The Issue At issue is whether Maritza Rios, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Petitioners, Hilda Rios and Jaime Rios, are the parents and natural guardians of Maritza Rios, a minor. Maritza was born a live infant on October 10, 2005, at Winter Haven Hospital, Inc., d/b/a Regency Medical Center, a licensed Florida hospital located in Winter Haven, Florida, and her birth weight exceeded 2,500 grams. Obstetrical services were delivered at Maritza's birth by Vincent W. Gatto, 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. "Notice pursuant to § 766.316, Fla. Stat., was properly given or excused, and is not an issue in this case." Maritza suffered an injury to the brain, caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in the hospital, which rendered her permanently and substantially physically impaired. The only remaining issue is whether such injury also rendered Maritza permanently and substantially mentally impaired. Findings related to Maritza's injury and her impairment At NICA's request, Donald Willis, M.D., an obstetrician/gynecologist, reviewed the medical records related to Maritza's birth and newborn course, and concluded that Maritza suffered an injury to the brain caused by oxygen deprivation occurring in the course of labor, delivery, and the immediately postdelivery period. Dr. Willis summarized the basis for his conclusion, as follows: I have reviewed the medical records for the above individual. The mother, Hilda Rios, was a 29 year old G4 P2103 with her first baby born by Cesarean section and then two vaginal births. Prenatal care was uncomplicated. She presented at 38 weeks with spontaneous rupture of the membranes. Vaginal birth after Cesarean section was planned. The fetal heart rate pattern had a normal baseline heart rate and was reactive on admission [to Winter Haven Hospital]. Some occasional variable decelerations were present since early in labor. About 45 minutes before delivery the patient had moderate vaginal bleeding and severe variable decelerations that continued until delivery. Cesarean section was done for the abnormal FHR pattern. A uterine rupture was documented at surgery. The fetal head was in the maternal abdomen and the placenta was completely separated from the uterus. No cord blood could be obtained due to the abruption. Birth weight was 3,329 grams or 7 lbs 5 ozs. The newborn was floppy, depressed and had no respiratory effort. [Apgar scores were noted as 1, 5, and 7, at one, five, and ten minutes respectively.] Bag and mask ventilation was done until the heart rate was >100 bpm. There was still no respiratory effort and intubation was required. The baby was taken to the NICU intubated and with depressed muscle tone. Initially, the baby did well, but shortly after birth, an attempt to take the baby off the ventilator failed. The baby became acidotic and hypoxic. Seizure activity was suspected based on facial grimacing. EEG was normal. Re-intubation was required. The baby remained on the ventilator for six days. Ultrasound of the head on the day after birth was normal. MRI . . . [showed abnormal signal within the thalami and basal ganglia] suspicious of hypoxic insult. A follow up MRI at 10 months of age was normal. Genetic evaluation was done and was normal. * * * In Summary, labor was complicated by a uterine rupture due to a prior Cesarean section. The baby was expelled into the maternal abdominal cavity and the placenta separated from the uterus. This event resulted in oxygen deprivation to the baby during labor, delivery and into the immediate post delivery period with resulting brain injury. I am not able to comment as to the extent of the brain injury. (Joint Exhibit 7). To address the nature and significance of Maritza's injury, the parties also offered the report and deposition testimony of Raymond Fernandez, M.D., a pediatric neurologist who, at NICA's request, evaluated Maritza on November 12, 2008, when she was a 3-year 1-month old infant. (Joint Exhibits 6 and 10). Based on his evaluation, review of the medical records, and the history he obtained from Maritza's parents, Dr. Fernandez, like Dr. Willis, was of the opinion that Maritza suffered a brain injury (within the thalami and basal ganglia) due to oxygen deprivation during labor and delivery, secondary to uterine rupture. As for the significance of her injury, Dr. Fernandez was of the opinion that Maritza's brain injury rendered her permanently and substantially physically impaired, but not permanently and substantially mentally impaired. Pertinent to Maritza's impairments, Dr. Fernandez documented the results of his evaluation, and Maritza's medical history following her discharge from Winter Haven Hospital on October 23, 2005, in his report, as follows: An independent medical examination was performed on 3-year 1-month-old Maritza Rios on November 12, 2008, at the request of Ms. Kathe Alexander, Florida Birth-Related Neurological Injury Compensation Association. Maritza was accompanied by her parents, Mr. and Mrs. Rios. * * * Maritza was referred to a pediatric neurologist on August 1, 2006, age 10 months, because of motor delay. She was not sitting or crawling. She had strabismus and was referred for physical therapy and occupational therapy. Brain MRI on August 21, 2006, reportedly was normal. Also normal were amino acids, organic acids, chromosomes, acylcarnitine profile, and testing for Angelman syndrome was negative. The next visit to pediatric neurology was on September 26, 2006, age 11 months. She was unable to sit, had mild tightness of heel cords, stood with support on her tiptoes, rolled over and said mama and papa. Plantar responses were extensor. On December 19, 2006, age 14 months, personal-social development was on target, fine motor development was at the 10 to 11 month age, language 14 months, and gross motor development 7 months. It was stated that lactate and ammonia were elevated. Muscle biopsy showed congenital fiber type disproportion but no details were given and nonspecific Z-band streaming on electron microscopy. [On March 15, 2007, at] 17 months of age, [a Speech-Language and Oral Motor Evaluation noted] auditory comprehension was at the 14- month level, and expressive communication was at the 9-month level. [The evaluation characterized Maritza's receptive language skills as within normal limits [WNL] and her expressive language skills as mildly to moderately delayed. Speech therapy, at 30 minutes twice weekly for 6 months was recommended.3] At 1 year and 11 months of age, gross and fine motor development was said to be at the 12-month level. Mr. and Mrs. Rios stated that Maritza was generally healthy. They have not observed seizures. They feel that she understands what is said to her at an age-appropriate level and that she interacts well with her sisters. Speech, while initially delayed, has improved significantly over the past 2 to 3 months. She now speaks numerous single words, phrases and sentences, mainly in Spanish. She sits independently but with a rounded back and with her head often deviated to 1 side or the other and sometimes flexed onto her chest. Head control is improving. She ambulates by bouncing on her knees. She pulls to stand, takes 2 or 3 independent steps and then falls if not supported. She began doing this about 2 months ago. Maritza has been enrolled in a physical therapy program and will begin an early learning program in public school in January of 2009. PHYSICAL EXAMINATION: Weight approximately 32 pounds. Pulse rate 92. Respiratory rate 20. Head circumference 48.5 cm (just below the 50th percentile). Maritza was alert and attentive. She was socially engaging. She smiled responsively and extended her hand to me when I greeted her. She told me her first name and age when asked. She told me her sisters' names. She also said in Spanish that "I don't want to walk because I cannot." Speech at times was indistinct [dysarthric4] but I was usually able to understand her. She identified 2 colors correctly, counted to 3 correctly, then skipped 4 and then counted from 5 to 8. She sang the alphabet song, although not completely. She pointed to most body parts correctly. She counted my fingers up to 3 correctly, then again skipped 4 and resumed counting at 5. Maritza was visually attentive and maintained good eye contact. Pupils were equal and reactive to light. Eyes were straight and moved fully. There was no ptosis. Face was symmetric. Hearing was grossly normal. Palate elevated symmetrically. Tongue midline. She swallowed well. There was no drooling. Muscle tone was reduced axially and in her limbs. She sat independently but with a rounded back, and her head was either flexed forward or deviated to either side. She pulled to stand with difficulty and took 2 unsteady steps, and then would have fallen if not supported. There was truncal instability. There was no obvious weakness of extremities in that she easily elevated her arms above her head and elevated her legs when on her mother's lap. Also, she supported her weight when standing but was unsteady, and I believe this is what would have caused her to fall rather than weakness of her legs. She reached with either hand with tremor and with some writhing movements of her arms distally. Deep tendon reflexes were 1+ in the arms, knees and ankles. Plantar responses were probably flexor. ENT exam was normal as were heart, lungs, and abdomen. There were no dysmorphic features or significant skin abnormalities. Maritza stacked three 1-inch cubes, although with difficulty because of her motor incoordination. She attempted to draw circles but had difficulty because of tremor. She handed objects to either parent correctly when asked to do so, and she also placed objects on the examining table next to her on request so that she understood these verbal requests. She correctly named pictures of animals and correctly described a picture of ducks and stated in Spanish that they were walking. IMPRESSION: Motor impairment that is substantial and consistent with deep brain injury (with basal ganglia) due to oxygen deprivation during labor and delivery, secondary to uterine rupture. However, I do not find evidence for substantial cognitive impairment at this time. Please note that Maritza might eventually prove to have learning difficulty, but this cannot be predicted based on current findings. She is improving, and this trend should continue. (Emphasis added). (Joint Exhibit 6). In his deposition testimony, Dr. Fernandez contrasted the history he obtained and the results of his examination of Maritza, with what he would expect to find if she were substantially mentally impaired, as follows: Well, a child with substantial cognitive mental impairment is a child who is not interactive, who is not attentive, who doesn't comprehend or understand spoken language, receptive language. A child that cannot carry out verbal requests because they don't understand what they are being asked to do. A child who might not speak at all. A child who doesn't understand, for example, prepositional commands to give something to that person, to give something to the mother, to the father, put something on the table. A child that cannot understand that. A child who has not learned and remembered colors at the age of three years. That's a three-year-old function. A child who cannot remember the shapes of symbols like circles. That's a three-year-old function, to know what a circle looks like and to draw it, or try to draw it in Maritza's case. She had trouble because of the motor problem that she has, but she made a definite attempt to make that circle. There are the things that a child with substantial mental cognitive impairment are not going to be able to do . . . . (Joint Exhibit 10, p. 116). In contrast, Dr. Fernandez was of the opinion that, by history and on evaluation, Maritza interacted at an age appropriate level, by conversing, understanding and following verbal requests; demonstrated expressive and receptive language skills at an age appropriate level; and had the ability to learn and be educated. In response to the observations and opinions of Dr. Fernandez, Intervenors offered the deposition testimony of Mr. and Mrs. Rios, as well as the deposition testimony of Elias Chalhub, M.D., a pediatric neurologist, to support a conclusion that Maritza was permanently and substantially mentally impaired. (Joint Exhibits 8, 9, and 11). However, such testimony was not compelling. From the testimony of Mr. and Mrs. Rios one learns that Maritza does not know her numbers, or can count only to 2; Maritza does not know the alphabet; Maritza knows only 3-5 words, but says more than 10; that six months earlier Maritza spoke only 1 word; Maritza does not speak in sentences; Maritza cannot converse; Maritza does not understand her parents; Maritza does not understand the television shows she watches (but, she watches in English, and speaks only Spanish); and Maritza does not understand stories her parents may read to her (but, they rarely read to her). However, Mr. and Mrs. Rios' testimony conflicts dramatically with the history they provided Dr. Fernandez, as well as Dr. Fernandez's personal and professional observations, and no credible explanation was offered to explain such discrepancy. From Dr. Chalhub we learn that in his opinion Maritza is permanently and substantially mentally impaired. However, Dr. Chalhub did not examine Maritza, and in reaching his opinion, Dr. Chalhub accepted, as true, the testimony of Mr. and Mrs. Rios regarding Maritza's presentation, and rejected or ignored the observations of Dr. Fernandez, without a persuasive explanation. Notably, the observations and opinions of Dr. Fernandez were logical, consistent with the record, and not shown to lack credibility. In contrast, the testimony of Mr. and Mrs. Rios, as well as Dr. Chalhub, was not compelling. Accordingly, it is resolved that, more likely than not, Maritza is not permanently and substantially mentally impaired.
