- Email: [email protected]
SUDDEN DEATH IN SQUASH PLAYERS
148
contentious issues which cannot be fully resolved without further information about the risks and financial costs that vaccination and tubercular disease incur and about the influence of age on these variables and on the effectiveness of vaccination. However, the policy of offering neonatal vaccination routinely at SMH appears to have led to less than half as high an incidence of childhood tuberculosis as would have occurred if the more usual policy of attempting to identify and vaccinate high-risk infants alone during the neonatal period had been followed. We thank Dr A. Elizabeth Jones, medical officer for environmental health,
City of Manchester, for a wealth of valuable advice and information, particularly about cases of tuberculosis notified to her; Dr Carolyn M. Johnson, specialist in community medicine, Central Manchester Health Authority, and many paediatricians, physicians, and other staff of what was then the Manchester Area Health Authority (Teaching), for giving us access to numerous data both on cases treated in hospital and on the related population; Mr Mahesh S. Patel and a group assembled by him, for identifying children
Occasional SUDDEN DEATH IN
Survey
SQUASH PLAYERS
ANTHONY D. B. EVANS ROBIN J. NORTHCOTE DAVID BALLANTYNE
Department of Medical Cardiology, Infirmary, Glasgow G42 9TY
Victoria
A series of thirty sudden deaths (twentynine men, one woman) associated with is squash playing described. The subjects’ mean age was 46· 7±SD 9·58 years (range 22-66). Necropsy results were available for twenty-seven subjects. Significant coronary heart disease (CHD) was found in twenty-three, valvular heart disease in three, and hypertrophic obstructive cardiomyopathy in one, and cardiac arrhythmia, in the absence of other pathology, was thought to have preceded death in two. One subject died from intracerebral haemorrhage. Twenty-two had reported prodromal symptoms, and of those with CHD, sixteen had had at least one identifiable CHD risk factor. Twelve subjects had been known by their family physician to have a medical disorder related to the cardiovascular system.
Summary
INTRODUCTION
runningl,2 and track and We been now report findings in have studied. sports3-5 thirty sudden deaths occurring during or shortly after squash playing. With rising public awareness of the benefits of physical exercise, squash, as well as other sports, has recently enjoyed a huge increase in popularity, particularly among middle-aged, executive men. Concern has mounted because of an increasing number of sudden deaths associated with the sport, but few reports of the physiological and metabolic responses to the game have been published. 6,7 In addition, the principal causes of such deaths have not been defined. This study was undertaken to investigate the causes of sudden death associated with squash and to identify factors which SUDDEN deaths associated with
field
may increase the risk. SUBJECTS
AND METHODS
Cases of sudden death associated with squash playing in the United Kingdom between 1977 and 1983 were identified by retrospective examination of media reports. A few cases were
with Bangladeshi, Indian, and Pakistani surnames; and Glaxo Pharmaceuticals Ltd for financial support.
Correspondence should be addressed to 1. L., Department of Community Medicine, Stopford Building, University of Manchester, Oxford Road, Manchester M13 9PT. REFERENCES
HG, Hitze KL. Does BCG vaccination protect the newborn and young infant? Bull Wld Hlth Org 1980; 58: 37-41. Anon. BCG vaccination in the newborn. Br Med J 1980; 281: 1445-46. Tuberculosis Prevention Trial. Trial of BCG vaccines in South India for tuberculosis prevention: first report. Bull Wld Hlth Org 1979; 57: 819-27. Griffiths MI. In: Health and Tuberculosis Conference 1962: Transactions of the Sixth Commonwealth Conference organised by the Chest and Heart Association. London: Chest and Heart Association, 1962: 47-52. Tuberculosis Vaccines Clinical Trials Committee of the Medical Research Council BCG and vole bacillus vaccines in the prevention of tuberculosis in adolescents: Second report to the Medical Research Council by their Tuberculosis Vaccines Clinical Trials Committee. Br Med J 1959; ii: 379-96. Clemens JD, Chuong JJH, Femstein AR. The BCG controversy: a methodological and statistical reappraisal. J Am Med Ass 1983; 249: 2362-69.
1. Ten Dam 2. 3. 4.
5.
6.
by witnesses or by officials from squash the next of kin was interviewed with a standard questionnaire, to establish the circumstances surrounding the sudden death and the presence of pre-morbid symptoms or coronary heart disease (CHD) risk factors, as defined by Kannel et al.8 Prodromal symptoms were defined as any change from usual health status considered important and reported to relatives.9 Next of kin were also invited to assess the level of physical fitness and psychological characteristics of the subject. We sought permission to approach witnesses to the event and the family physician. In addition, if the subject had had a medical examination for the purposes of employment or life insurance, we asked permission to approach the authority concerned for the results. Necropsy findings, if available, were reviewed and the results of any Coroner’s inquiry (England) or Procurator Fiscal investigation (Scotland) were taken into account. Sudden death has been defined as death occurring within 1-24 h of the onset of symptoms. 10,11 In this study, all subjects collapsed while playing squash or in the following hour, and all died within 6 h of playing. A diagnosis of CHD was made if necropsy evidence of severe or pronounced coronary atherosclerosis was present, as judged by the pathologist, or when the lumen had narrowed by more than 50%, with or without evidence of fresh thrombus, in the absence of other pathology. Pathological evidence of a healed myocardial infarction supported a diagnosis of CHD. reported directly
clubs. In each
to us
case
RESULTS
We identified thirty cases of sudden death associated with squash which occurred between January, 1977, and February, 1983. The mean age of the subjects was 46 -7±SD 9 -58 years (range 22-66 years). All were White, and only one was female. In each case, the onset of symptoms was rapid, and they culminated in collapse of the subject and unconsciousness. Twenty-two subjects collapsed on the squash court and eight in the first hour after play. In all but one case, death was almost instantaneous, and the subject did not reach hospital. The remaining subject collapsed 60 min after play, while driving, and died 6 h later in hospital. Two subjects collapsed while taking a hot shower after playing squash. Cardiopulmonary resuscitation was attempted in
twenty-nine cases. All the subjects had been playing squash for at least 2 years (10-89±7’45 years; range 2-30 years). The mean frequency of play was 2 -3--t1 - 26 visits to the squash court per week. Nine subjects had begun playing the game after they were 40 and only eight subjects had been playing since before they were 30. One subject (aged 60 years) had stopped playing squash 10 years earlier on medical advice and had recently restarted playing with his son.
