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 The issue in this case is whether Javier Saladrigas, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Threshold Facts Notice has been waived and is not a contested issue herein. (Stipulated). Elisa Saladrigas is the mother and natural guardian of Javier Saladrigas. (Stipulated). She holds a doctorate in psychology, and sometimes will be referred-to herein as "Dr. Saladrigas." Javier was born a live infant on December 14, 2006. Javier weighed at least 2,500 grams at birth and was the product of a single gestation. (Stipulated). Obstetrical services were delivered to Elisa Saladrigas in connection with the delivery of Javier Saladrigas by NICA- participating physicians in Baptist Hospital of Miami, Inc. (Baptist Hospital), which is a licensed hospital in Miami, Florida. (Stipulated). The Timing of Javier's Injury On the date of Javier's birth, Elisa Saladrigas was a 37-year-old G1 with an IVF pregnancy and history of hypothyroidism. On December 14, 2006, at 3:16 p.m., Javier was delivered, full term at 38 weeks and four days gestation, with thick meconium-stained amniotic fluid, following a 15-1/2 hour labor. During labor, Javier's fetal monitor strips showed variable decelerations that progressed to severe decelerations with loss of heart rate variability. Upon delivery, the umbilical cord was looped around Javier's neck. He was floppy, tachypnic (evidencing an increased rate of respiration), and grunting, with a weak respiratory effort and in respiratory distress. He required "vigorous resuscitation" in the delivery room in the form of bag and mask ventilation, oxygen support, oral suctioning, gastric suctioning, tracheal suctioning, and vigorous tactile stimulation. Subsequent to such resuscitation in the delivery room, Javier's Apgars were six at one minute, seven at five minutes, and nine at ten minutes. These scores are within normal limits. At 3:57 p.m., still requiring oxygen support and exhibiting low oxygen saturations, with a working diagnosis of possible sepsis (later confirmed by testing as Group B streptococcus acquired from the mother during labor and/or delivery), hypoglycemia, and respiratory distress, Javier was transferred to Baptist Hospital's newborn nursery. It is significant that Javier's respiratory distress continued even after he achieved acceptable Apgar scores, because case law provides that the statutory period for compensability may encompass an additional "extended period of time when a baby is delivered in a life threatening condition" only if "there are ongoing and continuous efforts of resuscitation," and that "both the incident of oxygen deprivation and the brain injury resulting from the oxygen deprivation must occur in this time period."2/ Newborn nursery examination notes indicate that at 4:30 p.m., Javier's overall status was "critical," with an unstable respiratory rate and unstable blood pressure, and describe his condition as "pale and tachypnic in severe respiratory distress." Based upon the evidence as a whole, particularly by comparison of this entry to other notations made in the record at or about the same time, it is probable that these notes were dictated earlier than 4:30 p.m., and closer in time to Javier's physical admission to the newborn nursery and simply were not dictated or typed until 4:30 p.m. Due to Javier's on-going respiratory distress and other indicators, Neonatologist Paul Fassbach, M.D., transferred Javier from the newborn unit to Baptist Hospital's Neonatal Intensive Care Unit (NICU) for treatment of meconium aspiration syndrome (MAS). At 4:53 p.m., Javier was admitted to the NICU with worsening respiratory distress and poor oxygen saturations. He was given increased respiratory support, including positive pressure ventilation by NCPAP. Javier subsequently was diagnosed with septicemia by group B streptococci (Group B strep sepsis); respiratory distress; and severe MAS, confirmed by X- ray, showing diffuse pulmonary opacities throughout both lungs. MAS occurs when a baby inhales his own feces which have been expelled during labor and/or delivery. These feces are extremely corrosive to the baby's lungs.3/ Javier continued to desaturate, despite continuous resuscitative measures in the NICU, and at 8:52 p.m., he was intubated and placed on a ventilator. Umbilical arterial and venous catheters were surgically inserted to enable closer monitoring of his metabolic and respiratory condition. Javier was administered IV antibiotics for sepsis, glucose for hypoglycemia, nutritional support, dopamine, dobutamine, and epinephrine for low blood pressure, and surfactant medication to improve his lung function, but his condition continued to deteriorate. At 7:21 a.m., on December 15, 2006, Javier suffered the first of two cardiac and respiratory arrests. At 9:04 a.m., December 15, 2006, he arrested a second time, while still being assisted for the first arrest. All of the testifying physicians who had an opinion on the subject agree that, more likely than not, Javier's subsequently-diagnosed brain injury occurred at or about the time of these two "codes" or that the brain injury began to evolve at that point in time and worsened thereafter. Resuscitation at the point of the cardiac arrests took about 40 minutes. Umbilical artery cord blood gas is indicative of whether or not there has been oxygen deprivation at birth, but Javier's umbilical artery cord blood gas was never drawn. Rather, arterial blood gas drawn about four hours after birth, via a heel pinprick, showed a pH of 7.12, with a base excess of minus 12.8, which is acidotic and indicative of some degree of acidosis. When the baby coded approximately 18 hours after birth, the pH was only 6.78, with a base excess of minus 21, which is profoundly acidotic. Together, the blood gases may be read to indicate progressive oxygen deprivation preceding the cardiac arrests. Petitioner presented the testimony of Daniel Castellanos, M.D., a child and adult psychiatrist, who did not opine on timing and causality of Javier's brain injury, and of Nicholas Suite, M.D., a neurologist. Intervenor presented by deposition the testimony of Dr. William Rhine, a neonatologist. Respondent NICA presented the testimony by deposition of Dr. Charles Willis, a board-certified obstetrician, with special competence in maternal-fetal medicine, and of Dr. Michael Duchowny, a pediatric neurologist.4/ Neonatologist Rhine opined that hypoxia (a deficiency of oxygen reaching the tissues of the body, including the brain) resulted in the foregoing blood gas values, which were profoundly acidotic. Obstetrician Willis testified much the same. See infra. The greater weight of the credible medical evidence as a whole, but most notably the testimony of Dr. Rhine, the only neonatologist to testify, Dr. Willis, Dr. Michael Duchowny, a board-certified pediatric neurologist retained by NICA, who performed a "hands-on" neurological examination of Javier on July 15, 2009, and Dr. Nicholas Suite, a neurologist appearing for Petitioner, who examined Javier in September 2010, support a finding that simultaneously or concurrently with the two cardiac arrests in close succession, Javier suffered loss of oxygen to his brain, resulting in physical damage to his brain, which damage subsequently became visible on MRI. That is not to say, however, that some brain damage due to loss of oxygen did not occur during labor and delivery and/or during resuscitation in the delivery room, because the various medical authorities concede that it takes only about six minutes for such brain damage to occur, killing brain tissue. Most particularly, Dr. Duchowny's formal report to NICA read: . . . The records provide evidence of meconium aspiration syndrome and cardiac arrest. As they both occurred in the postnatal period, I believe they are the consequence of factors operating during labor and delivery. Dr. Willis could not quantify the degree of respiratory distress at birth, and opined, without further explanation, that although there may have been some oxygen deprivation to the baby at birth, it did not appear sufficient to meet the HIE standards for hypoxic brain injury. Dr. Willis could not determine from the cold medical records whether the baby had strep B pneumonia at birth, but he acknowledged that there was as good a chance that the baby acquired strep B and MAS during labor and birth as prior thereto; that the baby had respiratory distress "at birth"; and that upon delivery, the baby immediately required some type of oxygen support. He further opined that if Javier did have strep B, then that could result in an inflammatory response in the lungs. The baby had respiratory distress at birth, which Dr. Willis thought was most likely caused by MAS, both irritating the lining of the lungs, and causing them to thicken and create mechanical obstruction of oxygen exchange in the lungs. He acknowledged that the baby's respiratory status deteriorated after the Apgars were recorded. He described the baby's condition on leaving the delivery room as only "improving somewhat." Dr. Willis testified, in pertinent part, as follows: * * * [Dr. Willis] A: . . . the baby went to the, left the delivery room, improving somewhat, but once the baby got to the nursery, began having more respiratory distress, and then was transferred to the neonatal intensive care nursery . . . about five or six hours after the baby was born that they had to intubate the baby because of worsening respiratory distress. * * * [Mr. Wolk] Q: All right. And respiratory distress worsens in the immediate post delivery period even after the baby's received supplemental oxygen and needed to be bagged. Also correct? A: Correct. Q: The respiratory distress continues worsening and the baby then needs to be intubated at five hours after birth? A: Yes. Q: Okay. This continuum of respiratory distress then continues. And I'm tracking the language on the first page of your report, Doctor. A: Uh-huh. Q: So about 18 hours after birth the baby codes in the NICU? A: Correct. Q: All right. All right. At this point would you -- do you have an opinion as to whether the cause of the code was related to group B--more related to group B stress [sic] or meconium aspiration, or a combination of the two? A: You know, I don't know. I believe by that time you're probably getting in more to a neonatal expertise then [sic] a maternal fetal medicine. I mean, I feel comfortable with the immediate postdelivery period, but, you know, hours into the nursery, I would prefer the neonatologist comment about that.[5/] Q: All right. We've got this continuing of worsening respiratory distress, starting with birth and then continuing to the code about 18 hours afterwards in the NICU, correct? A: Yes.[6/] Q: All right. Basically the summary in your report, baby requires CPR for 40 minutes and develops an anoxic brain injury from the code, correct? That's my assumption, yes. Q. When you say that's your assumption, what do you base that assumption on? A: Well, you know, the baby had a -- an ultrasound of the head done on the 15th, the day after birth, which would be, you know, after the code, and at that time they showed a moderate amount of cerebral edema, and that's often what we see as the earliest ultrasound findings for hypoxic ischemic brain injury, so -- Q: So more likely than not the edema shown on the head ultrasound was the result of a hypoxic brain injury? A: Right. And since the baby coded and required, you know, 40 minutes of CPR, it would certainly make sense that if there's, you know, brain injury, that it probably occurred, most of it, during that time. (Jt. Ex. 18, Willis Depo. pages 19-22) * * * [Mr. Solomon] Q: Okay. Would you agree with me that the passage of meconium and the meconium aspiration was an event which occurred sometime prior to the delivery of Javier . . . ? * * * A: . . . -- yes, it could occur at that time, but also you can get aspiration of meconium after the baby's born, when the baby takes the first few breaths as well. Q: Okay so it either occurred just prior to delivery or in the immediate post delivery period, correct? A: Correct. (Jt. Ex. 18, Willis Depo. pages 27-28) * * * Q: Okay. Is this child hypoglycemic at birth? A: Yes. The baby did have hypoglycemia, had low platelet counts, had a lot of problems, actually. Q: And all of these conditions would have existed at or around the time of birth, correct? A: Yes. (Jt. Ex. 18, Willis Depo. page 29) * * * Q: I mean, did this child always require some type of respiratory support? A: As far as I'm aware, yes.[7/] (Jt. Ex. 18, Willis Depo. pages 30-31) After his two "heart attacks," see Finding of Fact 16, Javier was transferred to Miami Children's Hospital at 10:30 a.m., on December 15, 2006, in critical condition with unstable heart rate, respiratory rate, and blood pressure. Javier's admitting diagnoses at Miami Children's Hospital included MAS, pulmonary hypertension, septic shock, hypertension, thrombocytopenia, and the need for continuous ventilator support. Javier was placed on extracorporeal membrane oxygenation (ECMO) due to severe respiratory distress and sepsis. ECMO is the equivalent of a heart/lung bypass machine which breathes for the infant and oxygenates his blood. At this point, ECMO "stabilized" Javier, but that is because it breathed for him. A brain ultrasound at Miami Children's Hospital at 1:33 p.m., on December 15, 2006, revealed "moderate diffuse brain edema." An EEG also showed abnormality. A brain ultrasound performed on January 9, 2007, was abnormal and showed signs of periventricular leukomalacia (PVL) within the brain's left frontal white matter, indicative of dead brain tissue. On February 14, 2007, a brain ultrasound showed a focal area of echogenicity in the white matter of Javier's brain. A CT scan of Javier's brain on April 3, 2007, showed permanent areas of calcification in the white matter of the left frontal lobe and an area of increased density in the white matter adjacent to the frontal horn of the left lateral ventricle. Encephalopathy and leukomalacia (signs of permanent brain injury resulting from loss of oxygen) were diagnosed on April 4, 2007, by Dr. William F. Carroll, a neonatologist at Miami Children's Hospital. He noted that Javier was oxygen dependent and required oxygen via nasal cannula; was at risk for developmental delay and required long term follow-up with physical, occupational, and speech therapies as well as frequent follow-up with the Early Intervention Team and multiple healthcare providers. A CT scan on April 3, 2007, showed that the cerebral edema was largely resolved and that only a "tiny area of increased density in white matter of the right frontal lobe remained, and this tiny area might constitute an area of calcification." See Finding of Fact 36. Javier remained at Miami Children's Hospital through April 24, 2007, when he was discharged by Dr. Manuel Campos, a neonatologist. When discharged, Javier had a doctor's authorization for "medically necessary" skilled nursing for 24 hours per day for one month, then 12 hours per day for two weeks. Thereafter, he transitioned into family care. The discharge diagnosis was thrombocytopenia, MAS, and pulmonary hypertension. Javier also had failed his hearing screening. However, a later test showed his hearing to be intact. See Finding of Fact 36. An MRI was recommended for further evaluation but was not performed until four years later, when it showed physical brain damage to Javier's hippocampus. See Finding of Fact 43. Although Petitioner and Intervenor have argued that oxygen deprivation to Javier's brain persisted through ECMO and further into the postnatal period, no finding regarding that period is necessary, because the greater weight of the competent evidence supports a finding that the injury to Javier's brain occurred during resuscitation in the immediate postdelivery period in Baptist Hospital no later than when Javier "coded" due to the cardiac arrests, and that the brain injury from oxygen deprivation had occurred at least by that point in time. Javier's Evaluations and Diagnoses Israel Alfonso, M.D., Director of Neonatal Neurology at Miami Children's Hospital, followed Javier's progress for some time. His reports, stipulated in evidence, addressed Javier's situation