Findings Of Fact Orlando Regional Healthcare System, Inc. ("ORHS") filed a letter of intent to apply for certificate of need ("CON") 8039 for the approval of a bone marrow transplantation program. ORHS also submitted a Notice of Filing the letter of intent for publication in The Orlando Sentinel newspaper. The notice, which is as follows, did not include the capital expenditure cost of the project. PUBLIC NOTIFICATION NOTICE OF FILING The applicant, Orlando Regional Healthcare System, Inc., which is authorized to operate Orlando Regional Medical Center, announces its intent to file a certificate of need application on March 22, 1995 with the Agency for Health Care Administration to establish Bone Marrow Transplantation Services at Orlando Regional Medical Center, located in Orlando, FL, the Agency's District 7, Orange County Subdistrict, which is designated as Organ Transplant Planning Area 3 by the Agency's Certificate of Need Program Office. The project, if granted is expected to become operational in 1996. Signed: /s/ Garry J. Singleton Garry J. Singleton Vice President of Acute Care Operations Orlando Regional Healthcare System, Inc. 1414 Kuhl Avenue Orlando, Fl. 32806 The Agency For Health Care Administration ("AHCA") is the state agency that administers the CON program. AHCA published notice of receiving ORHS' letter of intent in Vol. 21, Number 10 of Florida Administrative Weekly on March 10, 1995. AHCA's notices do not contain cost estimates. AHCA deemed ORHS' application incomplete and withdrew it from consideration due to omission of capital costs from the published notice in the newspaper. AHCA relied on the requirements on Rule 59C-1.008(1)(i) and (j), Florida Administrative Code. See, Conclusion of Law 11, infra. There is no evidence that The Orlando Sentinel made an error in the publication of the Notice of Filing. Capital expenditure costs, when estimated in letters of intent and in notices of filing letters of intent, are often inflated. That is done because CON applications, filed subsequently with higher capital expenditure costs than those stated in the letter of intent, are rejected. Rule 59C-1.008(1)(k)3, Florida Administrative Code. Because the capital costs are often inflated in letters of intent, ORHS' expert concluded that notices of capital expenditure costs are meaningless, and that the omission of such costs from the newspaper notice is insignificant. Therefore, he asserts that the ORHS' notice of filing its letter of intent substantially complied with the requirements of the rule. ORHS' expert also notes that the publication rule requires the notice to include eleven different items, and that ORHS' notice omitted only one of the eleven. AHCA does not always require letters of intent or newspaper notices. They are not required for expedited applications, and errors in notices are excused if made by the newspaper and not the applicant. However, there are no batching cycles or comparative review of expedited CON applications.
Recommendation Based on the foregoing Findings of Fact and Conclusions of Law, it is RECOMMENDED that AHCA enter a final order withdrawing from consideration CON application 8039 filed by ORHS. DONE AND ENTERED this 11th day of August, 1995, in Tallahassee, Leon County, Florida. ELEANOR M. HUNTER Hearing Officer Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-1550 (904) 488-9675 Filed with the Clerk of the Division of Administrative Hearings this 11th day of August, 1995. APPENDIX TO RECOMMENDED ORDER, CASE NO. 95-3059 To comply with the requirements of Section 120.59(2), Florida Statutes (1993), the following rulings are made on the parties' proposed findings of fact: ORHS' Proposed Findings of Fact. Accepted in Findings of Fact 1. Accepted in Findings of Fact 3. Subordinate to Findings of Fact 3. Accepted in Findings of Fact 3. Accepted in or subordinate to Findings of Fact 5 (as $5,000,000 each in proposed project costs in Exhibit 3 and approximately $5,000 total actual costs in Exhibit 4). Accepted in or subordinate to Findings of Fact 7. Accepted in Findings of Fact 5. Accepted in or subordinate to Findings of Fact 2 and conclusions of law 11. Accepted in Findings of Fact 5. Rejected in conclusions of law 13. 11-13. Accepted in Findings of Fact 5. Accepted in or subordinate to Findings of Fact 5 (as $5,000,000 each in proposed project costs in Exhibit 3 and approximately $5,000 total actual costs in Exhibit 4). Accepted in Findings of Fact 5 and Conclusions of Law 13. 16-17. Accepted in Findings of Fact 8. Accepted. Conclusion rejected in conclusions of law 11. See, 5 supra. AHCA's Proposed Findings of Fact. Accepted in Findings of Fact 2. Accepted in Findings of Fact 3 and 4. 3-5. Accepted in Findings of Fact 5-8. COPIES FURNISHED: John Gilroy, Esquire Senior Attorney Agency for Health Care Administration 2727 Mahan Drive Fort Knox Building 3, Suite 3431 Tallahassee, Florida 32308-5403 James M. Barclay, Esquire Cobb, Cole & Bell 131 North Gadsden Street Tallahassee, Florida 32301 R. S. Power, Agency Clerk Agency for Health Care Administration 2727 Mahan Drive Fort Knox Building 3, Suite 3431 Tallahassee, Florida 32308-5403 Tom Wallace Assistant Director Agency For Health Care Administration 2727 Mahan Drive Fort Knox Building 3, Suite 3431 Tallahassee, Florida 32308-5403
The Issue This matter concerns the amount of money to be reimbursed to the Agency for Health Care Administration for medical expenses paid on behalf of Gregory McElveen, a Medicaid recipient, following a settlement recovered from a third party.
Findings Of Fact This proceeding determines the amount the Agency should be paid to satisfy a Medicaid lien following Petitioner’s recovery of a $240,000.00 settlement from a third party. The Agency asserts that it is entitled to recover the full amount of its $72,907.93 lien. The incident that gave rise to this matter resulted from alleged medical malpractice. In 2016, Mr. McElveen saw his primary care physician complaining of pain and redness in his hand. The pain was ultimately traced to a metal shaving that had lodged in his finger. Despite repeated visits complaining of pain and swelling, however, Mr. McElveen’s physician failed to locate and remove the foreign object. In the meantime, his health worsened. On July 17, 2017, Mr. McElveen was admitted to the hospital, and was found to be critically ill with septic emboli. On August 15, 2017, Mr. McElveen died as a result of a systemic infection. He was survived by his wife and three daughters.3 2 By requesting a deadline for filing post-hearing submissions beyond ten days after receipt of the Transcript at DOAH, the 30-day time period for filing the Final Order was waived. See Fla. Admin. Code R. 28-106.216(2). 3 Although Mr. McElveen’s three daughters survived his death, in his subsequent wrongful death lawsuit, only one of his daughters was considered a “minor child” under the Florida Wrongful Death Act, because the other two were over the age of 25. § 768.18, Fla. Stat. The Agency, through the Medicaid program, paid a total of $72,907.93 for Mr. McElveen’s medical care, which was the full amount of his past medical expenses. In 2019, Mr. McElveen’s estate brought a wrongful death action against his treating physician.4 Charles T. Moore, Esquire, represented Petitioner’s estate and was the primary attorney handling the litigation. Ultimately, Mr. Moore was able to settle the wrongful death action for $240,000. The Agency was not a party to, nor did it intervene in, Petitioner’s wrongful death lawsuit. Under section 409.910, the Agency is to be repaid for its Medicaid expenditures out of any recovery from liable third parties. Accordingly, when the Agency was notified of the settlement of Petitioner’s lawsuit, it asserted a Medicaid lien against the amount Petitioner recovered. The Agency asserts that, pursuant to the formula set forth in section 409.910(11)(f), it should collect $72,907.93 to satisfy the medical costs it paid on Petitioner’s behalf. The Agency maintains that it should receive the full amount of its lien regardless of the fact that Petitioner settled for less than what Petitioner believes is the full value of his damages. Petitioner, on the other hand, argues that, pursuant to section 409.910(17)(b), the Agency should be reimbursed a lesser portion of the settlement than the amount the Agency calculated pursuant to the section 409.910(11)(f) formula. Petitioner specifically asserts that the Medicaid lien should be reduced proportionately, taking into account the full value of Petitioner’s damages. Otherwise, the application of the statutory formula would permit the Agency to collect more than that portion of the settlement that fairly represents Petitioner’s compensation for medical expenses. Petitioner insists that reimbursement of the full lien amount violates the federal Medicaid law’s anti-lien provision (42 U.S.C. § 1396p(a)(1)) and 4 Petitioner Daniel Hallup was appointed Personal Representative of Mr. McElveen’s estate. Florida common law. Petitioner requests that the Agency’s allocation from Petitioner’s recovery be reduced to $5,832.63. To establish the value of Mr. McElveen’s damages, Petitioner offered the testimony of Mr. Moore. Mr. Moore has practiced law for 24 years and is a partner with the law firm of Morgan & Morgan in Tampa, Florida. In his practice, Mr. Moore focuses exclusively on medical malpractice causes of action. Mr. Moore represented that he has taken a number of his cases to jury. As part of his practice, Mr. Moore routinely evaluates damages similar to those Petitioner suffered. This activity includes analyzing jury verdicts to keep current on case values, as well as discussing cases with other attorneys. In calculating the value of Mr. McElveen’s wrongful death claim, Mr. Moore reviewed Mr. McElveen’s medical records. Mr. Moore stated that, based on his professional assessment and experience, Mr. McElveen’s damages equaled between three to five million dollars which is the total monetary value of the survivors’ and estate’s wrongful death damages. Therefore, Mr. Moore opined that a conservative value of Mr. McElveen’s damages is $3,000,000. Based on his evaluation, Mr. Moore asserted that the $240,000 settlement was far less than the value of the actual damages Mr. McElveen suffered. Mr. Moore explained that Petitioner settled for a much lower amount because his potential recovery was limited due to the fact that the one potential defendant (Mr. McElveen’s physician) was retiring and carried minimal insurance coverage ($250,000). Mr. Moore also felt that the other possible liable parties (including the hospital) had met the appropriate standard of medical care when treating Mr. McElveen. Therefore, Mr. Moore believed that he had settled for the best deal he could under the circumstances, and Mr. McElveen’s estate was not likely to recover more. Finally, to support the Petition to reduce the amount of the Medicaid lien, Mr. Moore explained that Petitioner’s estate received only eight percent of the true value of Mr. McElveen’s damages ($3,000,000 divided by $240,000). Because only eight percent of the damages were recovered, in like manner, the $72,907.93 Medicaid lien should be reduced to eight percent, or $5,832.63, as a fair and reasonable allocation of the amount of Petitioner’s past medical expenses recovered the $240,000 settlement. The Agency did not present evidence or testimony disputing Mr. Moore’s valuation of the “true” value of Petitioner’s damages or his calculation of the amount of the settlement that should be allocated as Petitioner’s past medical expenses. Petitioner also offered the testimony of R. Vinson Barrett, Esquire, to established the value of Mr. McElveen’s damages. Mr. Barrett is a trial attorney with over 40 years’ experience. Mr. Barrett works exclusively in the area of plaintiff’s personal injury, medical malpractice, and medical products liability cases. He has also handled wrongful death cases. Mr. Barrett expressed that, as a routine part of his practice, he makes assessments concerning the value of damages suffered by injured parties. In addition, not only does he have personal experience with jury trials, but he stays current in recent jury verdicts and regularly discusses jury results with other attorneys. Mr. Barrett was accepted as an expert in the valuation of damages suffered by injured persons. Prior to testifying, Mr. Barrett familiarized himself with the facts and circumstances of Mr. McElveen’s injuries and death. He reviewed Petitioner’s exhibits, including Petitioner’s medical records. He also reviewed the sample jury verdicts Petitioner introduced as Petitioner’s Exhibit 8. Based on his valuation of Petitioner’s injuries, as well as his professional training and experience, Mr. Barrett placed a “very conservative value” on Petitioner’s injuries at $3,000,000. Mr. Barrett explained that injuries similar to Petitioner’s would result in jury awards averaging approximately $3.5 million dollars. Mr. Barrett supported Mr. Moore’s pro rata methodology of calculating a reduced portion of Petitioner’s $240,000 settlement to equitably and fairly represent past medical expenses. With injuries valued at $3,000,000, the $240,000 settlement only compensated Petitioner for eight percent of the total value of his damages. Therefore, the most “fair” and “reasonable” manner to apportion the $240,000 settlement is to apply that same percentage to determine Petitioner’s recovery of medical expenses. Petitioner asserts that applying the same ratio to the total amount of medical costs produces the definitive value of that portion of Petitioner’s $240,000 settlement that represents compensation for past medical expenses, i.e., $5,823.63 ($72,907.93 times eight percent). Similar to Mr. Moore’s testimony, Mr. Barrett’s expert testimony was unrebutted. Further, the Agency did not offer evidence or testimony proposing a more appropriate or different valuation of Mr. McElveen’s total damages, or contesting the methodology Petitioner used to calculate the portion of the $240,000 settlement fairly allocable to Petitioner’s past medical expenses. Based on the testimony from Mr. Moore and Mr. Barrett that the $240,000 settlement does not fully compensate Petitioner for Mr. McElveen’s damages, Petitioner argues that a lesser portion of the medical costs should be calculated to reimburse Medicaid, instead of the full amount of the lien. Petitioner proposes that a ratio be applied based on the true value of Petitioner’s damages ($3,000,000) compared to the amount that Petitioner actually recovered ($240,000). Using these numbers, Petitioner’s settlement represents approximately an eight percent recovery of the full value of Petitioner’s damages. In similar fashion, the Medicaid lien should be reduced to eight percent or approximately $5,832.63 ($72,907.93 times .08). Therefore, Petitioner asserts that $5,832.63 is the portion of his third-party settlement that represents the equitable, fair, and reasonable amount the Florida Medicaid program should recoup for its payments for Petitioner’s medical care. All of the expenditures Medicaid spent on Petitioner’s behalf are attributed to past medical expenses. No portion of the $72,907.93 Medicaid lien represents future medical expenses. The undersigned finds that the unrebutted testimony at the final hearing demonstrates that the full value of Petitioner’s damages from this incident equals $3,000,000. Further, based on the evidence in the record, Petitioner met his burden of proving, by clear and convincing evidence, that a lesser portion of Petitioner’s settlement should be allocated as reimbursement for medical expenses than the amount the Agency calculated using the formula set forth in section 409.910(11)(f).5 Accordingly, the undersigned finds that the competent substantial evidence adduced at the final hearing establishes that the Agency should be reimbursed in the amount of $5,832.63 from Petitioner’s recovery of $240,000 from a third party to satisfy the Medicaid lien.
The Issue At issue is whether Samuel Hess, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan).
