STATE OF FLORIDA
DIVISION OF ADMINISTRATIVE HEARINGS
JEFFERY A. HESS AND JEANMARIE HESS, ON BEHALF OF AND AS PARENTS AND NATURAL GUARDIANS OF SAMUEL HESS, A MINOR,
Petitioners,
vs.
FLORIDA BIRTH-RELATED NEUROLOGICAL INJURY COMPENSATION ASSOCIATION,
Respondent.
)
)
)
)
)
)
)
) Case No. 06-0187N
)
)
)
)
)
)
)
FINAL ORDER
Pursuant to notice, the Division of Administrative Hearings, by Administrative Law Judge William J. Kendrick, held a hearing in the above-styled case on October 27, 2006, in
Jacksonville, Florida.
APPEARANCES
For Petitioners: Michael S. Sharrit, Esquire
Brown, Terrell, Hogan, Ellis, McClamma, Yegelwel, P.A.
Blackstone Building, 8th Floor
233 East Bay Street Jacksonville, Florida 32202
For Respondent: M. Mark Bajalia, Esquire
Brennan, Manna & Diamond
76 South Laura Street, Suite 2110 Jacksonville, Florida 32202
STATEMENT OF THE ISSUE
At issue is whether Samuel Hess, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
PRELIMINARY STATEMENT
On January 6, 2006, Jeffrey and Jeanmarie Hess, on behalf of, and as parents and natural guardians of Samuel Hess (Samuel), a minor, filed a petition (claim) with the Division of Administrative Hearings (DOAH) for compensation under the Plan.
DOAH served the Florida Birth-Related Neurological Injury Compensation Association (NICA) with a copy of the claim on January 18, 2006,1 and on April 5, 2006, NICA responded to the petition and gave notice that it was of the view that Samuel did not suffer a "birth-related neurological injury," as defined by Section 766.302(2), Florida Statutes, and requested that a hearing be scheduled to resolve whether the claim was compensable. Such a hearing was initially scheduled for September 6, 2006, but at the parties' request was rescheduled for October 27, 2006.
At hearing, Petitioners offered the testimony of Jeanmarie Hess, and Exhibits 1-34 (the parties' Stipulated Record) were received into evidence.
The transcript of the hearing was filed November 14, 2006, and the parties were accorded 10 days from that date to file
proposed orders or written argument. The parties elected to file such proposals and they have been duly-considered.
FINDINGS OF FACT
Stipulated facts
Jeffrey Hess and Jeanmarie Hess are the natural parents of Samuel Hess, a minor. Samuel was born a live infant on January 7, 2002, at St. Vincent's Medical Center, a licensed hospital in Jacksonville, Florida, and his birth weight exceeded 2,500 grams.
The physician providing obstetrical services at Samuel's birth was Karen D. Bonar, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes.
Coverage under the Plan
Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat.
Here, Petitioners are of the view that Samuel suffered such an injury. More particularly, Petitioners believe Samuel's neurologic impairments are the result of a brain injury caused by hydrocephalus, secondary to an intraventricular hemorrhage (diagnosed at six days of life), that was precipitated by oxygen deprivation (a hypoxic ischemic insult), and which occurred during labor and delivery. In contrast, NICA is of the view that Samuel's impairments are most likely developmentally based, as opposed to birth related, and that, whatever the etiology of Samuel's impairments, he is not permanently and substantially physically impaired.
Samuel's birth and immediate newborn course
At or about 12:55 p.m., January 7, 2002, Mrs. Hess, with an estimated delivery date of January 21, 2002, and the fetus at 38 weeks' gestation, was admitted to St. Vincent's Medical Center, following spontaneous rupture of the membranes, with clear fluid noted, at 9:00 a.m. On admission, mild, irregular contractions were noted; vaginal examination revealed the cervix at 2 to 3 centimeters dilation, 60 percent effacement, and the fetus at -1 station; and fetal monitoring was reassuring for fetal well-being, with a baseline of 120 to
130 beats per minute. Given rupture of the membranes, Mrs. Hess was committed to deliver, and she was admitted for pitocin augmentation.
Following admission, an IV was started at 1:48 p.m.; an epidural was placed at 3:56 p.m.; pitocin drip was started at 4:05 p.m.; Mrs. Hess was noted as pushing at 9:24 p.m.; and Samuel was delivered spontaneously at 10:24 p.m., with "Nu[cal]/Hand" (the umbilical cord wrapped around the hand) noted. In the interim, staring at or about 8:00 p.m., monitoring revealed, over time, late decelerations; marked decelerations with slow return to baseline; and evidence of a hypertonic uterus (starting at 9:24 p.m., and persisting, following periods of relaxation, until 10:22 p.m.), with exaggerated fetal heart rate variability. Such a pattern is consistent with fetal stress, and raises concerns regarding fetal reserves and adequate oxygenation. However, at delivery, Samuel was not depressed; did not require resuscitation; was accorded normal Apgar scores of 8 and 9, at one and five minutes, respectively, reflective of a healthy newborn2; and no abnormalities were observed at birth, except pronounced molding.3
Following delivery, Samuel was transferred to the nursery, and ultimately discharged with his mother on
January 10, 2002. In the interim, Samuel's newborn course was normal, except for evidence of mild jaundice (diagnosed the morning of January 9, 2002), which did not require light therapy. However, on discharge, instructions were given to
follow-up the next day at the Seton Center for a repeat bilirubin check.