on April 30, 2007, July 23, 2007, March 24, 2008, and March 23, 2009. Dr. Alfonso's last narrative report, rendered when Javier was 27 months of age, describes a CT brain scan on April 3, 2007, showing a "[t]iny area of increased density in the white matter of the left frontal lobe that may represent an area of calcification," see Finding of Fact 31; a March 20, 2007, BAEP study, suggesting "normal precochlear and cochlear functions as well as normal conduction through both peripheral and central auditory pathways up to the level of the midbrain bilaterally"; a March 27, 2007, sacral ultrasound, showing a normal spinal cord; a VEEG study on January 22, 2007, represented as "Normal, . . . events non-epileptic in nature," and a January 15, 2007, normal EEG. His report further stated, ASSESSMENT: Neurological examination: minimal gross and fine motor developmental delay and hypotonia. IMPRESSION: static encephalopathy temporally related perinatal problems by history manifested by poor head growth (following a trend), minimal hypotonicity and feeding problems (improving). No craniofacial disproportion. Translated from "doctor-speak," the foregoing means that the neurologist associated with Javier for the longest time in a clinical setting, as opposed to a setting for litigation, who also is the neurologist who has had the most "hands on" association to date with Javier, diagnosed him at 27 months, as having minimal gross and fine motor developmental delay; permanent but non-progressing and unchanging encephalopathy; minimal loss of muscle tone; poor head growth; and feeding problems. Dr. Duchowny, NICA's pediatric neurologist, performed an independent medical examination of Javier on July 15, 2009, when Javier was about 31 months old. Deposed on April 12, 2010, Dr. Duchowny's ultimate opinion was that his examination of Javier did not reveal evidence of a substantial motor (physical) or mental impairment and consequently, Javier would not be compensable under the NICA statute. That said, Dr. Duchowny acknowledged that Javier had Attention Deficit Hyperactivity Disorder (ADHD), hypertonia and some fine motor impairment and developmental delays. He also noted that Javier's head was in the third deviation too small for his body and that the fontenelles of his skull had closed, and that as a result, Javier's brain would not grow as Javier grows physically. Dr. Duchowny did not view microcephaly as a "physical impairment," but as a "physical finding on neurological examination," and testified that, in his view, "an impairment would be some problem that prevents one from doing things." However, he also conceded that probably 90 percent of microcephalics have a lower IQ than normocephalics; more often than not, as they age, the majority of microcephalics have other motor or developmental issues, compared with normocephalic children; and for the majority of microcephalic children, these motor or developmental issues are permanent. Dr. Roberto F. Lopez-Alberola, Assistant Professor and Chief of the Section of Child Neurology, Pediatrics, at the University of Miami's Miller School of Medicine, wrote (in pertinent part) in a letter concerning his February 26, 2010, assessment of Javier, when Javier was approximately three-and-a- half years of age, that: PHYSICAL EXAMINATION VITAL SIGNS: . . . Head circumference of 46 cm, which is below the 2nd percentile. GENERAL: Awake, alert, fidgety, and hyperactive, yet very sociable and playful, interactive both physically and verbally. Well nourished. No dysmorphic features. HEENT: Microcephalic, atraumatic, pupils equally round and reactive to light and accommodation. Extraocular movements were full. Occasional eye blinking noted. No craniofacial asymmetry. CARDIOVASCULAR: Irregular rate and rhythm. RESPIRATORY: Clear to auscultation. ABDOMEN: No hepatosplenomegaly, soft and depressible. SKIN/EXTREMITIES: No rash or lesions. No joint deformity or limb asymmetry. No hypo or hyperpigmented skin areas. NEUROLOGIC: Cranial nerves II through XII grossly intact. SENSORY: Romberg was negative. Deep tendon reflexes symmetric. MOTOR: Slightly decreased tone throughout. Fair muscle bulk. No evidence of wasting or atrophy. No pronator drift. COORDINATION: No truncal titubation, however, decreased balance and coordination with slight dysmetria bilaterally. GAIT: No ataxia. ASSESSMENT: In summary, Javier is a 3-year-old young boy with complicated birth history with known developmental delay, making strides, microcephaly, abnormal movements, which are consistent with simple motor tics. Interestingly today, the patient's maternal grandfather accompanied mother and he also has a longstanding history of simple motor tics, which most likely then represent a familial trait. Nonetheless, the EEG which was ordered to rule out any epileptic activity, although these movements are not epileptic in nature, the EEG is not normal and does show epileptiform activity. . . . it is questionable whether the patient's microcephaly is acquired or if indeed was congenital. In terms of the patient's simple motor tic disorder, I have explained to mother the natural history of tics and as long as the tics are not bothering the patient psychologically or emotionally or in any physical form that treatment would be deferred. In terms of the patient's developmental delays, the patient most certainly would benefit from continued therapies including occupational and physical therapy, as the patient's coordination and balance as well as muscle tone are still impaired. I have also recommended aqua therapy. In terms of the patient's behavioral issues, I have recommended behavioral therapy and at some point if the patient's hyperactivity were to become an issue interfering with his behavior and his academic progress, would then consider pharmacotherapy. . . . (emphasis added). For purposes of assessing permanent impairments, the foregoing record appears to state that Javier's head is too small for his body, which may be a birth injury or congenital, and which is a condition that persisted at the date of final hearing, as also discussed by other physicians, including Respondent's expert neurologist, Dr. Duchowny, see Findings of Fact 39-40, that Javier has tics, which are as likely to be congenital or hereditary as they are to be the result of brain injury, and that are not epileptic in nature; that Javier has symmetrical and working limbs, muscles, and joints; and that he is without ataxia, meaning that he has some ability to coordinate body movements. Ataxia is sometimes associated with walking or cerebral palsy. This record also states that Javier evidences dysmeteria (an abnormal condition typically characterized by overestimating or underestimating the range of motion needed to place the limbs correctly during voluntary movement); that some of his muscles are somewhat flaccid; that he is without Romberg's sign8/; and that his gait (walking) is within normal limits. However, the record also states that upon report by his mother, Javier has developmental delays. Dr. Suite, a neurologist, examined Javier on September 17, 2010, and testified on behalf of Petitioner. He rendered a report of his examination, which, together with his testimony, shows that Javier's affect was dull and slow; that he had no history of epileptic seizures; that he could relate some of his history; and that his head circumference is microcephalic. Contrary to a previous treating evaluation, see Finding of Fact 37, some limitation of Javier's lateral spine and range of hip movement was found. Contrary to a previous treating evaluation, see Finding of Fact 41, Dr. Suite found a positive Romberg sign and abnormal gait. He also diagnosed developmental delay, attention deficit disorder, hypotonia, and behavioral difficulties. On August 26, 2011, a brain MRI of Javier (age four years, eight months) was done at Miami Children's Hospital. It concluded: Scattered foci of superatentorial signal abnormality, likely areas of gliosis or dysmyelination, the result of a remote insult. Bilateral hippocampal atrophy, on the left with associated sclerosis. Tiny physiologic pineal cyst and small choroidal fissure cyst. Dr. Castellanos, a board-certified child and adolescent psychiatrist, examined Javier at Dr. Saladrigas' request on October 31, 2011. He diagnosed Javier at approximately five years old, with cerebral palsy, ADHD, problems fulfilling activities of daily living (ADLs), developmental problems related to personal hygiene, and intermittent memory deficits currently manifesting as Javier being unable to remember from day to day where his pull-ups are stored; that he is supposed to place his school gear in his "cubby"; and his being unable to remember where, within his school, his "cubby" is located.9/ Significantly, Dr. Castellanos predicted that Javier's brain will not continue to grow, but the complexity of academic tasks required of him will increase and his ability to cope will diminish; he will become more frustrated; and in the future, he will be even less able to perform academically than at the present time. Ultimately, Dr. Castellanos deferred to psychologists for testing IQ and to teachers to determine what learning disabilities Javier may have. The Extent of Javier's Mental and Physical Impairments Under the NICA Plan, a "physical impairment" relates to impairment of the infant's "motor abnormalities" or "physical functions." "Mental impairment" also addresses functionality, as opposed to mere diagnosis. However, under NICA, the identification of a substantial mental impairment may include not only identifying significant cognitive deficiencies but can include, in a proper case, additional circumstances such as significant barriers to learning and social development.10/ As his parent, Javier's mother is better positioned than anyone else to observe Javier's day-to-day behavior.11/ In this case, Dr. Saladrigas is a licensed clinical psychologist, and accordingly, despite the inherent natural bias of every parent, her observations and impressions of Javier's functioning are entitled to some greater weight than might ordinarily be accorded a lay-parent.12/ That said, Javier's mother's testimony contains internal contradictions. On the one hand, she testified that she tested his IQ prior to his entering the academic year at St. Thomas Parish School in August 2010, at about age three, and found it to be in the normal range of IQ. On the other hand, she states that such testing does not have much validity until a child is six. She testified that Javier has never had an independent IQ test, but that he had IQ testing by Ketty Gonzalez, without any elaboration on what was determined. Under these circumstances, the undersigned is left with a perception of Javier's possessing a normal IQ at age three. Javier has epileptiform signals on various brain examination, but he has never been diagnosed with epileptic seizures. His mother believes his tics and eye-rolling signal seizures, but no physician or test has confirmed this perception. Javier is bilingual in Spanish and English, because his family speaks both languages. According to his mother, Javier started to speak first words "possibly" before he was one year old, and she considers that Javier met his normal developmental milestone in this regard and later with regard to when he first spoke in sentences. In the past, Dr. Saladrigas has been diligent in seeking out and providing private occupational, speech, and physical therapies for Javier, but at the present time, he is in an Exceptional Student Education (ESE) class in the public school system, which can provide all these therapies. Even now, his mother prefers to pay for occupational therapy in the private sector. She stated that at the present time, Javier's speech and the production of his speech is quite good, and his feeding problems have largely disappeared, so she has temporarily discontinued private speech therapy. At the present time, Javier is physically able to walk without assistance; to use the bathroom by himself, although he wets the bed most nights; to run around the playground when he chooses to do so; and to swing on the swings without assistance. He requires neither braces nor a wheelchair for ambulation. His mother reported that he started walking at thirteen months, which she perceives is a normal age for that developmental milestone. Dr. Castellanos observed that Javier talks a lot and is clumsy with his drawing. He has diagnosed Javier has having cerebral palsy, which is a physical or motor disability, arising in Javier's damaged brain, as opposed to a mental disability, but Dr. Castellanos agrees that Javier is very active and without physical problems ambulating. Javier's mother also commented on Javier's "floppy" aspect, that is, his mild hypotonia or muscle weakness, but she admitted that there is not much Javier cannot now do from a gross motor standpoint. Nonetheless, she perceives a difference in the quality of Javier's gross motor functions in comparison to those of her two-year-old son and her nephews of varying ages. She described Javier's susceptibility to pneumonia due to his lung damage from MAS, for which he has had 10 hospitalizations. He has poor appetite and a general fraility as a result of the lung damage. She uses a nebulizer with him and a "Shake Vest" to break up the congestion in his lungs. He uses oxygen when he travels. Next to his mother, Javier's teachers are probably best-suited to describe how Javier functions daily and how he learns.13/ Javier has been placed in a succession of five pre- schools where he has had little success and from which he was either asked to leave as a result of behavioral problems or was withdrawn by his mother because, according to her, the teachers in those schools, who were not ESE-qualified, "complained" about Javier's disruptive behaviors. Javier also had not been able to interact successfully with the other "normal" children in any of these locations. Dr. Saladrigas perceives Javier's socialization problems as related to hyperactivity; as not honoring the "personal space" boundaries required by other children; and as his withdrawal from interaction with other children when he is not successful socializing with them or getting their undivided attention. Her perceptions in this regard were echoed by Kitty Finneran, associate head of St. Thomas Parish School. Dr. Saladrigas placed Javier at St. Thomas Parish School's summer camp in June 2010, when he was three-and-a-half years old. She sought no special accommodation for him, and, in fact, withheld from school/camp staff some information regarding his difficulties in his prior pre-school environments, so that he would not be pre-judged. Initially, in the first part of the June 2010, summer camp, experienced school staff viewed Javier as being in the normal range for his development, based upon their observation and conversation with him and his mother. After a period of observing how Javier interacted with other children at camp, they recognized that he had the types of behavioral, social, and learning problems testified-to by his mother and Ms. Finneran. Kathleen Finneran is the associate head of St. Thomas Parish School. She has been associated with St. Thomas for 43 years and has been an administrator there for 17 years. Ms. Finneran presided over the summer camp activities when Javier was enrolled there in June 2010 and over the school year that began in August 2010. She described Javier as having no focus; doing inappropriate things; invading others' personal space; being unable to grasp "why" he was forbidden to "stomp" repeatedly on a teacher's foot, and persisting in such behavior despite being told not to do so. She described him as retreating to the swings from other playground play when he could not get other children to focus on playing with him or playing what he wanted them to play and as frightening them. Javier's mother described Javier's home play then, and at the present time, as being almost exclusively on the swings or dressing up, pretending to be a fictional character, and running around the house in costume. She maintained that he could parallel play with toys, but could not play with toys interactively with his brother or cousins. She indicated that Javier's role-playing had