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The uses of error
COMMENTARY
COMMENTARY
The uses of error The patient was a man in his early forties with vague chest discomfort. Neither he nor his wife spoke good English, and no translator was available that night. The patient’s only other medical history was Addison’s disease, for which he was on steroid-replacement therapy. To judge from a mix of hand signals, halfformed sentences, and nods, the discomfort did not seem to be the band-like, crushing, radiating pain of cardiac ischaemia. He seemed to agree when I asked whether the pain was worse when he lay down. He was sweating and very agitated and anxious. Physical examination revealed nothing relevant, although I persuaded myself of epigastric tenderness. The antiquarian electrocardiographic machine worked only if I kept moving the baseline control to keep the needle running on the paper—but the trace looked normal. All coronary-care beds were occupied. Kicking up a fuss and transferring a more stable patient to the ward to make way for a man with a probable diagnosis of gastro-oesophageal reflux would only have irritated the experienced nursing team and attracted derision from the cardiologists in the morning. I put the patient on a medical ward instead. When I reviewed him a few hours later, he had calmed down and seemed well. Thinking of his hypoadrenal state, I considered additional hydrocortisone, but I judged that I was over-reacting. The man had heartburn. He probably did not even need to be in hospital. At 0530 h a nurse making routine observations found him dead. I was stunned. I was sure that either he had died of a fatal arrhythmia secondary to an infarct that I had missed, or he had died from an Addisonian crisis that I could have prevented. When I presented the case on the following morning’s hectic ward round, no difficult questions were asked. A necropsy would have revealed all, and I was prepared for some serious interrogation later. But the family refused a necropsy on religious grounds. Errors in medicine are common. All doctors I have talked to about clinical mistakes admit them. Yet the present anxieties about medical malpractice and incompetence ignore the fact that error is an everyday event, a routine part of learning. Media outrage and public alarm over recent scares in the UK1 have put doctors on the defensive. A doctor’s perfection, seen by many as an important element in the securing of the public’s trust, is under attack. Fear of patients and of their work causes doctors to close ranks even more when a scandal erupts. How can this cycle of fear be broken? In the UK, the 422
General Medical Council has proposed that doctors “must be able to demonstrate on a regular basis that they are keeping themselves up to date and remain fit to practise in their chosen field”. The GMC’s concept of revalidation for doctors will be debated again next week. But stricter oversight alone will not make more open a culture that fosters secrecy and denial. Nor will performance league tables. Rather, the prevailing culture may become not one of defensiveness but one of aggression—naming, shaming, suspending, and punishing colleagues without proper investigation or due process. There is another way. Doctors can dismantle the notion that the only good doctor is a perfect doctor, and explain that in medicine, as in any other sphere of human activity, errors occur. Atul Gawande did so last week2 when he told of his own error. He pointed out how doctors have much to learn from engineers at the US Federal Aviation Administration about how to deal with error. The issue is not whether errors occur, but what doctors learn from them. The current wish to discourage discussion of doctors’ mistakes and to say that error concerns only a few and not the many will deepen the gulf between patients and their doctors. This tension will be deflated only by talking and writing honestly about errors and, most importantly, discussing the lessons that might be drawn from them. The profession can then make use of a valuable accumulation of clinical experience that is currently lost. My experience a decade ago raises questions not only about my judgment but also about the need for effective senior cover for younger colleagues on call, availability of coronary-care beds, provision of translators outside normal hours, and the value of necropsy as part of a continuum of clinical care. There are three immediate objections to such openness. First, the threat of litigation. Doctors must not fear the law. They can describe events in a suitably generalised way, thereby, as Gawande writes, “protecting the patient, [themselves], and the rest of the staff ”.2 Second, disclosure of errors may damage the public’s trust in doctors still further. I think it is hard to argue against the broad principle that “disclosure is good, secrecy is bad”. The prevailing climate, which encourages suppression of truth about medical error, is already harming public trust in doctors by exaggeration of patients’ fears whenever an isolated medical disaster is reported. Patients are more likely to be reassured by a profession that faces up to its mistakes than by one that
THE LANCET • Vol 353 • February 6, 1999
COMMENTARY
buries them. Finally, is it ethical to report medical mistakes without the patient’s consent? Ideally, consent should be obtained. But with insistence on consent, the present recourse to instant blame and recrimination by a highly sensitised public will stop doctors from telling the truth about the reality of clinical practice. Is the principle of consent so sacrosanct that it should over-ride the principle of disclosure and the opportunity to learn from mistakes? The arguments in favour of disclosure are sufficiently compelling to proceed cautiously. But this issue needs further and more careful exploration. Safe ways to admit error must be found. Doctors are under pressure to change—by patients finding their voice in the consultation, by the profession’s regulators keen to prevent new scandals, and by managers whose top agenda item is efficiency. One way to respond to these incursions—some justifiable, others not—on a doctor’s independence is to “promote those facets of professional autonomy likely to contribute to the common good”.3 How better to begin than with a debate initiated by doctors about the uses of error in medicine?
