STATE OF FLORIDA
DIVISION OF ADMINISTRATIVE HEARINGS
VANESSA M. ALICEA, on behalf of ) and as natural guardian of ) AIYMANI ARLYNNE EMMANUELLI )
ALICEA, a minor, )
)
Petitioner, )
)
vs. )
)
FLORIDA BIRTH-RELATED )
NEUROLOGICAL INJURY )
COMPENSATION ASSOCIATION, )
)
Respondent. )
Case No. 03-3657N
)
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 March 1, 2006, by video teleconference, with sites in Tallahassee and Jacksonville, Florida.
APPEARANCES
For Petitioner: Rodney S. Margol, Esquire
Margol & Pennington, P.A.
One Independent Drive, Suite 1700 Jacksonville, Florida 32202-5010
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 Aiymani Arlynne Emmanuelli Alicea, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
PRELIMINARY STATEMENT
On October 3, 2003, Vanessa M. Alicia, as the parent and natural guardian of Aiymani Arlynne Emmanuelli Alicea (Aiymani), 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 October 8, 2003, and on January 30, 2004, following an extension of time within which to do so, NICA responded to the claim, and gave notice that it was of the view that Aiymani 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.
A hearing to resolve whether the claim was compensable was initially scheduled for May 24, 2004; however, at the parties' request the hearing was canceled and the case was abated until May 24, 2005. Thereafter, the hearing was rescheduled for March 1, 2006.
At hearing, the parties stipulated to the facts set forth in paragraphs 1, 2, and 4 of the Findings of Fact, infra, and
Petitioner's Exhibits 1-10 and Respondent's Exhibits 1-16, were received into evidence.
The transcript of the hearing was filed March 16, 2006, and the parties were accorded 10 days from that date to file proposed orders. The parties elected to file such proposals and they have been duly-considered.
FINDINGS OF FACT
Preliminary findings
Vanessa M. Alicea is the natural mother and guardian of Aiymani Arlynne Emmanuelli Alicea, a minor. Aiymani was born a live infant on July 20, 2002, at Orange Park Medical Center, a hospital located in Orange Park, Florida, and her birth weight exceeded 2,500 grams.
The physician providing obstetrical services at Aiymani's birth was R. Roland Powers, 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."1 § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat.
Here, the parties have stipulated, and the proof is otherwise compelling, that Aiymani is permanently and substantially mentally and physically impaired. What remains to resolve is whether Aiymani's impairments resulted from an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period," as required for coverage under the Plan.
Aiymani's birth and immediate postnatal course
At or about 6:30 a.m., July 20, 2002, Ms. Alicea, with an estimated delivery date of July 15, 2002, and the fetus at 40 5/7 weeks' gestation, was admitted to Orange Park Medical Center, for induction of labor. At the time, it was noted that during her prenatal care (on June 18, 2002), Ms. Alicea had tested positive for Group B Streptococcus (GBS) in the vagina, and had been provided antibiotic treatment. Otherwise, her prenatal course was without apparent complication.
Upon admission, Ms. Alicea's membranes were intact; blood pressure was noted as 117/76; mild contractions were documented, at a frequency of 3-6 minutes, with a duration of 50-60 seconds; vaginal examination revealed the cervix at 1
centimeter dilation, 70 percent effacement, and the fetus at -2 station; and fetal monitoring revealed a reassuring fetal heart rate, with a baseline in the 140-beat per minute range. An IV was started at 7:20 a.m., antibiotics (Ampicillin) were started at 8:19 a.m., and Pitocin induction was started at 8:40 a.m.
Ms. Alicea's labor slowly progressed, and at
11:12 a.m., her membranes spontaneously ruptured, with a small amount of clear fluid noted. At the time, vaginal examination revealed the cervix at 3 centimeters dilation, 80 percent effacement, and the fetus at -1 station. Mild contractions continued to be documented, at a frequency of 2-6 minutes, with a duration of 50-60 seconds. However, beginning at 11:40 a.m., her contractions were noted as moderate, at a frequency of 2-4 minutes, with a duration of 60 seconds, and fetal monitoring continued to reveal a reassuring fetal heart rate, with a baseline in the 130 to 140-beat per minute range. Nevertheless, an occasional decrease in long-term variability was noted, as well as "subtle" late decelerations.
