Findings Of Fact Jamerious was born on January 1, 2014, at Winnie Palmer Hospital in Orlando, Florida. Attached to Respondent’s Motion for Summary Final Order is a certification of medical records from Dean Richey, Registered Health Information Administrator for Orlando Health, Inc., d/b/a Winnie Palmer Hospital. Said certification avers that the copies of the records attached to the certificate are true and accurate copies of the original records from Winnie Palmer Hospital related to Jamerious and Petitioner Terrese Franklin. The Discharge Summary from Winnie Palmer Hospital, dated February 14, 2014, documents that Jamerious’s birth weight was 1,152 grams. A Coding Summary from Winnie Palmer Hospital, concerning Petitioner Terrese Franklin, dated February 19, 2014, documents “Neonate bwt 1000-1249g w resp dist synd/oth maj resp or maj anom.” A review of the file reveals that no contrary evidence was presented to dispute the medical records from Winnie Palmer Hospital showing that Jamerious’s birth weight was less than 2,500 grams.
The Issue At issue in this proceeding is whether Adam Joseph Balash, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary matters Evan Balash and Terry Balash are the parents and natural guardians of Adam Joseph Balash (Adam), a minor. Adam was born a live infant on November 5, 1991, at Palms West Hospital, a hospital located in Palm Beach County, Florida, and his birth weight was in excess of 2500 grams. The physicians providing obstetrical services during the birth of Adam were Robert Chaitin, M.D., and Ronald Ackerman, M.D., who were, at all times material hereto, participating physicians in the Florida Birth-Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Mrs. Balash's antepartum course and Adam's birth Mrs. Balash's antepartum course was without apparent complication until November 5, 1991, when, with the fetus at 37 weeks gestation (estimated date of confinement November 20, 1991), she presented to her obstetrician/gynecologist. At the time, examination was reassuring with fetal movement and a fetal heart rate of 136 beats per minute; however, Mrs. Balash reported decreased fetal movement over the last few days. Consequently, she was referred to Palms West Hospital for a non- stress test (NST). Mrs. Balash presented to Palms West Hospital at or about 2:00 p.m. (1400 hours), November 5, 1991, and was placed on a fetal monitor for the NST at or about 2:04 p.m.3 Fetal heart rate (FHR) baseline was noted at 150 beats per minute and continued at that rate until about 2:25 p.m. when a period of bradycardia was shown to develop, down to approximately 90 beats per minute, and persist for approximately 5 minutes, with a return to baseline.4 Reassuringly, beat-to-beat variability and reactivity to Doppler were present, and no further episodes of bradycardia were noted during the course of Mrs. Balash's labor and delivery.5 Given the prolonged deceleration noted on the NST, Mrs. Balash was admitted to labor and delivery at 2:30 p.m. Vaginal examination revealed the cervix to be at 2-3 centimeters, effacement at 80 percent, and the fetus at station -2,6 with contractions at 1 to 2 minutes. Mrs. Balash complained of abdominal tenderness, and the abdomen palpated firm. No vaginal bleeding was noted. Dr. Chaitin was advised of Mrs. Balash's status, and intravenous (IV) fluids and lab work were ordered. At 3:00 p.m. the FHRs were noted as 140s, without accelerations, and at 3:20 p.m. vaginal examination revealed no change or progress. Dr. Chaitin was updated. At 3:34 p.m. Mrs. Balash was attended by Dr. Chaitin. His examination noted the fetus at station -3; however, dilation remained at 2 centimeters. The uterus was noted to be "rock hard without any relaxation," a presentation consistent with placental abruption. Consequently, Dr. Chaitin ruptured the membranes, yielding bright red amniotic fluid (further evidence of placental abruption).7 Internal fetal monitor was placed, revealing FHRs of 140s, with good variability and no decelerations.8 The fetus was noted to be in frank breech presentation. Given the evidence of fetal stress and probable placental abruption, Dr. Chaitin opted for a stat (immediate) cesarean section. Between 3:40 p.m. and 3:54 p.m., Mrs. Balash was prepared for surgery, anesthesia was started, and she was moved to the operating room. According to the labor and delivery summary, she was in the operating room at 3:55 p.m., the incision was made at 3:56 p.m., and Adam was delivered at 3:57 p.m., November 5, 1991. Pertinent to this case, the operative report reads as follows: . . . The uterus was noted to be rock hard in all quadrants. A low transverse incision was made with a scalpel. The uterine incision was extended bilaterally. The fetal breech was noted to be in frank breech position and with care, the butt was delivered and both arms were reduced appropriately. The fetal head was then removed, the baby was well bulb suctioned, and started crying extremely vigorously. [Infant dried and provided whiffs of oxygen, but no resuscitation required.] Cord was clamped, and neonatology present and baby evaluation was normal. A 6 pound, 12 ounce, baby boy was born with Apgar's 8/9. The cord ph was obtained which was 7.322 [normal]. The placenta was actively delivering, and was found to be 40% abrupted and was sent to pathology for evaluation. . . . The Apgar scores assigned to Adam are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, muscle tone, gag reflex, and color, with each category being assigned a score ranging from the lowest score of 0 through a maximum score of 2. As noted, at one minute Adam's Apgar score totalled 8, with heart rate, respiratory effort, muscle tone, and gag reflex being graded at 2 each, and color being graded at 0. At five minutes, his Apgar score totalled 9, with heart rate, respiratory effort, muscle tone, and gag reflex being graded at 2 each, and color being graded at 1. Such scores are grossly normal, as were Adam's newborn assessments, and he was admitted to the newborn nursery for routine care. (Petitioners' Exhibit 5, tabs 4 and 8). At approximately one hour of life (5:00 p.m.), Adam was observed to have turned dusky. One hundred percent oxygen via mask was applied, and Adam's color improved. Heart rate and respiratory rate were noted as stable. Adam was subsequently attended by Dr. Lerma Te, who noted nasal flaring, grunting, and retraction. Dr. Te's impression was "respiratory distress" and "rule out sepsis." Blood cultures were ordered, and intravenous Ampicillin and Claforan were started. Adam developed increasing oxygen requirements and at or about 6:40 p.m. he was intubated and assisted ventilation was begun. X-rays revealed "homogenous bilateral extensive ground glass appearance of the air bronchograms." Impression was that "[t]his either represents transient respiratory distress syndrome in the newborn or hyaline membrane disease."9 Given Adam's needs, he was transported to Good Samaritan Hospital, where he was admitted to the neonatal intensive care unit (NICU) at or about 10:25 p.m. Notably, notwithstanding his respiratory problems, Adam's neurological status remained essentially normal throughout his hospital stay. On November 20, 1991, Adam was discharged, in apparent good health, to his mother's care. His course at Good Samaritan Hospital noted no neurological problems, and is summarized on his discharge summary as follows: HISTORY: Mother is a 27 year old gravida 2, para 1, blood type 0 negative. Admitted at 37 weeks gestational age with abruptia placenta. Stat cesarean section was done and the baby was in breech position with Apgar score of eight and nine at one and five minutes respectively. Weight 2920 grams. The baby developed respiratory distress with increasing FI02 requirement. He was intubated and assisted ventilation started. Blood cultures were done. Intravenous Ampicillin and Claforan were started and the baby was transferred to Good Samaritan Hospital from Palm West. PHYSICAL EXAMINATION: Baby's weight 2920 grams, heart rate 156, respiratory rate 60, blood pressure 65/38. Premature 37 week male infant in respiratory distress. Head and Face: Anterior fontanelle flat. Oral cavity: No cleft plate noted. Chest: The baby is on assisted ventilation. Air entry heard both sides. Cardia: Heart sounds normal. Abdomen is soft. Umbilical cord has two vessels. Genitalia: Male. Extremities: No click at the hips. Central nervous system: Tone and reflexes equal on both sides. ASSESSMENT: Premature 37 weeks. Respiratory distress. Maternal complications, abruptia placenta. Cesarean section delivery. Suspected sepsis. Maternal history of herpes. HOSPITAL COURSE: Complete blood count, blood cultures x 7 were done. The baby continued on intravenous Ampicillin, endotracheal tube and cultures were sent for herpes. Umbilical catheter was inserted through the umbilicus about nine centimeters. He was started on Exosurf. The baby remained on assisted ventilation from 11/5 through 11/10/91 and was extubated on 11/10 and placed on Oxy-Hood. The baby was weaned from oxygen to room air by 11/18/91. The baby was also noted to be jaundiced and was started on photo therapy on 11/9/91 and was discontinued on 11/11/91 when the bilirubin declined. Echocardiogram done on 11/7/91 revealed moderate size patent ductus arteriosus and the baby was given Indocin and the patent ductus closed after the Indocin. The baby was on Ampicillin and Claforan for suspected sepsis and this was discontinued after a course of antibiotics of seven days. The baby was started on feedings on 11/18/91 and was advanced and IV's decreased. The baby tolerated adequate amounts of feedings and tolerated feeds well. The baby was discharged home at fifteen days of age when the baby weighed 6 lbs. 7.6 oz., was clinically stable and tolerating feedings well. DISCHARGE DIAGNOSIS: Premature 37 weeks male. Respiratory distress syndrome. Patent ductus arteriosus. Hyperbilirubinemia. Suspected sepsis. DISCHARGE PLAN: To be followed by Dr. Marineau in one week and Dr. Friedman for eye examination on 12/11/91. Brain stem auditory evoke potential examination to be done on 12/5/91 at Good Samaritan Hospital. Cranial ultrasound on 11/6 showed no evidence of [hydrocephalus or] intracranial bleeding. Adam's development Adam's early infancy was apparently unremarkable, and no problems were observed until approximately eight to ten months of age. At that time, developmental delay became evident and the parents