Charette v. Wexford Health Sources Inc.

1

ANGELA CHARETTE, Personal Representative of the Estate of Michael Anthony Miller, Plaintiff, v. WEXFORD HEALTH SOURCES, INC. et al., Defendants.

Civil Action No. GLR-19-33

United States District Court, D. Maryland

September 11, 2023

MEMORANDUM OPINION

George L. Russell, III, United States District Judge

THIS MATTER is before the Court on Defendants Wexford Health Sources, Inc. (“Wexford”), Nurse Bernard Alenda Dr. Gedion Atnafu, Dr. Melaku Ayalew, Dr. Zowie Barnes, Nurse Wondaye Deressa, Physician Assistant (“PA”) Robert Giangrandi, Dr. Kenneth Lee, PA Priscilla Momoh, Dr Ayoku Oketunji, Dr. Bolaji Onabajo, Nurse Titilayo Otunuga Nurse Jennifer Pope, and Dr. Kasahun Temesgen's (collectively, “Defendants”) Motion for Summary Judgment (ECF No. 115) and Plaintiff Angela Charette's Cross-Motion for Partial Summary Judgment (ECF No. 129). The Motions are ripe for disposition, and no hearing is necessary. See Local Rule 105.6 (D.Md. 2023). For the reasons outlined below, the Court will grant in part and deny in part Defendants' Motion for Summary Judgment. Additionally, the Court will deny Charette's Cross-Motion for Partial Summary Judgment.

I. BACKGROUND

A. Factual Background

Michael Miller spent the last two decades of his life caught in a revolving door of incarceration. (See Defs.' Ex. 1, Inmate Traffic History [“Inmate Traffic Hist.”], ECF No. 115-3). Miller's imprisonment was defined by cascading medical complications related to chronic cirrhosis, hepatitis B, and hepatitis C-conditions that ultimately caused his death. This dispute focuses mainly on Miller's medical care while incarcerated at Jessup Correctional Institution (“JCI”) between September 2, 2015 and March 24, 2017. During this time, Wexford, a private medical company, provided health care services to inmates in Maryland. The other thirteen Defendants are individual health care providers employed or contracted by Wexford. These individual Defendants each participated in Miller's care in some fashion. The Court recounts Miller's complicated medical history with attention to the care that was-or was not-provided by Defendants.

1. Miller's Early Detection of Hepatitis B and C

Miller first entered the Maryland state prison system in 1997. (Inmate Traffic Hist. at 8). He spent several years cycling between prison and mandatory supervision on release before starting a decade-long prison sentence in 2005. (Id.; see also Defs.' Ex. 2, Sentence Status Change Report [“Sentence Rep.”], ECF No. 115-4).^[1] Miller was likely infected with at least one form of hepatitis before his reimprisonment in 2005. (Defs.' Ex. 4, Kali Zhou, M.D., Dep. Tr. [“Dr. Zhou Dep.”] at 43:17-44:12, ECF No. 115-6). This was no secret to Miller, who believed he contracted hepatitis C in 1999. (Defs.' Ex. 10, Integris Medical Records [“Integris Med. Rs.”] at IMBC-SUB-000033, ECF No. 115-12). On October 12, 2007, Miller told a nurse practitioner he was infected with both hepatitis B and hepatitis C. (Defs.' Ex. 3, Wexford Medical Records [“Wexford Med. Rs.”] at DPSCS000038, ECF No. 115-5). Because nothing at that time corroborated Miller's belief, the nurse practitioner ordered lab reports and noted that she would follow-up with Miller once she received the results. (Id.).

It is worth pausing to discuss the risks associated with hepatitis B, hepatitis C, cirrhosis, and esophageal varices-each of which contributed to Miller's deteriorating health. Hepatitis B is a potentially-life threatening liver infection caused by the hepatitis B virus (“HBV”). HBV is generally transmitted through blood, sexual contact, or childbirth. See generally World Health Organization, Fact Sheet: Hepatitis B (June 24, 2022), https://www.who.int/news-room/fact-sheets/detail/hepatitis-b. Some symptoms associated with hepatitis B include “yellowing of the skin and eyes (jaundice), dark urine, extreme fatigue, nausea, vomiting, and abdominal pain.” Id. Hepatitis B can take on both acute and chronic forms. Id. While acute hepatitis B involves a short-term infection, a person has chronic hepatitis B when the virus remains active in a body for more than six months. (See Pl.'s Ex. O, Ryan D. Herrington, M.D., Expert Rep. [“Dr. Herrington Rep.”] at 18, ECF No. 127-15).

