The Issue At issue is whether Samuel Hess, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts Jeffrey Hess and Jeanmarie Hess are the natural parents of Samuel Hess, a minor. Samuel was born a live infant on January 7, 2002, at St. Vincent's Medical Center, a licensed hospital in Jacksonville, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Samuel's birth was Karen D. Bonar, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. Here, Petitioners are of the view that Samuel suffered such an injury. More particularly, Petitioners believe Samuel's neurologic impairments are the result of a brain injury caused by hydrocephalus, secondary to an intraventricular hemorrhage (diagnosed at six days of life), that was precipitated by oxygen deprivation (a hypoxic ischemic insult), and which occurred during labor and delivery. In contrast, NICA is of the view that Samuel's impairments are most likely developmentally based, as opposed to birth related, and that, whatever the etiology of Samuel's impairments, he is not permanently and substantially physically impaired. Samuel's birth and immediate newborn course At or about 12:55 p.m., January 7, 2002, Mrs. Hess, with an estimated delivery date of January 21, 2002, and the fetus at 38 weeks' gestation, was admitted to St. Vincent's Medical Center, following spontaneous rupture of the membranes, with clear fluid noted, at 9:00 a.m. On admission, mild, irregular contractions were noted; vaginal examination revealed the cervix at 2 to 3 centimeters dilation, 60 percent effacement, and the fetus at -1 station; and fetal monitoring was reassuring for fetal well-being, with a baseline of 120 to 130 beats per minute. Given rupture of the membranes, Mrs. Hess was committed to deliver, and she was admitted for pitocin augmentation. Following admission, an IV was started at 1:48 p.m.; an epidural was placed at 3:56 p.m.; pitocin drip was started at 4:05 p.m.; Mrs. Hess was noted as pushing at 9:24 p.m.; and Samuel was delivered spontaneously at 10:24 p.m., with "Nu[cal]/Hand" (the umbilical cord wrapped around the hand) noted. In the interim, staring at or about 8:00 p.m., monitoring revealed, over time, late decelerations; marked decelerations with slow return to baseline; and evidence of a hypertonic uterus (starting at 9:24 p.m., and persisting, following periods of relaxation, until 10:22 p.m.), with exaggerated fetal heart rate variability. Such a pattern is consistent with fetal stress, and raises concerns regarding fetal reserves and adequate oxygenation. However, at delivery, Samuel was not depressed; did not require resuscitation; was accorded normal Apgar scores of 8 and 9, at one and five minutes, respectively, reflective of a healthy newborn2; and no abnormalities were observed at birth, except pronounced molding.3 Following delivery, Samuel was transferred to the nursery, and ultimately discharged with his mother on January 10, 2002. In the interim, Samuel's newborn course was normal, except for evidence of mild jaundice (diagnosed the morning of January 9, 2002), which did not require light therapy. However, on discharge, instructions were given to follow-up the next day at the Seton Center for a repeat bilirubin check. As instructed, Mrs. Hess presented with Samuel at the Seton Center on January 11, 2002, for a repeat bilirubin check. At the time, Samuel was noted to be active, alert, and in no apparent distress; his temperature was recorded as normal (as it had been following delivery, and during his admission in the nursery at St. Vincent's Medical Center); his newborn examination, apart from evidence of jaundice, was within normal limits; and Mrs. Hess reported that Samuel had fed well.4 The results of the bilirubin test were obtained at or about 1:30 p.m., that afternoon, and called to a staff physician (Dr. Vaughn), who gave instructions to initiate phototherapy. Accordingly, later that afternoon, Samuel was put under the bilirubin lights at home, with instructions to monitor his temperature every two hours. On January 12, 2002, Samuel recorded a temperature of 100.6, and on the instructions of Dr. Vaughn, Samuel was taken to the emergency room at Wolfson Children's Hospital for evaluation.5 There, Samuel was received at 6:35 p.m., and triaged at 6:42 p.m. Chief complaint was jaundice, and temperature was noted as 100.7, otherwise no abnormalities were observed. Samuel's physical examination and immediate hospital course were documented, as follows: PHYSICAL EXAMINATION: His temperature is 100.7 in the ER. The rest of his vitals are normal. His weight is 2.7 kg. He is resting, easily aroused. Anterior fontanelle is soft and flat, with normal sutures. Has good red reflexes bilaterally. Ear canals are patent. Nose without congestion. Oropharynx is clear, no cleft. Heart is normal S1 and S2 without murmurs. Abdomen is soft and nontender. Chest is clear to auscultation. Extremities are without rashes, cyanosis, clubbing or edema. He does have good femoral pulses bilaterally, and no hip clicks. Neurologically, he is alert and active . . . . LABORATORY: . . . Total bilirubin on admission was 14.2, direct was 0.5. He was tapped, and had a white count in his spinal fluid of 2,500 and red count of 241,250. He had 65 segs, 17 lymphocytes and 18 monocytes, and the spinal fluid Gram stain showed no organisms, but an occasional leukocyte. IMPRESSION AND PLAN: My impression is that we have a six-day-old with fever and abnormal leukocytosis in his spinal fluid. He was placed on ampicillin, and gentamicin . . . . He was also cultured for herpes [, which was negative]. He was started on Acyclovir 20/kilo q.8 hours. He will continue to feed. A repeat spinal tap was attempted to clear up the meningitis issue on two occasions; however, both times they were bloody. We, therefore, are going to obtain a head CT with contrast to rule out an intracranial bleed. A CT of the head was done on January 13, 2002, and revealed a bilateral intraventricular hemorrhage (IVH) and a left posterior parietal cephalohematoma.6 The CT scan was read, as follows: FINDINGS: There is molding of the bones of the calvarium, compatible with recent vaginal delivery. Curvilinear area of increased density identified within the scalp soft tissues in the left posterior parietal region, compatible with a cephalohematoma. Increased densities identified within the lumen of the left lateral ventricle, predominantly involving the left choroid plexus, but also layering in the dependent portion of the lateral ventricle, compatible with intraventricular hemorrhage from the choroid plexus bleed. In addition, increased density is identified in the dependent portion of the right lateral ventricle consistent with intraventricular hemorrhage. No extra axial fluid collections are identified. Linear area of increased density is identified in the right frontal region, only seen on images #11, and therefore likely not due to subarachnoid hemorrhage. The ventricular system is not dilated. No focal parenchymal mass is identified. After contrast administration, there are no abnormal areas of parenchymal or meningeal enhancement identified. IMPRESSION: Left posterior parietal cephalohematoma Bilateral intraventricular hemorrhage, left greater than right, with the left intraventricular hemorrhage due to choroid plexus bleed. Molding of the bones of the calvarium compatible with history of recent vaginal delivery . . . . Given the abnormalities reported on the CT scan, Dr. Randell Powell, a neurosurgeon, was requested to see Samuel for neurosurgical input. That consultation occurred on January 16, 2002,7 and was reported, as follows: . . . I have been requested to see the child for neurosurgical input. I am informed that the baby is now doing well. Septic work-up was completely negative and antibiotics have since been discontinued and the baby is anticipating discharge later on today. PHYSICAL EXAMINATION: Reveals a beautiful, sleeping, male infant with a very soft head, a very soft fontanelle, no splitting of the sutures. The head circumference is measured to be slightly less than the 50th percentile for a newborn. There is no nuchal rigidity and bending the legs did not appear to cause irritation as well. The child has a bilateral red reflex. Pupils are equal and reactive. The Moro reflex is symmetric. Computed tomographic scan shows hemorrhage emanating from the choroid plexus and the trigone of the left lateral ventricle. There is mild ventricular dilatation. Follow-up ultrasound shows similar findings. IMPRESSION: Intraventricular hemorrhage. DISCUSSION: Intraventricular hemorrhages in the newborn perinatal period that are caused by choroid plexus hemorrhage generally have an excellent prognosis as no significant brain parenchyma is disrupted and these hemorrhages usually resolve without sequelae. However, there is roughly a 20% chance of developing post hemorrhagic hydrocephalus which in 50% of cases could require more aggressive treatment. That means the baby's chances of needing neurosurgical intervention is somewhat less than 10% and this was discussed extensively with the parents who were happy to hear this news. There are no overt signs of hydrocephalus at this time and in my opinion I think that we can safely follow the baby with serial physical examination consisting of palpation of the fontanelle and head circumference measurements. I would be glad to see the baby at age one month for follow- up, but I suspect a good prognosis here. Samuel was discharged from Wolfson Children's Hospital at 6:15 p.m., January 16, 2002, with instructions to monitor his head circumference once a week, and for follow-up appointments with Dr. Hamaty (his pediatrician at the time8) and Dr. Powell. Samuel's subsequent development Following discharge, Samuel was followed by Dr. Powell for mild posthemorrhagic hydrocephalus, that appeared to stabilize, but then got worse between ages four and six months.9 Serial studies showed progressive ventricular enlargement consistent with hydrocephalus, and after discussing treatment options Samuel's parents elected to proceed with endoscopic third ventriculostomy, which was performed on August 26, 2002. Initially, Samuel appeared to be doing reasonably well, but then he developed an accelerated head circumference (53.8 centimeters, which placed him above the 98th percentile), consistent with progressive hydrocephalus, and on December 6, 2002, a Codman programmable ventriculoperioneal shunt was placed. Since that time, Samuel has done fairly well, without symptoms related to increased intracranial pressure. However, he continues to evidence macrocrania (above the 98th percentile), ventriculomegaly (enlargement of the laterial ventricules), and atrophy of brain tissue.10 (Exhibit 34). Samuel's current presentation With regard to Samuel's current presentation, the parties agree, and the proof is otherwise compelling, that Samuel is permanently and substantially mentally impaired.11 As for his physical presentation, while there may be room for disagreement, the complexity of Samuel's difficulties support the conclusion that he is also permanently and substantially physically impaired. In so concluding, it is noted that on the Vineland Adoptive Behavior Scales Form (VABS), related to daily living skills and motor skills, Samuel scored in the mentally handicapped range. "He is not yet toilet trained despite intensive efforts in this regard"; "[h]e is able to assist with simple dressing and undressing tasks but is not yet independent with these skills"; and he "continues to display gross-motor, fine-motor, visual-motor, and motor planning impairment." (Exhibits 18 and 30). It is further noted that Samuel presents with impaired postural control (aggravated by his large head), impaired strength, hypotonia, and bilateral pronatal feet. As a result, Samuel has moderate to severe impairment in strength, endurance, postural control, balance responses (with unexpected falls), functional mobility, and activities of daily living. Notably, at approximately five years of age, Samuel requires a stroller for extended outings, and caregiver assistance for 90 percent of self care needs. (Exhibit 10). The cause of Samuel's impairments As for the cause of Samuel's neurologic impairments, the proof demonstrates that, more likely than not, they are the result of a brain injury, caused by hydrocephalus, secondary to the intraventricular hemorrhage (IVH) he suffered, and which was diagnosed at six days of life. What remains to resolve is the genesis of Samuel's IVH or, stated otherwise, whether the proof demonstrated, more likely than not, that the IVH was caused by oxygen deprivation, and occurred during labor, delivery or resuscitation. § 766.302(2), Fla. Stat. ("'Birth-related neurological injury' means injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period."); Nagy v. Florida Birth-Related Neurological Injury Compensation Association, 813 So. 2d 155 (Fla. 4th DCA 2002)(The oxygen deprivation and injury to the brain must occur during labor, delivery, or immediately afterward.). The genesis of Samuel's IVH Regarding the intraventricular hemorrhage Samuel suffered, the proof is compelling that an IVH in a term infant, such as Samuel, is a rare occurrence, and its cause frequently cannot be identified. Indeed, among the physicians who addressed the issue, there is apparent agreement that the majority of IVHs (approximately 50 percent) are related to oxygen deprivation (hypoxia-ischemia) or trauma, and the remainder fall into one of two groups, those with another identifiable cause (such as vascular malformation, infection, clotting disorder, venous infarct, or genetic disorder) and those of unknown etiology (idiopathic). To address the cause and timing of Samuel's IVH, the parties offered the deposition testimony of Julius Piver, M.D., J.D., a physician board-certified in obstetrics and gynecology (albeit one who has not practiced obstetrics for 20 years); Mary Edwards-Brown, M.D., a physician board-certified in radiology, with subspecialty certification in neuroradiology; David Hammond, M.D., a physician board-certified in pediatrics, neurology with special competence in child neurology, and clinical neurophysiology; Donald Willis, M.D., a physician board-certified in obstetrics and gynecology, and maternal-fetal medicine; and Michael Duchowny, M.D., a physician board- certified in pediatrics, neurology with special competence in child neurology, electroencephalography, and clinical neurophysiology.12 The testimony of Doctors Piver, Edwards- Brown, and Hammond were offered in support of Petitioners' view on causation, and testimony of Doctors Willis and Duchowny were offered in support of NICA's view on causation. Pertinent to the issue of causation, Doctors Piver, Edwards-Brown, and Hammond were of the opinion