Elawyers Elawyers
Ohio| Change
Find Similar Cases by Filters
You can browse Case Laws by Courts, or by your need.
Find 49 similar cases
SHEILA ADAME ON BEHALF OF AND AS MOTHER AND NATURAL GUARDIAN OF SHAYLA ADAME, A MINOR vs FLORIDA BIRTH-RELATED NEUROLOGICAL INJURY COMPENSATION ASSOCIATION, 00-001437N (2000)
Division of Administrative Hearings, Florida Filed:Miami, Florida Apr. 05, 2000 Number: 00-001437N Latest Update: Aug. 13, 2002

The Issue At issue in the proceeding is whether Shayla Adame, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.

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

Florida Laws (11) 120.68766.301766.302766.303766.304766.305766.309766.31766.311766.313766.314
# 3
ANGELINA JOHNSON AND JOHN T. JOHNSON, JR., INDIVIDUALLY AND AS THE PARENTS AND NATURAL GUARDIANS OF ADAM JOHNSON, A MINOR vs FLORIDA BIRTH-RELATED NEUROLOGICAL INJURY COMPENSATION ASSOCIATION, 20-002377N (2020)
Division of Administrative Hearings, Florida Filed:Cape Coral, Florida May 18, 2020 Number: 20-002377N Latest Update: Oct. 05, 2024

Findings Of Fact Adam was born on June 11, 2018, at HealthPark Medical Center, in Fort Myers, Florida. Adam was a single gestation and his weight at birth exceeded 2500 grams. Obstetrical services were delivered by a participating physician, Jane A. Daniel, M.D., in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital, HealthPark Medical Center. As set forth in greater detail below, the unrefuted evidence establishes that Adam did not sustain a “birth-related neurological injury,” as defined by section 766.302(2). Donald Willis, M.D., a board-certified obstetrician specializing in maternal-fetal medicine, was retained by Respondent to review the pertinent medical records of Ms. Johnson and Adam and opine as to whether Adam sustained an injury to his brain or spinal cord caused by oxygen deprivation or mechanical injury that occurred during the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital. In his affidavit, dated December 11, 2020, Dr. Willis summarized his opinions as follows: In summary, an abnormal FHR pattern developed during labor and resulted in a depressed newborn. Cord blood pH was 6.9 with a base excess of -18.6. Seizures began shortly after birth. The newborn hospital course was complicated by multi-system organ failures, consistent with birth-related oxygen deprivation. MRI on DOL 4 was suggestive of HIE, but findings improved with follow-up MRI. There was an apparent obstetrical event that resulted in oxygen deprivation to the brain during labor, delivery and continuing into the immediate post-delivery period. The oxygen deprivation resulted [in] a potential for brain injury, but the follow-up normal MRI suggests that no actual brain injury occurred. Respondent also retained Michael S. Duchowny, M.D., a pediatric neurologist, to review the medical records of Ms. Johnson and Adam, and to conduct an Independent Medical Examination (IME) of Adam. The purpose of his review and IME was to determine whether Adam suffered from a permanent and substantial mental and physical impairment as a result of an injury to the brain or spinal cord caused by oxygen deprivation or mechanical injury in the course of labor, delivery, or resuscitation in the immediate post- delivery period. Dr. Duchowny reviewed the pertinent medical records and, on October 20, 2020, conducted the IME. In his affidavit, dated December 16, 2020, Dr. Duchowny summarized his opinions as follows: In summary, Adam’s evaluation reveals findings consistent with a substantial motor but not mental impairment. He evidences a spastic diplegia, but with relative preservation of motor milestones, and age-appropriate receptive and expressive communication. Adam additionally has a severe behavior disorder, and has a sleep disorder and attentional impairment. His seizures are in remission. Review of the medical records reveals that Adam was the product of a 40 week gestation and was delivered vaginally with Apgar scores of 3, 6, 7 and 6 at one, five and 10 minutes. Terminal meconium was noted at delivery. Adam initially required positive pressure ventilation until his respirations were subsequently managed with nasal CPAP. His cord gas pH was 6.917 with a base excess of – 18.6. Adam developed seizures in the NICU and was intubated on the first day of life for apnea. Multiple seizures were documented on video/EEG monitoring. He was oliguric on the first day of life and had elevated liver function studies. An elevated lactic acid level was noted and there was a borderline elevation of DIC parameters. Adam was enrolled in a body hypothermia protocol on the first day of life. His blood pressure was maintained with dopamine. A head ultrasound on June 11 at 22:23 (DOL#2) was unremarkable. A brain MR imaging study performed on June 15, (DOL#5) revealed multifocal areas of restricted diffusion. Follow-up brain MR imaging study on July 5th revealed near-complete resolution of the previously observed diffusion abnormalities. A third MR imaging study obtained one month ago confirms the resolution of the DWI findings noted on the first brain MR imaging study. In conclusion, Dr. Duchowny opined that Adam does not have a substantial mental impairment, and, therefore, did not recommend that Adam be considered for inclusion in the Plan. The undisputed findings and opinions of Drs. Willis and Duchowny are credited. The undersigned finds that Adam did not sustain an injury to the brain or spinal cord caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital, which rendered him permanently and substantially mentally and physical impaired.

