Combined magnetic recanalization and laparoscopic antireflux surgery for complex esophageal comorbidities in an infant with congenital esophageal atresia

Abstract

BACKGROUND

Congenital esophageal atresia (CEA) is a critical neonatal anomaly requiring timely surgical intervention. Anastomotic stricture represents the most frequent long-term complication, affecting 30% to 50% of repaired cases. Refractory strictures are particularly challenging when compounded by concurrent gastroesophageal reflux disease (GERD) and hiatal hernia, as these conditions synergistically sustain local inflammation, impair healing, and promote recurrent fibrosis.

CASE SUMMARY

We describe a 7-month-old male infant with Gross type III CEA who developed a refractory anastomotic stricture after primary repair, unresponsive to seven sessions of endoscopic balloon dilation. Preoperative workup identified severe gastroesophageal reflux and a hiatal hernia as key perpetuating factors. The patient underwent a single-stage combined minimally invasive procedure, consisting of endoscopic magnetic compression anastomosis for stricture recanalization, followed by laparoscopic hiatal hernia repair and Nissen fundoplication. The procedure lasted 3.5 hours with negligible blood loss. The magnets were removed endoscopically at 32 days, revealing a well-healed anastomosis with a luminal diameter of approximately 8 mm. Mild restenosis occurred at 20 months postoperatively and was effectively managed with five additional dilations. At 3 years and 7 months of follow-up, the child maintained a normal oral diet, remained symptom-free, and exhibited growth and development appropriate for his age.

CONCLUSION

In this infant, single-stage magnetic recanalization combined with laparoscopic antireflux surgery proved feasible for refractory anastomotic stricture with GERD and hiatal hernia, achieving favorable medium-term patency and symptom control. This approach may interrupt the reflux-stricture cycle while avoiding open revision, though further study in larger series is needed.

Key Words: Magnetic compression anastomosis; Congenital esophageal atresia; Anastomotic stricture; Gastroesophageal reflux disease; Laparoscopic antireflux surgery; Hiatal hernia

Core Tip: We report a 7-month-old infant with congenital esophageal atresia who developed a refractory anastomotic stricture, hiatal hernia, and severe gastroesophageal reflux after primary repair. A single-stage combined procedure, consisting of endoscopic magnetic compression anastomosis followed by laparoscopic hiatal hernia repair and Nissen fundoplication, successfully restored esophageal patency and controlled reflux. At nearly 4 years of follow-up, the child exhibited normal growth and development. This integrated minimally invasive approach may offer a safe and effective alternative for complex esophageal comorbidities that fail conventional therapy, addressing multiple pathologies simultaneously while minimizing surgical trauma.

INTRODUCTION

Congenital esophageal atresia (CEA) is a severe neonatal gastrointestinal anomaly, with postoperative anastomotic stricture occurring in 30% to 50% of cases[1-3]. When anastomotic stricture coexists with hiatal hernia and gastroesophageal reflux disease (GERD), a vicious cycle ensues: Reflux acidifies and inflames the anastomotic site, promoting fibrotic scarring, while the stricture impairs esophageal clearance and exacerbates reflux[4,6,7]. This self-perpetuating mechanism often renders conventional balloon dilation ineffective. Beyond the local obstruction, persistent feeding difficulties place these children at sustained risk of malnutrition and growth retardation. Traditional staged procedures, including repeated endoscopic dilation[8] and reoperative thoracotomy[9], cannot address all concomitant pathologies in a single operation. Although early antireflux surgery can interrupt the vicious cycle[10,11], standardized minimally invasive protocols for such complex cases remain lacking.

Magnetic compression anastomosis (MCA) has recently emerged as a promising alternative for recanalizing refractory esophageal strictures, with encouraging results reported in pediatric series[12,13]. However, published experience with MCA has largely focused on stricture recanalization alone; its combination with concurrent laparoscopic hiatal hernia repair and fundoplication in a single anesthetic session has not been previously reported, to our knowledge, in infants with refractory anastomotic stricture. Herein, we report a case of refractory anastomotic stricture with hiatal hernia and severe GERD in an infant after CEA repair, successfully managed through a one-stage combined endoscopic-laparoscopic approach with magnetic recanalization and concomitant antireflux surgery.

