Diabetes Mellitus:- Part 7 – Diabetic Ketoacidosis and Ketone Bodies
- The ketones can be detected in blood and urine.
- The false-positive test may be seen in some medications.
- Prolonged exposure of the strips to air gives the false-negative result.
- Normally no ketones are present in the urine.
- Diabetic ketoacidosis is due to the presence of Ketone bodies in the blood and the urine.
- There is a presence of ketones in the blood and these are toxic acids.
- This is the complication in diabetic patients with hyperglycemia and massive fatty catabolism.
- The primary substrate for the ketone body formation is free fatty acids from adipose tissue.
- This is due to the lake of insulin in uncontrolled diabetes mellitus.
- These free fatty acids are substrates for the formation of ketone bodies.
- These free fatty acids when reesterified in the liver then give rise to triglycerides and low-density lipoproteins.
- When the body can not utilize carbohydrates or glucose can not enter the cells.
- In the blood samples mainly 78% is beta-hydroxybutyric acid and acetone is hardly 2%.
- Ketones are formed when the energy to the body is provided by the fats.
- Ketone bodies are:
- ketone bodies are the end product of fatty acid breakdown.
- The presence of ketones bodies in the urine indicates poorly controlled diabetes mellitus.
- When the body can not utilize the ketone bodies and, these are produced in excess, is called ketosis.
- These are excreted in the urine and is called ketonuria.
- The elevated level of ketones in the blood is called ketonemia.
- This overproduction of the keto acids leads to acidosis or lower the blood pH.
- Gerhardt’s ferric chloride reacts with acetoacetate only.
- Nitroprusside is 10 times more sensitive to acetoacetate than acetone.
- It has no reaction to β-hydroxybutyrate.
- For β-hydroxybutyrate, urine heated to convert β-hydroxybutyrate to acetone and acetoacetate by oxidation.
- Commercial kits are available to estimate the β-hydroxybutyrate.
Signs and Symptoms
- This condition is seen in carbohydrates deficiency or starvation or frequent vomiting.
- The patient will have a thirst and a dry mouth.
- Increased frequency of urine.
- There is easy fatigue.
- There may be nausea, vomiting, and abdominal pain.
- There is a fruity odor breath.
- Difficult in concentration and confusion.
- This condition may become very serious if not treated in time.
Typical findings in diabetic ketoacidosis
- Blood glucose = 300 to 500 mg/dL.
- Ketones = positive.
- Electrolytes =
- Sodium decreased.
- Potassium increased.
- The anion gap increased.
- Blood gasses =
- Total CO2 decreased.
- Metabolic acidosis =
- pH decreased (<_7.30 )
- Bicarbonate decreased (<_15 meq/L).
- Blood glucose: level is 300 to 500 mg/dL or higher.
- Ketones bodies: These are positive in the urine and their level in the blood is increased.
- Electrolytes: Sodium is decreased.
- Potassium is increased.
- Blood gasses: There is metabolic acidosis.
- The pH is low.
- Bicarbonate markedly decreased.
The complication of diabetic ketoacidosis:
- There is brain edema due to fluid accumulation.
- The patient may have a cardiac arrest.
- The patient may go into kidney failure.
- Start with saline for volume replacement.
- Insulin infusion (but delay if serum potassium level is low <_3.3 meq/L.
- Potassium replacement when the serum level is <5.5 meq/L.
- Glucose drip (5% dextrose with 0.45% saline when the plasma glucose level is <250 mg/dL).
- Continue glucose and insulin until the anion gap is <12 meq/L.