Kasongo v. United States (523 F. Supp. 2d 759, 2007)

MEMORANDUM OPINION AND ORDER

REBECCA R. PALLMEYER, District Judge.

Jacqueline Makombe, her husband Innocent Kasongo, and their three children emigrated to the United States after enduring civil war and ethnic strife in central Africa. Raped by soldiers in 1998 during the Second Congo War, Ms. Makombe contracted HIV and subsequently developed AIDS. After arriving in Chicago in July 2000, Ms. Makombe received treatment at Chicago Health Outreach Clinic (the “Clinic”), a federally-funded clinic that provides medical care and social services to HIV-positive refugees and their families. Ms. Makombe’s treatment included the AIDS drug Zerit. A rare but known side effect of Zerit is the often-fatal condition lactic acidosis. Although Ms. Makombe developed symptoms of lactic acidosis beginning in August 2001, medical staff at the Clinic did not diagnose the condition until October 22, 2001. By that time, the lactic acidosis was irreversible, and on October 24, 2001, Ms. Makombe died.

Mr. Kasongo, individually and on behalf of his children and his wife’s estate, brings this action against the Clinic pursuant to the Federal Tort Claims Act, 28 U.S.C. § 1346(b)(1), asserting claims for negligence under the Illinois wrongful death statute, 740 ILCS 180/1 et seq., and under the Illinois survival statute, 755 ILCS 5/27-6. Plaintiff contends that the Clinic and its employees breached the applicable standard of care by failing to timely diagnose lactic acidosis, and that that failure proximately caused Ms. Makombe’s death. The court conducted a bench trial in December 2006 and, for the reasons set forth below, now finds in Plaintiffs favor. The court awards Plaintiff $3.5 million in damages for the wrongful death claim, and $1 million in survival damages.

BACKGROUND

The basic facts of this case are undisputed. Beginning on July 24, 2000, Ms. Ma-kombe received treatment for HIV and AIDS at the Clinic. (UF ¶ 4.) That treatment included the antiretroviral drug Zer-it, which is the brand name for stavudine. (Id. ¶¶ 22-23.) On October 22, 2001, the Clinic referred Ms. Makombe to Weiss Memorial Hospital (‘Weiss”), where she was diagnosed with lactic acidosis. (Id. ¶¶ 25-26.) It is undisputed that the lactic acidosis was caused by Zerit, and that she died as a result of lactic acidosis on October 24, 2001. (Id. ¶¶ 27-28.) The disposi-tive issue in this ease, for purposes of liability, is whether the standard of care required the Clinic to have diagnosed lactic acidosis prior to October 22, 2001.

Plaintiff Innocent Kasongo, Ms. Ma-kombe’s surviving spouse, is the appointed, qualified and acting personal representative of Ms. Makombe’s estate, and has been authorized by Illinois courts to bring this action on behalf of their children Mois-és Kasongo, Ange Kasongo, and Sara Ka-songo. (Id. ¶¶ 7-8.) The federally-funded Clinic, and all its employees who provided care and treatment to Ms. Makombe, have been deemed by the Department of Health and Human Services (“DHHS”) to be employees of the United States for purposes of the Federal Tort Claims Act, 28 U.S.C § 1346(b)(1). (UF ¶¶ 5-6, 9-12.)

Clinic care providers and employees Dr. Marcia Katz, Mary Tornabene, Tamara Falk, Celine Boers, Mary Lynn Everson, and Heidi Nelson testified as adverse witnesses during Plaintiffs case-in-chief. Mr. Kasongo testified as well. Dr. Larry Ru-mans, Dr. Richard Novak, and Sheldon Fields testified as medical experts for Plaintiff, and Gerald Richard testified as an expert in the area of document examination. Dr. Harold Kessler and Bradford Farrington testified as medical experts on behalf of the United States.

A. The Parties

1. Jacqueline Makombe and Her Family

Ms. Makombe was born in what is now known as the Democratic Republic of the Congo on April 24, 1962. Although she was raised Congolese, her parents, who had emigrated from Rwanda in 1959, were of Tutsi descent. Mr. Kasongo was also born in the Congo and is Congolese. Mr. Kasongo and Ms. Makombe were married in 1987 in a folk ceremony, and renewed their vows in a civil ceremony in 1994. They settled in Kinshasa, the capital of the Congo, in 1989. Their three children are Moisés, who was born on April 13, 1991; Ange, born on November 19, 1993; and Sara, born on May 22, 1996. (Kasongo 12/13/06.)

Mr. Kasongo holds a diploma in economics and finance, and also received a diploma in “expert detective work” to assist with an accounting practice in which he investigated money laundering. His native language is French, and although he is able to communicate in English, he testified at trial through an interpreter. (Id.)

At trial, Mr. Kasongo told a harrowing tale of his family’s experiences in Africa during what are known as the First and Second Congo Wars. He explained that in 1996, the Tutsi Rwandan government funded a rebellion, led by Laurent Kabila, to overthrow Mobuto Sese Seko, the longtime ruler of the Congo (then known as Zaire). The war lasted six months. Because Ms. Makombe was Tutsi, she was in danger; Mr. Kasongo testified that in Kinshasa, Tutsi civilians were burned alive in the streets. He contacted the International Red Cross, which evacuated the family to Brazzaville, across the Congo River in the neighboring Republic of the Congo. Mr. Kasongo then brought the family to Rwanda, whose government had offered asylum to Congolese Tutsi. In Rwanda, however, Mr. Kasongo experienced difficulties because his physical experience led people to believe he was Hutu. After Ka-bila prevailed, ending the First Congo War, the family returned to Kinshasa, where Mr. Kasongo opened a grocery store and established businesses in transportation and construction to assist with rebuilding the country’s infrastructure. (Id.)

In August 1998, the Second Congo War began with a rebellion against Kabila. Mr. Kasongo described a scene in Kinshasa of massacres and generalized killings. One week after the war began, Mr. Kasongo received a phone call at work, informing him that soldiers had come to his house and taken his wife. A maid reported that thirteen or fourteen soldiers had come to the house, and that four had gone into Ms. Makombe’s bedroom, beaten her, and raped her. After learning that his wife was being held in a detention camp for Tutsi and Rwandans, Mr. Kasongo persuaded the camp’s commanding officer to allow him to take her. Because she was Tutsi, it was not safe to take her to a hospital; his cousin’s wife, however, was a medical student who helped care for her. (Id.)

The family hid in the house for the next fourteen months. Although Mr. Kasongo approached both the International Red Cross and Catholic Charities, they were unable to help the family escape Kinshasa because the borders were closed. Eventually, with the assistance of the United States government, the family was evacuated to a refugee center and ultimately to a transient camp in Cameroon. There, Ms. Makombe was diagnosed with HIV. According to Mr. Kasongo, she never knew how she had contracted the virus; in fact, he had been advised not to tell his wife that she had been raped during the soldiers’ assault, because the knowledge might prove too traumatic. (Id.)

In July 2000, the family came to Chicago and moved into a small one-bedroom apartment in the Uptown neighborhood. Ms. Makombe immediately began receiving treatment at the Clinic. (Id.)

