The Issue At issue is whether Dillon Campbell, a minor, is permanently and substantially physically impaired.
Findings Of Fact Fundamental findings Monique A. Campbell and Gregory P. Campbell are the parents and natural guardians of Dillon Campbell (also referred to as "Twin A" in the medical records), a minor. Dillon was born a live infant on November 18, 1996, at HCA Health Services of Florida, Inc., d/b/a Columbia Blake Medical Center (Blake Medical Center), a hospital located in Bradenton, Florida, and his birth weight exceeded 2500 grams. The physician providing obstetrical services during Dillon's birth was James S. Albin, 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. Women's Health Associates of Manatee, P.A., was at all times material hereto, Doctor Albin's professional association. Coverage under the Plan Pertinent to this case, coverage under the Plan is available when the claimant demonstrates, more likely than not, that the infant suffered an "injury to the brain . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post- delivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Here, Petitioners and Respondent were of the opinion that it was unlikely that the proof would support the conclusion that Dillon was permanently and substantially physically impaired and suggested, given the Plan requirement that the infant suffer both substantial mental and physical impairment for coverage to be afforded by the Plan [Florida Birth-Related Neurological Injury Compensation Association v. Florida Division of Administrative Hearings, 686 So. 2d 1349 (Fla. 1997)], that Dillon's physical presentation be addressed initially, with the view that unnecessary expense might be avoided in resolving the claim. Given the circumstances, it was resolved to bifurcate the issue of physical impairment from the other issues that would also have to be resolved were coverage to be accepted (i.e., the cause and timing of Dillon's brain injury, as well as whether he was also rendered permanently and substantially mentally impaired.) In this case, the proof supports Petitioners' and Respondent's view of the record that Dillon's physical impairments are not substantial, and it is unnecessary to reconvene to take proof with regard to any other issue on the claim. Dillon's birth and subsequent development Dillon was born at 3:28 p.m., November 18, 1998, at Blake Medical Center, and by 6:25 p.m., on the orders of Alberto Soto, M.D., was transferred to Manatee Memorial Hospital for neonatal intensive care. Dillon's birth and subsequent care at Manatee Memorial Hospital were described by Dr. Soto in his discharge summary, as follows: SUMMARY OF NURSERY STAY: Dillon Campbell was a newborn infant born at Columbia Blake Hospital on November 18, 1996. I was called to Blake Hospital for an emergency cesarean section that was being performed on Monique Campbell. She had twin gestation and it was noted that twin A [Dillon] had a decrease in fetal heart rate and also developed a non- reassuring strip and because of that emergency cesarean section was being undertaken. In the operating room, a quick check by one of the nurses could not [detect] heart tones on twin A . . . . On extraction, [twin A] had no pulse and no respiratory effort. Full cardiopulmonary resuscitation was started with positive pressure ventilation and cardiac compressions. The baby was intubated through endotracheal tube and given Epinephrine through the endotracheal tube as well as per the resuscitation protocol. At first Epinephrine dose got the heart rate to about 80 beats per minute; a second dose was given and that got us to a normal count of above 100. This was achieved at about 2 minutes of age. At that point, there still was no respiratory effort. The first attempt of the baby to breathe were observed at about 6 minutes of age. These appeared to be more like gasping than true breaths. Normal easy respiration's were seen at about 11 minutes of age. As part of our resuscitation, Plasmanate was given intravenously because of low blood pressure and slow capillary refill. Blood sugar was checked by chem strip; this was also low so a bolus of D10W was given IV push; these boluses were given by an umbilical venous catheter which was placed as part of resuscitation measures. After those two things were given, an umbilical arterial catheter was placed also. [Apgars were 1 at one minute and 3 five minutes.] I had done an initial venous blood gas from the umbilical vein and this showed a pH of 6.95, a pC02 of 80. Because it was done so quickly from the umbilical vein, I am assuming that this would be the equivalent of a cord blood venous gas. The first arterial blood gas has pC02 of 7.06, after which we gave sodium bicarbonate. Once we settled him in the nursery, we repositioned the tubes both endotracheal, oral gastric, and umbilical artery catheters. The blood sugar dropped again so a second bolus was given. Intravenous fluids were raised and increased from 7 cc per hour to 15 cc per hour of 10 percent Dextrose. A second dose of sodium bicarbonate was given. We gradually had a rising pH. The second pH was 7.32 and the third pH was 7.43. I then went on to get more routine labs and started antibiotics. On visual inspection of the twins, I saw that this baby looked ruddy or plethoric and that the other twin had looked pale. This made us suspect a twin to twin transfusion. I also contacted the Neonatal Intensive Care Unit at Manatee Memorial Hospital for transfer. Part of our initial physical assessment on Dillon was that there was . . . generalized edema noticed mostly at the posterior and all other parts of the body were also puffy. The abdomen appeared distended which we felt was possibly due to ascites but x-rays did not show evidence of that. Overall, we did not see any stigmata of genetic abnormalities or birth defects. No overt seizure activity was noted at Blake Hospital although we did observe a degree of obtundation. The baby was transferred then to Manatee Memorial Hospital for Neonatal Intensive Care as the baby was still on the respirator, suspected cause was a twin to twin transfusion with possibility of hydrops non-immune type. Other than the blood gases, additional laboratory analysis findings at Blake had an liver enzymes that were abnormally high, ALT was 231, AST was 935, and LDH was 2281. This was right after birth. Another unusual finding was that the laboratory reported a creatine kinase isoenzyme that is very rare. They found a mitral chondral CK isoenzyme which has been reported only on a handful of babys throughout the world. It seems to be, according to my research, originated in either the liver or the heart and so far in the handful of babys that have been described with this macro C2 creatinine kinase there seems to be no long-term sequelae. The official report on the x-rays from Blake Hospital have pleural effusion on the right and possible ascites. At about 2015 hours over at the Neonatal Intensive Care Unit we noticed some suspicious tongue thrusting movements with tremors, we considered it a possibility that it might be seizure activity and treated it as such with Phenobarbital. It was a brief episode but we knew that this baby was at risk for seizures so we went ahead and started loading the baby with Phenobarb dose of 30 milligrams. X-rays had showed that the umbilical arterial line was low. I had come back shortly after midnight and replaced the umbilical lines now with good placements for high lines. I stayed with the baby further because of acuity at 0220 hours, we observed movements of arms and posturing of the legs; this was more typical of seizure activity and Lorazepam was given for this episode. Further dose was required at 0355 hours. Shortly thereafter, the baby[']s blood pressure started to come down at 0435 hours [and] we started Dopamine drip which was able to maintain a normal mean arterial blood pressure. I was at the baby[']s bedside on and off throughout the night up to about 0500 hours. The day after the admission, we had no[] tonic or clonic activity but still an occasional fasciculation of the tongue was seen; these kinds of autonomatism are very difficult to control. We were getting also brown, thick secretions from the endotracheal tube which were suspicious of either pulmonary hemorrhage or pulmonary edema. We continued to fine tune treatment for the seizure activity because shortly after 1600 hours, we saw another small episodes of what could [be] tonic activity of one of the arms. Tongue thrusting continued on and off. The nurses had mentioned what they called cogwheel motion of arms. The baby was now on Phenobarbital, Dilantin and p.r.n. Ativan. We continued trying to determine if there are any other causes of all this symptomatology. We did TORCH titers, chromosome analysis and electroencephalogram. The electroencephalogram to my eyes was abnormal and consistent with deep seizure activity. Initially on admission, the mother had told me that her brother was a "bleeder". Eventually, we were able to find the actual charts on him and found him to have had a subacute type of idiopathic thrombocytopenia; this should not be an issue for these infants. During the baby[']s second day of stay, I had the ophthalmologist examine him. He had seen retinal hemorrhages and suggested coagulation studies which were done; these were abnormal an we started the baby treating him as DIC, that included fresh frozen plasma, cryoprecipitate and intravenous gamma globulins. That day #2, we had two episodes of seizure activities that was treated with intravenous Ativan. By day #3, the respirator was down to minimal settings, the oxygen was 25 percent only and the mechanical respirations were only 15 breaths per minute. X-rays already did not show any pleural effusions although the monogram of the abdomen did still reveal small effusions present. Still on Dopamine drip, we occasionally had myoclonic movement of the arms and legs and occasional small episodes of seizure activity. The DIC was still being treated by twice a day cryoprecipitant plasma. Also one transfusion of platelets was required. On day three, we did not give any more platelets but he did get one transfusion of fresh frozen plasma and one of cryoprecipitant and with one infusion of intravenous gamma globulin. The baby was still on Dopamine drip for low blood pressure and by the early morning of day number four, we were able to start cutting back on the Dopamine dosage. We had during day #4, labile blood pressures, we had to adapt and adjust with the Dopamine drip going up and down according to the measurements that we were getting. Late that evening, about 2000 hours, he had another seizure activity with sucking motions and jerky movements also blinking of the eyes. The left leg was rigid and arms were also clonic. We adjusted Phenobarbital level because the level was 27. Platelet count that day was 78. On day #5, we had mild metabolic alkalosis with mild C02 retention. The cardiac echo was reported as normal. The generalized edema was slightly improved, had a 15 second episode of seizure activity. Platelets were found to be low so full DIC profile was repeated. Platelets were ordered and given transfusion. Also repeat doses of cryo and FFP added as well. On day 6, blood levels of Phenobarbital were at 22 and Dilantin was 26. After the transfusion, the platelet count was now 98,000 and held both the Phenobarb and the Dilantin. On days 6, 7, and 8, no seizure activity was reported. We tried him on continuous positive airway pressure on day #8, hence we tried to wean him off the ventilator. In the late evening, day 8, into day 9, we transfused with platelets again because platelet count had dropped to 36,000. On day 9, we tried him off the respirator and extubated him at 1350 hours, started on oxygen by hood. The electroencephalogram was repeated and still was abnormal. By the early morning hours of day 10, we were able to get him completely off oxygen. Still no overt seizure activities once we had held the medications. By day 11, we were able to see that he had lost peripheral edema, no apneas were noted and no seizures either. By day #12, nurses were commenting that he looked more awake and on my physical examination, the only other thing I noted was that there is still neuromuscular irritability as evidenced by increased and clonus beats although they were symmetric. Extensor tone still also was slightly increased. On day #12, I removed the umbilical lines and started oral feedings. On days 13 and 14, we had him on 1/2 strength Nutramigen feeds by tube. Platelets counts were on the lower range of normal at 53 and 55,000. No overt seizure activity was noted but occasionally the nurses would still comment on tremors and occasional mild irritability. On day 15, I switched him to 1/2 strength Enfamil feeds, platelet count was still 53, the number of clonus beats at the ankles was normal but the deep tendon reflexes were still brisk. Again, no asymmetries were noted, no dystonias were noted either. On day 16, the platelet count was 91,000 and beyond that it was always above 100,000. Gradually, he started to tolerate feeds better. On day #16, he nipple fed all his feeds. We advanced him to full strength feeds and got him into an open crib. We did a hearing screen which he failed on both ears. On December 7, which was day #19, I repeated the[] DIC profile one more time and this time everything was normal. The blood counts including white blood cells and platelet counts were normal. The chemistry panel done that included liver enzymes were also fully normal. The baby was then discharged at 1600 hours on December 7, 1996, to the parents, told to be followed in about a week with the pediatrician. DISCHARGE PHYSICAL EXAMINATION: Discharge weight 5 pounds and 5.3 ounces. . . DISCHARGE VITAL SIGNS: Temperature 98.7, pulse 136, respirations 36. GENERAL APPEARANCE: Strong and vigorous. HEAD, EYES, EARS, NOSE AND THROAT: Anterior fontanel is flat, sutures feel normal to palpation. Examination of the eye grounds have good red reflexes bilaterally. There is no sign of nasopharyngeal infections, both nares are patent. There is no cleft of lip or palate. No signs of any congenital abnormalities or genetic traits. NECK: Good range of motion. Clavicles intact to palpation without callus formation. No lymph nodes palpable. No masses, no goiter. CHEST: Breathing effortlessly in room air. HEART: No murmurs. LUNGS: All lung fields clear. ABDOMEN: No organomegaly, no abnormal masses. Belly is soft and not tender. GENITALIA: Normal newborn male. Both testes palpable. The meatus is well placed. ANUS: Patent and well placed. EXTREMITIES: No hip clicks. NEUROLOGICAL: Get the impression, the baby[']s muscle tone is normal now which was true since about day 16. The deep tendon reflexes are still slightly brisk but there is no other evidence of neuromuscular irritability; for example, clonus beats at ankles are normal in terms of numbers and they are symmetric. Cannot detect any asymmetries in muscle tone nor in any of the reflexes. I do have a good Moro reflex, good Perez, and Galant reflexes with again no asymmetries, good placing and stepping reflexes with no focal findings. DISCHARGE DIAGNOSIS: Full term twin born by cesarean section. Cardiorespiratory arrest at birth. Hypoglycemia. Non-immune hydrops. Hypocalcemia. Hypokalemia. Low Apgar scores. Neonatal seizures. Hypothrombocytopenia. Disseminated intravascular coagulation. Feeding problems of the newborn. Apnea. PLAN: Discharged to the parents as noted above with follow-up Dr. Alfredo A. Giangreco. COMMENT: Areas that need follow-up: We need to repeat the hearing screen as the baby[']s hearing screen at discharge failed both ears. Long-term follow-up purposes should also include neuro developmental evaluations preferably by a pediatric neurologist; this may or may not include repeat electroencephalograms. This of course to be left up to the judgment of the pediatric neurologist. Perhaps a repeat monogram of the brain is warranted since the healing stages of any incidence before birth and after birth may not be visible on sonography of the brain until 6 to 8 weeks of age.2 Following discharge, Dillon was followed by Alfredo Giangreco, M.D., or other pediatricians associated with his practice. The medical records related to Dillon's first visit on December 12, 1996, reflect an alert, active 3-week-old infant in no apparent distress, with good Moro-suck, and good muscle tone or, stated otherwise, no hypertonia. Dillon's subsequent visits at 1 month of age (December 26, 1996), 2 months of age (January 17, 1997), and 3 months of age (February 19, 1997) were likewise unremarkable except that his 3-month visit reflects a clinical observation that his head was microcephalic (an abnormal smallness of the head.) Apart from the microcephalia, Dillon's remaining visits were unremarkable until his visit at 7 months of age (June 18, 1997), when the doctor noted a spastic paresis of the left arm and hand, as well as both legs. At the time, the parents disclosed that they planned to move to Rhode Island in 4 days, and the doctor recommended a follow-up on such findings and reminded them of the importance of a hearing evaluation (the parents had failed to pursue following Dillon's discharge from Manatee Memorial Hospital.) Following the family's move to Rhode Island, Dillon came under the primary care of Roxanne Simmons, M.D., a board- certified pediatrician. On her initial examination of March 11, 1998, Dr. Simmons noted "symmetrical decreased strength throughout all four extremities," as well as expressive language delay with disarticulation. Given the "global issues," which included microcephalia, Dr. Simmons referred Dillon to Dr. Maria Younes, a pediatric neurologist and, given his speech delay, referred Dillon for a hearing assessment. Dillon was also referred to the Earl Intervention Program for assessment, and occupational and physical therapy, as needed, to address his speech, language, and/or oral-motor delays. Dr. Younes' evaluation of Dillon will be discussed infra. As for Dillon's hearing assessment, testing on April 2, 1998, revealed a "moderate (probably conductive) hearing loss." Following that test, Dillon had "tubes inserted [in his ears]" by Dr. Blat, on referral by Dr. Simmons, and further assessment on July 13, 1998, found his "hearing is developmentally adequate." Dillon also received occupational and physical therapy through the Early Intervention Program with good results, as noted infra. Dr. Simmons continued to provide primary care for Dillon, and saw him as recently as June 9, 2000. As of that date, Dr. Simmons noted that Dillon now evidenced good strength in his extremities and no gross motor deficits. As for his fine motor skills, Dr. Simmons offered no opinion, and deferred to others more appropriately suited to make such an assessment. Currently, according to Dr. Simmons, the issues now confronting Dillon are behavioral, as evidenced by his aggressive character (otherwise described as an attention deficit, hyperactivity disorder,) and continued delay in his expressive language with disarticulation. As for any relationship between Dillon's current presentation and any injury to or anomaly in brain development, Dr. Simmons deferred to Dr. Younes. (Dr. Albin's Exhibit 1, pages 30 and 31.) Dillon's neurologic assessments Dillon was first seen by Dr. Younes on June 2, 1998. At the time, Dr. Younes noted the mother's concerns regarding his speech and language delays, a perceived mild delay in fine motor skills, and a possible mild left hemiparesis (a muscular weakness or partial paralysis affecting the left side of the body); however, Dr. Younes' examination did not reveal any significant difference in his muscle tone or the strength in his extremities. Nonetheless, Dr. Younes noted a working diagnosis of left hemiparesis and developmental delay and, given Dillon's microcephaly, his mother's concerns, and Dillon's birth history, ordered an MRI of the head. The MRI examination occurred on June 26, 1998, and the results of that examination were reported as follows: Axial T2 and FLAIR images demonstrate confluent hyperintense white matter signal abnormality predominantly involving the periatrial white matter of the bilateral cerebral hemispheres. In addition, there is periventricular white matter signal abnormality involving the bilateral frontal periventricular white matter, left greater than right. The MR imaging appearance is most consistent with periventricular leukomalacia. No evidence of hydrocephalus. No evidence of intracranial hemorrhage, mass, or midline shift. Normal vascular flow voids are present. IMPRESSION: MRI EXAMINATION DEMONSTRATES EXTENSIVE WHITE MATTER HYPERINTENSE SIGNAL ABNORMALITY PREDOMINANTLY INVOLVING PERIVENTRICULAR WHITE MATTER BILATERALLY. GIVEN THE CLINICAL HISTORY OF PERINASAL [SIC] ASPHYXIA, THE PATTERN IS MOST CONSISTENT WITH PERIVENTRICULAR LEUKOMALACIA. As read, the MRI results are consistent with an abnormality in brain development associated with prematurity or a brain injury associated with hypoxic insult.3 Following receipt of the MRI results, Dillon was further evaluated by Dr. Younes on August 23, 1999, and April 3, 2000. Based on her multiple examinations, Dr. Younes offered the following observations with regard to the physical impairments Dillon manifests, which she perceives are related to his periventricular leukomalacia: Q. I would ask you, of course, as you respond to questions that I put to you about this child's condition and the way you found him on April 3, 2000, if you need to draw upon your knowledge of him gained from August 23rd of 1999, 6/2/98, or certainly any tests that you ordered or information that you received such as from the school psychologist, that kind of thing. A. Yes. He was now three years and a half. Because school takes over services at age 3 here in Rhode Island, he had had a complete evaluation from Lincoln School Department, and he was found to have delays in his speech and language, occupational therapy, the most concerning a low IQ. IQ is 67.4 * * * Q. With regard to the speech impairment that Dillon Campbell has, do you have an opinion as to whether there is an element of motor dysfunction or motor deficit that is either causing or contributing to the child's speech deficit? A. He does have articulation problems, but he also has basically both expressive and receptive language delays. Q. Is the child's speech -- is the child's speech deficit permanent and substantial? A. He will continue to improve. He will be getting speech and language therapy, so some of these things will improve with time. Also as he continues to develop, he will continue to improve. Eventually his output could be very good, but his receptive language may be impaired long term. Q. At the current time, however, clearly the speech impairment that he has is now substantial? A. Yes. Q. Are you able to say to a reasonable medical probability that his speech impairment will completely abate, completely go away, or will there always be some speech impairment? A. There will always be some speech impairment -- impediment. * * * Q. Are you able to at this point, based upon the information you have, give an opinion held to a reasonable medical probability with regard to whether this child for sure does have or doesn't have impairments of fine motor skills? A. He has impairment of fine motor skills. Q. Do you believe that the impairment that he has of fine motor skills are substantial? A. No. Q. Do you believe that the impairments that he has in fine motor skills, if they do not get better, will affect him in later life? A. No. * * * Q. How has the periventricular leukomalasia affected this child in terms of his physical being outside of the brain? * * * Q. Has it affected or contributed to his speech deficit? A. Yes. Q. In what way has the . . . periventricular leukomalasia affected this child's speech? A. Significantly. I think the periventricular leukomalasia will be most significant for this child in the areas of cognitive ability. He is mentally retarded and his speech and language. His fine motor and gross motor will be fine. Q. In terms of periventricular leukomalasia that this child suffers from, is that periventricular leukomalasia consistent with speech difficulties that are motor related, motor function related? * * * A. Speech and language requires a lot of different parts of the brain, the left hemisphere, and it has a lot of different components, and the motor component to the ability of articulating words, he has a problem in that area; but he also has a problem understanding language and also expressing himself. * * * Q. Are you able to give an opinion as to how much of the child's speech problem or speech impairment is related to motor deficiency versus cognitive deficiency? A. It's a combination of both, but the cognitive is probably a greater component. * * * Q. The articulation problem that Dillon has, you indicated I believe that there could be several causes to it; is that correct? A. Yes. Q. One could be a cognitive dysfunction? A. Yes. Q. And the other could be a motor dysfunction? Q. Yes. Q. If I understand correctly, when asked by Mr. Marchbank, you said more likely than not it was more cognitive than motor; isn't that true? * * * A. I said it is a component of both, that most likely the articulation may improve with time, but the cognitive part may persist. Q. At the present time, what if anything do you find to enable you to continue, if you do, with the diagnosis of left hemiparesis? A. Could you ask the question again? Q. Yes. What is it in his physical condition right now that you have determined by examination that Dillon still has a persistent left hemiparesis? A. I don't think that's significant. I think it's only been picked up by an occupational therapist, by the mother after a lot of observation of her child, but not something that you could pick up just by looking at him. Q. In fact, in your examination of him when you see him grossly, it would appear to you that he has no gross motor impairment; is that true? A. Exactly. Notably, Dr. Younes was not requested to address and offered no opinion as to the gravity of Dillon's behavior disorder (also referred to as attention deficit, hyperactivity disorder), or whether there was any causal relationship between such disorder and the periventricular leukomalacia he suffered. In addition to Dr. Younes' evaluation, Dillon's neurologoic status was also assessed by Michael Duchowny, M.D., a pediatric neurologist associated with Miami Children's Hospital. Dr. Duchowny's examination occurred on February 17, 2000, and he reported the results of his evaluation as follows: HISTORY ACCORDING TO MRS. CAMPBELL: Dillon is a 3 year old right handed boy who is one of monozygotic twins. The family resides in Lincoln, Rhode Island. Mrs. Campbell began by explaining that Dillon is a "very loving child" and that he has been "making progress and wants to learn". His major difficulty centers over speech delay. He can communicate in single words, but the words are poorly articulated. Dillon has been working in speech therapy at the Fairlawn Early Learning Center where he is in a secluded classroom. He receives speech therapy once a week, as well as occupational therapy on a weekly basis. Mrs. Campbell also indicated that Dillon "has sensory stuff". She feels that he does not listen and is very active. She went on to express that Dillon is extremely aggressive and will throw things, have temper tantrums and bite indiscriminately . . . . The teachers have not yet recommended medication for his behavior, but Mrs. Campbell feels that this is likely in the near term . . . . Dillon's coordination has been a problem, in that he has had trouble walking up stairs. These difficulties have apparently resolved. His vision is good and his hearing has been tested on multiple occasions because he has bilateral tubes . . . . FAMILY HISTORY: The father is 31; the mother is a 30 year old, gravida 3, pare 4, ABO. A 13 year old brother and 16 year old sister are healthy. There is a strong family history of mental illness. The father suffers from depression, anxiety and an obsessive/compulsive disorder for which he takes Paxil and Xanax. A maternal brother suffers from a bipolar disorder and has a spinal cord injury. He also has been diagnosed as having borderline schizophrenia. The mother's family background is from Portugal. There are no family members with neurodegenerative illnesses or spinocerebellar ataxia. There is no history of familial dementia. Dillon had a single febrile seizure, but was not . . . been treated with medication. PRE- AND PERINATAL HISTORY: Dillon was the product of a 38-week gestation at Blake Memorial Hospital. His delivery was by emergency caesarean section and he required immediate resuscitation. His birth weight was 5-pounds, 15-ounces and he remained in the nursery for 19 days. He had recurrent seizures which were treated with 3 anti- epileptic drugs including phenobarbital and Phenytoin. GROWTH AND DEVELOPMENTAL MILESTONES: Dillon did not sit up until 8 months. He stood at 11 months and walked at 18 months. Dillon began saying single words at 15 months. He is not yet toilet trained. Dillon is fully immunized, has no significant allergies and has never undergone surgery. PHYSICAL EXAMINATION reveals Dillon to be an alert, but extremely active well proportioned child. His weight is 26-pounds and height 34-inches. Dillon's head circumference measures 46.8 cm, which is below standard percentiles for age matched controls and approximates the 50th percentile for age 15 months. The hair is brown and of normal texture. There are no cranial or facial anomalies or asymmetries. The neck is supple without masses, thyromegaly or adenopathy. The cardiovascular, respiratory and abdominal examinations are normal. The spine is straight without dysraphic features. Dillon's NEUROLOGIC EXAMINATION was significant for a high activity level and short attention span. His behavior was virtually uncontrollable for much of the evaluation and he required coaxing and stimulation to keep his interest. Dillon spoke in single words periodically, but these were poorly articulated and it was difficult to understand their meaning. The tongue movements were reasonably well coordinated and he did not drool. Dillon could interact at a very basic level and certainly understood simple commands. Cranial nerve examination revealed full visual fields to direct confrontation testing and a brief, but normal ocular fundoscopic examination. The pupils were 3 mm and reacted briskly to direct and consensually presented light. The uvula was midline and there were no facial movement asymetries. Motor examination revealed symmetric strength and bulk. The tone was slightly diminished for age. His gait was stable with symmetric arm swing. Dillon could run and jump without difficulty. The deep tendon reflexes were 1 to 2+ bilaterally with flexor planter responses. The stance was appropriately narrowly based. Sensory examination was deferred. Neurovascular examination revealed no cervical, cranial or ocular bruits and no temperature or pulse asymmetries. Dillon could build a tower of 5 cubes using primarily his right hand. He had well developed pincer grasp bilaterally. Dillon knew simple body parts, but could not identify pictures of animals. In SUMMARY, Dillon's neurologic examination is significant for a short attention span, high activity level and marked expressive language delay with disarticulation. He additionally manifests microcephaly and has a history of neonatal seizures. Dillon presently is on no medications. I regard Dillon's motor abilities to be within the normal range and he therefore has no evidence of a significant motor impairment . . . . The conclusion regarding Dillon's physical presentation To address whether Dillon is permanently and substantially physically impaired, the parties offered selected records relating to Mrs. Campbell's antepartum and intrapartum course, as well as for Dillon's birth and subsequent development. The parties also offered the opinions of three physicians and Mrs. Campbell, by deposition, to address the character of his physical presentation. Those physicians were Doctors Simmons, Younes, and Duchowny. The medical records and other proof, including the testimony of the physicians offered by the parties, have been carefully considered. So considered, it must be concluded that the proof does not demonstrate that, more likely than not, Dillon is permanently and substantially physically impaired. To the contrary, the proof reveals that the physicians most knowledgeable in the area (Doctors Younes and Duchowny) share strikingly similar and consistent opinions regarding the nature of Dillon's presentation, and that he is not permanently and substantially physically impaired.5
The Issue At issue in this proceeding is whether Joiner Abelove, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary matters John Abelove and Kathryn Abelove are the parents and natural guardians of Joiner Abelove (Joiner), a minor. Joiner was born a live infant on January 29, 1992, at Cape Canaveral Hospital, a hospital located in Cocoa Beach, Florida, and his birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Joiner was Fred Turner, M.D., who was, at all times material hereto, a participating physician in the Florida Birth- Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Mrs. Abelove's antepartum course and Joiner's birth Mrs. Abelove's antepartum course was without apparent complication; however, by late January 1992, the fetus was noted to be large for gestational age and her obstetrician/gynecologist proposed to induce labor. Mrs. Abelove presented to Cape Canaveral Hospital for a Prostin/Pitocin induction of labor at or about 8:30 a.m., January 28, 1992, and was immediately placed on a fetal monitor. Fetal heart rate (FHR) was reassuring, with a baseline of 148 to 154 beats per minute and good variability.1 Mrs. Abelove received her first Prostin gel, as the first step in the induction of labor, shortly after admission, her second at or about 12:30 p.m., and continued with Prostin until about 7:00 a.m., January 29, 1992, when mild contractions were noted. Membranes were artificially ruptured at 7:25 a.m., revealing clear fluid, and onset of labor was confirmed at 7:30 a.m. At 9:25 a.m., Pitocin was started, and Mrs. Abelove's labor slowly progressed until 7:15 p.m., when she began to push. Until that time, the fetal heart rate tracing was unremarkable or, stated differently, revealed a reassuring fetal heart rate, with normal/average long and short term variability. When Mrs. Abelove began to push, variable decelerations were noted to the 120s for 10 to 20 seconds, with a return to the FHR baseline of 150 to 160 beats per minute. Several other decelerations of a similar nature were noted prior to delivery, but not in sufficient number or intensity to reflect fetal compromise or injury. At 9:18 p.m., January 29, 1992, Joiner, the product of a spontaneous vaginal delivery, was born. Nuchal cord X 3 was noted; however, cord blood pH was 7.36 (normal). Joiner was Deelee suctioned to clear mucus, stimulated and administered oxygen by bag and mask; however, he "did not come around to stimulation [as expected]" and was transported to the neonatal intensive care unit for further management. Joiner was assigned Apgars of 5, 5, and 7, at one, five, and ten minutes, respectively. The Apgar scores assigned to Joiner 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 Joiner's Apgar score totalled 5, with heart rate being graded at 2; respiratory effort, muscle tone and reflex irritability being graded at 1 each; and color being graded at 0. At five minutes Joiner's Apgar score was unchanged. At ten minutes, his Apgar score totalled 7, with heart rate, muscle tone and reflex irritability being graded at 2 each, respiratory effort being graded at 1, and color being graded at 0. Joiner was admitted to the nursery at 9:25 p.m., and administered whiffs of oxygen. At the time, Joiner was noted to be flaccid (decreased tone); evidence general cyanosis; and exhibit flaring, grunting, and retracting (evidence of respiratory distress). Moist lungs, bilaterally, were also observed. Otherwise, Joiner's newborn infant exam was grossly normal. At 9:28 p.m., Joiner was placed in a oxyhood at 30 percent oxygen, and then increased to 50 percent. By 