As instructed, Mrs. Hess presented with Samuel at the Seton Center on January 11, 2002, for a repeat bilirubin check. At the time, Samuel was noted to be active, alert, and in no apparent distress; his temperature was recorded as normal (as it had been following delivery, and during his admission in the nursery at St. Vincent's Medical Center); his newborn examination, apart from evidence of jaundice, was within normal limits; and Mrs. Hess reported that Samuel had fed well.4
The results of the bilirubin test were obtained at or about 1:30 p.m., that afternoon, and called to a staff physician (Dr. Vaughn), who gave instructions to initiate phototherapy. Accordingly, later that afternoon, Samuel was put under the bilirubin lights at home, with instructions to monitor his temperature every two hours.
On January 12, 2002, Samuel recorded a temperature of 100.6, and on the instructions of Dr. Vaughn, Samuel was taken to the emergency room at Wolfson Children's Hospital for evaluation.5 There, Samuel was received at 6:35 p.m., and triaged at 6:42 p.m. Chief complaint was jaundice, and temperature was noted as 100.7, otherwise no abnormalities were observed. Samuel's physical examination and immediate hospital course were documented, as follows:
PHYSICAL EXAMINATION:
His temperature is 100.7 in the ER. The rest of his vitals are normal. His weight is 2.7 kg. He is resting, easily aroused. Anterior fontanelle is soft and flat, with normal sutures. Has good red reflexes bilaterally. Ear canals are patent. Nose without congestion. Oropharynx is clear, no cleft. Heart is normal S1 and S2 without murmurs. Abdomen is soft and nontender.
Chest is clear to auscultation. Extremities are without rashes, cyanosis, clubbing or edema. He does have good femoral pulses bilaterally, and no hip clicks.
Neurologically, he is alert and active . . . .
LABORATORY:
. . . Total bilirubin on admission was 14.2, direct was 0.5. He was tapped, and had a white count in his spinal fluid of 2,500 and red count of 241,250. He had 65 segs, 17 lymphocytes and 18 monocytes, and the spinal fluid Gram stain showed no organisms, but an occasional leukocyte.
IMPRESSION AND PLAN:
My impression is that we have a six-day-old with fever and abnormal leukocytosis in his spinal fluid. He was placed on ampicillin, and gentamicin . . . . He was also cultured for herpes [, which was negative]. He was started on Acyclovir 20/kilo q.8 hours. He will continue to feed. A repeat spinal tap was attempted to clear up the meningitis issue on two occasions; however, both times they were bloody. We, therefore, are going to obtain a head CT with contrast to rule out an intracranial bleed.
A CT of the head was done on January 13, 2002, and revealed a bilateral intraventricular hemorrhage (IVH) and a
left posterior parietal cephalohematoma.6 The CT scan was read, as follows:
FINDINGS: There is molding of the bones of the calvarium, compatible with recent vaginal delivery. Curvilinear area of increased density identified within the scalp soft tissues in the left posterior parietal region, compatible with a cephalohematoma. Increased densities identified within the lumen of the left lateral ventricle, predominantly involving the left choroid plexus, but also layering in the dependent portion of the lateral ventricle, compatible with intraventricular hemorrhage from the choroid plexus bleed.
In addition, increased density is identified in the dependent portion of the right lateral ventricle consistent with intraventricular hemorrhage. No extra axial fluid collections are identified. Linear area of increased density is identified in the right frontal region, only seen on images #11, and therefore likely not due to subarachnoid hemorrhage. The ventricular system is not dilated. No focal parenchymal mass is identified.
After contrast administration, there are no abnormal areas of parenchymal or meningeal enhancement identified.
IMPRESSION:
Left posterior parietal cephalohematoma
Bilateral intraventricular hemorrhage, left greater than right, with the left intraventricular hemorrhage due to choroid plexus bleed.
Molding of the bones of the calvarium compatible with history of recent vaginal delivery . . . .
Given the abnormalities reported on the CT scan,
Dr. Randell Powell, a neurosurgeon, was requested to see Samuel for neurosurgical input. That consultation occurred on
January 16, 2002,7 and was reported, as follows:
. . . I have been requested to see the child for neurosurgical input. I am informed that the baby is now doing well. Septic work-up was completely negative and antibiotics have since been discontinued and the baby is anticipating discharge later on today.
PHYSICAL EXAMINATION:
Reveals a beautiful, sleeping, male infant with a very soft head, a very soft fontanelle, no splitting of the sutures.
The head circumference is measured to be slightly less than the 50th percentile for a newborn. There is no nuchal rigidity and bending the legs did not appear to cause irritation as well. The child has a bilateral red reflex. Pupils are equal and reactive. The Moro reflex is symmetric.
Computed tomographic scan shows hemorrhage emanating from the choroid plexus and the trigone of the left lateral ventricle.
There is mild ventricular dilatation. Follow-up ultrasound shows similar findings.
IMPRESSION:
Intraventricular hemorrhage. DISCUSSION:
Intraventricular hemorrhages in the newborn perinatal period that are caused by choroid plexus hemorrhage generally have an excellent prognosis as no significant brain parenchyma is disrupted and these hemorrhages usually resolve without sequelae. However, there is roughly a 20%
chance of developing post hemorrhagic hydrocephalus which in 50% of cases could require more aggressive treatment. That means the baby's chances of needing neurosurgical intervention is somewhat less than 10% and this was discussed extensively with the parents who were happy to hear this news. There are no overt signs of hydrocephalus at this time and in my opinion I think that we can safely follow the baby with serial physical examination consisting of palpation of the fontanelle and head circumference measurements. I would be glad to see the baby at age one month for follow- up, but I suspect a good prognosis here.