2. The Clinic

The Clinic, which has been known since 2003 as Heartland Health Outreach, is a wholly owned subsidiary of Heartland Alliance for Human Needs and Human Rights (“Heartland”). (Nelson 12/12/06.) Heartland provides a number of programs and services, including primary medical care, mental health and addiction services, housing and homeless outreach services, and refugee resettlement programs. (Id.; see http://www.heartlandalliance.org/index. html.) The Clinic operates a community health center for the homeless and working poor, and an HIV/AIDS program that serves approximately 300 un- and under-insured patients. (Nelson 12/12/06; Tor-nabene 12/11/06.) The Clinic receives approximately two-thirds of its funding from the federal government. (Nelson 12/12/06.)

In 1999, Heartland and the Clinic instituted a program specifically for HIV-positive refugees. (Tornabene 12/11/06.) The Clinic’s Executive Director, Heidi Nelson, explained that in the late 1990s, the Clinton administration created a waiver program as an exception to a federal law that precludes individuals with communicable diseases from entering the United States. The waiver allowed HIV-positive refugees to apply for resettlement in the United States if a healthcare provider and refugee resettlement agency could provide care for them. Because Heartland already provided separate HIV primary care and refugee resettlement services, the Clinic was able to quickly set up the program. According to Nelson, the program has been successful at achieving dramatic medical improvements in HIV-positive refugees, and serves as a model for similar programs throughout the country. (Nelson 12/12/06.) In 2001, the program treated approximately 80 HIV-positive refugees and their families. (Tornabene 12/11/06.)

As of October 2001, the Clinic as a whole employed three doctors, five or six nurse practitioners, eight or nine registered nurses, and two midwives. (Tornabene 12/11/06.) At the times relevant to this lawsuit, Nelson was the Executive Director of the Clinic, and Mary Lynn Everson was the managing director; neither is a physician. (Nelson 12/12/06; Everson 12/12/06.) Dr. Katz was the Clinic’s medical director, and Tornabene, a licensed advanced practice nurse (“APN”), was the clinical director of primary care services. (Nelson 12/12/06; Tornabene 12/11/06.) Other relevant Clinic personnel include Celine Boers, an APN, (Boers 12/11/06), and Tammy Falk, a registered nurse (“RN”). (Falk 12/12/06.) Dr. Katz, Tornabene, Boers, and Falk all provided at least some degree of care to Ms. Makombe at the Clinic.

Tornabene was the primary healthcare provider for the majority of patients in the HIV-positive refugee program, including Ms. Makombe. (Tornabene 12/11/06.) In her testimony, Tornabene explained that treating HIV-positive refugees presents unique challenges, as many patients come from countries where they received little or no education, and may have endured torture and other trauma. (Id.) Falk was the nurse case manager for the HIV-positive refugee patients and their families, working primarily with Torna-bene. (Id.; Falk 12/12/06.) Falk’s role as a nurse and case manager included assisting patients with social service needs, such as housing issues. (Id.) She occasionally delivered medications to her patients’ homes, or picked up food for them. (Id.) Boers had no specific role in the HIV-positive refugee program. (Nelson 12/12/06.)

Tornabene practiced pursuant to a collaborative agreement (“CA”) with Dr. Katz, the scope of which is somewhat unclear. The CA states that an APN must obtain a consultation when presented with a clinical situation beyond his or her scope of practice, expertise or experience; and that in the event of disagreement between the APN and the collaborating physician regarding a patient’s diagnosis or treatment, the physician’s decision prevails. (Heartland Health Outreach Advanced Practice Nurse Collaborative Agreement, Pl.’s Ex. 8; Tornabene 12/11/06.) Tornabene testified that prior to Ms. Makombe’s admission to Weiss on October 22, 2001, shortly before her death, nothing in her care or treatment was beyond the scope of Torna-bene’s expertise as a nurse practitioner. (Tornabene 12/11/06.) Dr. Katz testified that she and Tornabene “worked as equals,” that they consulted with each other as needed, and that physician/nurse practitioner distinctions were “pretty much lost” in practice. (Katz 12/13/06.) Dr. Katz also noted that Tornabene had more experience working with HIV patients than she did. (Id.)

Tornabene and Dr. Katz gave somewhat inconsistent answers, however, when asked who was “ultimately responsible” for Ms. Makombe’s care and treatment at the Clinic under the CA. Tornabene testified that she was responsible for Ms. Makombe’s care; yet she acknowledged testifying in her deposition that Dr. Katz was “ultimately responsible for the care and treatment of Jacqueline Makombe with regard to doctors.” (Tornabene 12/11/06.) When asked in her deposition if she was ultimately responsible for Ms. Makombe’s care and treatment, Dr. Katz answered, “I don’t believe so”; and when asked that question at trial, replied that Ms. Ma-kombe “was not [her] patient,” and that Tornabene was “primarily responsible.” (Katz 12/13/06.) Dr. Katz further testified that she had no oversight obligations pursuant to the CA, was unclear as to the responsibility of a collaborating physician in 2001, and did not know who was ultimately responsible for Ms. Makombe’s care. (Id.) Plaintiffs expert, Dr. Rumans, testified that under the CA, Dr. Katz had the “ultimate responsibility” for Ms. Ma-kombe’s care, and was “primarily responsible.” (Rumans 12/14/06.)

Clinic Executive Director Nelson testified that Dr. Katz was primarily responsible for promulgating policies and procedures pertaining to care and treatment at the Clinic, and for ensuring that clinical guidelines relating to patient care were known by the medical staff. (Nelson 12/12/06.) Tornabene, as the clinical director of primary care services, was responsible for the “maintenance” of policies and procedures for primary care services in 2001, and for supervising the other APNs and RNs. (Id.) Nelson explained that nurse practitioners such as Tornabene are important to an outpatient medical clinic because they can perform the same tasks as physicians, can spend more time with patients and perhaps relate better to them, but command lesser salaries and are thus cost effective. (Id.)

Dr. Rumans and Bradford Farrington, an APN who testified for the government, each asserted that the standard of care is identical for a physician and a nurse practitioner. (Rumans 12/14/06; Farrington 12/15/06.) Neither party has argued to the contrary.

B. HIV/AIDS, Zerit, and Lactic Acidosis

1. HIV/AIDS and Zerit

Acquired immunodeficiency syndrome, or AIDS, results from infection with the human immunodeficiency virus, or HIV. See DoRland’s IllustRated Medioal Dictionary 1623 (28th ed. 1994) (“Dor-land’s”). An HIV-positive patient is diagnosed with AIDS upon the presence of either (1) an AIDS-defining illness, as defined by the Centers for Disease Control (“CDC”); or a T-cell count below 200. (Tornabene 12/11/06.) According to Tor-nabene, three classes of drugs were used in 2001 to treat AIDS: nucleoside reverse transcriptase inhibitors (“NRTIs”); non-nucleoside reverse transcriptase inhibitors; and protease inhibitors. (Id.) A common treatment is known as Highly Active Antiretroviral Therapy, or HAART, which consists of a combination of antire-troviral drugs from the different classes. See Treatment of HIV Infection, http:// www.niaid.nih.gov/factsheets/treat-hiv.htm.

