Recurrent Congenital Hiatal Hernia After Laparoscopic Repair Complicated by Gastric Perforation and Abdominal Compartment Syndrome

ABSTRACT

Complete excision of the hernial sac during congenital hiatal hernia repair may help prevent recurrence. This case also emphasizes the importance of early recognition and prompt management of abdominal compartment syndrome when progressive abdominal distension and organ dysfunction develop postoperatively.

1. Introduction

Congenital hiatal hernia is a rare condition, with clinical manifestations ranging from vomiting and respiratory infections to anemia and failure to thrive [1]. While laparoscopic repair is widely performed, recurrence remains an infrequent but clinically significant complication [2, 3].

Here, we report a case of recurrent congenital hiatal hernia after laparoscopic Nissen fundoplication, presenting with gastric perforation. The postoperative course was further complicated by perforation of the sigmoid colon and abdominal compartment syndrome (ACS). This case highlights the importance of complete hernial sac excision during the initial repair to reduce the risk of recurrent hiatal hernia and associated serious complications.

2. Case History/Examination

A previously healthy 7‐month‐old male infant presented with fever and cough. On physical examination, the abdomen was flat and soft, with no nausea or vomiting.

3. Investigations and Treatment

Chest radiography revealed an abnormal opacity in the right lower lung field. Chest–abdominal computed tomography (CT) revealed herniation of the stomach, small intestine, and colon through the esophageal hiatus, consistent with a Type IV hiatal hernia (Figure 1a). After enteral nutrition was established via a feeding tube, elective laparoscopic repair was performed.

FIGURE 1.

Radiography and intraoperative images. (a) Chest–abdominal computed tomography demonstrates herniation of the stomach, small intestine, and colon through the esophageal hiatus. (b) After reduction of the small intestine and colon into the abdominal cavity, the hiatal defect is identified. (c) The hernia sac is retracted into the abdominal cavity. It is large and associated with dense adhesions. (d) The hiatal defect is closed with interrupted sutures. (e) Chest–abdominal computed tomography reveals gastric volvulus with free air and ascites. (f) Plain abdominal radiography demonstrates dilated bowel loops consistent with ileus and elevation of the diaphragm. The intraoperative videos were recorded using an Olympus laparoscopic imaging system (Olympus, Tokyo, Japan) and saved in MP4 format. Still images were extracted using Microsoft Clipchamp (Microsoft Corporation, Redmond, WA, USA), and GIMP (GNU Image Manipulation Program) was used solely to adjust image resolution for publication. No adjustments were made to the brightness, contrast, color balance, saturation, or other aspects of the image appearance.

The entire stomach herniated into the thoracic cavity after reduction of the small intestine and colon (Figure 1b). Dense inflammatory adhesions were observed around the hiatus (Figure 1c). The hernial sac was resected as much as possible; however, complete excision was not feasible. A standard Nissen fundoplication was also performed. The crura were approximated with four interrupted 3‐0 nonabsorbable sutures, narrowing the hiatus to a size that allowed the insertion of a 5‐mm forceps (Figure 1d). A 2.5‐cm fundic wrap was then created and secured to the right crus using a single suture.

The patient resumed oral feeding on postoperative Day 3, and was discharged on Day 10. Seven months later, the patient developed intermittent vomiting and dysphagia. Imaging revealed recurrent hiatal hernia with intrathoracic stomach migration. Nine months postoperatively, the patient presented with shock while awaiting reoperation. CT revealed a gastric volvulus with free air and ascites, suggesting gastrointestinal perforation (Figure 1e).

Emergency surgery required conversion to open laparotomy because of the dense adhesions. The perforation at the gastric angle was repaired, and the residual hernia sac was completely excised. The hiatus was reconstructed in the same manner as during the initial operation, and a new fundoplication wrap was created. The histopathological examination revealed no evidence of connective tissue disease.

4. Outcome and Follow‐Up

Postoperatively, the patient developed abdominal distension, which was initially attributed to postoperative paralytic ileus secondary to opioid analgesia. However, the abdominal distension progressively worsened and was accompanied by respiratory deterioration (Figure 1f). Therefore, on postoperative Day 4, a transanal decompression tube was placed under fluoroscopic guidance and advanced to the ascending colon to relieve the abdominal distension.

Despite the placement of a transanal decompression tube, abdominal tension, oliguria, tachycardia, and respiratory compromise worsened by postoperative Day 6. There were no clear clinical or radiological findings suggestive of gastrointestinal perforation before emergency exploration; despite persistent high fever, the C‐reactive protein level had gradually declined, and serial abdominal radiographs showed no free intraperitoneal air. The initial intravesical pressure was 45 mmHg, confirming ACS. Emergency exploration revealed a 1.5‐cm perforation of the sigmoid colon. Segmental colectomy with primary anastomosis was performed, which reduced the intravesical pressure to 12 mmHg. Histopathological examination demonstrated marked lymphocytic and neutrophilic infiltration around the perforation site, with ischemic changes in the adjacent mucosa. The patient was discharged 1 month later, and has remained recurrence‐free after 5 years of follow‐up.

