The Issue At issue in this proceeding is whether Jonathan Trujillo, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Jonathan Trujillo (Jonathan) is the natural son of Odalis Merida and Antonio Trujillo. He was born a live infant on December 31, 1993, at Jackson Memorial Hospital, a teaching hospital located in Miami, Dade County, Florida, and his birth weight was in excess of 2500 grams. The physicians providing obstetrical services during the birth of Jonathan were Doctors Oliva and McGare, resident physicians in an approved training program, who were supervised by Gene Burkett, M.D., a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan (the "Plan"). Consequently, each physician who provided obstetrical services during the birth of Jonathan was a "participating physician" in the Plan. Sections 766.302(7) and 766.314(4)(c), Florida Statutes. The birth of Jonathan Trujillo At or about 5:20 p.m., December 31, 1993, Odalis Merida (Ms. Merida) was admitted to Jackson Memorial Hospital in active labor. Notably, Ms. Merida's prenatal course had been complicated by the development of Class B gestational diabetes, requiring insulin during the course of her pregnancy, and the development of severe preeclampsia, characterized by hypertension. Consequently, Ms. Merida's pregnancy was rated high risk. To address Ms. Merida's diabetes during labor and delivery, she was maintained on drip insulin, and to address her hypertension, she was administered magnesium sulfate. Ms. Merida's condition and the substances administered to address her condition, although apparently necessary and appropriate, were not without risk or side effect to the fetus. Notably, magnesium sulfate is a muscle relaxant which can induce "floppiness" in a new born, as well as respiratory distress. 1/ The presence of maternal diabetes portends the risk of infantile hypoglycemia, which occurred in the instant case. A clinical symptom of hypoglycemia is "floppiness" in the new born, which may be exaggerated when, as here, it is found in conjunction with ploycythemia, discussed infra. Upon admission, Jonathan was at term, with a gestational age of 41 weeks, and fetal heart monitoring, commenced at or about 5:25 p.m., revealed good fetal heart tone. A physical examination at 6:00 p.m. noted the cervix to be at 7 centimeters, effacement complete, and the fetus at station 0. Contractions were regular at 2 minutes, and when the membrane was ruptured clear amniotic fluid was observed. Ms. Merida progressed through labor without incident until approximately 8:45 p.m., following the administration of an epidural anesthesia, when late decelerations of the fetal heart beat with bradycardia were noted, as a consequence of epidural hypertension. More specifically, Ms. Merida's blood pressure was observed to drop from a base line rate of 200/150 to 98/45, and a few late decelerations of the infant's heart rate were observed from a baseline rate of 120 to 130 beats per minute to 80 beats per minute. Ms. Merida was repositioned to her left side, the infant's heart rate promptly recovered, and no further unusual incidents were observed during the course of her labor or delivery. Given the limited duration and isolated nature of the late decelerations and bradycardia, it was the opinion of the physicians who testified in this proceeding that such anomaly did not adversely affect the infant's oxygenation or, stated differently, did not result in a hypoxic/ischemic insult to the infant's brain. Such opinions are credited. At 9:40 p.m., December 31, 1993, Ms. Merida, as she had with her first child, spontaneously delivered Jonathan vaginally, without apparent complication. Notably, Jonathan was vigorous on delivery, breathed spontaneously, did not require resuscitation, and his apgar scores were 9 at one minute, five minutes and ten minutes. In all, Jonathan's presentation was reflective of a healthy, vigorous infant. 2/ Jonathan was admitted to the newborn nursery at 10:00 p.m. Physical assessment upon admission revealed a large infant, at 4040 grams, with a large head (above the 90th percentile), who was crying spontaneously, alert, pink in color, but with a "slight floppiness" in the extremities. Jonathan was noted to breath spontaneously, without flaring or grunting; heart rate was noted at 160 beats per minute, with regular rhythm; fontanel were soft and flat; and reflexes were present. In brief, Jonathan's presentation in the newborn nursery was that of a healthy, vigorous infant, with the only negative observation being a "slight floppiness" in his extremities. Such "floppiness" was, however, more likely than not, related to the magnesium sulfate administered to Ms. Merida during labor and delivery, the hypoglycemia Jonathan was subsequently diagnosed to have acquired, or a combination of the two, and does not detract from the conclusion that Jonathan had no apparent signs of distress at birth. Later in the day, following testing, Jonathan was diagnosed with moderate to severe hypoglycemia, polycythemia, and moderate thrombocytopenia. Such conditions, singularly, or in combination, placed the infant at risk. Hypoglycemia, low blood sugar, may place the infant at risk of seizures and, pertinent to this case, resultant brain hemorrhage. Here, the moderate to severe hypoglycemia that Jonathan suffered was apparently recurrent, although it did resolve over time, and was addressed each time it presented through the administration of glucose. Polycythemia is a disorder whereby the number of red blood cells are abnormally high, making the blood thicker (hyperviscous) than normal. Apparently, brain hemorrhage is often related to decreased blood flow on the venus side of the brain, and where the blood is hyperviscous it could help or contribute to a brain hemorrhage. Here, with a hematocrit of 64, Jonathan's condition met the definition of polycythemia, which is a hematocrit over 60; however, such condition was not, or was not shown to be, significant in the instant case. Thrombocytopenia is a disorder resulting in an abnormally low platelet count which could affect clotting and therefore predispose the infant to bleeding through, among other things, trauma. Here, Jonathan's thrombocytopenia, more likely than not isoimmune thrombocytopenia, was considered moderate, as opposed to severe, and serial testing reported his platelet count as follows for the date and time indicated: DATE TIME 3/ PLATELET COUNT 1/1/94 07:00 Platelet estimate 40,000-80,000 1/2/94 03:47 Platelet estimate 80,000-100,000 1/3/94 07:57 Platelet estimate 40,000-80,000 1/3/94 15:08 Platelet estimate 40,000-80,000 1/4/94 05:04 Platelet count 49,000 1/5/94 06:46 Platelet estimate 40,000-80,000 1/6/94 12:50 Platelet estimate 40,000-80,000 1/8/94 21:12 Platelet count 182,000 1/10/94 03:52 Platelet count 263,000 1/12/94 06:00 Platelet count 357,000 The normal platelet count for newborns, as with adults, is 150,000 to 400,000, and, as may be observed from the serial testing, Jonathan's thrombocytopenia resolved over time. While at risk, Jonathan's neonatal course in the nursery was uneventful until 26 hours of life when he was noted to have suffered a generalized seizure characterized by cyanosis, severe bradycardia (heart beat in the range of 40 beats per minute), and respiratory arrest (apnea), requiring intubation. At or about 1:00 a.m., January 1, 1994, Jonathan was transferred to the neonatal intensive care unit, where he was maintained on positive ventilation until approximately January 6, 1994. Examination, through EEG's and CT and MRI scans of the brain, revealed that Jonathan had suffered an intraventricular hemorrhage, Grade IV, characterized by a massive bleed, with dilation of the ventricles. 4/ Thereafter residual hypodensity of the white matter of the brain was observed, consistent with degeneration of the hemorrhage and, ultimately, hypodensity compatable with evolving encephalomalacia (swelling of the brain.) Subsequently, on February 2, 1994, developing hydrocephalus required the placement of an intraventricular shunt to relieve intracranial pressure. Currently, in the opinions of Dr. Robert Roth and Dr. Michael Duchowny, whose opinions are credited, Jonathan is permanently and substantially mentally and physically impaired. Such impairment is evidenced by, inter alia, cortical blindness, hypotonia and, more likely than not, mental retardation. It is further the opinion of such physicians, which is again credited, that the cause of Jonathan's neurologic impairment is the injury to the brain he suffered as a consequence of the Grade IV intraventricular hemorrhage. Given the foregoing, resolution of this claim resolves itself to an identification of the genesis of Jonathan's Grade IV intraventricular hemorrhage or, stated otherwise, whether the proof demonstrates, more likely than not, that the hemorrhage, which resulted in injury to Jonathan's brain and the ensuing neurological injuries, resulted from "oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period" in the hospital. Sections 766.302(2) and 766.309(1)(a), Florida Statutes. The cause of Jonathan's Grade IV intraventricular hemorrhage A Grade IV intraventricular hemorrhage in a term infant, such as Jonathan, is a rare occurrence, and its cause frequently cannot be identified. Notwithstanding, Jonathan did suffer such a hemorrhage, and he was shown to suffer from two conditions, isoimmune thrombocytopenia and hypoglycemia, which could offer some explanation for the hemorrhage. Here, petitioner contends that Jonathan, due to his large head, received an injury to his brain occasioned by the "mechanical" forces of labor and delivery, and that such injury resulted in a slow bleed which, because of his thrombocytopenia, progressed over