Findings Of Fact Tristan N. Thomas was born on August 12, 2009, at Baptist Medical Center in Jacksonville, Florida. Tristan weighed in excess of 2,500 grams. Donald Willis, M.D., was requested by NICA to review the medical records of Tristan. Based on his review of the medical records, Dr. Willis opined as follows: In summary, labor was complicated by hypertension and a placental abruption. This resulted in a depressed baby at birth. Full resuscitation was required. The initial blood gas after birth was consistent with severe acidosis with a pH of 6.6. Seizures developed shortly after birth. EEG and MRI were consistent with HIE. There was an apparent obstetrical event that resulted in loss of oxygen to the baby’s brain during labor, delivery, and continuing into the immediate post delivery period. This oxygen deprivation resulted in brain injury. I am not able to comment about the severity of the brain injury. Michael S. Duchowny, M.D., was requested by NICA to perform an independent medical evaluation of Tristan. The evaluation was done on January 22, 2014. Based on his evaluation, Dr. Duchowny opined as follows: In summary, Tristan’s neurologic examination reveals evidence of multiple developmental delays in the social, communication and behavioral domains. His findings are consistent with a clinical diagnosis of autism spectrum disorder and there are no specific focal or lateralizing findings to suggest structural brain damage. I had an opportunity to review medical records supplied to me which confirmed the history obtained from Tristan’s mother. Tristan was delivered at term at Baptist Medical Center. His mother suffered from preeclampsia and was treated with magnesium sulfate. Tristan was delivered by emergency cesarean section due to placental abruption, required resuscitation at birth and had Apgar scores of 0, 3, and 7 at 1, 5, and 10 minutes. His cord blood gases revealed severe acidosis and he was placed in a head cooling protocol for 72 hours following stabilization. However, an ultrasound of the brain on August 17, 2009 was negative as was an MRI scan performed on August 18, 2009. In summary, the findings on examination today together with the medical history did not provide evidence of significant brain damage and Tristan does not suffer from a substantial motor impairment. Furthermore, his neurological problems did not, in my opinion result from either mechanical injury or oxygen deprivation acquired in the course of labor and delivery. His autism spectrum disorder is a primary developmental disability of prenatal origin. I, therefore, believe that Tristan should not be considered for admission into the NICA program. A review of the file does not show any contrary opinion to Dr. Willis’ opinion that Tristan did sustain oxygen deprivation during labor, delivery, and resuscitation in the immediate post-delivery period Plan. Dr. Willis could not comment on the extent of any brain injury that resulted from the oxygen deprivation. Dr. Duchowny opines that Tristan does not suffer from significant brain damage and that Tristan does not have a substantial motor impairment. These opinions are not disputed and are credited.
The Issue At issue in this proceeding is whether Britney Palmero, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary matters Manuel Palmero and Mary Jane Palmero are the parents and natural guardians of Britney Palmero (Britney), a minor. Britney was born a live infant on January 11, 1993, at South Miami Hospital, a hospital located in South Miami, Dade County, Florida, and her birth weight exceeded 2500 grams. The physician providing obstetrical services during the birth of Britney was Julio Somoano, M.D., who was, at all times material hereto, a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Mrs. Palmero's antepartum course and Britney's birth On January 11, 1993, Mrs. Palmero was admitted to South Miami Hospital for induction of labor. At the time, her estimated date of confinement was January 19, 1993, and her antepartum course was without apparent complication; however, due to Mrs. Palmero's expressed discomfort during the later stage of pregnancy, and the size of the baby (over eight pounds), it was resolved to deliver the baby prior to its due date. Mrs. Palmero's initial admission on January 11, 1993, occurred at or about 7:50 a.m. Thereafter, at or about 8:00 a.m., external fetal monitoring commenced, and revealed a normal fetal heart rate pattern or, stated differently, reflected evidence of fetal well-being. Mrs. Palmero received her first Prostin gel, as the first step in the induction of labor, at 9:45 a.m., and her second at about 11:45 a.m. Following the second Prostin gel, mild irregular contractions were noted; however, her cervix did not progress (she did not go into labor), and at 2:00 p.m. Mrs. Palmero was sent home with instructions to call if she began to experience regular contractions, if the membranes ruptured, or if she observed any vaginal bleeding. During the period she was monitored, and until her discharge at 2:00 p.m., no vaginal bleeding was observed, and the fetal heart rate pattern continued to evidence fetal well-being. Mrs. Palmero returned to labor and delivery at or about 3:21 p.m. complaining of increased "intensity of cramps" and some bloody discharge. A small amount of red vaginal blood, with mucus, was noted; however, vaginal examination revealed the cervix (at 1 centimeter, effacement at 50 percent, and the fetus at station -2) to be unchanged. External fetal monitoring again revealed a reassuring fetal heart rate and, at 3:40 p.m., there being no evidence that she was yet in labor, the instructions previously given were reviewed and Mrs. Palmero was sent home. At or about 8:00 p.m., January 11, 1993, Mrs. Palmero returned to labor and delivery complaining of moderately bright red bleeding. According to Mrs. Palmero, her membranes ruptured at 7:00 p.m. with pinkish fluid noted. Vaginal examination revealed the cervix to be at 1 to 2 centimeters, effacement at 50 percent, and the fetus at station -2. A moderate amount of red fluid with occasional clots was observed by the nurse. Contractions were noted at a frequency of 1 1/2 to 3 minutes, with moderate intensity, and fetal heart rate was noted as stable, with good variability. At 8:45 p.m. it was noted that Mrs. Palmero continued to leak a large to moderate amount of red fluid from the vagina, but no clots were noted. Fetal heart rate remained stable. Dr. Somoano was notified by phone of the patient's status, and he announced he was enroute to the hospital. Dr. Somoano arrived at the hospital at or about 9:15 p.m. Vaginal examination revealed the cervix to be 3 centimeters, effacement complete, and the fetus at station - Fetal heart rate remained stable. Given Mrs. Palmero's presentation on admission, Dr. Somoano entertained the likelihood of abruptio placenta, but, there being no evidence of fetal distress, elected to proceed with a normal delivery. An epidural anesthetic was ordered. Following the epidural, Mrs. Palmero's contractions were less frequent. Given the stability of the fetal heart rate pattern, Dr. Somoano ordered Pitocin to augment labor. Pitocin was started at 10:45 p.m., which brought Mrs. Palmero's contractions closer together; however, given that she began bleeding more and her cervix had only progressed to 5 centimeters, Dr. Somoano elected to proceed by cesarean section to avoid the risk of a complete abruptio. Consequently, at 11:15 p.m., Pitocin was discontinued and Mrs. Palmero was moved to the operating room. During this period, apart from a few mild variable decelerations consistent with cord compression, and one variable deceleration about 45 minutes before delivery, the fetal heart rate remained stable and continued to evidence fetal well-being. The cesarean section was begun at 11:28 p.m., Britney was delivered at 11:29 p.m., and the procedure was complete at 11:45 p.m. During delivery, the cord was noted to be tight, around the baby's neck twice, and around the shoulder. Upon removal of the placenta, a marginal abruptio placenta, 15 to 20 percent, was observed. Following delivery, Britney was handed off to the attending neonatologist, who assigned her Apgar scores of 7 at one minute and 9 at five minutes. The