown to have suffered (on the CT scan of September 18, 2004), Dr. Willis agreed it was likely related to the vacuum-assisted delivery. As for the cause of the periventricular hemorrhage (brain injury/stroke) Elizabeth was shown to have suffered (on the MRI of September 22, 2004), Dr. Willis voiced no opinion, and deferred to the expertise of a pediatric neurologist. As for Petitioners' theory of the case, that a subgaleal hemorrhage can progress to cause bleeding within the brain as a result of hypovolemia, Dr. Willis agreed. However, he did not see evidence in this case to suggest such a causative connection. Dr. Willis expressed his opinion, as follows: Q. Tell me why you don't think, if you don't think, that her brain injury is related to the vacuum extraction? A. Well, subgaleal hemorrhage is between the skull and the skin on the outside of the skull, and that's very common with vacuum extractions. But the only way that that can cause a brain injury that I'm aware of is that if so much hemorrhage occurs into that hematoma that the baby becomes hypovolemic and has a stroke due to hypovolemia and low blood pressure related to blood loss. I am not aware that this child had a subgaleal hematoma that was to that extent. (Exhibit 18, pp. 17 and 18). See also Exhibit 18, p. 35. Dr. Duchowny evaluated Elizabeth on September 10, 2008. Based on his evaluation, as well as his review of the medical records, Dr. Duchowny was of the opinion that Elizabeth's impairments were likely the result of a meningoencephalitis (an "inflammation of the brain and meninges"11), resulting from a viral infection, albeit not HSV, as opposed to a brain injury caused by oxygen deprivation or mechanical injury occurring during labor or delivery. Dr. Duchowny was also of the opinion that Elizabeth was neither substantially mentally nor substantially physically impaired. (Exhibits 15 and 19). Dr. Duchowny described the results of his evaluation, and the bases for his opinions, as follows: Q. . . . During that examination did you obtain any medical history from Elizabeth's family? A. Yes. Q. What was the history that you obtained? A. I was able to speak to Elizabeth's mother, who was the person, the caretaker, bringing Elizabeth to my office; and she first talked about Elizabeth's seizures, which began shortly after birth, at age sixteen hours; and continued with a total of five seizures during her life. The seizures, although infrequent, were prolonged, and her mother indicated that they lasted between three and five hours, all of which, obviously, resulted in hospitalizations. They were terminated with rescue Diastat in order to stop the status epilepticus. All of Elizabeth's seizures began on the right side of her body but then would generalize to involve both arms and both legs, and most recently Elizabeth has been treated which Trileptal, which apparently has brought the seizures under control. Her mother then went on to describe mild weakness on the right side of Elizabeth's body. She commented that Elizabeth had trouble with fine motor coordination, particularly a pincer grasp, and as a result was a left hander. However, Elizabeth's overall motoric ability was good. She didn't have any specific limitations to her motor abilities, and she was fully functional for her age, which at that time was three years. On a positive note, her mother indicated that her mental development was going well, that there were no delays in her acquisition of speech and language, and that she was in the New Dimensions Preschool Program where she was attending a regular classroom. There has never been any regression of Elizabeth's abilities, and at the time that I evaluated Elizabeth in September, she did not have an ongoing need for either physical or occupational therapy. Otherwise, things were good; she was healthy. She was under the care of Dr. Harry Abrams at Nemours Children's Hospital. She continued to have abnormal EEGs, and her mother commented that her MRI scan of the brain revealed damage, primarily on the left side of her brain. Q. What information, if any, did you obtain regarding her birth? A. Well, again, this was information from Elizabeth's mother, and she told me that Elizabeth was born after a term gestation at St. Luke's Hospital. It was a natural delivery, but with the assistance of a vacuum for the extraction. Elizabeth weighed seven pounds, eleven ounces. She breathed well. She was not a jaundice baby, but that she remained in the NICU at St. Luke's Hospital for a treatment of suspected infection with the herpes simplex virus; so essentially, a herpes simplex encephalitis concern. Q. Thank you. Did you obtain any information with respect to Elizabeth's growth and development? A. Yes. Elizabeth rolled over and sat at six months and then was able to stand at age ten months. She was walking on her own by age thirteen months and began talking in single words between a year and age eighteen months. At the time I saw her she had not yet been toilet trained, but she received all of her immunizations and had no known allergies to medications. She had undergone surgery on two occasions for the ear tubes and, of course, there were the multiple hospitalizations for the recurrent bouts of status epilepticus. Q. Did you perform a physical examination of Elizabeth? A. Yes. Q. What were your findings upon that examination? A. When I saw her, she was actually quite cooperative so, socially, she was very appropriate for her age. She seemed appropriately nourished and developed. Her weight was recorded at thirty-five pounds. There was no abnormalities of her skin, neck and she had no abnormal aspects of her body which suggested a malformation. I noted that her spine was normal. Her head growth was good. She had a head circumference of 49.1 centimeters, which for age three years is within standard percentiles. There were no abnormalities