Findings Of Fact The Respondent is a state agency which initiated a proceeding with the filing of an Administrative Complaint against Marc Richman, D.O. The said complaint was assigned to the Division of Administrative Hearings pursuant to a request for Administrative Hearing pursuant to Chapter 120 and was assigned Division of Administrative Hearing Case Number 88-5258. On June 24, 1989, the Department of Professional Regulations issued a notice of voluntary dismissal in the above captioned proceeding and dismissed all charges against Marc Richman, D.O., in that case. Marc Richman, D.O. is a prevailing small business party within the meaning of Section 57.111(3)(c) and (d). The amount of attorney's fees and cost sought by the Petitioner in the Petition for Attorney's Fees is reasonable for the Representation of Marc Richman, D.O., in the defense of the Administrative Complaint through the date of issuance of the Notice of Dismissal. The Department of Professional Regulation maintains that the proceeds (sic) above-captioned were substantially justified at the time the Administrative Complaint was initiated by the state agency in that it maintains that there existed a reasonable basis in law and fact at the time of the filing of the Administrative Complaint. This position is disputed by the Petitioner, Marc Richman, D.O. The request for attorney's fees in the amount of $8,572.00 and costs of $563.96 for a total of $9,225.96 is reasonable for the representation of Petitioner throughout the instant proceeding. These proceedings were initiated by the filing of a complaint on September 16, 1986 with the Department of Professional Regulation (DPR), Petitioner in Case 88-5258, by the parents of G.H. who died October 18, 1984. G.H. was a long time patient of Dr. Jaffee, D.O. who called in Dr. Richman, an orthopedic surgeon to consult and perform an arthodesis on the left ankle of G.H. to relieve constant pain. G.H. was a 34 year old male accountant who had suffered from juvenile rheumatoid arthritis since the age of 4. Although badly crippled he was able to lead a relatively independent life. As a result of his malady G.H. had for years taken steroid and corticosteroid medications. These medications depress the body's immune system and the ability to fight off infections. Accordingly, G.H. was at more than normal risk anytime he was exposed to infectious diseases. After Petitioner explained the procedure and the risks to G.H., the latter elected to have Petitioner perform the arthodesis. This operation consists of grafting bone into the ankle to stabilize that joint. The donor site chosen for the bone to graft to the ankle was the crest of the left ilium of the patient. This operation was successfully performed on August 2, 1984 at Metropolitan General Hospital, Pinellas Park, Florida. In the hospital on August 9, 1984, while G.H. was being adjusted in his bed, he felt a pop in his left hip and a large hematoma developed over the wound at the donor site. It is not unusual for hematomas to develop over surgical wounds but it is important that such conditions be closely watched because hematomas are a fertile field for an infection. The hematoma on G.H.'s hip showed no evidence of infection and G.H. was discharged from the hospital August 12, 1984 and sent home. Arrangements were made by Petitioner for Robert's Home Health Services, Inc. of Pinellas Park to send a nurse 3 times per week to check on G.H., take his vital signs, dress his wounds and attend to any other medical needs he may have. Verbal reports were made by the nurse to Richman reporting the condition of G.H. While being helped from his wheel chair into bed by his parents on or about August 15, 1984, G.H. apparently fell and caused additional bleeding of the wound on the left hip. On August 16, 1984 the nurse reported to Richman the additional bleeding and she was directed to have G.H. taken to the hospital to be seen by Richman. On August 16, 1984, Petitioner examined the wound, noted the reports that the hematoma was neither inflamed nor more tender, and that G.H.'s temperature had remained normal since the hematoma developed. He sent G.H. back home without further tests. The classic signs and symptoms of infection are redness, swelling, heat and pain. Redness of the skin due to intense hyperemia, is seen only in infections of the skin itself. Swelling accompanies infection unless the infection is confined to the bone which cannot swell. Heat results from hyperemia and may be detected even in the absence of redness. Pain is the most universal sign of infection. Along with pain goes tenderness, or pain to the touch, which is greatest over the area of maximal involvement. (Exhibit 12, Principals of Surgery, Fourth Edition). The hematoma on G.H.'s left hip between its inception and September 13, 1984 never exhibited any sign of infection. On September 6, 1984, G.H. reported to the visiting nurse that he had a pain in his stomach and didn't feel well. The nurse described this as having flu-like symptoms. This was reported to Petitioner and the nurse received no additional orders. On the nurse's next visit on September 10, 1984, G.H. reported his abdomen was still hurting and he didn't feel good. At this time his temperature was elevated at 101. The nurse called Dr. Jaffee's office and was told to have the patient admitted to Metropolitan Hospital. Upon admission to the hospital on September 10, 1984, G.H. was nauseous, vomiting, and had a high fever (103). He had no complaints regarding his ankle or iliac crest and the hematoma had decreased greatly. On September 13, 1984, while G.H. continued showing signs of infection (high fever) Petitioner operated on G.H. to remove the hematoma. At this time aerobic and anaerobic cultures were obtained. Forty-eight and seventy-two hours later these cultures had grown no infectious substance. Further studies and tests revealed that G.H. had bleeding ulcers and surgery was required to patch the ulcers. At this time the spleen was also removed. Following this surgery G.H. was more debilitated and with the precarious condition of his immune system he continued to go down hill until he expired on September 18, 1984. Cause of death was cardiac pulmonary arrest caused by candida septicemia. During the initial stage of the investigation, which was initiated some two years after the death of G.H., the investigator interviewed the parents of G.H., who had filed the complaint, and assembled the medical records including those kept by the home health agency. The parents contended that when the hematoma was removed by Dr. Richman he told the parents that he had found infection at that site. Dr. Richman denies making any such statement to the parents of G.H. and the medical records support the conclusion that there was no infection in the hematoma on September 13, when the hematoma was excised. The parents complained of the treatment that G.H. received from Drs. Jaffee and Richman as well as Roberts Home Health Services. Accordingly the investigation started with both Jaffee and Richman charged with malpractice by the parents of G.H. The investigator selected an orthopedic surgeon, Dr. Richard M. Couch, D.O., from DPR's consulting list and forwarded to him on January 7, 1987, the patient records of G.H. and requested he review those records and give his opinion on whether Drs. Jaffee and Richman diagnoses and treatment of G.H. was appropriate. In this letter (Exhibit 1) the investigator advised Dr. Couch that following surgery a hematoma developed, that after G.H.'s discharge from the hospital the hematoma ruptured and that G.H. was taken back to the emergency room where Dr. Richman saw the patient but found nothing significant about the hematoma. He also told Dr. Couch that when Richman cleaned out the hematoma he advised the family (of G.H.) that infection was found, and that, after this G.H. started internal bleeding which ultimately resulted in the patient's death. Dr. Couch responded to this request with two letters, the first of February 16, 1987 and a second on March 6, 1987. In his first letter Dr. Couch concluded that the iliac wound began draining on or about August 14, 1984 and cultures of this wound were not secured until after G.H.'s hospitalization on September 10, 1984. Since the hematoma was a post-operative complication he opined that Richman failed to adhere to certain tenets regarding wound care in this situation. However, Dr. Couch suggested the records be referred to an internist who reviewed the treatment provided by Dr. Jaffee. In his second letter Dr. Couch opined that Richman was at fault for not incising, debriding and draining the hematoma when it developed and for not taking cultures when Richman saw G.H. in the emergency room on later dates. He also found Richman at fault for not referring G.H. to a consultant in infectious diseases. A letter similar to the letter sent to Dr. Couch was sent by the investigator to Neal B. Tytler, Jr., D.O., an internist. Although the investigator contends he submitted the records maintained by Roberts Home Health Services in this case to Dr. Tytler it is obvious that before he submitted his report on June 5, 1987, Dr. Tytler had not read those records and was concerned regarding the absence of medical records during the period between G.H.'s discharge from the hospital on August 12, 1984, and his readmission on September 10, 1984. In his report Dr. Tytler carefully noted G.H.'s long term medication for juvenile rheumatoid arthritis and the serious side effects, viz depression of the immune system, which results from long-term steroid therapy. Recognizing the risk to G.H. from any surgery Dr. Tytler questioned the wisdom of the arthodesis but recognized that this was more of an orthopedic problem than an internal medicine problem. From the records received, Dr. Tytler concluded that G.H. developed a hematoma after his departure from the hospital and before September 6, 1984. Significantly, Dr. Tytler reported "Of concern to me is the apparent lack of records to document the events which transpired between August 12, 1984 and September 10, 1984. In this one month period an abscess formed at the surgical site and led to disastrous consequences. Unfortunately it can only be