The Issue At issue in this proceeding is whether Daniel Jazon, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Daniel Jazon (Daniel) is the natural son of Elizabeth Jazon and William Jazon. He was born a live infant on May 8, 1993, at Baptist Hospital, a hospital duly licensed in the State of Florida and located in Miami, Dade County, Florida. Daniel's birth weight exceeded 2,500 grams. The physician providing obstetrical services during the birth of Daniel was George Battle, M.D., who was, at all times material hereto, a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Daniel's birth and subsequent condition A review of the medical records reveals that Daniel was born full term after an essentially uncomplicated pregnancy. Total labor time was approximately 17 hours, and progressed slowly. During the last hour variable decelerations occurred and brief episodes of fetal bradycardia, so delivery was assisted by vacuum and outlet forceps were used. Daniel cried and breathed immediately at birth, and his Apgar scores were noted as 7 at one minute and 9 at five minutes. He was noted to be mildly sluggish at birth, but improved with tactile stimulation and blow-by oxygen. Daniel was also noted not to move his left arm for approximately three minutes. Daniel was transferred to the regular nursery, but fed poorly. At approximately seven hours of age jitteriness was noted, followed by episodes of rhythmic jerking of the left arm and leg lasting up to nine minutes. Upon transfer to the neonatal intensive care unit, similar seizure activity was noted, so Daniel was loaded with phenobarbital. A CT scan of the brain revealed a right temporal parietal infarct. A neurological consultation by Kenneth Butler, M.D., on May 9, 1993, observed definite weakness in the left upper extremity and diminished reflexes on the left side. Daniel evidenced further focal seizure activity on May 10, 1993, involving the left chest, shoulder, arm and hand, and was started on Dilantin. Daniel remained seizure- free, and a CT scan of the brain on May 12, 1993, revealed the right temporal parietal infarct without any change, which demonstrated, more likely than not, that the infarct was old and predated labor and delivery. 1/ Daniel remained seizure free, and was discharged to the care of his mother on May 27, 1993. At discharge, his neurological examination remained abnormal, with hypotonia, hyperreflexia and ankle clonus. Following discharge, Daniel continued to be followed by Dr. Butler. His examinations of June 22, 1993, September 10, 1993, November 9, 1993, and March 10, 1994, reveal that the physical impairments Daniel suffered as a consequence of his right temporal infarct progressively resolved and, as of his last examination, no significant physical or neurologic deficits were observed.
Conclusions The Division of Administrative Hearings has jurisdiction over the parties to, and the subject matter of, these proceedings. Section 766.301, et seq., Florida Statutes. The Florida Birth-Related Neurological Injury Compensation Plan (the "Plan") was established by the Legislature "to provide compensation, on a no fault basis, for a limited class of catastrophic injuries, [defined as 'birth- related neurological injuries' in the Plan]" relating to births occurring on or after January 1, 1989. Humana of Florida, Inc. v. McKaughn, 20 Fla.L.Weekly D565, D567 (Fla. 2d DCA 1995), and Section 766.303(1), Florida Statutes. The injured "infant, his personal representative, parents, dependents, and next of kin," may seek compensation under the Plan by filing a claim for compensation with the Division of Administrative Hearings within five years of the infant's birth. Sections 766.302(3), 766.303(2), 766.305(1) and 766.313, Florida Statutes. The Florida Birth-Related Neurological Injury Compensation Association (NICA), which administers the Plan, has "45 days from the date of service of a complete claim . . . in which to file a response to the petition and to submit relevant written information relating to the issue of whether the injury is a birth-related neurological injury." Section 766.305(3), Florida Statutes. If NICA determines that the injury alleged in a claim is a compensable birth-related neurological injury, it may award compensation to the claimant, provided that the award is approved by the Hearing Officer to whom the claim has been assigned. Section 766.305(6), Florida Statutes. If, on the other hand, NICA disputes the claim, as it has in the instant case, the dispute must be resolved by the assigned Hearing Officer in accordance with the provisions of Chapter 120, Florida Statutes. Sections 766.304, 766.307, 766.309 and 766.31, Florida Statutes. In discharging this responsibility, the Hearing Officer must make the following determination based upon the available evidence: Whether the injury claimed is a birth- related neurological injury. If the claimant has demonstrated, to the satisfaction of the hearing officer, that the infant has sustained a brain or spinal cord injury caused by oxygen deprivation or mechanical injury and that the infant was thereby rendered permanently and substantially mentally and physically im- paired, a rebuttable presumption shall arise that the injury is a birth-related neurologi- cal injury as defined in s. 766.303(2). Whether obstetrical services were de- livered by a participating physician in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital; or by a certified nurse midwife in a teaching hospital supervised by a partici- pating physician in the course of labor, de- livery, or resuscitation in the immediate post-delivery period in a hospital. Section 766.309(1), Florida Statutes. 2/ An award may be sustained only if the Hearing Officer concludes that the "infant has sustained a birth-related neurological injury and that obstetrical services were delivered by a participating physician at birth." Section 766.31(1), Florida Statutes. Pertinent to this case, "birth-related neurological injury" is defined by Section 766.302(2), Florida Statutes, to mean: . . . injury to the brain or spinal cord of a live infant weighing at least 2,500 grams at birth caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immedi- ate post-delivery period in a hospital, which renders the infant permanently and substan- tially mentally and physically impaired. This definition shall apply to live births only and shall not include disability or death caused by genetic or congenital abnormality. Here, the proof demonstrated that Daniel was born a live infant, that his birth weight was in excess of 2,500 grams, and that the physician who provided obstetrical services during the course of his birth was a "participating physician" as that term is defined by Section 766.302(7), Florida Statutes. However the record developed in this case failed to demonstrate that Daniel suffered a "birth-related neurological injury," within the meaning of Section 766.302(2), Florida Statutes, since it failed to support the conclusion that Daniel suffered any injury to his brain or spinal cord caused by oxygen deprivation or mechanical injury during labor, delivery or resuscitation in the immediate post- delivery period which rendered him permanently and substantially mentally and physically impaired. Sections 766.302(2), 766.309(1) and 766.31(1), Florida Statutes. Rather, the proof demonstrated that the right temporal parietal infarct Daniel suffered occurred prior to labor and delivery, and that currently Daniel is not permanently and substantially mentally and physically impaired. Where, as here, the Hearing Officer determines that ". . . the injury alleged is not a birth-related neurological injury . . . he [is required to] enter an order [to such effect] and . . . cause a copy of such order to be sent immediately to the parties by registered or certified mail." Section 766.309(2), Florida Statutes. Such an order constitutes final agency action subject to appellate court review. Section 766.311(1), Florida Statutes.
Findings Of Fact Luke Z. Davis was born on March 27, 2014, at Shands at the University of Florida, Gainesville, Florida. Luke weighed 4,060 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Luke, 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 a medical report dated February 25, 2016, Dr. Willis described his findings in part as follows: There was an apparent obstetrical event, shoulder dystocia that resulted in loss of oxygen to the baby's brain during delivery and continuing into the immediate post delivery period. There was no trauma to the spinal cord. The oxygen deprivation to the brain resulted in some degree of brain injury, as identified by brain hemorrhage on MRI. The MRI reported no evidence of global brain injury. I am not able to comment about the severity of the brain injury. Dr. Willis reaffirmed his opinion in an affidavit dated May 25, 2016. NICA retained Laufey Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to examine Luke and to review his medical records. Dr. Sigurdardottir examined Luke on March 30, 2016. In her report dated March 30, 2016, Dr. Sigurdardottir opined in pertinent part as follows: Summary: Here we have a 2-year-old with a difficult birth due to shoulder dystocia leading to an acute hypoxic event lasting 13 minutes. The patient did receive cooling protocol, had evidence of a brain injury on MRI, although not severe, and is left with a significant motor impairment from a flaccid right arm, as well as expressive language delay . . . . [T]he patient is found to have substantial physical impairment, as his right upper extremity has little to no functional use. There is a possible mild mental impairment due to language delay, but his delays do not seem substantial at this time. [T]here is evidence of a hypoxic ischemic event occurring at birth resulting in neurologic depression at birth, as well as mechanical injury resulting in a severe paresis of right upper extremity. Both his hypoxic events, as well as his mechanical brachial plexopathy is birth related. 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 evidence of global brain injury or injury to the spinal cord. Dr. Willis’ opinion is credited. There are no expert opinions filed that are contrary to Dr. Sigurdardottir’s opinion that Luke does not suffer from a substantial mental impairment. Dr. Sigurdardottir’s opinion is credited.
