Findings Of Fact Dariel Antonio Molina Benitez was born on September 29, 2011, at Baptist Hospital in Miami, Florida. Dariel weighed in excess of 2,500 grams at birth. NICA retained Donald C. Willis, M.D. (Dr. Willis), to review Dariel’s medical records. In an affidavit dated October 17, 2016, Dr. Willis made the following findings and expressed the following opinion: In summary, Cesarean section was done for variable FHR decelerations during labor. The baby was not depressed at birth. Apgar scores were 9/9 and the baby stated to be vigorous after birth. The medical records do not suggest a birth related hypoxic event. 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’ opinion 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 is credited. Respondent retained Michael Duchowny, M.D., (Dr. Duchowny), a pediatric neurologist, to evaluate Dariel. Dr. Duchowny reviewed Dariel’s medical records and performed an independent medical examination on him on September 21, 2016. Dr. Duchowny made the following findings and summarized his evaluation as follows: IN SUMMARY Dariel’s general, physical and neurological examinations today are entirely within normal limits. There are no focal or lateralizing findings to suggest a structural brain injury. I have reviewed medical records for Dariel sent by your office on September 16, 2016. The records are primarily directed at long- term follow up and confirm that Dariel’s overall development has proceeded normally with a slight expressive language delay. An MRI scan of the brain on September 10, 2015, apparently revealed mild generalized cortical atrophy but was otherwise within normal limits. Dariel underwent a genetic workup including a chromosomal microarray that was normal. All other laboratory parameters were similarly within normal limits. An EEG obtained on April 1, 2014 was unremarkable. Given Dariel’s normal mental and physical status, I am not recommending him for compensation within the NICA program. Dr. Duchowny stated his ultimate opinion in an affidavit dated October 18, 2016, in which he opined, “Based on review of the medical records and the neurological evaluation and given Dariel’s normal and physical status, Dariel does not have a substantial and permanent mental or motor impairment, and I am not recommending him for compensation within the NICA program.” Dr. Duchowny’s opinion that Dariel does not have a substantial and permanent mental or motor 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. 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 Dariel does not have a substantial and permanent mental or motor impairment.
Findings Of Fact Neha was born on May 15, 2012, at Broward General Medical Center, located in Fort Lauderdale, Florida. Neha weighed six pounds nine ounces at birth. NICA retained Michael S. Duchowny, M.D., as its medical expert in pediatric neurology. Dr. Duchowny examined Neha on March 20, 2013, and reviewed her medical records. In an affidavit dated April 24, 2013, Dr. Duchowny opined as follows: Neha’s neurological examination is significant only for a mild degree of hypontia coupled with very slight motor development delay. In other regards, she seems to be developing quite well and I suspect that her language development will progress on schedule. There are no focal or lateralizing findings to suggest structural brain damage. A review of medical records reveals that Neha was born by stat cesarean section at Broward General Hospital due to fetal bradycardia. She was delivered with a full body nuchal cord and a true knot that was removed at birth. There was evidence of severe metabolic acidosis-arterial blood gases drawn 11 minutes after birth revealed a pH of 6.66, PC02 of 162, P02 of 11, and base excess of -32. These values were improved on a repeat series drawn at 12:27 PM. Thick meconium was suctioned below the vocal cords and Neha was diagnosed with meconium aspiration syndrome. Seizures occurred several after birth and were treated with phenobarbital and phenytoin. As previously stated by the family, Neha was immediately enrolled in a general hypothermia protocol. Of significance, a brain ultrasound exam obtained on May 15 at 6:46 PM, was normal and an MRI scan of the brain obtained on May 23 (DOL #8) was also within normal limits. Neha’s examination today does not reveal either a substantial mental or motor impairment, findings are consistent with the lack of significant MRI findings. I believe that the hypothermia protocol in all likelihood was neuro-protective and more likely than not, contributed to Neha’s positive outcome. Given Neha’s favorable outcome, I believe that she should not be considered for inclusion within the NICA program. As such, it is my opinion that Neha Kannikal is not permanently and substantially mentally impaired nor is she permanently and substantially physically impaired due to oxygen deprivation or mechanical injury occurring during the course of labor, delivery or the immediate post-delivery period in the hospital during the birth of Neha Kannikal. A review of the file does not show any opinion contrary to Dr. Duchowny's opinion that Neha does not have a substantial and permanent mental and physical impairment due to lack of oxygen or mechanical trauma is credited.
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/
The Issue The issue in this case is whether Reshnaya E. Francois suffered a birth-related injury as defined by section 766.302(2), Florida Statutes, for which compensation should be awarded under the Plan.
