Hyperosmolar hyperglycaemic state

Overview

HHS is a life-threatening metabolic emergency in type 2 diabetes: profound hyperglycaemia + hyperosmolality + NO significant ketosis/acidosis.

•JBDS diagnostic criteria - all four must be present:

•Hypovolaemia - clinically evident dehydration

•Hyperglycaemia - blood glucose >30 mmol/L

•Hyperosmolality - serum osmolality >320 mOsm/kg

•No significant hyperketonaemia (blood ketones <3 mmol/L) and no significant acidosis (pH >7.3, bicarbonate >15 mmol/L)

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Why no ketones? Residual basal insulin in type 2 diabetes is enough to suppress lipolysis and inhibit ketogenesis - even though it cannot control glucose. This is the key distinction from DKA.

Presentation

•Develops over days to weeks (unlike DKA which evolves over hours) - typically in older adults with type 2 diabetes

•Polyuria and polydipsia - osmotic diuresis from glucosuria

•Drowsiness and altered consciousness - correlates with degree of hyperosmolality; can progress to coma

•Weakness and fatigue

•Hypotension and tachycardia - severe hypovolaemia

•Headache, visual disturbance, papilloedema - CNS effects of hyperosmolality

•Notably absent: vomiting, abdominal pain, Kussmaul breathing - these suggest DKA

Investigations

•Bedside glucose - typically >30 mmol/L

•Ketones (blood/urine) - absent or minimal; significant ketosis suggests DKA

•Venous blood gas - pH near-normal (>7.3), bicarbonate normal; acidosis suggests concurrent DKA

•Calculated serum osmolality - >320 mOsm/kg confirms HHS

•Na⁺ - often raised; K⁺ - may appear normal/high despite total body depletion

•Urea and creatinine - commonly raised (pre-renal AKI from dehydration)

•FBC, CRP, blood cultures, urine MC&S - screen for precipitating infection

•ECG - arrhythmia (K⁺-related) and underlying MI as precipitant

Management

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Do NOT give insulin before adequate IV fluid resuscitation. Insulin drives glucose and water into cells, rapidly depleting the intravascular compartment - in severe hypovolaemia this can cause cardiovascular collapse. Fluids first - always.

•IV fluid resuscitation - 0.9% NaCl; target osmolality fall of 3-8 mOsm/kg/hour (must correct slowly)

•Potassium replacement - add to subsequent fluid bags per JBDS protocol (total body depletion despite normal serum level)

•Insulin - withhold until glucose fails to fall with fluids alone

•LMWH - thromboprophylaxis (high thromboembolic risk from hyperviscosity)

•Identify and treat precipitating cause

Complications

•Cerebral oedema - rare but fatal; risk increased by overly rapid correction of glucose/osmolality

•Thromboembolic events (DVT/PE) - hyperviscosity from dehydration and immobility

•Acute kidney injury - pre-renal from profound dehydration

•Cardiac arrhythmias - hypokalaemia or hyperkalaemia during treatment

•Mortality 10-20% - higher than DKA, reflecting older age and severity of precipitating illness

Serum osmolality formula

•Calculated serum osmolality = 2×Na⁺ + glucose + urea (all in mmol/L)

•Example: Na 152, glucose 36, urea 9.5 → (2×152) + 36 + 9.5 = 349.5 mOsm/kg (normal 278-305)

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This formula is directly tested in exams - know it cold.

Precipitants

Common precipitants

Infection - most common (UTI, pneumonia, gastroenteritis)

New diagnosis of type 2 diabetes - HHS may be first presentation

Corticosteroids

Thiazide diuretics

Antipsychotics (e.g. olanzapine)

Myocardial infarction or stroke

Poor fluid intake - frail/elderly patients