A case of non-immune hydrops fetalis and intrauterine transfusion. Perinatal Journal 2014;22(3):SE14
- İzmir Katip Çelebi Üniversitesi Tıp Fakültesi, Perinatoloji Kliniği- İzmir TR
- İzmir Katip Çelebi Üniversitesi Tıp Fakültesi, Kadın Hastalıkları ve Doğum Anabilim Dalı- İzmir TR
Emre Ekmekçi, İzmir Katip Çelebi Üniversitesi Tıp Fakültesi, Perinatoloji Kliniği- İzmir TR,
Conflicts of Interest
No conflicts declared.
Hydrops fetalis is excessive accumulation of fluid in extravascular compartmans which causes fluid collection in fetal body spaces and generalised soft tissue edema.Non immun hydrops fetalis is a high mortality rate disease that can be caused by chromosomal abnormalities cardiacanomalies, arrhythmia, fetalanemia and TORCH infections. In her first prenatal visit the patient who had gravida 2, paritiy 1 referred to our clinic to perform a combine test on her 12th week of pregnancy. Her blood type was A Rh positive and there was no consanguinity with her husband. Her combined test result was 1/10000. One month later, fetal caryotyping by amniocentesis was performed when fetal intestinal hyperechogenity and intracardiac echogenic focus in the left venticule were observed in the 17th week of pregnancy. TORCH screening was made and it was negative. Fetal caryotype was normal, fetal echocardiography was normal. In 27th week of pregnancy the fetus is examined again and ıt was observed that intestinal hyperechogenicity is persisted and additionally intraabdominal accumulation of fluid is found. Nuchal fold is measured as 8.3 mm. Enddiastolic reverse flow was diagnosed in umbilical artery. Scalp was edematous and skin thickness was measured as 8 mm. Cardiomegaly was observed in fetal echocardiography. A systolic regurgation flow with the peak velocity of 117cm/sec was measured in tricuspid valve. Indirect coombs test was negative. Parvovirus test was negative. Any additional abnormality was not observed in the anatomic examination. After five-day period of test results span, fetal hydrops advanced excessive acid accumulated in the abdomen, plevral effusion started and skin edema improved. Daily 25 mg Digoxine was prescribed. Fetal heart rate was 188/min and peak systolic velocity in MCA was measured 53cm/sec (1,57 MoM) suggesting fetal anemy. Because of fetal anemy intrauterin transfusion was planned. 250 cc, 0 Rh negative irradiated and locosyte filtered CMV negative, %80 hematocryte erithrocyte suspension was prepared. The fetal hematocryte before transfusion was 21. İntravasculer fetal transfusion was made by 180cc eriytrocyte suspension. After transfusion fetal hematocryte was 54 and increased, the peac systolic velocity in MCA was 0,82 MoM and it was decreased and fetal tacycardia was regressed. The daily 25 mg Digoxin therapy was continiued. After transfusion, in the first 20-hour period, fetal heart rate was normal. But in the 21st hour, it was observed that fetal heart beats was negative. After than, pregnancy was terminated through vagina. The etiology is usually unknown in NIHF. In INHF cases, after a detailed anatomic scan and fetal echocardiography evaluation for the fetal anemy should be made. Subgroup Rh incompatibility or any other etiolgic factors can be the cause of the fetal anemy. As in our case if hydrops occurs the prognosis in fetal anemy is poor even if the tratment is performed.
Hydrops fetalis, intrauterine transfusion
Hyperechogen intestine and hydrothorax
MCA Doppler PSV measure