The Issue The issue is whether Respondent is guilty of failing to practice medicine in accordance with the applicable standard of care by failing to assess adequately a patient's complaints, failing to provide an adequate diagnosis, failing to obtain a specialized consultation, and failing to pursue the appropriate treatment, in violation of Section 458.331(1)(t), Florida Statutes, and failing to keep adequate medical records to justify the use of Cardizem and document the drug's effect, in violation of Section 458.331(1)(m). If guilty of either of these offenses, an additional issue is the penalty that should be imposed.
Findings Of Fact At all material times, Respondent has been a licensed physician, holding license number ME 0048483. He is Board Certified in Emergency Medicine. On May 16, 1994, shortly after 2:00 PM, a 48-year-old male presented at the Naples Community Hospital emergency room with the chief complaints of a rapid heart rate and shortness of breath. He felt warm, but denied feeling nauseous or chest pain. He also reported that he had not had any previous cardiac problems or any head trauma. The patient's heart rate was rhythmic, though rapid at 132 beats per minute. His respiration rate was 24, and his blood pressure was 110/80. The nurse initially examining the patient applied a pulse oximeter and obtained an abnormally low reading of 70 percent on room air. The patient's grey color confirmed that this was not an erroneous reading. The nurse immediately placed the patient on oxygen. After the oxygen was started, Respondent saw the patient, whom he found not to appear sick. The patient's breathing, though rapid, was not labored. He explained that he had come to the hospital only at the insistence of his employer. Evidently, his color had quickly improved with the administration of oxygen. Thinking that this might be a case of tachycardia, which can cause a sensation of shortness of breath, Respondent appropriately ordered a chest x-ray, EKG, and cardiac labs. Respondent received the chest x-rays promptly. They were normal, precluding, among other things, a collapsed lung. The cardiac labs were also normal. Respondent ordered two more EKGs during the patient's hospitalization on May 16. The parties disagree as to the significance of the results of the three EKGs, which revealed some abnormalities. Petitioner failed to prove that the abnormalities revealed in the EKGs were material to a correct diagnosis. Respondent's expert testified that these abnormalities were common among adults and nonspecific. He added that they did not reveal that the patient was suffering from a pulmonary embolism. This detailed, unqualified testimony from an experienced physician is credited over the testimony of Petitioner's expert. Respondent ordered an intravenous access, which was established at 3:00 PM. Although still receiving oxygen, the patient's oxygen saturation was at 97 percent at 2:45 PM and 4:00 PM. Based on his tentative diagnosis of tachycardia, Respondent administered 20mg of Cardizem at 3:35 PM. Cardizem is a calcium channel blocker, which slows down the heart rate. Generally, the patient's condition improved following the administration of the oxygen. According to the nurses' notes, the patient's breathing had slowed down by 2:45 PM, and he reported that he was feeling better by 4:45 PM. Respondent saw the patient four times during his hospitalization and confirmed for himself the nurses' observations before discharging the patient by 6:00 PM. Respondent's discharge diagnosis was paroxysmal supraventricular tachycardia--resolved. He later amended the diagnosis to sinus tachycardia, but testified that he still would have discharged the patient with this diagnosis, under all of the circumstances. The patient returned to the hospital at 10:00 AM the next day, effectively dead on arrival. He had suffered an acute pulmonary saddle embolus. The sole question in this case turns on the adequacy of Respondent's diagnosis and treatment on May 16. Petitioner's expert conceded that there were no independent issues involving the adequacy of the medical records, and Petitioner's proposed recommended order makes no mention of this alleged violation. In hindsight, it is impossible to attribute to mere chance the events of May 16 when the patient died the next morning from an acute pulmonary saddle embolus. Something happened at work, and probably was still happening when the patient first arrived at the hospital, and this was related to what killed the patient the following day. However, Petitioner has not proved that whatever happened to the patient persisted long enough for Respondent to be able to diagnose it based on the data available to him on May 16 or, even if it had, that Respondent's failure to diagnose it was a departure from the applicable standard of care. The first potentially important piece of information collected by the hospital, apart from this history, was the abnormally low pulse oximeter reading. However, Petitioner failed to prove that Respondent was aware of this information, or reasonably should have been aware of this information, at the time that he was treating the patient. The hospital had recently instituted the practice, since discontinued, of separating the nurses' notes, where the low reading was recorded, from the remainder of the medical records for a patient. Ensuing pulse oximeter readings, of which Respondent was aware, were recorded in a different place in the records from the initial pulse oximeter reading. Moreover, it is unclear whether, if Respondent had been aware of the patient's abnormally low pulse oximeter reading, this knowledge would have materially changed what Respondent had to do to meet the applicable standard of care. Ensuing pulse oximeter readings were 96 and 97 percent. Prior to discharge and after discontinuation of the oxygen for a suitably long period of time to eliminate its effects, the patient's pulse oximeter reading remained in the high 90s. Petitioner's expert witness conceded that the pulse oximeter is not a diagnostic tool for a pulmonary embolism. He testified that the EKGs were not a diagnostic tool for a pulmonary embolism, but would give hints of this condition. His main argument was that the initial pulse oximeter reading of 70 percent at room air should have been followed by an arterial blood gas test, which "probably" would have been abnormal. An abnormal arterial blood gas reading should have been followed by a VQ scan, which he asserted should have been abnormal due to little emboli coming off the lungs. However, there is a large element of speculation in the testimony of Petitioner's expert concerning these two tests. It is as likely as not that the arterial blood gas results would have been normal. The VQ scan would almost certainly have been normal, as the autopsy revealed no profusion of emboli, but only an acute pulmonary saddle embolism as the cause of the patient's death. Respondent's expert conceded that a pulmonary arteriogram probably would have been useful, but, in 20 years' practice, he could not recall ordering such a test, which is relatively frequently done in large academic institutions, but not in community hospitals, due to the mortality associated with the procedure and the 2-3 percent of false negatives. Additionally, this record does not so clearly disclose the relationship between the incident on the afternoon of May 16 and the death on the morning of May 17 to permit even an inference that a pulmonary arteriogram would have detected an abnormality in the interim between these two points. Perhaps the most important fact in evaluating whether Respondent met the applicable standard of care is that the patient exhibited none of the predisposing factors for a pulmonary embolism. He had no cardiopulmonary disease. He had no chronic obstructive pulmonary disease. A cable television installer, he was not sedentary and had no stasis of the blood flow, such as from a prolonged immobilization. He was not obese. He had no relevant trauma or injury to the lower extremities. The diagnosis of a pulmonary embolism is very difficult even with predisposing factors; in the absence of such factors, the diagnosis is dauntingly difficult. As Respondent's expert testified, he has never encountered a case of pulmonary embolism without a predisposing factor. Under all of these circumstances, especially the absence of predisposing factors, Respondent's failure to order a pulmonary arteriogram or obtain a consultation was not a departure from the applicable standard of care, nor was his failure to diagnose a pulmonary embolism, if one in fact existed on May 16. Shortness of breath and rapid heart rate are nonspecific complaints. Respondent retained the patient in the hospital for four hours for observation and analysis of test results. Respondent examined the patient four times during this hospitalization. Respondent reasonably and correctly ruled out a variety of more common diseases and illnesses. Under all of the circumstances, the final diagnosis of tachycardia, which related the shortness of breath to tachycardia or possibly anxiety, was not a departure from the applicable standard of care. Petitioner has therefore failed to prove by clear and convincing evidence that Respondent failed to meet the applicable standard of care in any respect in his diagnosis or treatment of the patient on May 16.
Recommendation It is RECOMMENDED that the Board of Medicine enter a Final Order dismissing the Administrative Complaint. DONE AND ENTERED this 4th day of August, 1998, in Tallahassee, Leon County, Florida. ROBERT E. MEALE Administrative Law Judge Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-3060 (850) 488-9675 SUNCOM 278-9675 Fax Filing (850) 921-6847 Filed with the Clerk of the Division of Administrative Hearings this 4th day of August, 1998. COPIES FURNISHED: Gabriel Mazzeo, Senior Attorney Carol A. Lanfri, Staff Attorney Agency for Health Care Administration Post Office Box 14229 Tallahassee, Florida 32317-4229 William Partridge Grossman, Roth and Partridge SouthTrust Bank Plaza 1800 Second Street, Suite 777 Sarasota, Florida 34236 Angela T. Hall, Agency Clerk Department of Health Bin A02 2020 Capital Circle Southeast Tallahassee, Florida 32399-1703 Pete Peterson, General Counsel Department of Health Bin A02 2020 Capital Circle Southeast Tallahassee, Florida 32399-1703 Dr. Marm Harris, Executive Director Board of Medicine Department of Health 1940 North Monroe Street Tallahassee, Florida 32399-0792
The Issue The issue in this case is whether Layton Maloy suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Jessica and Josh Maloy are the natural parents of Layton Maloy. Layton was born on September 4, 2012, at Lakeland Regional Medical Center, Inc. (Lakeland Regional), which is a hospital located in Lakeland, Florida. Layton was a single gestation and weighed in excess of 2,500 grams at birth. Obstetrical services at Layton’s birth were provided by Dr. Jeffrey L. Puretz, who was a physician participating in the NICA program. Notice of NICA participation was provided to Petitioners by Dr. Puretz and by Lakeland Regional. Petitioners contend that Layton suffered a birth-related neurological injury and seek compensation under the NICA Plan. More specifically, Petitioners contend that Layton suffered a stroke during labor and delivery, which resulted in a brain injury, rendering Layton permanently and substantially mentally and physically impaired. Respondent contends that there was no event during labor and delivery which resulted in oxygen deprivation to Layton, and that any medical conditions suffered by Layton are not birth-related neurological injuries as defined in section 766.302(2), Florida Statutes. Respondent further contends that Layton is not permanently and substantially mentally and physically impaired. Intervenors take no position as to whether Layton suffered a birth-related neurological injury. Layton was born at approximately 9:22 p.m., via cesarean section secondary to non-reassuring fetal heart rate tracing following six hours of labor. Following receiving an epidural, Mrs. Maloy experienced hypotension for which she received two doses of Ephedrine to raise her blood pressure. Following the second dose of Ephedrine, the baby’s fetal heart tracing became non-reassuring and the mother and baby’s heart rate became tachycardic. Mrs. Maloy also received an amnioinfusion during labor. Layton was born crying, pink and vigorous. Layton’s one- minute Apgar score was 8, and his five-minute Apgar score was 9. He did not require resuscitation at birth, and was sent to the regular newborn nursery with “routine NB orders” where he was noted to be active, awake, with normal rooting and sucking reflexes. Layton was discharged from the hospital with his mother on day two of life. After returning home, Mrs. Maloy noticed what she believed to be Layton having abnormal movements described as episodes of arms and/or legs shaking. His two-week old check-up was normal. However, two or three days after that check-up, she returned to the pediatrician’s office where “Layton had an episode in front of Dr. Leviten.” Dr. Leviten admitted Layton to Lakeland Regional for evaluation and a neurological consultation. A VEEG obtained was interpreted to reveal frontal central spike and wave on a few occasions from the left hemisphere suspicious for seizure activity. Layton was subsequently placed on Phenobarbital. Layton was noted at this time to be clinically very stable, doing well, eating well, happy and alert, and interactive. Layton was transferred to All Children’s Hospital. Upon admission, he was noted to be bottle feeding, had normal tone and no focal deficits. Dr. Ena Andrews, a pediatric neurologist, first saw Layton on September 26, 2012, at All Children’s Hospital, where she reviewed his medical records from Lakeland Regional. Her impression included a history of focal seizures and a finding on MRI that “is suspicious for intrauterine stroke.” She conducted a neurological examination of Layton. There were no abnormal findings from her neurological examination. She also reviewed a CT performed at Lakeland Regional that was read as normal by a radiologist. However, she ordered an MRI to rule out an intrauterine stroke. The MRI was conducted and Dr. Andrews reviewed the results with Mrs. Maloy on September 27, 2012: IMAGING STUDIES: I reviewed images of the MRI with mom at the bedside. As suspected, after reviewing the head CT, there is an area on the right frontal lobe with hypodensity on T2 weighted images. The area is also hypodense on diffusion, indicating it is not an acute ischemic lesion. Ventricles enlarged on the left compared to the right. There is also a hypodense area on the right parietal. Finding appears to be limited to the white matter without clear involvement of the cortex. There is no enhancement. LABORATORY STUDIES: Phenobarbital level is 22.9 this morning. IMPRESSION: History of focal seizures, doing well without seizure recurrence. Phenobarbital is in low-therapeutic range. Hypodense lesion in the right frontal and parietal white matter, unclear etiology. Given prior investigations at outside hospital, including blood cultures and CSF cultures, infection is unlikely. No evidence of diffusion change to suggest acute stroke; however, this does not rule out the possibility of prenatal stroke. Differential also includes some other type of inflammatory lesion with edema. In her deposition which was taken on June 23, 2015, when Layton was less than 3 years old, Dr. Andrews explained that her use of the word “prenatal” referenced a stroke occurring before birth, and her use of the term “acute stroke” referenced a stroke occurring within 14 days of the September 26, 2012, MRI. Dr. Andrews was asked about the comments she wrote in her September 27, 2012, notes: Q: So by “acute stroke” in your September 27th note, do you mean no stroke occurring within 14 days? A: Yes. Q: Is that 9/26 MRI? A: Correct. Q: Is that your testimony? A: Yes. Q: Now, you have -- you did not -- you did not diagnose Layton Maloy with having suffered a stroke during labor and delivery, correct? A: That’s correct. Q: Based on your notes here, would you agree with me that the imaging that you looked at was suggestive potentially for -- or rather you weren’t able to rule out a stroke occurring just before -- sometime before birth, correct? A: Correct. I was not able to rule that out. * * * Q: So one -- you actually reviewed not only the MRI that was done on September 26, 2012, but you also reviewed the CT scan that was done prior to that, correct? A: Yes. Q: Okay. And when you reviewed the CT scan, even though the radiologist didn’t note some abnormality, you felt that there was a possible abnormality on that CT scan, correct? A: Correct. Q: And you felt there was an area on the right frontal lobe that caused you some concern, correct? A: Yes. Q: And . . . you felt that the area is also hypodense on diffusion, indicating it is not an acute ischemic lesion; is that correct? A: Yes. Q: And so by that you mean that it wasn’t an ischemic event, whether it’s a stroke or something else, that caused this lesion occurring within two weeks of the study being done, correct? A: Correct. Q: And so that acute ischemic lesion that you saw on the CT scan and then correlated on the MRI, that is something that could have occurred during labor? Ms. Gaffney: Form A: Yes. Layton was discharged from All Children’s Hospital on September 29, 2012, but Dr. Andrews and another pediatric neurologist, Dr. Joseph Casadonte, followed up the medical management of Layton’s seizures in their offices beginning on October 10, 2012. Layton continues to see Dr. Andrews for management of his seizures, and has had additional brain diagnostic testing and imaging through the years. A November 28, 2012, brain MRI was read to reveal the following findings in pertinent part: Findings: The previously seen signal abnormality in the right frontal and right parietal lobes is no longer identified. Lateral ventricles and third ventricle are mildly prominent, more so then on prior examination. There is persistent asymmetry with the left lateral ventricle being larger than the right lateral ventricle. The subarchachnoid spaces are increased in size when compared to prior examination. There is no mass effect or midline shift. No abnormal fluid collections are identified. The pons is decreased in size. The vermis also appears smaller than expected. It is also noted that the corpus callosum is thinned in appearance. Layton was admitted to St. Joseph’s Hospital in January 2013, for acute vomiting and rash, with a history of seizures. Radiology results from an MRI conducted at St. Joseph’s Hospital revealed the following: IMPRESSION: Generalized volume loss in the brain with prominence of the subarachnoid space in the lateral ventricles. No transependymal fluid migration to suggest increased intracranial pressure. No intracranial hemorrhage or mass effect. While at St. Joseph’s Hospital, Layton had an 18-hour video EEG monitoring which was normal. He also had a consultation with Dr. Jose Ferreira. Dr. Ferreira’s impression included history of suspected neonatal seizures; mild degree of hypotonia of unclear significance; suggestion of mild volume loss on MRI which he believed was borderline; and the possibility of disorders associated with seizures of continued concern. He noted that the MRI showed no signs of ischemia or hemorrhage. Dr. Andrews attributes Layton’s balance and coordination issues to his mild to moderate developmental delay. Her records reflect that Layton continues to improve with function overall, and her testimony is consistent with her records. Significantly, Dr. Andrews testified that she has not seen evidence of a mental impairment, but that he suffers from physical or motor impairment for which physical therapy was prescribed. She further explained that some of the factors, e.g., social interactions, language development, and higher cognitive functions, which she would use to evaluate any mental impairment cannot be determined until he is older. She also testified that he is improving from physical therapy. When asked whether Layton’s physical impairments were permanent, she answered that she “wouldn’t be able to say whether his impairment is permanent” at this time, as she does not know to what extent he will continue to make progress and at what point he may or may not plateau. Layton also has had difficulty feeding and is being seen by a gastroenterologist for that. Layton’s most recent brain MRI was conducted on February 9, 2015. The report from the MRI contained the following: IMPRESSION: Continued somewhat slightly dysmorphic appearance of the brain as discussed in detail with mildly prominent ventricles, left greater than right. The findings may suggest some degree of volume loss, potentially involving the left basal ganglia and thalamus with question for decreased white matter volume. While nonspecific, these may be the sequela of prior insult. Dr. Andrews agrees with the above impression. She believes that his epilepsy to be symptomatic from brain abnormalities that were seen on MRI. However, when specifically asked whether the seizure disorder that Layton has is consistent with a perinatal stroke, she responded, “his epilepsy, we believe to be symptomatic from brain abnormalities that we’ve seen on MRI.” She did not specifically testify that these brain abnormalities were consistent with a perinatal stroke. Petitioners retained James Balducci, M.D., to review Layton’s medical records. Dr. Balducci practices in obstetrics and gynecology and maternal fetal medicine in Arizona. In his deposition taken on April 13, 2015, Dr. Balducci stated his opinion that Layton did sustain a brain injury caused by oxygen deprivation during labor. Specifically, Dr. Balducci is of the opinion that Layton suffered oxygen deprivation to his brain shortly after a second dose of ephedrine was administered to his mother during labor and delivery, and that this caused Layton to have a stroke. He reached this opinion by examining the fetal heart tracings. Dr. Balducci explained the basis for his opinion as follows: A: This baby suffered oxygen deprivation to the brain shortly after the second dose of Ephedrine. So the effects of the Ephedrine caused a vasoconstriction in the fetal vessels in the brain, caused an intrapartum stroke to the baby’s brain, which was the source and the cause of this baby’s neurologic sequela which the baby suffers from today. Q: And is the basis for that opinion, Dr. Balducci, the fetal heart tracings that you’ve just gone over with me? A: Yes. The fact that the baby was completely reassuring prior to the two doses of Ephedrine, and the fact that the baby became completely non-reassuring after the second dose of the Ephedrine, with the maternal pulse raising up to 140, trying to get the mother’s blood pressure up, the Ephedrine had the effect, in the fetal physiology, of causing a fetal stroke in the kid’s brain. Q: And sir, are you able to say within a reasonable degree of medical probability that that is diagnosable from these fetal heart tracings? A: Yes, ma’am. And the reason is -- Q: And the timing of the -- I’m sorry. I didn’t mean to speak over you. A: Yes ma’am, because the tracing prior to the second dose of ephedrine was reassuring, and the -- the fetal heart rate tracing post Ephedrine was completely non-reassuring, and nothing else had changed. Q: Sir, would you agree with me that you can have a non-reassuring tracing and still deliver a viable infant with no hypoxic brain injury? A: Yes, ma’am. That happens a lot. Dr. Balducci is of the opinion that a local area of Layton’s brain was devoid of oxygen secondary to the administration of Ephedrine to his mother. According to Dr. Balducci, the effects of this type of stroke may not show up until a week or two later so the baby is not depressed at birth. At the request of Petitioners, Paul Kornberg, M.D., reviewed Layton’s medical records and performed a medical examination of Layton. Dr. Kornberg is a specialist in physical medicine and rehabilitation, specifically pediatric rehabilitation. He serves as Medical Director for Tampa General Hospital’s Pediatric Rehabilitation Program and works in an outpatient clinic. His practice includes treatment of children with Cerebral Palsy and who have had intrapartum strokes. He examined Layton and evaluated him on April 7, 2015, when Layton was approximately 2 1/2 years old. Dr. Kornberg believes that Layton is permanently and substantially neurologically and physically impaired. This opinion is based on Layton’s daily seizures and that, at the time of his examination, Layton was dependent on a feeding tube. Based upon the history he was given, he noted that Layton dragged his left leg when fatigued. Upon examination, however, Dr. Kornberg found that Layton’s tone and strength appeared to be normal. At the time of his examination, Layton was walking and putting words together at the level that would be expected at his age at the time of the examination. Dr. Kornberg has no opinion as to whether Layton’s impairments are related to oxygen deprivation occurring during labor and delivery. He noted that there are causes other than an event during labor and delivery that could cause Layton’s symptoms (e.g., seizures, functional neurologic impairments, sensory processing issues), including a variety of developmental abnormalities of the brain. Layton’s school records from the Polk County Public Schools contain an initial Individualized Education Plan (IEP) which was developed at an IEP meeting on September 1, 2015, just three days before Layton’s third birthday. In the domain of Curriculum and Learning, Layton scored in the mild developmental delay range in cognitive development and scored average in communication development. In the Social Emotional Behavior domain, Layton scored in the mild developmental delay range in personal-social development. In the Independent Functioning domain, Layton scored in the significant delay range in adaptive developmental quotient and average in the motor development quotient. The initial IEP indicates that the educational setting for Layton would be in an ESE Pre-K classroom. The IEP noted that he needed a health care plan but did not need assistive technology devices or strategies and did not need specially designed or adaptive physical education (PE). A physical therapy (PT) evaluation was performed by Polk County Public Schools on November 12, 2015. It reveals that Layton’s ESE teacher reported that, at that time, Layton was able to go up and down the steps to the portable classroom with one railing and close supervision; he pedaled a small tricycle on the playground sidewalk; and he was able to drink a can of Pediasure from a straw. The physical therapist notes that although a wooden chair with armrests was available in the classroom, Layton was sitting in a standard classroom chair at the time and appears to have functional balance. He was noted to walk independently within the classroom and needed verbal cuing to remind him not to run in the classroom which, apparently, he liked to do. By observation and teacher report, Layton was noted to want to run in the classroom and to need verbal cuing to slow down. Although observed to be mildly off balance at times, falls appeared to be rare. He was reported to be able to put away his lunchbox and was eating well. He was observed walking and running on the playground without falling. Nonetheless, the PT report recommended that Layton continue to wear his soft helmet for safety when playing on the playground or transitioning on campus, due to his history of seizures and falling. Layton’s most recent PT report, dated August 30, 2016, from his school states in pertinent part: Layton should be watched closely when he is outdoors to be sure he does not get overheated. Mother had previously noted that he had a high incidence of falling (greater than 10x) per day, however by teacher report, and undersigned therapist’s observation, his falls are currently rare. Layton has been wearing a soft helmet when he is outdoors at school (on the playground and in the halls). Layton has been able to walk with the undersigned PT from his classroom, to the far end of school and back, with supervision to handheld assistance. Layton is able to walk on the yellow lines (with helmet on) with minimal verbal cuing. He is able to walk at a good pace, and has only had rare stumbles (primarily when he stumbled on a doormat, but did not fall). Layton is able to ascend steps to the portable reciprocally with one railing, and is emerging in ascending the steps reciprocally without using the railing. He is able to descend the steps in a step to fashion, both with and without the railing. Layton is able to ascend and descend the ramp without the railing with verbal cuing to slow down by teacher report for ascent and observation of PT for descent. By Mrs. Stambaugh’s report, he is able to ride the tricycle independently with the helmet on. She reported that he has not had falls on the playground. Within the classroom, Layton does not wear the helmet. He sits in a wooden toddler chair with armrests to give some additional protection if he should have a seizure while sitting in his chair in the classroom. By teacher report, Layton is potty trained, and uses the standard toilet. She noted that he wears regular underwear, but still needs assistance with hygiene. Mrs. Stambaugh reported that he feeds himself with utensils. By report, Layton is a car rider in the am and pm, and does not currently need to negotiate bus steps. By Mrs. Stambaugh’s report, they go to the field at the front of the school for fire drills, and they hold Layton’s hand when they walk there. Mrs. Stambaugh reported that Layton only climbs on playground equipment with direct, close adult supervision. The PT report suggested that Layton continue to wear his soft helmet when on the playground or walking on campus, that he should be closely supervised on any playground equipment, and that he should not get overheated. His most recent IEP dated September 7, 2016, notes that Layton loves to dress up as a police officer or fireman, and loves to play with Legos and blocks. The IEP reflects that Mrs. Maloy has Layton on a waiting list for a regular Pre-K program. It also reflects that he no longer receives G-tube feedings at school because he is eating well. However, school staff has been trained to provide G-tube feedings to him in case Layton will not eat or drink his Pediasure. Testimony of Layton’s parents is consistent with the mental and physical abilities detailed in the school records. Mrs. Maloy is able to understand Layton and attend to his needs when he communicates with her. Although Layton tends to prefer a certain food repetitively for breakfast, lunch, and dinner, he eats regular food and his G-tube is used as a supplemental feed. Layton continues to have a seizure disorder for which he continues to be followed by Dr. Andrews and continues to take medicine. Mr. Maloy plays catch with Layton, and takes him to the water park. Mr. Maloy sometimes feeds Layton food from his own plate including meats and vegetables. NICA retained Dr. Donald Willis, a physician who is board-certified in maternal fetal medicine and obstetrics and gynecology. Dr. Willis reviewed the medical records related to Layton’s birth to determine whether Layton sustained an injury to the brain or spinal cord caused by oxygen deprivation or mechanical injury in the course of labor, delivery, or resuscitation in the immediate post-delivery period. In a report dated September 2, 2014, Dr. Willis referenced relevant parts of Layton’s records and stated in pertinent part: The mother was admitted at 39 weeks in labor with spontaneous rupture of the membranes. Amniotic fluid was clear. The fetal heart rate (FHR) monitor during labor was reviewed. The FHR had a normal baseline rate of 130 bpm on admission and normal heart rate variability. Late and variable FHR decelerations began about 90 minutes prior to delivery. This pattern was followed by a period of exaggerated FHR variability with some improvement in the overall pattern prior to delivery. Cesarean section was done for “intolerance to labor.” Birth weight was 3,319 grams (7 lbs 5 oz’s). The baby was not depressed at birth. Apgar scores were 9/9. The baby came out crying and required no resuscitation. The baby was taken to the normal newborn nursery after delivery. Umbilical cord blood gas was not done. Newborn hospital course was uneventful. The baby was discharged home with the mother two days after delivery. The baby apparently did well until about two weeks after birth, when some twitching movements were noted. Seizure activity was diagnosed. Head MRI at four months of age showed generalized volume loss. In summary, Cesarean section was done for a non-reassuring FHR pattern during labor. The baby was not depressed at birth and had a normal hospital course with discharge home two days after birth. Medical records suggest the baby did not suffer a birth related injury. