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
The Issue At issue is whether Daniel Irchai, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Stipulated facts Petitioners, Arnold Irchai and Irina Irchai, are the natural parents and guardians of Daniel Irchai, a minor. Daniel was born a live infant on February 14, 2003, at North Florida Regional Medical Center, a licensed hospital located in Gainesville, Alachua County, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Daniel's birth was Richard Brazzel, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. In this case, Petitioners are of the view that Daniel suffered a "birth-related neurological injury," as defined by the Plan. In contrast, NICA is of the view that Daniel did not suffer a "birth-related neurological injury" since the proof failed to support the conclusion that, more likely than not, Daniel suffered a brain injury "caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period" in the hospital and, regardless of the etiology of Daniel's brain injury, he was not rendered "permanently and substantially mentally and physically impaired." Daniel's birth and postnatal course At approximately 10:00 a.m., February 14, 2003, Mrs. Irchai was admitted to North Florida Regional Medical Center for an elective repeat cesarean section. According to the hospital records, pre op was complete at 11:00 a.m., Mrs. Irchai was moved to the operating room at 11:45 a.m., anesthesia was started at 11:50 a.m., surgery was started at 12:14 p.m., and Daniel was delivered, with vacuum assist, at 12:26 p.m. Of note, the records reveal maternal hypotension after the spinal anesthesia, with some fetal bradycardia before delivery, and at least three attempts with the vacuum extractor before Daniel was delivered. Following delivery, Daniel was slow to respond, and was "vigorus[ly]" stimulated and administered blow-by oxygen for 15 minutes. Apgar scores were recorded as 6 and 8, at one and five minutes, respectively,3 and cord pH was recorded as 6.89. Physical examination by Dr. Burchfield, the neonatalogist present at delivery, noted breath sounds with fine crackles, as well as intermittent grunting. At 12:41 p.m., Daniel was transported to the special care nursery where, at 12:45 p.m., he was assessed for abnormalities. Admission assessment was grossly normal, except for apparent respiratory problems, with evidence of slight nasal flaring, grunting, mild subcostal retractions, and diminished breath sounds. A cephalhematoma was also noted.4 Daniel initially responded well to blow-by oxygen, but grunting worsened and a stat consultation by neonatology was requested. On arrival at 1:50 p.m., Dr. Burchfield's physical examination revealed retractions, grunting, rales bilaterally, good skin perfusion, and open and flat fontanelle. Dr. Burchfield's impression was probable transitory tachypnea of the newborn (TTN), and his treatment plan included hood oxygen, IV fluids, blood cultures, and antibiotics (Ampicillin and Gentamicin). The nurses' progress notes reveal that between 3:00 p.m., and 3:40 p.m., Daniel continued under the oxygen hood, but was very fussy, and on one occasion was noted to secrete approximately 5 cc of blood from his mouth. The progress notes further reveal that between 3:40 p.m., and 3:50 p.m., when Dr. Burchfield was paged, Daniel was placed on NCPAP, and blood secretions from his mouth continued. Dr. Burchfield described the events in his progress notes, as follows: I was paged at 3:50 p.m. to say that this baby had vomited bright red blood [BRB] - baby's respiratory distress worsened & NCPAP started. OG placed & copious BRB came up. Baby had an estimate of 10-15 cc of blood. Upon arrival [at approximately 4:20 p.m.] baby was on NCPAP . . . . I intubated [with] 3.5 ET - initially no blood in ET. Attempt to place UAC unsuccessful. During this attempt, blood came up ET tube requiring suction. UVC placed & VBG sent, Coags sent (no heparin in line) & emergent T&C . . . . Imp[ression] - UGI bleed [hemorrhage] - ? sepsis . . . . P[lan] - Transfer to Shands UF Peds. Surgery Consult (already contacted ) ? Coags (pending) Stat T&C for transfusion Daniel was transferred to Shands at the University of Florida, where he was admitted at approximately 6:30 p.m. Following admission, the neonatalogist admission note, prepared by Dr. Burchfield, documented the presence of fresh blood in the ET tube and that "a subgaleal hemorrhage was becoming evident." Dr. Burchfield's impression was diffuse hemorrhagic disease of the newborn5; coagulopathy6; respiratory distress; pulmonary hemorrhage; suspect sepsis; and fetal distress. Dr. Burchfield's treatment plan was FFP 10 cc/kg; blood transfusion; NPO/IVF; antibiotics; and follow up with coagulation studies "to see if FFP corrects, [and] if it does, consider further deficiency." At 11:45 p.m., Dr. Burchfield made the following progress note: Baby is critically ill [with] evidence of bleeding diathesis —bleeding from GI track, lung, scalp. Emergency head US showed no bleed earlier this evening, but fontanelle is more tense now, so will repeat in a.m. Fibrinogen[7] was very low -26. This improved to 90 [with] FFP. Coags improved somewhat [with] FFP also . . . . Baby is having frequent desats and some posturing -its unclear if this is occluded ET and he's fighting, or if he is having seizures. We have given a dose of Ativan. This severe hypofibrinogenemia may be due to Liver disease 2) Congenital deficiency of Factor I 3) DIC [disseminated intravascular coagulation].