The Issue At issue is whether Jasmine Scott, 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 Temple Scott and Daryl Scott, are the parents and natural guardians of Jasmine Scott (Jasmine), a minor. Jasmine was born a live infant on November 7, 1997, at Columbia Memorial Hospital, a hospital located in Jacksonville, Florida, and her birth weight was in excess of 2500 grams. The physician providing obstetrical services during Jasmine's birth was Joan Macksey, M.D., who was at all times material hereto, a participating physician in the Florida Birth-Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Jasmine's birth At or about 9:15 a.m., November 6, 1997, Mrs. Scott was admitted to Columbia Memorial Hospital in labor, with onset of labor noted as having occurred at 6:00 a.m. At the time, Mrs. Scott's estimated date of delivery was noted as November 3, 1997 (by date of last menstrual period), or November 8, 1997 (by fetal/ultrasound assessment). On admission, vaginal examination revealed the membranes were intact; the cervix to be at 3 centimeters dilatation; effacement at 50 percent; and the fetus at station -1, with a vertex presentation. Fetal heart tone (FHT) was noted as 130 to 140 beats per minute, and contractions were observed at 1 1/2 to 3 minute intervals, lasting 40 to 60 seconds. Fetal monitoring from admission until approximately 5:31 p.m. revealed a FHT of 130 to 140 beats per minute, with average long-term variability. At 5:31 p.m., uterine contractions were noted at a frequency of 2 to 4 minutes, with a duration of 60 to 90 seconds and moderate intensity. Vaginal examination (at 5:33 p.m.) revealed the cervix to be at 6 to 7 centimeters dilatation, effacement at 100 percent, and the fetus still at station -1. At approximately 5:31 p.m. and extending through 5:35 p.m., the FHT was noted to decrease to the 90 beat-per- minute range, and at 5:37 p.m. to accelerate to the 180 beat per minute range. Mrs. Scott was repositioned and administered oxygen, and FHT returned to a baseline of 130 to 140 beats per minute. While fetal heart decelerations and occasional decreases in long-term variability were described between 6:00 p.m. and the end of the first stage of labor (10:20 p.m.), accelerations were also noted to accompany decelerations and overall long-term variability remained normal, a circumstance consistent with fetal reserve and continued wellbeing. At 10:20 p.m., vaginal assessment revealed complete dilatation and effacement (the onset of the second stage or, stated differently, the pushing stage of labor); however, the fetus had only progressed to station 0. Between 10:20 p.m. and midnight, FHT was noted in the 120 to 130/130 to 140 beat- per-minute range. Again, occasional decelerations were described (with Mrs. Scott being repositioned and administered oxygen); however, accelerations were also noted to accompany decelerations and overall long-term variability (as well as short-term variability) was maintained, a circumstance (as heretofore noted) consistent with fetal wellbeing. At midnight, late and variable decelerations were noted at each push and Mrs. Scott was administered oxygen and repositioned. FHT remained at 130 to 140 beats per minute, and long-term variability persisted. Subsequently, at 12:36 a.m., November 7, 1997, Dr. Macksey called for a cesarean section, secondary to arrest of descent, and at 12:57 a.m., Mrs. Scott was taken by bed to the operating room where Jasmine was delivered at 1:32 a.m. Dr. Macksey's operative report reads as follows: This is a 22-year-old female, G-1, P-0 approximately 40-3/7 weeks. Came in spontaneous labor on 11/6/97. She went on to progress to complete complete 0. She pushed for approximately two hours without any further progression and she was diagnosed secondary arrest of descent. She was explained the risks and benefits of a cesarean delivery plus full need for transfusion as necessary. She agreed to proceed. She was taken to the operating room, placed in the dorsal supine position with a leftward tilt. Epidural anesthesia was insured to be adequate. She was subsequently prepped and draped in the normal sterile fashion. A Pfannenstiel skin incision was made . . . [and, following entry], [a] low transverse incision was made on the uterus and carried out laterally with Mayo scissors. The fluid was noted to be clear. Efforts were made to deliver the baby, however, the head was firmly impacted into the pelvis, therefore help was needed with the nurse pushing up from the vaginal vault lifting, trying to elevate the head. A second attempt was made again to reinsert my hand into the uterus and deliver the child, however, the lower uterine segment had clamped down and it was very difficult to deliver the child at this point. Efforts to get the head out of the pelvis were very futile, therefore, the infant was delivered with a flexed head at the level of the scapulas almost in a curled up position and was immediately bulb suctioned and the cord clamped times two and cut and handed to the waiting neonatologist. . . . On delivery, Jasmine was bulb suctioned, and received free oxygen (blow by) for 4 minutes and oxygen by bag/mask for 1 minute. Her initial newborn exam revealed "no observable abnormalities," and cord pH was 7.10 arterial, with a normal bicarbonate component. While depressed (a "little lower than normal"), Jasmine's cord pH was not so low as one would typically associate with an acute hypoxic event during the course of labor and delivery. Moreover, with a normal bicarbonate component, Jasmine's cord pH failed to demonstrate the presence of metabolic acidosis, an absence of which is inconsistent with acute birth-related hypoxia. Apgar scores totaling 5 and 9 were assigned at one and five minutes, respectively. The Apgar scores assigned to Jasmine 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 Jasmine's Apgar score totalled 5, with respiratory effort and color being graded at 0 each; muscle tone being graded at 1; and heart rate and reflex irritability being graded at 2 each. At five minutes Jasmine's Apgar score totalled 9, with heart rate, respiratory effort, muscle tone, and reflex irritability being graded at 2 each, and color being graded at 1. While slightly depressed at birth, as reflected by the one-minute Apgar score of 5, her five-minute Apgar score (the more important of the two with regard to long-term neurologic outcome) was 9 or, stated differently, perfectly normal. Jasmine was transferred (carried) to the newborn nursery at 1:45 a.m. Upon admission to the nursery, newborn assessment was, with the exception of some discoloration of the skin (bruising on the left side and left side back) grossly normal. Jasmine's neonatal course in the nursery was unremarkable 1/ except for a slight case of jaundice (a syndrome characterized by hyperbilirubinemia and deposition of bile pigment in the skin with resulting yellow appearance of the patient), and on November 9, 1997, at two-days-old, she was discharged to the care of her parents. Jasmine's subsequent development In February 1998, at three-months-old, Jasmine was admitted to Baptist Medical Center and Wolfson Children's Hospital (Wolfson Children's Hospital), Jacksonville, Florida, for evaluation of possible seizure activity. There, Jasmine was seen by William R. Turk, M.D., for neurological evaluation, who reported his findings as follows: HISTORY: Jasmine a three-month-old seen for evaluation of possible seizures. I have reviewed her charts, spoken with Dr. Jada [Jasmine's primary care physician], and personally reviewed her history with her parents and grandparents. Apparently a question of seizures first arose last Wednesday, approximately five days ago, on Jasmine, when she had the first of now eight events. These events have occurred both during sleep and wakefulness and are characterized by the sudden onset of generalized stiffening, predominantly involving her upper extremities, as her hips are kept in a cast for a congenital hip dislocation. Her arms are either held extended or flexed. There is no clonic component, and it is bilaterally symmetrical. When she suddenly assumes this stiff posture, her eyes will be open and staring. They do not roll or flutter. No mouth movements have been noted. There are no autonomic changes in terms of cyanosis, pallor, or appearing erythematous. She does not stop breathing. There is no associated reflux. They have occurred both with and without stimuli, and generally last 15 seconds. Following the events she at times will briefly cry. When she is asleep at the onset, she will briefly open her eyes, appear alert, smile, then return to sleep. One was observed by the nursing staff as described in the notes, with bilateral stiffening lasting 30 seconds. In between these events recently she has been well. There has been no history of recent illness or trauma. PAST MEDICAL HISTORY: Reveals she is the 6 pound 1 ounce product of a term pregnancy complicated only by low maternal iron. She was delivered by emergency cesarean section due to some decelerations. However, she did well in the perinatal period. Her mother in retrospect denies any illnesses, flus, drug or toxin exposures during pregnancy. She since has been generally healthy, with no significant illnesses. . . . Jasmine was diagnosed at birth as having congenital hip dislocation and has been maintained in hip braces. Developmentally, she has not rolled over, which has been attributed to her hip braces. She has been very alert and social. On review of systems, her parents note occasionally her eyes will roll downward. There has been no consistent strabismus. She appears to hear normally. She has had no problems with chewing or swallowing. She has had no chronic cardiopulmonary complaints. She has rare modest reflux with being burped. She has had no choking or gagging. She has had no vomiting or diarrhea. No motor asymmetries have been noted, nor tremulousness. She has one café au lait patch on her right leg. She has had no recent fever, rashes, or irritability. * * * PHYSICAL EXAMINATION: She is an alert, pleasant, happy infant, in no apparent distress. She was afebrile. Her head circumference of 39.5 cm is on the 50th percentile, while her height and weight were approximately in the 15th percentile. There were no dysmorphic features, although she does have a scaphocephalic-appearing cranium. Her anterior fontanelle was soft. There were no cranial bruits. Her ears, eyes, nose, mouth, and