User:Sethbrautigam/sandbox

As a result of sharing a single placenta, the blood supplies of monochorionic twin fetuses, can become connected, so that they share blood circulation: although each fetus uses its own portion of the placenta, the connecting blood vessels within the placenta allow blood to pass from one twin to the other. It is thought that most monochorionic placentae have these "shared connections" that cross the placenta, with the net flow volumes being equal between them. This state is sometimes referred to as "flow balance". When the placenta has deep vein-artery connection this can cause blood flow to become unbalanced. Depending on the number, type and direction of the interconnecting blood vessels (anastomoses), blood can be transferred disproportionately from one twin (the "donor") to the other (the "recipient"), due to a state of "flow imbalance" imparted by new blood vessel growth across the placental "equator", the line that divides each baby's proportion of the shared placenta. This imbalance of blood flow causes the donor twin have poor growth and can be very small. The donor twin also has decreased blood volume, and also decreased urinary output, leading to a lower than normal level of amniotic fluid(becoming oligohydramnios). The blood volume of the recipient twin is increased, which can strain the fetus's heart and eventually lead to heart failure, and also higher than normal urinary output, which can lead to excess amniotic fluid (becoming polyhydramnios). The demise of the fetus is typically a result of ischemia related to the lack of blood flow. The lack of blood flow causes bowel atresia, brain damage, and renal failure.

TTTS usually develops during the period of peak placental growth, starting in week 16 and proceeding through week 25; after this point, the placenta's growth decelerates, essentially stopping just after week 30. While TTTS has occasionally been detected beyond this timepoint, it is thought that its occurrence beyond week 30 may be due to a placental embolism that upsets the flow balance of the shared connections between the babies. TTTS is potentially lethal to either or both twins, no matter when it is detected. However, when detected past week 25, emergency delivery may be considered to rescue the babies if the TTTS is severe.

Other than requiring a monochorionic twin (or higher multiple) pregnancy, the underlying causes of TTTS are not known. It is not known to be hereditary or genetic.

Effects to the Surviving Fetus
The fetal demise of one of the twins during the second trimester of a monochorionic pregnancy can result in serious complications to the surviving fetus. Complications include gangrenous limbs, hands and feet, cerebral palsy and IQ deficits, constriction rings of limbs and digits, reduced digits, skin defects, brain cysts, hydranencephaly, multicystic encephalmalacia, microencephaly, renal agenesis and bowel atresia. There are three hypotheses explaining these complications.

1.) Embolic Theory

- The demise of the donor twin allows necrotic tissue, presumably thrombosis-plastin like material, to pass through the vasculature of the surviving twin via the placental vessels. The necrotic tissue embolizes the surviving twin's mesenteric artery resulting bowel atresia, the renal artery resulting in renal agenesis, or the peripheral arteries resulting in limb ischemia and skin abnormalities.

2.) Ischemic Theory

- The demise of the donor twin creates a low pressure state resulting in the shunting of blood into the low resistance vascular system of the dead fetus. This state of low pressure acutely causes hypovolemia resulting in ischemia, and poor end organ perfusion.

3.) Placentation Theory

- The incidence of velamentous cord insertion, an abnormal insertion of the umbilical cord into the placenta, is higher in TTTS. The exact mechanism of effect this has on fetal damage is unknown.