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Uses of error: clinical and epidemiological
EPONYM
Germany. Fabry was born in 1860 and studied in Bern and Berlin. He worked at the dermatology department of the University Hospital in Bonn and later in Zurich. From 1889–1927, he was director of the dermatology department of the hospital in Dortmund, where he was elected as professor in 1919. In 1898, Fabry reported a 13-year-old boy who had had cutaneous lesions and proteinuria for over 3 years, which he described as angiokeratoma corporis diffusum. Many feel that although the condition is usually known as Fabry’s disease, it should really be called Anderson-Fabry’s disease. We are grateful to H F P Hillen for figure 1.
References 1
2 3
4
5
Nakao S, Takenaka T, Maeda M, et al. An atypical variant of Fabry’s disease in men with left ventricular hypertrophy. N Engl J Med 1995; 333: 288–93. Peters FPJ, Sommer A, Vermeulen A, et al. Fabry’s disease: a multidisciplinary disorder. Postgrad Med J 1997; 73: 710–12. Takena T, Qin G, Brady RO, et al. Circulating ␣-Galactosidase A derived from transduced bone marrow cells: relevance for corrective gene transfer for Fabry disease. Hum Gen Therap 1999; 10: 1931–39. Fan JQ, Satoshi I, Asano N, et al. Accelerated transport and maturation lysocomal ␣-galactosidase A in Fabry lymphoblasts by enzyme inhibitor. Nat Med 1999; 5: 112–15. Desnick RJ, Ioannou YA, Eng CM. ␣-Galactosidase A deficiency: Fabry disease. In: Scriver CR, Beaudet AL, Sly WS, Valle D, eds. The metabolic and molecular bases of inherited disease, 6th ed. New York: McGraw-Hill, 1996: 2741–84.
Uses of error: clinical and epidemiological After 30 years of clinical and public health practice, four errors stand out; three clinical and one epidemiological. On reflection, this surprisingly small number of (recognised) errors is more of a result of my career preoccupation with public health than my clinical competence. The first and most influential error occurred on a Sunday evening when, as a final year medical student, I was covering for a house surgeon. I admitted an elderly confused man from a residential hostel. I diagnosed pneumonia, consulted the registrar by phone, prescribed antibiotics, and went to bed. The post-mortem examination the next morning revealed a subdural haematoma. Subsequent questioning of hostel staff revealed a history of a recent fall. This patient died because of my over-confidence, ignorance, and the unrealistic expectations the profession had of medical students. From the recent experience of my daughter, as a final-year medical student, this is not a problem, at least in Auckland. The second error was less personal and more institutional and occurred on my first night on call in a London teaching hospital. Unbeknown to me, the hospital had a private wing. When I was called to a cardiac arrest in a private patient in the middle of the night, I couldn’t find an unlocked entrance to the private building. By the time I reached the patient, I was far too late. I didn’t attend the necropsy, but I doubt whether the impediments to emergency access were discussed. I’ve been prejudiced against class-based care ever since. The third and decisive clinical error was my failure to diagnose a transient ischaemic attack in a clinic patient. This error was fortunately not fatal, but made me realise that, even after all my training, I did not have the clinical competence that I felt I needed to act independently. Shortly thereafter, and with great relief, I gave up clinical practice. From a public-health perspective my major error was epidemiological. In 1981, we identified an epidemic of asthma deaths in New Zealand and pointed to a recent change in drug management as a likely cause. Instead of conducting a large-scale case-control study of medical therapy and asthma, I became involved in a large and detailed case study and a small case-control study run by clinicians. By the time the appropriate studies were conducted and the role of fenoterol clarified, many preventable deaths had occurred. The abiding lesson for me from this episode is the importance of focused and well-designed studies of adequate power. My clinical errors have influenced the evolution of my career; ironically the most significant error was epidemiological. My clinical errors could easily have been prevented; the epidemiological error was more complex. Judging from conversations with clinicians, my error experience is by no means unusual. Judging from conversations with friends, they would welcome openness in any form from the profession. Robert Beaglehole
140
THE LANCET • Vol 357 • January 13, 2001
For personal use only. Not to be reproduced without permission of The Lancet.