Richard Horton The Lancet, London WC1B 3SL, UK 1. Horton R. How should doctors respond to the GMC’s judgements on Bristol? Lancet 1998; 351: 1900–01. 2. Gawande A. When doctors make mistakes. New Yorker 1999, Feb 1: 40–55. 3. Bloche MG. Clinical loyalties and the social purposes of medicine. JAMA 1999; 281: 267–74.
New antithrombotic treatment in unstable coronary syndrome—for whom? See page 429 The range of antithrombotic drugs has expanded rapidly in the past few years. Most of these drugs have been assessed in unstable coronary disease—ie, unstable angina or myocardial infarction without ST elevation. Unstable coronary disease is an ideal clinical target for anti-thrombotic therapy, since most of the patients have a thrombotic coronary lesion as the main cause of the disease and a high risk of coronary events in the next few weeks.1 In the 1980s, aspirin in doses of 75 mg to 1300 mg daily was found to reduce the 7-day rates of death and myocardial infarction from about 10% down to 5% in unselected populations with unstable coronary artery disease.2 At the start of the 1990s, the addition to aspirin of 5–7 days of standard heparin or twice-daily subcutaneous injections of low-molecular-weight (LMW) heparin further reduced the 7-day rates of death and myocardial infarction to about 2·5% in similar populations.3,4 During the past few years, several trials have compared 3–8 days of standard heparin with twice daily subcutaneous injections of LMW heparin, both given in addition to aspirin. They have shown either that the two heparin regimens are similarly effective (FRIC,5 FRAX.I.S) or that LMW heparin is better (ESSENCE,6 TIMI 11B). A meta-analaysis of the enoxaparin trials (ESSENCE6, TIMI11B) showed that, compared with standard heparin, enoxaparin produces a 20% relative reduction in rates of death and myocardial infarction during the first 7–14 days. There have also been a few trials comparing standard heparin with the
THE LANCET • Vol 353 • February 6, 1999
synthetic glycoprotein IIb/IIIa blockers. These trials have shown that neither lamifiban (PARAGON7) nor tirofiban (PRISM8) affects death or myocardial infarction in the acute phase In today’s Lancet the OASIS-2 investigators present the results from a randomised study in 10 141 patients with unstable coronary artery disease assigned 72 h of intravenous hirudin or standard heparin. There was a 10–20% relative reduction in incidence of death or myocardial infarction with hirudin during the first 3–7 days. Thus, in unselected patients with unstable coronary artery disease, overall, the new antithrombotic agents, when given with aspirin, are 15–20% more effective than heparin in reducing the rate of death or myocardial infarction in the acute phase—from about 2·5% to 2·0%. Three recent trials have assessed the addition of a glycoprotein IIb/IIIa inhibitor to aspirin and heparin— ie, triple antithrombotic treatment. In the PURSUIT trial,9 9450 unselected patients with unstable coronary artery disease were randomised to 72 h infusion of the glycoprotein IIb/IIIa inhibitor integrilin or placebo, in addition to aspirin; the vast majority of patients were also given an infusion of standard heparin. Integrilin produced a 15–20% relative reduction in death and myocardial infarction. The other two trials (CAPTURE,10 PRISM PLUS11) focused on patients with high-risk unstable coronary artery disease as identified by continuing episodes of pain or ischaemia during standard treatment and need for early coronary procedures before termination of the intravenous antithrombotic treatment. In such patients the addition of glycoprotein IIb/IIIa inhibitors gave 40–50% relative reduction in death or myocardial infarction during treatment and before and during the revascularisation procedure, as well as a sustained absolute reduction of about 3–4% after 1 month. OASIS-2 and several of the glycoprotein IIb/IIIa trials9,10 have shown the downside to the more effective anti-thrombotic agents. In