At 1:21 p.m., an epidural anesthesia was started; moderate contractions continued, at a frequency of 1.5-5 minutes, with a duration of 50-60 seconds; and by 3:41 p.m., vaginal examination revealed the cervix at 4 centimeters, 80 percent effacement, and the fetus at -2 station. In the interim, at 2:02 p.m., postepidural hypotension was noted, and
addressed intravenously with ephedrine (at 2:02 p.m., 2:18 p.m., and 2:24 p.m.). Fetal monitoring continued to appear reassuring, with a baseline in the 130 to 140/140 to 150-beat per minute range. However, occasional decreases in long-term variability were noted, and addressed with position change, oxygen by mask, and IV bolus.
Ms. Alicea's labor continued, with moderate contractions, and at 4:08 p.m., vaginal examination revealed the cervix at 5 centimeters, 80 percent effacement, and the fetus at
-1 to -2 station. At the time, while fetal monitoring was otherwise reassuring (with a baseline of 140-150 beats per minute, and short and long-term variability present), variable decelerations were documented. Amnioinfusion, to relieve umbilical cord compression, was started at 4:26 p.m., but variable decelerations persisted; by 5:53 p.m., long-term variability had decreased; by 6:08 p.m., accelerations were no longer documented; and at 6:40 p.m., variable late decelerations were noted. In the interim, maternal blood pressure had fallen, fetal heart rate baseline had risen to 150-beats per minute, and at 6:14 p.m., vaginal examination revealed an arrest of active labor (with the cervix at 5 centimeters, 90 percent effacement, and the fetus at -2 station), and at 6:40 p.m., fetal heart rate was noted as "150's - 170's" beats per minute. At the time,
Pitocin was discontinued, and intervention included position change, oxygen by mask, and IV bolus.
According to the labor and delivery records, at
6:44 p.m., Dr. Powers was called to come to labor and delivery, and notified of fetal tachycardia, decreased long-term variability, late decelerations and low maternal blood pressure (hypotension). On his orders, Ms. Alicea was given an IV bolus, terbutaline, and ephedrine, and Ms. Alicea was taken to the operating room for stat cesarean section, secondary to arrest of active labor and nonreassuring fetal rhythm. Notably, at
6:57 p.m., a portable external fetal monitor was attached, and at 7:00 p.m., revealed a fetal heart rate as "110's - 120's," beats per minute, with accelerations up to "140's for 50 seconds."
Ms. Alicea was noted in the operating room at 7:05 p.m., surgery started at 7:15 p.m., and Aiymani was
delivered by cesarean section at 7:20 p.m., with Apgar scores of
8 and 9, or 7 and 9, depending on which records are consulted, at one and five minutes respectively.2 Aiymani's delivery was described in Dr. Powers' Operative Report, as follows:
. . . the fetal vertex [was] delivered with a vacuum extractor. The oropharynx and nasopharynx were bulb suctioned after nuchal cord x1 was reduced. (This was a loose nuchal cord.) The infant was placed out of the field where it was continued to be bulb suctioned with clear fluid noted. Cord was
doubly clamped and cut. The infant was handed to the nurse practitioner for further care and treatment. Cord blood and cord pH obtained . . . .
According to the medical records, resuscitation efforts included blowby oxygen, as well as bulb and deep suctioning, and cord pH (arterial) was reported as 7.089, and below the reference range of 7.1 to 7.4.
Following delivery, Aiymani was transferred to the newborn nursery, where she was admitted at 7:30 p.m., and remained until she was discharged with her mother at 8:00 p.m., July 22, 2002. Initial examination on admission to the nursery was grossly normal, and her subsequent newborn course was uncomplicated and without evidence of neurologic compromise. Aiymani's subsequent development
Following discharge from Orange Park Medical Center, Aiymani's development was without apparent complication until November 20, 2002, when, at 4 months of age, Ms. Alicea voiced concerns to Aiymani's pediatrician (Daya Patel, M.D.) that Aiymani was not holding her head up and was not bearing weight on her legs.3 Dr. Patel diagnosed generalized hypotonia and motor developmental delay, and referred Aiymani for physical therapy. However, no diagnostic workup was undertaken at this point.
On February 20, 2003, Aiymani was admitted to Wolfson Children's Hospital on referral from her pediatrician for difficulty breathing. The Admission Admitting Note concluded:
IMPRESSION:
Respiratory infection with mild wheezing.