Samuel was discharged from Wolfson Children's Hospital at 6:15 p.m., January 16, 2002, with instructions to monitor his head circumference once a week, and for follow-up appointments with Dr. Hamaty (his pediatrician at the time8) and Dr. Powell. Samuel's subsequent development
Following discharge, Samuel was followed by Dr. Powell for mild posthemorrhagic hydrocephalus, that appeared to stabilize, but then got worse between ages four and six months.9 Serial studies showed progressive ventricular enlargement consistent with hydrocephalus, and after discussing treatment options Samuel's parents elected to proceed with endoscopic third ventriculostomy, which was performed on August 26, 2002. Initially, Samuel appeared to be doing reasonably well, but then he developed an accelerated head circumference (53.8 centimeters, which placed him above the 98th percentile), consistent with progressive hydrocephalus, and on December 6,
2002, a Codman programmable ventriculoperioneal shunt was placed. Since that time, Samuel has done fairly well, without symptoms related to increased intracranial pressure. However, he continues to evidence macrocrania (above the 98th percentile), ventriculomegaly (enlargement of the laterial ventricules), and atrophy of brain tissue.10 (Exhibit 34).
Samuel's current presentation
With regard to Samuel's current presentation, the parties agree, and the proof is otherwise compelling, that Samuel is permanently and substantially mentally impaired.11 As for his physical presentation, while there may be room for disagreement, the complexity of Samuel's difficulties support the conclusion that he is also permanently and substantially physically impaired. In so concluding, it is noted that on the Vineland Adoptive Behavior Scales Form (VABS), related to daily living skills and motor skills, Samuel scored in the mentally handicapped range. "He is not yet toilet trained despite intensive efforts in this regard"; "[h]e is able to assist with simple dressing and undressing tasks but is not yet independent with these skills"; and he "continues to display gross-motor, fine-motor, visual-motor, and motor planning impairment." (Exhibits 18 and 30). It is further noted that Samuel presents with impaired postural control (aggravated by his large head), impaired strength, hypotonia, and bilateral pronatal feet. As a
result, Samuel has moderate to severe impairment in strength, endurance, postural control, balance responses (with unexpected falls), functional mobility, and activities of daily living.
Notably, at approximately five years of age, Samuel requires a stroller for extended outings, and caregiver assistance for
90 percent of self care needs. (Exhibit 10).
The cause of Samuel's impairments
As for the cause of Samuel's neurologic impairments, the proof demonstrates that, more likely than not, they are the result of a brain injury, caused by hydrocephalus, secondary to the intraventricular hemorrhage (IVH) he suffered, and which was diagnosed at six days of life. What remains to resolve is the genesis of Samuel's IVH or, stated otherwise, whether the proof demonstrated, more likely than not, that the IVH was caused by oxygen deprivation, and occurred during labor, delivery or resuscitation. § 766.302(2), Fla. Stat. ("'Birth-related neurological injury' means injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period."); Nagy v. Florida Birth-Related Neurological Injury Compensation Association, 813 So. 2d 155 (Fla. 4th DCA 2002)(The oxygen deprivation and injury to the brain must occur during labor, delivery, or immediately afterward.).
The genesis of Samuel's IVH
Regarding the intraventricular hemorrhage Samuel suffered, the proof is compelling that an IVH in a term infant, such as Samuel, is a rare occurrence, and its cause frequently cannot be identified. Indeed, among the physicians who addressed the issue, there is apparent agreement that the majority of IVHs (approximately 50 percent) are related to oxygen deprivation (hypoxia-ischemia) or trauma, and the remainder fall into one of two groups, those with another identifiable cause (such as vascular malformation, infection, clotting disorder, venous infarct, or genetic disorder) and those of unknown etiology (idiopathic).
To address the cause and timing of Samuel's IVH, the parties offered the deposition testimony of Julius Piver, M.D., J.D., a physician board-certified in obstetrics and gynecology (albeit one who has not practiced obstetrics for 20 years); Mary Edwards-Brown, M.D., a physician board-certified in radiology, with subspecialty certification in neuroradiology; David Hammond, M.D., a physician board-certified in pediatrics, neurology with special competence in child neurology, and clinical neurophysiology; Donald Willis, M.D., a physician
board-certified in obstetrics and gynecology, and maternal-fetal medicine; and Michael Duchowny, M.D., a physician board- certified in pediatrics, neurology with special competence in
child neurology, electroencephalography, and clinical neurophysiology.12 The testimony of Doctors Piver, Edwards- Brown, and Hammond were offered in support of Petitioners' view on causation, and testimony of Doctors Willis and Duchowny were offered in support of NICA's view on causation.
Pertinent to the issue of causation, Doctors Piver, Edwards-Brown, and Hammond were of the opinion that an infant can suffer a intraventricular hemorrhage during labor and delivery, as a result of a hypoxic-ischemic insult, and not show any clinical evidence in the immediate postnatal period. However, although offered the opportunity to do so, Dr. Hammond declined to offer an opinion as to the likely etiology (cause and timing) of Samuels IVH.13 Consequently, we are left to consider the testimony of Doctors Piver and Edwards-Brown with regard to Petitioners' view on causation.
As for the etiology of Samuel's IVH, it was
Dr. Piver's opinion, based on his review of the medical records, that Samuel's IVH was most likely caused by partial prolonged asphyxia, that was sufficient to cause a subtle, slow bleed during labor and delivery, which progressed to the significant IVH noted at 6 days of life, but that was initially insufficient to reveal itself (by clinical evidence of a bleed) in the immediate postnatal period.
