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Appeals : Arbitrator Decisions : #157 - August 23, 2004

D E C I S I O N

Claim No. 665

Province of Infection – Nova Scotia

1. The Claimant applied for compensation pursuant to Section 3.05 of the Transfused HCV Plan in her capacity as the personal representative of a Primarily Infected Person (the Claimant’s mother) who died prior to January 1, 1999.

2. By letter dated July 26, 2001, the Administrator denied the claim on the basis that the Claimant had not provided sufficient evidence to establish that the death of the Primarily Infected Person was caused by her infection with HCV.

3. The Claimant requested that the Administrator’s denial of the claim be reviewed by an Arbitrator.

4. Oral hearings were held on February 25 th, June 27 th and August 21 st, 2002 and written submissions were filed by Fund Counsel on January 9, 2002 and August 3, 2004.

5. The uncontested facts can be summarized as follows:

(i) The Primarily Infected Person underwent triple bypass surgery in December of 1987. She was 77 years old at the time and had suffered a myocardial infarction in 1985 with subsequent unstable angina. She also had a long history of Type 2 diabetes.

(ii) The Primarily Infected Person received blood products during or immediately following bypass surgery. Approximately a month later, she developed jaundice and her transaminase levels became highly elevated. She was diagnosed at the time as suffering from an acute infection with non-A, non-B viral hepatitis as a result of being transfused with contaminated blood.

(iii) The acute phase of the infection passed and by June of 1988 laboratory tests showed normal bilirubin and ALT levels. Subsequent transaminase and bilirubin measurements in 1989, 1996 and 1997 were all within normal limits. A physical exam report in 1989 indicated that the liver was not palpable and no other abnormalities were detected. An ultrasound in 1990 described the liver as being normal in appearance.

(iv) In 1996, Hepatitis C antibody testing and confirmatory RIBA measurement were positive. No Hepatitis C PCR test or biopsies were performed.

(v) The Primarily Infected Person’s last few years of life were characterized by fatigue, anorexia and weight loss. These symptoms were investigated on numerous occasions but without any definite diagnosis being made.

(vi) Despite receiving regular medical care, the Primarily Infected Person was never treated for Hepatitis C.

(vii) The Primarily Infected Person died in hospital on or about February 19, 1998.

(viii) The TRAN 2 form was completed by the Primarily Infected Person’s family physician of many years. He indicated on the TRAN 2 that her infection with HCV did not materially contribute to her death. In a later handwritten note, the doctor stated:

“This is to certify that I was the attending doctor for the above named patient who died on Feb. 19/98. She was an asymtomatic Hepatitis C patient who died of Congestive Heart Failure.”

6. Against the backdrop of the foregoing uncontested facts, there is a difference of medical opinion as to whether or not the Primarily Infected Person’s death was caused by her HCV infection. In this context, both the medical witnesses and the Administrator have proceeded on the assumption that, if HCV infection materially contributes to a person’s death, then the death can properly be said to have been caused by the infection. I propose to do likewise.

7. Dr. Ian Rendak has assisted the Claimant throughout the arbitration process. He is a diagnostic radiologist but does not have any special training or experience with respect to Hepatitis C. He never met the Primarily Infected Person and his opinion, therefore, is based strictly on a review of the medical file which he obtained from her family physician. Dr. Rendak’s opinion can be summarized as follows:

“...Reading the file, mostly the consults of Drs. Cookey and Dill, one must conclude that she developed acute hepatitis about five weeks after receiving a whole-blood transfusion in December 1987. She then developed signs of chronic hepatitis within a year and these persisted until her death. During those years she mainly had profound fatigue, flu-like symptoms and anorexia.

Her general health slowly plummeted and at the time she died she weighed less than one hundred pounds (from 180 lbs) due to chronic wasting. She had cardiac disease but Dr. Dill, heart specialist, repeatedly stated that he did not think her fatigue was due to her cardiac condition. Furthermore her type II diabetes was relatively mild not requiring insulin and apparently under control. Thyroid disease was ruled-out as a cause for her fatigue. During her last days in the hospital, there are no notes found to show that she was being treated for acute or even sub-acute congestive heart failure. In retrospect, it is very reasonable to conclude that she died from a slow progressive deterioration of her health with chronic hepatitis as a significant underlying factor.”

8. Under cross-examination by Fund Counsel, Dr. Rendak conceded that it is extremely difficult to say to what extent the HCV infection had contributed to the Primarily Infected Person’s death.

9. Dr. K. Peltekian is a specialist in liver disease and transplantation who practices in Halifax. He is recognized as an expert in the diagnosis and management of Hepatitis C. Like Dr. Rendak, Dr. Peltekian never treated the Primarily Infected Person and his opinion, therefore, is based entirely upon a review of her medical file. His opinion is contained in a written report dated January 8, 2004. In the report, Dr. Peltekian reviews the history of the initial infection and the subsequent symptoms experienced by the Primarily Infected Person. He notes that Hepatitis C is a slow, progressive disease but states that the process develops more quickly in persons who have a “high viral load” and are advanced in age at the time of infection. The report concludes as follows:

“The final events, no doubt, were independent of the liver disease. Patients in same age group with all the other problems without hepatitis C are at risk for dying. But, in my opinion, the hepatitis C in this patient did progress to more advanced level than what has been suggested. In that context hepatitis C contributed to the death but obviously was not the sole cause of it.”