Findings Of Fact Daniel Flint was born on May 3, 2014, at Bayfront Health Spring Hill in Spring Hill, Florida. Daniel weighed in excess of 2,500 grams at birth. NICA retained Donald C. Willis, M.D. (Dr. Willis), to review Daniel's medical records. In a medical report dated June 2, 2015, Dr. Willis made the following findings and expressed the following opinion: In summary, fetal bradycardia developed during labor and required emergency Cesarean delivery. The baby was severely depressed at birth with Apgar scores of 0 at one and five minutes. A heart rate was not present until after 10 minutes of vigorous resuscitation. The initial blood gas was consistent with acidosis. The base was -22. Seizures occurred within the first hour of life. The baby was diagnosed with HIE and managed with whole body cooling. The baby was found to have a single mutation for the Prothrombin II mutation. I do not believe this was a factor in the oxygen deprivation at birth. 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. Seizure activity shortly after birth would be consistent with brain injury as a result of the oxygen deprivation. I am unable to comment about the severity of the brain injury. Dr. Willis' opinion that 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, and that seizure activity shortly after birth would be consistent with brain injury as a result of oxygen deprivation is credited. Respondent retained Michael Duchowny, M.D. (Dr. Duchowny), a pediatric neurologist, to evaluate Daniel. Dr. Duchowny reviewed Daniel's medical records and performed an independent medical examination on him on May 13, 2015. Dr. Duchowny made the following findings and summarized his evaluation as follows: In SUMMARY Daniel's neurological examination reveals very mild plantar-grade foot positioning without corroborating evidence of increased muscle tone. The elevated (3+) knee jerks are consistent with an extremely mild spastic diparesis. He additionally evidences borderline microcephaly. I was surprised by this finding as his head appeared normal to inspection; I re-measured the head circumference several times to confirm. Daniel's motor impairment is judged to be mild and I did not find evidence of many [sic] mental impairment. A review of medical records sent on April 16th reveals that following Daniel's birth at Bayfront Health at Springhill Hospital at 38 4/7 weeks gestation he was transferred to All Children's Hospital. Because of concern over low Apgar scores of 0, 0, 2, 4 and 5 at 1, 5, 10, 15 and 20 minutes, lethargy and tremors, he was placed in a hypothermic protpocol at 1 hour of life which was formally implemented upon arrival at All Children's Hospital. Daniel underwent total body cooling for 3 days. He developed seizures within 35 minutes of delivery and was treated with phenobarbital. Dopamine and hydrocortisone were administered. His nursery course was complicated by MRSA colonization which stabilized. He was found to be heterozygous with a prothrombin gene mutation. An MRI scan of the brain obtained on May 12 revealed a questionable area of thrombosis but a repeat MRI scan on May 22 was significant only for enlarged extraaxial spaces. In summary, Daniel has done remarkably well and now has only a very mild motor impairment affecting his gait and to a lesser degree his oroalimentary coordination. His head growth is borderline. I believe the hypothermia protocol played a role in improving his long- term prognosis. Daniel does not have either a substantial mental or motor impairment and I am not recommending him for consideration within the NICA Program. Dr. Duchowny was deposed on January 15, 2015, wherein he testified in pertinent part as follows: Q. Okay. All right. And these records discuss and describe certain issues, and I know you said you read the mom's deposition. She raised some issues about the child's coordination running or about some of the swallowing issues. Is it fair to say that any issue that's been raised, either by Mom in her deposition or by any of the health care providers in the records that you reviewed or any issues that you noted in your report, are all related to this developmentally based disorder that was established in utero? A. That's what I believe, yes. Q. And is that your opinion within a reasonable degree of medical probability? A. It is. * * * Q. Doctor, are you familiar with the term or definition of birth-related neurological injury as it's used with Chapter 766 of the Florida Statutes? A. I believe so, yes. Q. Okay. So I want to ask you then: Do you have an opinion whether Daniel is permanently and substantially mentally and physically impaired? MS. DAWSON: Form THE WITNESS: I do BY MR. GRACE: Q. What's that opinion Doctor? A. I do not believe that he has a substantial mental or physical impairment. Q. And just in summary fashion – I'm not asking for you to re-testify about all your prior opinions. But in summary fashion, tell us the basis for that opinion and where you gathered your support. A. It's because I believe that Daniel's motor dysfunction is mild and primarily is associated with incoordination which will improve over time. And I also believe that his delayed expressive language development will also improve over time. So they're mild now and will continue to improve. Therefore, neither domain represents a substantial impairment. Q. Is that opinion given within a reasonable degree of medical probability? A. Yes. Q. Doctor, in response to Mr. Valenzuela's question, you briefly touched on MRI scans that were done. Did you review the actual films, or did you rely on the reports? A. I can't recall. I have not reviewed them recently. If I had to guess, I would say that I relied on the reports at that time, but I honestly can't recall. Q. Okay. There were two scans done. And with regard to those scans, you indicated in your report on page 5 there was a questionable area of thrombosis? A. Yes, that was on the first one I believe. Q. All right, what is thrombosis? A. Blood clot. Q. And are you able to tell us what you attribute that clot to? A. I don't know. Q. Then there was a repeat MRI scan done on May 22nd, correct? A. Yes sir. Q. All right. And what were the findings on that? A. That showed no abnormalities in the brain, no evidence of thrombosis, and an extra-axial collection of fluid, meaning a collection of fluid outside the brain, not within the brain substance itself. Q. With regard to your opinion that Daniel has not suffered a birth-related neurological injury, did you rely on these MRI's to formulate that opinion? A. Yes, that was one component. Q. Okay. And how did you rely on these? What's the significance? A. Well, I don't think it's -- that you can rely on any one aspect. What I did was factor the findings on the MRI with the history and with my findings on physical examination as well as the history of Daniel's development. Putting all of that information together, in my opinion, yields a consistent pattern and diagnosis of developmental delay. I thought Daniel's examination revealed developmental findings, as I've stated previously. And the fact that his follow-up MRI showed no evidence of a structural brain injury, in my opinion, supported that diagnosis. Dr. Willis is of the opinion that there was an apparent obstetrical event that resulted in loss of oxygen to the baby's brain during labor, delivery and continuing into the post- delivery period, and that seizure activity shortly after birth is consistent with brain injury as the result of oxygen deprivation. However, in order for a birth-related injury to be compensable under the Plan, the injury must meet the definition of a birth- related neurological injury and the injury must have caused both permanent and substantial mental and physical impairment. Dr. Duchowny's opinion that Daniel does not have a substantial mental or physical impairment is credited. 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. Duchowny that Daniel does not have a substantial mental and physical impairment. While Daniel has some deficits, these deficits do not render him permanently and substantially mentally and physically impaired.
Findings Of Fact Lukas Wilson was born on August 9, 2010, at Baptist Hospital located in Pensacola, Florida. Lukas weighed 2,699 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Lukas. Dr. Willis wrote a medical report dated December 2, 2015, and affirmed his opinion in an affidavit dated March 23, 2016, as follows: In summary, delivery occurred at 36 weeks due to preterm labor. The baby was not depressed at birth and had normal Apgar scores of 8/9. No resuscitation was required at birth. The child developed a seizure disorder with Autism and ADHD. Genetic evaluation was negative. MRI of the brain at about three years of age was normal. These findings do not suggest a birth related hypoxic brain injury. As such, it is my opinion that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the child’s brain or spinal cord occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period. NICA retained Laufey Y. Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to examine Lukas and to review his medical records. Dr. Sigurdardottir examined Lukas on February 17, 2016. Dr. Sigurdardottir wrote a medical report on the date of the examination regarding her independent medical examination of Lukas, and in an affidavit dated March 30, 2016, Dr. Sigurdardottir summarized her opinion as follows: The summary of the examination is as follows: Here we have a 5-year 5-month-old male born at 36 weeks via a somewhat traumatic vaginal delivery with vacuum extraction and a scalp hematoma. His Apgar scores were, however, 8 after 1, 9 and [sic] 5 minutes. He has declared himself as having mild delays both with early motor delays and mild language delays, delay in adaptive functioning and an autistic spectrum disorder. Neuroimaging has, however, been normal. An extensive metabolic and genetic workup has been normal. Review of birth records does not indicate serious problems during the delivery, although it was somewhat lengthy and patient had only mild abnormalities on blood gas performed shortly after birth. Therefore, our results are as follows: . . . The patient is found to have no permanent substantial physical impairments and to have mild to moderate mental impairment mainly in areas of autism spectrum disorder. . . . There is evidence of a slightly traumatic birth, but no evidence of a clear hypoxic ischemic injury as Apgar scores were normal and subsequent neuroimaging has been normal. As such, it is my opinion that the IME and record review do not support a finding that Lukas suffered a birth-related neurological injury. I therefore do not recommend consideration for inclusion within the NICA 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 or spinal cord occurring in the course of labor, delivery or resuscitation in the immediate post-delivery period. Dr. Willis’ opinion is credited. There are no contrary expert opinions filed that are contrary to Dr. Sigurdardottir’s opinion that Lukas is found to have no substantial physical impairment and has a mild to moderate mental impairment mainly in the area of autism spectrum disorder. Dr. Sigurdardottir’s opinion is credited.
The Issue The issue in this case is whether Amelia Ann Shold suffered a birth-related injury as defined by section 766.302(2), Florida Statutes, for which compensation should be awarded under the Plan.
Findings Of Fact Amelia Ann Shold was born on August 11, 2015, at Baptist Medical Center South located at 800 Prudential Drive, Jacksonville, Florida 32207. The Petition alleged that the child “suffered from brain damage as a result of a prolonged second stage labor.” The circumstances of the labor, delivery, and birth of the minor child are reflected in the medical records submitted to NICA in conjunction with the Petition. At all times material, both Baptist and Dr. Tanouye were active members under NICA pursuant to section 766.302(6) and (7). Petitioners contend that Amelia suffered a birth-related neurological injury and seeks compensation under the Plan. Respondent contends that Amelia has not suffered a birth-related neurological injury as defined by section 766.302(2). In order for a claim to be compensable under the Plan, certain statutory requisites must be met. Section 766.309 provides: The Administrative Law Judge shall make the following determinations based upon all available evidence: Whether the injury claimed is a birth- related neurological injury. If the claimant has demonstrated, to the satisfaction of the Administrative Law Judge, that the infant has sustained a brain or spinal cord injury caused by oxygen deprivation or mechanical injury and that the infant was thereby rendered permanently and substantially mentally and physically impaired, a rebuttable presumption shall arise that the injury is a birth-related neurological injury as defined in § 766.302(2). Whether obstetrical services were delivered by a participating physician in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital; or by a certified nurse midwife in a teaching hospital supervised by a participating physician in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital. * * * How much compensation, if any, is awardable pursuant to § 766.31. If the Administrative Law Judge determines that the injury alleged is not a birth-related neurological injury or that obstetrical services were not delivered by a participating physician at birth, she or he shall enter an order . . . . (Emphasis added). The term “birth-related neurological injury” is defined in section 766.302(2), Florida Statutes, as: [I]njury to the brain or spinal cord of a live infant weighing at least 2,500 grams for a single gestation or, in the case of a multiple gestation, a live infant weighing at least 2,000 grams at birth caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired. This definition shall apply to live births only and shall not include disability or death caused by genetic or congenital abnormality. (Emphasis added). In the instant case, NICA has retained Laufey Y. Sigurdardottir, M.D. (Dr. Sigurdardottir), as its medical expert specializing in pediatric neurology. Dr. Sigurdardottir reviewed the medical records and conducted an independent medical examination (IME) of the child on November 16, 2017. Dr. Sigurdardottir subsequently rendered a report and opined, in pertinent part, that: Summary: Patient is a 2-year-old girl with history of neonatal focal seizures and evidence of subdural and intraventricular hemorrhage along with several small foci of diffusion restriction in left frontal lobe after prolonged vaginal delivery. She has had a good developmental trajectory and currently exhibits mild right monoparesis and a mild expressive language delay. Substantial motor or mental delays are not noted. * * * In light of evidence presented I believe Amelia does not fulfill criteria of a substantial mental and physical impairment at this time. I do not feel that Amelia should be included in the NICA 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. Sigurdardottir. The opinion of Dr. Sigurdardottir that Amelia does not suffer from a substantial mental and physical impairment at this time is credited.