[8] We have sent LFT's to rule out #1). Platelet count is not extremely low, as one would see [with] DIC. Now that FFP is given, we can't accurately obtain other factor levels to study DIC (Factors V, VIII). We will give some cryoprecipitate to bring fibrinogen higher. On February 15, 2003, David Suhrbier, D.O., a pediatric neurologist, examined Daniel. Dr. Suhrbier summarized Daniel's history and his impressions, as follows: CHIEF COMPLAINT: Seizure activity and abnormal CT of the brain. HISTORY OF PRESENT ILLNESS: Baby boy Irchai is a one-day-old Caucasian male who was referred from North Florida Regional Medical Center due to respiratory distress requiring intubation and the development of hematemesis[9] and hemoptysis.[10] Upon arrival the infant demonstrated evidence of disseminated hemorrhage disorder of the newborn manifested by a subgaleal hematoma, continued hemoptysis from the ET tube, hematemesis from the OG tube and coagulopathy evaluation demonstrating thrombocytopenia,[11] decreased fibrinogen and prolonged PT measurement. The infant received fresh frozen plasma and red blood cells. Ampicillin and Gentamycin were initiated for potential septic etiology. Chest x-ray demonstrated evidence of bilateral "ground glass" appearance consistent with respiratory distress syndrome. Initial head ultrasound was unremarkable for intraventricular hemorrhage. Infant shortly after arrival . . . began to manifest paroxysmal spells of desaturation associated with tonic posturing of the extremity which was presumed to be seizure activity. The infant was treated with two doses of IV Ativan. Head CT demonstrated evidence of both intra-axial as well as extra-axial blood products. Review of the study demonstrates the presence of a cerebellar hematoma with mass-effect upon the fourth ventricle resulting in ventriculomegaly of the third and lateral ventricles. Subarachnoid blood is also noted along both tentorial planes. Intraparenchymal hemorrhages are noted, as well as a large subgaleal hemorrhage. The infant received a 10 mg/kg bolus of IV Phenobarbital. No further seizure activity has been witnessed since the administration of the Phenobarbital. * * * OBJECTIVE: . . . HEENT: No dysmorphic features, large right parietal cephalohematoma, anterior fontanel elevated, pulsatile. Sutures minimally displayed. OFC 37 cm. Pulmonary: Breath sounds equal bilaterally. Lung fields clear to auscultation . . . . . Neurologic: Mental status: Infant somnolent (however the infant has received two doses of Ativan and loading dose of Phenobarbital). Cranial nerves: Pupils equal, round, and reactive to light. Infant attempted to squeeze eyes shut in response to light stimulus. Deep tendon reflexes 2+ in the upper and lower extremities. Motor: Minimal spontaneous movement of the extremities upon stimulation. With cotton tip applicator the infant demonstrated the ability to flex arms against gravity. Withdrew lower extremities. IMPRESSION: Neonatal seizures. Cerebellar hematoma, subarachnoid hemorrhage, and intraparenchymal hemorrhage. Obstructive Hydrocephalus due to cerebellar hematoma. RECOMMENDATIONS: Follow OFC measurements on a daily basis. Carefully monitor infant for symptoms of Cushing's triad. Repeat CT of the brain in 24 hours. Maintain Phenobarbital on minimal maintenance dosing 3 mg/kg/day. Electroencephalogram on Monday. Should Phenobarbital fail, consider adjunctive Fosphenytoin. During the course of his admission at Shands, Daniel underwent multiple radiological studies, with the last study, a cerebral CT, performed February 25, 2003, approximately 10 days prior to his discharge. That study, performed to evaluate for interval changes from the previous study of February 17, 2003, was read as follows: The previous study demonstrated hemorrhage in the fourth ventricle, paramesencephalic cisterns, and right cerebellum with subarachnoid blood in the right sylvian region. A large cephalohematoma over the right posterior scalp at the high convexity was also present. The current exam demonstrates expected evolutionary changes of blood products. The region of hemorrhage shows decreased density from prior in the paramesencephalic cisterns and the right cerebellum. The subarachnoid blood at the right sylvian fissure is also decreased in density. The scalp hematoma also is decreased in density. There are no new regions of hemorrhage. The ventricles remain midline. They are enlarged but unchanged from prior. Again noted is transependymal fluid migration that is similar when compared to prior study. No new regions of hemorrhage are seen. IMPRESSION: Expected evolution of blood products in the previous regions of intracranial hemorrhage and scalp hematoma. Persistent hydrocephalus that is unchanged from the prior exam. No new regions of hemorrhage are seen. On March 6, 2003, Daniel's condition was stable, and he was discharged to his parents' care. Primary diagnosis on discharge was consumptive coagulopathy (DIC), and secondary diagnoses and complications were noted as ventriculomegaly/hydrocephalus, seizures, cerebellar hemorrhage, intracranial hemorrhage, and extracranial hemorrhage. Follow-up appointments were scheduled or recommended with Pediatric Neurosurgery, Pediatric Neurology, and Daniel's pediatrician (John Hellrung, M.D.). Daniel's subsequent development Following discharge, Daniel did