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Stage 2: Supporting Life > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What is AKI?

A

The syndrome arising from a rapidly falling GFR (drop in urine output)

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2
Q

What is AKI characterised by?

A

Retention of nitrogenous (urea and creatinine) and non-nitrogenous waste products, as well as disordered electrolytes

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3
Q

What are the 3 ways that AKI can be diagnosed?

A

1) Serum creatinine has increased by ≥26.5µmol/l in ≤48h
2) Serum creatinine has risen to ≥1.5-fold from baseline in the preceding 7 days
3) Urine output has been <0.5 ml/kg/h for 6 hours

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4
Q

How many stages of AKI are there?

A

3

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5
Q

What are the 3 diagnostic features of Stage 1 AKI?

A

1) Serum creatinine has increased by ≥26.5µmol/l in ≤48h
2) Serum creatinine has risen to ≥1.5-fold from baseline in the preceding 7 days
3) Urine output has been <0.5 ml/kg/h for 6 hours

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6
Q

What are the 2 diagnostic features of Stage 2 AKI?

A

1) Serum creatinine rises 2-2.9 times from baseline

2) Urine output has been <0.5 ml/kg/h for 12 hours

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7
Q

What are the 5 diagnostic features of Stage 3 AKI?

A

1) Serum creatinine rises ≥ 3 times from the baseline
2) Serum creatinine rises to ≥353.6µmol/l
3) RRT irrespective of serum creatinine
4) Urine output has been <0.3 ml/kg/h for ≥24h hours
5) Anuria for ≥12h

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8
Q

What diagnostic features are used in CKD but not AKI

A

Estimated GFR and proteinuria

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9
Q

Describe normal creatinine levels

A
  • Normal range is 50-80
  • However with lots of muscle mass can be higher e.g. 110 or if v thin 35 may be normal
  • If don’t know their normal or don’t know if they already have CKD, assume it is abnormal and have AKI if not in the normal range
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10
Q

What are the proximal tubules v susceptible to and why?

A

Hypotension and hypoxia → they are very vascular and receive 80% of the renal blood flow

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11
Q

What are the 3 classifications of AKI causes?

A

1) Pre-renal
2) Intrinsic (renal)
3) Post-renal

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12
Q

What are pre-renal causes of AKI related to?

A

Reduced BP or volume

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13
Q

What are 3 types of pre-renal causes of AKI?

A

1) Volume depletion
2) Decreased effective volume
3) Altered intrarenal haemodynamics → NSAIDs or ACEi-A2RB induced

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14
Q

What are intrinsic causes of AKI related to?

A

Diseases that affect blood vessels, glomerulus, tubules and cells

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15
Q

What are 5 types of intrinsic causes of AKI?

A

1) Acute tubular necrosis
2) Acute glomerulonephritis
3) Acute interstitial nephritis → inflammation e.g. drugs/sarcoidosis/autoimmune disease
4) Vasculitis
5) Drugs → damage tubular cells

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16
Q

What are 6 types of post-renal causes of AKI?

A

1) Ureteric obstruction e.g. stone in ureter, pelvis, bladder
2) Bladder outflow obstruction
3) Prostate hypertrophy
4) Pregnancy (v gravid e.g. twins)
5) Extrinsic e.g. retroperitoneal haematoma
6) Urethro valve obstruction

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17
Q

What is the most common cause of post-renal AKI in men and why does it lead to AKI?

A

Prostate hypertrophy → prostate can herniate and block off connection between the bladder and urethra

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18
Q

What is the most common cause of post-renal AKI in children?

A

Urethro valve obstruction

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19
Q

Describe what happens in a ureteric obstruction

A

Urine isn’t flowing leading to back pressure on the glomerulus so the kidneys don’t work

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20
Q

What are the 7 functions of kidneys?

A

1) Excretion of electrolytes
2) Clearance of waste products
3) Gluconeogenesis
4) Production of hormones
5) Control of water balance
6) Regulation of acid-base status (produce and reabsorb bicarbonate)
7) Receptor site for hormones

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21
Q

For what hormones does the kidney act as a receptor site for?

A

ADH, aldosterone, ANP, PTH, renin

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22
Q

What are the 5 consequences of AKI?

A

1) Fluid overload
2) Hyperkalaemia
3) Metabolic acidosis
4) Uraemia
5) Organ cross-talk

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23
Q

Why does fluid overload/accumulation occur in AKI?