Apgar scores assigned to Britney are a numerical expression of the condition of a newborn infant, and reflect the sum of 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 Britney's Apgar score totalled 7, with heart rate and respiratory effort being graded at 2 each, and muscle tone, reflex irritability and color being graded at one each.2 At five minutes, her Apgar score totalled 9, with heart rate, respiratory effort, muscle tone, and reflex irritability being graded at 2 each, and color being graded at 1. Such scores are normal and, while they do not rule out the presence of an existent brain injury or anomaly, the presentation represented by those scores is not consistent with a neurologic insult (injury to the brain) having occurred during the birth process. Britney's course and development subsequent to delivery Following delivery, Britney was transported to the newborn nursery, where she was admitted at "0000" January 12, 1993. Apart from the admitting nurse noting that Britney was a little lethargic and hypotonic, Britney's presentation appeared grossly normal. Dr. Jose Luis, the pediatrician, was notified of Britney's admission to the nursery at 12:40 a.m., January 12, 1993, and his physical examination on that date, as well as his examinations of January 13 and January 14, 1993, described a normal new-born girl without evidence of abnormality. During her stay in the nursery, Britney evidenced no problems, and her course was considered routine. She and her mother were discharged January 14, 1993.3 Britney's early infancy was characterized by good health, and no apparent problems were observed until approximately six to seven months of age. At that time, the parents observed that Britney's right hand was held in a closed fist position. The parents' concern was reported to Britney's pediatrician. He monitored Britney's progress, and in December 1993, referred her for a neurologic consult with Dr. Israel Alfonso at Miami Children's Hospital, Department of Neurology. Britney was examined by Dr. Alfonso on or about January 6, 1994. At the time, Dr. Alfonso noted Britney's general examination as normal; however, her neurological examination revealed the following: . . . neurological examination is characterized by a right hemiparesis that does not involve the face but it does involve the right arm, especially the right hand and also the right leg. Her deep tendon reflexes are within normal range in all four extremities. The right hand is somewhat smaller than the left, especially the thumb. The thumb is kept in a cortical position continuously. She did not use the right hand to grab any object while examined though she occasionally opens that hand at will. IMPRESSION: Right hemiparesis. Dr. Alfonso recommended an MRI of the brain to identify the most likely cause for Britney's presentation.4 The MRI was performed on January 7, 1994, and provided the following findings and conclusions: FINDINGS: There is focal signal abnormality seen in the left posterior frontal parietal region. This is reduced on the T1 weighted images and increased on the T2 weighted study. Also noted is enlargement of the left lateral ventricle. There is prominence of the sulcal folds in this region. Also, there is a discrepancy in the white matter volume with it being reduced on the left. There is a more immature myelin signal on the left particularly in the periventricular region. There is also noted thinning of the corpus callosum in the posterior body. The brain stem shows a reduction in size of the left cerebral peduncle. Evidence of mass effect, midline shift or hemorrhage is not seen. CONCLUSION: Findings as described in keeping cystic encephalomalacia involving the posterior, frontal and anterior parietal region. Secondary diaschisis involving the left cerebral peduncle is noted as well as the posterior body of the corpus callosum. There is signal abnormality identified of the white matter in the left periventricular region and associated with the posterior frontal parietal region. While this may represent delayed maturation of myelin, leukomalacia should also be considered. In addition, there is a reduction in volume of the white matter of the left cerebral hemisphere identified when compared with that on the right. These findings most likely represent a sequelae of a vascular insult. The infarct (loss of brain tissue) in the left cerebral hemisphere, near the left middle cerebral artery, depicted by the MRI is consistent with a vascular insult (cerebral vascular accident or stroke). The vascular insult resulted in focal damage to a selected region of the left hemisphere, and was clearly the cause of the prominent right hemiparesis, evidenced by spasticity of the right arm and leg, with which Britney presents.5 The dispute regarding compensability Given the proof, it cannot be subject to serious debate that Britney suffered an injury to her brain that resulted in neurologic impairment. What remains to resolve is the origin, nature and timing (genesis) of that injury or, more pertinent to these proceedings, whether the proof demonstrates, more likely than not, that the injury Britney suffered was "caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as opposed to some other genesis.6 Section 766.302(2), Florida Statutes. With regard to such issue, Petitioners contend that the brain injury was caused by oxygen deprivation (a hypoxic ischemic injury), consequent to placental abruption, which occurred during the course of labor, delivery, or resuscitation. In contrast, Respondent contends the proof is not consistent with a hypoxic ischemic injury occurring during the course of childbirth but, rather, with a brain injury resulting from a vascular insult or infarct,7 commonly referred to as a stroke, suffered in the antenatal (prenatal) period. Respondent's view of the proof has merit. The genesis of Britney's brain injury Britney's presentation is consistent with a group of persisting motor disorders appearing in young children, commonly referred to as cerebral palsy, that are characterized by delayed or abnormal motor development, such as spastic paraplegia, hemiplegia, or tetraplegia, which is often accompanied by mental retardation, seizures or ataxia. Such disorders result from brain damage caused by birth trauma, such as that which may result from oxygen deprivation or mechanical injury during labor or delivery, or may be associated with a intrauterine (antenatal) event or pathology, such as a vascular insult or stroke, genetic abnormality, or developmental abnormality.8 Here, the proof is compelling that Britney's brain injury resulted from a stroke suffered in the antenatal period, most likely after 30 weeks gestation and at least two weeks prior to delivery, and that it was not associated with any event occurring during the course of labor, delivery, or the immediate post-delivery period.9 In so concluding, it is initially observed that the results of the neuro-imaging study (MRI) are inconsistent with brain injury resulting from oxygen deprivation. Rather, the neuro-imaging study, as well as Britney's neurologic examination, are consistent with focal damage occasioned by a left hemisphere stroke, as opposed to the bilateral or global damage one would typically associate with an injury occasioned by oxygen deprivation. Moreover, Britney's course pre-delivery and post- delivery was inconsistent with hypoxic or ischemic damage occurring during the course of birth. First the stability of the fetal heart rate during labor and delivery affords objective proof that the marginal abruption Mrs. Palmero suffered did not adversely affect fetal oxygenation. Second, Britney's healthy presentation, as evidenced by her Apgar scores and uneventful hospital course, are inconsistent with the presentation and hospital course one would reasonably expect had the fetus suffered a brain injury, of the magnitude capable of producing the damage evidenced by Britney's MRI brain scan, during labor and delivery. Indeed, had such an event occurred, one would reasonably expect a severely depressed infant on delivery, with an absence of respiratory effort, and whose hospital course would be reflective of neurologic insult, to include a likely onset of seizure activity. Here, Britney presented with normal Apgars, good respiratory effort, and her hospital course reflected an essentially healthy new-born. In summary, the paucity of any evidence to suggest fetal compromise during labor and delivery, the conclusions reasonably drawn from the MRI scan, and Britney's presentation and hospital course present a picture that is wholly inconsistent with a birth-related injury. Moreover, the marginal nature of the placental abruption, given the evidence of fetal well-being during labor and delivery, renders it most unlikely that the abruption played any role in Britney's injury. Rather, giving due regard to the objective evidence, the conclusion is inescapable that the most likely cause of Britney's brain injury was a vascular insult or stroke, which occurred well prior to labor or delivery.10
