A 42 year-old-woman, gravida 3 para 2, at 21 weeks and three days of gestation with monochorionic/ diamniotic twins was diagnosed with twin-to-twin transfusion syndrome (TTTS). There was oligopolyhydramnios sequence with maximum vertical pocket less than 2 cm for the donor twin and 8.5 cm for the recipient twin as well as a non-visible bladder for the donor twin. The patient was counseled regarding her options and decided to have amnioreduction. One thousand milliliters of fluid were removed with a maximum vertical pocket of 9.6 cm at the end of the procedure. Follow-up at two days revealed normal fluid volumes in both sacs and a large and small bladder for the recipient and the donor twin, respectively. There was absent end-diastolic flow in the umbilical artery of the recipient twin.The patient was referred for a consultation for possible laser surgery. Laser surgery was not deemed necessary by the consultants but they did recommend a follow-up of myocardial function, amniotic fluid volumes, and Doppler studies [1]. At 22 weeks and two days, the bladder, amniotic fluid volume, and Doppler waveforms of umbilical artery and ductus venosus and myocardial function studies for both twins appeared normal. At 23 weeks and two days interspersing of the amniotic membranes secondary to amnioreduction and absent enddiastolic flow in the umbilical artery of the donor twin were noted. At 24 weeks the middle cerebral artery (MCA) Doppler waveform for twin B revealed brain sparing with Doppler ratios below the 95th percentile and normal velocity.The patient presented with decreased fetal movement at 25 weeks and one day and demise of the recipient twin was noted. The middle cerebral artery peak systolic velocity (MCA PSV) was above the 1.55 multiples of the median (MoM) for the donor twin B (Figure 1a). There was skin edema and polyhydramnios. The patient was counseled regarding the risks and benefits of intrauterine transfusion (IUT) and desired to proceed with the procedure. The procedure was performed within 24 hours from the diagnosis of single intrauterine fetal demise (SIUFD). The opening hematocrit was 12%. The closing hematocrit was 43% after 75 mL of blood transfusion. The post-procedure MCA PSV was within normal limits ( Figure 1b).Pleural effusion with polyhydramnios was noted two days after the transfusion (Figure 2). Those signs resolved at 26 weeks. The patient was followed with biweekly nonstress testing and ultrasound examinations. Biweekly MCA PSV Doppler measurements remained within normal levels after the IUT procedure. The patient presented in active labor at 31 weeks and delivered a 1940 g male infant with Apgar scores of 8
The patient was a 29-year multiparous woman, hospitalised in the 25 week of pregnancy because of fetal hydrops (ascites, polyhydramnios, placentomegaly) and cardiomegaly. The results of the physical and laboratory examinations of the mother were initially normal. MCA PSV in the fetus was 1.9 MoM. Diagnostic cordocentesis revealed profound fetal anemia with high erytroblastosis, thrombocytopenia and fetal PVB19 viremia (2.27 × 108 IU/ml). We transfused to the fetal umbilical vein 35 ml of packed red cells and 0.5 g IVIG. After the transfusion the MCA PSV normalised. In the fourth day after the transfusion the patient reported dyspnoea, oedema of lower extremities and rash on the palmar side of her hands. There was fluid in both pleural cavities. The fluid balance was positive (plus 9 kg in one week), the blood pressure was normal all the time, but the condition of the mother was deteriorating rapidly. The blood parameters showed surprisingly progressive hemodilution and the patient was gradually developing anemia and thrombocytopenia, with elevation of aminotransferases.In the next few days we observed dyspnoea at rest, continuous liver pain and enlargement and massive generalised oedema. The patient was given high doses of diuretics (i.v. furosemide up to 60 mg a day), antibiotics, steroids, IVIG (0.5 g/day) and FFP. After about one week of treatment the condition of the fetus and the mother started to improve and the oedema in both patients gradually disappeared. In the 30 week of pregnancy the patient left the hospital. There was PROM and premature delivery in the 31 week of pregnancy. She delivered a child 1750/45 g with minor ascites, but no important medical problems.Supporting information can be found in the online version of this abstract. SB presented as a 30 yo G1 at 11 weeks for an ultrasound (US) to confirm her EDC. US showed a viable extrauterine gestation in the right ovarian fossa, anterior to the uterus and adjacent to the bladder. Doppler examination showed large caliber blood supply from the iliac arteries. There was no pelvic free fluid and the patient was asymptomatic with a benign abdomen. She was extensively counseled regarding the pregnancy's poor prognosis and potential maternal morbidity and mortality. SB agreed to in-patient monitoring but declined to interrupt the pregnancy. MRI of the abdomen/pelvis confirmed the pregnancy's blood supply originated from bilateral iliac arteries (R>L) and the right ovarian artery. After continued counseling and input from a multispeciality team, SB consented to treatment. Fetal intracardiac KCl injection was followed by systemic MTX. Initial HCG was 99,313 and day 7 HCG returned 40,634. SB was discharged on day 8 in stable condition, but presented to the ED on day 11 with acute abdominal pain. Vital signs were stable and her abdominal exam was nonacute although tender. Her hemoglobin was 9.1 gm/dl (baseline 11.6) and a CT demonstrated a hematoma around the gestation. Angiography was performed given the concern for active intraabdominal bleeding, but no ...
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