The Issue At issue in this proceeding is whether Jillian Joyce, 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 Petitioners, Robert Joyce and Lillian Reyes Joyce, are the parents and natural guardians of Jillian Joyce (Jillian), a minor. Jillian was born a live infant on March 30, 1990, at St. Joseph's Hospital, a hospital located in Tampa, Hillsborough County, Florida, and her birth weight was in excess of 2,500 grams. The physician providing obstetrical services during the birth of Jillian was Rufus S. Armstrong, M.D., who was, at all time material hereto, a participating physician in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. At the commencement of hearing, the parties were unable to stipulate that Jillian was currently permanently and substantially mentally and physically impaired; however, as hereafter found, the proof compels such conclusion. Consequently, the gravamen of this case concerns whether Jillian's condition was the consequence of an injury to her brain caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery or resuscitation in the immediate post-delivery period in the hospital. For the convenience of the reader, it is noted that petitioners' theory of the case is that Jillian "was injured during a difficult labor which culminated in a forceps delivery and that, during labor or delivery, . . . [she] . . . suffered a stroke event which caused oxygen deprivation to her brain and produced the neurological injury at issue." [Petitioners' proposed final order, at page 2.] The respondent, on the other hand, views Jillian's anomalous brain development, and consequent impairments, as resulting from a congenital anomaly or stroke in-utero, unassociated with labor or delivery. [Respondent's proposed final order, paragraph 16, page 8.] Mrs. Joyce's antepartum course Mrs. Joyce's pregnancy was essentially unremarkable. She had no significant illnesses or injuries during her pregnancy; avoided substances, such as alcohol or tobacco, that could adversely affect her or the fetus; and, received prenatal care throughout her term. 2/ During the course of her antepartum care, Mrs. Joyce had a series of ultrasounds and an amniocentesis. Neither those tests nor any of her examinations revealed any abnormalities or cause for concern with the development of the fetus. Jillian's birth On March 30, 1990, at approximately 6:30 a.m., Mrs. Joyce's membrane spontaneously ruptured. At the time, her estimated date of confinement had been noted as April 2, 1990, and the fetus was at term, with a gestational age of 39+ weeks. Later that morning, Mrs. Joyce visited her doctor's office, and the leakage of amniotic fluid was confirmed. Consequently, she was referred to the hospital to await labor and delivery. Mrs. Joyce was admitted to St. Joseph's Hospital, labor and delivery, at or about 10:30 a.m., March 30, 1990. At the time, vaginal examination revealed the cervix to be at 2 centimeters, effacement at 80 percent, and the fetus at station -1. Fetal monitoring was commenced, which reflected evidence of fetal well-being. Apparently, labor did not progress, and that afternoon it was induced. By late afternoon, Mrs. Joyce began to experience labor pains, and her labor progressed uneventfully, with concomitant fetal well-being, until shortly before 9:00 p.m. At that time, the fetal monitor began to evidence signs of fetal "distress." The "distress" noted was fetal tachycardia, with heart rates in the 150 beat per minute range. Such "distress," among those physicians qualified to address the subject, would be consistent with, at most, some mild stress to the infant during birth. [Respondent's exhibit 1, page 27]. Dr. Armstrong, Mrs. Joyce's obstetrician, was promptly summoned, and he and his partner, Dr. J. Garcia, promptly responded. At 9:08 p.m., Jillian was delivered vaginally by Dr. Armstrong, with forceps assistance, while Dr. Garcia applied fundal pressure. Upon delivery Jillian apparently breathed spontaneously, and did not require resuscitation. Birth weight was 7 pounds, 1 ounce, and the nursing delivery record reflects no nuchal cord at birth, no observed abnormalities, and Apgar scores of 8 at one minute and 9 at five minutes. The Apgar scores assigned to Jillian 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 Jillian's Apgar score totaled 8, with heart rate, respiratory effort, muscle tone, and reflex irritability being graded at 2 each and color being graded at 0. At five minutes, Jillian's Apgar score totalled 9, with heart rate, respiratory effort, muscle tone, and reflex irritability being graded at 2 each and color being graded at 1. Such scores are, essentially, normal. While Jillian's Apgar scores and presentation were noted in the records as essentially normal, certain abnormalities did exist. These included mild bruising on both sides of Jillian's head as a consequence of forceps use, and the presence of a ptosis of the left upper eyelid and a small, reddish birth mark like change on the left upper lid. Moreover, the parents observed what they perceived to be rapid horizontal movement of Jillian's right eye, and that Jillian's right side appeared less reactive than her left side. The parent's observations were not apparently medically significant, since hospital staff, as well as her pediatrician (Dr. Lane France) noted no significant abnormalities at the time, and on April 2, 1990, following a two day stay in the nursery, Jillian was discharged to her parent's care. Jillian's subsequent development and medical care On April 6, 1990, Jillian was seen by Dr. France. At the time, Dr. France suspected a strabismus of the left eye but otherwise was of the impression that Jillian was a well infant, without abnormality. Mr. and Mrs. Joyce (the Joyces), concerned with the continued deviation of Jillian's left eye, sought an ophthalmologic consult on or about April 10, 1990. At the time, the physician noted some edema and erythema (redness of the skin) of the left upper lid, fontanels that were soft to palpitation, and the child blinked to light in both eyes. He apparently suspected exotropia (strabismus in which there is permanent deviation of the visual axis of one eye away from that of the other), that the child appeared otherwise morphologically sound, and recommended a re-evaluation in three to four months. On April 13, 1990, Jillian came under the care of a new pediatrician, Dr. Kathy Lewis. Dr. Lewis noted that Jillian's left eye was deviated, and diagnosed a "congenital ptosis [with] amblyopia." Otherwise, Dr. Lewis found Jillian to be doing well, and without abnormality. The Joyces sought a second ophthalmologic opinion from Dr. G.S. Guggino on April 23, 1990. External examination revealed a left upper lid ptosis and left exotropia. Further examination revealed, inter alia, the right pupil at 4 mm. and the left pupil at 3 mm., with both pupils fixed and not reactive to light. His impression was bilateral internal ophthalmoplegia (paralysis of the eye muscles) and external ophthaloplegia on the left. Dr. Guggino further observed the need to address or rule out an intracranial pathology including porencephalic cyst, tumor and CVA, as well as developmental abnormality, as a cause of Jillian's condition. An MRI brain scan was recommended. On April 26, 1990, Jillian was examined by Dr. Richard Gunderman, a pediatric neurologist, on referral of Dr. Guggino. Examination revealed that: . . . cranial nerves revealed the left eye to be deviated outward. The patient had no movement of the left eye whatsoever past the midline. The pupil was slightly large, did not seem to react, and there was ptosis of the left lid. The right eye actually demon- strated an anisocoria, with the right pupil being somewhat larger than the left and there was, I believe pupillary reaction to light on the right. I could not tell whether there was consensual reaction. The patient had full range of motion of the right eye. The patient had rapid movement of the right eye with some nystagmus, which I believe could be normal for a child of this age. I could not get the child to fixate well, with either eye. The remainder of her cranial nerves appeared in- tact. The motor examination revealed normal motor tone and strength and the reflexes were symmetric. The cerebellar function appeared grossly intact. The patient had an active moro and a minimal tonic neck response. Dr. Gunderman's impression was ophthalmoplegia, possibly third nerve palsy on the left, with ptosis, fixed pupil and deviation of the eye laterally, and an anisocoria of the right eye. Again, an MRI brain scan was recommended. An MRI brain scan was had on April 27, 1990, which detected enlargement of the third and lateral ventricles with rounded appearance of the frontal horns, compatible with hydrocephalus. 3/ Atrophy of the left cerebral peduncle and associated midbrain structures in this area were noted and considered secondary to dilation of the third ventricle, although the existence of a ventricular cyst causing the mass effect could not be completely ruled out. A flow void was identified within the cerebral aqueduct. The hydroplasia of the left portion of the midbrain appeared to involve the third cranial nerve nucleus and thereby account for Jillian's third nerve palsy. Marked thinning of the corpus callosum was noted. The fourth ventricle appeared normal, but the cerebellum was small and the posterior aspect of the posterior fossa was filled with cerebrospinal fluid. Most likely explanation was a large foramen magnum as opposed to posterior fossa cyst compatible with a Dandy-Walker variant. Impression was enlarged third and lateral ventricles compatible with hydrocephalus with what appeared to be a posterior fossa cyst, although a cyst in the third ventricle due to its asymmetric appearance and associated hydroplasis of the midbrain and cerebral peduncle could not be ruled out. Dr. Guggino discussed the abnormal results of the MRI with the Joyces, and it was agreed that Jillian should be seen by a neuro-ophthalmologist. Dr. J. Lawton Smith of the Bascom Palmer Eye Institute, University of Miami School of Medicine, was selected. Jillian was examined by Dr. Smith on or about May 4, 1990, and her MRI scan was reviewed with two neuroradiologists. Dr. Smith's initial observations were that: . . . we have a 5 week[] old baby girl, who was found to have a ptotic left upper lid at birth. This brought the child under medical scrutiny, and it is now the consensus of opinion that there is a congenital left III nerve paresis and an abnormal pupil on the right. Her development otherwise has been doing well; she moves all her extremities-- she has no seizures--her head is not part- icularly pathologically enlarged, she seems to be comfortable and developing well, otherwise. Dr. Smith was of the opinion that the enlargement of the third ventricle observed on the MRI scan would be adequate to account for the sluggish pupil on the right and the III nerve involvement on the left. As for her condition, Dr. Smith observed "[t]his is an unusual anomaly," and further MRI studies were recommended to study the flow in and out of the third ventricle. His impression was, as follows: Congenital left III nerve paresis, asso- ciated with an[] internal opthalmoplegia of the right eye, congenital, associated with an anomalous large fluid collection in the left posterior fossa, and an enlarged [third] ventricle, as a developmental anomaly. There does appear to be a hypoplasia of the cere- bellum as well. On August 1, 1990, Jillian was seen by Dr. Raymond Fernandez, a pediatric neurologist, on the referral of Jillian's pediatrician. His examination revealed: . . . Neurologically, Jillian was alert and she smiled responsively. I agree that she probably fixes with her left eye more often than right and tends to tilt her head up and to the right in order to do this. The left pupil measured about 3 mm. and the right 4 mm. Neither reacted very well, if at all, to light. I thought the optic nerves were normal. There was ptosis of the left upper eyelid, with good lid elevation on the right. The left eye was out, slightly down, and did not adduct beyond mid-line. The right eye moved fully horizon- tally with occasional coarse nystagmoid jerks to either side. I could not elicit much ver- tical eye movement. Corneal reflexes brisk. No evidence of facial weakness. She alerted to various sounds. Lower cranial nerves normal. Muscle tone was either normal or very only slightly increased, and I was more concerned about this latter possibility in the right upper extremity only. The right hand seemed to be closed more than the left, although this was subtle. She moved all limbs well, without evidence of focal or lateralized weakness. She readily withdrew all extremities when gently stimulated . . . The Moro response consisted only of very minimal abduction of the arms. There was some persistence of palmar grasping bilater- ally and this appeared to be symmetric. Stepping and placing could be demonstrated. Dr. Fernandez's impression was: . . . a four month old girl with a left third nerve palsy, but with pupillary abnor- mality of the right eye as well and only the suggestion of a spastic monoparesis involving the right upper extremity. Etiology is un- clear, but she appears to have a pre-natally acquired cerebral and mid-brain abnormality characterized by a smaller left hemisphere and dilatation of the third ventricle versus a cyst in the third ventricle. I should mention that the right upper extremity find- ing is not clear-but and with passage of time might prove to be either insignificant or possibly part of a right hemiparesis. Clinic- ally, she seems to be doing well, without evidence of increased intra-cranial pressure and no evidence of progressive expansion of ventricles or possible cyst on serial MRIs. With regard to overall development, she is visually attentive and socially responsive. Between May 4, 1990, when Jillian's initial MRI scan was reviewed by Dr. Smith and a number of neuroradiologists, Jillian had a second MRI scan. That scan, taken July 16, 1990, revealed: . . . Again noted is moderate ventricular enlargement unchanged from the previous exam- ination. There is a probable cyst within the posterior aspect of the third ventricle which is again unchanged from the previous study. There is a flow void noted within the cere- bral aqueduct suggesting a patency of this structure. There is a large fluid-containing space noted within the posterior fossa with no visible connection to the fourth ven- tricle. This most likely represents an enlarged cisterna magna. The left midbrain and left cerebral peduncle appears smaller than the comparable right side and this finding again is unchanged from the prior study. We are not certain whether this represents pressure effects from a cyst within the third ventricle or whether this is cong- enital in nature. This finding also remains unchanged when compared to the prior study. . The radiologist's impression was: Moderate ventriculomegaly not signifi- cantly changed when compared to the previous exam. Probable cyst within the posterior aspect of the third ventricle. A repeat MRI examination of the brain with Gadolinium in six months is recommended to exclude any change in this cystic lesion within the post- erior third ventricle. Prominent cisterna magna as described above. Immature myelinization pattern. This reversal of the gray/white matter signal intensity reflects immature myelinization and is commensurate with the patient's given age. On September 20, 1990, Dr. Smith rendered a progress note wherein the review of Jillian's first MRI was compared with her second MRI. The features noted and emphasized on the review of these two MRI scans by Dr. Smith and Dr. Robert Quencer, a neuroradiologist, were as follows: the center of interest relates to the abnormally enlarged third ventricle. Dr. Quencer suspects there may be an ependymal cyst in the III ventricle. The midbrain is definitely asymmetric with the smaller side being on the patient's left. The ventricles are asymmetric. The left temporal lobe is smaller than right. There appears to be some hemiatrophy of the entire left cerebrum. The foramen Monroe is enlarged and appears patent on the left. Dr. Quencer thought the ventricles were slightly larger now than on the first study, done at one month of age. Dr. Quencer still advises that a cine-MR study be done on this child to watch flow through the third ventricle. The point was raised today as to whether an in-utero ependymal cyst of 3rd ventricle existed, which enlarged and then compressed and subsequently occluded a paramedian perforator into the left side of midbrain of the child. Dr. Naidich had previously raised the ques- tion of an in-utero occlusion of a paramedian perforator into midbrain, but the question today proposed was if the child has an ependymal cyst of III ventricle, then the softening may have been "egg" rather than "chicken". His impression was: Congenital left III nerve palsy * * * Enlarged third ventricle--rule out in-utero developmental ependymal cyst of III ventricle. Atrophy of left midbrain--rule out in-utero occlusion of a paramedian perforating artery. A day later, on September 21, 1990, Jillian had a seizure-like episode lasting several seconds, and approximately one such episode each day for the ensuing three days. Consequently, Jillian was examined by Dr. Fernandez on September 26, 1990. That examination revealed: Her EEG was abnormal, showing frequent paroxysmal spike, multi-spike, and spike-wave discharges over the left hemisphere. These usually rose in generalized distribution over the left hemisphere, but on occasion were confined to the posterior quadrant. Less often, they arose further anteriorly. It is possible that she had at lest two independent foci, although this was not clear and I will review the record once again. Background over the left hemisphere was slow and not well- organized. In comparison, the right hemisp- here was normal. Dr. Fernandez's impression was: At least one definite seizure on September 21st and it is possible that she has had several subsequent subtle seizures occurring relatively infrequently. Based on Mrs. Joyce's observations, it is possible that Jillian is having myoclonic spasms, although this is not certain. Her EEG is abnormal over the left hemisphere in comparison to right which is completely normal. The left hemisphere is not hypsarrhythmic, but it is severely disorganized with frequent paroxysmal discharges which might be multi-focal, al- though I am not absolutely certain of this and I will get another opinion on the EEG. As an anti-convulsant treatment, Jillian was thereafter placed on ACTH, and her myoclonic seizures came under control by mid- October 1990. Following an MRI in January 1991, which revealed a moderate enlargement of the ventricles since the prior MRI, Dr. Smith conducted a further neuro-ophthalmologic examination of Jillian on January 7, 1991. A general, brief neurological examination "show[ed] that she ha[d] hyperreflexia throughout, but it [was] more marked on the right than the left and she ha[d] definitely more increased tone on her right upper extremity than the left." Addressing Jillian's presentation and the cause of her condition, Dr. Smith again observed that: . . . The baby was first seen May 4, 1990 at 5 weeks of age. For details see the note at that time. The problem in essence was that the child had presented with a cong- enital left III nerve palsy which prompted neuroimaging which showed significant effects. This primarily consisted of a large cystic structure in the posterior fossa, a dilated third ventricle, congenital hemispheral asymmetry with the left hemisphere smaller than the right primarily in the temporal lobe, and some asymmetry of the frontal horns. These were reviewed by excellent neuroradio- logists and the opinions varied between this being a congenital anomaly or perhaps a consequence of an in-utero vascular occlusion [blockage] with a mid-brain infarction. Dr. Smith concluded: There are two pragmatic questions that need to be resolved in the child at this point. (1) Is the dilatation of the ventricles due to a progressive hydrocephalus, due to an out- flow impairment, or is the ventricular enlarge- ment secondary to brain atrophy ("hydrocephalus - ex-vacuo")? Dr. Naidich feels that the child should have a cine MR as has been re- commended by Dr. Quencer, and I think this is obviously the prudent way to go to see if there is any flow obstruction in the third ventricle. The third ventricle is either dilated from a lack of substance around it, or the possibility exists that there is some outflow impairment--as a very small cyst in the third ventricle itself. We will try to arrange for this cine MR. . . . On January 8, 1991, a cine MRI of the brain was taken to determine whether there was an intraventricular cystic mass within the third ventricle or whether the third ventricle was enlarged simply because of ex-vacuo dilation. That MRI was inconclusive, but noted an: area within the superior aspect of the brain ventricle which fails to demonstrate normal CSF flow on the gated coronal cine study. This may represent an ependymal or intraventricular cyst. Alternatively, this may represent an area of stagnant flow or an area of loculation within the third ventricle which may or may not connect with the re- mainder of the ventricle system. A follow-up cine MRI on July 18, 1991, identified a cyst at the superior aspect of the third ventricle. The findings and impressions of that study was as follows: FINDINGS: Again noted is the cystic area at the superior aspect of the third ventricle which is grossly unchanged in size. The lateral ventricles remain enlarged. No focal intraparenchymal cerebral lesions are demon- strated. The cine images obtained in the sagittal plane demonstrate normal cerebral spinal fluid flow with patency of the aque- duct of Sylvius. No definite stream of CSF flow is demonstrated within the cystic area. IMPRESSION: Compared with January 1991, there are no significant changes. There remains a cyst at the superior aspect of the third ventricle as described above with dilatation of the lateral ventricles and normal CSF flow through the aqueduct of Sylvius. Although a third ventricle cyst was observed, no progressive enlargement of the ventricular system was noted between the January and July 1991, MRIs, and Dr. Fernandez's examinations of January 1991 and August 1991, noted no signs of increased intracranial pressure. Consequently, the previous enlargement of the ventricular system was felt to be due to atrophy rather than obstructive hydrocephalus. Jillian remained seizure free until November 9, 1991, when she was admitted to Tampa General Hospital because of a seizure that occurred in association with fever. A CT scan at the time did not show significant change in comparison to prior MRIs; however, her EEG showed left hemisphere slowing, but no epileptiform discharge. Jillian received anti-convulsant treatment during the acute seizure episode, promptly recovered, and remained under good control with ACTH injections until the fall of 1992 when she experienced three seizures from apparently mid-August to mid-October, each occurring about one month apart. Following the last episode, Jillian was treated with Phenobarbital, and remained seizure free until October 1993. Brain CT did not show progressive change in ventricular size or other progressive anatomic change; however, her EEG showed a left central spike focus which was not present on prior recordings. Thereafter, Jillian remained seizure free until the fall of 1994, when she experienced two seizures, one in mid- August and one in mid-October, with predominately right side involvement. Thereafter, in January 1995, Jillian began to exhibit sudden flexor spasms, and such have apparently continued, periodically, to date. Coincident with such spasms, Jillian's coordination deteriorated further. There was, however, no note of any progressive change in ventricular size or other progressive anatomic change. Jillian's current physical and mental condition Over time, Jillian's condition, mentally and physically, has deteriorated, albeit with occasional periods of improvement. She presently cannot walk on her own, feed herself, or go to the bathroom unattended. A neurological examination of Jillian on May 15, 1995, revealed that: . . . tongue movements were poorly coordi- nated and there was excessive drooling. Speech sounds were diminished and there was a lingual, labial and guttural dysarthria . . . Motor examination revealed evidence of bilateral compromise with much greater right- sided involvement. She demonstrated a right hemiparesis with arm greater than leg involve- ment and with the right arm held in a posture of internal rotation at the shoulder with flexation at the elbow and wrist. There was no individual finger dexterity of the right hand and the right thumb was fisted. Jillian grasped only with the left hand and did not transfer using the right only for gross palmar activities. The right hemidecorticate posturing becomes accentuated with gait. Jillian has a broad-based stance and shows evidence of bilateral gait and stability. In summary, neurologic examination revealed "evidence of substantial motor impairment with a right hemiparesis and milder . . . left motor problems as well." There was also noted "a complete left thalamoplegia and a significant communication disorder affecting both language and speech articulation." Given the proof of record, it cannot be subject to serious debate that Jillian is currently permanently and substantially mentally and physically impaired. What remains to be resolved is the genesis of her neurologic impairment or, more pertinent to these proceedings, whether the proof supports the conclusion that such condition was caused by "oxygen deprivation or mechanical injury occurring in the course of labor, delivery or resuscitation in the immediate post-delivery period" in the hospital, as required by Section 766.302(2), Florida Statutes. The cause of Jillian's condition At hearing, neither petitioners nor respondent elected to call or present testimony from any of Jillian's health care providers, including the physicians who provided obstetrical services at birth (Doctors Armstrong or Garcia), Jillian's pediatricians (Doctors France and Lewis), Jillian's pediatric neurologists (Doctors Gunderman and Fernandez), Jillian's neuro- ophthalmologist (Dr. Smith), any of the neuroradiologists who attended or were consulted regarding her condition or progress, or any of the other myriad of health care providers associated with her care, diagnosis and treatment. The parties did, however, introduce into evidence selected records dealing with Jillian's birth and subsequent evaluation and treatment and, presumably, those records adequately address the findings and opinions of those health care professionals. Such findings and opinions are addressed supra. Notably, among the observations and opinions of the physicians who evaluated and treated Jillian, there is not one suggestion that the events surrounding her delivery, whether through oxygen deprivation, mechanical injury or otherwise, resulted in, or contributed to, the onset of any of her present neurological deficits. Given the breadth of expertise employed to evaluate Jillian, the absence of such a hypothesis as to etiology is significant. Apart from the observations and opinions of the health care providers who have examined and treated Jillian, which are reflected in the medical records, the parties offered the testimony of three physicians as an aid to resolving whether Jillian's neurologic condition resulted from "oxygen deprivation or mechanical injury occurring in the course of labor [or] delivery." The physicians selected by petitioners to address the issue were Doctors Robert Martinez and Joseph Witek. Respondent selected Doctor Michael Duchowny to address the issue. None of these physicians could be characterized as treating physicians. Doctor Martinez is a board certified neurologist; however, he does not possess special competence in pediatric neurology, neonatology, pediatrics, or obstetrics, and was not shown to treat neonates. Doctor Witek is a board certified radiologist; however, he does not possess special competence in pediatric neuroradiology and does not review films of neonates. Compared with the experiences of these physicians, respondent's expert, Doctor Duchowny, was shown to possess special competence in the field of pediatric neurology (the subspecialty of medicine that is concerned with disorders affecting the central and peripheral nervous system of infants), as well as pediatrics, and routinely treats neonates in his association with Miami Children's Hospital, Miami, Florida. In considering the observations and opinions of these physicians, scrutiny has been accorded to, inter alia, their training and experience, the opportunity they had through examination or review of medical records or otherwise to be knowledgeable concerning Jillian's presentation at birth and subsequent development, and the reasonableness of their conclusions based on Jillian's presentation, development, and the observations of her numerous treating physicians. So considered, Dr. Duchowny's opinion that Jillian's neurological impairments are, more likely than not, the consequence of a developmental anomaly of the brain occurring during gestation (a congenital anomaly), as opposed to oxygen deprivation or a stroke suffered during the course of birth, is persuasive, and the opinions of Doctors Martinez and Witek, which seek to ascribe the cause of her impairments to a stroke suffered during the course of birth, are rejected as unpersuasive. In reaching the foregoing conclusion, it is worthy of note that Jillian's presentation at birth is not consistent with an acute insult, either oxygen deprivation, stroke or otherwise. In this regard it is noted that Jillian's condition, which may be characterized as a smaller left hemisphere of the brain and dilation of the third ventricle, is not consistent with hypoxic insult, which would manifest as a more global insult to the brain. Moreover, while her condition is not inconsistent with a stroke, her presentation at birth is inconsistent with an acute insult at that time. In this regard it is noted that Jillian breathed spontaneously, her heart rate, respiratory effort, muscle tone and reflex irritability were normal, and she did not thereafter evidence jitteriness, a high pitched cry or feeding problems. Finally, at birth, Jillian evidenced a congenital left III nerve paresis and curvature of the toes, all evidence of congenital malformation. 4/ It is further worthy of note that Dr. Duchowny's opinions are grossly consistent with the observations and opinions of the consultants and treating physicians who were called upon to attend Jillian's subsequent development. In this regard, the records reflect that Jillian's first MRI of April 27, 1990, reflected the smaller left hemisphere and a moderate third ventricle enlargement, but her second MRI, on July 16, 1990, noted that the ventricular enlargement was unchanged or not significantly changed. 5/ The enlargement evident in the MRIs is, in the opinion of Dr. Duchowny, consistent with a progressive manifestation of a developmental anomaly. Finally, the marked thinning of Jillian's corpus callosum and decreased myelinization of her left cerebral hemisphere are consistent with a developmental anomaly of the brain. Contrasted with the opinions of Dr. Duchowny, the opinions of Doctors Martinez and Witek do not enjoy a consistency with the opinions and observations of Jillian's consulting and treating physicians, their training and experience fails to evidence a firm foundation upon which to predicate opinions related to fetal or neonatal development or injuries, and their opinions otherwise suffer a lack of persuasiveness. For example, it was the opinion of Dr. Witek that an insult to Jillian's brain occurred at or after birth because of the progressive changes in the MRI scans, and that the ventricles would not have continued to expand if she had suffered a developmental problem or stroke in utero. [Transcript, pages 94, 95, and 98]. Apart from such precision in timing being suspect, Dr. Witek's opinion that Jillian's ventricle would not continue to expand subsequent to birth, whether consequent to developmental anomaly or in utero stroke, is contrary to the more well informed and credible evidence in this case. As for Dr. Martinez, he appears to rule out a developmental anomaly as the cause of Jillian's impairment because the abnormal formation of Jillian's brain is asymmetric, as opposed to symmetrical. [Transcript, pages 36, 37, and 50]. Again, such opinion is contrary to the more well informed and credible evidence of record. Given the proof, and the opinions of those most qualified to address the matter, it is found that the cause of Jillian's neurologic impairments is a congenital or developmental abnormality of her brain, acquired prenatally, and unrelated to any event during labor or delivery.