9:30 p.m., Joiner's oxygen saturation was noted at 100 percent, and his color improving (now pale pink). At or about 9:40 p.m., Joiner was examined by a Dr. Radu and lab work and a chest x-ray were ordered. At 10:00 p.m., following the results of the lab work, Dr. Radu lowered the oxygen to 30 percent. Joiner's oxygen saturation was noted at 98 percent, and he was described as pink with occasional retracting. Chest x-ray noted no acute cardiopulmonary disease, and he was diagnosed with respiratory distress syndrome of the newborn, which proved to be transitory. Course of treatment was continued oxygenation via oxyhood. At 10:30 p.m., Joiner continued to exhibit occasional flaring, grunting, and retracting; however, his color remained pink and he was observed to be active. By 11:30 p.m., Joiner's respirations were described as easy or unlabored, and his color continued pink. His condition remained stable through the night and at 8:20 a.m., January 31, 1992, oxygen was discontinued. At 11:20 a.m., cardiac and oxygen saturation monitors were also discontinued, and Joiner was transferred to the central nursery. There, he was bathed and placed under a warmer. At 12:45 p.m., the warmer was discontinued and Joiner was delivered to Mrs. Abelove where he was noted to latch on and nurse well. At 3:10 p.m., Joiner, in apparent good health, was discharged with his mother from the hospital. Joiner's subsequent development and medical care Joiner was followed at The Pediatric Group, by Dr. Thomas Fisk, for regular routine well-baby care following his discharge from the hospital, and his early infancy was apparently unremarkable; however, some mild delays in gross motor skills were observed at some point during his first year of life. At 13 months, Dr. Fisk saw Joiner for a physical examination, and his mother and grandmother expressed concern over his developmental progress, primarily his expressive language. Regarding these concerns, Dr. Fisk also noted: [His grandmother and mother] did report, however, at that time that he had some new found skills, was verbalizing a lot more, and we decided to watch him over the next few months and see him back at 15 months. Review of the record revealed that he had no vocalization at 9 months, so he had made some progress. At 13 months he was not walking and the only problem that I noticed was what appeared to be some trunkal hypotonia. Joiner was next seen by Dr. Fisk at 16 1/2 months and he observed that Joiner was still suffering from a delay in receptive language and gross motor development. Specifically, Dr. Fisk observed: . . . In receptive language, he does not seem to follow commands or simple instructions very well and he presently says only "mama" and "dada", "no", and has a rather unusual flow of speech. He does not have normal jargon and vocalizations are more grunting and non-fluid in nature. From a gross motor standpoint, is still cruising, but has not begun independent walking. Observation of his gait reveals what appears to be some generalized hypotonia but fairly good strength. Movements involving the upper and lower extremities, however, are also not very fluid and are awkward, however, I cannot put my finger on what seems to be wrong otherwise more specifically. Dr. Fisk's conclusion was generalized developmental delay, and he referred Joiner to Dr. Frank Lopez, a member of the Society of Developmental and Behavioral Pediatrics, to direct the developmental evaluation; however, Joiner was apparently not evaluated by Dr. Lopez until May 29, 1997, as discussed infra. Joiner had a computer tomogram (CT) of the brain on July 23, 1993, which was normal. More specifically, the report noted: No masses are detected. There are no intracranial calcifications. The ventricles are normal. No abnormal fluid collections are seen. At the request of Dr. Fisk, Joiner was seen by Dr. Michael Pollack, a pediatric neurologist on January 17, 1995. Dr. Pollack's report of that examination reads, in pertinent part, as follows: NEUROLOGICAL EXAMINATION: During the initial portion of the office visit, the patient makes minimal eye contact with the examiner. Subsequently he displays more social interaction both with the examiner and with his parents. He engages in mildly mischievous behavior and appears amused. He is not able to stack rings in order after demonstration and does not assemble a Gesell Form Board after demonstration. He does not point to body parts on request. He produces no intelligible words during the office visit and makes minimal attempt to communicate by gesture. He scribbles but does not attempt to copy a figure. Joiner is quite active and enjoys scattering rings about the room but displays no interest in representational play and very little interest in interactive play with the examiner. He does not vocalize abundantly. He does turn to voice. Pupils are equal and reactive to light. Limited view of the ocular fundi shows no abnormalities. There is a full range of conjugate, horizontal eye movement without nystagumus. No facial weakness or significant asymmetry are present. Gag reflex is preserved. Gait is normal. He is not able to cooperate for testing of strength or coordination but functional testing suggests normal strength in all limbs. Tendon reflexes are symmetrically ++ and plantar responses flexor. IMPRESSION: At a chronological age of almost 3 years, Jointer appears to be functioning below the 2 year level. He has facial features which raise the possibility of cerebral gigantism (Soto's syndrome), but these are relatively non-specific and it is noted that his facial features are similar to those of his father. In addition, multiple members of both families are tall as noted above. Although his most conspicuous delay is in the language sphere, other areas of cognitive development also appear to be affected. He has a number of features which fall in the autistic spectrum but does display the ability to interact socially as described above. He has had a variety of diagnostic studies, all of which have been normal. RECOMMENDATIONS: 1. Genetics consultation was suggested. 2. MRI scan of the head was also ordered since cerebral anomalies which are not evident on CT scan are sometimes demonstrated by MRI. The patient was referred to FDLRS and also to a speech/language pathologist. It is likely that he will benefit from medication to improve attention span and to reduce his high activity level, but, if the situation permits, it would be preferable to defer such medication for 1 or 2 years. His parents will call for the result of the MRI scan and the patient will return to the office for re-examination in one year. The results of the MRI scan and chromosome study were normal. Whether Joiner ever returned for re-examination by Dr. Pollack is not of record. Joiner continued to be followed by Dr. Fisk, who had resolved that Joiner suffered from pervasive developmental disorder. On Joiner's visit of June 4, 1996, at approximately 4 1/2 years of age, Dr. Fisk observed: . . . He attends Parton Elementary Pre-K program for children with developmental problems. Father indicates that he has made good progress especially with his expressive language over this last year, but he continues to be remarkably delayed. Expressive language skills are really at the 2-year level, and his visual attending is rated at the one-year level. He has very few skills above the 2-year level. He is extremely aggressive at school, very easily over stimulated, flaps his hands, stimulates himself, as is often seen in children with autism. He has much improvement when on his Ritalin with fair control over these particular symptoms, but the aggressive issue continues to be a major problem for the parents. Now that he is getting bigger, they literally can not go out of the house with him without getting into an aggressive situation. I have discussed in the past with these parents the need for him being involved with a specialist to manage his pervasive developmental delay. Insurance restrictions have preempted their attempts to do this, and they have been unwilling to see Dr. Frank Lopez here in town. I discussed his progress over the last year today in the office with the father. The last note of record by Dr. Fisk, relates to an office visit of February 27, 1997.2 At that time, Dr. Fisk observed: Patient well-known to me with pervasive developmental disorder. Joiner currently is in a developmental preschool situation and takes Ritalin. . . . Parents have noted a significant decrease in his aggressive tendencies and they have been helped out significantly by their present behavioral therapist who has gone to the school, come to their home, and tried to work a behavior program out for Joiner. He is much less aggressive, more cooperative in the classroom, settles down and does at least attend and participate, at least significantly more than he used to. He still has significant language problems, repeats a few words back when spoken to him, but is really still not putting words together in sentences; has significant communication difficulties. Has been feeling well over the time frame of the last several months. Mom was very reluctant originally to consider using Ritalin, but she has come to grips now with the fact that he seems to be doing well on it. They have not gotten involved with child psychiatrist, but have significant educational intervention ongoing. He does see OT and speech therapy as well. Been feeling well recently. Parents relate no medical problems. Uncooperative 5-year-old male who is tall for age, tends to cling to his dad in the office. He will ambulate, however, and cooperated with most of the exam until he had to lay down on the table. Even considering this, he was much better today than he has been in the past. . . . Chest is clear. Cardiovascular: normal. ABD: soft, nontender w/o organomegaly. GU: normal circumcised male. Testes descended. Back and extremities exam: essentially normal with normal gait. He has mild clinodactyly bilaterally. DTRs 2+ and symmetrical. Motor strength and tone equal and symmetrical as well. Hemoglobin today: 14.3. UA could not be obtained secondary to lack of cooperation - parents will be bringing that back. He could not cooperate with hearing or vision screen, but dad says he is scheduled to have his hearing retested next week. Joiner was seen by Dr. Frank Lopez on May 29, 1997. He observed, as follows: Joiner has been referred into this office by courtesy of Dr. Fisk. Joiner is here accompanied by his parents who serve as primary historians and report that he has been seen and had a work-up done by Dr. Colin Condron and Dr. Michael Pollack in the past. Their concerns are that they would like more information regarding Joiner's problems and "a more accurate diagnosis and supportive treatment plan." He has been diagnosed as Developmental Delay and Autistic Spectrum presentation. Mom and Dad are very concerned, not as much with the diagnostic category, but rather with how best to place and guide him. He is presently staffed into EMH at Partin Elementary and will be changing schools, going into TMH classroom due to his not keeping up. The Autistic Program has been considered, but the parents have not decided on its merits yet. Following consideration of Joiner's developmental history, family history, and physical examination, Dr. Lopez's impression was: Autism; Hypotonia; Dyspraxia. Given the proof, it cannot be subject to serious debate that Joiner suffers a serious neurologic impairment. What remains to resolve is the genesis of his impairment or, more pertinent to these proceedings, whether the proof supports the conclusion that his condition resulted from an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as required by Section 766.302(2), Florida Statutes, for coverage to be afforded by the Plan.3 With regard to such issue, Petitioners contend that Joiner suffered an injury to his brain caused by oxygen deprivation (an hypoxic event) during the course of resuscitation, and that such injury was the cause of Joiner's neurologic impairment. In contrast, Respondent contends the proof is not consistent with hypoxic ischemic injury occurring during or immediately following child birth, but is consistent with a pervasive developmental disorder or autism.4 Respondent's view of the proof has merit. The genesis of Joiner's neurologic impairment To address the genesis of Joiner's neurologic impairment, the parties offered selected medical records relating to Mrs. Abelove's antepartum and intrapartum course, as well as for Joiner's birth and subsequent development. Portions of those records have been addressed supra, and further salient portions will be addressed infra. The parties also offered the opinions of three physicians as to the likely cause of Joiner's disorder. The physician selected by Petitioners was Danuta Deeb, M.D., board certified in pediatrics. The physicians offered by Respondent were Edward Lance Wyble, M.D., board certified in pediatrics and neonatology, and Michael Duchowny, M.D., board certified in pediatric neurology, pediatrics, and clinical neurophysiology. The medical records and other documentary proof, as well as the testimony of the physicians offered by the parties have been carefully considered. So scrutinized, it must be concluded that the proof does not allow a conclusion to be drawn with any sense of confidence that, more likely than not, Joiner's neurologic impairment was associated with an injury to the brain caused by oxygen deprivation occurring during the course of labor, delivery, or resuscitation in the immediate post-delivery period. Rather, the proof demonstrates, convincingly, that Joiner's presentation is consistent with a pervasive developmental disorder, a disorder within the spectrum of childhood autism, which resulted from an anomaly in brain development, as opposed to a hypoxic ischemic injury during the birth process.5 In so concluding, it is observed that Joiner's course pre-delivery and post-delivery was inconsistent with hypoxic or ischemic injury having occurred during the course of labor, delivery, or resuscitation. First, the evidence documenting fetal heart rate during the course of labor and delivery does not support the conclusion that Joiner suffered an acute intrapartum event that led to hypoxic or ischemic injury.6 Further militating against the conclusion that Joiner's anomaly was caused by oxygen deprivation pre-delivery or new-onset hypoxia post-delivery, are the numerous inconsistencies between Joiner's presentation and development, and the clinical findings one would expect had he suffered hypoxic ischemic encephalopathy, secondary to perinatal asphyxia, during that period. Notably, Joiner's Apgar scores were 5, 5, and 7 at one, five, and ten minutes. Apgars of 5 do not represent a threatening situation to the brain, but provide a reflection of the infant's status where, as here, the infant is going through a 10-minute to 15-minute change process after birth. Importantly, the Apgar did not stay at 5, but progressed to 7 by ten minutes and the infant was essentially normal when examined by the pediatrician at 9:40 p.m. Clearly, the infant was improving over that period, which compels the conclusion that there was no ongoing insult.7 Had Joiner suffered an injury to his brain during or immediately following birth, there are a number of clinical findings one would reasonably expect to observe. An infant who has suffered a neurologic injury should demonstrate a 6-hour to 12-hour period of decreased tone, followed by evidence of hyperactivity and irritability. Moreover, in cases of substantial neurologic injury, the infant should generally evidence seizure activity within 8 to 24 hours. Beyond the first 24-hour period, the infant should demonstrate moderate to significant decreased tone, depending on the magnitude of the injury, and within the first 48-hour period the injured infant should evidence resistance to feeding. Here, Joiner's decreased tone was resolved by 9:40 p.m., there was no evidence of hyperactivity and irritability, and no evidence of seizure activity. Moreover, at approximately 15 hours of life, Joiner was shown to latch on and breast-feed well. It is further observed that, while he suffered respiratory distress, Joiner did not suffer respiratory arrest or failure, and did not require intubation or mechanical ventilation. Rather, his respiratory effort was adequate to ventilate and, as confirmed by pulse oximeter, he was adequately oxygenated. Also inconsistent with brain injury during or immediately following birth, there was no evidence of other system dysfunction, such as the heart or kidney8; no evidence of brain swelling within 24 hours of birth9; Joiner's lab studies were normal, including cord pH; and follow-up blood-gas studies did not reflect acidosis of substance. In sum, there was no clinical evidence in the newborn period that Joiner's neurologic presentation was abnormal or, stated differently, that he had suffered or was suffering a neurologic injury. Finally, it is observed that Joiner's presentation is consistent with pervasive developmental disorder, a disorder within the spectrum of childhood autism, a serious neurologic disorder in which affected children display abnormalities in socialization, behavior, language and, occasionally, stereotyped motor movements. Such disorder is developmental in origin (an anomaly in brain development), acquired prenatally, and is not associated with events that might occur during labor, delivery, or resuscitation. Given the proof, it cannot be concluded that, more likely than not, Joiner's neurologic impairment was associated with a brain injury caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period. Notably, Joiner's presentation at birth and his neonatal course were not consistent with an acutely acquired neurological injury, and it is improbable that he could have experienced an acute injury during labor and delivery, or immediately thereafter, without evidencing a single clinical symptom of such damage. Conversely, the existence of a prenatally acquired (predating labor and delivery) brain disorder (developmentally based) would be consistent with Joiner's presentation at birth and subsequent development.