inferred that the first recognition of any problem occurred on September 6, 1984, when the patient developed `flu-like symptoms'. He was not examined and no one perceived that his problems were serious." When the probable cause panel met on June 25, 1988 to consider the charges against Drs. Jaffee and Richman, no probable cause was found as to Jaffee. One of the two members of the probable cause panel disclosed at the opening of the panel meeting that he knew Dr. Richman socially and that Richman had been his treating physician for a finger injury. He was excused from further participation and the hearing was tabled regarding Dr. Richman. At a subsequent panel meeting by telephone conference call, after a substitute lay panel member was selected and had been furnished the medical records, a vote was taken to find probable cause. The excerpt from those proceedings (Exhibit 8) shows that the DPR attorney opened the conference call by stating that Richman was charged with medical conduct falling below acceptable minimal standards and "at the last probable cause panel meeting you voted to find probable cause, and asked that administrative complaint be issued. At this time the Department recommends that you do find probable cause to believe that this violation exists." Following receipt of this erroneous information regarding the previous probable cause panel meeting, the Chairman, Mr. Wheeler, stated that after reviewing the entire file he believes probable cause exists to file an Administrative Complaint. Dr. Barker concurred. The case against Dr. Richman began to unravel when the deposition of Dr. Tytler was taken on February 24, 1989. Prior to taking this deposition Dr. Tytler had been provided records from Metropolitan General Hospital, records from Roberts Home Health Services and a copy of the Administrative Complaint. In response to questions regarding the treatment of G.H. as afforded by Dr. Richman, Dr. Tytler stated that a review of all medical records clearly demonstrated that after the hematoma developed at the donor site for the transplant no indication of infection ever appeared; that considering the medical history of G.H. and his high susceptibility to infection it would be more dangerous to the patient to evacuate the hematoma and risk additional infection than it would to continue to observe the hematoma and let it cure itself; that the cultures taken on September 13, 1984, when the hematoma was evacuated clearly and unequivocally demonstrated that the hip wound was not the source of the infection that ultimately led to the demise of G.H.; and that the treatment rendered by Petitioner was in all respects in conformance with required medical standards and procedures. Dr. Tytler further opined that treating an immune compromised patient with antibiotics without a specific infection in mind "could lead to the very scenario that caused his (G.H.) death", namely secondary infection. Further, with respect to the contention of Dr. Couch regarding the failure of Petitioner to take cultures at the hematoma site before September 10, 1984, Dr. Tytler opined that indiscriminate taking of cultures when no evidence of infection is present could result in a positive culture unrelated to the wound but which the doctor would be called upon to treat. This could invite a major change in therapy and an inappropriate prescribing of an antibiotic. Following the deposition of Dr. Tytler, DPR referred the medical records to another orthopedic physician and this doctor concurred with the opinion of Dr. Tytler that Dr. Richman's treatment of G.H. was not below minimally acceptable standards, that no malpractice was involved and that the treatment was in accordance with acceptable medical standards. The Department then dismissed the Administrative Complaint. In his deposition the physician member of the probable cause panel, James H. Barker, D.O., emphasized that his conclusion that probable cause existed to go forward with the Administrative Complaint was significantly influenced by the fact that no culture was done at the hematoma site. From his subsequent testimony it is clear that Dr. Barker was unaware, when he voted to find probable cause, that the culture taken from the hematoma site on September 13, 1984 was negative. The record clearly shows this to be a fact. As stated by Dr. Tytler in his testimony "hematoma yes; infection no." Dr. Barker was also concerned, and perhaps rightly so, that any time that someone goes in for an elective procedure and he dies "that alone makes you think there may be probable cause here." However, there must be factual evidence to support a finding of probable cause and here there was no such evidence.
The Issue Whether Respondent's license as a physician should be disciplined for the alleged violation of Section 458.331(1)(t), Florida Statutes, in that 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, by failing to treat the patient's preoperative coagulopathy and/or failing to use an alternate vein that would have allowed visualization of the shunt placement into the vein thereby reducing the risk of causing a hemorrhage given the patient's preoperative history, and, if so, what penalty should be imposed. AS TO CASE NO. 01-4407PL Whether Respondent's license as a physician should be disciplined for the alleged violation of Section 458.331(1)(t), Florida Statutes, by failing to practice medicine with that level of care, skill, and treatment which is recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances by failing to distally clamp part of the arteries prior to manipulation of the aneurysm and by failing to ensure periodic monitoring of the patient's condition postoperatively for evidence of ischemia or other problems and, if so, what penalty should be imposed.
Findings Of Fact Based on the evidence adduced at the final hearing, and the entire record in this proceeding, the following findings of fact are made: FACTS COMMON TO BOTH CASES Petitioner is the state agency charged with regulating the practice of medicine pursuant to Section 20.42, Florida Statutes, Chapters 456 and 458, Florida Statutes. At all times relevant to this proceeding, Respondent was a licensed physician in the State of Florida, having been issued license number ME 0036360. Respondent is board-certified in thoracic and general surgery. FACTS RELATED TO CASE NO. 01-4406PL Patient D.J.P. was a 54-year-old female with a history of liver resection for carcinoma. Patient D.J.P. had contracted Hepatitis C in the 1960s from a blood transfusion, after being the victim of a gun shot wound during a robbery at a convenience store. Patient D.J.P. subsequently had developed cirrhosis secondary to the Hepatitis C. Cirrhosis is a scarring process of the liver that results in the displacement of the normally functioning liver tissue. A healthy liver processes lymphatic fluid back into the bloodstream. However, a cirrhotic liver cannot properly process the lymphatic fluid back into the bloodstream. Therefore, lymphatic fluid backs up within the liver and weeps out the covering over the liver and into the abdominal cavity. Patient D.J.P. presented to Respondent on February 1, 1994, after being referred to Respondent by Michael Carey, M.D., the primary care physician, for evaluation for implanting a peritoneal venous shunt. A venous shunt is a conduit designed to take ascitic fluid from the abdomen and put it back in the vascular system. The shunt removes the fluid from the abdominal cavity and transports it to the vascular system where it can be absorbed. The procedure is for the patient's comfort and does not prolong the patient's life. The procedure is for patients with end stage liver disease. After obtaining a medical history and conducting a physical examination, Respondent's assessment of the Patient D.J.P. was massive ascites secondary to cirrhosis and previous liver resection. Respondent believed that Patient D.J.P. was a candidate for a venous shunt procedure due to the fact that she was very symptomatic from her massive ascites and she was on the maximum medical therapy. The mortality rate for this type of procedure is between 5 and 25 percent or at the very least, one-in-twenty patients would die from this procedure. Complications associated with this type of procedure include disseminated intravascular coagulopathy (hereinafter referred to as "DIC") which may lead to the general worsening of the disease or death. The patient was informed of this mortality rate as well as of the complications associated with this procedure. Patient D.J.P. decided to think about the procedure and contact Respondent's office when she wanted the shunt inserted. On February 10, 1994, Patient D.J.P. called Respondent's office and asked to have the shunt inserted as soon as possible. Respondent scheduled the procedure for February 14, 1994, and signed the written surgical consent form. Prior to the surgery, lab tests were performed on Patient D.J.P. The lab report indicated that the patient's prothrombin time was 14.3, with a normal range being 10.7-12.8. Prothrombin time ("PT") is a measurement of one aspect of the blood clotting mechanism. This was considered slightly abnormal and not an indication of a clotting problem or coagulopathy. Respondent decided it was not necessary to address Patient D.J.P.'s abnormal PT prior to the procedure by preoperatively administering Vitamin K or fresh frozen plasma. On February 14, 1994, Patient D.J.P. was transported to the operating room at approximately 12:10 p.m. After Patient D.J.P. was placed under general anesthesia, Respondent began the venous shunt operation at approximately 12:34 p.m. Respondent attempted to access the right jugular vein to insert the shunt. He found this vein to be unusable because it was too scarred from previous surgeries. Respondent then proceeded to access the right subclavian area to insert the shunt. Once the shunt was inserted into the subclavian area, Respondent positioned it in the superior vena cava. The shunt was noted to be in position in the superior vena cava. Respondent then removed eight liters of ascitic fluid from the abdominal cavity. After removing the ascitic fluid, he then put one liter of saline into the abdominal cavity to dilute any remaining