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. 2026 Jul 28;118(8):e70097. doi: 10.1002/bdr2.70097

Fetal Superior Mesenteric Artery Peak Systolic Velocity as a Marker of Prenatal Bowel Inflammation in Gastroschisis: A Case–Control Study

Renata Jaczyńska 1,2,✉, Boyana Mikulska 1, Magda Rybak‐Krzyszkowska 3, Dariusz Mydlak 4, Ewa Sawicka 4, Anna Nimer 5, Tomasz Maciejewski 1
PMCID: PMC13414641  PMID: 42521617

ABSTRACT

Objective

This study aimed to evaluate whether peak systolic velocity (PSV) in the fetal extra‐abdominal superior mesenteric artery (SMA) is a useful prenatal marker of bowel inflammation in gastroschisis (GS), which manifests postnatally as bowel matting.

Methods

This case–control study included 30 fetuses with gastroschisis who underwent standardized bowel assessment and Doppler measurement of the extra‐abdominal SMA‐PSV. Postnatal bowel status was classified as normal or inflamed. The primary analysis examined the association between fetal SMA‐PSV and bowel inflammation, using linear models and generalized estimating equations for repeated measurements.

Results

Among 30 fetuses, bowel matting was identified postnatally in 10 cases (33.3%). These neonates had significantly lower birthweight percentiles (5.5 vs. 50.5; p = 0.002) and more frequent ultrasound inflammatory signs such as bowel wall oedema (80% vs. 15%; p = 0.002), bowel wall stiffness (50% vs. 5%; p = 0.004), and corrugation wall (60% vs. 5%; p = 0.004). PSV was strongly correlated with bowel wall thickness (r = 0.81) and significantly higher in fetuses with postnatally diagnosed bowel matting (p < 0.001). GEE models showed that higher prenatal PSV independently predicted the later occurrence of bowel matting. Incorporating the time × bowel matting interaction significantly improved model fit (adjusted R 2 = 0.460).

Conclusions

Fetal SMA‐PSV is significantly associated with prenatal/ultrasound and postnatal signs of bowel inflammation in gastroschisis, such as bowel wall thickening and bowel matting. This association appears independent of the simple/complex GS surgical classification, suggesting PSV as a functional marker of intestinal compromise. Although technically demanding, SMA‐PSV assessment may aid prenatal evaluation and perinatal planning, particularly in detecting evolving intestinal inflammatory cases.

Keywords: fetal doppler ultrasound, gastroschisis, peak systolic velocity, prenatal bowel inflammation, superior mesenteric artery

1. Introduction

Gastroschisis (GS) is a congenital abdominal wall defect in most cases situated to the right of the insertion of the umbilical cord, in which the intestine is located outside the abdominal cavity without any protective membrane (Prefumo and Izzi 2014). The prevalence of the GS is now 1.6 per 10,000 births, which classifies it as a rare disease (Orphanet 2024; European Commission 2025). Based on the absence or presence of additional intestinal complications, two forms of the defect were distinguished—simple gastroschisis (sCG) and complex gastroschisis (cGS) (Molik et al. 2001). Despite this binary classification, it has become increasingly evident that intrauterine bowel injury does not always correlate with surgical complexity. The bowel, continuously exposed to the amniotic fluid, is susceptible to inflammation, oedema, and vascular compromise, potentially leading to postnatal complications (Mazzoni et al. 2022; Cowan et al. 2012; Martillotti et al. 2015; Guibourdenche et al. 2006; Langer et al. 1989; Chabra et al. 2021). A key pathological feature frequently observed in both sGS and cGS is intestinal wall thickening and bowel matting, an ultrasound and postnatal manifestation of inflammatory changes of the bowel wall (Martillotti et al. 2015; Youssef et al. 2017; Dekonenko et al. 2021). The intensity of the inflammatory reaction is a defining factor in prognosis for neonates, from which springs the importance of identifying signs that may be associated with a worse prognosis and the possibility of their prenatal identification. Exposure to meconium‐stained amniotic fluid, fetal urine may trigger inflammation by inducing chemical irritation and vasoconstriction of the superior mesenteric artery (SMA), thereby compromising bowel perfusion (Karakuş et al. 2015; Luton et al. 2003). Additionally, the small size of the abdominal wall defect can amplify perfusion disturbance. The binary classification may not adequately capture the functional and inflammatory status of the bowel, as some cases of sGS may exhibit marked inflammation, while certain cGS cases proceed without significant bowel oedema or matting.

Only a few studies have analyzed bowel vascularization in gastroschisis and underlined the low predictive value of the superior mesenteric artery Doppler for neonatal outcome. Additionally, Doppler assessment of the SMA was not a useful parameter for differentiating between simple and complex gastroschisis cases (Martillotti et al. 2015; Lap et al. 2020; Abuhamad et al. 1997; Volumenie et al. 2001).