The Issue At issue is whether Noah Taber (Noah), a minor, suffered a "birth-related neurological injury," as defined by Section 766.302(2), Florida Statutes.1
Findings Of Fact Preliminary findings Dawn Tabor and Britt Tabor, are the parents and natural guardians of Noah Tabor, a minor. Noah was born a live infant on June 19, 1999, at Largo Medical Center, a hospital located in Largo, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Noah's birth was Ivelisse Ruiz-Robles, 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. Noah's presentation On April 23, 2002, following the filing of the claim for compensation, Noah was examined by Michael S. Duchowny, M.D., a pediatric neurologist associated with Miami Children's Hospital, Miami, Florida. Dr. Duchowny reported the results of his neurological evaluation, as follows: Noah's PHYSICAL EXAMINATION reveals Noah to be an alert, extremely active youngster. He weighs 25-pounds. The hair is blond and of normal texture. The head circumference measures 43.3 cm, which is several standard deviations below age level and median for age 5-month males. He has frequent tongue thrusting movements and drooling. There are no dysmorphic features and no cutaneous stigmata. The spine is straight. There is a small nevus flambeaus. The neck is supple without masses, thyromegaly or adenopathy. The cardiovascular, respiratory and abdominal examinations are normal. Noah's NEUROLOGIC EXAMINATION reveals a small child with a short attention span and high activity level. Noah is difficult to control and has poor social skills. He did not articulate words during the evaluation. Noah tends to engage in simple games and there is no evidence of overtly aggressive behavior. He will perform very simple commands. Noah would not identify body parts for me. Noah's MOTOR EXAMINATION reveals generalized hypotonia in all extremities, with a slight dynamic increase of tone on the right. He has exaggerated range of motion on the left side, with normal range of motion on the right. There is no evidence of spasticity. Noah demonstrates a clear left hand preference and will grasp with both hands on the right. He can clearly use the right hand to manipulate objects and transfer to the left. There is also diminished arm swing on the right side, compared to the left. His overall movement is clearly more fluid on the left side of his body. He has bilateral pes planus and there is no clear asymmetry of gait with regard to the lower extremities. Muscle bulk is symmetric throughout. The deep tendon reflexes are bilaterally brisk at 3+ and both plantar responses are in extension. He walks in a straightforward manner and turns crisply. He would not cooperate for formal finger-to-nose or heel- to-shin testing. A sensory examination is grossly intact to withdrawal all extremities to touch. The cardiovascular examination reveals no cervical, cranial, or ocular bruits and no temperature or pulse asymmetries. An AFO is appreciated over the right ankle. In SUMMARY, Noah's neurologic examination is significant for microcephaly and a prominent cognitive impairment. In contrast, his motor deficit is much less severe and it appears to be improving steadily. I am not sure that he needs an AFO, as he has good range of motion. Noah also suffers from epilepsy. Following his examination, Dr. Duchowny had the opportunity to review Noah's medical records and concluded that: Although Noah has a substantial mental impairment, his motor abilities are only mildly behind age level and I suspect that he will continue to improve over the next several years. For this reason, I do not believe that Noah is eligible for compensation under the Florida NICA statute. 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 a "injury to the brain . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." Section 766.302(2), Florida Statutes. See also Section 766.309(1)(a), Florida Statutes. Here, the medical records and the results of Dr. Duchowny's neurological evaluation demonstrate Noah suffered an injury to the brain caused by oxygen deprivation in the course of labor, delivery, or resuscitation in the immediate post- delivery period that rendered him permanently and substantially mentally impaired; however, physically, he was not similarly affected or, stated otherwise, he was not rendered permanently and substantially physically impaired.
The Issue Whether Deidre Denson has suffered an injury for which compensation should be awarded under the Florida Birth- Related Neurological Injury Compensation Plan, as alleged in the claim for compensation.
Findings Of Fact Preliminary matters Deidre Denson (Deidre) is the natural daughter of David and Linda Denson. She was born a live infant on October 8, 1991, at Bayfront Medical Center in St. Petersburg, Pinellas County, Florida, and her birth weight was in excess of 2500 grams. The physicians providing obstetrical services during the birth of Deidre were David Moreland, M.D., and Donna Miller, M.D., who were, at all times material hereto, participating physicians in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. The birth of Deidre Denson At or about 12:30 a.m., October 8, 1991, Linda Denson presented to Bayfront Medical Center, upon advice of her physician, following the spontaneous rupture of her membrane. At the time, Linda Denson was in active labor and Deidre, who was at term, was in a breach presentation. At approximately 1:09 a.m., Mrs. Denson was admitted to the labor room, and thick meconium was observed upon examination. External fetal monitoring was commenced, which initially reflected a fetal heart rate in the 80-90 beat per minute range; however, at or about 1:12 a.m., and continuing until approximately 1:18 a.m., the fetal heart rate was observed to fluctuate between the 80-90 rate and 60 beats per minute. This situation evidenced fetal distress and an urgent need for surgical intervention. Accordingly, at approximately 1:18 a.m. Mrs. Denson was taken to the operating room. Mrs. Denson was admitted to the operating room at 1:23 a.m., and Deidre was delivered by a cesarean section surgical procedure at 1:35 a.m. Upon delivery, Deidre's physical appearance was observed to be "blue" and her heart rate was below 30 beats per minute. Delivery room resuscitation included intubation, with suctioning of meconium below the vocal cords four times, and bagging with 100 percent oxygen. Spontaneous respirations were not observed in the infant until thirty minutes after birth, when they were noted as "slow" and continued to be noted as "slow" until 2:12 a.m. when she was transferred to the neonatal intensive care unit at All Children's Hospital. At birth, Deidre's Apgar scores at one, five and 10 minutes were one, four and five respectively. These scores are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of the heart rate, muscle tone, respiratory effort, color, and reflex irritability, with each category being assigned a score ranging from the lowest score of zero through a maximum score of two. As noted, at one minute, Deidre's Apgar score totaled one, with heart rate being graded at one ("slow, below 100"), and muscle tone, respiratory effort, color and reflex irritability being graded at zero. At five minutes, Deidre's Apgar score totaled four, with heart rate and color being graded at two each, respiratory effort being graded at one ("slow, irregular"), and muscle tone and reflex irritability being graded at zero each. At 10 minutes, Deidre's Apgar score totaled five, with heart rate and color again being graded at two each, and muscle tone, respiratory effort and reflex irritability being graded at one each. Such scores are consistent with Deidre having suffered a severe hypoxic insult (deprivation of oxygen) at birth. At approximately 2:25 a.m., October 8, 1991, Deidre was admitted to the neonatal intensive care unit at All Children's Hospital, and was placed on a ventilator until four days of age and remained with an endotracheal tube until six days of age. At 1:45 p.m., Deidre was observed to have developed seizure activity, secondary to perinatal depression, and an electroencephalogram (EEG) was ordered. That EEG was read as an "abnormal ictal EEG recording," and is consistent with diffuse cerebral disfunction. Dr. Kenneth Sassower, a pediatric neurologist, performed a consult on Deidre on October 8, 1991, and observed that the "differential diagnosis of neonatal seizures at this early age include fetal hypoxia; metabolic abnormalities . . . intracranial hemorrhage . . .; meningitis, etc." He recommended a cranial ultrasound, a "CT scan of the head without contrast, pending stable clinical status," a repeat EEG study, and certain other testing procedures designed to identify the cause of Deidre's seizure activity. The cranial ultrasound was taken on October 9, 1991, and was read as normal in that it failed to reflect any hemorrhage in or around the ventricles and did not reflect any displacement of the ventricles. Such findings do not, however, rule out the possibility that a bleed/intracranial hemorrhage existed in the frontal area, since such would not be picked up on ultrasound. Rather, a CT scan of the head without contrast would have been the preferred and more reliable testing procedure; however, due to the fragile nature of the infant's condition, ultrasound was employed as the first test to discern the presence of cerebral blood. As discussed infra, the first CT scan was performed December 3, 1991, after Deidre's discharge from All Children's Hospital, and evidenced a bleed in the frontal area. Other testing procedures ruled out metabolic abnormalities and meningitis as causative factors for Deidre's seizures. As with the EEG taken October 8, 1991, serial EEG's taken October 9, 14 and 23, 1991, were also read as abnormal and "indicative of diffuse cerebral dysfunction with bifocal dysfunction over both central regions." The proximity of Deidre's seizure activity to birth, and the abnormal EEGs, are consistent with diffuse brain injury as a consequence of hypoxic insult at birth. Given the absence of any other identifiable factor, it is found that Deidre's seizure activity was directly attributable to birth asphyxia. 1/ In addition to the foregoing abnormalities, Deidre was also diagnosed as suffering hypotension due to mycardial insufficiency, as well as renal (kidney) and liver damage, due to perinatal depression, and on neurologic consult to exhibit "evidence of generalized hypotonia and hyporeflexia." Such observations are consistent with hypoxic insult at birth. Deidre's condition was, however, managed and she was discharged from All Children's Hospital to the care of her parents on October 24, 1991. Currently, Deidre is, indisputedly, permanently and substantially mentally and physically impaired. Considering its quality, the proof is compelling that Deidre suffered a severe hypoxic insult at birth and that as a consequence of such oxygen deprivation suffered an injury to her brain which adversely impacted her mentally and physically. Notwithstanding, respondent, Florida Birth- Related Neurological Injury Compensation Association (NICA), contends that the seriousness of Deidre's current neurological deficit is not a product of the hypoxic insult she suffered at birth but, rather, was occasioned by head trauma suffered after her discharge from All Children's Hospital. For the reasons that follow, NICA's position is rejected, and it is found, based on the more compelling proof, that Deidre sustained an injury to the brain caused by oxygen deprivation in the course of labor, delivery or resuscitation in the immediate post-delivery period that rendered her permanently and substantially mentally and physically impaired. Events subsequent to Deidre's discharge from All Children's Hospital Following Deidre's discharge from All Children's Hospital, she was next neurologically examined by Dr. Kenneth Sassower on November 26, 1991. On examination, Dr. Sassower observed evidence of a mild to moderate spastic diparesis and hyperreflexia in the lower extremities, but noted that Deidre was currently seizure free on phenobarbital monotherapy without undue behavioral side effects noted. Based on his observations, Dr. Sassower proposed a reevaluation of Deidre in three to four months. 2/ On December 3, 1991, Deidre presented for a CT Scan of the brain without enhancement at the radiology department of All Children's Hospital. Such CT scan was an apparent follow-up to a recommendation made by Dr. Sassower when he examined Deidre on October 8, 1991, to address the cause of Deidre's seizure activity. [Petitioners' exhibits 16 and 18] The attending radiologist reported: Findings: As compared to the sonogram on 10-9-91, the frontal horns now seem slightly distended. This is seen in association with chronic bilateral subdural hematomas. There is also evidence of prominent sulci and cisterns with underlying leukomalacia. This is most pronounced in the frontal lobes. The 3rd and 4th ventricle are also slightly distended . . . No intracranial calcifications. The mastoid air cells are well aerated bilaterally. The anterior and posterior fontanelles are small for the patient's age. Otherwise, normal calvarial contour. IMPRESSION: 1. Status post development of bilateral subdural hematomas and brain atrophy with predominant frontal leukomalacia. This raises a question of intervening trauma. Recommend clinical correlation. Consequently, the radiologist telephoned Dr. Sassower at 10:15 a.m., December 3, 1991, and arranged for a neurological examination of Deidre at 12:00 p.m. Deidre was indeed examined by Dr. Sassower on December 3, 1991. During the course of that examination he concluded: . . . The CT scan reveals evidence of prominent cortical atrophy, along with what appears to be a suggestion of semi-acute bifrontal subdural hematomas. The exact extent of subdural blood is somewhat difficult to assess due to the presence of increased hypolucencies which at times appear continuous with areas of relative cortical atrophy. * * * During the course of the clinical examination, both parents deny any known recent head trauma, either accidental or otherwise. Both parents, who appear extremely reliable, have now reported leaving their child in the company of other caretakers since discharge from the nursery. I think in spite of the fact that both parents appear to be appropriately concerned, one needs to exercise a good deal of caution in this regard, and pursue careful clinical surveillance over the course of the ensuing weeks. In this regard, a repeat neurologic follow-up in 4-6 weeks time is suggested. A subdural hematoma, as observed in Deidre, is a collection of blood which has accumulated in the space between the dura matter, a thickened membrane which covers the brain, and the surface of the other membranes which cover the brain. Their presence raises the possibility that any existent brain damage may have been caused or exacerbated by trauma or the subdural hematoma itself. Notably, the trauma which tears the subdural veins and creates the subdural hematoma may be of sufficient force itself to cause brain damage or the hematoma itself may be of sufficient magnitude to compress the brain and cause brain damage. About 99 percent of subdural hematomas are due to trauma, which causes the veins crossing the subdural space into the dural sinuses to tear and thereby bleed. The other one percent of observed subdural hematomas are due to rare causes such as bleeding disorders. Under the circumstances, the presence of a subdural hematoma in Deidre certainly raised the possibility of secondary brain damage due to trauma or abuse. Here, the proof demonstrates that the subdural hematomas reflected by the CT scan of December 3, 1991, may be characterized as "chronic," and so defined, reflect a hematoma that had its genesis more than two weeks prior to its discovery. As for Deidre's hematomas, her neurosurgeon, whose opinion is credited, dates their occurance at two to four weeks prior to the CT scan of December 3, 1991. 3/ Regarding the cause of Deidre's subdural hematomas, the proof is, at best, unsatisfying. Deidre's birth was by cesarean section and therefore no mechanical maneuver or device, such as a vacuum extractor, forceps or a forced vaginal delivery, was utilized which could cause trauma. Moreover, the medical records are devoid of any indication of trauma to Deidre's head during delivery or the term of her hospitalization. Such does not, of course, completely rule of the possibility that trauma was induced during resuscitation efforts or at some other time in the hospital, but any such conclusion, absent a CT scan or other definitive testing during her admission, would be speculative. On the other hand, Deidre received routine follow-up after discharge by her pediatricians and Dr. Sassower, and they observed no evidence of trauma or abuse to Deidre, and a physical and ophthalmology consult revealed none. The absence of such physical evidence does not completely rule out the possibility of trauma or abuse, but its absence coupled with the ophthalmology consult and the reliability and character of the parents, as well as the other sole caregiver, renders it extremely unlikely that the subdural hematomas were a consequence of abuse or trauma suffered following Deidre's discharge from the hospital. The only other explanation offered at hearing for Deidre's subdural hematomas, other than a blood disorder which was ruled out, were the opinions offered by her physicians and experts, who suggested that because of the brain atrophy and the resultant shrinkage of the brain suffered as a consequence of the hypoxic insult at birth, the bridging veins which cross the subdural space into the dural sinuses were stressed and introduced a bleed, causing the hematomas. Given the conclusion that trauma or abuse was not the cause of Deidre's hematomas, and the elimination of a blood disorder as a possible cause, such opinions, based on the proof in this case, are the most likely explanation of Deidre's bleed, which resulted in the hematomas disclosed by the December 3, 1991 scan. Finally, the absence of any compelling proof to demonstrate that Deidre's hematomas were induced by trauma, and the absence of any compelling proof that the chronic subdural hematomas were of sufficient magnitude and existed for a sufficient period of time to compress the brain and cause significant brain damage, absent trauma, it is concluded that the atropy evidenced by the CT scan of December 3, 1991, was more likely than not, a product of the hypoxic insult that Deidre suffered at birth, and that such hypoxic insult rendered her substantially and permanently mentally and physically impaired. 4/
The Issue Whether Eman Mustafa, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan). If so, whether the hospital and the participating physician gave the patient notice, as contemplated by Section 766.316, Florida Statutes, or whether any failure to give notice was excused because the patient had an "emergency medical condition," as defined by Section 395.002(9)(b), Florida Statutes, or the giving of notice was not practicable.