follow-up with Pediatric Neurosurgery, with his last visit on April 9, 2003. At that time a CT scan was performed, which showed decreased ventricular size and resolution of the intracranial hemorrhage. Pediatric Neurology recommended monitoring of head circumference, and Daniel was placed on an as needed status for return to the clinic. Following discharge, Daniel also followed-up with Pediatric Neurology, with his first visit on May 15, 2003. At that time, Daniel was examined by Paul Carney, M.D., a pediatric neurologist, who reported the results of his evaluation to Daniel's pediatrician (Dr. Hellrung), by letter of the same date, as follows: Daniel Irchai was seen in the Pediatric Neurology Clinic this morning accompanied by his parents. As you know, he is a three- month-old who had an intracranial hemorrhage at birth, as well as a large right parietal cephalohematoma. He was last seen as an inpatient during his stay in the NICU. Pediatric Neurology was initially consulted as he experienced some abnormal posturing and possible seizure activity during his first week of life. He was loaded with Phenobarbital and has been maintained on Phenobarbital routine dose since that time . . . . Since his discharge, the Irchais have not noticed any seizure activity, no episodes of loss of tone, abnormal posturing, eye deviation or tonic/clonic activity. They are very eager to see if Phenobarbital can be weaned off as they are concerned how this is impacting his development. It is for this reason that they present in clinic today. * * * Developmental History: Now at three months, Daniel is noted to be awake and alert. He has had no difficulty tolerating the Phenobarbital therapy. He smiles, he is not a fuzzy [sic] baby, no irritability noted. He does respond to mom. What mom does report is that he, if looking straight on him, Daniel will smile, coo and interact. However, if she is away from him and she calls to him no matter what method she uses, he will not turn his head to find her. He has never done this. She does report that he is trying to hold his head up, has not rolled over completely yet, he does [12] with kicking and moving all extremities equally. When placed on his stomach, he will make attempts to lift his head up but does not get it completely up, will remain with his cheeks to the side, does appear to bring his knees up to try to move and will attempt to push up lifting the chest but does not completely make it. His appetite is good, he is breast-fed. He does not have any problems with choking, spitting up, drooling or controlling his secretions. * * * Review of Systems: Negative for nausea, vomiting, diarrhea, no fever, no seizures noted, no change in tone, no altered level of consciousness, staring or deviations of the eyes and generalized tonic/clonic activity. Appetite is good. He is breast- fed only, has been growing well. No recent colds, no past infections. Physical Exam: On exam today, . . . height was 61.5 cm, weight was 6.11 kg, head circumference 39.5 cm. Today he was plotted out compared to birth at two months and at three months and he is following a nice curve right below the 50th percentile for age . . . . Neurologically, Daniel was awake and alert. He had a social smile, would seem to track but would not turn his head to voice. He was examined initially supine. Anterior fontanel open, flat, soft. Face was symmetric. His tongue was midline, palate was symmetric. He had a good suck. Pupils were equal, round and reactive to light with accommodation. A red reflex was noted on funduscopic exam. He did have moderate head lag when raised to the seated position. He had strong finger grasps bilaterally. Supine, he was moving all extremities vigorously. Reflexes were 2+ on bilateral upper extremities, 3+ bilateral lower extremities but he did have a plantar grasp when toes were downgoing. He had a positive Moro. He did have decreased central tone, increased ventral suspension but otherwise had a nonfocal exam. No clonus was noted, no tremor was noted. * * * Plan: Today we have spent a great deal of time with the Irchais going over all the scans that have been done, his head plot and his neurological exam of today. We feel optimistic that Daniel will do well overall. We have reviewed the EEG that was completed as an inpatient with them. In light of the fact that he has not had any other further clinical events and has continued to make some strides despite having some of the motor that we are noting today, we feel it is reasonable to begin a slow Phenobarbital taper. It may be that the hypotonic features we are seen in his exam may be related to Phenobarbital therapy. We have given them instructions to wean by half a cc every week until he is off, this will take approximately seven weeks. If after his Phenobarbital has been tapered to off, Daniel continues to show some hypotonicity, it would be reasonable to start occupational and physical therapy at that time. We would like him to have a followup head MRI to be completed in the next three to four months to give them a better idea as to if any scarring or atrophy remains from his initial bleed . . . . As requested, Daniel had a follow-up head MRI on September 8, 2003. The results of that study were reported by the attending radiologist, as follows: Encephalomalacic changes with almost complete destruction of the upper vermis is present. Old blood products are present as well at this site which are also