Findings Of Fact Stipulated facts Jeffrey Hess and Jeanmarie Hess are the natural parents of Samuel Hess, a minor. Samuel was born a live infant on January 7, 2002, at St. Vincent's Medical Center, a licensed hospital in Jacksonville, Florida, and his birth weight exceeded 2,500 grams. The physician providing obstetrical services at Samuel's birth was Karen D. Bonar, M.D., who, at all times material hereto, was a "participating physician" in the Florida Birth-Related Neurological Injury Compensation Plan, as defined by Section 766.302(7), Florida Statutes. Coverage under the Plan Pertinent to this case, coverage is afforded by the Plan for infants who suffer a "birth-related neurological injury," defined as an "injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired." § 766.302(2), Fla. Stat. See also §§ 766.309 and 766.31, Fla. Stat. Here, Petitioners are of the view that Samuel suffered such an injury. More particularly, Petitioners believe Samuel's neurologic impairments are the result of a brain injury caused by hydrocephalus, secondary to an intraventricular hemorrhage (diagnosed at six days of life), that was precipitated by oxygen deprivation (a hypoxic ischemic insult), and which occurred during labor and delivery. In contrast, NICA is of the view that Samuel's impairments are most likely developmentally based, as opposed to birth related, and that, whatever the etiology of Samuel's impairments, he is not permanently and substantially physically impaired. Samuel's birth and immediate newborn course At or about 12:55 p.m., January 7, 2002, Mrs. Hess, with an estimated delivery date of January 21, 2002, and the fetus at 38 weeks' gestation, was admitted to St. Vincent's Medical Center, following spontaneous rupture of the membranes, with clear fluid noted, at 9:00 a.m. On admission, mild, irregular contractions were noted; vaginal examination revealed the cervix at 2 to 3 centimeters dilation, 60 percent effacement, and the fetus at -1 station; and fetal monitoring was reassuring for fetal well-being, with a baseline of 120 to 130 beats per minute. Given rupture of the membranes, Mrs. Hess was committed to deliver, and she was admitted for pitocin augmentation. Following admission, an IV was started at 1:48 p.m.; an epidural was placed at 3:56 p.m.; pitocin drip was started at 4:05 p.m.; Mrs. Hess was noted as pushing at 9:24 p.m.; and Samuel was delivered spontaneously at 10:24 p.m., with "Nu[cal]/Hand" (the umbilical cord wrapped around the hand) noted. In the interim, staring at or about 8:00 p.m., monitoring revealed, over time, late decelerations; marked decelerations with slow return to baseline; and evidence of a hypertonic uterus (starting at 9:24 p.m., and persisting, following periods of relaxation, until 10:22 p.m.), with exaggerated fetal heart rate variability. Such a pattern is consistent with fetal stress, and raises concerns regarding fetal reserves and adequate oxygenation. However, at delivery, Samuel was not depressed; did not require resuscitation; was accorded normal Apgar scores of 8 and 9, at one and five minutes, respectively, reflective of a healthy newborn2; and no abnormalities were observed at birth, except pronounced molding.3 Following delivery, Samuel was transferred to the nursery, and ultimately discharged with his mother on January 10, 2002. In the interim, Samuel's newborn course was normal, except for evidence of mild jaundice (diagnosed the morning of January 9, 2002), which did not require light therapy. However, on discharge, instructions were given to follow-up the next day at the Seton Center for a repeat bilirubin check. As instructed, Mrs. Hess presented with Samuel at the Seton Center on January 11, 2002, for a repeat bilirubin check. At the time, Samuel was noted to be active, alert, and in no apparent distress; his temperature was recorded as normal (as it had been following delivery, and during his admission in the nursery at St. Vincent's Medical Center); his newborn examination, apart from evidence of jaundice, was within normal limits; and Mrs. Hess reported that Samuel had fed well.4 The results of the bilirubin test were obtained at or about 1:30 p.m., that afternoon, and called to a staff physician (Dr. Vaughn), who gave instructions to initiate phototherapy. Accordingly, later that afternoon, Samuel was put under the bilirubin lights at home, with instructions to monitor his temperature every two hours. On January 12, 2002, Samuel recorded a temperature of 100.6, and on the instructions of Dr. Vaughn, Samuel was taken to the emergency room at Wolfson Children's Hospital for evaluation.5 There, Samuel was received at 6:35 p.m., and triaged at 6:42 p.m. Chief complaint was jaundice, and temperature was noted as 100.7, otherwise no abnormalities were observed. Samuel's physical examination and immediate hospital course were documented, as follows: PHYSICAL EXAMINATION: His temperature is 100.7 in the ER. The rest of his vitals are normal. His weight is 2.7 kg. He is resting, easily aroused. Anterior fontanelle is soft and flat, with normal sutures. Has good red reflexes bilaterally. Ear canals are patent. Nose without congestion. Oropharynx is clear, no cleft. Heart is normal S1 and S2 without murmurs. Abdomen is soft and nontender. Chest is clear to auscultation. Extremities are without rashes, cyanosis, clubbing or edema. He does have good femoral pulses bilaterally, and no hip clicks. Neurologically, he is alert and active . . . . LABORATORY: . . . Total bilirubin on admission was 14.2, direct was 0.5. He was tapped, and had a white count in his spinal fluid of 2,500 and red count of 241,250. He had 65 segs, 17 lymphocytes and 18 monocytes, and the spinal fluid Gram stain showed no organisms, but an occasional leukocyte. IMPRESSION AND PLAN: My impression is that we have a six-day-old with fever and abnormal leukocytosis in his spinal fluid. He was placed on ampicillin, and gentamicin . . . . He was also cultured for herpes [, which was negative]. He was started on Acyclovir 20/kilo q.8 hours. He will continue to feed. A repeat spinal tap was attempted to clear up the meningitis issue on two occasions; however, both times they were bloody. We, therefore, are going to obtain a head CT with contrast to rule out an intracranial bleed. A CT of the head was done on January 13, 2002, and revealed a bilateral intraventricular hemorrhage (IVH) and a left posterior parietal cephalohematoma.6 The CT scan was read, as follows: FINDINGS: There is molding of the bones of the calvarium, compatible with recent vaginal delivery. Curvilinear area of increased density identified within the scalp soft tissues in the left posterior parietal region, compatible with a cephalohematoma. Increased densities identified within the lumen of the left lateral ventricle, predominantly involving the left choroid plexus, but also layering in the dependent portion of the lateral ventricle, compatible with intraventricular hemorrhage from the choroid plexus bleed. In addition, increased density is identified in the dependent portion of the right lateral ventricle consistent with intraventricular hemorrhage. No extra axial fluid collections are identified. Linear area of increased density is identified in the right frontal region, only seen on images #11, and therefore likely not due to subarachnoid hemorrhage. The ventricular system is not dilated. No focal parenchymal mass is identified. After contrast administration, there are no abnormal areas of parenchymal or meningeal enhancement identified. IMPRESSION: Left posterior parietal cephalohematoma Bilateral intraventricular hemorrhage, left greater than right, with the left intraventricular hemorrhage due to choroid plexus bleed. Molding of the bones of the calvarium compatible with history of recent vaginal delivery . . . . Given the abnormalities reported on the CT scan, Dr. Randell Powell, a neurosurgeon, was requested to see Samuel for neurosurgical input. That consultation occurred on January 16, 2002,7 and was reported, as follows: . . . I have been requested to see the child for neurosurgical input. I am informed that the baby is now doing well. Septic work-up was completely negative and antibiotics have since been discontinued and the baby is anticipating discharge later on today. PHYSICAL EXAMINATION: Reveals a beautiful, sleeping, male infant with a very soft head, a very soft fontanelle, no splitting of the sutures. The head circumference is measured to be slightly less than the 50th percentile for a newborn. There is no nuchal rigidity and bending the legs did not appear to cause irritation as well. The child has a bilateral red reflex. Pupils are equal and reactive. The Moro reflex is symmetric. Computed tomographic scan shows hemorrhage emanating from the choroid plexus and the trigone of the left lateral ventricle. There is mild ventricular dilatation. Follow-up ultrasound shows similar findings. IMPRESSION: Intraventricular hemorrhage. DISCUSSION: Intraventricular hemorrhages in the newborn perinatal period that are caused by choroid plexus hemorrhage generally have an excellent prognosis as no significant brain parenchyma is disrupted and these hemorrhages usually resolve without sequelae. However, there is roughly a 20% chance of developing post hemorrhagic hydrocephalus which in 50% of cases could require more aggressive treatment. That means the baby's chances of needing neurosurgical intervention is somewhat less than 10% and this was discussed extensively with the parents who were happy to hear this news. There are no overt signs of hydrocephalus at this time and in my opinion I think that we can safely follow the baby with serial physical examination consisting of palpation of the fontanelle and head circumference measurements. I would be glad to see the baby at age one month for follow- up, but I suspect a good prognosis here. Samuel was discharged from Wolfson Children's Hospital at 6:15 p.m., January 16, 2002, with instructions to monitor his head circumference once a week, and for follow-up appointments with Dr. Hamaty (his pediatrician at the time8) and Dr. Powell. Samuel's subsequent development Following discharge, Samuel was followed by Dr. Powell for mild posthemorrhagic hydrocephalus, that appeared to stabilize, but then got worse between ages four and six months.9 Serial studies showed progressive ventricular enlargement consistent with hydrocephalus, and after discussing treatment options Samuel's parents elected to proceed with endoscopic third ventriculostomy, which was performed on August 26, 2002. Initially, Samuel appeared to be doing reasonably well, but then he developed an accelerated head circumference (53.8 centimeters, which placed him above the 98th percentile), consistent with progressive hydrocephalus, and on December 6, 2002, a Codman programmable ventriculoperioneal shunt was placed. Since that time, Samuel has done fairly well, without symptoms related to increased intracranial pressure. However, he continues to evidence macrocrania (above the 98th percentile), ventriculomegaly (enlargement of the laterial ventricules), and atrophy of brain tissue.10 (Exhibit 34). Samuel's current presentation With regard to Samuel's current presentation, the parties agree, and the proof is otherwise compelling, that Samuel is permanently and substantially mentally impaired.11 As for his physical presentation, while there may be room for disagreement, the complexity of Samuel's difficulties support the conclusion that he is also permanently and substantially physically impaired. In so concluding, it is noted that on the Vineland Adoptive Behavior Scales Form (VABS), related to daily living skills and motor skills, Samuel scored in the mentally handicapped range. "He is not yet toilet trained despite intensive efforts in this regard"; "[h]e is able to assist with simple dressing and undressing tasks but is not yet independent with these skills"; and he "continues to display gross-motor, fine-motor, visual-motor, and motor planning impairment." (Exhibits 18 and 30). It is further noted that Samuel presents with impaired postural control (aggravated by his large head), impaired strength, hypotonia, and bilateral pronatal feet. As a result, Samuel has moderate to severe impairment in strength, endurance, postural control, balance responses (with unexpected falls), functional mobility, and activities of daily living. Notably, at approximately five years of age, Samuel requires a stroller for extended outings, and caregiver assistance for 90 percent of self care needs. (Exhibit 10). The cause of Samuel's impairments As for the cause of Samuel's neurologic impairments, the proof demonstrates that, more likely than not, they are the result of a brain injury, caused by hydrocephalus, secondary to the intraventricular hemorrhage (IVH) he suffered, and which was diagnosed at six days of life. What remains to resolve is the genesis of Samuel's IVH or, stated otherwise, whether the proof demonstrated, more likely than not, that the IVH was caused by oxygen deprivation, and occurred during labor, delivery or resuscitation. § 766.302(2), Fla. Stat. ("'Birth-related neurological injury' means injury to the brain . . . caused by oxygen deprivation . . . occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period."); Nagy v. Florida Birth-Related Neurological Injury Compensation Association, 813 So. 2d 155 (Fla. 4th DCA 2002)(The oxygen deprivation and injury to the brain must occur during labor, delivery, or immediately afterward.). The genesis of Samuel's IVH Regarding the intraventricular hemorrhage Samuel suffered, the proof is compelling that an IVH in a term infant, such as Samuel, is a rare occurrence, and its cause frequently cannot be identified. Indeed, among the physicians who addressed the issue, there is apparent agreement that the majority of IVHs (approximately 50 percent) are related to oxygen deprivation (hypoxia-ischemia) or trauma, and the remainder fall into one of two groups, those with another identifiable cause (such as vascular malformation, infection, clotting disorder, venous infarct, or genetic disorder) and those of unknown etiology (idiopathic). To address the cause and timing of Samuel's IVH, the parties offered the deposition testimony of Julius Piver, M.D., J.D., a physician board-certified in obstetrics and gynecology (albeit one who has not practiced obstetrics for 20 years); Mary Edwards-Brown, M.D., a physician board-certified in radiology, with subspecialty certification in neuroradiology; David Hammond, M.D., a physician board-certified in pediatrics, neurology with special competence in child neurology, and clinical neurophysiology; Donald Willis, M.D., a physician board-certified in obstetrics and gynecology, and maternal-fetal medicine; and Michael Duchowny, M.D., a physician board- certified in pediatrics, neurology with special competence in child neurology, electroencephalography, and clinical neurophysiology.12 The testimony of Doctors Piver, Edwards- Brown, and Hammond were offered in support of Petitioners' view on causation, and testimony of Doctors Willis and Duchowny were offered in support of NICA's view on causation. Pertinent to the issue of causation, Doctors Piver, Edwards-Brown, and Hammond were of the opinion that an infant can suffer a intraventricular hemorrhage during labor and delivery, as a result of a hypoxic-ischemic insult, and not show any clinical evidence in the immediate postnatal period. However, although offered the opportunity to do so, Dr. Hammond declined to offer an opinion as to the likely etiology (cause and timing) of Samuels IVH.13 Consequently, we are left to consider the testimony of Doctors Piver and Edwards-Brown with regard to Petitioners' view on causation. As for the etiology of Samuel's IVH, it was Dr. Piver's opinion, based on his review of the medical records, that Samuel's IVH was most likely caused by partial prolonged asphyxia, that was sufficient to cause a subtle, slow bleed during labor and delivery, which progressed to the significant IVH noted at 6 days of life, but that was initially insufficient to reveal itself (by clinical evidence of a bleed) in the immediate postnatal period. In reaching his conclusion, Dr. Piver relied heavily on his evaluation of the fetal monitor strips, which he opined revealed, starting at 6:48 p.m. (18:48), and continuing for 30 to 35 minutes, evidence of marked loss of beat-to-beat variability; late decelerations at 8:01 p.m., 8:03 p.m., 8:05 p.m., 8:25 p.m., 8:28 p.m., 8:31 p.m., and 8:33 p.m.; a marked deceleration to a low of 70 beats per minute at 8:50 p.m., with a slow return to baseline at 8:56 p.m.; a marked deceleration from 180 beats per minute to 90 beats per minute between 9:14 p.m. to 9:20 p.m.; a late deceleration at 9:23 p.m.; and evidence of a hypertonic uterus starting at 9:24 p.m., and persisting to 9:42 p.m., again at 9:50 p.m., and persisting to 10:14 p.m., and again at 10:20 p.m. and persisting to 10:22 p.m., with exaggerated fetal heart rate variability. While acknowledging the bleed could have started at any time between the 7th of January (Samuel's delivery date) and the 