Metabolic acidosis

Definition: a primary fall in serum bicarbonate with a fall in blood pH, compensated by hyperventilation and a fall in pCO₂. Normal bicarbonate is 22–26 mEq/L; expected compensation is a fall in pCO₂ of about 1.2 mmHg for every 1 mEq/L fall in bicarbonate.

Classification is by anion gap = Na+ − (Cl− + HCO₃−), normally 8–12 mEq/L. High anion gap (added acid) — MUDPILES: Methanol, Uraemia, Diabetic ketoacidosis, Paraldehyde, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates. Normal anion gap (hyperchloraemic, bicarbonate loss): diarrhoea, renal tubular acidosis, carbonic anhydrase inhibitors, ureteric diversion, large-volume 0.9% saline.

Key geriatric physiology: older people take longer to reach peak proton excretion. After an acid load, maximal ammonia and titratable acid excretion is reached in 4 hours in the young but only at 6–8 hours in the old, so the elderly have greater difficulty handling states of acidosis even though their baseline acid excretion is normal.

Common causes in older adults: acute kidney injury and chronic kidney disease (retained acid and uraemia); sepsis, shock and dehydration (lactic acidosis); diarrhoea; diabetic ketoacidosis and mixed hyperglycaemic states; drugs, especially metformin-induced lactic acidosis; heat stroke, which causes metabolic acidosis with respiratory alkalosis.

A characteristic geriatric presentation is the "mixed" metabolic disturbance of older diabetics — neither classical ketoacidosis nor hyperosmolar coma, with glucose around 270–450 mg/dL, arterial pH 7.2–7.3 (not markedly acidotic), and without marked dehydration or altered consciousness.

Clinical features are often masked in the elderly: Kussmaul breathing, anorexia, vomiting, weakness, hypotension and arrhythmia from hyperkalaemia, and frequently delirium as the presenting feature. Acid–base disturbance is also a recognised metabolic cause of apparent depression in old age.

Chronic acidosis has geriatric consequences: muscle protein catabolism worsening sarcopenia, bone demineralisation worsening osteoporosis, and accelerated CKD progression — linking it directly to falls and fracture risk.

Investigations: arterial blood gas, electrolytes with calculated anion gap, serum bicarbonate, lactate, ketones, glucose, urea and creatinine, and where relevant urine pH and urine anion gap (for renal tubular acidosis) and osmolal gap (for toxic alcohols).

Management principle is to treat the cause, not the number: volume resuscitation and restoration of perfusion for lactic acidosis, insulin with fluids for ketoacidosis, withdrawal of metformin, relief of obstruction or dialysis in AKI, and treatment of sepsis.

Sodium bicarbonate is reserved for severe acidaemia (pH below about 7.1) or for associated hyperkalaemia. Use it cautiously in the elderly — the sodium load can precipitate heart failure and hypertension, and it can cause hypokalaemia, hypocalcaemia and volume overload. In advanced CKD, dialysis is indicated for refractory acidosis, and replacement therapy is needed when GFR falls below 10 mL/min.

Calculating the anion gap but forgetting to correct for albumin (add 2.5 mEq/L for every 1 g/dL fall below 4 g/dL) — hypoalbuminaemia is near-universal in frail elderly and masks a raised gap.

Giving bicarbonate reflexively in lactic acidosis instead of restoring perfusion.

Missing the delta-delta check for a coexisting normal-gap acidosis or metabolic alkalosis (common with vomiting or diuretics).

Forgetting that delirium may be the only presenting sign in an older patient.