This form of chronic fetofetal transfusion, referred to as TAPS, is characterized by significant hemoglobin diferences between donor and recipient twins. However, TAPS lacks the discrepancies in amnionic luid volumes typical of TTTS (Slaghekke, 2010). It is diagnosed ante natally by M CA peak systolic velocity (PSV) > 1.5 multiples of the median (MoM) in the donor and < 1.0 MoM in the recipient twin (Society for MaternalFetal Medicine, 2013). The spontaneous form of TAPS reportedly complicates 3 to 5 percent of monochorionic pregnancies, and it occurs in up to 13 percent of pregnancies after laser photocoagulation of the placenta. Spontaneous TAPS usually occurs after 26 weeks' gestation, and iatrogenic TAPS develops within 5 weeks of a procedure (Lewi, 2013). Although a staging system has been proposed by Slaghekke and colleagues (2010), further studies are necessary to better elucidate the natural history of TAPS and its management. In brief, evidence of fetal compromise or greater diferences in MCA PSV between twins raise the stage.
lso known as an acardiac twin, this is a rare but serious complication of monochorionic multifetal gestation. n estimated incidence is 1 case in 35,000 births. In the classic twin reversedarterial-perfusion (TRAP) sequence, there is a normally formed donor twin that shows features of heart failure and a recipient twin that lacks a heart (acardius) and other structures. In one theory, the TRAP sequence is caused by a large artery-to-artery placental shunt, often also accompanied by a vein-to-vein shunt
FIGURE 45-22 Twin reversed-arterial-perfusion sequence. In the TRAP sequence, there is usually a normally formed donor twin that has features of heart failure, and a recipient twin that lacks a heart. It has been hypothesized that the TRAP sequence is caused by a large artery-to-artery placental shunt, often also accompanied by a vein-to-vein shunt. Within the single, shared placenta, perfusion pressure of the donor twin overpowers that in the recipient twin, who thus receives reverse blood flow from its twin sibling. The "used" arterial blood that reaches the recipient twin preferentially goes to its iliac vessels and thus perfuses only the lower body. This disrupts growth and development of the upper body.
(Fig. 45-22). Within the single, shared placenta, arterial perfusion pressure of the donor twin exceeds that in the recipient twin, who thus receives reverse blood low containing deoxygenated arterial blood from its cotwin (Lewi, 2013). his "used" arterial blood reaches the recipient twin through its umbilical arteries and preferentially goes to its iliac vessels. Thus, only the lower body is perfused, and therefore disrupted growth and development of the upper body results. In these cases, failed head growth is called acardius acephalus; a partially developed head with identifiable limbs is called acardius myelacephalus; and failure of any recognizable structure to form is acardius amorphous, which is shown in Figure 45-23 (Faye-Petersen, 2006). Because of this vascular connection, the normal donor twin must not only support its own circulation but also pump blood through the underdeveloped acardiac recipient. This may lead to cardiomegaly and high-output heart failure in the normal twin (Fox, 2007).