Disorders of Glucose Metabolism
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meals composed of protein, fat, and carbohydrate to avoid the sensation of hypoglycemia.
Acute Complications of Diabetes Mellitus Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS) are acute complications of uncontrolled hyperglycemia with life-threatening consequences if not recognized and treated early. DKA typically occurs in the setting of hyperglycemia with relative or absolute insulin deficiency and an increase in counterregulatory hormones. Sufficient amounts of insulin are not present to suppress lipolysis and oxidation of free fatty acids, which results in ketone body production and subsequent metabolic acidosis. DKA occurs more frequently with type 1 diabetes, although 10% to 30% of cases occur in patients with type 2 diabetes. HHS occurs in the setting of partial insulin deficiency that is more typical of type 2 diabetes. There is sufficient insulin in patients with HHS to suppress lipolysis and production of ketone bodies, but inadequate amounts to prevent the hyperglycemia, dehydration, and hyperosmolality characteristic of HHS. Several risk factors can precipitate the development of extreme hyperglycemia: infection, intentional or inadvertent insulin therapy nonadherence, myocardial infarction, stress, trauma, and confounding medications, such as glucocorticoids or atypical antipsychotic agents. In addition, DKA may be the initial clinical presentation in some patients with previously undiagnosed type 1 or type 2 diabetes. An illness or event that leads to dehydration will often precipitate the hyperglycemia associated with HHS. Symptoms of extreme hyperglycemia in DKA and HHS include polyuria, polydipsia, unintentional weight loss, vomiting, weakness, and mentation changes. Dehydration and metabolic abnormalities worsen as hyperglycemia progresses, which can lead to respiratory failure, lethargy, obtundation, coma, and death. DKA can occur within several hours of the inciting event. The development of HHS is less acute than DKA and may take days to weeks to develop. HHS typically presents with more extreme hyperglycemia and mental status changes compared with DKA. The initial evaluation of severe hyperglycemia includes serologic studies (plasma glucose, serum ketones, blood urea nitrogen, creatinine, electrolytes, calculated anion gap, arterial blood gases, osmolality, complete blood count with differential, blood cultures), urine studies (ketones, urinalysis, urine culture), chest radiograph, and an electrocardiogram. Urine and serum ketones are elevated in DKA; however, a negative measurement initially does not exclude DKA. β-Hydroxybutyrate is the major ketone body in DKA, but
ketone laboratory measurements often use the nitroprusside reaction, which only estimates acetoacetate and acetone levels that may not be elevated initially. Although hyperglycemia is the typical finding at presentation with DKA, patients can present with a range of plasma glucose values, including those in the normal range (Figure 1). The anion gap is elevated. Stress-related mild leukocytosis is often present. Higher levels of leukocytosis may indicate an infectious process as the etiology of the hyperglycemia. Serum sodium levels can be low due to osmotic shifts of water from the intracellular to extracellular spaces. Normal or elevated serum sodium levels are indicative of severe volume depletion. Serum potassium levels may be elevated due to shifts from the intracellular to extracellular spaces due to ketoacidosis and the absence of sufficient insulin. Normal or low potassium levels on presentation indicate low potassium stores in the body with need for correction prior to initiation of insulin therapy to avoid cardiac arrhythmias. Serum amylase and lipase levels also can be elevated in the absence of pancreatitis. HHS typically presents with normal or small amounts of urine or serum ketones. Plasma glucose values in HHS are typically greater than in DKA and can exceed 1200 mg/dL (66.6 mmol/L). The serum osmolality is elevated greater than 320 mOsm/kg H2O. The serum bicarbonate level is greater than 18 mEq/L (18 mmol/L), and the pH remains greater than 7.3. Treatment of DKA and HHS requires correction of hyperglycemia with intravenous insulin infusions, frequent monitoring and replacement of electrolytes, correction of hypovolemia with intravenous fluids, and possible correction of acidosis (Table 11). The ICU is the best place for management of severe hyperglycemia because of the frequent monitoring required with intravenous insulin therapy, the need for monitoring for potential electrolyte-induced arrhythmias, and the potential for rapid decompensation. Plasma glucose levels should be monitored initially every hour while on insulin infusion therapy. Electrolytes should be monitored every 2 to 4 hours, depending on the initial electrolyte deficits and level of acidosis. Key Points
• The development of hyperglycemic hyperosmolar syndrome is less acute than that of diabetic ketoacidosis and may take days to weeks to develop; however, hyperglycemic hyperosmolar syndrome typically presents with more extreme hyperglycemia and mental status changes compared with diabetic ketoacidosis. • Treatment of diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome requires correction of hyperglycemia with intravenous insulin infusions, frequent monitoring and replacement of electrolytes, correction of hypovolemia with intravenous fluids, and possible correction of acidosis.
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