149
of Death Necropsy reports were available for twenty-seven subjects. Of the three others, symptoms of angina pectoris had developed in one a year before he died and he had significant ST depression on exercise electrocardiography at that time. One had had a history of myocardial infarction and documented aortic regurgitation in the 10 years before he died and one no features of CHD before the fatal episode. CHD was the probable cause of death in twenty-three cases. ’Of these, a firm pathological diagnosis was made in twenty cases, with severe or pronounced stenosis of at least Causes
In one subject, hypertrophic obstructive cardiomyopathy, disorder known to be associated with sudden death during strenuous exercise,13 was found in the absence of other pathology. This 37-year-old man was not known to his family physician, and his annual medical examinations at work had detected no abnormality. A right intracranial haemorrhage had occurred in one subject in whom symptoms developed 60 min after playing squash and who died in hospital 6 h later without regaining consciousness. In two cases, no pathological abnormality was found at necropsy and in both the pathologist certified that death resulted from a cardiac arrhythmia. This diagnosis should preferably be supported by thorough histopathological examination of the conduction system of the heart. 14 This was done for one subject, but no abnormality was detected. Since both deaths were instantaneous, it seems likely that the certified cause of death was correct. a
main coronary artery, and there was evidence of fresh thrombus formation in five cases. Although seven subjects had pathological evidence of a healed myocardial infarction, this had been diagnosed in only one subject during life. In sixteen of the cases of CHD an accurate description of the state of the coronary arteries was available from the necropsy report (table I). All sixteen had had severe disease of at least one major coronary artery. In one case (no necropsy), death was attributed to CHD, since the subject had a history of one
myocardial infarction. However, aortic regurgitation necessitating annual review at a cardiac clinic had been documented in this patient. TABLE I-SITE OF ATHEROMA IN SIXTEEN DYING OF CHD
SUBJECTS
Pre-morbid Conditions and Symptoms
Twenty-two victims had reported prodromal symptoms (table II). Only four subjects were known to have received medical advice about these symptoms, and a further two had arranged appointments to discuss the symptoms with their family physicians. Eight subjects had had more than one
prodromal symptom. Twelve subjects were
known to have had at least one medical disorder related to the cardiovascular system during life: ten (33% of whole group) had had documented hypertension, which had been confirmed on two or more occasions. Surprisingly, only one subject had received antihypertensive treatment. Three had had documented angina pectoris or myocardial infarction. Three were known have had valvular heart disease and three to
hypercholesterolaemia. Of the twenty-three subjects dying of CHD, sixteen had had at least 1 CHD risk factor, nine subjects 2 or more, two subjects at least 3, and three subjects more than 3 (table III). Physical Fitness Next of kin were asked to assess the physical fitness of the deceased in relation to the general population, in five I1
I
j
TABLE II-PRODROMAL SYMPTOMS
I
*MI = myocardial infarction; AW = anterior wall. -fRCA=right coronary artery; LAD = left anterior descending coronary artery; Cx = circumflex branch of left coronary artery; LMS = left mainstem coronary artery.
Valvular heart disease was implicated in three cases. The valvular lesions had been discovered during life in all three, but none had received medical advice against strenuous exercise. The first subject had had congenital prolapse of the mitral valve with atrial fibrillation during life. This abnormality was confirmed at necropsy and was accompanied by pronounced left-ventricular hypertrophy (the heart weighed 550 g) in the absence of significant CHD. The cause of death was certified as acute heart failure, possibly in association with a cardiac arrhythmia.12 Mitral stenosis resulting in acute heart failure was found in the second subject in the absence of significant CHD. The third subject had a calcified aortic valve, resulting in severe aortic stenosis, and calcified coronary arteries. However, the certifying pathologist judged that the aortic valve lesion was the principal cause of death.
*
One subject, who ran 1 mile every morning, had extreme breathlessness on 3 successive mornings before he died, but was not deterred from further strenuous exercise. tCause of death intracranial haemorrhage.
.
TABLE III-PREVALENCE OF CHD RISK FACTORS IN DYING OF CHD
SUBJECTS
_
150
categories. Twenty-one subjects were said to be very fit, eight fit, and one averagely fit. No subject was considered unfit or very unfit.
Occupation Each subject’s occupation was noted; none was, unemployed. Twelve subjects had been company directors or had worked in higher management. Six had worked in higher education (including two university professors). Four had been civil servants, two engineers, one a salesman, one a student, one a policeman, and three had worked in other occupations.