The Issue At issue in this proceeding is whether Morgan Farnum, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Preliminary findings Petitioners, Karen Farnum and James Farnum, are the parents and natural guardians of Morgan Farnum. Morgan was born a live infant on July 30, 1996, at Morton Plant Hospital, a hospital located in Clearwater, Florida, and her birth weight exceeded 2,500 grams. The physician providing obstetrical services at Morgan's birth was Patricia St. John, 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. Morgan's birth At or about 10:30 p.m., July 29, 1996, Mrs. Farnum (with an estimated date of delivery of July 20, 1996, and the fetus of 41 1/2 weeks gestation) experienced the onset of labor, and at 2:00 a.m., July 30, 1996, proceeded to Morton Plant Hospital, where she was admitted at 2:17 a.m. At the time, Mrs. Farnum reported her membranes had ruptured in route to the hospital (at 2:15 a.m.), and, following admission, meconium stained amniotic fluid was noted. Mrs. Farnum rapidly progressed through labor, and Morgan was born at 2:42 a.m. Apgar scores were noted as 2, 5, and 7, at one, five, and ten minutes, respectively, and umbilical cord pH was reported as normal (7.4). The Apgar scores assigned to Morgan 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 irritation, and skin color, with each category being assigned a score ranging from the lowest score of 0 through a maximum score of 2. As noted, at one minute, Morgan's Apgar score totaled 2, with heart rate being graded at 2, and respiratory effort, muscle tone, reflex irritation, and skin color being graded at 0. At five minutes, Morgan's Apgar scores totaled 5, with heart rate and respiratory effort being graded at 2 each, skin color being graded at 1, and muscle tone and reflex irritation being graded at 0. At ten minutes, Morgan's Apgar score totaled 7, with heart rate and respiratory effort being graded at 2 each, and muscle tone, reflex irritation and skin color being graded at 1 each. Such scores are abnormal, and consistent with severe depression at birth. Following resuscitation, Morgan was transferred to the neonatal intensive care unit, where she remained until 1:10 p.m., when she was transferred to All Children's Hospital for further evaluation and monitoring. The circumstances of Morgan's birth and subsequent course at Morton Plant Hospital are summarized in the Neonatal Transfer Summary, as follows: HISTORY: Baby Girl Farnum was born on 7/30/1996 with an estimated gestational age of 41 weeks and a birth weight of 3670 grams . . . . There was spontaneous rupture of membranes at 27 minutes prior to delivery with some meconium stained amniotic fluid noted. Labor was noted to be rapid with some variables. The infant was suctioned by the obstetrician prior to delivery. There was a true kno[t] in the cord noted, as well as the cord around the neck X 2 and around the arm X 1. The infant was suctioned below the cord for a small amount of meconium fluid. She required positive pressure ventilation with a Fi02 of 100% X 1 minute to initiate respiratory effort. She then required whiffs of oxygen until approximately 5 minutes of age. Her Apgars were 2, 5 and 7 at 1, 5 and 10 minutes respectively. The infant was noted initially to be hypotonic. She was transferred to the Neonatal Intensive Care unit for further evaluation and management. On admission to the intensive care unit her vital signs revealed a temperature of 97.2, pulse of 138, respiratory rate of 52 and blood pressure of 56/24. Her saturations were 80% in room air. She was placed in Fi02 of 100%, keeping saturations between 96 - 98%. Her physical exam was remarkable for hypotonicity. HEENT: pupils were constricted bilaterally, responding to light. Lungs: breath sounds were equal but coarse. Rhythm: normal heart sounds, no murmur was noted. Abdomen was soft. Impression at that time was term female infant, respiratory distress, perinatal depression and to rule out sepsis . . . . PROBLEM #1 Respiratory: The infant was maintained in an oxyhood of 100%. Her blood gases revealed a progressive respiratory acidosis. Prior to intubation the pH was 7.09, PC02 was 74, P02 was 68, bicarb was 22, basex was -9.3. Following intubation the pH was 7.29, PC02 was 35, P02 was 186, bicarb was 17, basex was -8.4. Chest x-rays are consistent with some mild transient tachypnea. The x-rays following intubation are pending at this time. PROBLEM #2 Metabolic Acidosis: The infant's initial blood gas following admission to the nursery with a Fi02 of 100% revealed a pH of 7.15, PC02 of 37, PO2 of 142, bicarb of 13.1 and basex of -50.1 (the core pH was reported 7.4). The infant has required 3 doses of sodium bicarb for correction of metabolic acidosis. The most recent bicarb is 17 with basex of -8.4. The electrolytes this morning revealed a bicarb of 16. PROBLEM #3 Sepsis: Blood cultures were obtained and then the infant was placed on antibiotics. Admission white count was 26,300 with 60 polys, 3 bands, 31 lymphs, 6 monos with an I/T ratio 0.5. HCT was 42, platelet count was 224,000. The infant is currently on ampicillin and gentamicin. PROBLEM #4 Metabolic Disorder: The infant's ALT is 601, AST is 1210. The blood ammonia level is 104. The questions of metabolic disease versus a viral infection versus perinatal depression as to the etiology for the derangements is in process right now. PROBLEM #5 Hypotension: The infant was started on 5 mcg of dopamine. The infant's blood pressure is with a systolic of 56 with a diastolic of 38. * * * IMPRESSION: At this time is a term female infant. Perinatal depression Respiratory distress (suspect transient tachypnea) Hypotension Rule Out Sepsis Metabolic Acidosis Rule Out Metabolic Disease Morgan remained at All Children's Hospital until August 16, 1996, when she was discharged to her parent's care. Morgan's course at All Children's was summarized in her Neonatal Discharge Summary, as follows: DISCHARGE DIAGNOSIS: Perinatal Depression Respiratory Distress HSV Infection; Ruled Out Increased Liver Function Tests - Resolved Acute Renal Failure Resolved Metabolic Acidosis Status Epilepticus Pulmonary Hypertension Tricuspid Regurgitation Diffuse Encephalopathy * * * RESPIRATORY/APNEA: The infant was admitted on 60% oxygen, rate of 35, and pressures of 17/5. The initial chest x-ray, at Morton Plant Hospital, was consistent with mild TTN. The first x-ray, at All Children's, showed the lungs well aerated. She was weaned from the ventilator to ET CPAP of 7 days of age and then weaned to room air at 8 days of age. The infant's clinical course was compatible with transient tachypnea of the newborn and respiratory depression secondary to CNS insult. CARDIOVASCULAR: The infant had hypotension due to perinatal depression and metabolic acidosis on newborn day of life and required treatment with dobutamine and dopamine. These were weaned and attempted to be discontinued at 3 days of age but the patient required restart of the dopamine for renal perfusion and was discontinued at 7 days of life. An echocardiogram was done on newborn day of life secondary to perinatal depression which showed normal anatomy and function but was significant for pulmonary hypertension and moderately severe tricuspid regurgitation. These clinically improved during the patient's hospital stay and no follow up is indicated at this time. INFECTIONS: Blood cultures were obtained at the referring hospital. ET tube for bacteria and virus, gastric cultures, urine cultures, and eye for virus cultures along with serum HSV,IgG, IgM, and PCR were obtained on admission. The infant was started on ampicillin, gentamicin, and acyclovir. The gentamicin was changed to Claforan on day of life 1 secondary to poor renal function. All cultures were negative and the antibiotics were stopped after 3 days, however, due to the risk of HSV infection the Acyclovir was continued for 7 days until the PCRs were negative. * * * HEMATOLOGY: The infant had a low fibrinogen on newborn day of age. This was treated with one unit of cryoprecipitate. This was felt to be due to perinatal asphyxia and it returned to normal by one day of age. RENAL: The baby developed oliguria on the first day of life. This was felt to be secondary to the perinatal depression. She was treated with dopamine, dobutamine, and fluid restriction. Urine output returned to normal by 3 days . . . . METABOLIC: The infant had persistent metabolic acidosis at newborn day of age felt to be secondary of perinatal depression. This responded to treatment with sodium bicarbonate and intubation. The infant later developed a transient alkalosis secondary to aggressive management of the acidosis. This resolved by 2 days of age. * * * CENTRAL NERVOUS SYSTEM: A CT scan done at newborn day of age for perinatal depression showed generalized low attenuation of supratentorial brain parenchymal, especially the white matter tracts, most pronounced frontally and a questionable association of edema as the ventricles were small but the basilar cisterns were widely patent. This was thought to be secondary to a previous ischemic event. Follow up CT scan at 6 days of life revealed diffuse cerebral edema slightly improved, but suspicious for a hypoxic event. Follow up CT at 16 days of life revealed continued diffuse severe low density brain with evidence of encephalomalacia or edema with good evidence of improvement not identified. This was thought to have a poor prognostic appearance and may result in severe cerebral deficiency. The infant developed seizures on newborn day of life. An EEG showed continuous seizure activity in both the left and right hemispheres. Follow up EEG at 1 day of life showed background slowing which is suggestive of a diffuse encephalopathic process and also repetitive discharge which was significant for subclinical electrographic seizures. The seizures were secondary to perinatal depression and were finally controlled with phenobarbital and Dilantin. A 24 hour continuous video EEG was started on the first day of life which initially had multiple clinical and subclinical seizures indicating the patient was in status epilepticus which decreased in frequency toward the end of the monitoring, revealing mostly severely depressed background without evidence of authentic or subclinical seizure activity. The dilantin was weaned and discontinued at 9 days of life. The phenobarbital was weaned but the patient will continue phenobarbital at discharge. Follow up EEG at 16 days of life was abnormal secondary to attenuation of the background voltage with also excessive activity of sharp transients, especially in the left frontal temporal region, but also seemed to occur in the right temporal region. This EEG was felt to be consistent with a diffuse encephalopathic process with an area of additional superimposed cerebral dysfunction, most predominantly in the left frontal temporal region, but also in the right temporal regions and these areas were felt to be potentially epileptogenic. This EEG, though, was improved from the previous tracing. * * * PHYSICAL EXAM AT DISCHARGE: Significant for a term female infant with generalized hypotonia, especially in the upper extremities . . . . Patient is slow to Moro, has a weak grasp . . . . On August 8, 2001, following the filing of the claim for compensability, Morgan was examined by Michael Duchowny, M.D., a physician board-certified in pediatrics, neurology with special competence in child neurology, and clinical neurophysiology. Dr. Duchowny reported the results of his evaluation, as follows: PHYSICAL EXAMINATION reveals Morgan to be wheelchair bound. Her weight is estimated at 35-pounds. The skin is warm and moist. Her hair is brown and of normal texture. Her head circumference measures 46.7 cm, which is well below standard percentiles for age. There is a backward sloping to her forehead. The fontanelles are closed. There are no dysmorphic features and no facial asymmetries. She has frequent tongue protrusions and drooling almost constantly. There is some gingival hypertrophy. The neck is supple without masses or thyromegaly. The cardiovascular examination is unremarkable. She has a clean indwelling G-tube in the left upper abdominal quadrant. There is no palpable organomegaly. The peripheral pulses are 2+ and symmetric. Morgan's NEUROLOGIC EXAMINATION is significant for a severe degree of neurologic impairment. Morgan does not make good eye contact. There are conjugate eye movements with left esotropia. She has both kyphosis and thoracolumbar scoliosis. This is mild. A brief fundoscopic examination is unremarkable. There is no persistent central gaze fixation and she does not conjugately follow. Morgan does brighten in response to music. Her pupils are 3 mm and react briskly to direct and consensually presented light. Motor examination reveals double hemiparesis, with flexion postures of the upper extremities and bilateral fisting of the thumbs, greater on the right side. She has marked spasticity of all extremities, but no fixed contractures. Her feet can be dorsiflexed just to neutrality. Morgan's spasticity is prominent in all four extremities. In vertical suspension she tends to maintain a plantar grade attitude, with slight scissoring. In the supine position she demonstrates bilateral tonic neck responses which are obligate. There is significant head lag on pull-to-sit maneuver. Hoffmann signs are positive bilaterally and she has bilateral Babinski signs. The deep tendon reflexes are 3+ in the upper extremities and 4+ in the lowers, with bilateral crossed adductor responses and Babinski signs. There is withdrawal of all extremities to touch. Morgan has frequent tongue thrusting and an overactive gag response. She did not speak in words at anytime during the evaluation and it was not clear that she understood simple commands. In SUMMARY, Morgan's neurologic examination is significant for a severe degree of mental and motor impairment. She is functioning at approximately age 2 to 3 months which puts her in the profoundly retarded range. She additionally demonstrates evidences of spastic tetraparesis, cortical inattentiveness and has a history of seizures, with startle myoclonus. Morgan additionally demonstrates microcephaly. 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 post- delivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." Section 766.302(2), Florida Statutes. See also Section 766.309(1)(a), Florida Statutes. Here, it is undisputed that Morgan suffered a injury to the brain, which rendered her permanently and substantially mentally and physically impaired. Consequently, with regard to the issue of compensability, what remains to resolve is whether the proof supports the conclusion that, more likely than not, Morgan's brain injury was "caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as required for coverage under the Plan. The cause and timing of Morgan's brain injury To address the cause and timing of Morgan's brain injury, the parties offered the medical records relating to Mrs. Farnum's antepartum course, as well as those associated with Morgan's birth and subsequent development. Additionally, Mrs. Farnum testified on her own behalf, and Respondent offered the deposition testimony of Dr. Donald Willis, a physician board-certified in obstetrics and gynecology, as well as maternal-fetal medicine, and the deposition testimony of Dr. Michael Duchowny, whose qualifications were previously discussed. As for the timing of Morgan's brain injury, it was Dr. Willis' opinion, based on his review of the medical records, that Morgan's brain injury occurred prior to the onset of labor. In so concluding, Dr. Willis noted that the time between the onset of labor and Morgan's delivery was brief; that following admission to the hospital, the fetal monitor strips did not reveal any significant abnormalities; the umbilical cord pH (a pH of 7.4, with a base excess of -4) was well within normal limits; and the CT scan, at approximately 15 hours of birth, already revealed evidence of hypoxic changes (damage). Consequently, Dr. Willis resolved that the most likely explanation for Morgan's depression at birth was a injury that predated the onset of labor.1 Also speaking to the timing of Morgan's brain injury was Dr. Duchowny who, based on his review of the medical records was likewise of the opinion that the injury Morgan suffered was attributable to events which occurred prior to labor. In reaching such conclusion, Dr. Duchowny noted that, based on his review of the CT scan done on July 30, 1996, at 5:30 p.m., the amount of edema evident would take a minimum of 24 hours, and as long as 48 hours, to develop. As for the cause of Morgan's injury, Dr. Duchowny noted the possibility of infection (since Mrs. Farnum was febrile on admission to the hospital), as well as the possibility of hypoxia (as a result of the tight nucal cord, and true knot), but did not express an opinion, within reasonable medical probability, as to the likely cause of Morgan's injury. In contrast to the proof offered by Respondent regarding the timing of Morgan's injury, Petitioners and Intervenor offered no expert testimony regarding the timing of Morgan's injury or its cause. Consequently, given that the opinions of Doctors Willis and Duchowny are logical and consistent with the other proof, it must be resolved that Morgan's injury occurred prior to the onset of labor. See, e.g., 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 ."). Moreover, given the lack of medical evidence as to causation, it must be resolved that the proof failed to demonstrate that Morgan's brain injury was caused by oxygen deprivation or mechanical injury, as required for coverage under the Plan. See, e.g., Thomas v. Salvation Army, supra, at page 749 ("It is an established rule that a workers' compensation claimant must prove the existence of a causal connection between the employment and injury for which benefits are sought, and the existence of causation must be based upon reasonable medical probability.")
The Issue Whether disciplinary action should be taken against Respondent's license to practice medicine based on allegations that Respondent violated the provisions of Subsections 458.331(1)(m) and (t), Florida Statutes, arising from his treatment and care of Patient M.R., as alleged in the Administrative Complaint in this proceeding.
