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 hyponatremia, hypernatremia, hypokalemia, hypophosphatemia, hypomagnesemia, increased serum urea nitrogen, increased serum creatinine, hypertriglyceridemia, and increased serum amylase may also be present. Increased lipase in the absence of pancreatitis may occur. Initially, potassium, magnesium, and phosphorus may be increased or normal; however, close monitoring is required because serum concentrations of these ions may decrease significantly with treatment as they move intracellularly, and total body depletion of one or more of these ions becomes manifest.
The degree of dehydration varies in DKA. Severe DKA (ie, severe ketoacidemia) does not necessarily mean that severe dehydration is present; the degree of ketonemia and the degree of dehydration should be individually assessed. Raised ICP is the most common cause of morbidity and mortality; thus, monitoring for neurologic symptoms is essential. Avoid excessive volume administration, which can exacerbate brain swelling. Efforts to assign a volume of deficit should be made (Table 14.1).