Laparoscopic one-stage repair of concurrent Morgagni hernia and hiatus hernia: A case report and review of literature

Abstract

BACKGROUND

Morgagni hernia (MH) is a rare congenital diaphragmatic defect that is extremely rare when concomitant with hiatus hernia (HH), and there are only a few cases reported in the world literature. Surgical treatment is the definitive treatment for MH, and in clinical practice, laparoscopic surgery is the first line of minimally invasive approach for diaphragmatic hernia repair.

CASE SUMMARY

A 73-year-old female patient, with heartburn and occasional dry cough for one year, was thought to have gastroesophageal reflux disease. Preoperative imaging and endoscopic examinations were completed in a comprehensive way, and the diagnosis of right-sided MH, sliding HH, and non-atrophic gastritis was made. She underwent laparoscopic tension-free one-stage repair of both diaphragmatic hernias combined with 270-degree Toupet fundoplication under general anesthesia. The operation went smoothly. To ensure safe gastrointestinal recovery, the patient was kept nil per os with exclusive parenteral nutrition on postoperative day one. Water was permitted on day two, followed by a liquid diet on day three, at which point parenteral nutrition was completely discontinued. She returned to a normal diet within one week. At her 12-month follow-up, she reported zero reflux symptoms, and scans showed no recurrence.

CONCLUSION

Concurrent Morgagni and HHs are safely resolved by single-stage laparoscopic repair using biological mesh and Toupet fundoplication.

Key Words: Morgagni hernia; Hiatus hernia; Laparoscopic repair; Toupet fundoplication; Biological mesh; Case report

Core Tip: Concurrent Morgagni hernia and hiatus hernia is an extremely rare clinical condition with limited reported cases globally. Laparoscopic one-stage tension-free repair with biological mesh combined with 270° Toupet fundoplication is safe, minimally invasive and clinically effective. It achieves ideal anatomical reconstruction of diaphragmatic defects, fully alleviates patient symptoms and maintains excellent long-term outcomes, and no hernia recurrence was detected during regular follow-up.

INTRODUCTION

Morgagni hernia (MH), also known as parasternal hernia, was first described by Giovanni Battista Morgagni in his anatomical monograph in 1761 and remains a rare congenital diaphragmatic anomaly, accounting for approximately 3% of all congenital diaphragmatic hernias[1,2]. Its pathogenic mechanism has not been fully elucidated to date. Adult MH is mostly asymptomatic and is often incidentally detected on chest imaging performed for other indications. Once diagnosed, surgical repair is routinely indicated to avoid life-threatening complications such as intestinal incarceration and obstruction[2].

Hiatus hernia (HH) is far more prevalent than MH. It has a prevalence of up to 60% in the population over 50 years of age[3]. The concurrence of these two conditions, one a rare retrosternal diaphragmatic defect and the other a common gastroesophageal junction anomaly, is an extremely rare clinical entity. Less than 20 cases of concurrence of MH and HH have been found in a literature review. Early English papers mainly described traditional open surgical cases, and detailed records remain scarce[4-8]. In recent decades, researchers have published several complex cases treated with minimally invasive surgery[9-13]. Scholars from Japan[14-16] and China[17,18] have also documented this rare combination of conditions in their studies. These defects have an underlying pathophysiological link. In elderly patients, the relentless age-related degradation of the phrenoesophageal membrane, combined with systemic collagen metabolic derangements, weakens the global diaphragmatic integrity. This progressive structural failure unmasks a dormant congenital Morgagni defect and, at the same time, allows the stomach to herniate through an acquired, widened esophageal hiatus[19].