Plaintiffs expert, Dr. Rumans, explained that HIV uses an enzyme, reverse tran-scriptase, to replicate itself by utilizing the DNA machinery in human cells. (Rumans 12/14/06.) NRTIs block that replication process by inserting themselves into the DNA replication chain, thereby preventing the virus from reproducing. (Id.) In the early 1980s, the NRTI drug AZT was the only treatment available for AIDS. (Ru-mans 12/14/06.) Zerit, or stavudine, is a newer NRTI that became available in 1994. (Id.) According to Plaintiffs expert Dr. Novak, who testified as to Ms. Ma-kombe’s life expectancy, HAART treatment that includes NRTIs such as Zerit has transformed HIV from a “death sentence” into a chronic disease, similar to diabetes, that “can be managed for an indefinite period of time.” (Novak 12/14/06.)

2. Lactic Acidosis

a. As Side Effect of Zerit

A rare but often lethal side effect of NRTIs, including Zerit and AZT, is a condition known as lactic acidosis. Lactic acidosis is “a metabolic acidosis occurring as a result of excess lactic acid in the blood, due to conditions causing impaired cellular respiration.” DoRlaNd’s, at 16. Dr. Ru-mans explained that lactic acidosis can occur when the energy process within human cells, a process known as the “Krebs cycle,” shifts from an aerobic to an anaerobic metabolism. (Rumans 12/14/06.) Ordinarily, mitochondria within cells metabolize glucose into energy; lactic acidosis results when the mitochondria are unable to take up the glucose, which instead turns into lactic acid (lactate). (Id.; Kessler 12/19/06.) NRTIs such as Zerit can cause lactic acidosis though mitochondrial toxicity, which occurs when the NRTIs bind themselves to cellular enzymes and shut down energy production within cells. (Ru-mans 12/14/06.) As a result of this mitochondrial dysfunction, the body is unable to eliminate the excess lactate, which continues to builds up in the bloodstream. (Kessler 12/19/06.) Elevated levels of lactic acid, referred to as hyperlactatemia, can lead to severe lactic acidosis if the catalyst for the elevated lactate, e.g., the Zerit, is allowed to continue. (Rumans 12/14/06.) Patients who die from lactic acidosis typically do so as a result of respiratory failure. (Id.)

b. Signs and Symptoms

The parties do not dispute the nature of the signs and symptoms of HAART-relat-ed lactic acidosis. Clinical guidelines published by the DHHS and available on the CDC’s website in August 2001, titled “Guidelines for the Use of Antiretroviral Agents in HIV-Infected Adults and Adolescents” (the “CDC Guidelines”), describe those signs and symptoms. (CDC Guidelines, Pl.’s Ex. 8, at 19.) According to the CDC Guidelines, the initial clinical presentation may include “nonspecific gastrointestinal symptoms” and dyspnea. (Id.) Dyspnea, both parties’ experts testified, means shortness of breath, or the patient’s perception or sensation thereof. (Rumans 12/14/01; Kessler 12/19/01.) Other symptoms “may include otherwise unexplained onset and persistence of abdominal distention, nausea, abdominal pain, vomiting, diarrhea, anorexia, generalized weakness, weight loss, and hepatomegaly” (enlarged liver). (CDC Guidelines, at 19).

Dr. Rumans provided a more detailed, and unchallenged, explanation of the progression of lactic acidosis. The initial symptoms are gastrointestinal: nausea, possibly vomiting, loss of appetite, and abdominal discomfort ranging from pain to “just an unpleasant feeling of fullness and distension.” (Rumans 12/14/06.) Weight loss may occur. (Id.) Next, the patient may complain of inadequate respiration. (Id.) Dr. Rumans explained that lactic acidosis effects an alteration in the respiratory system, but one that occurs slowly; thus, respiratory problems may not be “readily identifiable” to someone looking at the patient, but the patient nonetheless complains of feeling breathless. (Id.) As the condition progresses, the patient complains of fatigue and weakness, and begins to develop muscle aches and pains, or “myalgia,” due to excess lactate in the bloodstream. (Id.) Paresthesia, or numbness and tingling in the extremities, may develop and may mimic or become a type of peripheral neuropathy (numbness and pain resulting from nerve damage). (Id.)

Both parties’ experts agreed that despite the possibility of lactic acidosis, routine monitoring of lactate levels in patients taking NRTIs, through serum lactate blood testing, is unnecessary because these patients can have elevated lactate levels without showing signs of, or developing, acidosis. (Rumans 12/14/06; Kessler 12/19/06.) A serum lactate test is required once a patient shows signs and symptoms sufficient to place lactic acidosis on a differential diagnosis; if the test shows elevated lactate levels, then an arterial blood gas test can confirm the presence of the condition. (Rumans 12/14/06; Tornabene 12/11/06.) It is further undisputed that the treatment for lactic acidosis caused by Zerit is the immediate cessation of the use of Zerit. (Rumans 12/14/06; Katz 12/13/06.)

c. Frequency

The parties agree that lactic acidosis is a rare side effect of Zerit; the government characterizes it as exceedingly so. Torna-bene testified that lactic acidosis is a “very rare side effect” of antiretroviral drugs, and is “very uncommon”; she estimated its frequency at “somewhere around 3.2 cases per 1000 person years.” (Tornabene 12/11/06.) Dr. Katz referred to lactic acidosis as “incredibly rare” in 2001. (Katz 12/13/06.) Dr. Kessler called it a “very rare, rare disease,” and testified that of 681,000 prescriptions for Zerit issued in 1997, only thirty-nine cases of lactic acidosis were reported to the FDA. (Kessler 12/19/06.) He acknowledged, however, that there may have been other cases that were not reported to the FDA. (Id.)

Plaintiff, while not denying that lactic acidosis is rare, presented uncontradicted evidence that it was nonetheless a well-known side effect of Zerit by 2001 and probably for several years before that. Defendant’s expert, Dr. Kessler, acknowledged that there had been a “spike” in Zerit-related lactic acidosis in 1997, and that an article published by the FDA in 1999 had highlighted lactic acidosis as a side effect of Zerit. (Id.) Dr. Rumans testified that lactic acidosis had been linked to the NRTI drug AZT as far back as 1989, and that by the time Zerit appeared in 1994, lactic acidosis was a known side effect of NRTIs. (Rumans 12/14/06.) As early as 1996, according to Dr. Ru-mans, there had been reports of a link between lactic acidosis and Zerit specifically, and by 2000 there were warnings in the medical literature and at HIV care provider meetings. (Id.) By 2001, Dr. Rumans testified, the linkage between Zerit and lactic acidosis had thus been “clearly previously established” as far back as 1997 within the community of AIDS and HIV treatment providers. (Id.)

