Medicine chapters
DKA, HHS and diabetes during surgery
Recognition and step-by-step treatment of diabetic ketoacidosis and the hyperosmolar hyperglycaemic state, how they differ, and how to manage diabetes drugs and glucose around surgery.
- DKA = ketones ≥3 mmol/L, glucose >11 mmol/L (or known diabetes) and bicarbonate <15 mmol/L and/or pH <7.3; treat with 0.9% saline, potassium and a fixed-rate insulin infusion of 0.1 unit/kg/h.
- HHS = very high glucose and osmolality ≥320 mOsm/kg without major ketosis in older type 2 patients; correct slowly with fluids first and 0.05 unit/kg/h insulin only if needed.
- Around surgery, insulin users missing more than one meal need a variable-rate IV insulin infusion, while their long-acting insulin is continued.
On this page
Overview
The two hyperglycaemic emergencies are diabetic ketoacidosis (DKA) and the hyperosmolar hyperglycaemic state (HHS). They sit at two ends of one spectrum: DKA is driven by absolute insulin lack (ketones and acidosis), HHS by relative insulin lack with severe dehydration. Both kill if treated badly, and both have strict, protocol-based treatment that PGET questions test step by step. Surgery in a person with diabetes is the other common inpatient problem.
Diabetic ketoacidosis (DKA)
How it happens
- With no insulin, fat breaks down (lipolysis). The liver turns the released fatty acids into ketones (acetoacetate, β-hydroxybutyrate, acetone), causing a high anion gap metabolic acidosis.
- The liver also releases glucose without control, so glucose rises and causes an osmotic diuresis. Water, sodium, potassium and phosphate are lost. Vomiting adds to the losses.
- The typical water deficit is about 100 mL/kg (about 7 litres in a 70 kg adult).
Who gets it and why
- Mostly type 1 diabetes; it may be the first presentation.
- Triggers: infection, missed or reduced insulin, new diabetes, myocardial infarction, pancreatitis, pump failure, alcohol.
- Can occur in type 2 diabetes, especially on SGLT2 inhibitors, where the glucose may be only slightly raised (euglycaemic DKA).
Clinical features
- Polyuria, thirst, weight loss, nausea, vomiting, abdominal pain (may mimic an acute abdomen), weakness.
- Dehydration, tachycardia, hypotension.
- Kussmaul breathing (deep, sighing), ketone smell on the breath (like pear drops or nail-polish remover).
- Drowsiness; a few present in coma.
Diagnosis (all three needed)
| Component | Criterion |
|---|---|
| Ketones | Blood ketones ≥3 mmol/L or urine ketones 2+ or more |
| Glucose | >11 mmol/L (above 200 mg/dL), or the patient is already known to have diabetes |
| Acidosis | Bicarbonate <15 mmol/L and/or venous pH <7.3 |
Markers of severe DKA (needs HDU or ICU)
- Ketones >6 mmol/L, bicarbonate <5 mmol/L, pH <7.0.
- Potassium <3.5 mmol/L on admission.
- GCS <12, oxygen saturation <92% on air, systolic BP <90 mmHg, pulse >100 or <60.
- Anion gap >16.
Investigations
- Capillary glucose and blood ketones at the bedside; venous blood gas (pH, bicarbonate, potassium); urea, creatinine and electrolytes; full blood count; cultures; urine; ECG; chest X-ray if indicated.
- White cell count is often high even without infection, and fever is often absent even with infection. Look hard for a source.
- Serum amylase may be mildly raised without pancreatitis.
Serum potassium is often normal or high at presentation, yet total body potassium is low. Acidosis and insulin lack shift potassium out of cells. Once insulin starts, potassium falls fast.
Management
The aim is to replace fluid, give insulin to switch off ketone production, replace potassium and treat the cause.
First hour
- Assess severity; take the bloods above; attach a cardiac monitor.
- 0.9% sodium chloride 1 L over 1 hour (faster boluses if systolic BP is below 90 mmHg).
- Fixed-rate IV insulin infusion (FRIII): soluble insulin 0.1 unit/kg per hour (about 6–10 units/h). Estimate weight if needed. No bolus is needed.
- Continue the patient's usual long-acting basal insulin subcutaneously.
Hours 1–12: fluids with potassium
- Then 0.9% saline 1 L over 2 h, 1 L over 2 h, 1 L over 4 h, 1 L over 4 h, 1 L over 6 h, adjusted for age, heart and kidney disease.
- Potassium in each litre:
| Serum K+ (mmol/L) | Potassium per litre of fluid |
|---|---|
| >5.5 | None |
| 3.5–5.5 | 40 mmol/L |
| <3.5 | Senior review; more potassium needed (central line or HDU) |
Monitoring and targets (hourly glucose and ketones; venous gas at 1 h, 2 h and then regularly)
- Blood ketones should drop by 0.5 mmol/L or more each hour, or
- Bicarbonate should rise by at least 3 mmol/L per hour, or
- Glucose should fall by at least 3 mmol/L per hour.
- If not, increase insulin by 1 unit/h each hour until targets are met.