Findings Of Fact Stipulated facts Shiren Mustafa and Nehad Mustafa are the natural parents and guardians of Eman Mustafa, a minor. Eman was born a live infant on February 22, 2002, at University Community Hospital, a hospital located in Tampa, Florida, and her birth weight exceeded 2,500 grams. The physician providing obstetrical services at Eman's birth was Caryn L. Bray, 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. Eman's birth and immediate postnatal course At or about 8:00 p.m., February 21, 2002, Mrs. Mustafa, with an estimated delivery date of February 15, 2002, and the fetus at 40 6/7 weeks' gestation, was admitted to University Community Hospital, for induction of labor, and proposed vaginal birth, after prior cesarean section (VBAC). At the time, Mrs. Mustafa's membranes were intact; irregular contractions were noted; vaginal examination revealed the cervix closed, effacement at 60-70 percent, and the fetus at station -2; and fetal monitoring revealed a reassuring fetal heart rate, with a baseline in the 130-beat per minute range. At 9:00 p.m., Cervidil was placed to soften the cervix overnight, and by 7:15 a.m., February 22, 2002, vaginal examination revealed the cervix at 1-2 centimeters dilation, effacement at 90 percent, and the fetus at station -1. Cervidil was removed; at 7:40 a.m., the membranes spontaneously ruptured, with clear fluid noted; and Pitocin was started to augment labor. Fetal monitoring contained to reveal a reassuring fetal heart rate. Mrs. Mustafa's labor rapidly progressed and by 8:30 a.m., vaginal examination revealed the cervix at 5 centimeters,3 effacement complete and the fetus at station 0, and by 9:30 a.m., vaginal examination revealed complete dilation and effacement, and the fetus at station +2. Late decelerations were also noted at 9:30 a.m., but fetal heart rate was otherwise reassuring. Dr. Bray was paged at 9:32 a.m., and returned the page at 9:39 a.m. At the time, Dr. Bray was notified of Mrs. Mustafa's status and requested that the patient start pushing. However, due to the low station of the fetus, staff requested Dr. Bray's presence for pushing, and Dr. Bray stated she would be bedside in approximately 10 minutes. Thereafter, at 9:58 a.m., further decels were noted, and Pitocin was stopped. At 9:59 a.m., Dr. Bray was noted at bedside, oxygen was applied, fluid bolus started, and fetal heart rate decels to 60 beats per minute were documented. Thereafter, at 10:03 a.m., Mrs. Mustafa was pushing, complaining of pain when abdomen palpated, and fetal heart rate in the 50-beat per minute range was noted. Then, at 10:07 a.m., fetal heart rate in the 50s was noted, with brief accelerations to the 110-beat per minute range, and Dr. Bray requested a Kiwi vacuum. At 10:09 a.m., Kiwi vacuum-assisted delivery, with patient pushing, proved unsuccessful, and fetal heart rate was noted in the 110-beat per minute range, with deceleration back to the 60-beat per minute range. At 10:11 a.m., Dr. Bray requested fundal pressure, with patient pushing, but again Kiwi vacuum-assisted delivery was unsuccessful, despite three attempts. Medela vacuum was called for and at 10:17 a.m., two attempts at delivery with the Medela vacuum and fundal pressure proved unsuccessful. Then, at 10:19 a.m., with fetal heart rate remaining in the 60-beat per minute range, a stat cesarean section was called for non-reassuring fetal heart rate and suspected uterine rupture. At 10:22 a.m., Mrs. Mustafa was taken to the operating room, where she was admitted at 10:25 a.m.; surgery started at 10:30 a.m., at which time uterine rupture was confirmed; and Eman was delivered at 10:32 a.m., with Apgar scores of 1, 3, and 6, at one, five, and ten minutes respectively.4 According to the medical records, Eman required resuscitation at birth, with tracheal intubation, IPPV, and cardiac massage, and was then transferred to the neonatal intensive care unit (NICA), where she developed spontaneous respirations, and within two to three hours was weaned from the ventilator. Eman's subsequent newborn course was without incident or evidence of residual effects of birth trauma, and she was discharged with her mother on February 25, 2002. Eman's Discharge Summary included the following observations: PHYSICAL EXAMINATION: A term female infant, weight 3329 grams, length 51 cm, and hip circumference 32 cm. Temperature 97.3, heart rate 158, respiratory rate 62, blood pressure 51/48. HEENT: Normocephalic. Eyes examined at discharge: Pupils were reactive and the red reflex seen. No nasal flaring. Neck supple. Lungs: No retractions. Good air entry. Heart regular rate and rhythm. No murmur. Abdomen soft, no masses, three-vessel cord. Genitalia: Female. Extremities: Moving all limbs, hips stable. No rashes. Neurological: Good tone. INITIAL IMPRESSION: Term female infant. Perinatal depression. Maternal uterine rupture. Respiratory distress. At once (STAT) cesarean section. INITIAL TREATMENT: NICU admission. Pulse oximetry monitoring. Conventional mechanical ventilation. Nothing by mouth. Intravenous fluids. Sepsis workup. Antibiotics. Chest x-ray. PROGRESS: Respiratory: The infant was extubated and weaned to room air within approximately two to three hours of admission. Initial chest x-ray was not significant. Rule out sepsis: The infant was treated with antibiotics; namely, ampicillin and gentamicin for 48 hours. These were discontinued when the cultures remained negative. Fluids and electrolytes: On admission, the infant was given early intravenous fluids, approximately 24 to 48 hours enteral feeds were begun and increased progressively. At the present time the infant is breastfeeding only. She is voiding well, passing stools. Neurological: The infant has good tone and good reflexes, no clonus, and appears to be neurologically normal. SUMMARY: This is a term female infant who was delivered after having maternal uterine rupture. The infant did require neonatal resuscitation but recovered very quickly. At the present time the infant is doing well and feeding well. FINAL DIAGNOSIS: Term female infant. Cesarean section. Perinatal depression. Rule out sepsis. Respiratory distress. Eman's subsequent development Eman's early development was apparently without significant concern until approximately 19 months of age, when she was referred by her pediatrician (Issaam Albanna, M.D.) to Jose Ferreira, M.D., a physician board-certified in neurophysiology and neurology with special qualification in child neurology, for evaluation concerning "some gait disturbance with falling and some coordination problems." Pertinent to this case, Dr. Ferreira reported the results of his initial evaluation of October 6, 2003, as follows: I had the pleasure of seeing Eman for initial evaluation today accompanied by her mother and aunt. The main concern is some gait disturbance with falling and some coordination problems. They report that she started walking somewhat late at 14-15 months and was doing better initially and then seems to be falling more frequently recently and will walk on her toes at times. There is also some deficits with the coordination where she seems to be "clumsy" at times, hands "clinched" frequently and her muscles "give out" on her apparently more frequently then expected for age. She has been developing speech with about 5 words at this point. She tends to drool frequently She is potty training currently as she starts to talk with 5-6 words vocabulary . . . . PAST MEDICAL HISTORY: She was born at full term pregnancy. Birth weight was 7 lb 8 ounces. There was some traumatic delivery as she describes it with uterine rupture and labor requiring a stat cesarean section. She went home with her mother. There was no other problems noted initially. * * * GENERAL PHYSICAL EXAMINATION: HC: 45 cm (5th percentile) WT: 23 lb HR: 90 and regular. HEENT: Unremarkable. Normocephalic. . . . The extremities have full range of motion with no edema, deformities or joint tenderness. The midline back shows no midline defects and no point tenderness to percussion. The skin shows no neurocutaneous findings of significance and there was no dysmorphic features. NEUROLOGICAL EXAMINATION: Shows she was alert. She was initially showing significant stranger anxiety and then was more comfortable with the examiner as the interview took place. She was able to follow some simple commands from her mother. She did not say any words during the examination. The cranial nerve examination revealed full extraocular movements and visual fields full to confrontation. The pupils were equal and reactive. The funduscopic exam showed bilateral red reflex. The face is symmetric and the tongue midline with no fasciculations. There was some degree of drooling noted. Her motor exam shows she had no focal weakness. There is no significant increased resistance to pass of motion other than possibly the right upper extremities. She tended to maintain her hands fisted with some cortical thumbs at times specially when she walked. The gait shows she was somewhat stooped forward to a mild degree but otherwise wide based appropriate for age. She tended to fall occasionally. There was no asymmetry of the use of her extremities otherwise except that she tended to hold the right arm more flexed and the right hand more frequently closed and pronated. The deep tendon reflexes showed 2+. There is no sustained ankle clonus. The plantar responses were extensor bilaterally. Gait and coordination showed there was no tremors and no ataxia [failure of musculature coordination]5 of significance other than the tendency to fall which was somewhat limited coordination. The plantar responses were extensor bilaterally. IMPRESSION: 1. Gait disturbance associated with a mild degree of incoordination with her age with some mild upper motor neuron dysfunction signs as described above in the neurological examination. * * * RECOMMENDATIONS: She will have an MRI of the brain without contrast. She will have a metabolic screening including serum amino acids, ammonia levels, thyroid functions studies, total carnitine levels, ammonia and lactate and CPK levels. She will be seen for follow up here in approximately one and a half to two months or earlier if there is any acute changes. Physical and occupational therapy may be recommended at this point . . . . (Petitioners' Exhibit 2). Eman was reevaluated by Dr. Ferreira on December 15, 2003, and he reported the results of that visit, as follows: I had the pleasure of seeing Eman for follow up today accompanied by her parents. As you know, she has a history of difficulties with her gait and some developmental delay and coordination difficulties. She had an MRI of the brain, which was normal with the exception of some sinusitis. She also had a metabolic screen and had elevated T4[,] and T3 and TSH was normal. She continues having difficulties with her gait and coordination. She has had some drooling at times. Her speech has been somewhat delayed and she has approximately 10-15 word vocabulary but difficult to understand and does not show any signs to suggest regression. She has been sleeping and eating well. * * * HEENT: Unremarkable. . . . The extremities had full range of motion and no edema. NEUROLOGICAL EXAMINATION: She was alert and friendly. She was cooperative. Cranial nerve exam revealed full extraocular movements and visual fields grossly full to confrontation. The pupils are equal and reactive. The funduscopic exam shows bilateral red reflex. The face is symmetric and the tongue was midline with no fasciculations. The motor exams shows she had some difficulties with fine motor coordination. She did not have a good pincer grasp and she tended to keep her hands mostly in a pronated position and somewhat flexed at the elbow and especially when she walked. Her muscle tone was minimally increased in all extremities. Deep tendon reflexes were 2+/2+. The plantar responses were extensor bilaterally. Her gait was minimally spastic with a slightly wide base. She tended to walk somewhat stood forward to a mild degree. When she was sitting she also had some mild degree of truncal ataxia. IMPRESSION: History of developmental disorder with mild speech and language delay as well as some drooling. Mild degree of spasticity with gait disturbance. There is history of sinusitis. RECOMMENDATIONS: As her MRI did not show any intracranial pathology an EEG will be done to evaluate for any encephalopathic changes. She was referred to occupational, speech and physical therapy. The thyroid function (T4 was mildly elevated) will be repeated. She will be seen for follow up here in three to four months or earlier if there is any acute changes . . . . (Petitioners' Exhibit 2). Eman was last evaluated by Dr. Ferreira on February 11, 2004, and he reported the results of that visit, as follows: I had the pleasure of seeing Eman for follow up today accompanied by her parents for a history of gait disturbance with some developmental delay and coordination difficulties. She had an EEG done today which showed a mild abnormality with the right occipital rhythm being slightly lower voltage than the left. The EEG was otherwise normal. She is now in physical, occupational and speech therapy. This just started so it is difficult to say whether or not improvement has been noted. Her parents feel however that she has improved. She is learning new words and her parents feel that she is steadily showing improvement. She is falling still but is moving around better than she has previously. They also feel her drooling has improved. She is eating and sleeping well and they have no new concerns today. * * * HEENT: Unremarkable. . . . Extremities had full range of motion. NEUROLOGICAL EXAMINATION: She is awake and alert. She is very cooperative and friendly. She was speaking at times and was smiling. Cranial nerve and motor exams were unchanged from the last evaluation. Her pincer grasp was still not as good as expected for her age and she tended to keep her hands pronated when walking. Her muscle tone was still mildly increased. Deep tendon reflexes were 2+ and she was walking with a slightly wide based gait for age. She was sitting without assistance for short periods of time today but continued with a mild degree of truncal ataxia. RECOMMENDATIONS: The thyroid panel will be repeated as it was requested at the last visit but unable to be completed.