The Issue At issue in this proceeding is whether Alexandra Louise Biedenharn, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Deborah Biedenharn and Joseph Biedenharn are the parents and natural guardians of Alexandra Louise Biedenharn (Alexandra), a minor. Alexandra was born a live infant on March 17, 1997, at Lawnwood Regional Medical Center, a hospital located in Fort Pierce, Florida, and her birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Alexandra was Juliette Lomax-Homier, 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. Coverage under the Plan Pertinent to this case, coverage is afforded under the Plan when the claimant demonstrates, more likely than not, that the infant suffered an "injury to the brain or spinal cord . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Here, Alexandra's neurologic condition is dispositive of the claim and it is unnecessary to address the timing or cause of her condition. Alexandra's neurologic status On October 2, 1997, following the filing of the claim for compensation, Alexandra was examined by Michael Duchowny, M.D., a board-certified pediatric neurologist. Dr. Duchowny's examination of Alexandra revealed no evidence of a substantial motor deficit, but did reveal evidence of mild hypertonia, which has shown progressive improvement over time. Alexandra's social and cognitive function evidenced no compromise and, with regard to such matters, she was progressing at age level. In Dr. Duchowny's opinion, which is credited, Alexandra is not currently substantially mentally and physically impaired and, consequent to any events which may have occurred at birth, is not likely to be so impaired in the future.
The Issue At issue is whether Harper Dean Stever, a deceased minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts Laura Stever and Joseph Dean Stever, Jr., are the natural parents of Harper Dean Stever, a deceased minor, and Mrs. Stever is the Personal Representative of her deceased son's estate. Harper was born a live infant on October 16, 2004, at South Seminole Hospital, a licensed hospital located in Longwood, Florida, and died October 22, 2004. Harper's birth weight exceeded 2,500 grams. The physician providing obstetrical services at Harper's birth was Christopher Quinsey, 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. The hospital and the participating physician complied with the notice provisions of the Plan. § 766.316, Fla. Stat. Harper's birth and newborn course At or about 8:42 a.m., October 16, 2004, Mrs. Stever, with an estimated delivery date of October 10, 2004, and the fetus at 40 6/7 weeks' gestation, presented to South Seminole Hospital with complaints of contractions and blood-tinged fluid discharge since 6:00 a.m. At the time, moderate, regular contractions (at a frequency of 1 1/2 to 2 minutes) were noted; the membranes were intact; vaginal examination revealed the cervix at 2 centimeters dilation, 90 percent effacement, and the fetus at -1 station; and fetal monitoring was reassuring for fetal well-being, with a fetal heart rate in the 150s, with positive long-term variability, accelerations, and no decelerations. Following admission, Mrs. Stever was given morphine with Vistaril for pain (at 9:15 a.m.), and monitoring continued to reveal a reassuring fetal heart rate in the 150s and regular uterine contractions. However, at approximately 9:20 a.m., fetal monitoring began to evidence fetal tachycardia (with a fetal heart rate above 160 beats per minute), with some decrease in variability, and at 10:20 a.m., Mrs. Stever recorded a temperature of 100.2, with a fetal heart rate in the 170s. Mrs. Stever was given an IV for hydration (at 10:30 a.m.), Tylenol for her fever (at 10:40 a.m.), and Ampicillin for presumed early chroioamnionitis (at 10:42 a.m.). Nevertheless, fetal tachycardia continued, and at 11:30 a.m., the fetal heart rate was noted as 180 with decreasing long-term variability. Therefore, since the tachycardia had not responded to the hydration, antibiotics, and Tylenol, and notwithstanding Mrs. Stever's labor had progressed ("to 4 cm dilated, 90% effaced, with a bulging bag"), the decision was made (at 12:05 p.m.) to proceed with a cesarean section because of "extended fetal tachycardia with non-reassuring fetal surveillance." Mrs. Stever was prepared for surgery, and at 12:22 p.m., the external fetal monitor was removed and Mrs. Stever was moved to the operating room, where she was received at 12:27 p.m. Of note, when removed, the fetal monitor revealed a fetal heart tone of 175 to 180 beats per minute, minimal variability, no accelerations, and no decelerations. Of further note, the Intraoperative Nurses Notes reveal a fetal heart tone of 182 beats per minute at 12:36 p.m. (Intervenor's Exhibit 1, page 109.) At 12:43 p.m., the incision was made (surgery started), and at 12:48 p.m., Harper was delivered. According to the medical records, a copious amount of thick meconium stained fluid was extruded through the incision at the time of entry into the uterine cavity, and Harper's head was delivered without difficulty and his nose and mouth were DeLee suctioned by Dr. Quinsey on the abdomen. Then, the nuchal cord was reduced and the rest of Harper was delivered atraumatically, the cord was doubly clamped and cut (so the cord blood could be drawn, and the child's blood chemistry at the time of birth ascertained), and Harper was passed off to the awaiting resuscitation team. Harper was immediately placed in a preheated radiant warmer, dried briefly, and suctioned. Heart rate was initially noted at 100 and Harper was given free flow oxygen. However, he still did not breathe spontaneously, and his heart rate rapidly slowed to 60, requiring Ambu bag and mask, and chest compressions. At 12:50 p.m., with a heart rate still at 60 and Harper's color noted as cyanotic, a "Code Blue 45" was called. At 12:51 p.m., Harper was intubated (with an endotracheal tube), and his heart rate returned to 160 with 40 seconds of chest compressions and ventilation. At 12:55 p.m., heart rate remained at 160, color was noted as pink, and ventilation continued with Ambu and endotracheal tube (ET). By 1:05 p.m., the code ended, and Harper (with a heart rate above 140) was moved to the special care nursery by the code team, with continued ventilation by Ambu and ET. Notably, although successfully resuscitated (revived) in the operating room, the respiratory failure Harper suffered since birth persisted, and he would require continuous respiratory support to survive. Harper's Apgar scores were noted as 1, 5, and 7, at one, five, and ten minutes respectively. (Intervenor's Exhibit 1, page 91.) Cord blood was drawn at 1:00 p.m., and revealed an umbilical artery pH of 7.112, PC02 of 75.3, PO2 of 4.5, 02-SAT of 1.3%, and BE of -8.0. (Intervenor's Exhibit 1, page 9; Intervenor's Exhibit 2, page 677.) The Apgar scores assigned to Harper are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, reflex irritability, muscle tone, and color, with each category being assigned a score ranging from the lowest score of 0 through a maximum score of 2. See Dorland's Illustrated Medical Dictionary, 28th Edition, 1994; Intervenor's Exhibit 1, page 91. Such scores help the physician decide what resuscitative efforts may be required for the baby. (Respondent's Exhibit 1, page 41.) As noted, Harper's one minute Apgar score was 1, with heart rate being graded at 1 (under 100 beats per minute), and respiratory effort (none), reflex irritability (absent), muscle tone (flaccid), and color (central cyanosis) being graded at 0. At five minutes, Harper's Apgar score totaled 5, with heart rate being graded at 2 (above 100 beats per minute), reflex irritability (medium), muscle tone (lazy) and color (peripheral cyanosis) being graded at 1 each, and respiratory effort being graded at 0. At ten minutes, Harper's Apgar score totaled 7, with heart rate, reflex irritability (good), and color (pink) being graded at 2 each, muscle tone being graded at 1, and respiratory effort being graded at 0. (Intervenor's Exhibit 1, page 91.) Following admission to the special care nursery (at 1:05 p.m.) Harper was assessed and placed on a ventilator (full ventilatory support with endotracheal intubation). Newborn assessment noted a heart rate of 140, pale pink color, hypotonic tone, depressed activity, and no cry. Blood sugar at 1:20 p.m., was noted as 51 (hypoglycemic). (Intervenor's Exhibit 2, pages 601 and 675.) Given Harper's acute respiratory failure, an order was entered to transfer Harper to the neonatal intensive care unit (NICU) at Arnold Palmer Hospital for Children and Women, and at 1:50 p.m., the Arnold Palmer Hospital neonatal transport team arrived at South Seminole Hospital to assume responsibility for Harper's care. In the interim, the progress notes reveal Harper to have been fairly stable on the ventilator, with oxygen (02) saturations above 95 percent, color pale pink and responding to tactile stimulation. (Intervenor's Exhibit 2, pages 675.) When the transport team assumed Harper's care at 1:50 p.m., he appeared relatively stable, with a mean blood pressure of 49, and an 02 saturation level of 92 percent. (Intervenor Exhibit 2, page 285.) However, by 2:30 p.m., he appeared dusky with poor profusion, and his 02 saturation level was 85 percent. In response, Harper was given a volume expander (normal saline) and Ambu'd with 100 percent oxygen. However, while his 02 saturation level briefly improved to 99 percent, it remained unstable and over time, despite efforts to stabilize Harper (with Ambu ventilation, sodium bicarbonate for metabolic acidosis, volume expanders, Dobutamine, Fentanyl, Ampicillin, and Gentamicin) it dropped to the 70s (by 3:45 p.m.) and 60s (by 4:40 p.m.), and his mean blood pressure dropped into the 30s. Chest X-ray at 2:37 p.m., was reported as follows: FINDINGS: . . . Lungs are distinctly abnormal showing severe opacification bilaterally in a very diffuse pattern. On the first day of life I would not expect the child to present hyaline membrane disease. I do not see blunting of the costophrenic angles to suggest pleural fluid associated with Beta strep pneumonia. Pneumonia is not ruled out but I am more suspicious of edema from heart disease or meconium aspiration that is quite severe . . . . IMPRESSION: 1. Severe lung opacity bilaterally raising question of edema from meconium aspiration . . . . The transport team left South Seminole Hospital at 4:50 p.m. (with 02 saturations at 65 percent and mean blood pressure at 40) and arrived at Arnold Palmer Hospital at 5:30 p.m. (with 02 saturations at 57 percent and a mean blood pressure of 37). During transport, Harper was Ambu'd with Fi 02 100 percent. On admission to the neonatal intensive care unit at Arnold Palmer Hospital, Harper was noted to be cyanotic (pale gray), with saturations in the 50s despite positive pressure ventilation, poor perfusion, and adventitial breath sounds (rales and rhonchi) over all fields. Diagnoses on admission included hypotension, meconium aspiration syndrome, persistent pulmonary hypertension newborn, pneumonia-congenital, respiratory distress-newborn, and sepsis-newborn. Harper was started on high frequency oscillator ventilation (HFOV) and Dopamine was added to his interventions to support his blood pressure (BP). However, Harper's condition did not improve, and at 7:44 p.m., he was placed on veno-venous extracorporeal membrane oxygenation (V-V ECMO).3 Chest X-ray at 6:14 p.m. (pre-ECMO) revealed "[h]yperinflation, diffuse infiltrates and right pleural effusion," and chest X-ray at 10:27 p.m., revealed "[w]orsening diffuse pulmonary infiltrates, now severe." (Intervenor's Exhibit 2, pages 301 and 297.) Ultrasound Echoencephalogram pre-ECMO was read as normal, with the following findings: The ventricles are of normal size and