Gregg K. VandeKieft, MD

Mary’s father died last month. Mr B was an uncomplicated man who treated most ailments with an aspirin and a beer. This time, however, the ailment was worse and the therapy less benign. His lymphoma went into remission, but chemotherapy caused complications: congestive heart failure, bowel obstruction, ascites, and eventually sepsis and adult respiratory distress syndrome. Mary, a nurse for 20 years, attended her father’s clinic visits and sat at his bedside; she was his ambassador to the medical system that dominated his life. Her clinical experience, however, was not enough to prepare Mary for the debacle of her father’s death.

For Mr B the end began quickly, but it did not end quickly. Hospialized with multisystem failure, he became confused, so treatment decisions were turned over to his wife. Mary’s mother was not ready to stop treatment as long as there was hope for recovery, and no physician told her otherwise; it seemed too much like euthanasia. Two “successful” resuscitations prolonged his death, allowing him to spend his last weeks on a ventilator, rarely coherent.

Hospital staff touted Mr. B’s physician as one of the best in the world. And indeed he maintained all the right physiologic parameters. But Mary thought him less than zero. When it came time to turn off the ventilator, he assured the family that Mr B would be asleep, and it would all be over in less than 15 minutes. At the appointed time, Mr B’s family gathered at his bedside, said their good-byes, and steeled themselves for the imminent death of a husband and father. Hours later, the physician finally came back and said, “It’s too late in the day; we’ll do it tomorrow morning” …and left. Mr B’s family went home for a sleepless night and resumed their deathbed vigil in the morning. The physician came in and said, “See, he’s sleeping; he won’t know a thing,” and disconnected the ventilator. Mr B’s eyes flew open; he looked panicked. The physician laughed-laughed!-and said, “Well I guess that did get his attention.” Without further comment, he wheeled the ventilator from the room, never to be seen or heard from again. One of Mr B’s other physicians stuck his head in the door around midday and said, “Oh, he’s still holding on” …and then left. He also was never seen or heard from again.

Mary’s father gasped and looked about the room for 9 hours. No one sedated him or treated his respiratory distress; instead, he was merely given modest doses of pain relievers. And so the family waited…and watched…for 9 hours. Finally, he died.

Neither of the physicians contacted Mr B’s family after his death. A consultant peripherally involved in Mr B’s care sent a hand-written note saying what a special man Mr B had been, as witnessed by the loving and caring family he had raised. Mrs B cherished this simple caring gesture immeasurably. Why, she wondered, did none of the other physicians care for her husband in this way?

The end began quickly. The scars will last forever. Mary does not question the management of her father’s lymphoma. She knows that medical science cannot always provide a cure. But she never imagined that technologically skilled physicians would be so inept in the art of medicine. Contemporary end of life care guided by basic compassion and caring could have spared Mr B’s family the legacy of a botched death. Instead, their grief is intertwined with a profound sense of violation. Mary’s tears stemmed more from her helplessness than from the sadness of losing her father. Despite her nursing experience she could not protect her father and family from technology run amok, from incompetence in the fundamentals of palliative care of one of the best physicians in the world, or from the relational negligence of those entrusted to care for her father. Mr B’s death will live forever in Mary’s memory for all the wrong reasons.

When will we recognize this as malpractice?

Mary’s father died last month. Mr B was an uncomplicated man who treated most ailments with an aspirin and a beer. This time, however, the ailment was worse and the therapy less benign. His lymphoma went into remission, but chemotherapy caused complications: congestive heart failure, bowel obstruction, ascites, and eventually sepsis and adult respiratory distress syndrome. Mary, a nurse for 20 years, attended her father’s clinic visits and sat at his bedside; she was his ambassador to the medical system that dominated his life. Her clinical experience, however, was not enough to prepare Mary for the debacle of her father’s death.

For Mr B the end began quickly, but it did not end quickly. Hospialized with multisystem failure, he became confused, so treatment decisions were turned over to his wife. Mary’s mother was not ready to stop treatment as long as there was hope for recovery, and no physician told her otherwise; it seemed too much like euthanasia. Two “successful” resuscitations prolonged his death, allowing him to spend his last weeks on a ventilator, rarely coherent.