It is not surprising, because adverse changes in the intestinal wall (wall thickening, oedema, increased wall echogenicity) are not related to atresia, perforation, necrosis, or volvulus (cGS), but are rather a result of chronic inflammatory changes, covering the intestinal wall with fibrous tissue exposed to amniotic fluid. Therefore, this sign was visible in both sGS and cGS fetuses and may be a useful marker for identifying complicated cases (inflammatory process) in both groups of the defect (Guibourdenche et al. 2006; Dekonenko et al. 2021; Jaczyńska et al. 2024). During pregnancy, fundamental changes occur in splanchnic blood flow circulation even though the placenta performs the main function of the large intestine. The blood circulation of almost the whole intestine depends solely on a single vessel—the superior mesenteric artery, which implies that physiological circulation is essential in the development and function of the bowel. Therefore, the changes in blood flow in the SMA may affect physiological functions of the intestine (Visnovsky et al. 2016). These changes can be assessed prenatally, and knowledge of the physiological parameters of the splanchnic circulation may help detect pathological conditions. Peak systolic velocity (PSV), a parameter more directly linked to intravascular dynamics, may better reflect changes in bowel perfusion resulting from either mechanical obstruction at the abdominal wall defect or from inflammatory oedema within the herniated bowel and mesentery (Luton et al. 2003; Bhat et al. 2020). This study aims to evaluate the diagnostic value of PSV in the extra‐abdominal SMA for identifying fetuses with evident bowel inflammation in ultrasound, regardless of their classification as simple or complex GS. Specifically, we sought to assess the association between an elevated PSV and the presence of bowel inflammation, detected by ultrasound as bowel wall thickness and bowel matting confirmed during surgery, irrespective of the surgical classification as sGS or cGS. We hypothesized that elevated PSV in the fetal SMA reflects underlying bowel compromise and is associated with ultrasound and postnatal signs of intestinal inflammation in fetuses/newborns with gastroschisis.

2. Material and Methods

2.1. Study Design

This case–control study was conducted at a tertiary referral fetal medicine center and included fetuses with prenatally diagnosed GS. This report is written according to the STROBE Statement for a case–control study (von Elm et al. 2014).

2.2. Setting

Our study evaluated fetuses/newborns diagnosed, monitored at the Department of Obstetrics and Gynecology between January 2018 and December 2021, and treated at the Department of Pediatric and Adolescent Surgery of the Institute of Mother and Child in Warsaw (Poland).

All cases of prenatally diagnosed gastroschisis referred to the center during this period were systematically reviewed for eligibility.

2.3. Participants

The study population included 30 singleton pregnancies with a prenatal diagnosis of gastroschisis. Inclusion criteria comprised: (1) confirmed diagnosis of fetal gastroschisis on prenatal ultrasound; (2) availability of detailed intestinal evaluation, SMA Doppler assessment; and (3) complete postnatal follow‐up with accessible surgical records and neonatal outcomes.

Exclusion criteria encompassed multiple pregnancies, the presence of additional structural anomalies unrelated to gastroschisis, chromosomal abnormalities, and incomplete Doppler or outcome data.

2.4. Ultrasound Evaluation

All ultrasound examinations were performed using high‐resolution ultrasound machines (GE Voluson E8 and E10 with 4–8 MHz and RM6C transabdominal probes). Standardized fetal biometric, anatomical, Doppler, and intestinal ultrasound parameters assessments were conducted during each ultrasound exam.

The ultrasound examinations with assessment of SMA flow were performed from 26.0 weeks of pregnancy until delivery. The SMA was visualized in the sagittal (Figure 1a–c) and axial plane (Figure 1d). Color Doppler was used to identify the vessel and pulsed‐wave Doppler was applied to obtain velocity waveforms. Measurements of SMA peak systolic velocity (SMA‐PSV) were performed in the axial plane, at its extra‐abdominal segment, at around 1 cm from the abdominal wall defect. We used the lowest possible insonation angle with angle correction used when necessary, and it was below 30 degrees. PSV was measured at least three times during fetal quiescence and without fetal breathing. The highest PSV value from three technically satisfactory waveforms was recorded for analysis (Figure 1g,k). We measured extra‐abdominal bowel diameter and wall thickness, intra‐abdominal bowel dilatation, and gastric dilatation (Figure 1e,f). Measurements of extra‐abdominal bowel were performed separately for the small and large intestines. During ultrasound examination, we focused on the qualitative assessment of the bowel condition and signs suggesting inflammatory changes: bowel wall oedema, corrugated wall (swollen layer of the small bowel circular musculature), and bowel wall stiffness (Figure 1i,j) (Jaczyńska et al. 2024). All ultrasound assessments were performed by fetal medicine specialists with experience in prenatal diagnosis of abdominal wall defects.

FIGURE 1.