10. Dr. Curtis Cooper is a specialist in internal medicine and infectious diseases. For the past seven years, he has been associated with the Viral Hepatitis Clinic at The Ottawa Hospital-General Campus which follows approximately 1,000 patients with chronic viral hepatitis infection. Dr. Cooper also directs an active and productive viral hepatitis research program in Ottawa. Dr. Cooper reviewed the Primarily Infected Person’s medical file. He also reviewed the opinions of Drs. Rendak and Peltekian. Fund Counsel filed two reports from Dr. Cooper – one dated April 17, 2002 and a supplemental report dated May 10, 2004.

11. Dr. Cooper’s April 17, 2002 report describes the circumstances of the initial infection and subsequent medical history. It also discusses the results of the several liver-related investigations which were undertaken during the last decade of the Primarily Infected Person’s life.

12. Dr. Cooper notes in his report that the Primarily Infected Person suffered from renal insufficiency which can be caused by Hepatitis C infection. However, it was his opinion that the more probable cause in this case was diabetes and underlying vascular disease. Dr. Cooper also observes that fatigue, anorexia and weight loss can be symptoms of chronic Hepatitis C infection. Again, however, it was his opinion that the more probable causes of these symptoms in the present case were ischemic heart disease, congestive heart failure, chronic renal insufficiency and medications (beta-blockers which are well known for causing fatigue and anorexia).

13. Dr. Cooper’s April 17, 2002 report concludes with the following statement:

“Even if this patient was chronically infected with hepatitis C, I do not believe that chronic hepatitis C infection contributed to [her] clinical demise or death.”

14. In Dr. Cooper’s report of May 10, 2004, he disagrees with Dr. Peltekian that there is any correlation between the level of HCV viral load and the rate of liver fibrosis. Moreover, while he agrees with Dr. Peltekian that fibrosis generally progresses more rapidly in older patients infected with HCV, he goes on to state that it still takes decades before cirrhosis is reached. As in his earlier report, Dr. Cooper emphasizes the absence of clinical findings and reiterates his earlier opinion that the Primarily Infected Person’s fatigue, anorexia and weight loss during the latter years of her life were probably not attributable to chronic HCV. The report concludes as follows:

“In closing, it is my opinion that this patient was exposed to HCV in December 1987. We will never know if she remaining [sic] chronically infected. Even if you assume that she remained chronically infected, there is no evidence that this resulted in endstage liver disease. If you assume that she remained chronically infected, then it is possible that she experienced chronic fatigue as a result, but far more likely that other medical disorders accounted for all of this patient’s symptoms.”

15. As is readily apparent from the medical evidence, this is a difficult case. In the opinion of Drs. Rendak and Peltekian, the death of the Primarily Infected Person was caused or contributed to by her HCV infection. Dr. Cooper is of the contrary view, as was her family physician. Dr. Peltekian and Dr. Cooper are both acknowledged experts in the field of HCV infection.

16. The burden is on the Claimant to establish, on the balance of probabilities, that the death of the Primarily Infected Person was caused by HCV infection. Such proof is not required to be absolute but must meet the civil “balance of probabilities” test.

17. In the present case, there can be no real doubt that the Primarily Infected Person was infected with HCV as a result of being transfused with contaminated blood during the Class Period. The Claimant has also adduced evidence from two doctors to the effect that the Primarily Infected Person suffered chronic HCV infection which caused or materially contributed to her death. On the other side of the ledger, there is the TRAN 2 form completed by the family physician which indicates that the Primarily Infected Person died of congestive heart failure and that her HCV infection was not a contributing factor. More significantly, there is the opinion of Dr. Cooper that HCV infection did not contribute in any material way to the death.

18. Considering all of the evidence, I have concluded that the Claimant has not met the burden of establishing that the Primarily Infected Person’s death was probably caused by her HCV infection. In reaching this conclusion, I am influenced by the fact that the Primarily Infected Person was never diagnosed or treated for chronic HCV infection while she was alive. Furthermore, as pointed out in Dr. Cooper’s reports, liver-related investigations performed in 1989, 1996 and 1997 produced results which were within normal limits. It is also clear from the record that the Primarily Infected Person had a long history of vascular disease and Type 2 diabetes. Similarly, it does not appear to be disputed that the immediate cause of her death was congestive heart failure. As stated in Dr. Peltekian’s report, “The final events, no doubt, were independent of the liver disease.”

19. With deference to Dr. Peltekian, it is difficult to understand how HCV infection could be found to be a material contributing factor here if the “final events” were independent of liver disease.

20. In the result, while one cannot help but be sympathetic to the Claimant for her loss, the appeal must be dismissed.

DATED at Halifax, Nova Scotia, this 23rd day of August, 2004.

S. BRUCE OUTHOUSE, Q.C.

Arbitrator








 

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