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 Terrance Drake, Jr., was born on April 27, 2012, at Bayfront Medical Center in St. Petersburg, Florida. Respondent retained Laufey Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to evaluate Terrance. Dr. Sigurdardottir reviewed Terrance’s medical records, and performed an independent medical examination on him on October 14, 2015. In a neurology evaluation based upon this examination and an extensive medical records review, Dr. Sigurdardottir made the following findings and summarized her evaluation as follows: Summary: Here we have a 3-year-5-month-old boy with a near miraculous recovery after a near fatal bradycardia due to likely placental abruption during delivery. He is at this time physically healthy but has a mild microcephaly. He has no obvious motor impairment and likely but not established mild language delay. The patient is doing well compared to his extremely dire situation at birth. Results as to question 1: The patient is found to have no substantial physical or mental impairment. Results as to question 2: There is evidence of near terminal hypoxia at birth resulting in infant being declared deceased, but self resuscitation occurred followed by a period of critical illness. Presumed hypoxic neurologic injury is plausible and timing of injury is in immediate perinatal period. No evidence suggests his injury having occurred apart from the immediate perinatal period. Results as to question 3: We expect a full life expectancy and an excellent prognosis, although mild mental delays relating to attention span, language, and/or behavior cannot be ruled out at this time. In light of the above-mentioned details, and with lack of substantial physical and motor impairment, I do not recommend Terrance being included into the Neurologic Injury Compensation Association (NICA) Program and would be happy to answer additional questions. Dr. Sigurdardottir’s opinion was affirmed in her affidavit dated March 29, 2016. In order for a birth-related injury to be compensable under the NICA Plan, the injury must meet the definition of a birth-related neurological injury and the injury must have caused both permanent and substantial mental and physical impairment. Dr. Sigurdardottir’s opinion that Terrance does not have a substantial physical or mental impairment is credited. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Sigurdardottir that Terrance does not have a substantial physical or mental impairment.
The Issue At issue is whether Robert Donald Vose, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts Dawn Vose is the parent of Robert Donald Vose, a minor. Robert was born a live infant on August 15, 2001, at Baptist Hospital, Pensacola, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Robert's birth was Jill Prafke, M.D., who, at all times material hereto, was a "participating physician" in the 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 or spinal cord . . . 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. To resolve whether Robert suffered a "birth-related neurological injury," the parties offered the medical records related to Robert's birth and subsequent development (Respondent's Exhibit 3), as well as the opinions of Donald C. Willis, M.D., a physician who practices maternal-fetal medicine, and Michael Duchowny, M.D., a physician board-certified in pediatrics, neurology with special competence in child neurology, and clinical neurophysiology. (Respondent's Exhibits 1 and 2). With regard to injury, Dr. Willis was of the opinion that Robert suffered a brain injury (a venous sinus thrombosis and choroid plexus hemorrhage) at or around the time of delivery, that resulted in the development of hydrocephalus. However, he offered no opinion regarding the extent or significance of the brain damage. (Respondent's Exhibit 2). In contrast, Dr. Duchowny evaluated Robert on May 4, 2006, and concluded that his "normal neurological status together with a review of the accompanying medical records does not suggest that he has a substantial mental or motor impairment," as required for coverage under the Plan. (Respondent's Exhibit 1). Dr. Duchowny reported the results of his evaluation, and the basis for his opinion, as follows: I had the pleasure of evaluating Bobby Vose on May 4, 2006. Bobby is a 4-year-old, left-handed, prekindergarten student who was brought by his father for evaluation. This was conducted in my office at Miami Children's Hospital. HISTORY ACCORDING TO THE FATHER: Mr. Vose explained that Bobby was brought in order to "verify his abilities for NICA." He believes that Bobby is developing normally and in fact, is above average in several areas. He will be starting kindergarten in September and has done extremely well in his prekindergarten class setting. In fact, his language abilities are above average for age and he is bilingual with approximately 70 words of Spanish. He is a sociable boy who plays well with other children and his motor milestones have progressed normally. He sleeps through the night. His vision and hearing are intact. There has been no regression and no toxic or infectious exposure. Bobby is on no intercurrent medications. Bobby's PAST MEDICAL HISTORY is significant for placement of a ventriculoperitoneal shunt as a newborn. He apparently experienced an intercranial hemorrhage into the right ventricle and had a shunt placed from the anterior horn of the right ventricle into the peritoneal cavity. His shunt has functioned well and there have been no complications or revisions . . . . Otherwise, Bobby enjoys good health. He is not being followed for any chronic illnesses and has not required medical or surgical intervention subsequent to the newborn period. PERINATAL HISTORY: Bobby was born at Baptist Hospital in Pensacola at 