FIGURE 1

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Comparison of the prenatal ultrasound assessment (bowel and vascularity) with photographic documentation of the newborn's intestine. (a) Sagittal plane of fetal abdomen demonstrating small (short white arrow) and large (long white arrow) bowel in the abdomen wall defect (white arrow heads). Urinary blader (white asterisk). (b) Sagittal plane of fetal abdomen demonstrating truncus celiacus (short white arrow), superior mesenteric artery (long white arrow) raising from the aorta (white arrow heads). Urinary blader (white asterisk). (c) The superior mesenteric artery (SMA) (white long arrow) visible in the abdomen wall defect (white circle). (d) Extra‐abdominal bowel loops (white short arrows) and extra‐abdominal part of the superior mesenteric artery (white long arrow) (e) Extra‐abdominal small bowel in uncomplicated simple gastroschisis (sGS) with no bowel dilatation (small bowel diameter 7 mm, on the right) and normal appearance of the large bowel (on the left). Fetus at 34.0 weeks. US evaluation (e–g) was performed 4 days before the planned delivery. (f) Smal bowel wall thickness—1.9 mm, without bowel wall edema, stiffness and “corrugated” wall (g) SMA peak systolic velocity 42 cm/s—uncomplicated sGS. (h) Surgical macroscopic evaluation of the intestines in a newborn (prenatal assessment on (e–g)). Visible normal loops of small and large intestine without bowel matting. (i) Extra‐abdominal small bowel in complicated simple gastroschisis with bowel dilatation (small bowel diameter 12 mm), bowel wall edema (small bowel wall thickness—3.2 mm) and bowel wall stiffness (straightened bowel loops). Fetus examined at 33.6 weeks, describes as a Case 1 on Figure S1, US evaluation (i–k) was performed 1 day before planned delivery. (j) “Corrugated” wall visualized in longitudinal view of the small bowel loops in a plane tangential to the surface of the intestinal wall—swollen layer of the small bowel's circular musculature and thickened circular muscles (white short arrow). (k) SMA peak systolic velocity 104 cm/s—complicated sGS. (l) Surgical macroscopic evaluation of the intestines in a newborn (prenatal assessment on (i–k) with complicated sGS). Visible loops of small intestine with severe bowel matting. Look at the volume of the intestinal loops in comparison to the hand of the surgeon.

2.5. Surgeon Assessment

The newborns with gastroschisis were divided into two groups, by analyzing the data from the surgical bowel assessment: no bowel matting—normal bowel without inflammation (grade 0) and with bowel matting (grade 1—mild matting—slight inflammation/visible plaque on bowel wall surface or grade 2—severe bowel matting—moderate to massive inflammation with fibrous plague on bowel wall surface, stiffness of the bowel wall) (Figure 1h,l) (Cowan et al. 2012).

2.6. Variables and Outcomes

The primary explanatory variable was PSV in the fetal extra‐abdominal SMA, measured at multiple time points during gestation by Doppler ultrasound.

Covariates considered in the analysis included gestational age at delivery, birthweight, diagnosis of fetal growth restriction (FGR), Apgar scores at 1 and 5 min, type of surgical repair (primary closure or secondary closure/silo placement), and classification as simple or complex gastroschisis.

The primary outcome was bowel inflammation, defined as postnatal bowel matting grade 1 or 2. Follow‐up included time to full enteral feeding (TFEF), length of hospital stay (LOS), and neonatal sepsis. PSV trajectories and their associations with inflammatory findings were further modeled using generalized estimating equations (GEE) to account for repeated measures across gestation.

2.7. Statistical Analysis

Continuous variables were reported as medians with first and third quartiles for non‐normally distributed data, or as means with standard deviations (SD) for normally distributed data. The distribution of variables was assessed using graphical methods, including Q–Q plots and histograms. The normal distribution of PSV and other ultrasound parameters was confirmed.

Univariable and multivariable linear models were fitted to explore associations between PSV and outcome variables. Generalized estimating equations (GEE) were applied in selected models to address potential multicollinearity between correlated explanatory variables. Statistical significance was defined as a two‐tailed p‐value below 0.05. All analyses were performed in R using the RStudio environment (R Core Team, version 4.3).

3. Results

3.1. Population Characteristics

The study included 30 fetuses diagnosed prenatally with gastroschisis. In the no bowel matting group, there were 20 newborns, and in the bowel matting group, there were 10 newborns. The 6 of them presented mild and 4 moderate or severe bowel matting. Additional clinical variables, including gestational age at delivery, birth weight, and Apgar scores, are presented in Table 1.

TABLE 1.

Comparison of clinical characteristics between neonates with and without bowel matting.

Variable No bowel matting (N = 20) n/median (%)/[IRQ] Bowel matting (N = 10) n/median (%)/[IRQ] p
Gestational age at delivery (weeks) 34.0 [34.0–35.0] 34.0 [33.0–34.0] 0.045
Delivery time (days) 242.5 [240.75–246.0] 239.5 [234.0–242.75] 0.049
Birthweight (grams) 2410.0 [2197.5–2505.0] 1900.0 [1695.0–2112.5] < 0.001
Birthweight percentile 50.5 [20.25–72.75] 5.5 [2.75–11.25] 0.002
Apgar score = 10 18 (90.0%) 6 (60.0%) 0.154
Primary closure 20 (100.0%) 9 (90.0%) 0.719
Simple gastroscisis 19 (95.0%) 7 (70.0%) 0.184
Complex gastroschisis 1 (5.0%) 3 (30.0%)
Closing gastroschisis type B a 0 1 (10.0%) N/A
Intestinal complitations 1 (5%) 3 (30.0%) 0.095
IABD 2 (10.0%) 9 (90.0%) < 0.001
Corrugatted wall 1 (5.0%) 6 (60.0%) 0.004
Bowel wall oedema 3 (15.0%) 8 (80.0%) 0.002
Bowel wall stiffness 1 (5%) 5 (50%) 0.004
Neonatal sepsis 3 (15.0%) 3 (30.0%) 0.628
TFEF (days) 20.0 [15.25–26.75] 25.5 [20.5–35.0] 0.098
LOS (days) 28.5 [22.0–37.75] 42.0 [32.75–52.75] 0.094
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Abbreviations: FGR, fetal growth restriction; IABD, intra‐abdominal bowel dilatation; LOS, length of hospital stay; TFEF, time to full enteral feeding.

