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Some schools and colleges have already laid such plans. Tomlinson envisages a slower move to integration of the postgraduate schools into the faculties of medicine, the pace largely being dictated by changes in the organisation of London University and in funding for the special health authorities. He recommends that the HEFCE should monitor the links between the medical postgraduate institutions and multi-faculty colleges and review their effectiveness in consultation with the University in 5 years’ time when the reorganisation of the undergraduate medical schools should be nearly

complete. Many questions remain. Where will doctors come from to fill the expanded primary care sector? How will new staff be deployed to overcome the pressures exerted by lack of facilities in the most deprived areas? What guarantees are there that money saved from rationalisation will be directed into the community or that adequate transitional funds will be provided to secure the services necessary before hospital closures take place? The Government has accepted Tomlinson’s proposal of a special London Implementation Group to oversee the reforms, while delaying a detailed response to the report until early 1993. This response must include a statement on just how the community services are to be built up, and how the programme will be protected against erosion and cuts. Although Sir Bernard, in making his proposal, hastened to say that "none of us wishes to put ourselves forward for that task", perhaps he did not foresee that the Implementation Group would be part of the NHS Management Executive, to be chaired by Mr Tim Chessells, currently chairman of North East Thames Regional Health Authority. The success of all the proposed changes is hugely dependent on money "up front". The Secretary of State will need to lean heavily on the Treasury even to begin this task, for which the prevailing sorry state of the British economy does not bode well. 1. Editorial. The LCC and the MAB. Lancet 1920; ii: 359-60. 2. Tomlinson B. Report of the inquiry into London’s health service, medical education and research. London: HM Stationery Office, 1992. 3. King’s Fund Commission on the future of London’s acute health services. London health care 2010: changing the future of services in the capital. London: King’s Fund, 1992.

Nosocomial infection with respiratory syncytial virus

Respiratory syncytial virus (RSV) is a highly contagious paramyxovirus that spreads among infants and young children in the community and in hospital wards, causing upper and lower respiratory symptoms. The epidemiology of RSV infection resembles that of the parainfluenza viruses, both are widespread in older children but cause little discomfort. Attack rates in families are high but children with upper respiratory symptoms are usually nursed at home unless respiratory distress is bad

necessitate hospital admission. RSV is seasonal-a winter disease in temperate infection climates.1 The RSV season lasts about four months, with peaks in February or March. Two antigenically distinct groups of RSV may circulate concurrently in a community. Such is the pattern of respiratory disease that often a single case of bronchiolitis or pneumonia in a child under the age of two years heralds the onset of the RSV season and the burden of infection begins. Infants with underlying bronchopulmonary dysplasia and those who have congenital heart disease

enough

to

immunocompromised may get severe or even fatal RSV infection and require special attention.2 These at-risk infants are often cared for in special units appropriate to their underlying condition and are spared many of the cross-infection hazards that exist in general paediatric wards. Most infants cope well with their RSV infection but they may act as a focus for nosocomial spread. Some paediatric units have a well-rehearsed action plan based on rapid diagnosis, cohort nursing, and infection control strategies. These measures can be costly in terms of medical and nursing resources and need to be evaluated in carefully controlled prospective trials. The spread of RSV seems to require close contact with infectious respiratory secretions either by largeparticle aerosols or by fomites. The usual route of transmission is the nose or the eyes.3 Infected infants shed virus abundantly in respiratory secretions and the most likely vehicle of transmission is the unwashed/ ungloved hands of health care workers and family members. Infected ward staff should be discouraged from handling potentially susceptible infants. Although bronchiolitis is a common manifestation, RSV infection cannot be diagnosed on clinical grounds alone. The rapid antigen detection tests now readily available are both sensitive and specific for RSV.4 Infected respiratory epithelial cells obtained by nasopharyngeal aspiration or washings from the patient are stained directly with fluorescein-labelled specific RSV antibody. The results of the direct fluorescent antibody test are available within a few hours, thus permitting quick decisions about patient isolation. Respiratory secretions are usually inoculated on to HEp-2 or HeLa tissue cells for isolation of the virus; direct culture will yield a positive syncytial formation within 2-7 days of inoculation. Prevention of the nosocomial spread of RSV is important since infection by this means may result in appreciable morbidity and mortality.s Such are the difficulties in controlling the spread of RSV that cross-infection rates of over 30% have been recorded in high-risk infants with lengthy hospital stay. However, the median hospital stay of babies and children is usually less than the incubation period of RSV (ie, 5-8 days) and cross-infection rates are often between 15 and 20%. Several trials have been conducted to determine the best strategy for control of hospital spread of RSV infection but technical differences hinder comparisons. In this issue (p 1079), or are

