The Issue The issue in this case is whether Samuel Joseph Hereford suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Steven and Theresa Hereford are the natural parents of Samuel Joseph Hereford. Samuel was born on May 31, 2009, at Memorial Hospital, which is a licensed hospital located in Jacksonville, Florida. Samuel weighed in excess of 2,500 grams at birth. Obstetrical services at Samuel’s birth were provided by a physician participating in the NICA program. Samuel has permanent and substantial mental and physical impairments. Samuel is Mrs. Hereford’s fourth biological child. She chose to use the services of a midwife for Samuel’s birth, but to deliver at the hospital. Mrs. Hereford presented to Memorial Hospital at approximately 4:00 a.m., on May 31, 2009. When she was first examined, it was determined that she was dilated at 8 centimeters. Mrs. Hereford recalls that the nurse midwife asked her if she was “ready to get this over with.” When Mrs. Hereford replied “yes,” the nurse midwife ruptured Mrs. Hereford’s membranes. She immediately began experiencing intense pain, “a pain like I had never experienced before.” Samuel’s head was delivered and she continued to push while in extreme pain. At some point, she was turned over and Samuel was delivered. Samuel was born by vaginal delivery at 5:17 a.m. His delivery was complicated due to a shoulder dystocia that resulted in a six-minute delay between his head and the rest of his body being delivered. He did not cry when he was first delivered. Mrs. Hereford recalls seeing all of the medical personnel around Samuel’s bed and recalls maybe hearing a faint cry at some point. After an undetermined amount of time, Samuel was brought to her very briefly. She recalls that he was swaddled and that his face was blue. He was not crying or making noise. Mr. Hereford was present for Samuel’s delivery. He recalls that when Samuel was delivered, he looked lifeless. He was blue and did not make any noise. Samuel was taken to a table where the medical personnel began resuscitation. He recalls them performing chest compressions and putting an oxygen mask on him. Samuel looked swollen, blue, puffy and “like he had just been beat up.” He also recalls that Samuel was swaddled, taken to Mrs. Hereford briefly, then taken to the NICU. Samuel’s one-minute Apgar score was 3, his skin was pale and blue, his muscle tone was absent, and his heart rate was below He received “face mask ventilation x 2 minutes, blow by oxygen and cardiac compression. Began gasping less than 1 minute of age. HR over 100 by 90 seconds of age.” His five-minute Apgar was 8. At about six hours of life, Samuel was transported to Wolfson’s Children’s Hospital for further evaluation. Mr. Hereford described how Samuel looked when he first saw him at Wolfson’s: “Well, he still looked like he had been through trauma. He was still blue. He was still puffy. He was still bruised. I remember seeing a cut on his shoulder. That’s what I remember how he looked.” He stayed in the NICU at Wolfson’s for four days. After leaving Wolfson’s, the Herefords took him straight to the pediatrician’s office, which then referred them to Dr. Joyce, a board-certified pediatric cardiologist. Dr. James Joyce first examined Samuel on June 5, 2009. His notes from that first visit reflect history obtained from Samuel’s parents and from his examination of Samuel: CC Abnormal echocardiogram and cardiomegaly on chest X-ray HPI Discharged yesterday from Wolfson Children’s Hospital NICU after 4 day stay. Admitted in transfer from Memorial Hospital for cardiomegaly on initial chest X-ray performed for evaluation of oxygen requirement. Spontaneous vaginal delivery at -37 weeks gestation at Memorial Hospital complicated by shoulder dystocia, then initially low Apgars requiring resuscitation for the first few minutes of life. He stabilized on nasal prong oxygen and IV fluids with glucose. After transfer to WCH he required nasal oxygen and IV fluids for two days. He also had hypoglycemia on the first two days with low of 31 mg/dl at 5:30AM on 06/03/09. His pCO2 ranged from 45 to 53mmHg from 05/31/09 to 06/02/09. His hematocrit rose from 58.6 on 05/31/09 to high of 71.5 on 06/02/09, then fell to 59% on 06/02/09 before rising to 65.7% yesterday morning before discharge. Initial echocardiogram to evaluate CXR finding of cardiomegaly on 05/31/09 showed bidirectional flow across a “moderate-size” patent ductus arteriosus and mildly depressed LV systolic function with EF of 52% and FS of 25%. His second and last echocardiogram on 06/03/09 showed left to right shunting across the PFO, no residual PDA shunting, mild tricuspid regurgitation, mild residual pulmonary hypertension with estimated PASP -45mmHg, and decreased RV and LV systolic function with estimated EF -40% However, a Cardiology consult was not ordered. He was advanced to room air and p.o. feedings on the third day of life and jaundice developed with a peak total bilirubin of 20.8 on 06/03/09. His bilirubin decreased to 14 on the day of discharge 06/04/09, but increased to 15mg/dl last night after they had been having problems with his bililight bed at home. Today he was brought in by his parents without other complaint. He is breast feeding every 2 hours for about 30 minutes each time. Denied history of feeding difficulty, breathing difficulty, syncope, or sweats with feeds. ROS Mildly sleepy most of the time. Not as alert as previous babies. Bruising of shoulders from difficult delivery. Normal renal ultrasound yesterday. Entire review of systems was negative, except as above. PMH Gestation complicated by polyhydramnios, thick heart walls on OB ultrasound, and then preterm labor after 33 weeks gestation. Spontaneous vaginal delivery at -37 weeks gestation at Memorial Hospital complicated by shoulder dystocia. s/p early transient neonatal hypoglycemia. s/p early neonatal polycythemia. Neonatal jaundice Decreased RV and LV systolic function since first day of life. SH He lives with parents, sisters 16 and 18y/o, brothers 19y/o and 15 months. FH Parents alive and well. No family history of congenital heart disease, sudden cardiac death, pacemaker, or early (<age 40 yr.) myocardial infarction or stroke, grandparents have hypertension and high cholesterol with history of stroke and heart attacks. Allergies NKDA Meds No meds, but on home phototherapy for jaundice. Vitals Wt: 8.8 lb Ht: 21.5 in BP: 86/52 P: 127 RR:28 BMI: 13.2 PE Oxygen saturation in room air 98%. Awake and in no distress. Well developed, well nourished appearing. Mildly lethargic. Normocephalic, except for slight molding and mild bilateral ecchymosis of lower eyelids. Mild scleral icterus. No ear, nose or throat