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical injury to the baby’s brain during labor, delivery or the immediate post delivery period. In a deposition on February 24, 2015, Dr. Willis testified as to typical findings in an infant who suffered oxygen deprivation. If a stroke is caused by hypoxic injury to the baby during labor and delivery, then the entire brain is going to be affected by the hypoxia. “I mean, we don’t see an isolated stroke in a baby like of one small, little area in the brain due to hypoxic injuries during labor and delivery.” Normally, babies born with hypoxic brain injury are depressed at birth. Layton’s Apgar score was 9 at one minute and 9 at 5 minutes, and was not depressed at birth. He noted that the hospital progress notes stated that the baby came out crying and was vigorous, and went to the normal nursery. Two days after birth, the hospital notes stated that the newborn was progressing as expected. And, he noted that the baby was discharged home after two days, which is a routine time for discharge. When asked whether the fetal heart tracing was consistent with an in utero stroke, Dr. Willis testified that “well I don’t know that a tracing can tell me if a baby had a stroke in utero.” He further explained: A: I have been reviewing cases for NICA for 14, 15 years, and what I look at is oxygen deprivation that occurs during labor or delivery that results in brain injury. And those babies, as we said, are going to have problems at birth and be depressed. I have not considered a stroke that occurs spontaneously during labor as a hypoxic event resulting in brain injury. Q: Well -- A: I am not the judge. I’m just -- I’m just the doctor that’s reviewing the cases here, but that’s how I review them and that’s what -- and that’s how I reviewed the NICA case and that’s my interpretation of what it means by oxygen deprivation with brain injury. Q: Well, I want to go over that again then. An ischemic stroke occurring in utero during labor will cause oxygen deprivation to the part of the brain that’s affected by the ischemia, correct? A: That’s correct. Q: Okay. And as you sit here today, you’re not familiar with any such pathology, an intrauterine stroke occurring during labor not caused by hypoxia? A: I’m sure all things can occur, but for NICA, I read it as I stated. I mean, if you had a stroke due to the -- that wasn’t due to oxygen deprivation, again, where would you place when that stroke occurred if there’s no event to show you that here’s where the stroke occurred? I can’t say that the baby had a stroke during labor because an MRI afterwards shows the baby had brain injury. I don’t know where that stroke occurred. The only thing I can do is look at the fetal heart rate tracing and the baby after birth and the newborn course and try to determine if that baby had oxygen deprivation sufficient enough to cause brain injury. And that’s what I’ve done on my report. If baby had a stroke that you’re talking about, who knows -- you know, how would you -- I have no way of telling where or when that would have occurred if you have a stroke that leaves a baby without symptoms, because all the ones we see due to oxygen deprivation, those babies are depressed at birth. When asked whether Ephedrine poses a risk of harm to a baby, he replied “no.” When asked whether tachycardia can cause a stroke, he replied, “Tachycardia does not cause stroke as far as I’m aware.” When asked whether there is any way from reviewing an MRI to be able to tell when an injury occurred, he replied, “no.” Dr. Willis’ opinion that there was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor or delivery is credited. NICA also retained Dr. Michael Duchowny to evaluate Layton. Dr. Duchowny is board-certified in pediatrics, neurology, with special qualifications in child neurology, and in clinical neurophysiology. He is a senior staff attending at Nicklaus Children’s Hospital, and directs the neurology training program. Dr. Duchowny reviewed Layton’s medical records and performed an independent medical examination on Layton on January 7, 2015. In a medical report dated January 11, 2015, Dr. Duchowny expressed the following opinions: In Summary, Layton’s neurological examination is only significant for mild generalized hypotonia with oromotor dysfunction and an indwelling G-tube. His motor and cognitive development are both in the 18-24 months range which places him at a mild level of disability. He is doing well from the social and behavioral domains with no specific focal or lateralizing findings of significance. This examination therefore does not provide support for the presence of either a substantial mental or motor impairment. Review of the medical records reveals that Layton was born at 39 weeks gestation at Lakeland Regional Medical Center. He weighed 3320 grams at birth and had Apgar scores of 8 & 9 at 1 and 5 minutes. He was ultimately discharged in stable condition on day 3 of life. As documented by his mother, he was diagnosed with neonatal seizures which have persisted to the present time. Most of his current issues are related to a chronic medically resistant seizure disorder. Of note, Layton has never received pyridoxine, pyridoxal-5-phosphate or biotin. Layton’s MRI scan on January 3, 2013 was significant for prominent extra-axial spaces and generalized volume loss. There is no mention of a right frontal infarct pattern. I have not personally reviewed the scan. In view of Layton’s overall developmental progress, I do not believe he should be considered for inclusion within the NICA program. Dr. Duchowny routinely reviews and interprets brain imaging studies as a daily part of his practice. He explained that the MRI is the gold standard in terms of diagnosis of stroke, and that FHR tracings are of no clinical significance in diagnosing a stroke. Had Layton suffered a stroke during labor and delivery or at any time, Dr. Duchowny would expect to see findings of that on the neuroimaging studies performed on Layton’s brain. He did not see any clinical evidence of a stroke on any of the brain MRIs he reviewed. Dr. Duchowny attributes Layton’s seizure disorder to developmental abnormalities in his brain which were acquired in utero. He attributes Layton’s mild generalized hypotonia (low muscle tone) and oral-motor dysfunction (which has necessitated a G-tube for supplemental feeding) to prenatally acquired Cerebral Palsy. When asked about Dr. Ferreira’s use of the term “volume loss” regarding the January 2013 MRI, Dr. Duchowny disagrees that there was volume loss and noted an asymmetry of the ventricles. “It certainly is not a stroke.” Regarding his physical examination of Layton, Dr. Duchowny described Layton’s motor and cognitive development to be in the mild range of delay. He noted that there were “no local or lateralizing findings as one might expect to see in a stroke.” He described his findings to be consistent with a toddler with developmental delay. Dr. Duchowny described Layton as very sociable, noting his behavior to be “appropriate.” He described Layton as a “very cute boy” who is very interactive and progressing well in the social and behavioral domains. He noted that while Layton was poorly coordinated, he could take steps and walked into the examination room. He had a “button” on the left side of his abdomen for the G-tube. He also noted that in reviewing Dr. Andrews’ records, she initially noted “suspicion of perinatal or prenatal stroke” but that notation did not carry throughout her notes over time. That is, while she considered it, she did not diagnose Layton with a stroke. This is consistent with Dr. Andrews’ testimony. Moreover, when asked about Dr. Casadonte’s notation of “concern for intrauterine stroke,” Dr. Duchowny understands that to mean prenatally acquired. When asked if it is medically probable that based on his records review, his examination of Layton, and his review of the imaging studies, whether Layton suffered a stroke during labor and delivery, Dr. Duchowny replied, “No, I don’t believe so.” Dr. Duchowny’s opinion in this regard is credited. Dr. Duchowny wrote a supplemental report dated September 19, 2016, which addressed Layton’s February 9, 2015, MRI study. This report was one page in length and reads as follows: Pursuant to your request, I reviewed the MR imaging study on Layton Maloy performed on February 9, 2015, at All Children’s Hospital. As you know, Layton has been imaged extensively in the past including head CT studies on September 24, 2012, March 7, 2013, and September 13, 2013, brain MR Imaging on Sept. 26, 2012, November 28, 2013 and February 9, 2015, and head ultrasound on October 18, 2012. The brain MR imaging study of February 9, 2015 is the most recent imaging performed to date and was obtained when Layton was 2 ½ years old. This study reveals no areas of abnormality in the cerebral cortex or subcortical white matter. The deep gray matter structures (basal ganglia and thalami) are also normal. The hippocampi demonstrate no abnormality. The lateral ventricles are enlarged and dysmorphic in appearance. The occipital horns are larger than the frontal horns and evidence a colpocephalic configuration. There is a ventricular asymmetry favoring greater enlargement on the left. The corpus callosum is borderline thin. The posterior fossa contents are abnormal and reveal ponto-cerebellar hypoplasia and vermian hypoplasia with compensatory enlargement of the fourth ventricle. In summary, these imaging findings are consistent with prenatally acquired brain malformations and provide no evidence for acquired brain injury due to either intra- partum mechanical injury or oxygen deprivation. In response to Dr. Duchowny’s one-page supplemental report, Petitioners requested Dr. Daniel Adler review the February 9, 2015, MRI report, as well as his earlier imaging reports. Dr. Adler is a pediatric neurologist who practices in New York City. It is Dr. Adler’s opinion that the images from the February 9, 2015, MRI report demonstrate a progressive loss of tissue in the white matter of Layton’s brain and are not the result of a congenital problem. He concludes that the images reflect brain injury that happened to the fetus due to intrauterine hypoxia, of a type not manifested by encephalopathy. At NICA's request, Jay Goldsmith, M.D., reviewed Layton’s medical records and the reports of all diagnostic and neuroimaging studies performed on Layton, as well as Mrs. Maloy’s labor and delivery records. Dr. Goldsmith is a neonatologist who is board-certified in Pediatrics and Neonatal-Perinatal Medicine. He practices neonatology and is a professor of pediatrics at Tulane University Medical School. He diagnoses strokes in babies as part of his clinical practice and has been practicing neonatology for approximately 40 years. In his deposition which took place on September 26, 2016, Dr. Goldsmith noted that at birth, Layton was a fairly vigorous baby with good Apgar scores. No abnormal brain function, or encephalopathy, was noted in the newborn period, and Layton went home with his mother after two days. Dr. Goldsmith explained: That’s, probably, the most important thing to rule out; an intrapartum deprivation of oxygen; if there’s no encephalopathy, for the most part, there’s no injury that occurred during labor and delivery; the person who is injured, or a baby who is injured in -- a fetus who was injured in labor and delivery will, certainly, in the overwhelming number of cases, show signs of that injury as a newborn; and demonstrate it as an encephalopathy. The one exception to that is perinatal arterial stroke; and so that’s what, basically, this case has come down to; Layton came back at two to three weeks of age with seizures; had a work-up; and subsequently, I think, seven brain imaging studies, none of which showed arterial stroke. Now, perinatal arterial stroke is a neuroradiological diagnosis, pure and simple; you can think about it; you can put it on your differential diagnosis; but if you don’t see a stroke on the images, there’s no stroke; and, in fact, as this process evolved, over two and a half years or so, the MRIs showed that Layton has a developmental, or genetic, anomaly of his brain that has, certainly, defined itself on the brain imaging. Dr. Goldsmith considers MRI to be the gold standard in diagnosing a stroke, which is consistent with Dr. Duchowny’s testimony. He further noted that Layton transitioned well from intrauterine to extrauterine, and explained that babies injured in the womb during labor and delivery do not make this transition well, would not be vigorous at birth, would be acidotic, and may need resuscitation. Dr. Goldsmith is also of the opinion that the findings of the 2015 MRI suggest a developmental anomaly of the brain, showing that his brain was slightly dysmorphic with no evidence of stroke. When asked whether he would expect to see evidence of a stroke on the MRI findings, he answered, “Yes; unfortunately, the brain does not regenerate,” noting that with an ischemic stroke, that area of the brain will die and will not regenerate. “We will see a hole in the brain in that area.” It is Dr. Goldsmith’s ultimate opinion “to an extraordinary high degree of certainty” that Layton did not suffer a stroke during labor and delivery, and that his injuries were not a result of a neurological injury caused by oxygen deprivation that occurred during labor and delivery. Dr. Goldsmith’s opinion in this regard is credited. While Dr. Goldsmith is of the opinion that Layton is permanently and substantially mentally and physically impaired, he would defer to a neurologist, especially one who has examined Layton, to make that determination. The dispute in this case centers on what, more likely than not, was the primary cause of Layton’s impairments. That is, did Layton suffer a stroke during his mother’s labor that resulted in oxygen deprivation to a specific portion of Layton’s brain which caused his disabilities or is it more likely than not that they were caused by a prenatally acquired congenital or genetic disorder acquired in utero. Secondly, did any such injury result in Layton becoming permanently and substantially mentally and physically impaired. The undersigned finds the testimony of NICA’s experts to be compelling. The greater weight of the evidence establishes through the opinions of Dr. Willis and Dr. Goldsmith, together with Dr. Duchowny, that there was not an apparent obstetrical event that resulted in loss of oxygen to Layton’s brain during labor and delivery that resulted in brain injury. Moreover, the record evidence does not support a finding that Layton is permanently and substantially mentally and physically impaired. His treating physician, Dr. Andrews, noted Layton’s improvements over time and was not of the opinion that Layton has a mental impairment. Moreover, Dr. Kornberg’s opinion that Layton is substantially impaired, while deferring to the pediatric neurologists, was based in large part on Layton’s required use of the G-tube for feeding. He has clearly improved in this regard and now uses the G-tube to supplement his eating and use of Boost or Pediasure. Dr. Duchowny’s opinion that Layton’s disabilities are in the mild range, and not considered to be substantial, is consistent with Dr. Andrews’ assessment, and is credited.