Hospital staff touted Mr. B’s physician as one of the best in the world. And indeed he maintained all the right physiologic parameters. But Mary thought him less than zero. When it came time to turn off the ventilator, he assured the family that Mr B would be asleep, and it would all be over in less than 15 minutes. At the appointed time, Mr B’s family gathered at his bedside, said their good-byes, and steeled themselves for the imminent death of a husband and father. Hours later, the physician finally came back and said, “It’s too late in the day; we’ll do it tomorrow morning” …and left. Mr B’s family went home for a sleepless night and resumed their deathbed vigil in the morning. The physician came in and said, “See, he’s sleeping; he won’t know a thing,” and disconnected the ventilator. Mr B’s eyes flew open; he looked panicked. The physician laughed-laughed!-and said, “Well I guess that did get his attention.” Without further comment, he wheeled the ventilator from the room, never to be seen or heard from again. One of Mr B’s other physicians stuck his head in the door around midday and said, “Oh, he’s still holding on” …and then left. He also was never seen or heard from again.

Mary’s father gasped and looked about the room for 9 hours. No one sedated him or treated his respiratory distress; instead, he was merely given modest doses of pain relievers. And so the family waited…and watched…for 9 hours. Finally, he died.

Neither of the physicians contacted Mr B’s family after his death. A consultant peripherally involved in Mr B’s care sent a hand-written note saying what a special man Mr B had been, as witnessed by the loving and caring family he had raised. Mrs B cherished this simple caring gesture immeasurably. Why, she wondered, did none of the other physicians care for her husband in this way?

The end began quickly. The scars will last forever. Mary does not question the management of her father’s lymphoma. She knows that medical science cannot always provide a cure. But she never imagined that technologically skilled physicians would be so inept in the art of medicine. Contemporary end of life care guided by basic compassion and caring could have spared Mr B’s family the legacy of a botched death. Instead, their grief is intertwined with a profound sense of violation. Mary’s tears stemmed more from her helplessness than from the sadness of losing her father. Despite her nursing experience she could not protect her father and family from technology run amok, from incompetence in the fundamentals of palliative care of one of the best physicians in the world, or from the relational negligence of those entrusted to care for her father. Mr B’s death will live forever in Mary’s memory for all the wrong reasons.

When will we recognize this as malpractice?

Mary’s father died last month. Mr B was an uncomplicated man who treated most ailments with an aspirin and a beer. This time, however, the ailment was worse and the therapy less benign. His lymphoma went into remission, but chemotherapy caused complications: congestive heart failure, bowel obstruction, ascites, and eventually sepsis and adult respiratory distress syndrome. Mary, a nurse for 20 years, attended her father’s clinic visits and sat at his bedside; she was his ambassador to the medical system that dominated his life. Her clinical experience, however, was not enough to prepare Mary for the debacle of her father’s death.

For Mr B the end began quickly, but it did not end quickly. Hospialized with multisystem failure, he became confused, so treatment decisions were turned over to his wife. Mary’s mother was not ready to stop treatment as long as there was hope for recovery, and no physician told her otherwise; it seemed too much like euthanasia. Two “successful” resuscitations prolonged his death, allowing him to spend his last weeks on a ventilator, rarely coherent.

Hospital staff touted Mr. B’s physician as one of the best in the world. And indeed he maintained all the right physiologic parameters. But Mary thought him less than zero. When it came time to turn off the ventilator, he assured the family that Mr B would be asleep, and it would all be over in less than 15 minutes. At the appointed time, Mr B’s family gathered at his bedside, said their good-byes, and steeled themselves for the imminent death of a husband and father. Hours later, the physician finally came back and said, “It’s too late in the day; we’ll do it tomorrow morning” …and left. Mr B’s family went home for a sleepless night and resumed their deathbed vigil in the morning. The physician came in and said, “See, he’s sleeping; he won’t know a thing,” and disconnected the ventilator. Mr B’s eyes flew open; he looked panicked. The physician laughed-laughed!-and said, “Well I guess that did get his attention.” Without further comment, he wheeled the ventilator from the room, never to be seen or heard from again. One of Mr B’s other physicians stuck his head in the door around midday and said, “Oh, he’s still holding on” …and then left. He also was never seen or heard from again.

Mary’s father gasped and looked about the room for 9 hours. No one sedated him or treated his respiratory distress; instead, he was merely given modest doses of pain relievers. And so the family waited…and watched…for 9 hours. Finally, he died.

Neither of the physicians contacted Mr B’s family after his death. A consultant peripherally involved in Mr B’s care sent a hand-written note saying what a special man Mr B had been, as witnessed by the loving and caring family he had raised. Mrs B cherished this simple caring gesture immeasurably. Why, she wondered, did none of the other physicians care for her husband in this way?

The end began quickly. The scars will last forever. Mary does not question the management of her father’s lymphoma. She knows that medical science cannot always provide a cure. But she never imagined that technologically skilled physicians would be so inept in the art of medicine. Contemporary end of life care guided by basic compassion and caring could have spared Mr B’s family the legacy of a botched death. Instead, their grief is intertwined with a profound sense of violation. Mary’s tears stemmed more from her helplessness than from the sadness of losing her father. Despite her nursing experience she could not protect her father and family from technology run amok, from incompetence in the fundamentals of palliative care of one of the best physicians in the world, or from the relational negligence of those entrusted to care for her father. Mr B’s death will live forever in Mary’s memory for all the wrong reasons.

