Metabolic alkalosis
| Metabolic alkalosis | |
|---|---|
| Definition | A process increasing pH due to metabolic process |
| Symptoms | Usually asymptomatic |
| Complications | Seizures, coma |
| Types | Chloride-responsive and chloride-resistant type |
| Causes | Vomiting, diuretics, hypokalaemia |
| Treatment | Management of underlying cause. Correction of hypokalaemia. Dialysis or HCl if severe |
Metabolic alkalosis is an acid-base disorder characterised by a metabolic pathological process which increases the pH of the blood. If the alkalosis is severe, it can overcome the body's defense against alkalosis, causes the pH in the blood to increase beyond 7.45. This is called alkalaemia.
Respiratory alkalosis is similar but is rather due to a respiratory problem. Metabolic acidosis is sort of the opposite of metabolic alkalosis. Metabolic alkalosis is an uncommon acid-base disorder.
Etiology
Metabolic alkalosis can be caused by excessive loss of hydrogen ion or due to excessive administration or retention of alkali.
- Loss of hydrogen ions
- Vomiting or excessive nasogastric suction
- Diuretics (loop or thiazides)
- Hyperaldosteronism (primary or secondary)
- Hypokalaemia
- Villous adenoma
- Administration of alkali
- Multiple blood transfusions (they contain citrate which is metabolised to bicarbonate)
- Milk-alkali syndrome
- Excessive administration/intake of alkali
- Contraction alkalosis
- Diuretics
- Rare disorders
- Bartter syndrome
- Gitelman syndrome
The most common causes overall are vomiting, nasogastric suction, and diuretic therapy.
Hypokalaemia
Main article: Hypokalaemia
Hypokalaemia can both cause and maintain metabolic acidosis by increasing bicarbonate retention in the kidney. This is secondary to the kidney reabsorbing potassium in exchange for hydrogen ions.
Milk-alkali syndrome
Milk-alkali syndrome is a possible causes of metabolic alkalosis. It occurs when large amounts of calcium (in milk or otherwise) is consumed with an alkali like bicarbonate or carbonate. The calcium causes hypercalcaemia, which reduces the excretion of bicarbonate as well as volume depletion, both of which lead to metabolic alkalosis.
Contraction alkalosis
Loss of fluid which is rich in sodium chloride but low in bicarbonate concentration may cause a form of metabolic alkalosis called contraction alkalosis. The bicarconate concentration increases not because of increased bicarbonate but because of decreased bicarbonate-poor volume (concentration = solute/volume). Contraction alkalosis is usually not significant to cause alkalaemia alone and is therefore usually one etiology of multiple.
Bartter syndrome and Gitelman syndrome
Bartter syndrome is a disorder of the renal tubule (tubulopathy) and a genetic disorder where the Na-K-2Cl cotransporter in the thick ascending loop is impaired. This is the same cotransporter that loop diuretics inhibits, so Bartter syndrome mimics chronic loop diuretic treatment.
Gitelman syndrome is another tubulopathy and also a genetic disorder where the Na-Cl cotransporter in the distal convoluted tubule is impaired. This is the same cotransporter that thiazide diuretics inhibits, and so Gitelman syndrome mimics chronic thiazide treatment.
Both syndromes cause hypokalaemia, metabolic alkalosis, and a reduction in plasma volume. As a result, there is increased activity of RAAS with secondary hyperaldosteronism.
Types
One may distinguish between two types of metabolic alkalosis depending on whether administration of chloride is effective in the treatment. Chloride-responsive metabolic alkalosis occurs due to vomiting, contraction alkalosis, and diuretics. Chloride-resistant metabolic alkalosis occurs due to hypokalaemia, hyperaldosteronism, Bartter syndrome, and Gitelman syndrome.
Pathophysiology
Alkalaemia may cause plasma proteins to bind more free calcium ions, causing the level of free calcium in the serum to decrease, effectively causing hypocalcaemia.
Alkalaemia also shifts the haemoglobin-oxygen dissociation curve to the left, which decreases tissue oxygenation.
Compensation
The initial compensation occurs to intracellular buffers like the haemoglobin buffers, and is relatively modest.
The healthy kidney can compensate for metabolic alkalosis by increasing its excretion of bicarbonate to a large degree. As such, for metabolic alkalaemia to occur, there is often a loss of kidney function. Renal compensation begins soon after the alkalosis, but it takes up to five takes to become complete.
Clinical features
Metabolic alkalosis is often asymptomatic, unless there are symptoms of the underlying cause or of concomitant hypokalaemia. In severe cases, there may be agitation.
Diagnosis and evaluation
Arterial blood gas is essential in the evaluation of acid-base disorders. It will give the pH, bicarbonate level, pCO2, pO2, and lactate levels. In metabolic alkalosis, the bicarbonate level is abnormally high (> 26 mmol/L). If there is alkalaemia, the pH is > 7.45. Hypokalaemia is often present with metabolic alkalosis.
The cause of metabolic alkalosis is often apparent by the anamnesis. If not, rare causes like hyperaldosteronism and genetic syndromes should be sought. Measurement of urine chloride may be helpful to narrow down the causes. Chloride-responsive metabolic alkalosis has a urine chloride concentration < 20 mmol/L, while chloride-resistant type has a concentration > 40 mmol/L.
Management
As metabolic alkalosis is not a disease of itself but rather a consequence, the underlying disease must be identified and treated. This will reverse the metabolic alkalosis.
Because hypokalaemia may cause and maintain metabolic alkalosis, any concomitant hypokalaemia should be treated by potassium supplementation. It's important to keep in mind the possibility of the serum potassium level being normal but there being an intracellular potassium deficit.
In chloride-responsive metabolic alkalosis, administration of isotonic saline (0.9% NaCl) may help correct the alkalosis.
In the most severe cases, dialysis (RRT) or administration of HCl may be used.