Findings Of Fact Michael was born on June 27, 2014, at Jackson Memorial Hospital. Michael was a twin, a multiple gestation, weighing over 2,000 grams at birth. Respondent retained Donald Willis, M.D., an obstetrician specializing in maternal-fetal medicine, to review the medical records of Michael and his mother, Petitioner Maria Jose Morales Cannon, and opine as to whether there was an injury to his brain or spinal cord that occurred in the course of labor, delivery, or resuscitation in the immediate postdelivery period due to oxygen deprivation or mechanical injury. In his report, dated September 10, 2018, Dr. Willis set forth the following, in pertinent part: The mother was admitted to the hospital at about 32 weeks gestational age for steroids to enhance fetal lung maturity and intravenous MgSO4 as neuroprotection to help reduce the risk for intracranial bleed. Her cervix was dilated one centimeter, 20% effaced and posterior, consistent with an unlabored cervix. Primary Cesarean section was done at 32 weeks as pre management plan for TTTS.[2/] Biophysical profiles (BPP) were 8/8 for both fetuses prior to delivery, indicating neither fetus was in distress. Fetal heart rate tracing was stated to be reactive, again suggesting no distress prior to delivery. Michael Cannon was the larger of the twins, designated as twin A. Cesarean delivery was apparently uncomplicated. Birth weight was 2,090 grams. The baby was not depressed at birth. Apgar scores were 9/9/9. Essentially no resuscitation was required with only tactile stimulation and oral suctioning done after birth. * * * In summary, this child was born as twin A at 32 weeks gestational age. Delivery was by elective Cesarean selection. Birth weight was 2,090 grams. The mother was not in labor. Delivery was uncomplicated. The baby was not depressed at birth. Apgar scores were 9/9. No resuscitation was required. The initial platelet count was decreased at 96,000. However, Intracranial hemorrhage would be unlikely with this platelet count. Head ultrasound and MRI were consistent with periventricular leukomalacia. Brain injury was most likely related to prematurity and not oxygen deprivation or trauma at birth. There was no apparent obstetrical event that resulted in oxygen deprivation or mechanical trauma during labor, delivery or the immediate post-delivery period. Brain injury identified by head Ultrasound and MRI was more likely related to prematurity and not oxygen deprivation at birth. In his affidavit, dated November 30, 2018, Dr. Willis affirms, to a reasonable degree of medical probability, the above-quoted findings and opinions from his report. Respondent also retained Michael S. Duchowny, M.D., a pediatric neurologist, to review the pertinent medical records, conduct an Independent Medical Examination (IME) of Michael, and opine as to whether Michael suffers from a permanent and substantial mental and physical impairment as a result of a birth-related neurological injury. Dr. Duchowny reviewed the medical records, obtained historical information from Michael’s mother and aunt, and performed an IME on November 14, 2018. Respondent’s Motion for Partial Summary Final Order also relies upon the attached affidavit from Dr. Duchowny, dated November 28, 2018. In his affidavit, Dr. Duchowny testifies, in pertinent part, as follows: In summary, MICHAEL’s examination reveals neurological findings consistent with spastic diparetic cerebral palsy. He evidences dysarthic speech and refractory strabismus. Impairment primarily affecting his right upper extremity. In contrast, Michael has preserved cognitive function and social awareness. Review of MICHAEL’s medical records reveals that his mother’s twin pregnancy was complicated by intrauterine growth retardation and polyhdramnious. Corner over absent diastolic blood flow in MICHAEL’s twin brother prompted decision to deliver both twins at 32 weeks gestation. MICHAEL’s APGAR scores were 9, 9, and 9 at 1, 5 and 10 minutes. MICHAEL remained in the Jackson Memorial Hospital NICU for 28 days and was treated for apnea of prematurity and retinopathy of prematurity. Hyperechoic periventricular regions were noted on head ultrasound studies in the NICU, and a follow-up MR imaging study on January 7, 2015, revealed findings compatible with periventricular leukomalacia. Although MICHAEL has a substantial motor impairment, he is not currently evidencing a substantial cognitive impairment. I further believe that his neurological deficits are a consequence of prematurity and not acquired in the course of labor and delivery. I am therefore not recommending MICHAEL for consideration by the NICA program. In his affidavit, Dr. Duchowny testifies that his opinions are to a reasonable degree of medical probability. A review of the file reveals that no contrary evidence was presented to dispute the findings and opinions of Drs. Willis and Duchowny. Their opinions are credited.
The Issue At issue in this proceeding is whether Michael Chase Anwar, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary matters Lisa Anwar and Saeed Anwar are the parents and natural guardians of Michael Chase Anwar (Michael), a minor. Michael was born a live infant on September 11, 1995, at Florida Hospital, a hospital located in Orlando, Florida, and his birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Michael was Jorge Jesus Lense, M.D., who was, at all times material hereto, a participating physician in the Florida Birth-Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Mrs. Anwar's antepartum course and Michael's birth At or about 12:48 a.m., September 11,1995, Mrs. Anwar was admitted, in labor, to Florida Hospital. At the time, her estimated date of confinement was noted as September 22, 1995, and her antepartum course was without apparent complication; however, the fetus was noted to be large for gestational age. Onset of labor was noted as 11:15 p.m., September 10, 1995, with spontaneous rupture of the membranes, and clear amniotic fluid noted. Mrs. Anwar's obstetrical course from admission through Michael's delivery at 1:55 p.m., September 11, 1995, is detailed in Dr. Lense's delivery notes, as follows: The patient . . . presented with spontaneous rupture of membranes since 2315 hours on September 10, 1995. She was in active labor on admission. She progressed through labor to 8 cm dilatation at which time she had a prolonged fetal heart rate deceleration lasting approximately four minutes to fetal heart tones of 70s associated with a tetanic uterine contraction lasting approximately four minutes. This was relieved with terbutaline 0.125 mg subcutaneously and 0.125 mg intravenously. Fetal heart rate returned to normal with good variability and accelerations. She was having mild to moderate variable decelerations. She allowed labor to progress. She progressed rapidly to the anterior lip of the cervix to complete and +1 station. Because the fetal heart rate tracing was reassuring she was allowed to progress spontaneously to reach complete dilatation. However, the variable decelerations progressively worsened. She had temperature elevation of 100.5 [to 101.4]. She was begun on ampicillin 2 grams intravenously for presumed chorioamnionitis [an inflammation of female membranes]. She began pushing second stage labor. The variable decelerations worsened, and the decision was made to shorten second state of labor with vacuum assist. A vacuum was applied after the bladder was empty, complete, complete +3 station. The fetal head was delivered to complete, complete and +4 with the vacuum. However, it was difficult to maintain an adequate suction on the vacuum secondary to the thickness of the fetal hair. However, the patient was able to deliver the infant spontaneously without difficulty. Double nuchal cord was reduced. The rest of the infant was delivered without difficulty . . . The cord was doubly clamped and cut. The infant was noted to have poor respiratory effort and tone at the time of delivery. The neonatal resuscitation team and the neonatal intensive care unit neonatologists were called to the delivery. . . . At delivery Michael was intubated due to apnea (failure of the newborn infant to initiate pulmonary ventilation), and required positive pressure ventilation. Apgar scores of 2 at one minute, 3 at five minutes, and 5 at ten minutes were noted. Chord pH obtained on delivery was noted as 7.01, representing severe acidosis. The Apgar scores assigned to Michael are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, muscle tone, reflex irritability, and color, with each category being assigned a score ranging from the lowest score of 0 through a maximum score of 2. As noted, at one minute Michael's Apgar score totalled 1, with heart rate being graded at 2, and respiratory effort, muscle tone, reflex irritability, and color being graded at zero. At five minutes his Apgar score totalled 3, with heart rate being graded at 2, color being graded at 1, and respiratory effort, muscle tone, and reflex irritability being graded at zero. At ten minutes his Apgar score totalled 5, with heart rate being graded at 2, respiratory effort, reflex irritability and color being graded at 1 each, and muscle tone being graded at zero. Such scores are abnormal, and consistent with perinatal depression. Michael's course and development subsequent to delivery Following resuscitation, Michael was transferred to the neonatal intensive care unit in guarded condition. After admission, positive pressure ventilation was continued, and he was placed on ventilatory support. A blood culture, complete blood count, urine wellcogen and RPR were