Historically, open laparotomy was the mainstay for the treatment of combined diaphragmatic hernias, which is associated with severe postoperative pain and a prolonged recovery period. In contrast, laparoscopic surgery is more optimal in most cases with minimal tissue trauma, low complication rate, and accelerated postoperative recovery. Now it is the gold standard for the repair of complex diaphragmatic hernias[2,20]. Robotic-assisted surgery offers superior surgical precision in complex procedures, but its clinical application is limited by high costs and the requirement for specialized surgical training[12,21,22]. In this report, we present a case of a 73-year-old female with concurrent right-sided MH and sliding HH who received surgical treatment by laparoscopic one-stage tension-free repair with biological mesh augmentation and subsequent 270-degree Toupet fundoplication. A surgical video showing the important operative steps is attached to this report with the aim of giving a clinical reference in the management of similar complex cases (see Video).

CASE PRESENTATION

Chief complaints

A 73-year-old female Chinese patient presented to our department with a one-year history of persistent heartburn and intermittent dry cough.

History of present illness

The patient presented with heartburn and a dry cough onset one year ago. Clinical symptoms have progressively worsened recently, which has led to a hospital admission.

History of past illness

The patient denied any prior medical illnesses.

Personal and family history

The patient denied any personal and family history.

Physical examination

The vital signs were as follows: Body temperature, 36.5 °C; blood pressure, 132/81 mmHg; heart rate, 72 beats per minute; respiratory rate, 19 breaths per minute. Body mass index: 18.3 kg/m², height: 155 cm, weight: 44 kg. No abnormalities were found on physical examination.

Laboratory examinations

Comprehensive preoperative laboratory examinations were conducted on September 13, 2021, covering blood routine, blood grouping, coagulation function, serum biochemistry and infectious disease screening. The patient was blood type A with Rh-positive factor. Mild abnormalities included decreased neutrophil percentage, elevated monocyte and eosinophil counts, slightly lowered total protein and increased lactic acid. All other hematological, coagulation, hepatic, renal, lipid and electrolyte indicators were normal. Besides, all infectious disease screening results were negative.

Imaging examinations

As the first diagnostic modality, an upper gastrointestinal contrast study was performed. We noted a cystic lesion above the diaphragm with herniation of gastric mucosa, with normal esophageal peristalsis, which is highly suggestive of HH (Figure 1A). By fluoroscopy, we noted an abnormal soft tissue shadow at the right cardiophrenic angle, and we decided to perform the cross-sectional imaging in order to evaluate the mediastinal structure. Gastroscopy confirmed the diagnosis of sliding HH (Figure 1B) and also found the presence of non-atrophic gastritis and duodenal bulb inflammation. There was no active ulceration or neoplastic lesions in the upper gastrointestinal tract. Notably, no Helicobacter pylori testing was performed to evaluate these inflammatory mucosal changes during her preoperative evaluation. For further characterization of the cardiophrenic mass, enhanced chest computed tomography (CT) and magnetic resonance imaging were performed. These showed the 5.4 cm diaphragmatic defect at the retrosternal region. Herniation of the greater omentum and abdominal adipose tissue through the defect into the thoracic cavity formed a soft tissue mass measuring 5.9 cm × 6.2 cm × 6.3 cm (Figure 1C-E), and there were no signs of intestinal incarceration or strangulation. Detailed evaluation of the esophageal hiatus demonstrated widening of the bilateral diaphragmatic crura to about 4.5 cm and herniation of the gastric fundus into the posterior mediastinum (Figure 1F-H). The last image (Figure 1I) presents a picture obtained at postoperative day 7 showing the integrity of the retrosternal and esophageal hiatus repairs, with proper positioning of both biological meshes, and no significant fluid collection.

Figure 1 Pre- and postoperative imaging findings of the patient. A: Preoperative upper gastrointestinal contrast study; B: Preoperative gastroscopy; C-E: Preoperative chest computed tomography scans (axial, sagittal, and coronal planes); F-H: Preoperative chest magnetic resonance imaging scans demonstrating the two distinct diaphragmatic defects; I: Postoperative chest computed tomography scan at one week showing successful repair of both hernias.

