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Pediatric Diabetic Ketoacidosis Workup

  • Author: William H Lamb, MD, MBBS, FRCP(Edin), FRCP, FRCPCH; Chief Editor: Timothy E Corden, MD  more...
Updated: Apr 25, 2014

Approach Considerations

The following lab studies are indicated in patients with diabetic ketoacidosis:

  • Blood glucose
  • Blood gases
  • Potassium
  • Sodium
  • Blood urea and creatinine
  • Bicarbonate - Usually available from blood gas analysis
  • Capillary blood ketone
  • High glycosylated hemoglobin (HbA1c)
  • Full blood count
  • Urine
  • Insulin
  • Culture
  • Amylase
  • Serum osmolarity
  • Phosphate, calcium, and magnesium
  • Lipids

Imaging studies

Perform head computed tomography (CT) scanning if coma is present or develops. Concurrently, initiate appropriate measures to manage cerebral edema. Perform chest radiography if clinically indicated.


Check the patient’s consciousness level hourly for up to 12 hours, especially in a young child with a first presentation of diabetes. The Glasgow coma scale (see the image below) is recommended for this purpose.

Glasgow Coma Scale, modified for age of verbal res Glasgow Coma Scale, modified for age of verbal response.

The normal maximum score on the Glasgow coma scale is 15. A score of 12 or less implies significant impairment of consciousness. A falling score may signify the development of cerebral edema.


Laboratory Studies

Blood glucose

Capillary blood samples analyzed on any modern blood glucose meter are acceptable for monitoring changes in blood glucose levels as treatment progresses, but measure at least 1 whole blood glucose at presentation.

Check blood glucose at least hourly during the initial stages of treatment (more frequently if blood glucose levels fall quickly or if changes to insulin infusion rates are made).

Blood gases

Traditionally, arterial blood samples are used; however, free-flowing capillary or venous samples are as reliable as the arterial samples for monitoring acidosis, are much easier to collect, and are less traumatic for the child.[36]

The severity of diabetic ketoacidosis can be defined by blood gas results, as follows:

  • Mild diabetic ketoacidosis - pH level of less than 7.3, bicarbonate level of less than 15 mmol/L
  • Moderate diabetic ketoacidosis - pH level of less than 7.2, bicarbonate level of less than 10 mmol/L
  • Severe diabetic ketoacidosis - pH level of less than 7.1, bicarbonate level of less than 5 mmol/L


Initial blood potassium levels are usually normal or high, despite considerable deficits of total body potassium. This is because the acidosis encourages leakage of intracellular potassium. Insulin drives potassium back into the cells, and levels may drop very quickly with treatment.

Frequent checks of potassium levels (ie, every 1-2 h), together with electrocardiographic monitoring, may be required in the first hours of therapy.


Measured sodium values are likely to be low because of the dilutional effect of hyperglycemia. True sodium levels can be calculated by adding 1.6 mEq/L sodium for every 100 mg/dL glucose (ie, 1 mmol/L sodium for 3 mmol/L glucose).

Sodium levels should rise with treatment. Failure of sodium levels to rise is associated with an increased risk of cerebral edema.

Blood urea and creatinine

Some creatinine assays can be affected by the presence of ketones, thus giving falsely elevated results. Under these circumstances, blood urea may give a better measure of dehydration.

Capillary blood ketone

This can be measured using a handheld meter; the level is always elevated at presentation of diabetic ketoacidosis (>2 mmol/L). Two studies have proposed using serial measurements as a way of indicating the resolution of diabetic ketoacidosis when the pH level is more than 7.3 and the sequential capillary blood ketone level is less than 1 mmol/L.[37, 38]


This test is especially indicated in children with recurrent diabetic ketoacidosis, as an absence of measurable insulin can confirm omission. Caution is needed because not all assays measure the newer analogue insulins; insulin antibody levels can also affect the result.

Additional studies

Other lab studies include the following:

  • Bicarbonate (usually available from blood gas analysis) - This reflects the degree of acidosis
  • High glycosylated hemoglobin (HbA1c) - High results are expected in a patient with newly diagnosed diabetes and in patients with an established diagnosis who have poor compliance with treatment
  • Urine - Check all urine for glucose and ketones for at least 24 hours, particularly if capillary blood ketones are not available
  • Full blood count - The white blood cell (WBC) count is usually elevated, even in the absence of infection
  • Culture - Perform blood culture and other cultures as clinically indicated (eg, urine, throat swab)
  • Amylase - Blood amylase levels often are elevated in diabetic ketoacidosis and can be misleading in the presence of abdominal pain
  • Serum osmolarity - This is usually elevated
  • Phosphate, calcium, and magnesium - These levels are invariably reduced but without obvious clinical significance
  • Lipids - Extremely high triglyceride levels are sometimes present; this causes an artificial lowering of other blood values, such as those for glucose, sodium, and potassium


Ideally, insert a good-sized venous cannula into each arm, the first for fluid, electrolyte, and insulin replacement and the second for regular sampling.

