College Answer

Evaluation of causes of metabolic alkalosis requires a systematic approach involving history, examination and some specific investigations. Categories of aetiology include
• loss of hydrogen ions (gastrointestinal, renal)

• intracellular shift of hydrogen ions

• administration of alkali

• contraction alkalosis

•    History and examination will reveal, documented fluid losses

-(vomiting & gastric losses, laxative induced diarrhoea),

-signs of volume depletion (loss of bicarbonate free fluids),

- administered drugs (mineralocorticoids, diuretics , and antacids in renal failure) , alkali (bicarbonate, lactate, citrate etc)

• and recent hypercapnia.

• Blood investigations may reveal hypokalemia (with hydrogen shifting into cells), hypochloremia

•    Urinary findings may include excessive potassium excretion (reabsorbing hydrogen), alkaline pH (increased bicarbonate) and inappropriately elevated chloride excretion (diuretic therapy, hypokalaemia).

•          Using Stewart’s physicochemical approach, an isolated increase in Strong ion difference (SID) seen with the use of solutions such as plasmalyte or NaHCO3 or a reduction in ATOT seen with hypoalbuminemia can lead to metabolic alkalosis

Discussion

The diagnostic approach to metabolic alkalosis is discussed in more detail elsewhere.

Instead of a text excess, I will reproduce the diagnostic flowchart which was suggested by a Medscape article, and which seemed like a nice way of remembering this process.

This flowchart can be converted into the form of a point-form answer:

• History and examination
  • Recent exogenous bicarbonate administration
  • Milk-alkali syndrome
  • Hypercalcemia
  • β-lactam use
  • Cystic fibrosis
• Low urinary chloride
  • Recent diuretic therapy
  • Gastric losses via NG suction or vomiting,
  • Villous adenoma of colon
  • Post-hypercapneic (compensatory) alkalosis
• High urinary chloride and normal blood pressure
  • Ongoing diuretic therapy (must be effective, the blood pressure is normal...)
  • Bartter syndrome
  • Gitelman’s syndrome
  • Hypokalemia
  • Hypomagnesaemia
• High urinary chloride, hypertension and high renin activity
  • Ongoing diuretic therapy
  • Renal artery stenosis
  • Renin-secreting tumour
  • Malignant hypertension
• High urinary chloride, hypertension and normal renin-aldosterone axis
  • Cushing syndrome
  • Corticosteroid use
  • 17-hydroxylase deficiency
  • Liddle’s syndrome
  • Licorice overindulgeance
• High urinary chloride, hypertension and hyperaldosteronism without high renin levels
  • Adrenal adenoma
  • Adrenal hyperplasia
  • Aldosterone synthase hyperactivity

Thus, the following is a list of the necessary details one will need to determine from the patients history, physical examination, and biochemistry values:

Background history

• History of congential adrenal hypoplasia
• History of cystic fibrosis
• History of CCF (suggesting chronic exposure to diuretics)
• History of uncontrolled hypertension (malignant hypertension or renal artery stenosis)

Recent history

• Recent antacic consumption
• Recent use of calcium supplements
• β-lactam antibiotic use
• Massive abuse of licorice
• History of diarrhoea (villous adenoma) or vomiting (chloride loss)
• History of recent hypercapneic respiratory failure

Examination

• Clinically, findings consistent with severe hypertension (eg. retinal changes)
• Renal artery stenosis bruit
• Peripheral oedema (suggesting chronic exposure to diuretics)

Biochemistry

• Serum potassium
• Serum magnesium
• Urinary chloride
• Serum renin levels
• Serum aldosterone levels