Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Twin Reversed Arterial Perfusion Sequence
Introduction
Twin reversed arterial perfusion (TRAP) sequence is a rare complication specific to monochorionic twin pregnancies. As a result of early vascular disruption occurring during embryogenesis, a dysmorphic acardiac twin receives circulatory support from a pump twin via aberrant placental arterioarterial anastomoses. Because the acardiac twin is entirely dependent on perfusion from the pump twin, the pump twin is at risk of hemodynamic compromise.
Originally described as acardia, the condition was classified further according to the overall appearance of the acardiac fetus on postmortem and radiographic evaluation. The most common presentation, acardius acephalus, consists of a well-formed fetal pelvis and lower limbs without a head or skull and usually without thoracic organs and arms ( Fig. 163.1 ). However, this classification system has been supplanted by the broader, albeit less descriptive, TRAP acronym.
Disease
Prevalence and Epidemiology
The estimated occurrence of TRAP sequence is approximately 1 : 35,000 pregnancies, including 1 : 100 monozygotic twins and 1 : 30 monozygotic triplets. Most (74%) TRAP presentations occur within monochorionic diamniotic pregnancies, with the remaining cases monoamniotic. Although it is generally accepted that acardia is unique to monochorionic pregnancies, there are two reported cases within dichorionic twin pregnancies.
Etiology and Pathophysiology
Theories exist to explain disease pathogenesis; however, the precise etiology of TRAP is unknown. The most widely accepted theory is that the condition is the result of abnormal arterioarterial anastomoses established early in embryogenesis between twin fetuses sharing a single placenta. The acardiac mass lacks direct placental perfusion and is dependent on a retrograde arterial supply of relatively deoxygenated blood from the pump twin. Asymmetric circulation favoring caudal aspects of the acardiac fetus and tissue hypoxia are believed to contribute to resultant fetal dysmorphology. Excess circulatory workload can prove detrimental to the recipient twin, which is at increased risk of high-output cardiac failure. An alternative, although less widely supported, hypothesis for disease pathogenesis involves a primary defect in cardiac embryogenesis, which secondarily permits retrograde blood flow within the acardiac twin.
Manifestations of Disease
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here
