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Urology > Acute Kidney Injury (AKI) > Flashcards

Acute Kidney Injury (AKI) Flashcards

1
Q

How is AKI defined.

A

It is defined as a rapid reduction in kidney function over hours to days.

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2
Q

How is kidney function measured. (2)

A

Serum urea.

Serum creatinine.

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3
Q

What are the consequences of AKI. (3)

A

Failure to maintain fluid balance.
Failure to maintain electrolyte balance.
Failure to maintain acid-base homeostasis.

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4
Q

What percentage of hospitalized patients suffer from AKI. (2)

A

Up to 18%.

AKI is an independent risk factor for mortality.

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5
Q

What are the three main criteria for diagnosing AKI. (3)

A

Rise in creatinine >26 in 48h.
Rise in creatinine >1.5 from baseline.
Urine output

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6
Q

What staging system is used to stage AKI.

A

KDIGO staging system.

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7
Q

What two aspects are taken into consideration in the KDIGO staging system for AKI.

A

Serum creatinine.

Urine output.

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8
Q

What are the risk factors for AKI. (10)

A 
Age >75. 
Chronic kidney disease. 
Cardiac failure. 
Peripheral vascular disease. 
Chronic liver disease. 
Diabetes. 
Drugs (especially new ones started). 
Sepsis. 
Poor fluid intake/increased fluid losses. 
History of urinary symptoms.
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9
Q

What are some of the commonest causes of AKI. (3)

A

Ischaemia.
Sepsis.
Nephrotoxins.

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10
Q

What are the general causes of AKI. (3)

A

Pre renal.
Intrinsic renal.
Post renal.

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11
Q

What percentage of AKIs are due to pre renal causes.

A

40-70%.

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12
Q

What percentage of AKIs are due to intrinsic renal causes.

A

10-50%.

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13
Q

What percentage of AKIs are due to post renal causes.

A

10-25%.

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14
Q

What are some pre renal causes of AKI. (3)

A

Renal hypoperfusion (hypotension, renal artery stenosis, ACEi).

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15
Q

What are some intrinsic renal causes of AKI. (4)

A

Tubular damage.
Glomerular damage.
Interstitial damage.
Vascular damage.

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16
Q

What is the most common cause of tubular damage leading to AKI.

A

Acute tubular necrosis (ATN) is the most common renal cause of AKI.

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17
Q

What are some causes of ATN. (4)

A

Pre renal damage.
Nephrotoxins (drugs).
Radiological contrast.
Myoglobinuria in rhabdomyolisis.

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18
Q

What is another cause of tubular damage leading to AKI. (3)

A

Crystal damage.
Myeloma.
Raised calcium.

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19
Q

What are some glomerular causes of AKI (renal). (4)

A

Autoimmune (SLE, HSP).
Drugs.
Infections.
Primary glomerulonephritides.

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20
Q

What are some interstitial causes of AKI (renal). (3)

A

Drugs.
Infiltration (eg lymphoma).
Infection.
Tumour lysis syndrome following chemotherapy.

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21
Q

What are some vascular causes of AKI (renal). (5)

A

Vasculitis.
Malignant hypertension.
Thrombus or cholesterol emboli from angiography.
HUS/TTP.
Large vessel occlusion (eg dissection or thrombus).

22
Q

What are some post renal causes of AKI. (4)

A

Caused by urinary tract obstruction.
Luminal causes.
Mural causes.
Extrinsic compression.

23
Q

What are some luminal causes of AKI (post renal). (3)

A

Stones.
Clots.
Sloughed papillae.

24
Q

What are some mural causes of AKI (post renal). (3)

A

Malignancy (ureteric, bladder, prostate).
BPH.
Strictures.

25
Q

What are some extrinsic compression causes of AKI (post renal). (2)

A

Malignancy (especially pelvic).

Retroperitoneal fibrosis.

26
Q

What are some clinical signs of AKI. (5)

A

Palpable bladder.
Palpable kidneys (Polycystic kidney disease).
Abdominal/pelvic masses.
Renal bruits (signs of renovascular disease).
Rashes.

27
Q

What bedside test should you always do if you suspect AKI.

A

Urine dipstick.

28
Q

What is seen on a urine dipstick in infection. (2)

A

Leucocytes.

Nitrates.

29
Q

What is seen on a urine dipstick in golmerular disease. (3)

A

Blood.

