From the Guidelines

Rapid correction of hyperglycemia is not safe in Hyperosmolar Hyperglycemic State (HHS).

The mechanism of cerebral edema, a rare but frequently fatal complication of HHS, is thought to result from osmotically driven movement of water into the central nervous system when plasma osmolality declines too rapidly with treatment 1.
To avoid cerebral edema, prevention measures include gradual replacement of sodium and water deficits in patients who are hyperosmolar, with a maximal reduction in osmolality of 3 mOsm/kg/h 1.
In HHS, a glucose level of 250–300 mg/dl should be maintained until hyperosmolarity and mental status improve and the patient becomes clinically stable 1.
Fluid replacement should correct estimated deficits within the first 24 h, with the induced change in serum osmolality not exceeding 3 mOsm/kg/h 1.

Insulin therapy should be initiated with a low dose of 0.1 U/kg/h (5–7 U/h in adults) to decrease plasma glucose concentration at a rate of 50–75 mg/dl/h 1.
Dextrose should be added to the hydrating solution once blood glucose reaches 250 mg/dl to maintain a glucose level of 250–300 mg/dl until the patient is stable 1.

From the Research

The safety of rapid correction of hyperglycemia in Hyperosmolar Hyperglycemic State (HHS) is a topic of concern, as it may lead to complications such as osmotic demyelination syndrome (ODS) and cerebral edema 2, 3.
A study published in 1999 suggests that the goal of therapy is for the plasma glucose level to decline by at least 75 to 100 mg per dL (4.2 to 5.6 mmol per L) per hour, indicating the adequacy of therapy, especially rehydration 4.
However, more recent studies warn against rapid correction of hyperglycemia, highlighting the importance of cautious correction of serum hyperglycemia and monitoring serum sodium levels in patients with HHS 2, 3, 5.
The treatment of HHS involves replacement of the substantial fluid deficit with several liters of a physiological crystalloid solution, and serum potassium concentrations need to be carefully monitored to guide its substitution 6.
Guidelines for the management of HHS recommend monitoring the response to treatment, aiming to reduce osmolality by 3-8 mOsm/kg/h, and withholding insulin until the blood glucose level is no longer falling with i.v. fluids alone (unless ketonaemic) 5.

Osmotic demyelination syndrome (ODS) is a rare complication that can occur due to rapid correction of chronic hyponatremia, and has also been reported in patients with HHS 2.
Cerebral edema is another potential complication of rapid correction of hyperglycemia, and can result from overly-aggressive fluid resuscitation and rapid correction of hyperglycemia and hyperosmolarity 3.
Central pontine myelinolysis is also a potential complication of rapid changes in osmolality during treatment of HHS 5.