[6] She will continue in the therapies . . . . (Petitioners' Exhibit 2). According to Dr. Ferreira, as of the last time he saw Eman (February 11, 2004) she was still showing some neurologic deficits, which he described as a mild degree of spasticity (increased muscle tone), with gait disturbance; mild upper motor dysfunction, with a less than age-appropriate pincer grasp and tendency to pronate her hands when walking; and a mild speech and language delay. (See Dr. Ferreira's reports of December 15, 2003, and February 11, 2004, supra, and Petitioners' Exhibit 2, pages 15-21, 28-32, and 42). As for permanency, Dr. Ferreira declined (given the limited contact he had with Eman) to offer an opinion regarding the significance of any dysfunction that might persist. Moreover, Dr. Ferreira, who was not familiar with Eman's birth records or those medical records that predated his evaluation of October 6, 2003, offered no opinion, within a reasonable degree of medical certainty, as to the likely etiology of Eman's neurologic defects (i.e., whether they resulted from brain injury caused by oxygen deprivation or mechanical injury occurring during labor delivery or resuscitation, or another etiology) or whether Eman suffered any mental impairment. Subsequent neurologic evaluations On February 23, 2005, Eman was, at NICA's request, evaluated by Michael Duchowny, M.D., a pediatric neurologist associated with Miami Children's Hospital. Dr. Duchowny reported the results of his evaluation, as follows: PRE-AND PERINATAL HISTORY: Eman was born in Tampa at University Hospital after a full term gestation. Her birth weight was 7 pounds 9 ounces, and she remained in the nursery for three days. Eman walked at eighteen months and said single words at two years. She is just beginning toilet training. She is fully immunized and has no known allergies. She has never undergone surgery and has not been hospitalized after birth. PHYSICAL EXAMINATION reveals an alert, well- developed and well-nourished, cooperative 3- year-old girl. Eman weighs 36 pounds and is 45 inches tall. The skin is warm and moist. There are no neurocutaneous stigmata . . . The spine is straight. The head circumference measures 45.8 centimeters, which is below the 3rd percentile for age. There are no cranial or facial anomalies or asymmetries. The neck is supple without masses, thyromegaly or adenopathy. The cardiovascular examination is unremarkable, and the lung fields are clear. There is no palpable abdominal organomegaly. Peripheral pulses are 2+ and symmetric. Eman's NEUROLOGIC EXAMINATION reveals her to be socially interactive and cooperative. She has a good attention span and is quite inquisitive. She smiles frequently. She is able to understand commands and completes them very clearly. She is quite interactive playing games. She knows body parts. She is behaviorally intact. Cranial nerve examinations reveal full visual fields to confrontation testing. The pupils are 3mm and briskly reactive to direct and consensually presented light. There are full and conjugate extraocular movements. Funduscopic examination is unremarkable with well-defined optic disc margins. There are no significant facial asymmetries. The tongue movements are poorly coordinated. Drooling is noted intermittently. Motor examination reveals static hypotonia with a mild increase in tone in all extremities. There are no contractures and there is full range of motion in all joints. The gait is complex with the left heel being slightly elevated with a mild degree of circumduction at the hips and internal rotation at the ankles. Deep tendon reflexes are 1+ in the upper extremities, 3+ at the knees, and 1+ at the ankles. Plantar responses are downgoing. 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. (Petitioners' Exhibit 3). Based on his neurologic evaluation and review of the medical records, Dr. Duchowny was of the opinion that Eman's impairments were most likely developmentally based (the product of atypical brain development), as opposed to birth trauma (brain injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery or resuscitation). In so concluding, Dr. Duchowny noted that following delivery, Eman's hospital course was inconsistent with traumatic brain damage (there being an absence of significant prolonged respiratory depression, an absence of systemic organ involvement, and an absence of seizure activity), and her MRI scan of November 13, 2003, was normal. Dr. Duchowny also noted that Eman's presentation on February 23, 2005, with a pattern of immature muscle control and expressive language delay, was typical of children with developmental disabilities, as opposed to disabilities associated with birth trauma. Finally, Dr. Duchowny was of the opinion that Eman's expressive language delay was mild to moderate, and her motor disability was moderate, as opposed to substantial, and that her condition was likely to improve with time. (Petitioners' Exhibit 4; Respondent's Exhibit 1). Subsequently, on March 11, 2005, Eman was, at University Community Hospital's request, evaluated by S. Parrish Winesett, M.D. a physician board-certified in pediatrics and neurology with special qualification in child neurology. Dr. Winesett reported the results of his evaluation, as follows: PHYSICAL EXAMINATION: General: Shows a young lady who is alert, who is quite interactive. She smiles easily. She has no obvious dysmorphic features. She has normally placed eyes, ears, nose, philtrum and mouth. Her mental status is that she said single words during my exam. I did not really hear her say sentences. She was rather quiet for the most part. She seemed to follow directions well. Cranial nerve exam showed her pupils were equal and responsive to light. She seemed to have full visual fields. Her extraocular eye movements were intact. Range of motion in all directions was full. Face was symmetrical with good facial movements in both the upper and lower face. Tongue was midline without any fasiculations. Palate raised symmetrically. She shrugged her shoulders will. Motor exam seemed to show that she was strong in all four extremities. I could not get her to fully resist me and give her full effort in trying to resist me, but she did seem to be fairly strong in what resistance I could elicit. She does not seem to have any obvious atrophy of the muscles. She seemed to have normal tone and bulk. In particular, I did not detect any asymmetry of tone nor did I detect any hypertonia. Reflexes in the upper extremities were normal in the biceps, brachial radialis and triceps. In the lower extremities, she did not have any pathologic increase in reflexes, but her patella and ankle reflexes were brisk. Her motor coordination showed that in reaching with both hands, she seemed to be somewhat jerky and has a very slow approach in reaching for my tape measure. She did not seem to be particularly adept at pushing the buttons and pulling the tape as I would expect a child of three to be. She seemed to be very slow. Finger tapping also seemed to be slow and somewhat labored. She did not diminish her amplitude as she tapped. Sensation was not extensively tested, but she did seem to acknowledge being touched in all four extremities in a normal fashion. Her gait was clearly abnormal. Her hands while sitting never showed any adduction of the thumbs within the palms. When she walked, she immediately assumed a posture in which she pulled her arms close to her side, bent her elbows and brought her thumbs within her palm. This was seen each time she started to walk. She did not circumduct her legs but instead seemed to drag her lower extremities and have an almost slapping motion of her feet as she pulled her legs forward. She did not particularly scissor while she was walking. She did not space out her gait while she was walking. * * * Review of the medical records provided to me of both the child, as well as the mother . . . showed the following. The child was born on February 22, 2002 as the product of a 41 week pregnancy. There was an attempted vaginal birth after previous C-section. At approximately 10:02, the fetal heart rate was noticed to be decelerating. The obstetrician was called at that time. The child had heart deceleration during this period that was noted in the nurses notes to be down in the 50's and noted in the physician's notes to be in the 70's. The child was then taken to the operating room where the child was born at approximately 10:32. The child, at that time, was handed over to the neonatal resuscitation team who started resuscitation effort and gave the child Apgar scores of 1, 3 and 6 at 1, 5 and 10 minutes. The patient had been intubated by the 3rd Apgar score. The child was taken back to the NICU where at 10:45, a blood gas was performed which showed a pH of 7.31, a PC02 of 22 and a base excess of -18. The child recovered quite quickly and was extubated in approximately two hours. Review of the operating notes showed that there was reported 200 to 300 cc of blood in the uterus and that there was a uterine rupture noted by the physicians at the operation. The child was discharged from the NICU on February 25, 2002 with the neurological exam reported to be normal. The child has subsequently been seen by Dr. Jose Ferriera for the same complaints that they presented to me with. He has done an MRI which was read as normal by the Tampa Children's Hospital radiologist. Thyroid function tests were ordered and showed a mild elevation of T4. . . . A speech therapy evaluation including the Rossetti Infant Toddler Language Scale showed that she scored at the 15 month range at the age of 23 months for her speech skills. There was apparently some splintering of the scoring but mostly within the 15 to 18 month range. An auditory comprehension subtest, she scores at 23 months which is normal. She is also noted to have some oral motor speech difficulties. Physical and occupational therapy evaluations were reviewed but not as significantly to the data. IMPRESSION: Eman is a young lady who is presenting with predominantly problems in gait disturbance, as well as speech problems. Many of her speech problems could be related to problems in the coordination of her speech. There is a mild increase in reflexes in the lower extremities; however, it does not appear to be a significant degree of hypertonia. Overall, this child appears to have predominant problems with dyscoordination. This is not a typical presentation for a neonatal hypoxic ischemic encephalopathy syndrome. In addition, the fact that the child recovered so quickly and was extubated within two hours and was discharged within two days makes it highly unlikely that the hypoxia suffered at birth is the cause of the neurologic syndrome. (Petitioners' Exhibit 3). Based on his neurologic evaluation and review of the medical records, Dr. Winesett was of the opinion that, while of unknown etiology, it was unlikely Eman's neurologic problems were related to birth trauma. Dr. Winesett also described Eman's motor difficulties as moderate, as opposed to substantial, and offered no opinion regarding her cognitive function. (Petitioner's Exhibit 3, pages 18, 19, 22-26, and 36). Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired."7 § 766.302(2), Fla. Stat. See also §§ 766.309(1) and 766.31(1), Fla. Stat. The etiology and significance of Eman's impairments Here, among the physicians who have examined Eman, and who were particularly qualified to address the etiology and significance of her impairments, none concluded that Eman's impairments most likely resulted from brain injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitating in the immediate postdelivery period in the hospital, or that Eman was permanently and substantially mentally and physically impaired. See, e.g., Wausau Insurance Company v. Tillman, 765 So. 2d 123, 124 (Fla. 1st DCA 2000)("Because of the medical conditions which the claimant alleged had resulted from the workplace incident were not readily observable, he was obliged to present expert medical evidence establishing that causal connection."); Ackley v. General Parcel Service, 646 So. 2d 242 (Fla. 1st DCA 1995)(determining cause of psychiatric illness is essentially a medical question, requiring expert medical evidence); Thomas v. Salvation Army, 562 So. 2d 746, 749 (Fla. 1st DCA 1990)("In evaluating medical evidence, a judge of compensation claims may not reject uncontroverted medical testimony without a reasonable explanation."). Therefore, the proof fails to support the conclusion that Eman suffered a "birth-related neurological injury," as required for coverage under the Plan. The notice provisions of the Plan Given that Eman did not suffer an injury compensable under the Plan, it is unnecessary to address whether the healthcare providers complied with the notice provisions of the Plan. See, e.g., Galen of Florida, Inc. v. Braniff, 696 So. 2d 308, 309 (Fla. 1997)("[A]s a condition precedent to invoking the Florida Birth-Related Neurological Injury Compensation Plan as a patient's exclusive remedy, healthcare providers must, when practicable, give their obstetrical patients notice of their participation in the plan a reasonable time prior to delivery."); O'Leary v. Florida Birth-Related Neurological Injury Compensation Association, 757 So. 2d 624, 627 (Fla. 5th DCA 2000)("We recognize that lack of proper notice does not affect a claimant's ability to obtain compensation from the Plan. However, a healthprovider who disputes a plaintiff's assertion of inadequate notice is raising the issue of whether a claim can only be compensated under the plan.").