FINAL DIAGNOSIS

Combined with the patient’s medical history, our final diagnosis included a right-sided MH, a sliding HH, non-atrophic gastritis, duodenal bulb inflammation, and gastroesophageal reflux disease (GERD).

TREATMENT

Our plan was a single-stage laparoscopic tension-free repair of both hernias with a Toupet fundoplication.

Surgical procedure

After induction of general anesthesia and endotracheal intubation, the patient was placed in the supine position with a 30-degree reverse Trendelenburg tilt to facilitate caudal displacement of abdominal viscera by gravity. Pneumoperitoneum was established at an intra-abdominal pressure of 12 mmHg via a 10 mm umbilical trocar. Laparoscopic exploration revealed a diaphragmatic defect greater than 4 cm in diameter at the retrosternal region to the right of the falciform ligament, with the greater omentum as the only hernia content (Figure 2A). The hernia content was gently reduced into the peritoneal cavity with atraumatic graspers, and a well-defined 4 cm × 6 cm hernia orifice was seen.

Figure 2 Intraoperative laparoscopic findings and key operative steps. A: Laparoscopic exploration revealing a retrosternal right-sided diaphragmatic defect with the greater omentum as the hernia content; B: Primary suture closure of the Morgagni hernia defect; C: Fixation of the biological mesh for defect augmentation; D: Laparoscopic visualization of the sliding hiatus hernia; E: Complete reduction of the herniated gastric fundus into the abdominal cavity with full mobilization of the gastric fundus and distal esophagus; F: Primary suture reconstruction of the bilateral diaphragmatic crura; G: Augmentation repair of the esophageal hiatus with biological mesh; H: 270-degree “U” shaped Toupet fundoplication around the gastroesophageal junction.

Three additional 5 mm working trocars were placed in the upper abdomen. The MH defect was closed with a continuous 2/0 absorbable barbed suture in a medial-to-lateral fashion (Figure 2B). For durable repair and reduction of recurrence risk, we used a 13 cm × 15 cm porcine small intestinal submucosa biological mesh (Trade name: Inguinal Hernia Biological Mesh, Model: SIS-HRP-BL-13*15 manufactured by Beijing Biosis Healing Biological Technology Co., Ltd., Beijing, China; National Medical Products Administration registration No. 20183130498). The mesh was fixed with absorbable tacks at 1 cm intervals and further reinforced with a continuous 3/0 absorbable barbed suture along the mesh perimeter (Figure 2C).

Then the left hepatic lobe was retracted to expose the esophagogastric junction and esophageal hiatus. The esophageal hiatus was markedly dilated to about 3 cm in diameter with the herniation of a large part of the gastric fundus. After carefully reducing the herniated gastric fundus into the abdominal cavity, the distal 5 cm of the esophagus was fully mobilized to achieve tension-free fundoplication. We incised the gastrophrenic ligament, then subsequently ligated and divided the short gastric vessels and gastro-splenic ligament (Figure 2D-E).

Reconstruction of the bilateral diaphragmatic crura was performed with interrupted 2/0 non-absorbable sutures posterior to the esophagus (Figure 2F). To prevent postoperative re-widening of the esophageal hiatus and avoid neurovascular injury associated with tack fixation in this narrow anatomical region, a biological mesh was placed over the reconstructed diaphragmatic crura and reinforced with absorbable sutures and cyanoacrylate medical glue (Figure 2G).

For the management of GERD, the anatomical reconstruction of the gastroesophageal junction was completed with a 270-degree Toupet fundoplication (Figure 2H). The fully mobilized gastric fundus was passed posterior to the esophagogastric junction and fixed to the anterior and posterior walls of the distal esophagus with six interrupted 3/0 absorbable sutures, with the suture depth limited to the muscular layer to avoid mucosal injury. It is to be underlined that no intraoperative esophageal bougie and no endoscopic assistance were used for the crural closure or the subsequent fundoplication. The trocar sites were closed in layers after confirming no active bleeding and after completion of the instrument and sponge count. The total operative time was 120 minutes with an estimated blood loss of less than 20 mL. The key operative steps were recorded and compiled into a surgical video accompanying this report vignette (see Video).

