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]

DCE Short Case — Blood Gas Interpretation

Instruction

"Interpret this arterial blood gas and discuss your management. You have 4 minutes to interpret and 6 minutes for discussion." [1]

Provided data: pH 7.48, PaCO2 16 mmHg, bicarbonate 12 mmol/L, PaO2 95 mmHg on room air. Sodium 140, chloride 100, potassium 4.0, albumin 40 g/L. [1]

Presentation template

"I will interpret this gas in six steps. First, the pH is 7.48, which is alkalaemia. Second, the bicarbonate is 12 and the PaCO2 is 16; both are low, but the low bicarbonate would cause acidaemia, so it is not driving the alkalaemia — the very low PaCO2 is the primary process, a respiratory alkalosis. Third, I apply Winter's formula to the metabolic component: the expected PaCO2 for a bicarbonate of 12 is 1.5 times 12 plus 8, equals 26, plus or minus 2, so 24 to 28. The measured PaCO2 of 16 is far below the expected range, confirming a concurrent respiratory alkalosis on top of a metabolic acidosis. Fourth, the anion gap is 140 minus 100 minus 12, which is 28 — a high anion gap. Fifth, the delta-delta is 28 minus 12 equals 16, divided by 24 minus 12 equals 12, ratio 1.3, within the pure high anion gap range. Sixth, the osmolar gap is not given, but I would calculate it if a toxic alcohol were a possibility." [1]

"In summary, this is a mixed high anion gap metabolic acidosis and a primary respiratory alkalosis — the classic pattern of early salicylate toxicity. My immediate management is ABCDE, take a salicylate level, give activated charcoal if ingestion was recent, start intravenous sodium bicarbonate to alkalinise the urine and enhance elimination, and arrange haemodialysis for severe toxicity." [1]

Discussion

Examiner: "Name three causes of this mixed pattern other than salicylates." [1]

"Sepsis with lactic acidosis and hyperventilation; pulmonary embolism with shock causing lactic acidosis and hyperventilation; and hepatic failure with lactic acidosis and hyperventilation from portopulmonary stimulation. In each, the metabolic acidosis is from lactate and the respiratory alkalosis from hyperventilation. The discriminator is the salicylate level and the clinical context." [1]

Examiner: "What is the most dangerous error in interpreting a gas like this?" [1]

"Stopping at the primary disorder. A candidate who sees the low bicarbonate and 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, which completely changes the differential. 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." [1]

Examiner: "Name three causes of a high anion gap metabolic acidosis with a specific antidote or definitive treatment." [1]

"Methanol — fomepizole, folate, and haemodialysis, with the clue of visual symptoms and a high osmolar gap. Ethylene glycol — the same fomepizole-based approach, with thiamine and pyridoxine as cofactors, and the clue of renal failure and calcium oxalate crystals. Metformin-associated lactic acidosis — there is no drug antidote, but the definitive treatment is haemodialysis to remove the metformin and correct the acidosis. A fourth is salicylate toxicity, treated with urine alkalinisation and haemodialysis." [1]