ascitic fluid which allowed any remaining fluid to be more easily absorbed into the vascular system. The Patient's central venous pressure dropped from 8 to 2. Hespan and Albumin were then administered to replace any lost volume and it helped to increase the colloidomotic pressure. At this point, Patient D.J.P.'s central venous pressure (CVP) increased from 2 to 14 or 15. This is a faster than normal rate. Upon finding that the shunt was operating well, Respondent closed the abdominal portion and the patient was extubated. Petitioner claimed that fluoroscopy was not used to ensure that the shunt was positioned in the proper place. A Fluoroscope is like a real-time X-ray. A fluoroscope has two parts to it: a C-arm, which goes above the patient and underneath the bed, and two screens where the doctor can see what is going on. The C-arm is approximately 5-and-a-half feet tall. It is below the standard of care to do a venous shunt procedure without using a fluoroscope. It would enable Respondent to visualize the placement of the shunt. Felicia Whitmer, a scrub technician, and Rene Myers, a circulating nurse, prepared the operating room for Patient D.J.P.'s procedure on February 14, 1994. Both Felicia Whitmer and Rene Myers testified that there was no fluoroscope in the operating room on February 14, 1994. Respondent testified that there was a fluoroscope in the operating room on February 14, 1994, during Patient D.J.P.'s procedure and that he used it to assist him. The evidence is not clear and convincing that the fluoroscope was not used during the course of the operation. It is considered within the accepted standard of care to access the right subclavian vein to insert a shunt of this type because this vein follows a gentle curve or path. With this gentle curve in the vein, there is less risk of damage, i.e. puncture, to the vein. In contrast, the left jugular vein follows a more sharp-angled 70-degree bend-curve in the vein where one risks the danger of the shunt coming out of the bottom of the vein or perforation and, thereby, damaging the vein. Respondent ordered an X-ray to confirm placement of the shunt and catheter. The X-ray revealed that the shunt had good positioning but the right lung was filled with fluid. The patient was re-intubated and Respondent inserted a chest tube into the patient which would expand the patient's lung, oxygenate the patient and allow for fluid removal. Three or four liters of fluid were removed. The fluid was originally serous and pink tinged and shortly thereafter, turned bloody. Respondent noted that there was bruising around the wounds. Additionally, the patient's breathing became shallow and her blood pressure began to deteriorate. Resuscitative efforts were performed and Respondent re- entered the shunt area to clamp the shunt to prevent any ascites from flowing into the venous system and to prevent further coagulation and massive bleeding. Despite heroic resuscitative efforts, the patient's condition continued to deteriorate and the patient died. The cause of death was determined to be DIC and severe coagulopathy from drainage of the ascitic fluid into the venous system. Respondent made the determination that the patient did not have preoperative coagulopathy. Respondent testified that if the patient did have preoperative coagulopathy, he would not have performed the procedure because the patient would not be able to make the clotting factors well enough for problems that would occur after the shunt was inserted. It was Respondent's opinion that the patient did not have a serious clotting problem. Based on her lab report, Patient D.J.P. had a slightly abnormal PT and this was not an indication of a clotting problem. Respondent reviewed the lab reports and determined the PT (the measurement of one aspect of blood clotting mechanism), to be only slightly elevated. It measured 14.3 with a normal range being 10.7-12.8. Moreover, the PT International Normalized Ratio (INR) (which is the standardized measurement of PT) was 1.63 where the therapeutic range was 2-3. Therefore, this was slightly below average. Dr. Yahr testified that an abnormal clotting problem is a clinically evident problem and not an incident of a lab number. If Patient D.J.P. had a clotting abnormality, adverse conditions or symptoms would have been evident with the incisions that were made prior to the shunt being opened. Rather, normal clotting reactions occurred. Coagulation occurred right after the shunt was opened and the ascitic fluid began to flow into the atrium. Dr. Yahr testified that the etiology of the coagulation was the body's reaction to the ascitic fluid after the shunt was opened. Accordingly, it was Dr. Yahr's opinion that Respondent did not fail to treat the preoperative coagulopathy because upon his examination of the patient, he determined that no such preoperative coagulopathy existed prior to the procedure. Dr. Yahr testified that the patient did not have abnormal bleeding. Her liver failure was the result of scarring and abnormal liver function. Therefore, administration of clotting factors such as Vitamin K and fresh frozen plasma was not indicated or medically necessary. Petitioner presented the expert testimony of John W. Kilkenny, III, M.D. Dr. Kilkenny is board-certified in general surgery and has been for 11 years and is currently a professor with the University of Florida College of Medicine, Department of Surgery in Jacksonville, Florida, a position which he has held for the last six years. According to Dr. Kilkenny, Patient D.J.P.'s elevated PT was a cause for concern in that it was an indication that the patient's ability to clot or coagulate was diminished. It is not clear and convincing that the standard of care required that the elevated PT be treated by infusing fresh frozen plasma or Vitamin K. Respondent did not violate Section 458.331(1)(t), Florida Statutes, by failing to use an alternate vein that would allow visualization of the placement of the shunt. Respondent first attempted to access the right jugular vein to insert the shunt but found it be unusable because it was too scarred. Respondent, acting as a reasonably prudent physician and using sound medical judgment, accessed the right subclavian area to insert the shunt. After the shunt was inserted into he subclavian vein, Respondent claimed he was able to visualize the placement of the shunt by the use of fluoroscopy. Furthermore, the operative notes seemed to indicated that the procedure was performed under fluoroscopic control and the shunt was found to be in position. Therefore, Respondent accessed an appropriate alterative vein-the subclavian vein, which allowed visualization, with the assistance of fluoroscopy, of the placement of the shunt. As to the second issue, Dr. Kilkenny opined that the standard of care requires direct visualization for insertion of the shunt. By not accessing a vein under direct visualization, such as with Respondent's subclavian approach, the surgeon is, in essence, hunting for the vein, and risking damage to the wall of the vein that may not be evident immediately. The rapid rise in CVP from 2 to 14 or 15 was also a concern for Dr. Kilkenny because it was not normal, and did not mean that the shunt was placed correctly of that the shunt was functioning properly. Dr. Kilkenny noted that it was unlikely that the bleeding in the chest cavity was caused by damage to an intercostals vessel when the chest tube was inserted because the chest X-ray that was taken prior to insertion of the chest tube showed a complete opacification of the right side and a shifting of the major vessels within the middle of the chest over to the left side. According to Dr. Kilkenny, the chest X-ray indicated that there had already been some sort of bleeding in the right chest prior to the insertion of the chest tube. Dr. Kilkenny disputed Respondent's theory that Patient D.J.P. died as a result of DIC. Dr. Kilkenny asserted that Respondent fell below the standard lf care in that, given Patient D.J.P.'s rapid decompensation, he failed to consider whether the patient's subclavian vein had been damaged, a condition which could have been addressed surgically. Dr. Yahr opined that Patient D.J.P. died of DIC that occurred within a short period of time after Respondent opened up the shunt and ascitic fluid was introduced into the atrium of the heart. Although Dr. Yahr further admitted that the bleeding in the chest could have occurred as a result of damage to the subclavian vein, and that it was below the standard of care to access the subclavian vein without using fluoroscopy, the evidence is not clear and convincing that either event occurred. It is found that Petitioner has failed to establish by clear and convincing evidence that the standard of care required Respondent to use an access site that allowed direct visualization of the placement of the shunt into the vein, or that Respondent failed to use fluoroscopy in order to directly visualize insertion of the shunt into the subclavian vein. AS TO CASE NO. 01-4407PL On August 22, 1997, Patient H.H., a 55-year-old female, was diagnosed with an abdominal aortic aneurysm measuring approximately 4.5 cm transverse diameter and beginning approximately 1-2 cm below an enlargement or swelling, of a blood vessel resulting in a weakening or thinning out of the vessel wall. On November 28, 1997, Patient H.H.'s aneurysm had grown to 5 cm within a three-month period and was occluded with partial thrombosis with a true lumen around 2.7 cm and extended down to the bifurcation of the abdominal iliac. This put the patient at risk for rupture of the aneurysm. Thrombosis is a blood clot within a vessel or within the vascular system. It does not embolize (travel) from another part of the body. It starts in a particular vessel and causes its damage from there. It is an acute clot that occurs in the vessel secondary to stasis (non-moving ) or some kind of coagulation or clotting deficiency or abnormality. Thrombotic activity most often begins by occluding the smaller vessels in the vascular system, such as those smaller veins located in the feet. On December 2, 1997, Patient H.H. first met with Respondent, who performed a complete medical history and physical examination and