Paraduodenal Hernia With Intestinal Obstruction During Pregnancy

Introduction

An internal hernia is defined as the displacement of abdominal organs through normal or abnormal intraperitoneal foramina or defects into an abnormal compartment. In the narrow sense, it refers specifically to herniation of bowel loops through congenital pockets or openings in the visceral peritoneum. Clinically, the broad definition encompasses congenital and postoperative defects. Internal hernias are rare, with an autopsy incidence of 0.2% to 0.9%, and account for 0.6% to 5.8% of obstructions of the small bowel [1]. According to the incidence rate, Ghahremani classified internal hernias into: paraduodenal (50–55%), pericecal (10–15%), transmesenteric (8–10%), foramen of Winslow (6–10%), sigmoid (4–8%), and paravesical (<4%) hernias [2]. As the most common subtype, paraduodenal hernia (PDH) causes only 0.2% to 0.9% of intestinal obstructions. Based on anatomical characteristics and embryonic origin, PDH is categorized into 2 types: right-sided and left-sided paraduodenal hernias. Left-sided PDH occurs in Landzert’s fossa on the left abdomen, while right-sided PDH arises from Waldeyer’s fossa inferior to the duodenum and superior mesenteric artery. Right-sided PDH is rarer, accounting for approximately 25% of cases [3,4]. Due to its nonspecific clinical manifestations, PDH is often misdiagnosed or diagnosed late, potentially leading to bowel necrosis and peritonitis. When PDH is highly suspected, computed tomography (CT) of the abdomen should be performed for definitive diagnosis [5]. This report presents a case of right-sided PDH with intestinal obstruction in a pregnant woman that was successfully treated via laparoscopic surgery.

Case Report

A 33-year-old woman at 20 weeks 6 days gestation was admitted with “abdominal distension accompanied by nausea and vomiting for 2 weeks”. Half a month earlier, the patient developed intermittent abdominal distension and pain with nausea and vomiting, exacerbated by food intake. Emesis occurred 4 to 5 times daily, consisting of greenish fluid, with partial symptom relief after vomiting. Conservative management at an external hospital showed no improvement, prompting transfer to our institution. Since symptom onset, the patient maintained a normal mental status and urinary output but exhibited reduced defecation (once every 2–3 days) and flatus, poor dietary intake, and weight loss of 5 kg. During the patient’s prior pregnancy, she presented with analogous intractable vomiting, accompanied by abdominal distension and pain. The current pregnancy was terminated via medical abortion, using misoprostol. The patient reported that her symptoms subsequently resolved spontaneously, her clinical condition improved, and she was ultimately discharged from the hospital without a definitive diagnosis. The patient’s obstetric history was documented as G2P1A1L1 (gravida 2, para 1, abortion 1, living child 1). Her spouse and biological parents were in good health, and there was no family history of genetic disorders. Ten years earlier, the patient underwent a lower uterine segment cesarean delivery. She had no other past medical conditions and no known history of allergies.

Physical examination revealed vital signs were within the normal ranges. The abdomen was distended with palpable fullness and tenderness in the right upper quadrant, without rebound tenderness. Bowel sounds were diminished.

Laboratory test results showed leukocytosis (WBC: 13.83×109/L) and electrolyte disturbances (Na+: 127.4 mmol/L; Cl−: 85.6 mmol/L). Other parameters were unremarkable.

In the patient’s clinical course, nasogastric decompression yielded copious gastric contents. After 48 hours of conservative treatment with no improvement in symptoms, and with the abdominal pain and distension worsening, it was recommended to perform an enhanced abdominal CT scan. The patient provided informed consent regarding the fetal risks of CT. The CT scan revealed clustered small bowel loops forming a cystic dilatation superior to the transverse colon, absence of the third duodenal segment in its anatomical position, tortuous displacement of the superior mesenteric vein, and tortuous mesenteric vessels triggering collateral circulation development (Figure 1), consistent with right-sided PDH. The patient chose to terminate the pregnancy. During the conservative treatment period, the patient was instructed to maintain nil per os. Therapeutic interventions included parenteral nutrition support, inhibition of digestive juice secretion, prophylactic anti-infective treatment, correction of hyponatremia and hypochloremia, and potassium supplementation adjusted according to urine output. After the patient’s current acid-base imbalance and electrolyte disorders were corrected, she was transferred to the Department of Obstetrics and Gynecology for surgical intervention. Following pregnancy termination, the patient’s abdominal distension and other symptoms did not alleviate significantly; therefore, she was further transferred to the Department of Gastrointestinal Surgery for surgical management. The patient received oral contrast preoperatively and underwent a follow-up abdominal CT scan. The results showed that the gastric cavity and proximal duodenum were dilated and filled, a small amount of contrast medium was visible in the distal small intestine, and the mesenteric vessels were still tortuous (Figure 2).

