Recommended Citation
Capelli GP, Affi A. Gastroduodenal Fistula Stemming from a Prior Ulcer Amid NSAID Use. Presented at Scientific Day; May 21, 2025; Park Ridge, IL.
Abstract
Introduction/Background:
While the exact mechanism of fistula formation in cases of gastroduodenal fistulas (GDFs) is unclear, we present a case in which the primary suspect for GDF formation is fistulation originating from a previous gastric antral ulcer, compounded by persistent NSAID usage. This case also underscores the possibility of concomitant gastric ulcers along the GDF tract in individuals continuing NSAID therapy.
Description:
A 74-year-old male with a history of joint pain and non-steroidal anti-inflammatory (NSAID) use presented for weight loss. On physical examination, he appeared well without distress, abdominal pain, or discomfort. Laboratory findings showed a hemoglobin (Hb) level of 10.7 g/dL and mean corpuscular volume (MCV) of 86.0 fL. Esophagogastroduodenoscopy (EGD) revealed a 12mm Forrest III ulcer in the antrum. Biopsies revealed mild chronic gastritis, without evidence of H. pylori infection. The patient was told to stop NSAIDs and was prescribed twice daily PPI. An EGD three months later displayed a 3mm remnant ulcer with granulation tissue and patchy erythema in the antrum, indicative of mucosal healing. A year later, the patient presented with dizziness. He had been using supratherapeutic doses of NSAIDs for several months for knee pain. He denied nausea, vomiting, or abdominal pain, but reported melena. Laboratory findings showed a Hb of 4.3 g/dL and MCV of 76.0 fL. On examination, he appeared well without acute distress or abdominal pain. Repeat Hb following transfusion of three units of packed red blood cells was 8.3 g/dL. Repeat EGD identified a GDF at the previous ulcer site in the antrum. Additionally, a 3cm Forrest IIa ulcer was observed along the luminal wall of the fistula. Hemostasis was successfully achieved using epinephrine injection and bipolar electrocautery. Biopsies showed benign gastric mucosa without H. pylori infection. The patient experienced no post-procedural complications or recurrence of gastrointestinal hemorrhage. He was discharged with strict instructions to stop NSAIDs and was given twice daily PPI therapy.
Discussion:
While the exact mechanism of fistula formation in cases of GDFs is unclear, we present a case in which the primary suspect for GDF formation is fistulation originating from a previous gastric antral ulcer, compounded by persistent NSAID usage. This case also underscores the possibility of concomitant gastric ulcers along the GDF tract in individuals continuing NSAID therapy.
Presentation Notes
Presented at Scientific Day; May 21, 2025; Park Ridge, IL.
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Gastroduodenal Fistula Stemming from a Prior Ulcer Amid NSAID Use
Introduction/Background:
While the exact mechanism of fistula formation in cases of gastroduodenal fistulas (GDFs) is unclear, we present a case in which the primary suspect for GDF formation is fistulation originating from a previous gastric antral ulcer, compounded by persistent NSAID usage. This case also underscores the possibility of concomitant gastric ulcers along the GDF tract in individuals continuing NSAID therapy.
Description:
A 74-year-old male with a history of joint pain and non-steroidal anti-inflammatory (NSAID) use presented for weight loss. On physical examination, he appeared well without distress, abdominal pain, or discomfort. Laboratory findings showed a hemoglobin (Hb) level of 10.7 g/dL and mean corpuscular volume (MCV) of 86.0 fL. Esophagogastroduodenoscopy (EGD) revealed a 12mm Forrest III ulcer in the antrum. Biopsies revealed mild chronic gastritis, without evidence of H. pylori infection. The patient was told to stop NSAIDs and was prescribed twice daily PPI. An EGD three months later displayed a 3mm remnant ulcer with granulation tissue and patchy erythema in the antrum, indicative of mucosal healing. A year later, the patient presented with dizziness. He had been using supratherapeutic doses of NSAIDs for several months for knee pain. He denied nausea, vomiting, or abdominal pain, but reported melena. Laboratory findings showed a Hb of 4.3 g/dL and MCV of 76.0 fL. On examination, he appeared well without acute distress or abdominal pain. Repeat Hb following transfusion of three units of packed red blood cells was 8.3 g/dL. Repeat EGD identified a GDF at the previous ulcer site in the antrum. Additionally, a 3cm Forrest IIa ulcer was observed along the luminal wall of the fistula. Hemostasis was successfully achieved using epinephrine injection and bipolar electrocautery. Biopsies showed benign gastric mucosa without H. pylori infection. The patient experienced no post-procedural complications or recurrence of gastrointestinal hemorrhage. He was discharged with strict instructions to stop NSAIDs and was given twice daily PPI therapy.
Discussion:
While the exact mechanism of fistula formation in cases of GDFs is unclear, we present a case in which the primary suspect for GDF formation is fistulation originating from a previous gastric antral ulcer, compounded by persistent NSAID usage. This case also underscores the possibility of concomitant gastric ulcers along the GDF tract in individuals continuing NSAID therapy.
Affiliations
Aurora St. Luke's Medical Center