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Diabetic ketoacidosis/ketoacidemia (DKA) is an absolute or relative insulin deficiency resulting in ketone body production and decreased serum total CO2 concentration. This potentially life-threatening metabolic disturbance occurs most commonly in type 1 diabetics, but may also occur in type 2 diabetics.
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Absolute or relative insulin deficiency results in hyperglycemia, glycosuria, and intracellular starvation, leading to release of counterregulatory hormones (glucagon, epinephrine, cortisol, and growth hormone). This results in lipolysis, proteolysis, glycogenolysis, gluconeogenesis, and insulin resistance. Glycogenolysis and gluconeogenesis exacerbate the already-present hyperglycemia. A negative cycle of progressive ketoacidemia and insulin resistance, associated with a surge of counterregulatory hormones, leads to increasing insulin resistance, hyperglycemia, dehydration, electrolyte losses, potential brain swelling, and may result in metabolic death.
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Key findings include polyuria, nocturia, polydipsia, no change in appetite, polyphagia or decreased appetite, varying degrees of dehydration, weight loss, abdominal pain, vomiting, hyperventilation, Kussmaul breathing (which is clinically visible and may be confused with respiratory distress from primary respiratory diseases such as pneumonia), subnormal body temperature (in severe DKA; may also occur in sepsis), altered mental status (which may be caused by shock, profound ketoacidemia or raised intracranial pressure [ICP]), the fruity odor of ketones on the breath, and Candida infections (eg, vaginitis or perineal yeast). Typical laboratory findings include hyperglycemia (may only be modest with serum glucose <300 mg/dL), glycosuria, ketonemia, ketonuria, metabolic acidosis/acidemia, and compensatory hypocarbia. Enuresis, urinary incontinence, apparent or actual ...