37-weeks gestation. There was an attempt at a vaginal delivery but "the head was wedged" and Bobby was ultimately delivered by emergency cesarean section. He weighed 8 pounds and breathed well at birth. He remained in the hospital for approximately 11 days. GROWTH AND DEVELOPMENT: Bobby's father could not recall Bobby's motor or language milestones except to note that all occurred at the normal time. Bobby is fully immunized and has no known drug allergies. He has had a hernia repaired. * * * PHYSICAL EXAMINATION reveals an alert, well- developed, pleasant and cooperative 4-year- old boy. Bobby weighs 38 pounds. The skin is warm and moist. Bobby's head circumference measures 51.9 centimeters, which is within standard percentiles for age. The fontanels are closed. The ventriculoperitoneal shunt reservoir is palpated over the right frontal bone and shunt tubing is noted in the right anterior lateral neck region and across the thorax and abdomen. There is a healed right, upper quadrant abdominal scar. There are no cranial or facial anomalies or asymmetries. No dysmorphic features or cutaneous stigmata are noted. The neck is supple without masses, thyromegaly or adenopathy. The lung fields are clear and the heart sounds are normal. There is no palpable abdominal organomegaly. Peripheral pulses are 2+ and symmetric. NEUROLOGICAL EXAMINATION likewise discloses no significant findings. Bobby is alert, pleasant and cooperative. He answers all questions fluently with a good fund of information and an age appropriate stream of both thought and attention. He cooperated with all aspects of the evaluation. The cranial nerve examination reveals full visual fields to direct confrontation testing and normal ocular fundi. The optic disc margins are clearly demarcated and there is no optic pallor. There are no significant retinal findings. The extraocular movements are full and conjugate. The pupils are 3 mm and react briskly to direct and consensually presented light. There is blink to threat from both directions. The tongue is moist and papillated and moves well in all plains. The uvula is midline. The pharyngeal folds are symmetric. Motor examination reveals symmetric strength, bulk, and tone. There are no adventitious movements and no focal weakness or atrophy. The deep tendon reflexes are 2+ throughout. Plantar responses are downgoing. Station and gait are appropriate for age. The arm swing is symmetric. 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, Bobby's neurological examination in detail reveals no significant focal or lateralizing findings. The ventriculoperitoneal shunt is likely to be nonfunctional at this point. Bobby's normal neurological status together with a review of the accompanying medical records does not suggest that he has a substantial mental or motor impairment. . . . I, therefore, do not believe that he is eligible for compensation under the NICA statute.
The Issue At issue in this proceeding is whether Travis Chestnut, 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 Treena Chestnut and Terrance Chestnut are the parents and natural guardians of Travis Chestnut (Travis), a minor. Travis was born a live infant on July 26, 1994, at University Medical Center, a hospital located in Jacksonville, Florida, and his birth weight was in excess of 2,500 grams. The physician providing obstetrical services during the birth of Travis was James Lewis Jones, M.D., who was, at all time material hereto, a participating physician in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Mrs. Chestnut's antepartum course and Travis' delivery Prior to Mrs. Chestnut's admission to University Medical Center, her prenatal course had been essentially uncomplicated. Notwithstanding, she was noted at risk because of a prior cesarean section delivery for fetal distress, and when admitted Travis was slightly post-term at 41.5 weeks. At or about 2:00 a.m., July 25, 1994, Mrs. Chestnut was admitted to University Medical Center. At the time, Mrs. Chestnut was noted to be in labor, and vaginal examination revealed the cervix to be at 2 centimeters, effacement at 100 percent, and the fetus at station 0 with vertex presentation. The membranes were noted to be intact, and fetal heart tone was noted at 135 to 145 beats per minute, with good fetal movement. At 8:45 a.m., an epidural was inserted for analgesia, and at 9:05 a.m. Mrs. Chestnut's membranes spontaneously ruptured, with clear fluid noted. Vaginal examination revealed the cervix to be at 2 to 3 centimeters, effacement at 100 percent, and the fetus at station 0. A scalp electrode was placed, and fetal heart tone was noted to continue in the 135 to 145 beat per minute range. Mrs. Chestnut's labor progressed slowly through July 25, 1994. During that period, fetal heart tones evidenced good beat to beat variability (short-term and long-term) with accelerations and occasional variable decelerations. Commencing at or about 2:00 a.m. July 26, 1994, late decelerations were noted, and fetal heart tones began to demonstrate, with increasing intensity and duration, early variable and late decelerations, with rates as low as the 70's, as well as fetal tachycardia. At approximately 2:25 a.m., dilation was noted as complete, and Mrs. Chestnut was instructed to push. At 2:28 a.m. a supplemental dose of epidural analgesia was administered, and at 2:34 a.m. deep variable decelerations were noted and Mrs. Chestnut was taken, via bed, to the delivery room. Mrs. Chestnut was noted in the delivery room at 2:39 a.m., at which time fetal heart rate was recorded in the 90's, and she was prepared for delivery. Mrs. Chestnut continued to push, and fetal heart tone remained in the 90's. Three attempts to deliver the infant by vacuum were attempted and failed. Fetal heart tone dropped to the 80's and a scalp pH performed