Acid-Base Disorders — Written Clinical Reasoning

SAQ 1 — Integrated Acid-Base Interpretation and Management (20 marks, 30 minutes)

Prompt: Interpret this patient's acid-base disorder using the six-step algorithm, construct a problem list, and outline an integrated management plan with justification for each decision. [1]

Model Answer

Step-by-step interpretation (5 marks): [1]

1. pH 7.05 — severe acidaemia.
2. Primary disorder: bicarbonate 8 (low) and PaCO2 22 (low). A low PaCO2 would alkalinise, so it is compensation; the low bicarbonate is the primary metabolic acidosis.
3. Compensation — Winter's formula: expected PaCO2 = (1.5 x 8) + 8 = 20, range 18 to 22. The measured PaCO2 is 22, within the expected range — so respiratory compensation is appropriate with no concurrent respiratory disorder.
4. Anion gap — corrected: measured AG = 138 - 96 - 8 = 34, markedly elevated. Correct for albumin: 32 g/L is 3.2 g/dL, so add 2.5 x (4.0 - 3.2) = 2.0; corrected AG = 36. This is a high anion gap metabolic acidosis.
5. Delta-delta: delta AG = 36 - 12 = 24; delta bicarbonate = 24 - 8 = 16; ratio = 24/16 = 1.5. This is within the 1 to 2 range, consistent with a pure high anion gap acidosis — no concurrent metabolic alkalosis despite his vomiting (the acid load is overwhelming). This is an important point: the delta-delta is < 2, so the vomiting has not yet generated a dominant alkalosis.
6. Osmolar gap: measured 312 minus calculated 300 = 12, mildly elevated but not the 20 to 30 that would suggest a toxic alcohol. The gap is borderline and the clinical picture (diabetes, CKD, SGLT2 inhibitor, metformin, vomiting) is consistent with endogenous causes. [1]

Diagnosis: severe high anion gap metabolic acidosis from a combination of (a) euglycaemic diabetic ketoacidosis (raised beta-hydroxybutyrate, SGLT2 inhibitor, near-normal glucose) and (b) metformin-associated lactic acidosis (raised lactate, CKD, metformin), with a smaller contribution from uraemic acidosis. [1]

Problem list (3 marks): [1]

1. Severe high anion gap metabolic acidosis (pH 7.05) — metformin-associated lactic acidosis and euglycaemic DKA on a background of CKD.
2. Acute kidney injury, KDIGO stage 2, on chronic CKD stage 3b — pre-renal from vomiting and hypovolaemia, compounded by nephrotoxic medications.
3. Hyperkalaemia, K 6.4, with peaked T waves — a medical emergency requiring immediate stabilisation.
4. Possible intra-abdominal sepsis or mesenteric ischaemia as the precipitant (abdominal pain, high lactate, confusion) — demand urgent investigation.
5. Chronic multimorbidity (diabetes, CKD, ischaemic heart disease) — dictates drug choices and prognosis. [1]

Management plan (12 marks): [1]

1. Resuscitate and treat the hyperkalaemia first (3 marks): ABCDE, oxygen, two large-bore cannulae, continuous cardiac monitoring. Calcium gluconate 10 mL of 10% intravenously to stabilise the myocardium (onset seconds), then insulin (10 units) with 50 mL of 50% dextrose to shift potassium intracellularly, plus a beta-agonist (salbutamol nebuliser). Recheck potassium and the ECG. Do not give bicarbonate as a first-line potassium-shifting agent here unless the acidosis is to be addressed definitively. [1]

2. Stop the offending agents (2 marks): cease metformin and empagliflozin immediately — both are contributing to the acidosis (metformin via lactic acidosis, empagliflozin via euglycaemic DKA). Hold perindopril (hyperkalaemia, AKI). Continue frusemide only if volume overloaded; he is volume-depleted, so hold it. [1]

3. Fluid resuscitation (2 marks): he is hypovolaemic (dry mucous membranes, BP 92/58) — give balanced crystalloid (Plasma-Lyte or Hartmann's) in 500 mL boluses with reassessment. Avoid normal saline in large volumes as it causes hyperchloraemic acidosis and worsens renal vasoconstriction. [1]

