https://orcid.org/0009-0006-5857-5052
Abstract
A 38-year-old woman with a history of Roux-en-Y gastric bypass (RYGB) 2 years prior presented to the bariatric clinic on multiple occasions with postprandial abdominal pain and bloating and bilateral lower extremity edema. Abdominal pain did not improve despite antiacid medication and dietary recommendations. Computed tomography scan of the abdomen revealed an internal hernia (IH) through Petersen’s defect (a potential space between the Roux limb and transverse colon), with a mass effect on the inferior vena cava by herniated bowel. Diagnostic laparoscopy confirmed the diagnosis. Reduction of the hernia and defect closure resulted in full symptom resolution. This case highlights the importance of high clinical suspicion for IH in any patient with a history of RYGB and abdominal pain, even when symptoms are chronic and/or atypical. Early recognition is important for prompt treatment and prevention of bowel ischemia and necrosis.
Introduction
The Roux-en-Y gastric bypass (RYGB) procedure is a widely performed bariatric procedure and provides an effective long-term treatment for obesity [1]. Early recognition of post-operative complications improves outcomes. A feared complication of RYGB is an internal hernia (IH) through the mesojejunal and Petersen’s defects. Petersen’s defect is a potential space created between the Roux-limb mesentery and the transverse mesocolon. This complication is thought to occur after 2.1%–2.14% of procedures [2, 3]. Internal herniation through Petersen’s defect poses significant risks such as bowel ischemia and gangrene [4]. IH can present with non-specific symptoms, requiring high clinical suspicion from physicians treating post-RYGB patients.
Case presentation
A 38-year-old female with a history of RYGB (antecolic, antegastric; Roux limb 150 cm, biliopancreatic limb 50 cm) performed 2 years earlier presented for evaluation. Due to her high preoperative body mass index (BMI) of 58.5 kg/m2, she had been restarted on tirzepatide postoperatively and achieved significant weight loss. Her weight stabilized at 140 lb, down from a maximum of 330 lb, corresponding to a BMI of 25.1 kg/m2. Her maintenance tirzepatide dose was 12.5 mg weekly.
She presented to the obesity medicine and bariatric surgery clinic with bilateral lower-extremity edema, nonspecific abdominal discomfort, and bloating. The leg edema worsened later in the day. The abdominal bloating and discomfort were postprandial resulting in decreased oral intake and an additional 10-lb unintentional weight loss. She also reported lightheadedness upon standing.
On examination, her blood pressure was 99/62 mmHg, heart rate 65/min, and temperature 36.8°C. She had bilateral 2+ pitting edema without other abnormal findings on abdominal exam. Laboratory studies showed normal electrolytes, mildly elevated aspartate aminotransferase and alanine aminotransferase (77 and 105 U/L, respectively), low albumin (3.7 g/dL; normal 3.8–4.8); other nutritional markers were within normal limits. She was advised to increase dietary protein and undergo further evaluation. Obesity medicine initiated a workup for hepatic, renal, and nutritional etiologies and began discussions regarding reducing her tirzepatide dose. Ordered tests included serum protein electrophoresis, an acute hepatitis panel, iron studies, zinc, vitamin levels, peripheral smear review, urinary oxalate, urine protein/creatinine ratio, kappa/lambda free light chains, abdominal ultrasound, complete blood count, and differential. All lab results were within normal limit except hypogammaglobulinemia.
In 2-week follow-up, she had the same symptoms and had not responded to an addition of proton pump inhibitor therapy. Additional dietary recommendations were provided while considering tirzepatide dose reduction.
One week later, she presented to the emergency department with generalized food-related abdominal pain and worsening bloating for three days. A computed tomography (CT) scan was interpreted as showing no acute pathology, however, retrospective review revealed subtle mesenteric swirling suggestive of an IH. She was discharged with outpatient follow-up, but at her bariatric clinic visit three days later she reported ongoing symptoms. After referral back to the emergency department, a repeat CT scan demonstrated a clear mesenteric swirl sign [5] (Fig. 1) consistent with an IH through Petersen’s defect, with compression effect on the inferior vena cava (IVC) (Fig. 2).
Abdominal axial CT showing the mesenteric swirl sign from the small bowel internal hernia at approximately L2.
Sagittal abdominal CT showing internal hernia of the small bowel and associated compression of the IVC.
She was taken for diagnostic laparoscopy, which revealed herniation of the entirety of the jejunojejunostomy through Petersen’s defect. The hernia was reduced, and the defect was closed with a running nonabsorbable suture [6]. Recovery was uncomplicated and she was discharged on postoperative day two. At her 2- and 4- weeks follow-up visits, all symptoms including leg edema, abdominal pain and bloating, and 10-lb weight loss had resolved.
Discussion
Retrospective review of both CT scans demonstrated IH through Petersen’s defect, with associated compression of the IVC. This radiologic finding provides a plausible explanation for the patient’s initial symptoms of bilateral lower-extremity edema, as impaired venous return from IVC compression can clinically mimic peripheral venous congestion [7].
IH after RYGB is a known complication and can occur through the jejunojejunostomy mesenteric defect or the space between the Roux limb and transverse mesocolon [3] (Fig. 3). Common acute phase symptoms of internal hernias include nausea with or without emesis, and abdominal pain [8] which can vary in location but often correlates with the side in which the hernia occurred [9]. Our patient’s subacute presentation of bilateral lower extremity edema, however, appears to be less common. We suggest that the mechanism of symptomatology was likely due to herniation of the small bowel and jejunojejunostomy through Petersen’s defect with pressure effect on the IVC, causing partial IVC occlusion and thus lower-extremity venous congestion. A similar process has been described in cases of pancreatic pseudocyst causing IVC compression, suggesting that a mass effect close to that anatomical location could produce comparable hemodynamic consequences [10].
Locations for internal hernia through Petersen’s defect (arrow ‘2’) and the jejunojejunostomy mesenteric defect (arrow ‘1’) after an antecolic approach RYGB. Reproduced with permission from de Bakker JK, et al. [5].
This case highlights the importance of maintaining a high index of clinical suspicion for IH in post-RYGB patients, even when abdominal pain is not acute, associated symptoms are atypical, and imaging findings are initially subtle. Use of multi-detector CT is helpful for detection of IH due to its high sensitivity and specificity for the mesenteric swirl sign [4, 11]. Other CT findings can be mesenteric vascular congestion or edema, clustered small bowel loops, abnormal bowel positioning, mesenteric vessel engorgement, signs of small bowel obstruction, and in advanced cases, signs of bowel ischemia. Early recognition and timely surgical intervention are essential to resolve secondary vascular obstruction and to prevent progression to bowel ischemia [4, 12]. Routine closure of mesenteric defects, including Petersen’s space and the jejunojejunostomy defect is recommended to reduce the incidence of postoperative IH [13]. Prophylactic closure of Petersen’s defect is estimated to be completed by 78.68% of surgeons [14], has been shown to reduce the risk of internal herniation by close to 70% [13], and reduces risk of bowel ischemia [2, 15].
This patient presented with bilateral lower extremity edema, several weeks of non-specific abdominal pain, bloating, and this subacute presentation has not been well documented. This case highlights the importance of both prophylactic closure of Petersen’s space during the initial procedure and of high clinical suspicion for internal hernia in any patient with a history of RYGB, even when presenting symptoms seem to be non-specific or atypical.
Conflicts of interest
None.
Funding
There is no funding to disclose.
Conference presentation
This case report has been presented as a poster at the 2026 Annual Meeting of the American Society of Metabolic and Bariatric Surgery.
