First-trimester transabdominal fetal echocardiography

First-trimester transabdominal fetal echocardiography

CORRESPONDENCE 1 2 3 4 Douek M, Vaidya JS, Lakhani SR, Hall-Craggs MA, Baum M, Taylor I. Can magnetic-resonance imaging help elucidate natural hi...

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CORRESPONDENCE

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Douek M, Vaidya JS, Lakhani SR, Hall-Craggs MA, Baum M, Taylor I. Can magnetic-resonance imaging help elucidate natural history of breast cancer multicentricity? Lancet 1998; 351: 801–02. Mussurakis S, Buckley DL, Drew PJ, et al. Dynamic MR Imaging of the breast combined with analysis of contrast agent kinetics in the differentiation of primary breast tumours. Clin Rad 1997; 52: 516–26. Drew PJ, Turnbull LW, Kerin MJ, Carleton PJ, Fox JN. Multicentricity and recurrence of breast cancer. Lancet 1998; 349: 208–09. Heywang SH, Hahn D, Schmidt H, et al. MR imaging of the breast using gadoliniumDTPA. JCAT 1986; 10: 199–204.

do not get referred for a detailed cardiac scan until the second trimester, and this is commonly the reason for a later scan. These women should be referred earlier in pregnancy for detailed fetal echocardiography. First-trimester scans can be more time-consuming and, therefore, cannot realistically be offered to everyone. A subset of high-risk patients can be selected, however, for whom the reassurance provided at an early stage of pregnancy has immeasurable value. Gurleen Sharland

First-trimester transabdominal fetal echocardiography

Fetal Cardiology, Guy’s Hospital, London SE1 9RT, UK

Sir—Julene Carvalho and colleagues (April 4, p 1023)1 report the feasibility of first-trimester transabdominal scans. I agree that this technique can be used effectively in the first trimester, but it should be noted that in this study 27% of the women could not be reassured of normality, because the imaging was not of sufficient quality. Since 1993, we have done 223 transabdominal fetal echocardiograms at 13–14 weeks of gestation in highrisk pregnancies. We detected six major cardiac malformations at this early gestation, all of which were later confirmed, in addition to confirming normality in the remaining scans at a later gestation and after birth. Transvaginal echocardiography has been used to detect cardiac abnormalities as early as 11–12 weeks2–4 and normal structures defined at 9–10 weeks.5 In the detection of cardiac abnormalities, it is not the method of scanning used that is the most important factor, but the experience of the operator in interpreting the scan. Thus, an obstetrician may feel more comfortable with the transvaginal approach, whereas a paediatric cardiologist may prefer to use a transabdominal approach. The important issue is whether not being able to reassure about 30% of women in the first trimester is acceptable, compared with reassurance for the vast majority at 18 weeks of gestation, bearing in mind that the workload is increased by first-trimester scanning, since a follow-up scan is usually required. Early scans are needed in high-risk groups, especially women who have already lost a child with congenital heart disease, or those who have had a termination for congential heart disease in the fetus. Unfortunately, many of these women

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Carvalho JS, Moscoso G, Ville Y. Firsttrimester fetal echocardiography. Lancet 1998; 351: 1023–27. Bronshtein M, Zimmer EZ, Milo S, Ho SY, Lorber A, Gerlis L. Fetal cardiac abnormalities detected by transvaginal sonography at 12–16 weeks’ gestation. Am J Obstet Gynecol 1991; 78: 374–78. Gembruch U, Knopfle G, Chatterjee M, Bald R, Hansmann M. First trimester diagnosis of fetal congenital heart disease by transvaginal two-dimensional and Doppler echocardiography. Obstet Gynecol 1990; 75: 496–98. Timor-Trish IE, Monteagudo A, Peisner DB. High-frequency transvaginal sonographic examination for the potential malformation assessment of the 9 week to 14 week fetus. J Clin Ultrasound 1992; 20: 231–38. Allan LD, Santos R, Pexieder T. Anatomical and echocardiographic correlates of normal cardiac morphology in the late first trimester fetus. Heart 1997; 77: 68–72.

Severe childhood asthma Sir—Marco Rabusin and colleagues’ case report (Jan 3, p32)1 of a child with severe asthma contains several lessons, some arguably more important than the post-mortem diagnosis of Churg-Strauss syndrome. From the history given it is clear that the child was atopic and at risk of further attacks of acute asthma, having been admitted to hospital three times during the previous 6 months. The child had been treated at home with nebulised salbutamol and had received 20 mg over 12 h before his final and fatal admission. Regular use of ␤2-agonists alone is associated with down-regulation of the ␤2-receptor, which leads to a cycle of increased dependence on ␤2agonists and an increase in bronchial hyper-responsiveness. 2 Studies of the epidemics of asthma deaths from the 1960s and the 1980s showed that reliance on short-acting bronchodilators was associated with increased

risk of death, particularly when delivered by home nebuliser.3 The recently described Campbell and coworkers report of reduction in asthma mortality has been attributed to a rise in the use of inhaled corticosteroids. 4 A 2-year-old child with 3 recent hospital admissions for acute asthma should be treated with inhaled corticosteroids and oral steroids should be used early during exacerbations. In this situation it is vital for parents to understand the way these drugs should be used so that they do not allow their prejudices against the use of steroids to interfere with effective treatment of such a serious condition. A further point illustrated by this case relates to the availability and use of home nebulisers. Home nebulisers are useful for children who do not tolerate any other delivery system. Risks develop if nebulised bronchodilators are administered in higher than recommended doses (including more frequent administration than 4 h) and if hospital referral is not made when there is an inadequate response. There can be an inclination to give the child “just one more dose” to see if he “responds as he usually does”, but the child may become increasingly hypoxic with no monitoring of oxygen saturation available. Data from New Zealand suggest that inappropriate long-term use of a home nebuliser may delay institution of other effective therapy, in some cases of asthma deaths.5 A child with severe asthma must be treated with inhaled and sometimes oral corticosteroids. Home nebulisers may be extremely dangerous in this situation. These rules should apply to any child with severe asthma so that preventable deaths are avoided. Simon Langton Hewer Department of Child Health, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK 1

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Rabusin M, Lefore L, Constantinides F, Bussani R. A child with severe asthma. Lancet 1998; 351: 32. Vathensen AS, Knox AJ, Higgins BJ, et al. Rebound increase in bronchial responsiveness after treatment with inhaled terbutaline. Lancet 1988; i: 554–58. Mullen M, Mullen B, Carey M. The association between b-agonist use and death from asthma. JAMA 1993; 270: 1842–45. Campbell MJ, Cogman CR, Holgate ST, et al. Age specific trends in asthma mortality in England and Wales, 1983–1995: results of an observational study. BMJ 1997; 314: 1439–41. Sears MR, Rea HH, Beaglehole R, et al. Asthma mortality in New Zealand: a two year national study. NZ Med J 1985; 98: 271–75.

THE LANCET • Vol 351 • May 30, 1998