- Email: [email protected]
Global health status
CORRESPONDENCE
was confirmed in a prospective cohort study in twin pregnancies.5 Thus, gestational thrombocytopenia can be a precursor of the HELLP syndrome, rather than simply a mild transient manifestation of idiopathic thrombocytopenic purpura. HELLP syndrome is diagnosed by laboratory data but blood tests generally are done only when disorders such as pre-eclampsia and epigastralgia become evident. Patients at an advanced stage of the HELLP syndrome with severe thrombocytopenia require platelet transfusion.2 Prompt delivery is the only intervention that improves the clinical course of HELLP syndrome; women who are at increased risk of HELLP or are at an early stage of the syndrome must be identified as early as possible to avoid serious complications such as disseminated intravascular coagulation. We therefore urge that women with gestational thrombocytopenia be carefully monitored. *Hisanori Minakami, Ikuo Sato Department of Obstetrics and Gynaecology, Jichi Medical School, Tochigi 329-0498, Japan (e-mail: [email protected]) 1 2
3
4
5
George JN. Platelets. Lancet 2000; 355: 1531–39. Stone JH. HELLP syndrome: hemolysis, elevated liver enzymes, and low platelets. JAMA 1998; 280: 559–62. Minakami H, Kuwata T, Sato I. Gestational thrombocytopenia: is it new? Am J Obstet Gynecol 1996; 175: 1676–77. Minakami H, Kohmura Y, Izumi A, Watanabe T, Matsubara S, Sato I. Relation between gestational thrombocytopenia and the syndrome of hemolysis, elevated liver enzymes, and low platelet count (HELLP syndrome). Gynecol Obstet Invest 1998; 46: 41–45. Minakami H, Watanabe T, Izumi A, et al. Association of a decrease in antithrombin III activity with a perinatal elevation in aspartate aminotransferase in women with twin pregnancies: relevance to the HELLP syndrome. J Hepatol 1999; 30: 603–11.
Author’s reply Sir—Hisanori Minakami and Ikuo Sato suggest that mild but progressive thrombocytopenia during the third trimester predicts a greater risk of the HELLP syndrome, and they urge a diligent search for the cause of thrombocytopenia when it is noted. This recommendation is reasonable, but I would take assessment of mild thrombocytopenia during pregnancy to be sufficiently diligent if the patient is symptom-free, physical examination is normal, and the remainder of the blood counts and urine analysis are normal. In such women, I do not believe that more expensive laboratory assessment is necessary. If thrombo-
THE LANCET • Vol 356 • October 14, 2000
cytopenia becomes more severe, such as with a platelet count less than 50⫻109/L, or abdominal pain or other symptoms develop, or if anaemia exceeds the anticipated physiological level, then more extensive laboratory assessment would be appropriate.
3
4
James George University of Oklahoma Health Science Center, Haematology and Oncology Section, PO Box 26901, Oklahoma City, OK 73190, USA
Sir—James N George1 states: “Although patients with essential thrombocythaemia (ET) do not have the Philadelphia chromosome t(9;22), which defines chronic myelocytic leukaemia, the chimeric BCR-ABL transcript mRNA from this translocation has been identified in patients with clinically typical essential thrombocythaemia”. These findings have been detected, by D Blickstein and colleagues2 in 48% of 25 patients negative for the Philadelphia chromosome who had essential thrombocythaemia, investigated by two-step nested RT-PCR. Some workers have not, however, been able to confirm these data by the same technique, in 18 and 20 such patients, respectively.3,4 Moreover, others have shown the absence of the chimeric transcript in 41 patients with essential thrombocythaemia studied by the fluorescence in-situ hybridisation with a BCR-ABL probe.5 We investigated 112 patients who had essential thrombocythaemia with long follow-up, by RT-PCR, and detected the BCR-ABL transcript in only one patient who