Findings Of Fact Akeem Brown was born on May 15, 2012, at Memorial Hospital Jacksonville in Jacksonville, Florida. NICA retained Donald C. Willis, M.D. (Dr. Willis), to review Akeem’s medical records. In a medical report dated May 14, 2015, Dr. Willis made the following findings and expressed the following opinion: Spontaneous vaginal delivery was apparently uncomplicated. Birth weight was 3,626 grams or 8 lbs. The baby was not depressed. Apgar scores were 8/9. Newborn hospital course appears to be uncomplicated. Progress note on the day after birth recommended routine newborn care. Neurology evaluation at 20 months of age stated the baby had global developmental delay, hypotonia, and hyperreflexia. MRI at about 2 years of age showed bilateral motor cortex hyperintense FLAIR, suggestive of gliosis. A subsequent neurology note stated this finding was likely related perinatal ischemia. In summary, there was no apparent fetal distress during labor. Delivery was uncomplicated. The newborn was not depressed. Newborn hospital course was uncomplicated. The baby was subsequently found to have global developmental delay and an abnormal MRI as described above. There is nothing in the medical records to suggest this brain injury was related to hypoxia or trauma during the birth process. There was no apparent obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or the immediate post delivery period. Dr. Willis reaffirmed his opinion in an affidavit dated October 31, 2016. Dr. Willis’ opinion that there was no obstetrical event that resulted in loss of oxygen or mechanical trauma to the baby’s brain during labor, delivery or in the immediate post- delivery period is credited. Respondent retained Laufey Y. Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to evaluate Akeem. Dr. Sigurdardottir reviewed Akeem’s medical records, and performed an independent medical examination on him on October 21, 2015. Dr. Sigurdardottir made the following findings and summarized her evaluation as follows: Summary: Akeem is a 3-year 5-month-old black male who has a possible bilateral hemiplegic cerebral palsy following a fairly uncomplicated pregnancy and delivery. His MRI shows evidence of old hypoxia. After review of fairly extensive maternal records and labor and delivery records, it seems clear that timing his injury is difficult as he did not show any evidence of recent neurologic injury at the time of birth. Although sparse medical records of Akeem are made available to us, such as physical therapy or occupational therapy records, cognitive testing or language assessments and no additional neurologic evaluations are at hand it seems clear that Akeem has relatively spared cognitive abilities. Final result: Results of question 1: The patient is found to have a permanent substantial physical impairment, but to have relatively mild mental impairment mainly in the areas of language. Results of question 2: There is evidence on neuroimaging that Akeem’s difficulties could relate to hypoxic neurologic injury, but no clear evidence to suggest the timing of such an injury and, therefore, it cannot be established that it occurred in the immediate perinatal period. Results of question 3: We would expect full life expectancy, although a guarded prognosis for motor recovery and likely ongoing disability from his significant bilateral hemiplegia. We expect favorable recovery in areas of cognition and language. In light of the above-mentioned details, difficulty with clear timing of Akeem’s injury, we do not recommend Akeem to be included into the Neurologic Injury Compensation Association (NICA) Program and would be happy to answer additional questions. Dr. Sigurdardottir reaffirmed her opinions in an affidavit dated November 29, 2016. In order for a birth-related injury to be compensable under the Plan, the injury must meet the definition of a birth- related neurological injury and the injury must have caused both permanent and substantial mental and physical impairment. Dr. Sigurdardottir’s opinion that while Akeem has a substantial physical impairment, he has a relatively mild mental impairment, mainly in the area of language, is credited. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Sigurdardottir that Akeem does not have a substantial mental impairment.
Findings Of Fact Fundamental findings Austin Robert Pollard (Austin) is the natural son of Ann S. and James A. Pollard. He was born a live infant on October 26, 1992, at Morton Plant Hospital, a hospital located in Clearwater, Pinellas County, Florida, and his birth weight was in excess of 2500 grams. The physician providing obstetrical services during the birth of Austin was Glenn A. Helwig, 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. Austin's birth and subsequent condition At or about 5:00 p.m., October 25, 1992, Ann S. Pollard's membranes spontaneously ruptured, and at or about 7:45 p.m. she was admitted to Morton Plant Hospital. At the time, Mrs. Pollard was at term, and her prenatal course had been uncomplicated, except for hyperemesis gravidarium (pernicious vomiting of pregnancy) and a history of genital herpes (herpes simplex virus), although no outbreaks were reported during the course of her pregnancy. Upon admission, a vaginal exam revealed dilation of the cervix at 1 centimeter, effacement at 80 percent, and the fetus at station -2. Fetal heart monitoring revealed a fetal heart tone of 130 to 140 beats per minute upon admission and, notably, no fetal distress was documented during the course of labor or delivery. 2/ Mrs. Pollard progressed slowly through labor during the evening, and at 5:00 a.m., October 26, 1992, the cervix was noted to be at 6 centimeters and the fetus at zero station. By approximately 8:00 a.m. the cervix progressed to 9 centimeters and the fetus to station +1, augmentation was begun at 9:30 a.m. with the use of pitocin, and by 1:10 p.m. dilation of the cervix was noted to be complete and the fetus at station +1. Following completion of the first stage of labor, pushing was started; however, Mrs. Pollard was not able to push well, even though the epidural anesthesia was decreased, and she experienced a prolonged second stage of labor. Consequently, at or about 3:40 p.m., Dr. Helwig determined to use forceps to deliver the child, and Mrs. Pollard was prepared for delivery. The medical records reveal that Austin was delivered vaginally at 3:47 p.m., October 26, 1992, with forceps and a moderate left medial lateral episiotomy that extended to the third degree. 