inflammation. Mucosae pink and moist. Neck supple without lymphadenopathy, goiter, or jugular venous distention. Chest symmetrical without deformity. Lungs clear to auscultation. Heart with regular rhythm and normal rate. Normal first and second heart sounds. No click, gallop, murmur or rub heard. No lift or thrill felt. Abdomen nondistended, nontender, with normal bowel sounds and no evidence of hepatomegaly, splenomegaly or mass. No abdominal bruit heard. Polydactyly with 6th finger on right hand. No extremity edema. No joint swelling or tenderness. Pulses 2+ and equal in all four extremities. Normal skin temperature and furgor. Plethoric skin color with superimposed jaundice. No rash seen. No weakness, incoordination, or tremor. Grossly normal muscle tone. ECG: normal sinus rhythm, diffuse T wave inversion in inferior and anteroseptal leads and mildly prolonged QTc interval suggestive of ischemic myocardial injury. Echocardiogram: very mild Ebstein anomaly of the tricuspid valve with mild regurgitation, moderately dilated RV, severe RVH, other cardiac chambers of normal size, moderately decreased biventricular systolic function, LV EF -40%, trivial mitral valve regurgitation, no pericardial effusion, no residual PDA, no aortic coarctation. no AS, normal coronary artery origins. A/P #CHRONIC SYSTOLIC HEART FAILURE (428.22): EF -40%, mildly to moderately decreased left, probable cardiomyopathy, R/O ischemic CMP vs. noncompaction or other congenital CMP #EBSTEIN’S ANOMALY (746.2): Mild tricuspid regurgitation. # secondary Pulm Hin /OT Ch P Heart Disease (416.8): resolving primary pulmonary hypertension of the newborn. # POLYCYTHEMIA NEONATORUM (776.4): still plethoric appearing. # UNSPECIFIED FETAL AND NEONATAL JAUNDICE (774.6): still jaundiced appearing. # SPONTANEOUS ECCHYMOSES (782.7): ecchymosis of both lower eyelids, R/O IVH or basilar skull fracture. # POLYDACTYLY OF FINGERS (755.01): 6 fingers on right hand. I called and discussed case with Dr. Caron- Canas, her Pediatrician on-call. Working diagnoses and prognosis explained to parents. Therapeutic plan outlined. ADVISED/ORDERED: Admit Orders: Admit to Wolfson children’s hospital on telemetry to the service of Dr. James J. Joyce Diagnosis: chronic systolic heart failure, R/O cardiomyopathy, neonatal jaundice vital signs every 4 hours with BP accurate I & O, daily weights breast feedings per mother’s schedule Labwork now: CBC, complete metabolic profile, troponin, CK-MB PA and lateral Chest X-ray today (regarding CHF) Digoxin 16micrograms (0.32ml of 50mcg/ml oral solution p.o. now and every 12 hours thereafter Captopril 0.7 ml of 1 mg/ml oral solution) p.o. now and every 8 hours thereafter 12-lead ECG in the morning tomorrow please call Dr. J. Joyce when patient arrives on the ward (296-7771). In his deposition taken August 5, 2016, Dr. Joyce described Samuel when he first examined him, as having bruising of his lower eyelids, was plethoric (darkish pink) and had mild jaundice. Dr. Joyce performed an electrocardiogram (ECG) and an echocardiogram at his initial evaluation on June 5, 2009, and was asked about the findings from these tests: Q: Was that something that you performed? A: Here in the office, yes. Q: And what did you find as a result of that ECG? A: He had abnormal T-wave inversions inferiorly and from the anteroseptal leads and mildly prolonged QT intervals suggestive of ischemic injury. * * * Q: You said suggestive of ischemic myocardial injury. What does that mean in layman’s terms? A: Like an infarction. Well, like a heart attack or an injury to the muscle that is from low blood flow. That’s what ischemia is. Low blood flow to the muscle causing damage. Q: Then an echocardiogram was also performed; is that right? A: That’s correct. Q: And you found that he had a very mild Ebstein’s anomaly? A: Yes. That’s a deformity of the tricuspid valve, but it’s extremely mild. Very mild. Q: Very mild. Okay. And as a result of this workup you decided to admit him to Wolfson’s Children’s Hospital; is that right? A: Correct. Q: And at Wolfson’s what was your role in Sam Hereford’s care? Did you serve as his attending physician? A: As I recall, yes. I got a neurology consult and -- well, neurology in particular. I was very concerned about that because he was floppy or hypotonic. He had bruising on his head. And the history that I saw, the history from the time of delivery and thereafter. It was obvious in the record that he had a period of asphyxia. * * * And he [had] low sats, low oxygen saturation and thereafter had to be put on oxygen. Also blood pressure was low so they gave him a bolus of fluid. And that brought the blood pressure up. So this was a kid who was in distress at birth, quite clearly. * * * The bloodwork back when he was admitted the first time to Wolfson’s, he had -- at Memorial Hospital he had prolonged and extensive hypoglycemia. Low blood sugar. Q: What does that indicate to you? A: Well, it certainly can be increased insulin from maternal gestational diabetes, but there was no history of that here. Although with his weight being as heavy, as big as he was, that’s certainly a possibility. But when you have hypoxia or asphyxia you go into anaerobic metabolism and you use glucose up a lot quicker than you do with aerobic metabolism. So his asphyxia alone could cause hypoglycemia. He had very extensive and prolonged hypoglycemia. He also had thrombocytopenic where his platelet count was low. Then during the first couple of days in the hospital his creatinine elevated, which implies that he had injury to his kidneys. Acute tubular necrosis can be caused by asphyxia. Also he was polycythemic. His hematocrit actually went up to 71 percent, quite high. And that can also be due to asphyxia. Asphyxia’s a risk factor for polycythemia and elevated creatinine, hypoglycemia, and thrombocytopenia. So all of those are circumstantial pieces of evidence, along with the history of him being stuck for six minutes during a very difficult delivery, so that all led to that. And we did admit him. And, now, on my admission, what I did do, because I was suspicious because of the EKG and the history that he had, the hypoxic ischemic injury to his entire body, I figured it obviously would include that heart. So I checked for serum troponin and CPK or CK- MB, creatinine kinase myocardial band, or MB. And those were all positive. Those two were positive, showing that he did have injury and necrosis of his myocardium. These were specific for the myocardium. So those enzymes showed that he had myocardial necrosis. Q: So the troponins -- am I saying that right? A: Yes. Troponin I is the particular one he had. Q: So the troponin I showed that