Hyperosmolar hyperglycaemic state (HHS)

Background

Hyperosmolar hyperglycaemic state (HHS, previously known as hyperosmolar non-ketotic coma or HONK) is a syndrome characterised by extreme elevations in serum glucose concentrations, hyperosmolality and dehydration without significant ketosis.

Hyperosmolar hyperglycaemic state (HHS) occurs in people with type 2 diabetes and may develop over days or a number of weeks.


Pathophysiology
Hyperglycaemia causes osmotic diuresis with resulting hyperosmolality. Hyperosmolality causes osmotic shifts resulting in severe intracellular dehydration. Ketosis does not occur as insulin levels are sufficient to prevent ketogenesis but insufficient to reduce blood glucose.

It should be noted that proinflammatory cytokines increase two to threefold during acute episodes. This causes a temporary increase in prothrombotic event risk e.g. MI, DIC, stroke and artery thrombosis. In most cases risk returns to normal within 24 hours.

Clinical features

• Polyuria
• Polydipsia
• Nausea
• Clinical features of dehydration (hypotension, tachycardia, poor skin turgor)
• Lethargy
• Confusion
• Weakness

Precipitating factors

• Infection
• Inadequate diabetic treatment.
• Physiological stress (trauma, surgery, pancreatitis, MI etc).
• Drugs e.g. corticosteroids, diuretics, atypical antipsychotics, and sympathomimetic drugs such as salbutamol.

Initial investigations

• Capillary blood glucose
• Venous blood gas
• Urinalysis
• ECG (MI may precipitate or be a complication of HHS)
• Measure osmolality (or calculate osmolarity: (2 x Na+) + Glucose + Urea)

Management
Treatment aims to correct dehydration, hyperglycaemia, hyperosmolality, electrolyte disturbance as well as identify and treat any underlying cause. The patient will also require prophylactic anticoagulation due to transient hypercoagulable state

Care is needed in correction of plasma sodium and osmolality as there is a risk of cerebral oedema and osmotic demyelination syndrome which are both potentially fatal.

Key points:

• Use IV 0.9% sodium chloride solution as the principal fluid to restore circulating volume and reverse dehydration
• Consider switch to 0.45% sodium chloride solution if the osmolality is not declining despite adequate positive fluid balance. An initial rise in sodium is expected and is not itself an indication for hypotonic fluids.
• The rate of fall of plasma sodium should not exceed 10 mmol/L in 24 hours.
• The fall in blood glucose should be no more than 5 mmol/L/hour. A target blood glucose of between 10 and 15 mmol/L is a reasonable goal.
• Low-dose IV insulin (0.05 units/kg/hour) should only be commenced once the blood glucose is no longer falling with IV fluids alone OR immediately if there is significant ketonaemia (urine ketones > 2+ or 3β-hydroxy butyrate > 1 mmol/l)
• IV fluid replacement aims to achieve a positive balance of 3-6 litres by 12 hours and the remaining replacement of estimated fluid losses within next 12 hours, though complete normalisation of biochemistry may take up to 72 hours.
• Potassium replacement should be guided by potassium level as follows:

• 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 including fluid overload, cerebral oedema or central pontine myelinosis
• Underlying precipitants identified and treated.
• Prophylactic anticoagulation is required in most patients.
• All patients should be assumed to be at high risk of foot ulceration. The heels should be appropriately protected and daily foot checks undertaken.