Psychological Characteristics A high proportion of subjects, despite having prodromal symptoms or disorders, had played squash and ignored these factors. Next of kin
were
asked
to assess
the deceased’s
predominant psychological characteristics. In six cases the next of kin described a competitive, ambitious, hard-driving, perfectionist. Eleven subjects were considered very aggressive, two very competitive, and one obsessive about fitness; ten had no clear recognisable traits. DISCUSSION
This study shows that the major cause of sudden death associated with squash is cardiovascular disease and that the causes are similar to those reported in other studies concerned with various other sports.I-4 Although cardiopulmonary resuscitation was attempted in all but one of our cases, often in the presence of a physician or nurse, none was successful. We do not know whether the pronounced male preponderance in oui study reflects the proportions of men and women playing squash, the lower prevalence of CHD in women, or the intensity with which the game is played by each sex. The mean age of our subjects (46 -7±9’58 years) is similar to that reported for other sudden deaths, particularly those caused by CHD.15 Although it did not feature in other studies,4,5 valvular heart disease caused three deaths and contributed to another in our series. In the first three cases the valvular lesions had been discovered in life, but the subjects had never been advised to avoid strenuous exercise by their doctors. No case was associated with myopericarditis, which has been considered a possible cause of sudden death or collapse in sport. 16 It is unlikely that this disorder is a significant cause of sudden death in squash players. It is possible that many of these subjects, particularly those who began playing in their 40s, took up squash to benefit from any preventive effect of vigorous exercise on CHD. 17,18 However, it is unlikely that such exercise will be able to protect against or reverse existing coronary atheroma, 19 and it may even render the individual more susceptible to cardiac complications; vigorous exercise is known to precipitate cardiac arrhythmias in those with CHD20 and may be associated with sudden death.21 Twenty-two subjects in this series had had prodromal symptoms, the most common being chest pain, gastrointestinal complaints, and excessive fatigue or dyspnoea. Only four of these individuals had sought medical advice, and it is remarkable that none of them thought these symptoms should interfere with their exercise. Such denial of prodromal symptoms has been noted by others2,22 and may be a characteristic to which aggressive sportsmen are prone.3 It is noteworthy also that twelve subjects continued to play squash despite having medical disorders related to the cardiovascular
system and, to our knowledge, were never advised to avoid such vigorous exercise. It is impossible, from these data, to assess whether squash is more likely to precipitate sudden death than other sports. We were able to identify from media reports only seven sudden deaths associated with other sports between 1977 and 1983; this difference may be due to incomplete reporting or may reflect the greater popularity of squash, particularly in the coronary-prone age group. Attempts have been made to estimate the incidence of sudden death in other sportS.3,23 In the UK, however, collation of any series of squash deaths depends heavily on media reports, which may underestimate the problem. We would not disagree with Fowler’s estimate of twenty-seven a year in the UK,24 but we are unable to find evidence to support it. In our study the greatest number of deaths occurred in 1980 (twelve). Squash is a vigorous sport, able to raise heart rate to 90% of predicted maximum and to generate significant cardiac arrhythmias in a normal population.6 Both of these effects could be harmful in subjects already at risk through CHD or valvular heart disease. Eight subjects collapsed within 30 min of play, a period referred to as the post-exercise vulnerable period,25 during which there is raised ventricular ectopic activity.6,26 The reasons for the raised ventricular ectopic activity, in an individual who has been able to undertake severe exertion without collapse, are not clear. It is possible that after sudden cessation of activity, pooling of blood in the legs reduces venous return to the heart and results in coronary artery insufficiency. Free fatty acid and catecholamine levels may rise after exercise27 and can cause arrhythmias 28 and arterial thromboses,29 especially in the presence of coronary artery constriction. 30 Two of our subjects died while taking a hot shower. Such thermal stress also results in arrhythmias and increased heart rate.31 These factors may also be evident on squash courts, many of which are too warm and poorly ventilated. The high proportion of professional people in this group of sudden deaths may reflect the popularity of the sport in such individuals or may be related to their personality characteristics. Squash may be attractive to more aggressive individuals, who may already be more prone to CHD. Exercise may have a role in the prevention and therapy of CHD, as well as having other benefits,32 and it is not our purpose to discourage healthy, low-risk individuals from playing squash. We have identified the principal causes of sudden death in squash and have attempted to define those who may be at increased risk. The high prevalence of prodromal symptoms and known risk factors suggest that some of these deaths could have been prevented. We thank the Squash Rackets Association, the Coroners Society (England), and the Crown Office (Scotland) for their help in the collation of data; and the relatives and general practitioners of the deceased for their cooperation. The study was supported by a grant from the Chest, Heart and Stroke Association.
Correspondence should be
addressed
to
R. J. N.
REFERENCES
BF, Roberts WC. Sudden death while running, in conditioned runners aged 40 years or over. Am J Cardiol 1980, 45: 1292-300. Thompson PD, Stern MP, Williams P, Duncan K, Haskell W, Wood P Death during jogging or running, a study of 18 cases. JAMA 1979; 242: 1265-67. Opie LH Sudden death and sport. Lancet 1975; i. 263-66. Lynch P. Soldiers, sport and sudden death Lancet 1980; i: 1235-37. Maron BJ, Roberts WC, McAllister HA, Rosing DR, Epstein SE. Sudden death in young athletes Circulation 1980; 60: 218-29. Northcote RJ, MacFarlane P, Ballantyne D. Ambulatory electrocardiography in squash players. Br Heart J1983, 50: 372-77
1. Waller 2. 3. 4. 5. 6.
151
Hospital
retrospectively. Colonisation tively for 4 months.
Practice
AN OUTBREAK OF SERRATIA MARCESCENS INFECTION IN A NEONATAL UNIT
J. SMITH Department of Paediatrics,
D. S. K. BROOKFIELD
P.
North
Stoke-on- Trent
METHODS
Neonatal Unit This is a 30-bed ward divided into five rooms and an isolation cubicle. Neonates requiring intensive or care are nursed in one of three rooms and, when space permits, they are separated from well neonates and those who are recovering.
Case Definition
J. GRAY
Case-reports in which S marcescens was isolated were studied retrospectively. Symptom-free babies whose cultures yielded
Microbiology and Public Health Laboratory, North Staffordshire Hospital Centre
deemed to be colonised. Patients with infections were divided into two groups. Babies with major infections had clinical signs of septicaemia or pneumonia and positive cultures of blood or sputum, respectively. Minor infection was considered to be present in infants with purulent conjunctivitis or a sticky umbilicus yielding S marcescens.
