Esophageal Bleeding and Radiational Esophagitis Presenting as Acute Gastroesophageal Junction Obstruction

Abstract

Acute gastroesophageal junction obstruction is an uncommon condition that can raise concern for malignancy. We report a case of spontaneous esophageal bleeding of a patient on chronic anticoagulation who received radiation therapy 4 months prior, presenting with sudden-onset intractable nausea, vomiting, and abdominal pain. Imaging demonstrated marked esophageal dilation with distal obstruction. Endoscopy revealed a large friable, near-obstructing esophageal mass with extensive clot burden. Repeated biopsies showed necrotic debris, inflammation, and fungal elements without malignancy. Endoscopic removal led to complete symptom resolution.

Introduction

GEJ obstruction is commonly caused by malignancy or chronic stricture formation presented with progressive course. Acute gastroesophageal junction (GEJ) obstruction is rare and can be caused by foreign body impaction, severe motility disorders, vagal nerve injury, or hematoma. Radiation-induced esophageal injury is a complication of thoracic radiotherapy and can lead to mucosal inflammation, ulceration, and bleeding.¹ Acute GEJ obstruction caused by esophageal blood clot in the setting of radiational esophagitis has not been reported to our knowledge. We present a case of acute GEJ obstruction concerning obstructive esophageal malignancy that was ultimately found to represent a large, organized clot associated with severe esophageal inflammation.

Case Report

A 76-year-old woman with a past medical history of breast cancer status post left partial mastectomy, chemotherapy and radiation therapy (last treatment 4 month prior), hypertension, hyperlipidemia, type 2 diabetes mellitus, and recurrent venous thromboembolism on apixaban presented with 3 days of severe nausea, intractable vomiting, upper abdominal pain, and blood-tinged sputum following a precipitating mechanical event in which she remained on a bedpan for approximately 45 minutes with upper-body twisting. She experienced numerous subsequent episodes of emesis and an inability to tolerate solid food, without prior similar symptoms. Her history was notable for chronic constipation with bowel movements every 3 days, longstanding inability to undergo colonoscopy due to intolerance of bowel preparation, and a 70-lb unintentional weight loss over the preceding year associated with diminished appetite due to chemotherapy and radiation therapy. Computed tomography angiography of the chest, abdomen, and pelvis demonstrated marked dilation of the midthoracic esophagus with a transition point at the GEJ, raising concern for a distal obstructing lesion vs a severe motility disorder. Hemoglobin was stable at baseline (8.8 g/dL) after symptom onset.

Esophagogastroduodenoscopy (EGD) revealed a large friable mass extending 25–40 cm from the incisors, traversing the GEJ and nearly occluding the lumen (Figure 1A and B). The mass was coated with adherent clots and oozed with contact. The stomach was diffusely coated with old blood, and clots were noted in the cardia and fundus (Figure 1C and D). The duodenum appeared normal. The mass could not be cleared, and multiple biopsies were obtained. Attempt of inserting nasal gastric feeding tube was made but unsuccessful. Given the high aspiration risk and inability to fully clear esophageal obstruction, the patient remained intubated after EGD. Biopsy histology demonstrated necrotic debris, fibrin, chronic inflammatory cells, calcification, yeasts, and foreign-body material without viable tissue, dysplasia, or malignancy; multiple deeper levels and immunohistochemical stains for herpes simplex virus, cytomegalovirus, and Grocott methenamine silver yielded no evidence of infectious or neoplastic pathology.

Figure 1.

Large friable mass (A and B) and signs of bleeding in the gastric cardia and fundus (C and D) from the first esophagogastroduodenoscopy.

Two days later, a repeated EGD was performed with attempt of obtaining more biopsies and navigate feeding pathway. Persistent but markedly reduced lesion was seen, allowing passage of the endoscope without resistance (Figure 2A and B). The clot was broken down into pieces and dragged past the GEJ into the stomach by a cold snare, subsequently retrieved with a Roth net (Figure 2C). The esophagus was patent without any obstruction (Figure 2D). Inspection revealed half-circumferential ulceration, erythema, and nodularity involving the mid, distal esophagus, and GEJ, with minimal oozing (Figure 2E and F). Biopsies of underlying mucosa (arrows in Figure 2E and F) again demonstrated benign squamous and columnar epithelium with reactive changes, necrotic debris, acute and chronic inflammation, calcification without evidence of malignancy. The patient was successfully extubated 1 day later, with complete resolution of symptoms. She was discharged without complications on a 2-week course of fluconazole and pantoprazole 40 mg daily.