seen on diffusion weighted imaging as dark signal in the poster fossa. There is no evidence of vascular malformations. Otherwise, the brain density is appropriate for a young child. Brain formation is normal. Myelination is appropriate for age with evidence of myelination in corticospinal tracts, visual pathways and corpus callosum. Ventricular size and sulcal pattern are within normal limits. No evidence of acute hemorrhage. IMPRESSION: Encephalomalacia changes with old blood products in the posterior fossa as above. No evidence of vascular malformation. Daniel's next evaluation by Dr. Carney, and his most recent, was on September 18, 2003. Dr. Carney reported the results of that evaluation, as follows: I had the pleasure of seeing Daniel today in the Pediatric Neurology on followup. As you know, he is a 7-month-old boy who has a history of neonatal seizures secondary to a cerebellar hematoma with intracranial bleed and cephalohematoma[.] [W]hen I last saw him on 05/18/03 [sic] . . . [h]e was doing quite well. He had no recurrent seizures at that time therefore, the Phenobarbital was tapered and discontinued. At today's visit, his parents report that he is doing quite well. He has good head control if sitting with minimal support. His tracking laterally and vertically to mom's voice, dad's voice as well as to face and object recognition. He is cooing. They are concerned that he has had some head bobbing which on further questioning sounds like mild titubation. He has had no developmental regression. No seizures since I last saw him. He underwent a followup brain MRI which demonstrated a superior vermis encephalomalacic abnormality secondary to his neonatal intracranial hemorrhage. Ventricular sizes were not dilated nor were the basilar cisterns, and the third and fourth ventricles appeared open and patent. There were no recurrent bleeds, nor was there brain atrophy or cerebellar hemispheric atrophy. * * * Physical Examination: Weight 8.19 kg, head circumference 43 cm (50th percentile), height 73 cm, . . . . He was awake, alert, tracked laterally to moving object. He had good neck tone. When placed on his abdomen, he lifted his head and held it in a erect position for more than two minutes. He would sit with minimal support. He had no axial slippage. Resistance to passive manipulation was normal in both upper and lower extremities. Deep tendon reflexes were 2+ at the biceps, triceps, brachioradialis, knees and ankles. Optic discs were pink and flat. I saw no retinal abnormalities. No drooling. Tongue at the midline, palate rose symmetrically, cooed throughout the examination. General physical examination no adenopathy or thyromegaly. Chest clear to auscultation. Heart sounds were regular rate and rhythm without murmurs. Abdomen soft without signs of hepatosplenomegaly, abdominal masses, no skin rashes were noted. Genitalia - normal male. Assessment and Plan: A 7-month-old boy with neonatal cerebellar hemorrhage as outlined above and post hemorrhage encephalomalacic defect. Developmentally he has made good progress. For the most part, he is on track with the exception of some head titubation. His parents are very much interested in pursuing physical therapy and therefore, I am recommending this at this time. He will have a followup brain MRI in six months and will see me in clinic thereafter . . . . Following discharge from Shands, Daniel received routine care from his pediatrician, Dr. Hellrung, with his first visit on March 10, 2003, at 3 weeks of age, and his last visit on May 12, 2004, at 15 months of age. Dr. Hellrung's records do not reveal any significant findings or observations that are pertinent to this case, but do document, as noted by Petitioners in their proposed final order, "tremor of head," and that as of May 12, 2004, Daniel showed evidence of a delay in gross motor development, since he did not yet "Walk[] alone, stoop[], recover[]," and a delay in language development, since he was "not [yet] talking." On June 2, 2004, following the filing of the claim in this case, Daniel was, at Respondent's request, examined by Michael Duchowny, M.D., a pediatric neurologist. Dr. Duchowny reported the results of his neurologic examination, as well as his review of Daniel's medical records, as follows: I evaluated Daniel Irchai on June 02, 2004. The evaluation was performed at Miami Children's Hospital. Both parents were in attendance and supplied historical information. HISTORY ACCORDING TO MR. AND MRS. IRCHAI: Daniel is a 15-month-old boy who suffers from developmental delay. The parents indicated that Daniel is not yet walking or talking and has very poor balance. He has just started to stand while holding on but seems "wobbly." He is unable to walk independently. They note no present changes in his muscle tone, although his mother felt that he may have been excessively loose several months ago. Parents also indicated that Daniel's head may shake in a side-to- side manner when he is in the sitting position. This is particularly evident when he is reaching. They believe that these movements have diminished somewhat over the last several months. * * * Daniel is sociable and plays well with his older brother. He does not drool except while teething. There has been no behavioral regression. Daniel has recently been evaluated for physical therapy at the "Kids on the Move" Program. He has not yet been scheduled for a routine physical therapy exercise regime. Daniel's health is otherwise good. His vision is normal, although the left eye will occasionally "move up under the eyelid" on directed right gaze.