The Issue Whether Jael Sutton, a minor, qualifies for benefits under Florida's Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Petitioner, Senboya Sutton, is the natural parent of Jael Sutton (Jael). At all times material, Senboya Sutton was an obstetric patient of Intervenor, Mark Davis, M.D., who was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by section 766.302(7). Dr. Davis provided obstetrical services "in the course of labor, delivery and resuscitation in the immediate postdelivery period in a hospital," as related to this case. Jael was born on November 28, 2006. At birth, Jael weighed in excess of 2,500 grams. Jael was a single gestation. Jael was born live at St. Joseph's. St. Joseph's is a licensed hospital located in Tampa, Florida. The parties stipulated that all notice requirements of the statute have been met and that the notice requirement of section 766.316, is not at issue herein.2 Coverage is afforded by the plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat.3 Herein, it is undisputed that Jael is "permanently and substantially mentally and physically impaired." Also, as described more fully hereafter, all the testifying experts concur that Jael's underlying brain damage did not result from a mechanical injury, but did result from sepsis and/or meningitis. However, it remains for determination whether or not Jael's brain injury and permanent and substantial mental and physical impairment occurred in the course of "labor, delivery, or resuscitation in the immediate postdelivery period," hereafter referred to as "the statutory period."4 The following terms were defined within this record: "Hypoxia" means "not enough oxygen." "Cerebral ischemia" means "not enough blood is getting to the brain." "Perfusion," for purposes of the instant case, means "to pass blood through the brain to ensure adequate oxygen." For her pregnancy with Jael, Ms. Sutton was first seen by Dr. Davis on August 17, 2006. Her delivery date was estimated as January 25, 2007. On November 17, 2006, a vaginal culture was taken of Ms. Sutton. On November 25, 2006, it was reported as "positive" for Group B streptococcus (Group B-strep), a genus of bacteria that causes life-threatening infections in newborn infants.5 Dr. Chalhub testified that intrauterine infections are the leading cause of cerebral palsy in term infants. Jael was not a term infant, but cerebral palsy is one of the conditions with which he has been diagnosed. On November 27, 2006, at approximately noon,6 Ms. Sutton presented to St. Joseph's. She complained of a single episode of leaking fluid at 1:02 p.m. Hospital records characterized this as the onset of labor, despite Ms. Sutton's denial of contractions. The plan of treatment was to rule out spontaneous rupture of the membranes. A nitrazine test was performed to identify amniotic fluid outside the amniotic sac, and was negative. Dr. Davis was present and ordered a non- stress test. At 1:34 p.m., Ms. Sutton again complained of leaking fluid and mucus discharge was noted. At 1:58 p.m., Dr. Davis reviewed the fetal monitor strip and discharged Ms. Sutton. At approximately 5:50 p.m., on November 27, 2006, Ms. Sutton presented to UCH. Her membranes were noted as possibly ruptured, and she complained of small gushes of fluid since noon. Again, a nitrazine test was performed and was negative. A speculum vaginal examination was performed; fetal heart rate was monitored; and a non-stress test was performed. She was discharged home upon phone orders of the "on-call" physician and advised to follow up with her obstetrician. The next morning, before 10:00 a.m., Dr. Davis did an ultrasound in his office. The ultrasound showed what was believed to be decreased amniotic fluid; a 34-week, four day gestation; and ruptured membranes. Due to the Group B strep and the gestation in excess of 34 weeks, Dr. Davis initiated a plan of care to induce labor and perform a vaginal delivery. Later on November 28, 2006, Ms. Sutton was admitted to St. Joseph's. Examination by speculum showed positive nitrazine and a copious amount of fluid in the vaginal vault, which, in hindsight after Jael's birth, Dr. Davis recorded as "probably a high leak to begin with." A fern test for nitrazine was positive. The cervix was 2-3 centimeters dilated. Labor steadily progressed. At 11:32 a.m., a nurse noted a non- reassuring fetal heart rate. At 11:47 a.m., Dr. Davis reviewed fetal heart rate tracings from his office. These were better, without decelerations. Ms. Sutton was placed in a left lateral position and continuous face mask oxygen was maintained. At 11:49 a.m., another sterile vaginal exam was performed. The amniotic fluid was noted to be clear and of normal quantity. At 11:54 a.m., due to a non-reassuring fetal heartbeat, Dr. Davis called for an immediate Caesarean section. Jael's fetal heart rate was 160, just prior to the C-section. A low transverse uterine incision was performed at 12:16 p.m., and Jael was delivered. Throughout the C-section, under general anesthesia, Ms. Sutton's oxygen saturation levels remained at 100. There is no record of trauma or of mechanical injury to Jael during labor or delivery. Indeed, the parties agree that there was no mechanical injury to Jael during labor or delivery. See infra. The delivery record does not show checks or fill-ins for the following, but the following is printed or typed in on the delivery room record form: "suction bulb, suction catheter, tactile stimulation, oxygen/PPV[7], intubated, neonatologist present." Apgar scores were taken at one and five minutes after Jael's birth.8 Jael's one minute Apgar score showed: Heart rate 2 > 100 Respiratory effort 0 none Muscle tone 1 some flexion Activity 0 none Color 0 blue/pale Total 3 Jael's five minute Apgar score showed: Heart rate 2 > 100 Respiratory effort 2 good cry Muscle tone 1 some flexion Activity 1 grimace Color 1 extremities blue Total 7 It is a point of contention among the parties as to whether Jael was intubated in the delivery room or in the Neonatal Intensive Care Unit (NICU). It is more likely that intubation and administration of nitrous oxide began after he was stabilized, as evidenced by the good Apgar score at five minutes after birth. The "good cry" recorded at five minutes of life (12:21 p.m.) suggests that Jael was breathing on his own at that point, had stabilized, and was not intubated before his admission to the NICU at 12:40 p.m. Jael's cord blood gas was collected at ten minutes after birth at 12:26 p.m. Its pH measured 7.206. A cord blood of 7.2 or higher suggests absence of metabolic acidosis. Metabolic acidosis is a sign of a pathological condition, not of a mechanical injury or of oxygen deprivation.9 At 12:32 p.m., Jael was transferred by isolette from the delivery/operating room to NICU due to "post C-section respiratory status." It would be fair to say that, at this point, if not sooner, Jael's care passed from the NICA participating physician, who provided obstetrical services to the mother, to other health care professionals in the NICU. At 12:40 p.m., on November 28, 2006, Jael was admitted to the NICU. The records show that ventilation support was given, and Jael was intubated. No physician associated with Jael's delivery or NICU care testified. However, Dr. Katz, a pediatric neurologist, opined without refutation that intubation at that stage might have been for ventilation, but could as easily have been to keep Jael's airway open because he was born prematurely. The reasons that were contemporaneously documented for Jael's admission to NICU were "premi, 34 weeks, R/O sepsis." This notation most probably means, "34 week gestational, premature infant; rule out sepsis." "'Sepsis' refers to the presence in the blood or other tissues of pathogenic microorganisms or their toxins; the condition associated with such presence."10 As described more fully hereafter, all testifying medical experts, regardless of specialty, agreed that in the NICU, Jael suffered from vascular inflammation, decreased blood pressure, and diminished perfusion caused by infection. Where they disagree is whether it was sepsis or meningitis which was ultimately responsible for Jael's diminished blood supply to the brain. "'Meningitis' is an inflammation of the meninges, usually by either a bacterium (bacterial meningitis) or a virus (viral meningitis)."11 Upon admission to the NICU at 12:40 p.m., Jael's oxygen saturation levels were at 93 per cent, and despite continuing very low blood pressures, his oxygen saturation levels remained in the 80's and 90's until 6:40 p.m., that evening. Jael was not assessed again after NICU admission until 1:20 p.m. At that time, a nurse noted that she was unable to obtain his blood pressure in either leg, although no reason was given. Dr. Katz testified that this could mean anything, up to and including an ill-fitting blood pressure cuff. Jael's bedside glucose (BSG) was recorded as 10, and 50cc of D10 bolus were ordered. At 1:44 p.m., on November 28, 2006, the BSG was recorded as 43 and another bolus was administered. At 1:58 p.m., November 28, 2006, a blood culture was drawn which was not reported back until the next day, but when it was reported back, the blood culture was read as positive for Group B strep. 37. At 2:00 p.m. and 2:05 p.m., on November 28, 2006, boluses and antibiotics were ordered, but one or more antibiotics were not administered to Jael for the first time until considerably later. At 2:05 p.m., on November 28, 2006, orders were written for survanta and dopamine. Dr. Katz opined that Jael was in septic shock at this time. At 2:16 p.m. on November 28, 2006, Neonatologist Dr. Amaizu entered an NICU admission note that Jael was lethargic with decreased reactions to stimuli. Capillary reflex was > 2 sec. Jael had decreased tone and activity. Although perfusion was decreased, his skin was pink. The active diagnosis at that point was "hypoglycemia, prematurity, respiratory distress syndrome, R/O sepsis newborn." At 2:25 p.m., an NICU nursing assessment was done. Jael was described as withdrawn, flaccid, lethargic with absent reflexes (suck, rooting, moro, and grasp). Central cyanosis (blueness in the torso) was observed. At 3:07 p.m., dopamine was administered. On the following day, November 29, 2006, Terry Declue, M.D., performed an endocrinology consult on Jael, who was on nitrous oxide via an oscillatory ventilator. He noted hypoglycemia. Perfusion was noted as good with capillary refill one second. The chest appeared clear, and Jael moved spontaneously. Dr. Declue's diagnosis was: Severe metabolic acidosis Lactic acidosis Respiratory failure Gram positive cocci sepsis Pulmonary hypertension On December 1, 2006, three days post-birth, a cranial neuro-sonogram was performed. At that time, hospital Radiologists Steen Mandel, M.D., and John Rasmussen, M.D., read the sonogram as normal. On December 4, 2006, four days post-birth, Jael underwent a lumbar puncture. His cerebrospinal fluid showed a white blood count of 185, reference 0-5. The consulting neurologist diagnosed Strep Group B sepsis and meningitis. On December 10, 2006, a second cranial ultrasound was done. This second sonogram was read by Michael Shaw, M.D. He recorded that ventricular size and configuration was normal, with no evidence of germinal matrix or inter-ventricular bleed, but the ventricles appeared slightly (not significantly) more prominent than the prior December 1, 2006, study. On December 15, 2006, an MRI was performed and interpreted by radiologist Elaine Engleman, M.D. Her impression was: Extensive cystic encephalomalacia[12] involving both cerebral hemispheres throughout all vascular territories. There is slightly less extensive involvement in the posterior cerebral artery territories. There is preservation of parenchyma involving the basal ganglia, thalami and brainstem. Jael was discharged from St. Joseph's on January 5, 2007, with a diagnosis of: Prematurity at 34 weeks gestational age Respiratory distress syndrome Neonatal depression Severe metabolic acidosis Patent ductus arteriosis Cholestasis Lactic acidosis Respiratory failure Meningitis that was treated for three weeks and supraventricular tachycardia On August 1, 2007, another MRI was performed on Jael's brain and interpreted by Radiologist, James Hanner, M.D. His report opined: FINDINGS: There is extensive cystic encephalomalacia seen throughout in the frontal, temporal, and parieto-occipital lobes associated with significant ex vacuo enlargement of the occipital horns, bilaterally, left greater than right. There is some sparing of the medial frontal accident, hemorrhage, or extra-axial fluid collection is identified. The hindbrain structures are normal without developmental anomaly. There is wallerian degeneration of the cerebral peduncles bilaterally. IMPRESSION: Extensive supratentorial systic encephalomalacia associated with ex vacuo enlargement of the lateral ventricles and occipital horns, left greater than right. The volume loss has progressed when compared to the earlier examination. Despite some variant medical testimony, across all experts, to the effect that Jael was probably infected with Group B-strep from his mother before labor, during labor, or during delivery, Intervenors collectively submit that, ". . . Jael Sutton did not suffer from oxygen deprivation during labor or delivery . . ." (proposed finding of fact 54 of Intervenors' proposed final order). Due to this admission and the other parties' similar positions, it is not necessary for the undersigned to resolve when labor began; when "active" labor began; when the amniotic fluid began to leak; or even whether Jael's delivery by C-section undermines any medical opinions rendered herein in terms of acquisition of bacterial infection during Jael's passage through the birth canal. Therefore, the issue is further narrowed to whether or not Jael suffered from oxygen deprivation "occurring in the course of . . . resuscitation in the immediate postdelivery period . . . which render[ed] the infant permanently and substantially mentally and physically impaired." The parties presented medical experts in a variety of fields who offered their opinions, within reasonable medical probability, as to what happened to Jael and within which periods of time. All experts testified by deposition, but the undersigned has had the benefit of viewing DVDs of the depositions of Dr. Robert Zimmerman and Dr. Mary K. Edwards- Brown. Michael Duchowny, M.D., a Florida-licensed physician, is a professor of neurology at the University of Miami Leonard Miller School of Medicine; a clinical professor of neurology at Florida International University College of Medicine; and senior attending physician at Miami Children's Hospital. He is board- certified in pediatric neurology, with special competence in child neurology, clinical neurology, and clinical neuro- physiology. He performed a medical examination of Jael on February 17, 2010, and reviewed the mother's and the child's medical records, including the ultrasound study of December 1, 2006, and the MRI scans of December 15, 2006, and August 1, 2007. He did not read the December 10, 2006, ultrasound. Dr. Duchowny's testimony confirmed, without equivocation, that Jael is tragically and profoundly permanently and substantially mentally and physically impaired. It was his ultimate opinion that Jael did not suffer a birth-related neurological injury due either to mechanical injury or deprivation of oxygen supply or blood flow to the brain within the statutory period. He reached this conclusion because, in his expert opinion, no impairment occurred during the statutory period. Dr. Duchowny did not see, on the films he reviewed, any sign of damage during the statutory period. He diagnosed the cause of Jael's multiple problems as meningitis, and opined, in pertinent part, as follows: Q: . . . Do you have an opinion, within a reasonable degree of medical probability, whether or not he had an impairment that was acquired during labor, delivery or post- delivery? . . . A: If we're going to define it as impairment, I would say, no. Q: So what you're saying is that no damage was done, even if he had the infection, right? A: I am saying that, because I don't see any indication of damage at that time. Q: . . . You don't find him -- you don't find that he had a mechanical injury; is that right? A: That's correct. Q: And you don't find that there was deprivation of blood flow or oxygen, correct? A: That's correct. (Depo. 33-34). Dr. Duchowny testified concerning the meningitis diagnosis as follows: A. . . . Meningitis means -- it specifically refers to a bacterial infection of the membranes covering the brain. These are anatomically called the meninges, so that in its strictest sense, a meningitis is an infection and an inflammation of the membranes covering the brain, but, in point of fact, it spreads from the membranes usually directly to the brain itself, and that's where the problems come in. . . . * * * I don't believe that Jael's brain damage was due to either a mechanical injury or oxygen- -deprivation of oxygen supply or blood flow to the brain. I think that Jael's brain damage is primarily due to the effects of meningitis. * * * . . . the MRI findings are consistent with severe bacterial meningitis, in this case, Group B strep meningitis. The findings, also, to me, are supported by the fact that if one looks at the clinical course of Jael, there really is no specific hypoxic or ischemic event that would be in the records to explain the findings on neuroimaging and the neurologic outcome. . . . So although one can see findings on MRI that are consistent with hypoxic and ischemic damage, for example, cystic encephalomalacia, if one looks at the totality of the picture, meaning, put the clinical events together with the neuroimaging findings and the neurologic examination, I think that this pattern of evidence all supports the fact that