Acid-Base Disorders — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Hung Tran, 64 years old, retired plumber. ^[1]

Presenting complaint: Two days of vomiting, diffuse abdominal pain, and increasing confusion. His wife found him drowsy this morning. ^[1]

Past history: Type 2 diabetes for 20 years, chronic kidney disease stage 3b (baseline eGFR 38, creatinine 170), hypertension, ischaemic heart disease (NSTEMI 3 years ago). ^[1]

Current medications: Metformin 1 g BD, empagliflozin 10 mg daily, perindopril 10 mg daily, frusemide 40 mg daily, atorvastatin 80 mg, aspirin 100 mg. ^[1]

Examination findings (trainee elicits):

• GCS 13 (E3 V4 M6), drowsy but rousable
• BP 92/58, HR 110, regular; RR 28, deep and laboured (Kussmaul breathing)
• Dry mucous membranes, reduced skin turgor, flat JVP
• Soft, diffusely tender abdomen, no guarding; bowel sounds present
• No focal neurological deficit ^[1]

Investigations:

• Sodium 138, potassium 6.4, chloride 96, bicarbonate 8, urea 22, creatinine 230 (baseline 170)
• Glucose 9.2, lactate 9.5, beta-hydroxybutyrate 4.8 (raised), albumin 32 g/L
• Venous pH 7.04; arterial blood gas: pH 7.05, PaCO2 22 mmHg, PaO2 88 mmHg, bicarbonate 8
• ECG: peaked T waves, widened QRS
• Measured osmolality 312, calculated osmolality 300 ^[1]

Candidate's structured presentation (model)

Opening statement: ^[1]

"Mr Tran is a 64-year-old retired plumber who presents with two days of vomiting, abdominal pain and confusion. He has a background of type 2 diabetes for 20 years, chronic kidney disease stage 3b, hypertension and ischaemic heart disease, and he takes metformin, empagliflozin, perindopril, frusemide and atorvastatin." ^[1]

"His main problems are:

1. Severe high anion gap metabolic acidosis — a combination of metformin-associated lactic acidosis and euglycaemic diabetic ketoacidosis, on a background of chronic kidney disease
2. Acute kidney injury, KDIGO stage 2, on chronic CKD — pre-renal, compounded by nephrotoxic medications
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]

Acid-base interpretation: ^[1]

"His gas shows a pH of 7.05, a severe acidaemia. The bicarbonate is 8 and the PaCO2 is 22; both are low, so the low PaCO2 is compensation and the primary process is a metabolic acidosis. Winter's formula gives an expected PaCO2 of 1.5 times 8 plus 8, equals 20, plus or minus 2; his measured PaCO2 of 22 is within that range, so compensation is appropriate. The anion gap is 138 minus 96 minus 8, equals 34; corrected for his albumin of 32 grams per litre it is 36 — a high anion gap metabolic acidosis. The delta-delta ratio is 1.5, in the pure-acidosis range. The osmolar gap is 12, mildly elevated but not in the toxic alcohol range. The raised lactate and beta-hydroxybutyrate confirm lactic acidosis and ketoacidosis respectively." ^[1]

Management plan: ^[1]

1. Stabilise the potassium immediately: calcium gluconate 10 mL of 10% intravenously to protect the myocardium, then insulin (10 units) with 50 mL of 50% dextrose, and a salbutamol nebuliser to shift potassium intracellularly. Continuous cardiac monitoring.
2. Resuscitate: he is hypovolaemic — balanced crystalloid (Plasma-Lyte) in 500 mL boluses with reassessment.
3. Stop the offending agents: cease metformin (lactic acidosis), empagliflozin (euglycaemic DKA), and hold perindopril (hyperkalaemia, AKI).
4. Treat the DKA component: fixed-rate intravenous insulin at 0.1 units/kg/hour, with dextrose running because his glucose is only 9.2 — this is euglycaemic DKA, so dextrose is needed from the outset to allow insulin to run without hypoglycaemia. Replace potassium as the acidosis corrects.
5. Definitive removal — early haemodialysis: he meets multiple criteria — severe acidaemia (pH 7.05), hyperkalaemia with ECG changes, AKI on CKD, and a dialysable toxin in metformin. Discuss immediately with ICU and nephrology.
6. Investigate the precipitant: blood cultures, lipase, lactate trend, and a CT abdomen to exclude mesenteric ischaemia or intra-abdominal sepsis. Empirical broad-spectrum antibiotics within one hour if sepsis is suspected. ^[1]

Examiner discussion questions

Q: "Would you give sodium bicarbonate to this patient?" ^[1]

"Not as a standalone treatment. BICAR-ICU showed no overall mortality benefit from bicarbonate in severe metabolic acidaemia in the ICU, though there was a signal toward reduced renal replacement therapy in the severe-AKI subgroup. His definitive treatment is haemodialysis, which corrects the acidosis, removes metformin and addresses the potassium. I would reserve bicarbonate as a bridge to dialysis if his pH were to fall further or his haemodynamics to deteriorate. The principle is that his acidosis is a marker of metformin accumulation and hypoperfusion — I treat the cause and remove the toxin, not the number." ^[1]

Q: "How did the empagliflozin contribute, and what will you tell him on recovery?" ^[1]

"The empagliflozin causes glucosuria by blocking glucose reabsorption in the proximal tubule, which lowers plasma glucose, suppresses insulin secretion and raises glucagon. The high glucagon-to-insulin ratio drives ketogenesis, producing ketoacidosis with a near-normal glucose — euglycaemic DKA. This is a recognised risk of SGLT2 inhibitors, especially in the context of acute illness, reduced oral intake, surgery, or dehydration. On recovery I would teach him the sick-day rule: hold the empagliflozin, metformin, perindopril and frusemide during any acute illness with reduced intake, vomiting, diarrhoea or fever, and resume when recovered. I would not stop the SGLT2 inhibitor permanently, because its cardiovascular and renoprotective benefits are substantial — I would restart it once he is well, hydrated and eating." ^[1]

Q: "His delta-delta is 1.5 despite vomiting. Explain." ^[1]

"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. Here the acid load is so overwhelming — the lactic acidosis and ketoacidosis together — that any alkalinising effect from vomiting is being consumed to buffer the acid, so the ratio stays in the pure-acidosis range. If his vomiting were the dominant process with 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 contribution." ^[1]

Q: "What is the single most dangerous acid-base diagnosis to miss in a confused patient with a high anion gap acidosis?" ^[1]

"A toxic alcohol ingestion — methanol or ethylene glycol. Although his osmolar gap of 12 is only mildly elevated and his clinical picture fits metformin and DKA, I would explicitly take a collateral history about possible ingestion and, if there were any visual symptoms or renal failure out of proportion, I would give fomepizole empirically while awaiting levels. The danger is that the osmolar gap falls as the parent alcohol is metabolised, so a late presentation can have a normal osmolar gap with a severe high anion gap acidosis. Fomepizole is safe, and the cost of missing the diagnosis is blindness (methanol) or irreversible renal failure (ethylene glycol)." ^[1]