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Routine prenatal screening for congenital heart disease See page 854 Expertise in fetal echocardiography has continued to improve over the past 15 years. However, its usefulness as a screening tool has remained controversial. In this week’s Lancet Stümpflen and colleagues assess in a prospective study the detection rate of congenital heart disease by detailed fetal echocardiography. By separating low-risk from high-risk groups, they have mimicked both a “screening” and a “tertiary referral” situation. The study was well designed, and the diagnostic accuracy was high (sensitivity 88·5%, specificity and positive predictive value 100%) compared with that in similarly designed studies.1,2 Furthermore, these results reflect true sensitivity since they are based on follow-up information rather than prevalence estimates of congenital heart disease. Undoubtedly, the results are near “gold standard” for fetal cardiac diagnosis. However, they are also certain to rekindle the debate about several controversial issues in this field. First, how useful are these data for determining the efficacy of fetal echocardiography as a screening tool? They show what can be achieved in an ideal world, which far exceeds that currently achieved by routine screening practices in obstetric units incorporating the fourchamber view into routine prenatal ultrasound examinations.3,4 It has been estimated that 400 additional fetal cardiac specialists would be needed for the UK alone for every pregnant woman to undergo routine detailed fetal echocardiography3—clearly an impossibility in the present economic climate. The first step to improve the accuracy of screening is to continue to educuate obstetric ultrasonographers to obtain and correctly interpret the four-chamber view. Including the great arteries in the evaluation might increase the yield of detectable lesions, but the feasibility of doing so and its impact remain questionable. Even if detailed fetal echocardiography in all pregnant women were possible, what would be the outcome of such an undertaking? In many countries an increasing number of parents expect to have a choice of termination of pregnancy when severe fetal anomalies are detected. Apart from the debate of the ethics of abortion, there is the debate about appropriate counselling. There is little argument among cardiologists about the termination of a fetus with hypoplastic left heart syndrome, and a noticeable reduction in number of babies born with this lesion has been reported after a screening programme.5 Where, however, do we draw the line? Reports of postnatal outcomes for babies with antentally detected lesions have to be interpreted with caution, since they often reflect other factors, including the quality of postnatal care and the co-existence of extracardiac anomalies. Is truly non-directive counselling really possible or do we only like to think it is? Counselling in Stümpflen’s study involved a multidisciplinary team, an approach most likely to minimise biased information. It would also be useful for parents to know the best possible outcome and not only the locally relevant mortality figures. Improved care and planning, especially in the case of duct-dependent lesions and lesions that require intervention early in the neonatal period, is undoubtedly an advantage of prenatal cardiac screening. Cost-benefit 836
considerations in these circumstances3 seem artificial and inconsistent with high-technology medicine as it is practised in developed countries. Last but not least, the effect of parental reassurance, especially in high-risk cases, is of immeasurable value. The more optimistic and forward-looking perinatal specialists will add a further dimension to the debate—the possibility of intrauterine cardiac interventions.6 This is an attractive concept, since several lesions worsen, and abnormal flow haemodynamics lead to hypoplasia of cardiac chambers and great arteries. If early correction were feasible, the progression of some lesions might halted and the outcome improved. Such therapy is still in the experimental stage but will no doubt lead to even more controversial discussions.
Sabine Kleinert 75 Mount Ararat Road, Richmond, Surrey TW10 6PL 1 2 3 4
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Ott WJ. The accuracy of antenatal fetal echocardiography screening in high- and low-risk patients. Am J Obstet Gynecol 1995; 172: 1741–47. Rustico MA, Benettoni A, D’Ottavio G, et al. Fetal heart screening in low-risk pregnancies. Ultrasound Obstet Gynecol 1995; 6: 313–19. Wyllie J, Wren C, Hunter S. Screening for fetal cardiac malformations. Br Heart J 1994; 71 (suppl): 20–27. Sharland GK, Allan LD. Screening for congenital heart disease prenatally. Results of a 2As year study in the South East Thames Region. Br J Obstet Gynecol 1992; 99: 220–25. Allan LD, Cool A, Sullivan I, Sharland GK. Hypoplastic left heart syndrome: effects of fetal echocardiography on birth prevalence. Lancet 1991; 337: 959–61. Hanley FL. Fetal cardiac surgery. Adv Cardiac Surg 1994; 5: 47–74.