of her heart, her lungs, her abdomen, and her extremities or her peripheral pulses. Q. Did you also perform a neurological examination of Elizabeth? A. Yes. And once again, in terms of her social abilities, she actually was quite good for her age and she was appropriately verbal at her age level. She answered questions, she provided decent verbal content. I thought her speech sounds had a very mild disarticulation, but she knew her colors. She was able to identify parts of her body, and she was able to draw with a pencil using her left hand. No drooling was noted. Examination of her cranial nerves was essentially normal, and her motor examination revealed a well developed, age appropriate amount of muscle strength, bulk of her muscle and muscle tone. I was unable to detect any specific focal weakness, although, again, there was a difference in terms of her fine motor coordination. Even though she used both hands cooperatively, she clearly preferred her left hand, although I was able to demonstrate a pincer grasp bilaterally and reasonably good manual dexterity. Where I did think there was asymmetry had to do with her walking where her left arm would swing in a more prominent fashion on the left compared to the right. Also, there was a tendency actually for both feet to turn in, but this was more prominent, again, on the right side. I thought that Elizabeth's sensory examination was normal and that her gait was appropriate in terms of coordination, despite the asymmetric arm swing. Her deep tendon reflexes were normal and symmetric on both sides of the body, in other words, both arms and legs; and her plantar response, which is a reflex response to stroking the bottom of the feet, was normal. There were no abnormalities of her neurovascular examination, meaning that there were no asymmetries when a stethoscope was placed on her neck, head or over her eyes. The bones of her skull were closed, which was appropriate. Q. Okay. Thank you. Based upon your review of the medical records and documents which you identified earlier, and based upon your examination of Elizabeth and the findings from that examination, were you able to form an opinion as to the nature and extent of Elizabeth's neurological delays or developmental delays, if any, and the etiology of those delays? A. Well, there were some findings on the neurological exam with respect to Elizabeth's motor coordination, and my impression was that these findings were, at best, mild. I would characterize them really as very mild. Q. Specifically, what are those findings? A. The asymmetric arm swing, the establishment of handedness on the left and slightly decreased -- well, really, minimal, minimal change in dexterity. Really, the arm swing and the handedness. Q. And those delays that you've identified and, as I understand it, it's your opinion that you would characterize those as mild? A. Yes. Q. What functional impact, if any, do those mild delays have on Elizabeth based upon your examination of her when you saw her? A. Well, at present I would have predicted that there would be no compromise to her functionality, and that appeared to be the case. Q. With respect to her cognitive development, what were you able to conclude based upon your review of the medical records and your examination of her? A. My examination revealed normal cognitive development; in other words, a level of mental function, which was at age level. So I was, again, not surprised that she was in a regular class at the New Dimensions Preschool. Based upon your review of the medical records, were you able to form an opinion as to the etiology of any of those neurological problems that were identified? A. Well, from a review of the records, I think that there was a strong indication that Elizabeth had had some kind of meningoencephalitis in the first week of life, and I believe that her findings on neurological examination today are related to the previous bout of meningoencephalitis. Q. Do you have an opinion as to whether or not Elizabeth suffers from a substantial mental impairment? A. I do, and that is that I do not believe that Elizabeth has a substantial mental impairment. Q. Do you have an opinion as to whether or not Elizabeth suffers from a substantial physical impairment? A. I do not believe that Elizabeth has a substantial physical impairment either. * * * Q. . . . You mentioned the motor findings that you described as, at best, mild, or very mild, and you listed the asymmetrical arm swing, and the handedness on the left and the minimal loss of dexterity. I think your findings also included abnormalities in the gait, is that correct? A. Yes, that's true. There was a toe-in position bilaterally, but I didn't see that as a functional problem. She did that, but it didn't seem to contribute to any disability at all . . . . (Exhibit 19, pp. 7-16). When, as here, the medical condition is not readily observable, issues of causation are essentially medical questions, requiring expert medical evidence. 