A

Bc not making enough urine

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24
Q

What does fluid overload lead to?

A

Peripheral and pulmonary oedema

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25
Q

What is the life-threatening complication of AKI linked to fluid overload?

A

Pulmonary oedema → can’t breathe

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26
Q

What are the effects of sacral and ankle oedema?

A

Might be more susceptible to skin break down and ulcers

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27
Q

What does hyperkalaemia affect?

A

Conduction of the heart and therefore the ECG (arrhythmia)

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28
Q

What is the normal serum potassium level?

A

Up to 4.5 (4-5.5) mmol/L

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29
Q

What is the first sign of hyperkalaemia on an ECG?

A

Peaked T waves after the QRS complex

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30
Q

What would you see on an ECG with a serum potassium of 5.5-6.5?

A
  • Peaked T waves

- Prolonged PR segment

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31
Q

What would you see on an ECG with a serum potassium of 6.5-8?

A
  • Loss of P waves
  • Prolonged QRS complex
  • ST segment elevation
  • Ectopic beats and escape rhythms
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32
Q

What would you see on an ECG with a serum potassium of > 8?

A
  • Sine wave
  • Progressive widening of QRS complex
  • Ventricular fibrillation
  • Asystole
  • Axis deviations
  • Bundle branch blocks
  • Fascicular blocks
33
Q

What width of the QRS complex is abnormal?

A

> 3 small squares

34
Q

What is the immediate temporary solution to hyperkalaemia but why is it only temporary?

A
  • Giving dextrose insulin

- Just shifts potassium in cells (right thing to do in emergency) but it will come out of the cells again

35
Q

What can be given to briefly reduce the response to hyperkalaemia and what does it do?

A

Calcium chloride → stabilises cell membrane and makes it less irritable

36
Q

What do you need to organise for someone with hyperkalaemia?

A

Dialysis

37
Q

What can happen if someone goes untreated with hyperkalaemia?

A

Cardiac arrest → no CO → death

38
Q

What does hyperkalaemia + ECG changes mean?

A

An emergency

39
Q

What are the typical ABGs of someone with AKI?

A
  • pH < 7.3
  • pCO2 low
  • pO2 normal or high
  • HCO3 low
40
Q

Why might pO2 be high in someone with AKI/metabolic acidosis?

A

If they are breathing a lot

41
Q

What are the typical symptoms of metabolic acidosis?

A

1) Breathless/tachypneic
2) Nausea
3) Non-specifically unwell

42
Q

Why might someone be breathless/tachypneic with AKI/metabolic acidosis?

A

1) Pulmonary oedema

2) Urge to breathe faster to compensate for metabolic acidosis

43
Q

What is uraemia?

A

Retention of metabolic waste products e.g. urea, sulfate, creatinine, phosphate

44
Q

What are the effects of uraemia?

A

1) Pericarditis
2) Pleurisy
3) Encephalopathy

45
Q

Describe pericarditis

A
  • Causes pleuritic chest pain, worse on a deep breath → but cardiac function at this point should be fine
  • Both layers of the pericardium are inflamed and rubbing together, which can cause fluid to build up
  • This can lead to haemorrhagic pericarditis
  • Need to listen to check for murmur (crunchy, high pitched noise) to diagnose pericarditis
  • Needs to go on dialysis
46
Q

What is pleurisy and what can it lead to?

A

Inflammation of the pleura (pleural membrane) → pleural effusion

47
Q

Describe encephalopathy

A
  • Inflammation of the brain
  • Patients can present with different neurological symptoms (if gets too far can be uraemic coma)
  • Leakage and inflamed membranes
48
Q

How can AKI lead to organ cross-talk?

A

AKI affects other organs mainly as a result of uraemic toxin and fluid build up (gut, liver, bone marrow)

49
Q

What are the 4 domains of AKI management?

A

1) Exclude a life-threatening complication
2) Identify the aetiology of AKI
3) Supportive treatment
4) Avoidance of progression

50
Q

How do you exclude a life-threatening complication of AKI?

A

Check potassium, ECG, listen to chest and check breathlessness and keep checking up on these throughout treatment

51
Q

What do you do if a life-threatening complication is present in AKI?

A

Correct/treat immediately

52
Q

How do you treat if the is AKI due to hypovolaemia?

A

Give fluids

53
Q

How do you treat if the AKI is due to low BP?

A

Give fluids/medication

54
Q

How do you treat if the AKI is drug induced?

