1. Immediate Pressure Sump & Retrograde Exsanguination
The heart of the demised twin ceases pumping, converting its circulation into an open, low-resistance, flaccid vascular sump. Within seconds to minutes, massive volume shifts from the surviving co-twin into the dead twin across large arterio-arterial (AA) or veno-venous (VV) connections.
2. Transient Profound Hypotension & End-Organ Ischemia
Acute hypovolemia triggers acute systemic hypotension in the survivor. This watershed hypoperfusion preferentially inflicts ischemic injury on fragile neonatal brain territories—predisposing to periventricular leukomalacia (PVL), multicystic encephalomalacia, and porencephaly.
3. Dismantling the "Embolic Theory"
Historically, injury was attributed to thromboplastic material embolizing from the deceased twin. Contemporary hemodynamic Doppler and fetal autopsy evidence proves the primary culprit is acute exsanguination and hemodynamic shockwave at the moment of demise.
Dichorionic (DCDA) Contrast
In DCDA gestations, separate placental masses eliminate vascular sharing. Demise of Twin A does not produce acute hypovolemic shock in Twin B. Management focuses primarily on monitoring maternal coagulation profiles and avoiding unnecessary iatrogenic preterm delivery.
Acute exsanguination causes severe acute anemia in the surviving co-twin. Measurement of MCA Peak Systolic Velocity (MCA-PSV) is the validated non-invasive gold standard for detecting fetal anemia.