carried over to his annoying other visitors at Disney World when the family had gone there in the summer of 2011. On that trip, Javier imitated the cartoon character actors by blowing kisses and asking other park attendees to dance with him. Dr. Saladrigas, Ms. Finneran, and Dr. Castellanos commented on Javier's propensity to constantly sing to himself. His mother says he learns songs quickly. In August 2010, Javier began his three-year-old pre- school program at St. Thomas. He was not able to function in a regular class with two teachers and 15 other children. One teacher had to be assigned to exclusively manage him. Dr. Saladrigas was ultimately asked to remove Javier from St. Thomas Parish School, which she did. Javier is currently enrolled in an "inclusive" ESE program in the public school system. His mother is credible in her assertion that he has not yet been classified as to type of ESE student at this early grade level. However, so far, he seems to be functioning adequately in an ESE "inclusionary" class of 50 percent ESE students and 50 percent mainstream students. Analysis It is the child's ability to function mentally which must control a determination of permanent and substantial mental impairment or lack thereof. Javier has been diagnosed with ADHD, developmental delays, dull affect, slow speech, problems with ADLs, and memory deficits. Although he has been unsuccessful to date in mainstream educational environments, such as St. Thomas Parish pre-school and camp and in what appear to be other very informal pre-school environments, there are no standardized IQ or other intellectual tests whereby his degree of mental impairment or ability to learn can be assessed. In a proper case, proof that a child cannot learn once he is placed in an accredited ESE class could support a finding of permanent and substantial mental impairment, but there is no such proof here, and NICA reasonably points out that Javier has made good progress in private, one-on-one speech therapy, physical therapy, and occupational therapy. Even so, there can be no serious debate that Javier's microcephalic head constitutes a permanent abnormal physical condition, and that his closed fontenelles mean that his head and his brain will not continue to grow, as he otherwise physically grows and matures, or that he will have limited intellectual functioning as a result. These factors, together with his failure to understand correction, his inability to remember physical things and locations, his inability to sequence tasks, and his failure to process memory, compel a finding that Javier has, indeed, sustained a "permanent and substantial mental impairment." However, the evidence falls short of establishing that Javier has sustained a "permanent and substantial physical impairment." Petitioner asserts that because all of Javier's mental impairments arise from the physical injury to his brain, which injury is visible on MRI within the hippocampus, then it must follow that he is permanently and substantially physically impaired, as well as permanently and substantially mentally impaired. This argument is not persuasive. The language employed by the Legislature in enacting section 766.302(2), recognizes a distinction between "injury" and "impairment." It provides compensation only for an "injury to the brain or spinal cord . . . caused by oxygen deprivation or mechanical injury . . . which renders an infant permanently and substantially mentally and physically impaired." Because of the clear language selected by the enactors, "injury" and "impairment" cannot mean the same thing. By statutory context, the physical or mental "impairment" must come to pass because of the brain or spinal cord "injury." Moreover, "impairment" has, throughout the history of the Act, been equated with functional defect or loss of functionality.14/ Javier has lung damage and significant recurrent pneumonia, probably related to MAS and probably not related to his brain injury in the statutory period, but his lung problems have been considered as part of the sequelae of the brain injury which occurred in the statutory period. Even so, the treatments Javier has undergone and the maturation process seem to have lessened the physical problems with his lungs. Javier has cerebral palsy and mild, generalized hypertonia (decreased muscle tone) directly related to his brain injury in the statutory period. Yet, he can perform all of the physical demands of daily living. He has gross control of his head and use of his hands, arms, and legs, with only some mild leg-shaking. His tics and the rolling back of his eyes may or may not be congenital, but they are intermittant. His fine motor control development is stunted, but he is able to sit alone, stand alone, walk, run, swing, and play alone or with others. Javier can see, hear, smell, and speak. There is no evidence he has an impaired sense of touch. Javier met his early developmental milestones. There is no evidence suggesting that he cannot be trained to feed and groom himself, despite current personal hygiene issues. He is toilet trained, except at night, and his medical records show his amount and frequency of bedwettings do not amount to eurinesis. On its own, this scenario does not amount to permanent and substantial physical impairment. The record also does not support a finding that any or all of Javier's physical impairments present significant barriers to learning and social development.
The Issue At issue in this proceeding is whether Jonathan Trujillo, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Jonathan Trujillo (Jonathan) is the natural son of Odalis Merida and Antonio Trujillo. He was born a live infant on December 31, 1993, at Jackson Memorial Hospital, a teaching hospital located in Miami, Dade County, Florida, and his birth weight was in excess of 2500 grams. The physicians providing obstetrical services during the birth of Jonathan were Doctors Oliva and McGare, resident physicians in an approved training program, who were supervised by Gene Burkett, M.D., a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan (the "Plan"). Consequently, each physician who provided obstetrical services during the birth of Jonathan was a "participating physician" in the Plan. Sections 766.302(7) and 766.314(4)(c), Florida Statutes. The birth of Jonathan Trujillo At or about 5:20 p.m., December 31, 1993, Odalis Merida (Ms. Merida) was admitted to Jackson Memorial Hospital in active labor. Notably, Ms. Merida's prenatal course had been complicated by the development of Class B gestational diabetes, requiring insulin during the course of her pregnancy, and the development of severe preeclampsia, characterized by hypertension. Consequently, Ms. Merida's pregnancy was rated high risk. To address Ms. Merida's diabetes during labor and delivery, she was maintained on drip insulin, and to address her hypertension, she was administered magnesium sulfate. Ms. Merida's condition and the substances administered to address her condition, although apparently necessary and appropriate, were not without risk or side effect to the fetus. Notably, magnesium sulfate is a muscle relaxant which can induce "floppiness" in a new born, as well as respiratory distress. 1/ The presence of maternal diabetes portends the risk of infantile hypoglycemia, which occurred in the instant case. A clinical symptom of hypoglycemia is "floppiness" in the new born, which may be exaggerated when, as here, it is found in conjunction with ploycythemia, discussed infra. Upon admission, Jonathan was at term, with a gestational age of 41 weeks, and fetal heart monitoring, commenced at or about 5:25 p.m., revealed good fetal heart tone. A physical examination at 6:00 p.m. noted the cervix to be at 7 centimeters, effacement complete, and the fetus at station 0. Contractions were regular at 2 minutes, and when the membrane was ruptured clear amniotic fluid was observed. Ms. Merida progressed through labor without incident until approximately 8:45 p.m., following the administration of an epidural anesthesia, when late decelerations of the fetal heart beat with bradycardia were noted, as a consequence of epidural hypertension. More specifically, Ms. Merida's blood pressure was observed to drop from a base line rate of 200/150 to 98/45, and a few late decelerations of the infant's heart rate were observed from a baseline rate of 120 to 130 beats per minute to 80 beats per minute. Ms. Merida was repositioned to her left side, the infant's heart rate promptly recovered, and no further unusual incidents were observed during the course of her labor or delivery. Given the limited duration and isolated nature of the late decelerations and bradycardia, it was the opinion of the physicians who testified in this proceeding that such anomaly did not adversely affect the infant's oxygenation or, stated differently, did not result in a hypoxic/ischemic insult to the infant's brain. Such opinions are credited. At 9:40 p.m., December 31, 1993, Ms. Merida, as she had with her first child, spontaneously delivered Jonathan vaginally, without apparent complication. Notably, Jonathan was vigorous on delivery, breathed spontaneously, did not require resuscitation, and his apgar scores were 9 at one minute, five minutes and ten minutes. In all, Jonathan's presentation was reflective of a healthy, vigorous infant. 2/ Jonathan was admitted to the newborn nursery at 10:00 p.m. Physical assessment upon admission revealed a large infant, at 4040 grams, with a large head (above the 90th percentile), who was crying spontaneously, alert, pink in color, but with a "slight floppiness" in the extremities. Jonathan was noted to breath spontaneously, without flaring or grunting; heart rate was noted at 160 beats per minute, with regular rhythm; fontanel were soft and flat; and reflexes were present. In brief, Jonathan's presentation in the newborn nursery was that of a healthy, vigorous infant, with the only negative observation being a "slight floppiness" in his extremities. Such "floppiness" was, however, more likely than not, related to the magnesium sulfate administered to Ms. Merida during labor and delivery, the hypoglycemia Jonathan was subsequently diagnosed to have acquired, or a combination of the two, and does not detract from the conclusion that Jonathan had no apparent signs of distress at birth. Later in the day, following testing, Jonathan was diagnosed with moderate to severe hypoglycemia, polycythemia, and moderate thrombocytopenia. Such conditions, singularly, or in combination, placed the infant at risk. Hypoglycemia, low blood sugar, may place the infant at risk of seizures and, pertinent to this case, resultant brain hemorrhage. Here, the moderate to severe hypoglycemia that Jonathan suffered was apparently recurrent, although it did resolve over time, and was addressed each time it presented through the administration of glucose. Polycythemia is a disorder whereby the number of red blood cells are abnormally high, making the blood thicker (hyperviscous) than normal. Apparently, brain hemorrhage is often related to decreased blood flow on the venus side of the brain, and where the blood is hyperviscous it could help or contribute to a brain hemorrhage. Here, with a hematocrit of 64, Jonathan's condition met the definition of polycythemia, which is a hematocrit over 60; however, such condition was not, or was not shown to be, significant in the instant case. Thrombocytopenia is a disorder resulting in an abnormally low platelet count which could affect clotting and therefore predispose the infant to bleeding through, among other things, trauma. Here, Jonathan's thrombocytopenia, more likely than not isoimmune thrombocytopenia, was considered moderate, as opposed to severe, and serial testing reported his platelet count as follows for the date and time indicated: DATE TIME 3/ PLATELET COUNT 1/1/94 07:00 Platelet estimate 40,000-80,000 1/2/94 03:47 Platelet estimate 80,000-100,000 1/3/94 07:57 Platelet estimate 40,000-80,000 1/3/94 15:08 Platelet estimate 40,000-80,000 1/4/94 05:04 Platelet count 49,000 1/5/94 06:46 Platelet estimate 40,000-80,000 1/6/94 12:50 Platelet estimate 40,000-80,000 1/8/94 21:12 Platelet count 182,000 1/10/94 03:52 Platelet count 263,000 1/12/94 06:00 Platelet count 357,000 The normal platelet count for newborns, as with adults, is 150,000 to 400,000, and, as may be observed from the serial testing, Jonathan's thrombocytopenia resolved over time. While at risk, Jonathan's neonatal course in the nursery was uneventful until 26 hours of life when he was noted to have suffered a generalized seizure characterized by cyanosis, severe bradycardia (heart beat in the range of 40 beats per minute), and respiratory arrest (apnea), requiring intubation. At or about 1:00 a.m., January 1, 1994, Jonathan was transferred to the neonatal intensive care unit, where he was maintained on positive ventilation until approximately January 6, 1994. Examination, through EEG's and CT and MRI scans of the brain, revealed that Jonathan had suffered an intraventricular hemorrhage, Grade IV, characterized by a massive bleed, with dilation of the ventricles. 4/ Thereafter residual hypodensity of the white matter of the brain was observed, consistent with degeneration of the hemorrhage and, ultimately, hypodensity compatable with evolving encephalomalacia (swelling of the brain.) Subsequently, on February 2, 1994, developing hydrocephalus required the placement of an intraventricular shunt to relieve intracranial pressure. Currently, in the opinions of Dr. Robert Roth and Dr. Michael Duchowny, whose opinions are credited, Jonathan is permanently and substantially mentally and physically impaired. Such impairment is evidenced by, inter alia, cortical blindness, hypotonia and, more likely than not, mental retardation. It is further the opinion of such physicians, which is again credited, that the cause of Jonathan's neurologic impairment is the injury to the brain he suffered as a consequence of the Grade IV intraventricular hemorrhage. Given the foregoing, resolution of this claim resolves itself to an identification of the genesis of Jonathan's Grade IV intraventricular hemorrhage or, stated otherwise, whether the proof demonstrates, more likely than not, that the hemorrhage, which resulted in injury to Jonathan's brain and the ensuing neurological injuries, resulted from "oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period" in the hospital. Sections 766.302(2) and 766.309(1)(a), Florida Statutes. The cause of Jonathan's Grade IV intraventricular hemorrhage A Grade IV intraventricular hemorrhage in a term infant, such as Jonathan, is a rare occurrence, and its cause frequently cannot be identified. Notwithstanding, Jonathan did suffer such a hemorrhage, and he was shown to suffer from two conditions, isoimmune thrombocytopenia and hypoglycemia, which could offer some explanation for the hemorrhage. Here, petitioner contends that Jonathan, due to his large head, received an injury to his brain occasioned by the "mechanical" forces of labor and delivery, and that such injury resulted in a slow bleed which, because of his thrombocytopenia, progressed over the next 26 hours and ultimately manifested as a generalized seizure characterized by cyanosis, severe bradycardia and respiratory arrest. In support of such contention, petitioner offered the testimony of Robert S. Roth, M.D., a physician board certified in pediatrics and neonatal/perinatal medicine. Pertinent to this case, Dr. Roth observed that infants born with thrombocytopenia are at increased risk of suffering an intraventricular brain hemorrhage if subjected to the trauma occasioned by the mechanical forces of labor and vaginal delivery. In his opinion, Jonathan's medical records reveal a classic case of neonatal brain hemorrhage resulting from the mechanical forces of labor and vaginal delivery that occurred because of Jonathan's large head and thrombocytopenia. Those conditions, affected by the forces of labor and delivery, combined to "start the process of hemorrhage in the brain," resulting in "tissue changes and cell death and vascular pressure changes" over time, and culminating when it progressed to the "centers that control breathing," manifested by apnea or seizure- like activity that led to apnea. Notably, it was Dr. Roth's opinion that it was not Jonathan's large head alone or his thrombocytopenia alone, apparently because of its moderate nature, which occasioned the initial bleed and resulting hemorrhage but, rather, the two conditions acting in consort. There was, however, no injury to Jonathan's scalp or skull noted at delivery, nor any molding of his head consequent to the delivery. It is of further note, in evaluating Dr. Roth's opinion, that he also observed that, had Jonathan been delivered by cesarean section before the onset of labor, he would have had a "lower probability" of having a hemorrhage than had he undergone active labor and vaginal delivery. Such observation clearly implies that factors other than labor and delivery could have operated to induce Jonathan's hemorrhage. Finally, in considering Dr. Roth's opinion of progressive deterioration, it is worthy of note that, apart from the "slight floppiness" observed shortly after birth, Jonathan evidenced no symptoms of neurologic injury until 26 hours of life. As heretofore noted, the "slight floppiness" exhibited by Jonathan was reasonably attributed to the magnesium sulfate administered to Ms. Merida during labor and delivery, the hypoglycemia Jonathan was shown to have developed, or a combination of the two, as opposed to a symptom of neurologic injury. Consequently, there is no objective evidence or symptom, that one would otherwise expect to observe, to support Dr. Roth's opinion of progressive deterioration. Contrasted with the opinions of Dr. Roth, regarding the genesis of Jonathan's hemorrhage, are the opinions offered on behalf of NICA through Michael S. Duchowny, M.D., a physician board certified in pediatric neurology. Dr. Duchowny, although acknowledging that thrombocytopenia offered an increased risk of intraventricular hemorrhage to an infant through the forces of labor and delivery, was of the opinion that Jonathan's hemorrhage at 26 hours of life was a spontaneous event, unrelated to labor and delivery, and that the cause of that hemorrhage could not be identified with any reasonable degree of medical certainty or, stated differently, that any attempt to attribute a cause for Jonathan's hemorrhage was, at best, speculative. 