the next 26 hours and ultimately manifested as a generalized seizure characterized by cyanosis, severe bradycardia and respiratory arrest. In support of such contention, petitioner offered the testimony of Robert S. Roth, M.D., a physician board certified in pediatrics and neonatal/perinatal medicine. Pertinent to this case, Dr. Roth observed that infants born with thrombocytopenia are at increased risk of suffering an intraventricular brain hemorrhage if subjected to the trauma occasioned by the mechanical forces of labor and vaginal delivery. In his opinion, Jonathan's medical records reveal a classic case of neonatal brain hemorrhage resulting from the mechanical forces of labor and vaginal delivery that occurred because of Jonathan's large head and thrombocytopenia. Those conditions, affected by the forces of labor and delivery, combined to "start the process of hemorrhage in the brain," resulting in "tissue changes and cell death and vascular pressure changes" over time, and culminating when it progressed to the "centers that control breathing," manifested by apnea or seizure- like activity that led to apnea. Notably, it was Dr. Roth's opinion that it was not Jonathan's large head alone or his thrombocytopenia alone, apparently because of its moderate nature, which occasioned the initial bleed and resulting hemorrhage but, rather, the two conditions acting in consort. There was, however, no injury to Jonathan's scalp or skull noted at delivery, nor any molding of his head consequent to the delivery. It is of further note, in evaluating Dr. Roth's opinion, that he also observed that, had Jonathan been delivered by cesarean section before the onset of labor, he would have had a "lower probability" of having a hemorrhage than had he undergone active labor and vaginal delivery. Such observation clearly implies that factors other than labor and delivery could have operated to induce Jonathan's hemorrhage. Finally, in considering Dr. Roth's opinion of progressive deterioration, it is worthy of note that, apart from the "slight floppiness" observed shortly after birth, Jonathan evidenced no symptoms of neurologic injury until 26 hours of life. As heretofore noted, the "slight floppiness" exhibited by Jonathan was reasonably attributed to the magnesium sulfate administered to Ms. Merida during labor and delivery, the hypoglycemia Jonathan was shown to have developed, or a combination of the two, as opposed to a symptom of neurologic injury. Consequently, there is no objective evidence or symptom, that one would otherwise expect to observe, to support Dr. Roth's opinion of progressive deterioration. Contrasted with the opinions of Dr. Roth, regarding the genesis of Jonathan's hemorrhage, are the opinions offered on behalf of NICA through Michael S. Duchowny, M.D., a physician board certified in pediatric neurology. Dr. Duchowny, although acknowledging that thrombocytopenia offered an increased risk of intraventricular hemorrhage to an infant through the forces of labor and delivery, was of the opinion that Jonathan's hemorrhage at 26 hours of life was a spontaneous event, unrelated to labor and delivery, and that the cause of that hemorrhage could not be identified with any reasonable degree of medical certainty or, stated differently, that any attempt to attribute a cause for Jonathan's hemorrhage was, at best, speculative. 5/ In reaching his conclusion, Dr. Duchowny observed that there was no objective evidence or symptom of trauma or oxygen deprivation at birth, as one would expect had there been a neurologic insult during the course of labor and delivery, and that there was likewise no objective evidence or symptom of neurologic injury over the course of Jonathan's first 26 hours of life, as one would expect to observe were he suffering a progressive disorder, as opined by Dr. Roth. Dr. Duchowny was further of the opinion that, although moderately thrombocytopenic, Jonathan's platelet count was not sufficiently low, a level he described as 20,000 or less, to increase the likelihood that Jonathan would suffer a bleed. Resolving the conflict between the opinions of Doctors Roth and Duchowny is not an easy or lightly undertaken effort. Each physician is eminently qualified and the genuineness of the opinions they expressed is apparent. The seriousness of the resolution is further intensified by the obvious needs of a severely impaired infant; however, while such needs are significant, it cannot be overlooked that where, as here, responsibility for the care of the infant is sought to be imposed on the Plan, the proof must be compelling that, more likely than not, the infant suffered a "birth-related neurological injury" as defined by law. In this case, the proof falls short of meeting such standard. 6/ As heretofore noted, the labor and delivery of Jonathan was essentially normal and there was no obstetrical incident or identifiable event during labor and delivery that would evidence that he had suffered a hypoxic insult, mechanical injury or traumatic event. Indeed, although Jonathan did have a large head (above the 90th percentile), there was no cephalopelvic disproportion noted, no arrest of labor, no protracted labor, and no use of forceps or vacuum extraction in delivery. Upon delivery, no apparent cranial injuries were observed, no molding of the head was noted, and Jonathan presented as a vigorous infant with normal Apgars. In summary, there was no identifiable incident during the course of labor or delivery, or thereafter during Jonathan's first 26 hours of life, evidencing oxygen deprivation, mechanical injury, or other insult, that would account for the hemorrhage he suffered. In reaching the foregoing conclusion, it has not been overlooked that an infant suffering from thrombocytopenia is at increased risk of intraventricular hemorrhage through the forces of labor and delivery. Here, however, it was not suggested or shown that Jonathan's mild thrombocytopenia would, itself, foster a hemorrhage of the nature he suffered, rather petitioner's proof suggested that his large head and thrombocytopenic condition combined, when subjected to the trauma of labor and delivery, to precipitate a bleed that slowly progressed to a Grade IV intraventricular hemorrhage or precipitated a seizure that resulted in such a hemorrhage. Given the nature of the proffer, there being no apparent complication during labor and delivery, no objective sign of head trauma at birth, no symptoms of neurologic insult at birth, and no symptom of neurologic insult over the 26 hours prior to Jonathan's acute compromise, it must be concluded, as suggested by Dr. Duchowny, that any conclusion timing the genesis of Jonathan's hemorrhage to the events of labor and delivery is not supported by reasonable medical probability but is, at best, speculative. Consequently, it must be concluded, that petitioners have failed to demonstrate that Jonathan's hemorrhage was related to trauma, oxygen deprivation or mechanical injury occurring during the course of labor and delivery, as opposed to a spontaneous event, of unknown origin, occurring at Jonathan's twenty-sixth hour of life. 7/
Findings Of Fact Jordan Gonzalez was born on May 29, 2008, at North Shore Medical Center in Miami, Florida. Jordan weighed 2,530 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Jordan and his mother. In an affidavit dated February 19, 2013, Dr. Willis opined the following within a reasonable degree of medical probability: It is my opinion that in summary, fetal abnormalities were identified by ultrasound during pregnancy. The baby was delivered by Cesarean section due to the development of fetal ascites. The mother was not in labor. The baby had several congenital abnormalities including hypoplastic lungs, single umbilical artery, ascites, dilated ventricles in the brain, agenesis of the corpus callosum and a small phallus. MRI did not identify findings suggestive of hypoxic brain injury. As such, it is my opinion that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby's brain during delivery or during resuscitation in the immediate post delivery period in the hospital. The mother was not in labor. The fetus had known abnormalities identified by ultrasound during pregnancy. It is most likely the baby's brain abnormalities are congenital and not related to oxygen deprivation at birth. Jordan was examined and evaluated by Michael Duchowny, M.D. (Dr. Duchowny), on January 30, 2013. In an affidavit dated February 27, 2013, Dr. Duchowny found the following on his examination of Jordan: It is my opinion that the findings from the examination are consistent with both a substantial mental and motor impairment. Jordan is functioning at approximately age 2-3 month level and in addition to his global development delay manifests microcephaly, dynamic hypotonia and dynamic static hypotonia with hyperreflexia and pathological reflexes. However his examination reveals multiple congenital anomalies which together with the neuroimaging findings suggest that Jordan's neurological deficits were most likely acquired prior to birth. As such, it is my opinion that there is no evidence from his postnatal course or from his present physical findings to indicate that Jordan Gonzalez sustained an hypoxic or ischemic insults in the course of labor, delivery or the immediate neonatal period. I therefore am not recommending Jordan for inclusion into the NICA program. A review of the file does not show any contrary opinions to those of Dr. Willis and Dr. Duchowny. The opinions of Dr. Willis and Dr. Duchowny that Jordan did not suffer a neurological injury due to oxygen deprivation or mechanical trauma during labor, delivery, or resuscitation in the immediate postdelivery period are credited.