Findings Of Fact Reshnaya E. Francois was born on January 31, 2016, at Broward Health, in Coral Springs, Florida. Reshnaya weighed in excess of 2,500 grams at birth. The circumstances of the labor, delivery, and birth of the minor child are reflected in the medical records of Broward Health submitted with the Petition. At all times material, both Broward Health and Dr. Wajid were active members under NICA pursuant to sections 766.302(6) and (7). Reshnaya was delivered by Dr. Wajid, who was a NICA- participating physician, on January 31, 2016. Petitioners contend that Reshnaya suffered a birth- related neurological injury and seek compensation under the Plan. Respondent contends that Reshnaya has not suffered a birth- related neurological injury as defined by section 766.302(2). In order for a claim to be compensable under the Plan, certain statutory requisites must be met. Section 766.309 provides: The Administrative Law Judge shall make the following determinations based upon all available evidence: Whether the injury claimed is a birth- related neurological injury. If the claimant has demonstrated, to the satisfaction of the Administrative Law Judge, that the infant has sustained a brain or spinal cord injury caused by oxygen deprivation or mechanical injury and that the infant was thereby rendered permanently and substantially mentally and physically impaired, a rebuttable presumption shall arise that the injury is a birth-related neurological injury as defined in § 766.302(2). Whether obstetrical services were delivered by a participating physician in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital; or by a certified nurse midwife in a teaching hospital supervised by a participating physician in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital. How much compensation, if any, is awardable pursuant to § 766.31. If the Administrative Law Judge determines that the injury alleged is not a birth-related neurological injury or that obstetrical services were not delivered by a participating physician at birth, she or he shall enter an order . . . . The term “birth-related neurological injury” is defined in Section 766.302(2), Florida Statutes, as: . . . injury to the brain or spinal cord of a live infant weighing at least 2,500 grams for a single gestation or, in the case of a multiple gestation, a live infant weighing at least 2,000 grams at birth caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired. This definition shall apply to live births only and shall not include disability or death caused by genetic or congenital abnormality. (Emphasis added). In the instant case, NICA has retained Donald Willis, M.D. (Dr. Willis), as its medical expert specializing in maternal-fetal medicine and pediatric neurology. Upon examination of the pertinent medical records, Dr. Willis opined: The newborn was not depressed. Apgar scores were 8/8. Decreased movement of the right arm was noted. The baby was taken to the Mother Baby Unit and admission exam described the baby as alert and active. The baby had an Erb’s palsy or Brachial Plexus injury of the right arm. Clinical appearance of the baby suggested Down syndrome. Chromosome analysis was done for clinical features suggestive of Down syndrome and this genetic abnormality was confirmed. Chromosome analysis was consistent with 47, XX+21 (Down syndrome). Dr. Willis’s medical Report is attached to his Affidavit. His Affidavit reflects his ultimate opinion that: In summary: Delivery was complicated by a mild shoulder dystocia and resulting Erb’s palsy. There was no evidence of injury to the spinal cord. The newborn was not depressed. Apgar scores were 8/9. Chromosome analysis was consistent with Down syndrome. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain or spinal cord during labor, delivery or the immediate post delivery period. The baby has a genetic or chromosome abnormality, Down syndrome. 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. The opinion of Dr. Willis that Reshnaya did not suffer an obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain or spinal cord during labor, delivery, or the immediate post-delivery period is credited. In the instant case, NICA has retained Michael S. Duchowny, M.D. (Dr. Duchowny), as its medical expert in pediatric neurology. Upon examination of the child and the pertinent medical records, Dr. Duchowny opined: In summary, Reshnaya’s examination today reveals findings consistent with Down syndrome including multiple dysmorphic features, hypotonia, and hyporeflexia. She has minimal weakness at the right shoulder girdle and her delayed motor milestones are likely related to her underlying genetic disorder. There are no focal or lateralizing features suggesting a structural brain injury. Dr. Duchowny’s medical report is attached to his Affidavit. His Affidavit reflects his ultimate opinion that: Neither the findings on today’s evaluation nor the medical record review indicate that Reshnaya has either a substantial mental or motor impairment acquired in the course of labor or delivery. I believe that her present neurological disability is more likely related to Downs syndrome. For this reason, I am not recommending that Reshnaya be considered for compensation within the NICA program. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Duchowny. The opinion of Dr. Duchowny that Reshnaya did not suffer a substantial mental or motor impairment acquired in the course of labor or delivery is credited.