progressed to myeloid blastic crisis 12 years after diagnosis. Actually, whether essentialthrombocythaemia patients negative for the Philadelphia chromosome express the BCR-ABL transcript has been a matter of controversy for several years. In studies, the apparent essential thrombocythaemia carrying the Philadelphia anomaly, cytogenetically or molecularly should probably be considered as a variant of chronic myelocytic leukaemia with thrombocytosis and often long survival, with obvious clinical and therapeutical implications. *Giovanni Emilia, Mario Luppi, Roberto Marasca, Giuseppe Torelli Department of Medical Sciences, University of Modena, Policlinico, via del Pozzo 71, 41100 Modena, Italy (e-mail: [email protected])) 1 2
George JN. Platelets. Lancet 2000; 355: 1531–39. Blickstein D, Aviram A, Luboshitz J, et al. BCR-ABL transcripts in bone marrow
5
aspirates of Philadelphia-negative essential thrombocythemia patients: clinical presentations. Blood 1997; 90: 2768–71. Marasca R, Luppi M, Zucchini P, Longo G, Torelli G, Emilia G. Might essential thrombocythemia carry Ph anomaly? Blood 1998; 91: 3084 (letter). Hackwell S, Ross F, Cullis JO. Patients with essential thrombocythemia do not express BCR-ABL transcripts. Blood 1999; 93: 2420 (letter). Solé F, Florensa L, Espinet B, Besses C, Lloveras E, Woessner S. Absence of bcr/abl rearrangement in 41 patients with essential thrombocythemia. Haematologica 2000; 85: 214–15.`
Global health status Sir—Kasturi Sen and Ruth Bonita (Aug 12, p 577)1 refer to the double burden of disease as the epidemics of non-communicable diseases in countries that are struggling with old and new infectious diseases. They describe the increasing population of older people in lessdeveloped and more-developed countries, stating that more than half of the population older than 65 years lives in less-developed countries. Sen and Bonita argue that these rapid demo-graphic and risk-factor changes will lead to an increase in the heavy burden of non-communicable diseases in the absence of preventative action. We believe that non-communicable diseases are already well established in Our less-developed countries.2 calculations using data from 19983 show that the rates of noncommunicable diseases are similar in countries with high and low or middle incomes (table).2 The rates, expressed as disease-adjusted life years per 100 000 population, take into account the fact that low-income or middleincome countries contain 85% of the world’s population and account for at least 92% of the world’s disease burden. The rates for communicable conditions (including maternal and perinatal conditions, and malnutrition) and injuries are, respectively, thirteen and three times higher in low-income and middle-income countries than in high-income countries. Group
Low/middleincome countries
Highincome countries
Communicable diseases, maternal, perinatal, and nutritional disorders Non-communicable diseases Injuries
11 206
863
10 200 4198
9664 1403
Burden calculated as disease-adjusted life years per 100 000 population.
Rate of burden of disease by disease group and country income in 1998
1355
For personal use only. Not to be reproduced without permission of The Lancet.
CORRESPONDENCE
Existing interventions implemented in more-developed countries often cannot be transferred to lessdeveloped countries. The Global Forum for Health Research is working to help correct the imbalance in health research funding from projects benefiting fewer people to projects benefiting the large majority. Andres de Francisco Global Forum for Health Research, c/o WHO, 1211 Geneva 27, Switzerland (e-mail: [email protected]) 1
2
3
Sen K, Bonita R. 2000. Global health status: two steps forward, one step back. Lancet 2000; 356: 577–82. The 10/90 Report on Health Research 2000. Global Forum for Health Research. Geneva: WHO, 2000: 156. World Health Report 1999. Geneva: WHO, 2000: 121.
