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


Diabetic Ketoacidosis Workup

  • Author: Osama Hamdy, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
Updated: Jul 20, 2016

Approach Considerations

Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria.

While definitions vary, mild DKA can be categorized by a pH level of 7.25-7.3 and a serum bicarbonate level between 15-18 mEq/L; moderate DKA can be categorized by a pH between 7.0-7.24 and a serum bicarbonate level of 10 to less than 15 mEq/L; and severe DKA has a pH less than 7.0 and bicarbonate less than 10 mEq/L.[14] In mild DKA, anion gap is greater than 10 and in moderate or severe DKA the anion gap is greater than 12. These figures differentiate DKA from HHS where blood glucose is greater than 600 mg/dL but pH is greater than 7.3 and serum bicarbonate greater than 15 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 4-6 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.


Plasma Glucose Study

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


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.



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, however, measure beta-hydroxybutyrate, so the patient may appear to have "paradoxical worsening" as the latter is oxidized to acetoacetate in extrahepatic tissues with improved perfusion and better oxygenation.

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.[15] Using capillary beta hydroxybutyrate offers a distinct advantage of avoiding unnecessary workup.

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.[16, 17]



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.[18]


Arterial Blood Gases

In patients with DKA, arterial blood gases (ABGs) frequently show typical manifestations of metabolic acidosis, low bicarbonate, and low pH (less than 7.3).

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.[16, 17]

Venous pH may be used for repeat pH measurements.[19] Brandenburg and Dire found that pH on venous blood gas in patients with DKA was 0.03 lower than pH on ABG.[20] 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.


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.



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


Anion Gap

In patients with diabetic ketoacidosis, the anion gap is elevated ([Na + K] - [Cl + HCO3] greater than 10 mEq/L in mild cases and greater than 12 mEq/L in moderate and severe cases).


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 (greater than 15 X 109/L) or marked left shift may suggest underlying infection.


Renal Function Studies

BUN frequently is increased in patients with diabetic ketoacidosis.



Plasma osmolarity usually is increased (greater than 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.



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



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


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.


Chest Radiography

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



An MRI is helpful in detecting early cerebral edema; it should be ordered only if altered consciousness is present.[1]


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.



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.



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

Contributor Information and Disclosures

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

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

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: on advisory panel of Novo-Nordisk Inc, Astra-Zeneca Inc., Metagenics Inc<br/>Received research grant from: Metagenics Inc, USDA Dairy Council <br/>Have a 5% or greater equity interest in: HealthyMation LLC<br/>Received consulting fee from Merck Inc for speaking and teaching; Received consulting fee from Abbott Nutrition for consulting; Received grant/research funds from Metagenics for research support; Received grant/research funds from Neurometrix for research support.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.


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.

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for 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.

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, National Lipid Association, Royal College of Physicians, and The Endocrine Society

Disclosure: Nothing to disclose.

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

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, New Mexico Medical Society, New York Academy of Sciences, Society for Experimental Biology and Medicine, and The Endocrine Society

Disclosure: Nothing to disclose.

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 The Endocrine Society

Disclosure: Nothing to disclose.

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

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

  1. Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline].

  2. Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline]. [Full Text].

  3. Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients?. Diabet Med. 2012 Jan. 29(1):32-5. [Medline].

  4. Mrozik LT, Yung M. Hyperchloraemic metabolic acidosis slows recovery in children with diabetic ketoacidosis: a retrospective audit. Aust Crit Care. 2009 Jun 26. [Medline].

  5. Bowden SA, Duck MM, Hoffman RP. Young children (12 yr) with type 1 diabetes mellitus have low rate of partial remission: diabetic ketoacidosis is an important risk factor. Pediatr Diabetes. 2008 Jun. 9(3 Pt 1):197-201. [Medline].

  6. Potenza M, Via MA, Yanagisawa RT. Excess thyroid hormone and carbohydrate metabolism. Endocr Pract. 2009 May-Jun. 15(3):254-62. [Medline].

  7. Zargar AH, Wani AI, Masoodi SR, et al. Causes of mortality in diabetes mellitus: data from a tertiary teaching hospital in India. Postgrad Med J. 2009 May. 85(1003):227-32. [Medline].

