Kane v. Winn

Citation319 F.Supp.2d 162
Decision Date27 May 2004
Docket NumberNo. CIV.A.03-40116-WGY.,CIV.A.03-40116-WGY.
PartiesMichael KANE, Plaintiff, v. David L. WINN, Warden, F.M.C. Devens, Defendant.
CourtUnited States District Courts. 1st Circuit. United States District Courts. 1st Circuit. District of Massachusetts

Mark J. Grady, United States Attorney's Office, Boston, MA, for David L. Winn, Bhatti, S. Howard, Respondents.

MEMORANDUM

YOUNG, Chief Judge.

I. INTRODUCTION

If incarceration rates remain unchanged, 6.6% of U.S. residents born in 2001 will go to prison at some time during their lifetime.1

This memorandum explores the consequences of this statistic, which stark as it is, does not even account for incarceration in jails or growing incarceration rates. The particular action here involved a federal prisoner's allegations that his medical treatment fell short of what Bureau of Prisons ("BOP") regulations and the United States Constitution require, and that the BOP retaliated against him for requesting adequate medical care. The prisoner, Michael Kane ("Kane"), moved for appointment of counsel and requested a jury trial. Kane and Federal Medical Center-Devens Warden David L. Winn ("Warden") filed cross motions for summary judgment.

For the reasons discussed below, Kane's Motions for Appointment of Counsel [Doc. No. 14], for a Jury Trial [Doc. No. 5], and for Summary Judgment [Doc. No. 11] were DENIED, the Warden's Motion for Summary Judgment [Doc. No. 7] was ALLOWED, judgment was entered for the Warden, and no further filing fee was assessed.

II. BACKGROUND
A. Factual Background
1. Kane's Incarceration and Medical Condition

On March 23, 2000, the United States District Court for the Eastern District of Pennsylvania sentenced Kane to ten years in prison followed by five years of supervised release for distribution of methamphetamines, a violation of 21 U.S.C. 841(a)(1). Def.'s 56.1 Stmt. [Doc. No. 8] ¶ 1; id. Ex. 1, Attach. A.2 On January 4 2001, he was transferred to Federal Medical Center-Devens ("FMC-Devens") in Ayer, Massachusetts, where he remains incarcerated. Id. ¶ 1; id. Ex. 1, Attach. F.

Kane, a 47-year-old man, id. Ex. 2 (Letter from Hinendi and Guzman to Howard of 2/11/02) [hereinafter "Hinendi Letter"], has a history of hepatitis B and C, diabetes mellitus type I,3 seizure disorder, asthma, gastroesophageal reflux disease, and peptic ulcer disease. Id. Ex. 1, Attach. C (Response to Request for Administrative Remedy # 241172-F1 of 6/15/01). He has chronic hepatitis C, and was apparently first diagnosed with hepatitis C about five years ago. Id. Ex. 2. His hepatitis C virus ("HCV") genotype is 1 (1A, to be precise). Id. Ex. 1, Attach. G (Algorithm for Treatment of Hepatitis C/Approval Form of 3/6/03). He is overweight, has a history of heavy drinking, and smokes. Id.

2. Nature, Monitoring, and Treatment of Chronic Hepatitis C
a. Nature of Chronic Hepatitis C

An understanding of chronic hepatitis C is necessary to an evaluation of Kane's claims. HCV is an RNA virus, transmitted primarily through the blood, and which mainly impacts the liver. Def.'s 56.1 Stmt. Ex. 3, at 8 (National Institutes of Health Consensus Development Conference Statement — Management of Hepatitis C: 2002 (June 10-12, 2002), at 3-4, at http://odp.od.nih.gov/consensus/cons/116/116cdc_intro.htm (last modified Sept. 12, 2002) [hereinafter NIH Statement]). It is difficult for the body's immune system to eradicate. Id. Ex. 4 (Nelson Decl.) ¶ 5. It resides in liver cells (hepatocytes), where it replicates and causes cell death (necrosis). Id. Infection becomes chronic if it persists for at least six months. NIH Statement, supra, at 4.

According to the National Health and Nutrition Examination Survey of 19881994, as of 1994, 3.9 million Americans were infected with HCV, an estimated 2.7 million of whom were suffering from chronic infection. Id. at 3. That population-based household survey almost certainly underestimated levels of infection, as it did not include the incarcerated, the institutionalized, or the homeless, among all of whom the disease is more prevalent than in the population at large. Id. An estimated 35,000 new HCV infections occur every year, and HCV is the most common blood-borne infection nationwide. Id. at 4.