3/ Upon delivery, Austin was observed to have the umbilical "cord around [his] neck and shoulder x 1"; however, he promptly breathed and cried with stimulation, and his Apgar scores were 7 at one minute and 9 at five minutes. The newborn record further reflects no abnormalities at birth, with the exception of bruising of the face and neck associated with the forceps delivery, and a "dusky" left great toe. Following delivery, Austin was placed in the nursery and his progress was unremarkable until 6:00 p.m. that day, when the infant progress notes reveal that the discoloration of the left foot, "lateral side 1/2 to and including great toe" had not changed, and that the "infant is moving foot and toe actively." Such observations were reported to Deborah French, M.D., and she referred for a neonatology consult. At or about 7:15 p.m. that day, a neonatology consult was had. That examination revealed: Baby Pollard is a 7 number 11 oz white male infant born by low forceps delivery to a 33 4.0 g2p0 0 pos mother @ EGA 39 wks. Prenatal care via Dr. Helwig beginning @ 6 wks EGA. Labs: STS n/r, Rubella immune, HBsAg neg, random glucose 74, Hepatitis profile negative (husband [with] possible exposure to Hepatitis C). Maternal history significant for: (1) H/O genital HSV - one outbreak several years ago, nothing during this pregnancy (2) Occasional ETOH, denies tobacco, drugs (3) Hyperemesis gravidarum Rx'd [with] diet, Tigan, Transdarm Scop. ROM 24h 47 min [at] delivery. No fetal distress documented. Low forceps delivery [with] Apgars 7 [at 1 minute] -9 [at 5 minutes] - rec'd 02 X 1 min for color. Shoulder/nuchal cord x 1 . . . Skin: No rash. Bruising over eyelids, earlobes. Forceps marks over face. HEENT: Molaing present. Ant. font. soft & flat. Eyelids edematous & bruised . . . RESP: Resp. easy [with] BBS cl & equal. Symmetrical chest rise. Becomes tachypreic [with] stimulation, but quickly resolves . . . Great toe of L foot, medial aspect of plantar/ dorsum deeply cyanotic - blanches under pressure - irregular borders . . . Neuro: Quiet - responds to stimuli [with] L lateral arching & draws R arm over abdomen. Otherwise good tone. + Moro, but quickly arches. + Grasp, suck. L foot cyanosis resolved somewhat when R foot wrapped [with] warm compress. Based on that examination the doctor gleaned the following impressions: IMP: Prolonged ROM - 24 3/4 h - R/O sepsis Cyanotic toe/foot - R/O arteriospasm, R/O embolus, R/O polycythemia, R/O hyperviscosity Arching [with] unusual posturing Consequently, the doctor recommended, among other things, admission to "SCN for monitoring," blood work, and a cranial ultrasound in the morning. The cranial ultrasound, taken October 27, 1992, revealed: . . . A VERY SMALL (4 X 3 MM) CYST IN THE ANTERIOR ASPECT OF THE CHOROID PLEXUS ON THE RIGHT SIDE. OTHERWISE, THE STUDY IS NEGATIVE. THE VENTRICLES APPEAR NORMAL AND SYMMETRIC BILATERALLY. THERE IS NO INTRACRANIAL HEMORRHAGE. IMPRESSION: . . . 1. SMALL CYST IN THE CHOROID PLEXUS OF THE RIGHT LATERAL VENTRICLE. SUGGEST REPEAT ULTRASOUND IN 3-4 WEEKS FOR COMPARISON. OTHERWISE, NEGATIVE STUDY. At or about 10:30 p.m., October 27, 1992, Austin was observed to evidence seizure activity that included rhythmic jerking of both feet and lip smacking, which lasted for 4 minutes. Over the next 9-10 hours, Austin had increased episodes of seizure activity, primarily right sided, and at or about 4:00 a.m., October 28, 1992, he was also observed to have developed a deeply cyanotic area of approximately 3 X 4 centimeters over the left scrotum, similar to the area initially involving the left toe. At or about 9:35 a.m., October 28, 1992, Austin was transferred to All Children's Hospital for further evaluation and care. There, Austin came under the care of Robert Kropp, M.D., a pediatric neurologist. While at All Children's Hospital, a CT scan of the brain was performed on October 28, 1992. It revealed "multifocal low-density, spherical lesions in both the supra- and infratentorial region without mass effect or hemorrhage." The radiologist observed that the "areas are fairly well defined and may represent areas of edema or developing encephalomalacia," and that he "[w]ould suspect some type of thromboembolic origin." Otherwise, the anatomy of the brain appeared normal. An EEG on the same date revealed multi focal epileptic abnormalities. Dr. Kropp's initial consultation of October 28, 1992, observed evidence of peripheral embolization, which was reflected by the blue discoloration found in the left great toe and in the scrotum area. He suspected that Austin had an anti-thrombin-3 deficiency which created the thromboembolic phenomenon to his leg and scrotum, and that diagnosis was supported by the multiple low density lesions observed on the CT scan which were also consistent with the thromboembolic phenomenon. Dr. Kropp's differential diagnosis was as follows: The differential diagnosis includes anti- thrombin 3 deficiency. The CT abnormalities are also consistent with congenital infection, such as CMV, HIV, or VDRL-positive spirochetes. It also suggests vasculitis, such as congenital lupus or intrauterine procaine exposure. These are secondary considerations in view of peripheral embolization, but need to be considered if the appropriate coagulin studies do not confirm the suspected primary diagnosis. While in All Children's Hospital, Austin was also evaluated by Robert A. Good, M.D., the head of the hospital's division of clinical immunology and allergy. His consultation of November 5, 1992, observed: Hematology evaluated this patient and felt that the thromboembolic manifestations might be secondary to deficiency of anticoagulant proteins. This patient's antithrombin 3 was within normal limits, as well as PT, PTT, and fibrinogen. . . . His impressions were: This thromboembolic phenomenon may be seen with neonatal lupus. In many cases, sometimes the mother is unaware of her lupus and the manifestation in the infant leads to the diagnosis. Would recommend anti-Ro and anti-La, which are associated with infantile lupus. Would also obtain an anti-double-stranded DNA, as well as an ANA in the infant. Would perform an EKG to rule out a congenital heart block. It is also important to obtain anti-cardiolipin antibodies in the mother, as well as circulating lupus anticoagulants. The performance of a