Tests
1st tests to order
plasma glucose
Test
A plasma glucose test should be performed as an initial laboratory evaluation. In diabetic ketoacidosis (DKA), it is usually ≥200 mg/dL (≥11.1 mmol/L) with acidosis and ketonemia.
However, 10% of patients present with blood glucose <200 mg/dL (<11.1 mmol/L), which is termed euglycemic DKA.[1]
Result
elevated
ABG
Test
Acidosis is essential for the diagnosis of diabetic ketoacidosis (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.
Result
pH varies from <7.00 to 7.30; arterial bicarbonate ranges from <10 mEq/L (<10 mmol/L) in severe DKA to >15 mEq/L (>15 mmol/L) in mild DKA
capillary or serum ketones
Test
There are three main ketones that are produced in diabetic ketoacidosis (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 DKA diagnosis; hence a negative test for serum ketones does not exclude DKA. Acetone is rarely measured due to its volatile nature.[63] 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.[64] Blood concentrations of BOHB ≥3 mmol/L correlate well with acid-base changes, with >90% sensitivity and specificity for DKA.[1]
During the treatment of DKA, BOHB is converted to acetoacetate. 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 drugs. 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 judgment and other biochemical tests are required in patients who are receiving such drugs.[1]
Result
beta-hydroxybutyrate ≥3 mmol/L
urinalysis
Test
Glucose and ketones are typical findings in diabetic ketoacidosis (DKA).[1]
Reliance on urine ketone testing can underestimate the severity of ketonemia early in the course of DKA because of a lag in the formation of acetoacetate, and conversely overestimate its severity later in the course of DKA when beta-hydroxybutyrate (BOHB) is being cleared and converted into acetoacetate.[1] In addition, several sulfhydryl drugs (e.g., captopril) and other drugs such as valproic acid can give false-positive nitroprusside urine tests. Thus, direct measurement of serum or capillary BOHB is preferred for diagnosis and monitoring of the response to therapy.[1]
Result
typically positive for glucose and ketones; positive for leukocytes and nitrites in the presence of infection; in rhabdomyolysis, urine dipstick test will typically be positive for blood, even if red blood cells are not present on microscopic exam, indicating the presence of myoglobin (however, a negative dipstick does not rule out rhabdomyolysis as the test can be unreliable for detecting low levels of myoglobin)
serum BUN
Test
Typically increased due to volume depletion.[65]
Result
elevated
serum creatinine
Test
Increased due to volume depletion.[65]
Result
elevated
serum sodium
Test
Patients commonly present with hyponatremia due to osmotic reflux of water from the intracellular to extracellular space in the presence of hyperglycemia.[65] Total sodium deficit is usually 7-10 mEq/kg (7-10 mmol/kg).[66][76] Hypernatremia in the presence of hyperglycemia in DKA indicates profound volume depletion.[65]
Several estimating equations correct the measured serum sodium concentration to account for increased extracellular free water volume from hyperglycemia. The most common correction method is to increase the measured serum sodium concentration by 1.6 mEq/L (1.6 mmol/L) of serum sodium level for every 100 mg/dL (5.6 mmol/L) of serum glucose above 100 mg/dL (5.6 mmol/L).[67]
Result
usually low
serum potassium
Test
Total body potassium deficit is 3-5 mEq/kg (3-5 mmol/kg).[66] However, serum potassium is usually normal or elevated due to extracellular shift of potassium caused by insulin insufficiency, hypertonicity, and acidemia.[1] Therefore, low potassium level on admission indicates severe total-body potassium deficit.[1]
Result
usually normal or elevated
serum chloride
Test
Total chloride deficit is 3-5 mEq/kg (3-5 mmol/kg).[66]
Result
usually low
serum phosphate
Test
In diabetic ketoacidosis, there is a shift of phosphate from intracellular to extracellular fluid, with an excess urinary phosphate loss leading to hypophosphatemia. Whole-body losses can be up to 1 mmol/kg.[1] Despite this, serum phosphate is often normal or increased at presentation, but decreases with insulin therapy.[68]
Result
normal or elevated
anion gap calculation
Test
