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 Did the Respondent commit the violations alleged in the Amended Administrative Complaint dated March 2, 2001, and if so, what penalty should be imposed?
Findings Of Fact Upon consideration of the oral and documentary evidence adduced at the hearing, the following relevant findings of fact are made: The Board is the agency charged with regulating the practice of medicine in the State of Florida. Respondent, Carl W. Liebert, Jr., M. D. (Dr. Liebert) is and, at all times material hereto, has been licensed to practice medicine in the State of Florida, having been issued license number ME0047601. Respondent is Board-certified in surgery. On January 29, 1997, Respondent performed an abdominal aortic aneurysm repair and an aortobifemoral graft on E. T., a male patient, approximately 70 years of age. The site of the graft for the left femoral artery intruded partially upon the site of a previous graft of the femoral artery performed in 1986. This graft failed immediately after the procedure. Respondent sutured the graft at the left femoral artery partially into old scar tissue from the 1986-failed graft. After the surgery, on the Sunday before his release from the Naples Community Hospital (Hospital) on Thursday, February 6, 1997, E. T. suddenly and abruptly fell in his hospital room. Respondent was concerned about the possible damage this fall may have caused to the surgical repair. Although E. T. experienced pain in his left groin area, the location of one of the aortobifemoral grafts, while in the Hospital, there is no evidence that any harm resulted from the fall or that the pain was a result of the fall. After the surgery, during E. T.'s stay in the Naples Community Hospital (Hospital), there was lymphatic drainage, a pinkish colored fluid, from the incision in his left groin. While the lymphatic fluid may have been blood stained resulting in the pinkish color, the lymphatic drainage was not as described in the nurse's notes as being "a bloody discharge." On Thursday, February 6, 1997, E.T. was discharged from the Hospital. After E. T.'s discharge from the Hospital, his wife cared for him in their home in Naples, Florida. As expected by Dr. Liebert, the incision in E. T.'s left groin area continued to have lymphatic drainage after E. T.'s discharge from the Hospital. The incision in E. T.'s left groin area continued to drain a pinkish colored fluid. The lymphatic drainage from the incision in E. T.’s left groin continued over the weekend and on Monday, February 10, 1997, E. T.'s wife contacted Respondent's office to advise Respondent of the drainage and of the pain E. T. was experiencing. Although E. T.'s wife did not speak directly to Respondent, she assumed that the person to whom she spoke with over the telephone conveyed her message to Respondent. E. T.'s wife was given a prescription for Percocet for pain and told that Respondent would see E. T. in his office on Thursday, February 13, 1997. On Wednesday, February 12, 1997, while showering and cleansing the incision on his left groin, E. T. inadvertently disturbed the incision on his left groin, which caused the incision to drain profusely. After leaving the shower, E. T.'s wife assisted E. T. in drying-off his body and controlling the drainage from the incision. The wife stemmed the flow of the drainage with a towel and called the Collier County Emergency Medical Services (EMS) and Respondent's office. The wife explained to the person answering Respondent's telephone, the circumstances of the occurrence with E. T., and that she had called the Collier County EMS personnel. The wife also requested that Respondent come to the Hospital. On February 12, 1997, in response to E. T.'s wife's call, the Collier County EMS personnel responded to E. T.'s home at approximately 7:25 a.m., performed an initial treatment for the drainage from E.T.'s left groin and transported E. T. by ambulance to the Hospital. The EMS personnel noted that E. T. complained of bleeding and it was their initial impression that E. T. was bleeding from his femoral artery. However, the EMS personnel did not confirm that E. T. was bleeding from his left femoral artery. The EMS personnel also noted what they considered to be a large amount of thick, clotty blood, which they estimated to be approximately 1000 milliliters (ml's) or 1000 cubic centimeters (cc's), surrounding E. T. Based on the records of the EMS personnel and on E. T.'s description given to Dr. Mulert, E. T.'s wife's testimony that the incision spurted blood for approximately 3- 4 feet appears to be somewhat exaggerated. The EMS personnel, assuming that E. T. had recently loss blood, administered 300 cc of fluid intravenously to E. T. When the EMS personnel attempted to move E. T., the drainage from the incision started again, but was controlled with a trauma dressing and pressure applied by a sandbag. The EMS personnel presented E. T. at the Emergency Room (ER) of the Hospital at approximately 7:52 a.m. on February 12, 1997. The ER nurse noted that a pressure dressing along with a sandbag had been applied and that the drainage or bleeding was under control. The ER nurse drew blood from E. T. and noted in her record that it was for a "type and cross" in preparation for a blood transfusion should one become necessary. However, Dr. Robert Mulert, the ER physician who attended E. T. while in the ER, noted in his records that he had requested a "type and hold," a less elaborate procedure than a "type and cross," which requires checking the antibodies and making sure the blood in question is compatible blood. Based on his estimate of E. T.'s blood loss and E. T.'s vital signs and other health conditions, Dr. Mulert did not consider E. T. as a patient in need of a blood transfusion. Upon E. T.'s arrival at the Hospital, Dr. Mulert made a brief assessment of E. T.'s condition to confirm that there was no active bleeding and that the patient did not need emergent intervention. Although Dr. Mulert is not a vascular surgeon or even a general surgeon, he has one year of residency training in surgery and is a Board-certified emergency room physician who has been working as an emergency room physician for approximately 27 years. Dr. Mulert is qualified to examine patients such as E. T. and advise the primary treating physician of his findings. Dr. Liebert has worked with, and relied on, Dr. Mulert's expertise as an emergency room physician in treating many of his patients who are presented at the Hospital for emergency treatment for approximately 15 years. Dr. Mulert discussed E. T.'s condition by telephone with Dr. Liebert on two separate occasions during E. T.'s visit to the Hospital on February 12, 1997. The first occasion was shortly after E. T. was admitted to the Hospital ER. During this first occasion, Dr. Mulert advised Dr. Liebert that his patient, E. T. had been admitted to the Hospital with a reported acute hemorrhaging or bleeding of the incision in the area of his left groin and that E. T.'s wife was asking for Dr. Liebert. In some instances, the primary physician will assume treatment at this juncture. However, it is not unusual for the ER physician to continue treatment. The decision was for Dr. Mulert to continue treatment and to keep Dr. Liebert advised as to E. T.'s condition. There is nothing in the record to indicate Dr. Liebert's location on the morning of February 12, 1997; nor is there any evidence to indicate that Dr. Liebert was prevented from examining E. T. on the morning of February 12, 1997. Also, during this first discussion, Dr. Mulert advised Dr. Liebert, based on the information that he had gathered, that E. T.'s blood loss was approximately 500 cc's but that there was no active bleeding at that time. Dr. Mulert also advised Dr. Liebert that he intended to deal with the patient's problems by proceeding with his plan to assess E. T.'s blood count, to monitor E.T.'s vital signs, and to see if the patient met Dr. Mulert's criteria for stability: Can he get up? Can he walk? Can he talk? Does the patient make sense? Does the patient have discharge stability? Subsequent to this first discussion, Dr. Mulert made a more detailed examination of the wound to determine if the wound was infected, the depth of the wound, and the need to pack the wound with sterile dressing, etc. After reviewing the EMS personnel records, E. T.'s history, talking with E. T., and reviewing the results of his examination, Dr. Mulert's impression was that E. T. had a hematoma under a surgical wound; that the wound had come apart; and that the collection of blood (old blood) within the hematoma had expressed from that surgical wound. The blood within the hematoma is referred to as "old blood" in that it was no longer in the vascular system and was not being replenished with oxygen. While E. T.'s vital signs were low compared to his vital signs taken while in the Hospital on visits prior to February 12, 1997, they were not significantly lower and were within a normal range for a patient, such as E. T., who was on beta blockers. E. T.'s vital signs were inconsistent with an aggressive femoral graft leak. The hematocrit and hemoglobin values on February 12, 1997, were slightly lower than the hematocrit and hemoglobin values while in the hospital during his most recent visit in January 1997. However, based on the testimony of Dr. Liebert, which I find to be credible, that was to be expected since E. T. had been given a significant amount of auto-transfused blood during his surgery on January 29, 1997. Also, the lower values were consistent with a 500 cc or less blood loss by a patient that had just recently undergone surgery. During either the first or second conversation, Dr. Mulert advised Dr. Liebert that the surgical site had come apart. During his care of E. T., Dr. Mulert became aware that Dr. Liebert had performed an abdominal aortic aneurysm repair earlier in the year, and that the repair was under the nine-inch incision on E. T.’s left groin but did not know the exact location of the repair. If Dr. Liebert made a diagnosis, he did not convey such diagnosis to Dr. Mulert. Neither Dr. Liebert nor Dr. Mulert discussed or made a differential diagnosis. However, it was the testimony of both Dr. Mulert and Dr. Liebert, which I find to be credible, that based on the facts presented in respect to E. T. by Dr. Mulert, a differential diagnosis was unnecessary. A differential diagnosis is a mechanism physicians use to identify and evaluate possible alternative causes for observed symptoms. During the second telephone conversation, Dr. Mulert advised Dr. Liebert that the patient had been stable for approximately four hours, that his vital signs were within normal ranges, that his blood counts were basically unchanged, that there was no active bleeding and had not been any active bleeding