reported their concerns to Adam's pediatrician, who referred him for neurologic consult at the Palm Beach Neurological Group.10 Adam was examined by a Dr. Mate, at the Palm Beach Neurological Group, in 1992; however, those observations are not of record. What is of record are the observations of Luis Bello-Espinosa, M.D. (Dr. Bello), another neurologist associated with the Palm Beach Neurological Group, who first examined Adam in April 1994. Dr. Bello describes Adam's presentation as consistent with severe cerebral palsy (profound brain dysfunction), that is characterized by spastic quadriparesis (an abnormal motor development affecting all four extremities) and mental retardation. Here, there is no dispute that Adam's impairments, mental and physical, are permanent and substantial. In an effort to identify the etiology of Adam's dysfunction, he was referred to Paul J. Benke, M.D., for genetic consultation. The results of Dr. Benke's first consultation were reported on November 2, 1993, as follows: DIAGNOSTIC IMPRESSION: Chromosome Anomaly. GENETIC COUNSELING: The developmental delay, now performing at 11-12 months, is probably related to the chromosome anomaly. It could not be determined today whether the neonatal problems played a role. One cell strain, the 20 deletion with 2 normal 7 chromosomes, is probably derivative from the dominant strain with the apparently balanced translocation. This would mean that the translocated #7 broke and lost most of the translocated #20, or far more likely, the whole chromosome was lost, the normal #7 was duplicated, and the 2 #7 chromosomes are derived from 1 parent. Blood was taken today to see if 1 parent is a translocation carrier. A skin biopsy, with a presumably higher proportion of 20 p- cells, would be required to determined (sic) why the translocated 7 was lost. Dr. Benke recommended follow-up studies. The results of Dr. Benke's follow-up studies were reported on October 1, 1994, as follows: This boy . . . [has] a mosaic chromosome abnormality . . . We did a skin biopsy months ago to determine the proportion of cells with a derivative chromosome 20, partial trisomy 7 and deletion 20. Most of the sample (29/30) cells had the balanced 7:20 translocation, with the deriviative (sic) 20 in just 3 percent. This suggests also that the balanced translocation was probably the first genetic lesion. Compounding conclusions of etiology for slow development is that a new balanced translocation leads to slow development and birth defects 7-10 per cent of the time. Also, the derivative 20 chromosome could be responsible since the neurons with this anomaly may function poorly. Also, he had a delay in his C-section of more than one hour when there was a demonstrable disruption of the placenta, associated with attendant neonatal problems. It is tough to say which of the factors is most responsible, but I think that the balanced translocation is the least important. Interestingly, children with chromosome 20 deletion are not particularly dysmorphic, but are delayed, and have some findings similar to those found in Adam. . . . In sum, Dr. Benke's conclusion was that Adam suffered a chromosonal abnormality known as a balanced translocation affecting approximately 3 percent of his cells. This genetic abnormality generally does not lead to any clinical problems; however, in 7 to 10 percent of the cases involving this type of translocation there may be genetic predisposition to decreased neurological development or birth (genetic) defect. The dispute regarding compensability Here, it is not subject to serious debate that the cause of Adam's neurologic impairment is associated with brain dysfunction or anomaly.11 What is at issue is the cause and timing (genesis) of that anomaly (encephalopathy)12 or, more pertinent to these proceedings, whether the proof demonstrates, more likely than not, that Adam's neurologic impairment resulted from an "injury to the brain . . . caused by oxygen deprivation13 . . . occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as opposed to some other genesis. Section 766.302(2), Florida Statutes. With regard to such issue, Petitioners contend that Adam suffered an hypoxic event, consequent to the stresses of labor (placental abruption and uterine hypertonicity), which caused a microscopic brain injury, and that such injury was the cause of Adam's neurologic impairment. In contrast, Respondent contends the proof is not consistent with hypoxic ischemic injury occurring during the course of childbirth, and, therefore, Adam's disorder must be attributable to some other etiology. Respondent's view of the proof has merit. The genesis of Adam's brain anomaly To address the genesis of Adam's brain anomaly, the parties offered selected medical records relating to Mrs. Balash's antepartum and intrapartum course, as well as for Adam's birth and subsequent development. Portions of those records have been addressed supra, and further salient portions will be addressed infra. The parties also offered the opinions of five physicians as to the likely cause of Adam's birth disorder. The physicians selected by Petitioners were Paul J. Benke, M.D., a board certified clinical and biochemical geneticist; Luis J. Bello, M.D., a board certified neurologist; and, Barry D. Chandler, M.D., a board certified neonatologist. The physicians offered by Respondent were Charles Kalstone, M.D., a board certified obstetrician and gynecologist; and Lance E. Wyble, M.D., a board certified neonatologist. The medical records and other documentary proof, as well as the testimony of the physicians offered by the parties, have been scrutinized. So considered, it must be concluded that the proof does not allow a conclusion to be drawn with any sense of confidence, that, more likely than not, Adam's brain anomaly was associated with an injury caused by oxygen deprivation during labor, delivery, or resuscitation in the immediate post- delivery period, as opposed to some other etiology.14 In reaching the foregoing conclusion, neither the evidence of placental abruption nor fetal stress during labor has been overlooked. However, while the presence of such factors could lead one to assume a connection and attribute Adam's anomaly to hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, an examination of the clinical data and observations suggests that such would be a speculative and unlikely explanation for Adam's presentation. In so concluding, it is observed that Adam's course pre-delivery and post-delivery was inconsistent with hypoxic or ischemic injury having occurred during the course of birth. First, the evidence documenting fetal heart rate during the course of labor and delivery, particularly when compared with Adam's post-delivery presentation, does not support the conclusion that Adam suffered an acute intrapartum event that led to an hypoxic or ischemic injury. Notably, there was only one event of fetal heart rate deceleration and overall the monitoring tape was reassuring. Under such circumstances, it is unlikely that the partial abruption Mrs. Balash suffered adversely affected fetal oxygenation during labor and delivery. Further militating against the conclusion that Adam's anomaly was caused by oxygen deprivation during the course of labor and delivery are the numerous inconsistencies between Adam's presentation and the clinical findings one would expect had he suffered hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, during that period. Notably, had such an event occurred, one would reasonably expect a severely depressed infant on delivery, with an absence of respiratory effort; a depressed cord pH; and the onset of seizure activity during the neonatal period. Here, Adam was alert and active on delivery, with good respiratory effort; his Apgars were normal, as were his newborn assessments; his cord pH was normal; and no seizure activity was noted in the neonatal period. Also of note, within approximately 24 hours of birth, Adam was administered a cranial ultrasound, which proved negative for hemorrhage and edema. Edema is a clinically anticipated consequence of neurological injury, and is anticipated within 6 to 12 hours of the event. Subsequent brain studies (MRIs), at or about 11 and 18 months of age, were also read as normal or, stated differently, failed to reveal global or bilateral injury generally associated with hypoxic ischemic encephalopathy. Finally, had Adam suffered an hypoxic ischemic event during birth, one would reasonably expect damage to multiple organ systems. Included would be the kidneys, bone marrow, the liver, and the heart. Here, Adam's creatine levels and urine output remained normal throughout the neonatal period, indicating that his kidneys were not subjected to an acute hypoxic event. Additionally, Adam evidenced no myocardial injury, and his bone marrow reflected no evidence of lymphocrytosis, which one would anticipate had there been an acute hypoxic event.15 Finally, Adam's first CBC (complete blood count) at Palms West Hospital indicated an extremely elevated level of nucleated red blood cells, which would be consistent with the presence of a chronic injury, as opposed to an acute insult. Given the proof, it cannot be concluded that, more likely than not, Adam's brain disorder and resulting neurologic impairment was associated with a brain injury caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Notably, Adam's presentation at birth and his neonatal course were not consistent with an acutely acquired neurological injury, and it is improbable that he could have experienced an acute injury during labor and delivery without evidencing a single clinical symptom of such damage. Conversely, the existence of a prenatally acquired (predating labor and delivery) brain disorder (whether genetically or otherwise based) would be consistent with Adam's presentation at birth and during the neonatal period.
Findings Of Fact Spencer Heaton was born on August 17, 2015, at Florida Hospital in Orlando, Florida. He was a single gestation. NICA attached to its motion a certification of medical records signed by the Custodian of Records from Florida Hospital, and a four-page discharge record for Ashley and Spencer Heaton. The medical records show that Spencer Heaton’s birth weight was less than 2,500 grams. A review of the file reveals that no contrary evidence was presented to dispute the medical record from Florida Hospital showing that Spencer Heaton’s birth weight was less than 2,500 grams.
