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Renal > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What is the mortality for severe acute kidney injury?

A

Over 50% for most and up to 80% in the context of multi-organ failure needing dialysis

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2
Q

What can be looked at to help diagnose acute kidney injury?

A

Solute clearance = urea/creatine
Urine output = oliguria
Need for dialysis = increased urea or K+, fluid overload

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3
Q

What is acute kidney injury defined as?

A

Abrupt (<48hrs) reduction in kidney function = absolute increase in serum creatine by >26.4 micromol/l OR increase in creatine by >50% OR a reduction in urine output

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4
Q

What can be used to categorise acute kidney injury?

A

KDIGO staging

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5
Q

What are the patient risk factors for acute kidney injury?

A

Older age, CKD, diabetes, cardiac failure, liver disease, PVD, previous AKI

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6
Q

What are some exposure risk factors for acute kidney injury?

A

Hypotension, hypovolaemia, sepsis, deteriorating NEWS, recent contrast, exposure to certain medications

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7
Q

What are the causes of acute kidney injury split into?

A

Pre-renal (functional), renal (structural) and post-renal (obstruction)

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8
Q

What are the causes of pre-renal AKI?

A

Hypovolaemia = haemorrhage, volume depletion
Hypotension = cardiogenic shock, distributive shock
Renal hypoperfusion = NSAIDs, COX2, ACEi, ARB, hepatorenal syndrome

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9
Q

What is the underlying mechanism of pre-renal AKI?

A

Reversible volume depletion leading to oliguria and increase in creatine

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10
Q

What is the urine output of pre-renal AKI?

A

Oliguria = <0.5 ml/kg/hr

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11
Q

How much of the total body weight do the kidneys account for?

A

0.5% = receive 20% of cardiac output

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12
Q

What does pre-renal AKI lead to if left untreated?

A

Acute tubular necrosis = most common form of AKI in hospital

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13
Q

What causes acute tubular necrosis?

A

A combination of factors leading to decreased renal perfusion = sepsis, severe dehydration, rhabdomyolysis, drug toxicity

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14
Q

How can the hydration of a patient with pre-renal AKI be assessed?

A

BP, heart rate, urine output, JVP, capillary refill time, oedema, pulmonary oedema

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15
Q

How may a patient with pre-renal AKI undergo fluid challenging for hypovolaemia?

A

Crystalloid (0.9% NaCl) or colloid (Gelofusion), don’t use 5% dextrose, give bolus of fluid then reassess and repeat as necessary, if >1L IN and no improvement seek help

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16
Q

What is renal AKI?

A

Diseases causing damage or inflammation to cells = categorised by structure (blood vessels, glomerular, interstitial, tubular)

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17
Q

What are some causes of vascular renal AKI?

A

Vasculitis, renovascular disease

18
Q

What causes glomerular renal AKI?

A

Glomerulonephritis

19
Q

What are some causes of interstitial renal AKI?

A

Nephritis due to drugs, infection (TB) or systemic disease (sarcoid)

20
Q

What are some causes of tubular renal AKI?

A

Ischaemia (prolonged renal hypoperfusion), gentamicin, contrast, rhabdomyolysis

21
Q

What are some non-specific symptoms of renal AKI?

A

Anorexia, weight loss, fatigue/lethargy, nausea and vomiting, itch, oedema and SOB due to fluid overload

22
Q

What are some signs of renal AKI?

A

Hypertension, oedema, pleural/pulmonary effusion, uraemia (itch, pericarditis), oliguria

23
Q

What are some clues that AKI might have a renal cause?

A

Sore throat, rash, joint pain, diarrhoea, vomiting, haemoptysis, recent contrast, eosinophilia, vascular bruit

24
Q

What are some investigations done for renal AKI?

A

U & Es = marker for renal function, is K+ high?
FBC and clotting screen = abnormal clotting, anaemia
Urinalysis = haematoproteinuria
Immunology = ANCA, ANA, GBM
USS, protein electrophoresis, BJP

25
Q

How is renal AKI treated?

A

Establish good perfusion pressure = inotropes/vasopressors, fluid
Treat underlying cause and stop nephrotoxics
Dialysis if still uraemic/anuric

26
Q

What are some complications of renal AKI?

A

Hyperkalaemia, pulmonary oedema, fluid overload, severe acidosis (pH <7.5), uraemic pericardial effusion, severe uraemia (>40)

27
Q

What is the underlying mechanism of post-renal AKI?

A

Obstruction of urine flow leads to back pressure (hydronephrosis) and thus loss of concentrating ability

28
Q

What are some causes of post-renal AKI?

A

Calculi, cancer, strictures, extrinsic pressure

29
Q

How is post-renal AKI treated?

A

Relieve obstruction = catheter, nephrostomy

Refer to urology if ureteric stenting needed

30
Q

What is hyperkalaemia associated with?

A

Cardiac arrhythmias = peaked T waves on ECG

31
Q

What is the normal range for potassium?

A

3.5-5

32
Q

What is hyperkalaemia defined as?

A

Quantities >5.5

Life threatening if >6.5

33
Q

How is hyperkalaemia assessed?

A

ECG and muscle weakness

34
Q

How can the heart be protected from hyperkalaemia?

A

Protect the myocardium by giving 100ml of 10% of calcium gluconate (2-3 mins)

35
Q

How is hyperkalaemia treated?

A

Move K+ back into cells = insulin (actrapid 10 units) with 50ml of 50% dextrose (30 mins), nebulised salbutamol (90 mins)

36
Q

How is absorption of potassium from the GI tract during hyperkalaemia prevented?

A

Give calcium resonium (not in an acute setting)

37
Q

What are some urgent indications for haemodialysis?

A

Hyperkalaemia >7 or >6.5 if unresponsive to therapy
Severe acidosis = pH <7.15
Fluid overload
Urea >40 (pericardial rub/effusion)

38
Q

What is the mortality of AKI?

A

AKI alone = 10-30%
AKI with one other organ dysfunction = 30-50%
AKI as part of multi-organ failure = 70-90%

39
Q

What is the recovery rate of renal function after AKI?

A

10-15% have no recovery of renal function

5-10% recover but have progressive CKD

40
Q

Can dialysis reverse disease course?

A

No = it clears toxins but doesn’t alter the course of disease

Renal (36 decks)

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