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."); Ackley v. General Parcel Service, 646 So. 2d 242, 245 (Fla. 1st DCA 1994)("The determination of the cause of a non-observable medical condition, such as a psychiatric illness, is essentially a medical question."); 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 obligated to present expert medical evidence establishing that causal connection."). Here, the opinions of Doctors Willis and Duchowny were logical, consistent with the record, not controverted, and not shown to lack credibility. Consequently, it must be resolved that the cause of Elizabeth's impairments was most likely a meningoencephalitis, as opposed to a "birth-related neurological injury," and, regardless of the etiology of her impairments, she is not permanently and substantially mentally and physically impaired. See 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 Issue At issue in this proceeding is whether Allan Fils-Aime, 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 Rose Louis and Emmanual Fils-Aime, are the parents and natural guardians of Allan Fils-Aime (Allan), a minor. Allan was born a live infant on August 31, 1990, at Bethesda Memorial Hospital, a hospital located in Boynton Beach, Florida, and his birth weight was in excess of 2,500 grams. The physician providing obstetrical services during the birth of Allan was Allan Dinnerstein, 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. Rose Louis' antepartum course and Allan's delivery Rose Louis' (Ms. Louis') antepartum course was essentially uncomplicated; however, as of August 30, 1990, Allan was post-term at 42 weeks. At or about 7:10 p.m., August 30, 1990, Ms. Louis was admitted to Bethesda Memorial Hospital in labor. Vaginal examination revealed the cervix to be at 2 centimeters, effacement at 50 percent, and the fetus at station -2. The membranes were noted to be intact, and fetal heart tone was noted in the 150s and reactive. Ms. Louis' labor progressed slowly through August 30, 1990, and by 9:40 a.m., August 31, 1990, vaginal examination revealed the cervix to be at 4 to 5 centimeters, effacement complete, and the fetus at station 0. Fetal heart tone during labor was noted in the 140s, with good variability and occasional decelerations with uterine contractions. At or about 10:00 a.m., a variable deceleration to 80 was noted without uterine contractions, and Ms. Louis was repositioned, with a good return of fetal heart tone to baseline. Thereafter, at 10:30 a.m., variable decelerations, with a late component to 70, were noted with contractions, and Ms. Louis was given oxygen by mask. Fetal heart tone variability was noted as good. Vaginal examination at 10:58 a.m. revealed the cervix to be at 5 centimeters, effacement at 80 percent, and the fetus at station -1. Thereafter, variability was noted as average, and variable decelerations, with a late component of 90 to 100, were occasionally observed. At 12:35 p.m., fetal heart tone was noted to decrease to 60, with uterine contractions, and a slow return to baseline. Ms. Louis was repositioned, and fetal heart tone was noted as reactive, with average variability. At 1:00 p.m., heavy deep variables, with late components, were noted with each contraction. Vaginal examinations at 12:50 p.m. and 1:10 p.m. revealed the cervix to remain at 5 centimeters, effacement at 80 percent, and the fetus at station -1. Consequently, given Ms. Louis' failure to progress and the indications of fetal intolerance to labor, delivery by cesarean section was proposed. Ms. Louis was moved to the delivery room at 1:35 p.m., and at 1:59 p.m. Allan was delivered by cesarean section. Following delivery, Allan was suctioned2 and administered oxygen by mask for approximately one minute to establish regular respiratory effort. Apgar scores at one minute totaled 5, with heart rate, respiratory effort, muscle tone, reflex irritability, and color being graded at 1 each. Apgar scores at five minutes totaled 9, with heart rate, respiratory effort, muscle tone, and reflex irritability being graded at 2 each, and color being graded at 1. Initial physical examination revealed no abnormalities. Allan was admitted to the neonatal intensive care unit (NICU) at 2:20 p.m. for transient respiratory distress and received increased oxygen support for one and one-half days. Physical examination on admission was of "normal male," with "good generalized tone [and] good suck [and] grasp." Allan was weaned to room air at 5:00 a.m., September 1, 1990, and remained stable, with respiratory distress resolved. He remained under observation, however, and received a course of treatment for possible infection (sepsis). On September 9, 1990, Allan was discharged to his parents' care, with no apparent abnormalities. On discharge, Allan was noted as "pale pink, active [with] good tone." Allan's development Allan's early infancy was characterized by good health, and his parents observed no apparent problem until Allan was three to four months of age. At that time, the parents observed that Allan would not reach out or use his right hand. On March 5, 1991, at approximately six months of age, Allan presented to Children's Medical Services. At the time, Allan's right hand was noted to have a weak grasp, with a flexation contraction of the right thumb, and he was observed not to reach out with his right hand. Assessment was neurological deficit and muscle weakness of the right hand, and Allan was referred for further evaluation. On July 19, 1991, Allan received an orthopedic consult, which noted that "his whole right upper extremity is spastic," and recommended referral for neurologic examination. That referral occurred on August 21, 1991, and resulted in the following findings: PHYSICAL EXAMINATION: On examination, head circumference was 43.2 cm which is below the second percentile in the microcephalic range. The head is fairly symmetrical. No gross facial weakness or asymmetry. He is able to stand, bearing weight. The right leg is externally rotated. The muscle tone is clearly different and slightly increased on the right side, not only in the arm but in lower extremity. There is posturing of the right hand with a cortical thumb. DIAGNOSTIC IMPRESSION: CEREBRAL PALSY MANIFESTED BY RIGHT HEMIPARESIS, GREATER INVOLVEMENT OF THE ARM THAN THE LEG. OVERALL DEVELOPMENTAL DELAY. Further neurological work-up, consisting of an MRI, EEG, and auditory evoked response, was recommended. The neurological work-up was conducted in August 1991. Auditory evoked response disclosed preservation of hearing, and EEG disclosed no active seizure or paroxysmal activity. The MRI scan was, however, abnormal, and showed evidence of "an odd infarction in the distribution of the left middle