Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

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.

Consciousness

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.

Next

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

Potassium

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.

Sodium

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]

Insulin

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
Previous
Next

Procedures

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.

Previous
Next

Electrocardiography

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).
Previous
 
 
Contributor Information and Disclosures
Author

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.

Acknowledgements

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.

Acknowledgments

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

References
  1. Edge JA, Roy Y, Bergomi A, et al. Conscious level in children with diabetic ketoacidosis is related to severity of acidosis and not to blood glucose concentration. Pediatr Diabetes. 2006 Feb. 7(1):11-5. [Medline].

  2. Harris GD, Fiordalisi I. Physiologic management of diabetic ketoacidemia. A 5-year prospective pediatric experience in 231 episodes. Arch Pediatr Adolesc Med. 1994 Oct. 148(10):1046-52. [Medline].

  3. Wolfsdorf J, Craig ME, Daneman D, et al. Diabetic ketoacidosis. Pediatr Diabetes. 2007 Feb. 8(1):28-43. [Medline].

  4. Marshall SM, Walker M, Alberti KGMM. Diabetic Ketoacidosis and Hyperglycaemic non-ketotic coma. Alberti, Zimmet, Defronzo eds. International Textbook of Diabetes Mellitus. 1997. 1215-30.

  5. Fagan MJ, Avner J, Khine H. Initial fluid resuscitation for patients with diabetic ketoacidosis: how dry are they?. Clin Pediatr (Phila). 2008 Nov. 47(9):851-5. [Medline].

  6. Durr JA, Hoffman WH, Sklar AH, et al. Correlates of brain edema in uncontrolled IDDM. Diabetes. 1992 May. 41(5):627-32. [Medline].

  7. Hale PM, Rezvani I, Braunstein AW, et al. Factors predicting cerebral edema in young children with diabetic ketoacidosis and new onset type I diabetes. Acta Paediatr. 1997 Jun. 86(6):626-31. [Medline].

  8. Mel JM, Werther GA. Incidence and outcome of diabetic cerebral oedema in childhood: are there predictors?. J Paediatr Child Health. 1995 Feb. 31(1):17-20. [Medline].

  9. Silver SM, Clark EC, Schroeder BM, Sterns RH. Pathogenesis of cerebral edema after treatment of diabetic ketoacidosis [published erratum appears in Kidney Int 1997 May;51(5):1662]. Kidney Int. 1997 Apr. 51(4):1237-44. [Medline].

  10. Okuda Y, Adrogue HJ, Field JB, et al. Counterproductive effects of sodium bicarbonate in diabetic ketoacidosis. J Clin Endocrinol Metab. 1996 Jan. 81(1):314-20. [Medline].

  11. Glaser N. Cerebral injury and cerebral edema in children with diabetic ketoacidosis: could cerebral ischemia and reperfusion injury be involved?. Pediatr Diabetes. 2009 Dec. 10(8):534-41. [Medline].

  12. Musey VC, Lee JK, Crawford R. Diabetes in urban African-Americans. I. Cessation of insulin therapy is the major precipitating cause of diabetic ketoacidosis. Diabetes Care. 1995 Apr. 18(4):483-9. [Medline].

  13. Thompson CJ, Cummings F, Chalmers J, Newton RW. Abnormal insulin treatment behaviour: a major cause of ketoacidosis in the young adult. Diabet Med. 1995 May. 12(5):429-32. [Medline].

  14. Morris AD, Boyle DI, McMahon AD, et al. Adherence to insulin treatment, glycaemic control, and ketoacidosis in insulin-dependent diabetes mellitus. The DARTS/MEMO Collaboration. Diabetes Audit and Research in Tayside Scotland. Medicines Monitoring Unit. Lancet. 1997 Nov 22. 350(9090):1505-10. [Medline].

  15. Smaldone A, Honig J, Stone PW, et al. Characteristics of California children with single versus multiple diabetic ketoacidosis hospitalizations (1998-2000). Diabetes Care. 2005 Aug. 28(8):2082-4. [Medline]. [Full Text].

  16. Holstein A, Abel C, Zumwalde I. Recurrent severe diabetic ketoacidosis due to intoxication with synthetic drugs ('Ecstasy' and 'Speed'). Intensivmedizin und Notfallmedizin. 1997. 34(1):46-50.