Germany. Fabry was born in 1860 and studied in Bern and Berlin. He worked at the dermatology department of the University Hospital in Bonn and later in Zurich. From 1889–1927, he was director of the dermatology department of the hospital in Dortmund, where he was elected as professor in 1919. In 1898, Fabry reported a 13-year-old boy who had had cutaneous lesions and proteinuria for over 3 years, which he described as angiokeratoma corporis diffusum. Many feel that although the condition is usually known as Fabry’s disease, it should really be called Anderson-Fabry’s disease. We are grateful to H F P Hillen for figure 1.
References 1
2 3
4
5
Nakao S, Takenaka T, Maeda M, et al. An atypical variant of Fabry’s disease in men with left ventricular hypertrophy. N Engl J Med 1995; 333: 288–93. Peters FPJ, Sommer A, Vermeulen A, et al. Fabry’s disease: a multidisciplinary disorder. Postgrad Med J 1997; 73: 710–12. Takena T, Qin G, Brady RO, et al. Circulating ␣-Galactosidase A derived from transduced bone marrow cells: relevance for corrective gene transfer for Fabry disease. Hum Gen Therap 1999; 10: 1931–39. Fan JQ, Satoshi I, Asano N, et al. Accelerated transport and maturation lysocomal ␣-galactosidase A in Fabry lymphoblasts by enzyme inhibitor. Nat Med 1999; 5: 112–15. Desnick RJ, Ioannou YA, Eng CM. ␣-Galactosidase A deficiency: Fabry disease. In: Scriver CR, Beaudet AL, Sly WS, Valle D, eds. The metabolic and molecular bases of inherited disease, 6th ed. New York: McGraw-Hill, 1996: 2741–84.
Uses of error: clinical and epidemiological After 30 years of clinical and public health practice, four errors stand out; three clinical and one epidemiological. On reflection, this surprisingly small number of (recognised) errors is more of a result of my career preoccupation with public health than my clinical competence. The first and most influential error occurred on a Sunday evening when, as a final year medical student, I was covering for a house surgeon. I admitted an elderly confused man from a residential hostel. I diagnosed pneumonia, consulted the registrar by phone, prescribed antibiotics, and went to bed. The post-mortem examination the next morning revealed a subdural haematoma. Subsequent questioning of hostel staff revealed a history of a recent fall. This patient died because of my over-confidence, ignorance, and the unrealistic expectations the profession had of medical students. From the recent experience of my daughter, as a final-year medical student, this is not a problem, at least in Auckland. The second error was less personal and more institutional and occurred on my first night on call in a London teaching hospital. Unbeknown to me, the hospital had a private wing. When I was called to a cardiac arrest in a private patient in the middle of the night, I couldn’t find an unlocked entrance to the private building. By the time I reached the patient, I was far too late. I didn’t attend the necropsy, but I doubt whether the impediments to emergency access were discussed. I’ve been prejudiced against class-based care ever since. The third and decisive clinical error was my failure to diagnose a transient ischaemic attack in a clinic patient. This error was fortunately not fatal, but made me realise that, even after all my training, I did not have the clinical competence that I felt I needed to act independently. Shortly thereafter, and with great relief, I gave up clinical practice. From a public-health perspective my major error was epidemiological. In 1981, we identified an epidemic of asthma deaths in New Zealand and pointed to a recent change in drug management as a likely cause. Instead of conducting a large-scale case-control study of medical therapy and asthma, I became involved in a large and detailed case study and a small case-control study run by clinicians. By the time the appropriate studies were conducted and the role of fenoterol clarified, many preventable deaths had occurred. The abiding lesson for me from this episode is the importance of focused and well-designed studies of adequate power. My clinical errors have influenced the evolution of my career; ironically the most significant error was epidemiological. My clinical errors could easily have been prevented; the epidemiological error was more complex. Judging from conversations with clinicians, my error experience is by no means unusual. Judging from conversations with friends, they would welcome openness in any form from the profession. Robert Beaglehole
140
THE LANCET • Vol 357 • January 13, 2001
For personal use only. Not to be reproduced without permission of The Lancet.