An Atypical Case of Metastatic Esophageal Adenocarcinoma Causing Biliary Obstruction and Duodenal Infiltration Requiring EUS-Guided Choledochoduodenostomy

Introduction

Esophageal cancer (EC) is the ninth most common cancer and the sixth leading cause of cancer-related deaths worldwide, causing over 500 000 fatalities annually. ¹ It mainly presents as either esophageal squamous cell carcinoma (ESCC) or esophageal adenocarcinoma (EAC), with distinct clinical and epidemiological features. EAC, comprising about 20% of cases, is most prevalent among white populations in developed countries and typically affects the distal esophagus. ¹ While ESCC rates are declining, EAC incidence has steadily increased in Western nations over the past 40 years.^1,2 We report a 50-year-old male with metastatic esophageal adenocarcinoma presented with jaundice. Imaging revealed biliary dilation due to metastatic invasion of the distal bile duct. ERCP failed due to duodenal involvement, so endoscopic ultrasound-guided biliary drainage was performed with stent placement. Post-procedure, the patient developed pancreatitis, which was managed with IV fluids, leading to gradual clinical improvement.

Case Presentation

A 50-year-old male patient with a past medical history of testicular cancer in remission, EAC with metastasis to the liver, adrenal glands, lymph nodes, bones, lungs, and peritoneum, on pembrolizumab, trastuzumab, and folfox, presented for jaundice of 2 days duration. The patient reports no abdominal pain, nausea, vomiting, diarrhea, or fever. Physical exam was normal, showing no abdominal tenderness or bruits. Laboratory workup showed an elevated CRP of 42 mg/L, bilirubin of 142 µmol/L, direct bilirubin of 107 µmol/L, alkaline phosphatase of 958 IU/L, gamma glutamyl transferase of 1151 IU/L and mildly elevated AST and ALT. Complete blood count was normal along with electrolytes. On ultrasound of the abdomen, the common hepatic duct, cystic duct, intrahepatic ducts, and common bile duct (CBD) showed a dilation of 10.5 mm, with a transition zone seen following the CBD (Figure 1), due to metastatic invasion of the distal part of the biliary tree. Although the distal CBD obstruction was initially described as secondary to “metastatic invasion,” no direct histological confirmation from the biliary wall was obtained. Endoscopic ultrasound (EUS) demonstrated a hypoechoic irregular lesion contiguous with the known duodenal and peri-biliary metastatic disease, causing luminal narrowing of the distal CBD. Cross-sectional imaging revealed a clear transition point at the distal CBD with soft tissue density extending from adjacent metastatic deposits, supporting the likelihood of malignant involvement rather than isolated extrinsic compression. No EUS-guided fine needle aspiration (FNA) or biliary brush cytology was performed due to technical constraints and the urgent need for biliary decompression. Therefore, the diagnosis of metastatic biliary involvement was based on radiologic continuity with known metastatic sites and the overall disease burden, which represents a limitation of this report. During endoscopic retrograde cholangiopancreatography (ERCP), we failed to reach the biliary tree due to metastatic invasion of the second portion of the duodenum.

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Figure 1.

Abdominal ultrasound demonstrating intrahepatic and extrahepatic biliary dilation (CBD measuring approximately 10.5 mm) with a distal transition point, suggestive of malignant obstruction.

EUS-guided choledochoduodenostomy (EUS-CDS) was performed from the duodenal bulb using a linear-array echoendoscope. The dilated CBD was identified and accessed using a 19-gage EUS needle. A 0.035-inch guidewire was advanced into the biliary system under fluoroscopic guidance (Figure 2). The tract was subsequently dilated using a cystotome, followed by placement of a fully covered self-expandable metal stent (SEMS; Figure 3). The stent measured approximately 10 mm in diameter and 60 mm in length, allowing effective drainage between the CBD and the duodenal lumen. Fluoroscopy was used throughout the procedure to confirm correct positioning and contrast flow within the biliary tree. Electrocautery-enhanced devices were not utilized in this case. Prophylactic intravenous antibiotics were administered peri-procedurally. The procedure was performed by an experienced attending interventional endoscopist with significant expertise in EUS-guided biliary drainage techniques.

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Figure 2.

EUS-guided puncture of the common bile duct from the duodenal bulb using a linear echoendoscope (model not specified), with visualization of the dilated CBD (blue arrow).

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Figure 3.

Fluoroscopic image showing contrast opacification of the biliary tree following guidewire insertion and successful deployment of a fully covered metallic stent across the choledochoduodenostomy tract.

