Diabetic Ketoacidosis Workup

  • Author: Vasudevan A Raghavan, MBBS, MD, MRCP(UK); Chief Editor: George T Griffing, MD   more...
 
Updated: Jan 3, 2012
 

Approach Considerations

Diabetic ketoacidosis is typically characterized by hyperglycemia over 300 mg/dL, a bicarbonate level less than 15 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria.

While definitions vary, moderate DKA can be categorized by a pH less than 7.2 and a serum bicarbonate less than 10 mEq/L, whereas severe DKA has a pH less than 7.1 and bicarbonate less than 5 mEq/L.

Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows:

  • Blood tests for glucose every 1-2 h until patient is stable, then every 6 h
  • Serum electrolyte determinations every 1-2 h until patient is stable, then every 4-6 h
  • Initial blood urea nitrogen (BUN)
  • Initial arterial blood gas (ABG) measurements, followed with bicarbonate as necessary

Repeat laboratory tests are critical, including potassium, glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressive volume, glucose, and electrolyte management.

It is important to be aware that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels.

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Serum Glucose Study

The blood glucose level for patients with DKA usually exceeds 250 mg/dL. The clinician can perform a fingerstick glucose test while waiting for the serum chemistry panel.

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Urine Dipstick Testing

For patients with DKA, the urine dipstick test is highly positive for glucose and ketones. Rarely, urine is negative for ketones, due to the fact that most available laboratory tests can detect only acetoacetate, while the predominant ketone in severe untreated DKA is beta-hydroxybutyrate.

When the clinical condition improves with treatment, the urine test result becomes positive due to the returning predominance of acetoacetate. To detect underlying urinary infection, look for glycosuria and urine ketosis.

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Ketones

In patients with DKA, serum ketones are present. Blood beta-hydroxybutyrate levels measured by a reagent strip (Ketostix, N-Multistix, and Labstix) and serum ketone levels assessed by the nitroprusside reaction are equally effective in diagnosing DKA in uncomplicated cases.

The Acetest and Ketostix products measure blood and urine acetone and acetoacetic acid. They do not measure the more common ketone body, beta-hydroxybutyrate, so the patient may have paradoxical worsening as the latter is converted into the former during treatment.

Specific testing for beta-hydroxybutyrate can be performed by many laboratories. Diagnosis of ketonuria requires adequate renal function. Additionally, ketonuria may last longer than the underlying tissue acidosis.

One study suggests that routine urine testing for ketones is no longer necessary to diagnose DKA.[12] Using capillary beta hydroxybutyrate offers a distinct advantage of avoiding unnecessary work-up.

According to the 2011 Joint British Diabetes Societies (JBDS) guideline for the management of diabetic ketoacidosis, capillary blood ketones should be measured in order to monitor the response to DKA treatment. The method of choice is bedside measurement of blood ketones using a ketone meter. In the absence of blood ketone measurement, venous pH and bicarbonate should be used together with bedside blood glucose monitoring to evaluate treatment response.[13, 14]

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Beta-Hydroxybutyrate

Serum or capillary beta-hydroxybutyrate can be used to follow response to treatment in patients with DKA. levels greater than 0.5 mmol/L are considered abnormal, and levels of 3 mmol/L correlate with the need for treatment for DKA.[15]

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Arterial Blood Gases

In patients with DKA, arterial blood gases (ABGs) frequently show typical manifestations of metabolic acidosis, low bicarbonate, and low pH (< 7.2).

When monitoring the response to treatment, the 2011 JBDS guideline recommends the use of venous blood rather than arterial blood in blood gas analyzers, except where respiratory problems preclude using arterial blood.[13, 14]

Venous pH may be used for repeat pH measurements.[16] Brandenburg and Dire found that pH on venous blood gas in patients with DKA was 0.03 lower than pH on ABG.[17] Because this difference is relatively reliable and not of clinical significance, there is almost no reason to perform the more painful ABG. End tidal CO2 has been reported as a way to assess acidosis as well.

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Serum Electrolyte Panel

Serum potassium levels initially are high or within the reference range in patients with DKA. This is due to the extracellular shift of potassium in exchange of hydrogen, which is accumulated in acidosis, in spite of severely depleted total body potassium. This needs to be checked frequently, as values drop very rapidly with treatment. An ECG may be used to assess the cardiac effects of extremes in potassium levels.

The serum sodium level usually is low in affected patients. The osmotic effect of hyperglycemia moves extravascular water to the intravascular space. For each 100 mg/dL of glucose over 100 mg/dL, the serum sodium level is lowered by approximately 1.6 mEq/L. When glucose levels fall, the serum sodium level rises by a corresponding amount.