CASE PRESENTATION

Chief complaints

A 7-month-old full-term male infant presented with a 2-day history of recurrent non-projectile vomiting following oral feeding.

History of present illness

The patient received a diagnosis of Gross type III CEA (the most common variant, with a blind-ending upper esophageal pouch and a tracheoesophageal fistula from the lower pouch) shortly after birth, due to vomiting and tachypnea, and underwent transthoracic esophageal anastomosis with tracheoesophageal fistula closure on day 3 of life. The postoperative course was complicated by anastomotic leakage, which resolved with conservative management and nasogastric tube feeding. Secondary esophageal stenosis subsequently developed. At the 4-month follow-up, a hiatal hernia was identified, accompanied by poor weight gain. Despite seven sessions of endoscopic balloon dilation over the subsequent 7 months, the stricture remained refractory, with persistent vomiting.

History of past illness

The patient was born full-term via vaginal delivery with a birth weight of XX kg. No other significant medical conditions were recorded. He had no known drug or food allergies. Immunizations were up-to-date per the national schedule.

Personal and family history

No family history of similar diseases or congenital anomalies was reported. The patient had no other relevant medical history.

Physical examination

On admission, the infant appeared mildly malnourished, with a body weight of 7.0 kg. Vital signs were within normal limits. The abdomen was soft and non-distended, with no visible peristaltic waves or palpable masses. Bowel sounds were normoactive.

Laboratory examinations

Laboratory evaluation revealed hypoproteinemia, with total protein of 44.8 g/L (reference range 55-79 g/L), albumin of 30.5 g/L (reference range 36-50 g/L), and globulin of 14.3 g/L (reference range 20-40 g/L), consistent with chronic suboptimal oral intake. Alanine aminotransferase was mildly elevated at 97 U/L (reference range 4-35 U/L), and serum calcium was slightly decreased at 2.36 mmol/L (reference range 2.5-3.0 mmol/L). Bilirubin, renal function parameters (urea, creatinine), electrolytes (sodium, potassium, chloride), and carbon dioxide combining power were all within normal ranges.

Imaging examinations

Upper gastrointestinal contrast study demonstrated a 1.5-cm linear stricture at the T4 Level of the mid-upper esophagus, with a minimal luminal diameter of approximately 1 mm and marked proximal dilation up to 1.7 cm. The gastric cardia was elevated, and a portion of the gastric fundus had herniated into the thoracic cavity, consistent with hiatal hernia and severe GERD (Figure 1A). Gastroscopy revealed a cicatricial stenotic orifice located 14 cm from the incisors, measuring approximately 1 mm in diameter (Figure 1B), which precluded passage of a 5.5-mm scope. The surrounding mucosa appeared hyperemic and granular.

Figure 1 Preoperative imaging findings. A: Upper gastrointestinal contrast study showing severe anastomotic stricture, hiatal hernia, and gastroesophageal reflux; B: Gastroscopy revealing a cicatricial stenotic orifice with a luminal diameter of approximately 1 mm.

FINAL DIAGNOSIS

The final diagnoses were: (1) Refractory anastomotic stricture following repair of CEA; (2) Hiatal hernia; and (3) Severe GERD.

