The Issue Did Respondent's failure to intervene in the post-operative period immediately after learning the CT scan results of Patient C.O. near midnight on April 12, 1997, constitute treatment that fell below the standard of care and that he failed to practice medicine with that level of care, skill, and treatment which is recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances, in violation of Section 458.331(1)(t), Florida Statutes?
Findings Of Fact Petitioner is the state agency charged with regulating the practice of medicine in Florida. Respondent is a licensed physician in the State of Florida at all times material to the times alleged in the Complaint, having been issued license number ME 0070668. Respondent, as of May 2001, is board-certified in the area of neurological surgery. On April 3, 1997, Patient C.O., a 50-year-old male, presented to an Otolaryngologist (ear, nose and throat surgeon) with complaints of right side nasal polyps. On April 7, 1997, Patient C.O.'s surgeon ordered a radiological consult and a Coronal CT (up, down, front and back) scan of the right maxillary sinus. The CT scan revealed "complete opacification (blockage) of the left frontal, right ethmoid, right maxillary sinus, as well as the right nasal cavity with complete opacification of right sphenoid sinus." On April 9, 1997, Patient C.O. underwent a surgical procedure to remove nasal polyps. The surgeon removed an extremely large right nasal polyp, measuring approximately 10 cm in length. After removing the large mass, the surgeon noted smaller polyps and removed these also. After removing the polyps, the surgeon noted a "large pulsatile mass," which he biopsied. Biopsy results indicated that the "mass" was brain tissue. During the course of this procedure, the patient's cribriform plate had been pierced. This plate forms a barrier between the nasal cavity and the base of the brain. As a result of this puncture, the surgeon had removed a portion of Patient C.O.'s brain. The surgeon requested an intraoperative consult with Respondent. The surgeon and Respondent talked by telephone and Respondent recommended sealing off the brain tissue with a surgical flap and packing. An arteriogram was performed on Patient C.O. to determine if bleeding was from an artery or vein. It was determined that the bleeding was from a vein. He also, recommended placing Patient C.O. in the neurological intensive care unit, which was done, and the patient was stabilized. A CT scan, ordered by the surgeon, noted a right frontal hemorrhage and pneumoncephalus (air at the top of the skull). On April 10, 1997, drainage was noted from the right nostril of Patient C.O. Respondent noted that drainage was suspicious for cerebrospinal fluid (CSF). Respondent then considered various options in order to stop the leakage of CSF. On April 10, 1997, Respondent performed a surgical procedure which placed a spinal drain in Patient C.O. to control the intracranial pressure and to permit an outlet for the CSF. Respondent was attempting to allow the rupture to the cribriform plate to heal on its own. On April 11, 1997, a CT scan revealed large areas of air in the frontal areas of the skull. On April 12, 1997, it was determined that the rupture of the cribriform plate had not healed on its own. Patient C.O. had persistent drainage from the right nostril. He was taken to the operating room for a direct intracranial surgical repair of the defect. A CT scan demonstrated an increase in the frontal hemorrhage, a large left subdural hematoma, and brain swelling. On the afternoon of April 12, 1997, Respondent performed a bi- frontal craniotomy on Patient C.O. to close off the leaking of spinal fluid from the brain in the area behind the patient's forehead (CSF leak). The surgery began at 12:15 p.m. and anesthesia was initiated at approximately 12:30 p.m. on April 12, 1997, and surgery concluded at about 5:00 p.m. The procedure involved making an incision across the top of the scalp, from ear to ear, gaining access to the brain by making incisions in the cranium, then lifting the brain to allow access to the cribriform plate. This was accomplished without incident. During the post-operative period, the anticipated reaction of the patient was to return to post-operative status, or to improve neurologically beginning within two hours after the surgery ended. During the course of post-operative care, Patient C.O.'s vital signs and neurological statistics were constantly monitored. Patient C.O. did not show any improvements several hours after surgery as would be expected, but began to show signs of neurological deterioration. Because Patient C.O. did not improve neurologically after the surgery, Respondent, at about 9:30 p.m. on April 12, 1997, ordered a CT scan to be done immediately. Patient C.O. was taken for his CT scan around 10:45 p.m. The CT scan report by radiologist at Florida Hospital was called in to the hospital unit at 11:50 p.m. on April 12, 1997. Respondent was at home in bed, sleeping, when he was paged. Respondent called in and was told by telephone of the "wet read" results of the CT scan by the neuroradiologist. After obtaining the CT scan report, Respondent disagreed with the neuroradiologist's recommendations, ordered the continuation of the interventions which he had previously ordered, and issued no new medical orders. The April 12, 1997, CT scan results were reduced to writing and showed the following findings, when compared to the CT scan taken of Patient C.O., on April 11, 1997: Noncontrast examination shows numerous abnormal findings. Compared to the 04/11/97 study acute left subdural hemorrhage is similar. There is a large intraparenchymal frontal hemorrhage that has a similar appearance . . . . DIFFUSE INTRACEREBRAL SWELLING PROBABLY WORSE IN THE POSTERIOR FOSSA. OBLITERATED FOURTH VENTRICLE. VENTRICLE SIZE SIMILAR. INCREASED BLOOD FRONTAL REGION. UNCHANGED SUBDURAL LEFT POSTERIOR PAREITAL REGION. VENTRICULAR SIZE STABLE. PNEUMOCEPHALUS UNCHANGED. INTRAVENTRICULAR BLOOD STABLE. At 5:15 a.m. on April 13, 1997, Patient C.O.'s neurological status took a significant turn for the worse. The patient was interbated, and all appropriate measures were taken to attempt to revive the patient. Patient C.O. lapsed into coma and was unable to breathe sufficiently for himself; he sustained respiratory failure and coma. In the early morning hours of April 13, 1997, Patient C.O's neurological status was discussed with his family, and the decision was made to execute a do-not- resuscitate order. The patient never recovered and died two days later on April 15, 1997. Petitioner alleges that the standard of care required Respondent to take some affirmative or new action to intervene post-operatively on the night of April 12 through 13, 1997, to determine the cause of the deterioration and prevent irreversible brain damage. In support of Petitioner's position with regard to Respondent's standard of care, it presented the testimony of Dean C. Lohse, M.D. Dr. Lohse is a board-certified neurosurgeon who is licensed to practice medicine in the State of Florida. Dr. Lohse is a similar health care provider to Respondent, and he qualifies as an expert witness under Florida law. Dr. Lohse testified that he had several criticisms of the manner in which Respondent managed Patient C.O.'s post-operative care. Dr. Lohse was critical of the manner in which Respondent reacted to the information which was provided to him regarding the CT scan which was taken on the night of April 12, 1997, and which was communicated to Respondent at approximately midnight on that same night. In response to this information, Dr. Lohse was of the opinion that Respondent should have initiated some new intervention, including returning Patient C.O. to surgery, initiating medications to reduce swelling, introducing a pressure monitor, or changing the position of the lumbar drain. However, during the course of cross-examination, Dr. Lohse conceded that he could not say whether a return to surgery would have resulted in a different outcome for Patient C.O. Likewise, he could not state to within a reasonable degree of medical probability whether the introduction of medications to reduce the swelling would have worked. He could not state within a reasonable degree of medical probability whether the placement of a pressure monitor would have created a different result. Finally, he conceded that the issue of changing the lumbar drain was best left to the clinical judgment of the physician who is presiding over the care of the patient. Respondent testified on his own behalf at the final hearing. Respondent explained the April 12, 1997, craniotomy which he performed. He also explained the course of treatment which was followed with Patient C.O. in the hours subsequent to the conclusion of the craniotomy. Respondent explained his rationale behind ordering a stat CT scan, and he described the basis for his response to the information received at that time. Respondent testified that although he considered a return to surgery based upon the information contained within the CT scan, he decided against this option, as performing another surgery would only have been for the purpose of removing additional portions of Patient C.O.'s brain, including areas of the brain which are designed to control significant elements of an individual's personality. Respondent made the determination at that time that performing another surgical procedure would likely have caused more harm than good. Respondent testified that brain swelling reducing medication had been introduced previously and that the introduction of more or different brain swelling-reducing medications would not have addressed Patient C.O.'s condition. Respondent testified that the placement of a pressure monitor would have been pointless, given the information which he was able to obtain during the course of the craniotomy procedure. A pressure monitor is designed to measure increased levels of pressure on the brain. Patient C.O. was suffering from the opposite problem. Patient C.O.'s brain was actually flaccid, suffering from an absence, rather than an overabundance, of pressure. Therefore, the placement of a pressure monitor was never considered, as it would not have been of any use under the circumstances. Respondent testified that there was no need to change the aspect of the lumbar spinal drain. The lumbar spinal drain in this particular case was adequately controlled, at 5 ccs per hour. Thus, the use of the spinal drain was appropriate under the circumstances. Respondent's testimony is credible. Respondent also presented expert testimony, via deposition, of R. Patrick Jacob, M.D. Dr. Jacob is a board- certified neurosurgeon who currently works at the University of Florida in Gainesville. Dr. Jacob testified as to his education, training, and experience. He is a similar health care provider to Respondent, qualifies as an expert under Florida law, and can render expert medical opinions regarding the applicable standard of care in this case. Dr. Jacob testified that in his opinion, to within a reasonable degree of medical probability, Respondent met the applicable standard of care. He addressed each of the specific criticisms raised by Dr. Lohse. He specifically rejected the idea that another surgical procedure should have been performed, stating that to do so would have done more harm than good. He rejected Dr. Lohse's contention that the introduction of additional medications to reduce swelling would have been appropriate. Dr. Jacob disagreed with Dr. Lohse's suggestion that the placement of a pressure monitor would have been appropriate under the circumstances of this case. Finally, Dr. Jacob took issue with Dr. Lohse's opinion that a change in the lumbar spinal drain was warranted given Patient C.O.'s condition. On cross-examination, Dr. Jacob testified that he felt that Respondent's response to the information contained within the April 12, 1997, CT scan was appropriate. He was then presented with hypothetical questioning regarding whether doing nothing in response to the information contained within the CT scan would have been appropriate. Dr. Jacob testified that doing nothing in response to the information contained within the CT scan report may have constituted a deviation from the accepted standard of care. However, according to Dr. Jacob's review of the records, and Respondent's testimony at the final hearing, it is apparent that a decision was made by Respondent to continue with the interventions which had already been initiated, which under the circumstances of this case constitutes an affirmative act by Respondent to address the treatment and care of Patient C.O. Dr. Jacob's testimony is both credible and persuasive. The evidence is not clear and convincing that Respondent failed to intervene in the post-operative period immediately after learning the CT scan results of Patient C.O. around midnight on April 12, 1997. Respondent did not fail to take appropriate action after learning the results of the CT scan at midnight on April 12, 1997. Respondent ruled out several options and elected to continue with the interventions already initiated. Therefore, Respondent did not fall below the standard of care for similarly situated neurosurgeons and his actions on April 12 through 13, 1997, did not constitute a failure to practice medicine with that level of skill, care, and treatment recognized by a reasonably prudent similar neurosurgeon as being acceptable under similar conditions and circumstances.
