Post written by Sonmoon Mohapatra, MD, from the Division of Gastroenterology and Hepatology, Saint Peter’s University Hospital/Rutgers—RWJ Medical School, New Brunswick, New Jersey, USA.

A 65-year-old woman with a history of Barrett’s esophagus, decompensated alcoholic cirrhosis (MELD 8, Child Pugh class B) complicated by ascites, esophageal varices, gastric antral vascular ectasia, hepatic encephalopathy, and severe thrombocytopenia underwent a surveillance EGD for Barrett’s esophagus. EGD noted a nodular lesion arising from Barrett’s esophagus (BE) [C1M3], with a biopsy reading at least intramucosal cancer. Under endoscopic ultrasound, the lesion was not well visualized because of diffuse mucosal edema. Submucosal and extramural varices were seen in the distal esophagus. Computed tomography (CT) of the chest, abdomen, pelvis, with intravenous contrast showed no evidence of loco-regional lymphadenopathy or distant metastasis. Given the lesion size, and prior biopsy of at least intramucosal cancer, ESD was planned to offer accurate pathological diagnosis and curative resection for early BE adenocarcinoma. Because of her baseline low platelet count [30 k/µL], she was given Avatrombopag (thrombopoietin receptor agonist), 5 days prior to the procedure. The platelet count was 48K after receiving Avatrombopag. She received 1-unit platelet transfusion during the procedure. EGD demonstrated a 15- x 10-mm depressed lesion with disrupted surface pattern in the esophagogastric junction at 28 cm from the incisors. Thermocautery markings were placed 5 mm around the lesion edge. The area around the lesion was injected with mixed solution of hetastarch and methylene blue. Mucosal incision and submucosal dissection performed using a 2-mm dual knife JET [Olympus America, Center Valley, Pa, USA]. The lesion was noted to be hyper-vascularized. Major oozing and visualized blood vessel were controlled with coagulation forceps and minor bleeding was treated with close tip of the dual knife. A long, tortuous submucosal varix was identified which was procoagulated using coagulation forceps. The varix was cut after it was coagulated. The lesion was removed in en bloc fashion. She was admitted for observation and the postprocedural course was uneventful. Final pathologic examination revealed T1a esophageal adenocarcinoma, in a background of high-grade columnar epithelial dysplasia. Both lateral and deep margins were noted to be negative. No poorly differentiated component or lymphovascular invasion was identified. Curative resection was achieved and surveillance endoscopy and treatment of remaining BE was recommended.

To date, only small case series of esophageal ESDs especially for squamous cell carcinoma have been reported from Asia in patients with cirrhosis, but the included patients were well compensated with platelet count > 50k/µL. Here, we present a case of Barrett’s-associated adenocarcinoma in a patient with decompensated cirrhosis, platelet count < 50 k/µL, and EV, who was successfully treated with ESD.

Esophageal ESD is feasible for Barrett’s-associated superficial adenocarcinoma in a decompensated cirrhotic patient with esophageal varices and severe thrombocytopenia. Presence of esophageal varices, portal hypertension, or severe thrombocytopenia are not absolute contraindications for esophageal ESD, if performed carefully after proper medical optimization preprocedurally. Extra care should be taken to avoid inadvertent injury to submucosal varix for successful completion of the procedure.

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