The Issue At issue is whether Tyler Baker, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact 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. In contrast, NICA offered the testimony of Donald Willis, M.D., a physician board- certified in obstetrics and gynecology, as well as maternal- fetal medicine, and Michael Duchowny, M.D., a physician board- certified in pediatrics; neurology, with special competence in child neurology; and clinical neurophysiology. Dr. Duchowny is a pediatric neurologist associated with Miami Children's Hospital, who evaluated Tyler on January 16, 2008. Based on that evaluation, as well as his review of the medical records associated with Tyler's birth and subsequent development, Dr. Duchowny concluded that, although Tyler was permanently and substantially mentally and physically impaired, the cause of such impairment was likely a developmentally-based brain abnormality, as opposed to a brain injury caused by oxygen deprivation or mechanical injury during labor, delivery, or the immediate postdelivery period. Dr. Duchowny offered the following basis for his opinion: That opinion is based on several factors. If one looks through the records, it's clear that when Tyler was born, he had reasonably good Apgar Scores, and was actually relatively stable at birth. By that I mean, he didn't show evidence of any respiratory embarrassment. He did not require intubation and mechanical ventilation, and he did not show evidence of multi-system organ involvement of, for example, the heart, the liver or kidneys, as one would expect in a child who suffered from hypoxic ischemic damage or mechanical injury. Furthermore, Tyler's normal MRI scans of the brain argue strongly that there was no damage due to mechanical injury or oxygen deprivation at birth. Q. And why is that, Dr. Duchowny? A. If Tyler's neurological problems were caused by lack of oxygen at birth, one would expect to see changes on his MRI scan of the brain. Particularly, one would expect to see evidence of brain atrophy, enlargement of the ventricles deep within the brain or possibly abnormalities of white matter. None of these findings are evident in Tyler's MRI scan, suggesting that lack of oxygen at birth is simply not a realistic possibility. (Respondent's Exhibit 2, pp. 14 and 15). Similarly, Dr. Willis, based on his evaluation of the medical records, concluded that Tyler did not suffer a brain injury due to oxygen deprivation or mechanical injury occurring during labor, delivery, or resuscitation. Dr. Willis based his opinion on the fetal monitor strips, which did not reveal any significant abnormalities that would be suggestive of fetal distress; Tyler's Apgar score of 8 at five minutes, which was normal; and Tyler's newborn course, which was uncomplicated. The opinions of Doctors Duchowny and Willis were rationally based, and not contradicted. Consequently, it must be resolved that the cause of Tyler's neurologic impairments was likely a developmental brain disorder, as opposed to a birth- related brain injury. See 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."); 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 Tyler suffered a "birth-related neurological injury," as required for coverage under the Plan.
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 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 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 this proceeding is whether Shalyn L. Hayman, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Shalyn L. Hayman (Shalyn) is the natural daughter of Rosalee Hayman and Basil Hayman. She was born a live infant on January 6, 1993, at St. Mary's Hospital, a hospital located in West Palm Beach, Palm Beach County, Florida, and her birth weight was in excess of 2,500 grams. The physician providing obstetrical services during the birth of Shalyn was John Pauly, M.D., who was, at all time material hereto, a participating physician in the Florida Birth- Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. The parties have stipulated and the proof demonstrates, that Shalyn is permanently and substantially mentally and physically impaired. What is at issue is the cause and timing of the event or events giving rise to such impairment or, stated differently and pertinent to these proceedings, whether Shalyn's impairment resulted from an "injury to the brain or spinal cord . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery or resuscitation in the immediate post-delivery period in the hospital." Section 766.302(2), Florida Statutes. Mrs. Hayman's antepartum course and Shalyn's delivery Mrs. Hayman's pregnancy was essentially uncomplicated, except for being post-term. In this regard, it is noted that Mrs. Hayman's due date was established as December 25, 1992, at forty weeks gestation, and that when delivered on January 6, 1993, Shalyn was almost two weeks overdue, a high risk situation. At or about 5:30 a.m., January 6, 1993, Mrs. Hayman presented to St. Mary's Hospital. At the time, Mrs. Hayman was experiencing mild, irregular contractions, and vaginal examination revealed the cervix to be at 1 to 2 centimeters, effacement at 50 percent, and the fetus at station -1. The membrane was noted to be intact, and monitoring revealed a fetal heart tone in the 130's, with poor variability and no observed reactivity. Given the circumstances, Mrs. Hayman was admitted to the labor and delivery area at or about 6:00 a.m. At or about 7:50 a.m., Mrs. Hayman's contractions were still noted as irregular; however, vaginal examination revealed her cervix was changing, and it was recorded at 2 centimeters, effacement at 80 percent, and the fetus at station -3. Fetal monitoring reflected a fetal heart tone in the 140's, but an abnormal pattern, with decreased variability, lack of acceleration, and persistent late decelerations. That heart rate and pattern persisted through delivery. Mrs. Hayman's labor continued to progress slowly, and at 9:20 a.m. vaginal examination revealed the cervix to be 3 centimeters, with effacement at 80 percent, and at 10:44 a.m. the cervix was noted to be 4 to 5 centimeters. At 10:55 a.m., labor was augmented with Pitocin, and thereafter progressed fairly normally. At 1:55 p.m., January 6, 1993, Shalyn was delivered vaginally. Upon delivery thick meconium stained fluid was noted, but none was present below the cords. Shalyn initially required intubation and bagging with 100 percent oxygen for a low heart rate and poor respiratory effort, but was extubated at approximately 10 to 15 minutes of age in the delivery room. Her Apgar scores were 4, 7 and 8 at one, five and ten minutes. 3/ Shalyn was noted to have the physical stigmata of Down's syndrome, which was later substantiated by chromosomal analysis, and was ultimately transferred to the neonatal intensive care unit (NICU) for further care and management. Following admission to the NICU, Shalyn failed to maintain appropriate respirations or oxygenation, and she was re- intubated and placed on ventilator support. Her hospital course was consistent with severe persistent pulmonary hypertension of the newborn, and she required extensive ventilator support. Cardiac disease was ruled out by echocardiogram. Shalyn's initial hematocrit was 57 with a platelet count of 43,000. The reason for this thrombocytopenia was unknown, although Down's syndrome or perinatal depression were considered as possibilities. On January 7, 1993, Shalyn developed symptomatic polycythemia and a partial exchange transfusion was done. The same day, Shalyn suffered cardiac arrest, which responded to epinephrine and Bicarb. On January 8, 1993, Shalyn was noted to have developed seizure activity, which was treated with Phenobarbital, Dilantin and intermittent lorazepam before the seizures were under control. An electroencephalogram demonstrated bilateral spiked discharges. In response to the seizure activity, a neonatal head ultrasound was taken on January 8, 1993, to rule out intraventricular hemorrhage. The ultrasound was entirely normal, with no evidence of hemorrhage into the ventricular system or the tissue immediately surrounding the ventricle. Shalyn was slowly weaned from ventilatory support and by January 11, 1993, was on an oxygen hood, and by January 14, 1993, was on room air. Physical examination on January 12, 1993, revealed Shalyn to be alert and active under the oxygen hood, her anterior and posterior fontanelle open and flat, not bulging, and neurologically to demonstrate good activity, but decreased tone. On January 15, 1993, Shalyn underwent a CT brain scan to rule out congenital malformation. That scan revealed the following: There is a large right sided intracerebral hematoma involving the occipital area with mild mass effect on the right lateral ventricle. There is a much smaller area of intracerebral hematoma anterior to the larger one in the high frontal parietal area and there is a tiny intracerebral hematoma in the high left frontal parietal region. There is also some hemorrhage in the body of the left lateral ventricle and the ventricular system shows mild dilatation but no midline shift. There is no extra-axial fluid collections. IMPRESSION: There are bilateral intracerebral hematomas but the primary and largest one is located in the right parietal occipital region and causing mild mass effect on the ventricular system. There is minimal hydrocephalus with no midline shift. There is some extension into the ventricular system with blood in the left lateral ventricle. A follow-up head ultrasound was administered on January 23, 1993. In contrast to the head ultrasound conducted on January 8, 1993, the January 23rd ultrasound clearly demonstrated "a dilated ventricle system with bilateral intraventricular hemorrhage with large right occipital parenchymal bleed, essentially unchanged from the previous CT scan" of January 15, 1993. On January 25, 1993, Shalyn underwent a second brain CT scan. The January 25th scan indicated the hemorrhage was now resolving and had decreased in size. In place of the resolving hemorrhage, a resultant encephalomalacia was diagnosed. Subsequent CT scans have confirmed bilateral damage in the form of porencephalic cystic areas in the right temporal parietal and occipital lobes. These areas are consistent with the resolution of an infarct and hemorrhage. The focal damage to Shalyn's brain, evident from the CT scans, is consistent with an injury caused by an intraventricular hemorrhage, but is not consistent with the global changes to the structures of the brain associated with asphyxia. Shalyn was discharged from St. Mary's on January 30, 1993, with evident neurologic impairment. Currently, Shalyn is microcephalic, cortically blind, and has increased tone and spasticity of all four limbs, with very limited motor development. In sum, neurological examination reveals a severe degree of both mental and motor impairment, that is permanent in nature. The cause and timing of Shalyn's injury In addressing the cause and timing of Shalyn's injury, it is first observed that Shalyn has been diagnosed with Trisomy 21, also known as Down's Syndrome. Down's Syndrome is a genetic condition, which often results in mental and physical impairment. In Shalyn's case, however, her neurological impairments are significantly different and more severe than one would normally expect in a child suffering only from Down's Syndrome. Consequently, it must be concluded that Down's Syndrome is not the cause of Shalyn's current impairments. Having rejected Down's Syndrome as the cause of Shalyn's injury, the only logical conclusion to be drawn from the proof is that the injury Shalyn suffered to her brain was occasioned by a large intracerebral hemorrhage, and not asphyxia. In so concluding, it is observed that the pattern of her brain damage is focal, as opposed to the global damage one would attribute to asphyxia. Moreover, the medical records do not evidence associated organ damage, which would normally be present if Shalyn had suffered acute hypoxia. Finally, while the delivery records clearly reflect an abnormal fetal heart rate from the onset of labor, no pattern developed that would reflect acute hypoxia or an asphyxial state during labor or delivery and, as heretofore noted, there was no objective evidence of brain damage consistent with asphyxia. Consequently, it is unlikely that Shalyn suffered a hypoxic episode during labor or delivery. Having resolved that the cause of Shalyn's brain injury, and the resultant permanent and substantial mental and physical impairment, was the intracerebral hemorrhage she suffered, it becomes necessary to address the timing and origin of that hemorrhage. As for the timing, the proof demonstrates that Shalyn's ultrasound of January 8, 1993, demonstrated a normal ventricular system and no evidence of hemorrhage; however, the CT brain scan of January 15, 1993, did reveal the presence of such hemorrhage. Therefore, based on the medical evidence of record, it is reasonable to conclude that Shalyn experienced the disabling intracerebral hemorrhage sometime between January 8, 1993, and January 15, 1993, or, stated differently, after labor, delivery and resuscitation in the immediate post-delivery period. As for the cause of the hemorrhage, the proof demonstrates that, shortly after birth, Shalyn developed polycythemia, and that polycythemia is associated with hemorrhages, including hemorrhagic stroke. 4/ Given the proof, the opinion of Michael Duchowny, M.D., a board certified pediatric neurologist associated with Miami Children's Hospital, that Shalyn's hemorrhage most likely was associated with her polycythemia and was not related to any event during the birth process, is credited.