Recommendation Based on the foregoing, it is RECOMMENDED that the Board of Medicine issue a final order finding that Respondent has not violated Section 458.331(1)(t), Florida Statutes, and dismissing the Administrative Complaint. DONE AND ENTERED this 19th day of July, 2002, 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 19th day of July, 2002. COPIES FURNISHED: Michael R. D'Lugo, Esquire Wicker, Smith, O'Hara, McCoy, Graham & Ford, P.A. Post Office Box 2753 Orlando, Florida 32802-2753 Shirley J. Whitsitt, Esquire Agency for Health Care Administration 2727 Mahan Drive, Mail Stop 39-A Tallahassee, Florida 32308 William W. Large, General Counsel Department of Health 4052 Bald Cypress Way, Bin A02 Tallahassee, Florida 32399-1701 R. S. Power, Agency Clerk Department of Health 4052 Bald Cypress Way, Bin A02 Tallahassee, Florida 32399-1701 Tanya Williams, Executive Director Board of Medicine Department of Health 4052 Bald Cypress Way Tallahassee, Florida 32399-1701
The Issue At issue in this proceeding is whether Michael Chase Anwar, 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 Lisa Anwar and Saeed Anwar are the parents and natural guardians of Michael Chase Anwar (Michael), a minor. Michael was born a live infant on September 11, 1995, at Florida Hospital, a hospital located in Orlando, Florida, and his birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Michael was Jorge Jesus Lense, M.D., who was, at all times material hereto, a participating physician in the Florida Birth-Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Mrs. Anwar's antepartum course and Michael's birth At or about 12:48 a.m., September 11,1995, Mrs. Anwar was admitted, in labor, to Florida Hospital. At the time, her estimated date of confinement was noted as September 22, 1995, and her antepartum course was without apparent complication; however, the fetus was noted to be large for gestational age. Onset of labor was noted as 11:15 p.m., September 10, 1995, with spontaneous rupture of the membranes, and clear amniotic fluid noted. Mrs. Anwar's obstetrical course from admission through Michael's delivery at 1:55 p.m., September 11, 1995, is detailed in Dr. Lense's delivery notes, as follows: The patient . . . presented with spontaneous rupture of membranes since 2315 hours on September 10, 1995. She was in active labor on admission. She progressed through labor to 8 cm dilatation at which time she had a prolonged fetal heart rate deceleration lasting approximately four minutes to fetal heart tones of 70s associated with a tetanic uterine contraction lasting approximately four minutes. This was relieved with terbutaline 0.125 mg subcutaneously and 0.125 mg intravenously. Fetal heart rate returned to normal with good variability and accelerations. She was having mild to moderate variable decelerations. She allowed labor to progress. She progressed rapidly to the anterior lip of the cervix to complete and +1 station. Because the fetal heart rate tracing was reassuring she was allowed to progress spontaneously to reach complete dilatation. However, the variable decelerations progressively worsened. She had temperature elevation of 100.5 [to 101.4]. She was begun on ampicillin 2 grams intravenously for presumed chorioamnionitis [an inflammation of female membranes]. She began pushing second stage labor. The variable decelerations worsened, and the decision was made to shorten second state of labor with vacuum assist. A vacuum was applied after the bladder was empty, complete, complete +3 station. The fetal head was delivered to complete, complete and +4 with the vacuum. However, it was difficult to maintain an adequate suction on the vacuum secondary to the thickness of the fetal hair. However, the patient was able to deliver the infant spontaneously without difficulty. Double nuchal cord was reduced. The rest of the infant was delivered without difficulty . . . The cord was doubly clamped and cut. The infant was noted to have poor respiratory effort and tone at the time of delivery. The neonatal resuscitation team and the neonatal intensive care unit neonatologists were called to the delivery. . . . At delivery Michael was intubated due to apnea (failure of the newborn infant to initiate pulmonary ventilation), and required positive pressure ventilation. Apgar scores of 2 at one minute, 3 at five minutes, and 5 at ten minutes were noted. Chord pH obtained on delivery was noted as 7.01, representing severe acidosis. The Apgar scores assigned to Michael 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 Michael's Apgar score totalled 1, with heart rate being graded at 2, and respiratory effort, muscle tone, reflex irritability, and color being graded at zero. At five minutes his Apgar score totalled 3, with heart rate being graded at 2, color being graded at 1, and respiratory effort, muscle tone, and reflex irritability being graded at zero. At ten minutes his Apgar score totalled 5, with heart rate being graded at 2, respiratory effort, reflex irritability and color being graded at 1 each, and muscle tone being graded at zero. Such scores are abnormal, and consistent with perinatal depression. Michael's course and development subsequent to delivery Following resuscitation, Michael was transferred to the neonatal intensive care unit in guarded condition. After admission, positive pressure ventilation was continued, and he was placed on ventilatory support. A blood culture, complete blood count, urine wellcogen and RPR were obtained, and Michael was started on ampicillin and gentamicin to address the risk of sepsis or infection. Possible seizure activity was noted during the first day of life, with tonic-clonic movements of all four extremities, and he was loaded with phenobarbital. An electroencephalogram was obtained and read as an abnormal neonatal recording characterized by diffuse depression of background cerebral activity; however, no electrographic seizures or lateralized epileptiform discharges were observed, and motion and electrical artifact were noted to be present. Michael was extubated the morning of September 12, 1995, following which he was noted to be "breathing spontaneously, receiving oxygen via nasal cannula." However, overnight he was noted as "quite irritable, jittery, with back arching," and required occasional sedation with Fentanyl. A head ultrasound completed on September 12, 1995, revealed the following: THERE IS A SMALL BLEED IN CHOROID PLEXUS NOTED BILATERALLY. IT COULD BE WORSE ON THE RIGHT THAN ON THE LEFT. THE VENTRICLES ARE NORMAL IN SIZE. THERE IS NO INTRAVENTRICULAR BLEED. NO OTHER ABNORMALITY. IMPRESSION: SMALL CHOROID PLEXUS BLEED NOTED BILATERALLY, WITH THE LEFT BEING MORE EXTENSIVE THAN THE RIGHT. Stated differently, the ultrasound revealed a bilateral grade one intraventricular hemorrhage (IVH). Between the afternoon of September 11, 1995, and the afternoon of September 12, 1995, Michael's hematocrit was noted to drop from 46 percent to 29 percent. Hemoglobin likewise dropped from 15.6 to 10.0. Consequently, due to his anemic condition, Michael was transfused on September 12, 1995. On September 12, 1995, Michael was examined by a consulting physician, most likely to address his neurologic condition. That examination, by Prashant M. Desai, M.D., reported the following observations, impressions, and recommendations: PHYSICAL EXAMINATION GENERAL: Weight is approximately 3.5 kg. Head circumference was 36.75 cm. Anterior fontanel is soft. The infant is lying supine in an open warmer, receiving oxygen via nasal cannula. He looks healthy, well-developed and well-hydrated. No clear dysmorphic features are noted. No apparent significant congenital skin lesions. He is sleeping comfortably. When disturbed, he becomes jittery and extremely irritable. He is difficult to console. He arches his neck and back. He keeps his hands fisted, flexes the elbows, and displays hand tremoring. BACK & SPINE: Appear normal. EXTREMITIES: There is mild stiffness of the extremities. Reflexes