Additionally, serum chloride levels and phosphorus levels always are low in these patients.

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Bicarbonate

Use bicarbonate levels in conjunction with the anion gap to assess the degree of acidosis that is present.

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Anion Gap

In patients with diabetic ketoacidosis, the anion gap is elevated ([Na + K] - [Cl + HCO3] >13 mEq/L).

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CBC Count

Even in the absence of infection, the CBC count shows an increased white blood cell (WBC) count in patients with diabetic ketoacidosis. High WBC counts (>15 X 109/L) or marked left shift may suggest underlying infection.

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Renal Function Studies

BUN frequently is increased in patients with diabetic ketoacidosis.

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Osmolarity

Plasma osmolarity usually is increased (>290 mOsm/L) in patients with diabetic ketoacidosis. If plasma osmolarity cannot be measured directly, it may be calculated with the following formula: plasma osmolarity = 2 (Na + K) + BUN/3 + glucose/18. Urine osmolarity also is increased in affected patients.

Patients with diabetic ketoacidosis who are in a coma typically have osmolalities greater than 330 mOsm/kg H2 O. If the osmolality is less than this in a patient who is comatose, search for another cause of obtundation.

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Cultures

Urine and blood culture findings help to identify any possible infecting organisms in patients with diabetic ketoacidosis.

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Amylase

Hyperamylasemia may be seen in patients with diabetic ketoacidosis, even in the absence of pancreatitis.

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Phosphate, Calcium, and Magnesium

If the patient is at risk for hypophosphatemia (eg, poor nutritional status, chronic alcoholism), then the serum phosphorous level should be determined.

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Chest Radiography

Chest radiography should be used to rule out pulmonary infection such as pneumonia.

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MRI

An MRI is helpful in detecting early cerebral edema; it should be ordered only if altered consciousness is present.[8]

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CT Scanning

The threshold should be low for obtaining a head CT scan in children with diabetic ketoacidosis who have altered mental status, as this may be caused by cerebral edema.

Many of the changes may be seen late on head imaging and should not delay administration of hypertonic saline or mannitol in those pediatric cases where cerebral edema is suspected.

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Electrocardiography

DKA may be precipitated by a cardiac event, and the physiological disturbances of DKA may cause cardiac complications. An ECG should be performed every 6 hours during the first day, unless the patient is monitored. An ECG may reveal signs of acute myocardial infarction that could be painless in patients with diabetes, particularly in those with autonomic neuropathy.

An ECG is also a rapid way to assess significant hypokalemia or hyperkalemia. T-wave changes may produce the first warning sign of disturbed serum potassium levels. Low T wave and apparent U wave always signify hypokalemia, while peaked T wave is observed in hyperkalemia.

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Telemetry

Consider telemetry in patients with comorbidities (especially cardiac), known significant electrolyte abnormalities, severe dehydration, or profound acidosis.

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Contributor Information and Disclosures
Author

Vasudevan A Raghavan, MBBS, MD, MRCP(UK)  Director, Cardiometabolic and Lipid (CAMEL) Clinic Services, Division of Endocrinology, Scott and White Hospital, Texas A&M Health Science Center College of Medicine

Vasudevan A Raghavan, MBBS, MD, MRCP(UK) is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Heart Association, Endocrine Society, National Lipid Association, and Royal College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Howard A Bessen, MD  Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Program Director, Harbor-UCLA Medical Center

Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Osama Hamdy, MD, PhD, FACE  Medical Director, Obesity Clinical Program, Director of Inpatient Diabetes Management, Joslin Diabetes Center; Assistant Professor of Medicine, Harvard Medical School

Osama Hamdy, MD, PhD, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists and American Diabetes Association

Disclosure: Merck Inc Honoraria Speaking and teaching

Donald W Rucker, MD, MBA, MS  Clinical Assistant Professor of Emergency Medicine, University of Pennsylvania School of Medicine

Donald W Rucker, MD, MBA, MS is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians, American Medical Association, American Medical Informatics Association, and Society for Academic Emergency Medicine

Disclosure: Siemens Healthcare Salary Employment

Erik D Schraga, MD  Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Specialty Editor Board

David S Schade, MD  Chief, Division of Endocrinology and Metabolism, Professor, Department of Internal Medicine, University of New Mexico School of Medicine and Health Sciences Center

David S Schade, MD is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, New Mexico Medical Society, New York Academy of Sciences, and Society for Experimental Biology and Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Don S Schalch, MD  Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics

Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP  Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD  Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

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