12th of January, when Samuel presented to Wolfson Children's Hospital, Dr. Piver was of the opinion, given his review of the fetal monitor strips, that Samuel's bleed was most likely caused by hypoxia, and that it began during labor and delivery. Dr. Piver variously noted the likely onset of the bleed as "[b]etween 2030 and 2130 hours"; "around 2000 hours"; "from 2000 hours to 2130 hours"; "between 1800 and 2224 hours"; "between 1800 and 2100 hours"; and "the 21:24 to 22:20 time interval." (Exhibit 23, pages 34, 48, 49, 57, 80, 82; Exhibit 23, deposition Exhibit 6). Dr. Edwards-Brown, like Dr. Piver, was of the opinion that Samuel's IVH was most likely caused by hypoxia, that caused a slow bleed during labor and delivery, but an insufficient bleed to reveal evidence of brain damage during the immediate postnatal period. Dr. Edwards-Brown's opinion was explained, as follows: Q How are you able to determine, based on the films that you reviewed, that the hemorrhage began during labor and delivery? A Based on the films alone, we can't make that determination. It's simply the path of physiology of the hemorrhages and the hospital course as well as the labor and delivery records that allow me to make that conclusion. * * * Q Are you able to look at the effect of the hemorrhage on the brain structures to determine or time when the hemorrhage may have occurred? A What I see is a large hemorrhage wherein the ventricle that is pretty bright and that hemorrhage is causing hydrocephalus; and the hydrocephalus, I'm sure, is causing symptoms, but hemorrhages don't cause hydrocephalus initially. It takes some time before that occurs. So all I can say is yes, the hemorrhage is having an effect on the brain, and that effect is hydrocephalus and ischemia, and it could have occurred sometime from the time of labor and delivery until the time that film was obtained. Q It could have occurred at any time in between there? A. The hydrocephalus and the ischemia. Q But not the hemorrhage? A Certainly the hemorrhage could have occurred after birth, but I would have expected some evidence of that in the clinical history. I would have expected evidence that this child had suffered a profound hypoxic injury as one might see if this child had had a code or a profound drop in his oxygen status. None of that is in the record; therefore, I don't think it's a post natal event. * * * Q Okay. How are you able to rule out in this case that the hemorrhage did not begin on January 9th, 10th, 11th or 12th? A Several things. Number one, I don't have evidence on the 9th, 10th, 11th, or 12th of January that this child suffered any hypoxic injury. Q Hemorrhage [can] be caused by something other than hypoxic injury? A It can. Q Okay, and what are the other possible causes? A Intraventricular hemorrhage might result from a tumor, might result from a vascular malformation, it could result from an infection, but it usually results from hypoxia. Q We sometimes do not know what causes intraventricular hemorrhage? A I think when we don't know what causes intraventricular hemorrhage, it is a reasonable presumption that there was hypoxia at a time when someone was not looking, as in the prenatal or labor and delivery period. If there wasn't a fetal heart monitoring strip obtained during that period and the child is born with -- excuse me, with intraventricular hemorrhage, I think the presumption should be that there was hypoxia during that time. But certainly there may be some times when we don't have an answer. Q Sometimes we simply don't know what caused the hemorrhage? A That is undeniably true; however, one should not make that presumption until we have excluded the usual causes. And in this case, based on Dr. Piver's testimony that there was evidence of hypoxia during labor and delivery, one must assume that that was the cause. We don't make the diagnosis of an idiopathic cause. That means we don't have the answer when we have evidence of a reasonable cause, which we have here. Q In your letter to Mr. Sharrit that we referred to earlier, you state on Page No. 2 further down that, "The absence of symptoms in the three days following birth is not unusual since bleeding begins small and increases with time." What do you mean by that? A That's the nature of bleeding. I'm sure you know this. We have all bled. You don't -- Well, bleeding -- unless it's the result of an aneurism -- is not so massive initially. It starts out as a leak in the vessels, and the longer it bleeds the more it accumulates . . . . (Exhibit 27, pages 39, 41, 42, 44-46). Contrasted with the opinion held by Doctors Piver, Edwards-Brown, and Hammond, Doctors Willis and Duchowny were of the opinion that if a hypoxic event is significant enough to cause an intraventricular hemorrhage during labor and delivery, there will be clinical evidence in the immediate newborn period. Dr. Willis expressed his observations on the medical records, as well as the basis of his opinions on causations, as follows: Q . . . Dr. Willis, in reviewing the records and the fetal heart tracings, were you able to identify any intervals, any intervals of concern, I suppose, or any that you thought that may have been hypoxic intervals? A Well, the fetal heart rate monitor strip looks pretty good until about an hour and a half before delivery, and then there are fetal heart rate decelerations that pretty much continue until the time of birth. Q And what was the significance of those intervals that you're talking about, to you? A Well, the decrease in fetal heart rate usually means that there's some decrease in oxygen supply to the baby. Q Okay. A Or umbilical cord compression, which could lead to that same thing. Q So are you saying you found intervals that were suspicious for oxygen compromise? A That's correct. Q Did you identify intervals of lack of beat-to-beat variability that you thought were of concern? A Well, I'll look, but most of what I saw were fetal heart rate decelerations along with really exaggerated fetal heart rate variability, which usually you see with umbilical cord compression. Q Well, are you saying, then, that there were episodes in this case where you felt there was significant cord compression? A Well, the fetal heart rate tracing certainly is consistent with umbilical cord compression. Q And over what time period would you say the fetal heart tracings are consistent with cord compression? A Well, off and on for the last hour and a half prior to birth. Q And could that create a scenario, an hypoxic scenario that could lead to some kind of vascular insult within the brain? A Now, let me be sure I understand the question. Are you asking me if I believe this fetal heart rate pattern, the abnormalities that I see led to that or can abnormalities in fetal heart rate pattern in general lead to brain injury? Q I guess my question would be, the pattern that you've identified in this case, is that consistent with a pattern that can lead to injury, vascular injury within the brain? A Well, I think it shows that there's probably some lack of oxygen during that time period. Now, the question then is, you know, did that lack of oxygen lead to brain damage. And in this case, you know, my feeling is or my opinion is that it did not lead to brain damage. Q Let's break that up a little bit. Without knowing, without looking at the final result -- I presume you're looking at the early neonatal period right after birth to help you make that conclusion. Am I correct? A Yes. Q If we for the moment put aside the early clinical course of the child, just by looking at the heart tracings and the patterns that you've identified, are those consistent with or perhaps suspicious for the kind of pattern that could lead to a fetal compromise, brain compromise? A Well, I don't know if anyone could predict fetal brain damage simply based on a fetal heart rate pattern. You really have to look at the baby, the condition of the baby after birth to be able to say whether or not the abnormalities in the fetal heart rate pattern resulted in oxygen deprivation and brain injury. * * * Q Now, you did, no doubt, note that the child did return to the hospital after discharge and was found to have a bloody spinal tap, and ultimately it was determined that it had an intraventricular hemorrhage? A That's correct. That's, I believe, on the fifth day after birth. Q Well, having identified hypoxic consistent patterns within the fetal heart tracings, how is it that you can say that perhaps did not lead to a vascular insult that slowly progressed over a period of four or five days into an extensive hemorrhage? * * * A . . . I think that it's pretty clear that if you're going to have an hypoxic injury to the brain that's substantial enough to cause brain injury then the baby really is going to be depressed at time of birth and is going to have an unstable newborn period. Simply having an abnormal fetal heart rate pattern is not enough to say that any lack of oxygen that occurred during labor caused brain damage. Q . . . And I guess you're saying across the board and without exception there can be no slowly progressing brain damage that can occur due to labor and delivery hypoxia? A Well, in order to have an hypoxic event during labor or delivery that would be substantial enough to cause an hypoxic- related brain injury, then really the baby is going to have to be depressed at birth. Now, I mean, you can have intracranial hemorrhages, choroid plexus bleeds in babies that have normal, spontaneous vaginal births with normal-looking fetal heart rate tracings. I mean, there are spontaneous hemorrhages that can occur during labor, delivery, at some point after the baby is born, in the newborn period. But what I'm saying is that if you're going to have an intracranial hemorrhage due to an hypoxic event during labor or delivery, then the baby really should be depressed at time of birth and have an unstable newborn course. Q When you say depressed after the birth, do you put any outer limit on the time frame during which the baby might become depressed? A Well, usually, by the newborn -- by the immediate post-delivery period they mean immediately after birth and until the baby is essentially stabilized after birth. For instance, in this case the baby had Apgar scores of eight and nine, required no resuscitation at all. So, you know, we really don't have anything to suggest that there's a problem in the immediate newborn period. And then during the hospital stay, other than the jaundice, the baby did not really have any problems. The baby breast-fed. It did not have any neurologic findings that were abnormal, didn't have renal failure, did not have seizures, you know, the types of things that we see with babies that suffer an hypoxic insult during labor or delivery. * * * Q I know that your opinion is that if an hypoxic event is significant enough to cause a brain damage, then you're going to have to necessarily see signs of depression at birth or shortly after birth. Am I stating that correctly? A Very nicely. Q Okay. What if we're not talking about brain damage or encephalopathy in the broad sense but we're just talking about a very small insult to one of the blood vessels in the brain that doesn't readily turn into brain damage but, rather, becomes a progressive problem over a period of several days? Is that a possible scenario? A I guess most things are possible, but that seems unlikely to me. Q It seems unlikely to you that you could have a weakening of a blood vessel or some injury that lessens the integrity of the blood vessel and that the brain damage is then latent and that's perhaps the reason why it would not negatively impact the early clinical course? A Well, let me say -- and I think we kind of went over this before -- that you can have intracranial hemorrhages on babies that have no apparent problems at all during labor, delivery. Just for reasons unknown you can have intracranial hemorrhage and blood vessels can rupture. But I guess what we're talking about is brain injury due to lack of oxygen or mechanical trauma. And my point being that if you're going to get a hemorrhage due to lack of oxygen or mechanical trauma, then the baby really should be depressed at time of birth (Exhibit 28, pages 23-30). Dr. Duchowny expressed his observations of the medical records, as well as his opinions on causation, as follows: Q. Let me at this time suggest a brain injury pathway that has been offered by others in this case for Samuel Hess and ask you to comment on that. Others have suggested that in this case there was labor and delivery hypoxia that resulted in a choroid plexus bleed and was associated with an isolated -- excuse me, where the blood was isolated -- the bleed was isolated within the ventricles during the pre-natal course and that that later produced hydrocephalus -- MR. BAJALIA: Pre-natal? MR. SHARRIT: Yes, in the first few days after birth. Q. Are you with me, doctor? A. Yes, I am, but I think you mean post- natal course. Q. I'm sorry, I'm sorry. I do. Thank you. Labor and delivery hypoxia, the choroid plexus bleed isolated within the ventricles during the post-natal course that later produced hydrocephalus and increased the internal cranial pressure that later after - - well after discharge from the hospital resulted in periventricular white matter damage. Is that a reasonable interpretation for Samuel Hess' brain injury? A. No. Q. Why not? A. There's no evidence of hypoxia. * * * Q. . . . [Y]ou don't think that they are a result of hypoxia because you don't discern evidence of hypoxia on the fetal monitor strips? A. There are abnormalities on the fetal monitoring strips. As I said before, I don't think they are associated with hypoxia. * * * Q. I understand your testimony to the contrary, but if -- if it turned out that after reviewing Samuel's fetal monitor strips you decided that there was evidence of hypoxia, would that be a reasonable link to the hemorrhage that was diagnosed? A. No, because Samuel didn't show any of the signs of hypoxia at birth so I don't believe he had any type of hypoxic damage. * * * Q. Do you not find any evidence at all of hypoxia on the fetal monitor strips? A. I believe the fetal monitoring strips indicate some fetal stress and that's all. Q. As opposed to distress? A. It just shows stress to the fetus during the inter-partum experience. That's all. Q. How do you define stress? A. I think the decelerations indicate, you know, stress on -- you know, stress is being placed on the fetus. Q. . . . [But] can't late decelerations be an indication of hypoxia? A. It's possible. Q. Could bradycardia in the 60 to 70 be[at]s per minute range be an indication of hypoxia? A. It's possible but not necessarily. * * * Q. . . . If you have an intraventricular hemorrhage that you attribute to a hypoxic ischemic insult that resulted during the course of labor and delivery and late in delivery, as has been suggested in this case, wouldn't you expect to see some clinically recognizable neurologic dysfunction in the neonate during the immediate newborn period? A. Yes, you would. Q. Even if the hemorrhage was, to use opposing counsel's words, isolated? A. Yes. If you're claiming that the neurologic problems are related to hypoxia, you would expect to see clinical signs of hypoxia at the time. Q. Even if the hemorrhage was isolated? A. Yes. Q. Can you explain that? A. You would see clinical manifestations in some way. You know, there would be some compromise in respiratory status, evidence of compromise in organ function because the lack of oxygen would affect not only the brain but other organ systems as well. You might see elevation of cardiac enzymes, liver enzymes, changes in renal function, changes in mental status, seizures, changes in blood pressure, respirations, etcetera. Q. And just so I'm clear, that is true even if the hemorrhage was isolated just within the ventricle? A. Yes, if you're attributing it to hypoxia. * * * Q. And based upon your review of the medical records, did you see any indication that Samuel had any such clinically recognizable neurological impairment or dysfunction during the immediate newborn period? A. No, I did not. Q. Did you note what his APGAR scores were? A. Yes, I believe he had normal APGAR scores. I believe they were eight and nine and one at five minutes. Q. Is that consistent with Samuel having suffered an isolated intraventricular hemorrhage that was the result of a hypoxic ischemic insult that occurred late in delivery -- A. No. Q. -- labor and delivery? A. I don't believe so. Q. Is the fact that there was no documented evidence of impaired neurologic function in Samuel during the immediate newborn period consistent with Samuel having suffered an isolated intraventricular hemorrhage that occurred late in labor and delivery? A. No. (Exhibit 29, pages 17, 18, 20-23, and 36-39). Here, there is no apparent reason to credit the testimony of Petitioners' witnesses on the issue of causation over the testimony of NICAs witnesses. Indeed, as among those who spoke to the issue of causation, Doctors Willis and Duchowny are the more qualified to address the issue, and their testimony the more persuasive.
