Findings Of Fact Elaina was born on July 23, 2018, at St. Vincent’s Hospital, located in Duval County, Florida. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Elaina. In a medical report dated August 13, 2020, Dr. Willis summarized his findings and opined, in pertinent part, as follows: In summary, pregnancy was essentially uncomplicated. Spontaneous vaginal birth resulted in a healthy newborn with Apgar scores of 8/9. The newborn hospital course was uncomplicated. MRI at about one year of age showed cerebral volume loss, consistent with prior brain injury. The brain injury was apparently not due to birth related oxygen deprivation or trauma. As such, it is my opinion that there was no apparent obstetrical event that resulted in oxygen deprivation and or mechanical trauma to the brain or spinal cord during labor, delivery or in the immediate post-delivery period. NICA retained Raj D. Sheth, M.D. (Dr. Sheth), a medical expert specializing in pediatric neurology, to examine Elaina and to review her medical records. Dr. Sheth examined Elaina on June 17, 2020. In a medical report dated June 17, 2020, Dr. Sheth summarized his examination of Elaina and opined, in pertinent part, as follows: Elaina Howe does suffer from substantial physical impairment and substantial mental impairment as manifest by delays in gross motor, and fine motor, language and personal social skills. Elaina Howe mental and physical impairments are likely to be permanent although there is likely to be some improvement with time. The mental and physical impairments are not consistent with an injury to the brain or spinal cord acquired due to oxygen deprivation or mechanical injury occurring during labor and delivery or immediate post delivery period. The permanent and substantial impairments from the records provided and this evaluation do not appear to have occurred during labor, delivery or the immediate post-delivery period. NICA filed a Supplemental Affidavit of Dr. Willis on December 21, 2020, in which he offered an opinion on the fetal heart tracing records submitted by Petitioners. Dr. Willis opined as follows: The FHR tracing during labor was reassuring (no distress), consistent with my previous opinion, dated 6/17/20, that there was no apparent obstetrical event that resulted in oxygen deprivation and or mechanical trauma to the brain or spinal cord during labor, delivery or in the immediate post delivery period. The Opinions se[t] forth in my Affidavit executed July 21, 2020 remain the same and are not modified by my review of the additional medical records as indicated herein. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Willis that it is unlikely that any significant oxygen deprivation occurred prior to the birth of Elaina. Dr. Willis’s opinion is credited. There are no expert opinions filed that are contrary to Dr. Sheth’s opinion that Elaina should not be considered for inclusion in the NICA program. Dr. Sheth’s opinion is credited. Petitioners have failed to respond to the Motion or the undersigned’s Second Order to Show Cause.
Findings Of Fact On December 13, 2018, Petitioner filed a Petition for Benefits Pursuant to Florida Statute Section 766.301 et seq. for benefits pursuant to sections 766.301-766.316, Florida Statutes, otherwise known as the Plan. The baby was born on April 1, 2018, at Winnie Palmer Hospital for Women and Babies (Hospital). The circumstances of the labor, delivery, and birth of the minor child are reflected in the medical records the Hospital submitted with the Petition. In the instant case, NICA has retained Donald C. Willis, M.D. as its medical expert specializing in maternal- fetal medicine. Upon examination of the pertinent medical records, Dr. Willis opined: There was no apparent obstetrical event that resulted in oxygen deprivation or mechanical trauma to the baby's brain or spinal cord during labor, delivery or the immediate post-delivery period. Dr. Willis’s medical report dated February 25, 2019, (which reviews additional medical records), are attached to his Affidavit, with the Affidavit being attached to the motion as Exhibit “1”. His Affidavit reflects his ultimate opinion that: The baby suffered cerebral infarction, which appear to have occurred after the period of stabilization during the immediate post delivery period. Medical records do not suggest the cerebral infarction occurred during labor, delivery or the immediate post delivery period. As such, it is my ultimate opinion that there was no apparent obstetrical event that resulted in oxygen deprivation or mechanical trauma to the baby's brain or spinal cord during labor, delivery or the immediate post-delivery period. In the instant case, NICA has retained Michael S. Duchowny, M.D. as its medical expert in pediatric neurology. Upon examination of the child and the pertinent medical records, Dr. Duchowny opined: I reviewed medical records which document Elias's birth at 37 weeks' gestation at Winnie Palmer Hospital. The pregnancy was complicated by pre-eclampsia, asthma, GERD and obesity. The mother had a fever to 101 degrees at time of delivery and was diagnosed with chorioamnionitis. Elias was born vaginally with a birth weight of 5 pounds 10 ounces (2547 grams). Apgar scores were 8 and 9 at 1 and 5 minutes. Elias was admitted to the NICU and found to have a blood glucose of 35. His NICU stay was further complicated by apnea and desaturation that raised concerns for seizures; he was started on Keppra, Elias was never intubated or mechanically ventilated and was maintained on room air. An MRI scan of the brain on DOL #2 revealed multiple ischemic infarcts involving the left lateral temporal lobe, left posterior thalamus and left hippocampal formation. There was adjacent extra-axial hemorrhage over the left temporal lobe. The findings were felt to most likely represent areas of venous infarction. Dr. Duchowny’s medical report is attached to his Affidavit, with the Affidavit being attached to the motion as Exhibit “2”. His Report reflects his ultimate opinion that: A consideration of the findings from today's evaluation and record review lead me to recommend that Elias not be considered for compensation within the NICA program. He has normal motor functions and his stroke was likely acquired prenatally. There is no evidence of either mechanical injury or oxygen deprivation in the course of labor, delivery or the immediate post-delivery period. The Affidavits of Dr. Willis and Dr. Duchowny are the only evidence of record relating to the issue of whether the subject claim is compensable as defined by the statute. As noted, Petitioner did not file a response to the motion, nor submit countervailing affidavits. The Petition, along with the Affidavits attached to the motion, establish that there are no genuine issues of material fact regarding the compensability of this claim.
Other Judicial Opinions Review of a final order of an administrative law judge shall be by appeal to the District Court of Appeal pursuant to section 766.311(1), Florida Statutes. Review proceedings are governed by the Florida Rules of Appellate Procedure. Such proceedings are commenced by filing the original notice of administrative appeal with the agency clerk of the Division of Administrative Hearings within 30 days of rendition of the order to be reviewed, and a copy, accompanied by filing fees prescribed by law, with the clerk of the appropriate District Court of Appeal. See § 766.311(1), Fla. Stat., and Fla. Birth-Related Neurological Injury Comp. Ass'n v. Carreras, 598 So. 2d 299 (Fla. 1st DCA 1992).
Findings Of Fact Lennox Wiles was born on May 11, 2014, at Tallahassee Memorial Hospital located in Tallahassee, Florida. Lennox weighed in excess of 2,500 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Lennox, to determine whether an injury occurred 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 an affidavit dated January 23, 2017, Dr. Willis set forth his findings and opinion in pertinent part as follows: It is my opinion the mother was not in labor, so the injury did not occur during labor. Delivery was by Cesarean section, so hypoxic brain injury did not occur during delivery. The baby was crying at birth, again suggesting there was no significant brain injury during delivery. Respiratory distress occurred shortly after delivery and required bag and mask ventilation for 30 seconds. Apgar score was 9 by 5 minutes. Spontaneous respiratory activity resumed and the baby was left with the Labor and Delivery staff. Once the NICU staff left the baby with the L & D staff, this would indicate the baby was stable and would end the immediate post- delivery period. It would be unlikely that significant hypoxic brain injury occurred during post-delivery period, which would be the brief period from delivery until the baby was left with the L & D staff. Based on this information, it does not appear this child suffered oxygen deprivation sufficient to cause brain injury during the labor, delivery or the immediate post delivery period. In conclusion, there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post delivery period. NICA retained Laufey Y. Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to examine Lennox and to review his medical records. Dr. Sigurdardottir examined Lennox on October 19, 2016. In an affidavit dated January 19, 2017, Dr. Sigurdardottir summarized her findings from the medical evaluation and opined as follows: Lennox is found to have substantial motor and mental impairment at this time. At the age of [2-1/2], he is dependent on his caretakers for all care and although he can grab toys and indicate wants and needs in a very simple manner, he has what seem to be significant cognitive delays. His motor disability is significant. There is evidence of decreased fetal movement and nonreassuring fetal heart rate. This led to his cesarean section. The patient did have signs of ischemia including coagulopathy at birth and went into a persistent pulmonary hypertension suggestive of fetal distress. His current clinical picture is that of cerebral palsy. The injury is likely to have occurred prenatally, prompting decreased fetal movements. The mother was however not in active labor at time of delivery. At this time, Lennox’s prognosis for life expectancy is excellent, but for full recovery is extremely guarded as he has substantial mental and physical impairment and is not sitting at this time. In light of the above details, and the absence of active labor at time of delivery, I do not recommend Lennox being included in the Neurologic Injury Compensation Association Program. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Willis that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post- delivery period. Dr. Willis’ opinion is credited. There are no expert opinions filed that are contrary to Dr. Sigurdardottir’s opinion that while Lennox has substantial motor and mental impairment, Lennox’s cerebral palsy is likely to have occurred prenatally and there was no active labor at the time of delivery. Dr. Sigurdardottir’s opinion is credited.