The Issue At issue in the proceeding is whether Shayla Adame, 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, Sheila Adame, is the mother and natural guardian of Shayla Adame, a minor. Shayla was born a live infant on April 1, 1996, at University Medical Center, a hospital located in Jacksonville, Florida, and her birth weight exceeded 2,500 grams. The physicians providing obstetrical services during the birth of Shayla included Drs. Pierce, Murray, and Sanchez, who were at all times material hereto "participating physician[s]" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Sections 766.302(7) and 766.314(4)(c), Florida Statutes. Ms. Adame's antenatal course and Shayla's birth Ms. Adame's antepartum course was without any apparent prenatal complication of significance; however, on November 17, 1995, at 17 weeks and 6 days gestation, the fetus was noted in a breech presentation (presentation of the buttocks of the fetus to the cervix), with placenta anterior, a condition that would persist through the course of Ms. Adame's pregnancy.1 Given the breech presentation, an external cephalic version (a manipulation of the fetal body applied through the abdominal wall of the mother to convert a breech presentation to a head presentation), referred to as an ECV in the medical records, was attempted on two occasions. The first procedure occurred on March 22, 1996, at 37 weeks gestation, and despite three attempts proved unsuccessful. The second procedure occurred on March 29, 1996, and, with one attempt, likewise proved unsuccessful. The progress notes of that attempt reveal the following: . . . ECV attempted but buttocks (presenting part) engaged and unable to elevate to perform ECV . . . [Patient] desires TOL [Trial of Labor]. CT pelvimetry [measurement of the dimensions and capacity of the pelvis to assess clinical adequacy] ordered for 4/1/06 . . . . At the time, the cervix was noted as closed and thick. At 7:35 a.m., March 31, 1996, Ms. Adame telephoned University Medical Center, the entity that provided her antenatal care, and reported that she had "[s]tarted vag[inal] bleeding last night more than spotting, less than period. Bright Red." Shortly thereafter, at 7:45 a.m., the duty nurse returned Ms. Adame's telephone call, and was informed by Ms. Adame that she was now having contractions. In response, the duty nurse told Ms. Adame to come to the hospital immediately if she experienced any more evidence of bleeding, if she experienced decreased fetal movement or no fetal movement in 2 hours, or if she experienced regular uterine contractions for 2 to 3 hours of 30 seconds duration, with 6 or more an hour. Approximately 4 1/2 hours later, at 12:15 p.m., March 31, 1996, Ms. Adame presented at University Medical Center complaining of vaginal bleeding and lower abdominal pain (described as "cramps"). External fetal monitor (EFM) and tocograph (TOCO), an instrument for measuring uterine contractions, were applied. At the time, fetal monitoring revealed a fetal heart rate of 140 to 150 beats per minute, positive long term variability and no decelerations. TOCO revealed no evidence of contractions. Vaginal examination showed the cervix at 1 centimeter dilatation, effacement at 50 percent, and the fetus high posterior. Assessment was term breach, latent labor, and the plan was to proceed with the CT pelvimetry previously scheduled for April 1, 1996. At 2:00 p.m., Ms. Adame was discharged home, with labor precautions. A little less than 6 hours later, at 7:42 p.m., March 31, 1996, Ms. Adame (with an estimated date of delivery of April 13, 1996) again presented at University Medical Center, this time complaining of spontaneous rupture of membranes (SROM) at 7:00 p.m., with "green fluid" (meconium stained fluid), and some uterine contractions. EFM and TOCO were applied, and revealed a stable fetal heart rate and positive uterine contractions. Subsequent vaginal examination revealed the cervix at 2 centimeters dilatation, effacement complete, and the fetus at station-1, with a moderate amount of "green fluid pouring from the os [ostium uteri]". CT pelvimetry revealed a clinically adequate pelvis and it was resolved to proceed with a vaginal breech delivery. Ms. Adame's labor progressed steadily until at or about 10:30 a.m., April 1, 1996, when dilatation and effacement were noted as complete, and the fetus at station +2. In the interim, fetal monitoring was reassuring, although there were occasional declarations noted and an increase in the fetal heart tone base line to 160-190 beats per minute (described in the records as protracted accelerations or persistent fetal tachycardia) associated with a slow rise in maternal temperature, which was noted to peak at 100.6 degrees Fahrenheit at 8:31 a.m., April 1, 1996. Given the elevation in temperature, blood cultures were ordered, and Ms. Adame was accorded ampicillin and gentamycin. Ms. Adame's second stage of labor was not prolonged, extending from approximately 10:30 a.m., until 11:36 a.m., when Shayla was delivered. As for the delivery, the delivery summary describes a delivery which, albeit a breech vaginal delivery, was easy and without incident. The summary further reflects that on delivery of the infant's head she was Delee suctioned, while the cord was clamped and cut, and accorded free flow oxygen. Following delivery, Shayla was handed off to the pediatrician, who noted that upon presentation Shayla was cyanotic with poor respiratory effort; however, following suctioning, stimulation, and positive pressure ventilation (PPV) for 15 seconds Shayla turned pink and cried spontaneously. Apgar scores were recorded as 3 at one minute and 8 at five minutes. The Apgar scores assigned to Shayla 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 Shayla's Apgar score totaled 3, with heart rate, respiratory effort, and reflex/irritability being graded at 1 each, and muscle tone and color being graded at 0. At five