The Issue The issue in this proceeding is how much of Petitioner’s settlement proceeds should be paid to Respondent, Agency for Health Care Administration (“AHCA”), to satisfy AHCA's Medicaid lien under section 409.910, Florida Statutes.1/
Findings Of Fact On July 31, 2012, Luca Weedo’s natural mother, who was 30 weeks pregnant with Luca, was walking on the sidewalk on the east shoulder of Airport Pulling Road in Naples, Florida. At the same time, a Jeep Wrangler was traveling on Airport Pulling Road. As the Jeep Wrangler approached Luca’s natural mother, the left front tire and wheel separated from the Jeep Wrangler. The separated wheel bounced along the roadway at a high rate of speed, crossing the median and northbound lane of Airport Pulling Road. The wheel approached Luca’s natural mother at such a high rate of speed that she was unable to avoid it. She was struck by the wheel and knocked to the ground, which caused her to lose consciousness and suffer a ruptured placenta. Luca’s natural mother was transported to Lee Memorial Hospital. Upon admission, she underwent emergency surgery due to abdominal trauma. Luca was delivered via emergency C-section. Luca was born with extreme fetal immaturity and catastrophic brain damage. Luca remained in the hospital for three months, undergoing numerous medical procedures associated with his serious medical needs and brain damage. Luca now suffers from catastrophic brain damage and a seizure disorder that causes him to have multiple seizures every day. He is unable to ambulate, speak, eat, toilet, or care for himself in any manner. Prior to Luca’s birth, his natural mother had decided to place Luca up for adoption. Accordingly, when Luca was discharged from the hospital, the Florida Department of Children and Families asked Debra and Kenneth Weedo to take Luca into their home as a foster child. Kenneth Weedo is a retired truck driver and his wife Debra is a foster parent for medically needy children. Debra and Kenneth Weedo took Luca into their home and adopted him on May 2, 2013. Luca’s past medical expenses related to his injuries were paid by Medicaid, which provided $319,188.20 in benefits. This $319,188.20 paid by Medicaid constituted Luca’s entire claim for past medical expenses. Luca, through his parents and guardians, Debra and Kenneth Weedo, brought a personal injury action to recover all his damages. The lawsuit was initially brought against the owner/driver of the Jeep Wrangler. However, through discovery, it was determined that the party responsible for the wheel separating from the Jeep Wrangler was the tire and rim shop that installed the wheel on the Jeep Wrangler approximately a year prior to the accident (“Tire Shop”). The Tire Shop maintained insurance with a policy limit of $1 million. The Tire Shop’s insurance company tendered the $1 million insurance policy limit, which was accepted by Debra and Kenneth Weedo in settlement of Luca’s claim for damages against the Tire Shop. The General Release and Hold Harmless Agreement (“Release”), executed on December 21, 2015, memorialized the settlement with the Tire Shop as follows, in relevant part: Although it is acknowledged that this settlement does not fully compensate LUCA ALECZANDER WEEDO for all of the damages that he has allegedly suffered, this settlement shall operate as a full and complete Release as to Second Parties without regard to this settlement only, compensating LUCA ALECZANDER WEEDO for a fraction of the total monetary value of his alleged damages. LUCA ALECZANDER WEEDO has alleged his damages have a value in excess of $25,000,000, of which $319,188.20 represents LUCA ALECZANDER WEEDO’s claim for past medical expenses. Given the facts, circumstances, and nature of LUCA ALECZANDER WEEDO’s injuries and allegations, $12,767.53 of this settlement has been allocated to LUCA ALECZANDER WEEDO for LUCA ALECZANDER WEEDO’s claim for past medical expenses and the remainder of the settlement towards the satisfaction of claims other than past medical expenses. LUCA ALECZANDER WEEDO alleges that this allocation is reasonable and proportionate based on the same ratio this settlement bears to the total monetary value of all LUCA ALECZANDER WEEDO’s damages. Further, LUCA ALECZANDER WEEDO acknowledges that he may need future medical care related to his injuries, and some portion of this settlement may represent compensation for future medical expenses that LUCA ALECZANDER WEEDO will incur in the future. However, LUCA ALECZANDER WEEDO alleges that his family and/or others on his behalf have not made payments in the past or in advance for LUCA ALECZANDER WEEDO’s future medical care and LUCA ALECZANDER WEEDO has not made a claim for reimbursement, repayment, restitution, indemnification, or to be made whole for payments made in the past or in advance for future medical care. Accordingly, it is LUCA ALECZANDER WEEDO’s contention that no portion of this settlement represents reimbursement for future medical expenses. Because Luca was a minor, Court approval of the settlement was required. Accordingly, on February 17, 2016, Collier County Circuit Court Judge James Shenko approved the settlement by entering an Agreed Order on Petitioner’s Unopposed Petition to Approve Minor’s Settlement. As a condition of his eligibility to receive Medicaid benefits, Luca assigned to AHCA his right to recover from liable third-parties medical expenses paid by Medicaid. See 42 U.S.C. § 1396a(a)(25)(H) and § 409.910(6)(b), Fla. Stat. AHCA was notified of Luca’s personal injury action during its pendency. Through its collections contractor, Xerox Recovery Services, AHCA has asserted a Medicaid lien in the amount of $314,747.23 against Luca’s cause of action and settlement of the personal injury action. This is the amount that the Medicaid program spent on behalf of Luca for his past medical expenses.2/ Application of the formula set forth in section 409.910(11)(f) requires that AHCA be reimbursed for the full $314,747.23 Medicaid lien. Neither Luca nor others on his behalf made payments in the past or in advance for his future medical care. No claim for damages was made for reimbursement, repayment, restitution, indemnification, or to be made whole for payments made in the past or in advance for future medical care. Debra Ann Weedo attended the final hearing along with Luca. Ms. Weedo is a foster parent for medically needy children. She testified that she currently has four children in her home: three-year-old Luca; a six-year-old in more or less the same condition as Luca; a five-year-old who is “basically normal”; and an autistic eight-year-old. Ms. Weedo first met Luca in the hospital during his post-birth hospitalization. She was asked to take him as a foster child and visited him several times in the hospital before taking him home at age three months. Ms. Weedo stated that when she brought Luca home, the whole family fell in love with him and “he became our family.” As soon as it was possible, Ms. Weedo and her husband adopted Luca. Ms. Weedo testified that Luca’s siblings interact with him and that Luca knows the voices of his caregivers and “will kind of try to talk to us.” At the hearing, the undersigned observed that Luca is somewhat aware of his surroundings and responsive to voices. Ms. Weedo testified that her family does everything together. Luca travels, goes on vacations, and goes out to eat as part of the family. Ms. Weedo testified that Luca requires 24-hour supervision and that his condition will become progressively worse as he ages. Luca has been on oxygen since December 2014. He must use a BiPAP (Bilevel Positive Airway Pressure) machine when he sleeps because the oxygen saturation level in his blood tends to be perilously low. He receives his nutrition through a gastrostomy tube. Civil trial attorney Todd Rosen testified on behalf of Petitioner as a fact witness and an expert on the valuation of damages. Mr. Rosen has been an attorney for 15 years and is the principal of the Todd Rosen Law Group in Coral Gables. Mr. Rosen stated that his practice is exclusively devoted to representing plaintiffs in personal injury cases. Mr. Rosen is a member of the American Association for Justice, the Florida Justice Association, the American Trial Lawyers Association, and the Dade County Bar Association. Mr. Rosen has handled many jury trials and has represented plaintiffs who have suffered catastrophic brain injuries. A daily part of his practice is to assess the value of damages to injured persons. He stays abreast of jury verdicts in his area and routinely “round-tables” legal issues and damage valuations with other attorneys. Mr. Rosen testified that he was hired by Luca Weedo’s parents to investigate the potential claims they might have on behalf of their son. Mr. Rosen reviewed thousands of pages of Luca’s medical records, the accident report, and insurance policies for the defendants. The records indicated that Luca suffered catastrophic brain damage as a result of placental abruption and that this injury had a permanent and devastating impact on the child’s life. Mr. Rosen explained that he could not file a lawsuit until the adoption process was complete, about eight months after the accident. He initially brought the suit against the driver of the Jeep, who had only PIP and property damage insurance and no collectable assets. Mr. Rosen interviewed the Jeep owner and learned the name of the Tire Shop. He made a demand for payment of the Tire Shop’s $1 million insurance policy. The full policy amount was tendered very soon after Mr. Rosen’s demand. Mr. Rosen testified that no life care plan or economist’s report was prepared in this case because the case settled so quickly. He believed that it would have been imprudent to spend money out of the $1 million settlement on a life care plan when the Weedos were not facing the prospect of a jury trial. Mr. Rosen testified that Luca’s past medical care related to the accident was paid by Medicaid. He testified that Medicaid provided $319,188.20 in benefits, representing Luca’s entire claim for past medical expenses. Mr. Rosen testified that Luca, or others on his behalf, did not make payments in the past or in advance for future medical care and no claim was brought to recover reimbursement for past payments for future medical care. Mr. Rosen opined that Luca’s damages had a value “well in excess of” $25 million. Mr. Rosen explained that based on his experience in other cases, he believed the value of Luca’s future life care needs “would be well in excess of at least 10 to 15 million dollars” and that Luca’s non-economic damages would have a high value. Mr. Rosen noted that a jury would also take into account how “wonderful” Debra and Kenneth Weedo are to have devoted their lives to caring for Luca and other children in similar circumstances. Mr. Rosen believed that the $25 million valuation on Luca’s damages was “very conservative.” Mr. Rosen stated that the Tire Shop’s insurance counsel believed they had a strong argument that the owner of the Jeep must have done something to the tires after the Tire Shop put them on the car. However, despite the contested liability, the insurance company readily agreed during informal settlement discussions to pay the policy limits because the lawyers believed they were facing a verdict of up to $50 million. Mr. Rosen testified that the biggest cost factor in assessing Luca’s damages is the 24-hour attendant care that he will require for the rest of his life. Depending on how many caregivers are employed, the skill level required, and the location, attendant care may range from $25 to $40 per hour. Mr. Rosen estimated that a life care plan for Luca would be in the neighborhood of $10 million, including attendant care, nursing, and medical expenses. Mr. Rosen testified that the $1 million settlement did not come close to fully compensating Luca for the full value of his damages. Based on the conservative valuation of all Luca’s damages at $25 million, the $1 million settlement represented a recovery of four percent of the value of Luca’s damages. Mr. Rosen testified that because Luca only recovered four percent of the value of his damages in the settlement, he only recovered four percent of his $319,188.20 claim for past medical expenses, or $12,767.53.3/ Mr. Rosen noted that the settling parties agreed in the Release that Luca’s damages had a value in excess of $25 million, as well as to the allocation of $12,767.53 to past medical expenses. Mr. Rosen testified that the allocation of $12,767.53 of the settlement to past medical expenses was reasonable, rational, and more than fair because it was based on a conservative estimate of Luca’s damages. He stated, “Me, personally, I believe it should be less, but yes, that is fair just being conservative.” Mr. Rosen testified that because no claim was made to recover reimbursement for past payments for future medical care, no portion of the settlement represented reimbursement for past payments for future medical care. He noted that the parties agreed in the Release that no claim was made for reimbursement of past payments for future medical care, and no portion of the settlement represented reimbursement for future medical expenses. Because Luca was a minor, court approval of his settlement was required. The court appointed another experienced attorney to act as Luca’s Guardian ad Litem to review the terms of the settlement and make a report to the court as to its appropriateness. The Guardian ad Litem recommended approval of the settlement, and the court adopted that recommendation. Also testifying on behalf of Petitioner as an expert in the valuation of damages was R. Vinson Barrett, a partner in the Tallahassee firm of Barrett, Fasig and Brooks, which Mr. Barrett described as a mid-sized firm that exclusively undertakes personal injury and products liability cases. Mr. Barrett stated that he has been a trial lawyer for 40 years and for the last 15 years has confined his practice to medical malpractice, medical products liability, and pharmaceutical products liability cases. Mr. Barrett testified that he has done many jury trials. He discussed the importance of accurately estimating the value of the damages suffered by his clients because of the heavy investment that a trial firm must make in a complex case. Mr. Barrett stated that a firm can easily spend a quarter of a million dollars on experts and discovery, as well as life care plans, economic analyses, and vocational rehabilitation analyses, among other items required to establish damages. He stated that it is essential not to spend so much money in putting on the case that the client has nothing left after the verdict. Mr. Barrett stated that he has reviewed dozens of life care plans and economist reports, many for children with the same kind of injuries suffered by Luca Weedo. Mr. Barrett testified that he was familiar with Luca’s injuries and had reviewed the accident report, hospital birth records, records from a second hospitalization, medical records from Luca’s neurologist, the Guardian ad Litem report, the court order approving the settlement, Mr. Rosen’s demand letter to the insurance carrier, and each of Petitioner’s exhibits. He had also spoken to Debra Weedo by phone concerning Luca’s medical condition. Mr. Barrett gave a detailed explanation of Luca’s injuries and extent of his disability. He concluded that Luca’s injury “is as bad an injury as you can possibly receive and stay alive . . . . It could not be more catastrophic.” The medical records indicate that Luca will not get better and his prognosis is poor. Mr. Barrett opined that Luca’s life care plan alone would probably exceed $25 million. He conceded “that seems like a huge, huge, huge amount of money,” but explained that it really is not such a large sum when one considers that Luca is supposed to have 24-hour attendant care throughout his lifetime. Life care plans are not limited to the cost of services provided by Medicaid, which is a safety net that “takes care of things that are absolutely essential to keep on breathing.” However, Medicaid does not cover many things that medically needy children require for quality of life, such as wheelchair-equipped vans. The life care plan includes all of the child’s needs. Mr. Barrett testified that a life care planner accounts for every cost, “pill by pill, wheelchair replacement by wheelchair replacement,” then reduces it to present value. Mr. Barrett testified that based on his experience working with life care planners in trial preparation, and his extensive experience in evaluating damages in cases similar to that of Luca Weedo, he had no doubt that $25 million is a conservative estimate of Luca’s pure losses. Mr. Barrett testified that the settlement did not come close to compensating Luca for the full value of his damages. Using $25 million as the conservative measure of all his damages, Luca had recovered only four percent of the value of his damages. Mr. Barrett testified that “by equity and basically, now by federal law, you look at the same ratio for the lien that you look at [for] the claimant.” Accordingly, Mr. Barrett testified that the settlement provided Luca with only four percent of Medicaid’s $319,188.20 claim for past medical expenses, or $12,767.53. Mr. Barrett testified that the settling parties’ allocation of $12,767.53 of the settlement to past medical expenses was reasonable, rational, and conservative. Both Mr. Rosen and Mr. Barrett testified at some length about comparable jury verdicts and prior DOAH Medicaid lien cases involving children with catastrophic brain injuries. This discussion had some value in establishing that $25 million was by no means an unreasonable estimate of Luca Weedo’s damages, but was secondary and supplemental to the directly expressed expert opinions of Mr. Rosen and Mr. Barrett. AHCA presented the testimony of attorney James Bruner, who was accepted as an expert for the limited purpose of comparing the jury verdicts in the cases cited by Petitioner to the facts of the instant case. Mr. Bruner correctly noted that it can be misleading to cite the numbers from a jury verdict without reference to later reductions made on appeal or via settlement pending appeal. Mr. Bruner also effectively demonstrated that there is never a precise correlation between the facts of one case and those of another, and therefore that there cannot be a precise comparison of damages from one case to another.4/ However, the undersigned did not look to the comparative verdicts for such a strict comparison, but simply for the purpose of establishing a range of reasonableness in broadly similar cases. AHCA called no witness to directly contest the valuation of damages made by Mr. Rosen or to offer an alternative methodology to calculate the allocation to past medical expenses. No evidence was presented that the settlement agreement was not reasonable given all the circumstances of the case. It does not appear that the parties colluded to minimize the share of the settlement proceeds attributable to Medicaid’s payment of costs for Petitioner’s medical care. In fact, the evidence established that the settlement was conservative in its valuation of Petitioner’s claim and that the settling parties could have reasonably apportioned less to Medicaid than they actually did. AHCA was not a party to the settlement of Petitioner’s claim. AHCA correctly computed the lien amount pursuant to the statutory formula in section 409.910(11)(f). Deducting the 25 percent attorney’s fee, or $250,000, as well as $8,112.70 in taxable costs, from the $1 million recovery, leaves $741,887.30, half of which is $370,943.65. That figure exceeds the actual amount expended by Medicaid on Petitioner’s medical care. Application of the formula would provide sufficient funds to satisfy the Medicaid lien of $314,747.23. Petitioner proved by clear and convincing evidence that the $25 million total value of the claim was a reasonable, even somewhat conservative, amount. Petitioner proved by clear and convincing evidence, based on the strength and sympathy of his case and on the fact that it was limited only by the inability to collect the full amount of the likely judgment, that the amount agreed upon in settlement of Petitioner’s claims constituted a fair settlement, including the portion attributed to the Medicaid lien for medical expenses.
The Issue Whether Jennifer Peterson, a minor, qualifies for coverage under the Florida Birth-Related Neurological Injury Compensation Plan (Plan). Whether the hospital's failure to give notice, as contemplated by Section 766.316, Florida Statutes, was excused because the patient had an "emergency medical condition," as defined by Section 395.002(9)(b), Florida Statutes, or the giving of notice was not practicable.
