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Clinical Manifestations

Diabetes mellitus is characterized by hyperglycemia and glycosuria arising from an absolute or relative deficiency of insulin or insulin responsiveness. Diabetes is classified in multiple ways. Type 1 (insulin-requiring due to endogenous insulin deficiency) and type 2 (insulin-resistant) diabetes are the most common and well known. The diagnosis is based on an elevated fasting plasma glucose greater than 126 mg/dL or glycated hemoglobin (HgbA1c) of 6.5% or greater. Long-term complications of diabetes include retinopathy, kidney disease, hypertension, coronary artery disease, peripheral and cerebral vascular disease, and peripheral and autonomic neuropathies. Patients with diabetes who are also hyperglycemic have an increased susceptibility to infections.

There are three life-threatening acute complications of diabetes and its treatment—diabetic ketoacidosis (DKA), hyperosmolar nonketotic coma, and hypoglycemia—in addition to other acute medical problems (such as sepsis) in which the presence of diabetes makes treatment more difficult. Decreased insulin activity allows the catabolism of free fatty acids into ketone bodies (acetoacetate and β-hydroxybutyrate), some of which are weak acids. Accumulation of these organic acids results in DKA, an anion-gap metabolic acidosis. DKA can easily be distinguished from lactic acidosis; lactic acidosis is identified by elevated plasma lactate (>6 mmol/L) and the absence of urine and plasma ketones. DKA is associated with type 1 diabetes mellitus, but a rare individual with DKA may appear phenotypically to have type 2 diabetes mellitus. Alcoholic ketoacidosis can follow binge drinking in a nondiabetic patient and may include a normal or slightly elevated blood glucose level. Such patients may also have a disproportionate increase in β-hydroxybutyrate compared with acetoacetate, in contrast to those with DKA.

Clinical manifestations of DKA include tachypnea (respiratory compensation for the metabolic acidosis), abdominal pain, nausea and vomiting, and changes in sensorium. The treatment of DKA should include correcting the often substantial hypovolemia, hyperglycemia, and total body potassium deficit. This is typically accomplished with a continuous infusion of isotonic fluids with potassium and an insulin infusion.

Ketoacidosis is not a feature of hyperosmolar nonketotic coma, possibly because enough insulin is available to prevent ketone body formation. Instead, a hyperglycemia-induced diuresis leads to dehydration and hyperosmolality and may ultimately lead to kidney failure, lactic acidosis, and disseminated intravascular coagulation. Hyperosmolality (frequently exceeding 360 mOsm/L) dehydrates neurons, causing altered mental status and seizures. Severe hyperglycemia causes factitious hyponatremia: each 100 mg/dL increase in plasma glucose lowers plasma sodium concentration by 1.6 mEq/L. Treatment includes fluid resuscitation with normal saline, small doses of insulin, and potassium supplementation.

Hypoglycemia in a patient with diabetes is the result of an absolute or relative excess of insulin relative to carbohydrate intake and exercise. Furthermore, patients with diabetes are incompletely able to counter hypoglycemia despite secreting glucagon or epinephrine (counterregulatory failure). The brain depends on glucose as an energy source, and it is the organ ...

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