- Email: [email protected]
Myocarditis
883
LEADING ARTICLES
THE
LANCET
LONDON 22 APRIL
Design
of
1967
Operating-theatres
practice in Great Britain were operating-theatres in which the essential elements were a large room with a commodious gallery, a large side window admitting a lot of daylight, and a sort of open stage upon which the operative ritual was enacted. The origins of this design were probably several, and the one which springs most readily to mind is the dissecting-room of the Hunterian era. Dissection of cadavers was an exercise attended not only by young surgeons in training but also by laymen who regarded anatomy simply as a branch of human knowledge appropriate to any educated person. The type of building most suited to this purpose was not unlike the Elizabethan theatre, with its open stage, circular gallery, and overhead daylight. Since most anatomists were also surgeons who earned fees for teaching apprentices, it is not unreasonable to suppose that they modelled their MOST surgeons
now
in
trained in
theatres on their own dissection rooms. The advent of antisepsis, asepsis, and anaesthesia in the mid-19th century revolutionised the scope of surgery, but it made little difference to the general design until after the 1914-18 war, when the idea emerged of grouping all the necessaries of surgery in one suite. The advantages of centralisation--of instrument storage, sterilisation, and staff-were quickly recognised, and by the mid-1920s most new hospitals, particularly in the United States, incorporated this arrangement. The next step was related not so much to administrative convenience as to bacteriological idealism-a bacteria-tree environment in which wounds could be safely made and repaired. The isolation concept, established in the late 1930s, was closely related to the barrier nursing practised in fever hospitals and paediatric wards. The essential feature was a barrier zone between the hospital and the theatres, beyond which only the few people concerned in the operation could pass (suitably clad). Some years later came the idea of central sterilisation of all instruments and equipment used in the operating-theatres. The most modern and expensive sterilisation techniques could be employed, and human error could be virtually eliminated. About the same time, forced ventilation with filtered air was introduced. By this method a one-way air-flow from theatre to hospital could be maintained, and from there it was a short step to full control of air temperature, humidity, and flow-in fact, the airconditioning which is taken for granted in parts of the world with extremes of climate. Increasing technical complexity in both surgical and anarsthetic practice dictated other changes, notably the provision of anzesthetic and recovery rooms and monitoring laboratories.
The Ministry of Health, in its recommendations for the design of operating-theatre suites, comes down firmly on the side of the central sterile supply department2 and subsidiary theatre sterile supply unit in the theatre suite. No sterilising should be done in individual theatre complexes. Many surgeons will feel a little uneasy about this,2 but it is in line with recommendations of the Medical Research Council’s subcommittee on operating-theatre hygiene. The recommendations on zoning and patient transfer are welcome, and so are those on the location of the theatre suite and its functional relation with other departments. But it is disappointing to read that air-conditioning is not essential; for, even in Britain, theatres can become unbearably hot and humid in summer, and it surely is excessively parsimonious not to provide complete air-conditioning as a routine. It is also discouraging to find that most service lines are to be brought to the wall of the theatre, so that tubes and wires will have to trail across the floor, interfering with the movements of staff and equipment. The portable X-ray set is also to be perpetuated, with its cumbersome trolley and linen-clad head. The recommended theatre size is, at 400-480 sq. ft., small for ease of movement, especially when complex apparatus like heart-lung machines or monitoring equipment is in use. Finally, no research laboratories of any kind are provided in the theatre suite. This decision seems unimaginative when one considers, for instance, the great advances in patient care which have been derived from research into homoeostasis during and after operations. The memorandum is a sound and detailed guide for architects and surgeons, but it is neither forward-looking nor stimulating. It should not be accepted as the last word in operating-theatre design.
Myocarditis of preoccupation with the of haemodynamics congenital and acquired heart-disease, many cardiologists are now showing revived interest in the myocardium. Myocardial disorders, however, other than those secondary to such well-recognised causes as rheumatic or ischaemic heart-disease, are a large and mixed group about which remarkably little is known. Myocarditis, for example, a popular diagnosis at the end of the last century,3 has until lately been very much out of favour. Though it is present in many well-defined conditions, it is often said to be non-specific, and GORE and SAPHIR4 could make no firm aetiological diagnosis in 75% of their 1042 cases. The terms used to define it are often descriptive, reflecting ignorance of its origin and in this way resembling that other great protean group, the cardiomyopathies. Many organisms directly attack the myocardium (bacteria, viruses, rickettsix, spirochxtes, parasites, and AFTER twenty years
Ministry of Health Hospital Building Note, no. 26. H.M. Stationery Office. 1967. Pp. 44 and appendix. 6s. 6d. 2. See Lancet, April 15, 1967, p. 830. 3. Fiedler, A. in Festschrift zur Feier des Fünfzigjährigen Besrehens des Stadtkrankenhauses zu Dresden-Friedrichstadt; part 2, p. 3. Dresden, 1.