The Issue At issue in this proceeding is whether Andrew Fullerton, 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 Maureen Fullerton and James Fullerton are the parents and natural guardians of Andrew Fullerton (Andrew), a minor. Andrew was born a live infant on June 10, 1995, at Tallahassee Memorial Regional Medical Center, a hospital located in Tallahassee, Florida, and his birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Andrew was David O'Bryan, 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. Coverage under the Plan Pertinent to this case, coverage is afforded under the Plan when the claimant demonstrates, more likely than not, that the infant suffered 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 renders the infant permanently and substantially mentally and physically impaired." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Here, Andrew's neurologic condition is dispositive of the claim and it is unnecessary to address the timing or cause of his condition. Andrew's neurologic status On November 2, 1998, following the filing of the claim for compensation, Andrew was examined by Michael Duchowny, M.D., a board-certified pediatric neurologist. The results of Dr. Duchowny's examination were reported as follows: PHYSICAL EXAMINATION reveals a well developed, but shy 3 year old boy. The weight is 37-pounds and height 40-inches. The skin is warm and moist without neurocutaneous stigmata. There are no digital, skeletal or palmar abnormalities. The head circumference measure 52.3 cm, which is at the 70th percentile for age. There are no cranial or facial anomalies or asymmetries. The hair is blonde and of normal texture. The neck is supple without masses, thyromegaly or adenopathy. The cardiovascular, respiratory and abdominal examinations are normal. Andrew's NEUROLOGIC EXAMINATION reveals him to be immature and shy. His speech seemed reasonably fluent and well articulated. He can answer questions with a verbal content that was appropriate for age. There is good central gaze fixation with conjugate following movements. The pupillary light responses are intact to direct and consentually presented light. The pupillary diameter was 2 to 3 mm. A fundoscopic examination was brief, but disclosed no obvious abnormalities. Motor examination revealed symmetric strength, bulk and tone. There were no adventitious movements and no focal weakness or atrophy. The arm swing is symmetric with his gait and his stance is relatively narrow based. He has good individual finger dexterity. He tends to manipulate objects with both hands and with thumb/finger opposition bimanually. There was no tiptoe walking or plantar grade attitude was noted. Deep tendon reflexes were 1 to 2+ bilaterally with flexor plantar responses. The sensory examination is deferred. Andrew holds his outstretched hands with appropriate posturing. Neurovascular examination revealed no cervical, cranial or ocular bruits. There are no temperature or pulse asymmetries. In SUMMARY, Andrew's neurologic examination reveals evidence of immature socialization skills and a borderline delay in linguistic functioning. He has seizures by history and these are well controlled. There is also a history of mood swings and impulsivity, but it is difficult to be certain that at least some of his symptoms are not secondary to phenobarbital administration. I have had an opportunity to review the medical records on Andrew. His past medical history and present evaluation indicate that Andrew does not have a substantial motor or mental impairment. . . . In Dr. Duchowny's opinion, which is credited, Andrew is not currently substantially mentally and physically impaired and, notwithstanding any events which may have occurred at birth, is not likely to be so impaired in the future.
The Issue Whether Hunter Lewis, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Petitioners, Angel Lewis and Jerry Lewis, are the parents and natural guardians of Hunter Lewis, a minor. Hunter was born a live infant on June 2, 2000, at Tallahassee Memorial Hospital, a hospital located in Tallahassee, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Hunter's birth was Arthur S. Clements, 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.1 Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. The cause and timing, as well as the significance of Hunter's neurologic impairment To address the cause and timing of Hunter's neurologic impairment, as well as its significance, Petitioners offered selected medical records relating to Hunter's birth and subsequent development (Petitioners' Exhibit 1); the Verified Medical Opinion of Richard J. Inwood, M.D., a neonatologist (Petitioners' Exhibit 2); and the deposition of Donald C. Willis, M.D., an obstetrician (Petitioners' Exhibit 3). In turn, Respondent offered the deposition of Paul R. Carney, M.D., a pediatric neurologist (Respondent's Exhibit 1). As for the significance of Hunter's impairments, it was Dr. Carney's opinion, based on the results of his neurologic evaluation of November 21, 2002, that Hunter's assessment "indicates substantial cognitive and language impairment," but "very mild long tract neurological findings." Dr. Carney described Hunter's developmental delay as static, as opposed to progressive, and he ventured no opinion as to the cause or timing of Hunter's impairments. As for Dr. Inwood, he was of the opinion that: . . . Hunter Lewis [ ] was delivered by induced labor prior to 38 weeks and had immature lungs. Because of the immaturity of the lungs he suffered hypoxic insult and, to a reasonable degree of medical probability, sustained significant neurological injury. This injury would not have occurred had his delivery been delayed until he had demonstrated lung maturity. His problems are not congenital and did not occur during labor or delivery, but rather after delivery . . . . Notably, Dr. Inwood did not further address Hunter's neurologic injury or, stated otherwise, did not speak to whether in his opinion, Hunter suffered both cognitive and motor impairment and, if so, the significance of each. As for Dr. Willis, he was of the opinion that the medical records revealed no evidence of oxygen deprivation or other trauma associated with labor, delivery, or resuscitation immediately following Hunter's birth. Significantly, the medical records are consistent with the opinions of Doctors Inwood and Willis that the cause and timing of Hunter's impairment was not associated with labor, delivery, or resuscitation, and with the opinion of Dr. Carney that, while Hunter may demonstrate substantial cognitive delay, his motor impairment is mild. Given the record, it must be concluded that the proof demonstrated, more likely than not, that Hunter's impairments were not occasioned by an injury to the brain caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital, and that he is not permanently and substantially physically impaired.
The Issue At issue in this proceeding is whether Susan Lapidus, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary matters Paul Lapidus and Lori Beth Lapidus are the parents and natural guardians of Susan Lapidus (Susan), a minor. Susan was born a live infant on November 5, 1993, at Good Samaritan Medical Center, a hospital located in West Palm Beach, Florida, and her birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Susan was Ronald Koch, M.D., who was at all times material hereto, a participating physician in the Florida Birth- Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Mrs. Lapidus' antepartum course and Susan's birth At or about 1:00 p.m., November 4, 1993, Mrs. Lapidus was admitted to Good Samaritan Medical Center for an oxytocin challenge test (a contraction stress test), with suspected intrauterine growth retardation (IUGR), to assess fetal well- being. At the time, the fetus was at 39 weeks gestation, with an estimated date of delivery of November 17, 1993, and Mrs. Lapidus' antepartum course had not been without complication or risk. Regarding those risk factors, the proof demonstrates that at the time of Susan's conception Mrs. Lapidus (date of birth November 1, 1955) was 37 years of age, with a history of five previous pregnancies. Of those pregnancies, four were aborted (one "therapeutic" in 1979, and the balance "spontaneous" in January 1985, October 1985, and 1990) and one was carried to term and produced a normal, healthy boy (Michael, date of birth, October 21, 1988). Further complicating her pregnancy, the proof demonstrated that (to the extent conceded by Mrs. Lapidus), she smoked approximately 10 cigarettes per day and drank white wine daily (1 glass with dinner) throughout her pregnancy. 1/ Because of her age and other risk factors, Mrs. Lapidus underwent a number of tests during the course of her pregnancy, including an amniocentesis and multiple sonograms which revealed (within the limits of testing accuracy) no apparent cause for concern. Finally, during the month preceding her admission to Good Samaritan Medical Center, Mrs. Lapidus underwent non-stress testing, and ultimately contraction stress testing by oxytocin challenge test (OCT), to assess fetal well-being. 2/ The non- stress tests and oxytocin challenge tests that were administered to Mrs. Lapidus prior to November 4, 1993, were apparently reassuring for fetal well-being and placental integrity. As heretofore noted, Mrs. Lapidus was admitted to Good Samaritan Medical Center at 1:00 p.m., November 4, 1993, for an OCT, which extended until 3:55 p.m., when Pictocin was discontinued. During the test some decelerations were observed late in contractions (late decelerations), consistent with placental aging/diminishing function, and Dr. Koch resolved it would be prudent to admit Mrs. Lapidus for observation overnight and induction of labor in the morning. Mrs. Lapidus was admitted to labor and delivery at about 5:30 p.m., November 4, 1993. External fetal monitoring revealed a fetal heart rate (FHR) of 120 to 130 beats per minute (normal), and mild, irregular uterine contractions (most likely symptomatic of the prior administration of Pictocin). At 5:50 p.m. Mrs. Lapidus was repositioned, and external fetal monitor was positive for accelerations and continued mild, irregular uterine contractions. Assessment at 7:30 p.m. noted continued mild contractions, as well as "variable decelerations [at] intervals but not consistently [with each] contraction," however, beat-to- beat variability was noted to be present. Continued monitoring overnight revealed occasional variable decelerations, but continued beat-to-beat variability. At 7:10 a.m., external fetal monitoring revealed a FHR of 110 to 120 beats per minute, with spontaneous accelerations. Pictocin was administered to induce labor, at 7:30 a.m. contractions commenced (labor began), and an FHR deceleration to 90 to 110 beats per minute for 2 1/2 minutes was observed. Mrs. Lapidus was repositioned to her left side, intravenous fluids (IV) were increased, and FHR returned to a 110 to 120 beat per minute baseline. Beat-to-beat variability in fetal heart rate persisted, and at 8:20 a.m. the membranes were artificially ruptured with clear fluid noted. At or about 9:00 a.m., a FHR deceleration with contraction was noted. Mrs. Lapidus was again repositioned, intravenous fluids increased and FHR accelerated to 150 beats per minute following the contraction. A late deceleration was again noted with the next contraction. At 9:40 a.m., the nurses' notes reveal 3 late decelerations were observed, and Pictocin was discontinued; FHR continued at 130 to 140 beats per minute, with moderate beat-to- beat variability. Vaginal examination at 9:50 a.m. revealed the cervix to be 5 centimeters dilated, effacement at 80 percent, and the fetus at station -2. Contractions were noted as moderate in intensity, with 3 to 5 minute frequency, and a duration of 60 to 70 seconds. At or about 10:10 a.m., an epidural was placed and at 11:45 a.m., with no further decelerations having been observed, Pictocin was restarted. At 11:50 a.m., Mrs. Lapidus' bladder was noted as distended and a foley was inserted to help her void. Contemporaneously, FHR was noted to decelerate to the 60 beat per minute range for 30 seconds. When Mrs. Lapidus was repositioned, FHR returned to the 140 beat per minute range, with accelerations. At 12:29 p.m., the fetal monitor again revealed a late deceleration with contraction; however, it also noted continued moderate beat-to-beat variability and spontaneous acceleration. At 12:50 p.m. another late deceleration was noted and Mrs. Lapidus was repositioned to her right side. FHR remained in the 130 beat per minute range, with moderate beat-to- beat variability. Vaginal examination at 1:25 p.m. revealed dilatation and effacement to be complete and the fetus at station -1. FHR was noted in the 130 to 140 beat per minute range, with moderate beat-to-beat variability. At 1:40 p.m. Mrs. Lapidus began pushing, and at 1:50 p.m. Susan was delivered (6 hours and 20 minutes after labor commenced). Susan had a weak cry and was dusky at birth, and was placed on a warmer, dried, and given oxygen via blow-by. Apgars of 7 and 8 were assigned at one and five minutes, respectively. Cord specimen was obtained, and, when subsequently analyzed, revealed that, at delivery, Susan presented with a normal pH of 7.318. The Apgar scores assigned to Susan are a numeric expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, muscle tone, reflex response, and color, with each category being assigned a score ranging from the lowest score of 0 through a maximum score of 2. As noted, at one minute Susan's Apgar score totalled 7, with heart rate, muscle tone and reflex response being graded at 2 each; respiratory effort being graded at 1; and color being graded at 0. At five minutes, Susan's Apgar score totalled 8 with heart rate, respiratory effort, muscle tone, and reflex response being graded at 2 each, and color being graded at 0. Such scores were normal, and consistent with the delivery of a healthy, vigorous infant. Following delivery, Susan developed slight retractions and coarse respirations, as well as a temperature of 100.2, and was transferred to the neonatal intensive care unit (NICU) for further evaluation and treatment. There, physical examination revealed the following: HEAD: The head is normocephalic. The anterior fontanel is soft. ENT: There is no nasal flaring. The ears are well set. The nasal choanae are patent. Slight protruding tongue. THORAX: The chest is symmetric. There is [sic] subcostal retractions. LUNGS: There are coarse breast sounds. There is audible grunting present. HEART: There is a normal regular rhythm with no murmurs. ABDOMEN: The abdomen is non-distended. There is no organomegaly. The umbilical cord has three vessels. EXTREMITIES: The extremities are symmetric. The hips are normal, without any dislocation or subluxation. The pulses are equal bilaterally. Bilateral simian creases. SKIN: There is no cyanosis, and no rashes are present. There is good capillary refill. GENITALIA: There are no anomalies noted. CNS: The baby is active and alert. There is good muscular tone. Admitting diagnosis (impression) was as follows: 1.- Term 38 weeks appropriate for gestational age female. 2.- Respiratory distress. 3.