OUTCOME AND FOLLOW-UP

Recovery on the ward was smooth. We adopted a very conservative nutritional recovery protocol, given her very advanced age and very frail constitution. The patient was kept strictly nil per os regimen and on total parenteral nutrition on postoperative day one. On day two, she was allowed to drink water, which she tolerated very well without nausea. On day three, she was advanced to a liquid diet, and parenteral nutrition was discontinued completely at the end of that day. She went on a regular diet during the one-week hospitalization period.

A follow-up chest CT scan at seven days postoperatively confirmed that the integrity of the retrosternal and esophageal hiatus repairs, with proper positioning of both biological meshes, and no significant fluid collection (Figure 1I). The patient was discharged with complete resolution of preoperative symptoms. During the 12-month follow-up period, the patient had a normal diet and daily activities and no recurrence of GERD or respiratory symptoms. In the 12-month follow-up, the patient also had a follow-up imaging, which showed durable repair with no sign of hernia recurrence. The clinical data of this case are arranged in a timeline (Table 1).

Table 1 Information from this case reportorganized into a timeline.

Date	Key clinical events
September 12, 2021	The patient was admitted to the hospital due to related symptoms
September 12, 2021	Chest CT examination was completed
September 13, 2021	Routine blood laboratory tests were completed
September 14, 2021	Magnetic resonance imaging (MRI) was performed for further evaluation
September 15, 2021	A definitive clinical diagnosis was established based on imaging and laboratory findings
September 20, 2021	Surgical treatment was conducted
September 27, 2021	The patient recovered and was discharged

CT: Computed tomography; MRI: Magnetic resonance imaging.

DISCUSSION

Diaphragmatic hernias most commonly occur at congenital weak points of the diaphragmatic muscle, including the sternocostal triangle (foramen of Morgagni) and the esophageal hiatus[2,3]. In spite of the protective effect of the right hepatic lobe, more than 90% of MH cases are in the right sternocostal triangle. Horton et al[23] suggested that the left diaphragmatic dome has additional structural support of the pericardium, which can explain the predominance of right MH[23].

In adult patients, the hernia sac of MH may contain a variety of intra-abdominal structures, with the greater omentum (31%) and colon (29%) being the most common hernia contents[23]. Increased intra-abdominal pressure due to central obesity and chronic pulmonary disease is considered a predisposing factor for the clinical manifestation of MH, but congenital diaphragmatic developmental deficiency is the primary etiology[2]. Our case supports this notion: The patient presented with a large 5.4 cm diaphragmatic defect in the absence of obesity or abdominal trauma, which confirms a congenital origin of the defect[23,24].

Pediatric MH typically presents with acute respiratory compromise, while adult MH is mostly asymptomatic with insidious onset, allowing for adaptive compensation of the thoracic cavity[2,23]. However, the lack of clinical symptoms masks the potential risk of life-threatening complications such as intestinal volvulus and ischemic necrosis. Therefore, surgical repair is recommended for all diagnosed cases of MH regardless of symptom status[2,20,24].

High-resolution chest CT is still the gold standard for the diagnosis of MH, and it allows to clearly visualize the retrosternal defect and the hernia contents[2,23]. In the present case, the patient had non-specific GERD symptoms; a multimodality imaging approach, in the form of upper gastrointestinal contrast study, chest CT, and magnetic resonance imaging, is indispensable. If only one of these imaging modalities would have been used, the patient would have had a missed diagnosis of the asymptomatic parasternal diaphragmatic defect.

Since the concurrent MH and HH is so extremely rare, there is no present standard surgical guideline for this condition[24]. For the management of the MH sac, both complete resection and simple reduction are acceptable surgical options. In our case, the hernia sac contained only non-adherent greater omentum, so a simple reduction was performed. This approach achieved effective defect repair, shortened operative time, and avoided the risk of bleeding associated with sac resection[20,24].

