申し訳ありません、このコンテンツはただ今　English　のみです。

Here, I present two patients with a peculiar mechanism that provokes debilitating postprandial vomiting. Neither patient was able to maintain their weight, despite the first patient having a nasojejunal tube. Even the slightest filling of the GI tract with food provoked nausea, headaches and vomiting. In the second patient, it also caused yellowish discolouration of the visual field, followed by postprandial blindness (amaurosis fugax).

The unifying characteristic was severe nutcracker syndrome, whereby the left renal vein is compressed while crossing the aorta, resulting in the development of a broad collateral pathway towards the spinal canal (tronc réno-rachidien). This collateral pathway chronically increased intraspinal and, consequently, intracranial pressure. The patients developed headaches, but the inability to be nourished by mouth or tube was even more debilitating, as any volume inside the GI tract would promptly induce vomiting.

A detailed functional ultrasound of the GI tract and blood vessels after food uptake demonstrates the causal relationship responsible for vomiting. The enlarging stomach or small bowel exerts additional pressure on the left renal vein. This subsequently increases the influx into the spinal canal via the renal-rachidian trunk and produces pressure waves travelling up to the brain, resulting in increased intracranial pressure, headaches and vomiting.

The first patient in the following medical video underwent surgery involving shielding of the left renal vein to reduce external pressure. Post-operatively, the vomiting stopped immediately. The patient was able to eat a slice of pizza and stop taking her pain medication.