at 2:54 a.m. was 6.95 (reflective of fetal acidosis). Given the circumstances, an emergency cesarean section was ordered, the incision started at 3:00 a.m., and Travis was delivered at 3:05 a.m. During delivery, difficulty was experienced elevating the infant's head, as he was deep in the pelvis, and a cord prolapse was noted. On delivery, Travis was atonic, with a heart rate of less than 60 and no respiratory effort. He was dried for 10 seconds, then begun on positive pressure ventilation with bag and mask. Heart rate increased to greater than 100 within 10 seconds, and color became pink within 20 seconds. Travis required support until 10 minutes of age, when regular sustained respiratory effort was noted. First gasp occurred between 1 and 2 minutes of age, and was progressively more frequent through 15 minutes of age. Shallow regular respirations began at about 5 minutes of age, and were adequate and sustained by 10 minutes of age. Slight tone was developed in the extremities by 10 minutes, and spontaneous movement of the extremities developed by 12 minutes. Apgars were 4, 5, 7, 7, and 8 at one, two, five, ten, and fifteen minutes, respectively.1 Cord gas at delivery reflected a pH of 6.76. Arterial blood gas at 20 minutes of age on blow by oxygen included a pH of 7.04. Neurologic impression at birth was severe neonatal depression/fetal distress and severe metabolic acidosis. At 20 minutes of life, Travis was transferred to the neonatal intensive care unit (NICU) for further management. At about three-and-one-half hours of age seizures were noted, and phenobarbital was started. Also noted, were lip smacking, eye deviation, spasticity, and hypertonic extremities. CT scan showed left parietal infarct and left post-occipital subdural hematoma. The EEG was markedly abnormal. MRI on August 3, 1994, reflected high signal gyral areas in both parietal and occipital lobes, consistent with cortical injury or hemorrhage. Travis remained in the intensive care unit until August 19, 1994, when he was discharged to the care of his parents. On discharge, he was noted to be doing well clinically, with no reported seizures while on maintenance phenobarbital. Physical examination revealed positive blink and suck, and symmetric motor patterns, although with increased tone. Neurologic impression on discharge was "perinatal encephalopathy - improved[,] neonatal seizures well controlled [and] developmentally at risk." The genesis and timing of Travis' neurologic insult Here, the proof that is pertinent to the nature and timing of Travis' neurologic insult is consistent with a brain- related injury caused by oxygen deprivation occurring in the course of labor, delivery, and the immediate post-delivery period. In this regard, it is observed, inter alia, that Mrs. Chestnut's prenatal course was uneventful; on admission to the hospital, the fetus evidenced reassuring fetal heart tones and fetal movement; only after protracted labor did the fetus begin to evidence multiple variable decelerations; prior to delivery, Travis suffered a period of prolonged bradycardia; prior to and following delivery, Travis was severely acidotic; upon delivery, Travis evidenced profound neurologic depression; and, following delivery, Travis developed seizure activity. Consequently, the proof supports the conclusion, more likely than not, that Travis suffered an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital." Section 766.302(2), Florida Statutes. Having resolved the genesis and timing of Travis' neurologic insult, it remains to resolve its significance or, stated differently, whether the proof supports the conclusion that Travis' injury rendered him "permanently and substantially mentally and physically impaired," as required by Sections 766.302(2) and 766.309(1), Florida Statutes. The significance of Travis' neurologic impairment The proof offered by Petitioners to quantify the significance of Travis' impairment was less than compelling. In this regard, it is observed that Petitioners offered the affidavit of Stuart C. Edelberg, M.D., (Petitioners' Exhibit 2), an apparent expert in obstetrics and gynecology, who opined, based on his record review, that Travis' "impairment is permanent and substantial, both mentally and physically." Notably, Dr. Edelberg was not shown to have examined Travis, and his affidavit is hearsay, subject to the limitations imposed by Section 120.57(1)(c), Florida Statutes (1996 Supp.). Compared to the proof offered by Petitioners, Respondent offered the testimony, through deposition, of Michael Duchowny, M.D., an expert in pediatric neurology. (Respondent's Exhibit 1.) Dr. Duchowny examined Travis on July 16, 1996, and on January 24, 1997. Dr. Duchowny's examinations revealed that Travis did suffer some impairment of motor function, as evidenced by increased muscle tone, increased deep tendon reflexes, and diminished fine motor coordination; however, he walked independently and without support in a stable fashion. As for his cognitive abilities, Dr. Duchowny did observe expressive disfluency, but Travis' receptive skills were good, he could communicate non-verbally, and mental functioning was in the normal or near normal range. It was Dr. Duchowny's opinion that, although Travis does suffer some permanent mental and physical impairment, it is not substantial and, based on improvements observed between the examinations of July 16, 1996, and January 24, 1997, further improvement is most likely. Dr. Duchowny's observations and opinions are most consistent with the records offered into evidence (Petitioners' Exhibit 1), and are credited.2 Based on the proof, it cannot be concluded that Travis' injury has rendered him permanently and substantially mentally and physically impaired. Rather, the competent and persuasive proof is to the contrary.