A

Stop drugs

55
Q

What is an example of a drug that can cause AKI?

A

Gentamicin → overdose or on it for too long

56
Q

How do you treat if the AKI is sepsis induced (most common cause of AKI in hospital setting)?

A

Treat sepsis

57
Q

What is supportive treatment given in AKI?

A
  • Nutrition

- Ulcer prophylaxis

58
Q

How do you avoid progression of AKI?

A

Avoid nephrotoxic drugs, hypovolaemia and hypotension

59
Q

What treatment is a life threatening complication of AKI an indication for?

A

Renal replacement therapy (RRT)

60
Q

What are 5 examples of life threatening complications of AKI that are an indication for RRT?

A

1) Life threatening pulmonary oedema
2) Severe metabolic acidosis
3) Severe hyperkalaemia, esp. if ECG changes
4) Uraemic pericarditis
5) Uraemic encephalopathy

61
Q

Why is severe metabolic acidosis life threatening?

A

pH < 7.1 → cardiac function affected, risk of arrhythmia

62
Q

Why is uraemic pericarditis life threatening?

A

Risk of fluid accumulation and bleeding into cardiac space → cardiac arrest

63
Q

Describe RRT

A
  • Uses filter that acts as an artificial kidney
  • Hair sized tiny columns that blood goes through
  • Can correct AKI emergencies
  • Effluent is like urine
  • Dual lumen catheters → one lumen removes blood and in the other one it comes back
64
Q

Where are the insertion sites for RRT?

A

To be effective needs to be a big vein → internal jugular, femoral, subclavian

65
Q

Describe RRT as part of multi-organ support

A
  • Routine life support

- Can combine with ECMO → artificial oxygenation + cleaning of blood

66
Q

Describe how cancer/chemotherapy can lead to AKI

A
  • Chemotherapy can lead to tumour lysis syndrome
  • This is when tumour cells are killed, releasing intracellular electrolytes (potassium) and substances (toxicity from chemo)
  • This can lead to diarrhoea and vomiting → hypovolaemia
  • This patient population is v high risk for this, look out for it, can’t prevent, just give RRT
67
Q

What do you need to do if someone has high potassium?

A

An ECG

68
Q

What treatment do you give if you have excluded a life-threatening cause but creatinine is high, potassium is a bit high but ECG is normal?

A

IV fluids

69
Q

What treatment do you give to someone with high potassium and ECG changes?

A

Calcium, dextrose insulin and call ICU/renal team to start RRT

70
Q

What are the sub-classifications of AKI causes?

A

1) Pre-renal AKI
2) Renal artery
3) Small vessel disease
4) Glomerular disease
5) Acute tubular necrosis
6) Acute interstitial nephritis
7) Intra-tubular obstruction
8) Post-renal obstruction

71
Q

What are 3 causes of pre-renal AKI?

A

1) Hypovolaemia e.g. ruptured aneurysm or trauma bleeding
2) Cardiac failure
3) Hepatorenal syndrome

72
Q

What are 2 causes of renal artery related AKI?

A

1) Renal artery occlusion

2) Large/medium vessel vasculitis

73
Q

What are 3 causes of small vessel disease?

A

1) Thrombotic microangiopathy
2) Renal atheroembolism
3) Small vessel vasculitis

74
Q

What are 7 causes of glomerular disease?

A

1) Anti-GBM disease
2) Lupus nephritis
3) Post-infectious glomerulonephritis
4) Infective endocarditis
5) Membrano-proliferative glomerulonephritis
6) Cryoglobulinemia
7) IgA nephropathy/HSP

75
Q

What are the 8 causes of acute tubular necrosis (mainly drugs)?

A

1) Amphotericin
2) Aminoglycosides
3) Antiretrovirals
4) Cisplatin
5) Paracetamol (acetaminophen)
6) Radiocontrast
7) Organic solvents
8) IV immunoglobulin

76
Q

What are 3 causes of acute interstitial nephritis?

A

1) Drugs
2) Infection
3) Systemic disease

77
Q

What are 3 causes of intra-tubular obstruction?

A

1) Cast nephropathy (kidney injury in myeloma)
2) Drugs
3) Crystalluria (benign, side effect of sulfonamides and penicillins)

78
Q

What are 5 causes of post-renal obstruction?

A

1) Papillary necrosis
2) Tumours
3) Retroperitoneal fibrosis
4) Renal calculi
5) Urinary retention

Stage 2: Supporting Life (30 decks)

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