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al report the results of a prospective controlled study designed to evaluate the most effective infection control procedures in preventing nosocomial infection with RSV. They conclude that, in combination with rapid laboratory diagnosis, cohort nursing and the wearing of gowns and gloves reduced the cross-infection rate from a high of 26% to a mean of 9-5%. The second figure may have been an underestimate, because the researchers deliberately did not follow-up babies who were discharged from hospital within the RSV incubation period. It is entirely possible that RSV infection occurred after hospital discharge but was not severe enough to require readmission. Isolation of patients with acute respiratory infection in a single room is the preferred method of restricting nosocomial spread of RSV infection but this may not be feasible for every patient. Isolation alone is not sufficient to contain RSV and other measures must be put in place. Madge et al examined earlier studies and conclude that the use of gowns and gloves, handwashing and cohort isolation, and screening for RSV with cohort nursing did not reduce the risks of cross-infection significantly. Complex measures need increased resources and hamper routine management of infants in hospital, but simple measures also have drawbacks. Handwashing is the single most important procedure in the prevention of nosocomial infections, including respiratory infection, yet it remains the most violated of all infection control procedures.6 Numerous studies have documented poor compliance with handwashing instructions; even with effective and socially acceptable skin disinfectants such as chlorhexidine gluconate 4% w/v and 60% isopropyl alcohol with emollients, handwashing rates can be as low as 30%.’Handwashing has been repeatedly associated with reduced risks of transmission of infectious diseases including those spread by the routed respiratory Unfortunately, repeated handwashing may result in a greater frequency of chapped, irritated skin for health care givers and this deters the practice. Education and persuasion do not generally lead to sustained improvement in handwashing compliance.6Nevertheless, every effort should be made to encourage health care workers to wash their hands after handling RSV babies with respiratory secretions. The chances of increasing handwashing compliance are improved if a single ward is used for cohort isolation with self-policing by staff and relatives. Since handwashing practices are thought to be inadequate in most hospitals, gloves are a practical means of preventing transient hand colonisation and spread of some infections.9However, gloves may give a false sense of security, leading wearers to neglect handwashing. Hands may become contaminated through holes in the gloves or when the gloves are removed. Nurses do not like wearing gloves for very long and will not spend as much time with a baby if

