THE HANDOVER CLUB
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The handover sheet for student nurses and new grads: what it is, why it happens, how to spot it, and what you'll be doing on shift.
With no insulin, the cells can't use glucose, so the body burns fat for fuel. That makes ketones, which are acids. They build up until the blood becomes acidic.
Mostly people with type 1 diabetes, and sometimes it's how type 1 is first diagnosed. It can also happen in type 2, especially on an SGLT2 inhibitor (the "-gliflozins").
DKA is a medical emergency. The danger isn't only the sugar: it's the acid, the dehydration and the potassium shifts.
On an SGLT2 inhibitor (dapagliflozin, empagliflozin)? DKA can happen with a near normal BGL. If they look unwell, check ketones anyway.
Insulin is the key that lets glucose into the cells. Without it, glucose stays in the blood and the cells are starving next to a full plate.
Stress hormones (glucagon, cortisol, adrenaline) tell the liver to release even more glucose. The BGL keeps climbing.
The body breaks down fat for energy. The liver turns it into ketones. Ketones are acids.
Ketones use up the bicarbonate (the blood's buffer). pH falls, HCO₃⁻ falls, anion gap rises. This is metabolic acidosis.
Above roughly 10 mmol/L, glucose spills into the urine and drags water, sodium and potassium with it. Result: polyuria, thirst, severe dehydration.
Deep, fast breathing (Kussmaul) blows off CO₂ to bring the pH back up. Fruity breath = acetone, a ketone you can smell.
Diabetes
BGL > 11 mmol/L
(or known diabetes)
Ketones
blood ketones ≥ 3 mmol/L
Acidosis
pH < 7.3 and/or
HCO₃⁻ < 15 mmol/L
Commonly used thresholds (e.g. JBDS). Exact cut-offs vary between Australian hospitals, so check your local protocol.
| BGL | High (often > 11, but see euglycaemic DKA on page 1) |
| Ketones | High (≥ 3 mmol/L) |
| pH / HCO₃⁻ | Low: metabolic acidosis |
| Anion gap | High: Na⁺ − (Cl⁻ + HCO₃⁻), the ketones are the "unmeasured" acids |
| K⁺ | Normal or high at first, even though total body K⁺ is low |
| Na⁺ | Can look low because the high glucose pulls water into the blood |
| Urea / creatinine | Often up from dehydration |
Fluids fix the dehydration. Insulin (usually a fixed-rate IV infusion) switches off ketone production. Potassium is replaced because insulin pushes K⁺ into the cells. When the BGL comes down, glucose is added so the insulin can keep running safely.
| Check | Usually |
|---|---|
| BGL | Hourly |
| Blood ketones | Hourly at first |
| VBG: pH, HCO₃⁻, K⁺ | Regularly, often 2-hourly at first, then less often as they improve |
| Obs and neuro obs (GCS) | Hourly, or as the patient's condition needs |
| Strict fluid balance | Hourly urine output (may need an IDC) |
| Cardiac monitoring | If K⁺ is abnormal |
Frequencies differ between hospitals. Follow your local DKA protocol and chart.
Headache or a drop in GCS (think cerebral oedema, especially in younger patients) · K⁺ out of range · a hypo · ketones not falling or HCO₃⁻ not rising · poor urine output · any Q-ADDS or local MET criteria.
That's why the insulin keeps running after the BGL is normal: it's still clearing ketones.
Serum K⁺ can drop fast once insulin starts. Know the K⁺ before and during the infusion.
Fluids are usually the first thing started. Most patients are several litres down.
Glucose goes into the fluids so the insulin can keep working without a hypo.
Long-acting insulin is usually continued during DKA treatment. A person with type 1 should never stop it, even when sick and not eating.
SGLT2 inhibitors can cause DKA with a near normal BGL.
Many protocols use blood ketones < 0.6 mmol/L and pH > 7.3, but criteria vary between hospitals. When switching to subcutaneous insulin, the IV infusion is usually kept running for a while after the first subcut dose, so there's never a gap in insulin.
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