The Issue Whether Madison McCorkle, III, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan). Whether the notice provisions of the Plan were satisfied by the participating physician.
Findings Of Fact Preliminary Findings Petitioner, Rebekah Leah Scarfone, now Rebekah Scarfone Jackson, is the mother and natural guardian of Madison McCorkle, III, a minor. Madison was born a live infant on June 2, 1999, at Morton Plant Hospital, a hospital located in Pinellas County, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Madison's birth was Stanley E. Rosewater, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan. Madison's Birth At or about 1:15 a.m., June 2, 1999, Ms. Scarfone (with an estimated date of delivery of June 3, 1999, and the fetus at term) presented to Morton Plant Hospital, in labor. At the time, Ms. Scarfone's membranes were noted as intact, and vaginal examination revealed the cervix at three centimeters dilation, effacement at 90 percent, and the fetus at -1 station. Contractions were noted at a frequency of four minutes, with a duration of 70-80 seconds, and fetal monitoring revealed a reassuring fetal heart rate, with a baseline of 125-130 beats per minute. From 1:15 a.m. until 3:48 p.m., when she was first evaluated by Dr. Rosewater, Ms. Scarfone's labor progress was slow, but steady, and fetal monitoring continued to reveal a reassuring fetal heart rate. At 3:48 p.m., Dr. Rosewater's vaginal examination revealed the cervix at nine centimeters, effacement at 100 percent, and the fetus at 0 station. Thereafter, commencing at or about 4:35 p.m., and continuing until 6:00 p.m., when the fetal heart rate was noted at 50-60 beats per minute and Ms. Scarfone was moved to the operating room for a stat forceps delivery, a pattern of deceleration in fetal heart rate developed. Following admission to the operating room, at 6:13 p.m., the fetal heart rate was noted in the 160 beat per minute range, anesthesia was started at 6:15 p.m., forceps were applied by Dr. Rosewater at or about 6:25 p.m., and Madison was delivered at 6:29 p.m. According to the delivery notes, the cord was observed around the baby's shoulder during delivery, and reduced, and following delivery the baby was bulb suctioned on the perineum and taken to a warmer for resuscitation by the neonatology team. At delivery, Madison was depressed (limp, without spontaneous respiration), and required positive pressure ventilation for about one minute before spontaneous respiration was achieved. Apgar scores were recorded as 2, 7, and 7, at one, five and ten minutes, respectively.2 Following delivery, Madison was transferred to the neonatal intensive care unit (NICU) and at or about 10:15 a.m., June 3, 1999, with evidence of seizure activity, he was transported to All Children's Hospital for further management. On discharge from All Children's Hospital on July 1, 1999, Madison's Neonatal Discharge Summary described his history as follows: Discharge Diagnoses: Term Male Infant Perinatal Depression Hypoxic Ischemic Encephalopathy Seizures Right Optic nerve Hypoplasia and Left Macular Edema Acute Tubular Necrosis Evolving Encephalomalacia Right Submandibular Fat Necrosis * * * HISTORY: Baby Boy Scarfone was born by a forceps delivery with a vertex presentation to a 20 year old G1P0 mother. Apgars were 2,7, and 7 and 1, 5, and 10 minutes respectively. Birth weight was 3210 gms and estimated gestational age was term. Maternal history was significant for: blood type A+, HBS Ag-, RPR nonreactive, and Group B strep negative. During labor there were deep variable decelerations. The mother took prenatal vitamins and received Pitocin. This was a forceps delivery and the cord was noted to be around the body. Delivery room resuscitation included whiffs of oxygen and positive pressure ventilation via mask. Care at the referring hospital included intubation and ventilation, peripheral IV fluids, umbilical arterial catheter placement, Dopamine, normal saline boluses x 3, and sodium bicarbonate were given. Cranial ultrasound was performed.[3] Blood cultures were drawn and Ampicillin and Gentamicin initiated. The infant was noted to have 4 episodes of seizure activity and was started on Phenobarbital. The infant was transferred to All Children's Hospital for perinatal depression and seizures. RESPIRATORY: The infant was admitted on room air. The initial chest x-ray showed clear lung fields. The infant developed stridor, with feedings, at 21 days of life. A Pulmonology consult was obtained. An OPMS study was recommended. No evidence of aspiration or suck, [s]wallow, incoordination was noted. The pulmonologist did not feel a bronchoscopy was needed at this time. The infant had a sleep study performed with pH probe at 21 days of life. There were numerous central apneas and transient desaturations. There was no evidence of reflux. The infant was also studied in a car seat which showed intermittent central apnea, mixed apnea, and a few obstructive apneas and desaturations. The infant will be discharged home with an apnea monitor. He will also receive oxygen and when traveling will be placed in a car bed. He will have Pulmonology follow up 2 weeks after hospital discharge. CARDIOVASCULAR: The infant had hypotension due to perinatal depression at newborn day of age and required treatment with volume expansion and Dopamine for 4 days. * * * INFECTION: Blood cultures were obtained at the referring hospital. The infant was started on Ampicillin and Gentamicin. Gentamicin was discontinued due to increased creatinine level. Ampicillin was continued for a total of 3 days. * * * CENTRAL NERVOUS SYSTEM: The infant was admitted with a diagnosis of seizures which were treated with Phenobarbital, Dilantin, and Ativan. The infant was evaluated by Neurology. A CT scan at 1 day of age for perinatal depression revealed bra[i]n edema in the left parietal/occipital region. A MRI, at 5 days, revealed probably left cerebellar intraparenchymal subacute hemorrhage, abnormal signal in the left hemisphere and basal ganglia probably representing infarction. The infant was evaluated by Ophthalmology on 6/4/99 for retinal (macular) edema and right optic nerve hypoplasia. [H]e will be followed by Ophthalmology. A repeat CT scan, at 19 days of life, revealed evolving encephalomalacia. A follow up EEG at 22 days of age was within normal limits. At the time of hospital discharge the infant is receiving Phenobarbital with the last level 14.4. He will be followed by Neurology and have a follow up Phenobarbital level in one week. Due to the history of perinatal depression the infant will require developmental follow up, occupational therapy, and physical therapy intervention. . . . Discharge planning included follow-up with his pediatrician at Mother and Child Care (Dr. K. Adnan); Ophthalmology (Dr. J. Bruce Hess); Neurology (Pediatric Neurology Associates, P.A.); occupational therapy/physical therapy (Morton Plant Hospital - Barrett Center, Outpatient Rehabilitative Services); and the Early Intervention Program. Madison's Subsequent Development Madison received a physical therapy evaluation at the Barrett Center on July 13, 1999, and an occupational therapy evaluation on August 10, 1999, to assess his need for rehabilitative services. Assessment on physical therapy evaluation was, as follows: Musculoskeletal Status Madison presents normal to mild high tone. Range of motion marked by tightness in hip and knee flexion; range of motion of feet within normal limits for his age, but Madison has a tendency to maintain feet dorsiflexed. Madison has increased flexion recoil of lower extremities during range of motion testing and when placed in various positions. Recommendation was "[s]tart Physical Therapy services once a week; re-evaluation in six months." Assessment on occupational therapy evaluation was, as follows: Madison had normal tone in his upper extremities. He had the age appropriate grasp reflex. Passive and active range of motion of the upper extremities was within normal limits. Under the circumstances, occupational therapy was not recommended, but follow-up screening in three months to monitor progress was suggested. Thereafter, by February 8, 2000, Madison was also receiving occupational therapy. Madison had his first evaluation under the Early Intervention Program on August 2, 1999. The results of that evaluation were reported, as follows: Neurological Dubowitz is done with the patient in quiet alert state. Although he cries to aversive stimuli, he consoles readily with holding and a nipple. Movement and tone reveals symmetric arm and leg recoil. Flexion responses are initial in upper and lower extremities. There is some increase in tone in the lower extremities. Although head lags behind the body when brought from supine to sitting, in supported sitting he attempts to bring head upright from both anterior and posterior positions. In prone, he rolls head to the side and brings hand to shoulder level. No abnormal movements are noted. Reflexes indicate symmetric Moro response. Walking reflex is present. Palmar grasp is maintained. Suck is regular with good stripping. Neurobehavior includes conjugate eye movements, turning toward a rattle, and following a bright object horizontally and vertically. * * * Dubowitz Neonatal Neurological Examination is suspicious due to increased tone in the lower extremities. * * * EARLY INTERVENTION PROGRAM PLAN: * * * Recommend continuing with physical therapy on weekly basis. Madison was re-evaluated under the Early Intervention Program on May 12, 2000. According to standardized testing, Madison's cognitive skills were considered at risk for delay for his chronological age of 11 months 10 days; however, communication screening indicated his receptive and expressive language skills were age-appropriate. Neurological examination revealed that tone was mildly low, movements symmetrical. Recommendation was to