Acute Kidney Injury Flashcards

1
Q

What is acute kidney injury?

A

Rapid reduction in kidney function

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2
Q

What is acute kidney injury based on?

A
  • Rise in creatinine (reduction in removal by kidneys)

- Decreases in urine output

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3
Q

What is the serum creatinine criteria for stage 1 AKI?

A

SCr increase ≥26 µmol/L within 48 hrs

or

­SCr increase 1.5–1.9 fold from baseline

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4
Q

What is the urine output for stage 1 AKI?

A

<0.5 mL/kg/hr for 6 consecutive hrs

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5
Q

What is the serum creatinine criteria for stage 2 AKI?

A

SCr increase 2–2.9 fold from baseline

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6
Q

What is the urine output for stage 2 AKI?

A

<0.5 mL/kg/hr for 12 hrs

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7
Q

What is the serum creatinine criteria for stage 3 AKI?

A

SCr increase ≥3 fold from baseline

or

SCr increase ≥354 µmol/L
or

initiated on RRT (irrespective of stage at time of initiation)

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8
Q

What is the urine output for stage 3 AKI?

A

<0.3 mL/kg/hr for 24 hr

or
anuria for 12 hr

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9
Q

What are the 3 broad types of AKI?

A
  1. Pre-renal
  2. Post-renal
  3. Intrinsic

According to which part of the renal system is primarily affected

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10
Q

What is pre-renal AKI?

A

Drop in blood flow to kidneys so kidneys cannot remove creatinine (in health, around 20% of cardiac output is directed to kidneys)

No cellular injury unless left untreated

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11
Q

What are the common causes of pre-renal AKI?

A
  • Severe sepsis (vasodilation)
  • Toxins
  • Haemorrhage
  • Hypotension (vomiting, diuretics, haemorrhage, diarrhoea, medication)
  • Over diuresis with diuretics
  • Burns (excessive fluid loss through skin)
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12
Q

What is intrinsic AKI?

A
Structural damage to the kidney tissue (glomeruli/tubules/interstitium). 
Cellular injury (necrosis) can release intracellular contents that damages surrounding cells

This is commonly 2ary to pre-renal AKI

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13
Q

What are the most common causes of intrinsic AKI?

A
  • Prolonged pre-renal AKI
  • Acute tubular injury
  • Nephrotoxins (e.g. gentamicin, contrast media)
  • Interstitial nephritis (e.g. NSAIDs)
  • Vasculitis
  • Glomerulonephritis
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14
Q

What is post-renal AKI?

A

Occurs after an acute obstruction of urinary flow. This increases intra-tubular pressure and decreases GFR

Examples:

  • Kidney stones
  • Prostatic hypertrophy
  • Tumours (bladder carcinoma, cervical carcinoma)
  • Retroperitoneal fibrosis
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15
Q

What are common causes of post-renal AKI?

A

Caused by obstruction to the renal tract - this can be anywhere from the renal pelvis to the urethra.

If the kidney’s drainage is blocked this will lead to damage of kidney tissue

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16
Q

Where are 80% of the glomeruli found?

A

In the cortex

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17
Q

What structures are found in the outer medulla?

A

Proximal straight tubule

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18
Q

Describe the proximal straight tubule?

A

Very dense network of blood vessels (25% of cardiac output)

Filtrate being produced

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19
Q

When blood pressure drops, where do kidneys divert blood? What does this pose risk to?

A

To the cortex to preserve the glomeruli (glomeruli cannot recover after injury)

Poses risk to outer medulla (proximal straight tubule)

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20
Q

What is reperfusion injury?

A

Tissue damage (exacerbation of cellular death) following restoration of blood flow and oxygen after a period of ischaemia or lack of oxygen (anoxia or hypoxia)

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21
Q

How is apoptosis unique?

A

When cells die, their contents are not released so do not damage surroundings

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22
Q

How might a patient present acutely ill / post-major surgery?

A
  • Hypovolaemia / hypotensive

- Sepsis (infection)

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23
Q

What are the risk factors for AKI?

A
  • Age
  • Pre existing CKD
  • Previous AKI
  • Heart failure
  • Liver diseases
  • Diabetes
  • Hypotension
  • Sepsis
  • Nephrotoxins
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24
Q

What are the complications of AKI?

A
  • Hyperkalaemia
  • Acidaemia
  • Pulmonary oedema
  • Uraemia
  • GI effects
  • Haematological effects
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25
Q

What can hyperkalaemia lead to?

A

Cardiac arrest

26
Q

What can acidaemia lead to?

A

Vascular instability

27
Q

What can pulmonary oedema lead to?

A
  • Usually iatrogenic

- Respiratory arrest

28
Q

What is uraemia?

A

A raised level of urea, and other nitrogenous waste compounds that are normally removed by the kidneys, in the blood

29
Q

What can uraemia lead to?

A
  • Pericarditis (inflammation of the pericardium)

- Encephalopathy (damage or disease that affects brain - confusion)

30
Q

What are the GI effects of AKI?

A
  • Nausea/vomiting
  • Gastritis
  • Malnutrition
31
Q

What are the haematological effects of AKI?

A
  • Anaemia

- Bleeding

32
Q

What investigations should be taken during AKI?

A

Full blood count (FBC)

U&Es (urea and electrolytes)

C-reactive protein (CRP)

Liver function tests

Calcium and phosphate

Immunological screen (rarer form of AKI)

Creatine kinase (enzyme released by muscle during muscle breakdown in trauma)

Urinalysis (prior to urinary catheter, looking for blood/protein)

Virology (to look for potential cause e.g. HIV, hep B/C)

33
Q

What is rhabdomyolysis?

