• Severe hyperglycaemia in the absence of ketosis
  • Characteristic of Type 2 diabetes
  • Common precipitating factors include;
  • Consumption of glucose rich fluids
  • Concurrent medication such as thiazide diuretics and steroids
  • Intercurent illness
  • Endogenous insulin is sufficient to prevent hepatic ketogenesis

 

Clinical presentation

  • Dehydration
  • Stupor/coma
  • Impairment of consciousness is related to degree of hyperosmolarity
  • Hyperosmolar state may predispose to stroke, MI or arterial insufficiency in lower limbs

 

Biochemical presentation

  • Blood glucose is high, often higher than that seen in ketoacidosis
  • Na is high
  • Potassium levels are often raised but total body potassium can be normal
  • Urea high due to dehydration
  • Serum osmolality is very high
  • Arterial pH is not normally raised

 

Treatment

  • Generally treat similarly to diabetic ketoacidosis, however;
  • Patient may be normo- or hypernatraemic therefore hypotonic fluid replacement may be required
  • There is increased risk of prothrombotic events therefore prophylactic anticoagulation may be necessary
  • Bicarbonate therapy is unnecessary and smaller amounts of potassium are required
  • Blood glucose levels are extremely high so restoration of normal levels may take many hours, too quick a reestablishment can lead to effects of osmotic disequilibrium on the CNS

 

 

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