skin biopsy to rule out vasculitis is not useful. Another entity that may be considered is HIV infection, acquired early in gestation, which may certainly present as a thromboembolic phenomenon. To work this up, we suggest HIV ELISA, as well as PCR P24 antigen, and HIV culture. Other entities which have also been considered are congenitally-acquired viral infections, such as syphilis and herpes, or CMV. Would also consider leptospirosis. Austin was discharged from All Children's Hospital on November 13, 1992, to his parents' care. The diagnosis on discharge was seizures and peripheral thrombo embolization. The discharge summary further observed: INFECTIONS: Blood culture was done at the referring hospital. CBC was within normal limits. The infant was started on Ampicillin and Gentamicin. An LP was performed. CSF and viral cultures were obtained. All cultures were negative. The anti- biotics were discontinued after 7 days. There was a maternal history of herpes in the past although no outbreaks were reported during this pregnancy. NP and eye viral cultures were negative for herpes. Stool for echovirus and enterovirus were also negative. TORCH IgMs were obtained from the referring hospital and were reported as negative. On day 9 an Immunology consult was requested to rule out a vasculitis. Infantile lupus work up on the infant was negative. Maternal PT, PTT, protein, C&S, and lupus anticoagulant were all negative. Paternal PT, PTT, protein, C&S were normal. * * * HEMATOLOGY: Due to the peripheral thromboembolic manifestations a Hematology consult was obtained. The infant was evaluated for a deficiency of anticoagulant proteins. The infant was started on daily FFP administration. The antithrombin 3, FSP, PT, PTT, and fibrinogen were all within normal. Proteins S and C were normal. Urine amino acids are pending. FFP administration was discontinued on day 15 when the proteins S&C were reported normal. The infant was closely observed and there was no reoccurrence of cyanosis or thrombosis noted. The infant's mother was instructed to call a physician if cyanosis or purpura was seen. The infant will be followed by Dr. Bagtas in 2 weeks. The etiology for the suspected thromboembolic event is unknown at this time. * * * CENTRAL NERVOUS SYSTEM; Due to the seizure activity a cranial ultrasound was done at the referral hospital at 1 day of age and was normal except for a small right choroid cyst. Due to seizures a CT of the brain was performed at 2 days of age at All Children's. This revealed multifocal low density spherical lesions in both supra and infra tentorial region without mass effect or hemorrhage. This may represent edema or encephalomalacia of thromboembolic origin. An EEG, completed on the same date, revealed multifocal epileptic form abnormalities. These seizures were controlled with Phenobarbital. . . . As of the date of discharge, the etiology or cause for the suspected thromboembolic event was unknown. The cause and timing of Austin's neurologic insult. Here, the proof demonstrates, more likely than not, that the deficits Austin suffers, discussed infra, were the consequence of a spontaneous left thalamic hemorrhage, generically referred to as a stroke in these proceedings, which occurred subsequent to birth, but during the first 48 hours of life. Consequently, the injury Austin suffered to his brain occurred during the neonatal period, which is defined as the time period subsequent to birth and through the first 30 days of life, as opposed to occurring during labor, delivery or the immediate post-delivery period. As for the cause of Austin's stroke, the objective evidence, as reflected by the blue discoloration found in his left great toe and in the scrotum area, as well as the multiple low density lesions observed on the CT scan, is consistent with a thromboembolic phenomenon, a hematologic phenomenon, as opposed to oxygen deprivation or mechanical injury suffered during the course of labor, delivery or the immediate post-delivery period. Consequently, while the underlying cause for the hematologic phenomenon which precipitated Austin's stroke has not been definitively established, it must be concluded that, based on the record developed in this case, the injury he sustained was unrelated to the actual birthing process. In concluding that the proof fails to demonstrate that Austin's neurologic insult was occasioned by oxygen deprivation or mechanical injury during the birthing process, it is first observed that the competent medical testimony does not suggest that Austin suffered any fetal distress, occasioned by oxygen deprivation or mechanical injury, during the course of labor or delivery which would have resulted in the subject injury but, rather, points to a hematologic phenomenon as the origin of Austin's stroke. That testimony is consistent with the medical records which, facially, did not reflect fetal distress during labor or delivery, the fact that following delivery Austin was suctioned and received whiffs of oxygen for color but was not intubated nor ventilated, that upon delivery Austin's Apgar scores were 7 and 9, which is not indicative of perinatal distress, and the consistency of the objective evidence regarding his subsequent condition with a hematologic phenomenon as the cause of his distress. Finally, although the use of forceps to deliver Austin did cause some bruising in or about the facial area, no physician who testified in this case suggested such injury caused or contributed to Austin's neurologic insult. To the contrary, the testimony demonstrated that the discoloration on the great left toe and scrotum area, as well as the cerebral infarcts, were unrelated to the use of forceps. 