he had a myocardial injury, an injury to his heart. A: Yeah. An infarction. Actually death of the cells. It gets released into the blood. Q: And myocardial infarction is death of heart tissue; correct? A: Right. From low blood flow. From inadequate nutrition, blood flow, or oxygenation, or both. Q: And the troponin levels that you noted, were they high? A: They were high. Because, again, he was five days old at that time, five or six days old. Q: Six days old, I believe. A: Yes. He was old enough that it was on its way down. It went down. On recheck a couple of days later it was dropping. Q: Does -- A: For it to still be high six days after birth meant that it was pretty darn high earlier. Because it bumps up and then it comes down over time. * * * All this being consistent with a watershed or diffuse myocardial infarction, which would go along with the history of the birth injury, and the low Apgar, the resuscitation, et cetera. Again, I’m inferring asphyxia from all the evidence. * * * Q: So, if I understand you, and tell me if I don’t, from what you are saying, all of his records that you were able to see from his birth and also the evaluation of him and the following of him in the hospital led you to believe that he suffered a hypoxic ischemic event during birth; is that right? A: Yes. * * * Q: So after you admitted him to the hospital, and I believe in your note you were indicating that you were attempting to at least rule out an ischemic CMP versus non-compaction or other congenital CMP. What does that mean? A: Cardiomyopathy. He does have evidence of non-compaction cardiomyopathy. Q: What is that? A: It’s an abnormality of the heart muscle. The form of the heart muscle is more trabeculated. It’s not as compact. That’s where the word non-compaction comes in. But there’s many different forms—different degrees of non-compaction. Mild, moderate, severe. There’s also many different known genetic origins for that and many that we don’t have genetic origins for. We don’t know. Dr. Joyce explained that cardiomyopathy can make someone more sensitive to a hypoxic ischemic event, but it was not the reason for the event. “In other words, it can make things worse than they would be otherwise, but it’s not the main reason that you’re going to have that malfunction.” When asked whether non- compaction syndrome, as a prenatally acquired congenital disorder, can cause a child to have a myocardial infarction post-delivery, he replied, “Not in and of itself, no.” He continued: Q Had that hypoxic ischemic event not occurred, let’s say, in your opinion, could Samuel still have the heart problems he had as a result of the prenatally acquired congenital heart abnormalities we know he had? A He wouldn’t have had the extent of dysfunction and he wouldn’t have had positive troponin and CK-MB. Q Based on the non-compaction cardiomyopathy alone? A Correct. Q What other factors, other than a hypoxic ischemic could contribute to the non- compaction cardiomyopathy that would lead a child to have heart conditions like Samuel had post-delivery. * * * A You’re asking what else can do this. There isn’t a whole lot more in a newborn baby. You have to really use your imagination to come up with why you’re going to have a diffuse subendocardial myocardial infarction in a newborn baby, other than hypoxic ischemic encephalopathy and some other wild things. Prolonged shock. High dose epinephrine. Those kind of things. You have to come up with that. Dr. Joyce was also asked about Ebstein’s anomaly: Q . . . Were you able to determine whether or not that Ebstein’s anomaly caused the myocardial infarction? A No, it did not. Q How do you know that? A Ebstein’s anomaly, what it is, is an abnormality of the tricuspid valve. A valve is a door. It’s just a simple door, a doorway. The tricuspid valve has three doors to the doorway. He had a slight abnormality to the door. The door wasn’t quite normal. But it was a very mild abnormality. His regurgitation at birth was listed as mild. No, I’m sorry, moderate. It was moderate at birth and then it quickly became mild by day four. The second echocardiogram was mild. That was associated -- when it was moderate, and even mild, it was associated with pulmonary hypertension that was severe and moderate. So at birth he had severe pulmonary hypertension and moderate tricuspid valve regurgitation. By day five or so, the second echocardiogram in his initial hospitalization, the pulmonary hypertension was down to moderate and his tricuspid valve regurgitation was down to mild. And the reason is because the pulmonary hypertension, that high pressure, is back against that right sided pumping chamber, the one that has the tricuspid valve. We commonly see it in kids with normal tricuspid valves that have pulmonary hypertension, we will see more severe tricuspid valve regurgitation. So the tricuspid regurgitation wasn’t significantly out of proportion to the pulmonary hypertension. And it certainly was not enough to cause heart failure. Q Right. I have a copy here of -- A And just as an aside, you will notice that, if you look at the record, the echocardiograms that were reported in the hospital, they didn’t mention non-compaction, they didn’t mention Ebstein’s anomaly on their echo reports. The reason was because both of them were relatively mild. Again, I did an extra year of training in echocardiography. I used to run the echocardio- -- the echo lab at Wolfson Children’s Hospital. I’m a fellow of the American Society of Echocardiography. I see more detail in echocardiograms than most cardiologists because of that background. Q So -- A Again, these were mild, mild abnormalities. And unfortunately, you go, oh, there’s Ebstein’s anomaly, that must be the reason for heart failure. Well, Ebstein’s can be very, very mild or very severe. And it can have all sorts of forms and problems with function. But, again, this was a very mild one. And the non-compaction is relatively mild. Because it also was missed. Q Okay. So what you’re saying is there were echocardiograms that were taken before you were involved but they missed the Ebstein’s anomaly -- A Correct. Q -- and they missed the cardio -- the non- compaction? A Correct. Q And -- A Because they were so mild. Q Because they were so mild. A Exactly. Q Fair enough. Have you seen any evidence that the Ebstein’s -- the very mild Ebstein’s anomaly was causing him any issues prenatally? A No. Q Have you seen any evidence from treating him and his medical records that he developed non-immune hydrops as a result of the Ebstein’s anomaly? A No. He had no evidence of hydrops. Most importantly, when he was born he did not have skin edema, according to the history and