Findings Of Fact The Respondent, Stephen L. Watson, M.D., has been practicing medicine in Lakeland, Florida, since 1945. Since 1950, he has been board-certified in obstetrics and gynecology. Until this case, he has not been the subject of any Board of Medicine disciplinary proceeding. He recently closed his practice of medicine due to his own poor health. The Respondent saw B. D., as a gynecology patient, for the first time in December, 1983. She was 33 years old at the time and was obese, weighing 184 pounds and standing only approximately five feet, four inches. She also had borderline high blood pressure, at 140/90. On the patient's second visit in July, 1984, the Respondent discussed her weight and gave her a book on diet and weight loss entitled, "The Lighter Side of Life, the Doctor's Program that Really Works." He discussed the contents of the book with her, emphasizing certain parts of it. He also prescribed a month's supply of an appetite suppressant called Fastin, to be taken in conjunction with the diet recommendations, along with a diuretic. The patient's next visit was a weight conference on January 2, 1987. On this visit the patient weighed 212; her blood pressure was 140/90. The Respondent again discussed weight and diet with the patient and prescribed a month's supply of another appetite suppressant called Didrex, to be taken in conjunction with the diet recommendations, along with a diuretic. Didrex contains the anorectic agent benzphetamine hydrochloride. It is a sympathomimetic amine with pharmacologic activity similar to the prototype drugs of this class used in obesity, the amphetamines. Actions include some central nervous system stimulation and elevation of blood pressure. Didrex is contraindicated in patients with moderate to severe hypertension, and caution is to be exercised in prescribing amphetamines for patients with even mild hypertension. At the visit on January 2, 1987, it also was arranged that the Respondent would have blood work done on January 6, a pelvic examination on January 7, and another weight conference on January 29, 1987. As often would happen during the long doctor-patient relationship, the patient missed all three appointments and did not request a refill of her medications. The patient's next visit was for another weight conference on February 10, 1987. She had lost 12 pounds (down to 200), and her blood pressure reading was down to 130/88. The Respondent's course of treatment seemed to be effective. The Respondent prescribed another month's supply of Didrex, to be taken in conjunction with the diet recommendations, along with a diuretic. Ten days later, the patient came in complaining of "nerves" after taking her medications. The Respondent discontinued the Didrex and the diuretic and scheduled the patient for another weight conference for March 10, 1987. The patient missed the March 10, 1987, appointment as well as the next two rescheduled appointments, and she did not request a refill of her medications. Finally, the patient kept the third rescheduled appointment for a weight conference, for May 6, 1987. By this time, the patient's weight was back up to 208. Her blood pressure reading was 120/80. The Respondent prescribed a month's supply of another appetite suppressant called Ionamin, to be taken in conjunction with the diet recommendations, along with a diuretic. The patient missed her weight conference scheduled for June 3, 1987, and did not request a refill of her medications. The patient kept her rescheduled appointment for a weight conference, for June 11, 1987. This time, her weight was back down, to 197, and her blood pressure reading was 120/80. The Respondent's course of treatment seemed to be effective. The Respondent prescribed another month's supply of Ionamin, to be taken in conjunction with the diet recommendations, along with a diuretic. The patient again missed her next scheduled weight conference, for July 9, 1987, and did not request a refill of her medications. The patient kept her rescheduled appointment for a weight conference, for July 13, 1987. This time, her weight was down further, to 187, and her blood pressure reading again was 120/80. The Respondent's course of treatment continued to seem to be effective. The Respondent prescribed another month's supply of Ionamin, to be taken in conjunction with the diet recommendations, along with a diuretic. The patient's next weight conference was on August 17, 1987. Her weight was down a little more, to 183.5, and her blood pressure reading remained at 120/80. The Respondent's course of treatment continued to seem to be effective, although the patient's rate of weight loss was decreasing. The Respondent prescribed another month's supply of Ionamin, to be taken in conjunction with the diet recommendations, but discontinued the diuretic apparently due to a bladder problem. The patient missed her next scheduled weight conference, for September 15, 1987, and did not request a refill of her medications. The patient's next rescheduled weight conference was on October 9, 1987. Her weight was up a little, to 184.75. Her blood pressure reading again was 120/80. The Respondent prescribed another month's supply of Ionamin, to be taken in conjunction with the diet recommendations, along with a diuretic. The patient missed her next scheduled weight conference, for November 6, 1987, and did not request a refill of her medications. The patient's next rescheduled weight conference was on December 7, 1987. Her weight was down a little, to 183. Her blood pressure reading again was 120/80. The Respondent prescribed another month's supply of Ionamin, to be taken in conjunction with the diet recommendations, along with a diuretic. The patient missed her next scheduled weight conference, for January 5, 1988, and did not request a refill of her medications. The patient's next rescheduled weight conference was on February 18, 1988. Her weight was up a little, to 187.5. Her blood pressure reading was 130/80. The Respondent prescribed a month's supply of another appetite suppressant called Tenuate Dospan, to be taken in conjunction with the diet recommendations, along with a diuretic. Tenuate Dospan contains the anorectic agent diethylpropion hydrochloride. Like Didrex, it is a sympathomimetic amine with some pharmacologic activity similar to that of the prototype drugs of this class used in obesity, the amphetamines. Actions include some central nervous system stimulation and elevation of blood pressure. It is contraindicated in patients with severe hypertension, and caution is to be exercised in prescribing it for any patient with hypertension. The Respondent did not see the patient again for weight control, or prescribe any more medication, until May 3, 1988, when the patient was seen for bladder problems. Her weight was down a little, to 181.5, and her blood pressure reading was 120/80. The Respondent prescribed another month's supply of Ionamin, to be taken in conjunction with the diet recommendations, but discontinued the diuretic again apparently due to a bladder problem. The patient preferred Tenuate Dospan, and the Respondent changed the prescription to another month's supply of Tenuate Dospan. The patient missed the next two conferences, scheduled for August 8 and rescheduled for August 9, 1988, and did not request a refill of her medications. She did not see the Respondent or get any more medications from him until a weight conference on December 2, 1988. Her weight was up a little, to 185. Her blood pressure reading was 130/80. The Respondent prescribed a month's supply of Tenuate Dospan, to be taken in conjunction with the diet recommendations, along with a diuretic. The patient missed her next four scheduled appointments and did not request a refill of her medications. She did not see the Respondent or get any more medications from him until a blood pressure conference on June 28, 1989. Her weight was up significantly, to 200, and her blood pressure reading was up significantly, to 140/100. Although the patient still was relatively young (approximatly 39), and the Respondent believed there was a causal connection between the patient's weight and blood pressure, the Respondent prescribed only a month's supply of Enduron, a medication for hypertension. The patient missed her next two scheduled blood pressure conferences and did not request a refill of her blood pressure medications, or request any other medications. She did not see the Respondent or get any more medications from him until she saw him for blood in the urine on October 3, 1989, and had a urinalysis and conference. At the time, her weight was up a little more, to 203, and her blood pressure reading was 140/90. The Respondent prescribed an antibiotic and, for reasons not apparent from the evidence, a month's supply of a mild antidepressant, called Elavil. On or about October 23, 1989, the patient telephoned for a refill of her Enduron prescription, which was about to run out, and the Respondent prescribed another month's supply. The patient again missed her next weight conference scheduled for October 30, 1989, and did not request any other medications. She did not see the Respondent or get any more medications from him until a rescheduled weight conference on December 11, 1989. By this time her weight was up to 217, and her blood pressure reading was 140/98. The Respondent was aware that amphetamine-like appetite suppressants should be used with caution with patients having moderately high blood pressure, as the patient had by December 11, 1989. But he also continued to believe that there was a causal connection between the patient's weight and blood pressure and that, given the patient's relative youth and the past success with the treatment, it was worth trying appetite suppressants, in conjunction with diet recommendations, to help reduce both the patient's weight and her blood pressure. He prescribed a month's supply of Tenuate, to be taken in conjunction with the diet recommendations, along with a diuretic. (Tenuate is essentially the same drug as Tenuate Dospan but is shorter lasting.) On January 5, 1990, the patient telephoned the Respondent with a complaint of "nerves." The Respondent prescribed another month's supply of Elavil, with authority for two refills. The patient's next weight conference was on January 24, 1990. Her weight was up a little more, to 220, and her blood pressure reading was 160/98. At that point, it seemed that perhaps the Tenuate Dospan was not effective. Although there could be other explanations why the patient was not losing weight, and it was possible that all appetite suppressants had become ineffective, the Respondent decided to switch the patient to Didrex, which seemed to have been effective in the past, and prescribed a month's supply, to be taken in conjunction with the diet recommendations, along with a diuretic. He also changed her blood pressure medication to Wytensin. The patient missed her next weight conference, scheduled for January 31, 1990, and did not request any additional medications. The patient did not see the Respondent again, or get any additional medications from him, until March 21, 1990, when she saw him to get a letter for employment purposes certifying that she was disease-free. Her weight was up to 226, and her blood pressure was 164/96. The Respondent prescribed another month's supply of Didrex, to be taken in conjunction with the diet recommendations, along with a diuretic and another month's supply of Wytensin. The patient did not see the Respondent again, or get any additional medications from him until August 28, 1991, when she saw him to complain of blood in the urine. At this time, her weight was 234, and her blood pressure reading was 140/90. In addition to treating the urine problem, the Respondent prescribed a month's supply of Tenuate, to be taken in conjunction with the diet recommendations, along with a diuretic and a month's supply of Wytensin. The patient missed her appointment for a pelvic examination on September 5, 1991, and did not see the Respondent, or get any additional medications from him until she went to a weight conference on December 11, 1989. Her weight was 234.5, and her blood pressure reading was 140/94. The Respondent prescribed a month's supply of Tenuate, to be taken in conjunction with the diet recommendations, along with a diuretic. (It is not clear from the evidence why no blood pressure medication was prescribed.) The patient missed her appointment for a pelvic exam on December 17, 1991, and missed scheduled weight conferences for February 10, 11, and 19, 1992. She did not request any additional medications during this time. The patient made her next scheduled appointment on March 16, 1992, when the Respondent discussed her weight, blood pressure and complaint of headaches. Both her weight and her blood pressure were at their highest: weight, 237; blood pressure reading, 150/110. At this point, there was a real question whether the appetite suppressants still were effective in controlling the patient's weight and thereby helping reduce the patient's blood pressure. On the other hand, the patient continued to miss weight conferences and not follow through on the Respondent's instructions, and it was not clear whether the patient ever had followed the Respondent's weight control treatment long enough to give it a fair chance to work. The patient's blood pressure now was moderately to severely high; on the other hand, she still was only about 42 years of age, and her weight still could have been contributing to her high blood pressure. Nonetheless, the Respondent decided to prescribe only Wytensin on March 16; he also scheduled a complete physical for March 20, 1992. On March 20, 1992, the Respondent had the patient undergo a complete physical. Her weight still was 237, and her blood pressure reading was 160/120. He switched her blood pressure medication to Accupril and decided not to prescribe any appetite suppressants at that time. He scheduled the patient for a weight conference on April 3, 1992. On April 3, 1992, the patient's weight still was 237, but her blood pressure reading was 150/110. Although the patient's blood pressure still was moderately to severely high, the Respondent decided to try an appetite suppressant to reduce her weight in the hopes of, together with the blood pressure medication, effecting a lasting reduction in her blood pressure. He prescribed a month's supply of Tenuate Dospan, to be taken in conjunction with the diet recommendations, along with a diuretic. On April 14, 1992, the patient telephoned the Respondent to report that her blood pressure still was up and that she continued to suffer from headaches. The Respondent decided that it was time to refer the patient to a specialist in internal medicine and made an appointment for her. The patient missed her next scheduled weight conference on April 16, 1992, and missed the appointment with the internist which the Respondent had scheduled for her. She never saw the internist. The patient's next appointment was on May 6, 1992. The Respondent discussed the patient's weight and her hypertension. Her weight was 236, and her blood pressure reading was down to 144/100. The Respondent decided to prescribe a month's supply of Tenuate, to be taken in conjunction with the diet recommendations, along with a diuretic. The patient overdosed on a pain medication (not the appetite suppressant) and was hospitalized on June 4, 1992. She missed the next scheduled weight conference on June 15, 1992. She did not request any additional medications. The patient's next appointment with the Respondent was on June 18, 1992. She weighed 230, and her blood pressure reading was 140/110. The Respondent prescribed only Accupril and an iron supplement. The Respondent only saw the patient once more, on July 17, 1992, for gynecological problems, and referred the patient to a specialist. He did not prescribe any medications. The patient's blood pressure was 130/100. Her weight was not recorded. The evidence does not reflect that the patient, B. D., grew progressively dependent on the appetite suppressants the Respondent prescribed for her. There was no evidence that the patient ever asked for a refill or new prescription early. She often missed scheduled appointments, resulting in gaps of time between prescriptions when the patient presumably had no appetite suppressants available to her. There also were extended periods of time between visits during which time the patient presumably had no appetite suppressants available to her. Some reputable physicians now seriously question the use of appetite suppressants. There is some evidence that patients lose as much weight and maintain as much weight loss without them as with them. The trend in the late 1980s and early 1990s has been to treat patients for obesity with behavior modification (essentially, diet and exercise) only. But there is no evidence that it is below the level of care, skill and treatment which is recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances to treat patients for obesity by prescribing appetite suppressants in conjunction with diet recommendations. It is true that the Respondent prescribed appetite suppressants for longer periods of time than recommended in the medical and pharmaceutical literature. The literature recommends using appetite suppressants only during the early weeks of a weight reduction program. The reasons are twofold and related: first, the patient generally builds a tolerance to the appetite suppressant, making them less effective; second, the patient can become dependent on them. The goal is to use appetite suppressants to begin reducing caloric intake for initial weight loss, while changing eating habits for long term reduction in caloric intake and weight. The problem confronting the Respondent in this case lay in the nature of the patient's noncompliance. She would begin the program but not follow it or continue with it for long. When she returned to the Respondent after a long hiatus, it was like starting the program over again. The evidence did not prove that it was below the level of care, skill and treatment which is recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances for the Respondent to repeatedly restart his treatment for obesity, namely by prescribing appetite suppressants in conjunction with diet recommendations. There were occasions when the Respondent prescribed an appetite suppressant when the patient's blood pressure reading was high. According to the medical and pharmaceutical literature and the expert medical testimony, caution should be exercised in prescribing these medications for patients with high blood pressure. But the exercise of that caution is a matter of medical judgment, based on an overall knowledge and understanding of the patient and circumstances involved. Only once, on April 3, 1992, did the Respondent prescribe an appetite suppressant (Tenuate Dospan) when the patient's blood pressure reading was so high (150/110) as to clearly contraindicate the use of the appetite suppressant. On all other occasions, the patient's blood pressure would be considered mildly or moderately high, requiring the Respondent to exercise caution, which he did. In all cases, the Respondent believed that there was a causal connection between the patient's weight and blood pressure and that, given the patient's relative youth and the past success with the treatment, it was worth trying appetite suppressants, in conjunction with diet recommendations, to help reduce both the patient's weight and her blood pressure. Although some physicians would disagree with the Respondent's medical judgments, except for April 3, 1992, it was not proven that the Respondent's medical judgment in this case fell below the level of care, skill and treatment which is recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances. However, it is found that it was below the level of care, skill and treatment which is recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances for the Respondent to prescribe Tenuate Dospan on April 3, 1992. It was not proven that it was below the level of care, skill and treatment which is recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances for the Respondent not to refer the patient to a specialist for hypertension before April 14, 1992. The first evidence of severe hypertension appeared on her visit on March 16, 1992. But the Respondent had not seen the patient since December, 1991, due to missed appointments, and it was reasonable at that point for the Respondent not to refer immediately. It could be argued that he should have referred the patient after one of the next two visits, but the delay until April 14, 1992, was fairly short. It was not the Respondent's fault that the patient did not keep the appointment with the specialist which he made for her. It should be noted that the patient does not complain about the level of care and treatment given by the Respondent. Nor is there any evidence that the Respondent's care and treatment harmed the patient. Apparently, while the patient was hospitalized for overdosing on pain medication unrelated to the Respondent's care and treatment, the patient's medical records were brought to the attention of the predecessor of the AHCA, and it appeared to that agency (and to the AHCA) that the Respondent was guilty of worse practice of medicine than ultimately was proven in this case.
