The hyperglycaemic hyperosmolar state (HHS) occurs most commonly in older people with type 2 diabetes. HHS is different from diabetic ketoacidosis (DKA) and treatment requires a different approach. Whilst DKA presents within hours of onset, HHS comes on over many days, and consequently the dehydration and metabolic disturbances are more extreme.
Presents with polyuria, polydipsia, weakness, weight loss, tachycardia, dry mucous membranes, poor skin turgor, hypotension, and, in severe cases, shock.
Acute cognitive impairment (lethargy, disorientation, stupor) is common with osmolalities over 330 mosmol/kg.
Neurological Symptoms
Severe hyperosmolality (>330 mOsm/kg) can cause seizures, focal neurological deficits, and decreased level of consciousness that may mimic stroke.
Fluid Resuscitation
- IV 0.9% NaCl initially
- 1-2L in first 2 hours
- Monitor osmolality hourly
- Switch to 0.45% NaCl if needed
Insulin Therapy
- Start after fluids
- 0.05 units/kg/hr IV
- Target glucose 10-15 mmol/L
- Max fall 5 mmol/L per hour
Electrolyte Management
- Monitor K⁺ every 2-4 hours
- Replace if < 5.5 mmol/L
- Watch for hypophosphataemia
- Consider magnesium if symptomatic
Fluid Replacement
Key Principle
Rapid changes in osmolality may be harmful. Use intravenous (IV) 0.9% sodium chloride solution as the principle fluid to restore circulating volume and reverse dehydration.
- Measurement or calculation of osmolality should be undertaken every hour initially and the rate of fluid replacement adjusted to ensure a positive fluid balance sufficient to promote a gradual decline in osmolality.
- Fluid replacement alone (without insulin) will lower blood glucose which will reduce osmolality causing a shift of water into the intracellular space.
- Rising sodium is only a concern if the osmolality is NOT declining concurrently. Rapid changes must be avoided – a safe rate of fall of plasma glucose of between 4 and 6 mmol/hr is recommended.
- The aim of treatment should be to replace approximately 50% of estimated fluid loss within the first 12 hours and the remainder in the following 12 hours though this will in part be determined by the initial severity, degree of renal impairment and co-morbidities such as heart failure.
Clinical Tip
Ideally patients will recover quickly enough to replace the water deficit themselves by taking fluids orally. However, if the osmolality is no longer declining despite adequate fluid replacement with 0.9% sodium chloride solution AND an adequate rate of fall of plasma glucose is not being achieved then 0.45% sodium chloride solution should be substituted.
Insulin Therapy
Important Warning
Insulin treatment prior to adequate fluid replacement may result in cardiovascular collapse as water moves out of the intravascular space, with a resulting decline in intravascular volume.
- Low dose IV insulin (0.05 units/kg/hr) should only be commenced once the blood glucose is no longer falling with IV fluids alone OR immediately if there is significant ketonaemia.
- A fall of glucose at a rate of up to 5 mmol/L per hour is ideal and once the blood glucose has ceased to fall following initial fluid resuscitation, reassessment of fluid intake and evaluation of renal function must be undertaken.
Electrolyte Replacement
- Patients with HHS are potassium deplete but less acidotic than those with DKA so potassium shifts are less pronounced.
- Hypophosphataemia and hypomagnesaemia are common in HHS. As with the management of DKA there is no evidence of benefit of treatment with phosphate infusion.
- Magnesium replacement has also not been shown to be beneficial so should only be considered if the patient is symptomatic or has symptomatic hypocalcaemia.
General Principles
- A target blood glucose of between 10 and 15 mmol/L is a reasonable goal. Complete normalisation of electrolytes and osmolality may take up to 72 hours.
- The patient should be encouraged to drink as soon as it is safe to do so and an accurate fluid balance chart should be maintained until IV fluids are no longer required.
- Assessment for complications of treatment e.g. fluid overload, cerebral oedema or central pontine myelinolysis (as indicated by a deteriorating conscious level) must be undertaken frequently (every 1-2 hours).
- Underlying precipitants must be identified and treated. An infective source should be sought on clinical history and examination and C-reactive protein may be helpful.
- Patients in HHS have an increased risk of arterial and venous thromboembolism. All patients should receive prophylactic low molecular weight heparin (LMWH) for the full duration of admission unless contraindicated.
- All patients should be assumed to be at high risk of foot ulceration if obtunded or uncooperative - the heels should be appropriately protected and daily foot checks undertaken.