Acute Kidney Injury Flashcards

1
Q

Define Acute Kidney Injury

A
  • Clinical syndrome
  • Decline in renal excretory function over hours/days (<3/12)
  • Resulting in failure to maintain homeostasis of:
    • Fluid
    • Electrolyte
    • Acid-base
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the KDIGO criteria for AKI Stage I?

A

Any of:

  • Serum creatinine 1.5-1.9x baseline
  • Serum creatinine increase of ≥0.3 mg/dl within 48h
  • Urine output <0.5 ml/kg/hr for 6-12h
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the KDIGO criteria for AKI Stage II?

A

Either:

  • Serum creatinine 2.0-2.9x baseline
  • Urine output <0.5 ml/kg/h for ≥12h
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the KDIGO criteria for Stage 3 AKI?

A

Any of:

  • Serum creatinine 3x of baseline
  • Serum creatinine increase of ≥4.0 mg/dl
  • Initiation of renal replacement therapy
  • Urine output <0.3 ml/kg/hr for ≥24h
  • Anuria ≥12h
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Classify the aetiology of acute kidney injury

A
  • Pre-renal (commonest)
  • Intrinsic renal: includes pre- or post-renal causes damaging renal cells
  • Post-renal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

List five causes of pre-renal AKI

A
  • Hypovolaemia:
    • Dehydration
    • Haemorrhage
    • DaV; third space losses; renal losses
    • Burns
  • Reduced CO: cardiac failure; liver failure; sepsis
  • Renal artery stenosis
  • NSAIDs; Coxibs; ACEi; loop diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Explain how NSAIDs and Coxibs cause AKI

A
  • Both inhibit COX enzymes needed for prostaglandin (PG) synthesis
  • PG is a vasodilator which can act on the afferent arteriole
  • Inhibition causes afferent vasoconstriction and renal hypoperfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

List five causes of intrinsic renal AKI

A
  • Tubular:
    • Acute tubular necrosis (80-90%)
    • Acute interstitial nephritis (rare): 4-7d after starting abx
    • Rhabdomyolysis: CK >10,000
    • Multiple myeloma
  • Nephrotoxins: abx; contrast; chemotherapy
  • Sepsis
  • Glomerular: glomerulonephritis; SLE; haemolytic-uraemic syndrome
  • Vasculitis; renal artery stenosis; thrombosis; dissection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain the pathophysiology of acute tubular necrosis

A

Almost any cause of pre-renal AKI if prolonged to the point at which renal autoregulation fails, will lead to ischaemic ATN

  • Sustained hypoperfusion of renal tubules ➔ tubular cell death
  • Nephrotoxins causing direct injury and tubular cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is haemolytic uraemic syndrome?

A

Commonest cause of AKI in children

Toxins associated with E. coli O157:H7

Triad of:

  • Microangiopathic haemolytic anaemia: Coomb’s -ve
  • Thrombocytopenia
  • AKI

Supportive treatment

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

List four causes of post-renal AKI

A
  • Ureteric: bilateral renal stones, retroperitoneal fibrosis, GU tumours
  • Bladder: acute urinary retention, blocked catheter
  • Urethral: prostate enlargement, renal stones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give five risk factors for AKI

A
  • Aged 65+
  • Hx of AKI
  • CKD Stage 3+ (eGFR <60)
  • Symptoms or Hx of urological obstruction
  • Chronic conditions: heart failure; liver disease; diabetes
  • Neurological or cognitive impairment
  • Sepsis
  • Oliguria
  • Nephrotoxic drugs or contrast agents within 1/52
  • Immunocompromised; cancer therapy; toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Provide three complications of AKI

A
  • Hyperkalaemia
  • Hyponatraemia
  • Hypermagnesaemia; hyperphosphataemia
  • Hypocalcaemia
  • Metabolic acidosis
  • Volume overload: peripheral and pulmonary oedema
  • Uraemia
  • CKD and ESRD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name three clinical features of suspected AKI

A
  • NaV; diarrhoea; evidence of dehydration
  • Reduced urine output; changes in urine colour
  • Confusion; fatigue; drowsiness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List three signs seen in AKI

A
  • HTN
  • Dehydration: prolonged CRT; tachycardia; postural hypotension
  • Sepsis: eg. fever; respiratory signs; indwelling urinary catheter
  • Urinary retention: enlarged bladder or prostate
  • Fluid overload: raised JVP, peripheral and pulmonary oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How can the risk of AKI be reduced?

A
  • Early identification
  • Avoid pre- and peri-operative hypovolaemia
  • Continuous monitoring of fluid status during IV fluids
  • Avoid nephrotoxins where possible: NSAIDs, aminoglycosides, contrast
    • NaCl 0.9% for 12h pre- and post-contrast
  • Prompt treatment of suspected sepsis
17
Q

Request three investigations for suspected AKI

A
  • U+Es
  • Urinalysis
  • USS KUB
  • FBC; LFTs; bone profile; CRP; glucose
  • Clotting screen
  • Blood cultures
  • ECG
  • CXR
  • Medication review
18
Q

Outline the management of AKI

A

AKI Care Bundle

  • Monitor: 4hrly EWS; hourly urine output; fluid balance; daily weight
  • Routine U+Es; bone profile; VBG
  • Identify and treat reversible causes
  • Optimise fluid balance using IVI; consider catheterisation
  • Medication review
  • Referral for RRT and nephrology where appropriate
19
Q

What are the indications for renal replacement therapy for AKI?

A
  • Hyperkalaemia unresponsive to medical treatment
  • Fluid overload unresponsive to medical treatment
  • Persistent or worsening metabolic acidosis
  • Uraemic symptoms: Intractable vomiting; confusion; twitching
  • Evidence of pericardial effusion
20
Q

Outline the emergency treatment of hyperkalaemia

A

10ml of 10% calcium gluconate IV: cardioprotective IV insulin actrapid + dextrose Dialysis if persistent hyperkalaemia

21
Q

What ECG changes are seen with hyperkalaemia?

A

Tall tented T waves Small/absent p waves Increased PR interval Widened QRS Sine wave pattern Asystole

22
Q

List three clinical features of uraemia

A
  • Anorexia; intractable NaV
  • Uraemic polyneuropathy; restless legs
  • Pruritus
  • Pericarditis
  • Encephalopathy
    • Intellectual clouding; drowsiness
    • Seizures
    • Coma
  • Haemorrhage: abnormal platelet adhesion
  • ‘Uraemic frost’: acummulation in skin
23
Q

Define contrast nephropathy

A
  • 25% increase in creatinine
  • Within 2 days of IV administration of contrast media
24
Q

How is contrast nephropathy best prevented?

A

IV 0.9% sodium chloride for 12h pre- and post-op

25
Q

What follow-up monitoring should be done after an episode of AKI?

A

Monitor for development or progression of CKD for at least 2-3 years after AKI