cerebral artery associated with porencephalic changes." A CT scan of the brain on October 24, 1994, was consistent, revealing "a large area of encephalomalacia in the left hemisphere, maximal over the parietal region, indicative of a previous middle cerebral artery stroke."3 Allan was examined by Michael Duchowny, M.D., a pediatric neurologist, on August 25, 1995. That examination provided the following observations: NEUROLOGICAL EXAMINATION revealed an obvious right hemisyndrome consisting of right hemiparesis with arm involvement greater than face and leg, right hemidecorticate posturing and hemihypotrophy. Alan walked with an obvious hemiparetic gait and the arm was adducted and internally rotated at the shoulder, flexed at the elbow and wrist with a markedly fisted thumb. He used his left hand exclusively for functional tasks and did not use the right hand in assistance. There was no evidence of transferring. When asked to perform with the right hand, Alan will grasp the right hand with the left and move it around in order to reach a target. He could move the fingers slightly, but tended to keep the fingers flexed and had great difficulty extending them on command. There was obvious smallness to the right upper extremity, particularly involving the fingers and I would doubt that Alan can wear the same size glove on both hands. By contrast, the lower extremities appeared to be symmetric, although the right leg was externally rotated at the hip with a foot eversion and slight plantar grade attitude. There was a pelvic tilt on walking and hemidecorticate posturing became exaggerated as he tried to run. He does not fall. There was also a facial asymmetry with relative increase in the right palpebral fissure compared to the left. His sensory examination was deferred due to lack of cooperation. There was right-sided hyperreflexia, but there was an increase in the deep tendon reflexes on the left side as well particularly at the knee. Both plantar responses were extensor, the right being more so. Alan could perform finger-to-nose and heel-to-shin testing on the left side without difficulty. Neurovascular examination was unremarkable. Alan had a marked deficiency in both expressive and receptive language skills. He spoke in single words and there was a strong tendency toward echolalia. He could identify body parts, but did not know colors and often had trouble following one-step commands with any degree of accuracy. His speech sound[s] were poorly articulated particularly for labile consonants. His fund of information was obviously diminished. I found his behavior to be appropriate and he was socially interactive. Alan was unable to build a tower of cubes with an individual finger grasp on the right and had some difficulty on the left as well. IN SUMMARY, Alan's neurological examination reveals him to be a mentally retarded boy with a prominent right hemisyndrome. He also has evidence of left-sided involvement, although clearly this is relatively minor in contrast to his right-sided involvement which includes evidence of right spastic hemiparesis and decrease in size of the upper extremities. I should add that there is evidence of a right visual neglect, although I could not formally demonstrate a homonomous hemianopic field cut. Not other cranial nerve findings are noted. I regard Alan's findings as being permanent and he clearly has a substantial deficit both with regard to mental and motor functioning. Here, there is no dispute, as the proof demonstrates, that Allan is permanently and substantially mentally and physically impaired. What is at issue is the cause and timing of the brain injury giving rise to such impairment, or, stated differently, whether Allan's impairment resulted from an injury to the brain "caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery or resuscitation in the immediate post-delivery period," as contended by Petitioners, or whether Allan's impairment was the product of an insult predating and unrelated to labor and delivery, as contended by Respondent. The genesis and timing of Allan's brain disorder Allan's presentation is consistent with a group of persisting motor disorders appearing in young children, commonly referred to as cerebral palsy, that are characterized by delayed or abnormal motor development and often accompanied by mental retardation, seizures, or ataxia. Such disorders result from brain damage which may be intrapartum (occurring during child birth) or antenatal in origin.4 Here, the proof is compelling that Allan's brain injury resulted from a stroke suffered in the antenatal period, most likely prior to 30 weeks gestation, and that it was not associated with any event occurring during the course of labor, delivery, or the immediate post-delivery period. In so concluding, it is first observed that the neuro- imaging studies are inconsistent with brain injury resulting from oxygen deprivation during the birth process, and suggest strongly that brain damage occurred prior to 30 weeks gestation. In this regard, the neuro-imaging studies, as well as neurologic examination, are consistent with a focal left hemisphere stroke and porencephaly, as opposed to bilateral or generalized injury, with associated atrophy, one would typically associate with oxygen deprivation suffered during the course of birth. Moreover, the absence of a significant glial response in the brain scan suggests strongly that the brain damage was acquired prior to 30 weeks gestation.5 In addition to the foregoing, Allan's clinical course post-delivery is inconsistent with hypoxic or ischemic damage occurring during the course of birth. In this regard, it is observed that, at birth, Allan evidenced good Apgar scores, no significant respiratory depression, no signs of systemic or organ damage (such as renal failure or cardiac decompensation), no depression of consciousness, and no seizure activity. In sum, Allan's immediate post-delivery course evidenced no neurologic compromise, and his presentation was inconsistent with a brain injury occurring during the course of labor, delivery, or resuscitation in the immediate post-delivery period.