Protein (look out for Bence Jones proteins).

30
Q

What blood tests should be done in a patient suspected of having AKI. (10)

A 
UandEs. 
FBC. 
Clotting screen. 
SK, ESR, CRP. 
ABG for acid base assessment. 
Blood cultures if signs of infection. 
Consider blood film and renal immunology if systemic cause suspected.
Autoantibodies (ANCA, ANA). 
Complement (C3/C4). 
Paraprotein electrophoresis.
31
Q

What is the use of a renal ultrasound. (3)

A

It can help distinguish obstruction and hydronephrosis.
Can look for abnormalities such as cysts, small kidneys, masses.
Assess corticomedullary differentiation.

32
Q

What does complete anuria suggest in AKI.

A

It is an unusual finding, but if present suggests an obstructive cause.

33
Q

What can be seen on a CTKUB of the renal system in suspected obstructive AKI (above prostate).

A

Obstructing masses or calculi.

34
Q

When should you suspect chronic kidney damage. (5)

A 
Small kidneys on ultrasound. 
Anaemia. 
Low calcium. 
High PO4. 
Definite sign of chronic kidney disease is previous blood result showing high creatinine/low GFR.
35
Q

What are the indications for dialysis. (6)

A

Refractory pulmonary oedema.
Persistent hyperkalaemia.
Severe metabolic acidosis.
Ureamic complications (eg encephalopathy).
Uraemic pericarditis.
Drug overdose (BLAST: barbiturates, lithium, alcohol, salicylates, theophyline).

36
Q

How do you assess volume status in a patient with AKI. (6)

A 
Low urine volume. 
Non-visible JVP. 
Poor tissueturgor. 
Low BP. 
High HR.
Signs of fluid overload.
37
Q

What are some signs of fluid overload. (5)

A 
Raised BP. 
Raised JVP. 
Lung crepitations. 
Peripheral oedema. 
Gallop rhythm.
38
Q

What fluid status are you aiming for in a patient with AKI.

A

Euvolaemia.

39
Q

What general measures should you taken when treating a patient with AKI. (5)

A

Assess fluid status.
Aim for euvolaemia.
Stop nephrotoxic drugs.
Monitoring (UandEs, fluid balance chart, etc…).
Nutrition (aim for normal calorie intake).

40
Q

What are some nephrotoxic drugs that should be stopped in a patient with AKI. (5)

A 
Metformin. 
NSAIDs. 
ACEi. 
Gentamicin. 
Amphotericin.
41
Q

How do you treat pre renal causes of AKI. (3)

A

Correct volume depletion.
Treat sepsis.
Consider referral to ICU if signs of shock.

42
Q

How do you treat post renal causes of AKI. (3)

A

Catheterise.
Consider CTKUB.
Urology referral if obstructive cause (cystoscopy, retrograde stents, nephrostomy insertion).

43
Q

How do you treat intrinsic renal causes of AKI.

A

Refer early to nephrology if concerns.

44
Q

What concerns in intrinsic causes of AKI would lead you to refer the patient to nephrology. (4)

A

Tubulointerstitial or glomerular pathology.
Signs of systemic disease.
Signs of multi-organ involvement.
Indications for dialysis.

45
Q

What are the complications of AKI. (4)

A

Hyperkalaemia.
Pulmonary oedema.
Uraemia.
Acidaemia.

46
Q

How is AKI treated after the initial assessment, treatment of the underlying cause and complications have been dealt with.

A

Renal replacement therapy.

47
Q

What are the RRT options for patients with AKI. (2)

A

Haemodialysis.

Haemofiltration.

48
Q

What is the prognosis for patients with AKI. (3)

A

Depends on early recognition and intervention.
The more prolonged the insult, the less likely full recover of function is.
Mortality can be as high as 80% and as low as 10%.

49
Q

What ECG changes are seen in hyperkalaemia. (6)

A 
Tall tented T waves. 
Small or absent P waves. 
Increased PR interval. 
Widened QRS complex. 
'Sine wave' pattern. 
Asystole.
50
Q

How is pulmonary oedema treated in AKI. (6)

A 
Oxygen. 
Venous vasodilator. 
Furosemide IV. 
Haemodialysis or haemofiltration if no response. 
CPAP. 
IV nitrates may be useful.

Urology (11 decks)

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