5/ In reaching his conclusion, Dr. Duchowny observed that there was no objective evidence or symptom of trauma or oxygen deprivation at birth, as one would expect had there been a neurologic insult during the course of labor and delivery, and that there was likewise no objective evidence or symptom of neurologic injury over the course of Jonathan's first 26 hours of life, as one would expect to observe were he suffering a progressive disorder, as opined by Dr. Roth. Dr. Duchowny was further of the opinion that, although moderately thrombocytopenic, Jonathan's platelet count was not sufficiently low, a level he described as 20,000 or less, to increase the likelihood that Jonathan would suffer a bleed. Resolving the conflict between the opinions of Doctors Roth and Duchowny is not an easy or lightly undertaken effort. Each physician is eminently qualified and the genuineness of the opinions they expressed is apparent. The seriousness of the resolution is further intensified by the obvious needs of a severely impaired infant; however, while such needs are significant, it cannot be overlooked that where, as here, responsibility for the care of the infant is sought to be imposed on the Plan, the proof must be compelling that, more likely than not, the infant suffered a "birth-related neurological injury" as defined by law. In this case, the proof falls short of meeting such standard. 6/ As heretofore noted, the labor and delivery of Jonathan was essentially normal and there was no obstetrical incident or identifiable event during labor and delivery that would evidence that he had suffered a hypoxic insult, mechanical injury or traumatic event. Indeed, although Jonathan did have a large head (above the 90th percentile), there was no cephalopelvic disproportion noted, no arrest of labor, no protracted labor, and no use of forceps or vacuum extraction in delivery. Upon delivery, no apparent cranial injuries were observed, no molding of the head was noted, and Jonathan presented as a vigorous infant with normal Apgars. In summary, there was no identifiable incident during the course of labor or delivery, or thereafter during Jonathan's first 26 hours of life, evidencing oxygen deprivation, mechanical injury, or other insult, that would account for the hemorrhage he suffered. In reaching the foregoing conclusion, it has not been overlooked that an infant suffering from thrombocytopenia is at increased risk of intraventricular hemorrhage through the forces of labor and delivery. Here, however, it was not suggested or shown that Jonathan's mild thrombocytopenia would, itself, foster a hemorrhage of the nature he suffered, rather petitioner's proof suggested that his large head and thrombocytopenic condition combined, when subjected to the trauma of labor and delivery, to precipitate a bleed that slowly progressed to a Grade IV intraventricular hemorrhage or precipitated a seizure that resulted in such a hemorrhage. Given the nature of the proffer, there being no apparent complication during labor and delivery, no objective sign of head trauma at birth, no symptoms of neurologic insult at birth, and no symptom of neurologic insult over the 26 hours prior to Jonathan's acute compromise, it must be concluded, as suggested by Dr. Duchowny, that any conclusion timing the genesis of Jonathan's hemorrhage to the events of labor and delivery is not supported by reasonable medical probability but is, at best, speculative. Consequently, it must be concluded, that petitioners have failed to demonstrate that Jonathan's hemorrhage was related to trauma, oxygen deprivation or mechanical injury occurring during the course of labor and delivery, as opposed to a spontaneous event, of unknown origin, occurring at Jonathan's twenty-sixth hour of life. 7/
Findings Of Fact 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 is whether Eliana Redwine, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts1 Petitioner, Aimee Redwine, is a parent and natural guardian of Eliana Redwine. Eliana was born a live infant on October 10, 2006, at Shands at AGH, a licensed Florida hospital located in Gainesville, Florida, and her birth weight exceeded 2,500 grams. Obstetrical services were delivered at Eliana's birth by George Buchanan, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired."2 § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. Here, it is undisputed that Eliana suffered a brain- damaging event, which rendered her permanently and substantially mentally and physically impaired. What must be resolved is whether the record supports the conclusion that, more likely than not, such injury was "caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period" in the hospital, as required for coverage under the Plan. § 766.302(2), Fla. Stat.; Nagy v. Florida Birth-Related Neurological Injury Compensation Association, 813 So. 2d 155, 160 (Fla. 4th DCA 2002)("According to the plain meaning of the words as written, the oxygen deprivation or mechanical injury to the brain must take place during labor or delivery, or immediately afterward."). Eliana's birth and immediate newborn course At or about 11:43 a.m., October 10, 2006, Mrs. Redwine, with an estimated delivery date of October 17, 2006, and the fetus at 39 3/7 weeks' gestation by ultrasound (US), was admitted to Shands at AGH for induction of labor due to preeclampsia. There, fetal monitoring revealed an overall reassuring fetal heart rate in the 140 beat per minute range, and vaginal examination revealed the cervix at 2-3 centimeters dilation, effacement at 50 percent, and the fetus high. Mrs. Redwine was induced with Petocin, starting at 2:36 p.m.; progressed to complete dilation by 9:58 p.m.; and at 10:05 p.m., Eliana was born by spontaneous vaginal delivery. In the interim, at 6:16 p.m., Mrs. Redwine's membranes were artificially ruptured, with clear fluid noted, and fetal monitoring remained reassuring. At delivery, a single nuchal cord was noted, and relieved. According to the medical records, Eliana cried spontaneously following delivery; was bulb-suctioned, dried, and stimulated; and was assigned Apgar scores of 8 and 8, at one and five minutes, respectively. However, Eliana subsequently showed evidence of respiratory distress (retractions and grunting)3 and, at or about 10:20 p.m., a Neonatal Intensive Care Nurse (NICU) nurse (Melissa Decker, R.N.) was called to observe her. (Joint Exhibit 1B, Tab 14, Bate Stamp p. 408). The NICU nurse arrived at labor and delivery when Eliana was 20 minutes of age (10:25 p.m.), and noted moderate subcostal retractions, with grunting; some central cyanosis; significant facial bruising; and oxygen being provided via blow- by. Eliana was suctioned by catheter, with a copious amount of thick mucous returned, and transported to the neonatal intensive care unit for continued care via transport isolette, with blow- by oxygen provided during transport. (Joint Exhibit 1B, Tab 14, Bate Stamp p. 408). Eliana was received in the neonatal intensive care unit at or about 10:35 p.m., and placed on a radient warmer (RW) bed. Oxygen saturation was noted as 92% with blow-by. Eliana was placed under an oxyhood, with oxygen started at 90%, and a decrease in cyanosis was noted. By 12:15 a.m., October 11, 2006, no further grunting or retractions were noted, oxygen saturation was noted as 100%, and Eliana was described as pink and well-perfused. Orders were received to begin weaning, and by 1:30 a.m., Eliana was weaned to room air, with oxygen saturation noted as 98%. Eliana experienced no further respiratory difficulties, and was discharged with her mother on October 13, 2006. Eliana's subsequent development On April 5, 2007, Eliana was seen by Myra Alfino, M.D., a pediatrician associated with the University of Florida, for developmental delay. Dr. Alfino noted a number of abnormalities, including microcephaly (37.8 cm), eyes not tracking, and hypotonia, and ordered a brain MRI. The MRI, done April 11, 2007, was reported, as follows: Findings: This study is abnormal. There is advanced global atrophy. There is diffuse leukomalacia of the white matter of the cerebrum and of the dentate nuclei of the cerebellum and Wallerian degeneration in long tracks. Patient motion precludes evaluation of the optic nerve size. There is compensatory extra-axial fluid. There is a focal intradural blood collection of acute to subacute nature along the posterior falx. The corpus callosum is small. The paranasal sinuses and oto-mastiod air cells are normally developed and aerated without evidence of acute or chronic mucoperiosteal thickening or intrasinus fluid. IMPRESSION: Post anoxic brain damage producing microcephaly and extensive leukomalacia. Small subacute intradural hemorrhage as above. Following the MRI, Eliana was seen by Dr. Omid Rabbani, a resident doing a 3-month rotation in pediatric neurology, and Dr. Edgar Andrade, a physician board-certified in neurology with special competence in child neurology, and Assistant Professor in the College of Medicine, Department of Pediatrics, Division of Pediatric Neurology, who was Dr. Rabbani's attending (supervising) physician. Dr. Andrade included the following attending attestation to Dr. Rabbani's report: I have spoke with the caregivers and have examined the patient and have formulated a join[t] history, physical assessment and plan of care, as Dr. Rabbani has documented it. The patient reportedly suffered anoxic brain injury at the time of birth.[4] Neurological exam was significant for poor head control, diffuse hypotonia, hyperreflexia and a brisk Moro response. Brain MRI supports the notion of post anoxic brain damage. I have educated the family about potential complications of such findings included but not limited to cerebral palsy and developmental delay. I have recommended enrolling the patient in a comprehensive multidisciplinary program where she can receive physical, occupational and speech therapy. Follow up in the clinic in 3-4 months. Notably, neither Dr. Rabbani nor Dr. Andrade expressed an opinion regarding the cause or timing of Eliana's brain injury. (Petitioner's Exhibit 1; Respondent's Exhibit 3). The likely cause and timing of Eliana's brain injury To address the likely etiology of Eliana's brain injury, NICA offered the deposition testimony of Donald Willis, M.D., a physician board-certified in obstetrics and gynecology, and maternal-fetal medicine, and Raymond Fernandez, M.D., a pediatric neurologist. Dr. Willis reviewed the medical records associated with Eliana's birth and newborn course and concluded that, more likely than not, Eliana did not suffer a brain injury caused by oxygen deprivation or mechanical injury during labor, delivery, or resuscitation in the immediate postdelivery period.5 In so concluding, Dr. Willis observed that fetal monitoring during labor was reassuring; the baby's Apgar scores were good (8 at one and five minutes); the baby did not require any significant resuscitation at birth; and there was no clinical evidence of an acute brain injury during Eliana's immediate newborn course. (Respondent's Exhibit 4). Dr. Fernandez evaluated Eliana on October 1, 2008. Based on that evaluation, as well as his review of the medical records, Dr. Fernandez was of the opinion that Eliana was permanently and substantially mentally and physically impaired, and that the cause of such neurologic impairment was the brain damaging event revealed by the MRI scan of April 11, 2007. As for the etiology of the brain injury, Dr. Fernandez was of the opinion that, while its cause could not be identified,6 the injury most likely occurred in utero, weeks or months before the onset of labor, and not during labor, delivery, or resuscitation in the immediate postdelivery period. (Respondent's Exhibit 2). In expressing, his opinion, Dr. Fernandez noted that, at birth, Eliana presented with a congenital microcephaly, a head circumference of 30.5 centimeters (cm) that was way below the third percentile for age matched controls; that such condition is consistent with long-standing growth retardation of the brain during the course of pregnancy; and that when he examined Dr. Eliana, at almost two years of age, her head circumference, at 39.5 cm, was still well below the third percentile. Moreover, Dr. Fernandez, like Dr. Willis, was of the opinion that there was no clinical evidence to support the conclusions that, more likely than not, Eliana suffered a significant brain injury during labor, delivery, or immediately thereafter. (Respondent's Exhibit 2). Notably, when a medical condition is not readily observable, issues of causation are essentially medical questions, requiring expert medical evidence. See, e.g., Vero Beach Care Center v. Ricks, 476 So. 2d 262, 264 (Fla. 1st DCA 1985)("[L]ay testimony is legally insufficient to support a finding of causation where the medical condition involved is not readily observable."); Ackley v. General Parcel Service, 646 So. 2d 242, 245 (Fla. 1st DCA 1994)("The determination of the cause of a non-observable medical condition, such as a psychiatric illness, is essentially a medical question."); Wausau Insurance Company v. Tillman, 765 So. 2d 123, 124 (Fla. 1st DCA 2000)("Because the medical conditions which the claimant alleged had resulted from the workplace incident were not readily observable, he was obligated to present expert medical evidence establishing that causal connection."). Here, Petitioner offered no expert testimony to support a finding regarding the cause or timing of Eliana's brain injury, and the opinions of Doctors Willis and Duchowny were logical, consistent with the record, not controverted, and not shown to lack credibility. Consequently, it must be resolved that Eliana's brain injury represents a congenital abnormality, that predated the onset of labor, as opposed to a "birth-related neurological injury." See Thomas v. Salvation Army, 562 So. 2d 746, 749 (Fla. 1st DCA 1990)("In evaluating medical evidence, a judge of compensation claims may not reject uncontroverted medical testimony without a reasonable explanation.").