are brisk. He will not allow flexion of his neck, and instead, he resists it by neck arching and back arching. He will transiently open his eyes. Face is symmetric. Tongue is midline. Gag reflex is present. IMPRESSION: FULL-TERM ONE-DAY-OLD NEWBORN INFANT WITH PERINATAL DEPRESSION AND HYPOXIC-ISCHEMIC ENCEPHALOPATHY. RECENT DROP IN HEMOGLOBIN AND HEMATOCRIT MAY INDICATE INTRACRANIAL HEMORRHAGE. SUBARACHNOID HEMORRHAGE IS POSSIBLE, AND WOULD BE COMPATIBLE WITH CLINICALLY NOTED NECK AND BACK ARCHING, JITTERINESS AND EXTREME IRRITABILITY. HE HAS BEEN LOADED WITH PHENOBARBITAL AND PLACED ON MAINTENANCE PHENOBARBITAL SECONDARY TO SOME SEIZURE-LIKE ACTIVITY YESTERDAY. ELECTROENCEPHALOGRAM SHOWS DIFFUSE DEPRESSION OF BACKGROUND CEREBRAL ACTIVITY. THIS WOULD BE COMPATIBLE WITH HISTORY OF PERINATAL DEPRESSION. RECOMMENDATIONS: Head computerized axial tomography scan when feasible. Continue Phenobarbital at 4-5 mg/kg/day in two divided doses. He may require p.r.n. sedation with Fentanyl, given his irritability. Obtain a repeat electroencephalogram prior to hospital discharge. Duration of anticonvulsant treatment will depend on his hospital course. If his seizures recur and, in particular, if his extreme irritability persists, a metabolic work-up might be indicated. A CT (computerized tomography) brain scan of September 13, 1995, was read as "probably within normal limits." The scan was read and reported as follows: FINDINGS: THE DURAL VENOUS SINUSES AND THE VEIN OF GALEN ARE RELATIVELY DENSE COMPARED TO BRAIN. THIS IS PROBABLY RELATED TO THIS CHILD'S AGE AND THE COMPARATIVE LOW ATTENUATION OF THE UNMYELINATED BRAIN. THIS APPEARANCE CAN ALSO BE SEEN WITH ELEVATED HEMATOCRIT. WHILE THIS CAN ALSO BE SEEN WITH DURAL SINUS THROMBOSIS, THIS WOULD IMPLY THAT THE ENTIRE DURAL SINUS SYSTEM AS WELL AS THE VEIN OF GALEN WERE THROMBOSED. THAT IS UNLIKELY IN THIS SITUATION ESPECIALLY SINCE NO ASSOCIATED PARENCHYMAL CHANGES ARE NOTED. NO FOCAL PARENCHYMAL ATTENUATION ABNORMALITY IS NOTED. IMPRESSION: THE EXAM IS PROBABLY WITHIN NORMAL LIMITS. THE POSSIBILITY OF AN ELEVATED HEMATOCRIT IS RAISED. On September 14, 1995, Michael was noted to have an increased temperature. To further address the risk of sepsis or infection he was accorded a regimen of Vanco and Claforan for three days. Blood culture, urine, and CSF (cerebrospinal fluid) studies were reported as negative. Phenobarbital was discontinued September 16, 1995, and ampicillin and gentamicin were discontinued September 18, 1995. All intervening culture studies were reported as negative. A repeat electroencephalogram of September 20, 1995, was read as a "mildly abnormal neonatal recording due to some mild diffuse suppression of background cerebral activity." However, consistent with improvement in Michael's status, the recording was noted to be "considerably improved from [the] previous electroencephalogram performed on day 1" of life. On September 25, 1995, Michael had a second CT brain scan.1 That scan, unlike the first scan, was apparently read as abnormal, reflecting a presentation consistent with hypoxic- ischemic encephalopathy2 or, stated differently, brain injury occasioned by oxygen deprivation. (Discharge Summary for Michael Anwar, at page 2). Michael was discharged at 4:45 p.m., September 25, 1995, to the care of his parents.3 At the time, he was noted to exhibit "diffusely poor tone" ("infant limp, floppy tone"), and "little spontaneous movement" or, stated differently, "little spontaneous arousal." However, positive suck, positive blink, and positive gag were present, and Michael was free of seizure activity. Discharge diagnosis was, as follows: DISCHARGE DIAGNOSIS: 35 weeks appropriate for gestational age male Perinatal depression Sepsis, ruled out Seizures, ruled out Hypoxic-Ischemic Encephalopathy Bilateral Grade 1 Intraventricular hemorrhage Anemia On February 27, 1998, following the filing of the claim for compensation, Michael was examined by Michael Duchowny, M.D., a board certified pediatric neurologist. Dr. Duchowny's examination revealed the following: PHYSICAL EXAMINATION reveals a small 2 1/2 year old, appropriately proportioned boy. The weight is 25 pounds. The skin is warm and moist without neurocutaneous stigmata. There are no gross dysmorphisms. No digital, skeletal or palmar abnormalities are noted. The head circumference measures 48.6 centimeters which approximates the 3rd percentile for age. There are no cranial or facial anomalies or asymmetries, and the fontanels are closed. The neck is supple without masses, thyromegaly or adenopathy and the cardiovascular, respiratory and abdominal examinations are normal. NEUROLOGIC EXAMINATION reveals an alert boy who is socially interactive and has only a few words. There is an abundant amount of babbling sounds which suggest the emergence of speech patterns. Michael is in fact able to identify all of his body parts and knows both primary and secondary colors. He is quite alert and his socialization skills are well developed. He maintains good central gaze fixation with conjugate following movements and the ocular fundi are normal. There are full and conjugate extraocular movements with blink to threat from both directions. There are no significant facial asymmetries. The tongue movements are poorly coordinated and drooling is a prominent feature. Motor examination reveals a static generalized hypotonia with a dynamic increase in tone and bilateral upper extremity posturing. Michael is grossly ataxic [uncoordinated], both for axial and appendicular musculature [both truncal stability as well as all four limbs (arms and legs)] and his gait shows marked instability and a tendency to fall in all directions. Romberg sign could not be tested. He is unable to perform alternating movement sequences and he had poor dexterity for individual finger movements. The DTR's are present and 2 to 3+ bilaterally and plantar responses are downgoing. Sensory examination is intact to withdrawal of extremities to touch and pin, and a neurovascular examination discloses no cervical, cranial or ocular bruits. There are no temperature or pulse asymmetries. IN SUMMARY: Michael's neurologic examination reveals findings consistent with ataxic cerebral palsy. I believe that his cognitive and social skills are actually quite good but [are] restricted as a result of his motor deficit. I suspect that Michael will continue to improve in the future and that he will walk independently within the next 12 to 18 months. The dispute regarding compensability Given the proof, it cannot be subject to serious debate that Michael suffered an injury or anomaly in brain development that has resulted in neurologic impairment. What remains to resolve is the cause and timing (genesis) of the event which led to Michael's anomalous brain development or, more pertinent to these proceedings, whether the proof demonstrates, more likely than not, that the anomaly Michael suffers was "caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period," as opposed to some other genesis. Section 766.302(2), Florida Statutes. Also at issue is whether, if such an injury occurred, Michael was rendered "permanently and substantially mentally and physically impaired." Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Here, the nature and significance of Michael's impairment is dispositive of the claim, and it is unnecessary to resolve the dispute regarding the cause and timing of the event which led to Michael's anomalous brain development.4 Regarding the nature and significance of Michael's impairment, the proof demonstrates that the physical impairment he suffers may best be described as moderate, as opposed to severe, and that his physical impairment is not static, but improving. As for Michael's mental status, it has been observed to be at or near age level, and, consequently, there is no evidence of any mental impairment.5
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).
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.