A

The breakdown of damaged skeletal muscle, causing the release of myoglobin into the bloodstream. If you have too much myoglobin in your blood, it can cause kidney damage.

34
Q

What % of kidney function is lost before serum creatinine rises above normal range?

A

50% (hence why you can lose a kidney)

Therefore, not a good marker of injury

35
Q

When is an ultrasound of renal tract required?

A

Within 24 hours if:

  • Obstruction suspected
  • Rare cause suspected requiring a kidney biopsy
36
Q

What is STOP method used to treat AKI?

A

S: Sepsis (treat)

T: Toxins (avoid)

O: Optimise BP/Volume status

P: Prevent harm:

  • Identify cause
  • Treat complications
  • Review medication doses
  • Review fluid prescription
37
Q

What is the ABCDE approach?

A

Airway (e.g. patent)

Breathing (breaths per minute, crackles)

Circulation (heart rate, blood pressure)

Disability/dysfunction (e.g. confused, verbal response, blood sugar)

Exposure (e.g. no rash)

38
Q

What is C reactive protein an indicator of?

A

Inflammation and infection

39
Q

What is sepsis 6?

A

To be applies to anyone over age of 12 with suspected or confirmed Red Flag Sepsis within 1 hour

  1. Administer O2
  2. Take blood cultures
  3. Give IV antibiotics
  4. Give IV fluids
  5. Check serial lactates
  6. Measure urine output
40
Q

What is sepsis?

A

Caused by the body’s response to an infection. The body normally releases chemicals into the bloodstream to fight an infection. Sepsis occurs when the body’s response to these chemicals is out of balance, triggering changes that can damage multiple organ system

41
Q

When is a rarer cause of AKI suspected?

A

If the AKI is not 2ary to sepsis, toxins or haemodynamic compromise/hypovolaemia

42
Q

What is effect of hyperkalaemia on ECG?

A

Tented T wave (after QRS complex)

Loss of P wave

43
Q

How is pulmonary oedema treated?

A

Sit up

O2 high flow via reservoir mask

(High dose furosemide)
only if volume replete
do not persist if unresponsive

Intravenous nitrates (specific situations)

Renal Replacement Therapy

44
Q

If kidney function reduces, so does drug clearance which can lead to toxicity.

What are dangers of reduced clearance of antibiotics?

A

E.g. penicillins –> seizures

45
Q

What are dangers of reduced clearance of opioids?

A

E.g. morphine –> pinpoint pupils, respiratory depression

46
Q

What are dangers of reduced clearance of metformin?

A

Lactic acidosis

47
Q

What are dangers of reduced clearance of digoxin?

A

Cardiac toxicity

48
Q

Which drugs can cause harm directly?

A

Aminoglycosides (gentamicin)

NDAIDS (ibuprofen, voltarol)

49
Q

What is gentamicin?

A

Antibiotic

50
Q

What are the indications that renal replacement therapy (RRT) is required?

A
  1. Hyperkalaemia unresponsive to medical therapy
  2. Pulmonary oedema unresponsive to medical therapy
  3. Severe acidaemia pH < 7.1
  4. Uraemic complications (encephalopathy, pericarditis)
51
Q

What is intermittent RRT?

A

Indicated for patients who are haemodynamically stable

  • haemodialysis
  • peritoneal dialysis
52
Q

What is continuous RRT?

A

Indicated for patients who are haemodynamically unstable

CVVHD (continuous veno-venous haemodialysis)

53
Q

A patient presents with vomiting and diarrhoea with a SCr of 250 µmol/L. 1 month earlier their SCr was 85 µmol/L. What stage AKI do they have?

A

SCr has risen 2.9 fold from baseline and therefore have stage 2 AKI

54
Q

What can acutely obstructed kidneys (post-renal AKI) lead to?

A

Kidneys can swell under increased pressure (hydronephrosis)

Kidneys look large on ultrasound (important to request renal tract ultrasound on anyone with AKI)

55
Q

What are potential causes for AKI?

A
  • Reduced fluid intake (nausea)
  • Increases fluid losses (vomiting and diarrhoea)
  • Urinary tract symptoms (prostatic disease-obstruction)
  • Recent drug ingestion (overdose-paracetamol)
56
Q

What are systemic clinical features of AKI?

A
  • Fever (vasculitis)
  • Rash (vasculitis)
  • Joint pains (vasculitis)
57
Q

What is renovascular disease?

A

The narrowing of the artery to one or both kidneys

Can cause hypertension and reduced kidney function (AKI or CKD)

58
Q

What are the signs of renovascular disease?

A
  • Audible bruits

- Impalpable peripheral pulses

59
Q

How can some cases of AKI be prevented?

A

Volume repletion

Withholding ant-hypertensive medication if hypotensive

Discontinuing and/or avoiding certain potentially nephrotoxic agents e.g. NSAIDs

Earlier recognition of conditions causing rapid progression of AKI

60
Q

What does AKI therapy include?

A

Adequate volume replacement – IV fluids

Treatment of the underlying medical condition (e.g. sepsis, haemorrhage)

Avoidance of nephrotoxic medications

61
Q

What are the rarer forms of AKI?

A

Glomerulonephritis vasculitis, interstitial nephritis, Lupus nephritis

62
Q

Why must drugs be used carefully in AKI?

A

Kidneys remove drugs, if function is impaired then risk of toxicity