Severe generalized hypotonia of prenatal onset. Her wheezing seems to not require much in the way of treatment. Since she is on day 3, even if this is an RSV infection she seems to be handling it reasonably well. On the other hand, given her weakness and hypotonia, she will have to be watched more carefully. As far as the hypotonia, it is severe and early onset without detectable reflexes, the most likely cause would be spinal muscular atrophy Type I. Other possibilities would be severe cerebral palsy, myotonic dystrophy, hypothyroidism, congenital syndrome such as Prader-Willi or major CNS malformations. Primary muscle disease is possible as well as diseases of neuromuscular junction. We will involve Neurology early in this admission in order to be efficient in finding the diagnosis. We will do some basic labs and check the neonatal screening for thyroid problems. Other consultations will be obtained as suggested by Neurology.
As proposed, neurology was involved early in the admission when Daniel Shanks, M.D., of Nemours Children's Clinic, was called for consultation. Dr. Shanks evaluated Aiymani on February 21, 2003, and reported the results of his consultation, as follows:
REASON FOR CONSULTATION: Evaluation of hypotnoia
Mother reports that the decrease in overall movement pattern may date back to the third trimester, when she was poorly active in utero. They have been particularly concerned over the last 2 to 3 months with poor head control, poor movement patterns, and very prominent hypotonia. Her mother does report that perhaps she is a little more active over the last couple of months. She has been in physical therapy through Nemours in Orange park. No diagnostic workup has been undertaken to this point.
She cannot roll. She can left her legs against gravity to a limited degree. She has had good p.o. feeding. She has had no significant respiratory events other than the present URI symptoms, for which she is admitted. She has not been critically ill or hospitalized.
She is the 7 pound 4 ounce product of a term infancy [sic], that was generally unremarkable, other than the decreased movements. She was discharged by 2 days of age, and has had no significant hospitalizations, surgeries, or serious injuries.
* * *
FAMILY HISTORY:
There is no history of neurologic, neurodevelopmental or neuromuscular abnormalities, and specifically no history of infants with severe hypotonia.
REVIEW OF SYSTEMS:
Generally unremarkable, other than her low tone and movement patterns. She is alert, interactive. There are no constitutional,
HEENT, cardiac, respiratory, GI, GU, musculoskeletal, hematologic, endocrinologic, or immunologic concerns.
* * *
On physical examination, height 67 cm; weight 8.15 kg; head circumference 42.5 cm (50th percentile); weight for height is approximately 90th percentile. Generally, she is a well appearing, alert, socially interactive infant. She lays in a very hypotonic frog-leg posture. Anterior fontanelle is 1 x 2 cm and flat. Cranium appears normal. Neck is supple. There are no chest deformities. Abdomen is benign.
Extremities have full range of motion, no deformities or asymmetries, and in fact range of motion is mildly exaggerated due to the hypotonia. Back is without midline lesions, and no significant neurocutaneous lesions are noted.
NEUROLOGIC EXAM:
She is visually attentive and socially interactive. Cranial nerves: Pupils equal, round and reactive to light. Red reflexes are intact bilaterally. Extraocular movements are full and conjugate. Facial muscle movements are symmetric. She responds to auditory stimulation. There are no overt oral motor abnormalities and no fasciculations are noted in the tongue.
Motor exam shows profound hypotonia and apparent weakness. She has very minimal anti-gravity movement. She has little movement when trying to pull her extremity away from a noxious stimulus. She is areflexic. Sensory exam appears grossly intact, and there are no adventitial movements. She has essentially no head control and negative support reflex. She is hypotonic both truncally and peripherally.
She has limited mobility, in that she can do very little anti-gravity, and has no ability to get from one point to another.
IMPRESSION:
Likely profound hypotonia due to neuromuscular disease and anterior horn cell disease would be statistically the most likely. One cannot exclude other neuromuscular processes, however. I think it would be reasonable to send SMN DNA test to Athena, as well as to obtain baseline CPK and a nerve conduction study. Further evaluations can be based on these. If they are unrevealing, then proceeding to muscle biopsy and other metabolic work-up will be considered.