  8. 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].

  9. Lin SF, Lin JD, Huang YY. Diabetic ketoacidosis: comparisons of patient characteristics, clinical presentations and outcomes today and 20 years ago. Chang Gung Med J. 2005 Jan. 28(1):24-30. [Medline].

  10. Pugliese G, Zanuso S, Alessi E, et al. Self glucose monitoring and physical exercise in diabetes. Diabetes Metab Res Rev. 2009 Sep. 25 Suppl 1:S11-7. [Medline].

  11. Weber C, Kocher S, Neeser K, et al. Prevention of diabetic ketoacidosis and self-monitoring of ketone bodies: an overview. Curr Med Res Opin. 2009 May. 25(5):1197-207. [Medline].

  12. Crossen SS, Wilson DM, Saynina O, Sanders LM. Outpatient Care Preceding Hospitalization for Diabetic Ketoacidosis. Pediatrics. 2016 Jun. 137 (6):[Medline].

  13. Jessup AB, Grimley MB, Meyer E, et al. Effects of Diabetic Ketoacidosis on Visual and Verbal Neurocognitive Function in Young Patients Presenting with New-Onset Type 1 Diabetes. J Clin Res Pediatr Endocrinol. 2015 Sep. 7 (3):203-10. [Medline]. [Full Text].

  14. Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in diabetes. Diabetes Care. 2004 Jan. 27 Suppl 1:S94-102. [Medline].

  15. Arora S, Henderson SO, Long T, Menchine M. Diagnostic Accuracy of Point-of-Care Testing for Diabetic Ketoacidosis at Emergency-Department Triage: {beta}-Hydroxybutyrate versus the urine dipstick. Diabetes Care. 2011 Apr. 34(4):852-4. [Medline]. [Full Text].

  16. Savage MW, Dhatariya KK, Kilvert A, Rayman G, Rees JA, Courtney CH, et al. Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabet Med. 2011 May. 28(5):508-15. [Medline].

  17. Joint British Diabetes Societies Inpatient Care Group. The Management of Diabetic Ketoacidosis in Adults. March 2010. Available at Accessed: June 27, 2011.

  18. Wallace TM, Matthews DR. Recent advances in the monitoring and management of diabetic ketoacidosis. QJM. 2004 Dec. 97(12):773-80. [Medline].

  19. Ma OJ, Rush MD, Godfrey MM, Gaddis G. Arterial blood gas results rarely influence emergency physician management of patients with suspected diabetic ketoacidosis. Acad Emerg Med. 2003 Aug. 10(8):836-41. [Medline].

  20. 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].

  21. Goyal N, Miller JB, Sankey SS, Mossallam U. Utility of initial bolus insulin in the treatment of diabetic ketoacidosis. J Emerg Med. 2010 May. 38(4):422-7. [Medline].

  22. [Guideline] Wolfsdorf J, Craig ME, Daneman D, Dunger D, Edge J, Lee WR, et al. Diabetic ketoacidosis. Pediatr Diabetes. 2007 Feb. 8(1):28-43. [Medline].

  23. Glaser NS, Wootton-Gorges SL, Buonocore MH, Marcin JP, Rewers A, Strain J, et al. Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosis. Pediatr Diabetes. 2006 Apr. 7(2):75-80. [Medline].

  24. 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].

  25. Hom J, Sinert R. Evidence-based emergency medicine/critically appraised topic. Is fluid therapy associated with cerebral edema in children with diabetic ketoacidosis?. Ann Emerg Med. 2008 Jul. 52(1):69-75.e1. [Medline].

  26. Bradley P, Tobias JD. An evaluation of the outside therapy of diabetic ketoacidosis in pediatric patients. Am J Ther. 2008 Nov-Dec. 15(6):516-9. [Medline].

  27. Chandu A, Macisaac RJ, Smith AC, Bach LA. Diabetic ketoacidosis secondary to dento-alveolar infection. Int J Oral Maxillofac Surg. 2002 Feb. 31(1):57-9. [Medline].