Recommendation Based on the foregoing Findings of Fact and Conclusions of Law, it is recommended that the Board of Medicine enter a final order: (1) finding the Respondent guilty of a single violation, on April 3, 1992, of Section 458.331(1)(t), which also resulted in a technical violation of Section 458.331(1)(q), Fla. Stat. (1993); (2) requiring the Respondent to notify the Board or the AHCA if he reopens his practice of medicine; (3) placing the Respondent on probation on appropriate terms in the event the Respondent reopens his practice; and (4) fining the Respondent $500. RECOMMENDED this 15th day of November, 1994, in Tallahassee, Florida. J. LAWRENCE JOHNSTON Hearing Officer Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-1550 (904) 488-9675 Filed with the Clerk of the Division of Administrative Hearings this 15th day of November, 1994. APPENDIX TO RECOMMENDED ORDER, CASE NO. 94-2375 To comply with the requirements of Section 120.59(2), Fla. Stat. (1993), the following rulings are made on the parties' proposed findings of fact: Petitioner's Proposed Findings of Fact. 1.-8. Accepted and incorporated to the extent not subordinate or unnecessary. Rejected as not proven. Rejected as not proven. (The Respondent testified.) Accepted but subordinate and unnecessary. Accepted. First sentence, subordinate to facts contrary to those found; second sentence, subordinate to facts found. Rejected as not proven that the patient's hypertension was severe. Otherwise, accepted but subordinate to facts contrary to those found. 14.-19. Accepted and incorporated. Rejected as not proven, except for patients with severe hypertension. First sentence, rejected as not proven. (He believed it permissible because the patient's blood pressure was not stable.) Second sentence, accepted but subordinate to facts contrary to those found. Third sentence, accepted but subordinate to facts contrary to those found, and unnecessary. First sentence, accepted but subordinate to facts contrary to those found. Second sentence, rejected as not proven. Accepted. Subordinate to facts found. Accepted but subordinate to facts contrary to those found. First sentence, accepted but subordinate to facts contrary to those found. Second sentence, rejected as not proven as to Didrex after 1990; otherwise, accepted and incorporated. First sentence, accepted and incorporated. Second sentence, accepted but subordinate to facts contrary to those found, and unnecessary. (The AHCA did not charge inadequate records.) 27.-29. Accepted and incorporated to the extent not subordinate or unnecessary. Rejected as not proven. Accepted but subordinate to facts contrary to those found. Accepted and incorporated to the extent not subordinate or unnecessary. (The question is not whether a referral would have been appropriate but rather whether not referring was inappropriate.) Accepted and incorporated. Rejected as not proven that referral was required in 1984 or that the patient's weight and blood pressure did not respond to treatment before 1988. Otherwise, accepted and incorporated to the extent not subordinate or unnecessary. (The question is not whether a referral would have been appropriate but rather whether not referring was inappropriate.) Accepted but subordinate and unnecessary. Rejected. They knew it to the extent that it is the same as for an internist. 37.-38. Accepted but subordinate and unnecessary. 39. Rejected as not proven and as contrary to the facts found. Respondent's Proposed Findings of Fact. 1.-4. Accepted and incorporated to the extent not subordinate or unnecessary. 5. Accepted but subordinate and unnecessary. 6.-20. Accepted and incorporated to the extent not subordinate or unnecessary. Rejected as contrary to the greater weight of the evidence. Accepted but subordinate and unnecessary. 23.-28. Accepted and incorporated to the extent not subordinate or unnecessary. Other than evidence that she may have become nervous on occasion from the appetite suppressants, accepted and incorporated to the extent not subordinate or unnecessary. Accepted. The second occasion is irrelevant, having occurred after the events in issue in this case. The first is accepted and incorporated to the extent not subordinate or unnecessary. 31.-32. Accepted and incorporated to the extent not subordinate or unnecessary. Rejected as contrary to the greater weight of the evidence. Accepted and incorporated. Accepted but subordinate and unnecessary. 36.-37. Accepted and incorporated. 38.-40. Accepted. Subordinate to facts found. First sentence, accepted and incorporated. Second sentence, accepted but subordinate and unnecessary. Accepted (that it is not necessarily inappropriate) and incorporated. Accepted. First two sentences, incorporated; second, subordinate to facts found. Accepted. Subordinate to facts found. Rejected as to April 3, 1992, as contrary to facts found and to the greater weight of the evidence. Otherwise, accepted but subordinate to facts found. 46.-47. Accepted and incorporated. 48. Rejected as to April 3, 1992, as contrary to facts found and to the greater weight of the evidence. Otherwise, accepted and incorporated. COPIES FURNISHED: Alex D. Barker, Esquire Elaine Lucas, Esquire Agency for Health Care Administration 7960 Arlington Expressway Suite 230 Jacksonville, Florida 32211-7466 John A. Naser, Esquire 1401 South Florida Avenue Suite 201 Lakeland, Florida 33802 Dr. Marm Harris Executive Director, Board of Medicine Agency for Health Care Administration Northwood Centre 1940 North Monroe Street Tallahassee, Florida 32399-0792 Harold D. Lewis, Esquire Agency for Health Care Administration The Atrium, Suite 301 325 John Knox Road Tallahassee, Florida 32303
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 The issue in this case is whether Respondent, Charles R. Thompson, M.D., 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 as alleged in an Administrative Complaint entered November 3, 1993.
Findings Of Fact The Parties. Petitioner, the Agency for Health Care Administration (hereinafter referred to as the "Agency"), is the state agency charged with regulating the practice of medicine in the State of Florida pursuant to Section 20.165, Florida Statutes, Chapter 455, Florida Statutes, and Chapter 458, Florida Statutes. (Stipulated Fact). Respondent, Charles R. Thompson, M.D., is, and has been at all times material hereto, a licensed physician in the State of Florida. Dr. Thompson was issued license number ME 0053590. Dr. Thompson's last known address is 8333 North Davis Highway, Pensacola, Florida 32514. (Stipulated Facts). Dr. Thompson specializes in internal medicine. Dr. Thompson is not, however, Board certified in internal medicine. (Stipulated Facts). At all times relevant to this proceeding, Dr. Thompson was a shareholder/employee of the Hodnette Medical Center Clinic, a/k/a The Medical Center Clinic, P.A. (hereinafter referred to as the Medical Center Clinic"), in Pensacola, Florida. Dr. Thompson has not been the subject of any disciplinary action against his license to practice medicine, other than the subject proceeding, and has had no medical malpractice claims asserted against him. Patient Number 1, K. M.. Patient Number 1, K. M., was a 27 year old female. (Stipulated Fact). K. M. had a history of severe insulin dependent diabetes mellitus, severe hypertension, blindness due to diabetic retinopathy, and chronic renal failure. K. M. had lost a toe due to gangrene. (Stipulated Facts). She suffered from fluctuating blood sugars, recurring problems with headaches, recurring problems with nausea and vomiting, recurring instances of non- compliance with physicians' orders, recurring episodes or phases of anemia and recurring periods during which she suffered from diabetic ketoacidosis. K. M. was also suspected of suffering from coronary artery disease, due to the severity and duration of her diabetes and the resulting peripheeral vascular disease. She was also suspected to suffer from diabetic gastroparesis, a condition that affects the function of the stomach and digestive tract. Dr. Thompson had become K. M.'s primary treating physician around October of 1989. She had been a patient at the Medical Center Clinic prior to becoming Dr. Thompson's patient. Emergency Room Visits Prior to September, 1990. During the year 1990, K. M. went to the Emergency Department of West Florida Regional Medical Center (hereinafter referred to as "West Florida Regional"), on eight different occasions prior to September 16, 1990. On some of the 1990 Emergency Department visits, K. M. presented with symptoms similar to those which she presented with at the time of the hospitalization which is the subject of this proceeding. The symptoms she presented with included headaches, nausea and vomiting, hypertension and manifestations of kidney dysfunction. Dr. Thompson was consulted on three of these occasions. K. M. was hospitalized from July 9, 1990 through July 19, 1990. She was under the care of Dr. Thompson during this hospitalization. K. M. was treated for insulin dependent mellitus, nausea and vomiting secondary to probable gastroparesis, hypertension, dehydratin and anemia. During K. M.'s July, 1990, hospitalization, she received IV fluids, blood pressure medications, and medication to treat nausea and vomiting and the effects of diabetic gastroparesis. She was discharged in stable condition on July 19, 1990. K. M.'s Hospitalization in September of 1990. On or about September 16, 1990, K. M. presented to the Emergency Department of West Florida Regional with complaints of headache, nausea and uncontrolled vomiting. K. M. was vomiting blood. (Stipulated Facts). Dr. Thompson, K. M.'s primary care physician, was consulted by the Emergency Department physician. Dr. Thompson examined K. M. and noted that she was dehydrated with no diarrhea or edema, had clear lungs and a regular heart rate and rhythm. K. M. had a blood pressure of 218/137. (Stipulated Facts). Dr. Thompson diagnosed K. M. with dehydration, nausea, probably due to chronic renal failure, and possible tear ("Mallory-Weis") to the esophagus due to severe vomiting. (Stipulated Facts). Dr. Thompson's assessment also included the following findings: (a) insulin-dependent diabetes mellitus; (b) hypertension; (c) chronic renal failure secondary to diabetic nephropathy; (d) migraine headaches; (e) mild diabetic ketoacidosis; (f) anemia; (g) poorly controlled blood sugars; and (h) tachycardia. At the time of her admission to West Florida Regional, K. M. was critically ill. A component of K. M.'s illness was her volume status. Dr. Thompson admitted K. M. to the Critical Care Unit (hereinafter referred to as the "CCU"), of West Florida Regional, administered Catapres intravenously to lower her blood pressure, and issued orders for intravenous rehydration and insulin therapy. (Stipulated Facts). Dr. Thompson also ordered Bicitra for K. M.'s acidosis. Dr. Thompson's full admitting orders are recited in Respondent's proposed finding of fact 8. The protocol for the CCU included orders for the contemporaneous recording of all intake and output of a patient receiving IV fluids, such as K. M. The protocol also included orders for the taking of vital signs, including pulse, respiration and blood pressure on a frequent and regular basis. The protocol orders were followed for K. M. K. M. was admitted to the CCU by Dr. Thompson because he believed she would receive more constant nursing supervision and attention than on the regular hospital floor. There was one nurse to every one or two patients on the CCU, a much higher nurse staffing ration than on the regular floor. On September 17, 1990, Dr. Thompson's physical examination of K. M. revealed that her nausea persisted with some vomiting. The bleeding, however, had decreased. Dr. Thompson's medical records reflect that K. M. refused an upper endoscopy to determine the cause of the bleeding. K. M. also declined Dr. Thompson's suggestion that she could benefit from a blood transfusion. Dr. Thompson also noted no edema. (Stipulated Facts). At 3:00 p.m., on September 17, 1990, Dr. Thompson ordered Demerol, 25 mg IM or IV every four hours PRN for pain. At 5:55 p.m. Dr. Thompson ordered 14 units of insulin, SQ stat. Dr. Thompson later ordered the following: Please begin clear liquids - ADA SMA-7, CBC in AM MG SO4 8 mg IV over 6 hrs (in N/S) Notify Dr. Wayne Miller of admit & location Stools for blood, X 3 Bicitra 15 cc po BID On September 18, 1990, Dr. Thompson examined K. M. Dr. Thompson found the following: Continues with nausea, vomiting. Some coffee-ground material. Afebrile, Vital Signs Stable. Exam--unchanged. Blood sugars fluctuating 35-400. Hematocrit down to 22.4 last p.m., 23 this a.m. Patient refuses transfusion and endoscopy. Will continue to monitor H & H and B.S. If Hematocrit continues to fall, will have to convince to have transfusion and endoscopy. Based upon Dr. Thompson's examination of K. M. on September 18, 1990, he ordered: (a) Hematocrit and hemoglobin be changed every 8 hours, instead of every 12 hours--call if Hematrocirt goes below 22; and (b) SMA-7, CBC in a.m. On or about September 19, 1990, Dr. Thompson examined K. M. and noted 1+ edema in the hands and feet. Edema is swelling and is an indication that a person is retaining excessive fluids. Dr. Thompson ordered 20 mg. of Lasix, a diuretic, and reduced K. M.'s fluid intake. According to Dr. Thompson's records he also found no S3 Gallup and that her lungs were clear. (Stipulated Facts). Dr. Thompson's observations of the results of his examination of September 19, 1990, were as follows: Patient confused yesterday and this a.m. Still with some dry heaves. Afebrile--vital signs stable. Lungs: clear CV: regular rate and rhythm without S3 gallop Abdomen: positive bowel signs, no increased organomegaly Extremities: 1+ edema feet and hands Intate/Output markedly positive Hematocrit 24.6 this a.m. Blood Sugars 100-250 Plan: Will transfer to floor--watch blood sugars and Hematocrit and Hemoglobin-- as long as stable Hematocrit and Hemoglobin, will try to hold on Endoscopy, but if nausea, gagging continue, will need to look at stomach. Give Lasix and decrease IV fluids. Check labs in a.m. Dr. Thompson ordered the following: Please transfer to floor, no monitor needed. Decrease Hematocrit and Hemoglobin checks to every 12 hours. SMA-18, CBC in a.m. Lasix 20 mg IV now. Decrease IV fluids to 100 CCs per hour [down from 150]. Decrease Zantac to 50 mg IV. After Dr. Thompson examined K. M. on September 19, 1990, he visited briefly with her parents. Dr. Thompson then checked out of the hospital and went home because he was ill. Pursuant to protocol, another physician was to cover for Dr. Thompson. On or about September 19, 1990, K. M. suffered cardiac arrest and revived. K. M. expired after multiple episodes of cardiac arrest. (Stipulated Facts). K. M. first sustained an acute myocardial infarction at approximately 3:00 p.m. This was the first time that K. M. first evidenced shortness of breath. Three separate Code 3 procedures were administered to K. M. During the Code 3 procedures she received additional fluids. The autopsy report on K. M. dated September 20, 1990 indicates that K. M. suffered from acture bilateral bronchopneumonia of the lower lobes with severe pulmonary edema and bilateral pleural effusions, severe artherosclerosis, and marked abdominal ascites. The cause of K. M.'s death was an acute myocardial infarction. (Stipulated Facts). To the extent that K. M. experienced a fluid overload, that condition did not cause the myocardial infarction she suffered. Fluid overload had nothing to do with the myocardial infarction. E. Monitoring K. M.'s Fluids. K. M.'s condition required that her fluids be monitored. K. M. was receiving rehydration therapy. She was also receiving medication to control her hypertension. These are opposing therapies and, therefore, more strict monitoring was required. While K. M. was dehydrated and needed fluids, the condition of her kidneys caused her to be less able to handle fluids. It is preferrable, however, that a patient such as K. M. experience some fluid overload as opposed to being dehydrated. Nonetheless, if a patient receives and retains excessive fluids it can be detrimental to the patient. For example, a patient that receives and retains excessive fluids may develop pulmonary edema. Dr. Thompson monitored K. M.'s rehydration progress through "gross methods". Dr. Thompson used physical examination, including listening to K. M.'s heart and lungs with a stethescope and physically and visually checking for swelling or the absence thereof. K. M.'s fluid intake and output was also recorded and reviewed by Dr. Thompson. K. M.'s intake and output of fluids was monitored and recorded on a continuing basis each day that she was hospitalized, consistent with protocols. Fluid intake was recorded by IV fluid, IV medication and oral consumption. Fluid output was recorded as urine, bowel movements and emesis. Measuring fluid intake and output is not completely accurate. Dr. Thompson monitored K. M.'s intake and output, he examined K. M. daily, he looked for pulmonary or cardiac signs of fluid overload, he reviewed nurses notes, graphic sheets recording pulse rate, respiration and blood pressure, and reviewed lab results. These items did not suggest that K. M. was experiencing fluid overload. Dr. Thompson was alert for any signs of edema. There was, in fact, no sign of edema until the morning of September 19, 1990, and Dr. Thompson took steps to alleviate what he concluded was mild edema. Until that time, K. had not evidenced any shortness of breath, which would have suggested pulmonary edema and a possible fluid overload. Dr. Thompson did not order the use of a Swan-Ganz catheter or a central venous line. These are both invasive devices designed to measure fluids. Dr. Thompson also did not order daily weighing of K. M. Weighing a patient can provide information about fluids levels by monitoring weight gain. Dr. Thompson also did not order daily x-rays of K. M.'s lungs to determine if she had fluid in her lungs. Dr. Thompson relied on listening to her lungs with a stethoscope. K. M. Experienced Excessive Fluids. K. M. experienced excessive fluids, or a "fluid overload", while under Dr. Thompson's care. The terms "fluid overload" refer to the condition of the body when excessive fluids are retained in the body. While hospitalized, K. M. received approximately 8,120 cc.'s of fluid in excess of what her intake and output measurements indicated she was excreting. On the second day of her hospitalization, K. M. received three times the amount of fluids she excreted. On the morning of September 19, 1990, a nurse caring for K. M. telephoned Dr. Thompson and expressed concern to Dr. Thompson over the amount of fluids K. M. was receiving. It was after this telephone call that Dr. Thompson noted K. M.'s edema and ordered a reduction in her fluids and that she be given Lasix, a diuretic. Although K. M. did not have any signs of fluid overload until the morning of September 19, 1990, the results of her autopsy indicate that she had begun suffering a fluid overload one or two days earlier. The autopsy also revealed that K. M. had bilateral pneumonia. This condition was not detected by Dr. Thompson during his clinical assessment of her. Did Dr. Thompson Fail to Adequately Monitor K. M.'s Fluid Level? The evidence failed to prove that there is a single, standard method of monitoring the fluid status of a patient such as K. M. The physicians called as witnesses by the Agency all agreed that Dr. Thompson failed to adequately monitor K. M.'s fluid levels. All three physicians disagreed, however, about the method of monitoring that should have been employed. The physicians called as witnesses by Dr. Thompson all agreed that Dr. Thompson's efforts to monitor K. M.'s fluid levels were adequate. The explanations provided by the Agency's witnesses of their opinions as to Dr. Thompson's treatment were inadequate to support a finding that the opinions as to Dr. Thompson's treatment provided by Dr. Thompson and his witnesses were inaccurate. The weight of the evidence failed to prove that Dr. Thompson deviated from the appropriate standard of care by failing to adequately monitor K. M.'s condition. The weight of the evidence failed to prove that Dr. Thompson failed to practice medicine with an acceptable level of care, skill, and treatment which a reasonably prudent similar physician recognizes as acceptable under similar conditions.
