# Challenges of Retained Thoracoamniotic Shunts in the Neonatal Period: A Case Report

**Authors:** Alejandro Madurga, María Victoria López Canelada, María Velayos, Carlos De la Torre, Eugenia Antolín Alvarado, Jose Luis Encinas, María Álvarez Barrial

PMC · DOI: 10.3390/children13020182 · 2026-01-28

## TL;DR

A case report shows that retained thoracoamniotic shunts can cause postnatal complications, requiring timely surgical removal for effective treatment.

## Contribution

Highlights the need for active intervention and thoracoscopic removal in managing retained thoracoamniotic shunts causing neonatal complications.

## Key findings

- Retained thoracoamniotic shunts can lead to delayed complications like recurrent pleural effusions.
- Thoracoscopic removal is a safe and effective treatment for postnatal complications caused by retained shunts.

## Abstract

What are the main findings?
•Thoracoamniotic shunting can successfully resolve fetal hydrops and allow favorable perinatal outcomes, even in severe pleural effusions.•Retained or migrated thoracoamniotic shunts may cause delayed postnatal complications, including recurrent pleural effusions, despite initial neonatal stability.

Thoracoamniotic shunting can successfully resolve fetal hydrops and allow favorable perinatal outcomes, even in severe pleural effusions.

Retained or migrated thoracoamniotic shunts may cause delayed postnatal complications, including recurrent pleural effusions, despite initial neonatal stability.

What are the implications of the main findings?
•Conservative observation is not always sufficient for retained thoracoamniotic shunts, and clinical deterioration should prompt active intervention.•Thoracoscopic removal represents a safe, effective, and minimally invasive definitive treatment when postnatal complications arise.

Conservative observation is not always sufficient for retained thoracoamniotic shunts, and clinical deterioration should prompt active intervention.

Thoracoscopic removal represents a safe, effective, and minimally invasive definitive treatment when postnatal complications arise.

Background: Thoracoamniotic shunting (TAS) is a well-established fetal therapy for severe pleural effusions complicated by hydrops. Although survival in selected cases exceeds 60%, retained or migrated shunts can pose significant postnatal management challenges. Case presentation: We report a neonate with intrathoracic migration of a Somatex® shunt placed at 26 weeks’ gestation for hydropic pleural effusion. Although initially asymptomatic, the infant developed recurrent pleural effusions requiring multiple readmissions. Thoracoscopic retrieval on day 76 of life allowed safe removal despite dense adhesions, leading to complete clinical resolution. Discussion: Retained thoracoamniotic shunts may remain asymptomatic or cause recurrent effusions, pneumothorax, or other complications. This case highlights the limitations of conservative management in the presence of clinical deterioration and supports timely surgical removal. Standardized criteria for intervention are lacking and urgently needed. Conclusions: In infants with retained TAS, recurrence of effusions or respiratory compromise should prompt active removal. Thoracoscopic retrieval is a safe and effective minimally invasive option.

## Linked entities

- **Diseases:** fetal hydrops (MONDO:0015193)

## Full-text entities

- **Genes:** PTPN11 (protein tyrosine phosphatase non-receptor type 11) [NCBI Gene 5781] {aka BPTP3, CFC, JMML, METCDS, NS1, PTP-1D}
- **Diseases:** lung injury (MESH:D055370), hydrops (MESH:D004487), pulmonary pathologies (MESH:D008171), pleural damage (MESH:D010995), chylothorax (MESH:D002916), inflammatory (MESH:D007249), injury to (MESH:D014947), pulmonary hypoplasia (MESH:C562992), respiratory distress (MESH:D012128), hydrothorax (MESH:D006876), fetal hydrops (MESH:D015160), CMV (MESH:D003586), pleural effusion (MESH:D010996), respiratory compromise (MESH:D012131), pneumothorax (MESH:D011030), air leak (MESH:D004618), effusion (MESH:D000080324), adhesion (MESH:D000267), polyhydramnios (MESH:D006831), heart failure (MESH:D006333)
- **Chemicals:** Carbon dioxide (MESH:D002245)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12939657/full.md

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Source: https://tomesphere.com/paper/PMC12939657