When will we recognize this as malpractice?

CLINICAL QUESTION: Does therapy with an angiotensin-converting-enzyme (ACE) inhibitor reduce the rate of cardiovascular events in high-risk patients with no known left ventricular (LV) dysfunction or heart failure?

BACKGROUND: The renin-angiotensin-aldosterone system is an important contributor to the pathogenesis of cardiovascular disease. ACE inhibitors improve outcomes in patients with LV dysfunction (with or without heart failure). This study assessed whether therapy with an ACE inhibitor, ramipril, reduced the rate of cardiovascular events in high-risk patients with no known LV dysfunction or heart failure.

POPULATION STUDIED: From December 1993 through June 1995, the Heart Outcomes Prevention Evaluation (HOPE) investigators recruited patients from 277 centers in Canada, the United States, Argentina, Brazil, Mexico, and 14 western European countries. The final study population included 9297 patients at high risk for a cardiovascular event. All patients were aged 55 years or older and had either evidence of vascular disease or diabetes mellitus plus one other cardiovascular risk factor. Exclusion criteria included known history of heart failure or low LV ejection fraction (<40%), use of an ACE inhibitor or vitamin E, uncontrolled hypertension, overt nephropathy, and myocardial infarction or stroke in the 4 weeks before the study began.

STUDY DESIGN AND VALIDITY: The study was part of a double-blinded 2-by-2 factorial randomized trial evaluating both ramipril and vitamin E. This paper reports the placebo-controlled study of ramipril 10 mg per day compared with placebo. Allocation of patients to ramipril or placebo was adequately concealed. Treatments were compared using the log-rank test, and subgroup analyses were conducted using tests for interactions in the Cox regression model. Treatment was scheduled to last 5 years, but an independent monitoring board recommended termination of the study after 4 years because of clear evidence of a beneficial effect of ramipril.

OUTCOMES MEASURED: The primary study outcome was a composite of myocardial infarction, stroke, or death from cardiovascular causes. Secondary outcomes were death from any cause, the need for revascularization, hospitalization for unstable angina or heart failure, diabetes-related complications, and each of the primary outcomes reported individually.

RESULTS: Compared with controls, treatment with ramipril reduced the combined rate of myocardial infarction, stroke, or death from cardiovascular causes (relative risk reduction [RRR]=21%, absolute risk reduction [ARR]=3.8%, number needed to treat [NNT]=27). It also reduced the rates of the secondary outcomes, including death from any cause (RRR=15%, ARR=1.9%, NNT=54), revascularization procedures (RRR=13%, ARR=2.3%, NNT=43), cardiac arrest (RRR=38%, ARR=0.5%, NNT=200), heart failure (RRR=22%, ARR=2.5%, NNT=40), and complications related to diabetes (RRR=16%, ARR=1.2%, NNT=83). All these reductions in risk were statistically significant. Reduction in blood pressure was not felt to be a major factor in the improved outcomes; the majority of patients did not have underlying hypertension and the treatment group’s mean reduction in blood pressure was minimal (3/2 mm Hg).

CLINICAL QUESTION: Does therapy with an angiotensin-converting-enzyme (ACE) inhibitor reduce the rate of cardiovascular events in high-risk patients with no known left ventricular (LV) dysfunction or heart failure?

BACKGROUND: The renin-angiotensin-aldosterone system is an important contributor to the pathogenesis of cardiovascular disease. ACE inhibitors improve outcomes in patients with LV dysfunction (with or without heart failure). This study assessed whether therapy with an ACE inhibitor, ramipril, reduced the rate of cardiovascular events in high-risk patients with no known LV dysfunction or heart failure.

POPULATION STUDIED: From December 1993 through June 1995, the Heart Outcomes Prevention Evaluation (HOPE) investigators recruited patients from 277 centers in Canada, the United States, Argentina, Brazil, Mexico, and 14 western European countries. The final study population included 9297 patients at high risk for a cardiovascular event. All patients were aged 55 years or older and had either evidence of vascular disease or diabetes mellitus plus one other cardiovascular risk factor. Exclusion criteria included known history of heart failure or low LV ejection fraction (<40%), use of an ACE inhibitor or vitamin E, uncontrolled hypertension, overt nephropathy, and myocardial infarction or stroke in the 4 weeks before the study began.

