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Metabolic Alkalosis

Updated : January 2, 2024





Background

  • Metabolic alkalosis is an increase in the body’s pH of over 7.45. It is primarily caused by a rise in serum bicarbonate (HCO3-) concentration, which may result from either a loss of hydrogen ions (H+) or a gain of bicarbonate. This may be caused by several circumstances, including severe vomiting, the use of certain drugs (e.g., diuretics), or excessive consumption of alkali substances.  
  • Alveolar hypoventilation increases arterial CO2 tension (PaCO2) in metabolic alkalosis. This rise in PaCO2 helps to minimize the change in pH that would otherwise occur. The expected increase in PaCO2 is approximately 0.5-0.7 mm Hg for every 1 mEq/L increase in plasma bicarbonate concentration. If the change in PaCO2 deviates from this range, it indicates a mixed acid-base disturbance. 

Epidemiology

  • Most acid-base disturbances, or around 50%, are caused by metabolic alkalosis, which is most often seen in hospitalized patients. A 7.55 pH in the arterial blood has been linked to a 45% mortality rate, while a 7.65 pH has been linked to an 80% mortality rate.
  • The exact illness or conditions that caused metabolic alkalosis can affect the prognosis. 

Anatomy

Pathophysiology

The pathophysiology of metabolic alkalosis involves alterations in acid-base balance, primarily characterized by an increase in serum bicarbonate (HCO3-) concentration and a resulting elevation of the body’s pH.

This can occur due to various underlying factors: 

  • Loss of Hydrogen Ions (H+): Metabolic alkalosis can occur when the body has excessive loss of hydrogen ions. This can happen through conditions such as prolonged vomiting, gastric suctioning, or diuretic medications that promote the loss of hydrogen ions through the kidneys. 
  • Gain of Bicarbonate (HCO3-): Another cause of metabolic alkalosis is the excessive gain or accumulation of bicarbonate. This can occur due to excessive intake of alkali substances (e.g., bicarbonate-containing medications) or intravenous bicarbonate solutions. 

Etiology

The different etiologies of metabolic alkalosis: 

Hydrogen Ion Loss in Excess:  

  • Gastric Losses: Gastric acid and hydrogen ions may be lost during prolonged, serious gastric aspiration or vomiting. 
  • Congenital chloridorrhea: This uncommon genetic condition causes excessive chloride ion loss in the intestines, which results in metabolic alkalosis.

Increase in the bicarbonate rate: 

  • Excessive Ingestion or Administration of Bicarbonate:  Consumption or administration of substances containing bicarbonate or alkali can increase the bicarbonate concentration in the body. 

Diuretic-Induced Alkalosis: 

  • Thiazide and Loop Diuretics: To prevent metabolic alkalosis, these diuretics boost proximal tubular bicarbonate absorption by blocking salt and chloride reabsorption. 

Genetics

Prognostic Factors

  • Severity of metabolic alkalosis: The degree of bicarbonate elevation may impact prognosis.  
  • Underlying cause: The primary condition or disease-causing metabolic alkalosis may influence the prognosis.  
  • Associated electrolyte and fluid imbalances: Concurrent electrolyte abnormalities, such as hypokalemia or hypocalcemia, can affect the prognosis of metabolic alkalosis.  
  • Organ dysfunction: The presence of pre-existing organ dysfunction, particularly renal or cardiovascular impairment, may contribute to a poorer prognosis in cases of metabolic alkalosis. 
  • Timely recognition and management: The prompt identification and appropriate management of metabolic alkalosis can influence outcomes.  

Clinical History

Age group: Metabolic alkalosis can occur across all ages, from infants to older adults. The specific age group affected may depend on the underlying etiology.  

Physical Examination

  • Neurological symptoms: Metabolic alkalosis can affect the central nervous system, leading to manifestations such as confusion, lethargy, irritability, and even seizures in severe cases. 
  • Muscular manifestations: Patients may experience muscle weakness, twitching, cramps, and tetany due to alterations in calcium and potassium levels. 
  • Respiratory changes: Compensatory mechanisms may cause respiratory changes, such as hypoventilation, as the body attempts to retain carbon dioxide (CO2) to offset alkalosis. 

