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Hyperosmolar Hyperglycemic State (HHS) Hyperosmolar hyperglycemic state (HHS) is a serious metabolic derangement that is fatal in 10% to 20% of patients. Some research cites the fatality rate as much higher—up to 40% or 50% in some cases. It is less common that diabetic ketoacidosis, although findings of both conditions are exhibited in one-third of patients. HHS usually occurs in older patients (60 years of age is the average) who have type 2 diabetes and an illness leading to decreased fluid intake. Infection, certain medications, noncompliance, undiagnosed diabetes, substance abuse, and coexisting disease can lead to HHS. In one study of an urban population, the three leading causes were poor compliance with medication, ethanol ingestion, and cocaine use. Long-term steroid use and gastroenteritis are common causes of HHS in children. HHS is sometimes reported in people with type 1 diabetes, but this is uncommon. HHS affects approximately 1 in 500 individuals with diabetes. In 30% to 40% of cases, HHS is a person’s first presenting symptom of diabetes. HHS results from a reduction in effective circulating insulin and an increase in counterregulatory hormones. The four major counterregulatory hormones are epinephrine, glucagon, growth hormone, and cortisol; they cause insulin resistance and levels increase during acute illness or stress. In HHS, the kidneys are not able to clear the glucose from the blood, and the peripheral tissues are not able to use the glucose effectively, which results in hyperglycemia. The glucosuria impairs the concentrating capacity of the kidney, leading to even greater water loss. The loss of more water than sodium leads to hyperosmolarity; this triggers the release of antidiuretic hormone and stimulates thirst. The hypovolemia that occurs in HHS if the individual is unable to compensate by drinking more fluids will lead to hypotension and impaired tissue perfusion. Coma results from these severe electrolyte imbalances and hypotension. People with HHS may present with: Plasma glucose level of ≥600 mg/dL Effective serum osmolarity of ≥320 mOsm/kg Profound dehydration Serum pH >7.30 Bicarbonate concentration >15 mEq/L Small ketonuria and absent-to-low ketonemia Some alteration in consciousness; confusion Tachycardia Elevated creatinine, BUN, and hematocrit levels Potassium in the serum may run normal or high, but total body potassium is depleted Convulsions Weight loss Lethargy and weakness Nausea and vomiting Fever Treatment of HHS may include: Fluid replacement (the average patient requires 9 L in 48 hours) Electrolyte replacement Airway management Crystalloid administration IV insulin Treatment of underlying disease Complications of HHS include: Acute circulatory collapse (shock) Blood clot formation Cerebral edema Lactic acidosis BUN=concentration of nitrogen in the form or urea in the blood, dL=deciliter, IV=intravenous, kg=kilogram, L=liter, mEq=milliequivalent, mg=milligram, mOsm=milliosmol References and recommended readings Hemphill RR. Hyperosmolar hyperglycemic state. Medscape Web site. http://emedicine.medscape.com/article/1914705-overview. Updated August 2, 2012. Accessed February 20, 2014. MedlinePlus. Diabetic hyperglycemic hyperosmolar syndrome. US National Library of Medicine, National Institutes of Health Web site. http://www.nlm.nih.gov/medlineplus/ency/article/000304.htm. Updated June 12, 2012. Accessed February 20, 2014. Stoner GD. Hyperosmolar hyperglycemic state. Am Fam Physician. 2005;71(9):1723-1730. http://www.aafp.org/afp/2005/0501/p1723.html. Accessed February 20, 2014. Contributed by Elaine Koontz, RDN, LD/N Review Date 2/14 D-0680