Florida Laws (8) 766.302766.303766.304766.305766.309766.31766.311766.316 DOAH Case (1) 20-2377N
# 5
TRISTEN ONOFRY, A MINOR BY AND THROUGH HIS PARENTS AND NEXT BEST FRIENDS, VICTORIA HILL AND KEITH ONOFRY, AND VICTORIA HILL AND KEITH ONOFRY, INDIVIDUALLY vs FLORIDA BIRTH-RELATED NEUROLOGICAL INJURY COMPENSATION ASSOCIATION, 04-002538N (2004)
Division of Administrative Hearings, Florida Filed:Tallahassee, Florida Jul. 20, 2004 Number: 04-002538N Latest Update: May 01, 2006

The Issue At issue is whether Tristen Onofry, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).

Findings Of Fact Stipulated facts Victoria Hill and Keith Onofry are the parents of Tristen Onofry, a minor. Tristen was born a live infant on July 29, 2002, at Tallahassee Memorial Regional Medical Center, Tallahassee, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Tristen's birth was Minal K. Krishnamurphy, 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 and 766.31, Fla. Stat. To resolve whether Tristen suffered a "birth-related neurological injury," the parties offered the medical records related to Tristen's birth and subsequent development (Joint Exhibit 1), and the opinions of Michael Duchowny, M.D., a physician board-certified in pediatrics; neurology, with special competence in child neurology; and clinical neurophysiology (Joint Exhibit 2). Notably, Dr. Duchowny evaluated Tristen on October 6, 2004, and reported the results of his evaluation, as follows: PHYSICAL EXAMINATION reveals an[] alert and cooperative, well developed, well-nourished, 2-year-old, left-handed boy. Tristen weighs 23 pounds and is 32 inches tall. His head circumference measures 46.4 centimeters, placing him at the 10th percentile for age match controls. There are no dysmorphic features and no cranial or facial anomalies . . . [or] asymmetries. There are no neurocutaneous stigmata. The neck is supple without masses, thyromegaly, or adenopathy. The cardiovascular, respiratory and abdominal examinations are normal. Tristen's NEUROLOGIC EXAMINATION reveals him to be cooperative but with no speech output. He does know colors by pointing. He does not interact with meaningful speech sounds. He seems to enjoy the examination and actively participated. There are prominent tongue thrusting movements and intermittent drooling. The cranial nerve examination reveals full visual fields to direct confrontation testing. Funduscopic examination reveals sharply demarcated disc margins without optic pallor. There is no retinopathy. Pupils are 3 mm and react briskly to direct and consensually presented light. The extraocular movements are conjugate and full in all planes of gaze. The motor examination reveals a static hypotonia with dynamic hypertonicity most prominent in the lower extremities. At rest, Tristen demonstrates an overly full range of motion at all joints. He will then stiffen with activated movement. There are bilateral AFO's in place. Tristen shows no evidence of stable weightbearing and has poor head control with the head flopping forward. He has a wide based stance and demonstrates truncal ataxia. He is able to grasp objects only with a palmar grasp and has no evidence of developed pincher grasp in either hand. He tends to grasp cubes but cannot transfer and drops them readily. He cannot build a tower of cubes. There are no pathological reflexes. The deep tendon reflexes are 2+ in the upper extremities but 3+ at both knees and 3+ at the ankles. There are bilateral Babinski responses. The spine is straight without dysraphic features. Tristen maintains a plantar grade attitude when held in the vertical position. His shoulder girdle seems to slip through the examiner's hands. Sensory examination is intact to withdrawal of all extremities to stimulation. The neurovascular examination reveals no cervical, cranial, or ocular bruits and no temperature or pulse asymmetries. As for the etiology of Tristen's impairments, it was Dr. Duchowny's opinion, based on the results of his neurologic evaluation of Tristen and review of the medical records, that, while of unknown etiology, Tristen's impairments were most likely developmentally based, and not associated with oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or the immediate postpartum period. In so concluding, Dr. Duchowny observed that the impairments demonstrated by Tristen are consistent with the syndrome of ataxic cerebral palsy, a developmentally-based brain disorder acquired before the onset of labor. Dr. Duchowny was also of the opinion that the medical records did not reveal evidence of a substantial mechanical or hypoxic event having occurred during labor and delivery. As for the significance of Tristen's impairments, it was Dr. Duchowny's opinion that Tristen is permanently and substantially physically impaired. However, mentally, Tristen is not similarly affected or, stated otherwise, he is not permanently and substantially mentally impaired. Notably, Dr. Duchowny's opinions were uncontroverted, grossly consistent with the record, and credible.