symmetrical bilaterally. No intracerebral hemorrhages or other intracranial abnormalities are apparent. Harper continued to require increasing pressor support with little effect (i.e., a "mean BP of 40 and arterial saturations of 75% on maximal ventilatory support"). Accordingly, given Harper's continued deterioration, he was changed from V-V ECMO to veno-arterial (V-A) ECMO on October 17, 2004, at 2:15 p.m. Oxygen saturations were noted to rise to 85 percent and blood pressure rose to a mean of 70. Ultrasound Echoencephalogram on October 17, 2004, was normal. On October 18, 2004, Harper remained on V-A ECMO, with saturations in the 90s, and on Dopamine and Dobutamine, with a mean BP of 58. At 7:30 a.m., twitching was noted, consistent with seizure activity, and again at 2:30 p.m., and 10:15 p.m. (Intervenor's Exhibit 2, page 630.) Phenobarbital was prescribed. Ultrasound Echoencephalogram revealed "[s]mall bilateral Grade I germinal matrix hemorrhages." On October 19, 2004, Harper remained on V-A ECMO, with saturations in the mid 90s, and on Dopamine and Dobutamine, with a mean BP of 44-49. Seizure episodes continued, as did treatment with Phenobartital. Ultrasound Echoencephalogram revealed "[s]table bilateral Grade I intracranial hemorrhages," and no new hemorrhages. On October 20, 2004, Harper remained on V-A ECMO, with saturations in the mid 90s, and on Dopamine and Dobutamine, with a mean BP of 40-50s. Seizure activity continued, and Harper was treated with Phenobarbital and Fosphenytoin. Ultrasound Echoencephalogram revealed a "[s]uspected bilateral Grade II intracranial hemorrhage." On October 21, 2004, Harper remained on V-A ECMO, with saturations in the mid 90s, and on Dopamine and Dobutamine, with a mean BP of 50-60s. Some increase in acidosis over the last 24 hours was noted. Seizure activity continued, as did treatment with Phenobarbital and Fosphenytoin. Ultrasound Echoencephalogram revealed "[s]uspect bilateral choroid plexus hemorrhages." On October 22, 2004, neurologic evaluation noted that Harper continued with frequent seizure episodes, and near continuous clonic, jerking activity of the lower extremities. Harper was noted to be acidotic, with generalized edema, jaundice, no spontaneous movement, boggy scalp, and decreased movement. Ultrasound Echoencephalogram revealed "a new 1.5 x 2.1 cm hemorrhagic cyst within the right parietal cerebral parenchyma . . . equivalent to a Grade IV germinal matrix hemorrhage." Given Harper's heparinization4 and contraindications of ECMO with severe intracranial hemorrhage, Harper was removed from ECMO and died soon thereafter, at 12:40 p.m., October 22, 2004. At the time, active diagnoses included hypotension, intraventricular hemorrhage, meconium aspiration syndrome, persistent pulmonary hypertension newborn, pneumonia-congenital, and sepsis-newborn. An autopsy was performed October 22, 2004. The report included the following anatomic findings: RESPIRATORY SYSTEM: Hyaline membrane disease. Acute bronchopneumonia with large areas of necrosis. Fungal lung abscess with secondary cyst formation. CENTRAL NERVOUS SYSTEM: Intraventricular hemorrhage. Arachnoidal congestion and hemorrhage. Cerebellar fungal infarct. Periventricular leukomalacia. PLACENTA (S-04-31353) Large for gestational age placenta, three vessel cord, no acute chorioamnionitis is seen.[5] The likely cause and timing of Harper's brain injury To address the cause and timing of Harper's brain injury, the parties offered the medical records related to Mrs. Stever's antepartal course, as well as those associated with Harper's birth and subsequent development. Additionally, the parties offered the deposition testimony of William D. Rhine, M.D., a physician board-certified in pediatrics, and neonatal-perinatal medicine; Charles B. Brill, M.D., a physician board-certified in pediatrics, and neurology with special competence in child neurology; and Donald C. Willis, M.D., a physician board-certified in obstetrics and gynecology, and maternal-fetal medicine.6 The medical records and the testimony of the parties' experts have been thoroughly reviewed. Having done so, it must be resolved that among the physicians who addressed the cause and timing of Harper's brain injury, Dr. Rhine was the more qualified to address the issues, and his testimony most candid and compelling.7 Dr. Rhine expressed his opinions on the likely cause and timing of Harper's brain injury, as follows: [Examination by Mr. Grace] A. [Harper suffered] [p]rocesses during birth, including meconium aspiration during labor and delivery, that led to respiratory failure and ultimately to his death. Along with that, that respiratory failure that was obviously caused by . . . meconium in his lungs [, were] bouts of low oxygen and low blood pressure in the first couple hours of life that led to ongoing resuscitative efforts and escalation of care until he finally got onto ECMO bypass. I think before he got onto ECMO bypass, that more likely than not, he had suffered substantial injury from his low oxygen and low blood pressure. Ultimately, that substantial injury was impacted by him being on ECMO and was a significant or proximate cause of his having bleeding into his brain, which led to the decision for the cessation of ECMO and his death thereafter. Q. . . . Let's back up for a minute, Doctor. Did an hypoxic event occur? A. Did a hypoxic event occur? Q. Yes, sir. A. Yes. Actually, I mean several events occurred. Q. Were you talking about several hypoxic events? A. Yes. Q. Will you take me through them and point out each hypoxic event as you have found in the records. A. I think even before birth, there was enough hypoxic event to lead to this child having pulmonary hypertension and passage of meconium. Okay? Q. Uh-huh. A. And then there was a transient hypoxic event right at birth . . . . And then in the hours after he was born, as his care was escalated and they still tried to stabilize his respiratory or pulmonary status, he had basically prolonged episodes of low oxygen and low blood pressure until he finally got onto ECMO in the evening of the 16th of October. * * * Q. Now, with regard to this first hypoxic event that you have identified sometime before birth, as you termed it, did it actually lead to injury to the child? A. Yes. Q. And what was the injury? A. Well, it led to meconium -- the passage of meconium, which led to meconium aspiration and the evolution of pulmonary hypertension. * * * Q. Okay. Was there a brain injury when the child was born? A. I don't know. that? Q. You have no opinion with regard to A. Not to a reasonable medical probability, no. Q. Do you have an opinion, Doctor, if the child did in fact suffer a brain injury during labor and delivery? A. Again, I don't know. Q. Do you have an opinion whether the child suffered a brain injury at any time prior to being placed on ECMO? A. Yes, I do have an opinion. Q. What is that opinion? A. That he did suffer a brain injury in the hours after delivery and before he got put on ECMO. Q. And at what point did the child suffer the brain injury? Are you able to pinpoint that for us? A. Not with precision in terms of time. I can describe the physiologic events that I think were associated with the brain injury, and that itself describes the timeframe. Q. Okay. A. So there is -- first of all, I think that there is a compromise of blood and oxygen flow in the minutes after birth, and there is limited improvement physiologically thereafter, and then within two and a half hours, he starts having the onset of low levels of oxygen and low levels of blood pressure that more likely than not are going to lead to brain -- that did lead to brain injury. Q. And this is two and a half hours after birth, Doctor? A. Yes. Q. Is that the first event you could look at that your opinion would lead to brain injury? A. No. I talked to someone about the compromise right around birth. That -- you know, the fact that he needed to be resuscitated, gets cardiac compressions, gets intubated, et cetera, that's going to be an initial insult. I can't say whether or not that alone, in and of itself, would have caused substantial injury, but it contributed to the injury that I did think became substantial later on that afternoon once his saturations and blood pressures fell again. Q. Okay. And how did it contribute? A. Well, basically, the way that the brain responds to low blood and oxygen levels is that you can have a compromise of oxygen to the tissues, and then if it's repeated and recurrent, you are that much more susceptible to oxygen and blood deprivation within the next couple of hours or so. * * * Q. Do you place any significance on the cord gas ph in terms of ruling in or out neurological injury? A. Yes. Q. Okay. And in terms of this child, what was the cord gas ph? A. . . . [I]t is 7.11. So the one that's collected at 13:07, that one?[8] Q. Yes, sir. A. Okay. . . . assuming it's umbilical artery, the oxygen level is quite low, but it is not profoundly acidotic, and the acidosis is both a mixed, metabolic and respiratory. * * * Q. What about the base excess level, Doctor? A. . . . The base axis is minus eight. Q. So my question is going to be do you place any significance on the base excess level being minus eight? A. Yes. Q. And what significance do you attach to that? A. [F]irst of all, I should say this is very minimal metabolic acidosis. . . . [I]f this is an umbilical arterial gas, there is probably not enough acidosis to be associated with brain injury at that time. Q. And that is at the time the cord gas level is taken, correct? A. Well, it's actually at the time of birth. It took about 19 minutes for them to get over to the cord and to draw it or something. But the cord gas reflects what's happened at birth. * * * Q. At any time in your review of this case -- or did you review the fetal monitor strips? A. Yes. Q. And would you agree that the only abnormality was fetal tachycardia and decreased variability? A. Yes. Q. Can a maternal infection alone cause fetal tachycardia? A. Yes. Q. And do you have an opinion whether maternal infection here caused the fetal tachycardia? A. I think it contributed to it. Q. So you do think there is a maternal infection? A. Well, again, mom had a fever, and I think that that temperature is associated with the fetal -- had at least some contribution to the fetal tachycardia. Q. Okay. Is it still your opinion, though, you don't know one way or the other whether there was a maternal infection? A. Correct. * * * Q. Doctor, a minute ago, you talked about . . . an ischemic event versus an hypoxic event. You talked about narrowing down the definitions, or did I have that wrong? A. No. No. I did mention that. Q. Okay. Tell me what you were referring to with regard to this specific case when you brought that up. A. I just wanted to point out that there are basically two ways of getting brain injury from oxygen deprivation, and that is your oxygen level can be low in your blood [hypoxia]; or you can have not enough blood circulating [ischemia] . . . . Q. And in terms of not having enough blood circulation, do you have an opinion as to whether that was applicable to Harper Stever, the baby in this case? A. Yes. Q. What's that opinion? A. I think that there were two episodes, one when he was first born and had a low heart rate, that is, that there was an abnormal amount of blood being delivered to his brain during that time, and then later on in the afternoon of the 16th, he is profoundly hypotensive, and that, too, is associated with inadequate blood and oxygen delivery to the brain. Q. Okay. Do you see when the child had a low heart rate? A. Yes. Q. When did that occur, specifically? A. At birth. Q. And where is that reflected, Doctor? A. Well, in the code record and by the fact that he got cardiac compressions. Q. Okay. And when the