Jael's neurologic damage is primarily due to bacterial meningitis. (Depo. 20-26). Michael Katz, M.D., is a pediatric neurologist, and board-certified in pediatrics, pediatric neurology, and neuro- developmental disabilities. He is based at Hackensack University Medical Center, New Jersey. He examined Jael on September 14, 2009, and testified on behalf of Petitioners by a November 19, 2010, deposition. He considered the "resuscitative period" in Jael's case to be "until the Apgar is normalized at five minutes when the Apgar was seven," and opined that the injury to Jael's brain did not take place in that period. He concluded that the cause of Jael's permanent and substantial mental and physical impairment was a "strep B meningitis." More specifically, Dr. Katz testified: Q: In your opinion within a reasonable degree of medical probability, was there any injury to Jael Sutton's brain caused by oxygen deprivation occurring during labor or delivery or resuscitation in the immediate postdelivery period? A: No. * * * Q: What significant history did you elicit that leads you to reach that diagnosis and opinion of causation? * * * A: . . . First is that Mom was group B strep positive. The second was that mom had premature ruptured membranes. . . . Jael had a clinical deterioration, essentially went into shock and required pressors and resuscitation. And the ultimate, and probably most important fact, is when he was finally clinically stable, we were able to do a lumbar puncture, and we drew out group B strep spinal bacteria in his spinal fluid, along with a diagnosis of group B strep meningitis. (Depo. 11-12). Robert Zimmerman, M.D., is a professor of radiology of the division of neurosurgery at Children's Hospital of Pennsylvania. He has been chief of pediatric neurology there since 1989. He is licensed to practice medicine in Pennsylvania, New Jersey, and Israel, and has been board- certified in diagnostic radiology and neuroradiology. In Dr. Zimmerman's opinion, after having read the two ultrasounds (December 1, 2006 and December 10, 2006) and the two MRIs (December 15, 2006 and August 1, 2007) performed on Jael, the first ultrasound was abnormal and clearly showed decreased oxygen (hypoxia) and decreased blood flow (ischemia), and the remaining studies showed advancing stages of brain injury (the brain turning to "swiss cheese") due to lack of oxygen and lack of blood flow. This was cystic encephalomalacia. He acknowledged that a hypoglycemic event could possibly have contributed to the situation, but he perceived no traumatic event and no mechanical injury. As to timing, Dr. Zimmerman indicated that the progression of the ischemia possibly started intrauterine, even before delivery, but the best he could place a point of injury was, "in and around the time that the kid was being delivered, the day of birth or a little earlier, or perhaps right after birth, but somewhere in that vicinity . . . . Sometime around the 28th." He believed that hypoxic ischemia caused the holes in Jael's brain, and that the condition first began to develop more than 1-6 days before the first ultrasound of December 1, 2006. He indicated that sepsis was probably the cause of the oxygen insufficiency and ruled out bacterial meningitis, but he ultimately conceded he would defer those decisions to a clinician, such as a pediatric neurologist. Dr. Zimmerman's opinion is diminished by his vascillations on placing the time of injury and his disclaimers, and by there being no indication he reviewed any medical information on Jael other than the four films. Mary K. Edwards-Brown M.D., is a neuro-radiologist with a subspecialty interest in pediatric neuroradiology. She is board-certified in radiology and in neuroradiology. She is also a full professor of radiology at Indiana University and practices at Riley Children's Hospital, Riley, Indiana. She also teaches medical professionals at many levels, including preparation for specialty boards. Dr. Edwards-Brown also reviewed the history and all four of Jael's films (December 1, 2006; December 10, 2006; December 15, 2006, and August 1, 2007). She, unlike Dr. Zimmerman, considered the first ultrasound to be normal. In the December 10, 2006, MRI, she found non-specific brain damage by tissue destruction. In the December 15, 2006, MRI, she, like Dr. Zimmerman, found massive brain damage and diffused cystic encephalomalacia, which she also considered non-specific. According to Dr. Edwards-Brown, the most common cause for this condition is that insufficient oxygen was getting to the brain, which can occur by not enough oxygen being present, by infection, or by trauma. Dr. Edwards-Brown ultimately opined that: . . . [Jael] was suffering from a profound meningitis, which caused the pattern of hypoxic-ischemic encephalitis -- encephalomalacia. And it was a mechanism of meningitis that induced hypoglycemia and brain injury that happened after this child was born. * * * Given that Jael was born with Apgars of 3 and 7, and a pH of 7.2, those are signs that -- most children who have those Apgars and that non-acidotic pH at birth generally do very well, and certainly don't have a pattern of injury as we've seen here. And given the fact that the ultrasound of December 1st looks normal to me it is my opinion that this injury occurred after the time of birth [November 28, 2006]. And most likely, the bulk of the injury occurred after December 1st, that first ultrasound that looks so very normal. Doctors Duchowny, Katz, and Edwards-Brown concurred, in varying terminology, that Jael's situation was a slow- evolving brain injury not consistent with a sentinel hypoxic insult occurring during resuscitation in the immediate postdelivery period. Dr. Zimmerman also could not point to any specific sentinel event. Elias Chalhub, M.D., testified by a deposition taken November 26, 2010. Dr. Chalhub is board-certified in pediatrics, psychiatry, and neurology, but he has not done research or published in over 20 years. Based on a records review, and without examining Jael, he testified that Jael's Group B strep sepsis occurred within an hour and a half of birth when the child was in the NICU in septic shock. He noted the records of Jael's pale, blue color (cyanosis) but also agreed that the baby had reasonably good Apgars and normal cord gas before transfer to the NICU. He stated Jael deteriorated rapidly after the good Apgars, which, in his opinion, is consistent with septic shock. However, Dr. Chalhub conceded that the baby was stable at five minutes after birth; that there was nothing in the nursing notes at 1:00 p.m., on December 28, 2006, that alerted to a problem; that there was no indication about an inability to get blood pressures before 1:20 p.m.; that thereafter, the baby became hypotensive, and that the first abnormal blood pressure reading was at 1:52 p.m., an hour and 36 minutes after birth. Dr. Chalhub opined that between birth at 12:16 p.m. and 2:00 p.m., on November 28, 2006, there was sepsis and decreased perfusion that resulted in Jael's injury. He was satisfied that the Group B-strep, which may have been acquired before labor or during birth, resulted in sepsis and that the brain injury occurred before the sepsis became meningitis, but conceded the meningitis, which came later, could have contributed to Jael's brain damage. He stated he did not believe that hypoglycemia, detected at 1:20 p.m., contributed to the brain damage. That said, Dr. Chalhub, in asserting compensability, also set the "immediate postdelivery period in a hospital" at an arbitrary "six hours from birth," without even relating the six hour period to acts of "resuscitation" or to the facts of this case. He claimed "six hours" would be what neonatologists would say constituted the "immediate post-resuscitative period," but he quoted no neonatal authority for the proposition. Clearly, his arbitrary concept is not the understanding of the greater medical community as evidenced by the other testifying physicians, nor is it the status of Florida law.13 Accordingly, I have discounted his opinion that the oxygen deprivation occurred during the statutory period. It might have been helpful to have heard testimony from a perfusionist or neonatologist, but herein radiologists' opinions have been compared with each other and neurologists' opinions have been compared with those of other neurologists. Dr. Chalhub's opinion is less persuasive than some other witnesses for the reasons related supra. The opinions of the physicians who actually examined Jael are more persuasive than those of physicians who only did a records review. Finally, the logic and reasoning of all experts have been compared and weighed and one common theme appears: whether characterized as "sepsis" or "meningitis," the Group B-strep resulted in a plethora of diagnoses, culminating in ultimate brain cell death. Within these parameters, and upon the credible evidence as a whole, it is found that more likely than not, Jael did not suffer brain injury due to oxygen deprivation that occurred during labor, delivery or resuscitation in the immediate postdelivery period in a hospital. Rather, it is more likely than not that Jael suffered brain damage after he was initially stabilized and after he was removed to the NICU due to his premature birth status. Based on the credible evidence as a whole, it appears that wherever and whenever Jael was intubated, he probably was not intubated until after the Apgars and after the immediate resuscitative period ended. Due to Jael's "good cry" immediately after delivery, the increasingly good Apgars, the good cord blood report, and the fact that there was no indication of oxygen deprivation to the brain at least until the first ultrasound of December 1, 2006, three days after delivery, the more compelling evidence supports a finding that Jael did not suffer from oxygen deprivation during labor or delivery and did not suffer injury to the brain during that period, either. As to his intubation in NICU, it is as likely that his airway was being protected by intubation as it is that he suffered any problem breathing or any oxygen deprivation before 2:00 p.m., on November 28, 2006, when he went into shock. Accordingly, the record fails to support a finding that there was an hypoxic or ischemic event during the statutory period (labor, delivery, or resuscitation in the immediate postdelivery period in a hospital). Alternatively, it is conceivable, but not proven, that Jael suffered oxygen deprivation at some unspecified point in time which occurred after 2:00 p.m., on December 28, 2006, and after he had arrived in NICU, which still is not within the statutory period. Since both the oxygen deprivation and the injury cannot be placed in the statutory period, Petitioners cannot prevail.
The Issue At issue in the proceeding is whether Ashley Wilkinson, 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 Petitioners, George Wilkinson and Kimberly Wilkinson, are the parents and natural guardians of Ashley C. Wilkinson, a minor. Ashley was born a live infant on July 13, 1996, at Spring Hill Regional Hospital, a hospital located in Spring Hill, Florida, and her birth weight exceeded 2,500 grams. The physician providing obstetrical services at Ashley's birth was Thomas J. Armbruster, 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. Mrs. Wilkinson's antepartum course and Ashley's birth Mrs. Wilkinson's antepartum course was without significant complication until July 10, 1996, when, at 6:40 p.m., with the fetus at 38 and 4/7 weeks gestation (estimated date of delivery July 20, 1996), she presented at Spring Hill Regional Hospital complaining of "bleeding [and] low pressure," and was admitted to rule out labor. At the time, external fetal monitoring revealed a reassuring fetal heart rate in the 130-beat per minute range, and no contractions. Vaginal examination revealed the cervix at 1 centimeter, effacement at 20 percent, and the fetus at station -3, with the membranes intact. Dr. Armbruster was paged, and at 7:15 p.m., visited briefly with Mrs. Wilkinson. At that time, Dr. Armbruster instructed staff to watch for contractions for another 30 minutes and if none were observed, Mrs. Wilkinson could be discharged. Thereafter, at 8:45 p.m., there being no evidence of contractions or other change in status, Mrs. Wilkinson was discharged, with mother and fetus noted to be stable. Insofar as the record reveals, Mrs. Wilkinson's antepartum course continued without apparent complication until approximately 12:01 a.m., July 13, 1996, when, while at home in bed, her membranes ruptured and, either contemporaneously or shortly thereafter, she evidenced seizure activity (possibly eclampic) and severe vaginal bleeding.2 Mrs. Wilkinson's husband immediately called 911. Pasco County Fire Rescue responded to the emergency call. On arrival, fire rescue personnel witnessed Mrs. Wilkinson thrashing about in bed, and observed a large amount of blood on the bed and in her vaginal area. The Pasco County Fire Rescue personnel further noted that: . . . [Patient] combative, swinging arms [and] attempting to bite . . . ABD firm, soft. Restraints bilat[eral] wrists to protect [patient]. O2 by NRB held near face. [Patient] remained combative, unable to attempt IV. S[pring] H[ill] Reg[ional] ER called to advise of possible emergent C Section during response . . . . Mrs. Wilkinson was transported by Pasco County Fire Rescue to the Spring Hill Regional Hospital emergency room (ER) where she arrived shortly after 1:00 a.m., July 13, 1996.3 Upon arrival, Mrs. Wilkinson was described as combative (scratching, kicking and screaming), with no eye contact. At the time, heavy bright red vaginal bleeding was noted, and Mrs. Wilkinson's cervix was described as 1 to 2 centimeters dilated. Fetal monitoring (from approximately 1:10 a.m. to 1:20 a.m.) revealed a fetal heart rate of 120 to 130 beats per minute, with no accelerations, and no evidence of uterine contractions; however, because monitoring was sporatic and brief, the monitor strips provide no compelling evidence as to the well-being of the fetus or whether Mrs. Wilkinson was or was not in labor. At approximately 1:20 a.m., ER personnel advised Dr. Ambruster by phone, at home, of Mrs. Wilkinson's status. Dr. Armbruster ordered that preparations be made for a stat cesarean section. At 1:45 a.m., Mrs. Wilkinson was taken to the operating room, and at 2:11 a.m., Ashley was delivered by cesarean section. Pertinent to this case, Dr. Armbruster's operative report noted that: . . . there appeared to be an approximately 30% abruptio placenta at the time of delivery and also that the amniotic fluid was port wine stained and that would be consistent with the abruptio placenta. Whether the cause be a straight abruptio or the eclampic seizure was unknown. Otherwise the uterus, tubes and ovaries were noted to be normal. On delivery, Ashley was handed off to Dr. Mari Doherty, the pediatrician in attendance. Dr. Doherty's progress notes include the following observations: . . . [On delivery, the baby] was bathed in blood. [S]uctioned blood from mouth [and] nares. Baby delivered [and] placed under radient warmer [and] because of no respirations [and] limp, the baby was given PPV [with] 100 [percent] BVM for about 4-5 min[utes] intermittently . . . Baby's breathing was labored [and] grunting; more suctioning and chest PT improved the baby. Suctioning done in between breaths . . . Baby transported from the OR to the Nursery [with] O2 by mask . . . . Apgars scores were recorded as 4, 7, and 8, at one, five, and ten minutes respectively. The Apgar scores assigned to Ashley 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, Ashley's Apgar score totaled 4, with heart rate being graded at 2, muscle tone and reflex/irritability being graded at 1 each, and respiratory effort and color being graded at 0 each. At five minutes, Ashley's Apgar score totaled 7, with heart rate and reflex/irritability being graded at 2 each, and respiratory effort, muscle tone, and color (with her body pink, but extremities blue) being graded at 1 each.4 At 2:30 a.m., Ashley was transported from the operating room to the nursery. On admission, Ashley was placed on an EKG/Apnea monitor; ABG, blood culture, and blood sugar testing was ordered; and IV was started. At 2:45 a.m., when her oxygen saturation levels were noted to fall, Ashley was deep suctioned and given increased oxygen. Between 2:45 a.m., and 7:55 a.m., Ashley's oxygen saturation levels continued to drop periodically, and she was noted to be cyanotic on occasion. At 5:30 a.m., Ashley was again suctioned, producing approximately 5cc of bloody mucus, and during the early morning hours was noted to be very jittery and irritable, with occasional arching of the back and stiff extremities, and was medicated with Phenobarbital. Given her condition, Ashley was transferred, at or about 7:55 a.m., to All Children's Hospital where she was reportedly in a coma for two weeks.5 Currently, Ashley presents with static encephalopathy (status post hypoxic ischemic encephalopathy), characterized by spastic quadriplegia, global developmental delay, and seizure disorder, as well as gastroesophageal reflux. 