obtained, and Michael was started on ampicillin and gentamicin to address the risk of sepsis or infection. Possible seizure activity was noted during the first day of life, with tonic-clonic movements of all four extremities, and he was loaded with phenobarbital. An electroencephalogram was obtained and read as an abnormal neonatal recording characterized by diffuse depression of background cerebral activity; however, no electrographic seizures or lateralized epileptiform discharges were observed, and motion and electrical artifact were noted to be present. Michael was extubated the morning of September 12, 1995, following which he was noted to be "breathing spontaneously, receiving oxygen via nasal cannula." However, overnight he was noted as "quite irritable, jittery, with back arching," and required occasional sedation with Fentanyl. A head ultrasound completed on September 12, 1995, revealed the following: THERE IS A SMALL BLEED IN CHOROID PLEXUS NOTED BILATERALLY. IT COULD BE WORSE ON THE RIGHT THAN ON THE LEFT. THE VENTRICLES ARE NORMAL IN SIZE. THERE IS NO INTRAVENTRICULAR BLEED. NO OTHER ABNORMALITY. IMPRESSION: SMALL CHOROID PLEXUS BLEED NOTED BILATERALLY, WITH THE LEFT BEING MORE EXTENSIVE THAN THE RIGHT. Stated differently, the ultrasound revealed a bilateral grade one intraventricular hemorrhage (IVH). Between the afternoon of September 11, 1995, and the afternoon of September 12, 1995, Michael's hematocrit was noted to drop from 46 percent to 29 percent. Hemoglobin likewise dropped from 15.6 to 10.0. Consequently, due to his anemic condition, Michael was transfused on September 12, 1995. On September 12, 1995, Michael was examined by a consulting physician, most likely to address his neurologic condition. That examination, by Prashant M. Desai, M.D., reported the following observations, impressions, and recommendations: PHYSICAL EXAMINATION GENERAL: Weight is approximately 3.5 kg. Head circumference was 36.75 cm. Anterior fontanel is soft. The infant is lying supine in an open warmer, receiving oxygen via nasal cannula. He looks healthy, well-developed and well-hydrated. No clear dysmorphic features are noted. No apparent significant congenital skin lesions. He is sleeping comfortably. When disturbed, he becomes jittery and extremely irritable. He is difficult to console. He arches his neck and back. He keeps his hands fisted, flexes the elbows, and displays hand tremoring. BACK & SPINE: Appear normal. EXTREMITIES: There is mild stiffness of the extremities. Reflexes are brisk. He will not allow flexion of his neck, and instead, he resists it by neck arching and back arching. He will transiently open his eyes. Face is symmetric. Tongue is midline. Gag reflex is present. IMPRESSION: FULL-TERM ONE-DAY-OLD NEWBORN INFANT WITH PERINATAL DEPRESSION AND HYPOXIC-ISCHEMIC ENCEPHALOPATHY. RECENT DROP IN HEMOGLOBIN AND HEMATOCRIT MAY INDICATE INTRACRANIAL HEMORRHAGE. SUBARACHNOID HEMORRHAGE IS POSSIBLE, AND WOULD BE COMPATIBLE WITH CLINICALLY NOTED NECK AND BACK ARCHING, JITTERINESS AND EXTREME IRRITABILITY. HE HAS BEEN LOADED WITH PHENOBARBITAL AND PLACED ON MAINTENANCE PHENOBARBITAL SECONDARY TO SOME SEIZURE-LIKE ACTIVITY YESTERDAY. ELECTROENCEPHALOGRAM SHOWS DIFFUSE DEPRESSION OF BACKGROUND CEREBRAL ACTIVITY. THIS WOULD BE COMPATIBLE WITH HISTORY OF PERINATAL DEPRESSION. RECOMMENDATIONS: Head computerized axial tomography scan when feasible. Continue Phenobarbital at 4-5 mg/kg/day in two divided doses. He may require p.r.n. sedation with Fentanyl, given his irritability. Obtain a repeat electroencephalogram prior to hospital discharge. Duration of anticonvulsant treatment will depend on his hospital course. If his seizures recur and, in particular, if his extreme irritability persists, a metabolic work-up might be indicated. A CT (computerized tomography) brain scan of September 13, 1995, was read as "probably within normal limits." The scan was read and reported as follows: FINDINGS: THE DURAL VENOUS SINUSES AND THE VEIN OF GALEN ARE RELATIVELY DENSE COMPARED TO BRAIN. THIS IS PROBABLY RELATED TO THIS CHILD'S AGE AND THE COMPARATIVE LOW ATTENUATION OF THE UNMYELINATED BRAIN. THIS APPEARANCE CAN ALSO BE SEEN WITH ELEVATED HEMATOCRIT. WHILE THIS CAN ALSO BE SEEN WITH DURAL SINUS THROMBOSIS, THIS WOULD IMPLY THAT THE ENTIRE DURAL SINUS SYSTEM AS WELL AS THE VEIN OF GALEN WERE THROMBOSED. THAT IS UNLIKELY IN THIS SITUATION ESPECIALLY SINCE NO ASSOCIATED PARENCHYMAL CHANGES ARE NOTED. NO FOCAL PARENCHYMAL ATTENUATION ABNORMALITY IS NOTED. IMPRESSION: THE EXAM IS PROBABLY WITHIN NORMAL LIMITS. THE POSSIBILITY OF AN ELEVATED HEMATOCRIT IS RAISED. On September 14, 1995, Michael was noted to have an increased temperature. To further address the risk of sepsis or infection he was accorded a regimen of Vanco and Claforan for three days. Blood culture, urine, and CSF (cerebrospinal fluid) studies were reported as negative. Phenobarbital was discontinued September 16, 1995, and ampicillin and gentamicin were discontinued September 18, 1995. All intervening culture studies were reported as negative. A repeat electroencephalogram of September 20, 1995, was read as a "mildly abnormal neonatal recording due to some mild diffuse suppression of background cerebral activity." However, consistent with improvement in Michael's status, the recording was noted to be "considerably improved from [the] previous electroencephalogram performed on day 1" of life. On September 25, 1995, Michael had a second CT brain scan.1 That scan, unlike the first scan, was apparently read as abnormal, reflecting a presentation consistent with hypoxic- ischemic encephalopathy2 or, stated differently, brain injury occasioned by oxygen deprivation. (Discharge Summary for Michael Anwar, at page 2). Michael was discharged at 4:45 p.m., September 25, 1995, to the care of his parents.3 At the time, he was noted to exhibit "diffusely poor tone" ("infant limp, floppy tone"), and "little spontaneous movement" or, stated differently, "little spontaneous arousal." However, positive suck, positive blink, and positive gag were present, and Michael was free of seizure activity. Discharge diagnosis was, as follows: DISCHARGE DIAGNOSIS: 35 weeks appropriate for gestational age male Perinatal depression Sepsis, ruled out Seizures, ruled out Hypoxic-Ischemic Encephalopathy Bilateral Grade 1 Intraventricular hemorrhage Anemia On February 27, 1998, following the filing of the claim for compensation, Michael was examined by Michael Duchowny, M.D., a board certified pediatric neurologist. Dr. Duchowny's examination revealed the following: PHYSICAL EXAMINATION reveals a small 2 1/2 year old, appropriately proportioned boy. The weight is 25 pounds. The skin is warm and moist without neurocutaneous stigmata. There are no gross dysmorphisms. No digital, skeletal or palmar abnormalities are noted. The head circumference measures 48.6 centimeters which approximates the 3rd percentile for age. There are no cranial or facial anomalies or asymmetries, and the fontanels are closed. The neck is supple without masses, thyromegaly or adenopathy and the cardiovascular, respiratory and abdominal examinations are normal. NEUROLOGIC EXAMINATION reveals an alert boy who is socially interactive and has only a few words. There is an abundant amount of babbling sounds which suggest the emergence of speech patterns. Michael is in fact able to identify all of his body parts and knows both primary and secondary colors. He is quite alert and his socialization skills are well developed. He maintains good central gaze fixation with conjugate following movements and the ocular fundi are normal. There are full and conjugate extraocular movements with blink to threat from both directions. There are no significant facial asymmetries. The tongue movements are poorly coordinated and drooling is a prominent feature. Motor examination reveals a static generalized hypotonia with a dynamic increase in tone and bilateral upper extremity posturing. Michael is grossly ataxic [uncoordinated], both for axial and appendicular musculature [both truncal stability as well as all four limbs (arms and legs)] and his gait shows marked instability and a tendency to fall in all directions. Romberg sign could not be tested. He is unable to perform alternating movement sequences and he had poor dexterity for individual finger movements. The DTR's are present and 2 to 3+ bilaterally and plantar responses are downgoing. Sensory examination is intact to withdrawal of extremities to touch and pin, and a neurovascular examination discloses no cervical, cranial or ocular bruits. There are no temperature or pulse asymmetries. IN SUMMARY: Michael's neurologic examination reveals findings consistent with ataxic cerebral palsy. I believe that his cognitive and social skills are actually quite good but [are] restricted as a result of his motor deficit. I suspect that Michael will continue to improve in the future and that he will walk independently within the next 12 to 18 months. The dispute regarding compensability Given the proof, it cannot be subject to serious debate that Michael suffered an injury or anomaly in brain development that has resulted in neurologic impairment. What remains to resolve is the cause and timing (genesis) of the event which led to Michael's anomalous brain development or, more pertinent to these proceedings, whether the proof demonstrates, more likely than not, that the anomaly Michael suffers was "caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as opposed to some other genesis. Section 766.302(2), Florida Statutes. Also at issue is whether, if such an injury occurred, Michael was rendered "permanently and substantially mentally and physically impaired." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Here, the nature and significance of Michael's impairment is dispositive of the claim, and it is unnecessary to resolve the dispute regarding the cause and timing of the event which led to Michael's anomalous brain development.4 Regarding the nature and significance of Michael's impairment, the proof demonstrates that the physical impairment he suffers may best be described as moderate, as opposed to severe, and that his physical impairment is not static, but improving. As for Michael's mental status, it has been observed to be at or near age level, and, consequently, there is no evidence of any mental impairment.5