The Issue At issue is whether Eli Joe Arellano, Jr., a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts Cathy Arellano and Eli Joe Arellano, Sr., are the natural parents of Eli Joe Arellano, Jr., a minor. Joe was born a live infant on February 17, 1999, at Fort Walton Beach Medical Center, a hospital located in Fort Walton Beach, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Joe's birth was Thomas H. Moraczowski, 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 or spinal cord . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." §§ 766.302(2), Fla. Stat. See also §§ 766.309(1) and 766.31(1). In this case, Petitioners are of the view that Joe suffered a "birth-related neurological injury" because it is their "belief . . . [based on] the medical records and injuries sustained at birth [such as bruises on top of the head and face and broken collarbone] . . . Joe has sustained a spinal cord or brain injury resulting in Cerebral Palsy Hypotonia." (Pre- Hearing Stipulation, paragraph B1) In contrast, NICA is of the view that Joe did not suffer a "birth-related neurological injury" because his impairments were not occasioned by an "injury to the brain or spinal cord . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation" and, regardless of the etiology of Joe's impairments, he is not "permanently and substantially mentally and physically impaired." (Pre-Hearing Stipulation, paragraph B2). Here, Respondent's view is most consistent with the proof. Joe's birth and immediate postnatal course At or about 3:30 p.m., February 16, 1999, Mrs. Arellano, with an estimated delivery date of February 21, 1999, and the fetus at 39 2/7 weeks gestation, presented to Fort Walton Beach Medical Center, in labor. At the time, Mrs. Arellano's membranes were noted as intact, and vaginal examination revealed the cervix at 5-6 centimeters dilation, effacement at 75 percent, and the fetus at -3 station. Uterine contractions were described as moderate, at a frequency of 5-7 minutes, and fetal monitoring revealed a reassuring fetal heart rate, with a baseline in the 130-beat per minute range. Mrs. Arellano was admitted to labor and delivery at 4:15 p.m.; an IV was started at 5:18 p.m.; her membranes were artificially ruptured at 5:22 p.m., with clear fluid noted; and Petocin augmentation was started at 6:20 p.m. Thereafter, Mrs. Arellano's labor slowly progressed until 1:55 a.m., February 17, 1999, when complete cervical dilation was noted, and Joe was delivered vaginally at 2:01 a.m. Notably, fetal monitoring revealed a reassuring fetal heart rate throughout the course of labor, but, at 10 pounds 7 ounces, Joe was large for gestational age (LGA), and delivery was complicated by a shoulder dystocia, which was relieved by hyperflexion of the legs to the maternal abdomen, suprapubic pressure, and corkscrew rotation of the infant's posterior shoulder to the anterior plane. Nevertheless, although not diagnosed at the time, Joe suffered a fractured clavicle during delivery, which healed without apparent complication. At delivery, Joe was reported to be "healthy and vigorous," and did not require resuscitation. Cord blood pH was reported as normal (7.25), as were Joe's Apgar scores, which were noted as 9 and 9, at one and five minutes, respectively.1 Following delivery, Joe was transported to the regular newborn nursery, where he was received at 2:30 a.m. Newborn assessment noted "L[igh]t bruising to forehead/top of head" and "mild" molding, observations that were not shown to have any clinical significance in this case. Otherwise, Joe's newborn assessment was unremarkable, as was the remainder of his postnatal course, and he was discharged with his mother on February 19, 1999. Joe's subsequent development Following discharge from Fort Walton Beach Medical Center, Joe's early development was age appropriate; however, over time, his mother voiced a number of concerns about his development, and in December 2000 he was referred by his pediatrician to the Child Neurology Center of Northwest Florida for evaluation. There, Joe was initially seen for a neurology consultation by Tim S. Livingston, M.D., who reported the results of his January 4, 2001, evaluation, as follows: REASON FOR CONSULTATION: Hypotonia. PRESENT ILLNESS "Joe" is a 22-month-old, possibly left- handed young boy who presents with his family for evaluation of the above concerns. His mother indicates she has several concerns about his development. She is most concerned about his gait. She indicates that ever since he has been walking he has had a tendency to in-toe (right greater than left). This was not significantly disabling and did not significantly impair attainment of his milestones. However, over the last month she feels this has worsened and that he has more frequent falls. She does not notice any diurnal variation of this gait or any apparent dystonia. She also indicates that she has concerns about his speech. She indicates that he said his first words at 12 months and knows approximately 10 words at the present. However, she feels the words he does know are poorly articulated. He is able to point to some body parts and understands "yes" and "no." He does make good eye contact with family members and others and is variably affectionate. He does not have significant ritualistic behavior or any apparent stereotypes. She is also concerned about his fine motor and gross motor coordination. She indicates that he is able to throw a ball but remains incoordinated when he attempts to feed himself. He does not always know how to properly hold utensils. She denies any apparent . . . regression of milestones. PAST HISTORY Antenatal: He was born to his mother after a pregnancy complicated by weight loss and gestational diabetes. There is no apparent hypertension, infection, bleeding, drug use or alcohol use. Birth: He was felt to be born at term and weighed 10 pounds, 7 ounces. His mother reports he did not have any significant immediate perinatal difficulties. Neonatal: She indicates that he did not have significant jaundice, cyanotic episodes, respiratory distress, or other problems. However, she does indicate that since the newborn period he has had constipation. Development: Held head up at 2 months, sat alone at 4 months, walked at 13 months, fed himself at 1 year. The remainder of development as per History of Present Illness. Behavior: He has frequent episodes of crying. He is somewhat shy but is affectionate when he is familiar with people. She does indicate that he does not sleep well at all. * * * NEUROLOGICAL EXAMINATION General: Healthy, alert young boy in no apparent distress. Skull: Occipitofrontal circumference 50 centimeters (75th percentile). Normocephalic, without evidence of cranial trauma. Fontanel is closed. No boney abnormalities or bruits. Neck and Spine: Supple, full range of motion, no meningeal signs. Speech and Language: As per above. Mental Status: The child was awake, alert. He follows simple commands. He was not fully compliant with language or speech testing, though spontaneous language seemed age appropriate. * * * Motor: Tone - Spontaneous observation demonstrates hypotonic posture (i.e., exaggerated kyphosis, mild froglegging), also passive range of motion demonstrates reduced tone in a generalized distribution which is mildly greater in truncal musculature. Power - there is no asymmetry of movement. He moved all extremities appropriately and symmetrically. Coordination - He was able to hold a ball appropriately and throw it. There is no obvious incoordination. Cerebellar - No apparent ataxia with spontaneous reaching and hand movements or spontaneous movements of the lower extremities. Involuntary movements - no obvious tics, tremors, chorea, athetosis or other abnormal movements. Reflexes: His tendon reflexes were 0 to 1+ at biceps, triceps, radialis, knee jerks, and ankle jerks (reduced in a generalized distribution). Gait and Stance: Spontaneous observation of his gait demonstrated bilateral in-toeing (right greater than left). His gait was not abnormally wide-based or ataxic. Heel walking and toe walking was appropriate. He was not able to comply with tandem gait. Sensation: Intact to temperature, light touch and vibration throughout. * * * ASSESSMENT Generalized hypotonia. Abnormal gait (in-toeing). Possible developmental articulation difficulties. Based on the history, I suspect that "Joe" is suffering from mild developmental hypotonia which may be benign in nature. However, potential causes such as hypothyroidism and inborn errors of metabolism need to be considered. Furthermore, abnormalities of myelinization should be considered. I am not entirely convinced that his abnormal gait is directly related to his hypotonia. It is possible that he is suffering from tibial torsion or femoral anteversion. Regardless, I do not think his gait is significantly abnormal to warrant orthopedic evaluation. His parents do give a history of significant difficulty with articulation which was difficult to confirm at bedside testing. Regardless, his cognitive and receptive language skills appear to be normal, as do most of his other developmental milestones. It is possible that he has a mild developmental speech disorder. I have discussed the above in detail with his mother and she wishes to proceed as outlined below at my recommendation. PLAN Magnetic resonance imaging of the brain with sedation. Blood work for TSH, amino acids and ammonia. Urine amino and organic acids. Physical therapy, occupational therapy and speech therapy. Return in 1 month. Over the years, Joe has had multiple consults at the Child Neurology Center, initially with Dr. Livingston and then, beginning in 2003, with Dr. J.B. Renfroe. Those consults ultimately produced an assessment of static encephalopathy, developmental delay, and initially, cerebral palsy hypotonia and later, autism/pervasive developmental disorder (PDD).2 Over the years, Joe has also undergone multiple studies to identify the etiology of his neurologic deficits, without success. Such studies have included multiple blood and urine studies, including genetic and metabolic analyses, which have been unrevealing; an MRI of the brain on February 5, 2001, which was normal; an MRI of the cervical spine on March 28, 2002, which was normal; electroencephalograms (EEGs) on February 21, 2002, and October 30, 2003, which were normal; and a video EEG on June 11 and 12, 2002, which demonstrated an abnormal generalized slowing of background activity, consistent with encephalopathy, but nonspecific with regard to etiology, and no epileptiform abnormalities or seizure activity. On March 24, 2004, following the filing of the claim for compensation, Joe was examined by Michael S. Duchowny, M.D., a physician board-certified in pediatrics, neurology with special competence in child neurology, electroencephalography, and child neurophysiology. The results of that evaluation were reported, as follows: PHYSICAL EXAMINATION reveals an alert, reasonably cooperative, well developed and well nourished 5-year-old boy. Joe weighs 73 pounds and is 47 inches tall. The skin is warm and moist. There are no cutaneous stigmata. The neck is supple without masses, thyromegaly or adenopathy. There are no cranial or facial anomalies or asymmetries. The head circumference measures 53.1 cm, which is within standard percentiles. The cardiovascular, respiratory and abdominal examinations are unremarkable. There is bilateral pes planus. Peripheral pulses are 2+ and symmetric. NEUROLOGICAL EXAMINATION reveals a boy with a pleasant disposition, but poor eye contact and diminished social skills. Joe rarely speaks spontaneously. He is dysarthric for lingual and labial sounds. He does know his colors, body parts and pictures of animals. He does not drool. He understands simple commands, but his cooperation is limited. He is able to build a tower of tubes. MOTOR EXAMINATION reveals mild generalized hypotonia. Joe is able to use both hands, but prefers the right. He has well- developed pincer grasp and uses his hands bimanually. He exhibits intermittent hand waiving sterotype movements. There are no other adventitious movements and no focal weakness or atrophy. The deep tendon reflexes are 1+ and symmetric. Plantar responses are downgoing. The stance is reasonably based and he walks with symmetric arm swing. He has trouble doing tandem walk and tends to posture his upper extremities. 