[13] Daniel's hearing is good and his appetite has been stable. He is on no intercurrent medications but did take phenobarbital for the first five-months of life. * * * Daniel rolled over at four-months and sat at eight-months. He began standing with support at thirteen-months but cannot walk independently or talk in words. He is not yet toilet trained. Daniel is fully immunized and has no known allergies. He has never undergone surgery or been hospitalized after the neonatal period. * * * PHYSICAL EXAMINATION reveals an alert, well- developed and well-nourished 15-month-old boy. Daniel weighs 23 pounds. The hair is blond and of normal texture. The eyes are blue. There is a nevus flammeus below the occipital hairline. There are no other cutaneous markings and no dysmorphic features. The head circumference measures 46.1 centimeters, which approximates the 20th percentile for age. The fontanels are closed. There are no cranial or facial anomalies or asymmetries. The neck is supple without masses, thyromegaly or adenopathy. The cardiovascular examination reveals normal heart sounds and the lung fields are clear. The abdomen is soft and non-tender. There is no palpable organomegaly. Peripheral pulses are 2+ and symmetric. NEUROLOGICAL EXAMINATION reveals an initially quiet infant sitting in his father's lap. However, Daniel is quite fearful and defensive and began crying inconsolably when approached. He did not speak in words at anytime during the evaluation but at least initially followed simple commands. Cranial nerve examination reveals full visual fields to direct confrontation testing and normal ocular fundi, which were seen only briefly. The pupils are 3 mm and react briskly to direct and consensually presented light. No facial asymmetries. The tongue and palate move well. The uvula is midline. Motor examination reveals mild generalized hypotonia for both axial and appendicular musculature. There were no tremors or evidence of adventitious movements. Daniel's head control was stable. Daniel is able to stand with minimal support but is unable to take steps independently. He did not fall. The deep tendon reflexes are slightly exaggerated at 2-3+ bilaterally. Plantar responses are downgoing. There are no pathological reflexes. Sensory examination is intact to withdrawal of all extremities to stimulation. Neurovascular examination reveals no cervical, cranial, or ocular bruits and no temperature or pulse asymmetries. In SUMMARY, Daniel's neurologic examination reveals very slight delays in motor and language development with excessive behavioral irritability. He demonstrates no findings to suggest structural brain damage and his seizures are in complete remission. A review of Daniel's medical records further indicates that Daniel's postnatal circumstances did not result from intrapartum oxygen deprivation or mechanical injury . . . . The cause and timing of Daniel's brain injury, as well as the significance of Daniel's impairment Given Dr. Duchowny's opinion that "Daniel's neurologic evaluation reveals very slight delays in motor and language development," and the absence of any contrary opinion or facts of record that would compel a contrary conclusion, it must be resolved that Daniel suffers neither a substantial mental impairment nor a substantial physical impairment, much less a permanent and substantial mental and physical impairment as required for coverage under the Plan. See Thomas v. Salvation Army, 562 So. 2d 746, 749 (Fla. 1st DCA 1990)("In evaluating medical evidence, a judge of compensation claims may not reject uncontroverted medical testimony without a reasonable explanation.") Moreover, given Dr. Duchowny's opinion "that Daniel's postnatal circumstances did not result from intrapartum oxygen deprivation or mechanical injury," and the absence of any contrary opinion or facts of record that would compel a contrary conclusion, it must be resolved that the proof fails to support the conclusion that Daniel's deficits resulted from a brain injury that occurred during labor, delivery, or resuscitation, as opposed to some other etiology (i.e.: the bleeding he experienced postdelivery). See Thomas v. Salvation Army, supra; Wausau Insurance Company v. Tillman, 765 So. 2d 123, 124 (Fla. 1st DCA 2000)("Because the medical conditions which the claimant alleged had resulted from the workplace incident were not readily observable, he was obliged to present expert medical evidence establishing that causal connection."); Nagy v. Florida Birth-Related Neurological Injury Compensation Association, 813 So. 2d 155, 160 (Fla. 4th DCA 2002)("[T]he oxygen deprivation or mechanical injury to the brain must take place during labor or delivery, or immediately afterward . . . . The fact that a brain injury from oxygen deprivation could be traced back to a mechanical injury outside the brain resulting in subgaleal hemorrhaging does not satisfy the requirement that the oxygen deprivation or mechanical injury to the brain occur during labor or delivery.") Consequently, the proof failed to support the conclusion that, more likely than not, Daniel suffered a "birth- related neurological injury," as defined by the Plan.
The Issue The issue in this case is whether Kayla Mackenzie Stowers sustained a birth-related neurological injury.
