15. AKI Flashcards

1
Q

What is AKI?

A

A rapid (within hours to days) fall in glomerular filtration rate (GFR) which impedes the kidney’s normal functions

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2
Q

how does the kidney work?

A

unfiltered blood in, filtered at glomeruli, filtered blood out

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3
Q

sites of filtration

A

bowman’s capsule 100% filtrate produced
proximal tubule 80% filtrate reabsorbed -active and passive reabsorption
Loop of henle - 6% of filtrate reabsorbed - H20 and salt conservation
Distal tubule - 9% of filtrate reabsorbed, variable reabsorption, active secretion
Collecting tubule - 4% filtrate reabsorbed, variable salt and H2O reabsorption

urine vol is 1% of total filtrate vol

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4
Q

AKI stage 1

A

Increase in serum creatinine of 26 micromol/litre or more within 48 hours
OR1.5 to 2-fold increase from baseline

Urine output less than 0.5 ml/kg/hour for more than 6 hours*

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5
Q

AKI stage 2

A

Increase in serum creatinine to more than 2 to 3-fold from baseline

Urine output less than 0.5 ml/kg/hour for more than 12 hours

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6
Q

AKI stage 3

A

Increase in serum creatinine to more than 3-fold from baseline
OR
Serum creatinine more than 354 micromol/litre with an acute increase of at least 44 micromol/ litre

urine output less than 0.3 ml/kg/hour for 24 hours or anuria for 12 hours

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7
Q

What is creatinine?

A

a normal, non-toxic product of muscle turnover
transported by blood and excreted by kidneys

Used as a surrogate marker for glomerular filtration.
Less filtration => less creatinine removed => a creatinine rise

GFR is estimated from creatinine results

creatinine ranges differ based on muscle mass, age, pregnancy

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8
Q

Oliguria

A

<0.5ml/Kg/Hour urine output

Usually <500ml/24 hours in adults

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9
Q

Anuria

A

Anuria
Officially would mean no urine output
Softly defined as <100ml/24 hours

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10
Q

AKI natural time course

A
Four Phases
Onset phase
Oliguric/Anuric phase
Polyuric/Diuretic phase
Recovery phase
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11
Q

Onset phase

A

Commonly triggered by significant blood loss, burns, fluid loss, diabetes insipidus.
Renal blood flow 25% of normal
tissue oxygenation 25% of normal
urine output below 0.5mL/kg/hr

Lasts hours to days

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12
Q

Oliguric (anuric) phase

A

urine output below 400mL/day, possible as low as 100mL/day
Increases in blood urea nitrogen (BUN) and creatinine levels
Kidney unable to excrete water so:
Electrolyte disturbances, acidosis, and fluid overload

Lasts 8 to 14 days or longer depending on the AKI itself and initiation of dialysis

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13
Q

Diuretic phase

A
occurs when cause of AKI is corrected
renal tubule scarring and oedema
increased GFR
Daily urine output above 400mL
possible electrolyte depletion from excretion of more water and osmotic effects of high BUN

lasts 7 to 14 days

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14
Q

Recovery phase

A

decreased oedema
normalisation of fluid and electrolyte balance
return of GFR to 70% or 80% of normal

Several months to 1 year

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15
Q

Normal kidney functions

A
Excretion of toxins – urea etc
Electrolyte balance – Na+/K+ etc
Acid base balance
Fluid balance 
BP control
Control of bone metabolism, vit D activation, phosphate excretion
Production of erythropoietin
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16
Q

Hyperkalaemia

A

K+ > 6.0 = bad
K+ > 6.5 = medical emergency

Progressive ECG changes:
reduced P wave and widened QRS
tented (higher) T wave
Sine wave pattern (PRECARDIAC ARREST)

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17
Q

What can AKI lead to which will kill you first?

A

hyperkalaemia

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18
Q

What is the danger of fluid overload?

A

pulmonary oedema -> severe tissue hypoxia

19
Q

Fluid overload in AKI

A

symptoms: breathlessness, orthopnoea, limb swelling

Danger - pulmonary oedema-> severe tissue hypoxia

If patient is oliguric/anuric they can’t get rid of this excess water

20
Q

What are the indications for dialysis in olig/anuric AKI?

A
4 main indications:
Refractory hyperkalaemia
Pulmonary oedema
Refractory acid/base disturbance
uraemic complications (coma, pericarditis)
21
Q

What causes AKI?

