ICU · Endocrine & metabolic emergencies
Diabetic Ketoacidosis (DKA) & Hyperosmolar Hyperglycaemic State (HHS)
Also known as Diabetic ketoacidosis · DKA · Hyperosmolar hyperglycaemic state · HHS · Hyperosmolar non-ketotic coma · HONK · Fixed-rate intravenous insulin infusion · FRIII · Euglycaemic DKA · Hyperglycaemic crisis · Ketonaemia · Beta-hydroxybutyrate
DKA and HHS are the two hyperglycaemic emergencies on a spectrum of insulin deficiency. DKA (typically type 1) is the triad of hyperglycaemia, ketonaemia and a high-anion-gap metabolic acidosis — the biochemical mirror of HHS, which is defined by ketonaemia at or under 3.0 mmol/L, pH above 7.3 and bicarbonate at or above 15. HHS (typically type 2, elderly) is marked hypovolaemia with hyperglycaemia (30 mmol/L or more by JBDS, 33.3 by ADA), osmolality 320 mOsm/kg or more (2 x Na + glucose + urea) and estimated fluid losses of 100-220 mL/kg; pooled mortality 21.1 per cent. Management is fluid first (0.9% saline to restore circulating volume), a fixed-rate insulin infusion (DKA 0.1 unit/kg/h, de-escalating to 0.05 once glucose is under 14 mmol/L; HHS 0.05 unit/kg/h by JBDS or 0.1 by ADA), potassium addressed before insulin drives it lower, gradual osmolality correction (3.0-8.0 mOsm/kg/h JBDS), and identification plus treatment of the precipitant. The DKA resolution target is ketone clearance, NOT glucose normalisation.
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- DKA resolution is defined by KETONE clearance — the intravenous insulin infusion continues until ketonaemia resolves, not until glucose normalises; stopping early leaves the ketoacidosis untreated (a named management pitfall).
- Address potassium before or with insulin — current guidance runs continuous IV insulin only once fluid status is restored and potassium levels have been achieved; hypokalaemia was common enough under the previous UK regimen to help drive the 2022 JBDS rewrite.
- Once glucose falls under 14 mmol/L, do NOT stop insulin — start a 5% or 10% glucose infusion (JBDS HHS pathway) and consider de-escalating the DKA infusion from 0.1 to 0.05 units/kg/h (JBDS DKA update).
- Routine bicarbonate is discouraged — it can worsen ketosis and hypokalaemia and carries cerebral-oedema risk (bicarbonate treatment was associated with cerebral oedema in children, relative risk 4.2). Consider IV bicarbonate only if pH falls below 6.9, or peri-intubation with pH below 7.2 and bicarbonate below 10 mEq/L.
- Cerebral oedema is the devastating complication of DKA in children — independently associated with lower initial PaCO2 (severity of acidosis), higher urea nitrogen (dehydration) and bicarbonate treatment.
- HHS is a high-mortality emergency (pooled mortality 21.1 per cent, roughly ten times DKA) — VTE prevention is a named pathway aim; let osmolality fall gradually (3.0-8.0 mOsm/kg/h JBDS, under 3 mOsm/kg/h ADA).
Meet the patient
A 24-year-old man with type 1 diabetes is brought to the emergency department drowsy and breathing deeply and rapidly, his mucous membranes dry and his face sunken, after a flu-like illness and 36 hours of omitted insulin (infection and non-adherence are the classic precipitants). Glucose 34 mmol/L, venous pH 7.02, bicarbonate 6, beta-hydroxybutyrate 8.2, ketonuria triple-positive — admission biochemistry of exactly this order is typical of published DKA cohorts (glucose about 40 mmol/L, pH about 7.1, bicarbonate about 7 mmol/L).[23][7]
The diagnosis is immediate; the question is the order of the next four moves. The therapeutic order never changes and is the whole topic: fluids first, insulin second, potassium third, treat the trigger fourth. Hold that order and every guideline slots into place — and remember the single trap that kills: DKA resolves when the ketones clear, not when the glucose normalises.[1]
References23ShowHide
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