TREATMENT

Following parental informed consent, the patient underwent a single-stage combined minimally invasive procedure under general anesthesia. The magnetic rings were custom-fabricated from NdFeB N45 magnets and coated with titanium nitride for corrosion resistance. The two rings were configured with opposite magnetic poles, each measuring 12 mm × 8 mm × 3 mm (outer diameter × inner diameter × thickness). Under endoscopic guidance, a guidewire was navigated across the stenotic segment and exteriorized through a small anterior gastrotomy. A 6-F gastric tube was passed retrogradely across the stricture into the proximal esophagus and exteriorized via the oral cavity. Magnetic ring A was attached to the proximal end of the gastric tube and positioned endoscopically at the superior margin of the stricture (Figure 2A). Subsequently, magnetic ring B was advanced retrogradely along the guidewire to the inferior margin of the stricture (Figure 2B). Magnetic attraction between the two rings delivered sustained compressive force across the scar tissue, effecting anastomosis. Proper alignment of the paired magnetic rings was confirmed on postoperative radiography (Figure 2C). The gastric and abdominal wall incisions were subsequently closed in layers with absorbable sutures.

Figure 2 Intraoperative magnetic recanalization. A: Magnetic ring A was delivered orally and positioned at the superior margin of the stricture under endoscopic guidance; B: Magnetic ring B was advanced retrogradely through a small anterior gastrotomy to the inferior margin of the stricture; C: Postoperative chest radiograph confirming proper alignment of the paired magnetic rings, hiatal hernia repair, and a smooth diaphragmatic contour.

Laparoscopic exploration followed. The distal esophagus and hernia sac were adequately mobilized, and the bilateral diaphragmatic crura were approximated and sutured to repair the esophageal hiatus. Following complete anatomical restoration, a Nissen fundoplication was performed to construct an antireflux barrier. The total operative time was 3.5 hours, with negligible blood loss.

Postoperatively, the patient received antibiotics, acid suppression, and nutritional support.

OUTCOME AND FOLLOW-UP

A contrast study on postoperative day 10 showed partial restoration of esophageal patency with no evidence of leakage, allowing initiation of tube feeding. The magnetic rings were removed endoscopically via the original gastrotomy on postoperative day 32 (Figure 3A). Upper gastrointestinal contrast study at that time revealed a well-healed anastomosis with a luminal diameter of approximately 8 mm (Figure 3B).

Figure 3 Postoperative magnet removal and outcome. A: The magnetic rings were removed through the original gastrotomy at postoperative day 32, revealing complete excision of scar tissue within the crateriform depression; B: Upper gastrointestinal contrast study after magnet removal demonstrating restored esophageal patency (upper circle), with the gastric fundus situated below the diaphragm and resolution of gastroesophageal reflux (lower circle).

At 20 months postoperatively, the patient developed restenosis, which was successfully managed with five additional balloon dilation sessions. Potential contributing factors included the introduction of a solid diet, which increased mechanical stress at the anastomotic site, and gradual attenuation of the fundoplication’s antireflux effect over time. At the final follow-up, 3 years and 7 months after the procedure, the child was tolerating a normal diet with no recurrence of vomiting or dysphagia. His weight was 17.1 kg (40^th-50^th percentile) and height 105.7 cm (25^th-50^th percentile), consistent with age-appropriate growth.

DISCUSSION

Postoperative anastomotic stricture remains the most common long-term complication after CEA repair, affecting 30% to 50% of patients[1-3]. Its development is driven by multiple factors, including anastomotic tension, local ischemia, and, crucially, persistent chemical injury from reflux[2,6]. Children with CEA are particularly vulnerable to severe GERD due to inherent esophageal dysmotility and an obtuse angle of His, with reflux documented in up to 50% of cases[5,6]. The pathogenic sequence is well delineated: Reflux of acid and bile onto the anastomosis incites transmural inflammation, submucosal collagen deposition, and progressive fibrosis, culminating in stricture formation[6,7]. Once a stricture narrows the lumen, esophageal clearance deteriorates, prolonging mucosal exposure to refluxate and locking the patient into a self-reinforcing cycle that resists intervention targeting either component alone[8].