A

Three big categories:
pre-renal causes
renal causes
post-renal

most commonly prerenal

22
Q

Prerenal causes

A

decrease in perfusion pressure resulting in ischaemia or infarction:

  • bleeding
  • septic shock
  • dehyrdration
  • myocardial infarction
  • iatrogenic?
  • renal artery stenosis
23
Q

Renal causes

A

Intrinsic

Direct toxic effects e.g. drugs, calcium and other metals

Overproduction leading to blockage of the tubules - rhabdomyolysis, myeloma

inflammation in the kidney - GN, interstitial nephritis, acute tubular necrosis (ATN)

24
Q

post-renal causes

A

relatively likely but not as common as prerenal

plumbing problem/outflow obstruction:
stones
-ureteric/urethral strictures
-BPH
-prostate cancer
-urinary retention e.g. neurogenic, constipation
25
Q

Prerenal AKI causes

A
hypovolaemia
Decreased cardiac output- 
Decreased effective circulating volume
- congestive heart failure
-liver failure

Impaired renal autoregulation
-NSAIDS
-ACE-i/ARB
cyclosporine

26
Q

Intrinsic causes of AKI

A

Glomerular - acute GN
vascular - vasculitis, malignant hypertension, TTP-HUS
tubules and interstitium
Tubules and interstitium: ischaemia, sepsis/infection, nephrotoxins e.g. iodianated contrast, rhabdomyolysis

27
Q

Why is AKI bad news?

A

increased mortality, increased length of stay and costs

AKI is present in 50% of ITU admissions
independent risk factor for mortality
if requires haemofiltration/dialysis 50% mortality

28
Q

Chronic risks of AKI

A
elderly
CKD
cardiac failure
liver disease
diabetes
vascular disease
background nephrotoxic medications
29
Q

Acute risks of AKI

A

STOP

Sepsis and hypoperfusion
toxins
obstruction
parenchyma

30
Q

How to predict/prevent AKI

A

4 M’s
Monitor - Obs/NEWS, regular blood tests, fluid balance charts, pathology alerts

Maintain circulation - hydration, resuscitation, oxygenation

Minimise kidney insults - nephrotoxic meds, surgery, contrast, hospital acquired infection

Manage the acute illness - sepsis, heart failure, liver failure

31
Q

What to do after identifying AKI?

A

Make patient safe:
ABCDE if required
K+ level?
Volume status?

If hypovolaemic - think HR, BP, JVP, cap refill - give fluid - 250/500ml bolus of saline

Monitoring - consider a catheter. Strict fluid input/output. VBG to see acid/base balance

Investigate AKI cause - urine dip, bladder scan/USS KUB. Detailed Hx and exam, medications review

32
Q

History red flags

A

haemoptysis
rashes (if outside rashes, kidney rashes too)
joint pain/swelling
ENT - crusting of nose/acute hearing impairment
Significant acute limb swelling
noticable urine frothiness
jaundice

33
Q

Urine dip in prerenal AKI

A

Blood -/+
Protein -
Leukocytes -
Nitrites -

34
Q

Urine dip in renal AKI

A

Blood +++
Protein ++>+++
Leukocytes ++>+++
Nitrites -

35
Q

Urine dip in post renal AKI

A

Blood +
Protein +
Leukocytes -
Nitrites -

36
Q

Urine dip in UTI

A

Blood ++
Protein +
Leukocytes ++
Nitrites +++

37
Q

Initial fluid assessment

A
Focused Hx - is pt thirsty?
Capillary refill time
mucous membranes
skin turgor
pulse rate
BP (relative and postural)
resp rate
Central vs peripheral temp
JVP
lung auscultation
oedema - peripheral and sacral
CXR - pulmonary oedema/iniltrates
fluid balance charts/urine output
Invasive methods - catheter, arterial line, central line
38
Q

Drugs to hold in AKI

A
ACE inhibitors
ARBs
NSAIDS: ibuprofen, diclofenac, naproxen
any diuretics
metformin (theoretically)
39
Q

How to treat someone w urinary retention?

A

Put in a urinary catheter

40
Q

polyuria causes

A

known and commonphase of AKI of any cause
Post relief of obstruction
diabetes mellitus
psychogenic
beer potomania
rare endocrine causes e.g. diabetes insipidus

41
Q

Managing polyuria

A

Encourage the pt to drink
Depending on fluid balance assessment:
-provide IV fluids to match output +/- additional input if dry
-Once renal function is beginning to improve, reduce to 75% of urine output

42
Q

Managing oliguria

A

Depending on your assessment of fluid balance

If you have given 2-3 litres and can’t see blood on the floor, ask for help

43
Q

heavy proteinuria >3.5g/day
Hypoalbuminaemia <30g/L
peripheral oedema
dyslipidaemia

A

minimal change disease, acute nephrotic syndrome