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. Joe can perform finger-to-nose and heel-to-shin movements at an age appropriate level. In SUMMARY, Joe's neurological examination, in detail, reveals evidence of immature social skills, poor eye contact, short attention span, mild generalized hypotonia and delayed speech and language development. He demonstrates no focal or lateralizing findings. Joe's neurologic findings fit best within the autistic spectrum. Findings from my evaluation together with a review of medical records . . . indicate that Joe does not suffer from a permanent or substantial mental or physical impairment and that his neurologic findings did not result from oxygen deprivation or mechanical injury at birth . . . . The etiology and significance of Joe's impairments To address the cause and timing of Joe's impairments, the parties offered, inter alia, medical records related to Mrs. Arellano's antepartum course; those associated with Joe's birth and subsequent development; and the opinions of Dr. Duchowny and Dr. Donald Willis, a physician board-certified in obstetrics and gynecology, as well as maternal-fetal medicine, regarding the likely etiology and significance of Joe's impairments. As for the etiology of Joe's impairments, it was Dr. Duchowny's opinion, based on the results of his neurologic evaluation of Joe on March 24, 2004, and review of the medical records, that, while of unknown etiology, Joe's impairments were most likely developmentally based, and not associated with oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation. In so concluding, Dr. Duchowny observed that contrary to the clinical evidence one would expect if Joe had suffered a severe hypoxic event or mechanical injury during labor or delivery, Joe's Apgar scores were normal, his cord blood gases were normal, his neonatal course was normal, his neuro-imaging studies were within normal limits, and his EEGs were normal. As for Dr. Willis, he, like Dr. Duchowny, was of the opinion that the medical records failed to reveal any evidence of neurologic injury having occurred during the course of labor, delivery, or the immediate postdelivery period. In so concluding, Dr. Willis observed that the fetal heart rate was reassuring throughout the course of labor; Joe was reported to be healthy and vigorous at birth, and did not require resuscitation; Joe's Apgar scores were normal, as were his cord blood gases; and Joe's newborn course and subsequent neuro-imaging studies were normal. Finally, the medical records, including the observations of the physicians who have treated Joe, while unrevealing as to etiology, also point to the likelihood of a developmental disorder, as opposed to birth trauma, as the likely cause of Joe's impairments. As for the significance of Joe's impairments, it was Dr. Duchowny's opinion, based on his neurologic evaluation of Joe and review of the medical records, that Joe does not suffer from a substantial mental or physical impairment. Notably, Dr. Duchowny's opinion was uncontroverted, grossly consistent with the record, and credible. Given the record, it must be resolved that Joe's impairments were, more likely than not, occasioned by a developmental abnormality, that preceded the onset of labor, and not by an injury to the brain or a spinal cord occurring in the course of labor, delivery, or resuscitation, and, regardless of the etiology of Joe's impairments, he is not permanently and substantially mentally or physically impaired. See, e.g., 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."); Ackley v. General Parcel Service, 646 So. 2d 242 (Fla. 1st DCA 1995)(determining cause of psychiatric illness is essentially a medical question, requiring expert medical evidence); 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 Daniel S. Merklinger, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary findings Lorna Merklinger and Scott Merklinger are the natural parents and guardians of Daniel S. Merklinger, a minor. Daniel was born a live infant on November 17, 2001, at Florida Hospital Waterman, a hospital located in Eustis, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Daniel's birth was Jose Ramon Gonzalez, 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. Daniel's birth and postnatal course At or about 6:50 a.m., November 16, 2001, Mrs. Merklinger, with an estimated delivery date of November 23, 2001, and the fetus at 39 weeks gestation, presented to Florida Hospital Waterman, for induction of labor. At the time, Mrs. Merklinger's membranes were noted as intact, and vaginal examination revealed the cervix at fingertip dilation, effacement at 60 percent, and the fetus at -1 station. Uterine contractions were noted as mild, irregular and with a duration of 60 seconds, and external fetal monitoring revealed a reassuring fetal heart rate, with a baseline at 130 to 140 beats per minute. Pitocin induction was started at or about 7:00 a.m., and continued until 3:51 p.m., when it was discontinued following a vaginal examination that revealed no progress in cervical dilation.3 Given the lack of progress, Cytotec was inserted vaginally at 4:34 p.m., and again at 1:10 a.m., November 17, 2001. From 8:18 a.m., when Pitocin induction was restarted, until 7:00 p.m., when Dr. Gonzalez ordered Mrs. Merklinger prepared for delivery, Mrs. Merklinger's labor progress was slow, but, until 6:20 p.m., when prolonged decelerations in the 90 to 102 beat per minute range were noted, fetal monitoring continued to reveal a reassuring fetal heart rate. Starting at 7:25 p.m., vacuum delivery was attempted on three occasions, unsuccessfully, and between 7:30 p.m., and 7:32 p.m., forceps were applied three times. Then, after delivery of Daniel's head, a right shoulder dystocia was noted, and relieved with suprapubic pressure and McRoberts maneuver, and Daniel was delivered at 7:42 p.m. At delivery, Daniel was depressed (limp, with poor respiratory effort), and required resuscitation measures, including oxygen and bag/mask for four to five minutes. Apgar scores were recorded as 3, 6, and 8, at one, five, and ten minutes, respectively.4 Following delivery, Daniel was transported to the nursery, where he remained until approximately 6:10 p.m., November 18, 2001, when he was transferred via ambulance to the neonatal intensive care unit at Arnold Palmer Hospital for Children & Women. Reason for transfer was noted as fractured skull and subdural hematoma. Daniel's history and diagnoses at Florida Hospital Waterman were summarized by his attending physician (Dr. Thomas Carlson) in Daniel's discharge summary, as follows: HISTORY OF PRESENT ILLNESS: Baby boy Merklinger is a product of a pregnancy complicated by a maternal age of 41, maternal chronic hypertension and asthma. Labor was induced with Pitocin. Toward the termination of delivery, the child became distressed and delivery was urgent . . . . Mother suffered a third degree laceration in the rapid delivery, and the child's head was quite bruised . . . . I was called at the time of delivery and was in Orlando. I transferred the call to the doctor on call, Dr. Burgos. When she was reached, the baby had already been born and was breathing, so she elected not to go in at that time. The baby was born at 1958 [sic] hours. My examination was complete and note written at 2130 hours. The child was, according to the nurse, bagged for approximately 5 minutes postpartum, but then did well. When I saw the baby under the warmer, I immediately noticed severe bruising and abrasions of the forehead, on through the occiput with large quantity of subcutaneous blood under the scalp. The right cornea was noted to be cloudy. The chest was clear. Heart regular without murmur. The child was breathing well with good oxygen saturation, good capillary refill on room air. There was also noted an apparent fracture of the right clavicle, and the left arm had some decreased movement probably from pulling of the nerve plexus at birth. Impression at that time was traumatic birth doing well . . . . The following morning, it was noted that the hemoglobin and hematocrit were dropping . . . . It was noted that the head circumference was growing . . . . Intravenous antibiotics and fluids were begun. I ordered a CT of the head, chest x-ray and came in to see the child. IV antibiotics were begun. The chest x-ray showed mildly displaced right clavicular fracture. The heart and lungs appeared normal. No pneumothorax identified. CT of the brain without contrast revealed a frontal subdural hematoma, 11 mm in thickness with mild mass effect and midline shift. Scalp hematoma noted on physical exam was also present. [Mildly] depressed left frontal skull fracture, minimally displaced left posterior fossa fracture at the lambdoid suture inferiorly. A right anterolateral scalp hematoma with slight suture separation at coronal suture, and a minimally depressed fracture extending back towards the right lambdoid. No intraventricular hemorrhage. With this finding, it was elected to immediately transfer the child to Arnold Palmer Hospital because a neuro surgeon was needed. The child was then transferred out. DIAGNOSES Traumatic birth. Multiple skull injuries with depressed fractures and subdural hematomas. Traumatized right cornea. Mild Erb's palsy on the left. Fractured right clavicle. At approximately 7:11 p.m., November 18, 2001, Daniel was admitted to Arnold Palmer Hospital. Upon admission, Daniel was examined by Dr. Michael McMahan, who noted that: . . . On arrival of the team, tonic colonic motions of the lower extremity noted, could not be suppressed. Phenobarbital . . . given . . . . Ampicillin and Claforan begun after blood culture obtained The infant has been feeding well, but with question of seizures infant was made n.p.o. and placed on IV fluids PHYSICAL EXAM: . . . Irritable. Molding. Severe bruising of the scalp. Very large caput as well as cephalohematomas. Question of subgaleal bleed. Fontanelle is full. Eyes are open. Cloudy right cornea . . . . Chest: Right clavicle with palpable fracture/crepitus . . . . Neuro: Normal tone and motor strength, moves all extremities . . . . Bruises on chest. IMPRESSION: Term AGA male Intracranial bleed. Possible seizures. Rule out sepsis On November 18 and 19, 2001,5 with a diagnosis of "depressed left temporal skull fracture with underlying epidural hematoma," Daniel underwent a "[l]eft temporal craniotomy for elevation of skull fracture and evacuation of epidural hematoma," and "[p]lacement of left frontal external ventricular drain with Codman monitor." The surgeon was Eric Trumble, M.D., a pediatric neurosurgeon, who noted that Daniel "tolerated the procedure well, was sent to NICU postoperatively." On November 27, 2001, at 10 days of age, Daniel was discharged home on Phenobarbital, with instructions to follow up with his pediatrician within one week, Dr. Trumble in 2-3 weeks, and the development center. Discharge examination noted: . . . active, alert, no distress. Head and neck: Large cephalohematoma. Incision healing. Chest clear. No murmur. Abdomen soft. Normal motor strength. Slightly decreased tone left