pharynx were unrevealing. Her neck was supple. I could appreciate no meningismus. Her chest was clear. I could appreciate no cardiac murmur. Her abdomen was benign. She was wearing her hip brace, which was removed. She appeared to have full range of motion of her joints. She had one café au lait patch in her right groin. There were some areas of irregular depigmentation in a nonspecific pattern. There were no acute rashes. On neurological examination, her pupils were equal, round, and reactive to light. Here extraocular movements were conjugate and full, and she would fix, follow, and socialize visually. Multiple fleeting glimpses of her disc and retina were unrevealing. Her facial movements were symmetrical. She localized auditory stimuli bilaterally. Her gag was intact, and her cry was loud and lusty. MOTOR EXAMINATION: Demonstrated equal and symmetrical muscle bulk, tone, and strength. She had vigorous spontaneous movements of all extremities without abnormal posturing. She did appear to have a mild to moderate head lag when pulled to a sitting position. Deep tendon reflexes were diffusely 2+, with flexor plantar responses. She withdrew briskly and symmetrically to noxious stimuli. No tremulousness was noted. * * * IMPRESSION: Jasmine is a three-month-old with a history of congenital hip dislocation who in the last five days has had eight episodes of generalized (bilateral, predominantly upper extremity) stiffening. This has been either in an extensor or flexor posture. This has been associated with her eyes being open but no other motor manifestations have been noted. There are no associated autonomic changes, distress, cyanosis, or regurgitation. These events as described are suggestive of seizures, although it is unusual in an infant of this age to have generalized tonic seizures due to the relative immaturity of their cerebral circuitry. She did have an EEG performed that did demonstrate some left parietal sharp waves that are potentially epileptogenic, but these would be more suggestive of a partial rather than generalized seizure process. She does not appear to be acutely ill and is otherwise an alert, active infant whose only remarkable finding on examination is some mild head lag. Thus, it is unclear clinically whether she is having seizures or whether these stiffening spells reflect either a startle or arousal type phenomena. . . . A February 10, 1998, MRI scan was read as normal, and disclosed no evidence of brain damage. Jasmine was apparently started on Phenobarbital therapy for a perceived seizure disorder. Notwithstanding, on March 16, 1998, her seizure activity persisted and her primary care physician (Dr. Jada) referred her to Carlos Gama, M.D., for neurologic evaluation. 2/ Dr. Gama's diagnosis and recommendations were as follows: Diagnosis: Infantile spasms. Encephalopathy. 3/ Seizure disorder. Developmental delay. Recommendations: 1. Admit to Baptist Medical Center [Wolfson Children's Hospital] for further diagnostic workup and appropriate treatment. Comments: Jasmine is a four month old female infant who comes today with her parents and paternal grandmother for evaluation of a seizure disorder, which has been diagnosed in the recent month by Dr. William Turk and started on Phenobarbital therapy. However, the present visit is precipitated by the fact that she is now displaying a different type of seizure activity described as clusters of startle like movements, which tend to occur primarily during the morning time when the patient is tired. These have been present since last weekend and suggestive of infantile spasms. The past medical history reveals that Jasmine was born to a 22 year old G1 Para 0 mother at 40 weeks gestational age, uncomplicated pregnancy. Delivery was difficult and the fetus had an erratic heart rate, and possibly a cephalopelvic disproportion. The infant was delivered by c-section. The apgars were five at one minute and nine at five minutes. The infant went to the normal nursery and fed well with no significant difficulties, except parents report that for the first few weeks Jasmine was not a very active infant. They deny any evidence of hypotonia. The developmental history is remarkable for the fact that she has not obtained developmental milestones properly. Medications include Phenobarbital 3mls in the morning and 4mls at nighttime. Vaccines are remarkable for the fact that she received the first round of vaccines with no complications. The family history was negative, except for epilepsy in a paternal uncle and two maternal cousins. The neurological examination reveals that the patient's head circumference is in the 50th percentile. Her weight and height were within the normal percentiles. The baby was drowsy during the examination, however, she was able to arouse, but did not have appropriate eye contact. Red reflex was present bilaterally. Pupils were equal and reactive to light stimulation. Cranial nerve examination was normal. The motor examination was remarkable for the fact that she kept her hands fisted. She had poor traction response with very poor head control. Moro was absent. Tone and neck reflex was absent. Palmar and Plantar reflexes were present. The muscle tone seemed to be somewhat decreased. The patient was able to support weight in her lower extremities. The rest of the neurological examination was noncontributory. No obvious organomegalies, skin abnormalities or dysmorphic features were observed. Therefore it is my opinion that Jasmine has infantile spasms with a progressive encephalopathy and developmental delay. In view of the present history it is recommended that she be admitted to Baptist Medical Center for further evaluation of her seizure disorder and initiation of appropriate treatment. Jasmine was admitted to Wolfson Children's Hospital on March 17, 1998, and discharged to the care of her parents on March 25, 1998. Dr. Gama's discharge summary contained the following diagnoses and recommendations: DIAGNOSES: Infantile spasms. Partial complex seizures. Developmental delay. Iron deficiency anemia. Vitamin B6 deficiency. Congenital deformity of the hip joint. * * * PAST MEDICAL HISTORY: Basically noncontributory. Developmental history has been abnormal. FAMILY HISTORY: A paternal uncle with epilepsy as well as two maternal cousins with epilepsy. NEUROLOGICAL EXAMINATION: Examination was characterized by the fact the baby was hypotonic, delayed with no dysmorphic features per se and in no acute distress. The patient was witnessed to have had some infantile spasms. Therefore, she is admitted for further neurological work-up. The baby underwent an EEG which [was abnormal] and reveal[ed] a hypsarrhythmic pattern. During this EEG, she received Pyridoxine 50 mg IV which seemed to have improved the background of these tests. Positive pattern of vitamin B6 deficiency was considered. The patient was treated with this medication for 24-48 hours, but the symptoms persisted in spite of the fact that she was receiving high dose of vitamin B6. In view of this, it was decided to treat her with ACTH. After appropriate discussion with the family, this medication was agreed upon and was started at 40 units IM q. day. She was maintained on her Phenobarbital 4 ml p.o. q.h.s. and 3 ml in the morning. The patient also was noted to have anemia and iron deficiency and therefore she was started on Fer-In-Sol. The baby tolerated procedures well. She also had metabolic studies obtained which were unrevealing. The patient was therefore discharged to the care of her parents on 03-25-98 with the following recommendations. DISCHARGE INSTRUCTIONS: Diet is regular for age. Activity regular. ACTH 40 units IM q. day for five days and then to decrease this to 20 units IM thereafter. Pyridoxine 100 mg p.o. q. day. FOLLOW-UP: The patient is to be seen in my office in one week for re-evaluation and further recommendations regarding the ACTH therapy. Return to my office as recommended. Jasmine returned to Dr. Gama on March 31, 1998, for a follow-up neurological evaluation. The following were his diagnosis and recommendations: Diagnosis: Infantile spasms. Idiopathic [of unknown origin]. Severe encephalopathy. Iron deficiency anemia. Recommendations: Continue ACTH 20 units IM q day. Continue Phenobarbital 20mg/5mls 4mls po BID. Obtain EET. . . . Comments: Jasmine returns for her post hospital follow-up visit. She has been on the ACTH for approximately 8-9 days, 20 units q day. She continues having infantile spasms and there has not been any significant change in her overall encephalopathy. . . . Her examination shows that head circumference is 41.5cm. She is alert, but does not track the examiner. The patient's pupils are equal and reactive. Her motor response is absent. Traction is negative. Head control is poor and her muscle tone overall is decreased. Deep tendon reflexes were +2. The rest of the examination was noncontributory. In summary it is my opinion that Jasmine is not responding to ACTH as expected. I am concerned because this usually will carry poor prognosis overall if we are unable to control her seizures. In view of this I recommend that we obtain an EEG to further assess the electroencephalographic pattern and effectiveness of this. Jasmine was again seen by Dr. Gama on April 6, 1998, for a follow-up evaluation. The following were his diagnosis and recommendations: Diagnosis: Infantile spasms. Responding to ACTH. Encephalopathy. Recommendations: Continue ACTH 20 units qod IM. Phenobarbital 5 mls po BID. . . . * * * Comments: Jasmine underwent EEG, which reveals improvement of the background, although there was evidence [of] occipital spike discharges. Her grandmother reports occasional staring spells, which may represent seizures, but this is unclear. This may be related to partial seizures rather than to infantile spasms. No evidence of myoclonic jerks is described during today's visit. The grandmother also describes Jasmine of being more sociable, laughing more and being more playful. The examination shows that head circumference is 41.5 cm. She was alert and seems to be able to focus, and maybe starting to track but this was quite inconsistent. Her muscle tone is decreased throughout. Deep tendon reflexes were hypoactive. The patient remained with no evidence of a traction response, poor head control and absent tone and neck reflex. Therefore it is my opinion that Jasmine seems to be responding to the ACTH therapy at this point. She may be having