Acid-Base Disorders Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Tran is a 64-year-old man with type 2 diabetes for 20 years, chronic kidney disease stage 3b, and ischaemic heart disease, who presents with two days of vomiting, abdominal pain, and confusion. He takes metformin, empagliflozin, perindopril, frusemide and atorvastatin. His arterial blood gas shows a pH of 7.05 with a bicarbonate of 8 and a PaCO2 of 22, a corrected anion gap of 36, a lactate of 9.5 and a beta-hydroxybutyrate of 4.8, with potassium 6.4 and peaked T waves on the ECG." [1]

"His main problems are:

1. Severe high anion gap metabolic acidosis, most likely a combination of metformin-associated lactic acidosis and euglycaemic diabetic ketoacidosis precipitated by his SGLT2 inhibitor and acute illness
2. Acute kidney injury, KDIGO stage 2, on chronic CKD
3. Severe hyperkalaemia with ECG changes — a medical emergency
4. A possible intra-abdominal precipitant — abdominal pain and a high lactate demand urgent investigation
5. Chronic multimorbidity dictating drug choices and prognosis." [1]

"My immediate priorities are to stabilise the potassium, resuscitate, stop the offending medications, and arrange definitive removal by haemodialysis, while investigating for sepsis or mesenteric ischaemia." [1]

Examiner probing questions and model answers

Q1: "Take me through your six-step interpretation of this gas." [1]

"Step one, the pH is 7.05 — severe acidaemia. Step two, the bicarbonate is 8 and the PaCO2 is 22; both are low, but a low PaCO2 would alkalinise, so it is compensation and the primary process is a metabolic acidosis. Step three, I apply Winter's formula: the expected PaCO2 is 1.5 times the bicarbonate plus 8, which is 1.5 times 8 plus 8, equals 20, plus or minus 2. The measured PaCO2 is 22, within the expected range, so compensation is appropriate and there is no concurrent respiratory disorder. Step four, the anion gap is sodium 138 minus chloride 96 minus bicarbonate 8, which is 34; correcting for his albumin of 32 grams per litre adds 2, giving a corrected gap of 36 — a high anion gap metabolic acidosis. Step five, the delta-delta: the delta anion gap is 36 minus 12 equals 24, the delta bicarbonate is 24 minus 8 equals 16, the ratio is 1.5, within the 1 to 2 range for a pure high anion gap acidosis. Step six, the osmolar gap is 312 minus 300 equals 12, mildly elevated but not in the toxic alcohol range." [1]

Q2: "What is causing his acidosis?" [1]

"There are three contributors. First, metformin-associated lactic acidosis: he has chronic kidney disease and is acutely unwell with vomiting and hypovolaemia, which is the classic setting for metformin to accumulate and inhibit mitochondrial complex I, shifting metabolism to anaerobic glycolysis — hence the lactate of 9.5. Second, euglycaemic diabetic ketoacidosis: the empagliflozin causes glucosuria, lowering insulin and raising glucagon, which drives ketogenesis; his glucose is only 9.2 but the beta-hydroxybutyrate is 4.8, confirming ketoacidosis. Third, a smaller contribution from uraemic acidosis given his CKD and acute kidney injury. I have stopped the metformin and the SGLT2 inhibitor." [1]

Q3: "Would you give sodium bicarbonate?" [1]

"Not as a standalone treatment. The BICAR-ICU trial showed no overall mortality benefit from sodium bicarbonate in severe metabolic acidaemia in the ICU, although a pre-specified subgroup with severe acute kidney injury showed a reduced need for renal replacement therapy. In this patient, the definitive treatment is haemodialysis, which removes metformin, corrects the acidosis by providing bicarbonate in the dialysate, and addresses the potassium. I would use bicarbonate only as a bridge to dialysis in conjunction with ICU if his pH were to fall further or his haemodynamics to deteriorate. The fundamental point is that his acidosis is a marker of metformin accumulation and hypoperfusion — I treat the cause, not the number." [1]

Q4: "His delta-delta is 1.5. He has been vomiting. Why is there no metabolic alkalosis?" [1]