Recommendation Based upon the foregoing Findings of Fact and Conclusions of Law, it is RECOMMENDED that the Agency for Health Care Administration enter a Final Order dismissing all charges in the Administrative Complaint entered against Charles R. Thompson, M.D. DONE and ENTERED this 1st day of July, 1996, in Tallahassee Florida. LARRY J. SARTIN, Hearing Officer Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-1550 (904) 488-9675 Filed with the Clerk of the Division of Administrative Hearings this 1st day of July, 1996. APPENDIX TO RECOMMENDED ORDER, CASE NO. 94-6437 The parties have submitted proposed findings of fact. It has been noted below which proposed findings of fact have been generally accepted and the paragraph number(s) in the Recommended Order where they have been accepted, if any. Those proposed findings of fact which have been rejected and the reason for their rejection have also been noted. The Agency's Proposed Findings of Fact Accepted in 2. Accepted in 3. Accepted in 6-7. Accepted in 14. Accepted din 14-15 and 18. See 16 and 19. Hereby accepted. Accepted in 8. 9-10 Accepted in 18. Accepted in 32. Hereby accepted. Accepted in 34-36. Accepted in 35. 15-16 Not supported by the weight of the evidence. 17 Accepted in 33. 18-19 Accepted in 32. Hereby accepted. Not supported by the weight of the evidence. See 26. Accepted in 27. Hereby accepted. See 20. 26-27 Not supported by the weight of the evidence. 28 Accepted in 40. 29-30 Accepted in 41. The last sentence of proposed finding of fact 30 is not supported by the weight of the evidence. 31 See 42. 32-33 Accepted in 25. 34 See 25 and 42-43. Accepted in 25 and 27. See 27 and hereby accepted. Accepted in 29. Not supported by the weight of the evidence. Accepted in 30 and 43. Accepted in 32. Accepted in 26. 42-43 Accepted in 43. 44-50 Not supported by the weight of the evidence. Dr. Thompson's Proposed Findings of Fact Accepted in 2-4 and hereby accepted. Accepted in 9. Accepted in 7-8. Accepted in 10-11 and hereby accepted. Accepted in 12-13 and hereby accepted. Accepted in 14-16 and 18. Accepted in 17. Accepted in 19 and hereby accepted. Accepted in 21 and hereby accepted. 10-11 Accepted in 21. Accepted in 22. Accepted in 23. Accepted in 24. Accepted in 26 and hereby accepted. Accepted in 27. Although generally correct, this charge was dismissed by Petitioner. Accepted in 35 and hereby accepted. Accepted in 28 and hereby accepted. Accepted in 29 and hereby accepted. Accepted in 30. Statement of the issues. Paragraph 22(a) was dismissed by Petitioner. Hereby accepted. Accepted in 35. See 34-36. Restatement of previously proposed findings. Accepted in 37-39. See 44-49. These proposed findings constitute an accurate summary of testimony. See 45-49. These proposed findings constitute an accurate summary of testimony. 29-30 These proposed findings constitute an accurate summary of testimony. See 45-49. These proposed findings constitute an accurate summary of testimony. These proposed findings constitute an accurate summary of testimony. 33-34 These proposed findings are generally correct but are irrelevant. 35-36 These proposed findings constitute an accurate summary of testimony. See 45-49. These proposed findings constitute an accurate summary of testimony. These proposed findings constitute an accurate summary of testimony and argument. These proposed findings are a repeat of previous proposed findings. Hereby accepted. Accepted in 36. These proposed findings are a repeat of previous proposed findings. Hereby accepted. 44 See 45-49. COPIES FURNISHED: Britt Thomas, Esquire Agency for Health Care Administration Northwood Centre, Suite 60 1940 North Monroe Street Tallahassee, Florida 32399-0792 James M. Wilson, Esquire 307 Palafox Street Pensacola, Florida 32501 Dr. Marm Harris, Executive Director Agency for Health Care Administration Board of Medicine 1940 North Monroe Street Tallahassee, Florida 32399-0792 Douglass M. Cook, Director Agency for Health Care Administration 2727 Mahan Drive Tallahassee, Florida 32308 Jerome W. Hoffman, Esquire 2727 Mahan Drive Tallahassee, Florida 32309
The Issue The issue is whether Respondent's license as a medical doctor should be disciplined for the reasons given in the Administrative Complaint filed on October 25, 2000.
Findings Of Fact Based upon all of the evidence, the following findings of fact are determined: Background At all times material hereto, Respondent, David Lowell Williams (Respondent or Dr. Williams), was a licensed medical doctor having been issued license number ME 0035686 by Petitioner, Department of Health, Board of Medicine (Board). The Board is charged with the responsibility of regulating the practice of medicine in the State of Florida. Respondent is board-certified in cardiovascular disease and internal medicine and has practiced his specialty in Ormond Beach, Florida, since 1983. In 1990, Respondent accepted a position as a cardiologist with Florida Health Care Plan, Inc. Except for the charges raised in this proceeding, there is no evidence that Respondent has ever been involved in a prior disciplinary action. Based on a complaint filed with the Board by an attorney representing the family of a former patient, S.T., on October 25, 2000, the Department of Health, acting on behalf of the Board, filed an Administrative Complaint against Respondent generally alleging that in April 1995 he had failed to practice medicine with the level of skill and care required of a reasonably prudent physician, and that he failed to keep written medical records justifying the course of treatment of S.T. Respondent has denied the charges and contends that he practiced medicine within the standard of care and that the documentation related to the patient justified the course of treatment. In determining whether a deviation from the appropriate standard has occurred, the undersigned has considered the conflicting testimony presented by the witnesses and has accepted the more credible evidence, as reflected in the findings below. In doing so, the undersigned has discounted Petitioner's contention that Respondent's expert, Dr. Henderson, is a close friend of Respondent and therefore his testimony is clearly biased. Although the two once practiced together for a few years in the 1980's, Dr. Henderson acknowledged that they "don't get along very well right now." The treatment of the patient Over a period of years, S.T. was treated by several doctors, including Respondent, who participated in the Florida Health Care Plan, Inc. network. The medical records for that treatment have been received in evidence as Joint Exhibit No. Because they are not in chronological order, contain matters relating to treatment by physicians other than Respondent, and include some partially illigible pages, the records are somewhat difficult for the reader to navigate. They do show, however, that S.T. occasionally cancelled appointments, would not always accept his doctor's advice, sometimes refused to take prescribed medications, and was perhaps not totally candid at all times with the treating physician regarding his symptoms. The records reflect that Respondent first began treating S.T. on March 29, 1989, on referral from his primary care doctor, Dr. Moussly, due to complaints of "burning in chest with exercise." S.T., then a sixty-year-old male, underwent a stress test on the treadmill which was terminated after three and one-half minutes due to fatigue and shortness of breath. The test revealed "significant ST segment depression" and was consistent with ischemia (inadequate blood flow to the heart). Respondent prescribed Lopressor (a beta- blocking agent used in the treatment of hypertension and angina) and a Nitro-patch (transdermal nitroglycerin delivery system). Dr. Williams also recommended that the patient have a cardiac catherization. Even though the records show that the patient was "reluctant to do this at this point in time," they indicate that a coronary angiogram was performed by Respondent on April 26, 1989, and that "a high-grade stenosis of approximately 90 [percent] . . . with deeply ulcerated plaque" was exhibited in the left anterior descending artery. S.T. was again referred by Dr. Moussly to Respondent on March 7, 1990, "on an urgent basis." However, S.T. cancelled his appointment and accepted another appointment on April 4, 1990. Despite the urgency of the referral, S.T. reported to Dr. Williams that he was doing well with no symptoms since his last visit one year earlier. His records reflect that his blood pressure was 136/86, his weight 258, his pulse was 60 and regular, his lungs were clear, and a cardiovascular examination was unremarkable. Dr. Williams concluded that S.T. was stable at that time with minimal chest discomfort, and he recommended that S.T. undergo a routine treadmill exercise test to further evaluate his coronary heart disease. A stress test was performed on May 11, 1990, but it was terminated after three minutes due to shortness of breath. Another stress test was conducted on July 5, 1990, the results of which were "significant for ischemia." Although a cardiac catherization was recommended, "[t]he patient again refuses at this point in time." On May 1, 1991, S.T. was again seen by Respondent (after cancelling an earlier appointment) at which time he indicated he was feeling well and was essentially asymptomatic. He specifically denied having any shortness of breath, light-headedness, dizziness, or chest pain, and he reported that he had skipped taking his prescribed Cardizem on numerous occasions without undergoing any significant change in his symptoms. On that date, his blood pressure was 150/90, his weight 259, his lungs were clear, and the cardiovascular examination revealed no murmur. Dr. Williams concluded that the patient "seems to be stable at this point in time," and allowed S.T. to discontinue Cardizem as a therapeutic trial, and if he had no further symptoms, he would continue on Lopressor only. Otherwise, he would need to start up on that medication again. Finally, Dr. Williams offered S.T. the opportunity to participate in a beta blocker angina trial for which he would be evaluated the following week. The patient apparently declined this offer. The patient did not return to Respondent's office until December 21, 1994, or more than three years later, after he was given a "[r]outine referral for a stress test" by Dr. Moussly. S.T. had seen Dr. Moussly on a "routine followup" on December 1, 1994, at which time he denied having chest pain or shortness of breath. On his visit with Respondent, S.T. underwent another treadmill test that was terminated after two minutes due to the development of ST- segment depression. S.T. also experienced tightness in his chest. The treadmill tests were positive for ischemia "at low exercise tolerance." Based on the above results, S.T. agreed to undergo cardiac catherization. On December 28, 1994, Respondent performed the cardiac catherization on S.T., which revealed that the main coronary artery was very short, but was essentially normal. The left anterior descending artery (one of the three main arteries to the heart) exhibited a proximal 90 percent stenosis (stricture of a canal or narrowing of a cardiac valve). A second 75 percent stenosis was present in the distal portion of the artery. No other significant lesions were noted. The left circumflex artery was a large and dominant system. A stenosis in the distal portion of the parent circumflex of approximately 30 percent was present with no other significant lesions noted. The right coronary artery was a nondominant artery with no significant lesions noted. Based upon the results of the cardiac catherization, Dr. Williams concluded that P.T. demonstrated mild coronary artery disease in the left circumflex artery and "rather severe disease" in the left anterior descending artery. Respondent advised S.T. that he was a candidate for angioplasty (reconstitution or recanalization of a blood vessel) of the left anterior descending artery. On January 4, 1995, Respondent performed the angioplasty of S.T.'s left anterior descending artery, which contained two lesions. The proximal lesion was reduced from approximately 95 percent stenosis to around 10 percent, and the distal lesion was likewise reduced from approximately 75 percent stenosis to around 10 percent. On February 8, 1995, S.T. made a follow-up visit to Respondent's office. According to the patient notes, S.T.'s vital signs were normal, and he stated that he was "doing very well." Respondent's plan of treatment was to have him follow- up on an as-needed basis. In addition, Respondent discussed the "signs and symptoms of recurrence of chest discomfort" and the importance of stopping smoking as well as having good dietary practice and daily exercise. On March 7, 1995, Dr. Moussly again referred S.T. to Dr. Williams for a stress test due to the patient's "having very non[-]specific chest discomfort; non[-]exertional, non[-] radiating [pain that was] apparently . . . different than the pain he had prior to his angioplasty." Dr. Moussly also noted in his records that even though the patient had elevated cholesterol, he refused to take Pravachol, which had been prescribed by Dr. Moussly on December 1, 1994. Pursuant to the referral, on March 15, 1995, S.T. made a follow-up visit to Respondent complaining of "chest discomfort." He underwent another treadmill test which was terminated after three minutes due to chest discomfort and ST- segment depression. The test was positive for ischemia, which meant that restenosis of an artery had likely occurred. Respondent recommended repeat cardiac catheterization and angioplasty. Given S.T.'s age, progression of disease, and risk factors, which included "virtually every one known to man," restenosis was not particularly surprising since Respondent's expert established that "the restenosis rate for this [type of] patient was probably in excess of 50 percent." On March 17, 1995, Respondent performed a second angioplasty of S.T.'s left anterior descending artery and reduced the stenosis from 75 percent to 10 percent in both the proximal and distal lesions. There were no complications from this procedure, which S.T. tolerated well. On April 3, 1995, S.T. visited Respondent's office for a follow-up at which time he complained of chest discomfort. At that time, S.T. was "very vague about his discomfort" in terms of how often it occurred, how long it lasted, whether there were accompanying symptoms present, and whether the Nitroglycerin provided relief. S.T. did acknowledge, however, that the discomfort was "very infrequent." The records for that visit read as follows: Mr. T. since his last visit is having some chest discomfort, although, it has been better. He has taken some sublingual Nitroglycerin on a number of occasions, but is unable to recall exactly how often. His episodes are not exertionally related, different in type and severity than prior to his angioplasty. I feel he may be having coronary spasm, although, I cannot totally rule out restenosis. In any event, his symptoms are relatively mild. I have asked him to continue as we're doing. He wil [sic] return in two more weeks for follow-up examination. I have asked him to call should he get worse and he has, otherwise, been asked to keep a diary so that we can more objectively quantify his Nitroglycerin usage. Although S.T.'s vital signs are not recorded in the above note, Dr. Williams performed a physical