Hyperosmolar hyperglycemic state (HHS) is an acute metabolic complication of both diabetes mellitus type 1 and type 2. Although HHS accounts for only 1% of diabetic-related hospital admissions, HHS-related mortality is greater than that of diabetic ketoacidosis. This increased mortality is due to a greater severity of dehydration as well as the older age and concurrent comorbid conditions of patients with HHS.

The term "hyperosmolar hyperglycemic state" has replaced "hyperglycemic hyperosmolar nonketotic state" and "hyperglycemic hyperosmolar nonketotic coma," since the condition may present with varying degrees of ketosis and with altered mental status in the absence of coma.

HHS is due to ineffective action of insulin and elevated counter-regulatory hormones with increased hepatic glucose production and impaired peripheral utilization, resulting in dehydration and electrolyte abnormalities due to osmotic diuresis by glycosuria.

The most common precipitating factors for HHS are inadequate insulin therapy and the presence of infection. Other potential precipitants include acute coronary syndromes, drugs (steroids in particular), pulmonary embolism, stroke, and alcohol abuse.

HHS is marked by signs of dehydration and glucosuria (polydipsia, polyuria, decreased skin turgor, and tachycardia) and altered mental status (severity relates to degree of hyperosmolality). Coma may be present in 25%-50% of cases. Some patients with HHS may present with hemiparesis, hemianopsia, or even seizures.

Metabolic derangements include hyperglycemia, hyperosmolarity, hyponatremia, and hyperkalemia. Blood urea and creatinine may be elevated. Unlike diabetic ketoacidosis, bicarbonate is >20 mEq/L, pH is >7.3, and there are negative ketone bodies in urine and plasma.