4/ Austin's mental and physical condition Austin has undergone two developmental evaluations through All Childrens' Hospital. The first took place on October 18, 1993, when Austin was 11 months, twenty-two days old. The evaluation revealed that he had cognitive development to an age equivalent level of 10 months, motor development to an age equivalent of 8.9 months, and communication development to an age equivalent level of 10.5 months. Such scores reflected that Austin's "cognitive skills [were] delayed for his chronological age," his motor development was "below age-appropriate for his chronological age, primarily due to slightly abnormal muscle tone in his trunk and extremities," but that he "present[ed] with communication skills that [were] within a range of normal limits for his age." He was referred to a developmental preschool, as well as for occupation and physical therapy. No speech therapy was recommended. The second developmental evaluation took place on June 20, 1994, and June 22, 1994, when Austin was approximately 20 months old. The evaluation revealed that he had cognitive development to an age equivalent level of 16 months, motor development to an age equivalent level of 17 months, and communication development to an age equivalent level of 18 months (receptive) and 17.25 months (expressive). Such scores revealed that Austin's cognitive skills continued to be delayed for his chronological age, that his motor development (gross and fine) was below age-appropriate for his chronological age, and that his communication skills were "suspect . . . [when evaluated because he] presented as shy and quiet for the majority of the evaluation; therefore, information was obtained via parent report." Austin has continued to be followed by Dr. Robert Kropp, as his primary pediatric neurologist, since his first admission to All Children's Hospital. In the opinion of Dr. Kropp, which is credited, Austin has been set back mentally and physically "from what would be described as normal development as it relates to a child of his age" due to complications from the stroke he suffered and resulting seizures. [Petitioners' exhibit 19, page 25]. As for Austin's physical condition, Dr. Kropp observed that he had a residual right sided weakness, which the doctor ascribed as the cause of Austin's internally rotated left foot, and a tendency for the right arm to posture when Austin ran. Consequently, Austin had difficulty climbing, as well as turning and negotiating uneven surfaces. Austin also evidenced a balance problem, and tremors bilaterally, with the right worse than the left. To address his balance and coordination problem, Dr. Kropp prescribed Amantadine, which alters the biochemical functioning of the cerebellum, the balance organ of the brain. By observation, Austin's balance and coordination improved on the medication compared to off the medication. As for Austin's mental condition, Dr. Kropp did not elaborate beyond his conclusion that Austin's mental development was not age- appropriate. Concerning the significance and permanency of Austin's physical and mental delays, Dr. Kropp was of the opinion, as evidenced by his last consult of October 11, 1994, that Austin's developmental delays were very moderate and improving. Such conclusion is consistent with the opinion of Michael S. Duchowny, M.D., who examined Austin on March 2, 1995, and concluded: . . . Austin has evidence of a very mild residual asymmetry of motor postures primarily evidenced in the right arm. There is no evidence of spasticity. I believe that the internal rotation of the left lower extremity is more likely to be orthopedic in origin, possibly related to his hip joint. Certainly it does not fit with his past history of possible left hemisphere damage. I thing that his social and cognitive skills are quite good and the future prognosis would appear promising. Notably, among neurologists, mental and physical impairments are routinely classified as mild, moderate or severe. Here, Austin's developmental delays have been classified as "very moderate," a classification far below what would be considered severe.
The Issue The issues are whether Respondent failed to practice medicine with that level of care, skill, and treatment which is recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances, and, if so, what penalty, if any, should be imposed.
Findings Of Fact 1. Stipulated Facts Petitioner is the state agency charged with regulating the practice of medicine pursuant to Section 20.30 and Chapters 455 and 458, Florida Statutes. Respondent is a licensed physician in Florida holding license number ME 0009772. Respondent's last known address is 9430 Turkey Lake Road, Orlando, Florida 32819-8015. Respondent is Board certified in orthopedic surgery. Respondent provided medical treatment to two male patients between 1990 and 1991. Patient 1 was treated from approximately April 29, 1991, through August 12, 1991. At the time, Patient 1 was approximately 34 years old. Patient 2 was treated from approximately May 14, 1990, through June 20, 1991. Patient 2 was approximately 29 years old. Patient 1 Patient 1 had a history of hip dislocation with aseptic necrosis, chronic back and leg pain, and foot numbness associated with degenerative disc disease and lumbar stenosis. Lumbar stenosis is compression of the spine. Spine compression was particularly significant between the fifth lumbar and first sacral vertebrae. Prior to April 29, 1991, Patient 1's treatment was conservative and nonsurgical. On April 29, 1991, Patient 1 presented to Respondent to explore alternative therapy. Patient 1 complained of pain and numbness in his back, hip, and legs. Respondent diagnosed Patient 1 with lumbar spinal stenosis and possible disc herniation. Respondent recommended a myelogram. A myelogram was performed on May 13, 1991. The myelogram confirmed Respondent's diagnosis of lumbar spinal stenosis and possible disc herniation. The myelogram revealed a disc defect on the right side of L5-S1 as well as severe spinal and lateral recess stenosis. On June 11, 1991, Respondent performed a laminectomy on Patient 1, an L5-S1 disc excision, and an internal spinal stabilization using Harrington rods attached with lamina hooks. Use of lamina hooks resulted in the compression of Patient 1's underlying neural tissue. Compression of the underlying neural tissue caused Patient 1 to suffer perineal numbness. Respondent's medical records of June 17, 1991, show that Respondent knew Patient 1's perineal numbness was a result of compression of the sacral nerve root at L5-S1. On June 17, 1991, Respondent again performed surgery on Patient 1. Respondent replaced the lamina hooks with alar hooks. Respondent also replaced and adjusted the tension of the Harrington rods. On August 1, 1991, Patient 1 was admitted to Sandlake/Orlando Regional Medical Center ("ORMC") for surgical removal of the implanted hooks and Harrington rods. Respondent surgically removed the Harrington rods and attachment hooks. On August 12, 1991, Respondent's medical records showed that Patient 1 suffered from persistent numbness of the sacral nerve root areas. The area of