Findings Of Fact Isabella Delvalle was born on January 17, 2012, at Orange Park Medical Center in Orange Park, Florida. Isabella weighed in excess of 2,500 grams at birth. NICA retained Donald C. Willis, M.D. (Dr. Willis), to review Isabella’s medical records. In a medical report dated May 30, 2015, Dr. Willis made the following findings and expressed the following opinion: Additional medical records from Baptist Hospital were reviewed (pages 618-1546). As discussed in the previous report, dated 04/07/2015, the baby was delivered by Cesarean section following failed attempt at vacuum delivery. Apgar scores were reported as 8/9. Cord blood gas had a normal pH of 7.26. This would suggest there was no oxygen deprivation during labor or delivery. An ARNP was present at delivery to manage the newborn. The baby was felt to be stable enough that the nurse left the delivery room at about two minutes after delivery to assist with another delivery. When she returned after about five minutes, the baby was having some respiratory distress. The baby was transferred to the NICU for observation. Seizure activity developed within about 24 hours of life. EEG was abnormal and consistent with seizure activity. MRI on DOL 3 was reported as normal. Two additional MRI’s over the next few months were also reported as normal. However, MRI at four months of age showed enlargement of the lateral ventricles since the prior exam and was consistent with brain volume loss. Genetic evaluation was negative. Microarray was negative. There was no apparent obstetrical event that resulted in oxygen deprivation or mechanical trauma to the baby’s brain during labor or delivery. I do not have any opinion about oxygen deprivation during the immediate post delivery period. Dr. Willis’ opinion that there was no apparent obstetrical event that resulted in oxygen deprivation or mechanical trauma to the baby’s brain during labor or delivery is credited. Respondent retained Raymond Fernandez, M.D. (Dr. Fernandez), a pediatric neurologist, to evaluate Isabella. Dr. Fernandez reviewed Isabella’s medical records and performed an independent medical examination on her on February 2, 2015. Dr. Fernandez made the following findings and summarized his evaluation as follows in a medical report dated February 10, 2015: IMPRESSION: There is ample evidence for substantial mental and motor impairment that is likely to be permanent, but etiology is unknown. Based on record review, history and physical examination, etiology cannot be determined at this time. There is no evidence in the medical record made available to me for brain or spinal cord injury due to oxygen deprivation or mechanical injury during labor, delivery, or the immediate post delivery period of resuscitation. However, note that I have not yet reviewed the Wolfson’s Children’s Hospital NICU admission, nor have I reviewed brain imaging studies presumably performed while at Wolfson’s. Records and imaging studies have been requested and an addendum to this report will be sent to NICA upon further review. On April 12, 2015, Dr. Fernandez wrote an addendum to the above medical report after reviewing additional records: I recently received records from Wolfson Children’s Hospital where Isabella was admitted on January 18, 2012 and discharged on May 24, 2012 and two additional admissions to the hospital were reviewed. Also reviewed were brain imaging studies, including two brain CTs and four brain MRIs. * * * In conclusion, as previously states [sic] there is ample evidence for substantial mental and physical impairment that likely will be premanent. However, etiology is unknown. There is no evidence in the record for oxygen deprivation or mechanical injury during labor, delivery, or the immediate post delivery period of resuscitation to be the explanation for Isabella’s substantial mental and motor impairment. There was a small amount of subdural blood within the posterior fossa, but this was not of clinical significance. This bleeding probably occurred during labor and delivery and was possibly due to the attempted vacuum extraction that was unsuccessful. Again, this is not felt to be clinically significant. There is no evidence for parenchymal brain hemorrhage, brain swelling, or brain injury due to oxygen deprivation or mechanical injury. Dr. Fernandez’s opinion that there is no evidence of oxygen deprivation or mechanical injury during labor, delivery or the immediate post-delivery period of resuscitation to be the explanation of Isabella’s substantial mental and 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 opinions of Dr. Willis and Dr. Fernandez that there was no obstetrical event that resulted in oxygen deprivation or mechanical injury to the baby’s brain during labor, delivery or the immediate post-delivery period.
Findings Of Fact Calise L. Muniz was born on May 2, 2015, at Holmes Regional Medical Center, located in Melbourne, Florida. Calise weighed in excess of 2,500 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Calise. In a medical report dated January 24, 2017, Dr. Willis opined in pertinent part as follows: In summary, the mother apparently became hypotensive after placement of epidural anesthesia with resulting fetal distress. The baby was depressed at birth. The initial ABG was consistent with metabolic acidosis. Cooling protocol was initiated for HIE. EEG was normal for age. No MRI or CT scan was done during the newborn hospital course. There was an apparent obstetrical event that resulted in loss of oxygen during labor and delivery. However, there was no documentation of actual brain injury. NICA retained Laufey Y. Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to examine Calise and to review her medical records. Dr. Sigurdardottir examined Calise on February 1, 2017. In a medical report dated February 1, 2017, Dr. Sigurdardottir summarized her examination of Calise and opined in pertinent part as follows: Summary: Calise is a 21-month-old female who was born via emergency cesarean section after nonreassuring fetal heart rate tracings were noted after a high spinal anesthesia. She had poor Apgars of 2, 4 and 5 after 1, 5 and 10 minutes, and was treated with cooling protocol. She did not have any neonatal seizures and the only neuroimaging available is a head ultrasound on day of life 1 that was normal. On neurologic exam today she is normal, both with her motor skills and cognition and language development. There are no signs of autistic features. Results as to question 1: Calise is not found to have substantial physical or mental impairment at this time. Results as to question 2: In review of available documents, she does have the clinical picture of an acute birth-related hypoxic injury. Results as to question 3: The prognosis for full motor and mental recovery is excellent and her life expectancy is full. In light of the normal cognitive abilities and normal neurologic exam, I do not feel that Calise should be included in the NICA program. If needed, I will be happy to answer additional questions. 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 while there was an apparent obstetrical event that resulted in loss of oxygen to the baby's brain during labor and delivery, there was no documentation of actual brain injury. Dr. Willis’ opinion is credited. There are no expert opinions filed that are contrary to Dr. Sigurdardottir’s opinion that Calise does not have a substantial physical or mental impairment. Dr. Sigurdardottir’s opinion is credited.