The Issue At issue in this proceeding is whether Michael Chase Anwar, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary matters Lisa Anwar and Saeed Anwar are the parents and natural guardians of Michael Chase Anwar (Michael), a minor. Michael was born a live infant on September 11, 1995, at Florida Hospital, a hospital located in Orlando, Florida, and his birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Michael was Jorge Jesus Lense, M.D., who was, at all times material hereto, a participating physician in the Florida Birth-Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Mrs. Anwar's antepartum course and Michael's birth At or about 12:48 a.m., September 11,1995, Mrs. Anwar was admitted, in labor, to Florida Hospital. At the time, her estimated date of confinement was noted as September 22, 1995, and her antepartum course was without apparent complication; however, the fetus was noted to be large for gestational age. Onset of labor was noted as 11:15 p.m., September 10, 1995, with spontaneous rupture of the membranes, and clear amniotic fluid noted. Mrs. Anwar's obstetrical course from admission through Michael's delivery at 1:55 p.m., September 11, 1995, is detailed in Dr. Lense's delivery notes, as follows: The patient . . . presented with spontaneous rupture of membranes since 2315 hours on September 10, 1995. She was in active labor on admission. She progressed through labor to 8 cm dilatation at which time she had a prolonged fetal heart rate deceleration lasting approximately four minutes to fetal heart tones of 70s associated with a tetanic uterine contraction lasting approximately four minutes. This was relieved with terbutaline 0.125 mg subcutaneously and 0.125 mg intravenously. Fetal heart rate returned to normal with good variability and accelerations. She was having mild to moderate variable decelerations. She allowed labor to progress. She progressed rapidly to the anterior lip of the cervix to complete and +1 station. Because the fetal heart rate tracing was reassuring she was allowed to progress spontaneously to reach complete dilatation. However, the variable decelerations progressively worsened. She had temperature elevation of 100.5 [to 101.4]. She was begun on ampicillin 2 grams intravenously for presumed chorioamnionitis [an inflammation of female membranes]. She began pushing second stage labor. The variable decelerations worsened, and the decision was made to shorten second state of labor with vacuum assist. A vacuum was applied after the bladder was empty, complete, complete +3 station. The fetal head was delivered to complete, complete and +4 with the vacuum. However, it was difficult to maintain an adequate suction on the vacuum secondary to the thickness of the fetal hair. However, the patient was able to deliver the infant spontaneously without difficulty. Double nuchal cord was reduced. The rest of the infant was delivered without difficulty . . . The cord was doubly clamped and cut. The infant was noted to have poor respiratory effort and tone at the time of delivery. The neonatal resuscitation team and the neonatal intensive care unit neonatologists were called to the delivery. . . . At delivery Michael was intubated due to apnea (failure of the newborn infant to initiate pulmonary ventilation), and required positive pressure ventilation. Apgar scores of 2 at one minute, 3 at five minutes, and 5 at ten minutes were noted. Chord pH obtained on delivery was noted as 7.01, representing severe acidosis. The Apgar scores assigned to Michael are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, muscle tone, reflex irritability, and color, with each category being assigned a score ranging from the lowest score of 0 through a maximum score of 2. As noted, at one minute Michael's Apgar score totalled 1, with heart rate being graded at 2, and respiratory effort, muscle tone, reflex irritability, and color being graded at zero. At five minutes his Apgar score totalled 3, with heart rate being graded at 2, color being graded at 1, and respiratory effort, muscle tone, and reflex irritability being graded at zero. At ten minutes his Apgar score totalled 5, with heart rate being graded at 2, respiratory effort, reflex irritability and color being graded at 1 each, and muscle tone being graded at zero. Such scores are abnormal, and consistent with perinatal depression. Michael's course and development subsequent to delivery Following resuscitation, Michael was transferred to the neonatal intensive care unit in guarded condition. After admission, positive pressure ventilation was continued, and he was placed on ventilatory support. A blood culture, complete blood count, urine wellcogen and RPR were obtained, and Michael was started on ampicillin and gentamicin to address the risk of sepsis or infection. Possible seizure activity was noted during the first day of life, with tonic-clonic movements of all four extremities, and he was loaded with phenobarbital. An electroencephalogram was obtained and read as an abnormal neonatal recording characterized by diffuse depression of background cerebral activity; however, no electrographic seizures or lateralized epileptiform discharges were observed, and motion and electrical artifact were noted to be present. Michael was extubated the morning of September 12, 1995, following which he was noted to be "breathing spontaneously, receiving oxygen via nasal cannula." However, overnight he was noted as "quite irritable, jittery, with back arching," and required occasional sedation with Fentanyl. A head ultrasound completed on September 12, 1995, revealed the following: THERE IS A SMALL BLEED IN CHOROID PLEXUS NOTED BILATERALLY. IT COULD BE WORSE ON THE RIGHT THAN ON THE LEFT. THE VENTRICLES ARE NORMAL IN SIZE. THERE IS NO INTRAVENTRICULAR BLEED. NO OTHER ABNORMALITY. IMPRESSION: SMALL CHOROID PLEXUS BLEED NOTED BILATERALLY, WITH THE LEFT BEING MORE EXTENSIVE THAN THE RIGHT. Stated differently, the ultrasound revealed a bilateral grade one intraventricular hemorrhage (IVH). Between the afternoon of September 11, 1995, and the afternoon of September 12, 1995, Michael's hematocrit was noted to drop from 46 percent to 29 percent. Hemoglobin likewise dropped from 15.6 to 10.0. Consequently, due to his anemic condition, Michael was transfused on September 12, 1995. On September 12, 1995, Michael was examined by a consulting physician, most likely to address his neurologic condition. That examination, by Prashant M. Desai, M.D., reported the following observations, impressions, and recommendations: PHYSICAL EXAMINATION GENERAL: Weight is approximately 3.5 kg. Head circumference was 36.75 cm. Anterior fontanel is soft. The infant is lying supine in an open warmer, receiving oxygen via nasal cannula. He looks healthy, well-developed and well-hydrated. No clear dysmorphic features are noted. No apparent significant congenital skin lesions. He is sleeping comfortably. When disturbed, he becomes jittery and extremely irritable. He is difficult to console. He arches his neck and back. He keeps his hands fisted, flexes the elbows, and displays hand tremoring. BACK & SPINE: Appear normal. EXTREMITIES: There is mild stiffness of the extremities. Reflexes are brisk. He will not allow flexion of his neck, and instead, he resists it by neck arching and back arching. He will transiently open his eyes. Face is symmetric. Tongue is midline. Gag reflex is present. IMPRESSION: FULL-TERM ONE-DAY-OLD NEWBORN INFANT WITH PERINATAL DEPRESSION AND HYPOXIC-ISCHEMIC ENCEPHALOPATHY. RECENT DROP IN HEMOGLOBIN AND HEMATOCRIT MAY INDICATE INTRACRANIAL HEMORRHAGE. SUBARACHNOID HEMORRHAGE IS POSSIBLE, AND WOULD BE COMPATIBLE WITH CLINICALLY NOTED NECK AND BACK ARCHING, JITTERINESS AND EXTREME IRRITABILITY. HE HAS BEEN LOADED WITH PHENOBARBITAL AND PLACED ON MAINTENANCE PHENOBARBITAL SECONDARY TO SOME SEIZURE-LIKE ACTIVITY YESTERDAY. ELECTROENCEPHALOGRAM SHOWS DIFFUSE DEPRESSION OF BACKGROUND CEREBRAL ACTIVITY. THIS WOULD BE COMPATIBLE WITH HISTORY OF PERINATAL DEPRESSION. RECOMMENDATIONS: Head computerized axial tomography scan when feasible. Continue Phenobarbital at 4-5 mg/kg/day in two divided doses. He may require p.r.n. sedation with Fentanyl, given his irritability. Obtain a repeat electroencephalogram prior to hospital discharge. Duration of anticonvulsant treatment will depend on his hospital course. If his seizures recur and, in particular, if his extreme irritability persists, a metabolic work-up might be indicated. A CT (computerized tomography) brain scan of September 13, 1995, was read as "probably within normal limits." The scan was read and reported as follows: FINDINGS: THE DURAL VENOUS SINUSES AND THE VEIN OF GALEN ARE RELATIVELY DENSE COMPARED TO BRAIN. THIS IS PROBABLY RELATED TO THIS CHILD'S AGE AND THE COMPARATIVE LOW ATTENUATION OF THE UNMYELINATED BRAIN. THIS APPEARANCE CAN ALSO BE SEEN WITH ELEVATED HEMATOCRIT. WHILE THIS CAN ALSO BE SEEN WITH DURAL SINUS THROMBOSIS, THIS WOULD IMPLY THAT