Findings Of Fact Akeem Brown was born on May 15, 2012, at Memorial Hospital Jacksonville in Jacksonville, Florida. NICA retained Donald C. Willis, M.D. (Dr. Willis), to review Akeem’s medical records. In a medical report dated May 14, 2015, Dr. Willis made the following findings and expressed the following opinion: Spontaneous vaginal delivery was apparently uncomplicated. Birth weight was 3,626 grams or 8 lbs. The baby was not depressed. Apgar scores were 8/9. Newborn hospital course appears to be uncomplicated. Progress note on the day after birth recommended routine newborn care. Neurology evaluation at 20 months of age stated the baby had global developmental delay, hypotonia, and hyperreflexia. MRI at about 2 years of age showed bilateral motor cortex hyperintense FLAIR, suggestive of gliosis. A subsequent neurology note stated this finding was likely related perinatal ischemia. In summary, there was no apparent fetal distress during labor. Delivery was uncomplicated. The newborn was not depressed. Newborn hospital course was uncomplicated. The baby was subsequently found to have global developmental delay and an abnormal MRI as described above. There is nothing in the medical records to suggest this brain injury was related to hypoxia or trauma during the birth process. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post delivery period. Dr. Willis reaffirmed his opinion in an affidavit dated October 31, 2016. Dr. Willis’ opinion that there was no obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or in the immediate post- delivery period is credited. Respondent retained Laufey Y. Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to evaluate Akeem. Dr. Sigurdardottir reviewed Akeem’s medical records, and performed an independent medical examination on him on October 21, 2015. Dr. Sigurdardottir made the following findings and summarized her evaluation as follows: Summary: Akeem is a 3-year 5-month-old black male who has a possible bilateral hemiplegic cerebral palsy following a fairly uncomplicated pregnancy and delivery. His MRI shows evidence of old hypoxia. After review of fairly extensive maternal records and labor and delivery records, it seems clear that timing his injury is difficult as he did not show any evidence of recent neurologic injury at the time of birth. Although sparse medical records of Akeem are made available to us, such as physical therapy or occupational therapy records, cognitive testing or language assessments and no additional neurologic evaluations are at hand it seems clear that Akeem has relatively spared cognitive abilities. Final result: Results of question 1: The patient is found to have a permanent substantial physical impairment, but to have relatively mild mental impairment mainly in the areas of language. Results of question 2: There is evidence on neuroimaging that Akeem’s difficulties could relate to hypoxic neurologic injury, but no clear evidence to suggest the timing of such an injury and, therefore, it cannot be established that it occurred in the immediate perinatal period. Results of question 3: We would expect full life expectancy, although a guarded prognosis for motor recovery and likely ongoing disability from his significant bilateral hemiplegia. We expect favorable recovery in areas of cognition and language. In light of the above-mentioned details, difficulty with clear timing of Akeem’s injury, we do not recommend Akeem to be included into the Neurologic Injury Compensation Association (NICA) Program and would be happy to answer additional questions. Dr. Sigurdardottir reaffirmed her opinions in an affidavit dated November 29, 2016. 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. Sigurdardottir’s opinion that while Akeem has a substantial physical impairment, he has a relatively mild mental impairment, mainly in the area of language, 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. Sigurdardottir that Akeem does not have a substantial mental impairment.
The Issue The issue is whether Petitioner's request for eligibility for developmental services should be approved.
Findings Of Fact Based upon all of the evidence, the following findings of fact are determined: In this dispute over the provision of developmental services, Petitioner, Mark J. Haley, who is 36 years of age, seeks to establish eligibility for such services. Respondent, Department of Children and Family Services (DCFS), which administers that program, has denied the request on the ground that Petitioner's medical condition does not qualify him for services. Under guidelines established in Section 393.063, Florida Statutes (2000), in order to qualify for DCFS services, an applicant must demonstrate that he or she has a developmental disability. That term is defined in part in Subsection (12) as "a disorder or syndrome that is attributable to . . . Prader-Willi [S]yndrome and that constitutes a substantial handicap that can reasonably be expected to continue indefinitely." Subsection (34) of the same statute goes on to define Prader-Willi Syndrone (PWS) as "an inherited condition typlified by neonatal hypotonia with failure to thrive, hyperphagia or an excessive drive to eat which leads to obesity usually at 18 to 36 months of age, mild to moderate retardation, hypogonadism, short stature, mild facial dysmorphism, and a characteristic neurobehavior." (Emphasis added) When he was 18 years old, Petitioner stood six feet, three inches tall and weighed 190 pounds. He was an honor student and merit scholar. Tragically, however, he was diagnosed with a tumor affecting his hypothalumus (an area of the brain), which required surgery and radiation. Over time, and due to damage to his hypothalumus, Petitioner has acquired the symptoms of PWS, which include obesity, uncontrolled appetite, a lack of testosterone, and short temper with poor short-term memory. In April 1999, Petitioner was examined by a University of Florida physician who specializes in genetics. He confirmed that Petitioner's "[a]quired [PMS] is not the result of a genetic defect, but [is] due to damage to the hypothalamus . . . because of his brain tumor." Contrary to an assertion by Petitioner, there is no persuasive medical evidence of record that the tumor was present from a very early age and therefore his condition can be characterized as inherited. Rather, a Texas neurosurgeon simply opined that the tumor was "slow growing," and "was most likely present for more than a year before he was first seen and operated on in 1983," when Petitioner was 18 years old. While living in Texas, Petitioner's weight ballooned to 525 pounds. Because of parental concern, in January 1999 Petitioner relocated to Volusia County, Florida, where his parents reside in a retirement community. The parents' intention was to place their son under strict supervision and dietary control in the hopes of reducing his weight. Their efforts have been somewhat successful as Petitioner has lost approximately 100 pounds in the last year and now weighs around 425 pounds. Petitioner's condition is permanent. He suffers from uncontrolled appetite and other deficits which necessitate full-time supervision. He is unable to care for himself. Suffice it to say that Petitioner's elderly parents have encountered difficulty in providing the necessary supervision that he requires. In March 2000, Petitioner filed a request with the DCFS seeking developmental services for his condition. The request was eventually denied on the ground that state law requires that a person have inherited, and not acquired, PWS in order to qualify for services. If services are approved, clients are typically placed in a facility that specializes in the full-time treatment and care of persons with PWS. One such facility is ARC of Alachua County, Inc. (ARC), which has 42 PWS patients under its care at this time. Petitioner points out that 4 clients at the facility have acquired PWS, and therefore there is precedent for his receiving services. However, those 4 also have a primary diagnosis of mental retardation, which qualifies them for developmental services, irrespective of the PWS condition. Petitioner does not have mild to moderate retardation. Petitioner's elderly parents are legitimately concerned that once they are gone, there will be no one to care for their son, who requires constant supervision, and that his modest social security disability check is insufficient to pay for services at ARC, which cost around $50,000.00 per year. Besides that, the full-time job of supervising their son is a taxing one, and they are not sure how long they can continue to do this. An ARC representative confirmed that the job of caring for a person with PWS is extremely difficult, and he praised the parents for their perserverance. Notwithstanding these genuine concerns, however, there is no relief available in this proceeding.