a

Perrone et al. (2019).

Significant differences were observed between neonates with and without bowel matting. Neonates in the bowel matting group had a significantly lower median birthweight (1900 g [IQR 1695–2112.5] vs. 2410 g [IQR 2197.5–2505]; p < 0.001) and birthweight percentile (5.5 [IQR 2.75–11.25] vs. 50.5 [IQR 20.25–72.75]; p = 0.002). They were also delivered slightly earlier (median 34.21 weeks [IQR 33.43–34.68] vs. 34.64 weeks [IQR 34.39–35.14]; p = 0.049).

Ultrasound inflammatory signs were notably more frequent in the bowel matting group, including bowel wall oedema (80.0% vs. 15.0%; p = 0.002), corrugated wall (60.0% vs. 5.0%; p = 0.004), and bowel wall stiffness (50% vs. 5%; p = 0.004).

Intra‐abdominal bowel dilatation (IABD) as an ultrasound sign of bowel atresia or bowel compression was significantly more frequent in the bowel matting group (90.0% vs. 10.0%; p < 0.001).

Although time to full enteral feeding (median 25.5 days [IQR 20.5–35.0] vs. 20.0 days [IQR 15.25–26.75]; p = 0.098) and length of hospital stay (median 42.0 days [IQR 32.75–52.75] vs. 28.5 days [IQR 22.0–37.75]; p = 0.094) were longer in the bowel matting group, these differences did not reach statistical significance.

SMA‐PSV correlated positively with bowel wall thickness, strongest for the small bowel (r = 0.81, p < 0.001) and moderate for the large bowel (r = 0.56, p < 0.001), indicating that higher PSV is consistently associated with prenatal signs of bowel inflammation.

To evaluate gestational age‐dependent changes in Doppler measurements, linear regression models including both linear and quadratic gestational age terms were constructed for each variable. A significant increase over time was observed in PSV and bowel wall thickness, although the magnitude and consistency of these trends varied between measures.

PSV values showed a non‐significant linear trend with gestational age (p = 0.066), but a significant quadratic component (p = 0.030), indicating an accelerated increase in later gestational weeks. Small bowel wall thickness demonstrated a quadratic effect (p = 0.061 for time, p = 0.022 for time2), while large bowel wall thickness similarly exhibited a significant quadratic component (p = 0.066 for time, p = 0.030 for time2) (Table 2, Figure S1).

TABLE 2.

Linear regression models for bowel wall thickness and SMA‐PSV with gestational age and its quadratic term.

Term Estimate Standard error t value p R 2
Extra‐abdominal small bowel wall thickness
Intercept 10 5.78 1.73 0.086 0.423
Time −0.102 0.0542 −1.88 0.061
Time2 0.00029 0.00013 2.31 0.022
Extra‐abdominal large bowel wall thickness
Intercept 258 155 1.67 0.097 0.284
Time −2.68 1.45 −1.85 0.066
Time2 0.00742 0.00338 2.2 0.03
SMA peak systolic velocity
Intercept 258 155 1.67 0.097 0.327
Time −2.68 1.45 −1.85 0.066
Time2 0.00742 0.00338 2.2 0.03
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Abbreviation: SMA‐PSV, superior mesenteric artery peak systolic velocity.

In the first, generalized estimating equations model, PSV was modeled as a function of gestational age (time), time squared, and the presence of bowel matting. The presence of bowel matting was significantly associated with higher PSV values (Estimate = 9.70; p < 0.001), independently of gestational age. In contrast, both the linear (p = 0.016) and quadratic (p = 0.006) time components were statistically significant, although PSV remained a stronger predictor of bowel matting (Table 3).

TABLE 3.

Generalized estimating equation models evaluating the association between prenatal SMA‐PSV values and the postnatal occurrence of bowel matting across gestational time.

Term Model A Model B
Intercept 320.51 (145.25); p = 0.029 358.04 (138.65); p = 0.011
Time −3.30 (1.36); p = 0.016 −3.51 (1.30); p = 0.008
Time2 0.00889 (0.00317); p = 0.006 0.00907 (0.00302); p = 0.003
Bowel Matting 9.70 (1.94); p < 0.001 −96.12 (25.05); p < 0.001
Time × Bowel Matting — 0.482 (0.114); p < 0.001
Adjusted R 2 0.405 0.460
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Note: Model A includes time, time2, and bowel matting as predictors; Model B additionally incorporates the interaction term time × bowel matting. Values are presented as Estimate (SE); p‐value.

