Acute Kidney Injury Flashcards

1
Q

When is a patient in AKI?

A

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

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2
Q

When is a patient in AKI stage 2

A

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.

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3
Q

When is a patient in AKI stage 3

A

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.

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4
Q

AKI can be pre - renal. What does this mean and how is it caused and treated?

A

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.

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5
Q

AKI can be post-renal. What does this mean and how is it caused and treated?

A

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.

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6
Q

Intrinsic AKI is due to….

A

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.

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7
Q

symptoms of AKI

A
unwell
oliguric - reduced urine flow
anuric - no urine flow
hypotensive - if dehydrated
hypertensive - if overloaded
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8
Q

How is AKI prevented?

A

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.

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9
Q

What should systolic BP be to maintain renal perfusion?

A

> 110mmHg

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10
Q

if overloaded loop diuretics may be used

A

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.

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11
Q

Management of AKI essentially covers three areas

A

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.

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12
Q

ACE’s, ARB’s and NSAIDs effect the kidney how

A

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.

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13
Q

is eGFR/CrCL accurate in AKI?

A

No

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14
Q

Can we give full dose ABx in AKI?

A

Yes - may be the infection causing the AKI

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15
Q

Does AKI have a high or low mortality rate?

A

High

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16
Q

what is the prevalence of the causes of AKI?

A

80% pre renal and tubular necrosis
10% intrinsic
10% post renal

17
Q

post renal causes of AKI include

A

BPH
prostate cancer
retroperitoneal fibrosis
renal calculi

18
Q

intrinsic causes of AKI include (damage to the functional tissues of the kidney)

A
  • acute interstitial nephritis (cause by hypersensitivity reaction and often drug induced)
  • myeloma
  • immunological renal disease including vasculitis and glomerulonephritis
  • rhabdomyolysis
19
Q

signs of hypovolaemia include

A

reduced jugular venous pressure
reduced central venous pressure
reduced BP
increased HR

20
Q

sings of hypervolaemia include

A
raised jugular venous pressure
raised central venous pressure
raised HR
increased of decreased BP
reduced oxygen saturation
increased RR
21
Q

Risk factors for AKI include

A

Age

Long-term disease (CKD, DM, HF, Liver, vascular)

Surgical procedures

Medication

22
Q

Points about NSAIDS

A
  • They inhibit prostaglandin synthesis
  • They cause proteinuria
  • They should be avoided in patients with AKI
  • They can cause interstitial nephritis
23
Q

Causes of intrinsic AKI include

A

myeloma
rhabdomyolysis
vasculitis

24
Q

Medicines known to cause acute tubular necrosis include

A

calcineurin inhibitors
ciprofloxacin
aciclovir

25
Q

Pre-renal AKI

A
  • responds to fluid administration
  • can be cause by laxative abuse
  • can be differentiated from intrinsic causes of AKI through urinalysis
26
Q

Points about loop diuretics

A
  • gut oedema can reduce their absorption
  • if high doses do not induce diuresis in fluid-overloaded patients they should be stopped
  • they can cause interstitial nephritis
27
Q

CANDA stands for

A

Contrast media

ARB/ACE

NSAIDS

Diuretics

Aminoglycosides

28
Q

CRCL is reduced in

  • pregnancy
  • AKI
  • cachetic patient (muscle waste)
A

True