As Harrison's Principles of Internal Medicine, a medical treatise that both Kane and the Warden cite as an accurate scientific reference, describes: "Milder forms [of chronic hepatitis] are nonprogressive or only slowly progressive, while more severe forms may be associated with scarring and architectural reorganization, which, when advanced, lead ultimately to cirrhosis." Jules L. Dienstag & Kurt J. Isselbacher, Chronic Hepatitis, in 2 Harrison's Principles of Internal Medicine 1742, 1742 (Eugene Braunwald et al. eds., 15th ed.2001) [hereinafter Chronic Hepatitis]. Twenty percent of those with chronic transfusion-associated hepatitis C (a class that may include Kane) progress to cirrhosis. Id. at 1747. Hepatocellular carcinoma ("HCC") can follow,4 as can end-stage liver disease and liver failure. NIH Statement, supra, at 4; Chronic Hepatitis, supra, at 1747. At least 10,000 to 12,000 deaths result from hepatitis C each year. NIH Statement, supra, at 5.

Progression of liver disease in chronic hepatitis C patients is more likely "in patients with older age, longer duration of infection, advanced histologic stage and grade, genotype 1 (especially type 1b), more complex quasispecies diversity,5 and increased hepatic iron." Chronic Hepatitis, supra, at 1747 (footnote added). Duration of infection appears to be the most important of this set of variables, and several of the other factors, such as quasispecies diversity and hepatic iron accumulation, "probably reflect disease duration to some extent." Id. Of lesser but still substantial significance is the severity of grade and stage; patients with mild grade and stage tend not to progress to cirrhosis, whereas for patients with moderate or severe grade and stage, "progression to cirrhosis is highly likely over the course of 10 to 20 years." Id. Patients who simultaneously suffer from other liver processes, such as chronic hepatitis B,6 alcoholic liver disease, and hemochromatosis, are also prone to greater severity of chronic hepatitis and faster progression of chronic liver disease. Id.

Still, for the majority of patients, the long-term prognosis is "relatively benign":

Mortality over 10 to 20 years among patients with transfusion-associated chronic hepatitis C has been shown not to differ from mortality in a matched population of transfused patients in whom hepatitis C did not develop.... Overall, then, chronic hepatitis tends to be very slowly and insidiously progressive, if at all, in the vast majority of patients ....

Id."Among patients with compensated cirrhosis associated with hepatitis C, the 10-year survival is close to 80 percent ...." Id.

b. Classification and Monitoring of Chronic Hepatitis

"Classification of chronic hepatitis is based upon (1) its cause, (2) its histologic activity, or grade, and (3) its degree of progression, or stage." Id. The available classifications by cause include: "chronic viral hepatitis, caused by hepatitis B, hepatitis B plus D, hepatitis C, or potentially other unknown viruses; autoimmune hepatitis, including several subcategories; types 1, 2, and 3, based on serologic distinctions; drug-associated chronic hepatitis; and a category of unknown cause, or cryptogenic chronic hepatitis." Id. at 1742-43.

"Grade, a histologic assessment of necroinflammatory activity, is based upon examination of the liver biopsy." Id. at 1743. At least in clinical practice, grade is typically categorized as "mild," "moderate," or "severe," based on "[a]n assessment of important histologic features," translated into a numerical score based on one of several available scoring systems. Id. Typically, the histologic features to be measured include:

periportal necrosis and the disruption of the limiting plate of periportal hepatocytes by inflammatory cells (so-called piecemeal necrosis or interface hepatitis); the degree of confluent necrosis that links or forms bridges between vascular structures — between portal tract and central vein — referred to as bridging necrosis; the degree of hepatocyte degeneration and focal necrosis within the lobule; and the degree of portal inflammation.

Id.7 Of the available scoring systems, "the most popular is the numerical histological activity index (HAI), based on the work of Knodell and Ishak." Id. Although the HAI primarily measures grade, it "also includes an assessment of fibrosis, which is currently used to categorize stage of the disease." Id.

Classification by stage "reflects the level of progression of the disease, [and] is based on the degree of fibrosis." Id."When fibrosis is so extensive that fibrous septa surround the parenchymal nodules and alter the normal architecture of the liver lobule, the histologic lesion is defined as cirrhosis. There are five stages:

0 = no fibrosis

1 = mild fibrosis

2 = moderate fibrosis

3 = severe fibrosis, including bridging fibrosis

4 = cirrhosis"

Id.

Michael B. Nelson, Chief of Health Programs for the BOP's Health Services Division ("Division Chief Nelson"), states that "[t]he liver has the capacity to reverse fibrosis up until the development of stage 4." Def.'s 56.1 Stmt. Ex. 4, ¶ 6 (Nelson Decl.). Division Chief Nelson further states that "[i]t is extremely unlikely that an individual will progress more than one stage of fibrosis every ten years." Id. ¶ 6. Kane disputes both these statements. He urges that "[t]he precise point at which fibrosis becomes irreversible is unclear," although he cites no medical authority to support his contention. Pl.'s Summ. J. Opp'n at 5-6. Kane's filings also suggest that he considers the typical rate of progression of the disease irrelevant, because numerous factors (such as his age and his hepatitis B) make his liver disease apt to progress...

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