Hyperchloraemic Metabolic Acidosis

Hyperchloraemic metabolic acidosis is a normal anion gap metabolic acidosis in which bicarbonate is lost or acid is retained without the accumulation of unmeasured anions. Electroneutrality is maintained by a compensatory rise in chloride, which is what gives the disorder its name.

The distinction from raised anion gap acidosis is the first and most useful step in any metabolic acidosis, because the two have entirely different differential diagnoses. A normal anion gap points toward bicarbonate loss or a renal acidification defect; a raised gap points toward added acid such as lactate, ketones or toxins.

Causes divide into gastrointestinal bicarbonate loss (diarrhoea, which is by far the commonest, alongside high-output stomas, ileostomies, pancreatic and biliary fistulae, and ureteric diversion), renal causes (renal tubular acidosis types 1, 2 and 4, early chronic kidney disease, carbonic anhydrase inhibitors, hypoaldosteronism), and iatrogenic causes, principally large-volume 0.9% saline resuscitation, which is a common and under-recognised contributor in hospital practice.

• Calculate the anion gap: Na − (Cl + HCO₃), normal range approximately 8–12 mmol/L. Correct for albumin, adding roughly 2.5 mmol/L for every 10 g/L that albumin falls below 40 g/L, since hypoalbuminaemia masks a raised gap and can make a mixed picture look like a pure normal-gap acidosis
• Urinary anion gap (Na + K − Cl) is the key discriminating test once a normal anion gap acidosis is confirmed:
• A negative urinary anion gap indicates appropriate renal ammonium excretion, pointing to a gastrointestinal cause such as diarrhoea
• A positive urinary anion gap indicates impaired renal ammonium excretion, pointing to renal tubular acidosis
• Urine pH: a pH above 5.5 in the presence of systemic acidosis suggests a distal (type 1) renal tubular acidosis, since the distal tubule should be able to acidify maximally
• Potassium helps subclassify: low in types 1 and 2 renal tubular acidosis, and high in type 4, which is the commonest form in adults and is typically associated with diabetes, chronic kidney disease, and drugs including ACE inhibitors, ARBs, spironolactone and trimethoprim
• Review the fluid chart specifically for saline volume, and the drug chart for acetazolamide and topiramate
• Venous blood gas with electrolytes, renal function and albumin

• Treat the underlying cause, which is the definitive step in almost every case: manage diarrhoea, address the stoma or fistula output, review and stop contributing drugs, and switch from 0.9% saline to a balanced crystalloid where ongoing resuscitation is required
• Bicarbonate replacement is considered for severe acidosis (pH below approximately 7.1–7.2, or bicarbonate below 10–12 mmol/L), for symptomatic patients, and in chronic renal causes where sustained acidosis contributes to bone disease, muscle wasting and progression of chronic kidney disease
• Oral sodium bicarbonate is used for chronic replacement, particularly in renal tubular acidosis and chronic kidney disease
• Intravenous bicarbonate is reserved for severe acute acidosis, with the recognised caveats that it can worsen intracellular acidosis, cause hypokalaemia as potassium shifts into cells, cause hypocalcaemia, and produce sodium and volume loading
• Correct potassium alongside, and anticipate the direction: in types 1 and 2 renal tubular acidosis potassium falls further as bicarbonate is given, whereas type 4 requires management of hyperkalaemia
• In type 4 renal tubular acidosis, fludrocortisone is used where hypoaldosteronism is the mechanism, alongside dietary potassium restriction and review of contributing drugs
• Monitor gas, electrolytes and renal function during correction

Referral: nephrology for renal tubular acidosis, and for acidosis complicating chronic kidney disease; gastroenterology for high-output stoma or fistula management.