Recommendation Based on the foregoing Findings of Fact and Conclusions of Law, it is RECOMMENDED that the Department of Children and Family Services enter a final order denying Petitioner's request for a determination that he is eligible for developmental services. DONE AND ENTERED this 6th day of March, 2001, in Tallahassee, Leon County, Florida. ___________________________________ DONALD R. ALEXANDER Administrative Law Judge Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-3060 (850) 488-9675 SUNCOM 278-9675 Fax Filing (850) 921-6847 www.doah.state.fl.us Filed with the Clerk of the Division of Administrative Hearings this 6th day of March, 2001. COPIES FURNISHED: Virginia A. Daire, Agency Clerk Department of Children and Family Services Building 2, Room 204B 1317 Winewood Boulevard Tallahassee, Florida 32399-0700 Richard E. Haley 193 La Colina Drive Edgewater, Florida 32141 Cathy B. McAllister, Esquire Department of Children and Family Services 210 North Palmetto Avenue, Suite 210 Daytona Beach, Florida 32114-3269 Josie Tomayo, General Counsel Department of Children and Family Services Building 2, Room 204 1317 Winewood Boulevard Tallahassee, Florida 32399-0700
The Issue The issue to determine in this matter is whether Ashton Payne suffered a "birth-related neurological injury" as defined by section 766.302(2), Florida Statutes, for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Ashton was born on January 19, 2018. Ashton was delivered at Winter Park Hospital. Petitioner Michele Mark is Ashton's mother. Petitioners are Ashton's natural parents and legal guardians. Michele M. Cabrera, M.D., delivered Ashton at Winter Park Hospital. Dr. Cabrera was a "participating physician" in the Plan at the time she rendered obstetrical services on January 19, 2018. See § 766.302, Fla. Stat. Dr. Cabrera provided her obstetrical services in the course of Ashton's delivery, and the resuscitation in the immediate post-delivery period. Ashton weighed 3310 grams at birth. The parties do not dispute that Ashton has suffered an injury to his brain due to oxygen deprivation which has left him permanently and substantially mentally and physically impaired. The parties do not dispute that the NICA notice requirements, as set forth in section 766.316, were met. Ashton was born under very challenging circumstances. At approximately 1:11 a.m. on January 19, 2018, Ms. Mark appeared at Winnie Palmer.3/ Ms. Mark, who was at 37 weeks' gestation, complained of contractions and severe pain. At Winnie Palmer, a triage nurse evaluated Ms. Mark. The examination revealed that Ms. Mark was experiencing intermittent contractions. The nurse also recorded that Ms. Mark's cervix was one centimeter dilated and 100 percent effaced. Ms. Mark informed the nursing staff that an ultrasound two days earlier revealed that the fetus was breech. However, apparently because the birth was not imminent, Ms. Mark was discharged from Winnie Palmer at 2:33 a.m. Back at her home, at approximately 3:19 a.m., Ms. Mark experienced a spontaneous rupture of her fetal membranes (her "water broke"). The rupture immediate resulted in an umbilical cord prolapse. A cord prolapse means that the umbilical cord dropped down through the cervix before the baby. This complication can cause the umbilical cord to be occluded, or squeezed, which can severely diminish the flow of oxygen to the fetus. Later, Ms. Mark relayed that she felt her baby's foot in her vagina (a "footling" breech). Sitting on her bathroom floor, with the umbilical cord protruding from the birth canal, Ms. Mark called 911. At 3:30 a.m., Emergency Medical Service personnel ("EMS") responded to Ms. Mark's home. When EMS reached Ms. Mark, they found her seated with approximately 15 inches of umbilical cord exposed. Initially, EMS was unable to feel a pulse in the umbilical cord. Once Ms. Mark was lifted and repositioned onto a stretcher, however, EMS was able to detect a faint pulse in the cord. EMS also noted that Ms. Mark was experiencing contractions "2 minutes apart." EMS transported Ms. Mark, in an ambulance, to Winter Park Hospital. EMS departed Ms. Mark's home at 3:41 a.m., and arrived at Winter Park Hospital at 3:53 a.m. At 3:58 a.m., Ms. Mark reached the Labor and Delivery Operating Room. There, she underwent an emergency C-section. Prior to the operation, the triage nurse palpated pulsation in the prolapsed cord. Ms. Mark was still experiencing contractions at two to three minutes apart. Dr. Cabrera conducted the emergency C-section. Ashton was delivered at 4:04 a.m. Dr. Cabrera's notes record "fetal distress cord prolapse, fetal malposition footling breech." A "footling breech" indicates that one or both of the baby's feet were positioned in the birth canal instead of the pelvis. Upon Ashton's delivery, Winter Park Hospital initiated a "Code Blue." Dr. Cabrera immediately started emergency resuscitative measures. At delivery, Ashton was not breathing, with a recorded heart rate of only 30 beats per minute. Ashton required full cardiorespiratory resuscitation. Ashton was emergently intubated at 4:06 a.m. Chest compressions were initiated "@ 20-30 seconds of life" and stopped at 4:08 a.m. At 4:08 a.m., Ashton's heart rate had reached 104 beats per minute. The Code Blue lasted from 4:04 a.m. to 4:29 a.m. By 4:29 a.m., Ashton's heart rate had risen to 144 beats per minute. The last oxygen saturation level recorded during the Code Blue was 77 percent at 4:19 a.m., indicating severe hypoxia. ("Hypoxia" means partial loss of oxygen to the fetus. "Anoxia" means total loss of oxygen to the fetus. The normal oxygen saturation range is 97-100 percent.) Ashton's APGAR ("Appearance, Pulse, Grimace, Activity, Respiration") scores following delivery were 1/2/4/4 at 1, 5, 10, and 15 minutes, respectively. (Scores of 7 to 10 are considered normal.) At 4:29 a.m., Ashton was transferred to the Neonatal Intensive Care Unit ("NICU"). Ashton was still unable to breath on his own. NICU noted "no respiratory effort and seizures." NICU placed Ashton on a mechanical ventilator in a continued effort to resuscitate him. At 4:41 a.m., the initial Arterial Blood Gas ("ABG") Report showed that Ashton was experiencing severe metabolic acidosis. The ABG Report recorded a pH level of 6.809 (critical) with a base excess of negative 25. This score signified a severely acidotic child with both a metabolic and respiratory acidotic condition. The acidotic condition required immediate medical treatment to correct. At 5:14 a.m., approximately 70 minutes after Ashton's birth, a second ABG Report showed a pH level of 7.034 (critical) with a base excess of negative 19. These values indicated that Ashton was continuing to experience severe metabolic acidosis. At 7:15 a.m., Ashton was transferred to the NICU at Florida Hospital Orlando. Although Ashton's oxygen saturation level had reached 99 percent, he was still unable to breathe on his own. He remained on a ventilator. Ashton also experienced repeated seizure activity. A progress report on January 21, 2018 (two days after his delivery), noted two episodes of seizures on that day. Ashton remained on a ventilator until January 26, 2018 (seven days after his delivery), when he was extubated. Petitioners argue that Ashton did not suffer a "birth- related neurological injury" which would entitle him to an award under the Plan. Section 766.302(2) defines the term to mean: njury to the brain or spinal cord of a live infant weighing at least 2,500 grams for a single gestation . . . 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. Petitioners do not dispute that Ashton's case presents an injury to the brain of a live infant weighing at least 2,500 grams. Neither do Petitioners contest that Ashton's injury was caused by oxygen deprivation which renders him permanently and substantially mentally and physically impaired. What Petitioners challenge is whether Ashton's injury occurred "in the course of labor, delivery, or resuscitation in the immediate postdelivery period." Petitioners assert that Ashton's neurological impairment directly resulted from the umbilical cord prolapse in Ms. Mark's home at 3:19 a.m. Petitioners contend that Ashton's brain injury (due to oxygen deprivation) manifested before the time Ms. Mark reached Winter Park Hospital (3:53 a.m.). Consequently, Ashton's injury did not develop during his delivery at 4:04 a.m. or any subsequent postdelivery resuscitation efforts. Petitioners further argue that Ms. Mark was never in labor at any point during Ashton's birth. Therefore, they contend that Ashton's brain injury did not occur "in the course of labor, delivery, or resuscitation," and Ashton does not qualify for coverage under the Plan. To support their argument, at the final hearing, Petitioners presented the (deposition) testimony of Jason James, M.D., and Ariel Sherbany, M.D. Dr. James is a board-certified obstetrician/ gynecologist. Dr. James testified that, in his opinion, Ashton did not sustain a qualifying "birth-related" injury because Ms. Mark was not in labor at any point prior to Ashton's delivery at 4:04 a.m. Initially, Dr. James commented that it is "impossible to say" with any certainty whether Ms. Mark was in labor at the time of the umbilical cord prolapse at her home or prior to Ashton's delivery. Dr. James defined labor as "progressive cervical change in response to contractions." He relayed that, "In order for me to say a patient's in labor, I would need to see progressive cervical change in the presence of contractions, and we don't see that." Dr. James explained that, even with Ms. Mark dilated at one centimeter at Winnie Palmer, he saw "no documentation of any cervical change, whether