Hyperosmolar hyperglycaemic state (HHS)
Severe hyperglycaemia + hyperosmolality without significant ketosis
Overview
A type 2 diabetes emergency of profound hyperglycaemia, hyperosmolality and severe dehydration WITHOUT significant ketoacidosis (residual insulin suppresses ketogenesis). Onset is slower than DKA; fluid replacement is the mainstay and insulin is used cautiously.
Recognise
- Marked hyperglycaemia (often >30), severe dehydration, hypovolaemia
- Reduced consciousness/confusion; osmolality typically >320
- Minimal ketones/acidosis (unlike DKA); high VTE risk
Red flags
- Profound dehydration/hypovolaemic shock, reduced GCS, very high osmolality; high thrombosis risk
Differentials & how to tell them apart
Investigations
Glucose, osmolality (or calculated), U&E, ketones (low), venous gas, FBC/CRP, search for precipitant (infection, MI).
Management
IV 0.9% saline (cautious rehydration) first; low-dose insulin only if needed; VTE prophylaxis
- 1Cautious IV 0.9% saline rehydration (the priority); glucose often falls with fluids alone. Give VTE prophylaxis.Gate: Start insulin only once glucose stops falling with fluids (or if significant ketones) — early/aggressive insulin risks dangerous osmotic shifts
- 2Correct electrolytes gradually; treat the precipitant; aim for a slow correction of osmolality/glucose.
Key points
Slower, gentler than DKA: fluids first and insulin later/lower. Rapid osmotic shifts risk cerebral oedema and central pontine myelinolysis. VTE risk is high.
Monitor & prognosis
Glucose, osmolality, U&E, fluid balance, GCS — aim for gradual correction.
Higher mortality than DKA (older, comorbid); good if corrected slowly.
Source: JBDS-IP (HHS guideline)