As noted, the CDC Guidelines specifically warned of HAART-related lactic acidosis in 2001. In addition, the FDA-approved package insert for Zerit in 1999, as replicated in the Physicians’ Desk Reference (“PDR”), contained a “black box” warning of reported cases of fatal lactic acidosis with the use of NRTIs including Zerit. (1999 PDR, PL’s Ex. 52; Kessler 12/19/06.) The same black box warning appeared in package inserts in 2000 and 2001. (2000 PDR, Pl.’s Ex. 51; 2001 PDR, Pl.’s Ex. 50.) The 1999 and 2000 versions, in a separate “Warnings” section, added that the majority of reports involved women, and the 2001 version elaborated that obesity and prolonged NRTI exposure were additional risk factors. (2001 PDR, Pl.’s Ex. 50.) Plaintiff additionally points to an article in the Journal of the Association of Nurses in AIDS Care, published in the fall of 2000, that specifically addressed lactic acidosis as a side effect of NRTI medications. (Patricia M. Caffrey, Lactic Acidosis Associated With Nucleoside Reverse Transcriptase Inhibitors, 11 J. Assoc. NuRSes AIDS Cabe 91 (2000), Pl.’s Ex. 43.) The article, written by an RN, discusses early nursing intervention, including early identification and symptom management of lactic acidosis. (Id.)

C. Ms. Makombe’s Treatment at the Clinic

1. Treatment between July 2000 and August 10, 2001

Ms. Makombe first came to the Clinic on July 24, 2000, immediately after her arrival in the United States, at which time her condition was evaluated and a nurse took her personal and medical history. (Torna-bene 12/11/06; 000004-08, 000017-19.) Although she had no AIDS-defining illness, her T-cell (CD4) count was 48, indicating a diagnosis of AIDS, and her viral load was more than 90,000. (Tornabene 12/11/06; 000010.) Mary Tornabene, who testified that she was Ms. Makombe’s primary healthcare provider throughout her treatment, first saw her on August 15, 2000. (Tornabene 12/11/06.) Tornabene’s August 15 treatment notes state that Ms. Makombe felt “sad” and “depressed,” but that she denied the “usual problems” associated with AIDS, such as sores in the mouth or chest pain. (000013.) Tornabene prescribed Zithromax and Bactrim as prophylactic antibiotics to protect against pneumonia and other infections. (Falk 12/12/06; 000019.)

At her next visit to the Clinic on September 19, 2000, Ms. Makombe reported no side effects from the medications. (000019.) She began HAART treatment with a combination of AZT and Sustiva. (Falk 12/12/06; 000021.) On September 26, 2000, she complained of a “slightly queasy stomach” after taking the Bactrim, but reported that the feeling went away when she drank a glass of water. (000021-22.) On October 24, 2000, Tornabene noted “side effects from [the] Zithromax” including nausea; Tornabene discontinued that medication, and gave instructions to take the Bactrim with food and a large glass of water. (000022-23.) After routine blood tests revealed that the AZT was causing a low neutrophil count, Torna-bene on October 26, 2000 switched Ms. Makombe from AZT to Zerit. (000023-24; Tornabene 12/11/06.) From that point until April 2001, Ms. Makombe presented with no serious problems; nurse Falk testified that she reported only “run of the mill complaints.” (Falk 12/12/06.) Ms. Makombe responded well to the Zerit. By January 23, 2001, her T-cell count was up to 112, and her viral load was less than 50, or undetectable. (000009.)

On April 17, 2001, Ms. Makombe reported dizziness and blackouts when she had “a lot of things to do at one time” or when she felt “overwhelmed.” (000028-29.) Through a French interpreter, she described having been beaten unconscious during wartime in the Congo. (Id.) In her subjective assessment, Tornabene wrote “Prayer is treatment of choice for this person.” (000029.) Tornabene made an assessment of post-traumatic stress disorder (“PTSD”) and offered a mental health referral, which Ms. Makombe refused. (000029.)

Also on April 17, Tornabene completed a “Report of Incapacity” for the Illinois Department of Human Services. (000164-000167.) Tornabene listed AIDS and PTSD as the “chief complaints of patient.” (000164.) In the section concerning limitations on activities, she indicated that Ms. Makombe had a 20-50% reduced capacity in the activities of walking, bending, turning, standing, climbing and stooping; reduced capacity of up to 20% in sitting, speaking, pushing, travel, and grasping manipulations; and a lifting limit of ten pounds. (000167.) Where the form called for observations of mental status, Torna-bene made a notation that Ms. Makombe suffered from “severe PTSD” and depression, and further wrote: “needs intensive therapy — refusing at present.” (Id.) These mental impairments resulted, in Tornabene’s estimation, in a reduced capacity of more than 50% in activities of daily living, in social functioning, and in concentration, persistence, and pace. (Id.)

On May 14, 2001, nurse Falk went to Ms. Makombe’s home after receiving a phone call in which the caller, whom Falk does not recall, reported that Ms. Ma-kombe had experienced dizzy spells and had fallen. (Falk 12/12/06.) Falk testified that she made the home visit out of concern for Ms. Makombe, and that she found Ms. Makombe sleepy yet easily aroused. (Id.) Her written assessment contains the notation “PTSD?”. (000035.) Ms. Ma-kombe came to the Clinic the following day, and saw both Falk and Tornabene. (Tornabene 12/11/06.) Tornabene noted that Ms. Makombe complained that she “gets to feeling ‘too much’ and then gets dizzy and passes out.” (Id.; 000035.) Tornabene assessed her symptoms as “probably PTSD,” and referred Ms. Ma-kombe to two Heartland programs for refugees that have experienced torture or other trauma, the Kovler Center and Refugee Mental Health. (Id.; 000036.) Tornabene testified that she wanted Ms. Makombe to be evaluated by a psychiatrist at Kovler, but that Ms. Makombe never was evaluated. (Tornabene 12/11/06.)

Ms. Makombe returned to the Clinic on May 29, 2001 for a refill of her medications, seeing only nurse Falk, and reporting no complaints. (Falk 12/12/06.) On July 17, 2001, again seeing only Falk, she reported, through an interpreter, having fainted while doing dishes, and that Mr. Kasongo had had difficulty reviving her for several hours afterward. (Id.; 000036.) Falk scheduled an EEG for July 19, the results of which showed a possible mild HIV-related encephalopathy, which according to Tornabene can cause various neurological problems, including dementia. (Tornabene 12/11/06.) Tornabene scheduled an MRI, but Ms. Makombe was unable to complete it; she could not tolerate the test due to its closeness and sounds that resemble gunfire. (Id.)

Plaintiff does not assert that any of Ms. Makombe’s above complaints or presenting symptoms, prior to August 10, 2001, constituted signs and symptoms of lactic acidosis.

2. Clinic Visits on August 10 and August 28, 2001

On August 10, 2001, Ms. Makombe presented at the Clinic complaining of nausea, gastrointestinal (“GI”) discomfort, and feelings of fullness and tenderness in both breasts. (000039.) She saw only nurse Falk, whom she told that she wanted no more tests, and that her symptoms were “God’s way of telling me not to take meds anymore.” (Id.) Ms. Makombe denied missing any doses of her medication, however. (Id.) Falk did a pregnancy test, which was negative, and offered over-the-counter antacids for the “GI discomfort.” (Id.) Falk did not consult with Tornabene or another provider on August 10. (Falk 12/12/06.)

