Diagnosis of Metabolic Alkalosis
Once it has been determined that a patient has metabolic alkalosis, the etiology is usually obvious from the history. If there is no pertinent history, then one can assume that the alkalosis is due to one of the three most common causes: 1) vomiting, 2) diuretics, 3) mineralocorticoid excess. To differentiate between these conditions, it is usually helpful to measure the urinary chloride concentration.
In causes of metabolic alkalosis associated with a reduction in the ECV, there will be a stimulus for avid Na and Cl reabsorption to replenish extracellular volume. In these setting urinary Cl should be expected to be very low, less than 25 meq/L.
Urinary Na is not a reliable measure of extracellular volume in this setting because if the alkalosis is such that not all of the filtered HCO3- can be reabsorbed, then some will be excreted with Na and the urinary Na may be high. Thus, it may appear that the volume status is euvolemic or hypervolemic when it is not.
If the urinary Cl is low, indicating a hypovolemic state, then administration of NaCl and water to replenish the extracellular volume should stop the stimulus for aldosterone production and in turn should lead to appropriate excretion of excess HCO3- and improvement of hypokalemia. Thus, leading to correction of the metabolic alkalosis. Such causes of metabolic alkalosis are said to be saline responsive. See table below.
In contrast, states of mineralocorticoid excess are associated with an expanded volume and sometimes hypertension. The urinary Cl will be high (> 40 meq/L). In these patients, administration of saline would further expand the extracellular volume and worsen hypertension. It would not correct the alkalosis which is primarily due to hypokalemia. Such causes of metabolic alkalosis are said to be saline resistant.
|Urine Cl < 25 meq/L
|Urine Cl > 40 meq/L
Causes of saline resistant metabolic alkalosis can further be distinguished based on whether or not the patient is hypertensive. Mineralocorticoid excess states tend to be associated with hypertension while exogenous alkali load, Barrters and Gitelman's syndrome are associated with normal blood pressure.
Saline - Responsive metabolic alkalosis
- Re-expand volume with Normal Saline ( Primary Therapy)
- Supplement with Potassium to treat hypokalemia (alkalosis associated with severe hypokalemia will be resistant to volume resuscitation until K is repleted)
- H+ blockers or PPIs if vomiting/NG suction to prevent further losses in H+ ions
- Discontinue diuretics
- Acetazolamide if NS contraindicated due to CHF. (Monitor for hypokalemia)
- HCl or NH4Cl in emergency. (HCl can cause hemolysis, NH4Cl should not be used in liver disease)
- Hemodialysis in patients with marked renal failure
Saline – Unresponsive metabolic alkalosis (Mineraldocorticoid excess)
- Surgical removal of mineralocorticoid producing tumor
- Aldosterone inhibitor
- ACE inhibitor.
- Discontinue steroids
- Potassium repletion (only intervention needed to treat the alkalosis)