# Prenatal ultrasound diagnosis of fetal upper gastrointestinal bleeding in a monochorionic twin pregnancy: a case report

Arthur Gavotto, Arthur Gaudaire, Florent Fuchs

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Arthur Gavotto, Arthur Gaudaire, Florent Fuchs. Prenatal ultrasound diagnosis of fetal upper gastrointestinal bleeding in a monochorionic twin pregnancy: a case report. BMC Pregnancy and Childbirth, In press, 10.1186/s12884-026-08826-7. [https://hal.science/hal-05516376v1](https://hal.science/hal-05516376v1)

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# Prenatal ultrasound diagnosis of fetal upper gastrointestinal bleeding in a monochorionic twin pregnancy: a case report

Received: 2 November 2025

Accepted: 12 February 2026

Published online: 17 February 2026

Cite this article as: Gavotto A., Gaudaire A. & Fuchs F. Prenatal ultrasound diagnosis of fetal upper gastrointestinal bleeding in a monochorionic twin pregnancy: a case report. BMC Pregnancy Childbirth (2026). https://doi.org/10.1186/s12884-026-08826-7

Arthur Gavotto, Arthur Gaudaire & Florent Fuchs

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# Prenatal ultrasound diagnosis of fetal upper gastrointestinal bleeding in a monochorionic twin pregnancy: a case report.

**Short title:** Urgent C-Section for fetal gastric bleeding

Arthur Gavotto, MD, PhD<sup>a,b</sup> ; Arthur Gaudaire<sup>a,b</sup> ; Florent Fuchs, MD, PhD<sup>c,d,e</sup>

<sup>a</sup>Department of Neonatal Medicine, Pediatric Intensive Care, Pediatric Emergency Transport Service, Arnaud de Villeneuve Hospital, Montpellier University Hospital Centre, University of Montpellier, Montpellier, France.

<sup>b</sup>PhyMedExp, University of Montpellier, CNRS, INSERM, Montpellier, France

<sup>c</sup>Department of Obstetrics and Gynecology. University Hospital Center. 371 Avenue du Doyen Gaston Giraud, Montpellier, France.

<sup>d</sup>Inserm, CESP Center for research in Epidemiology and Population Health, U1018, Reproduction and child development, Villejuif, France.

<sup>e</sup>Desbrest Institute of Epidemiology and Public Health (IDESP), Univ Montpellier, INSERM, (CHU Montpellier), Montpellier, France

**Corresponding author:**

Pr. Arthur Gavotto, Department of Neonatal Medicine, Pediatric Intensive Care, Neonatal and Pediatric Emergency Transport Service, Arnaud de Villeneuve Hospital, Montpellier University Hospital Centre, 371 Avenue du Doyen Giraud, 34295 Montpellier cedex 5, France.

Email: a-gavotto@chu-montpellier.fr ; tel.: +33 4 67 33 66 39; fax: +33 4 67 33 21 29.

ORCID: https://orcid.org/0000-0001-6485-7634
Words count: 1000

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**Abstract**

**Background**

Fetal upper gastrointestinal bleeding (UGIB) is an exceptionally rare condition. We report a case of antenatally detected UGIB in a monochorionic diamniotic twin pregnancy, emphasizing key ultrasound features that enabled timely delivery and a favorable neonatal outcome.

**Case presentation**

A 23-year-old woman with a monochorionic diamniotic twin pregnancy complicated by Stage II twin-to-twin transfusion syndrome (TTTS) underwent fetoscopic laser ablation at 23 + 1 weeks. At 33 + 5 weeks' gestation, routine ultrasound revealed marked gastric and intestinal dilatation with echogenic intraluminal material and echogenic amniotic fluid in the recipient twin, along with elevated middle cerebral artery (MCA) peak systolic velocity (1.53 MoM) suggesting fetal anemia. An emergency cesarean section was performed. The neonate, born in bloody amniotic fluid, presented with hemorrhagic shock due to hemorrhagic gastritis confirmed by endoscopy. After intensive resuscitation, the infant recovered fully and was discharged on Day 23.

