Discussion 
Gastrosplenic fistula due to type V gastric ulcer complicated by massive GIB is rare. There are five types of benign gastric ulcers including true gastric ulcers at incisura angularis (type I), combined gastric and duodenal ulcers (type II), Pyloric and pre-pyloric ulcers (type III), ulcers high along lesser curvature within 1-2cm of gastroesophageal junction (type IV) and gastric ulcers anywhere secondary to medications (type V)5. The incidence of type V ulcers is <5%. The proposed pathogenic mechanism of GSF are progressive infiltrative, erosive, and penetrating lesions of spleen and/or adjacent gastric wall. A subset of patients with GSF, present with GIB due to necrosis of underlying blood vessel in splenic parenchyma, gastric wall and gastrosplenic ligament that contains short gastric, and left gastroepiploic vessels6.
In our case the patient had significant drop in hemoglobin from his baseline and evidence of GSF on cross-sectional radiologic images that was the source of GIB. Abdominal CT was negative for splenic abscess, ischemia, lymphadenopathy or mass concerning for malignancy. Although patient was hemodynamically stable on admission and there was no active bleeding on CT scan, an embolization of the main splenic artery, right gastroepiploic, and left omental artery was performed by interventional radiology prior to EGD to prevent procedural related risks of iatrogenic bleeding as biopsy of gastric ulcer was essential to rule out malignancy and other etiologies of GSF7. Gastric biopsies were negative for H-pylori, malignancy, however demonstrated non-specific findings of mild chronic inflammation and reactive gastropathy that may be seen in patients with GSF and its sequalae. Operative findings and pathology of operative specimen demonstrated transmural granulation tissue and acute inflammation with acute serositis and mucosal ulceration consistent with type V gastric ulcer. The risk factor of type V gastric ulcer in our patient was chronic NSAID’s use intermittently for back pain which may results in fistulation due to chronic inflammation involving transmural gastric wall ulceration.
Prior to definitive surgical management of GSF, an EGD evaluation of other causes of upper GIB is crucial to establish etiology by obtaining tissue diagnosis. Surgical resection of GSF is curative treatment. The choice of surgical resection depends on patient’s hemodynamic stability, extension of underlying disease and surgeons’ preferences. Laparoscopic partial gastrectomy with or without splenectomy is common method of surgical resection with favorable outcomes1,2,8. Non-surgical management of GSF with chemotherapy has also been reported effective in several cases of DLBCL8-10.