After providing written informed consent for surgery, the patient underwent laparoscopic exploration. During the procedure, in the right upper abdomen, loops of the small intestine and part of the ascending colon were found herniated through the right PDH orifice (in the region of the Waldeyer’s fossa) (Figure 3A). The herniated intestinal segments showed dilation and serosal hyperemia, with no transmural necrosis or perforation noted. No physiological adhesive fixation was present between the right colonic mesentery and the posterior peritoneum, and the ascending colon appeared as an “intraperitoneal organ” with a significantly increased degree of mobility (Figure 3B). A wide gap (hernia orifice) existed between the root of the right colonic mesentery and the posterior peritoneum, through which the intestinal loops herniated into the lateral space of the ascending part of the duodenum. The duodenal bulb and descending segment were densely adherent to the surrounding posterior peritoneum and colonic mesentery, resulting in angular distortion; the proximal duodenum was dilated (with a diameter of approximately 3.5 cm). The incarceration was relieved, and all herniated contents (small intestine and ascending colon) were completely reduced. After reduction, the intestinal segments were observed to have a bright red color, smooth serosa, good mesenteric vascular pulsation, and recovered peristalsis, ruling out ischemic injury. The ultrasonic scalpel was used for meticulous dissection of the adhesions between the duodenal bulb, descending duodenum, posterior peritoneum, and colonic mesentery. This eliminated the angular deformity and restored the natural course of the intestinal tract. The dilation of the proximal duodenum was relieved, and the patency of the intestinal lumen was restored. The operation was completed successfully. The patient remained hemodynamically stable and was returned to the ward. Recovery was satisfactory: liquid diet was tolerated on postoperative day 3 without discomfort, and discharge occurred on postoperative day 5. Three-month follow-up showed no symptoms.