The Issue The issue in this case is whether Jeffrey D’Angelo, Jr. (Jeffrey), suffered a birth-related neurological injury as defined by section 766.302(2), Florida Statutes (2014), for which compensation should be awarded under the Florida Birth- Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact On February 22, 2014, in her 37th week of pregnancy, Petitioner, Katis D’Angelo, had a spontaneous rupture of her membranes. She presented to Bayfront and, at approximately 11:00 p.m., was evaluated in the labor suite. Upon initial examination, her cervix was noted to be “1 cm dilated, 50 percent effaced with the vertex at a -2 station.” The fetus’s heart tones were normal; however, Mrs. D’Angelo was not having an active labor pattern. Accordingly, Mrs. D’Angelo was admitted to the hospital. Dr. Dieffenbach had been Mrs. D’Angelo’s obstetrician throughout her pregnancy and, upon admission to Bayfront, was the primary and attending obstetrician. To assist in the progression of her labor, Dr. Dieffenbach ordered a low dose of Pitocin. Mrs. D’Angelo’s labor progressed and her cervix dilated to about five centimeters; however, it “got hung up for about 5 hours.” She was reexamined about an hour later with no changes noted. Due to her failure to progress, Dr. Dieffenbach recommended a Cesarean section delivery. Dr. Dieffenbach’s Clinical and Operative Notes provide, in pertinent part, as follows: CLINICAL NOTE: . . . At this point, cesarean delivery was recommended. Risks were explained and accepted. The labor was dysfunctional. Pitocin was up to about 14 milliunits. The fetal heart tones were in the normal range, but failed to show a great deal of variability. No decelerations were noted. Fluids were changed to D5 and Ringers to see if that would help stimulate the baby. OPERATIVE NOTE: . . . Uterine incision was extended laterally by stretching. The baby was noted to be in a ROT position. The infant was LGA, weighing 7 pounds 14 ounces at 37 weeks. The extraction was difficult. This was a male weighing 7 pounds 14 ounces, 3575 grams. Apgars were 2, 6, and 8. The infant was noted to have cord wrapped around the legs with several loops and also around the abdomen, possibly accounting for the fetal heart rate changes. The nares and orpharynx were suctioned with bulb syringe. Cord was clamped and severed. The infant was given to the nurse for further care at the isolette . . . . Both mother and baby did well. The baby is currently in the NICU, stable. Jeffrey was born at 1:52 p.m., on February 23, 2014. At delivery, he was noted to be “depressed.” At one minute of life, Jeffrey’s Apgar score was a 2.1/ A Neonatal Intensive Care Unit (NICU) Registered Nurse (RN) was requested to provide assistance in the operating room and the RN arrived within four minutes. Due to his depressed state, resuscitative efforts were required in the first several minutes of life. These efforts included positive pressure ventilation (for five minutes), oxygen, and chest compressions for 30 seconds. It appears the resuscitative efforts were administered by the respiratory therapist and operating room nurse prior to the NICU RN’s arrival.2/ The NICU RN documented that, upon arrival, Jeffrey had poor color and tone. By his tenth minute of life, Jeffrey had responded well to the oxygen, his color had improved, and he had spontaneously cried. At 2:10 p.m., Jeffrey was transitioned and admitted to the Bayfront NICU. At the NICU, Jeffrey was noted to have decreased tone, facial bruising, petechiae, and a low blood glucose level. He was noted to have a strong suck (for feeding), however, he had desaturations during feeding attempts, with a recorded apnea. At 3:45 p.m., Jeffrey was noted to have a significant apneic episode (ceased breathing for more than 15 seconds), he became cyanotic, and “very aggressive stimulation was needed,” in addition to mask oxygen. At that time, his oxygen saturation level was low at 58. At approximately 7:00 p.m., Jeffrey was placed on a nasal cannula for oxygen (vapotherm 2 LPM 23%). Jeffrey had several additional apneic episodes during his first day of life. On three occasions, the apnea lasted for more than 15 seconds, he became cyanotic, and required gentle or vigorous stimulation. Due to these incidents, on February 24, 2014, an echoencephalograph (EEG) was performed. The EEG finding and impression were as follows: FINDING: Transcranial head ultrasound was performed with gray scale imaging via anterior fontanelle. This demonstrates normal brain parenchymal echogenicity. There is a normal germinal matrix and cord plexus. There is no hydrocephalus or intraparenchymal hemorrhage. Impression: Normal transcranial head ultrasound as above. Jeffrey remained at the Bayfront NICU until March 5, 2014. During his NICU stay, he had a cranial ultrasound which was interpreted as normal; he was noted as having frequent arching and possible posturing; and continued to have poor feeding coordination. On March 5, 2014, he was transferred to All Children’s Hospital to obtain a brain MRI, neurology consultation, and a speech therapy consultation. On March 6, 2014, the brain MRI was conducted. The MRI was interpreted as showing a brain with normal signal intensity, including gray and white matter on multiple sequences. Ultimately, Jeffrey was discharged from All Children’s Hospital after approximately three days.3/ Following his discharge, Jeffrey exhibited developmental delays. When Jeffrey was approximately nine months old, he was evaluated by Elizabeth Barkoudah, M.D., the attending physician for the Neurodevelopmental Disabilities Department at Children’s Hospital in Boston, Massachusetts. Her report documents his post discharge history as follows: Concerns with Jeffrey were first noted in the neonatal period given low tone. This has prompted him to be seen by various specialties in Florida including Neurology, Neurosurgery, Physiatry, Genetics, Ophthalmology and Neuro-opthalmology. He has had a head ultrasound at 5 months of age which showed increased frontal lobe fluid. A brain MRI was repeated at 7 months of age including a cervical MRI. Again this showed the increased fluid. He was seen by Neurosurgery who did not feel that shunting was needed. His cervical MRI showed some narrowing with persistent SCF flow around the spinal cord. This MRI was obtained after papillodema was found on his examination. This examination was recommended due to “choppy visual tracking.” Over time it was felt that this was not truly papilledema and is simply elevated optic nerves. Visual assessment at the time showed weaknesses left more than right. In regards to evaluations, he has also been seen by Genetics who has obtained a chromosomal microarray which was unremarkable. He had thyroid testing and CPK levels which were normal. He has been seen by Physiatry who recommended ongoing therapy. They have provided him with a Benik trunk brace which now he only uses with exercises. He has been receiving Early Interventions services including PT two times per week, OT one time per week and speech therapy one time per week. Dr. Barkoudah’s impression was that Jeffrey’s low muscle tone was “likely central in origin and related to his gross motor delays.” She did not recommend any further assessments. Dr. Barkoudah opined in her report that the average age for diagnosis of cerebral palsy is two years of age, and, therefore, Jeffrey did not currently meet the diagnostic requirement. At approximately 13 months of age, Jeffrey was referred to Radhakrishna K. Rao, M.D., D.C.H., M.S., at Bay Regional & International Institute of Neurology, for a neurological evaluation. After conducting an examination of Jeffrey, Dr. Rao’s report documented his clinical impression as follows: Patient has a complex medico-neurological condition of severe complexity. Patient had difficult neonatal period as described above. Developmentally child is making progress at a slower pace without any regression. In my opinion, the loose umbilical cord wrapped around his legs and abdomen may have contributed to initially for persistent transverse lie and later descent for normal vaginal birth. This also might have contributed for respiratory depression and low Apgar score resulting in intermittent hypoxia. This appears to be the reason for his development of generalized hypotonia, gross motor and fine motor developmental delay and hypotonic cerebral palsy. Dr. Rao recommended an additional EEG to document any underlying neuronal dysfunction and seizure activity. An EEG was conducted several days later and was interpreted as within normal limits for Jeffrey’s age, and there was no definite seizure activity seen. Jeffrey presented to Dr. Rao again on April 21, 2015. On this occasion, among other medical concerns, Dr. Rao diagnosed Jeffrey with hypotonic cerebral palsy. Jeffrey continued to treat with Dr. Rao through August 2015. On June 21, 2017, Jeffrey (at age three years, four months) presented to the neurology clinic at All Children’s Hospital for follow-up of his history of hypotonia and global development delay. According to the clinical note, he had been diagnosed previously with congenital hypotonia, and had developmental delays including expressive speech delays. It was further documented that Jeffrey has a history of abnormal signal intensities on brain MRI. The clinical note described Jeffrey’s developmental delays as follows: Parents relate today that he is making steady for developmental progress, although slowly. Parents are very involved with a home regimen of multiple therapies which they engage in with him on a daily basis. Presently, he is able to walk independently. He continues to be unsteady and falls frequently. He is not able to stoop to pick up an object and then stand back up alone without holding onto something. He is not yet running. He can pick up a Cheerio or small object with a pincer grasp: not able to yet hold onto a crayon and scribble. Expressive language reveals approximately 15-20 independent words, although these are inconsistent. He knows (approximately) 8 signs and uses these appropriately. He is not able to identify pictures in books; does not know body parts. He waves “bye bye” and initiates some activities. He is not potty trained. He wears glasses and does vision therapy. Developmental level at this time by Denver Developmental Assessment is gross motor: (approximately) 15 mo.; fine motor/adaptive: (approximately) 10 mo.; language: (approximately) 15 mo.; personal/social: (approximately) 15 mo. The All Children’s clinical note again documented Jeffrey as having congenital hypotonia and concluded that he is globally delayed, but making slow gains with “a lot of intervention/therapy.” As indicated in the preceding paragraphs, Petitioners have commendably sought advice, treatment, and evaluations from multiple health care providers and specialists in an effort to care for Jeffrey. At the time of Mrs. D’Angelo’s deposition on September 17, 2018, Jeffrey was four years, seven months old. Mrs. D’Angelo credibly testified about a “day in the life” of Jeffrey, his development, and his limitations. Jeffrey is currently receiving multiple therapies on a daily basis at Petitioners’ home. Mrs. D’Angelo credibly testified that Jeffrey receives physical therapy once per week, occupational therapy twice per week, speech therapy three times per week, music therapy twice per week, and Applied Behavioral Analysis therapy for 40 hours per week. His various therapies essentially begin at 8:00 a.m., and continue throughout the day until 5:00 p.m. Mrs. D’Angelo explained that, in physical therapy, the primary goal at this time is for Jeffrey to be able to transition stairs. Over the last 4.5 years of physical therapy, there has been some slight improvement in that 1) he no longer has to wear a medical helmet; 2) he no longer has a walker; 3) his leg braces were previously from the knee down and now they are only ankle braces; 4) and he can walk independently indoors with adult supervision with mats on the floor to protect him from falls. At this time, he does not walk independently without the mats due to the potential fall risk. Concerning his occupational therapy goals, Mrs. D’Angelo credibly testified that they are working on his prewriting skills. The team is working on his ability to draw a line. At present, he does not have the ability to independently hold a pencil or a crayon correctly. Mrs. D’Angelo explained that he continues to require speech therapy, as he is functioning at a one-year-old level. Although Jeffrey may be able to say 20-25 words, they are approximations. Essentially, he can say “mom,” “dad,” and “hi” clearly. Mrs. D’Angelo further credibly testified concerning other limitations. Jeffrey wears diapers and is not potty- trained. He can follow very limited one-task directions, but rarely two-step directions. Jeffrey cannot and does not play with other children. While he can use a “sippy cup,” he cannot use an open cup to drink and cannot use utensils to feed himself. In April 2018, Jeffrey was diagnosed with an undisputedly rare genetic disorder referred to as CHAMP 1. The undersigned finds that there was insufficient evidence presented by the parties concerning this disorder to make any findings as to whether Jeffrey’s impairments are caused by genetic or congenital abnormality. NICA retained Donald C. Willis, M.D., an obstetrician specializing in maternal-fetal medicine, to review the medical records of Jeffrey and Mrs. D’Angelo, 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 postdelivery period due to oxygen deprivation or mechanical injury. Dr. Willis made the following findings and expressed the following opinions in a report, dated March 27, 2017: I have reviewed [the] medical records for the above individual. The mother, Katis D’Angelo was a 25 year old G1 with a history of successful treatment for preterm labor at 32 weeks. Prenatal course was otherwise without complications. The Mother was admitted at 37 weeks gestational age with spontaneous rupture of the membranes. Her cervix was dilated 1 cm. She was not in labor. Pitocin induction of labor was initiated for rupture of membranes. The fetal heart rate (FHR) monitor tracing was reviewed. There was no fetal distress. Cesarean section was done for failure to progress. Birth weight was 3,575 grams (7 lbs 14 oz’s). Extraction of the fetal head during Cesarean section was described as difficult. Several loops of umbilical cord were around the body of the fetus. Apgar scores were 2/6/8. Positive pressure ventilation was given for 5 minutes and chest compressions for 30 seconds. The baby was taken to the NICU for evaluation and management. NICU evaluation noted overall reduced motor activity and a rapid respiratory rate. X-ray showed bilateral vascular markings, compatible with transient tachypnea vs pneumonia. Several episodes of apnea occurred. Capillary blood gas at 5 hours of age was normal with a pH of 7.36. Antibiotics were started and continued for 7 days. Blood cultures were negative. Initial platelet count was low at 84,000. A short tongue frenulum, Ankyloglossia was present. This birth defect was later surgical[ly] corrected. Orogastric tube feedings were required for poor feeding coordination. Frequent body arching and posturing episodes developed. EEG on DOL 2 was normal. Head ultrasound was also normal. The baby was transferred to All Children’s Hospital due to possible seizure activity and poor feeding. Genetic testing, including microarray studies were negative. The child continue[d] to have hypotonia after hospital discharge. Neurology evaluation for hypotonia and motor developmental delay was done with the impression of a “complex medico-neurological condition of severe complexity.” EEG at about one year of age was normal. Sleep studies suggested upper airway obstruction. MRI found mild cervical spine narrowing, but no brain injury. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain or spinal cord that resulted in injury during labor, delivery and the immediate post delivery period. Dr. Willis’s findings and opinions were confirmed and verified in an affidavit dated September 1, 2017. At his deposition, Dr. Willis testified, in pertinent part, as follows: Q. Okay. What is your opinion as to whether or not Jeffrey D’Angelo suffered a birth-related neurological injury? A. I do not believe that there was any apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery, or the immediate post-delivery period. * * * Q. Would you briefly summarize your findings and basis for your opinion? A. Yes. Q. And refer to the report if necessary. A. Yeah. The mother was admitted to the hospital at 37 weeks gestational age with spontaneous rupture of the membranes. Labor was induced. She progressed to about 5 centimeters dilation and then had failure to dilate after that point. Cesarean section was then done for failure to dilate. And the – let me back up a moment. I did see the fetal heart rate tracings. And there was a nice set of fetal heart rate tracings during labor. I reviewed those. The fetal heart rate tracing did not show anything to me that suggested fetal distress during labor. It appeared to be a reassuring fetal heart rate pattern. Delivery was done by Cesarean section. Delivery was stated to be complicated or difficult because the umbilical cord was around the baby’s body. And the – and the delivery was stated to be difficult. When the baby was born, it was depressed. Apgar scores were 2 at 1 minute, 6 at 5 minutes, and 8 at 10 minutes. The baby did require positive-pressure ventilation for approximately 5 minutes. And chest compressions were approximately 30 seconds. The baby was taken to the neonatal intensive care unit. Chest x-ray showed – had some bilateral vascular markings which were compatible with transient tachypnea of the newborn. Shortly after birth the baby had some episodes of apnea. A capillary blood gas was done about 5 hours after birth, and it was normal. The pH was 7.36. EEG was done on day of life two, which was normal. Head ultrasound was also normal. The baby was transferred to All Children’s Hospital because – from what I gather from the records because they wanted to do an MRI. The MRI was done about two weeks after birth and was – and was normal. With respect to Jeffrey’s Apgar scores, Dr. Willis testified, in relevant part, as follows: Q. What did those Apgar scores mean or indicate to you in the context of your review of this case? A. Right. Well, usually we say that the one Apgar – the 1-minute Apgar score tells you what resuscitation is required. So Apgar score of 2 would be a low Apgar score. And that would mean that some resuscitation would be required after birth. The 5-minute Apgar score tells you a little bit more about what the baby’s acid base status, oxygen deprivation status would be. And that was 6. We consider the Apgar to be low if it is below 7. So the 5-minute Apgar was slightly lower than expected. By 10 minutes it was 8. So that would be within normal limits’ score for an Apgar. With respect to the diagnostic studies performed during the newborn period, Dr. Willis testified, in relevant part, as follows: Q. What is the purpose of an EEG? A. Purpose of the EEG is to determine if there’s any electrical brain injury. Q. Okay, and that’s a diagnostic study to determine if the brain is functioning properly? A. Correct. Q. And in this case on the second day of life an EEG was done and it was read as normal? A. Correct. Q. If J.D. in this case had suffered oxygen deprivation significant enough to cause brain damage in the course of labor and delivery, would you expect an EEG on day of life two to be normal? A. No. You would expect some abnormalities in that EEG. Q. So this EEG, correct me if I am wrong, would be inconsistent with . . . J.D. having suffered oxygen deprivation significant enough to cause brain injury at the time of labor and delivery in this case? A. Correct. * * * Q. And then you mentioned that an MRI was done at approximately 2 weeks of age? A. Correct. Q. And are you referring to the MRI that was dated March 6, 2014? A. Correct. Q. And what did that MRI reflect? A. That MRI was read as normal. So nothing on that MRI that suggested hypoxic or ischemic brain injury. And I felt that was very important in my – in my final disposition of this case because the delivery was somewhat difficult. And the baby was depressed at birth and required resuscitation. So that made me somewhat concerned about oxygen deprivation at birth. However, if the baby has oxygen deprivation at birth enough to cause brain injury, then the EEG will be abnormal and for sure the MRI at two weeks is going to show abnormalities. With a normal MRI at two weeks after birth, it really confirms that there was no oxygen deprivation during labor or delivery or the immediate post delivery period that was substantial enough to cause identifiable brain injury. Q. Okay. Is it fair to say, just to follow up on that MRI at two weeks, that the findings on that MRI are inconsistent with J.D. in this case having suffered oxygen deprivation significant enough to cause brain injury at the time of labor and delivery? Q. Correct. Dr. Willis’s findings and opinion that there was not a brain injury caused by oxygen deprivation or mechanical injury in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital are credited. NICA also retained Laufey Y. Sigurdardottir, M.D., a pediatric neurologist, to review Jeffrey’s medical records, conduct an independent medical examination (IME), and opine as to whether he suffers from a permanent and substantial mental and physical impairment as a result of a birth-related neurological injury. Dr. Sigurdardottir reviewed Jeffrey’s medical records and performed an IME on March 29, 2017. Dr. Sigurdardottir made the following findings and summarized her evaluation as follows: Pregnancy and Birth Summary: Jeffrey was born at 37 weeks 3 days to a 25-year-old G1, P0 serology negative mother after normal, noncomplicated, pregnancy. She did have premature labor at 32 weeks that resolved and then spontaneous rupture of membranes at 11 p.m. on 02/22/2014. Jeffrey’s mother presented shortly before midnight to Bayfront Health Labor and Delivery Ward, was found to have 1 cm cervical dilation and was admitted. She was not felt to be in active labor at that time. Labor was augmented with Pitocin but an emergent C-section was performed at 1 p.m. on 02/23/2014 due to failure to progress and arrested of fetal head. Fetal heart rate strips are available for our review and no fetal heart decelerations are noted. During the Cesarean section, the infant was found to be in a ROT position and large for gestational age. The extraction was difficult. The umbilical cord was noted to be wrapped around the legs with several loops and also around the abdomen. The infant was depressed at birth with Apgars of 2, 6 and 8 at 1,5 and 10 minutes. The infant was delivered at 1352 on 02/23/2014 weighing 3570g, length 51 cm and head circumference of 33cm. The infant did receive chest compressions for 30 seconds and positive pressure ventilation. Infant was noted to have respiratory distress and was admitted to Bayfront NICU for further evaluation. Infant had initial exam on admission suggestive of perinatal depression. His neurologic examination on admission revealed decreased muscle tone, decreased motor activity, symmetric Moro reflex, response to stimuli and no tremor. The infant had recovery of neurologic status apart from continued hypotonia and difficulty feeding. Infant was worked up with labs including a capillary blood gas at 5 hours of life showing a pH of 7.36 and a base excess of - 0.6. PCo2 was 48. Initial creatinine measurement was 1 and had a steady decline after that. AST and ALT were found to be normal. Initial platelets were found to be 84,000 with recovery to 165,000 by 6 a.m. on 02/24/201[4]. EEG performed on day of life 2 was found to be normal with no indication of a lowered seizure threshold and no abnormality on background activity. Head ultrasound was also performed and found to be normal. Infant had transient tachypnea, tongue ankyloglossia, possible sepsis and was treated with antibiotics. Nutritional status was found to include initial low blood glucose and episodes of arching with feeding. The patient did require partial gavage feeding prior to discharge. Discharge was on 03/05/201[4]. Developmental and Medical History: Jeffrey continued to exhibit delays in neurologic development. Per parents’ report, he had poor feeding abilities, was found to have low muscle tone and required therapies, occupational, physical, and speech therapy, from a very early age. He sat around 14 months, crawled at 15 months and walked unassisted at 22 months. He has had significant language delays, although at this time he has 20-25 words. He has been found to have apraxia of speech. The patient has had ophthalmologic abnormality including a downward eye deviation that the parents report and was seen at Boston Children’s Hospital at the age of 9 months for a second opinion of the underlying etiology for his delays. He has had genetic workup including microarray and Prader-Willi has also been ruled out. Patient has had multiple neuro radiologic evaluations of brain and spinal cord. The initial MRI was performed on 03/06/2014 and found to have a brain that seems normal in signal intensity including gray and white matter on multiple sequences. Vascular structures appear grossly normal. The second evaluation is a brain ultrasound on 07/29/2014 which shows mild increased CSF fluid spaces. A second MRI was performed in September 2014 and showed increased bifrontal temporal extraaxial convexity, effusion and mild ventricular dilation as compared to study from 03/06/2014. This was considered to be suggestive of a communicating hydrocephaly with impaired drainage at the level of the arachnoid granulations. An MRI of the cervical spine was also performed and showed mild C3-C5 spinal canal stenosis. A follow up MRI was then performed on 01/26/2015 with no interval change in the spinal stenosis at C3-C5 and no significant change in appearance of the extraaxial fluid or ventricular size. A 3rd follow up MRI then performed in May 2015 which showed possible increased in kyphosis of cervical region but no clear change in ventricular size and possible decrease in amount of extraaxial CSF spaces. Final MRI was then performed on July 2016 which continues to show mild bilateral and lateral ventricular dilation and bifrontal temporal convexity, extraaxial fluid. This was deemed to be stable. In the final MRI there are noted small foci of bifrontal white matter increased FLAIR signal without associated mass effect. Jeffrey has been treated with vigorous therapy, both with therapy providers as well as with his parents and has undergone hyperbaric oxygen therapy. Parents feel that he continues to be significantly delayed as compared to his peers. But now he is more responsive to them. He has been evaluated for possible autism and found to be negative for such symptoms on 3 occasions, as per parents’ report. * * * Physical Examination: Jeffrey is 17.7 kg, 91.4 cm and his head circumference is 51 cm. This places his growth parameters to be at the 95th percentile for weight, at the 13th percentile for length and his head circumference to be at the 59th percentile. His general exam is as follows: Head and Neck: There are no obvious dysmorphic features, although mouth tends to be open. He does have conjugate eye movement. Lungs: Clear to auscultation. Cardiovascular exam reveals first and second heart tones, no noted heart murmurs, no rhythm abnormalities. Abdomen is soft, no hepatosplenomegaly. GU normal. Musculoskeletal: He does have some increased joint laxity. Skin is without abnormal markings. Neurologic Examination: Mental status: The patient is interactive with his parents often needing multiple requests to comply with their requests for him. He does wave bye-bye. He does clap and does have occasional words that are difficult for this examiner to understand. His eye contact seems at times to be poor. No repetitive behavior is noted. Cranial nerves: His pupils are equal, reactive to light. He has full visual fields. Extraocular movements are conjugate. His facial expression is somewhat diminished. His hearing seems intact to voice. Motor exam reveals generalized hypotonia with some increased joint laxity, but full strength. Reflexes are difficult to elicit but present. Balance and coordination is delayed for age, although fine motor skills assessment is not performed. Summary: Jeffrey is a 3-year 1-month-old boy with motor and speech delays from birth. There is documented fetal depression but no clear documented fetal heart rate disturbance after the onset of active labor. His current status is improved from early in life and he is now able to ambulate without support and has started speaking in single words. There are no signs of autistic features. Result as to question 1: Jeffrey is not found to have a substantial physical impairment at this time. He is found to have a substantial language impairment at this time. Result as to question 2: In review of available documents, although having neurologic depression requiring some resuscitation at birth, there is no clear acute hypoxic event, and fetal heart rate strips were relatively benign. MRI performed in the neonatal period, EEG performed in the neonatal period did not support an acute encephalopathy. No laboratory evidence of multisystem hypoxic changes were noted in postnatal period. Result as to question 3: The prognosis for full motor and mental recovery is guarded but his life expectancy is full. Due to absence of evidence of hypoxic event during active labor, absence of secondary findings supportive of a hypoxic encephalopathy (MRI, laboratory or EEG) and his ongoing motor and cognitive progress, I do not feel that he should be included in the NICA program. (JE I, P. 1-3). Dr. Sigurdardottir confirmed and verified her opinions in an affidavit dated August 31, 2017. Dr. Sigurdardottir also testified, in relevant part, during her deposition on February 14, 2018, as follows: Q. And what were your conclusions to those questions (asked by NICA)? A. The conclusions are the following: Jeffrey is not found to have a substantial physical impairment at this time. He is found to have a substantial language impairment at this time. That is question one. So question one, he does not fulfill the criteria having both a substantial physical impairment and mental impairment. Result of the question two, that although having neurologic depression requiring some resuscitation at birth there is no clear precipitating acute hypoxic event that we can establish with the available records that we have, including fetal heart restrict, as well as in the neonatal post natal period there was no evidence of multi- system organ failure that often goes along with hypoxic ischemic events. So there was an MRI performed within the first two weeks, an EEG that was performed in a neonatal period, and then no laboratory evidence of multisystem hypoxic injury. On cross examination by Mr. D’Angelo, Dr. Sigurdardottir further explained her opinions and analysis as follows: Q. So what do you personally think was just the resuscitation he needed at birth likely? And I understand we’re not dealing in terms of absolutes, but was the likely cause of my son’s injury due to low amounts of oxygen at birth? A. Well, I would say it’s clear he had neurologic depression at birth. Then, we start looking for signs that would indicate that that would happen, such as the fetal heart rate [t]racing, that was benign. There was nothing in that that indicated there was lack of oxygen. And then after birth, even though he had neurologic depression, we did not have any of the hard evidence that he had significant hypoxic ischemic encephalopathy, is what we call it, and that’s when you have other systems involved, like the liver test becomes abnormal, the creatine continues to rise, his active base balance at the age of five hours looked fairly good, did not show a metabolic acidosis. And then an MRI that was performed, I believe, on day of life 10 or 11, that did not show any abnormality at that point that indicated an acute ischemic injury. So we have little that supports it from all of the laboratory results that we have and the fetal heart rate [tracing]. Dr. Sigurdardottir’s findings and opinion that Jeffrey has a substantial language impairment is undisputed and credited. Her opinion that Jeffrey does not have a substantial physical impairment is not credited for the reasons discussed below in the Conclusions of Law. Dr. Sigurdardottir’s opinion that there is evidence of fetal depression, but insignificant evidence (at birth) to establish significant hypoxic ischemic encephalopathy is supported by the evidence and is credited. Petitioners submitted a notarized statement from Jeffrey Huber in support of their position that Jeffrey sustained a birth-related neurological injury. It appears that Mr. Huber was the respiratory therapist in the operating room at the time of delivery. Mr. Huber’s statement provides, inter alia, that Jeffrey had a “lack of ventilation for longer than 2 minutes.” Although Mr. Huber’s statement has been considered, it constitutes hearsay and cannot support independently any finding of fact. Additionally, Dr. Willis and Dr. Sigurdardottir, the only qualified medical experts who have testified in this matter, both represented that Mr. Huber’s statement was duly considered by them and did not change any of their opinions and ultimate conclusions. Specifically, Dr. Willis testified, in relevant part, as follows: Q. Did that report [and] statement from Mr. [H]uber have any impact on your ultimate opinions and conclusions? A. No. No, it did not. Most of the things that he – that he talked about in there were part of the medical records. The fact that the baby required resuscitation, required chest compressions was all in the medical records. So nothing new there. He does not state exactly what his position is, but I assume from what I’ve read he must be somehow involved with respiratory therapy. So nothing new as far as what was in the medical records in his report.