Findings Of Fact Preliminary findings Jon Petersen and Kimberly Petersen are the natural parents of Jennifer Petersen, a minor. Jennifer was born a live infant on December 20, 2001, at Tallahassee Memorial Hospital, a hospital located in Tallahassee, Florida. The physician providing obstetrical services at Jennifer's birth was Jana M. Bures Forsthoefel, 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 . . . of a live infant weighing at least 2,500 grams for a single gestation or, in the case of a multiple gestation, a live infant weighing at least 2,000 grams at birth caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in a hospital, which renders the infant permanently and substantially mentally and physically impaired . . . . In this case, it is undisputed that Jennifer suffered an injury to the brain caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate postdelivery period in the hospital, which rendered her permanently and substantially mentally and physically impaired. What is disputed is whether Jennifer weighed at least 2,500 grams at birth. As to that issue, Petitioners were of the view that "[b]ased on the evidence presented . . . it cannot be established what Jennifer Petersen's 'actual' birth weight was at the time of her birth" or, alternatively, that it was most likely less than the 2,500 grams recorded on admission to the newborn intensive care unit (NICU), after she had been intubated. (Petitioners' proposed order, page 4.) In contrast, the other parties were of the view that the weight recorded in the NICU, which they chose to characterize as the "official birth weight," should be accepted as Jennifer's birth weight, without consideration of any weight attributable to the endotracheal tube that was inserted after delivery. (See Respondent's and Intervenors' post-hearing submittals.) Notably, when it has been shown "that the infant has sustained a brain . . . injury caused by oxygen deprivation or mechanical injury and that the infant was thereby rendered permanently and substantially mentally and physically impaired, a rebuttable presumption . . . [arises] that the injury is a birth-related neurological injury, as defined [by the Plan]." § 766.309(1)(a), Fla. Stat. Under the circumstances of this case, the presumption is that Jennifer's birth weight was 2,500 grams or greater. Consequently, to be resolved is whether there was credible evidence produced to support a contrary conclusion and, if so, whether absent the aid of the presumption the record demonstrates, more likely than not, that Jennifer's birth weight met or exceeded 2,500 grams.1 The proof regarding Jennifer's birth weight Pertinent to Jennifer's birth weight, the proof demonstrates that when delivered at 12:42 a.m., December 20, 2001, at 33 4/7 weeks gestation, Jennifer was severely depressed, and was immediately intubated and given cardiopulmonary resuscitation. At 3 minutes of life, a heart rate greater than 100 beats per minute was achieved, and at 5 minutes of life the endotracheal tube was secured and she was transferred to the NICU, where she was admitted at 12:50 a.m. Following admission to the NICU, Jennifer was weighed for the first, and insofar as the record reveals, the only time.2 That process was credibly described at hearing by Stacie Forbes, R.N., one of two nurses on duty in the newborn intensive care unit at the time, as follows: Q. Okay. Ma'am, what I'm going to . . . show you is . . . [a document that's] identified as Bates stamp 0309 [the Newborn ICU Admission Assessment form3] and get you to tell the Judge, if you can, what that document is. A. Okay. This document is our standard admission document for the newborn intensive care unit. When a baby comes into our unit, this is our initial assessment, the very first thing we do. * * * Q. All right. Now, . . . did you write the entries on that form? A. Yes. Q. And that's your signature down below? A. Yes. Q. Were you present when this baby Jennifer Peterson was weighed? A. Yes. * * * Q. How much did that baby weigh? A. 2500 grams, or 2.5 kilograms. Q. What did you . . . write down how much it weighed? A. I wrote 2.500. Q. All right. Now, I would like for you, if you would, to just briefly describe to us how you go about weighing a baby to get that weight. A. Okay. The baby comes in. As soon as the baby is stable, the first thing we do is we put the baby on the radiant warmer, we zero the warmer out, and then we lay the baby on the warmer and the grams comes up on the scale, on the bed scale. Q. All right. So when you put the baby on the bed scale, the weight in grams appears on a digital display? A. Yes. Q. So it's digital, 2500? A. Yes. Q. You don't have to do any kind of conversion at all? A. No. Q. Okay. Is it always the grams weight that comes up first in every case? A. Yes. Q. All right. Now, if you look on that form that you are looking at, it's got a weight in pounds [5 pounds 8.1 ounces] next to it? A. Yes. Q. Would you explain to the Court how you go about getting weight in pounds? A. As soon as the grams comes up, there is a button on the scale that you push that converts it to pounds. Q. Okay. And so, do you, as the nurse, have to do any sort of mathematical calculation or computation? A. No. Q. Who does that -- or how is that done? A. It's done by the radiant warmer. Q. Which is where the scale is? A. Yes, the scale. * * * Q. . . . Now, the 2500 grams that you recorded on the newborn admission form? A. Yes. Q. Is that the official birth weight of the baby? A. Yes. Q. . . . [H]ow is that used later on, in terms of the care of the baby? A. We do all of our medications, all of our IV fluids, blood transfusions, anything, any medical care, we use grams or kilograms, so, for the baby. We don't use the pounds. Q. All right. So, in other words, then you take that weight and when you have to figure out how much medicine you are going to give them, it's based many times on the weight of the baby? A. Yes. Q. And the weight that you use for that is 2500 grams? A. Yes, that's correct. * * * Q. Was [the baby] intubated when . . . [she] was admitted to the newborn ICU? A. Yes. * * * Q. Okay. Was the baby intubated when it was weighed? A. Yes. Q. Do you know what the weight of a standard 3.5 intubation tube is? A. No. Q. Did you deduct anything for the intubation tube? A. No. (Transcript, pages 15-19, 22 and 23.) There is no reason to question Nurse Forbes' testimony that Jennifer's initial weight, as displayed by the bed scale, was 2,500 grams. However, since the scale calculated an equivalent in pounds and ounces as 5 pounds 8.1 ounces, when the correct figure would have been (5 pounds 8.185 ounces), closer to 5 pounds 8.2 ounces, and since only a weight of approximately 2,497.60 grams would produce an equivalent weight of 5 pounds 8.1 ounces, there is cause to question the reliability of the bed scale. Consequently, since no reasonable explanation for the discrepancy was offered at hearing, and since a plausible explanation is malfunction or improper calibration, the weight of 2,500 grams noted for Jennifer on her initial examination cannot be accepted as reliable. Similarly, since the weight of 2,500 grams is not reliable, a reduction of that weight by the weight of the endotracheal tube, if shown,4 would likewise not produce an accurate reflection of Jennifer's birth weight.5 Consequently, there being no other evidence of her birth weight, there was no credible evidence produced to rebut the presumption that Jennifer weighed at least 2,500 grams at birth. The notice provisions of the Plan With regard to notice, Petitioners have stipulated that "Dr. Forsthoefel provided notice to the Petitioners pursuant to Section 766.316, Florida Statutes," but contend the hospital, although it had a reasonable opportunity to do so, did not. (Amended Pre-Hearing Stipulation.) In contrast, while acknowledging that notice was never given, the hospital and NICA contend the giving of notice was not required because, when Mrs. Petersen presented to the hospital on December 18, 2001, she had an "emergency medical condition as defined in s. 395.002(9)(b)," Florida Statutes. Petitioners dispute such contention. Therefore, it must be resolved whether the giving of notice was not required.6 At all times material hereto, Section 766.316, Florida Statutes (2001), prescribed the notice requirements of the Plan, as follows: Each hospital with a participating physician on its staff and each participating physician, other than residents, assistant residents, and interns deemed to be participating physicians under s. 766.314(4)(c), under the Florida Birth- Related Neurological Injury Compensation Plan shall provide notice to the obstetrical patients as to the limited no-fault alternative for birth-related neurological injuries. Such notice shall be provided on forms furnished by the association and shall include a clear and concise explanation of a patient's rights and limitations under the plan. The hospital or the participating physician may elect to have the patient sign a form acknowledging receipt of the notice form. Signature of the patient acknowledging receipt of the notice form raises a rebuttable presumption that the notice requirements of this section have been met. Notice need not be given to a patient when the patient has an emergency medical condition as defined in s. 395.002(9)(b) or when notice is not practicable. Section 395.002(9)(b), Florida Statutes, defines "emergency medical condition" to mean: (b) With respect to a pregnant woman: That there is inadequate time to effect safe transfer to another hospital prior to delivery; That a transfer may pose a threat to the health and safety of the patient or fetus; or That there is evidence of the onset and persistence of uterine contractions or rupture of the membranes. The Plan does not define "practicable." However, "practicable" is a commonly understood word that, as defined by Webster's dictionary, means "capable of being done, effected, or performed; feasible." Webster's New Twentieth Century Dictionary, Second Edition (1979). See Seagrave v. State, 802 So. 2d 281, 286 (Fla. 2001)("When necessary, the plain and ordinary meaning of words [in a statute] can be ascertained by reference to a dictionary.") Here, the hospital does not suggest that, and the record would not support a conclusion that, the giving of notice was not practicable. Consequently, the sole issue is whether Mrs. Petersen had an "emergency medical condition." Findings related to the hospital and notice At 2:33 a.m., December 18, 2001, Mrs. Petersen, with an estimated delivery date of February 3, 2002, and the fetus at 33 2/7 weeks' gestation, presented to Tallahassee Memorial Hospital, where she was initially assessed in Labor and Delivery Triage. Of note, history revealed Mrs. Petersen had been seen in Triage the previous afternoon, on referral from her obstetrician's office for monitoring because of perceived cervical change. At that time, she complained of feeling menstrual-like cramping, but no cervical change was noted (cervical dilation was recorded at 1.5 centimeters dilation, effacement at 80 percent, and the fetus at -3 station), and nitrazine test was negative. Mrs. Petersen was treated with stat doses of terbutaline (to forestall preterm labor), stabilized, and discharged. During the night, Mrs. Petersen began to feel increasing discomfort, and returned to the hospital (at 2:33 a.m., December 18, 2001) where assessment revealed the cervix at 1.5 centimeters, effacement at 90 percent, and the fetus at station B (Ballott). Mild uterine activity was noted to have begun at 2:00 a.m., but regular or persistent uterine contractions were not noted.7 Nevertheless, given evidence of early (preterm) cervical change and risk for preterm delivery, Mrs. Petersen was admitted for preterm labor pathway and tocolysis (inhibilation of uterine contractions). (Joint Exhibit 2, Tabs 3, 4, 23, and 27.) At 3:30 a.m., Mrs. Petersen was transferred from Triage to Labor and Delivery, where she was received at 3:45 a.m. External fetal monitor [EFM] was applied, which revealed a reassuring fetal heart rate and no uterine contractions. Moreover, no uterine contractions were charted until 7:30 a.m., and those that were subsequently charted were irregular until well after 10:00 a.m., December 19, 2001, when Mrs. Petersen's membranes spontaneously ruptured, and she was committed to deliver. At that time, the decision was made to discontinue tycolysis, and to augment labor with Petocin, in anticipation of vaginal delivery. (Joint Exhibit 2, Tabs 7 and 23, Transcript, pages 50, 51, 61, and 62.) Petocin augmentation started at 1:40 p.m., and Mrs. Petersen's labor slowly progressed. Vaginal examination at 6:45 p.m., revealed the cervix at 2 centimeters dilation, effacement at 90 percent, and the fetus at station O, and vaginal examination at 10:11 p.m., revealed the cervix at 3.5 centimeters dilation, effacement at 95 percent, and the fetus at station O. (Joint Exhibit 2, Tab 23.) At 11:55 p.m., Mrs. Petersen requested an epidural for pain management. Dr. Forsthoefel described the events that subsequently unfolded in her Operative Report, as follows: [Patient] [r]equesting pain management in the form of an epidural. Had received Stadol X 2 with stable fetal heart tones, occasional variable decels with an inadequate pattern of labor with frequent contractions, but not of the intensity required for adequate progress. During the period of the epidural placement, was laid down immediately after the epidural placement and at that point fetal heart tones could not be identified. Immediately I was called and came to the room from Room #1 where there had also been fetal distress. At the time of entry in Room #4 for evaluation, epidural was in place. Blood pressure had dropped immediately after dosing of the epidural and was felt to be secondary to epidural dosing. Fetal heart tones were felt to be in the 70s and 80s, again felt to be secondary to epidural. However, exam was immediately done. Patient was noted to be 4-5 cm, complete vertex at -1 and 0 station. A forebag was once again palpated and ruptured. At this point, bloody fluid was noted from the rupturing of the forebag. IUPC that was present was removed for the possibility of reinsertion for re- evaluation. Scalp electrode was applied and at that time, fetal heart tones were again felt to be between 75 and 80, initially thought perhaps secondary to positioning and low blood pressure. Call to Anesthesia for ephedrine had been made and was in the process of being given. Patient was tilted from right and left rapidly with no response to fetal heart tones. Maternal heart tones were in the 100s and this was felt to be possible fetal. However, a moment later, it was noted the maternal heart rate was at 80 and what appeared to be the fetal heart was at the exact same rate. Concern that there was misjudgment of fetal tracing interpretation that heart rate had been lost on the fetus and that actual maternal heart rate was being picked up was considered and although etiology of the event could not be determined at that immediate moment, call for immediate cesarean section was made. Patient was rushed to the operating room and patient had general anesthesia and patient was prepped and draped for an abdominal procedure. Incision was made with the knife and extended through the fascia with the deep knife. The fascia was incised with the knife and extended in lateral fashion with both blunt and sharp dissection. Fascia was dissected from the underlying rectus muscles using sharp dissection. Rectus muscles were dissected laterally using blunt dissection. Peritoneum was entered with blunt dissection. Immediately on entry, there was noted to be bloody fluid in the abdominal cavity. Examination of the lower uterine segment, however, quickly revealed no evidence of a defect of the lower uterine segment. Therefore an incision was made rapidly in the lower uterine segment and a transverse incision was made extended with bandage scissors. The infant was delivered [at 12:42 a.m., December 20, 2005] from a vertex presentation. Cord was clamped in two places and cut. Infant was suctioned and was limp. Handed to the Neonatal Team in sterile fashion for resuscitation. * * * FINAL ASSESSMENT: Intrauterine pregnancy at 33+ weeks with spontaneous rupture of membranes. In the face of preterm labor, magnesium sulfate discontinued. Patient positive for beta Strep, now contracting. Plan for delivery was made with Pitocin augmentation, intrauterine pressure catheter was placed. Fetal distress requiring immediate cesarean section with evidence of ruptured uterus at the fundus in a bivalve fashion compatible with previous classical incision. To resolve whether Mrs. Petersen had an "emergency medical condition," the parties presented Joint Exhibit 2, which included the medical records related to Mrs. Petersen's admission of December 18, 2001, addressed supra. The hospital also presented the testimony of Dr. Forsthoefel, Mrs. Petersen's obstetrician, and Petitioners presented the testimony of Dr. Giles, a physician board-certified in obstetrics and gynecology, as well as maternal-fetal medicine. On the issue of "emergency medical condition," it was Dr. Forsthoefel's opinion that on presentation to the hospital, Mrs. Petersen was having persistent uterine contractions, and that those contractions persisted despite efforts to stop them. It was further Dr. Forsthoefel's opinion that Mrs. Petersen was not medically stable when she presented to the hospital, or thereafter, and that a transfer might have compromised patient safety. In contrast, it was Dr. Giles' opinion that on presentation to the hospital, Mrs. Petersen was not having persistent uterine contractions, and that she never evidenced persistent contractions until well after her membranes spontaneously ruptured. It was further Dr. Giles' opinion that Mrs. Petersen was medically stable on presentation to the hospital; that she remained medically stable until she entered the active phase of labor, some time after her membranes ruptured; that the fetus evidenced good fetal heart rate status; and that a transfer would not have posed a threat to the safety of Mrs. Petersen or the fetus. Here, Dr. Giles' testimony, is credited, as most consistent with the proof. Consequently, it is resolved that Mrs. Petersen was not having persistent uterine contractions when she presented to the hospital; that Mrs. Petersen did not evidence persistent uterine contractions until after her membranes ruptured; and that Mrs. Petersen was medically stable at and following admission, and a transfer would not have posed a threat to the safety of Mrs. Petersen or the fetus. Therefore, Mrs. Petersen did not have an "emergency medical condition," as that term is defined by Section 395.002(9)(b), Florida Statutes, and the hospital was required to give notice, during the course of Mrs. Petersen's December 18, 2001, admission.
The Issue The issue is the amount of Petitioner’s $800,000 personal injury settlement payable to Respondent, Agency for Health Care Administration (“AHCA”), to satisfy AHCA’s $187,950.01 Medicaid lien.