An MR Brain scan of February 21, 2003, concluded:
FINDINGS: Midline structures of corpus callosum, pituitary gland and cerebellar vermis are within normal limits. Mega cisterna magna is present. There is no mass effect or midline shift. The ventricles have a slightly undulating contour, particularly involving the bodies of the lateral ventricles. The periventricular white matter volume is decreased. Because of the patient's age of 7 months, bright signal is seen on the T2-weighted images in the periventricular and subcortical white matter, but this is expected for the degree of myelination at this age. It is difficult, therefore, to evaluate for true signal abnormality or normal lack of myelination at this age. The decreased white matter volume may represent periventricular leukomalacia. Imaging followup when the patient is 2 years of age or older is suggested to evaluate for periventricular white matter signal abnormality.
Mildly prominent extra-axial CSF spaces adjacent to the frontal and parietal lobes bilaterally is a normal finding for the patient's age . . . .
IMPRESSION:
Abnormal contour of the bodies of the lateral ventricles with decrease in volume of periventricular white matter as discussed above. Finding may be secondary to periventricular leukomalacia, although presence of signal abnormality in the periventricular white matter is difficult to assess at this age due to normal bright signal in the periventricular white matter from lack of myelination. Imaging followup is recommended when the patient is 2 years of age to determine presence of abnormal periventricular white matter signal.[4]
Mega cisterna magna.
No other structional anomalies are identified.
The myelination pattern of the white matter is compatible with the patient's age of 7 months.
A motor and sensory nerve conduction study of February 25, 2003, was reported normal for Aiymani's age, with "[n]o evidence of neuropathy at the sites tested."
Aiymani was seen at Nemours Children's Clinic for follow-up by Dr. Shanks on March 18, 2003. At the time, Dr. Shanks noted the following:
PE: . . . GENERAL APPEARANCE: alert,
healthy, not in distress. HEAD: atraumatic, normorcephalic. NECK: supple with full range of motion.
EXTREMITIES: no asymmetries or deformities. NEUROLOGICAL EXAM: On neurological exam,
. . . muscle tone was severely decreased in
extremities and trunk. There is little
antigravity movement and I suspect diminished strength. Deep tendon reflexes were absent bilaterally. Sensation
was normal to light touch.
IMPRESSION: Congenital hypotonia which is significant and appears associated with weakness. Neuromuscular hypotonia which most likely represents anterior horn cell disease. Unfortunately, the critical test is not paid by Medicaid. Athena (the only lab available for the test) is to be in touch with the family to see if arrangements can be made. Alternatively, we may have to proceed with muscle biopsy as another potentially confirmatory test. I will see her back when this is settled. She should continue with PT and oral feeding competence will need to be monitored.
Aiymani continued to be followed at Nemours Children's Clinic by neurology (Dr. Shanks, and following his retirement, Dr. David Hammond), genetics (Dr. Pamela Arn), and multiple Nemours sub-specialists. However, despite multiple studies, no etiology or unifying diagnosis for Aiymani's severe hypotonia and developmental delay was identified, and at no time did her treating physicians postulate that a likely cause for Aiymani's neurologic impairments was a brain injury (hypoxic or otherwise) suffered during the course of birth.
The parties' experts
Apart from the medical records related to Aiymani's birth and subsequent development, salient portions of which have been addressed supra, the parties offered the opinions of three physicians to address the likely etiology of Aiymani's
neurologic impairment. These physicians' statements were brief, and in written format. (Petitioner's Exhibit 1; Respondent's Exhibits 12-16).
Offered on behalf of Petitioner was the statement of Dr. James O'Leary, a physician board-certified in obstetrics and gynecology, and maternal-fetal medicine. Dr. O'Leary wrote:
I have evaluated the medical care rendered to Vanessa Alicea and her 7 pound, 4 ounce daughter. At this time, I am prepared to provide you with my opinions concerning the relationship of that care to the adverse outcome. These opinions are based on the standard care applicable at the time the events in this case occurred, namely 2002 and they are expressed in terms of a reasonable degree of medical certainty.
It is my opinion that the permanent neurologic damage sustained by her daughter, Aiymani, which left her brain damaged, occurred during the course of labor, on
July 20, 2002, because of the delay in proper treatment of postepidural hypotension and fetal distress which complicated her labor. In addition, Dr. Powers should have performed an emergency cesarean section much sooner.
The prenatal care was within accepted standards of care. The ultrasound examinations have excluded any possible intrauterine causes of brain damage.