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.
The Issue At issue in the proceeding is whether Ashley Wilkinson, 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 Petitioners, George Wilkinson and Kimberly Wilkinson, are the parents and natural guardians of Ashley C. Wilkinson, a minor. Ashley was born a live infant on July 13, 1996, at Spring Hill Regional Hospital, a hospital located in Spring Hill, Florida, and her birth weight exceeded 2,500 grams. The physician providing obstetrical services at Ashley's birth was Thomas J. Armbruster, 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. Mrs. Wilkinson's antepartum course and Ashley's birth Mrs. Wilkinson's antepartum course was without significant complication until July 10, 1996, when, at 6:40 p.m., with the fetus at 38 and 4/7 weeks gestation (estimated date of delivery July 20, 1996), she presented at Spring Hill Regional Hospital complaining of "bleeding [and] low pressure," and was admitted to rule out labor. At the time, external fetal monitoring revealed a reassuring fetal heart rate in the 130-beat per minute range, and no contractions. Vaginal examination revealed the cervix at 1 centimeter, effacement at 20 percent, and the fetus at station -3, with the membranes intact. Dr. Armbruster was paged, and at 7:15 p.m., visited briefly with Mrs. Wilkinson. At that time, Dr. Armbruster instructed staff to watch for contractions for another 30 minutes and if none were observed, Mrs. Wilkinson could be discharged. Thereafter, at 8:45 p.m., there being no evidence of contractions or other change in status, Mrs. Wilkinson was discharged, with mother and fetus noted to be stable. Insofar as the record reveals, Mrs. Wilkinson's antepartum course continued without apparent complication until approximately 12:01 a.m., July 13, 1996, when, while at home in bed, her membranes ruptured and, either contemporaneously or shortly thereafter, she evidenced seizure activity (possibly eclampic) and severe vaginal bleeding.2 Mrs. Wilkinson's husband immediately called 911. Pasco County Fire Rescue responded to the emergency call. On arrival, fire rescue personnel witnessed Mrs. Wilkinson thrashing about in bed, and observed a large amount of blood on the bed and in her vaginal area. The Pasco County Fire Rescue personnel further noted that: . . . [Patient] combative, swinging arms [and] attempting to bite . . . ABD firm, soft. Restraints bilat[eral] wrists to protect [patient]. O2 by NRB held near face. [Patient] remained combative, unable to attempt IV. S[pring] H[ill] Reg[ional] ER called to advise of possible emergent C Section during response . . . . Mrs. Wilkinson was transported by Pasco County Fire Rescue to the Spring Hill Regional Hospital emergency room (ER) where she arrived shortly after 1:00 a.m., July 13, 1996.3 Upon arrival, Mrs. Wilkinson was described as combative (scratching, kicking and screaming), with no eye contact. At the time, heavy bright red vaginal bleeding was noted, and Mrs. Wilkinson's cervix was described as 1 to 2 centimeters dilated. Fetal monitoring (from approximately 1:10 a.m. to 1:20 a.m.) revealed a fetal heart rate of 120 to 130 beats per minute, with no accelerations, and no evidence of uterine contractions; however, because monitoring was sporatic and brief, the monitor strips provide no compelling evidence as to the well-being of the fetus or whether Mrs. Wilkinson was or was not in labor. At approximately 1:20 a.m., ER personnel advised Dr. Ambruster by phone, at home, of Mrs. Wilkinson's status. Dr. Armbruster ordered that preparations be made for a stat cesarean section. At 1:45 a.m., Mrs. Wilkinson was taken to the operating room, and at 2:11 a.m., Ashley was delivered by cesarean section. Pertinent to this case, Dr. Armbruster's operative report noted that: . . . there appeared to be an approximately 30% abruptio placenta at the time of delivery and also that the amniotic fluid was port wine stained and that would be consistent with the abruptio placenta. Whether the cause be a straight abruptio or the eclampic seizure was unknown. Otherwise the uterus, tubes and ovaries were noted to be normal. On delivery, Ashley was handed off to Dr. Mari Doherty, the pediatrician in attendance. Dr. Doherty's progress notes include the following observations: . . . [On delivery, the baby] was bathed in blood. [S]uctioned blood from mouth [and] nares. Baby delivered [and] placed under radient warmer [and] because of no respirations [and] limp, the baby was given PPV [with] 100 [percent] BVM for about 4-5 min[utes] intermittently . . . Baby's breathing was labored [and] grunting; more suctioning and chest PT improved the baby. Suctioning done in between breaths . . . Baby transported from the OR to the Nursery [with] O2 by mask . . . . Apgars scores were recorded as 4, 7, and 8, at one, five, and ten minutes respectively. The Apgar scores assigned to Ashley are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, muscle tone, reflex/irritability, and color, with each category being assigned a score ranging from the lowest score of 0 through a maximum score of 2. As noted, at one minute, Ashley's Apgar score totaled 4, with heart rate being graded at 2, muscle tone and reflex/irritability being graded at 1 each, and respiratory effort and color being graded at 0 each. At five minutes, Ashley's Apgar score totaled 7, with heart rate and reflex/irritability being graded at 2 each, and respiratory effort, muscle tone, and color (with her body pink, but extremities blue) being graded at 1 each.4 At 2:30 a.m., Ashley was transported from the operating room