Findings Of Fact Eleanor was born on August 28, 2017, at Lower Keys Medical Center in Key West, Florida. Eleanor was a single gestation weighing over 2,500 grams at birth. Respondent retained Donald Willis, M.D., an obstetrician specializing in maternal-fetal medicine, to review the medical records of Eleanor and her mother, Laura Ann Ontiveros, and opine as to whether there was an injury to her brain or spinal cord that occurred in the course of labor, delivery, or resuscitation in the immediate postdelivery period due to oxygen deprivation or mechanical injury. In his report, dated September 9, 2018, Dr. Willis set forth the following: The mother was admitted to the hospital at 37 weeks gestational age in labor. A fetal heart rate (FHR) monitor tracing during labor was reviewed and showed no fetal distress. Delivery was by Cesarean section for arrest of dilation. Birth weight was 2,857 grams. Amniotic fluid was clear. The baby was not depressed at birth. Apgar scores were 8/9. No resuscitation was required. Newborn physical exam states “Healthy Term Newborn.” The baby failed the newborn hearing test in one ear. Newborn hospital course was otherwise uncomplicated and the baby was discharged home on DOL 2. Hearing evaluation after hospital discharge identified hearing loss in one ear. Records also indicate the child had Torticollis and limited mobility. MRI at 7 months of age identified a small Arachnoid cyst, slightly increased extra axial fluid and a simple pineal cyst. There were mention of findings suggestive of hypoxic ischemic encephalopathy (HIE). In summary, pregnancy was essentially uncomplicated. Cesarean section was done during labor for Arrest of Dilation. The baby was not depressed at birth with Apgar scores of 8/9. No resuscitation was required. The baby was discharged home on DOL 2. MRI at 7 months of age did not describe findings consistent with HIE. There was no apparent obstetrical event that resulted in oxygen deprivation or mechanical trauma during labor, delivery or in the immediate post-delivery period. Respondent’s Motion also relies upon Dr. Willis’s January 14, 2019, affidavit, wherein he affirms, to a reasonable degree of medical probability, the above-quoted findings and opinions from the report. Respondent also retained Michael S. Duchowny, M.D., a pediatric neurologist, to review the medical records of Eleanor and her mother, conduct an Independent Medical Examination (IME) of Eleanor, and opine as to whether Eleanor suffers from a permanent and substantial mental and physical impairment as a result of a birth-related neurological injury, as that term is defined in Section 766.302(2), Florida Statutes. Dr. Duchowny reviewed the medical records, obtained historical information from Eleanor’s mother, and performed an IME on November 28, 2018. Respondent’s Motion also relies upon the attached affidavit from Dr. Duchowny, dated January 14, 2019. In his affidavit, Dr. Duchowny testifies, as follows: It is my opinion that: In summary, Eleanor’s examination reveals neurological findings consistent with a diagnosis of ataxic hypotonic cerebral palsy associated with sensorineural and conductive hearing losses. Eleanor has preserved social awareness. It is premature to adequately assess cognitive functioning although her speech output is obviously delayed. She evidences dysmorphism characterized by epicanthal folds and a saddle nasal bridge. A review of the medical records does not disclose any significant risk factors during labor or delivery. Eleanor’s Apgar scores were 8 and 9 at 1 and 5 minutes, and her post-natal course in the newborn nursery was unremarkable. MR imaging performed on April 26, 2018 revealed benign cysts of the right anterior temporal and pineal regions. Based on today’s evaluation and record review, I believe that Eleanor’s neurological disabilities were acquired prior to birth and did not result from either oxygen deprivation or mechanical injury in the course of labor or delivery. In his affidavit, Dr. Duchowny testifies that his opinions are to a reasonable degree of medical probability. A review of the file, including Petitioner’s Response, reveals that no contrary evidence was presented to dispute the findings and opinions of Drs. Willis and Duchowny. Their opinions are credited.1/
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.
Findings Of Fact Jer’Donis Pringle was born on June 24, 2011, at Heart of Florida Regional Medical Center located in Davenport, Florida. Jer’Donis weighed 3,004 grams at birth. NICA retained Donald Willis, M.D., a Florida board- certified obstetrician and gynecologist specializing in maternal- fetal medicine to review the medical records of Jer’Donis. In an affidavit dated July 2, 2013, Dr. Willis opined as follows: Based upon my education and experience, it is my professional opinion, within a reasonable degree of medical probability that the pregnancy was complicated by Maternal Diabetes, that fetal testing at 34 weeks suggested fetal distress, that based on available medical records, the mother did not appear to be in labor at time of delivery by Cesarean section, and that the baby suffered severe oxygen deprivation and resulting brain damage. Overall findings suggest that severe brain injury occurred at some time prior to hospital admission and, therefore, prior to delivery. A review of the file does not show any opinion contrary to Dr. Willis’ opinion that Sherita Leeks was not in labor prior to delivery and that Jer’Donis suffered severe oxygen deprivation resulting in brain injury prior to admission to the hospital and delivery is credited.
The Issue At issue in this proceeding is whether Susan Lapidus, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary matters Paul Lapidus and Lori Beth Lapidus are the parents and natural guardians of Susan Lapidus (Susan), a minor. Susan was born a live infant on November 5, 1993, at Good Samaritan Medical Center, a hospital located in West Palm Beach, Florida, and her birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Susan was Ronald Koch, M.D., who was at all times material hereto, a participating physician in the Florida Birth- Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Mrs. Lapidus' antepartum course and Susan's birth At or about 1:00 p.m., November 4, 1993, Mrs. Lapidus was admitted to Good Samaritan Medical Center for an oxytocin challenge test (a contraction stress test), with suspected intrauterine growth retardation (IUGR), to assess fetal well- being. At the time, the fetus was at 39 weeks gestation, with an estimated date of delivery of November 17, 1993, and Mrs. Lapidus' antepartum course had not been without complication or risk. Regarding those risk factors, the proof demonstrates that at the time of Susan's conception Mrs. Lapidus (date of birth November 1, 1955) was 37 years of age, with a history of five previous pregnancies. Of those pregnancies, four were aborted (one "therapeutic" in 1979, and the balance "spontaneous" in January 1985, October 1985, and 1990) and one was carried to term and produced a normal, healthy boy (Michael, date of birth, October 21, 1988). Further complicating her pregnancy, the proof demonstrated that (to the extent conceded by Mrs. Lapidus), she smoked approximately 10 cigarettes per day and drank white wine daily (1 glass with dinner) throughout her pregnancy. 1/ Because of her age and other risk factors, Mrs. Lapidus underwent a number of tests during the course of her pregnancy, including an amniocentesis and multiple sonograms which revealed (within the limits of testing accuracy) no apparent cause for concern. Finally, during the month preceding her admission to Good Samaritan Medical Center, Mrs. Lapidus underwent non-stress testing, and ultimately contraction stress testing by oxytocin challenge test (OCT), to assess fetal well-being. 