A small bowel fistula causes a metabolic acidosis by decreasing the strong ion difference, due to the loss of a large amount of strong cations (sodium and potassium) with a relatively small loss of chloride.
The reason for this is the relatively large amount of bicarbonate (and thus small amount of chloride) in the fluid at this part of the gut. Pancreatic secretions play a role, as already discussed- these bring the pH of the gastric output back to a more tolerable 7.0, by secreting a bicarbonate-rich, chloride-poor fluid.
On top of this, the duodenum contains Brunner’s glands, which secrete an alkaline mucus. Thus, in essence, the pathophysiology underlying the development of metabolic acidosis from a duodenal fistula is the same as that of a pancreatic fistula- it is basically the same secretions being lost.
Not so for the jejunum. This segment both secretes and absorbs fluid, but absorption generally predominates. This process is driven by the co-absorption of sodium and chloride. As the sodium is exchanged for a hydrogen ion, the bicarbonate in the lumen combines with it, and is gradually converted into carbon dioxide and water.
Thus, in the small intestine, the strong ions which were lost to produce gastric and pancreatic secretions are reclaimed.
So, by the time the gut content arrives at the terminal ileum, it has lost 80% of its volume, and is slightly richer in chloride. Therefore, one can expect an ileostomy (when it is working properly and producing 500-1000ml/day) not to cause any particularly threatening acid-base disturbances- while glomerular filtration remains adequate, the kidneys will be able to adapt to the mild chloride retention by excreting a little more chloride in the tubule.
However, a high output fistula or a high output ileostomy would result in a more rapid increase in the strong ion difference, as well as a diminished ability to compensate (with dehydration and decreased glomerular filtration rate).
How high is high output?
To be classified as a “high output fistula” it has to produce more than 500ml per day.
To add weirdness to this situation, ileostomies can also produce a large volume of chloride-rich output, giving rise to a severe metabolic alkalosis. Not only that, but if the bowel is preserved in a short-gut patient, colonic bacteria can have a party with the undigested carbohydrate and generate enough D-lactate to produce a high anion gap metabolic acidosis.