by the EMS or by the hospital staff at Winter Park." Dr. James further expounded that the 100 percent effacement observed at Winnie Palmer was not necessarily related to labor. "Effacement is one of the cervical changes that we do see, but there are things that can cause cervical effacement that are not associated with labor." Accordingly, Dr. James did not see sufficient evidence to conclude that Ms. Mark was in labor before Ashton's delivery. Regarding the exact time Ashton's brain injury occurred, Dr. James testified that Ashton's brain injury resulted from oxygen deprivation due to the umbilical cord prolapse. He opined that the majority of the oxygen deprivation occurred during the 34 minutes from the "moments . . . the cord prolapse occurred" (3:19 a.m.) to the time Ms. Mark arrived at Winter Park Hospital (3:53 a.m.). Dr. James stated that: [T]he amount of brain damage that occurred prior to even the patient arriving at the hospital was substantial and permanent, and I think that the die was cast. . . . Was there ongoing and further damage? Yes. I will agree that there was ongoing and further damage, but I think that to say that that was the portion that resulted in permanent impairment is a mischaracterization. Accordingly, Dr. James supported Petitioners' position that Ashton's brain injury did not occur in the course of labor, delivery, or resuscitation in the immediate postdelivery period because "this baby already had substantial and permanent brain damage on arrival." Despite this assertion, Dr. James conceded that Ashton did suffer oxygen deprivation during the 11 minutes between the time Ms. Mark was admitted to Winter Park Hospital (3:53 a.m.) and his delivery at 4:04 a.m. Dr. James also accepted that Ashton continued to incur brain damage through the one hour and 10-minute time frame after his birth.4/ Dr. James further acknowledged that the hypoxia (partial lack of oxygen) Ashton experienced after 3:53 a.m. could have resulted in significant brain impairment. Finally, Dr. James disclosed that, in his opinion, Ashton was never anoxic (total lack of oxygen to the fetus) during the 34 minutes prior to Ms. Mark's arrival at Winter Park Hospital. Dr. Sherbany is a pediatric neurologist. Dr. Sherbany offered no opinion as to whether Ms. Mark was actually in labor at the time of the umbilical cord prolapse. Regarding the time period during which Ashton's brain injury due to oxygen deprivation occurred, Dr. Sherbany testified that Ashton's "brain-damaged fate was already predetermined before he arrived." Dr. Sherbany believed that the umbilical cord prolapse caused anoxia, or complete loss of oxygen to the fetus. Dr. Sherbany opined that this period of anoxia lasted 11 minutes until EMS repositioned Ms. Mark on a stretcher. Thereafter, the fetus experienced hypoxia (partial loss of oxygen) until Ms. Mark was admitted to the hospital. Dr. Sherbany explained that the "bulk of [Ashton's] oxygen deprivation really occurred" during the 34-minute time period before Ms. Mark presented at Winter Park Hospital. Dr. Sherbany expressed that, "The damage was determined at the time of that anoxic event. . . . In those 34 minutes, basically, this unfortunate child suffered his fate." In Dr. Sherbany's opinion, Ashton sustained the "majority of the insult to the brain stem . . . during that anoxic period." Like Dr. James, however, Dr. Sherbany conceded that Ashton continued to suffer oxygen deprivation, which resulted in additional brain injury, in the first 11 minutes after Ms. Mark arrived at Winter Park Hospital up to and through the four minutes of cardiac massage administered to Ashton after his delivery. Although Dr. Sherbany limited the immediate postdelivery resuscitation period to four minutes after birth, he acknowledged that Ashton was not medically stable until he was transported to the NICU unit at Florida Hospital Orlando at 7:15 a.m., three hours and 11 minutes after delivery. Dr. Sherbany also recognized that Ashton did not breathe on his own, without the assistance of a mechanical ventilator, for six days after his birth. Upon receiving Petitioners' Petition for NICA benefits, NICA conducted an evaluation to determine whether Petitioners' claim was compensable under the Plan. Unlike Petitioners, however, NICA concluded that Ashton did suffer a "birth-related neurological injury" within the meaning of section 766.302(2) and should be covered by the Plan. NICA does not dispute Petitioners' claim that Ashton suffered oxygen deprivation beginning as early as 3:19 a.m. (the moment of the umbilical cord prolapse) through 3:53 a.m. (All medical experts agree that Ashton experienced oxygen deprivation, as well as brain injury, between 3:19 a.m. and 3:53 a.m.) However, NICA asserts that Ms. Mark was in labor at the time of the cord prolapse. NICA also argues that Ashton continued to experience oxygen deprivation (which resulted in brain injury) through his delivery and postdelivery resuscitation at Winter Park Hospital. Therefore, NICA contends that Ashton's medical condition meets the statutory definition of "birth-related neurological injury" because his neurological injury occurred "in the course of labor, delivery, or resuscitation." To support its position, NICA presented the (deposition) testimony of Donald C. Willis, M.D., and Laufey Y. Sigurdardottir, M.D. Dr. Willis is board-certified in both obstetrics and maternal fetal medicine. Dr. Willis opined, within his medical expertise, that Ms. Mark went into labor shortly before or just after 3:19 a.m. Dr. Willis explained that "when EMS came [at 3:30 a.m.], [Ms. Mark] was having regular contractions, so I would assume that she was either in labor before that time or labor initiated with rupture of the membranes. . . . I would assume that her labor began somewhere right around 3:19 a.m." Dr. Willis concurred with Petitioners' medical experts that oxygen deprivation occurred at the moment of the umbilical cord prolapse at 3:19 a.m. Dr. Willis explained that "oxygen deprivation can lead to brain injury." Accordingly, Dr. Willis agreed that "there was some degree of brain injury [to Ashton] during that time period [3:19 a.m. through 3:53 a.m.]." However, unlike Dr. James and Dr. Sherbany, Dr. Willis declared that Ashton experienced an ongoing and continuing injury from the cord prolapse through at least 70 minutes after he was delivered at 4:04 a.m. Dr. Willis explained that oxygen deprivation continues until the oxygen returns to the bloodstream and reaches the organs and tissues. Consequently, Ashton's neurological injury progressed through his delivery and into the immediate postdelivery resuscitation period, at least through the time that Ashton continued to experience metabolic acidosis (5:14 a.m.). Accordingly, in Dr. Willis' opinion, Ashton's brain injury due to oxygen deprivation undoubtedly occurred during the labor, delivery, and the immediate postdelivery resuscitation period. However, while agreeing that Ashton began experiencing oxygen deprivation with the umbilical cord prolapse (3:19 a.m.), Dr. Willis testified that he did not "have any way to gauge" the amount of oxygen deprivation between 3:19 a.m. and 3:53 a.m. Therefore, he would not quantify when exactly Ashton's brain injury reached the level of permanent and substantial mental and physical impairment. On the other hand, Dr. Willis was certain Ashton continued to suffer brain injury due to oxygen deprivation during the resuscitation efforts in the immediate postdelivery period. Finally, Dr. Willis refuted Dr. Sherbany's statement that Ashton experienced complete anoxia for any prolonged period (11 minutes) after the umbilical cord prolapse. Dr. Willis did not believe that Ashton would have lived through that situation. Dr. Sigurdardottir is a pediatric neurologist. Alone among the expert witnesses, Dr. Sigurdardottir performed an independent medical evaluation of Ashton on June 27, 2018. Similar to Dr. Willis, Dr. Sigurdardottir testified that the "very, very substantial part" of Ashton's brain injury occurred at Winter Park Hospital in the final couple of minutes just prior to his delivery. Dr. Sigurdardottir declared that Ashton endured a continuum of brain injury due to oxygen deprivation. Dr. Sigurdardottir explained that brain injuries from oxygen deprivation occur exponentially, with the most critical period of injury "at the tail end of the hypoxic ischemic event." Dr. Sigurdardottir opined that the most severe part of Ashton's neurological injury occurred in the few minutes right before his delivery, and extended through the immediate post resuscitative period when Ashton experienced metabolic acidosis. Dr. Sigurdardottir further stated that Ashton's brain injury continued to evolve "within the first week" of his life, when he was most unstable. Dr. Sigurdardottir also commented that, given that hypoxia existed for some undetermined time prior to Ms. Mark's arrival at a hospital, it is difficult, if not impossible, to determine the full extent of the oxygen deprivation that occurred prior to 3:53 a.m. Therefore, it is difficult, if not impossible, to conclude that Ashton incurred a permanent and substantial brain injury prior to his delivery. Accordingly, Dr. Sigurdardottir concluded that Ashton's irreversible brain injury occurred during the final minutes prior to his birth at Winter Park Hospital, and in the hours and days after his delivery. In addition, contrary to Dr. Sherbany and similar to Dr. Willis, Dr. Sigurdardottir unequivocally stated that Ashton did not experience complete lack of oxygen (anoxia) prior to his delivery. Dr. Sigurdardottir rejected any suggestion that the fetus had no