What is diabetic ketoacidosis❓❓❓

One of the most common acute complications of diabetes is diabetic
ketoacidosis. The fatality rate of diabetic ketoacidosis in elderly patients with diabetes is as high as 5 to 16%. Therefore, we should master the diagnosis and treatment of diabetic ketoacidosis.

What are ketone bodies?

Fats are broken down into glycerol and fatty acids. Fatty acids are oxidatively broken down in the liver to form acetone, β-hydroxybutyric acid and acetoacetic acid. These three intermediate products are collectively referred to as ketone bodies. Since both acetoacetic acid and beta-hydroxybutyric acid are acidic substances, they can cause acidosis when they accumulate in large amounts in the body. In the blood, acetone accounts for only about 2% of the total ketone bodies, acetoacetic acid accounts for 28% and β-hydroxybutyric acid accounts for 70%. The blood concentration of β-hydroxybutyrate can directly reflect the ketone bodies in the body. However, the urine ketone measurement method can only measure acetone and acetoacetic acid, but not β-hydroxybutyric acid. 

What are the main causes of diabetic ketoacidosis?

Infection is the most common cause of diabetic ketoacidosis. Inappropriate dose reduction or interruption of insulin therapy is also a common cause of it. Insulin promotes the synthesis of fatty acids and glycerol into fat. When a patient's insulin is acutely deficient, it accelerates the breakdown of fat and increases the concentration of free fatty acids. Increased free fatty acid concentrations are oxidatively broken down in the liver to generate large amounts of ketone bodies. It will cause ketoacidosis.

How can a patient be diagnosed with diabetic ketoacidosis?

A lack of insulin in diabetics can increase blood sugar and accelerate fat breakdown. Hyperglycemia can cause osmotic diuresis. It causes dehydration and electrolyte loss in patients. Accelerated lipolysis increases free fatty acids in the patient's body. The oxidation and decomposition of fatty acids into ketone bodies will also increase. It can cause acidosis in patients.

Laboratory tests:

Blood sugar > 13.9 mmol/L.

Blood ketone ≥ 3 mmol/L or urine ketone(++).

Blood pH < 7.3 and/or HCO₃- < 18 mmol/L.

Diabetic ketoacidosis can be diagnosed with the above test results. The normal blood ketone value is 0.03 to 0.5 mmol/L. Plasma pH is normal 7.35 to 7.45. Serum HCO₃^- normal value is 22 to 27mmol/L. The clinical manifestations of diabetic ketoacidosis are lethargy, headache, abdominal pain, nausea, vomiting and rapid breathing (the exhaled breath will smell like rotten apples with acetone). Severe cases can cause dehydration, varying degrees of disturbance of consciousness and even coma.

What is the treatment for diabetic ketoacidosis?

Rehydration therapy: It is the primary treatment for patients with diabetic ketoacidosis. 0.9% Sodium Chloride Injection is the recommended treatment of choice. In principle, the rehydration treatment should be fast first and then slow. 1.0 to 1.5 L of normal saline should be infused during the first hour, and pre-estimated fluid losses should be replenished within the first 24 hours.

Insulin therapy: Insulin doesn't just lower a patient's blood sugar. It also reduces fat breakdown and inhibits the production of ketone bodies. Insulin is recommended as a continuous intravenous infusion of 0.1 U/kg/h. Insulin will generally correct ketosis more slowly than hyperglycemia. Therefore, when the patient's blood glucose was lowered to 11.1 mmol/L, the insulin input needed to be reduced and the patient started to be given 5% dextrose. It can maintain the patient's blood sugar at 8.3 to 11.1 mmol/L until the diabetic ketoacidosis is relieved.

Potassium supplementation therapy: If the patient's serum potassium is less than 3.3mmol/L, potassium supplementation therapy should be given priority to the patient. Insulin therapy should be started when the patient's serum potassium rises to 3.3 mmol/L. Cell membrane Na+-K⁺-ATPase is activated by insulin. It increases the intracellular potassium concentration, thereby reducing the blood potassium concentration. If the patient has normal urine output but serum potassium is less than 5.2 mmol/L after starting rehydration therapy and insulin, the patient should receive intravenous potassium supplementation. In general, 1.5 to 3.0 g of potassium chloride is added to each liter of infusion solution to maintain the patient's serum potassium level between 4 and 5 mmol/L.

Correction of acidosis: lipolysis is inhibited by insulin. It reduces the production of ketone bodies so that the acidosis is corrected. If the patient's circulation is not depleted, they generally do not need additional alkaline supplements. Generally, the use of 5% sodium bicarbonate solution for alkaline supplementation is only considered in the case of patients whose pH is less than or equal to 6.9.