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Question 26 - Answer: D
Cautious fluid resuscitation with insulin infusion at 0.1 unit/kg/h until ketonaemia resolves.
Clinical Reasoning
Diagnosis: Severe Diabetic Ketoacidosis (DKA)
This 17-year-old presents with the classic triad of DKA:
| Feature | This Patient | Significance |
|---|
| pH 6.89 | < 7.0 | Severe acidosis |
| HCO3 4 mmol/L | Very low | Severe base deficit |
| Ketonuria on dipstick | Positive | Ketonaemia confirmed |
| Glucose 41 mmol/L | Markedly raised | Hyperglycaemia |
| Kussmaul breathing | "Rapid, deep, sighing" | Respiratory compensation |
| Na+ 114 mmol/L | Low | Osmotic dilution effect |
| K+ 6.9 mmol/L | Elevated | Shift due to acidosis |
This is severe DKA (pH < 7.0, HCO3 < 10 mmol/L) by standard diagnostic criteria.
Why D is Correct
The cornerstone of DKA management is:
-
Fluid resuscitation first - restores circulating volume and tissue perfusion. Fluid losses of 5-10 litres are common in DKA. Initial treatment is 0.9% NaCl (isotonic saline) at 2-4 L in the first 2-4 hours - Goldman-Cecil Medicine, p. 2484
-
Fixed-rate IV insulin at 0.1 units/kg/hour - started as soon as the diagnosis is confirmed. This suppresses lipolysis, ketogenesis, and gluconeogenesis. Insulin dose is NOT adjusted to glucose level (that is a sliding scale approach, which is wrong here) - Goldman-Cecil Medicine, p. 2484
-
Continue insulin until ketonaemia resolves - the endpoint is clearance of ketones, not normalisation of blood glucose (glucose is given alongside as dextrose once BG falls below 250 mg/dL to allow insulin to continue)
Why Each Other Option is Wrong
A - Immediate intubation and ventilation
The patient has a GCS of 13/15 (mild impairment, not coma), is maintaining saturations at 99%, and has a normal BP. The rapid deep breathing (Kussmaul respiration) is a critical physiological compensation for severe acidosis - intubating and paralysing this patient would abolish the respiratory compensation and precipitously worsen the pH, which can be fatal. Intubation is reserved for GCS <8 or airway compromise.
B - Urgent haemofiltration
Haemofiltration/haemodiafiltration is not indicated for DKA. The acidosis is metabolic (ketoacid accumulation from insulin deficiency) and reverses with insulin + fluids. Haemofiltration could actually worsen haemodynamic instability. It is very rarely considered in refractory lactic acidosis, not DKA.
C - IV bicarbonate slow infusion
Bicarbonate is generally not recommended in DKA even with very low pH. The risks include paradoxical CNS acidosis (CO2 crosses blood-brain barrier while HCO3 does not), worsening hypokalemia (bicarb drives K+ into cells), and rebound alkalosis. Bicarbonate is considered only if pH remains < 7.0 and the patient is not responding to insulin and fluids - Goldman-Cecil Medicine, p. 2484. Even then, the threshold is < 7.0 and it is not first-line.
E - Insulin sliding scale adjusted to blood glucose
This is the approach used for routine hyperglycaemia management, NOT DKA. In DKA, insulin must run at a fixed rate (0.1 units/kg/h) regardless of glucose level, because the goal is to clear ketones. Sliding scale insulin titrated to glucose level would lead to premature insulin reduction as glucose falls, allowing ongoing ketosis and acidosis. As per Goldman-Cecil Medicine: "a fixed-rate intravenous insulin infusion should start at 0.1 units/kg/hour as soon as the diagnosis is made."
Key DKA Management Principles
- Fluid first, then insulin (after K+ ≥ 3.5 mEq/L is confirmed - never start insulin if K+ is very low)
- The patient here has K+ 6.9 - this is high due to acidosis. It will drop rapidly once insulin starts (K+ shifts back into cells). Watch for hypokalaemia during treatment.
- Add 10% dextrose once BG falls below ~14 mmol/L to allow insulin to continue clearing ketones
- Monitor for cerebral oedema in young patients (risk with overly rapid fluid correction)
- Do NOT use bicarbonate routinely
The answer is D. - Goldman-Cecil Medicine, International Edition, Chapter 210