Findings Of Fact Based on the stipulations of the parties, evidence adduced at hearing, and the record as a whole, the following Findings of Fact are made: Background On July 13, 2008, Carissa Gaudio (Carissa), then 26 years old, suffered severe physical injury and catastrophic brain damage when her car was struck by a train. Carissa received extensive medical intervention to save her life and address her injuries. Eventually, her medical condition stabilized and she was discharged to her parent’s home. While Carissa demonstrated consciousness and awareness, due to her catastrophic brain damage, she was unable to speak, ambulate, eat, toilet or care for herself in any manner. She was totally dependent on others for every aspect of her daily care. Carissa’s past medical expenses related to her injuries suffered on July 13, 2008, were paid by private health insurance through Blue Cross Blue Shield of Florida, Medicare, and Medicaid. Blue Cross Blue Shield of Florida provided $494,868.51 in benefits, Medicare provided $6,364.89 in benefits, and Medicaid provided $187,950.01 in benefits. The combined amount of these benefits is $689,183.41, and this $689,183.41 represented Carissa’s entire claim for past medical expenses. Carissa, or others on her behalf, did not make payments in the past or in advance for Carissa’s future medical care, and no claim for damages was made for reimbursement, repayment, restitution, indemnification, or to be made whole for payments made in the past or in advance for future medical care. Due to Carissa’s incapacity, Carissa’s mother, Roseann Gaudio, was appointed her legal guardian. Roseann Gaudio, as Carissa’s mother and guardian, brought a personal injury action in Broward County, Florida to recover all of Carissa’s damages against the railway company and train engineer (“Tortfeasor”). On January 10, 2015, Roseanne Gaudio, as Carissa’s mother and guardian, settled Carissa’s personal injury lawsuit for $800,000. In making this settlement, the settling parties agreed that: 1) the settlement did not fully compensate Carissa for all her damages; 2) Carissa’s damages had a value in excess of $16,000,000, of which $689,183.41 represents her claim for past medical expenses; and 3) allocation of $34,459.17 of the settlement to Carissa’s claim for past medical expenses was reasonable and proportionate. Because Carissa was incapacitated, her settlement required Court approval. Accordingly, by Order Approving Settlement dated February 11, 2015, the Circuit Court Judge, Honorable Jack Tuter, approved Carissa’s settlement. As a condition of Carissa’s eligibility for Medicaid, Carissa assigned to AHCA her right to recover from liable third- parties medical expenses paid by Medicaid. See 42 U.S.C. § 1396a(a)(25)(H) and § 409.910(6)(b), Fla. Stat. During the pendency of Carissa’s lawsuit, AHCA was notified of the lawsuit and AHCA, through its collections contractor, Xerox Recovery Services Group, asserted a $187,950.01 Medicaid lien against Carissa’s cause of action and future settlement of that action. By letter of February 17, 2015, Carissa’s personal injury attorney notified AHCA of the settlement and provided AHCA with a copy of the executed Final Release and a copy of the Order Approving Settlement. This letter requested AHCA to advise as to the amount AHCA would accept in satisfaction of the Medicaid lien. AHCA did not respond to Carissa’s attorney’s letter of February 17, 2015. AHCA did not file an action to set aside, void, or otherwise dispute Carissa’s settlement with the Tortfeasor. The Florida Medicaid program spent $187,950.01 on behalf of Carissa, all of which represents expenditures paid for Carissa’s past medical expenses. Carissa died on August 12, 2015 (Death Certificate filed by Petitioner on September 11, 2015). No portion of the $187,950.01 paid by the Medicaid program represents expenditures for future medical expenses, and AHCA did not make payments in advance for medical care. AHCA has determined that of Carissa’s $226,478.73 in litigation costs, $210,463.10 are taxable costs for purposes of the section 409.910(11)(f) formula calculation. Based on $210,463.10 in taxable costs, the section 409.910(11)(f) formula applied to Carissa’s $800,000 settlement, requires payment of $194,768.45 to AHCA in satisfaction of its $187,950.01 Medicaid lien. Since $187,950.01 is less than the $194,768.45 amount required to be paid to AHCA under the section 409.910(11)(f) formula, AHCA is seeking reimbursement of $187,950.01 from Carissa’s $800,000 settlement in satisfaction of its Medicaid lien. The full Medicaid lien amount has been deposited into an interest-bearing account pending an administrative determination of AHCA’s rights, and this constitutes “final agency action” for purposes of chapter 120, pursuant to section 409.910(17)(b). At hearing, Petitioner called Joseph J. Slama, a board-certified civil trial lawyer. Mr. Slama handles aviation crash, products liability, roadway defect, and automobile accident cases, including handling catastrophic brain injury cases through jury trial. He stays abreast of jury verdicts through review of publications and participation in trial attorney organizations. He testified that he routinely evaluates his client’s injuries and makes assessments concerning the value of their damages, and he explained his process for making these determinations based on his experience and training. Mr. Slama was accepted as an expert in the valuation of damages suffered by injured parties. Mr. Slama testified that he represented Carissa in relation to her personal injury action. He explained that he first met with Carissa and her mother after she was discharged home from the hospital. Mr. Slama testified that he had reviewed the accident report, Carissa’s medical records, taken depositions of witnesses and experts, and reviewed the Life Care Plan prepared by Craig H. Lichtblau, M.D. Mr. Slama explained in great detail the facts and circumstances of Carissa’s accident. He explained that Carissa’s car became stuck on the railroad tracks. Unfortunately, a train approached and shortly before impact, Carissa exited her vehicle. Her vehicle was struck by the train and she was propelled 167 feet from the point of impact. Mr. Slama testified that as a result of the accident, Carissa suffered catastrophic physical injury and brain damage. He testified that due to this catastrophic brain injury, Carissa was left in a semi-vegetative state and was unable to ambulate. While she was conscious and aware of her condition, she was unable to communicate other than with limited facial expressions. She lived in her parents’ living room where she received around the clock care, provided by her family, until her recent death. Mr. Slama testified that through his representation of Carissa, interactions with her, review of her medical records and reports, and based on his training and experience in similar cases, it was his opinion that the “minimum reasonable value” of Carissa’s damages was $16,000,000. He testified that this $16,000,000 would be the amount a jury would award in damages if the question of damages alone was presented to the jury, and he would be disappointed in this result because he would ask for much more in damages. Mr. Slama explained that the basis of his opinion was her past expenses, her need for future life care needs, and her non-economic damages, including pain and suffering, which would have been awarded from the date of her injury by a jury and would be a huge amount. Mr. Slama explained that Carissa’s lawsuit to recover all her damages had issues related to comparative negligence and disputed facts that called into question the responsibility of the defendants to pay for Carissa’s damages. He testified that based on these issues, Carissa’s lawsuit was settled for $800,000. Mr. Slama testified that this $800,000 settlement did not fully compensate Carissa for the full value of her damages and that based on the $16,000,000 valuation of all Carissa’s damages, the $800,000 settlement represented a five percent recovery of Carissa’s damages. He testified that because she only recovered five percent of her damages in the settlement, she “only recovered 5 percent of each and every element of her damages, including only 5 percent of her $689,183.41” claim for past medical expenses, or $34,459.17. R. Vincent Barrett has been a trial attorney since 1977 and is a partner with the Tallahassee law firm of Barrett, Fasig & Brooks. He practices in the area of medical malpractice and medical and pharmaceutical product liability. He has handled catastrophic injury cases and handled numerous jury trials. Mr. Barrett stays abreast of jury verdicts by reviewing Jury Verdict Reports, talking with other lawyers, and attending seminars. He testified that as a routine part of his practice, he ascertains the value of damages suffered by injured parties and has served as an expert in the valuation of damages in civil cases. Mr. Barrett was accepted as an expert in the valuation of damages suffered by injured parties. Mr. Barrett testified that he was very familiar with Carissa’s injuries and had reviewed a substantial amount of Carissa’s medical records, the Life Care Plan, accident report, before and after pictures of Carissa, Day in the Life Video, the Second Amended Complaint, the Release, and the Order Approving Settlement. Mr. Barrett explained that he was familiar with the type of injury suffered by Carissa because he had handled a number of traumatic brain and orthopedic injury cases with injuries similar to Carissa’s. He testified that with respect to virtually every injury that Carissa suffered, he had handled a case that involved one or more of those injuries. Mr. Barrett stated that Carissa’s case is “one of the worst cases I’ve ever seen,” and he described Carissa’s accident and extensive injuries. Mr. Barrett explained that Carissa’s injuries were “horrible” and “dramatic” and that “tractor trailer versus car, train versus car, those kinds of cases are worth in a jury trial generally twice as much as in a regular car accident just because of the dramatic traumatic nature of the impact it has on jurors.” Mr. Barrett testified that Carissa’s damages had a value of at least up in the $30,000,000 range and that the valuation of her damages at $16,000,000 was extremely conservative. He explained that he had reviewed jury verdicts in developing his opinion as to the value of Carissa’s damages, and he compared a number of the verdicts he had reviewed with Carissa’s case, including the Mosley 2014 Broward verdict for $75,543,527, noting that the Mosley plaintiff, unlike Carissa, was left with limited verbal language and the ability to walk short distances with assistance. Mr. Barrett stated in relation to the $16,000,000 valuation of Carissa’s damages that, “in Broward County for a pretty, young, 26-year old, gainfully employed, Hispanic lady, who was engaged, it’s got to be the limit. I mean, some of those verdicts were $75 million and some of those people weren’t hurt as bad as Carissa. So, yes, it’s very conservative.” The testimony of Mr. Slama and Mr. Barrett that the minimum reasonable value of Carissa’s damages was $16,000,000 was unrebutted, and is credible. Respondent’s position is that it should be reimbursed for its Medicaid expenditures on behalf of Petitioner pursuant to the formula set forth in section 409.910(11)(f). Under the statutory formula, the lien amount is computed by deducting a 25 percent attorney’s fee ($200,000) and taxable costs ($210,463.10) from the $800,000 recovery, which yields a sum of $389,536.90, then dividing that amount by two, which yields a result of $194,768.45. Under the statute, Respondent is limited to recovery of the amount derived from the statutory formula or the amount of its lien, whichever is less. Since the Medicaid lien amount is $187,950.01, which is less than the $194,768.45 amount required to be paid to AHCA under the section 409.910(11)(f) formula, AHCA is seeking reimbursement of $187,950.01 from Carissa’s $800,000 settlement in satisfaction of its Medicaid lien. Petitioner’s position is that reimbursement for past medical expenses should be limited to the same ratio as Petitioner’s recovery amount to the total value of damages. Petitioner urges Respondent should be reimbursed $34,459.17 in satisfaction of its Medicaid lien. The settlement amount of $800,000 is five percent of the reasonable total value ($16 million) of Petitioner’s damages. By the same token, five percent of $689,183.41 (Petitioner’s past medical expenses paid by both Medicaid and private insurance) is $34,459.17. Petitioner proved by clear and convincing evidence that a lesser portion of the total recovery should be allocated as reimbursement for past medical expenses than the amount calculated by Respondent pursuant to the formula set forth in section 409.910(11)(f).
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
The Issue At issue in this proceeding is whether Cody Byrne, a deceased minor, suffered an injury for which compensation should be awarded under the Florida Birth-Related Neurological Injury Compensation Plan.
Findings Of Fact Fundamental findings John Byrne, Jr. and Theresa Byrne are the parents and natural guardians of Cody Byrne (Cody), a deceased minor. Cody was born a live infant on June 4, 1995, at Orange Park Medical Center, a hospital located in Orange Park, Florida, and his birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Cody was Meng-Shu Lin, M.D., who was at all times material hereto, a participating physician in the Florida Birth- Related Neurological Injury Compensation Plan (the Plan), as defined by Section 766.302(7), Florida Statutes. Mrs. Byrne's antepartum course and Cody's delivery Mrs. Byrne's prenatal course was essentially uncomplicated; however, as of June 2, 1995, she was slightly post-term, with an estimated date of confinement of May 31, 1995. Consequently, on June 2, 1995, her obstetrician, Dr. Robert Bazley, admitted her to Orange Park Medical Center for a non- stress test to assess the well-being of the fetus. Mrs. Byrne was admitted at 7:20 a.m. At the time, the fetal heart rate base line was noted at 125 to 135 beats per minute. Vaginal examination revealed the cervix to be at 2 centimeters, the same as disclosed on her last office visit of May 31, 1995; however, effacement and station were not noted on the record. The membranes were intact, and mild, occasional contractions were noted. The non-stress test was reactive, consistent with fetal well-being, with good fetal heart rate accelerations noted with fetal movement. Following the non-stress test, Mrs. Byrne was discharged to return home, with instructions to notify her physician if there was "any change in fetal movements that seem out of the ordinary," "leaking or rupture of membranes," "regular contractions," "any progressive discomfort," or "bright red bleeding." At the time, induction of labor was planned for June 6, 1995, absent intervening changes. At or about 7:30 p.m., June 3, 1995, Mrs. Byrne began to experience unusual or rhythmic fetal activity, initially thought to be hiccups. However, the activity persisted, and at about 9:00 p.m. she and her husband presented to Orange Park Medical Center, where she was admitted at 9:30 p.m. for observation/evaluation of fetal status. Assessment on admission revealed a fetal heart rate baseline of 150 beats per minute. Vaginal examination revealed the cervix to be at 2 centimeters, effacement at 50 percent, and the fetus at station -3. The membranes were intact, and mild, occasional contractions were noted. 1/ Initially, difficulty was experienced in acquiring and tracking fetal heart rate by fetal monitor; however, audible monitoring revealed a fetal heart rate of 150 to 160 beats per minute which was non-reactive. Several spontaneous contractions were noted, with questionable variable decelerations, and at or about 10:10 p.m. a biophysical profile was ordered. Vaginal examination at 10:31 p.m. revealed no change in dilation, effacement or station. Continued fetal monitoring revealed a non-reactive fetal heart rate of 150 to 160 beats per minute. The biophysical profile was completed and reported to Dr. Lin at 12:16 a.m., June 4, 1995. The test was abnormal, reflecting unusual fetal breathing movements ("repetitive jerky movements of the diaphragm" at a rate of 30 per minute during the exam), no gross body movement, and no tone. Vaginal examination at 12:43 a.m. again revealed no change in dilation, effacement, or station. The membranes were artificially ruptured, revealing dark, thick meconium stained fluid. Digital fetal scalp stimulation produced no acceleration, and fetal heart tone persisted at about 160 beats per minute. Pitocin was started at 12:57 a.m. and, thereafter, variable decelerations were noted, with mild contractions. Pitocin was discontinued, and at 1:03 a.m. an emergency primary cesarean section was called for by Dr. Lin. At 1:28 a.m. Mrs. Byrne was moved to the operating room, and at 1:46 a.m. Cody was delivered by cesarean section. During delivery, the umbilical cord was observed to be "very twisted like [a] cork screw" or "very tightly coiled," and wrapped tight around the infant's neck. Upon delivery, Cody was limp, with minimum respiratory effort. Meconium stained fluid was suctioned from below the cords and, following positive pressure ventilation for approximately 30 seconds, Cody began to gasp. Continuous tremor of the lower jaw was noted. A sustained grunting, shallow respiration was achieved by 2 minutes of age. Cody remained pink with good heart rate on blow-by oxygen. Apgars were 4, 6, and 6 at one, five, and ten minutes, respectively. 