Findings Of Fact Tatiana C. Stowers and Robert M. Stowers are the natural parents of Kayla Mackenzie Stowers, a minor. Kayla was born a live infant on October 12, 2009, at Orange Park Medical Center, a licensed hospital located in Orange Park Florida. Eric J. Edelenbos, M.D., provided obstetric services at the birth of Kayla, and at all times material to this proceeding, was a “participating physician” as defined in section 766.302(7), Florida Statutes. Kayla weighed 3,078 grams at birth. On October 12, 2009, Mrs. Stowers, who was at full term, was admitted to Orange Park Medical Center at 6:28 a.m., for induction of labor. Her prenatal course had been uneventful. The baby?s baseline fetal heart rate on admission was 150 bpm, and the fetal heart rate monitor did not show any fetal distress during labor or delivery. At 8:05 a.m., Pitocin was administered to augment Mrs. Stowers? labor. During her labor, the dosage of Pitocin was increased. At 1:48 p.m., Dr. Edelenbos ruptured Mrs. Stowers? membranes, and the medical records indicate that the amniotic fluid was clear and odorless. At 9:40 p.m., Mrs. Stowers delivered Kayla by normal spontaneous vaginal delivery. At birth, Kayla?s mouth and nose were suctioned, but no other resuscitative measures were needed or administered in the delivery room. No complications were noted at her birth, and she was in stable condition. Kayla?s Apgar scores at one and five minutes were eight and nine respectively. At 10:30 p.m., Kayla was noted to have respiratory distress. Her left nasal passage was tight and her right nare was patent. She was transferred to the hospital?s neonatal intensive care unit. On October 13, 2009, at 12:05 a.m., Kayla was placed on a nasal cannula and an IV was started. Antibiotics were given at 12:20 p.m., and Neo-Synephrine was administered for nasal stuffiness. By 3:45 p.m., on October 13, 2009, Kayla had increased retractions and grunting and was placed on neonatal CPAP at 100% oxygen. During the evening of October 13, 2009, Kayla experienced two apneic episodes with jerking movements of her arms and leg. On October 14, 2009, Kayla was on CPAP for four hours and then intubated due to the apneic episodes the previous evening. A chest X-ray taken of Kayla on October 13, 2009, was within normal limits. On October 14, 2009, Kayla had a normal neonatal head ultrasound. On October 15, 2009, it was noted that Kayla had not experienced any abnormal movements for 24 hours. At 6:00 p.m., on October 17, 2009, Kayla experienced periodic episodes of jerking of hands and legs, in addition to the arching of her back. On October 18, 2009, Kayla had jerky movements of all extremities, including her eyes rolling back. The movements stopped with restraint, but were not typical seizure-like movements. On October 19, 2009, due to suspected seizures, respiratory distress, and suspected sepsis, Kayla was transferred from Orange Park Medical Center to Wolfson Children?s Hospital for further workup. An EEG performed on Kayla on October 20, 2009, was within normal limits. A follow-up video EEG on November 4, 2009, was normal. An MRI was done on Kayla on October 21, 2009, and the followings findings were reported: Moderate image degradation secondary to patient?s motions. Normal variant cavum septus pellucidum and cavas vergae. Prominent extra-axial fluid at the anterior aspect of both middle fossae, and with „apparent? suboptimal opoerculation of the Sylvian fissures ? clinical signicance. Followup US may be helpful for further evaluation. Remainder of the examination appears otherwise unremarkable. Kayla?s attending physician at Wolfson Children?s Hospital indicated in her discharge summary dated November 10, 2009, that the MRI was normal. On December 9, 2009, Kayla was taken to the emergency room at Wolfson Children?s Hospital. While in the emergency room, Kayla experienced apneic episodes that required intubation. She was admitted to Wolfson Children?s Hospital. While admitted to Wolfson Children's Hospital, Kayla had abnormal movements that were nonspecific and not due to seizures. Kayla was discharged on December 22, 2009. In his discharge summary, Clifford David, M.D., summarized the hospital course as it related to the seizure-like activities. Neurology-wise, the patient was again worked up for this possible seizure-like activity, which was possibly due to reflux. This workup included another EEG and MRI. The CT of the head that was done on admission was reported as positive for a remote area of ischemia involving the basal ganglia but repeat MRI on admission showed no area of acute ischemia. The patient was witnessed to have back arching and head extension with some clenching of the arms and chest, again unsure whether this was seizure versus reflux versus obstructive airway. Neurology examined the patient and EEG showed no epileptiform discharges although was limited secondary to movement artifact. The repeat MRI referenced in Dr. David?s discharge summary was done on December 12, 2009. The findings of this MRI indicated that there was no acute ischemic event. Respondent retained Donald C. Willis, M.D., to review the medical records for Kayla. Dr. Willis reviewed the fetal heart rates of Kayla as recorded by the fetal heart rate monitor during labor. It is Dr. Willis? opinion that the fetal heart rate monitor did not show any fetal distress during labor. On the issue of whether there was an obstetrical event which resulted in loss of oxygen or mechanical trauma to Kayla during labor or delivery, Dr. Willis opined: In summary, there was no fetal distress during labor. The baby was not in distress at birth. Apgar scores were 8/9. Immediately after delivery, the baby was placed on the mother?s abdomen for bonding. The newborn course was complicated by a complex history of apnea episodes, respiratory distress and possible seizures. EEG?s and MRI studies were normal. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby?s brain during labor or delivery. Raymond J. Fernandez, M.D., a pediatric neurologist, reviewed Kayla?s medical records and examined Kayla on April 30, 2013. He opined as follows: There is ample evidence for substantial mental and motor impairment, but this is of unknown etiology. There is no evidence in the medical record for oxygen deprivation or mechanical injury of brain or spinal cord during labor, delivery, or the immediate post delivery period that explains Kayla?s substantial and global impairment. Petitioners have presented no expert opinions that refute the opinions of Dr. Willis and Dr. Fernandez. The opinions of Dr. Willis and Dr. Fernandez that Kayla?s mental and motor impairments are not due to oxygen deprivation or mechanical injury of the brain or spinal cord during labor, delivery, or the immediate post delivery period are credited.
