aki Flashcards
aki consequences
increased mortality (over double)
cost
increased length of hospital stay
increased creatinine
def of aki
abrupt (<48hrs) reduction in kindye function defined as
- absolute increase in serum creatinine by > 26.4 micrmol/l
OR increase in creatinine by >50%
OR reduction in UO
can only be applied following adequate fluid resuscitation & exclusion of obstruction
KDIGO staging classification
risk factors for AKI
older age
ckd
diabetes
cardiac failure
liver disease
pvd
previous aki
risk faCtors - exposure
hypotension
hypovolaemia
sepsis
deteriorating NEWS
recent contrast
exposure to certain meds
causes of aki
pre renal (functional)
renal (structural)
post renal (obstructional)
pre-renal aki causes
HYPOvolaemia
- haemorrhage
- volume depletion (e.g D&V, burns)
HYPOtension
- cardiogenic shock
- distributive shock (e.g. sepsis, anaphylaxis)
renal hypoperfusion
- NSAIDs / COX-2
- ACEi / ARBs
- hepatorenal syndrome
pre renal aki
reversible volume depletion leading to oliguria & increase in creatinine
normal urine output
- 0.5ml/kg/hr
- 30mls/hr if 60kg or 50mls/hr if 100kgs
oliguria
- <0.5mls/kg/hr
renal perfusion
kidneys are 0.5% of body weight
kidneys receive 20% CO
untreated pre renal AKI leads to ______
acute tubular necrosis
acute tubular necrosis
comment form of aki in hospital
due to a combination of factors leading to decreased renal perfusion
common causes include sepsis and severe hydration
other important causes include rhabdomyolysis and drug toxicity
treatment of pre renal aki
assess for hydration
- obs (BP, HR, UO)
- jvp, cap refill, oedema
- pulm oedema
fluid challenge for hypovolaemia
- crystalloid (0.9% nacl) or colloid (gelofusin)
- DO NOT USE 5% dextrose
- give bolus of fluid then reassess and repeat as necessary
- if > 1000mls IN and no improvement, seek help
renal aki
diseases cauasing inflammation or damage to cells causing aki
split by structure
- blood vessels
- glomerular disease
- interstitial injury
- tubular injury
causes of renal aki
- vascular
- vasculitis, renovascular disease - glomerular
- glomerulonephritis - interstitial nephritis
- drugs
- infection (TB)
- systemic (sarcoid) - tubular injury
- ischaemia (prolonged renal hypoperfusion)
- drugs (gentamicin)
- contrast
- rhabdomyolysis
signs & symptoms aki
- non specific
- constitutional (anorexia, weight loss, fatigue, lethary)
- N&V
- itch
- fluid overload (oedema, sob) - signs
- fluid overload (inc HTN, oedema, pulm oedema, pleural & pulm effusions)
- uraemia incl itch, pericarditis
- oliguria
clues to renal cause
- hx (sore throat, rash, joint pains, d&v, haemoptysis)
- urinalysis
- drug chart
- recent contrast
- blood results (eosinophilia, ck)
- vascular bruits
aki initial invstgns
- U&Es (high K?)
- FBC & coag screen (clotting, Hb)
- urinalysis (haematoproteinuria)
- uss (obstruction size?)
- immunology (ANA, ANCA, GBM)
- protein electrophoresis & BJP (myeloma)
further treatment of aki
- good perfusion pressure (fluid resus, if still not adequte BP - inotropes/vasopressors)
- treat underlying cause (ABs if sepsis)
- stop nephrotoxics
- dialysis if anuric & uraemia (can require urgent dialysis)
life threatening comps of aki
- hyperkalaemia
- fluid overload (pulm oedema)
diuretics dont work help!! - severe acidosis (ph<7.15)
- uraemic pericardial effusion
- severe uraemia (ur > 40)
post renal aki (obstruction)
aki due to obstruction of urine flow leading to back pressure (hydronephrosis) and loss of conc ability
obstruction causes
stones, cancers, strictures, extrinsic pressure
treatment post renal
relieve obstruction
- catheter
- nephrostomy
- refer to urology if ureteric stenting required
hyperkalaemia values and assessment
> 5.5
life threating = >6.5
ECG or muscle weakness
ECG hyperkalaemia
peaked T waves, flattened P wave, prolonged PR interval, depressed ST segment, peaked T wave, atrial standstill, prolonged QRS duration, further peaking T waves, sine-wave pattern