2/ At approximately 2:00 a.m., Cody was transported to the special care nursery and placed in a 100 percent oxygen hood. Arterial blood gas on 100 percent oxihood showed a pH of 7.35 and base excess of -5.4. Umbilical cord pH, at delivery, was 7.22 and base excess -6.6. Cody was noted to be very lethargic, with decreased responsiveness, and Narcan was given without change in status. At approximately 1 1/2 hours of age he was again noted to have continuous tremors of the upper extremities and lower jaw. Phenobarbital was administered. Cody began desaturating, with shallow respirations, and was placed on mechanical ventilation. Further seizure activity was noted, and Phenobarbital was again administered. Finally, at or about 6:00 a.m., Cody was transferred to the neonatal intensive care unit at University Medical Center. Cody's course at University Medical Center is aptly summarized in his discharge resume, as follows: Central Nervous System: . . . the infant had seizure activity noted at Orange Park Medical Center and received Phenobarbital prior to transfer to University Medical Center. Once at University Medical Center, the infant had an extensive neurological and metabolic workup performed. Pediatric neurology was involved. The Phenobarbital level was monitored and the Phenobarbital doses were adjusted per neurology. . . . The infant was unresponsive on admission and remained so. No improvement was noted in his neurological status during his hospitalization. The initial electroencephalogram was grossly abnormal. Seizure activity was controlled with Phenobarbital. However on July 21, 1995 the infant was noted to have multiple episodes of rhythmic movements primarily of the upper extremities. Dr. Shanks was involved and an electroencephalogram done during the above rhythmic motion showed movement artifact and no electrographic evidence of seizures. CT scan on June 6, 1995 showed diffuse increased densities throughout. Repeat CT scan on June 13, 1995 showed diffuse low attenuation throughout the brain with preserved densities in the basal ganglia and posterior fossa. There was hyperintensity of the cortex of several areas, possibly hemorrhagic. No mass effect or midline shift was seen. These findings were consistent with anoxic encephalopathy. . . . At the time of discharge the infant is still followed by the neurology department. He was seen by Dr. Shanks on August 1, 1995. His impression at that time was encephalopathy with cerebral palsy/spastic quadriplegia. The infant is on Phenobarbital and the last level obtained was 24.6 on July 31, 1995 at which time the dose was increased. At the time of discharge the infant has no suck or swallow reflex. The infant has hypertonicity in all extremities and the spine. He has splints on the wrists and forearms bilaterally. He has intermittent rhythmic "jerking" motions primarily of the upper extremities. The plan is to discharge the infant home with his parents to be followed by Dr. Shanks at Nemours neurology clinic. He will have early intervention program in Gainesville with Sharon Henessey on September 7, 1995 at 10:30. He will be discharged to home on Phenobarbital 38 mg b.i.d. via jejunostomy tube. . . . Cody was discharged from University Medical Center to the care of his parents on August 2, 1995, and expired on November 12, 1995. Cause of death was noted as respiratory failure due to severe ischemic encephalopathy. Cody's neurologic injury and its timing Here, the competent proof is compelling, and not subject to serious debate, that Cody suffered an injury to his brain caused by oxygen deprivation that rendered him permanently and substantially mentally and physically impaired, and led inevitably to his death. Indeed, Respondent's own expert, Charles Kalstone, M.D., upon review of the medical records, was of the opinion that Cody suffered a hypoxic insult, most likely associated with umbilical cord compression, that resulted in severe brain damage. What is disputed, and must be resolved, is the timing of Cody's injury or, stated otherwise, whether such injury "occurr[ed] in the course of labor, delivery, or resuscitation in the immediate post-delivery period." Section 766.302(2), Florida Statutes. In addressing the timing of Cody's injury, it is worthy of note that where, as here, the proof demonstrates that the infant suffered an injury to the brain caused by oxygen deprivation which rendered him permanently and substantially mentally and physically impaired, the Petitioner/Claimant is entitled to the benefit of a rebuttable presumption that the injury occurred in the course of labor, delivery, or resuscitation in the immediate post-delivery period in the hospital. Section 766.309(1)(a), Florida Statutes. 3/ Consequently, absent persuasive proof that, as contended by Respondent, Cody's injury predated Mrs. Byrne's admission to the hospital and without the onset of labor, it must be concluded that he suffered a "birth-related neurological injury" as defined by law, and that the subject claim is compensable. Sections 766.302(2) and 766.309(1)(a), Florida Statutes. Addressing first the timing of Cody's injury, it must be concluded that, more likely than not, his injury occurred after the positive non-stress test of June 2, 1995, and prior to Mrs. Bryne's admission to Orange Park Medical Center the evening of June 3, 1995, and that upon admission he was already severely compromised. In so concluding, it is observed that fetal heart monitoring from the time of admission to the hospital reflected fetal tachycardia at approximately 160 beats per minute without reactivity, and that the fetal heart rate remained essentially unchanged through the course of monitoring until variable decelerations were observed following the administration of Pitocin. The stark contrast between the tracing of June 2, 1995, and the tracing of June 3, 1995, is strong evidence that during the intervening period the fetus had suffered a substantial insult, resulting in neurologic damage as evidenced by the altered, tachycardic heart rate. Moreover, the umbilical cord pH, at delivery, was noted as 7.22 and the base excess as -6.6. These are normal values, and do not reflect metabolic acidosis, which would be expected had the fetus suffered an acute hypoxic insult around the time of birth. Finally, it is noted that Cody exhibited evidence of seizure activity at least as early as 1 1/2 hours of life. Such activity is inconsistent with hypoxic injury at birth and dates the injury as prior to Mrs. Byrne's admission. Turning now to the issue of labor, it is, as heretofore noted, Respondent's contention that at the time of Cody's injury Mrs. Byrne was not in labor. Respondent's position is premised on the observation that no change in Mrs. Byrne's cervical dilatation occurred between June 2, 1995, when occasional contractions were observed, and her presentation to Orange Park Medical Center on June 3, 1995, when occasional contractions were also observed. Based on such facts, Respondent's expert, Dr. Kalstone, defining labor as "contractions that become painful, more regular, more frequent, and lead to a progressive change in dilatation and effacement of the uterine cervix," concluded Mrs. Byrne was not in labor when Cody's injury occurred. (Respondent's Exhibit 1, at pages 14 and 15) In response, Petitioner suggests that Dr. Kalstone has overlooked the fact that labor is generally accepted to be divided into stages, and that with dilatation and effacement present Mrs. Byrne was, by definition, in stage one labor. 4/ Conversely, were the contractions she suffered false labor, no dilatation would be present. Essentially, all the proof shows, according to Petitioner, is that Mrs. Byrne's labor failed to progress, and not that she was without labor. (Petitioner's letter dated May 19, 1997, filed May 22, 1997.) Moreover, according to Petitioner, Mrs. Byrne's obstetrician noted her to be in "spontaneous labor" on admission to the hospital. 5/ There is merit to Petitioner's response. The Legislature has not chosen to define "labor," as that word is used in the phrase "in the course of labor, delivery, or resuscitation in the immediate post-delivery period." When words used in a statute are not defined, "they must be construed according to their plain and ordinary meaning, or according to the meaning assigned to the terms by the class of persons within the purview of the statute." Florida East Coast Industries, Inc. v. Department of Community Affairs, 677 So. 2d 357, 362 (Fla. 1st DCA 1996). See, Southeastern Fisheries Association, Inc. v. Department of Natural Resources, 453 So. 2d 1351 (Fla. 1984). If necessary, the plain, ordinary meaning of a word can be found by looking in a dictionary. Gardner v. Johnson, 451 So. 2d 477 (Fla. 1984), and Hernando County v. Florida Public Service Commission, 685 So. 2d 48 (Fla. 1st DCA 1996). Pertinent to this case, Webster's New Twentieth Century Dictionary, Unabridged, Second Edition, describes the meaning of "labor" as follows: . . . in medicine, the process of childbirth; parturition; especially, the muscular contractions of giving birth. To like effect, but more pertinent to the usage of the word in medicine, is the meaning ascribed to "labor" by Dorland's Illustrated Medical Dictionary, Twenty-eighth Edition, as follows: . . . the function of the female organism by which the product of conception is expelled from the uterus through the vagina to the outside world. Labor may be divided into four stages: The first (the stage of cervical dilatation) begins with the onset of regular uterine contractions and ends when the os is completely dilated. The second stage (stage of expulsion) extends from the end of the first stage until the expulsion of the infant is completed. The third stage (placental stage) extends from the expulsion of the child until the placenta and membranes are expelled. The fourth stage denotes the hour or two after delivery, when uterine tone is established. Called also childbirth, delivery, and parturition. See also labor pains, under pain. Dorland's further describes the meaning of false labor pains and labor pains as follows: false p's, ineffective pains which resemble labor pains, but which are not accompanied by effacement and dilatation of the cervix. * * * labor p's, the rhythmic pains of increasing severity and frequency, caused by contractions of the uterus during childbirth. Accord, Taber's Cyclopedic Medical Dictionary (1997), and Mosby's Medical Dictionary, Fourth Edition (1994). 6/ Given the commonly understood meaning of the term "labor," and the absence of any further explanation from Respondent, it must be concluded that, at best, Respondent's proof merely demonstrates that Mrs. Byrne's labor failed to progress, not the absence of labor. Consequently, Respondent has failed to rebut the presumption, as well as the credible proof, that at the time of Cody's neurologic insult Mrs. Byrne was in labor.
The Issue Whether the Respondent committed the violations alleged in the Administrative Complaint dated May 23, 2000, and, if so, the penalty that should be imposed.
Findings Of Fact Based on the oral and documentary evidence presented at the final hearing and on the entire record of this proceeding, the following findings of fact are made: The Department of Health, Board of Medicine, is the state agency charged with regulating the practice of medicine in Florida. Section 20.43; Chapters 455 and 458, Florida Statutes (2000). Dr. Sadarangani is, and was at the times material to this proceeding, a physician licensed to practice medicine in Florida, having been issued license number ME 0041985. He maintained a private practice in Fort Lauderdale, Florida, from 1984 until 1997. He was board certified in 1981 in cardio- thoracic surgery by the American Board of Thoracic Surgery and was re-certified in 1990. In his practice, Dr. Sadarangani performed between 20 and 25 aneurysm repairs each year. Dr. Sadarangani has not practiced surgery since 1997 because of his health. General anatomy of the abdominal blood vessels. The arterial system. The aorta is the main blood vessel leaving the heart and going through the chest and pelvic area. The aorta carries the majority of the blood to the body and provides blood to the body's main organs. The renal arteries branch off of the aorta and provide blood to the kidneys. In the pelvic area, the aorta branches into two iliac arteries that carry blood to the pelvic organs and to the legs. The iliac arteries are referred to as the common femoral arteries when they reach the groin. As they descend into the leg, the common femoral arteries branch into the superficial femoral arteries, which continue below the knee and into the lower leg, and into the profundus femoris arteries, which provide blood to the muscles of the thighs. The lumbar arteries extend in pairs from the posterior of the aorta in the abdomen to the lumbar musculature. The venous system. The vena cava is the very large vein in the abdominal cavity that drains blood from the legs and the abdominal organs and returns it to the heart. It is located on the right side of the aorta. In very rare cases, a person is born with two vena cavas, one located on the left side of the aorta and one on the right side, into which blood drains from the left and right kidneys, respectively. The renal veins are the main venous structures that carry blood from the kidneys to the vena cava. There are normally two renal veins, one draining the right kidney into the vena cava, and one draining the left kidney into the vena cava. The renal veins are two of the largest veins in the body, and, because the kidneys absorb 20 percent of the heart's output of blood, the renal system contains a high volume of blood. The right renal vein is short and is not located near the aorta because it attaches to the vena cava to the right of the aorta. The left renal vein normally crosses over the anterior, or front, surface of the aorta to join the vena cava. In rare cases, the left renal vein crosses posterior to, or in back of, the aorta to join the vena cava; such a vein is referred to as a retroaortic renal vein. Aortic aneurysms. An aortic aneurysm is an area of the aorta where the vessel wall has dilated and expanded abnormally, like a balloon; it appears as a markedly enlarged blood vessel. A normal aorta is between 1.5 and two centimeters in diameter; if an area of the aorta expands to between 2.5 and three centimeters, it is referred to as a dilated aorta. It is only after the aorta has dilated to four centimeters that the area of dilation is referred to as an aneurysm. An aneurysm is often life threatening because it can burst, resulting in massive blood loss and, in many cases, death. The repair of an aneurysm involves the replacement of the part of the blood vessel that is aneurysmal with a bypass graft. The graft is an artificial prosthesis that is pre-made and comes as a straight tube or a bifurcated tube, that is, a tube that splits into two smaller tubes. Once in place, the graft allows the blood to flow through the area where the aneurysm is located, but the aneurysm is no longer a part of the blood vessel, and there is no danger that the aneurysm will rupture. The repair of an aortic aneurysm that is located in the abdomen is a major surgical procedure. There are three types of bypass procedures used to repair abdominal aortic aneurysms: An aortic tube bypass is appropriate when the aneurysm is limited to the aorta. In this procedure, a tube graft is attached to the aorta above the aneurysm and below the aneurysm, and the walls of the aneurysm are sutured closed over the graft. With this type of procedure, the surgeon first makes an incision in the abdomen and enters the abdominal cavity. After retractors are placed and the bowel is moved to the side, the blood vessels above and below the aneurysm are separated, or dissected, from the surrounding fatty and connective tissue using both sharp and blunt instruments. Although it is possible to tear blood vessels, especially veins, using blunt dissection techniques, the use of good surgical techniques will minimize the number of vessel tears.1 An aortic-biiliac bypass is appropriate when the aneurysm extends into the upper iliac arteries or when there is a blockage of the upper iliac arteries. In this procedure, the aneurysm is replaced with a bifurcated tube graft attached to the aorta above the aneurysm and to each iliac artery below the aneurysm or blockage. When performing an aortic-biiliac bypass, the surgeon proceeds in the same manner as when performing an aortic tube bypass, but extends the abdominal incision to dissect the iliac arteries in the pelvic area. The iliac arteries lie very deep and must be dissected from the veins that lie next to these arteries and from the ureter. An aortic-bifemoral bypass is appropriate when the patient has occlusive disease, or a blockage, of the iliac arteries or when it would be difficult to work in the pelvic area where the iliac arteries are located as a result of significant scarring. The iliac arteries are bypassed in this procedure, and a bifurcated tube graft is attached to the aorta above the aneurysm and to each common femoral artery below the blockage. When performing an aortic-bifemoral bypass, the surgeon usually begins with incisions in each side of the groin and dissection of the common femoral arteries. The abdominal incision and dissection of the aorta is done after the common femoral arteries are dissected in order to reduce the amount of time the abdomen is open. Prior to surgery, an aortogram, or arteriogram, is performed to establish the anatomy of the patient's arteries. An arteriogram is a procedure in which a dye is injected into the aorta by means of a catheter, and X-rays are taken showing the pathway of the dye through the arteries from the diaphragm to the feet so that any blockages or abnormalities in the vessels can be identified. An arteriogram is the most accurate way of determining that blood is flowing through a particular blood vessel, and the type of bypass to be performed is determined on the basis of the anatomy of the patient's arteries as revealed by the arteriogram. Patient W.R. Patient W.R. was a 71-year-old male who was referred to Dr. Sadarangani after he was diagnosed with an abdominal aortic aneurysm. W.R. had a history of coronary artery disease, diabetes mellitus, high blood pressure, and mild chronic obstructive pulmonary disease. He weighed approximately 212 pounds at the time Dr. Sadarangani first examined him. An ultrasound indicated that W.R.'s aneurysm was increasing in size, and Dr. Sadarangani recommended surgery to repair the aneurysm. Because of W.R.'s weight and his medical history, Dr. Sadarangani did not classify him as a normal patient, and he was a medium-level anesthesiology risk. In a letter dated August 3, 1993, W.R.'s cardiologist cleared him for surgery based on the results of a cardiac catheterization and a thallium stress test. In his letter, W.R.'s cardiologist stated that W.R. had coronary artery disease of the right coronary system and that, during surgery, "careful attention [should be] paid to hemodynamic status "2 W.R.'s fitness for surgery was also evaluated by a pulmonologist, who cleared W.R. for the surgery based on the results of a pulmonary function test. On August 12, 1993, W.R. underwent an abdominal aortogram and bilateral lower extremity runoff arteriogram in order to establish the anatomy of the arteries in his abdomen and legs. The aortogram revealed a fusiform aneurysm of the distal abdominal aorta that was 5.7 centimeters in diameter; the craniocaudel length of the aneurysm was approximately seven centimeters. It was noted in the report of the aortogram that "[b]oth renal arteries are well demonstrated. The aneurysm originates approximately 5 cm. below the origin of the lowest renal artery. The iliac arteries are not involved. Aortic bifurcation is normal." The bilateral lower extremity runoff arteriogram revealed that the "internal iliac and external iliac arteries bilaterally show normal liminal [sic] filling with no abnormality. The common femoral arteries are also normal." It was noted in the report of the arteriogram that the superficial femoral arteries filled normally, but bilateral segmental stenosis, or occlusive disease, of the distal superficial femoral arteries was observed, with 80-to-90 percent stenotic lesion in the left distal superficial femoral artery and 50-to-60 percent stenotic lesion in the right distal superficial femoral artery. Because the aortogram and arteriogram revealed that the aneurysm ended above the point where the aorta bifurcated into the iliac arteries and because they revealed that there were no abnormalities in the iliac arteries, an aortic tube bypass to repair W.R.'s aneurysm would be the indicated procedure. This was the type of bypass Dr. Sadarangani intended to perform when he began the surgery. Anesthesia was administered to W.R. at 8:15 a.m. and, after W.R. was prepared, Dr. Sadarangani began surgery at 9:10 a.m. Dr. Sadarangani first made an incision into the abdomen and dissected into the abdominal cavity. After isolating and putting aside the abdominal organs, Dr. Sadarangani, as is his usual practice, dissected and isolated the iliac arteries. He then dissected up around each side of the aorta until he reached the neck, or upper edge, of the aneurysm. Dr. Sadarangani did not visualize the left renal vein as he dissected around the sides of the aorta, and he remarked on this to Dr. Robert McGuire, the surgeon who was assisting with the procedure. The left renal vein is the first blood vessel the surgeon must locate after the aorta has been exposed. It is crucial for the left renal vein to be identified for two reasons. First, it