The Issue At issue in this proceeding is whether Jenna Kemper, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Nancy Kemper and Jeffery Kemper are the parents and natural guardians of Jenna Kemper (Jenna), a minor. Jenna was born a live infant on March 27, 1996, at Lakeland Regional Medical Center, a hospital located in Lakeland, Polk County, Florida, and her birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Jenna was Keith Bernard Paredes, 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. Jenna's delivery at Lakeland Regional Medical Center on March 27, 1996, was apparently difficult due to her large birth weight, and when delivered she was noted to have suffered an injury to her upper right brachial plexus, an Erb's palsy, which affected the range of motion on the upper right extremity, and is evidenced by diminished range of motion at the right elbow and an inability to freely elevate the right arm above neutrality at the shoulder. Jenna's brachio-plexus injury may reasonably be described as mild to moderate, and her impairment is most likely permanent. A brachial plexus injury, such as that suffered by Jenna during the course of her birth, is not, anatomically, a brain or spinal cord injury, and does not affect her mental abilities. Moreover, apart from the brachial plexus injury, Jenna was not shown to have suffered any other injury during the course of her birth. Consequently, the proof fails to demonstrate that Jenna suffered an injury to the brain or spinal cord caused by oxygen deprivation or mechanical injury during the course of labor or delivery, and further fails to demonstrate that she is presently permanently and substantially, mentally and physically impaired.
Findings Of Fact Andy was born on November 2, 2015, at Tampa General located in Tampa, Florida. Based on the available evidence, Alyssa J. Brown, M.D., was the delivering physician for Andy’s birth. Dr. Brown was a “participating physician” under the Plan at the time Andy was born. See § 766.302(7), Fla. Stat. Upon receiving the Petition, NICA retained Donald Willis, M.D., a board-certified obstetrician/gynecologist specializing in maternal-fetal medicine, as well as Laufey Y. Sigurdardottir, M.D., a pediatric neurologist, to review Andy’s medical condition. NICA sought to determine whether Andy suffered a “birth-related neurological injury” as defined in section 766.302(2). Specifically, NICA requested its medical experts opine whether Andy experienced 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; and, if so, whether this injury rendered Andy permanently and substantially mentally and physically impaired. Dr. Willis reviewed Andy’s medical records and described Andy’s birth as follows: [V]acuum assisted vaginal delivery at term resulted in a newborn with normal Apgar scores and a normal umbilical cord blood gas. [Andy] did not require resuscitation. Dr. Willis then opined: There was no apparent obstetrical event that would have resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post delivery period. Dr. Sigurdardottir also reviewed Andy’s medical records, as well as conducted an independent medical exam of Andy on May 2, 2018. Dr. Sigurdardottir commented that “Andy is found to have substantial delays in motor and mental abilities. . . . [T]here is no evidence of impairment consistent with a neurologic injury to the brain or spinal cord acquired due to oxygen deprivation or mechanical injury.” Dr. Sigurdardottir further opined: In light of evidence presented, I believe Andy does fulfill criteria of a substantial mental and physical impairment at this time, but it is likely due to a genetic condition and not to be from birth related injury. I do not feel that Andy should be included in the NICA program. A review of the file reveals no contrary evidence to dispute the findings and opinions of Dr. Willis and Dr. Sigurdardottir. Their opinions are credible and persuasive. Based on the opinions and conclusions of Dr. Willis and Dr. Sigurdardottir, NICA determined that Petitioner’s claim was not compensable. NICA subsequently filed the Unopposed Motion for Summary Final Order asserting that Andy has not suffered a “birth-related neurological injury” as defined by section 766.302(2). Petitioners do not oppose NICA’s motion.
Findings Of Fact Alexander was born on August 28, 2015, at South Miami Hospital. Alexander was a single gestation, weighing over 2,500 grams at birth. NICA retained Donald Willis, M.D., an obstetrician specializing in maternal-fetal medicine, to review the medical records of Alexander and his mother, Petitioner Evelyn Machado Valdes, and opine as to whether there was an injury to his brain or spinal cord that occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period due to oxygen deprivation or mechanical injury. In his report, dated February 19, 2018, Dr. Willis set forth the following: In summary, umbilical cord prolapse occurred during labor. Emergency Cesarean section was done with delivery of a healthy newborn. The baby was not depressed at birth. Apgar scores were 9/9. No resuscitation was required. The baby left the delivery room stable and well. Episodes of cyanosis occurred several hours after birth. Cerebral infarction was diagnosed by MRI. The baby suffered a stroke at some time around the episodes of cyanosis that occurred several hours after birth. This would be well after the post-delivery resuscitation period. The baby was born active and required no resuscitation at birth, indicating there was no oxygen deprivation during labor, delivery of [sic] the post- delivery period. * * * There was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain or spinal cord during labor, delivery or the immediate post delivery period. The baby did suffer a stroke during the perinatal period, but this was not related to oxygen deprivation or mechanical trauma during labor, delivery or the immediate post-delivery period. Dr. Willis affirms in his amended affidavit, dated September 24, 2018, the above-quoted opinions from his report and further opines that: [I]n that there was no oxygen deprivation or mechanical injury occurring in the course of labor, delivery or resuscitation in the immediate post-delivery period in this Hospital, then accordingly, there was no causal event which would have rendered Alexander Pinera permanently and substantially mentally and physically impaired as a result of the same. NICA also retained Michael S. Duchowny, M.D., a pediatric neurologist, to review the pertinent medical records, conduct an Independent Medical Examination (IME) of Alexander, and opine as to whether Alexander suffers from a permanent and substantial mental and physical impairment as a result of a birth-related neurological injury. Dr. Duchowny reviewed the medical records, obtained historical information from Alexander’s mother, Evelyn Machado, and performed an IME on June 13, 2018. In a report authored after the IME, Dr. Duchowny summarized his findings, in pertinent part, as follows: In SUMMARY, Alex’s neurological examination reveals subtle right upper extremity weakness characterized by left hand preference and posturing of his right upper extremity while walking. There is no objective weakness and his fine motor coordination is preserved. His speech is age-appropriate. * * * Although Alex had a major cerebral vascular accident that affected his left cerebral hemisphere, he has made a remarkable recovery and now evidences only minimal deficits on his neurological examination. In view of his stable general physical and neurological status at birth, it is most likely that the cerebral vascular accident occurred prior to the onset of labor. * * * Based on the medical record review and today’s evaluation, I am not recommending Alexander for inclusion in the NICA program. NICA’s Motion for Partial Summary Final Order also relies upon the attached affidavit from Dr. Duchowny, dated September 4, 2018. In his affidavit, he affirms his findings and opinions contained in his report to a reasonable degree of medical probability. A review of the file reveals that no contrary evidence was presented to dispute the findings and opinions of Dr. Willis and Dr. Duchowny. Their opinions are credited.
The Issue Whether the injury claimed is a birth-related neurological injury and qualifies for coverage under the Florida Birth- Related Neurological Injury Compensation Plan.