THE ENTIRE DURAL SINUS SYSTEM AS WELL AS THE VEIN OF GALEN WERE THROMBOSED. THAT IS UNLIKELY IN THIS SITUATION ESPECIALLY SINCE NO ASSOCIATED PARENCHYMAL CHANGES ARE NOTED. NO FOCAL PARENCHYMAL ATTENUATION ABNORMALITY IS NOTED. IMPRESSION: THE EXAM IS PROBABLY WITHIN NORMAL LIMITS. THE POSSIBILITY OF AN ELEVATED HEMATOCRIT IS RAISED. On September 14, 1995, Michael was noted to have an increased temperature. To further address the risk of sepsis or infection he was accorded a regimen of Vanco and Claforan for three days. Blood culture, urine, and CSF (cerebrospinal fluid) studies were reported as negative. Phenobarbital was discontinued September 16, 1995, and ampicillin and gentamicin were discontinued September 18, 1995. All intervening culture studies were reported as negative. A repeat electroencephalogram of September 20, 1995, was read as a "mildly abnormal neonatal recording due to some mild diffuse suppression of background cerebral activity." However, consistent with improvement in Michael's status, the recording was noted to be "considerably improved from [the] previous electroencephalogram performed on day 1" of life. On September 25, 1995, Michael had a second CT brain scan.1 That scan, unlike the first scan, was apparently read as abnormal, reflecting a presentation consistent with hypoxic- ischemic encephalopathy2 or, stated differently, brain injury occasioned by oxygen deprivation. (Discharge Summary for Michael Anwar, at page 2). Michael was discharged at 4:45 p.m., September 25, 1995, to the care of his parents.3 At the time, he was noted to exhibit "diffusely poor tone" ("infant limp, floppy tone"), and "little spontaneous movement" or, stated differently, "little spontaneous arousal." However, positive suck, positive blink, and positive gag were present, and Michael was free of seizure activity. Discharge diagnosis was, as follows: DISCHARGE DIAGNOSIS: 35 weeks appropriate for gestational age male Perinatal depression Sepsis, ruled out Seizures, ruled out Hypoxic-Ischemic Encephalopathy Bilateral Grade 1 Intraventricular hemorrhage Anemia On February 27, 1998, following the filing of the claim for compensation, Michael was examined by Michael Duchowny, M.D., a board certified pediatric neurologist. Dr. Duchowny's examination revealed the following: PHYSICAL EXAMINATION reveals a small 2 1/2 year old, appropriately proportioned boy. The weight is 25 pounds. The skin is warm and moist without neurocutaneous stigmata. There are no gross dysmorphisms. No digital, skeletal or palmar abnormalities are noted. The head circumference measures 48.6 centimeters which approximates the 3rd percentile for age. There are no cranial or facial anomalies or asymmetries, and the fontanels are closed. The neck is supple without masses, thyromegaly or adenopathy and the cardiovascular, respiratory and abdominal examinations are normal. NEUROLOGIC EXAMINATION reveals an alert boy who is socially interactive and has only a few words. There is an abundant amount of babbling sounds which suggest the emergence of speech patterns. Michael is in fact able to identify all of his body parts and knows both primary and secondary colors. He is quite alert and his socialization skills are well developed. He maintains good central gaze fixation with conjugate following movements and the ocular fundi are normal. There are full and conjugate extraocular movements with blink to threat from both directions. There are no significant facial asymmetries. The tongue movements are poorly coordinated and drooling is a prominent feature. Motor examination reveals a static generalized hypotonia with a dynamic increase in tone and bilateral upper extremity posturing. Michael is grossly ataxic [uncoordinated], both for axial and appendicular musculature [both truncal stability as well as all four limbs (arms and legs)] and his gait shows marked instability and a tendency to fall in all directions. Romberg sign could not be tested. He is unable to perform alternating movement sequences and he had poor dexterity for individual finger movements. The DTR's are present and 2 to 3+ bilaterally and plantar responses are downgoing. Sensory examination is intact to withdrawal of extremities to touch and pin, and a neurovascular examination discloses no cervical, cranial or ocular bruits. There are no temperature or pulse asymmetries. IN SUMMARY: Michael's neurologic examination reveals findings consistent with ataxic cerebral palsy. I believe that his cognitive and social skills are actually quite good but [are] restricted as a result of his motor deficit. I suspect that Michael will continue to improve in the future and that he will walk independently within the next 12 to 18 months. The dispute regarding compensability Given the proof, it cannot be subject to serious debate that Michael suffered an injury or anomaly in brain development that has resulted in neurologic impairment. What remains to resolve is the cause and timing (genesis) of the event which led to Michael's anomalous brain development or, more pertinent to these proceedings, whether the proof demonstrates, more likely than not, that the anomaly Michael suffers was "caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as opposed to some other genesis. Section 766.302(2), Florida Statutes. Also at issue is whether, if such an injury occurred, Michael was rendered "permanently and substantially mentally and physically impaired." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Here, the nature and significance of Michael's impairment is dispositive of the claim, and it is unnecessary to resolve the dispute regarding the cause and timing of the event which led to Michael's anomalous brain development.4 Regarding the nature and significance of Michael's impairment, the proof demonstrates that the physical impairment he suffers may best be described as moderate, as opposed to severe, and that his physical impairment is not static, but improving. As for Michael's mental status, it has been observed to be at or near age level, and, consequently, there is no evidence of any mental impairment.5
Findings Of Fact Melina Antunes was born on August 27, 2015, at Florida Hospital, located in Orlando, Florida. Melina weighed in excess of 2,500 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Melina. In a medical report dated December 12, 2016, Dr. Willis summarized his findings and opined in pertinent part as follows: In summary, induction of labor was complicated by a spontaneous uterine rupture. The baby and placenta were expelled into the maternal abdomen. The baby was depressed at birth with low Apgar scores and a cord blood gas consistent with acidosis (pH 6.65). MRI was consistent with HIE. There was an apparent obstetrical event (uterine rupture) that resulted in loss of oxygen to the baby’s brain during labor, delivery, and continuing into the immediate post delivery period. The oxygen deprivation resulted in brain injury. NICA retained Laufey Y. Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to examine Melina and to review her medical records. Dr. Sigurdardottir examined Melina on February 15, 2017. In a medical report dated February 15, 2017, Dr. Sigurdardottir summarized her examination of Melina and opined in pertinent part as follows: Summary: Here we have a 17-month-old born after a sudden uterine rupture during active labor. The patient had neurologic depression at birth, significant acidosis with a pH of 6.6 and required active cooling as well as supportive medication for seizures in the neonatal period. She did have well documented injury on MRI but has made a remarkable recovery. Neurologic exam today, has mild abnormalities, but no standardized developmental testing is available for our review. Result as to question 1: Melina is not found to have substantial physical or mental impairment at this time. Results as to question 2: In review of available documents, Melina does have the clinical picture of an acute birth related hypoxic injury with both the clinical features of hypoxic encephalopathy and electrographic and MRI evidence to suggest hypoxic injury. Result as to question 3: The prognosis for full motor and mental recovery currently is excellent and her life expectancy is full. In light of her normal cognitive abilities and near normal neurologic exam, I do not feel that Melina should be included in the NICA program. If needed, I will be happy to answer additional questions or review further documentation of her developmental status. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Willis that there was an apparent obstetrical event that resulted in loss of oxygen to the baby's brain during labor, delivery and the post-delivery period which resulted in brain injury. Dr. Willis’ opinion is credited. There are no expert opinions filed that are contrary to Dr. Sigurdardottir’s opinion that Melina does not have a substantial physical or mental impairment. Dr. Sigurdardottir’s opinion is credited.
