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Management of twin-to-twin transfusion syndrome
  1. Tara J Selman1,
  2. R Katie Morris1,2,
  3. Mark D Kilby1,2
  1. 1Fetal Medicine Centre, Birmingham Women's Hospital NHS Foundation Trust, Birmingham, UK
  2. 2Department of Fetal Medicine, School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK
  1. Correspondence to Professor Mark D Kilby, Department of Fetal Medicine, School of Clinical and Experimental Medicine, University of Birmingham, Birmingham Women's NHS Foundation Trust, Birmingham B15 2TG, UK; m.d.kilby{at}bham.ac.uk

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Twin-to-twin transfusion (TTTS) syndrome complicates approximately 10–15% of all monochorionic twin pregnancies. The pathogenesis of this condition is primarily placental in origin, with unidirectional arteriovenous anastomoses being implicated in the development of the condition and secondary fetoplacental endocrine disturbance compounding the clinical presentation. If untreated, this condition ends in pregnancy loss in over 90% of cases by 26 weeks, and survivors have high rates of neurodevelopmental delay. Fetoscopic laser ablation is the treatment of choice in severe TTTS and increases perinatal survival significantly, while reducing long-term neurodevelopmental morbidity in childhood survivors. Such monochorionic twin pregnancies though, even after ‘successful therapy’, remain high risk in utero and the need for specialist and careful ultrasound surveillance and multidisciplinary care is mandatory.

Monochorionic twin pregnancies constitute 20–30% of all twin pregnancies but compared with dichorionic twins are associated with up to a 10-fold increase in fetal loss rates, perinatal mortality and morbidity.1 2 All monochorionic placentae have intertwin vascular anastomoses, which may predispose the twins to acute and chronic haemodynamic disequilibrium increasing perinatal mortality and morbidity.3 However, in between 10% and 15% of monochorionic twins, the intertwin vascular anastomoses are ‘unidirectional’ leading to relative hyperperfusion within the ‘recipient twin’ causing polyuria, hydramnios and cardiac dysfunction while the co-twin, the ‘donor’, is hypoperfused, with oliguria, oligohydramnios with features of increased fetoplacental impedence.4 It is these clinical features, diagnosed using ultrasound that constitutes the diagnosis of TTTS, a condition if untreated (or unrecognised) that is associated with over 90% perinatal loss and neurodevelopmental morbidity in over 50% of cases.5 This morbid prenatal condition (rarely associated with an intertwin discordancy of haemoglobin concentration) is to be contrasted with acute haemodynamic shifts through placental anastomoses, often associated with uterine contractions, and leading to profound haemodynamic and haemoglobin differences between the fetuses noted at …

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