Findings Of Fact The parties' Pre-Hearing Stipulation stipulated as fact that: Nealy and John Munoz are the parents of minor Giovanni Munoz. Giovanni Munoz was born on March 18, 2006, at Memorial Regional Hospital, Hollywood, Florida. His was a live birth, and he weighed in excess of 2500 grams at birth. The physician providing obstetrical services during labor and delivery of Giovanni was Violetta Lyra, M.D. Dr. Lyra was a participating physician in the NICA program in 2006.[3] Nealy and John Munoz, as parents and natural guardians of Giovanni Munoz have filed a Petition with the State of Florida, Division of Administrative Hearings, seeking a determination that injuries sustained by Giovanni Munoz constitute a birth-related neurological injury. The record evidence supports the foregoing stipulated facts, and the record also supports findings that Giovanni was a single gestation and that Memorial Regional Hospital is a "hospital" as defined in Section 766.302(6), Florida Statutes. The Plan affords coverage 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 § 766.31, Fla. Stat. At hearing, the parties stipulated orally, and the proof is otherwise compelling, that Giovanni suffered an injury to the brain caused by oxygen deprivation, which injury resulted in a permanent and substantial mental and physical impairment. Accordingly, the issue for resolution herein was narrowed to whether or not Giovanni's permanent and substantial mental and physical impairment caused by oxygen deprivation occurred "in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital[.]" Expert medical testimony was rendered herein via the depositions of Dr. Michael Duchowny, Dr. Donald C. Willis, and Dr. Tatyana Dubrovsky. Dr. Duchowny is board-certified in pediatric neurology, a sub-specialty of medicine involved with the diagnosis and treatment of disorders of the nervous system in children, with special competence in clinical neurophysiology. Dr. Willis is board-certified in obstetrics, gynecology, and maternal-fetal medicine. Dr. Dubrovsky is board-certified in pediatric neurology. Dr. Dubrovsky has been Giovanni's treating neurologist since he was seven months' old, when Giovanni's parents noted that he was not meeting his milestones. Notably, the parties did not present testimony from a neonatologist. Wherever the medical experts' testimony is relied-upon or referred-to herein, it is only those portions of their testimony which have been rendered within reasonable medical probability or certainty, and the undersigned has not relied upon any responses by deponents to unrelated or incomplete hypothetical questions or where the deponents have been asked to speculate upon events not recorded or facts not in evidence. Giovanni is the product of a 38-week gestation. His mother, Nealy Munoz, denied that any major problems occurred with the pregnancy during the first 36 weeks. On March 3, 2006, in the thirty-sixth week of an uneventful pregnancy, Mrs. Munoz presented to Memorial Regional Hospital as an outpatient for a biophysical profile (BPP). She had been referred there by her treating obstetrician, Dr. Lyra, due to "decreased fetal movement." A BPP is used to determine the well-being of a fetus and uses numerical points for certain criteria. There are a total of eight points attainable on a BPP. Either two points or zero are given for each of four categories: fetal breathing, body movement, fetal tone, and sufficiency of amniotic fluid. Although Mrs. Munoz' testimony gave no particular reason for the March 3, 2006, BPP, it is apparent from the medical records that her physician ordered the March 3, 2006, BPP due to lack of, or decrease in, fetal movement. Mrs. Munoz also provided that same reason to Dr. Duchowny as part of his independent medical examination of Giovanni. For the first BPP on March 3, 2006, Giovanni scored six out of eight points, with no points for fetal breathing. Fetal breathing movements (FBM) are a reflection of adequate oxygenation to the baby's brain. However, they are intermittent, and fetal breathing movements sometimes are not observed within the 30-minute window for a BPP, so repeating such a test on sequential days was appropriate. On March 4, 2006, the BPP was repeated, and Giovanni again scored 6 of 8, with no points for fetal breathing. However, a non-stress test (NST) also was done the same day, and the NST showed that Giovanni was "reactive," which information was somewhat reassuring. On March 5, 2006, the BPP was repeated a third time, and Giovanni scored eight out of eight. On the second NST, which was also done that date, Giovanni was again found to be "reactive." All three physicians who testified believed something had happened to Giovanni in utero at or about March 3- 5, 2006. Drs. Duchowny and Willis also opined that the oxygen deprivation that impaired Giovanni's brain probably occurred outside the statutory time frame for compensability but within the 24 hours before his mother presented to the hospital two weeks later on March 17, 2006. (See Finding of Fact 38.) No assessment of fetal brain injury was undertaken March 3-5, 2006. Classically, assessments of brain injury are not performed until after birth. On March 15, 2006, another BPP and another NST were performed, and Giovanni scored 8/8 on the BPP and had a "reactive" NST. Apparently, there was no absence of fetal breathing or oxygen deprivation at that point in time, but again, there also was no assessment of possible brain injury to Giovanni that may already have occurred. Mrs. Munoz experienced no further pregnancy problems until two days later, on the morning of March 17, 2006. That morning, she arose and dressed for work, noting that there was no fetal movement and that Giovanni felt "hard." At hearing, she described this sensation as, "When they [a fetus/baby] are moving there is a softer feeling in the belly, and it just felt as if it was hard, like it was a ball, very stiff." Mrs. Munoz made similar statements to Dr. Duchowny, as part of his examination of Giovanni. Because Giovanni did not move from the time Mrs. Munoz awakened the morning of March 17, 2006, until 2:00 p.m., that afternoon, she phoned her obstetrician. Dr. Lyra told her to go home, rest, eat, and drink something sugary "to get things going." Mrs. Munoz did as she was told. Mrs. Munoz utilized a fetal Doppler heart monitor two or three times on the morning of March 17, 2006, before calling her physician, and also used it in the afternoon, after talking to her physician. This type of fetal heart monitor measures the fetus/baby's heart beat, but there is no evidence that it measures oxygen to the baby's brain. There was still no fetal movement by late evening on March 17, 2006, so about 10:00 p.m., Mrs. Munoz again phoned her obstetrician, who told her to go to the hospital, which she did. The hospital records show that on March 18, 2006, Mrs. Munoz was admitted to Memorial Regional Hospital on an emergency basis for a labor check, decreased fetal movement (fetal distress), and probable caesarean section. Mrs. Munoz did not testify to the time she awakened on the morning of March 17, 2006, except that it was "morning." Therefore, even if she had awakened as late as 11:59 a.m., that day, which is very unlikely, and allowing for delays in admission between the time she testified she arrived at the hospital on March 17, 2006, and the March 18, 2006, date on her admission documents, by the time she checked into the hospital, there had been no fetal movement for a minimum of 10 hours and probably for a much longer period of time. At no time did medical personnel check the degree of dilation of Mrs. Munoz' cervix, or chart that she was in labor. Dr. Duchowny testified that he had never heard of an absence of fetal movement being indicative of the onset of labor. At 2:28 a.m., March 18, 2006, fetal heart rate (FHR) decelerations were recorded. Decelerations show that the fetus was in distress. Mrs. Munoz testified that in the hospital, she had some weak contractions, lasting a half minute, about nine minutes apart, but the BPP and hospital records reflect the following activity: At 2:55 a.m. March 18, 2006, a contraction of mild intensity lasting 40-50 seconds was recorded. At 3:00 a.m., accelerations were absent, and there were intermittent late decelerations recorded. At 3:15 a.m., Giovanni scored only two out of eight points, with zero points for fetal breathing, zero points for body movement, zero points for fetal tone, and two points for sufficiency of amniotic fluid. There also was an abnormally high resistance to umbilical cord artery flow in the placenta and a NST showed that Giovanni was non-reactive. At 3:30 a.m., left and right reflexes were absent, contraction intensity was