heartbeat from 3:19 a.m. until EMS felt a pulse around 3:31 a.m. Dr. Sigurdardottir explained that if Ashton had no heartbeat for 12 minutes prior to his birth, then relieving pressure on the umbilical cord would not have made a difference; Ashton would have been dead at his delivery. However, because EMS was able to detect a pulse after repositioning Ms. Mark on the stretcher, Dr. Sigurdardottir believed that Ashton's heart was beating between 3:19 a.m. and 3:31 a.m. Dr. Sigurdardottir further posited that, if Ashton had been utterly deprived of oxygen (anoxic) prior to 3:53 a.m., some meconium would have been present in the amniotic fluid. However, the EMS personnel who first treated Ms. Mark did not document any meconium from the rupture of membranes. In addition, the operative report from Ashton's delivery at Winter Park Hospital noted that the amniotic fluid was "clear." Therefore, Dr. Sigurdardottir refuted Dr. Sherbany's conclusion that Ashton experienced anoxia (total loss of oxygen) rather than hypoxia (partial loss of oxygen). Winnie Palmer joined NICA in arguing that Ashton suffered a "birth-related neurological injury" as defined in section 766.302. Winnie Palmer presented the expert (deposition) testimony of Donald Null, M.D., and Harry Farb, M.D. Dr. Null is a board-certified neonatologist. In his practice, Dr. Null provides care and treatment to critically ill infants just after delivery. In Dr. Null's opinion, Ms. Mark was experiencing some form of labor, though not "active" labor, when she visited Winnie Palmer at 1:11 a.m. on January 19, 2018. Dr. Null based his opinion on the fact that Ms. Mark was noted to have contractions and "minor" changes in her cervix. Dr. Null explained that active labor is when contractions start happening at a regular and consistent basis, and there is a change in the cervix. Dr. Null believed that Winnie Palmer released Ms. Mark at 2:33 a.m. because her contractions and cervical changes were not progressing. Dr. Null further remarked that Ms. Mark was clearly in labor at the time she presented to Winter Park Hospital at 3:53 a.m. However, Dr. Null qualified his comment by conceding that "I don't really have an opinion of when [Ms. Mark] was or wasn't in labor." Regarding the timing of Ashton's neurologic injury, in Dr. Null's opinion, Ashton had only suffered "mild insult" when Ms. Mark arrived at Winter Park Hospital. Dr. Null explained that a footling breech typically does not result in "total occlusion" of the umbilical cord, only "partial occlusion." In other words, Ashton only experienced hypoxia (partial loss of oxygen to the fetus) not anoxia (total loss of oxygen to the fetus) prior to 3:53 a.m. Dr. Null further opined that the hypoxia was not as severe before Ms. Mark's admission to the hospital as it was during the delivery and resuscitation efforts. Dr. Null testified that Ashton suffered a continuing brain injury from the time of the cord prolapse (3:19 a.m.) until his metabolic acidosis was rectified approximately 70 minutes after his delivery (5:14 a.m.). Dr. Null concluded that Ashton suffered a profound neurological injury, which he referred to as hypoxic ischemic encephalopathy ("HIE"), from the time Ms. Mark arrived at Winter Park Hospital until the time the postdelivery resuscitation efforts concluded. Dr. Null based his opinion on the fact that Ashton's heartrate was measured at 30 beats per minute at delivery, and was most likely at that level at the time Ms. Mark arrived at the hospital. Dr. Null also referred to the fact that Ashton required continuing resuscitation to correct his metabolic acidosis. Dr. Null opined that the HIE was significant enough to cause Ashton's substantial brain injury. Agreeing with Dr. Willis, Dr. Null testified that it is "impossible to quantify" the extent of the oxygen deprivation Ashton suffered between 3:19 a.m. and 3:53 a.m. However, agreeing with Dr. Sigurdardottir, Dr. Null testified that if Ashton had experienced "profound" oxygen deprivation (anoxia) or "a very profound injury prior to arrival" at Winter Park Hospital, he "probably would not have survived the rest of the labor and the resuscitation." Therefore, in concert with Dr. Sigurdardottir's opinion, Dr. Null believed that Ashton sustained the "more substantial portion of his brain injury" after the time Ms. Mark presented at the hospital (3:53 a.m.) and during delivery and postdelivery resuscitation. Dr. Farb is board-certified in both obstetrics and maternal fetal medicine. In Dr. Farb's opinion, the vast majority of Ashton's brain injury occurred after Ms. Mark arrived at Winter Park Hospital. Initially, Dr. Farb testified that Ms. Mark was in labor, "with a qualifier," when she arrived at Winter Park Hospital at 3:53 a.m. Dr. Farb defined labor as "contractions in association with cervical dilation [or change]." Dr. Farb commented that Ms. Mark's "contractions every two minutes could certainly be consistent with labor." However, he did not have any information on the presence of cervical change. Therefore, Dr. Farb issued a "qualified" conclusion that, if Ms. Mark was not in the active phase of labor, then she was at least in the "latent phase of labor." Regarding when Ashton's neurological injury occurred, Dr. Farb acknowledged that some hypoxia occurred prior to Ms. Mark's arrival at the hospital. However, Dr. Farb agreed with the assessments of Dr. Willis, Dr. Sigurdardottir, and Dr. Null that the actual amount of oxygen deprivation cannot be determined. That being said, Dr. Farb, again agreeing with Dr. Willis, Dr. Sigurdardottir, and Dr. Null, believed that "the substantial part of the injury occurred after arrival [at 3:53 a.m.] and into the immediate neonatal resuscitation period." Dr. Farb estimated that "90 percent of the injury at least occurred at and after admission to the hospital." Dr. Farb based his opinion on several factors, including: a footling breech does not cause total umbilical cord occlusion; Ashton's condition worsened from the time of his presentation to the hospital (3:53 a.m.) until delivery (4:04 a.m.); and Ashton experienced "continuous seizure activity" for at least 70 minutes after delivery (through 5:14 a.m.). Dr. Farb further commented that the second ABG draw at 5:14 a.m. showed that Ashton was still severely acidotic, which meant that his brain injury was still progressing. Dr. Farb also explained that a fetus does not immediately suffer a neurological injury at the moment of an umbilical cord prolapse. A fetus has a reserve of oxygen that must be depleted before injury to the brain occurs. Dr. Farb explained that oxygen deprivation (and any resulting brain injury) may not have commenced in Ashton until 10 to 18 minutes after the ruptured membranes and prolapsed cord. Like Dr. Sigurdardottir, Dr. Farb explained that oxygen deprivation is progressive in nature and exacerbates over time. Accordingly, "the severity of the oxygen deprivation was much worse at [Ms. Mark's] admission and [Ashton's] delivery." There was no question in Dr. Farb's mind "that the severity of the oxygen deprivation and the brain injury . . . occurs much closer to the time of delivery because things are progressive and as well as continuing in the immediate resuscitation period." Specifically, Ashton's brain injury continued to occur up to an hour and 10 minutes after his delivery as revealed by his severe metabolic acidosis at 5:14 a.m. In addition, Dr. Farb stated that Ashton's brain was also injured due to constant seizure episodes after his delivery while he was still being resuscitated. Based on the competent substantial evidence in the record, the preponderance of the evidence establishes that Ashton suffered a "birth-related neurological injury" as defined in section 766.302(2). The evidence demonstrates that Ashton began experiencing oxygen deprivation at the time of the umbilical cord prolapse which continued through delivery and immediate postdelivery resuscitation. This oxygen deprivation caused Ashton to sustain a brain injury which has rendered him permanently and substantially mentally and physically impaired. The evidence does not prove that Ms. Mark was in labor prior to Ashton's birth. However, based on the more persuasive medical testimony, the evidence establishes that Ashton suffered injury to his brain, caused by oxygen deprivation, in the course of his delivery and resuscitation in the immediate postdelivery period at Winter Park Hospital. Accordingly, Ashton is eligible for an award of compensation under the Plan.
The Issue The ultimate issues to be resolved in this matter are whether the Respondent has violated provisions of law relating to the practice of optometry and, if so, what penalty should be imposed. The Respondent has been specifically charged with violating Section 463.016(1)(g), Florida Statutes, in connection with his examination and treatment of Karilyn Boggan Peterson. The Respondent contends that his treatment of Peterson was in accordance with accepted standards of optometric practice. In resolving the issues, it has been necessary to resolve conflicting testimony given by the Respondent and Karilyn Boggan Peterson. In resolving the conflicting evidence, due regard has been given to the demeanor of the witnesses at the hearing and the extent to which their testimony is corroborated by other evidence. In most instances, the conflicting testimony has been resolved in favor of the witness Peterson and against the Respondent. The witness Peterson's testimony has been deemed credible. In many respects, the Respondent's testimony is not corroborated even by the Respondent's own records. His testimony has not been deemed credible.
