Vomiting or nasogastric tube (NG) decompression can lead to metabolic alkalosis, often associated with hypokalemia. When asked what the source of the K loss is, most people assume it is lost in the gastric fluid. However, gastric fluid only contains about 9 mEq/L of potassium, hardly enough to lead to profound hypokalemia. While it is true that cellular shift due to alkalosis could explain some of the hypokalemia, the primary source of potassium loss is via the urine. Metabolic alkalosis induced by GI loss leads to volume depletion. In this setting, secondary hyperaldosteronism ensues, leading to sodium retention and potassium wasting, hence the hypokalemia. Further, such GI losses are also associated with chloride depletion. Maintenance of electroneutrality usually obligates chloride reabsorption along with sodium retention. But in chloride depleted states, this is not possible. Instead the lumen-negative gradient (due to sodium reabsorption without chloride following) obligates cation excretion, usually potassium or hydrogen ions. Additionally, the hyperaldosteronism increases H+ excretion via effects on the H-ATPase. Together these explain the paradoxical aciduria associated with GI loss-induced metabolic alkalosis as hydrogen is excreted despite alkalemia. The chloride depleted state, as well as the sodium retention induced by volume depletion, also lead to maintenance of the alkalosis by limiting bicarbonate excretion by a variety of mechanisms. It is for this reason that such alkaloses are termed saline responsive, indicated by a low urine chloride - administration of saline leads to correction of hypovolemia and therefore removes the stimulus to aldosterone, while at the same time chloride replenishment allows for the excretion of bicarbonate while minimizing H+ excretion, leading to an appropriately alkaline urine and rapid correction of the electrolyte abnormalities.
But is metabolic alkalosis the only acid-base disturbance that results from NG decompression? Some anecdotal experience suggests not. As noted above gastric fluid contains little potassium and almost no bicarbonate. So at first glance the answer seems to be no. However, there is a not-so-infrequent clinical scenario where NG decompression can result in metabolic acidosis. More distal fluids, such as bile, pancreatic secretions, and small bowel fluids all have high concentrations of bicarbonate (45, 92, and 50 mEq/L respectively). When NG suction is employed to decompress a small bowel obstruction, more distal fluids can be suctioned, leading to bicarbonate loss. In general though, the suctioned fluid will also contain gastric acid and there will be limited net change in acid-base status. However, if gastric acid production is limited by a proton pump inhibitor, metabolic acidosis can ensue. This was the case with a patient we were consulted on with a metabolic acidosis and bicarbonate of 13 in the setting of NG decompression for a partial small bowel obstruction. The patient was also on a PPI. He was not having diarrhea. To test our theory, we checked the pH of his NG fluid (pH testing was more readily available than electrolytes). The pH was 6.9, far above what would be expected from a PPI alone. We suggested holding his PPI. His acidosis resolved quickly, though in the context of discontinuation of NG decompression and bicarbonate administration, so we can't say for sure that holding the PPI during NG decompression solved the problem. Nonetheless, sharing our case with other colleagues revealed similar anecdotal experiences, suggesting that the phenomenon of metabolic acidosis resulting from upper GI loss of bicarbonate in the setting of partial or complete small bowel obstruction, NG decompression, and concomitant PPI administration should at least be kept in the back of the mind.
Here is a little more detailed explanation incorporated into the original post for those wanting it, courtesy of Dr. Julian Seifter......
ReplyDeleteInitially, as blood bicarbonate is raised due to gastric acid loss, the bicarbonate spills into the urine, accompanied by sodium and potassium. The urine is alkaline, K losses gradually increase due to the bicarbonaturia, and sodium losses contribute to the volume depletion while the high Na concentration of urine belies the ECF depletion. Metabolic alkalosis induced by gastric loss is associated with extracellular volume depletion and a fall in GFR. In this setting, increased AII and secondary hyperaldosteronism ensue, leading to sodium retention and further potassium wasting,. The GI losses are also associated with chloride depletion and hypochloremia. Chloride reabsorption in the setting of gastric Cl losses results in low urinary Cl concentrations. Sodium reabsorption through the epithelial Na channels in the principal cells of the collecting segments and cortical collecting duct, create a greater lumen-negativity that enhances K secretion and H+ secretion. The result is maintainence of alkalosis, steady increases in bicarbonate reabsorption and continued urinary K losses. Ultimately, due to enhanced Na and HCO3 reabsorption in the proximal and distal nephron (due to hypokalemia, hypovolemia and aldosterone, meatbolic alkalosis persists while all filtered bicarbonate is reabsorbed. The steady state is reached and urinary Na is appropriately low, and urinary pH is acid, a condition known as paradoxical aciduria in metabolic alkalemia. Such alkaloses are termed saline responsive, as administration of saline leads to correction of hypovolemia and therefore removes the stimulus to proximal NaHCO3 reabsorption and aldosterone, while at the same time chloride replenishment allows for the excretion of bicarbonate, leading to an appropriately alkaline urine and rapid correction of the electrolyte abnormalities as long as the K deficit is corrected with Cl salts.