irregular, and accelerations and decelerations were absent. Contractions of 20-40 seconds with irregular intensity were recorded with absent accelerations and variable decelerations. This recorded activity is not sufficient to meet the definition of "labor."4 Dr. Lyra was contacted by phone, and she ordered an immediate cesarean section. Giovanni Munoz was delivered by emergency cesarean section at approximately 4:04 a.m., on March 18, 2006. The membranes were ruptured at the time of delivery. There was no placental detachment. Drs. Duchowny and Willis were of the opinion that Mrs. Munoz never went into labor, and Dr. Dubrovsky deferred on this issue. Upon delivery, Giovanni's skin was peeling and he was not breathing on his own. However, he only required suction of his nose and mouth with a bulb syringe, mask bag ventilation for 60 seconds, and vigorous stimulation. As Giovanni responded to mask oxygen and vigorous stimulation, his color and heart rate improved and his Apgar scores reflected that improvement.5 Giovanni was not intubated or placed on a ventilator due to lack of oxygen. According to Dr. Willis, if a baby does not have chemical pneumonia or chemical pneumonitis, then not intubating would not have any effect on oxygen consumption or oxygenation. Giovanni did not evidence either of these problems, which most often arise from meconium6 aspiration syndrome (MAS). Giovanni's Apgar scores were taken at one minute, five minutes and ten minutes, and recorded as four, six and eight, respectively. An Apgar score of seven or below is considered "low," but according to Dr. Duchowny, an Apgar score at one minute is more a reflection of the trauma of delivery itself, rather than an indicator of an infant's well-being at the moment of delivery or whether there is an ongoing hypoxic event. Dr. Willis stated that Giovanni's one-minute Apgar score signaled how much resuscitation was needed. According to Dr. Duchowny, Giovanni's rising Apgar scores in so short a period "reflected a reasonable, moderately good physiologic adjustment to the extra-uterine environment," and were not Apgar scores associated with a severe hypoxic ischemic insult acquired during labor and delivery. If Giovanni had been asphyxiated during labor and delivery, Dr. Duchowny would have expected his Apgar scores to be considerably lower than they were. Dr. Willis also testified that Giovanni's rapid response to bulb syringe suctioning and one minute of mask bag resuscitation was better than normally seen if a baby has suffered an acute hypoxic event. At birth, there was meconium in the amniotic sac, and Giovanni's fingernails were meconium-stained. Meconium in the amniotic fluid does not signal a hypoxic event. If meconium gets into a baby's posterior pharynx just below the vocal cords, then intubation and suctioning can be used to remove it, but if meconium gets into the lungs, intubation or suctioning will not solve the problem, and the baby can suffer meconium aspiration syndrome (MAS), leading to chemical pneumonia or chemical pneumonitis, and finally, brain injury by loss of oxygen. Although Giovanni had sufficient respiratory distress to require 60 seconds of mask bag oxygenation, there is no persuasive evidence that he suffered chemical pneumonia, chemical pneumonitis, or MAS. Dr. Dubrovsky testified that she could not state one way or another, or with full clarity, when the brain injury to Giovanni occurred.7 A baby's fingernails will not be stained with meconium just because there is meconium in the amniotic fluid shortly before delivery. Therefore, Giovanni's stained fingernails demonstrated that a hypoxic event had occurred remote in time from his delivery. Dr. Willis testified that when a newborn's fingernails become meconium stained, it usually means that the meconium was present for at least four to six hours prior to birth, and that herein, the hypoxic event must have occurred at some point prior to Giovanni's March 18, 2006, delivery. In his opinion, Giovanni's situation "would be consistent with having a hypoxic insult at some time remote from delivery." Moreover, Dr. Duchowny found Giovanni's nucleated red blood cells also to be indicative of a hypoxic event more than 24 hours, and probably much longer, prior to any labor. He further testified that none of Giovanni's widespread systems were compromised as would be expected of a hypoxic event during labor or delivery. There was no systemic compromise, renal failure, cardiovascular failure or liver enzyme abnormalities noted in Giovanni's medical records. However, Giovanni's umbilical cord gas had an abnormal pH of 6.97 and a BE of "minus 13" [-13]. He had prenatal depression, mild hypoglycemia (low blood sugar), thrombocytopenia (decreased platelets) and jaundice. Giovanni was immediately removed to the Neonatal Intensive Care Unit (NICU) for five days until he and Mrs. Munoz were simultaneously released to go home. Mrs. Munoz's hospital records from this point on reflect that she was recovering from the cesarean section and that Giovanni had problems breast feeding. None of the expert medical physicians who testified addressed what Giovanni's being in NICU might mean in relation to oxygen deprivation, if any. However, according to the records, Giovanni's oxygen problems were resolved on March 18, 2006 (presumably by the suction and mask bag ventilation), and according to Dr. Duchowny, Giovanni's postnatal course was not complicated in the same way as that of a baby with oxygen deprivation during the statutory period (labor, delivery, or resuscitation in the immediate postdelivery period in a hospital) would be.
The Issue At issue in this proceeding is whether Jacqueline LaPoint, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary matters Catherine LaPoint is the mother and natural guardian of Jacqueline LaPoint (Jacqueline), a minor. Jacqueline was born a live infant on July 2, 1994, at Holy Cross Hospital, a hospital located in Fort Lauderdale, Florida, and her birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Jacqueline was Marsh McEachrane, M.D., who was, at all times material hereto, a participating physician in the Florida Birth-Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Mrs. LaPoint's antepartum course and Jacqueline's birth At or about 1:00 a.m., July 2, 1994, Mrs. LaPoint's membranes spontaneously ruptured (while she was at home), with clear fluid noted, and contractions commenced approximately one to two hours later. At the time her estimated date of delivery had been noted as July 24, 1994, and, apart from the borderline prematurity of the fetus at the time labor commenced, her antepartum course was without apparent complication; however, Mrs. LaPoint did present with a number of risk factors, including a history of chronic smoking; obesity3 (a risk factor of gestational diabetes4); four previous cesarean sections (representing a risk of uterine compromise or rupture); and a large for gestational age fetus. Given the previous uterine surgery, Mrs. LaPoint had been scheduled for a repeat cesarean section. At or about 4:45 a.m., Mrs. LaPoint presented to Holy Cross Hospital in active labor. On presentation, contractions were noted as moderate (with a frequency of 3 to 4 minutes and a duration of 40 to 60 seconds), and vaginal examination revealed the cervix to be at 5 to 6 centimeters, effacement at 80 to 90 percent, and the fetus at station -3. External fetal monitor revealed a normal fetal heart tone (FHT) baseline of 150 to 160 beats per minute. Given her history of previous cesarean sections (uterine surgery) and her presentation of active labor, Mrs. LaPoint was admitted at or about 4:49 a.m. for a repeat cesarean section. FHT was monitored by external fetal monitor from admission until 5:26 a.m., when it was disconnected and Mrs. LaPoint was transported to the operating room (OR). During that period, FHT baseline remained consistent at 150 to 160 beats per minute, except for one episode of variable/late deceleration to the 90-beat per minute range at about 3:00 a.m., but with good beat-to-beat variability and recovery to baseline was noted. One other variable deceleration was noted shortly thereafter to the 120-beat per minute range with spontaneous recovery to baseline. Notably, while the tape reveals some diminished long term variability with contractions, it does not reveal a pattern of persistent deceleration. Mrs. LaPoint was transported to the OR at 5:26 a.m., at which time FHT was noted as 150 beats per minute, and contractions were noted as moderate (with a frequency of 2 minutes and a duration of 40 to 60 seconds). Anesthesia was noted to commence at 5:50 a.m., the operation started at 6:08 a.m., and Jacqueline was delivered at 6:14 a.m. Cord specimen