Gastrointestinal metastases are rare causes of GIB (Bhatia et al., 2006). GI involvement can be due to direct extension of primary or recurrent tumor in the renal bed or from hematogenous metastasis (Fidelman et al., 2010). Duodenum is the most common site of GI involvement, given its close proximity to the right kidney (Ouellet et al., 2018). Clinical symptoms of GI involvement are usually related to the tumor-related hemorrhage including melena (Ohmura et al., 2000; Ali et al., 2013), hematemesis (Blake et al., 1995), hematochezia (Ali et al., 2013), haemobilia (Lynch-Nyhan et al., 1987) and iron-deficiency anemia (Kobak et al., 2006), or bowel obstruction (Sadler et al., 2007). Sixty-nine percent of patients with solitary GI metastasis from RCC present with GIB, but massive GIB is a rare occurrence (Ohmura et al., 2000). An ulcerative metastatic mass in the duodenum is the main cause of GIB (Rustagi et al., 2011; Chang et al., 2004; Cherian et al., 2011). Duodenal involvement with pseudoaneurysm formation as the cause of GI bleeding has also been reported in patients with clinical history of RCC in the literature (Blake et al., 1995).
Management of patients with solitary metastatic RCC to the duodenum depends upon the extent and location of duodenal lesion and general conditions of the patient and should be individualized for each patient (Thyavihally et al., 2005). Endoscopic hemostatic control of GIB is usually difficult and in selected cases, intractable GI bleeding can be controlled by endovascular embolization of the tumor-supplying artery (Barth, 1991). This is only a palliative treatment and collateral vessels which have potential for re-bleeding may eventually develop at the site of metastatic lesion. It is also important to keep in mind that small bowel arteries embolization carries a risk of bowel ischemia and infarction (Blake et al., 1995; Lynch-Nyhan et al., 1987). To the best of our knowledge, in all reported cases of GIB secondary to RCC metastasis treated with endovascular approach, a tumor-supplying artery (including mesenteric, celiac, lumbar or intercostal branches) was embolized for hemostatic control. The present case is unique in the way that a pseudoaneurysm from the remaining accessory renal artery (not the tumor-supplying artery) formed a fistulous communication with duodenal lumen and caused massive GI bleeding. Endovascular embolization and coiling of the pseudoaneurysm was performed as an emergent life-saving procedure.
This case report highlights the importance of high index suspicion in post-nephrectomy patients for RCC, presenting with new symptoms. Aggressive gastrointestinal workup and adequate awareness of available minimally-invasive endovascular options for controlling GIB in these patients, are of paramount importance.