physical by attending physician neonatologist. He also -- his chest x-ray at the original hospital did not show pulmonary edema and did not show pleural effusions. His echocardiogram on day one at Wolfson Children’s Hospital did not show a pericardial effusion. Hydrops fetalis is -- the non-immune hydrops that’s due to a heart condition is basically congestive heart failure. In order to diagnose hydrops you have to have multiple fluid collections. You have to have skin edema and/or one of the following three things. Or two of the following three things. Pleural effusion, pericardial effusion, ascites. They didn’t check for ascites so I don’t know about that. But I do know in his first day of life he did not have skin edema, according to the history of all the physicians who examined him. He did not have pleural effusion per the chest x-ray reports. And he did not have pericardial effusion according to the echo report. So he therefore did not have hydrops. Q Would a large -- well, would a loss of weight from 10.3 pounds to 8.7 be enough evidence to make a finding that he had had - A No. Q -- non-immune hydrops -- A No. Because you would lose weight from the acute tubular necrosis. As you recover from acute tubular necrosis, the injury to the kidneys, you go through a polyuric phase where you can actually diurese, get rid of the excess fluid. In fact, when I saw him on day six of life he was dry. I had to give him volume. Q And because he had to give him volume -- that’s fluids? A Right. Fluid volume. Yes. That was day six. But I’m just giving an example. I think he dried out. And that could be from the injury to the kidneys, which he had evidence of that by his creatinine going up after birth. Q And babies often lose weight after they’re born? A Oh yeah. Of course. They commonly lose up to 15 percent of their body weight in the first few days or week of life. Dr. Joyce readmitted Samuel to Wolfson’s on June 5, 2009, for initiation of cardiac medications and further diagnostic workup. While at Wolfson’s for this second hospital stay, his records reflect that he had a chest x-ray, a head ultrasound, an EEG, a head MRI, and ECGs. The results of the EEG were abnormal: IMPRESSION: This is an abnormal EEG because of excessive sharp waves, asynchrony, and excessive suppression. This would be consistent with encephalopathic process but is not specific with regard to etiology. Clinical correlation is advised. An MRI was also performed on June 8, 2009: IMPRESSION: Linear T1 hyperintensity in the region of the straight sinus, the totcula and the right sigmoid sinus is most likely the sequelle of recent birth although if there is clinical concern for sinus thrombosis, an MRV could be performed. Possible punctuate focus of intraparenchymal hemorrhage in the right frontal lobe. I personally discussed these findings with Dr. Ceron-Canas (primary care physician) on 6/9/09 at 11:45 hours. Dr. Joyce requested a neurology consultation during the second hospital stay. The consulting neurologist, Dr. Hammond, raised the issues of both Samuel’s risk of hypoxic ischemic brain injury, as well as a recommendation for genetics consultation due to Samuel’s dysmorphic features (“wide upper extremity polydactyly as well as suspected mild low-set ears.”). His hospital discharge summary dated June 8, 2009, reflect the following diagnoses: Diffuse non-Q wave myocardial infarction with secondary decreased ventricular systolic function, clinically improving. Neonatal jaundice exacerbated by recent neonatal polycythemia plus bruising from shoulder dystocia, improving. Possible hypoxic ischemic encephalopathy. Ebstein’s anomaly of the tricuspid valve. Mild dehydration, resolved. Samuel’s pediatrician, Dr. Miles, referred him for a neurology consult with Dr. Harry Abram, which took place when Samuel was approximately six months old. Dr. Abram noted “global delay” and made a referral for the parents to seek occupational, physical, and speech therapies for Samuel. He also recommended a genetics referral and careful monitoring for seizures, with a follow-up with neurology in six months. In May 2010, Samuel’s pediatrician, Dr. Miles, referred the Herefords to Dr. Anthony Perszyk, a geneticist with the University of Florida Pediatric Multispecialty Center. Noting Samuel’s history of hypotonia, polydactyly, and cardiomyopathy, Dr. Perszyk ordered lab work and genetics testing to begin to explore whether there was a genetic basis for Samuel’s impairments. Following this initial testing, Dr. Perszyk wrote to Dr. Miles in June 2010, regarding the test results, and stated in relevant part: Labs that we obtained at the end of May have now been completed. An extensive microarray or genetic analysis of the boy’s chromosomes is reported as within normal limits. There does not seem to be additional deletions or duplications of his chromosome material that accounts for hypotonia or developmental delay. Some specific regions would be on chromosome 17; this did not show up in the testing. There may be other tests we might do, but at the present time, this is adequate for ruling out many of the common disorders that give a child low muscle tone and developmental delays. Dr. Perszyk addressed Samuel’s possible seizure activity and wanted to follow up the following month. He also noted Samuel had been taken off some dietary supplements and wanted certain lab work to be repeated to determine its effect on mitochondrial function. Dr. Perszyk further noted that while Samuel was large for gestational age, he is close in weight to the Herefords’ other children. Dr. Perszyk saw Samuel again in July 2010, and again wrote a letter to Dr. Miles, which stated in relevant part: Previous genetic testing so far has not revealed a specific genetic abnormality. A DNA microarray testing as well as a metabolic testing have all been within normal limits. Initially fatty acid oxidation abnormalities were suspected with abnormality seen on initial screening laboratories. However, discontinuing the use of additional oils such as omega 3 or FISH oil has allowed his levels to improve amino acids from the urine, and plasma amino acids, are all within normal limits now at this time. Also acylcarnitine profile is improved with better utilization at the mitochondrial level of all his fatty acids. CK level is 55. While Dr. Perszyk noted that there may be consideration of additional DNA testing, he did not order it. Moreover, Mrs. Hereford recalls that Dr. Perzyk mentioned to them that an additional genetic test would cost $20,000, as insurance would not cover it. The record does not reflect any order for additional genetic testing from Dr. Perszyk. On February 1, 2011, Dr. Perszyk