follow-up in six months to monitor Madison's growth and development. Madison's next evaluation under the Early Intervention Program was on November 10, 2000, at age 17 months 8 days. At the time, assessment was "[c]ognitive skills are delayed at a 13 month age level"; [m]otor skills are within normal limits at a 16 month age level"; and "[c]ommunication skills are in an at risk category with both receptive and expressive language at a 14 month level." Based on such evaluation, a homebound teacher was recommended one hour per week to work on cognitive and communication skills, and physical or occupational therapy were no longer deemed developmentally necessary. Nevertheless, according to the records of Pediatric Neurology Associates, discussed infra, physical and occupational therapy continued. Subsequently, in early 2001, Madison was also accorded speech therapy. Madison's initial evaluation at Pediatric Neurology Associates, was on August 2, 1999. The results of that evaluation were noted, as follows: This 2 month old was seen for a hospital follow-up for experiencing difficulties at birth. He has suffered perinatal depression and then neonatal seizures. There have been no seizures since hospitalization. * * * PHYSICAL EXAMINATION: The patient is a well- developed, well-nourished 2 month old white male. Head circumference is 38.5 centimeters, which is at the 50th percentile. There are no skin rashes noted. Anterior fontanel is soft and flat. Head and facies are symmetric without dysmorphic features. He does track objects. The pupils are equal, round, and respond to light, and constrict, bilaterally, to light. The conjunctivae are pink. The funduscopic examination demonstrates a positive red reflex. Tongue and palate are symmetric. There is upper respiratory congestion. Neck is supple without lymphadenopathy. Chest is clear to auscultation, bilaterally. Heart demonstrates regular rate and rhythm with normal S1 and S2. Spine is straight without masses, lesions, or dimples. Abdomen is soft and round without hepatosplenomegaly or tenderness. Full range of motion noted. There are no motor asymmetries identified. Tone is within normal limits. Deep tendon reflexes are +2. Response to plantar stimulation is withdrawal, bilaterally. LABORATORIES: EEG, performed 06/04/99, is abnormal because of excessive sharp transients in the left posterior and central vertex region. EEG, performed 06/22/99, is normal. CT of the brain, 06/21/99, demonstrates peripheral foci of abnormal low density within the left parietal occipital region. High left parietal convexity and possibly more anteriorly within the left parietal lobe, as above. These regions likely represent evolving and encephalomalacia, possibly secondary to infarction, infection, or other brain insult. MRI of the brain, 06/07/99, demonstrates probably left cerebellar intraparenchymal early subacute hemorrhage. Abnormal signal in the left hemisphere, especially parietal occipital and in the basal ganglia (especially right thalamus) probably represents infarction. Phenobarbital level, 06/14/99, is 19.2 (15 to 40). IMPRESSION: Hypoxic ischemic encephalopathy. Seizures, which are currently under control. Perinatal depression. Right optic nerve hypoplasia. PLAN: Will obtain Dr. Hess' ophthalmologic report.[4] Will begin weaning Phenobarbital . . . . Madison was also seen at Pediatric Neurology Associates (or Children's Medical Services Clinic) on November 12, 1999, February 8, 2000, November 27, 2001, and June 26, 2002. Initially, Ms. Scarfone reported no evidence of seizure activity, abnormal movements, or altered consciousness; however, on November 27, 2001, she reported a paroxysmal episode ("a spasm or seizure") had occurred, about two weeks previous. A CT of the brain on November 30, 2001, demonstrated: Small focal area of decreased attenuation in the high left parietal area peripherally. This probably represents a small area of encephalomalacia. No definite additional areas of abnormal attenuation are identified. Specifically, the fairly prominent area of low attenuation seen in the left posterior parietal area on the previous study of 06/21/99 is no longer seen. No new abnormalities are appreciated. Subsequently, on June 26, 2002, Ms. Scarfone reported paroxysmal episodes, at one episode per month for the previous four to five months. At the time, the "Plan" included "[f]ollow- up in C[hildren's] M[edical] S[ervices] within the next two to four months," "[i]n the meantime, obtain a CT of the brain, noncontrast and repeat the EEG," and "[i]f episodes should continue, may consider an empirical trial of anticonvulsant therapy." On October 3, 2002, Madison had a prolonged seizure. At the time, the head CT scan was negative; however, EEG of October 4, 2002, was abnormal, and Madison was placed on maintenance Dilantin, which, given allergic reaction, was changed to Depakene and then to Keppra. Madison's follow-up visit at Pediatric Neurology Associates on December 18, 2002, was reported, as follows: This 3 year old returns for a follow-up for history of hospitalization for seizure exacerbation. His mother reports his seizures usually start with waking up out of his sleep with coughing and then vomiting. He will stare and then go into tonic-clonic activity. The last event was one to two weeks ago. DEVELOPMENT: He is in multimodal therapies at school for a history of developmental delay. PAST MEDICAL HISTORY: He has a history of anoxic encephalopathy and seizures. PHYSICAL EXAMINATION: The patient is a 3 year old, male weighing 43 pounds (19.5 kilograms). Height 39-3/4 inches. Blood pressure is 86/44. Heart rate is 108. There are no skin rashes noted. * * * The extraocular movements are full and intact without nystagmus noted. The pupils are equal, round, and respond to light, and constrict bilaterally to light. Convergence is positive. Conjunctivae are pink. The funduscopic exam demonstrates discs of normal color and sharp margins with no hemorrhage or exudates. He is slightly impulsive during the exam. The neck is supple without lymphadenopathy. The heart demonstrates regular rate and rhythm with normal S1 and S2. Full range of motion. Tone is slightly low. Reflexes are +2. Gait is without ataxia. * * * IMPRESSION: Seizure reoccurrence. PLAN: 1. Continue with Keppra . . . . 3. Follow-up will be in the CMS Clinic with Dr. Casadonte . . . Dr. Casadonte reported the results of his follow-up of April 18, 2003, as follows: Madison McCorkel [sic] presents to the CMS clinic. He's a child with seizures secondary to anoxic encephalopathy experienced at birth. He's on Keppra . . . . Mom reports he's had only one event in two months. The events are stereotypically where he awakens from his sleep. He coughs and stares. They last several minutes and then he's sleepy afterwards. He is three years 10 months . . . . He's alert. Pupils are equal and reactive. His face is symmetric. He moves his extremities equally. He attends Fuguitt Elementary through the FDLRS program. The plan is to continue Keppra . . . . Notably, Madison's medical records fail to support a conclusion that he is substantially mentally or physically impaired, much less permanently impaired, and none of his treating physicians has expressed such an opinion. It is also worthy of note that, while Respondent presented the testimony of Dr. Michael Duchowny, discussed infra, to address the issues, neither Petitioner nor Intervenors, although they had the burden to prove Madison suffered a birth-related neurological injury, offered any expert testimony to establish that Madison's current deficits resulted from a brain injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation, or that Madison was permanently and substantially mentally and physically impaired. Dr. Duchowny, a physician board certified in pediatrics, neurology with special competence in child neurology, and clinical neurophysiology, examined Madison, at NICA's request, on September 11, 2002, and reported the results of his evaluation, as follows: Madison's NEUROLOGIC EXAMINATION reveals him to be overactive, inattentive, and impulsive. He maintains poor eye contact and it is difficult to keep him on track for the evaluation. He is quite defensive and, for example, fends off attempts to have his fundi looked at in detail. There are marked imitative gestures and repetitive movements. He tends to wave goodbye throughout the evaluation in a semi-repetitive fashion. The speech sounds are poorly articulated for lingual, labial, and guttural consonance and it is very difficult to understand his speech output. He tends to speak in one or two words. He could identify some body parts but not others and was not able to articulate colors in any specific fashion. It was difficult to keep his attention span on track. The cranial nerve examination reveals full visual fields to direct confrontation testing. He blinks to threat in both directions and reacts to sound in all planes. The pupils are 3mm and briskly reactive to direct and consensually presented light. I could not get a full fundoscopic evaluation. The tongue and palate move well. The uvula is midline. Motor examination reveals symmetric strength and bulk. His tone is slightly diminished throughout and his movements are uncoordinated. He postures his outstretched hands in a very marked fashion and there is marked decomposition of rapid alternating movement sequences. He has distal career from movements as well. There is no focal weakness or atrophy. The deep tendon reflexes are 1+ bilaterally. His gait and station are stable. There is pesplanus bilaterally. He did not fall while walking. The spine is straight without dysraphism. There is withdrawal of all extremities to provocation. Neurovascular examination discloses no cervical, cranial or ocular bruits, and there are no temperature or pulse asymmetries. IN SUMMARY, Madison's neurologic examination is significant for