The Issue At issue in this proceeding is whether Charles Caleb Padgett, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Initial observations As observed in the preliminary statement, neither petitioner nor anyone on her behalf appeared at hearing, and no proof was offered to support her claim. Ordinarily, such failing would be dispositive of the case; however, notwithstanding petitioner's failure of proof, respondent elected to offer into evidence the medical records filed with DOAH on February 8, 1995, which relate to Sandra Padgett's prenatal care, the birth of Charles Caleb Padgett (Caleb) and Caleb's subsequent development, as well as the opinions of Charles Kalstone, M.D., a board certified obstetrician, and Michael Duchowny, M.D., a board certified pediatric neurologist, to affirmatively resolve the issue as to whether Caleb had suffered a "birth-related neurological injury," within the meaning of Section 766.302(2), Florida Statutes. Ms. Padgett's antepartum course and Caleb's birth The records relating to Ms. Padgett's antepartum course fail to demonstrate any complication other than polyhydramnios (an abnormal collection of amniotic fluid). Such complication did, however, place her pregnancy at risk, and she was routinely the subject of non-stress testing to assess the well being of the fetus, and periodic ultrasounds. On November 10, 1992, with an estimated date of confinement of November 19, 1992, Ms. Padgett underwent a routine non-stress test and ultrasound. The non-stress test was reactive, a positive sign of fetal well-being; however, the ultrasound suggested that the infant was macrosomic, with an estimated fetal weight of over nine pounds. 1/ Based on the ultrasound results, and considering that Ms. Padgett had previously undergone a cesarean section at term, her physician decided against a trial of labor and recommended that she be admitted for a repeat cesarean delivery. At or about 10:55 a.m., November 11, 1992, Ms. Padgett was admitted to Lawnwood Regional Medical Center, Fort Pierce, Florida, for the repeat cesarean section heretofore noted. At the time, Ms. Padgett was not in labor, and was not thereafter noted to have entered labor. At 3:50 p.m., November 11, 1992, Caleb was delivered by cesarean section. Upon delivery, copious clear fluid was aspirated from his oropharynx and stomach, and resuscitation was noted to consist of tactile stimulation, suctioning, and oxygen blow-by. Apgars were noted as 7 and 8, at 1 and 5 minutes respectively. Notwithstanding resuscitation, Caleb was noted to become dusky (pale) each time oxygen was withdrawn, and developed grunting and retractions. Consequently, Caleb was transferred to the nursery where he was initially placed on a 50 percent oxyhood. Subsequent assessment revealed transient tachypnea of the newborn (TTN), and chest x-ray revealed bilateral haziness of the lungs. Therefore, Caleb was intubated and, over the course of the next 10 hours, weaned well and was extubated to room air without further respiratory complications. Neurologically, Caleb was noted to have decreased tone since birth, with some arching, and small fontanelle. The arching resolved within the first 48 hours, but the hypotomia persisted. A CT study of the brain at 48 hours of age was noted to be within normal limits. In this regard, it is observed that there was no demonstrated evidence of intracranial hemorrhage, significant mass effect or shift to the midline structures. The ventricular system appeared patent and normal for age, and there was no evidence of extra axial fluid collections. There were, however, diffuse low attenuation changes throughout the white matter which was thought to represent immature white matter, normal for age, but other etiologies could not be entirely excluded. Caleb's hospital course was otherwise uneventful, and he was discharged to his mother's care on November 15, 1992. Caleb's development Subsequent to discharge, Caleb was followed medically, and ultimately diagnosed with a very mild right hemiparesis and developmental disorder, probably mild cerebral palsy. In an effort to identify the cause of Caleb's disorder, a number of radiological studies were performed. A CT of the brain taken on July 13, 1993, revealed: . . . encephalomalacia immediately lateral to the left caudate nucleus, manifested by linear low attenuation in the white matter and compensatory dilation of the frontal horn of the left lateral ventricle. This indicates an old unilateral vascular insult, which may well have occurred in utero. The remainder of the brain including the right hemisphere is within normal limits. There is no hydrocephalus, intracranial hemorrhage nor intracranial calcification. An MRI of the brain on November 29, 1993, revealed the following: The cerebellum and brain stem appeared normal in configuration. There is altered contour in the left basal ganglia and internal, external capsular region suggestive of an old infarct with signal changes in this region compensatory. There are areas of gliosis as well as porencephalic changes in the frontal horn and body of the lateral ventricle on the left compensatory to the infarct. There is some thickening of the ethmoid and maxillary sinus regions notable. IMPRESSION: Abnormal MRI of the brain as noted by the changes suggestive of old left basal ganglia, internal capsule and external capsular region infarct with compensatory ventricular changes of the frontal horn and body of the lateral ventricle of porencephalic nature with gliottic changes throughout this region. . . . Electroencephalograms of January 5, 1994, and May 3, 1994, were essentially normal, with no evidence of seizure activity. Although the medical records indicate that Caleb suffered some oxygen deprivation at birth, the proof fails to support the conclusion that such event caused the injury to his brain which resulted in his neurological impairment. Rather, the proof, as demonstrated by Caleb's presentation at birth, hospital course, and radiological studies, indicates that Caleb's neurological impairments, more likely than not, derive from an intra-uterine stroke which significantly predated his mother's admission to the hospital or his birth. In so concluding, it is first observed that the radiological studies do not demonstrate evidence of a brain injury at or about the time of birth but, rather, prenatally. Second, the focal nature of Caleb's brain injury, with resultant right-sided hemiparesis, is not generally associated with hypoxic insult. Rather, hypoxic insult generally evidences as a global injury to the brain, as opposed to the focal injury Caleb suffered. Finally, Caleb presented with dysmorphic features, an abnormality suggesting Caleb did not develop appropriately in utero. Such developmental abnormality is a risk factor, and can lead to developmental problems with motor function, language function and cerebral palsy. Turning now to the significance of Caleb's neurologic impairments, it must be concluded that the proof fails to demonstrate that Caleb is permanently and substantially, mentally and physically impaired. Rather, the proof demonstrates that Caleb's physical impairment can best be described as mild, as opposed to substantial, and there is no evidence that he suffered any loss of cognitive function.
