It's the difference between insulin resistance and complete absence of insulin.
Without talking about the whole pathophys of the disease processes, the basal level of insulin produced in a T2DM patient is usually enough to prevent severe ketosis. The hyperosmolarity is due to the hyperglycemia and resulting osmotic diuresis. This results in the hyperosmolar hyperglycemic non-ketotic syndrome.
Since T1DM has no insulin production, their metabolism becomes wholly dependent on lipolysis and ketosis. Again the hyperosmolarity is due to the hyperglycemia and resulting osmotic diuresis.
Keep in mind that this is more a rule of thumb than anything else: T1DM usually develop DKA and T2DM usually develop HHS.