The Issue Whether Deidre Denson has suffered an injury for which compensation should be awarded under the Florida Birth- Related Neurological Injury Compensation Plan, as alleged in the claim for compensation.
Findings Of Fact Preliminary matters Deidre Denson (Deidre) is the natural daughter of David and Linda Denson. She was born a live infant on October 8, 1991, at Bayfront Medical Center in St. Petersburg, Pinellas County, Florida, and her birth weight was in excess of 2500 grams. The physicians providing obstetrical services during the birth of Deidre were David Moreland, M.D., and Donna Miller, M.D., who were, at all times material hereto, participating physicians in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. The birth of Deidre Denson At or about 12:30 a.m., October 8, 1991, Linda Denson presented to Bayfront Medical Center, upon advice of her physician, following the spontaneous rupture of her membrane. At the time, Linda Denson was in active labor and Deidre, who was at term, was in a breach presentation. At approximately 1:09 a.m., Mrs. Denson was admitted to the labor room, and thick meconium was observed upon examination. External fetal monitoring was commenced, which initially reflected a fetal heart rate in the 80-90 beat per minute range; however, at or about 1:12 a.m., and continuing until approximately 1:18 a.m., the fetal heart rate was observed to fluctuate between the 80-90 rate and 60 beats per minute. This situation evidenced fetal distress and an urgent need for surgical intervention. Accordingly, at approximately 1:18 a.m. Mrs. Denson was taken to the operating room. Mrs. Denson was admitted to the operating room at 1:23 a.m., and Deidre was delivered by a cesarean section surgical procedure at 1:35 a.m. Upon delivery, Deidre's physical appearance was observed to be "blue" and her heart rate was below 30 beats per minute. Delivery room resuscitation included intubation, with suctioning of meconium below the vocal cords four times, and bagging with 100 percent oxygen. Spontaneous respirations were not observed in the infant until thirty minutes after birth, when they were noted as "slow" and continued to be noted as "slow" until 2:12 a.m. when she was transferred to the neonatal intensive care unit at All Children's Hospital. At birth, Deidre's Apgar scores at one, five and 10 minutes were one, four and five respectively. These scores are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of the heart rate, muscle tone, respiratory effort, color, and reflex irritability, with each category being assigned a score ranging from the lowest score of zero through a maximum score of two. As noted, at one minute, Deidre's Apgar score totaled one, with heart rate being graded at one ("slow, below 100"), and muscle tone, respiratory effort, color and reflex irritability being graded at zero. At five minutes, Deidre's Apgar score totaled four, with heart rate and color being graded at two each, respiratory effort being graded at one ("slow, irregular"), and muscle tone and reflex irritability being graded at zero each. At 10 minutes, Deidre's Apgar score totaled five, with heart rate and color again being graded at two each, and muscle tone, respiratory effort and reflex irritability being graded at one each. Such scores are consistent with Deidre having suffered a severe hypoxic insult (deprivation of oxygen) at birth. At approximately 2:25 a.m., October 8, 1991, Deidre was admitted to the neonatal intensive care unit at All Children's Hospital, and was placed on a ventilator until four days of age and remained with an endotracheal tube until six days of age. At 1:45 p.m., Deidre was observed to have developed seizure activity, secondary to perinatal depression, and an electroencephalogram (EEG) was ordered. That EEG was read as an "abnormal ictal EEG recording," and is consistent with diffuse cerebral disfunction. Dr. Kenneth Sassower, a pediatric neurologist, performed a consult on Deidre on October 8, 1991, and observed that the "differential diagnosis of neonatal seizures at this early age include fetal hypoxia; metabolic abnormalities . . . intracranial hemorrhage . . .; meningitis, etc." He recommended a cranial ultrasound, a "CT scan of the head without contrast, pending stable clinical status," a repeat EEG study, and certain other testing procedures designed to identify the cause of Deidre's seizure activity. The cranial ultrasound was taken on October 9, 1991, and was read as normal in that it failed to reflect any hemorrhage in or around the ventricles and did not reflect any displacement of the ventricles. Such findings do not, however, rule out the possibility that a bleed/intracranial hemorrhage existed in the frontal area, since such would not be picked up on ultrasound. Rather, a CT scan of the head without contrast would have been the preferred and more reliable testing procedure; however, due to the fragile nature of the infant's condition, ultrasound was employed as the first test to discern the presence of cerebral blood. As discussed infra, the first CT scan was performed December 3, 1991, after Deidre's discharge from All Children's Hospital, and evidenced a bleed in the frontal area. Other testing procedures ruled out metabolic abnormalities and meningitis as causative factors for Deidre's seizures. As with the EEG taken October 8, 1991, serial EEG's taken October 9, 14 and 23, 1991, were also read as abnormal and "indicative of diffuse cerebral dysfunction with bifocal dysfunction over both central regions." The proximity of Deidre's seizure activity to birth, and the abnormal EEGs, are consistent with diffuse brain injury as a consequence of hypoxic insult at birth. Given the absence of any other identifiable factor, it is found that Deidre's seizure activity was directly attributable to birth asphyxia. 1/ In addition to the foregoing abnormalities, Deidre was also diagnosed as suffering hypotension due to mycardial insufficiency, as well as renal (kidney) and liver damage, due to perinatal depression, and on neurologic consult to exhibit "evidence of generalized hypotonia and hyporeflexia." Such observations are consistent with hypoxic insult at birth. Deidre's condition was, however, managed and she was discharged from All Children's Hospital to the care of her parents on October 24, 1991. Currently, Deidre is, indisputedly, permanently and substantially mentally and physically impaired. Considering its quality, the proof is compelling that Deidre suffered a severe hypoxic insult at birth and that as a consequence of such oxygen deprivation suffered an injury to her brain which adversely impacted her mentally and physically. Notwithstanding, respondent, Florida Birth- Related Neurological Injury Compensation Association (NICA), contends that the seriousness of Deidre's current neurological deficit is not a product of the hypoxic insult she suffered at birth but, rather, was occasioned by head trauma suffered after her discharge from All Children's Hospital. For the reasons that follow, NICA's position is rejected, and it is found, based on the more compelling proof, that Deidre sustained an injury to the brain caused by oxygen deprivation in the course of labor, delivery or resuscitation in the immediate post-delivery period that rendered her permanently and substantially mentally and physically impaired. Events subsequent to Deidre's discharge from All Children's Hospital Following Deidre's discharge from All Children's Hospital, she was next neurologically examined by Dr. Kenneth Sassower on November 26, 1991. On examination, Dr. Sassower observed evidence of a mild to moderate spastic diparesis and hyperreflexia in the lower extremities, but noted that Deidre was currently seizure free on phenobarbital monotherapy without undue behavioral side effects noted. Based on his observations, Dr. Sassower proposed a reevaluation of Deidre in three to four months. 2/ On December 3, 1991, Deidre presented for a CT Scan of the brain without enhancement at the radiology department of All Children's Hospital. Such CT scan was an apparent follow-up to a recommendation made by Dr. Sassower when he examined Deidre on October 8, 1991, to address the cause of Deidre's seizure activity. [Petitioners' exhibits 16 and 18] The attending radiologist reported: Findings: As compared to the sonogram on 10-9-91, the frontal horns now seem slightly distended. This is seen in association with chronic bilateral subdural hematomas. There is also evidence of prominent sulci and cisterns with underlying leukomalacia. This is most pronounced in the frontal lobes. The 3rd and 4th ventricle are also slightly distended . . . No intracranial calcifications. The mastoid air cells are well aerated bilaterally. The anterior and posterior fontanelles are small for the patient's age. Otherwise, normal calvarial contour. IMPRESSION: 1. Status post development of bilateral subdural hematomas and brain atrophy with predominant frontal leukomalacia. This raises a question of intervening trauma. Recommend clinical correlation. Consequently, the radiologist telephoned Dr. Sassower at 10:15 a.m., December 3, 1991, and arranged for a neurological examination of Deidre at 12:00 p.m. Deidre was indeed examined by Dr. Sassower on December 3, 1991. During the course of that examination he concluded: . . . The CT scan reveals evidence of prominent cortical atrophy, along with what appears to be a suggestion of semi-acute bifrontal subdural hematomas. The exact extent of subdural blood is somewhat difficult to assess due to the presence of increased hypolucencies which at times appear continuous with areas of relative cortical atrophy. * * * During the course of the clinical examination, both parents deny any known recent head trauma, either accidental or otherwise. Both parents, who appear extremely reliable, have now reported leaving their child in the company of other caretakers since discharge from the nursery. I think in spite of the fact that both parents appear to be appropriately concerned, one needs to exercise a good deal of caution in this regard, and pursue careful clinical surveillance over the course of the ensuing weeks. In this regard, a repeat neurologic follow-up in 4-6 weeks time is suggested. A subdural hematoma, as observed in Deidre, is a collection of blood which has accumulated in the space between the dura matter, a thickened membrane which covers the brain, and the surface of the other membranes which cover the brain. Their presence raises the possibility that any existent brain damage may have been caused or exacerbated by trauma or the subdural hematoma itself. Notably, the trauma which tears the subdural veins and creates the subdural hematoma may be of sufficient force itself to cause brain damage or the hematoma itself may be of sufficient magnitude to compress the brain and cause brain damage. About 99 percent of subdural hematomas are due to trauma, which causes the veins crossing the subdural space into the dural sinuses to tear and thereby bleed. The other one percent of observed subdural hematomas are due to rare causes such as bleeding disorders. Under the circumstances, the presence of a subdural hematoma in Deidre certainly raised the possibility of secondary brain damage due to trauma or abuse. Here, the proof demonstrates that the subdural hematomas reflected by the CT scan of December 3, 1991, may be characterized as "chronic," and so defined, reflect a hematoma that had its genesis more than two weeks prior to its discovery. As for Deidre's hematomas, her neurosurgeon, whose opinion is credited, dates their occurance at two to four weeks prior to the CT scan of December 3, 1991. 3/ Regarding the cause of Deidre's subdural hematomas, the proof is, at best, unsatisfying. Deidre's birth was by cesarean section and therefore no mechanical maneuver or device, such as a vacuum extractor, forceps or a forced vaginal delivery, was utilized which could cause trauma. Moreover, the medical records are devoid of any indication of trauma to Deidre's head during delivery or the term of her hospitalization. Such does not, of course, completely rule of the possibility that trauma was induced during resuscitation efforts or at some other time in the hospital, but any such conclusion, absent a CT scan or other definitive testing during her admission, would be speculative. On the other hand, Deidre received routine follow-up after discharge by her pediatricians and Dr. Sassower, and they observed no evidence of trauma or abuse to Deidre, and a physical and ophthalmology consult revealed none. The absence of such physical evidence does not completely rule out the possibility of trauma or abuse, but its absence coupled with the ophthalmology consult and the reliability and character of the parents, as well as the other sole caregiver, renders it extremely unlikely that the subdural hematomas were a consequence of abuse or trauma suffered following Deidre's discharge from the hospital. The only other explanation offered at hearing for Deidre's subdural hematomas, other than a blood disorder which was ruled out, were the opinions offered by her physicians and experts, who suggested that because of the brain atrophy and the resultant shrinkage of the brain suffered as a consequence of the hypoxic insult at birth, the bridging veins which cross the subdural space into the dural sinuses were stressed and introduced a bleed, causing the hematomas. Given the conclusion that trauma or abuse was not the cause of Deidre's hematomas, and the elimination of a blood disorder as a possible cause, such opinions, based on the proof in this case, are the most likely explanation of Deidre's bleed, which resulted in the hematomas disclosed by the December 3, 1991 scan. Finally, the absence of any compelling proof to demonstrate that Deidre's hematomas were induced by trauma, and the absence of any compelling proof that the chronic subdural hematomas were of sufficient magnitude and existed for a sufficient period of time to compress the brain and cause significant brain damage, absent trauma, it is concluded that the atropy evidenced by the CT scan of December 3, 1991, was more likely than not, a product of the hypoxic insult that Deidre suffered at birth, and that such hypoxic insult rendered her substantially and permanently mentally and physically impaired. 4/
The Issue Did Respondent's failure to intervene in the post-operative period immediately after learning the CT scan results of Patient C.O. near midnight on April 12, 1997, constitute treatment that fell below the standard of care and that he failed to practice medicine with that level of care, skill, and treatment which is recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances, in violation of Section 458.331(1)(t), Florida Statutes?