1899.
4.
Gore, I., Saphir,
O. Am. Heart J. 1947,
34,
827.
884
have all been incriminated); and it seems likely that other organisms and various immunity reactions may also damage the myocardium. The true incidence of inflammatory lesions of the myocardium is hard to judge because, while careful pathologists often find these lesions, most patients with myocardial involvement in infections do not succumb, and myocarditis is not a common clinical diagnosis. Even when suspected, it is difficult to prove, for the diagnosis depends on possible transient non-specific electrocardiographic changes and extensive bacteriological or biochemical investigations that are likely to be helpful only in an early phase of the illness. To add to the difficulty many of these tests are of value only when positive; negative results do not exclude active disease. Acute myocarditis often arises during the course of the acute infectious diseases, and patients who are isolated in special hospitals for contagious illness are a group that lends itself to intensive study. BENGTSSON and LAMBERGER,3 who followed a series of such patients with myocardial involvement for five years, found that 20% still had subjective symptoms (fatigue, dyspnoea,
fungi
precordial pain, impaired physical condition), 15-20% had abnormal electrocardiograms, 30% had abnormal exercise tests, and 40% had low working capacities. These figures were highly significant when compared with two other groups-one with doubtful myocarditis and one with no evidence of myocarditis. Although approximately 50% of the affected patients had had hxmolytic streptococcal infections (such as rheumatic fever or scarlet fever), symptoms and abnormal signs in this group after five years than in a group who had had aseptic meningitis (20% in both); and they were much less frequent than in the group with miscellaneous infectious diseases, in whom every second patient had sequelx of one sort or another. Myocardial involvement in generalised infections is probably commoner than is generally appreciated, and this Swedish work suggests that it almost certainly has greater prognostic significance. The Coxsackie viruses were no commoner
established as cardiac pathogens s-8; and recent work has shown that rubella is not only teratogenic but also a possible cause of clinical myocarditis in the newborn.9 Further advances in microbiology will undoubtedly reveal the cause of other types of "idiopathic" cardiac disorders-perhaps along the lines pursued by BRAIMBRIDGE and his colleagues.10o That a great deal remains to be explained about the causes of most of these conditions is beyond question and is reflected in the present interest in the many and bizarre forms of heart-disease that are becoming increasingly recognised in the tropics. Heart-muscle diseases nutritional heart-disease,12 cryptogenic heart-
are now
firmly
Bengtsson, E., Lamberger, B. ibid. 1966, 72, 751. Montgomery, J., Gear, J., Prinsloo, F. R., Kahn, M., Kirsch, Z. G. S. Afr. med. J. 1955, 29, 608. 7. Fletcher, E., Brennan, C. F. Lancet, 1957, i, 913. 8. Smith, W. G. Br. Heart J. 1966, 28, 204. 9. Ainger, L. E., Lawyer, N. G., Fitch, C. W. ibid. p. 691. 10. Braimbridge, M. V., Oarracott, S., Chayen, J., Bitensky, L., Poulter, L. W. Lancet, Jan. 28, 1967, p. 171. 11. Edington, G. M., Jackson, J. G. J. Path. Bact. 1963, 86, 333. 12. Gillanders, A. D. Br. Heart J. 1951, 13, 177. 5. 6.