again saw Samuel and again wrote Dr. Miles regarding the office visit. Dr. Perszyk referenced Samuel’s significant visual problems and the need for ophthalmology examination. Again, he referenced “a plan to consider” further testing, including a video EEG, brain MRI and other DNA testing, but there is no reference to additional orders for genetic tests. Moreover, Mrs. Hereford credibly testified that “we did exactly what he asked us to do. I am not aware of anything that he says that you’re saying that he ordered that we did not do.” Samuel was admitted to Wolfson’s Children’s Hospital by Dr. Perszyk on February 21, 2011, for “workup for seizure disorder,” including brain MRI, video EEG, brain MRI spectroscopy, and lab tests. He again consulted with Dr. Abrams. The MRI report initially stated that other than sinus disease and prominent frontal extraaxial fluid, the MRI was otherwise normal. However, an addendum, stated, “The images were again reviewed. The patient has a history of grand mal seizure and [is] also on seizure medication. In this clinical context, the findings could represent diffuse global cortical atrophy with prominence of the sylvian fissure and lateral ventricles. However one-year followup recommended for continued assessment.” Samuel was discharged on February 24, 2011, with a prescription for seizure medication and vitamin B6. While it is not entirely clear from the record if any additional genetic testing was completed, Dr. Perszyk saw Samuel in May 2016, and wrote a letter in conjunction with the office visit addressed “To Whom it May Concern” regarding Samuel. This letter was written at the request of the Herefords, who were unfamiliar with the typical process for filing such claims, at the time they were making application for NICA benefits. The letter, which appears to summarize his care for Samuel over the years, states as follows: Samuel Hereford is a 6 year old male that I have followed since infancy. He has had long standing hypotonia and developmental delays since birth. Samuel has had abnormal reflexes and spasticity during the first several years of life. He has the clinical features of cerebral palsy. This has always been the main concern with Samuel since his hypotonia was recognized and therapy was begun. He had events around the time of delivery that would be the etiological basis of the cerebral palsy. This is documented in his medical record. As a geneticist, I have followed him and tested him for other causes for his hypotonia and did not find any other cause. He continues to grow slowly and has markedly delayed motor and language skills. His growth is also slow with weight and length near the bottom of the growth curves. Dr. Dawn Duss is a pediatric ophthalmologist and is Samuel’s treating ophthalmologist. She is board-certified in ophthalmology and completed fellowship training in the sub- specialty of pediatric ophthalmology. Dr. Duss first examined Samuel in 2014 to evaluate him for poor visual behavior, and reviewed his medical records. She diagnosed him with cortical visual impairment, which is abnormal visual behavior which cannot be explained by an anatomical deficit in the eyeball, so, she explained, that deficit has to be somewhere along the optic pathways or occipital lobe. She further explained that there is nothing pathognomic about cortical visual impairment. The anatomy of the eye does not reflect the level of visual behavior in the child. Dr. Duss explained that Samuel has poor visual attention. He cannot match a shape to a chart, he is unable to maintain visual attention for any amount of time, and he does not have depth perception. Dr. Duss has treated hundreds of children who have cortical visual impairment as a result of hypoxic ischemic events. According to Dr. Duss, a hypoxic ischemic event is the number one cause of cortical visual impairment. In reviewing Samuel’s medical records, Dr. Duss noted that his 2011 MRI revealed diffuse global cortical atrophy with prominence of a Sylvian fissure and lateral ventricles. Dr. Duss explained that diffuse cortical atrophy on an MRI is a very typical finding in cortical visual impairment caused by a hypoxic ischemic event. She further noted that the fact that this did not show up in earlier MRIs is typical in a hypoxic ischemic birth because the atrophy has to have time to develop after the traumatic event. It is Dr. Duss’ opinion that the hypoxic ischemic event that Samuel suffered at birth is the sole cause of Samuel’s visual impairments. NICA retained Dr. Donald Willis, a board-certified obstetrician specializing in maternal fetal medicine, who reviewed the medical records related to Samuel’s birth and subsequent development to determine whether Samuel sustained an injury to the brain or spinal cord caused by oxygen deprivation or mechanical injury in the course of labor, delivery, or resuscitation in the immediate post-delivery period. In a report dated May 9, 2014, Dr. Willis referenced relevant parts of Samuel’s records and stated in pertinent part: The mother presented to the hospital in active labor at 36 weeks gestational age. Cervical dilation was 8 cms. Amniotic fluid was clear. No fetal heart rate (FHR) monitor tracing during labor was available for review. There was no mention of suspected fetal distress during labor. Delivery was complicated by a shoulder dystocia with a six-minute delay in delivery. The baby was large-for-gestational age with a birth weight of 4,688 grams. An extra digit was noted on the right hand. The newborn was described as depressed, floppy and apnic at birth. Chest compressions were initiated. A heart rate of >100bpm was established by 90 seconds. Bag and mask ventilation was required for about two-minutes. Cord blood gas showed a pH of 7.22 and a base excess of only -2. The baby was taken to the NICU for evaluation. Nasal cannula oxygen was required for respiratory distress. A chest x-ray showed an enlarged heart. Muscle tone was decreased. The initial blood gas in the NICU was at about four hours of age. The pH was 7.35 with a base excess of -6. The baby was transferred to Baptist Hospital at six hours of age due to respiratory distress and an enlarged heart. Admission to Baptist Hospital indicated the baby was in critical and unstable condition. There was minimal muscle tone. Platelet count dropped to 88,000. Nasal cannula oxygen was required until DOL 3. Antibiotics were given, but cultures returned as no growth. Cardiac ECHO showed severe pulmonary hypertension and decreased ventricular function. No seizure activity was described. The baby was discharged on DOL 4. EEG on DOL 8 was abnormal and consistent with encephalopathy. MRI on the same