Acute Kidney Injury Flashcards

1
Q

Define acute kidney injury

A

Sudden loss of renal function, characterised by either abnormal urine output or increased urea and creatinine in the urine.

May be reversible (while CKD is not)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the KDIGO staging for acute kidney injury

A

Serum creatinine
1: 1.5-1.9x baseline or 0.3 mg/dl increase
2: 2.0-2.9x baseline
3: 3.0x baseline OR increase >4.0mg/dl

Urine output
1: <0.5ml/kg/h for 6-12 hours
2: <0.5ml/kg/h for >12 hours
3: <0.5ml/kg/h for >24 hours OR anuria >12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the causes of AKI

A

Pre-renal (most common):
- Shock or circulatory failure
- Hypovolaemia (sepsis, major haemorrhage, burns, vomiting/diarrhoea e.g. gastroenteritis, HF)
- Trauma
- Nephrotic syndrome
- Renal artery stenosis
- Drugs e.g. NSAIDs, ACEi

Renal:
- Glomerular: Glomerulonephritis
- Interstitial: interstitial nephritis, pyelonephritis
- Tubular: acute tubular necrosis, ischaemia, toxic, obstructive
- Drugs
- Nephrotoxic contrast from imaging
- Vascular: HUS, vasculitis, emboli, renal vein thrombosis

Post-renal:
- Kidney stones,
- Calcified ureter
- Cancer
- Fibrosis
- Urethral stricture, posterior urethral valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the most common causes of renal failure in the UK

A

HUS and acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Symptoms of AKI

A

Oliguria/anuria
Oedema (feet, legs, abdomen) → weight gain
Brown/red urine
Fatigue, lethargy, malaise, anorexia
N&V
Pruritus
Dizziness/orthostatic symptoms
Drowsiness, convulsions, coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does presentation differ between pre-, renal, and post-renal AKI

A

Pre-renal: tachycardia (hypovolaemia)
Renal: Hx RFs, rash/petechiae/ecchymoses, signs of nephritic syndrome
Post-renal: Urgency, frequency, hesitance, flank pain, haematuria. distended/palpable bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do you differentiate between acute and chronic kidney disease

A

Consider the presentation
Anaemia (Check FBC) will suggest chronic (anaemia of chronic disease)
US: Kidneys smaller than <9cm on USS will suggest chronic
PMH will give clues e.g. HTN, DM
Hypocalcaemia and hyperphosphatemia suggests chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What investigations should be done for AKI

A

Bedside:
- Urine dip: protein + haematuria +
- Urinalysis: low fractional Na+ excretion (pre-renal failure)
- Urine output: sustained reduction
- ECG: tented T/flat P/PR prolongation

Bloods:
- U&Es: acute rise in serum creatinine
- FBC: normal Hb, deranged WCC
- ABG/VBG: metabolic acidosis
- Film: exclude MAHA (schistocytes)
- Bone profile
- Albumin

Other:
- US: large, bright kidneys with loss of cortical medullar differentiation + exclude post-renal obstruction
- Bladder scan: <150ml (>150 → bladder obstruction)
- CXR: ?fluid overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the management for AKI

A
  1. Find and treat cause (e.g. US scan to check for obstruction)
  2. Stop renotoxic drugs
  3. IV fluid treatment (depending on severity)
  4. Treat any complications e.g. hyperkalaemia, acidosis
  5. Consider dialysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which drugs are renotoxic

A

Diuretics
Aminoglycosides (gentamicin) and ACE inhibitors
Metformin
NSAIDs.
Spironolactone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the treatment for the following in AKI:
Metabolic acidosis
Hyperphosphataemia
Hyperkalaemia
Hypovolaemia
Cardiac decompensation

A

Metabolic acidosis → sodium bicarbonate

Hyperphosphatemia → Calcium carbonate + dietary restriction

Hyperkalaemia → calcium gluconate + salbutamol nebs/IV + dietary restriction + calcium exchange resin + glucose and insulin + renal replacement therapy

Hypovolaemia → IV fluids

Cardiac decompensation → venovenous haemofiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When should dialysis be given in AKI

A

A: Severe acidosis (pH<7.2)
E: Persistently high potassium that is refractory to medical treatment | Severe hyponatremia or hypernatremia
I: Drug overdose (e.g. BLAST: barbiturates, lithium, alcohol, salicylates, theophylline)
O: Fluid overload → Refractory pulmonary oedema
U: Symptomatic uraemia (pericarditis, encephalopathy, nausea, pruritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the specific management for pre-renal AKI

A

Fluid replacement (IV fluids)
Circulatory support

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the specific management for renal AKI

A

Supportive: Monitor water and electrolyte balance
High calorie, normal protein feed (decreases catabolism, uraemia and hyperkalaemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the specific management for post-renal AKI

A

Refer if there are complications:
- Pyonephrosis
- Obstructed solitary kidney
- Bilateral upper urinary tract obstruction
- Complications of AKI caused by urological obstruction
Requires assessment of the site of obstruction under nephrostomy or bladder catheterisation
Urology referral, may require surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the complications of AKI

A

Metabolic acidosis
Water retention: Pulmonary/peripheral oedema, ascites, raised JVP
Hyperkalaemia and check potassium levels every 4 hours
Hyponatraemia
Toxin accumulation e.g. urea
Blood pressure: normal in AKI, raised in CKD
EPO: normal in AKI, raised in CKD
Vitamin D: normal in AKI, raised in CKD

17
Q

What is the prognosis for AKI in children

A

Generally has a GOOD prognosis unless it is complicating a more serious condition e.g. severe infection, following cardiac surgery