was obtained, and when subsequently analyzed revealed that, at delivery, Jacqueline presented with a pH of 7.085, PCO2 of 90.3, PO2 of 19.2, HCO3 of 27, and a Base Excess (BE) of -6. During delivery amniotic fluid was noted to be thin merconium stained, and oropharyngeal suctioning was done before the shoulders were delivered. Jacqueline was noted as limp (hypotonic) and apnic at birth, and intermittent positive pressure ventilation was given by bag and mask for about one minute. Laryngoscopy revealed cords were clear. Apgars of 4 and 8 were assigned at one and five minutes, respectively. The Apgar scores assigned to Jacqueline are a numeric expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, muscle tone, reflex irritability, and skin color, with each category being assigned a score ranging from the lowest score of 0 through a maximum score of 2. As noted, at one minute Jacqueline's Apgar score totalled 4, with heart rate being graded at 2; respiratory effort and color being graded at 1 each; and muscle tone and reflex irritability being graded at 0. At five minutes, Jacqueline's Apgar score totalled 8, with heart rate, respiratory effort, and reflex irritability being graded at 2 each, and muscle tone and color being graded at 1 each. While the one minute Apgar was low,5 the five minute Apgar was quite normal or, stated otherwise, not predictive of neurologic complications.6 Following stabilization, Jacqueline continued to evidence respiratory difficulty and, at or about 6:30 a.m., she was admitted to the neonatal intensive care unit (NICU) for further evaluation and management. Initial assessment on admission evidenced an unusual neurologic and respiratory presentation. Neurologically, Jacqueline was noted as lethargic, floppy, and jittery. As for her respiratory presentation, although her breathing rate was regular, she evidenced rales, grunting, flaring, and moderate retractions. Dextrostix (a reagent strip designed for determination of blood-glucose levels with the use of fingertip venous blood) on admission was low, at 26, and immediate glucose testing was ordered and also reported as critically low at 24. Diagnosis was respiratory distress syndrome (RDS) and possible hypoglycemia (an abnormally diminished concentration of glucose in the blood). Respiratory support (for RDS) and intravenous (IV) glucose (for hypoglycemia) were ordered. For respiratory support, Jacqueline was initially placed in an Oxyhood (on an infant warmer bed) with 96 percent oxygen; however, when she continued to require a high oxygen concentration to maintain her gases and saturation levels within normal limits she was intubated (at or about 8:15 a.m.) and ventilator support was provided. Thereafter, her oxygenation was maintained within normal limits without difficulty.7 While Jacqueline's RDS was successfully managed, without apparent harm (by oxygen deprivation or otherwise) to the infant, her hypoglycemia proved refractory or, stated differently, recalcitrant or not responsive to treatment. Indeed it was not until the afternoon of July 4, 1994, that her condition started to resolve, and then only after progressively intensive intervention.8 Here, Jacqueline may reasonably be described as an infant of a diabetic mother9 (IDM)--a hyperglycemic mother--who, consequently, presented with hyperinsulinism, resulting in hypoglycemia.10 Such presentation is clearly demonstrated by elevated readings of insulin in Jacqueline's blood (of 24.7 at 7:00 p.m. on July 3, 1994),11 as well as the severe hypoglycemia she developed subsequent to delivery. Jacqueline was noted as "jittery" throughout the course of treatment; however, the most pronounced period of physiological abnormality was noted at or about 8:00 a.m., July 4, 1994. At that time, an apnic episode was noted during assessment, and tone was flaccid, color pale, and lips dusky. Jacqueline was accorded tactile stimulation without response, and manual breaths were given from the ventilator for approximately 30 seconds before a response was noted. Jacqueline was noted as jittery and diaphoretic (evidencing profuse perspiration). Other apnic episodes, with similar observations, were noted and addressed at 8:15 a.m., 8:18 a.m., and 8:30 a.m. Neurologic consult was called, and an EEG was recommended to rule out seizures, and an ultrasound to rule out possible intraventricular hemorrhage. The EEG was read as normal and the head ultrasound was read as within normal limits, as follows: "No evidence of intraventricular or subpendymal hemorrhage. The ventricles appear normal in size, left slightly larger than right." Jacqueline was started on a course of antibiotics to address the possible presence of sepsis. At or about 4:00 p.m., July 4, 1994, Jacqueline's urinary output was noted to be diminished. Her output continued as diminished and at or about 5:40 p.m., given such development, as well as her continued complex metabolic problems, her treating physician ordered Jacqueline transferred to the Level III Neonatal ICU at Broward General Medical Center for continued evaluation and management. Final diagnosis on discharge was, as follows: Prematurity. Large for gestational age. Respiratory distress syndrome. Hyperglycemia. Hypocalcemia. Hypomagnesemia. Rule out hypoparathyroidism. Seizure disorder. Ventriculoseptal hypertrophy. Jacqueline was discharged from Holy Cross Hospital at or about 8:30 p.m., July 4, 1994, and transported to Broward General Medical Center, where she was admitted at or about 9:18 p.m. in stable condition. There, Jacqueline's condition progressively improved and on July 11, 1994, she was discharged in her mother's care. Jacqueline's course at Broward General Medical Center is reasonably stated in her discharge summary as follows: Admission diagnoses: 36 week white female Large for gestational age Grandmultiparity Respiratory distress R/O RDS I, RDS II, Pneumonia R/O Sepsis R/O Meconium aspiration syndrome R/O Congenital heart disease R/O Pulmonary hypertension R/O Seizures R/O Hyperparathyroid R/O Hypoglycemia, hypocalcemia Transfer from Holy Cross CLINICAL PROBLEMS: Respiratory: RDS I Persistent pulmonary hypertension was diagnosed. The highest delivered FI02 was 0.46, with time spent in increased oxygen = 3 days (total). The infant was intubated and on intermittent mandatory ventilation for approximately 3 days (at BGMC). Cardiac: A cardiac consultation was performed on 7/5/94 by Dr. Miller to reassess previous consult of 7/2/94 at Holy Cross. Echocardiogram revealed hypertrophied left ventricular septum and left posterior wall, turbulance of the left ventricular outflow tract, a PDA with bidirectional shunting and increased pulmonary reistance. Dr. Millers impression as that of RDS with evidence of pulmonary hypertension and hypertrophic cardiomyopathy. Metabolic: Hypoglycemia - treated with IV glucose. Hyponatremia. IV sodium was given. Hypocalcemia. There was treatment with IV calcium. Endocrine: A consultation was performed by Dr. Motkin- Kalia on 7/5/94. Findings were most likely consistent with IDM although there was no maternal history of diabetes/gestational diabetes. Infection: A septic workup was performed on 7/2/94 at Holy Cross Hospital. There was antibiotic treatment with Ampicillin and Gentamicin for 10 days (total) due to clinical evidence of sepsis. Neurologic: Dr. Epstein was consulted on 7/5/94 due to report of seizure at Holy Cross Hospital. Most probable etiology [of seizures] was felt to be hypocalcemia. There was no further seizure activity, infant was treated with phenobarbital X 1 dose after the seizure noted on 7/4/94 An EEG was performed on 7/5/94. It was reported as within normal limits. * * * Final Discharge Diagnoses: 36 week white female Large for gestational age RDS I PFC Hypoglycemia Hyponatremia Hypocalcemia Seizure Clinical sepsis Probable IDM Condition on discharge - Recovered. Jacqueline's subsequent development Jacqueline's early infancy was apparently unremarkable until around the age of 5 to 6 months when she was noted to have visual inattention. Around the same time she was also noted to have intermittent deviation of the head downwards without any associated symptoms. On May 5, 1995, Jacqueline was evaluated by Jaime L. Baquero, M.D., a pediatric neurologist. His neurologic evaluation revealed the following: PHYSICAL EXAM: . . . she indeed appeared visually inattentive . . . [and] did have intermittent downward head deviation which was not fixed and was not associated with any other signs or symptoms. There were no overt dysmorphic features or evidence of neurocutaneous signs. The appendicular muscle tone was felt to be normal, although her axial tone diminished. No other abnormalities were noted on examination. IN SUMMARY, based on