Diagnosis And Treatment Of Metabolic Alkalosis

Metabolic alkalosis is a common acid-base balance disorder, especially in hospitalized patients. The main features of metabolic alkalosis are increased serum bicarbonate, and increased pH, often accompanied by hypokalemia. When the patient's arterial blood pH value was ≥7.55, the risk of death increased significantly. The kidney is an important organ to maintain acid-base balance, so metabolic alkalosis is often associated with kidney disease.

 

 

 

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On May 4, 2022, AJKD magazine released its 2022 core curriculum - the pathogenesis, diagnosis, and treatment of metabolic alkalosis. This article summarizes the classification, clinical manifestations, diagnosis, and treatment of it.

Classification of metabolic alkalosis

Depending on the patient's blood volume status, metabolic alkalosis can be divided into two types: hypervolemic (with hypochloremia) and hypovolemic (with hypokalemia). There are two special cases worth noting, gastric acid loss and diuretic overuse.

1. Gastric Acid Loss

Gastric outlet obstruction or severe vomiting can lead to loss of stomach acid and fluid. Gastric acid is hydrochloric acid (HCl) produced by the combination of H+ and Cl- secreted by parietal cells. However, during the production of HCl, parietal cells will produce a large amount of bicarbonate, that is, excess alkaline substances, which are called alkaline tides.

The alkaline tide produced by ordinary vomiting is usually transient and will not have a great impact on the blood volume, chloride ion, and potassium ion concentration of the human body. However, excessive loss of gastric fluid (eg, severe vomiting) will result in decreased extracellular fluid, elevated pH, and hypochloremia. Not only that, to replenish the lost gastric acid, the body will also activate the renin-angiotensin-aldosterone system (RAAS), enhance the excretion of potassium ions, and lead to hypokalemia.

2. Overuse of diuretics

Extensive use of diuretics can inhibit the reabsorption of chloride ions, produce metabolic alkalosis, and disrupt the patient's ion and fluid balance, accelerating fluid excretion. Different types of diuretics have different effects on the human body. Thiazide diuretics can cause mild metabolic alkalosis, while loop diuretics can cause severe metabolic acidosis.

The metabolic alkalosis induced by loop diuretics is related to 3 mechanisms: first, salt consumption causes volume depletion and RAAS activation; second, salt consumption increases the reabsorption of sodium and chloride ions, and The secretion of ions is affected; finally, the above two stages have a significant impact on aldosterone, which in turn has a direct impact on the excretion of hydrogen ions. Of note, carbonic anhydrase inhibitors (eg, acetazolamide) often result in hyperchloremia, hypokalemia, and metabolic acidosis. Therefore, not all diuretics cause metabolic alkalosis.

 

In addition, metabolic alkalosis may also occur if the patient has impaired renal function while ingesting many absorbable alkaline drugs/substances (such as sodium bicarbonate). Sodium bicarbonate is commonly used to correct metabolic acidosis in patients with CKD, as well as to promote uric acid excretion. Therefore, attention should be paid to the dosage of sodium bicarbonate in clinical practice.

Clinical Manifestations of Metabolic Alkalosis

Metabolic alkalosis affects several systems, organs, or tissues of the body, including the central nervous system (confusion or coma), peripheral nervous system (tingling, numbness), heart muscle (arrhythmia), and skeletal muscle (weakness or convulsions). )Wait. Some signs and symptoms are related to hypokalemia, hypophosphatemia, and changes in calcium ion binding ratio caused by metabolic alkalosis.

 

The first signs of metabolic alkalosis are markedly elevated plasma pH and bicarbonate levels. In addition, many patients with metabolic alkalosis have hypokalemia, which results from excessive potassium excretion/loss. It is worth noting that almost all patients with metabolic alkalosis will have elevated RAAS levels.

 

Metabolic alkalosis due to vomiting or loss of gastric juices may also cause hypochloremia, a transfer of chloride ions from the blood to the gastric juices.

 

In addition, not all patients with metabolic alkalosis will be hypovolemic, and some patients will be hypervolemic. Therefore, metabolic alkalosis does not necessarily mean hypotension or hypovolemia, but a small number of patients may develop hypertension.

Diagnosis of metabolic alkalosis

In patients with suspected metabolic alkalosis, blood volume status and pH should be checked first. The diagnostic criteria for metabolic alkalosis are a high serum bicarbonate concentration and a pH ≥ 7.44. If the diagnosis is in doubt, arterial or venous blood gas analysis is needed to confirm.

 

It is worth noting that almost all patients with metabolic alkalosis and hypovolemia will develop hypochloremia and renal hypoperfusion, that is, decreased glomerular filtration rate (GFR). The decline in GFR will further lead to persistent hypovolemia and is associated with hypochloremia, hypokalemia, and aldosterone excess. Furthermore, in some patients, hypovolemia persists for a prolonged period and may persist even through the recovery phase.

Levels of chloride ions, potassium ions, magnesium ions, creatinine, and aldosterone should be tested, and sodium ions should be tested if necessary, to understand the patient's blood and clinical symptoms as soon as possible and make relevant preparations for the determination of subsequent treatment plans. Finally, the patient's medical history and medication history should also be clarified to ensure that the patient stops taking acid-losing drugs (diuretics or licorice) and alkaline drugs (sodium bicarbonate).

Treatment of Metabolic Alkalosis

The first step in treatment is to correct the abnormal state. Once the patient's hypovolemia, chloride, or potassium levels are corrected, and the cause is controlled (eg, vomiting stops), the patient enters the recovery phase. Drugs that can cause acid loss or basic drugs should continue to be discontinued at this stage.

 

After correcting the patient's acute state, a more comprehensive history can be scheduled. In addition to medication history, medical history can also provide some clues, such as primary aldosteronism, cystic fibrosis, and the use of penicillin, etc. may be related to metabolic alkalosis. After obtaining medical history information, a comprehensive analysis of sodium, potassium, chloride, magnesium ions, and creatinine levels is performed to assess renal function and may provide clues to determine the cause of alkalosis.

In addition, patients with metabolic alkalosis can be classified as chlorine-sensitive (urine chlorine <20 mmol/L) or non-sensitive (urine chlorine >20 mmol/L) based on systemic blood pressure and urine test results. At the same time, based on other medical history or clinical features, the etiology of the patient can be speculated.

 

Intervention according to the etiology can reduce the risk of recurrence of metabolic alkalosis and help improve the prognosis of patients. However, it must be clear that some patients have high calcium ion levels, but at this time diuretics should not be used to enhance calcium ion excretion. At this time, increasing blood volume is the best treatment option for these patients.

 

In general, metabolic alkalosis has various etiologies. Physicians need to pay attention to the patient's clinical manifestations, complete the examination as soon as possible, and ask about the medical history in detail, to correct the metabolic alkalosis urgently and treat the cause at the same time, reducing the risk of recurrence of the patient.

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