minutes, Shayla's Apgar score totaled 8, with heart rate, respiratory effort, and reflex/irritability being graded at 2 each, and muscle tone and color being graded at 1 each. Notably, while Shayla's one-minute Apgar was below normal, such occurrence is not uncommon with a breech delivery, and her five-minute Apgar score, which is most predictive of neurologic outcome, was normal. Shayla was admitted to the newborn nursery at 12:00 (noon). Admission assessment and physical were essentially normal. Generally, she was described as pink, active, and with good cry; respiration as regular and unlabored; mouth with good suck and no cleft; spine straight with no apparent abnormality; and neurologic examination revealed good symmetrical muscle tone, positive suck, and positive moro. Notwithstanding, Shayla was noted with poor feeding by the third day of admission, with persistent hypotonia and occasional irritability and arching. Shayla's course in the newborn nursery from date of admission (April 1, 1996) to date of discharge (April 29, 1996) is reasonably summarized in her resume, as follows: ADMISSION DIAGNOSES: Term female appropriate for gestational age 38 weeks. BO isommunization. Rule out sepsis. Feeding difficulties. Breech delivery. Floppy infant. DISCHARGE DIAGNOSES: Term female appropriate for gestational age. BO isoimmunization. Ruled out sepsis. Feeding difficulties improved. Breech delivery. Floppy infant, etiology unknown yet. PROCEDURES: 1. Lumbar puncture. Head CT scan. Video swallow test. EEG. HISTORY: This is a 38 weeks' AGA infant born from 18-year-old gravida 2, para 0-0-1-0 white female with prenatal care at Clinic C with 0 positive blood, hepatitis B surface antigen negative, HIV negative, RPR nonreactive, rubella immune, mother who has been positive for Chlamydia on 9/22/95 which later on became negative, several times UTI with Proteus mirabilis which was treated during pregnancy, otherwise unremarkable pregnancy. Breech presentation with less fetal movement according to mom. Rupture of membranes about 16 hours prior to delivery. Mom had chorioamnionitis, temperature of 100.6. She received antibiotics prior to delivery . . . . [Baby was born by SVD] Apgars reported at 3 and 8 secondary to hypotonia, low respiratory effort and color. Mom denied drugs, alcohol or cigarette smoking during pregnancy. Mother had one elective abortion at 9 weeks of pregnancy in 1994 with different father. Father is a black male who has not been involved after pregnancy. HOSPITAL COURSE: Baby had poor p.o. feeding on the third day of admission noticed, not improving her tone and mostly floppy with occasional irritability and arching. With initial prolonged rupture of membranes and mother's known history of chorio, blood cultures, CBC, urine and CIE were done, and the patient was started on antibiotics, ampicillin and gentamicin. On the third day due to poor feeds LP was done too, and continued antibiotics until 72 hours of negative cultures. The infant continued to be floppy with generalized hypotonia and occasional arching especially neck and back accompanied with opisthotonos and extension of extremities with irritability and inconsolable. This problem continued during the past 28 days of newborn nursery. Her hypotonia did not progress, and at the same time did not improve or improved a little bit. Her irritability and arching to some extent decreased. These days she is most of the time resting with less irritability but the problem of hypotonicity and lethargy continued. Problem #1. Fluids/electrolytes/nutrition: On the first three days of life she continued with the regular care with p.o. feeding. Initially it was decided by mom to breast- feed but since she was not eating enough or not sucking enough continued with bottle feeding, namely Enfamil with Iron, but on the third day it was noticed that she was not taking enough or not sucking enough, and at the same time was getting easily tired. It was decided to continue with p.o. and at the same time NG feeding but her feeding pattern did not improve and most of the time she was dependent on NG feeding due to decreased or insufficient sucking reflex and swallowing problem. Speech therapy was consulted. Video swallow was done which showed incoordination of the muscle, and at the same time although there was no frank aspiration but was high risk for aspiration. Continued NG feeding most of the time and with OT and physical therapy with speech therapy daily arrangement this problem somehow resolved. Accordingly, it has been about a week that the patient is eating by p.o. without any need for NG. The last video swallow which was done about a week ago, namely on 4/24 showed improved swallowing mechanism but still is at risk for aspiration. No aspiration was noticed during this test. Accordingly, she is taking about 75 cc Enfamil with Iron and rice cereal is added to it . . . for thickening and decreased risk for aspiration. Problem #2. Floppy baby, hypotonia, occasional arching and irritability: The patient was born with breech presentation with history of prenatal decreased fetal movement with Apgars of 3 and 8. She continued to be hypotonic which was not improving and occasional arching which was significant. Initially sepsis was ruled out including lumbar puncture done which was normal and antibiotics were discontinued based on negative cultures. CT scan of the head was done which was normal. Neurology consult was done from Nemours Children's Clinic. Dr. Shank followed this patient. Their impression was hypotonia that appeared to be prenatal due to breech presentation and decreased fetal movement. Dr. Shanks suspected that it