day showed finding “most likely represents sequellae of recent birth trauma” with possible punctuate interparenchymal hemorrhage. Genetic evaluation was done due to an extra digit, hypotonia, cardiomyopathy at birth, visual cortical impairment, possible seizures and developmental delay. Chromosome analysis and microarray were normal. No specific genetic diagnosis was made. In summary, delivery was complicated by a shoulder dystocia that resulted in a depressed newborn, requiring chest compressions and bag and mask ventilation. Despite the initial depression with an Apgar score of only 3 at one minute, the baby’s condition improved with an Apgar score of 8 at five minutes. The newborn hospital course was complicated by respiratory distress, poor muscle tone, cardiomegaly and thrombocytopenia. EEG on DOL 8 was abnormal and consistent with encephalopathy. Based on the above history, some degree of oxygen deprivation at birth would be expected. However, the umbilical cord gas was normal (ph 7.22). Newborn depression at birth, severe enough to require cardiac compression would be unexpected with a cord pH of 7.22. It is likely the cord blood pH reflects the acid-base status of the fetus prior to the shoulder dystocia and not the actual status after delivery was completed six minutes later. This is reasonable since the blood flow through the umbilical cord ceases after the head is delivered. So for six minutes the baby was oxygen deprived, which may not be reflected in the blood cord gas findings. The other complicating issue is the possibility of an underlying genetic problem that could cause or contribute to the developmental delay. I am not aware of any specific diagnosis, but this issue could be better addressed by Pediatric Neurology. There was an obstetrical event (shoulder dystocia) that resulted in loss of oxygen to the baby’s brain during delivery. The oxygen deprivation resulted in brain injury. I am not able to comment about the extent of the injury. In a deposition on November 13, 2015, Dr. Willis further explained how shoulder dystocia causes oxygen deprivation. Once a baby’s head is delivered, the umbilical cord is compressed, so there is no real oxygen supply to the baby after the head is delivered until the delivery is completed. In Samuel’s case, the remainder of his body was delivered six minutes after his head, so he did not receive oxygen for that period of time. Additionally, because the medical records reflect that his first gasp was less than one minute and sustained respiration was in two minutes, it was likely that Samuel experienced more than six minutes of oxygen deprivation. Dr. Willis further explained with a shoulder dystocia, that the pH of the blood in the umbilical cord reflects what the baby’s acid-base status was just prior to delivery and not the acid-base status when the delivery is completed. Therefore, Samuel’s blood cord pH is not an accurate indicator of the pH following delivery with a shoulder dystocia. He described Samuel’s blood cord gas as “relatively normal” and that indicated the baby was not in distress prior to delivery. There were no fetal heart rate strips available for him to review. Samuel’s Apgar score was 3 at one minute and 8 at 5 minutes. Dr. Willis explained that the one-minute Apgar score tells what resuscitative measures may be necessary. The five- minute Apgar score tells more about the baby’s overall response and degree of hypoxia and acidosis. Samuel’s five-minute Apgar score of 8 is a normal score, and that the neurologic outcome of babies “is probably better reflected by the five-minute Apgar score, not the one-minute Apgar score, the long-term neurologic development.” However, when asked whether the MRI taken of Samuel on June 8, 2009, had findings with an acute hypoxic ischemic event, he replied “yes.” Specifically, he noted that the MRI report described punctuate or small pinpoint hemorrhages within the brain which is consistent with birth trauma. When asked whether the findings of the EEG taken on June 8, 2009, of excessive sharp waves, asynchrony, and excessive suppression is consistent with a hypoxic ischemic brain injury, he replied “yes.” It is Dr. Willis’s opinion that Samuel did sustain brain injury due to oxygen deprivation. He addressed the possible role of Samuel’s heart problems: A: Well, this baby had -- had birth defects, congenital heart defects, congenital birth defects. There was the enlarged heart, and the subsequent echoes after birth showed poor cardiac function. That was all present at birth. That was not something that developed after birth. The baby did have a sixth digit on the right hand, so there were birth defects present. And I guess where -- where I say any, you know, genetic diagnosis, there can also be just developmental abnormalities that can cause neurologic injury that may not have specific DNA probes to identify the defect or may not have a gross abnormality in the chromosomes. So what I’m trying to say is that this baby obviously had certain congenital birth defects, and I’m not sure if there were congenital birth defects that could have contributed to the oxygen deprivation to result in his eventual neurologic outcome. Q: Okay. Well, doctor, let me ask you about the poor cardiac function that you describe in the echocardiogram. Can that poor cardiac function that you see – and maybe this goes beyond the scope of your expertise, but that poor cardiac function could have been caused by damage to the heart tissue as a result of a hypoxic brain injury; correct? A: Well, I guess -- I guess that’s possible, but the baby -- we knew the baby had thick myocardial tissue prior to delivery, and that’s what was found after delivery so that’s a preexisting problem. That’s a congenital birth defect. Q: Now, babies that have those types of valves or the enlarged heart that you describe are born without problems all the time; correct? Mr. Bajalia: Objection to form. The witness: Well. I’m not -- I’m not sure how to answer that. I mean, we know babies with congenital heart defects have a higher incidence of neurologic problems. I mean, that -- that, we’ve known for some time. So I’m not sure. Maybe if you ask me that question again, I’ll try to answer. Mr. Nowak: Well, let me ask a little different, Doctor. You don’t have an opinion in this case one way or another as to what causes Sam -- caused Sam Hereford’s developmental delays, correct – A: Correct. Q:- -the congenital problem or the hypoxic brain -- the hypoxic brain event we’ve been talking about; correct? A: Correct. My – my review of the case – I am not asked to comment as to the severity of the injury, only if there was any brain injury due to