The Issue At issue in this proceeding is whether Cortina Fountain, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Ann Williams' prenatal course and the birth of Cortina Fountain Due to a paucity of proof, little is known of Ann Williams' prenatal care except that at or about 6:10 a.m., August 3, 1992, she was seen at Waterman Medical Center, Eustis, Florida, for a prenatal progress check. 1/ At the time, Ms. Williams complained of contractions at 15 minute intervals, dilation was noted to be "1-2, thick, high;" and fetal heart tone was noted to be in the 130 beat per minute range. The midwife was called, and upon receipt of her orders Ms. Williams was discharged home with instructions "to call Tavares Clinic today to be seen." At 12:15 p.m. that day, Ms. Williams, while at home, precipitously delivered her child, Cortina Fountain (Cortina), in the toilet. Emergency medical services were called, and Ms. Williams and Cortina were taken by ambulance to Waterman Medical Center, where they were admitted at 1:10 p.m. that day. 2/ Upon admission to the hospital, physical examination revealed Cortina to be a viable female infant, with normal activity and no overt abnormalities. No evidence of trauma, cyanosis or poor oxygenation function, or cardiac function was observed, and Cortina exhibited all normal neurologic reflexes, such as Moro, suck, and grasp. Moreover, no abnormality of the anterior fontanel of the infant was noted. Cortina remained in the hospital until August 5, 1992, when she was discharged to the care of her mother. During her two day residence in the hospital, Cortina did not evidence any abnormalities. Rather, she fed well and gained weight, did not demonstrate any bruising or trauma, and did not demonstrate any neurologic changes or other abnormalities. Cortina's subsequent development and readmission to the hospital Cortina was readmitted to Waterman Medical Center, through the emergency room, at or about 6:35 p.m., September 11, 1992. At the time, history reflected that her development was apparently uneventful until one or two days prior to admission. During that time, Cortina stopped taking her formula, became progressively lethargic, vomited, and experienced episodes of diarrhea. For the twenty four hour period prior to her admission, Cortina was noted to be febrile. Upon admission, Cortina was noted to be extremely emaciated, having a weight of 4 pounds 3 ounces compared to her birth weight of 5 pounds 12 ounces. She was also noted to be listless, markedly dehydrated, and with bulging anterior fontanelle and a temperature of 104 degrees Farenheit. Testing revealed electrolyte imbalance and metabolic acidosis. Such symptomology was consistent with central nervous system infection, and Cortina was started on oxygen, intravenous fluids, including dextrose, and Rocephin. At or about 10:35 p.m., September 11, 1992, she was transferred by helicopter to the neonatal intensive care unit at Florida Hospital Medical Center (Florida Hospital) in Orlando, Florida. Cortina remained at Florida Hospital until October 2, 1992, when she was discharged to the care of her mother. Her course at Florida Hospital was adequately set forth in her discharge summary as follows: PHYSICAL EXAMINATION: Physical examination on arrival at Florida Hospital Medical Center, pediatric intensive care unit, revealed a marasmic, somewhat listless, black female who was markedly dehydrated. Temperature was 103 degrees Fahrenheit. Heart rate ranged between 170 and 190, and blood pressure was 83/53. She was intubated, and the anterior fontanelle was somewhat sunken at this time. IMPRESSION ON ADMISSION: FEVER WITH A POSSIBILITY OF SEPSIS. BORDERLINE HYPOGLYCEMIA. SEVERE DEHYDRATION. MARASMUS. RULE OUT A METABOLIC DISORDER OR A VIRAL ENCEPHALOPATHY. HOSPITAL COURSE: Upon admission, a central line was placed, and patient was placed on assisted ventilation. The fontanelle was initially sunken but after adequate hydration was noted to be bulging during the night. A computerized axial tomo- graphy scan of the brain was obtained on an emergency basis, and this revealed diffuse brain swelling. The patient was started on hyperventilation with the addition of intravenous mannitol. Additional laboratory data that was obtained included a liver profile which showed her albumin to be 2.0, SGPT was 52, SGOT 39, GGT 350, serum ammonia 161 which is increased, serum lactase was 6.5 which is also increased. Reticulocyte count was 3.7 [percent] and hemoglobin and hematocrit were decreased to 5.8 and 18.0 respectively. Endotracheal tube aspirate that was sent for respiratory syncytial virus came back negative. Hospital course will be further discussed on the problem list. PROBLEM [NO.] 1: ENCEPHALOPATHY WITH BRAIN SWELLING AND SEIZURE DISORDER. After the initial presentation and the finding of cerebral swelling, the patient was started on hyperventilation with intravenous mannitol. She was noted to have fisting of the hands and occasional jerky movements that were associated with bradycardia, and an electroencephalogram that was done revealed seizure activity. Hence, she was started on intravenous phenobarbital which was slowly increased over 24 hours until clinical control of the seizures was obtained. Subsequent electroencephalograms that were done on September 14, 1992, still showed frequent multifocal epileptiform discharges, although there was no clinical evidence of seizure disorder. In light of this, her dose of phenobarbital was increased after an initial minibolus. A pheno- barbital level in the upper 20s to lower 30s was maintained with a dose of phenobarbital 6 mg b.i.d. Repeat electroencephalograms done on September 17, 1992, and September 25, 1992, were abnormal, as manifested by diffuse sharp and slow wave discharges in the waking state which got accentuated by sleep. . . . on September 12, 1992, the patient was also started on intravenous acyclovir because of the possibility of herpes encephalitis. A lumbar puncture was not repeated for further cerebrospinal fluid studies because of the presence of the cerebral swelling, but an attempt to obtain cerebrospinal fluid via a subdural tap was futile. The patient was slowly weaned off the ventilator and finally extubated on September 17, 1992. The mannitol was weaned off over the next four days and discontinued on September 20, 1992. The Rocephin was continued for a total of 10 days and the acyclovir for a total of 14 days. At the time of discharge and for at least one week prior to discharge, she was able to track very well, was feeding well, and had essentially a normal neurologic examination. Auditory brain stem evoked response studies that were done revealed normal hearing in both ears. A computerized axial tomography scan of the brain that was done on September 22, 1992, showed diffuse, decreased density within the cerebral hemispheres bilaterally with preservation of the basal ganglia and thalamus. There was interval volume loss in the cerebral hemispheres which was felt to be consistent with resolution of the cerebral edema. PROBLEM [NO.] 2: DEHYDRATION AND ELECTROLYTE ANOMALIES. On the day of admission, the patient had a BUN of 38 with a creatinine of 1.2 and a glucose of 60. She was placed on D10 one-quarter normal saline and the dehydration was corrected slowly over 48 hours. Over the ensuing week, she developed anasarca, mostly due to hypoalbuminemic state, but this resolved at least one to two weeks prior to discharge. A Chem-21 that was done on September 29, 1992, showed a sodium of 137, potassium 5.2, chloride 106, CO2 20.6, glucose 96, creatinine 0.5, BUN 13. The rest of the Chem-21 profile was essentially with normal limits. Specifically, the albumin had risen to 3.5 on September 29, 1992. PROBLEM [NO.] 3: ANEMIA. At the time of her admission, the patient's hematrocrit was 22 [percent] but this dropped to 18 [percent] after she was rehydrated. She was transfused on two occasions, and after this she maintained a reasonable hematocrit until the time of discharge. A complete blood count that was done on September 29, 1992, showed a white blood cell count of 13,800, hemoglobin 14.0, hematocrit 40.8, platelet count 151,000. There were 41 segs, 1 band, 43 lymphs, 13 monos and 2 eosinophils. * * * PROBLEM [NO.] 4: HEPATOPATHY WITH HYPERLACTASEMIA AND HYPERAMMONEMIA. It was felt that the patient's hepatopathy and abnormal laboratory data related to the liver function was probably due to a viral or metabolic problem. Urine for amino acid screen was essen- tially negative, and urine for organic acid screen came back showing an abnormal peak with octeny- lsuccinic acid. It was felt by Dr. McReynolds that this is an emulsifier that is used in certain infant formulas, and repeat testing for this purpose has been scheduled on an outpatient basis. The metabolic studies that are pending at the time of discharge include blood amino acid profile and also serum isocarnitine profile. PROBLEM [NO.] 5: MALNUTRITION. Patient looked significant marasmic on the date of admission and had an admission weight of 4 lb. 3 oz. At the time of discharge, she was toler- ating full-strength Pregestimil and was gaining weight daily. Her discharge weight is 6 lb. 7 oz. (2.9 kg). Her head circumference was 35.5 cm at the time of discharge. PROBLEM [NO.] 6: INFECTIOUS DISEASE. In spite of the septic workup, there was no identifiable causative organism, although a viral etiology could not be totally ruled out. Blood for herpes simplex IgM titers was un- revealing. In spite of the negative studies, the patient was given the benefit of the doubt and treated with meningitic doses of Rocephin for 10 days and meningitic doses of acyclovir for 14 days. . . . Cortina's discharge diagnoses were "severe encephalopathy with cerebral edema and epilepticus," "ongoing seizure disorder," and "anemia with abnormal peripheral smear." The cause and severity of Cortina's neurologic injury Although the proof demonstrates that Cortina suffered some neurologic impairment, as a consequence of events at or about the time of her readmission to the hospital on September 11, 1992, it is quite unrevealing as to the severity of that impairment. Consequently, the proof fails to support the conclusion that any neurologic injury Cortina suffered rendered her permanently and substantially mentally and physically impaired. Regarding the timing and cause of Cortina's neurologic injury, the proof is compelling that, notwithstanding the circumstances of her delivery, Cortina was, at birth, a normal, vigorous infant, with no apparent abnormalities. Her development thereafter was likewise uneventful, until one to two days prior to September 11, 1992, when she was readmitted to the hospital, at approximately five weeks of age. In the opinion of Lance Wyble, M.D., a board certified neonatologist, Cortina's presentation on September 11, 1992, was most consistent with a viral etiology which, given her history, had its genesis within the 24 to 48 hour period immediately preceding her admission on September 11, 1992. It was further Dr. Wyble's opinion that such was the most likely cause of any neurologic injury Cortina suffered, and that any injury she suffered was wholly unrelated to the birthing process or her delivery. Of a similar opinion was Charles Kalstone, M.D., a board certified obstetrician. The opinions of Doctors Wyble and Kalstone are grossly consistent with the proof of record regarding Cortina's birth and her subsequent readmission to the hospital on September 11, 1992, and are credited.