confirmed the presence of a 5 cm abdominal aneurysm. Patient H.H. was a 55-year-old female who smoked 1- and-a-half packs of cigarettes per day, had a blood pressure of 182/104 despite the fact that she was taking 50 mg Atenolol for hypertension (high blood pressure), and had a 30 percent blockage of the coronary artery. Previously, she had a cardiac catheterization, followed by an angioplasty of the femoral vessel in her left leg. Patient H.H. advised Respondent that her legs gave out on her after she walked two blocks, but that she did not have associated chest pain. Respondent confirmed earlier diagnosis of Patient H.H.'s medical condition as single vessel coronary artery disease, abdominal aortic aneurysm, hypertension, and claudication with femoral occlusive disease. Respondent also found diminished femoral pulses and palpable Dorsal pedal pulses present in both feet. Patient H.H.'s medical records indicated that this smoker of 30 years suffered from diabetes, peripheral vascular disease, intermittent clottication of the leg, hypertension, atherosclerotic disease, hypercoagulopathy, anthithrombin III deficiency, high cholesterol, and diminished protein and pH levels. Respondent prescribed prescription medication, Procardia to lower Patient H.H.'s blood pressure and Zyban to help her stop smoking. He recommended that the patient return in a week for follow-up. On December 15, 1997, Respondent continued to prepare Patient H.H for surgery. He again advised her to stop smoking and to purchase and take medication to help her stop smoking. Patient H.H.'s blood pressure was lower, 144/84, and although she had not purchased or taken the medication, she reduced her smoking down to one-half pack of cigarettes per day. Respondent then advised Patient H.H. to make plans to undergo the abdominal aortic aneurysm ("AAA") repair. Patient H.H. informed Respondent that she wanted to wait a little longer while she made financial arrangements to pay for the surgery. Respondent advised Patient H.H. to completely quit smoking before the surgery and advised her to return in one month for additional preoperative evaluation. On January 12, 1998, Respondent continued to prepare Patient H.H. for surgery by ordering a cardiac clearance (thallium evaluation) of the patient's heart to ensure she could tolerate the surgery before attempting the AAA repair. On February 3, 1998, Patient H.H. presented for the thallium evaluation of the heart and, on February 9, 1998, obtained cardiac clearance for repair of the AAA. On February 11, 1998, Respondent continued to prepare Patient H.H. for AAA surgery and suggested she donate two units of blood which would be used during the surgical procedure. Respondent scheduled AAA repair surgery for March 6, 1998. Respondent advised Patient H.H. of the risks associated with AAA surgery and specifically mentioned the risk of a heart attack, bleeding, kidney damage and loss of legs. He also advised that the risks associated with intra-operative AAA repair include spontaneous rupture, embolization of material from the wall distally, myocardial infarction, bleeding, injury to viscera of the small vessels, devascularization of the colon causing ischemic colitis, death, kidney blockage. Patient H.H. indicated she understood the risks and despite the risks associated with this type of surgical procedure, including the risk of death, she agreed to the procedure. Preoperative testing by angiogram was not required for Patient H.H. The aneurysm was a massive aneurysm presenting a very serious health risk of imminent rupture. The size of Patient H.H.'s aneurysm (5 cm) made AAA repair an emergency in a sense because there was almost a 100 percent chance of rupture with in the next six months. Any findings determined by angiogram would not have changed the outcome of the case because Respondent had to definitively treat the aneurysm first. Additionally, an angiogram is a very expensive test and Patient H.H. expressed a concern about her financial situation with respect to the AAA repair. It is reasonable to not do studies that a physician does not feel are absolutely necessary. The patient's financial concerns are part of the pathology. On March 6, 1998, Patient H.H. was admitted to Winter Haven Hospital and filled out and signed the Special Authorization for Medical and/or Surgical Treatment form indicating her consent to the surgical procedure which Respondent was to perform. She indicated that she understood the risks associated with such surgical procedure. Paragraph two of the informed consent form states in pertinent part: I hereby certify that I have given complete and informed consent for the above named operation and/or procedures, and Dr. L. Thomas has explained to me the reason why the above-named operation and/or procedure are considered appropriate, its advantages and possible complication, if any, as well as possible alternative modes of treatment. I also certify that no guarantee or assurance has been made as to the results that may be obtained. The operative procedure on the consent form was signed by Patient H.H. at 6:10 a.m. on March 6, 1998. Surgery indicated on the consent form was for a resection abdominal aortic aneurysm (AAA repair). After Patient H.H. was taken to the operating room and administration of anesthesia began, Respondent performed his routine preoperative check of femoral and pedal pulses. Checking for femoral and pedal pulses is the type of preoperative work-up Respondent routinely performs while he waits for the anesthesia to take its effect on the patient. The operative report indicates that the abdominal aneurysm was "very large" extending quite high within 1-2 cm from the renal vein and down to and involving the common and hypogastric arteries and noted to be "quite saccular" with "impending rupture in the near future at the neck." The common iliacs were noted to be "quite large and aneurysmatic." The external iliacs were soft but extremely small, "approximately 4-5 mm in size, certainly less than half, more like 1/4 the size of a normal iliac" but nevertheless usable vessels to make his anastomosis. As Respondent was bluntly dissecting (separating the tissues using the fingers) the aortic aneurysm from the venous plexus to position his proximal clamp when one of the lumbar veins was encountered and mass bleeding occurred. The venous plexus is a grouping of veins located under the aorta that can best be described as a wagon wheel. The system has a hub and all the veins in the grouping extend outward from the hub. If one of the veins in the grouping is injured, it will bleed heavily, but the bleeding is controllable. The lumbar veins are part of the venous plexus and a tear of the lumbar vein is a known risk during this type of surgery. Patient H.H. suffered the loss of three times the amount of blood as would have been routinely expected. The sudden blood loss caused the patient's condition to rapidly deteriorate. Dr. Wickstrom-Hill, Anesthesiologist, testified that had Respondent not controlled the blood loss, and had not maintained Patient H.H.'s vital signs, she would have died. Using sound medical judgment, Respondent elected to bypass the aneurysmatic common iliacs and make his anastomosis of the graft to the external iliacs in order to not disconnect or separate the aortic or common iliac aneurysms from the iliac vein. This is a very fragile vessel and could have resulted in further massive bleeding and possible death of the patient. A reasonable prudent physician faced with a similar circumstance and situation would not attempt to mobilize the aneurysm further if doing so would cause additional massive blood loss and possible death of the patient. The hypogastric arteries (a/k/a the internal iliacs) serve to provide the pelvic viscera (bladder, rectum, etc.) with blood. During the AAA repair, Respondent performed an embolectomy on both legs following manipulation of the aneurysm. The purpose of this procedure was to remove any debris which may have dislodged from the aneurysm and flowed distally to the legs. The procedure involves running a Fogarty catheter down the femoral arteries as far as the catheter will go, then inflating a balloon located at the end of the catheter. Once the balloon is inflated, the surgeon will extract the catheter, pulling the debris out of the artery. This process is repeated as necessary to remove all debris. Fresh clot was obtained from both legs, indicating a lack of debris. Prior to completing the anastomosis of the bifurcated graft to the aorta and external iliacs respectively, Respondent ran a Fogarty catheter down proximal (back into the graft itself), to remove any debris in the graft itself. Finally, he back-bled the graft (allowed blood to flow out of the graft, to, again, ensure that there existed no debris in the graft). On March 7, 1998, Patient H.H.'s medical condition stabilized such that Respondent felt it safe to return Patient H.H. to the operating room to undergo an additional embolectomy of the legs and an endarterectomy of the right femoral artery. The record demonstrates that Respondent believed he collected embolic debris from the femoral arteries. However, based upon the pathology report and the testimony of Dr. Zeller, the debris removed from Patient H.H. during this procedure was acute blood clots and atherosclerotic plaque. This finding is consistent with thrombotic material and not a result of debris coming from another location as it tends to demonstrate that Patient H.H. had a clotting disorder consistent with her medical history. The record also demonstrates that upon completion of the procedure, Patient H.H. was noted to have excellent pulses in the superficial and profunda femoral arteries distal to the anastomosis with good emptying and filing of the vessels. Before, during, and after the AAA repair, Respondent used Heparin (an anti-clotting drug) in an effort to prevent the formation of clots throughout Patient H.H.'s vascular system. Intraoperatively, on March 3, 1998, Respondent administered 10,000 units of Heparin. Normally a patient will respond to 5,000 units. Despite giving Patient H.H. twice the normal amount of Heparin, Patient H.H. continued to have a lowered clotting time. It is noted in the medical