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 post-delivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Here, there is no serious dispute that Ashley suffered an injury to the brain, caused by oxygen deprivation, secondary to placental abruption. There is likewise no serious dispute that the injury Ashley suffered rendered her permanently and substantially mentally and physically impaired.6 What is at issue, is whether the asphyxia which precipitated her injury occurred "in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital," as required to qualify for coverage under the Plan. To address the issue, the parties offered selected medical records relating to Mrs. Wilkinson's antepartum course, as well as those associated with Ashley's birth and subsequent development. Additionally, Petitioners offered the deposition testimony of Radhakrishna Rao, M.D., a pediatric neurologist (board-eligible in pediatrics and pediatric neurology). Petitioners also offered the testimony of Mrs. Wilkinson which, if credited, would demonstrate that commencing at or about noon, July 12, 1996, she began to experience regular uterine contractions approximately 10 minutes apart, and that the contractions continued throughout the day progressing to approximately 8 minutes apart by 3:30 p.m., and approximately 6 minutes apart by 7:30 p.m. Respondent offered the deposition testimony of Charles Kalstone, M.D., a physician board-certified in obstetrics and gynecology, and Intervenor Armbruster offered his own testimony, as well as the testimony of Robert Yelverton, M.D., a physician board-certified in obstetrics and gynecology. The medical records and the testimony of the physicians and other witnesses offered by the parties have been carefully considered. So considered, it must be concluded, by application of the presumption established by Section 766.309(1)(a), Florida Statutes, or otherwise, that the brain injury suffered by Ashley was caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital.7 In reaching such conclusion, it has been helpful to initially identify those matters on which the medical experts share a commonality of opinion. Such matters include an opinion that Ashley's brain injury was caused by oxygen deprivation, secondary to placental abruption; that such deprivation started at some time following abruption and continued until she was resuscitated, following delivery; and that, given the record in this case, one cannot resolve where on that time line (whether at the onset of the abruption or at some other definitive point through resuscitation) hypoxia of a sufficient magnitude occurred to account for the severe brain injury Ashley suffered. The experts are also in agreement that the hospital records relating to Ashley's birth provide little or no help in resolving the issue of whether Mrs. Wilkinson was in labor at the time of placental abruption or thereafter. In this regard, it is noted that there is no serious disagreement that the fetal monitoring which occurred following Mrs. Wilkinson's arrival at the emergency room (from approximately 1:10 a.m. to 1:20 a.m.) was inadequate to provide any compelling evidence as to whether Mrs. Wilkinson was or was not in labor. Moreover, it is worthy of note that the experts agree that, given the emergent nature of Mrs. Wilkinson's presentation, it was not pertinent to her clinical management to resolve whether she was in labor but, rather, to delivery Ashley as soon as possible. Consequently, the absence of evidence in the hospital records regarding labor is not meaningful.8 Having explored the areas on which the experts are in agreement, it is timely to consider, without reference to Mrs. Wilkinson's testimony regarding the onset of labor, the opinions of the experts offered on behalf of Intervenor Armbruster regarding the onset of labor, contrasted with the opinions of the expert offered by Respondent.9 As will be noted, there is little in the testimony of these physicians to credibly resolve, without reference to Mrs. Wilkinson's testimony, when, if ever Mrs. Wilkinson entered labor. Dr. Yelverton, an expert called by Intervenor Armbruster, expressed his opinion on the question of labor, as follows: Q. Did you find any evidence in the record, Dr. Yelverton, that the patient was in labor with respect to any of the health care providers that had been treating her at the hospital? * * * A. There's one comment on the summary of the labor and delivery which states that the patient was in labor and the labor began 0001 hours on July 13th, 1996. This was a summary of the labor and delivery record that was recorded by a registered nurse whose name is illegible to me.[10] * * * Q. In addition to the nurse's note that you've pointed out to Judge Kendrick about labor, did you find any other evidence in the record that the mother was in labor, including the fact that she had an abruptio placenta? A. Well, I think given a more likely than not scenario in this case, when events of this nature occur at home, or even in the hospital, and they result in a spontaneous rupture of membranes with a great deal of blood present at the time, either there were some contractions that disrupted the placenta or a spontaneous rupture in the membrane which resulted in the contraction of the uterus itself which resulted in the abruption. Either way, more likely than not, there was some uterine activity that resulted in either spontaneous rupture of the membranes or the abruption itself. Q. Do you have an opinion within reasonable medical probability or more likely than not, based upon your background, training and experience and your review of the materials about whether or not Ms. Wilkinson was, in fact, in labor? A. I think more likely than not, she was in labor. I failed to mention also that she was two centimeters dilated when she arrived at the hospital with ruptured membrane, vaginal bleeding. It would be very unusual to find that particular scenario with a patient not having uterine contractions. [Transcript of September 13, 2001, hearing, at pages 48, 49, 52 and 53.] Dr. Yelverton's opinion that, without consideration of Mrs. Wilkinson's testimony, Mrs. Wilkinson was in labor at the time of abruption is not persuasive. First, it is noted that at admission to the ER, Mrs. Wilkinson was not noted to be 2 centimeters dilated but, rather 1 to 2 centimeters dilated. Given that she was 1 centimeter dilated on July 10, 1996, and not in labor; the subjective nature of the examination; the circumstances under which it was done; and the fact that the examination of July 13, 1996, noting a range of 1 to 2 centimeters was apparently made by a different person than the one who made the observation on July 10, 1996; the difference in dilations is not compelling evidence of labor. Second, Dr. Yelverton's suggestion that "some uterine activity" must have "resulted in either spontaneous rupture of the membranes or the abruption itself," is hardly persuasive evidence of labor (the onset of regular uterine contractions), and ignores, inter alia, the equally plausible alternative that the abruption was spontaneous or that it was precipitated by the seizure Mrs. Wilkinson suffered. Dr. Armbruster, who testified on behalf of himself, expressed his opinion on the question of labor, as follows: Q. . . . [W]as there any evidence in the records that you're aware of that . . . indicate[d] that . . . the mother . . . was in labor, or have you had a chance to re- review the records recently? A. Yes. One, she did complain of abdominal pain, which, of course, is associated with labor, and, two, her cervix had dilated. She was two centimeters from one centimeter when she came in two days prior, and she had effaced. Her cervix had thinned out from 20 percent to 80 percent, therefore, some sort of labor had to be going on during the two intervening days. Q. Would you explain that in a little bit more detail by the progression of cervical dilatation and progression of effacement in the face of contractions indicating to you that labor was ongoing? A. All right. We have many definitions of what labor is or we discuss what labor is, but most doctors agree true labor is the changing of a cervix in dilatation and the effacing or thinning out of a cervix. So most doctors or most obstetrician/gynecologists will agree upon the fact that if there is a change in the cervix, whether it be effacement or dilatation, that is the definition of labor. In this case, Ms. Wilkinson showed both a change in dilatation and effacement. Q. Do you have an opinion within a reasonable medical probability, based upon your background, training and experience, your involvement with this patient and your review of the records about whether or not Ms. Wilkinson was in true labor from the time that the abruptio placenta occurred up through the delivery of the child? A. In my opinion, she was in labor from the time of the abruptio to the time I did the C section, both with the pain she showed and also the change in the cervix and with effacement and dilatation, that is correct. * * * Q. But based upon the records alone, do you believe that she was in labor? A. Without a doubt, I believe she was in labor at the time of the abruption of the placenta. Q. And regardless of the records, just based on your own experience with patients with abruptio placentas and the consequent bleeding causing uterine irritability and contraction, do you believe she was in labor based on that experience? A. I believe that she was in labor for two reasons, and I've stated them prior: One, she did complain of abdominal pain, and; two, that there was a change in the cervix with both -- in change of dilatation and effacement . . . . [Transcript of September 13, 2001, hearing, pages 89-92.] Dr. Armbruster's opinion that, without consideration of Mrs. Wilkinson's testimony, Mrs. Wilkinson was in labor at the time of abruption is also not persuasive. First, Mrs. Wilkinson was not, as Dr. Armbruster states, 2 centimeters dilated when she presented to the ER on July 13, 1996, and, for reasons heretofore noted, the change in dilation noted is not persuasive proof of labor. Second, Dr. Armbruster's testimony that on presentation to the ER on July 13, 1996, "[h]er cervix had thinned out from 20 percent [noted on July 10, 1996] to 80 percent" finds no record support, and his testimony that he has a clear recollection of her effacement on July 13, 1996, without benefit of any contemporaneous notation of such observation, is improbable and unworthy of belief.11 Dr. Kalstone, who testified on behalf of NICA, expressed his opinion on the question of labor, as follows: Q. . . . Doctor, based upon your training and experience and review of this file, were you able to reach any conclusions whether or not the records demonstrated to you that Ashley Wilkinson sustained oxygen deprivation during the course of her delivery or immediate resuscitation? A. Yes. My opinion was that she was not in labor, essentially, and therefore, she didn't suffer from oxygen deprivation during labor, and certainly during labor or resuscitation in the immediate post-delivery period. Q. Doctor, please explain the basis for that opinion. A. The patient was at approximately 39 weeks pregnant and her husband woke up to find her having a major seizure, it sounds like, in bed, and simultaneously her membranes ruptured spontaneously. She had severe hemorrhage from the vagina, which later turned out to be proven to be from a placental abruption. There is no mention that the patient was in labor or that she was having contractions, by anyone that took care of her or was with her. She was transported in a timely way to Spring Hill Regional Hospital where the nurse who admitted her noticed that she was actively bleeding and that she was agitated and combative. She was prepared for an emergency cesarean section. * * * Now, in the doctor's written and dictated notes, including the summary, there doesn't seem to be any mention or consideration that she was in labor, and there was nothing in the nurses' notes that would lead me to believe that she was in labor, either. The doctor said that the cervix was one to two centimeters dilated when checked in the emergency room. She had one previous vaginal delivery and one to two centimeters doesn't mean necessarily that the patient was in labor. There is no mention as to whether the cervix was effaced. * * * So, in reviewing all this information, there was no reason to suggest that the patient was in labor. * * * Q. Doctor, did you have an occasion to review the fetal monitor strips? A. Yes. On the fetal monitoring strips -- they start monitoring shortly before 1:10 a.m., and ended shortly before 1:20. On the fetal monitor strips the fetal heart wasn't recorded continuously. The rate was around 120 to 130. There were no accelerations, but the fetus was monitored for a short period of time. So, I can't really tell if that tracing is normal or abnormal. In regards to the uterine-activity part of the tracing, that was monitored for part of that time and I didn't see any evidence of uterine contractions that were recorded on these fetal monitor strips for the time that the patient was on the monitor. Q. Doctor, do you believe that the abruption of the placenta occurred before Mrs. Wilkinson commenced labor? Yes. I don't think she really commenced labor. The placenta definitely abrupted at home. It was a sudden event, catastrophic event that occurred while she was in bed, maybe concomitant with when the membranes ruptured, that they both happened about the same time. Placentas do abrupt during labor, but they can also abrupt without labor, and it is my opinion that this patient went to bed fine, essentially, and then had two major things happen to her. One, she had a seizure; and two, her placenta abrupted. Simultaneously, the membranes ruptured . . . * * * Q. Based upon your review of the records, more likely than not did the baby's mother actually go into labor at all before she was born? * * * As I said before, there is really no evidence that I can see from nursing notes, the doctor's dictation or the patient history that was obtained, through the husband mostly, I think, to suggest that labor was the culprit or that she was in labor . . . . [Respondent's Exhibit 1, pages 7-12] Dr. Kalstone's opinion that, based on the available antepartum records, Mrs. Wilkinson was not in labor when she presented at Spring Hill Regional Hospital is credible; however, given that the records are limited in scope, given the emergent nature of Mrs. Wilkinson's presentation, and given the absence of any reason to document labor, any opinion based on those records is inadequate to rebut the presumption of labor established by Section 766.309(1)(a), Florida Statutes. Finally, addressing Mrs. Wilkinson's testimony regarding the onset of labor at or about noon, July 12, 1996, it must be resolved, contrary to Respondent's contention, that there is no compelling reason to reject her testimony as less than credible. Consequently, it may be said that the record supports the conclusion that, by application of the presumption established by Section 766.309(1)(a), Florida Statutes, or otherwise, that the brain injury Ashley suffered was caused by oxygen deprivation occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital.
The Issue At issue in this proceeding is whether Wilkens Jolimer, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Initial observations As observed in the preliminary statement, neither Petitioners nor anyone on their behalf appeared at hearing, and no proof was offered to support their claim. Ordinarily, such failing would be dispositive of the case; however, notwithstanding Petitioners' failure of proof, Respondent elected to offer into evidence the medical records filed with DOAH on December 16, 1996, which included records relating to Wilkens Jolimer's (Wilkens') birth, as well as the opinion of Michael Duchowny, M.D., a board certified pediatric neurologist, to affirmatively resolve the issue as to whether Wilkens had suffered a "birth-related neurological injury," within the meaning of Section 766.302(2), Florida Statutes. Wilkens' birth and development Wilkens was born July 11, 1996, at Florida Hospital, Orlando, Florida. On January 23, 1997, following the filing of the claim for compensation, Wilkens was examined by Michael Duchowny, M.D., a board certified pediatric neurologist. Dr. Duchowny's physical and neurologic examination revealed the following: PHYSICAL EXAMINATION reveals an alert, pleasant and cooperative, well-developed, well-nourished, six-month-old, black male infant. The skin is warm and moist. There are no neurocutaneous stigmata. No digital, skeletal or palmar abnormalities are noted. There is a mild cranial asymmetry, with prominence of the left parietal region. The anterior and posterior fontanelle are patent and flat. Head circumference measures 44.7 cm, which approximates the 60th percentile for age. There is no frontal bossing. The neck is supple without masses, thyromegaly or adenopathy. There are four teeth. The cardiovascular, respiratory and abdominal examinations are normal. NEUROLOGIC EXAMINATION reveals Wilkins to be an active six-month-old with a well- developed curiosity and active vocalizations. He maintains good central gaze fixation and conjugately follows without difficulty. There is good visual tracking. There is blink to threat from both directions. The fundi are benign. Pupils are 3 mm and react briskly to direct and consensually presented light. The tongue and palate move well and there are no facial asymmetries. Motor examination reveals symmetric strength, bulk and tone. There are no adventitious movements, focal weakness or atrophy. Wilkins is able to sit without falling and he stands briefly, but cannot bear weight [which is consistent with a six-month-old infant and entirely normal]. There are no movement asymmetries. The deep tendon reflexes are 2+ and symmetric and the plantar responses are downgoing. Sensory examination is intact to withdrawal of all extremities to pin. Neurovascular examination discloses no cervical, cranial or ocular bruits and there are no temperature or pulse asymmetries. In Dr. Duchowny's opinion, which is credited, Wilkens' neurologic examination was entirely normal, and he evidenced no motor or cognitive deficits. Moreover, it was also Dr. Duchowny's opinion, which is likewise credited, that the records relating to Wilkens' birth do not reveal any untoward events occurring in the course of labor, delivery or the immediate post-delivery period which would have caused or contributed to neurological injury.