to the nursery. On admission, Ashley was placed on an EKG/Apnea monitor; ABG, blood culture, and blood sugar testing was ordered; and IV was started. At 2:45 a.m., when her oxygen saturation levels were noted to fall, Ashley was deep suctioned and given increased oxygen. Between 2:45 a.m., and 7:55 a.m., Ashley's oxygen saturation levels continued to drop periodically, and she was noted to be cyanotic on occasion. At 5:30 a.m., Ashley was again suctioned, producing approximately 5cc of bloody mucus, and during the early morning hours was noted to be very jittery and irritable, with occasional arching of the back and stiff extremities, and was medicated with Phenobarbital. Given her condition, Ashley was transferred, at or about 7:55 a.m., to All Children's Hospital where she was reportedly in a coma for two weeks.5 Currently, Ashley presents with static encephalopathy (status post hypoxic ischemic encephalopathy), characterized by spastic quadriplegia, global developmental delay, and seizure disorder, as well as gastroesophageal reflux. Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Here, there is no serious dispute that Ashley suffered an injury to the brain, caused by oxygen deprivation, secondary to placental abruption. There is likewise no serious dispute that the injury Ashley suffered rendered her permanently and substantially mentally and physically impaired.6 What is at issue, is whether the asphyxia which precipitated her injury occurred "in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital," as required to qualify for coverage under the Plan. To address the issue, the parties offered selected medical records relating to Mrs. Wilkinson's antepartum course, as well as those associated with Ashley's birth and subsequent development. Additionally, Petitioners offered the deposition testimony of Radhakrishna Rao, M.D., a pediatric neurologist (board-eligible in pediatrics and pediatric neurology). Petitioners also offered the testimony of Mrs. Wilkinson which, if credited, would demonstrate that commencing at or about noon, July 12, 1996, she began to experience regular uterine contractions approximately 10 minutes apart, and that the contractions continued throughout the day progressing to approximately 8 minutes apart by 3:30 p.m., and approximately 6 minutes apart by 7:30 p.m. Respondent offered the deposition testimony of Charles Kalstone, M.D., a physician board-certified in obstetrics and gynecology, and Intervenor Armbruster offered his own testimony, as well as the testimony of Robert Yelverton, M.D., a physician board-certified in obstetrics and gynecology. The medical records and the testimony of the physicians and other witnesses offered by the parties have been carefully considered. So considered, it must be concluded, by application of the presumption established by Section 766.309(1)(a), Florida Statutes, or otherwise, that the brain injury suffered by Ashley was caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital.7 In reaching such conclusion, it has been helpful to initially identify those matters on which the medical experts share a commonality of opinion. Such matters include an opinion that Ashley's brain injury was caused by oxygen deprivation, secondary to placental abruption; that such deprivation started at some time following abruption and continued until she was resuscitated, following delivery; and that, given the record in this case, one cannot resolve where on that time line (whether at the onset of the abruption or at some other definitive point through resuscitation) hypoxia of a sufficient magnitude occurred to account for the severe brain injury Ashley suffered. The experts are also in agreement that the hospital records relating to Ashley's birth provide little or no help in resolving the issue of whether Mrs. Wilkinson was in labor at the time of placental abruption or thereafter. In this regard, it is noted that there is no serious disagreement that the fetal monitoring which occurred following Mrs. Wilkinson's arrival at the emergency room (from approximately 1:10 a.m. to 1:20 a.m.) was inadequate to provide any compelling evidence as to whether Mrs. Wilkinson was or was not in labor. Moreover, it is worthy of note that the experts agree that, given the emergent nature of Mrs. Wilkinson's presentation, it was not pertinent to her clinical management to resolve whether she was in labor but, rather, to delivery Ashley as soon as possible. Consequently, the absence of evidence in the hospital records regarding labor is not meaningful.8 Having explored the areas on which the experts are in agreement, it is timely to consider, without reference to Mrs. Wilkinson's testimony regarding the onset of labor, the opinions of the experts offered on behalf of Intervenor Armbruster regarding the onset of labor, contrasted with the opinions of the expert offered by Respondent.9 As will be noted, there is little in the testimony of these physicians to credibly resolve, without reference to Mrs. Wilkinson's testimony, when, if ever Mrs. Wilkinson entered labor. Dr. Yelverton, an expert called by Intervenor Armbruster, expressed his opinion on the question of labor, as follows: Q. Did you find any evidence in the record, Dr. Yelverton, that the patient was in labor with respect to any of the health care providers that had been treating her at the hospital? * * * A. There's one comment on the summary of the labor and delivery which states that the patient was in labor and the labor began 0001 hours on July 13th, 1996. This was a summary of the labor and delivery record that was recorded by a registered nurse whose name is illegible to me.