S
Over a 15-month period 732 babies were admitted to a neonatal unit, and Serratia marcescens was isolated from 153 (21%). In one-fifth (34) a clinical infection (9 major and 25 minor) developed. Major infection was associated with high mortality and morbidity and 2 cases presented after the neonatal period. No environmental reservoir was found. Colonised symptom-free neonates were considered to be the source, with transmission
Summary
by staff-baby contact despite adequate hand-washing. Overcrowding was believed to be responsible for the difficulties experienced in eradicating this transmission. INTRODUCTION Serratia marcescens,
as a biological marker for recognised as an important opportunistic pathogen.’ Most infections have been reported in adults but one of the earliest descriptions was of urinarytract infection in children.2 Other reported outbreaks have implicated contaminated saline bottles,3 scalp-vein needles,4 and nail brushes. Christensen et al emphasised the importance of symptom-free colonised infants as the major reservoir of infection. We report a further epidemic of
once
pathogenicity studies, is
S
in
used
now
neonatal unit. S marcescens was first isolated from babies in the neonatal unit at Stoke-on-Trent in August, 1981, and was subsequently shown to be a cause of potentially serious infection in some neonates. The morbidity and mortality over a 15-month period in these neonates was studied marcescens
evaluated prospec-
high-dependency
Staffordshire Hospital Centre,
D. A. SHAW
rates were
a
TD, Cowling JR, Gevers W, Van Niekerk JPDeV. The metabolic response to squash including the influence of pre-exercise carbohydrate ingestion. S Afr Med J
marcescens were
Bacteriological Sampling During the early part of the investigation environmental samples taken with moistened cotton-wool swabs which were incubated overnight in glucose brothand subcultured on MacConkey agar. Items sampled included the blood-gas analyser, breast pumps, incubators, humidifiers, suction jars, and various ointments, hand creams, and antiseptics in use on the unit. Hand cultures were taken from members of the staff on several occasions by means of a moistened 5 x5 cm gauze square, which was rubbed over both hands, incubated overnight in glucose broth, and subcultured on MacConkey agar. For the latter part of the survey, after June, 1982, the nose and throat of all babies newly admitted to the unit were swabbed twice weekly with damp cotton-wool swabs. The isolates were identified by conventional methods. Antibiotic sensitivity testing was performed by a rotary Stokes method. Selected isolates were phage-typed and serotyped. were
-
Ward Observations
’
Members of the infection control team used the cover provided by the bacteriological surveys to observe the hand-washing techniques of the medical and nursing staff on the unit. The team also made unannounced visits to the ward at irregular intervals throughout the outbreak.
7. Noakes
1982, 62: 721-23. 8. Kannel WB, Doyle JT, McNamara PM, Quikenton P, Gordon T. Precursors of sudden coronary death. Factors related to the incidence of sudden death. Circulation 1975; 51: 606-13 9. Alonzo AA, Simon
AB, Feinlab M. Prodromata of myocardial infarction and sudden deaths Circulation 1975; 52: 1056-62. 10. Kuller L, Lillienfield A, Fisher R. An epidemiological study of sudden and unexpected deaths in adults. Medicine 1967, 46: 341-61. 11. Friedman M, Manwarmg JH, Rosenman RH, Donlon G, Ortega P, Grube SM Instantaneous and sudden deaths: clinical and pathological differentation in coronary artery disease. JAMA 1973; 225: 1319-28 12 Mills P, Rose J, Hollingsworth J, Amara I, Craige E. Long term prognosis of mitral valve prolapse N Engl J Med 1977; 297: 13-18 13 Maron BJ, Roberts WC, Edwards JE, McAllister HA, Foley DD, Epstein SE Sudden death in patients with hypertrophic cardiomyopathy: characterisation of 26 patients without previous functional limitation. Am J Cardiol 1978; 41: 803-10 14. James TN, Froggatt P, Marshall TK Sudden death in young athletet. Ann Intern Med 1967, 67: 1013-21. 15. Northcote RJ, 1357-59
Ballantyne
D. Sudden cardiac death
in
sport Br
Med J 1983;
287:
16. Barlow JB Exercise, rugby football and infection. S Afr Med J 1976, 50: 1351 17 Turner R, Ball K Prevention of coronary heart-disease. A counterblast to present inactivity. Lancet 1973; ii: 1137-40. 18. Opie LH. Exercise training, the myocardium, and ischaemic heart disease. Am Heart J
1974; 88: 539-41. 19.
Jokl E Sudden
death of a rugby international after a test game. In eds. Medicine and sport. Basel: S Krager, 1971 153-58.
Jokl E,
Culver
EH,
20. Gordon T, Kannel WB, McGee D, et al. Death and coronary attacks in men after giving up cigarette smoking. A report from the Framingham study. Lancet 1974; ii: 1345-48. 21. Moritz AR, Zamcheck N. Sudden and unexpected deaths in young soldiers. Arch Pathol 1946; 42: 459-93. 22 Nixon PGF, Bethell HJN Preinfarction ill health. Am J Cardiol 1974; 33: 446-49. 23. Thompson PD, Funk EJ, Carleton RA, Sturner WQ. Incidence of death during jogging m Rhode Island from 1975 through 1980. JAMA 1982, 18: 2535-38. 24. Fowler AW. Cause of death on squash courts. On Call 1980; 14: 7. 25. Adams CW. Symposia on exercise and the heart. Introduction. Am J Cardiol 1972; 30: 713-15. 26. Goldschlager N, Cake D, Cohn K. Exercise-induced ventricular arrhythmias in
patients with coronary artery disease: their relation to angiographic findings. Am J Cardiol 1973; 31: 434-40. 27. Johnson RH, Walton JL, Krebs HA, Williamson DM. Metabolic fuels during and after severe exercise in athletes and non-athletes. Lancet 1969, ii: 452-55. 28. Kurien VA, Yates PA, Oliver MF. The role of free fatty acids in the production of ventricular atthythmias after acute coronary artery occlusion. Eur J Clin Invesr 1971; 1: 225-41. 29. Hoak JC, Poole JCF, Robinson DS. Thrombosis associated with mobilization of fatty acids. Am J Pathol 1963; 43: 987-98. 30. Raab W, Van Lith P, Lepeschin E, Herrlich HC. Catecholamine induced myocardial hypoxia in the presence of impaired coronary dilatability independent of external cardiac work Am J Cardiol 1962; 9: 455-70. 31. Taggart P, Parkinson P, Carruthers M Cardiac responses to thermal, physical and emotional stress. Br Med J 1972; iii: 71-76. 32. Clark RS, Ballantyne D. Physical activity and coronary heart disease. Scot Med J 1981; 26: 15-20.
