An acute complication, DKA requires rapid intervention to prevent cellular starvation and profound dehydration. Although DKA usually occurs in patients with Type 1 diabetes, it can strike a patient with Type 2 diabetes.The three major causes of DKA are undiagnosed diabetes, insufficient insulin therapy, and physical or emotional stress.
How Diabetic ketoacidosis Develops
Without sufficient insulin, the cells can’t use glucose for energy. The body, sensing this energy decrease, begins to release and break down its stores of fat. Lipolysis creates glycerol and fatty acids. Glycerol is converted into glucose, and the liver converts fatty acids to ketone bodies. As ketone bodies accumulate, metabolic acidosis develops.
As a last resort, the body begins breaking down protein to create glucose for energy. This increases circulating glucose and nitrogen. In the ongoing absence of available insulin, however, glucose can’t enter the cells, and the blood glucose level continues to rise. Eventually, the blood glucose level rises to between 300 and 800 mg/dl.
The increase in blood glucose level and ketone bodies leads to a severe loss of water and electrolytes. The kidneys respond to the increase in circulating glucose by increasing the glomerular filtration rate. As the body tries to remove the excess glucose, urine output climbs. In many cases, it reaches 5 to 8 liters a day.
This excessive diuresis results in a loss of sodium, potassium, chloride, bicarbonate and, to a lesser degree, magnesium and phosphate. As sodium and bicarbonate are lost because of osmotic diuresis, acidosis develops. Acidosis leaves the rising level of carbonic acid (a by-product of ketosis) unchallenged. To compensate, the patient develops Kussmaul’s respirations (deep rapid breathing) to blow off the carbonic acid.
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How Diabetic ketoacidosis Develops
Without sufficient insulin, the cells can’t use glucose for energy. The body, sensing this energy decrease, begins to release and break down its stores of fat. Lipolysis creates glycerol and fatty acids. Glycerol is converted into glucose, and the liver converts fatty acids to ketone bodies. As ketone bodies accumulate, metabolic acidosis develops.
As a last resort, the body begins breaking down protein to create glucose for energy. This increases circulating glucose and nitrogen. In the ongoing absence of available insulin, however, glucose can’t enter the cells, and the blood glucose level continues to rise. Eventually, the blood glucose level rises to between 300 and 800 mg/dl.
The increase in blood glucose level and ketone bodies leads to a severe loss of water and electrolytes. The kidneys respond to the increase in circulating glucose by increasing the glomerular filtration rate. As the body tries to remove the excess glucose, urine output climbs. In many cases, it reaches 5 to 8 liters a day.
This excessive diuresis results in a loss of sodium, potassium, chloride, bicarbonate and, to a lesser degree, magnesium and phosphate. As sodium and bicarbonate are lost because of osmotic diuresis, acidosis develops. Acidosis leaves the rising level of carbonic acid (a by-product of ketosis) unchallenged. To compensate, the patient develops Kussmaul’s respirations (deep rapid breathing) to blow off the carbonic acid.