Findings Of Fact Effective July 1, 1997, Petitioner is the state agency charged with regulating the practice of medicine pursuant to Section 20.43, Florida Statutes, and Chapters 456 and 458, Florida Statutes. Respondent is and has been at all times material hereto a licensed physician in the State of Florida, having been issued license number ME 0077248. Respondent is a vascular surgeon, who is not board-certified in his area of practice. On November 27, 2000, Patient M.R., a 70-year-old male, was admitted to ORMC for a right-side carotid endarterectomy. Patient M.R. initially presented to Respondent in October 2000 with a number of health conditions, including chronic obstructive pulmonary disease (related to a 54-year history of smoking), cerebral vascular disease, atherosclerotic changes, and hypertension. Patient M.R. had a significant cardiac condition which resulted in a bypass procedure. It was determined at that time that Patient M.R. had significant stenosis in both carotid arteries which would require Patient M.R. to undergo two separate procedures, known as carotid endarterectomies. The left carotid artery was the subject of the first procedure in October 2000. Patient M.R. tolerated this procedure with no complications. Subsequent to the first carotid endarterectomy, but prior to the second, Patient M.R. suffered a transient ischemic attack (TIA), which is commonly referred to as a "mini-stroke." The symptomatic clinical presentation placed Patient M.R. in a high-risk category for peri-operative stroke. Respondent performed a right carotid endarterectomy on Patient M.R. on November 27, 2000. This requires the clamping of the artery in two locations, using a shunt to allow for the flow of blood. The incision must be made length wise in the controlled portion of the artery using an instrument to clear out the interior or lumen of the artery. This is done to reduce the stenosis and allow for better blood flow, without disbodying any particle from the wall of the artery. Once this is completed, the incision is patched, the clamps and shunt are removed, and the outer skin incision is closed. During the course of the above-described carotid endarterectomy, Respondent used a patch angioplasty with intra- operative shunt, which was manufactured from a pediatric feeding tube, and peri-operative neurologic monitoring. Immediately after the operation, the patient appeared to tolerate the procedure well, but was lethargic. Patient M.R. exhibited good movement in all four extremities and appeared to be neurologically intact, although he underwent extreme fluctuation in blood pressure. Patient M.R. was placed on ventilator support. The next morning, November 28, 2000, Patient M.R. had swelling and a hematoma in his neck on the right side, in the area of the incision. Respondent returned Patient M.R. to surgery, for exploration and evacuation of the hematoma. During the course of this second operation, Respondent observed a lot of swelling and edema in the operative site, but not much blood. Respondent evacuated the hematoma, and the carotid artery was found to have good blood flow. Later in the evening on November 28, 2000, Patient M.R. developed an acute neurologic deficit and was returned to the intensive care unit (ICU) at ORMC. Respondent ordered a Computerized Tomographry Scan (CT Scan) of the patient and an arteriogram. The results of the CT Scan showed a probable right occiptal infarct (stroke). The arteriogram showed significant occlusion of the right carotid artery extending to the carotid siphon. Patient M.R. was returned to the operating room in the early morning hours of November 29, 2000. Respondent made the decision to reopen the surgical area in an effort to resume blood flow in the right carotid artery that was seen to be occluded on the angiogram. Assisting Respondent on this November 29, 2000, procedure were John Horowitz, M.D., a board- certified vascular surgeon with nine years of experience, and Joseph Muller, M.D., a third-year general surgical resident at ORMC. During the November 29, 2000, procedure, Respondent reopended the previous incision in the skin and partially opened the patch that had previously been used over the carotid artery itself. Respondent performed a thrombectomy using a Fogarty "balloon" catheter in an effort to extract any debris that was causing the stenosis in the carotid artery. The balloon is placed into the carotid artery itself and is pushed up into the artery until it has passed whatever occlusion is present. Then the balloon is inflated and pulled back out, pulling with it any debris that is located within the artery. Near the conclusion of this November 29, 2000, procedure, a small piece of tubing was discovered in the surgical field. The piece of tubing was handed to Dr. Horowitz, who examined it and then placed it on the surgical tray. This piece of tubing was the same size, slope, and material cut from the feeding tube which was used as a shunt in the first surgery on November 27, 2000. There is conflicting testimony regarding the precise size and location of this piece of tubing that will be discussed below. What remains undisputed based upon the record in this case is that Respondent completed the surgical procedure on November 29, 2000, by closing the incision in the carotid artery and also in the skin of the neck. Dr. Muller is currently a surgical resident at ORMC, as he was at the time of the November 29, 2000, procedure. Dr. Muller testified that he had approximately two years and five months of residency training prior to the procedure in question. He estimated that he had observed approximately ten to 15 carotid endarterectomies. Dr. Muller testified that he observed a clear and slightly opaque piece of pediatric feeding tube coming out of the lumen of the artery as Respondent was evacuating debris after the inflation of the Fogarty balloon catheter and after about three passes of the catheter. Dr. Muller also testified that the piece of tubing in question was two or three centimeters in length. The other witnesses to this event testified that the piece in question was two to three millimeters in length. Dr. Muller's description of the position of the surgeon and assistant surgeon was also contrary to that of the other witnesses. Dr. Muller also testified that he did not know Patient M.R.'s medical history or his previous hospital course of treatment. Dr. Horowitz, the senior physician assisting, is a board-certified vascular surgeon who has performed several hundred carotid endarterectomies. He testified that he was called in by Respondent to assist on the surgical procedure which took place in the early morning hours of November 29, 2000. He found the piece of tubing located somewhere within the surgical field, remote from the carotid artery. He was certain that it was after Respondent had cleared the artery with the use of the Fogarty balloon catheter and had cleared the surgical wound. Dr. Horowitz testified that he saw a piece of tubing among the debris that had been evacuated from the surgical wound. It was not in the lumen of the artery. He picked up the piece of tubing in question with his thumb and forefinger and examined it. He testified that it was approximately two to three millimeters in length. He agreed that the material was consistent with the pediatric feeding tube that was used to create a shunt for the first procedure. Dr. Horowitz's testimony is credible and persuasive. Dr. Horowitz also gave his opinion that based upon his observation of the November 29, 2000, procedure, he did not believe that Respondent deviated from the standard of care in his treatment and care of Patient M.R. Patient M.R. was returned to the ICU, where he deteriorated and showed evidence of complete lack of brain stem reflexes. Patient M.R. was later pronounced brain dead, and he subsequently died on November 30, 2000. Gregory Schreiber, M.D., was the anesthesiologist who was present for a portion of the November 29, 2000, procedure. Dr. Schreiber testified that he was present during the beginning portion and the end portion of the procedure, when anesthesia is introduced and when anesthesia is abated. He was not present in the operating room when the piece of tubing was found. Further, there was a drape that separates the operative field from the anesthesiologist during the course of this procedure, which would have prevented Dr. Schreiber or his assistant from being able to see into the operative field directly. Dr. Schreiber noted that Patient M.R. was considered a very high-risk patient, whose multiple co-existent diseases posed a constant threat to his life when he presented for this surgery. In addition to the testimony outlined above, Petitioner also introduced three affidavits into evidence. One affidavit was that of Lata Bansal, M.D., a neurologist who was brought in for consultation after the November 29, 2000, procedure. Dr. Bansal swore in her affidavit that when she first saw Patient M.R. he was already brain dead. She otherwise did not have specific recollection of Patient M.R. The affidavit of Peter D. Taylor, M.D., a cardiac specialist, stated that he recommended a Thallium stress test for Patient M.R. prior to carotid surgery. The stress test was conducted on October 17, 2000, and revealed no ischemia but moderately decreased left ventricle function. Because he had no ischemia, Dr. Taylor opined that Patient M.R. was at an increased but acceptable risk for carotid surgery. The affidavit of Marita Lu, Registered Nurse, who was present during the November 29, 2000, procedure, stated that she could remember very few details of Patient M.R.'s case, other than she has the "impression" that something was recovered from the wound and that when she asked whether there was a specimen, she was told there was no specimen. Nothing in her affidavit indicates to whom she asked this question regarding the specimen nor is there any indication who responded to her question. Respondent is a board-certified general surgeon who is eligible for a special certification in vascular surgery and who was working at a vascular surgery group in Orlando, Florida, as of October and November of 2000. Respondent no longer practices in the State of Florida. He currently is an assistant professor of surgery and director of endovascular surgery at Creighton University in Omaha, Nebraska. Respondent described in detail each of the three procedures he performed. On November 27, 2000, the original procedure on the right carotid artery proceeded in routine fashion. Respondent provided an exemplar, which was admitted into evidence, of a pediatric feeding tube which is substantially similar to the pediatric feeding tube utilized in the November 27, 2000, procedure on Patient M.R. He utilizes a portion of the pediatric feeding tube as a shunt in his carotid endarterectomy procedures. He demonstrated at the final hearing that the pediatric feeding tube itself is so flexible as to be incapable of breaking. The only means of cutting it down is through the use of surgical instruments. He also indicated that there was no way to further cut down the tubing once it had been placed. The scrub technician cut the pediatric feeding tube into the appropriate length to be used as a shunt during the November 27, 2000, procedure. Respondent recalled that prior to this particular procedure, the tubing in question was not originally cut down to the appropriate size. It had to be cut down while in the operating room. It is during this cutting of the tubing that a tiny sliver, approximately two to three millimeters in length, was removed from the larger piece of tubing and entered the surgical field. Respondent did not know and did not have any way of knowing that the piece of tubing had entered the surgical field, as he was focused on preparing the artery itself for its incision while this tubing was cut. Respondent testified that the pediatric feeding tube in question was cut down to size before any incision was made in the carotid artery itself. Respondent performed the November 27, 2000, procedure as he normally does. After the procedure, Patient M.R. experienced extreme fluctuations in blood pressure. This can occur in patients due to multiple factors involving the nervous tissue and blood flow in the carotid artery, but there is no specific explanation for why it does happen. Subsequent to the November 27, 2000, procedure, Respondent monitored Patient M.R., addressing the extreme fluctuations in blood pressure along with the consulting physicians referred to above. Respondent noted that Patient M.R. developed a hematoma subsequent to the first procedure. He made a determination that the best course for Patient M.R. would be to evacuate the hematoma. In Respondent's opinion, evacuating the hematoma would speed up the healing process. Respondent performed this procedure on November 28, 2000. Patient M.R. tolerated this procedure well, and there was nothing remarkable about the procedure itself. Respondent palpated Patient M.R.'s artery during the course of this procedure and used the Doppler to reinforce his findings on palpation. A Doppler signal gives more specific information about the varied nature of blood flow in the internal and external carotid arteries. It was not Respondent's standard practice, nor is it necessary, to create a medical record that palpation of the artery has occurred, since it is such a basic and common occurrence that its notation on the record is not deemed to be necessary. Respondent continued to follow Patient M.R. subsequent to the November 28, 2000, procedure. When it was determined that Patient M.R. had suffered a stroke, Respondent was left with a choice of either doing nothing, or reopening the artery in an effort to save Patient M.R.'s life. Respondent chose to reopen the artery in an effort to determine whether anything could be done to save Patient M.R. Respondent opened the prior incision in the carotid artery on November 29, 2000, and inserted the Fogarty catheter in order to evacuate any debris that was located within the carotid artery. Respondent testified that it was at about this time that the piece of tubing was found; however, he further testified that he did not see the tubing in question come from the lumen of the carotid artery. Respondent's testimony is credible. It was Respondent's opinion testimony that the piece of tubing in question was located in the subcutaneous tissue outside of the artery. Its exact location within the various layers of subcutaneous tissue was not observed during the procedure. It was not possible for the piece of tubing in question to have entered the artery at this time. There was no evidence to suggest that the piece could have migrated into the artery at a later time. James Dennis, M.D., is a board-certified vascular surgeon who is the chief of the vascular surgery department at the University of Florida in Jacksonville, Florida. Dr. Dennis has sufficient education, training, and experience to qualify as an expert in vascular surgery under Florida law. Dr. Dennis testified that he reviewed all of the pertinent medical records concerning the treatment and care provided by Respondent to Patient M.R. and that based upon his review of these records and based upon his education, training, and experience, it was his opinion to within a reasonable degree of medical probability that Respondent deviated from the accepted standard of care in his treatment and care of Patient M.R., which constituted a violation of Subsection 458.331(1)(t), Florida Statutes. Dr. Dennis also testified that in his opinion, Respondent violated Subsection 458.331(1)(m), Florida Statutes, in that he failed to compile appropriate medical records reflecting the treatment and care provided to Patient M.R. Dr. Dennis' standard of care opinions were based on several factors. First, it was Dr. Dennis' opinion that based upon the contents of the chart, the only time that the piece of pediatric feeding tube could have entered Patient M.R. was during the course of the November 27, 2000, procedure. Dr. Dennis testified that in his opinion, Respondent deviated from the standard of care in allowing the piece of pediatric feeding tube to enter Patient M.R.'s body. This would be his opinion even if Respondent did not see the sliver of tubing in question enter Patient M.R.'s body and even if the piece of tubing in question were so small and translucent as to be practically invisible. Dr. Dennis also testified that in his opinion, Respondent deviated from the standard of care during the November 28, 2000, procedure in that he failed to adequately palpate the carotid artery. Dr. Dennis was critical of Respondent's use of a Doppler to assess Patient M.R.'s pulse. In Dr. Dennis' opinion, the use of the Doppler was indicative a weakening pulse rate and that the proper practice would have been to palpate the artery by touch rather than by using a Doppler instrument. Dr. Dennis was also critical of Respondent during the November 28, 2000, procedure for his failure to find the piece of tubing in question. It is Dr. Dennis' opinion that the piece of tubing had to have been located within the lumen of the artery and that had Respondent adequately palpated the entire length of the carotid artery during the November 28, 2000, procedure, he would have located the piece of tubing within the artery and could have taken appropriate steps to remove the piece of tubing before Patient M.R. suffered his stroke later that night or during the early morning hours of November 29, 2000. Dr. Dennis' opinion that the piece of tubing in question had to have been located in the lumen of the artery was also based upon his assessment of the procedures performed. He discounted the theory that the piece of tubing was located within subcutaneous tissue outside of the artery because, in his opinion, the piece of tubing would have been discovered either during the November 28, 2000, procedure or earlier in the November 29, 2000, procedure if it had been outside the artery. However, according to Dr. Dennis, based upon the timing of when the piece of tubing was found, the tubing itself had to have been located within the lumen of the artery until it was removed in the November 29, 2000, procedure. Dr. Dennis also rendered the opinion that not only was the piece of tubing located within the lumen of the carotid artery, but that the piece of tubing is directly related to the stroke which Patient M.R. suffered later that day or the following morning, which caused his death. Dr. Dennis testified that the piece of tubing became lodged in Patient M.R.'s carotid artery and that as blood flowed by it, platelets attached to the tubing, slowly building up with the carotid artery, until Patient M.R. experienced 100 percent stenosis in the right carotid artery, leading to his stroke. In sum, Dr. Dennis' opinion was that Respondent deviated from the standard of care by allowing a piece of tubing to enter Patient M.R.'s carotid artery and that it was this tubing which lead to Patient M.R.'s stroke and ultimately his death. This is in spite of the fact that Dr. Dennis was not able to state within any degree of medical probability how the sliver of tubing could have entered the artery. Dr. Dennis also rendered an opinion during his final hearing testimony that Respondent deviated from the standard of care because he did not secure the piece of tubing at issue in this case and see to it that the tubing was sent to the pathology laboratory at ORMC for analysis. Morris Kerstein, M.D., a board-certified vascular surgeon, reviewed all of the pertinent medical records reflecting the treatment and care Respondent provided to Patient M.R. Dr. Kerstein had been practicing for 35 years, and he is currently the chief of the vascular surgery department at the Veteran's Administration Hospital in Philadelphia, Pennsylvania. Dr. Kerstein has sufficient education, training, and experience to qualify as an expert in vascular surgery under Florida law. Dr. Kerstein's opinion based upon his education, training, and experience is that Respondent did not deviate from the standard of care in his treatment of Patient M.R. First, Dr. Kerstein testified that in his opinion, Respondent's conduct during all three procedures at issue was appropriate. As to the November 27, 2000, procedure, there was no way for Respondent to be aware that the piece of pediatric feeding tube had entered the operative field. It was too small to be noticed, and it was of a translucent color which made locating it extremely difficult. He was not critical of Respondent for not cutting the tubing himself. He testified that if, in fact, the sliver of tubing entered the surgical area as a result of the scrub technician cutting the tubing, and a two to three millimeter fragment jettisoned into the surgical field, this would not constitute a deviation from the standard of care by Respondent. Dr. Kerstein testified that he felt the November 28, 2000, procedure was performed appropriately as well. He testified that it was not a deviation for Respondent to use a Doppler to feel for pulses in the arteries, and to the contrary, it reveals that Respondent was being meticulous beyond what the standard of care requires. He opined that Respondent certainly would have palpated the arteries in question, and to suggest otherwise based on the absence of a note to that effect is not an appropriate conclusion to draw. Dr. Kerstein rendered the opinion that he did not believe that the piece of tubing in question was located within the lumen of the artery of Patient M.R. He testified that there was no way for the tubing to enter the artery because the sliver in question came off of the longer tubing before an incision was made in the carotid artery. There is therefore no reasonable explanation as to how the piece in question could have entered the carotid artery in the first place. Dr. Kerstein also disputed the theory that not only was the piece of tubing located within the lumen of the artery, but also the piece in question actually caused Patient M.R.'s stroke. Dr. Kerstein relied principally on the radiographic studies. Both the CT Scan of the brain and the angiogram taken late in the evening of November 28, 2000, revealed a right posterior occipital infarct. The posterior of the brain is the back of the brain, and if the infarct was located there, it means that the cause of the stroke had to be something other than an occlusion in the carotid artery. This is because the arteries that feed the back portion of the brain are the basilar and vertebral arteries, not the carotid artery. Therefore, there could be no possible causal connection between the sliver in question and Patient M.R.'s stroke. Dr. Kerstein's opinion as to the cause of Patient M.R.'s stroke focused on his personal history rather than on the events of November 27, 2000. He noted that Patient M.R. presented with severe atherosclerotic changes, indicative of an advanced disease process. He noted that Patient M.R. suffered from chronic obstructive pulmonary disease, which was the product of his 54-year smoking history. He also noted Patient M.R.'s significant cerebrovascular disease. He also stated that thrombosis (or clotting of the blood) is a known complication of this procedure and can happen for several plausible reasons other than a sliver of tubing in the artery. All of these conditions conspired to predispose Patient M.R. to suffer a significant event such as the stroke he suffered on November 28 through 29, 2000. Dr. Kerstein also noted that the piece of tubing was completely inert, and given its size and its location in the subcutaneous tissue outside of the carotid artery, the tubing would have had no impact whatsoever on Patient M.R.'s prognosis. The tubing in question is an example of inert material that can remain inside the body, such as the case of a bullet which is located too close to the spinal cord to allow for an operation to remove it, without causing the body any harm. Dr. Kerstein had no criticism of the medical records Respondent kept regarding the treatment he provided to Patient M.R. He specifically noted that the records were accurate and honestly reflected what had occurred during the procedure. The fact that no foreign object was noted in the first two procedures was appropriate because at that point, he had no reason to suspect the presence of a foreign object. The lack of reference to a cause of Patient M.R.'s atypical post-operative course was appropriate because in fact Respondent could not have defined a single reason why Patient M.R. was reacting the way he did. Finally, the operative note from the November 29, 2000, procedure was appropriate, as it also honestly and accurately depicted what had occurred; he made a specific comment on Respondent's note that the sliver was not indeed from the lumen, but that the exact location was unclear, finding this to be an unambiguous statement of fact. Dr. Kerstein also disagreed with the state's position with regard to the responsibility for maintaining possession of the piece of tubing post-operatively. Dr. Kerstein testified that it was the responsibility of the circulating nurse, an employee of the hospital, to arrange for the piece of tubing to be sent to the pathology lab for examination. The evidence is insufficient to support Petitioner's contention that the pediatric feeding tube sliver at issue caused Patient M.R. to suffer a stroke because of its location within the carotid artery itself. Radiographic studies were performed on Patient M.R. after the stroke. A CT Scan performed on November 28, 2000, revealed an acute right posterior cerebral artery distribution infarct. Further, a cerebral angiogram was performed on November 28, 2000, and revealed "markedly diseased circulation particularly in the right vertebral and basilar arteries." This note also revealed: "Severely diseased posterior fossa circulation." Based upon the location of the infarct in Patient M.R.'s brain, the cause of the stroke had to have been either the vertebral or basilar arteries that supply blood to the posterior part of the brain. In view of all the evidence, the expert testimony of Dr. Kerstein, together with that of Dr. Horowitz, was more persuasive than that of Dr. Dennis in regard to the standard of care and Respondent's actions in this matter.
Recommendation Based on all the evidence of record, it is RECOMMENDED that the Board of Medicine enter a final order holding that the evidence is not clear and convincing that Respondent has violated either Subsections 458.331(t) or (m), Florida Statutes, in his treatment of Patient M.R. and that the Administrative Complaint be dismissed. DONE AND ENTERED this 9th day of June, 2003, in Tallahassee, Leon County, Florida. DANIEL M. KILBRIDE Administrative Law Judge Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-3060 (850) 488-9675 SUNCOM 278-9675 Fax Filing (850) 921-6847 www.doah.state.fl.us Filed with the Clerk of the Division of Administrative Hearings this 9th day of June, 2003. COPIES FURNISHED: Michael D'Lugo, Esquire Wicker, Smith, O'Hara, McCoy, Graham & Ford, P.A. 390 North Orange Avenue Suite 1000 Orlando, Florida 32802 Daniel Lake, Esquire Department of Health 4052 Bald Cypress Way Bin C-65 Tallahassee, Florida 32399-3265 William W. Large, General Counsel Department of Health 4052 Bald Cypress Way, Bin A02 Tallahassee, Florida 32399-1701 Larry McPherson, Executive Director Board of Medicine Department of Health 4052 Bald Cypress Way Tallahassee, Florida 32399-1701
Findings Of Fact George Selis holds certificate of registration Number 695-04-73 to fit and sell hearing aids in the State of Florida, and this certificate of registration was issued by the Department of Health and Rehabilitative Services. On August 9, 1976, George Selis did fit and sell a hearing aid to Daisy Binder. On that date George Selis examined the ears of Daisy Binder prior to giving her a hearing test and according to his testimony observed a quantity of cerumen, or ear wax, in her ears. At that time, according to Selis, the ear canal was not blocked or impacted by the cerumen. In accordance with his experience and training, it was not improper for Selis to test an individual's hearing when cerumen was observed in the ear canal as long as the ear canal was not blocked. On August 24, 1976, Daisy Binder was examined by Dr. Herbert King, M.D., who determined that both of her ears were impacted with cerumen. In Dr. King's medical opinion, from the quantity of wax present on August 24, 1976, an excessively large quantity of wax would have been present on August 9, 1976, when Daisy Binder's ears were examined by George Selis. Dr. King's medical opinion is buttressed by the medical records of Binder which show she had had her ears irrigated and impacted cerumen removed roughly every two years for four years prior to August, 1976. George Selis sold and fitted a hearing aid to Augusta Miller on or about August 24, 1975. Regarding the testing of hearing of his client, Selis explained that prior to every test he explained to the client the way the test was conducted and what the results meant. The handwritten lines and annotations on the hearing test of Augusta Miller, Exhibit 20, had a diagram on the back of this test relating to Selis' explanation of the test and its operation on the ear. In this explanation Selis explained that a hearing loss of 30 decibels or less is normal, that a hearing loss between 30 decibels and 80 decibels may not be correctable. Selis also explained the fact that hearing aids cannot help certain hearing losses and that certain types of hearing losses can be treated medically. Regarding the type of loss which a hearing aid can help, Selis explained that the use of the hearing aid does not stop the loss and that the loss may continue to the extent that the hearing aid will no longer offer any assistance. Selis represented that it was this explanation which he gave to Augusta Miller on August 24, 1975, when he fitted and sold her a hearing aid.