For diaphragmatic defects larger than 3 cm, primary suture closure alone is insufficient, and mesh augmentation is necessary to distribute tension and reduce recurrence risk[2,24]. The selection of mesh material is important for the long-term success of the repair. Non-absorbable synthetic meshes have a high tensile strength but are rigid and may induce chronic foreign body reactions, particularly when in contact with mobile structures such as the esophagus and stomach[25]. Complications of the synthetic mesh that have been reported are severe adhesions, postoperative dysphagia, and visceral erosion[26]. Biological meshes, such as the porcine small intestinal submucosa mesh used in our case, are acellular collagen scaffolds with excellent biocompatibility and promote rapid neovascularization and tissue ingrowth with minimal chronic inflammation[27]. There is now evidence that the biological meshes have a comparable recurrence rate with the synthetic meshes, with a lower incidence of early postoperative complications such as early satiety, dysphagia, and esophageal erosion[22,28]. Considering the patient's advanced age, poor nutritional status (Body mass index: 18.3 kg/m²), and attenuated native tissue quality, the biological mesh augmentation was the optimal choice, providing good support for the large diaphragmatic defects without excessive tension and minimizing the risk of visceral injury.

The management of sliding HH is the restoration of the incompetent lower esophageal sphincter function[3], which should be done in a concurrent way for the management of sliding HH. The 360-degree Nissen fundoplication is the traditional anti-reflux “procedure”, but in this case 270-degree Toupet fundoplication was selected. A complete fundoplication has the risk of postoperative dysphagia in elderly patients, and the Toupet procedure has effective anti-reflux control with the superior postoperative gastrointestinal functional results[3].

The anatomical nuances of concurrent diaphragmatic hernias fix a very specific fixation strategy. For the anterior Morgagni defect, the diaphragm is the tissue that is going to have a very robust respiratory excursion, so absorbable tacks combined with running sutures provide crucial initial mechanical pull-out strength. Conversely, the esophageal hiatus is bounded by highly critical neurovascular structures, including the aorta, vagus nerves, and pericardium. In this anatomically unforgiving posterior “triangle of doom”, mechanical tacking would carry the risk of catastrophic risks of vascular injury, pericardial penetration, or chronic neuropathic pain. Therefore, the use of cyanoacrylate medical glue for hiatal mesh fixation is an atraumatic, safe, and equally effective alternative[29].

We deliberately picked a biological mesh for both repairs. Placing rigid synthetic plastic mesh next to the dynamic esophagus and stomach in a thin 73-year-old carries a known, prohibitive risk of long-term visceral erosion and dense fibrotic strictures[25,26]. Biological meshes avoid these risks. They are an acellular scaffold that promotes rapid neovascularization and host tissue ingrowth, with the end result being constructive tissue remodeling rather than foreign-body scarring[30].

We also had to fix the sliding HH with an anti-reflux procedure[3]. We performed a 270-degree Toupet wrap instead of a 360-degree Nissen, without any intraoperative bougie and gastroscopic assistance, only with the surgical visualization. In elderly patients, it is often difficult to swallow if one makes a full Nissen wrap. The Toupet is controlling the acid reflux very, very well, but it is much more tolerant of the esophageal motility[3].

A PubMed literature review confirms that concurrent MH and HH is an extremely rare clinical entity[4]. Most cases reported are of elderly female patients in their seventies, with non-specific gastrointestinal or respiratory symptoms that predispose to misdiagnosis[6,11,13]. Open surgery was the historical treatment of choice, but minimally invasive approaches have now become the mainstay. Both conventional laparoscopic surgery[5,11] and robotic-assisted one-stage repair[12,21] have been reported, with favorable safety and efficacy outcomes. However, due to the steep learning curve and high costs associated with robotic surgery, laparoscopic tension-free repair as performed in our case, remains the most cost-effective and safe option for the one-stage management of concurrent MH and HH[2,20]. A summary of recent literature that details simultaneous minimally invasive repairs is provided in Table 2.

