We described a case where gastric remnant necrosis developed after a distal gastrectomy. To the best of our knowledge, this is the first report of gastric remnant necrosis after gastrectomy caused by CCE. This case is instructive because 1) gastric necrosis can be a presentation of CCE, in addition to kidney and skin involvement, and 2) the mortality of gastric remnant necrosis after gastrectomy is very high; therefore, it is essential to manage this risk before and during surgery.
CCE, also referred to as atheroembolism or cholesterol embolization syndrome, is a rare manifestation of atherosclerotic disease . It occurs when an atherosclerotic plaque in the aorta or another major artery ruptures and releases cholesterol crystals and atheroma debris into the bloodstream, eventually occluding small arteries and arterioles, and resulting in severe end-organ damage . CCE can be induced after iatrogenic mechanical trauma such as vascular surgery, angiography, or angioplasty, or as a side-effect of medications (anticoagulants or thrombolytics) targeting the coagulation system . This patient developed CCE after percutaneous coronary intervention. The incidence of CCE has been reported to be 1.4% after coronary catheterization .
CCE affects multiple organs, especially those vulnerable to low blood perfusion such as the skin, kidneys, gastrointestinal system, and brain . The gastrointestinal tract is the third-most frequent organ affected (13.4%) next to the skin (15.5%) and kidneys (31.5%) . Within the gastrointestinal tract, the stomach is also the third-most common site (12.3%), next to the small intestine (33%) and colon (42.3%) . Two patterns of presentation of CCE in the digestive tract are recognized: 1) acute catastrophic multiorgan disorder with poor prognosis and 2) chronic indolent gastrointestinal diseases such as abdominal pain, diarrhea, and gastrointestinal bleeding secondary to ischemic colitis  . A catastrophic case of CCE leading to postoperative bowel infarction has been described . However, no previous case of gastric necrosis after gastrectomy caused by CCE has been reported.
The stomach has a rich blood supply and an extensive submucosal plexus. Gastric necrosis in patients with CCE may not have been reported because of the stomach’s abundant blood flow. Nevertheless, in our case, transient reduction of blood supply into the gastric remnant occurred during surgery, eventually leading to a postoperative catastrophe. The mortality associated with gastric remnant necrosis has been reported to be as high as 70% .
The main arterial feeders of the remnant stomach after distal gastrectomy with D2 lymph node dissection are the short gastric artery, the posterior gastric artery, and the left subphrenic artery. When these arteries are preserved, blood flow to the gastric remnant is usually sufficient. However, this was not the case here. Interruption of the blood flow to the gastric remnant causes necrosis. Several reported cases have occurred secondary to splenic infarction . However, some cases with a preserved splenic artery, as in the present case, have also been reported . The patient in our case suffered subtotal necrosis of the remnant stomach, revealing severe blood flow reduction. The general etiology of interruption of blood flow include arteriosclerosis, atrial fibrillation, sepsis, or venous thrombosis . In our patient, CCE obstructed the small arteries and arterioles within the submucosal plexus, and the resultant insufficient blood perfusion to the gastric mucosa led to necrosis of the remnant stomach.
Because the mortality of gastric remnant necrosis is very high, prevention is essential. CT angiography can be used to assess preoperative perfusion from the large vessels of the gastric walls . However, given that CCE occludes the small arteries and arterioles, CT angiography might not have been revealing. It is possible that it would have been preferable to perform total gastrectomy initially. We hypothesize that arterial flow to the jejunum is preserved because there is no resected vasculature of the jejunum. In contrast, blood flow to the lower part of the esophagus is supplied by esophageal branches of the left gastric artery, left subphrenic artery, and proper esophagus arteries. To sustain sufficient esophageal blood flow, we should preserve these vessels during the total gastrectomy operation. In addition, a systematic review of the literature suggested the effectiveness of indocyanine green fluorescence angiography for intraoperative assessment of gastrointestinal anastomotic perfusion . In this case, we should have assessed the risk of low blood flow of the remnant stomach; intraoperative indocyanine green fluorescence angiography would have been the preferred imaging modality. In addition, upper gastrointestinal endoscopy could be preferable to detect this rare complication early.
In conclusion, we encountered a case of gastric remnant necrosis caused by CCE after distal gastrectomy. Gastric necrosis can be a gastrointestinal presentation of CCE, and perioperative/intraoperative risk assessments may help prevent this complication.