baby was coded and had this low heart rate, you testified to, do you have an opinion on whether it caused brain injury? A. Well, I think what I said before, I think in light of what happened later that day, I think it contributed to it. Whether or not it would have caused it on its own, I don't -- I don't know, and actually, I would dare say probably not. Q. Okay. Then move on, if you will. Tie it into what happened later on that day. A. Well, he continues to have ongoing care to try to stabilize him -- Q. Uh-huh. A. -- in the post delivery period, and that care includes prolonged artificial ventilation, if you will, as well as support of his circulation, and despite that, he has episodes of drops in his saturations and ultimately in his blood pressure, as well, before he goes onto ECMO bypass. * * * Q. And in terms of meconium aspiration, Doctor, do you know whether the baby actually aspirated the meconium in utero or whether it was perhaps after birth? A. It's usually a combination of both. Q. But there is generally no way to know; is that correct? A. Well, severe meconium aspiration, there is usually a component of it that has occurred before a baby is born. Q. Okay. In severe meconium aspiration? A. Yes. Q. In this particular case, would you categorize it as severe meconium aspiration? A. Yes. Q. And what do you base that opinion on, Doctor? A. Well, the fact that there was such respiratory failure, as well as the radiographic changes seen. * * * [Examination by Mr. Blystone] Q. . . . Next, if you would turn to page 285 of the medical record of Baby Stever, which is entitled a "Neonatal Transport Flow Sheet." Do you see that? A. Yes. Q. Okay. Now, correct me if I'm wrong. Is this at the point when the neonatal transport team arrives and takes over the care of Harper Dean Stever until his ultimate delivery to Arnold Palmer Hospital? A. Yes. Q. Is there anything clinically significant to you on this record as far as Harper Dean Stever's vital signs and oxygen saturation level and so forth are concerned? A. Yes. Normal saturation for babies is going to be in the 90s, and yet they can tolerate saturations down to the 80s or even usually into the 70s without sustaining injury to their vital organs, including their brain. However, persistent levels below 70 are going to be associated with neurologic injury, and the fact that the first dip is at 15:15, and at 16:40 drops below 70 and stays below 70 until he's left that unit or, you know, and soon thereafter, he arrives at Arnold Palmer. Q. In your opinion as a neonatologist, would significant brain damage be occurring in Harper Dean Stever when his oxygen saturation levels drop and stay below the 80 mark? A. 70. I'm not going to say 80, but I think staying below 70, also in concert with blood pressures -- again, the normal mean blood pressure for a baby is going to be 40 or more. So when it drops down as low as 30 in conjunction with a saturation of 68 percent, that's likely to be adding to his injury, and that continues on to Arnold Palmer for the next couple hours, as well, before he goes onto ECMO, which sort of is the continuation of those type of vital signs. * * * Q. On page 287 of that same neonatal transport flow sheet, I note that at 15:20, and then again at 15:30, Harper Dean was administered sodium bicarb. What was the reason for that? A. To compensate for acidosis. Q. What type of acidosis? A. Metabolic acidosis. Q. At the time that Harper Dean Stever was being administered sodium bicarb, you stated that he then -- that was because he was having metabolic acidosis at the time? A. Yes. Q. And when a child such as Harper Dean Stever is having metabolic acidosis, that they had risk for brain injury? A. Yes, because that reflects inadequate blood and oxygen delivery to their body. Q. Now, you were pointing out to me before, I think, that Harper Dean Stever's oxygen saturation levels continued to be below the 70 mark by the time of the admission to the neonatal intensive care unit at Arnold Palmer Hospital, correct? A. Correct. * * * Q. And it appears that generally, his 02 saturation levels were staying in the 60s[9] to 60s range. Is that fair to say? A. Yes. There is a brief increase at 17:52 to 17:55. But by 18:10, it's back below 65, where it stays for over half an hour, and then it goes up to 69, 75, and back down to 63, and then 59 percent. Q. And this is from the timeframe of 17:30 through 19:00 on October 16th, correct? A. Correct. Q. And how was Harper Dean Stever's blood pressure doing during that timeframe? A. Well, unfortunately, it was even worse than it had been before, with his blood pressure means falling into as low as 24. Q. So in your opinion as a neonatologist, from the time of Harper Dean Stever's arrival to Arnold Palmer Hospital at 17:30, through this time period, 19:00, represented on this neonatal intensive care flow sheet, was he suffering significant brain damage during that time? A. Yes. Q. And why is that? A. . . . Because there is other evidence -- there is evidence that he still has ongoing metabolic acidosis. He has blood gasses that instead of being only minimally metabolically acidotic, they are going up to the moderate to severe range, and that is after the administration of bicarb, which should, in theory, counteract that metabolic acidosis. So he clearly is having inadequate blood and oxygen delivery. He is clearly becoming acidotic. He clearly has a level of cardiac performance and -- or cardiac poor performance and inadequate oxygen to sustain his vital physiology, including his brain function. And then ultimately, one thing that should be mentioned is that his ultimate autopsy does show periventricular leukomalacia, which would be the type of injury that would arise from this pattern of low blood pressure and low oxygen level that he really doesn't sustain anywhere else during his run, during his hospital course once he gets stabilized by virtue of going on ECMO. * * * Q. Dr. Rhine, had Harper Dean Stever not passed away, do you have an opinion within a reasonable degree of medical probability whether he would have been substantially, permanently mentally and physically impaired as a result of his brain injury to which you testified to? A. Yes. My opinion is that he would have had substantial neurologic impairment. * * * Q. Dr. Rhine, do you have an opinion as to when Harper Dean Stever was undergoing metabolic acidosis to the extent that it was causing significant brain injury? A. As I mentioned before in the afternoon of the 16th after his birth, during that resuscitation and attempted stabilization, I think that's when it occurred. Dr. Willis was of the opinion that the medical records failed to support the conclusion that Harper suffered a lack of oxygen substantial enough to cause brain injury during labor, delivery, or resuscitation immediately following delivery, and that the tachycardia Harper experienced was most likely related to maternal infection. As for the likely cause of Harper's respiratory failure, Dr. Willis was of the opinion it was most likely the result of infection and meconium aspiration. As for whether Harper suffered a significant brain injury after he was transported to the special care nursery, Dr. Willis deferred to the neonatologists and pediatric neurologists. Contrasted with the opinions of Doctors Rhine and Willis, Dr. Brill was of the opinion that Harper suffered two hypoxic injuries. The first being present at birth, and the second an ongoing injury from the time Harper was an hour old (when Dr. Brill notes poor profusion and duskiness is documented) until he died.10 As for the timing of the first injury, Dr. Brill was of the opinion it occurred within 24 hours preceding birth, and probably shortly before delivery. As for the cause of the injury, Dr. Brill was of the opinion it was most likely caused by a profusely hemorrhagic placenta, which resulted in oxygen deprivation (hypoxia) to the baby. Dr. Brill's conclusion that Harper presented with a profound brain injury at birth was premised on "several features: Number one is . . . the placenta is described as profusely hemorrhagic, so that there's a cause for lack of oxygen to the baby; and that event had abnormal fetal monitoring strips; was born with meconium stained fluid; and had very low Apgar to begin with; and persistent apnea." (Intervenor's Exhibit 6, page 19.) As for the cord pH of 7.112, Dr. Brill acknowledged it was only mildly depressed, but was of the opinion it was taken "when the baby was 12 minutes old after he had been resuscitated." (Intervenor's Exhibit 6, pages 22, 23, and 60.) Dr. Brill was also of the opinion that had the cord pH been taken within the first two minutes of life it would likely have been below 7. (Intervenor's Exhibit 6, pages 41 and 42.) Dr. Brill's observations regarding Harper's cord pH are not credible. The Blood Gas Summary reveals that the blood sample was drawn from the umbilical cord, and not the infant. (Intervenor's Exhibit 2, page 677.) The cord pH reflects the infant's pH and other chemistry at birth, not following resuscitation. (Intervenor's Exhibit 5, page 26; Respondent's Exhibit 1, pages 50 and 51.) See also "Blood," "cord b." ("blood contained within the umbilical vessels at the time of delivery of the infant."), Dorland's Illustrated Medical Dictionary, 28th Edition, 1994). Dr. Brill's observations to the contrary detract from the credibility of his testimony regarding the presence of a hypoxic brain injury at delivery. However, except for the onset of the injury, Dr. Brill's observations regarding brain injury following the arrival of the transport team are consistent with those of Dr. Rhine, and are credited. As for the onset of the injury, Dr. Rhine's conclusion that it began at two and a half hours of life (2:30 p.m.) is the more credible. (See Endnote 10.) Given the proof, it is resolved that, more likely than not, Harper did not suffer brain injury due to oxygen deprivation that occurred during labor, delivery, or resuscitation immediately following delivery. Rather, it is most likely that Harper began to suffer hypoxic ischemic brain damage (due to low oxygen saturation levels and low blood pressure) following the arrival of the transport team at South Seminole Hospital, when evidence of profound pulmonary hypotension was noted, at about two and a half hours of life, and that his brain injury progressively worsened until a point in time, likely prior to his placement on ECMO, when the injury was so severe permanent and substantial mental and physical impairment would necessarily ensure. Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired."11 § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. Here, it has been resolved that Harper did suffer an injury to the brain caused by oxygen deprivation that rendered him permanently and substantially mentally and physically impaired. However, it was also resolved that Harper's brain injury began about two and a half hours after birth, following the arrival of the transport team at South Seminole Hospital. Nevertheless, Petitioners and Intervenor were of the view that Harper's brain injury occurred "in the immediate postdelivery period," because Harper had required continuous respiratory support since birth. In contrast, NICA was of the view that while Harper required continuous respiratory support, his brain injury postdated the "immediate postdelivery period," and therefore does not qualify for coverage. The ultimate goal in construing a statutory provision is to give effect to legislative intent. BellSouth Telecomms, Inc. v. Meeks, 863 So. 2d 287 (Fla. 2003) "In attempting to discern legislative intent, we first look to the actual language used in the statute." Id., at 289. "If the statutory language is unclear, we apply rules of statutory construction and explore legislative history to determine legislative intent." Id., at 289. "Ambiguity suggests that reasonable persons can find different meanings in the same language." Forsythe v. Longboat Key Beach Erosion Control District, 604 So. 2d 452, 455 (Fla. 1992). "If the language of the statute under scrutiny is clear and unambiguous, there is no reason for construction beyond giving effect to the plain meaning of the statutory words." Crutcher v. School Board of Broward County, 834 So. 2d 228, 232 (Fla. 1st DCA 2002). In enacting the Florida Birth-Related Neurological Injury Compensation Plan, the Legislature expressed its intent, as follows: It is the intent of the Legislature to provide compensation, on a no-fault basis, for a limited class of catastrophic injuries that result in unusually high costs for custodial care and rehabilitation. This plan shall apply only to birth-related neurological injuries. § 766.302(2), Fla. Stat. In defining "birth-related neurological injury," the Legislature chose to limit coverage to brain injuries that occurred during "labor, delivery, or resuscitation in the immediate postdelivery period." § 766.302(2), Fla. Stat. However, the Legislature did not define "resuscitation in the immediate postdelivery period," and the term has no technical significance.12 (Respondent's Exhibit 1, pages 43 and 44; Intervenor's Exhibit 5, page 30.) "When necessary, the plain and ordinary meaning of words in a statute can be ascertained by reference to a dictionary." Seagrave v. State, 802 So. 2d 281, 286 (Fla. 2001). "Resuscitate" is commonly understood to mean "[t]o return to life or consciousness; revive." The American Heritage Dictionary of the English Language, New College Edition, 1979. Dorland's Illustrated Medical Dictionary, 28th Edition, 1994, defines "resuscitation" as "the restoration to life or consciousness of one apparently dead; it includes such measures as artificial respiration and cardiac massage." "Immediate" is commonly understood to mean "[n]ext in line or relation[;] . . . [o]ccuring without delay[;] . . . [o]f or near the present time[;] . . . [c]lose at hand; near." The American Heritage Dictionary of the English Language, New College Edition, 1979. Finally, "period" is commonly understood to mean "[a]n interval of time characterized by the occurrence of certain conditions or events." The American Heritage Dictionary of the English Language, New College Edition, 1979. Under the statutory scheme then, the brain injury must occur during labor, delivery, or immediately thereafter. Nagy v. Florida Birth-Related Neurological Injury Compensation Association, 813 So. 2d 155, 160 (Fla. 4th DCA 2002)("According to the plain meaning of the words written, the oxygen deprivation or mechanical injury must take place during labor, delivery, or immediately thereafter."). Such conclusion is also consistent with "the requirement that statutes which are in derogation of the common law be strictly construed and narrowly applied." Nagy, 813 So. 2d at 159; Humana of Florida, Inc. v. McKaughn, 652 So. 2d 852, 859 (Fla. 2d DCA 1995)("Because of the Plan . . . is a statutory substitute for common law rights and liabilities, it should be strictly construed to include only those subjects clearly embraced within its terms."), approved, Florida Birth-Related Neurological Injury Compensation Association v. McKaughn, 668 So. 2d 974, 979 (Fla. 1996). Under the facts of this case, resuscitation in the immediate postdelivery period ended not later than 1:05 p.m., when the code ended and Harper was transferred to the special care nursery. By then, Harper had been successfully resuscitated (revived), and his circulation restored. However, nothing further could be done to establish spontaneous respirations (until the cause of his respiratory failure could be addressed), and he would remain on respiratory support for the remainder of his life. Harper's subsequent brain injury, which began at about two and a half hours of life, post-dated his "resuscitation in the immediate postdelivery period."
The Issue The issue in this case is whether Eric Ryan Birnie has suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan, as alleged in the Petition for Compensation.
Findings Of Fact Based upon the oral and documentary evidence adduced at the final hearing and the entire record in this proceeding, the following findings of fact are made: 1. Eric Ryan Birnie (Eric) is the natural son of Fred and Judith Birnie. He was born a live infant on March 12, 1989, at Halifax Hospital in Daytona Beach, Florida. His birth weight was in excess of 2500 grams. 2. The parties have stipulated that the physician(s) providing obstetrical services during the birth of Eric were, at all times material hereto, participating physician(s) in the Florida Birth-Related Neurological Injury Compensation Plan (hereinafter referred to as the "NICA Plan), as defined by Section 766.302(7), Florida Statutes. 3. Eric is the fifth child of Judith and Fred Birnie. The four older children are normal and healthy and they were all vaginally delivered without any significant problems. 4. At the time Eric was born, Judith Birnie was 35 years old. There is no evidence of any problems or complications during her pregnancy prior to the day Eric was born. 5. On the day Eric was born, Judith Birnie went to the hospital at approximately 7:00 in the morning. She was put on electronic fetal monitoring to monitor the heart rate of the fetus in conjunction with the contractions of the mother. 6. During the first 24 hours that Judith Birnie was in the hospital, the fetal heart monitor reflected a relatively constant fetal heart rate of approximately 150 beats per minute. Beginning at approximately 9:55 a.m., the fetal heart monitor began to register variable, recurrent decelerations to approximately 60 to 70 beats per minute for periods of 25-40 seconds. 7. At approximately 12:40 p.m., there was an abrupt change in the fetal heart monitor without a return to the baseline indicating a strong likelihood of fetal stress. Around this same time, Judith Birnie began to experience severe pain in the fundus of the uterus. The delivery room nurse called the attending physician who conducted a vaginal examination and determined that it was necessary to try and deliver the baby immediately. The physician twice attempted vacuum extraction of the fetus without success. At approximately 1:10 p.m., the doctor ordered a cesarean section ("C-section). The mother was induced for anesthesia about 1:15 p.m. and the baby was delivered by C- Section at 1:29 p.m. 8. During the operation, the attending physician noticed a collection of blood in the uterus and determined that there had been an abruption of the placenta, in other words, a separation of the placenta from the uterine wall. Even a partial abruption of the placenta can lead to fetal hypoxia. In this case, it appears that the abruption occurred at least 39 minutes before the baby was delivered. 9. The abruption of the placenta was subsequently confirmed by a pathology report which contained the following diagnosis: Placenta and umbilical cord with edema and hemorrhage between the amnion and corium infibrin deposition on the maternal surface of the cotyledons as may be seen with premature separation. 10. The Operative Report prepared by Dr. deGarcia, confirms severe fetal bradycardia and multiple variable decelerations as well as an abruption of the placenta. Similarly, the Discharge Summary for Judith Birnie prepared by Dr. Trelsar noted ". , fetal distress, severe... abruptio placentae. ..." ll. At the time of delivery, the baby was floppy and not breathing. Eric's head size at birth was normal which tends to belie the presence of any gross abnormality. 12. Delivery room resuscitation included intubation, with suctioning of meconium, and "bagging" with 100 percent oxygen. It appears that there was some meconium aspiration which is an indication of fetal asphyxiation. 13. Eric's Apgar score at one minute was two and at five minutes it was four. 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, Eric's Apgar score totaled two, with heart rate and color being graded at one. Muscle tone, respiratory effort, and reflex irritability were graded at zero. At five minutes, Eric's Apgar score totaled four, with heart rate and color being graded at two each; respiratory effort, muscle tone and reflex irritability being graded at zero each. Such scores are consistent with Eric having suffered a severe hypoxic insult (deprivation of oxygen) at birth. 14. Eric's initial cord blood, i.e., the blood that was taken off the umbilical cord itself showing the condition of his blood at the time of birth, was recorded at a PH of 7.13. Anything under 7.2 is considered an asphyxiated condition. The baby was given sodium bicarbonate which is reflective of a determination that he was acidotic, a condition that could have been caused by hypoxia. 15. The progress notes made after the delivery indicate “cord around neck X2." The notes also indicate "perinatal asphyxia . . . hypoxic ischemia encephalopathy." Hypoxic encephalopathy is the loss of Oxygen to the brain. 16. Shortly after his birth, Eric was admitted to the neonatal intensive care unit at Halifax Hospital, where he was extubated. While in this unit, Eric was observed to display signs of seizure activity, and an electroencephalogram (EEG) was ordered. The first EEG was taken on March 13, 1989, and was read as normal. 17. A second EEG was taken on March 21, 1989. That EEG was read as follows: This is an abnormal tracing because of the presence of sharp spike and occasionally slow wave activity seen emanating out of the left hemisphere, particularly left temporal region. Occasionally there is some mild slowing. Seems to be a little greater in the right hemisphere but I think that is probably artifactual in nature. IMPRESSION: abnormal tracing. This is consistent with an underlying cerebral irritability involving the left hemisphere, particularly with the left temporal central region. It is also consistent with the diagnosis of seizures. 18. While in the hospital, Eric was placed on phenobarbital and dilantin to control the seizures. He was weaned from dilantin shortly thereafter. He continued on phenobarbital for approximately a 1% years until approximately July of 1990 when he was taken off the drug because he had not demonstrated any further seizures. There is no indication that Eric has had any subsequent seizures. The lack of and/or control of his seizures does not, however, suggest that any damage to Eric's brain has been remedied. Once brain cells are destroyed, they are not replaced. 19. During the first couple days of life, Eric was noted to have oliguria, i.e., decreased or diminished urine output. In addition to scant urine output, Eric's urine tested positive for blood and protein. These conditions could have been caused by tubular necrosis of the kidneys secondary to loss of oxygen to the organs during the late stages of labor. The existence of these kidney problems close to birth tends to confirm that Eric suffered an hypoxic injury that occurred at or close to birth. The oliguria cleared up within a few days, which is consistent with an hypoxic injury. 20. Eric was discharged from Halifax Hospital to the care of his parents on March 24, 1989. 21. The discharge summary prepared by the attending physician in the neonatal intensive care unit listed the principal diagnosis as follows: 1. Depressed newborn. 2. Post hypoxic encephalopathy with seizures. 3. Oliguria. 