The Issue At issue in this proceeding is whether Travis Chestnut, a minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings Treena Chestnut and Terrance Chestnut are the parents and natural guardians of Travis Chestnut (Travis), a minor. Travis was born a live infant on July 26, 1994, at University Medical Center, a hospital located in Jacksonville, Florida, and his birth weight was in excess of 2,500 grams. The physician providing obstetrical services during the birth of Travis was James Lewis Jones, 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. Mrs. Chestnut's antepartum course and Travis' delivery Prior to Mrs. Chestnut's admission to University Medical Center, her prenatal course had been essentially uncomplicated. Notwithstanding, she was noted at risk because of a prior cesarean section delivery for fetal distress, and when admitted Travis was slightly post-term at 41.5 weeks. At or about 2:00 a.m., July 25, 1994, Mrs. Chestnut was admitted to University Medical Center. At the time, Mrs. Chestnut was noted to be in labor, and vaginal examination revealed the cervix to be at 2 centimeters, effacement at 100 percent, and the fetus at station 0 with vertex presentation. The membranes were noted to be intact, and fetal heart tone was noted at 135 to 145 beats per minute, with good fetal movement. At 8:45 a.m., an epidural was inserted for analgesia, and at 9:05 a.m. Mrs. Chestnut's membranes spontaneously ruptured, with clear fluid noted. Vaginal examination revealed the cervix to be at 2 to 3 centimeters, effacement at 100 percent, and the fetus at station 0. A scalp electrode was placed, and fetal heart tone was noted to continue in the 135 to 145 beat per minute range. Mrs. Chestnut's labor progressed slowly through July 25, 1994. During that period, fetal heart tones evidenced good beat to beat variability (short-term and long-term) with accelerations and occasional variable decelerations. Commencing at or about 2:00 a.m. July 26, 1994, late decelerations were noted, and fetal heart tones began to demonstrate, with increasing intensity and duration, early variable and late decelerations, with rates as low as the 70's, as well as fetal tachycardia. At approximately 2:25 a.m., dilation was noted as complete, and Mrs. Chestnut was instructed to push. At 2:28 a.m. a supplemental dose of epidural analgesia was administered, and at 2:34 a.m. deep variable decelerations were noted and Mrs. Chestnut was taken, via bed, to the delivery room. Mrs. Chestnut was noted in the delivery room at 2:39 a.m., at which time fetal heart rate was recorded in the 90's, and she was prepared for delivery. Mrs. Chestnut continued to push, and fetal heart tone remained in the 90's. Three attempts to deliver the infant by vacuum were attempted and failed. Fetal heart tone dropped to the 80's and a scalp pH performed at 2:54 a.m. was 6.95 (reflective of fetal acidosis). Given the circumstances, an emergency cesarean section was ordered, the incision started at 3:00 a.m., and Travis was delivered at 3:05 a.m. During delivery, difficulty was experienced elevating the infant's head, as he was deep in the pelvis, and a cord prolapse was noted. On delivery, Travis was atonic, with a heart rate of less than 60 and no respiratory effort. He was dried for 10 seconds, then begun on positive pressure ventilation with bag and mask. Heart rate increased to greater than 100 within 10 seconds, and color became pink within 20 seconds. Travis required support until 10 minutes of age, when regular sustained respiratory effort was noted. First gasp occurred between 1 and 2 minutes of age, and was progressively more frequent through 15 minutes of age. Shallow regular respirations began at about 5 minutes of age, and were adequate and sustained by 10 minutes of age. Slight tone was developed in the extremities by 10 minutes, and spontaneous movement of the extremities developed by 12 minutes. Apgars were 4, 5, 7, 7, and 8 at one, two, five, ten, and fifteen minutes, respectively.1 Cord gas at delivery reflected a pH of 6.76. Arterial blood gas at 20 minutes of age on blow by oxygen included a pH of 7.04. Neurologic impression at birth was severe neonatal depression/fetal distress and severe metabolic acidosis. At 20 minutes of life, Travis was transferred to the neonatal intensive care unit (NICU) for further management. At about three-and-one-half hours of age seizures were noted, and phenobarbital was started. Also noted, were lip smacking, eye deviation, spasticity, and hypertonic extremities. CT scan showed left parietal infarct and left post-occipital subdural hematoma. The EEG was markedly abnormal. MRI on August 3, 1994, reflected high signal gyral areas in both parietal and occipital lobes, consistent with cortical injury or hemorrhage. Travis remained in the intensive care unit until August 19, 1994, when he was discharged to the care of his parents. On discharge, he was noted to be doing well clinically, with no reported seizures while on maintenance phenobarbital. Physical examination revealed positive blink and suck, and symmetric motor patterns, although with increased tone. Neurologic impression on discharge was "perinatal encephalopathy - improved[,] neonatal seizures well controlled [and] developmentally at risk." The genesis and timing of Travis' neurologic insult Here, the proof that is pertinent to the nature and timing of Travis' neurologic insult is consistent with a brain- related injury caused by oxygen deprivation occurring in the course of labor, delivery, and the immediate post-delivery period. In this regard, it is observed, inter alia, that Mrs. Chestnut's prenatal course was uneventful; on admission to the hospital, the fetus evidenced reassuring fetal heart tones and fetal movement; only after protracted labor did the fetus begin to evidence multiple variable decelerations; prior to delivery, Travis suffered a period of prolonged bradycardia; prior to and following delivery, Travis was severely acidotic; upon delivery, Travis evidenced profound neurologic depression; and, following delivery, Travis developed seizure activity. Consequently, the proof supports the conclusion, more likely than not, that Travis suffered an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period in a hospital." Section 766.302(2), Florida Statutes. Having resolved the genesis and timing of Travis' neurologic insult, it remains to resolve its significance or, stated differently, whether the proof supports the conclusion that Travis' injury rendered him "permanently and substantially mentally and physically impaired," as required by Sections 766.302(2) and 766.309(1), Florida Statutes. The significance of Travis' neurologic impairment The proof offered by Petitioners to quantify the significance of Travis' impairment was less than compelling. In this regard, it is observed that Petitioners offered the affidavit of Stuart C. Edelberg, M.D., (Petitioners' Exhibit 2), an apparent expert in obstetrics and gynecology, who opined, based on his record review, that Travis' "impairment is permanent and substantial, both mentally and physically." Notably, Dr. Edelberg was not shown to have examined Travis, and his affidavit is hearsay, subject to the limitations imposed by Section 120.57(1)(c), Florida Statutes (1996 Supp.). Compared to the proof offered by Petitioners, Respondent offered the testimony, through deposition, of Michael Duchowny, M.D., an expert in pediatric neurology. (Respondent's Exhibit 1.) Dr. Duchowny examined Travis on July 16, 1996, and on January 24, 1997. Dr. Duchowny's examinations revealed that Travis did suffer some impairment of motor function, as evidenced by increased muscle tone, increased deep tendon reflexes, and diminished fine motor coordination; however, he walked independently and without support in a stable fashion. As for his cognitive abilities, Dr. Duchowny did observe expressive disfluency, but Travis' receptive skills were good, he could communicate non-verbally, and mental functioning was in the normal or near normal range. It was Dr. Duchowny's opinion that, although Travis does suffer some permanent mental and physical impairment, it is not substantial and, based on improvements observed between the examinations of July 16, 1996, and January 24, 1997, further improvement is most likely. Dr. Duchowny's observations and opinions are most consistent with the records offered into evidence (Petitioners' Exhibit 1), and are credited.2 Based on the proof, it cannot be concluded that Travis' injury has rendered him permanently and substantially mentally and physically impaired. Rather, the competent and persuasive proof is to the contrary.
The Issue At issue is whether Samuel Hess, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts Jeffrey Hess and Jeanmarie Hess are the natural parents of Samuel Hess, a minor. Samuel was born a live infant on January 7, 2002, at St. Vincent's Medical Center, a licensed hospital in Jacksonville, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Samuel's birth was Karen D. Bonar, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. Here, Petitioners are of the view that Samuel suffered such an injury. More particularly, Petitioners believe Samuel's neurologic impairments are the result of a brain injury caused by hydrocephalus, secondary to an intraventricular hemorrhage (diagnosed at six days of life), that was precipitated by oxygen deprivation (a hypoxic ischemic insult), and which occurred during labor and delivery. In contrast, NICA is of the view that Samuel's impairments are most likely developmentally based, as opposed to birth related, and that, whatever the etiology of Samuel's impairments, he is not permanently and substantially physically impaired. Samuel's birth and immediate newborn course At or about 12:55 p.m., January 7, 2002, Mrs. Hess, with an estimated delivery date of January 21, 2002, and the fetus at 38 weeks' gestation, was admitted to St. Vincent's Medical Center, following spontaneous rupture of the membranes, with clear fluid noted, at 9:00 a.m. On admission, mild, irregular contractions were noted; vaginal examination revealed the cervix at 2 to 3 centimeters dilation, 60 percent effacement, and the fetus at -1 station; and fetal monitoring was reassuring for fetal well-being, with a baseline of 120 to 130 beats per minute. Given rupture of the membranes, Mrs. Hess was committed to deliver, and she was admitted for pitocin augmentation. Following admission, an IV was started at 1:48 p.m.; an epidural was placed at 3:56 p.m.; pitocin drip was started at 4:05 p.m.; Mrs. Hess was noted as pushing at 9:24 p.m.; and Samuel was delivered spontaneously at 10:24 p.m., with "Nu[cal]/Hand" (the umbilical cord wrapped around the hand) noted. In the interim, staring at or about 8:00 p.m., monitoring revealed, over time, late decelerations; marked decelerations with slow return to baseline; and evidence of a hypertonic uterus (starting at 9:24 p.m., and persisting, following