In reaching his conclusion, Dr. Piver relied heavily on his evaluation of the fetal monitor strips, which he opined revealed, starting at 6:48 p.m. (18:48), and continuing for 30 to 35 minutes, evidence of marked loss of beat-to-beat variability; late decelerations at 8:01 p.m., 8:03 p.m.,
8:05 p.m., 8:25 p.m., 8:28 p.m., 8:31 p.m., and 8:33 p.m.; a
marked deceleration to a low of 70 beats per minute at
8:50 p.m., with a slow return to baseline at 8:56 p.m.; a marked deceleration from 180 beats per minute to 90 beats per minute between 9:14 p.m. to 9:20 p.m.; a late deceleration at
9:23 p.m.; and evidence of a hypertonic uterus starting at
9:24 p.m., and persisting to 9:42 p.m., again at 9:50 p.m., and persisting to 10:14 p.m., and again at 10:20 p.m. and persisting to 10:22 p.m., with exaggerated fetal heart rate variability.
While acknowledging the bleed could have started at any time between the 7th of January (Samuel's delivery date) and the 12th of January, when Samuel presented to Wolfson Children's Hospital, Dr. Piver was of the opinion, given his review of the fetal monitor strips, that Samuel's bleed was most likely caused by hypoxia, and that it began during labor and delivery.
Dr. Piver variously noted the likely onset of the bleed as "[b]etween 2030 and 2130 hours"; "around 2000 hours"; "from 2000 hours to 2130 hours"; "between 1800 and 2224 hours"; "between 1800 and 2100 hours"; and "the 21:24 to 22:20 time interval."
(Exhibit 23, pages 34, 48, 49, 57, 80, 82; Exhibit 23,
deposition Exhibit 6).
Dr. Edwards-Brown, like Dr. Piver, was of the opinion that Samuel's IVH was most likely caused by hypoxia, that caused a slow bleed during labor and delivery, but an insufficient bleed to reveal evidence of brain damage during the immediate postnatal period. Dr. Edwards-Brown's opinion was explained, as follows:
Q How are you able to determine, based on the films that you reviewed, that the hemorrhage began during labor and delivery?
A Based on the films alone, we can't make that determination. It's simply the path of physiology of the hemorrhages and the hospital course as well as the labor and delivery records that allow me to make that conclusion.
* * *
Q Are you able to look at the effect of the hemorrhage on the brain structures to determine or time when the hemorrhage may have occurred?
A What I see is a large hemorrhage wherein the ventricle that is pretty bright and that hemorrhage is causing hydrocephalus; and the hydrocephalus, I'm sure, is causing symptoms, but hemorrhages don't cause hydrocephalus initially. It takes some time before that occurs.
So all I can say is yes, the hemorrhage is having an effect on the brain, and that effect is hydrocephalus and ischemia, and it could have occurred sometime from the time
of labor and delivery until the time that film was obtained.
Q It could have occurred at any time in between there?
A. The hydrocephalus and the ischemia.
Q But not the hemorrhage?
A Certainly the hemorrhage could have occurred after birth, but I would have expected some evidence of that in the clinical history. I would have expected evidence that this child had suffered a profound hypoxic injury as one might see if this child had had a code or a profound drop in his oxygen status. None of that is in the record; therefore, I don't think it's a post natal event.
* * *
Q Okay. How are you able to rule out in this case that the hemorrhage did not begin on January 9th, 10th, 11th or 12th?
A Several things.
Number one, I don't have evidence on the 9th, 10th, 11th, or 12th of January that this child suffered any hypoxic injury.
Q Hemorrhage [can] be caused by something other than hypoxic injury?
A It can.
Q Okay, and what are the other possible causes?
A Intraventricular hemorrhage might result from a tumor, might result from a vascular malformation, it could result from an infection, but it usually results from hypoxia.
Q We sometimes do not know what causes intraventricular hemorrhage?
A I think when we don't know what causes intraventricular hemorrhage, it is a reasonable presumption that there was hypoxia at a time when someone was not looking, as in the prenatal or labor and delivery period. If there wasn't a fetal heart monitoring strip obtained during that period and the child is born with -- excuse me, with intraventricular hemorrhage, I think the presumption should be that there was hypoxia during that time. But certainly there may be some times when we don't have an answer.
Q Sometimes we simply don't know what caused the hemorrhage?
A That is undeniably true; however, one should not make that presumption until we have excluded the usual causes. And in this case, based on Dr. Piver's testimony that there was evidence of hypoxia during labor and delivery, one must assume that that was the cause. We don't make the diagnosis of an idiopathic cause. That means we don't have the answer when we have evidence of a reasonable cause, which we have here.
Q In your letter to Mr. Sharrit that we referred to earlier, you state on Page No. 2 further down that, "The absence of symptoms in the three days following birth is not unusual since bleeding begins small and increases with time."
What do you mean by that?
A That's the nature of bleeding. I'm sure you know this. We have all bled. You don't
-- Well, bleeding -- unless it's the result of an aneurism -- is not so massive initially. It starts out as a leak in the
vessels, and the longer it bleeds the more it accumulates . . . .
(Exhibit 27, pages 39, 41, 42, 44-46).
Contrasted with the opinion held by Doctors Piver, Edwards-Brown, and Hammond, Doctors Willis and Duchowny were of the opinion that if a hypoxic event is significant enough to cause an intraventricular hemorrhage during labor and delivery, there will be clinical evidence in the immediate newborn period.
