PubMed · 13812354
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J L COULOMB. 1960. [Chorionic gonadotropin tests].. https://pubmed.ncbi.nlm.nih.gov/13812354/
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The twin-twin transfusion syndrome (TTTS) is a severe complication of monochorionic twin pregnancies caused by a net transfusion of blood from one twin (the donor) to the other (the recipient) through placental anastomoses. To examine the pathophysiology of TTTS evolving through clinical stages I to IV, we extended our mathematical model to include pulsating circulations propagating along the arterial tree as well as placental and cerebral vascular resistances, and arterial wall thickness and stiffness. The model demonstrates that abnormal umbilical arterial flow (TTTS stage III) in the donor twin results from increased placental resistance as well as reduced resistance in the cerebral arteries. In contrast, recipient twin abnormal umbilical arterial flow requires a significantly greater increase in placental resistance, resulting from the compressive effects of high amniotic fluid pressure. Thus simulated abnormalities of donor umbilical arterial pulsations occur in the donor more commonly and earlier than in the recipient. The "normal" staging sequence (I, II, III, IV) correlates with the presence of compensating placental anastomoses, constituting the majority of monochorionic twin placentas. However, TTTS stage III may occur before manifestations of stage II (lack of donor bladder filling), in our model correlating with severe TTTS from a single arteriovenous anastomosis, an infrequent occurring placental angioarchitecture. In conclusion, this mathematical model describes the onset and development of the four stages of TTTS, reproduces a variety of clinical manifestations, and may contribute to identifying the underlying pathophysiology of the staging sequence in TTTS.
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OBJECTIVE: This study was undertaken to detect missed anastomoses on the chorionic surface as well as hidden connections in the depth of the cotyledons in placentas after laser coagulation for twin-to-twin transfusion syndrome (TTTS) and to correlate these findings to clinical outcome. STUDY DESIGN: All cord vessels were injected with dyed barium sulphate. A digital photograph of the chorionic surface angioarchitecture and single-shot digital X-ray (Rx) angiograms were made. The presence and diameter of any missed anastomoses on the chorionic surface and of any hidden angiographic connections were determined. RESULTS: Fifty placentas were analyzed, 7 of double intrauterine fetal death (IUFD) and 43 of double survivors. In 9 of 43 (21%) cases with double survival and in all 7 cases of double IUFD, missed anastomoses were identified that should have been ablated by laser coagulation (P < .001). There appeared to be a correlation between the type and diameter of missed anastomoses on the chorionic surface and the clinical outcome. Placentas with missed large arteriovenous/venoarterial anastomoses (AV/VA) (N = 8) were from cases with recurrent TTTS or double IUFD (unless compensated by a large arterioarterial anastomosis [AA]). Next, missed small AV/VA (N = 4) without AA resulted in isolated (ie, without TTTS) discordant hemoglobin levels requiring intrauterine transfusion. Finally, when there were no missed anastomoses (N = 34), TTTS had resolved in all cases and outcome was good, although 1 case had discordant hemoglobin values treated with a single intrauterine transfusion and 4 others had discordant hemoglobin at birth. On Rx angiography, potential hidden connections were present, all but 1 case. CONCLUSION: Coagulation of all anastomoses visible on the chorionic surface seems adequate to treat TTTS. However, hidden connections in the depth of the cotyledon could not be excluded and may be involved in lesser degrees of intertwin transfusion.