numbness included the perineum, scrotum, and penis. Respondent did not perform an L5-S1 bone fusion during any surgery. Patient 2 On May 14, 1990, Patient 2 presented to the Emergency Room ("ER") at ORMC with primary complaints of back and right leg pain. The ER physician diagnosed Patient 2 with a herniated nucleus pulposus at L4-L5. The nucleus pulposus is the soft central portion of the intervertebral disc. Respondent admitted Patient 2 on May 14, 1990, and treated him with intravenous muscle relaxants. On May 15, 1990, a computerized axial tomography ("CAT") scan revealed a bulging, herniating disc at L4-L5. On May 17, 1990, Respondent discharged Patient 2 with instructions regarding back care and an exercise program. On August 24, 1990, Patient 2 presented to Respondent with recurrent disabling sciatic pain. A magnetic resonance imaging ("MRI") scan was performed on August 28, 1990. The MRI revealed a prominent disc bulging at L4-L5 with material intruding into the spinal cord. On September 7, 1990, Respondent performed a lumbar laminectomy and disc excision at L4-L5. Respondent discharged Patient 2 on September 12, 1990. On December 11, 1990, Patient 2 presented to Respondent with recurrent back and right leg pain. Respondent prescribed analgesics including Soma with codeine and Naprosyn. On January 14, 1991, Patient 2 presented to Respondent with back and right leg pain. Patient 2 underwent a CAT scan to determine if recurrent disc herniation was present. The CAT scan failed to indicate any obvious asymmetric changes which would confirm Respondent's diagnosis of recurrent disc herniation. On January 21, 1991, Respondent performed a decompressive laminectomy on Patient 2. Respondent's operative report for January 21, 1991, indicates that Respondent found no evidence of a herniated disc. On February 26, 1991, Patient 2 presented to Respondent with complaints of recurrent leg and back pain. Respondent referred Patient 2 to Dr. William Bradford for treatment utilizing epidural blocks. On April 16, 1991, Patient 2 again presented to Respondent. Respondent placed Patient 2 in a molded, fiberglass body jacket. Back and leg pain subsided while Patient 2 wore the fiberglass jacket. On May 14, 1991, Respondent performed surgical stabilization of the lower lumbar spine utilizing Harrington rods. On June 17, 1991, Patient 2 presented to Respondent with persistent numbness of the perineal area as well as bowel and bladder incontinence. Respondent determined that the numbness and incontinence were caused by sacral nerve root irritation associated with the Harrington rod hooks. Respondent surgically adjusted the Harrington rods on June 20, 1991. Respondent did not perform vertebral bone fusion during any surgery. 2. Standard Of Care Respondent failed to practice medicine in his treatment of Patient 1 with that level of care, skill, and treatment which is recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances. Respondent improperly seated lamina hooks in Patient 1. As a result, Patient 1 suffered compression of underlying neural tissue. Respondent improperly used Harrington rods and hooks to achieve transient spinal decompression without performing essential vertebral bone fusion. Use of Harrington rods in the lumbar spine is an obsolete technology. It is fraught with dangers. Among other things, it eliminates the lordosis, or natural spinal curvature. Respondent failed to practice medicine in his treatment of Patient 2 with that level of care, skill, and treatment which is recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances. Respondent performed numerous surgeries on Patient 2 when CAT scans and other examinations failed to confirm recurrent disc herniation. In addition, Respondent failed to perform essential vertebral bone fusion on Patient 2. 3. Proximate Cause And Severity Of Injury Respondent's failure to practice medicine with that level of care, skill, and treatment which is recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances was the proximate cause for permanent neurological damage to Patient's 1 and 2. Both patients suffered sacral nerve root paralysis. Sacral nerve roots feed functions in the pelvis, bladder bowel, and sphincter. Both patients suffered permanent incontinency, including loss of bladder and bowel function. Each patient requires a colostomy and must wear diapers. Patient 1 has suffered sexual dysfunction in that he has lost the sensation necessary for a natural erection. The neurologic injuries to Patients 1 and 2 are major and permanent. Nothing can restore the functional loss suffered by either patient.
Recommendation Based upon the foregoing Findings of Fact and Conclusions of Law, it is RECOMMENDED that Respondent enter a Final Order finding Respondent guilty of violating Section 458.331(1)(t) in his treatment of Patients 1 and 2, imposing an administrative fine of $7,500, and restricting Respondent's practice as follows: Respondent shall not perform any spinal surgery on patients unless and until Respondent appears before the Board of Medicine and demonstrates to the satisfaction of the Board that he is able to do so with skill and safety; and The Board of Medicine may place other reasonable conditions on Respondent's practice of orthopedic surgery at such time as the restriction in the preceding paragraph is lifted. DONE AND ENTERED in Tallahassee, Leon County, Florida, this 6th day of October, 1994. DANIEL MANRY Hearing Officer Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-1550 (904) 488-9675 Filed with the Clerk of the Division of Administrative Hearings this 6th day of October, 1994. APPENDIX TO RECOMMENDED ORDER, CASE NO. 93-3966 Petitioner's Proposed Findings of Fact 1. -39. Accepted as stipulated fact 40.-41. Rejected as recited testimony Accepted in substance Rejected as recited testimony Accepted in substance 45.-51. Rejected as recited testimony Respondent's Proposed Findings of Fact Respondent stipulated to Petitioner's proposed findings of fact, paragraphs 1- 39. Respondent's only additional proposed finding of fact is unnumbered and is rejected as not supported by persuasive evidence. COPIES FURNISHED: Dr. Marm Harris, Executive Director Department of Business and Professional Regulation Board of Medicine Northwood Centre 1940 North Monroe Street Tallahassee, Florida 32399-0792 Harold D. Lewis, Esquire Agency For Health Care Administration The Atrium, Suite 301 325 John Knox Road Tallahassee, FL 32303 Kenneth J. Metzger, Esquire Agency For Health Care Administration 1940 North Monroe Street Tallahassee, Florida 32399-0792 Jack L. Gresham, M. D. 9430 Turkey Lake Road Orlando, Florida 32819-8015