developmental delays in multiple areas. He is clearly delayed in terms of his expressive and receptive language skills, and has a speech articulation defect. He also has a short attention span, high activity level, and an impulsive behavioral style. Marked dyspraxia is also noted. Apart from these developmental findings, there are no focal or lateralizing features to suggest structural brain damage and I believe that Madison most likely has a pervasive developmental disorder and is at risk for falling within the autistic spectrum in the future. . . . I have not as yet had an opportunity to review Madison's medical records and will issue a final report once the review process is complete. Following review of the medical records, Dr. Duchowny concluded: A review of the medical records suggests that the pregnancy with Madison was complicated by a probable vira[l] infection, as evidenced by the placental pathology, ophthalmology findings, elevated liver function tests, and neuro-imaging findings. The findings on Madison's neurologic examination are most consistent with the developmental syndrome of pervasive developmental disorder, and I strongly suspect that Madison will ultimately be diagnosed with childhood autism. Given these findings, I do not believe that Madison suffers from a substantial motor or mental impairment, or that h[is] problems were acquired in the course of labor, deliver, or the immediate post partum period. Stated otherwise, while Dr. Duchowny acknowledged that Madison's birth was stressful, and resulted in a number of problems that had to be managed post-delivery, he was of the opinion that the deficits Madison currently exhibits are "developmentally based, meaning that they have to do with abnormalities during the formation of the brain as opposed to consequences of hypoxia, ischemia or trauma." (Respondent's Exhibit 3, at page 30.) As for Dr. Duchowny's opinion that Madison does not suffer from a substantial motor or mental impairment, it is worthy of note that, although they had the opportunity to do so during the course of his deposition, the parties did not challenge or otherwise question his opinion. Finally, pertinent to a current assessment of Madison's neurologic presentation is the deposition testimony of Ms. Scarfone, taken July 21, 2003. (Hospital Exhibit 2.) At the time, Ms. Scarfone offered the following observations: Q Is Madison currently enrolled in any school or educational program? A Yes. Q Where? A Fuguitt elementary in the FDLRS Program. Q What is the FDLRS Program? A It's for kids that have developmental problems, autistic children, for kids that are developmentally delayed. Q Is that a year-round program? A Yes. He was in pre-K, and he's going to be in pre-K again. Q Has he been diagnosed as suffering from autism? A No. Q What kind of developmental delays does he have? A Speech. He's four. They say that he's at age three. So I guess that would be developmental altogether. Q What other developmental delays does he have other than speech? A He's not like other kids. I mean, he's behind. I don't know what - what it would be called. I mean, he's four years old, and he acts as if he's three. I mean, healthwise, I mean, his vision is bad in his left eye, and he has seizures. Q Describe the seizures for me. A Before he was not placed on the medicine, he would wake up from a nap, and he would have convulsions. Since he's been placed on the medicine, he will just wake up with the gagging effect, and he'll just stare off. And he'll last maybe like a minute or two, and then he'll - it will go away, and he'll just want to go to sleep. Q How often does he have these seizures? A Since he's been on the medicine, he usually has maybe one to every three months. Q Does he have any problem with swallowing? A No. Q Does he have any motor problems? A Motor skills? Q Yes, ma'am. A I was told that he did, yes. Q By whom were you told? A I don't recall. Plenty of people have told me, but it was a certain program that I used to take him to. I was told by his occupational therapist that he had, and I don't remember what it was called. Q Is he currently enrolled in any programs designed to assist him with any motor problems? A No. Q What kind of motor problems has he had in the past? A He was delayed when he was young. He, like, wasn't sitting up when he should. They had to - I had to take him to therapy to set him up because his - when he was born, his legs were bowed up. I had to take him to therapy to stretch his legs. He was late sitting up and crawling, walking, stuff like that. Q Does he currently have any motor deficits? A No. Q He is able to walk, run, jump? A Yes. Q Skip? A Yes. Q As far as you're concerned, whatever motor problems he's had in the past with his legs have resolved? A Yes. Q Does he have any motor problems with his hands or arms? A No. * * * Q Fuguitt Elementary is a public school? A Yes. Q And he's going to be repeating the pre-K program? A Yes. Q Is he in school today? A No. He starts back when school starts back. Q Has he been off for the summer? A Yes. Q What has he been doing? A Stays home with me. Q And his brother? A Yes. A And his two stepsisters? A Yes. . . . Q Okay, Has he had any sort of therapy this summer? A Yes, he takes speech therapy in FDLRS. Q So even though school is not ongoing, that particular program provides some sort of summer therapy? A Oh, I'm sorry, no, not for the summer. No, he hasn't done anything in that. Q He hasn't had any kind of therapy since school let out in May? A No. Q Other than that which he receives at school, is he receiving any sort of therapy? A No. * * * Q Has anyone suggested to you now that he is in school, that he needs anything in addition to that which the school is providing? A No. I did sign - well, I did sign a paper for his school for vision. They wanted to see if he qualifies for vision class or vision therapy. Q You said it's the one eye that's bad, the left - A The left eye. * * * Q . . . Other than the problem with his left eye and the problems he has with respect to speech, are there any other objective problems that you, as his mother, have observed? A He's very active, very hyper. Q Has he been treated for that hyperactivity? A No. Coverage Under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post- delivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired."5 Section 766.302(2).6 See also Section 766.309. Here, given the proof, it must be resolved that Madison suffers neither a substantial mental impairment nor a substantial physical impairment, much less a permanent and substantial mental and physical impairment required for coverage under the Plan. Moreover, given Dr. Duchowny's observations, and the paucity of proof to the contrary, it cannot be resolved, as suggested by Intervenors, that the cause of Madison's deficits resulted from a brain injury caused by oxygen deprivation or mechanical injury that occurred during labor, delivery, or resuscitation, as opposed to a developmental abnormality, that preceded the onset of labor. See Wausau Insurance Company v. Tillman, 765 So. 2d 123, 124 (Fla. 1st DCA 2000)("Because the medical conditions which the claimant alleged had resulted from the workplace incident were not readily observable, he was obliged to present expert medical evidence establishing that causal connection."); Thomas v. Salvation Army, 562 So. 2d 746, 749 (Fla. 1st DCA 1990)("In evaluating medical evidence, a judge of compensation claims may not reject uncontroverted medical testimony without a reasonable explanation.") The Notice Provisions of the Plan Pertinent to this case, at the time of Madison's birth, Section 766.316, Florida Statutes (1998), prescribed the notice requirement, as follows: Each hospital with a participating physician on its staff and each participating physician, other than residents, assistant residents, and interns deemed to be participating physicians under s. 766.314(4)(c), under the Florida Birth-Related Neurological Injury Compensation Plan shall provide notice to the obstetrical patients as to the limited no-fault alternative for birth-related neurological injuries. Such notice shall be provided on forms furnished by the association and shall include a clear and concise explanation of a patient's rights and limitations under the plan. The hospital or the participating physician may elect to have the patient sign a form acknowledging receipt of the notice form. Signature of the patient acknowledging receipt of the notice form raises a rebuttable presumption that the notice requirements of this section have been met. Notice need not be given to a patient when the patient has an emergency medical condition as defined in s. [395.002(9)(b)][7] or when notice is not practicable. Here, there being no proof to support a contrary conclusion, Dr. Rosewater presumably did not provide Ms. Scarfone notice. See Balino v. Department of Health and Rehabilitative Services, 348 So. 2d 349, 350 (Fla. 1st DCA 1977)("[T]he burden of proof, apart from statute, is on the party asserting the affirmative issue before an administrative tribunal.") However, at the time, he was not required to do so. Notably, Section 766.316, Florida Statutes (1998), describes those circumstances under which notice need not be given, as follows: . . . Notice need not be given to a patient when the patient has an emergency medical condition as defined in [s. 395.002(9)(b)] or when notice is not practicable. Pertinent to this case, Section 395.002(9)(b), defines "emergency medical condition" to mean: (b) With respect to a pregnant woman: * * * 3. That there is evidence of the onset and persistence of uterine contractions or rupture of the membranes. Here, on presentation to Morton Plant Hospital, there was clear evidence of the onset and persistence of uterine contractions. Consequently, Dr. Rosewater was not required to provide Ms. Scarfone with notice.