Findings Of Fact Brandon Santiago was born on January 28, 2008, at Health Central in Ocoee, Florida. Brandon weighed 2,750 grams at birth. NICA retained Donald C. Willis, M.D., as its expert in maternal fetal medicine. After having reviewed the medical records of Brandon and his mother, Dr. Willis opined in an affidavit dated June 26, 2013, as follows: The fetal heart rate (FHR) monitor tracing during labor was not available for review. However, the operative report stated “repetitive variable decelerations to the 60’s" were present. Cesarean section delivery was done for the abnormal FHR pattern and failure to progress in labor. Amniotic fluid was clear at delivery. Birth weight was 2,750 grams. The newborn was not depressed. Apgar scores were 7/9/9. Cord blood gas did not suggest acidosis. The pH was 7.26 with abase [sic] excess of only -3. Decreased fetal tone was present after birth and attributed to maternal MgS04 administration during labor. The baby had an uneventful hospital course and was discharged home two days after birth. Subsequently, the baby was noted to have poor muscle tone and developmental delay. Genetic evaluation was done but no obvious genetic condition was identified. In summary, Cesarean section was done for abnormal FHR pattern. The baby was not depressed at birth. Decreased muscle tone was noted, but otherwise the newborn hospital course was uneventful. The baby was discharged home with the mother two days after birth. These findings do not suggest oxygen deprivation during the birthing process. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to Brandon Santiago’s brain during labor, delivery, or the immediate post delivery period. NICA retained Michael S. Duchowny, M.D., as its medical expert in pediatric neurology. Dr. Duchowny examined Brandon and reviewed his medical records. In an affidavit dated July 9, 2013, Dr. Duchowny opined as follows: Brandon’s neurological examination reveals evidence of severe motor delay with virtually no progress past the newborn level. This disorder affects all limbs in a symmetric fashion and has likely compromised his bulbar musculature, as well. Cognitive testing is difficult to assess due to the profound motor impairment. A review of the medical records confirms his mother’s impression of only transient difficulties at birth and in fact, Brandon was born only with a brief period of absent respirations which responded immediately in the delivery room. His Apgar scores were 7, 9, 9 at 1, 5, and 10 minutes and Brandon’s hospital course stabilized rapidly allowing him to be discharged on the second day of life. These facts do not support the acquisition of a neurological injury to the brain or spinal cord due to oxygen deprivation or mechanical injury during labor or delivery. While Brandon does evidence a substantial motor impairment, he is likely suffering from an unknown neuromuscular disorder. The history of seizures obviously suggests that the underlying diagnosis also involves the central nervous system and is therefore more complex, but his caretakers have so far been unable to ascertain a definitive diagnosis. * * * It is my opinion that BRANDON SANTIAGO does have a substantial motor impairment. However, I do not regard Brandon’s neurological presentation as consistent with a neurological injury to the brain or spinal cord acquired due to oxygen deprivation or mechanical injury occurring during the course of labor, delivery, or the immediate post- delivery period in the hospital during the birth of BRANDON SANTIAGO. I, therefore, do not believe that BRANDON SANTIAGO is compensable within the NICA program. A review of the file does not show any opinions contrary to the opinions of Dr. Duchowny and Dr. Willis that Brandon did not suffer a neurological injury due to oxygen deprivation or mechanical injury during labor, delivery, or resuscitation in the immediate post-delivery period are credited.
Findings Of Fact Tristan N. Thomas was born on August 12, 2009, at Baptist Medical Center in Jacksonville, Florida. Tristan weighed in excess of 2,500 grams. Donald Willis, M.D., was requested by NICA to review the medical records of Tristan. Based on his review of the medical records, Dr. Willis opined as follows: In summary, labor was complicated by hypertension and a placental abruption. This resulted in a depressed baby at birth. Full resuscitation was required. The initial blood gas after birth was consistent with severe acidosis with a pH of 6.6. Seizures developed shortly after birth. EEG and MRI were consistent with HIE. There was an apparent obstetrical event that resulted in loss of oxygen to the baby’s brain during labor, delivery, and continuing into the immediate post delivery period. This oxygen deprivation resulted in brain injury. I am not able to comment about the severity of the brain injury. Michael S. Duchowny, M.D., was requested by NICA to perform an independent medical evaluation of Tristan. The evaluation was done on January 22, 2014. Based on his evaluation, Dr. Duchowny opined as follows: In summary, Tristan’s neurologic examination reveals evidence of multiple developmental delays in the social, communication and behavioral domains. His findings are consistent with a clinical diagnosis of autism spectrum disorder and there are no specific focal or lateralizing findings to suggest structural brain damage. I had an opportunity to review medical records supplied to me which confirmed the history obtained from Tristan’s mother. Tristan was delivered at term at Baptist Medical Center. His mother suffered from preeclampsia and was treated with magnesium sulfate. Tristan was delivered by emergency cesarean section due to placental abruption, required resuscitation at birth and had Apgar scores of 0, 3, and 7 at 1, 5, and 10 minutes. His cord blood gases revealed severe acidosis and he was placed in a head cooling protocol for 72 hours following stabilization. However, an ultrasound of the brain on August 17, 2009 was negative as was an MRI scan performed on August 18, 2009. In summary, the findings on examination today together with the medical history did not provide evidence of significant brain damage and Tristan does not suffer from a substantial motor impairment. Furthermore, his neurological problems did not, in my opinion result from either mechanical injury or oxygen deprivation acquired in the course of labor and delivery. His autism spectrum disorder is a primary developmental disability of prenatal origin. I, therefore, believe that Tristan should not be considered for admission into the NICA program. A review of the file does not show any contrary opinion to Dr. Willis’ opinion that Tristan did sustain oxygen deprivation during labor, delivery, and resuscitation in the immediate post-delivery period Plan. Dr. Willis could not comment on the extent of any brain injury that resulted from the oxygen deprivation. Dr. Duchowny opines that Tristan does not suffer from significant brain damage and that Tristan does not have a substantial motor impairment. These opinions are not disputed and are credited.
The Issue At issue in this proceeding is whether Britney Palmero, 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 Manuel Palmero and Mary Jane Palmero are the parents and natural guardians of Britney Palmero (Britney), a minor. Britney was born a live infant on January 11, 1993, at South Miami Hospital, a hospital located in South Miami, Dade County, Florida, and her birth weight exceeded 2500 grams. The physician providing obstetrical services during the birth of Britney was Julio Somoano, 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. Palmero's antepartum course and Britney's birth On January 11, 1993, Mrs. Palmero was admitted to South Miami Hospital for induction of labor. At the time, her estimated date of confinement was January 19, 1993, and her antepartum course was without apparent complication; however, due to Mrs. Palmero's expressed discomfort during the later stage of pregnancy, and the size of the baby (over eight pounds), it was resolved to deliver the baby prior to its due date. Mrs. Palmero's initial admission on January 11, 1993, occurred at or about 7:50 a.m. Thereafter, at or about 8:00 a.m., external fetal monitoring commenced, and revealed a normal fetal heart rate pattern or, stated differently, reflected evidence of fetal well-being. Mrs. Palmero received her first Prostin gel, as the first step in the induction of labor, at 9:45 a.m., and her second at about 11:45 a.m. Following the second Prostin gel, mild irregular contractions were noted; however, her cervix did not progress (she did not go into labor), and at 2:00 p.m. Mrs. Palmero was sent home with instructions to call if she began to experience regular contractions, if the membranes ruptured, or if she observed any vaginal bleeding. During the period she was monitored, and until her discharge at 2:00 p.m., no vaginal bleeding was observed, and the fetal heart rate pattern continued to evidence fetal well-being. Mrs. Palmero returned to labor and delivery at or about 3:21 p.m. complaining of increased "intensity of cramps" and some bloody discharge. A small amount of red vaginal blood, with mucus, was noted; however, vaginal examination revealed the cervix (at 1 centimeter, effacement at 50 percent, and the fetus at station -2) to be unchanged. External fetal monitoring again revealed a reassuring fetal heart rate and, at 3:40 p.m., there being no evidence that she was yet in labor, the instructions previously given were reviewed and Mrs. Palmero was sent home. At or about 8:00 p.m., January 11, 1993, Mrs. Palmero returned to labor and delivery complaining of moderately bright red bleeding. According to Mrs. Palmero, her membranes ruptured at 7:00 p.m. with pinkish fluid noted. Vaginal examination revealed the cervix to be at 1 to 2 centimeters, effacement at 50 percent, and the fetus at station -2. A moderate amount of red fluid with occasional clots was observed by the nurse. Contractions were noted at a frequency of 1 1/2 to 3 minutes, with moderate intensity, and fetal heart rate was noted as stable, with good variability. At 8:45 p.m. it was noted that Mrs. Palmero continued to leak a large to moderate amount of red fluid from the vagina, but no clots were noted. Fetal heart rate remained stable. Dr. Somoano was notified by phone of the patient's status, and he announced he was enroute to the hospital. Dr. Somoano arrived at the hospital at or about 9:15 p.m. Vaginal examination revealed the cervix to be 3 centimeters, effacement complete, and the fetus at station - Fetal heart rate remained stable. Given Mrs. Palmero's presentation on admission, Dr. Somoano entertained the likelihood of abruptio placenta, but, there being no evidence of fetal distress, elected to proceed with a normal delivery. An epidural anesthetic was ordered. Following the epidural, Mrs. Palmero's contractions were less frequent. Given the stability of the fetal heart rate pattern, Dr. Somoano ordered Pitocin to augment labor. Pitocin was started at 10:45 p.m., which brought Mrs. Palmero's contractions closer together; however, given that she began bleeding more and her cervix had only progressed to 5 centimeters, Dr. Somoano elected to proceed by cesarean section to avoid the risk of a complete abruptio. Consequently, at 11:15 p.m., Pitocin was discontinued and Mrs. Palmero was moved to the operating room. During this period, apart from a few mild variable decelerations consistent with cord compression, and one variable deceleration about 45 minutes before delivery, the fetal heart rate remained stable and continued to evidence fetal well-being. The cesarean section was begun at 11:28 p.m., Britney was delivered at 11:29 p.m., and the procedure was complete at 11:45 p.m. During delivery, the cord was noted to be tight, around the baby's neck twice, and around the shoulder. Upon removal of the placenta, a marginal abruptio placenta, 15 to 20 percent, was observed. Following delivery, Britney was handed off to the attending neonatologist, who assigned her Apgar scores of 7 at one minute and 9 at five minutes. The Apgar scores assigned to Britney are a numerical expression of the condition of a newborn infant, and reflect the sum of 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 Britney's Apgar score totalled 7, with heart rate and respiratory effort being graded at 2 each, and muscle tone, reflex irritability and color being graded at one each.2 At five minutes, her Apgar score totalled 9, with heart rate, respiratory effort, muscle tone, and reflex irritability being graded at 2 each, and color being graded at 1. Such scores are normal and, while they do not rule out the presence of an existent brain injury or anomaly, the presentation represented by those scores is not consistent with a neurologic insult (injury to the brain) having occurred during the birth process. Britney's course and development subsequent to delivery Following delivery, Britney was transported to the newborn nursery, where she was admitted at "0000" January 12, 1993. Apart from the admitting nurse noting that Britney was a little lethargic and hypotonic, Britney's presentation appeared grossly normal. Dr. Jose Luis, the pediatrician, was notified of Britney's admission to the nursery at 12:40 a.m., January 12, 1993, and his physical examination on that date, as well as his examinations of January 13 and January 14, 1993, described a normal new-born girl without evidence of abnormality. During her stay in the nursery, Britney evidenced no problems, and her course was considered routine. She and her mother were discharged January 14, 1993.3 Britney's early infancy was characterized by good health, and no apparent problems were observed until approximately six to seven months of age. At that time, the parents observed that Britney's right hand was held in a closed fist position. The parents' concern was reported to Britney's pediatrician. He monitored Britney's progress, and in December 1993, referred her for a neurologic