Following the attempted ERCP, the patient developed mild acute pancreatitis, diagnosed based on abdominal discomfort, elevation of serum lipase to more than 3 times the upper limit of normal, and supportive clinical findings. No evidence of necrosis or organ failure was noted, consistent with mild pancreatitis according to the revised Atlanta classification. Prophylactic rectal nonsteroidal anti-inflammatory drugs (NSAIDs) were not administered prior to ERCP due to institutional practice variability, and pancreatic duct stenting was not feasible given failed cannulation. The patient was managed conservatively with intravenous fluid resuscitation, analgesia, and close monitoring, resulting in gradual clinical improvement without the need for intensive care unit admission. Anticoagulation was not in use at the time of the procedure. Post-procedural monitoring included serial laboratory assessment and clinical observation. Biliary drainage remained clinically effective, with progressive normalization of bilirubin levels over the subsequent days, indicating sustained stent patency during short-term follow-up. Table 1 summarizes the clinical course and events that occurred with the patient during his hospital stay.

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Table 1.

Timeline of Clinical Course.

Time point	Clinical event
Day 0	Onset of jaundice
Day 2	Hospital presentation
Day 2-3	Laboratory evaluation and imaging confirming biliary obstruction
Day 3	Attempted ERCP (unsuccessful due to duodenal invasion)
Day 3 (same session)	EUS-guided choledochoduodenostomy performed
Day 4	Development of post-procedure pancreatitis
Following days	Clinical improvement with conservative management
Within several days	Patient discharged

Following successful biliary decompression, the patient was evaluated for continuation of systemic therapy with palliative intent. Restoration of biliary drainage allowed consideration of resuming chemotherapy, highlighting the importance of effective biliary intervention in maintaining oncologic treatment pathways in advanced disease.

Discussion

The 2 primary histological subtypes of EC are ESCC and EAC, each with distinct epidemiology and clinical features. ² EAC often develops from Barrett’s esophagus (BE), with gastroesophageal reflux disease (GERD) being the strongest risk factor. However, up to 40% of EAC patients report no reflux. Obesity, especially central obesity, and smoking also elevate risk. EAC is more prevalent in men, potentially due to hormonal and physiological differences. Interestingly, Helicobacter pylori infection appears protective, while alcohol consumption has no clear association.^{2 -4} Dysphagia and weight loss are common symptoms, affecting 79% and 53% of patients, respectively.^4,5

EAC may arise through gradual accumulation of genetic mutations, with early CDKN2A and later TP53 mutations, or via TP53-mutant cells acquiring genomic instability and oncogenic amplifications. Notch1 and TP53 mutations are observed in normal esophageal epithelium, suggesting early carcinogenic pressure. Genetic susceptibility loci such as FOXF, BARX1, and ABCC5 are linked to BE and EAC risk. ¹

BE progresses through metaplasia to dysplasia and eventually EAC. Early detection and surveillance are essential, as EAC prognosis remains poor at advanced stages. Surveillance of BE reduces EAC incidence and improves outcomes.^4,6 Chemoprevention with PPIs, aspirin, and NSAIDs may reduce risk via anti-inflammatory pathways.^4,7 Novel BE screening tools include the cytosponge, transnasal endoscopy, and breath tests.^6,8 Endoscopic biopsy remains the diagnostic gold standard. ⁶ Accurate TNM staging is crucial, with PET/CT and endoscopic ultrasound recommended for advanced disease, although limited in early-stage EAC. Endoscopic resection is preferred for T1a tumors, requiring precise staging to avoid overtreatment. ⁶

Treatment is stage-dependent. Non-dysplastic BE is managed with PPIs and surveillance, while dysplasia is treated with EMR and RFA. ⁴ Early EAC may be treated endoscopically or surgically. ⁹ Locally advanced disease is managed with neoadjuvant chemoradiotherapy (CROSS) or perioperative chemotherapy (FLOT), followed by surgery. ⁴ Metastatic EAC is treated with systemic therapy per NCCN guidelines, with Lonsurf approved for late-line treatment. Currently, only HER2, VEGFR2, and PD-1 are validated molecular targets, underscoring the need for novel therapies. ⁴

Over the past 2 decades, endoscopic ultrasound (EUS) has evolved from a diagnostic tool into a versatile therapeutic platform, particularly through the development of EUS-guided biliary drainage (EUS-BD). This minimally invasive technique provides an effective alternative to percutaneous and transpapillary approaches, especially in cases where endoscopic retrograde cholangiopancreatography (ERCP) fails due to anatomical alterations, malignant infiltration, or surgically altered anatomy. EUS-BD is now routinely employed in both benign and malignant biliary obstructions, including distal and hilar strictures secondary to pancreatic cancer, cholangiocarcinoma, and metastatic disease.^9,10

