Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content + Download Section PDF Listen ++ For further information, see CMDT Part 27-04: Hyperglycemic Hyperosmolar State + Key Features Download Section PDF Listen +++ +++ Essentials of Diagnosis ++ Hyperglycemia, serum glucose > 600 mg/dL (33.3 mmol/L) Serum osmolality > 310 mOsm/kg No acidosis; blood pH > 7.3 Serum bicarbonate > 15 mEq/L Normal anion gap (< 14 mEq/L) +++ General Considerations ++ Frequently occurs with mild or occult diabetes mellitus Infection, myocardial infarction, stroke, or recent operation is often a precipitating event Drugs (phenytoin, diazoxide, corticosteroids, and diuretics) or procedures associated with glucose loading such as peritoneal dialysis can also precipitate the syndrome Acute kidney dysfunction develops from hypovolemia, leading to increasingly higher blood glucose concentrations Underlying chronic kidney disease or heart failure is common, and the presence of either worsens the prognosis +++ Demographics ++ Rarer than diabetic ketoacidosis even in older age groups Affects middle-aged to elderly + Clinical Findings Download Section PDF Listen +++ +++ Symptoms and Signs ++ Onset may be insidious over days or weeks, with weakness, polyuria, and polydipsia The lack of features of diabetic ketoacidosis may delay recognition until dehydration becomes more profound than in ketoacidosis Fluid intake is usually reduced from inappropriate lack of thirst, nausea, or inaccessibility of fluids to bedridden patients Lethargy and confusion develop as serum osmolality exceeds 310 mOsm/kg Convulsions and coma can occur if osmolality exceeds 320–330 mOsm/kg Physical examination shows profound dehydration, lethargy, or coma without Kussmaul respirations +++ Differential Diagnosis ++ Diabetic ketoacidosis Cerebrovascular accident or head trauma Hypoglycemia Sepsis Diabetes insipidus + Diagnosis Download Section PDF Listen +++ +++ Laboratory Tests ++ Severe hyperglycemia (serum glucose 800–2400 mg/dL [44.4 to 133.2 mmol/L]) When dehydration is less severe, dilutional hyponatremia as well as urinary sodium losses may reduce serum sodium to 120–125 mEq/L As dehydration progresses, serum sodium can exceed 140 mEq/L, producing serum osmolality readings of 330–440 mOsm/kg Ketosis and acidosis are usually absent or mild Prerenal azotemia with blood urea nitrogen elevations > 100 mg/dL (35.7 mmol/L) typical + Treatment Download Section PDF Listen +++ +++ Medications +++ Fluid Replacement ++ Fluid replacement paramount to correct fluid deficits of 6–10 L In hypovolemic oliguric hypotension, initiate fluid resuscitation with isotonic 0.9% saline Otherwise, hypotonic (0.45%) saline preferred because of hyperosmolality As much as 4–6 L of fluid may be required in first 8–10 h Once blood glucose reaches 250 mg/dL (13.9 mmol/L), add 5% dextrose to either water, 0.45% saline solution, or 0.9% saline solution at a rate to maintain serum glucose levels of 250–300 mg/dL (13.9 to 16.7 mmol/L) to reduce risk of cerebral edema Goal of fluid therapy is to restore urinary output to ≥ 50 mL/h +++ Insulin ++ Less insulin is required than in diabetic ketoacidotic coma Fluid replacement alone can reduce hyperglycemia by increasing glomerular filtration and renal excretion of glucose Insulin treatment should therefore be delayed unless the patient has significant ketonemia (β-hydroxybutyrate > 1 mmol/L) Start the insulin infusion rate at 0.05 units/kg/h (bolus is not needed) and titrate to lower blood glucose levels by 50–70 mg/dL per hour (2.8–3.9 mmol/L/h) Once patient has stabilized and the blood glucose falls to around 250 mg/dL (13.9 mmol/L), insulin can be given subcutaneously +++ Potassium ++ Add potassium chloride (10 mEq/L) to initial fluids if serum potassium is not elevated. Adjust subsequent potassium replacement based on serum potassium level +++ Phosphate ++ If severe hypophosphatemia (serum phosphate < 1 mg/dL [0.32 mmol/L]) develops during therapy, phosphate replacement can be given as its potassium salt To minimize the risk of tetany from an overload of phosphate replacement, an average deficit of 40–50 mmol phosphate should be replaced by intravenous infusion at a rate not to exceed 3–4 mmol/h in a 60- to 70-kg person A stock solution (Abbott Laboratories) provides a mixture of 1.12 g KH2PO4 and 1.18 g KH2PO4 in a 5-mL single-dose vial representing 22 mmol potassium and 15 mmol phosphate; 5 mL of this stock solution in 2 L of 0.45% saline or 5% dextrose in water, infused at 400 mL/h, will replace the phosphate at the optimal rate of 3 mmol/h and provide 4.4 mEq potassium per hour If serum phosphate remains < 2.5 mg/dL, a repeat 5-h infusion can be given +++ Therapeutic Procedures ++ Using a flow sheet, document vital signs, time sequence of laboratory values (arterial pH, plasma glucose, acetone, bicarbonate, blood urea nitrogen, electrolytes, serum osmolality) in relation to therapy + Outcome Download Section PDF Listen +++ +++ Complications ++ Myocardial infarction, stroke, pulmonary embolism, mesenteric vein thrombosis, and disseminated intravascular coagulation May result from severe dehydration and low output state Fluid replacement remains the primary approach to preventing these complications Rhabdomyolysis should be looked for and treated +++ Prognosis ++ The overall mortality rate is > 10 times that of diabetic ketoacidosis because of its higher incidence in older patients and greater dehydration When prompt therapy is instituted, the mortality rate can be reduced from nearly 50% to that related to the severity of coexistent disorders +++ When to Admit ++ Altered mental status Severe volume depletion + References Download Section PDF Listen +++ + +Fayfman M et al. Management of hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Med Clin North Am. 2017 May;101(3):587–606. [PubMed: 28372715] + +Scott AR; Joint British Diabetes Societies (JBDS) for Inpatient Care; JBDS hyperosmolar hyperglycaemic guidelines group. Management of hyperosmolar hyperglycaemic state in adults with diabetes. Diabet Med. 2015 Jun;32(6):714–24. [PubMed: 25980647]