periods of relaxation, until 10:22 p.m.), with exaggerated fetal heart rate variability. Such a pattern is consistent with fetal stress, and raises concerns regarding fetal reserves and adequate oxygenation. However, at delivery, Samuel was not depressed; did not require resuscitation; was accorded normal Apgar scores of 8 and 9, at one and five minutes, respectively, reflective of a healthy newborn2; and no abnormalities were observed at birth, except pronounced molding.3 Following delivery, Samuel was transferred to the nursery, and ultimately discharged with his mother on January 10, 2002. In the interim, Samuel's newborn course was normal, except for evidence of mild jaundice (diagnosed the morning of January 9, 2002), which did not require light therapy. However, on discharge, instructions were given to follow-up the next day at the Seton Center for a repeat bilirubin check. As instructed, Mrs. Hess presented with Samuel at the Seton Center on January 11, 2002, for a repeat bilirubin check. At the time, Samuel was noted to be active, alert, and in no apparent distress; his temperature was recorded as normal (as it had been following delivery, and during his admission in the nursery at St. Vincent's Medical Center); his newborn examination, apart from evidence of jaundice, was within normal limits; and Mrs. Hess reported that Samuel had fed well.4 The results of the bilirubin test were obtained at or about 1:30 p.m., that afternoon, and called to a staff physician (Dr. Vaughn), who gave instructions to initiate phototherapy. Accordingly, later that afternoon, Samuel was put under the bilirubin lights at home, with instructions to monitor his temperature every two hours. On January 12, 2002, Samuel recorded a temperature of 100.6, and on the instructions of Dr. Vaughn, Samuel was taken to the emergency room at Wolfson Children's Hospital for evaluation.5 There, Samuel was received at 6:35 p.m., and triaged at 6:42 p.m. Chief complaint was jaundice, and temperature was noted as 100.7, otherwise no abnormalities were observed. Samuel's physical examination and immediate hospital course were documented, as follows: PHYSICAL EXAMINATION: His temperature is 100.7 in the ER. The rest of his vitals are normal. His weight is 2.7 kg. He is resting, easily aroused. Anterior fontanelle is soft and flat, with normal sutures. Has good red reflexes bilaterally. Ear canals are patent. Nose without congestion. Oropharynx is clear, no cleft. Heart is normal S1 and S2 without murmurs. Abdomen is soft and nontender. Chest is clear to auscultation. Extremities are without rashes, cyanosis, clubbing or edema. He does have good femoral pulses bilaterally, and no hip clicks. Neurologically, he is alert and active . . . . LABORATORY: . . . Total bilirubin on admission was 14.2, direct was 0.5. He was tapped, and had a white count in his spinal fluid of 2,500 and red count of 241,250. He had 65 segs, 17 lymphocytes and 18 monocytes, and the spinal fluid Gram stain showed no organisms, but an occasional leukocyte. IMPRESSION AND PLAN: My impression is that we have a six-day-old with fever and abnormal leukocytosis in his spinal fluid. He was placed on ampicillin, and gentamicin . . . . He was also cultured for herpes [, which was negative]. He was started on Acyclovir 20/kilo q.8 hours. He will continue to feed. A repeat spinal tap was attempted to clear up the meningitis issue on two occasions; however, both times they were bloody. We, therefore, are going to obtain a head CT with contrast to rule out an intracranial bleed. A CT of the head was done on January 13, 2002, and revealed a bilateral intraventricular hemorrhage (IVH) and a left posterior parietal cephalohematoma.6 The CT scan was read, as follows: FINDINGS: There is molding of the bones of the calvarium, compatible with recent vaginal delivery. Curvilinear area of increased density identified within the scalp soft tissues in the left posterior parietal region, compatible with a cephalohematoma. Increased densities identified within the lumen of the left lateral ventricle, predominantly involving the left choroid plexus, but also layering in the dependent portion of the lateral ventricle, compatible with intraventricular hemorrhage from the choroid plexus bleed. In addition, increased density is identified in the dependent portion of the right lateral ventricle consistent with intraventricular hemorrhage. No extra axial fluid collections are identified. Linear area of increased density is identified in the right frontal region, only seen on images #11, and therefore likely not due to subarachnoid hemorrhage. The ventricular system is not dilated. No focal parenchymal mass is identified. After contrast administration, there are no abnormal areas of parenchymal or meningeal enhancement identified. IMPRESSION: Left posterior parietal cephalohematoma Bilateral intraventricular hemorrhage, left greater than right, with the left intraventricular hemorrhage due to choroid plexus bleed. Molding of the bones of the calvarium compatible with history of recent vaginal delivery . . . . Given the abnormalities reported on the CT scan, Dr. Randell Powell, a neurosurgeon, was requested to see Samuel for neurosurgical input. That consultation occurred on January 16, 2002,7 and was reported, as follows: . . . I have been requested to see the child for neurosurgical input. I am informed that the baby is now doing well. Septic work-up was completely negative and antibiotics have since been discontinued and the baby is anticipating discharge later on today. PHYSICAL EXAMINATION: Reveals a beautiful, sleeping, male infant with a very soft head, a very soft fontanelle, no splitting of the sutures. The head circumference is measured to be slightly less than the 50th percentile for a newborn. There is no nuchal rigidity and bending the legs did not appear to cause irritation as well. The child has a bilateral red reflex. Pupils are equal and reactive. The Moro reflex is symmetric. Computed tomographic scan shows hemorrhage emanating from the choroid plexus and the trigone of the left lateral ventricle. There is mild ventricular dilatation. Follow-up ultrasound shows similar findings. IMPRESSION: Intraventricular hemorrhage. DISCUSSION: Intraventricular hemorrhages in the newborn perinatal period that are caused by choroid plexus hemorrhage generally have an excellent prognosis as no significant brain parenchyma is disrupted and these hemorrhages usually resolve without sequelae. However, there is roughly a 20% chance of developing post hemorrhagic hydrocephalus which in 50% of cases could require more aggressive treatment. That means the baby's chances of needing neurosurgical intervention is somewhat less than 10% and this was discussed extensively with the parents who were happy to hear this news. There are no overt signs of hydrocephalus at this time and in my opinion I think that we can safely follow the baby with serial physical examination consisting of palpation of the fontanelle and head circumference measurements. I would be glad to see the baby at age one month for follow- up, but I suspect a good prognosis here. Samuel was discharged from Wolfson Children's Hospital at 6:15 p.m., January 16, 2002, with instructions to monitor his head circumference once a week, and for follow-up appointments with Dr. Hamaty (his pediatrician at the time8) and Dr. Powell. Samuel's subsequent development Following discharge, Samuel was followed by Dr. Powell for mild posthemorrhagic hydrocephalus, that appeared to stabilize, but then got worse between ages four and six months.9 Serial studies showed progressive ventricular enlargement consistent with hydrocephalus, and after discussing treatment options Samuel's parents elected to proceed with endoscopic third ventriculostomy, which was performed on August 26, 2002. Initially, Samuel appeared to be doing reasonably well, but then he developed an accelerated head circumference (53.8 centimeters, which placed him above the 98th percentile), consistent with progressive hydrocephalus, and on December 6, 2002, a Codman programmable ventriculoperioneal shunt was placed. Since that time, Samuel has done fairly well, without symptoms related to increased intracranial pressure. However, he continues to evidence macrocrania (above the 98th percentile), ventriculomegaly (enlargement of the laterial ventricules), and atrophy of brain tissue.10 (Exhibit 34). Samuel's current presentation With regard to Samuel's current presentation, the parties agree, and the proof is otherwise compelling, that Samuel is permanently and substantially mentally impaired.11 As for his physical presentation, while there may be room for disagreement, the complexity of Samuel's difficulties support the conclusion that he is also permanently and substantially physically impaired. In so concluding, it is noted that on the Vineland Adoptive Behavior Scales Form (VABS), related to daily living skills and motor skills, Samuel scored in the mentally handicapped range. "He is not yet toilet trained despite intensive efforts in this regard"; "[h]e is able to assist with simple dressing and undressing tasks but is not yet independent with these skills"; and he "continues to display gross-motor, fine-motor, visual-motor, and motor planning impairment." (Exhibits 18 and 30). It is further noted that Samuel presents with impaired postural control (aggravated by his large head), impaired strength, hypotonia, and bilateral pronatal feet. As a result, Samuel has moderate to severe impairment in strength, endurance, postural control, balance responses (with unexpected falls), functional mobility, and activities of daily living. Notably, at approximately five years of age, Samuel requires a stroller for extended outings, and caregiver assistance for 90 percent of self care needs. (Exhibit 10). The cause of Samuel's impairments As for the cause of Samuel's neurologic impairments, the proof demonstrates that, more likely than not, they are the result of a brain injury, caused by hydrocephalus, secondary to the intraventricular hemorrhage (IVH) he suffered, and which was diagnosed at six days of life. What remains to resolve is the genesis of Samuel's IVH or, stated otherwise, whether the proof demonstrated, more likely than not, that the IVH was caused by oxygen deprivation, and occurred during labor, delivery or resuscitation. § 766.302(2), Fla. Stat. ("'Birth-related neurological injury' means injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period."); Nagy v. Florida Birth-Related Neurological Injury Compensation Association, 813 So. 2d 155 (Fla. 4th DCA 2002)(The oxygen deprivation and injury to the brain must occur during labor, delivery, or immediately afterward.). The genesis of Samuel's IVH Regarding the intraventricular hemorrhage Samuel suffered, the proof is compelling that an IVH in a term infant, such as Samuel, is a rare occurrence, and its cause frequently cannot be identified. Indeed, among the physicians who addressed