- Perinatal sepsis suspected. Susan remained in the hospital until November 13, 1993, when she was discharged in satisfactory condition to her parents' care. While in the hospital Susan evidenced the following problems: RESPIRATORY: The patient developed respiratory distress that required no oxygen, and that subsided rapidly. The results of the CXR [chest x-ray] showed no infiltrate, congestion, pneumothorax or other pathology. The heart size is within normal limits. She developed inspiratory stridor. This was considered to be related to a certain degree of laryngomalacia [flacidity of the epiglottis and aryepiglottic folds (a softening of the cartilage in the upper airway), as in congenital laryngral stridor]. 3/ R/O SEPSIS: In view of the initial presentation, the possibility of sepsis was considered. The patient was placed on antibiotics, ampicillin and Claforan in appropriate doses. Results of the cultures were negative. The antibiotics were discontinued on 11/12/93. DYSMORPHIC FEATURES: In view of the dysmorphic features, and the possibility of this has been associated with chromosomes pending, a new chromosome studies was sent on 11/12/93 for extended banding. 4/ Also a renal ultrasound was done on 11/10/93 and the result was negative. Notably, Susan evidenced no neurologic problems or sequela during the course of her admission. Final diagnosis on discharge was as follows: 1.- Term 38 weeks appropriate for gestational age female. 2.- Transient respiratory distress. 3.- Dysmorphic facies. 4.- Bilateral simian creases. 5.- Perinatal sepsis suspected. 6.- Mild degree of laryngomalacia. 7.- Slow feeder. Susan's subsequent development Susan's early infancy was apparently unremarkable until around 10 months of age when her parents became concerned that her development (mental and physical) appeared delayed. Consequently, they sought the advice of Susan's pediatrician and, over time, Susan was referred to, and examined by, a number of medical specialists to assess her condition and to identify its etiology. On June 5, 1995, Susan was evaluated by Amanda Naguiat, M.D., Assistant Professor of Clinical Neurology, University of Miami Children's Hospital Center. Dr. Naguiat's assessment was as follows: . . . Susan appears to have global development delay with relative strength in social interaction. Her exam is significant for diffuse hypotonia and probably some associated weakness, dysmorphic features and depressed deep tendon reflexes. Her yellowish discoloration is secondary to carotenemia. So far, I cannot put her in a definite syndrome, although phenotypically, the only thing that comes to mind here is some of the rhizomelic forms of chondrodysplasia, belonging to the group of peroxisomal disorders. There is a definite need to find etiology for all of these. As discussed with her parents, I would like for her to have an MRI of the brain to look for any malformations or any white matter anomalies that would guide us to further testing. I would like to have some initial metabolic testing, which would include serum quantitative amino acids, urine organic, acids, carnitine total and free levels, and thyroid function tests. I have referred her to Dr. Benke, who they will see this coming Saturday, on June 10, in his clinic up in West Palm Beach, to see if he can shed light on any type of syndrome in view of her dysmorphic features. I concur with the recommendations for her to have early intervention in the form of speech, occupational and physical therapy. As discussed with her parents, I do not believe that her condition will be 'outgrown' and if we do not find any etiology, I would assume that she will follow a static encephalopathy with improvement over time but with persistent impairments. If a cerebral cause for her problems are not found, she should have further investigation for neuromuscular disease, as I am concerned that there might be a concomitant peripheral nervous system problem in view of her hypotonia and weakness and depressed reflexes. I will arrange a followup with them as soon as all these tests are done. On July 17, 1995, an MRI of the brain without contrast was performed and interpreted by Walter H. Forman, M.D. The MRI was considered normal and revealed no changes or anomalies one would associate with hypoxic injury. Specifically the MRI revealed that: The ventricles are normal in size and position. No masses or mass effects are identified. I don't see any areas of abnormal signal. The myeline maturation appears to be normal for age. On October 7, 1995, Susan was seen by Paul Benke, M.D., Ph.D., Director, Clinical Genetics, University of Miami School of Medicine, for a second time in a follow-up visit. 5/ Dr. Benke reported the results of that visit as follows: I saw this 23 mo old girl with minor anomalies and developmental delay in genetic clinic in Palm Beach Gardens on this date in follow-up. She has made a lot of progress; she can now stand and is starting to talk, she has about 10 words and a sense of humor, and has made up a lot of ground. She has not been sick. The two chromosome studies (including amnio) were sent in to me, and were of sufficient quality that a routine repeat chromosome study would not be helpful. I asked the parents to bring in pictures, since they claimed that pictures of the father, taken as a child, were similar, and I thought there was small, not large resemblance. To my delight (and surprise) the family was quite right about this, and the father had a prominent forehead, low set ears, and slightly small chin as a child. He also had some speech delay, but is very normal now, and these features minimally evident. She has had a lot of OT, PT and speech therapy for the past 3 1/2 months, and the parents attribute a lot of her gains to that. But I think that they have done a lot as well, and have had a positive attitude about her development. She has not been sick, and has had no fever, seizures or other problems. Importantly, she had tracheomalacea, and high pitched breathing, and grew out of it by 1 yr, and the father has a retarded brother. PHYSICAL FINDINGS: Interactive girl with lots of personality, mild dysmorphic features. She is very interactive today. HT: 29 in(?) WT: 22 1/2 lb. HC: 48 cm Head: prominent forehead Eyes: mongoloid slant IC: 3.5, IP: 6.0, IP: 9.5 (mild increase) Ears: +/-low set Nose: slight depressed nasal bridge Chin: small chin, high arched palate Chest: clear, no rales. Heart: [n]o murmur. Abdomen: neg, no masses, organomegaly Genitals: neg. Spine: no scoliosis. Extremities: small hands and feet, hypoplastic 5th toe nail. She is hyperextensible. She has fusiform fingers. Skin: negative Neurological: tone a little better. poor DTR. No localizing finding. Diagnosis: Multiple Minor Anomalies, Probable FG (Optiz Frias) Syndrome. Counseling: Deferred Pending testing. The Opitz Frias is a very variable disorder, compatible with normal intelligence, and mild-moderate effects on intelligence. Affected patients frequently have tracheomalacea or feeding problems, frontal prominence, low set ears, hypertelorism and other findings. Recent research suggests a microdeletion of chromosome #22, determinable by Florescence-in-situ-hybridization (FISH) testing. She has greatly improved, and is functioning at a 12-14 month level today. Recommendations: 1) Fish Testing of chromosome #22. We should be able to have blood sent off to the researchers who do this testing. 2. Get pictures of Paul's retarded brother. 3. See in clinic after testing. . . . A second genetics evaluation of Susan was conducted on January 21, 1998, by Parul Jayakar, M.D., a clinical geneticist associated with the Genetics Center of South Florida. Dr. Jayaker's report of that examination reads as follows: Susan Lapidus came to our office accompanied by her parents, Lori and Paul Lapidus, for a genetics evaluation because she has speech and developmental delay. The patient was born by NSVD at term to a 37 year old gravida 8 para 1061 (2 TAb, 4 SAb) woman. An amniocentesis done because of advanced maternal age was normal, 46,XX. The patient's mother states that she was put on progesterone during her pregnancy because of her history of multiple miscarriages. She also smoked approximately 10 cigarettes per day and drank white wine daily throughout her pregnancy. The patient remained in the NICU for 1 week after delivery because she had a strep infection. The patient has not had any major hospitalizations or illnesses. An MRI of the brain was normal at approximately 2 1/2 years of age. Her vision and hearing have both been evaluated and are reportedly normal. * * * Physical Examination: Height of 39 inches (90%), weight 31 lb. (25%), head circumference 48.5 cm (5%). Patient was awake, alert and active, pupils equal and reactive to light, no ectropien, with temporal receding hairline, good hair growth, prominent glabella, slight hypertelorism, flat long philtrum, thin upper lip (? familial), slightly high arched palate, broad nasal root. Chest - no heart murmur; abdomen - soft, no hepatosplenomegaly; genitalia female. Extremities - right single palmar crease, slightly hypoplastic toenails. Neurologically - vocabulary limited to monosyllables, no obvious cranial nerve palsies. Impression: 4 year old with Speech and developmental delay Minor dysmorphic features Susan, in the past, has been seen by Dr. Benke who contemplated the diagnosis of Optiz syndrome. At the moment I do not feel that she meets the clinical criteria for Opitz syndrome and the chromosomes done revealed a 46,XX, normal female karyotype and the FISH for chromosome 22 microdeletion was normal. 6/ She was seen also, in June of 1995, by Dr. Naguiat at that time the Mom reports that a significant workup was done including MRI of the brain and hearing test which were all normal (verbal report, I do not have these reports in hand). As Mom tells me, an ophthalmology evaluation was also done which was also normal. She has been receiving OT, PT and speech therapy since 17 months of age but lately her speech therapy has been discontinued in her recent school. I feel she is in great need of speech therapy to be able to increase her vocabulary for day to day life. Based on her clinical features I do not feel that she has characteristics of any particular syndrome, the only things which come to mind is the hypoplastic toenails, the long philtrum and the thin upper lip which may be reminiscent of ? Fetal Alcohol Effects (Mom had 1 glass of white wine with dinner every day). I do not think this amount of alcohol intake would cause full blown Fetal Alcohol Syndrome. Certainly some of her facial characteristics also appears to be familial. Therefore, I feel that right now I am unable to label her in any definite syndrome. 7/ As explained to the family, she clinically does not seems to have a progressive neural degenerative condition since she has not have [sic] regression of milestones and seems to be doing much better. The dispute regarding compensability Here, there is no dispute that Susan suffers neurologic dysfunction, mental and physical. What is at issue is whether that dysfunction may reasonably be described as permanent and substantial and, more fundamentally, whether the cause (etiology) of such dysfunction is, more likely than not, attributable to "an injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as required for coverage to be afforded under the Plan. Section 766.302(2), Florida Statutes. With regard to the issue of causation and timing, Petitioners are of the view that Susan's presentation is consistent with a brain injury caused by oxygen deprivation which occurred during the course of labor and delivery. In contrast, Respondent is of the view that the proof is not consistent with brain injury caused by oxygen deprivation during or immediately following birth and must, therefore, be attributable to some other etiology. Respondent's view of the proof has merit, and it is unnecessary to address whether Susan's neurologic dysfunction is permanent and substantial. The etiology (genesis) of Susan's neurologic dysfunction To address the etiology of Susan's neurological dysfunction, the parties offered selected records relating to Mrs. Lapidus' antepartum and intrapartum course, as well as for Susan's birth and subsequent development. Portions of those records have been addressed supra, and further salient portions will be addressed infra. The parties also offered the opinions of three physicians, at hearing, to address the likely etiology of Susan's presentation. Those physicians were Seth J. Herbst, M.D., a board-certified obstetrician and gynecologist; Jaime Baquero, M.D., a pediatric neurologist, board-certified in pediatrics and board-eligible in neurology; and Charles Kalstone, M.D., a board-certified obstetrician and gynecologist. 8/ The medical records and other proof, including the testimony of the physicians offered by the parties, have been carefully considered. So considered, it must be concluded that the proof does not demonstrate (or allow a conclusion to be drawn with any sense of confidence) that, more likely than not, Susan's neurologic dysfunction is related to an "injury to the brain . . . caused by oxygen deprivation . . . [which] occurr[ed] in the course of labor, delivery, or resuscitation in the immediate post-delivery period." In reaching such conclusion, it is observed that Susan's course pre-delivery and post-delivery was inconsistent with hypoxic or ischemic injury having occurred during the course of labor, delivery, or resuscitation. First, the evidence documenting fetal heart rate from admission through the period of labor and delivery does not support the conclusion that Susan suffered an acute intrapartum event that led to hypoxic or ischemic injury. Notably, while there were multiple late decelerations (which evidenced periods of diminished oxygenation or, stated differently, periods of transient hypoxia) the fetal monitoring tape also provided reassuring evidence of fetal wellbeing (by documenting good beat-to-beat variability, spontaneous accelerations, normal FHR baseline, and the absence of a progressive or persistent pattern of decelerations). Given such positive evidence of fetal reserve, it is unlikely that fetal oxygenation was significantly adversely affected during labor and delivery. Further militating against the conclusion that Susan's impairments were caused by oxygen deprivation during labor or delivery are the numerous inconsistencies between Susan's presentation and development, and the clinical findings one would expect had she suffered hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, during that period. For example, Susan's Apgars were within the normal range; her breathing at birth was essentially stable; cord pH was normal; and she did not evidence neurologic problems in the neonatal course. Finally, the results of Susan's MRI were normal and inconsistent with an hypoxic ischemic brain injury. Given the proof, it cannot be concluded that Susan's neurologic dysfunction resulted from a brain injury caused by oxygen deprivation or that it was related to an event which may have occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Notably, Susan's presentation and neonatal course were not consistent with an acutely acquired neurological injury caused by oxygen deprivation, and it is improbable that she could have experienced an acute event during labor and delivery, or immediately thereafter, without evidencing clinical symptoms of such damage. Conversely, Susan's presentation, and Mrs. Lapidus' prenatal history, suggest a genetic or congenital anomaly (or syndrome) as the more likely etiology for Susan's presentation.