,
contentious issues which cannot be fully resolved without further information about the risks and financial costs that vaccination and tubercular disease incur and about the influence of age on these variables and on the effectiveness of vaccination. However, the policy of offering neonatal vaccination routinely at SMH appears to have led to less than half as high an incidence of childhood tuberculosis as would have occurred if the more usual policy of attempting to identify and vaccinate high-risk infants alone during the neonatal period had been followed. We thank Dr A. Elizabeth Jones, medical officer for environmental health,
City of Manchester, for a wealth of valuable advice and information, particularly about cases of tuberculosis notified to her; Dr Carolyn M. Johnson, specialist in community medicine, Central Manchester Health Authority, and many paediatricians, physicians, and other staff of what was then the Manchester Area Health Authority (Teaching), for giving us access to numerous data both on cases treated in hospital and on the related population; Mr Mahesh S. Patel and a group assembled by him, for identifying children
Occasional SUDDEN DEATH IN
Survey
SQUASH PLAYERS
ANTHONY D. B. EVANS ROBIN J. NORTHCOTE DAVID BALLANTYNE
Department of Medical Cardiology, Infirmary, Glasgow G42 9TY
Victoria
A series of thirty sudden deaths (twentynine men, one woman) associated with is squash playing described. The subjects’ mean age was 46· 7±SD 9·58 years (range 22-66). Necropsy results were available for twenty-seven subjects. Significant coronary heart disease (CHD) was found in twenty-three, valvular heart disease in three, and hypertrophic obstructive cardiomyopathy in one, and cardiac arrhythmia, in the absence of other pathology, was thought to have preceded death in two. One subject died from intracerebral haemorrhage. Twenty-two had reported prodromal symptoms, and of those with CHD, sixteen had had at least one identifiable CHD risk factor. Twelve subjects had been known by their family physician to have a medical disorder related to the cardiovascular system.
Summary
INTRODUCTION
runningl,2 and track and We been now report findings in have studied. sports3-5 thirty sudden deaths occurring during or shortly after squash playing. With rising public awareness of the benefits of physical exercise, squash, as well as other sports, has recently enjoyed a huge increase in popularity, particularly among middle-aged, executive men. Concern has mounted because of an increasing number of sudden deaths associated with the sport, but few reports of the physiological and metabolic responses to the game have been published. 6,7 In addition, the principal causes of such deaths have not been defined. This study was undertaken to investigate the causes of sudden death associated with squash and to identify factors which SUDDEN deaths associated with
field
may increase the risk. SUBJECTS
AND METHODS
Cases of sudden death associated with squash playing in the United Kingdom between 1977 and 1983 were identified by retrospective examination of media reports. A few cases were
with Bangladeshi, Indian, and Pakistani surnames; and Glaxo Pharmaceuticals Ltd for financial support.
Correspondence should be addressed to 1. L., Department of Community Medicine, Stopford Building, University of Manchester, Oxford Road, Manchester M13 9PT. REFERENCES
HG, Hitze KL. Does BCG vaccination protect the newborn and young infant? Bull Wld Hlth Org 1980; 58: 37-41. Anon. BCG vaccination in the newborn. Br Med J 1980; 281: 1445-46. Tuberculosis Prevention Trial. Trial of BCG vaccines in South India for tuberculosis prevention: first report. Bull Wld Hlth Org 1979; 57: 819-27. Griffiths MI. In: Health and Tuberculosis Conference 1962: Transactions of the Sixth Commonwealth Conference organised by the Chest and Heart Association. London: Chest and Heart Association, 1962: 47-52. Tuberculosis Vaccines Clinical Trials Committee of the Medical Research Council BCG and vole bacillus vaccines in the prevention of tuberculosis in adolescents: Second report to the Medical Research Council by their Tuberculosis Vaccines Clinical Trials Committee. Br Med J 1959; ii: 379-96. Clemens JD, Chuong JJH, Femstein AR. The BCG controversy: a methodological and statistical reappraisal. J Am Med Ass 1983; 249: 2362-69.
1. Ten Dam 2. 3. 4.
5.
6.
by witnesses or by officials from squash the next of kin was interviewed with a standard questionnaire, to establish the circumstances surrounding the sudden death and the presence of pre-morbid symptoms or coronary heart disease (CHD) risk factors, as defined by Kannel et al.8 Prodromal symptoms were defined as any change from usual health status considered important and reported to relatives.9 Next of kin were also invited to assess the level of physical fitness and psychological characteristics of the subject. We sought permission to approach witnesses to the event and the family physician. In addition, if the subject had had a medical examination for the purposes of employment or life insurance, we asked permission to approach the authority concerned for the results. Necropsy findings, if available, were reviewed and the results of any Coroner’s inquiry (England) or Procurator Fiscal investigation (Scotland) were taken into account. Sudden death has been defined as death occurring within 1-24 h of the onset of symptoms. 10,11 In this study, all subjects collapsed while playing squash or in the following hour, and all died within 6 h of playing. A diagnosis of CHD was made if necropsy evidence of severe or pronounced coronary atherosclerosis was present, as judged by the pathologist, or when the lumen had narrowed by more than 50%, with or without evidence of fresh thrombus, in the absence of other pathology. Pathological evidence of a healed myocardial infarction supported a diagnosis of CHD. reported directly
clubs. In each
to us
case
RESULTS
We identified thirty cases of sudden death associated with squash which occurred between January, 1977, and February, 1983. The mean age of the subjects was 46 -7±SD 9 -58 years (range 22-66 years). All were White, and only one was female. In each case, the onset of symptoms was rapid, and they culminated in collapse of the subject and unconsciousness. Twenty-two subjects collapsed on the squash court and eight in the first hour after play. In all but one case, death was almost instantaneous, and the subject did not reach hospital. The remaining subject collapsed 60 min after play, while driving, and died 6 h later in hospital. Two subjects collapsed while taking a hot shower after playing squash. Cardiopulmonary resuscitation was attempted in
twenty-nine cases. All the subjects had been playing squash for at least 2 years (10-89±7’45 years; range 2-30 years). The mean frequency of play was 2 -3--t1 - 26 visits to the squash court per week. Nine subjects had begun playing the game after they were 40 and only eight subjects had been playing since before they were 30. One subject (aged 60 years) had stopped playing squash 10 years earlier on medical advice and had recently restarted playing with his son.
