Hyperglycemia and Diabetic Ketoacidosis

(Diabetic Ketoacidosis) DKA
Diabetic Ketoacidosis occurs as a result of severe insulin insufficiency and an excess of counter-regulatory hormones (e.g glucagon).  It usually presents itself with the gradual onset of polyuria and drowsiness (pre-coma), which may, over a day or more progress to coma.
Diagnosis: Common symptoms include;
  • Vomiting.
  • Vague abdominal pain without localizing signs.
  • Hyperventilation, Shock or Coma.
  • Symptoms of Diabetes Mellitus.
Laboratory Investigations Reveal
  • Elevated plasma glucose
  • Metabolic acidosis – (ABG)
  • Urinalysis – ketone bodies, sugar +++
  • Hyponatremia, hyperkalemia and elevated serum amylase.
Supportive Measures
For patients in shock or coma, supportive measures should proceed without delay. e.g. O2 , I/V fluids.
Monitoring of Therapy:
Frequent measures of glucose and electroytes are essential to assess response to therapy in Diabetic Ketoacidosis (DKA.).  Ketonuria can persist after correction of acidosis and urine ketones are of only limited use in following therapy.
Fluid Management: Initial fluid should include isotonic (0.9%) saline or Ringer lactate solution.  Patients with normal cardiac function should receive the first liter of fluid rapidly.  Volume replacement may then proceed at 1 liter/hr (or more) until intravascular deficit has been corrected.  An osmotic diuresis is common when fluid is started and may show progress towards a positive fluid balance.
  1. Monitoring of Volume:  Frequent assessment of the heart rate, B.P. and urinary output is important to guide volume replacement.
  2. Maintenance Fluids: When the intravascular volume has been restored a maintenance infusion 0.45 % saline at a rate of 150-250 ml/hr is appropriate for most patients.
Bicarbonate Therapy:
Bicarbonate therapy should be considered initially when DKA is accompanied by:
Shock or coma
Arterial pH less then 7.1, or
Severe hyperkalemia.   (Two ampoules of soda bicarbonate in a liter of 0.45% saline.)
Potassium Replacement:
Replacement of potassium is a fundamental part of therapy for DKA.  Life-threatening hypokalemia can develop during insulin treatment.  Potassium should be given at an initial rate of 10 mEq/hr.  Plasma potassium levels may be used as guide to potassium administration.
Insulin Treatment
1. Initial dose 10-15 units of regular insulin (or 0.15 units/kg) I/V as bolus.
2. Continuous I/V insulin infusion:  Administration of 10 units/hr or 0.1 units/kg/hr is appropriate initially.
Adjustments of Insulin Dosage: Should be guided initially by blood glucose levels.  After the first hours of treatment, the glucose level should fall by at least 50 mg/dl/hr.  If slower response, dosages of I/V insulin should be increased by 50-100% in hourly increments.
When oral intake is resumed, S/C insulin may be given and I/V insulin discontinued.
Dextrose Administration:
Fall in blood glucose level caused by insulin treatment is usually more prompt than the resolution of ketoacidosis.  Dextrose administration is necessary during therapy.
Initiation of Oral Intake:
Nausea, vomiting and abdominal pain usually resolve during the first few hours of treatment.  Patients may eat when they can tolerate food.
Ketoacidosis should be corrected before full diet is resumed.