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Laparoscopic, Trans-Gastric Endoscopic Removal of Gastroesophageal Junction Gastrointestinal Stromal Tumors (GIST)

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract, believed to derive from the interstitial cells of Cajal in the gastrointestinal myenteric plexus, emanating from esophagus to anus. More than half of GIST tumors involve the stomach, but the small bowel and rectum are also frequently affected. Clinical presentation is often an asymptomatic incidental finding but symptomatology is variable including pain, nausea, indigestion, vomiting, and blood loss. GIST tumors are often encountered via endoscopy as a smooth submucosal mass that endophytically occupies space within the visceral lumen. But, it can also present as an ulcerated, ruptured, full-thickness, or serosally pedunculated mass.1 An endoscopic ultrasound guided needle biopsy will generally show spindle cell histology, which can be immunohistochemically characterized. Preoperative biopsy is not mandatory in the surgical management of gastric GIST tumors, but it is often undertaken to verify the diagnosis of GIST and proactively triage the extent of any anatomical lymphatic exploration that would be necessary if the tumor was neuroendocrine or carcinomatous in nature. Sufficient preoperative staging for GIST is done with contrast-enhanced CT of the chest, abdomen, and pelvis where the GIST is usually seen as an encapsulated mass often with heterogeneous enhancement secondary to internal necrosis.1 Nonmetastatic lesions are brought to the operating room for resection with grossly negative margins. There has been a failure to demonstrate any improved outcome or recurrence rate with increasing surgical margin width. The key pathological parameters of a resected gastric GIST include tumor site, size, focality, mitotic rate, immunohistochemical status, margin status, and molecular genetic studies. The American Joint Committee on Cancer seventh edition staging system separates gastric and omental GIST tumors from nongastric GIST tumors. Validated tools available for predicting postoperative prognosis include the Memorial Sloan Kettering Cancer Center nomogram and the National Institutes of Health criteria, both of which heavily weigh tumor size and mitotic rate. These predictors of outcome are routinely used to assess the need for adjuvant therapy with a tyrosine kinase inhibitor such as imatinib.1 A 74-year-old woman with renal cell carcinoma of her right kidney and an endoscopic ultrasound biopsyproven GIST on the posterior aspect of the gastric cardia near the gastroesophageal (GE) junction was referred for simultaneous surgical treatment of both tumors. Preoperative CT evaluation elucidated a mass at the inferior pole of her right kidney and an encapsulated mass with homogenous enhancement at the posterior gastric wall near the GE junction. Preoperative upper endoscopy showed a 2-cm endophytic gastric mass intermittently protruding through the lower esophageal sphincter, deemed the source of her presentation with dyspepsia and reflux. Needle biopsy showed spindle cell histology consistent with GIST and no mitotic activity was visualized, consistent with a very low-risk lesion. The 5-mm right hypogastric and 10-mm umbilical trocars used during the laparoscopic right radical nephrectomy were recycled as extragastric ports for the resection of her GIST. After the patient was repositioned supine, another “exogastric” left hypogastric 5-mm port was placed. The stomach was endoscopically insufflated and control stitches were placed into the gastric parenchyma to mobilize it toward the abdominal wall. With the stomach abutting the abdominal wall, two 5-mm and one 12-mm balloon trocars were penetrated through the abdominal wall and the anterior gastric wall into the lumen Video Presented at the Southeastern Surgical Congress 2017 Annual Meeting, February 27, 2017, Nashville, TN. Address correspondence and reprint requests to Aaron Lee Wiegmann, B.S., Department of Surgery, Rush University Medical Center, 1725 West Harrison Street 810, Chicago, IL 60612. E-mail: aaron_L_wiegmann@rush.edu.