Findings Of Fact At all times relevant to this proceeding, the Respondent has been licensed to practice optometry in the State of Florida. He holds License No. 0000668 issued by the Florida State Board of Optometry. The Respondent has practiced optometry in Gainesville, Florida, since 1960. He has a good educational background and is an active member in several professional organizations. During June, 1979, Karilyn Boggan, who since then has married and changed her name to Karilyn Boggan Peterson, visited the Respondent's office in Gainesville, Florida. She had bought a pair of nonprescription sunglasses from the Respondent a year prior to that, and she wanted to purchase a new pair of sunglasses and to have her eyes examined. She had not previously worn prescription glasses. She was experiencing some difficulties with her eyes. When she read for long periods, her eyes would get irritated, and she would get drowsy. The problem appeared to be getting worse. Boggan visited the Respondent's office on June 28, 1979, and related these problems to him. The Respondent examined Boggan and advised her that she had an astigmatism and that she would benefit from wearing prescription glasses. She asked if he would write a prescription so that she could have it filled at a place where glasses were available at less cost. Respondent advised her that he would need to charge her an additional $15 if she did not buy the glasses from him. She then requested that the Respondent fill the prescription. Respondent advised Boggan that persons with astigmatisms were generally sensitive to light, and he asked if she wanted "tinted" or "photogray" lenses. She said that she did. On July 14, 1979, Boggan returned to the Respondent's office to be fitted for her new glasses. The only instructions that the Respondent gave her about the glasses were that she should wash them in soap and water. Boggan paid the Respondent for the examination and the glasses. Approximately one month later, Boggan contacted the Respondent by telephone and advised him that she did not notice a lot of difference in her vision when she used the prescription glasses. She asked the Respondent if she should wear them at all times, or just when she read. The Respondent advised Boggan that she should wear the glasses all of the time. Prior to then, Boggan had been wearing the glasses irregularly. Thereafter, she wore them faithfully nearly all of the time. Boggan visited the Respondent's office on one or two occasions thereafter to have the frames adjusted. Other than that, she had no further contact with the Respondent. Except for the tinting, things appeared the same to Boggan with or without the glasses. Nonetheless, she continued to wear them until May, 1982. At that time, she was working as a proofreader and was having the same symptoms she experienced before, only more profoundly. A coworker suggested that she visit an ophthalmologist. She visited an ophthalmologist on May 21, 1982. The ophthalmologist examined her and the glasses that had been prescribed by Respondent. He concluded that she had a muscle control problem which he called "convergence insufficiency." He advised her that the glasses were of no benefit to her, and he sent her to an orthoptist, a person trained in treating eye muscle problems. The orthoptist prescribed an eye muscle exercise program. Boggan has followed the program, albeit not vigorously, and has observed some lessening of the sumptoms she experienced. The Respondent's testimony about his examination of Boggan is not supported by his own records, and his testimony about it has not been deemed credible. The Respondent did determine that she exhibited slight farsightedness and a slight astigmatism. He determined that she had a slight exophoria at distance, which was nothing to be concerned about, and a normal vertical phoria at distance. The Respondent did some near point testing to determine near point phorias and the accommodative capacity, which he determined to be normal. The Respondent utilized a "fogging technique" to determine the maximum amount of plus lens that Boggan could utilize, both distance and near, without experiencing blurry vision. He determined that she could wear a +.12 diopter lens on her right eye and a +.37 diopter lens on her left eye without experiencing blurriness. A "diopter" is a measurement of the refractive correction in a lens. The Respondent sold Boggan glasses with that prescription. He did not suggest the need for any follow-up visits. Generally, lenses with a refractive correction of +1 diopter or less are considered low power lenses. Lenses of +.12 diopter and +.37 diopter are very low power lenses which offer very little corrective value. Except for the tint in the glasses the Respondent sold Boggan, the glasses served no function at all for her. They did not correct any visual deficiency, nor does it appear that they were designed to do that. The Respondent prescribed the glasses solely on the basis of Boggan's complaints that her eyes would get irritated and drowsy when she read a lot and upon the "fogging test" which determined the maximum plus lens that she could wear without experiencing blurriness. There is a legitimate difference of opinion among practicing optometrists as to the value of low plus power glasses. Some optometrists would never prescribe them; others prescribe them routinely. Whatever the philosophy of a given optometrist, the prescribing of low plus power glasses would be justified only if numerous tests were conducted and the results evaluated. A proper eye examination conducted by an optometrist in 1979 in Gainesville, Florida, would have begun with the taking of the patient's medical history and a consideration of the patient's complaints. The patient's visual acuity would be measured to get an objective determination of refractive error. Muscle balance is tested either through a "cover test," or through "phorias" to determine the position of one eye relative to the other. This is done at distance, infinity and at near. If these findings are normal, a "vertical phoria" is done to determine the position of the eyes in a vertical position, as opposed to a horizontal position. The "amplitude of accommodation" is then tested by changing lenses in front of the patient's eyes and making the patient focus, or by having the patient fixate on small print and moving it toward the patient and asking him when it gets blurry. An "ophthalmoscopy" is conducted to observe the inside of the eye, and the outside is observed. A "slit lamp examination" is conducted to evaluate the interior portion of the eyes, the cornea, the iris and the lens. A tonometry is done to measure the pressure inside the eye. A "cover test" is also used to determine whether there is any area in the patient's field of vision where he cannot see. The minimum procedures for a vision analysis conducted by an optometrist have been prescribed by a rule adopted by the Department of Professional Regulation, Board of Optometry. Rule 210-3.07, Florida Administrative, Code, prescribes these minimum procedures. The rule was not in effect at the time that the Respondent conducted his examination of Boggan. The minimum procedures set out in the rule are, however, in concert with the minimum standards followed by optometrists in the State of Florida, including Gainesville, Florida, during 1979. The Respondent's examination and prescription of glasses for Boggan did not comport with these minimum requirements. An organization known as the Optometric Extension Program ("OEP") advocates the prescription of low plus power glasses. The Respondent is a member of that organization and agrees with its philosophy. To justify a low power prescription under the OEP theory, numerous near point tests need to be conducted. The results of these tests are placed in a formula, and a prescription is determined based upon the formula. The Respondent did not arrive at his prescription for Boggan in this manner. The prescribing of very low power glasses based solely upon a patient's complaints and upon a "fogging test" is not in accord with the OEP system. If the results of other tests show no abnormalities as they did for Boggan insofar as the tests were conducted, there would be no justification other than a commercial one for prescribing glasses and selling them. The prescribing and selling of glasses to Boggan does not comport with generally accepted and prevailing standards of optometric practice in Florida and specifically in Gainesville, Florida, at the present or at the time that the Respondent examined and prescribed glasses for Boggan. Prescribing glasses in that manner constitutes incompetence and misconduct in the practice of optometry. The manner in which the Respondent prescribed glasses for Karilyn Boggan was not an isolated occurrence in the Respondent's practice. The Respondent would conduct the same sort of examination and, with the same complaints and the same test results, issue the same prescription today. It is the sort of examination and prescription that the Respondent routinely makes in his practice. A "probable cause panel" of the Florida State Board of Optometry was convened to consider whether an administrative complaint should be issued in this matter. The panel determined that probable cause existed to justify issuing an administrative complaint against the Respondent. The attorney who prosecuted this matter on behalf of the Department of Professional Regulation appeared at the probable cause panel meeting. The attorney made recommendations to the panel, some of which were followed. It does not appear that the attorney was providing legal services to the probable cause panel, but rather that he was making recommendations as a prosecutor. To the extent that his recommendations could be considered the providing of legal services to the panel, it does not appear that the fairness of the probable cause proceeding nor the correctness of the action they took was impaired. During 1978, the Board of Optometry issued an Administrative Complaint against the Respondent in a different proceeding. The attorneys for the Board and the attorney for the Respondent entered into a stipulation through which the Respondent agreed to reimburse a patient; that the charges against him, if true, constituted unprofessional conduct; to pay a fine and costs; and to submit to a period of probation for one year. The stipulation was executed on January 26, 1979. The file before the Division of Administrative Hearings was closed based upon the stipulation. It does not appear that the Board of Optometry ever approved the stipulation, nor that the Respondent actually paid the fine, nor that the period of probation ever commenced. It cannot be determined, based upon the evidence presented, whether the Respondent was on probation at the time that he examined Karilyn Boggan.
The Issue The issue in this case is whether Everett Luis Northup sustained a birth-related neurological injury.
