Hyperosmolar Hyperglycaemic State (HHS)

HHS was formerly known as HONK (Hyperosmolar Non-Ketotic State)

  • HHS = Severe hyperglycemia (>50mmol/L) without significant hyperketonaemia or acidosis
    • Normal ketones
    • Normal ph
    • Normal bicarbonate
    • Osmolality >320mOsm
  • HHS is indicative of poor glycaemic control in type 2 patients
    • May be the first presentation
    • Typically affects patients 55-70 years old (unlike DKA)
      • F>M
  • 10x less common than DKA

  • High glucagon and low insulin activity => high glycogenolysis => hyperglycaemia
  • No ketosis because:
    1. Gluconeogenesis is inhibited by insulin which is still present (only a little insulin is required to prevent it)
    2. Gluconeogenesis is also inhibited by the significant dehydration
    3. Liver responds to insulin better than other tissue

Aetiology (Precipitants)
  • Drugs
    • Steroids
    • Diuretics
  • Social isolation
  • Acute illnesses – e.g. infections causing cortisol release
    • Sepsis
    • MI, Stroke


Signs & Symptoms:

  • Subacute onset over about a week
    • This is much longer than DKA
    • Initial symptoms may be undetected as these patients are old and less perceptive of thirst
  • Severe hyperglycaemia results in profound osmotic diuresis
    • => Profound polyuria + polydipsia
      • => Severe dehydration and hyperosmolality of blood
    • Neurological symptoms develops when osmolality >340mosm/kg (normal is 280-300)
      • This is because the brain also becomes dehydrated
      • Typically present with disturbed consciousness
      • May present with focal neurology – often mistaken for other conditions
      • NB no seizures
  • Occlusive events  – e.g. DVT, Stroke, MI – are much more likely in HHS than in DKA (greater degree of dehydration)

Differences in HHS vs DKA

  • HHS has:
    • Slower onset – days vs hours
    • Greater glucose increase (>50mmol/L) in HONK
      • Greater hyperosmolarity and more dehydration due to this
        • Greater risk of occlusive events
        • Hypernatremia is more likely
        • Hypokalemia is also very likely
    • No change in pH or ketones
      • Therefore there are ketotic/acidotic symptoms
    • Insulin is more effective in these patients

  • Consider acute management and secondary prevention

Acute management (RIPA)

  • Escalate if there is imminent organ failure
  • Aims:
    • Drop osmolality by 3-8mOsm/hr doing so quicker than this can cause cerebral oedema
    • Drop glucose by ≤5mmol/hr
  • Rehydration – fluid deficit is higher in HHS than DKA
    • 0.9% Saline is given more slowly (over 48/72 hours)
    • Monitor CVP and plasma Na+ and glucose
  • Insulin infusion  (Fixed rate)
    • Wait 1 hour before starting – only use this if rehydration alone is not adequate
    • Use at half the rate of DKA (0.05 units/kg/hr = weight in kg/20)
  • Potassium replacement is required (as in DKA)
    • These patients are often hypokalemic in the first place due to high osmolality/normal insulin (rather than being iatrogenic as in DKA)
  • Prophylactic Anticoagulants to prevent occlusive events are very important due to the especially high risk of thromboembolism
    • I.e. LMWH

Long-term management

  • Look for a precipitant and treat it if possible
    • Consider the patient’s compliance with treatment
    • In a first-time patient something causing an increase in BGL like acute illness can be treated
  • Most of these patients can then be discharged and managed without insulin