Findings Of Fact Jamal White was born on August 19, 2010, at St. Joseph Women and Children's Hospital in Tampa, Florida. Jamal weighed 3,530 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Jamal and his mother. In an affidavit dated February 22, 2013, Dr. Willis opined the following within a reasonable degree of medical probability: In summary, delivery was complicated by a shoulder dystocia. Cord blood pH was within normal limits with pH of 7.08. The baby suffered a brachial plexus injury. Hospital course was otherwise normal. Labor was complicated by a shoulder dystocia that resulted in a difficult delivery and a brachial plexus injury. However, the shoulder dystocia did not result in brain injury. There is no obstetrical event that resulted in oxygen deprivation or mechanical trauma to the brain or spinal cord during labor, delivery, or the immediate postdelivery period. Jamal was examined and evaluated by Raymond J. Fernandez, M.D. (Dr. Fernandez), on May 30, 2012. In an affidavit dated February 25, 2013, Dr. Fernandez found the following on his examination of Jamal: Jamal has mild weakness of his left arm, but in spite of this, he has good use of the arm, proximally and distally. The left arm weakness was due to a mechanical injury of his left brachial plexus during delivery that was complicated by shoulder dystocia. There was no evidence for substantial and permanent mental and physical impairment due to brain or spinal cord injury due to lack of oxygen or mechanical trauma. A review of the file does not show any contrary opinion, and Petitioner has no objection to the issuance of a summary final order finding that the injury is not compensable under Plan. The opinion of Dr. Willis that Jamal did not suffer a neurological injury due to oxygen deprivation or mechanical injury during labor, delivery, or resuscitation in the immediate postdelivery period is credited. The opinion of Dr. Fernandez that Jamal does not have a substantial and permanent mental and physical impairment due to lack of oxygen or mechanical trauma is credited.
Findings Of Fact Josue A. Solis was born on December 12, 2013, at Plantation General Hospital in Plantation, Florida. Josue weighed in excess of 2,500 grams at birth. NICA retained Donald C. Willis, M.D. (Dr. Willis), to review Josue’s medical records. In a medical report dated August 17, 2016, Dr. Willis made the following findings and expressed the following opinion: In summary, labor was induced at 39 weeks. There was no fetal distress during labor. The baby was delivered by spontaneous vaginal birth without complications. The baby was not depressed and had normal Apgar scores of 9/9. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post delivery period. Dr. Willis reaffirmed his ultimate opinion in an affidavit dated February 24, 2017. Dr. Willis’ opinion that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical injury to the baby’s brain during labor, delivery or the immediate post-delivery period is credited. Respondent retained Michael Duchowny, M.D. (Dr. Duchowny), a pediatric neurologist, to evaluate Josue. Dr. Duchowny reviewed Josue’s medical records and performed an Independent Medical Evaluation on him on February 1, 2017. In a medical report dated February 7, 2017, Dr. Duchowny made the following findings and summarized his evaluation as follows: IN SUMMARY Josue’s physical examination reveals evidence of hypotonia and ataxia with delayed language development. I believe his presentation is most consistent with ataxic hypotonic cerebral palsy. I believe his motor skills will improve in the future and it is unlikely that he will ultimately have a substantial motor impairment. In all likelihood, Josue will continue to have a delayed language development. Ataxic cerebral palsy is a prenatally acquired syndrome and there is no evidence from the records that Josue’s neurological difficulties were acquired in the course of labor or delivery. Furthermore, there is no support for either mechanical injury or oxygen deprivation as contributing factors. I am therefore not recommending Josue for inclusion in the NICA program. Dr. Duchowny reaffirmed his ultimate opinion in an affidavit dated February 27, 2017, in which he opined, “it is my opinion that IME and record review do not provide a basis to find that Josue’s neurological difficulties were acquired in the course of labor, delivery or resuscitation in the immediate postdelivery period. I therefore do not recommend consideration for inclusion within the NICA program.” Dr. Duchowny’s opinion that ataxic cerebral palsy is a prenatally acquired syndrome and that there was no basis found in the records or in his Independent Medical Evaluation that Josue’s neurological difficulties were acquired in the course of labor, delivery or resuscitation in the immediate post-delivery period is credited. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Willis that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post- delivery period. There are no expert opinions filed that are contrary to Dr. Duchowny’s opinion that ataxic cerebral palsy is a prenatally acquired syndrome and that there is no indication that Josue’s neurological difficulties were acquired in the course of labor, delivery or resuscitation in the immediate post- delivery period.
The Issue The issue in this case is whether Daquan T. Smith, Jr. (Daquan) suffered a birth-related injury as defined by section 766.302(2), Florida Statutes, for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan (the Plan).
Findings Of Fact Daquan was born on November 22, 2015, at Florida Hospital, 601 East Altamonte Drive, Altamonte Springs, Florida. The pregnancy, labor, and delivery of his mother, Verdale T. Robinson, were managed by employees of Florida Hospital and Dr. Norma Waite. At all times material, both Florida Hospital and Dr. Waite were active members under NICA pursuant to sections 766.302(6) and (7). Daquan was born a live infant on November 22, 2015. Daquan was a single gestation, weighing 2,730 grams at birth. Daquan was delivered by Dr. Waite, who was a NICA participating physician on November 22, 2015. Petitioners contend that Daquan suffered a birth- related neurological injury and seek compensation under the NICA Plan. Respondent contends that Daquan has not suffered a birth- related neurological injury as defined by section 766.302(2). The medical records reviewed by Dr. Willis reflect that Daquan’s mother was admitted to the hospital at 36 6/7 weeks gestational age with vomiting, pain, and blood in the urine. She was started on antibiotics for a suspected UTI and observed. Her blood pressure began to elevate, and she was transferred to Florida Hospital for high-risk consultation. Labor was induced for suspected preeclampsia. The fetal heart rate (FHR) monitor during labor was reviewed. The initial FHR pattern showed a normal baseline rate and normal FHR variability. Variable decelerations with decreased variability developed about 30 minutes prior to delivery. Daquan’s delivery was by spontaneous vaginal birth. Daquan was initially depressed with Apgar scores 5/7/9. At birth, there was no respiratory effort, but heart rate was stated to be good. Bag and Mask ventilation was started without improvement. Daquan required intubation for respiratory distress and quickly improved, allowing extubation to nasal CPAP. Daquan started crying and his muscle tone improved. At this point Daquan was transferred to the NICU. The initial blood gas was a venous gas done about 15 minutes after birth and the pH level was 7.23, with a normal base excess. The initial arterial blood gas was done 90 minutes after birth, again with a normal pH level of 7.4. Apnea and bradycardia occurred with onset of seizure activity about 14 hours after birth. Oxygen desaturations were in the ‘70s. Bag and mask ventilation was required for a short period of time, followed by nasal oxygen. Phenobarb was started to control seizure activity. Daquan’s EEG readings were abnormal, confirming seizure activity. Head Ultrasound was normal. CT scan on DOL 2 showed minimal acute intraventricular hemorrhage and a subdural hemorrhage. MRI at seven weeks showed evidence of brain injury with volume loss. At the request of NICA, Dr. Willis, who is board- certified in obstetrics and gynecology and maternal-fetal medicine, reviewed the medical records relating to Daquan’s birth. In his report dated June 21, 2017, Dr. Willis opined that, [t]here was no apparent obstetrical event that resulted in loss of oxygen to the baby's brain during labor, delivery or the immediate post delivery period. At the request of NICA, Laufey Y. Sigurdardottir, M.D., who is board-certified in neurology, reviewed Daquan’s medical records and performed an independent medical examination of Daquan on May 17, 2017. Dr. Sigurdardottir opined, in pertinent part, that: Daquan is a 17 month old with history of neonatal seizures, after induced labor for maternal hypertension and pyelonephritis. No evidence of acute hypoxic episode during active labor and blood gas within hour after birth did not indicate significant asphyxia. MRI performed at 6 weeks of age does have some findings consistent with hypoxic ischemic injury but timing is hard to determine as being within active labor and delivery. Patient has delays in his development but as he is able to walk unassisted (short distances) at 17 months and is using gestures for yes and no, I do not feel that he has established permanent substantial motor and mental disability at this time. Result of question 1 [Does the child suffer from a permanent and substantial mental and physical impairment?]: Daquan is found to have delays in motor and language development but is making progress and is walking independently at this time therefore a permanent and substantial physical and mental impairment cannot be determined at this juncture. Result of question 2 [If so, was such an impairment consistent with a neurologic injury to the brain or spinal cord acquired due to oxygen deprivation or mechanical injury? If so, is injury felt to be labor and birth related?]: In review of available documents, although having respiratory distress shortly after birth, there is no clear acute hypoxic event during labor and/or delivery, and fetal heart rate strips were benign. Laboratory tests were not indicative of an acute hypoxic injury. Neonatal seizures were seen but this does not give us a clear timeframe for timing of injury. Result as to question 3 [What is the prognosis and estimate of life expectancy?]: The prognosis for full motor and mental recovery is guarded but his life expectancy is full. Dr. Sigurdardottir's Affidavit reflects her ultimate opinion that "the IME and record review do not support a finding that Daquan suffered a 'birth-related neurological injury.'” Dr. Willis's and Dr. Sigurdardottir's opinions both support a finding that there was no injury to the brain or spinal cord of the infant caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period, which rendered the infant permanently and substantially mentally and physically impaired. Petitioners did not submit or introduce into evidence any expert reports rebutting the opinions of Dr. Willis or Dr. Sigurdardottir.