Discussion

PDH was first described in 1786 by Neubaur, who attributed it to a peritoneal developmental defect [6]. Moynihan proposed that PDH results from physiological adhesions formed during intestinal re-entry into the abdominal cavity and fusion of the dorsal mesentery with the posterior abdominal wall, leading to the development of fusion folds and physiological recesses. Right-sided PDH occurs due to a congenital anomaly, where the ascending colonic mesentery fails to fuse with the parietal peritoneum. This results in a rare defect occurring in the proximal mesenteric root of the jejunum, observed in no more than 1% of autopsies [7,8]. Current consensus indicates PDH occurs as a result of midgut malrotation and defective fusion between the mesentery and retroperitoneum. Studies classify right-sided PDH into 3 types, based on embryology and anatomy: type 1 (most common) features a morphologically intact duodenum with normal horizontal/ascending segments and an anatomically normal Treitz ligament; type 2 involves partial entry of the horizontal duodenum into the hernial sac with absence of the Treitz ligament; and type 3 includes type 2 characteristics with additional extension of Ladd’s band from anomalous cecal sites to the peritoneum or liver, where this band traverses and compresses the duodenum or small bowel, predisposing to obstruction [9]. PDH manifests with nonspecific gastrointestinal symptoms. Abdominal pain (96.7%) is most frequent, followed by vomiting (66.7%), nausea (34.0%), signs of bowel obstruction (32.7%), and fever (6.5%), with no significant difference between left- and right-sided PDH presentations [10]. In clinical practice, when a patient presents with chronic abdominal pain, abdominal distension, or acute abdominal pain, a high degree of suspicion for internal hernia should be raised. Due to the lack of specific clinical manifestations of internal hernia, misdiagnosis or delayed diagnosis often occurs; internal hernia is easily confused with acute abdominal conditions such as gastrointestinal perforation and appendicitis in emergency settings [11]. In the present case, the patient had received conservative treatment for intractable hyperemesis gravidarum at an external hospital, while the occurrence of an internal hernia was overlooked. Abdominal CT is the preferred imaging modality for diagnosing internal hernias and conducting preoperative evaluations. Compared with traditional imaging techniques, CT offers distinct advantages in localizing the obstruction site, identifying the cause of obstruction, and assessing ischemic changes in the intestinal tract. By virtue of high-quality 3-dimensional post-processing techniques, such as multiplanar reconstruction, maximum-intensity projection, and volume rendering, CT can clearly visualize the small intestine and its surrounding structures, thereby improving the diagnostic accuracy of localizing the obstruction transition zone. A small-bowel obstruction caused by internal hernias is mostly a closed-loop obstruction, which refers to the simultaneous obstruction at 2 adjacent points of a segment of the intestinal tract. The direct CT signs of this condition mainly include fluid-distended intestinal loops presenting a U-shaped or C-shaped appearance, and distended intestinal loops arranged in a radial pattern, accompanied by traction and thickening of mesenteric blood vessels that converge toward a central point. If clusters of distended intestinal loops in an abnormal anatomical location or a “cystic” aggregation of the small intestine are observed within the hernia sac, it highly suggests the possibility of an internal hernia. Therefore, the main CT methods for diagnosing internal hernias include detecting intestinal closed loops, identifying the hernia sac neck, and analyzing the abnormal displacement of the hernia sac neck, surrounding structures, and key blood vessels [12,13]. In the absence of contraindications, all patients should undergo abdominal contrast-enhanced CT with intravenous contrast medium. Contrast enhancement can also evaluate the blood flow of hernial contents and assess the severity of small-bowel strangulation. Additionally, it enables clearer visualization of the mesenteric blood vessels – landmark vessels that pass through or enter the hernia sac neck and surrounding structures – which helps confirm the diagnosis of internal hernia and identify its type. Among the abdominal CT signs, a hallmark of right-sided PDH is a cluster of encapsulated small-bowel loops localized in the right mid-abdomen, lateral to the descending segment of the duodenum, with the superior mesenteric artery and superior mesenteric vein extending along the anteromedial margin of Waldeyer’s fossa [5]. Over half of PDH cases progress to bowel obstruction (with or without strangulation), having a mortality risk of 20% to 50% [14,15]. Obstruction represents the terminal evolution, necessitating surgical intervention [16]. Surgical approaches for PDH are selected based on anatomical characteristics and include the following: (1) enlargement of the hernial orifice followed by anatomical reduction (most common), (2) primary closure of the defect, with or without mesh reinforcement, and (3) hernial sac excision followed by defect closure [10]. Regardless of approach, bowel resection is mandatory when strangulated segments are identified. In the present case, we performed enlargement of the hernial orifice with adhesiolysis between the ring and small bowel mesentery. This allowed reduction of hernial contents to their normal intraperitoneal position without defect closure. This decision was based on the patient’s complete absence of the ascending mesocolon and failure of physiological retroperitoneal attachment, resulting in extreme mobility of the ascending colon and formation of a large hernia sac. To avoid injury to the superior mesenteric artery and vein, which could cause massive hemorrhaging, we deliberately refrained from further opening or resection of the hernia sac [6,17]. Studies indicate that laparoscopic surgery reduces postoperative pain, shortens hospitalization, and lowers perioperative morbidity, in comparison with open surgery [10,18]; conversion to laparotomy is advised when bowel necrosis or intestinal distension compromises the operative space.

Conclusions

In conclusion, although PDH is rare, it causes intestinal obstruction and complications in over 50% of cases. Its nonspecific clinical manifestations frequently lead to misdiagnosis or delayed diagnosis, warranting particular clinical attention during management. For patients with suspected internal hernia or unexplained intestinal obstruction, prompt abdominal CT examination is essential. Once PDH is diagnosed, timely surgical intervention is required. With advancements in laparoscopic techniques, early diagnosis followed by laparoscopic intervention offers improved clinical outcomes and lower complication rates.