is central due to fair muscular strength, but at the same time it was complicated by absence of deep tendon reflex. [Dr. Shank observed that the differential diagnosis was extensive (chromosome, metabolic, syndromic mostly likely)]. He suggested to do chromosomal workup, metabolic, and other syndromes which can cause the same hypotonia and his recommendation was followed. High resolution chromotrope was normal. Basic chemistry including sodium, potassium, calcium, phosphate, magnesium, liver function tests, and CPK were normal. Serum blood test was normal. Serum very long chain fatty acid was done which is followed by genetics, the result of the test is mentioned below. Urine metabolic screening was done too. Thyroid function was normal which was recommended also by neurology. EEG was done on 4/16/96. The patient had episodes of suspicious lip smacking. To rule out possibility of seizure EEG was done the same day which was normal. Ophthalmology consult was done on 4/10/96 to rule out possibly of some metabolic abnormalities, infectious, or other finding by routine lens evaluation. Ophthalmology examination was entirely normal at this time. The patient was also followed by DEI (developmental early intervention) and also by OT, PT and ST on the basis of p.r.n. Genetics: The patient was seen today by Dr. Perszyk from Nemours Children's Clinic after having all the metabolic screening and results from plasma amino acid, urine amino acid, urine organic acid and other tests . . . [At the time, Dr. Persyk's differential diagnosis included mitochodrial disease, lactic acidosis, or congenital myopathy (central core disease).] Problem #3. Social: Mom is an 18-year-old white female. Father is black but has not been involved. There is no history of any genetic abnormality, muscular disease, neurologic abnormality or seizures in the family on the maternal side. We do not know anything about the father's side. Mom had prenatal care . . . [at University Medical Center, Clinic C]. PHYSICAL EXAMINATION ON ADMISSION: Weight 2,915 g which is equal to 25-50th percentile, height 45.7 cm equal to 10th percentile, head circumference 34.5 cm equal to 75th percentile. On admission vital signs were stable. Pulse 150, respiratory rate 48, blood pressure 58/30. Generally she was described as pink and active without any facial dysmorphism. Eyes with red reflex without discharge. Ears no tags, no sinus, no external abnormality. Mouth without any cleft. Neurological exam has been described as symmetric muscle tone and active. PHYSICAL EXAMINATION ON DISCHARGE (DAY #28): Weight 3,181 g. She has been responsive to touch, pain, stimuli, but still has arching movements and opisthotonos but to a lesser extent. HEENT showed anterior fontanelle open and flat. Head circumference 36.5 cm. Positive red reflex. Pupils equal, round and reactive to light, but at this time is not focusing which is expected. Lungs clear to auscultation bilaterally. Cardiovascular with rate and rhythm regular without murmurs. Good peripheral pulses. Abdomen soft, no mass, no hepatosplenomegaly. Liver edge is palpable about 1.5 to 2 cm below right costal margin and it is soft. Genitourinary without any hip click. Extremities with generalized hypotonia but is moving with pain and stimuli. Neurological exam showed generalized hypotonia. She cannot move her head at all. She has some flexion of extremity but is purposeless. Mild grasp reflex. No deep tendon reflex. No clonus. Has good sucking reflexes but there is no rooting reflex. No Moro reflex. SIGNIFICANT LABORATORY FINDINGS: Baby is B positive, Coombs' positive. Mom is 0 positive. Blood culture negative. Chloric metabolites negative. Group B Strep urine negative. CSF result showed glucose of 38, protein 58, with 3 white blood cells. CSF culture negative. Total bilirubin increased to maximum 7.3 with direct of 0.2. Chem-20 was done on 4/11/96 which showed glucose of 45, sodium 134, potassium 4.1, chloride 99, BUN 6, creatinine 0.6, calcium 10, phosphorus 7.1, total protein 6.2, albumin 4, total bilirubin 2.1, SGOT 22.7, alkaline phosphatase 190, SGPT 14, triglycerides 154, uric acid 3.2, LDH 439, cholesterol 101, anion gap 12. Hematocrit 43.4, white blood cells 11.3. T4 16, TSH 1.97, CK 313. All of the above has been in normal range. Repeated Chem-20 on 4/15/96 showed glucose of 63, chemistry within normal limits, total protein 5.4, albumin 3.5, liver function tests within normal limits, hematocrit 46, LDH 306, cholesterol 91, anion gap 9, magnesium 2. Ammonia showed 41 and CK 193. Lactic acid 2.6. UA showed normal with pH of 6.5, with no ketones. Urine CMV was negative. [Her] stool pH was 7, no reduce in substance. IgM was done on 4/24/96 which was 30.6 and IgG was 832 which was within normal limits. PKU was normal. Galactosemia normal. Hemoglobin electrophoresis normal and 17-hydroxy was 27.2 which is within normal limits. A very long chain fatty acid showed mildly elevated on 4/26 which is 0.034. Creatinine was normal, free creatinine was normal too. Amino acid panel was done. A copy of the result is sent to genetics, Dr. Perszyk, and also a copy of the urine amino acid and urine organic acid - at this time not significant finding. Chest x-ray was done which was normal. IMPRESSION: In summary, this is a floppy child who was born at 38 weeks of gestation with AGA with history of breech presentation with no genetics or prenatal complication. Her floppiness did not progress, at the same time it did not improve significantly either. Metabolic screening was done which at this time is not significant and needs to be followed up with other clinical findings. Neurological abnormality could