Chloride Sensitive Metabolic Alkalosis

The main surgical cause of metabolic alkalosis is loss of gastrointestinal secretions. This mainly occurs from the gastro-intestinal tract in the form of vomiting, naso-gastric losses and diarrhoea. Rarely the problem may be a fistula or a tumor.

Upper gastrointestinal fluid losses occur in two main forms;

Pyloric stenosis

Here there is a failure of the stomach to empty its contents into the duodenum. In infants this may be due to Infantile pyloric stenosis. In adults it may be due to scarring from previous benign ulceration related to peptic ulcer disease, or to encroachment of the pyloric canal by a tumor, most commonly distal gastric cancer.

Intestinal obstruction

This will not usually cause metabolic alkalosis because HCO is lost as well as Cl and Na .

The classical metabolic disturbance in surgery is that due to loss of gastric secretions due to an obstructed pylorus. This causes hypo-chloremic, hypo-kalemic, metabolic alkalosis.

In pyloric stenosis, gastric fluid is lost, see table 2. The fluid lost from the stomach will have Cl as the major anion. The cations that are secreted to balance this will be either [H ] or Na . If the patient is receiving acid suppressant therapy then the main cation lost will be Na . The patient becomes alkalotic and deficient in fluid and Cl . Thus the patient will have a Cl sensitive metabolic alkalosis. The kidney and lung will try to compensate for this metabolic derangement.

The kidney will try to reabsorb sodium to restore fluid. For each Na ion that is absorbed it is necessary to reabsorb a negatively charged ion such as Cl or HCO As there is deficiency of Cl the kidney must reabsorb HCO with the Na . The renal response therefore aggrevates the accumulation of HCO , and worsens tha alkalosis. Urinary Cl is characteristically low. In the distal convuluted tubule Na reabsorbtion occurs in exchange for either K or [H ]. If there is not too severe a deficiency in K the kidney looses K and the urine is alkaline ([H ] is conserved). Later on when the K deficiency becomes severe the urine becomes acid because there is no K to exchange for the Na so [H ] must be lost, this is termed paradoxical aciduria.

The lungs respond to the alkalosis by reducing alveolar ventilation. But, this is limited by the need to maintain the pO2 . Indeed, it would be unusual for the paCO2 to rise above 6.6 kPa in response to metabolic alkalosis.

$$P_{a_{CO_2}}\ rises\ by\ 1\ kPa = 10 mmol/l\ rise\ in\ HCO\ensuremath{_3^-}$$ (7)

A good way to assess the adequacy of fluid and electrolyte replacement in these patients is to monitor the Cl .

In intestinal obstruction, the pattern of response is a bit different because HCO is lost from pancreatico-biliary secrertions. The patient will get less metabolic alkalosis than a patient with pyloric stenosis. Often the patient will just exhibit severe dehydration with contraction of the ECF . There will not be a metabolic alkalosis, but if the dehydration is severe there may be a metabolic acidosis with an increase in the anion gap, due to the accumulation of lactate.

Non surgical casuses of chloride sensitive metabolic alkalosis include; diuretics (thiazides, loop, metolazone) and upon the relief of chronic hypercapnia.