This case exemplifies that refractory trajectory. The infant developed stricture within months of primary repair and remained unresponsive to seven dilations-surpassing the conventional threshold for refractoriness (failure after five or more appropriately timed sessions)[3]. Imaging uncovered a concurrent hiatal hernia, a mechanical disruptor of lower esophageal sphincter function and a well-recognized driver of pathologic reflux[10]. Together, these findings form a pathogenic triad: The hernia sustains reflux, reflux inflames and fibroses the stricture, and the stricture impedes clearance, which in turn amplifies reflux. Serial dilation alone cannot dismantle this triad; indeed, repeated instrumentation may further compromise the antireflux barrier and paradoxically accelerate the cycle[8,10].

Historically, surgical options for refractory anastomotic stricture have centered on reoperative thoracotomy with resection and re-anastomosis[9]. But in infants, this approach carries high stakes, including recurrent stricture, leak, and adjacent tissue injury, with re-stenosis rates of 30% to 50% in some series[9]. It also leaves abdominal pathology, such as hiatal hernia, unaddressed. MCA offers a fundamentally different tactic. By positioning paired magnets across the scarred segment, the compressive force induces pressure necrosis of the interposed tissue, followed by re-epithelialization along a sutureless tract[13,14]. The result is a more compliant anastomosis with less foreign-body reaction than surgical revision. In a multicenter pediatric series, magnetic stricturoplasty achieved durable patency in most refractory cases, albeit with a median of two to three subsequent dilations[15].

The role of antireflux surgery in this population has also shifted. Where fundoplication was once reserved as a last resort after multiple dilation failures, current evidence favors earlier deployment to interrupt the reflux-stricture cycle before it becomes entrenched[5,10]. François et al[10] showed that early fundoplication reduced dilation burden and improved growth. Mokka et al[11] first validated the concept of combining intraoperative dilation with antireflux repair in adults, and Li et al[12] later extended it to children with dilatable reflux strictures, demonstrating superior outcomes over dilation or fundoplication alone. Crucially, however, Li's study excluded strictures too narrow for guidewire passage-precisely the subset our patient represents, leaving a defined therapeutic gap.

Our strategy was designed to fill that gap. In a single anesthetic session, we performed magnetic recanalization, hiatal cruroplasty, and Nissen fundoplication. Each component addressed a distinct element of the triad: The magnet reopened the lumen, the cruroplasty corrected the hiatal defect, and the wrap restored an antireflux barrier. Performing these concurrently offers a specific synergistic benefit, as reflux control protects the freshly epithelialized magnet tract during healing and reduces the likelihood of acid-driven refibrosis[6]. In this infant, the postoperative course was uneventful. Although restenosis emerged at 20 months, consistent with the known trajectory after magnetic anastomosis in children[15], it responded predictably to five additional dilations. At the final follow-up of nearly 4 years, the child has achieved full oral feeding with normal growth parameters and remains free of vomiting or dysphagia.

Several limitations of this report should be acknowledged. The magnet dimensions, compressive force, and removal timing were chosen empirically, guided by surgical judgment in the absence of a standardized pediatric protocol for this combined approach. Moreover, while medium-term outcomes are favorable, the durability of both the anastomotic patency and the antireflux barrier can only be confirmed with follow-up through adolescence and beyond, particularly given the elevated lifetime risk of Barrett's esophagus and adenocarcinoma in CEA survivors. Larger, prospective studies are needed to refine patient selection, magnet specifications, and operative timing for the varied presentations of complex esophageal comorbidity.

CONCLUSION

For infants with refractory anastomotic stricture complicated by hiatal hernia and severe GERD after CEA repair, the single-stage combined approach of endoscopic magnetic recanalization with laparoscopic hiatal hernia repair and Nissen fundoplication proved feasible in this case, achieving favorable medium-term patency and symptom control. This integrated strategy addressed both the luminal obstruction and the underlying reflux mechanism in a single anesthetic session, potentially interrupting the pathogenic cycle while avoiding open surgical revision. Although these results are promising, the broader applicability of this approach requires further evaluation in larger cohorts with extended follow-up.