Recommendation Based upon the foregoing Findings of Fact and Conclusions of Law, the Hearing Officer recommends that the certificate of registration of George Selis be suspended for a period of 30 days. DONE and ORDERED this 3rd day of August, 1977, in Tallahassee, Florida. STEPHEN F. DEAN, Hearing Officer Division of Administrative Hearings Room 530, Carlton Building Tallahassee, Florida 32304 (904) 488-9675 COPIES FURNISHED: Robert Eisenberg, Esquire Department of Health and Rehabilitative Services Post Office Box 2417 F Jacksonville, Florida 32231 Louis Ossinsky, Jr., Esquire Ossinsky and Krol 411 Main Street Post Office Drawer E Daytona Beach, Florida 32018
The Issue The issue is whether Respondent's license as a medical doctor should be disciplined for the reasons given in the Administrative Complaint filed on October 25, 2000.
Findings Of Fact Based upon all of the evidence, the following findings of fact are determined: Background At all times material hereto, Respondent, David Lowell Williams (Respondent or Dr. Williams), was a licensed medical doctor having been issued license number ME 0035686 by Petitioner, Department of Health, Board of Medicine (Board). The Board is charged with the responsibility of regulating the practice of medicine in the State of Florida. Respondent is board-certified in cardiovascular disease and internal medicine and has practiced his specialty in Ormond Beach, Florida, since 1983. In 1990, Respondent accepted a position as a cardiologist with Florida Health Care Plan, Inc. Except for the charges raised in this proceeding, there is no evidence that Respondent has ever been involved in a prior disciplinary action. Based on a complaint filed with the Board by an attorney representing the family of a former patient, S.T., on October 25, 2000, the Department of Health, acting on behalf of the Board, filed an Administrative Complaint against Respondent generally alleging that in April 1995 he had failed to practice medicine with the level of skill and care required of a reasonably prudent physician, and that he failed to keep written medical records justifying the course of treatment of S.T. Respondent has denied the charges and contends that he practiced medicine within the standard of care and that the documentation related to the patient justified the course of treatment. In determining whether a deviation from the appropriate standard has occurred, the undersigned has considered the conflicting testimony presented by the witnesses and has accepted the more credible evidence, as reflected in the findings below. In doing so, the undersigned has discounted Petitioner's contention that Respondent's expert, Dr. Henderson, is a close friend of Respondent and therefore his testimony is clearly biased. Although the two once practiced together for a few years in the 1980's, Dr. Henderson acknowledged that they "don't get along very well right now." The treatment of the patient Over a period of years, S.T. was treated by several doctors, including Respondent, who participated in the Florida Health Care Plan, Inc. network. The medical records for that treatment have been received in evidence as Joint Exhibit No. Because they are not in chronological order, contain matters relating to treatment by physicians other than Respondent, and include some partially illigible pages, the records are somewhat difficult for the reader to navigate. They do show, however, that S.T. occasionally cancelled appointments, would not always accept his doctor's advice, sometimes refused to take prescribed medications, and was perhaps not totally candid at all times with the treating physician regarding his symptoms. The records reflect that Respondent first began treating S.T. on March 29, 1989, on referral from his primary care doctor, Dr. Moussly, due to complaints of "burning in chest with exercise." S.T., then a sixty-year-old male, underwent a stress test on the treadmill which was terminated after three and one-half minutes due to fatigue and shortness of breath. The test revealed "significant ST segment depression" and was consistent with ischemia (inadequate blood flow to the heart). Respondent prescribed Lopressor (a beta- blocking agent used in the treatment of hypertension and angina) and a Nitro-patch (transdermal nitroglycerin delivery system). Dr. Williams also recommended that the patient have a cardiac catherization. Even though the records show that the patient was "reluctant to do this at this point in time," they indicate that a coronary angiogram was performed by Respondent on April 26, 1989, and that "a high-grade stenosis of approximately 90 [percent] . . . with deeply ulcerated plaque" was exhibited in the left anterior descending artery. S.T. was again referred by Dr. Moussly to Respondent on March 7, 1990, "on an urgent basis." However, S.T. cancelled his appointment and accepted another appointment on April 4, 1990. Despite the urgency of the referral, S.T. reported to Dr. Williams that he was doing well with no symptoms since his last visit one year earlier. His records reflect that his blood pressure was 136/86, his weight 258, his pulse was 60 and regular, his lungs were clear, and a cardiovascular examination was unremarkable. Dr. Williams concluded that S.T. was stable at that time with minimal chest discomfort, and he recommended that S.T. undergo a routine treadmill exercise test to further evaluate his coronary heart disease. A stress test was performed on May 11, 1990, but it was terminated after three minutes due to shortness of breath. Another stress test was conducted on July 5, 1990, the results of which were "significant for ischemia." Although a cardiac catherization was recommended, "[t]he patient again refuses at this point in time." On May 1, 1991, S.T. was again seen by Respondent (after cancelling an earlier appointment) at which time he indicated he was feeling well and was essentially asymptomatic. He specifically denied having any shortness of breath, light-headedness, dizziness, or chest pain, and he reported that he had skipped taking his prescribed Cardizem on numerous occasions without undergoing any significant change in his symptoms. On that date, his blood pressure was 150/90, his weight 259, his lungs were clear, and the cardiovascular examination revealed no murmur. Dr. Williams concluded that the patient "seems to be stable at this point in time," and allowed S.T. to discontinue Cardizem as a therapeutic trial, and if he had no further symptoms, he would continue on Lopressor only. Otherwise, he would need to start up on that medication again. Finally, Dr. Williams offered S.T. the opportunity to participate in a beta blocker angina trial for which he would be evaluated the following week. The patient apparently declined this offer. The patient did not return to Respondent's office until December 21, 1994, or more than three years later, after he was given a "[r]outine referral for a stress test" by Dr. Moussly. S.T. had seen Dr. Moussly on a "routine followup" on December 1, 1994, at which time he denied having chest pain or shortness of breath. On his visit with Respondent, S.T. underwent another treadmill test that was terminated after two minutes due to the development of ST- segment depression. S.T. also experienced tightness in his chest. The treadmill tests were positive for ischemia "at low exercise tolerance." Based on the above results, S.T. agreed to undergo cardiac catherization. On December 28, 1994, Respondent performed the cardiac catherization on S.T., which revealed that the main coronary artery was very short, but was essentially normal. The left anterior descending artery (one of the three main arteries to the heart) exhibited a proximal 90 percent stenosis (stricture of a canal or narrowing of a cardiac valve). A second 75 percent stenosis was present in the distal portion of the artery. No other significant lesions were noted. The left circumflex artery was a large and dominant system. A stenosis in the distal portion of the parent circumflex of approximately 30 percent was present with no other significant lesions noted. The right coronary artery was a nondominant artery with no significant lesions noted. Based upon the results of the cardiac catherization, Dr. Williams concluded that P.T. demonstrated mild coronary artery disease in the left circumflex artery and "rather severe disease" in the left anterior descending artery. Respondent advised S.T. that he was a candidate for angioplasty (reconstitution or recanalization of a blood vessel) of the left anterior descending artery. On January 4, 1995, Respondent performed the angioplasty of S.T.'s left anterior descending artery, which contained two lesions. The proximal lesion was reduced from approximately 95 percent stenosis to around 10 percent, and the distal lesion was likewise reduced from approximately 75 percent stenosis to around 10 percent. On February 8, 1995, S.T. made a follow-up visit to Respondent's office. According to the patient notes, S.T.'s vital signs were normal, and he stated that he was "doing very well." Respondent's plan of treatment was to have him follow- up on an as-needed basis. In addition, Respondent discussed the "signs and symptoms of recurrence of chest discomfort" and the importance of stopping smoking as well as having good dietary practice and daily exercise. On March 7, 1995, Dr. Moussly again referred S.T. to Dr. Williams for a stress test due to the patient's "having very non[-]specific chest discomfort; non[-]exertional, non[-] radiating [pain that was] apparently . . . different than the pain he had prior to his angioplasty." Dr. Moussly also noted in his records that even though the patient had elevated cholesterol, he refused to take Pravachol, which had been prescribed by Dr. Moussly on December 1, 1994. Pursuant to the referral, on March 15, 1995, S.T. made a follow-up visit to Respondent complaining of "chest discomfort." He underwent another treadmill test which was terminated after three minutes due to chest discomfort and ST- segment depression. The test was positive for ischemia, which meant that restenosis of an artery had likely occurred. Respondent recommended repeat cardiac catheterization and angioplasty. Given S.T.'s age, progression of disease, and risk factors, which included "virtually every one known to man," restenosis was not particularly surprising since Respondent's expert established that "the restenosis rate for this [type of] patient was probably in excess of 50 percent." On March 17, 1995, Respondent performed a second angioplasty of S.T.'s left anterior descending artery and reduced the stenosis from 75 percent to 10 percent in both the proximal and distal lesions. There were no complications from this procedure, which S.T. tolerated well. On April 3, 1995, S.T. visited Respondent's office for a follow-up at which time he complained of chest discomfort. At that time, S.T. was "very vague about his discomfort" in terms of how often it occurred, how long it lasted, whether there were accompanying symptoms present, and whether the Nitroglycerin provided relief. S.T. did acknowledge, however, that the discomfort was "very infrequent." The records for that visit read as follows: Mr. T. since his last visit is having some chest discomfort, although, it has been better. He has taken some sublingual Nitroglycerin on a number of occasions, but is unable to recall exactly how often. His episodes are not exertionally related, different in type and severity than prior to his angioplasty. I feel he may be having coronary spasm, although, I cannot totally rule out restenosis. In any event, his symptoms are relatively mild. I have asked him to continue as we're doing. He wil [sic] return in two more weeks for follow-up examination. I have asked him to call should he get worse and he has, otherwise, been asked to keep a diary so that we can more objectively quantify his Nitroglycerin usage. Although S.T.'s vital signs are not recorded in the above note, Dr. Williams performed a physical examination of the patient that day, and he recorded the vital signs on a separate office record entitled "Vital Sign Sheet." He also maintained a separate patient medication chart, which reflected the various medications taken by all his patients; however, due to its age, that chart has been purged in the normal course of business. A stress test was not ordered by Respondent since he considered the patient's chest discomfort to be "very mild," and the patient described the pain as "completely different" than his previous angina. Also, the pain was not exertionally related, and restenosis was unlikely "at this early date following an angioplasty." Dr. Williams concluded that more than likely the pain was a coronary spasm (a muscular contraction of the wall of the artery), which typically occurs up to 30 to 60 days after the procedure, and he would wait "to see if [the symptoms are going] to go away . . . [w]hich they frequently do after an angioplasty." Finally, Respondent noted that the cardinal indicators of ischemic heart disease (a blockage) were not present - - exertional pain, relief from Nitroglycerin, and a similarity with pain experienced before the angioplasty was performed. He accordingly advised S.T. to continue his present course of treatment and to follow-up in two weeks, or if his condition worsened, to return sooner or go to an emergency room. On Friday, April 7, 1995, S.T. went to the Halifax Hospital Emergency Room in Daytona Beach, Florida, complaining of chest pressure, accompanied by an episode of dizziness, weakness, diaphoresis, and nausea. He also advised that he had been taking several Nitroglycerines on a regular basis. Respondent was not present at the facility, and was not the on-call cardiologist on this date. S.T. was seen by Dr. David E. Stibbins, who observed that S.T. was bradycardic and had low blood pressure. Like the information given to Dr. Williams on April 3, here the patient gave vague information regarding his chest discomfort. The records suggest that Dr. Stibbins opined that the patient's discomfort was not cardiac related and was probably due to anxiety. A cardiac consultation was requested, but not conducted, and S.T. was kept in the hospital overnight for observation. Around 1:15 a.m., S.T. reported a few "twinges" in his chest to the nurse, but he told her the pain was not serious enough to wake up his doctor. After denying that he had experienced any chest pain other than the few twinges described above, on the afternoon of April 8, 1995, S.T. was discharged from the hospital in stable condition (without ever being seen by a cardiologist) and advised to follow-up with Respondent in two days (the following Monday). On Sunday, April 9, 1995, the patient suffered a cardiac event and expired. The cause of death on his certificate of death is probable sudden death as a result of coronary artery disease, but neither expert in this case could give a precise reason for S.T.'s demise. The standard of care In the aftermath of an angioplasty, a variety of things can occur causing chest discomfort in the patient. While the beneficial effects of an angioplasty "can last . . . [up] to 20 years," three to five percent of patients experience an acute closure within a matter of minutes or hours, which is the sudden and complete obstruction of the artery. Because of this risk, after a procedure is performed, patients are kept in the hospital at least over night for observation. An acute closure often occurs in patients with a 70 to 80 percent narrowing of the artery. During the first few weeks after a procedure, acute thrombosis to the vessel at the site of the injury sometimes occurs, but a patient with that condition would experience "intense discomfort that's exactly the same as the patient's pre-intervention discomfort." Without such symptoms, that diagnosis would be "down [on] the list of considerations" by the treating physician. Between six and eight weeks and four months after the procedure, up to a third of balloon angioplasty patients experience a subacute closure (or restenosis) of the artery. Typically, these patients return to the physician's office with clinical symptoms of angina chest pain (similar to that experienced before the procedure) and require a repeat procedure. If restenosis has occurred, the patient is at risk for additional cardiac complications, such as myocardial infarction (heart attack). In some cases, within 30 to 60 days after a procedure, a patient will experience a "different type of sensation" in the chest due to the mechanical stretching of the vessel wall during the procedure. Other patients experience an artery spasm (cramping of the vessel wall), which occurs when the muscle cells go into spasm and constrict the artery. In both of these situations, the discomfort is dissimilar to that experienced before the procedure. Given the foregoing, if a patient presents himself to the doctor within a matter of weeks after an angioplasty with vague, non-ischemic related chest discomfort, it is not a deviation from the standard of care for the physician to choose a course of treatment consisting of "medical management" of the patient, that is, the close monitoring of the patient in the following days and weeks, and treating the patient with beta blockers, nitrates, and aspirin to ameliorate his symptoms. Conversely, if a patient presents himself to the physician with chest discomfort which is ischemic in nature, the ordering of further tests, including an exercise EKG, would be appropriate, with possible referral to a hospital for another cardiac catherization. Other considerations in determining the appropriate course of treatment of a patient include the cardiologist's familiarity with the patient's prior symptoms and history and the symptoms presented at the current time. In addition, the physician must rely upon his experience, knowledge, and education in the field. Taking into account all of these circumstances and considerations, the more convincing evidence establishes that Respondent did not deviate from the standard of care. c. The adequacy of the patient's records The Board has also alleged that Respondent failed to keep adequate medical records on the April 3, 1995, office visit in that he failed to document a physical examination or the results of any ancillary tests, and that the records as a whole fail to justify the course of treatment of the patient. The criticisms of Dr. Williams are based upon the testimony of the Board's expert, Dr. Dormois, who presented deposition testimony in this matter. In his deposition, however, Dr. Dormois withdrew his earlier criticisms of the records, and he indicated that the records provided by Dr. Williams "are generally adequate." He also concluded that this case "is not an issue of a medical record deficiency," but rather is "a deficiency of [a] failure to make clinical decisions." When these admissions are coupled with the testimony of Dr. Henderson, who concluded that the records were adequate, it is found that the Respondent kept written medical records justifying the course of treatment of the patient.
Recommendation Based on the foregoing Findings of Fact and Conclusions of Law, it is RECOMMENDED that the Board of Medicine enter a final order dismissing, with prejudice, the Administrative Complaint. DONE AND ENTERED this 30th day of August, 2001, in Tallahassee, Leon County, Florida. ___________________________________ DONALD R. ALEXANDER Administrative Law Judge Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-3060 (850) 488-9675 SUNCOM 278-9675 Fax Filing (850) 921-6847 www.doah.state.fl.us Filed with the Clerk of the Division of Administrative Hearings this 30th day of August, 2001. COPIES FURNISHED: Kim M. Kluck, Esquire Agency for Health Care Administration Post Office Box 4229 Tallahassee, Florida 32317-4229 Michael R. D'Lugo, Esquire Wicker, Smith, Tutan, O'Hara, McCoy, Graham & Ford, P.A. Bank of America Center, Suite 1000 390 North Orange Avenue Orlando, Florida 32802-1646 Tanya Williams, Executive Director Board of Medicine Department of Health 1940 North Monroe Street Tallahassee, Florida 32399-0750 William W. Large, General Counsel Department of Health 4052 Bald Cypress Way Bin A02 Tallahassee, Florida 32399-1701
Findings Of Fact The decedent, James C. Daniels, was employed as a fire fighter with the Village of Miami Shores, Florida, in April of 1972. The Miami Shores Fire Department was subsequently assimilated by Metropolitan Dade County, Florida, and at the time of the decedent's death on July 20, 1976, he was employed by Dade County as a fire fighter/emergency medical technician. On November 4, 1975, the decedent received a physical examination which showed no evidence of heart disease, and an electrocardiogram, the results of which were within "normal" limits. The decedent had no history of heart disease or circulatory problems, did not drink, and began smoking only in 1974 or 975. At the time of his death, the decedent's customary work routine involved 24 hours on duty, from 7:00 a.m. to 7:00 a.m., followed by 48 hours off duty. The decedent's duties included answering emergency calls along with his partner in a rescue vehicle. These calls included such incidences as automobile accidents, fires, violent crimes involving injuries to persons, and various and sundry other emergency situations. Upon answering an emergency call, the decedent was required by his job to carry heavy equipment, sometimes weighing as much as 80 pounds, to the place where the injured person was located. On occasion, the decedent would transport injured persons from the scene to local hospitals. At the time of his death, the decedent appeared outwardly to be in good physical condition. In fact, he engaged in a regular program of physical exercise. During the approximately two months prior to his death, the decedent participated in a busy work schedule which often included numerous rescues, in addition to false alarms and other drills required of his unit. In fact, only four days prior to his death, the decedent and his partner during one twenty- four hour shift, were involved in 13 rescues and one building fire. During that day, the decedent worked for 24 straight hours, apparently without sleep. On July 19, 1976, at 7:00 a.m., the decedent began his last work shift prior to his death. During that day, the decedent's unit participated in two rescues and two drills. That evening, several of decedent's fellow workers noticed that he looked "bad", "tired" or "drawn out". During the night, decedent was observed getting out of bed from three to five times, and holding his left arm, left side or armpit. At 7:00 a.m. on July 20, 1976, the decedent went off duty and returned home. Upon returning home, he ate breakfast, and later washed down a new brick fireplace at his home. After showering, resting and eating a lunch, he joined several other men near his home whom he had agreed to help in pouring cement for some new construction. The decedent mentioned pains in his neck and shoulder to these men before the truck carrying the cement arrived. The decedent mentioned that he had been under a lot of tension and pressure as a result of the busy work schedule at the fire station. When the cement truck arrived, cement was poured into several wheelbarrows and several of the men, including the decedent, pushed the wheelbarrows to the rear of the structure on which they were working. It appears that the decedent pushed approximately four wheelbarrow loads of cement weighing about 75 pounds each to the rear of the structure. Approximately one-half hour elapsed during the time that the decedent was engaged in this activity. Soon thereafter, the decedent was observed to collapse and fall to the ground. He was given emergency medical treatment and transported to Palmetto General Hospital, where he was pronounced dead at 5:24 p.m. on July 20, 1976. An autopsy was performed on the deceased on July 21, 1976 by Dr. Peter L. Lardizabal, the Assistant Medical Examiner for Dade County, Florida. In pertinent part, the autopsy showed moderate arteriosclerosis of the aorta, and severe occlusive arteriosclerosis of the proximal third of the anterior descending coronary artery in which the lumen, or opening, through which the blood passes through the artery was hardly discernible. The remaining coronary arteries appeared unaffected by the arteriosclerosis. The decedent's certificate of death, which was also signed by Dr. Lardizabal, listed the immediate cause of death as acute myocardial infarction due to severe occlusive arteriosclerosis of the left coronary artery. Dr. Lardizabal performed the autopsy examination of the decedent by "gross" observation, that is, without the benefit of microscopic analysis. However, microscopic slides were made during the course of the autopsy which were subsequently examined by other physicians whose testimony is contained in the record of this proceeding. Findings contained in the autopsy report, together with an evaluation of the aforementioned microscopic slides, establish that the myocardial infarction suffered by the decedent occurred at least 24 hours, and possible as many as 48 hours, prior to the decedent's death. This conclusion is based upon the existence of heart muscle necrosis, or tissue death, which would not have been discernible had the decedent died immediately following a coronary occlusion. In fact, for a myocardial infarction to he "grossly" observable at autopsy, that is, without the benefit of microscopic examination, it appears from the record that such an infarction would have to occur a substantial period of time prior to the death of the remainder of the body. Otherwise, the actual necrosis of heart muscle tissue would not be susceptible to observation with the naked eye. Although it appears probable from the evidence that the decedent went into a type of cardiac arrhythmia called ventricular fibrillation which led to his death, the actual proximate cause of his death was the underlying myocardial infarction, which in turn was a result of arteriosclerosis which had virtually shut off the supply of blood to the affected area of his heart. Although the causes of arteriosclerosis are not presently known to A medical science, it appears clear from the record that acute myocardial infarctions can be caused by emotional or physical stress, and that the decedent's myocardial infarction was, in fact, caused by the stress and strain of his job as a fire fighter and emergency medical technician. In fact, it appears from the medical testimony in this proceeding that the decedent was having a heart attack which led to the myocardial infarction on the night of July 19, 1976, or in the early morning hours of July 20, 1976, while he was still on duty. It further appears that, although physical exertion, such as the pushing of the wheelbarrow loads of cement by the decedent, might act as a "triggering mechanism" for ventricular fibrillation, the decedent's activities on the afternoon of July 20, 1976, had very little to do with his death. The type of lesion present in the decedent's heart, which had occurred as much as 48 hours prior to his death, was of such magnitude that he would likely have died regardless of the type of physical activity in which he engaged on July 20, 1976. Petitioner, Dolores A. Daniels, is the surviving spouse of James C. Daniels.