[10] * * * Q. In addition to the nurse's note that you've pointed out to Judge Kendrick about labor, did you find any other evidence in the record that the mother was in labor, including the fact that she had an abruptio placenta? A. Well, I think given a more likely than not scenario in this case, when events of this nature occur at home, or even in the hospital, and they result in a spontaneous rupture of membranes with a great deal of blood present at the time, either there were some contractions that disrupted the placenta or a spontaneous rupture in the membrane which resulted in the contraction of the uterus itself which resulted in the abruption. Either way, more likely than not, there was some uterine activity that resulted in either spontaneous rupture of the membranes or the abruption itself. Q. Do you have an opinion within reasonable medical probability or more likely than not, based upon your background, training and experience and your review of the materials about whether or not Ms. Wilkinson was, in fact, in labor? A. I think more likely than not, she was in labor. I failed to mention also that she was two centimeters dilated when she arrived at the hospital with ruptured membrane, vaginal bleeding. It would be very unusual to find that particular scenario with a patient not having uterine contractions. [Transcript of September 13, 2001, hearing, at pages 48, 49, 52 and 53.] Dr. Yelverton's opinion that, without consideration of Mrs. Wilkinson's testimony, Mrs. Wilkinson was in labor at the time of abruption is not persuasive. First, it is noted that at admission to the ER, Mrs. Wilkinson was not noted to be 2 centimeters dilated but, rather 1 to 2 centimeters dilated. Given that she was 1 centimeter dilated on July 10, 1996, and not in labor; the subjective nature of the examination; the circumstances under which it was done; and the fact that the examination of July 13, 1996, noting a range of 1 to 2 centimeters was apparently made by a different person than the one who made the observation on July 10, 1996; the difference in dilations is not compelling evidence of labor. Second, Dr. Yelverton's suggestion that "some uterine activity" must have "resulted in either spontaneous rupture of the membranes or the abruption itself," is hardly persuasive evidence of labor (the onset of regular uterine contractions), and ignores, inter alia, the equally plausible alternative that the abruption was spontaneous or that it was precipitated by the seizure Mrs. Wilkinson suffered. Dr. Armbruster, who testified on behalf of himself, expressed his opinion on the question of labor, as follows: Q. . . . [W]as there any evidence in the records that you're aware of that . . . indicate[d] that . . . the mother . . . was in labor, or have you had a chance to re- review the records recently? A. Yes. One, she did complain of abdominal pain, which, of course, is associated with labor, and, two, her cervix had dilated. She was two centimeters from one centimeter when she came in two days prior, and she had effaced. Her cervix had thinned out from 20 percent to 80 percent, therefore, some sort of labor had to be going on during the two intervening days. Q. Would you explain that in a little bit more detail by the progression of cervical dilatation and progression of effacement in the face of contractions indicating to you that labor was ongoing? A. All right. We have many definitions of what labor is or we discuss what labor is, but most doctors agree true labor is the changing of a cervix in dilatation and the effacing or thinning out of a cervix. So most doctors or most obstetrician/gynecologists will agree upon the fact that if there is a change in the cervix, whether it be effacement or dilatation, that is the definition of labor. In this case, Ms. Wilkinson showed both a change in dilatation and effacement. Q. Do you have an opinion within a reasonable medical probability, based upon your background, training and experience, your involvement with this patient and your review of the records about whether or not Ms. Wilkinson was in true labor from the time that the abruptio placenta occurred up through the delivery of the child? A. In my opinion, she was in labor from the time of the abruptio to the time I did the C section, both with the pain she showed and also the change in the cervix and with effacement and dilatation, that is correct. * * * Q. But based upon the records alone, do you believe that she was in labor? A. Without a doubt, I believe she was in labor at the time of the abruption of the placenta. Q. And regardless of the records, just based on your own experience with patients with abruptio placentas and the consequent bleeding causing uterine irritability and contraction, do you believe she was in labor based on that experience? A. I believe that she was in labor for two reasons, and I've stated them prior: One, she did complain of abdominal pain, and; two, that there was a change in the cervix with both -- in change of dilatation and effacement . . . . [Transcript of September 13, 2001, hearing, pages 89-92.] Dr. Armbruster's opinion that, without consideration of Mrs. Wilkinson's testimony, Mrs. Wilkinson was in labor at the time of abruption is also not persuasive. First, Mrs. Wilkinson was not, as Dr. Armbruster states, 2 centimeters dilated when she presented to the ER on July 13, 1996, and, for reasons heretofore noted, the change in dilation noted is not persuasive proof of labor. Second, Dr. Armbruster's testimony that on presentation to the ER on July 13, 1996, "[h]er cervix had thinned out from 20 percent [noted on July 10, 1996] to 80 percent" finds no record support, and his testimony that he has a clear recollection of her effacement on July 13, 1996, without benefit of any contemporaneous notation of such observation, is improbable and unworthy of belief.11 Dr. Kalstone, who testified on behalf of NICA, expressed his opinion on the question of labor, as follows: Q. . . . Doctor, based upon your training and experience and review of this file, were you able to reach any