Ms. Makombe returned to the Clinic for another scheduled appointment on August 28, 2001, seeing both Falk and Tornabene. (Tornabene 12/11/06; 000041.) She complained of “continued GI distress,” especially when eating spicy food, but reported that the antacids helped. (Id.) She reported a continued feeling of fullness in her breasts. (000041.) Tornabene’s notes indicate that Ms. Makombe reported “100% adherence to HAART” and denied missing any doses. (Id.)

Tornabene ordered pituitary gland tests to see if a pituitary discovery could be the source of Ms. Makombe’s breast enlargement and weight gain. (Tornabene 12/11/06; Falk 12/12/06.) According to her “HIV Flowsheet,” Ms. Makombe weighed 153 lbs. in September 2000; she weighed 179 lbs. in March 2001, and 194 lbs. on August 28, 2001. (000009; Falk 12/12/06.) Tornabene testified that the weight gain was “a good thing.” (Tornabene 12/11/06.) Ms. Makombe had not been weighed at the Clinic between March and August, and after the pituitary tests results came back normal, no follow-up was done with regard to her weight. (Falk 12/12/06.)

Ms. Makombe also came to the Clinic on September 7, 2001 for a tetanus shot. (Id.) She told nurse Falk at that time that her breast swelling and tenderness had decreased. (Id.; 000043.)

3. September 18 and September 26, 2001

On September 18, 2001, Ms. Makombe returned to the Clinic for a scheduled appointment, seeing both Falk and Torna-bene. (000042, 000044.) She reported doing “generally well,” and that she no longer had headaches or blackouts. (000042; Tornabene 12/11/06.) She also reported, however, a “scant amount” of yellow bilious emesis (vomit), as well as abdominal pain in the upper left quadrant. (000042.) Tornabene found Ms. Makombe’s abdomen large and firm. (Tornabene 12/11/06.) An X-ray showed a normal abdomen. (Id.) To rule out gallbladder disease, Tornabene scheduled an ultrasound of the gallbladder, spleen, liver, and pancreas. (Id.; 000044.)

On September 26, 2001, Ms. Makombe arrived at the Clinic without an appointment and was triaged by nurse Falk. (000046; Tornabene 12/11/06.) Ms. Ma-kombe complained of throat pain while swallowing, and reported that she had vomited three times the night before. (000046.) Falk’s assessment on the triage form indicated “probable viral flu (Indigestion),” and Falk recommended rest, clear liquids, a bland diet, and antacids. (Id.) Neither Tornabene nor any other provider examined Ms. Makombe on September 26. (Tornabene 12/11/06.)

4. October 1, 2001

Ms. Makombe again came to the Clinic without an appointment on October 1, 2001, and was again triaged by nurse Falk. (000047; Tornabene 12/11/06.) No interpreter was present. (000047.) The triage form notes a “continued” complaint of “no eating,” abdominal pain in the mid epigas-tric area (below the breast bone), vomiting, and constipation. (Id.) Falk also wrote that Ms. Makombe “states ‘respirations are low.’ ” (Id.) According to Falk, Ms. Makombe made this comment in “not terribly broken” English. (Falk 12/12/06.)

Falk testified that she took vital signs: temperature, blood pressure, pulse, and respiratory rate. (Id.) The triage form notes a respiratory rate of 22, which Tor-nabene testified is normal. (000047; Tor-nabene 12/11/06.) Falk found no bowel obstruction that could have been causing abdominal pain. (000047; Falk 12/12/06.) Falk indicated “NAD”, or “no apparent distress,” on the triage form. (000047.) The box labeled “shortness of breath” is unchecked on the form, (id.), and no pulse oximeter test (finger test) was done to measure the level of oxygenation in Ms. Makombe’s blood. (Tornabene 12/11/06.)

Although Ms. Makombe was Torna-bene’s patient, Tornabene was not contacted on October 1; instead, Falk consulted with Celine Boers, another APN. (Id.; Falk 12/12/06.) Boers diagnosed constipation and gave instructions for treatment with Milk of Magnesia. (Boers 12/11/06.) Beyond that diagnosis, the extent of Falk’s consultation with Boers is unclear. It is undisputed that Boers did not examine Ms. Makombe on October 1; Boers further testified that she has no recollection even of talking to Falk on October 1. (Id.) Falk testified that she told Boers about the constipation, but that she also showed Boers the triage form, which noted other symptoms, including vomiting. (Falk 12/12/06.) Boers does not remember the conversation, nor ever seeing the triage form, and testified that she would not be likely to diagnose constipation, or to prescribe Milk of Magnesia, for a patient who was vomiting. (Boers 12/11/06.)

Boers also ordered liver function tests (“LFTs”). (000047.) Although neither Boers nor Falk testified as to why LFTs were ordered, Falk made the notation “?Lft’s” in her nursing assessment on the triage form, (id.), suggesting that perhaps Falk proposed the tests to Boers, who agreed.

Falk’s consultation with Boers on October 1 amounted to Boers’ only involvement in the care and treatment of Ms. Ma-kombe. (Boers 12/11/06.)

5. October 3, 2001

Ms. Makombe made a third unscheduled visit to the Clinic on October 3, 2001. (000048.) Her caseworker Martine was present to interpret. (Id.) Falk’s triage form notes complaints of vomiting, decreased appetite, weakness, dizziness, shortness of breath, and increased breast size and tenderness. (Id.) Falk again took vital signs; Ms. Makombe’s respiratory rate was 20, which was still normal. (Id.; Tornabene 12/11/06.) Falk also noted on the form that she had called for the results of the ultrasound scan that had been conducted on October 1; that test showed that Ms. Makombe had gallstones and that her liver was normal. (000048; 000092; Torna-bene 12/11/06.) As her “nursing assessment,” Falk recorded that Ms. Makombe suffered from gallstones, “possible gastric inflammation,” and depression, though the latter observation was preceded by a question mark. (000048.) Falk again indicated “NAD” on the triage form. (Id.) She also recommended that Ms. Makombe see a nutritionist for help with the decreased appetite, and made a referral for home help. (Id.; Falk 12/12/06.) Ms. Makombe refused the home help referral, telling Falk that her husband “might get mad.” (Falk 12/12/06.)

Falk consulted with Dr. Katz on October 3; Tornabene again was not contacted. (Falk 12/12/06; Tornabene 12/11/06.) Falk testified that she described all of Ms. Ma-kombe’s signs and symptoms in her conversation with Dr. Katz. (Falk 12/12/06.) Dr. Katz herself did not examine Ms. Ma-kombe, and did not review Ms. Makombe’s medical records. (Katz 12/13/06.) Dr. Katz prescribed Ranitidine, a drug used to treat gastroesophageal reflux disease (“GERD”), and instructed Falk to schedule an appointment for Ms. Makombe with a surgeon for a gallbladder evaluation. (Id.; 000048.) Falk testified that Dr. Katz also instructed her to do a pulse oximeter test; the test showed an oxygenation rate (SP 02) of 98%, which is normal. (Falk 12/12/06; Tornabene 12/11/06.)