megalovirus isolates resistant to ganciclovir under selective pressure during exposure to valaciclovir5 has never been formally documented. For these reasons, we suggest that for now and until valganciclovir becomes available, oral valaciclovir should be the first-choice drug for prevention of cytomegalovirus disease, at least in kidney recipients. Christophe Legendre Service de Néphrologie, Hôpital Saint-Louis, 75010 Paris, France 1
2
3
Ganciclovir-resistant cytomegalovirus Sir—Ajit P Limaye and colleagues (Aug 19, p 645)1 report the emergence of ganciclovir-resistant cytomegalovirus strains as a non-unexpected consequence of the wide use of oral ganciclovir to prevent cytomegalovirus disease in organ-transplant recipients. Ganciclovir-resistant cytomegalovirus disease occurred late in the course of transplantation and led to serious clinical complications. We do not think that the role of valaciclovir, in at least kidney transplant recipients, was clearly enough outlined as a well documented, efficient, and safe alternative to prevent cytomegalovirus disease in the discussion, nor in W Lawrence Drew’s commentary (Aug 19, p 609).2 In the original study,3 involving 306 patients who received a 90-day course of oral valaciclovir, cytomegalovirus disease that did not respond to ganciclovir was not reported and in only one patient whose death was attributed to cytomegalovirus could not be excluded. Our experience with oral valaciclovir (more than 200 kidney and kidney-pancreas recipients) agrees with the original study: we have encountered no case of ganciclovirresistant cytomegalovirus disease, which was not the case with oral ganciclovir used as a maintenance prevention.4 Moreover, antigen or PCR-guided oral or intravenous ganciclovir use has never been proven to be more or even as efficient as valaciclovir prophylaxis in a well designed trial. Finally, the theoretical possibility of emergence of cyto-
1356
4
5
Limaye AP, Corey L, Koelle DM, Davis CL, Boeckh M. Emergence of ganciclovir-resistant cytomegalovirus disease among recipients of solid-organ transplants. Lancet 2000; 356: 645–49. Drew WL. Ganciclovir resistance: a matter of time and titre. Lancet 2000; 356: 609–10. Lowance D, Neumayer HH, Legendre Ch, et al. Valacyclovir for the prevention of cytomegalovirus disease after renal transplantation. N Engl J Med 1999; 340: 1462–70. Bienvenu B, Thervet E, Bedrossian J, et al. Development of cytomegalovirus resistance to gancicovir after oral maintenance treatment in a renal transplant recipient. Transplantation 2000; 69: 182–84. Erice A. Resistance of human cytomegalovirus to antiviral drugs. Clin Microbiol Rev 1999; 12: 286–97.
Hospital mortality and staff workload Sir—W O Tarnow-Mordi and colleagues (July 15, p 185)1 relate mortality in intensive care (ICU) to high patient occupancy. They support the intuitive deductions of many clinicians but also give some possible examples of medical error identified by the Institute of Medicine in the More importantly, the USA.2 researchers show possible causes and measurable effects of nursing error. Tarnow-Mordi and co-workers concentrate appropriately on quantitative data. However, any qualitative data on concerns expressed by the nursing or medical staff about the busy, high-risk shifts is important. These data might have been available from shift reports, handover documentation, and risk-management activities, such as critical-incident and near-miss reporting by nursing or Additionally, medical staff.3 documented meetings with, or correspondence to, the clinical directors and hospital management might have helped to confirm that clinical impressions of increased risk at times of high ICU occupancy were
apparent before the data in the paper became available. Expressions of concern probably antedated confirmation of the excess mortality, as they did in the Bristol The and Winnipeg cases.3,4 involvement of medically qualified managers in the process of reporting potentially unsafe services gives them an immediate/legal responsibility for the safety of patients in that service.5 The implications of limited human or financial resources in this context have not been legally tested. Ethically, the decision must be to manage patients in the safest environment possible. Stephen Bolsin Barwon Health, Geelong Hospital, Geelong, Victoria 3220, Australia (e-mail: [email protected]) 1
2
3
4
5
Tarnow-Mordi WO, Hau C, Warden A, Shearer AJ. Hospital mortality in relation to staff workload: a 4-year study in an adult intensive-care unit. Lancet 2000; 356: 185–89. Kohn CT, Corrigan JM, Donaldson MS. To Err is human: building a safer health system. Washington: Institute of Medicine, 1999: 1–16. Bolsin SN. Routes to quality assurance. International Journal for Quality in Healthcare 2000; 12 (5): accepted for publication. Sibbald B. Twelve deaths in Winnipeg: judge must ponder 48 000 pages of testimony. Can Med Assoc J 1998; 159 (10): 1285–87. Roylance v General Medical Council. London: 3 WLR, 1999: 541.
Sir—W O Tarnow-Mordi and colleagues’ report1 is a warning for politicians and administrators of public-health-care funding. As suspected by several physicians working in public hospitals, excessive workload for health carers in ICUs is accompanied by increased mortality. Similarly, M C Blunt and K R Burchet demonstrate that the lack of 24 h availability of specialists in ICUs is also associated with increased mortality.2 Patients who present to accident and emergency departments could be also put at increased risk when nursing or medical workload is high because of potential increments in iatrogenic complications, human errors, or both, decreased supervision, or excessive delays in medical assistance or drug administration. We suggest that overcrowding in accident and emergency departments leads to a decline in the quality of health care, shown by mortality.3 We gathered weekly data on deaths in the internal medicine unit (IMU) of our accident and emergency department for 200 consecutive weeks
THE LANCET • Vol 356 • October 14, 2000
For personal use only. Not to be reproduced without permission of The Lancet.