OASIS-2, the frequency of major bleeds was higher with hirudin (1·2% vs 0·7% with heparin), as was the frequency of minor bleeds (4·5% vs 7·6%.) Thus, the balance between gains and losses needs further exploration—eg, by longer followup. Patients with unstable coronary artery disease are heterogeneous in risk of future events. On the basis of recent findings,12,13 higher-risk patients are identifiable by a combination of clinical background factors (age, male sex, diabetes mellitus, hypertension, previous myocardial damage), clinical presentation (less than 12 h since last episode of pain), and signs of ischaemia or myocardial damage (ST-depression in the electrocardiogram at rest or during continuous monitoring, or raised concentrations of biochemical markers of myocardial damage, such as troponin). The lower-risk patients can safely be treated with aspirin and LMW heparin until a decision is made on the need for early coronary angiography, based on continuous observation and, commonly, a stress-test before discharge.12,13 These patients have a very small chance of further benefit with the more intensive treatments. By contrast, the risks of bleeding and the treatment costs will be unduly raised without much chance of change in either the short-term or the long-term outcome The higher-risk patients will benefit from more 423
COMMENTARY
The uses of error The patient was a man in his early forties with vague chest discomfort. Neither he nor his wife spoke good English, and no translator was available that night. The patient’s only other medical history was Addison’s disease, for which he was on steroid-replacement therapy. To judge from a mix of hand signals, halfformed sentences, and nods, the discomfort did not seem to be the band-like, crushing, radiating pain of cardiac ischaemia. He seemed to agree when I asked whether the pain was worse when he lay down. He was sweating and very agitated and anxious. Physical examination revealed nothing relevant, although I persuaded myself of epigastric tenderness. The antiquarian electrocardiographic machine worked only if I kept moving the baseline control to keep the needle running on the paper—but the trace looked normal. All coronary-care beds were occupied. Kicking up a fuss and transferring a more stable patient to the ward to make way for a man with a probable diagnosis of gastro-oesophageal reflux would only have irritated the experienced nursing team and attracted derision from the cardiologists in the morning. I put the patient on a medical ward instead. When I reviewed him a few hours later, he had calmed down and seemed well. Thinking of his hypoadrenal state, I considered additional hydrocortisone, but I judged that I was over-reacting. The man had heartburn. He probably did not even need to be in hospital. At 0530 h a nurse making routine observations found him dead. I was stunned. I was sure that either he had died of a fatal arrhythmia secondary to an infarct that I had missed, or he had died from an Addisonian crisis that I could have prevented. When I presented the case on the following morning’s hectic ward round, no difficult questions were asked. A necropsy would have revealed all, and I was prepared for some serious interrogation later. But the family refused a necropsy on religious grounds. Errors in medicine are common. All doctors I have talked to about clinical mistakes admit them. Yet the present anxieties about medical malpractice and incompetence ignore the fact that error is an everyday event, a routine part of learning. Media outrage and public alarm over recent scares in the UK1 have put doctors on the defensive. A doctor’s perfection, seen by many as an important element in the securing of the public’s trust, is under attack. Fear of patients and of their work causes doctors to close ranks even more when a scandal erupts. How can this cycle of fear be broken? In the UK, the 422