Anion gap is calculated by subtracting the sum of serum chloride and bicarbonate from measured sodium concentration. [ Anion Gap Opens in new window ] It gives an estimate of the unmeasured anions in plasma, which in diabetic ketoacidosis (DKA) are ketoacids. An anion gap >12 mEq/L (>12 mmol/L) indicates the presence of a high anion gap metabolic acidosis consistent with DKA.[1]
While most people with DKA present with a high anion gap metabolic acidosis, mixed acid-base disorders are present in about one third because of hyperglycemia-induced osmotic diuresis and natriuresis, nausea and vomiting leading to volume contraction and metabolic alkalosis, and a compensatory respiratory alkalosis caused by hyperventilation due to rapid and/or deep breathing (Kussmaul respiration).[1] In addition, hyperchloremic normal anion gap acidosis is commonly seen following successful treatment of DKA and may delay transition back to subcutaneous insulin if mistaken for persistent DKA.[1] The anion gap is therefore not recommended as a first-line diagnostic or resolution criterion, but may still have some utility in resource settings where ketone measurement is unavailable.[1]
Result
typically elevated (>12 mEq/L [>12 mmol/L])
serum lactate
LFT
Test
Usually normal, and are used to screen for an underlying hepatic precipitant. Abnormal LFTs indicate underlying diseases such as fatty liver or congestive heart failure. Chronic liver disease is a risk factor for euglycemic DKA.[69]
Result
usually normal
serum amylase
serum lipase
Test
Serum lipase may be beneficial in differentiating pancreatitis in patients with elevated amylase levels. However, elevated lipase, traditionally thought to be more specific for pancreatitis, may also accompany DKA and does not necessarily denote concomitant pancreatic inflammation.[35][70][71]
Result
usually normal; may be elevated in some patients
serum osmolality
Test
The serum osmolality is variable in DKA but is >320 mOsm/kg (>320 mmol/kg) in hyperosmolar hyperglycemic state.[1]
Result
variable
CBC
Test
Leukocytosis is present in hyperglycemic crises and correlates with blood ketone levels. However, leukocytosis >25,000/microliter (25 × 10⁹/L) may indicate infection and requires further evaluation.[65]
Result
elevated white cell count
ECG
Test
Should be performed to assess for evidence of biochemically induced repolarization abnormalities, such as peaked T waves or U waves from hyperkalemia.[1]
May also aid in identification of precipitating cardiovascular events such as myocardial infarction (MI).[1] Evidence of MI includes Q waves or ST segment changes.
Result
may show evidence of MI or hyper- or hypokalemia
Tests to consider
serum creatine kinase (CK)
Test
Rhabdomyolysis is common in cocaine users with concurrent diabetic ketoacidosis (DKA).[39] CK level should be assessed in patients with DKA if clinically indicated; for example, if acute kidney injury is present and/or a known or suspected history of cocaine use. Establishing a diagnosis of rhabdomyolysis is based primarily on a marked elevation in serum CK level or the appearance of myoglobin in the urine (myoglobinuria).[72] After muscle injury, plasma myoglobin increases rapidly and is cleared quickly through renal excretion, and a normal level is reestablished within 24 hours. In contrast, serum CK levels rise 2-12 hours after onset of muscle injury, peak at 3-5 days after injury, and decline over the subsequent 6-10 days.[72] Given that not all patients present within 24 hours of muscle damage, measurement of CK levels may provide the most reliable biochemical marker of rhabdomyolysis and its severity.[72] CK elevation five times the upper limit of normal is considered as the defining biochemical abnormality for this condition.[72]
Result
elevated in rhabdomyolysis
CXR
high sensitivity cardiac troponin
Test
Underlying cardiovascular events, particularly myocardial infarction (MI), provoke the release of counter-regulatory hormones that may result in DKA in patients with diabetes.[1]
Result
may be elevated in the presence of MI
blood, urine, or sputum cultures
Test
Should be obtained if there are signs of infection such as chills, constitutional upset (e.g., fatigue, confusion, anxiety), or symptoms and signs of specific infections.[13] The most common precipitating infections are pneumonia and urinary tract infections.[13] Patients are usually normothermic or hypothermic due to peripheral vasodilation, so fever may not be seen.[9]
Result
positive in the presence of infection
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