consult with Dr. Israel Alfonso at Miami Children's Hospital, Department of Neurology. Britney was examined by Dr. Alfonso on or about January 6, 1994. At the time, Dr. Alfonso noted Britney's general examination as normal; however, her neurological examination revealed the following: . . . neurological examination is characterized by a right hemiparesis that does not involve the face but it does involve the right arm, especially the right hand and also the right leg. Her deep tendon reflexes are within normal range in all four extremities. The right hand is somewhat smaller than the left, especially the thumb. The thumb is kept in a cortical position continuously. She did not use the right hand to grab any object while examined though she occasionally opens that hand at will. IMPRESSION: Right hemiparesis. Dr. Alfonso recommended an MRI of the brain to identify the most likely cause for Britney's presentation.4 The MRI was performed on January 7, 1994, and provided the following findings and conclusions: FINDINGS: There is focal signal abnormality seen in the left posterior frontal parietal region. This is reduced on the T1 weighted images and increased on the T2 weighted study. Also noted is enlargement of the left lateral ventricle. There is prominence of the sulcal folds in this region. Also, there is a discrepancy in the white matter volume with it being reduced on the left. There is a more immature myelin signal on the left particularly in the periventricular region. There is also noted thinning of the corpus callosum in the posterior body. The brain stem shows a reduction in size of the left cerebral peduncle. Evidence of mass effect, midline shift or hemorrhage is not seen. CONCLUSION: Findings as described in keeping cystic encephalomalacia involving the posterior, frontal and anterior parietal region. Secondary diaschisis involving the left cerebral peduncle is noted as well as the posterior body of the corpus callosum. There is signal abnormality identified of the white matter in the left periventricular region and associated with the posterior frontal parietal region. While this may represent delayed maturation of myelin, leukomalacia should also be considered. In addition, there is a reduction in volume of the white matter of the left cerebral hemisphere identified when compared with that on the right. These findings most likely represent a sequelae of a vascular insult. The infarct (loss of brain tissue) in the left cerebral hemisphere, near the left middle cerebral artery, depicted by the MRI is consistent with a vascular insult (cerebral vascular accident or stroke). The vascular insult resulted in focal damage to a selected region of the left hemisphere, and was clearly the cause of the prominent right hemiparesis, evidenced by spasticity of the right arm and leg, with which Britney presents.5 The dispute regarding compensability Given the proof, it cannot be subject to serious debate that Britney suffered an injury to her brain that resulted in neurologic impairment. What remains to resolve is the origin, nature and timing (genesis) of that injury or, more pertinent to these proceedings, whether the proof demonstrates, more likely than not, that the injury Britney suffered was "caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as opposed to some other genesis.6 Section 766.302(2), Florida Statutes. With regard to such issue, Petitioners contend that the brain injury was caused by oxygen deprivation (a hypoxic ischemic injury), consequent to placental abruption, which occurred during the course of labor, delivery, or resuscitation. In contrast, Respondent contends the proof is not consistent with a hypoxic ischemic injury occurring during the course of childbirth but, rather, with a brain injury resulting from a vascular insult or infarct,7 commonly referred to as a stroke, suffered in the antenatal (prenatal) period. Respondent's view of the proof has merit. The genesis of Britney's brain injury Britney'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, such as spastic paraplegia, hemiplegia, or tetraplegia, which is often accompanied by mental retardation, seizures or ataxia. Such disorders result from brain damage caused by birth trauma, such as that which may result from oxygen deprivation or mechanical injury during labor or delivery, or may be associated with a intrauterine (antenatal) event or pathology, such as a vascular insult or stroke, genetic abnormality, or developmental abnormality.8 Here, the proof is compelling that Britney's brain injury resulted from a stroke suffered in the antenatal period, most likely after 30 weeks gestation and at least two weeks prior to delivery, and that it was not associated with any event occurring during the course of labor, delivery, or the immediate post-delivery period.9 In so concluding, it is initially observed that the results of the neuro-imaging study (MRI) are inconsistent with brain injury resulting from oxygen deprivation. Rather, the neuro-imaging study, as well as Britney's neurologic examination, are consistent with focal damage occasioned by a left hemisphere stroke, as opposed to the bilateral or global damage one would typically associate with an injury occasioned by oxygen deprivation. Moreover, Britney's course pre-delivery and post- delivery was inconsistent with hypoxic or ischemic damage occurring during the course of birth. First the stability of the fetal heart rate during labor and delivery affords objective proof that the marginal abruption Mrs. Palmero suffered did not adversely affect fetal oxygenation. Second, Britney's healthy presentation, as evidenced by her Apgar scores and uneventful hospital course, are inconsistent with the presentation and hospital course one would reasonably expect had the fetus suffered a brain injury, of the magnitude capable of producing the damage evidenced by Britney's MRI brain scan, during labor and delivery. Indeed, had such an event occurred, one would reasonably expect a severely depressed infant on delivery, with an absence of respiratory effort, and whose hospital course would be reflective of neurologic insult, to include a likely onset of seizure activity. Here, Britney presented with normal Apgars, good respiratory effort, and her hospital course reflected an essentially healthy new-born. In summary, the paucity of any evidence to suggest fetal compromise during labor and delivery, the conclusions reasonably drawn from the MRI scan, and Britney's presentation and hospital course present a picture that is wholly inconsistent with a birth-related injury. Moreover, the marginal nature of the placental abruption, given the evidence of fetal well-being during labor and delivery, renders it most unlikely that the abruption played any role in Britney's injury. Rather, giving due regard to the objective evidence, the conclusion is inescapable that the most likely cause of Britney's brain injury was a vascular insult or stroke, which occurred well prior to labor or delivery.10
The Issue Whether Isaac Castro and David Castro, deceased minors, qualify for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts Milagros Magaly Castro and William Marcelo Castro are the natural parents of Isaac Castro and David Castro, deceased minors, and the Personal Representatives of their deceased sons' estates. Isaac and David were the product of a multiple (twin) gestation, and were born live infants on November 25, 2004, at Palmetto General Hospital, a hospital located in Hialeah, Florida, each with a birth weight exceeding 2,000 grams. David died December 7, 2004, and Isaac died January 12, 2005. The physician providing obstetrical services at Isaac's and David's birth was Monica Daniel, 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. Isaac's and David's birth At or about 1:50 p.m., October 11, 2004, Mrs. Castro, aged 40, with an estimated delivery date of December 30, 2004, and the twins at 28+ weeks' gestation, presented to Palmetto General Hospital on referral from her perinatologist for inpatient management, with concerns of elevated blood pressure (suspected pregnancy induced hypertension), and increased creatinine levels. At the time, Mrs. Castro's pregnancy was considered high risk, with advanced maternal age and twin gestation, and was further complicated by insulin dependent gestational diabetes and hypothyroidism. Nevertheless, numerous assessments during the term of her pregnancy were reassuring for fetal well-being, as was her initial assessment at Palmetto General Hospital. Mrs. Castro was admitted to the hospital at 3:00 p.m., that day, and her pregnancy was managed without apparent adverse incident until November 24, 2004, when, with the twins at 34 6/7 weeks' gestation, Mrs. Castro demonstrated severe preeclampsia, with increasing creatinine levels (worsening renal status). Notably, however, fetal monitoring between 1:01 p.m., and approximately 4:07 p.m., that afternoon,5 provided reassuring evidence of continued fetal well-being.6 Given her condition, Dr. Daniel ordered Mrs. Castro admitted to labor and delivery, where she was received at 9:10 p.m., for cesarean section delivery. Notably, Dr. Daniel's admission orders included a requirement for external fetal monitoring. However, that order was not followed, and no fetal monitor strips exist that would aid in assessing fetal status subsequent to 4:07 p.m., November 24, 2004. The progress notes do, however, include a few entries that bear on the issue. At 9:10 p.m., on admission to labor and delivery, the nurse noted that Mrs. Castro reported normal fetal movement, and denied pain, vaginal discharge, or blurred vision. Thereafter, at 10:30 p.m., the nurse noted that Mrs. Castro showed abnormal lung sounds, with crackles bilaterally to the bases, and dyspnea (difficult or labored breathing). Mrs. Castro was provided supplemental oxygen by nasal cannula (NC). At 1:00 a.m., November 25, 2004, while being prepared for surgery, the nurse noted that Mrs. Castro was slightly dyspneic and still receiving supplemental oxygen, NC at 2 liters. Assessment revealed reassuring fetal heart tones, with "FHT's via US on right upper quadrant in the 130's [and] FHT's via US on lower left upper quadrant in the 120's." Otherwise, the records provide no information regarding fetal status until the twins were delivered.7 At 1:35 a.m., Mrs. Castro was noted in the operating room, with an oxygen saturation level of 92 percent. She was given oxygen by mask, and by 1:45 a.m., her saturation levels were at 100 percent. No fetal heart tones were obtained "due to maternal instability," and, at 1:56 a.m., the incision was made (delivery began), and at 2:01 a.m., Isaac (identified as Twin A in the medical records) and at 2:02 a.m., David (identified as Twin B in the medical records) were delivered, severely depressed. Isaac's Apgar scores were noted as 1, 2, 2, 2, 2, 2, and 5, at one, five, ten, fifteen, twenty, twenty-five, and twenty-eight minutes, respectively.8 David's Apgar scores were noted as 3, 5, and 6, at one, five, and ten minutes, respectively.9 Isaac's delivery and hospital course are documented in his Death Summary, as follows: BIRTH DATE: 11/25/2004 [TIME 02:01 hours] WEIGHT: 2.275kg GEST AGE: 35 weeks GROWTH: AGA Amniotic fluid was meconium stained. Presentation was vertex. The patient was born in the delivery room by emergent cesarean section under spinal anesthesia for maternal hypertension and increasing creatinine. The patient was born first of twins. Apgar scores were 1 at 1 minute, 2 at 5 minutes and 2 at 10 minutes. At delivery, the patient was cyanotic, floppy, apneic and bradycardic. Treatment at delivery included oxygen, stimulation, oral suctioning, bag and mask ventilation, endotrachcal tube ventilation, epinephrine and cardiac compression. At birth baby was cyanotic, absent breathing effort, bradycardic (in the 20's-30's). Baby noticed to have particulate meconium. Oropharynx was suctioned by wall upon head delivery. Bag mask ventilation was started with no improvement in respiratory effort. Baby was intubated and epinephrine was given x 3 by EET but still no improvement in heart rate (in the 20's-30's). UAC line was placed while baby continued being bagged, and epinephrine was given IV x 2. Also 6 Meq of sodium bicarbonate was given x 2 plus one bolus of 4.5 Meq. Saline solution bolus of 20cc was given x1 . . . . On minute number 28-29 of life an adequate heart beat was finally noticed with improvement in color. Tone and activity still poor and no response to pain stimuli. ABG form UAC showed a pH=6.7 PCO2=47 PO2-380 BE=-31 HC03=5.6 . . . . ADMISSION DATE: 11/25/04 The patient was admitted immediately following delivery. Indications for admission included metabolic acidosis, possible sepsis, respiratory distress, prematurity and perinatal depression. Upon admission to NICU mechanical ventilation was started. Chest XR compatible with HMD vs. pneumonia. No air leak. Infasurf was given x 1 with good response, and several HCO3 corrections were needed. ADMISSION PHYSICAL EXAM . . . OVERALL STATUS: Critical - initial NICU day. BED: Radiant warmer. TEMP: Stable. HR: Stable. RR: Unstable. BP: Stable . . . . CONDITION: Acrocyanotic and depressed, intubated, hypertonic extremities. HEENT: Soft fontanelles, sluggish pupil reaction to light, ETT in place. RESPIRATORY: Minimally depressed air exchange and decreased breath sounds bilaterally (improved after surfactant administration). CARDIAC: Normal sinus rhythm . . . . NEUROLOGIC: Depressed mental status. Severely decreased muscle tone initially and hypertonicity noticed after NICU admission. Seizures noticed (lip smacking and tonic- clonic seizures on all 4 extremities > on the R hand) . . . . * * * RESOLVED DIAGNOSES DIAGNOSIS #1: RESPIRATORY DISTRESS ONSET: 11/25/2004 RESOLVED: 1/12/2005 * * * COMMENTS: Developed respiratory distress at birth. Chest Xrays compatible with HMD vs pneumonia. Initially severe respiratory acidosis. Improved with Infasurf x 1. On vent since birth, self-extubated during nursing touch-time on 12/5, was