record that Patient H.H. had an Antithrombin III deficiency. Antithrombin III is one of the factors that control how blood in the human body clots. Patient H.H.'s Antithrombin III deficiency is a hereditary defect that contributed significantly to her continued clotting despite the use of pharmacological intervention (substantial amount of Heparin). Respondent testified that in his medical training and experience, Patient H.H.'s Antithrombin III deficiency level was near fatal. Because Patient H.H. was hypercoagulative, thus causing the small vessels to clot off, on March 13, 1998, Patient H.H. underwent bilateral above the knee amputations. Hypercoagulopathy is a tendency to clot without anything being done - the blood just clots. This can be caused by a lower-than- normal blood pressure for a period of time and by having an Antithrombin III deficiency. Respondent observed during the surgery that this patient was hypercoagulative because he could see the blood clotting in the wound despite the fact that Patient H.H. was on twice the normal amount of Heparin. Respondent practiced within the standard of care at all times during the treatment of Patient H.H. Blood-flow going retrograde back into the common and iliac aneurismal sacs did not place Patient H.H. at a risk of rupture. The operative report clearly demonstrates that the aortic aneurysm involved the common iliacs and extended below the hypogastric arteries. The operative report also demonstrates that the external iliacs were extremely small, approximately one-quarter of the normal size. A reasonable and prudent surgeon, faced with a similarly situated patient with a massive sized aneurysm and the extremely small size of the distal external iliacs, would conclude that the pressure gradient now being carried to the graft rather than to the aneurysm would diminish flow to the aneurysms making the possibility of rupture unlikely. Moreover, the aneurysms were filled with calcified atherosclerotic plaque and other thrombotic (non-mobile) material. Dr. Begelman testified that calcified aneurysms do not tend to rupture as much. On direct examination, Dr. Begelman, Petitioner's expert, could not conclusively determine whether Respondent's surgical treatment of Patient H.H. fell below the standard of care and that distal clamping is an intra-operative decision to be made by the surgeon. Dr. Begelman who testified that he accepted Respondent's opinion that the iliacs were too large or too thin walled and could not distally clamp the aneurysm and that such decisions are those made by the surgeon on the case. Drs. Begelman and Seller and Respondent testified that it is usual and customary during this type of surgical procedure to distally clamp the aorta and that it is expected of a reasonable and prudent surgeon to make every attempt to do so. Nevertheless, all three doctors recognized that there are times when you cannot or should not distally clamp if to do so would cause further injury to the patient or death. Patient H.H. presented with very massive aneurysms of both the aorta and common iliacs making distal clamping impossible without sacrificing the hypogastric arteries thus placing Patient H.H. at risk for further injury or death. Petitioner's expert accepted Respondent's assessment of the condition of the iliacs and that Respondent did not want to dissect the iliacs off the iliac vein, which one needs to do in order to tie off distally. Dr. Begelman testified that he could not ascertain whether Respondent fell below the standard of care with respect to Respondent's treatment of Patient H.H. intraoperatively. Respondent acted within the standard of care and, therefore, did not violate Section 458.331(1)(t), Florida Statutes, when he did not clamp the distal arteries before manipulation of the aneurysm. Respondent did not violate Section 458.331(1)(t), Florida Statutes, by sewing the bifurcated graft to the external iliacs and making no attempt to disconnect the aneurysm from the common and internal (a/k/a hypogastric) iliacs. The common and internal iliac tissues were also diseased because of their involvement with the aneurysms coupled with the fact that the aneurysm and surrounding tissue was inflamed. Inflammation causes the tissues of the surrounding viscera to become sticky and by that, stick together making separation difficult and more prone to bleeding on manipulation. Normally, the surgeon must bluntly dissect (lift up) the distal end of the aorta in order to place the distal clamps on the aorta below the aneurysm. However, the inflammation present in Patient H.H.'s aorta made it impossible to mobilize (lift up) the distal aorta for clamping because the tissue was stuck to the iliac vein which could have caused Patient H.H. to suffer a lethal blood loss. Normally, blood loss associated with this type of surgery amounts to 500 ccs for the total surgery. Patient H.H. lost 1500 ccs during the manipulation of the aortic aneurysm to place the proximal clamp and a total of 2400 ccs during the entire surgery which represented a blood loss of nearly 25-40 percent respectively of her estimated total blood volume. Respondent used sound medical judgment by making no attempt to dissect the common iliac from the subordinate tissue because, in his training and experience, the separation of tissues would have caused further, possible lethal bleeding. Drs. Begelman and Zeller, experts for Petitioner and Respondent respectively, testified that a reasonably prudent surgeon would not clamp below the common iliacs if to do so would sacrifice the hypogastric arteries and thereby cause irreparable harm or death to the patient. Dr. Zeller testified that the hypogastric arteries are of such importance that not clamping them, even at the risk of embolization, would nevertheless be within the standard of care. Respondent closely monitored Patient H.H. postoperatively. A reasonable and prudent surgeon is not expected to remain in the recovery room with his post-surgical patient until the patient becomes stable. Rather, the reasonable and prudent surgeon is expected to utilize the nursing staff who are charged with attending to the patient and to keep the physician updated on the patient's medical condition. Petitioner's witness, Doris Gutierrez, was the recovery room nurse on duty on March 6, 1998. Her duties included monitoring and reporting changes in Patient H.H.'s condition to Respondent. The record demonstrates that Respondent closely monitored Patient H.H. postoperatively by being in contact with the nursing staff and thereby giving orders for care and treatment to the nursing staff, either by telephone orders ("TO") or in person by verbal orders ("VO") to stabilize the patient. While in the recovery room, Patient H.H. was intubated, on a respirator. Petitioner's witnesses, Doris Gutierrez, confirmed Respondent's monitoring of Patient H.H. when she testified that she called Respondent several times to provide updates on Patient H.H.'s condition. The record demonstrates that postoperatively on March 6, 1998, Respondent wrote his initial order to the nursing staff at 12:30 p.m. while sitting in post-surgical recovery with Patient H.H. Thereafter, Respondent continued to monitor Patient H.H.'s condition and remained in communication with the nursing staff and wrote orders at 1:30 p.m., 2:30 p.m., 3:25 p.m., 5:00 p.m., 5:15 p.m., 8:15 p.m., and again on March 7, 1998 at 12:24 a.m. Following his TO on March 7, 1998, at 12:24 a.m., Respondent next saw Patient H.H. 7 1/2 hours later, at 8:00 a.m., prior to taking Patient H.H. to the surgery room to perform the endarterectomy and embolectomy. Ms. Gutierrez testified that she does not always note when the doctor comes back into the recovery room to give orders. She could not testify as to events that took place after Patient H.H. was transferred to the Surgical Intensive Care Unit ("SICU"). She also stated she did not know how many times Respondent went to SICU because she did not work in SICU when Patient H.H. was transferred out of the recovery room. Ms. Gutierrez was also unable to testify as to when the last time was that Respondent came to the recovery room. Respondent testified that there is a difference between a TO and a VO, the latter indicating that the physician was present in the room at the time he gave his order to the nurse. The evidence is not clear and convincing that Respondent did not provide appropriate postoperative monitoring of Patient H.H.
Recommendation Based on the foregoing Findings of Fact and Conclusions of Law, it is RECOMMENDED that the Board of Medicine: Enter a final order dismissing with prejudice the Administrative Complaint filed against Respondent in DOAH Case No. 01-4406PL, and DOH Case No. 1994-12341. Enter a final order dismissing with prejudice the Administrative Complaint filed against Respondent in DOAH Case No. 01-4407PL, and DOH Case No. 1999-57795. DONE AND ENTERED this 8th day of August, 2002, 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 8th day of August, 2002. COPIES FURNISHED: William R. Huseman, Esquire Romualdo C. Marquinez, Esquire Huseman, Marquinez & Schlegal, P.A. 6320 St. Augustine Road, Building 12 Jacksonville, Florida 32217 Kim Kluck, Esquire Richard J. Shoop, Esquire Agency for Health Care Administration Post Office Box 14229, Mail Stop 39A Tallahassee, Florida 32317-4229 Dr. John O. Agwunobi, Secretary Department of Health 4052 Bald Cypress Way, Bin A00 Tallahassee, Florida 32399-1701 William W. Large, General Counsel Department of Health 4052 Bald Cypress Way, Bin A02 Tallahassee, Florida 32399-1701 R. S. Power, Agency Clerk Department of Health 4052 Bald Cypress Way, Bin A02 Tallahassee, Florida 32399-1701 Tanya Williams, Executive Director Board of Medicine Department of Health 4052 Bald Cypress Way Tallahassee, Florida 32399-1701
The Issue This is a license discipline case in which the Petitioner seeks to take disciplinary action against the Respondent on the basis of alleged violations of Section 458.331(l)(m) and (t), Florida Statutes. In this regard it is alleged that the Respondent failed to keep medical records justifying the course of treatment of a patient and also failed to practice medicine with an acceptable level of care, skill and treatment.