  17. Rewers A, Klingensmith G, Davis C, et al. Presence of diabetic ketoacidosis at diagnosis of diabetes mellitus in youth: the Search for Diabetes in Youth Study. Pediatrics. 2008 May. 121(5):e1258-66. [Medline].

  18. Smith CP, Firth D, Bennett S, et al. Ketoacidosis occurring in newly diagnosed and established diabetic children. Acta Paediatr. 1998 May. 87(5):537-41. [Medline].

  19. Rewers A, Chase HP, Mackenzie T, et al. Predictors of acute complications in children with type 1 diabetes. JAMA. 2002 May 15. 287(19):2511-8. [Medline].

  20. Levy-Marchal C, Patterson CC, Green A. Geographical variation of presentation at diagnosis of type I diabetes in children: the EURODIAB study. European and Dibetes. Diabetologia. 2001 Oct. 44 Suppl 3:B75-80. [Medline].

  21. Edge JA, Dunger DB. Variations in the management of diabetic ketoacidosis in children. Diabet Med. 1994 Dec. 11(10):984-6. [Medline].

  22. Neu A, Hofer SE, Karges B, Oeverink R, Rosenbauer J, Holl RW. Ketoacidosis at diabetes onset is still frequent in children and adolescents: a multicenter analysis of 14,664 patients from 106 institutions. Diabetes Care. 2009 Sep. 32(9):1647-8. [Medline]. [Full Text].

  23. Usher-Smith JA, Thompson MJ, Sharp SJ, Walter FM. Factors associated with the presence of diabetic ketoacidosis at diagnosis of diabetes in children and young adults: a systematic review. BMJ. 2011 Jul 7. 343:d4092. [Medline].

  24. Fritsch M, Rosenbauer J, Schober E, Neu A, Placzek K, Holl RW. Predictors of diabetic ketoacidosis in children and adolescents with type 1 diabetes. Experience from a large multicentre database. Pediatr Diabetes. 2011 Jun. 12(4 Pt 1):307-12. [Medline].

  25. Delamater AM, Shaw KH, Applegate EB, et al. Risk for metabolic control problems in minority youth with diabetes. Diabetes Care. 1999 May. 22(5):700-5. [Medline]. [Full Text].

  26. Cohn BA, Cirillo PM, Wingard DL, et al. Gender differences in hospitalizations for IDDM among adolescents in California, 1991. Implications for prevention. Diabetes Care. 1997 Nov. 20(11):1677-82. [Medline].

  27. Quinn M, Fleischman A, Rosner B, et al. Characteristics at diagnosis of type 1 diabetes in children younger than 6 years. J Pediatr. 2006 Mar. 148(3):366-71. [Medline].

  28. Ghetti S, Lee JK, Sims CE, Demaster DM, Glaser NS. Diabetic ketoacidosis and memory dysfunction in children with type 1 diabetes. J Pediatr. 2010 Jan. 156(1):109-14. [Medline].

  29. Edge JA, Ford-Adams ME, Dunger DB, et al. Causes of death in children with insulin dependent diabetes 1990-96. Arch Dis Child. 1999 Oct. 81(4):318-23. [Medline]. [Full Text].

  30. Neu A, Willasch A, Ehehalt S, et al. Ketoacidosis at onset of type 1 diabetes mellitus in children--frequency and clinical presentation. Pediatr Diabetes. 2003 Jun. 4(2):77-81. [Medline].

  31. Warner DP, McKinney PA, Law GR, Bodansky HJ. Mortality and diabetes from a population based register in Yorkshire 1978-93. Arch Dis Child. 1998 May. 78(5):435-8. [Medline]. [Full Text].

  32. Hoffman WH, Locksmith JP, Burton EM, et al. Interstitial pulmonary edema in children and adolescents with diabetic ketoacidosis. J Diabetes Complications. 1998 Nov-Dec. 12(6):314-20. [Medline].

  33. Holsclaw DS Jr, Torcato B. Acute pulmonary edema in juvenile diabetic ketoacidosis. Pediatr Pulmonol. 1997 Dec. 24(6):438-43. [Medline].