STUDY DESIGN AND VALIDITY: The study was part of a double-blinded 2-by-2 factorial randomized trial evaluating both ramipril and vitamin E. This paper reports the placebo-controlled study of ramipril 10 mg per day compared with placebo. Allocation of patients to ramipril or placebo was adequately concealed. Treatments were compared using the log-rank test, and subgroup analyses were conducted using tests for interactions in the Cox regression model. Treatment was scheduled to last 5 years, but an independent monitoring board recommended termination of the study after 4 years because of clear evidence of a beneficial effect of ramipril.

OUTCOMES MEASURED: The primary study outcome was a composite of myocardial infarction, stroke, or death from cardiovascular causes. Secondary outcomes were death from any cause, the need for revascularization, hospitalization for unstable angina or heart failure, diabetes-related complications, and each of the primary outcomes reported individually.

RESULTS: Compared with controls, treatment with ramipril reduced the combined rate of myocardial infarction, stroke, or death from cardiovascular causes (relative risk reduction [RRR]=21%, absolute risk reduction [ARR]=3.8%, number needed to treat [NNT]=27). It also reduced the rates of the secondary outcomes, including death from any cause (RRR=15%, ARR=1.9%, NNT=54), revascularization procedures (RRR=13%, ARR=2.3%, NNT=43), cardiac arrest (RRR=38%, ARR=0.5%, NNT=200), heart failure (RRR=22%, ARR=2.5%, NNT=40), and complications related to diabetes (RRR=16%, ARR=1.2%, NNT=83). All these reductions in risk were statistically significant. Reduction in blood pressure was not felt to be a major factor in the improved outcomes; the majority of patients did not have underlying hypertension and the treatment group’s mean reduction in blood pressure was minimal (3/2 mm Hg).

CLINICAL QUESTION: Does therapy with an angiotensin-converting-enzyme (ACE) inhibitor reduce the rate of cardiovascular events in high-risk patients with no known left ventricular (LV) dysfunction or heart failure?

BACKGROUND: The renin-angiotensin-aldosterone system is an important contributor to the pathogenesis of cardiovascular disease. ACE inhibitors improve outcomes in patients with LV dysfunction (with or without heart failure). This study assessed whether therapy with an ACE inhibitor, ramipril, reduced the rate of cardiovascular events in high-risk patients with no known LV dysfunction or heart failure.

POPULATION STUDIED: From December 1993 through June 1995, the Heart Outcomes Prevention Evaluation (HOPE) investigators recruited patients from 277 centers in Canada, the United States, Argentina, Brazil, Mexico, and 14 western European countries. The final study population included 9297 patients at high risk for a cardiovascular event. All patients were aged 55 years or older and had either evidence of vascular disease or diabetes mellitus plus one other cardiovascular risk factor. Exclusion criteria included known history of heart failure or low LV ejection fraction (<40%), use of an ACE inhibitor or vitamin E, uncontrolled hypertension, overt nephropathy, and myocardial infarction or stroke in the 4 weeks before the study began.

STUDY DESIGN AND VALIDITY: The study was part of a double-blinded 2-by-2 factorial randomized trial evaluating both ramipril and vitamin E. This paper reports the placebo-controlled study of ramipril 10 mg per day compared with placebo. Allocation of patients to ramipril or placebo was adequately concealed. Treatments were compared using the log-rank test, and subgroup analyses were conducted using tests for interactions in the Cox regression model. Treatment was scheduled to last 5 years, but an independent monitoring board recommended termination of the study after 4 years because of clear evidence of a beneficial effect of ramipril.

OUTCOMES MEASURED: The primary study outcome was a composite of myocardial infarction, stroke, or death from cardiovascular causes. Secondary outcomes were death from any cause, the need for revascularization, hospitalization for unstable angina or heart failure, diabetes-related complications, and each of the primary outcomes reported individually.

RESULTS: Compared with controls, treatment with ramipril reduced the combined rate of myocardial infarction, stroke, or death from cardiovascular causes (relative risk reduction [RRR]=21%, absolute risk reduction [ARR]=3.8%, number needed to treat [NNT]=27). It also reduced the rates of the secondary outcomes, including death from any cause (RRR=15%, ARR=1.9%, NNT=54), revascularization procedures (RRR=13%, ARR=2.3%, NNT=43), cardiac arrest (RRR=38%, ARR=0.5%, NNT=200), heart failure (RRR=22%, ARR=2.5%, NNT=40), and complications related to diabetes (RRR=16%, ARR=1.2%, NNT=83). All these reductions in risk were statistically significant. Reduction in blood pressure was not felt to be a major factor in the improved outcomes; the majority of patients did not have underlying hypertension and the treatment group’s mean reduction in blood pressure was minimal (3/2 mm Hg).