that an infant can suffer a intraventricular hemorrhage during labor and delivery, as a result of a hypoxic-ischemic insult, and not show any clinical evidence in the immediate postnatal period. However, although offered the opportunity to do so, Dr. Hammond declined to offer an opinion as to the likely etiology (cause and timing) of Samuels IVH.13 Consequently, we are left to consider the testimony of Doctors Piver and Edwards-Brown with regard to Petitioners' view on causation. As for the etiology of Samuel's IVH, it was Dr. Piver's opinion, based on his review of the medical records, that Samuel's IVH was most likely caused by partial prolonged asphyxia, that was sufficient to cause a subtle, slow bleed during labor and delivery, which progressed to the significant IVH noted at 6 days of life, but that was initially insufficient to reveal itself (by clinical evidence of a bleed) in the immediate postnatal period. In reaching his conclusion, Dr. Piver relied heavily on his evaluation of the fetal monitor strips, which he opined revealed, starting at 6:48 p.m. (18:48), and continuing for 30 to 35 minutes, evidence of marked loss of beat-to-beat variability; late decelerations at 8:01 p.m., 8:03 p.m., 8:05 p.m., 8:25 p.m., 8:28 p.m., 8:31 p.m., and 8:33 p.m.; a marked deceleration to a low of 70 beats per minute at 8:50 p.m., with a slow return to baseline at 8:56 p.m.; a marked deceleration from 180 beats per minute to 90 beats per minute between 9:14 p.m. to 9:20 p.m.; a late deceleration at 9:23 p.m.; and evidence of a hypertonic uterus starting at 9:24 p.m., and persisting to 9:42 p.m., again at 9:50 p.m., and persisting to 10:14 p.m., and again at 10:20 p.m. and persisting to 10:22 p.m., with exaggerated fetal heart rate variability. While acknowledging the bleed could have started at any time between the 7th of January (Samuel's delivery date) and the 12th of January, when Samuel presented to Wolfson Children's Hospital, Dr. Piver was of the opinion, given his review of the fetal monitor strips, that Samuel's bleed was most likely caused by hypoxia, and that it began during labor and delivery. Dr. Piver variously noted the likely onset of the bleed as "[b]etween 2030 and 2130 hours"; "around 2000 hours"; "from 2000 hours to 2130 hours"; "between 1800 and 2224 hours"; "between 1800 and 2100 hours"; and "the 21:24 to 22:20 time interval." (Exhibit 23, pages 34, 48, 49, 57, 80, 82; Exhibit 23, deposition Exhibit 6). Dr. Edwards-Brown, like Dr. Piver, was of the opinion that Samuel's IVH was most likely caused by hypoxia, that caused a slow bleed during labor and delivery, but an insufficient bleed to reveal evidence of brain damage during the immediate postnatal period. Dr. Edwards-Brown's opinion was explained, as follows: Q How are you able to determine, based on the films that you reviewed, that the hemorrhage began during labor and delivery? A Based on the films alone, we can't make that determination. It's simply the path of physiology of the hemorrhages and the hospital course as well as the labor and delivery records that allow me to make that conclusion. * * * Q Are you able to look at the effect of the hemorrhage on the brain structures to determine or time when the hemorrhage may have occurred? A What I see is a large hemorrhage wherein the ventricle that is pretty bright and that hemorrhage is causing hydrocephalus; and the hydrocephalus, I'm sure, is causing symptoms, but hemorrhages don't cause hydrocephalus initially. It takes some time before that occurs. So all I can say is yes, the hemorrhage is having an effect on the brain, and that effect is hydrocephalus and ischemia, and it could have occurred sometime from the time of labor and delivery until the time that film was obtained. Q It could have occurred at any time in between there? A. The hydrocephalus and the ischemia. Q But not the hemorrhage? A Certainly the hemorrhage could have occurred after birth, but I would have expected some evidence of that in the clinical history. I would have expected evidence that this child had suffered a profound hypoxic injury as one might see if this child had had a code or a profound drop in his oxygen status. None of that is in the record; therefore, I don't think it's a post natal event. * * * Q Okay. How are you able to rule out in this case that the hemorrhage did not begin on January 9th, 10th, 11th or 12th? A Several things. Number one, I don't have evidence on the 9th, 10th, 11th, or 12th of January that this child suffered any hypoxic injury. Q Hemorrhage [can] be caused by something other than hypoxic injury? A It can. Q Okay, and what are the other possible causes? A Intraventricular hemorrhage might result from a tumor, might result from a vascular malformation, it could result from an infection, but it usually results from hypoxia. Q We sometimes do not know what causes intraventricular hemorrhage? A I think when we don't know what causes intraventricular hemorrhage, it is a reasonable presumption that there was hypoxia at a time when someone was not looking, as in the prenatal or labor and delivery period. If there wasn't a fetal heart monitoring strip obtained during that period and the child is born with -- excuse me, with intraventricular hemorrhage, I think the presumption should be that there was hypoxia during that time. But certainly there may be some times when we don't have an answer. Q Sometimes we simply don't know what caused the hemorrhage? A That is undeniably true; however, one should not make that presumption until we have excluded the usual causes. And in this case, based on Dr. Piver's testimony that there was evidence of hypoxia during labor and delivery, one must assume that that was the cause. We don't make the diagnosis of an idiopathic cause. That means we don't have the answer when we have evidence of a reasonable cause, which we have here. Q In your letter to Mr. Sharrit that we referred to earlier, you state on Page No. 2 further down that, "The absence of symptoms in the three days following birth is not unusual since bleeding begins small and increases with time." What do you mean by that? A That's the nature of bleeding. I'm sure you know this. We have all bled. You don't -- Well, bleeding -- unless it's the result of an aneurism -- is not so massive initially. It starts out as a leak in the vessels, and the longer it bleeds the more it accumulates . . . . (Exhibit 27, pages 39, 41, 42, 44-46). Contrasted with the opinion held by Doctors Piver, Edwards-Brown, and Hammond, Doctors Willis and Duchowny were of the opinion that if a hypoxic event is significant enough to cause an intraventricular hemorrhage during labor and delivery, there will be clinical evidence in the immediate newborn period. Dr. Willis expressed his observations on the medical records, as well as the basis of his opinions on causations, as follows: Q . . . Dr. Willis, in reviewing the records and the fetal heart tracings, were you able to identify any intervals, any intervals of concern, I suppose, or any that you thought that may have been hypoxic intervals? A Well, the fetal heart rate monitor strip looks pretty good until about an hour and a half before delivery, and then there are fetal heart rate decelerations that pretty much continue until the time of birth. Q And what was the significance of those intervals that you're talking about, to you? A Well, the decrease in fetal heart rate usually means that there's some decrease in oxygen supply to the baby. Q Okay. A Or umbilical cord compression, which could lead to that same thing. Q So are you saying you found intervals that were suspicious for oxygen compromise? A That's correct. Q Did you identify intervals of lack of beat-to-beat variability that you thought were of concern? A Well, I'll look, but most of what I saw were fetal heart rate decelerations along with really exaggerated fetal heart rate variability, which usually you see with umbilical cord compression. Q Well, are you saying, then, that there were episodes in this case where you felt there was significant cord compression? A Well, the fetal heart rate tracing certainly is consistent with umbilical cord compression. Q And over what time period would you say the fetal heart tracings are consistent with cord compression? A Well, off and on for the last hour and a half prior to birth. Q And could that create a scenario, an hypoxic scenario that could lead to some kind of vascular insult within the brain? A Now, let me be sure I understand the question. Are you asking me if I believe this fetal heart rate pattern, the abnormalities that I see led to that or can abnormalities in fetal heart rate pattern in general lead to brain injury? Q I guess my question would be, the pattern that you've identified in this case, is that consistent with a pattern that can lead to injury, vascular injury within the brain? A Well, I think it shows that there's probably some lack of oxygen during that time period. Now, the question then is, you know, did that lack of oxygen lead to brain damage. And in this case, you know, my feeling is or my opinion is that it did not lead to brain damage. Q Let's break that up a little bit. Without knowing, without looking at the final result -- I presume you're looking at the early neonatal period right after birth to help you make that conclusion. Am I correct? A Yes. Q If we for the moment put aside the early clinical course of the child, just by looking at the heart tracings and the patterns that you've identified, are those consistent with or perhaps suspicious for the kind of pattern that could lead to a fetal compromise, brain compromise? A Well, I don't know if anyone could predict fetal brain damage simply based on a fetal heart rate pattern. You really have to look at the baby, the condition of the baby after birth to be able to say whether or not the abnormalities in the fetal heart rate pattern resulted in oxygen deprivation and brain injury. * * * Q Now, you did, no doubt, note that the child did return to the hospital after discharge and was found to have a bloody spinal tap, and ultimately it was determined that it had an intraventricular hemorrhage? A That's correct. That's, I believe, on the fifth day after birth. Q Well, having identified hypoxic consistent patterns within the fetal heart tracings, how is it that you can say that perhaps did not lead to a vascular insult that slowly progressed over a period of four or five days into an extensive hemorrhage? * * * A . . . I think that it's pretty clear that if you're going to have an hypoxic injury to the brain that's substantial enough to cause brain injury then the baby really is going to be depressed at time of birth and is going to have an unstable newborn period. Simply having an abnormal fetal heart rate pattern is not enough to say that any lack of oxygen that occurred during labor caused brain damage. Q . . . And I guess you're saying across the board and without exception there can be no slowly progressing brain damage that can occur due to labor and delivery hypoxia? A Well, in order to have an hypoxic event during labor or delivery that would be substantial enough to cause an hypoxic- related brain injury, then really the baby is going to have to be depressed at birth. Now, I mean, you can have intracranial hemorrhages, choroid plexus bleeds in babies that have normal, spontaneous vaginal births with normal-looking fetal heart rate tracings. I mean, there are spontaneous hemorrhages that can occur during labor, delivery, at some point after the baby is born, in the newborn period. But what I'm saying is that if you're going to have an intracranial hemorrhage due to an hypoxic event during labor or delivery, then the baby really should be depressed at time of birth and have an unstable newborn course. Q When you say depressed after the birth, do you put any outer limit on the time frame during which the baby might become depressed? A Well, usually, by the newborn -- by the immediate post-delivery period they mean immediately after birth and until the baby is essentially stabilized after birth. For instance, in this case the baby had Apgar scores of eight and nine, required no resuscitation at all. So, you know, we really don't have anything to suggest that there's a problem in the immediate newborn period. And then during the hospital stay, other than the jaundice, the baby did not really have any problems. The baby breast-fed. It did not have any neurologic findings that were abnormal, didn't have renal failure, did not have seizures, you know, the types of things that we see with babies that suffer an hypoxic insult during labor or delivery. * * * Q I know that your opinion is that if an hypoxic event is significant enough to cause a brain damage, then you're going to have to necessarily see signs of depression at birth or shortly after birth. Am I stating that correctly? A Very nicely. Q Okay. What if we're not talking about brain damage or encephalopathy in the broad sense but we're just talking about a very small insult to one of the blood vessels in the brain that doesn't readily turn into brain damage but, rather, becomes a progressive problem over a period of several days? Is that a possible scenario? A I guess most things are possible, but that seems unlikely to me. Q It seems unlikely to you that you could have a weakening of a blood vessel or some injury that lessens the integrity of the blood vessel and that the brain damage is then latent and that's perhaps the reason why it would not negatively impact the early clinical course? A Well, let me say -- and I think we kind of went over this before -- that you can have intracranial hemorrhages on babies that have no apparent problems at all during labor, delivery. Just for reasons unknown you can have intracranial hemorrhage and blood vessels can rupture. But I guess what we're talking about is brain injury due to lack of oxygen or mechanical trauma. And my point being that if you're going to get a hemorrhage due to lack of oxygen or mechanical trauma, then the baby really should be depressed at time of birth (Exhibit 28, pages 23-30). Dr. Duchowny expressed his observations of the medical records, as well as his opinions on causation, as follows: Q. Let me at this time suggest a brain injury pathway that has been offered by others in this case for Samuel Hess and ask you to comment on that. Others have suggested that in this case there was labor and delivery hypoxia that resulted in a choroid plexus bleed and was associated with an isolated -- excuse me, where the blood was isolated -- the bleed was isolated within the ventricles during the pre-natal course and that that later produced hydrocephalus -- MR. BAJALIA: Pre-natal? MR. SHARRIT: Yes, in the first few days after birth. Q. Are you with me, doctor? A. Yes, I