Madge

et

they are required to wear gloves continuously throughout the work period. Gloves should be changed between patients, otherwise cross-infection occurs. Use of gowns may be advisable during periods of close body contact in which an infant’s secretions are apt to contaminate the clothing. The use of masks does not result in measurable benefit in terms of infection control; eye and nose goggles offer some protection although their use is low. Parainfluenza viruses survive in the environment, especially on non-absorptive surfaces such as stainless steel, laminated plastics, and skin. to Environmental contamination by RSV is likely in the vicinity of an infected child and thorough cleaning is essential. Work surfaces can be disinfected by wiping with an alcohol-impregnated cloth. Hypochlorites are active against viruses but may damage metal equipment if applied liberally. Baby incubators should be thoroughly cleaned with warm water and detergent followed by a wipe over with a freshly prepared solution of (1000 ppm) hypochlorite. What is the best strategy for the prevention of nosocomial RSV infection? None of the trials to date has produced a clear picture. Prospective, controlled, crossover trials are very difficult to do on paediatric wards and should be designed to test one hypothesis at a time. Meanwhile, busy paediatric units will soon be faced with the RSV season. What can be done now? Babies with acute respiratory symptoms should be admitted to a cubicle on an admitting ward. Microbiological samples should be collected without delay and the direct fluorescent antibody test carried out. Rapid results will allow RSV positive patients to be transferred to a designated RSV ward. Cohort isolation with or without other infection control measures will be confmed to one ward, thereby freeing up other wards and sparing them the additional expense and work. Designated staff should be assigned to the RSV ward and these individuals should not nurse newly admitted unscreened infants or known RSV-negative infants. Respiratory syncytial virus. In: Zuckerman AJ, Banatvala JE, Pattison JR, eds. Principles and practice of clinical virology, 2nd ed. Chichester: Wiley, 1990: 253-66. 2. Hall CB, Powell KP, MacDonald NE, et al. Respiratory syncytial virus infection m children with compromised immune function. N Engl J Med 1986; 815: 77-80. 3. Hall CB, Douglas RG, Schnabel KC, Geiman JM. Infectivity of respiratory syncytial virus by various routes of inoculation. Infect Immun 1981; 33: 779-83. 4. Jacobsen D, Ackerman P, Payne NR. Rapid identification of respiratory syncytial virus infections by direct fluorescent antibody testing: reliability as a guide to patient cohorting. Am J Infect Control 1991; 19: 73-78. 5. Hall CB. The nosocomial spread of respiratory syncytial virus infections. Annu Rev Med 1983; 34: 311-19. 6. Conly JM, Hill S, Ross J, Lertzman J, Louie TJ. Handwashing practices in an intensive care unit: the effects of an educational programme and its relationship to infection rates. Am J Infect Control 1987; 17: 330-39. 7. Doebbeling BN, Stanley GL, Scheetz CT, et al. Comparative efficacy of alternative handwashing agents in reducing nosocomial infections in intensive care units. N Engl J Med 1992; 327: 88-93. 8. Gwalmey JM, Moskalski PB, Hendlye JO. Hand-to-hand transmission of rhinovirus colds. Ann Intern Med 1978; 88: 463-67. 9. Garner JS, Simmons BP. Guideline for isolation precautions in hospitals. Infect Control 1983, 4 (suppl): 245-325. 1. Hall CB.

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10. Brady MT, Evans J, Cuartas J. Survival and disinfection of parainfluenza viruses on environmental surfaces. Am J Infect Control 1990; 18: 18-23.

Endometriosis: time for reappraisal Endometriosis is the presence of tissue histologically similar to endometrium outside the uterine cavity and myometrium. The original of blue-black or "powder-burn" lesions, or ovarian cysts containing dark brown "chocolate" material. By causing an inflammatory reaction endometriosis precipitates pain and local damage that can ultimately lead to tubal occlusion or ovarian enclosure by fibrous tissue, and infertility. Until lately the condition was diagnosed only in those patients undergoing a laparotomy for a pelvic mass or pain. These women were a highly selected subgroup with an obvious mass or pain severe enough to warrant an invasive procedure, and the disease was perceived as uncommon. Use of laparoscopy early in the investigation of patients with infertility, pelvic or lower abdominal pain, and for sterilisation greatly enhanced our ability to inspect the pelvis and the new information generated has led to a reappraisal of

descriptions

were

endometriosis. Small lesions can be seen at laparoscopy in many women both with and without symptoms. The condition is commoner in those with infertility or the reported frequency in women being sterilised is risingi-an indication that doctors are increasingly sensitive to the diagnosis. Moreover, we now know that histological evidence of endometriosis can be found in many types of lesions other than the classic blue-black variety; for instance,endometriosis tissue has been found in over 50% of biopsy specimens from vesicular, haemorrhagic, and papular lesions, areas of fibrous scarring, and peritoneal defects.2 Histological evidence of endometriosis has even been found in up to 13% of peritoneal specimens that were apparently normal at biopsy.3 As a result of these observations some researchers have questioned whether endometriosis is a disease at all.4,5 If endometriosis is a common condition, visual diagnosis alone does not constitute a requirement to treat. The evidence that successful medical treatment of endometriosis in infertile women does not improve their fertility accords with this view.6,7 Although laparoscopic diagnosis of symptomless endometriosis is commoner in infertile women than in fertile controls, a group of European experts5 lately concluded that there can be no support for drug treatment of mild endometriosis in infertile women. Early reports of placebo-controlled trials suggested that the disease progressed in some patients and that, since progression was unpredictable, all patients should be treated.8 Subsequent studies showed that in over 50% of untreated patients the disease either improves or does not deteriorate/,1Q so there is little justification for such a therapeutic strategy. Furthermore, there is evidence that endometriosis