2/ The non- stress tests and oxytocin challenge tests that were administered to Mrs. Lapidus prior to November 4, 1993, were apparently reassuring for fetal well-being and placental integrity. As heretofore noted, Mrs. Lapidus was admitted to Good Samaritan Medical Center at 1:00 p.m., November 4, 1993, for an OCT, which extended until 3:55 p.m., when Pictocin was discontinued. During the test some decelerations were observed late in contractions (late decelerations), consistent with placental aging/diminishing function, and Dr. Koch resolved it would be prudent to admit Mrs. Lapidus for observation overnight and induction of labor in the morning. Mrs. Lapidus was admitted to labor and delivery at about 5:30 p.m., November 4, 1993. External fetal monitoring revealed a fetal heart rate (FHR) of 120 to 130 beats per minute (normal), and mild, irregular uterine contractions (most likely symptomatic of the prior administration of Pictocin). At 5:50 p.m. Mrs. Lapidus was repositioned, and external fetal monitor was positive for accelerations and continued mild, irregular uterine contractions. Assessment at 7:30 p.m. noted continued mild contractions, as well as "variable decelerations [at] intervals but not consistently [with each] contraction," however, beat-to- beat variability was noted to be present. Continued monitoring overnight revealed occasional variable decelerations, but continued beat-to-beat variability. At 7:10 a.m., external fetal monitoring revealed a FHR of 110 to 120 beats per minute, with spontaneous accelerations. Pictocin was administered to induce labor, at 7:30 a.m. contractions commenced (labor began), and an FHR deceleration to 90 to 110 beats per minute for 2 1/2 minutes was observed. Mrs. Lapidus was repositioned to her left side, intravenous fluids (IV) were increased, and FHR returned to a 110 to 120 beat per minute baseline. Beat-to-beat variability in fetal heart rate persisted, and at 8:20 a.m. the membranes were artificially ruptured with clear fluid noted. At or about 9:00 a.m., a FHR deceleration with contraction was noted. Mrs. Lapidus was again repositioned, intravenous fluids increased and FHR accelerated to 150 beats per minute following the contraction. A late deceleration was again noted with the next contraction. At 9:40 a.m., the nurses' notes reveal 3 late decelerations were observed, and Pictocin was discontinued; FHR continued at 130 to 140 beats per minute, with moderate beat-to- beat variability. Vaginal examination at 9:50 a.m. revealed the cervix to be 5 centimeters dilated, effacement at 80 percent, and the fetus at station -2. Contractions were noted as moderate in intensity, with 3 to 5 minute frequency, and a duration of 60 to 70 seconds. At or about 10:10 a.m., an epidural was placed and at 11:45 a.m., with no further decelerations having been observed, Pictocin was restarted. At 11:50 a.m., Mrs. Lapidus' bladder was noted as distended and a foley was inserted to help her void. Contemporaneously, FHR was noted to decelerate to the 60 beat per minute range for 30 seconds. When Mrs. Lapidus was repositioned, FHR returned to the 140 beat per minute range, with accelerations. At 12:29 p.m., the fetal monitor again revealed a late deceleration with contraction; however, it also noted continued moderate beat-to-beat variability and spontaneous acceleration. At 12:50 p.m. another late deceleration was noted and Mrs. Lapidus was repositioned to her right side. FHR remained in the 130 beat per minute range, with moderate beat-to- beat variability. Vaginal examination at 1:25 p.m. revealed dilatation and effacement to be complete and the fetus at station -1. FHR was noted in the 130 to 140 beat per minute range, with moderate beat-to-beat variability. At 1:40 p.m. Mrs. Lapidus began pushing, and at 1:50 p.m. Susan was delivered (6 hours and 20 minutes after labor commenced). Susan had a weak cry and was dusky at birth, and was placed on a warmer, dried, and given oxygen via blow-by. Apgars of 7 and 8 were assigned at one and five minutes, respectively. Cord specimen was obtained, and, when subsequently analyzed, revealed that, at delivery, Susan presented with a normal pH of 7.318. The Apgar scores assigned to Susan 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 a maximum score of 2. As noted, at one minute Susan's Apgar score totalled 7, with heart rate, muscle tone and reflex response being graded at 2 each; respiratory effort being graded at 1; and color being graded at 0. At five minutes, Susan's Apgar score totalled 8 with heart rate, respiratory effort, muscle tone, and reflex response being graded at 2 each, and color being graded at 0. Such scores were normal, and consistent with the delivery of a healthy, vigorous infant. Following delivery, Susan developed slight retractions and coarse respirations, as well as a temperature of 100.2, and was transferred to the neonatal intensive care unit (NICU) for further evaluation and treatment. There, physical examination revealed the following: HEAD: The head is normocephalic. The anterior fontanel is soft. ENT: There is no nasal flaring. The ears are well set. The nasal choanae are patent. Slight protruding tongue. THORAX: The chest is symmetric. There is [sic] subcostal retractions. LUNGS: There are coarse breast sounds. There is audible grunting present. HEART: There is a normal regular rhythm with no murmurs. ABDOMEN: The abdomen is non-distended. There is no organomegaly. The umbilical cord has three vessels. EXTREMITIES: The extremities are symmetric. The hips are normal, without any dislocation or subluxation. The pulses are equal bilaterally. Bilateral simian creases. SKIN: There is no cyanosis, and no rashes are present. There is good capillary refill. GENITALIA: There are no anomalies noted. CNS: The baby is active and alert. There is good muscular tone. Admitting diagnosis (impression) was as follows: 1.- Term 38 weeks appropriate for gestational age female. 2.- Respiratory distress. 3.- Perinatal sepsis suspected. Susan remained in the hospital until November 13, 1993, when she was discharged in satisfactory condition to her parents' care. While in the hospital Susan evidenced the following problems: RESPIRATORY: The patient developed respiratory distress that required no oxygen, and that subsided rapidly. The results of the CXR [chest x-ray] showed no infiltrate, congestion, pneumothorax or other pathology. The heart size is within normal limits. She developed inspiratory stridor. This was considered to be related to a certain degree of laryngomalacia [flacidity of the epiglottis and aryepiglottic folds (a softening of the cartilage in the upper airway), as in congenital laryngral stridor]. 3/ R/O SEPSIS: In view of the initial presentation, the possibility of sepsis was considered. The patient was placed on antibiotics, ampicillin and Claforan in appropriate doses. Results of the cultures were negative. The antibiotics were discontinued on 11/12/93. DYSMORPHIC FEATURES: In view of the dysmorphic features, and the possibility of this has been associated with chromosomes pending, a new chromosome studies was sent on 11/12/93 for extended banding. 4/ Also a renal ultrasound was done on 11/10/93 and the result was negative. Notably, Susan evidenced no neurologic problems or sequela during the course of her admission. Final diagnosis on discharge was as follows: 1.- Term 38 weeks appropriate for gestational age female. 2.- Transient respiratory distress. 3.- Dysmorphic facies. 4.- Bilateral simian creases. 5.- Perinatal sepsis suspected. 6.- Mild degree of laryngomalacia. 7.