am, but I think you mean post- natal course. Q. I'm sorry, I'm sorry. I do. Thank you. Labor and delivery hypoxia, the choroid plexus bleed isolated within the ventricles during the post-natal course that later produced hydrocephalus and increased the internal cranial pressure that later after - - well after discharge from the hospital resulted in periventricular white matter damage. Is that a reasonable interpretation for Samuel Hess' brain injury? A. No. Q. Why not? A. There's no evidence of hypoxia. * * * Q. . . . [Y]ou don't think that they are a result of hypoxia because you don't discern evidence of hypoxia on the fetal monitor strips? A. There are abnormalities on the fetal monitoring strips. As I said before, I don't think they are associated with hypoxia. * * * Q. I understand your testimony to the contrary, but if -- if it turned out that after reviewing Samuel's fetal monitor strips you decided that there was evidence of hypoxia, would that be a reasonable link to the hemorrhage that was diagnosed? A. No, because Samuel didn't show any of the signs of hypoxia at birth so I don't believe he had any type of hypoxic damage. * * * Q. Do you not find any evidence at all of hypoxia on the fetal monitor strips? A. I believe the fetal monitoring strips indicate some fetal stress and that's all. Q. As opposed to distress? A. It just shows stress to the fetus during the inter-partum experience. That's all. Q. How do you define stress? A. I think the decelerations indicate, you know, stress on -- you know, stress is being placed on the fetus. Q. . . . [But] can't late decelerations be an indication of hypoxia? A. It's possible. Q. Could bradycardia in the 60 to 70 be[at]s per minute range be an indication of hypoxia? A. It's possible but not necessarily. * * * Q. . . . If you have an intraventricular hemorrhage that you attribute to a hypoxic ischemic insult that resulted during the course of labor and delivery and late in delivery, as has been suggested in this case, wouldn't you expect to see some clinically recognizable neurologic dysfunction in the neonate during the immediate newborn period? A. Yes, you would. Q. Even if the hemorrhage was, to use opposing counsel's words, isolated? A. Yes. If you're claiming that the neurologic problems are related to hypoxia, you would expect to see clinical signs of hypoxia at the time. Q. Even if the hemorrhage was isolated? A. Yes. Q. Can you explain that? A. You would see clinical manifestations in some way. You know, there would be some compromise in respiratory status, evidence of compromise in organ function because the lack of oxygen would affect not only the brain but other organ systems as well. You might see elevation of cardiac enzymes, liver enzymes, changes in renal function, changes in mental status, seizures, changes in blood pressure, respirations, etcetera. Q. And just so I'm clear, that is true even if the hemorrhage was isolated just within the ventricle? A. Yes, if you're attributing it to hypoxia. * * * Q. And based upon your review of the medical records, did you see any indication that Samuel had any such clinically recognizable neurological impairment or dysfunction during the immediate newborn period? A. No, I did not. Q. Did you note what his APGAR scores were? A. Yes, I believe he had normal APGAR scores. I believe they were eight and nine and one at five minutes. Q. Is that consistent with Samuel having suffered an isolated intraventricular hemorrhage that was the result of a hypoxic ischemic insult that occurred late in delivery -- A. No. Q. -- labor and delivery? A. I don't believe so. Q. Is the fact that there was no documented evidence of impaired neurologic function in Samuel during the immediate newborn period consistent with Samuel having suffered an isolated intraventricular hemorrhage that occurred late in labor and delivery? A. No. (Exhibit 29, pages 17, 18, 20-23, and 36-39). Here, there is no apparent reason to credit the testimony of Petitioners' witnesses on the issue of causation over the testimony of NICAs witnesses. Indeed, as among those who spoke to the issue of causation, Doctors Willis and Duchowny are the more qualified to address the issue, and their testimony the more persuasive.
The Issue Whether Faith Lapp, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary findings Linda J. Davidson Lapp is the natural mother and guardian of Faith Lapp, a minor. Faith was born a live infant on January 27, 1998, at Arnold Palmer Hospital for Children & Women (Arnold Palmer Hospital), a division of Orlando Regional Healthcare System, Inc., a hospital located in Orlando, Florida, and her birth weight exceeded 2,500 grams. The physicians providing obstetrical services at Faith's birth were Penny A. Danna, M.D., and Steven Carlan, M.D., who, at all times material hereto, were "participating physician[s]" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Faith's birth At or about 1:25 a.m., January 27, 1998, Mrs. Lapp (with an estimated date of delivery of January 22, 1998, and the fetus at 40+ weeks gestation) presented to Arnold Palmer Hospital, in labor. At the time, Mrs. Lapp's membranes were noted as intact, and vaginal examination revealed the cervix at 4 centimeters dilation, effacement complete, and the fetus at -1 station. Contractions were noted as mild, at a frequency of 2-3 minutes, with a duration of 40 seconds, and fetal monitoring revealed a reassuring fetal heart rate, with a baseline in the 130 beat per minute range. From 1:25 a.m. until 5:00 a.m., when her membranes spontaneously ruptured, Mrs. Lapp's labor progress was steady, and fetal monitoring continued to reveal a reassuring fetal heart rate. Thereafter, to 7:05 a.m., when vaginal examination revealed Mrs. Lapp complete, monitoring continued to reveal a reassuring fetal heart rate, with a baseline in the 150 beat per minute range, and variable decelerations, with contractions, and a good return to baseline. At 7:20 a.m., Mrs. Lapp was noted as pushing, with contractions, and variable decelerations continued without significant change until approximately 8:40 a.m., one hour prior to delivery, when fetal heart rate decelerations became persistent. Thereafter, at 9:25 a.m., the baby was noted to crown; at 9:34 a.m., the baby was noted as bradycardic with a fetal heart rate in the 70 beat per minute range; and at 9:36 a.m., the baby's head was noted as delivered, with the fetal heart rate continuing in the 70 beat per minute range. Delivery was complicated by a shoulder dystocia, and at 9:38 a.m., the labor and delivery record reveals the baby was not yet delivered, and the fetal heart rate was persisting in the 70 beat per minute range. Thereafter, at 9:40 a.m., Faith was delivered. At delivery, Faith was severely depressed (without respiratory effort, reflex, or muscle tone; a color consistent with central cyanosis; and a heart rate under 60 beats per minute), and required resuscitation (ambu bagging with 100 percent oxygen, cardiac compression for 20 seconds, and intubation). Apgar scores were recorded as 1 and 6, at one and five minutes, respectively,1 and cord pH was recorded at 7.28. Following delivery, Faith was transported to the neonatal intensive care unit (NICU), where she remained until January 31, 1998, when she was discharged to her parent's care. Faith's hospital course was summarized in her Clinical Resume (discharge summary), as follows: History . . . . Term newborn female, birth weight 4449 gm, born on 01/27/98 at APHCW. Mother is a 39- year-old gravida 2, para 1, 0 positive, maternal screens negative, uncomplicated gestation, 40+ weeks gestation, rupture of membranes 4 hr., 40 min. prior to delivery. Difficult extraction, vaginal delivery, epidural anesthesia, nuchal cord times one. During process of extraction, left fracture of the humerus. Baby cyanotic and apneic, heart rate 40-60, Ambu bagged with 100%, cardiac compressions given, intubated at one to 1-1/2 min. of life, with 3.5 cm ET tube, responded with 100% 02 by bagging, re- intubated due to air leak with 4.0 ET tube at 7-10 min. of age. Apgars 1 at one min., 6 at five min., cord pH 7.28, birth weight 4449 gm, temperature 98.8?, Accu-Chek 72, mean blood pressure low 30s. Hematocrit 49%. PHYSICAL EXAMINATION: Alert, molding of the head, bruising of the scalp. Pupils reactive to light. Nose and throat normal. Lungs coarse. No murmur. Abdomen soft. Liver 2 cm below right costal margin. Cord - 2 arteries, 1 vein. Female genitalia. Anus patent. Passing meconium. Spine normal. Left arm with swelling and tenderness at fracture site. Decreased tone and reflexes. Poor perfusion. IMPRESSION: Post mature, 41 weeks female Neonatal depression, post difficult delivery. Aspiration. Rule out sepsis. Hypovolemia. Left humerus fracture. PROBLEM LIST: Problem #1: Post mature, 41 weeks female. Problem #2: Neonatal depression. Infant required 100%, pressures of 23/3 and an IMV of 30; pH 7.4, pCO2 22, PO2 393, base excess -8.1. Weaned and extubated to room air by day one. No apnea nor bradycardia. Monitor discontinued. Problem #3: Rule out sepsis. Treated with ampicillin and gentamicin times 72 hr. Blood culture negative. Problem #4: Fracture of the left humerus. Orthopaedic consult obtained, infant was splinted, now is positioned with left upper extremity pinned across chest and is comfortable. For follow-up with Dr. Topoleski. Problem #5: Neurologic. A CT scan of the head shows some central subdural bleeding along tentorium and falx cerebri, small amount, slightly prominent extra-axial space left temporal region.[2] Problem #6: Miscellaneous. Passed ABR hearing screening exam. Annual follow-up is recommended. Infant screening was done 01/28/97. Problem #7: Fluids/electrolytes/nutrition. Feedings were begun on day 2, and advanced. Infant is tolerating ad lib feedings of maternal breast milk or Similac-20 with iron, and nippling well. Physical examination, 01/31/98: Four days of age. Weight 4555 gm, head circumference 33.25 cm. Pink. Anterior fontanelle soft. No murmur. Lungs clear. Abdomen soft and full. Neurologic appropriate. Left arm positioned as noted above. * * * FINAL DIAGNOSIS: Post term, 41 weeks female. Neonatal depression. Rule out sepsis. Left fractured humerus. Subdural bleeding. Follow-up CT scan on March 25, 1998, showed resolution of the subdural hemorrhage. Specifically, the CT scan was read, as follows: The ventricles are normal in size and configuration. There is no midline shift. The attenuation characteristics of the brain are within normal limits for the patient's age and state of maturity. No extra-axial fluid collections are identified. The hemorrhagic changes described on the study of 01/30 have cleared. IMPRESSION: CT appearance of brain within normal limits. Faith's subsequent development Following discharge from Arnold Palmer Hospital, Faith was followed for a number of evolving irregularities. Pertinent to this case, insight into the complexity of her presentation can be gleaned from some observations by a few of Faith's physicians: Michael Pollack, M.D., a pediatric neurologist; Eric Trumble, M.D., a pediatric neurosurgeon; and Harry Flynn, Jr., M.D., an ophthalmologist. Dr. Pollack initially evaluated Faith on March 30, 1998, and described his impressions, as follows: . . . Parents have observed that the patient does not follow although she appears to respond to light. She has been evaluated by Dr. Gold and Dr Richmond and apparently has retinal detachment . . . . A recent film of the patient's left arm apparently demonstrated that her humeral fracture is healing satisfactorily. * * * A recent CT scan of the head shows resolution of posterior fossa hemorrhage. In addition, the fluid collection over the left temporal region has largely disappeared but the left-sided subarachnoid space does remain larger than the right. Physical examination includes a weight of 14 pounds and a head circumference of 35.5 cm. The forehead appears underdeveloped and the head is small in relation to the face. Anterior fontanel is closed. There is ridging of coronal and sagittal sutures. Slight flattening of the right occiput is present and there is corresponding alopecia . . . . IMPRESSION: Perinatal craniocerebral trauma and probable hypoxic ischemic encephalopathy. Retinopathy by history. Evolving microcephaly versus craniosynostosis: Primary microcephaly (failure of the head to grow because of poor brain growth) appears more likely than craniosynostosis . . . . Dr. Pollack summarized his September 29, 1998, evaluation, as follows: Faith is an 8-month-old girl who was initially evaluated in my office 3/98 because of visual impairment and suspected seizures. Her diagnoses include perinatal craniocerebral trauma and a possible hypoxic ischemic encephalopathy. In addition, she had a congenital retinopathy. Her diagnoses at Bascom Palmer Institute were: (1) congenital bilateral retinal detachment and (2) variation of persistent hyperplastic primary vitreous or persistent fetal vasculature bilaterally. Her MRI scan of the head showed an abnormality of the rostrum of the corpus callosum which was thought to fall in the spectrum of septo- optic dysplasia. Her condition, therefore, appears to be due to a combination of congenital anomalies and perinatal factors . . . . In the past few months, the patient has undergone . . . [repair of metopic synostosis]. Although the shape of her head has improved, her head circumference has remained below the 5th percentile, supporting the view that primary microcephaly rather than craniosynostosis was responsible for the small head size in this patient. In addition, ptosis of the right upper lid developed postoperatively. * * * PHYSICAL EXAMINATION: Includes a length of 26.5 inches, weight 18-3/4 pounds, head circumference 38.5 cm. The head appears small in relation to the face. There is unilateral occipital flattening . . . . IMPRESSION: Severe nonprogressive encephalopathy due to perinatal factors as outlined above and a congenital anomaly of the central nervous system. There is severe visual impairment which is due to a retinal anomaly . . . . Her residual microcephaly suggests that deficient brain growth rather than craniosynostosis was responsible for her small head size . . . . Development is globally delayed. The combination of microcephaly, congenital CNS anomalies, visual impairment and global developmental delay in this patient suggests that she is likely to function in the trainable mentally handicapped range. Her motor attainment to date implies that she will walk independently. Following September 29, 1998, Faith was seen by Dr. Pollack on July 21, 1999; April 3, 2000; and July 17, 2001, during which there was no apparent change in Dr. Pollack's impression. Thereafter, the record suggests that following Faith's last visit with Dr. Pollock, her