pain;

medical therapy is stopped-ie, the probably suppressing the disease rather than drugs it. 11 eradicating Thus, although endometriosis can unquestionably cause severe pelvic pain and destruction, lesions detected at laparoscopy may be incidental. It is therefore important to assess whether the patient’s symptoms are typical of endometriosis before attributing causality. Pain in endometriosis is usually cyclical and is precipitated by intercourse or defaecation. Physical signs such as a mass or tenderness are important confirmatory findings. In a patient with this constellation of features, medical and surgical approaches can undoubtedly be effective in relieving pelvic and abdominal pain. Length of treatment is arbitrarily set at six months. Symptomatic improvement should be evident by three months, since there is good evidence of substantial intracellular changes within the endometriosis lesions by then.12 What about ablative therapy at laparoscopy via either electrocautery or laser? A few groups have compared returns once are

this treatment with no treatment in infertile women, but no firm conclusions can be drawn about efficacy. There is a good case for initiating large randomised trials of these techniques. The pathogenesis of endometriosis still eludes us. The close similarity to endometrium suggests that the tissue is of epithelial origin, so implantation on the surface of pelvic organs probably occurs when menstrual blood refluxes down the fallopian tubes. Another possibility is that peritoneal mesothelium undergoes metaplasia to an endometrial-like epithelium. The importance of determining the correct mechanism will extend beyond the study of endometriosis per se since this condition is the only common "metastatic" disease that is benign. 1. Thomas EJ, Prentice A. The aetiology and pathogenesis of endometriosis. Reprod Med Rev 1992; 1: 21-36. 2. Jansen RP, Russell P. Non pigmented endometriosis: clinical, laparoscopic and pathologic definition. Am J Obstet Gynecol 1986; 155: 1154-59. 3. Nissole M, Paindaveine B, Bourdon A, et al. Histologic study of peritoneal endometriosis in infertile women. Fertil Steril 1990; 53: 984-88. 4. Vercellini P, Bocciolone L, Crosignani PG. Is endometriosis always a disease? Human Reprod 1992; 7: 627-29. 5. Audebert A, Backstrom T, Barlow DH, et al. Endometriosis 1991: a discussion document. Human Reprod 1992; 7: 432-35. 6. Bayer SR, Seibel MM, Saffan DS, Berger MJ, Taymor ML. Efficacy of danazol treatment for minimal endometriosis in infertile women. J Reprod Med 1988; 33: 179-83. 7. Telimaa S. Danazol and medroxyprogesterone acetate inefficacious in the treatment of infertility in endometriosis. Fertil Steril 1988; 50: 872-75. 8. Thomas EJ, Cooke ID. Impact of gestrinone on the course of asymptomatic endometriosis. BMJ 1987; 294: 272-74. 9. Telimaa S, Puolakka J, Ronnberg L, Kauppilla A. Placebo-controlled comparison of danazol and high-dose medroxyprogesterone acetate in the treatment of endometriosis. Gynecol Endocrinol 1987; 1: 13-23. 10. Mahmood TA, Templeton A. The impact of treatment on the natural history of endometriosis. Human Reprod 1990; 5: 965-70. 11. Evers J. The second look laparoscopy for the evaluation of the results of medical treatment of endometriosis should not be performed during ovarian suppression. Fertil Steril 1987; 47: 502-04. 12. Brosens IA, Verleyen A, Cornillie F. The morphologic effect of short term medical therapy of endometriosis. Am J Obstet Gynecol 1987; 157: 1215-21.

Nosocomial infection with respiratory syncytial virus.

1071 Some schools and colleges have already laid such plans. Tomlinson envisages a slower move to integration of the postgraduate schools into the fa...
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