for approximately four hours, that the patient was up and walking around the ER, that the patient was asymptomatic when vertical that the patient was not orthostatic when walking, that the patient wanted to go home, and that the incision in the left groin area needed to be repaired. There was no discussion between Dr. Mulert and Dr. Liebert concerning the admission of E. T. to the Hospital for the purpose of further examining the possibility of arterial bleeding. Ultrasound and computerized tomography (CT) were available to patients at the Hospital. While these tests don't always "rule out" internal bleeding or suture line disruptions, they can, in certain instances, "rule in" these conditions. Based on the facts in respect to E. T.'s condition presented by Dr. Mulert on February 12, 1997, particularly that they were dealing with an open wound, and Dr. Liebert's feelings as to the somewhat limited use of these tests in this type situation, there was no ultrasound or CT scan performed. Based on the facts in respect to E. T.'s condition as presented by Dr. Mulert on February 12, 1997, the failure of Dr. Liebert to utilize the ultrasound or CT scan to further examine E. T. in regard to arterial bleeding does not constitute the failure to practice medicine with that level of care, skill, and treatment which is recognized by a reasonable prudent similar physician as being acceptable under similar conditions and circumstances, notwithstanding the testimony of Michael J. Cohen, M.D. to the contrary. Subsequently, Dr. Mulert sewed up the incision which had come apart. Dr. Liebert did not personally examine E. T. at any time while he was in the ER to evaluate the cause of E. T.'s problem in relation to arterial bleeding, but relied on Dr. Mulert to provide him with facts surrounding E. T.'s condition based on Dr. Mulert's examination of E. T. and his assessment of E.T.'s problem. Based on the facts in respect to E. T.'s condition in relation to arterial bleeding as presented by Dr. Mulert on February 12, 1997, the failure of Dr. Liebert to personally examine E. T. prior to his discharge or to delay E. T.'s discharge so as to allow time for Dr. Liebert personally examine E. T. to determine for himself E. T.'s problem in relation to arterial bleeding does not constitute the failure to practice medicine with that level of care, skill, and treatment which is recognized by a reasonable prudent similar physician as being acceptable under similar conditions and circumstances, notwithstanding the testimony of Michael J. Cohen, M.D. to the contrary. 38. E. T. was discharged from the Hospital at approximately 12:00 noon on February 12, 1997. After his discharge on February 12, 1997, E. T. had an uneventful afternoon and evening. After getting out of his bed on the morning of February 13, 1997, E. T. walked from his bedroom into the kitchen and as he stood in the kitchen the left groin incision erupted again, hemorrhaging blood onto the kitchen floor. The EMS personnel were called responded to the call around 5:30 a.m. Prior to the arrival of the EMS personnel the bleeding had stopped. The EMS personnel noticed a moderate blood loss. The EMS personnel dressed the left groin wound, administered fluids and transported E. T. to the Hospital where he was admitted to the ER at approximately 6:00 a.m. Although E. T. received blood and fluids, his condition deteriorated rapidly and E. T. expired at approximately 7:24 a.m. on February 13, 1997. No autopsy was performed. However, the cause of death was most likely myocardial infarction that resulted from a loss of blood.
Recommendation Based on the foregoing Findings of Fact and Conclusions of Law, it is recommended that the Board enter a final order dismissing the Amended Administrative Complaint dated March 2, 2001. DONE AND ENTERED this 1st day of August, 2001, in Tallahassee, Leon County, Florida. ___________________________________ WILLIAM R. CAVE 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) 921-6947 www.doah.state.fl.us Filed with the Clerk of the Division of Administrative Hearings this 1st day of August, 2001. COPIES FURNISHED: Robert C. Byerts, Esquire Agency for Health Care Administration Post Office Box 14229 Tallahassee, Florida 32317-4229 Ralph L. Marchbank, Jr., Esquire Post Office Box 3979 Sarasota, Florida 34230 Tanya Williams, Executive Director Board of Medicine Department of Health Northwood Centre 1940 North Monroe Street Tallahassee, Florida 32399-0750 William W. Large, General Counsel Department of Health 4052 Bald Cypress Way Bin A00 Tallahassee, Florida 32399-1701 Theodore M. Henderson, Agency Clerk Department of Health 4052 Bald Cypress Way Bin A00 Tallahassee, Florida 32399-1701
The Issue The issue in this case is whether the license of Allen B. Erde, M.D., should be disciplined by the Florida Board of Medicine based upon actions he is alleged to have taken, or failed to have taken, between August and November, 1986, in the care and treatment of his patient, C.W.
Findings Of Fact At all times material hereto, Respondent has been licensed as a physician in the State Of Florida, having been issued license number ME-0008625. Respondent was C.W.'s obstetrician during her pregnancy in 1986, and initially examined her on August 26, 1986, when she was six weeks pregnant. During this initial visit, C.W. was informed by Respondent that her pregnancy was progressing normally. At her second visit, on September 23, 1986, Respondent detected no fetal heartbeat. However, he informed C.W. that this was not a problem. He requested that she bring her husband with her for her third visit so that they both could hear the heartbeat. Prior to her third visit, C.W. saw Respondent in his office on October 6, 1986, complaining of urinary problems, and a stiff neck and back. Respondent treated her for a urinary tract infection. Later that same day she began to bleed vaginally, passed clots and experienced cramping pains. She then saw Respondent at the Winter Haven Hospital emergency room, but was told that nothing seemed wrong. Respondent advised her simply to go home, put her feet up, and rest. There were several other occasions during October, 1986, when C.W. experienced cramping and vaginal bleeding. She called Respondent each time to express her concerns, but was told simply to lie down, and keep her feet up. On October 22, 1986, C.W. and her husband visited Respondent for her third scheduled visit. No heartbeat was heard. Respondent again told C.W. that there was no cause for concern, the baby was just small and probably behind her pelvic bone. C.W. was presumably 14 weeks pregnant at this time, but Respondent's office records indicate that the fetus was decreasing in size, there was no weight gain, and no heartone. C.W. continued to experience pain and bleeding, sometimes accompanied by clots. She was not gaining weight, and had none of the other indications of pregnancy which she had experienced in her prior pregnancies. C.W. continued to express concern to Respondent, but his advice remained simply to lie down, and keep her feet up. In response to a five day episode of bleeding, C.W. saw Respondent in his office on November 12, 1986. Although she was 17 weeks pregnant at that time, Respondent's office records indicate a fetus 14 weeks in size. Respondent did not order any fetal viability tests, and there is no evidence in his office record that he considered any testing of the fetus. C.W. saw Respondent for her fourth scheduled visit on November 19, 1986, and, again, no fetal heartbeat was detected. She was still experiencing vaginal bleeding. Her uterus was only 10-12 weeks in size, although she was presumably 19 weeks pregnant at this time. C.W. was distraught, and expressed great concern to Respondent that she was presumably almost five months pregnant and no fetal heartbeat had ever been detected. C.W. demanded that Respondent do something. He then ordered a quantitative Beta-subunit Human Chorionic Gonadotropin blood test to determine her hormone level. On November 2l, 1986, Respondent called C.W. at her place of employment, and informed her that her hormone levels were extremely low, and that she might not have a viable pregnancy. He told her she should keep her next regularly scheduled appointment with him, but if she experienced any severe bleeding or cramping to call him. C.W. left work and became increasingly upset. She contacted him later on that same day for a more complete explanation of what she should expect. Respondent told her that the fetus was "reversing itself and was losing weight instead of gaining." C.W. was not informed by Respondent that the fetus was not viable, and she took his advice to mean that if she was extremely careful there was still a chance of carrying the pregnancy to term. Respondent admitted to the Petitioner's investigator, Jim Bates, that he knew the fetus was dead at this time, but he was trying to let nature take its course, and if she did not abort in two or three months, he would take the fetus. Because she was extremely upset and her friends were concerned about the advice she was receiving from the Respondent, an appointment with another obstetrician, Dr. Vincent Gatto, was made for C.W. by one of her friends. Dr. Gatto saw C.W. on or about November 21, 1986, and after examining her he immediately diagnosed her as having had a missed abortion. A sonogram confirmed this diagnosis. A dilation and curettage was performed on C.W., and subsequent pathological reports revealed remnants of an 8-week fetus. The medical records which Respondent maintained of his care and treatment of C.W. are incomplete and contain discrepancies concerning his evaluation of the patient. They do not reflect C.W.'s numerous telephone calls, or that she was increasingly upset over the course of her pregnancy. There is no delineation of a plan of treatment in these records, or any explanation of the type of treatment he was pursuing for her. There is no explanation or justification in these records of Respondent's failure to order a sonogram or test, other than the one Beta-subunit Human Chorionic Gonadotropin, for C.W., although she repeatedly reported vaginal bleeding and cramping, and there was a continuing inability to detect a fetal heartbeat. Respondent failed to carry out the correct tests on C.W., and therefore, he failed to make a correct diagnosis of missed abortion, or to treat her correctly. He allowed her to carry a dead fetus for almost two months. Retention of the products of a non-viable pregnancy can lead to several complications, including infection, blood clotting and psychological trauma. In fact, this experience caused C.W. severe emotional anguish. In his care and treatment of C.W., Respondent failed to meet the standard of care that is required of a physician practicing under similar conditions and circumstances.
