Diagnosis, pathophysiology, and treatment of chronic twin-to-twin transfusion syndrome.

Abstract

The discovery of a 'stuck twin' during an ultrasound examination has often been equated with twin-to-twin transfusion based to a great extent on postnatal confirmation of discordant fetal size and hemoglobin concentration. However, the diagnosis of twin-to-twin transfusion cannot be made with certainty after birth since virtually all monochorionic gestations have placental anastomoses and there are many causes of growth deficiency and abnormal hemoglobin concentration. The purpose of this study is to investigate the pathophysiology of chronic twin-to-twin transfusion syndrome and apply the findings to the development of a management algorithm. In 42 twin gestations with stuck twin associated with acute hydramnios, we performed targeted ultrasound cordocentesis in each fetus and therapeutic amniocentesis. The diagnosis of chronic twin-to-twin transfusion syndrome required: sonographic evidence of monochorionicity; rapid reaccumulation of fluid after amniocentesis; discordant fetal size, and divergent fetal hematocrit measurements with at least one above or below the 95% confidence interval for gestational age. These criteria were met in 20 of 42 (48%) pregnancies. The mean gestation was 23.8 +/- 2 weeks (range 21-27 weeks). In 4 pregnancies, the transfer of adult RBCs from the donor to the recipient was documented. Monochorionicity was confirmed in all postnatally. All recipients had polycythemia and hyperproteinemia. Hydrops developed only in the recipient twin (6 of 20) and was associated with an elevated umbilical venous pressure. All pregnancies were treated with aggressive serial therapeutic amniocenteses. There was no objective evidence that amniocentesis altered the magnitude of the shunt.(ABSTRACT TRUNCATED AT 250 WORDS)