Why does diarrhoea cause acidosis

As a strong cation, it increases the strong ion difference of colonic contents. Therefore, the loss of vast volumes of diarrhoea is the loss of fluid with a large strong ion difference, which tends to decrease the strong ion difference of the remaining body fluids. Interestingly, the change in the strong ion difference can be offset by an oral rehydration solution containing both sodium and glucose.

A sodium-glucose co-transporter facilitates the absorption of sodium, thereby increasing the strong ion difference. Rosner, Mitchell H. Molla, A. Majid, et al. Gennari, F. John, and Wolfgang J. J Clin Invest 51 — , Shah, G. Heitzmann, Dirk, and Richard Warth. Diarrhoea as a cause of normal anion gap acidosis. Treatment is aimed at the health problem causing the acidosis. In some cases, sodium bicarbonate the chemical in baking soda may be given to reduce the acidity of the blood.

Often, you will receive lots of fluids through your vein. Diabetic ketoacidosis can be prevented by keeping type 1 diabetes under control. Disorders of acid-base balance. Brenner and Rector's The Kidney. Philadelphia, PA: Elsevier; chap Palmer BF. Metabolic acidosis. Comprehensive Clinical Nephrology.

Seifter JL. Acid-base disorders. Goldman-Cecil Medicine. Updated by: David C. Editorial team. Metabolic acidosis is a condition in which there is too much acid in the body fluids.

Hyperchloraemic metabolic acidosis tends to be associated with acute infective diarrhoea. This is the classical finding in patients with cholera. The problem is an excessive loss of bicarbonate in the diarrhoeal fluid. The acid-base situation with severe diarrhoea can be complicated by other factors see Table below and it may not be possible to completely sort out all the factors in the acid-base disturbance in an individual case.

Hypovolaemia causing peripheral circulatory failure Type A lactic acidosis Hypovolaemia causing an increase in plasma protein concentration increased unmeasured anion Increased anion gap Vomiting Metabolic alkalosis due loss of gastric HCl Abdominal pain Hyperventilation respiratory alkalosis Villous adenoma This can cause hypokalaemia.

Acid-base disorders may also occur: this is:. If hypovolaemia occurs, this may cause a metabolic acidosis. Loss of these secretions can cause a hyperchloraemic acidosis due to the high bicarbonate levels in these secretions. The frequency and severity depend on the daily volume of secretions lost. Pharmacological treatments eg somatostatin which decrease the volume lost by high output fistulae are effective at preventing the acidosis. In patients with a small bowel obstruction, these losses can be predominantly of bile and pancreatic secretions and cause an acidosis rather than an alkalosis as is usual with severe vomiting.

Patients on proton pump inhibitors or H2-blockers may also be more likely to lose predominantly alkaline secretions. Implantation of the ureters into the sigmoid colon or a vesicocolic fistula can result in a hyperchloraemic acidosis due to absorption of Cl - in exchange for HCO3 - across the bowel mucosa. Some of these patients develop renal failure related to infection, stones or urinary obstruction.

This can result in uraemic acidosis or renal tubular acidosis as well. Incidence data from Cruz, This is because the continuous external drainage from the ileal conduit usually results in a short dwell time in the conduit with minimal time for Cl - -HCO3 - exchange. Hyperchloraemic metabolic acidosis commonly develops during therapy of diabetic ketoacidosis. The mechanisms involved have been discussed in Section 8. The mechanism is effectively renal loss of base even though it is not bicarbonate which is lost in the urine.

The actual loss is of ketoacids keto-anions and water. When therapy commences, the ketoacids are metabolised in the liver resulting in the production of equal amounts of bicarbonate.

If excessive ketoacids have been lost in the urine and fluid therapy is initially with normal saline, there is a deficiency of bicarbonate precursors and a surfeit of chloride to replace bicarbonate.

Correction of the acidosis will now involve renal excretion of chloride and its replacement with bicarbonate. This is a slower process than metabolism of ketoacids to regenerate bicarbonate. The net result then is that full correction of the acidosis is much slower when a hyperchloraemic acidosis develops. In patients receiving acetazolamide or other carbonic anhydrase inhibitors , proximal reabsorption of bicarbonate is decreased and distal delivery is increased.