The Issue The issue in this case is whether Oliver Bender has suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Tyler Dyal is the natural mother of Oliver Bender. Oliver was born a live infant at Orange Park Medical Center in Orange Park, Florida, on September 26, 2011. Orange Park Medical Center was a hospital licensed in Florida on September 26, 2011. The physician providing obstetrical services at the time of Oliver’s birth was Dr. Edelenbos. At all material times, Dr. Eric Edelenbos, North Florida Obstetrical and Gynecological Associates, P.A., was a participating physician in the Plan. Oliver weighed in excess of 2,500 grams at birth. None of the parties dispute that Oliver sustained an injury to the brain caused by oxygen deprivation during resuscitation in the immediate post-delivery period. Donald C. Willis, M.D., NICA's expert, opined: In summary, labor was complicated by an abnormal FHR pattern and resulted in a depressed newborn. Umbilical cord blood gas was consistent with birth hypoxic with a pH of 6.87. The newborn hospital course was complicated by respiratory depression, apnea episodes and seizures. MRI identified hypoxic ischemic encephalopathy. There was an apparent obstetrical event that resulted in loss of oxygen to the baby’s brain during labor, delivery, and continuing into the immediate post delivery period. The oxygen deprivation resulted in brain injury. I am not able to comment about the extent of the brain injury. At the time of Oliver’s birth, his Apgar scores were 3 at one minute, 6 at five minutes, and 8 at ten minutes, and he required resuscitation in the delivery room. His arterial cord gas pH was 6.872 with a base deficit of over 20, indicating that he had metabolic acidosis and had experienced hypoxia during labor and delivery. Intubation was attempted but was not successful; however, Oliver improved and did not require intubation thereafter. Oliver began having dusky spells around 24 hours of age with reported “staring” and tight tone. He also demonstrated jitteriness and irritability. By September 28, 2011, Oliver had begun to have seizures, which were treated with Phenobarbital. Oliver was transferred to Wolfson’s Children’s Hospital, where he continued to have stiffening of his extremities with arching and eye staring. On September 29, 2011, Oliver had an MRI which showed the following: FINDINGS: There are felt to be diffusion abnormalities present. These are more conspicuous on the B200 (more heavily diffusion weighted) images. These involve predominantly the gray matter involving the left frontoparietal region and the left MCA distribution. In addition there is slight restricted diffusion in the basal ganglia bilaterally. There is restricted diffusion along the calcarine fissures greater on the right than the left. There is a small amount of restricted diffusion in the right frontal lobe along the inferior aspect of the sylvian fissure and extending slightly superiorly. There is also slight restricted diffusion bilaterally felt to localize to the gray matter along in the gray matter of the occipital tips. The cerebellum appears preserved. These diffusion abnormalities are accompanied by subtle T2 prolongation of FLAIR images as well. There is otherwise no space-occupying lesion, mass effect or midline shift. There is no hydrocephalus. The corpus callosum appears well formed. The intracerebral flow voids on the T2 cube images appear preserved and symmetric. The patient appears to have a complete circle of Willis. IMPRESSION Areas of restricted diffusion in distribution as described above. The study discussed with Dr. Driscoll and overall the findings are felt to be consistent with hypoxic ischemic encephalopathy. No obvious focal vascular abnormalities are seen on the T2 cube images. As such this is likely secondary to somewhat global ischemic etiology rather than embolic phenomenon. There is no evidence of hemorrhage. Oliver was discharged from Wolfson’s Children’s Hospital on October 5, 2011, with no further seizure activity being noted. He was continued with Phenobarbital and still remains on the medication. When Oliver was five weeks old, he was seen by Dr. Alana Salvucci at Nemours. Dr. Salvucci’s assessment of Oliver revealed the following: Since Oliver has been at home, he has made good developmental progress. He is making eye contact and tracks. He startles to loud sounds. He moves both of his extremities equally and spontaneously. He smiles. Overall, his grandmother describes him as stiff, tending to hold his hands in a fisted position, but will open and grasp objects. He is on phenobarbital 2 mL twice a day, which is approximately 3.5 mg/kg per day. He has had no further events of stiffening concerning for seizure. However, he does have episodes where he stares off, typically to the right with no change in tone, lasting 1 to 2 minutes, occurs at least once a day. There are several times where caretakers can get his attention; however, most of the time, he will not respond to tactile or verbal stimuli. There are no associated oral automatisms or eye flutter. * * * Oliver has overall been doing well with no stiffening or jerking episodes, he has been smiling, and tracking and milestones have been appropriate for his age. Dr. Salvucci recommended that Oliver’s mother and grandmother videotape Oliver’s episodes of staring off and send the tape to Nemours for review. She arranged for a prolonged, at least four-hour, video EEG in hopes of capturing the staring episodes described by Oliver’s mother and grandmother. On December 29, 2011, Oliver had a four-hour, sleep-deprived EEG, which was normal with no clinical events during the EEG recording. No evidence was presented that established Oliver’s mother followed Dr. Salvucci’s recommendation to videotape one of Oliver’s staring episodes. On March 22, 2012, Oliver returned to Nemours and was seen by Dr. Harry Abrams. Dr. Abrams noted that Oliver had made good developmental progress since his discharge from Wolfson’s Children’s Hospital. Oliver had begun sitting up in a tripod position. He used both hands equally, reaching for objects and transferring objects. According to his mother, Oliver’s stiffness had significantly improved, but Oliver still had tight heel cords, making him tend to stand on his toes when bearing weight. Although not babbling, Oliver was making good eye contact, smiling, and tracking. During the visit, Oliver’s mother reported that at least twice a day Oliver had episodes where his arms stiffened and flexed at the elbow and that he was having jerking movements. She indicated that Oliver had been staring off, and there appeared to be transient episodes of unresponsiveness that lasted several seconds. Dr. Abrams recommended that an eight-hour video EEG be done in hopes of capturing one of the events with the upper extremity jerking. This recommendation was not followed. On January 17, 2013, Oliver was admitted to Wolfson’s Children’s Hospital for seizures accompanying a fever and cough. The seizure was a single episode in which Oliver was unresponsive for one minute and nonresponsive to verbal or tactile stimulation. The seizure caused grogginess, and Oliver slept afterwards. The seizure was characterized as generalized and staring. The postical symptom was confusion. His mother reported that this was the first seizure that Oliver had had since he was an infant. Oliver was treated with Klonopin and discharged the next day in stable condition. Oliver visited Dr. Abrams on April 16, 2013. Dr. Abrams noted that Oliver was doing well. Oliver had no significant evidence of delay. Oliver’s family advised that Oliver had done well, but at times Oliver would