Atresia esofágica tipo A (brecha amplia): reparación diferida y manejo con stent esofágico. Reporte de caso

Type I (long-gap) esophageal atresia: delayed repair and esophageal stent placement. A case report

Introducción. La atresia esofágica (AE) es una anomalía congénita del aparato digestivo que puede o no estar asociada a una fístula traqueoesofágica (FTE). La AE tipo I (aislada sin FTE) se caracteriza por una discontinuidad esofágica amplia que impide la anastomosis primaria, lo cual representa un desafío quirúrgico.

Presentación del caso. Recién nacido pretérmino (36 semanas y 1 día) con diagnóstico prenatal de AE tipo A que fue sometido a 7 intervenciones, incluyendo medición seriada de cabos esofágicos, gastrostomía y reparación toracoscópica diferida con anastomosis término-terminal. En el posoperatorio presentó fuga anastomótica y estenosis, por lo que requirió colocación de un stent esofágico autoexpandible, dilataciones esofágicas y tratamiento médico para reflujo gastroesofágico. Durante su estancia hospitalaria presentó bacteriemia asociada a dispositivo intravascular que fue tratada con antibiótico escalonado. A los 4 meses de edad se le realizó un esofagograma contrastado de control que mostró integridad de la anastomosis, por lo que se procedió al retiro endoscópico del stent y, tras una evolución favorable y adecuada tolerancia a la vía oral, fue dado de alta. Sin embargo, un mes después reingresó por estenosis anastomótica y reflujo gastroesofágico grado II, por lo cual se realizó recambio de la gastrostomía por botón gástrico, con resolución de la sintomatología. Se restableció la vía oral y se indicó seguimiento ambulatorio, en el cual se evidenció evolución adecuada.

Conclusiones. La AE tipo A requiere un enfoque de atención integral desde el diagnóstico prenatal hasta la reconstrucción esofágica. El uso de stents esofágicos autoexpandibles es una alternativa eficaz para el manejo de complicaciones postoperatorias como la fuga anastomótica y la estenosis.

Introduction: Esophageal atresia (EA) with or without tracheoesophageal fistula (TEF) is a rare congenital anomaly with diverse anatomical variations. Type I EA, accounting for 5-8% of cases, involves a long esophageal gap exceeding three vertebral bodies, posing a major surgical challenge.

Case report: During his clinical course, the patient required multiple interventions, including serial measurement of the esophageal segments, gastrostomy, and delayed thoracoscopic repair with end-to-end anastomosis. The postoperative period was complicated by an anastomotic leak and stricture, which required stent placement and esophageal dilations. In the pediatric intensive care unit, he received escalated antibiotic therapy and medical management for gastroesophageal reflux and metabolic disturbances.

Conclusions: Type I EA demands an early diagnosis and tailored surgical strategy. Thoracoscopic repair is preferred over open surgery due to its lower postoperative morbidity and favorable cosmetic outcomes.

Type A (Long-Gap) Esophageal Atresia: Delayed Repair and Esophageal Stent Placement. A Case Report

Laura González-Hakspiel1, Luis Augusto Zárate-Suárez1

1 Universidad Autónoma de Bucaramanga - Faculty of Health Sciences - Bucaramanga, Santander - Colombia.

Open access

Received: 04/09/2025

Accepted: 06/04/2026

Corresponding author: Laura González-Hakspiel. Facultad de Ciencias de la Salud, Universidad Autónoma de Bucaramanga. Santander. Colombia. E-mail: lgonzalez884@unab.edu.co.

Keywords: Esophageal Atresia; Tracheoesophageal Fistula; Congenital Abnormalities; Minimally Invasive Surgical Procedures; Thoracoscopy.

Palabras clave: Atresia Esofágica; Fístula Traqueoesofágica; Anomalías Congénitas; Procedimientos Quirúrgicos Mínimamente Invasivos; Toracoscopia

How to cite: González-Hakspiel L, Zárate-Suárez LA. Type A (Long-Gap) Esophageal Atresia: Delayed Repair and Esophageal Stent Placement. A Case Report. Case reports. 2026;12:e121265. English. doi: https://doi.org/10.15446/cr.v12.121265.

Cómo citar: González-Hakspiel L, Zárate-Suárez LA. Atresia esofágica tipo A (brecha amplia): reparación diferida y manejo con stent esofágico. Reporte de caso. Case Reports. 2026;12:e121265. doi: https://doi.org/10.15446/cr.v12.121265.