neurology issues were followed in Miami; however, there is no evidence of record regarding those evaluations, if any.3 Following discharge from Arnold Palmer Hospital, Faith was also seen by Dr. Trumble and had serial workups for craniosynostosis. That diagnosis was rejected July 9, 1998, when "a head CT with 3-D reconstruction . . . revealed all sutures to be open with the exception of her metopic suture, which was supposed to be closed at this age." Faith did, however, have "metopic synostosis with a small palpable ridge," which was repaired on July 29, 1998. Faith apparently did well post-operatively, with the exception of right eye ptosis. Of note, an uncontrasted CT scan was reviewed by Dr. Trumble in March 1999, which he noted: "identifies normal morphology without evidence of increased CSF spaces or definite atrophy." On April 20, 1998, Faith's ophthalmologic problems were evaluated by Dr. Flynn, professor of ophthalmology at Bascom Palmer Eye Institute, Miami, Florida. Dr. Flynn described his impressions as follows: . . . [Faith] was examined on 4/20/98 regarding her retinal detachments in both eyes. . . . [The patient] had a traumatic delivery that involved extensive facial, cranial and subconjunctival hemorrhages. The patient has brought with her multiple studies including X-rays, CT scans and other studies that have been reviewed and are present on the chart. The patient is being referred regarding the possibility of any surgical therapy for this patient with bilateral retinal detachments. The ocular examination showed no recordable visual acuity although there did appear to be a response to light in each eye. The pupillary reaction showed a 1+ response to direct light in each eye. The tension by palpation was normal in both eyes. The anterior segment examination showed a white plague-like structure on the back surface of the lens in both eyes. The vitreous cavity was clear with no visible hemorrhage in either eye. The posterior segment examination showed total retinal detachment with dragging of the retina toward the inferior temporal quadrant in both eyes. The retinal folds were drawn forward as well to fibrous tissue inserting on the back surface of the lens. IMPRESSION: Congenital bilateral retinal detachment both eyes. Variation of persistent hyperplastic primary vitreous or persistent fetal vasculature both eyes. RECOMMENDATION: I discussed my findings with the patient [sic] and husband. I indicated that the retinal detachments were inoperable. I indicated that the changes present in the back of the eye could not have taken place in 2 1/2 months in spite of the extent of the trauma at delivery.[4] Apart from the impressions of Faith's treating physicians, some insight into Faith's development may also be gleaned from certain evaluations and testing by the Seminole County Public Schools; including a Report of Adoptive Behavior Testing, dated August 21, 2003. On that test, administered at age 5 years, 7 months, Faith's ability to care for herself and interact with others ("Broad Independence") was measured based on an average of four areas of adaptive functioning: motor skills, social interaction and communication skills, personal living skills, and community living skills. There, Faith's motor skills, which included gross and fine motor proficiency tasks involving mobility, fitness, coordination, eye-hand coordination, and precise movements were said to be comparable to an individual at age 3-1 (3 years, one month). However, the examiner noted the basis for such conclusion, as follows: When presented with age-level tasks, Faith's gross-motor skills are age-appropriate. Age-level tasks involving balance, coordination, strength, and endurance will be manageable for her. When presented with age-level tasks, Faith's fine-motor skills are very limited. Age- level tasks requiring eye-hand coordination using the small muscles of the fingers, hands, and arms will be extremely difficult for her. (Emphasis added.) (Intervenor's Exhibit 4.) Faith's motor skills were also evaluated by the Seminole Public County Schools, and noted in a Physical Therapy Assessment/Evaluation report, dated October 2, 2003, as follows: OBSERVATIONS: Faith was evaluated in a variety of educational settings. She was observed in the classroom, during an obstacle course in another classroom, on the playground and around the school campus. During the obstacle course observation, Faith was participating in tunnel creeping, rockerboard activities, basketball and balance beam walking. Throughout the evaluation, it appeared that Faith had difficulty with some motor tasks due to body and spatial awareness as well as with her speed and intensity of her movements. With this evaluator, Faith followed all directions and seemed eager to please. * * * FUNCTIONAL MOBILITY: Faith ambulates indepen[den]tly in all directions demonstrating a forward lurch, hiking type of gait pattern, head is bent forwards. She is able to walk in the halls, on ramps and on sand on the playground without falling. She is able to creep and knee walk independently. Rises from the floor using a half kneel pattern or through a backwards crab type of pattern. Lowers self to floor with control. Transfers in/out of all chairs independently but teacher reports she often trips over her own feet. Ascends the stairs using a reciprocal pattern without holding the rail, descends using step to step pattern holding the rail. GROSS MOTOR: Faith sits on the floor with good balance in a criss cross position or sidesit position. She low kneels but weight bears on her right side more than her left and high kneels with good balance. She squats to pick an item up off the floor. Is able to jump off the floor and jumps on the trampoline at least 5 times in a row. She is able to walk on the balance beam taking 3 steps independently and attempts to walk backwards on it. On the playground, she is able to climb all structures independently with supervision. Within the school environment, Faith is able to push/pull her exterior doors and turn knobs of all interior doors. FINE MOTOR/VISUAL MOTOR: . . . According to notes from OCPS records, Faith may exhibit some visual motor issues as well as the visual impairment already noted. (Intervenor's Exhibit 4.) Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as in "injury to the brain . . . caused by oxygen deprivation or mechanical injury, occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. In this case, Petitioner and Intervenor are of the view that Faith suffered a "birth-related neurological injury," as defined by the Plan. In contrast, NICA is of the view that Faith did not suffer a "birth-related neurological injury" since her neurologic impairments are, more likely than not, prenatal (developmental) in origin, and resulted from cerebral malformation, as opposed to brain injury caused by oxygen during labor, delivery, or resuscitation. Moreover, NICA is of the view that Faith is not permanently and substantially mentally and physically impaired. The cause and timing, as well as the significance of Faith's impairment To address the cause and timing of Faith's impairments, as well as their significance, the parties offered the records related to Faith's birth and subsequent development, portions of which have been addressed supra (Joint Exhibits 1-4, and Intervenor's Exhibit 2); a color photograph of Faith taken several hours after her birth (Petitioner's Exhibit 1); the deposition of Leon Charash, M.D., a physician board-certified in pediatrics, who practices pediatric neurology (Intervenor's Exhibit 1); the deposition of Donald Willis, M.D., a physician board-certified in obstetrics and gynecology, as well as maternal-fetal medicine (Respondent's Exhibit 1); and the deposition of Michael Duchowny, M.D., a physician board- certified in pediatrics, neurology with special competence in child neurology, and clinical neurophysiology. (Respondent's Exhibit 2.) Dr. Willis, whose deposition was offered on behalf of NICA, was of the opinion that the birth records failed to support a conclusion that Faith suffered a brain injury from oxygen deprivation during labor or delivery, but offered no opinion regarding the likelihood of brain injury from oxygen deprivation during the course of resuscitation or from trauma associated with Faith's delivery. Dr. Willis expressed the basis for his opinions, as follows: BY MS. WRIGHT: * * * Q. After reviewing the records in this case, do you have an opinion within a reasonable degree of medical probability as to whether or not Faith Lapp qualifies for compensation under the NICA criteria you just described? * * * A. Yes, it was my opinion that there did not appear to be a loss of oxygen that occurred during labor or delivery that would result in this child's injury. * * * Q. Doctor, would you tell us how it is that you reached such an opinion as that? A. Yes. I reviewed the fetal heart rate monitor strips, which do show fetal heart rate decelerations during the latter few hours of labor. Although they're not persistent decelerations until about the last hour before delivery, and then the fetal heart rate tracing does show persistent variable decelerations . . . . The Apgar scores that the baby had were low, the Apgar score was one and six. Of course, the baby had -- there was a shoulder dystocia at birth resulting in a very difficult delivery. However, the umbilical cord blood gas was normal with a pH of 7.28. And the baby had a course in the hospital that did not suggest an ischemic event during labor or delivery. In other words, did not have seizures in the post-delivery period, no other organ failure like renal failure, hypotension, those types of things, and was discharged home on the fourth day. So looking at all of that, I felt there was not oxygen deprivation during labor or delivery. Q. . . . What is the significance of the fetal heart rate monitoring strips? A. Well, the fetal heart rate monitor strips are consistent with some degree of umbilical cord compression or variable decelerations prior to delivery, and all fetuses react differently to that. But certainly if the fetal heart rate decelerations persist and are significant, then it can lead to a baby that has lack of oxygen at birth. * * * Q. Dr. Willis, can you tell us the significance of the cord blood pH which you referenced earlier as being normal at 7.28? A. Right. Well, if a baby is born with a lack of oxygen, then they will have lack of oxygen and acidosis, which the two go together. And if the baby has lack of oxygen acidosis, then the cord pH should be low. If the umbilical cord blood pH is within normal limits, it would suggest that for whatever fetal heart rate decelerations or whatever Apgar scores that were present, that that wasn't a result of or did not cause or was not a result of lack of oxygen to the baby. * * * Q. Would you anticipate the pH to be abnormal if the deceleration that you saw on the fetal heart monitoring strips had continuously occurred? A. Well, the fetal heart rate monitor strip shows you that in a way that the baby is being stressed, but it doesn't really tell you if the baby is in distress. So different babies tolerate different amounts of fetal heart rate deceleration. So the bottom line here was the umbilical cord pH being normal. I felt that I could not say that those fetal heart rate decelerations that were present in that hour prior to birth really resulted in lack of oxygen to the baby. Q. In other words, you would have anticipated the pH score to be abnormal if the infant had been severely affected by the deceleration? A. That is correct. * * * Q. And the significance of the Apgar scores? A. Well, the Apgar score at one minute tells you how much resuscitation is going to be required for the newborn, and the one was simply one point for fetal heart rate. The baby at birth had no spontaneous respiration, it was pale and it was not moving, and the only points that the baby got -- therefore, was depressed at that time, and the Apgar score was one. The one- minute Apgar score is not a very good indicator of long-term neurologic development though. The five- and the 10 minute Apgar scores are better indicators for that. The Apgar score at five minutes was listed at six. That's still low. We consider Apgar score to be low if it is under seven. So a six is just under the cut-off. If the baby had an Apgar score of seven at five minutes, then it would have been considered a normal score . . . . * * * BY MS. LAPP: Q. [D]o you normally . . . [limit yourself as you did in this case]? A. Normally -- normally, in most cases, I don't limit myself as much as I am with your case. Q. You found that my case was -- A. I found it a little bit confusing. If I saw the fetal heart rate tracing that I saw here and the Apgar scores that I saw and if the cord pH was abnormal, or I didn't see a cord pH, then I would have assumed that there would have been hypoxia to this baby at birth. But the fact that the cord pH was so normal, I really have to stop and question that. So then with that -- and this happens in other cases. So with that then, I have to look and see what else. And from doing this for several years and practicing in my subspecialty, I know that babies that have hypoxic injury to the brain at time of birth or during labor frequently have seizures during the first hour or two after birth and many of the other things that we've talked about. So, for instance, if your baby would have had a seizure disorder an hour or two hours after birth and would have been hypotensive, I might have in that circumstance decided that I would have simply ignored the cord pH result because it wouldn't have fit everything that I see. Q. Could it be possible that . . . [it was] human error . . . ? A. That is why I look at many different things. Again, if I would have seen other things that would have been consistent with hypoxic injury to the brain at birth, then I would have said I am going to discard this cord pH because it just doesn't fit the rest of the picture. And so that is the reason I kind of limited myself to labor and delivery, because the baby is depressed after birth, and I really can't explain that. * * * Q. . . . When would she have had these seizures? A. It would have been after birth, relatively in a short period after birth. I guess what I'm trying to say is from a maternal fetal standpoint, the medicine that I practice, if I see a poor fetal heart rate tracing and a baby with low Apgars and then seizures two hours after birth and then a CT scan done at five or six days of life which shows a cystic structure -- shows maybe brain edema consistent with hypoxic injury, then that all becomes a very, very clear picture for me. In this case, unfortunately, the picture just was not so clear. Because of that, I wanted