**Conclusion**

The coexistence of echogenic bowel content, echogenic amniotic fluid, and increased MCA Doppler should alert clinicians to possible in-utero gastrointestinal bleeding. Early recognition within standardized high-risk pregnancy surveillance protocols may allow life-saving intervention

**Keywords:** upper gastrointestinal bleeding; fetus; monochorionic twins; ultrasound; Doppler; twin-to-twin transfusion syndrome
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**Background**

Fetal upper gastrointestinal bleeding is an exceedingly rare diagnosis, with only a few cases reported in the literature. Its antenatal recognition is challenging, as findings are non-specific and may mimic other intra-abdominal pathologies. However, in high-risk pregnancies such as monochorionic twins, systematic ultrasound and Doppler monitoring may enable early detection of subtle but critical abnormalities, allowing timely intervention before irreversible fetal compromise occurs.

**Case report**

We report the case of a spontaneous monochorionic diamniotic twin pregnancy in a 23-year-old woman with a non-consanguineous partner. She had no significant medical history, except for a prior abortion. Non-invasive prenatal testing returned normal results. Given the chorionicity, the patient was enrolled in a high-risk pregnancy surveillance program, as per international guidelines¹ for monochorionic diamniotic twin pregnancies. This included frequent detailed ultrasound assessments (every two weeks) for complications such as twin-to-twin transfusion syndrome (TTTS) and twin anemia-polycythemia sequence (TAPS).

A moderate fetal weight discordance had been noted since 18 weeks' gestation, with estimated fetal weights around the 60th and 15th percentiles, respectively, without evidence of fetal growth restriction. The pregnancy remained uncomplicated until 22+1 weeks of gestation, when a discrepancy in amniotic fluid levels was noted: polyhydramnios in Twin A (patient concerned-Recipient Twin) and oligohydramnios in Twin B (Donor Twin). At 23+1 weeks' gestation, this discrepancy progressed to bladder
discrepancy, consistent with Stage II TTTS. Fetal growth was appropriate
in both twins. The pregnancy was associated with an anterior placenta. At
23+2 week's gestation, selective fetoscopic laser photocoagulation of four
arterio-venous anastomoses was performed at our tertiary referral center
(Montpellier University Hospital), followed by completion of the Solomon
technique along the placental vascular equator and 1.8L amnioreduction
in recipient twin. The procedure duration was 35 minutes, and it was
completed without intraoperative complications and with favorable
immediate outcome for both twins. The mother received intrarectal
indomethacin (100 mg, twice over 24 hours) for tocolysis according to
protocol before and after laser therapy. Thereafter weekly follow-up scan
of both fetuses showed normalization of the amniotic fluid, normal bladder
size and normal Doppler waveform for both fetuses.

At 32+3 weeks, the patient presented with painful uterine contractions.
Ultrasound examination confirmed fetal viability with normal Doppler
studies in both twins, and normal cervical length allowing discharge at
home.

At 33+5 weeks, during routine ultrasound follow-up, marked dilatation of
the stomach and small intestine was observed in Twin A (ex-recipient
twin), accompanied by echogenic intraluminal content and echogenic
amniotic fluid (Figure 1). In contrast, Twin B had a normal
gastrointestinal tract and amniotic fluid (Figure 2). Middle cerebral artery
(MCA) Doppler in Twin A showed elevated peak systolic velocity (1.53
MoM), suggestive of fetal anemia (Figure 3), whereas MCA peak systolic
velocity in Twin B remained within the normal range (1.27 MoM). All other
fetal Doppler parameters (umbilical, ductus venosus, MCA of co-twin) were within normal ranges. Maternal blood tests showed a normal complete blood count and coagulation profile, and fetal red blood cell screening was negative (<0.05%). Cardiotocography performed prior to delivery showed reassuring fetal heart rate tracings in both fetuses. Twin A showed no signs of chronic fetal anemia, including normal cardiothoracic ratio (0.32), absence of hydrops, and preserved fetal movements; MCA peak systolic velocity was repeated on several occasions and consistently remained above 1.5 MoM.