some underlying partial seizures, secondary to her occipital spike discharge. We will reassess her in two weeks in this office. On April 20, 1998, at five-months-old, Jasmine returned to Dr. Gama for a follow-up evaluation. The following were his diagnosis and recommendations: Diagnosis: Infantile spasms. Idiopathic. Iron deficiency anemia. Hypotonia. Central. Hip dislocation. Recommendations: Start weaning off schedule of ACTH by decreasing the dosage. . . . Continue Phenobarbital 5mls po BID. Refer to Easter Seals for early intervention program. * * * Comments: Jasmine seems to be doing well on the ACTH with no recurrent myoclonic spasms. The grandmother reports no significant staring spells or other seizure types. Her Phenobarbital level on 4/13/98 was 31. The patient's electrolytes are stable, as well as her CBC/diff. Jasmine is described as being more vocal, more active and seems to be starting to track more than before. She is rolling over from her back to her stomach. She seems to be pleasant and with no irritability. She is feeding well and thriving. The examination shows that her head circumference is 41 cm (in the 50th percentile). Anterior fontanel is soft and normal tense. The patient is alert and she seems to track the examiner more consistently than in the past, but still no more than a 90 degree range. The patient's muscle tone is decreased. Her traction is improved, as well as head control, but still remains abnormal for her age. The motor examination shows deep tendon reflexes of +3. No clonus was seen. General muscle tone was slow as described before. The rest of the examination was noncontributory. . . . Jasmine was next seen by Dr. Gama for a follow-up evaluation on May 5, 1998. At the time, his diagnosis and recommendations were as follows: Diagnosis: Infantile spasms. Partial seizures. Hypotonia. Developmental delay. Recommendations: Continue decreasing ACTH, now to 15 units IN every other day, and progress according to schedule. Change Phenobarbital to tablets, 30mg 1 1/2 tab qHS. * * * Comments: Jasmine is doing well. She is now more alert and attentive. She seems to be laughing and more interactive than in the past. The grandparent's report no recurrent myoclonic seizures. She is scheduled to be evaluated by the Early Intervention Program in the next few weeks. Her vaccines have been on hold until she completes her ACTH therapy, which will [be] in approximately six weeks, after which she should be starting her regular schedule. The patient's examination shows that she is alert and attentive. She tracks well. Her traction response seems to be improved. Her control is also better. Her muscle tone remains low. Deep tendon reflexes are +2. The patient seems to be improving clinically. . . . Jasmine's next follow-up evaluation with Dr. Gama was on June 3, 1998. At the time, Dr. Gama made the following diagnosis and recommendations: Diagnosis: Infantile spasms. Partial seizures. Hypotonia. Developmental delay. Recommendations: Discontinue ACTH. Phenobarbital 30mg 2 tabs qHS. Continue Pyridoxine for now. * * * Comments: Jasmine is doing extremely well. She is seizure-free and tolerating Phenobarbital well. Her most recent level was 34. She seems to be interacting more with her parents. She is more playful and sociable. She has mild estropia and continues to be hypotonic, especially in her axial musculature. Moro reflex is absent. Her traction is decreased. Her head control is also decreased. Deep tendon reflexes were +3. The rest of the examination was noncontributory. She remains developmentally delayed. However, I feel that Jasmine's infantile spasms are resolved and her partial seizures seem to be under control on present dosage of Phenobarbital. On August 27, 1998, at nine-months-old, Jasmine returned to Dr. Gama for a follow-up evaluation. The results of that examination were as follows: Diagnosis: Infantile spasms. Decreased activity in the morning times by parent's report. Rule out recurrent seizures. Hypotonia. Developmental delay. Recommendations: Continue Phenobarbital 30mg 2 tabs qHS. Discontinue Pyridoxine. * * * Comments: Jasmine returns for an early appointment because of concerns regarding the fact that in the morning time she has not been as active as usual. Father reports some irritability in the last several days. She has had some nasal congestion, but no other symptoms. No nausea, vomiting or fever. Parent's also feel that she is not moving her right arm very well, and that she is not be [sic] rolling over as frequently as before. The patient continues to feed well. She has no difficulties swallowing. The examination today demonstrates that she is alert and playful. She smiles and socially relates to the examiner. The patient's cranial nerve examination shows mild esotropia of the eyes with no pupillary abnormalities. Her motor examination is unchanged, with significant hypotonia, poor traction response and poor head control, however this is not new to the examiner. The deep tendon reflexes were present. The patient is unable to support weight in the lower extremities. No pinpoint tenderness of the bones in her arms or joints is elicited. Passive range of motion is normal with no pain. No evidence of injury is seen during the examination. In general she seems to be at baseline in her neurological examination. . . . It is my opinion that Jasmine is stable neurologically, although she is developmentally delayed with severe hypotonia and an underlying seizure disorder. . . . Jasmine next saw Dr. Gama at twelve-months-old for a follow-up evaluation on November 16, 1998. The results of that evaluation were as follows: Diagnosis: Seizure disorder. Stable on Phenobarbital (infantile spasms, partial seizures). Psychomotor developmental delay. Improving. Hypotonia. Improving. Recommendations: 1. Continue Phenobarbital 60 mg 1 tab qHS. * * * 3. Continue physical and speech therapy. * * * Comments: Jasmine is doing extremely well. She has been seizure free for several months. She is starting to gain some milestones. She is now more alert, talkative and interactive with environment. She is still hypotonic, and she is getting physical therapy on a regular basis. She will be starting speech therapy. The mother has no specific complaints. . . . The examination reveals that her head circumference is 44cm. She is alert and attentive. Her head size and shape is within normal limits. The cranial nerve examination demonstrates mil[d] esotropia. The patient has a good traction response and head control, but her muscle tone is decreased axially. She is still not able to sit up by herself. The patient does not pull up to a standing position. Her muscle tone in the lower extremities tend to be somewhat increased. Deep tendon reflexes were within normal limits. The patient tends to keep her upper extremities in a semi-flex posture. No fisting was seen. The Denver Developmental Screen Test demonstrates that she is at approximately 6-8 months in her gross motor skills. She seems to be appropriate in the language area. She is approximately 9 months of age in personal/social skills. . . . Insofar as the record reflects, Jasmine was last seen by Dr. Gama for a follow-up evaluation on March 15, 1999, at sixteen-months-old. The results of that evaluation were as follows: Diagnosis: Seizure disorder. Stable on Phenobarbital. S/P Infantile spasms. Hypotonia. Developmental delay. Recommendations: Continue Phenobarbital 60mg qHS. Continue supportive therapies. Return to this office in four months for reevaluation. Comments: Jasmine is doing well, with no recurrent seizures. Her Phenobarbital level in December was 32. A repeat study is recommended. The patient is having physical therapy. She is going to the Early Intervention Program and doing well. She is making good progress. The examination reveals that her head circumference is 43.7cm. She is alert. She has good eye contact. She has mild esotropia of the right eye. The cranial nerve examination was otherwise unremarkable. Muscle tone shows hypotonia. The deep tendon reflexes were present and +2. The patient has made some advances in her milestones. Therefore, she is to continue present regimen of medication as well as support therapies. . . . Given the proof, it is apparent that Jasmine suffered some anomaly which adversely affected brain development, as evidenced by her current neurologic impairment (mental and physical). However, the records of her treating and consulting physicians, consistent with her perinatal and neonatal records from Columbia Memorial Hospital, contain no suggestion that her presentation is associated with any event which may have occurred during labor, delivery, or resuscitation. Indeed, while her consulting neurologist (Dr. Gama) evidently sought to identify the cause of her presentation, he concluded that her past medical history was "[b]asically noncontributory" and that her infantile spasms were of unknown origin ("idiopathic"). The dispute regarding compensability Here, there is no dispute that Jasmine suffers neurologic dysfunction, mental and physical. What is at issue is whether that dysfunction may reasonably be described as permanent and substantial and, more fundamentally, whether the cause (etiology) of such dysfunction is, more likely than not, attributable to "an injury to the brain . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post- delivery period," as required for coverage to be afforded under the Plan. Section 766.302(2), Florida Statutes. With regard to the issue of causation or timing, Petitioners are of the view that Jasmine's hospital course and subsequent development is consistent with a brain injury caused by oxygen deprivation or mechanical injury which occurred during the course of labor, delivery, or resuscitation. In contrast, Respondent is of the view that the proof is not consistent with a brain injury cause by oxygen deprivation or mechanical deprivation which occurred during or immediately following birth and must, therefore, be attributable to some other etiology. Respondent's view of the proof has merit, and it is unnecessary to address whether Jasmine's neurologic dysfunction is permanent and substantial. The etiology (genesis) of Jasmine's dysfunction To address the etiology of Jasmine's neurological dysfunction, the parties offered selected records relating to Mrs. Scott's intrapartum course, as well as for Jasmine's birth and subsequent development. Portions of those records have been addressed supra, and further salient portions will be addressed infra. The parties also offered the opinions of three physicians to address the likely etiology of Jasmine's presentation. The physician selected by Petitioners was Daria F. Marranzini, M.D., a pediatric neurologist. The physicians selected by Respondent were Michael S. Duchowny, M.D., a pediatric neurologist, and Charles Kalstone, M.D., a board- certified obstetrician and gynecologist. Here, the medical records and other proof, including the opinions of the physicians offered by the parties, have been carefully considered. So considered, the analysis and opinions of Doctors Kalstone and Duchowny were shown to rest on a logical premise, were grossly consistent with the record, and have been accepted as credible and persuasive. Consequently, it must be concluded that the proof does not demonstrate (or allow conclusion to be drawn with any sense of confidence) that, more likely than not, Jasmine's neurologic dysfunction is related to 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." 