149
of Death Necropsy reports were available for twenty-seven subjects. Of the three others, symptoms of angina pectoris had developed in one a year before he died and he had significant ST depression on exercise electrocardiography at that time. One had had a history of myocardial infarction and documented aortic regurgitation in the 10 years before he died and one no features of CHD before the fatal episode. CHD was the probable cause of death in twenty-three cases. ’Of these, a firm pathological diagnosis was made in twenty cases, with severe or pronounced stenosis of at least Causes
In one subject, hypertrophic obstructive cardiomyopathy, disorder known to be associated with sudden death during strenuous exercise,13 was found in the absence of other pathology. This 37-year-old man was not known to his family physician, and his annual medical examinations at work had detected no abnormality. A right intracranial haemorrhage had occurred in one subject in whom symptoms developed 60 min after playing squash and who died in hospital 6 h later without regaining consciousness. In two cases, no pathological abnormality was found at necropsy and in both the pathologist certified that death resulted from a cardiac arrhythmia. This diagnosis should preferably be supported by thorough histopathological examination of the conduction system of the heart. 14 This was done for one subject, but no abnormality was detected. Since both deaths were instantaneous, it seems likely that the certified cause of death was correct. a
main coronary artery, and there was evidence of fresh thrombus formation in five cases. Although seven subjects had pathological evidence of a healed myocardial infarction, this had been diagnosed in only one subject during life. In sixteen of the cases of CHD an accurate description of the state of the coronary arteries was available from the necropsy report (table I). All sixteen had had severe disease of at least one major coronary artery. In one case (no necropsy), death was attributed to CHD, since the subject had a history of one
myocardial infarction. However, aortic regurgitation necessitating annual review at a cardiac clinic had been documented in this patient. TABLE I-SITE OF ATHEROMA IN SIXTEEN DYING OF CHD
SUBJECTS
Pre-morbid Conditions and Symptoms
Twenty-two victims had reported prodromal symptoms (table II). Only four subjects were known to have received medical advice about these symptoms, and a further two had arranged appointments to discuss the symptoms with their family physicians. Eight subjects had had more than one
prodromal symptom. Twelve subjects were
known to have had at least one medical disorder related to the cardiovascular system during life: ten (33% of whole group) had had documented hypertension, which had been confirmed on two or more occasions. Surprisingly, only one subject had received antihypertensive treatment. Three had had documented angina pectoris or myocardial infarction. Three were known have had valvular heart disease and three to
hypercholesterolaemia. Of the twenty-three subjects dying of CHD, sixteen had had at least 1 CHD risk factor, nine subjects 2 or more, two subjects at least 3, and three subjects more than 3 (table III). Physical Fitness Next of kin were asked to assess the physical fitness of the deceased in relation to the general population, in five I1
I
j
TABLE II-PRODROMAL SYMPTOMS
I
*MI = myocardial infarction; AW = anterior wall. -fRCA=right coronary artery; LAD = left anterior descending coronary artery; Cx = circumflex branch of left coronary artery; LMS = left mainstem coronary artery.
Valvular heart disease was implicated in three cases. The valvular lesions had been discovered during life in all three, but none had received medical advice against strenuous exercise. The first subject had had congenital prolapse of the mitral valve with atrial fibrillation during life. This abnormality was confirmed at necropsy and was accompanied by pronounced left-ventricular hypertrophy (the heart weighed 550 g) in the absence of significant CHD. The cause of death was certified as acute heart failure, possibly in association with a cardiac arrhythmia.12 Mitral stenosis resulting in acute heart failure was found in the second subject in the absence of significant CHD. The third subject had a calcified aortic valve, resulting in severe aortic stenosis, and calcified coronary arteries. However, the certifying pathologist judged that the aortic valve lesion was the principal cause of death.
*
One subject, who ran 1 mile every morning, had extreme breathlessness on 3 successive mornings before he died, but was not deterred from further strenuous exercise. tCause of death intracranial haemorrhage.
.
TABLE III-PREVALENCE OF CHD RISK FACTORS IN DYING OF CHD
SUBJECTS
_
150
categories. Twenty-one subjects were said to be very fit, eight fit, and one averagely fit. No subject was considered unfit or very unfit.
Occupation Each subject’s occupation was noted; none was, unemployed. Twelve subjects had been company directors or had worked in higher management. Six had worked in higher education (including two university professors). Four had been civil servants, two engineers, one a salesman, one a student, one a policeman, and three had worked in other occupations.
