Type I diabetes is characterised by destruction of beta cells in the pancreatic islets and, therefore, a complete lack of insulin. In the absence of insulin glucose cannot enter the peripheral tissues resulting in hyperglycaemia. In contrast, type II diabetes is due to a resistance of the peripheral tissues to insulin action. The resistance to insulin action resides largely in skeletal muscle and adipocytes. The effect on glucose levels is the same, hyperglycaemia. However, in the type II patient with HHS at least some insulin is present to prevent the action of  glucagon on the liver, that is to antagonise the full expression of the ‘starvation response’. So, in theory at least, in type II diabetes, ketoacidosis with all it’s attendant problems does not develop.

However, the prognosis of HHS is, if anything, worse than that of DKA. This may reflect the difference in the age profile of patients affected by type I and type II diabetes. Co-morbidity may be a factor but also a difference in physiology. A young type I diabetic with an osmotic diuresis will avidly seek out water. However, the thirst mechanism declines with age and an elderly type II diabetic may fail to increase oral intake in response to the osmotic diuresis induced by hyperglycaemia. Hence, the later present with marked dehydration and associated hypernatremia secondary to free water loss in the kidneys. Also, as they are profoundly dehydrated, tissue perfusion may be compromised and they usually develop a secondary lactic acidosis.

In reality in type II diabetics, one sometimes encounters a mixture of lactic acidosis in the setting of HHS combined with a degree of ketoacidosis. Equally, in a young patient with DKA, vomiting and or altered conscious level may reduce the ability to take in fluids and this combined with the ongoing osmotic diuresis may result in hypernatremia.

The key points of treatment remain the same, replace fluids, give insulin and deal with any underlying trigger.

back to course menu