arm. Discharge summary noted the following problems addressed during Daniel's hospitalization: Depressed skull fracture: Neurosurgery consult obtained. Infant was taken to OR on November 18 for left temporal craniotomy and evacuation of EDH. CT scan of the head on November 19 showed extensive scalp swelling, multiple nondepressed skull fractures, small amount of intracranial hemorrhage, question status of intracranial pressure with low density changes inferiorly raising possibility of increased intracranial pressure. Infant continued on phenobarbital. Skull incision clean and healing. Large cephalohematomas remain present. MRI was done on November 27. This showed scalp hematoma which crosses the midline over the vertex, evidence for parenchymal hemorrhage adjacent to the atria/occipital horn, right lateral ventricle mixed signal intensity consistent with evolving hemorrhage. Additionally, posterior extra-axial hemorrhage is appreciated, likely subdural hemorrhage. Small amount of hemorrhage also seen along the interhemispheric fissure towards the vertex. Small areas of parenchymal signal abnormality seen in the left periventricular parenchyma likely related to ventricular shunt placement. An increased signal intensity is seen on both ADC and T2 weighted sequences within the white matter of the right parieto-occipital region likely reflecting edema. No midline shift. Midline structures intact. No ventriculomegaly. Infant has slightly decreased tone in the left arm compared to the right. No seizure activity noted. He is discharged home on phenobarbital 6 mg p.o.q. 12 hours for follow up with Dr. Trumble in 2-3 weeks . . . . Possible sepsis: Treated with ampicillin and Claforan times seven days. Blood culture negative. * * * 5. Ophthalmology: Eye exam on November 20 with diffuse hemorrhage OU. Follow up on November 27 improved, but still significant hemorrhage present. Guarded visual prognosis OD. For recheck in three weeks with Dr. Gold. Final diagnoses were: Term AGA (appropriate for gestational age) male. Depressed skull fracture, status post evacuation of hematoma. Possible seizures. Possible sepsis. Left corneal opacification. Anemia. Daniel's subsequent development Following discharge from Arnold Palmer Hospital, Daniel was referred to Pediatric Neuroscience, P.A., where he was initially followed by Dr. Trumble, who had performed his surgery. Dr. Trumble first examined Daniel on December 20, 2001, and in a letter to Daniel's pediatrician (Thomas Carlson, M.D.) reported his impressions, as follows: I have just had the opportunity to see Daniel with his mother in the neurosurgery clinic today. As you know, he is a 1-month- old child whose last neurosurgery intervention was a craniotomy for evacuation of epidural hematoma on 11/19/01. He has been doing very well since that time without headaches, nausea or vomiting and meeting developmental milestones. On examination, Daniel is bright, alert, and interactive. He weighs 9 pounds 8 ounces and has a head circumference of 37.25 cm. His incision is well healed. He remains neurologically intact. Eom's are intact. Disc margins are sharp bilaterally. His anterior fontanelle is soft and flat. He does have a bony ridge palpable about the posterior aspect of the left craniotomy and a scalp ridge in the right occipital region. I am pleased with the improvement Daniel has had thus far. I would like to see him back in the neurosurgery clinic in 3/02 with a repeat head CT for routine follow-up. He may discontinue all neuro-active medications from my stand-point, including anti- convulsants. Dr. Trumble next examined Daniel on March 14, 2002, at which time he noted that Daniel had a "progressive right occipital flatness with the right ear anterior to the left and subtle right frontal bossing," and prescribed an occipital molding band. Otherwise, there was no change in Dr. Trumble's impression of Daniel's progress, and he noted the "repeat head CT done at Arnold Palmer Hospital on 3/5/02 . . . was intracranially normal. The fractures healing well." Following March 14, 2002, Daniel was seen by Dr. Trumble on June 10, 2002; July 22, 2002; and September 26, 2002, during which time Daniel's occipital flatness improved and Dr. Trumble remained pleased with Daniel's progress. Dr. Trumble's impressions for this time period may be gleaned from the text of his letter to Daniel's pediatrician of September 26, 2002, as follows: I have just had the opportunity to see Daniel with his mother in the neurosurgery clinic today. As you know, he is a 10- month-old child whose last neurosurgical intervention was a craniotomy for evacuation of epidural hematoma on 11/19/01. He has been doing very well since that time without headaches, nausea or vomiting and meeting developmental milestones. His right occipital flatness has improved since he obtained his occipital molding band, initially in 3/02 with a replacement in late 5/02. He comes in for routine follow-up today. Mother notes that he was recently developmentally graded advanced.[6] On examination, Daniel is bright, alert, and interactive. He weighs 16 pounds, 12 ounces and has a head circumference of 44.3 cm. His left temporal incision is well healed. He remains neurologically intact. Eom's are intact. Disc margins are sharp bilaterally. His anterior fontanelle is soft and flat. He has mild right occipital flatness, with his right ear anterior to his left and mild, compensatory right frontal bossing. These findings are very subtle and much improved since he was placed in the occipital molding band. As part of his ongoing work-up, Daniel had a repeat head CT that was intracranially normal. His bone flap is integrating well. I am pleased with the improvement Daniel has had thus far. I do not feel that neurosurgical intervention is warranted at this time. We will be happy to see them back at any time but don't feel that they need[] routine neurosurgical follow-up. Following Dr. Trumble's September 26, 2002, evaluation, Daniel has been followed by Ronald Davis, M.D., a pediatric neurologist. Dr. Davis first evaluated Daniel on June 27, 2003, and reported the results of his evaluation to Daniel's pediatrician, as follows: I had the opportunity to evaluate Daniel. As you well know, he is a 19-month-old who was born with a delivery complicated by multiple skull fractures and subdurals as a result of forceps delivery. He subsequently had some transient seizure activity and was on Phenobarb, but was able to wean off. He underwent a number of surgical repairs, but developmentally has done well. Over the course of the last number of weeks he had events where he vomits out of the blue, turns pale, cold and clammy. He has some eye deviation and becomes unresponsive and still. It lasts for a number of minutes and he can be sleepy afterwards. He has had somewhere between 7-8 of these events. They are very discrete events without any clear tonic or clonic activity. They have been occurring on a cycle range about every 4-8 days. As a result of this he has had an EEG. It actually demonstrated the presence of right frontotemporal sharp wave discharges. Interestingly, in the past mother had wondered whether or not he had also had some headache like activities where he would seem to grab his head and wince in pain. Though he has had a number of CT scans he has not had an MRI. He has not been started on any medications. PAST MEDICAL HISTORY: Otherwise notable for the subdurals and the fractures. He has some right facial injury and a right orbital injury. * * * ON EXAM: General: He is a well-developed, healthy- appearing male with some slight facial asymmetry, right over left HEENT, patient is normocephalic. Pupils are reactive . . . . . NEUROLOGICAL EXAM: Mental Status: He was awake, alert, oriented. He was attentive and interactive. His speech was fluent. He had no anomia. He could follow directions appropriately. He had good right-left orientation. Cranial nerves II-XII: Intact. Full EOM's. Fundi were sharp bilaterally. Tongue was midline. Motor Exam: Normal tone and bulk with 5/5 strength. He did not have a drift. Sensory Exam: Intact to light touch, vibration and cold. Reflexes: 2+. Toes: Down. Coordination and Gait: No primary ataxia, dysmetria or tremor. He had appropriate gait for age. IMPRESSION: Daniel is a 19-month-old with seizure-like episodes, likely partial in nature with an abnormal EEG with trauma as the most likely inciting event. PLAN: At this point I am going to arrange for an MRI to rule out any structural abnormality. I have given them Diastat 5 mg to use for any prolonged events and they are going to think over the use of long-term antiepileptic medication. The side effects and risks of going on medicine as well as not going on antiepileptic medication on a routine basis were reviewed. Following an MRI, Daniel had a follow-up visit with Dr. Davis on August 26, 2003. Dr. Davis reported the results of that evaluation, as follows: I had the opportunity to follow-up with Daniel. As you well know, he is our nearly 2-year-old who suffered traumatic fractures as a result of delivery by forceps, as well as the presence of subdurals. Since his last visit he has had an MRI and EEG. His EEG had, of course, demonstrated the presence of frontotemporal sharp wave discharges on the right. This did correlate with MRI abnormality. The MRI actually demonstrated thickening cortex in that region, as well as focal cystic encephalomalacia there, as well as in the right gyrus rectus and the basal ganglia. Additionally, there was periventricular leukomalacia noted bilaterally. He continues to do well developmentally. There are some mild delays, but he continues to advance without any evidence of regression or plateauing. * * * NEUROLOGICAL EXAM: Mental Status: He was awake, alert, attentive and interactive. His speech is mildly disarticulate, but fluent. He is able to engage appropriately. Cranial nerves II-XII: Intact with some estropia of the right. Motor Exam: Demonstrates symmetric movement. Reflexes: 1+ Coordination and Gait: No primary ataxia. IMPRESSION: Daniel is a nearly 2-year-old with traumatic injury was described with resultant mild developmental delay, periventricular leukomalacia and an abnormal EEG. PLAN: At this point we will just continue to have the Diastat 5 mg to use for any breakthrough seizures. We will continue to hold off on any routine antiepileptic medication as he has not had any breakthrough seizures. Dr. Davis continues to follow Daniel's progress. On his most recent evaluation of July 19, 2004, Dr. Davis noted: I had the opportunity to follow-up with Daniel. As you well know, he is our young man with history of traumatic fractures from delivery by forceps and subdural hematoma. He has abnormal EEG and periventricular leukomalacia on MRI. He continues to do relatively well. He has not had any significant seizure activity, though mother does relate a time when he appeared to be having some type of partial spell in the face of being overheated. Interestingly, the grandfather also reports that he sees Daniel put his head down at times as if he has some transient and/or paroxysmal head pain which can last for a number of seconds. However, he did have a repeat EEG back in June which continued to demonstrate the presence of left frontocentral spike and wave discharges, as well as independent right frontocentral spike and wave discharges. Cognitively he continues to advance. There appears to be no regression. ON EXAMINATION: General: He is well developed and healthy appearing. . . . HEENT. patient is normocephalic. Pupils are reactive . . . . NEUROLOGIC EXAM: Mental Status: He was awake, alert, attentive, interactive and engaging. His speech was mildly disarticulate, but fluent. Cranial nerves II-XII: Intact. Full EOM's, though mild esotropia