clinical history and examination, it does appear that Jacqueline is experiencing significant visual impairment which at this point in my view is very difficult to distinguish whether this is a congenital blindness or delayed visual maturation. The possibility of optic nerve hypoplasia should be entertained being that the mother has possible maternal gestational diabetes, and in addition manifestations of hypoglycemia and hypocalcemia were seen in the neonatal period with seizures accompanying this metabolic deficit. It is known that there is a higher incidence of septal optic dysplasia associated with infants born to diabetic mothers. This sometimes is accompanied by hypopituitarism, therefore, I would recommend obtaining an MRI of the brain to R/O that possibility. In addition, I would like to obtain an EEG because of the concern with this startle and jerking which is seen more often in the morning. In addition, I would like to obtain a Visual Evoked Response to evaluate the integrity of the visual pathways, although if her visual deficits would be cortical, it could still be within normal limits. At some point she would deserve an endocrinologic evaluation to R/O the presence or absence of hypopituitarism. Obviously, being that her APGARS were somewhat low and that she was ventilated, the optic atrophy associated with hypoxic ischemia encephalopathy is still a possibility. I discussed all these different diagnoses with Mrs. LaPointe and we will sit down in a follow-up visit to discuss these issues after the tests have been obtained. Consistent with Dr. Baquero's suggestion, Jacqueline was admitted to Broward General Medical Center on June 6, 1995. The Visual Evoke Response test was normal, "suggesting normal conduction of the pathway between the retina and the occipital lobes bilaterally." The electroencephalogram (EEG) was read as abnormal "due to the presence of intermittent polymorphic slowing noted primarily in the left posterior quadrant but with a field extending sometimes to the right posterior quadrant with admixed spike discharges. These findings are indicative of a regional disturbance of cerebral function that is potentially epiteptogenic maximally noted in the left posterior quadrant."12 On June 14, 1995, Jacqueline was referred to Broward General Medical Center for evaluation of "daily episodes of upper extremity rapid 'jerks'" (possible new onset seizure activity). No seizures were noted on the 24-hour video EEG and on June 15, 1995, Jacqueline was discharged. On June 20, 1995, an MRI of the brain was finally obtained. That MRI revealed the following: FINDINGS CONSISTENT WITH PERIVENTRICULAR LEUKOMALACIA. DELAYED MYELINATION SEEN THROUGHOUT THE CEREBRAL CORTEX AS DESCRIBED ABOVE. THERE ARE NO MRI FINDINGS SEEN TO SUGGEST SEPTAL OPTIC DYSPLASIA. The dispute regarding compensability Here, there is no dispute that Jacqueline suffered an injury to her brain which has resulted in permanent and substantial mental and physical impairment. Indeed, the record reflects, without contradiction, that Jacqueline presents with severe spastic diplegia, is wheelchair dependent for all community mobility, and suffers cortical blindness. What is subject to dispute is the cause and timing (genesis) of Jacqueline's brain injury or, pertinent to these proceedings, whether the proof demonstrates, more likely than not, that her neurologic impairment resulted from an "injury to the brain . . . caused by oxygen deprivation or mechanical injury, occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as opposed to some other genesis. With regard to such issue, Petitioner is of the view that, while there is no dispute that Jacqueline suffered (post- delivery) a significant brain injury caused by severe hypoglycemia, Jacqueline also suffered pre-natal or immediate post-natal oxygen deprivation which caused, or operating in concert with her subsequent hypoglycemia caused, her brain injury. (Petitioner's Proposed Final Order, at page 18.) In contrast, Respondent is of the view that the proof is not consistent with brain injury caused by oxygen deprivation occurring during or immediately following birth and must, therefore, be attributable to Jacqueline's hypoglycemia. Respondent's view of the proof has merit. The genesis of Jacqueline's injury To address the genesis of Jacqueline's brain injury, the parties offered selected records relating to Mrs. LaPoint's antepartum and intrapartum course, as well as for Jacqueline's birth and subsequent development.13 Portions of those records have been addressed supra, and further salient portions will be addressed infra. The parties also offered the opinions of six physicians to address the likely cause of Jacqueline's injury. The physicians offered by Petitioner were Marsh McEachrane, M.D., a board certified obstetrician and gynecologist; Michael Tidwell, M.D., a board certified orthopedist; Lalit Shah, M.D., a board certified neonatologist; and Jaime Baquero, M.D., a pediatric neurologist, board certified in pediatrics and board eligible in neurology. The physicians offered by Respondent were Charles Kalstone, M.D., a board certified obstetrician and gynecologist; and Edward Lance Wyble, M.D., a board certified neonatologist. The medical records and other proof, including the testimony of the physicians offered by the parties, have been carefully considered. So considered, it must be concluded that the proof does not support (or allow a conclusion to be drawn with any sense of confidence) that, more likely than not, Jacqueline's brain injury was caused by oxygen deprivation occurring during the course of labor, delivery, or resuscitation in the immediate post-delivery period. Rather, the proof demonstrates, more likely than not, that Jacqueline's brain injury was directly related to the severe and intractable hypoglycemia she suffered following delivery and that it was not associated with any event which may have occurred during the course of labor, delivery, or resuscitation in the immediate post-delivery period.14 In so concluding, it is observed that Jacqueline's course pre-delivery and post-delivery was inconsistent with hypoxic or ischemic injury having occurred during the course of labor, delivery, or resuscitation. First, the evidence documenting fetal heart rate during the course of labor and delivery does not support the conclusion that Jacqueline suffered an acute intrapartum event that led to hypoxic or ischemic injury. Notably, there were only two variable decelerations (one to 90 beats per minute and the other to 120 beats per minute), but with good beat-to-beat variability and spontaneous recovery to baseline, and no persistent or pattern of persistent decelerations. Under such circumstances, the monitoring tape was reassuring and it is unlikely, based on such tape, that fetal oxygenation was adversely affected during labor and delivery.15 Further militating against the conclusion that Jacqueline's brain injury was caused (in whole or part) by oxygen deprivation pre-delivery, or new-onset hypoxia post-delivery, is the lack of trauma associated with Mrs. LaPoint's labor and delivery (labor was short, approximately 5 hours, and delivery was by cesarean section), and the numerous inconsistencies between Jacqueline's presentation and development, and the clinical findings one would expect had she suffered hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, during that period.16 Notably, Jacqueline's Apgar scores were 4 at one minute and 8 at five minutes. While an Apgar of 4 at one minute is less than average or not normal, it is but a reflection of the infant's status where, as here, the infant is going through the change process after birth. Importantly, the Apgar did not remain depressed, as it would have had she suffered an acute intrapartum event, but progressed to 8 (a very normal Apgar score) by five minutes. Clearly, the infant was improving over that period, which also compels the conclusion that there was no new or ongoing insult. Also inconsistent with brain injury during or immediately following birth, there was no evidence of metabolic acidosis on the cord blood sample and, consequently, no evidence to support an ongoing hypoxic process during the course of labor. Moreover, had Jacqueline suffered an injury to her brain during or immediately following birth, there are a number of other clinical findings one would reasonably expect to observe that were absent in her case. For example, an infant who suffered a hypoxic ischemic injury during such period would not only present with initial depression (more severe than Jacqueline evidenced), but would continue to demonstrate severe depression at one, five, and ten minutes. Additionally, in cases of substantial neurologic injury, the