Chronic TTTS results from unidirectional low through deep arteriovenous anastomoses. Deoxygenated blood from a donor placental artery is pumped into a cotyledon shared by the recipient (see Fig. 45-19). Once oxygen exchange is completed in the chorionic villus, the oxygenated blood leaves the cotyledon via a placental vein of the recipient twin. Unless compensatedtypically through superficial arterioarterial anastomoses-this unidirectional low leads to an imbalance in blood volumes (Lewi, 2013). Clinically important TTTS frequently is chronic and results from significant vascular volume diferences between the twins. Even so, the pathogenesis is more complex than a net transfer of red blood cells from one twin to another. Indeed, in most monochorionic twin pregnancies with the syndrome, hemoglobin concentrations between the donor and recipient twin do not difer (Lewi, 2013).
TTTS typically presents in midpregnancy when the donor fetus becomes oliguric from decreased renal perfusion (Society for Maternal-Fetal Medicine, 2013). This fetus develops oligohydramnios, and the recipient fetus develops severe hydramnios, presumably due to increased urine production. Virtual absence of amnionic fluid in the donor sac prevents fetal motion, giving rise to the descriptive term stuck twin or poyhydramnios-oligohydramnios syndrome-'poy-oli. " This amnionic fluid imbalance is associated with growth restriction, contractures, and pulmonary hypoplasia in the donor twin, and premature rupture of the membranes and heart failure in the recipient.
Fetal Brain Damage. Cerebral palsy, microcephaly, porencephaly, and multicystic encephalomalacia are serious complications associated with placental vascular anastomoses in multifetal gestation. he exact pathogenesis of neurological damage is not fully understood but is likely caused by ischemic necrosis leading to cavitary brain lesions (Fig. 45-20). In the donor twin, ischemia results from hypotension, anemia, or both. In the recipient, ischemia develops from blood pressure instability and episodes of profound hypotension (Lopriore, 2011). Cerebral lesions may also be due to postnatal injury associated with preterm delivery (Chap. 34, p. 639). In one review of315 liveborn fetuses from pregnancies with TTTS, cerebral abnormalities were found in 8 percent (Quarello, 2007).
If one twin of an afected pregnancy dies, cerebrl pathology in the survivor probably results from acute hypotension. A less likely cause is emboli of thromboplastic material originating from the dead fetus. Fusi and coworkers (1990, 1991) observed that with the death of one twin, acute twin-twin anastomotic transusion from the high-pressure vessels of the living twin to the lowresistance vessels of the dead twin leads rapidly to hypovolemia and ischemic antenatal brain damage in the survivor. In one review of 343 twin pregnancies complicated by single fetal demise, the risk of neurodevelopmental morbidity in monochorionic twins was 26 percent compared with 2 percent in dichorionic twins (Hillman, 2011). This morbidity was related to the gestational age at the death of the cotwin. If the death occurred between 28 and 33 weeks' gestation, monochorionic twins had an almost eightfold risk of neurodevelopmental morbidity compared with dichorionic twins of the same gestational age. With fetal death ater 34 weeks, the likelihood dramaticlly decreased-odds ratio 1.48.