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."
Findings Of Fact Tobias was born on May 3, 2019, at Memorial located in Pembroke Pines, Florida. The Petition alleges that Suzette M. Rodriguez, M.D., was the medical professional who participated in Tobias's birth. No evidence was presented to the ALJ establishing whether Dr. Rodriguez was a "participating physician" under the Plan at the time Tobias was born. See §§ 766.302(7) and 766.314(4), Fla. Stat. Upon receiving the Petition, NICA retained Donald Willis, M.D., a board-certified obstetrician/gynecologist specializing in maternal-fetal medicine, as well as Michael S. Duchowny, M.D., a pediatric neurologist, to review Tobias's medical records and condition. NICA sought to determine whether Tobias suffered a "birth-related neurological injury" as defined in section 766.302(2). Specifically, NICA requested its medical consultants opine whether Tobias experienced an injury to the brain or spinal cord caused by oxygen deprivation or mechanical injury which occurred in the course of labor, delivery, or resuscitation in the immediate postdelivery period. And, if so, whether this injury rendered Tobias permanently and substantially mentally and physically impaired. Dr. Willis reviewed Tobias's medical records and opined, within a reasonable degree of medical probability: The maternal history of decreased fetal movement prior to delivery and an abnormal [fetal heart rate] tracing for admission with no acidosis on the initial blood gas studies would be most consistent with a stroke (brain injury) occurring prior to birth. There was no obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby's brain during labor or delivery. The baby suffered a stroke due to an occluded right carotid artery. It appears this event occurred prior to delivery. The mother was not in labor. Dr. Duchowny also reviewed Tobias's medical records, as well as personally examined Tobias (via Zoom video conference) on December 22, 2020. Dr. Duchowny noted that: Tobias was diagnosed with cerebral palsy at age 1 year. He has extremely limited motor functions although his left hand is better than his right. He moves all limbs but none are functional. * * * Tobias had seizures in the NICU and remains on anti-seizure medications. He was formerly suspected of having infantile spasms but his EEG did not reveal hypsarrhythmia. * * * Tobias has not encountered respiratory difficulties or pneumonia. He has not been hospitalized since birth. His head has grown normally. * * * In summary, Tobias's examination reveals findings consistent with a substantial mental and motor impairment. He has four-limb spasticity, greater on the right, axial hypotonia, generalized hyper- reflexia with pathological reflexes and absent verbal communication. * * * A review of Tobias's medical records reveals that he was born at Memorial West Hospital at 38 4/7 week's gestation. His mother had noted decreased fetal movement the day before admission and presented for evaluation. Following a non- reassuring fetal heart rate assessment Tobias was delivered by Caesarian section. He weighed 2.87 kg. at birth and had Apgar scores of 4, 5, and 9 at 1, 5 and 10 minutes of life. * * * Seizures were noted on the first day of life and treated with Keppra and phenobarbital. Tobias was discharged from the NICU after two weeks. * * * An MRI scan of the brain obtained on May 4th (DOL # 1) revealed diffuse [Hypoxic Ischemic Encephalopathy] findings involving both cerebral hemispheres in the right and left anterior and middle cerebral artery and the right internal carotid territories. … Follow-up MR imaging revealed the presence of a thrombus in the right common and internal carotid arteries with decreased flow in the right middle cerebral artery and stenosis of the left middle cerebral artery with retrograde perfusion of the right internal carotid artery. Following his independent medical examination, Dr. Duchowny opined, within a reasonable degree of medical probability, that, "Despite Tobias's substantial delays, a review of the medical records reveals that his deficits were likely acquired prior to birth and were not due to mechanical injury or oxygen deprivation during labor, delivery, or the post-delivery period." Therefore, Dr. Duchowny concluded: "I am not recommending that Tobias be considered for inclusion into the NICA program." A review of the records filed in this matter reveals no contrary evidence to dispute the findings and opinions of Dr. Willis and Dr. Duchowny. Their opinions are credible and persuasive.
