Mechanism of visceral damage in fetofetal transfusion syndrome.

Rehan, Virender K.; Menticoglou, S. M.

doi:10.1136/fn.73.1.f48

Cited by 5 publications

(6 citation statements)

References 24 publications

(2 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Instead of alleviating the shunting between the fetuses, the situation is made worse and hence hastens their demise 9. If the laser coagulation is successful, however, the pregnancy should be prolonged and there will be interruption of the haemodynamic events which predispose the twins to visceral damage including cerebral injury,27 which may account for the relatively low reported incidence of neurodevelopmental disabilities. With improvements to the laser technique, however, it may be possible to decrease the procedure related loss rate.…”

Section: Discussionmentioning

confidence: 99%

Long term outcome of twin-twin transfusion syndrome

Cincotta

Gray²,

Phythian³

et al. 2000

Archives of Disease in Childhood - Fetal and Neonatal Edition

128

View full text Add to dashboard Cite

Aims-To compare the perinatal mortality and morbidity of infants with twintwin transfusion syndrome (TTTS) with those of gestation matched twin controls and to assess the neurodevelopmental outcome of surviving twins with TTTS. Methods-A cohort of 17 consecutive pregnancies with TTTS was enrolled over three years together with gestation matched twin pregnancies unaVected by TTTS. Serial amnioreduction for the TTTS pregnancies was performed as appropriate. Perinatal death and neonatal morbidities were recorded for both the TTTS cohort and controls. The TTTS survivors had neurodevelopmental follow up to at least 2 years of age. Results-In 12 of the pregnancies, serial amniocenteses were performed, but, in five, the infants were born before intervention. The mean gestational age at delivery was 29.1 weeks (range 23-36). There were five intrauterine deaths in the TTTS cohort and six neonatal deaths (survival 68%). In the control group, there was one intrauterine death and five neonatal deaths (survival 82%). Infants in the TTTS group had a greater requirement for inotropes (p = 0.04) and a higher incidence of renal failure (p = 0.005). Periventricular leucomalacia and cerebral atrophy were seen in 17% of the TTTS group, but none of the controls (p = 0.03). The 23 surviving TTTS infants were all followed up, with 22% having significant neurological morbidity: cerebral palsy and global developmental delay. Conclusions-Twins with TTTS have high perinatal mortality and neonatal morbidity, and long term neurodevelopmental morbidity in survivors is high. Further investigation into the pathogenesis and management of TTTS is required. (Arch Dis Child Fetal Neonatal Ed 2000;83:F171-F176)

show abstract

Section: Discussionmentioning

confidence: 99%

Long term outcome of twin-twin transfusion syndrome

Cincotta

Gray²,

Phythian³

et al. 2000

Archives of Disease in Childhood - Fetal and Neonatal Edition

128

View full text Add to dashboard Cite

show abstract

“…Twin-twin transfusion syndrome (TTTS) occurs in approximately 15% of monochorionic diamniotic gestations and is characterized by placental shunting of blood from a small growth-restricted donor to a large plethoric recipient [1,2]. This mismatched circulation has a significant impact on the developing visceral organs of both the donor and the recipient [3,4]. With volume overload, the heart of the recipient dilates and becomes a less effective pump [5].…”

Section: Introductionmentioning

confidence: 99%

Renal Tubular Dysgenesis in Twin-Twin Transfusion Syndrome

et al. 1999

View full text Add to dashboard Cite

In twin-twin transfusion syndrome (TTTS), the disparity in circulation is reflected in discordant fetal growth, urine output, and amniotic fluid accumulation. The effect of uneven shunting of the growth factor and nutrient-rich vasculature on development and differentiation of the kidney has not been well studied. We analyzed renal tubular growth and differentiation in 25 fetal autopsies with TTTS (13 donors and 12 recipients, including 9 sibling pairs) between 18 and 33 weeks gestation. Immunohistochemical markers for fumarylacetoacetate hydrolase (FAH), Leu-M1, and Lotus tetragonolobus (LTA) were used to identify proximal convoluted tubules, and epithelial membrane antigen (EMA) was used to demonstrate distal convoluted and collecting tubules. FAH appeared to be more specific and reliable than either Leu-M1 or LTA in the identification of proximal tubules. Donors tended to demonstrate a paucity of proximal tubules with crowding of glomeruli characteristic of renal tubular dysgenesis (RTD). The degree of dysgenesis was greater in later gestations and associated with more severe growth restriction. Donors in TTTS are at risk for the development of RTD. Several authors suggest ischemia as the underlying cause of "acquired" RTD. However, in this setting there is no evidence of cell death or necrosis, and we suggest that hypoperfusion leading to decreased glomerular filtration is the underlying etiology, with the severity of RTD related to the degree of shunting.

show abstract

“…It occurs in about 15% of monochorionic twin pregnancies [22], however the prevalence in triplet gestations is not known. The unbalanced blood flow via the placental arteriovenous anastomoses causes hypovolaemia/hypotension in one/two fetus (es) (donor) and hypervolaemia/hypertension in another fetus (es) (recipient) [23]. This haemodynamic instability can lead to multiple organ damage particularly the brain, and death.…”

Section: Discussionmentioning

confidence: 99%

Multicystic encephalomalacia and gastrointestinal injury following single fetal death in first trimester and subsequent fetofetal transfusion syndrome in a monochorionic triplet pregnancy: a case report

Yeung

et al. 2019

BMC Pregnancy Childbirth

View full text Add to dashboard Cite

Background Monochorionic multifetal pregnancies are at increased risk of adverse perinatal outcome because of placental vascular anastomoses. We present a case of multicystic encephalomalacia and gastrointestinal injury in two surviving fetuses following single fetal death in first trimester and subsequent fetofetal transfusion syndrome in a monochorionic triplet pregnancy. Case presentation A 31-year-old nulliparous woman had a spontaneous monochorionic triamniotic triplet pregnancy. Three live fetuses with single placenta were seen at 8-week ultrasound scan. One fetus demised at 11 weeks and 3 days of gestation. Dilated echogenic bowel and ascites were found in one surviving fetus at 23 weeks of gestation. At 28 weeks of gestation, the pregnancy was complicated by fetofetal transfusion syndrome in which discordant amniotic fluid volumes were found. Two days later, emergency Caesarean section was performed because of worsening of fetal Doppler and biophysical profile. One baby was found to have jejunal atresia requiring surgery at 4 days old. He had periventricular leukomalacia and intracranial haemorrhage, but subsequent normal neurological development. Another baby had gastric perforation requiring surgery at 2 days old. He was confirmed to have multicystic encephalomalacia by cranial ultrasound and magnetic resonance imaging. He suffered from developmental delay, epilepsy and cerebral palsy. Conclusion This case alerts the obstetricians the possible hypoxic-ischemic injury to the survivors of monochorionic triplet pregnancy after the co-triplet death in the first trimester and fetofetal transfusion syndrome. Antenatal assessment and postnatal follow-up are important for these high-risk multiple pregnancies.

show abstract

Mechanism of visceral damage in fetofetal transfusion syndrome.

Cited by 5 publications

References 24 publications

Long term outcome of twin-twin transfusion syndrome

Long term outcome of twin-twin transfusion syndrome

Renal Tubular Dysgenesis in Twin-Twin Transfusion Syndrome

Multicystic encephalomalacia and gastrointestinal injury following single fetal death in first trimester and subsequent fetofetal transfusion syndrome in a monochorionic triplet pregnancy: a case report

Contact Info

Product

Resources

About