The Issue At issue in this proceeding is whether Joiner Abelove, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary matters John Abelove and Kathryn Abelove are the parents and natural guardians of Joiner Abelove (Joiner), a minor. Joiner was born a live infant on January 29, 1992, at Cape Canaveral Hospital, a hospital located in Cocoa Beach, Florida, and his birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Joiner was Fred Turner, M.D., who was, at all times material hereto, a participating physician in the Florida Birth- Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Mrs. Abelove's antepartum course and Joiner's birth Mrs. Abelove's antepartum course was without apparent complication; however, by late January 1992, the fetus was noted to be large for gestational age and her obstetrician/gynecologist proposed to induce labor. Mrs. Abelove presented to Cape Canaveral Hospital for a Prostin/Pitocin induction of labor at or about 8:30 a.m., January 28, 1992, and was immediately placed on a fetal monitor. Fetal heart rate (FHR) was reassuring, with a baseline of 148 to 154 beats per minute and good variability.1 Mrs. Abelove received her first Prostin gel, as the first step in the induction of labor, shortly after admission, her second at or about 12:30 p.m., and continued with Prostin until about 7:00 a.m., January 29, 1992, when mild contractions were noted. Membranes were artificially ruptured at 7:25 a.m., revealing clear fluid, and onset of labor was confirmed at 7:30 a.m. At 9:25 a.m., Pitocin was started, and Mrs. Abelove's labor slowly progressed until 7:15 p.m., when she began to push. Until that time, the fetal heart rate tracing was unremarkable or, stated differently, revealed a reassuring fetal heart rate, with normal/average long and short term variability. When Mrs. Abelove began to push, variable decelerations were noted to the 120s for 10 to 20 seconds, with a return to the FHR baseline of 150 to 160 beats per minute. Several other decelerations of a similar nature were noted prior to delivery, but not in sufficient number or intensity to reflect fetal compromise or injury. At 9:18 p.m., January 29, 1992, Joiner, the product of a spontaneous vaginal delivery, was born. Nuchal cord X 3 was noted; however, cord blood pH was 7.36 (normal). Joiner was Deelee suctioned to clear mucus, stimulated and administered oxygen by bag and mask; however, he "did not come around to stimulation [as expected]" and was transported to the neonatal intensive care unit for further management. Joiner was assigned Apgars of 5, 5, and 7, at one, five, and ten minutes, respectively. The Apgar scores assigned to Joiner are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, muscle tone, reflex irritability, and color, with each category being assigned a score ranging from the lowest score of 0 through a maximum score of 2. As noted, at one minute Joiner's Apgar score totalled 5, with heart rate being graded at 2; respiratory effort, muscle tone and reflex irritability being graded at 1 each; and color being graded at 0. At five minutes Joiner's Apgar score was unchanged. At ten minutes, his Apgar score totalled 7, with heart rate, muscle tone and reflex irritability being graded at 2 each, respiratory effort being graded at 1, and color being graded at 0. Joiner was admitted to the nursery at 9:25 p.m., and administered whiffs of oxygen. At the time, Joiner was noted to be flaccid (decreased tone); evidence general cyanosis; and exhibit flaring, grunting, and retracting (evidence of respiratory distress). Moist lungs, bilaterally, were also observed. Otherwise, Joiner's newborn infant exam was grossly normal. At 9:28 p.m., Joiner was placed in a oxyhood at 30 percent oxygen, and then increased to 50 percent. By 9:30 p.m., Joiner's oxygen saturation was noted at 100 percent, and his color improving (now pale pink). At or about 9:40 p.m., Joiner was examined by a Dr. Radu and lab work and a chest x-ray were ordered. At 10:00 p.m., following the results of the lab work, Dr. Radu lowered the oxygen to 30 percent. Joiner's oxygen saturation was noted at 98 percent, and he was described as pink with occasional retracting. Chest x-ray noted no acute cardiopulmonary disease, and he was diagnosed with respiratory distress syndrome of the newborn, which proved to be transitory. Course of treatment was continued oxygenation via oxyhood. At 10:30 p.m., Joiner continued to exhibit occasional flaring, grunting, and retracting; however, his color remained pink and he was observed to be active. By 11:30 p.m., Joiner's respirations were described as easy or unlabored, and his color continued pink. His condition remained stable through the night and at 8:20 a.m., January 31, 1992, oxygen was discontinued. At 11:20 a.m., cardiac and oxygen saturation monitors were also discontinued, and Joiner was transferred to the central nursery. There, he was bathed and placed under a warmer. At 12:45 p.m., the warmer was discontinued and Joiner was delivered to Mrs. Abelove where he was noted to latch on and nurse well. At 3:10 p.m., Joiner, in apparent good health, was discharged with his mother from the hospital. Joiner's subsequent development and medical care Joiner was followed at The Pediatric Group, by Dr. Thomas Fisk, for regular routine well-baby care following his discharge from the hospital, and his early infancy was apparently unremarkable; however, some mild delays in gross motor skills were observed at some point during his first year of life. At 13 months, Dr. Fisk saw Joiner for a physical examination, and his mother and grandmother expressed concern over his developmental progress, primarily his expressive language. Regarding these concerns, Dr. Fisk also noted: [His grandmother and mother] did report, however, at that time that he had some new found skills, was verbalizing a lot more, and we decided to watch him over the next few months and see him back at 15 months. Review of the record revealed that he had no vocalization at 9 months, so he had made some progress. At 13 months he was not walking and the only problem that I noticed was what appeared to be some trunkal hypotonia. Joiner was next seen by Dr. Fisk at 16 1/2 months and he observed that Joiner was still suffering from a delay in receptive language and gross motor development. Specifically, Dr. Fisk observed: . . . In receptive language, he does not seem to follow commands or simple instructions very well and he presently says only "mama" and "dada", "no", and has a rather unusual flow of speech. He does not have normal jargon and vocalizations are more grunting and non-fluid in nature. From a gross motor standpoint, is still cruising, but has not begun independent walking. Observation of his gait reveals what appears to be some generalized hypotonia but fairly good strength. Movements involving the upper and lower extremities, however, are also not very fluid and are awkward, however, I cannot put my finger on what seems to be wrong otherwise more specifically. Dr. Fisk's conclusion was generalized developmental delay, and he referred Joiner to Dr. Frank Lopez, a member of the Society of Developmental and Behavioral Pediatrics, to direct the developmental evaluation; however, Joiner was apparently not evaluated by Dr. Lopez until May 29, 1997, as discussed infra. Joiner had a computer tomogram (CT) of the brain on July 23, 1993, which was normal. More specifically, the report noted: No masses are detected. There are no intracranial calcifications. The ventricles are normal. No abnormal fluid collections are seen. At the request of Dr. Fisk, Joiner was seen by Dr. Michael Pollack, a pediatric neurologist on January 17, 1995. Dr. Pollack's report of that examination reads, in pertinent part, as follows: NEUROLOGICAL EXAMINATION: During the initial portion of the office visit, the patient makes minimal eye contact with the examiner. Subsequently he displays more social interaction both with the examiner and with his parents. He engages in mildly mischievous behavior and appears amused. He is not able to stack rings in order after demonstration and does not assemble a Gesell Form Board after demonstration. He does not point to body parts on request. He produces no intelligible words during the office visit and makes minimal attempt to communicate by gesture. He scribbles but does not attempt to copy a figure. Joiner is quite active and enjoys scattering rings about the room but displays no interest in representational play and very little interest in interactive play with the examiner. He does not vocalize abundantly. He does turn to voice. Pupils are equal and reactive to light. Limited view of the ocular fundi shows no abnormalities. There is a full range of conjugate, horizontal eye movement without nystagumus. No facial weakness or significant asymmetry are present. Gag reflex is preserved. Gait is normal. He is not able to cooperate for testing of strength or coordination but functional testing suggests normal strength in all limbs. Tendon reflexes are symmetrically ++ and plantar responses flexor. IMPRESSION: At a chronological age of almost 3 years, Jointer appears to be functioning below the 2 year level. He has facial features which raise the possibility of cerebral gigantism (Soto's syndrome), but these are relatively non-specific and it is noted that his facial features are similar to those of his father. In addition, multiple members of both families are tall as noted above. Although his most conspicuous delay is in the language sphere, other areas of cognitive development also appear to be affected. He has a number of features which fall in the autistic spectrum but does display the ability to interact socially as described above. He has had a variety of diagnostic studies, all of which have been normal. RECOMMENDATIONS: 1. Genetics consultation was suggested. 