- Slow feeder. Susan's subsequent development Susan's early infancy was apparently unremarkable until around 10 months of age when her parents became concerned that her development (mental and physical) appeared delayed. Consequently, they sought the advice of Susan's pediatrician and, over time, Susan was referred to, and examined by, a number of medical specialists to assess her condition and to identify its etiology. On June 5, 1995, Susan was evaluated by Amanda Naguiat, M.D., Assistant Professor of Clinical Neurology, University of Miami Children's Hospital Center. Dr. Naguiat's assessment was as follows: . . . Susan appears to have global development delay with relative strength in social interaction. Her exam is significant for diffuse hypotonia and probably some associated weakness, dysmorphic features and depressed deep tendon reflexes. Her yellowish discoloration is secondary to carotenemia. So far, I cannot put her in a definite syndrome, although phenotypically, the only thing that comes to mind here is some of the rhizomelic forms of chondrodysplasia, belonging to the group of peroxisomal disorders. There is a definite need to find etiology for all of these. As discussed with her parents, I would like for her to have an MRI of the brain to look for any malformations or any white matter anomalies that would guide us to further testing. I would like to have some initial metabolic testing, which would include serum quantitative amino acids, urine organic, acids, carnitine total and free levels, and thyroid function tests. I have referred her to Dr. Benke, who they will see this coming Saturday, on June 10, in his clinic up in West Palm Beach, to see if he can shed light on any type of syndrome in view of her dysmorphic features. I concur with the recommendations for her to have early intervention in the form of speech, occupational and physical therapy. As discussed with her parents, I do not believe that her condition will be 'outgrown' and if we do not find any etiology, I would assume that she will follow a static encephalopathy with improvement over time but with persistent impairments. If a cerebral cause for her problems are not found, she should have further investigation for neuromuscular disease, as I am concerned that there might be a concomitant peripheral nervous system problem in view of her hypotonia and weakness and depressed reflexes. I will arrange a followup with them as soon as all these tests are done. On July 17, 1995, an MRI of the brain without contrast was performed and interpreted by Walter H. Forman, M.D. The MRI was considered normal and revealed no changes or anomalies one would associate with hypoxic injury. Specifically the MRI revealed that: The ventricles are normal in size and position. No masses or mass effects are identified. I don't see any areas of abnormal signal. The myeline maturation appears to be normal for age. On October 7, 1995, Susan was seen by Paul Benke, M.D., Ph.D., Director, Clinical Genetics, University of Miami School of Medicine, for a second time in a follow-up visit. 5/ Dr. Benke reported the results of that visit as follows: I saw this 23 mo old girl with minor anomalies and developmental delay in genetic clinic in Palm Beach Gardens on this date in follow-up. She has made a lot of progress; she can now stand and is starting to talk, she has about 10 words and a sense of humor, and has made up a lot of ground. She has not been sick. The two chromosome studies (including amnio) were sent in to me, and were of sufficient quality that a routine repeat chromosome study would not be helpful. I asked the parents to bring in pictures, since they claimed that pictures of the father, taken as a child, were similar, and I thought there was small, not large resemblance. To my delight (and surprise) the family was quite right about this, and the father had a prominent forehead, low set ears, and slightly small chin as a child. He also had some speech delay, but is very normal now, and these features minimally evident. She has had a lot of OT, PT and speech therapy for the past 3 1/2 months, and the parents attribute a lot of her gains to that. But I think that they have done a lot as well, and have had a positive attitude about her development. She has not been sick, and has had no fever, seizures or other problems. Importantly, she had tracheomalacea, and high pitched breathing, and grew out of it by 1 yr, and the father has a retarded brother. PHYSICAL FINDINGS: Interactive girl with lots of personality, mild dysmorphic features. She is very interactive today. HT: 29 in(?) WT: 22 1/2 lb. HC: 48 cm Head: prominent forehead Eyes: mongoloid slant IC: 3.5, IP: 6.0, IP: 9.5 (mild increase) Ears: +/-low set Nose: slight depressed nasal bridge Chin: small chin, high arched palate Chest: clear, no rales. Heart: [n]o murmur. Abdomen: neg, no masses, organomegaly Genitals: neg. Spine: no scoliosis. Extremities: small hands and feet, hypoplastic 5th toe nail. She is hyperextensible. She has fusiform fingers. Skin: negative Neurological: tone a little better. poor DTR. No localizing finding. Diagnosis: Multiple Minor Anomalies, Probable FG (Optiz Frias) Syndrome. Counseling: Deferred Pending testing. The Opitz Frias is a very variable disorder, compatible with normal intelligence, and mild-moderate effects on intelligence. Affected patients frequently have tracheomalacea or feeding problems, frontal prominence, low set ears, hypertelorism and other findings. Recent research suggests a microdeletion of chromosome #22, determinable by Florescence-in-situ-hybridization (FISH) testing. She has greatly improved, and is functioning at a 12-14 month level today. Recommendations: 1) Fish Testing of chromosome #22. We should be able to have blood sent off to the researchers who do this testing. 2. Get pictures of Paul's retarded brother. 3. See in clinic after testing. . . . A second genetics evaluation of Susan was conducted on January 21, 1998, by Parul Jayakar, M.D., a clinical geneticist associated with the Genetics Center of South Florida. Dr. Jayaker's report of that examination reads as follows: Susan Lapidus came to our office accompanied by her parents, Lori and Paul Lapidus, for a genetics evaluation because she has speech and developmental delay. The patient was born by NSVD at term to a 37 year old gravida 8 para 1061 (2 TAb, 4 SAb) woman. An amniocentesis done because of advanced maternal age was normal, 46,XX. The patient's mother states that she was put on progesterone during her pregnancy because of her history of multiple miscarriages. She also smoked approximately 10 cigarettes per day and drank white wine daily throughout her pregnancy. The patient remained in the NICU for 1 week after delivery because she had a strep infection. The patient has not had any major hospitalizations or illnesses. An MRI of the brain was normal at approximately 2 1/2 years of age. Her vision and hearing have both been evaluated and are reportedly normal. * * * Physical Examination: Height of 39 inches (90%), weight 31 lb. (25%), head circumference 48.5 cm (5%). Patient was awake, alert and active, pupils equal and reactive to light, no ectropien, with temporal receding hairline, good hair growth, prominent glabella, slight hypertelorism, flat long philtrum, thin upper lip (? familial), slightly high arched palate, broad nasal root. Chest - no heart murmur; abdomen - soft, no hepatosplenomegaly; genitalia female. Extremities - right single palmar crease, slightly hypoplastic toenails. Neurologically - vocabulary limited to monosyllables, no obvious cranial nerve palsies. Impression: 4 year old with Speech and developmental delay Minor dysmorphic features Susan, in the past, has been seen by Dr. Benke who contemplated the diagnosis of Optiz syndrome. At the moment I do not feel that she meets the clinical criteria for Opitz syndrome and the chromosomes done revealed a 46,XX, normal female karyotype and the FISH for chromosome 22 microdeletion was normal. 6/ She was seen also, in June of 1995, by Dr. Naguiat at that time the Mom reports that a significant workup was done including MRI of the brain and hearing test which were all normal (verbal report, I do not have these reports in hand). As Mom tells me, an ophthalmology evaluation was also done which was also normal. She has been receiving OT, PT and speech therapy since 17 months of age but lately her speech therapy has been discontinued in her recent school. I feel she is in great need of speech therapy to be able to increase her vocabulary for day to day life. Based on her clinical features I do not feel that she has characteristics of any particular syndrome, the only things which come to mind is the hypoplastic toenails, the long philtrum and the thin upper lip which may be reminiscent of ? Fetal Alcohol Effects (Mom had 1 glass of white wine with dinner every day). I do not think this amount of alcohol intake would cause full blown Fetal Alcohol Syndrome. Certainly some of her facial characteristics also appears to be familial. Therefore, I feel that right now I am unable to label her in any definite syndrome. 