Investigations

1st investigations to order

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A plasma glucose test should be performed as an initial laboratory evaluation. In DKA, it is usually >250 mg/dL with acidosis and ketonemia.

However, 10% of DKA patients present with blood glucose <250 mg/dL, which is termed euglycemic DKA.[1]

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elevated

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Acidosis is essential for the diagnosis of DKA. Arterial pH measurement is necessary for diagnosis of DKA, but venous pH is recommended for monitoring treatment, due to the pain and risk of infection in obtaining frequent arterial samples. A venous pH sample is usually 0.03 units lower than arterial pH, and this difference should be considered.

In hyperosmolar hyperglycemic state, the arterial pH is usually >7.30 and the arterial bicarbonate is >15 mEq/L.[1]

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pH varies from 7.00 to 7.30 in DKA; arterial bicarbonate ranges from <10 mEq/L in severe DKA to >15 mEq/L in mild DKA

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There are three main ketones that are produced in DKA that can be measured: acetone, acetoacetate, and beta-hydroxybutyrate (BOHB).

In early DKA, acetoacetate concentration is low, but it is a major substrate for ketone measurement by many laboratories (nitroprusside reaction method). Therefore, serum ketone measurement by usual laboratory techniques has a high specificity, but low sensitivity for the diagnosis of DKA; hence a negative test for serum ketones does not exclude DKA. Acetone is rarely measured due to its volatile nature.[41] Conversely, BOHB is an early and abundant ketoacid that can be the first signal of the development of DKA. Point-of-care BOHB testing is widely available and is highly sensitive and specific for the diagnosis of DKA.[42]

During the treatment of DKA, BOHB is converted to acetoacetate, which is detected by the nitroprusside method. Therefore, the increase in acetoacetate during the treatment of DKA may mistakenly indicate a worsening of ketonemia.

Another potential source of error in detecting ketone bodies is the patient's medications. Some drugs, such as the ACE inhibitor captopril, contain sulfhydryl groups that can react with the reagent in the nitroprusside test and give a false-positive result. Therefore, clinical judgement and other biochemical tests will be required in patients who are receiving such medications.[1]

Result

beta-hydroxybutyrate elevated ≥3.8 mmol/L in adults or ≥3.0 mmol/L in children

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Glucose and ketones are typical findings in DKA.[1]

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positive for glucose and ketones; positive for leukocytes and nitrites in the presence of infection

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Increased due to volume depletion.[1]

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elevated

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Increased due to volume depletion.[1]

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elevated

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Serum sodium is usually low due to osmotic reflux of water from the intracellular to extracellular space in the presence of hyperglycemia. Total sodium deficit is 7 to 10 mEq/kg. Hypernatremia in the presence of hyperglycemia in DKA indicates profound volume depletion. Alternately, in the presence of high serum chylomicron concentration, pseudonormoglycemia and pseudohyponatremia may occur in DKA.

The corrected serum sodium level should be evaluated as this is used to guide appropriate fluid replacement. The equation for conventional units is: corrected sodium (mEq/L) = measured sodium (mEq/L) + 0.016 (glucose [mg/dL] - 100).[1][18]

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usually low

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Total potassium deficit is 3 to 5 mEq/kg. Serum potassium is usually elevated due to extracellular shift of potassium caused by insulin insufficiency, hypertonicity, and acidemia, but the total body potassium concentration is low due to increased diuresis. Therefore, low potassium level on admission indicates severe total-body potassium deficit.[1][18]

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usually elevated

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Total chloride deficit is 3 to 5 mEq/kg.[1][18]

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usually low

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Total body deficit of magnesium is usually 1 to 2 mEq/kg.[1][18]

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usually low

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Total body calcium deficit is usually about 1 to 2 mEq/kg.[1][18]

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usually low

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Despite the total body phosphate deficit averaging 1.0 mmol/kg, serum phosphate is often normal or increased at presentation, but decreases with insulin therapy.[1][18]

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normal or elevated

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Anion gap is calculated by subtracting the sum of serum chloride and bicarbonate from measured sodium concentration.[ Anion Gap ][1]

Result

elevated anion gap (>10-12 mEq/L)

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In patients with history of cocaine abuse and DKA, rhabdomyolysis is common; therefore, checking creatine phosphokinase level can be initially assessed in patients with DKA if clinically indicated.

In rhabdomyolysis, pH and serum osmolality are usually mildly elevated and plasma glucose and ketones are normal. Myoglobinuria and/or hemoglobinuria are detected in urinalysis.[1][18]

Result

elevated in rhabdomyolysis

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Plasma glucose and serum ketones are normal in lactic acidosis. Serum lactate is >5 mmol/L in lactic acidosis.[1]

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elevated in lactic acidosis

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Used to identify underlying diseases such as fatty liver or congestive heart failure.[1]

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usually normal

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Amylase is elevated in majority of patients with DKA, but this may be due to nonpancreatic sources such as parotid glands.[1]

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usually elevated due to extrapancreatic sources

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Serum lipase may be beneficial in differentiating pancreatitis in patients with elevated amylase level. However, mildly elevated serum lipase level in the absence of pancreatitis has also been reported in patients with DKA.[1]

Result

usually normal

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The serum osmolality is variable in DKA but is >320 mOsm/kg in hyperosmolar hyperglycemic state.[1]

Result

variable

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Leukocytosis is present in hyperglycemic crises and correlates with blood ketone levels. However, leukocytosis >25,000/microliter may indicate infection and requires further evaluations.[1]

Result

elevated white cell count

Investigations to consider

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The most common infections are pneumonia and urinary tract infections.[1]

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may be compatible with pneumonia

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If clinically indicated, should be performed for identification of the precipitating cardiovascular diseases, such as myocardial infarction (MI) or severe electrolyte abnormalities.[1]

Evidence of MI includes Q waves or ST segment changes.

Evidence of hypokalemia (U waves) or hyperkalemia (tall T waves) may be present.[1]

Result

may show evidence of MI or hyper- or hypokalemia

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MI is a common precipitant of DKA in diabetic patients.[1]

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may be elevated in the presence of MI

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If indicated clinically, further sepsis workup should be performed.[1]

Result

positive in the presence of infection

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