Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State, or HHS, is a serious and life-threatening complication of type 2 diabetes mellitus. It is characterized by three main features: severe hyperglycemia, profound dehydration, and elevated serum osmolality, all occurring without significant ketoacidosis.

HHS typically develops in older adults or individuals with limited access to fluids. This may result from illness, cognitive impairment, or medications such as diuretics or corticosteroids. These factors reduce fluid intake, and when combined with osmotic diuresis triggered by very high blood glucose levels, they cause substantial volume loss and a rise in serum osmolality.

In contrast to diabetic ketoacidosis, or DKA, where a lack of insulin promotes fat breakdown and ketone production, individuals with HHS still produce enough insulin to suppress ketogenesis but not enough to prevent dangerous elevations in blood glucose. As a result, ketones are usually absent or minimal, and metabolic acidosis is generally not present. Although mild ketonuria may appear in cases of prolonged fasting or coexisting illness, it is not characteristic of HHS and does not reflect the primary disease mechanism.

As blood glucose levels rise, often exceeding 600 milligrams per deciliter, the kidneys become unable to reabsorb all the glucose. This leads to substantial fluid loss in the urine, which further concentrates the blood and elevates serum osmolality to above 320, and occasionally beyond 330, milliosmoles per kilogram.

Water then shifts from inside cells into the bloodstream in an attempt to balance the concentration gradient. Brain cells are particularly sensitive to this shift, leading to neurologic symptoms such as confusion, lethargy, seizures, and coma. In some instances, these symptoms can resemble those of a stroke, making rapid blood glucose testing essential for proper diagnosis.