4/ In reaching such conclusion, it is observed that Jasmine's course pre-delivery and post-delivery was inconsistent with a brain injury associated with a hypoxic/ischemic event or mechanical injury having occurred during the course of labor, delivery, or resuscitation. Notably, while there were multiple late decelerations during the second stage of labor (which evidenced periods of diminished oxygenation or, stated differently, periods of transient hypoxia) the fetal monitoring tape also provided reassuring evidence of fetal wellbeing/reserve (by documenting good beat-to-beat variability, spontaneous accelerations, and recovery (following deceleration) to FHT baseline. Further militating against the conclusion that Jasmine's impairments are associated with an injury caused by oxygen deprivation or mechanical injury during labor or delivery are the numerous inconsistencies between Jasmine's perinatal and neonatal course, and the clinical findings one would expect had she suffered a brain injury secondary to oxygen deprivation (perinatal asphyxia) or mechanical injury during that period. For example, Jasmine's five-minute Apgar score was normal; cord pH, while below normal, was not consistent with an acute insult or with metabolic acidosis; and Jasmine did not evidence symptoms (such as seizure activity within the first 48 hours of birth, continued poor tone, or renal failure) one would typically associate with an acute neurologic insult caused by oxygen deprivation or mechanical injury during the birth process. Moreover, Jasmine presented without apparent abnormality, her hospital course was essentially uneventful, and she was discharged to her parents' care (as a well baby) at two days of age. Finally, Jasmine's MRI, at three-months-old (February 10, 1998), was read as normal or, stated differently, failed to reflect any brain damage one would typically associate with an injury caused by oxygen deprivation or mechanical injury. Consequently, while Jasmine clearly suffered some trauma because of a difficult extraction during the cesarean section (occasioned by the baby's head being impacted in the pelvis), as well as transient periods of hypoxia, the objective proof regarding Jasmine's perinatal and neonatal course was not consistent with an acutely acquired neurologic injury caused by oxygen deprivation or mechanical injury, and it is improbable that she could have experienced an acute event during labor and delivery, or immediately thereafter, without evidencing clinical symptoms of such damage. Consequently, given the proof, it cannot be concluded that Jasmine's neurologic dysfunction resulted from a brain injury caused by oxygen deprivation or mechanical injury which occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period, as opposed to some intrauterine event (i.e., a developmental, genetic, or other congenital abnormality). (See Exhibit E.)
The Issue Whether Ashley Villarreal has suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan, as alleged in the claim for compensation.
Findings Of Fact Preliminary matters Ashley Villarreal (Ashley) is the natural daughter of Roy Villarreal and Carmen Luna. She was born a live infant on January 2, 1989, at Bethesda Memorial Hospital in Palm Beach County, Florida, and her birth weight was 3090 grams. The physician delivering obstetrical services during the birth of Ashley was Allen Dinnerstein, M.D., who was, at all times material hereto, a participating physician in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. The birth of Ashley Villarreal At or about 4:15 p.m., January 2, 1989, Carmen Luna was admitted to Bethesda Memorial Hospital. At the time, Carmen Luna was in active labor, and Ashley was post term with a gestational age of 41 weeks. Otherwise, Carmen Luna's pregnancy had been without complication. External fetal monitoring was commenced at 4:50 p.m. and indicated that the fetal heart tone was sporadically within the 60 beat per minute level, with a slow return to baseline; a level sufficient to indicate occasional fetal bradycardia and fetal distress. 1/ This situation evidenced a need for surgical intervention, and at 5:20 p.m. Carmen Luna was taken to the operating room. Anesthesia commenced at 5:25 p.m., a cesarean section surgical procedure was commenced at 5:39 p.m., and Ashley was delivered at 5:44 p.m. The operative report reflects that the following occurred during the course of the procedure: . . . a transverse incision was made into the uterus releasing meconium stained fluid. The vertex was delivered and the baby suctioned with DeLee. A loop of cord over the neck was removed and the baby then delivered completely continually being suctioned as the cord was double clamped and severed and the infant given to the neonatologist for care . . . . The delivery records likewise reflect that Ashley had a blue appearance at delivery, the presence of meconium staining, and the following resuscitation measures: "Stimulation," "Bulb Suction," "DeLee Suction," "Mech Suction" and "Whiffs Oz." When delivered, Ashley presented Apgar scores of 6 at one minute and 8 at five minutes. These scores are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of the heart rate, 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, Ashley's Apgar score totaled 6, with respiratory effort and reflex irritability being graded at 2 each, heart rate and muscle tone being graded at 1 each, and color being graded at 0. At 5 minutes, Ashley's Apgar score totaled 8, with heart rate, respiratory effort and reflex irritability being graded at 2 each, and muscle tone and color at 1 each. Such total scores could be characterized by an obstetrician as "good." Pertinent to this case, color, heart rate and respiratory effort are primarily related to the cardiovascular system, and color is the least significant indicator of an infant's brain or neurological status at birth. The categories of reflex irritability and muscle tone are, however, neurological assessments, which offer the greatest insight into the neurological condition of an infant at birth. Ashley's Apgar scores relative to those categories which reflect neurological status at birth were collectively a total of 3 out of a possible 4 at both 1 and 5 minutes. Under the circumstances, Ashley's Apgar scores, either globally or discretely, fail to reflect a hypoxic event at birth. At 6:00 p.m., following delivery, Ashley was admitted to the neonatal intensive care unit due to respiratory distress, possibly secondary to meconium aspiration. Ashley was accorded extra oxygen, via oxygen hood, for two days, and her meconium aspiration was successfully treated with antibiotics. During her admission, no clinical observations were noted that one would typically expect in a child undergoing hypoxic encephalopathy, and no neurological consult was ordered. 2/ On January 7, 1989, Ashley was discharged as an apparently well baby. Subsequent developments On July 29, 1989, Ashley was seen by M. Arenstein, D.O., for a "well baby visit," and no abnormalities were noted; however, on September 6, 1989, Ashley was again seen by Dr. Arenstein at which time the parents expressed their concern regarding Ashley "not sitting up, crawling, etc." Consequently, Dr. Arenstein referred Ashley for a pediatric consult with Jeffrey Perelman, M.D. Ashley was seen by Dr. Perelman on September 19, 1989, and he diagnosed her as developmentally delayed, and ultimately referred her to David Ross, M.D., for a neurological evaluation. Dr. Ross saw Ashley on July 2, 1990, and concluded: The patient has some mild facial dysmorphism with developmental delay in all fields associated with an abnormal neurologic exam with persistence of postural reflexes and hyperreflexia. The spectrum of findings is consistent with mental retardation of a mild to moderate degree probably due to cerebral palsy. 3/ Dr. Ross' ultimate diagnosis was mental retardation, and he recommended that Ashley have a full evaluation, including "an image of the brain either with CT scan or MRI (an EEG, torch titers, chromosome analysis)." Ashley was referred in August 1990, for a CT brain scan and an EEG. The CT scan is a neuroimaging study which can identify structural brain abnormalities occasioned by an hypoxic insult, as well as other causes. The EEG is a device used to detect abnormalities of the electrical currents of the brain such as seizure activity, which is often a manifestation of hypoxic insult at birth, and the death of neuronal cells. Here, both the CT scan and EEG were within normal limits. Ashley continued to be treated by Dr. Perelman through June 1991; however, on August 14, 1991, she came under the care of Miguel Simo, M.D., another pediatrician, because the parents were apparently dissatisfied with Dr. Perelman. Upon examination, Dr. Simo diagnosed Ashley as developmentally delayed, and referred her to Laszlo Mate', M.D., a physician practicing child neurology, for evaluation. Dr. Mate' examined Ashley on August 29, 1991, and observed: . . . a small, dysmorphic female in no apparent distress. Her head circumference is 47 cm which is in the 25th percentile. She doesn't have any neurocutaneous abnormalities. Her palmer creases are somewhat abnormal, but not of simian nature. Her fingers are slightly abnormal, extra long, and she seems to have a proximal displacement of both thumbs. Her ears are malformed with very small earlobes. The ears are somewhat posterior rotated and low set. Her eyes are almond shape but in view of her Indian heritage, that's probably normal. Both parents seem to have similar shaped eyes. The child has a somewhat prominent nose. The mouth is somewhat fishmouth in character and she has fairly shallow temporal area. She doesn't have any eyelashes on her lower eyelid. Dr. Mate's impression was: This is a markedly abnormal child with a developmental quotient in the 30's. She's currently is 30 months old and she functions around a 9-10 month level. She has multiple minor malformations which made the diagnosis of cerebral palsy somewhat unlikely. I suspect we are dealing with some prenatal etiology, either genetic or pregnancy related. 