to limit myself to labor and delivery because I could not make such a clear picture of what happened after that. (Respondent's Exhibit 1.) Dr. Duchowny, whose deposition was also offered on behalf of NICA, was of the opinion, based on his review of the records and his neurologic evaluation of Faith on March 12, 2003, that Faith's impairments, more likely than not, resulted from cerebral malformation, as opposed to brain injury caused by oxygen deprivation during labor, delivery, or resuscitation, and that, regardless of the cause, Faith was not permanently and substantially mentally and physically impaired. Dr. Duchowny expressed the basis for his opinions, as follows: BY MS. WRIGHT: * * * Q. Could you tell me, after reviewing the records concerning the records of both Linda Lapp and also Faith Lapp, your review of all the records you've just named and your examination of Faith Lapp, if you have reached an opinion which is in the reasonable degree of medical probability as to whether or not Faith Lapp sustained permanent mental and physical impairment as a result of her labor and delivery? A. Yes. I believe that Faith does not have a substantial mental or motor impairment and that her neurologic disabilities were acquired in utero and not the result of a birth related neurological injury that occurred during labor, delivery or resuscitation in the immediate post delivery period. Q. Could you tell me what you base that opinion on, Doctor? A. That opinion is based on the medical records which indicated that Faith's labor and delivery were complicated by a fractured left humerus, but that her cord blood pH was normal; her Apgar scores of 1 and 6 were reasonably good; that she did not have findings in the post natal period which are consistent with either mechanical injury or severe hypoxia; and that her evaluations, including my examination, all suggested that the types of neurologic disabilities that she has resulted from developmental abnormalities which occurred during the time that the brain was forming in interuterine life. Q. Doctor, in examining Faith's records, would you comment on the blood cord results? A. Well, her cord pH of the blood gas was 7.28, which is essentially normal. There is no indication of any hypoxia at that point in time when the blood gases were drawn from the cord. Q. Would you comment--you said earlier that her Apgar was relatively normal at 1 and 6. What did you mean by that? A. An Apgar score of 1 at one minute is not an unusual finding in normal deliveries. It reflects obstetrical medication; and I think the important Apgar score is at five minutes, which for Faith was 6. While not being perfect, it certainly is a decent Apgar score and inconsistent with asphyxia. * * * Q. Well, you indicated after that, if I heard you correctly, that you didn't see any post delivery signs of hypoxia. A. That's correct. Faith did require some ventilatory support for the first day, but she never developed systemic signs of hypoxia, which might produce abnormalities of her heart, liver, kidney, lungs, or cardiovascular system. * * * Q. You indicate further that there was no evidence of mechanical injury. Could you tell us for the record what you mean by "mechanical injury?" A. Well, there was no evidence of mechanical injury to the central nervous system, meaning there was no trauma to the brain or spinal cord. Faith did have a left Erb's palsy, which indicates dysfunction in the brachial plexus. I believe this was mechanically induced, but it was outside the central nervous system. * * * Q. Let's now turn to your opinion that Faith does not suffer from a substantial and permanent mental or physical impairment. Could you comment on the reasons why you believe that to be your opinion? A. Yes. At the time that I evaluated Faith last March, she was five years old. She did have a short attention span, and she was an overactive child, but she was able to talk. Albeit with a speech delay, she was able to talk. In fact, could speak in short phrases. She seemed to be socially appropriate. And with some effort, one could actually complete the examination because there would be some interaction between Faith and myself. She wouldn't cooperate for all testing but much of the testing did in fact get done. * * * BY MR. THOMPSON: * * * Q. . . . [Y]ou . . . [agree] that you believe there are neurologic abnormalities. Correct? A. Yes. Q. When you say that they were acquired in utero, you think that those were something that developed prior to the birthing process? A. Yes. Q. Is that what you mean? A. Yes. Q. Do you have a name for whatever that process was that caused that? A. I believe it is cerebral malformation. Q. And is that a chromosomal problem? A. Not usually. Q. What's usually the cause of that? A. Unknown interuterine acquired factors. Q. You have stated that you agree that there were mechanical injuries to this child during the labor and delivery process, correct? A. Yes. Q. You said one evidence of that was the fractured humerus. Correct? A. Yes. Q. She had some abnormalities on CT scan, I believe, some sort of--I can look for it, but you may remember what it was. I've got it right here. "A central subdural bleeding along the tentorium and faux cerebrum of a small amount." Do you recall that CT scan of the head that was taken shortly after her birth? A. Yes. Q. Would you agree that that was the result of a mechanical injury to her head? A. Yes. * * * Q. Would you agree that the pH of 7.28 in the cord blood may not represent what her true level of acidosis was? A. No, I wouldn't agree with that statement. Q. Could that be a lab error? * * * A. Well, anything is possible; but given the Apgar score and given her ultimate clinical findings, I regard that cord blood pH as being accurate. Q. What do you account for her being cyanotic? A. She already had brain dysfunction in utero. So, if you take a newborn, whose brain is not normal, and you provide stress, their response is often abnormal. Q. . . . Would you agree that Faith's laboratory work after her birth did show evidence of problems with her liver? A. No. Q. Are you familiar with what her LDH was? A. Yes. It was elevated, but the rest of her liver functions were normal. Q. Was her AST normal? A. I would have to check. I don't believe it was significantly elevated. Q. Was her ALT abnormal? A. Again, there were mild elevations that I don't think were significant, as I recall. Q. I may have asked you this. I apologize if I have. You do agree that her hydrocephaly is a result of secondary atrophy, as opposed to some other reason? A. No, I don't agree with that. Q. But you disagree with Dr. Trumbull [sic] when he said that in his report of July 9th, 1998?[5] A. Well, you would have to ask Dr. Trumbull [sic] what he meant by that. But my understanding is that there were findings, there were abnormalities, but they would not be classified as atrophy. It would really be failure to develop, which is different. Q. How can you distinguish between atrophy and failure to develop? A. Well, atrophy implies at one point all the brain structures were normal, and then something happened to damage those structures. Developmental problems imply that they never developed correctly in the first place so they never assumed normal proportions. The findings that Faith had on her MRI are more consistent with developmental abnormalities to her brain, so I would not classify them as atrophy. (Respondent's Exhibit 2.) Dr. Charash, whose deposition was offered by Intervenor, and whose testimony was supportive of Petitioner's claim, did not examine Faith, although he was accorded the opportunity to do so,6 but based on the records, he was of the opinion that Faith suffered a "birth-related neurological injury." With regard to brain injury, Dr. Charash was of the opinion that Faith's injury had two components, lack of oxygen and trauma (mechanical injury). As for oxygen deprivation being a likely course of brain injury, Dr. Charash noted Faith's one-minute Apgar score, which reflected severe depression; the need for resuscitation; an increased number of nucleated red cells; a low bicarb; a likely false pH, since Faith was given a bolus of sodium bicarb on delivery without adverse effect; and evidence of kidney malfunction, with transient abnormalities in her liver enzymes. As for trauma, Dr. Charash noted the subdural hemorrhage (cephalohematoma), observed on CT scan at 3 days of age, a likely result of trauma during delivery, as well as the severe bruising of the head documented following delivery. Finally, as further evidence of likely brain injury, Dr. Charash noted that on delivery, Faith's head, at 33 1/4 centimeters, was normal, but within a matter of months failed to grow as one would expect, and that she is now microcephalic. Consequently, Dr. Charash concluded that Faith likely suffered brain injury during labor, delivery, and resuscitation caused by oxygen deprivation and mechanical injury. (Intervenor's Exhibit 1, page 18.) As for the neurological consequences associated with such injury, Dr. Charash offered the following observations: EXAMINATION BY MR. TOWNSEND: * * * Q. Did . . . the lack of oxygen or the trauma affect her mentally in any way? A. Yes. I think it has left her with certain physical stigmata and certain intellectual stigmata. She has certain physical injuries based upon her birth difficulties and she's been left with behavioral and cognitive and learning difficulties; yes. Q. And that's clearly set forth in the records that you've reviewed, the cognitive and the physical problems? A. Yes. Let me deal with them one at a time, if I may. Q. All right, sir. A. The Orange County Public Schools have evaluated her and they find her functioning at percentiles which are far below age expectations. For example, there's a report of the Highland Elementary School in kindergarten described on 8/21/03, it's one of many reports, but this brings us up to five years and seven months . . . . At this point in time she's five years and seven months old. Her ability for functional independence is that of a three-year old which puts her in the lower one tenth of one percent of the population, 0.1, which means that 99 people out of a hundred outscore her in that area. They give her a rating for motor skills. They think her motor skills are three years and one month at an age of five years and seven months, which, again, puts her in the profoundly retarded area in terms of her motor skills, precise movements, coordination, fitness, etc. They have another score of social interaction and communication. Again, she's equivalent in one area to a three year one month old, another area she can pass tests at two years and two months, she has great difficulty with tasks that approach four years and eight months. And so it goes. They basically conclude that in every area she averages out three years and no months. She's five years and seven months. This gives her a quotient of an aggregate of all other adaptive performance in the range of retardation . . . . There is a psychoeducational evaluation done at the Seminole County Public Schools. This is carried out when she's five years and seven months. . . . The conclusion here . . . is . . . that the child is performing in areas that range from the very low category in the WJ-111 cognitive battery. She's considered to be significantly deficient. She's in the second percentile in the Bracken, B-R-A-C-K- E-N, basic concept scale. She's in the fourth percentile in some other test. On the Stanford Binet, in her verbal ability she does better, she's at the 12th percentile, and that's not retarded. . . . Now, her physical problems are of great significance here and, frankly, I think they relate to what I've mentioned before, her problems with balance, equilibrium, coordination, some of which may be tangentially a consequence of her visual impairments, but it is my opinion within a reasonable degree of medical certainty that her major physical problem aside from the structural change in her brain which makes it abnormally very, very small is her blindness or her severe visual impairments. As noted, Dr. Charash was of the opinion that Faith's principal physical injury was her visual impairment, which rendered her substantially physically impaired, and that Faith's visual impairment resulted from bilateral retinal detachment that was caused by mechanical injury during delivery.7 (Intervenor's Exhibit 1, pages 21-31.) Consequently, if credited, Dr. Charash's testimony would support the conclusion that Faith suffered bilateral retinal detachment caused by mechanical injury that rendered her substantially physically impaired, and that such impairment did not result from a brain injury. Notably, other physicians who have examined Faith, as well as the Seminole County School System, have concluded that Faith's gross and fine motor skills, except to the extent they may be diminished because of her visual impairment, are age appropriate. Consequently, given the record, there is no competent proof to support a conclusion that Faith is permanently and substantially physically impaired, because of a brain injury. Here, the opinions of the experts offered by the parties, as well as the other proof of record, have been carefully considered. So considered, it must be resolved that, while Faith's delivery was traumatic and there is evidence to suggest that she may have suffered oxygen deprivation during labor, delivery and resuscitation, as well as mechanical injury, as evidenced by the cephalhematoma, the proof fails to support the conclusion that, more likely than not, any oxygen deprivation or mechanical injury she may have suffered resulted in significant brain injury, or that she is permanently and substantially physically impaired. In so concluding, it is noted that Faith's hospital course post-delivery was not consistent with Faith having suffered an acute brain injury; that the imaging studies do not reveal brain injury, (i.e., evidence of atrophy) and are therefore most consistent with cerebral malformation; that Faith's current deficits have a congenital basis, at least in part; that Dr. Duchowny, as opposed to Dr. Charash, examined Faith, and based on his training and experience is most qualified to address the neurologic issues in this case; and that Dr. Duchowny, as opposed to Dr. Charash, was most candid, and his opinions were most consistent with the other proof of record. Consequently, it is resolved that the more credible proof demonstrates that Faith's impairment, more likely than not, resulted from cerebral malformation, as opposed to brain injury caused by oxygen deprivation or mechanical injury during labor, delivery or resuscitation, and that, regardless of the cause, Faith is not permanently and substantially physically impaired.