Age group

Associated comorbidity

The presence of comorbidities or specific activities can contribute to the development of metabolic alkalosis or influence its clinical presentation. Some examples include: 

  • Chronic lung disease: Chronic obstructive pulmonary disease (COPD) or cystic fibrosis patients may develop metabolic alkalosis due to chronic respiratory acidosis and compensatory renal bicarbonate retention. 
  • Diuretic use: Excessive or prolonged use of loop diuretics or thiazide diuretics can lead to volume depletion, hypokalemia, and subsequent metabolic alkalosis. 
  • Hormonal disorders: Conditions such as primary hyperaldosteronism or Cushing syndrome can cause mineralocorticoid excess, leading to sodium and bicarbonate retention and metabolic alkalosis. 

Associated activity

Acuity of presentation

  • In some cases, it may develop slowly, such as in chronic diuretic use or hormonal disorders. It can also present acutely, especially in severe vomiting or gastric loss.
  • The acuity of the presentation can influence the severity of symptoms and the need for urgent medical intervention. 

Differential Diagnoses

The ordinary differential diagnoses of metabolic alkalosis include: 

  • Congenital chloride-losing diarrhea (chloridorrhea): It is a rare genetic disorder characterized by excessive chloride loss in the intestines, leading to metabolic alkalosis. 
  • Cushing’s syndrome: Excess production of cortisol in Cushing’s syndrome can cause increased renal reabsorption of sodium and increased excretion of potassium, resulting in metabolic alkalosis. 
  • Gitelman syndrome: Another rare genetic disorder affecting the renal tubules, causing increased renal reabsorption of sodium, chloride, and magnesium, leading to metabolic alkalosis. 
  • Milk-alkali syndrome: Excessive calcium and absorbable alkali intake, often in the form of calcium carbonate and milk products, can lead to metabolic alkalosis. 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

  • Discontinuation or modification of any medications or substances contributing to alkalosis, such as diuretics or excess bicarbonate intake. 
  • Correction of volume depletion or dehydration by providing intravenous fluids. 

  • If hypokalemia (low potassium levels) is present, supplementation with potassium chloride may be necessary to restore normal potassium levels and correct the alkalosis. 
  • Calcium replacement may be needed if there is concurrent hypocalcemia (low calcium levels). 
  • In cases of severe metabolic alkalosis, where an acid-base balance needs to be restored quickly, intravenous administration of normal saline or ammonium chloride may be considered under appropriate medical supervision. 

  • Metabolic alkalosis is related to excessive mineralocorticoid activity; interventions such as surgical removal of adrenal tumors or targeted therapies may be required. 

  • Acute Phase: In the acute phase, the focus is on identifying and addressing any life-threatening complications, correcting electrolyte imbalances, and stabilizing the patient’s condition. 
  • Subacute/Chronic Phase: Once the acute phase is managed, the emphasis shifts to identifying the underlying cause and implementing long-term management strategies.  

Medication

 

ammonium chloride 

Indicated for Metabolic Alkalosis and Hypochloremic States:


mEq of chloride ion (NH4Cl) = [0.2 L/kg X Body weight(kg)] X [103 - measured serum chloride]; provide 50% of the dosage over 12 hours and reassess.
The typical range for serum chloride concentration is 103 mEq/L, while the distribution volume for chloride is 0.2 L/kg.



lysine 

10 g orally everyday divided doses of upto 5 days



Dose Adjustments

Dosing modifications
Kidney Impairment
dosage adjustment is not necessary
Hepatic Impairment
dosage adjustment is not necessary

 

ammonium chloride 

Indicated for Metabolic Alkalosis and Hypochloremic States:


mEq of chloride ion (NH4Cl) = [0.2 L/kg X Bodyweight (kg)] X [103 - measured serum chloride]; provide 50% of the dosage over 12 hours and reassess.
The typical range for serum chloride concentration is 103 mEq/L, while the distribution volume for chloride is 0.2 L/kg.



