DKA/HHS Flashcards
hebenstreit
general pathogenesis
reduction of circulating insulin
elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, growth hormones)
pathophysiology of DKA
precipitating factors eventually leads to triglycerides –> glycerol and free fatty acids –> ketones
DKA – goals of treatment
restore circulatory volume
inhibit ketogenesis and return of normal glucose metabolism
correct electrolyte imbalances
DKA – IV insulin initiation
start 0.1 units/kg/hour +/- a bolus of 0.1 units/kg
DKA – IV insulin continuation
when plasma glucose reaches 200 mg/dL
- decrease infusion rate to 0.02 to 0.05 units/kg/hr
- change fluids from NS to 1/2 NS + D5W
- decrease fluid rate to 150 - 250 mL/hour
DKA – transitioning insulin
blood glucose level below 200 mg/dL AND need two of the following:
- anion group closes
- bicarbonate level above 15
- venous pH above 7.3
DKA – transitioning insulin in naive patient
start basal/bolus regimen of a TDD of 0.5 to 0.8 units/kg/day divided 50/50 between basal and bolus
DKA – transitioning insulin in insulin-dependent patient
add up total amount of IV insulin required by patient
convert to estimated daily requirement using basal/bolus or every 6 hours NPH insulin
DKA – transitioning insulin RULE
overlap IV and SQ by 2-4 hours to prevent rebound ketoacidosis and hyperglycemia
anion gap equation
Na - (Chloride + Bicarbonate)
anion gap closure
when under 12
can consider transitioning from IV to SQ insulin
when should insulin not be started?
when potassium is under 3.3 mmol/L
DKA – potassium
maintain a K of 4-5 mmol/L
anything above 5 is considered acidosis and needs to be corrected with fluids and insulin
euglycemic DKA
rare form of DKA where bg is normal/slightly elevated but still urine positive for ketones
may be caused by SGLT2 inhibitors
DKA symptoms
NV
abdominal cramps
dehydration
polys
AMS
coma
DKA patients
new diagnosis T1DM
non-adherence to insulin
possible infection