The decision to proceed with emergency cesarean section (3h after the ultrasound) was based on an integrated assessment combining ultrasound findings, Doppler abnormalities including the MCA peak systolic velocity, and the overall clinical context. Taken together, these findings raised concern for ongoing intrauterine gastrointestinal bleeding as a potential cause of acute fetal anemia in twin A. Twin A, a male infant weighing 2600 g (appropriate for gestational age), was delivered in bloody amniotic fluid, with an Apgar score of 1, 2, and 3 at 1, 5, and 10 minutes, normal arterial (7.35) and venous pH (7.41), normal lactates (1.9 mmol/l) and initial hemoglobin was 12.6 g/dL. For Twin B, amniotic fluid was clear, his weight was 1910g with an Apgar score of 6,7 and 7 at 1, 5, and 10 minutes, normal arterial and venous pH, normal lactates and hemoglobin was 13.4 g/dL. There was no macroscopic evidence of placental abruption, retroplacental hematoma or umbilical cord rupture at delivery.

Twin A neonate exhibited profuse bleeding from the mouth, nose, and rectum (consistent with a massive UGIB), associated with marked pallor
and bradycardia (<60 bpm), prompting immediate resuscitation². Despite an initial hemoglobin level within the normal ranges, the clinical presentation was consistent with hemorrhagic shock (hemodynamic compromise), requiring immediate volume expansion and blood transfusion. An umbilical venous catheter was placed at 8 minutes, followed by 10 ml/kg of saline and 20 ml/kg of red blood cells. These interventions led to heart rate normalization (>100 bpm) and a mean arterial pressure of 38 mmHg.

Due to persistent hypoxemia despite manual ventilation with 100% $FiO_2$, orotracheal intubation was attempted but proved difficult because of massive blood expulsion from the esophagus and giottis. Intubation was finally achieved at 40 minutes. A diagnosis of hyaline membrane disease and blood aspiration syndrome was suspected. Surfactant (200 mg/kg) was administered at one hour of life with subsequent clinical improvement.

Resuscitation focused on hemorrhagic shock management with a second red blood cell transfusion, platelets, fresh frozen plasma, fibrinogen, and tranexamic acid. Vasopressors were not required.

Further evaluation included: (i) Abdominal ultrasound: normal liver, no signs of hemochromatosis; (ii) Gastroscopy (Day 1): isolated hemorrhagic gastritis without ulceration or varices (Figure 4); (iii) Hemostasis panel altered by acute blood loss (fibrinogen 1.24 g/L, aPTT ratio 1.87, reduced factors II, V, VII, and X), all normalized by day 1; (iv) Normal pre-transfusion platelet count; (v) Blood type A-negative, negative direct antiglobulin test; (vi) no intracranial hemorrhage on cranial ultrasound; (vii) Post-transfusion hemoglobin level of 20.1 g/dL.
The final diagnosis was perinatal hemorrhagic shock secondary to upper gastrointestinal bleeding from hemorrhagic gastritis. A proton pump inhibitor (1 mg/kg/day) was prescribed for one month. No recurrence occurred. The infant was discharged on Day 23.

Discussion

This case demonstrates the critical role of prenatal ultrasound in the detection of fetal gastrointestinal bleeding, a rare and potentially fatal condition. The combination of dilated bowel loops with echogenic content, echogenic amniotic fluid, and elevated MCA Doppler was key to identifying a significant fetal complication in an otherwise asymptomatic pregnancy. Previous case reports have described similar findings, although very few include signs of fetal anemia.<sup>3-5</sup> None of these cases was complicated by hemorrhagic shock. In our case, these sonographic abnormalities, detected during routine surveillance of a high-risk monochorionic pregnancy, prompted emergency delivery and effective neonatal resuscitation, likely preventing intrauterine demise.