 

Media Gallary

Metabolic Alkalosis

Updated : January 2, 2024




  • Metabolic alkalosis is an increase in the body’s pH of over 7.45. It is primarily caused by a rise in serum bicarbonate (HCO3-) concentration, which may result from either a loss of hydrogen ions (H+) or a gain of bicarbonate. This may be caused by several circumstances, including severe vomiting, the use of certain drugs (e.g., diuretics), or excessive consumption of alkali substances.  
  • Alveolar hypoventilation increases arterial CO2 tension (PaCO2) in metabolic alkalosis. This rise in PaCO2 helps to minimize the change in pH that would otherwise occur. The expected increase in PaCO2 is approximately 0.5-0.7 mm Hg for every 1 mEq/L increase in plasma bicarbonate concentration. If the change in PaCO2 deviates from this range, it indicates a mixed acid-base disturbance. 
  • Most acid-base disturbances, or around 50%, are caused by metabolic alkalosis, which is most often seen in hospitalized patients. A 7.55 pH in the arterial blood has been linked to a 45% mortality rate, while a 7.65 pH has been linked to an 80% mortality rate.
  • The exact illness or conditions that caused metabolic alkalosis can affect the prognosis. 

The pathophysiology of metabolic alkalosis involves alterations in acid-base balance, primarily characterized by an increase in serum bicarbonate (HCO3-) concentration and a resulting elevation of the body’s pH.

This can occur due to various underlying factors: 

  • Loss of Hydrogen Ions (H+): Metabolic alkalosis can occur when the body has excessive loss of hydrogen ions. This can happen through conditions such as prolonged vomiting, gastric suctioning, or diuretic medications that promote the loss of hydrogen ions through the kidneys. 
  • Gain of Bicarbonate (HCO3-): Another cause of metabolic alkalosis is the excessive gain or accumulation of bicarbonate. This can occur due to excessive intake of alkali substances (e.g., bicarbonate-containing medications) or intravenous bicarbonate solutions. 

The different etiologies of metabolic alkalosis: 

Hydrogen Ion Loss in Excess:  

  • Gastric Losses: Gastric acid and hydrogen ions may be lost during prolonged, serious gastric aspiration or vomiting. 
  • Congenital chloridorrhea: This uncommon genetic condition causes excessive chloride ion loss in the intestines, which results in metabolic alkalosis.

Increase in the bicarbonate rate: 

  • Excessive Ingestion or Administration of Bicarbonate:  Consumption or administration of substances containing bicarbonate or alkali can increase the bicarbonate concentration in the body. 

Diuretic-Induced Alkalosis: 

  • Thiazide and Loop Diuretics: To prevent metabolic alkalosis, these diuretics boost proximal tubular bicarbonate absorption by blocking salt and chloride reabsorption. 
  • Severity of metabolic alkalosis: The degree of bicarbonate elevation may impact prognosis.  
  • Underlying cause: The primary condition or disease-causing metabolic alkalosis may influence the prognosis.  
  • Associated electrolyte and fluid imbalances: Concurrent electrolyte abnormalities, such as hypokalemia or hypocalcemia, can affect the prognosis of metabolic alkalosis.  
  • Organ dysfunction: The presence of pre-existing organ dysfunction, particularly renal or cardiovascular impairment, may contribute to a poorer prognosis in cases of metabolic alkalosis. 
  • Timely recognition and management: The prompt identification and appropriate management of metabolic alkalosis can influence outcomes.  

Age group: Metabolic alkalosis can occur across all ages, from infants to older adults. The specific age group affected may depend on the underlying etiology.  

  • Neurological symptoms: Metabolic alkalosis can affect the central nervous system, leading to manifestations such as confusion, lethargy, irritability, and even seizures in severe cases. 
  • Muscular manifestations: Patients may experience muscle weakness, twitching, cramps, and tetany due to alterations in calcium and potassium levels. 
  • Respiratory changes: Compensatory mechanisms may cause respiratory changes, such as hypoventilation, as the body attempts to retain carbon dioxide (CO2) to offset alkalosis. 

