eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic

Diabetic Ketoacidosis

Author: Donald W Rucker, MD, MBA, MS, Clinical Assistant Professor of Emergency Medicine, University of Pennsylvania School of Medicine
Contributor Information and Disclosures

Updated: Jul 1, 2009

Introduction

Background

Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism. The most common causes are underlying infection, disruption of insulin treatment, and new onset of diabetes.

Diabetic ketoacidosis is typically characterized by hyperglycemia over 300 mg/dL, low bicarbonate level (<15 mEq/L), and acidosis (pH <7.30) with ketonemia and ketonuria. While definitions vary, moderate DKA can be categorized by pH <7.2 and serum bicarbonate <10 mEq/L, whereas severe DKA has pH <7.1 and bicarbonate <5 mEq/L. Mental status changes can be seen with mild-to-moderate DKA with more severe deterioration in mental status typical with moderate-to-severe DKA. 

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Pathophysiology

Many of the underlying pathophysiologic disturbances in diabetic ketoacidosis (DKA) are directly measurable by the clinician and need to be monitored throughout the course of treatment. Close attention to clinical laboratory data allows for tracking of the underlying acidosis and hyperglycemia as well as prevention of common potentially lethal complications such as hypoglycemia, hyponatremia, and hypokalemia.

The absence of insulin, the primary anabolic hormone, means that tissues such as muscle, fat, and liver do not take up glucose. Counterregulatory hormones, such as glucagon, growth hormone, and catecholamines, enhance triglyceride breakdown into free fatty acids and gluconeogenesis, which is the main cause for the elevation in serum glucose level in diabetic ketoacidosis. Beta-oxidation of these free fatty acids leads to increased formation of ketone bodies. Overall, metabolism in diabetic ketoacidosis shifts from the normal fed state characterized by carbohydrate metabolism to a fasting state characterized by fat metabolism.

Secondary consequences of the primary metabolic derangements in diabetic ketoacidosis include an ensuing metabolic acidosis as the ketone bodies produced by beta-oxidation of free fatty acids deplete extracellular and cellular acid buffers. The hyperglycemia-induced osmotic diuresis depletes sodium, potassium, phosphates, and water as well as ketones and glucose. Patients are often profoundly dehydrated and have a significantly depleted potassium level (as high as 5 mEq per kg of body weight). A normal or even elevated serum potassium concentration may be seen due to the extracellular shift of potassium in acidotic conditions, and this very poorly reflects the patient's total potassium stores. The serum potassium concentration can drop precipitously once insulin treatment is started, so great care must be taken to repeatedly monitor serum levels. Urinary loss of ketoanions with brisk diuresis and intact renal function may also lead to a component of hyperchloremic metabolicacidosis.

Frequency

United States

Diabetic ketoacidosis occurs primarily in patients with type 1 diabetes. The incidence is roughly 2 episodes per 100 patient years of diabetes, with about 3% of patients with type 1 diabetes initially presenting with diabetic ketoacidosis. It can occur in patients with type 2 diabetes as well; however, this is less common.

Mortality/Morbidity

With modern fluid management, the mortality rate of diabetic ketoacidosis is about 2% per episode. Before the discovery of insulin in 1922, the mortality rate was 100%.

Sex

No sex predilection exists for diabetic ketoacidosis.

Age

Diabetic ketoacidosis tends to occur in individuals younger than 19 years, but it may occur in patients with diabetes at any age.

Clinical

History

  • Classic symptoms of hyperglycemia
    • Thirst
    • Polyuria, polydipsia
    • Nocturia
  • Other symptoms
    • Generalized weakness
    • Malaise/lethargy
    • Nausea/vomiting
    • Decreased perspiration
    • Fatigue
    • Anorexia or increased appetite
    • Confusion
  • Symptoms of associated infections and conditions
    • Fever
    • Dysuria
    • Chills
    • Chest pain
    • Abdominal pain
    • Shortness of breath

Physical

  • General signs
    • Ill appearance
    • Dry skin
    • Labored respirations
    • Dry mucous membranes
    • Decreased skin turgor
    • Decreased reflexes
  • Vital signs
    • Tachycardia
    • Hypotension
    • Tachypnea
    • Hypothermia
    • Fever, if infection
  • Specific signs
    • Ketotic breath (fruity, with acetone smell)
    • Confusion
    • Coma
    • Abdominal tenderness

Causes

  • The most common scenarios for diabetic ketoacidosis are underlying or concomitant infection (40%), missed insulin treatments (25%), and newly diagnosed, previously unknown diabetes (15%). Other associated causes make up roughly 20% in the various series.
  • Urinary tract infections (UTIs) are the single most common infection associated with diabetic ketoacidosis, but many other associated illnesses need to be considered as well.
    • Myocardial infarction
    • Cerebrovascular accident
    • Complicated pregnancy
    • Trauma
    • Stress
    • Cocaine
    • Surgery
    • Heavy use of concentrated carbohydrate beverages such as sodas and sports drinks
    • Acromegaly
    • Idiopathic (20-30%)
    • Dental abscess1

More on Diabetic Ketoacidosis

Overview: Diabetic Ketoacidosis
Differential Diagnoses & Workup: Diabetic Ketoacidosis
Treatment & Medication: Diabetic Ketoacidosis
Follow-up: Diabetic Ketoacidosis
References
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References

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

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Further Reading

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Keywords

DKA, diabetic ketoacidosis, insulin, ketones, diabetic ketoacidosis symptoms, diabetic ketoacidosis treatment, diabetic ketoacidosis causes, diabetes, diabetes mellitus, insulin deficiency, hyperglycemia, low bicarbonate, acidosis, ketonemia, ketonuria, type 1diabetes, type 1 diabetes mellitus, insulin-dependent diabetes, IDD, insulin-dependent diabetes mellitus, IDDM, childhood diabetes, childhood diabetes mellitus, childhood-onset diabetes, childhood-onset diabetes mellitus, diabetes in childhood, diabetes mellitus in childhood, juvenile-onset diabetes, juvenile-onset diabetes mellitus, ketosis-prone diabetes, autoimmune diabetes mellitus, brittle diabetes mellitus, maturity-onset diabetes of the young, MODY, chamber-pot dropsy, thirst disease, sugar disease, sugar sickness, ketotic breath, coma, diabetes complications, diabetes care, incretin hormones

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Contributor Information and Disclosures

Author

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

Medical Editor

Erik D Schraga, MD, Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Howard A Bessen, MD, Professor of Medicine, Department of Emergency Medicine, UCLA 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.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

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

 
 
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