Florida Laws (9) 120.68766.301766.302766.303766.304766.305766.309766.31766.311
# 7
DENISE DAVIDSON, ON BEHALF OF AND AS PARENT AND NATURAL GUARDIAN OF EMMANUEL HOOKS, A MINOR vs FLORIDA BIRTH-RELATED NEUROLOGICAL INJURY COMPENSATION ASSOCIATION, 01-003909N (2001)
Division of Administrative Hearings, Florida Filed:Panama City, Florida Oct. 09, 2001 Number: 01-003909N Latest Update: May 22, 2002

The Issue At issue in this proceeding is whether Emmanuel Hooks, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.

Findings Of Fact Fundamental findings Petitioner, Brianna Denise Davidson, is the mother and natural guardian of Emmanuel Hooks, a minor. Emmanuel was born a live infant on July 26, 1999, at Gulf Coast Medical Center, a hospital located in Panama City, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Emmanuel's birth was Steven G. Smith, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Emmanuel's birth At or about 9:10 p.m., July 25, 1999, Ms. Davidson (with an estimated date of delivery of July 26, 1999, and the fetus at 40 weeks gestation) presented to Gulf Coast Medical Center in labor. Initial vaginal examination revealed the cervix at 2-3 centimeters dilation, effacement as "thin," and the fetus at station -3. External fetal monitoring revealed a reassuring fetal heart rate (of 140-150 beats per minute), with accelerations. Ms. Davidson was continually monitored, and at 11:00 p.m., she was admitted to labor and delivery. At the time, uterine contractions were noted at 3-5 minute intervals, and vaginal examination revealed the cervix at 3 centimeters, effacement at 90 percent, and the fetus at station -3. Ms. Davidson's labor apparently did not progress, and at 2:49 a.m., July 26, 1999, she was started on Pitocin. Thereafter, Ms. Davidson's labor progressed slowly, and at 6:45 a.m., vaginal examination revealed the cervix at 5 centimeters, effacement at 90 percent, and the fetus at station -1. In the interim, external fetal monitoring continued to reveal a reassuring fetal heart rate. Ms. Davidson's labor continued to slowly progress, and by 9:00 a.m., vaginal examination revealed the cervix at 8 centimeters, effacement at 100 percent, and the fetus at station -1. In the interim, at 8:48 a.m., Ms. Davidson's membranes spontaneously ruptured, with clear fluid noted. Thereafter, variable decelerations were noted with each contraction, consistent with umbilical cord compression, and fetal heart base line remained reassuring (in the 140-beat minute range). From 9:00 a.m. to 11:45 a.m., Ms. Davidson's labor failed to progress (with the cervix at 8 centimeters, effacement at 100 percent, and the fetus at station -1), and at 11:45 a.m., Ms. Davidson was transported to the operating room for delivery by caesarean section. Notably, between 9:00 a.m., and 11:45 a.m., while variable decelerations continued, the fetal heart rate base line remained in the 140-beat per minute range, and fetal electrode revealed the presence of short term variability. According to the records, Ms. Davidson was in the operating room at 11:45 a.m., anesthesia started at 11:45 a.m., surgery started at 12:32 p.m., and Emmanuel was delivered at 12:35 p.m. Of note, the "nucal cord x 1" observed during delivery was described as "loose," and fetal heart monitoring in the operating room and immediately prior to the caesarean section revealed a reassuring fetal heart rate. On delivery, Emmanuel was bulb-suctioned, but did not require resuscitation. Initial newborn assessment noted no apparent abnormalities, and Apgar scores were recorded as 8 at one minute and 9 at 5 minutes. The Apgar scores assigned to Emmanuel are a numeric expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, muscle tone, reflex response, and color, with each category being assigned a score ranging from the lowest score of 0 through maximum score of 2. As noted, at one minute, Emmanuel's Apgar score totaled 8, with heart rate, respiratory effort, muscle tone, and reflect response being graded at 2 each, and color being graded a 0. At five minutes, Emmanuel's Apgar score totaled 9, with heart rate, respiratory effort, muscle tone, and reflex response again graded at 2 each, and color now graded at 1. Such scores are considered normal, and inconsistent with recent hypoxic insult or