Dr. Willis expressed his observations on the medical records, as well as the basis of his opinions on causations, as follows:
Q . . . Dr. Willis, in reviewing the records and the fetal heart tracings, were you able to identify any intervals, any intervals of concern, I suppose, or any that you thought that may have been hypoxic intervals?
A Well, the fetal heart rate monitor strip looks pretty good until about an hour and a half before delivery, and then there are fetal heart rate decelerations that pretty much continue until the time of birth.
Q And what was the significance of those intervals that you're talking about, to you?
A Well, the decrease in fetal heart rate usually means that there's some decrease in oxygen supply to the baby.
Q Okay.
A Or umbilical cord compression, which could lead to that same thing.
Q So are you saying you found intervals that were suspicious for oxygen compromise?
A That's correct.
Q Did you identify intervals of lack of beat-to-beat variability that you thought were of concern?
A Well, I'll look, but most of what I saw were fetal heart rate decelerations along with really exaggerated fetal heart rate variability, which usually you see with umbilical cord compression.
Q Well, are you saying, then, that there were episodes in this case where you felt there was significant cord compression?
A Well, the fetal heart rate tracing certainly is consistent with umbilical cord compression.
Q And over what time period would you say the fetal heart tracings are consistent with cord compression?
A Well, off and on for the last hour and a half prior to birth.
Q And could that create a scenario, an hypoxic scenario that could lead to some kind of vascular insult within the brain?
A Now, let me be sure I understand the question. Are you asking me if I believe this fetal heart rate pattern, the abnormalities that I see led to that or can abnormalities in fetal heart rate pattern in general lead to brain injury?
Q I guess my question would be, the pattern that you've identified in this case, is that consistent with a pattern that can lead to injury, vascular injury within the brain?
A Well, I think it shows that there's probably some lack of oxygen during that time period. Now, the question then is, you know, did that lack of oxygen lead to brain damage. And in this case, you know, my feeling is or my opinion is that it did not lead to brain damage.
Q Let's break that up a little bit. Without knowing, without looking at the final result -- I presume you're looking at the early neonatal period right after birth to help you make that conclusion. Am I correct?
A Yes.
Q If we for the moment put aside the early clinical course of the child, just by looking at the heart tracings and the patterns that you've identified, are those consistent with or perhaps suspicious for the kind of pattern that could lead to a fetal compromise, brain compromise?
A Well, I don't know if anyone could predict fetal brain damage simply based on a fetal heart rate pattern. You really have to look at the baby, the condition of the baby after birth to be able to say whether or not the abnormalities in the fetal heart rate pattern resulted in oxygen deprivation and brain injury.
* * *
Q Now, you did, no doubt, note that the child did return to the hospital after discharge and was found to have a bloody spinal tap, and ultimately it was determined that it had an intraventricular hemorrhage?
A That's correct. That's, I believe, on the fifth day after birth.
Q Well, having identified hypoxic consistent patterns within the fetal heart
tracings, how is it that you can say that perhaps did not lead to a vascular insult that slowly progressed over a period of four or five days into an extensive hemorrhage?
* * *
A . . . I think that it's pretty clear that if you're going to have an hypoxic injury to the brain that's substantial enough to cause brain injury then the baby really is going to be depressed at time of birth and is going to have an unstable newborn period.
Simply having an abnormal fetal heart rate pattern is not enough to say that any lack of oxygen that occurred during labor caused brain damage.
Q . . . And I guess you're saying across the board and without exception there can be no slowly progressing brain damage that can occur due to labor and delivery hypoxia?
A Well, in order to have an hypoxic event during labor or delivery that would be substantial enough to cause an hypoxic- related brain injury, then really the baby is going to have to be depressed at birth.
Now, I mean, you can have intracranial hemorrhages, choroid plexus bleeds in babies that have normal, spontaneous vaginal births with normal-looking fetal heart rate tracings. I mean, there are spontaneous hemorrhages that can occur during labor, delivery, at some point after the baby is born, in the newborn period.
But what I'm saying is that if you're going to have an intracranial hemorrhage due to an hypoxic event during labor or delivery, then the baby really should be depressed at time of birth and have an unstable newborn course.
Q When you say depressed after the birth, do you put any outer limit on the time frame during which the baby might become depressed?
A Well, usually, by the newborn -- by the immediate post-delivery period they mean immediately after birth and until the baby is essentially stabilized after birth. For instance, in this case the baby had Apgar scores of eight and nine, required no resuscitation at all.
So, you know, we really don't have anything to suggest that there's a problem in the immediate newborn period. And then during the hospital stay, other than the jaundice, the baby did not really have any problems. The baby breast-fed. It did not have any neurologic findings that were abnormal, didn't have renal failure, did not have seizures, you know, the types of things that we see with babies that suffer an hypoxic insult during labor or delivery.
* * *
Q I know that your opinion is that if an hypoxic event is significant enough to cause a brain damage, then you're going to have to necessarily see signs of depression at birth or shortly after birth. Am I stating that correctly?
A Very nicely.
Q Okay. What if we're not talking about brain damage or encephalopathy in the broad sense but we're just talking about a very small insult to one of the blood vessels in the brain that doesn't readily turn into brain damage but, rather, becomes a progressive problem over a period of several days? Is that a possible scenario?
A I guess most things are possible, but that seems unlikely to me.
Q It seems unlikely to you that you could have a weakening of a blood vessel or some injury that lessens the integrity of the blood vessel and that the brain damage is then latent and that's perhaps the reason why it would not negatively impact the early clinical course?