is noted of the right. He has some mild asymmetry of his facies. Motor Exam: Normal tone and symmetric movement. Reflexes: 1+. Coordination and Gait: No primary movement disorder. IMPRESSION: Daniel is a young man with traumatic brain injury in the face of periventricular leukomalacia with mild developmental issues and abnormal EEG. PLAN: At this point I am concerned a little bit about these events that are both described by the grandfather, as well as the single event noted by the mother. Should these recur and/or persist I am going to arrange for a more prolonged ambulatory study. In the meantime we will continue to have the Diastat available and monitor him closely. On February 9, 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 neurology examination, as follows: PHYSICAL EXAMINATION reveals an alert, cooperative, well-developed and well- nourished 2-year-old boy. Daniel weighs 24 pounds and is 34 inches tall. The skin is warm and moist. There is one café-au-lait spot on the right thigh. There are no other neurocutaneous stigmata and no somatic dysmorphic features. The head circumference measures 48.5 cm, which is at the 50th percentile for age match controls. A bony ridge is palpated over the right skull vault and there is also a small area of depression. There are no facial asymmetries. There is some reddening beneath the eyes compatible with an allergic diathesis. The neck is supple without masses or thyromegaly. Bilateral anterior and posterior cervical adenopathy is palpated as well as small post auricular lymph nodes. The lungs' fields are clear and the heart sounds reveal a grade 2/6 innocent ejection systolic murmur. There is no palpable abdominal organomegaly. The abdomen is soft and non-tender. Peripheral pulses are 2+ and symmetric. NEUROLOGICAL EXAMINATION reveals an alert, well developed, cooperative and sociable 2- year-old. Daniel interacts very well and shows a very high level of curiosity. He was not overly defensive and cooperated fully for the evaluation. Daniel has an appropriate attentional span for his age and spoke in long phrases. He articulated his needs well. He also anticipated maneuvers and assisted in getting himself dresse[d] and undressed. Cranial nerve examination reveals full visual fields to direct confrontation testing. I can see no evidence of corneal scarring. The pupils are 2 to 3 mm and react briskly to direct and consensually presented light. A brief funduscopic examination was unremarkable. The extraocular movements are full and conjugate. There are no facial asymmetries. The tongue and palate move well. The uvula is midline. Motor examination reveals symmetric strength, bulk and tone. There are no adventitious movements and no focal weakness or atrophy. The deep tendon reflexes are 2+ and symmetric and there are no pathologic reflexes. Both plantar responses are downgoing. Daniel's stance is narrowly based and he walks with good stability and symmetric arm swing. He turns crisply. He is able to get up from a sitting position without difficulty. Sensory examination is intact to the withdrawal of all extremities to stimulation. Neurovascular examination reveals no cervical, cranial or ocular bruits. There are no temperature or pulse asymmetries. Daniel is able to grasp with either hand and transfers readily. In SUMMARY, Daniel's neurological examination reveals no significant findings. He does have some cranial dysmorphism secondary to his previous skull fractures and surgery. However, Daniel does not show evidence of a substantial mental or motor impairment . . . . 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 in "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 and NICA are of the view that Daniel suffered an injury to the brain caused by the forceps delivery, but that he was not rendered permanently and substantially mentally and physically impaired. In contrast, Intervenors are of the view that Daniel's brain injury did result in permanent and substantial mental and physical impairment. The significance of Daniel's impairment To address the significance of any impairment Daniel may have suffered, the parties offered the records related to Daniel's birth and subsequent development, pertinent portions of which have been addressed supra (Respondent's Exhibits A-G); a color photograph of Daniel taken within the first 24 hours of birth (Intervenors' Exhibit 1); the deposition of Michael Duchowny, M.D., an expert in pediatric neurology (Respondent's Exhibit H); the deposition of Ronald Davis, M.D., an expert in pediatric neurology (Respondent's Exhibit K); the deposition of Petitioner Lorna Merklinger (Respondent's Exhibit I); the deposition of Petitioner Scott Merklinger (Respondent's Exhibit J); the deposition of Loren Mann, Daniel's maternal grandmother (Intervenors' Exhibit 3); the deposition of Ruth Merklinger, Daniel's paternal grandmother (Intervenors' Exhibit 4); and the deposition of George Merklinger, Daniel's paternal grandfather (Intervenors' Exhibit 2). Dr. Duchowny, as revealed in his deposition, was of the opinion, based on his review of the medical records and his neurologic evaluation of Daniel on February 9, 2004, that Daniel was neither mentally nor physically impaired, much less substantially mentally and physically impaired, as required for coverage under the Plan. Dr Duchowny described his evaluation and conclusions, as follows: Q. Doctor, when you examined Daniel Merklinger, what physical and neurological exams did you conduct on him specifically? What did you have him do or what did you observe? A. Well, his weight and height were recorded. I looked at his skin. I looked at his head. I felt his head, measured his head circumference. Observed his face, his mouth, his throat. I looked at and palpated his neck. I listened to his chest. I listened and felt his abdomen, looking for his internal organs, and palpated his extremities and his peripheral pulses. On the neurological examination, I observed his behavior and his communication patterns, both expressive and receptive. I looked at his attention span, his social abilities, his ability to engage me in both the examination and in conversation. I looked at his ability to participate in the expected activities of daily living within a limited sense; for example, how he dressed or undressed himself. I certainly observed his behavior, both with respect to me and with respect to his family. I performed a cranial nerve examination, which included an examination of the eyes, of the facial movements, and an observation of his hearing abilities. I also looked at the way his mouth moved, how he swallowed, how his tongue moved, whether or not there was any drooling. I further looked at his motor abilities, including the movements of his extremities, his arm and legs. I evaluated his muscle tone. I looked to see if there was any atrophy, any abnormal movement, any lack of movement, any stiffness in any of his limbs. I made sure that his gait was stable, that it was symmetric, that his coordination was appropriate for his age, that his hand use was appropriate, and that he had bimanual dexterity, that he transferred between hands, that he had good, fine motor coordination and pincer grasp. I looked at his ability to show evidence of good muscle strength; for example, getting up from a sitting position, his ability to walk and turn and show coordinated movements. I examined him for sensation, just looking at the way he moved his arms and legs in response to my touch and pressure, and also examined the patterns of the blood flow to his head by checking his neck and head for temperature, for the pulses, making sure there were no abnormalities or asymmetries. I also listened to his neck and head to make sure that there were no abnormal sounds emanating from the vessels supplying blood to his head. Q. Was his behavior age appropriate? A. I thought so, yes. Q. Was his communication ability age appropriate? A. Yes. Q. Was his motor ability and coordination age appropriate? A. Yes. Q. Did you see anything during your examination that led you to believe that he was physically impaired? A. No. Q. Did you see anything in your examination that led you to believe he was mentally impaired? A. No. Q. Do you have an opinion regarding whether or not he is substantially and permanently physically impaired? A. Yes. I do not belie[ve] he is substantially impaired, mentally or physically. (Respondent's Exhibit H, pages 34-37). Dr. Davis, as revealed in his deposition, was of the opinion that Daniel suffered some developmental delays, but articulated no findings from which one could reasonably conclude that Daniel was either substantially mentally or physically impaired. Regarding Daniel's developmental delays, Dr. Davis described them as follows: Q. Okay. And have you noticed . . . [any developmental issues] in your treatment of Daniel? A. He has some disarticulation of his speech. In other words, his speech is difficult to understand. There is some slight inconsistencies in his motor skills, so you would see that. But then, also, when you go through some of the -- just the typical other developmental learning issues, he has some difficulty with that as well. * * * Q. . . . [W]hen I was asking you about developmental delays, could you be more specific about what it is that you base that upon as a clinical symptom? A. In particular for Daniel or -- Q. Yes, yes. Specifically for Daniel. A. He has some difficulty with his speech, which is the motor component of the way he moves his mouth, if you will, that sort of formation of words. There is some movement abnormalities noted in his face, some asymmetry there. And then his gait is a little -- this is more from recollection than from others, because I don't remember documenting it. But his -- he's a little bit wide based in his stance, so there are more subtle degrees there of his motor difficulties. But the more prominent is his disarticulation of speech, that formation, the mechanical formation of words. * * * Q. All right. Earlier, I believe you described his -- the motor dysfunction he's currently displaying as mild; is that correct? A. I think that's in my note, yes. * * * Q. You . . . mentioned that the -- that Daniel has some developmental delays. What were you referring to? Was it just the speech and the -- A. And the motor, yes. Q. Okay. And could you -- I think you've already gone over this a couple times, but for the motor dysfunction, other than the asymmetry in his face and speech disarticulation, was it anything other than the widened gait? A. Not that I have documented here, no. (Respondent's Exhibit K, pages 24, 29, 64, 65, and 69). Notably, Dr. Davis did not opine that, or disclose any findings that would support a conclusion that, more likely than not, Daniel was mentally impaired, that Daniel was substantially physically impaired, or that Daniel's brain injury would, at any time in the future, result in substantial mental or physical impairment. As for the deposition testimony of Daniel's parents and grandparents, with regard to his current mental and physical presentation, they were all of the opinion, to the extent they were called upon to express one, that Daniel's mental and physical development were age appropriate. Their concerns for Daniel, to the extent they expressed them, were speculative in nature, and premised on their uncertainty as to whether Daniel's brain injury would, either through the manifestation of persistent seizure activity or developmental deficiencies, adversely affect him in the future. Such concerns are certainly natural, but insufficient to support a conclusion that, more likely than not, Daniel's brain injury has rendered him, or will render him, permanently and substantially mentally and physically impaired.