Abbreviation: SMA‐PSV, superior mesenteric artery peak systolic velocity.

Visual inspection of residuals (Figure S2a) revealed heteroscedasticity, with increasing residual variance at higher PSV values, suggesting potential limitations in model fit.

In the second mode, an interaction term between time and bowel matting was introduced to evaluate whether PSV trajectories differed by inflammation status. This extended model showed that the interaction between time and bowel matting was statistically significant (p < 0.001), with a better model fit (adjusted R 2 = 0.460) (Table 3). The inclusion of an interaction term between gestational time and bowel matting significantly improved model fit, as evidenced by a higher adjusted R 2 (0.460 vs. 0.405). This suggests that fetuses with bowel matting follow a distinct PSV trajectory compared to those without, particularly in late gestation. The interaction indicates a steeper rise in PSV among affected fetuses, supporting its potential use as a dynamic marker of inflammatory bowel involvement. As shown in Figure S2b, PSV values increased more steeply in fetuses with bowel matting, especially beyond 30 weeks of gestation.

Figure 2 illustrates the expected PSV values across gestation as estimated from the final GEE model incorporating both a quadratic time component and a time × bowel matting interaction. While PSV values increased progressively in both groups, the growth trajectory was markedly steeper among fetuses with bowel matting, with a notable divergence becoming apparent after 30 weeks of gestation. These findings support the potential utility of PSV as a prenatal marker of intestinal inflammation in fetuses with gastroschisis.

FIGURE 2.

FIGURE 2

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Predicted SMA‐PSV values by bowel matting group across gestation NOTE: SMA‐PSV—Superior Mesenteric Artery Peak Systolic Velocity; GEE—Generalized Estimating Equations. Bar chart illustrating model‐derived SMA‐PSV predictions over gestational time for fetuses with (red) and without (blue) bowel matting, based on a GEE model with quadratic time and time × bowel matting interaction. The model predicts a steeper increase in SMA‐PSV values for the bowel matting group, particularly in late gestation.

4. Discussion

This study investigated the clinical utility of fetal SMA‐PSV as a prenatal marker of bowel compromise in fetuses with gastroschisis. We found that PSV values increased slightly with advancing gestational age in uncomplicated cases, whereas in fetuses with prenatal/ultrasound (bowel wall thickening) and postnatal/intraoperative (bowel matting) signs of bowel inflammation, PSV values increased progressively and reached significantly higher levels.

When contrasted with longitudinal reference data from healthy fetuses, the steep late‐gestational rise in PSV observed in our gastroschisis cohort clearly exceeds the physiological trajectory described by Achiron et al. and Ebbing et al., reinforcing its pathological nature (Achiron et al. 1998; Ebbing et al. 2009). PSV showed a strong correlation with small bowel wall thickness and remained independently associated with inflammatory signs even after adjustment for gestational age. Pearson's correlations between PSV and small bowel wall thickness were positive and statistically significant. Notably, PSV did not discriminate between fetuses classified as simple versus complex gastroschisis, and it was not associated with isolated structural complications such as atresia, necrosis, volvulus, or perforation. These findings suggest that PSV may serve as a more refined biomarker for fetal bowel compromise than the traditional binary classification based solely on postnatal surgical outcomes. PSV assessment may offer a more clinically relevant perspective on prenatal bowel injury in gastroschisis by focusing on ultrasound evidence of inflammation rather than solely on intestinal complications (atresia, necrosis, perforation, volvulus).

The primary determinant of outcome in infants with gastroschisis is the extent of intestinal injury that occurs during fetal life (Bhat et al. 2020).

Three main mechanisms underlie the development of intestinal complications in fetuses and neonates with GS. The first is the presence of atresia, necrosis, volvulus, and perforation in neonates with complex GS, as defined by its diagnostic criteria (Molik et al. 2001). The second mechanism is the occurrence of inflammatory changes in the bowel, which may arise in both simple and complex GS and manifest as bowel matting and, in severe cases, peel formation. These inflammatory alterations likely involve not only the bowel itself but also its mesentery (Guibourdenche et al. 2006; Youssef et al. 2017; Dekonenko et al. 2021; Luton et al. 2003). The third mechanism is narrowing or premature closure of abdominal wall defect (AWD), leading to bowel compression at the defect site and resulting in the ischemia of the extra‐abdominal bowel, which may progress to extensive necrosis and even bowel resorption (closing/closed/vanishing GS) (Perrone et al. 2019). A constricted abdominal wall defect affects the mesentery and its arterial, venous, and lymphatic vessels, causing ischemia and adverse changes in the intestine (Bhat et al. 2020). This mechanism may also contribute to intestinal atresia at the site of AWD due to direct compression and bowel dilatation located proximal to the AWD and manifested as IABD (Bergholz et al. 2012).