Copyright: ©2025 The Author(s). This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, as long as the original author and source are credited.

Abstract

Introduction: Esophageal atresia (EA) is a congenital anomaly of the digestive tract that may occur with or without a tracheoesophageal fistula (TEF). Type A EA (isolated, without TEF) is characterized by a long esophageal gap that prevents primary anastomosis, presenting a surgical challenge.

Case report: A preterm newborn (36 weeks and 1 day) with a prenatal diagnosis of type A EA underwent 7 procedures, including serial esophageal pouch measurement, gastrostomy, and delayed thoracoscopic repair with end-to-end anastomosis. After surgery, the patient developed an anastomotic leak and stricture, requiring placement of a self-expanding esophageal stent, esophageal dilations, and medical treatment for gastroesophageal reflux. During his hospital stay, the patient developed intravascular device-related bacteremia, which was treated with escalated antibiotic therapy. At 4 months of age, a follow-up contrast-enhanced esophagogram was performed, showing an intact anastomosis. Consequently, the stent was removed endoscopically, and the patient was discharged following a favorable course and adequate tolerance to oral feeding. However, one month later, he was readmitted due to anastomotic stenosis and grade II gastroesophageal reflux. The gastrostomy was exchanged for a gastric button, resolving the symptoms. Oral intake was restarted, and outpatient follow-up was recommended, showing adequate progress

Conclusions: Type A EA requires a comprehensive care approach from prenatal diagnosis to esophageal reconstruction. Self-expanding esophageal stents are an effective alternative for managing postoperative complications such as anastomotic leaks and stenosis.

Resumen

Case report

Introduction

Esophageal atresia (EA) is a congenital malformation of the digestive tract characterized by a partial or complete interruption of esophageal continuity, which may occur with or without a tracheoesophageal fistula (TEF) (1). Its etiology is not fully understood and is likely multifactorial (2). Identifying a specific genetic cause for EA remains extremely challenging because many genes, including Shh, SOX2, CHD7, MYCN, and FANCB, are affected by chromosomal duplications or deletions, leaving the causal genes unidentified (1,2).

The estimated global prevalence of EA varies from 1 case per 2 500 to 4 500 live births (2), being more frequent in males than in females, with a male-to-female ratio of 1.26:1 (3). EA and TEF are present together in approximately 90% of cases (4). EA is classified into 5 types depending on the presence and location of the TEF: type A: isolated EA without TEF (prevalence: 8%); type B: EA with proximal TEF (prevalence: 1%); type C: proximal EA with distal TEF (prevalence: 84%); Type D: AE with proximal and distal TEF (prevalence: 3%); and Type E: isolated TEF without associated EA, also known as Type “H” (prevalence: 4%) (2,5) (Figure 1).

Figure 1. Esophageal atresia/tracheoesophageal fistula classification.

Source: Own elaboration.

Type A EA (equivalent to Type I in other classifications) is characterized by a complete interruption of esophageal continuity without TEF. Since the lower pouch of this type of EA is not anchored to the trachea, it usually retracts into the abdomen and creates a gap between the pouches of >3 vertebral bodies, defining it as a long-gap condition (6). This extreme distance generates excessive tension that makes primary anastomosis impossible, so a delayed surgical approach and elongation techniques are frequently required (7). The thoracoscopic approach is a minimally invasive alternative for EA repair, as it offers better visualization, requires a much smaller incision than that needed for open surgery, and is less invasive for the patient. It also yields outcomes comparable to open surgery in specialized centers (8,9).

The following report describes the case of a newborn with a prenatal diagnosis of type A EA who underwent delayed thoracoscopic repair. The report describes the therapeutic decisions, postoperative complications (particularly anastomotic leak), management with an esophageal stent, and the clinical outcomes achieved.

Case presentation

A male newborn, the second child of a 27-year-old mother (G2P2) with a history of two cesarean deliveries, who had received adequate prenatal care and had a TORCH profile with serological markers indicating no active infection was born at a tertiary care hospital in Bucaramanga, Colombia, on May 11, 2020 (36 weeks and 1 day of gestation) via cesarean section scheduled by the perinatology service due to ultrasound findings suggestive of type A EA (absence of gastric bubble and severe polyhydramnios) reported at 30 weeks of gestation (Figure 2) and which persisted in all follow-up ultrasounds until birth.

