DKA and HHS Flashcards
DKA and HHS
2 of the most serious acute complications of DM
DKA = ketoacidosis and hypergly, <800, 350 - 450 (earlier tm)
HHS = more severe hypergly w/o ketoacidosis, >1000
rf: DKA
<65, type 1, type 2 under extreme conditions (bc still make insulin; infection, trauma, CV)
tend to be younger and have higher GFR (greater capacity to excrete glucose), often present earlier with s of ketoacidosis (SOB, abd pain, n/v) rather than hyperosmol
rf: HHS
mostly type 2
>65
normal response to hypergly
extracellular gly [] regulated by insulin and glucagon
glucose -> pancreas -> insulin release
insulin diminishes hepatic glucose production
glycogenolysis and gluconeogenesis decrease
also increase uptake by skeletal muscle and adipose tissue
glycogenolysis
glycogen -> glucose
gluconeogenesis
non carb (lactate, AA, glycerol) into glucose
hypergly patho
insulin def and/or resistance (decreased net effective action to insulin)
DKA > HHS
DKA = decreased secretion; dehydrated and e abn bc osmotic diuresis from glycosuria
HHS = ineffective insulin
glucagon excess
DKA patho
increased gluconeogenesis, lipolysis, ketogenesis, decreased glycolysis
hypergly patho: other factors
increased catecholamines, increased cortisol
increased hepatic glucose production, impaired glucose utilization in peripheral tissues
glucosuria
initially decreased rise in serum glucose via osmotic diuresis -> v depletion and decreased GFR, limits further glucose excretion (more pronounced in HHS)
ketone production
insulin def and resistance: cant get glu into cells, so use fat for E -> enhanced lipolysis in DKA
lipolysis of peripheral fat stores releases free FA and glycerol
FA transported to liver (hepatocytes) -> activated
activated FA converted to acetyl coa and enter ketogenic met -> ketone bodies
ketone bodies accumulate -> decrease pH (met acidosis)
not with HHS bc sufficient insulin to decrease lipolysis but not enough to block gluconeogenesis
anion gap met acidosis
DKA typically presents with increased anion gap (differences btw - and + ions Na-Cl and bicarb) from production and accumulation of ketones (B hydroxygutyrate - main met product of ketoacidosis)
severity of acidosis and increase of anion gap factors
rate and duration of ketoacid production
rate of metabolism of ketoacids
rate of loss of ketoacid anions in urine -> depend on V status and renal function: increase when treated w/ isotonic fluids to correct hypovol
plasma osmol and Na
higher with HHN
always elevated
hypergly -> pull H2O out of cells, expand ecf, decreased plasma Na (dilutional hypoNa)
Na, K, H2O loss w/ glycosuria
K
both present with hypoK: GI losses, increased urinary loss (with normal kidney function)
serum K normal d/t hyperosmol and insulin def: H2O out of cells, insulin normally promotes K uptake -> may be hyperK initially, only treat if s/s
w/ correction: H ions out of cell, K in
cellular compensation: DKA
increase in H [] seen with acidosis: H in, K out, neutral, temp correction of pH
process will reverse with normalization of pH: but, if kidneys working, they will excrete K -> can have depletion
precipitating factors
infection w/o insulin adjust
acute major illness or inflam process -> MI, CVA, sepsis, pancreatitis
new onset type 1
drugs that affect carb met (glucocorticoids, thiazide diuretic)
SGLT2I: type 2 but also off label type 1
cocaine or substance abuse
poor compliance with insulin regimen or faulty SQ infusion device -> run A1C
DKA cm
rapid onset over 24 hrs
polyuria, polydipsia
GI: n/v, abd pain (delayed gastric emptying or ileus from met acidosis
may have neuro s/s -> obtunded (severe acidosis)
v depletion: decreased turgor, dry oral mucosa, tachy, hypoT, decreased UO
fruity breath (exhaled acetone - nail polish remover)
kussmal resp -> deep resp, comp hypervent
HHS: cm
higher mortality
insidious (several days): polyuria, polydipsia, weight loss
as glu continues to increase, more common neuro s/s bc increased hyperosmol: lethargy, obtunded, coma
s of v depletion similar to DKA
tm
replace fluids 1st bc need renal function and to pee out excess, CV collapse, worse in elderly
fluids expand ecf, hemodynamic stability, 0.9 NS
correct e imbalance -> K, replace ~4, replace before insulin bc insulin will drive back into cells
insulin infusion
Na bicarb if DKA w acidosis (<7.2), difficulty breathing
dextrose may be added when <200 if anion gap still present: DKA
resolved
DKA: anion gap closed, ketoacidosis resolved
HHS: mentally alert, plasma osmol 315
pt can eat and transition back to SQ insulin
