By Annette R. Karnash, R.N., M.N.
Two life threatening acute metabolic complications of diabetes that require immediate medical attention are Diabetic Ketoacidosis (DKA) and Hyperglycemic Hyperosmolar Nonketotic Coma (HHNC). Acute insulin deficits and increased levels of blood glucose precipitate these complications.
Diabetic Ketoacidosis occurs most often in patients with type I diabetes and may be the first evidence of disease. The causes can be: (1) illness, (2) infection – most often viral, mumps, rubella or adenovirus, (3) physical or emotional stress, which can cause prolonged elevation in stress hormone levels of cortisol, glucagon, epinephrine or growth hormone, which in turn raises the blood glucose and increases demands on the pancreas, (4) hormones or drugs that may inhibit the release of insulin and (5) failure to take insulin or with patients on the pump – pump failure or insulin leakage.
Hyperglycemic Hyperosmolar Nonketotic Coma (HHNC) occurs primarily in type 2 diabetics, but also in those undergoing a stressed insulin tolerance, hemo- and peritoneal dialysis, tube feedings, or total parenteral nutrition (TPN).
Because there is inadequate insulin, glucose is unable to enter the fat and muscle cells to be converted into heat and energy. Glucose therefore accumulates in the blood causing the blood sugar to rise. Consequently, the liver, recognizing the cells are starved of energy, converts the stored glycogen to glucose and releases it into the blood, causing the blood glucose to rise to an even higher level. When the blood glucose exceeds the renal threshold, glycosuria results – higher in HHNC than in DKA because blood glucose levels are higher in HHNC.
Because the insulin deprived cells are still unable to utilize the glucose, protein is rapidly metabolized, causing the loss of intracellular potassium and phosphorus and the liberation of an excess amount of amino acids, which are then converted into urea and glucose by the liver. Once again the glucose levels in the blood become profoundly elevated causing high levels of glycosuria and serum osmolarity, leading to osmotic diuresis.
Dehydration, with fluid and electrolyte imbalance results, due to the vast volume of fluid loss from osmotic diuresis. Water loss, far greater than the loss of glucose and electrolytes, contributes to hyperosmolarity, which perpetuates dehydration, thus reducing the rate of glomerular filtration and the amount of glucose excreted in the urine. This leads to a deadly cycle. Diminished glucose excretion further raises the blood glucose, producing hyperosmolarity, dehydration that can continue into shock, coma and even death.
In DKA, to obtain energy, cells convert fats into glycerol and fatty acids because of the insulin deficiency. Fatty cells begin to accumulate in the liver, where they are converted into ketones, because they are unable to be metabolized as fast as they are released. Acidosis, resulting from the buildup of ketones in the blood and urine, leads to the breakdown of tissue, additional ketosis and acidosis and ultimately shock, coma and death.
The same basic principles are used to treat these complications; rehydration, electrolyte replacement, restoration of Insulin/glucose ration, and prevention/treatment of circulatory collapse. In the treatment of DKA, insulin is the key, whereas in HHNC, water is the key. Diagnostic procedures to identify and plan the treatment for these conditions are similar, with differences in the frequency performed.
