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.