Conclusions The attending nurse's actions and inactions fell below the standard of professional care applicable under the circumstances. The consequences of a below normal fetal heart rate are so critical that, even if the nurse was suspicious that the monitor was not working properly, her proper response should have been to take immediate steps to determine whether the fetus was in distress, to intervene with resuscitation measures if needed, and to alert a doctor. Her failure to take appropriate action was negligence and was the proximate cause of the injuries suffered by Janaria. South Broward Hospital District, doing business as Memorial Regional Hospital, is liable as the nurse's employer. There are many reasons for entering into a settlement agreement other than the perceived merits of the claim and, therefore, I am not precluded from reviewing the terms of the parties' settlement agreement in this matter and determining whether they are reasonable under the totality of the circumstances. In this case, the settlement amount is far less than the usual jury verdict for injuries of this nature. Had this case involved a private hospital, the settlement amount would probably have been much larger. Therefore, I believe it would be fair and reasonable for the Senate to pay an award of $550,000 (or 50 percent more than the agreed settlement amount). ATTORNEY’S FEES AND LOBBYIST’S FEES: In compliance with s. 768.28(8), F.S., the Claimants' attorneys will limit their fees to 25 percent of any amount awarded by the Legislature. However, Claimants’ attorneys did not acknowledge their awareness of the provision of the bill that limits attorney’s fees, lobbyist’s fees, and costs to 25 percent of the award. They propose a lobbyist's fee that would be an additional 6 percent of any award. OTHER ISSUES: The bill should be amended to correct the name of the defendant to South Broward Hospital District. Of the two annuity options presented by the Claimants' attorney, I believe the option that guarantees payment for 40 years is the better option. In addition, because Shakima Brown received nothing in the settlement, I believe the bill should specify that, in the event that Janaria dies before the trust fund is exhausted, the balance in the trust fund should go to Ms. Brown. The District stated that paying a claim in the amount of $300,000 would not impair its ability to provide normal services. RECOMMENDATIONS: For the reasons set forth above, I recommend that Senate Bill 38 (2008) be reported FAVORABLY, as amended. Respectfully submitted, cc: Senator Ted Deutch Representative Kelly Skidmore Faye Blanton, Secretary of the Senate Bram D. E. Canter Senate Special Master House Committee on Constitution and Civil Law Tony DePalma, House Special Master Counsel of Record
Findings Of Fact Jose Alfredo Lopez-Martinez was born on September 29, 2004, at Manatee Memorial Hospital in Bradenton, Florida. He weighed 3,125 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Jose. In a report dated May 24, 2012, Dr. Willis opined as follows: I have reviewed the records for [Jose Lopez- Martinez]. The mother, Natividad Martinez was a 22 year old G2 P1 with late pregnancy care. Pregnancy care was started during the third trimester. She was admitted to the hospital in labor at term. Her cervix was dilated 4 cms on admission. Amniotic membranes were ruptured with clear fluid. Fetal heart rate (FHR) monitor during labor shows a normal baseline heart rate of 130 bpm. FHR variability is reactive. FHR monitor tracing does not suggest fetal distress during labor. Spontaneous vaginal delivery was accomplished without complications. Birth weight was 3,125 grams. The newborn was not depressed. Apgar scores were 9/9. The baby cried and had spontaneous respiratory effort at birth. No resuscitation was required. The baby had a normal newborn hospital course and discharged home on DOL 2. * * * In summary, Labor and delivery were uncomplicated. FHR monitor did not suggest fetal distress during labor. The baby was not depressed at birth. The newborn hospital course was uncomplicated. 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. 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. The opinion of Dr. Willis that Jose did not suffer a neurological injury due to oxygen deprivation or mechanical injury during labor, delivery, or immediate post- delivery period is credited.
The Issue The issue in this case is whether Kayla Mackenzie Stowers sustained a birth-related neurological injury.
Findings Of Fact Tatiana C. Stowers and Robert M. Stowers are the natural parents of Kayla Mackenzie Stowers, a minor. Kayla was born a live infant on October 12, 2009, at Orange Park Medical Center, a licensed hospital located in Orange Park Florida. Eric J. Edelenbos, M.D., provided obstetric services at the birth of Kayla, and at all times material to this proceeding, was a “participating physician” as defined in section 766.302(7), Florida Statutes. Kayla weighed 3,078 grams at birth. On October 12, 2009, Mrs. Stowers, who was at full term, was admitted to Orange Park Medical Center at 6:28 a.m., for induction of labor. Her prenatal course had been uneventful. The baby?s baseline fetal heart rate on admission was 150 bpm, and the fetal heart rate monitor did not show any fetal distress during labor or delivery. At 8:05 a.m., Pitocin was administered to augment Mrs. Stowers? labor. During her labor, the dosage of Pitocin was increased. At 1:48 p.m., Dr. Edelenbos ruptured Mrs. Stowers? membranes, and the medical records indicate that the amniotic fluid was clear and odorless. At 9:40 p.m., Mrs. Stowers delivered Kayla by normal spontaneous vaginal delivery. At birth, Kayla?s mouth and nose were suctioned, but no other resuscitative measures were needed or administered in the delivery room. No complications were noted at her birth, and she was in stable condition. Kayla?s Apgar scores at one and five minutes were eight and nine respectively. At 10:30 p.m., Kayla was noted to have respiratory distress. Her left nasal passage was tight and her right nare was patent. She was transferred to the hospital?s neonatal intensive care unit. On October 13, 2009, at 12:05 a.m., Kayla was placed on a nasal cannula and an IV was started. Antibiotics were given at 12:20 p.m., and Neo-Synephrine was administered for nasal stuffiness. By 3:45 p.m., on October 13, 2009, Kayla had increased retractions and grunting and was placed on neonatal CPAP at 100% oxygen. During the evening of October 13, 2009, Kayla experienced two apneic episodes with jerking movements of her arms and leg. On October 14, 2009, Kayla was on CPAP for four hours and then intubated due to the apneic episodes the previous evening. A chest X-ray taken of Kayla on October 13, 2009, was within normal limits. On October 14, 2009, Kayla had a normal neonatal head ultrasound. On October 15, 2009, it was noted that Kayla had not experienced any abnormal movements for 24 hours. At 6:00 p.m., on October 17, 2009, Kayla experienced periodic episodes of jerking of hands and legs, in addition to the arching of her back. On October 18, 2009, Kayla had jerky movements of all extremities, including her eyes rolling back. The movements stopped with restraint, but were not typical seizure-like movements. On October 19, 2009, due to suspected seizures, respiratory distress, and suspected sepsis, Kayla was transferred from Orange Park Medical Center to Wolfson Children?s Hospital for further workup. An EEG performed on Kayla on October 20, 2009, was within normal limits. A follow-up video EEG on November 4, 2009, was normal. An MRI was done on Kayla on October 21, 2009, and the followings findings were reported: Moderate image degradation secondary to patient?s motions. Normal variant cavum septus pellucidum and cavas vergae. Prominent extra-axial fluid at the anterior aspect of both middle fossae, and with „apparent? suboptimal opoerculation of the Sylvian fissures ? clinical signicance. Followup US may be helpful for further evaluation. Remainder of the examination appears otherwise unremarkable. Kayla?s attending physician at Wolfson Children?s Hospital indicated in her discharge summary dated November 10, 2009, that the MRI was normal. On December 9, 2009, Kayla was taken to the emergency room at Wolfson Children?s Hospital. While in the emergency room, Kayla experienced apneic episodes that required intubation. She was admitted to Wolfson Children?s Hospital. While admitted to Wolfson Children's Hospital, Kayla had abnormal movements that were nonspecific and not due to seizures. Kayla was discharged on December 22, 2009. In his discharge summary, Clifford David, M.D., summarized the hospital course as it related to the seizure-like activities. Neurology-wise, the patient was again worked up for this possible seizure-like activity, which was possibly due to reflux. This workup included another EEG and MRI. The CT of the head that was done on admission was reported as positive for a remote area of ischemia involving the basal ganglia but repeat MRI on admission showed no area of acute ischemia. The patient was witnessed to have back arching and head extension with some clenching of the arms and chest, again unsure whether this was seizure versus reflux versus obstructive airway. Neurology examined the patient and EEG showed no epileptiform discharges although was limited secondary to movement artifact. The repeat MRI referenced in Dr. David?s discharge summary was done on December 12, 2009. The findings of this MRI indicated that there was no acute ischemic event. Respondent retained Donald C. Willis, M.D., to review the medical records for Kayla. Dr. Willis reviewed the fetal heart rates of Kayla as recorded by the fetal heart rate monitor during labor. It is Dr. Willis? opinion that the fetal heart rate monitor did not show any fetal distress during labor. On the issue of whether there was an obstetrical event which resulted in loss of oxygen or mechanical trauma to Kayla during labor or delivery, Dr. Willis opined: In summary, there was no fetal distress during labor. The baby was not in distress at birth. Apgar scores were 8/9. Immediately after delivery, the baby was placed on the mother?s abdomen for bonding. The newborn course was complicated by a complex history of apnea episodes, respiratory distress and possible seizures. EEG?s and MRI studies were normal. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby?s brain during labor or delivery. Raymond J. Fernandez, M.D., a pediatric neurologist, reviewed Kayla?s medical records and examined Kayla on April 30, 2013. He opined as follows: There is ample evidence for substantial mental and motor impairment, but this is of unknown etiology. There is no evidence in the medical record for oxygen deprivation or mechanical injury of brain or spinal cord during labor, delivery, or the immediate post delivery period that explains Kayla?s substantial and global impairment. Petitioners have presented no expert opinions that refute the opinions of Dr. Willis and Dr. Fernandez. The opinions of Dr. Willis and Dr. Fernandez that Kayla?s mental and motor impairments are not due to oxygen deprivation or mechanical injury of the brain or spinal cord during labor, delivery, or the immediate post delivery period are credited.