stare off and at other times, when he was drowsy or sleepy, he would put his fingers in his ears and shake his head back and forth. Dr. Abrams recommended that Oliver’s dosage of Phenobarbital begin to be tapered. In May 2013, Oliver had another seizure. Again, this seizure was accompanied by a high fever. His mother was about to give him Tylenol when Oliver suddenly stiffened and jerked for several minutes. The episode stopped spontaneously. As a result, Oliver’s dosage of Phenobarbital was increased. Oliver has not had another episode similar to the one he had in May 2013. His mother and grandmother report that he continues to have episodes in which he stares off and becomes confused. However, he returns to baselines after the staring episodes. Oliver is an active child; he can run, walk, and play. He is able to throw a ball and can drive a power-wheel car by pushing the pedal to drive it. He plays with other children. Oliver likes to play with his Hot Wheels cars. He can pull off his hats, socks, and clothes. He is able to turn pages in a book, and he can stack blocks. Oliver scribbles on paper with pens, pencils, and crayons. He can feed himself with utensils and drinks from a sippy cup. He can also drink from a straw. He can put his arms inside his sleeves when he is being dressed. When asked to point to his body parts, including his eyes, ears, hair, feet, hands, and belly button, he is able to do so. As of October 15, 2013, Oliver could speak approximately eight single words meaningfully and had not spoken any two-word phrases. His speech development at that time was not age appropriate. However, Oliver is able to use nonverbal communications effectively. When he is hungry, he smacks his lips and holds out his hands, indicating that he wants something to eat. He is able to understand and carry out verbal requests. He makes good eye contact. He can identify objects in pictures such as a ball, airplane, and ice cream cone by pointing to the objects. He is not receiving any type of therapy, such as physical, occupational, or speech therapy. Respondent retained Raymond Fernandez, M.D., to evaluate Oliver. Dr. Fernandez is board-certified in pediatrics and neurology together with child neurology and has been practicing pediatric neurology for 37 years. Dr. Fernandez reviewed Oliver’s medical records and performed independent medical examinations on Oliver on September 25, 2012, and October 15, 2013. After Dr. Fernandez’s examination on September 25, 2012, he felt that it would be appropriate to reexamine Oliver in six to nine months in order to track his developmental progress before coming to a final conclusion. After his second evaluation, Dr. Fernandez summarized his evaluation as follows: There is no evidence at this time, of substantial mental and motor impairment due to oxygen deprivation sustained during labor and delivery. Oliver has made good progress with his fine and gross motor skills and at this time, there is no convincing evidence for spasticity or cerebral palsy that was noted earlier. There is no reason to anticipate any reversal or regression in his motor skills, strength, or coordination. Expressive speech development has been delayed, but he is improving at a steady pace and this trend should continue. Receptive language skills are also improving steadily. Delay in speech and language skills, even when improving, is sometimes an early indicator of later learning difficulty in the classroom setting. Whether or not this will prove to be a problem for Oliver remains to be determined. It is a potential problem that should not be insurmountable with appropriate input from his teachers. At the time of Dr. Fernandez’s examination on October 15, 2013, Oliver was able to run without falling and had no abnormality in his gait. Intervenor, Orange Park Medical Center, retained Trevor Resnick, M.D., to evaluate Oliver. He is board-certified in pediatrics and neurology with a special competence in child neurology. Dr. Resnick reviewed Oliver’s medical records and examined Oliver. He opined Oliver’s staring spells and resulting confusion were partial complex seizures. These seizures have not been confirmed with a video EEG and have been witnessed only by his family. However, given the long history of these episodes, more likely than not, the episodes are partial complex seizures. When Oliver experiences a staring episode and resulting confusion, he will return to his baseline condition and is able to carry on with the activities previously described. The episodes are transient in nature; thus, any physical or mental impairment that occurs during the episode is not permanent. Dr. Fernandez’s opinion that Oliver does not have a substantial, permanent physical and mental impairment is credited.
The Issue Whether Daniel Espinoza has suffered an injury for which he and his mother, Maria L. Espinoza, should be awarded compensation under the Florida Birth-Related Neurological Injury Compensation Plan, as Ms. Espinoza has alleged in her claim for compensation filed on behalf of Daniel?
Findings Of Fact Based upon the evidence adduced at the July 14, 1994, Division-conducted hearing in this case, and the record as a whole, the following Findings of Fact are made: Daniel Espinoza is the natural son of Petitioner. He was born on January 6, 1991, at Jackson Memorial Hospital (hereinafter referred to as "Jackson") in Dade County, Florida. Daniel was the product of a full term pregnancy. His birth weight was in excess of 2500 grams. Daniel was delivered by Erin Colleen Dawson, M.D. At the time of Daniel's birth, Dr. Dawson was a participant in the Florida Birth-Related Neurological Injury Compensation Plan. The delivery was uneventful. Daniel was a "vigorous" baby at birth. He had a "good" Apgar score of 9 at one, five, and ten minutes after birth. There was no resuscitation required in the immediate postdelivery period. Approximately five hours after the initial evaluation, Daniel appeared to be "grunting" and suffering from "cyanosis." As a result, he was transferred to Jackson's neonatal intensive care unit, where he had a seizure and experienced respiratory distress. Daniel's C.S.F. (cerebrospinal fluid) was bloody and had a white blood cell count of 19000. An initial diagnosis of meningitis was made. On January 7, 1991, an EEG (electroencephalogram) was done. It revealed "no epileptiform phenomena." A CT (computerized tomography) scan of Daniel's brain was performed on January 8, 1991. The report of the scan read as follows: HISTORY- TWO DAY OLD WITH SEPSIS. 