Two life threatening acute metabolic complications of Diabetes, Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Non-ketotic Syndrome (HHNS), require immediate medical attention. Diabetic Ketoacidosis (DKA) is an acute complication of hyperglycemia that occurs most often in patients with type I diabetes and may be the fist evidence of disease. Acute insulin deficiency precipitates this condition, which can be caused by illness, infection - most often viral such as rubella, mumps, CMV and adenovirus, physical or emotional stress, which can cause prolonged elevation in stress hormone levels of cortisol, glucagon, epinephrine, and GH, which in turn raises the blood glucose and increases demands on the pancreas.
Hyperosmolar Hyperglycemic Nonketotic Syndrome occurs most often with type II diabetes, but can occur in those whose insulin tolerance is stressed and in those who have undergone certain procedures such as peritoneal dialysis, tube feedings or total parenteral nutrition (TPN). Acute insulin deficiency precipitates this condition as well and is caused by illness, infection and stress.
Inadequate insulin hinders the uptake of glucose by fat and muscle cells, resulthing in the accumulation of glucose by fat and muscle cells, resulting in the accumulation of glucose by fat and blood. The liver then responds to the demands of the energy-starved cells by converting glycogen to glucose and releasing it into the bloodstream. Consequently, the blood glucose level rises even further and when it exceeds the renal threshold, glycosuria results.
Because the insulin deprived cells are unable to utilize the glucose, protein is rapidly metabolized.
Intracellular potassium, phosphorus and excess liberation of amino acids, which are converted into glucose and urea by the liver, are lost. Glucose levels in the blood become grossly elevated causing an increased serum osmolarity and glucosuria, leading to osmotic diuresis. Because blood glucose is higher in HHNS than in DKA, glucosuria is higher in HHNS.
Fluids and electrolyte imbalance and dehydration can occur due to the vast volume loss of fluid from osmotic diuresis. Water loss, being far greater than the loss of glucose and electrolytes, contribute to hyperosmolarity, which perpetuates dehydration, reducing the amount of glucose excreted in the urine and decreasing the rate of glomerular filtration. This leads to a deadly cycle. A decreased excretion of glucose then raises the blood glucose, producing dehydration, hyperosmolarity, resulting in shock, coma and even death.
The absolute insulin deficiency found in DKA cause a further complication by converting the fat cells into glycerol and fatty acids to obtain energy. The fatty acids accumulate in the liver where they are converted into ketones because the can’t be metabolized as rapidly as they are released. Acidosis, which results in the accumulation of ketones in the blood and urine, lead to further tissue breakdown, additional acidosis and ketones and eventually shock, come and death.