Chronic hepatitis B infects cells within the liver, causing an “inflammatory response that injures or ‘scars' the liver,” a process called “fibrosis.” (Id. at 17). While healthy livers can regenerate, “long-term inflammation/injury from presence of HBV in the liver leads to progression of fibrosis until there is so much scar tissue the liver can no longer regenerate and begins to fail - the time point called cirrhosis.” (Id.). A person may eventually experience “decompensated cirrhosis,” which happens when complications related to liver failure start appearing. (Id.). These complications include “bleeding from varices (dilated esophageal veins from excess pressure in liver vessels), ascites (fluid in abdomen), and encephalopathy (confusion due to toxic ammonia build-up).” (Id.). A hepatitis B infection may move between an inactive state (with an undetectable viral load) and an active state (with a detectable viral load) throughout a patient's life. (Id. at 19).

Like hepatitis B, hepatitis C is a viral disease that affects the liver. And just as hepatitis B has both acute and chronic forms, so too does hepatitis C. Chronic hepatitis C similarly presents risks of fibrosis, cirrhosis, and liver failure.

On May 2, 2010, Miller took serology tests for hepatitis A, hepatitis B, and hepatitis C. (Defs.' Ex. 5, BioReference Laboratory Report [“BioReference Lab'y Rep.”] at BIO000011, ECF No. 115-7).^[2] Although Miller tested negative for hepatitis A, he tested positive for hepatitis B surface antigen. (Id.). A positive surface antigen test signifies a person currently has a hepatitis B infection. Miller also tested positive for hepatitis C antibodies. (Id.). Antibodies indicate a person has been infected with hepatitis B in the past. As a follow-up, on May 17, 2010, Miller underwent genotype and quantitative PCR testing for hepatitis C viral RNA. (Id. at BIO000013). Those tests revealed Miller did not have detectable levels of hepatitis C viral RNA. (Id.). Taken together, these results established that Miller did not have an active, treatable hepatitis C infection in May 2010, despite having been exposed to hepatitis C at some point. (Dr. Zhou Dep. at 41:17-18, 42:3-9). Miller did, however, have an active hepatitis B infection at that time.

On May 19, 2010, two days after Miller's provider tested his hepatitis C viral load but one day before the prison received those test results, Miller saw an infection control nurse. During that visit, the nurse (1) educated Miller about hepatitis C and the possibility for treatment; (2) obtained Miller's signed consent to receive hepatitis C treatment and to participate in the chronic care clinic; and (3) administered the first of three doses of the Twinrix vaccine for hepatitis A and hepatitis B. (Wexford Med. Rs. at DPSCS000170-72). Miller received the second and third dose of the Twinrix vaccine on June 9, 2010, and November 19, 2010, respectively. (Id. at DPSCS0000175, DPSCS000220).

2. Miller's Initial Gastrointestinal Bleeding

In late February 2012, Miller had his first episode of bleeding esophageal varices. Miller began vomiting blood on February 27, 2012. (Id. at DPSCS000434). The next day, he complained of chills, bloody diarrhea, black stool, and fatigue-all while continuing to vomit blood. (Id. at DPSCS000436). Miller was sent to an emergency room, where an esophagogastroduodenoscopy (“EGD”) revealed that Miller's bleeding was caused by esophageal varices. (Id. at DPSCS000439-42).^[3] Bleeding esophageal varices suggest a patient has end-stage liver disease from a decompensated liver. (Dr. Zhou Dep. at 56:1015). While at the hospital, Miller was prescribed Protonix and propranolol to treat the portal hypertension underlying his esophageal varices. (Wexford Med. Rs. at DPSCS000442).^[4] Miller's bleeding was resolved by March 1, 2012. (Id.). The doctor's notes related to this event, however, list only one chronic condition: hepatitis C. (Id.).

Miller started vomiting blood again just days after returning to prison. (Pl.'s Ex. R, Miller Medical Records [“Miller Med. Rs.”] at DPSCS000473, ECF No. 127-18). So, on March 4, 2012, Miller returned to the emergency room where he underwent a second EGD. (Id. at DPSCS000485). The hospital provider expressed concern that Miller's “history of HCV and HBV” would make his varices worse. (Id.). Miller was advised that he may need surgery “at some later time.” (Id.). These concerns were memorialized in a note by Ava Joubert, MD, after Miller returned to the prison infirmary on March 8, 2012. (Id. at DPSCS000485, DPSCS000501).

Dr. Joubert, according to this note, requested that Miller receive “specialty service” from infectious disease (“ID”) personnel. (Id. at DPSCS000486). Dr. Joubert explained she would “push for ID to see [Miller] regarding Hep B and Hep C status/treatment options.” (Id.). Over the next four days, Miller stayed in the prison infirmary and complained of severe pain. (Id. at DPSCS000493, DPSCS000498). Although Miller was discharged from the infirmary on March 12, 2012, he was sent to the hospital later that month due to abdominal pain and vomiting. (Id. at DPSCS000501, DPSCS000524). With no signs of active gastrointestinal (“GI”) bleeding, Miller was returned to the infirmary on March 21, 2012, and discharged to the general prison population on March 22, 2012. (Id. at DPSCS000524).

Concerns related to Miller's hepatitis were not forgotten during this time. On March 28, 2012, Sandra Pryor, LPN, reviewed Miller's medical records after learning that...