4. Treat the DKA component (2 marks): fixed-rate intravenous insulin infusion (0.1 units/kg/hour), with dextrose supplementation as the glucose is only 9.2 (euglycaemic DKA — start dextrose early to allow insulin to run without hypoglycaemia). Replace potassium as the acidosis corrects. [1]

5. Definitive removal — early haemodialysis (2 marks): this patient meets multiple criteria for renal replacement therapy: severe acidaemia (pH 7.05) refractory to initial therapy, refractory or recurrent hyperkalaemia with ECG changes, and a dialysable toxin (metformin). Discuss immediately with ICU and nephrology. Intermittent haemodialysis removes metformin efficiently and corrects the acidosis and potassium. [1]

6. Investigate the precipitant (1 mark): blood cultures, lactate trend, venous gas, lipase, abdominal imaging (CT abdomen) for mesenteric ischaemia or intra-abdominal sepsis given the abdominal pain. Empirical broad-spectrum antibiotics within one hour if sepsis is suspected. [1]

Communication and safety: explain to the family that the immediate priority is to stabilise the potassium and acid, and that dialysis is the fastest way to correct both. Document the sick-day rule education for recovery (hold metformin, SGLT2 inhibitor, ACE inhibitor and diuretics during any acute illness with reduced intake, vomiting, diarrhoea or fever). [1]

SAQ 2 — Distinguishing the Renal Tubular Acidoses (10 marks, 20 minutes)

Prompt: A 55-year-old woman is found incidentally to have a metabolic acidosis. Bloods: sodium 138, potassium 2.8, chloride 115, bicarbonate 17, anion gap 6 (normal). Urinary pH 6.5 (cannot acidify below 5.5 despite systemic acidosis). She has a history of Sjogren's syndrome and recurrent calcium phosphate kidney stones. Outline the diagnosis, the mechanism, and the management. [1]

Model Answer

This is distal (type 1) renal tubular acidosis. The diagnostic triad is a normal anion gap (hyperchloraemic) metabolic acidosis, hypokalaemia, and a urine pH that remains inappropriately high (above 5.5) despite systemic acidosis — the kidney cannot acidify the urine. The Sjogren's syndrome is the cause: autoimmune destruction of the alpha-intercalated cells of the collecting duct impairs the H+-ATPase proton pump, so hydrogen ion cannot be secreted into the tubular lumen [5].

Why the potassium is low: failure of H+ secretion forces the distal nephron to excrete potassium instead to maintain electroneutrality (enhanced distal Na reabsorption creates a lumen-negative gradient that drags potassium out), and secondary hyperaldosteronism from mild volume depletion worsens potassium wasting. [1]

Why she has kidney stones: chronic metabolic acidosis mobilises bone buffer, causing hypercalciuria; the persistently alkaline urine (pH above 5.5) favours precipitation of calcium phosphate, producing nephrocalcinosis and recurrent calcium phosphate stones. This is the classic presentation of distal RTA. [1]

Distinguishing from the other RTAs: [1]

Management: [1]

1. Oral alkali supplementation — oral bicarbonate or potassium citrate at 1 to 2 mmol/kg/day to correct the acidosis and the hypokalaemia. Citrate is metabolised to bicarbonate and is often better tolerated than sodium bicarbonate (less bloating); potassium citrate also corrects the potassium.
2. Correction of potassium is essential — citrate is preferred as it treats both.
3. Treat the underlying cause — immunosuppression for active Sjogren's may help the extrarenal manifestations but rarely reverses the tubular defect.
4. Surveillance — monitor for nephrocalcinosis and osteomalacia; ensure adequate citrate to reduce stone formation.
5. Patient education — adherence to alkali therapy prevents bone disease and stones; the condition is chronic. [1]

The principle: a hypokalaemic, normal anion gap metabolic acidosis with an inappropriately alkaline urine (pH above 5.5) in a patient with an autoimmune disease is distal RTA until proven otherwise. The serum potassium is the first branch point in the RTA differential — hypokalaemia narrows the field to type 1 or type 2, and the urine pH (and the search for Fanconi features) distinguishes them. [1]