Findings Of Fact The Respondent graduated from the University of Maryland Medical School in 1981 and then went on to State University of New York at Stoney Brook where he did an internship and residency for four years in general surgery. He was licensed in Florida in 1985 and, since then, has been practicing emergency medicine in Florida. In January 1992, patient H. G. was hospitalized at Parkway Regional Medical Center (Parkway) under the care of Malcolm G. Goldsmith, a board certified colorectal surgeon. The patient had been a patient of Dr. Goldsmith’s for two or three months prior to admission. The patient was hospitalized for the purpose of reconnecting his intestine after a prior colostomy with detachment of the rectum. Dr. Goldsmith admitted the patient and performed surgery on him. The patient was discharged from Parkway six days after the surgery. At that time he was on a regular diet, was having bowel movements and was ambulatory. The patient, upon discharge on January 27, 1992, remained the patient of Dr. Goldsmith and was given instructions regarding diet, activity, wound care, and pain medications, and was told to return in two weeks for removal of the staples or sutures. He was also instructed to let Dr. Goldsmith know about any unusual difficulties or problems. In the early morning of January 28, 1992, the Respondent was working the 7:00 p.m. to 7:00 a.m. shift at Pembroke Pines Hospital (PPH) when the patient presented with severe abdominal pain and nausea without emesis. The patient stated that he had recently had abdominal surgery, had been released the previous afternoon from the hospital, had been having bowel movements and had been tolerating food for a couple of days. The patient was awake, alert, and able to provide his history to the Respondent. The Respondent obtained a history from the patient and noted that he had a fever of 100.8. He then physically examined the patient’s abdomen noting in the medical record, “abdomen bowel sounds positive but decreased. Firm, distended diffused tenderness.” The Respondent also ordered a complete blood count (CBC) and an x-ray of the abdomen. Although he did not note his findings in the medical record, the Respondent read the x-ray as showing the patient had some dilated small bowel loops with some air-fluid levels which he interpreted as an ileus, a lack of proper motion of the small intestine. The Respondent read the CBC which showed a shift to the left which the Respondent interpreted as showing the patient having either an infeciton or aon inflammatory process going on. A shift to the left could be caused by sepsis which could be caused by a wound infection, which is not an unusual postsurgical event. At 5.55 a.m., after examination of the patient and reading the x-ray and laboratory report, the Respondent telephoned Dr. Goldsmith and consulted with him about the patient. He told Dr. Goldsmith of the results of his physical exam, the blood test results and his interpretation of the x-ray. After discussing the matter, the two physicians agreed that the patient should see Dr. Goldsmith later that same morning at Dr. Goldsmith’s office. Dr. Goldsmith did not have privileges at PPH. The Respondent then gave the patient a pain medication shot (effective for about four hours duration) and told the patient to follow up in four hours with Dr. Goldsmith or Dr. Schalen (the surgeon who was on call that day and on the staff at PPH). The Respondent then authorized the discharge of the patient, noting his diagnosis in the medical records as, “Abdominal pain secondary to surgery.” At discharge, the patient signed the following statement in his medical record: I acknowledge that I have been informed of and understand all of the instructions given to me and have received a copy thereof. I have been instructed to contact a physician as soon as possible for continued medical diagnosis and care, if indicated. I do not have any more questions at this time, but understand that I may call the Emergency Service Department at any time should I have any further questions or need assistance in obtaining follow up care. After being discharged from PPH, the patient delayed in contacting Dr. Goldsmith and was not seen by Dr. Goldsmith until 4:00 or 5:00 p.m. on January 28, 1992. At that time he was obviously sick primarily, in Dr. Goldsmith’s opinion, because he was dehydrated. Dr. Goldsmith ordered laboratory findings which showed a normal white cell count of 8,000 and a very minimal shift to the left. The patient did not have a fever and there were no signs in Dr. Goldsmith’s examination of the patient’s abdomen suggesting a peritoneal inflammatory process. According to both Dr. Mead and Dr. Goldsmith, the minimal shift to the left, late in the afternoon of the 28th is inconsistent with a diagnosis of sepsis. Sometime after being admitted to Parkway, and while under Dr. Goldsmith’s care, the patient died. His proximate cause of death was that he vomited, aspirated the vomitus into his lungs and sustained a cardiac arrest. Petitioner’s expert, Dr. Meade, agrees that Respondent is not responsible for the proximate cause of death of the patient. The Respondent went off duty at PPH at 7:00 a.m. Sometime after 8:00 a.m., after conducting an “overreading” of the x-ray, a PPH radiologist interpreted the x-ray as a probable 4444distal colonic obstruction, an interpretation different from that of the Respondent’s. The radiologist’s interpretation is inconsistent with the patient’s history of having bowel movements and tolerating food. The fact that the radiologist had a different interpretation of the x-ray is not proof of any deviation by Respondent from the standard of care required in this case. The Respondent was not notified of the radiologist’s interpretation and was not responsible for notification or recall of the patient after going off duty. PPH had a method for notification and recall of patients in such a situation. That system involved contacting the ER doctor on duty. The medical record shows that PPH staff left a message with the family late in the afternoon of January 28, after the patient had already been readmitted to Parkway Hospital, and spoke to the wife that evening regarding the radiologist’s findings. In his care of the patient, Dr. Galitz was responsible for judging the severity of the abdominal pain, the acuteness of the condition, and for determining whether to admit the patient to the hospital or release him. His physical examination and the tests and x-rays ordered were all appropriate. He appropriately undertook a “consultation” with the patient’s surgeon, Dr. Goldsmith, obtained his recommendation and advice and then decided to discharge the patient. If the patient is stable, it is appropriate to discharge him with a recommendation that he follow up in the morning with his doctor. At the time that the Respondent discharged the patient, he reasonably believed that the patient was stable and that discharge of the patient would not compromise his safety. It is clear from the evidence in this case that the Respondent secured and took into account all of the relevant facts available regarding the patient’s medical condition, consulted with the patient’s surgeon, and then made a reasonable and appropriate decision to discharge the patient to see his surgeon within four hours. The examination, consultation, test interpretations and decisions of Dr. Galitz in this case were consistent with the standard of care recognized by a reasonably prudent similar physician as being acceptable under similar conditions and circumstances.
Recommendation On the basis of all of the foregoing, it is RECOMMENDED that the Board of Medicine issue a Final Order in this case dismissing all charges against the Respondent. DONE AND ENTERED this 20th day of December, 1996, in Tallahassee, Florida. MICHAEL M. PARRISH Administrative Law Judge Division of Administrative Hearings The DeSoto Building 1230 Apalachee Parkway Tallahassee, Florida 32399-3060 (904) 488-9675 SUNCOM 278-9675 Filed with the Clerk of the Division of Administrative Hearings this 20th day of December, 1996.
The Issue The issues in this case for determination are whether Respondent Samuel Cox, M.D., committed the violations of Chapter 458, Florida Statutes, as alleged in an Administrative Complaint filed by the Department of Health on November 18, 2006; and, if so, what disciplinary action should be taken against his license to practice medicine in Florida.
Findings Of Fact The Parties. Petitioner, the Department of Health (hereinafter referred to as the "Department"), is the agency of the State of Florida charged with the responsibility for the investigation and prosecution of complaints involving physicians licensed to practice medicine in Florida. § 20.43 and Chs. 456 and 458, Fla. Stat. Respondent, Samuel Cox, M.D., is, and was at the times material to this matter, a physician licensed to practice medicine in Florida, having been issued license number ME 77851 on April 22, 1999. Dr. Cox's mailing address of record at all times relevant to this matter is 2438 East Commercial Boulevard, Fort Lauderdale, Florida 33308. Dr. Cox is a board-certified general surgeon who has specialized his practice to bariatric surgery. He has performed bariatric surgery since 1985, performing approximately 3,000 such surgeries since that time. Dr. Cox has performed approximately 214 Roux-en Y procedures in Florida. No evidence that Dr. Cox has previously been the subject of a license disciplinary proceeding was offered. Bariatric Surgery. Bariatric surgery, also known as gastro-bypass surgery, is a type of surgery performed on morbidly obese patients to assist them in losing weight. In order to be found to be morbidly obese and, therefore, to be considered a candidate for the procedure, a patient must be found to have a Body Mass Index greater than 40. Body Mass Index is a measure of body fat based on height and weight (weight in kilograms divided by the square of height in meters). For example, a six-foot-tall individual weighing 296 pounds would have a Body Mass Index of 40.1. See http://www.nhlbisupport.com/bmi/. A patient with a Body Mass Index of 35 may also be considered a candidate for the surgery if they present with certain comorbidities associated with obesity. Comorbidities are physical problems associated with obesity and include diabetes, lung problems, heart problems, and high blood pressure. The more comorbidities a patient has, the higher the risk is to that patient from bariatric surgery. While there is more than one type of bariatric surgery, at issue in this case is a procedure known as Roux-en-Y gastric- bypass surgery (hereinafter referred to as "RNY Surgery"). RNY Surgery is a surgical method of creating a reduced-sized stomach. This reduced-sized stomach is created by removing a small portion of the stomach, where the esophagus (which brings food from the mouth to the stomach) attaches to the stomach, from the larger remaining portion of the stomach. The small portion of the stomach attached to the esophagus is then formed into a pouch, creating a much smaller stomach. The remaining larger portion of the stomach is completely by-passed. Often a device called a silastic ring