Other Judicial Opinions A party who is adversely affected by this final order is entitled to judicial review pursuant to Sections 120.68 and 766.311, Florida Statutes. Review proceedings are governed by the Florida Rules of Appellate Procedure. Such proceedings are commenced by filing the original of a notice of appeal with the Agency Clerk of the Division of Administrative Hearings and a copy, accompanied by filing fees prescribed by law, with the appropriate District Court of Appeal. See Section 766.311, Florida Statutes, and Florida Birth-Related Neurological Injury Compensation Association v. Carreras, 598 So. 2d 299 (Fla. 1st DCA 1992). The notice of appeal must be filed within 30 days of rendition of the order to be reviewed. 10
The Issue At issue is whether Melody N. Smith, 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 1. Irwin C. Smith and Kristelle K. Smith are the parents and natural guardians of Melody N. Smith (Melody), a minor. Melody was born a live infant on October 16, 1989, at Baptist Medical Center, a hospital located in Jacksonville, Florida, and her birth weight was in excess of 2,500 grams. 2. The physician providing obstetrical services at birth was Ernest Ferrelle, M.D., who was, at all times material hereto, a “participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. 3. Here, there is no dispute that Melody is permanently and substantially mentally and physically impaired, consequent to a brain anomaly. What is at issue is the cause and timing of Melody's brain anomaly or, pertinent to these proceedings, whether her neurologic impairment resulted from an "injury to the brain . . . caused by oxygen deprivation. . . occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period ina hospital."* — — The cause-and timing of Melody's brain anomaly 4. On September 12, 1989, approximately one month before Melody's delivery, Mrs. Smith underwent an amniocentesis,’ following a diagnosis of polyhydramniosis,* to test for congenital abnormality. The test revealed the fetus suffered a common congenital abnormality known as Turner's Syndrome. 5. Turner's Syndrome, the hallmark of which is the presence of 45 chromosomes, as opposed to the normal 46 chromosomes, in every cell of the fetus, is a severe congenital abnormality that results in abortion or fetal loss among 99 percent of affected fetuses. Typical defects associated with the syndrome include cardiac, renal, and lymphatic abnormalities. Additionally, apart from those abnormalities typically associated with the syndrome, such infants are also known to present with other deficits, including developmental abnormalities of the brain. Compounding the complexity of risks associated with fetal development in this case, Mrs. Smith was diagnosed with chorioamnionitis, an inflammation of the fetal membranes, suggesting the presence of an infectious process. 6. At approximately 6:45 p.m., October 15, 1989, Mrs. Smith was admitted to Baptist Medical Center in labor. Fetal heart monitoring was started shortly after admission and revealed a fetal heart rate within normal limits. 7. At 3:00 a.m., October 16, 1989, an amniotomy (a deliberate rupture of the fetal membranes) was performed to drain excessive fluid. Upon rupture of the membranes, meconium stained amniotic fluid was noted; however, the fetal heart rate continued — we within normal limits, without any sign of fetal distress .* 8, Following the amniotomy, the fetal head stayed high and Mrs. Smith's physician elected to proceed with delivery by cesarean section. Consequently, Mrs. Smith was moved to the operating room at 8:11 a.m., and Melody was delivered at 8:41 a.m., October 16, 1989. 9. Upon delivery, Melody was DeLee suctioned and received oxygen by ambu bag for "a few seconds." Apgars were 3 at one minute and 9 at five minutes, consistent with infant well-being.* Umbilical cord pH, at delivery, was subsequently reported as 7.28, well within normal limits. 10. Following delivery, Melody was transported to the neonatal intensive care unit, where she was admitted in mild respiratory distress.* Admission chest x-ray was hazy, with fluid noted in the fissures, and the heart was noted to be enlarged, consistent with congenital heart disease. 11. Melody was initially on room air; however, at 18 hours of life, secondary to a bath, she inexplicably became hypothermic and required an oxihood. By day 2 of life, Melody was weaned to the equivalent of room air, and the oxihood was discontinued on day 3 of life. 12. On October 23, 1989, at day 7 of life, a computerized tomography (CT) brain scan was performed on Melody. The results of the scan were abnormal and provided "nonspecific findings" (not definitive for any particular diagnosis), suggesting atrophic changes in the brain. As a preliminary assessment, Melody's physicians noted these changes as consistent with those WwW —_ tw associated with a hypoxic ischemic insult; however, they were unsure, and were not shown to have ultimately resolved, the etiology and timing of Melody's anomaly. 