conclusions whether or not the records demonstrated to you that Ashley Wilkinson sustained oxygen deprivation during the course of her delivery or immediate resuscitation? A. Yes. My opinion was that she was not in labor, essentially, and therefore, she didn't suffer from oxygen deprivation during labor, and certainly during labor or resuscitation in the immediate post-delivery period. Q. Doctor, please explain the basis for that opinion. A. The patient was at approximately 39 weeks pregnant and her husband woke up to find her having a major seizure, it sounds like, in bed, and simultaneously her membranes ruptured spontaneously. She had severe hemorrhage from the vagina, which later turned out to be proven to be from a placental abruption. There is no mention that the patient was in labor or that she was having contractions, by anyone that took care of her or was with her. She was transported in a timely way to Spring Hill Regional Hospital where the nurse who admitted her noticed that she was actively bleeding and that she was agitated and combative. She was prepared for an emergency cesarean section. * * * Now, in the doctor's written and dictated notes, including the summary, there doesn't seem to be any mention or consideration that she was in labor, and there was nothing in the nurses' notes that would lead me to believe that she was in labor, either. The doctor said that the cervix was one to two centimeters dilated when checked in the emergency room. She had one previous vaginal delivery and one to two centimeters doesn't mean necessarily that the patient was in labor. There is no mention as to whether the cervix was effaced. * * * So, in reviewing all this information, there was no reason to suggest that the patient was in labor. * * * Q. Doctor, did you have an occasion to review the fetal monitor strips? A. Yes. On the fetal monitoring strips -- they start monitoring shortly before 1:10 a.m., and ended shortly before 1:20. On the fetal monitor strips the fetal heart wasn't recorded continuously. The rate was around 120 to 130. There were no accelerations, but the fetus was monitored for a short period of time. So, I can't really tell if that tracing is normal or abnormal. In regards to the uterine-activity part of the tracing, that was monitored for part of that time and I didn't see any evidence of uterine contractions that were recorded on these fetal monitor strips for the time that the patient was on the monitor. Q. Doctor, do you believe that the abruption of the placenta occurred before Mrs. Wilkinson commenced labor? Yes. I don't think she really commenced labor. The placenta definitely abrupted at home. It was a sudden event, catastrophic event that occurred while she was in bed, maybe concomitant with when the membranes ruptured, that they both happened about the same time. Placentas do abrupt during labor, but they can also abrupt without labor, and it is my opinion that this patient went to bed fine, essentially, and then had two major things happen to her. One, she had a seizure; and two, her placenta abrupted. Simultaneously, the membranes ruptured . . . * * * Q. Based upon your review of the records, more likely than not did the baby's mother actually go into labor at all before she was born? * * * As I said before, there is really no evidence that I can see from nursing notes, the doctor's dictation or the patient history that was obtained, through the husband mostly, I think, to suggest that labor was the culprit or that she was in labor . . . . [Respondent's Exhibit 1, pages 7-12] Dr. Kalstone's opinion that, based on the available antepartum records, Mrs. Wilkinson was not in labor when she presented at Spring Hill Regional Hospital is credible; however, given that the records are limited in scope, given the emergent nature of Mrs. Wilkinson's presentation, and given the absence of any reason to document labor, any opinion based on those records is inadequate to rebut the presumption of labor established by Section 766.309(1)(a), Florida Statutes. Finally, addressing Mrs. Wilkinson's testimony regarding the onset of labor at or about noon, July 12, 1996, it must be resolved, contrary to Respondent's contention, that there is no compelling reason to reject her testimony as less than credible. Consequently, it may be said that the record supports the conclusion that, by application of the presumption established by Section 766.309(1)(a), Florida Statutes, or otherwise, that the brain injury Ashley suffered was caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital.
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.
Findings Of Fact Jer’Donis Pringle was born on June 24, 2011, at Heart of Florida Regional Medical Center located in Davenport, Florida. Jer’Donis weighed 3,004 grams at birth. NICA retained Donald Willis, M.D., a Florida board- certified obstetrician and gynecologist specializing in maternal- fetal medicine to review the medical records of Jer’Donis. In an affidavit dated July 2, 2013, Dr. Willis opined as follows: Based upon my education and experience, it is my professional opinion, within a reasonable degree of medical probability that the pregnancy was complicated by Maternal Diabetes, that fetal testing at 34 weeks suggested fetal distress, that based on available medical records, the mother did not appear to be in labor at time of delivery by Cesarean section, and that the baby suffered severe oxygen deprivation and resulting brain damage. Overall findings suggest that severe brain injury occurred at some time prior to hospital admission and, therefore, prior to delivery. A review of the file does not show any opinion contrary to Dr. Willis’ opinion that Sherita Leeks was not in labor prior to delivery and that Jer’Donis suffered severe oxygen deprivation resulting in brain injury prior to admission to the hospital and delivery is credited.