The Issue At issue in this proceeding is whether Halle Cohen Martinez, III, a minor, qualifies for coverage under the Florida Birth- Related Neurological Injury Compensation Plan.
Findings Of Fact Petitioners, Barbara Mary Martinez and Halle Martinez, Jr., are the natural parents and guardians of Halle Cohen Martinez, III, a minor. Halle was born a live infant on November 12, 2001, at Leesburg Regional Medical Center, a hospital located in Leesburg, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Halle's birth was Wendell Courtney, 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 address the cause, timing, and significance of Halle's impairment, Petitioners offered selected medical records relating to Halle's birth and subsequent development, as well as the testimony of Mr. and Mrs. Martinez. In turn, Respondent offered the affidavits and the reports of Doctors Donald C. Willis and Paul R. Carney. The cause and significance of Halle's neurologic impairment At birth, Halle suffered a left brachial plexus injury, with resultant left arm brachial plexus palsy, and a left posterior dislocated shoulder, secondary to the birth brachial plexus palsy. Thereafter, at age 5 months, Halle underwent corrective surgery of the brachial plexus using sural nerve grafts, and at 8 months he underwent corrective surgery to improve the function of his left shoulder. The operations resulted in functional improvements; however, as of the date of hearing, Halle continued to suffer impairments of his left arm and hand, which are likely to be permanent, with notable atrophy within the left upper extremity. Apart from the physical impairment Halle exhibits in his left upper extremity, he is otherwise neurologically sound, without evidence of impairment in his right upper extremity or lower extremities; without evidence of cognitive delay; and without evidence of vision or hearing impairment. Accordingly, although Halle evidences a significant birth-related left brachial plexus injury, he is not, on balance, substantially physically impaired, and evidences no mental impairment. Therefore, for reasons appearing fully in the Conclusions of Law, the claim is not compensable, and it is unnecessary to address whether Halle's brachial plexus injury is, anatomically, an injury to the spinal cord.
Findings Of Fact Addyson Tilka was born on June 22, 2012, at Bayfront Medical Center, Inc., located in St. Petersburg, Florida. Addyson weighed in excess of 2,500 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Addyson. In an affidavit dated August 3, 2016, Dr. Willis opined as follows: In summary, the baby was delivered prematurely at 34 weeks due to premature rupture of the membranes. Apgar scores were 5/8. The baby had respiratory distress syndrome of prematurity. Oxygen and ventilation support was required for respiratory distress. Neurologic exam was appropriate for gestational age. The baby did not have seizures. No head imaging studies were done during the newborn hospital course. There was no apparent obstetrical event that resulted in loss of oxygen deprivation or mechanical trauma to the baby’s brain during labor, delivery or the immediate post delivery period. NICA retained Laufey Y. Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to examine Addyson and to review her medical records. Dr. Sigurdardottir examined Addyson on January 20, 2016. In an affidavit dated August 5, 2016, Dr. Sigurdardottir summarized her examination of Addyson and opined as follows: NEUROLOGICAL EXAM: Mental status: Addyson is a beautiful, interactive girl who speaks in full sentences with minor pronunciation difficulties. She has no autistic features and seems age appropriate in all aspects. Cranial nerves are intact. Pupils are equal and reactive to light. Visual fields are full. There is nystagmus, no amblyopia, no strabismus. Her facial expressions are symmetric. There is no hearing abnormality noted. Her motor exam reveals normal muscle tone, motor strength, symmetric reflexes are present. Balance and coordination seems grossly intact for age. ASSESSMENT AND PLAN: In summary, here we have a 3 year 6 month old girl who was born premature at 34 weeks and needed a neonatal intensive care unit (NICU) stay due to respiratory compromise. There are, however, no clear concerns of her development at this time. No suggestions of physical impairment. There is nothing on history or record review that suggests neurologic injury to the brain or spinal cord acquired due to oxygen deprivation or mechanical injury. Results as to question 1: The patient is found to have no substantial physical or mental impairment. Results as to question 2: there is no evidence of perinatal neurologic depression and no evidence of ischemic injury at birth or in the immediate postnatal period. Results as to question 3: We would expect full life expectancy as no noted abnormalities are found on exam. In light of the above-mentioned details, I do not recommend Addyson to be included in the Neurologic Injury Compensation Association program and will be happy to answer additional questions. All of my opinions are within a reasonable degree of medical probability. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Willis that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby's brain during labor, delivery or the immediate post- delivery period. Dr. Willis’ opinion is credited. There are no expert opinions filed that are contrary to Dr. Sigurdardottir’s opinion that Addyson does not have a substantial physical or mental impairment. Dr. Sigurdardottir’s opinion is credited.
The Issue At issue in this proceeding is whether Jacqueline LaPoint, 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 Catherine LaPoint is the mother and natural guardian of Jacqueline LaPoint (Jacqueline), a minor. Jacqueline was born a live infant on July 2, 1994, at Holy Cross Hospital, a hospital located in Fort Lauderdale, Florida, and her birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Jacqueline was Marsh McEachrane, M.D., who was, at all times material hereto, a participating physician in the Florida Birth-Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Mrs. LaPoint's antepartum course and Jacqueline's birth At or about 1:00 a.m., July 2, 1994, Mrs. LaPoint's membranes spontaneously ruptured (while she was at home), with clear fluid noted, and contractions commenced approximately one to two hours later. At the time her estimated date of delivery had been noted as July 24, 1994, and, apart from the borderline prematurity of the fetus at the time labor commenced, her antepartum course was without apparent complication; however, Mrs. LaPoint did present with a number of risk factors, including a history of chronic smoking; obesity3 (a risk factor of gestational diabetes4); four previous cesarean sections (representing a risk of uterine compromise or rupture); and a large for gestational age fetus. Given the previous uterine surgery, Mrs. LaPoint had been scheduled for a repeat cesarean section. At or about 4:45 a.m., Mrs. LaPoint presented to Holy Cross Hospital in active labor. On presentation, contractions were noted as moderate (with a frequency of 3 to 4 minutes and a duration of 40 to 60 seconds), and vaginal examination revealed the cervix to be at 5 to 6 centimeters, effacement at 80 to 90 percent, and the fetus at station -3. External fetal monitor revealed a normal fetal heart tone (FHT) baseline of 150 to 160 beats per minute. Given her history of previous cesarean sections (uterine surgery) and her presentation of active labor, Mrs. LaPoint was admitted at or about 4:49 a.m. for a repeat cesarean section. FHT was monitored by external fetal monitor from admission until 5:26 a.m., when it was disconnected and Mrs. LaPoint was transported to the operating room (OR). During that period, FHT baseline remained consistent at 150 to 160 beats per minute, except for one episode of variable/late deceleration to the 90-beat per minute range at about 3:00 a.m., but with good beat-to-beat variability and recovery to baseline was noted. One other variable deceleration was noted shortly thereafter to the 120-beat per minute range with spontaneous recovery to baseline. Notably, while the tape reveals some diminished long term variability with contractions, it does not reveal a pattern of persistent deceleration. Mrs. LaPoint was transported to the OR at 5:26 a.m., at which time FHT was noted as 150 beats per minute, and contractions were noted as moderate (with a frequency of 2 minutes and a duration of 40 to 60 seconds). Anesthesia was noted to commence at 5:50 a.m., the operation started at 6:08 a.m., and Jacqueline was delivered at 6:14 a.m. Cord specimen was obtained, and when subsequently analyzed revealed that, at delivery, Jacqueline presented with a pH of 7.085, PCO2 of 90.3, PO2 of 19.2, HCO3 of 27, and a Base Excess (BE) of -6. During delivery amniotic fluid was noted to be thin merconium stained, and oropharyngeal suctioning was done before the shoulders were delivered. Jacqueline was noted as limp (hypotonic) and apnic at birth, and intermittent positive pressure ventilation was given by bag and mask for about one minute. Laryngoscopy revealed cords were clear. Apgars of 4 and 8 were assigned at one and five minutes, respectively. The Apgar scores assigned to Jacqueline 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 irritability, and skin 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 Jacqueline's Apgar score totalled 4, with heart rate being graded at 2; respiratory effort and color being graded at 1 each; and muscle tone and reflex irritability being graded at 0. At five minutes, Jacqueline's Apgar score totalled 8, with heart rate, respiratory effort, and reflex irritability being graded at 2 each, and muscle tone and color being graded at 1 each. While the one minute Apgar was low,5 the five minute Apgar was quite normal or, stated otherwise, not predictive of neurologic complications.6 Following stabilization, Jacqueline continued to evidence respiratory difficulty and, at or about 6:30 a.m., she was admitted to the neonatal intensive care unit (NICU) for further evaluation and management. Initial assessment on admission evidenced an unusual neurologic and respiratory presentation. Neurologically, Jacqueline was noted as lethargic, floppy, and jittery. As for her respiratory presentation, although her breathing rate was regular, she evidenced rales, grunting, flaring, and moderate retractions. Dextrostix (a reagent strip designed for determination of blood-glucose levels with the use of fingertip venous blood) on admission was low, at 26, and immediate glucose testing was ordered and also reported as critically low at 24. Diagnosis was respiratory distress syndrome (RDS) and possible hypoglycemia (an abnormally diminished concentration of glucose in the blood). Respiratory support (for RDS) and intravenous (IV) glucose (for hypoglycemia) were ordered. For respiratory support, Jacqueline was initially placed in an Oxyhood (on an infant warmer bed) with 96 percent oxygen; however, when she continued to require a high oxygen concentration to maintain her gases and saturation levels within normal limits she was intubated (at or about 8:15 a.m.) and ventilator support was provided. Thereafter, her oxygenation was maintained within normal limits without difficulty.7 While Jacqueline's RDS was successfully managed, without apparent harm (by oxygen deprivation or otherwise) to the infant, her hypoglycemia proved refractory or, stated differently, recalcitrant or not responsive to treatment. Indeed it was not until the afternoon of July 4, 1994, that her condition started to resolve, and then only after progressively intensive intervention.8 Here, Jacqueline may reasonably be described as an infant of a diabetic mother9 (IDM)--a hyperglycemic mother--who, consequently, presented with hyperinsulinism, resulting in hypoglycemia.10 Such presentation is clearly demonstrated by elevated readings of insulin in Jacqueline's blood (of 24.7 at 7:00 p.m. on July 3, 1994),11 as well as the severe hypoglycemia she developed subsequent to delivery. Jacqueline was noted as "jittery" throughout the course of treatment; however, the most pronounced period of physiological abnormality was noted at or about 8:00 a.m., July 4, 1994. At that time, an apnic episode was noted during assessment, and tone was flaccid, color pale, and lips dusky. Jacqueline was accorded tactile stimulation without response, and manual breaths were given from the ventilator for approximately 30 seconds before a response was noted. Jacqueline was noted as jittery and diaphoretic (evidencing profuse perspiration). Other apnic episodes, with similar observations, were noted and addressed at 8:15 a.m., 8:18 a.m., and 8:30 a.m. Neurologic consult was called, and an EEG was recommended to rule out seizures, and an ultrasound to rule out possible intraventricular hemorrhage. The EEG was read as normal and the head ultrasound was read as within normal limits, as follows: "No evidence of intraventricular or subpendymal hemorrhage. The ventricles appear normal in size, left slightly larger than right." Jacqueline was started on a course of antibiotics to address the possible presence of sepsis. At or about 4:00 p.m., July 4, 1994, Jacqueline's urinary output was noted to be diminished. Her output continued as diminished and at or about 5:40 p.m., given such development, as well as her continued complex metabolic problems, her treating physician ordered Jacqueline transferred to the Level III Neonatal ICU at Broward General Medical Center for continued evaluation and management. Final diagnosis on discharge was, as follows: Prematurity. Large for gestational age. Respiratory distress syndrome. Hyperglycemia. Hypocalcemia. Hypomagnesemia. Rule out hypoparathyroidism. Seizure disorder. Ventriculoseptal hypertrophy. Jacqueline was discharged from Holy Cross Hospital at or about 8:30 p.m., July 4, 1994, and transported to Broward General Medical Center, where she was admitted at or about 9:18 p.m. in stable condition. There, Jacqueline's condition progressively improved and on July 11, 1994, she was discharged in her mother's care. Jacqueline's