Making real sense of MRSA Methicillin-resistant Staphylococcus aureus (MRSA) is now a common organism in many hospitals worldwide. In US hospitals, the prevalence of MRSA increased from 2·4% in 1975 to 29% in 1991.1 Perhaps more importantly, the increase has occurred not only in large tertiary-care teaching hospitals but also in small community hospitals.1 MRSA nasal carriage rates among patients in acute-care wards range from 1 to 10% and may be higher in patients with risk factors such as chronic haemodialysis, HIV infection, or intensive care.2 A considerable percentage of inpatients who become colonised by MRSA will develop an MRSA infection such as pneumonia, bacteraemia, or wound infection.2 And, whereas a single or predominant strain of MRSA used to be present in one setting, clonal diversity is now being reported.3,4 Moreover, MRSA can no longer be considered just a nosocomial organism. Nor is community-acquired MRSA limited to injecting drug users.3,4 In long-term-care facilities, nasal or wound colonisation rates range from 8 to 34%.2 However, MRSA infection is much less likely here than in acute-care facilities. In view of this evolving epidemiology of MRSA, what measures should be used to control nosocomial MRSA infection? A recent study from Spain by Pujol et al5 has shown that in an intensive-care unit nasal carriers of MRSA were at higher risk of MRSA bacteraemia than were carriers of methicillin-susceptible S aureus (38% vs 9·5%). The authors suggest that nasal eradication of MRSA might have been worthwhile for their ICU patients. The authors further observe, however, that this study was conducted during an MRSA outbreak at their institution. Most of the MRSA isolates belonged to a single clonal strain, which suggested cross-transmission. In addition, many of the bloodstream infections were deemed to be catheter related,
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COMMENTARY hence the suggestion for improved care of intravascular catheters. Specific measures could include the use of silverimpregnated catheters, aseptic insertion, chlorhexidine antisepsis, and, during a staphylococcal outbreak, mupirocin ointment as a catheter dressing. The study raises the issue of what control measures, if any, are warranted for nosocomial MRSA infection. Approaches for control of MRSA have ranged from the draconian to the laissez-faire. Control strategies must be developed by each health-care facility on the basis of factors such as whether an outbreak of MRSA is occurring, the MRSA endemic rate, the patient population, the type of facility, and resources for infection control. Surveillance cultures of patients for MRSA, as done by Pujol and colleagues, may be useful during an outbreak, but they are not recommended as a routine measure. Standard precautions such as hand washing and the use of barriers against contact with body fluids or blood,6 will prevent most cross-transmissions without having to identify individual carriers. Surveillance cultures of personnel may be justified during an outbreak if initial epidemiological investigations suggest that the carrier is a member of staff. When surveillance cultures are used for outbreak control, mupirocin is usually given for nasal eradication of MRSA.2 If mupirocin resistance is known or suspected, mupirocin susceptibility should be checked and an alternative agent given if needed.2 Although standard precautions are usually adequate in most settings, contract precautions6 may be needed during outbreaks. These involve the use of barriers (gown and gloves) for any contact with MRSA-infected or colonised patients. A mask is not necessary unless the patient has MRSA pneumonia. Acute-care patients colonised or infected by MRSA usually do not require isolation unless the patient is uncooperative, has poor personal hygiene, has an MRSA wound infection that cannot be controlled, or has MRSA pneumonia. During an outbreak isolation of colonised or infected patients, or grouping them together, may be necessary. Grouping may also be done in long-term care facilities although roommate transmission here is uncommon. Microbiological surveillance for MRSA is useful in many institutions for determining baseline endemic rate and location of carriers or infected patients. Departure from baseline pattern, especially clustering, calls for a focused investigation. Whether the organisms are nosocomial or present on admission to hospital should be determined, and they should undergo molecular typing. If most of the isolates are of the same clonal strain, outbreak measures should be implemented to prevent cross-transmission. If they are distinct strains, efforts can be focussed instead on standard precautions. Since human beings are the primary reservoir for this organism, special housekeeping efforts are usually not warranted except in the burn or the dermatology ward, where environmental reservoirs have been implicated.21 Certainly, if an outbreak of MRSA is occurring, stringent control measures are required. Intervention should focus not only on MRSA, but on sites of infection as well. For instance, in the study by Pujol et al, improving catheter care was an important additional control measure. If the rate of MRSA infection does not increase over a baseline endemic rate, if it is not associated with severe infections,
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and if molecular typing shows that nosocomial isolates are found distinct rather than clonal , standard precautions may be sufficient.
