Enlarged stomach
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Enlarged stomach

Disclaimer: The following explanation is focused on vascular compression syndromes. Of course, and more frequently other explanations may apply. In any case, please turn to your doctor or ask here.

 

An enlarged stomach may be a consequence of delayed emptying and accumulation of food which stays there  for many hours. The emptying of the stomach is a fine tuned process which relies on the intricate cooperation of the amount and type of nutrients, the nervous stimulation of the stomach by the vagus nerve, the secretion of intestinal hormones and enzymes, the function of the pancreas and last but not least the ability to propel the food into the small intestine.

This transport may become disturbed due to mechanical or intrinsically muscular or neural disorders of the stomach and the upper intestines.

A very important mechanical obstacle is the compression of the duodenum by the aorta which pushes the horizontal part of the duodenum against the superior mesenteric artery. This disorder is known as Wilkie syndrome and may be corrected by an operation.

The peristalsis is the motor function of the bowel and stomach. It needs to be slow enough to give the bowel time to absorb nutrients and it needs to be fast enough to transport digested food towards the anus. If the peristalsis is too slow, the stomach remains full, often many hours after a meal and dilates progressively. Sometimes such a development is described as gastroparesis. The stomach enlarges and not rarely extends down into the pelvis.

A disturbed peristalsis, also leading to a gastric enlargement, may be very annoying and substantially interferes with the social life. A weak peristalsis may have a variety of reasons, one of them may be a disturbed innervation of the muscle layers of the stomach and intestines. The innervation of the intestines is an area of intense research and functional disorders due to neural diseases are incompletely understood today. Genetic disorders, degeneration of intestinal neurons, metabolic disorders and mitochondrial diseases are known causes for such problems.

One example for a disturbed innervation of stomach and duodenum is the median arcuate ligament syndrome. The pressure of the arcuate ligament onto the nervous plexus surrounding the coeliac artery, the coeliac plexus aka solar plexus, disturbs the normal activity of this important vegetative nervous network. The normal function of the coeliac plexus consists among others to orchestrate the timely action of food uptake, secretion of digestive fluids and enzymes and a useful, propulsive peristalsis.

In the median arcuate ligament syndrome aka MALS or Dunbar syndrome a weak peristalsis may occur due to the mechanical damage of the coeliac plexus. The often long-lasting pressure of the ligament onto the nervous plexus produces an irritation in its beginning and a loss of function due to scarring after years of persisting pressure. Thus, diarrhoea may occur in early phases as a sign of irritation with an accelerated peristalsis. Later due to scarring a slow or lacking peristalsis may become the leading complaint. This is felt as bloating and constipation.

 

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