DKA Flashcards
DKA
DKA =
DM (usually type 1) + ↑↑↑gluc + ↓insulin + ↑ketones.
DKA pts ∼100 ml/kg fluid depleted.
DKA
ASAP:
ABCs, 2 LB IVs, O2, monitor, VS
DKA
DKA Hx:
Polyuria, polydipsia, fatigue, N/V, abd pain, HA/AMS; prev DKA / EtOH / AKA; meds
DKA
The 7 I’s (causes):
Infection
Ischemia
Intoxication
Infraction/intolerance- not taking insulin, insulin pump problem
Iatrogenic - steroids, surgery
Initial Presentation
Impregnation
DKA
Physical:
Dry, ↑HR, ↑RR (compensation for acidosis), Kussmaul resp (deep rapid breathing), lethargy, abd ttp, acetone odor
DKA
Labs:
Labs: Accu✓, VBG w lytes, CBC, BMP, Ca/Mg/Phos, ketones, lactate, lipase, LFTs, blood cx; UA w cx, hCG; CXR, ± EKG (for ↑K or ischemia)
DKA
Flowsheet:
q 1 hr VS, BMP, strict I/Os; q 4 h Ca, Mg, Phos
DKA
Treatment Fluids :
NS bolus, then NS 1-2 ml/kg/hr (or 20 mL/kg in peds) add Dextrose once gluc < 250 mg/dl. can switch to ½ NS.
→ NS causes non anion-gap hyperchloremic metabolic acidosis. Can cause already low bicarb to decrease. Consider using LR instead.
DKA
Treatment Insulin :
-0.1 u/kg/hr. Change to SC insulin when AG closed, tol PO, and pH > 7.2 (2 hr overlap required).
-Hold if K < 3.5; do not drop gluc > 100 mg/dl/hr. No bolus in peds.
→ Consider starting long acting insulin early
DKA
Treatment Electrolytes :
Electrolytes:
“K+: add 20-40 mEq/L to IVF til K > 4.5 K (corr) = expect drop of 0.6 mEq per 0.1 pH of acidosis (hypo K = #1 cause of death) (insulin and correcting acidosis will shift K into cell)
Phos: replete if < 1.0
Na (corr) = add 1.6 per 100 of gluc > 200
Bicarb: unless pH <7 or concomitant lactic acidosis and refractory hypotension
→ Consider isotonic bicarb infusion when ketoacidosis almost fixed. Especially if have low bicarb.
Predicted bicarb = Na -Cl - 10”
DKA
Treatment if Cerebral Edema :
S/Sx: HA/AMS, N/V, papilledema, sz
Rads: Head CT
Tx: Mannitol 1 g/kg IV, Intubate PRN (CE risk fx: kids and severe lab abnormalities)
DKA
Pathology:
acetoacetate,beta-hydroxybutyrate, acetone. can only detect acetoacetate. in vol deficient shifts to beta
Insulin deficiency (secretion or production) and elevated counter-regulatory hormones → decreased cellular uptake, increased liver
gluconeogenesis and lipolysis → hyperglycemia, anion-gap metabolic acidosis, ketonemia