is a major vein carrying a substantial blood flow from the left kidney, and it must be visualized so that the surgeon can avoid injuring it. Second, the aorta must be clamped below the renal arteries, and the left renal vein marks the spot where the renal arteries branch off of the aorta.3 If the left renal vein is not visualized in front of the aorta, the surgeon must assume that the patient has either a duplicate vena cava or a retroaortic renal vein. In such a circumstance, the surgeon must be very careful not to tear the left renal vein when dissecting out the aorta from the surrounding tissues and veins. Even though he had not located the left renal vein, Dr. Sadarangani followed his usual procedure when dissecting the aorta at the neck of the aneurysm, and he ran his thumb along one side of the aorta and his finger along the other side, pulling the aorta forward to clear it from the tissues behind it. Dr. Sadarangani continued to work his thumb and finger around the aorta, pulling the vessel forward, until his thumb and finger met behind the aorta and it pulled free from the vessels and tissue surrounding it. In choosing to use this technique, Dr. Sadarangani relied on his experience that there normally are no adhesions or scar tissue present in the tissues surrounding the aorta. As soon as Dr. Sadarangani removed his fingers from around W.R.'s aorta, he noticed bleeding that appeared to originate behind the aorta. He did not know the source of the bleeding but believed that it might originate in the lumbar veins because he observed only a small amount of blood. Dr. Sadarangani inserted a four-by-four sponge in the area of the bleeding and applied pressure for about five minutes. He removed the sponge, and the area again filled with blood. Dr. Sadarangani then tried to stop the bleeding by applying a mixture of gel foam and Thrombin to the area, and he applied pressure with a four-by-four sponge for an additional five minutes at the location of the bleeding. Dr. Sadarangani repeated this procedure two or three times and was not able to stop the bleeding. Dr. Sadarangani still did not know the source of the bleeding, although he knew it was venous blood because of its dark color, and he thought the bleeding might be coming from a lumbar vein.4 The only thing Dr. Sadarangani knew for certain was that the bleeding was coming from behind the aneurysm, so he moved it to the right in an attempt to see the source of the bleeding. As soon as he did so, blood gushed from W.R.'s abdomen, and his blood pressure dropped precipitously. Dr. Sadarangani moved the aneurysm back to its original position and applied pressure on the top of the aneurysm to stop the bleeding. At the same time, the anesthesiologist began transfusing blood and fluids. After about five to seven minutes, Dr. Sadarangani decided to move the aneurysm to the left to see if he could find the source of the bleeding. As soon as he moved the aneurysm to the left, blood gushed again, W.R.'s blood pressure dropped, and, according to Dr. Sadarangani, "the anesthesiologist started screaming." Dr. Sadarangani moved the aneurysm back to its original position and again applied pressure to the top of the aneurysm to stop the bleeding. Dr. Sadarangani was not able to stop the bleeding. Because he still had not identified the source of the bleeding, he decided to clamp the aorta above the aneurysm, sever the aorta below the clamp, and peel back the aneurysm to expose the structure behind it. Before undertaking this procedure, because he would be handling the aneurysm and did not want to dislodge any clotted material from the aneurysm into the blood stream, Dr. Sadarangani ordered the anesthesiologist to administer 7,000 units of Heparin to W.R., about three-quarters of the dose he would normally have given a patient of W.R.'s size. On Dr. Sadarangani's orders, the anesthesiologist administered the Heparin at 11:02 a.m. Heparin is an anticoagulant blood thinner used to prevent the formation of blood clots whenever a blood vessel is clamped off and the blood flow in the vessel stopped. Dr. Sadarangani was not concerned about giving a blood thinner and anticoagulant to W.R. even though he was experiencing severe blood loss because W.R.'s blood was being collected by the cell saver5 and re-transfused. In addition to the cell saver, Dr. Sadarangani had ordered six units of blood typed and cross- matched for W.R. Before he clamped the aorta, he told the anesthesiologist to order all six units of blood to the operating room and to tell the blood bank to type and cross- match more blood. After the Heparin was administered and the blood ordered, Dr. Sadarangani clamped off the iliac arteries, and then, at 11:08 a.m., he clamped off the aorta above the neck of the aneurysm. The aneurysm became soft with the decrease in pressure, and the blood flow from behind the aneurysm increased because the aneurysm no longer exerted pressure on the vessels behind it. Dr. Sadarangani then cut horizontally through the aorta and retracted down the aneurysmic portion of the aorta. At this, W.R.'s abdominal cavity began filling with blood. Dr. Sadarangani suctioned the blood into the cell saver, and he was able to see that there was a large amount of blood coming from both the right and the left side of the abdomen. There was also some bleeding from behind the aneurysm, and Dr. Sadarangani deflected the aneurysm down further and saw bleeding from another vein. Once he had suctioned the blood out of the abdominal cavity, Dr. Sadarangani was able to see that one source of bleeding was a long tear in the left renal vein, which was located behind the aorta; blood was also draining from what Dr. Sadarangani described as an abnormally large lumbar vein joining the left renal vein. The left renal vein was completely open behind the aorta, and the blood was coming from both the vena cava and from the left kidney. Dr. Sadarangani theorized that the lumbar vein and the renal vein had been adhered to the back of the aneurysm and had torn when he manipulated the aneurysm to the left and right. Normally, the aneurysm itself is not manipulated or resected because there is a lot of tissue adhering to the back portion of the aneurysm. Dr. Sadarangani temporarily controlled the bleeding by clamping the left renal vein to the right of the aorta, at the point where it joined the vena cava; clamping the left renal vein to the left of the aorta, distal to, or in front of, the adrenal vein and the testicular vein, both of which branch off the left renal vein before it enters the left kidney; and clamping the lumbar vein where it joined the left renal vein. Although the clamps stopped the bleeding from the veins, there was bleeding from the lumbar arteries that attached to the aneurysmic portion of the aorta. Consequently, Dr. Sadarangani removed the plaque and clotted material from the wall of the aneurysm, and he sutured the bleeding lumbar arteries. This procedure took between ten and 15 minutes. Dr. Sadarangani then had to decide how to repair the left renal vein and the lumbar vein. The renal vein was not very tense after Dr. Sadarangani finished suturing the lumbar arteries, and he noticed that the adrenal and testicular veins were becoming larger. He concluded, therefore, that the blood from the left kidney was draining through the adrenal and testicular veins. Dr. Sadarangani decided to excise the torn portion of the left renal vein and to suture it closed both at the point where it joined the vena cava and at the point distal to the adrenal and testicular veins.6 Dr. Sadarangani also sutured closed the bleeding lumbar vein. Dr. Sadarangani worked for several hours to stop the bleeding from the left renal and lumbar veins. During this time, W.R.'s blood pressure dropped precipitously several times, and W.R. suffered severe hypovolemia, that is, severe shock. With the bleeding controlled, Dr. Sadarangani proceeded with the repair of the aneurysm. He completed the anastomosis, or connection of the graft to the aorta, above the aneurysm. He then tested the anastomosis to ensure that there was no bleeding and clamped off the two limbs of the bifurcated tube graft he had chosen to use for the bypass. Dr. Sadarangani had originally intended to use an aortic tube bypass to repair W.R.'s aneurysm, but when he palpated the aorta below the aneurysm, the aorta felt hard. Dr. Sadarangani also noted that the iliac arteries below the bifurcation of the aorta also felt hard. He decided that it would take too long to remove the plaque from the walls of the aorta and abandoned the idea of using a tube bypass. Dr. Sadarangani felt along the iliac arteries until he reached soft spots on the anterior of both the left and right iliac arteries. He made a small incision in the soft spot on the right iliac artery, below the clamp, and noted that there was no retrograde bleeding from the artery.7 He inserted his forceps inside the artery to be sure the walls were separated, and, when he removed the forceps, he saw blood clots inside the artery. Dr. Sadarangani was surprised to see blood clots, and, because it had been several hours since the initial 7,000 units of Heparin had been administered, Dr. Sadarangani ordered the anesthesiologist to administer an additional 2,000 units of Heparin. This dose of Heparin was administered at 1:15 p.m. Dr. Sadarangani concluded from the lack of retrograde bleeding and from the presence of clots in the iliac artery that W.R. had blood clots in his lower leg that were blocking the blood flow. Accordingly, Dr. Sadarangani passed a small Fogarty catheter into the right iliac artery several times.8 Dr. Sadarangani chose a small catheter because he wanted the catheter to pass through W.R.'s iliac artery and the femoral artery into the arteries serving the leg, all the way to W.R.'s ankle. Even though he was unable to pass the catheter to the ankle, he brought up blood clots with the first two or three passes of the Fogarty catheter through the right iliac artery, but he did not bring up any clots on the next two or three passes of the catheter. Dr. Sadarangani noted some retrograde bleeding from the right iliac artery after he removed blood clots with the catheter, but the bleeding quickly stopped. Dr. Sadarangani inferred from this that there were more blood clots deeper in the femoral artery. Dr. Sadarangani opened the left iliac artery. He could not pass a Fogarty catheter to W.R.'s ankle through the left iliac artery, but he did bring up blood clots from that artery. The difficulty could be attributed to the fact that the iliac arteries follow a very tortuous path. The difficulty could also be attributed to the fact that the pre-operative arteriogram established that W.R. had some blockage in the femoral arteries. Because of the blood clots and his inability to pass the Fogarty catheter deep into W.R.'s leg, Dr. Sadarangani decided to do an aortic-bifemoral bypass instead of an aortic- biiliac bypass. He reasoned that, once he dissected out and opened up the common femoral artery, he would be able to visualize the deep femoral artery and the superficial femoral artery and pass a Fogarty catheter directly into those arteries to eliminate any blood clots in W.R.'s legs. Dr. Sadarangani was particularly concerned about leaving blood clots in W.R.'s arteries because, if clots of a significant size are left in the arteries, they can block blood flow once it is re-established after the bypass graft is attached and the clamps released. If clots block the blood flow in the graft or in the legs, it is necessary to perform another surgical procedure to remove the clots, and Dr. Sadarangani believed that W.R. could not tolerate a second surgical procedure. Dr. Sadarangani anticipated that it would take between ten and 15 minutes to open up W.R.'s groin and to expose and get control of the common femoral arteries; it would normally take between ten and 15 minutes per side, but Dr. Sadarangani intended to have Dr. McGuire open the left groin. In Dr. Sadarangani's opinion, this procedure would be quicker than a biiliac bypass because the iliac arteries are deep, and it is difficult to complete the anastomoses. Unfortunately, Dr. Sadarangani and Dr. McGuire unexpectedly encountered severe scar tissue when dissecting down to the common femoral arteries, and it took approximately 45 minutes to isolate these arteries. Once Dr. Sadarangani and Dr. McGuire had visualized and dissected out the common femoral arteries, Dr. Sadarangani inserted a Fogarty catheter into the right and then the left superficial femoral arteries, all the way to W.R.'s ankles and assured himself that there were no clots present in W.R.'s legs. Dr. Sadarangani performed the same procedure with the Fogarty catheter into the profundus femoris arteries and into the deep femoral arteries and assured himself that there were no clots below the incisions in the common femoral arteries. When performing an aortic-bifemoral bypass, it is necessary for the surgeon to make tunnels from the abdominal cavity to the femoral arteries through which the ends of the graft are passed. This is accomplished by the surgeon inserting one finger in the groin and one finger in the abdominal cavity and penetrating the retroperitoneal tissue until the fingers touch. Once the surgeon's fingers touch, a clamp and umbilical tape are passed through the tunnels, the bypass grafts are passed into each side of the groin, and the ends of the grafts are sewn onto the femoral arteries using the same procedure as that used for the iliac arteries with an aortic-biiliac bypass. After he made the tunnel to the right common femoral artery, Dr. Sadarangani completed the anastomosis and restored blood flow to the right leg. Between 30 and 35 minutes later, Dr. Sadarangani finished the anastomosis on the left common femoral artery, and he unclamped the left femoral artery at 2:55 p.m. Dr. Sadarangani estimates that it took him approximately 30 minutes longer to complete the aortic-bifemoral bypass than it would have taken him to complete an aortic-biiliac bypass. After blood flow was restored, Dr. Sadarangani flushed W.R.'s groin and abdominal cavity with antibiotic solution, returned his abdominal organs to their proper positions, and closed the incisions. W.R. was under anesthesia from 8:15 a.m. until 5:10 p.m.; W.R. was actually in surgery from 9:10 a.m. until 4:50 p.m.9 W.R. became hypovolemic approximately three hours into the surgery, when he suffered massive blood loss, and he suffered ongoing complications from the hypovolemia. W.R.'s total estimated blood loss was 8,600 milliliters of blood, IAT (Intraoperative Autologous Transfusion); W.R. received transfusions of 3,200 milliliters of blood during surgery, and his actual blood loss was 5,400 milliliters.10 W.R. was taken from surgery directly to intensive care. His condition deteriorated, and he died on the evening of August 24, 1993, from hyperkalemia with renal failure.11 The blood loss W.R. experienced during surgery, and the resulting hypovolemia, contributed to the renal failure. No matter how good the surgical technique, there is always some blood loss during the repair of an abdominal aortic aneurysm. Because of the need to create tunnels through the retroperitoneal tissue in the groin, an aortic-bifemoral bypass increases the amount of blood loss during surgery, especially in a patient who has received an anticoagulant. The most critical factor affecting a patient's ability to survive the repair of an abdominal aortic aneurysm is the amount of time the aorta is clamped shut, with the blood flow through the body interrupted. Stress is placed on the heart because there is higher pressure in the upper body because the heart is profusing only half of the body while the aorta is clamped. In addition, half of the body is not receiving significant blood flow, which leads to pooling of blood and metabolic stresses that can decrease cardiac output. In this case, W.R.'s aorta was clamped shut from approximately 11:00 a.m. until approximately 3:00 p.m., a period of four hours. Normally, the aorta is clamped approximately two to three hours during an aortic-bifemoral bypass. Summary. The evidence presented by the Department is sufficient to establish that a reasonably prudent cardio-thoracic surgeon would have located the left renal vein before beginning to dissect around the aorta and separate it from the surrounding tissues. In this case, Dr. Sadarangani did not visualize the left renal vein when he dissected down to the aorta. Even though he knew it was possible that W.R. had a retroaortic left renal vein, Dr. Sadarangani nonetheless proceeded with the blunt dissection of the aorta at the neck of the aneurysm, slipping his fingers behind the aorta and pulling it forward. Dr. Sadarangani also failed to recognize that the bleeding from behind the aorta might have originated from the left renal vein. By moving the aneurysm to the left and then to the right, Dr. Sadarangani most likely exacerbated the tear in the renal vein, and by retracting the aneurysm forward, he completely opened that portion of the left renal vein lying behind the aneurysm. While this latter procedure was necessary to expose the source of the bleeding in order to ultimately control it, Dr. Sadarangani should have identified the left renal vein before dissecting forward the aorta at the neck of the aneurysm. The evidence presented by the Department is sufficient to establish that a reasonably prudent cardio-thoracic surgeon would not have administered Heparin to a patient who was experiencing massive blood loss as a result of a torn left renal vein. It is not appropriate to administer Heparin to a patient who is experiencing or has experienced uncontrolled bleeding. Massive blood loss during surgery is life threatening, and the surgeon's foremost concern should be controlling the bleeding. Administering a blood thinner when a patient is bleeding uncontrollably is contraindicated, especially since massive blood loss in itself thins the blood. It should also be noted that Dr. Sadarangani had manipulated the aneurysm by moving it to the left and the right before he told the anesthesiologist to administer the Heparin. The evidence presented by the Department is not sufficient to establish that a reasonably prudent cardio- thoracic surgeon, under the circumstances presented to Dr. Sadarangani, would have performed an aortic-biiliac bypass rather than an aortic-bifemoral bypass. It was not unreasonable for Dr. Sadarangani to be concerned about blood clots in W.R.'s legs given the lack of retrograde bleeding and the presence of blood clots in the iliac arteries. Both the lack of retrograde bleeding and the presence of blood clots could be indicative of clots further down in the leg, and Dr. Sadarangani's decision to perform an aortic-bifemoral bypass was not unreasonable since he was unable to insert the Fogarty catheter far enough into W.R.'s arteries to assure himself that no clots were present in W.R.'s lower legs. Dr. Sadarangani's decision was based on the particular circumstances he encountered in this case, and the Department has failed to establish that his decisions departed from the acceptable standard of care.
Recommendation Based on the foregoing Findings of Fact and Conclusions of Law, it is RECOMMENDED that the Board of Medicine enter a final order finding that Nari T. Sadarangani, M.D., violated Section 458.331(1)(t), Florida Statutes (1993), issuing a reprimand to Dr. Sadarangani, and imposing an administrative fine in the amount of $1,200.00 DONE AND ENTERED this 29th day of March, 2001, in Tallahassee, Leon County, Florida. PATRICIA HART MALONO 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 29th day of March, 2001.