Findings Of Fact Katrina Northup (formerly Katrina McGuff) and Richard Northup are the natural parents of Everett Luis Northup. At all times material to this proceeding, Katrina Northup was an obstetrical patient of Wayne Blocker, M.D., and Dr. Blocker was a "participating physician" as defined in section 766.302(7), Florida Statutes. Dr. Blocker provided obstetrical services in the course of labor and delivery at the birth of Everett. Ms. Northup did not experience any significant problems during her prenatal course. On August 21, 2009, she presented to Brandon Regional Hospital, which is a licensed Florida hospital. She was 34.1 weeks pregnant. Beginning at 8:58 a.m., Ms. Northup was started on Pitocin. By 2:23 p.m., the baby's station was -1. At 3:50 p.m., Ms. Northup's membranes ruptured. At 4:41 p.m., the baby was experiencing increasing fetal tachycardia, and the mother's efforts at pushing were nonproductive. A decision was made to use vacuum extraction to facilitate the delivery. Dr. Blocker applied a KIWI vacuum extractor to the baby's head, but a seal could not be achieved. A soft cup vacuum extractor was used to deliver the baby's head to the perineum so that Ms. Northup could push the baby out. Four pulls, two of which were pop offs, were used. Ms. Northup was able to push the baby out after the use of the vacuum extractor. The baby experienced shoulder dystocia during delivery. This means that there was a delay in descent because the baby's shoulder was impinged on the mother's pubic bone. The shoulder dystocia was corrected using a MacRoberts maneuver, which is flexing the mother's hips to give more room in the pelvis. The shoulder dystocia did not require additional force from the vacuum extractor. Everett was born live on August 21, 2009, at 4:45 p.m. He weighed 3,875 grams at birth. Everett was large for his gestational age. The hospital's admission summary for Everett described his condition at time of delivery as follows: Infant was delivered pale, floppy, and with a poor respiratory effort. Infant was suctioned PO and nasally and stimulated . The initial HR was <100 but exceeded 100 by 1 minute of age. Respirations became more regular and color became ruddy with a rapid HR. Tone remained poor and there was bruising of the left arm and ballotable fluid in the scalp. After delivery, Everett's mouth, nose and pharynx were suctioned and he was given blow-by oxygen for two minutes. Everett's Apgar score at one minute of age was recorded as seven and, at five minutes of age, was eight. Apgar scores are designed to define a baby's responsiveness and cover five different categories: heart rate, respiration, color, reflex activity or reflex responsiveness, and muscle tone. Each of the categories can be scored a zero, a one, or a two. At one minute of life, Everett's heart rate was greater than 100 beats per minute; he had a good cry; there was some flexion of the extremities; he had a grimace; and his body was pink and extremities were blue. At five minutes of life, Everett's heart rate was greater than 100 beats per minute; he had a good cry; he had active motion; he had a cry or active withdrawal; and he was blue/pale. Everett's initial blood gases were recorded as a pH of 7.20, which is considered a mild to moderate metabolic acidosis. Everett was admitted to the Neonatal Intensive Care Unit (NICU). His admission summary describes the findings of the admission physical examination as follows: CONDITION: Pink, quiet and responsive. HEENT: Anterior fontanelle soft, open, and flat, red reflexes present bilaterally, subgaleal bleed with ballotable fluid, nares patent and palate intact. CARDIAC: Normal sinus rhythm with tachypnea, weak pulses and poor perfusion, CRT -5 seconds, precordium quiet and no murmur. Abdomen: Soft and nondistended abdomen, good bowel sounds, 3-vessel cord and liver edge palpable at the costal margin. GU: Normal male features for gestational age, testes descended bilaterally and patent anus. NEUROLOGIC: Quiet and responsive with fair muscle tone and reflexes for age. SPINE: Neck supple without masses, spine straight and intact, no sacral dimple noted and no clavicular fracture palpated bilaterally. EXTREMITIES: Symmetrical movements and no hip clicks. SKIN: Bruising over left arm. Everett's heart rate was recorded on August 21, 2009, as 208 at 5:00 p.m., 166 at 5:30 p.m., 172 at 6:00 p.m., and 168 at 8:30 p.m. Blood pressures taken at the same time intervals were 55/20, 48/20, 45/28, and 70/47. The initial glucose level for Everett was 29. This hypoglycemia was corrected with a DIOW bolus of 3 ml/kg. Everett had a respiratory distress syndrome, which was attributed to his premature lungs. This syndrome was corrected with intubation and the use of surfactant. He was intubated for approximately nine hours and then placed on room air. On August 27, 2009, Everett was discharged from the NICU. When Everett was 11 months old, his parents expressed concerns to his pediatrician that Everett was not meeting his developmental milestones. The pediatrician referred Everett to a pediatric neurology specialist, who prescribed an MRI. The MRI showed a "symmetric increased T2 signal within the periventricular white matter with associated atrophy of the corpus callosum, likely related to leukomalacia secondary to prematurity." On February 1, 2012, pediatric neurologist, Francis Filloux, M.D., notes her diagnostic impressions: Cerebral palsy with a spastic diplegia pattern or possible spastic triplegia, with the best function in the left upper extremity. Periventricular leukomalacia, by report from the prior MRI scan. Associated neurodevelopmental impairments. History of very mild prematurity. Everett is permanently and substantially mentally and physically impaired. Everett did not suffer an injury to the brain during resuscitation in the immediate post delivery period in a hospital. Petitioners retained Jeffrey Koren, M.D., and Stephen Glass, M.D., as expert witnesses. Respondent retained Donald Willis, M.D., and Michael Duchowny, M.D., as its expert witnesses. Dr. Glass is board-certified in neurology with a special competence in child neurology, and he is board-certified in pediatrics. He has been practicing as a pediatric neurologist for 32 years. Dr. Glass is currently an associate professor of neurology and pediatrics at the University of Washington. Dr. Glass opined that Everett sustained an injury to the brain caused by mechanical injury, due to the multiple vacuum extractions which occurred in the course of labor which rendered Everett permanently and substantially physically and mentally impaired. He believes that the injury to the brain caused by the use of the vacuum extraction device used during the delivery process caused a reduction of blood flow to the periventricular areas of the brain which caused periventricular leukomalacia (PVL), which led to cerebral palsy. Dr. Koren is board-certified in gynecology and has been practicing obstetrics and gynecology for over 30 years. He opined that the use of the vacuum extraction caused a traumatic injury to the scalp of Everett causing a subgaleal bleed and a diminished blood flow to the periventricular areas of the brain, which caused the PVL. Dr. Willis is fellowship trained in maternal fetal medicine and board-certified in obstetrics and gynecology and maternal fetal medicine. He began in private practice in 1980 and has taught at several universities. Since 2000, he has been doing consultations in maternal fetal medicine. Dr. Willis is of the opinion that Everett did not suffer a brain injury which was mechanical or due to oxygen deprivation during labor and delivery. Based on his readings of Everett's fetal heart-rate monitor, there was no evidence of fetal distress. Everett's Apgar scores were normal with a score of seven at one minute and eight at five minutes. The umbilical cord pH was not consistent with acidosis or hypoxia that would be significant enough to cause significant brain injury. The subgaleal hematoma caused by the use of the vacuum extractor was not clinically significant. Everett did not require a transfusion, and he was not anemic. By the second day of Everett's life, he had a hematocrit of 53, which is normal for a newborn. Dr. Duchowny is a pediatric neurologist who directs the neurology training program at Miami Children's Hospital. He is a professor of neurology and pediatrics at the University of Miami School of Medicine and is a full professor at the Florida International University School of Medicine. His clinical practice is based out of Miami Children's Hospital. Dr. Duchowny is board-certified in pediatrics, neurology with special qualification in child neurology, and clinical neurophysiology. He performed an independent medical examination of Everett on December 12, 2011. Dr. Duchowny opined that Everett did not suffer a brain or spinal cord injury caused by oxygen deprivation or mechanical injury during the course of labor, delivery or resuscitation in the immediate post delivery period. He explained the basis for his opinion as follows: [A]lthough Everett's neurological problems were substantial in both, the mental and motor domains, a review of his medical records did not support the belief that these abnormalities were, in fact, acquired during the labor or delivery. Everett was a pre-term infant. He was large for gestational age, but he was born at 34 weeks gestation, but if you look through the neonatal course, it's clear that his was relatively benign. For example, Everett's Apgar scores seven and eight at one and five minutes of life. These scores were quite good. His cord blood gases also were mildly abnormal, but really very little evidence of any significant problem. His cord pH was 7.18. He had a base excess of minus 10.3, and these are mild findings, and consistent with his overall neonatal course, during which he actually did very well. For example, there was no evidence of overall systemic involvement, apart from some transient hypoglycemia that was adequately treated, and he did not have multi-organ system failure, liver involvement, cardiovascular collapse. He certainly wasn't comatosed. He was transiently intubated but did not require a prolonged course of ventilator support. Sepsis was suspected, and he was treated with antibiotics, but ultimately his cultures were negative, and he went home without any significant problems or complications in the newborn period. Given the fact that his MRI scan of the brain ultimately revealed damage in the form of periventricular leukomalacia, and thinning of the corpus callosum, it would appear that his deficits could not have been acquired in the course of labor, delivery or the immediate post-partum period. Rather, I believe that Everett's brain injury was acquired prior to birth, likely as a consequence of his prematurity. Had it been acquired during labor and delivery, I would have expected a much more severe postnatal course, given the MRI findings and his neurological examination. The opinions of Dr. Willis and Dr. Duchowny are credited. Everett did experience a subgaleal hematoma during the birthing process. In order for a subgaleal hematoma to cause brain damage, it would have to be a substantial loss of circulating blood volume which would lead to hypovolemic shock. Everett did not have hypovolemic shock nor did Everett experience any seizures. If the subgaleal hematoma had been clinically significant, Everett would have been given a blood transfusion. He was not given a blood transfusion and he was not anemic. The subgaleal fluid collection was small and easily reabsorbed. Both Dr. Glass and Dr. Koren opined that the Apgar scores were incorrect and should have been substantially lower. However, their opinions are based on the descriptions of Everett at the time of delivery, which were pale, floppy, and with poor respiratory effort. At delivery, Everett's heart rate was less than 100 beats per minute. After he was suctioned and stimulated, Everett's heart rate was greater than 100 beats per minute and his color was ruddy. Everett had a difficult birth, which was reflected in the descriptions of him at delivery. However, within a minute of delivery he had bounced back and had a normal Apgar score. The greater weight of the evidence establishes that Everett did not suffer an injury to the brain during labor and delivery due to oxygen deprivation or mechanical injury. More likely than not the PVL and thinning of the corpus collosum are findings associated with Everett's prematurity and not a result either directly or indirectly of the vacuum extraction delivery and the resultant subgaleal hematoma.
