The opinion of the court was delivered by: Neal P. McCURN, Senior District Court Judge
Introduction . . . . . . . . . 4
Findings of Fact . . . . . . . . . 5
I. July 1997 . . . . . . . . . 5
A. July 7th -10th SVAMC Hospitalization . . . . 6
B. July 23rd Cardiac Clinic Visit . . . . . 8
C. July 31st TEE . . . . . . . . 9
II. August 1997 . . . . . . . . . 9
A. Cardioversion. . . . . . . . . 9
B. Stress Test. . . . . . . . . 10
C. Holter Monitor . . . . . . . 12
D. Cardiac Catheterization . . . . . . 13
III. September 1997 - Mitral Valve Repair . . . . . 14
IV. October 1997 - Cardiac Clinic Visit . . . . . 15
V. November1997 . . . . . . . . 16
A. November 24th Cardiac Clinic Visit . . . . 16
B. Roxbury Hospitalization . . . . . . 18
VI. December 1997 . . . . . . . . 18
A. December 11th Cardiac Clinic Visit . . . . 18
B. Mid-December - Dr. Brand . . . . . 20
C. December 24th - Cardiac Clinic Visit . . . . 20
D. December 29th Cardiac Catheterization . . . . 21
E. December 31st Coumadin Clinic Call . . . . 21
VII. January 1998 . . . . . . . . 22
A. January 13th - 18th Roxbury Hospitalization . . . 22
B. January 21st - Cardiac Clinic Follow-up . . . 22
VIII. February 1998 . . . . . . . . 24
A. February 12th Stress Test. . . . . . . 24
B. February 23rd - SVAMC Hallway Encounter. . . . 25
IX. March 1998 . . . . . . . . . 26
A. March 6th Addendum. . . . . . . 26
B. March 19th - SVAMC Hallway Encounter . . . 27
C. March 20th - Dr. Brand . . . . . . 32
D. March 21st - 28th SVAMC Hospitalization. . . . 32
Conclusions of Law . . . . . . . . 33
I. Governing Legal Standards . . . . . . . 33
A. Which Law Applies?. . . . . . . 33
B. Medical Malpractice Elements . . . . . 34
1. Proximate Cause. . . . . . . 35
C. Burden of Proof . . . . . . . 36
II. Application of Governing Legal Standards . . . . 39
A. Failure to "Make a Reasonable Investigation" . . 39
1. January 21, 1998 . . . . . . 39
2. January 22 - February 16, 1998 . . . . 42
3. February 17, 1998 - March 21, 1998 . . . 43
B. Failure to Reinstate Anticoagulant Therapy . . . 44
1. Standard of Care . . . . . . 44
2. Departure from Standard of Care? . . . 48
III. Proximate Cause . . . . . . . . 51 Conclusion . . . . . . . . . . 53
MEMORANDUM-DECISION AND ORDER
On March 21, 1998, plaintiff Robert Gerace, a 46 year old Caucasian male, presented at the emergency room ("ER") of the Syracuse Veteran's Administration Medical Center ("SVAMC"), where he was diagnosed has having had a stroke.
In this action, brought pursuant to the Federal Tort Claims Act ("FTCA"), 28 U.S.C. § 2671 et seq., plaintiff is seeking to recover nearly ten million dollars from the United States of America. Plaintiff alleges that Dr. Kishor V. Phadke, his cardiologist at the SVAMC, "ignored and discounted plaintiff's symptoms and complaints, on a regular basis, and failed to institute appropriate anti-coagulation" when he was "suffering from paroxysmal atrial fibrillation[.]"*fn1 Co. at 9, ¶46 (citation omitted) and ¶ 45 (footnote added). This alleged failure to diagnose and treat plaintiff supposedly caused his to have a stroke which resulted in, among other things, "permanent and irreversible brain damage[.]" Id. at 45.
Prior to trial, the United States sought bifurcation of the issues of liability and damage, a request which the court granted. Doc. #68. Following a five day non-jury trial confined to the issue of liability, the parties filed proposed findings of fact and conclusions of law. After careful consideration of same, as well as the record evidence, the court makes the following findings of fact and conclusions of law as Fed. R. Civ. P. 52(a) requires.
Prior to his stroke, plaintiff had a history of cardiac problems. In 1987, he was first diagnosed with mitral valve prolapse ("MVP"). Pl. exh. 17 at 1; Def. exh. A(17) at 135; and Pl. exh. 3 at 1; Def. exh. A(2) at 2. MVP is "[a] valvular heart disorder in which one or both mitral valve*fn2 flaps close incompletely[.]" Ct. exh. 1 (footnote added). Dr. Nash, the defendant's expert cardiologist, classified plaintiff's disorder as being of "significant severity[.]" Doc. 84 at 13. Plaintiff had a "very leaky mitral valve[.]" Id. That is a "bad problem to have[,]" according to Dr. Nash, because such a person will "have symptoms that will eventually go into heart failure[.]" Id.