13. As to etiology, the record developed in this case does not permit a conclusion to be drawn. Notably, there were many forces at work and risks present during the course of fetal development that could have caused or contributed to Melody's presentation, including congenital abnormality and infection. Moreover, the possibility of hypoxic insult cannot be discounted. There is, however, no compelling basis to prefer one factor over another as the cause of Melody's anomaly or, stated otherwise, to conclude that Melody's anomaly is attributable to hypoxic insult, as opposed to the other risks present during the course of her development . 14. While the proof does not permit a conclusion to be drawn as to the cause of Melody's brain anomaly, it does support the conclusion that, whatever its cause, it was not consequent to an injury to the brain caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period.’ 15. In reaching such conclusion, it is first observed that there was no evidence of fetal stress during the course of labor and delivery. Rather, the fetal heart tracings were normal throughout labor, and delivery by cesarean section was not traumatic. 16. Melody's presentation was likewise not consistent with hypoxic insult during labor and delivery. First, her umbilical ~ ~~ cord pH was normal. Had she undergone a hypoxic ischemic injury during birth, the pH would have reflected metabolic acidosis. Second, she did not require intubation and ventilation at birth, and her five-minute Apgar score was normal. 17. Melody's clinical course was likewise not consistent with hypoxic insult during labor or delivery. There was no evidence of multiple organ system dysfunction, which one would expect had Melody suffered a hypoxic ischemic event during birth. Moreover, no seizure activity developed in the immediate postpartum period. 18. Finally, the anomaly Melody was shown to suffer, as represented on the CT scan of October 23, 1989, at 7 days of life, was inconsistent with a hypoxic ischemic insult during labor and delivery. Rather, the progress or atrophic nature of the presentation, assuming a hypoxic ischemic etiology as opposed to congenital abnormality, dates the insult at least 4 to 6 weeks prior to the CT scan.
Conclusions For Petitioners: Robert J. Winicki, Esquire Winicki Law Firm 10161 Centurion Parkway North, Suite 190 Jacksonville, Florida 32256 For Respondent: W. Douglas Moody, Jr., Esquire Graham & Moody, P.A. 101 North Gadsden Street Tallahassee, Florida 32301
Other Judicial Opinions A party who is adversely affected by this Final Order is entitled to judicial review pursuant to Sections 120.68 and 766.311, Florida Statutes. Review proceedings are governed by the Florida Rules of Appellate Procedure. Such proceedings are commenced by filing one copy of a Notice of Appeal with the Agency Clerk of the Division of Administrative Hearings and a second copy, accompanied by filing fees prescribed by law, with the appropriate District Court of Appeal. See, Section 120.68(2), Florida Statutes, and Florida Birth-Related Neurological Injury Compensation Association v. Carreras, 598 So. 2d 299 (Fla. ist DCA 1992). The Notice of Appeal must be filed within 30 days of rendition of the order to be reviewed.
The Issue At issue in this proceeding is whether Wilgen Wandique, Jr., a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Wilgen Wandique and Concepcion Wandique, are the parents and natural guardians of Wilgen Wandique, Jr. (Wilgen), a minor. He was born a live infant on August 21, 1996, at Hialeah Hospital, a hospital located in Dade County, Florida, and his birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Wilgen was Gustavo Ruiz, 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. Wilgen's delivery at Hialeah Hospital on August 21, 1996, was apparently difficult due to his large birth weight, and was complicated by a shoulder dystocia. Following delivery, Wilgen was noted having evidence of a mild to moderate compromise of the upper right brachial plexus, an Erb's palsy, which affected the range of motion on the upper right extremity, including the arm, forearm, and hand. Otherwise, Wilgen's presentation was unremarkable, and he evidenced no abnormalities with regard to his mental status and, as hereafter noted, no motor abnormalities of central nervous system origin. A brachial plexus injury, such as that suffered by Wilgen during the course of his birth, is not, anatomically, a brain or spinal cord injury, and does not affect his mental abilities. Moreover, as heretofore noted, apart from the brachial plexus injury, Wilgen was not shown to suffer any other injury during the course of his birth. Consequently, the proof fails to demonstrate that Wilgen suffered an injury to the brain or spinal cord caused by oxygen deprivation or mechanical injury during the course of labor or delivery, and further fails to demonstrate he is presently permanently and substantially, mentally and physically impaired.