Findings Of Fact Petitioner is the state agency charged with regulating the practice of medicine in Florida. Respondent is a licensed physician in the State of Florida at all times material to the times alleged in the Complaint, having been issued license number ME 0070668. Respondent, as of May 2001, is board-certified in the area of neurological surgery. On April 3, 1997, Patient C.O., a 50-year-old male, presented to an Otolaryngologist (ear, nose and throat surgeon) with complaints of right side nasal polyps. On April 7, 1997, Patient C.O.'s surgeon ordered a radiological consult and a Coronal CT (up, down, front and back) scan of the right maxillary sinus. The CT scan revealed "complete opacification (blockage) of the left frontal, right ethmoid, right maxillary sinus, as well as the right nasal cavity with complete opacification of right sphenoid sinus." On April 9, 1997, Patient C.O. underwent a surgical procedure to remove nasal polyps. The surgeon removed an extremely large right nasal polyp, measuring approximately 10 cm in length. After removing the large mass, the surgeon noted smaller polyps and removed these also. After removing the polyps, the surgeon noted a "large pulsatile mass," which he biopsied. Biopsy results indicated that the "mass" was brain tissue. During the course of this procedure, the patient's cribriform plate had been pierced. This plate forms a barrier between the nasal cavity and the base of the brain. As a result of this puncture, the surgeon had removed a portion of Patient C.O.'s brain. The surgeon requested an intraoperative consult with Respondent. The surgeon and Respondent talked by telephone and Respondent recommended sealing off the brain tissue with a surgical flap and packing. An arteriogram was performed on Patient C.O. to determine if bleeding was from an artery or vein. It was determined that the bleeding was from a vein. He also, recommended placing Patient C.O. in the neurological intensive care unit, which was done, and the patient was stabilized. A CT scan, ordered by the surgeon, noted a right frontal hemorrhage and pneumoncephalus (air at the top of the skull). On April 10, 1997, drainage was noted from the right nostril of Patient C.O. Respondent noted that drainage was suspicious for cerebrospinal fluid (CSF). Respondent then considered various options in order to stop the leakage of CSF. On April 10, 1997, Respondent performed a surgical procedure which placed a spinal drain in Patient C.O. to control the intracranial pressure and to permit an outlet for the CSF. Respondent was attempting to allow the rupture to the cribriform plate to heal on its own. On April 11, 1997, a CT scan revealed large areas of air in the frontal areas of the skull. On April 12, 1997, it was determined that the rupture of the cribriform plate had not healed on its own. Patient C.O. had persistent drainage from the right nostril. He was taken to the operating room for a direct intracranial surgical repair of the defect. A CT scan demonstrated an increase in the frontal hemorrhage, a large left subdural hematoma, and brain swelling. On the afternoon of April 12, 1997, Respondent performed a bi- frontal craniotomy on Patient C.O. to close off the leaking of spinal fluid from the brain in the area behind the patient's forehead (CSF leak). The surgery began at 12:15 p.m. and anesthesia was initiated at approximately 12:30 p.m. on April 12, 1997, and surgery concluded at about 5:00 p.m. The procedure involved making an incision across the top of the scalp, from ear to ear, gaining access to the brain by making incisions in the cranium, then lifting the brain to allow access to the cribriform plate. This was accomplished without incident. During the post-operative period, the anticipated reaction of the patient was to return to post-operative status, or to improve neurologically beginning within two hours after the surgery ended. During the course of post-operative care, Patient C.O.'s vital signs and neurological statistics were constantly monitored. Patient C.O. did not show any improvements several hours after surgery as would be expected, but began to show signs of neurological deterioration. Because Patient C.O. did not improve neurologically after the surgery, Respondent, at about 9:30 p.m. on April 12, 1997, ordered a CT scan to be done immediately. Patient C.O. was taken for his CT scan around 10:45 p.m. The CT scan report by radiologist at Florida Hospital was called in to the hospital unit at 11:50 p.m. on April 12, 1997. Respondent was at home in bed, sleeping, when he was paged. Respondent called in and was told by telephone of the "wet read" results of the CT scan by the neuroradiologist. After obtaining the CT scan report, Respondent disagreed with the neuroradiologist's recommendations, ordered the continuation of the interventions which he had previously ordered, and issued no new medical orders. The April 12, 1997, CT scan results were reduced to writing and showed the following findings, when compared to the CT scan taken of Patient C.O., on April 11, 1997: Noncontrast examination shows numerous abnormal findings. Compared to the 04/11/97 study acute left subdural hemorrhage is similar. There is a large intraparenchymal frontal hemorrhage that has a similar appearance . . . . DIFFUSE INTRACEREBRAL SWELLING PROBABLY WORSE IN THE POSTERIOR FOSSA. OBLITERATED FOURTH VENTRICLE. VENTRICLE SIZE SIMILAR. INCREASED BLOOD FRONTAL REGION. UNCHANGED SUBDURAL LEFT POSTERIOR PAREITAL REGION. VENTRICULAR SIZE STABLE. PNEUMOCEPHALUS UNCHANGED. INTRAVENTRICULAR BLOOD STABLE. At 5:15 a.m. on April 13, 1997, Patient C.O.'s neurological status took a significant turn for the worse. The patient was interbated, and all appropriate measures were taken to attempt to revive the patient. Patient C.O. lapsed into coma and was unable to breathe sufficiently for himself; he sustained respiratory failure and coma. In the early morning hours of April 13, 1997, Patient C.O's neurological status was discussed with his family, and the decision was made to execute a do-not- resuscitate order. The patient never recovered and died two days later on April 15, 1997. Petitioner alleges that the standard of care required Respondent to take some affirmative or new action to intervene post-operatively on the night of April 12 through 13, 1997, to determine the cause of the deterioration and prevent irreversible brain damage. In support of Petitioner's position with regard to Respondent's standard of care, it presented the testimony of Dean C. Lohse, M.D. Dr. Lohse is a board-certified neurosurgeon who is licensed to practice medicine in the State of Florida. Dr. Lohse is a similar health care provider to Respondent, and he qualifies as an expert witness under Florida law. Dr. Lohse testified that he had several criticisms of the manner in which Respondent managed Patient C.O.'s post-operative care. Dr. Lohse was critical of the manner in which Respondent reacted to the information which was provided to him regarding the CT scan which was taken on the night of April 12, 1997, and which was communicated to Respondent at approximately midnight on that same night. In response to this information, Dr. Lohse was of the opinion that Respondent should have initiated some new intervention, including returning Patient C.O. to surgery, initiating medications to reduce swelling, introducing a pressure monitor, or changing the position of the lumbar drain. However, during the course of cross-examination, Dr. Lohse conceded that he could not say whether a return to surgery would have resulted in a different outcome for Patient C.O. Likewise, he could not state to within a reasonable degree of medical probability whether the introduction of medications to reduce the swelling would have worked. He could not state within a reasonable degree of medical probability whether the placement of a pressure monitor would have created a different result. Finally, he conceded that the issue of changing the lumbar drain was best left to the clinical judgment of the physician who is presiding over the care of the patient. Respondent testified on his own behalf at the final hearing. Respondent explained the April 12, 1997, craniotomy which he performed. He also explained the course of treatment which was followed with Patient C.O. in the hours subsequent to the conclusion of the craniotomy. Respondent explained his rationale behind ordering a stat CT scan, and he described the basis for his response to the information received at that time. Respondent testified that although he considered a return to surgery based upon the information contained within the CT scan, he decided against this option, as performing another surgery would only have been for the purpose of removing additional portions of Patient C.O.'s brain, including areas of the brain which are designed to control significant elements of an individual's personality. Respondent made the determination at that time that performing another surgical procedure would likely have caused more harm than good. Respondent testified that brain swelling reducing medication had been introduced previously and that the introduction of more or different brain swelling-reducing medications would not have addressed Patient C.O.'s condition. Respondent testified that the placement of a pressure monitor would have been pointless, given the information which he was able to obtain during the course of the craniotomy procedure. A pressure monitor is designed to measure increased levels of pressure on the brain. Patient C.O. was suffering from the opposite problem. Patient C.O.'s brain was actually flaccid, suffering from an absence, rather than an overabundance, of pressure. Therefore, the placement of a pressure monitor was never considered, as it would not have been of any use under the circumstances. Respondent testified that there was no need to change the aspect of the lumbar spinal drain. The lumbar spinal drain in this particular case was adequately controlled, at 5 ccs per hour. Thus, the use of the spinal drain was appropriate under the circumstances. Respondent's testimony is credible. Respondent also presented expert testimony, via deposition, of R. Patrick Jacob, M.D. Dr. Jacob is a board- certified neurosurgeon who currently works at the University of Florida in Gainesville. Dr. Jacob testified as to his education, training, and experience. He is a similar health care provider to Respondent, qualifies as an expert under Florida law, and can render expert medical opinions regarding the applicable standard of care in this case. Dr. Jacob testified that in his opinion, to within a reasonable degree of medical probability, Respondent met the applicable standard of care. He addressed each of the specific criticisms raised by Dr. Lohse. He specifically rejected the idea that another surgical procedure should have been performed, stating that to do so would have done more harm than good. He rejected Dr. Lohse's contention that the introduction of additional medications to reduce swelling would have been appropriate. Dr. Jacob disagreed with Dr. Lohse's suggestion that the placement of a pressure monitor would have been appropriate under the circumstances of this case. Finally, Dr. Jacob took issue with Dr. Lohse's opinion that a change in the lumbar spinal drain was warranted given Patient C.O.'s condition. On cross-examination, Dr. Jacob testified that he felt that Respondent's response to the information contained within the April 12, 1997, CT scan was appropriate. He was then presented with hypothetical questioning regarding whether doing nothing in response to the information contained within the CT scan would have been appropriate. Dr. Jacob testified that doing nothing in response to the information contained within the CT scan report may have constituted a deviation from the accepted standard of care. However, according to Dr. Jacob's review of the records, and Respondent's testimony at the final hearing, it is apparent that a decision was made by Respondent to continue with the interventions which had already been initiated, which under the circumstances of this case constitutes an affirmative act by Respondent to address the treatment and care of Patient C.O. Dr. Jacob's testimony is both credible and persuasive. The evidence is not clear and convincing that Respondent failed to intervene in the post-operative period immediately after learning the CT scan results of Patient C.O. around midnight on April 12, 1997. Respondent did not fail to take appropriate action after learning the results of the CT scan at midnight on April 12, 1997. Respondent ruled out several options and elected to continue with the interventions already initiated. Therefore, Respondent did not fall below the standard of care for similarly situated neurosurgeons and his actions on April 12 through 13, 1997, did not constitute a failure to practice medicine with that level of skill, care, and treatment recognized by a reasonably prudent similar neurosurgeon as being acceptable under similar conditions and circumstances.