The labor progress was not normal. The rate of dilation was abnormal. There was also an arrest of dilation at 5 cm/minus two station at 6:14 p.m. based upon SVE documentation.
Review of the fetal monitoring tracings reveals evidence of late decelerations and
an increasing baseline heart rate, variable decelerations and a decrease in the number of accelerations.
The standard of care required that the persistent hypotensive episode be rapidly treated and the Pitocin stopped. The failure to do this led to worsening of the fetal heart rate abnormalities, and the ultimate ischemic brain damage from persistent utero-placental insufficiency.
Had the physician and nurse midwife properly treated the hypotension and stopped the Pitocin, the fetal distress would have resolved and Aiymani's neurological injuries would not have occurred.
In contrast, Dr. Donald Willis, also an expert in obstetrics and maternal-fetal medicine, whose observations were offered on behalf of Respondent, wrote:
I have reviewed the medical records for the above named individual. The mother was a 20 year old admitted for induction of labor due to post dates. Cesarean delivery was done for a non-reassuring fetal heart rate pattern and failure to progress. Amniotic fluid was clear. The birth weight was 3,290 grams. The newborn was not depressed.
Apgar scores were 8/9. The baby was described as "term, pink, alert, strong cry." The newborn hospital course was uncomplicated and the baby was discharged home with the mother at 48 hours.
There was no apparent Obstetrical incident that led to this child's injury.
Stated otherwise, Dr. Willis concluded:
As such; it is my opinion that there was not an injury to the brain or spinal cord caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery,
or resuscitation in the immediate postdelivery period in a hospital as required by Section 766.302(2), Florida Statutes, for a claim to qualify for compensation under Sections 766.301 through 766.316, Florida Statutes.
Finally, Dr. Michael Duchowny, a physician board- certified in neurology with special competence in child neurology, and associated with Miami Children's Hospital, offered observations on behalf of Respondent. Notably, Dr. Duchowny examined Aiymani on January 14, 2004, and on
October 19, 2005, and based on the results of his examinations and review of the medical records, was of the opinion that Aiymani suffered a substantial mental and physical impairment. However, similar to Aiymani's treating physicians at Nemours Children's Clinic, Dr. Duchowny was of the opinion that Aiymani's neurologic impairments were most likely developmentally based, and not birth-related. Dr. Duchowny concluded:
. . . medical records provide [] no support for believing that Aiymani's neurologic impairments resulted from either oxygen deprivation or mechanical injury at the time of birth. [Moreover,] I believe that Aiymani most likely has ataxic cerebral palsy which was acquired prenatally and therefore do not believe that she is compensable under the NICA statute.
The likely etiology of Aiymani's neurologic impairments
Given the record, it must be resolved that the cause of Aiymani's neurologic impairments, while yet unidentified, was most likely developmentally based, as opposed to birth-related. In so concluding, it is noted that the medical records reveal that Aiymani was not depressed at birth and her immediate postnatal course was uneventful. Moreover, among the physicians who have examined or treated Aiymani, and were well qualified to address the cause of her impairments, there appears to be no disagreement that the likely cause of her impairments was developmentally based, and not birth-related. Consequently, Dr. O'Leary's opinion regarding causation is rejected, as unlikely. Moreover, given the studies that have been done to identify the cause of Aiymani's impairments, as well as the conclusion that the cause of her impairments was most likely developmentally based, Dr. O'Leary's observation that "[t]he [prenatal] ultrasound examinations have excluded any possible intrauterine cause of brain damage" is less than 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 Petitioner to demonstrate that Aiymani 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, Aiymani'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, Aiymani 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 Vanessa M. Alicea, as the parent and natural guardian of Aiymani Arlynne Emmanuelli Alicea, a minor, is dismissed with prejudice.
DONE AND ORDERED this 13th day of April, 2006, 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 13th day of April, 2006.
ENDNOTES
1/ The definition of "birth-related neurological injury" also includes an "injury to the brain . . . caused by . . . 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," as well as an "injury to the
. . . spinal cord . . . caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat.
However, in this case there is no contention or proof to support a conclusion that the infant suffered an injury to the brain caused by mechanical injury or an injury to the spinal cord.
Indeed, the parties have stipulated that the only issue is whether Aiymani's impairments were caused by an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period." (Prehearing Stipulation, filed
February 28, 2006; Transcript, pages 4-6.)