2. MRI scan of the head was also ordered since cerebral anomalies which are not evident on CT scan are sometimes demonstrated by MRI. The patient was referred to FDLRS and also to a speech/language pathologist. It is likely that he will benefit from medication to improve attention span and to reduce his high activity level, but, if the situation permits, it would be preferable to defer such medication for 1 or 2 years. His parents will call for the result of the MRI scan and the patient will return to the office for re-examination in one year. The results of the MRI scan and chromosome study were normal. Whether Joiner ever returned for re-examination by Dr. Pollack is not of record. Joiner continued to be followed by Dr. Fisk, who had resolved that Joiner suffered from pervasive developmental disorder. On Joiner's visit of June 4, 1996, at approximately 4 1/2 years of age, Dr. Fisk observed: . . . He attends Parton Elementary Pre-K program for children with developmental problems. Father indicates that he has made good progress especially with his expressive language over this last year, but he continues to be remarkably delayed. Expressive language skills are really at the 2-year level, and his visual attending is rated at the one-year level. He has very few skills above the 2-year level. He is extremely aggressive at school, very easily over stimulated, flaps his hands, stimulates himself, as is often seen in children with autism. He has much improvement when on his Ritalin with fair control over these particular symptoms, but the aggressive issue continues to be a major problem for the parents. Now that he is getting bigger, they literally can not go out of the house with him without getting into an aggressive situation. I have discussed in the past with these parents the need for him being involved with a specialist to manage his pervasive developmental delay. Insurance restrictions have preempted their attempts to do this, and they have been unwilling to see Dr. Frank Lopez here in town. I discussed his progress over the last year today in the office with the father. The last note of record by Dr. Fisk, relates to an office visit of February 27, 1997.2 At that time, Dr. Fisk observed: Patient well-known to me with pervasive developmental disorder. Joiner currently is in a developmental preschool situation and takes Ritalin. . . . Parents have noted a significant decrease in his aggressive tendencies and they have been helped out significantly by their present behavioral therapist who has gone to the school, come to their home, and tried to work a behavior program out for Joiner. He is much less aggressive, more cooperative in the classroom, settles down and does at least attend and participate, at least significantly more than he used to. He still has significant language problems, repeats a few words back when spoken to him, but is really still not putting words together in sentences; has significant communication difficulties. Has been feeling well over the time frame of the last several months. Mom was very reluctant originally to consider using Ritalin, but she has come to grips now with the fact that he seems to be doing well on it. They have not gotten involved with child psychiatrist, but have significant educational intervention ongoing. He does see OT and speech therapy as well. Been feeling well recently. Parents relate no medical problems. Uncooperative 5-year-old male who is tall for age, tends to cling to his dad in the office. He will ambulate, however, and cooperated with most of the exam until he had to lay down on the table. Even considering this, he was much better today than he has been in the past. . . . Chest is clear. Cardiovascular: normal. ABD: soft, nontender w/o organomegaly. GU: normal circumcised male. Testes descended. Back and extremities exam: essentially normal with normal gait. He has mild clinodactyly bilaterally. DTRs 2+ and symmetrical. Motor strength and tone equal and symmetrical as well. Hemoglobin today: 14.3. UA could not be obtained secondary to lack of cooperation - parents will be bringing that back. He could not cooperate with hearing or vision screen, but dad says he is scheduled to have his hearing retested next week. Joiner was seen by Dr. Frank Lopez on May 29, 1997. He observed, as follows: Joiner has been referred into this office by courtesy of Dr. Fisk. Joiner is here accompanied by his parents who serve as primary historians and report that he has been seen and had a work-up done by Dr. Colin Condron and Dr. Michael Pollack in the past. Their concerns are that they would like more information regarding Joiner's problems and "a more accurate diagnosis and supportive treatment plan." He has been diagnosed as Developmental Delay and Autistic Spectrum presentation. Mom and Dad are very concerned, not as much with the diagnostic category, but rather with how best to place and guide him. He is presently staffed into EMH at Partin Elementary and will be changing schools, going into TMH classroom due to his not keeping up. The Autistic Program has been considered, but the parents have not decided on its merits yet. Following consideration of Joiner's developmental history, family history, and physical examination, Dr. Lopez's impression was: Autism; Hypotonia; Dyspraxia. Given the proof, it cannot be subject to serious debate that Joiner suffers a serious neurologic impairment. What remains to resolve is the genesis of his impairment or, more pertinent to these proceedings, whether the proof supports the conclusion that his condition resulted from an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as required by Section 766.302(2), Florida Statutes, for coverage to be afforded by the Plan.3 With regard to such issue, Petitioners contend that Joiner suffered an injury to his brain caused by oxygen deprivation (an hypoxic event) during the course of resuscitation, and that such injury was the cause of Joiner's neurologic impairment. In contrast, Respondent contends the proof is not consistent with hypoxic ischemic injury occurring during or immediately following child birth, but is consistent with a pervasive developmental disorder or autism.4 Respondent's view of the proof has merit. The genesis of Joiner's neurologic impairment To address the genesis of Joiner's neurologic impairment, the parties offered selected medical records relating to Mrs. Abelove's antepartum and intrapartum course, as well as for Joiner's birth and subsequent development. Portions of those records have been addressed supra, and further salient portions will be addressed infra. The parties also offered the opinions of three physicians as to the likely cause of Joiner's disorder. The physician selected by Petitioners was Danuta Deeb, M.D., board certified in pediatrics. The physicians offered by Respondent were Edward Lance Wyble, M.D., board certified in pediatrics and neonatology, and Michael Duchowny, M.D., board certified in pediatric neurology, pediatrics, and clinical neurophysiology. The medical records and other documentary proof, as well as the testimony of the physicians offered by the parties have been carefully considered. So scrutinized, it must be concluded that the proof does not allow a conclusion to be drawn with any sense of confidence that, more likely than not, Joiner's neurologic impairment was associated with an injury to the brain caused by oxygen deprivation occurring during the course of labor, delivery, or resuscitation in the immediate post-delivery period. Rather, the proof demonstrates, convincingly, that Joiner's presentation is consistent with a pervasive developmental disorder, a disorder within the spectrum of childhood autism, which resulted from an anomaly in brain development, as opposed to a hypoxic ischemic injury during the birth process.5 In so concluding, it is observed that Joiner's course pre-delivery and post-delivery was inconsistent with hypoxic or ischemic injury having occurred during the course of labor, delivery, or resuscitation. First, the evidence documenting fetal heart rate during the course of labor and delivery does not support the conclusion that Joiner suffered an acute intrapartum event that led to hypoxic or ischemic injury.6 Further militating against the conclusion that Joiner's anomaly was caused by oxygen deprivation pre-delivery or new-onset hypoxia post-delivery, are the numerous inconsistencies between Joiner's presentation and development, and the clinical findings one would expect had he suffered hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, during that period. Notably, Joiner's Apgar scores were 5, 5, and 7 at one, five, and ten minutes. Apgars of 5 do not represent a threatening situation to the brain, but provide a reflection of the infant's status where, as here, the infant is going through a 10-minute to 15-minute change process after birth. Importantly, the Apgar did not stay at 5, but progressed to 7 by ten minutes and the infant was essentially normal when examined by the pediatrician at 9:40 p.m. Clearly, the infant was improving over that period, which compels the conclusion that there was no ongoing insult.7 Had Joiner suffered an injury to his brain during or immediately following birth, there are a number of clinical findings one would reasonably expect to observe. An infant who has suffered a neurologic injury should demonstrate a 6-hour to 12-hour period of decreased tone, followed by evidence of hyperactivity and irritability. Moreover, in cases of substantial neurologic injury, the infant should generally evidence seizure activity within 8 to 24 hours. Beyond the first 24-hour period, the infant should demonstrate moderate to significant decreased tone, depending on the magnitude of the injury, and within the first 48-hour period the injured infant should evidence resistance to feeding. Here, Joiner's decreased tone was resolved by 9:40 p.m., there was no evidence of hyperactivity and irritability, and no evidence of seizure activity. Moreover, at approximately 15 hours of life, Joiner was shown to latch on and breast-feed well. It is further observed that, while he suffered respiratory distress, Joiner did not suffer respiratory arrest or failure, and did not require intubation or mechanical ventilation. Rather, his respiratory effort was adequate to ventilate and, as confirmed by pulse oximeter, he was adequately oxygenated. Also inconsistent with brain injury during or immediately following birth, there was no evidence of other system dysfunction, such as the heart or kidney8; no evidence of brain swelling within 24 hours of birth9; Joiner's lab studies were normal, including cord pH; and follow-up blood-gas studies did not reflect acidosis of substance. In sum, there was no clinical evidence in the newborn period that Joiner's neurologic presentation was abnormal or, stated differently, that he had suffered or was suffering a neurologic injury. Finally, it is observed that Joiner's presentation is consistent with pervasive developmental disorder, a disorder within the spectrum of childhood autism, a serious neurologic disorder in which affected children display abnormalities in socialization, behavior, language and, occasionally, stereotyped motor movements. Such disorder is developmental in origin (an anomaly in brain development), acquired prenatally, and is not associated with events that might occur during labor, delivery, or resuscitation. Given the proof, it cannot be concluded that, more likely than not, Joiner's neurologic impairment was associated with a brain injury caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Notably, Joiner's presentation at birth and his neonatal course were not consistent with an acutely acquired neurological injury, and it is improbable that he could have experienced an acute injury during labor and delivery, or immediately thereafter, without evidencing a single clinical symptom of such damage. Conversely, the existence of a prenatally acquired (predating labor and delivery) brain disorder (developmentally based) would be consistent with Joiner's presentation at birth and subsequent development.
The Issue At issue in this proceeding is whether Respondent's proposal to accept the subject claim for compensation under the Florida Birth-Related Neurological Injury Compensation Plan should be approved and, if so, the amount and manner of payment (lump sum or periodic) of the parental award and the appropriate apportionment of the award between the parents.