Recommendation Based upon the foregoing, it is recommended that Florida Board of Medicine enter a Final Order suspending Respondent's license to practice medicine for a period of five years, and imposing an administrative fine of $3,000. DONE AND ENTERED this 21st day of August, 1989 in Tallahassee, Florida. DONALD D. CONN Hearing Officer Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-1550 Filed with the Clerk of the Division of Administrative Hearings this 21st day of August, 1989. APPENDIX (DOAH CASE NO. 88-4785) Rulings on the Petitioner's Proposed Findings of Fact: Adopted in Finding l. Adopted in Finding 2. Adopted in Finding 3. Adopted in Finding 4. Adopted in Finding 5. 6-7. Adopted in Finding 6. Adopted in Finding 7. Adopted in Finding 8. Adopted in Finding 9. Adopted in Finding 10. Adopted in Finding 11. Rejected as irrelevant. 14-17. Adopted in Finding 13. 18-21. Adopted in Finding 12. 22. Adopted in Finding 14. The Respondent did not file Proposed Findings of Fact. COPIES FURNISHED: Mary B. Radkins, Esquire Northwood Centre, Suite 60 1940 North Monroe Street Tallahassee, FL 32399-0792 Allen B. Erde, M.D. P. O. Box 1817 Winter Haven, FL 33883-1817 Allen B. Erde, M.D. 198 First Street, South Winter Haven, FL 33880 Dorothy Faircloth Executive Director Northwood Centre 1940 North Monroe Street Tallahassee, FL 32399-0792 Kenneth Easley, General Counsel Northwood Centre 1940 North Monroe Street Suite 60 Tallahassee, FL 32399-0729
The Issue Whether disciplinary action should be taken against Respondent's license to practice medicine based on allegations that Respondent violated the provisions of Subsections 458.331(1)(m) and (t), Florida Statutes, arising from his treatment and care of Patient M.R., as alleged in the Administrative Complaint in this proceeding.
Findings Of Fact Effective July 1, 1997, Petitioner is the state agency charged with regulating the practice of medicine pursuant to Section 20.43, Florida Statutes, and Chapters 456 and 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 number ME 0077248. Respondent is a vascular surgeon, who is not board-certified in his area of practice. On November 27, 2000, Patient M.R., a 70-year-old male, was admitted to ORMC for a right-side carotid endarterectomy. Patient M.R. initially presented to Respondent in October 2000 with a number of health conditions, including chronic obstructive pulmonary disease (related to a 54-year history of smoking), cerebral vascular disease, atherosclerotic changes, and hypertension. Patient M.R. had a significant cardiac condition which resulted in a bypass procedure. It was determined at that time that Patient M.R. had significant stenosis in both carotid arteries which would require Patient M.R. to undergo two separate procedures, known as carotid endarterectomies. The left carotid artery was the subject of the first procedure in October 2000. Patient M.R. tolerated this procedure with no complications. Subsequent to the first carotid endarterectomy, but prior to the second, Patient M.R. suffered a transient ischemic attack (TIA), which is commonly referred to as a "mini-stroke." The symptomatic clinical presentation placed Patient M.R. in a high-risk category for peri-operative stroke. Respondent performed a right carotid endarterectomy on Patient M.R. on November 27, 2000. This requires the clamping of the artery in two locations, using a shunt to allow for the flow of blood. The incision must be made length wise in the controlled portion of the artery using an instrument to clear out the interior or lumen of the artery. This is done to reduce the stenosis and allow for better blood flow, without disbodying any particle from the wall of the artery. Once this is completed, the incision is patched, the clamps and shunt are removed, and the outer skin incision is closed. During the course of the above-described carotid endarterectomy, Respondent used a patch angioplasty with intra- operative shunt, which was manufactured from a pediatric feeding tube, and peri-operative neurologic monitoring. Immediately after the operation, the patient appeared to tolerate the procedure well, but was lethargic. Patient M.R. exhibited good movement in all four extremities and appeared to be neurologically intact, although he underwent extreme fluctuation in blood pressure. Patient M.R. was placed on ventilator support. The next morning, November 28, 2000, Patient M.R. had swelling and a hematoma in his neck on the right side, in the area of the incision. Respondent returned Patient M.R. to surgery, for exploration and evacuation of the hematoma. During the course of this second operation, Respondent observed a lot of swelling and edema in the operative site, but not much blood. Respondent evacuated the hematoma, and the carotid artery was found to have good blood flow. Later in the evening on November 28, 2000, Patient M.R. developed an acute neurologic deficit and was returned to the intensive care unit (ICU) at ORMC. Respondent ordered a Computerized Tomographry Scan (CT Scan) of the patient and an arteriogram. The results of the CT Scan showed a probable right occiptal infarct (stroke). The arteriogram showed significant occlusion of the right carotid artery extending to the carotid siphon. Patient M.R. was returned to the operating room in the early morning hours of November 29, 2000. Respondent made the decision to reopen the surgical area in an effort to resume blood flow in the right carotid artery that was seen to be occluded on the angiogram. Assisting Respondent on this November 29, 2000, procedure were John Horowitz, M.D., a board- certified vascular surgeon with nine years of experience, and Joseph Muller, M.D., a third-year general surgical resident at ORMC. During the November 29, 2000, procedure, Respondent reopended the previous incision in the skin and partially opened the patch that had previously been used over the carotid artery itself. Respondent performed a thrombectomy using a Fogarty "balloon" catheter in an effort to extract any debris that was causing the stenosis in the carotid artery. The balloon is placed into the carotid artery itself and is pushed up into the artery until it has passed whatever occlusion is present. Then the balloon is inflated and pulled back out, pulling with it any debris that is located within the artery. Near the conclusion of this November 29, 2000, procedure, a small piece of tubing was discovered in the surgical field. The piece of tubing was handed to Dr. Horowitz, who examined it and then placed it on the surgical tray. This piece of tubing was the same size, slope, and material cut from the feeding tube which was used as a shunt in the first surgery on November 27, 2000. There is conflicting testimony regarding the precise size and location of this piece of tubing that will be discussed below. What remains undisputed based upon the record in this case is that Respondent completed the surgical procedure on November 29, 2000, by closing the incision in the carotid artery and also in the skin of the neck. Dr. Muller is currently a surgical resident at ORMC, as he was at the time of the November 29, 2000, procedure. Dr. Muller testified that he had approximately two years and five months of residency training prior to the procedure in question. He estimated that he had observed approximately ten to 15 carotid endarterectomies. Dr. Muller testified that he observed a clear and slightly opaque piece of pediatric feeding tube coming out of the lumen of the artery as Respondent was evacuating debris after the inflation of the Fogarty balloon catheter and after about three passes of the catheter. Dr. Muller also testified that the piece of tubing in question was two or three centimeters in length. The other witnesses to this event testified that the piece in question was two to three millimeters in length. Dr. Muller's description of the position of the surgeon and assistant surgeon was also contrary to that of the other witnesses. Dr. Muller also testified that he did not know Patient M.R.'s medical history or his previous hospital course of treatment. Dr. Horowitz, the senior physician assisting, is a board-certified vascular surgeon who has performed several hundred carotid endarterectomies. He testified that he was called in by Respondent to assist on the surgical procedure which took place in the early morning hours of November 29, 2000. He found the piece of tubing located somewhere within the surgical field, remote from the carotid artery. He was certain that it was after Respondent had cleared the artery with the use of the Fogarty balloon catheter and had cleared the surgical wound. Dr. Horowitz testified that he saw a piece of tubing among the debris that had been evacuated from the surgical wound. It was not in the lumen of the artery. He picked up the piece of tubing in question with his thumb and forefinger and examined it. He testified that it was approximately two to three millimeters in length. He agreed that the material was consistent with the pediatric feeding tube that was used to create a shunt for the first procedure. Dr. Horowitz's testimony is credible and persuasive. Dr. Horowitz also gave his opinion that based upon his observation of the November 29, 2000, procedure, he did not believe that Respondent deviated from the standard of care in his treatment and care of Patient M.R. Patient M.R. was returned to the ICU, where he deteriorated and showed evidence of complete lack of brain stem reflexes. Patient M.R. was later pronounced brain dead, and he subsequently died on November 30, 2000. Gregory Schreiber, M.D., was the anesthesiologist who was present for a portion of the November 29, 2000, procedure. Dr. Schreiber testified that he was present during the beginning portion and the end portion of the procedure, when anesthesia is introduced and when anesthesia is abated. He was not present in the operating room when the piece of tubing was found. Further, there was a drape that separates the operative field from the anesthesiologist during the course of this procedure, which would have prevented Dr. Schreiber or his assistant from being able to see into the operative field directly. Dr. Schreiber noted that Patient M.R. was considered a very high-risk patient, whose multiple co-existent diseases posed a constant threat to his life when he presented for this surgery. In addition to the testimony outlined above, Petitioner also introduced three affidavits into evidence. One affidavit was that of Lata Bansal, M.D., a neurologist who was brought in for consultation after the November 29, 2000, procedure. Dr. Bansal swore in her affidavit that when she first saw Patient M.R. he was already brain dead. She otherwise did not have specific recollection of Patient M.R. The affidavit of Peter D. Taylor, M.D., a cardiac specialist, stated that he recommended a Thallium stress test for Patient M.R. prior to carotid surgery. The stress test was conducted on October 17, 2000, and revealed no ischemia but moderately decreased left