Psychological Characteristics A high proportion of subjects, despite having prodromal symptoms or disorders, had played squash and ignored these factors. Next of kin
were
asked
to assess
the deceased’s
predominant psychological characteristics. In six cases the next of kin described a competitive, ambitious, hard-driving, perfectionist. Eleven subjects were considered very aggressive, two very competitive, and one obsessive about fitness; ten had no clear recognisable traits. DISCUSSION
This study shows that the major cause of sudden death associated with squash is cardiovascular disease and that the causes are similar to those reported in other studies concerned with various other sports.I-4 Although cardiopulmonary resuscitation was attempted in all but one of our cases, often in the presence of a physician or nurse, none was successful. We do not know whether the pronounced male preponderance in oui study reflects the proportions of men and women playing squash, the lower prevalence of CHD in women, or the intensity with which the game is played by each sex. The mean age of our subjects (46 -7±9’58 years) is similar to that reported for other sudden deaths, particularly those caused by CHD.15 Although it did not feature in other studies,4,5 valvular heart disease caused three deaths and contributed to another in our series. In the first three cases the valvular lesions had been discovered in life, but the subjects had never been advised to avoid strenuous exercise by their doctors. No case was associated with myopericarditis, which has been considered a possible cause of sudden death or collapse in sport. 16 It is unlikely that this disorder is a significant cause of sudden death in squash players. It is possible that many of these subjects, particularly those who began playing in their 40s, took up squash to benefit from any preventive effect of vigorous exercise on CHD. 17,18 However, it is unlikely that such exercise will be able to protect against or reverse existing coronary atheroma, 19 and it may even render the individual more susceptible to cardiac complications; vigorous exercise is known to precipitate cardiac arrhythmias in those with CHD20 and may be associated with sudden death.21 Twenty-two subjects in this series had had prodromal symptoms, the most common being chest pain, gastrointestinal complaints, and excessive fatigue or dyspnoea. Only four of these individuals had sought medical advice, and it is remarkable that none of them thought these symptoms should interfere with their exercise. Such denial of prodromal symptoms has been noted by others2,22 and may be a characteristic to which aggressive sportsmen are prone.3 It is noteworthy also that twelve subjects continued to play squash despite having medical disorders related to the cardiovascular
system and, to our knowledge, were never advised to avoid such vigorous exercise. It is impossible, from these data, to assess whether squash is more likely to precipitate sudden death than other sports. We were able to identify from media reports only seven sudden deaths associated with other sports between 1977 and 1983; this difference may be due to incomplete reporting or may reflect the greater popularity of squash, particularly in the coronary-prone age group. Attempts have been made to estimate the incidence of sudden death in other sportS.3,23 In the UK, however, collation of any series of squash deaths depends heavily on media reports, which may underestimate the problem. We would not disagree with Fowler’s estimate of twenty-seven a year in the UK,24 but we are unable to find evidence to support it. In our study the greatest number of deaths occurred in 1980 (twelve). Squash is a vigorous sport, able to raise heart rate to 90% of predicted maximum and to generate significant cardiac arrhythmias in a normal population.6 Both of these effects could be harmful in subjects already at risk through CHD or valvular heart disease. Eight subjects collapsed within 30 min of play, a period referred to as the post-exercise vulnerable period,25 during which there is raised ventricular ectopic activity.6,26 The reasons for the raised ventricular ectopic activity, in an individual who has been able to undertake severe exertion without collapse, are not clear. It is possible that after sudden cessation of activity, pooling of blood in the legs reduces venous return to the heart and results in coronary artery insufficiency. Free fatty acid and catecholamine levels may rise after exercise27 and can cause arrhythmias 28 and arterial thromboses,29 especially in the presence of coronary artery constriction. 30 Two of our subjects died while taking a hot shower. Such thermal stress also results in arrhythmias and increased heart rate.31 These factors may also be evident on squash courts, many of which are too warm and poorly ventilated. The high proportion of professional people in this group of sudden deaths may reflect the popularity of the sport in such individuals or may be related to their personality characteristics. Squash may be attractive to more aggressive individuals, who may already be more prone to CHD. Exercise may have a role in the prevention and therapy of CHD, as well as having other benefits,32 and it is not our purpose to discourage healthy, low-risk individuals from playing squash. We have identified the principal causes of sudden death in squash and have attempted to define those who may be at increased risk. The high prevalence of prodromal symptoms and known risk factors suggest that some of these deaths could have been prevented. We thank the Squash Rackets Association, the Coroners Society (England), and the Crown Office (Scotland) for their help in the collation of data; and the relatives and general practitioners of the deceased for their cooperation. The study was supported by a grant from the Chest, Heart and Stroke Association.
Correspondence should be
addressed
to
R. J. N.
REFERENCES
BF, Roberts WC. Sudden death while running, in conditioned runners aged 40 years or over. Am J Cardiol 1980, 45: 1292-300. Thompson PD, Stern MP, Williams P, Duncan K, Haskell W, Wood P Death during jogging or running, a study of 18 cases. JAMA 1979; 242: 1265-67. Opie LH Sudden death and sport. Lancet 1975; i. 263-66. Lynch P. Soldiers, sport and sudden death Lancet 1980; i: 1235-37. Maron BJ, Roberts WC, McAllister HA, Rosing DR, Epstein SE. Sudden death in young athletes Circulation 1980; 60: 218-29. Northcote RJ, MacFarlane P, Ballantyne D. Ambulatory electrocardiography in squash players. Br Heart J1983, 50: 372-77
1. Waller 2. 3. 4. 5. 6.
151
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Practice
AN OUTBREAK OF SERRATIA MARCESCENS INFECTION IN A NEONATAL UNIT
J. SMITH Department of Paediatrics,
D. S. K. BROOKFIELD
P.
North
Stoke-on- Trent
METHODS
Neonatal Unit This is a 30-bed ward divided into five rooms and an isolation cubicle. Neonates requiring intensive or care are nursed in one of three rooms and, when space permits, they are separated from well neonates and those who are recovering.
Case Definition
J. GRAY
Case-reports in which S marcescens was isolated were studied retrospectively. Symptom-free babies whose cultures yielded
Microbiology and Public Health Laboratory, North Staffordshire Hospital Centre
deemed to be colonised. Patients with infections were divided into two groups. Babies with major infections had clinical signs of septicaemia or pneumonia and positive cultures of blood or sputum, respectively. Minor infection was considered to be present in infants with purulent conjunctivitis or a sticky umbilicus yielding S marcescens.