Recommendation Based on the foregoing, it is RECOMMENDED that the Board of Medicine issue a final order finding that Respondent has not violated Section 458.331(1)(t), Florida Statutes, and dismissing the Administrative Complaint. DONE AND ENTERED this 19th day of July, 2002, in Tallahassee, Leon County, Florida. DANIEL M. KILBRIDE Administrative Law Judge Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-3060 (850) 488-9675 SUNCOM 278-9675 Fax Filing (850) 921-6847 www.doah.state.fl.us Filed with the Clerk of the Division of Administrative Hearings this 19th day of July, 2002. COPIES FURNISHED: Michael R. D'Lugo, Esquire Wicker, Smith, O'Hara, McCoy, Graham & Ford, P.A. Post Office Box 2753 Orlando, Florida 32802-2753 Shirley J. Whitsitt, Esquire Agency for Health Care Administration 2727 Mahan Drive, Mail Stop 39-A Tallahassee, Florida 32308 William W. Large, General Counsel Department of Health 4052 Bald Cypress Way, Bin A02 Tallahassee, Florida 32399-1701 R. S. Power, Agency Clerk Department of Health 4052 Bald Cypress Way, Bin A02 Tallahassee, Florida 32399-1701 Tanya Williams, Executive Director Board of Medicine Department of Health 4052 Bald Cypress Way Tallahassee, Florida 32399-1701
The Issue At issue is whether Daniel Irchai, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Stipulated facts Petitioners, Arnold Irchai and Irina Irchai, are the natural parents and guardians of Daniel Irchai, a minor. Daniel was born a live infant on February 14, 2003, at North Florida Regional Medical Center, a licensed hospital located in Gainesville, Alachua County, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Daniel's birth was Richard Brazzel, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. In this case, Petitioners are of the view that Daniel suffered a "birth-related neurological injury," as defined by the Plan. In contrast, NICA is of the view that Daniel did not suffer a "birth-related neurological injury" since the proof failed to support the conclusion that, more likely than not, Daniel suffered a brain injury "caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period" in the hospital and, regardless of the etiology of Daniel's brain injury, he was not rendered "permanently and substantially mentally and physically impaired." Daniel's birth and postnatal course At approximately 10:00 a.m., February 14, 2003, Mrs. Irchai was admitted to North Florida Regional Medical Center for an elective repeat cesarean section. According to the hospital records, pre op was complete at 11:00 a.m., Mrs. Irchai was moved to the operating room at 11:45 a.m., anesthesia was started at 11:50 a.m., surgery was started at 12:14 p.m., and Daniel was delivered, with vacuum assist, at 12:26 p.m. Of note, the records reveal maternal hypotension after the spinal anesthesia, with some fetal bradycardia before delivery, and at least three attempts with the vacuum extractor before Daniel was delivered. Following delivery, Daniel was slow to respond, and was "vigorus[ly]" stimulated and administered blow-by oxygen for 15 minutes. Apgar scores were recorded as 6 and 8, at one and five minutes, respectively,3 and cord pH was recorded as 6.89. Physical examination by Dr. Burchfield, the neonatalogist present at delivery, noted breath sounds with fine crackles, as well as intermittent grunting. At 12:41 p.m., Daniel was transported to the special care nursery where, at 12:45 p.m., he was assessed for abnormalities. Admission assessment was grossly normal, except for apparent respiratory problems, with evidence of slight nasal flaring, grunting, mild subcostal retractions, and diminished breath sounds. A cephalhematoma was also noted.4 Daniel initially responded well to blow-by oxygen, but grunting worsened and a stat consultation by neonatology was requested. On arrival at 1:50 p.m., Dr. Burchfield's physical examination revealed retractions, grunting, rales bilaterally, good skin perfusion, and open and flat fontanelle. Dr. Burchfield's impression was probable transitory tachypnea of the newborn (TTN), and his treatment plan included hood oxygen, IV fluids, blood cultures, and antibiotics (Ampicillin and Gentamicin). The nurses' progress notes reveal that between 3:00 p.m., and 3:40 p.m., Daniel continued under the oxygen hood, but was very fussy, and on one occasion was noted to secrete approximately 5 cc of blood from his mouth. The progress notes further reveal that between 3:40 p.m., and 3:50 p.m., when Dr. Burchfield was paged, Daniel was placed on NCPAP, and blood secretions from his mouth continued. Dr. Burchfield described the events in his progress notes, as follows: I was paged at 3:50 p.m. to say that this baby had vomited bright red blood [BRB] - baby's respiratory distress worsened & NCPAP started. OG placed & copious BRB came up. Baby had an estimate of 10-15 cc of blood. Upon arrival [at approximately 4:20 p.m.] baby was on NCPAP . . . . I intubated [with] 3.5 ET - initially no blood in ET. Attempt to place UAC unsuccessful. During this attempt, blood came up ET tube requiring suction. UVC placed & VBG sent, Coags sent (no heparin in line) & emergent T&C . . . . Imp[ression] - UGI bleed [hemorrhage] - ? sepsis . . . . P[lan] - Transfer to Shands UF Peds. Surgery Consult (already contacted ) ? Coags (pending) Stat T&C for transfusion Daniel was transferred to Shands at the University of Florida, where he was admitted at approximately 6:30 p.m. Following admission, the neonatalogist admission note, prepared by Dr. Burchfield, documented the presence of fresh blood in the ET tube and that "a subgaleal hemorrhage was becoming evident." Dr. Burchfield's impression was diffuse hemorrhagic disease of the newborn5; coagulopathy6; respiratory distress; pulmonary hemorrhage; suspect sepsis; and fetal distress. Dr. Burchfield's treatment plan was FFP 10 cc/kg; blood transfusion; NPO/IVF; antibiotics; and follow up with coagulation studies "to see if FFP corrects, [and] if it does, consider further deficiency." At 11:45 p.m., Dr. Burchfield made the following progress note: Baby is critically ill [with] evidence of bleeding diathesis —bleeding from GI track, lung, scalp. Emergency head US showed no bleed earlier this evening, but fontanelle is more tense now, so will repeat in a.m. Fibrinogen[7] was very low -26. This improved to 90 [with] FFP. Coags improved somewhat [with] FFP also . . . . Baby is having frequent desats and some posturing -its unclear if this is occluded ET and he's fighting, or if he is having seizures. We have given a dose of Ativan. This severe hypofibrinogenemia may be due to Liver disease 2) Congenital deficiency of Factor I 3) DIC [disseminated intravascular coagulation].[8] We have sent LFT's to rule out #1). Platelet count is not extremely low, as one would see [with] DIC. Now that FFP is given, we can't accurately obtain other factor levels to study DIC (Factors V, VIII). We will give some cryoprecipitate to bring fibrinogen higher. On February 15, 2003, David Suhrbier, D.O., a pediatric neurologist, examined Daniel. Dr. Suhrbier summarized Daniel's history and his impressions, as follows: CHIEF COMPLAINT: Seizure activity and abnormal CT of the brain. HISTORY OF PRESENT ILLNESS: Baby boy Irchai is a one-day-old Caucasian male who was referred from North Florida Regional Medical Center due to respiratory distress requiring intubation and the development of hematemesis[9] and hemoptysis.[10] Upon arrival the infant demonstrated evidence of disseminated hemorrhage disorder of the newborn manifested by a subgaleal hematoma, continued hemoptysis from the ET tube, hematemesis from the OG tube and coagulopathy evaluation demonstrating thrombocytopenia,[11] decreased fibrinogen and prolonged PT measurement. The infant received fresh frozen plasma and red blood cells. Ampicillin and Gentamycin were initiated for potential septic etiology. Chest x-ray demonstrated evidence of bilateral "ground glass" appearance consistent with respiratory distress syndrome. Initial head ultrasound was unremarkable for intraventricular hemorrhage. Infant shortly after arrival . . . began to manifest paroxysmal spells of desaturation associated with tonic posturing of the extremity which was presumed to be seizure activity. The infant was treated with two doses of IV Ativan. Head CT demonstrated evidence of both intra-axial as well as extra-axial blood products. Review of the study demonstrates the presence of a cerebellar hematoma with mass-effect upon the fourth ventricle resulting in ventriculomegaly of the third and lateral ventricles. Subarachnoid blood is also noted along both tentorial planes. Intraparenchymal hemorrhages are noted, as well as a large subgaleal hemorrhage. The infant received a 10 mg/kg bolus of IV Phenobarbital. No further seizure activity has been witnessed since the administration of the Phenobarbital. * * * OBJECTIVE: . . . HEENT: No dysmorphic features, large right parietal cephalohematoma, anterior fontanel elevated, pulsatile. Sutures minimally displayed. OFC 37 cm. Pulmonary: Breath sounds equal bilaterally. Lung fields clear to auscultation . . . . . Neurologic: Mental status: Infant somnolent (however the infant has received two doses of Ativan and loading dose of Phenobarbital). Cranial nerves: Pupils equal, round, and reactive to light. Infant attempted to squeeze eyes shut in response to light stimulus. Deep tendon reflexes 2+ in the upper and lower extremities. Motor: Minimal spontaneous movement of the extremities upon stimulation. With cotton tip applicator the infant demonstrated the ability to flex arms against gravity. Withdrew lower extremities. IMPRESSION: Neonatal seizures. Cerebellar hematoma, subarachnoid hemorrhage, and intraparenchymal hemorrhage. Obstructive Hydrocephalus due to cerebellar hematoma. RECOMMENDATIONS: Follow OFC measurements on a daily basis. Carefully monitor infant for symptoms of Cushing's triad. Repeat CT of the brain in 24 hours. Maintain Phenobarbital on minimal maintenance dosing 3 mg/kg/day. Electroencephalogram on Monday. Should Phenobarbital fail, consider adjunctive Fosphenytoin. During the course of his admission at Shands, Daniel underwent multiple radiological studies, with the last study, a cerebral CT, performed February 25, 2003, approximately 10 days prior to his discharge. That study, performed to evaluate for interval changes from the previous study of February 17, 2003, was read as follows: The previous study demonstrated hemorrhage in the fourth ventricle, paramesencephalic cisterns, and right cerebellum with subarachnoid blood in the right sylvian region. A large cephalohematoma over the right posterior scalp at the high convexity was also present. The current exam demonstrates expected evolutionary changes of blood products. The region of hemorrhage shows decreased density from prior in the paramesencephalic cisterns and the right cerebellum. The subarachnoid blood at the right sylvian fissure is also decreased in density. The scalp hematoma also is decreased in density. There are no new regions of hemorrhage. The ventricles remain midline. They are enlarged but unchanged from prior. Again noted is transependymal fluid migration that is similar when compared to prior study. No new regions of hemorrhage are seen. IMPRESSION: Expected evolution of blood products in the previous regions of intracranial hemorrhage and scalp hematoma. Persistent hydrocephalus that is unchanged from the prior exam. No new regions of hemorrhage are seen. On March 6, 2003, Daniel's condition was stable, and he was discharged to his parents' care. Primary diagnosis on discharge was consumptive coagulopathy (DIC), and secondary diagnoses and complications were noted as ventriculomegaly/hydrocephalus, seizures, cerebellar hemorrhage, intracranial hemorrhage, and extracranial hemorrhage. Follow-up appointments were scheduled or recommended with Pediatric Neurosurgery, Pediatric Neurology, and Daniel's pediatrician (John Hellrung, M.D.). Daniel's subsequent development Following discharge, Daniel did follow-up with Pediatric Neurosurgery, with his last visit on April 9, 2003. At that time a CT scan was performed, which showed decreased ventricular size and resolution of the intracranial hemorrhage. Pediatric Neurology recommended monitoring of head circumference, and Daniel was placed on an as needed status for return to the clinic. Following discharge, Daniel also followed-up with Pediatric Neurology, with his first visit on May 15, 2003. At that time, Daniel was examined by Paul Carney, M.D., a pediatric neurologist, who reported the results of his evaluation to Daniel's pediatrician (Dr. Hellrung), by letter of the same date, as follows: Daniel Irchai was seen in the Pediatric Neurology Clinic this morning accompanied by his parents. As you know, he is a three- month-old who had an intracranial hemorrhage at birth, as well as a large right parietal cephalohematoma. He was last seen as an inpatient during his stay in the NICU. Pediatric Neurology was initially consulted as he experienced some abnormal posturing and possible seizure activity during his first week of life. He was loaded with Phenobarbital and has been maintained on Phenobarbital routine dose since that time . . . . Since his discharge, the Irchais have not noticed any seizure activity, no episodes of loss of tone, abnormal posturing, eye deviation or tonic/clonic activity. They are very eager to see if Phenobarbital can be weaned off as they are concerned how this is impacting his development. It is for this reason that they present in clinic today. * * * Developmental History: Now at three months, Daniel is noted to be awake and alert. He has had no difficulty tolerating the Phenobarbital therapy. He smiles, he is not a fuzzy [sic] baby, no irritability noted. He does respond to mom. What mom does report is that he, if looking straight on him, Daniel will smile, coo and interact. However, if she is away from him and she calls to him no matter what method she uses, he will not turn his head to find her. He has never done this. She does report that he is trying to hold his head up, has