extubated for 19 hrs on nasal cannula but was reintubated on 12/6 for PC02 70 felt to be secondary to mucous plug. He has no gag reflex and has poor control of respiratory secretions reason why he has been kept on mechanical ventilation. He is still ventilator dependent, was on ETT CPAP+5 and after an extubation attempt on 1/2 he failed oxyhood and was reintubated on 1/3/05. now extubated to nasal cannula. * * * DIAGNOSIS #3: POSSIBLE SEPSIS ONSET: 11/25/2004 RESOLVED: 12/6/2004 * * * COMMENTS: Completed a 10 day course of antibiotics for suspect sepsis due to unknown GBS, respiratory distress, and severe metabolic and respiratory acidosis. There is no clinical evidence of sepsis at this time. * * * DIAGNOSIS #10: SEVERE HYPOXIC-ISCHEMIC BRAIN INJURY ONSET: 11/25/2004 RESOLVED: 1/12/2005 PROCEDURES: cranial ultrasound on 11/25/2004 (unofficially no bleed); MRI scan on 12/3/2004 (findings suggesting ischemic encephalopathy, normal size ventricles, no mass effects or midline shift) COMMENTS: Adequate heart rate not obtained till 28-29 minutes of life. He presented with seizures and an abnormal neurologic exam and abnormal EEG findings. The pediatric neurologist impression was of a severe hypoxic ischemic encephalopathy with multifocal seizures. No clinical neurologic deterioration has been noted recently. The MRI was compatible with ischemic encephalopathy. Ped neurologist has been following the baby with us. No neurological improvement has been noted recently. . . . Baby remains unresponsive, fixed pupils, minimal spontaneous breathing, does not have any spontaneous movement. No new changes noted recently. The baby has been unstable and recommended MRI of the brain was able to be done due to the critical condition of the infant. DIAGNOSIS #11: SEIZURES ONSET: 11/25/2004 RESOLVED: 1/12/2005 * * * COMMENTS: The pediatric neurologist impression is of a severe hypoxic ischemic encephalopathy with multifocal seizures. Baby was initially noted to be lip-smacking shortly after admission to NICU then started with tonic-clonic movement of all four extremities > on the R hand. Initially treated with phenobarbital and Versed. Phenobarb discontinued 11/26. No clinical seizure activity on PE but on 11/29 EEG showed diffuse electrical sz. Phenobarb and Cerebryx started. EEG on 12/1 was unchanged but occasional correlation with subtle finger movement. 12/2 with decerebrate posturing of UE to deep painful stimuli. EEG from 12/3 showed seizure activity but some improvement was reported. Phenobarbital given x1 then held 2nd level elevated Cerebryx continued till 12/9 discontinued per pedi-neuro. Depacon added on 12/6 as recommended by pediatric neurologist no change before discontinued 12/10. Phenobarb was resumed on 12/8. level 42.3 on 12/11. The dose has been adjusted as per neurologist. No recent new neurological changes or improvement noted. He continues on phenobarb w/occasional clinical seizure noted . . . . * * * DIAGNOSIS #13: SEVERE METABOLIC ACIDOSIS ONSET: 11/25/2004 RESOLVED: 12/2/2004 COMMENTS: Severe metabolic acidosis at birth pH 6.7 HCO3=5.6. Baby received HCO3 bolus x 3 in the OR and several corrections upon admission to NICU. * * * DEATH INFORMATION DISPOSITION: The patient died on 1/12/2005 at 00:52 hours. The cause of death was Cardio-respiratory arrest. Baby Boy "A" Castro is an 48 d/o w/Hypoxic- ischemic-encephalopathy, seizures, s/p 28-29 min full resuscitation, initially w/o a heart rate; who has been in a vegetative neurological state, w/intractable seizures since birth 11/25/04. Baby never tolerated any feeds and remained in TPN, was extubated to n/c w/(+) spontaneous breathing but NO gag and unable to clear secretions since baby never had any spontaneous voluntary movement. Tonight while parents visited baby was having desaturations and bradycardia that required IPPB, to improve heart rate and O2 sats. Parents requested to stop the IPPB, and requested to hold baby w/O2 N/C. Baby expired almost immediately of cardiorespiratory arrest at 12:52 a.m. . . . . David's delivery and hospital course are documented in his Death Summary, as follows: BIRTH DATE: 11/25/2004 TIME: 02:02 hours WEIGHT: 2.150kg GEST AGE: 35 weeks GROWTH: AGA RUPTURE OF MEMBRANES: At delivery. AMNIOTIC FLUID: Clear. PRESENTATION: Vertex. DELIVERY: Born in the delivery room by emergent cesarean section under spinal anesthesia for maternal hypertension with increasing creatinine. BIRTH ORDER: Second of twins. APGARS: 3 at 1 minute, 5 at 5 minutes and 6 at 10 minutes. CONDITION AT DELIVERY: Cyanotic and floppy. TREATMENT AT DELIVERY: Stimulation, oxygen, oral suctioning, bag and mask ventilation and endotrachael tube ventilation. At birth baby was cyanotic, no respiratory effort, floppy, bradycardic in the 50's. Mouth was suctioned with bulb, and bag mask ventilation was started for about 5 minutes before improvement in color and activity were seen. Baby was intubated aprox on min of life 4-5 by pediatrician Dr. Torres. No medication was needed during intervention, and baby responded well to intubation, oxygen and ambu bag ventilation. Baby noticed to be floppy despite color and heart rate improvement. Transferred stable to NICU. Initial ABG's showed severe metabolic acidosis pH=6.9 HCO3=7.4 BE=-25. ADMISSION DATE: 11/25/2004 ADMISSION TYPE: Immediately following delivery. ADMISSION INDICATIONS: Metabolic acidosis, respiratory distress, possible sepsis, prematurity and perinatal depression. Upon admission to NICU mechanical ventilation was stated. Chest XR showed reticulogranular pattern and air bronchograms compatible with HMD vs. pneumonia. No air leak. Infasurf was given x 1 with good response. Na bicarbonate corrections were needed x 3. ADMISSION PHYSICAL EXAM OVERALL STATUS: Critical - initial NICU day. BED: Radiant warmer. TEMP: Stable. HR: Stable. RR: Unstable: BP: Stable. URINE OUTPUT: Stable. CONDITION: on PRVC, breathing above the ventilator (tachypneic), pink color, mild acrocyanosis. HEENT: Pupils reactive to light, soft fontanelles, no bulging. RESPIRATORY: Minimally decreased air exchange, initially decreased breath sounds, improved after Infasurf and mechanical ventilator sounds heard equally bilaterally. CARDIAC: Normal sinus rhythm . . . . NEUROLOGIC: Depressed mental status and decreased muscle tone. * * * RESOLVED DIAGNOSES DIAGNOSIS #1: SEVERE RESPIRATORY DISTRESS ONSET: 11/25/2004 RESOLVED: 12/7/2004 * * * COMMENTS: Respiratory distress at birth. Chest XR compatible with HMD vs pneumonia. Received Infasurf x 1 with adequate response. In room air but requiring vent support due to no spontaneous respirations breathing with the vent. Poor respiratory effort more likely due to hypoxic ischemic encephalopathy but no deterioration in respiratory status. He remains critically ill and on high ventilatory support, unstable and deteriorating due to DIC and sepsis. During the course of the day the baby continued to deteriorate clinically and presented episodes of bradycardia and decreased SAO2 requiring higher ventilatory support and multiple doses of epinephrine. Later in the afternoon he became bradycardic and did not respond to resuscitative measures and was declared dead at 3:25 PM. . . . DIAGNOSIS #2: METABOLIC ACIDOSIS ONSET: 11/25/2004 RESOLVED: 11/29/2004 MEDICATIONS: Sodium bicarbonate on 11/25/2004. COMMENTS: Upon admission required Na bicarbonate corrections x3. Initial ABG's showed a pH=6.9 HCO3=7.4 BE=-25, currently stable. * * * DIAGNOSIS #6: POSSIBLE SEPSIS ONSET: 11/25/2004 RESOLVED: 12/5/2004 * * * COMMENTS: Completing a 10 day course of antibiotics for suspect sepsis secondary to maternal GBS unknown, respiratory distress at birth, severe metabolic acidosis. The blood culture was negative and there is no clinical evidence of sepsis at this time. * * * DIAGNOSIS #10: HYPOXIC-ISCHEMIC BRAIN INJURY ONSET: 11/25/2004 RESOLVED: 12/7/2004 PROCEDURES: cranial ultrasound from 11/25/2004 till 12/7/2004(normal) COMMENTS: Perinatal depression, required bag mask ventilation, intubation and oxygen in order to improve. Apgar scores were 3/5/6. The baby had presented seizures and systemic failure and the assessment of the pediatric neurologist was of severe hypoxic and ischemic encephalopathy. Neurologically he has not changed recently and continues with an abnormal neurological exam and no improvement in neuro condition. DIAGNOSIS #11: SEIZURES ONSET: 11/25/2004 RESOLVED: 12/7/2004 * * * COMMENTS: Shortly after admission to NICU he started with generalized tonic-clonic seizures. Persistent Sz activity on phenobarb and Cerebryx correlates with independent clonic movements of UE, extensor posturing of UE R>L and gaze deviation per neurologist Dr. Bustamante. Last EEG from 12/3 showed worsening EEG with seizure activity and burst suppression. The pediatric neurologist impression was of a severe hypoxic ischemic encephalopathy with multifocal seizures. Phenobarbital on hold since 12/1 for level 61.8 down to 29.5 will not resume per neuro and phosphenytoin level 18.8 on maintenance dose 2.5 mg/kg q 12. An MRI was not done due to the critical and unstable condition of the infant. * * * DEATH INFORMATION DISCHARGE TYPE: Died. DATE OF DEATH: 12/7/2004. TIME OF DEATH: 15:25 hours. CAUSE OF DEATH: Respiratory failure, sepsis and multisystemic failure . . . . Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. Here, it is undisputed that Isaac and David suffered an injury to the brain caused by oxygen deprivation, which rendered them permanently and substantially mentally and physically impaired. What is disputed is whether the injury occurred "in the course of labor, delivery, or resuscitation in the immediate postdelivery period," as required for coverage under the Plan. § 766.302(2), Fla. Stat.; Nagy v. Florida Birth-Related Neurological Injury Compensation Association, 813 So. 2d 155 (Fla. 4th DCA 2002). As to that issue, Petitioners are of the view that the brain injury occurred before delivery, and since it is undisputed that Mrs. Castro was never in labor the injury is not covered by the Plan. In contrast, NICA and the hospital are of the view that the injury either occurred during, or continued through, delivery and resuscitation, and is therefore compensable. As an aid to resolving such issue, Section 766.309(1)(a), Florida Statutes, provides that when, as here, the proof demonstrates "that the infant has sustained a brain . . . injury caused by oxygen deprivation . . . and that the infant was thereby rendered permanently and substantially mentally and physically impaired, a rebuttable presumption . . . [arises] that the injury is a birth-related neurological injury, as defined [by the Plan]." Here, since Mrs. Castro was never in labor, the presumption is that Isaac's and David's brain injury occurred in the course of delivery or resuscitation in the immediate postdelivery period. See Orlando Regional Healthcare Systems, Inc. v. Alexander, 909 So. 2d 582 (Fla. 5th DCA 2005). Consequently, to be resolved is whether there was credible evidence produced to support a contrary conclusion and, if so, whether, absent the presumption, the record demonstrates, more likely than not, that Isaac's and David's brain injury occurred during delivery or resuscitation in the immediate postdelivery period.10 The timing of the twins' brain injury To address the timing of the twins' brain injury, the parties offered the medical records relating to Mrs. Castro's antepartal course, as well as those associated with the twins' birth and subsequent development. (Petitioners' Exhibit A, tabs 8-11, and Exhibit B). Additionally, the parties offered the deposition testimony of Dr. Daniel, a physician board-certified in obstetrics and gynecology; Adré du Plessis, M.D., a physician board-certified in pediatrics, and neurology with special competence in child neurology; Steven Chavoustie, M.D., a physician board-certified in obstetrics and gynecology; Michael Katz, M.D., a physician board-certified in obstetrics and gynecology, and maternal-fetal medicine; and Donald Willis, M.D., a physician board-certified in obstetrics and gynecology, and maternal-fetal medicine. (Petitioners' Exhibit A, tabs 3-7) The testimony of Doctors Daniel, du Plessis, and Chavoustie was supportive of Petitioners' view, and the testimony of Doctors Katz and Willis was supportive of the views of NICA and the hospital. The medical records and the testimony of the parties' experts have been carefully considered. So considered, it must be resolved that there was credible evidence (through the testimony of Doctors Daniel, du Plessis, and Chavoustie) to rebut the presumption established by Section 766.309(1)(a), Florida Statutes, and that, absent the presumption, the record failed to demonstrate, more likely than not, that any injury the twins may have suffered during delivery or immediate postdelivery resuscitation contributed significantly to the profound neurologic impairment they suffered. Indeed, the more compelling proof supports a contrary conclusion. In so concluding, it is notable that the twins' brain injury started sometime after 4:07 p.m., November 24, 2004, when fetal reserves were lost, and the twins ability to compensate for a lack of oxygen failed, and that, given the severe depression the twins demonstrated at birth (cyanotic, apneic, floppy, and profoundly bradycardic), consistent with injury to the brain stem, the more robust level of a newborn brain; the need for intensive delivery room resuscitation (with intubation and, in the case of Isaac, advanced CPR), likewise consistent with injury to the brain stem; and the profound acidotic state in which they presented, it is likely, more so than not, that the twins suffered profound brain damage well prior to delivery (which was quick and without complication), that accounts for the severe neurological impairment (mental and physical) they demonstrated at birth. Consequently, since Mrs. Castro was not in labor when the profound brain injury most likely occurred, the twins were not shown to have suffered a "birth-related neurological injury," as defined by the Plan.
