The patient is a 22 year old male, asthenic, asthenic, slim and thin, who has been coming to our health centre repeatedly in the last month due to stabbing epigastric pain associated with nausea and postprandial vomiting that relieves the pain. The episodes have been occurring for 7 years, for which reason she has consulted the emergency services on multiple occasions, but no acute pathology has ever been found.
She was admitted 3 years ago for one of these episodes, undergoing gastroscopy with gastric biopsy which was positive for H. pylori; she underwent eradication treatment with current triple therapy (omeprazole, amoxicillin and clarithromycin), with a subsequent negative breath test for H. pylori infection. Due to persistent symptoms, treatment was started with antiemetics and multiple proton pump inhibitors, with no long-term response. On admission, he was assessed by the Mental Health Service, as the symptoms of acute pain persisted, which subsided with vomiting, and he was diagnosed with an anxious-depressive syndrome with poor follow-up and non-compliance with treatment. He had no food or drug allergies. Currently, the pain subsided in the genupectoral position and with cannabis consumption.
On examination we found a patient with stable vitals, with a BMI of 17.7. The abdomen was excavated, tympanic, soft and slightly painful on deep palpation in the epigastrium, with no palpable masses, adenopathies or megaliths.
Laboratory tests showed no abnormalities; no anaemia, negative inflammatory response markers, no liver or electrolyte abnormalities, total protein 5.8 g/dL (normal value 6.4 to 8.3 g/dL). The abdominal X-ray showed no signs of intestinal obstruction.
A total abdominal ultrasound was performed in the supine decubitus position, with no evidence of relevant findings, for which reason we decided to consult the Digestive Service, where, after being assessed, a barium bowel transit was requested, with a delay of more than 8 hours due to slow gastric emptying due to a permanent decrease in calibre in the 3rd duodenal portion, suggestive of extrinsic compression, which did not prevent the distal passage of contrast, all compatible with vascular compression. In view of this finding, a CT angiography of the abdomen was performed, with the result of a vascular clamp that produced compression of the 3rd portion of the duodenum. The mesenteric clamp affected the duodenum and the left renal vein, producing compression and pre- and post-compression dilatation.