4/ Dr. Simo also referred Ashley for an MRI of the brain. An MRI, as with a CT scan, is a neuroimaging study which can identify structural abnormalities occasioned by hypoxic insult, as well as other causes. The MRI, performed September 20, 1991, was abnormal, evidencing "poor and decreased white matter myelinization extending to the frontal, occipital, and parietal cortex and decrease in white matter content in the centrum semiovale." Such damage could be reflective of birth asphyxia, developmental immaturity of the brain, or a myriad of other causes. Finally, Dr. Simo referred Ashley to Oscar Febles, M.D., a physician practicing genetics. Dr. Febles examined Ashley on November 1, 1991, and rendered a diagnosis of "psychomotor retardation of unknown etiology." Concluding, Dr. Febles observed: The clinical findings in this patient are not diagnostic of a particular genetic syndrome . . . In conclusion, this patient presents a clinical picture characterized by psychomotor retardation that cannot be diagnosed on the clinical findings and/or testing done. The fact that she presents diffuse demyelinization on the MRI would favor the diagnosis of cerebral palsy and/or a CNS degenerative disease. It is my recommendation that an MRI be repeated in approximately 6 months to see if the demyelinization process of the cortex previously seen is progressive or static. If found to be progressive it would indicate a CNS degenerative disease (e.g. leukodystrophies) and if static the diagnosis of cerebral palsy is most likely. In addition, it is also recommended . . . Genetic re-evaluation in 1 year. Whether, consistent with Dr. Febles' recommendation, an MRI was repeated or Ashley had a subsequent genetic re- evaluation does not appear of record. Notably, however, while Ashley was genetically tested and found to have a normal karyotype, such test does not rule out the preponderance of genetic disorders which manifest themselves in microscopic point mutations within a chromosome as opposed to total chromosomal malformation. The medical experts at hearing As to whether Ashley had sustained permanent and substantial mental and physical impairment as a result of an injury to her brain resulting from oxygen deprivation during the course of labor, delivery or resuscitation in the immediate post-delivery period, petitioners offered the testimony of Dr. David Ross, who, although a board certified neurologist, does not regularly treat neonates. Dr. Ross examined Ashley on July 2, 1990, and March 2, 1994. It was Dr. Ross' opinion that Ashley suffered a substantial and permanent mental and physical impairment as a consequence of oxygen deprivation during the course of labor and delivery. Compared with the opinion of Dr. Ross, the respondent offered the testimony of Dr. Michael Duchowny. Dr. Duchowny is a child neurologist who is board certified in pediatrics, neurology with special competence in child neurology and clinical neurophysiology. Dr. Duchowny is associated with the department of neurology at Miami Children's Hospital and routinely treats neonates suspected of having suffered a hypoxic event at birth. Dr. Duchowny examined Ashley on September 21, 1992, as well as observed her at hearing, and was familiar, as was Dr. Ross, with the pertinent medical records. It was Dr. Duchowny's opinion that Ashley was substantially and permanently mentally impaired, but that her physical impairment could best be described as mild to moderate. As to causation, it was Dr. Duchowny's opinion that the cause (etiology) of Ashley's mental and physical impairment (neurologic syndrome) was a developmental problem of in utero (prenatal) or genetic origin, and that any fetal distress she may have suffered at birth was not substantial and did not contribute to her condition. [Tr. 97] Here, I accept the testimony and opinion of Dr. Duchowny as being the more credible and substantial as to whether Ashley sustained a substantial and permanent mental and physical impairment, and the cause of such dysfunction. Dr. Duchowny's opinions are credible, supported by the observations of other physicians as heretofore noted, and are most consistent with conclusions to be drawn or inferences raised by the medical records received into evidence.
The Issue At issue in this proceeding is whether Sarah Massey, 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 Gina R. Massey and James Massey, are the parents and natural guardians of Sarah Massey (Sarah), a minor. Sarah was born a live infant on March 14, 1993, at St. Joseph's Women's Hospital (St. Joseph's), a hospital located in Tampa, Florida, and her birth weight was in excess of 2,500 grams. The physician providing obstetrical services during the birth of Sarah was Steven Ira Arkin, M.D., who was, at all time material hereto, a participating physician in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Mrs. Massey's antepartum course and Sarah's birth At the time of Sarah's birth, Mrs. Massey was 28 years of age, and Sarah was to be her first child. Her estimated date of confinement was established as March 20, 1993, and her pregnancy was uncomplicated. On March 13, 1993, Mrs. Massey started to experience contractions, and at or about 7:00 p.m. her membranes spontaneously ruptured. Following her physician's advice, Mrs. Massey presented to St. Joseph's Women's Hospital at or about 9:00 p.m. By 5:30 a.m., March 14, 1993, Mrs. Massey's cervix had dilated to four centimeters; however, she failed to progress and at approximately 8:00 a.m. Pitocin was started. Thereafter labor continued, but without progress, until 9:20 a.m., at which time Pitocin was discontinued and Dr. Arkin decided, for reasons hereafter discussed, to proceed with a caesarean section. Pertinent to this case, starting at 5:30 a.m., March 14, 1996, and extending until delivery, the fetal heart rate was monitored by fetal scalp electrode. Such monitoring revealed, overtime, repetitive variable and late decelerations; a reflection of fetal stress. Based on such indicia of fetal distress and Mrs. Massey's failure to progress, Dr. Arkin elected to proceed by caesarean section. Mrs. Massey was taken to the operating room at 9:30 a.m., anesthesia was started at 9:35 a.m., and surgery commenced at 9:56 a.m. At 10:01 a.m., Sarah was delivered. Upon delivery Sarah breathed spontaneously, and did not require resuscitation. The delivery record reveals no abnormalities observed at birth; however, Sarah was noted to have a temperature of 102.5 degrees. Her Apgar scores were noted as 8 at one minute and 9 at five minutes. Such scores are considered good or normal. 3/ Sarah was transferred to the well baby nursery at 10:20 a.m. where, upon admission she was noted to exhibit grunting and nasal flaring, as well as a continued pale color and poor lung exchange of air. By 10:50 a.m. Sarah's color had improved; however she continued to grunt intermittently. Considering Sarah's presentation, the initial concern was of infection, given the mother's and child's elevated temperatures at birth, as opposed to hypoxic insult. Consequently, Sarah was placed on a seven-day regimen of antibiotics as a precautionary measure. 12. During the 11:00 p.m. (March 15, 1996) to 7:00 a.m. (March 16, 1996) shift, Sarah exhibited some right-sided twitching consistent with seizure activity. Following such report, initial physical examination by her treating physician failed to observe any jitteriness; however, questionable eye deviation to the left was noted. Consequently, an electroencephalogram (EEG) and cranial ultrasound were ordered, and a neurologic consult was placed. The EEG of March 16, 1993, was abnormal, and demonstrated active electrical seizure activity in the left hemisphere. The cranial ultrasound of the same date likewise demonstrated an abnormality. That study found: . . . There is an echogenic, amorphous area located within the left basal ganglion region. . . . The findings are nonspecific, but given the presentation and age of the infant, a hemorrhage would be most likely. No germinal matrix, hemorrhage or abnormality is seen and no periventricular white matter abnormality is seen to suggest hypoxic/ ischemic brain injury. Of note, color Doppler ultrasound of the area was performed, and no abnormal vascularity to the echogenic area was seen. This would support a hemorrhage over a tumor . . . since no vascularity was seen. Still, computer tomography of the head is recommended to further evaluate this abnormality if appropriate. No other abnormalities are seen. The brain is structurally normal. The ventricles are normal in size. Conclusion: Amorphous, echogenic mass in the left lentiform nucleus and external capsule region which most likely represents an intracerebral hemorrhage. Computer tomography at some point is recommended. No other abnormalities are seen. No germinal matrix abnormality, ventricular enlargement, or evidence of hypoxic/ischemic injury to the periventricular white matter is seen. Sarah was transferred from the well baby nursery to the neonatal intensive care unit (NICU) at approximately 3:00 p.m., March 16, 1993. Following admission, a brain CT scan was ordered. The brain CT scan of March 16, 1993, revealed extensive low attenuation throughout the left cerebral hemisphere, including the basal ganglia, suggesting a large cerebrovascular accident (CVA). No significant midline shift was observed, and no hemorrhage was seen to correlate with the echogenic area observed on the ultrasound performed earlier that day. Neurologic consult was of the impression that Sarah had a seizure disorder, probably secondary to an intra-uterine CVA, and a mild right-sided hemiparesis. Sarah was begun on Phenobarbital and her seizures