Hyperglycemic hyperosmolar syndrome (HHS) is a metabolic disorder resulting from a relative insulin deficiency initiated by an illness or physiologic stressor (e.g., infection, surgery, cerebrovascular disease or myocardial infarction [MI]) that raises demand for insulin.

This condition occurs most frequently in older adults (50 to 70 years of age) who have no known history of diabetes or who have type 2 diabetes. The acute development of the condition can be traced to some precipitating event, such as an acute illness (e.g., pneumonia, stroke), medications (e.g., thiazides) that exacerbate hyperglycemia, or treatments such as dialysis.

HHS is a serious condition in which hyperglycemia and hyperosmolarity predominate with alterations of consciousness (sense of awareness). Ketosis is minimal or absent. The basic biochemical defect is lack of effective insulin (insulin resistance). Persistent hyperglycemia causes osmotic diuresis, resulting in water and electrolyte losses. Although there is not enough insulin to prevent hyperglycemia, the small amount of insulin present is enough to prevent fat breakdown.

• History of days to weeks of polyuria with adequate fluid intake
• Hypotension, tachycardia
• Profound dehydration (dry mucous membranes, poor skin turgor)
• Variable neurologic signs (alterations of consciousness, seizures, hemiparesis)

• Laboratory tests, including blood glucose, electrolytes, blood urea nitrogen (BUN), complete blood cell (CBC) count, serum osmolality, and arterial blood gasses (ABGs)
• Clinical picture of severe dehydration

The overall treatment of HHS is similar to that of diabetic ketoacidosis (DKA): fluids, electrolytes, and insulin. Because patients with HHS are typically older, close monitoring of volume and electrolyte status is important for prevention of fluid overload, heart failure, and cardiac dysrhythmias. Fluid treatment is started with 0.9% sodium chloride or NaCl (normal saline) or 0.45% sodium chloride (half-strength normal saline), depending on the patient's sodium level and the severity of volume depletion. Central venous or hemodynamic pressure monitoring guides fluid replacement. Potassium is added to IV fluids when urinary output is adequate and is guided by continuous electrocardiography (ECG) monitoring and frequent laboratory determinations of potassium. Insulin is usually given at a continuous low rate to treat hyperglycemia, and dextrose is added to replacement fluids when the glucose level decreases to 250 to 300 mg/dL. Other therapeutic modalities are determined by the underlying illness and results of continuing clinical and laboratory evaluation, and treatment is continued until metabolic abnormalities are corrected; it may take 3 to 5 days for neurologic symptoms to resolve.

See “Nursing Management” under Diabetes in Section D and “Nursing Process: The Patient With DKA” under Diabetic Ketoacidosis in Section D for additional information.

• Assess vital signs, fluid status, and laboratory values. Fluid status and urine output are closely monitored because of the high risk of kidney failure secondary to severe dehydration.
• Blood glucose should be checked hourly.
• Because HHS tends to occur in older patients, the physiologic changes that occur with aging should be considered.
• Careful assessment of cardiovascular, pulmonary, and renal function throughout the acute and recovery phases of HHS is important.

For more information, see Chapter 51 in Hinkle, J. L., & Cheever, K. H. (2018). Brunner and Suddarth's textbook of medical-surgical nursing (14th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.