The Issue Compensability, to wit: Whether the injury claimed is a birth-related neurological injury and whether obstetrical services were delivered by a participating physician in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital. Whether notice was accorded the patient, as contemplated by Section 766.316, Florida Statutes, or whether the failure to give notice was excused because the patient had an emergency medical condition, as defined in Section 395.002 (8)(b), Florida Statutes, or the giving of notice was not practicable.
Findings Of Fact Latasha Williams Russell is the natural mother of Perry Russell, Jr. (Perry, Jr.). Perry Russell, Sr., is the natural father of Perry, Jr. Perry, Jr., was born a live infant on May 7, 2008. Perry, Jr., was born at Bay Medical Center, a licensed hospital located in Panama City, Florida. Perry, Jr.'s, birth weight was in excess of 2,500 grams. The physician providing obstetrical services at the time of Perry, Jr.'s, birth was Bryce Vincent Jackson. M.D. At all times material, Dr. Jackson was a participating physician in the Florida Birth-Related Neurological Injury Compensation Plan. Latasha Williams signed a Notice to Obstetric Patient (NICA notice form) stating that Bryce Vincent Jackson, M.D., is a "participating physician in the program" on November 20, 2007. Bay Medical Center acknowledged at hearing that it had never given pre-delivery notice of NICA participation/limitation to Ms. Williams. On May 7, 2008, Perry, Jr., suffered a brain injury caused by oxygen deprivation. As a result of the oxygen deprivation, Perry, Jr., was permanently and substantially mentally and physically impaired. Perry, Jr., subsequently died on October 8, 2008. Perry Jr.'s, death was caused by the brain injury resulting from the oxygen deprivation. The term, "resuscitation in the immediate postdelivery period" is not defined in the NICA Statute. §§ 766.301-766.316, Fla. Stat. Other Facts Found The term, "resuscitation in the immediate postdelivery period" is not uniformly defined in the medical community. Latasha Williams Russell was an obstetrical patient of Dr. Jackson at North Florida Obstetric and Gynecologic Center, beginning on November 20, 2007. Her expected delivery date was May 11, 2008. Labor began for Ms. Williams at approximately 0200 [2:00 a.m.] on May 7, 2008.5 At 0840 [8:40 a.m.], she was admitted to Bay Medical Center, experiencing active contractions every 2-3 minutes for 60-80 seconds, four centimeters dilated, with the baby 100 percent effaced and fetal heart rate of 135 with variability present. Accompanied by female family and friends, Ms. Williams was placed in a Labor/Delivery/Recovery/Post-Partum Room (LDRP), and prepped for delivery. Although her female support team varied a little in composition in the beginning of her hospitalization, at all times material, Ms. Williams' mother and sister and at least one other woman were present in the LDRP room with her. Ms. Williams' complete cervical dilation was reported at 1145 [11:45 a.m.]. At 1215 [12:15 p.m.], Dr. Jackson ruptured the membranes and found 3+ meconium-stained amniotic fluid. Meconium at 3+ would be of a putty-like consistency. 20. From 1220 [12:20 p.m.] to 1250 [12:50 p.m.], Ms. Williams pushed through her uterine contractions, and Perry, Jr.'s, fetal heart rate was sustained between 120 and 130 beats per minute through this period. At 12:50 p.m., Ms. Williams delivered Perry Russell, Jr., a live, 2605-gram boy, via normal spontaneous vaginal delivery, assisted by a right medial and lateral episiotomy performed by Dr. Jackson. Despite the episiotomy, Ms. Williams suffered a fourth-degree laceration, requiring repair. Dr. Jackson's narrative record reads: PROCEDURE PERFORMED: Normal spontaneous vaginal delivery on May 7, 2008. Right Medial and Lateral episiotomy. Fourth-degree laceration repair. PROCEDURE DESCRIPTION: The patient underwent a NSVD[6] at 1250 on May 7, 2008, over a right medial lateral episiotomy. She delivered a male infant that had Apgars[7] of 6 and 9, and weight equals 5 pounds plus 11.8 ounces (2606 g.) The amniotic fluid was 3+ meconium stained. The baby's airway was suctioned with a bulb syringe as well a [sic] #10 French pediatric suction cannula connected to the wall suction by intermittent suction technique prior to delivery of the thorax. The placenta delivered spontaneously and was found to be intact. There were three umbilical cord vessels. The placenta mass was also small. The uterine cavity was then manually explored and found to be intact with no retained products of conception. Post- delivery examination of the episiotomy site revealed an approximately 12mm inlet vertically oriented laceration into the rectal mucosa. The anal sphincter was intact. One carefully identified the proximal and distal end of the laceration and closed the defect with a 4-0 chromic suture in a continuous fashion. The second layer of closure was then done over the first layer, again using a 4-0 chromic suture in a continuous fashion. The remainder of the laceration was sutured in normal episiotomy repair fashion using 3-0 and 2-0 chromic sutures. Estimated blood loss was estimated at 250 mL. Anesthesia equaled epidural. The mother and baby were left in LDRP in good stable condition. (emphasis added). There is no further written evaluation of the child by Dr. Jackson, and he did not testify. Upon the foregoing obstetrician's record and the testimony of the mother, the grandmother, and an aunt who were present, it is found that Dr. Jackson suctioned Perry, Jr's, mouth by bulb and wall cannula while Perry, Jr.'s, head was out of the birth canal and his thorax remained inside, and then delivered the remainder of Perry, Jr.'s, body. Perry, Jr.'s, time of birth was recorded as 12:50 p.m. After delivering the whole of the baby,8 Dr. Jackson again suctioned him and "handed off" Perry, Jr., to one of two nurses, who took the baby to the LDRP crib/warmer and who examined and worked to stimulate him. The mother heard the baby cry when passed to the nurse. (Ex. K-522). Meanwhile, Dr. Jackson directed his primary attention to the repair of Ms. Williams' episiotomy tear. By all accounts, one or two nurses were present in the LDRP room at least until shortly before Dr. Jackson finished the episiotomy repair. At the LDRP's crib, a nurse bulb-suctioned Perry, Jr.'s, mouth and nose again (Ex. L-596, TR-74), but he would not suck her finger and was not very responsive to her vigorous stimulation by rubbing. She wiped him off and wrapped him in a swaddling blanket, but he still had meconium staining on his face and ears. Perry, Jr.'s, Apgar scores at one and five minutes were documented by one of the nurses as 6 and 9 as follows: Heart Rate Respiratory Rate Muscle Tone Reflex Irritability Skin Color Total 1 Min. 1 1 1 2 1 6 5 Min. 2 2 2 2 1 9 Out of a possible "10," or perfect Apgar score, Perry, Jr., improved from 6 to 9, in a four-minute period. The testifying medical experts, Dr. Berto Lopez (live and by deposition) and Dr. Donald C. Willis (by deposition only), agreed that these Apgar scores are inconsistent with a baby who has previous thereto suffered an injury to the brain. Entries by a nurse on a form entitled, "Possible Problems Typical of Age-Weight Categories," at 10 minutes post- birth and at 25 minutes post-birth, respectively, read as follows: [1:00 p.m.] [1:15 p.m.] (1300) (1315) Temperature 98.9R[9] 97.5AX[10] Pulse 140 140 Respiration Rate 60 52 Respiratory Pattern Unlabored Unlabored Nasal Flaring None None Expiratory Grunt None None Retractions None None Color Pink Pink Abdomen Normal Normal Cry Normal Normal Activity Normal Normal The foregoing nurse assessments did not include oxygen saturation of the blood, blood pressure, or assessment of acidosis in the arterial blood gases. If such assessments had been made at that point and if acidosis had been found, it would have been an indicator of an hypoxic event. The foregoing assessment form required that the nurses watch for asphyxia and meconium aspiration. None of the nurses' recorded assessments denote asphyxia, mechonium aspiration, hypoxia, or ischemia. "Hypoxia" denotes a low oxygen level in the blood. "Ischemia" occurs when there is not enough blood circulating in the body.11 If meconium gets below the baby's vocal cords and is aspirated into his lungs, there can be oxygen deprivation, possibly followed by meconium aspiration syndrome. Dr. Lopez testified that 10 percent of all babies are born with meconium, and of those 10 percent, perhaps five percent develop meconium aspiration syndrome. The foregoing nurse assessments required by the form are among the conditions that medical personnel look for, in an effort to determine whether or not a newborn is experiencing asphyxia, oxygen deprivation, or meconium aspiration syndrome. All of the foregoing recorded signs or symptoms existing at 10 minutes of life and 25 minutes of life suggest that Perry, Jr., had experienced no hypoxia, asphyxia, or meconium aspiration syndrome up to those points in time and that his transition from the uterus to the outside world had been successful. No party presented testimony by any medical personnel present at the labor or delivery, or present during the initial obstetrician and nurse resuscitations, already described, which occurred immediately after delivery. Dr. Berto Lopez faulted the sufficiency of the foregoing nurse assessments, maintained that they fall below recognized medical record-keeping standards, and are not the equivalent of a physician's evaluation of the child. The "Possible Problems Typical of Age-Weight Categories" form, itself, provided space for the nurses to periodically make, and record, new assessments at intervals at least four more times, but no further nurse assessments were recorded on this form after 1315 [1:15 p.m.], on May 7, 2008, and no further medical records of any kind were generated until 1412 [2:12 p.m.]. Nonetheless, Apgar scores and the 10-minute and 25-minute post- delivery nurse observations/assessments (see Finding of Fact 31) have not been shown to be other than the actual observations of the medical personnel at the times stated on them, and the medical experts testifying herein have considered those assessments, as well as the Apgar scores, in rendering their respective opinions. After Dr. Jackson completed the episiotomy repair, the family was left alone with the newborn in the LDRP. The baby was passed from woman to woman, each of whom examined and admired him. Hospital records next show that at 2:12 p.m., Perry, Jr., suffered a cardiopulmonary event, became apneic (ceased breathing), and required intubation, chest compressions, and administration of epinephrine. There is no documentation by any medical personnel of Perry, Jr.'s, condition between 1:15 p.m. and 2:12 p.m. Also, no party presented testimony by any medical personnel present during the resuscitative efforts hereafter described, which occurred at 2:12 p.m. Based on the time of Perry, Jr.'s, delivery recorded by Dr. Jackson (12:50 p.m.) Perry, Jr.'s, cardiopulmonary event at 2:12 p.m., occurred one hour and 22 minutes after his delivery at 12:50 p.m. Based on the time of the last nurse assessment as recorded on the "Possible Problems Typical of Age- Weight Categories" form (1:15 p.m.), Perry, Jr.'s, cardiopulmonary event at 2:12 p.m., occurred 57 minutes after the obstetrician and attending nurses had left him in the LDRP in what Dr. Jackson believed to be "good, stable" condition. Based on the testimony of the female relatives, the cardiopulmonary event at 2:12 p.m., occurred within 20-25 minutes of the time Dr. Jackson exited the LDRP room. The timing of precisely when Perry, Jr., became apneic is in dispute. Despite the foregoing health care professionals' records stating the cardiopulmonary event occurred at 2:12 p.m., Perry, Jr.'s, mother, grandmother, and aunt maintain that Perry, Jr., was continually struggling for breath while they were alone with him in the LDRP and that he ceased breathing within 20-25 minutes of Dr. Jackson's exiting the LDRP room. While these witnesses' testimony as to chronology of events and time elapsed is consistent with each other's testimony, they all base their time calculations on the recollection of the four women sequentially holding the baby for an estimated 4-5 minutes apiece as they passed him around, and they all concur that they were not sufficiently alarmed by his breathing on the day in question to immediately call for medical assistance. In challenging the medical personnel's recordation that the cardiopulmonary event occurred at 2:12 p.m., Petitioners put forth the premise that all notations in the medical records are misleading, because they had to have been written down subsequent to the events or conditions recorded. For instance, the family believes that 2:12 p.m., is when the cardiopulmonary event was recorded/charted, not when it occurred. This premise, that the medical notations were written down after the event recorded, is accepted, for what it is worth, because clearly, medical personnel cannot record events which have not yet taken place and cannot record them simultaneously with performing the medical procedures. However, the premise, by itself, does not establish either that the events recorded in the medical records did not ever occur or that those events occurred so far in advance of their being recorded as to prevent the records' content (including timing) from being credible. The accuracy of the family's testimony as to timing is also diminished by their not being medically trained and their testifying in retrospect, without any notes made contemporaneously with the events. Also, as might be expected, in the joy and excitement of holding a new family member, none of Petitioners' witnesses looked at a watch or clock to time events, and if the 2:12 p.m., cardiopulmonary event and subsequent events occurred somewhat before the times written down, then all the events recorded as occurring prior to Dr. Jackson exiting the LDRP room also must have occurred somewhat prior to the time stated in the records, so that the span of time from delivery until Perry, Jr., suffered the hypoxic event would still be about an hour and 22 minutes post- delivery and about 57 minutes after the delivery team exited the LDRP room, believing that Perry, Jr., had been stabilized. On the other hand, the consistent testimony of the mother, grandmother, and aunt that after they were alone with Perry, Jr., he opened his eyes as they admired him; that he later closed his eyes, stopped breathing, and went limp as the mother held him the second time; that the grandmother ran, carrying him, to the nurse's station for help; and that it was a nurse who returned him to the LDRP's crib/warming unit where resuscitation occurred, is accepted over the small amount of contrary hearsay contained in Dr. Mohamed's discharge summary quoted infra at Finding of Fact 54. Concerning Perry, Jr.'s, cardiopulmonary event at 2:12 p.m., a nurse recorded in the "Health Care Professionals' Progress Notes," in pertinent part, as follows: 5/7/08 1412: arrived to labor room 302. Observed infant on open warmer apneic and intubation performed per B. Miller with 3.0 ET tube PPV with 100% FI02. See Dr. Maniscalco progress notes. To newborn nursery via warmer with PPB en route with chest compression 2.6 cc epinephrine via ET tube. CPR continues ETC 11.5 cm @ lip HR54 . . . (Ex. C-103). It is also accepted that because of the run out/run in period, the note at 2:12 p.m., may actually show the hypoxic event as occurring a minute or two later than it actually occurred, but such a small delay is immaterial, given the rest of the evidence. Dr. Maniscalco's (surgeon's) progress note at 1455 [2:55 p.m.], reads, in pertinent part: 5/7/08 1455: Called stat to postpartum newborn in full arrest. CPR in progress. Intubated B. Miller . . . No IV access. Epinephrine/Atropin per ETT. HR 80's [to] 122+ palpable pulse. Dr. Azam in. IV established. Fluid bolus given. Pet. Color improved but . . . Dr. Azam to place UVC and assuming patient care. (Ex. C-81). After resuscitating Perry, Jr., at approximately 2:55 p.m., and moving him to the newborn nursery on mechanical ventilation, a chest X-ray was taken. Radiologist Billingsley's report, printed at 1604 [4:04 p.m.], on May 7, 2008, reads: INDICATION: Intubated, decreased breath sounds COMPARISON: None FINDINGS: The endotracheal tube tip is in the left mainstream bronchus. There is complete opacification of the right hemithorax likely due to inefficient aeration of the right lung. In the left lung there is patchy parenchymal opacification which may be due to . . . meconium aspiration in a term infant. (emphasis added). (Ex. C-97; see also Ex. C-99-100). Repeated X-rays thereafter also diagnosed "meconium aspiration syndrome." Arterial blood gas printouts showed severe acidosis as follows: Time pH pCO2 pO2 1520[3:20 p.m.] 6.549 65.4 152.3 1623[4.23 p.m.] 6.894 30.4 133.9 1755[5:55 p.m.] 7.096 32.5 76.5 At 1754 [5:54 p.m.], Perry, Jr., was noted as having tremors of the lips and facial tremors. Ahmed Baker Mohamed, M.D., was notified of the infant's seizure(s) and phenobarbital was administered at 6:12 p.m. At 1813 [6:13 p.m.], Perry, Jr., was air-lifted to Sacred Heart Hospital's Neonatal Intensive Care Unit (NICU). A discharge summary by Dr. Mohamed reads, in pertinent part: REASON FOR TRANSFER: Respiratory failure HISTORY OF PRESENT ILLNESS: This is a newborn, 1 day old, born in Bay Medical Hospital on May 7, 2008, as per report normal vaginal delivery with no reported complications during pregnancy or labor. After one hour from delivery, the baby was in the mother's room who asked for help because the baby stopped breathing and moving. The nurse rushed to the mother's room and found the baby pale, not moving and not breathing. The Ambu bag was started and called anesthesia who intubated the baby. Dr. Azam was called to evaluate the patient. She ordered epinephrine, IV fluid bolus and the patient was put on mechanical ventilation. It was reported that during the suction, meconium came out in a moderate amount. The patient was moved to the nursery on mechanical ventilation. Sacred Heart neonatal intensive care was called and arrangements were made to transport the patient to the neonatal intensive care. Prenatal labs were unremarkable. *** IMPRESSION: A one day newborn with respiratory failure, rule out sepsis, rule out aspiration, rule out pneumonia. (emphasis added). (Ex. C-73). Perry, Jr., stayed at Sacred Heart Hospital in Pensacola from May 7, 2008, to October 1, 2008, and was subsequently seen in other facilities. On July 2, 2008, and September 10, 2008, Perry, Jr., was seen by C. Anthony Hughes, M.D. (pediatric otolaryngologist). Dr. Hughes diagnosed Perry, Jr., as having hepatic encephalopathy, bilateral cortical injury secondary to hypoxic ischemic encephalopathy. On September 24, 2008, Perry, Jr., was seen by Kristin Van Hook, M.D., a pediatric pulmonologist, who diagnosed him at four months of age, with static encephalopathy and seizure disorder secondary to arrest shortly after birth from having suffered a severe anoxic injury at one hour of age. Coverage under the plan and the statutory presumption. Coverage is afforded under the Plan for infants who suffer a "birth-related neurological injury," which for our purposes here, is defined as: . . . injury to the brain . . . of a live infant . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." See § 766.302(2), Fla. Stat. Normally, Petitioners, as the proponents of the issue, would have the burden to demonstrate that Perry, Jr., suffered a "birth-related neurological injury." See Balino v. Dep't of Health and Rehab. Servs., 348 So. 2d 349, 350 (Fla. 1st DCA 1977)("[T]he burden of proof, apart from statute, is on the party asserting the affirmative of an issue before an administrative tribunal."); Galen of Fla., Inc. v. Braniff, 696 So. 2d 308, 311 (Fla. 1997)("[T]he assertion of NICA exclusivity is an affirmative defense."); Tabb v. Fla. Birth-Related Neurological Injury Compensation Ass'n, 880 So. 2d 1253, 1260 (Fla. 1st DCA 2004)("As the proponent of the issue, the burden rested on the health care providers to demonstrate, more likely than not, that the notice provisions of the Plan were satisfied."). However, herein, Petitioners have the benefit of a stipulation regarding notice issues and also that the statutory presumption contained in Section 766.309(1)(a) applies in this case. For our purposes here, the presumption reads: If the claimant has demonstrated, to the satisfaction of the administrative law judge, that the infant has sustained a brain . . . injury caused by oxygen deprivation . . . and that the infant was thereby rendered permanently and substantially mentally and physically impaired, a rebuttable presumption shall arise that the injury is a birth-related neurological injury as defined in s. 766.302 (2). The parties have stipulated that, as a matter of law, Petitioners are entitled to a rebuttable presumption that Perry, Jr., suffered a birth-related neurological injury, and it is undisputed herein, that Perry, Jr., suffered an injury to his brain caused by oxygen deprivation which rendered him permanently and substantially mentally and physically impaired and which ultimately resulted in his death. What remains for determination is whether or not the oxygen deprivation and the brain injury together occurred "in the course of labor, delivery, or resuscitation in the immediate postdelivery period." NICA suggests that the statutory presumption has been rebutted, asserting that the evidence demonstrates that the oxygen deprivation and injury to Perry, Jr.'s, brain and his subsequent neurologic impairment did not occur during "labor, delivery, or resuscitation in the immediate postdelivery period in a hospital" (the statutory period), because both the hypoxic insult which created the brain injury and the resultant brain injury itself did not occur until more than an hour after Perry, Jr., had been stabilized in the LDRP. NICA claims that both Perry, Jr.'s, oxygen deprivation and brain injury occurred when Perry, Jr., became apneic and was intubated, with chest compressions, and administration of epinephrine at 2:12 p.m. The likely timing of Perry, Jr.'s, brain injury. The statutory period is not defined under the Plan. Similarly, the medical experts herein acknowledged that this period is not defined within the medical community, but they agreed that this period would last until the infant was stabilized. Dr. Willis testified that although the term "resuscitation in the immediate post-delivery period" is not defined under the NICA Plan, the statute, or within the medical community, it was his opinion that it should be defined as follows: [W]hen the baby's born, once the baby is stabilized and no longer requires medical attention, care to maintain adequate oxygenation, to maintain adequate blood pressure, when the baby is surviving on its own without intervention, then, as far as I'm concerned, the immediate resuscitative period is over. (Ex. N-779). Dr. Lopez's definition was not very different. He testified: I would imagine the immediate postdelivery period would be what some doctors and many (TR-129). organizations call the fourth stage of labor, which is the period of time after the complete delivery of the baby until the baby has been stabilized and is no longer under observation. Orlando Regional Health Care System, Inc. v. Florida Birth-Related Neurological Injury Plan, 997 So. 2d 426 (Fla. 5th DCA 2008), instructs that the determination of what is "immediate" is a factual determination upon which medical testimony should guide the Administrative Law Judge. The medical experts, Dr. Willis and Dr. Lopez, are agreed that meconium only becomes an issue once the membranes are ruptured (during labor and delivery); the progress of meconium aspiration syndrome, if it occurs, is that the meconium is inhaled into the baby's lungs, creating an inability to take in enough oxygen to permit normal brain function, and eventually not enough oxygen is let in to sustain life. Dr. Lopez credibly testified that the alveoli of the lungs swell, cutting off the oxygen and causing cardiac arrest and oxygen deprivation. Dr. Willis is a Florida-licensed, board-certified obstetrician-gynecologist and a maternal-fetal medicine specialist. In this capacity, he focuses on providing consultative care to women with high risk pregnancies. He has not delivered a baby within the last ten years. Because meconium becomes an issue only after a patient's membranes are ruptured and the meconium becomes evident, Dr. Willis has not personally dealt with a meconium aspiration event in at least 10 years, and he was unable to give an opinion within reasonable medical probability as to whether meconium aspiration syndrome caused Perry, Jr.'s, hypoxic event and brain injury. However, he did opine that Perry, Jr.'s, brain injury did not occur within the statutory period so as to make it compensable under the NICA Plan. Dr. Berto Lopez has been a Florida-licensed, board- certified obstetrician for 23 years. He currently has privileges at four hospitals, delivers 30 babies per month, and is part of a high-risk perinatal transfer team at St. Mary's Hospital, Palm Beach, Florida. As such, it is found that Dr. Lopez was more qualified than Dr. Willis to address the issues of this particular case. Dr. Lopez faulted Dr. Jackson's records and failure to "evaluate" the child and further faulted the hospital's failure to monitor the child. He opined summarily that Perry, Jr.'s, loss of oxygen was an undiagnosed continuing insult that began at birth with aspiration of a moderate amount of thick meconium, and with loss of oxygen continuing through incomplete immediate resuscitative efforts in the LDRP, and that the remaining meconium, some of which was pumped out when Perry, Jr., was resuscitated at 2:12 p.m., had created a sequela of events, including loss of oxygen, brain damage, and full cardiopulmonary arrest at that time, approximately an hour after birth. Therefore, he concluded that the postdelivery resuscitative period extended through the 2:12 p.m., episode. However, upon closer questioning relevant to the issue of whether Perry, Jr.'s, oxygen deprivation and/or brain injury occurred within the statutory period of "labor, delivery, or resuscitation in the immediate postdelivery period in a hospital," Dr. Lopez testified as follows: [Questions by Mr. Bajalia] Q: And based on your review of the fetal monitor strips, you agree that there was no hypoxic insult or injury to Perry Russell, Jr.'s brain during labor? A: That's correct. (TR-145). *** Q: . . . Regardless of what you think of what Dr. Jackson did or didn't do, his assessment and his determination was that the baby was in good and stable condition; you agree with that? A: That's correct. (TR-148). *** Q: So it's your testimony that he [Perry, Jr.] was never in good and stable condition at any point in time? A: I'm not saying that he wasn't stable for a period of time. Q: There was a point in time, you're testifying here today, that he was in fact stabilized? A: He was stable, yes. (TR-149). *** Q: The one-minute Apgar score is inconsistent with a baby who has suffered an injury to the brain at that particular point in time? A: That's correct. Q: That one-minute Apgar score is not indicative of hypoxia or brain injury? A: Correct. Q: Now Perry's five-minute score was recorded as what? A: Nine. Q: And is that normal? A: Yes. But, it's normal, but the resuscitation not only included bulb and suction catheter. That also under oxygen, this baby has a nine when it's given 80 percent