This case recalls that an initially normal hemoglobin level may be misleading in the setting of acute hemorrhage, as hemorrhagic shock is primarily a clinical diagnosis and may precede biological changes; hemoglobin concentration may remain temporarily unchanged until intravascular-interstitial fluid equilibration occurs, as previously described <sup>6</sup>.

While the mother had received indomethacin 10 weeks prior, no definitive link can be established. NSAIDs are known to affect gastrointestinal mucosal integrity in neonates,<sup>7-9</sup> but no direct association with antenatal
hemorrhagic gastritis has been reported. A case of gastrointestinal bleeding in a neonate following maternal mesalazine has been described, though an immunologic mechanism was suspected.¹⁰

Other hypotheses such as prenatal intestinal hyperechogenicity associated with intrauterine growth restriction may suggest a mesenteric ischemia mechanism, particularly in the context of gastrointestinal bleeding. However, in our case, normal fetal growth and the absence of suggestive endoscopic findings do not support this hypothesis¹¹. Furthermore, the rectal bleeding was interpreted as distal intestinal passage of blood originating from massive upper gastrointestinal bleeding rather than evidence of a primary lower gastrointestinal source, as rapid intestinal transit may occur in neonates and is also well described in cases of severe upper gastrointestinal hemorrhage.

Thus, this idiopathic case provides valuable teaching points for the interpretation of fetal gastrointestinal echogenicity and the integration of MCA Doppler in the evaluation of suspected intrauterine bleeding.

## Conclusion

This case illustrates a rare presentation of antenatally detected upper gastrointestinal bleeding confirmed by endoscopy. Prenatal identification of echogenic intestinal content, echogenic amniotic fluid, and elevated MCA Doppler velocity should prompt consideration of fetal anemia and in-utero hemorrhage. Early diagnosis through systematic high-risk pregnancy monitoring allowed prompt delivery and effective neonatal care, resulting in a favorable outcome despite severe presentation.
**Declarations**

*Ethics approval and consent to participate*

Not applicable.

*Consent for publication*

Written informed consent for publication of this case report and accompanying images was obtained from the patient's parents.

*Competing interests*

The authors declare that they have no competing interests.

*Funding*

No funding was received for this work.

*Acknowledgments*

We thank the teams from the Departments of Obstetrics, Neonatology, and Pediatric Gastroenterology at Montpellier University Hospital for their contribution to patient care.
References

1. D'Antonio F, Odibo A, Berghella V, et al. Perinatal mortality, timing of delivery and prenatal management of monoamniotic twin pregnancy: systematic review and meta-analysis. *Ultrasound Obstet Gynecol Off J Int Soc Ultrasound Obstet Gynecol*. 2019;53(2):166-174.
doi:10.1002/uog.20100

2. Madar J, Roehr CC, Ainsworth S, et al. European Resuscitation Council Guidelines 2021: Newborn resuscitation and support of transition of infants at birth. *Resuscitation*. 2021;161:291-326.
doi:10.1016/j.resuscitation.2021.02.014

3. Matsumoto K, Yamaguchi M, Nonaka T, Enomoto T, Takakuwa K. Fetal Anemia Caused by Prenatal Gastrointestinal Bleeding: A Case Report. *Open J Obstet Gynecol*. 2016;06(07):385-389.
doi:10.4236/ojog.2016.67050

4. Decoret E, Sibony O, Vuillard E, et al. Prenatal diagnosis of in utero fetal gastrointestinal bleeding. *Fetal Diagn Ther*. 1994;9(4):252-255.
doi:10.1159/000263942

5. Bedu A, Faure C, Sibony O, Vuillard E, Mougenot JF, Aujard Y. Prenatal gastrointestinal bleeding caused by esophagitis and gastritis. *J Pediatr*. 1994;125(3):465-467. doi:10.1016/s0022-3476(05)83297-4

6. Treml B, Kleinsasser A, Knotzer J, Breitkopf R, Velik-Salchner C, Rajsic S. Hemorrhagic Shock: Blood Marker Sequencing and Pulmonary Gas Exchange. *Diagnostics*. 2023;13(4).
doi:10.3390/diagnostics13040639