disease.,13 and cardiovascular collagenosis 14 all show lesions in some way reminiscent of myocarditis, and a review of endomyocardial fibrosis 15 in Europeans who have been living in tropical Africa 16 favours an infective agent as a possible cause. Whether this affects the heart muscle directly or by some sensitivity or immunity reaction is still far from clear, 17 but this and other forms of myocarditis " are certain to take up much future cardiological time and space. "
Polymyositis THE difficulties of defining a " disease " and its cause are seldom more apparent than in the condition now universally known as polymyositis. The new work of ROSE and WALTON 18 is mainly concerned with epidemiology and response to treatment, but their initial survey of diagnostic criteria confirms that we are still in the stage of definition in clinical terms. Laboratory aids may be invaluable in proving that weakness is due to primary muscle disease, but the results are neither constant nor always specific and they may be hard to interpret. A rise in either the aldolase or creatine-kinase level in the serum indicates active muscle destruction and is therefore found in acute untreated disease or when relapse ensues during treatment-but it is not specific for any disease process. Muscle biopsy may be entirely normal in the presence of gross weaknessa finding usually attributed to the uneven distribution of the lesions. The interpretation of minor " abnormalities " is notoriously unreliable, and ROSE and WALTON found acceptable evidence of myositis in 34 out of 54 patients in whom biopsy was performed. The characteristic electromyographic appearance is a myopathic pattern during voluntary activity with a surprisingly high incidence of fibrillation potentials.l9 The recognition of a grossly myopathic pattern is not difficult, but minor degrees require precise analytical methods not everywhere available.20 Nevertheless, in conjunction with the clinical findings, the skilled use of these investigations will usually distinguish polymyositis from other causes of muscle weakness. The recognition of associated disease, while indisputably relevant, does not establish the " cause " of polymyositis. With our present knowledge a diagnosis of polymyositis is rather less specific than that of polyneuritis-in which at least some direct toxic agents can be incriminated. There is a curious resemblance between the two conditions in that both may arise in association with carcinoma and the collagen diseases, yet in most patients no associated disease or cause " can be found. In two of ROSE and WALTON’S patients both polymyositis and polyneuritis developed in succes"
13. 14. 15. 16. 17. 18. 19. 20.
Higginson, J., Isaacson, C., Simson, I. Archs. Path. 1960, 70, 497. Becker, B. J. P., Chatgidakis, C. B., van Lingen, B. Circulation, 1953, 7, 345. Davies, J. N. P. E. Afr. med. J. 1948, 25, 10. Brockington, I. F., Olsen, E. G. J., Goodwin, J. F. Lancet, March 18, 1967, p. 583. Shaper, A. G., Kaplan, M. H., Foster, W. D., Macintosh, D. M., Wilks, N. E. ibid. p. 598. Rose, A. L., Walton, J. N. Brain, 1966, 89, 747. Buchtal, F., Pinelli, P. Neurology, Minneap. 1953, 3, 424. Willison, R. G. Proc. R. Soc. Med. 1966, 59, 998.
LEADING ARTICLES
THE
LANCET
LONDON 22 APRIL
Design
of
1967
Operating-theatres
practice in Great Britain were operating-theatres in which the essential elements were a large room with a commodious gallery, a large side window admitting a lot of daylight, and a sort of open stage upon which the operative ritual was enacted. The origins of this design were probably several, and the one which springs most readily to mind is the dissecting-room of the Hunterian era. Dissection of cadavers was an exercise attended not only by young surgeons in training but also by laymen who regarded anatomy simply as a branch of human knowledge appropriate to any educated person. The type of building most suited to this purpose was not unlike the Elizabethan theatre, with its open stage, circular gallery, and overhead daylight. Since most anatomists were also surgeons who earned fees for teaching apprentices, it is not unreasonable to suppose that they modelled their MOST surgeons
now
in
trained in
theatres on their own dissection rooms. The advent of antisepsis, asepsis, and anaesthesia in the mid-19th century revolutionised the scope of surgery, but it made little difference to the general design until after the 1914-18 war, when the idea emerged of grouping all the necessaries of surgery in one suite. The advantages of centralisation--of instrument storage, sterilisation, and staff-were quickly recognised, and by the mid-1920s most new hospitals, particularly in the United States, incorporated this arrangement. The next step was related not so much to administrative convenience as to bacteriological idealism-a bacteria-tree environment in which wounds could be safely made and repaired. The isolation concept, established in the late 1930s, was closely related to the barrier nursing practised in fever hospitals and paediatric wards. The essential feature was a barrier zone between the hospital and the theatres, beyond which only the few people concerned in the operation could pass (suitably clad). Some years later came the idea of central sterilisation of all instruments and equipment used in the operating-theatres. The most modern and expensive sterilisation techniques could be employed, and human error could be virtually eliminated. About the same time, forced ventilation with filtered air was introduced. By this method a one-way air-flow from theatre to hospital could be maintained, and from there it was a short step to full control of air temperature, humidity, and flow-in fact, the airconditioning which is taken for granted in parts of the world with extremes of climate. Increasing technical complexity in both surgical and anarsthetic practice dictated other changes, notably the provision of anzesthetic and recovery rooms and monitoring laboratories.
