Blood gas, electrolyte and acid-base interpretation — formative SAQs

SAQ 1 — The five-step method on a high-anion-gap metabolic acidosis (15 marks, 15 minutes)

A three-year-old is brought in breathing deeply and rapidly with the smell of ketones on the breath. A capillary gas shows pH 7.07, PaCO2 14 mmHg, bicarbonate 4 mmol per litre, sodium 132, chloride 96, and glucose 24 mmol per litre. [6] [11]

Question. Interpret the gas using the five-step systematic method. Name the primary disturbance, judge the compensation with the appropriate formula, calculate the anion gap and classify the metabolic acidosis, and list the differential of a high-gap acidosis.

Model answer

Step 1 — pH (2 marks). The pH of 7.07 is well below 7.35, so this is a severe acidaemia. The primary disturbance is an acidosis. [11]

Step 2 — PaCO2 (2 marks). PaCO2 is 14 mmHg, which is below the normal range of 35 to 45. A low PaCO2 is a compensatory alkalosis, not the primary driver, because it moves against the acidaemia. [4]

Step 3 — Bicarbonate (2 marks). Bicarbonate is 4 mmol per litre, far below 22 to 26. A low bicarbonate with a low pH is a metabolic acidosis, and this is the primary disturbance. [6]

Step 4 — Compensation, Winter's formula (4 marks). For metabolic acidosis the expected PaCO2 is 1.5 times the bicarbonate plus 8, within plus or minus 2. Here that is 1.5 times 4 plus 8, equals 14, within the band of 12 to 16. The measured PaCO2 of 14 falls inside the band, so the respiratory compensation is appropriate and there is no additional respiratory disorder. [11]

Step 5 — Anion gap and classification (3 marks). The anion gap is sodium minus chloride plus bicarbonate: 132 minus 96 plus 4, equals 32 mmol per litre. The normal gap is 8 to 12, so this is a high-gap metabolic acidosis. The differential of a high gap is KULT — ketones, uraemia, lactate, toxins. Given the ketotic breath and the glucose of 24, this is diabetic ketoacidosis. [6]

Reasoning (2 marks). The five-step method holds the interpretation together: a high-gap metabolic acidosis with appropriate respiratory compensation, in a child whose history and glucose confirm DKA. The corrected sodium would guide the fluid plan, and the structured DKA protocol now drives management. [7]

SAQ 2 — A venous gas in diabetic ketoacidosis and the danger of cerebral oedema (12 marks, 12 minutes)

A nine-year-old with new-onset type 1 diabetes arrives drowsy with deep sighing respiration. A venous gas shows pH 7.12, bicarbonate 7 mmol per litre, glucose 28 mmol per litre, sodium 128, potassium 5.6, and base excess negative eighteen. [6]

Question. State the corrected sodium and why it matters, outline the structured fluid and insulin plan, and explain why bicarbonate is not routinely given and why cerebral oedema is feared.

Model answer

Corrected sodium (3 marks). The measured sodium is falsely low because the high glucose draws water into the vascular space. The corrected sodium is the measured value plus 1.6 mmol per litre for every 5.5 mmol per litre of glucose above normal. With glucose of 28 the rise is 1.6 times (28 minus 5.5) divided by 5.5, which is about 6.5, giving a corrected sodium of about 134.5 mmol per litre. It matters because the fluid plan is built on the corrected value, not the measured one, and a falling corrected sodium during treatment is an early warning of cerebral oedema. [1]

Fluid and insulin plan (4 marks). Give an initial 10 to 20 mL per kilogram of 0.9 per cent saline over one to two hours to restore perfusion, then continue with isotonic fluids. Start insulin as an infusion at 0.05 to 0.1 unit per kilogram per hour after the fluid bolus, not before, and do not give an insulin bolus. Replace potassium once the level begins to fall, because insulin drives potassium into the cell. Aim for a gradual fall in glucose of 3 to 5 mmol per litre per hour, and add dextrose when the glucose reaches 14 to 17. [7]

Why bicarbonate is not routine (2 marks). Bicarbonate lowers the cerebrospinal fluid pH paradoxically, generates carbon dioxide that the lung must clear, and does not address the cause (the ketoacids). It is reserved for the child with a pH below 7 and haemodynamic collapse, and even then it is given slowly and cautiously. [6]

Cerebral oedema (3 marks). Cerebral oedema is the feared complication of paediatric DKA and carries a high mortality. It is driven by rapid fluid shifts, a falling corrected sodium, and the osmotic gradient between plasma and brain. Watch for headache, drowsiness, bradycardia and a falling conscious level; if it appears, slow the fluids, give mannitol or hypertonic saline, raise the head of the bed, and consider intubation for airway protection. The venous gas tracks the trend well because venous pH sits within 0.03 of arterial and bicarbonate tracks closely, so an arterial stick is not needed to follow the acidosis. [4] [7]