6. October 9, 2001

On October 9, 2001, Ms. Makombe came to the Clinic for a scheduled appointment. (Tornabene 12/11/06.) No interpreter was present. (Id.) She saw both Tornabene and Falk. (Id.) To Falk, she complained of pain deep inside both legs from the knees to the soles of her feet, and reported that the skin on both legs felt numb. (000049.) She told Falk that her breasts were “bothering [her] very much.” (Id.) Falk wrote that Ms. Makombe “still feels that breathing is very low.” (Id.) Ms. Makombe also reported that her appetite and eating had improved; Falk noted, however, that Ms. Makombe had lost “10 lbs.” since August. (Id.) Falk measured a respiratory rate of 20; neither Falk nor Tornabene did a pulse oximeter test. (Id.; Tornabene 12/11/06.)

Tornabene noted “multiple somatic [complaints] including bilateral leg soreness” with “some paresthesias,” and that Ms. Makombe “feels breathing so heavy because breasts are so big.” (000050.) Tornabene then conducted a physical exam, which she described in her testimony as “almost a complete exam.” (Torna-bene 12/11/06.) She found Ms. Makombe’s lungs clear, her mouth fine, and her abdomen soft, not tender. (Id.) Tornabene recalled that Ms. Makombe “looked great on that day. She looked really really good.” (Id.) Tornabene assessed AIDS, PTSD, and gallstones, and told Ms. Makombe to return in one to two weeks because she wanted to keep a “close eye” on Ms. Ma-kombe’s complaints. (Id.)

Tornabene testified, and her treatment notes indicate, that she considered stopping the Zerit treatment on October 9. (Id.; 000050.) This was not out of concern about lactic acidosis, however. Tornabene testified that paresthesia is a common side effect of Zerit, and that there had been (unidentified) warnings by 2001 of peripheral neuropathy, a symptom that might be alleviated by removal of Zerit. (Torna-bene 12/11/06.) Dr. Rumans similarly testified that paresthesia caused by a neuro-pathy was a well-recognized side effect of Zerit in 2001, (Rumans 12/14/01), and the 1999, 2000, and 2001 package inserts for Zerit warned of peripheral neuropathy. (PDRs, Pl.’s Ex. 50-52.) Tornabene testified that she considered stopping the Zerit because it might be causing a neuropathy, and that she discussed this with Ms. Ma-kombe. (Tornabene 12/11/06.) According to Tornabene, Ms. Makombe was unwilling to stop taking the Zerit, and instead told Tornabene that she had a friend with tuberculosis who took vitamin B6 for a neu-ropathy. (Id.) Tornabene agreed that taking B6 would do no harm, and that Ms. Makombe could continue the Zerit treatment because Zerit had been effective at keeping her viral load down and her T-cell count stable. (Id.)

Tornabene further testified that as of October 9, she was aware of the results of the LFTs that Boers had ordered on October 1. (Id.) She did not explain when she reviewed those results, and there is no mention of them in her October 9 notes. (000050.) Those results, which measured liver enzyme levels, indicate an ALT (alanine am i notransfe rase) of 45 and an AST (aspartate aminotransferase) of 53; normal range for both is between zero and 40. (Tornabene 12/11/06; 000090.) In her testimony, Tornabene nevertheless characterized these results as “essentially normal” because elevated AST and ALT levels are common with HIV. (Tornabene 12/11/06.) In Tornabene’s view, only a reading as high as 80 would be cause for concern. (Id.) She acknowledged, however, that patients with lactic acidosis can have elevated liver enzymes. (Id.)

On October 15, 2001, Ms. Makombe saw Dr. Gerald Kaplan for the gallstone evaluation that Dr. Katz had ordered on October 3. (000090.) Dr. Kaplan recommended an upper GI endoscopy to rule out GERD. (Id.) The record from this visit appears to consist entirely of the referral form, on which Dr. Kaplan’s brief remarks note no complaints other than the GI complaints that were the basis for the referral. (000090.)

7. October 22, 2001

Ms. Makombe came to the Clinic at 10:30 a.m. on October 22, 2001 without an appointment, complaining of shortness of breath that “feels like suffocating,” severe pain in her ankles and the soles of her feet, and “burning” epigastric pain. (000051.) She reported that she had not been eating or sleeping. (Id.) Falk’s notes on the triage form also include vomiting, dizziness, weakness, and increased abdomen size. (Id.) October 22 was a Monday; Ms. Ma-kombe told Falk that she had been feeling poorly all weekend, but that the Clinic had been closed. (Falk 12/12/06.) Despite Ms. Makombe’s complaints, Falk did not believe she was in distress because her vital signs were normal. (Id.)

After the initial triage, Falk spoke with Tornabene, who did not examine Ms. Ma-kombe. (Id.) Falk testified that Torna-bene could see Ms. Makombe in an examination room from where Tornabene was sitting at the nurses’ station. (Id.) Torna-bene testified that she saw Ms. Makombe from several feet away and that she “looked awful.” (Tornabene 12/11/06.) Tornabene told Falk to send Ms. Ma-kombe to the outpatient lab at Weiss for a STAT serum lactate test and for STAT LFTs, and to stop the HAART medications. (Id,.; 000051-000052.) She also told Falk to do a pulse oximeter test, which again showed an SP 02 level of 98%. (Falk 12/12/06; 000051.) By this point, lactic acidosis was on the differential diagnosis, (Tornabene 12/11/06); Tornabene’s notes from October 22 state that her assessment was to rule out lactic acidosis. (000052.)

According to Tornabene, she wanted Ms. Makombe to go the outpatient lab at Weiss, rather than to the emergency room (“ER”), because the test results would come back more quickly. (Id.) Falk testified that when she told Ms. Makombe to go to the outpatient lab, which was several blocks away, Ms. Makombe replied that she would rather go to the ER, asking, “do you want me to die in the street?” (Falk 12/12/06.) Falk testified that because Ms. Makombe was able to walk, she did not call an ambulance. (Id.) Ms. Makombe’s caseworker Martine accompanied her to Weiss. (Id.)

The Weiss lab collected blood at 12:10 p.m. on October 22. (000093.) The results, indicating highly elevated lactate levels, were faxed to the clinic at 2:17 p.m. (Tor-nabene 12/11 /06.) An arterial blood gas test was done at Weiss at 2:16 p.m. (000094.) Ms. Makombe was seen at the ER at Weiss at 4:10 p.m.; ER intake records state that Dr. Katz referred her there. (000157.) The ER had the results of the serum lactate and arterial blood gas tests. (Tornabene 12/11/06.) The ER records indicate that Ms. Makombe’s oxygenation rate was 100%, that she was ambulatory, and that her condition was “non-urgent.” (000157.) She was subsequently admitted to the hospital. (Tornabene 12/11/06.)