2/ The Apgar scores assigned to Aiymani 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. Here, according to the mother's labor and delivery records (Petitioner's Exhibit 5, Respondent's Exhibit 1), at one minute, Aiymani's Apgar score totaled 8, with heart rate, respiratory effort, and reflex irritability being graded at 2 each, and muscle tone and color being graded at 1 each. At five minutes, Aiymani's Apgar score was noted as 9, with heart rate, respiratory effort, muscle tone, and reflex irritability being graded at 2 each, and color being graded at
According to the newborn records (Petitioner's Exhibit 4, Respondent's Exhibit 5), at one minute, Aiymani's Apgar score totaled 7, with heart rate, respiratory effort, and reflex irritability being graded at 2 each, muscle tone being graded at 1, and color being graded at 0. At five minutes, Aiymani's Apgar score was noted as 9, and scored consistent with the labor and delivery records. Aiymani's Apgar scores were acceptable, and inconsistent with depression at birth.
3/ See Respondent's Exhibit 6, examinations of July 24, 2002, through November 20, 2002.
4/ An MR Brain scan without and with contrast was performed on June 14, 2005, and compared with the follow-up exam that had been recommended (and performed on August 3, 2004). The results of that brain scan were consistent with end stage periventricular leukomalacia, and reported as follows:
FINDINGS: Stable appearance of the corpus callosum which is intact but thin.
Pituitary gland and cerebellar vermis are within normal limits. Mega cisterna magna is identified with a stable configuration when compared to the prior study.
There is stable ventricular asymmetry with left lateral ventricle slightly larger than the right. There is an irregular configuration of the lateral walls of the lateral ventricles. The scalloped border of the lateral ventricles is secondary to loss of volume of the periventricular white matter and there is abnormal bright signal in the periventricular white matter bilaterally. Findings are compatible with end stage periventricular leukomalacia.
There is stable prominence of the cortical sulci and the extraaxial CSF spaces. They are symmetric in size. No focal parenchymal mass. No midline shift.
No abnormal configuration or signal intensity in the hippocampi.
Visualized paranasal sinuses and mastoid air cells are clear. The orbital structures are symmetric and within normal limits.
After contrast administration, no abnormal parenchymal or meningeal enhancement.
MR BRAIN/W/WO CONTRAST I
Unenhanced and enhanced MRI examination of the brain demonstrating stable configuration of end stage periventricular leukomalacia.
Remainder of the examination is unremarkable.
COPIES FURNISHED:
(Via Certified Mail)
Rodney S. Margol, Esquire Margol & Pennington, P.A.
One Independent Drive, Suite 1700 Jacksonville, Florida 32202-5010
(Certified Mail No. 7005 1820 0002 9840 6871)
Kenney Shipley, Executive Director Florida Birth Related Neurological
Injury Compensation Association 2360 Christopher Place, Suite 1
Tallahassee, Florida 32308
(Certified Mail No. 7005 1820 0002 9840 6888)
M. Mark Bajalia, Esquire Brennan, Manna & Diamond
76 South Laura Street, Suite 2110 Jacksonville, Florida 32202
(Certified Mail No. 7005 1820 R. Roland Powers, Jr., M.D. 1605 Kingsley Avenue Orange Park, Florida 32073 | 0002 | 9840 | 6895) |
(Certified Mail No. 7005 1820 | 0002 | 9840 | 6901) |
Sharon Jones, ARNP, CNM | |||
Orange Park Medical Center 2001 Kingsley Avenue Orange Park, Florida 32073 (Certified Mail No. 7005 1820 | 0002 | 9840 | 6918) |
Orange Park Medical Center 2001 Kingsley Avenue Orange Park, Florida 32073 | |||
(Certified Mail No. 7005 1820 | 0002 | 9840 | 6925) |
Charlene Willoughby, Director Consumer Services Unit - Enforcement Department of Health
4052 Bald Cypress Way, Bin C-75 Tallahassee, Florida 32399-3275
(Certified Mail No. 7005 1820 0002 9840 6932)
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 |
---|---|---|
Apr. 13, 2006 | DOAH Final Order | While the infant was substantially impaired, the proof demonstrated that the cause of her impairments was most likely developmentally based and not birth-related. Therefore, the claim is denied. |