Table 2 Summary of recent literature on the minimally invasive repair of concurrent Morgagni and hiatus hernias.

Ref.	Patient characteristics	Repair methods of the Morgagni hernia	Repair methods of hiatal hernia	Combined anti-reflux and fixation surgery	Prognosis/follow-up
Cokmez et al[8], 2003	Missing	Laparoscopic	Suture repair	Not explained in detail	Recover smoothly
Szentkereszty et al[5], 2006	68 years old/female	Laparoscopic	Suture repair	Toupet fundoplication (270°)	No recurrence after surgery
Zhou et al[11], 2016	73 years old/female	Laparoscopic	Direct suture closure	No fundoplication performed	No recurrence for 6 months
Mittal et al[13], 2018	71 years old/male	Laparoscopic	Composite patch reinforcement (mesh)	Nissen 360-degree fundoplication	No recurrence of torsion after surgery
Fu et al[12], 2018	65 years old/female	Robotic	Biological patch (surgisis)	Nissen 360-degree fundoplication	No recurrence for 4 months
Radulski et al[31], 2026	77 years old/female	Laparoscopy (emergency)	Direct suture of the defect	Anterior gastropexy	Discharge after remission

Limitations and long-term prognosis

To draw massive conclusions from one case report is inherently limited. The long-term prognosis of using biological meshes should be objectively and critically considered. Although they are the most biocompatible, they have an important intrinsic drawback regarding their long-term structural integrity. The functional success of a biological prosthesis relies on a delicate physiological balance: The acellular scaffold must maintain its mechanical tensile strength long enough for native collagen-producing cells to fully infiltrate and deposit mature, load-bearing connective tissue. The big clinical disadvantage is that the enzymatic degradation of the biological matrix by host macrophages and matrix metalloproteinases is often faster than the rate of native tissue regeneration[31]. If the mesh degrades too rapidly before complete native collagen ingrowth and consolidation can occur, the repair site suffers a critical loss of mechanical support. This “remodeling mismatch” is the primary pathophysiological driver for the higher incidence of late anatomical hernia recurrences observed with biological meshes, particularly in high-tension areas like the diaphragm[32,33]. Contemporary long-term trials confirm that the biological meshes have a slightly higher long-term radiological recurrence rate in comparison to the synthetic ones; these recurrences are mainly asymptomatic according to Oelschlager et al[22], 5-year follow-up data. For an elderly, underweight patient, the clinical consensus is to put safety first: Accepting a marginal increase in late asymptomatic recurrence is a highly justified trade-off to absolutely eliminate the life-threatening risks of synthetic mesh erosion and intractable dysphagia. Evaluating this patient at the 5-year mark remains essential to truly validate the durability of this repair. Any conclusions drawn from one case report should be validated in large-scale multicenter prospective studies. Another point is that, if the 12-month follow-up is favorable for the short term, long-term follow-up of more than five years is needed to evaluate the durability of biological mesh augmentation in the simultaneous one-stage diaphragmatic repair.

CONCLUSION

Concurrent MH and HH is an extremely rare clinical condition. The diagnosis of this condition requires a high index of clinical suspicion and comprehensive multimodality imaging. Laparoscopic one-stage tension-free repair with biological mesh augmentation combined with a 270-degree Toupet fundoplication is a safe and effective therapeutic strategy for this complex condition. This customized minimally invasive approach gives precise anatomical reconstruction and functional restoration with minimal surgical trauma, so that the patient has rapid postoperative recovery and durable symptom relief.

ACKNOWLEDGEMENTS

The authors extend their sincere gratitude to the medical and nursing staff of the Department of Gastrointestinal and Hernia Surgery, The First Affiliated Hospital of Kunming Medical University, for their indispensable support during the patient's operative and postoperative care.