The Issue Whether Deidre Denson has suffered an injury for which compensation should be awarded under the Florida Birth- Related Neurological Injury Compensation Plan, as alleged in the claim for compensation.
Findings Of Fact Preliminary matters Deidre Denson (Deidre) is the natural daughter of David and Linda Denson. She was born a live infant on October 8, 1991, at Bayfront Medical Center in St. Petersburg, Pinellas County, Florida, and her birth weight was in excess of 2500 grams. The physicians providing obstetrical services during the birth of Deidre were David Moreland, M.D., and Donna Miller, M.D., who were, at all times material hereto, participating physicians in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. The birth of Deidre Denson At or about 12:30 a.m., October 8, 1991, Linda Denson presented to Bayfront Medical Center, upon advice of her physician, following the spontaneous rupture of her membrane. At the time, Linda Denson was in active labor and Deidre, who was at term, was in a breach presentation. At approximately 1:09 a.m., Mrs. Denson was admitted to the labor room, and thick meconium was observed upon examination. External fetal monitoring was commenced, which initially reflected a fetal heart rate in the 80-90 beat per minute range; however, at or about 1:12 a.m., and continuing until approximately 1:18 a.m., the fetal heart rate was observed to fluctuate between the 80-90 rate and 60 beats per minute. This situation evidenced fetal distress and an urgent need for surgical intervention. Accordingly, at approximately 1:18 a.m. Mrs. Denson was taken to the operating room. Mrs. Denson was admitted to the operating room at 1:23 a.m., and Deidre was delivered by a cesarean section surgical procedure at 1:35 a.m. Upon delivery, Deidre's physical appearance was observed to be "blue" and her heart rate was below 30 beats per minute. Delivery room resuscitation included intubation, with suctioning of meconium below the vocal cords four times, and bagging with 100 percent oxygen. Spontaneous respirations were not observed in the infant until thirty minutes after birth, when they were noted as "slow" and continued to be noted as "slow" until 2:12 a.m. when she was transferred to the neonatal intensive care unit at All Children's Hospital. At birth, Deidre's Apgar scores at one, five and 10 minutes were one, four and five respectively. These scores are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of the heart rate, muscle tone, respiratory effort, color, and reflex irritability, with each category being assigned a score ranging from the lowest score of zero through a maximum score of two. As noted, at one minute, Deidre's Apgar score totaled one, with heart rate being graded at one ("slow, below 100"), and muscle tone, respiratory effort, color and reflex irritability being graded at zero. At five minutes, Deidre's Apgar score totaled four, with heart rate and color being graded at two each, respiratory effort being graded at one ("slow, irregular"), and muscle tone and reflex irritability being graded at zero each. At 10 minutes, Deidre's Apgar score totaled five, with heart rate and color again being graded at two each, and muscle tone, respiratory effort and reflex irritability being graded at one each. Such scores are consistent with Deidre having suffered a severe hypoxic insult (deprivation of oxygen) at birth. At approximately 2:25 a.m., October 8, 1991, Deidre was admitted to the neonatal intensive care unit at All Children's Hospital, and was placed on a ventilator until four days of age and remained with an endotracheal tube until six days of age. At 1:45 p.m., Deidre was observed to have developed seizure activity, secondary to perinatal depression, and an electroencephalogram (EEG) was ordered. That EEG was read as an "abnormal ictal EEG recording," and is consistent with diffuse cerebral disfunction. Dr. Kenneth Sassower, a pediatric neurologist, performed a consult on Deidre on October 8, 1991, and observed that the "differential diagnosis of neonatal seizures at this early age include fetal hypoxia; metabolic abnormalities . . . intracranial hemorrhage . . .; meningitis, etc." He recommended a cranial ultrasound, a "CT scan of the head without contrast, pending stable clinical status," a repeat EEG study, and certain other testing procedures designed to identify the cause of Deidre's seizure activity. The cranial ultrasound was taken on October 9, 1991, and was read as normal in that it failed to reflect any hemorrhage in or around the ventricles and did not reflect any displacement of the ventricles. Such findings do not, however, rule out the possibility that a bleed/intracranial hemorrhage existed in the frontal area, since such would not be picked up on ultrasound. Rather, a CT scan of the head without contrast would have been the preferred and more reliable testing procedure; however, due to the fragile nature of the infant's condition, ultrasound was employed as the first test to discern the presence of cerebral blood. As discussed infra, the first CT scan was performed December 3, 1991, after Deidre's discharge from All Children's Hospital, and evidenced a bleed in the frontal area. Other testing procedures ruled out metabolic abnormalities and meningitis as causative factors for Deidre's seizures. As with the EEG taken October 8, 1991, serial EEG's taken October 9, 14 and 23, 1991, were also read as abnormal and "indicative of diffuse cerebral dysfunction with bifocal dysfunction over both central regions." The proximity of Deidre's seizure activity to birth, and the abnormal EEGs, are consistent with diffuse brain injury as a consequence of hypoxic insult at birth. Given the absence of any other identifiable factor, it is found that Deidre's seizure activity was directly attributable to birth asphyxia. 1/ In addition to the foregoing abnormalities, Deidre was also diagnosed as suffering hypotension due to mycardial insufficiency, as well as renal (kidney) and liver damage, due to perinatal depression, and on neurologic consult to exhibit "evidence of generalized hypotonia and hyporeflexia." Such observations are consistent with hypoxic insult at birth. Deidre's condition was, however, managed and she was discharged from All Children's Hospital to the care of her parents on October 24, 1991. Currently, Deidre is, indisputedly, permanently and substantially mentally and physically impaired. Considering its quality, the proof is compelling that Deidre suffered a severe hypoxic insult at birth and that as a consequence of such oxygen deprivation suffered an injury to her brain which adversely impacted her mentally and physically. Notwithstanding, respondent, Florida Birth- Related Neurological Injury Compensation Association (NICA), contends that the seriousness of Deidre's current neurological deficit is not a product of the hypoxic insult she suffered at birth but, rather, was occasioned by head trauma suffered after her discharge from All Children's Hospital. For the reasons that follow, NICA's position is rejected, and it is found, based on the more compelling proof, that Deidre sustained an injury to the brain caused by oxygen deprivation in the course of labor, delivery or resuscitation in the immediate post-delivery period that rendered her permanently and substantially mentally and physically impaired. Events subsequent to Deidre's discharge from All Children's Hospital Following Deidre's discharge from All Children's Hospital, she was next neurologically examined by Dr. Kenneth Sassower on November 26, 1991. On examination, Dr. Sassower observed evidence of a mild to moderate spastic diparesis and hyperreflexia in the lower extremities, but noted that Deidre was currently seizure free on phenobarbital monotherapy without undue behavioral side effects noted. Based on his observations, Dr. Sassower proposed a reevaluation of Deidre in three to four months. 2/ On December 3, 1991, Deidre presented for a CT Scan of the brain without enhancement at the radiology department of All Children's Hospital. Such CT scan was an apparent follow-up to a recommendation made by Dr. Sassower when he examined Deidre on October 8, 1991, to address the cause of Deidre's seizure activity. [Petitioners' exhibits 16 and 18] The attending radiologist reported: Findings: As compared to the sonogram on 10-9-91, the frontal horns now seem slightly distended. This is seen in association with chronic bilateral subdural hematomas. There is also evidence of prominent sulci and cisterns with underlying leukomalacia. This is most pronounced in the frontal lobes. The 3rd and 4th ventricle are also slightly distended . . . No intracranial calcifications. The mastoid air cells are well aerated bilaterally. The anterior and posterior fontanelles are small for the patient's age. Otherwise, normal calvarial contour. IMPRESSION: 1. Status post development of bilateral subdural hematomas and brain atrophy with predominant frontal leukomalacia. This raises a question of intervening trauma. Recommend clinical correlation. Consequently, the radiologist telephoned Dr. Sassower at 10:15 a.m., December 3, 1991, and arranged for a neurological examination of Deidre at 12:00 p.m. Deidre was indeed examined by Dr. Sassower on December 3, 1991. During the course of that examination he concluded: . . . The CT scan reveals evidence of prominent cortical atrophy, along with what appears to be a suggestion of semi-acute bifrontal subdural hematomas. The exact extent of subdural blood is somewhat difficult to assess due to the presence of increased hypolucencies which at times appear continuous with areas of relative cortical atrophy. * * * During the course of the clinical examination, both parents deny any known recent head trauma, either accidental or otherwise. Both parents, who appear extremely reliable, have now reported leaving their child in the company of other caretakers since discharge from the nursery. I think in spite of the fact that both parents appear to be appropriately concerned, one needs to exercise a good deal of caution in this regard, and pursue careful clinical surveillance over the course of the ensuing weeks. In this regard, a repeat neurologic follow-up in 4-6 weeks time is suggested. A subdural hematoma, as observed in Deidre, is a collection of blood which has accumulated in the space between the dura matter, a thickened membrane which covers the brain, and the surface of the other membranes which cover the brain. Their presence raises the possibility that any existent brain damage may have been caused or exacerbated by trauma or the subdural hematoma itself. Notably, the trauma which tears the subdural veins and creates the subdural hematoma may be of sufficient force itself to cause brain damage or the hematoma itself may be of sufficient magnitude to compress the brain and cause brain damage. About 99 percent of subdural hematomas are due to trauma, which causes the veins crossing the subdural space into the dural sinuses to tear and thereby bleed. The other one percent of observed subdural hematomas are due to rare causes such as bleeding disorders. Under the circumstances, the presence of a subdural hematoma in Deidre certainly raised the possibility of secondary brain damage due to trauma or abuse. Here, the proof demonstrates that the subdural hematomas reflected by the CT scan of December 3, 1991, may be characterized as "chronic," and so defined, reflect a hematoma that had its genesis more than two weeks prior to its discovery. As for Deidre's hematomas, her neurosurgeon, whose opinion is credited, dates their occurance at two to four weeks prior to the CT scan of December 3, 1991. 3/ Regarding the cause of Deidre's subdural hematomas, the proof is, at best, unsatisfying. Deidre's birth was by cesarean section and therefore no mechanical maneuver or device, such as a vacuum extractor, forceps or a forced vaginal delivery, was utilized which could cause trauma. Moreover, the medical records are devoid of any indication of trauma to Deidre's head during delivery or the term of her hospitalization. Such does not, of course, completely rule of the possibility that trauma was induced during resuscitation efforts or at some other time in the hospital, but any such conclusion, absent a CT scan or other definitive testing during her admission, would be speculative. On the other hand, Deidre received routine follow-up after discharge by her pediatricians and Dr. Sassower, and they observed no evidence of trauma or abuse to Deidre, and a physical and ophthalmology consult revealed none. The absence of such physical evidence does not completely rule out the possibility of trauma or abuse, but its absence coupled with the ophthalmology consult and the reliability and character of the parents, as well as the other sole caregiver, renders it extremely unlikely that the subdural hematomas were a consequence of abuse or trauma suffered following Deidre's discharge from the hospital. The only other explanation offered at hearing for Deidre's subdural hematomas, other than a blood disorder which was ruled out, were the opinions offered by her physicians and experts, who suggested that because of the brain atrophy and the resultant shrinkage of the brain suffered as a consequence of the hypoxic insult at birth, the bridging veins which cross the subdural space into the dural sinuses were stressed and introduced a bleed, causing the hematomas. Given the conclusion that trauma or abuse was not the cause of Deidre's hematomas, and the elimination of a blood disorder as a possible cause, such opinions, based on the proof in this case, are the most likely explanation of Deidre's bleed, which resulted in the hematomas disclosed by the December 3, 1991 scan. Finally, the absence of any compelling proof to demonstrate that Deidre's hematomas were induced by trauma, and the absence of any compelling proof that the chronic subdural hematomas were of sufficient magnitude and existed for a sufficient period of time to compress the brain and cause significant brain damage, absent trauma, it is concluded that the atropy evidenced by the CT scan of December 3, 1991, was more likely than not, a product of the hypoxic insult that Deidre suffered at birth, and that such hypoxic insult rendered her substantially and permanently mentally and physically impaired. 4/