examination of the patient that day, and he recorded the vital signs on a separate office record entitled "Vital Sign Sheet." He also maintained a separate patient medication chart, which reflected the various medications taken by all his patients; however, due to its age, that chart has been purged in the normal course of business. A stress test was not ordered by Respondent since he considered the patient's chest discomfort to be "very mild," and the patient described the pain as "completely different" than his previous angina. Also, the pain was not exertionally related, and restenosis was unlikely "at this early date following an angioplasty." Dr. Williams concluded that more than likely the pain was a coronary spasm (a muscular contraction of the wall of the artery), which typically occurs up to 30 to 60 days after the procedure, and he would wait "to see if [the symptoms are going] to go away . . . [w]hich they frequently do after an angioplasty." Finally, Respondent noted that the cardinal indicators of ischemic heart disease (a blockage) were not present - - exertional pain, relief from Nitroglycerin, and a similarity with pain experienced before the angioplasty was performed. He accordingly advised S.T. to continue his present course of treatment and to follow-up in two weeks, or if his condition worsened, to return sooner or go to an emergency room. On Friday, April 7, 1995, S.T. went to the Halifax Hospital Emergency Room in Daytona Beach, Florida, complaining of chest pressure, accompanied by an episode of dizziness, weakness, diaphoresis, and nausea. He also advised that he had been taking several Nitroglycerines on a regular basis. Respondent was not present at the facility, and was not the on-call cardiologist on this date. S.T. was seen by Dr. David E. Stibbins, who observed that S.T. was bradycardic and had low blood pressure. Like the information given to Dr. Williams on April 3, here the patient gave vague information regarding his chest discomfort. The records suggest that Dr. Stibbins opined that the patient's discomfort was not cardiac related and was probably due to anxiety. A cardiac consultation was requested, but not conducted, and S.T. was kept in the hospital overnight for observation. Around 1:15 a.m., S.T. reported a few "twinges" in his chest to the nurse, but he told her the pain was not serious enough to wake up his doctor. After denying that he had experienced any chest pain other than the few twinges described above, on the afternoon of April 8, 1995, S.T. was discharged from the hospital in stable condition (without ever being seen by a cardiologist) and advised to follow-up with Respondent in two days (the following Monday). On Sunday, April 9, 1995, the patient suffered a cardiac event and expired. The cause of death on his certificate of death is probable sudden death as a result of coronary artery disease, but neither expert in this case could give a precise reason for S.T.'s demise. The standard of care In the aftermath of an angioplasty, a variety of things can occur causing chest discomfort in the patient. While the beneficial effects of an angioplasty "can last . . . [up] to 20 years," three to five percent of patients experience an acute closure within a matter of minutes or hours, which is the sudden and complete obstruction of the artery. Because of this risk, after a procedure is performed, patients are kept in the hospital at least over night for observation. An acute closure often occurs in patients with a 70 to 80 percent narrowing of the artery. During the first few weeks after a procedure, acute thrombosis to the vessel at the site of the injury sometimes occurs, but a patient with that condition would experience "intense discomfort that's exactly the same as the patient's pre-intervention discomfort." Without such symptoms, that diagnosis would be "down [on] the list of considerations" by the treating physician. Between six and eight weeks and four months after the procedure, up to a third of balloon angioplasty patients experience a subacute closure (or restenosis) of the artery. Typically, these patients return to the physician's office with clinical symptoms of angina chest pain (similar to that experienced before the procedure) and require a repeat procedure. If restenosis has occurred, the patient is at risk for additional cardiac complications, such as myocardial infarction (heart attack). In some cases, within 30 to 60 days after a procedure, a patient will experience a "different type of sensation" in the chest due to the mechanical stretching of the vessel wall during the procedure. Other patients experience an artery spasm (cramping of the vessel wall), which occurs when the muscle cells go into spasm and constrict the artery. In both of these situations, the discomfort is dissimilar to that experienced before the procedure. Given the foregoing, if a patient presents himself to the doctor within a matter of weeks after an angioplasty with vague, non-ischemic related chest discomfort, it is not a deviation from the standard of care for the physician to choose a course of treatment consisting of "medical management" of the patient, that is, the close monitoring of the patient in the following days and weeks, and treating the patient with beta blockers, nitrates, and aspirin to ameliorate his symptoms. Conversely, if a patient presents himself to the physician with chest discomfort which is ischemic in nature, the ordering of further tests, including an exercise EKG, would be appropriate, with possible referral to a hospital for another cardiac catherization. Other considerations in determining the appropriate course of treatment of a patient include the cardiologist's familiarity with the patient's prior symptoms and history and the symptoms presented at the current time. In addition, the physician must rely upon his experience, knowledge, and education in the field. Taking into account all of these circumstances and considerations, the more convincing evidence establishes that Respondent did not deviate from the standard of care. c. The adequacy of the patient's records The Board has also alleged that Respondent failed to keep adequate medical records on the April 3, 1995, office visit in that he failed to document a physical examination or the results of any ancillary tests, and that the records as a whole fail to justify the course of treatment of the patient. The criticisms of Dr. Williams are based upon the testimony of the Board's expert, Dr. Dormois, who presented deposition testimony in this matter. In his deposition, however, Dr. Dormois withdrew his earlier criticisms of the records, and he indicated that the records provided by Dr. Williams "are generally adequate." He also concluded that this case "is not an issue of a medical record deficiency," but rather is "a deficiency of [a] failure to make clinical decisions." When these admissions are coupled with the testimony of Dr. Henderson, who concluded that the records were adequate, it is found that the Respondent kept written medical records justifying the course of treatment of the patient.
Recommendation Based on the foregoing Findings of Fact and Conclusions of Law, it is RECOMMENDED that the Board of Medicine enter a final order dismissing, with prejudice, the Administrative Complaint. DONE AND ENTERED this 30th day of August, 2001, in Tallahassee, Leon County, Florida. ___________________________________ DONALD R. ALEXANDER Administrative Law Judge Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-3060 (850) 488-9675 SUNCOM 278-9675 Fax Filing (850) 921-6847 www.doah.state.fl.us Filed with the Clerk of the Division of Administrative Hearings this 30th day of August, 2001. COPIES FURNISHED: Kim M. Kluck, Esquire Agency for Health Care Administration Post Office Box 4229 Tallahassee, Florida 32317-4229 Michael R. D'Lugo, Esquire Wicker, Smith, Tutan, O'Hara, McCoy, Graham & Ford, P.A. Bank of America Center, Suite 1000 390 North Orange Avenue Orlando, Florida 32802-1646 Tanya Williams, Executive Director Board of Medicine Department of Health 1940 North Monroe Street Tallahassee, Florida 32399-0750 William W. Large, General Counsel Department of Health 4052 Bald Cypress Way Bin A02 Tallahassee, Florida 32399-1701
Findings Of Fact The decedent, James C. Daniels, was employed as a fire fighter with the Village of Miami Shores, Florida, in April of 1972. The Miami Shores Fire Department was subsequently assimilated by Metropolitan Dade County, Florida, and at the time of the decedent's death on July 20, 1976, he was employed by Dade County as a fire fighter/emergency medical technician. On November 4, 1975, the decedent received a physical examination which showed no evidence of heart disease, and an electrocardiogram, the results of which were within "normal" limits. The decedent had no history of heart disease or circulatory problems, did not drink, and began smoking only in 1974 or 975. At the time of his death, the decedent's customary work routine involved 24 hours on duty, from 7:00 a.m. to 7:00 a.m., followed by 48 hours off duty. The decedent's duties included answering emergency calls along with his partner in a rescue vehicle. These calls included such incidences as automobile accidents, fires, violent crimes involving injuries to persons, and various and sundry other emergency situations. Upon answering an emergency call, the decedent was required by his job to carry heavy equipment, sometimes weighing as much as 80 pounds, to the place where the injured person was located. On occasion, the decedent would transport injured persons from the scene to local hospitals. At the time of his death, the decedent appeared outwardly to be in good physical condition. In fact, he engaged in a regular program of physical exercise. During the approximately two months prior to his death, the decedent participated in a busy work schedule which often included numerous rescues, in addition to false alarms and other drills required of his unit. In fact, only four days prior to his death, the decedent and his partner during one twenty- four hour shift, were involved in 13 rescues and one building fire. During that day, the decedent worked for 24 straight hours, apparently without sleep. On July 19, 1976, at 7:00 a.m., the decedent began his last work shift prior to his death. During that day, the decedent's unit participated in two rescues and two drills. That evening, several of decedent's fellow workers noticed that he looked "bad", "tired" or "drawn out". During the night, decedent was observed getting out of bed from three to five times, and holding his left arm, left side or armpit. At 7:00 a.m. on July 20, 1976, the decedent went off duty and returned home. Upon returning home, he ate breakfast, and later washed down a new brick fireplace at his home. After showering, resting and eating a lunch, he joined several other men near his home whom he had agreed to help in pouring cement for some new construction. The decedent mentioned pains in his neck and shoulder to these men before the truck carrying the cement arrived. The decedent mentioned that he had been under a lot of tension and pressure as a result of the busy work schedule at the fire station. When the cement truck arrived, cement was poured into several wheelbarrows and several of the men, including the decedent, pushed the wheelbarrows to the rear of the structure on which they were working. It appears that the decedent pushed approximately four wheelbarrow loads of cement weighing about 75 pounds each to the rear of the structure. Approximately one-half hour elapsed during the time that the decedent was engaged in this activity. Soon thereafter, the decedent was observed to collapse and fall to the ground. He was given emergency medical treatment and transported to Palmetto General Hospital, where he was pronounced dead at 5:24 p.m. on July 20, 1976. An autopsy was performed on the deceased on July 21, 1976 by Dr. Peter L. Lardizabal, the Assistant Medical Examiner for Dade County, Florida. In pertinent part, the autopsy showed moderate arteriosclerosis of the aorta, and severe occlusive arteriosclerosis of the proximal third of the anterior descending coronary artery in which the lumen, or opening, through which the blood passes through the artery was hardly discernible. The remaining coronary arteries appeared unaffected by the arteriosclerosis. The decedent's certificate of death, which was also signed by Dr. Lardizabal, listed the immediate cause of death as acute myocardial infarction due to severe occlusive arteriosclerosis of the left coronary artery. Dr. Lardizabal performed the autopsy examination of the decedent by "gross" observation, that is, without the benefit of microscopic analysis. However, microscopic slides were made during the course of the autopsy which were subsequently examined by other physicians whose testimony is contained in the record of this proceeding. Findings contained in the autopsy report, together with an evaluation of the aforementioned microscopic slides, establish that the myocardial infarction suffered by the decedent occurred at least 24 hours, and possible as many as 48 hours, prior to the decedent's death. This conclusion is based upon the existence of heart muscle necrosis, or tissue death, which would not have been discernible had the decedent died immediately following a coronary occlusion. In fact, for a myocardial infarction to he "grossly" observable at autopsy, that is, without the benefit of microscopic examination, it appears from the record that such an infarction would have to occur a substantial period of time prior to the death of the remainder of the body. Otherwise, the actual necrosis of heart muscle tissue would not be susceptible to observation with the naked eye. Although it appears probable from the evidence that the decedent went into a type of cardiac arrhythmia called ventricular fibrillation which led to his death, the actual proximate cause of his death was the underlying myocardial infarction, which in turn was a result of arteriosclerosis which had virtually shut off the supply of blood to the affected area of his heart. Although the causes of arteriosclerosis are not presently known to A medical science, it appears clear from the record that acute myocardial infarctions can be caused by emotional or physical stress, and that the decedent's myocardial infarction was, in fact, caused by the stress and strain of his job as a fire fighter and emergency medical technician. In fact, it appears from the medical testimony in this proceeding that the decedent was having a heart attack which led to the myocardial infarction on the night of July 19, 1976, or in the early morning hours of July 20, 1976, while he was still on duty. It further appears that, although physical exertion, such as the pushing of the wheelbarrow loads of cement by the decedent, might act as a "triggering mechanism" for ventricular fibrillation, the decedent's activities on the afternoon of July 20, 1976, had very little to do with his death. The type of lesion present in the decedent's heart, which had occurred as much as 48 hours prior to his death, was of such magnitude that he would likely have died regardless of the type of physical activity in which he engaged on July 20, 1976. Petitioner, Dolores A. Daniels, is the surviving spouse of James C. Daniels.
The Issue Should discipline be imposed on Respondent's license to practice medicine in Florida?