were well controlled. Following the seven day regimen of antibiotics heretofore noted, Sarah was believed stable, and on March 21, 1993, she was discharged to the care of her parents. The ultimate neurologic result of Sarah's intra- uterine CVA (stroke) was a mild right-sided hemiparesis, evidenced by spastic weakness primarily of her right arm; however, there is also some diminution of motor function in Sarah's right leg. As for her mental status, Sarah's mental functioning currently appears age appropriate and, although it cannot be conclusively stated at this juncture in her life, it appears more likely than not that she has not suffered any diminution of cognitive function. The timing and cause of Sarah's intra-uterine CVA Although the medical records indicate that during labor Sarah underwent fetal stress, as evidenced by fetal heart decelerations, the proof fails to support the conclusion that those events contributed to her neurological deficits. Rather, the proof, as demonstrated by Sarah's presentation at birth, relatively stable condition during hospitalization, and radiological studies, indicates that Sarah's neurological impairments derive from an intra-uterine stroke which significantly predated the onset of labor, as opposed to hypoxic insult during the course of labor or delivery. Apart from Sarah's presentation and progress during hospitalization, the radiological studies, done within two days of her birth, provide compelling proof as to the nature and timing of her injury. First, such studies do not demonstrate evidence of an acute brain injury which could have occurred during the course of labor and delivery. In this regard, it is observed that there was no evidence of edema (a condition of swelling which accompanies an acute brain injury) and no evidence of a recent (acute) hemorrhage (the presence of blood). Second, the area of diffuse low attenuation observed on radiologic study was most likely a presentation of dead or injured brain cells in the area of the hemorrhage which had undergone organic changes over time, and could properly be described as presenting in a chronic state (persisting over a long period of time), as opposed to acute. Finally, the focal nature of Sarah's brain injury, with resultant right-sided hemiparesis, is not generally associated with hypoxic insult. In this regard, it is noted that hypoxic insult generally evidences as a global injury to the brain, as opposed to the focal injury Sarah suffered, with a resultant effect, to varying degrees, on all neurologic function, as compared to the limited neurologic loss Sarah suffered. Given the record, the opinion of Michael Duchowny, M.D., a board certified pediatric neurologist associated with Miami Children's Hospital, that the cause of Sarah's brain injury and her ensuing neurologic impairment was an intra- uterine stroke, which predated labor by as much as one week, is credited as most consistent with the proof. Likewise credited, based on the consistency of his testimony with the proof of record, is Dr. Duchowny's opinion that Sarah's physical impairment can best be described as mild, as opposed to substantial, and that she evidences no loss of cognitive function.
The Issue At issue is whether Maxwell Hubmann, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts related to compensability Petitioners, Roger and Sara Hubmann, are the parents of Maxwell Hubmann, a minor. Maxwell was born a live infant on March 25, 2008, at Sacred Heart Hospital, a hospital located in Pensacola, Florida, and his birth weight exceeded 2,500 grams. Obstetrical services were delivered at Maxwell's birth by Brian Sontag, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by . . . 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. Here, the parties have stipulated, and the proof is otherwise compelling, that Maxwell suffered a traumatic brain injury during the delivery process. (Transcript, pp. 9 and 10; Respondent's Exhibits 1-4). What remains to resolve is whether such injury rendered Maxwell permanently and substantially mentally and physically impaired. To address the nature and significance of Maxwell's injury, NICA offered the affidavit and report of Michael Duchowny, M.D., a physician board-certified in pediatrics, neurology with special competence in child neurology, and clinical neurophysiology, who evaluated Maxwell on January 28, 2009. Based on his evaluation, as well as his review of the medical records, Dr. Duchowny was of the opinion that while Maxwell suffered a traumatic brain injury during delivery, his mental function was normal and his motor deficit was quite mild. In so concluding, Dr. Duchowny documented the results of his examination, as well as his conclusions, as follows: PHYSICAL EXAMINATION today reveals an alert, well-developed and cooperative, well- nourished 10-month-old infant. Maxwell weighs 24 pounds and is 30 inches in height. The skin is warm and moist. There are no neurocutaneous stigmata. The hair is blond and of normal texture. The spine is straight without dysraphism. The head circumference measures 46.1 centimeters which is within standard percentiles. The anterior and posterior fontanels are patent and flat. There are no cranial or facial anomalies or asymmetries. The tongue and palate are moist. The neck is supple without masses, thyromegaly or adenopathy. The cardiovascular, respiratory, and abdominal examinations are unremarkable. Maxwell's NEUROLOGICAL EXAMINATION reveals him to be alert, cooperative and fully attentive. He is quite sociable and maintains an age appropriate stream of attention. He has good central gaze fixation with conjugate following movements. The pupils are 3 mm and react briskly to direct and consensually presented light. Funduscopic examination revealed no abnormal retinal findings. There are no significant facial asymmetries of movement. The uvula is midline and the pharyngeal folds are symmetric. Tongue movements are full in all planes. Motor examination reveals an asymmetry of movement with relatively greater movement on the right side. The left upper extremity has mild stiffness but has full range of motor. There is fine motor dexterity of both hands but Maxwell demonstrates a right arm preference and will preferentially reach for an object with the right hand. When an object is moved to the left, he will ultimately offer the left and readily transfers between hands. He has symmetrical movement of both legs. He has well-developed traction and grasp responses and good head control for age. The deep tendon reflexes are slightly exaggerated being 3+ at the knees and biceps. There are no pathologic reflexes. Plantar responses are downgoing. He can stand and bear weight with good axial tone and support does not take steps independently. He has good sitting balance as well. Sensory examination is intact to withdrawal of all extremities to stimulation. Neurovascular examination reveals no cervical, cranial or ocular bruits and no temperature or pulse asymmetries. In SUMMARY, Maxwell's neurological examination reveals that his motor developmental milestones are on time despite a very mild asymmetry of movement and muscle tone in the upper extremities. He is preferentially a right hander due to the motoric asymmetry. In other respects, Maxwell's neurologic status is quite good and his overall level of mental functioning appears to be on target at age level. I have had an opportunity to fully review the medical records which were mailed on January 12, 2009. The records indicate that Maxwell's neurologic problems at birth were the result of mechanical injury acquired during the delivery process. However, he has made remarkable progress and his mental function is normal and his motor deficit is quite mild . . . . (Respondent's Exhibits 3 and 4). Here, the opinions of Dr. Duchowny were logical, consistent with the record, not controverted, and not shown to lack credibility. Consequently, it must be resolved that Maxwell's brain injury did not render him permanently and substantially mentally and physically impaired. See Thomas v. Salvation Army, 562 So. 2d 746, 749 (Fla. 1st DCA 1990)("In evaluating medical evidence, a judge of compensation claims may not reject uncontroverted medical testimony without a reasonable explanation.").
The Issue At issue in this proceeding is whether Jonathan Trujillo, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Jonathan Trujillo (Jonathan) is the natural son of Odalis Merida and Antonio Trujillo. He was born a live infant on December 31, 1993, at Jackson Memorial Hospital, a teaching hospital located in Miami, Dade County, Florida, and his birth weight was in excess of 2500 grams. The physicians providing obstetrical services during the birth of Jonathan were Doctors Oliva and McGare, resident physicians in an approved training program, who were supervised by Gene Burkett, M.D., a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan (the "Plan"). Consequently, each physician who provided obstetrical services during the birth of Jonathan was a "participating physician" in the Plan. Sections 766.302(7) and 766.314(4)(c), Florida Statutes. The birth of Jonathan Trujillo At or about 5:20 p.m., December 31, 1993, Odalis Merida (Ms. Merida) was admitted to Jackson Memorial Hospital in active labor. Notably, Ms. Merida's prenatal course had been complicated by the development of Class B gestational diabetes, requiring insulin during the course of her pregnancy, and the development of severe preeclampsia, characterized by hypertension. Consequently, Ms. Merida's pregnancy was rated high risk. To address Ms. Merida's diabetes during labor and delivery, she was maintained on drip insulin, and to address her hypertension, she was administered magnesium sulfate. Ms. Merida's condition and the substances administered to address her condition, although apparently necessary and appropriate, were not without risk or side effect to the fetus. Notably, magnesium sulfate is a muscle relaxant which can induce "floppiness" in a new born, as well as respiratory distress. 