the issue, there is apparent agreement that the majority of IVHs (approximately 50 percent) are related to oxygen deprivation (hypoxia-ischemia) or trauma, and the remainder fall into one of two groups, those with another identifiable cause (such as vascular malformation, infection, clotting disorder, venous infarct, or genetic disorder) and those of unknown etiology (idiopathic). To address the cause and timing of Samuel's IVH, the parties offered the deposition testimony of Julius Piver, M.D., J.D., a physician board-certified in obstetrics and gynecology (albeit one who has not practiced obstetrics for 20 years); Mary Edwards-Brown, M.D., a physician board-certified in radiology, with subspecialty certification in neuroradiology; David Hammond, M.D., a physician board-certified in pediatrics, neurology with special competence in child neurology, and clinical neurophysiology; Donald Willis, M.D., a physician board-certified in obstetrics and gynecology, and maternal-fetal medicine; and Michael Duchowny, M.D., a physician board- certified in pediatrics, neurology with special competence in child neurology, electroencephalography, and clinical neurophysiology.12 The testimony of Doctors Piver, Edwards- Brown, and Hammond were offered in support of Petitioners' view on causation, and testimony of Doctors Willis and Duchowny were offered in support of NICA's view on causation. Pertinent to the issue of causation, Doctors Piver, Edwards-Brown, and Hammond were of the opinion that an infant can suffer a intraventricular hemorrhage during labor and delivery, as a result of a hypoxic-ischemic insult, and not show any clinical evidence in the immediate postnatal period. However, although offered the opportunity to do so, Dr. Hammond declined to offer an opinion as to the likely etiology (cause and timing) of Samuels IVH.13 Consequently, we are left to consider the testimony of Doctors Piver and Edwards-Brown with regard to Petitioners' view on causation. As for the etiology of Samuel's IVH, it was Dr. Piver's opinion, based on his review of the medical records, that Samuel's IVH was most likely caused by partial prolonged asphyxia, that was sufficient to cause a subtle, slow bleed during labor and delivery, which progressed to the significant IVH noted at 6 days of life, but that was initially insufficient to reveal itself (by clinical evidence of a bleed) in the immediate postnatal period. In reaching his conclusion, Dr. Piver relied heavily on his evaluation of the fetal monitor strips, which he opined revealed, starting at 6:48 p.m. (18:48), and continuing for 30 to 35 minutes, evidence of marked loss of beat-to-beat variability; late decelerations at 8:01 p.m., 8:03 p.m., 8:05 p.m., 8:25 p.m., 8:28 p.m., 8:31 p.m., and 8:33 p.m.; a marked deceleration to a low of 70 beats per minute at 8:50 p.m., with a slow return to baseline at 8:56 p.m.; a marked deceleration from 180 beats per minute to 90 beats per minute between 9:14 p.m. to 9:20 p.m.; a late deceleration at 9:23 p.m.; and evidence of a hypertonic uterus starting at 9:24 p.m., and persisting to 9:42 p.m., again at 9:50 p.m., and persisting to 10:14 p.m., and again at 10:20 p.m. and persisting to 10:22 p.m., with exaggerated fetal heart rate variability. While acknowledging the bleed could have started at any time between the 7th of January (Samuel's delivery date) and the 12th of January, when Samuel presented to Wolfson Children's Hospital, Dr. Piver was of the opinion, given his review of the fetal monitor strips, that Samuel's bleed was most likely caused by hypoxia, and that it began during labor and delivery. Dr. Piver variously noted the likely onset of the bleed as "[b]etween 2030 and 2130 hours"; "around 2000 hours"; "from 2000 hours to 2130 hours"; "between 1800 and 2224 hours"; "between 1800 and 2100 hours"; and "the 21:24 to 22:20 time interval." (Exhibit 23, pages 34, 48, 49, 57, 80, 82; Exhibit 23, deposition Exhibit 6). Dr. Edwards-Brown, like Dr. Piver, was of the opinion that Samuel's IVH was most likely caused by hypoxia, that caused a slow bleed during labor and delivery, but an insufficient bleed to reveal evidence of brain damage during the immediate postnatal period. Dr. Edwards-Brown's opinion was explained, as follows: Q How are you able to determine, based on the films that you reviewed, that the hemorrhage began during labor and delivery? A Based on the films alone, we can't make that determination. It's simply the path of physiology of the hemorrhages and the hospital course as well as the labor and delivery records that allow me to make that conclusion. * * * Q Are you able to look at the effect of the hemorrhage on the brain structures to determine or time when the hemorrhage may have occurred? A What I see is a large hemorrhage wherein the ventricle that is pretty bright and that hemorrhage is causing hydrocephalus; and the hydrocephalus, I'm sure, is causing symptoms, but hemorrhages don't cause hydrocephalus initially. It takes some time before that occurs. So all I can say is yes, the hemorrhage is having an effect on the brain, and that effect is hydrocephalus and ischemia, and it could have occurred sometime from the time of labor and delivery until the time that film was obtained. Q It could have occurred at any time in between there? A. The hydrocephalus and the ischemia. Q But not the hemorrhage? A Certainly the hemorrhage could have occurred after birth, but I would have expected some evidence of that in the clinical history. I would have expected evidence that this child had suffered a profound hypoxic injury as one might see if this child had had a code or a profound drop in his oxygen status. None of that is in the record; therefore, I don't think it's a post natal event. * * * Q Okay. How are you able to rule out in this case that the hemorrhage did not begin on January 9th, 10th, 11th or 12th? A Several things. Number one, I don't have evidence on the 9th, 10th, 11th, or 12th of January that this child suffered any hypoxic injury. Q Hemorrhage [can] be caused by something other than hypoxic injury? A It can. Q Okay, and what are the other possible causes? A Intraventricular hemorrhage might result from a tumor, might result from a vascular malformation, it could result from an infection, but it usually results from hypoxia. Q We sometimes do not know what causes intraventricular hemorrhage? A I think when we don't know what causes intraventricular hemorrhage, it is a reasonable presumption that there was hypoxia at a time when someone was not looking, as in the prenatal or labor and delivery period. If there wasn't a fetal heart monitoring strip obtained during that period and the child is born with -- excuse me, with intraventricular hemorrhage, I think the presumption should be that there was hypoxia during that time. But certainly there may be some times when we don't have an answer. Q Sometimes we simply don't know what caused the hemorrhage? A That is undeniably true; however, one should not make that presumption until we have excluded the usual causes. And in this case, based on Dr. Piver's testimony that there was evidence of hypoxia during labor and delivery, one must assume that that was the cause. We don't make the diagnosis of an idiopathic cause. That means we don't have the answer when we have evidence of a reasonable cause, which we have here. Q In your letter to Mr. Sharrit that we referred to earlier, you state on Page No. 2 further down that, "The absence of symptoms in the three days following birth is not unusual since bleeding begins small and increases with time." What do you mean by that? A That's the nature of bleeding. I'm sure you know this. We have all bled. You don't -- Well, bleeding -- unless it's the result of an aneurism -- is not so massive initially. It starts out as a leak in the vessels, and the longer it bleeds the more it accumulates . . . . (Exhibit 27, pages 39, 41, 42, 44-46). Contrasted with the opinion held by Doctors Piver, Edwards-Brown, and Hammond, Doctors Willis and Duchowny were of the opinion that if a hypoxic event is significant enough to cause an intraventricular hemorrhage during labor and delivery, there will be clinical evidence in the immediate newborn period. Dr. Willis expressed his observations on the medical records, as well as the basis of his opinions on causations, as follows: Q . . . Dr. Willis, in reviewing the records and the fetal heart tracings, were you able to identify any intervals, any intervals of concern, I suppose, or any that you thought that may have been hypoxic intervals? A Well, the fetal heart rate monitor strip looks pretty good until about an hour and a half before delivery, and then there are fetal heart rate decelerations that pretty much continue until the time of birth. Q And what was the significance of those intervals that you're talking about, to you? A Well, the decrease in fetal heart rate usually means that there's some decrease in oxygen supply to the baby. Q Okay. A Or umbilical cord compression, which could lead to that same thing. Q So are you saying you found intervals that were suspicious for oxygen compromise? A That's correct. Q Did you identify intervals of lack of beat-to-beat variability that you thought were of concern? A Well, I'll look, but most of what I saw were fetal heart rate decelerations along with really exaggerated fetal heart rate variability, which usually you see with umbilical cord compression. Q Well, are you saying, then, that there were episodes in this case where you felt there was significant cord compression? A Well, the fetal heart rate tracing certainly is consistent with umbilical cord compression. Q And over what time period would you say the fetal heart tracings are consistent with cord compression? A Well, off and on for the last hour and a half prior to birth. Q And could that create a scenario, an hypoxic scenario that could lead to some kind of vascular insult within the brain? A Now, let me be sure I understand the question. Are you asking me if I believe this fetal heart rate pattern, the abnormalities that I see led to that or can abnormalities in fetal heart rate pattern in general lead to brain injury? Q I guess my question would be, the pattern that you've identified in this case, is that consistent with a pattern that can lead to injury, vascular injury within the brain? A Well, I think it shows that there's probably some lack of oxygen during that time period. Now, the question then is, you know, did that lack of oxygen lead to brain damage. And in this case, you know, my feeling is or my opinion is that it did not lead to brain damage. Q Let's break that up a little bit. Without knowing, without looking at the final result -- I presume you're looking at the early neonatal period right after birth to help you make that conclusion. Am I correct? A Yes. Q If we for the moment put aside the early clinical course of the child, just by looking at the heart tracings and the patterns that you've identified, are