oxygen by -- with something called blow-by. Blow-by is an open tube of oxygen that's usually attached to a wall oxygen dispenser. . . . *** Q Is the fact that Perry Russell as part of the initial resuscitative efforts received blow-by oxygen, is that in and of itself indicative of him sustaining a brain injury at that particular point in time? A: No. Q: Now back to the Apgar score. You testified his Apgar score at five minutes was nine? A: Yes. Q: And that's normal? A: Yes. Q: And Perry's five minute Apgar score is, in your opinion, inconsistent with hypoxic [sic]? A: Correct. Q: It's inconsistent with him having suffered an injury to the brain at that particular point in time? A: Correct. Q: Now, I'm going to show you what's been marked and identified as Joint Exhibit C, and it's part of the records you have in front of you, page 107 of the stipulated record. Are you familiar with that document? A: Yes. Q: What is it? A: It is the nurse evaluation form for part of the postpartum period. Q: And in fact it's titled possible problems typical of age/weight categories? A: That's what it's labeled, yes. Q: And this appears to be an assessment of Perry's condition by the nurses charged with his care with respect to possible problems he may be experiencing; do you agree with that? A: Yes. Q: And one of these problems that is identified on this record is asphyxia and/or meconium aspiration? A: Correct. Q: Okay. So those are the things that they're specifically looking for in an effort to determine whether or not Perry Russell, at these particular points in time, was experiencing asphyxia, oxygen deprivation, or meconium aspiration, or meconium aspiration syndrome; you would agree with that? A: Yes. (TR-150-153). *** Q: Okay. And so despite the fact that Perry received some initial resuscitative efforts, which you described as suctioning and some blow-by oxygen, at 13:00, ten minutes after birth, based on what we've been through thus far, he seems to be looking pretty good? A: Yes. (TR-155). *** Q: Okay. Based on this assessment, at ten minutes after birth you described I think Perry Russell in your deposition as a rock star; do you remember that? A: Yeah, he's a rock star, looks good. Q: Appears to be stabilized? A: Yeah. Q: On this assessment Perry didn't appear to be experiencing or suffering from asphyxia from meconium aspiration; you agree with that? A: Correct. Q: And he doesn't appear to have any difficulty breathing? A: Correct. Q: He's apparently breathing on his own? A: Correct. Q: He is not in respiratory failure? A: Correct. Q: Okay. This assessment is inconsistent with hypoxia at that particular point in time? A: That's -- if we accept this as accurate, this photograph says at this moment things are looking great. (TR-155-156). *** Q: Based on what's documented here, Perry apparently had no injury to his brain at this particular point in time? A: Correct. Q: At 13:00, based on what's documented there, Perry Russell is in good and stable condition? A: Yes. Q: He didn't appear to have any life- threatening condition at that point in time? A: Correct. Q: He appeared -- it appeared that he had made a safe transition from utero life to life outside the uterus? A: Yes. Q: Based on what's documented at 13:00, there were no active resuscitative measures being administered to Perry Russell? A: Correct. (TR-157). *** Q: Now let's talk about the assessment that was done at 13:15. Perry was born at 12:50. At 13:15, that's 25 minutes postdelivery? A: Correct. (TR-158). *** Q: At 25 minutes of life Perry Russell doesn't appear to be having any difficulty breathing? A: Correct. Q: At 25 minutes of life he's breathing on his own? A: Correct. Q: At 25 minutes of life he doesn't appear to be in respiratory distress? A: Correct. Q: At 25 minutes of life, based on what's documented there, this assessment would be inconsistent with a baby who has experienced hypoxia? A: Correct. Q: It would be inconsistent with a baby that's acidotic? A: Correct. Q: It would be inconsistent with a baby suffering from asphyxia? A: Correct. Q: It's inconsistent with a baby that has sustained an injury to the brain? A: Correct. Q: At 13:15, 25 minutes after he was born, it would appear that Perry was in good and stable condition? A: Yes. Q: It would appear that he had no life- threatening conditions? A: Correct. Q: It would appear that there were no active resuscitative measures being administered to Perry Russell at that time? A: Correct. Q: And it would appear none were needed? A: Correct. (TR-160-161). *** Q: Okay. And you told me at the beginning of this -- of my examination that just because a baby is experiencing an ongoing spectrum of oxygen deprivation, that doesn't mean that he has sustained an injury to the brain? A: Not - at certain points in time. It's a spectrum that may start as okay and then go - progress to hypoxia and brain damage. Q: Exactly, but the mere fact - my point is, the mere fact that Perry may have been experiencing a spectrum of oxygen deprivation, it doesn't mean he has a brain injury at 13:00? A: Correct. Q: It doesn't mean he had a brain injury at 13:15? A: That's right. Q: In fact, based on what's documented in the records and what we know with respect to what occurred at 14:12 an hour and 20 minutes after birth, that is when he probably and most likely incurred an injury to the brain? A: No. *** A: It was my opinion it occurred before that. Q: Before 14:12 [2:12 p.m.]? A: Right. Q: Okay. But you have no idea when? A: I could not pinpoint it to the exact minute or time. What we see at 14:12 [2:12 p.m.] is in fact that the baby is in full cardiopulmonary arrest, requiring extensive resuscitation. (TR-162-163). *** Q: All right. And regardless of whether you think the nurses could have, should have done more with respect to their assessments of Perry Russell at 13:00 and 13:15 [1:00 p.m. and 1:15 p.m.], it is, in your opinion, what they documented at 13:00 and 13:15 you would agree would indicate he was not in respiratory distress? A: Yes. Q: Was not having any problems breathing? A: That's right. Q: And that he had not suffered an injury to his brain at that particular point in time? A: Correct. (TR-165). Overall, it is most probable that the oxygen deprivation that caused Perry, Jr.'s, brain injury did not happen until the code was called at 2:12 p.m., well beyond the time he was stabilized in the LDRP. Given the proof, it is resolved that, more likely than not, Perry, Jr., did not suffer brain injury due to oxygen deprivation that occurred during labor, delivery, or resuscitation immediately following delivery. Rather, it is more likely than not that Perry, Jr., suffered hypoxic ischemic brain damage sometime after the statutory period had ended, that is, after the obstetrician and nurses left him in stable condition in the LDRP. It is most likely that the damage was done when he became apneic and had to be resuscitated about an hour later. (See Findings of Fact 31 and 38). Alternatively, it is conceivable, but not proven, that Perry, Jr., suffered oxygen deprivation from some unspecified point after being stabilized at 1:15 p.m., and the oxygen deprivation continued undetected until he went into cardiac arrest at 2:12 p.m., but either way, he did not suffer brain damage during the statutory period.
The Issue Whether the Respondent committed the violations alleged in the Administrative Complaint dated October 22, 2001, and, if so, the penalty that should be imposed.
Findings Of Fact Based on the oral and documentary evidence presented at the final hearing and on the entire record of this proceeding, the following findings of fact are made: The Department is the state agency responsible for the investigation and prosecution of complaints involving physicians licensed to practice medicine in Florida. See Section 455.225, Florida Statutes. The Board of Medicine is the entity responsible for regulating the practice of medicine in Florida and for imposing penalties on physicians found to have violated the provisions of Section 458.331(1), Florida Statutes. See Section 458.331(2), Florida Statutes. Dr. Pliskow is, and was at the times material to this proceeding, a physician licensed to practice medicine in Florida, having been issued license number ME 0054211, and he is Board-certified in Obstetrics, Gynecology, and Forensic Medicine. At the times material to this proceeding, Dr. Pliskow practiced obstetrics and gynecology with three other physicians, Dr. Ackerman, Dr. Herbst, and Dr. Aqua, under the name "Advanced Women's Healthcare." In 1996, Dr. Pliskow, Dr. Ackerman, and Dr. Herbst established the Comprehensive Weight Loss & Nutrition Center ("Center") as a separate corporation. Kimberly Payne, an A.R.N.P., was the administrative director of the Center, and, in addition to administrative duties, her job responsibilities included supervision of the nursing staff working in the Center, direct patient care, and staff training. The four physicians practicing at Advanced Women's Healthcare were the designated supervising physicians for staff of the Center. Bariatrics is the subspecialty dealing with the medical treatment of obesity, and the four physicians supervising the Center, as well as Nurse Payne, were members of the American Society of Bariatric Physicians. As members of this organization, the physicians and Nurse Payne received two monthly journals, a biweekly newsletter, a monthly magazine, and faxes and e-mails containing updates on standard-of-care issues, medication changes, updates from the Federal Drug Administration, and suggested treatment changes and recommendations. The organization also provided educational programs and training opportunities for its members. In accordance with the recommendations of the American Society of Bariatric Physicians, the Center's weight loss program included a behavior modification program; a diet providing between 1200 and 1400 kilocalories per day; and an exercise program designed for each of its patients. In addition, if the patient was an appropriate candidate, the Center prescribed anorectic medications, including the combination of the drugs Phentermine and Fenfluramine commonly known as "Phen/Fen." Weight Loss Protocol At the times material to this proceeding, A.R.N.P.s were allowed under Florida law to practice independently under the general supervision of a physician who was accessible to them if they needed a consultation or evaluation of a patient. See Sections 464.003(3)(c) and 464.012(3), Florida Statutes (1995); Rule 64B8-35.002, Florida Administrative Code. Among other things, A.R.N.P.s were allowed to perform physical examinations of patients, to take medical histories, to initiate treatment programs, to prescribe certain types of drugs, and to evaluate patients for signs and symptoms of side effects associated with medications. A.R.N.P.s could not, however, prescribe drugs that were classified as controlled substances. Nurse Payne, and another A.R.N.P. subsequently hired to work at the Center, practiced under the general supervision of Dr. Pliskow, Dr. Ackerman, Dr. Herbst, and Dr. Aqua and in accordance with a protocol setting forth the respective duties of the A.R.N.P.s and of the physicians in the various areas of practice at Advanced Women's Healthcare. The protocol was filed with the appropriate state agency. Section Four of the protocol dealt with weight loss. Pursuant to the general guidelines, the A.R.N.P.s working at the Center were "responsible for the assessment and management of overweight individuals in a comprehensive weight reduction program including nutritional counseling, exercise management, and use of anorectic medications when appropriate." Patient selection criteria were as follows: Any individual who is over their ideal body weight may participate in the nutrition and exercise portions of the program. In order to qualify to participate in the medication portion of the program, the individual must meet the following criteria: Between the ages of 18 and 65 (any person between the ages of 61 and 65 must have medical clearance from their PCP [primary care physician]). Minimum of 20% over ideal body weight. No present history of heart disease, uncontrolled hypertension, cardiac arrhythmia, glaucoma, uncontrolled diabetes, hyperthyroidism, psychotic illness, drug or alcohol abuse, pregnancy, breastfeeding, or impending surgery requiring general anesthesia. Any deviation from these criteria requires collaboration with physician. The following was the General Condition of the weight loss protocol: The A.R.N.P. should consult with the physician on all patients exhibiting abnormal findings which might affect their weight loss management and refer for physician evaluation as needed. Patient C.B. Patient C.B. learned of the Center's weight loss program from her daughter, who had participated in the program and taken weight loss medication. C.B. had an initial consultation at the Center on October 23, 1996. At the time, as recorded on the Center's Weight Reduction Intake Form, C.B. was 62 years of age, her weight was 165 pounds, her height was five feet and four inches, she had a medium frame, her blood pressure was 138/82, and her pulse was 72 beats per minute. The intake form also included her body measurements as of October 23, 1996. As part of the initial consultation, C.B. completed the Center's Weight Reduction Program Questionnaire, in which she stated that she considered her ideal weight to be 135 pounds, that her biggest obstacle to losing weight was staying on a diet, and that she was interested in using medication in her weight loss program. C.B. indicated that she had no limitations on exercise and played tennis regularly. She disclosed her current medications, and she indicated that she did not then, nor had she ever, had the following conditions: heart disease, irregular heartbeat, high blood pressure, glaucoma, diabetes, psychotic illness, or alcohol or drug abuse. Nurse Payne reviewed the Weight Reduction Program Questionnaire with C.B. and completed the intake form. She noted on the intake form that C.B.'s ideal weight was between 120 and 135 pounds, that her weight goal was 135 pounds, and that her body mass index ("BMI") was 28.1 Nurse Payne reviewed with C.B. the information C.B. provided on the questionnaire, including her medical history, current medications, and drug allergies, and Nurse Payne noted on the intake form that C.B. reported arthritis as her only significant medical history. Nurse Payne and C.B. discussed the 1200-calorie exchange diet that was part of the program, and Nurse Payne developed an exercise plan for C.B. that included walking in the pool twice each week and incorporated C.B.'s usual routine of playing tennis three times each week. Nurse Payne noted on the intake form that Dr. Ira Fine was C.B.'s primary care physician. Nurse Payne also discussed medication options with C.B., including the benefits and risks of medications. The intake form included a printed section on medications, in which the first entry was "Pondimin2 20 mg. po bid and Phentermine 37.5 mg. po qd" and the second entry was "Other." Nurse Payne indicated on the intake form that C.B. would be started on "Phen/Fen pending medical clearance [by] Dr. Fine & EKG." Nurse Payne also advised C.B. that she would need to obtain medical clearance from Dr. Fine before medication would be prescribed. During the initial consultation on October 23, 1996, Nurse Payne provided C.B. with a Consent for Diet Program form and discussed with C.B. in detail the information in the consent form. The consent form contained descriptions of both Phentermine and Fenfluramine, together with the contraindications to their use, and Nurse Payne provided C.B. with an excerpt from the Physician's Desk Reference for Phentermine and the packet insert for Pondimin.3 C.B. signed the consent form on October 23, 1996. A blood specimen was drawn from C.B. on October 23, 1996, and Nurse Payne scheduled C.B. for an EKG on October 26, 1996. Nurse Payne telephoned Dr. Fine's office on October 25, 1996, and spoke with "Betty" about medical clearance for C.B. to participate in the weight loss program; she specifically told Dr. Fine's office the program would include the use of Phen/Fen. Nurse Payne was later advised by Dr. Fine's office that Dr. Fine had medically cleared C.B. to participate in the Center's weight loss program.4 Once medical clearance was obtained for a patient and the results of the blood work and EKG were received, the standard procedure at the Center was for the A.R.N.P. to present the patient's chart to one of the supervising physicians.5 The physician would review the test results and the patient's medical history and determine whether it was appropriate to prescribe medications for the patient. If so, the physician wrote the prescriptions, which were then given to the patient. Neither Dr. Pliskow nor Nurse Payne can recall specifically that this procedure was followed in C.B.'s case, but there is nothing in the record to indicate a deviation from this procedure with respect to C.B. C.B. was cleared for participation in the weight loss program and for the use of Phen/Fen based the results of her blood work and her EKG and on the criteria set out in the weight loss protocol: Her primary care physician had given medical clearance; her weight was 20 percent above her ideal body weight; and she had reported no present history of the conditions identified in paragraph II.B.3 of the protocol. Her blood pressure and pulse were normal. The results of her EKG showed no significant abnormality, and there was nothing in the results of the blood work done on October 23, 1996, that would prevent C.B. from participating in the weight loss program or from taking Phen/Fen. C.B.'s initial prescriptions for Phen/Fen were written on October 28, 1996 and, as noted in her chart, were for Pondimin in the dosage of "20 mg. [milligrams] po [orally] bid [twice daily]" and for Phentermine in the dosage of "37.5 mg. [milligrams] po [orally] qd [daily]."6 The medications and dosage prescribed for C.B. remained the same throughout the time she participated in the Center's weight loss program, and no further notations regarding dosage was included in her chart. C.B. initially visited the Center each week; in late November 1996, the frequency of her visits was decreased to once every two weeks, and then, in early February 1997, to once every four weeks. At each visit, a member of the nursing staff at the Center would note C.B.'s blood pressure, pulse, and weight on the progress forms in her chart, together with the amount of weight lost since her last visit. The chart also contained the notes of Nurse Payne or the other A.R.N.P. working at the Center reporting on C.B.'s success in staying on the diet and exercise plans; noting that her medication was "P/F"; and summarizing C.B.'s general progress, anything unusual she reported, and the plan she would follow until the next visit. C.B. also completed at each visit a Follow-Up Questionnaire in which she was asked to report whether, since her last visit, she had experienced chest pain, shortness of breath, dizziness, light-headedness, visual problems, palpitations, abdominal pain, bowel changes, fatigue, difficulty sleeping, depression, irritability, difficulty concentrating, memory loss, tremors, or increased appetite. The Center's standard procedure was for the A.R.N.P. meeting with the patient to discuss the answers in the questionnaire with the patient and to question the patient regarding any problems he or she might be having with the program. Once the A.R.N.P. had examined the patient and completed the patient's progress report, the A.R.N.P. would take the chart to the supervising physician, who would review the chart and write the prescriptions for Phen/Fen. None of the prescriptions for Phen/Fen dispensed at the Center were pre-signed. Patients in the weight loss program received new prescriptions for Phen/Fen at each visit to the Center. Because Phentermine and Fenfluramine are controlled substances, there could be no refills on a prescription, so the prescriptions were written for a sufficient number of pills to last until the patient's next visit to the Center. Although the prescriptions were written and signed by one of the supervising physicians, the physicians did not sign the patient's chart. After the supervising physician wrote the prescriptions, the A.R.N.P. would take the prescriptions to the patient, who could have them filled at the pharmacy in the offices of Advanced Women's Healthcare or at a pharmacy elsewhere. There is nothing in the record to indicate that this practice was not followed with respect to the prescriptions issued to C.B.7 On November 4, 1996, her first visit after beginning the program, C.B. reported one episode of light-headedness. Otherwise, C.B. reported none of the symptoms identified in the questionnaire and reported no problems with the program. Had C.B. reported experiencing anything abnormal, Nurse Payne would have called in one of the physicians supervising the Center for a consultation. C.B. participated in the Center's weight loss program through April 7, 1997, which was the date of her last visit. C.B. lost weight on the Center's program at a slow but steady rate, usually between one and four pounds between visits, until, on April 7, 1997, she weighed 141 pounds. C.B.'s treatment with Phen/Fen ended before May 1997, when the Florida Board of Medicine published stricter limitations on the use of these medications.8 Although Dr. Pliskow was not present in the office on October 28, 1996, when C.B.'s first prescriptions for Phen/Fen were written, he was present in the office during four of C.B.'s ten visits to the Center. Because at least one other physician was also present in the office during these four visits, Dr. Pliskow may or may not have reviewed C.B.'s chart and written her prescriptions.9 Summary The evidence presented by the Department is not sufficient to support a finding that Dr. Pliskow practiced medicine below the level of care considered acceptable by a reasonably prudent physician under similar circumstances or to support a finding that Dr. Pliskow failed to document in C.B.'s medical records justification for the course of her treatment in the weight loss program and the dosage of the medications prescribed for her. The evidence is not sufficient to establish clearly and convincingly that the prevailing standard of care required the physician supervising the Center's A.R.N.P.s personally to perform a physical examination of C.B. prior to her being cleared for receiving medication as part of her weight loss program or personally to obtain C.B.'s medical history. Rather, it was appropriate for Nurse Payne and the other A.R.N.P. working at the Center to perform physical examinations and to take medical histories of persons seeking to participate in the Center's weight loss program. In addition, the evidence is not sufficient to establish clearly and convincingly that it was inconsistent with the prevailing standard of care for the Center's supervising physicians to rely on C.B.'s primary care physician to provide medical clearance for her to participate in the weight loss program. Dr. Fine was familiar with C.B.'s overall medical condition as a result of his examination of her on September 12, 1996, and he was, therefore, competent to assess the overall risks of her participation in a weight loss program incorporating the use of anorectic medications. Furthermore, the evidence fails to establish that it was inconsistent with the prevailing standard of care to rely on the verbal medical clearance conveyed to Nurse Payne through Dr. Fine's office; rather, the persuasive evidence suggests that it was the normal practice for clearance to be given in this manner.10 And, significantly, Dr. Fine's medical clearance was not the only basis for C.B.'s clearance to take anorectic medications: C.B.'s vital signs were recorded on the intake form by the Center's nursing staff, and Nurse Payne compiled C.B.'s medical history from C.B.'s answers to questions on the Weight Loss Program Questionnaire and from discussions with C.B; an EKG and extensive blood work were ordered for C.B., and a physician reviewed C.B.'s chart and the results of these tests before writing C.B. prescriptions for anorectic medications.11 The evidence is not sufficient to establish that the physicians practicing at Advanced Women's Healthcare failed to provide the appropriate level of supervision to the A.R.N.P.s who worked in the Center. A.R.N.P.s are independent practitioners, and they are subject only to the general supervision of a physician. The evidence failed to establish that the prevailing standard of care for physicians supervising A.R.N.P.s required anything more than that the physician be available for consultation. At least one physician was available in the Advanced Women's Healthcare offices at all times for consultation and/or patient evaluation if an A.R.N.P. working at the Center determined that a patient was experiencing any complications or if a patient reported any unusual symptoms. The evidence is not sufficient to establish clearly and convincingly that the type and scope of information collected during C.B.'s regular visits to the Center and the on-going care provided to C.B. were not appropriate under the prevailing standard of care for monitoring patients on weight loss programs such as C.B.'s. The prescriptions for C.B.'s weight loss medications were written by a physician at each of C.B.'s visits, but only after the physician reviewed her chart, which included the A.R.N.P.'s progress notes and C.B.'s answers on the Follow-Up Questionnaires she completed at each visit, to determine whether it was appropriate to continue C.B. on anorectic medications.12 The evidence also fails to establish that the prevailing standard of care required a supervising physician to sign a chart prepared by an A.R.N.P. to indicate that it had been reviewed.13 The evidence is not sufficient to establish that C.B. was not an appropriate candidate for a weight loss program using Phen/Fen under the prevailing standard of care in 1996 and early 1997.14 Adequate justification for the treatment of C.B. with anorectic medications was included in C.B.'s medical records: She was considered obese by 1996 standards because her weight of 165 pounds was more than 20 percent higher than her ideal body weight of 120-to-135 pounds and because her BMI was 28 and she wanted to lose weight. In addition, nothing in the medical history C.B. provided to Nurse Payne or in her tests results indicated that she would be an inappropriate candidate for anorectic medications, and she reported no complications during her follow-up visits.15 The evidence is not sufficient to establish clearly and convincingly that the dosages of Phen/Fen prescribed for C.B. were inappropriate or excessive under the prevailing standard of care in 1996 and early 1997. Rather, the dosages prescribed for C.B. were in the lower range of dosages recommended at the time by the American Society of Bariatric Physicians and in the medical literature in general for the use of Phentermine and Fenfluramine in combination.16 The dosage of both medications was printed on the intake form completed during C.B.'s initial visit to the Center, and the dosages did not change during the time C.B. participated in the Center's weight loss program; in accordance with normal practice, no further notations were made regarding dosages in C.B.'s chart. New prescriptions were written each time C.B. visited the Center, and no refills were permitted, which is also in accordance with the standard practice in dispensing controlled substances.
