July 27, 2017
Metabolic Alkalosis Minimize

Metabolic Alkalosis

Metabolic alkalosis is characterised by a primary increase in HCO3 with or without an increase in pCO2; [H+] may be low or nearly normal.

Aetiology

Metabolic alkalosis is HCO3 accumulation from acid loss, alkali administration, intracellular shift of hydrogen ion (as occurs in hypokalaemia), or HCO3 retention. Regardless of initial cause, persistence of metabolic alkalosis indicates that the kidneys have increased their HCO3 reabsorption, because HCO3 is normally freely filtered by the kidneys and hence excreted. Volume depletion and hypokalaemia are the most common stimuli for increased HCO3 reabsorption, but any condition that elevates aldosterone or mineralocorticoids (which enhance Na reabsorption and K and H+ excretion) can elevate HCO3. Hypokalaemia is both a cause and a frequent consequence of metabolic alkalosis.

The most common causes are volume depletion (particularly when involving loss of gastric acid and Cl from recurrent vomiting or nasogastric suction) and diuretic use.

Causes of metabolic alkalosis

GI acid loss

 

Vomiting or gastric aspiration

Congenital chloridorrhoea

Villous adenoma

Renal acid loss

Primary or secondary hyperaldosteronism

glycyrrhizin-containing compounds eg liquorice, carbenoxolone.

Bartter’s syndrome

Gitelman’s syndrome

Diuretics

Hypokalaemia and hypomagnesaemia

Bicarbonate excess

Milk alkali syndrome

Oral bicarbonate therapy

Contraction alkalosis

Dehydration due to diuretics or sweat loss

Other

Resolution of starvation ketosis or acidosis with improved cellular function

Laxative abuse

Symptoms and Signs

Symptoms and signs of mild alkalaemia are usually related to the underlying disorder. More severe alkalaemia increases protein binding of ionized Ca++, leading to hypocalcaemia and subsequent headache, lethargy, and neuromuscular excitability, sometimes with delirium, tetany, and seizures. Alkalaemia also lowers threshold for anginal symptoms and arrhythmias. Concomitant hypokalaemia may cause weakness.

Diagnosis

  1. Diagnosis of the cause is usually clinical
  2. Arterial blood gases and serum electrolytes
  3. Sometimes, measurement of urinary Cl and K+

Common causes can often be determined by history and physical examination. If history is unrevealing and renal function is normal, urinary Cl− and K+ concentrations are measured (values are not diagnostic in renal insufficiency). Urinary Cl < 20 mmol/L indicates significant renal Cl reabsorption and hence a Clresponsive cause. Urinary Cl > 20 mmol/L suggests a Cl unresponsive form.

Urinary K and presence or absence of hypertension help differentiate Clunresponsive alkaloses. Urinary K < 30 mmol/day signifies hypokalaemia or laxative misuse. Urinary K > 30 mmol/day without hypertension suggests diuretic abuse or Bartter or Gitelman's syndrome. Urinary K > 30 mmol/day with hypertension requires evaluation for hyperaldosteronism, mineralocorticoid excess, and renovascular disease.

JHB 19 Nov 2009

  

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