Insulin Deficiency is the primary defect in patients with DKA
Breakdown of storage forms of energy to meet energy needs. (Catabolism)
Gluconeogenesis (from amino acids, lipids)
Glucagon unopposed by Insulin stimulates this catabolic reaction
Skeletal and cardiac tissues are able to use free fatty acids and ketone bodies as an energy source.
Glucose can not be used by these tissues in the absence of insulin.
The brain is an insulin-independent tissue and continues to use available glucose.
Hyperglycemia is worsened by further intake of glucose.
Excess Ketone bodies from Lipolysis
Ratio of hydroxybutyrate (BHB)/Acetoacetate (AA) normally 3:1 is driven to 15:1 in severe DKA
Hyperglycemia acts as an osmotic diuretic with obligatory loss of water and electrolytes.
Ketosis/hyperglycemia stimulate vomiting with aggravation of dehydration
Hypovolemia secondary to dehydration can promote decreased tissue perfusion with anaerobic metabolism and elevated lactate production
Total fluid deficit in severe DKA usually averages around 10% of the total body weight
Clinical Findings in DKA
Polyuria, Polydipsia, Polyphagia
Dehydration + orthostasis
Küssmaul respiration if pH < 7.2
Temperature usually normal or low, if elevated think infection!
Abdominal pain present in at least 30%.
Clinical Findings of Hyperosmolarity
Hyperosmolar coma is the first sign of diabetes in 50-60 % of adult patients.
Hyperglycemia usually > 700-800mg/dl
Osmolarity above 340 mOsm/L is required for coma to be present.