Findings Of Fact Eleanor Breen Zayas was born on May 8, 2015, at University of South Florida Health, South Tampa Center, in Tampa, Florida. Donald Willis, M.D. (Dr. Willis), was requested by NICA to review the medical records for Eleanor. In an affidavit dated October 28, 2016, Dr. Willis described his findings in pertinent part as follows: In summary, delivery was complicated by a prolonged FHR deceleration about 8 hours prior to delivery, maternal chrioamnionitis and fetal tachycardia. Cesarean section was done with thick Meconium present. The baby was not depressed at birth. Cord blood gas pH was normal (pH 7.36). However, oxygen desaturation occurred at 5 hours after birth with seizure activity following shortly after. MRI within 24-hours of birth showed acute cerebral infarction. The baby suffered a cerebral infarction. The exact timing of the infarction is difficult to determine. However, it is possible the infarction occurred during the severe and prolonged FHR deceleration 8 hours prior to birth. It appears the baby recovered from this hypoxic event during the remaining 8 hours of labor. Therefore, the cord blood gas was not abnormal at birth and the baby was not depressed at birth. Infection (Choriomnionitis) could be a contributing factor. The other opinion would be the infarct occurred after delivery, primarily related to infection. There was an apparent obstetrical event that may have resulted in loss of oxygen to the baby’s brain during labor. Oxygen deprivation resulted in brain injury. I am unable to comment about the severity of the injury. Dr. Willis’ opinion that there was an apparent obstetrical event that may have resulted in loss of oxygen to the baby’s brain during labor is credited. Respondent retained Laufey Sigurdardottir, M.D. (Dr. Sigurdardottir), a pediatric neurologist, to evaluate Eleanor. Dr. Sigurdardottir reviewed Eleanor’s medical records, and performed an independent medical examination on her on August 10, 2016. In a neurology evaluation based upon this examination and a medical records review, Dr. Sigurdardottir made the following findings and summarized her evaluation as follows: Summary: Here we have a 14-month-old girl with a sinus vein thrombosis at birth, focal seizures and possible subsequent infarction. This is likely a birth related injury. Her recovery has been remarkable and neurologic exam today is suggestive of mild expressive language delay, but no focal motor abnormalities are found. Results as to Question 1: The patient is found to have no substantial physical or mental impairment at this time. Results as to Question 2: Eleanor’s injury is a neurologic injury to the brain occurred [sic] due to oxygen deprivation and is felt to be birth related. Results as to Question 3: Eleanor’s prognosis for full recovery is extremely good and mild expressive delays are not likely to have any lasting ill effect. In light of the above-mentioned details, although clear evidence is that Eleanor’s infarct and thrombosis was due to a difficult prolonged birth with chrioamnionitis and recurrent decelerations, she has made such good recovery that at this time I do not recommend Eleanor being included into the Neurologic Injury Compensation Association (NICA) Program and would be happy to answer additional questions. In order for a birth-related injury to be compensable under the NICA Plan, the injury must meet the definition of a birth-related neurological injury and the injury must have caused both permanent and substantial mental and physical impairment. Dr. Sigurdardottir’s opinion that Eleanor does not have a substantial physical or mental impairment is credited. A review of the file in this case reveals that there have been no expert opinions filed that are contrary to the opinion of Dr. Sigurdardottir that Eleanor does not have a substantial physical or mental impairment.
The Issue Whether Daniel Espinoza has suffered an injury for which he and his mother, Maria L. Espinoza, should be awarded compensation under the Florida Birth-Related Neurological Injury Compensation Plan, as Ms. Espinoza has alleged in her claim for compensation filed on behalf of Daniel?
Findings Of Fact Based upon the evidence adduced at the July 14, 1994, Division-conducted hearing in this case, and the record as a whole, the following Findings of Fact are made: Daniel Espinoza is the natural son of Petitioner. He was born on January 6, 1991, at Jackson Memorial Hospital (hereinafter referred to as "Jackson") in Dade County, Florida. Daniel was the product of a full term pregnancy. His birth weight was in excess of 2500 grams. Daniel was delivered by Erin Colleen Dawson, M.D. At the time of Daniel's birth, Dr. Dawson was a participant in the Florida Birth-Related Neurological Injury Compensation Plan. The delivery was uneventful. Daniel was a "vigorous" baby at birth. He had a "good" Apgar score of 9 at one, five, and ten minutes after birth. There was no resuscitation required in the immediate postdelivery period. Approximately five hours after the initial evaluation, Daniel appeared to be "grunting" and suffering from "cyanosis." As a result, he was transferred to Jackson's neonatal intensive care unit, where he had a seizure and experienced respiratory distress. Daniel's C.S.F. (cerebrospinal fluid) was bloody and had a white blood cell count of 19000. An initial diagnosis of meningitis was made. On January 7, 1991, an EEG (electroencephalogram) was done. It revealed "no epileptiform phenomena." A CT (computerized tomography) scan of Daniel's brain was performed on January 8, 1991. The report of the scan read as follows: HISTORY- TWO DAY OLD WITH SEPSIS. 