Acute Kidney Injury Flashcards
When is a patient in AKI?
When there serum creatinine rises by 26micromol/L in 48 hours or by 50% over 7 days
urine output may fall below 0.5ml/kg/hour for more than 6 hours
This is AKI stage 1
When is a patient in AKI stage 2
when serum creatinine is 2-2.9 greater than baseline and bring output is below 0.5ml/kg/hour and is maintained for more than 12 hours.
When is a patient in AKI stage 3
When there serum createnine is >3 times baseline or has reached 354micromol/L or the patient needs dialysis. AKI staged three can also be characterised by a urine output of <0.3ml/kg/hour for more than 24 hours or no urine at all for 12 hours.
AKI can be pre - renal. What does this mean and how is it caused and treated?
Renal perfusion
This could be due to haemorrhage, dehydration, hypovolaemia, heart failure, drugs (NSAIDS, ACE-I, ARBS)
Removal of nephrotoxic drugs and hydration can lead to recovery.
AKI can be post-renal. What does this mean and how is it caused and treated?
Outflow obstruction
This could be due to stones, prostatic hypertrophy & tumours
This will resolve once the kidney can be drained, by catheter or nephrostomy tube.
Intrinsic AKI is due to….
acute interstitial nephritis
direct damage to the kidney - due to drugs or toxic processes within the body including immunological problems, rhabdomyolysis, prolonged uraemia from other causes of AKI.
Try to rectify the cause of the AKI.
symptoms of AKI
unwell oliguric - reduced urine flow anuric - no urine flow hypotensive - if dehydrated hypertensive - if overloaded
How is AKI prevented?
Maintaining hydration
Treat infections
Good nursing of vital signs, fluid input and output
avoidance of nephrotoxic drugs unless essential and then
Used only with careful monitoring.
What should systolic BP be to maintain renal perfusion?
> 110mmHg
if overloaded loop diuretics may be used
but if they don’t work then they need to be stopped as patient will become toxic. The kidney is temporarily incapable of producing fluid output.
Management of AKI essentially covers three areas
1) Identification of cause and deal with it
2) Removal of nephrotoxic drugs
3) maintain fluid and pH homeostasis, management of biochemical derangements especially hyperkalaemia.
ACE’s, ARB’s and NSAIDs effect the kidney how
they impair the perfusion of the kidney and should be withheld.
ACE/ARB will increase potassium even when pre-renal hypoerfusion is not the cause of the AKI.
is eGFR/CrCL accurate in AKI?
No
Can we give full dose ABx in AKI?
Yes - may be the infection causing the AKI
Does AKI have a high or low mortality rate?
High
what is the prevalence of the causes of AKI?
80% pre renal and tubular necrosis
10% intrinsic
10% post renal
post renal causes of AKI include
BPH
prostate cancer
retroperitoneal fibrosis
renal calculi
intrinsic causes of AKI include (damage to the functional tissues of the kidney)
- acute interstitial nephritis (cause by hypersensitivity reaction and often drug induced)
- myeloma
- immunological renal disease including vasculitis and glomerulonephritis
- rhabdomyolysis
signs of hypovolaemia include
reduced jugular venous pressure
reduced central venous pressure
reduced BP
increased HR
sings of hypervolaemia include
raised jugular venous pressure raised central venous pressure raised HR increased of decreased BP reduced oxygen saturation increased RR
Risk factors for AKI include
Age
Long-term disease (CKD, DM, HF, Liver, vascular)
Surgical procedures
Medication
Points about NSAIDS
- They inhibit prostaglandin synthesis
- They cause proteinuria
- They should be avoided in patients with AKI
- They can cause interstitial nephritis
Causes of intrinsic AKI include
myeloma
rhabdomyolysis
vasculitis
Medicines known to cause acute tubular necrosis include
calcineurin inhibitors
ciprofloxacin
aciclovir