Findings Of Fact The claim for compensation Petitioner, Crystal Waddell, and Intervenor, William Davis, are the natural parents of Chelsey Davis (Chelsey), a minor. Chelsey was born a live infant on August 23, 1997, at University Medical Center, a hospital located in Jacksonville, Florida, and her birth weight was in excess of 2500 grams. Ms. Waddell and Mr. Davis are not now, nor have they ever been, husband and wife. The physician providing obstetrical services during the birth of Chelsey was Edward Illions, M.D., who was, at all times material hereto, a participating physician in the Florida Birth- Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Here, the parties agree that Chelsey suffered a "birth- related neurological injury" as defined by Section 766.302(2), Florida Statutes, in that she suffered an injury to the brain caused by oxygen deprivation in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital, which rendered her permanently and substantially, mentally and physically impaired. The medical records filed with DOAH on June 15, 1998, as well as the report of neurological evaluation by Michael S. Duchowny, M.D., filed with DOAH on September 28, 1998, are consistent with the parties' agreement. Consequently, it is accepted that Chelsey suffered a "birth- related neurological injury," as defined by Section 766.302(2), Florida Statutes. Given the compensability of the claim, NICA agreed as follows: 8. The Association agrees to pay $100,000.00 as follows: Ms. Crystal Waddell has requested that $6,000.00 be paid to Ms. Cheryl Chieves as reimbursement for funds which she has loaned Ms. Waddell. The Association has no objection to this payment. The Association and Ms. Waddell also request that the Administrative Law Judge schedule a hearing as soon as feasible to determine the entitlement of the mother and/or father, if any, to the parental award. The Association will pay all benefits, past and future, as authorized by Section 766.31, Florida Statutes. . . . The Association agrees that $3,753.25, which includes fees and expenses incurred in the representation of the Claimant in this case, will be paid to Merrill C. Tunsil, Esquire, the attorney for the claimant. (Stipulation filed December 22, 1998.) Consequently, at the commencement of hearing, the parties stipulated that the only issues which remained for resolution were the apportionment of the $100,000.00 award between the parents, and whether such award should be made in lump sum or by periodic payment. (Transcript, page 8.) Background Chelsey's mother, Crystal Waddell (Ms. Waddell), was born May 30, 1979, and was 18 years of age when Chelsey was born.3 Chelsey, born August 23, 1997, was the product of Ms. Waddell's first pregnancy. According to the proof, Ms. Waddell's formal education ceased following her completion of the 11th grade. Thereafter, she was employed by Arby's and, subsequently, by McDonald's in the years preceding Chelsey's birth. Following Chelsey's birth, Ms. Waddell, with the assistance of her mother, dedicated herself to Chelsey's care; however, recently, Ms. Waddell resumed her formal education, with the aim of completing her high school education. Chelsey's father, William Davis (Mr. Davis), was born March 31, 1980, and was 17 years of age when Chelsey was born. At the time, Chelsey was the second child Mr. Davis had fathered without the benefit of marriage. According to the proof, Mr. Davis abandoned his formal education during the 8th grade and, since that time, has been periodically employed in various unskilled positions. Such employment has included a term at McDonald's (where he and Ms. Waddell met); a period of approximately 6 weeks at John Rigsby Painting Company, Raleigh, North Carolina, at and shortly after Chelsey's birth; a term at Top Choice Poultry, following Chelsey's birth and his return to Jacksonville, Florida; and, most recently (since approximately September 1998), employment by Bill Williams Heating and Air Conditioning, where he nets approximately $180.00 each week. As of the date of hearing, Mr. Davis announced that he had recently (that week) started a program designed to achieve his GED and, if successful, hoped to begin an apprenticeship program with his current employer. The nature of Mr. Davis' current employment or the apprenticeship program is not of record. Approximately one year preceding Chelsey's birth, Ms. Waddell and Mr. Davis met while employed at a McDonald's restaurant in Jacksonville, Florida. Apparently, their relationship blossomed and, based on a perceived foundation of love and devotion, they designed to have a child and Chelsey was conceived. While Ms. Waddell and Mr. Davis may have initially felt a sense of purpose or closeness, their relationship proved to be tempestuous. Moreover, while they initially professed commitment and sought parenthood, the couple was never capable of sustaining themselves, much less an infant. Indeed, throughout the course of their relationship, and to this date, Ms. Waddell has continued to reside with her mother, Cheryl Chieves (Ms. Chieves). As Ms. Waddell's delivery date neared, Mr. Davis, who was apparently unemployed at the time, elected to go to Raleigh, North Carolina. According to Mr. Davis, the reason for the trip was two-fold. One reason was to visit his son (the issue of a previous relationship). The other reason was "I had a job waiting there to get some money up, you know." (Transcript, page 131.) As for the duration of the trip, the record reflects that Mr. Davis remained in Raleigh for 3 months, returning at the end of November 1997 when Chelsey was 3 months old. As for the promised job, the proof reflects that Mr. Davis was employed by John Rigsby Painting Company for the first 6 weeks of his stay in Raleigh, but was otherwise unemployed. At or about 10:54 p.m., August 22, 1997, Ms. Waddell was admitted to University Medical Center in labor, and at 12:30 a.m., August 23, 1997, her membranes spontaneously ruptures, with clear fluid noted. Ms. Waddell's labor and delivery was noted in her discharge summary as follows: The patient was admitted to Labor and Delivery . . . with a term intrauterine pregnancy and spontaneous rupture of membranes. The patient's cervix at the time of admission was 6, complete, -3 and vertex presentation. The patient had a protracted, active phase, and was started on Pitocin augmentation. At 7 centimeters, the patient had an intrauterine pressure catheter which showed an adequate contraction pattern x one hour. Her fetal heart tracing showed some subtle decelerations . . . . Later on that day, the patient developed a temperature to 101.2 degrees and she was diagnosed with chorioamnionitis and started on clindamycin and gentamicin. The patient was allergic to penicillin. She continued to make no progress with her cervical examination. A scalp pH was performed [at 6:50 p.m.] and came back 7.29 which showed reassurance. The patient was continued with Pitocin augmentation. A repeat scalp pH [performed at 11:10 p.m.] was 7.05 and [at 11:20 p.m. was] 6.86 [consistent with metabolic acidosis], so the patient was taken to the operating room for a stat cesarean section [and the infant was delivered at 11:36 p.m.]. . . . Apgars were 3 at one minute, 5 at five minutes and 6 at 10 minutes. Findings at the time of surgery showed a live born baby with a terminal meconium. Postoperatively, the baby was taken to the Neonatal Intensive Care Unit. . . . Ms. Waddell was discharged August 30, 1997, and Chelsey was ultimately discharged to the care of her mother on September 12, 1997. Chelsey's course was noted in her discharge summary as follows: HISTORY OF PRESENT ILLNESS: This 3075 gram female infant was born by cesarean section at 38 weeks gestation for decreased fetal heart rate and a scalp pH of 6.8. . . . Rupture of membranes was approximately 18 hours prior to delivery. There was a history of maternal fever and the mother received Clindamycin and Gentamicin. The amniotic fluid was meconium stained and 0.5 cc of thick meconium stained fluid was suctioned from below the cords. Apgars were 3 at one minute, 5 at five minutes and 6 at ten minutes, after receiving positive pressure ventilation and then blow- by oxygen. The infant was transported to the neonatal intensive care unit. PHYSICAL EXAMINATION: Neurological examination showed decreased tone with symmetrical movement and no focal neurological deficits. ADMISSION LABORATORY DATA: The infant is A+ and Coomb's positive. Arterial blood gas on 100% blow-by oxygen revealed a pH of 7.08, pC02 of 18, p02 of 479 and a base excess of -23. ADMISSION DIAGNOSES: Term female. Respiratory depression. Metabolic acidosis. ABO incapability. Sepsis surveillance. HOSPITAL COURSE AND PROBLEM LIST: * * * Respiratory: Initially she had metabolic acidosis and received sodium bicarbonate. A chest x-ray was consistent with retained fetal lung fluid and she was placed on nasal cannula. Initially she had tachypnea which slowly resolved. The nasal cannula was discontinued on day three and she had no further respiratory distress and required no further oxygen. This problem is considered resolved. * * * Central Nervous System: On August 24, 1997 she developed seizure activity at less than 12 hours of age. She was placed on Phenobarbital. An electroencephalogram (EEG) showed "status", although clinically no seizures were noted after the initial episode of seizure activity. . . . Neurology was consulted and she was seen by Dr. Shanks whose impression was acute encephalopathy and recurrent electrographic seizures from multiple-foci despite Phenobarbital therapy. . . . [P]henobarbital was given until maximal serum levels were achieved. She was then started on Dilantin. A head ultrasound on August 25, 1997 was normal. A CT scan on August 26, 1997 showed extensive cerebral low attenuation suggesting anoxic injury. Phenobarbital and Dilantin levels were followed closely and doses were adjusted appropriately. Follow up electroencephalogram (EEG) on September 2, 1997 showed no electrographic seizures and marked suppression except for bursts of excessive sharp waves. The Dilantin was discontinued. No change in the neurological status was noted. Plan: Discharge home on Phenobarbital 12 mg.b.i.d. and follow up Phenobarbital level two weeks after discharge. . . . * * * Discharge Physical Examination: . . . Neurological examination shows symmetrical decreased tone, otherwise no gross neurological deficits were noted. DISCHARGE DIAGNOSES: Term female, 38 weeks gestation. Neonatal asphyxia, resolved. Neonatal seizures ABO incompatibility with hemolysis. Metabolic acidosis, resolved. Anemia. Hyponatremia, resolved. Hypoxic ischemic encephalopathy. . . . Since her discharge, Chelsey has been cared for by Ms. Waddell and her mother (Ms. Chieves), initially in an apartment leased by Ms. Chieves and more recently in a single family residence purchased by Ms. Chieves. Ms. Waddell and Ms. Chieves have jointly shared the responsibility for Chelsey's care and, apart from Aid For Dependent Children (AFDC), which Ms. Waddell started to receive at or about three months after Chelsey's birth, and Medicaid assistance, all financial support for the family has been provided by Ms. Chieves.4 More recently, Ms. Chieves has added her daughter and Chelsey as dependents to her health insurance coverage, which she enjoys as an employee of the State of Florida. The attendant responsibilities and sacrifices inherently associated with Chelsey's daily care may be gleaned from