ventricle function. Because he had no ischemia, Dr. Taylor opined that Patient M.R. was at an increased but acceptable risk for carotid surgery. The affidavit of Marita Lu, Registered Nurse, who was present during the November 29, 2000, procedure, stated that she could remember very few details of Patient M.R.'s case, other than she has the "impression" that something was recovered from the wound and that when she asked whether there was a specimen, she was told there was no specimen. Nothing in her affidavit indicates to whom she asked this question regarding the specimen nor is there any indication who responded to her question. Respondent is a board-certified general surgeon who is eligible for a special certification in vascular surgery and who was working at a vascular surgery group in Orlando, Florida, as of October and November of 2000. Respondent no longer practices in the State of Florida. He currently is an assistant professor of surgery and director of endovascular surgery at Creighton University in Omaha, Nebraska. Respondent described in detail each of the three procedures he performed. On November 27, 2000, the original procedure on the right carotid artery proceeded in routine fashion. Respondent provided an exemplar, which was admitted into evidence, of a pediatric feeding tube which is substantially similar to the pediatric feeding tube utilized in the November 27, 2000, procedure on Patient M.R. He utilizes a portion of the pediatric feeding tube as a shunt in his carotid endarterectomy procedures. He demonstrated at the final hearing that the pediatric feeding tube itself is so flexible as to be incapable of breaking. The only means of cutting it down is through the use of surgical instruments. He also indicated that there was no way to further cut down the tubing once it had been placed. The scrub technician cut the pediatric feeding tube into the appropriate length to be used as a shunt during the November 27, 2000, procedure. Respondent recalled that prior to this particular procedure, the tubing in question was not originally cut down to the appropriate size. It had to be cut down while in the operating room. It is during this cutting of the tubing that a tiny sliver, approximately two to three millimeters in length, was removed from the larger piece of tubing and entered the surgical field. Respondent did not know and did not have any way of knowing that the piece of tubing had entered the surgical field, as he was focused on preparing the artery itself for its incision while this tubing was cut. Respondent testified that the pediatric feeding tube in question was cut down to size before any incision was made in the carotid artery itself. Respondent performed the November 27, 2000, procedure as he normally does. After the procedure, Patient M.R. experienced extreme fluctuations in blood pressure. This can occur in patients due to multiple factors involving the nervous tissue and blood flow in the carotid artery, but there is no specific explanation for why it does happen. Subsequent to the November 27, 2000, procedure, Respondent monitored Patient M.R., addressing the extreme fluctuations in blood pressure along with the consulting physicians referred to above. Respondent noted that Patient M.R. developed a hematoma subsequent to the first procedure. He made a determination that the best course for Patient M.R. would be to evacuate the hematoma. In Respondent's opinion, evacuating the hematoma would speed up the healing process. Respondent performed this procedure on November 28, 2000. Patient M.R. tolerated this procedure well, and there was nothing remarkable about the procedure itself. Respondent palpated Patient M.R.'s artery during the course of this procedure and used the Doppler to reinforce his findings on palpation. A Doppler signal gives more specific information about the varied nature of blood flow in the internal and external carotid arteries. It was not Respondent's standard practice, nor is it necessary, to create a medical record that palpation of the artery has occurred, since it is such a basic and common occurrence that its notation on the record is not deemed to be necessary. Respondent continued to follow Patient M.R. subsequent to the November 28, 2000, procedure. When it was determined that Patient M.R. had suffered a stroke, Respondent was left with a choice of either doing nothing, or reopening the artery in an effort to save Patient M.R.'s life. Respondent chose to reopen the artery in an effort to determine whether anything could be done to save Patient M.R. Respondent opened the prior incision in the carotid artery on November 29, 2000, and inserted the Fogarty catheter in order to evacuate any debris that was located within the carotid artery. Respondent testified that it was at about this time that the piece of tubing was found; however, he further testified that he did not see the tubing in question come from the lumen of the carotid artery. Respondent's testimony is credible. It was Respondent's opinion testimony that the piece of tubing in question was located in the subcutaneous tissue outside of the artery. Its exact location within the various layers of subcutaneous tissue was not observed during the procedure. It was not possible for the piece of tubing in question to have entered the artery at this time. There was no evidence to suggest that the piece could have migrated into the artery at a later time. James Dennis, M.D., is a board-certified vascular surgeon who is the chief of the vascular surgery department at the University of Florida in Jacksonville, Florida. Dr. Dennis has sufficient education, training, and experience to qualify as an expert in vascular surgery under Florida law. Dr. Dennis testified that he reviewed all of the pertinent medical records concerning the treatment and care provided by Respondent to Patient M.R. and that based upon his review of these records and based upon his education, training, and experience, it was his opinion to within a reasonable degree of medical probability that Respondent deviated from the accepted standard of care in his treatment and care of Patient M.R., which constituted a violation of Subsection 458.331(1)(t), Florida Statutes. Dr. Dennis also testified that in his opinion, Respondent violated Subsection 458.331(1)(m), Florida Statutes, in that he failed to compile appropriate medical records reflecting the treatment and care provided to Patient M.R. Dr. Dennis' standard of care opinions were based on several factors. First, it was Dr. Dennis' opinion that based upon the contents of the chart, the only time that the piece of pediatric feeding tube could have entered Patient M.R. was during the course of the November 27, 2000, procedure. Dr. Dennis testified that in his opinion, Respondent deviated from the standard of care in allowing the piece of pediatric feeding tube to enter Patient M.R.'s body. This would be his opinion even if Respondent did not see the sliver of tubing in question enter Patient M.R.'s body and even if the piece of tubing in question were so small and translucent as to be practically invisible. Dr. Dennis also testified that in his opinion, Respondent deviated from the standard of care during the November 28, 2000, procedure in that he failed to adequately palpate the carotid artery. Dr. Dennis was critical of Respondent's use of a Doppler to assess Patient M.R.'s pulse. In Dr. Dennis' opinion, the use of the Doppler was indicative a weakening pulse rate and that the proper practice would have been to palpate the artery by touch rather than by using a Doppler instrument. Dr. Dennis was also critical of Respondent during the November 28, 2000, procedure for his failure to find the piece of tubing in question. It is Dr. Dennis' opinion that the piece of tubing had to have been located within the lumen of the artery and that had Respondent adequately palpated the entire length of the carotid artery during the November 28, 2000, procedure, he would have located the piece of tubing within the artery and could have taken appropriate steps to remove the piece of tubing before Patient M.R. suffered his stroke later that night or during the early morning hours of November 29, 2000. Dr. Dennis' opinion that the piece of tubing in question had to have been located in the lumen of the artery was also based upon his assessment of the procedures performed. He discounted the theory that the piece of tubing was located within subcutaneous tissue outside of the artery because, in his opinion, the piece of tubing would have been discovered either during the November 28, 2000, procedure or earlier in the November 29, 2000, procedure if it had been outside the artery. However, according to Dr. Dennis, based upon the timing of when the piece of tubing was found, the tubing itself had to have been located within the lumen of the artery until it was removed in the November 29, 2000, procedure. Dr. Dennis also rendered the opinion that not only was the piece of tubing located within the lumen of the carotid artery, but that the piece of tubing is directly related to the stroke which Patient M.R. suffered later that day or the following morning, which caused his death. Dr. Dennis testified that the piece of tubing became lodged in Patient M.R.'s carotid artery and that as blood flowed by it, platelets attached to the tubing, slowly building up with the carotid artery, until Patient M.R. experienced 100 percent stenosis in the right carotid artery, leading to his stroke. In sum, Dr. Dennis' opinion was that Respondent deviated from the standard of care by allowing a piece of tubing to enter Patient M.R.'s carotid artery and that it was this tubing which lead to Patient M.R.'s stroke and ultimately his death. This is in spite of the fact that Dr. Dennis was not able to state within any degree of medical probability how the sliver of tubing could have entered the artery. Dr. Dennis also rendered an opinion during his final hearing testimony that Respondent deviated from the standard of care because he did not secure the piece of tubing at issue in this case and see to it that the tubing was sent to the pathology laboratory at ORMC for analysis. Morris Kerstein, M.D., a board-certified vascular surgeon, reviewed all of the pertinent medical records reflecting the treatment and care Respondent provided to Patient M.R. Dr. Kerstein had been practicing for 35 years, and he is currently the chief of the vascular surgery department at the Veteran's Administration Hospital in Philadelphia, Pennsylvania. Dr. Kerstein has sufficient education, training, and experience to qualify as an expert in vascular surgery under Florida law. Dr. Kerstein's opinion based upon his education, training, and experience is that Respondent did not deviate from the standard of care in his treatment of Patient M.R. First, Dr. Kerstein testified that in his opinion, Respondent's conduct during all three procedures at issue was appropriate. As to the November 27, 2000, procedure, there was