not rolled over completely yet, he does [12] with kicking and moving all extremities equally. When placed on his stomach, he will make attempts to lift his head up but does not get it completely up, will remain with his cheeks to the side, does appear to bring his knees up to try to move and will attempt to push up lifting the chest but does not completely make it. His appetite is good, he is breast-fed. He does not have any problems with choking, spitting up, drooling or controlling his secretions. * * * Review of Systems: Negative for nausea, vomiting, diarrhea, no fever, no seizures noted, no change in tone, no altered level of consciousness, staring or deviations of the eyes and generalized tonic/clonic activity. Appetite is good. He is breast- fed only, has been growing well. No recent colds, no past infections. Physical Exam: On exam today, . . . height was 61.5 cm, weight was 6.11 kg, head circumference 39.5 cm. Today he was plotted out compared to birth at two months and at three months and he is following a nice curve right below the 50th percentile for age . . . . Neurologically, Daniel was awake and alert. He had a social smile, would seem to track but would not turn his head to voice. He was examined initially supine. Anterior fontanel open, flat, soft. Face was symmetric. His tongue was midline, palate was symmetric. He had a good suck. Pupils were equal, round and reactive to light with accommodation. A red reflex was noted on funduscopic exam. He did have moderate head lag when raised to the seated position. He had strong finger grasps bilaterally. Supine, he was moving all extremities vigorously. Reflexes were 2+ on bilateral upper extremities, 3+ bilateral lower extremities but he did have a plantar grasp when toes were downgoing. He had a positive Moro. He did have decreased central tone, increased ventral suspension but otherwise had a nonfocal exam. No clonus was noted, no tremor was noted. * * * Plan: Today we have spent a great deal of time with the Irchais going over all the scans that have been done, his head plot and his neurological exam of today. We feel optimistic that Daniel will do well overall. We have reviewed the EEG that was completed as an inpatient with them. In light of the fact that he has not had any other further clinical events and has continued to make some strides despite having some of the motor that we are noting today, we feel it is reasonable to begin a slow Phenobarbital taper. It may be that the hypotonic features we are seen in his exam may be related to Phenobarbital therapy. We have given them instructions to wean by half a cc every week until he is off, this will take approximately seven weeks. If after his Phenobarbital has been tapered to off, Daniel continues to show some hypotonicity, it would be reasonable to start occupational and physical therapy at that time. We would like him to have a followup head MRI to be completed in the next three to four months to give them a better idea as to if any scarring or atrophy remains from his initial bleed . . . . As requested, Daniel had a follow-up head MRI on September 8, 2003. The results of that study were reported by the attending radiologist, as follows: Encephalomalacic changes with almost complete destruction of the upper vermis is present. Old blood products are present as well at this site which are also seen on diffusion weighted imaging as dark signal in the poster fossa. There is no evidence of vascular malformations. Otherwise, the brain density is appropriate for a young child. Brain formation is normal. Myelination is appropriate for age with evidence of myelination in corticospinal tracts, visual pathways and corpus callosum. Ventricular size and sulcal pattern are within normal limits. No evidence of acute hemorrhage. IMPRESSION: Encephalomalacia changes with old blood products in the posterior fossa as above. No evidence of vascular malformation. Daniel's next evaluation by Dr. Carney, and his most recent, was on September 18, 2003. Dr. Carney reported the results of that evaluation, as follows: I had the pleasure of seeing Daniel today in the Pediatric Neurology on followup. As you know, he is a 7-month-old boy who has a history of neonatal seizures secondary to a cerebellar hematoma with intracranial bleed and cephalohematoma[.] [W]hen I last saw him on 05/18/03 [sic] . . . [h]e was doing quite well. He had no recurrent seizures at that time therefore, the Phenobarbital was tapered and discontinued. At today's visit, his parents report that he is doing quite well. He has good head control if sitting with minimal support. His tracking laterally and vertically to mom's voice, dad's voice as well as to face and object recognition. He is cooing. They are concerned that he has had some head bobbing which on further questioning sounds like mild titubation. He has had no developmental regression. No seizures since I last saw him. He underwent a followup brain MRI which demonstrated a superior vermis encephalomalacic abnormality secondary to his neonatal intracranial hemorrhage. Ventricular sizes were not dilated nor were the basilar cisterns, and the third and fourth ventricles appeared open and patent. There were no recurrent bleeds, nor was there brain atrophy or cerebellar hemispheric atrophy. * * * Physical Examination: Weight 8.19 kg, head circumference 43 cm (50th percentile), height 73 cm, . . . . He was awake, alert, tracked laterally to moving object. He had good neck tone. When placed on his abdomen, he lifted his head and held it in a erect position for more than two minutes. He would sit with minimal support. He had no axial slippage. Resistance to passive manipulation was normal in both upper and lower extremities. Deep tendon reflexes were 2+ at the biceps, triceps, brachioradialis, knees and ankles. Optic discs were pink and flat. I saw no retinal abnormalities. No drooling. Tongue at the midline, palate rose symmetrically, cooed throughout the examination. General physical examination no adenopathy or thyromegaly. Chest clear to auscultation. Heart sounds were regular rate and rhythm without murmurs. Abdomen soft without signs of hepatosplenomegaly, abdominal masses, no skin rashes were noted. Genitalia - normal male. Assessment and Plan: A 7-month-old boy with neonatal cerebellar hemorrhage as outlined above and post hemorrhage encephalomalacic defect. Developmentally he has made good progress. For the most part, he is on track with the exception of some head titubation. His parents are very much interested in pursuing physical therapy and therefore, I am recommending this at this time. He will have a followup brain MRI in six months and will see me in clinic thereafter . . . . Following discharge from Shands, Daniel received routine care from his pediatrician, Dr. Hellrung, with his first visit on March 10, 2003, at 3 weeks of age, and his last visit on May 12, 2004, at 15 months of age. Dr. Hellrung's records do not reveal any significant findings or observations that are pertinent to this case, but do document, as noted by Petitioners in their proposed final order, "tremor of head," and that as of May 12, 2004, Daniel showed evidence of a delay in gross motor development, since he did not yet "Walk[] alone, stoop[], recover[]," and a delay in language development, since he was "not [yet] talking." On June 2, 2004, following the filing of the claim in this case, Daniel was, at Respondent's request, examined by Michael Duchowny, M.D., a pediatric neurologist. Dr. Duchowny reported the results of his neurologic examination, as well as his review of Daniel's medical records, as follows: I evaluated Daniel Irchai on June 02, 2004. The evaluation was performed at Miami Children's Hospital. Both parents were in attendance and supplied historical information. HISTORY ACCORDING TO MR. AND MRS. IRCHAI: Daniel is a 15-month-old boy who suffers from developmental delay. The parents indicated that Daniel is not yet walking or talking and has very poor balance. He has just started to stand while holding on but seems "wobbly." He is unable to walk independently. They note no present changes in his muscle tone, although his mother felt that he may have been excessively loose several months ago. Parents also indicated that Daniel's head may shake in a side-to- side manner when he is in the sitting position. This is particularly evident when he is reaching. They believe that these movements have diminished somewhat over the last several months. * * * Daniel is sociable and plays well with his older brother. He does not drool except while teething. There has been no behavioral regression. Daniel has recently been evaluated for physical therapy at the "Kids on the Move" Program. He has not yet been scheduled for a routine physical therapy exercise regime. Daniel's health is otherwise good. His vision is normal, although the left eye will occasionally "move up under the eyelid" on directed right gaze.[13] Daniel's hearing is good and his appetite has been stable. He is on no intercurrent medications but did take phenobarbital for the first five-months of life. * * * Daniel rolled over at four-months and sat at eight-months. He began standing with support at thirteen-months but cannot walk independently or talk in words. He is not yet toilet trained. Daniel is fully immunized and has no known allergies. He has never undergone surgery or been hospitalized after the neonatal period. * * * PHYSICAL EXAMINATION reveals an alert, well- developed and well-nourished 15-month-old boy. Daniel weighs 23 pounds. The hair is blond and of normal texture. The eyes are blue. There is a nevus flammeus below the occipital hairline. There are no other cutaneous markings and no dysmorphic features. The head circumference measures 46.1 centimeters, which approximates the 20th percentile for age. The fontanels are closed. There are no cranial or facial anomalies or asymmetries. The neck is supple without masses, thyromegaly or adenopathy. The cardiovascular examination reveals normal heart sounds and the lung fields are clear. The abdomen is soft and non-tender. There is no palpable organomegaly. Peripheral pulses are 2+ and symmetric. NEUROLOGICAL EXAMINATION reveals an initially quiet infant sitting in his father's lap. However, Daniel is quite fearful and defensive and began crying inconsolably when approached. He did not speak in words at anytime during the evaluation but at least initially followed simple commands. Cranial nerve examination reveals full visual fields to direct confrontation testing and normal ocular fundi, which were seen only briefly. The pupils are 3 mm and react briskly to direct and consensually presented light. No facial asymmetries. The tongue and palate move well. The uvula is midline. Motor examination reveals mild generalized hypotonia for both axial and appendicular musculature. There were no tremors or evidence of adventitious movements. Daniel's head control was stable. Daniel is able to stand with minimal support but is unable to take steps independently. He did not fall. The deep tendon reflexes are slightly exaggerated at 2-3+ bilaterally. Plantar responses are downgoing. There are no pathological reflexes. Sensory examination is intact to withdrawal of all extremities to stimulation. Neurovascular examination reveals no cervical, cranial, or ocular bruits and no temperature or pulse asymmetries. In SUMMARY, Daniel's neurologic examination reveals very slight delays in motor and language development with excessive behavioral irritability. He demonstrates no findings to suggest structural brain damage and his seizures are in complete remission. A review of Daniel's medical records further indicates that Daniel's postnatal circumstances did not result from intrapartum oxygen deprivation or mechanical injury . . . . The cause and timing of Daniel's brain injury, as well as the significance of Daniel's impairment Given Dr. Duchowny's opinion that "Daniel's neurologic evaluation reveals very slight delays in motor and language development," and the absence of any contrary opinion or facts of record that would compel a contrary conclusion, it must be resolved that Daniel suffers neither a substantial mental impairment nor a substantial physical impairment, much less a permanent and substantial mental and physical impairment as required for coverage under the Plan. See Thomas v. Salvation Army, 562 So. 2d 746, 749 (Fla. 1st DCA 1990)("In evaluating medical evidence, a judge of compensation claims may not reject uncontroverted medical testimony without a reasonable explanation.") Moreover, given Dr. Duchowny's opinion "that Daniel's postnatal circumstances did not result from intrapartum oxygen deprivation or mechanical injury," and the absence of any contrary opinion or facts of record that would compel a contrary conclusion, it must be resolved that the proof fails to support the conclusion that Daniel's deficits resulted from a brain injury that occurred during labor, delivery, or resuscitation, as opposed to some other etiology (i.e.: the bleeding he experienced postdelivery). See Thomas v. Salvation Army, supra; Wausau Insurance Company v. Tillman, 765 So. 2d 123, 124 (Fla. 1st DCA 2000)("Because the medical conditions which the claimant alleged had resulted from the workplace incident were not readily observable, he was obliged to present expert medical evidence establishing that causal connection."); Nagy v. Florida Birth-Related Neurological Injury Compensation Association, 813 So. 2d 155, 160 (Fla. 4th DCA 2002)("[T]he oxygen deprivation or mechanical injury to the brain must take place during labor or delivery, or immediately afterward . . . . The fact that a brain injury from oxygen deprivation could be traced back to a mechanical injury outside the brain resulting in subgaleal hemorrhaging does not satisfy the requirement that the oxygen deprivation or mechanical injury to the brain occur during labor or delivery.") Consequently, the proof failed to support the conclusion that, more likely than not, Daniel suffered a "birth- related neurological injury," as defined by the Plan.