is used at the bottom of the newly created stomach to help the pouch maintain the desired size and prevent it from stretching into a larger pouch. A portion of the small intestine is attached to the bottom of the newly created stomach. Approximately 150 centimeters down the small intestine, the excluded or removed portion of the stomach, the liver, and the pancreas are connected back to the intestine. This allows digestion of food to continue, but reduces the amount of digestion that previously occurred in the 150 centimeters of the intestine which are bypassed. RNY Surgery allows a patient to lose weight in two ways: first, by limiting the amount of food the patient can eat; and secondly, by reducing the absorption of nutrients by bypassing part of the intestine. The most common and serious complication of RNY Surgery is a leak at the gastrojejunal anastomosis, or the point where the newly created stomach pouch (the gastro) is connected to the intestine (the jejunal)(a gastrojejunal anastomosis leak will hereinafter be referred to simply as a "Leak"). This complication may be evidenced by several symptoms exhibited by a patient. Surgeons performing bariatric surgery must look for these symptoms. The typical symptoms of a Leak include left shoulder pain (caused by pooling of the leakage under the diaphragm which causes irritation which manifests as left shoulder pain), decreased urine output, fever, shortness of breath, and high heart rate. Some manifestations of a Leak, such as atrial fibrillation, are indirect signs of a Leak in that they are associated with the stress on the body caused by the Leak. Dr. Cox's Treatment of Patient W.T. Patient W.T. presented to Dr. Cox for bariatric surgery. W.T., a male, was 47 years of age at the time and was morbidly obese. W.T. weighed 458 pounds and had a Body Mass Index of Because his Body Mass Index exceeded 50, he was considered "super" morbidly obese. He also had the following comorbidities: high blood pressure, sleep apnea, congestive heart failure, thrombophlebitis, pulmonary eboli, diabetes, and gatroesophageal reflux disease. There is no dispute that W.T. was an appropriate candidate for bariatric surgery. W.T. underwent RNY Surgery on August 31, 2005. During the surgery, Dr. Cox experienced difficulty seeing, due to the size of W.T.'s liver, the staples which he used to connect the intestine to the bottom of the newly formed stomach. Instead of confirming the placement of the staples, he was required to assess the staples with his fingers. This should have made him more sensitive to the possibility of a Leak. Before ending the surgery, Dr. Cox performed a test called a methylene blue test. To perform this test, an anesthesiologist puts medicine down a tube which passes through the patient's nose and into the new stomach. The physician then looks for any sign of a leak where the physician has sewn or stapled the small intestine to the stomach. With W.T., the methylene blue test did not disclose any leaks. The day after W.T.'s bariatric surgery, September 1, 2005, W.T. began to complain of pain in his left shoulder which is an important symptom of a Leak. W.T. also experienced decreased urine output during the night (he had, however, "responded well to fluid increases and diuretics"), and a low- grade fever, which are also indicators of a Leak. Although pain is a normal response to any operation, pain in the shoulder for the type of non-laparoscropic bariatric surgery performed by Dr. Cox should have made Dr. Cox more concerned than he apparently was as to the cause. The normal pain response to the type of operation Dr. Cox performed would be expected where the incision was made, but not in the shoulder. Dr. Cox treated W.T.'s shoulder pain with narcotic analgesia by a patient-controlled analgesia pump. He treated the decreased urine output with increased fluids and a diuretic (Mannitol). The fever was treated with Tylenol. Although the left shoulder pain, decrease in urine output, and low-grade fever could have been indicative of a Leak, Dr. Cox made no note in the patient records that he had considered the possibility that W.T. had a Leak, prematurely ruling out the possibility of a Leak. Dr. Cox suggested that the left shoulder pain was related to a diaphragmatic irritation caused by the use of surgical instruments on the diaphragm and that the urine output decline could have been attributable to the impact on W.T.'s kidneys by his diabetes. While these might have been appropriate considerations at the time, Dr. Cox could have not known for sure what was causing W.T.'s symptoms and, therefore, should have considered all the possible causes of these symptoms, especially the possibility of a Leak. On the second post-operative day, September 2, 2005, W.T. exhibited an abnormal heart rhythm, called atrial fibrillation. With a normal heart rhythm, the atrial (the first two of the four heart chambers) contracts, followed by contraction of the ventricles (the other two heart chambers). Atrial fibrillation is an abnormal heart rhythm characterized by a failure of the atria to completely contract. The fact that W.T., who had no prior history of atrial fibrillation, was evidencing atrial fibrillation on post-operative day two should have raised a concern about what was happening to W.T., including, but not limited to, the possibility of a Leak. W.T. was also experiencing an abnormally high heart rate of 148, which could have also been indicative of a Leak. Dr. Cox continued to treat W.T.'s shoulder pain with narcotic analgesia and the decreased urine output with increased fluids and Mannitol. He treated the elevated heart rate with Cardizem, a medicine used to slow the heart. W.T.'s shoulder pain appeared to decrease, which was to be expected given the course of treatment ordered by Dr. Cox. Dr. Cox had not, however, appropriately determined the cause of the pain. Again, nothing in Dr. Cox's medical records indicates that he considered the possibility that W.T.'s various symptoms might be indicative of a Leak. Nor did he take any action, such as an upper gastrointestinal test, to rule out the possibility of a Leak. To perform a gastrointestinal test, a patient drinks a water-soluble contrast called Gastrografin and a radiologists takes serial pictures of the patient, which show the contrast as it moves down the esophagus and then crosses through the anastomosis of the pouch and intestine. From these pictures, it can be determined whether the anastomosis is open and functioning properly and whether any of the contrast leaks outside of the new stomach-intestine path. The test is not fool-proof, but it is an appropriate diagnostic tool for Leaks. Dr. Cox suggests that the atrial fibrillation and high heart rate could have simply been a recognized complication of any stress W.T., with his borderline cardiac status, was experiencing. Again, while these might have been appropriate considerations at the time, Dr. Cox could have not known for sure what was causing W.T.'s symptoms and, therefore, should have considered all the possible causes of these symptoms, especially the possibility of a Leak. On the third post-operative day, September 3, 2005, air and serosanguinous fluid were observed seeping from W.T.'s abdominal incision. The existence of air may be evidence of a Leak. Although some air gets into the abdominal cavity during surgery, it is usually absorbed by the body very, very quickly. Air coming from an incision on post-operative day three suggests a hole in the intestine. Dr. Cox responded to the finding of air coming from the abdominal incision by ordering a methylene blue swallow, where W.T. swallowed a small amount of blue dye. Blue dye was then seen either coming out of the incision or drains placed in W.T.'s abdomen. Either way, the test was "positive" indicating a leak in W.T.'s intestine. Dr. Cox correctly took W.T. back into surgery. He discovered and corrected a Leak which had been caused by failure of the staples used in W.T.'s surgery. Although much was made as to when the staples failed, that evidence was not conclusive nor is it necessary to resolve the dispute. Whether the staples failed immediately after surgery or at some later time does not excuse Dr. Cox's failure to appropriately react to signs exhibited by W.T. which could have indicated that W.T. had a Leak. This case does not turn on whether a Leak actually existed. It turns on whether Dr. Cox appropriately considered the possibility of a Leak and took the steps medically necessary. With W.T., he did not. Dr. Cox's error was not in failing to find the Leak earlier; it was in failing to properly consider the possibility of a Leak when W.T. exhibited signs that should have prevented Dr. Cox from, with reasonable medical certainty, ruling out the possibility that a Leak was present. For this reason, the fact that a Leak was ultimately found is of little importance in deciding whether the charges leveled against him in the Administrative Complaint are accurate. Even if no Leak had ultimately been found, Dr. Cox's failure to properly respond to the potential of a Leak evidenced by W.T.'s symptoms was inconsistent with the standard of care. Dr. Cox's Treatment of Patient J.L. Patient J.L. presented to Dr. Cox for bariatric surgery. J.L., a male, was 35 years of age at the time and was morbidly obese. J.L. weighed 417 pounds and had a Body Mass Index of Because his Body Mass Index exceeded 50, he was considered "super" morbidly obese. He also had the following comorbidities: high cholesterol, stress incontinence, depression, anxiety, high blood pressure, gastroesophageal reflux disease, and shortness of breath on exertion associated with asthma. There is no dispute that J.L. was an appropriate candidate for bariatric surgery. J.L. underwent RNY Surgery on August 4, 2005. Dr. Cox also removed J.L.'s gallbladder. Before ending the surgery, Dr. Cox performed a methylene blue test. The methylene blue test performed on J.L. did not disclose any leaks. On the first post-operative day, August 4, 2005, J.L.'s heart rate was as high as 155 (anything over 120 is problematic), was experiencing decreased oxygen saturation of 89 percent (95 percent to 98 percent are considered normal saturation levels), had increased BUN and creatinine levels, and his urine output was borderline low. The increased BUN and creatinine, indicative of a problem with the kidneys, were are not being perfused well. J.L. was also complaining of right shoulder pain. Dr. Cox's note concerning the right shoulder pain specifically notes that it was not the "left" shoulder, which suggests that Dr. Cox was aware of the significance of left shoulder pain. J.L.'s high heart rate and low oxygen saturation level were considered significant enough to return him to the intensive care unit. On the second post-operative day, August 5, 2005, J.L.'s BUN and creatinine levels rose higher. That evening J.L. had a high heart rate. His urine output level, which Dr. Cox had treated with a diuretic and increased fluids, had improved. J.L. also became agitated and restless. He began to constantly request water. Dr. Cox eventually ordered, however, that J.L. not be given water. Dr. Cox failed to note in his records that he