5 MM AXIAL SECTIONS WERE OBTAINED THROUGH THE BRAIN WITHOUT CONTRAST. THERE IS A SMALL LUCENT DEFECT IN THE LEFT OCCIPITAL BONE SEEN ON IMAGE #5. ALTHOUGH NO SOFT TISSUE SWELLING IS SEEN, CANNOT DEFINITELY EXCLUDE THIS BEING A LINEAR NONDEPRESSED FRACTURE VERSUS OTHER ETIOLOGY SUCH AS A VASCULAR GROOVE. WE SUGGEST CORRELATION WITH THE PLAIN FILM. THERE IS A HUGE AMOUNT OF BLOOD IN THE RIGHT POSTERIOR FOSSA EXTENDING ACROSS THE MIDLINE AND INSINUATING ON THE RIGHT TENTORIAL INCISURA SUPRATENTORIALLY. BLOOD IS ALSO SEEN ALONG THE POSTERIOR INTERHEMISPHERIC FISSURE DIFFUSELY IN THE EXTRA-AXIAL SPACE, AND A SMALL AMOUNT OF BLOOD IN THE OCCIPITAL HORNS OF THE LATERAL VENTRICLES. WITH SUCH A TREMENDOUS AMOUNT OF BLOOD PRESENT IN THE POSTERIOR FOSSA, IT IS DIFFICULT TO SAY HOW MUCH IS PARENCHYMAL VERSUS EXTRA-AXIAL. THERE IS MASS EFFECT UPON THE MID BRAIN PONS AND MEDULLA AND ON THE FOURTH VENTRICLE CAUSING OBSTRUCTING HYDROCEPHALUS. IMPRESSION LARGE ACUTE INTRACRANIAL HEMORRHAGE, AS DESCRIBED ABOVE, WITH THE EPICENTER BEING IN THE RIGHT POSTERIOR FOSSA. THE DIFFERENTIAL DIAGNOSIS INCLUDES NEOPLASM, TRAUMA, RUPTURED ANEURYSM OR ARTERIOVENOUS MALFORMATION, COAGULOPATHY, ETC. CONTRAST STUDY OR MRI MAY BE OF HELP FOR FURTHER EVALUATION TO TRY TO DETERMINE THE UNDERLYING ETIOLOGY. On January 9, 1991, Daniel underwent an echoencephalogram, which, according to the report of the study, indicated the following: ROUTINE ECHOENCEPHALOGRAM REVEALED DILATION OF THE LATERAL AND THIRD VENTRICLES. THERE IS A BILATERAL LUMPY CHOROID PLEXUS NOTED. ADDITIONAL TRANSTEMPORAL VIEWS REVEAL AN ECHOGENIC AREA SEEN IN THE INFRATENTORIAL REGION, WITH INCREASE IN THE ECHOGENICITY OF THE BASAL CISTERNS. THE FINDINGS ARE SIMILAR TO THOSE SEEN ON PREVIOUS CT SCAN, WHICH SHOWED EVIDENCE OF A CEREBRAL HEMORRHAGE WITH SUBARACHNOID BLEED. THE NORMAL STRUCTURES OF THE POSTERIOR FOSSA ARE ILL-DEFINED. IMPRESSION: MODERATE HYDROCEPHALIC CHANGES OF THE LATERAL AND THIRD VENTRICLES. SUBARACHNOID HEMORRHAGE WITH A POSTERIOR FOSSA HEMORRHAGE, AS DESCRIBED IN A PREVIOUS CT SCAN OF THE BRAIN. Another CT brain scan was performed on January 23, 1994, the report of which stated the following: THE PATIENT IS A TWO WEEK OLD MALE WITH A HISTORY OF INTRACRANIAL HEMORRHAGE. AXIAL IMAGES WERE OBTAINED THROUGH THE BRAIN AT 5MM INTERVALS FOLLOWING INTRAVENOUS ADMINISTRATION OF CONTRAST. COMPARED TO THE PRIOR STUDY OF 1-8-91, THERE HAS BEEN SUBSTANTIAL RESORPTION OF BLOOD IN THE REGION OF THE SUBDURAL, SUBARACHNOID AND INTRAVENTRICULAR HEMORRHAGE. THERE ALSO HAS BEEN MARKED DECREASE IN THE VENTRICULAR SIZE. THERE IS LESS ASSOCIATED MASS EFFECT, ESPECIALLY IN THE POSTERIOR FOSSA WITH PERSISTENT SUBDURAL HEMORRHAGE IN THE RIGHT SIDE OF THE POSTERIOR FOSSA DISPLACING THE CEREBELLUM ANTERIORLY AND TO THE LEFT. THE FOURTH VENTRICLE IS NOW VISUALIZED, HOWEVER. NO NEW AREAS OF HEMORRHAGE ARE SEEN. THERE ARE NO BONY ABNORMALITIES. THE MAXILLARY AND ETHMOID SINUSES AND MASTOID AIR CELLS ARE CLEAR. IMPRESSION SIGNIFICANT RESORPTION OF SUBDURAL, SUBARACHNOID WITH INTRAVENTRICULAR HEMORRHAGE SINCE THE PRIOR STUDY OF 1-8-91 WITH LESS MASS EFFECT, ESPECIALLY UPON THE CEREBELLUM AND BRAIN STEM. MARKED DECREASE IN VENTRICULAR SIZE HAS ALSO OCCURRED. On January 25, 1991, Daniel underwent a second echoencephalogram, the report of which read as follows: FOLLOW-UP BRAIN HEMORRHAGE. COMPARISON IS MADE TO PREVIOUS STUDY FROM 1/8/91. THERE HAS BEEN MARKED INTERVAL RESOLUTION OF THE PREVIOUSLY DEFINED RIGHT POSTERIOR FOSSA HEMORRHAGE. IN ADDITION, THE VENTRICULAR SIZE HAS DECREASED SIGNIFICANTLY SINCE THE PREVIOUS EXAM. THERE CONTINUES TO BE SLIGHT INCREASED ECHOGENICITY WITHIN THE SYLVIAN FISSURES BILATERALLY, WHICH MAY REPRESENT SOME RESIDUAL SUBARACHNOID HEMORRHAGE. NO EVIDENCE OF NEW OR ACUTE HEMORRHAGE IS IDENTIFIED. IMPRESSION: THERE HAS BEEN SIGNIFICANT INTERVAL IMPROVEMENT IN THE DEGREE OF VENTRICULAR DILATION AND THE PREVIOUSLY DEFINED HEMORRHAGE, WHEN COMPARED TO THE STUDY OF 1/8/91. Daniel was discharged from Jackson on January 31, 1991. At present, in terms of meeting expected language milestones, Daniel is mildly delayed, primarily in the area of expressive language. The delay is developmental in nature and Daniel will likely improve in this area over time. Otherwise, his mental functioning is relatively well preserved. Physically, Daniel is only very mildly impaired. He has a slight decrease in muscle tone and some incoordination, but he does not suffer from spasticity or contracture and he is able to move both of his arms well and to walk without losing his balance. He is even able to run, although he has a tendency to lean to the right and appear as if he is about to fall when he does so. In short, Daniel suffers from no permanent and substantial mental or physical impairment. 2/
Findings Of Fact Asher was born on April 20, 2017, at Memorial Hospital located in Pembroke Pines, Florida. Upon receiving the Petition, NICA retained Michael S. Duchowny, M.D., a pediatric neurologist, to review Asher’s case. NICA sought to obtain an opinion whether there was an injury to Asher’s brain or spinal cord at birth caused by oxygen deprivation or mechanical injury occurring in the course of labor, delivery, or resuscitation in the immediate post-delivery period, and whether that injury rendered Asher permanently and substantially mentally and physically impaired. Dr. Duchowny reviewed Asher’s medical records, as well as examined Asher on October 10, 2018. Dr. Duchowny opined, within a reasonable degree of medical probability: [I]t is my opinion that ASHER’s neurological examination reveals neurological findings consistent with a mild motor impairment primarily affecting his right upper extremity. In contrast, Asher has preserved cognitive function and social awareness. He evidences slightly decreased muscle tone in the right distal upper and lower extremities and slightly increased deep tendon reflexes. As such, it is my opinion that despite ASHER’s abnormal MR imaging studies at birth which document prominent hemorrhagic infarction in territories supplied by the left middle and posterior cerebral arteries with a smaller region of right middle cerebral artery infarction, and bilateral parieto-occipital areas of increased signal, he has recovered to a point where he no longer evidences either substantive mental or physical impairment. Based upon my evaluation and record review, as ASHER is developing normally, I am not recommending him for acceptance into the NICA program. A review of the records filed in this matter reveals no contrary evidence to dispute the findings and opinion of Dr. Duchowny. His opinion is credible and persuasive. Based on the opinion and conclusion of Dr. Duchowny, NICA determined that Petitioners’ claim was not compensable. NICA subsequently filed the Motion for Partial Summary Final Order asserting that Asher has not suffered a “birth-related neurological injury” as defined by section 766.302(2). Petitioners do not oppose NICA’s motion.