EUS-BD can be performed via intrahepatic or extrahepatic routes using several techniques: hepaticogastrostomy (EUS-HGS), EUS-CDS, antegrade transpapillary stenting, and EUS-guided rendezvous (EUS-RV). Technique selection is guided by the site of obstruction, degree of ductal dilation, access to the papilla, and operator experience. ⁹

EUS-CDS is preferred for distal malignant biliary obstruction when the common bile duct (CBD) is dilated and accessible from the duodenal bulb. It involves EUS-guided puncture of the CBD with a 19G needle, followed by guidewire insertion, tract dilation, and stent placement between the CBD and duodenum. The advent of electrocautery-enhanced lumen-apposing metal stents (EC-LAMS) has enhanced procedural efficiency by allowing single-step access, dilation, and stenting. Technical and clinical success rates exceed 93%, with adverse events ranging from 10% to 14%, including stent misdeployment, bile leakage, and late stent occlusion.^9,11 This technique was used in our case after failure to perform an ERCP, where at the level of duodenal bulb through the guidewire we drained the CBD under fluorescence and we succeeded in inserting a regular metallic stent.

EUS-HGS is typically used when EUS-CDS is not feasible—such as when the CBD is not dilated, the duodenum is inaccessible, or tumor invasion blocks papillary access. It is particularly useful in proximal or hilar malignant biliary obstruction, such as Bismuth II to IV strictures requiring bilateral drainage. The left intrahepatic bile duct (segment 2 or 3) is punctured via the stomach, a guidewire is advanced into the biliary system, the tract is dilated (commonly with a 6-Fr cystotome), and a self-expandable metal stent (SEMS) is deployed to form a fistula. Segment 2 offers better guidewire control but poses a higher risk of mediastinal injury. Partially covered SEMS (PC-SEMS) are now preferred due to their anti-migration design. Clinical success ranges from 80% to 100%, with technical success rates as high as 100%, though EUS-HGS is associated with higher complication and reintervention rates compared to EUS-CDS.^10,11

EUS-guided antegrade stenting is another alternative, especially when transpapillary stenting is needed but ERCP cannulation has failed. It involves puncture of a dilated intrahepatic duct, guidewire passage through the obstruction and papilla (or anastomosis), and antegrade SEMS deployment. This technique preserves physiologic biliary flow, making it valuable in altered anatomy. However, its technical difficulty lies in guidewire manipulation, and it carries a 92% technical success rate with ~14% adverse events.^9,12

EUS-guided rendezvous (EUS-RV) is an option when the papilla is reachable but biliary cannulation fails. After EUS-guided bile duct access, the guidewire is advanced through the papilla and retrieved endoscopically to facilitate ERCP. EUS-RV is favored in benign obstructions, with success rates of 72% to 98% and adverse event rates of 13% to 34%, the latter higher when intrahepatic access is used.^9,12

In select scenarios where both ERCP and standard EUS-BD approaches fail, EUS-guided gallbladder drainage (EUS-GBD) may be used, particularly in patients with malignant distal obstruction and a patent cystic duct. Using EC-LAMS, a cholecysto-enteric fistula is created via the gastric antrum or duodenal bulb. Meta-analyses show technical success of 99.2% and clinical success of 88.1%, with 13.7% experiencing mostly mild to moderate complications. EUS-GBD is now preferred over percutaneous drainage in high-risk surgical candidates with acute cholecystitis and has growing indications in malignant settings. ⁹

For patients with Roux-en-Y gastric bypass, the EDGE (EUS-directed transgastric ERCP) procedure allows ERCP access via a temporary gastrogastrostomy created with LAMS. Once the tract is dilated (~18 mm), a duodenoscope is passed to complete ERCP. Though effective, EDGE carries risks such as stent migration and persistent fistula, requiring careful procedural technique and follow-up. ¹²

Mengistie et al also highlights the critical importance of careful multimodality imaging in identifying atypical patterns of disease spread and guiding intervention. As demonstrated in other rare clinical scenarios, including atypical imaging presentations in unrelated conditions, meticulous imaging interpretation can prevent misdiagnosis and directly influence management decisions. ¹³

Management of malignant distal biliary obstruction typically begins with ERCP; however, failure rates increase significantly in the presence of duodenal obstruction or tumor infiltration, as observed in this case. Alternative approaches include PTBD, surgical bypass, and EUS-BD. PTBD has historically been the standard rescue technique following failed ERCP but is associated with higher morbidity, including infection risk, catheter-related complications, and reduced patient quality of life due to external drainage. Surgical bypass, while effective, is generally reserved for patients with longer life expectancy due to its invasive nature and associated perioperative risks. EUS-BD, particularly EUS-CDS, offers a minimally invasive internal drainage option with high technical and clinical success rates. In our patient, EUS-CDS was preferred over PTBD due to the presence of extensive metastatic disease, the need for rapid palliation, avoidance of external drainage, and the availability of local expertise in advanced endoscopy.