"A fair question. Vomiting generates a metabolic alkalosis by loss of gastric hydrochloric acid, and I would expect the delta-delta to rise above 2 if the alkalosis were dominant. In his case the acid load is so overwhelming — the lactic acidosis and ketoacidosis together — that the metabolic alkalosis is being consumed to buffer the acid, so the ratio remains in the pure-acidosis range. If his vomiting were the dominant process in a milder acidosis, the ratio would be higher. The lesson is that a normal delta-delta does not exclude vomiting; it tells me the acid load currently exceeds the alkalinising effect." [1]

Q5: "How would you decide between haemodialysis and continued medical therapy?" [1]

"He meets several indications for renal replacement therapy: severe acidaemia with a pH of 7.05, hyperkalaemia with ECG changes that may not resolve with shifting alone, acute kidney injury on chronic CKD, and a dialysable toxin in metformin. The decision is straightforward — he needs haemodialysis. If his pH were 7.25 with a mild acidosis and the potassium settled with shifting, I would pursue medical therapy with fluids, insulin for the DKA component, and time for the metformin to be renally cleared. The threshold for dialysis in metformin-associated lactic acidosis is lower than in most other acidoses because the toxin is dialysable and the acidosis can be profound." [1]

Short Case Discussion

Scenario: "Interpret this arterial blood gas"

Candidate presentation (model): [1]

"I will interpret this gas in six steps. The pH is 7.48 — alkalaemia. The PaCO2 is 16 and the bicarbonate is 12. The bicarbonate is low, which would cause acidaemia, so it is not driving the alkalaemia; the very low PaCO2 is the primary process — this is a respiratory alkalosis. For the metabolic component, I apply Winter's formula: the expected PaCO2 for a bicarbonate of 12 is 1.5 times 12 plus 8, equals 26, plus or minus 2. The measured PaCO2 of 16 is far below the expected range, confirming a concurrent respiratory alkalosis on top of a metabolic acidosis. The anion gap is sodium 140 minus chloride 100 minus bicarbonate 12, which is 28 — a high anion gap. So this is a mixed high anion gap metabolic acidosis and a respiratory alkalosis." [1]

Examiner: "What diagnosis does that mixed pattern suggest, and why?" [1]

"The combination of a high anion gap metabolic acidosis and a respiratory alkalosis, especially with a PaCO2 far below what compensation would predict, is the classic pattern of early salicylate toxicity. Salicylates directly stimulate the medullary respiratory centre, causing hyperventilation and a respiratory alkalosis, and they uncouple oxidative phosphorylation, driving a high anion gap metabolic acidosis from lactate and ketoacid production. Other causes of the same mixed pattern are sepsis (lactic acidosis plus hyperventilation), pulmonary embolism with shock, and hepatic failure with lactic acidosis. I would take a salicylate level, a lactate, and a careful history of ingestion, and I would treat with activated charcoal if early, intravenous sodium bicarbonate to alkalinise the urine and enhance salicylate elimination, and haemodialysis for severe toxicity." [1]

Examiner: "Name three causes of a high anion gap metabolic acidosis that you must not miss because they have specific antidotes." [1]

"First, methanol — treated with fomepizole to inhibit alcohol dehydrogenase, folate as a cofactor, and haemodialysis; the clue is visual symptoms with a high anion gap and osmolar gap. Second, ethylene glycol — the same fomepizole-based approach, with the clues being renal failure and calcium oxalate crystals. Third, metformin-associated lactic acidosis — there is no drug antidote, but the definitive treatment is haemodialysis to remove the metformin. A fourth, if you will allow, is salicylate toxicity, treated with urine alkalinisation and haemodialysis." [1]

Examiner: "What is the most common error candidates make when interpreting this kind of gas?" [1]

"Stopping at the primary disorder. A candidate who sees the low bicarbonate and the low PaCO2 may call it a 'metabolic acidosis with compensation' and miss that the PaCO2 is far too low to be compensation alone — there is a second, primary respiratory alkalosis. The defence is always to calculate Winter's formula and compare the measured PaCO2 to the predicted range. If the measured value is outside the range, a mixed disorder is present and the differential changes completely." [1]