Recommendation Based on the foregoing Findings of Fact and Conclusions of Law, it is RECOMMENDED that the Board of Medicine enter a final order dismissing in its entirety the Administrative Complaint against Steven Pliskow, M.D. DONE AND ENTERED this 30th day of April, 2002, in Tallahassee, Leon County, Florida. PATRICIA HART MALONO Administrative Law Judge Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-3060 (850) 488-9675 SUNCOM 278-9675 Fax Filing (850) 921-6847 www.doah.state.fl.us Filed with the Clerk of the Division of Administrative Hearings this 30th day of April, 2002.
The Issue The issue is whether Respondent is guilty of failing to practice medicine in accordance with the applicable standard of care by failing to assess adequately a patient's complaints, failing to provide an adequate diagnosis, failing to obtain a specialized consultation, and failing to pursue the appropriate treatment, in violation of Section 458.331(1)(t), Florida Statutes, and failing to keep adequate medical records to justify the use of Cardizem and document the drug's effect, in violation of Section 458.331(1)(m). If guilty of either of these offenses, an additional issue is the penalty that should be imposed.
Findings Of Fact At all material times, Respondent has been a licensed physician, holding license number ME 0048483. He is Board Certified in Emergency Medicine. On May 16, 1994, shortly after 2:00 PM, a 48-year-old male presented at the Naples Community Hospital emergency room with the chief complaints of a rapid heart rate and shortness of breath. He felt warm, but denied feeling nauseous or chest pain. He also reported that he had not had any previous cardiac problems or any head trauma. The patient's heart rate was rhythmic, though rapid at 132 beats per minute. His respiration rate was 24, and his blood pressure was 110/80. The nurse initially examining the patient applied a pulse oximeter and obtained an abnormally low reading of 70 percent on room air. The patient's grey color confirmed that this was not an erroneous reading. The nurse immediately placed the patient on oxygen. After the oxygen was started, Respondent saw the patient, whom he found not to appear sick. The patient's breathing, though rapid, was not labored. He explained that he had come to the hospital only at the insistence of his employer. Evidently, his color had quickly improved with the administration of oxygen. Thinking that this might be a case of tachycardia, which can cause a sensation of shortness of breath, Respondent appropriately ordered a chest x-ray, EKG, and cardiac labs. Respondent received the chest x-rays promptly. They were normal, precluding, among other things, a collapsed lung. The cardiac labs were also normal. Respondent ordered two more EKGs during the patient's hospitalization on May 16. The parties disagree as to the significance of the results of the three EKGs, which revealed some abnormalities. Petitioner failed to prove that the abnormalities revealed in the EKGs were material to a correct diagnosis. Respondent's expert testified that these abnormalities were common among adults and nonspecific. He added that they did not reveal that the patient was suffering from a pulmonary embolism. This detailed, unqualified testimony from an experienced physician is credited over the testimony of Petitioner's expert. Respondent ordered an intravenous access, which was established at 3:00 PM. Although still receiving oxygen, the patient's oxygen saturation was at 97 percent at 2:45 PM and 4:00 PM. Based on his tentative diagnosis of tachycardia, Respondent administered 20mg of Cardizem at 3:35 PM. Cardizem is a calcium channel blocker, which slows down the heart rate. Generally, the patient's condition improved following the administration of the oxygen. According to the nurses' notes, the patient's breathing had slowed down by 2:45 PM, and he reported that he was feeling better by 4:45 PM. Respondent saw the patient four times during his hospitalization and confirmed for himself the nurses' observations before discharging the patient by 6:00 PM. Respondent's discharge diagnosis was paroxysmal supraventricular tachycardia--resolved. He later amended the diagnosis to sinus tachycardia, but testified that he still would have discharged the patient with this diagnosis, under all of the circumstances. The patient returned to the hospital at 10:00 AM the next day, effectively dead on arrival. He had suffered an acute pulmonary saddle embolus. The sole question in this case turns on the adequacy of Respondent's diagnosis and treatment on May 16. Petitioner's expert conceded that there were no independent issues involving the adequacy of the medical records, and Petitioner's proposed recommended order makes no mention of this alleged violation. In hindsight, it is impossible to attribute to mere chance the events of May 16 when the patient died the next morning from an acute pulmonary saddle embolus. Something happened at work, and probably was still happening when the patient first arrived at the hospital, and this was related to what killed the patient the following day. However, Petitioner has not proved that whatever happened to the patient persisted long enough for Respondent to be able to diagnose it based on the data available to him on May 16 or, even if it had, that Respondent's failure to diagnose it was a departure from the applicable standard of care. The first potentially important piece of information collected by the hospital, apart from this history, was the abnormally low pulse oximeter reading. However, Petitioner failed to prove that Respondent was aware of this information, or reasonably should have been aware of this information, at the time that he was treating the patient. The hospital had recently instituted the practice, since discontinued, of separating the nurses' notes, where the low reading was recorded, from the remainder of the medical records for a patient. Ensuing pulse oximeter readings, of which Respondent was aware, were recorded in a different place in the records from the initial pulse oximeter reading. Moreover, it is unclear whether, if Respondent had been aware of the patient's abnormally low pulse oximeter reading, this knowledge would have materially changed what Respondent had to do to meet the applicable standard of care. Ensuing pulse oximeter readings were 96 and 97 percent. Prior to discharge and after discontinuation of the oxygen for a suitably long period of time to eliminate its effects, the patient's pulse oximeter reading remained in the high 90s. Petitioner's expert witness conceded that the pulse oximeter is not a diagnostic tool for a pulmonary embolism. He testified that the EKGs were not a diagnostic tool for a pulmonary embolism, but would give hints of this condition. His main argument was that the initial pulse oximeter reading of 70 percent at room air should have been followed by an arterial blood gas test, which "probably" would have been abnormal. An abnormal arterial blood gas reading should have been followed by a VQ scan, which he asserted should have been abnormal due to little emboli coming off the lungs. However, there is a large element of speculation in the testimony of Petitioner's expert concerning these two tests. It is as likely as not that the arterial blood gas results would have been normal. The VQ scan would almost certainly have been normal, as the autopsy revealed no profusion of emboli, but only an acute pulmonary saddle embolism as the cause of the patient's death. Respondent's expert conceded that a pulmonary arteriogram probably would have been useful, but, in 20 years' practice, he could not recall ordering such a test, which is relatively frequently done in large academic institutions, but not in community hospitals, due to the mortality associated with the procedure and the 2-3 percent of false negatives. Additionally, this record does not so clearly disclose the relationship between the incident on the afternoon of May 16 and the death on the morning of May 17 to permit even an inference that a pulmonary arteriogram would have detected an abnormality in the interim between these two points. Perhaps the most important fact in evaluating whether Respondent met the applicable standard of care is that the patient exhibited none of the predisposing factors for a pulmonary embolism. He had no cardiopulmonary disease. He had no chronic obstructive pulmonary disease. A cable television installer, he was not sedentary and had no stasis of the blood flow, such as from a prolonged immobilization. He was not obese. He had no relevant trauma or injury to the lower extremities. The diagnosis of a pulmonary embolism is very difficult even with predisposing factors; in the absence of such factors, the diagnosis is dauntingly difficult. As Respondent's expert testified, he has never encountered a case of pulmonary embolism without a predisposing factor. Under all of these circumstances, especially the absence of predisposing factors, Respondent's failure to order a pulmonary arteriogram or obtain a consultation was not a departure from the applicable standard of care, nor was his failure to diagnose a pulmonary embolism, if one in fact existed on May 16. Shortness of breath and rapid heart rate are nonspecific complaints. Respondent retained the patient in the hospital for four hours for observation and analysis of test results. Respondent examined the patient four times during this hospitalization. Respondent reasonably and correctly ruled out a variety of more common diseases and illnesses. Under all of the circumstances, the final diagnosis of tachycardia, which related the shortness of breath to tachycardia or possibly anxiety, was not a departure from the applicable standard of care. Petitioner has therefore failed to prove by clear and convincing evidence that Respondent failed to meet the applicable standard of care in any respect in his diagnosis or treatment of the patient on May 16.
Recommendation It is RECOMMENDED that the Board of Medicine enter a Final Order dismissing the Administrative Complaint. DONE AND ENTERED this 4th day of August, 1998, in Tallahassee, Leon County, Florida. ROBERT E. MEALE Administrative Law Judge Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-3060 (850) 488-9675 SUNCOM 278-9675 Fax Filing (850) 921-6847 Filed with the Clerk of the Division of Administrative Hearings this 4th day of August, 1998. COPIES FURNISHED: Gabriel Mazzeo, Senior Attorney Carol A. Lanfri, Staff Attorney Agency for Health Care Administration Post Office Box 14229 Tallahassee, Florida 32317-4229 William Partridge Grossman, Roth and Partridge SouthTrust Bank Plaza 1800 Second Street, Suite 777 Sarasota, Florida 34236 Angela T. Hall, Agency Clerk Department of Health Bin A02 2020 Capital Circle Southeast Tallahassee, Florida 32399-1703 Pete Peterson, General Counsel Department of Health Bin A02 2020 Capital Circle Southeast Tallahassee, Florida 32399-1703 Dr. Marm Harris, Executive Director Board of Medicine Department of Health 1940 North Monroe Street Tallahassee, Florida 32399-0792
The Issue The issue in this case is whether Layton Maloy suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Jessica and Josh Maloy are the natural parents of Layton Maloy. Layton was born on September 4, 2012, at Lakeland Regional Medical Center, Inc. (Lakeland Regional), which is a hospital located in Lakeland, Florida. Layton was a single gestation and weighed in excess of 2,500 grams at birth. Obstetrical services at Layton’s birth were provided by Dr. Jeffrey L. Puretz, who was a physician participating in the NICA program. Notice of NICA participation was provided to Petitioners by Dr. Puretz and by Lakeland Regional. Petitioners contend that Layton suffered a birth-related neurological injury and seek compensation under the NICA Plan. More specifically, Petitioners contend that Layton suffered a stroke during labor and delivery, which resulted in a brain injury, rendering Layton permanently and substantially mentally and physically impaired. Respondent contends that there was no event during labor and delivery which resulted in oxygen deprivation to Layton, and that any medical conditions suffered by Layton are not birth-related neurological injuries as defined in section 766.302(2), Florida Statutes. Respondent further contends that Layton is not permanently and substantially mentally and physically impaired. Intervenors take no position as to whether Layton suffered a birth-related neurological injury. Layton was born at approximately 9:22 p.m., via cesarean section secondary to non-reassuring fetal heart rate tracing following six hours of labor. Following receiving an epidural, Mrs. Maloy experienced hypotension for which she received two doses of Ephedrine to raise her blood pressure. Following the second dose of Ephedrine, the baby’s fetal heart tracing became non-reassuring and the mother and baby’s heart rate became tachycardic. Mrs. Maloy also received an amnioinfusion during labor. Layton was born crying, pink and vigorous. Layton’s one- minute Apgar score was 8, and his five-minute Apgar score was 9. He did not require resuscitation at birth, and was sent to the regular newborn nursery with “routine NB orders” where he was noted to be active, awake, with normal rooting and sucking reflexes. Layton was discharged from the hospital with his mother on day two of life. After returning home, Mrs. Maloy noticed what she believed to be Layton having abnormal movements described as episodes of arms and/or legs shaking. His two-week old check-up was normal. However, two or three days after that check-up, she returned to the pediatrician’s office where “Layton had an episode in front of Dr. Leviten.” Dr. Leviten admitted Layton to Lakeland Regional for evaluation and a neurological consultation. A VEEG obtained was interpreted to reveal frontal central spike and wave on a few occasions from the left hemisphere suspicious for seizure activity. Layton was subsequently placed on Phenobarbital. Layton was noted at this time to be clinically very stable, doing well, eating well, happy and alert, and interactive. Layton was transferred to All Children’s Hospital. Upon admission, he was noted to be bottle feeding, had normal tone and no focal deficits. Dr. Ena Andrews, a pediatric neurologist, first saw Layton on September 26, 2012, at All Children’s Hospital, where she reviewed his medical records from Lakeland Regional. Her impression included a history of focal seizures and a finding on MRI that “is suspicious for intrauterine stroke.” She conducted a neurological examination of Layton. There were no abnormal findings from her neurological examination. She also reviewed a CT performed at Lakeland Regional that was read as normal by a radiologist. However, she ordered an MRI to rule out an intrauterine stroke. The MRI was conducted and Dr. Andrews reviewed the results with Mrs. Maloy on September 27, 2012: IMAGING STUDIES: I reviewed images of the MRI with mom at the bedside. As suspected, after reviewing the head CT, there is an area on the right frontal lobe with hypodensity on T2 weighted images. The area is also hypodense on diffusion, indicating it is not an acute ischemic lesion. Ventricles enlarged on the left compared to the right. There is also a hypodense area on the right parietal. Finding appears to be limited to the white matter without clear involvement of the cortex. There is no enhancement. LABORATORY STUDIES: Phenobarbital level is 22.9 this morning. IMPRESSION: History of focal seizures, doing well without seizure recurrence. Phenobarbital is in low-therapeutic range. Hypodense lesion in the right frontal and parietal white matter, unclear etiology. Given prior investigations at outside hospital, including blood cultures and CSF cultures, infection is unlikely. No evidence of diffusion change to suggest acute stroke; however, this does not rule out the possibility of prenatal stroke. Differential also includes some other type of inflammatory lesion with edema. In her deposition which was taken on June 23, 2015, when Layton was less than 3 years old, Dr. Andrews explained that her use of the word “prenatal” referenced a stroke occurring before birth, and her use of the term “acute stroke” referenced a stroke occurring within 14 days of the September 26, 2012, MRI. Dr. Andrews was asked about the comments she wrote in her September 27, 2012, notes: Q: So by “acute stroke” in your September 27th note, do you mean no stroke occurring within 14 days? A: Yes. Q: Is that 9/26 MRI? A: Correct. Q: Is that your testimony? A: Yes. Q: Now, you have -- you did not -- you did not diagnose Layton Maloy with having suffered a stroke during labor and delivery, correct? A: That’s correct. Q: Based on your notes here, would you agree with me that the imaging that you looked at was suggestive potentially for -- or rather you weren’t able to rule out a stroke occurring just before -- sometime before birth, correct? A: Correct. I was not able to rule that out. * * * Q: So one -- you actually reviewed not only the MRI that was done on September 26, 2012, but you also reviewed the CT scan that was done prior to that, correct? A: Yes. Q: Okay. And when you reviewed the CT scan, even though the radiologist didn’t note some abnormality, you felt that there was a possible abnormality on that CT scan, correct? A: Correct. Q: And you felt there was an area on the right frontal lobe that caused you some concern, correct? A: Yes. Q: And . . . you felt that the area is also hypodense on diffusion, indicating it is not an acute ischemic lesion; is that correct? A: Yes. Q: And so by that you mean that it wasn’t an ischemic event, whether it’s a stroke or something else, that caused this lesion occurring within two weeks of the study being done, correct? A: Correct. Q: And so that acute ischemic lesion that you saw on the CT scan and then correlated on the MRI, that is something that could have occurred during labor? Ms. Gaffney: Form A: Yes. Layton was discharged from All Children’s Hospital on September 29, 2012, but Dr. Andrews and another pediatric neurologist, Dr. Joseph Casadonte, followed up the medical management of Layton’s seizures in their offices beginning on October 10, 2012. Layton continues to see Dr. Andrews for management of his seizures, and has had additional brain diagnostic testing and imaging through the years. A November 28, 2012, brain MRI was read to reveal the following findings in pertinent part: Findings: The previously seen signal abnormality in the right frontal and right parietal lobes is no longer identified. Lateral ventricles and third ventricle are mildly prominent, more so then on prior examination. There is persistent asymmetry with the left lateral ventricle being larger than the right lateral ventricle. The subarchachnoid spaces are increased in size when compared to prior examination. There is no mass effect or midline shift. No abnormal fluid collections are identified. The pons is decreased in size. The vermis also appears smaller than expected. It is also noted that the corpus callosum is thinned in appearance. Layton was admitted to St. Joseph’s Hospital in January 2013, for acute vomiting and rash, with a history of seizures. Radiology results from an MRI conducted at St. Joseph’s Hospital revealed the following: IMPRESSION: Generalized volume loss in the brain with prominence of the subarachnoid space in the lateral ventricles. No transependymal fluid migration to suggest increased intracranial pressure. No intracranial hemorrhage or mass effect. While at St. Joseph’s Hospital, Layton had an 18-hour video EEG monitoring which was normal. He also had a consultation with Dr. Jose Ferreira. Dr. Ferreira’s impression included history of suspected neonatal seizures; mild degree of hypotonia of unclear significance; suggestion of mild volume loss on MRI which he believed was borderline; and the possibility of disorders associated with seizures of continued concern. He noted that the MRI showed no signs of ischemia or hemorrhage. Dr. Andrews attributes Layton’s balance and coordination issues to his mild to moderate developmental delay. Her records reflect that Layton continues to improve with function overall, and her testimony is consistent with her records. Significantly, Dr. Andrews testified that she has not seen evidence of a mental impairment, but that he suffers from physical or motor impairment for which physical therapy was prescribed. She further explained that some of the factors, e.g., social interactions, language development, and higher cognitive functions, which she would use to evaluate any mental impairment cannot be determined until he is older. She also testified that he is improving from physical therapy. When asked whether Layton’s physical impairments were permanent, she answered that she “wouldn’t be able to say whether his impairment is permanent” at this time, as she does not know to what extent he will continue to make progress and at what point he may or may not plateau. Layton also has had difficulty feeding and is being seen by a gastroenterologist for that. Layton’s most recent brain MRI was conducted on February 9, 2015. The report from the MRI contained the following: IMPRESSION: Continued somewhat slightly dysmorphic appearance of the brain as discussed in detail with mildly prominent ventricles, left greater than right. The findings may suggest some degree of volume loss, potentially involving the left basal ganglia and thalamus with question for decreased white matter volume. While nonspecific, these may be the sequela of prior insult. Dr. Andrews agrees with the above impression. She believes that his epilepsy to be symptomatic from brain abnormalities that were seen on MRI. However, when specifically asked whether the seizure disorder that Layton has is consistent with a perinatal stroke, she responded, “his epilepsy, we believe to be symptomatic from brain abnormalities that we’ve seen on MRI.” She did not specifically testify that these brain abnormalities were consistent with a perinatal stroke. Petitioners retained James Balducci, M.D., to review Layton’s medical records. Dr. Balducci practices in obstetrics and gynecology and maternal fetal medicine in Arizona. In his deposition taken on April 13, 2015, Dr. Balducci stated his opinion that Layton did sustain a brain injury caused by oxygen deprivation during labor. Specifically, Dr. Balducci is of the opinion that Layton suffered oxygen deprivation to his brain shortly after a second dose of ephedrine was administered to his mother during labor and delivery, and that this caused Layton to have a stroke. He reached this opinion by examining the fetal heart tracings. Dr. Balducci explained the basis for his opinion as follows: A: This baby suffered oxygen deprivation to the brain shortly after the second dose of Ephedrine. So the effects of the Ephedrine caused a vasoconstriction in the fetal vessels in the brain, caused an intrapartum stroke to the baby’s brain, which was the source and the cause of this baby’s neurologic sequela which the baby suffers from today. Q: And is the basis for that opinion, Dr. Balducci, the fetal heart tracings that you’ve just gone over with me? A: Yes. The fact that the baby was completely reassuring prior to the two doses of Ephedrine, and the fact that the baby became completely non-reassuring after the second dose of the Ephedrine, with the maternal pulse raising up to 140, trying to get the mother’s blood pressure up, the Ephedrine had the effect, in the fetal physiology, of causing a fetal stroke in the kid’s brain. Q: And sir, are you able to say within a reasonable degree of medical probability that that is diagnosable from these fetal heart tracings? A: Yes, ma’am. And the reason is -- Q: And the timing of the -- I’m sorry. I didn’t mean to speak over you. A: Yes ma’am, because the tracing prior to the second dose of ephedrine was reassuring, and the -- the fetal heart rate tracing post Ephedrine was completely non-reassuring, and nothing else had changed. Q: Sir, would you agree with me that you can have a non-reassuring tracing and still deliver a viable infant with no hypoxic brain injury? A: Yes, ma’am. That happens a lot. Dr. Balducci is of the opinion that a local area of Layton’s brain was devoid of oxygen secondary to the administration of Ephedrine to his mother. According to Dr. Balducci, the effects of this type of stroke may not show up until a week or two later so the baby is not