S
Over a 15-month period 732 babies were admitted to a neonatal unit, and Serratia marcescens was isolated from 153 (21%). In one-fifth (34) a clinical infection (9 major and 25 minor) developed. Major infection was associated with high mortality and morbidity and 2 cases presented after the neonatal period. No environmental reservoir was found. Colonised symptom-free neonates were considered to be the source, with transmission
Summary
by staff-baby contact despite adequate hand-washing. Overcrowding was believed to be responsible for the difficulties experienced in eradicating this transmission. INTRODUCTION Serratia marcescens,
as a biological marker for recognised as an important opportunistic pathogen.’ Most infections have been reported in adults but one of the earliest descriptions was of urinarytract infection in children.2 Other reported outbreaks have implicated contaminated saline bottles,3 scalp-vein needles,4 and nail brushes. Christensen et al emphasised the importance of symptom-free colonised infants as the major reservoir of infection. We report a further epidemic of
once
pathogenicity studies, is
S
in
used
now
neonatal unit. S marcescens was first isolated from babies in the neonatal unit at Stoke-on-Trent in August, 1981, and was subsequently shown to be a cause of potentially serious infection in some neonates. The morbidity and mortality over a 15-month period in these neonates was studied marcescens
evaluated prospec-
high-dependency
Staffordshire Hospital Centre,
D. A. SHAW
rates were
a
TD, Cowling JR, Gevers W, Van Niekerk JPDeV. The metabolic response to squash including the influence of pre-exercise carbohydrate ingestion. S Afr Med J
marcescens were
Bacteriological Sampling During the early part of the investigation environmental samples taken with moistened cotton-wool swabs which were incubated overnight in glucose brothand subcultured on MacConkey agar. Items sampled included the blood-gas analyser, breast pumps, incubators, humidifiers, suction jars, and various ointments, hand creams, and antiseptics in use on the unit. Hand cultures were taken from members of the staff on several occasions by means of a moistened 5 x5 cm gauze square, which was rubbed over both hands, incubated overnight in glucose broth, and subcultured on MacConkey agar. For the latter part of the survey, after June, 1982, the nose and throat of all babies newly admitted to the unit were swabbed twice weekly with damp cotton-wool swabs. The isolates were identified by conventional methods. Antibiotic sensitivity testing was performed by a rotary Stokes method. Selected isolates were phage-typed and serotyped. were
-
Ward Observations
’
Members of the infection control team used the cover provided by the bacteriological surveys to observe the hand-washing techniques of the medical and nursing staff on the unit. The team also made unannounced visits to the ward at irregular intervals throughout the outbreak.
7. Noakes
1982, 62: 721-23. 8. Kannel WB, Doyle JT, McNamara PM, Quikenton P, Gordon T. Precursors of sudden coronary death. Factors related to the incidence of sudden death. Circulation 1975; 51: 606-13 9. Alonzo AA, Simon
AB, Feinlab M. Prodromata of myocardial infarction and sudden deaths Circulation 1975; 52: 1056-62. 10. Kuller L, Lillienfield A, Fisher R. An epidemiological study of sudden and unexpected deaths in adults. Medicine 1967, 46: 341-61. 11. Friedman M, Manwarmg JH, Rosenman RH, Donlon G, Ortega P, Grube SM Instantaneous and sudden deaths: clinical and pathological differentation in coronary artery disease. JAMA 1973; 225: 1319-28 12 Mills P, Rose J, Hollingsworth J, Amara I, Craige E. Long term prognosis of mitral valve prolapse N Engl J Med 1977; 297: 13-18 13 Maron BJ, Roberts WC, Edwards JE, McAllister HA, Foley DD, Epstein SE Sudden death in patients with hypertrophic cardiomyopathy: characterisation of 26 patients without previous functional limitation. Am J Cardiol 1978; 41: 803-10 14. James TN, Froggatt P, Marshall TK Sudden death in young athletet. Ann Intern Med 1967, 67: 1013-21. 15. Northcote RJ, 1357-59
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20. Gordon T, Kannel WB, McGee D, et al. Death and coronary attacks in men after giving up cigarette smoking. A report from the Framingham study. Lancet 1974; ii: 1345-48. 21. Moritz AR, Zamcheck N. Sudden and unexpected deaths in young soldiers. Arch Pathol 1946; 42: 459-93. 22 Nixon PGF, Bethell HJN Preinfarction ill health. Am J Cardiol 1974; 33: 446-49. 23. Thompson PD, Funk EJ, Carleton RA, Sturner WQ. Incidence of death during jogging m Rhode Island from 1975 through 1980. JAMA 1982, 18: 2535-38. 24. Fowler AW. Cause of death on squash courts. On Call 1980; 14: 7. 25. Adams CW. Symposia on exercise and the heart. Introduction. Am J Cardiol 1972; 30: 713-15. 26. Goldschlager N, Cake D, Cohn K. Exercise-induced ventricular arrhythmias in
patients with coronary artery disease: their relation to angiographic findings. Am J Cardiol 1973; 31: 434-40. 27. Johnson RH, Walton JL, Krebs HA, Williamson DM. Metabolic fuels during and after severe exercise in athletes and non-athletes. Lancet 1969, ii: 452-55. 28. Kurien VA, Yates PA, Oliver MF. The role of free fatty acids in the production of ventricular atthythmias after acute coronary artery occlusion. Eur J Clin Invesr 1971; 1: 225-41. 29. Hoak JC, Poole JCF, Robinson DS. Thrombosis associated with mobilization of fatty acids. Am J Pathol 1963; 43: 987-98. 30. Raab W, Van Lith P, Lepeschin E, Herrlich HC. Catecholamine induced myocardial hypoxia in the presence of impaired coronary dilatability independent of external cardiac work Am J Cardiol 1962; 9: 455-70. 31. Taggart P, Parkinson P, Carruthers M Cardiac responses to thermal, physical and emotional stress. Br Med J 1972; iii: 71-76. 32. Clark RS, Ballantyne D. Physical activity and coronary heart disease. Scot Med J 1981; 26: 15-20.
,