The Issue At issue in this proceeding is whether Bradley John Thomas, 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 Bradley John Thomas (Bradley) is the natural son of Scott G. Thomas and Mary E. Thomas. He was born a live infant on July 8, 1989, at Baptist Hospital, a hospital located in Pensacola, Florida, and his birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Bradley was Bo H. Bagenholm, 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. The birth of Bradley Thomas At or about 2:10 a.m., July 8, 1989, Mary Thomas was admitted to a labor room at Baptist Hospital. At the time, Mrs. Thomas was in active labor, having experienced a spontaneous rupture of the membranes with the emission of clear amniotic fluid at approximately 1:30 a.m., and Bradley was slightly post- term with a gestational age of approximately 41 weeks. Otherwise, Mrs. Thomas' pregnancy had been without complication. External fetal heart monitoring was commenced at approximately 2:15 a.m. and indicated a good base line with fetal heart tone between 125 and 140 beats per minute. From 2:30 a.m. to 2:45 a.m., the fetal heart tone was 120 to 150 beats per minute, from 2:45 a.m. to 3:00 a.m., the fetal heart tone was 115 to 145 beats per minute, and from 3:00 a.m. to 3:15 a.m., the fetal heart tone was 110 to 120 beats per minute with occasional acceleration to 160. In all, for such period, the fetal heart rate was normal, and no cause for concern. 4/ At approximately 3:15 a.m., Mrs. Thomas was removed from the monitor, provided a urine sample, and was given an enema, with good results. At 4:01 a.m., the fetal heart monitor was reapplied, and the nurse conducted a vaginal exam, at which point Mrs. Thomas was found to be 3 cm dilated. When the vaginal exam occurred, the fetal heart tone was recorded to be 120 to 130 beats per minute, with a reflex acceleration to 160 and deceleration to 60 following stimulation of the infant. Such heart rate was normal, and the reflex not unusual or ominous given the fetal heart tone recovery to the normal base line rate. 5/ Following the 4:01 a.m. vaginal examination, the fetal heart base line continued in the 120 to 160 or normal base line range until 12:14 p.m. when the fetal monitor was removed and the mother was taken to the delivery room via bed. During that period, an occasional acceleration and variable decelerations were noted, but such were not unusual or ominous given there was no persistent tachycardia or persistent decelerations. Indeed, the data recorded was consistent with the baby's reaction to examination, contractions or umbilical cord compression, and evidenced no fetal compromise. 6/ At 10:19 a.m., following an earlier epidural replacement, Dr. Bagenholm examined Mrs. Thomas and found the epidural effective and her cervical dilatation at rim. At 11:28 a.m., the nurse conducted a vaginal exam, found the mother's cervical dilation complete, and instructed her on pushing. At 12:00 p.m. (noon) the baby was noted to be at the +1/+2 station, at 12:07 p.m. to be at the +2 station, and at 12:14 p.m., the monitor was removed and the mother taken to the delivery room. Upon admission to the delivery room, the fetus continued to be monitored by doppler and evidenced fetal heart tones of 130-140 beats per minute. At 1:33 p.m., with the assistance of fundal pressure occasioned by the mother's reduced expulsion efforts, Bradley was delivered. When delivered, no meconium was present and Bradley presented with Apgar scores of 8 at one minute and 10 at five minutes. These scores are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, respiratory effort, muscle tone, reflex irritability, and color, with each category being assigned a score ranging from the lowest score of 0 through a maximum score of 2. As noted, at one minute Bradley's Apgar score totaled 8, with heart rate, respiratory effort, muscle tone and reflex irritability being graded 2 each and color being graded 0. At five minutes, Bradley's Apgar score totalled 10, with all categories being graded at 2 each. Bradley's Apgar scores are reflective of a healthy, vigorous infant. Indeed, on presentation, Bradley evidenced all the signs of a healthy newborn, with spontaneous respiration, a strong cry, no visible signs of trauma, good heart rate and good muscle tone. At or about 2:30 p.m., following routine suctioning and administration of oxygen, Bradley was admitted to the newborn nursery. Upon admission, Bradley's physical assessment revealed, inter alia, moderate molding of the head, not unusual in an infant delivered vaginally; soft and flat fontanelle, evidencing no intercranial pressure such as one might associate with a significant bleed; strong reflexes; a pink color; and, an alert and active infant. Bradley's first twenty-five hours of life were essentially uneventful, and he evidenced the normal signs of a healthy infant including the presence of soft and flat fontanelle, at least as late as 8:00 a.m., July 9, 1989. Bradley roomed-in with his mother from 10:30 a.m. to 2:30 p.m., July 9, 1989, when he was returned to the nursery, and during that time he reflected the signs of a healthy baby. 7/ Upon his return to the nursery at 2:30 p.m., Bradley was observed to be "gaggy" and "spit up." Shortly thereafter, at approximately 2:45 p.m., Bradley suddenly turned cyanotic, facial and trunk. The nurse promptly turned Bradley over, stimulated him, and Bradley responded with a "lusty cry" and "pinked up"; however, it was noted that he had a "fixed stare" and "does not blink to threat." At 4:30 p.m., another cyanotic episode was noted and, thereafter, evidence of seizure activity appeared. Dr. Jenkins, Bradley's pediatrician, ordered a blood culture to rule out infection and at 5:15 p.m. he performed a lumbar puncture, which evidenced bloody spinal fluid. Arrangements were made to transfer Bradley to the neonatal intensive care unit at Sacred Heart Hospital, and at 7:28 p.m., Bradley left Baptist Hospital with the transport team. At Sacred Heart Hospital, a physical examination of Bradley revealed that his fontanelle were full and, thereafter, he was diagnosed to have suffered a grade IV intraventricular hemorrhage, which evidenced at approximately his twenty-fifth hour of life. That hemorrhage caused profound injury to Bradley's brain, which has rendered him "permanently and substantially mentally and physically impaired," as that term is used in Section 766.302(2), Florida Statutes. The cause of Bradley's grade IV intraventricular hemorrhage Given the foregoing, resolution of this claim resolves itself to an identification of the genesis of Bradley's grade IV intraventricular hemorrhage or, stated otherwise, whether the proof demonstrated, more likely than not, that the hemorrhage, which resulted in injury to Bradley's brain and the ensuing neurological injuries, resulted from "oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post deliver period." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. 8/ Considering the proof, for the reasons that follow, it must be concluded that petitioners have failed to demonstrate, by the requisite standard, that the injury to Bradley's brain was the consequence of "oxygen deprivation or mechanical injury" and therefore failed to demonstrate that Bradley suffered a "birth-related neurological injury," as defined by law. Sections 766.302(2), Florida Statutes. Here, the proof is compelling that a grade IV intraventricular hemorrhage in a term infant, such as Bradley, is a rare occurrence, and that its cause is often not definable. Indeed, among the physicians who testified, there is apparent agreement that approximately 25 percent of grade IV intraventricular hemorrhages have identifiable causes such as sepsis, a blood disorder, an AV malformation, genetic disorder or an identifiable prenatal event; that approximately 50 percent are related to oxygen depravation or trauma in the intrapartum period; and, that approximately 25 percent can be attributed to no known cause. As for Bradley, when Mrs. Thomas was admitted to the labor and delivery room, he was assessed to be a viable fetus with no evident signs of stress. Indeed, Mrs. Thomas' pregnancy was without complications, and any prenatal events or other known causes of a grade IV intraventricular hemorrhage, such as sepsis, a genetic disorder, a blood disorder or an AV malformation have been examined and rejected as an identifiable cause of Bradley's hemorrhage. As for the labor and delivery of Bradley, the proof demonstrates that it was essentially normal and that there was no obstetrical incident or identifiable event during labor and delivery that would evidence that Bradley had suffered a hypoxic insult or mechanical injury. Indeed, Bradley, although large, was not large for his gestational age, given the use of an epidural there was no prolonged labor, there was no cephalopelvic disproportion, no untoward molding of the head, no use of forceps or vacuum extraction in delivery, and the use of fundal pressure was appropriate and not shown to be excessive. Upon delivery, no meconium was present, no apparent cranial injuries were observed, and Bradley presented as a vigorous infant with normal Apgars. In summary, there was no identifiable incident during the course of labor or delivery, or thereafter during Bradley's first twenty-five hours of life, evidencing oxygen deprivation, mechanical injury, or other insult, that would account for the hemorrhage he suffered at approximately his twenty-fifth hour of life. Indeed, the neonatologist, Dr. Dworsky, and neurologist, Dr. Miller, who offered testimony on behalf of petitioners, acknowledged that the labor and delivery of Bradley was fairly normal with no identifiable problems that would account for the hemorrhage. Moreover, Dr. Miller concluded that in the 50 percent of hemorrhages attributable to birth trauma, the literature suggests clear evidence at birth of compromise to the infant. Notwithstanding, there being no other traumatic event known, they theorize that Bradley failed to tolerate the stress associated with labor and delivery and that, through the mechanism of changes in venous or arterial blood pressure occasioned by variable decelerations caused by compression of the umbilical cord and from compression of the head associated with delivery, Bradley suffered an insult to the intracranial blood vessels which ultimately manifested as a grade IV intraventricular hemorrhage In their opinion, such insult was the product of oxygen deprivation and trauma associated with the stress of labor and delivery. 9/ The opinions of Doctors Dworsky and Miller regarding the probable cause of Bradley's hemorrhage are rejected as unpersuasive. Such opinions are largely speculative, being based on the assumption that the birth process was the only known traumatic event in Bradley's life, ignore that percentage of cases in which it is acknowledged that the cause of hemorrhage can never be known, and are not supported by any objective evidence of trauma or oxygen deprivation of record. Indeed, given the relatively uneventful labor and delivery, as well as Bradley's vigor at birth, the opinion of Dr. Duchowny that "this baby fits into the group of term infants with an intraventricular hemorrhage for which no cause is ever identified" is most credible and is, therefore, accepted.10
Findings Of Fact At all material times, Respondent has been currently licensed as a physician in Florida, holding license ME 0033496. Patient 1 was a 32 year old female who was admitted to Lykes Memorial Hospital on March 24, 1988, due to upper and lower abdominal pain, vomiting, and early signs of dehydration. Respondent placed Patient 1 on intravenous fluids and administered medications to control the vomiting. Patient 1 underwent diagnostic studies, including an upper gastrointestinal series, and received medication for the abdominal pain. After five days of hospitalization and tests, the source of the pain had not yet been identified. However, the lower abdominal pain had ceased, and the upper abdominal pain had lessened considerably. In general, the patient had improved during the hospitalization. At this point, Respondent discharged Patient 1 from the hospital with a final diagnosis of acute gastroenteritis. Respondent directed Patient 1 to return to his office for a follow-up visit. Five or six days after discharge, Patient 1 called Respondent and told him that her symptoms, which she now linked with taking birth control pills, had disappeared. Respondent advised her not to resume taking the pills, but to return to her gynecologist. With respect to Patient 1, Respondent practiced medicine with that level of care, skill, and treatment that is recognized by a reasonably prudent similar physician as being unacceptable under similar circumstances. Patient 2 was a 37 year old male who was admitted to Lykes Memorial Hospital on May 9, 1988, after having been found by a relative in a state of semi-consciousness. The admitting diagnosis was a probable overdose of lithium and possibly Thorazine. Respondent treated the drug toxicity during Patient 2's three-day hospitalization. Respondent became increasingly lucid during his hospitalization, and Respondent successfully managed the event of drug toxicity. Respondent tried to elicit from Patient 2 a medical and psychiatric history, but Patient 2 would or could not cooperate. Respondent was unable to identify any relatives or friends of Patient 2, including the person who brought him to the hospital. Respondent could not even find out where Patient 2 obtained the lithium and Thorazine that he was taking. Respondent treated the altered mental status that Patient 2 presented. There was no need during the short period of hospitalization to obtain a psychiatric consultation. Resumption of psychotropic medication so soon after the drug intoxication would have been imprudent. Consistent with the policy of Lykes Memorial Hospital, which has no psychiatrists on staff, Respondent referred Patient 2 to the Hernando County Mental Health Center. He directed Patient 2 not to take lithium or Thorazine until instructed to do so by a psychiatrist or other physician at the mental health center. Respondent and the hospital ensured that Patient 2 got to the mental health center following discharge. With respect to Patient 2, Respondent practiced medicine with that level of care, skill, and treatment that is recognized by a reasonably prudent similar physician as being unacceptable under similar circumstances. Patient 3 was a 49 year old male who was admitted to Lykes Memorial Hospital on or about February 5, 1988, with complaints of difficulty breathing. At the time, Patient 3 had been diagnosed with lung cancer that had metastasized to the spine and had undergone maximum radiation therapy. He was paralyzed from the waist down and in the last year of his life. He steadfastly refused all diagnosis or treatment involving radiation. By his own request, Patient 3's standing medical orders were "Do Not Resuscitate." He only wanted to be made comfortable. The acute illness resulting in Patient 3's admission was pulmonary congestion. There is some likelihood that the symptoms of infectious bronchitis with which he presented at time of admission were exacerbated by his chronic obstructive pulmonary disease. There is a possibility that some of Patient 3's discomfort was caused by mucous plugs in the lungs, whose capacity had already been diminished by the other diseases. However, mucous plugs were not affecting Patient 3 at the time of discharge. Respondent discussed with Patient 3 the possibility of cleaning out his lungs with a bronchoscope, but Patient 3 refused. Respondent treated Patient 3's discomfort with oxygen, diuretics, and increased steroids. Patient 3 had been receiving steroids due to a spinal disorder resulting from the cancer. Patient 3 was already receiving bronchodilators at the time of his admission. There is also a possibility that Patient 3 suffered from superior vena cava syndrome in which one or more tumors would block veins of the thorax. However, diagnosis of the condition would have been invasive, and Patient 3 refused such interventions. Treatment of such a condition would likely have required radiation, and Patient 3 would not tolerate additional radiation treatment. Respondent discussed with Patient 3 the possibility of superior vena cava syndrome and the possible treatment, but Patient 3 declined this intervention. Patient 3 received no EKG while in the hospital. The emergency medical services team transporting Patient 3 to the hospital performed a rhythm strip, which provides information about limited cardiac functions. Although Patient 3's potassium levels were slightly below normal at discharge, they had improved during hospitalization. With respect to Patient 3, Respondent practiced medicine with that level of care, skill, and treatment that is recognized by a reasonably prudent similar physician as being unacceptable under similar circumstances. Respondent's medical records represent the bare minimum required by law to justify the course of treatment. Matters discussed with Patient 3 were not always recorded. Patient 3's decisions concerning diagnosis and treatment were likewise not always recorded. But, on balance, the medical records adequately documented the course of treatment of Patient 3 while under Respondent's care at the hospital. Patient 4 was a 68 year old male who was admitted to Lykes Memorial Hospital on or about February 14, 1988, with complaints of a persistent cough and some gastric upset. He was suffering from exacerbation of chronic obstructive pulmonary disease. Respondent appropriately treated Patient 4's conditions. Patient 4 experienced problems with certain medications, which interfered with his progress, but he was drinking and eating without difficulty prior to his discharge. X-rays taken at admission and discharge revealed no significant change in Patient 4's condition during his eight-day hospitalization. At discharge, Respondent ordered Patient 4 to return for an office visit in two weeks. Patient 4's condition continued to improve following discharge. With respect to Patient 4, Respondent practiced medicine with that level of care, skill, and treatment that is recognized by a reasonably prudent similar physician as being unacceptable under similar circumstances.