Figure 2. Obstetric ultrasound at gestational week 30. Fetal biometry at 30 weeks and 4 days. Estimated fetal weight: 1 664 g (26th percentile for gestational age); amniotic fluid index: 29 cm (consistent with polyhydramnios). No fetal gastric bubble visible.

1: vein; 2: absence of gastric bubble; 3: aorta; 4: spine.

Source: Image obtained while conducting the study.

At birth, the patient presented with apnea and bradycardia (heart rate <100 bpm) that did not respond to tactile stimulation, requiring positive pressure ventilation. On initial physical examination, the inability to advance the orogastric tube confirmed the suspected diagnosis of EA. Anthropometric measurements revealed birth weight of 2 155 g, length of 51 cm, and head circumference of 32 cm. Blood typing was A, Rh-positive.

On his first day of life, he was admitted to the pediatric intensive care unit (PICU), where an evaluation protocol for VACTERL association was initiated. The echocardiogram identified no structural heart diseases, the renal ultrasound was normal, and the chest X-ray showed an esophageal blind pouch at the level of the second thoracic vertebra (T2). Given the suspicion of type A EA, on the second day of life, the pediatric surgery service performed a diagnostic surgical exploration by introducing bougies into the proximal and distal esophageal pouches, finding a gap of >7 vertebral bodies, confirming a long-gap condition (Figure 3). As this extreme distance contraindicates primary esophageal anastomosis, a gastrostomy tube was placed for enteral feeding, and total parenteral nutrition was requested.

Figure 3. Intraoperative chest and abdominal X-ray showing the delineation of the esophageal gap using bougies. The ends show a separation of more than seven vertebral bodies.

Source: Image obtained while conducting the study.

On the seventh day of life, trophic enteral feedings were initiated with adequate tolerance, and mixed nutrition (enteral and parenteral) was started 5 days later. During this period, the patient presented with episodes of desaturation associated with bronchial hypersecretion that required supplemental oxygen. Given the persistence of these respiratory events, laboratory tests were performed on the 12th day of life, reporting an absolute neutrophil count of 5 178/mL (60%), elevated C-reactive protein (CRP) levels (17.01 mg/L), ionized calcium levels at the upper limit of normal (1 402 mmol/L), and serum sodium levels within the normal range (143 mmol/L).

Considering the laboratory results, an infection was suspected, and empirical antibiotic therapy with intravenous (IV) oxacillin (130 mg every 8 hours for 3 days) was initiated on the same day. Blood cultures drawn through the femoral catheter were positive after 48 hours of incubation and tested positive for pan-susceptible Enterobacter cloacae. Consequently, on the 14th day of life, the catheter was removed, and the antibiotic regimen was switched to IV meropenem (52 mg every 8 hours for 4 days). A barium swallow test performed on the 13th day of life ruled out any leaks or extravasation through the gastrostomy.

On the 16th day of life, the patient showed signs of persistent sepsis characterized by tachycardia (heart rate of 174 bpm) and grade 3 edema in the lower extremities. Given the lack of clinical improvement with meropenem treatment, coverage for Gram-positive bacteria was added with IV vancomycin (30 mg every 8 hours for 7 days), and new blood cultures were drawn.

Follow-up laboratory tests taken on the 17th day of life reported hypoalbuminemia (2.36 g/dL), so 10% albumin (30 mL) and furosemide (3 mg at the start and end of the infusion) were administered to manage fluid overload. Follow-up blood cultures were negative after 7 days of incubation (24th day of life), allowing the discontinuation of antibiotic treatment.

On the 29th day of life, the patient underwent another surgical procedure to measure the distance between the esophageal pouches, noting a reduction in the gap to 3 vertebral bodies (Figure 4). During the procedure, the azygos vein was ligated.

Figure 4. Intraoperative chest X-ray in which the approximation of the bougies shows a reduction in the gap between the pouches to three vertebral bodies.

Source: Image obtained while conducting the study.

Over the following days, the patient experienced further clinical deterioration compatible with a respiratory infection. On the 44th day of life, a bronchoscopic culture was obtained, which tested positive for multidrug-resistant Pseudomonas aeruginosa. Consequently, that same day, combination antibiotic therapy was initiated with IV vancomycin (32 mg every 8 hours for 7 days) and IV meropenem (65 mg every 8 hours for 3 days). Following the administration of meropenem, the patient developed urticaria; therefore, the drug was discontinued, and the therapy was adjusted to IV cefepime (160 mg every 12 hours for 7 days) based on the antibiogram susceptibility. A chest X-ray performed on the 53rd day of life showed right atelectasis, for which targeted respiratory therapy was instituted.

