Laboratory

Almost all patients with DKA present with blood glucose greater than 300 mg/dL. Patients who present just after receiving insulin or who have impaired gluconeogenesis (e.g., in alcohol abuse or liver failure) may have lower initial serum glucose levels. 2 Elevated serum levels of bHB and AcAc cause acidosis and ketonuria. The nitroprusside reagent normally used to detect urine and serum ketones only detects AcAc. Acetone is only weekly reactive and bHB not at all. NADH accumulation in mitochondria, as may occur with lactic acidosis or alcohol metabolism, favors the bHB side of the equation noted earlier. The enzymatic test for bHB is reliable but not widely available. Paradoxically, ketone levels will increase as the patient is being treated and improve as the body converts the more acidic bHB to AcAc. Therefore, ketones need only be checked initially. Serum electrolytes should be carefully examined for multiple metabolic abnormalities. Elevated serum ketones lead to a high anion gap metabolic acidosis. Hyperchloremic acidosis also occurs on the basis of ketoanion exchange for chloride in the urine; this is especially true in patients who maintain good hydration status and thus their glomerular filtration rate despite ketoacidosis. Metabolic alkalosis also can occur due to vomiting, osmotic diuresis, and concomitant diuretic use. Some patients with DKA may present with "normal" appearing [HCO 3-] or even alkalemia if these other processes are severe enough to mask the acidosis. In such situations, an elevated anion gap may be the only clue to the presence of an underlying metabolic acidosis otherwise masked by the concomitant volume contraction-related metabolic alkalosis.

Arterial blood gases (ABG) have traditionally been used to help determine precise acid-base status in order to direct treatment. A very low P co2 usually reflects respiratory compensation for metabolic acidosis, but may also reflect a primary respiratory alkalosis, which may be an early indication of pulmonary disease (e.g., pneumonia, pulmonary embolus) as a possible trigger of the DKA. Chapter^.! details how compensatory changes in Pco2 can be distinguished from a primary respiratory alkalosis. Recent studies have shown a strong correlation between venous and arterial pH in patients with DKA. 9 Venous pH obtained during routine phlebotomy can potentially be used to avoid ABGs, which are painful and may cause arterial vascular complications.

Total body potassium is depleted by renal losses. However, measured serum potassium is normal or elevated in most patients 10 because of two important factors: extracellular shift of potassium secondary to acidemia and increased intravascular osmolarity caused by hyperglycemia. 11 Prerenal azotemia also contributes by interfering with kaliuresis. Osmotic diuresis leads to excessive renal losses of sodium chloride in the urine. However, the presence of hyperglycemia tends to artificially lower the serum sodium levels. The standard correction is by adding 1.6 meq to the reported sodium value for every 100 mg of glucose over 100 mg/dL. Osmotic diuresis also causes urinary losses and total body depletion of phosphorous, calcium, and magnesium. Be aware that hemoconcentration frequently leads to initial artificially elevated levels. As therapy progresses lower serum levels of each will be evident.

Serum creatinine will frequently be artificially elevated because AcAc interferes with the laboratory assay. Liver function studies may be elevated because of fatty infiltration of the liver, which corrects as the acidosis is treated. CPK and amylase are also frequently elevated at the time of presentation. Leukocytosis is often present because of hemoconcentration and stress. However, an elevated band count of 10 or more has been shown to reliably predict infection in this population. 12

Electrocardiographic changes of hyperkalemia or hypokalemia may be seen. These changes are often very transient because of the rapidly changing metabolic status. The cardiogram should also be evaluated for ischemia as myocardial infarction may precipitate DKA. The underlying rhythm is usually sinus tachycardia.

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