7/ As explained to the family, she clinically does not seems to have a progressive neural degenerative condition since she has not have [sic] regression of milestones and seems to be doing much better. The dispute regarding compensability Here, there is no dispute that Susan suffers neurologic dysfunction, mental and physical. What is at issue is whether that dysfunction may reasonably be described as permanent and substantial and, more fundamentally, whether the cause (etiology) of such dysfunction is, more likely than not, attributable 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," as required for coverage to be afforded under the Plan. Section 766.302(2), Florida Statutes. With regard to the issue of causation and timing, Petitioners are of the view that Susan's presentation is consistent with a brain injury caused by oxygen deprivation which occurred during the course of labor and delivery. In contrast, Respondent is of the view that the proof is not consistent with brain injury caused by oxygen deprivation during or immediately following birth and must, therefore, be attributable to some other etiology. Respondent's view of the proof has merit, and it is unnecessary to address whether Susan's neurologic dysfunction is permanent and substantial. The etiology (genesis) of Susan's neurologic dysfunction To address the etiology of Susan's neurological dysfunction, the parties offered selected records relating to Mrs. Lapidus' antepartum and intrapartum course, as well as for Susan's birth and subsequent development. Portions of those records have been addressed supra, and further salient portions will be addressed infra. The parties also offered the opinions of three physicians, at hearing, to address the likely etiology of Susan's presentation. Those physicians were Seth J. Herbst, M.D., a board-certified obstetrician and gynecologist; Jaime Baquero, M.D., a pediatric neurologist, board-certified in pediatrics and board-eligible in neurology; and Charles Kalstone, M.D., a board-certified obstetrician and gynecologist. 8/ The medical records and other proof, including the testimony of the physicians offered by the parties, have been carefully considered. So considered, it must be concluded that the proof does not demonstrate (or allow a conclusion to be drawn with any sense of confidence) that, more likely than not, Susan's neurologic dysfunction is related to an "injury to the brain . . . caused by oxygen deprivation . . . [which] occurr[ed] in the course of labor, delivery, or resuscitation in the immediate post-delivery period." In reaching such conclusion, it is observed that Susan's course pre-delivery and post-delivery was inconsistent with hypoxic or ischemic injury having occurred during the course of labor, delivery, or resuscitation. First, the evidence documenting fetal heart rate from admission through the period of labor and delivery does not support the conclusion that Susan suffered an acute intrapartum event that led to hypoxic or ischemic injury. Notably, while there were multiple late decelerations (which evidenced periods of diminished oxygenation or, stated differently, periods of transient hypoxia) the fetal monitoring tape also provided reassuring evidence of fetal wellbeing (by documenting good beat-to-beat variability, spontaneous accelerations, normal FHR baseline, and the absence of a progressive or persistent pattern of decelerations). Given such positive evidence of fetal reserve, it is unlikely that fetal oxygenation was significantly adversely affected during labor and delivery. Further militating against the conclusion that Susan's impairments were caused by oxygen deprivation during labor or delivery are the numerous inconsistencies between Susan's presentation and development, and the clinical findings one would expect had she suffered hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, during that period. For example, Susan's Apgars were within the normal range; her breathing at birth was essentially stable; cord pH was normal; and she did not evidence neurologic problems in the neonatal course. Finally, the results of Susan's MRI were normal and inconsistent with an hypoxic ischemic brain injury. Given the proof, it cannot be concluded that Susan's neurologic dysfunction resulted from a brain injury caused by oxygen deprivation or that it was related to an event which may have occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Notably, Susan's presentation and neonatal course were not consistent with an acutely acquired neurological injury caused by oxygen deprivation, and it is improbable that she could have experienced an acute event during labor and delivery, or immediately thereafter, without evidencing clinical symptoms of such damage. Conversely, Susan's presentation, and Mrs. Lapidus' prenatal history, suggest a genetic or congenital anomaly (or syndrome) as the more likely etiology for Susan's presentation.
The Issue Whether Jackson White (Jackson) suffered a birth-related neurological injury, as defined by section 766.302(2), Florida Statutes; and, if so, how much compensation, if any, is awardable pursuant to section 766.31.
Findings Of Fact Jackson was born on August 1, 2014, at Bayfront, in St. Petersburg, Florida. Jackson was a single gestation, weighing over 2,500 grams at birth. Jose Prieto, M.D., was the physician who provided obstetric services at Jackson’s birth. Jackson’s mother, Megan White (Mrs. White), was admitted to Bayfront and her labor was thereafter induced with Pitocin. Her membranes were artificially ruptured 15 hours prior to delivery, with clear fluid present. Delivery was initially attempted vaginally; however, delivery was altered to Cesarean section due to late decelerations and failure to descend and dilate. The records reflect that fetal heart rate decelerations may also have been present. Jackson was delivered in a vertex presentation. Upon delivery, out of a possible score of 10, his Apgar scores were 5, 7, and 8 at one, five, and ten minutes, respectively. Of concern was that his score for “color” was 0 for the first five minutes of life. He was not pink, but rather blue or pale. Additionally, he was not actively responding, but merely grimacing, at the first minute of life. The medical records document that Jackson was experiencing respiratory distress with desaturation. Accordingly, he initially received bulb suctioning, drying, stimulation, and whiffs of oxygen. As he continued to have poor color and perfusion, with grunting and retractions, continuous positive airway pressure by mask was applied. While there was improvement in the oxygen saturation after doing so, Jackson continued to have respiratory distress. Within two hours of birth, Jackson was transferred and admitted to the Neonatal Intensive Care Unit at All Children’s Hospital (All Children’s) for further management. Upon admission to All Children’s, it was documented that his oxygen saturations ranged from 96 percent to 100 percent while utilizing a Continuous Positive Airway Pressure (CPAP) system. His physical examination revealed that he was alert, active, responsive and pink in color. Jackson’s neurologic evaluation upon admission to All Children’s revealed that he was alert, active and responsive with good tone for age; there was symmetrical movement of all four extremities; his reflexes were intact; and that his “[n]eurological examination is appropriate for the baby’s gestational age.” At All Children’s, several chest X-rays were obtained from August 1 through August 3, 2014. Ultimately, the scans revealed that Jackson had a left pneumothorax. Accordingly, the CPAP was discontinued and an “oxyhood was initiated for nitrogen wash out which was discontinued after 22 hours.” Concerned with possible sepsis, Jackson also received seven days of antibiotics. Jackson was discharged home on August 8, 2014. Jackson failed his newborn hearing screen and subsequently underwent repeated testing where he was found to have mild-to-moderate sensorineural hearing loss bilaterally. Jackson has been wearing hearing aids since six months of age. Respondent retained Donald Willis, M.D., who is board- certified in obstetrics, gynecology, and maternal-fetal medicine, to review the available medical records of Jackson and his mother, and opine as to whether there was an injury to Jackson’s brain or spinal cord that occurred in the course of labor, delivery, or resuscitation in the immediate postdelivery period due to oxygen deprivation or mechanical injury. In his report, dated July 26, 2018, Dr. Willis set forth the following, in pertinent part: The mother was admitted for induction of labor at term. Amniotic membranes were ruptured with clear fluid. Fetal heart rate (FHR) monitor tracing was not available for review. Cesarean section delivery was apparently done for failure to decent [sic], but NICU notes suggest fetal heart decelerations were also present. Birth weight was 3,630 grams. Apgar scores were 5/7/8. Respiratory distress was present after birth with poor color, grunting and retractions. Bag and Mask ventilation was required and the baby transferred to All Children’s Hospital for respiratory distress. Grunting and retractions continued at All Children’s Hospital. Chest X-Ray identified a left pneumothorax. 