trauma. Following the initial newborn assessment, Emmanuel was transported to the regular nursery, where he remained until he was discharged with his mother on July 29, 1999. Notably, the newborn nursery admission assessment was grossly normal, and there is no evidence of any complication during Emmanuel's stay. Emmanuel's subsequent development On December 10, 2001, following the filing of the subject claim, Emmanuel was examined by Dr. Michael Duchowny, a physician board-certified in pediatrics, neurology with special competence in child neurology, electroencephalography, and clinical neurophysiology. Dr. Duchowny reported the results of his neurology evaluation, as well as the history he obtained from the parents, as follows: HISTORY ACCORDING TO MR. AND MRS. HOOKS: Emmanuel is a 2 1/2 year old boy who the parents indicated suffers from cerebral palsy and brain injury. They began by explaining that Emmanuel suffered brain injury at birth due to a cord being wrapped around his neck. He was delivered by emergency caesarean section. They noted that Emmanuel's MRI has shown periventricular leukomalacia and furnished a copy of the MRI report. Emmanuel's growth and developmental milestones have been slow. He did not rollover until 9 months, nor did he sit until a year of age. He stood at 14 months, walked at 18 months and said his first word at age 2. He now has a lexicon of only one word ("ma-ma"). Emmanuel is not toilet trained. He is described as being extremely active. He does not sit still at anytime during the day and it is difficult to examine him or provide therapy. He attends a wellness center where he receives physical, speech and occupational therapy on a twice weekly basis. Communication is a particular problem area for him. Emmanuel's appetite has also been diminished and he is now "only starting to eat". His mother indicated that Emmanuel suffers from "low muscle tone" and that he drools frequently. She also mentioned that he wakes up frequently at night and is just beginning to sleep more consistently. Emmanuel does not play with other children at school. His activity level and intrusiveness have precluded meaningful peer interactions. The parents are aware that his eye contact is poor. The parents stated that Emmanuel "had seizures", but then went on to explain that 2 EEG's were normal and he was never placed on medication. The events were described as "getting into a trance". He has not had motor convulsions. FAMILY HISTORY: Both parents are healthy. A 4 year brother had no medical problems and there are no family members with degenerative illnesses, mental retardation or cerebral palsy. Emmanuel was born at Gulf Coast Medical after a 39 week gestation. He weighed 8-pounds, 9- ounces at birth and breathed well. He was discharged from the nursery at 3 days of age. Emmanuel is fully immunized, has no significant drug allergies and never been hospitalized or undergone surgery. His vision and hearing are said to be excellent. PHYSICAL EXAMINATION reveals an alert, but extremely active and well developed 2 1/2 year old toddler. Emmanuel weighs 39-pounds. His head circumference measures 50.2 cm and there are no cranial or facial anomalies or asymmetries. Emmanuel's neck is supple without masses, thyromegaly or adenopathy. The cardiovascular, respiratory and abdominal examinations are normal. Emmanuel's NEUROLOGIC EXAMINATION is difficult to complete, as he is constantly in motion. The physical examination requires restraint from his father, as he continually tries to touch things and pull items off the desktop and shelves. Emanuel has very poor eye contact and did not communicate in words at anytime during the session. It was difficult for him to follow commands as well, as his attention span constantly shifted. He drooled intermittently. The tongue movements are poorly coordinated. Cranial nerve examination reveals full visual fields to direct confrontation testing. There is blink to threat from either direction. I could not perform a fundoscopic examination. There are no facial asymmetries. Motor examination reveals mild generalized hypotonia with full range of motion. There are no adventitious movements, aside from the high activity level and no evidence of focal weakness or atrophy. Emmanuel's gait is stable, but slightly wide- based