DKA

Initial eval glucose, BMP, CBCd, serum osm, UA/ketones, serum ketones, ABG, EKG o then BS q1, BMP q2-4, venous pH q2-4 Therapy o Fluid replacement expand intravascular volume and restore renal perfusion, correct hyperosmolar state (average 6L down) Correct initially with NS aim to correct fluid deficit in 1st 24 Replace K+ when levels ~4.5 change to NS as KCL is osmotically active Change to D5NS when BS<250 until AG closes insulin needed to fix AG o Insulin hepatic glucose production, ketone production by lipolysis & glucagon secretion, & augment ketone utilization (insulin deficitlipolysisrelease of ketonesAG) 0.1 unit/kg/ drip initially (no bolus) Goal fall in BS > 50-70 in 1st hour Decrease drip rate when BS <200 Overlap SQ therapy 1-2 prior to d/c drip o Bicarb (controversial) if pH <7.0 o Phosphate if serum <1.0 mg/dL (may be harmful if higher) Initially normal or elevated d/t movement of phosphate out of cells Creatinine is elevated out of proportion to decrease in GFR b/c acetoacetate artifactually increases measured creatinine in the assay All patients develop NAGA after resolution of ketoacidosis (unless advanced CKD) o Bicarb goes to replace bone and buffer stores, therefore NAGA o Ketoacid anions disappear with correction of AG, however, ketonemia and ketonuria persist ~36 d/t slower removal of acetone Potassium o Renal loss from glucose osmotic diuresis + hypovolemia-induced hyperaldosteronism o Cellular shifts out of cell d/t insulin deficit + hyperosmolality, but insulin causes rapid movement back into cells therefore K+ Sodium o Corrected serum Na+ = measured Na+ + (1.6x every 100 BS over 150) o Elevated serum osm (glucose) results in water movement out of cells o After glucose corrected, water moves back into cells and [Na+] corrects ADA guidelines say may change insulin from gtt to SQ when: o BS < 200 o HCO3 > 18 o AG < 12 o Venous pH > 7.30