Figure 2.

Mass with reduced size (A and B) in the second esophagogastroduodenoscopy, retrieved with a Roth net (C). Patent esophagus (D) with ulceration, erythema, and nodularity involving the mid, distal esophagus, and gastroesophageal junction which were biopsied (arrows in E and F).

Discussion

Acute obstruction of the GEJ can be caused by a broad spectrum of mechanical, inflammatory, and functional processes. While progressive GEJ obstruction is commonly caused by malignancy or chronic stricture formation, sudden-onset obstruction is comparatively uncommon in the absence of obvious causes such as foreign body injections or surgical injury of the vagal nerve.

Sudden GEJ obstruction may arise from nonneoplastic etiologies, including intramural esophageal hematoma (IEH), localized infectious masses, or inflammatory processes. IEH typically presents with abrupt onset of chest or epigastric pain, dysphagia, hematemesis, and is commonly associated with trauma, endoscopic instrumentation, or severe retching.² Cases of spontaneous IEH were also reported in the absence of antecedent trauma, either with or without anticoagulant therapy, and can be mistaken for other causes of luminal narrowing.3, 4, 5 Severe IEH could mimic malignancy on imaging with rapid worsening of dysphagia which requires emergent surgical intervention.⁶

Infectious etiologies represent another potential cause of sudden GEJ obstruction. Although Candida esophagitis classically presents as white mucosal plaques in immunocompromised individuals, a rare case described esophageal candidiasis forming a bulky pseudotumor that mimics malignancy, including positron emission tomography–avid lesions, with full-thickness resection ultimately excluding cancer.⁷ EGD with biopsy remains the gold standard for diagnosis in such cases, given the similarity in clinical and endoscopic presentation to neoplastic disease. Histopathology often reveals necrotic and inflammatory material without viable neoplastic cells.⁸ This pattern was observed in the present case, in which repeated biopsies demonstrated inflammatory debris, yeasts, and calcification in the absence of malignancy despite the concerning endoscopic findings.

Rarer causes of sudden GEJ obstruction include new-onset achalasia and hematoma formation arising from benign or malignant esophageal tumors. The estimated incidence and prevalence of achalasia are approximately 1 to 5 and 7 to 32 per 100,000 individuals, respectively, with a mean age at diagnosis greater than 50 years.⁹ Benign esophageal tumors account for fewer than 1% to 5% of all esophageal tumors, and bleeding represents one of their rarest complications.^10,11 Esophageal carcinoma remains the most common malignant esophageal tumor, and tumor ulceration has been reported to account for 53.8% of bleeding episodes in a prior multicenter study.¹² To our knowledge, hematoma formation causing acute obstruction in esophageal carcinoma or other malignant esophageal tumors have not been previously reported.

A unique aspect of this case is the recent radiation therapy for breast cancer. Radiation esophagitis (RE) is a recognized complication of thoracic irradiation, with up to 42% of patients experiencing RE following radiation therapy.¹ Acute RE typically develops within 2 to 3 weeks of initiating radiation therapy, whereas late-onset injury may occur months later. Mild cases may remain asymptomatic or self-limited after completion of therapy, while severe cases can be complicated by stricture formation, dysmotility, ulceration, bleeding, or tracheoesophageal fistula formation. Patients with severe RE may present with nausea, vomiting, dysphagia, weight loss, anorexia, or odynophagia.¹³ In the present case, the patient likely experienced mild RE manifested by weight loss, which was initially attributed to chemotherapy-related anorexia. The episode of prolonged upper-body twisting may have served as a precipitating mechanical stressor, triggering acute bleeding from inflamed or ulcerated esophageal mucosa. Diagnostic assessment was challenged by the absence of gastrointestinal symptoms following radiation therapy and the history of breast cancer, which raised the concern for esophageal malignancy. Ultimately, repeated biopsies confirmed esophageal bleeding with organized clot formation as the cause of acute GEJ obstruction.

Conclusion

Acute GEJ obstruction may result from hematomas or infectious masses that mimic malignant disease. Recognition of IEH and infectious pseudotumor as potential etiologies is essential to avoid misdiagnosis and unnecessary oncologic intervention. Sequential diagnostic evaluation including repeat endoscopy following clearance of obstructive material, comprehensive histologic assessment, and careful clinical correlation is critical to guiding appropriate management.