From the Guidelines
Metabolic alkalosis should be managed by addressing the underlying cause and correcting fluid and electrolyte imbalances, rather than using sodium bicarbonate, which can lead to complications such as calcium phosphate precipitation and xanthine-obstructive uropathies, as evidenced by the lack of clear benefit in preventing tumor lysis syndrome 1. When considering the management of metabolic alkalosis, it is crucial to understand that the condition arises from an imbalance in acid-base homeostasis, often due to excessive bicarbonate retention or acid loss. Key causes include:
- Prolonged vomiting
- Excessive diuretic use
- Hypokalemia
- Endocrine disorders like Cushing's syndrome Treatment strategies should focus on:
- Correcting the underlying cause
- Replenishing fluids, typically with normal saline to help re-establish normal electrolyte balances
- Potassium supplementation, as hypokalemia is both a cause and a consequence of metabolic alkalosis, with dosages often in the range of 40-80 mEq/day divided into multiple doses
- In cases where diuretics are the culprit, discontinuing the offending agent and considering the use of acetazolamide to enhance bicarbonate excretion, with doses ranging from 250-500mg orally Given the potential for sodium bicarbonate to exacerbate conditions like metabolic alkalosis, as noted in the context of tumor lysis syndrome management 1, its use is not recommended for preventing or treating this condition, highlighting the importance of careful patient management to prevent complications associated with severe alkalosis.
From the Research
Definition and Pathogenesis of Metabolic Alkalosis
- Metabolic alkalosis is a widespread acid-base disturbance characterized by the primary elevation of serum bicarbonate and arterial pH, along with a compensatory increase in Pco2 consequent to adaptive hypoventilation 2.
- The pathogenesis of metabolic alkalosis involves either a loss of fixed acid or a net accumulation of bicarbonate within the extracellular fluid 2, 3.
- 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 2, 3.
Clinical States Associated with Metabolic Alkalosis
- Major clinical states associated with metabolic alkalosis include vomiting, aldosterone or cortisol excess, licorice ingestion, chloruretic diuretics, excess calcium alkali ingestion, and genetic diseases such as Bartter syndrome, Gitelman syndrome, and cystic fibrosis 2, 3.
- Metabolic alkalosis can be divided into four categories: chloride depletion alkalosis, mineralocorticoid excess syndromes, apparent mineralocorticoid excess syndromes, and excess alkali administration 4.
Factors that Maintain Metabolic Alkalosis
- Factors that interfere with the kidney's mechanisms to eliminate excess bicarbonate include volume contraction, low glomerular filtration rate, potassium deficiency, hypochloremia, aldosterone excess, and elevated arterial carbon dioxide 2, 3.
- Factors that help maintain metabolic alkalosis include decreased glomerular filtration rate, volume contraction, hypokalemia, hypochloremia, and aldosterone excess 3.
Treatment and Management of Metabolic Alkalosis
- Treatment of metabolic alkalosis is usually supportive and based on the cause of the alkalosis 4, 5.
- Therapy consists of reversing the contributory factors that are promoting the alkalosis and, in severe cases, administration of carbonic anhydrase inhibitors, acid infusion, and low bicarbonate dialysis 3.
- Taking a mechanistic approach to etiologies and management can be very helpful in understanding and treating metabolic alkalosis 5.