not be ruled out at this time and needs to be followed up by neurology. Her p.o. feeding improved. This patient never had any life-threatening event during the 28 days in newborn nursery. She has never been on any monitors. She is still at risk for aspiration, and we instructed the parent about the feeding; they are CPR trained. VNA nursing, OT, PT and speech therapy are following the case. Primary care doctor, Dr. Cedres, is aware of the situation, and the plan is to follow closely by genetics, neurology and primary care physician for further workup. FOLLOWUP: 1. Dr. Cedres . . . . He is the primary care physician . . . . Dr. Perszyk, Nemours Children's Clinic, Division of Genetics, in two weeks . . . . Dr. Shanks, Nemours Children's Clinic, Division of Neurology, for the followup of the patient's neurological evaluation, improvement or drugs. 4. EIP (early intervention program) for followup for occupational, physical and speech therapy . . . . Shayla's subsequent development Following her discharge from University Medical Center, the medical records reveal that Shayla was followed at Nemours Children's Clinic at least through July 28, 1998. There, Shayla was under the care of, among others, Daniel E. Shanks, M.D., a pediatric neurologist, and Anthony Perszyk, M.D., a pediatric geneticist, both of whom had consulted on her care at University Medical Center. Such continuum of care was initially directed toward establishing an etiology that would explain her hypotonia, manifest at birth (described as congenital) and failure to thrive (poor feeding), but later came to include a more complex symptomatology (including discoordination of movement, gastroesophageal reflux, developmental delay (motor and cognitive), absence of deep tendon reflexes, indifference to pain, and absence of tears) that slowly manifested. Over time, Shayla underwent extensive diagnostic evaluations, including genetic, metabolic, structural, and infectious disease testing, which failed to reveal any abnormality to explain her presentation, and on August 4, 1997, Dr. Shanks summarized his thoughts, as follows: IMPRESSION: Presumed static encephalopathy of unclear etiology in a youngster who has a number of somewhat unusual features for a typical cerebral palsy. Though she has central hypotonia, she is developing some increased tone distally but has reflexes that I cannot elicit. She seems to have a decrease in her sensory responsivity. The possibility of a congenital neuropathy in addition to her encephalopathy is raised. Additionally, concerns regarding possible high cord lesion cannot be excluded. Consequently, Dr. Shanks recommended that they obtain "a C-spine and brain MRI, as well as nerve conduction studies." The spinal MRI did not reveal any abnormality. The brain MRI, taken September 5, 1997, was read, as follows: Minimal squaring of the frontal horns can be defined with prominent ventricular system involving the lateral, third as well as fourth ventricles. Minimal increase in extraaxial fluid can also be demonstrated. These findings are nonspecific. The lateral ventricles are slightly asymmetric, more so on the right. These findings are nonspecific. A focal signal or structural abnormality cannot be demonstrated. The myelination pattern is within normal limits. Minimal increase in CSF volume can be seen in the posterior fossa, the finding should represent a giant cisterna magnum. Incidental finding of abnormal increase in T2 signal intensity in the ethmoid, as well as maxillary sinuses. Correlation with clinical findings would be helpful. The results of the MRI brain scan are consistent with periventricular leukomalacia (PVL) which, as an isolated finding, is nonspecific or, stated otherwise, not diagnostic. Of note, PVL, which demonstrates as "a tiny bit of scarring in the infant's ventricles," may be seen in infants who have suffered ischemic brain disease, as well as in normal term and pre-term infants. (Respondent's Exhibit 1, pages 26 and 27). More helpful to establishing an etiology for Shayla's neurologic presentation, the nerve conduction studies, performed November 19, 1997, demonstrated abnormalities consistent with a severe sensory neuropathy, likely the group HSAN (hereditary, sensory and autonomic neuropathy), also referred to as congenital sensorimotor neuropathy during the course of this proceeding. To confirm such impression, Dr. Shanks ordered a seral nerve biopsy, which was performed in January 1998, and unequivocally identified the presence of a neuropathic process, characterized by severe loss of myelinated fibers. On March 13, 1998, at the request of Dr. Shanks, Shayla was seen by David Hammond, M.D., Director of Neuromuscular and MDA Clinics, Nemours Children's Clinic. The results of that consultation were reported, as follows: I saw Shayla in consultation in neurology clinic at Nemours today as requested by her regular neurologist, Dr. Shanks. History was obtained from Shayla's mother and grandmother. CHIEF COMPLAINT: 23-month old with developmental delay and truncal hypotonia, etc. INTERIM HISTORY OF PRESENT ILLNESS: Very slow if any developmental advances. She is not yet sitting. Her language skills are behind for age although there has been no apparent plateau or regression. Family has noted unexplained fevers. Additionally, an apparent insensitivity to pain persists. The parents have noted no significant abnormalities in terms of sweating, lacrimation, GI changes or pallor or skin mottling. REVIEW OF SYSTEMS, MEDICAL HISTORY, FAMILY HISTORY, SOCIAL/DEVELOPMENTAL HISTORY: Data as detailed in Dr. Shanks' notes on 8/4/97 and previous. No family history of