General Medical Council has proposed that doctors “must be able to demonstrate on a regular basis that they are keeping themselves up to date and remain fit to practise in their chosen field”. The GMC’s concept of revalidation for doctors will be debated again next week. But stricter oversight alone will not make more open a culture that fosters secrecy and denial. Nor will performance league tables. Rather, the prevailing culture may become not one of defensiveness but one of aggression—naming, shaming, suspending, and punishing colleagues without proper investigation or due process. There is another way. Doctors can dismantle the notion that the only good doctor is a perfect doctor, and explain that in medicine, as in any other sphere of human activity, errors occur. Atul Gawande did so last week2 when he told of his own error. He pointed out how doctors have much to learn from engineers at the US Federal Aviation Administration about how to deal with error. The issue is not whether errors occur, but what doctors learn from them. The current wish to discourage discussion of doctors’ mistakes and to say that error concerns only a few and not the many will deepen the gulf between patients and their doctors. This tension will be deflated only by talking and writing honestly about errors and, most importantly, discussing the lessons that might be drawn from them. The profession can then make use of a valuable accumulation of clinical experience that is currently lost. My experience a decade ago raises questions not only about my judgment but also about the need for effective senior cover for younger colleagues on call, availability of coronary-care beds, provision of translators outside normal hours, and the value of necropsy as part of a continuum of clinical care. There are three immediate objections to such openness. First, the threat of litigation. Doctors must not fear the law. They can describe events in a suitably generalised way, thereby, as Gawande writes, “protecting the patient, [themselves], and the rest of the staff ”.2 Second, disclosure of errors may damage the public’s trust in doctors still further. I think it is hard to argue against the broad principle that “disclosure is good, secrecy is bad”. The prevailing climate, which encourages suppression of truth about medical error, is already harming public trust in doctors by exaggeration of patients’ fears whenever an isolated medical disaster is reported. Patients are more likely to be reassured by a profession that faces up to its mistakes than by one that
THE LANCET • Vol 353 • February 6, 1999
COMMENTARY
buries them. Finally, is it ethical to report medical mistakes without the patient’s consent? Ideally, consent should be obtained. But with insistence on consent, the present recourse to instant blame and recrimination by a highly sensitised public will stop doctors from telling the truth about the reality of clinical practice. Is the principle of consent so sacrosanct that it should over-ride the principle of disclosure and the opportunity to learn from mistakes? The arguments in favour of disclosure are sufficiently compelling to proceed cautiously. But this issue needs further and more careful exploration. Safe ways to admit error must be found. Doctors are under pressure to change—by patients finding their voice in the consultation, by the profession’s regulators keen to prevent new scandals, and by managers whose top agenda item is efficiency. One way to respond to these incursions—some justifiable, others not—on a doctor’s independence is to “promote those facets of professional autonomy likely to contribute to the common good”.3 How better to begin than with a debate initiated by doctors about the uses of error in medicine?
Richard Horton The Lancet, London WC1B 3SL, UK 1. Horton R. How should doctors respond to the GMC’s judgements on Bristol? Lancet 1998; 351: 1900–01. 2. Gawande A. When doctors make mistakes. New Yorker 1999, Feb 1: 40–55. 3. Bloche MG. Clinical loyalties and the social purposes of medicine. JAMA 1999; 281: 267–74.