100% hood oxygen was started. Intubation was not required. Cultures were obtained to r/o sepsis and antibiotics given for 7 days. Bacterial and viral (HSV) cultures were negative. The newborn hearing screen was failed. No seizures occurred during the hospital stay. Head imaging studies were not done during the newborn hospital course. The baby was discharged home on DOL 8. Hearing evaluation subsequently diagnosed a sensorineural hearing loss. Genetic testing was negative for familial deafness genes. Developmental delay became a concern at about 10 months of age. Genetic evaluation, including microarray, Fragile-X and metabolic work/up was negative. MRI showed delayed myelination. Etiology was uncertain, but a statement indicated “a very subtle degree of remote insult could be considered.” Follow up MRI at 2 1/2 years of age found similar findings. Neurology evaluation gave a diagnosis of chronic static encephalopathy. MRI of the lumbar spine was normal. In summary, the baby had respiratory distress after Cesarean section delivery. Chest X-Ray identified a pneumothorax. Oxygen was given for respiratory distress, but the baby did not require intubation. No head imaging studies were done during the newborn hospital stay. There were no seizures. Sensorineural hearing loss was diagnosed. MRI for developmental delay showed only some delay in myelination. There was no apparent obstetrical event that resulted in oxygen deprivation or mechanical trauma to the brain or spinal cord during labor, delivery and the immediate post- delivery period. After authoring the initial report, Dr. Willis received a copy of the fetal heart rate monitoring strips. After reviewing the same, on August 30, 2018, he authored an addendum to his report, which provides, in full, as follows: The fetal heart rate (FHR) monitor tracing during labor was reviewed. The tracing begins at about 05:17 on 08/01/2014. The baseline FHR was normal at 130 bpm. Uterine contractions were about every 5 minutes. The FHR tracing at about one hour prior to delivery is somewhat difficult to interpret due to attempt to place a fetal scalp electrode (FSE). FHR tracing ends at about 21:18 with delivery about 30 minutes after monitor is discontinued. The FHR tracing just prior to removal of the monitor does not suggest fetal distress. Review of the FHR tracing does not change the opinions stated in the letter above, dated 7/26/2014. There was no apparent obstetrical event that would have resulted in oxygen deprivation sufficient to cause brain injury. Dr. Willis was deposed on May 20, 2019. At his deposition, Dr. Willis affirmed the factual findings and medical opinions in the above noted report. In support of his opinion that Jackson did not sustain an injury to his brain or spinal cord in the course of labor, delivery, or resuscitation in the immediate postdelivery period due to oxygen deprivation or mechanical injury, Dr. Willis credibly testified that: 1) Mrs. White’s amniotic membranes were ruptured with clear fluid; 2) the fetal heart rate tracing did not suggest fetal distress; 3) the Apgar scores, although initially low, quickly improved and were inconsistent with an infant that sustained oxygen deprivation or acidosis; 4) Jackson did not exhibit any seizure activity; 5) aside from failing his hearing screen, Jackson did not experience any other organ system failures; and 6) the available MRI reports are inconsistent with Jackson suffering a brain injury at the time of labor and delivery. On May 12, 2017, Jackson presented to Himali Renuka Jayakody, M.D., for a neurological examination. Dr. Jayakody’s office note documents that, “[d]evelopmentally, he had initial normal development but starting around 10 months when he started standing, he appeared very clumsy and was falling over a lot.” After conducting the examination, Dr. Jayakody’s assessment was that Jackson had developmental delay, sensorineural hearing loss, and chronic static encephalopathy. His note further documented that, “[a]part from signal abnormality suggestive of hypomyelination mostly affecting the posterior white matter on MRI, we have not identified any other abnormalities. Clinically, he does not seem to have a progressive disease and has always made improvement over time suggestive of static encephalopathy/cerebral palsy.” NICA also retained Laufey Y. Sigurdardottir, M.D., a pediatric neurologist, to review Jackson’s medical records, conduct an Independent Medical Examination (IME), and opine as to whether he suffers from a permanent and substantial mental and physical impairment as a result of a birth-related neurological injury. Dr. Sigurdardottir reviewed the available medical records, obtained a full historical account from Mrs. White, and conducted and IME on Jackson on August 24, 2018. In her IME report, Dr. Sigurdardottir set forth her factual findings and opinions, which have to be admitted in this matter as part of the stipulated evidentiary record. Her summary findings and opinions are as follows: Summary: Patient is a 4 year old with history of being born via stat C-section due to fetal distress. No clear evidence was present of a neonatal hypoxic ischemic encephalopathy but he has since been diagnosed with cerebral palsy with corresponding MRI findings. His delays are mild in nature. Result as to question 1: Jackson is not found to have substantial delays in motor and mental abilities. Result as to question 2: In review of available documents, there is evidence of fetal distress but no neonatal encephalopathy consistent with a neurologic injury to the brain or spinal cord acquired due to oxygen deprivation or mechanical injury is reported in neonatal period apart from failing newborn hearing screen. Result as to question 3: The prognosis for full motor and mental recovery is good and the life expectancy is full. In light of evidence presented, I believe Jackson does not fulfill criteria of a substantial mental and physical impairment at this time. Petitioner neither testified nor presented any testimony to refute the findings and opinions of Drs. Willis and Sigurdardottir. Their findings and opinions are credited.
Conclusions This cause came before the undersigned upon the parties’ Joint Motion to Submit Stipulated Factual Record in Lieu of a Contested Hearing (Joint Motion), which was granted on May 22, 2019, and the parties’ proposed final orders.
Other Judicial Opinions Review of a final order of an administrative law judge shall be by appeal to the District Court of Appeal pursuant to section 766.311(1), Florida Statutes. Review proceedings are governed by the Florida Rules of Appellate Procedure. Such proceedings are commenced by filing the original notice of administrative appeal with the agency clerk of the Division of Administrative Hearings within 30 days of rendition of the order to be reviewed, and a copy, accompanied by filing fees prescribed by law, with the clerk of the appropriate District Court of Appeal. See § 766.311(1), Fla. Stat., and Fla. Birth-Related Neurological Injury Comp. Ass'n v. Carreras, 598 So. 2d 299 (Fla. 1st DCA 1992).