was confirmed in a prospective cohort study in twin pregnancies.5 Thus, gestational thrombocytopenia can be a precursor of the HELLP syndrome, rather than simply a mild transient manifestation of idiopathic thrombocytopenic purpura. HELLP syndrome is diagnosed by laboratory data but blood tests generally are done only when disorders such as pre-eclampsia and epigastralgia become evident. Patients at an advanced stage of the HELLP syndrome with severe thrombocytopenia require platelet transfusion.2 Prompt delivery is the only intervention that improves the clinical course of HELLP syndrome; women who are at increased risk of HELLP or are at an early stage of the syndrome must be identified as early as possible to avoid serious complications such as disseminated intravascular coagulation. We therefore urge that women with gestational thrombocytopenia be carefully monitored. *Hisanori Minakami, Ikuo Sato Department of Obstetrics and Gynaecology, Jichi Medical School, Tochigi 329-0498, Japan (e-mail: [email protected]) 1 2
3
4
5
George JN. Platelets. Lancet 2000; 355: 1531–39. Stone JH. HELLP syndrome: hemolysis, elevated liver enzymes, and low platelets. JAMA 1998; 280: 559–62. Minakami H, Kuwata T, Sato I. Gestational thrombocytopenia: is it new? Am J Obstet Gynecol 1996; 175: 1676–77. Minakami H, Kohmura Y, Izumi A, Watanabe T, Matsubara S, Sato I. Relation between gestational thrombocytopenia and the syndrome of hemolysis, elevated liver enzymes, and low platelet count (HELLP syndrome). Gynecol Obstet Invest 1998; 46: 41–45. Minakami H, Watanabe T, Izumi A, et al. Association of a decrease in antithrombin III activity with a perinatal elevation in aspartate aminotransferase in women with twin pregnancies: relevance to the HELLP syndrome. J Hepatol 1999; 30: 603–11.
Author’s reply Sir—Hisanori Minakami and Ikuo Sato suggest that mild but progressive thrombocytopenia during the third trimester predicts a greater risk of the HELLP syndrome, and they urge a diligent search for the cause of thrombocytopenia when it is noted. This recommendation is reasonable, but I would take assessment of mild thrombocytopenia during pregnancy to be sufficiently diligent if the patient is symptom-free, physical examination is normal, and the remainder of the blood counts and urine analysis are normal. In such women, I do not believe that more expensive laboratory assessment is necessary. If thrombo-
THE LANCET • Vol 356 • October 14, 2000
cytopenia becomes more severe, such as with a platelet count less than 50⫻109/L, or abdominal pain or other symptoms develop, or if anaemia exceeds the anticipated physiological level, then more extensive laboratory assessment would be appropriate.
3
4
James George University of Oklahoma Health Science Center, Haematology and Oncology Section, PO Box 26901, Oklahoma City, OK 73190, USA
Sir—James N George1 states: “Although patients with essential thrombocythaemia (ET) do not have the Philadelphia chromosome t(9;22), which defines chronic myelocytic leukaemia, the chimeric BCR-ABL transcript mRNA from this translocation has been identified in patients with clinically typical essential thrombocythaemia”. These findings have been detected, by D Blickstein and colleagues2 in 48% of 25 patients negative for the Philadelphia chromosome who had essential thrombocythaemia, investigated by two-step nested RT-PCR. Some workers have not, however, been able to confirm these data by the same technique, in 18 and 20 such patients, respectively.3,4 Moreover, others have shown the absence of the chimeric transcript in 41 patients with essential thrombocythaemia studied by the fluorescence in-situ hybridisation with a BCR-ABL probe.5 We investigated 112 patients who had essential thrombocythaemia with long follow-up, by RT-PCR, and detected the BCR-ABL transcript in only one patient who progressed to myeloid blastic