At approximately 60 days of life, a third surgery was performed to measure the distance between the esophageal pouches, revealing a gap of <2 vertebral bodies (Figure 5). Based on this finding, a thoracoscopic esophageal repair was scheduled and performed at 2 months and 11 days of life.

Figure 5. Intraoperative chest X-ray showing a distance of one vertebral body between the esophageal pouches.

Source: Image obtained while conducting the study.

The procedure was performed with the patient in the left lateral decubitus position. The thoracoscopic approach was carried out by placing three trocars: one 5-mm trocar for the scope, inserted 1 cm below the inferior angle of the scapula, and two 3-mm trocars placed symmetrically relative to the scapular line, oriented toward the anterior and posterior axillary lines (Figure 6). A 30° scope was used, and a meticulous dissection of the esophagus was performed from the diaphragm to the upper pouch; both esophageal ends were then sectioned until viable mucosa was observed.

Subsequently, an end-to-end single-layer anastomosis was performed using interrupted sutures of 5-0 absorbable polyglactin 910 (Vicryl® 5-0), employing a mixed technique with 4 posterior, 2 lateral, and 3 anterior stitches. Adequate approximation of the pouches without significant tension was verified, as well as satisfactory hemostasis. A 14 Fr Nelaton-type pleural drain connected to a water-seal system (Pleur-evac®) was placed for postoperative monitoring, along with an orogastric tube for continuous decompression. In the immediate postoperative period, the patient experienced an episode of vomiting, which raised suspicion of an anastomotic leak.

Figure 6. Representation of the surgical approach. Intervention using three trocars.

1: 5-mm optical trocar; 2 and 3: 3-mm trocars.

Source: Own elaboration.

On the 80th day of life, a contrast esophagram was performed, showing a persistent leak of the contrast medium associated with the formation of a collection and gastroesophageal reflux (grade IV), as well as anatomical changes consistent with a pseudodiverticulum at the suture site. Given these findings, conservative management was immediately initiated, consisting of strict fasting, maintenance of a patent pleural drain, and exclusive enteral nutritional support via gastrostomy. Concurrently, speech-language pathologists began myofunctional therapy to improve swallowing coordination and reduce the risk of aspiration.

Due to the persistence of the leak, acid suppression treatment with IV omeprazole (4 mg every 24 hours) was started on the 87th day of life. In addition, a consultation with the pediatric gastroenterology service was requested, and the patient was evaluated on the 88th day of life. To treat the leak and protect the anastomosis, a self-expanding esophageal stent was placed endoscopically on the 90th day of life (Figure 7).

Figure 7. Endoscopic placement of a self-expanding stent.

1: esophageal diverticulum; 2 and 3: stent placement.

Source: Image obtained while conducting the study.

On the 117th day of life (27 days after the endoscopic placement of the self-expanding esophageal stent), blood cultures drawn through the catheter turned positive for Enterococcus faecalis. Given the diagnosis of a catheter-related bloodstream infection, targeted antibiotic therapy was initiated with IV vancomycin (40 mg every 6 hours for 14 days) combined with IV piperacillin/tazobactam (320 mg every 6 hours for 14 days), resulting in an adequate clinical response and the subsequent sterilization of follow-up blood cultures.

At 120 days of age, a follow-up contrast esophagogram was performed, which showed an intact anastomosis with no contrast extravasation. Given this finding, the stent was endoscopically removed without complications on the 131st day of life. After confirming adequate oral tolerance, hemodynamic stability, and infectious parameters within normal limits, the patient was discharged from the hospital at 140 days of life, with instructions to attend a follow-up appointment a month later.

At 163 days of life, the infant was brought to the emergency department due to sialorrhea and postprandial vomiting. Upon physical examination at admission, the following findings were documented: the patient was hemodynamically stable, irritable, with adequate peripheral perfusion and signs of moderate dehydration, but without signs of respiratory distress. Given the symptoms and surgical history, an anastomotic stricture was suspected. The patient was hospitalized for monitoring, and management was initiated with strict fasting, peripheral venous cannulation, intravenous hydration, and aspiration of secretions due to the persistent sialorrhea.

One month after readmission, a consultation with the pediatric surgery service was requested, and an esophagogram was performed, showing a significant anastomotic stenosis (a 70% reduction in luminal diameter) with proximal dilation, no signs of an active leak, and grade II gastroesophageal reflux.