- Keep potassium 4.0–5.5 mmol/L.
- When glucose falls below 14 mmol/L, add 10% glucose at 125 mL/h alongside the saline. Do not stop or cut the insulin: insulin is still needed to clear ketones.
Other measures
- Catheter if no urine after 2–4 hours or if incontinent; NG tube if drowsy or persistently vomiting (aspiration risk).
- LMWH thromboprophylaxis unless contraindicated.
- Antibiotics if infection is suspected (after cultures).
- Bicarbonate is rarely used: it can worsen intracellular and CSF acidosis and may add to cerebral oedema risk; consider only in extreme acidosis with senior input.
Resolution and switching back
- DKA has resolved when ketones are below 0.6 mmol/L and venous pH is above 7.3.
- When the patient can eat and drink, give subcutaneous rapid-acting insulin with a meal and stop the infusion 30 minutes later (basal insulin should already be on board).
- Find out why it happened and educate on sick-day rules (never stop insulin; check ketones; drink fluids).
Glucose is 12 mmol/L after six hours but ketones are still 3.5 mmol/L and pH 7.21. The answer is add 10% dextrose and continue (or increase) insulin, not stop the insulin. Glucose falls long before ketosis clears.
Hyperchloraemic acidosis often appears late in treatment because large volumes of saline are given. Bicarbonate stays low while the anion gap and ketones normalise. It is not treatment failure; judge recovery by ketones.
Complications
- Hypokalaemia (and arrhythmias), hypoglycaemia, hypophosphataemia.
- Cerebral oedema: mainly children and young adults, linked to over-rapid fluid or glucose correction. Headache, falling GCS, bradycardia and rising BP during treatment. Treat with mannitol or hypertonic saline and senior help.
- Aspiration pneumonia, ARDS, thromboembolism.
- Rhino-orbital mucormycosis: acidosis frees iron from transferrin, helping the fungus; black eschar in the nose or palate needs urgent debridement and amphotericin.
DKA management order, "Fluids, Insulin, Potassium, Glucose (at 14), Cause": FIP-GC.
Hyperosmolar hyperglycaemic state (HHS)
Who and why
- Typically older people with type 2 diabetes, often previously undiagnosed.
- There is enough insulin to stop ketone production but not enough to stop the liver making glucose.
- Develops over days to weeks, so dehydration is far worse than in DKA.
- Triggers: infection, sugary drinks, thiazides, steroids, stroke, myocardial infarction, poor fluid intake in the frail.
Diagnosis
- Hypovolaemia
- Marked hyperglycaemia, usually ≥30 mmol/L
- Osmolality ≥320 mOsm/kg
- No significant ketonaemia (below 3 mmol/L) and no acidosis (pH above 7.3, bicarbonate above 15 mmol/L)
Clinical features
- Severe dehydration, confusion, drowsiness or coma (closely linked to the osmolality), focal neurological signs or seizures.
- High risk of stroke, myocardial infarction, limb ischaemia, DVT and heel ulcers.
Management
- Fluids are the main treatment: 0.9% saline first. Use 0.45% saline only if osmolality is not falling despite good fluid balance.
- Correct slowly: plasma sodium should fall by no more than 10 mmol/L in 24 hours; glucose by at most 5 mmol/L each hour. Fast shifts risk cerebral oedema and osmotic demyelination.
- Sodium may rise at first as glucose falls (water moves back into cells). This is expected if osmolality is falling.
- Insulin only if glucose stops falling with fluids alone, or if there is significant ketonaemia: 0.05 unit/kg per hour (half the DKA dose). Many patients are very sensitive to insulin.
- Prophylactic LMWH, foot protection, treat the trigger, careful potassium replacement.
- Prognosis: mortality can reach 15–20% because patients are old and ill. Survivors may later manage on diet and tablets; long-term insulin is not automatic.
DKA versus HHS
| Feature | DKA | HHS |
|---|---|---|
| Usual patient | Young, type 1 | Older, type 2 |
| Onset | Hours to a day | Days to weeks |
| Glucose | Raised (may be near normal on SGLT2 inhibitors) | Very high (often >30 mmol/L) |
| Ketones | ≥3 mmol/L | Low |
| pH / bicarbonate | <7.3 / <15 | >7.3 / >15 |
| Osmolality | Raised moderately | ≥320 mOsm/kg |
| Insulin rate | 0.1 unit/kg/h from the start | 0.05 unit/kg/h, only if needed |
| Main danger | Hypokalaemia, cerebral oedema (children) | Thrombosis, stroke, too-rapid correction |
| Mortality | Low with good care | Higher (up to 15–20%) |
DKA: Na 136, K 5.0, Cl 98, HCO3 8 mmol/L
Anion gap = (Na + K) − (Cl + HCO3) = (136 + 5) − (98 + 8) = 35 → high (normal below about 17 with K included)
HHS: Na 150, K 4.5, glucose 45, urea 14 mmol/L
Osmolality = 2(Na + K) + glucose + urea = 2(154.5) + 45 + 14 = 368 mOsm/kg → well above 320
Insulin: 0.1 × 70 = 7 units per hour (soluble insulin, fixed rate)
Estimated water deficit: 100 mL/kg × 70 kg = 7 litres
Other acidotic emergencies to tell apart
- Lactic acidosis (metformin-associated): severe high anion gap acidosis without much hyperglycaemia or ketosis, usually with renal failure, sepsis or shock. Mortality is high (over half). Stop metformin, rehydrate, treat the cause; dialysis may be needed.