crisis 12 years after diagnosis. Actually, whether essentialthrombocythaemia patients negative for the Philadelphia chromosome express the BCR-ABL transcript has been a matter of controversy for several years. In studies, the apparent essential thrombocythaemia carrying the Philadelphia anomaly, cytogenetically or molecularly should probably be considered as a variant of chronic myelocytic leukaemia with thrombocytosis and often long survival, with obvious clinical and therapeutical implications. *Giovanni Emilia, Mario Luppi, Roberto Marasca, Giuseppe Torelli Department of Medical Sciences, University of Modena, Policlinico, via del Pozzo 71, 41100 Modena, Italy (e-mail: [email protected])) 1 2
George JN. Platelets. Lancet 2000; 355: 1531–39. Blickstein D, Aviram A, Luboshitz J, et al. BCR-ABL transcripts in bone marrow
5
aspirates of Philadelphia-negative essential thrombocythemia patients: clinical presentations. Blood 1997; 90: 2768–71. Marasca R, Luppi M, Zucchini P, Longo G, Torelli G, Emilia G. Might essential thrombocythemia carry Ph anomaly? Blood 1998; 91: 3084 (letter). Hackwell S, Ross F, Cullis JO. Patients with essential thrombocythemia do not express BCR-ABL transcripts. Blood 1999; 93: 2420 (letter). Solé F, Florensa L, Espinet B, Besses C, Lloveras E, Woessner S. Absence of bcr/abl rearrangement in 41 patients with essential thrombocythemia. Haematologica 2000; 85: 214–15.`
Global health status Sir—Kasturi Sen and Ruth Bonita (Aug 12, p 577)1 refer to the double burden of disease as the epidemics of non-communicable diseases in countries that are struggling with old and new infectious diseases. They describe the increasing population of older people in lessdeveloped and more-developed countries, stating that more than half of the population older than 65 years lives in less-developed countries. Sen and Bonita argue that these rapid demo-graphic and risk-factor changes will lead to an increase in the heavy burden of non-communicable diseases in the absence of preventative action. We believe that non-communicable diseases are already well established in Our less-developed countries.2 calculations using data from 19983 show that the rates of noncommunicable diseases are similar in countries with high and low or middle incomes (table).2 The rates, expressed as disease-adjusted life years per 100 000 population, take into account the fact that low-income or middleincome countries contain 85% of the world’s population and account for at least 92% of the world’s disease burden. The rates for communicable conditions (including maternal and perinatal conditions, and malnutrition) and injuries are, respectively, thirteen and three times higher in low-income and middle-income countries than in high-income countries. Group
Low/middleincome countries
Highincome countries
Communicable diseases, maternal, perinatal, and nutritional disorders Non-communicable diseases Injuries
11 206
863
10 200 4198
9664 1403
Burden calculated as disease-adjusted life years per 100 000 population.
Rate of burden of disease by disease group and country income in 1998
1355
For personal use only. Not to be reproduced without permission of The Lancet.
CORRESPONDENCE
Existing interventions implemented in more-developed countries often cannot be transferred to lessdeveloped countries. The Global Forum for Health Research is working to help correct the imbalance in health research funding from projects benefiting fewer people to projects benefiting the large majority. Andres de Francisco Global Forum for Health Research, c/o WHO, 1211 Geneva 27, Switzerland (e-mail: [email protected]) 1
2
3
Sen K, Bonita R. 2000. Global health status: two steps forward, one step back. Lancet 2000; 356: 577–82. The 10/90 Report on Health Research 2000. Global Forum for Health Research. Geneva: WHO, 2000: 156. World Health Report 1999. Geneva: WHO, 2000: 121.