and he has generalized hypotonia. The deep tendon reflexes are 2+ bilaterally and plantar responses are in flexion. There is withdrawal of all extremities to touch. Neurovascular examination reveals no cervical, cranial or ocular bruits and no temperature or pulse asymmetries. Cerebellar testing could not be completed due to poor cooperation. In SUMMARY, Emmanuel's neurologic examination is significant for multiple areas of developmental delay. He is extremely overactive and inattentive, and has a significant behavior and communication problem. He additionally demonstrates poor eye contact and has a significant social disability. There are no specific focal or lateralizing findings to suggest a structural brain lesion. The findings on Emmanuel's neurologic examination suggests a diagnosis of a pervasive developmental disorder. Emmanuel fits within the autistic spectrum and this was communicated to the family . . . . The cause and timing of Emmanuel's neurological impairment To address the issue of whether Emmanuel's impairments were associated with an "injury to the brain or spinal cord . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital," as required for coverage under the Plan, Petitioner offered selected medical records relating to Ms. Davidson's antepartum course, as well as those associated with Emmanuel's birth and subsequent development. Additionally, Emmanuel's parents testified on their own behalf, and Respondent offered the deposition testimony of Dr. Duchowny, whose qualifications were previously noted, and the deposition testimony of Dr. Donald Willis, a physician board-certified in obstetrics and gynecology, as well as maternal-fetal medicine. As for the cause and timing of Emmanuel's impairments, it was Dr. Duchowny's opinion, based on the results of his neurology evaluation and review of the medical records, that Emmanuel's impairments are not related to perinatal asphyxia or trauma. More particularly, Dr. Duchowny expressed his views, as follows: Q. Based on your review of the records and your evaluation of Emmanuel Hooks, can you give us an overview of his condition? A. Yes. I thought that Emmanuel's neurologic examination revealed evidence of developmental neurologic impairment. He was hyperactive and had an attention deficit disorder and additionally had significant behavior, social and communication problems. All of this suggested he had developmental problems in multiple areas, consistent with a diagnosis of pervasive developmental disorder. Many of the children with pervasive developmental disorder go on to develop childhood autism as they get older. * * * Q. In this particular case, do you believe that Emmanuel's condition was acquired during the course of labor-delivery in the immediate post-delivery period? A. No, I do not. Q. What is the basis for that opinion? A. The basis for my opinion is that autism is a developmental disorder which results from unknown factors operating in utero prior to the onset of labor and delivery and is not a recognized complication of birth asphysia or birth trauma. Q. I take it your opinion is that Emmanuel Hooks did not acquire whatever neurological deficits he had as a result of any oxygen deprivation or mechanical injury occurring during labor-delivery or the immediate post- delivery period? A. That's correct. Q. In fact, was there any evidence in the medical records of any oxygen deprivation that occurred during the course of labor- delivery or resuscitation during the immediate post-delivery period? A. No. Q. Was there any evidence of mechanical injury occurring during the course of labor- delivery or the immediate post-delivery resuscitative period? A. No, there was not? Q. In your opinion, were Emmanuel's problems acquired prior to the course of labor- delivery? A. Yes. As for Dr. Willis, he was also of the opinion that the medical records revealed no evidence of oxygen deprivation or other trauma associated with Emmanuel's birth. The medical records, as well as the testimony of the physicians and the parents, have been carefully considered. So considered, it must be concluded that the proof failed to demonstrate that any impairment Emmanuel suffers was occasioned by an injury to the brain or spinal cord injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period.