5. Discussion

Hiatal hernias are classified into Type I (sliding) and Types II–IV (paraesophageal) hernias [1]. In a relatively large series of congenital hiatal hernias treated laparoscopically (n = 136), the recurrence rate was found to be 3.8%, and four patients required conversion to open surgery [2]. No significant difference in recurrence was observed between Nissen–Rossetti fundoplication (2.8%) and Thal fundoplication (5.0%) [2]. Cheng et al. reported a recurrence rate of 12.7% among 79 pediatric patients undergoing laparoscopic fundoplication for hiatal hernias, with no significant differences between Type I and Types II–IV hernias [3]. In contrast, a large adult study suggested that recurrence and postoperative complications were more frequent in patients with Type II–IV hernias [4].

Cheng et al. reported that the most common causes of recurrence were inadequate closure of the enlarged hiatus and loosening of crural sutures [3]. Complete excision of the hernial sac is generally recommended during paraesophageal hiatal hernia repair because it facilitates adequate mediastinal mobilization of the esophagus and tension‐free positioning of the distal esophagus and stomach within the abdominal cavity [5, 6, 7, 8]. Conversely, incomplete excision of the hernial sac may result in persistent tension or traction on the hiatus, thereby facilitating hernia recurrence. In the present case, the hiatus appeared adequately narrowed during the initial operation, and no loosening of the crural sutures was observed during reoperation. In contrast, residual hernial sac tissue was found and completely excised during the second procedure. Although direct evidence is limited, the residual hernial sac may have contributed to recurrence by maintaining tension or traction on the hiatus and providing a potential pathway for re‐herniation into the thoracic cavity.

The precise cause of the sigmoid colon perforation remains uncertain. Marked bowel distension has been reported to cause intestinal ischemia and subsequent perforation [9, 10]. In the present case, marked bowel distension persisted postoperatively; moreover, histopathological examination revealed ischemic changes in the mucosa surrounding the perforation. These findings suggest that the bowel distension may have caused localized ischemic injury, predisposing the bowel wall to perforation. Additional mechanical stress from the transanal decompression tube may also have contributed to the perforation.

ACS is a rare but life‐threatening condition characterized by sustained elevation of intra‐abdominal pressure and organ dysfunction. Gastrointestinal perforation, peritonitis, ileus, and postoperative abdominal complications are recognized risk factors [11]. Management of ACS includes gastrointestinal decompression (nasogastric drainage, rectal or colonic decompression, enemas, and prokinetic agents), fluid management, and surgical decompression when conservative measures fail [11, 12]. In our case, before the diagnosis of ACS, progressive abdominal distension necessitated escalation of ventilatory support. Given that transanal decompression using a rectal tube is an established approach for relieving bowel distension in pediatric conditions such as Hirschsprung disease [13], we selected transanal tube decompression in this case.

In children, intra‐abdominal hypertension (IAH) is defined as a sustained or repeated elevation in intra‐abdominal pressure > 10 mmHg, whereas ACS is defined as intra‐abdominal pressure > 10 mmHg associated with new or worsening organ dysfunction attributable to elevated IAP [12]. In the present case, intestinal perforation likely occurred on postoperative Days 5–6 and subsequently contributed to the development of ACS. The initial intravesical pressure measurement revealed a markedly elevated pressure of 45 mmHg, enabling prompt diagnosis and timely surgical intervention before irreversible organ injury could occur. However, marked abdominal distension had persisted before the diagnosis of ACS. Persistent or progressive abdominal distension after abdominal surgery should prompt early measurement of intra‐abdominal pressure, which may allow recognition and intervention at the stage of IAH before progression to ACS.

This case has several limitations. First, although the residual hernial sac may have contributed to recurrence, a direct causal relationship cannot be established; moreover, other factors contributing to recurrence cannot be completely excluded. Second, the precise mechanism of the sigmoid colon perforation remains uncertain. Although histopathological findings suggested ischemic injury associated with marked bowel distension, additional mechanical stress from the transanal decompression tube may also have contributed. Nevertheless, this case provides clinically relevant insights into potential mechanisms of recurrent congenital hiatal hernia and emphasizes the importance of early recognition of IAH in postoperative patients with progressive abdominal distension.

6. Conclusion

This case highlights the importance of complete hernial sac excision during primary repair of congenital hiatal hernia to reduce the risk of recurrence. It also emphasizes that early measurement of intra‐abdominal pressure should be considered in postoperative patients with persistent or progressive abdominal distension, to allow early recognition of IAH and timely intervention before progression to ACS and irreversible organ injury.

Author Contributions

Takayuki Fujii: conceptualization, data curation, visualization, funding acquisition, writing – original draft, investigation. Yui Noguchi: supervision, project administration. Nanami Harada: supervision, project administration. Hiroto Katami: supervision, project administration. Aya Tanaka: supervision, writing – review and editing.

Funding

This work was supported by JSPS KAKENHI (grant number JP 23K07313).

Consent

Written informed consent from the patient was obtained according to journal guidelines.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

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