Recommendation Based on the foregoing, it is hereby RECOMMENDED that the Department of Business and Professional Regulation enter a final order dismissing the administrative complaint. ENTERED on October 11, 1993, in Tallahassee, Florida. ROBERT E. MEALE Hearing Officer Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, FL 32399-1550 (904) 488-9675 Filed with the Clerk of the Division of Administrative Hearings on October 11, 1993. APPENDIX Treatment Accorded Proposed Findings of Petitioner 1-5: adopted or adopted in substance. 6: rejected as unsupported by the appropriate weight of the evidence. 7-12: adopted or adopted in substance. 13: rejected as unsupported by the appropriate weight of the evidence. The pain or discomfort had lessened considerably. 14: adopted. 15: rejected as unsupported by the appropriate weight of the evidence. 16-17: rejected as irrelevant and unnecessary. 18: rejected as unsupported by the appropriate weight of the evidence. and 21-23: adopted or adopted in substance. and 24: rejected as unsupported by the appropriate weight of the evidence. 25: adopted except that Respondent and the hospital ensured that the patient was referred to a mental health treatment center as soon as his condition was sufficiently stabilized to allow discharge from the hospital. 26: rejected as unsupported by the appropriate weight of the evidence. 27: adopted or adopted in substance. 28: rejected as unsupported by the appropriate weight of the evidence. The record does not suggest how a psychiatrist would obtain a history from an unwilling patient. 29: adopted with respect to the period of the hospitalization through the point at which the patient could recommence active psychiatric treatment. 30: rejected as unsupported by the appropriate weight of the evidence. Respondent duly referred the patient to an appropriate facility for the treatment of the patient's underlying mental health problems. 31: rejected as recitation of evidence and subordinate. 32: rejected as legal argument and unsupported by the appropriate weight of the evidence. 33-36: adopted or adopted in substance. 37-38: rejected as unsupported by the appropriate weight of the evidence. 39: rejected as subordinate. 40: rejected as unsupported by the appropriate weight of the evidence. 41-43 (through third sentence): adopted or adopted in substance. 43 (fourth sentence): rejected as unsupported by the appropriate weight of the evidence with respect to this patient. 44-48 (first sentence): adopted or adopted in substance. 48 (except first sentence)-50: rejected as irrelevant and subordinate. 51-52 and 54: adopted or adopted in substance. 53: rejected as unsupported by the appropriate weight of the evidence. 55-56: adopted or adopted in substance. 57-59: rejected as unsupported by the appropriate weight of the evidence. Treatment Accorded Proposed Findings of Respondent 1-6: adopted or adopted in substance. 7: rejected as legal argument. 8: rejected as recitation of evidence. 9: rejected as legal argument and recitation of evidence. 10: adopted or adopted in substance. 11: rejected as recitation of evidence. 12: rejected as recitation of evidence and subordinate. 15: adopted or adopted in substance. 16 (first sentence): rejected as legal argument. 16 (second and third sentences): adopted or adopted in substance. (fourth sentence): rejected as recitation of evidence. (first sentence): rejected as legal argument. 17 (second sentence): adopted or adopted in substance. 17 (third sentence)-19 (first sentence): rejected as recitation of evidence. 19 (second sentence): adopted or adopted in substance. 20: rejected as recitation of evidence. 21: rejected as legal argument and recitation of evidence. 22: rejected as legal argument and recitation of evidence. 23: rejected as subordinate. 24: rejected as recitation of evidence. 27: adopted or adopted in substance. 28-31 (second sentence): rejected as legal argument and recitation of evidence. 31 (third sentence): adopted or adopted in substance. 32-34: rejected as legal argument and recitation of evidence. 38: adopted or adopted in substance. 39-43: rejected as legal argument, recitation of evidence, and subordinate. COPIES FURNISHED: Dorothy Faircloth Executive Director Board of Medicine 1940 North Monroe Street Tallahassee, FL 32399-0792 Jack McRay, General Counsel Department of Business and Professional Regulation 1940 North Monroe Street Tallahassee, FL 32399-0792 Barbara Whalin Makant, Staff Attorney Department of Business and Professional Regulation Northwood Center, Suite 60 1940 N. Monroe St. Tallahassee, FL 32399-0972 William B. Taylor, IV Macfarlane Ferguson P.O. Box 1531 Tampa, FL 33618
Findings Of Fact Elian O. Morales Galindo was born on October 27, 2012, at Winnie Palmer Hospital for Women and Babies located in Orlando, Florida. Elian weighed 3,849 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Elian to determine whether an injury occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital due to oxygen deprivation or mechanical injury. Dr. Willis described his findings as follows in an affidavit dated January 14, 2015: It is my opinion, in summary, spontaneous vaginal delivery was complicated by nuchal cord x2 and avulsion of the cord during reduction for delivery. Despite a normal cord blood pH, the baby was depressed at birth and required bag and mask ventilation for six minutes. The baby recovered quickly and was on room air within 24-hours after delivery. The initial blood gas after birth had a base excess of -12, which is consistent with some degree of acidosis. Head ultrasound was normal. EEG, CT scan and MRI were not done during newborn hospital course. Avulsion of the umbilical cord can occur when a tight nuchal cord is being reduced to allow delivery. The only risk related to cord rupture is neonatal blood loss and resulting hypotension. The baby’s blood counts were normal with a Hematocrit of 47% which would suggest the baby did not have a significant blood loss at time [sic] or cord rupture. This does not appear to be a factor in the outcome. There was an apparent obstetrical event that resulted in some degree of oxygen loss during delivery and continuing into the immediate post-delivery period. This is based primarily on the low Apgar scores and an initial blood gas with a based excess of -12. I am unable to comment about oxygen deprivation during labor without review [sic] the FHR monitor tracing. No imaging studies were done during the newborn hospital course to determine if this oxygen deprivation caused any brain injury. Thereafter, I reviewed the additional medical records, which include the mother’s hospital course during labor and delivery, the fetal heart rate (FHR) tracing during labor and an emergency room visit for the mother at 7 weeks gestational age for nausea. The FHR tracing during labor was reviewed. The baseline FHR on admission was normal at 130 bpm with normal heart rate variability. The FHR monitor tracing does not suggest fetal distress during labor. Accordingly, it is my opinion that there was no obstetrical event that resulted in oxygen deprivation or brain injury to the baby during labor. NICA retained Raymond J. Fernandez, M.D. (Dr. Fernandez), a pediatric neurologist, to examine Elian and to review his medical records. Dr. Fernandez examined Elian on February 11, 2015. In the medical report attached to Respondent’s Supplemental Motion for Summary Final Order, Dr. Fernandez opined as follows: CONCLUSION: There is no evidence for substantial motor or physical impairment. Elian walked on time and gross and fine motor skills are improving at a steady pace based on history and this trend should continue. Expressive speech and receptive language development is delayed, but improving and this trend should continue. While speech and language delay is a predictor of later learning difficulty, he is improving and we do not have convincing evidence, at this time, for substantial mental impairment that will be permanent. There was transient physical depression immediately after birth and there was transient respiratory distress, but he improved within a reasonable period of time. There was no clear evidence for neonatal encephalopathy or multi-organ involvement. Therefore, there is no clear evidence in the record for brain or spinal cord injury during labor, delivery, or the immediate post delivery period of resuscitation. While Dr. Willis and Dr. Fernandez are of the same opinion that an obstetrical event causing oxygen deprivation did not occur during labor, Dr. Willis’ opinion is somewhat at odds with Dr. Fernandez’s opinion regarding whether an obstetrical event occurred that resulted in some degree of oxygen loss during delivery and continuing into the immediate post-delivery period. However, there are no opinions filed contrary to Dr. Fernandez's opinion that there is no evidence of substantial motor or physical impairment or convincing evidence at this time of substantial mental impairment that will be permanent. Dr. Fernandez’s opinion is credited.
Findings Of Fact Allison Paige Blackshear was born on July 20, 2009, at University Community Hospital located in Tampa, Florida. Allison weighed 3,900 grams at birth. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Allison to determine whether an injury occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital due to oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Dr. Willis described his findings as follows in his medical report: She [Mrs. Blackshear] was admitted to the hospital at term for elective repeat Cesarean section delivery. She was not in labor. Fetal heart rate (FHR) monitor prior to delivery shows a normal baseline fetal heart rate of 130 bpm and a reactive pattern. The FHR monitor tracing prior to delivery does not suggest fetal distress. The operative report indicates that the repeat Cesarean delivery was “uncomplicated.” Birth weight was 8 lbs 9 oz’s (3,900 grams). The newborn was not depressed. Apgar scores were 9/9. No resuscitation was required. The baby was taken to the normal nursery. The baby breast fed twice and was in apparent good health until four hours after birth. While in the mother’s arms, the baby stopped breathing and turned blue. The baby was taken to the NICU for evaluation and management. Persistent apnea required intubation. Seizure activity was noted about 24-hours after birth. EEG confirmed seizure activity. Head ultrasound was negative. MRI on DOL 2 showed an extensive acute ischemic infarction in the area of the left middle cerebral artery. In summary, there was no fetal distress noted by FHR monitor prior to delivery. Delivery was by uncomplicated repeat Cesarean section. The newborn was not depressed at birth with Apgar scores of 9/9. About four hours after delivery, apnea developed, which was followed by seizure activity. MRI confirmed an acute cerebral infarction. The cerebral infarction apparently developed several hours after birth and was not related to any obstetrical event. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during delivery or the immediate post delivery period. NICA retained Raymond J. Fernandez, M.D. (Dr. Fernandez), a pediatric neurologist, to examine Allison and to review her medical records. Dr. Fernandez examined Allison on April 10, 2012. In the affidavit attached to the Motion for Summary Final Order, Dr. Fernandez opined as follows: I examined Allison on April 10, 2012. At that time, she was 2 years and 9 months old. Based on my examination of her and my review of the available records at that time, I concluded that Allison had a permanent and substantial motor (or physical) impairment. I also stated that she was likely to experience substantial mental (cognitive and behavioral) impairment due to her large perinatal stroke and associated left hemisphere atrophy. In addition, it was my opinion that the cause of Allison's perinatal stroke was unclear, but it was not due to an acute obstetrical event that caused systemic oxygen deprivation during delivery. See, Independent Medical Examination report dated April 10, 2012, a true and accurate copy of which is attached hereto as Exhibit A. Subsequently, on May 12, 2012, I prepared an addendum to my initial report. In that addendum, I explained that it was my opinion that irrespective of the timing of Allison's stroke, it was not due to systemic oxygen deprivation or mechanical injury during labor, delivery or resuscitation in the immediate post-delivery period and as result did not meet the criteria for coverage under the NICA plan. Allison's stroke was due to reduction in left middle cerebral artery blood flow. In addition, Allison was stable immediately after birth and had Apgar scores of 9 and 9, and she did not need or require any resuscitation in the delivery room or immediately thereafter and remained stable until approximately four hours after her birth, at which point the first apneic episode occurred. See, Addendum to The Independent Medical Examination of April 10, 2012, a true and accurate copy of which is attached hereto as Exhibit B. It remains my opinion today that Allison does not qualify for coverage under the NICA plan as her stroke was not caused by oxygen deprivation or mechanical injury during labor, delivery or resuscitation in the immediate post-delivery period and because the [sic] was no need for any active or ongoing resuscitation after delivery. Her first apneic episode did not occur until approximately four hours after birth, well after it had been determined that she was in good and stable condition. Irrespective of the timing of Allison's stroke and resulting brain injury, it is my opinion that she does not qualify for coverage under the NICA plan because she does not have a permanent and substantial mental impairment. Although I indicated in my initial report that substantial mental impairment was likely, I also noted that Allison's early speech delay (which some times can be predictive of substantial mental impairment) was improving. Subsequent to my initial report, I was provided additional medical records reflective of Allison's growth and development since the time that I examined her. In addition, I was provided the deposition transcripts of Allison's parents, Matt and Stacie Blackshear. Having reviewed this additional information, it is clear that Allison has developed and progressed much better than expected and currently does not have a permanent or substantial mental impairment. 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 delivery or the immediate post-delivery period. Dr. Willis’ opinion is credited. There are no expert opinions filed that are contrary to Dr. Fernandez’s opinion that, as there was no need for resuscitation at the time of delivery and Allison was stable until approximately four hours of age, the NICA criterion for brain injury to be caused by oxygen deprivation or mechanical injury in the course of labor, delivery or resuscitation in the immediate post-delivery period is not met. Moreover, there are no contrary opinions filed to Dr. Fernandez's opinion that Allison currently does not have a permanent or substantial mental impairment. Dr. Fernandez’s opinion is credited.