The presence of comorbidities or specific activities can contribute to the development of metabolic alkalosis or influence its clinical presentation. Some examples include: 

  • Chronic lung disease: Chronic obstructive pulmonary disease (COPD) or cystic fibrosis patients may develop metabolic alkalosis due to chronic respiratory acidosis and compensatory renal bicarbonate retention. 
  • Diuretic use: Excessive or prolonged use of loop diuretics or thiazide diuretics can lead to volume depletion, hypokalemia, and subsequent metabolic alkalosis. 
  • Hormonal disorders: Conditions such as primary hyperaldosteronism or Cushing syndrome can cause mineralocorticoid excess, leading to sodium and bicarbonate retention and metabolic alkalosis. 
  • In some cases, it may develop slowly, such as in chronic diuretic use or hormonal disorders. It can also present acutely, especially in severe vomiting or gastric loss.
  • The acuity of the presentation can influence the severity of symptoms and the need for urgent medical intervention. 

The ordinary differential diagnoses of metabolic alkalosis include: 

  • Congenital chloride-losing diarrhea (chloridorrhea): It is a rare genetic disorder characterized by excessive chloride loss in the intestines, leading to metabolic alkalosis. 
  • Cushing’s syndrome: Excess production of cortisol in Cushing’s syndrome can cause increased renal reabsorption of sodium and increased excretion of potassium, resulting in metabolic alkalosis. 
  • Gitelman syndrome: Another rare genetic disorder affecting the renal tubules, causing increased renal reabsorption of sodium, chloride, and magnesium, leading to metabolic alkalosis. 
  • Milk-alkali syndrome: Excessive calcium and absorbable alkali intake, often in the form of calcium carbonate and milk products, can lead to metabolic alkalosis. 

  • Discontinuation or modification of any medications or substances contributing to alkalosis, such as diuretics or excess bicarbonate intake. 
  • Correction of volume depletion or dehydration by providing intravenous fluids. 

  • If hypokalemia (low potassium levels) is present, supplementation with potassium chloride may be necessary to restore normal potassium levels and correct the alkalosis. 
  • Calcium replacement may be needed if there is concurrent hypocalcemia (low calcium levels). 
  • In cases of severe metabolic alkalosis, where an acid-base balance needs to be restored quickly, intravenous administration of normal saline or ammonium chloride may be considered under appropriate medical supervision. 

  • Metabolic alkalosis is related to excessive mineralocorticoid activity; interventions such as surgical removal of adrenal tumors or targeted therapies may be required. 

  • Acute Phase: In the acute phase, the focus is on identifying and addressing any life-threatening complications, correcting electrolyte imbalances, and stabilizing the patient’s condition. 
  • Subacute/Chronic Phase: Once the acute phase is managed, the emphasis shifts to identifying the underlying cause and implementing long-term management strategies.  

ammonium chloride 

Indicated for Metabolic Alkalosis and Hypochloremic States:


mEq of chloride ion (NH4Cl) = [0.2 L/kg X Body weight(kg)] X [103 - measured serum chloride]; provide 50% of the dosage over 12 hours and reassess.
The typical range for serum chloride concentration is 103 mEq/L, while the distribution volume for chloride is 0.2 L/kg.



lysine 

10 g orally everyday divided doses of upto 5 days



Dose Adjustments

Dosing modifications
Kidney Impairment
dosage adjustment is not necessary
Hepatic Impairment
dosage adjustment is not necessary

ammonium chloride 

Indicated for Metabolic Alkalosis and Hypochloremic States:


mEq of chloride ion (NH4Cl) = [0.2 L/kg X Bodyweight (kg)] X [103 - measured serum chloride]; provide 50% of the dosage over 12 hours and reassess.
The typical range for serum chloride concentration is 103 mEq/L, while the distribution volume for chloride is 0.2 L/kg.



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