considered the possibility that J.L. had a Leak. Instead, Dr. Cox focused on the possibility that J.L. was suffering from rhabdomyolysis, a malfunction of the kidneys caused by the breakdown, as a result of surgery, of muscle tissue into cells too large in size for the kidneys to process. Dr. Cox ordered a CK test which found elevated creatine phosphor kinase or CPK, a marker of muscle death. Dr. Cox then consulted with a nephrologists. While the symptoms evidenced by J.L. could have very well been a result of rhadbodmyolysis, they also could have been symptomatic of a Leak. Dr. Cox did not have adequate information on August 5, 2005, to conclusively find that J.L. was suffering from rhadbodmyolysis and, more importantly, not from a Leak. As of the second post-operative day, J.L. was exhibiting a high heart rate, low urine output, pain in his right shoulder, a worsening oxygen saturation level and hunger for air, and a changed mental status (anxiety and combativeness). Due to these symptoms, Dr. Cox should have considered the possibility of a Leak, rather than merely concluding that J.L. was suffering from rhabdomyolysis and treating J.L.'s individual symptoms. On the third post-operative day, August 6, 2005, J.L.'s condition worsened. His agitation and combativeness due to his thirst and air hunger worsened. J.L. was treated with Haldol, a psychiatric medication. Dr. Cox continued to suspect rhadbdomyolysis and to ignore the possibility of a Leak. On the fourth post-operative day, August 7, 2005, at approximately 15:30, pink-tinged fluid was seen draining from J.L.'s incision. A pulmonologist consulting on J.L.'s case was the first to suggest the possibility of a Leak, questioning whether the entire clinical picture pointed to intra-abdominal sepsis due to a Leak. It was not until the drainage from J.L.'s incision that Dr. Cox first considered the possibility of a Leak. Even then, Dr. Cox did not return J.L. to surgery until August 7, 2005, where a Leak was found and repaired. Dr. Cox's error in his treatment of J.L., like his error in his treatment of W.T., was not in failing to find the Leak earlier, but in failing to properly consider the possibility of a Leak when J.L. exhibited signs which should have prevented Dr. Cox from, with reasonable medical certainty, ruling out the possibility that a Leak was present. For this reason, the fact that a Leak was ultimately found is of little importance in deciding whether the charges leveled against him in the Administrative Complaint are accurate. Even if no Leak had ultimately been found, Dr. Cox's failure to properly respond to the potential of a Leak, evidenced by J.L.'s symptoms, was inconsistent with the standard of care. Dr. Cox's explanation at hearing as to why he waited from August 5, 2005, when it was apparent that J.L. had a Leak, until August 7, 2005, to repair the Leak, is not contained in Dr. Cox's medical records. The Standard of Care. The Department's expert, Christian Birkedal, M.D., credibly opined that Dr. Cox failed to practice medicine in accordance with the level of care, skill, and treatment recognized in general law related to health care licensure in violation of Section 458.331(1)(t), Florida Statutes (hereinafter referred to as the "Standard of Care"), in his treatment of W.T. and J.L. In particular, it was Dr. Birkedal's opinion that Dr. Cox violated the Standard of Care as to W.T. by failing to recognize W.T.'s signs and symptoms of a Leak and by failing to perform a post-operative upper gastrointestinal test on W.T. once he evidenced those signs. Dr. Birkedal's opinion is credited and accepted. As to J.L., Dr. Birkedal's opinion that Dr. Cox violated the Standard of Care by failing to recognize the signs and symptoms of a Leak for two days post-operatively is credited and accepted. The opinions to the contrary offered by Dr. Cox and his witnesses as to W.T. and J.L. are rejected as not convincing and as not addressing the issue precisely enough. The opinions offered by Dr. Cox and his witnesses with regard to both patients were essentially that the various symptoms pointed to by Dr. Birkedal were not "evidence" of a Leak. Those opinions do not specifically address the issue in this case. Dr. Cox and his witnesses based their opinions on whether Dr. Cox should have "known" there was a Leak at the times in issue. That is not the charge of the Administrative Complaint or the basis for Dr. Birkedal's opinion. The question was, not whether Dr. Cox should have known there was a Leak, but whether he should have considered a Leak as a possible cause for the symptoms exhibited by W.T. and J.L. Additionally, and finally, Dr. Birkedal based his opinions, not by looking at the record as a whole, as did Dr. Cox and his experts, but by looking at only those records in existence at the times relevant to this matter. In this way, Dr. Birkedal limited himself to a consideration of what Dr. Cox knew about his patients at the times relevant in the Administrative Complaint.
Recommendation Based on the foregoing Findings of Fact and Conclusions of Law, it is RECOMMENDED that the a final order be entered by the Board of Medicine finding that Samuel Cox, M.D., has violated Section 458.331(1)(m) and (t), Florida Statutes, as alleged in Counts I, II, and III of the Administrative Complaint; issuing a reprimand; placing his license on probation for two years, with terms to be established by the Board; and imposing a fine of $15,000. DONE AND ENTERED this 19th day of June, 2007, in Tallahassee, Leon County, Florida. S LARRY J. SARTIN 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 19th day of June, 2007. COPIES FURNISHED: Patricia Nelson, Esquire Assistant General Counsel Prosecution Services Unit Department of Health 4052 Bald Cypress Way, Bin C-65 Tallahassee, Florida 32399-3250 Jonathon P. Lynn, Esquire Marci Strauss, Esquire Stephens, Lynn, Klein 301 East Las Olas Boulevard, Suite 800 Fort Lauderdale, Florida 33301 Larry McPherson, Executive Director Board of Medicine Department of Health 4052 Bald Cypress Way Tallahassee, Florida 32399-1701 Josefina M. Tamayo, General Counsel Department of Health 4052 Bald Cypress Way, Bin A02 Tallahassee, Florida 32399-1701 Dr. Ana M. Viamonte Ros, Secretary Department of Health 4052 Bald Cypress Way, Bin A00 Tallahassee, Florida 32399-1701
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.
Findings Of Fact Respondent is a physician licensed to practice medicine in Florida. His office is located on Sanibel Island in Lee County. A Sanibel Island tourist, Mrs. Marion Wallace, presented herself as a patient at Respondent's office on the morning of March 2, 1981. She complained of abdominal pain and swelling. Mrs. Wallace was seen by Mr. Kern Barrow, a physician's assistant employed by Respondent. Barrow conducted a physical examination of Mrs. Wallace's abdominal region and took her medical history, noting abdominal distension, abdominal pain, anorexia, nausea, vomiting and dysuria. She had not been feeling well for several days and had experienced some nausea and vomiting in the early morning hours of March 2, 1981. Barrow conducted a routine physical examination that included examination of the abdominal region, neck, mouth and throat. No medical tests were ordered or conducted by Barrow other than a urinalysis. Barrow's preliminary diagnosis was viral gastroenteritis or urinary tract infection. He administered ampicillan and prescribed donnagel for her cramping and gaviscon for the abdominal distension or gas. He administered an injection of compazine to prevent further nausea and vomiting. Barrow could not remember consulting with Respondent concerning Mrs. Wallace on March 2, but told her to come back if her condition did not improve. He described Mrs. Wallace as looking ill, but not mortally ill. Respondent did not see Mrs. Wallace on March 2, but reviewed and initialed the chart prepared by Barrow. Respondent prescribed the medication "Tagamet," but did so only because the patient requested it, claiming to have received relief for gastritus from this medication. Mrs. Wallace returned to Respondent's office on the morning of March 3, continuing to complain of abdominal pain and swelling. Respondent examined the patient at that time, but did not perform a rectal examination. He did not order a blood test, barium enema or x-ray. He noted "observe" on her chart, but did not schedule a return visit. He tentatively diagnosed her condition as diverticulitis. Mrs. Wallace, who did not testify in this proceeding, claimed that her condition had worsened between her visits to Respondent's office on March 2 and March 3. This fact was not established by direct evidence. However, on March 4 she presented herself to another Fort Myers area physician who sent her to the hospital emergency room where her condition was diagnosed as "acute abdomen" necessitating immediate surgery. During the surgery performed on March 4, it was discovered that Mrs. Wallace had a perforated gangrenous appendicitis with abscess formation, peritonitis, and a small bowel obstruction. These are serious and dangerous medical conditions. The testimony of Respondent and the other physicians who testified in this proceeding established that his tentative diagnosis was not inappropriate given the patient's symptoms. However, his failure to perform tests (such as a blood test for white blood cell count, x-ray, rectal examination or barium enema) was a serious lapse in view of her condition and his tentative diagnosis. His prescribing of Tagamet was not shown to have been improper. Respondent's use of a physician's assistant for the initial examination was likewise not shown to have been improper. However, Respondent's inability to note any progression of her symptoms between March 2 and 3 resulted from his overreliance on the physician's assistant and failure to conduct even a minimal examination of her on March 2.
Recommendation From the foregoing, it is RECOMMENDED: That petitioner enter a Final Order (1) finding Respondent guilty of 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; and (2) reprimanding and fining Respondent $1,000. DONE and ENTERED this 21st day of January, 1983, in Tallahassee, Florida. R. T. CARPENTER, Hearing Officer Division of Administrative Hearings The Oakland Building 2009 Apalachee Parkway Tallahassee, Florida 32301 (904) 488-9675 Filed with the Clerk of the Division of Administrative Hearings this 21st day of January, 1983. COPIES FURNISHED: J. Riley Davis, Esquire Post Office Box 1796 Tallahassee, Florida 32302 Leonard A. Carson, Esquire Post Office Box 1528 Tallahassee, Florida 32302 Dorothy Faircloth, Executive Director Board of Medical Examiners Dept. of Professional Regulation 130 North Monroe Street Tallahassee, Florida 32301 Samuel R. Shorstein, Secretary Dept. of Professional Regulation 130 North Monroe Street Tallahassee, Florida 32301 ================================================================= AGENCY FINAL ORDER ================================================================= BEFORE THE BOARD OF MEDICAL EXAMINERS DEPARTMENT OF PROFESSIONAL REGULATION, BOARD OF MEDICAL EXAMINERS, Petitioner, vs. CASE NO. 82-815 STANLEY P. WEGRYN, M.D., License Number: 23028, Respondent. /