no way for Respondent to be aware that the piece of pediatric feeding tube had entered the operative field. It was too small to be noticed, and it was of a translucent color which made locating it extremely difficult. He was not critical of Respondent for not cutting the tubing himself. He testified that if, in fact, the sliver of tubing entered the surgical area as a result of the scrub technician cutting the tubing, and a two to three millimeter fragment jettisoned into the surgical field, this would not constitute a deviation from the standard of care by Respondent. Dr. Kerstein testified that he felt the November 28, 2000, procedure was performed appropriately as well. He testified that it was not a deviation for Respondent to use a Doppler to feel for pulses in the arteries, and to the contrary, it reveals that Respondent was being meticulous beyond what the standard of care requires. He opined that Respondent certainly would have palpated the arteries in question, and to suggest otherwise based on the absence of a note to that effect is not an appropriate conclusion to draw. Dr. Kerstein rendered the opinion that he did not believe that the piece of tubing in question was located within the lumen of the artery of Patient M.R. He testified that there was no way for the tubing to enter the artery because the sliver in question came off of the longer tubing before an incision was made in the carotid artery. There is therefore no reasonable explanation as to how the piece in question could have entered the carotid artery in the first place. Dr. Kerstein also disputed the theory that not only was the piece of tubing located within the lumen of the artery, but also the piece in question actually caused Patient M.R.'s stroke. Dr. Kerstein relied principally on the radiographic studies. Both the CT Scan of the brain and the angiogram taken late in the evening of November 28, 2000, revealed a right posterior occipital infarct. The posterior of the brain is the back of the brain, and if the infarct was located there, it means that the cause of the stroke had to be something other than an occlusion in the carotid artery. This is because the arteries that feed the back portion of the brain are the basilar and vertebral arteries, not the carotid artery. Therefore, there could be no possible causal connection between the sliver in question and Patient M.R.'s stroke. Dr. Kerstein's opinion as to the cause of Patient M.R.'s stroke focused on his personal history rather than on the events of November 27, 2000. He noted that Patient M.R. presented with severe atherosclerotic changes, indicative of an advanced disease process. He noted that Patient M.R. suffered from chronic obstructive pulmonary disease, which was the product of his 54-year smoking history. He also noted Patient M.R.'s significant cerebrovascular disease. He also stated that thrombosis (or clotting of the blood) is a known complication of this procedure and can happen for several plausible reasons other than a sliver of tubing in the artery. All of these conditions conspired to predispose Patient M.R. to suffer a significant event such as the stroke he suffered on November 28 through 29, 2000. Dr. Kerstein also noted that the piece of tubing was completely inert, and given its size and its location in the subcutaneous tissue outside of the carotid artery, the tubing would have had no impact whatsoever on Patient M.R.'s prognosis. The tubing in question is an example of inert material that can remain inside the body, such as the case of a bullet which is located too close to the spinal cord to allow for an operation to remove it, without causing the body any harm. Dr. Kerstein had no criticism of the medical records Respondent kept regarding the treatment he provided to Patient M.R. He specifically noted that the records were accurate and honestly reflected what had occurred during the procedure. The fact that no foreign object was noted in the first two procedures was appropriate because at that point, he had no reason to suspect the presence of a foreign object. The lack of reference to a cause of Patient M.R.'s atypical post-operative course was appropriate because in fact Respondent could not have defined a single reason why Patient M.R. was reacting the way he did. Finally, the operative note from the November 29, 2000, procedure was appropriate, as it also honestly and accurately depicted what had occurred; he made a specific comment on Respondent's note that the sliver was not indeed from the lumen, but that the exact location was unclear, finding this to be an unambiguous statement of fact. Dr. Kerstein also disagreed with the state's position with regard to the responsibility for maintaining possession of the piece of tubing post-operatively. Dr. Kerstein testified that it was the responsibility of the circulating nurse, an employee of the hospital, to arrange for the piece of tubing to be sent to the pathology lab for examination. The evidence is insufficient to support Petitioner's contention that the pediatric feeding tube sliver at issue caused Patient M.R. to suffer a stroke because of its location within the carotid artery itself. Radiographic studies were performed on Patient M.R. after the stroke. A CT Scan performed on November 28, 2000, revealed an acute right posterior cerebral artery distribution infarct. Further, a cerebral angiogram was performed on November 28, 2000, and revealed "markedly diseased circulation particularly in the right vertebral and basilar arteries." This note also revealed: "Severely diseased posterior fossa circulation." Based upon the location of the infarct in Patient M.R.'s brain, the cause of the stroke had to have been either the vertebral or basilar arteries that supply blood to the posterior part of the brain. In view of all the evidence, the expert testimony of Dr. Kerstein, together with that of Dr. Horowitz, was more persuasive than that of Dr. Dennis in regard to the standard of care and Respondent's actions in this matter.
Recommendation Based on all the evidence of record, it is RECOMMENDED that the Board of Medicine enter a final order holding that the evidence is not clear and convincing that Respondent has violated either Subsections 458.331(t) or (m), Florida Statutes, in his treatment of Patient M.R. and that the Administrative Complaint be dismissed. DONE AND ENTERED this 9th day of June, 2003, in Tallahassee, Leon County, Florida. DANIEL M. KILBRIDE Administrative Law Judge Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-3060 (850) 488-9675 SUNCOM 278-9675 Fax Filing (850) 921-6847 www.doah.state.fl.us Filed with the Clerk of the Division of Administrative Hearings this 9th day of June, 2003. COPIES FURNISHED: Michael D'Lugo, Esquire Wicker, Smith, O'Hara, McCoy, Graham & Ford, P.A. 390 North Orange Avenue Suite 1000 Orlando, Florida 32802 Daniel Lake, Esquire Department of Health 4052 Bald Cypress Way Bin C-65 Tallahassee, Florida 32399-3265 William W. Large, General Counsel Department of Health 4052 Bald Cypress Way, Bin A02 Tallahassee, Florida 32399-1701 Larry McPherson, Executive Director Board of Medicine Department of Health 4052 Bald Cypress Way Tallahassee, Florida 32399-1701
Findings Of Fact Dr. Jose A. Mijares is a general and thoracic surgeon who has practiced medicine in Tampa, Florida since 1967. He received his medical degree from the University of Havana in 1943. He served a five-year residency at Tampa General Hospital which was completed in 1967. He is Board certified in general surgery and limits his practice to that field. He is licensed to practice medicine in Florida and was so licensed at all relevant times herein. (Testimony of Respondent, stipulation) In 1977, Respondent was on the staffs of five hospitals in the Tampa area, including Centro Asturiano Hospital. The allegations of the Administrative Complaints deal with Respondent's treatment of six patients at Centro Asturiano Hospital at various times during the period 1977 to 1979. Ricardo Larzabal This sixteen-year-old patient was admitted to the hospital by Dr. A.B. Perez on May 12, 1977, with a diagnosis of abdominal pain and nausea. At admission, the patient's white blood count was slightly elevated at 11,000, but was at a normal range of 10,500 the following day. Respondent was called in for consultation on May 13. His impression was abdominal pain with possible appendical colic, and recommended a barium enema. The results of the barium enema showed that only about on-third of the appendix filled. On May 16, Respondent performed an exploratory laparotomy and appendectomy. He found the appendix kinked with a band in the proximal third of the appendix and fecalith in the distal two-thirds of the appendix. The pathological report reflected a congested vermiform appendix with lymphoid hyperplasia. Respondent's discharge diagnosis was "Abdominal pains. Appendical colic due to fecalith in the appendix. Chronic appendicitis." (Testimony of Respondent, Petitioner's Exhibit 4) Vivian Morejon Dr. C. Castellanos admitted this seventeen-year-old patient to the hospital on May 15, 1977, with a diagnosis of epigastric pain and colitis. On admission, the patient had a normal white blood county of 9,000. A barium enema was administered and reflected no abnormality. Respondent was called in for consultation on May 18 and his impression was "Abdominal pain, appendical colic." He performed an exploratory laparatomy and appendectomy on May 19, at which time he found blood in the peritoneal cavity caused by a ruptured follicle of an ovary. The appendix was retrocecal and covered by adhesions as in chronic appendicitis. His final diagnosis was "Abdominal pain, appendical colic due to chronic appendicitis, and ruptured follicle of the right ovary." The pathology report reflected that the patient had a vermiform appendix with lymphoid hyperplasia. (Testimony of Respondent, Petitioner's Exhibit 7) Ramiro Companioni, Jr. This fourteen-year-old patient was admitted to the hospital by Dr. C. Castellanos on September 24, 1977, due to pain in the right lower quadrant which had not been relieved with medication, and vomiting for two days prior to admission. The patient had been admitted to the hospital during the previous February with the same condition. At time of admission, he had a white blood count of 5,200 which was slightly lower than normal. Respondent was consulted on the day of admission and his impression was abdominal pain, appendical colic. A barium enema was ordered, but the appendix could not be observed. On September 27, Respondent performed an exploratory laparatomy and appendectomy. He found that the appendix was congested, edematous with fecalith in mid-portion covered by adhesions. The pathology report showed a microscopic diagnosis of acute appendicitis, as did Respondent's discharge diagnosis. The patient recovered without complications. (Testimony of Respondent, Petitioner's Exhibit 6) Shirley Alvarez This fifteen-year-old patient was admitted to the hospital by Dr. C. Castellanos