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Hyperosmolar Hyperglycaemic State (HHS)Emergency
Endocrinology · Ward Pathways · Locked — free with a referral
By Dr Javed Akhtar · Last reviewed 2 October 2026
Presentation Elderly type 2 diabetes, 1 week of polyuria then confusion; very dry; glucose 980 mg/dL, Na⁺ 148, effective osmolality 345 mOsm/kg, pH 7.34, BOHB 1.1 mmol/L
Red flags Osmolality >350 mOsm/kg Seizures, focal deficit, GCS <12 Oliguria despite fluids Chest pain or ECG change (MI as precipitant) Limb ischaemia or DVT
Differential diagnosis DKA or mixed DKA–HHS Stroke, meningitis, encephalitis (confusion) Hypernatraemic dehydration without diabetes Sepsis with stress hyperglycaemia
When to admit, call ICU or discharge Admit: All HHSICU/HDU: Osmolality >350, Na⁺ >160, GCS <12, hypotension, hypothermia, AKI, severe comorbidity (JBDS)
Key points HHS carries higher mortality than DKA — older patients with comorbidities; mortality is from the precipitant, thrombosis and over-rapid correction. Fluid alone brings glucose down; insulin is added only when that stops (or if ketotic). Watch osmolality, not just glucose — plot it every 2 hours for the first 6 hours.
Never Start insulin at 0.1 U/kg/h before fluids have been given — glucose and osmolality crash, fluid shifts intracellularly Drop Na⁺ by >10 mmol/L in 24 h Use hypotonic fluid as the first fluid Forget VTE prophylaxis and heel protection
Common mistakes Treating it like DKA with high-dose insulin Correcting Na⁺ or osmolality too fast Missing the precipitant No thromboprophylaxis
Disposition and follow-up HDU for severity markers; otherwise ward with hourly monitoring for the first 24 h. Diabetes team before discharge; insulin often needed temporarily.
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