depressed at birth. At the request of Petitioners, Paul Kornberg, M.D., reviewed Layton’s medical records and performed a medical examination of Layton. Dr. Kornberg is a specialist in physical medicine and rehabilitation, specifically pediatric rehabilitation. He serves as Medical Director for Tampa General Hospital’s Pediatric Rehabilitation Program and works in an outpatient clinic. His practice includes treatment of children with Cerebral Palsy and who have had intrapartum strokes. He examined Layton and evaluated him on April 7, 2015, when Layton was approximately 2 1/2 years old. Dr. Kornberg believes that Layton is permanently and substantially neurologically and physically impaired. This opinion is based on Layton’s daily seizures and that, at the time of his examination, Layton was dependent on a feeding tube. Based upon the history he was given, he noted that Layton dragged his left leg when fatigued. Upon examination, however, Dr. Kornberg found that Layton’s tone and strength appeared to be normal. At the time of his examination, Layton was walking and putting words together at the level that would be expected at his age at the time of the examination. Dr. Kornberg has no opinion as to whether Layton’s impairments are related to oxygen deprivation occurring during labor and delivery. He noted that there are causes other than an event during labor and delivery that could cause Layton’s symptoms (e.g., seizures, functional neurologic impairments, sensory processing issues), including a variety of developmental abnormalities of the brain. Layton’s school records from the Polk County Public Schools contain an initial Individualized Education Plan (IEP) which was developed at an IEP meeting on September 1, 2015, just three days before Layton’s third birthday. In the domain of Curriculum and Learning, Layton scored in the mild developmental delay range in cognitive development and scored average in communication development. In the Social Emotional Behavior domain, Layton scored in the mild developmental delay range in personal-social development. In the Independent Functioning domain, Layton scored in the significant delay range in adaptive developmental quotient and average in the motor development quotient. The initial IEP indicates that the educational setting for Layton would be in an ESE Pre-K classroom. The IEP noted that he needed a health care plan but did not need assistive technology devices or strategies and did not need specially designed or adaptive physical education (PE). A physical therapy (PT) evaluation was performed by Polk County Public Schools on November 12, 2015. It reveals that Layton’s ESE teacher reported that, at that time, Layton was able to go up and down the steps to the portable classroom with one railing and close supervision; he pedaled a small tricycle on the playground sidewalk; and he was able to drink a can of Pediasure from a straw. The physical therapist notes that although a wooden chair with armrests was available in the classroom, Layton was sitting in a standard classroom chair at the time and appears to have functional balance. He was noted to walk independently within the classroom and needed verbal cuing to remind him not to run in the classroom which, apparently, he liked to do. By observation and teacher report, Layton was noted to want to run in the classroom and to need verbal cuing to slow down. Although observed to be mildly off balance at times, falls appeared to be rare. He was reported to be able to put away his lunchbox and was eating well. He was observed walking and running on the playground without falling. Nonetheless, the PT report recommended that Layton continue to wear his soft helmet for safety when playing on the playground or transitioning on campus, due to his history of seizures and falling. Layton’s most recent PT report, dated August 30, 2016, from his school states in pertinent part: Layton should be watched closely when he is outdoors to be sure he does not get overheated. Mother had previously noted that he had a high incidence of falling (greater than 10x) per day, however by teacher report, and undersigned therapist’s observation, his falls are currently rare. Layton has been wearing a soft helmet when he is outdoors at school (on the playground and in the halls). Layton has been able to walk with the undersigned PT from his classroom, to the far end of school and back, with supervision to handheld assistance. Layton is able to walk on the yellow lines (with helmet on) with minimal verbal cuing. He is able to walk at a good pace, and has only had rare stumbles (primarily when he stumbled on a doormat, but did not fall). Layton is able to ascend steps to the portable reciprocally with one railing, and is emerging in ascending the steps reciprocally without using the railing. He is able to descend the steps in a step to fashion, both with and without the railing. Layton is able to ascend and descend the ramp without the railing with verbal cuing to slow down by teacher report for ascent and observation of PT for descent. By Mrs. Stambaugh’s report, he is able to ride the tricycle independently with the helmet on. She reported that he has not had falls on the playground. Within the classroom, Layton does not wear the helmet. He sits in a wooden toddler chair with armrests to give some additional protection if he should have a seizure while sitting in his chair in the classroom. By teacher report, Layton is potty trained, and uses the standard toilet. She noted that he wears regular underwear, but still needs assistance with hygiene. Mrs. Stambaugh reported that he feeds himself with utensils. By report, Layton is a car rider in the am and pm, and does not currently need to negotiate bus steps. By Mrs. Stambaugh’s report, they go to the field at the front of the school for fire drills, and they hold Layton’s hand when they walk there. Mrs. Stambaugh reported that Layton only climbs on playground equipment with direct, close adult supervision. The PT report suggested that Layton continue to wear his soft helmet when on the playground or walking on campus, that he should be closely supervised on any playground equipment, and that he should not get overheated. His most recent IEP dated September 7, 2016, notes that Layton loves to dress up as a police officer or fireman, and loves to play with Legos and blocks. The IEP reflects that Mrs. Maloy has Layton on a waiting list for a regular Pre-K program. It also reflects that he no longer receives G-tube feedings at school because he is eating well. However, school staff has been trained to provide G-tube feedings to him in case Layton will not eat or drink his Pediasure. Testimony of Layton’s parents is consistent with the mental and physical abilities detailed in the school records. Mrs. Maloy is able to understand Layton and attend to his needs when he communicates with her. Although Layton tends to prefer a certain food repetitively for breakfast, lunch, and dinner, he eats regular food and his G-tube is used as a supplemental feed. Layton continues to have a seizure disorder for which he continues to be followed by Dr. Andrews and continues to take medicine. Mr. Maloy plays catch with Layton, and takes him to the water park. Mr. Maloy sometimes feeds Layton food from his own plate including meats and vegetables. NICA retained Dr. Donald Willis, a physician who is board-certified in maternal fetal medicine and obstetrics and gynecology. Dr. Willis reviewed the medical records related to Layton’s birth to determine whether Layton sustained an injury to the brain or spinal cord caused by oxygen deprivation or mechanical injury in the course of labor, delivery, or resuscitation in the immediate post-delivery period. In a report dated September 2, 2014, Dr. Willis referenced relevant parts of Layton’s records and stated in pertinent part: The mother was admitted at 39 weeks in labor with spontaneous rupture of the membranes. Amniotic fluid was clear. The fetal heart rate (FHR) monitor during labor was reviewed. The FHR had a normal baseline rate of 130 bpm on admission and normal heart rate variability. Late and variable FHR decelerations began about 90 minutes prior to delivery. This pattern was followed by a period of exaggerated FHR variability with some improvement in the overall pattern prior to delivery. Cesarean section was done for “intolerance to labor.” Birth weight was 3,319 grams (7 lbs 5 oz’s). The baby was not depressed at birth. Apgar scores were 9/9. The baby came out crying and required no resuscitation. The baby was taken to the normal newborn nursery after delivery. Umbilical cord blood gas was not done. Newborn hospital course was uneventful. The baby was discharged home with the mother two days after delivery. The baby apparently did well until about two weeks after birth, when some twitching movements were noted. Seizure activity was diagnosed. Head MRI at four months of age showed generalized volume loss. In summary, Cesarean section was done for a non-reassuring FHR pattern during labor. The baby was not depressed at birth and had a normal hospital course with discharge home two days after birth. Medical records suggest the baby did not suffer a birth related injury. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical injury to the baby’s brain during labor, delivery or the immediate post delivery period. In a deposition on February 24, 2015, Dr. Willis testified as to typical findings in an infant who suffered oxygen deprivation. If a stroke is caused by hypoxic injury to the baby during labor and delivery, then the entire brain is going to be affected by the hypoxia. “I mean, we don’t see an isolated stroke in a baby like of one small, little area in the brain due to hypoxic injuries during labor and delivery.” Normally, babies born with hypoxic brain injury are depressed at birth. Layton’s Apgar score was 9 at one minute and 9 at 5 minutes, and was not depressed at birth. He noted that the hospital progress notes stated that the baby came out crying and was vigorous, and went to the normal nursery. Two days after birth, the hospital notes stated that the newborn was progressing as expected. And, he noted that the baby was discharged home after two days, which is a routine time for discharge. When asked whether the fetal heart tracing was consistent with an in utero stroke, Dr. Willis testified that “well I don’t know that a tracing can tell me if a baby had a stroke in utero.” He further explained: A: I have been reviewing cases for NICA for 14, 15 years, and what I look at is oxygen deprivation that occurs during labor or delivery that results in brain injury. And those babies, as we said, are going to have problems at birth and be depressed. I have not considered a stroke that occurs spontaneously during labor as a hypoxic event resulting in brain injury. Q: Well -- A: I am not the judge. I’m just -- I’m just the doctor that’s reviewing the cases here, but that’s how I review them and that’s what -- and that’s how I reviewed the NICA case and that’s my interpretation of what it means by oxygen deprivation with brain injury. Q: Well, I want to go over that again then. An ischemic stroke occurring in utero during labor will cause oxygen deprivation to the part of the brain that’s affected by the ischemia, correct? A: That’s correct. Q: Okay. And as you sit here today, you’re not familiar with any such pathology, an intrauterine stroke occurring during labor not caused by hypoxia? A: I’m sure all things can occur, but for NICA, I read it as I stated. I mean, if you had a stroke due to the -- that wasn’t due to oxygen deprivation, again, where would you place when that stroke occurred if there’s no event to show you that here’s where the stroke occurred? I can’t say that the baby had a stroke during labor because an MRI afterwards shows the baby had brain injury. I don’t know where that stroke occurred. The only thing I can do is look at the fetal heart rate tracing and the baby after birth and the newborn course and try to determine if that baby had oxygen deprivation sufficient enough to cause brain injury. And that’s what I’ve done on my report. If baby had a stroke that you’re talking about, who knows -- you know, how would you -- I have no way of telling where or when that would have occurred if you have a stroke that leaves a baby without symptoms, because all the ones we see due to oxygen deprivation, those babies are depressed at birth. When asked whether Ephedrine poses a risk of harm to a baby, he replied “no.” When asked whether tachycardia can cause a stroke, he replied, “Tachycardia does not cause stroke as far as I’m aware.” When asked whether there is any way from reviewing an MRI to be able to tell when an injury occurred, he replied, “no.” Dr. Willis’ opinion that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor or delivery is credited. NICA also retained Dr. Michael Duchowny to evaluate Layton. Dr. Duchowny is board-certified in pediatrics, neurology, with special qualifications in child neurology, and in clinical neurophysiology. He is a senior staff attending at Nicklaus Children’s Hospital, and directs the neurology training program. Dr. Duchowny reviewed Layton’s medical records and performed an independent medical examination on Layton on January 7, 2015. In a medical report dated January 11, 2015, Dr. Duchowny expressed the following opinions: In Summary, Layton’s neurological examination is only significant for mild generalized hypotonia with oromotor dysfunction and an indwelling G-tube. His motor and cognitive development are both in the 18-24 months range which places him at a mild level of disability. He is doing well from the social and behavioral domains with no specific focal or lateralizing findings of significance. This examination therefore does not provide support for the presence of either a substantial mental or motor impairment. Review of the medical records reveals that Layton was born at 39 weeks gestation at Lakeland Regional Medical Center. He weighed 3320 grams at birth and had Apgar scores of 8 & 9 at 1 and 5 minutes. He was ultimately discharged in stable condition on day 3 of life. As documented by his mother, he was diagnosed with neonatal seizures which have persisted to the present time. Most of his current issues are related to a chronic medically resistant seizure disorder. Of note, Layton has never received pyridoxine, pyridoxal-5-phosphate or biotin. Layton’s MRI scan on January 3, 2013 was significant for prominent extra-axial spaces and generalized volume loss. There is no mention of a right frontal infarct pattern. I have not personally reviewed the scan. In view of Layton’s overall developmental progress, I do not believe he should be considered for inclusion within the NICA program. Dr. Duchowny routinely reviews and interprets brain imaging studies as a daily part of his practice. He explained that the MRI is the gold standard in terms of diagnosis of stroke, and that FHR tracings are of no clinical significance in diagnosing a stroke. Had Layton suffered a stroke during labor and delivery or at any time, Dr. Duchowny would expect to see findings of that on the neuroimaging studies performed on Layton’s brain. He did not see any clinical evidence of a stroke on any of the brain MRIs he reviewed. Dr. Duchowny attributes Layton’s seizure disorder to developmental abnormalities in his brain which were acquired in utero. He attributes Layton’s mild generalized hypotonia (low muscle tone) and oral-motor dysfunction (which has necessitated a G-tube for supplemental feeding) to prenatally acquired Cerebral Palsy. When asked about Dr. Ferreira’s use of the term “volume loss” regarding the January 2013 MRI, Dr. Duchowny disagrees that there was volume loss and noted an asymmetry of the ventricles. “It certainly is not a stroke.” Regarding his physical examination of Layton, Dr. Duchowny described Layton’s motor and cognitive development to be in the mild range of delay. He noted that there were “no local or lateralizing findings as one might expect to see in a stroke.” He described his findings to be consistent with a toddler with developmental delay. Dr. Duchowny described Layton as very sociable, noting his behavior to be “appropriate.” He described Layton as a “very cute boy” who is very interactive and progressing well in the social and behavioral domains. He noted that while Layton was poorly coordinated, he could take steps and walked into the examination room. He had a “button” on the left side of his abdomen for the G-tube. He also noted that in reviewing Dr. Andrews’ records, she initially noted “suspicion of perinatal or prenatal stroke” but that notation did not carry throughout her notes over time. That is, while she considered it, she did not diagnose Layton with a stroke. This is consistent with Dr. Andrews’ testimony. Moreover, when asked about Dr. Casadonte’s notation of “concern for intrauterine stroke,” Dr. Duchowny understands that to mean prenatally acquired. When asked if it is medically probable that based on his records review, his examination of Layton, and his review of the imaging studies, whether Layton suffered a stroke during labor and delivery, Dr. Duchowny replied, “No, I don’t believe so.” Dr. Duchowny’s opinion in this regard is credited. Dr. Duchowny wrote a supplemental report dated September 19, 2016, which addressed Layton’s February 9, 2015, MRI study. This report was one page in length and reads as follows: Pursuant to your request, I reviewed the MR imaging study on Layton Maloy performed on February 9, 2015, at All Children’s Hospital. As you know, Layton has been imaged extensively in the past including head CT studies on September 24, 2012, March 7, 2013, and September 13, 2013, brain MR Imaging on Sept. 26, 2012, November 28, 2013 and February 9, 2015, and head ultrasound on October 18, 2012. The brain MR imaging study of February 9, 2015 is the most recent imaging performed to date and was obtained when Layton was 2 ½ years old. This study reveals no areas of abnormality in the cerebral cortex or subcortical white matter. The deep gray matter structures (basal ganglia and thalami) are also normal. The hippocampi demonstrate no abnormality. The lateral ventricles are enlarged and dysmorphic in appearance. The occipital horns are larger than the frontal horns and evidence a colpocephalic configuration. There is a ventricular asymmetry favoring greater enlargement on the left. The corpus callosum is borderline thin. The posterior fossa contents are abnormal and reveal ponto-cerebellar hypoplasia and vermian hypoplasia with compensatory enlargement of the fourth ventricle. In summary, these imaging findings are consistent with prenatally acquired brain malformations and provide no evidence for acquired brain injury due to either intra- partum mechanical injury or oxygen deprivation. In response to Dr. Duchowny’s one-page supplemental report, Petitioners requested Dr. Daniel Adler review the February 9, 2015, MRI report, as well as his earlier imaging reports. Dr. Adler is a pediatric neurologist who practices in New York City. It is Dr. Adler’s opinion that the images from the February 9, 2015, MRI report demonstrate a progressive loss of tissue in the white matter of Layton’s brain and are not the result of a congenital problem. He concludes that the images reflect brain injury that happened to the fetus due to intrauterine hypoxia, of a type not manifested by encephalopathy. At NICA's request, Jay Goldsmith, M.D., reviewed Layton’s medical records and the reports of all diagnostic and neuroimaging studies performed on Layton, as well as Mrs. Maloy’s labor and delivery records. Dr. Goldsmith is a neonatologist who is board-certified in Pediatrics and Neonatal-Perinatal Medicine. He practices neonatology and is a professor of pediatrics at Tulane University Medical School. He diagnoses strokes in babies as part of his clinical practice and has been practicing neonatology for approximately 40 years. In his deposition which took place on September 26, 2016, Dr. Goldsmith noted that at birth, Layton was a fairly vigorous baby with good Apgar scores. No abnormal brain function, or encephalopathy, was noted in the newborn period, and Layton went home with his mother after two days. Dr. Goldsmith explained: That’s, probably, the most important thing to rule out; an intrapartum deprivation of oxygen; if there’s no encephalopathy, for the most part, there’s no injury that occurred during labor and delivery; the person who is injured, or a baby who is injured in -- a fetus who was injured in labor and delivery will, certainly, in the overwhelming number of cases, show signs of that injury as a newborn; and demonstrate it as an encephalopathy. The one exception to that is perinatal arterial stroke; and so that’s what, basically, this case has come down to; Layton came back at two to three weeks of age with seizures; had a work-up; and subsequently, I think, seven brain imaging studies, none of which showed arterial stroke. Now, perinatal arterial stroke is a neuroradiological diagnosis, pure and simple; you can think about it; you can put it on your differential diagnosis; but if you don’t see a stroke on the images, there’s no stroke; and, in fact, as this process evolved, over two and a half years or so, the MRIs showed that Layton has a developmental, or genetic, anomaly of his brain that has, certainly, defined itself on the brain imaging. Dr. Goldsmith considers MRI to be the gold standard in diagnosing a stroke, which is consistent with Dr. Duchowny’s testimony. He further noted that Layton transitioned well from intrauterine to extrauterine, and explained that babies injured in the womb during labor and delivery do not make this transition well, would not be vigorous at birth, would be acidotic, and may need resuscitation. Dr. Goldsmith is also of the opinion that the findings of the 2015 MRI suggest a developmental anomaly of the brain, showing that his brain was slightly dysmorphic with no evidence of stroke. When asked whether he would expect to see evidence of a stroke on the MRI findings, he answered, “Yes; unfortunately, the brain does not regenerate,” noting that with an ischemic stroke, that area of the brain will die and will not regenerate. “We will see a hole in the brain in that area.” It is Dr. Goldsmith’s ultimate opinion “to an extraordinary high degree of certainty” that Layton did not suffer a stroke during labor and delivery, and that his injuries were not a result of a neurological injury caused by oxygen deprivation that occurred during labor and delivery. Dr. Goldsmith’s opinion in this regard is credited. While Dr. Goldsmith is of the opinion that Layton is permanently and substantially mentally and physically impaired, he would defer to a neurologist, especially one who has examined Layton, to make that determination. The dispute in this case centers on what, more likely than not, was the primary cause of Layton’s impairments. That is, did Layton suffer a stroke during his mother’s labor that resulted in oxygen deprivation to a specific portion of Layton’s brain which caused his disabilities or is it more likely than not that they were caused by a prenatally acquired congenital or genetic disorder acquired in utero. Secondly, did any such injury result in Layton becoming permanently and substantially mentally and physically impaired. The undersigned finds the testimony of NICA’s experts to be compelling. The greater weight of the evidence establishes through the opinions of Dr. Willis and Dr. Goldsmith, together with Dr. Duchowny, that there was not an apparent obstetrical event that resulted in loss of oxygen to Layton’s brain during labor and delivery that resulted in brain injury. Moreover, the record evidence does not support a finding that Layton is permanently and substantially mentally and physically impaired. His treating physician, Dr. Andrews, noted Layton’s improvements over time and was not of the opinion that Layton has a mental impairment. Moreover, Dr. Kornberg’s opinion that Layton is substantially impaired, while deferring to the pediatric neurologists, was based in large part on Layton’s required use of the G-tube for feeding. He has clearly improved in this regard and now uses the G-tube to supplement his eating and use of Boost or Pediasure. Dr. Duchowny’s opinion that Layton’s disabilities are in the mild range, and not considered to be substantial, is consistent with Dr. Andrews’ assessment, and is credited.