Mr. Kasongo testified that he had been worried when his wife had not returned from the Clinic. (Kasongo 12/13/06.) After receiving a phone call around 5 p.m. that she was at Weiss, he left the children with a neighbor and went to the ER. (Id.) He found Ms. Makombe in the waiting room, where she told him of “heat rising from her stomach to her mouth.” (Id.) She told her husband to go home and care for the children, and that she would be coming home in a couple of days. (Id.) He testified that when he left, he did not believe that his wife was going to die. (Id.)

Ms. Makombe’s condition in fact deteriorated rapidly after her admission to Weiss. (Tornabene 12/11/06; Discharge Summary, 000140.) At around 10:00 p.m. on the night of October 22, a doctor at Weiss called Mr. Kasongo and told him that Ms. Makombe was having difficulty breathing and was in intensive care; when Mr. Ka-songo asked to speak to his wife, the doctor informed him that it was impossible. (Kasongo 12/13/06.) On October 24, Weiss doctors told him that Ms. Makombe was on life support, could remain in the same condition for months with no change, and was unlikely to recover. (Id.) Tornabene testified that Ms. Makombe was brain dead. (Tornabene 12/11/06.) Mr. Kason-go testified that after speaking with his wife’s brother in Belgium, he “took the responsible decision of liberating her.” (Id.) Falk, Tornabene, and Dr. Katz were present with Mr. Kasongo when Ms. Ma-kombe was taken off the ventilator. (Tor-nabene 12/11/06; Falk 12/12/06.)

D. Testimony

As noted, it is undisputed in this case that Ms. Makombe died on October 24, 2001 from lactic acidosis that was caused by Zerit. (UF ¶¶ 27-28.) The dispute centers around whether the standard of care required the Clinic to have diagnosed her lactic acidosis prior to her coming to the Clinic on October 22, 2001. Plaintiff, to this end, presented the testimony of medical experts and of Ms. Makombe’s healthcare providers at the Clinic. The government called two experts. In an effort to support an argument that certain medical records had been altered, Plaintiff also called an expert in the area of document examination. Plaintiff further presented evidence relating to damages, including testimony as to Ms. Makombe’s life expectancy and the loss experienced by Mr. Kasongo and his children. The court here presents relevant portions of this testimony.

1. Testimony Concerning Document Alteration

Gerald Richard, a former FBI agent and chief of the FBI document operations and research unit, testified as an expert in the area of document examination. (Richard 12/14/06.) He examined four documents in this case: the October 1 triage form completed by Falk (000047); the October 3 triage form, also completed by Falk (000048); the second page of October 9 treatment notes, written by Tornabene (000050); and Falk’s October 22 triage form (000051). He testified that he used techniques including infrared reflectance, infrared luminescence, and dichroic filter examination. (Id.)

Richard testified that Falk’s writing on the October 1 triage form consisted of two different pen ink formulations. (Id.) Specifically, the vital sign entries for blood pressure and pulse rate, and the indication “NAD”, were written in a different pen from the entries on the rest of the document. (Id.) Similarly, the entries on the October 3 form for blood pressure and SP 02, and the “NAD” indication, were written in a different pen from the pen used on the rest of the form; those entries, moreover, were “similar in all observable respects” to the entries written by the second pen on the October 1 triage form. (Id.)

The second page of treatment notes from Ms. Makombe’s October 9, 2001 appointment, in which Tornabene wrote that she was considering stopping the Zerit but that Ms. Makombe had requested vitamin B6 instead, indeed is dated “10/9.” (000050.) Richard testified, however, that the date had been altered, but that the original date was indeterminable because the ink formulations were similar. (Richard 12/14/06.) That ink formulation, which was used on the entire page, was similar to that of the second pen used on the October 1 and October 3 triage forms. (Id.)

With respect to the October 22 triage form, Richard testified that three different ink formulations had been used, with the majority of the document written in an ink formulation similar to that of the second pen on the October 1 triage form, the October 3 triage form, and the second page of October 9 treatment notes.

Although the government generally did not dispute Richard’s findings, both Falk and Tornabene offered explanations for why certain entries may have been made by different pens. Falk testified that she might, for example, have two pens in her pocket; or she might take a chart to a provider with whom she was consulting, and use a different pen at that time; or she might hand a pen to a patient to fill something out and then use a different pen to continue writing. (Falk 12/12/06.) When asked why the “NAD” indication on the October 1 triage form appears to be written at a different angle from other entries, Falk testified that she remembered taking the form with her when consulting with Boers, who asked her if Ms. Makombe was in distress; when Falk said no, she reached over the desk at which Boers was sitting and wrote “NAD.” (Id.) Falk denied doctoring the medical records in any way — a denial the court found fully credible.

As for why the differing group of entries may have had similar ink formulations, Tornabene testified that “drug reps” frequently hand out pens at the Clinic; indeed, such pens are “all over the clinic.” (Tornabene 12/11/06.) Richard testified that pens from the same manufacturer might have the same or similar ink formulations. (Richard 12/14/06.) From the court’s perspective, the most plausible explanation for the alteration of the date on the second page of October 9 treatment notes is simply that the original entry was mistaken and then corrected. Moreover, any suggestion that that page had been written at a different time, possibly in an attempt to alter the records, is belied by the fact that in the first page of October 9 notes, Falk wrote that Tornabene had indeed instructed her to provide vitamin B6 for Ms. Makombe. (000049.)

Because the evidence does not support any finding that Ms. Makombe’s records were doctored or altered after the fact, the court declines to further consider any argument in that regard.

2. Testimony Concerning the Standard of Care

a. Testimony of Clinic Healthcare Providers and Employees

i. Mary Tornabene (12/11/06)

Tornabene began working at the Clinic as an RN in 1990 before obtaining her APN license. She testified that she has received specialized HIV training, has lectured on HIV-related topics including an-tiretroviral drugs, and completes 16-20 hours per year in continuing education in the HIV field. She has many HIV patients at the Clinic.

Tornabene testified that she knew in 2001 that NRTIs had the known side effect of lactic acidosis. She further testified that the standard of care in 2001 required her to know the signs and symptoms of lactic acidosis, and acknowledged that she, as a treatment provider, was responsible to be on guard for signs and symptoms of potentially fatal side effects of medications.

Tornabene acknowledged that the updated CDC Guidelines, warning of HAART-related lactic acidosis, had been published on August 13, 2001, and that the standard of care required her to know of any such updates. Those guidelines, according to Tornabene, were available on the CDC’s website, and on “every HIV treatment web site.” All charting stations at the Clinic, Tornabene testified, had binders containing all the latest clinical guidelines, and “everybody knew they were there.”

Tornabene further testified as to her knowledge of the specific signs and symptoms of lactic acidosis that she had seen Ms. Makombe beginning to exhibit in August 2001. She acknowledged that Ms. Makombe’s complaints of nausea and GI discomfort on August 10, 2001, were signs and symptoms of lactic acidosis, as were Ms. Makombe’s complaints on September 18 of vomiting, abdominal pain in the upper left quadrant, and the fact that her abdomen was large and firm. Similarly, Ms. Makombe’s complaints on October 1, 2001 of vomiting, lack of appetite, and mid-epigastric pain were signs and symptoms of lactic acidosis. Tornabene further acknowledged that a complaint of shortness of breath would also be a sign of lactic acidosis; she denied, however, that Ms. Makombe’s statement that “respirations are low” signified “shortness of breath.” According to Tornabene, “shortness of breath” means “inability to breathe” or to “feel like you are breathing adequately,” and a statement that “respirations are low” does not qualify.