A Well, let me say -- and I think we kind of went over this before -- that you can have intracranial hemorrhages on babies that have no apparent problems at all during labor, delivery. Just for reasons unknown you can have intracranial hemorrhage and blood vessels can rupture.
But I guess what we're talking about is brain injury due to lack of oxygen or mechanical trauma. And my point being that if you're going to get a hemorrhage due to lack of oxygen or mechanical trauma, then the baby really should be depressed at time of birth
(Exhibit 28, pages 23-30).
Dr. Duchowny expressed his observations of the medical records, as well as his opinions on causation, as follows:
Q. Let me at this time suggest a brain injury pathway that has been offered by others in this case for Samuel Hess and ask you to comment on that.
Others have suggested that in this case there was labor and delivery hypoxia that resulted in a choroid plexus bleed and was associated with an isolated -- excuse me, where the blood was isolated -- the bleed was isolated within the ventricles during the pre-natal course and that that later produced hydrocephalus --
MR. BAJALIA: Pre-natal?
MR. SHARRIT: Yes, in the first few days after birth.
Q. Are you with me, doctor?
A. Yes, I am, but I think you mean post- natal course.
Q. I'm sorry, I'm sorry. I do. Thank you. Labor and delivery hypoxia, the choroid plexus bleed isolated within the ventricles during the post-natal course that later produced hydrocephalus and increased the internal cranial pressure that later after -
- well after discharge from the hospital resulted in periventricular white matter damage. Is that a reasonable interpretation for Samuel Hess' brain injury?
A. No.
Q. Why not?
A. There's no evidence of hypoxia.
* * *
Q. . . . [Y]ou don't think that they are a result of hypoxia because you don't discern evidence of hypoxia on the fetal monitor strips?
A. There are abnormalities on the fetal monitoring strips. As I said before, I don't think they are associated with hypoxia.
* * *
Q. I understand your testimony to the contrary, but if -- if it turned out that after reviewing Samuel's fetal monitor strips you decided that there was evidence of hypoxia, would that be a reasonable link to the hemorrhage that was diagnosed?
A. No, because Samuel didn't show any of the signs of hypoxia at birth so I don't believe he had any type of hypoxic damage.
* * *
Q. Do you not find any evidence at all of hypoxia on the fetal monitor strips?
A. I believe the fetal monitoring strips indicate some fetal stress and that's all.
Q. As opposed to distress?
A. It just shows stress to the fetus during the inter-partum experience. That's all.
Q. How do you define stress?
A. I think the decelerations indicate, you know, stress on -- you know, stress is being placed on the fetus.
Q. . . . [But] can't late decelerations be an indication of hypoxia?
A. It's possible.
Q. Could bradycardia in the 60 to 70 be[at]s per minute range be an indication of hypoxia?
A. It's possible but not necessarily.
* * *
Q. . . . If you have an intraventricular hemorrhage that you attribute to a hypoxic ischemic insult that resulted during the course of labor and delivery and late in delivery, as has been suggested in this case, wouldn't you expect to see some clinically recognizable neurologic dysfunction in the neonate during the immediate newborn period?
A. Yes, you would.
Q. Even if the hemorrhage was, to use opposing counsel's words, isolated?
A. Yes. If you're claiming that the neurologic problems are related to hypoxia, you would expect to see clinical signs of hypoxia at the time.
Q. Even if the hemorrhage was isolated?
A. Yes.
Q. Can you explain that?
A. You would see clinical manifestations in some way. You know, there would be some compromise in respiratory status, evidence of compromise in organ function because the lack of oxygen would affect not only the brain but other organ systems as well. You might see elevation of cardiac enzymes, liver enzymes, changes in renal function, changes in mental status, seizures, changes in blood pressure, respirations, etcetera.
Q. And just so I'm clear, that is true even if the hemorrhage was isolated just within the ventricle?
A. Yes, if you're attributing it to hypoxia.
* * *
Q. And based upon your review of the medical records, did you see any indication that Samuel had any such clinically recognizable neurological impairment or dysfunction during the immediate newborn period?
A. No, I did not.
Q. Did you note what his APGAR scores were?
A. Yes, I believe he had normal APGAR scores. I believe they were eight and nine and one at five minutes.
Q. Is that consistent with Samuel having suffered an isolated intraventricular hemorrhage that was the result of a hypoxic ischemic insult that occurred late in delivery --
A. No.
Q. -- labor and delivery?
A. I don't believe so.
Q. Is the fact that there was no documented evidence of impaired neurologic function in Samuel during the immediate newborn period consistent with Samuel having suffered an isolated intraventricular hemorrhage that occurred late in labor and delivery?
A. No.
(Exhibit 29, pages 17, 18, 20-23, and 36-39).
Here, there is no apparent reason to credit the testimony of Petitioners' witnesses on the issue of causation over the testimony of NICAs witnesses. Indeed, as among those who spoke to the issue of causation, Doctors Willis and Duchowny are the more qualified to address the issue, and their testimony
the more persuasive.
CONCLUSIONS OF LAW
The Division of Administrative Hearings has jurisdiction over the parties to, and the subject matter of, these proceedings. § 766.301, et seq., Fla. Stat.
The Florida Birth-Related Neurological Injury Compensation Plan was established by the Legislature "for the purpose of providing compensation, irrespective of fault, for birth-related neurological injury claims" relating to births occurring on or after January 1, 1989. § 766.303(1), Fla. Stat.
