Diabetic Ketoacidosis (DKA) definition, symptoms, diagnosis, treatement

Definition: DKA is a potentially fatal acute metabolic complication of diabetes mellitus. It is characterized by the biochemical triad of hyperglycemia, ketonemia, and metabolic acidosis.

DKA is typically associated with type 1 diabetes but may also occur in type 2 diabetes during periods of infection, trauma, cardiovascular injury, or other emergencies. It is more common in young people with type 1 diabetes and in females. It may be the presenting manifestation of diabetes.

Precipitating factors

  • Inadequate dosing of insulin
  • Cardiovascular disorders (myocardial infarction, stroke)
  • Infection.
  • Drug use (steroids, diuretics, vasopressors, antipsychotics, cocaine).


DKA results from severe alterations in carbohydrate, protein, and lipid metabolism. In simple terms, it is the consequence of severe cell starvation and death resulting from a relative or complete deficiency of insulin needed to transport glucose into the cells. Increased gluconeogenesis, increased glycogenolysis, and decreased use of glucose by the muscles, liver, and fat lead to profound metabolic derangements. Insulin deficiency promotes lipolysis. Lipolysis also plays a key role in promoting metabolic decompensation by providing the substrate for the formation of ketone bodies (acetone, beta-hydroxybutyric acid, and acetoacetic acid). Decreased clearance of ketone bodies leads to ketonemia and results in an anion gap metabolic acidosis. There are also elevated levels of proinflammatory cytokines and procoagulant factors (C-reactive protein and interleukin-6 and -8) that predispose the patient to thrombosis.

Clinical Manifestation and Diagnosis

Severe disease can develop in less than 24 hours after the onset of ketosis.Clinical manifestations include:
  • Polyuria, polydipsia, polyphagia, and weakness.
  • Manifestation of dehydration (dry mucous membranes, flattened neck veins, tachycardia, hypotension, and orthostasis).
  • Nausea and vomiting are common, occurring in up to 80% of patients.
  • A fruity odor to their breath, resulting from elevated serum acetone.
  • Kussmaul respirations (rhythmic, gasping deep respirations with normal or reduced frequency). as a compensatory response to the underlying metabolic acidosis seen in this disorder.
  • Altered mental status. The spectrum can vary from mild confusion to coma.

N.B. In short, DKA is nearly universally associated with  profound intravascular volume depletion and restoration of this is a cornerstone of therapy.


  1. Serum ketones
  2. Widened anion gap metabolic acidosis.
  3. Hyperglycemia is almost always seen but is not required for the diagnosis, and clinically significant DKA can occur in patients with normal serum glucose levels.
  4. Most patients have elevations in the blood urea nitrogen and serum creatinine concentration,
  5. Hyponatremia results from the osmotic diuresis
  6. Hyperkalemia results from insulin deficiency
  7. Hemoglobin A1C measurement may be useful in determining whether the episode is an acute exacerbation of previously controlled diabetes or the first manifestation of undiagnosed diabetes. However, level of hemoglobin A1C should not be relied on to diagnose or initiate treatment for DKA.
  8. Evaluation for underlying infectious causes should be undertaken because of the common associations with DKA.

Treatment strategies

  • Normalization of the serum glucose and electrolytes(especially in potassium, magnesium, and phosphorous).
  • Restoration of the intravascular volume.
  • Resolution of the metabolic acidosis (closure of the anion gap).
  • Treatment of the precipitating factor e.g.sepsis.



  • An initial intravenous bolus of regular insulin at 0.1 U/kg body weight
  • Followed by a continuous infusion of regular insulin at a dose of 0.1 U/kg/hour.
  • Long-acting and oral preparations should be strictly avoided during the initial treatment of this disorder as rapid fluctuations in serum glucose levels may be experienced and are more easily managed with regular insulin.
  • The insulin drip should be continued until the anion gap closes and not when the serum glucose level normalizes.
  • Glucose should initially be measured hourly, with appropriate adjustments to the insulin drip. If the serum glucose level becomes normal or low in the face of a persistently widening anion gap
  • Intravenous dextrose should be given and the insulin drip rate reduced but not stopped.

Initial fluid therapy

  • Up to 6 liters to adequately replete intracellular volume.
  • Caution must be taken during fluid repletion as rapid reduction in plasma osmolality can precipitate cerebral edema.
  • Isotonic saline is the initial resuscitative fluid of choice.

- Rate= 15-20 mL/kg/hour for the first several    hours.
- Once the serum glucose level is below 200-250 mg/dL, the fluids should be changed to one-half normal saline with dextrose (D5 1/2NS). 

N.B.   Fluid therapy &insulin infusion should be continued till normalization of anion gap (reflects recovery from metabolic acidosis).

Causes of death in Diabetic Ketoacidosis

  • Cerebral edema.
  • Shock.
  • Electrolyte abnormalities (esp hypokalemia induced by insulin therapy).
  • The underlying precipitant for DKA, especially sepsis. 


DKA is preventable complication of diabetes ,so patients must be educated about insulin compliance and encouraged to seek medical attention in the early coarse of illness. 
Diabetic Ketoacidosis (DKA) definition, symptoms, diagnosis, treatement
Dr.Tamer Mobarak


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