Complications
Encephalopathy, athetoid cerebral palsy, and/or sensorineural deafness may result from deposition of bilirubin into the basal ganglia.
Postnatal treatment consists of intensive phototherapy and exchange transfusions to reduce bilirubin levels and prevent kernicterus.
The most common complication of intrauterine transfusion is fetal bradycardia during transfusion (8%).[65] Fetal bradycardia and vasospasm are more frequent when accidental intra-arterial transfusion is given. Immediate interruption of the transfusion is therapeutic in most cases.
Although short-term neurological outcome is normal in >90% of infants, neurodevelopmental abnormalities have been reported in a few studies with small patient numbers.[63] In one study, 4.8% of the children treated by intrauterine transfusion developed neurodevelopmental impairment. Fetal hydrops was the strongest predictor for impaired outcome.[66]
Hydrops fetalis is defined as abnormal accumulation of fluid in two or more fetal compartments. It is a major fetal complication in RhD disease that will develop when a haemoglobin deficit of 70 g/L (7 g/dL) is exceeded.
Hydrops fetalis is diagnosed with ultrasound. Intrauterine fetal transfusion is life-saving and can reverse fetal hydrops. Cardiac decompensation is often seen in hydrops.[63] Perinatal mortality in fetal hydrops is 50%.[64]
Characterised by reduced reticulocyte count and low serum erythropoietin levels.
Diagnosed when haemoglobin falls <8 g/dL and is treated with transfusion. Erythropoietin has been used to prevent anaemia and reduce transfusions. Iron supplementation is not recommended.[63]
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