1/ The presence of maternal diabetes portends the risk of infantile hypoglycemia, which occurred in the instant case. A clinical symptom of hypoglycemia is "floppiness" in the new born, which may be exaggerated when, as here, it is found in conjunction with ploycythemia, discussed infra. Upon admission, Jonathan was at term, with a gestational age of 41 weeks, and fetal heart monitoring, commenced at or about 5:25 p.m., revealed good fetal heart tone. A physical examination at 6:00 p.m. noted the cervix to be at 7 centimeters, effacement complete, and the fetus at station 0. Contractions were regular at 2 minutes, and when the membrane was ruptured clear amniotic fluid was observed. Ms. Merida progressed through labor without incident until approximately 8:45 p.m., following the administration of an epidural anesthesia, when late decelerations of the fetal heart beat with bradycardia were noted, as a consequence of epidural hypertension. More specifically, Ms. Merida's blood pressure was observed to drop from a base line rate of 200/150 to 98/45, and a few late decelerations of the infant's heart rate were observed from a baseline rate of 120 to 130 beats per minute to 80 beats per minute. Ms. Merida was repositioned to her left side, the infant's heart rate promptly recovered, and no further unusual incidents were observed during the course of her labor or delivery. Given the limited duration and isolated nature of the late decelerations and bradycardia, it was the opinion of the physicians who testified in this proceeding that such anomaly did not adversely affect the infant's oxygenation or, stated differently, did not result in a hypoxic/ischemic insult to the infant's brain. Such opinions are credited. At 9:40 p.m., December 31, 1993, Ms. Merida, as she had with her first child, spontaneously delivered Jonathan vaginally, without apparent complication. Notably, Jonathan was vigorous on delivery, breathed spontaneously, did not require resuscitation, and his apgar scores were 9 at one minute, five minutes and ten minutes. In all, Jonathan's presentation was reflective of a healthy, vigorous infant. 2/ Jonathan was admitted to the newborn nursery at 10:00 p.m. Physical assessment upon admission revealed a large infant, at 4040 grams, with a large head (above the 90th percentile), who was crying spontaneously, alert, pink in color, but with a "slight floppiness" in the extremities. Jonathan was noted to breath spontaneously, without flaring or grunting; heart rate was noted at 160 beats per minute, with regular rhythm; fontanel were soft and flat; and reflexes were present. In brief, Jonathan's presentation in the newborn nursery was that of a healthy, vigorous infant, with the only negative observation being a "slight floppiness" in his extremities. Such "floppiness" was, however, more likely than not, related to the magnesium sulfate administered to Ms. Merida during labor and delivery, the hypoglycemia Jonathan was subsequently diagnosed to have acquired, or a combination of the two, and does not detract from the conclusion that Jonathan had no apparent signs of distress at birth. Later in the day, following testing, Jonathan was diagnosed with moderate to severe hypoglycemia, polycythemia, and moderate thrombocytopenia. Such conditions, singularly, or in combination, placed the infant at risk. Hypoglycemia, low blood sugar, may place the infant at risk of seizures and, pertinent to this case, resultant brain hemorrhage. Here, the moderate to severe hypoglycemia that Jonathan suffered was apparently recurrent, although it did resolve over time, and was addressed each time it presented through the administration of glucose. Polycythemia is a disorder whereby the number of red blood cells are abnormally high, making the blood thicker (hyperviscous) than normal. Apparently, brain hemorrhage is often related to decreased blood flow on the venus side of the brain, and where the blood is hyperviscous it could help or contribute to a brain hemorrhage. Here, with a hematocrit of 64, Jonathan's condition met the definition of polycythemia, which is a hematocrit over 60; however, such condition was not, or was not shown to be, significant in the instant case. Thrombocytopenia is a disorder resulting in an abnormally low platelet count which could affect clotting and therefore predispose the infant to bleeding through, among other things, trauma. Here, Jonathan's thrombocytopenia, more likely than not isoimmune thrombocytopenia, was considered moderate, as opposed to severe, and serial testing reported his platelet count as follows for the date and time indicated: DATE TIME 3/ PLATELET COUNT 1/1/94 07:00 Platelet estimate 40,000-80,000 1/2/94 03:47 Platelet estimate 80,000-100,000 1/3/94 07:57 Platelet estimate 40,000-80,000 1/3/94 15:08 Platelet estimate 40,000-80,000 1/4/94 05:04 Platelet count 49,000 1/5/94 06:46 Platelet estimate 40,000-80,000 1/6/94 12:50 Platelet estimate 40,000-80,000 1/8/94 21:12 Platelet count 182,000 1/10/94 03:52 Platelet count 263,000 1/12/94 06:00 Platelet count 357,000 The normal platelet count for newborns, as with adults, is 150,000 to 400,000, and, as may be observed from the serial testing, Jonathan's thrombocytopenia resolved over time. While at risk, Jonathan's neonatal course in the nursery was uneventful until 26 hours of life when he was noted to have suffered a generalized seizure characterized by cyanosis, severe bradycardia (heart beat in the range of 40 beats per minute), and respiratory arrest (apnea), requiring intubation. At or about 1:00 a.m., January 1, 1994, Jonathan was transferred to the neonatal intensive care unit, where he was maintained on positive ventilation until approximately January 6, 1994. Examination, through EEG's and CT and MRI scans of the brain, revealed that Jonathan had suffered an intraventricular hemorrhage, Grade IV, characterized by a massive bleed, with dilation of the ventricles. 4/ Thereafter residual hypodensity of the white matter of the brain was observed, consistent with degeneration of the hemorrhage and, ultimately, hypodensity compatable with evolving encephalomalacia (swelling of the brain.) Subsequently, on February 2, 1994, developing hydrocephalus required the placement of an intraventricular shunt to relieve intracranial pressure. Currently, in the opinions of Dr. Robert Roth and Dr. Michael Duchowny, whose opinions are credited, Jonathan is permanently and substantially mentally and physically impaired. Such impairment is evidenced by, inter alia, cortical blindness, hypotonia and, more likely than not, mental retardation. It is further the opinion of such physicians, which is again credited, that the cause of Jonathan's neurologic impairment is the injury to the brain he suffered as a consequence of the Grade IV intraventricular hemorrhage. Given the foregoing, resolution of this claim resolves itself to an identification of the genesis of Jonathan's Grade IV intraventricular hemorrhage or, stated otherwise, whether the proof demonstrates, more likely than not, that the hemorrhage, which resulted in injury to Jonathan's brain and the ensuing neurological injuries, resulted from "oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period" in the hospital. Sections 766.302(2) and 766.309(1)(a), Florida Statutes. The cause of Jonathan's Grade IV intraventricular hemorrhage A Grade IV intraventricular hemorrhage in a term infant, such as Jonathan, is a rare occurrence, and its cause frequently cannot be identified. Notwithstanding, Jonathan did suffer such a hemorrhage, and he was shown to suffer from two conditions, isoimmune thrombocytopenia and hypoglycemia, which could offer some explanation for the hemorrhage. Here, petitioner contends that Jonathan, due to his large head, received an injury to his brain occasioned by the "mechanical" forces of labor and delivery, and that such injury resulted in a slow bleed which, because of his thrombocytopenia, progressed over the next 26 hours and ultimately manifested as a generalized seizure characterized by cyanosis, severe bradycardia and respiratory arrest. In support of such contention, petitioner offered the testimony of Robert S. Roth, M.D., a physician board certified in pediatrics and neonatal/perinatal medicine. Pertinent to this case, Dr. Roth observed that infants born with thrombocytopenia are at increased risk of suffering an intraventricular brain hemorrhage if subjected to the trauma occasioned by the mechanical forces of labor and vaginal delivery. In his opinion, Jonathan's medical records reveal a classic case of neonatal brain hemorrhage resulting from the mechanical forces of labor and vaginal delivery that occurred because of Jonathan's large head and thrombocytopenia. Those conditions, affected by the forces of labor and delivery, combined to "start the process of hemorrhage in the brain," resulting in "tissue changes and cell death and vascular pressure changes" over time, and culminating when it progressed to the "centers that control breathing," manifested by apnea or seizure- like activity that led to apnea. Notably, it was Dr. Roth's opinion that it was not Jonathan's large head alone or his thrombocytopenia alone, apparently because of its moderate nature, which occasioned the initial bleed and resulting hemorrhage but, rather, the two conditions acting in consort. There was, however, no injury to Jonathan's scalp or skull noted at delivery, nor any molding of his head consequent to the delivery. It is of further note, in evaluating Dr. Roth's opinion, that he also observed that, had Jonathan been delivered by cesarean section before the onset of labor, he would have had a "lower probability" of having a hemorrhage than had he undergone active labor and vaginal delivery. Such observation clearly implies that factors other than labor and delivery could have operated to induce Jonathan's hemorrhage. Finally, in considering Dr. Roth's opinion of progressive deterioration, it is worthy of note that, apart from the "slight floppiness" observed shortly after birth, Jonathan evidenced no symptoms of neurologic injury until 26 hours of life. As heretofore noted, the "slight floppiness" exhibited by Jonathan was reasonably attributed to the magnesium sulfate administered to Ms. Merida during labor and delivery, the hypoglycemia Jonathan was shown to have developed, or a combination of the two, as opposed to a symptom of neurologic injury. Consequently, there is no objective evidence or symptom, that one would otherwise expect to observe, to support Dr. Roth's opinion of progressive deterioration. Contrasted with the opinions of Dr. Roth, regarding the genesis of Jonathan's hemorrhage, are the opinions offered on behalf of NICA through Michael S. Duchowny, M.D., a physician board certified in pediatric neurology. Dr. Duchowny, although acknowledging that thrombocytopenia offered an increased risk of intraventricular hemorrhage to an infant through the forces of labor and delivery, was of the opinion that Jonathan's hemorrhage at 26 hours of life was a spontaneous event, unrelated to labor and delivery, and that the cause of that hemorrhage could not be identified with any reasonable degree of medical certainty or, stated differently, that any attempt to attribute a cause for Jonathan's hemorrhage was, at best, speculative. 