Tornabene acknowledged that Ms. Ma-kombe did exhibit shortness of breath on October 3, 2001, which, along with her complaints of weakness, decreased appetite, and vomiting, were signs and symptoms of lactic acidosis. Tornabene testified that Ms. Makombe’s additional symptom on October 9 of pain in her legs was also a sign and symptom of lactic acidosis, but that paresthesia, which Ms. Makombe also presented with on October 9, is a “common” side effect of Zerit that has “nothing to do with” lactic acidosis. With respect to Ms. Ma-kombe’s reporting on October 9 that her appetite and eating had improved, Torna-bene admitted that it was possible that the Ranitidine, which Dr. Katz had prescribed for GERD on October 3, had masked Ms. Makombe’s epigastric pain sufficiently that she was able to eat.

As noted, lactic acidosis was on Torna-bene’s differential diagnosis on October 22, when Ms. Makombe presented with shortness of breath that “feels like suffocating,” pain in her ankles and the soles of her feet, lack of appetite, and epigastric pain. She maintained that the standard of care did not require lactic acidosis to have been on the differential diagnosis before then, on October 1 or on October 9. She admitted that when asked in her deposition what else would have been needed on October 1 for lactic acidosis to have been on the differential diagnosis, she had answered, “shortness of breath and leg pain.” When asked at trial whether lactic acidosis should have been on the differential diagnosis on October 9, when Ms. Makombe did exhibit both those symptoms, Torna-bene answered, “I wish I had, but no ... no. She was fine ... she looked good.” Significantly, Tornabene acknowledged that the complaints Ms. Makombe experienced on October 22, which did result in Tornabene’s differential diagnosis of lactic acidosis, had been ongoing since at least October 9.

When asked if her process of developing a differential diagnosis consisted of looking at the signs and symptoms and charting possible diagnoses from the most severe to the least severe, Tornabene testified that that was not a “complete definition” of a differential diagnosis; in her deposition, however, she had answered “correct” when asked the question. Tornabene further testified that had lactic acidosis been part of the differential diagnosis before October 22, she would have ordered a serum lactate test, which cost $20. Tornabene also testified that had she discontinued the Zerit on October 9, the outcome may have been different; however, there was “no guarantee” because other NRTIs (which presumably would have been substituted for Zerit) had the same side effect of lactic acidosis. Ultimately, Tornabene defended her actions by testifying that lactic acidosis is “an incredibly difficult thing to diagnose.” She stated that she felt “incredibly awful that this woman got sick and died. She had incredibly good care. She had complaints in her gut. We looked in her gut, we addressed everything that she had

ii. Tammy Falk (12/12/06)

Falk, an RN, started working at the Clinic in October 2000. Before that, she was a nurse at Illinois Masonic, where she cared for many patients with HIV. Shortly after starting at the Clinic, she attended a training course at the Midwest Aids Training and Educational Center (“MATEC”). Falk worked primarily with Tornabene at the Clinic, and as the nurse case manager of the HIV-positive refugee program, had a specific caseload of HIV-positive refugees and their families. Falk testified that her job as a nurse was to identify a patient’s signs and symptoms and present those signs and symptoms to a physician or to an APN.

At trial, Falk could not remember whether she knew in October 2001 that lactic acidosis was a side effect of Zerit, but acknowledged that at the time of her deposition, she did not believe she did. She further testified that she did not know in October 2001 that not eating, vomiting, epigastric pain, abdominal pain, muscle pain, and shortness of breath were signs and symptoms of lactic acidosis. She testified that she was not sure whether the standard of care required her to know the side effects of Zerit in 2001; but she admitted that she was required to educate Ms. Makombe about the side effects of Zerit, and that her role in educating patients about their medication including going over common side effects.

Falk acknowledged that the Clinic followed clinical guidelines from the CDC. She testified that those guidelines were available at the nurses’ station in the Clinic, but admitted stating in her deposition that she did not know if she ever accessed them there; at trial, she explained that she “[did] them on line” because going to the CDC website was “the most up-to-date way to get those guidelines.” She further testified that she did not know in 2001 that the CDC Guidelines indicated that lactic acidosis could be a known side effect of Zerit.

Falk also testified that in 2001, the Journal of the Association of Nurses in AIDS Care, was available on fine, and that she had looked up articles pertaining to AIDS and HIV treatment. As noted, that Journal published an article in 2000 that specifically addressed lactic acidosis as a side effect of NRTIs. Falk was not asked at trial whether she had in fact seen the specific article.

iii. Dr. Marcia Katz (12/13/06)

Dr. Katz, the medical director of the Clinic in 2001 and a staff physician, testified that she had no independent recollection of Ms. Makombe prior to October 22, 2001. She asserted that Ms. Makombe was not her patient, that Tornabene was Ms. Makombe’s primary care provider and was thus “primarily responsible” for her care and treatment, and that she had provided no direct care with respect to Ms. Makombe until October 22, 2001, when Ms. Makombe was admitted to Weiss.

Dr. Katz was aware in 2001 of case reports of lactic acidosis occurring with patients who were taking Zerit. She testified that vomiting, dizziness, nausea, GI discomfort, upper GI pain, weakness, and shortness of breath are all potential signs and symptoms of lactic acidosis, but that she did not believe that paresthesia is a sign or symptom. Unlike Tornabene, Dr. Katz testified that a statement that “breathing is very low” could be a sign or symptom of lactic acidosis, and that Falk’s indication on the October 1 triage form that Ms. Makombe’s “respirations are low” was a new and different sign and symptom that would make her more suspicious of lactic acidosis.

Dr. Katz acknowledged that Ms. Ma-kombe on October 1, 2001 was exhibiting at least five signs and symptoms of lactic acidosis, including decreased appetite, GI pain, vomiting, low respirations, abdominal pain, and indigestion. In her testimony at trial, she nevertheless answered “no” when asked whether a diagnosis of lactic acidosis should have been made on October 1, whether lactic acidosis should have been on a differential diagnosis, and whether a failure to diagnose lactic acidosis at that time was a deviation from the standard of care. This testimony was inconsistent with her deposition testimony, in which she testified that lactic acidosis could have been diagnosed “at the very earliest” on October 1, answered “correct” when asked if it should have been on the differential diagnosis, and answered “yes” when asked if it was more probably true than not that it was a deviation from the standard of care not to have diagnosed lactic acidosis on October 1. Similarly, Dr. Katz testified at trial that she did not believe that a lactate level test should have been done on October 1, but admitted answering to the contrary in her deposition.

With respect to October 3, when Falk consulted with her, Dr. Katz acknowledged that she did not personally examine Ms. Makombe, and that she never looked at Ms. Makombe’s medical records. She defended not seeing Ms. Makombe herself, explaining, “I depend on someone to tell me that they think something is different.” Moreover, she testified, she would not have ordered