Only a few studies have analyzed SMA Doppler assessment in fetuses with gastroschisis and have shown that pulsatility index (PI) was a poor predictor of simple and complex forms of the defect and adverse neonatal outcomes. Abuhamad et al. reported no significant difference noted in the superior mesenteric artery pulsatility index between the good‐neonatal‐outcome and poor‐neonatal‐outcome groups (p = 0.99). About 50% of cases had SMA‐PI below the normal range, which underlined the low predictive value of SMA Doppler for neonatal outcome. Both blood‐flow velocimetry of the intra‐ and extra‐abdominal SMA were unable to differentiate between good and poor neonatal outcomes. Interestingly, in the pregnancy that ended with a fetal death, the superior mesenteric artery pulsatility index was above normal reference range a week before, which may indicate an association between changes in bowel vascularization and fetal demise (Abuhamad et al. 1997).

Similarly, Lap et al. reported that SMA‐PI was on average significantly lower in fetuses with gastroschisis than in normal controls, especially with advancing gestation, and both the intra‐ and extra‐abdominal SMA were unable to differentiate between simple and complex gastroschisis cases and did not seem to be related to neonatal morbidity (Lap et al. 2020).

Martillotti et al. conducted a retrospective study that found a higher incidence of perturbed mesenteric circulation in cases with complex gastroschisis; however, the measurement method and the definition of abnormal Doppler were not described (Martillotti et al. 2015).

Volumenie et al. analyzed the influence of amnioinfusion on Doppler velocimetry of the SMA in cases of gastroschisis and reported a significant positive correlation between the extra‐abdominal SMA‐PI before amnioinfusion and maximal bowel dilatation and length of stay in the neonatal intensive care unit; no other correlations with neonatal outcome were found. A significant improvement of diastolic flow was observed in the extra‐abdominal superior mesenteric artery after amnioinfusion (Volumenie et al. 2001).

These findings highlight the limited diagnostic value of PI, whereas PSV may more directly capture perfusion changes induced by inflammation or mechanical distortion of the mesenteric artery. In our study, fetuses with the highest value of SMA‐PSV presented three main mechanisms underlying the development of intestinal complications.

The surgical procedure after birth is rather simple but may be hampered by bowel dilatation and wall thickening with the presence of a fibrous peel, which may render the primary closure of the abdominal defect impossible (Luck et al. 1985). Therefore, the most important factor in determining the possibility of primary abdominal wall closure is the “state of pathology of the bowel”, which is displaced outside the abdominal cavity, and the coexistence of other bowel defects. Short and long‐term neonatal outcomes for the neonate born with gastroschisis are generally dependent on the bowel condition at birth (Cowan et al. 2012; Youssef et al. 2017; Jaczyńska et al. 2023; Moore et al. 1999).

Guibourdenche demonstrated in bowel histology that the thickness of the muscularis intestinalis and the serous layer increased 2‐fold. Within and below the serous layer, fibrosis was associated with mild infiltration by polymorphonuclear leukocytes and mononuclear cells. Gastroschisis may be associated with a subchronic inflammatory process of variable intensity. Neonates with gastroschisis have perivisceritis due to aseptic peritonitis, prolonged exposure of the bowel to amniotic fluid, resulting from contact between the bowel and amniotic fluid (Guibourdenche et al. 2006; Langer et al. 1989). This inflammation is restricted to the bowel and appears as an oedema, fibrin deposition, and inflammatory cell infiltration of the intestinal wall. The degree of inflammation should be used to evaluate intestinal damage (Cowan et al. 2012; Morrison et al. 1998).

According to Tibboel et al., perivisceritis in fetus does not occur before 30 weeks' gestation because of a modification of amniotic fluid consisting of an increase in the concentration of urea and creatine and a decrease in osmolality and sodium (Tibboel et al. 1986). However, one cannot ignore that all fetuses with gastroschisis have their bowel bathed by amniotic fluid and urine, yet they have a spectrum of bowel matting from none to severe (Deans et al. 1999; Bargy and Beaudoin 2014). This suggests that there are several mechanisms of intestinal damage in GS.

Some authors have suggested that components of the amniotic fluid involved in this reaction are controversial, but others have demonstrated that high levels of digestive enzymes can aggressively affect the intestine, findings supported by experimental results (Guibourdenche et al. 2006; Langer et al. 1989; Api et al. 2001; Akgür et al. 1998).

Guibourdenche et al. claimed that there is no reliable way to predict the degree of perivisceritis or postnatal digestive function before birth (Guibourdenche et al. 2006).

However, in our previous studies we have demonstrated that it is possible to assess the intestinal wall by ultrasound and to recognize adverse signs suggesting postnatal bowel matting with high predictive value (Jaczyńska et al. 2024, 2023).

In our study, PSV in the fetal superior mesenteric artery showed a strong association with ultrasound markers of intestinal inflammation, most notably bowel wall thickening. This finding is consistent with earlier evidence that increased echogenicity and bowel wall thickening on prenatal ultrasound reflect underlying inflammatory injury to extra‐abdominal bowel loops (Martillotti et al. 2015).

Lap et al. demonstrated that the SMA‐PI was significantly lower in fetuses with gastroschisis, a finding they attributed to vasodilatation caused by progressive chronic inflammation, leakage of albumin from the vessel wall, hypovolemia due to reduced serum protein concentration, and hypoperfusion of the exposed bowel (Lap et al. 2020).