Findings Of Fact Melina Antunes was born on August 27, 2015, at Florida Hospital, located in Orlando, Florida. Melina weighed in excess of 2,500 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Melina. In a medical report dated December 12, 2016, Dr. Willis summarized his findings and opined in pertinent part as follows: In summary, induction of labor was complicated by a spontaneous uterine rupture. The baby and placenta were expelled into the maternal abdomen. The baby was depressed at birth with low Apgar scores and a cord blood gas consistent with acidosis (pH 6.65). MRI was consistent with HIE. There was an apparent obstetrical event (uterine rupture) that resulted in loss of oxygen to the baby’s brain during labor, delivery, and continuing into the immediate post delivery period. The oxygen deprivation resulted in brain injury. NICA retained Laufey Y. Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to examine Melina and to review her medical records. Dr. Sigurdardottir examined Melina on February 15, 2017. In a medical report dated February 15, 2017, Dr. Sigurdardottir summarized her examination of Melina and opined in pertinent part as follows: Summary: Here we have a 17-month-old born after a sudden uterine rupture during active labor. The patient had neurologic depression at birth, significant acidosis with a pH of 6.6 and required active cooling as well as supportive medication for seizures in the neonatal period. She did have well documented injury on MRI but has made a remarkable recovery. Neurologic exam today, has mild abnormalities, but no standardized developmental testing is available for our review. Result as to question 1: Melina is not found to have substantial physical or mental impairment at this time. Results as to question 2: In review of available documents, Melina does have the clinical picture of an acute birth related hypoxic injury with both the clinical features of hypoxic encephalopathy and electrographic and MRI evidence to suggest hypoxic injury. Result as to question 3: The prognosis for full motor and mental recovery currently is excellent and her life expectancy is full. In light of her normal cognitive abilities and near normal neurologic exam, I do not feel that Melina should be included in the NICA program. If needed, I will be happy to answer additional questions or review further documentation of her developmental status. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Willis that there was an apparent obstetrical event that resulted in loss of oxygen to the baby's brain during labor, delivery and the post-delivery period which resulted in brain injury. Dr. Willis’ opinion is credited. There are no expert opinions filed that are contrary to Dr. Sigurdardottir’s opinion that Melina does not have a substantial physical or mental impairment. Dr. Sigurdardottir’s opinion is credited.
Other Judicial Opinions A party who is adversely affected by this final order is entitled to judicial review pursuant to Sections 120.68 and 766.311, Florida Statutes. Review proceedings are governed by the Florida Rules of Appellate Procedure. Such proceedings are commenced by filing the original of a notice of appeal with the Agency Clerk of the Division of Administrative Hearings and a copy, accompanied by filing fees prescribed by law, with the appropriate District Court of Appeal. See Section 766.311, Florida Statutes, and Florida Birth-Related Neurological Injury Compensation Association v. Carreras, 598 So. 2d 299 (Fla. 1st DCA 1992). The notice of appeal must be filed within 30 days of rendition of the order to be reviewed.
Findings Of Fact Josue A. Solis was born on December 12, 2013, at Plantation General Hospital in Plantation, Florida. Josue weighed in excess of 2,500 grams at birth. NICA retained Donald C. Willis, M.D. (Dr. Willis), to review Josue’s medical records. In a medical report dated August 17, 2016, Dr. Willis made the following findings and expressed the following opinion: In summary, labor was induced at 39 weeks. There was no fetal distress during labor. The baby was delivered by spontaneous vaginal birth without complications. The baby was not depressed and had normal Apgar scores of 9/9. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post delivery period. Dr. Willis reaffirmed his ultimate opinion in an affidavit dated February 24, 2017. Dr. Willis’ opinion that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical injury to the baby’s brain during labor, delivery or the immediate post-delivery period is credited. Respondent retained Michael Duchowny, M.D. (Dr. Duchowny), a pediatric neurologist, to evaluate Josue. Dr. Duchowny reviewed Josue’s medical records and performed an Independent Medical Evaluation on him on February 1, 2017. In a medical report dated February 7, 2017, Dr. Duchowny made the following findings and summarized his evaluation as follows: IN SUMMARY Josue’s physical examination reveals evidence of hypotonia and ataxia with delayed language development. I believe his presentation is most consistent with ataxic hypotonic cerebral palsy. I believe his motor skills will improve in the future and it is unlikely that he will ultimately have a substantial motor impairment. In all likelihood, Josue will continue to have a delayed language development. Ataxic cerebral palsy is a prenatally acquired syndrome and there is no evidence from the records that Josue’s neurological difficulties were acquired in the course of labor or delivery. Furthermore, there is no support for either mechanical injury or oxygen deprivation as contributing factors. I am therefore not recommending Josue for inclusion in the NICA program. Dr. Duchowny reaffirmed his ultimate opinion in an affidavit dated February 27, 2017, in which he opined, “it is my opinion that IME and record review do not provide a basis to find that Josue’s neurological difficulties were acquired in the course of labor, delivery or resuscitation in the immediate postdelivery period. I therefore do not recommend consideration for inclusion within the NICA program.” Dr. Duchowny’s opinion that ataxic cerebral palsy is a prenatally acquired syndrome and that there was no basis found in the records or in his Independent Medical Evaluation that Josue’s neurological difficulties were acquired in the course of labor, delivery or resuscitation in the immediate post-delivery period is credited. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Willis that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post- delivery period. There are no expert opinions filed that are contrary to Dr. Duchowny’s opinion that ataxic cerebral palsy is a prenatally acquired syndrome and that there is no indication that Josue’s neurological difficulties were acquired in the course of labor, delivery or resuscitation in the immediate post- delivery period.