Findings Of Fact Michael was born on June 27, 2014, at Jackson Memorial Hospital. Michael was a twin, a multiple gestation, weighing over 2,000 grams at birth. Respondent retained Donald Willis, M.D., an obstetrician specializing in maternal-fetal medicine, to review the medical records of Michael and his mother, Petitioner Maria Jose Morales Cannon, and opine as to whether there was an injury to his brain or spinal cord that occurred in the course of labor, delivery, or resuscitation in the immediate postdelivery period due to oxygen deprivation or mechanical injury. In his report, dated September 10, 2018, Dr. Willis set forth the following, in pertinent part: The mother was admitted to the hospital at about 32 weeks gestational age for steroids to enhance fetal lung maturity and intravenous MgSO4 as neuroprotection to help reduce the risk for intracranial bleed. Her cervix was dilated one centimeter, 20% effaced and posterior, consistent with an unlabored cervix. Primary Cesarean section was done at 32 weeks as pre management plan for TTTS.[2/] Biophysical profiles (BPP) were 8/8 for both fetuses prior to delivery, indicating neither fetus was in distress. Fetal heart rate tracing was stated to be reactive, again suggesting no distress prior to delivery. Michael Cannon was the larger of the twins, designated as twin A. Cesarean delivery was apparently uncomplicated. Birth weight was 2,090 grams. The baby was not depressed at birth. Apgar scores were 9/9/9. Essentially no resuscitation was required with only tactile stimulation and oral suctioning done after birth. * * * In summary, this child was born as twin A at 32 weeks gestational age. Delivery was by elective Cesarean selection. Birth weight was 2,090 grams. The mother was not in labor. Delivery was uncomplicated. The baby was not depressed at birth. Apgar scores were 9/9. No resuscitation was required. The initial platelet count was decreased at 96,000. However, Intracranial hemorrhage would be unlikely with this platelet count. Head ultrasound and MRI were consistent with periventricular leukomalacia. Brain injury was most likely related to prematurity and not oxygen deprivation or trauma at birth. There was no apparent obstetrical event that resulted in oxygen deprivation or mechanical trauma during labor, delivery or the immediate post-delivery period. Brain injury identified by head Ultrasound and MRI was more likely related to prematurity and not oxygen deprivation at birth. In his affidavit, dated November 30, 2018, Dr. Willis affirms, to a reasonable degree of medical probability, the above-quoted findings and opinions from his report. Respondent also retained Michael S. Duchowny, M.D., a pediatric neurologist, to review the pertinent medical records, conduct an Independent Medical Examination (IME) of Michael, and opine as to whether Michael suffers from a permanent and substantial mental and physical impairment as a result of a birth-related neurological injury. Dr. Duchowny reviewed the medical records, obtained historical information from Michael’s mother and aunt, and performed an IME on November 14, 2018. Respondent’s Motion for Partial Summary Final Order also relies upon the attached affidavit from Dr. Duchowny, dated November 28, 2018. In his affidavit, Dr. Duchowny testifies, in pertinent part, as follows: In summary, MICHAEL’s examination reveals neurological findings consistent with spastic diparetic cerebral palsy. He evidences dysarthic speech and refractory strabismus. Impairment primarily affecting his right upper extremity. In contrast, Michael has preserved cognitive function and social awareness. Review of MICHAEL’s medical records reveals that his mother’s twin pregnancy was complicated by intrauterine growth retardation and polyhdramnious. Corner over absent diastolic blood flow in MICHAEL’s twin brother prompted decision to deliver both twins at 32 weeks gestation. MICHAEL’s APGAR scores were 9, 9, and 9 at 1, 5 and 10 minutes. MICHAEL remained in the Jackson Memorial Hospital NICU for 28 days and was treated for apnea of prematurity and retinopathy of prematurity. Hyperechoic periventricular regions were noted on head ultrasound studies in the NICU, and a follow-up MR imaging study on January 7, 2015, revealed findings compatible with periventricular leukomalacia. Although MICHAEL has a substantial motor impairment, he is not currently evidencing a substantial cognitive impairment. I further believe that his neurological deficits are a consequence of prematurity and not acquired in the course of labor and delivery. I am therefore not recommending MICHAEL for consideration by the NICA program. In his affidavit, Dr. Duchowny testifies that his opinions are to a reasonable degree of medical probability. A review of the file reveals that no contrary evidence was presented to dispute the findings and opinions of Drs. Willis and Duchowny. Their opinions are credited.