Florida Laws (10) 120.68766.301766.302766.303766.304766.305766.309766.31766.311766.313
# 9
FAYE CURRY, ON BEHALF OF AND AS PARENT AND NATURAL GUARDIAN OF LAWRENCE CURRY, A MINOR vs FLORIDA BIRTH-RELATED NEUROLOGICAL INJURY COMPENSATION ASSOCIATION, 16-007025N (2016)
Division of Administrative Hearings, Florida Filed:Health Care, Florida Nov. 28, 2016 Number: 16-007025N Latest Update: Oct. 06, 2017

Findings Of Fact Lawrence Curry was born on September 8, 2015, at Baptist Medical Center in Jacksonville, Florida. NICA retained Donald Willis, M.D., an obstetrician specializing in maternal-fetal medicine, to review Lawrence’s medical records and opine as to whether there was an injury to Lawrence’s brain or spinal cord that occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period due to oxygen deprivation or mechanical injury. In a report dated May 8, 2017, Dr. Willis described his findings in pertinent part as follows: In summary, the pregnancy was complicated by maternal hypertension and poorly controlled Gestational Diabetes. Fetal compromise (oxygen deprivation) was likely present prior to delivery based on decreased fetal movement and a non-reactive NST for several days prior to delivery. Emergency Cesarean section was done for suspected fetal distress based on fetal testing. The mother was not in labor. The baby was large-for-gestational age (LGA), consistent with maternal Diabetes. Significant depression was present at birth with a cord blood gas pH of only 6.95. The newborn hospital course was complicated by multi-system organ failure. Head ultrasound and MRI some degree of intraventricular hemorrhage. Discharge diagnosis included HIE. The baby suffered some degree of oxygen deprivation and resulting brain injury. The injury likely occurred primarily prior to delivery and does not appear to be birth related. The brain injury would include the IVH as identified by head Ultrasound and MRI. The mother was not in labor, so injury during labor would not be an issue. Attached to Respondent’s Motion for Summary Final Order is the affidavit of Dr. Willis, dated July 20, 2017. In his affidavit, Dr. Willis affirms his May 8, 2017, report and maintains that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to Lawrence’s brain or spinal cord occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period. NICA also retained Laufey Y. Sigurdardottir, M.D., a pediatric neurologist, to review Lawrence’s records and conduct an Independent Medical Examination and opine as to whether Lawrence suffers from a permanent and substantial mental and physical impairment as a result of a birth-related neurological injury. Dr. Sigurdardottir reviewed the medical records, obtained a full historical account from Faye Curry, and performed a full neurologic evaluation on May 24, 2017. In a report authored after the neurologic evaluation, Dr. Sigurdardottir summarized his findings as follows: Lawrence is a 20 month old with history of hypoxic ischemic encephalopathy, neonatal seizures, pulmonary hypertension and bilateral grade 1 IVH. He was born via emergency C section and had 2 month long NICU stay. He has made remarkable recovery and has minimal developmental delays at this time. Result as to question 1: Lawrence is not found to have permanent substantial physical and mental impairments at this time. Result as to question 2: In review of the available documents, Lawrence had early evidence of neurologic injury due to hypoxic ischemic event, which was birth related. Mother was not in active labor at time of delivery. Result as to question 3: The prognosis for full motor and mental recovery is good and his life expectancy is full. Due to the absence of clear mental and motor impairments at this time I do not recommend Lawrence to be included in the NICA Program. . . . Respondent’s Motion for Summary Final Order also relies upon the attached affidavit from Dr. Sigurdardottir, dated July 21, 2017. In his affidavit, he affirms the findings contained in his report. It is his ultimate opinion that “the IME and record review do not support a finding that Lawrence suffered a ‘birth-related neurological injury.’” A review of the file reveals that no contrary evidence was presented to dispute the findings and opinions of Dr. Willis and Dr. Sigurdardottir. Their opinions are credited.

Florida Laws (7) 766.301766.302766.303766.305766.309766.311766.316
# 10

Can't find what you're looking for?

Post a free question on our public forum.
Ask a Question
Search for lawyers by practice areas.
Find a Lawyer