The injured infant, her or his personal representative, parents, dependents, and next of kin, may seek compensation under the Plan by filing a claim for compensation with the Division of Administrative Hearings. §§ 766.302(3), 766.303(2), and 766.305(1), Fla. Stat. The Florida Birth- Related Neurological Injury Compensation Association, which administers the Plan, has "45 days from the date of service of a complete claim . . . in which to file a response to the petition and to submit relevant written information relating to the issue of whether the injury is a birth-related neurological injury."
§ 766.305(4), Fla. Stat.
If NICA determines that the injury alleged in a claim is a compensable birth-related neurological injury, it may award compensation to the claimant, provided that the award is approved by the administrative law judge to whom the claim has been assigned. § 766.305(7), Fla. Stat. If, on the other hand, NICA disputes the claim, as it has in the instant case, the dispute must be resolved by the assigned administrative law
judge in accordance with the provisions of Chapter 120, Florida Statutes. §§ 766.304, 766.309, and 766.31, Fla. Stat.
In discharging this responsibility, the administrative law judge must make the following determination based upon the available evidence:
Whether the injury claimed is a birth-related neurological injury. If the claimant has demonstrated, to the satisfaction of the administrative law judge, that the infant has sustained a brain or spinal cord injury caused by oxygen deprivation or mechanical injury 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. 766.303(2).
Whether obstetrical services were delivered by a participating physician in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital; or by a certified nurse midwife in a teaching hospital supervised by a participating physician in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital.
§ 766.309(1), Fla. Stat. An award may be sustained only if the administrative law judge concludes that the "infant has sustained a birth-related neurological injury and that obstetrical services were delivered by a participating physician at birth." § 766.31(1), Fla. Stat.
Pertinent to this case, "birth-related neurological injury" is defined by Section 766.302(2), Florida Statutes,
to mean:
injury to the brain or spinal cord of a live infant weighing at least 2,500 grams for a single gestation or, in the case of a multiple gestation, a live infant weighing at least 2,000 grams at birth caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired. This definition shall apply to live births only and shall not include disability or death caused by genetic or congenital abnormality.
As the proponent of the issue, the burden rested on Petitioners to demonstrate that Samuel suffered a "birth-related neurological injury." § 766.309(1)(a), Fla. Stat. See also
Balino v. Department of Health and Rehabilitative Services, 348 So. 2d 349, 350 (Fla. 1st DCA 1997)("[T]he burden of proof, apart from statute, is on the party asserting the affirmative issue before an administrative tribunal.").
Here, the proof failed to support the conclusion that, more likely than not, Samuel's neurologic impairment was the result of a brain or spinal cord injury caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in the hospital. Consequently, given the provisions of
Section 766.302(2), Florida Statutes, Samuel does not qualify for coverage under the Plan. See also §§ 766.309(1) and 766.31(1), Fla. Stat.; Humana of Florida, Inc. v. McKaughan, 652 So. 2d 852, 859 (Fla. 5th DCA 1995)("[B]ecause the Plan . . . is a statutory substitute for common law rights and liabilities, it should be strictly constructed to include only those subjects clearly embraced within its terms."), approved, Florida Birth- Related Neurological Injury Compensation Association v.
McKaughan, 668 So. 2d 974, 979 (Fla. 1996).
Where, as here, the administrative law judge determines that ". . . the injury alleged is not a birth-related neurological injury . . . she or he [is required to] enter an order [to such effect] and . . . cause a copy of such order to be sent immediately to the parties by registered or certified mail." § 766.309(2), Fla. Stat. Such an order constitutes final agency action subject to appellate court review.
§ 766.311(1), Fla. Stat.
CONCLUSION
Based on the foregoing Findings of Fact and Conclusions of Law, it is
ORDERED the claim for compensation filed by Jeffrey and Jeanmarie Hess, on behalf of, and as parents and natural guardians of Samuel Hess, a minor, is dismissed with prejudice.
DONE AND ORDERED this 24th day of January, 2007, in Tallahassee, Leon County, Florida.
S
WILLIAM J. KENDRICK
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 24th day of January, 2007.
ENDNOTES
1/ The delay in serving NICA was occasioned by Petitioners' failure to submit the required filing fee until January 17, 2006.
2/ The Apgar scores assigned to Samuel are a numerical expression of the condition of a newborn infant, and reflect the sum points gained on assessment of heart rate, muscle tone, respiratory effort, reflex irritability, and color, with each category being assigned a score ranging from the lowest score of
0 through a maximum score of 2. See Dorland's Illustrated Medical Dictionary, 28th Edition, 1994. Here, at one minute, Samuel's Apgar score totaled 8, with heart rate, muscle tone, respiratory effort, and reflex irritability being graded at 2 each, and color being graded at 0. At five minutes, Samuel's Apgar score totaled 9, with heart rate, muscle tone, respiratory effort, and reflex irritability being graded at 2 each, and color being graded at 1.
3/ At birth, Samuel was described as a "conehead" or as having a head similar in shape to that of a football.
4/ See the two-page record of Infant Assessment, dated
January 11, 2002, St. Vincent's Medical Center Seton Center for Women's & Infant's Health, included in Exhibit 6.
5/ Fever is a nonspecific symptom, but is consistent with, inter alia, infection and intraventricular hemorrhage.
6/ A "cephalohematoma" is "a subperiosteal hemorrhage limited to the surface of one cranial bone, a usually benign condition seen frequently in the newborn as a result of bone trauma." See "cephalhematoma," Dorland's Illustrated Medical Dictionary, 28th Edition, 1994. See also Exhibit 23, pages 76 and 77.