neuropathy. GENERAL EXAMINATION, HIGHER INTEGRATIVE FUNCTIONS, CRANIAL NERVES, SENSORY, MOTOR, REFLEXES, COORDINATION, GAIT: Data as detailed in Dr. Shanks' letter of 8/4/97 and previous except/with height 79.8 cm, weight 10 kg, head circumference 46.5 cm. She is irritable but appears otherwise appropriate in terms of her social interaction when calm. No expressive language detected in the course of the examination. She does appear to respond well to simple directions from parent or grandparent. Truncal tone is decreased. Her lower extremity tone which was felt to be increasing on previous exams is difficult to evaluate because of her resistance to examination today. Areflexia. No response to noxious stimuli. No tears are noted when she is irritable and crying. Cardiac exam shows no apparent murmurs and a regular rhythm with a rate (while irritable) of 120. Abdominal examination is benign. No tongue fasciculations. She has vigorous movements of each of the four extremities as she resists examination. She is unable to sit or stand independently. DATA REVIEWED: MRI of brain (9/97) minimal squaring of the frontal horns with prominent ventricular system involving lateral third as well as fourth ventricle. Minimal increase in extra-axial fluid. Posterior fossa findings suggestive of a giant cisterna magna. Nerve conduction EMG (11/97) compatible with electrophysiologically severe sensory neuropathy. R1 blink reflexes were not elicitable. Sensory nerve action potentials are absent throughout. Motor conduction studies normal. Sural nerve biopsy (1/98) severe decrease in density of myelinated fibers which is diffuse. An unequivocal neuropathic process is present characterized by severe loss of myelinated fibers. Consider congenital neuropathy. Other available medical records as summarized above. ASSESSMENT: Child with a number of problems. 1. Indifference to pain, truncal hypotonia, gross motor delay and areflexia. The clinical constellation and the laboratory data are consistent with the diagnosis of hereditary, sensory and autonomic neuropathy (HSAN). HSAN Type IV is generally distinguished from HSAN Type II based on the presence of more significant cognitive involvement and more severe anhydrosis. Given the history suggestive of language and cognitive delay and the history of unexplained fevers, HSAN Type IV appears somewhat more likely diagnosis in this case than HSAN Type II. 2. Suggestion of possible autonomic involvement related to #1 in terms of her unexplained fevers. Would also recommend screening for cardiac arrhythmia with an EKG. 3. At risk unrecognized trauma skin ulcerations, etc. related to her HSAN. 4. Cognitive delay, changes on MRI scan as outlined above, changes in tone which have been noted in the past. Question of possible encephalopathic components unrelated to her HSAN. Would defer to Dr. Shanks in term of further evaluation and recommendations in this regard. According to the medical records, Shayla's last consultation with Dr. Shanks was June 8, 1998, "for followup of her hereditary sensory autonomic neuropathy type IV most likely." Dr. Shanks' notes of that visit do not speak to an encephalopathic component unrelated to Shayla's HSAN, but conclude with his "Impression: Encephalopathy associated with hereditary sensory autonomic neuropathy."2 On May 22, 2000, Thayla was examined by Michael S. Duchowny, M.D., a pediatric neurologist associated with Miami Children's Hospital. The results of that neurologic evaluation were reported by Dr. Duchowny, as follows: I evaluated Shayla Adame on May 22, 2000. Shayla is a four year old developmentally delayed girl who is brought for an evaluation of development problems. HISTORY ACCORDING TO MRS. ADAME: Mrs. Adame began by explaining that Shayla has been diagnosed with hereditary sensory and autonomic neuropathy type . . . [IV]. In this regard she has a congenital absence of sensitivity to pain in conjunction with other abnormalities. Her lack of pain perception has caused her to scratch her eyes and she has already required a right eye corneal transplant due to trauma. This has been accentuated by Shayla's inability to generate tears and she appears to lack the ability to generate secretions in a generalized sense. The diagnosis of this rare disorder was made at Nemours Children's Clinic at age 2 years when Shayla had a seral nerve biopsy. The results are not available today. Shayla is developmentally delayed with regard to her language and tends to speak in single words, but occasionally puts several together to talk in phrases or sentences. Her hearing is said to be intact. She drools frequently and has been diagnosed with "cerebral palsy". She has a scoliosis and is fitted with a brace, but this is not present today. Shayla has suffered from intermittent muscle spasms and has had a total of 2 or 3 febrile seizures lifelong. She was hospitalized in March of this year for pneumonia and was sent home on cardiac monitoring. Shayla required a G-tube which was placed at a year of age. This was withdrawn at age 2 years and she is now able to sustain herself through oral intake. She had neuroimaging studies as a infant which apparently were normal. Shayla presently takes artificial tears, but is on no other medications. She receives various therapies which have been beneficial. There is a history of unexplained fever which appears to be related to environmental temperatures and she has had temperatures as high as 106 degrees. Shayla has pervasive absence of sweating and apparently is scheduled for a sweat test in the near term. She has also had tongue biting episodes with the right lateral border of her tongue sustaining a