Paradoxical aciduria: The biochemical changes that occurs in gastric outlet obstruction
Paradoxical aciduria is a situation where a patient having metabolic alkalosis continues to make acidic urine instead of alkaline urine. This situation occurs typically in prolonged and persistent vomiting from gastric outlet obstruction
In a patient having GOO (gastric outlet obstruction), the biochemical changes varies with time, however in a patient with gastric outlet obstruction accompanied by protracted non-bilious vomiting ( persistently loosing gastric acid) or prolonged gastric suctioning. The final picture of the biochemical changes is as listed below:
- Hypochloremia
- Hyponatremia
- Hypokalemia
- Metabolic alkalosis and formation /excretion of acidic urine (urine with low PH, PH less than 5.5), due to loss of hydrogen ions in the urine
In a patient that has metabolic alkalosis, the loss of acid in urine is not consistent with the expected response which is the excretion of alkaline urine while conserving hydrogen ions in order to reverse the metabolic alkalosis. Therefore, the renal excretion of acidic urine is paradoxical, hence phenomenon is termed PARADOXICAL ACIDURIA.
The pathophysiology of the biochemical changes
Following persistent vomiting of gastric juice which is rich in water, acid (HCL about 150mmol/L). The initial derangement is dehydration, hypochloremia and metabolic alkalosis.
hyponatremia soon becomes added gastric secretion contains about 60-100mmol/L,
Hypokalemia is delayed because of the low concentration of potassium in the gastric juice(5-10mmol/L) and because there is repletion of lost serum potassium by egress of potassium from the intracellular reservoir (the intracellular potassium is about 140mmol/L )
(summary: the earliest changes in persistent vomiting will be Dehydration , hypochloremia, hyponatremia and metabolic alkalosis )
Because of the hypovolemia and hyponatremia there is activation of the Renin-Angiotensin-Aldosterone system to retain sodium and water.
In the renal tubules sodium is reabsorbed and a positively charged ion (preferably potassium) is excreted. The compensatory mechanism of RAAS in addition to vomiting means that potassium is now los from two fronts. (in gastric juice and in urine) leads to depletion of extracellular potassium.
The extracellular potassium is replenished initially by egress of potassium from the intracellular space into the extracellular fluid until the intracellular potassium is also depleted.
Upon depletion of total body potassium, another positively charge ion will have to be exchange for sodium in urine in order to sustain the reabsorption of sodium and water. The next available cation that will replace potassium in this system happens to be hydrogen ion, this forced excretion of hydrogen ion in urine in exchange for sodium and water reabsorption leads to production of acidic urine in the presence of metabolic alkalosis – “paradoxical aciduria”
NOTE
In addition to the loss of the serum acidity due to secretion of hydrochloric acid in the gastric juice, for every millimole of chloride secreted into the gastric juice, an equivalent amount of bicarbonate is reabsorbed into circulation in the stomach worsening the alkalosis.
Also, in the renal tubules, sodium is reabsorbed as sodium bicarbonate. These two sources of increasing serum bicarbonate lead to worsening of the metabolic alkalosis.
The alkalosis leads to functional hypocalcaemia because reduced concentration of ionized calcium which is the functional/ active form of serum calcium
