Diabetic Ketoacidosis (DKA): Pathophysiology and Treatment
Diabetic Ketoacidosis is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including the production of serum acetone.
It can occur in both Type I Diabetes and Type II Diabetes
In type II diabetics with insulin deficiency/dependence.
The presenting symptom for ~ 25% of Type I Diabetics.
Causes of Diabetic Ketoacidosis
- The stressful precipitating event that results in increased catecholamines, cortisol, glucagon.
- Infection (pneumonia, UTI)
- Alcohol, drugs
- Myocardial Infarction
- Medications (steroids, thiazide diuretics)
- Non-compliance with insulin
Essentials of diagnosis OF DKA
- Acidosis with blood pH <7.3
- Serum bicarbonate < 15mEq/L
- Serum positive for ketones
- Elevated anion gap
- Variable, may occur without a gap.
- Hyperglycemia > 250
No correlation between the severity of hyperglycemia and severity of ketoacidosis
Clinical manifestations of diabetic ketoacidosis
polydipsia and urination
Nausea and vomiting
Generalized weakness and fatigability
Altered consciousness is common (stupor or coma).
Symptoms of associated intercurrent illness
Physical Assessment findings
Signs of dehydration -tachycardia, hypotension.
Acetone odor(fruity breath odor)
Signs of acidosis
Shallow rapid breathing or air hunger (Kussmaul or sighing respiration)
Abdominal tenderness and abdominal pain.
Disturbance of consciousness
Signs of intercurrent illness.
Diabetic Ketoacidosis Treatment
Management of DKA includes:
3) Electrolyte replacement.
Glucose osmotic diuresis causes dehydration therefore in your management you should give between 4-6 liters, then reassess (caution in CHF). Fluids help decrease blood glucose levels.
Always start with isotonic normal saline fluids. Give as a bolus and then a steady rate (i.e. 150cc/hr). Switch to 0.45% NS when “corrected” sodium within normal limits.
Add 1.6 mEq to sodium for every 100 glucose is above 100. Switch to Dextrose 5% 1/2 Normal Saline when glucose between 200-250.
Administer intravenous insulin drip as a bolus approx 10 units (or 0.1 to o.15 units/kg), then initiate drip at 0.1 unit/kg/hr. Ideally, you should decrease glucose 50-100 mg/dl per hour. Avoid bolus if the potassium level is above 3.3mEq.
Replete potassium before starting a drip. Insulin drives potassium into the cells so if potassium starts off very low can make hypokalemia life-threatening.
Switch to subcutaneous insulin when the anion gap closed signifying acidosis cleared.
Subcutaneous insulin must overlap with an insulin drip over 2 hours. Use the patient’s outpatient insulin dose several hours prior to stopping the insulin drip or In insulin-naive patients, a multi-dose insulin regimen should be started at a dose of 0.5 to 0.8 U/kg per day, including bolus and basal insulin until an optimal dose is established OR
Calculate 24-hour insulin requirements and use 50% as long-acting. Once the anion gap closes, can feed the patient. Remember to add sliding scale insulin (preferably lispro) with meals in addition to basal SC insulin dose.
Bicarbonate: If pH<6.9 (controversial) or K>6 with ECG changes
Potassium: If potassium < 5.3, you give 20-60 meq/L of ½ normal saline when K <5.3 with severe acidosis
Phosphate: If phosphate is below 1, especially if muscle weakness. When needed 20-30mEQ/L of potassium phosphate can be added to replacement fluids. Be sure to check q1hour glucose checks and q2-4hrs BMP to monitor anion gap and acidosis
Pitfalls of diabetic ketoacidosis treatment
High serum glucose levels may lead to dilutional hyponatremia
Triglyceride levels may lead to fictitious low glucose;
High levels of ketone bodies may lead to factitious elevation of creatinine.
If the potassium level is greater than 6 mEq/L, do not administer potassium supplementation.
If the potassium level is 4.5-6 mEq/L, administer 10 mEq/h of potassium chloride.
If the potassium level is 3-4.5 mEq/L, administer 20 mEq/h of potassium chloride. Monitor serum potassium levels hourly, and the infusion must stop if the potassium level is greater than 5 mEq/L.
Complications of DKA
Hypophosphatemia occurs after aggressive hydration/treatment
Monitor phosphorus and replete as needed to keep more than 1
Cerebral edema is rare but life-threatening. Usually in pediatric, adolescent patients
Symptoms of cerebral edema are Headache, altered mental status. It is treated with mannitol, hyperventilation
Deep vein thrombosis/Pulmonary Embolism,