Findings Of Fact Neha was born on May 15, 2012, at Broward General Medical Center, located in Fort Lauderdale, Florida. Neha weighed six pounds nine ounces at birth. NICA retained Michael S. Duchowny, M.D., as its medical expert in pediatric neurology. Dr. Duchowny examined Neha on March 20, 2013, and reviewed her medical records. In an affidavit dated April 24, 2013, Dr. Duchowny opined as follows: Neha’s neurological examination is significant only for a mild degree of hypontia coupled with very slight motor development delay. In other regards, she seems to be developing quite well and I suspect that her language development will progress on schedule. There are no focal or lateralizing findings to suggest structural brain damage. A review of medical records reveals that Neha was born by stat cesarean section at Broward General Hospital due to fetal bradycardia. She was delivered with a full body nuchal cord and a true knot that was removed at birth. There was evidence of severe metabolic acidosis-arterial blood gases drawn 11 minutes after birth revealed a pH of 6.66, PC02 of 162, P02 of 11, and base excess of -32. These values were improved on a repeat series drawn at 12:27 PM. Thick meconium was suctioned below the vocal cords and Neha was diagnosed with meconium aspiration syndrome. Seizures occurred several after birth and were treated with phenobarbital and phenytoin. As previously stated by the family, Neha was immediately enrolled in a general hypothermia protocol. Of significance, a brain ultrasound exam obtained on May 15 at 6:46 PM, was normal and an MRI scan of the brain obtained on May 23 (DOL #8) was also within normal limits. Neha’s examination today does not reveal either a substantial mental or motor impairment, findings are consistent with the lack of significant MRI findings. I believe that the hypothermia protocol in all likelihood was neuro-protective and more likely than not, contributed to Neha’s positive outcome. Given Neha’s favorable outcome, I believe that she should not be considered for inclusion within the NICA program. As such, it is my opinion that Neha Kannikal is not permanently and substantially mentally impaired nor is she permanently and substantially physically impaired due to oxygen deprivation or mechanical injury occurring during the course of labor, delivery or the immediate post-delivery period in the hospital during the birth of Neha Kannikal. A review of the file does not show any opinion contrary to Dr. Duchowny's opinion that Neha does not have a substantial and permanent mental and physical impairment due to lack of oxygen or mechanical trauma is credited.
Findings Of Fact Elaina was born on July 23, 2018, at St. Vincent’s Hospital, located in Duval County, Florida. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Elaina. In a medical report dated August 13, 2020, Dr. Willis summarized his findings and opined, in pertinent part, as follows: In summary, pregnancy was essentially uncomplicated. Spontaneous vaginal birth resulted in a healthy newborn with Apgar scores of 8/9. The newborn hospital course was uncomplicated. MRI at about one year of age showed cerebral volume loss, consistent with prior brain injury. The brain injury was apparently not due to birth related oxygen deprivation or trauma. As such, it is my opinion that there was no apparent obstetrical event that resulted in oxygen deprivation and or mechanical trauma to the brain or spinal cord during labor, delivery or in the immediate post-delivery period. NICA retained Raj D. Sheth, M.D. (Dr. Sheth), a medical expert specializing in pediatric neurology, to examine Elaina and to review her medical records. Dr. Sheth examined Elaina on June 17, 2020. In a medical report dated June 17, 2020, Dr. Sheth summarized his examination of Elaina and opined, in pertinent part, as follows: Elaina Howe does suffer from substantial physical impairment and substantial mental impairment as manifest by delays in gross motor, and fine motor, language and personal social skills. Elaina Howe mental and physical impairments are likely to be permanent although there is likely to be some improvement with time. The mental and physical impairments are not consistent with an injury to the brain or spinal cord acquired due to oxygen deprivation or mechanical injury occurring during labor and delivery or immediate post delivery period. The permanent and substantial impairments from the records provided and this evaluation do not appear to have occurred during labor, delivery or the immediate post-delivery period. NICA filed a Supplemental Affidavit of Dr. Willis on December 21, 2020, in which he offered an opinion on the fetal heart tracing records submitted by Petitioners. Dr. Willis opined as follows: The FHR tracing during labor was reassuring (no distress), consistent with my previous opinion, dated 6/17/20, that there was no apparent obstetrical event that resulted in oxygen deprivation and or mechanical trauma to the brain or spinal cord during labor, delivery or in the immediate post delivery period. The Opinions se[t] forth in my Affidavit executed July 21, 2020 remain the same and are not modified by my review of the additional medical records as indicated herein. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Willis that it is unlikely that any significant oxygen deprivation occurred prior to the birth of Elaina. Dr. Willis’s opinion is credited. There are no expert opinions filed that are contrary to Dr. Sheth’s opinion that Elaina should not be considered for inclusion in the NICA program. Dr. Sheth’s opinion is credited. Petitioners have failed to respond to the Motion or the undersigned’s Second Order to Show Cause.
Findings Of Fact 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.