Findings Of Fact Stipulated Facts and Admitted Facts: Petitioner is the state agency charged with regulating the practice of medicine pursuant to Section 20.43, Florida Statutes; Chapter 456, Florida Statutes; and Chapter 458, Florida Statutes. Respondent is and has been at all times material hereto a licensed physician in the State of Florida, having been issued License No. ME0063587. Respondent's mailing address is 1834 Southwest 1st Avenue, Ocala, Florida 34474. Respondent is board certified in Internal Medicine with a sub-specialty in Pulmonary Disease and Critical Care Medicine. On July 21, 1999, Patient F.C. presented to Respondent for the bronchoscopy and biopsy of his left lung. The results of the biopsy performed on July 21, 1999, by Respondent were benign. The final diagnosis on the cytology of the biopsy performed on July 21, 1999, by Respondent showed malignancy not identified. Additional Facts: F.C. was born on December 12, 1939. In January of 1997 he was diagnosed with small cell carcinoma of the lung with brain metastasis. He received Carboplatinum and VP-16 to treat the condition. He had a DVT in January of 1998. In 1999 F.C. was the patient of Thumati Jagalur, M.D. Dr. Jagalur referred F.C. to Anju Vasudevan, M.D., for an oncology consult. As of July 16, 1999, Dr. Vasudevan determined that given F.C.'s status two and a half years post- diagnosis, it would be worthwhile to obtain a biopsy through bronchoscopy. Dr. Vasudevan made Dr. Jagalur aware of this plan in correspondence dated July 16, 1999. This report from Dr. Vasudevan to Dr. Jagalur made mention of the results of a CT scan of the chest that had been done on F.C., in which a multi-lobular soft tissue density mass, left intrahilar posteriorly with respect to the hilum had been identified. The mass was approximately 3.5 x 4cm in diameter, according to Dr. Vasudevan's remarks to Dr. Jagalur. The CT scan did not reveal any definite metastatic disease in the abdomen or brain pan. Dr. Vasudevan anticipated that the bronchoscopy would be performed by Nagesh Kohli, M.D., a physician practicing pulmonary medicine with Ocala Lung and Critical Care Associates in Ocala, Florida. Respondent was also a member of that practice. In anticipation of the bronchoscopy, Dr. Kohli gave pre-bronchoscopy orders on July 19, 1999. The bronchoscopy was scheduled to be conducted on July 21, 1999. These orders did not make mention of the location of the soft tissue density mass that had been previously identified in the CT scan of the chest, left intrahilar posteriorly with respect to the hilum. The bronchoscopy to be performed on patient F.C. was to take place in the Ocala Regional Medical Center, Ocala, Florida. The procedure was performed by Respondent, who substituted for Dr. Kohli. The procedure took place as scheduled at Ocala Regional Medical Center. In the records from the Ocala Regional Medical Center in the operative report, Respondent describes the pre- operative diagnosis as right lower lobe mass. The post- operative diagnosis states "No endobronchial lesions. Biopsies taken from the right lower lobe as well as right hilar Wang aspiration." The procedures were described in the report as bronchoscopy and biopsy. The report by Respondent goes on to describe examination of the trachea, the carina, and the main bronchi. These features were found to be normal. The report describes examination of the main stem bronchus left and right and other aspects of the left and right bronchus with no abnormalities found. The report further describes that "transbronchial biopsies were obtained from the right lower lobe, multiple biopsies were taken from various segments. Wang aspiration was performed times 3 from the right hilum." In his post-bronchoscopy orders Respondent referred to the specimen biopsy sites as right trans-bronchial biopsies associated with the pathology. In correspondence from Dr. Vasudevan to Dr. Jagalur following the negative results obtained in the biopsy performed by Respondent, Dr. Vasudevan expressed her belief that the biopsy done on July 21, 1999, by Respondent was in relation to the right lung, not the left lung as intended. In the correspondence from Dr. Vasudevan to Dr. Jagalur she goes on to describe how there were no indobronchial lesions noted on either side. As explained in the correspondence, Dr. Vasudevan, with F.C.'s consent, determined to arrange a CT scan guided biopsy of the left lung mass, to be followed by a repeat bronchoscopy with biopsy of the left side if the results obtained from the guided biopsy of the left lung mass were negative. The patient F.C. returned to Ocala Regional Medical Center on July 26, 1999, and the CT scan biopsy needle guided was performed, in which the spinal needle was inserted into the mass lesion in the left lower lung field. The pathology from this biopsy was negative. On August 16, 1999, patient F.C. returned to the Ocala Regional Medical Center. At that time Dr. Kohli performed a bronchoscopy with biopsy of the left lower lobe lung mass. No indobronchial lesions were seen. During the procedure the trans-bronchial biopsies performed by Dr. Kohli were in the superior segment of the left lower lobe and posteria segment of the left lower lobe. The results of the specimens revealed a grade IV carcinoma. Patient F.C. died sometime around the end of June 2001. Respondent is board certified in pulmonary medicine and critical care medicine. He performed the bronchoscopy and biopsy on F.C. as part of his practice in pulmonary medicine. Before performing the bronchoscopy and biopsy he had reviewed radio-graphic studies which revealed the mass in the left lung. No other mass was evident in the studies. The review of the film was made with the aid of a view box. In particular, when Respondent did the bronchoscopy on July 21, 1999, he displayed the aforementioned CT scans on the view box. The CT scan available to Respondent when performing the bronchoscopy had been made on July 14, 1999. Although no mention is made in the operative report prepared by Respondent on July 21, 1999, Respondent used fluoroscopy to assist in obtaining the biopsies. The procedure performed on July 21, 1999, was video- taped and available for viewing on a television screen through a live picture, to include the use of fluoroscopy. Kristine Sittrick, R.N., was employed by the Ocala Regional Medical Center on the date Respondent performed the bronchoscopy with biopsy on F.C. She had involvement in the procedure in the capacity of respiratory care therapist. At the time and at present Ms. Sittrick served as supervisor for the pulmonary lab where the procedure was being performed. During the procedure Ms. Sittrick told Respondent that F.C.'s history of cancer was on the left side. She told Respondent this because she observed that Respondent ". . . was going into, on the right side. . . . He was looking in the area that wasn't . . . ." When asked if Respondent was performing procedures on the side that was not implicated by F.C.'s history of cancer, Ms. Sittrick stated "I believe he did." Ms. Sittrick did not recall in her testimony what exactly Respondent may have done on the right side. Ms. Sittrick further describes her concern that Respondent "knew the man's history of what was on the left . . . because he was doing the procedure for Dr. Kohli, and that was a limitation as well. I just wanted to make sure he knew the tissue was on the left." Consistent with Respondent's instructions, Ms. Sittrick wrote on the specimen labels the location that Respondent said the specimen was obtained from. That information Respondent imparted was that the specimen came from the right lung, leading to the pathology report reflecting findings in the right lung, transbronchial biopsies. When Respondent concluded the bronchoscopy with biopsy for patient F.C. he immediately dictated his operative report indicating that transbronchial biopsies were obtained from the right lower lobe. Notwithstanding contrary evidence, Respondent biopsied the mass in question from the left lung as he claimed in his testimony. The expectation in the case is that the biopsy should have been performed on the left lung. All Respondent's records prepared in association with the procedure say otherwise. Consequently, the medical record prepared by Respondent fails to justify in any manner the course of treatment involving the left lung where the biopsies were taken. Instead, the records justify the biopsies in the right lung that were not actually performed. Those are circumstances that violated the standard of care for physicians, as established through the opinion of George Schoonover, M.D., who is board certified in internal medicine and pulmonary diseases with a special qualification in critical care medicine. Dr. Schoonover's opinion is premised upon the fact that the record reflects Respondent biopsied the right lung, which was an erroneous medical record.
Recommendation Upon consideration of the facts found and conclusions of law reached, it is RECOMMENDED: That a final order be entered dismissing Count I, and finding Respondent in violation of Count II in the Administrative Complaint, issuing a letter of reprimand, imposing a $5,000.00 administrative fine, and the cost of investigation and prosecution in the amount of $3,630.50. DONE AND ENTERED this 15th day of February, 2002, in Tallahassee, Leon County, Florida. CHARLES C. ADAMS 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 15th day of February, 2002. COPIES FURNISHED: Ephraim D. Livingston, Esquire Agency for Health Care Administration Fort Knox Building II, Suite 1100 2727 Fort Knox Boulevard, Mail Stop 39-A Tallahassee, Florida 32308-6287 Paul A. Nugent, Esquire O'Hara Law Firm First Sanford Tower, Suite 600 312 West First Street Sanford, Florida 32771 Gary C. Simons, Esquire Savage, Krim, Simons and Jones 121 Northwest Third Street Ocala, Florida 34475 Tanya Williams, Executive Director Board of Medicine Department of Health 4052 Bald Cypress Way, Bin A02 Tallahassee, Florida 32399-1701 Theodore M. Henderson, Agency Clerk Department of Health 4052 Bald Cypress Way, Bin A02 Tallahassee, Florida 32399-1701
The Issue The issues for determination in this proceeding are whether Respondent committed the acts alleged in the Administrative Complaint and, if so, what disciplinary action, if any, should be taken against Respondent's license.
Findings Of Fact Petitioner is the state agency charged with regulating the practice of medicine pursuant to Section 20.30, Florida Statutes, and Chapters 455 and 459, Florida Statutes. Respondent is licensed as a physician in the State of Florida pursuant to license number ME 0032342. Respondent's address is 4100 South Hospital Drive, Suite 202, Plantation, Florida 33317. Patient L.M.A. (the "Patient") was seen by Dr. Burkhart in September, 1985, prior to the Patient's initial examination by Respondent. Dr. Burkhart examined the Patient's throat and found an unidentified mass in the Patient's throat. Dr. Burkhart advised the Patient that a throat scan should be performed. The Patient consulted Respondent on September 28, 1985. The Patient complained of a sore throat, hypertension, excessive weight, and marginal diabetes. Physical findings included some redness of the throat and slight edema on the soft palate. The Patient informed Respondent of her history of cancer of the uvula and of what Dr. Burkhart had said to her regarding the mass in her throat and the need for a throat scan. Respondent told the Patient that there was no need for a throat scan. Respondent provided medical care and treatment for the Patient from September 28, 1985, until March 28, 1988. During the time Respondent provided medical care and treatment to the Patient, Respondent knew that the Patient had cancer of the uvula in 1974. Respondent examined the Patient approximately 19 times over a period of 11 months during 1986. The Patient's chief complaints involved upper respiratory symptoms and throat problems. On January 13 and 27, 1986, and on March 26, 1986, Respondent prescribed throat lozenges for the Patient. The medical records disclose that the Patient complained of upper respiratory symptoms including coughing, a runny nose, and watery eyes. Throat lozenges, however, are customarily prescribed for a sore throat. On April 7, 1986, Respondent found that the Patient had a sore, reddened throat and coughing. Respondent prescribed antibiotics in the form of intramuscular Penicillin and 500 mg. of Penicillin four times a day for ten days. Dr. Burkhart's office called the Patient sometime in April, 1986, and reminded her that it was important for her to have a throat scan performed. The Patient told Respondent, and Respondent told the Patient that she did not need a throat scan. The Patient saw Respondent on May 1, 1986, complaining of a sore throat, coughing, and difficulty swallowing. Respondent prescribed Penicillin parenterally and 500 mg. orally for 10 days. When the Patient returned to Respondent on May 13, 1986, complaining of a sore throat and a lump in her throat, Respondent prescribed antibiotics in the form of 400 mg. of Erythromycin orally for ten days, Septa (a sulfa drug), and Chloraseptic. The Patient saw Respondent on June 19 and 25, 1986. The medical records indicate that the Patient had no complaints but that the Respondent again told the Patient to take Chloraseptic lozenges. The Patient saw Respondent on August 4, 1986, complaining that she could feel something in her throat. The Respondent prescribed more antibiotics in the form of Penicillin and Ampicillin, Probenecid, and more Chloraseptic. 2/ Respondent advised the patient to see a throat specialist but did not arrange a consultation or a referral. The Patient saw Respondent on August 8, 1986, complaining of a sore, reddened throat, infected tonsils, and a cough. Respondent prescribed ten more days of Penicillin 500 mg. The Patient saw Respondent again on August 21, 1986. The Patient's throat was red and Respondent prescribed Chloraseptic lozenges. In September, 1986, the Patient had difficulty swallowing. Her throat was raw and sore. Upon self-examination, she saw that her uvula was raw. On October 16, 1986, the Patient complained of vague throat symptoms including a "sensation" in her throat. The Respondent prescribed antibiotics in the form of 250 mg. of Erythromycin three times a day and Chloraseptic lozenges. On November 19, 1986, the Patient's throat was sore and reddened. The Respondent prescribed antibiotics in the form of intramuscular Penicillin and oral Penicillin. On December 6, 1986, the Patient's throat remained sore and reddened. Respondent prescribed antibiotics in the form of Erythromycin and also prescribed Chloraseptic. Respondent's medical records indicate that a referral to Dr. Ramos, an otolaryngologist, was considered by Respondent. On December 16, 1986, the Patient told Respondent that she felt that she had cancer again and that she would not take any more antibiotics. Respondent made an appointment for the Patient to see Dr. Ramos. Dr. Ramos performed a biopsy on the Patient in December, 1986. The Patient was found to have a schema-cell carcinoma of the soft palate. The Patient was diagnosed as having cancer of the uvula and treated with radiation therapy. The radiation therapy dried up the Patient's saliva glands. Respondent failed to practice medicine with that level of care, skill, and treatment which is recognized by a reasonably prudent physician as being acceptable under similar circumstances. The Patient's complaints of sore throat were related to her underlying cancer. Respondent was under the impression that an infectious process was involved and prescribed antibiotics. Respondent failed to document the existence of an infectious process either by the presence of a fever or by a culture of the throat. 3/ Respondent's examination of the Patient's head and neck was incomplete. Respondent failed to document that a mirror examination was performed on the soft palate, including the back of the Patient's uvula, hypopharynx, and larynx. 4/ The Patient had a higher than average chance of getting cancer in the throat area due to the fact that she had cancer of the uvula in the past and had been a smoker. Appropriate medical treatment requires that cancer be ruled out as a cause of repeated sore throats, even in patients without prior histories of cancer, before concluding that an infectious process is the cause of the sore throats. The Patient either had cancer or Erythroplasia of Queyrat when she first visited Respondent on September 28, 1985, which Respondent improperly interpreted as an infectious process. 5/ Respondent failed to keep written medical records justifying the course of treatment in three respects. First, the records failed to justify the initial use of antibiotics. Second, the records failed to justify the continued use of antibiotics when they did not resolve the condition. Third, the records failed to justify the failure to consult with or refer the patient to a specialist in a timely manner. Respondent prescribed, dispensed, and administered, legend drugs inappropriately and not in the best interest of the Patient. Respondent treated the Patient with antibiotics when such treatment was not justified.
Recommendation Based upon the foregoing Findings of Fact and Conclusions of Law, it is RECOMMENDED that Petitioner enter a final order finding the Respondent guilty of violating Sections 458.331(1)(m), (q), and (t), Florida Statutes, and imposing the following disciplinary action: a reprimand; an administrative fine in the amount of $5,000; and three years of probation in accordance with terms to be determined by Petitioner. DONE AND ORDERED in Tallahassee, Leon County, Florida, this 20th day of August 1991. DANIEL MANRY Hearing Officer Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-1550 (904) 488-9675 Filed with the Clerk of the Division of Administrative Hearings this 20th day of August 1991.