A focused literature review was conducted using PubMed and Google Scholar databases, searching for combinations of terms including “esophageal adenocarcinoma,” “biliary obstruction,” “metastasis,” and “EUS-guided drainage” up to 2025. This search revealed only a very limited number of reported cases of EAC metastasizing to the biliary tree, and even fewer requiring EUS-guided biliary drainage following failed ERCP. This underscores the exceptional rarity of our case.

This case presents a rare and unique manifestation of metastatic EAC with biliary obstruction due to metastatic invasion of the distal biliary tree, a complication scarcely reported in the literature. While EAC commonly metastasizes to the liver, lungs, adrenal glands, and bones, direct involvement of the biliary tract is exceptionally unusual. ¹⁴ Even more distinctive is the failure of conventional ERCP due to metastatic infiltration of the second portion of the duodenum, necessitating echo-endoscopic drainage a technically challenging and less commonly employed intervention. Differentiating intrinsic biliary invasion from extrinsic compression or a second primary malignancy remains challenging in advanced oncologic cases. In our patient, the diagnosis of metastatic involvement of the distal CBD was based on multimodal imaging demonstrating continuity between peri-duodenal metastatic disease and the biliary obstruction, in the absence of histologic confirmation. While tissue diagnosis would have strengthened diagnostic certainty, the imaging pattern and clinical context strongly supported metastatic infiltration. This case is further complicated by the patient’s extensive metastatic burden involving the liver, adrenal glands, lymph nodes, lungs, peritoneum, and bones, alongside prior history of testicular cancer, making it a diagnostically and therapeutically complex scenario. The development of post-ERCP pancreatitis adds another layer of clinical difficulty. This constellation of features highlights not only the aggressive nature of EAC but also the importance of personalized, multidisciplinary approaches in managing advanced disease with atypical metastatic patterns. To our knowledge, reports of biliary tree obstruction due to EAC metastases—requiring endoscopic ultrasound-guided biliary stenting because of duodenal involvement are extremely limited, making this a notably rare and educationally valuable case in oncologic gastroenterology.

A number of limitations should be acknowledged in this report. First, this is a single case report, which inherently limits the generalizability of the findings and precludes drawing firm conclusions regarding optimal management strategies or outcomes. Second, the diagnosis of biliary involvement by metastatic esophageal adenocarcinoma was not confirmed histologically. Although multimodal imaging strongly suggested direct metastatic invasion of the distal common bile duct, the absence of tissue confirmation (via EUS-guided fine needle aspiration or biliary brush cytology) introduces a degree of diagnostic uncertainty, particularly in differentiating true intraductal metastasis from extrinsic compression. Third, the short duration of follow-up limits assessment of long-term stent patency, delayed complications, and overall clinical outcomes after EUS-guided biliary drainage. Additionally, procedural details such as the lack of prophylactic rectal NSAIDs and inability to perform pancreatic duct stenting may have contributed to post-ERCP pancreatitis, highlighting variability in practice patterns that could influence outcomes. Finally, as this intervention was performed in a specialized center with advanced endoscopic expertise, the reproducibility of this approach may be limited in settings with less experience in EUS-guided biliary drainage techniques. Despite these limitations, this case provides valuable insight into a rare metastatic presentation and supports the role of EUS-guided biliary drainage as an effective rescue therapy in complex malignant biliary obstruction.

Conclusion

In conclusion, this case highlights an exceptionally rare presentation of esophageal adenocarcinoma with extensive metastatic spread, including direct invasion of the biliary tree and duodenum. The resulting biliary obstruction, unmanageable through conventional ERCP, required advanced echo-endoscopic intervention, underscoring the complexity of care in advanced EAC. Such unusual metastatic patterns emphasize the need for heightened clinical awareness and individualized, multidisciplinary treatment strategies. Given the scarcity of similar reports in the literature, this case contributes valuable insight into the diverse metastatic behavior of EAC and reinforces the importance of adaptable endoscopic techniques in managing complicated oncologic presentations.