The Issue At issue in this proceeding is whether Emmanuel Hooks, 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 Petitioner, Brianna Denise Davidson, is the mother and natural guardian of Emmanuel Hooks, a minor. Emmanuel was born a live infant on July 26, 1999, at Gulf Coast Medical Center, a hospital located in Panama City, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Emmanuel's birth was Steven G. Smith, 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. Emmanuel's birth At or about 9:10 p.m., July 25, 1999, Ms. Davidson (with an estimated date of delivery of July 26, 1999, and the fetus at 40 weeks gestation) presented to Gulf Coast Medical Center in labor. Initial vaginal examination revealed the cervix at 2-3 centimeters dilation, effacement as "thin," and the fetus at station -3. External fetal monitoring revealed a reassuring fetal heart rate (of 140-150 beats per minute), with accelerations. Ms. Davidson was continually monitored, and at 11:00 p.m., she was admitted to labor and delivery. At the time, uterine contractions were noted at 3-5 minute intervals, and vaginal examination revealed the cervix at 3 centimeters, effacement at 90 percent, and the fetus at station -3. Ms. Davidson's labor apparently did not progress, and at 2:49 a.m., July 26, 1999, she was started on Pitocin. Thereafter, Ms. Davidson's labor progressed slowly, and at 6:45 a.m., vaginal examination revealed the cervix at 5 centimeters, effacement at 90 percent, and the fetus at station -1. In the interim, external fetal monitoring continued to reveal a reassuring fetal heart rate. Ms. Davidson's labor continued to slowly progress, and by 9:00 a.m., vaginal examination revealed the cervix at 8 centimeters, effacement at 100 percent, and the fetus at station -1. In the interim, at 8:48 a.m., Ms. Davidson's membranes spontaneously ruptured, with clear fluid noted. Thereafter, variable decelerations were noted with each contraction, consistent with umbilical cord compression, and fetal heart base line remained reassuring (in the 140-beat minute range). From 9:00 a.m. to 11:45 a.m., Ms. Davidson's labor failed to progress (with the cervix at 8 centimeters, effacement at 100 percent, and the fetus at station -1), and at 11:45 a.m., Ms. Davidson was transported to the operating room for delivery by caesarean section. Notably, between 9:00 a.m., and 11:45 a.m., while variable decelerations continued, the fetal heart rate base line remained in the 140-beat per minute range, and fetal electrode revealed the presence of short term variability. According to the records, Ms. Davidson was in the operating room at 11:45 a.m., anesthesia started at 11:45 a.m., surgery started at 12:32 p.m., and Emmanuel was delivered at 12:35 p.m. Of note, the "nucal cord x 1" observed during delivery was described as "loose," and fetal heart monitoring in the operating room and immediately prior to the caesarean section revealed a reassuring fetal heart rate. On delivery, Emmanuel was bulb-suctioned, but did not require resuscitation. Initial newborn assessment noted no apparent abnormalities, and Apgar scores were recorded as 8 at one minute and 9 at 5 minutes. The Apgar scores assigned to Emmanuel are a numeric expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, muscle tone, reflex response, and color, with each category being assigned a score ranging from the lowest score of 0 through maximum score of 2. As noted, at one minute, Emmanuel's Apgar score totaled 8, with heart rate, respiratory effort, muscle tone, and reflect response being graded at 2 each, and color being graded a 0. At five minutes, Emmanuel's Apgar score totaled 9, with heart rate, respiratory effort, muscle tone, and reflex response again graded at 2 each, and color now graded at 1. Such scores are considered normal, and inconsistent with recent hypoxic insult or trauma. Following the initial newborn assessment, Emmanuel was transported to the regular nursery, where he remained until he was discharged with his mother on July 29, 1999. Notably, the newborn nursery admission assessment was grossly normal, and there is no evidence of any complication during Emmanuel's stay. Emmanuel's subsequent development On December 10, 2001, following the filing of the subject claim, Emmanuel was examined by Dr. Michael Duchowny, a physician board-certified in pediatrics, neurology with special competence in child neurology, electroencephalography, and clinical neurophysiology. Dr. Duchowny reported the results of his neurology evaluation, as well as the history he obtained from the parents, as follows: HISTORY ACCORDING TO MR. AND MRS. HOOKS: Emmanuel is a 2 1/2 year old boy who the parents indicated suffers from cerebral palsy and brain injury. They began by explaining that Emmanuel suffered brain injury at birth due to a cord being wrapped around his neck. He was delivered by emergency caesarean section. They noted that Emmanuel's MRI has shown periventricular leukomalacia and furnished a copy of the MRI report. Emmanuel's growth and developmental milestones have been slow. He did not rollover until 9 months, nor did he sit until a year of age. He stood at 14 months, walked at 18 months and said his first word at age 2. He now has a lexicon of only one word ("ma-ma"). Emmanuel is not toilet trained. He is described as being extremely active. He does not sit still at anytime during the day and it is difficult to examine him or provide therapy. He attends a wellness center where he receives physical, speech and occupational therapy on a twice weekly basis. Communication is a particular problem area for him. Emmanuel's appetite has also been diminished and he is now "only starting to eat". His mother indicated that Emmanuel suffers from "low muscle tone" and that he drools frequently. She also mentioned that he wakes up frequently at night and is just beginning to sleep more consistently. Emmanuel does not play with other children at school. His activity level and intrusiveness have precluded meaningful peer interactions. The parents are aware that his eye contact is poor. The parents stated that Emmanuel "had seizures", but then went on to explain that 2 EEG's were normal and he was never placed on medication. The