Hypoglycemia Flashcards
reduced metformin clearance is worsened by
lactic acidosis, metabolic acidosis, renal impairment (AKI), poor perfusion
what is the relationship between metformin clearance and creatinine clearance?
proportionally decrease
metformin toxicity symptoms
non-specific
ab pain, N/V, malaise, myalgia
blindness, hypothermia, hypotension, respiratory insufficiency
mechanisms of metformin metabolic acidosis
- interfere with cellular aerobic metabolism by inhibiting ETC, thus shifting to anaerobic metabolism –> lactic acidosis
- suppresses hepatic gluconeogenesis from pyruvate, decreases hepatic pH and lactate uptake –> lactic acidosis
metformin toxicity treatment
ABCDs, vasopressors, fluids
Extracorporeal treatment (intermittent hemodialysis preferred)
When is extracorporeal treatment recommended for metformin toxicity?
- lactate concentration > 20 mmol/L
- pH =< 7
- failure of standard supportive measures
- comorbid conditions - shock, liver/kidney failure, decreased consciousness
How long should ECTR be done?
until lactate conc < 3 mmol/L
AND
pH > 7.35
insulin toxicity management
initial bolus (D10W at 75 mL/hr and titrate)
maintenance infusion (D5W or D10W)
how to proceed transitioning off dextrose in insulin toxicity management?
consider measuring C-peptide (bc insulin will not be accurate)
or trial octreotide
target BG range for maintaining euglycemia
100-150 mg/dL
when to consider central venous access
- dextrose conc greater than or equal to D10W
- large volume administrations
what to monitor for peripheral
glucose every 30 min to 1 hr initially, then less frequently
serum phosphate levels
serum potassium levels
maximum peripheral dextrose concentrations (IV bolus)
adult = D50W
children = D25W
infants = D10W
which hypoglycemia causing agents are highly protein bound and cannot be removed via dialysis?
sulfonylurea (glimepiride, glipizide, glyburide)
sulfonylurea MoA
- inhibit K+/ATP channels on beta cells –> prevents efflux of K
- cellular depolarization
- calcium influx via opening of Ca channels
- insulin release
how does sulfonylurea toxicity cause prolonged hypoglycemia?
long duration of action causes prolonged cell depolarization, thus prolonged insulin release
in sulfonylurea toxicity, how long is the delayed onset of hypoglycemia
1st gen = up to 48 hrs
2nd gen = up to 24 hrs
sulfonylurea toxicity: further insulin release after dextrose infusion can cause
rebound hypoglycemia
sulfonylurea toxicity causes failure of counterregulatory mechanisms such as
adrenalin, cortisol, growth hormone, glucagon
sulfonylurea toxicity management
ABCDs, activated charcoal, dextrose (only for correction), octreotide (for maintenance)
octreotide MoA
mimics somatostatin, inhibits release of insulin, glucagon, secretin, motilin by decreasing cytoplasmic calcium
octreotide dosing
50 mcg as single dose SUBQ/IV
repeatable every 6 hours
octreotide dosing for refractory hypoglycemia
continuous infusion up to 125 mcg/hr
when to use octreotide
when euglycemic and high risk for prolonged, delayed, or rebound hypoglycemia
