Pathophysiology of Diabetic Ketoacidosis : Animation

When the rate of synthesis of ketone bodies exceeds the rate of utilization, their concentration in blood increases, this is known as ketonemia. This is followed by ketonuria – excretion of ketone bodies in urine. The overall picture of ketonemia and ketonuria is commonly referred to as ketosis.


  1. Hyperglycaemia occurs due to decreased glucose uptake in fat and muscle cells due to insulin deficiency Lipolysis in fat cells now occurs promoted by the insulin deficiency releasing 
  2. Free fatty acids (FFA) into the blood which provide substrate to the liver 
  3. A switch in hepatic lipid metabolism occurs due to the insulin deficiency and the glucagon excess, so the excess FFA is metabolised resulting in excess production of acetyl CoA 
  4. The excess hepatic acetyl CoA (remaining after saturation of TCA cycle) is converted to ketone bodies which are released into the blood 
  5. Ketoacidosis and hyperglycaemia both occur due to the lack of insulin and the increase in glucagon and most of the clinical effects follow from these two factors 
1.    ↓ Insulin, ↑Glucogon (glycogen à glucose)
-  Glucose 500-700 mg/dl
2.    Glucose-derived osmotic diuresis
3.    ↑ Glucagon
-  ↑ FFA esterfied à ketone bodies à acidosis

Diagnostic tests:
  1. Blood glucose greater than 250 mg/dL 
  2. Blood pH less than 7.3 
  3. Blood bicarbonate less than 15 mEq/L 
  4. Ketones present in blood (exceeds 90 mg/dl) 
  5. Ketones excreted in urine exceeds 5000 mg/24 hrs 

Signs and Symptoms:
  1. Kussmal's respiration 
  2. Fruity odor of breath 
  3. Nausea and abdominal pain 
  4. Dehydration 
  5. Lethargy 
  6. Coma 
  7. Polydipsia, polyuria, polyphagia