infant should generally evidence seizure activity within 8 to 24 hours. Finally, inconsistent with brain injury during or immediately following birth, there was no evidence (within 5 or 6 hours of delivery) of other or multi- organ system dysfunction, including kidney dysfunction. Evidence of such dysfunction would be reflected in decreased urine out-put and on biochemical analysis of blood with elevated serum creatinine levels. No such dysfunction was present in the hours immediately following Jacqueline's birth. Contrasted with the paucity of compelling evidence of perinatal asphyxia as the cause for Jacqueline's brain injury, the medical records and other persuasive proof clearly demonstrate the presence of severe and untractable hypoglycemia and support the conclusion that Jacqueline's brain injury was caused, post-delivery, by the presence of such metablic derangement. Supportive of such conclusion, it is observed that contemporaneously with the observed on-set of hypoglycemia (at or about 6:30 a.m., following admission to the neonatal ICU), Jacqueline was observed to be jittery, lethargic, and floppy, clinical symptoms typically associated with hypoglycemia. Such presentation persisted as Jacqueline's hypoglycemia proved severe and intractable, and at or about 8:00 a.m., July 4, 1994, Jacqueline was noted to undergo an apnic episode, and her tone was flaccid, color pale, and lips dusky. Such events are clinical evidence of the on-set of seizure activity which, given its timing, is compelling proof of brain injury associated with hypoglycemia and not any event associated with labor or delivery, which occurred over 48-hours previously. Further supporting the timing and cause of Jacqueline's insult, is evidence of kidney dysfunction (diminished urine output) at or about 4:00 p.m., July 4, 1994. Given the proof, it cannot be concluded that, more likely than not, Jacqueline's brain injury, and resultant neurologic impairment, was caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Notably, Jacqueline's presentation and neonatal course were not consistent with an acutely acquired neurologic injury, and it is improbable that she could have experienced an acute injury during labor and delivery, or immediately thereafter, without evidencing clinical symptoms of such damage. Conversely, a brain injury, resulting from hypoglycemia acquired post-delivery, would be consistent with Jacqueline's presentation at birth and subsequent development.
Findings Of Fact Jaliyah was born on March 7, 2017, at Lakeland Regional Medical Center. With respect to Jaliyah’s birth, obstetrical services were delivered by Maria Martino, M.D., a NICA participating physician, in the course of labor, delivery, or resuscitation in the immediate postdelivery period. NICA retained Donald Willis, M.D., an obstetrician specializing in maternal-fetal medicine, to review Jaliyah’s medical records and opine as to whether there was an injury to her brain or spinal cord that occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period due to oxygen deprivation or mechanical injury. In his report and subsequent affidavit (attached to NICA’s Motion), Dr. Willis opines that “there was an obstetrical event that resulted in loss of oxygen to the baby’s brain during labor, delivery and continuing into the immediate post deliver [sic] period. The oxygen deprivation resulted in brain injury.” NICA also retained Laufey Y. Sigurdardottir, M.D., a pediatric neurologist, to review Jaliyah’s medical records, conduct an Independent Medical Examination (IME), and opine as to whether she suffers from a permanent and substantial mental and physical impairment as a result of a birth-related neurological injury. Dr. Sigurdardottir reviewed the available medical records, obtained a full historical account from Petitioner, and conducted an IME of Jaliyah on December 13, 2017. Dr. Sigurdardottir’s affidavit, attached to NICA’s Motion, provides in pertinent part, as follows: Based upon my education, training and experience, it is my professional opinion, within a reasonable degree of medical probability that although there is evidence of impairment consistent with a neurologic injury to the brain or spinal cord acquired due to oxygen deprivation or mechanical injury, Jaliyah is not found to have substantial delays in motor and mental abilities. Her prognosis for full motor and mental recovery is excellent and her life expectancy is full. A review of the file reveals that no contrary evidence was presented to refute the findings and opinions of Dr. Willis and Dr. Sigurdardottir. Their unrefuted opinions are credited.
The Issue At issue in this proceeding is whether Blane Earl Pearson, Jr., 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, Blane Earl Pearson and Janet Pearson, are the parents and natural guardians of Blane Earl Pearson, Jr., a minor. Blane was born a live infant on October 5, 1998, at Shands at AHG (Alachua General Hospital), a hospital located in Gainesville, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Blane's birth was Bradley Williams, 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 under 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." Sections 766.302(2) and 766.301(1)(a), Florida Statutes. Here, the parties have stipulated, and the proof otherwise demonstrates, that Blane is permanently and substantially mentally and physically impaired. What remains to resolve is whether Blane's impairment is related to an injury to the brain caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the hospital. Blane's birth At or about 6:30 a.m., October 5, 1998, Mrs. Pearson (with an estimated date of delivery of October 10, 1998, and the fetus at 39+ weeks gestation) presented to Alachua General Hospital for induction of labor. At the time, Mrs. Pearson's membranes were noted as intact, and no contractions or vaginal bleeding were observed. External fetal monitoring, which began at 6:41 a.m., revealed a reassuring fetal heart rate. Pitocin drip was started at 7:59 a.m., and by 9:19 a.m., Mrs. Pearson was experiencing irregular contractions. In the interim, external fetal monitoring revealed a reassuring fetal heart rate (in the 130 beat per minute range), with good reactivity and variability.3 Mrs. Pearson's labor progressed steadily, and at or about 11:50 a.m., vaginal examination revealed the cervix at 3 centimeters dilation, effacement at 80 percent, and the fetus at station -1. At that time, the membranes were artificially ruptured, with clear fluid noted, and Dr. Williams authorized an epidural anesthesia.4 Mrs. Pearson's labor continued to progress steadily, and at 1:04 p.m., with the cervix at 10 centimeters dilation, effacement at 100 percent, and the fetus at station +1, Dr. Williams was called and advised that Mrs. Pearson was "complete and wanting to push." Dr. Williams announced he was "on his way," arrived in the labor and delivery room at 1:18 p.m., and at 1:20 p.m., Blane was delivered spontaneously, without incident. On delivery, Blane was bulb-suctioned, accorded blowby oxygen, dried, and moved to a radiant warmer. Initial newborn assessment noted no apparent abnormalities. Apgar scores were recorded as 8 at one minute and 9 at five minutes. The Apgar scores assigned to Blane are a numeric expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, muscle tone, reflex irritability, and 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, Blane's Apgar score totaled 8, with heart rate, respiratory effort, muscle tone, and reflex irritability being graded at 2 each, and color being graded at 0. At five minutes, Blane's Apgar score totaled 9, with heart rate, respiratory effort, muscle tone, and reflex irritability again being graded at 2 each, and color now being graded at 1. Such score is considered good, and inconsistent with recent hypoxic insult or trauma. Following the initial newborn assessment, Blane was examined by Karen Dees, an advanced registered nurse practitioner (ARNP). On examination, Ms. Dees noted Blane as "active," and her physical examination as "unremarkable" or stated otherwise, within normal limits (WNL). Ms. Dees completed her examination at or about 1:45 p.m., and executed the standard orders for Blane's admission to the newborn nursery. Blane transitioned for a brief period with his mother in the labor and delivery room and was then transferred to the newborn nursery, where he apparently did well until 5:20 p.m., when he was noted with tachypnea (at a respiratory rate of 68), slight nasal flaring, and respirations that appeared irregular. Questionable circumoral cyanosis was noted, with quick return to pink. Blane was transported to the neonatal intensive care unit (NICU) for evaluation by NICU staff. At the