events were described as "getting into a trance". He has not had motor convulsions. FAMILY HISTORY: Both parents are healthy. A 4 year brother had no medical problems and there are no family members with degenerative illnesses, mental retardation or cerebral palsy. Emmanuel was born at Gulf Coast Medical after a 39 week gestation. He weighed 8-pounds, 9- ounces at birth and breathed well. He was discharged from the nursery at 3 days of age. Emmanuel is fully immunized, has no significant drug allergies and never been hospitalized or undergone surgery. His vision and hearing are said to be excellent. PHYSICAL EXAMINATION reveals an alert, but extremely active and well developed 2 1/2 year old toddler. Emmanuel weighs 39-pounds. His head circumference measures 50.2 cm and there are no cranial or facial anomalies or asymmetries. Emmanuel's neck is supple without masses, thyromegaly or adenopathy. The cardiovascular, respiratory and abdominal examinations are normal. Emmanuel's NEUROLOGIC EXAMINATION is difficult to complete, as he is constantly in motion. The physical examination requires restraint from his father, as he continually tries to touch things and pull items off the desktop and shelves. Emanuel has very poor eye contact and did not communicate in words at anytime during the session. It was difficult for him to follow commands as well, as his attention span constantly shifted. He drooled intermittently. The tongue movements are poorly coordinated. Cranial nerve examination reveals full visual fields to direct confrontation testing. There is blink to threat from either direction. I could not perform a fundoscopic examination. There are no facial asymmetries. Motor examination reveals mild generalized hypotonia with full range of motion. There are no adventitious movements, aside from the high activity level and no evidence of focal weakness or atrophy. Emmanuel's gait is stable, but slightly wide- based and he has generalized hypotonia. The deep tendon reflexes are 2+ bilaterally and plantar responses are in flexion. There is withdrawal of all extremities to touch. Neurovascular examination reveals no cervical, cranial or ocular bruits and no temperature or pulse asymmetries. Cerebellar testing could not be completed due to poor cooperation. In SUMMARY, Emmanuel's neurologic examination is significant for multiple areas of developmental delay. He is extremely overactive and inattentive, and has a significant behavior and communication problem. He additionally demonstrates poor eye contact and has a significant social disability. There are no specific focal or lateralizing findings to suggest a structural brain lesion. The findings on Emmanuel's neurologic examination suggests a diagnosis of a pervasive developmental disorder. Emmanuel fits within the autistic spectrum and this was communicated to the family . . . . The cause and timing of Emmanuel's neurological impairment To address the issue of whether Emmanuel's impairments were associated with an "injury to the brain or spinal cord . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital," as required for coverage under the Plan, Petitioner offered selected medical records relating to Ms. Davidson's antepartum course, as well as those associated with Emmanuel's birth and subsequent development. Additionally, Emmanuel's parents testified on their own behalf, and Respondent offered the deposition testimony of Dr. Duchowny, whose qualifications were previously noted, and the deposition testimony of Dr. Donald Willis, a physician board-certified in obstetrics and gynecology, as well as maternal-fetal medicine. As for the cause and timing of Emmanuel's impairments, it was Dr. Duchowny's opinion, based on the results of his neurology evaluation and review of the medical records, that Emmanuel's impairments are not related to perinatal asphyxia or trauma. More particularly, Dr. Duchowny expressed his views, as follows: Q. Based on your review of the records and your evaluation of Emmanuel Hooks, can you give us an overview of his condition? A. Yes. I thought that Emmanuel's neurologic examination revealed evidence of developmental neurologic impairment. He was hyperactive and had an attention deficit disorder and additionally had significant behavior, social and communication problems. All of this suggested he had developmental problems in multiple areas, consistent with a diagnosis of pervasive developmental disorder. Many of the children with pervasive developmental disorder go on to develop childhood autism as they get older. * * * Q. In this particular case, do you believe that Emmanuel's condition was acquired during the course of labor-delivery in the immediate post-delivery period? A. No, I do not. Q. What is the basis for that opinion? A. The basis for my opinion is that autism is a developmental disorder which results from unknown factors operating in utero prior to the onset of labor and delivery and is not a recognized complication of birth asphysia or birth trauma. Q. I take it your opinion is that Emmanuel Hooks did not acquire whatever neurological deficits he had as a result of any oxygen deprivation or mechanical injury occurring during labor-delivery or the immediate post- delivery period? A. That's correct. Q. In fact, was there any evidence in the medical records of any oxygen deprivation that occurred during the course of labor- delivery or resuscitation during the immediate post-delivery period? A. No. Q. Was there any evidence of mechanical injury occurring during the course of labor- delivery or the immediate post-delivery resuscitative period? A. No, there was not? Q. In your opinion, were Emmanuel's problems acquired prior to the course of labor- delivery? A. Yes. As for Dr. Willis, he was also of the opinion that the medical records revealed no evidence of oxygen deprivation or other trauma associated with Emmanuel's birth. The medical records, as well as the testimony of the physicians and the parents, have been carefully considered. So considered, it must be concluded that the proof failed to demonstrate that any impairment Emmanuel suffers was occasioned by an injury to the brain or spinal cord injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period.