megalovirus isolates resistant to ganciclovir under selective pressure during exposure to valaciclovir5 has never been formally documented. For these reasons, we suggest that for now and until valganciclovir becomes available, oral valaciclovir should be the first-choice drug for prevention of cytomegalovirus disease, at least in kidney recipients. Christophe Legendre Service de Néphrologie, Hôpital Saint-Louis, 75010 Paris, France 1
2
3
Ganciclovir-resistant cytomegalovirus Sir—Ajit P Limaye and colleagues (Aug 19, p 645)1 report the emergence of ganciclovir-resistant cytomegalovirus strains as a non-unexpected consequence of the wide use of oral ganciclovir to prevent cytomegalovirus disease in organ-transplant recipients. Ganciclovir-resistant cytomegalovirus disease occurred late in the course of transplantation and led to serious clinical complications. We do not think that the role of valaciclovir, in at least kidney transplant recipients, was clearly enough outlined as a well documented, efficient, and safe alternative to prevent cytomegalovirus disease in the discussion, nor in W Lawrence Drew’s commentary (Aug 19, p 609).2 In the original study,3 involving 306 patients who received a 90-day course of oral valaciclovir, cytomegalovirus disease that did not respond to ganciclovir was not reported and in only one patient whose death was attributed to cytomegalovirus could not be excluded. Our experience with oral valaciclovir (more than 200 kidney and kidney-pancreas recipients) agrees with the original study: we have encountered no case of ganciclovirresistant cytomegalovirus disease, which was not the case with oral ganciclovir used as a maintenance prevention.4 Moreover, antigen or PCR-guided oral or intravenous ganciclovir use has never been proven to be more or even as efficient as valaciclovir prophylaxis in a well designed trial. Finally, the theoretical possibility of emergence of cyto-
1356
4
5
Limaye AP, Corey L, Koelle DM, Davis CL, Boeckh M. Emergence of ganciclovir-resistant cytomegalovirus disease among recipients of solid-organ transplants. Lancet 2000; 356: 645–49. Drew WL. Ganciclovir resistance: a matter of time and titre. Lancet 2000; 356: 609–10. Lowance D, Neumayer HH, Legendre Ch, et al. Valacyclovir for the prevention of cytomegalovirus disease after renal transplantation. N Engl J Med 1999; 340: 1462–70. Bienvenu B, Thervet E, Bedrossian J, et al. Development of cytomegalovirus resistance to gancicovir after oral maintenance treatment in a renal transplant recipient. Transplantation 2000; 69: 182–84. Erice A. Resistance of human cytomegalovirus to antiviral drugs. Clin Microbiol Rev 1999; 12: 286–97.
Hospital mortality and staff workload Sir—W O Tarnow-Mordi and colleagues (July 15, p 185)1 relate mortality in intensive care (ICU) to high patient occupancy. They support the intuitive deductions of many clinicians but also give some possible examples of medical error identified by the Institute of Medicine in the More importantly, the USA.2 researchers show possible causes and measurable effects of nursing error. Tarnow-Mordi and co-workers concentrate appropriately on quantitative data. However, any qualitative data on concerns expressed by the nursing or medical staff about the busy, high-risk shifts is important. These data might have been available from shift reports, handover documentation, and risk-management activities, such as critical-incident and near-miss reporting by nursing or Additionally, medical staff.3 documented meetings with, or correspondence to, the clinical directors and hospital management might have helped to confirm that clinical impressions of increased risk at times of high ICU occupancy were
apparent before the data in the paper became available. Expressions of concern probably antedated confirmation of the excess mortality, as they did in the Bristol The and Winnipeg cases.3,4 involvement of medically qualified managers in the process of reporting potentially unsafe services gives them an immediate/legal responsibility for the safety of patients in that service.5 The implications of limited human or financial resources in this context have not been legally tested. Ethically, the decision must be to manage patients in the safest environment possible. Stephen Bolsin Barwon Health, Geelong Hospital, Geelong, Victoria 3220, Australia (e-mail: [email protected]) 1
2
3
4
5
Tarnow-Mordi WO, Hau C, Warden A, Shearer AJ. Hospital mortality in relation to staff workload: a 4-year study in an adult intensive-care unit. Lancet 2000; 356: 185–89. Kohn CT, Corrigan JM, Donaldson MS. To Err is human: building a safer health system. Washington: Institute of Medicine, 1999: 1–16. Bolsin SN. Routes to quality assurance. International Journal for Quality in Healthcare 2000; 12 (5): accepted for publication. Sibbald B. Twelve deaths in Winnipeg: judge must ponder 48 000 pages of testimony. Can Med Assoc J 1998; 159 (10): 1285–87. Roylance v General Medical Council. London: 3 WLR, 1999: 541.
Sir—W O Tarnow-Mordi and colleagues’ report1 is a warning for politicians and administrators of public-health-care funding. As suspected by several physicians working in public hospitals, excessive workload for health carers in ICUs is accompanied by increased mortality. Similarly, M C Blunt and K R Burchet demonstrate that the lack of 24 h availability of specialists in ICUs is also associated with increased mortality.2 Patients who present to accident and emergency departments could be also put at increased risk when nursing or medical workload is high because of potential increments in iatrogenic complications, human errors, or both, decreased supervision, or excessive delays in medical assistance or drug administration. We suggest that overcrowding in accident and emergency departments leads to a decline in the quality of health care, shown by mortality.3 We gathered weekly data on deaths in the internal medicine unit (IMU) of our accident and emergency department for 200 consecutive weeks
THE LANCET • Vol 356 • October 14, 2000
For personal use only. Not to be reproduced without permission of The Lancet.