time, he again evidenced circumoral cyanosis, as well as an apneic episode, and was provided blowby oxygen and stimulation, with quick return to pink. Blane was admitted to NICU (for further management and observation), and placed on monitors and under an oxyhood. Labs were ordered (BC, ABG, and CBC with differential), and antibiotics (ampicillen and gentamicin) were prescribed for suspected sepsis. During the late afternoon and early evening, Blane was noted with several more apneic episodes, followed by tachypnea. And, at 8:00 p.m., Blane was noted to exhibit extensioned extremities, hypotonia, weak grasp, and deep to shallow irregular non-labored respirations. At 9:00 p.m., Blane experienced a long apneic spell requiring stimulation. No obvious seizure activity was noted, but his eyes deviated to the left. The impression was apnea of unknown etiology, respiratory distress of unknown etiology, and possibly intraventricular hemorrhage (IVH), seizures, and hypocalcemia. The Plan was to continue antibiotics and to perform a cranial ultrasound (to rule out a bleed). The cranial ultrasound was done at 11:00 p.m., and read as follows: HISTORY: Apneic spells and possible seizure activity. Evaluation for intracranial hemorrhage in a full term, newborn infant. FINDINGS: The intracranial, supratentorial structures are well delineated and exhibit no apparent hemorrhage or mass effect. The ventricles are not enlarged. The posterior fossa structures are seen best sagittally and appear unremarkable. IMPRESSION: NO HEMORRHAGE IDENTIFIED During the ultrasound, Blane had another apneic episode, requiring ambu bagging. At 1:00 a.m., October 6, 1998, Blane was given phenobarbital for suspected seizure activity, and at 1:30 a.m., he was intubated and placed on a ventilator because of multiple apneic episodes. Later that morning, at or about 9:00 a.m., Blane was transferred to Shands Hospital at the University of Florida (Shands Hospital), a level 3 neonatal intensive care facility, where he remained until October 17, 1998, when he was discharged to his mother's care. While admitted to Shands Hospital, Blane underwent a number of studies to identify the cause of his difficulties (seizures/apnea). Among those studies was an EEG, as well as CT of the head, done on October 6, 1998. The EEG was read, as follows: IMPRESSION: This is an abnormal EEG because of the presence of sharp waves seen over the frontocentral and temporal regions. This is consistent with but not diagnostic of a seizure disorder. In addition, positive sharp waves are also noted over both temporal regions. This is consistent with a diagnosis of intraventricular hemorrhage or periventricular leukomalacia. The CT of the head was reported, as follows: The peripheral cortical areas in the ACA and MCA distributions bilaterally have markedly decreased attenuation and loss of cortical sulci. These changes are most pronounced on the right. There is no evidence for intracranial hemorrhage. There is no evidence of herniation at this time. The basal ganglia, thalamus, and cerebellum are intact. IMPRESSION: The peripheral cortical territories in the ACA and MCA artery distributions bilaterally have decreased attenuation and loss of cortical sulci. These changes are most pronounced on the right and are compatible with an anoxic brain injury. A head UMR study was obtained on October 7, 1998, and compared with the CT exam of October 6, 1998. The results were reported, as follows: FINDINGS: Cerebral M.R. study was obtained 10/7/98 and compared to the 10/6/98 CT exam. There is diffuse cytogenic edema which is comparable on the two studies and is not evolved. The edema corresponds to lateral cortical areas on the right side in the middle cerebral artery zone and involves the anterior suprasylvian, the anterior infrasylvian and basal ganglion region on the left side. This also appears to be involving much of the middle cerebral artery zone on the left side. The remainder of the brain has less edema or no edema. The T1-weighted images are hyperintense in the basal ganglion region on the right side, indicative of coagulative necrosis in blood products, but not distinct hematoma. The findings are compatible with perfusion defects in the middle cerebral artery zones bilaterally. They do not appear to correspond to areas of cortex to suggest trauma since the patient is recently delivered. The remainder of the examination is unremarkable. There is no midline shift or downward herniation. IMPRESSION: Evidence of diffuse cytogenic edema in the middle cerebral artery zones bilaterally as described above. Etiology is not apparent. Regarding the results of the scan, the attending neonatologist noted "CT scan . . . grossly abnormal -- [consistent with] . . . diffuse hypoxic/ischemic insult, of recent timing, although it is not possible to pin down the exact timing." Finally, at 7:57 a.m., October 15, 1998, Blane had a final CT of the head to reassess his cerebral edema. That exam was reported, as follows: COMPARISON: Continuous axial CT images were obtained of the brain. Those dated 10/15/98 are directly compared to prior dated 10/6/98. FINDINGS: Again seen is ischemic encephalopathy. Multiple vascular territories show areas of ischemia/infarct. The ischemic core now contains blood products and radiographic appearance consistent with coagulative necrosis. No hematoma is seen. When compared to prior images there is decreased edema with now visualization of the lateral ventricles. Decreased mass effect when compared to prior images is seen. IMPRESSION: Known ischemic encephalopathy with blood products now seen in the ischemic core. Decreased edema. Less mass effect. The cause and timing of Blane's brain injury To address the issue of whether Blane's brain injury was "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," as required for coverage under the Plan, Petitioners offered medical records relating to Mrs. Pearson's antepartum and intrapartum course, as well as Blane's birth and subsequent development. (Petitioners' Exhibits 1 and 2). Portions of those records have been addressed supra, and other salient portions of those records will be addressed infra. Additionally, Petitioner Janet Pearson testified on her own behalf, and offered the testimony of Janet Luna (Mrs. Pearson's mother) and the deposition testimony of Laura Law (Mrs. Pearson's sister). Respondent offered the deposition testimony of Dr. Michael Duchowny, a physician board- certified in pediatric neurology, and Dr. Charles Kalstone, a physician board-certified in obstetrics and gynecology. As for the cause and timing of Blane's brain injury, it was Dr. Duchowny's opinion that the injury Blane suffered was, more likely than not, intrauterine acquired, and attributable to events which occurred prior to labor and delivery. In so concluding, Dr. Duchowny observed that contrary to what one would expect if Blane had suffered a recent neurological injury, his Apgar scores were good, his arterial blood gases were normal, and he required no assistance other than blowby oxygen. It was also Dr. Duchowny's opinion that Blane's brain injury was not caused by oxygen deprivation or mechanical injury. (Respondent's Exhibit 1, pages 25 and 26). As for the cause of Blane's injury, it was Dr. Duchowny's opinion that it was most likely associated with a stroke or series of strokes suffered late in term. (Respondent's Exhibit 1, pages 23 and 24). For similar reasons, Dr. Kalstone, like Dr. Duchowny, was of the opinion, based on his review of the medical records, including the fetal monitor strips, that Blane's presentation (during labor and delivery) was not consistent with a brain injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation. As for the cause, as well as the timing of Blane's injury, Dr. Kalstone deferred to others, such as a pediatric neurologist, who were more suited to address that issue. (Respondent's Exhibit 2, page 14). Petitioners did not offer any expert testimony to support their view that Blane's brain injury was occasioned by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post- delivery period in the hospital. Petitioners did, however, offer the testimony of Petitioner Janet Pearson, Janet Luna and Laura Law on two matters: the actions of the nursing staff, which they perceived to be an effort to forestall Blane's delivery; and their opinions regarding Blane's condition on delivery. These matters, Petitioners believe, were not considered by Respondent's experts (because they were not contained within the medical records), and they contend such matters compel the conclusion that Blane's injury was occasioned by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period. With regard to the first matter, Petitioner Janet Pearson