7. Grimaldi-Bensouda L, Abenhaim L, Michaud L, et al. Clinical features and risk factors for upper gastrointestinal bleeding in children: a case-crossover study. *Eur J Clin Pharmacol*. 2010;66(8):831-837.
doi:10.1007/s00228-010-0832-3

8. Evans P, O'Reilly D, Flyer JN, Soll R, Mitra S. Indomethacin for symptomatic patent ductus arteriosus in preterm infants. *Cochrane Database Syst Rev*. 2021;1(1):CD013133.
doi:10.1002/14651858.CD013133.pub2

9. G AG, Im U, Ah N. Indomethacin in pregnancy: applications and safety. *Am J Perinatol*. 2012;29(3). doi:10.1055/s-0031-1284227

10. Nii K, Okazaki K, Okada H, Kuboi T. Maternal mesalazine-induced neonatal gastrointestinal bleeding. *BMJ Case Rep*. 2021;14(4):e238743. doi:10.1136/bcr-2020-238743

11. Vena F, Mazza A, Bartolone M, et al. Hyperechogenic fetal bowel: Current evidence-based prenatal diagnosis and management. *J Clin Ultrasound JCU*. 2023;51(7):1172-1178. doi:10.1002/jcu.23528
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FIGURES

**Figure 1:** Obstetrical ultrasound performed (33+^5^ weeks' GA) on twin A

Legend: marked dilatation of (A) stomach (arrow) and (B) small intestine (arrows) with echogenic sludge in the lumen.

**Figure 2:** Obstetrical ultrasound performed (33+^5^ weeks' GA) on twin B

Legend: normal sonographic appearance of the gastrointestinal tract

**Figure 3:** Middle cerebral artery doppler (MCA) performed on twin A (33+^5^ weeks' GA)

Legend: peak systolic velocity Doppler in the MCA was increased (1.53MoM) corresponding to fetal anemia

**Figure 4:** Upper gastrointestinal endoscopy in Twin A on Day 1 of life.

Legend: diffuse petechiae and erythema of the gastric fundus (circle), with fibrinous deposits and brownish residue suggestive of digested blood (arrow). No ulcers were identified.
GA=33s5d

Tls 0.1

Tlb 0.1

MI 1.0

RM7C

19Hz/17.2cm

75°/1.1

1 Trim./OB

HI H PI 9.60 - 3.90

Gn 10

C7.0/M7

FF3/E3

Radiant min

SRI II 3/CRI 3

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CA
AG=33s5j

Tls 0.4

Tlb 1.2

MI 0.3

RM7C

<figure><img src="image_2.png" /></figure>

A Drt ACM-Syst. 73.44cm/s

A Drt ACM-Diasto. 13.50cm/s

A Drt ACM-S/D 5.44

A Drt ACM-IP 1.80

A Drt ACM-IR 0.82

A Drt ACM-TAmax 33.21cm/s

A Drt ACM-FC 147bpm

Gn 0.6

Frq low

Qual norm

WMF low2

PRF 1.4kHz

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<figure><img src="image_3.png" /></figure>
GA=33s5d

Tis 0.2
Tib 0.2
MI 0.8

RM7C
22Hz/14.0cm
75°/1.1

1 Trim./0B
HI H PI 9.60 - 3.90
Gn 10
C7.0/M7
FF3/E3
Radiant min
SRI II 3/CRI 3

A

<figure><img src="image_4.png" /></figure>

B

<figure><img src="image_5.png" /></figure>

GA=33s5d

Tis 0.2
Tib 0.2
MI 0.8

RM7C
22Hz/14.0cm
75°/1.1
1 Trim./0B
HI H PI 9.60 - 3.90
Gn 10
C7.0/M7
FF3/E3
Radiant min
SRI II 3/CRI 3

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<figure><img src="image_6.png" /></figure>

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