A 78‐year‐old male presented for a second opinion of 4 months of recurrent nausea, vomiting, and abdominal cramping with an inability to tolerate solid foods. He had early satiety and abdominal distension with a 17‐pound weight loss. Previous admissions with recurrent bouts of gastric and colonic distension had required nasogastric decompressions and decompressive colonoscopies. A previous colonoscopy showed hepatic flexure narrowing, and abdominal CT revealed scattered inflammation in the hepatic flexure and ascending colon. Simultaneous with these symptoms, he was diagnosed with an enterococcal UTI and ARF with bilateral hydronephrosis (severe on the right) requiring percutaneous nephrostomy tubes placement. Cystoscopies revealed bilateral stenotic ureters, but no obvious cause was noted, and he persisted with mild hydronephrosis. An ex‐smoker, he had a history of NSCLC 5 years ago requiring left lower lobectomy. On examination, he had mild abdominal distension, epigastric tenderness, and hyperactive bowel sounds but no signs of an acute abdomen. He had mild anemia and an albumin of 3.5 g/dL. Initial CT abdomen only revealec moderate stranding around the second and third portions of Itie duodenum. EGD showed grade C esophagitis, severely dilated stomach, and edematous mucosa of the second portion of the duodenum. Colonoscopy showed narrowing at the hepatic flexure/ascending colon with no mucosal irregularities. Agastric emptying study confirmed severe gastroparesis. However, the workup failed to provide an etiology. Realizing that bilateral ureters, second and third parts of the duodenum, hepatic flexure, and ascending colon were all retroperitoneal structures, MRI of the abdomen with contrast was done. It suggested inflammatory changes in the right retroperitoneum, concerning for fibrosis. He had no history of granulomatous, connective tissue, or autoimmune disease. A CT guided retroperitoneal biopsy revealed metastatic non‐small cell carcinoma. His paraneoplastic panel showed high titers of antistriational antibodies, indicating lung cancer as likely primary. Because of his declining functional status, he was offered palliative care.
Nonsarcomatous malignancy can affect the retroperitoneum in 2 ways. Malignancy at distant sites (lung, breast, colon, testicles) generally produces retroperitoneal disease by hematogenous spread, whereas malignancy in surrounding organs can induce a secondary retroperitoneal fibrosis. Retroperitoneal involvement without overt primary disease presents in the late stages with obstruction of retroperitoneal organs or infiltration of the neurovascular structures. Our patient had struggled with recurrent obstructive symptoms for 4 months without a unifying diagnosis until the anatomical relationship of the structures involved was explored.
Good anatomical knowledge of the retroperitoneum can lead to an earlier diagnosis of infiltrative or fibrosing retroperitoneal disease which can probably help change the overall outcome.
M. Patel, none; A. Prabhakaran, none.