  28. Ai D, Roper TA, Riley JA. Diabetic ketoacidosis and clozapine. Postgrad Med J. 1998 Aug. 74(874):493-4. [Medline].

  29. Amemiya S. Constant infused glucose regimen during the recovery phase of diabetic ketoacidosis in children and adolescents with IDDM. Diabetes Care. 1998 Apr. 21(4):676-7. [Medline].

  30. Bohan JS. Chemical measurements in ketoacidosis. Arch Intern Med. 1999 Sep 27. 159(17):2089. [Medline].

  31. Brink SJ. Diabetic ketoacidosis: prevention, treatment and complications in children and adolescents. Diabetes Nutr Metab. 1999 Apr. 12(2):122-35. [Medline].

  32. Carroll MA, Yeomans ER. Diabetic ketoacidosis in pregnancy. Crit Care Med. 2005 Oct. 33(10 Suppl):S347-53. [Medline].

  33. Catalano C, Fabbian F, Di Landro D. Acute pulmonary oedema occurring in association with diabetic ketoacidosis in a diabetic patient with chronic renal failure. Nephrol Dial Transplant. 1998 Feb. 13(2):491-2. [Medline].

  34. Charfen MA, Fernández-Frackelton M. Diabetic ketoacidosis. Emerg Med Clin North Am. 2005 Aug. 23(3):609-28, vii. [Medline].

  35. 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].

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

  37. Fearon DM, Steele DW. End-tidal carbon dioxide predicts the presence and severity of acidosis in children with diabetes. Acad Emerg Med. 2002 Dec. 9(12):1373-8. [Medline].

  38. Fisken RA. Severe diabetic ketoacidosis: the need for large doses of insulin. Diabet Med. 1999 Apr. 16(4):347-50. [Medline].

  39. Glaser N, Barnett P, McCaslin I, Nelson D, Trainor J, Louie J, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med. 2001 Jan 25. 344(4):264-9. [Medline].

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

  41. Grimberg A, Cerri RW, Satin-Smith M, Cohen P. The "two bag system" for variable intravenous dextrose and fluid administration: benefits in diabetic ketoacidosis management. J Pediatr. 1999 Mar. 134(3):376-8. [Medline].

  42. Guenette MD, Hahn M, Cohn TA, Teo C, Remington GJ. Atypical antipsychotics and diabetic ketoacidosis: a review. Psychopharmacology (Berl). 2013 Mar. 226(1):1-12. [Medline].

  43. Hjort U, Christensen JH. Diabetic ketoacidosis and compliance. Lancet. 1998 Feb 28. 351(9103):674-5. [Medline].

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

  45. Kannan CR. Bicarbonate therapy in the management of severe diabetic ketoacidosis. Crit Care Med. 1999 Dec. 27(12):2833-4. [Medline].

  46. Kaufman FR, Halvorson M. The treatment and prevention of diabetic ketoacidosis in children and adolescents with type I diabetes mellitus. Pediatr Ann. 1999 Sep. 28(9):576-82. [Medline].

  47. Kaufman FR, Halvorson M, Fisher L, Pitukcheewanont P. Insulin pump therapy in type 1 pediatric patients. J Pediatr Endocrinol Metab. 1999. 12 Suppl 3:759-64. [Medline].

  48. Kitabchi AE, Nyenwe EA. Hyperglycemic crises in diabetes mellitus: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Endocrinol Metab Clin North Am. 2006 Dec. 35(4):725-51, viii. [Medline].

  49. Kreshak A, Chen EH. Arterial blood gas analysis: are its values needed for the management of diabetic ketoacidosis?. Ann Emerg Med. 2005 May. 45(5):550-1. [Medline].

  50. Laffel L. Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes. Diabetes Metab Res Rev. 1999 Nov-Dec. 15(6):412-26. [Medline].

  51. Liss DS, Waller DA, Kennard BD, McIntire D, Capra P, Stephens J. Psychiatric illness and family support in children and adolescents with diabetic ketoacidosis: a controlled study. J Am Acad Child Adolesc Psychiatry. 1998 May. 37(5):536-44. [Medline].

  52. Mahoney CP, Vlcek BW, DelAguila M. Risk factors for developing brain herniation during diabetic ketoacidosis. Pediatr Neurol. 1999 Oct. 21(4):721-7. [Medline].