on September 26, 1977, with acute abdominal pain in the right side with nausea and vomiting, which was diagnosed as possible appendicitis. Her white blood count was 6,900 and a barium enema did not visualize the appendix. Respondent was consulted on September 28, and his impression was that the patient had abdominal pain, appendiceal colic. He performed an exploratory laparotomy and appendectomy on September 29. The appendix was retrocecal and covered with adhesions as in chronic appendicitis. The pathology report showed on microscopic diagnosis a vermiform appendix with multiple serosal adhesions. The patient was discharged with a final diagnosis of chronic appendicitis. (Testimony of Respondent, Petitioner's Exhibit 8) Luisa Areu This forty-two year old patient was admitted by Respondent to the hospital on July 18, 1978, complaining of abdominal pain in the right flank. On examination, Respondent's impression was cervical polyp and possible enlarged uterus. The patient had experienced an exploratory laparotomy some 10 years before, but no records were available to determine the cause or results of the operation. On July 21, 1978, Respondent performed a dilation and four quadrant biopsy of the cervix. Although no polyp was found, there was severe chronic cervicitis and the uterus on palpation was enlarged. Respondent determined that a hysterectomy was advisable due to the enlargement of the uterus and the advanced severe chronic cervicitis. On July 27, Respondent removed the uterus, both fallopian tubes, and the appendix. The ovaries were not removed. The uterus was found to be of normal size, but both tubes were congested and edematous as in salpingitis. The pathology report confirmed the diagnosis of chronic cervicitis but found no significant abnormalities with the patient's tubes or appendix. Respondent's discharge diagnosis was severe chronic cervicitis. His discharge summary stated that in spite of the pathological report that the tubes looked normal, both tubes were congested and edematous like chronic salpingitis. (Testimony of Respondent, Petitioner's Exhibit 1) Deborah Fisher This 22-year-old patient was admitted by Respondent to the hospital on February 4, 1979, complaining of lower abdominal pain. Approximately seven months prior to her admission, she had had a tubal ligation and had experienced pain and occasional vomiting thereafter. The patient's history indicated that intercourse was very painful and that she had not had menstrual periods since September, 1978. Respondent's impression was "lower abdominal pain, rule out chronic pelvic inflammatory disease." All laboratory and other tests of the patient were negative. On February 8, 1979, Respondent performed a total abdominal hysterectomy, bilateral salpingectomy, and appendectomy. He found the tubes to be congested and edematous as in sub-acute salpingitis. The pathology report on microscopic diagnosis showed chronic cervicitis, mild with reserve call hyperplasia and slight dysplasia. No patholgoical diagnosis was found as to the fallopian tubes and appendix. (Testimony of Respondent, Petitioner's Exhibit 2, Respondent's Exhibit 1) It is difficult to diagnose acute appendicitis, particularly in the case of children between 12 and 18 years of age. About 70% to 85% of appendices removed incident to an operating diagnosis of appendicitis are pathologically acute. This generally is because physicians are reluctant to permit the possibility of appendices developing abscesses and perforations if appendectomies are forestalled for too long a period. It is particularly difficult to diagnose acute appendicitis in females between the ages of 14 and 18 because they often have other causes for pain, such as an ovarian cyst. It is an accepted and customary practice to remove a normal appendix in conjunction with other surgery in the right lower quadrant, unless there are contra- indicating problems. This precludes the later possibility of appendicitis attacks, and also lessens the probability of erroneous diagnosis later because of the presence of a lower incision scar. (Testimony of Myers, [Deposition- Respondent's Exhibit 4], Mason [Deposition-Respondent's Exhibit 5] Respondent) In cases that are difficult to diagnose, particularly in young children, the use of the barium enema as a diagnostic tool for appendicitis is accepted medical practice. It helps to determine if an appendix is normal. If the appendix fills completely, it is considered to be normal, but if it does not fill normally and there is also swelling and other complaints, a physician can imply pathology in the area near the appendix. (Testimony of Respondent, Myers, Ferris, Respondent's Composite Exhibit 2, 4) Expert testimony at the hearing established that all six of the operations in question were necessary and proper, and that the care and treatment rendered by Respondent to the patients met acceptable and medical standards in the community. In the case of patient Larrabal, although his white blood count had subsided on the second day of admission, his prior history, coupled with the fact that the barium enema only partially filled the appendix, showed, in the opinion of one expert, that there was a "diagnostic dilemma" which justified the operation after waiting an appropriate time. Although the pathology report reflected a normal appendix, the fact that lymphoid hyperplasia was also found indicated the presence of an abnormality. As to patient Companioni, Respondent testified that he saw no need to operate immediately because the white blood count was normal which could have indicated the presence of viral rather than bacterial infection. Again, however, the barium enema only partially filled the appendix, thus justifying the operation when considered along with the patient's complaints and other indications. Expert opinion established that Respondent's delay was justified in waiting an appropriate time to determine if the patient's illness was minor in nature or acute. The exploratory laparotomy which Respondent performed on patient Morejon was justified in that it was impossible to determine in advance whether the pain she had experienced was caused by appendicitis or something else. It was discovered upon operating that she had had a ruptured follicle of the ovary which was the source of pain. The removal of her normal appendix as incident to the surgery was necessary and proper under the circumstances. Even Petitioner's expert testified that it had been a "close call" as to whether or not to operate on the patient, and he agreed that the appendix should have been removed as incidental to the surgery. As to patient Alvarez, the fact that the appendix didn't "visualize" as a result of the barium enema indicated something was blocking the appendix and warranted the operation. The fact that fibrous adhesions were found showed that the appendix was abnormal. Although Petitioner's expert, Dr. Charles F. James, testified that the presence of adhesions indicated that the patient had probably had previous attacks of appendicitis, he felt that the operation was unjustified because there was no acute inflammation. However, he acknowledged that it is common to remove an appendix in such a case and could not be considered improper. (Testimony of Respondent, Myers, Mason, James, Respondent's Exhibit 4, 5) Petitioner's expert had reviewed the records of 15 appendectomy cases of Respondent, including the four which are the subject of charges herein. He testified that, although his opinion might be different from that of Respondent as to the treatment in question, none of the cases justified disciplinary action. (Testimony of James) There was conflicting expert testimony at the hearing with regard to the property and necessity of Respondent's surgical procedures regarding patients Area and Fisher, but the opinions expressed in the testimony of Dr. Robert W. Withers are accepted. He found that patient Areu's complaints, past medical history, and the fact that a sonogram reflected that she had an enlarged uterus indicated that the only reasonable location for her pain was in the uterus. It was therefore his opinion that such pain related to the uterus is best cured in someone who has had previous surgery in that area by the surgical procedures performed by Respondent. As to patient Fisher, similar surgical procedures performed by Respondent. As to patient Fisher, similar surgical procedures performed by Respondent were considered indicated and proper by Dr. Withers based on the patient's complaints and the prior history of tubal ligation which had resulted in the existence of post-tubal sterilization syndrome. In the opinion of Dr. Withers, there could be no other effective treatment for the patient to relieve her problem than the surgical procedures employed by Respondent. Additionally, it was found that the patient had a precancerous condition known as dysplasia, indicative that Respondent's operative procedures were fortuitous and to the patient's benefit. (Testimony of Respondent, Withers)
Recommendation That Petitioner dismiss the Administrative Complaints herein. DONE AND ENTERED this 3rd day of February, 1983, in Tallahassee, Florida. THOMAS C. OLDHAM Hearing Officer Division of Administrative Hearings 2009 Apalachee Parkway Tallahassee, Florida 32301 (904) 488-9675 Filed with the Clerk of the Division of Administrative Hearings this 3rd day of February, 1983. COPIES FURNISHED: Grover C. Freeman, Esquire Freeman and Lopez, P.A. 4600 West Cypress, Suite 410 Tampa, Florida 33607 Tony Cunningham, Esquire Wagner, Cunningham, Vaughan and McLaughlin, P.A. 708 Jackson Street Tampa, Florida 33602 Dorothy Faircloth, Executive Director Board of Medical Examiners 130 North Monroe Street Tallahassee, Florida 32301 ================================================================= AGENCY FINAL ORDER ================================================================= BEFORE THE BOARD OF MEDICAL EXAMINERS DEPARTMENT OF PROFESSIONAL REGULATION, BOARD OF MEDICAL EXAMINERS, Petitioner, vs. CASE NOS. 81-3183 82-823 JOSE A. MIJARES, M.D., License Number: 12114, Respondent. /
