Diabetic Coma: The Lurking Danger
Diabetic patients can suffer different types of comas. The most common, insulin shock develops rapidly and is the result of an excess of injected insulin or other sugar-lowering medication that causes a depletion of blood sugar (hypoglycemia). Another type of coma results from inadequate insulin, which leads to too much blood sugar (hyperglycemia) and a build-up of toxic substances called ketoacids (ketoacidosis) in the blood.
Diabetic coma is loss of consciousness, an extremely dangerous condition, which is the result of severe mismanagement of food and liquid intake. This can occur in individuals with diabetes unless proper care is not taken in controlling the diet and subsequent blood sugar control.
As mentioned above, 3 different types of comas are associated with diabetes, namely the ketoacidotic, the hyperosmolar, and the hypoglycemic coma. The ketoacidotic coma is more prevalent in Type1 diabetic patients than in those with Type2. Similarly the possibility of occurrence of hypoglycemic coma is more in those patients using insulin for blood sugar control. The hyperosmolar coma occurs primarily due to excessive loss of fluids from the body.
Ketoacidotic coma occurs when the body is in ketosis. Ketosis is the condition where excessive ketone (toxic substance) bodies are in circulation in the blood. This occurs when the body utilizes excessive fat instead of carbohydrates for the primary energy requirements and leads to a lowering of blood PH .
Basically ketoacidotic coma occurs when the metabolic focus shifts away from the use of glucose for energy. The brain cannot function properly in such a situation and goes into coma, which could be life threatening. Dehydration, brain cell starvation and an unbalanced blood PH are all potential risk factors that can trigger a ketoacidotic coma.
Hyperosmolar coma occurs when the body loses unusual amounts of fluid due to excessive amounts of glucose in the blood. If the diabetic person misses his regular insulin shot, or increase food intake without adequate exercise, the blood glucose level shoots up dangerously high. Responding to the crisis situation, the kidneys pull out glucose, sodium, and other molecules out of the circulating system in an attempt to stabilize the blood sugar levels. These different molecules are pushed out of the body along with large quantities of water by means of urination.
Rapid dehydration is the next stage in diabetic hyperosmolarity (a condition where blood has excessively high concentrations of sodium, glucose, and other molecules due to the excessive loss of water in diabetes). It has to be kept in mind that the diabetic person is unable to adequately rehydrate himself or herself. This is mainly due to the increasing rate at which the dehydration of the body occurs. Unless intravenous (IV) fluids are administered quickly massive cell damage can result. Complicating the situation, the brain shuts down at this critical juncture and creates a life-threatening situation.
Hypoglycemic coma is the loss of consciousness, which occurs as blood glucose falls significantly below normal levels. This condition is prevalent in people who need close glucose monitoring and insulin intake. Hypoglycemic coma occurs when large amount of insulin is injected and is not balanced by the amount of glucose in the blood. Consequently, glucose levels fall rapidly as cells absorb all available sugars leading to brain cell starvation, the precursor of coma.
Usual symptoms of insulin shock are tremors, palpitations, sweating and excessive hunger. For counteracting extreme hypoglycemic reactions, a swift dose of glucagon is beneficial. Glucagon stops the insulin reaction occurring within the body by rapidly increasing the blood glucose levels. Intravenous administration of glucose would also help in counteracting the effects of severe insulin shock. Experts are of the opinion that oral medication should not be administered when a person is in a comatose state. Immediate medical assistance can significantly reduce the risk of serious damage.
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Modified : Oct 16, 2002. |
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