Dr. Michael Duchowny's report of neurological evaluation of August 18, 1998, as follows: HISTORY ACCORDING TO CHELSEY'S FAMILY: Chelsey is an almost 1 year old female who "has cerebral palsy and is legally blind". Ms. Waddell began by explaining that Chelsey has severe motor delay and has essentially made no progress past the newborn level. Chelsey is unable to roll over or sit on her own and requires almost constant feeding. She had an indwelling gastrostomy for the first few months of life, but is now able to mouth and swallow on her own. Still, Chelsey's oromotor problems limit her caloric intake. She is quite small for her age and now weighs only 15 pounds, 14 ounces with a length of 27 inches. Ms. Waddell feels that Chelsey's motor problems effect [sic] all extremities. Chelsey is also "legally blind". By that, her mother indicated that Chelsey is unable to understand what she sees and therefore has little visual information. She can respond to her mother's voice and apparently is hyper alert. She sleeps through the night. Chelsey also suffers from recurrent seizures. These apparently are a marked problem and Chelsey has between 10 and 20 brief tonic seizures per day. Her head and eyes tend to be deviated to the right side with stiffening of the upper extremities. She takes phenobarbital 8 cc b.i.d. and is under the care of Dr. Daniel Shanks in Jacksonville. Chelsey receives physical therapy on a once weekly basis and speech therapy twice weekly. Occupational therapy is administered on one occasion every 2 weeks. . . . * * * NEUROLOGIC EXAMINATION reveals an infant who lies supine with fixed postures in a right tonic neck response. Chelsey demonstrates a startle myoclonus. She has intermittent tongue thrusting movements. There is no drooling. The head is deviated to the right side, but can be passively rotated to the left. There is no central gaze fixation. Chelsey does have brief limited conjugate following. The funduscopic examination is unremarkable. Motor examination reveals increased tone in all extremities indicative of a spastic hemiparesis. The tonic neck response is obligate and can be obtained in both directions through passive movement of the head. There is a positive jaw jerk, sucking and snouting responses. The limbs are small with diminished muscle bulk. Fisting of the thumbs is noted bilaterally. There is evidence of guided reaching. The deep tendon reflexes are brisk at 3+ in all extremities with crossed adductor responses. There are florid bilateral Babinski responses with the large toes being held in passive Babinski attitudes. Sustained ankle and knee clonus are easily elicited. The jaw jerk and facial jerks are both hyperactive. The spine shows a slight curvature convex to the right. The neurovascular examination is unremarkable. In SUMMARY, Chelsey's neurologic examination reveals evidence of severe motor and cognitive delay. Chelsey is showing little progress past the newborn period and her microcephaly suggests that there has been little brain growth since birth. At the same time, Chelsey manifests cortical blindness and startle myoclonus. Chelsey additionally has medically resistant seizures of probable left frontal lobe origin. . . . As heretofore noted, Mr. Davis did not return to Jacksonville, or visit his daughter, until Chelsey was 3 months of age. Thereafter, apart from the first week he was in town and resided with Ms. Waddell and Ms. Chieves, Mr. Davis has lived apart from his daughter and Ms. Waddell, and his participation in his daughter's care, as well as any contribution to his daughter's support, has been de minimus.5 Mr. Davis' interest in Chelsey was stated by him at hearing to be as follows: Q. . . . You're not telling this Court that you want custody of this baby and that you're capable of taking care of it; are you? A. No, sir. I just want it where I can see her when I want to and I ain't got to go through so much trouble, you know, just to see her. Apportionment and manner of payment (lump sum or periodic payment) of the parental award As the primary caretaker for Chelsey, the demands placed on Ms. Waddell as the custodial parent, are, and will continue to be onerous. Clearly, without the support of her mother, the demands placed on Ms. Waddell for Chelsey's care would have left her little or no time for other activities or pursuits, and those demands greatly exceed, and will continue to exceed, those assumed by the parent of an infant not so impaired. In contrast, Mr. Davis has accepted none of the responsibilities (financial or otherwise) associated with Chelsey's care, and has evidenced no sincere inclination to do so. Under the circumstances, it is apparent that, as between them, the loss suffered by Ms. Waddell as a consequence of Chelsey's injury has been grossly disproportionate to that suffered by Mr. Davis, and that such disparity warrants a similar distinction, as between them, in the apportionment of the parental award. As for the method of payment, lump sum or periodic, it should not be subject to serious debate that Ms. Waddell and Mr. Davis have evidenced poor judgment in the past, and that, given their positions in life and young ages, they cannot be relied upon to make sound decisions in the immediate future. Consequently, except for the lump sums hereafter awarded, it is resolved that, absent further order, the bulk of the parental award should be paid periodically to the custodial parent. Given the foregoing considerations, as well as the legal principles discussed infra, it is resolved that of an award of $100,000, Ms. Waddell and Mr. Davis are each eligible to receive $2,500 in lump sum, and that the balance of $95,000 be paid to the custodial parent, retroactive to August 23, 1997, at the rate of $500 per month. Ms. Waddell, as the current and past custodial parent, shall receive the retroactive payment in lump sum and, absent a change in the custodial arrangement, the sum of $500 each month thereafter absent further order or until the principle is exhausted.
The Issue At issue in this proceeding is whether Halle Cohen Martinez, III, a minor, qualifies for coverage under the Florida Birth- Related Neurological Injury Compensation Plan.
Findings Of Fact Petitioners, Barbara Mary Martinez and Halle Martinez, Jr., are the natural parents and guardians of Halle Cohen Martinez, III, a minor. Halle was born a live infant on November 12, 2001, at Leesburg Regional Medical Center, a hospital located in Leesburg, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Halle's birth was Wendell Courtney, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth- Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury" defined as an "injury to the brain or spinal cord . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat. See also, §§ 766.309 and 766.31, Fla. Stat. To address the cause, timing, and significance of Halle's impairment, Petitioners offered selected medical records relating to Halle's birth and subsequent development, as well as the testimony of Mr. and Mrs. Martinez. In turn, Respondent offered the affidavits and the reports of Doctors Donald C. Willis and Paul R. Carney. The cause and significance of Halle's neurologic impairment At birth, Halle suffered a left brachial plexus injury, with resultant left arm brachial plexus palsy, and a left posterior dislocated shoulder, secondary to the birth brachial plexus palsy. Thereafter, at age 5 months, Halle underwent corrective surgery of the brachial plexus using sural nerve grafts, and at 8 months he underwent corrective surgery to improve the function of his left shoulder. The operations resulted in functional improvements; however, as of the date of hearing, Halle continued to suffer impairments of his left arm and hand, which are likely to be permanent, with notable atrophy within the left upper extremity. Apart from the physical impairment Halle exhibits in his left upper extremity, he is otherwise neurologically sound, without evidence of impairment in his right upper extremity or lower extremities; without evidence of cognitive delay; and without evidence of vision or hearing impairment. Accordingly, although Halle evidences a significant birth-related left brachial plexus injury, he is not, on balance, substantially physically impaired, and evidences no mental impairment. Therefore, for reasons appearing fully in the Conclusions of Law, the claim is not compensable, and it is unnecessary to address whether Halle's brachial plexus injury is, anatomically, an injury to the spinal cord.
The Issue At issue in this proceeding is whether Gordon Quinn Kowlessar, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Carmen L. Diaz and Andrew Kowlessar are the parents and natural guardians of Gordon Quinn Kowlessar (Gordon), a minor. Gordon was born a live infant on August 26, 1997, at Halifax Medical Center, a hospital located in Daytona Beach, Florida, and his birth weight was in excess of 2500 grams. The physicians providing obstetrical services during the birth of Gordon were Linda Hensley, M.D., assisted by Julia Harris, M.D., and they were, at all times material hereto, participating physicians in the Florida Birth-Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Coverage under the Plan Pertinent to this case, coverage is afforded under the Plan when the claimant demonstrates, more likely than not, that the infant suffered an "injury to the brain or spinal cord . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Here, the parties agree that Gordon suffered an injury to his brain caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post- delivery period which rendered him permanently and substantially physically impaired. Consequently, the sole issue to resolve is whether such injury likewise resulted in permanent and substantial mental impairment. As to that issue, Petitioners are of the opinion that Gordon's mental development is age appropriate, and Respondent is of the opinion that, at the present time, Gordon's mental status can not be adequately assessed. Gordon's neurologic condition On October 23, 1998, following the filing of the claim for compensation, Gordon was examined by Michael Duchowny, M.D., an expert in pediatric neurology. At the time, Dr. Duchowny was unable to reach an opinion regarding Gordon's mental status for two reasons. First, Gordon was quite young to perform such an assessment. Second, Gordon had a significant motor impairment which made, at his age, the assessment of mental status difficult. Consequently, Dr. Duchowny was unable to offer an opinion as to whether Gordon's brain injury also produced permanent and substantial mental impairment. The infant's mother, Carmen L. Diaz, based on her observations and experience, expressed the opinion that Gordon's mental status or function was normal or, stated differently, age appropriate. Such opinion was premised on Gordon's language development, as well as his reaction/interaction with others and his environment, which in Ms. Diaz's opinion failed to reveal any delay in development of his mental functions. Apart from the observations of Dr. Duchowny and Ms. Diaz, the parties also offered certain medical records pertaining to Gordon's birth and subsequent development (Petitioners' Exhibit 1); however, these records do not provide any meaningful assessment of Gordon's mental status. Indeed, consistent with Dr. Duchowny's observations, they reveal that due to Gordon's motor impairment, a meaningful assessment of his mental status, at the time, was difficult.