Findings Of Fact The Respondent, Charles P. Shook, M.D., is a medical doctor having been issued license number 0020414, pursuant to Chapter 458, Florida Statutes. He is board certified in the areas of general and peripheral vascular surgery and practices in those specialty areas in Fort Myers, Lee County, Florida. He has been practicing in Lee County since 1973. The Petitioner is an agency of the State of Florida, charged with enforcing the licensure and practice standards embodied in Chapter 458, Florida Statutes and related statutes and rules and imposing disciplinary measures for departure from those standards by physicians licensed in Florida when such are proven. Mrs. Betty A. Fiore, at times pertinent hereto, was an obese, 47-year old female, with a history of thrombo-phlebitis and progressively enlarging and painful bilaterial varicosities of the veins in her right and left legs. She was admitted to Fort Myers Community Hospital on January 28, 1979, by the Respondent, for performance of a bilateral "vein-stripping" surgical procedure. Her medical history reflected that she had had a similar vein-stripping procedure performed over 20 years previously. The patient was operated on by the Respondent on January 29, 1979, beginning at approximately 9:25 a.m. The procedure was quite lengthy due to certain complications and lasted until 1:25 p.m. that day. After normal preparations, under general anesthesia, the Respondent began the operation by performing an oblique groin incision on the left leg just below the inquinal liagment, approximately ten centimeters in length. The incision penetrated the subcutaneous tissue and, as the "fossa-ovalis" was approached, the Respondent noted a significant amount of scar tissue, apparently related to the earlier surgical procedure, which obliterated and concealed much of the normal anatomy and structure in the area of surgery. It was of such a dense nature that only a faintly palpable pulse could be felt in the vessel. The Respondent dissected out the various venous branches in the area and individually ligated them. During his dissection process, the distal common femoral artery was injured by being slightly nicked with the surgical instrument. Repair procedures for the injury to the artery were carried out as will be described below. In any event, the "codman stripper" was employed in carrying out the stripping operation on the vein in question and additionally, several incisions were made around the calf of the leg to alleviate smaller varicosities. One large perforating vein in the malleolar area had to be ligated after the superficial portion had been stripped away. The Respondent then began to perform a similar procedure on the right leg, in spite of the initial difficulties he had had on the left leg, because he did not expect such severe scar tissue involvement with the anatomical structures in the area of incision on both legs. When he carried out the incision on the right leg however, he found that the anatomy of the right leg was essentially the same as that of the left and that substantial scar tissue reaction had occurred, related to prior surgery, with obliteration of much of the normal anatomy, including concealment of the femoral artery. Due in large part to these anatomical changes and complications involved in dissecting out the various venous branches involved in the stripping procedure, the right femoral artery was also slightly nicked by the scalpel. The Respondent attempted to suture the femoral arteries nicked in both legs at the time these injuries occurred, but the sutures would not hold in the arteries due to some then unknown, medical condition. After the same failure to hold sutures was encountered with regard to both femoral arteries, the Respondent sent samples of the arteries to the pathologist for evaluation. The pathologist report indicated that the arteries were "normal." Parenthetically it should he noted that the "complaining witness," Mrs. Fiore, has been found to exhibit symptoms of diabetes mellitus. Her testimony was somewhat evasive concerning the degree to which she may suffer from this malady, which can have a detrimental effect on the vascular system. In any event, when working first on the left leg, the Respondent elected to resect back along the artery for approximately a half-inch on each side of the wound and after that resection, to repair the femoral artery with the insertion of a 6 millimeter gortex graft. Likewise, with regard to the right leg, the Respondent found the sutures would not hold in the damaged artery (which was of a "cheese-like" consistency). He therefore performed a similar resection and insertion of a 6 millimeter gortex graft to repair the injury. The surgical procedure was then successfully concluded. Post-operatively the patient encountered some complications involving infection in the groin area, requiring two additional admissions to Fort Myers Community Hospital. Subsequently, she was transferred to Methodist Hospital in Houston, Texas, where she underwent two additional surgical procedures. The Petitioner presented the opinions of two expert witnesses, Dr. Alexander Braze and Dr. E. William Reiber. Dr. Braze's expert opinion is predicated on the review of Mrs. Fiore's office records from the Respondent's office, the hospital charts for her three admissions to Fort Myers Community Hospital, and summaries of her two admissions to the Methodist Hospital in Houston, Texas. His opinion is not based on any examination of the patient involved. Dr. Braze thus opined that because of the previous surgery on the greater saphenous vein, bilaterally, there would be obvious and considerable scarring and scar tissue in the subcutaneous area which would distort and conceal the individual anatomical structures. He himself has never nicked a femoral artery while doing a vein-stripping operation but, although he acknowledges it is an "uncommon complication, he has heard of it occurring. He was unable to render an opinion concerning whether or not the operation was performed properly because this was not a typical vein ligation and stripping procedure, due to the presence of extensive scar tissue, and resulting difficulty involved. The dense scar tissue precluded identification of the structures in the area of the surgical incision and meant that the Respondent had to proceed slowly and very meticulously with a careful dissection, deviation from which careful procedure could cause difficulty. The doctor's procedure was slow and meticulous. The procedure (for both legs) took approximately four hours. Although the Respondent proceeded with care, he nicked the arteries anyway. Dr. Braze could not state that such a complication, albeit uncommon, constituted a departure from standards normally recognized in the medical community. With regard to the doctor's judgmental decision to proceed to the right leg after nicking and repairing the artery in the left leg and completing the vein stripping procedure in the left leg. Dr. Braze opined that he was acting as a reasonable physician in proceeding to the other leg since he had already corrected the initial injury, especially since it was the leg in which she was having her chief complaints. In any event, Dr. Braze was unable to render an opinion as to whether or not the procedure up to the point of nicking the artery was properly or improperly done, although he acknowledged that the lengthy time taken to perform the total procedure indicates that the doctor was proceeding slowly and with greater than normal difficulties. In any event, after the arteries were nicked, the procedure followed by the Respondent was excellent and the repair work was competently and efficiently performed. Dr. Reiber, Petitioner's other expert witness, testified by deposition, which was stipulated into evidence. His expert opinion was based on a review of the deposition of the Respondent, the Fort Myers Community Hospital records of the patient, and the depositions of the patient, Betty Fiore, Arnold Flare and Quillen Jones. Additionally, he reviewed the records dealing with Mrs. Flare's treatment in Houston, Texas. He thus opined that the Respondent made two technical errors when he injured the arteries in each leg and he felt that it was an error in judgment to have performed the procedure on the right leg after having encountered difficulty in the initial procedure on the left leg. He was unable to opine however, that the treatment rendered the patient by Respondent fell below the appropriate standard of care accepted by similar physicians in the community. Moreover, he also opined that the Respondent's treatment after nicking the arteries affirmatively met the standard of care for reasonably prudent physicians in such circumstances. The expert witnesses presented on behalf of the Respondent were Drs. Peter M. Sidell and Luis A. Ruilova. Both witnesses opined, in effect, that, given the obesity of the patient and the difficult surgical process that alone entailed, coupled with the significant involvement of scar tissue in the area of the incision, that the complications associated with this procedure could occur in the hands of even the most renowned surgeon. The fact that the Respondent experienced these complications does not render his practice in this regard to be below the standard of care for vascular surgeons in that community or area of practice. They further opined that it is a matter of personal judgment on whether to proceed to the other leg after encountering these difficulties. A reasonable judgment would have been to explore the groin area on the other side, after accomplishing repair of the first injured artery, which was done. The initial arterial injury having been repaired in a successful manner, both of the Respondent's experts opined that, the patient then being stabilized, the Respondent was justified in proceeding to the other leg and performing the procedure on that side. The main purpose of the operation was to remove the veins of the patient since the patient was symptomatic with varicosities. It therefore would be poor judgment to simply repair the nicked artery and proceed no further, since the symptomatic vein would remain uncorrected. In short, both experts for Respondent opined that neither the vein-stripping procedure, the repair of the damaged arteries nor post-operative management for which Respondent was responsible were performed in a manner below the appropriate standard of care of reasonably prudent physicians in the community. Thus, although the patient unfortunately experienced difficulties during a procedure involving the accidental nicking of her femoral arteries and, after the grafts repairing those injured arteries were performed, later suffered an infection at the operative site necessitating further hospitalization, no expert witness could describe the treatment and care afforded this patient as being below the appropriate standard of care exercised by a reasonably prudent physician performing such vascular surgical practice in the Fort Myers community or area. The Respondent has never encountered this difficulty either before or since this occasion in his practice, which is characterized by frequent vascular surgical procedures. Additionally, Dr. Ruilova established that the nicking of the femoral arteries during such a procedure, although not a common occurrence, is well documented in the literature and not at all unheard of. Indeed, Dr. Ruilova, when assisting a distinguished surgeon who was chief of surgery at the Mayo Clinic at the time, observed that expert surgeon nick a femoral artery in a vein- stripping procedure on two occasions. Finally, it is noted that the Respondent's practice has been characterized by a high level of professional expertise, competence and compassion in caring for his patients, both before and since the occasion in question. He has never before been subjected to disciplinary action.