New antithrombotic treatment in unstable coronary syndrome—for whom? See page 429 The range of antithrombotic drugs has expanded rapidly in the past few years. Most of these drugs have been assessed in unstable coronary disease—ie, unstable angina or myocardial infarction without ST elevation. Unstable coronary disease is an ideal clinical target for anti-thrombotic therapy, since most of the patients have a thrombotic coronary lesion as the main cause of the disease and a high risk of coronary events in the next few weeks.1 In the 1980s, aspirin in doses of 75 mg to 1300 mg daily was found to reduce the 7-day rates of death and myocardial infarction from about 10% down to 5% in unselected populations with unstable coronary artery disease.2 At the start of the 1990s, the addition to aspirin of 5–7 days of standard heparin or twice-daily subcutaneous injections of low-molecular-weight (LMW) heparin further reduced the 7-day rates of death and myocardial infarction to about 2·5% in similar populations.3,4 During the past few years, several trials have compared 3–8 days of standard heparin with twice daily subcutaneous injections of LMW heparin, both given in addition to aspirin. They have shown either that the two heparin regimens are similarly effective (FRIC,5 FRAX.I.S) or that LMW heparin is better (ESSENCE,6 TIMI 11B). A meta-analaysis of the enoxaparin trials (ESSENCE6, TIMI11B) showed that, compared with standard heparin, enoxaparin produces a 20% relative reduction in rates of death and myocardial infarction during the first 7–14 days. There have also been a few trials comparing standard heparin with the
THE LANCET • Vol 353 • February 6, 1999
synthetic glycoprotein IIb/IIIa blockers. These trials have shown that neither lamifiban (PARAGON7) nor tirofiban (PRISM8) affects death or myocardial infarction in the acute phase In today’s Lancet the OASIS-2 investigators present the results from a randomised study in 10 141 patients with unstable coronary artery disease assigned 72 h of intravenous hirudin or standard heparin. There was a 10–20% relative reduction in incidence of death or myocardial infarction with hirudin during the first 3–7 days. Thus, in unselected patients with unstable coronary artery disease, overall, the new antithrombotic agents, when given with aspirin, are 15–20% more effective than heparin in reducing the rate of death or myocardial infarction in the acute phase—from about 2·5% to 2·0%. Three recent trials have assessed the addition of a glycoprotein IIb/IIIa inhibitor to aspirin and heparin— ie, triple antithrombotic treatment. In the PURSUIT trial,9 9450 unselected patients with unstable coronary artery disease were randomised to 72 h infusion of the glycoprotein IIb/IIIa inhibitor integrilin or placebo, in addition to aspirin; the vast majority of patients were also given an infusion of standard heparin. Integrilin produced a 15–20% relative reduction in death and myocardial infarction. The other two trials (CAPTURE,10 PRISM PLUS11) focused on patients with high-risk unstable coronary artery disease as identified by continuing episodes of pain or ischaemia during standard treatment and need for early coronary procedures before termination of the intravenous antithrombotic treatment. In such patients the addition of glycoprotein IIb/IIIa inhibitors gave 40–50% relative reduction in death or myocardial infarction during treatment and before and during the revascularisation procedure, as well as a sustained absolute reduction of about 3–4% after 1 month. OASIS-2 and several of the glycoprotein IIb/IIIa trials9,10 have shown the downside to the more effective anti-thrombotic agents. In OASIS-2, the frequency of major bleeds was higher with hirudin (1·2% vs 0·7% with heparin), as was the frequency of minor bleeds (4·5% vs 7·6%.) Thus, the balance between gains and losses needs further exploration—eg, by longer followup. Patients with unstable coronary artery disease are heterogeneous in risk of future events. On the basis of recent findings,12,13 higher-risk patients are identifiable by a combination of clinical background factors (age, male sex, diabetes mellitus, hypertension, previous myocardial damage), clinical presentation (less than 12 h since last episode of pain), and signs of ischaemia or myocardial damage (ST-depression in the electrocardiogram at rest or during continuous monitoring, or raised concentrations of biochemical markers of myocardial damage, such as troponin). The lower-risk patients can safely be treated with aspirin and LMW heparin until a decision is made on the need for early coronary angiography, based on continuous observation and, commonly, a stress-test before discharge.12,13 These patients have a very small chance of further benefit with the more intensive treatments. By contrast, the risks of bleeding and the treatment costs will be unduly raised without much chance of change in either the short-term or the long-term outcome The higher-risk patients will benefit from more 423