Upon confirming the diagnosis, the pediatric surgery and pediatric gastroenterology services initiated a joint endoscopic management plan involving serial esophageal dilations. As part of the comprehensive care provided during this same hospitalization, the gastrostomy tube was replaced with a gastric button. The patient progressed satisfactorily, showing symptom improvement and progressive restoration of oral intake; therefore, at 171 days of age, he was discharged with the following indications: pharmacological management for gastroesophageal reflux with oral domperidone (2 mL every 8 hours for 15 days) and oral esomeprazole 20 mg (diluted in 5 mL of water, administering 1.5 mL every 24 hours for 10 days).

During regular outpatient follow-up, a favorable clinical course was documented. At his last follow-up visit at the time of writing this case report, it was noted that the patient presented optimal feeding tolerance, adequate weight gain, and no new complications, maintaining a satisfactory outcome.

Discussion

EA is a congenital disease caused by an incomplete embryonic division of the foregut, which results in esophageal discontinuity and may occur with or without TEF (10,11). It is often accompanied by other anomalies, primarily VACTERL association, and has multiple long-term health implications (1,2,10,11).

Type A EA is a rare variant that poses a clinical challenge due to the wide gap between the esophageal pouches (usually >3 vertebral bodies) (2,6), limiting the possibility of a safe primary anastomosis and necessitating delayed or staged surgical strategies (2,5). In the present case, due to the initial inter-pouch distance (>7 vertebral bodies), delayed esophageal reconstruction was performed via a thoracoscopic approach.

Since the first thoracoscopic repair described by Lobe et al. (9) in 1999, this technique has evolved significantly and is now a safe and effective alternative with outcomes comparable to those of thoracotomy in terms of survival, complications, and functional outcomes, and is associated with less postoperative pain and faster recovery (8,9,12).

The patient in this case report developed major infectious complications during the postoperative period, including sepsis due to E. cloacae and E. faecalis, highlighting the high risk of nosocomial infections in neonatal patients undergoing invasive procedures with multiple vascular accesses. These complications increase morbidity and mortality, prolong hospital stays, and delay clinical recovery (13,14).

One of the main surgical complications following EA repair is anastomotic leak (2,4,15), which occurs in 10–25% of operated children (4) and constitutes a risk factor for mortality (15). The initial management of anastomotic leaks is usually conservative, including drainage, antibiotic therapy, and parenteral nutrition (4). Endoscopic vacuum therapy (EVAC), which involves placing a vacuum system over the wound at the site of the leak, is a novel and promising technique for treating esophageal perforations in the pediatric population that serves as an adjunct to help control the source of anastomotic leaks and achieve their closure (4,16). In our patient, the persistence of the anastomotic leak despite conservative management and the use of negative pressure therapy led to the placement of an esophageal stent.

The use of self-expanding esophageal stents is a minimally invasive therapeutic option for anastomotic leaks that proves effective with a single application in selected cases (17). Nonetheless, endoscopic treatment is the most commonly used strategy, in both children and adults, for the management of EA (18). In our patient, the placement of a self-expanding esophageal stent allowed for complete resolution of the anastomotic leak, avoiding a repeat surgical intervention and promoting clinical recovery. This reinforces the utility of this type of prosthesis in complex scenarios, particularly in patients with type A EA undergoing delayed repair. It is important to bear in mind that the use of stents is not without complications—such as migration and general patient discomfort (pain and nausea) (16)—thereby requiring close clinical and radiological follow-up during its implementation.

Finally, our patient’s favorable outcome underscores the importance of implementing a multidisciplinary care approach that integrates pediatric surgery, pediatric intensive care, pediatric gastroenterology, and interdisciplinary rehabilitation, with the aim of optimizing clinical outcomes for patients.

Conclusions

Type A EA poses a therapeutic challenge that requires a staged, multidisciplinary approach to care. The use of self-expanding esophageal stents is an effective option for managing postoperative complications such as anastomotic leak and stricture, as it promotes healing, maintains esophageal patency, and reduces the need for repeat surgical procedures.

Ethical considerations

Informed consent was obtained from the patient’s legal guardian for the preparation of this case report; the guardian expressly authorized the publication of the clinical data and images included in this article.

Conflicts of interest

None stated by the authors.

Funding

None stated by the authors.

Acknowledgments

None stated by the authors.

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