those consistent with or perhaps suspicious for the kind of pattern that could lead to a fetal compromise, brain compromise? A Well, I don't know if anyone could predict fetal brain damage simply based on a fetal heart rate pattern. You really have to look at the baby, the condition of the baby after birth to be able to say whether or not the abnormalities in the fetal heart rate pattern resulted in oxygen deprivation and brain injury. * * * Q Now, you did, no doubt, note that the child did return to the hospital after discharge and was found to have a bloody spinal tap, and ultimately it was determined that it had an intraventricular hemorrhage? A That's correct. That's, I believe, on the fifth day after birth. Q Well, having identified hypoxic consistent patterns within the fetal heart tracings, how is it that you can say that perhaps did not lead to a vascular insult that slowly progressed over a period of four or five days into an extensive hemorrhage? * * * A . . . I think that it's pretty clear that if you're going to have an hypoxic injury to the brain that's substantial enough to cause brain injury then the baby really is going to be depressed at time of birth and is going to have an unstable newborn period. Simply having an abnormal fetal heart rate pattern is not enough to say that any lack of oxygen that occurred during labor caused brain damage. Q . . . And I guess you're saying across the board and without exception there can be no slowly progressing brain damage that can occur due to labor and delivery hypoxia? A Well, in order to have an hypoxic event during labor or delivery that would be substantial enough to cause an hypoxic- related brain injury, then really the baby is going to have to be depressed at birth. Now, I mean, you can have intracranial hemorrhages, choroid plexus bleeds in babies that have normal, spontaneous vaginal births with normal-looking fetal heart rate tracings. I mean, there are spontaneous hemorrhages that can occur during labor, delivery, at some point after the baby is born, in the newborn period. But what I'm saying is that if you're going to have an intracranial hemorrhage due to an hypoxic event during labor or delivery, then the baby really should be depressed at time of birth and have an unstable newborn course. Q When you say depressed after the birth, do you put any outer limit on the time frame during which the baby might become depressed? A Well, usually, by the newborn -- by the immediate post-delivery period they mean immediately after birth and until the baby is essentially stabilized after birth. For instance, in this case the baby had Apgar scores of eight and nine, required no resuscitation at all. So, you know, we really don't have anything to suggest that there's a problem in the immediate newborn period. And then during the hospital stay, other than the jaundice, the baby did not really have any problems. The baby breast-fed. It did not have any neurologic findings that were abnormal, didn't have renal failure, did not have seizures, you know, the types of things that we see with babies that suffer an hypoxic insult during labor or delivery. * * * Q I know that your opinion is that if an hypoxic event is significant enough to cause a brain damage, then you're going to have to necessarily see signs of depression at birth or shortly after birth. Am I stating that correctly? A Very nicely. Q Okay. What if we're not talking about brain damage or encephalopathy in the broad sense but we're just talking about a very small insult to one of the blood vessels in the brain that doesn't readily turn into brain damage but, rather, becomes a progressive problem over a period of several days? Is that a possible scenario? A I guess most things are possible, but that seems unlikely to me. Q It seems unlikely to you that you could have a weakening of a blood vessel or some injury that lessens the integrity of the blood vessel and that the brain damage is then latent and that's perhaps the reason why it would not negatively impact the early clinical course? A Well, let me say -- and I think we kind of went over this before -- that you can have intracranial hemorrhages on babies that have no apparent problems at all during labor, delivery. Just for reasons unknown you can have intracranial hemorrhage and blood vessels can rupture. But I guess what we're talking about is brain injury due to lack of oxygen or mechanical trauma. And my point being that if you're going to get a hemorrhage due to lack of oxygen or mechanical trauma, then the baby really should be depressed at time of birth (Exhibit 28, pages 23-30). Dr. Duchowny expressed his observations of the medical records, as well as his opinions on causation, as follows: Q. Let me at this time suggest a brain injury pathway that has been offered by others in this case for Samuel Hess and ask you to comment on that. Others have suggested that in this case there was labor and delivery hypoxia that resulted in a choroid plexus bleed and was associated with an isolated -- excuse me, where the blood was isolated -- the bleed was isolated within the ventricles during the pre-natal course and that that later produced hydrocephalus -- MR. BAJALIA: Pre-natal? MR. SHARRIT: Yes, in the first few days after birth. Q. Are you with me, doctor? A. Yes, I am, but I think you mean post- natal course. Q. I'm sorry, I'm sorry. I do. Thank you. Labor and delivery hypoxia, the choroid plexus bleed isolated within the ventricles during the post-natal course that later produced hydrocephalus and increased the internal cranial pressure that later after - - well after discharge from the hospital resulted in periventricular white matter damage. Is that a reasonable interpretation for Samuel Hess' brain injury? A. No. Q. Why not? A. There's no evidence of hypoxia. * * * Q. . . . [Y]ou don't think that they are a result of hypoxia because you don't discern evidence of hypoxia on the fetal monitor strips? A. There are abnormalities on the fetal monitoring strips. As I said before, I don't think they are associated with hypoxia. * * * Q. I understand your testimony to the contrary, but if -- if it turned out that after reviewing Samuel's fetal monitor strips you decided that there was evidence of hypoxia, would that be a reasonable link to the hemorrhage that was diagnosed? A. No, because Samuel didn't show any of the signs of hypoxia at birth so I don't believe he had any type of hypoxic damage. * * * Q. Do you not find any evidence at all of hypoxia on the fetal monitor strips? A. I believe the fetal monitoring strips indicate some fetal stress and that's all. Q. As opposed to distress? A. It just shows stress to the fetus during the inter-partum experience. That's all. Q. How do you define stress? A. I think the decelerations indicate, you know, stress on -- you know, stress is being placed on the fetus. Q. . . . [But] can't late decelerations be an indication of hypoxia? A. It's possible. Q. Could bradycardia in the 60 to 70 be[at]s per minute range be an indication of hypoxia? A. It's possible but not necessarily. * * * Q. . . . If you have an intraventricular hemorrhage that you attribute to a hypoxic ischemic insult that resulted during the course of labor and delivery and late in delivery, as has been suggested in this case, wouldn't you expect to see some clinically recognizable neurologic dysfunction in the neonate during the immediate newborn period? A. Yes, you would. Q. Even if the hemorrhage was, to use opposing counsel's words, isolated? A. Yes. If you're claiming that the neurologic problems are related to hypoxia, you would expect to see clinical signs of hypoxia at the time. Q. Even if the hemorrhage was isolated? A. Yes. Q. Can you explain that? A. You would see clinical manifestations in some way. You know, there would be some compromise in respiratory status, evidence of compromise in organ function because the lack of oxygen would affect not only the brain but other organ systems as well. You might see elevation of cardiac enzymes, liver enzymes, changes in renal function, changes in mental status, seizures, changes in blood pressure, respirations, etcetera. Q. And just so I'm clear, that is true even if the hemorrhage was isolated just within the ventricle? A. Yes, if you're attributing it to hypoxia. * * * Q. And based upon your review of the medical records, did you see any indication that Samuel had any such clinically recognizable neurological impairment or dysfunction during the immediate newborn period? A. No, I did not. Q. Did you note what his APGAR scores were? A. Yes, I believe he had normal APGAR scores. I believe they were eight and nine and one at five minutes. Q. Is that consistent with Samuel having suffered an isolated intraventricular hemorrhage that was the result of a hypoxic ischemic insult that occurred late in delivery -- A. No. Q. -- labor and delivery? A. I don't believe so. Q. Is the fact that there was no documented evidence of impaired neurologic function in Samuel during the immediate newborn period consistent with Samuel having suffered an isolated intraventricular hemorrhage that occurred late in labor and delivery? A. No. (Exhibit 29, pages 17, 18, 20-23, and 36-39). Here, there is no apparent reason to credit the testimony of Petitioners' witnesses on the issue of causation over the testimony of NICAs witnesses. Indeed, as among those who spoke to the issue of causation, Doctors Willis and Duchowny are the more qualified to address the issue, and their testimony the more persuasive.
The Issue Whether Daniel Espinoza has suffered an injury for which he and his mother, Maria L. Espinoza, should be awarded compensation under the Florida Birth-Related Neurological Injury Compensation Plan, as Ms. Espinoza has alleged in her claim for compensation filed on behalf of Daniel?
