Abstract
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are the two major hyperglycemic emergencies that complicate diabetes mellitus. DKA develops when an excess of counterregulatory hormones relative to insulin trigger unchecked lipolysis that drives ketoacid synthesis. DKA is often catalyzed by a physiologic stressor such as infection but may also result from insulin nonadherence. Excessive circulating ketoacids results in severe perturbations in acid-base status, manifesting on labs as a high anion-gap metabolic acidosis, and volume depletion in addition to underlying hyperglycemia. Symptoms classically include abdominal pain, nausea/vomiting, polyuria/polydipsia, and blurry vision. Mental status may be normal or altered. Treatment of DKA requires aggressive fluid resuscitation and intravenous insulin at a high rate, targeted to closure of the anion gap and resolution of hyperglycemia. Treatment of any provoking underlying conditions is essential. Intensive insulin treatment may be complicated by hypokalemia, and thus potassium supplementation may also be necessary. HHS occurs when significant hyperglycemia (>600 mg/dL) results in hyperosmolality (>320 mOsm/kg) that causes alteration of mental status. This can range from mild confusion to obtundation or coma. HHS is also associated with volume depletion but not typically with acid-base disturbances. Treatment of HHS is similar to that of DKA but is aimed at normalization of mental status and of serum osmolality instead of closure of an anion gap. HHS treatment can be complicated by cerebral edema if serum osmolality is corrected too rapidly.
Published Version
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