significant injury. FAMILY HISTORY: Shayla is an only child. Her father[']s whereabouts are unknown. There is no family history of sensory or motor neuropathy and no history of any neurodegenerative illnesses. PRE- AND PERINATAL HISTORY: Shayla was born at term by frank breech presentation at University Hospital. Her birth weight was 6- pounds, 6-ounces. She remained in the hospital for a total of 29 days. Shayla is not walking, although she can pull to a stand. Toilet training is "in process." * * * PHYSICAL EXAMINATION reveals an alert small child, but in proportion. Her weight is 27- pounds and height 27-inches. The head circumference measures 48.4 cm and the fontanelles are closed. There are no cranial asymmetries. Shayla has a large area of depigmentation on her right posterior lateral buttock region. There is an asymmetry of her eye with a skin tag linking the upper and lower lids on the right lateral aspect of her eye where she had the corneal transplant. A small traumatic cataract is noted in the left eye as well. There are thick callouses over the knees from crawling. She has multiple ulcerations of her toes and fingers where she has picked at sores to the point of thick soft tissue overgrowth. Shayla has only a few teeth and several stainless steel replacement caps. Multiple gingival abscissa are noted. There is a scoliosis convexed to the left. The cardiovascular, respiratory and abdominal examinations are normal. The healed G-tube scar is noted. The limbs appear warm and there are full and bounding periphereal pulses. NEUROLOGIC EXAMINATION reveals Shayla to have delayed language development. She speaks primarily in 1 or 2 word phrases with thick dysarthric speech that frequently required interpretation. Drooling is remarkably prominent. There is central gaze fixation with conjugate following movements. The pupils are 3 mm and react sluggishly to light. I was unable to visualize the fundi of either eye due to opachification. Shayla can clearly see objects in all visual spheres and tracks actively. There is no facial asymmetry. The tongue is moist and appears to be papillated with several traumatic lacerations on the lateral grooves. Motor examination reveals symmetric strength and bulk. The tone is slightly diminished throughout. There is generalized areflexia of both upper and lower extremities. Sensory examination reveals absence of withdrawal to painful pinching of all extremities. She does appear to feel however, although pain is not specifically perceived. Shayla sits with a stable balance and without head titubation, but can not stand without support. Neurovascular examination reveals no cervical, cranial or ocular bruits and no temperature or pulse asymmetries. In SUMMARY, Shayla's neurologic examination is consistent with type IV hereditary sensory and autonomic neuropathy, a rare disorder that is often associated with mental retardation. This disorder is likely to be genetic in origin, although direct linkage has not been established. The cause (etiology) and timing of Shayla's neurologic dysfunction To address the cause and timing of Shayla's neurologic dysfunction, the parties offered the medical records relating to Ms. Adame's antepartum and intrapartum course, as well as those associated with Shayla's birth and subsequent development. Portions of those records have been discussed supra, and further salient portions will be addressed infra. Additionally, Petitioner offered the deposition testimony of Paul R. Summers, M.D., an expert in obstetrics and gynecology, and Respondent offered the deposition testimony of Michael S. Duchowny, M.D., an expert in pediatric neurology, and Charles Kalstone, M.D., an expert in obstetrics and gynecology. The medical records and the testimony of the physicians offered by the parties have been carefully considered. So considered, it must be concluded that Shayla's neurologic dysfunction resulted from a Type IV hereditary, sensory and autonomic neuropathy (a congenital sensorimotor neuropathy) unassociated with any intrapartum injury, hypoxic or traumatic in nature.3 In reaching such conclusion, the evidence regarding the bleed Ms. Adame suffered the evening of March 30, 1996 (which Dr. Summers alone opined evidenced a partial placental abruption, with resultant hypoxic brain injury and serious neurologic damage) has not been overlooked; however, it is also noted that when Ms. Adame presented at University Medical Center at 12:15 p.m., and later at 7:42 p.m., March 31, 1996, fetal heart monitoring was reassuring for fetal wellbeing, and that monitoring throughout the course of labor evidenced no significant abnormalities. Moreover, Ms. Adame's labor was essentially normal, the second stage of labor was not protracted, and Shayla's delivery, including her head, was without apparent delay or other difficulty. Further, it is noted that on delivery, Shayla presented with hypotonia, a cord pH of 7.182 and a base excess of -4.5 (a result inconsistent with significant deficit in oxygenation), a normal five-minute Apgar, and no evidence of seizure activity in the immediate postnatal period. Finally, it is noted that by presentation, development, and a seral nerve biopsy, it has been demonstrated that Shayla's neurologic presentation is consistent with a Type IV hereditary, sensory and autonomic neuropathy, as opposed to any intrapartum injury. In sum, as observed by Drs. Duchowny and Kalstone, whose testimony is most consistent with the medical records and the observation of Shayla's treating physicians, the record does not evidence an acute event during labor and delivery as the cause of Shayla's neurologic impairment.4