The Issue At issue in the proceeding is whether Demetrios Robertson, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Petitioner, Carmina Gilliam, is the mother and natural guardian of Demetrios Robertson, a minor. Demetrios was born a live infant on August 4, 1996, at University Medical Center, a hospital located in Jacksonville, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services during the birth of Demetrios was Michael T. Valley, 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 when the claimant demonstrates, more likely than not, that the infant suffered an "injury to the brain . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital which renders the infant permanently and substantially mentally and physically impaired." Section 766.302(2), Florida Statutes. Here, the proof failed to demonstrate that Demetrios suffered a permanent and substantial mental and physical impairment. Consequently, it is unnecessary to address whether he suffered an injury to the brain caused by oxygen deprivation or mechanical injury and, if so, whether such injury occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Demetrios' current mental and physical presentation To address the character of Demetrios' neurologic presentation, Petitioner offered selected medical records relating to Demetrios' birth and subsequent development, as well as the opinions of Demetrios' treating pediatric neurologist, Daniel E. Shanks, M.D. In turn, Respondent offered the opinions of Michael Duchowny, M.D., a pediatric neurologist who examined Demetrios on January 17, 2001. As noted, on January 17, 2001, following the filing of the claim for compensation, Demetrios was examined by Dr. Duchowny. Pertinent to this case, the results of that evaluation were reported as follows: PHYSICAL EXAMINATION reveals Dem[e]trios to be alert, pleasant and cooperative. His weight is 55 pounds and height 32 inches. There is a single cafe-au-lait spot over the left midabdominal region. There are no dysmorphic features and no other cutaneous stigmata. The spine is straight without dysraphism. The head circumference measures 50.4 cm and there are no craniofacial anomalies or asymmetries. The fontanelles are closed. The neck is supple, without masses, thyromegaly or adenopathy and the cardiovascular, respiratory and abdominal examinations are unremarkable. Peripheral pulses are 2+ and symmetric. NEUROLOGICAL EXAMINATION: Dem[e]trios' neurological examination reveals him to be quiet but cooperative. He does have a short attention span but he is easily engaged and tends to complete requests without flinching. His speech output is noticeably diminished and he tends to speak in short phrases with poorly articulated words. He does not know primary or secondary colors and has a limited command of knowing the names of animals. He does identify body parts well. There is no evidence of overactivity. Cranial nerve examination reveals full visual fields to direct confrontation testing and normal ocular fundi. The pupils are 4 mm, react briskly to direct and consensually presented light. The optic disc margins are well- marginated with normal coloring. The tongue and palate move well and there is no drooling. Medical examination reveals mild spasticity of the lower extremities with some tightening of the heel cords. Dem[e]trios barely dorsiflexes the feet past neutrality and he has slight Babinski attitudes of the big toes. In contrast, the tone in the upper extremities is relatively normal. He has trouble with rapid alternating movement sequences and demonstrates mild decomposition. There is no focal weakness or atrophy. Dem[e]trios walks in a single fashion although there is eversion of his feet. The deep tendon reflexes are brisk and 2+ at the knees, brachioradialis and biceps. There are one or two beats or reduplication at the ankles and quite positive Babinski signs. There is no abductor spasticity. His gait is stable but he tends to posture both arms. He has difficulty walking on tip toes or heels. Romberg sign is absent. The neurovascular examination reveals no cervical, cranial, ocular bruits and no temperature or pulse asymmetries. Sensory examination was deferred. IN SUMMARY, Dem[e]trios' neurologic examination reveals evidence of moderate developmental delay, particularly in the area of language functioning. He additionally has evidence of mild lower extremity spasticity indicating a mild spastic diparesis. At a deposition held August 28, 2001, and received in evidence as Respondent's Exhibit 1, Dr. Duchowny expanded on the results of his examination and conclusions regarding the character of Demetrios' presentation, as follows: BY MR. CULPEPPER: * * * Q. . . . What were your conclusions regarding Demetrios' neurological condition? A. Having performed the evaluation and reviewing the medical records, I felt that Demetrios has neither a substantial mental nor motor impairment. Q. . . . Is Demetrios impaired? A. I believe that he does have evidence of impairment, yes. * * * Q. . . . Does Demetrios have a permanent injury? A. Yes, I believe he does. Q. Is he mentally impaired? A. I think he has developmental delay. I am using the term to distinguish it from brain damage. I think his language is behind age level, but will probably progress and continue to improve. Q. I will focus on the context of NICA. How would you quantify the seriousness of Demetrios' mental impairment? A. I would call it mild to moderate. Q. Okay. So you would not consider Demetrios' mental impairment, quote, unquote, "significant" in terms of NICA? A. That's correct. Q. Why not? A. Because he probably functions within a high -- in the high end of kids with disabilities. He basically would be mild to moderately impaired by school standards, and he is not mentally retarded. Q. To follow up, describe what you would consider a, quote, unquote, "significant" mental impairment in terms of the NICA statute? A. Well, he would have to be -- function within the mentally retarded range, and I regard him more as having evidence of language delay. Otherwise, he seems socially intact and he does well. Q. Now I'll turn to Demetrios' physical condition. Is Demetrios suffering from a physical impairment? A. Yes. Q. In the context of NICA, how would you quantify the seriousness of Demetrios' physical impairment? A. I believe he has a mild physical impairment of his legs. Q. Again, in the context of the NICA statute, would you consider Demetrios' physical impairment, quote, unquote, "significant" MR. SCHACK: Let me object to the language and the form of the question. You keep using the word "significant," and I think the language is "substantial." MR. CULPEPPER: I apologize, and thank you for pointing that out. Let me switch the words then. Q. (By Mr. Culpepper) Do you consider his impairment substantial in terms of NICA? A. No. Q. And why not? A. Because in the spectrum of what we see of motor impairment, this is simply not a substantial motor impairment. He would have to be more spastic, more involved with greater compromise of his functionality. Q. And then to clean up my error, going back to mental impairment, would you consider Demetrios' mental impairment "substantial," quote, unquote, in terms of the NICA statute? A. No, I would not. BY MR. SCHACK: * * * * * * Q. . . . When you use the terms mild, moderate, and severe, is that medical terminology? A. Well, it's not a medical dictionary word, but I think it is a modifier that tries to categorize a patient within the scope of disability that we see. Q. Well, Doctor, if this was your patient, would you just describe the neurological findings and the problems the child had rather than trying to modify it by an adjective? A. No. We always modify with an adjective. Q. Okay. A. Apart from NICA, we do that. * * * Q. It appears in this case to me, correct me if I am wrong, that regardless of whether you describe it as mild, moderate, or severe, that Demetrios has some motor difficulties that might impact on his ability to live a normal life. A. You mean lifespan or just life functions? Q. That was a -- life function. A. They might, yes. Q. Okay. He at the present time has lower motor problems, lower extremity motor problems; is that correct? A. Yes. Q. And exactly what is his problem? A. He has spasticity, mild, of his legs. Q. What does that prevent him from doing? A. Being agile, running fast, being a competitive athlete. Q. Okay. Does it give him difficulty walking? A. Yes. Q. Okay. And he can't stand straight? A. Right. Q. All right. Would you say that is a substantial problem for a child such as Demetrios? A. I think he's going to get better with time. I think he's going to be able to do most of the things he wants to do. Q. But at the present time he's unable to do things he wants to do; is that correct? A. I'm sure that's true . . . . Demetrios was last examined by his pediatric neurologist, Dr. Shanks, on October 18, 2001. Dr. Shanks reported the results of that evaluation, as follows: . . . [Demetrios] has always had a tendency to walk up on his toes since he began walking at approximately 14 months of age. It has not progressed over time. He may be a little tighter in the right than the left and he did go through physical therapy during earlier years. * * * On physical examination, height 105 cm (10th to 25th %); weight 22 kg (75th to 90th %); head circumference 51 cm (50th %). Generally, he is a well-appearing, alert youngster who is generally cooperative. There are no cranial or carotid bruits noted. Neck is supple with full range of motion. He has full primary dentition. There are no chest deformities other than a well-healed scar on his left infrascapular region inside. Abdomen is mildly obese. Extremities have full range of motion with the exception of ankles that have slight restriction in dorsiflexion, right slightly more so than the left, and there is a little bit of tightness in hip adductors. There are no asymmetries of his extremities. Back is without midline lesions. He has two hyperpigmented macular lesions, one of his abdomen and one on his back. NEUROLOGIC EXAM: Speech is fluent but mostly just one to two-word utterances. He does follow simple commands readily. Cranial nerves pupils equal, round and reactive to light; discs are sharp with normal appearing vessels. Extraocular movements are full and conjugate. Facial muscle movements full and asymmetric. Hearing is normal to low-level stimulation bilaterally. Palate elevates symmetrically; sternomastoids are strong and tongue is midline. Motor exam shows normal tone with the exception of his distal lower extremities and a possible slight spastic catch in his hip adductors. Upper extremity tone feels relatively normal. Deep tendon reflexes are 2+ in the upper extremities, 3- 4+ lower extremities with crossed adductors. Ankle jerks are 1+ and toes are upgoing bilaterally, more strongly on the right than the left. With gait, he does have a tendency to get up on his toes slightly but is very functionally mobile. Sensory exam is intact to touch, cold and vibration. He has no cerebellar signs or adventitial movements. IMPRESSION: Likely mild spastic diplegia with overall relatively good prognosis for functional capabilities. He also seems to have significant cognitive delays . . . . Considering the proof, it must be resolved that Petitioner has failed to demonstrate, more likely than not, that Demetrios is permanently and substantially mentally and physically impaired.1 Notably, Doctors Duchowny and Shanks share strikingly similar views regarding the characterization of Demetrios' physical presentation, and concur that his physical impairment can best be described as mild. With regard to Demetrios' mental impairment, Dr. Duchowny was of the view that Demetrios was developmentally delayed, but would likely improve, and that his impairment could best be described as mild to moderate. In contrast, Dr. Shank's was of the view that Demetrios "seems to have significant cognative delays"; but did not otherwise characterize Demetrios' impairment. Stated otherwise, Dr. Shank's did not express an opinion as to whether Demetrios' mental impairment could best be described as mild, moderate, or severe, and expressed no opinion as to whether Demetrios' impairment was or was not likely to improve.
