Acute Kidney Injury Flashcards

1
Q

What is definition of acute renal failure?

A
  • Rapid loss of glomerular filtration and tubular function over hours to days
  • Retention of urea/creatinine -> Failure of homeostasis
  • Oliguric / non-oliguric
  • Potentially recoverable
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2
Q

What is the definition of acute kidney injury?

A

Increase in serum creatinine
• ≥ 26.5 μmol/l within 48 hours; or
• ≥ 1.5 times baseline, which has occurred within the prior 7 days; or

Urine volume <0.5 ml/kg/h for 6 hours

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3
Q

What is the range for stage AKI 1?

A
  • Serum creatinine: x1.5-1.9 baseline

* Urine: <0.5 for 6-12hrs

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4
Q

What is the range for stage AKI 2?

A
  • Serum creatinine: x2-2.9 baseline

* Urine: <0.5 for > 12hrs

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5
Q

What is the range for stage AKI 3?

A
  • Serum creatinine: x3 baseline

* Urine: <0.3 for > 24hrs

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6
Q

What are the immediate dangerous consequences of AKI?

A
A - acidosis (can cause cardiac arrest)
E - electrolyte imbalance
I - intoxication TOXINS 
O - overload of fluid and pulmonary oedema --> cardiac arrest 
U - uraemic complications
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7
Q

What is the danger of electrolyte imbalance?

A

Hyperkalaemia can cause cardiac arrest

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8
Q

What is the danger of toxin build up?

A

Opiates can cause respiratory (and the cardiac) arrest

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9
Q

What are the three types of causes of AKI?

A
  • Pre-renal - blood flow to kidney
  • Renal (intrinsic) - damage to renal parenchyma
  • Post-renal - obstruction
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10
Q

How do pre-renal causes cause AKI?

A

Reduce circulative volume causing renal hypoperfusion
• Volume deplete (haemorrhage, dehydration)
• Hypotension / shock
• Congestion cardiac failure / liver failure

  • Arterial Occlusion
  • Vasomotor: NSAIDs/ACEi
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11
Q

How do renal (intrinsic) causes cause AKI?

A
Consider after pre-renal and obstruction is ruled out:
• Acute tubular necrosis 
• Drugs (NSAIDs, gentamicin)
• Radiocontrast 
• Acute interstitial nephritis  
• Myeloma
• Acute glomerulonephritis
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12
Q

How do post-renal causes cause AKI?

A

Obstruction
• Intraluminal (calculus, clot, sloughed papilla)
• Intramural (malignancy, ureteric stricture, radiation fibrosis, prostate disease)
• Extramural (RPF, malignancy)

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13
Q

What is the most common cause of AKI?

A

Poor perfusion leading to established tubule damage

Failure of the circulation (loss of volume and/or pressure) to provide sufficient plasma flow to maintain blood chemistry and fluid balance

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14
Q

What investigations are used for AKI?

A
  • History and examination (fluid status)
  • Urine dip stick
  • FBC
  • USS
  • Blood gas (A/B status, potassium and lactate)
  • Renal biopsy (histology)
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15
Q

What blood tests are carried out for AKIs?

A
  • U+Es, Bicarb, LFTs, bone
  • FBC
  • Clotting
  • ABG
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16
Q

How are patients at risk of AKI identified?

A

S - Sepsis: if suspected screen and treat
T -Toxins: avoid (gentamicin, NSAIDs)
O - Optimise BP and volume status
P - Prevent harm: daily U+Es, fluid balance and med review

17
Q

What is the supportive management of acute kidney injury?

A
  • Fluid balance (restriction if overload)
  • Optimise blood pressure (give fluid and stop ACEi)
  • Stop nephrotoxic drugs (i.e. NSAIDs, aminoglycoside)
18
Q

What are the ECG changes of hyperkalaemia?

A
  • Peaked T waves (tall tented T waves)
  • P wave widen
  • PR segment lengthens
  • P waves eventually disappear
19
Q

What is the treatment of hyperkalaemia?

A

• Stabilise myocardium (calcium gluconate)
• Shift K+ into cells (salbutamol, insulin-dextrose)
• Remove K+
- Diuresis
- Dialysis
- Anion exchange resins

20
Q

What is the most common cause of the established tubule damage?

A

Prerenal (hypotension, hypovolemia):
Failure of the circulation (loss of volume and/or pressure) to provide sufficient plasma flow to maintain blood chemistry and fluid balance –> Acute Tubular Necrosis