course at Broward General Medical Center is reasonably stated in her discharge summary as follows: Admission diagnoses: 36 week white female Large for gestational age Grandmultiparity Respiratory distress R/O RDS I, RDS II, Pneumonia R/O Sepsis R/O Meconium aspiration syndrome R/O Congenital heart disease R/O Pulmonary hypertension R/O Seizures R/O Hyperparathyroid R/O Hypoglycemia, hypocalcemia Transfer from Holy Cross CLINICAL PROBLEMS: Respiratory: RDS I Persistent pulmonary hypertension was diagnosed. The highest delivered FI02 was 0.46, with time spent in increased oxygen = 3 days (total). The infant was intubated and on intermittent mandatory ventilation for approximately 3 days (at BGMC). Cardiac: A cardiac consultation was performed on 7/5/94 by Dr. Miller to reassess previous consult of 7/2/94 at Holy Cross. Echocardiogram revealed hypertrophied left ventricular septum and left posterior wall, turbulance of the left ventricular outflow tract, a PDA with bidirectional shunting and increased pulmonary reistance. Dr. Millers impression as that of RDS with evidence of pulmonary hypertension and hypertrophic cardiomyopathy. Metabolic: Hypoglycemia - treated with IV glucose. Hyponatremia. IV sodium was given. Hypocalcemia. There was treatment with IV calcium. Endocrine: A consultation was performed by Dr. Motkin- Kalia on 7/5/94. Findings were most likely consistent with IDM although there was no maternal history of diabetes/gestational diabetes. Infection: A septic workup was performed on 7/2/94 at Holy Cross Hospital. There was antibiotic treatment with Ampicillin and Gentamicin for 10 days (total) due to clinical evidence of sepsis. Neurologic: Dr. Epstein was consulted on 7/5/94 due to report of seizure at Holy Cross Hospital. Most probable etiology [of seizures] was felt to be hypocalcemia. There was no further seizure activity, infant was treated with phenobarbital X 1 dose after the seizure noted on 7/4/94 An EEG was performed on 7/5/94. It was reported as within normal limits. * * * Final Discharge Diagnoses: 36 week white female Large for gestational age RDS I PFC Hypoglycemia Hyponatremia Hypocalcemia Seizure Clinical sepsis Probable IDM Condition on discharge - Recovered. Jacqueline's subsequent development Jacqueline's early infancy was apparently unremarkable until around the age of 5 to 6 months when she was noted to have visual inattention. Around the same time she was also noted to have intermittent deviation of the head downwards without any associated symptoms. On May 5, 1995, Jacqueline was evaluated by Jaime L. Baquero, M.D., a pediatric neurologist. His neurologic evaluation revealed the following: PHYSICAL EXAM: . . . she indeed appeared visually inattentive . . . [and] did have intermittent downward head deviation which was not fixed and was not associated with any other signs or symptoms. There were no overt dysmorphic features or evidence of neurocutaneous signs. The appendicular muscle tone was felt to be normal, although her axial tone diminished. No other abnormalities were noted on examination. IN SUMMARY, based on clinical history and examination, it does appear that Jacqueline is experiencing significant visual impairment which at this point in my view is very difficult to distinguish whether this is a congenital blindness or delayed visual maturation. The possibility of optic nerve hypoplasia should be entertained being that the mother has possible maternal gestational diabetes, and in addition manifestations of hypoglycemia and hypocalcemia were seen in the neonatal period with seizures accompanying this metabolic deficit. It is known that there is a higher incidence of septal optic dysplasia associated with infants born to diabetic mothers. This sometimes is accompanied by hypopituitarism, therefore, I would recommend obtaining an MRI of the brain to R/O that possibility. In addition, I would like to obtain an EEG because of the concern with this startle and jerking which is seen more often in the morning. In addition, I would like to obtain a Visual Evoked Response to evaluate the integrity of the visual pathways, although if her visual deficits would be cortical, it could still be within normal limits. At some point she would deserve an endocrinologic evaluation to R/O the presence or absence of hypopituitarism. Obviously, being that her APGARS were somewhat low and that she was ventilated, the optic atrophy associated with hypoxic ischemia encephalopathy is still a possibility. I discussed all these different diagnoses with Mrs. LaPointe and we will sit down in a follow-up visit to discuss these issues after the tests have been obtained. Consistent with Dr. Baquero's suggestion, Jacqueline was admitted to Broward General Medical Center on June 6, 1995. The Visual Evoke Response test was normal, "suggesting normal conduction of the pathway between the retina and the occipital lobes bilaterally." The electroencephalogram (EEG) was read as abnormal "due to the presence of intermittent polymorphic slowing noted primarily in the left posterior quadrant but with a field extending sometimes to the right posterior quadrant with admixed spike discharges. These findings are indicative of a regional disturbance of cerebral function that is potentially epiteptogenic maximally noted in the left posterior quadrant."12 On June 14, 1995, Jacqueline was referred to Broward General Medical Center for evaluation of "daily episodes of upper extremity rapid 'jerks'" (possible new onset seizure activity). No seizures were noted on the 24-hour video EEG and on June 15, 1995, Jacqueline was discharged. On June 20, 1995, an MRI of the brain was finally obtained. That MRI revealed the following: FINDINGS CONSISTENT WITH PERIVENTRICULAR LEUKOMALACIA. DELAYED MYELINATION SEEN THROUGHOUT THE CEREBRAL CORTEX AS DESCRIBED ABOVE. THERE ARE NO MRI FINDINGS SEEN TO SUGGEST SEPTAL OPTIC DYSPLASIA. The dispute regarding compensability Here, there is no dispute that Jacqueline suffered an injury to her brain which has resulted in permanent and substantial mental and physical impairment. Indeed, the record reflects, without contradiction, that Jacqueline presents with severe spastic diplegia, is wheelchair dependent for all community mobility, and suffers cortical blindness. What is subject to dispute is the cause and timing (genesis) of Jacqueline's brain injury or, pertinent to these proceedings, whether the proof demonstrates, more likely than not, that her neurologic impairment resulted from 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 opposed to some other genesis. With regard to such issue, Petitioner is of the view that, while there is no dispute that Jacqueline suffered (post- delivery) a significant brain injury caused by severe hypoglycemia, Jacqueline also suffered pre-natal or immediate post-natal oxygen deprivation which caused, or operating in concert with her subsequent hypoglycemia caused, her brain injury. (Petitioner's Proposed Final Order, at page 18.) In contrast, Respondent is of the view that the proof is not consistent with brain injury caused by oxygen deprivation occurring during or immediately following birth and must, therefore, be attributable to Jacqueline's hypoglycemia. Respondent's view of the proof has merit. The genesis of Jacqueline's injury To address the genesis of Jacqueline's brain injury, the parties offered selected records relating to Mrs. LaPoint's antepartum and intrapartum course, as well as for Jacqueline's birth and subsequent development.13 Portions of those records have been addressed supra, and further salient portions will be addressed infra. The parties also offered the opinions of six physicians to address the likely cause of Jacqueline's injury. The physicians offered by Petitioner were Marsh McEachrane, M.D., a board certified obstetrician and gynecologist; Michael Tidwell, M.D., a board certified orthopedist; Lalit Shah, M.D., a board certified neonatologist; and Jaime Baquero, M.D., a pediatric neurologist, board certified in pediatrics and board eligible in neurology. The physicians offered by Respondent were Charles Kalstone, M.D., a board certified obstetrician and gynecologist; and Edward Lance Wyble, M.D., a board certified neonatologist. The medical records and other proof, including the testimony of the physicians offered by the parties, have been carefully considered. So considered, it must be concluded that the proof does not support (or allow a conclusion to be drawn with any sense of confidence) that, more likely than not, Jacqueline's brain injury was caused by oxygen deprivation occurring during the course of labor, delivery, or resuscitation in the immediate post-delivery period. Rather, the proof demonstrates, more likely than not, that Jacqueline's brain injury was directly related to the severe and intractable hypoglycemia she suffered following delivery and that it was not associated with any event which may have occurred during the course of labor, delivery, or resuscitation in the immediate post-delivery period.14 In so concluding, it is observed that Jacqueline's course pre-delivery and post-delivery was inconsistent with hypoxic or ischemic injury having occurred during the course of labor, delivery, or resuscitation. First, the evidence documenting fetal heart rate during the course of labor and delivery does not support the conclusion that Jacqueline suffered an acute intrapartum event that led to hypoxic or ischemic injury. Notably, there were only two variable decelerations (one to 90 beats per minute and the other to 120 beats per minute), but with good beat-to-beat variability and spontaneous recovery to baseline, and no persistent or pattern of persistent decelerations. Under such circumstances, the monitoring tape was reassuring and it is unlikely, based on such tape, that fetal oxygenation was adversely affected during labor and delivery.15 Further militating against the conclusion that Jacqueline's brain injury was caused (in whole or part) by oxygen deprivation pre-delivery, or new-onset hypoxia post-delivery, is the lack of trauma associated with Mrs. LaPoint's labor and delivery (labor was short, approximately 5 hours, and delivery was by cesarean section), and the numerous inconsistencies between Jacqueline's presentation and development, and the clinical findings one would expect had she suffered hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, during that period.16 Notably, Jacqueline's Apgar scores were 4 at one minute and 8 at five minutes. While an Apgar of 4 at one minute is less than average or not normal, it is but a reflection of the infant's status where, as here, the infant is going through the change process after birth. Importantly, the Apgar did not remain depressed, as it would have had she suffered an acute intrapartum event, but progressed to 8 (a very normal Apgar score) by five minutes. Clearly, the infant was improving over that period, which also compels the conclusion that there was no new or ongoing insult. Also inconsistent with brain injury during or immediately following birth, there was no evidence of metabolic acidosis on the cord blood sample and, consequently, no evidence to support an ongoing hypoxic process during the course of labor. Moreover, had Jacqueline suffered an injury to her brain during or immediately following birth, there are a number of other clinical findings one would reasonably expect to observe that were absent in her case. For example, an infant who suffered a hypoxic ischemic injury during such period would not only present with initial depression (more severe than Jacqueline evidenced), but would continue to demonstrate severe depression at one, five, and ten minutes. Additionally, in cases of substantial neurologic injury, the infant should generally evidence seizure activity within 8 to 24 hours. Finally, inconsistent with brain injury during or immediately following birth, there was no evidence (within 5 or 6 hours of delivery) of other or multi- organ system dysfunction, including kidney dysfunction. Evidence of such dysfunction would be reflected in decreased urine out-put and on biochemical analysis of blood with elevated serum creatinine levels. No such dysfunction was present in the hours immediately following Jacqueline's birth. Contrasted with the paucity of compelling evidence of perinatal asphyxia as the cause for Jacqueline's brain injury, the medical records and other persuasive proof clearly demonstrate the presence of severe and untractable hypoglycemia and support the conclusion that Jacqueline's brain injury was caused, post-delivery, by the presence of such metablic derangement. Supportive of such conclusion, it is observed that contemporaneously with the observed on-set of hypoglycemia (at or about 6:30 a.m., following admission to the neonatal ICU), Jacqueline was observed to be jittery, lethargic, and floppy, clinical symptoms typically associated with hypoglycemia. Such presentation persisted as Jacqueline's hypoglycemia proved severe and intractable, and at or about 8:00 a.m., July 4, 1994, Jacqueline was noted to undergo an apnic episode, and her tone was flaccid, color pale, and lips dusky. Such events are clinical evidence of the on-set of seizure activity which, given its timing, is compelling proof of brain injury associated with hypoglycemia and not any event associated with labor or delivery, which occurred over 48-hours previously. Further supporting the timing and cause of Jacqueline's insult, is evidence of kidney dysfunction (diminished urine output) at or about 4:00 p.m., July 4, 1994. Given the proof, it cannot be concluded that, more likely than not, Jacqueline's brain injury, and resultant neurologic impairment, was caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Notably, Jacqueline's presentation and neonatal course were not consistent with an acutely acquired neurologic injury, and it is improbable that she could have experienced an acute injury during labor and delivery, or immediately thereafter, without evidencing clinical symptoms of such damage. Conversely, a brain injury, resulting from hypoglycemia acquired post-delivery, would be consistent with Jacqueline's presentation at birth and subsequent development.
