![]() ![]() Potassium is variable based on the degree of acidosis and the time of presentation of the DKA.ĭKA usually occurs quickly, over hours to days. Sodium tends to be low secondary to the fact that glucose is osmotically active and will draw fluids into the extracellular space. Many of the other symptoms may result from the pro-inflammatory state of DKA, and elevated cytokines have been documented during diabetic ketoacidosis. Polydipsia results from the hyperosmolarity after osmoreceptors are triggered in the brain. Water losses are typically greater than electrolyte losses, and thus there is an increased serum osmolality. However, the expansion of the extra-cellular compartment is short lived as the ability to reabsorb glucose at the level of the renal tubule is limited and osmotic diuresis occurs. Elevated blood glucose shifts water into the extracellular compartment. Many of the remaining problems with DKA are from the resultant osmotic diuresis. Furthermore, with the pre-renal azotemia that ensues, there is retention of other acids besides ketoacids. Because of this buffering, there is an increase in unmeasured anions that cause a gapped metabolic acidosis. Increased ketone production results in the attempt for the body to buffer with bicarbonate. Symptoms of ketosis include nausea, vomiting, abdominal pain, and respiratory insufficiency. In HHNK, blood sugars are usually higher as ketoacidosis produces more severe symptoms and presentation is usually earlier. Conversely, in HHS there is usually enough insulin to suppress ketogenesis, but not control blood sugars. Unfortunately, with ketone overproduction, peripheral tissues cannot utilize these molecules and ketosis predominates. These free fatty acids are then transported across the mitochondrial membrane, and they are eventually used for synthesis of ketones, namely in the form of acetoacetic acid, which is oxidized to form betahydroxybutyrate or decarboxylated to form acetone. Also, glucagon itself will stimulate hormone-sensitive lipase, which in turn mobilizes adipose stores and converts triglycerides to free fatty acids. ![]() Thus there is both overproduction and underutilization of ketones in an insulin-deficient state. Insulin also increases oxidation of ketones in the peripheral tissues. Insulin will inhibit lipolysis and oxidation of free fatty acids. Insulin is normally the most important regulator in production and utilization of ketones. While elevated blood glucose from the increased glycogenolysis and gluconeogenesis is certainly a major problem, the cornerstone of DKA lies in ketogenesis. In a stressed state, such as infection, myocardial infarction, intoxication, pregnancy, or stroke there is an increased demand for insulin, but a diminished supply by the stress put on the pancreas. Growth hormone also has a similar role as epinephrine and cortisol. Epinephrine acts to block the action of insulin and stimulates the release of glucagon. In a so-called “stressed state,” there is a relative abundance of epinephrine and cortisol. Moreover, the risk of DKA increases with any increased stress state. The situation is complicated by the fact that in this more catabolic state there is breakdown of proteins to form new amino acids that in turn are used to build glucose. To add to the overall hyperglycemic state, there is also a concomitant decreased utilization of glucose in peripheral tissues. With the lack of insulin, there is decreased storage of glucose, increased breakdown of glycogen stores, and increased synthesis of glucose in both the liver and kidney. In diabetic ketoacidosis (DKA), the balance between catabolism and anabolism is, in a sense, broken. This is a catabolic state, which allows for sustenance in times when nutrition is not available. Conversely, in a state of starvation, there is an increase in counter regulatory hormones such as glucagon in which stores are appropriately mobilized and glucose production increased. With this surge of insulin, the production of new glucose is suppressed appropriately. Normally, with elevated blood glucose, as occurs after a digested meal, there is production and release of insulin by the beta cells in the islets of Langerhans. Both of the crises result in subsequent glucagon and counter-regulatory hormone excess from lack of suppression from insulin. ![]() ![]() Diabetic ketoacidosis primarily results from insulin deficiency and hyperglycemic hyperosmolar state (HHS) from severe insulin resistance. There are ~120,000 admissions for diabetic ketoacidosis and hyperglycemic hyperosmolar state per year in the United States alone. There are two major hyperglycemic crises associated with diabetes: diabetic ketoacidosis and the hyperosmotic hyperglycemic state. ![]()
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