Findings Of Fact Based upon the evidence adduced at the July 14, 1994, Division-conducted hearing in this case, and the record as a whole, the following Findings of Fact are made: Daniel Espinoza is the natural son of Petitioner. He was born on January 6, 1991, at Jackson Memorial Hospital (hereinafter referred to as "Jackson") in Dade County, Florida. Daniel was the product of a full term pregnancy. His birth weight was in excess of 2500 grams. Daniel was delivered by Erin Colleen Dawson, M.D. At the time of Daniel's birth, Dr. Dawson was a participant in the Florida Birth-Related Neurological Injury Compensation Plan. The delivery was uneventful. Daniel was a "vigorous" baby at birth. He had a "good" Apgar score of 9 at one, five, and ten minutes after birth. There was no resuscitation required in the immediate postdelivery period. Approximately five hours after the initial evaluation, Daniel appeared to be "grunting" and suffering from "cyanosis." As a result, he was transferred to Jackson's neonatal intensive care unit, where he had a seizure and experienced respiratory distress. Daniel's C.S.F. (cerebrospinal fluid) was bloody and had a white blood cell count of 19000. An initial diagnosis of meningitis was made. On January 7, 1991, an EEG (electroencephalogram) was done. It revealed "no epileptiform phenomena." A CT (computerized tomography) scan of Daniel's brain was performed on January 8, 1991. The report of the scan read as follows: HISTORY- TWO DAY OLD WITH SEPSIS. 5 MM AXIAL SECTIONS WERE OBTAINED THROUGH THE BRAIN WITHOUT CONTRAST. THERE IS A SMALL LUCENT DEFECT IN THE LEFT OCCIPITAL BONE SEEN ON IMAGE #5. ALTHOUGH NO SOFT TISSUE SWELLING IS SEEN, CANNOT DEFINITELY EXCLUDE THIS BEING A LINEAR NONDEPRESSED FRACTURE VERSUS OTHER ETIOLOGY SUCH AS A VASCULAR GROOVE. WE SUGGEST CORRELATION WITH THE PLAIN FILM. THERE IS A HUGE AMOUNT OF BLOOD IN THE RIGHT POSTERIOR FOSSA EXTENDING ACROSS THE MIDLINE AND INSINUATING ON THE RIGHT TENTORIAL INCISURA SUPRATENTORIALLY. BLOOD IS ALSO SEEN ALONG THE POSTERIOR INTERHEMISPHERIC FISSURE DIFFUSELY IN THE EXTRA-AXIAL SPACE, AND A SMALL AMOUNT OF BLOOD IN THE OCCIPITAL HORNS OF THE LATERAL VENTRICLES. WITH SUCH A TREMENDOUS AMOUNT OF BLOOD PRESENT IN THE POSTERIOR FOSSA, IT IS DIFFICULT TO SAY HOW MUCH IS PARENCHYMAL VERSUS EXTRA-AXIAL. THERE IS MASS EFFECT UPON THE MID BRAIN PONS AND MEDULLA AND ON THE FOURTH VENTRICLE CAUSING OBSTRUCTING HYDROCEPHALUS. IMPRESSION LARGE ACUTE INTRACRANIAL HEMORRHAGE, AS DESCRIBED ABOVE, WITH THE EPICENTER BEING IN THE RIGHT POSTERIOR FOSSA. THE DIFFERENTIAL DIAGNOSIS INCLUDES NEOPLASM, TRAUMA, RUPTURED ANEURYSM OR ARTERIOVENOUS MALFORMATION, COAGULOPATHY, ETC. CONTRAST STUDY OR MRI MAY BE OF HELP FOR FURTHER EVALUATION TO TRY TO DETERMINE THE UNDERLYING ETIOLOGY. On January 9, 1991, Daniel underwent an echoencephalogram, which, according to the report of the study, indicated the following: ROUTINE ECHOENCEPHALOGRAM REVEALED DILATION OF THE LATERAL AND THIRD VENTRICLES. THERE IS A BILATERAL LUMPY CHOROID PLEXUS NOTED. ADDITIONAL TRANSTEMPORAL VIEWS REVEAL AN ECHOGENIC AREA SEEN IN THE INFRATENTORIAL REGION, WITH INCREASE IN THE ECHOGENICITY OF THE BASAL CISTERNS. THE FINDINGS ARE SIMILAR TO THOSE SEEN ON PREVIOUS CT SCAN, WHICH SHOWED EVIDENCE OF A CEREBRAL HEMORRHAGE WITH SUBARACHNOID BLEED. THE NORMAL STRUCTURES OF THE POSTERIOR FOSSA ARE ILL-DEFINED. IMPRESSION: MODERATE HYDROCEPHALIC CHANGES OF THE LATERAL AND THIRD VENTRICLES. SUBARACHNOID HEMORRHAGE WITH A POSTERIOR FOSSA HEMORRHAGE, AS DESCRIBED IN A PREVIOUS CT SCAN OF THE BRAIN. Another CT brain scan was performed on January 23, 1994, the report of which stated the following: THE PATIENT IS A TWO WEEK OLD MALE WITH A HISTORY OF INTRACRANIAL HEMORRHAGE. AXIAL IMAGES WERE OBTAINED THROUGH THE BRAIN AT 5MM INTERVALS FOLLOWING INTRAVENOUS ADMINISTRATION OF CONTRAST. COMPARED TO THE PRIOR STUDY OF 1-8-91, THERE HAS BEEN SUBSTANTIAL RESORPTION OF BLOOD IN THE REGION OF THE SUBDURAL, SUBARACHNOID AND INTRAVENTRICULAR HEMORRHAGE. THERE ALSO HAS BEEN MARKED DECREASE IN THE VENTRICULAR SIZE. THERE IS LESS ASSOCIATED MASS EFFECT, ESPECIALLY IN THE POSTERIOR FOSSA WITH PERSISTENT SUBDURAL HEMORRHAGE IN THE RIGHT SIDE OF THE POSTERIOR FOSSA DISPLACING THE CEREBELLUM ANTERIORLY AND TO THE LEFT. THE FOURTH VENTRICLE IS NOW VISUALIZED, HOWEVER. NO NEW AREAS OF HEMORRHAGE ARE SEEN. THERE ARE NO BONY ABNORMALITIES. THE MAXILLARY AND ETHMOID SINUSES AND MASTOID AIR CELLS ARE CLEAR. IMPRESSION SIGNIFICANT RESORPTION OF SUBDURAL, SUBARACHNOID WITH INTRAVENTRICULAR HEMORRHAGE SINCE THE PRIOR STUDY OF 1-8-91 WITH LESS MASS EFFECT, ESPECIALLY UPON THE CEREBELLUM AND BRAIN STEM. MARKED DECREASE IN VENTRICULAR SIZE HAS ALSO OCCURRED. On January 25, 1991, Daniel underwent a second echoencephalogram, the report of which read as follows: FOLLOW-UP BRAIN HEMORRHAGE. COMPARISON IS MADE TO PREVIOUS STUDY FROM 1/8/91. THERE HAS BEEN MARKED INTERVAL RESOLUTION OF THE PREVIOUSLY DEFINED RIGHT POSTERIOR FOSSA HEMORRHAGE. IN ADDITION, THE VENTRICULAR SIZE HAS DECREASED SIGNIFICANTLY SINCE THE PREVIOUS EXAM. THERE CONTINUES TO BE SLIGHT INCREASED ECHOGENICITY WITHIN THE SYLVIAN FISSURES BILATERALLY, WHICH MAY REPRESENT SOME RESIDUAL SUBARACHNOID HEMORRHAGE. NO EVIDENCE OF NEW OR ACUTE HEMORRHAGE IS IDENTIFIED. IMPRESSION: THERE HAS BEEN SIGNIFICANT INTERVAL IMPROVEMENT IN THE DEGREE OF VENTRICULAR DILATION AND THE PREVIOUSLY DEFINED HEMORRHAGE, WHEN COMPARED TO THE STUDY OF 1/8/91. Daniel was discharged from Jackson on January 31, 1991. At present, in terms of meeting expected language milestones, Daniel is mildly delayed, primarily in the area of expressive language. The delay is developmental in nature and Daniel will likely improve in this area over time. Otherwise, his mental functioning is relatively well preserved. Physically, Daniel is only very mildly impaired. He has a slight decrease in muscle tone and some incoordination, but he does not suffer from spasticity or contracture and he is able to move both of his arms well and to walk without losing his balance. He is even able to run, although he has a tendency to lean to the right and appear as if he is about to fall when he does so. In short, Daniel suffers from no permanent and substantial mental or physical impairment. 2/
Conclusions Sovereign immunity extends to “corporations primarily acting as instrumentalities . . . of the state, county, or municipalities.” See § 68.28(2), F.S.; Pagan v. Sarasota County Public Hospital Board, 884 So.2d 257 (Fla. 2d DCA 2004). MRHS was deemed to be an instrumentality of the hospital district by the Attorney General in an opinion dated December 8, 2006 and the circuit court in Marion County has reached the same conclusion in several cases. As a result, MRHS is entitled to sovereign immunity under § 768.28, F.S. The public policy basis for extending sovereign immunity to private entities such as MRHS has recently been questioned by two appellate courts. See University of Florida Board of Trustees v. Morris, 32 Fla. L. Weekly D1803 (Fla 2d DCA July 27, 2007) (Altenbernd, J., concurring), rev. denied, 2008 Fla LEXIS (Fla. Jan. 7, 2008); Andrews v. Shands at Lakeshore, Inc., 33 Fla. L. Weekly D30 (Fla 1st DCA Dec. 20, 2007). The nurses are employees of MRHS and they were acting within the scope of their employment when providing services to Tyler. As a result, the nurses’ negligence is attributable to MRHS. The nurses had a duty to provide competent medical care to Tyler. They breached this duty and violated the standards of care for nursing personnel by failing to report the cyanotic episodes to Dr. Pierre and by failing to properly perform the four-extremity blood pressure test. The nurses’ actions and inactions contributed to the delayed diagnosis of Tyler’s heart condition. However, Dr. Pierre’s failure to order an immediate cardiology consultation when she detected a heart murmur shortly after Tyler’s birth also contributed to the delayed diagnosis of Tyler’s heart condition. The delayed diagnosis of Tyler’s heart condition led to his “crash” on December 16 because it is more likely than not that Tyler would have been transferred to Shands or another tertiary facility had his condition been diagnosed sooner. Tyler was not a candidate for the second and third stages of the Norwood procedure because of the damage caused by the “crash,” and he also suffered brain damage during the “crash” that caused his developmental delay. The amount of damages agreed to by MRHS is reasonable, even though Dr. Pierre likely shares some of the responsibility for Tyler’s condition. Indeed, the life care plan prepared for Tyler reflects that the cost of a transplant is between $650,000 and $700,000 and Tyler is expected to require multiple transplants over the course of his life. Moreover, the non-economic damages (e.g., pain and suffering) of Tyler and his parents could very well have exceeded the settlement amount had the case gone to jury trial. LEGISLATIVE HISTORY: This is the first year that this claim has been presented to the Legislature. ATTORNEYS’ FEES AND LOBBYIST’S FEES: The claimants’ attorney provided an affidavit stating that that attorney’s fees will be capped at 25 percent of the amount awarded by the claim bill in accordance with §768.28(8), F.S. Lobbyist’s fees are not included in the 25 percent attorney’s fees. Lobbyist’s fees will be an additional 4 percent of the amount awarded by the claim bill, which would be $28,000 based upon the $700,000 claim. The Legislature is free to limit the fees and costs paid in connection with a claim bill as it sees fit. See Gamble v. Wells, 450 So. 2d 850 (Fla. 1984). The bill does so by stating that “[t]he total amount paid for attorney’s fees, lobbying fees, costs and other similar expenses relating to this claim may not exceed 25 percent of the amount awarded [by the bill].” If this language remains in the bill (and the bill is amended as recommended below to reflect the allocation approved by the circuit court), the claimants will receive a total of $525,000, with $393,750 going into Tyler’s special needs trust and $131,250 going to his parents. The remaining $175,000 will go to attorney’s fees, costs, and lobbyist’s fees. If this language was not in the bill (and the bill is amended as recommended below to reflect the allocation approved by the circuit court), the claimants would receive approximately $362,000, with approximately $271,500 going into Tyler’s special needs trust and approximately $90,500 going to his parents. The claimants’ attorney would receive a total of approximately $310,000 ($175,000 for attorney’s fees and approximately $135,000 for costs), and the lobbyist would receive $28,000. OTHER ISSUES: The bill identifies the Marion County Hospital District as the entity responsible for payment of the claim. The parties agree, and I recommend that the bill be amended to reflect MRHS as the entity responsible for payment because it is responsible for operating the hospital pursuant to a lease from the hospital district. The bill requires the entire claim to be paid into Tyler’s special needs trust. The parties agree, and I recommend that the bill be amended to require payment of the claim in accordance with the allocation approved by the circuit court, i.e., 75 percent into Tyler’s special needs trust and 25 percent to his parents. The bill requires any funds remaining in Tyler’s special needs trust upon his death to revert to the General Revenue Fund. The parties agree, and I recommend that the bill be amended to remove this language because the bill is being paid from the hospital’s funds, not State funds. The bill should be also amended to include the standard language requiring payment of Medicaid liens prior to disbursing any funds to the claimants. See § 409.910, F.S. RECOMMENDATIONS: For the reasons set forth above, I recommend that Senate Bill 68 (2008) be reported FAVORABLY, as amended. Respectfully submitted, cc: Senator Charlie Dean Representative Marcelo Llorente Faye Blanton, Secretary of the Senate T. Kent Wetherell Senate Special Master House Committee on Constitution and Civil Law Tony DePalma, House Special Master Counsel of Record
