In the last 50 years we have seen tremendous advances in the management of fetal haemolytic anaemia. What was once a disease of high perinatal mortality and morbidity has become a condition readily amenable to antenatal diagnosis and intrauterine fetal therapy. Prior to the 1960s, the management of severe fetal anaemia relied on preterm delivery and subsequent therapy in the neonatal period. In 1961, Liley 1 described the use of amniocentesis to predict the severity of fetal haemolytic anaemia. Amniotic fluid bilirubin concentrations, reflecting the degree of fetal haemolysis, gave indirect assessment of fetal anaemia. The first therapeutic intervention for fetal anaemia was again described by Liley in 1963 2 . He performed the first intrauterine transfusion via the intraperitoneal route. The introduction of real‐time ultrasound facilitated needle‐guided intraperitoneal transfusion in 1977 3 . The first intravascular transfusion, performed fetoscopically, was carried out by Rodeck in 1981 4 . Developments in imaging technology mean that intravascular transfusion is now routinely performed with the aid of ultrasound guidance, and success rates of 92–94% can be expected for the non‐hydropic anaemic fetus 5 , 6 . In the last twenty years we have witnessed another milestone in the management of fetal haemolytic disease. Prediction of fetal anaemia by the non‐invasive method of middle cerebral artery Doppler has revolutionised the assessment of rhesus sensitised pregnancies, and provides the focus of discussion for this article. Rationale for middle cerebral artery Doppler studies in fetal anaemia The physiological response of a fetus to anaemia is an increase in stroke volume and hence an increase in cardiac output. As a result, the fetus develops a hyperdynamic circulation. Blood flow is redistributed to vital end organs, including brain, heart and adrenals, following changes in vascular resistance and a reduction in blood viscosity. The utility of Doppler studies in the assessment of fetal anaemia relies on the premise that provided the cross‐sectional area of a blood vessel remains constant, blood velocity is directly proportional to blood flow. In addition, decreased blood viscosity results in increased blood flow 7 , 8 . The increase in cardiac output, and reduced blood viscosity will both lead to in an increase in blood flow, and hence blood velocity, in the anaemic fetus. In the middle cerebral artery this is reflected by an increase in peak systolic velocity. The middle cerebral artery is the vessel of choice for assessment because it is accessible, and sensitive to the effects of hypoxia. The technique for middle cerebral artery peak systolic velocity measurement has been described in detail by Mari, et al. 9 , 10 . An axial section through the fetal head that includes the thalami and cavum septum pellucidum is obtained and the circle of Willis visualised with colour or power Doppler. The middle cerebral artery is examined close to its origin from the internal carotid artery. The sample volume should be placed in the centre of the vessel and the angle between the ultrasound beam and the direction of blood flow kept as close to 00 as possible. Angle correction can be used if required. The highest peak systolic waveform is measured, in the absence of fetal breathing movements. Open in a separate window Fig. 1 Insonation of middle cerebral artery, with angle correction. Measurement of peak systolic velocity (cm/s).
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Dec 1, 2013
Miroslaw Wielgos + 1