Arterial cannulation is appropriate for patients who require mechanical ventilation or for those who need intensive care for conditions such as coma, shock, or severe acidosis.

Insert a nasogastric tube and aspirate the gastric contents for all patients with impaired consciousness and for children with repeated vomiting.

Consider urinary catheterization for children with impaired consciousness. This allows accurate calculation of urinary losses, particularly in the early hyperosmolar phases of diabetic ketoacidosis in which osmotic diuresis can lead to massive urinary losses, even in the presence of dehydration.

Manage cerebral edema with intubation and mechanical ventilation in addition to osmotic diuresis.



Electrocardiography (ECG) is a useful adjunct to monitor potassium status. Characteristic changes appear with extremes of potassium status. Characteristic changes of hypokalemia as represented on ECG (see the image below) are as follows:

  • Apparent prolongation of QT interval
  • ST segment depression
  • Flat or diphasic T waves
  • Prominent U waves
  • Prolongation of PR interval
  • Sinoatrial block
    A graphical representation of the electrocardiogra A graphical representation of the electrocardiographic changes of hypokalemia.

Hyperkalemia may develop due to overcorrection of potassium loss, with electrocardiographic changes occurring as follows (see the image below):

  • Broadening of the QRS
  • Peaked T waves
  • Prolonged PR interval
  • Disappearance of P wave
  • Diphasic QRS complex
  • Asystole
    A graphical representation of the electrocardiogra A graphical representation of the electrocardiographic changes of hyperkalemia (due to overcorrection of potassium loss).
Contributor Information and Disclosures

William H Lamb, MD, MBBS, FRCP(Edin), FRCP, FRCPCH Consultant Paediatric Diabetologist, The Great North Children's Hospital, The Royal Victoria Infirmary; Honorary Clinical Lecturer, University of Newcastle upon Tyne; Honorary Clinical Lecturer, University of Durham, UK

William H Lamb, MD, MBBS, FRCP(Edin), FRCP, FRCPCH is a member of the following medical societies: British Medical Association, Royal College of Physicians, Royal College of Paediatrics and Child Health, British Society of Paediatric Endocrinology and Diabetes, International Society for Pediatric and Adolescent Diabetes

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Eli Lily and Company.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.


G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami, Leonard M Miller School of Medicine; Medical Director, Palliative Care Team, Director, Pediatric Critical Care Transport, Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Manager, FEMA, Urban Search and Rescue, South Florida, Task Force 2; Pediatric Medical Director, Tilli Kids – Pediatric Initiative, Division of Hospice Care Southeast Florida, Inc

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.


The author would like to thank Debbie Matthews and Tim Cheetham for reading the manuscript and for all of their support.

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Glasgow Coma Scale, modified for age of verbal response.
A graphical representation of the electrocardiographic changes of hypokalemia.
A graphical representation of the electrocardiographic changes of hyperkalemia (due to overcorrection of potassium loss).
Diabetic ketoacidosis treatment and results chart (page 1 of 4).
Diabetic ketoacidosis treatment and results chart (page 2 of 4).
Diabetic ketoacidosis treatment and results chart (page 3 of 4).
Diabetic ketoacidosis treatment and results chart (page 4 of 4).
Carbs for Kids-Count Them In: The Constant Carbohydrates Diet.
Diabetes Sick Day Rules.
Taking Diabetes Back to School.
Table 1. Clinical Assessment of Dehydration
  Mild (< 3%) Moderate


Severe (8%) and

Shock (>10%)

Appearance Thirsty, alert Thirsty, lethargic Drowsy, cold
Tissue turgor Normal Absent Absent
Mucous membranes Moist Dry Very dry
Blood pressure Normal Normal or low Low for age
Pulse Normal Rapid Rapid and weak
Eyes Normal Sunken Grossly sunken
Anterior fontanelle Normal Sunken Grossly sunken
Table 2. Suggested Daily Maintenance Fluid Replacement Rates
Weight Infusion rate
0-12.9 kg 80 mL/kg/24 h
13-19.9 kg 65 mL/kg/24 h
20-34.9 kg 55 mL/kg/24 h
35-59.9 kg 45 mL/kg/24 h
Adult (>60 kg) 35 mL/kg/24 h
Table 3. Infusion Rates of Potassium Chloride
Serum/Plasma K+ (mEq/L) Potassium Chloride (KCL) Dose in Infusion Fluids
< 2.5 mEq/L Carefully monitored administration of 1 mEq/kg body weight by separate infusion over 1 h
2.5-3.5 mEq/L 40 mEq/L
3.5-5 mEq/L 20 mEq/L
5-6 mEq/L 10 mEq/L (optional)
Over 6 mEq/L Stop K+ and repeat level in 2 h
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