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Week 227 - AKI > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What is the mortality rate in AKI?

A

40-60% in critically ill patients

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2
Q

What factors affect the outcome of AKI?

A 
Age
DM
Hypertension
Congestive cardiac failure
Pre-existing renal disease
Acute MI
Sepsis
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3
Q

List some of the extra-renal effects of AKI

A

Pulmonary function
CNS function
Cardiac function

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4
Q

What are the three main categories of acute kidney injury?

A

Pre-renal AKI
Intrinsic AKI
Post-renal AKI

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5
Q

Describe the pathophysiology of pre-renal AKI

A

Reduced GFR as a result of haemodynamic disturbances that decrease glomerular perfusion

  • absence of cellular injury
  • normalisation of renal function with reversal of altered haemodynamic factors
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6
Q

List four causes of pre-renal AKI?

A

Intravascular volume depletion

Decreased effective blood volume

Altered intrarenal haemodynamics

Third space sequestration (intravascular fluid loss to interstitium)

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7
Q

What are the causes of third space sequestration?

A

Bowel obstruction, peritonitis, pancreatitis, ascites

  • third space results, hypovolaemia occurs
  • raised intra-abdo pressure comprising renal blood flow
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8
Q

Why must medication not be used to treat oedema in third space sequestration?

A

Medication has negative effects

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9
Q

How must third space sequestration be treated?

A

Abdominal decompression (AKI usually recovers after)

  • paracentesis if massive ascites
  • surgical decompression
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10
Q

How should pre-renal AKI be treated?

A 
Treat cause(s)
Treat complications
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11
Q

What are the four main pathologies associated with intrinsic AKI?

A

Acute tubular necrosis

Acute tubulo-intersitial nephritis

Acute glomerulonephritis

Acute vascular syndrome

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12
Q

What are the causes of Acute tubular necrosis?

A

Ischaemic (HTN, hypovolaemia, sepsis) = 50%

Nephrotoxic (radio-contrast, drug-induced, pigment nephropathy) = 35%

Multifactorial

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13
Q

Give two examples causing pigment nephropathy?

A

Intravascular haemolysis

Rhabdomyolsis

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14
Q

Profound ischaemic injury may cause what?

A

Bilateral cortical necrosis

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15
Q

Describe the recovery of the kidney after acute ischaemic or toxic injury?

A

Able to restore its structure and function by de-differentiation and proliferation of remaining viable tubular epithelial cells

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16
Q

What is the pathogenesis behind radio-contrast causing AKI?

A

Hypertonic agent that induces transient vasodilation followed by prolonged vasoconstriction
=> renal ischaemia => reactive oxygen species release
=> direct tubular toxicity

17
Q

What are the causes of tubulo-interstitial nephritis?

A

Drug-induced (Many ABX, NSAIDs, furosemide)

Infection-related (bacterial, viral, rickettsia disease, TB)

18
Q

What are the features of tubulo-interstitial nephritis?

A

Arthralgia, Eosinophilia, Eosinophiluria, Biopsy (cell infiltrates)

19
Q

How do you treat tubulo-intersitial nephritis?

A

Withdrawal offending agent

Steroids => excellent outcome

20
Q

What are the main causes of post-renal AKI?

A

Intrinsic (stone, papillary necrosis, clot, TCC)

Extrinsic (retroperitoneal fibrosis, AAA, malignancy)

Lower obstruction (urethral stricture, BPH, Prostate Ca,..)

21
Q

Describe the pathophysiology of post-renal AKI

A

Tubular dysfunction in obstruction

  • loss of concentration capacity (polyuria)
  • loss of acidification capacity (more alkaline urine)
  • causes metabolic acidosis
22
Q

How should post-renal AKI be treated?

A

Treat the cause

After obstruction relief:

  • Monitor post-obstructive diuresis
  • Monitor for electrolyte loss with polyuria
  • Treat metabolic acidosis
23
Q

List three life-threatening complications of AKI?

A

Metabolic acidosis

Hyperkalaemia

Acute Pulmonary Oedema

24
Q

What is the clinical effect of metabolic acidosis?

A 
Muscle weakness
Altered mental sate
Kussmaul breathing
Hyperkalaemia
Negative inotropic effect => HTN
25
Q

How should metabolic acidosis be treated?

A

Treat cause
Volume expansion
IV sodium bicarbonate (only in severe MA)
Dialysis

26
Q

What are the risks of treating acidosis with sodium bicarbonate?

A 
Hypokalaemia (by shifting K+ into cell)
Symptomatic hypocalcaemia (by decreasing Ca2+)
27
Q

What is the pathophysiology with hyperkalaemia ?

A

Acidosis causes H+ to move into cell => K+ moves out of cell

28
Q

What are the clinical effects of hyperkalaemia?

A

Muscle weakness
Constipation
Cardiac arrhythmias

29
Q

What ECG changes can occur with hyperkalaemia?

A 
P wave loss
AV block
Broad QRS
Tented T waves
Bradycardia
Ventricular tachycardia
Asystole
30
Q

How should hyperkalaemia be treated?

A 
Treat cause
IV fluid
Cardiac protection (Calcium gluconate 10% 10mL 10mins)
IV insulin dextrose
Correct acidosis
IV salbutamol (Beta-agonist) - shifts K+ into cell
Cation exchange resin
Dialysis

Week 227 - AKI (7 decks)

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