- Alcoholic ketoacidosis: binge drinking followed by vomiting and starvation; normal or low glucose, high anion gap acidosis with ketones. Treat with fluids, glucose and thiamine (not insulin).
- Starvation ketosis: mild ketosis, near-normal bicarbonate.
Diabetes during surgery
Both high and low glucose around surgery increase infection, heart attack, length of stay and death.
Before admission
- Optimise control in primary care and the pre-assessment clinic. Many guidelines suggest postponing elective surgery if HbA1c is well above target (around 69 mmol/mol, 8.5%) when it is safe to do so.
- Put the patient first on the morning list to shorten fasting.
On the day: drugs
| Treatment | What to do |
|---|---|
| Long-acting basal insulin | Continue (often at a slightly reduced dose); prevents rebound hyperglycaemia and DKA |
| Short-acting or premixed insulin | Omit or reduce while fasting; replace with VRIII if needed |
| Sulphonylureas | Omit on the morning of surgery (hypoglycaemia risk while fasting) |
| Metformin | Can often continue for short fasts; withhold if more than one meal will be missed, if contrast is given or if renal function is impaired |
| SGLT2 inhibitors | Withhold before surgery (usually from the day before) because of the risk of euglycaemic DKA |
| DPP-4 inhibitors, GLP-1 agonists | Usually omitted on the day of surgery |
Variable-rate IV insulin infusion (VRIII)
- Needed for insulin-treated patients who will miss more than one meal, for type 1 diabetes having anything but the shortest procedure, for emergency surgery with poor control, and in labour.
- Soluble insulin by syringe pump, with the rate adjusted to hourly capillary glucose, given with a glucose-containing fluid (and potassium) so the patient is not starved of substrate.
- Typical target glucose 6–10 mmol/L (wider range acceptable).
- Keep the long-acting basal insulin going. Stop the VRIII only after the first subcutaneous mealtime dose has been given and the patient is eating.
- The old term "sliding scale" is no longer preferred.
Use a fixed-rate infusion for DKA and HHS and a variable-rate infusion for surgery, nil by mouth, acute coronary syndrome, stroke, labour, critical illness and high-dose steroid hyperglycaemia.
Stopping all insulin in a fasting type 1 patient before surgery can precipitate DKA within hours. Type 1 patients always need some insulin.
After surgery
- Restart usual treatment when eating and drinking normally (metformin once renal function is confirmed normal).
- Check feet and pressure areas; give a clear discharge plan.
Expect: the three DKA criteria and markers of severity; why potassium is given despite a normal first value; the fixed-rate insulin dose (0.1 unit/kg/h) and continuing basal insulin; when to add 10% dextrose (glucose below 14) and the trap of stopping insulin too early; resolution criteria; cerebral oedema in children; HHS criteria (osmolality 320, glucose 30, no ketosis), slow sodium and glucose correction and the lower insulin dose; anion gap and osmolality calculations; euglycaemic DKA with SGLT2 inhibitors; alcoholic and lactic acidosis; and which diabetes drugs to stop or continue around surgery and when to use a variable-rate infusion.
Quick revision
- DKA: ketones ≥3, glucose >11 (or known DM), HCO3 <15 and/or pH <7.3.
- Severe: ketones >6, HCO3 <5, pH <7.0, K <3.5, GCS <12.
- 0.9% saline 1 L in first hour; FRIII 0.1 unit/kg/h; continue basal insulin.
- KCl 40 mmol/L if K 3.5–5.5; none if >5.5; senior help if <3.5.
- Glucose <14 → add 10% dextrose 125 mL/h and keep insulin going.
- Resolved: ketones <0.6 and pH >7.3.
- HHS: osmolality ≥320, glucose ≥30, no ketosis; Na fall ≤10/24 h; glucose fall ≤5/h; insulin 0.05 unit/kg/h if needed.
- Surgery: VRIII if more than one meal missed; omit sulphonylurea and SGLT2 inhibitor; keep basal insulin.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
Why is insulin given as a fixed rate in DKA?
A fixed weight-based rate reliably switches off ketone production; the glucose is then held up with 10% dextrose rather than by lowering the insulin.
Why is bicarbonate not routinely given in DKA?
Insulin and fluids correct the acidosis on their own, and bicarbonate can worsen acidosis inside cells and the CSF and may contribute to cerebral oedema.
Why does HHS need slower correction than DKA?
The brain has adapted to a very high osmolality over days, so a rapid fall in glucose or sodium can cause cerebral oedema or osmotic demyelination.
Should long-acting insulin be stopped before surgery?
No. It is usually continued, sometimes at a slightly lower dose, to prevent rebound hyperglycaemia and ketosis when the intravenous insulin is stopped.