5 MM AXIAL SECTIONS WERE OBTAINED THROUGH THE BRAIN WITHOUT CONTRAST. THERE IS A SMALL LUCENT DEFECT IN THE LEFT OCCIPITAL BONE SEEN ON IMAGE #5. ALTHOUGH NO SOFT TISSUE SWELLING IS SEEN, CANNOT DEFINITELY EXCLUDE THIS BEING A LINEAR NONDEPRESSED FRACTURE VERSUS OTHER ETIOLOGY SUCH AS A VASCULAR GROOVE. WE SUGGEST CORRELATION WITH THE PLAIN FILM. THERE IS A HUGE AMOUNT OF BLOOD IN THE RIGHT POSTERIOR FOSSA EXTENDING ACROSS THE MIDLINE AND INSINUATING ON THE RIGHT TENTORIAL INCISURA SUPRATENTORIALLY. BLOOD IS ALSO SEEN ALONG THE POSTERIOR INTERHEMISPHERIC FISSURE DIFFUSELY IN THE EXTRA-AXIAL SPACE, AND A SMALL AMOUNT OF BLOOD IN THE OCCIPITAL HORNS OF THE LATERAL VENTRICLES. WITH SUCH A TREMENDOUS AMOUNT OF BLOOD PRESENT IN THE POSTERIOR FOSSA, IT IS DIFFICULT TO SAY HOW MUCH IS PARENCHYMAL VERSUS EXTRA-AXIAL. THERE IS MASS EFFECT UPON THE MID BRAIN PONS AND MEDULLA AND ON THE FOURTH VENTRICLE CAUSING OBSTRUCTING HYDROCEPHALUS. IMPRESSION LARGE ACUTE INTRACRANIAL HEMORRHAGE, AS DESCRIBED ABOVE, WITH THE EPICENTER BEING IN THE RIGHT POSTERIOR FOSSA. THE DIFFERENTIAL DIAGNOSIS INCLUDES NEOPLASM, TRAUMA, RUPTURED ANEURYSM OR ARTERIOVENOUS MALFORMATION, COAGULOPATHY, ETC. CONTRAST STUDY OR MRI MAY BE OF HELP FOR FURTHER EVALUATION TO TRY TO DETERMINE THE UNDERLYING ETIOLOGY. On January 9, 1991, Daniel underwent an echoencephalogram, which, according to the report of the study, indicated the following: ROUTINE ECHOENCEPHALOGRAM REVEALED DILATION OF THE LATERAL AND THIRD VENTRICLES. THERE IS A BILATERAL LUMPY CHOROID PLEXUS NOTED. ADDITIONAL TRANSTEMPORAL VIEWS REVEAL AN ECHOGENIC AREA SEEN IN THE INFRATENTORIAL REGION, WITH INCREASE IN THE ECHOGENICITY OF THE BASAL CISTERNS. THE FINDINGS ARE SIMILAR TO THOSE SEEN ON PREVIOUS CT SCAN, WHICH SHOWED EVIDENCE OF A CEREBRAL HEMORRHAGE WITH SUBARACHNOID BLEED. THE NORMAL STRUCTURES OF THE POSTERIOR FOSSA ARE ILL-DEFINED. IMPRESSION: MODERATE HYDROCEPHALIC CHANGES OF THE LATERAL AND THIRD VENTRICLES. SUBARACHNOID HEMORRHAGE WITH A POSTERIOR FOSSA HEMORRHAGE, AS DESCRIBED IN A PREVIOUS CT SCAN OF THE BRAIN. Another CT brain scan was performed on January 23, 1994, the report of which stated the following: THE PATIENT IS A TWO WEEK OLD MALE WITH A HISTORY OF INTRACRANIAL HEMORRHAGE. AXIAL IMAGES WERE OBTAINED THROUGH THE BRAIN AT 5MM INTERVALS FOLLOWING INTRAVENOUS ADMINISTRATION OF CONTRAST. COMPARED TO THE PRIOR STUDY OF 1-8-91, THERE HAS BEEN SUBSTANTIAL RESORPTION OF BLOOD IN THE REGION OF THE SUBDURAL, SUBARACHNOID AND INTRAVENTRICULAR HEMORRHAGE. THERE ALSO HAS BEEN MARKED DECREASE IN THE VENTRICULAR SIZE. THERE IS LESS ASSOCIATED MASS EFFECT, ESPECIALLY IN THE POSTERIOR FOSSA WITH PERSISTENT SUBDURAL HEMORRHAGE IN THE RIGHT SIDE OF THE POSTERIOR FOSSA DISPLACING THE CEREBELLUM ANTERIORLY AND TO THE LEFT. THE FOURTH VENTRICLE IS NOW VISUALIZED, HOWEVER. NO NEW AREAS OF HEMORRHAGE ARE SEEN. THERE ARE NO BONY ABNORMALITIES. THE MAXILLARY AND ETHMOID SINUSES AND MASTOID AIR CELLS ARE CLEAR. IMPRESSION SIGNIFICANT RESORPTION OF SUBDURAL, SUBARACHNOID WITH INTRAVENTRICULAR HEMORRHAGE SINCE THE PRIOR STUDY OF 1-8-91 WITH LESS MASS EFFECT, ESPECIALLY UPON THE CEREBELLUM AND BRAIN STEM. MARKED DECREASE IN VENTRICULAR SIZE HAS ALSO OCCURRED. On January 25, 1991, Daniel underwent a second echoencephalogram, the report of which read as follows: FOLLOW-UP BRAIN HEMORRHAGE. COMPARISON IS MADE TO PREVIOUS STUDY FROM 1/8/91. THERE HAS BEEN MARKED INTERVAL RESOLUTION OF THE PREVIOUSLY DEFINED RIGHT POSTERIOR FOSSA HEMORRHAGE. IN ADDITION, THE VENTRICULAR SIZE HAS DECREASED SIGNIFICANTLY SINCE THE PREVIOUS EXAM. THERE CONTINUES TO BE SLIGHT INCREASED ECHOGENICITY WITHIN THE SYLVIAN FISSURES BILATERALLY, WHICH MAY REPRESENT SOME RESIDUAL SUBARACHNOID HEMORRHAGE. NO EVIDENCE OF NEW OR ACUTE HEMORRHAGE IS IDENTIFIED. IMPRESSION: THERE HAS BEEN SIGNIFICANT INTERVAL IMPROVEMENT IN THE DEGREE OF VENTRICULAR DILATION AND THE PREVIOUSLY DEFINED HEMORRHAGE, WHEN COMPARED TO THE STUDY OF 1/8/91. Daniel was discharged from Jackson on January 31, 1991. At present, in terms of meeting expected language milestones, Daniel is mildly delayed, primarily in the area of expressive language. The delay is developmental in nature and Daniel will likely improve in this area over time. Otherwise, his mental functioning is relatively well preserved. Physically, Daniel is only very mildly impaired. He has a slight decrease in muscle tone and some incoordination, but he does not suffer from spasticity or contracture and he is able to move both of his arms well and to walk without losing his balance. He is even able to run, although he has a tendency to lean to the right and appear as if he is about to fall when he does so. In short, Daniel suffers from no permanent and substantial mental or physical impairment. 2/
Findings Of Fact Coleman McMillan was born on December 12, 2012, at Baptist Medical Center South located in Jacksonville, Florida. Coleman weighed 3,690 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Coleman, to determine whether an injury occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital due to oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Dr. Willis described his findings as follows: In summary: The mother had well-controlled hypertension during pregnancy. She was followed twice weekly for fetal testing. There was no documentation of fetal distress prior to labor. The baby was depressed at birth, requiring resuscitation. A cord blood gas was apparently not done. The initial blood gas in the NICU was consistent with acidosis. Abnormal fetal tone was noted shortly after delivery. MRI on DOL 2 was consistent with anoxic brain injury. There was an apparent obstetrical event that resulted in loss of oxygen to the baby’s brain during delivery and continuing into the immediate post delivery period. Oxygen deprivation was likely present during labor, but without reviewing the FHR tracing I am reluctant to make a statement concerning this issue. After a review of the fetal heart rate monitor tracing, Dr. Willis concluded that there was no significant oxygen deprivation during labor. NICA retained Raymond J. Fernandez, M.D., a pediatric neurologist, to examine Coleman and to review his medical records. Dr. Fernandez examined Coleman on May 29, 2014, and made the following findings: Coleman was active and energetic during much of the examination. He usually turned when his name was called, and maintained good eye contact. Towards the end of the examination Coleman sat calmly on his father’s lap and again maintained good eye contact. He displayed appropriate stranger anxiety. He pointed and made grunting sounds. No words were spoken. He carried out age-appropriate verbal requests. He opened the door on request without visual cues, looked up at the light when I asked him where is the light, lifted his shirt when I asked him to show me his shirt and pointed to his father’s nose when I asked him to touch his nose. He scribbled with pen and paper and pushed the button on the pen before he handed it back to me. He stacked four, one-inch cubes using either hand in well-coordinated fashion. He walked and ran well. He was able to squat, pick up objects and shift to stand without difficulty. He was able to throw a ball overhand. Muscle tone was normal. He reached accurately with either hand. There was no tremor, ataxia or involuntary movement. Deep tendon reflexes were 2+ throughout. There were no pathologic reflexes. Limited funduscopic examination was normal. Eye movement was normal and he was visually attentive. Face was symmetric. He swallowed well. Palate elevated at midline. Tongue was midline. Based on his review of the medical records and his examination of Coleman, Dr. Fernandez opined as follows: There is no evidence for substantial motor impairment. Coleman’s motor examination is normal, both with regard to fine and gross motor control and muscle tone is normal. There is no evidence for substantial mental impairment at this time. Expressive speech is delayed, but he displays normal or age- appropriate preverbal skills and he appears to have age-appropriate comprehension of language. Expressive speech will probably improve within a reasonable period of time. Coleman sustained an hypoxic brain injury, probably during labor and delivery, but there is no evidence for substantial mental and motor impairment that will be permanent. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinions of Dr. Willis and Dr. Fernandez that there was an obstetrical event that resulted in loss of oxygen to the brain. Their opinions are credited. There are no contrary expert opinions filed that are contrary to Dr. Fernandez’s opinion that there is no evidence for a substantial motor or mental impairment that will be permanent. Dr. Fernandez’s opinion is credited.
