Hyperglycemic Hyperosmolar State

Key Features

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

Symptoms and Signs

• Onset may be insidious over days or weeks, with weakness, polyuria, and polydipsia

• The lack of features of ketoacidosis may retard 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

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

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)

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