5/ In reaching his conclusion, Dr. Duchowny observed that there was no objective evidence or symptom of trauma or oxygen deprivation at birth, as one would expect had there been a neurologic insult during the course of labor and delivery, and that there was likewise no objective evidence or symptom of neurologic injury over the course of Jonathan's first 26 hours of life, as one would expect to observe were he suffering a progressive disorder, as opined by Dr. Roth. Dr. Duchowny was further of the opinion that, although moderately thrombocytopenic, Jonathan's platelet count was not sufficiently low, a level he described as 20,000 or less, to increase the likelihood that Jonathan would suffer a bleed. Resolving the conflict between the opinions of Doctors Roth and Duchowny is not an easy or lightly undertaken effort. Each physician is eminently qualified and the genuineness of the opinions they expressed is apparent. The seriousness of the resolution is further intensified by the obvious needs of a severely impaired infant; however, while such needs are significant, it cannot be overlooked that where, as here, responsibility for the care of the infant is sought to be imposed on the Plan, the proof must be compelling that, more likely than not, the infant suffered a "birth-related neurological injury" as defined by law. In this case, the proof falls short of meeting such standard. 6/ As heretofore noted, the labor and delivery of Jonathan was essentially normal and there was no obstetrical incident or identifiable event during labor and delivery that would evidence that he had suffered a hypoxic insult, mechanical injury or traumatic event. Indeed, although Jonathan did have a large head (above the 90th percentile), there was no cephalopelvic disproportion noted, no arrest of labor, no protracted labor, and no use of forceps or vacuum extraction in delivery. Upon delivery, no apparent cranial injuries were observed, no molding of the head was noted, and Jonathan presented as a vigorous infant with normal Apgars. In summary, there was no identifiable incident during the course of labor or delivery, or thereafter during Jonathan's first 26 hours of life, evidencing oxygen deprivation, mechanical injury, or other insult, that would account for the hemorrhage he suffered. In reaching the foregoing conclusion, it has not been overlooked that an infant suffering from thrombocytopenia is at increased risk of intraventricular hemorrhage through the forces of labor and delivery. Here, however, it was not suggested or shown that Jonathan's mild thrombocytopenia would, itself, foster a hemorrhage of the nature he suffered, rather petitioner's proof suggested that his large head and thrombocytopenic condition combined, when subjected to the trauma of labor and delivery, to precipitate a bleed that slowly progressed to a Grade IV intraventricular hemorrhage or precipitated a seizure that resulted in such a hemorrhage. Given the nature of the proffer, there being no apparent complication during labor and delivery, no objective sign of head trauma at birth, no symptoms of neurologic insult at birth, and no symptom of neurologic insult over the 26 hours prior to Jonathan's acute compromise, it must be concluded, as suggested by Dr. Duchowny, that any conclusion timing the genesis of Jonathan's hemorrhage to the events of labor and delivery is not supported by reasonable medical probability but is, at best, speculative. Consequently, it must be concluded, that petitioners have failed to demonstrate that Jonathan's hemorrhage was related to trauma, oxygen deprivation or mechanical injury occurring during the course of labor and delivery, as opposed to a spontaneous event, of unknown origin, occurring at Jonathan's twenty-sixth hour of life. 7/
The Issue At issue is whether Robert Donald Vose, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts Dawn Vose is the parent of Robert Donald Vose, a minor. Robert was born a live infant on August 15, 2001, at Baptist Hospital, Pensacola, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Robert's birth was Jill Prafke, M.D., who, at all times material hereto, was a "participating physician" in the 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. To resolve whether Robert suffered a "birth-related neurological injury," the parties offered the medical records related to Robert's birth and subsequent development (Respondent's Exhibit 3), as well as the opinions of Donald C. Willis, M.D., a physician who practices maternal-fetal medicine, and Michael Duchowny, M.D., a physician board-certified in pediatrics, neurology with special competence in child neurology, and clinical neurophysiology. (Respondent's Exhibits 1 and 2). With regard to injury, Dr. Willis was of the opinion that Robert suffered a brain injury (a venous sinus thrombosis and choroid plexus hemorrhage) at or around the time of delivery, that resulted in the development of hydrocephalus. However, he offered no opinion regarding the extent or significance of the brain damage. (Respondent's Exhibit 2). In contrast, Dr. Duchowny evaluated Robert on May 4, 2006, and concluded that his "normal neurological status together with a review of the accompanying medical records does not suggest that he has a substantial mental or motor impairment," as required for coverage under the Plan. (Respondent's Exhibit 1). Dr. Duchowny reported the results of his evaluation, and the basis for his opinion, as follows: I had the pleasure of evaluating Bobby Vose on May 4, 2006. Bobby is a 4-year-old, left-handed, prekindergarten student who was brought by his father for evaluation. This was conducted in my office at Miami Children's Hospital. HISTORY ACCORDING TO THE FATHER: Mr. Vose explained that Bobby was brought in order to "verify his abilities for NICA." He believes that Bobby is developing normally and in fact, is above average in several areas. He will be starting kindergarten in September and has done extremely well in his prekindergarten class setting. In fact, his language abilities are above average for age and he is bilingual with approximately 70 words of Spanish. He is a sociable boy who plays well with other children and his motor milestones have progressed normally. He sleeps through the night. His vision and hearing are intact. There has been no regression and no toxic or infectious exposure. Bobby is on no intercurrent medications. Bobby's PAST MEDICAL HISTORY is significant for placement of a ventriculoperitoneal shunt as a newborn. He apparently experienced an intercranial hemorrhage into the right ventricle and had a shunt placed from the anterior horn of the right ventricle into the peritoneal cavity. His shunt has functioned well and there have been no complications or revisions . . . . Otherwise, Bobby enjoys good health. He is not being followed for any chronic illnesses and has not required medical or surgical intervention subsequent to the newborn period. PERINATAL HISTORY: Bobby was born at Baptist Hospital in Pensacola at 37-weeks gestation. There was an attempt at a vaginal delivery but "the head was wedged" and Bobby was ultimately delivered by emergency cesarean section. He weighed 8 pounds and breathed well at birth. He remained in the hospital for approximately 11 days. GROWTH AND DEVELOPMENT: Bobby's father could not recall Bobby's motor or language milestones except to note that all occurred at the normal time. Bobby is fully immunized and has no known drug allergies. He has had a hernia repaired. * * * PHYSICAL EXAMINATION reveals an alert, well- developed, pleasant and cooperative 4-year- old boy. Bobby weighs 38 pounds. The skin is warm and moist. Bobby's head circumference measures 51.9 centimeters, which is within standard percentiles for age. The fontanels are closed. The ventriculoperitoneal shunt reservoir is palpated over the right frontal bone and shunt tubing is noted in the right anterior lateral neck region and across the thorax and abdomen. There is a healed right, upper quadrant abdominal scar. There are no cranial or facial anomalies or asymmetries. No dysmorphic features or cutaneous stigmata are noted. The neck is supple without masses, thyromegaly or adenopathy. The lung fields are clear and the heart sounds are normal. There is no palpable abdominal organomegaly. Peripheral pulses are 2+ and symmetric. NEUROLOGICAL EXAMINATION likewise discloses no significant findings. Bobby is alert, pleasant and cooperative. He answers all questions fluently with a good fund of information and an age appropriate stream of both thought and attention. He cooperated with all aspects of the evaluation. The cranial nerve examination reveals full visual fields to direct confrontation testing and normal ocular fundi. The optic disc margins are clearly demarcated and there is no optic pallor. There are no significant retinal findings. The extraocular movements are full and conjugate. The pupils are 3 mm and react briskly to direct and consensually presented light. There is blink to threat from both directions. The tongue is moist and papillated and moves well in all plains. The uvula is midline. The pharyngeal folds are symmetric. 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+ throughout. Plantar responses are downgoing. Station and gait are appropriate for age. The arm swing is symmetric. Sensory examination is intact to withdrawal of all extremities to stimulation. Neurovascular examination reveals no cervical, cranial, or ocular bruits and no temperature or pulse asymmetries. In SUMMARY, Bobby's neurological examination in detail reveals no significant focal or lateralizing findings. The ventriculoperitoneal shunt is likely to be nonfunctional at this point. Bobby's normal neurological status together with a review of the accompanying medical records does not suggest that he has a substantial mental or motor impairment. . . . I, therefore, do not believe that he is eligible for compensation under the NICA statute.