7/ Dr. Powell's Consultation Report notes the date of consultation as January 17, 2002. However, that notation is evidently a scrivener's error, since the medical records clearly date his consultation to have occurred on January 16, 2002, before Samuel's discharge at 6:15 p.m.
8/ Dr. Hamaty provided pediatric care until July 10, 2002, and, insofar as the record reveals, Kenneth Horm, M.D., provided pediatric care starting on July 1, 2002. (Exhibits 6 and 8).
9/ Samuel's head circumference was within normal limits until age four months, but by six months it was at the 90th percentile. Head ultrasound on February 11, 2002, revealed "[p]rogressive increase in ventricular size," and a brain MRI on May 28, 2002, revealed "[i]terval dilation of the lateral and third ventricles with moderate to severe dilation of the lateral and third ventricles with normal caliber of the fourth ventricle, . . . consistent with hydrocephalus with no transependymal migration of fluid." Follow-up head ultrasound on July 2, 2002, was reported, as follows:
Sonographic evaluation of the intracranial contents performed via the anterior fontanel and compared with 02/11/02 previous head ultrasound, and compared with 05/28/02 brain MR.
Lateral and third ventricles are quite dilated, with thinning of the cerebral hemisphere parenchyma. The ventricles have definitely increased in size since the prior ultrasound and appear larger than on the MR, but direct comparison with the MR is difficult. No acute intracranial
hemorrhage. Echogenic material in the ventricles is probably partially . . . choroid although old clot is possible as well as previous intraventricular hemorrhage has been documented. No extra-axial collection. No acute intracranial hemorrhage and no midline shift. Posterior fossa normal.
10/ Samuel was last evaluated by Dr. Powell on May 21, 2003, and has since been followed by Hector James, M.D., a pediatric neurosurgeon associated with the University of Florida, Health Science Center, Jacksonville, Florida. (Exhibits 7 and 15).
11/ Samuel has a myriad of deficits, including significant cognitive, behavioral, emotional, and language impairments that have persisted despite intensive therapy. These deficits include mentation, problem solving, information processing, comprehension and reasoning skills, as well as attention and behavioral problems. (Exhibit 30).
12/ See, e.g., Wausau Insurance Company v. Tillman, 765 So. 2d 123, 124 (Fla. 1st DCA 2000)("Because the medical conditions which the claimant alleged had resulted from the workplace incident were not readily observable, he was obligated to present expert medical evidence establishing that causal connection."); Ackley v. General Parcel Service, 646 So. 2d 242 (Fla. 1st DCA 1994)(determining cause of psychiatric illness is essentially a medical question, requiring expert medical evidence).
13/ In Petitioners' Proposed Findings of Fact, filed November 22, 2006, at page 7, Petitioners addressed
Dr. Hammond's refusal to offer an opinion regarding the cause of Samuel's IVH, as follows: "Due to hospital-employer policy, Dr. Hammond declined to offer a specific opinion regarding the origin of Sam's IVH." Notably, there is no citation to the record to support such statement, and nothing in Dr. Hammond's testimony to support such statement. (Exhibit 26).
COPIES FURNISHED:
(Via certified mail)
Kenney Shipley, Executive Director Florida Birth Related Neurological
Injury Compensation Association 2360 Christopher Place, Suite 1
Tallahassee, Florida 32308
(Certified Mail No. 7099 3400 0010 4399 2536)
M. Mark Bajalia, Esquire Brennan, Manna & Diamond
76 South Laura Street, Suite 2110 Jacksonville, Florida 32202
(Certified Mail No. 7099 3400 0010 4399 2529)
Michael S. Sharrit, Esquire
Brown, Terrell, Hogan, Ellis, McClamma, Yegelwel, P.A.
Blackstone Building, 8th Floor
233 East Bay Street Jacksonville, Florida 32202
(Certified Mail No. 7099 3400 | 0010 | 4399 | 2512) |
Karen Bonar, M.D. North Florida OB/GYN 1820 Barrs Street, Suite 310 Jacksonville, Florida 32204 | |||
(Certified Mail No. 7099 3400 | 0010 | 4399 | 2505) |
St. Vincent's Medical Center 1800 Barrs Street Jacksonville, Florida 32204 (Certified Mail No. 7099 3400 | 0010 | 4399 | 2499) |
Charlene Willoughby, Director Consumer Services Unit - Enforcement Department of Health
4052 Bald Cypress Way, Bin C-75 Tallahassee, Florida 32399-3275
(Certified Mail No. 7099 3400 0010 4399 2482)
NOTICE OF RIGHT TO JUDICIAL REVIEW
A party who is adversely affected by this Final Order is entitled to judicial review pursuant to Sections 120.68 and 766.311, Florida Statutes. Review proceedings are governed by the Florida Rules of Appellate Procedure. Such proceedings are commenced by filing the original of a notice of appeal with the Agency Clerk of the Division of Administrative Hearings and a copy, accompanied by filing fees prescribed by law, with the appropriate District Court of Appeal. See Section 766.311, Florida Statutes, and Florida Birth-Related Neurological Injury Compensation Association v. Carreras, 598 So. 2d 299 (Fla. 1st DCA 1992). The notice of appeal must be filed within 30 days of rendition of the order to be reviewed.
| Issue Date | Document | Summary |
|---|---|---|
| Jan. 24, 2007 | DOAH Final Order | The proof failed to demonstrate that the infant`s intrventricular hemorrhage was caused by oxygen deprivation, and that it occurred during labor and delivery. The claim is denied. |