  53. Martin SL, Hoffman WH, Marcus DM, Passmore GG, Dalton RR. Retinal vascular integrity following correction of diabetic ketoacidosis in children and adolescents. J Diabetes Complications. 2005 Jul-Aug. 19(4):233-7. [Medline].

  54. McDonnell CM, Pedreira CC, Vadamalayan B, Cameron FJ, Werther GA. Diabetic ketoacidosis, hyperosmolarity and hypernatremia: are high-carbohydrate drinks worsening initial presentation?. Pediatr Diabetes. 2005 Jun. 6(2):90-4. [Medline].

  55. Moller N, Foss AC, Gravholt CH, Mortensen UM, Poulsen SH, Mogensen CE. Myocardial injury with biomarker elevation in diabetic ketoacidosis. J Diabetes Complications. 2005 Nov-Dec. 19(6):361-3. [Medline].

  56. Newton CA, Raskin P. Diabetic ketoacidosis in type 1 and type 2 diabetes mellitus: clinical and biochemical differences. Arch Intern Med. 2004 Sep 27. 164(17):1925-31. [Medline].

  57. Paton RC, Sathiavageeswaran M. Severe diabetic ketoacidosis. Diabet Med. 1999 Oct. 16(10):884. [Medline].

  58. Reichel A, Rietzsch H, Kohler HJ, Pfutzner A, Gudat U, Schulze J. Cessation of insulin infusion at night-time during CSII-therapy: comparison of regular human insulin and insulin lispro. Exp Clin Endocrinol Diabetes. 1998. 106(3):168-72. [Medline].

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

  60. Timmons JA, Myer P, Maturen A, et al. Use of beta-hydroxybutyric acid levels in the emergency department. Am J Ther. 1998 May. 5(3):159-63. [Medline].

  61. Umpierrez GE, Cuervo R, Karabell A, Latif K, Freire AX, Kitabchi AE. Treatment of diabetic ketoacidosis with subcutaneous insulin aspart. Diabetes Care. 2004 Aug. 27(8):1873-8. [Medline].

  62. Umpierrez GE, Smiley D, Kitabchi AE. Narrative review: ketosis-prone type 2 diabetes mellitus. Ann Intern Med. 2006 Mar 7. 144(5):350-7. [Medline].

  63. Viallon A, Zeni F, Lafond P, et al. Does bicarbonate therapy improve the management of severe diabetic ketoacidosis?. Crit Care Med. 1999 Dec. 27(12):2690-3. [Medline].

  64. Wagner A, Risse A, Brill HL, et al. Therapy of severe diabetic ketoacidosis. Zero-mortality under very-low-dose insulin application. Diabetes Care. 1999 May. 22(5):674-7. [Medline].

  65. Warner EA, Greene GS, Buchsbaum MS, Cooper DS, Robinson BE. Diabetic ketoacidosis associated with cocaine use. Arch Intern Med. 1998 Sep 14. 158(16):1799-802. [Medline].

  66. Whiteman VE, Homko CJ, Reece EA. Management of hypoglycemia and diabetic ketoacidosis in pregnancy. Obstet Gynecol Clin North Am. 1996 Mar. 23(1):87-107. [Medline].

  67. Wolfsdorf J, Glaser N, Sperling MA. Diabetic ketoacidosis in infants, children, and adolescents: A consensus statement from the American Diabetes Association. Diabetes Care. 2006 May. 29(5):1150-9. [Medline].

  68. Yan SH, Sheu WH, Song YM, Tseng LN. The occurrence of diabetic ketoacidosis in adults. Intern Med. 2000 Jan. 39(1):10-4. [Medline].

  69. Younis N, Austin MJ, Casson IF. A respiratory complication of diabetic ketoacidosis. Postgrad Med J. 1999 Dec. 75(890):753-4. [Medline].

  70. Taylor SI, Blau JE, Rother KI. SGLT2 Inhibitors May Predispose to Ketoacidosis. J Clin Endocrinol Metab. 2015 Aug. 100 (8):2849-52. [Medline].

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