Jan Evans Patterson Department of Medicine (Infectious Diseases) and Pathology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78284-7881, USA 1
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Panlilio AL, Culver DH, Gaynes RP, et al. Methicillin-resistant Staphylococcus aureus in US hospitals, 1975–1991. Infect Control Hosp Epidemiol 1992: 13: 582. Mulligan ME, Murray-Leisure KA, Ribner BS, et al. Methicillinresistant Staphylococcus aureus: a consensus review of the microbiology, pathogenesis, and epidemiology with implications for prevention and management. Am J Med 1993; 94: 313–26. Layton MC, Hierholzer WJ Jr, Patterson JE. The evolving epidemiology of methicillin-resistant Staphylococcus aureus at a university hospital. Infect Control Hosp Epidemiol 1995; 16: 12–17. Moreno F, Crisp C, Jorgensen JH, Patterson JE. Methicillin-resistant Staphylococcus aureus as a community organism. Clin Infect Dis 1995; 21: 1308–12. Pujol M, Pena C, Pallares R, et al. Nosocomial Staphylococcus aureus bacteremia among nasal carriers of methicillin-resistant and methicillinsusceptible strains. Am J Med 1996; 100: 509–16. Hospital Infection Control Practices Advisory Committee. Centers for Disease Control and Prevention. Guideline for isolation precautions in hospitals. Am J Infect Control 1996; 24: 24–52.
Mild cytological atypia in women with HIV infection The addition of invasive cervical cancer to the definition of AIDS was an acknowledgment of its relevance to women infected with human immunodeficiency virus (HIV), 80% of whom will die of the cancer once acquired.1 Furthermore, it is clear that HIV-infected women are at high risk of the precursor lesions, cervical intraepithelial neoplasia (CIN) and human papillomavirus (HPV) infection.2,3 In many countries women now account for the highest percentage increase in HIV-infected individuals. Thus the number of HIV-infected women who present with abnormal Papanicolaou (Pap) smears can be expected to rise. As in immunocompetent women, low-grade abnormalities are the commonest finding.2 Despite recognition of this risk of cytological abnormalities, management of these cervical lesions has not been standardised. Part of the difficulty arises from a lack of agreement on management of these lesions in the immunocompetent population, for whom more is known about the biology of atypia and CIN.4 Debate persists about the appropriate management of low-grade cervical lesions, which include atypical squamous cells of uncertain significance (ASCUS), mild cytological atypia, severe inflammation with reparative atypia, and low-grade squamous intraepithelial lesions (LGSIL). However, the National Cancer Institute has made a start to pull things together.Implicit in these guidelines was the possibility for revision as new information became available, especially with regards to HPV testing, as well as the recognition that a different set of standards was required for high-risk patients—ie, those women with previous abnormal Pap smears, those who do not comply with follow-up, and immunodeficient women.4 Lack of universal endorsement of the Bethesda System nomenclature and the consequent difficulty in interpretation and comparison of results from population studies contribute to the confusion over management of 837