# The impact of delayed evacuation on the quality of human fetal tissue

## TL;DR

This study examines how delaying fetal tissue removal affects tissue quality, finding that warm ischemia after circulation stoppage causes significant degradation.

## Contribution

The study is the first to systematically assess the impact of delayed evacuation and digoxin on human fetal tissue quality.

## Key findings

- Delayed evacuation leads to structural disruption, reduced cell proliferation, and increased apoptosis in fetal tissues.
- RNA integrity is significantly reduced when tissues are exposed to warm ischemia and digoxin.
- DNA remains stable even after delayed evacuation, making it suitable for PCR analysis.

## Abstract

Agents such as digoxin and potassium chloride are frequently administered to arrest fetal circulation prior to termination procedures. Although this practice is common, the impact of delayed evacuation on human fetal tissue quality has not been systematically assessed. High-quality tissue is essential for accurate diagnosis of fetal abnormalities and for biomedical research.

To evaluate the effects of induced fetal demise and delayed evacuation on human fetal tissue quality across multiple organ systems, and to determine whether digoxin independently contributes to tissue degradation.

Tissue was collected from second-trimester dilation and evacuation procedures performed either after induced demise with digoxin or potassium chloride followed by evacuation 19–25 hours later, or without prior induction (immediate evacuation). Brain, lung, kidney, liver, and muscle were evaluated for morphology, proliferation, apoptosis, cell viability, culture success, and nucleic acid integrity. To model in utero conditions, tissues were incubated at 37 °C or 4 °C for up to 18 hours, with and without digoxin.

Delayed evacuation was associated with structural disruption, reduced proliferation, increased apoptosis, diminished fibroblast viability, and reduced RNA integrity compared to immediate evacuation. DNA integrity remained robust, with all samples suitable for PCR. Digoxin alone did not significantly alter RNA quality; however, when combined with prolonged incubation at 37 °C, RIN and DV200 values were significantly reduced across multiple tissues.

Warm ischemia following circulatory arrest is the principal driver of tissue degradation, with RNA and cell viability most affected and DNA relatively preserved. Digoxin alone has minimal effect but accelerates degradation under warm conditions. Minimizing the interval between circulatory arrest and evacuation, and avoiding prolonged exposure to body temperature, may preserve tissue integrity and improve the diagnostic and research utility of HFT.