hypoxia at birth. Q Okay. And you concluded that there was; correct? A Correct. Dr. Willis’ opinion that there was an apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post-delivery period is credited. NICA also retained Dr. Michael Duchowny to evaluate Samuel. Dr. Duchowny is board-certified in pediatric neurology, with special qualifications in child neurology and in clinical neurophysiology. He is a senior staff attending at Nicklaus Children’s Hospital, and directs the neurology training program. Dr. Duchowny reviewed Samuel’s medical records and performed an independent medical examination on Samuel on June 18, 2014. In a medical report dated June 18, 2014, Dr. Duchowny stated the following: In Summary, Samuel’s neurological evaluation reveals evidence of global developmental delay which includes a substantial mental and motor impairment. He additionally manifests multiple dysmorphic features including midfacial compression, polydactyly, and a dysmorphic dental pattern. There is abundant self-stimulatory activity including blindisms and a lack of social interaction consistent with an autistic presentation. In contrast, there are no specific focal or lateralizing neurologic findings. Samuel’s medical records confirm his parent’s history of significant problems at birth. He was delivered at Memorial Hospital Jacksonville via delivery complicated by shoulder dystocia with the head [sic] being delivered 6 minutes later. The pregnancy had previously been complicated by macrosomia, polyhydramnios and left renal pyelectasis. Samuel was depressed at birth; a heart rate less than 100 was noted and he was floppy and apneic. The heart rate increased to 100 by 90 seconds of age and his Apgar score of 3 at 1 minute increased to 8 at 5 minutes. Cord blood gases were perfectly normal with a pH of 7.22 and base excess of -2. Samuel had significant cardiomegaly and had an in depth cardiac workup. He also suffered from respiratory distress, thrombocytopenia, and severe pulmonary hypertension. Of note, an MRI scan of the brain performed on June 8th revealed increased signal in the straight sinus and a punctate area of signal in the right frontal region. An EEG on the 8th day of life was consistent with encephalopathy. There was additional evidence of borderline polycythemia and hypoglycemia. Although Samuel has substantial mental and motor impairment, today’s evaluation and review of the medical records does not suggest that his neurological injury occurred in the course of labor or delivery. More likely, Samuel has neurological problems that were acquired prenatally and his delays are therefore likely to be on a developmental basis. For this reason, I am not recommending Samuel for compensation within the NICA program. Dr. Duchowny reaffirmed his opinions contained in his June 2014 written report when he was deposed on November 10, 2015. Dr. Duchowny agreed that Samuel suffered birth trauma and some degree of oxygen deprivation, but disagrees that the oxygen deprivation suffered by Samuel resulted in brain injury. Dr. Duchowny is of the opinion that none of the findings on the MRI are the cause of Samuel’s problems because the findings are small and would not be expected to produce the pattern of deficits that he has. Instead, Dr. Duchowny is of the opinion that Samuel’s deficits were acquired prenatally. To diagnose a hypoxic ischemic brain injury, Dr. Duchowny considers the history, lab and image findings, and physical examination. Regarding Samuel’s abnormal EEG, Dr. Duchowny noted that while that means there is abnormal brain function, the cause is essentially unknown based on the EEG findings. Further, Dr. Duchowny noted that Samuel’s five-minute Apgar score was 8, which typically would not be indicative of a severe hypoxic brain injury, and that while Samuel needed resuscitation, he appeared to respond to them by the five-minute Apgar determination. Overall, Dr. Duchowny is of the opinion that the clinical picture of Samuel following delivery is inconsistent with an encephalopathic process that was caused by hypoxic ischemic brain injury at the time of delivery. He described Samuel as having a “whole complex of findings, and one of them is prenatally acquired cerebral palsy, and that would include hypotonia, the hyporeflexia and the motor developmental delay, but additionally he has severe visual impairment, which, again I think is brain based.” As for Samuel’s heart issues, Dr. Duchowny agrees that Samuel suffered a myocardial injury. But he attributed that most likely to congenital cardiomyopathy and congenital valvular problems. When asked whether oxygen deprivation can cause the type of myocardial injury that Dr. Joyce was describing, he testified that he had never seen that but it was possible in theory, noting that he was not an expert in cardiology. Nancy Rodgers-Neame (Dr. Rodgers) is a board-certified neurologist and epilepsy specialist with sub-specialties in pediatric neurology and epilepsy. She is Director of the Florida Comprehensive Epilepsy and Seizure Disorders Center in Tampa, and Medical Director of Neurodiagnostics, at Florida Hospital, Tampa Bay Division. After reviewing Samuel’s medical records, letters from his treating physicians, and the reports of Dr. Willis and Dr. Duchowny, she stated her opinion in an affidavit dated January 19, 2016, as follows: It is my opinion that Samuel Hereford suffered a birth-related neurological injury, as defined by Section 766.302(2), Florida Statutes, as a result of shoulder that caused a period of oxygen deprivation during delivery which led to a hypoxic-ischemic event that resulted in brain damage to Samuel Hereford. Although there are multiple possible contributing factors to Samuel Hereford’s neurologic disability, including congenital complications and anomalies, it is my opinion that the hypoxic birth-related neurological injury suffered by Samuel Hereford is the primary cause of his neurologic disability and rendered him permanently and substantially mentally and physically impaired. Following this records review, she performed an independent medical examination and evaluation on Samuel on March 30, 2016. She is not one of Samuel’s treating physicians, but is an expert witness on behalf of Petitioners. In Dr. Rodgers opinion, Samuel was acidotic at birth. While she acknowledged that Samuel’s MRIs of his brain are not typical of someone who had suffered such an event, she noted that an MRI is not always going to show a structural injury that coordinates with the functional problems that the child has. She acknowledged that Samuel has dysmorphic features which were prenatally acquired. She characterized them as “minor” and noted that