The Issue At issue in the proceeding is whether Clayton Kenneth Hunter Cochran (Hunter), a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Jean Ann Cochran and Clayton Leon Cochran, are the parents and natural guardians of Clayton Kenneth Hunter Cochran (Hunter). Hunter was born a live infant on June 12, 1997, at Orlando Regional Health Care System, Inc., d/b/a South Seminole Hospital, a hospital located in Longwood, Florida, and his birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Hunter was John V. Parker, 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(2), Florida Statutes. Pertinent to this case, coverage is afforded under the Plan, when the claimants demonstrate, more likely than not, that the infant suffered an "injury to the brain or spinal cord . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Here, Hunter's mental and physical presentation are dispositive of the claim and it is unnecessary to address the cause or timing of any injury he may have suffered. To address Hunter's current physical and mental status, Petitioners offered the opinions of Michael S. Duchowny, M.D., a pediatric neurologist, as well as the results of Hunter's recent occupational therapy evaluations by the Easter Seal Program of Volusia and Flagler Counties. Notably, Dr. Duchowny examined Hunter on March 20, 2000, and reported the results of his neurological evaluation as follows: NEUROLOGIC EXAMINATION reveals Hunter to be alert and socially oriented. He tends toward non-fluency, but can communicate some thoughts in words. Hunter has a speech articulation defect. He can talk in phrases and short sentences. There is good central gaze fixation with conjugate following movements. The pupils are 3 mm and briskly reactive. There are no fundoscopic findings and no significant facial asymmetries. The tongue and palate move well without drooling. Motor examination reveals symmetric strength, bulk and tone. There are no adventitious movements, focal weakness or atrophy. The outstretched hands are markedly postured. His gait is stable and reasonably narrow based. The deep tendon reflexes are 2+ and symmetric. The plantar responses are downgoing. Neurovascular examination reveals no cervical, cranial or ocular bruits and no temperature or pulse asymmetries. The sensory and cerebellar examinations are deferred. In SUMMARY, Hunter presents as a 2 1/2 year old boy with an expressive language delay and speech dysfluency. In contrast, he has mild fine motor incoordination, but his examination is otherwise non-focal. I have not as yet had an opportunity to review Hunter's records and will issue a final report once the review process is complete. Subsequently, Dr. Duchowny had an opportunity to review the medical records, and on April 11, 2000, reported his conclusions as follows: A review of medical records and the medical evaluation of Clayton "Hunter" Cochran leads me to believe that he does not have significant neurologic impairment. His neurologic examination reveals evidence of an expressive language delay and some fine motor incoordination. Both of these findings are developmentally based and indicate acquisition in utero, long before the onset of labor and delivery. These findings are mild and there certainly is no evidence of substantial mental or motor impairment. Furthermore, Hunter's developmental delay would be expected to improve over time and therefore is not permanent. Dr. Duchowny's deposition testimony and the results of recent occupational therapy evaluations by the Easter Seal Program are consistent with the opinions heretofore expressed by Dr. Duchowny. Consequently, it must be resolved that the proof failed to demonstrate that Hunter was "permanently and substantially mentally and physically impaired," as required for coverage under the Plan.
The Issue At issue is whether Eliana Redwine, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts1 Petitioner, Aimee Redwine, is a parent and natural guardian of Eliana Redwine. Eliana was born a live infant on October 10, 2006, at Shands at AGH, a licensed Florida hospital located in Gainesville, Florida, and her birth weight exceeded 2,500 grams. Obstetrical services were delivered at Eliana's birth by George Buchanan, 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 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."2 § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. Here, it is undisputed that Eliana suffered a brain- damaging event, which rendered her permanently and substantially mentally and physically impaired. What must be resolved is whether the record supports the conclusion that, more likely than not, such injury was "caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period" in the hospital, as required for coverage under the Plan. § 766.302(2), Fla. Stat.; Nagy v. Florida Birth-Related Neurological Injury Compensation Association, 813 So. 2d 155, 160 (Fla. 4th DCA 2002)("According to the plain meaning of the words as written, the oxygen deprivation or mechanical injury to the brain must take place during labor or delivery, or immediately afterward."). Eliana's birth and immediate newborn course At or about 11:43 a.m., October 10, 2006, Mrs. Redwine, with an estimated delivery date of October 17, 2006, and the fetus at 39 3/7 weeks' gestation by ultrasound (US), was admitted to Shands at AGH for induction of labor due to preeclampsia. There, fetal monitoring revealed an overall reassuring fetal heart rate in the 140 beat per minute range, and vaginal examination revealed the cervix at 2-3 centimeters dilation, effacement at 50 percent, and the fetus high. Mrs. Redwine was induced with Petocin, starting at 2:36 p.m.; progressed to complete dilation by 9:58 p.m.; and at 10:05 p.m., Eliana was born by spontaneous vaginal delivery. In the interim, at 6:16 p.m., Mrs. Redwine's membranes were artificially ruptured, with clear fluid noted, and fetal monitoring remained reassuring. At delivery, a single nuchal cord was noted, and relieved. According to the medical records, Eliana cried spontaneously following delivery; was bulb-suctioned, dried, and stimulated; and was assigned Apgar scores of 8 and 8, at one and five minutes, respectively. However, Eliana subsequently showed evidence of respiratory distress (retractions and grunting)3 and, at or about 10:20 p.m., a Neonatal Intensive Care Nurse (NICU) nurse (Melissa Decker, R.N.) was called to observe her. (Joint Exhibit 1B, Tab 14, Bate Stamp p. 408). The NICU nurse arrived at labor and delivery when Eliana was 20 minutes of age (10:25 p.m.), and noted moderate subcostal retractions, with grunting; some central cyanosis; significant facial bruising; and oxygen being provided via blow- by. Eliana was suctioned by catheter, with a copious amount of thick mucous returned, and transported to the neonatal intensive care unit for continued care via transport isolette, with blow- by oxygen provided during transport. (Joint Exhibit 1B, Tab 14, Bate Stamp p. 408). Eliana was received in the neonatal intensive care unit at or about 10:35 p.m., and placed on a radient warmer (RW) bed. Oxygen saturation was noted as 92% with blow-by. Eliana was placed under an oxyhood, with oxygen started at 90%, and a decrease in cyanosis was noted. By 12:15 a.m., October 11, 2006, no further grunting or retractions were noted, oxygen saturation was noted as 100%, and Eliana was described as pink and well-perfused. Orders were received to begin weaning, and by 1:30 a.m., Eliana was weaned to room air, with oxygen saturation noted as 98%. Eliana experienced no further respiratory difficulties, and was discharged with her mother on October 13, 2006. Eliana's subsequent development On April 5, 2007, Eliana was seen by Myra Alfino, M.D., a pediatrician associated with the University of Florida, for developmental delay. Dr. Alfino noted a number of abnormalities, including microcephaly (37.8 cm), eyes not tracking, and hypotonia, and ordered a brain MRI. The MRI, done April 11, 2007, was reported, as follows: Findings: This study is abnormal. There is advanced global atrophy. There is diffuse leukomalacia of the white matter of the cerebrum and of the dentate nuclei of the cerebellum and Wallerian degeneration in long tracks. Patient motion precludes evaluation of the optic nerve size. There is compensatory extra-axial fluid. There is a focal intradural blood collection of acute to subacute nature along the posterior falx. The corpus callosum is small. The paranasal sinuses and oto-mastiod air cells are normally developed and aerated without evidence of acute or chronic mucoperiosteal thickening or intrasinus fluid. IMPRESSION: Post anoxic brain damage producing microcephaly and extensive leukomalacia. Small subacute intradural hemorrhage as above. Following the MRI, Eliana was seen by Dr. Omid Rabbani, a resident doing a 3-month rotation in pediatric neurology, and Dr. Edgar Andrade, a physician board-certified in neurology with special competence in child neurology, and Assistant Professor in the College of Medicine, Department of Pediatrics, Division of Pediatric Neurology, who was Dr. Rabbani's attending (supervising) physician. Dr. Andrade included the following attending attestation to Dr. Rabbani's report: I have spoke with the caregivers and have examined the patient and have formulated a join[t] history, physical assessment and plan of care, as Dr. Rabbani has documented it. The patient reportedly suffered anoxic brain injury at the time of birth.[4] Neurological exam was significant for poor head control, diffuse hypotonia, hyperreflexia and a brisk Moro response. Brain MRI supports the notion of post anoxic brain damage. I have educated the family about potential complications of such findings included but not limited to cerebral palsy and developmental delay. I have recommended enrolling the patient in a comprehensive multidisciplinary program where she can receive physical, occupational and speech therapy. Follow up in the clinic in 3-4 months. Notably, neither Dr. Rabbani nor Dr. Andrade expressed an opinion regarding the cause or timing of Eliana's brain injury. (Petitioner's Exhibit 1; Respondent's Exhibit 3). The likely cause and timing of Eliana's brain injury To address the likely etiology of Eliana's brain injury, NICA offered the deposition testimony of Donald Willis, M.D., a physician board-certified in obstetrics and gynecology, and maternal-fetal medicine, and Raymond Fernandez, M.D., a pediatric neurologist. Dr. Willis reviewed the medical records associated with Eliana's birth and newborn course and concluded that, more likely than not, Eliana did not suffer a brain injury caused by oxygen deprivation or mechanical injury during labor, delivery, or resuscitation in the immediate postdelivery period.5 In so concluding, Dr. Willis observed that fetal monitoring during labor was reassuring; the baby's Apgar scores were good (8 at one and five minutes); the baby did not require any significant resuscitation at birth; and there was no clinical evidence of an acute brain injury during Eliana's immediate newborn course. (Respondent's Exhibit 4). Dr. Fernandez evaluated Eliana on October 1, 2008. Based on that evaluation, as well as his review of the medical records, Dr. Fernandez was of the opinion that Eliana was permanently and substantially mentally and physically impaired, and that the cause of such neurologic impairment was the brain damaging event revealed by the MRI scan of April 11, 2007. As for the etiology of the brain injury, Dr. Fernandez was of the opinion that, while its cause could not be identified,6 the injury most likely occurred in utero, weeks or months before the onset of labor, and not during labor, delivery, or resuscitation in the immediate postdelivery period. (Respondent's Exhibit 2). In expressing, his opinion, Dr. Fernandez noted that, at birth, Eliana presented with a congenital microcephaly, a head circumference of 30.5 centimeters (cm) that was way below the third percentile for age matched controls; that such condition is consistent with long-standing growth retardation of the brain during the course of pregnancy; and that when he examined Dr. Eliana, at almost two years of age, her head circumference, at 39.5 cm, was still well below the third percentile. Moreover, Dr. Fernandez, like Dr. Willis, was of the opinion that there was no clinical evidence to support the conclusions that, more likely than not, Eliana suffered a significant brain injury during labor, delivery, or immediately thereafter. (Respondent's Exhibit 2). Notably, when a medical condition is not readily observable, issues of causation are essentially medical questions, requiring expert medical evidence. See, e.g., Vero Beach Care Center v. Ricks, 476 So. 2d 262, 264 (Fla. 1st DCA 1985)("[L]ay testimony is legally insufficient to support a finding of causation where the medical condition involved is not readily observable."); Ackley v. General Parcel Service, 646 So. 2d 242, 245 (Fla. 1st DCA 1994)("The determination of the cause of a non-observable medical condition, such as a psychiatric illness, is essentially a medical question."); Wausau Insurance Company v. Tillman, 765 So. 2d 123, 124 (Fla. 1st DCA 2000)("Because the medical conditions which the claimant alleged had resulted from the workplace incident were not readily observable, he was obligated to present expert medical evidence establishing that causal connection."). Here, Petitioner offered no expert testimony to support a finding regarding the cause or timing of Eliana's brain injury, and the opinions of Doctors Willis and Duchowny were logical, consistent with the record, not controverted, and not shown to lack credibility. Consequently, it must be resolved that Eliana's brain injury represents a congenital abnormality, that predated the onset of labor, as opposed to a "birth-related neurological injury." See Thomas v. Salvation Army, 562 So. 2d 746, 749 (Fla. 1st DCA 1990)("In evaluating medical evidence, a judge of compensation claims may not reject uncontroverted medical testimony without a reasonable explanation.").
The Issue At issue is whether Tyler Baker, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact As observed in the Preliminary Statement, neither Petitioners nor anyone on their behalf appeared at hearing, and no proof was offered to support their claim. In contrast, NICA offered the testimony of Donald Willis, M.D., a physician board- certified in obstetrics and gynecology, as well as maternal- fetal medicine, and Michael Duchowny, M.D., a physician board- certified in pediatrics; neurology, with special competence in child neurology; and clinical neurophysiology. Dr. Duchowny is a pediatric neurologist associated with Miami Children's Hospital, who evaluated Tyler on January 16, 2008. Based on that evaluation, as well as his review of the medical records associated with Tyler's birth and subsequent development, Dr. Duchowny concluded that, although Tyler was permanently and substantially mentally and physically impaired, the cause of such impairment was likely a developmentally-based brain abnormality, as opposed to a brain injury caused by oxygen deprivation or mechanical injury during labor, delivery, or the immediate postdelivery period. Dr. Duchowny offered the following basis for his opinion: That opinion is based on several factors. If one looks through the records, it's clear that when Tyler was born, he had reasonably good Apgar Scores, and was actually relatively stable at birth. By that I mean, he didn't show evidence of any respiratory embarrassment. He did not require intubation and mechanical ventilation, and he did not show evidence of multi-system organ involvement of, for example, the heart, the liver or kidneys, as one would expect in a child who suffered from hypoxic ischemic damage or mechanical injury. Furthermore, Tyler's normal MRI scans of the brain argue strongly that there was no damage due to mechanical injury or oxygen deprivation at birth. Q. And why is that, Dr. Duchowny? A. If Tyler's neurological problems were caused by lack of oxygen at birth, one would expect to see changes on his MRI scan of the brain. Particularly, one would expect to see evidence of brain atrophy, enlargement of the ventricles deep within the brain or possibly abnormalities of white matter. None of these findings are evident in Tyler's MRI scan, suggesting that lack of oxygen at birth is simply not a realistic possibility. (Respondent's Exhibit 2, pp. 14 and 15). Similarly, Dr. Willis, based on his evaluation of the medical records, concluded that Tyler did not suffer a brain injury due to oxygen deprivation or mechanical injury occurring during labor, delivery, or resuscitation. Dr. Willis based his opinion on the fetal monitor strips, which did not reveal any significant abnormalities that would be suggestive of fetal distress; Tyler's Apgar score of 8 at five minutes, which was normal; and Tyler's newborn course, which was uncomplicated. The opinions of Doctors Duchowny and Willis were rationally based, and not contradicted. Consequently, it must be resolved that the cause of Tyler's neurologic impairments was likely a developmental brain disorder, as opposed to a birth- related brain injury. See Ackley v. General Parcel Service, 646 So. 2d 242, 245 (Fla. 1st DCA 1994)("The determination of the cause of a non-observable medical condition, such as a psychiatric illness, is essentially a medical question."); Thomas v. Salvation Army, 562 So. 2d 746, 749 (Fla. 1st DCA 1990)("In evaluating medical evidence, a judge of compensation claims may not reject uncontroverted medical testimony without a reasonable explanation."). Therefore, the proof fails to support the conclusion that Tyler suffered a "birth-related neurological injury," as required for coverage under the Plan.
