Gastroparesis or delayed gastric emptying occurs when the stomach is paralyzed and gastric emptying is impaired. As a result, patients report bloating, nausea, vomiting, and pain. The underlying pathophysiology of gastroparesis is poorly understood. The cause of gastroparesis is also unknown. When patients with diabetes develop gastroparesis, the condition is called diabetic gastroparesis. It appears that in diabetic patients enteric nerve damage results in gastric dysmotility. However, the relationship between diabetes and gastroparesis is far more complex than a simple neuropathy. Normally, rising blood sugar levels halt gastric emptying as a protective measure against further nutrient passage into the intestines and sugar absorption. In type 2 diabetic patients abnormal gastric emptying may be the cause of diabetes rather than the result. In fact, type 2 Diabetes may be looked at as a gastro-intestinal motility disorder resulting in insulin resistance. Dr. Mason, the father of bariatric surgery, is an avid proponent of this theory. The early resolution of type 2 Diabetes immediately following gastric bypass and sleeve surgery is partly secondary to faster delivery of food to the distal small bowel. Gastric sleeve increases gastric emptying allowing food particles to reach the distal bowel to stimulate more L cells leading to increased GLP-1 secretion. L cells are specialized cells that react to glucose in ingested food and secrete several hormones like GLP-1 that affect glucose metabolism. GLP-1 stimulates insulin secretion and blocks glucagon secretion hence improving post-prandial blood sugar levels.
Several studies have shown that gastric sleeve surgery increases gastric emptying. Few years ago, I used this concept to treat a severe case of diabetic gastroparesis in a 45-year-old male. I performed a longitudinal gastrectomy to mimic the effects of gastric sleeve and improve gastric emptying. I also added a duodeno-jejunostomy to promote duodenal emptying. The patient immediately improved and was tolerating regular diet few days after surgery. Interestingly, his diabetes resolved immediately after surgery. This observation shows again that type 2 Diabetes is primarily a gastro-intestinal motility disorder. I did not consider a gastric bypass in this particular patient because the stomach was massively dilated. Gastric remnant secretion would accumulate in the stomach causing symptoms. A recent study from the Cleveland Clinic showed that gastric bypass surgery is effective in morbidly obese gastroparesis patients and safer than subtotal gastrectomy. The series was small (7 patients) and the follow up was short. Two patients were converted to subtotal gastrectomy for persistent gastroparesis related symptoms following gastric bypass surgery. In my opinion, gastroparesis is a generalized motility disorder that affects the duodenum and sometimes the entire small bowel. Simply bypassing the stomach and proximal bowel may not resolve the symptoms especially in severe cases. A modified gastric sleeve or longitudinal gastrectomy is a more effective option that addresses the underlying problem. By resecting the gastric fundus and most of the greater curvature, stomach compliance decreases leading to improved gastric emptying. Furthermore, the malfunctioning gastric pacemaker that is located along the greater curvature is eliminated and potentially leading to increased motility. I recommend leaving the antrum intact as it represents the gastric pump and may help promote gastric emptying.
In summary, gastrointestinal motility affects many functions in the body and contributes to many diseases like acid reflux, diabetes and obesity. Gastric motility patterns are highly coordinated and still poorly understood. Lessons learned in gastric sleeve surgery may be applied to severe refractory gastroparesis cases. Future studies are needed to establish longitudinal gastrectomy as an effective treatment modality for gastroparesis.