and her witnesses testified that a nurse gloved-up, placed her hand inside Mrs. Pearson's vagina, and placed her hand on Blane's head to forestall delivery until the doctor could arrive. Petitioners suggest the nurse's act was improper and may have resulted in injury to Blane; however, they offered no competent proof to support such contention. Indeed, the only testimony on the matter was given by Doctors Kalstone and Duchowny who observed that, under the circumstances of this case, the nurse's action was unlikely to have caused any injury to Blane. In this regard, Dr. Kalstone, responding to questions by counsel for Petitioners observed: Q. Let me ask you, Doctor, hypothetically, assuming that at sometime during the labor that Blane was manipulated by one or more nurses in such a fashion as to push his head back into or farther up the birth canal, assuming that type of manipulation, is that the type of motor force that could cause an injury? * * * If the nurses were trying to hold the baby in, so to speak, then I wouldn't expect it would cause significant damage like this baby has. The kinds of damage that that thing, that that kind of action can cause, although I've never seen it, would be if there was like intracranial hemorrhage that caused the problem, that is actual trauma, and its hard to traumatize a baby's head by pushing it back up, but that would be one mechanism, that if you caused an intracranial hemorrhage, so to speak, and I didn't see any evidence of that in the record, in the CT scan. There was nothing suspicious in the baby's records that I could tell that that was a brain hemorrhage, but that would be one possible mechanism that one at least would look for. And the other would be if that in some way can cause an oxygen deprivation, which I've never seen it . . . [do] that, again, I haven't seen this done that often, sometimes we intentionally push a baby's head up when the cord prolapses to keep them off the cord. There's a decrease in the fetal heart sometimes by reflex when you push on the baby's head, but it usually wouldn't cause brain damage or significant problem, and if it did, I would expect it, that the baby would come out in poor condition if this occurred right before the doctor arrived, but this baby was born with an APGAR of 8 and 9 at one and five minutes, which were normal, so I would think that if there was anything that the nurses did that caused the oxygen deprivation, that, first of all, I would think that would be unlikely that it would cause that, just what they could be able to do with their hands. And second of all, I would think it wouldn't have been the kind of thing that would have damaged the baby and then the baby came out without showing signs of being asphyxiated. [Respondent's Exhibit 2, pages 15-17]. Dr. Duchowny's opinions on the matter were strikingly similar to those of Dr. Kalstone. (Respondent's Exhibit 1, pages 20-22, 24, and 32). With regard to the second matter, Mrs. Pearson and her witnesses testified as to their observations regarding Blane's condition on delivery, which they contend supports an Apgar score substantially lower than the score recorded at birth.5 Petitioners also suggest that the Apgar scores recorded by the nurse were most likely inflated because of a "certain self- interest motive . . . , if, and in the event, that they indeed were pushing him back in, holding him, . . . to wait for the doctor to get there." (Petitioners' proposed final order, paragraph 28). Consequently, since Respondent's experts relied on the Apgar scores of record in rendering their opinions, Petitioners suggest their opinions should be rejected, and a conclusion drawn that Blane's injury was caused by oxygen deprivation that occurred during the course of labor, delivery, or resuscitation. Petitioners' contention is rejected. In rejecting Petitioners' contention, it is initially observed that, where, as here, there was no showing that the nursing staff acted improperly, or that their actions could reasonably cause injury to the infant, there was no compelling reason for fabrication. Moreover, following delivery, Blane was also examined by Ms. Dees, who discerned no apparent abnormality, and Blane's course in the newborn nursery did not raise any concern until approximately 4 hours of age. Under such circumstances, it is doubtful that Blane's initial Apgar scores were inflated by the nursing staff at delivery. Additionally, it is observed that, while Petitioners offered testimony which, if credited, might warrant a reassessment of Blane's Apgar scores, they failed to offer any expert testimony or other competent proof as to what that score would be. Consequently, any reassessment of Blane's Apgar scores would be founded on speculation. Finally, it is observed that the opinions of Doctors Duchowny and Kalstone were not predicted simply on Blane's Apgar scores. Rather, their opinion that Blane's injury was not caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation, was also premised on evidence which demonstrated that Blane's arterial blood gases were normal, he required no assistance at birth other than blowby oxygen, and the fetal monitor strips failed to reveal any event consistent with fetal compromise. Accordingly, it must be concluded that the proof failed to demonstrate that Blane suffered a "birth-related neurological injury" since the proof failed to demonstrate that, more likely than not, his impairments were associated with a brain or spinal cord injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital.
Findings Of Fact By stipulation filed November 8, 1995, petitioners and respondent stipulated as follows: That pursuant to Chapter 766.301 - 766.316, Florida Statutes, a claim was filed on behalf of the above-styled infant against the Florida Birth-Related Neurological Injury Compensation Association (the Association) by Susan Petty Rogers and Calyvin Rogers (the petitioners) for benefits under Chapter 766.301 - 766.316, F.S. That a timely filed claim for benefits complying with the requirements of F.S. 766.305 was filed by Petitioners and a timely denial was filed on behalf of the Association. That the Division of Administrative Hearings has jurisdiction of the parties and the subject matter of this claim That the parties agree the medical records of Chelsea Rogers reveal that she suffers form an injury to the right brachial plexus. A brachial plexus injury is not, however, a brain or spinal cord injury. Chelsea has also been diagnosed by T. Wayne Conger, Ph.D., a neuropsychologist, as having a cognitive disorder which may be related to her birth. The cognitive disorder is not, however, a brain injury " which renders the infant permanently and substantially mentally and physically impaired." Therefore, Chelsea does not fit within the strict definition of claims covered by the Florida Birth-Related Neurological Injury Compensation Association under Section 766.302.(2), Florida Statutes. That the infant, Chelsea Rogers was born at Tallahassee Memorial Hospital on April 5, 1990, and that the said hospital was a licensed Florida hospital. The participating physician who was present at the birth and delivered obstetrical services was A. J. Brickler, M.D. That the infant, Chelsea Rogers, weighed 4,510 grams which is in excess of 2,500 grams. WHEREFORE, based upon the above stipulated set of facts, it is respectfully requested that the Division of Administrative Hearings approve the stipulations as being consistent with the evidence in this cause and enter an order denying the claim against the Association on the basis that Chelsea Rogers did not suffer a birth-related neurological injury as defined by Section 766.302(2), Florida Statutes. The medical records and other documentation of record in this case reveal, consistent with the parties' stipulation, that Chelsea Rogers suffered a right brachial plexus injury at birth. A brachial plexus injury is not, however, a brain or spinal cord injury and such injury did not render her substantially physically impaired. Moreover, while Chelsea Rogers may have a cognitive disorder, she is not substantially mentally impaired.
Recommendation Based on the foregoing Findings of Fact and Conclusions of Law, it is ORDERED that the petition for compensation filed by Susan Petty Rogers and Calyvin Rogers, as parents and natural guardians of Chelsea Rogers, a minor, be and the same is hereby denied with prejudice. DONE AND ORDERED this 14th day of November 1995 in Tallahassee, Leon County, Florida. ___________________________________ WILLIAM J. KENDRICK Hearing Officer Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-1550 (904) 488-9675 Filed with the Clerk of the Division of Administrative Hearings this 14th day of November 1995.
