Pulse oximetry screening for critical congenital heart defects

Pulse oximetry screening for critical congenital heart defects

Correspondence 1 2 Ma C, An Z, Hao L, et al. Progress toward measles elimination in the People’s Republic of China, 2000–2009. J Infect Dis 2011; 2...

40KB Sizes 0 Downloads 14 Views

Correspondence

1

2

Ma C, An Z, Hao L, et al. Progress toward measles elimination in the People’s Republic of China, 2000–2009. J Infect Dis 2011; 204: S447–54. De Serres G, Boulianne N, Defay F, et al. Higher risk of measles when the first dose of a 2-dose schedule of measles vaccine is given at 12–14 months versus 15 months of age. Clin Infect Dis 2012; 55: 394–402.

Pulse oximetry screening for critical congenital heart defects Shakila Thangaratinam and colleagues (June 30, p 2459)1 report a systematic review to assess pulse oximetry as a screening method for critical congenital heart defects (CCHD) in asymptomatic newborn babies. They found that pulse oximetry was highly specific and moderately sensitive in the detection of CCHD, and this they cite as compelling evidence to introduce pulse oximetry as a screening test in asymptomatic newborn babies. We agree that the introduction of such screening would lead to a reduction in morbidity and mortality associated with CCHD. These disorders accounted for an estimated 219 000 deaths in 20042—about 2% of child deaths worldwide (and a higher proportion in rich countries where child mortality rates are lower). However, this point raises the issue that many disorders characterised by hypoxaemia have a higher burden of neonatal and child mortality and morbidity than do CCHD, but are not screened for with pulse oximetry. Globally 64% of the 7·6 million deaths in children younger than 5 years are due to infectious causes, most of which involve hypoxaemia—notably pneumonia (18% of child deaths), diarrhoea (11%), malaria (7%), and neonatal sepsis (5%).3 There are an estimated 1·5–2·7 million cases of hypoxaemic pneumonia annually.4,5 Additionally, preterm birth is the second leading cause of child death (1·1 million per year),3 mainly through respiratory distress syndrome, which requires oxygen therapy and has a www.thelancet.com Vol 380 October 13, 2012

narrow therapeutic index necessitating pulse oximetry to minimise the risk of retinopathy of prematurity. If hypoxaemia is missed in these patients, treatment and referral can be delayed, and mismanagement of oxygen therapy can lead to continued morbidity or irreversible damage. In prioritising a global reduction in neonatal and child mortality, an effort needs to be made to target the major killers and to ensure that pulse oximetry is available to identify all who would benefit from oxygen therapy and to monitor those receiving such therapy. Poorer countries have a greater need for appropriate pulse oximetry than do rich ones, and further research and innovation is also required in these settings. We are all involved with Powerfree Education and Technology—a not-for-profit organisation to test robust, low-cost health-care devices.

*Sarah Crede, Joy Lawn, David Woods, John Wyatt [email protected] Powerfree Education and Technology, Cape Town, South Africa (SC, JL, DW, JW); Saving Newborn Lives/Save the Children, London, UK (JL); University of Cape Town, Cape Town, South Africa (DW); and University College London, London, UK (JW) 1

2

3

4

5

Thangaratinam S, Brown K, Zamora J, Khan KS, Ewer AK. Pulse oximetry screening of critical congenital heart defects in asymptomatic newborn babies: a systematic review and meta-analysis. Lancet 2012; 379: 2459–64. WHO. The global burden of disease: 2004 update. Geneva: World Health Organization, 2008. Liu L, Johnson HL, Cousens S, et al, for the Child Health Epidemiology Reference Group of WHO and UNICEF. Global, regional, and national causes of child mortality: an updated systematic analysis for 2010 with time trends since 2000. Lancet 2012; 379: 2151–61. Duke T, Graham SM, Cherian MN, et al. Oxygen is an essential medicine: a call for international action. Int J Tuberc Lung Dis 2010; 14: 1362–68. Subhi R, Adamson M, Campbell H, Weber M, Smith K, Duke T. The prevalence of hypoxaemia among ill children in developing countries: a systematic review. Lancet Infect Dis 2009; 9: 219–27.

in a universal newborn screening programme. The role of hereditary variant haemoglobins in artifactually low SpO2 is worthy of mention. Artifactually low SpO2 is attributed to altered light absorption properties of the variant haemoglobins at 660 nm and 940 nm (the two wavelengths used to calculate estimated SaO2 by pulse oximetry). A review2 has reported 45 patients with 21 different hereditary variant haemoglobins that were associated with asymptomatic low SpO2. 11 of the index cases were infants. Lowoxygen-affinity variant haemoglobins such as haemoglobin Bassett3 cause true hypoxaemia and low SpO2. However, most variant haemoglobins associated with asymptomatic low SpO2 have normal arterial oxygen saturation (SaO2) by co-oximetry. In one report,4 a neonate had SpO2 of 85% and was investigated extensively. The baby’s mother and grandmother also had asymptomatic low SpO2. They were later found to be heterozygous for an α-globin chain variant, haemoglobin Titusville. Although hereditary variant haemoglobins are likely to be rare causes of asymptomatic low SpO2 in neonates, they should be included in the diagnostic work-up of these infants if universal newborn screening is implemented. In one survey,5 in 40 neonates found to have low SpO2 but no congenital heart defect, 12 were healthy. Measurement of SpO2 in parents, haemoglobin analysis by highperformance liquid chromatography, and, when indicated, measurement of SaO2 can be helpful to rule out artefactually low SpO2 caused by variant haemoglobins. We declare that we have no conflicts of interest.

Shakila Thangaratinam and colleagues1 report that measurement of oxygen saturation (SpO2) by pulse oximetry is highly specific for the detection of critical congenital heart defects and should be included

*Madeleine M Verhovsek, David H K Chui [email protected] Department of Medicine, McMaster University, Hamilton, ON L8N 4A6, Canada (MMV); and Department of Medicine, Boston University, Boston, MA, USA (DHKC)

1305