4. Hypokalecemia 5. Meconium aspiration 22. The following clinical problems were noted: 1... . hypoxic encephalopathy with seizures. This infant manifested early signs of hypoxic encephalopathy with seizures requiring initially phenobarbital and later dilantin intravenously for complete control. Electroencephalograms were performed. The one done of 3/13/89 was reported as normal. However the one performed on 3/21/89, showed that the tracing was abnormal consistent with an underlined cerebral irritability. The CAT scan performed on 3/13/89 was also regarded as probably normal by the Radiologists, as was the MRI performed on 3/24/89 . infant also developed an extensive soft tissue swelling in the scalp on the second day presumably because of a subgaleal hematoma or a cephal hematoma. The 23. Prior to discharge, there was an "Early Intervention Assessment" included in the progress notes which noted the fetal bradycardia and multiple decelerations, the abruption of the placenta, and the cord wrapped around the infant's neck. In view of these complications, the Early Intervention Assessment noted that Eric was "at high risk for developmental delay." It was recommended that Eric be referred to Easter Seals upon discharge and that the parents be provided with Support to help them cope with the problems they were likely to encounter because of Eric's condition. 24. After Eric was discharged from the hospital, he was evaluated by Dr. James Nealis, a pediatric neurologist. Dr. Nealis first evaluated Eric on March 29, 1989. Under his direction, a number of tests and evaluations were conducted. A Genetics tests did not reveal any abnormalities. Similarly, a 10 urine metabolic screen and thyroid function study did not reveal any problems. 25. An EEG report dated April 17, 1989 stated as follows: {nJormal tracing for age. There is some non- specific sharp activity seen that is of questionable significance, and there is asymmetry noted a voltage, which may be artifactual in nature. Clinical correlation is indicated. No definite evidence of paroxysmal epileptiform activity is seen. 26. Dr. Nealis continued to prescribe phenobarbital for Eric through July of 1990. Dr. Nealis' records indicate that an CAT scan, an EEG and a MRI performed in September/October of 1989 did not reveal any abnormalities. In addition, his records indicate that an MRI performed on January 12, 1990, was "negative." An EEG taken on June 14, 1990, was also read as normal. 27. An examination of Eric on January 11, 1990, indicated that he was experiencing some developmental delay. He had poor control of his head and he could not sit alone. 28. Eric began a special program at Easter Seals at approximately 11 months of age. At the time, Eric's gross motor skills were evaluated at 4 months and his fine motor skills were thought to be 4% months. At 16 months of age, Eric's motor development was still at 4 months. He could not sit alone and could not crawl. 29. A July 19, 1990 MRI report included the following: . {Tjhere are areas of abnormal T2 hyperintensity identified in the thalami and posterior putamen bilaterally. In retrospect, these were noted on the prior examination although they appear slightly more prominent on the present study li The significance is uncertain. These could represent focal areas of gliosis, hamartomatous change, focal areas of dysmyelination, or focal areas of prior ischemic change .. . Focal areas of abnormal patchy T2 hyperintensity in the thalamin putamen bilaterally which remains stable compared to the prior examination. These most likely represent focal areas of gliosis hamartomatous. The possibility of an abnormality in myelination or a prior ischemic injury can not entirely be excluded 30. On August 1, 1990, Eric was evaluated at the Nemours Children's Clinic in Jacksonville, Florida. Dr. William R. Turk performed the evaluation. He noted that Eric's gross motor development was severely limited and concluded that Eric had a static but evolving encephalopathy. 31. Dr. Turk also noted in his August 1, 1990 evaluation that: "{Eric's] history is not suggestive of a typical chronic metabolic encephalopathy. An issue has been raised in regard to Eric's serial MRI scan which questionably show a progression of changes in the basal ganglia. I have only been able to briefly review these studies, and have forwarded them to,Dr. Wismer for a comprehensive reading. However, my initial impression is that these scans demonstrate findings consistent with the prior hypoxic ischemic insult. 32. Dr. Turk summarized his findings in a letter to Eric's pediatrician dated September 25, 1990. That letter indicates that Dr. Turk reviewed Eric's "sequential neuroadiologic studies” and concludes that Eric has "a static encepholopathy manifest[ed] by a dystonic quadriplegia" as the result of "an evolving but remote hypoxic ischemic insult.” 33. Dr. Turk referred Eric to the Genetics Clinic fora second genetics evaluation. That study found "no clinically 12 significant cytogenetic abnormalities." The genetics report noted that Judith Birnie had a chorionic villus sampling procedure performed during her pregnancy with Eric at 17 weeks and that study was reported as a normal male karyotype. 34. Dr. Charlotte Ziskin Lafer performed the genetics study and also examined Eric. She advised the family that Eric's delayed development was most likely due to an hypoxic event. 35. In his 35 month evaluation conducted by Easter Seals, it was noted that Eric was functioning at an age equivalent of 8 months in gross motor skills. Eric was approximately age equivalent in receptive language skills, but he was functioning at only 24 months in expressive language skills. Eric was also demonstrating significant delay in oral motor skills. He had limited tongue mobility and was unable to lateralize, raise or lower his tongue. He was only able to produce a small number of vowel and consonant sounds. 36. On February 10, 1993, the Volusia County School Board administered a number of tests to Eric in order to evaluate him for placement in their exceptional student program. At the time of the evaluation, Eric was not able to stand, his manual dexterity was limited and special effort and attention was necessary to understand his verbal communications. Because of Eric's profound physical handicaps, the tests were specially selected and administered. The test results indicated that Eric was average or even above in his cognitive skills and preacademic skills. As a result, the School Board anticipates that Eric will ultimately be educated in a mainstream classroom with 13 nonhandicapped students of his own age group. He will, however, need special accommodations within the classroom to address his physical handicaps and limitations. 37. The evidence established that it is very difficult to accurately assess the intellectual ability of a young child, especially a severely handicapped child such as Eric. While it is impossible to determine whether Eric's intellectual test results would have been higher if he had not suffered an hypoxic insult at birth, it is likely that the limitations on his exploratory capabilities caused by his physical handicaps have impaired his intellectual development to some degree. 38. At the time of the hearing in this case, Eric was 4% years old. He was unable to stand up, walk or crawl. His only method of independent mobility was to roll over. The use of his hands and arms was very limited. He also had great difficulty talking and/or communicating and he must take long pauses to formulate a response to any inquiry. 39. Eric's brain dysfunction is permanent. Because Eric's speech is greatly impacted by his condition, it is virtually certain that he will always be severely limited in his verbal expression and other communication skills. While continued therapy may help him to communicate better and to become somewhat more mobile, he will almost certainly never be able to walk, feed, groom or toilet himself. 40. The evidence established that Eric's problems are the result of damage to the basal ganglia deep inside his brain. Although it can not be determined conclusively, it is more likely 14 than not that the "white matter" surrounding the basal ganglia have also been damaged to some degree which may impact his perceptual and processing abilities. 41. The opinions of the eminently qualified physicians who testified in the case as to the cause of Eric's brain dysfunction are diametrically opposed. Petitioners' expert claims that Eric suffered a severe hypoxic insult at birth and that, as a consequence of the resultant oxygen deprivation, Eric suffered an injury to his brain which has dramatically impacted his development. Petitioners’ expert contends that the isolated nature of the brain injury was a function of the duration of the hypoxic event and Eric's individual sensitivities. 42. Respondent's expert suggests that the seriousness of Eric's current neurological deficit is not a product of an hypoxic insult suffered at birth, but, rather, was occasioned by some unspecified prenatal problem. He believes that an hypoxic injury to the brain would have necessarily resulted in more global damage to the brain. 43. After considering all of the evidence , it is concluded that the more compelling proof in this case is that Eric sustained an injury to the brain caused by oxygen deprivation in the course of labor, delivery or resuscitation in the immediate post-delivery period. The injuries and disabilities which have been manifested by Eric since his birth are consistent with and have repeatedly been attributed to brain damage from loss of oxygen during labor and delivery. The proximity of Eric's seizure activity to birth and the abnormal EEGs are also is consistent with a brain injury as a consequence of an hypoxic insult at birth. Given the absence of any other identifiable factor, it is concluded that Eric's condition is attributable to birth asphyxia. This conclusion is accordant with the opinion of the neonatologist who treated Eric in the neonatal intensive care unit. He believes that Eric suffered fetal distress due to the partial abruption of the placenta during labor and delivery. He also believes that Eric suffered hypoxic encephalopathy as the result of the umbilical cord being wrapped around his neck. 44. Eric is indisputably permanently and substantially physically impaired. Respondent contends, however, that Eric and his parents are not entitled to compensation under the NICA Plan because he is not substantially mentally impaired. This issue is addressed in more detail in the Conclusions of Law below. As noted above, Eric's condition is the result of damage to his brain. As a direct result of his injury, Eric will not be able to communicate, attend school or otherwise learn and develop intellectually without substantial accommodation. His social and vocational development have unquestionably been significantly impaired.
Conclusions For Petitioners: Larry Sands, Esquire 760 White Street Daytona Beach, Florida 32115-2010 For Respondent: W. Douglas Moody, Jr., Esquire Taylor, Brion, Buker & Greene 225 South Adams Street, Suite 250 Tallahassee, Florida 32301
Other Judicial Opinions A party who is adversely affected by this final order is entitled to judicial review pursuant to Sections 120.68 and 766.311, Florida Statutes. Review proceedings are governed by the Florida Rules Of Appellate Procedure. Such proceedings are commenced by filing one copy of a notice of appeal with the Agency Clerk Of The Division Of Administrative Hearings and a second copy, accompanied by filing fees prescribed by law, with the appropriate District Court of Appeal. See, Section 120.68(2), Florida Statutes, and Florida Birth-Related Neurological Injury Compensation Association v. Carreras, 598 So.2d 299 (Fla. lst DCA 1992). The notice of appeal must be filed within 30 days of rendition of the order to be reviewed. 29
The Issue Whether Jackson White (Jackson) suffered a birth-related neurological injury, as defined by section 766.302(2), Florida Statutes; and, if so, how much compensation, if any, is awardable pursuant to section 766.31.