The Issue At issue in this proceeding is whether Jonathan Trujillo, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Jonathan Trujillo (Jonathan) is the natural son of Odalis Merida and Antonio Trujillo. He was born a live infant on December 31, 1993, at Jackson Memorial Hospital, a teaching hospital located in Miami, Dade County, Florida, and his birth weight was in excess of 2500 grams. The physicians providing obstetrical services during the birth of Jonathan were Doctors Oliva and McGare, resident physicians in an approved training program, who were supervised by Gene Burkett, M.D., a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan (the "Plan"). Consequently, each physician who provided obstetrical services during the birth of Jonathan was a "participating physician" in the Plan. Sections 766.302(7) and 766.314(4)(c), Florida Statutes. The birth of Jonathan Trujillo At or about 5:20 p.m., December 31, 1993, Odalis Merida (Ms. Merida) was admitted to Jackson Memorial Hospital in active labor. Notably, Ms. Merida's prenatal course had been complicated by the development of Class B gestational diabetes, requiring insulin during the course of her pregnancy, and the development of severe preeclampsia, characterized by hypertension. Consequently, Ms. Merida's pregnancy was rated high risk. To address Ms. Merida's diabetes during labor and delivery, she was maintained on drip insulin, and to address her hypertension, she was administered magnesium sulfate. Ms. Merida's condition and the substances administered to address her condition, although apparently necessary and appropriate, were not without risk or side effect to the fetus. Notably, magnesium sulfate is a muscle relaxant which can induce "floppiness" in a new born, as well as respiratory distress. 1/ The presence of maternal diabetes portends the risk of infantile hypoglycemia, which occurred in the instant case. A clinical symptom of hypoglycemia is "floppiness" in the new born, which may be exaggerated when, as here, it is found in conjunction with ploycythemia, discussed infra. Upon admission, Jonathan was at term, with a gestational age of 41 weeks, and fetal heart monitoring, commenced at or about 5:25 p.m., revealed good fetal heart tone. A physical examination at 6:00 p.m. noted the cervix to be at 7 centimeters, effacement complete, and the fetus at station 0. Contractions were regular at 2 minutes, and when the membrane was ruptured clear amniotic fluid was observed. Ms. Merida progressed through labor without incident until approximately 8:45 p.m., following the administration of an epidural anesthesia, when late decelerations of the fetal heart beat with bradycardia were noted, as a consequence of epidural hypertension. More specifically, Ms. Merida's blood pressure was observed to drop from a base line rate of 200/150 to 98/45, and a few late decelerations of the infant's heart rate were observed from a baseline rate of 120 to 130 beats per minute to 80 beats per minute. Ms. Merida was repositioned to her left side, the infant's heart rate promptly recovered, and no further unusual incidents were observed during the course of her labor or delivery. Given the limited duration and isolated nature of the late decelerations and bradycardia, it was the opinion of the physicians who testified in this proceeding that such anomaly did not adversely affect the infant's oxygenation or, stated differently, did not result in a hypoxic/ischemic insult to the infant's brain. Such opinions are credited. At 9:40 p.m., December 31, 1993, Ms. Merida, as she had with her first child, spontaneously delivered Jonathan vaginally, without apparent complication. Notably, Jonathan was vigorous on delivery, breathed spontaneously, did not require resuscitation, and his apgar scores were 9 at one minute, five minutes and ten minutes. In all, Jonathan's presentation was reflective of a healthy, vigorous infant. 2/ Jonathan was admitted to the newborn nursery at 10:00 p.m. Physical assessment upon admission revealed a large infant, at 4040 grams, with a large head (above the 90th percentile), who was crying spontaneously, alert, pink in color, but with a "slight floppiness" in the extremities. Jonathan was noted to breath spontaneously, without flaring or grunting; heart rate was noted at 160 beats per minute, with regular rhythm; fontanel were soft and flat; and reflexes were present. In brief, Jonathan's presentation in the newborn nursery was that of a healthy, vigorous infant, with the only negative observation being a "slight floppiness" in his extremities. Such "floppiness" was, however, more likely than not, related to the magnesium sulfate administered to Ms. Merida during labor and delivery, the hypoglycemia Jonathan was subsequently diagnosed to have acquired, or a combination of the two, and does not detract from the conclusion that Jonathan had no apparent signs of distress at birth. Later in the day, following testing, Jonathan was diagnosed with moderate to severe hypoglycemia, polycythemia, and moderate thrombocytopenia. Such conditions, singularly, or in combination, placed the infant at risk. Hypoglycemia, low blood sugar, may place the infant at risk of seizures and, pertinent to this case, resultant brain hemorrhage. Here, the moderate to severe hypoglycemia that Jonathan suffered was apparently recurrent, although it did resolve over time, and was addressed each time it presented through the administration of glucose. Polycythemia is a disorder whereby the number of red blood cells are abnormally high, making the blood thicker (hyperviscous) than normal. Apparently, brain hemorrhage is often related to decreased blood flow on the venus side of the brain, and where the blood is hyperviscous it could help or contribute to a brain hemorrhage. Here, with a hematocrit of 64, Jonathan's condition met the definition of polycythemia, which is a hematocrit over 60; however, such condition was not, or was not shown to be, significant in the instant case. Thrombocytopenia is a disorder resulting in an abnormally low platelet count which could affect clotting and therefore predispose the infant to bleeding through, among other things, trauma. Here, Jonathan's thrombocytopenia, more likely than not isoimmune thrombocytopenia, was considered moderate, as opposed to severe, and serial testing reported his platelet count as follows for the date and time indicated: DATE TIME 3/ PLATELET COUNT 1/1/94 07:00 Platelet estimate 40,000-80,000 1/2/94 03:47 Platelet estimate 80,000-100,000 1/3/94 07:57 Platelet estimate 40,000-80,000 1/3/94 15:08 Platelet estimate 40,000-80,000 1/4/94 05:04 Platelet count 49,000 1/5/94 06:46 Platelet estimate 40,000-80,000 1/6/94 12:50 Platelet estimate 40,000-80,000 1/8/94 21:12 Platelet count 182,000 1/10/94 03:52 Platelet count 263,000 1/12/94 06:00 Platelet count 357,000 The normal platelet count for newborns, as with adults, is 150,000 to 400,000, and, as may be observed from the serial testing, Jonathan's thrombocytopenia resolved over time. While at risk, Jonathan's neonatal course in the nursery was uneventful until 26 hours of life when he was noted to have suffered a generalized seizure characterized by cyanosis, severe bradycardia (heart beat in the range of 40 beats per minute), and respiratory arrest (apnea), requiring intubation. At or about 1:00 a.m., January 1, 1994, Jonathan was transferred to the neonatal intensive care unit, where he was maintained on positive ventilation until approximately January 6, 1994. Examination, through EEG's and CT and MRI scans of the brain, revealed that Jonathan had suffered an intraventricular hemorrhage, Grade IV, characterized by a massive bleed, with dilation of the ventricles. 4/ Thereafter residual hypodensity of the white matter of the brain was observed, consistent with degeneration of the hemorrhage and, ultimately, hypodensity compatable with evolving encephalomalacia (swelling of the brain.) Subsequently, on February 2, 1994, developing hydrocephalus required the placement of an intraventricular shunt to relieve intracranial pressure. Currently, in the opinions of Dr. Robert Roth and Dr. Michael Duchowny, whose opinions are credited, Jonathan is permanently and substantially mentally and physically impaired. Such impairment is evidenced by, inter alia, cortical blindness, hypotonia and, more likely than not, mental retardation. It is further the opinion of such physicians, which is again credited, that the cause of Jonathan's neurologic impairment is the injury to the brain he suffered as a consequence of the Grade IV intraventricular hemorrhage. Given the foregoing, resolution of this claim resolves itself to an identification of the genesis of Jonathan's Grade IV intraventricular hemorrhage or, stated otherwise, whether the proof demonstrates, more likely than not, that the hemorrhage, which resulted in injury to Jonathan's brain and the ensuing neurological injuries, resulted from "oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period" in the hospital. Sections 766.302(2) and 766.309(1)(a), Florida Statutes. The cause of Jonathan's Grade IV intraventricular hemorrhage A Grade IV intraventricular hemorrhage in a term infant, such as Jonathan, is a rare occurrence, and its cause frequently cannot be identified. Notwithstanding, Jonathan did suffer such a hemorrhage, and he was shown to suffer from two conditions, isoimmune thrombocytopenia and hypoglycemia, which could offer some explanation for the hemorrhage. Here, petitioner contends that Jonathan, due to his large head, received an injury to his brain occasioned by the "mechanical" forces of labor and delivery, and that such injury resulted in a slow bleed which, because of his thrombocytopenia, progressed over the next 26 hours and ultimately manifested as a generalized seizure characterized by cyanosis, severe bradycardia and respiratory arrest. In support of such contention, petitioner offered the testimony of Robert S. Roth, M.D., a physician board certified in pediatrics and neonatal/perinatal medicine. Pertinent to this case, Dr. Roth observed that infants born with thrombocytopenia are at increased risk of suffering an intraventricular brain hemorrhage if subjected to the trauma occasioned by the mechanical forces of labor and vaginal delivery. In his opinion, Jonathan's medical records reveal a classic case of neonatal brain hemorrhage resulting from the mechanical forces of labor and vaginal delivery that occurred because of Jonathan's large head and thrombocytopenia. Those conditions, affected by the forces of labor and delivery, combined to "start the process of hemorrhage in the brain," resulting in "tissue changes and cell death and vascular pressure changes" over time, and culminating when it progressed to the "centers that control breathing," manifested by apnea or seizure- like activity that led to apnea. Notably, it was Dr. Roth's opinion that it was not Jonathan's large head alone or his thrombocytopenia alone, apparently because of its moderate nature, which occasioned the initial bleed and resulting hemorrhage but, rather, the two conditions acting in consort. There was, however, no injury to Jonathan's scalp or skull noted at delivery, nor any molding of his head consequent to the delivery. It is of further note, in evaluating Dr. Roth's opinion, that he also observed that, had Jonathan been delivered by cesarean section before the onset of labor, he would have had a "lower probability" of having a hemorrhage than had he undergone active labor and vaginal delivery. Such observation clearly implies that factors other than labor and delivery could have operated to induce Jonathan's hemorrhage. Finally, in considering Dr. Roth's opinion of progressive deterioration, it is worthy of note that, apart from the "slight floppiness" observed shortly after birth, Jonathan evidenced no symptoms of neurologic injury until 26 hours of life. As heretofore noted, the "slight floppiness" exhibited by Jonathan was reasonably attributed to the magnesium sulfate administered to Ms. Merida during labor and delivery, the hypoglycemia Jonathan was shown to have developed, or a combination of the two, as opposed to a symptom of neurologic injury. Consequently, there is no objective evidence or symptom, that one would otherwise expect to observe, to support Dr. Roth's opinion of progressive deterioration. Contrasted with the opinions of Dr. Roth, regarding the genesis of Jonathan's hemorrhage, are the opinions offered on behalf of NICA through Michael S. Duchowny, M.D., a physician board certified in pediatric neurology. Dr. Duchowny, although acknowledging that thrombocytopenia offered an increased risk of intraventricular hemorrhage to an infant through the forces of labor and delivery, was of the opinion that Jonathan's hemorrhage at 26 hours of life was a spontaneous event, unrelated to labor and delivery, and that the cause of that hemorrhage could not be identified with any reasonable degree of medical certainty or, stated differently, that any attempt to attribute a cause for Jonathan's hemorrhage was, at best, speculative. 5/ In reaching his conclusion, Dr. Duchowny observed that there was no objective evidence or symptom of trauma or oxygen deprivation at birth, as one would expect had there been a neurologic insult during the course of labor and delivery, and that there was likewise no objective evidence or symptom of neurologic injury over the course of Jonathan's first 26 hours of life, as one would expect to observe were he suffering a progressive disorder, as opined by Dr. Roth. Dr. Duchowny was further of the opinion that, although moderately thrombocytopenic, Jonathan's platelet count was not sufficiently low, a level he described as 20,000 or less, to increase the likelihood that Jonathan would suffer a bleed. Resolving the conflict between the opinions of Doctors Roth and Duchowny is not an easy or lightly undertaken effort. Each physician is eminently qualified and the genuineness of the opinions they expressed is apparent. The seriousness of the resolution is further intensified by the obvious needs of a severely impaired infant; however, while such needs are significant, it cannot be overlooked that where, as here, responsibility for the care of the infant is sought to be imposed on the Plan, the proof must be compelling that, more likely than not, the infant suffered a "birth-related neurological injury" as defined by law. In this case, the proof falls short of meeting such standard. 6/ As heretofore noted, the labor and delivery of Jonathan was essentially normal and there was no obstetrical incident or identifiable event during labor and delivery that would evidence that he had suffered a hypoxic insult, mechanical injury or traumatic event. Indeed, although Jonathan did have a large head (above the 90th percentile), there was no cephalopelvic disproportion noted, no arrest of labor, no protracted labor, and no use of forceps or vacuum extraction in delivery. Upon delivery, no apparent cranial injuries were observed, no molding of the head was noted, and Jonathan presented as a vigorous infant with normal Apgars. In summary, there was no identifiable incident during the course of labor or delivery, or thereafter during Jonathan's first 26 hours of life, evidencing oxygen deprivation, mechanical injury, or other insult, that would account for the hemorrhage he suffered. In reaching the foregoing conclusion, it has not been overlooked that an infant suffering from thrombocytopenia is at increased risk of intraventricular hemorrhage through the forces of labor and delivery. Here, however, it was not suggested or shown that Jonathan's mild thrombocytopenia would, itself, foster a hemorrhage of the nature he suffered, rather petitioner's proof suggested that his large head and thrombocytopenic condition combined, when subjected to the trauma of labor and delivery, to precipitate a bleed that slowly progressed to a Grade IV intraventricular hemorrhage or precipitated a seizure that resulted in such a hemorrhage. Given the nature of the proffer, there being no apparent complication during labor and delivery, no objective sign of head trauma at birth, no symptoms of neurologic insult at birth, and no symptom of neurologic insult over the 26 hours prior to Jonathan's acute compromise, it must be concluded, as suggested by Dr. Duchowny, that any conclusion timing the genesis of Jonathan's hemorrhage to the events of labor and delivery is not supported by reasonable medical probability but is, at best, speculative. Consequently, it must be concluded, that petitioners have failed to demonstrate that Jonathan's hemorrhage was related to trauma, oxygen deprivation or mechanical injury occurring during the course of labor and delivery, as opposed to a spontaneous event, of unknown origin, occurring at Jonathan's twenty-sixth hour of life. 7/
