In general, the body is shifted into a major catabolic state with breakdown of glycogen stores, hydrolysis of triglycerides from adipose tissues, and mobilization of amino acids from muscle.
Diabetic ketoacidosis is an extreme metabolic state caused by insulin deficiency. Insulin deficiency stimulates the elevation of the counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). This type of hormonal imbalance enhances hepatic gluconeogenesis and glycogenolysis resulting in severe hyperglycaemia. Without the ability to use glucose, the body needs alternative energy sources.
Lipase activity increases, causing a breakdown of adipose tissue that yields free fatty acids. These components are converted to acetyl coenzyme A, some of which enter the Krebs cycle for energy production; the remainder are broken down into ketones (acetone, acetoacetate, and β-hydroxybutyrate).
This results in accumulation of large quantities of ketone bodies and subsequent metabolic acidosis. Ketones include acetone, 3-beta-hydroxybutyrate, and acetoacetate. The predominant ketone in diabetic ketoacidosis is 3-beta-hydroxybutyrate.
Diabetic ketoacidosis usually develops quickly, within 24 hours. Typically, patients develop polyuria and polydipsia along with vomiting, dehydration, and, if severe, an altered mental state, including coma. Signs of the underlying cause may also be present—for example, infection. Abdominal pain is a common feature of diabetic ketoacidosis and may be part of the acute episode or, less often, represent an underlying cause.
Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years.
The main causes of mortality in the adult population include severe hypokalaemia, adult respiratory distress syndrome, and co-morbid states such as pneumonia, acute myocardial infarction and sepsis.
Diabetic ketoacidosis: how it happened?