The Ministry of Health, in its recommendations for the design of operating-theatre suites, comes down firmly on the side of the central sterile supply department2 and subsidiary theatre sterile supply unit in the theatre suite. No sterilising should be done in individual theatre complexes. Many surgeons will feel a little uneasy about this,2 but it is in line with recommendations of the Medical Research Council’s subcommittee on operating-theatre hygiene. The recommendations on zoning and patient transfer are welcome, and so are those on the location of the theatre suite and its functional relation with other departments. But it is disappointing to read that air-conditioning is not essential; for, even in Britain, theatres can become unbearably hot and humid in summer, and it surely is excessively parsimonious not to provide complete air-conditioning as a routine. It is also discouraging to find that most service lines are to be brought to the wall of the theatre, so that tubes and wires will have to trail across the floor, interfering with the movements of staff and equipment. The portable X-ray set is also to be perpetuated, with its cumbersome trolley and linen-clad head. The recommended theatre size is, at 400-480 sq. ft., small for ease of movement, especially when complex apparatus like heart-lung machines or monitoring equipment is in use. Finally, no research laboratories of any kind are provided in the theatre suite. This decision seems unimaginative when one considers, for instance, the great advances in patient care which have been derived from research into homoeostasis during and after operations. The memorandum is a sound and detailed guide for architects and surgeons, but it is neither forward-looking nor stimulating. It should not be accepted as the last word in operating-theatre design.
Myocarditis of preoccupation with the of haemodynamics congenital and acquired heart-disease, many cardiologists are now showing revived interest in the myocardium. Myocardial disorders, however, other than those secondary to such well-recognised causes as rheumatic or ischaemic heart-disease, are a large and mixed group about which remarkably little is known. Myocarditis, for example, a popular diagnosis at the end of the last century,3 has until lately been very much out of favour. Though it is present in many well-defined conditions, it is often said to be non-specific, and GORE and SAPHIR4 could make no firm aetiological diagnosis in 75% of their 1042 cases. The terms used to define it are often descriptive, reflecting ignorance of its origin and in this way resembling that other great protean group, the cardiomyopathies. Many organisms directly attack the myocardium (bacteria, viruses, rickettsix, spirochxtes, parasites, and AFTER twenty years
Ministry of Health Hospital Building Note, no. 26. H.M. Stationery Office. 1967. Pp. 44 and appendix. 6s. 6d. 2. See Lancet, April 15, 1967, p. 830. 3. Fiedler, A. in Festschrift zur Feier des Fünfzigjährigen Besrehens des Stadtkrankenhauses zu Dresden-Friedrichstadt; part 2, p. 3. Dresden, 1.
1899.
4.
Gore, I., Saphir,
O. Am. Heart J. 1947,
34,
827.
884
have all been incriminated); and it seems likely that other organisms and various immunity reactions may also damage the myocardium. The true incidence of inflammatory lesions of the myocardium is hard to judge because, while careful pathologists often find these lesions, most patients with myocardial involvement in infections do not succumb, and myocarditis is not a common clinical diagnosis. Even when suspected, it is difficult to prove, for the diagnosis depends on possible transient non-specific electrocardiographic changes and extensive bacteriological or biochemical investigations that are likely to be helpful only in an early phase of the illness. To add to the difficulty many of these tests are of value only when positive; negative results do not exclude active disease. Acute myocarditis often arises during the course of the acute infectious diseases, and patients who are isolated in special hospitals for contagious illness are a group that lends itself to intensive study. BENGTSSON and LAMBERGER,3 who followed a series of such patients with myocardial involvement for five years, found that 20% still had subjective symptoms (fatigue, dyspnoea,
fungi
precordial pain, impaired physical condition), 15-20% had abnormal electrocardiograms, 30% had abnormal exercise tests, and 40% had low working capacities. These figures were highly significant when compared with two other groups-one with doubtful myocarditis and one with no evidence of myocarditis. Although approximately 50% of the affected patients had had hxmolytic streptococcal infections (such as rheumatic fever or scarlet fever), symptoms and abnormal signs in this group after five years than in a group who had had aseptic meningitis (20% in both); and they were much less frequent than in the group with miscellaneous infectious diseases, in whom every second patient had sequelx of one sort or another. Myocardial involvement in generalised infections is probably commoner than is generally appreciated, and this Swedish work suggests that it almost certainly has greater prognostic significance. The Coxsackie viruses were no commoner