Further complicating matters, in 1994 plaintiff had an EKG which showed "evidence of moderate mitral regurgitation[.]" Pl. exh. 5 at 1. Mitral regurgitation ("MR") is the "[b]ackward flow of blood into the atrium due to mitral insufficiency." Ct. exh. 1. Mitral insufficiency, in turn, means that the mitral valve is unable "to close perfectly, permitting blood to flow back into the atrium[.]" Id. That 1994 diagnosis of mitral regurgitation was reaffirmed in early 1997. See Pl. exh. 5 at 1. Thus it stands to reason that when Dr. Phadke saw plaintiff for "new onset atrial fibrillation[,]" on July 24, 1997, he noted that plaintiff "clearly had significant MR for a period of time[.]" Id.
In January 1997, a private physician prescribed Acebutolol for plaintiff's complaints of heart palpitations. Pl. exh. 3 at 1; Def. exh. A(2) at 2. Later that year, in July 1997, plaintiff began to experience a "worsening of symptoms in terms of shortness of breath and episodes of palpitations which [were] increasing in frequency."
Id. On July 2, 1997, while working as a registered nurse ("R.N.") at the SVAMC, plaintiff performed an EKG on himself. Id.; see also Def. exh. A-1. Although the EKG revealed that plaintiff had atrial fibrillation, Def. exh. A-1 at 1; Pl. exh. 2, he did not consult with a cardiologist or seek any type of medical attention at that time.
The following Monday, July 7, 1997, plaintiff returned to work at the SVAMC. While Wendy Ryan, another R.N., was reporting on the night shift which she had just completed, she noticed that plaintiff was gray in pallor. Ms. Ryan testified that when she touched plaintiff's arm, he felt very sweaty. She took his pulse and found it to be "irregular." According to his chart, plaintiff was "dizzy, cold[,] clammy" and "light-headed." Pl. exh. 1; Def. exh. A(2) at 6. Nurse Ryan speculated that perhaps plaintiff's blood sugar was low. She walked him to the ER. Even though plaintiff was unsteady, Ryan testified that he refused to be transported by wheelchair.
A. July 7th -10th SVAMC Hospitalization
After being seen in the ER on July 7, 1998, plaintiff was admitted to the SVAMC where he stayed for three days. His diagnosis was "new onset atrial fibrillation[,]" which was "increasing in irregularity or increasing in frequency of attacks[.]" Pl. exh. 3 at 2; Def. exh. A(2) at 3. To treat this atrial fibrillation "Cardiology" was "consulted" and "the plan was to heparinize" plaintiff and "anticoagulate him enough" until he could be "start[ed] on Coumadin[.]" Id.
Although heparin and Coumadin are both anti-coagulants, they are administered differently and react somewhat differently in the body. Heparin is a fast-acting and "relatively short-lived" anti-coagulant. Doc. 84 at 9. It is a "parenteral[;]" it is given intravenously. Id. at 8. In layperson's terms, heparin "thin[s] the blood." Id. More accurately, however, heparin is "used to prevent further clot formation[,]" or "to prevent a clot from forming in the first place." Id. at 8 and 10 (emphasis added). What heparin does not do is dissolve pre-existing clots. Id. at 8 and 9. As Dr. Nash succinctly put it, "heparin buys . . . time while our body dissolves the . . . clot itself." Id. at 10. Thus, as Dr. Nash testified, "[t]heoretically[,]" if a patient presents with a clot and is then placed on heparin, "that clotting process stops" and "the body self-destroys or breaks down slowly much of the more friable form of thrombus." Id. at 11. Significantly, the body's natural clot dissolving mechanism does not take place "immediately[.]" Id. Dr. Nash frankly stated that he "would suspect" that natural process "takes multiple days at a minimum." Id.
Coumadin is an oral anti-coagulant which "is a slightly different mechanism than heparin[,]" and typically is administered after heparin. Doc. 84 at 9. As Dr. Debra A. Buchan, the Medical Director of the Anticoagulation Center at the State University of New York ("SUNY") Upstate Medical University and a Clinical Associate Professor of Medicine there explained it, Coumadin acts more gradually than does heparin. She further explained that Coumadin is a vitamin K antagonist so that it decreases the production of protein, which in turn makes it less likely that a person will develop a blood clot - an explanation which Dr. Nash endorsed. See Doc. 84 at 9.
Coumadin is not without risks, however. In fact because of the serious risks associated with it, a person on Coumadin requires regular monitoring. See id. at 48. Regular monitoring is necessary so that a therapeutic level of anticoagulation is achieved, i.e. enough so that a person is "safe from thromboembolism[,]" but not so much that a person has a stroke due to "excessive anticoagulation[.]" Doc. 81 at 133; see also Doc. 84 at 52. So even though Coumadin "lowers the risk of a blood-clot-derived stroke[,]" it "raises the risk of a bleeding type stroke." Id. Indeed, the "most feared complication," according to Dr. Buchan is intercranial bleeding. If a person does not die from that, "most of the time they will end up with horrible neurological deficits." Perhaps that is why Dr. Buchan somberly described the risks associated with Coumadin in this way: "Clotting is an act of God, but bleeding is my fault."
According to the discharge summary, after plaintiff had maintained therapeutic levels with the Coumadin, he was to "return in 2-4 weeks maximum to" have a transesophageal echocardiogram ("TEE"). Pl. exh. 3 at 2; Def. exh. A(2) at 3. A TEE is done using "an ultrasound probe [which] is passed orally into the patient's esophagus, producing very clear images of the heart structures and valves[.]" Ct. exh. 1. If the TEE did not show "any thrombi in the left atrium," Pl. exh. 3 at 2; Def. ...