The observed increase in SMA‐PSV in our analysis could also reflect mesenteric compression from inflammatory oedema.

The effect of vascular compression in adults is known as mesenteric stenosis and results in insufficient blood flow to the small intestine, causing chronic intestinal ischemia. The symptom and diagnostic criterion are an increased velocity in SMA (Bhatt 2004).

A similar phenomenon occurs in some fetuses with gastroschisis. However, “stenosis” at the AWD site is caused by vessel compression by a too‐small defect and/or oedema of the structures located in the AWD. The presence of IABD in 90% of fetuses in the bowel matting group in our study is consistent with the described mechanism.

Changes in splanchnic blood flow can be assessed prenatally, and knowledge of the physiological parameters of splanchnic circulation may help detect pathological conditions.

During normal pregnancy, PSV values measured at the origin of the SMA from the aorta remain relatively stable throughout the third trimester. Visnovsky et al. found that SMA systolic velocity slightly increases and reaches its highest value in the 21st week of gestation, which is about the end of the second phase of the trophoblastic invasion (Visnovsky et al. 2016). In the next period, the systolic velocity was almost constant and showed no significant variations across the different weeks of pregnancy; finally, at the end of pregnancy, the PSV decreased after the 35th week (Visnovsky et al. 2016; Matasova et al. 2011). Our study demonstrated lower PSV values, especially in the uncomplicated cases. The higher PSV values reported in Visnovsky's study compared to ours are attributable to measurements performed directly at the vessel's origin from the aorta, whereas in our study, measurements were taken around 1 cm beyond the AWD, several centimeters distally from the measurement point in Visnovsky's study.

Meconium‐induced vasoconstriction of the superior mesenteric artery can precipitate transient ischaemia (Karakuş et al. 2015). Volumenie et al. showed that diluting inflammatory mediators with amnioinfusion promptly resulted in a significant improvement in diastolic flow and lowered the extra‐abdominal SMA‐PI (0.75 → 0.64; p < 0.001), confirming the haemodynamic reversibility of this process (Volumenie et al. 2001).

Inflammatory oedema of the extra‐abdominal bowel and its mesentery may result in thickness and stiffness of the bowel wall and compress mesenteric vessels, thereby raising PSV in the mesenteric artery before overt structural damage becomes visible. Mechanical narrowing of the SMA at the abdominal‐wall defect reduces the vessel's cross‐sectional area and accelerates blood flow through a Venturi‐type effect (Munson et al. 1998).

The impaired mesenteric blood flow and intestinal injury were first highlighted by Rickham. Shaw et al. related the bowel lesions to constriction of the loops at the AWD ring and pointed out that this process is enhanced by bowel oedema. Additionally, the lack of normal mesenteric attachment may also cause the bowel to twist resulting in volvulus and, secondary to this, impaired intestinal blood supply (Rickham 1963; Shaw 1975).

Similarly, Beaudoin et al. noticed that in case of severe bowel matting in many patients, a mesenteric root was fixed in torsion by the thickened peritoneum and pointed out that, more to a true constriction within AWD, partial volvulus may impair lymphatic and venous drainage of the bowel, leading to swelling and enlargement of mesenteric lymph nodes observed in cases presenting intestinal peels (Beaudoin 2018).

During pregnancy complicated by fetal growth restriction, the blood flow in SMA may undergo changes, affecting intestinal perfusion and redistributes fetal circulation in response to hypoxia or hypovolemia. Kivilevitch et al. reported lower PI values for the superior mesenteric artery in IUGR fetuses, and interestingly, in these fetuses intestinal perfusion showed a protective effect from developing NEC. However, reduced intestinal blood supply is associated with an increased risk of necrotizing enterocolitis (NEC) in the neonatal period. In growth‐restricted pregnancies, studies showed that extreme SMA‐PI (> 97.5th centile) identified all neonates who subsequently developed necrotizing enterocolitis (Korszun et al. 2002; Kivilevitch et al. 2011).

In our analysis, neonates in the bowel matting group had a significantly lower median birthweight and birthweight percentile. These results show that bowel inflammation is not limited to the intestine but affects global fetal development. None developed NEC.

Our findings contribute to a growing body of evidence suggesting that traditional structural classification of gastroschisis into simple and complex types may be insufficient for guiding prenatal counseling and predicting neonatal outcomes. In our study, a substantial proportion of fetuses classified as sGS presented with pronounced signs of inflammation, manifesting postnatally as bowel matting, highlighting the importance of functional assessment beyond surgical classification alone (Jaczyńska et al. 2023; Botelho et al. 2022; Merritt 2022).

4.1. Practical Implications

In the late second and third trimester the fetal spine is often on the left or right side of the uterine cavity—the course of the SMA extends horizontally on the US resulting in an insonation angle close to 90 degrees. These imaging conditions can substantially affect SMA velocity measurements. Obtaining reliable measurements may require waiting for or actively encouraging a change in fetal position.

