About This Page
This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
Key points
- HHS (previously HONK) = glucose >30 mmol/L + osmolality >320 mOsm/kg + NO significant ketonaemia/acidosis
- Typically elderly T2DM patients. Precipitants: infection (most common), MI, stroke, new diagnosis, drugs (steroids, thiazides)
- Severe dehydration (average fluid deficit 100–220 mL/kg — much more than DKA)
- Treatment: cautious IV 0.9% NaCl rehydration is the PRIORITY (not insulin). Low-dose insulin only if glucose not falling with fluids alone
- VTE prophylaxis MANDATORY — high risk of thromboembolism (hyperviscosity)
- Mortality 15–20% (much higher than DKA ~1%). Complications: cerebral oedema (if corrected too rapidly), VTE, rhabdomyolysis
Overview
Hyperosmolar hyperglycaemic state (HHS) is a life-threatening metabolic emergency of type 2 diabetes characterised by severe hyperglycaemia, hyperosmolality, and profound dehydration without significant ketoacidosis. Unlike DKA, there is sufficient residual insulin to prevent lipolysis and ketogenesis, but not enough to control glucose. The profound hyperglycaemia causes osmotic diuresis leading to massive fluid and electrolyte losses over days to weeks. The insidious onset and population affected (elderly, often with comorbidities) contribute to the high mortality (15–20%). Serum osmolality is calculated as: 2(Na⁺ + K⁺) + glucose + urea (all in mmol/L).
Epidemiology
HHS accounts for approximately 1% of diabetes-related hospital admissions but carries a disproportionately high mortality. It typically affects elderly patients with T2DM, often with limited access to fluids (nursing home residents, dementia, immobility). Common precipitants include infection (pneumonia, UTI), acute illness (MI, stroke), medications (corticosteroids, thiazides), and new diabetes diagnosis. It may be the first presentation of T2DM. Mixed DKA-HHS occurs in approximately 15% of cases and carries the highest risk.
Clinical Features
Symptoms
Gradual onset over days to weeks (unlike DKA which is hours to days)
Profound thirst and polyuria (initially — then reduced as dehydration worsens)
Confusion, drowsiness, altered consciousness — often the presenting feature
Nausea, vomiting
Weakness and lethargy
Visual disturbance
Symptoms of precipitant (cough/fever if infection, chest pain if MI)
Signs
Severe dehydration: dry mucous membranes, reduced skin turgor, sunken eyes
Tachycardia, hypotension
Altered consciousness or coma (correlates with osmolality)
NO Kussmaul breathing (unlike DKA — no significant acidosis)
NO ketotic breath (unlike DKA)
Focal neurological deficits (seizures, hemiparesis — may mimic stroke)
Investigations
First-line
Blood glucose>30 mmol/L (often >50 mmol/L). Much higher than typical DKA
Serum osmolality>320 mOsm/kg (calculate: 2[Na⁺ + K⁺] + glucose + urea). Correlates with level of consciousness
Blood ketones<3.0 mmol/L (no significant ketonaemia). If >3.0 or pH <7.3 → consider mixed DKA/HHS
ABG/VBGpH usually >7.3. Bicarbonate usually >15 mmol/L. If acidotic → mixed picture or lactic acidosis
Second-line
U&EsSodium may be falsely low (pseudohyponatraemia from hyperglycaemia). Calculate corrected sodium. Potassium: may be high initially then falls with treatment
FBCRaised WCC (infection or stress response). Haemoconcentration
Blood cultures, urine culture, CXRLook for precipitant — infection is the most common trigger
ECGExclude MI (common precipitant). Monitor potassium changes
Specialist
CT headIf focal neurology or failure to improve — exclude stroke (precipitant or complication)
CKRhabdomyolysis is a recognised complication — from severe dehydration and immobility
1
Fluid resuscitation (THE PRIORITY)
- IV 0.9% NaCl is the fluid of choice. Average deficit 100–220 mL/kg (8–15 L)
- Aim: replace 50% of estimated fluid deficit in first 12 h, remainder in next 12–24 h
- Typical rate: 1 L in first hour, then 500 mL/h for 4 h, then 250 mL/h — adjust for cardiac function
- Aim for glucose fall of 4–6 mmol/L per hour. Aim for osmolality fall of 3–8 mOsm/kg per hour
- AVOID overly rapid correction — risk of cerebral oedema and central pontine myelinolysis
- Switch to 0.45% NaCl only if osmolality not declining despite adequate fluid replacement
2
Insulin
- Do NOT start insulin immediately unless blood ketones >1.0 mmol/L or mixed DKA/HHS
- Fluids alone will lower glucose in most cases. Start low-dose insulin ONLY if glucose not falling with fluids
- If insulin needed: fixed-rate IV insulin infusion (FRII) 0.05 units/kg/h (HALF the DKA dose)
- Early insulin risks precipitous glucose/osmolality fall → cerebral oedema
3
Potassium replacement
- Monitor potassium closely (falls rapidly with rehydration and any insulin given)
- K⁺ >5.5: no replacement. K⁺ 3.5–5.5: add 40 mmol KCl per litre of IV fluid. K⁺ <3.5: urgent replacement before insulin
4
VTE prophylaxis
- LMWH (e.g. enoxaparin) for ALL patients unless contraindicated — high VTE risk from hyperviscosity
- Continue throughout admission and for duration of immobility
5
Monitoring
- Hourly glucose, osmolality every 2 h, U&Es every 4–6 h
- Fluid balance chart, urinary catheter if oliguric or altered consciousness
- Senior review if not improving within 6 hours, or deteriorating neurologically
Complications
- Venous thromboembolism: DVT/PE from hyperviscosity — major cause of mortality. Prophylactic LMWH essential
- Cerebral oedema: From overly rapid correction of osmolality — devastating and often fatal
- Stroke and MI: Both precipitants and complications (thrombotic tendency)
- Rhabdomyolysis: From severe dehydration + immobility → AKI, hyperkalaemia
- Seizures: Osmotic shifts during treatment
- Death: Mortality 15–20%, much higher than DKA. Often related to comorbidities and age
UKMLA Exam Tips
- 1HHS vs DKA: HHS = glucose >30, osmolality >320, NO significant ketosis. DKA = glucose >11, pH <7.3, ketones ≥3.0
- 2HHS = FLUIDS first, insulin cautiously later. DKA = fluids AND insulin together from the start
- 3Insulin dose in HHS is HALF that of DKA (0.05 vs 0.1 units/kg/h) — to avoid rapid osmolality shifts
- 4VTE prophylaxis is MANDATORY in HHS — test favourite: patient with HHS who develops PE
- 5Focal neurology in HHS can mimic stroke — check glucose before diagnosing stroke
- 6Mixed DKA/HHS carries the HIGHEST mortality — treat as DKA but with extreme caution on fluid rates
Put your reading into practice
Topic-specific question practice is not linked for this article yet.
Choose UKMLA questions from the existing bank. General exam practice covers your selected topics; it is not filtered to this article. Your usual question-bank access applies.
Choose UKMLA practiceAfter your session, return to this section to revisit the reading and choose your next review.
Verified Sources & References
related resources
Save your place and choose what comes next
Endocrine & Metabolic · Article 14 of 25