From the Guidelines
Metabolic alkalosis is primarily caused by excessive vomiting or nasogastric suction, diuretic use, particularly loop and thiazide diuretics, excessive alkali intake, severe potassium depletion, and certain endocrine disorders. The main causes of metabolic alkalosis can be broken down into several key categories, including:
- Excessive vomiting or nasogastric suction, which removes stomach acid and leads to a loss of hydrogen ions 1
- Diuretic use, particularly loop and thiazide diuretics like furosemide and hydrochlorothiazide, which increase bicarbonate reabsorption and can lead to metabolic alkalosis, especially when used in high doses 1
- Excessive alkali intake, such as from antacids containing calcium carbonate or sodium bicarbonate
- Severe potassium depletion, which can occur due to various mechanisms, including diuresis, potassium-free intravenous fluids, and other endocrine and renal mechanisms 1
- Certain endocrine disorders like Cushing's syndrome or primary hyperaldosteronism
- Contraction alkalosis, which can develop when the body loses fluid but retains bicarbonate It's worth noting that hypokalemic metabolic alkalosis can also occur in rare genetic disorders, such as Bartter syndrome, which is characterized by inherited hypokalemia and salt-losing tubulopathy 1. In clinical practice, it's essential to identify and address the underlying cause of metabolic alkalosis to prevent complications and improve patient outcomes.
From the Research
Causes of Metabolic Alkalosis
Metabolic alkalosis is defined by the increase of both plasma HCO3- level (>26 mmol/L) and blood arterial pH (>7.43) [ 2 ]. The causes of metabolic alkalosis can be divided into several categories:
- Generation of alkalosis: This may be due to excessive hydrogen ion loss by the gastrointestinal tract (e.g., vomiting) or by the kidney (e.g., use of loop diuretics) or may be due to exogenous base gain [ 2 ].
- Maintenance of alkalosis: This reflects the inability of the kidney to excrete the excess of bicarbonate because of hypovolemia, chloride depletion, hypokalemia, hyperaldosteronism, renal failure, or a combination of these factors [ 2 ].
Clinical States Associated with Metabolic Alkalosis
Several clinical states are associated with metabolic alkalosis, including:
- Vomiting [ 2 , 3 , 4 , 5 ]
- Mineralocorticoid excess [ 3 , 4 , 5 ]
- Licorice ingestion [ 3 , 4 , 5 ]
- Diuretic administration [ 3 , 4 , 5 ]
- Bartter's and Gitelman's syndromes [ 3 , 4 , 5 ]
Pathogenesis of Metabolic Alkalosis
The pathogenesis of metabolic alkalosis involves either a loss of fixed acid or a net accumulation of bicarbonate within the extracellular fluid [ 4 ]. The loss of acid may be via the gastrointestinal tract or the kidney, whereas the sources of excess alkali may be via oral or parenteral alkali intake [ 4 ]. Factors that interfere with the kidney's ability to eliminate excess bicarbonate will impair the ability of the kidney to eliminate excess bicarbonate, therefore promoting the generation or impairing the correction of metabolic alkalosis [ 4 ].