by the time children are six years old, their dysmorphic features have to do with the fact that they are “not getting adequate input from their brain to the rest of their body. So the fact that he is confined to -- essentially unable to walk and confined to a wheelchair is significant in that it is going to cause some changes to the musculature in the legs and the musculature in the face and the arms and everything else.” Dr. Rodgers is of the opinion that the hypoxic event at Samuel’s birth was a significant contributor to his neurologic disability. Moreover, she is of the opinion that it is impossible to tell what his physical and mental condition would have been had he not suffered the hypoxic ischemic event during birth. She noted that the results of the EEG performed on Samuel when he was eight days old, noting “an excessive number of sharp waves, asynchrony and successive suppression is most consistent with an hypoxic ischemic event.” NICA presented the testimony of Dr. Jay Goldsmith, a board-certified neonatologist who is licensed in Louisiana, Florida and Virginia. He is a full professor at Tulane University School of Medicine, has an active clinical practice, and has been practicing neonatology for approximately 40 years. After reviewing the medical records in this case, Dr. Goldsmith wrote a report dated March 25, 2016, and summarized his conclusions as follows: In summary, this young man had a difficult delivery, but also has signs of a pre- existing condition prior to birth. It is my opinion to a reasonable degree of medical probability that the events at delivery did not cause or contribute to his condition today. The events in the first few days of life do not meet the criteria for intrapartum hypoxic-ischemic encephalopathy (low Apgar scores at 5 minutes, severe acidosis in the cord blood gases, seizures, multiple system organ involvement, etc.) and the cardiomyopathy seen at birth was probably due to non-immune hydrops from some intra-uterine condition. The rapid recovery of the heart and huge weight loss in the first 4 days of life would support this opinion. Babies who are asphyxiated will usually have oliguria and gain weight over the first several days of life. Moreover, the dysmorphic features suggest an intra-uterine etiology. The MRIs also are not consistent with the patterns seen after hypoxia-ischemia (watershed pattern or basil ganglia injury). The traumatic findings in the brain imaging most often resolve without sequelae. Therefore it is my belief that Samuel does not qualify for compensation under the Florida NICA statute. Dr. Goldstein’s ultimate opinion is that Samuel suffered prenatally from a condition called non-immune hydrops, also known as hydrops fetalis. He explained that hydrops fetalis is not really a diagnosis but is “a symptom complex secondary to another diagnosis,” which in his opinion is the congenital heart defect of mild Ebstein’s anomaly. Non-immune hydrops is a collection of fluid around areas of the body, and the neonate loses the fluid (and weight) after good systolic function of the heart is reestablished. He is of the opinion that Samuel’s cardiomyopathy at birth was part of the process with the Epstein’s anomaly that caused him to suffer congestive heart failure in utero, which caused him to develop non-immune hydrops. He further explained that this process results in a lack of perfusion or oxygenation to Samuel’s organs, including his brain, and ultimately led to the development of brain damage. He acknowledged that Samuel suffered a myocardial infarction, but attributed it to congestive heart failure due to congenital heart defects. Dr. Goldsmith was of the opinion that the findings on Samuel’s MRI were not consistent with long-term neurological deficits. He acknowledged that Samuel was born floppy, apneic and depressed, but noted that his five-minute Apgar score was 8 and that “minutes to first gasp” was recorded as less than one minute. With respect to the blood gases, Dr. Goldstein is of the opinion that just because the baby had a shoulder dystocia and a six-minute head to body birth interval, that it does not necessarily mean that there is total obstruction of the umbilical cord. These opinions are in disagreement with Dr. Willis’ testimony regarding the blood gases or the cord compression. As is common in cases which involve a “battle of the experts,” all of the physicians testified credibly as to their individual medical opinions. Dr. Goldstein’s testimony was consistent with some opinions of the other doctors testifying in this case, and inconsistent with others. He appears to be the only doctor who believes that Samuel had hydrops. It was not noted on any ultrasound during Mrs. Hereford’s pregnancy and is not a diagnosis that was ever mentioned to the Herefords by any of Samuel’s many treating doctors. Dr. Joyce unequivocally testified that Samuel did not have hydrops. While he and Dr. Willis agreed that a five-minute Apgar score is not typical for a baby with acute birth asphyxia, they disagreed as to whether or not the cord compression for six minutes resulted in lack of oxygen to the infant. The ultimate opinions of the two pediatric neurologists are obviously in disagreement. As Dr. Duss testified, this case is not “clear cut.” There is no dispute that Samuel has permanent physical and mental impairments. There is no real dispute that Samuel had a traumatic birth and that he was deprived of oxygen for a period of time, which led to some brain injury. There is no real dispute that Samuel has some dysphormic features, albeit generally considered mild. The dispute centers on what, more likely than not, was the primary cause of Samuel’s impairments. That is, was the hypoxic ischemic event that occurred at Samuel’s birth the cause of his disabilities, or is it more likely than not that they were caused by a prenatally acquired congenital or genetic disorder acquired in utero. The undersigned finds the testimony of two of Samuel’s treating physicians, Dr. Joyce and Dr. Duss, in separate specialties to be compelling. That is, these two specialists testified credibly that the hypoxic ischemic event which occurred at birth was the primary cause of Samuel’s impairments. Dr. Duss’ testimony that a hypoxic ischemic event is the number one cause of cortical visual impairment was not rebutted. The greater weight of the evidence establishes through the opinions of Dr. Joyce and Dr. Duss, together with Dr. Rodgers, that there was an apparent obstetrical event that resulted in loss of oxygen to Samuel’s brain during delivery that resulted in brain injury, which rendered him permanently and substantially mentally and physically impaired.