Findings Of Fact Jackson was born on August 1, 2014, at Bayfront, in St. Petersburg, Florida. Jackson was a single gestation, weighing over 2,500 grams at birth. Jose Prieto, M.D., was the physician who provided obstetric services at Jackson’s birth. Jackson’s mother, Megan White (Mrs. White), was admitted to Bayfront and her labor was thereafter induced with Pitocin. Her membranes were artificially ruptured 15 hours prior to delivery, with clear fluid present. Delivery was initially attempted vaginally; however, delivery was altered to Cesarean section due to late decelerations and failure to descend and dilate. The records reflect that fetal heart rate decelerations may also have been present. Jackson was delivered in a vertex presentation. Upon delivery, out of a possible score of 10, his Apgar scores were 5, 7, and 8 at one, five, and ten minutes, respectively. Of concern was that his score for “color” was 0 for the first five minutes of life. He was not pink, but rather blue or pale. Additionally, he was not actively responding, but merely grimacing, at the first minute of life. The medical records document that Jackson was experiencing respiratory distress with desaturation. Accordingly, he initially received bulb suctioning, drying, stimulation, and whiffs of oxygen. As he continued to have poor color and perfusion, with grunting and retractions, continuous positive airway pressure by mask was applied. While there was improvement in the oxygen saturation after doing so, Jackson continued to have respiratory distress. Within two hours of birth, Jackson was transferred and admitted to the Neonatal Intensive Care Unit at All Children’s Hospital (All Children’s) for further management. Upon admission to All Children’s, it was documented that his oxygen saturations ranged from 96 percent to 100 percent while utilizing a Continuous Positive Airway Pressure (CPAP) system. His physical examination revealed that he was alert, active, responsive and pink in color. Jackson’s neurologic evaluation upon admission to All Children’s revealed that he was alert, active and responsive with good tone for age; there was symmetrical movement of all four extremities; his reflexes were intact; and that his “[n]eurological examination is appropriate for the baby’s gestational age.” At All Children’s, several chest X-rays were obtained from August 1 through August 3, 2014. Ultimately, the scans revealed that Jackson had a left pneumothorax. Accordingly, the CPAP was discontinued and an “oxyhood was initiated for nitrogen wash out which was discontinued after 22 hours.” Concerned with possible sepsis, Jackson also received seven days of antibiotics. Jackson was discharged home on August 8, 2014. Jackson failed his newborn hearing screen and subsequently underwent repeated testing where he was found to have mild-to-moderate sensorineural hearing loss bilaterally. Jackson has been wearing hearing aids since six months of age. Respondent retained Donald Willis, M.D., who is board- certified in obstetrics, gynecology, and maternal-fetal medicine, to review the available medical records of Jackson and his mother, and opine as to whether there was an injury to Jackson’s brain or spinal cord that occurred in the course of labor, delivery, or resuscitation in the immediate postdelivery period due to oxygen deprivation or mechanical injury. In his report, dated July 26, 2018, Dr. Willis set forth the following, in pertinent part: The mother was admitted for induction of labor at term. Amniotic membranes were ruptured with clear fluid. Fetal heart rate (FHR) monitor tracing was not available for review. Cesarean section delivery was apparently done for failure to decent [sic], but NICU notes suggest fetal heart decelerations were also present. Birth weight was 3,630 grams. Apgar scores were 5/7/8. Respiratory distress was present after birth with poor color, grunting and retractions. Bag and Mask ventilation was required and the baby transferred to All Children’s Hospital for respiratory distress. Grunting and retractions continued at All Children’s Hospital. Chest X-Ray identified a left pneumothorax. 100% hood oxygen was started. Intubation was not required. Cultures were obtained to r/o sepsis and antibiotics given for 7 days. Bacterial and viral (HSV) cultures were negative. The newborn hearing screen was failed. No seizures occurred during the hospital stay. Head imaging studies were not done during the newborn hospital course. The baby was discharged home on DOL 8. Hearing evaluation subsequently diagnosed a sensorineural hearing loss. Genetic testing was negative for familial deafness genes. Developmental delay became a concern at about 10 months of age. Genetic evaluation, including microarray, Fragile-X and metabolic work/up was negative. MRI showed delayed myelination. Etiology was uncertain, but a statement indicated “a very subtle degree of remote insult could be considered.” Follow up MRI at 2 1/2 years of age found similar findings. Neurology evaluation gave a diagnosis of chronic static encephalopathy. MRI of the lumbar spine was normal. In summary, the baby had respiratory distress after Cesarean section delivery. Chest X-Ray identified a pneumothorax. Oxygen was given for respiratory distress, but the baby did not require intubation. No head imaging studies were done during the newborn hospital stay. There were no seizures. Sensorineural hearing loss was diagnosed. MRI for developmental delay showed only some delay in myelination. There was no apparent obstetrical event that resulted in oxygen deprivation or mechanical trauma to the brain or spinal cord during labor, delivery and the immediate post- delivery period. After authoring the initial report, Dr. Willis received a copy of the fetal heart rate monitoring strips. After reviewing the same, on August 30, 2018, he authored an addendum to his report, which provides, in full, as follows: The fetal heart rate (FHR) monitor tracing during labor was reviewed. The tracing begins at about 05:17 on 08/01/2014. The baseline FHR was normal at 130 bpm. Uterine contractions were about every 5 minutes. The FHR tracing at about one hour prior to delivery is somewhat difficult to interpret due to attempt to place a fetal scalp electrode (FSE). FHR tracing ends at about 21:18 with delivery about 30 minutes after monitor is discontinued. The FHR tracing just prior to removal of the monitor does not suggest fetal distress. Review of the FHR tracing does not change the opinions stated in the letter above, dated 7/26/2014. There was no apparent obstetrical event that would have resulted in oxygen deprivation sufficient to cause brain injury. Dr. Willis was deposed on May 20, 2019. At his deposition, Dr. Willis affirmed the factual findings and medical opinions in the above noted report. In support of his opinion that Jackson did not sustain an injury to his brain or spinal cord in the course of labor, delivery, or resuscitation in the immediate postdelivery period due to oxygen deprivation or mechanical injury, Dr. Willis credibly testified that: 1) Mrs. White’s amniotic membranes were ruptured with clear fluid; 2) the fetal heart rate tracing did not suggest fetal distress; 3) the Apgar scores, although initially low, quickly improved and were inconsistent with an infant that sustained oxygen deprivation or acidosis; 4) Jackson did not exhibit any seizure activity; 5) aside from failing his hearing screen, Jackson did not experience any other organ system failures; and 6) the available MRI reports are inconsistent with Jackson suffering a brain injury at the time of labor and delivery. On May 12, 2017, Jackson presented to Himali Renuka Jayakody, M.D., for a neurological examination. Dr. Jayakody’s office note documents that, “[d]evelopmentally, he had initial normal development but starting around 10 months when he started standing, he appeared very clumsy and was falling over a lot.” After conducting the examination, Dr. Jayakody’s assessment was that Jackson had developmental delay, sensorineural hearing loss, and chronic static encephalopathy. His note further documented that, “[a]part from signal abnormality suggestive of hypomyelination mostly affecting the posterior white matter on MRI, we have not identified any other abnormalities. Clinically, he does not seem to have a progressive disease and has always made improvement over time suggestive of static encephalopathy/cerebral palsy.” NICA also retained Laufey Y. Sigurdardottir, M.D., a pediatric neurologist, to review Jackson’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 the available medical records, obtained a full historical account from Mrs. White, and conducted and IME on Jackson on August 24, 2018. In her IME report, Dr. Sigurdardottir set forth her factual findings and opinions, which have to be admitted in this matter as part of the stipulated evidentiary record. Her summary findings and opinions are as follows: Summary: Patient is a 4 year old with history of being born via stat C-section due to fetal distress. No clear evidence was present of a neonatal hypoxic ischemic encephalopathy but he has since been diagnosed with cerebral palsy with corresponding MRI findings. His delays are mild in nature. Result as to question 1: Jackson is not found to have substantial delays in motor and mental abilities. Result as to question 2: In review of available documents, there is evidence of fetal distress but no neonatal encephalopathy consistent with a neurologic injury to the brain or spinal cord acquired due to oxygen deprivation or mechanical injury is reported in neonatal period apart from failing newborn hearing screen. Result as to question 3: The prognosis for full motor and mental recovery is good and the life expectancy is full. In light of evidence presented, I believe Jackson does not fulfill criteria of a substantial mental and physical impairment at this time. Petitioner neither testified nor presented any testimony to refute the findings and opinions of Drs. Willis and Sigurdardottir. Their findings and opinions are credited.
Conclusions This cause came before the undersigned upon the parties’ Joint Motion to Submit Stipulated Factual Record in Lieu of a Contested Hearing (Joint Motion), which was granted on May 22, 2019, and the parties’ proposed final orders.
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).
The Issue At issue in this proceeding is whether Ernest Hall, Jr., a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Initial observations As observed in the preliminary statement, neither petitioners nor anyone on their behalf appeared at hearing, and no proof was offered to support their claim. Ordinarily, such failing would be dispositive of the case; however, notwithstanding petitioners' failure of proof, respondent elected to offer into evidence the medical records filed with DOAH on May 15, 1996, which included records relating to Ernest Hall, Jr.'s (Ernest's) birth and subsequent development, as well as the opinions of Charles Kalstone, M.D., a board certified obstetrician, and Michael Duchowny, M.D., a board certified pediatric neurologist, to affirmatively resolve the issue as to whether Ernest had suffered a "birth-related neurological injury," within the meaning of Section 766.302(2), Florida Statutes. Ernest's birth and development Ernest was delivered vaginally at 2:17 a.m., June 1, 1991, at Shands Hospital, the University of Florida, Gainesville, Florida. His Apgars were normal at birth (9 at one minute and 9 at five minutes) and arterial pH from the umbilical cord was normal at 7.19. Earnest's newborn course was characterized by anemia, transient thrombcytopenia, and prenatally acquired cytomegalovirus. Where, as here, the cytomegalovirus (CMV) was acquired prenatally, it has the potential to cause brain damage in the fetus, as well as hearing impairment, chorioretinitis (inflammation of the eye) and other central nervous system abnormalities. Consequently, Ernest was placed on a ten day regimen of Ampicillin and Gentamicin. A head CT taken on June 5, 1991, revealed periventricular calcification and probably parenchymal calcification consistent with a prenatal infection such as CMV. Notably, following insult, it would require several weeks for such calcifications to occur. Due to the high risk factor associated with CMV, Ernest's auditory brain stem response was evaluated on June 7, 1991. At the time, his response was noted to be within normal limits; however, follow-up was recommended in six months since he was at risk for hearing loss due to CMV. Ernest was discharged to his parents care on June 10, 1991. On February 28, 1994, Ernest was re-evaluated, and those results indicated a severe sensorineural hearing loss in the sound field. On June 19, 1996, Ernest was examined by Michael Duchowny, M.D., a pediatric neurologist associated with Miami Children's Hospital. Dr. Duchowny's neurologic examination revealed evidence of marked hearing impairment with both expressive and receptive language delay, a left ptosis (drooping of the upper eyelid) and exotropia (a deviation of the visual axis of one eye away from that of the other) with chorioretinitis (inflammation of the choroid and retina). In Dr. Duchowny's opinion, which is credited, such findings were consistent with early CMV exposure, and placed Ernest at risk for significant cognitive delay, accentuated by his hearing impairment. Ernest's motor abilities were, however, noted to be age appropriate. As for the cause of Ernest's neurological injury, it must be concluded that the proof fails to demonstrate that it resulted from a brain or spinal cord injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation. Rather, the proof demonstrates, more likely than not, that Ernest's neurologic impairments derive from a congenital CMV infection, which predated his birth by several weeks.