established as cardiac pathogens s-8; and recent work has shown that rubella is not only teratogenic but also a possible cause of clinical myocarditis in the newborn.9 Further advances in microbiology will undoubtedly reveal the cause of other types of "idiopathic" cardiac disorders-perhaps along the lines pursued by BRAIMBRIDGE and his colleagues.10o That a great deal remains to be explained about the causes of most of these conditions is beyond question and is reflected in the present interest in the many and bizarre forms of heart-disease that are becoming increasingly recognised in the tropics. Heart-muscle diseases nutritional heart-disease,12 cryptogenic heart-
are now
firmly
Bengtsson, E., Lamberger, B. ibid. 1966, 72, 751. Montgomery, J., Gear, J., Prinsloo, F. R., Kahn, M., Kirsch, Z. G. S. Afr. med. J. 1955, 29, 608. 7. Fletcher, E., Brennan, C. F. Lancet, 1957, i, 913. 8. Smith, W. G. Br. Heart J. 1966, 28, 204. 9. Ainger, L. E., Lawyer, N. G., Fitch, C. W. ibid. p. 691. 10. Braimbridge, M. V., Oarracott, S., Chayen, J., Bitensky, L., Poulter, L. W. Lancet, Jan. 28, 1967, p. 171. 11. Edington, G. M., Jackson, J. G. J. Path. Bact. 1963, 86, 333. 12. Gillanders, A. D. Br. Heart J. 1951, 13, 177. 5. 6.
disease.,13 and cardiovascular collagenosis 14 all show lesions in some way reminiscent of myocarditis, and a review of endomyocardial fibrosis 15 in Europeans who have been living in tropical Africa 16 favours an infective agent as a possible cause. Whether this affects the heart muscle directly or by some sensitivity or immunity reaction is still far from clear, 17 but this and other forms of myocarditis " are certain to take up much future cardiological time and space. "
Polymyositis THE difficulties of defining a " disease " and its cause are seldom more apparent than in the condition now universally known as polymyositis. The new work of ROSE and WALTON 18 is mainly concerned with epidemiology and response to treatment, but their initial survey of diagnostic criteria confirms that we are still in the stage of definition in clinical terms. Laboratory aids may be invaluable in proving that weakness is due to primary muscle disease, but the results are neither constant nor always specific and they may be hard to interpret. A rise in either the aldolase or creatine-kinase level in the serum indicates active muscle destruction and is therefore found in acute untreated disease or when relapse ensues during treatment-but it is not specific for any disease process. Muscle biopsy may be entirely normal in the presence of gross weaknessa finding usually attributed to the uneven distribution of the lesions. The interpretation of minor " abnormalities " is notoriously unreliable, and ROSE and WALTON found acceptable evidence of myositis in 34 out of 54 patients in whom biopsy was performed. The characteristic electromyographic appearance is a myopathic pattern during voluntary activity with a surprisingly high incidence of fibrillation potentials.l9 The recognition of a grossly myopathic pattern is not difficult, but minor degrees require precise analytical methods not everywhere available.20 Nevertheless, in conjunction with the clinical findings, the skilled use of these investigations will usually distinguish polymyositis from other causes of muscle weakness. The recognition of associated disease, while indisputably relevant, does not establish the " cause " of polymyositis. With our present knowledge a diagnosis of polymyositis is rather less specific than that of polyneuritis-in which at least some direct toxic agents can be incriminated. There is a curious resemblance between the two conditions in that both may arise in association with carcinoma and the collagen diseases, yet in most patients no associated disease or cause " can be found. In two of ROSE and WALTON’S patients both polymyositis and polyneuritis developed in succes"
13. 14. 15. 16. 17. 18. 19. 20.
Higginson, J., Isaacson, C., Simson, I. Archs. Path. 1960, 70, 497. Becker, B. J. P., Chatgidakis, C. B., van Lingen, B. Circulation, 1953, 7, 345. Davies, J. N. P. E. Afr. med. J. 1948, 25, 10. Brockington, I. F., Olsen, E. G. J., Goodwin, J. F. Lancet, March 18, 1967, p. 583. Shaper, A. G., Kaplan, M. H., Foster, W. D., Macintosh, D. M., Wilks, N. E. ibid. p. 598. Rose, A. L., Walton, J. N. Brain, 1966, 89, 747. Buchtal, F., Pinelli, P. Neurology, Minneap. 1953, 3, 424. Willison, R. G. Proc. R. Soc. Med. 1966, 59, 998.