Therefore, SMA assessment requires additional examination time and repeated Doppler acquisitions at a clearly defined point of measurement during each examination. Measurements should be accepted only after several high‐quality, reproducible waveforms have been obtained for each fetus. Based on our experience, operators familiar with Doppler assessment of fetal vessels other than the umbilical artery and middle cerebral artery should be able to acquire interpretable SMA Doppler measurements after supervised assessment in a limited number of fetuses. However, during the learning curve, serial SMA assessment in each fetus is recommended, with particular attention to gate size, insonation angle correction, wall filter settings, noise reduction, image magnification, and potential interference from the umbilical artery signal.

4.2. Limitations

This study has several limitations. First, the sample size was relatively small, which may limit the generalizability of the findings and the statistical power to detect subtle associations. Second, the retrospective design inherently introduces the risk of selection and information bias, as data collection depends on the accuracy and completeness of existing medical records. Third, Doppler assessment of the extra‐abdominally located superior mesenteric artery—especially the measurement of PSV—requires technical expertise and is highly dependent on fetal position and insonation angle. The SMA assessment is difficult due to the position of the fetus's lower limbs and the course of the vessel being assessed close to the umbilical arteries at the AWD site.

The strength of this study is the material from a single tertiary center, in which fetal monitoring was performed using a consistent protocol and uniform evaluation throughout the entire study period. In addition, ultrasound examinations were performed by the same team throughout the study, which may increase the subjectivity of the assessment and results and also increases the likelihood of uniformity. The last ultrasound examination was performed shortly before delivery. We had photographic records of newborns taken immediately after birth, which allowed us to thoroughly analyze and compare the ultrasound images with macroscopic evaluation of the intestines.

5. Conclusions

Fetal SMA‐PSV is significantly associated with prenatal and postnatal signs of bowel inflammation in gastroschisis, such as wall thickening and bowel matting. This association appears independent of the simple/complex surgical classification. This supports the concept that PSV captures functional intestinal compromise rather than additional intestinal complications alone. Although technically demanding, SMA‐PSV may aid in prenatal risk stratification and delivery planning for selected cases of gastroschisis. Prospective multicenter studies with larger cohorts are now needed to confirm these findings and refine the clinical utility of PSV as a biomarker of fetal bowel inflammation.

Author Contributions

Renata Jaczyńska and Ewa Sawicka: conceptualization. Renata Jaczyńska, Boyana Mikulska, Anna Nimer, Tomasz Maciejewski, Dariusz Mydlak, and Ewa Sawicka: methodology. Renata Jaczyńska and Magda Rybak‐Krzyszkowska: software. Tomasz Maciejewski, Magda Rybak‐Krzyszkowska, and Ewa Sawicka: validation. Renata Jaczyńska, Anna Nimer, Dariusz Mydlak, and Boyana Mikulska: formal analysis. Renata Jaczyńska: investigation. Renata Jaczyńska, Boyana Mikulska, Anna Nimer, Magda Rybak‐Krzyszkowska, and Dariusz Mydlak: data curation. Renata Jaczyńska: writing – original draft preparation. Dariusz Mydlak, Anna Nimer, Boyana Mikulska, Ewa Sawicka, Magda Rybak‐Krzyszkowska, and Tomasz Maciejewski: writing – review and editing. Tomasz Maciejewski and Ewa Sawicka: supervision. Renata Jaczyńska: project administration. All authors have read and agreed to the published version of the manuscript.

Funding

The authors have nothing to report.

Ethics Statement

This study was conducted in accordance with the principles of the Declaration of Helsinki and adhered to all applicable standards of medical research ethics. The analyzed dataset consisted exclusively of anonymized clinical and sonographic records. As a retrospective analysis, the study does not meet the definition of a medical experiment under Article 21 of the Polish Act on the Medical Profession (consolidated text: Journal of Laws 2021, item 790), nor does it fulfill the criteria of a clinical trial as defined by Article 2(2)(2) of Regulation (EU) No. 536/2014, as incorporated into Polish law under the Act of 9 March 2023 on Clinical Trials of Medicinal Products for Human Use. Therefore, under the applicable national legislation, formal approval by a bioethics committee was not required for this project.

Consent

Written informed consent was obtained from the parents or legal guardians of the newborns for publication of the images and associated clinical data. All identifying information has been anonymized to protect patient privacy.

Conflicts of Interest

The authors declare no conflicts of interest.

Supporting information

Figure S1: Temporal analysis of SMA‐PSV values with fitted curves for fetuses with (red) and without (blue) bowel matting.

Figure S2: Predicted SMA‐PSV values in fetuses with (red) and without (blue) bowel matting based on GEE models.

BDR2-118-e70097-s001.docx (182.6KB, docx)

Acknowledgments

During the preparation of this work, the authors used ChatGPT by OpenAI to improve language clarity. The authors reviewed and edited the content and take full responsibility for it.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Figure S1: Temporal analysis of SMA‐PSV values with fitted curves for fetuses with (red) and without (blue) bowel matting.

Figure S2: Predicted SMA‐PSV values in fetuses with (red) and without (blue) bowel matting based on GEE models.

BDR2-118-e70097-s001.docx (182.6KB, docx)

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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