  34. Muir AB, Quisling RG, Yang MC, Rosenbloom AL. Cerebral edema in childhood diabetic ketoacidosis: natural history, radiographic findings, and early identification. Diabetes Care. 2004 Jul. 27(7):1541-6. [Medline].

  35. Sottosanti M, Morrison GC, Singh RN, Sharma AP, Fraser DD, Alawi K, et al. Dehydration in children with diabetic ketoacidosis: a prospective study. Arch Dis Child. 2012 Feb. 97(2):96-100. [Medline].

  36. Brandenburg MA, Dire DJ. Comparison of arterial and venous blood gas values in the initial emergency department evaluation of patients with diabetic ketoacidosis. Ann Emerg Med. 1998 Apr. 31(4):459-65. [Medline].

  37. Wiggam MI, O'Kane MJ, Harper R, et al. Treatment of diabetic ketoacidosis using normalization of blood 3- hydroxybutyrate concentration as the endpoint of emergency management. A randomized controlled study. Diabetes Care. 1997 Sep. 20(9):1347-52. [Medline].

  38. Noyes KJ, Crofton P, Bath LE, et al. Hydroxybutyrate near-patient testing to evaluate a new end-point for intravenous insulin therapy in the treatment of diabetic ketoacidosis in children. Pediatr Diabetes. 2007 Jun. 8(3):150-6. [Medline].

  39. Fiordalisi I, Novotny WE, Holbert D, Finberg L, Harris GD. An 18-yr prospective study of pediatric diabetic ketoacidosis: an approach to minimizing the risk of brain herniation during treatment. Pediatr Diabetes. 2007 Jun. 8(3):142-9. [Medline].

  40. Puttha R, Cooke D, Subbarayan A, Odeka E, Ariyawansa I, Bone M. Low dose (0.05 units/kg/h) is comparable with standard dose (0.1 units/kg/h) intravenous insulin infusion for the initial treatment of diabetic ketoacidosis in children with type 1 diabetes-an observational study. Pediatr Diabetes. 2009 Jul 6. [Medline].

  41. Butkiewicz EK, Leibson CL, O'Brien PC, Palumbo PJ, Rizza RA. Insulin therapy for diabetic ketoacidosis. Bolus insulin injection versus continuous insulin infusion. Diabetes Care. 1995 Aug. 18(8):1187-90. [Medline].

  42. Della Manna T, Steinmetz L, Campos PR, Farhat SC, Schvartsman C, Kuperman H. Subcutaneous use of a fast-acting insulin analog: an alternative treatment for pediatric patients with diabetic ketoacidosis. Diabetes Care. 2005 Aug. 28(8):1856-61. [Medline].

  43. Green SM, Rothrock SG, Ho JD, et al. Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emerg Med. 1998 Jan. 31(1):41-8. [Medline].

  44. Hale PJ, Crase J, Nattrass M. Metabolic effects of bicarbonate in the treatment of diabetic ketoacidosis. Br Med J (Clin Res Ed). 1984 Oct 20. 289(6451):1035-8. [Medline].

  45. White H, Cook D, Venkatesh B. The use of hypertonic saline for treating intracranial hypertension after traumatic brain injury. Anesth Analg. 2006 Jun. 102(6):1836-46. [Medline].

  46. Vanelli M, Chiari G, Ghizzoni L, et al. Effectiveness of a prevention program for diabetic ketoacidosis in children. An 8-year study in schools and private practices. Diabetes Care. 1999 Jan. 22(1):7-9. [Medline]. [Full Text].

  47. [Guideline] Miller SG. Family therapy for recurrent diabetic ketoacidosis: Treatment guidelines. Family Systems Medicine. 1996. 14(3):303-14.

  48. Douglas D. Isotonic Fluids Helpful in Diabetic Ketoacidosis in Kids: Study. Medscape. Apr 4 2013. Available at http://www.medscape.com/viewarticle/781938. Accessed: April 16, 2013.

  49. White PC, Dickson BA. Low Morbidity and Mortality in Children with Diabetic Ketoacidosis Treated with Isotonic Fluids. J Pediatr. 2013 Mar 15. [Medline].

 
Previous
Next
 
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



(3-8%)



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
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.