Recommendation Having considered the foregoing Findings of Fact, Conclusions of Law, the evidence of record, the candor and demeanor of the witnesses and the pleadings and arguments of the parties, it is, therefore RECOMMENDED that a Final Order be entered by the Board of Medical Examiners dismissing the complaint in its entirety. DONE and ENTERED this 11th day of October, 1984, in Tallahassee, Florida. P. MICHAEL RUFF Hearing Officer Division of Administrative Hearings The Oakland Building 2009 Apalachee Parkway Tallahassee, Florida 32301 (904)488-9675 FILED with the Clerk of the Division of Administrative Hearings this 11th day of October, 1984. COPIES FURNISHED: Barbara K. Hobbs, Esquire Department of Professional Regulation 130 North Monroe Street Tallahassee, Florida 32301 Dorothy Faircloth, Executive Director Board of Medical Examiners 130 North Monroe Street Tallahassee, Florida 32301 Patrick Geraghty, Esquire HENDERSON, FRANKLIN, STARNES & HOLT Post Office Box 280 Fort Myers, Florida 33902 Fred M. Roche, Secretary Department of Professional Regulation 130 North Monroe Street Tallahassee, Florida 32301
The Issue The issue in this case is whether Jose Rosado, M.D., (Respondent), violated Section 458.331(1)(t), and, if so, what penalty should be imposed.
Findings Of Fact Petitioner is the state agency charged with regulating the practice of medicine pursuant to Florida law. At all times material to these proceedings, Respondent has been a licensed physician in the State of Florida, having been issued license number ME 0068035. Respondent is board-certified in internal medicine and cardiovascular diseases. On March 10, 1997, Patient W.B.C., a 72-year-old man, arrived at the Leesburg Regional Medical Center (LRMC) emergency room. He complained of a sudden onset of weakness in his left hand and arm with numbness and tingling. Respondent was Patient W.B.C.'s primary care physician. Respondent admitted Patient W.B.C. with a diagnosis of cerebrovascular accident, mitral regurgitation, sick sinus syndrome and a history of myocardial infarction. Respondent ordered that Patient W.B.C. undergo a head CT scan, carotid Doppler, 2-D echocardiogram, an electroencephalogram, and a neurological consultation. Based on the test results and the consultation, Respondent diagnosed Patient W.B.C. with right cerebrovascular accident, mitral regurgitation, sick sinus syndrome, and history of myocardial infarction. Respondent then discharged the patient with Ticlid, a medication to prevent further cerebrovascular accidents and aspirin. On March 16, 1997, Patient W.B.C. was admitted to LRMC complaining of weakness, dizziness and a fever. His vital signs revealed a temperature of 103.0 F, a pulse of 118, and a blood pressure of 139/75. The emergency room physician ordered a chest x-ray, EKG, and urine and blood cultures. The chest x-ray revealed no acute cardiopulmonary abnormality. Urine tests revealed features consistent with the possibility of urosepsis. Blood work showed a white blood count of 9.15, elevated but within the normal range. Also on March 16, Respondent ordered that antibiotics be given prophylactically until the blood cultures came back from the laboratory. The cultures came back positive for staphylococcus aureus (staph). Staph is a notoriously “bad bug” and Staphylococci aureus bacteremia has a high mortality rate. Staph aureus can originate from several possible sources including infections through the urinary tract system, IV sites, aspiration into the lungs, and pneumonia (although not very common). Staphylococci in the bloodstream is known as bacteremia. Bacteremia can lead to endocarditis which is an infection of the inner lining of the heart and the heart valves. Endocarditis is a life-threatening condition that can quickly damage the heart valves and lead to heart failure or even death. Patients with certain cardiac conditions such as mitral valve regurgitation have a higher risk of developing endocarditis. Patient W.B.C. had such a history. On March 17, 1997, Patient W.B.C. was started on intravenous antibiotics by Respondent. Patient W.B.C. continued to receive the intravenous antibiotics for four days from March 17, 1997, through March 20, 1997. Respondent then switched Patient W.B.C. to oral antibiotics and kept the patient in the hospital one more day prior to discharging him with instruction to continue on the oral antibiotics for another ten days. Patient W.B.C. was discharged on March 21, 1997. He was not referred to an infectious disease specialist nor had Respondent obtained a consultation with any specialist to determine the length of time that the patient's infection should be treated. Respondent felt that he was adequately qualified to treat this patient, and the treatment appeared to work. Respondent thought the bacteria growing in the patient's blood "likely" originated from a lung infection. An infectious disease specialist should have been consulted to give guidance as to how long to treat the infection. The standard of care for treating a staph aureus infection where there is a known source of infection requires 14 days of intravenous antibiotics. Where the source is not known, then four to six weeks of antibiotics is recommended. In this case, the infection, a resistant staph infection found in the patient's blood, could have originated from several sources. While such staph could have sprung from a source in the lung, this is by no means likely and the infection could have originated from another source. The standard of care required that Respondent contact an infectious disease specialist for an evaluation and/or that he treat Patient W.B.C.’s staphylococcus with a minimum of 10 to days of intravenous antibiotics. On or about April 11, 1997, Patient W.B.C., presented to the emergency room at LRMC complaining of congestion, shortness of breath, fever of 100.3° F, and a cough. The emergency room physician performed a physical exam which revealed vital signs of a temperature of 101.3° F, a pulse of 104, and a blood pressure of 90/54. A chest x-ray, blood work and a urine culture were ordered. Patient W.B.C. was then admitted on April 11, 1997, with a diagnosis of pneumonia, an old cerebrovascular accident and coronary artery disease. The ER physician started Patient W.B.C. on a plan of treatment which included intravenous antibiotics, Vancomycin, IV fluids, and blood cultures. A physical examination on the patient revealed a temperature of 101.3° F, a pulse of 104 and blood pressure of 91/53. The attending physician diagnosed him with probable sepsis with pneumonia. On April 12, 1997, the blood cultures came back positive for Staphylococcus aureus bacteremia. On April 15, 1997, Patient W.B.C. was afebrile (without fever) and his white blood cell count was 10.23, which is within the normal range of 4.0 to 11.0. The patient continued in this condition through April 18, 1997, despite suffering from sepsis. On April 18, 1997, Respondent approved Patient W.B.C. for transfer to another institution for consideration for urgent mitral valve replacement. On April 19, 1997, Patient W.B.C. arrested and was pronounced dead at 5:53 a.m. Petitioner’s expert, Carlos Sotolongo, M.D., is board- certified in internal medicine, cardiovascular disease and nuclear cardiology. As established by Dr. Sotolongo's testimony, Respondent practiced below the standard of care by failing to treat Patient W.B.C. with a sufficient number of days of intravenous antibiotics and by failing to consult an infectious disease specialist. According to Dr. Sotolongo, there is a difference in the way that an uncomplicated pneumonia is treated as opposed to a pneumonia complicated by bacteremia. The latter must be treated more aggressively. Based on the foregoing, Respondent violated Section 458.331(1)(t), by failing 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.
Recommendation Based on the foregoing, it is recommended that a Final Order be entered finding that Respondent violated Section 458.331(1)(t), and imposing a penalty which includes a formal reprimand, payment of an Administrative Fine in the amount of $5,000.00 within 180 days, and eight hours of Continuing Medical Education (CME) to be completed within the next 12 months dealing with the diagnosis and treatment of infections and/or risk management. DONE AND ENTERED this 1st day of October, 2003, in Tallahassee, Leon County, Florida. S DON W. DAVIS 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 1st day of October, 2003. COPIES FURNISHED: William M. Furlow, Esquire Katz, Kutter, Alderman, Bryant & Yon, P.A. Post Office Box 1877 Tallahassee, Florida 32302-1877 Kim M. Kluck, Esquire Department of Health 4052 Bald Cypress Way, Bin C-65 Tallahassee, Florida 32399-3265 R. S. Power, Agency Clerk Department of Health 4052 Bald Cypress Way, Bin A02 Tallahassee, Florida 32399-1701 Larry McPherson, Executive Director Board of Medicine Department of Health 4052 Bald Cypress Way Tallahassee, Florida 32399-1701
