Acute Kidney Injury

Acute kidney injury (AKI) is a common, but often predictable and avoidable complication post-operatively. It should be considered a medical emergency and therefore requires early diagnosis, investigation and management.


Definition

Acute kidney injury can be defined (as per KDIGO and RIFLE criteria) as any of the following:

  • ≥50% rise in serum creatinine from baseline within last 7 days
  • Increase in serum creatinine by ≥26.5mmol/l within 48 hours
  • Urine output <0.5mls/kg/hour (oliguria) for more than 6hrs
Fig 1 – The internal structure of the kidney

Fig 1 – The internal structure of the kidney

The severity of AKI can be classified by creatinine level relative to baseline:

  • Stage 1: 1.5 – 2.0 times the baseline
  • Stage 2: 2 – 3 times the baseline
  • Stage 3: >3 times the baseline

Causes of Acute Kidney Injury

The causes of acute kidney injury can be categorised into pre-, intra- or post- renal causes. Perioperatively, pre-renal causes are the most common but it is still important to consider and exclude the other causes (most common causes have been placed in bold)

Pre-renal

  • Sepsis
  • Dehydration (including pre-operative NBM or bowel preparation)
  • Haemorrhage
  • Cardiac failure
  • Liver failure (causing a hepatorenal syndrome)

Important to remember that any intra-operative damage to the renal arteries can also cause pre-renal AKI. This is common in vascular procedures, such as from accidental graft occlusion, endovascular emboli, or proximal aortic clamp applied for too long.

Intra-renal

  • Nephrotoxins:
    • NSAIDS

      Fig 1 - Pathological kidney specimen from a patient with AKI. Necrosis of the cortex can be seen.

      Fig 2 – Pathological kidney specimen from a patient with AKI. Necrosis of the cortex can be seen.

    • ACEi (or ARBs)
    • Aminoglycosides
    • IV Contrast
  • Parenchymal Disease:
    • Glomerulonephritides
    • Acute tubulointerstitial nephritis
    • Rhabdomyolysis
    • Haemolytic uraemic syndrome (HUS)
    • Multiple myeloma

Post-renal

  • Ureteric:
    • Retroperitoneal fibrosis
    • Bilateral renal stones*
    • Tumours (either mural or extra-mural)

*Beware the patient with one kidney, renal stones and signs of infection, this is a true urological emergency

  • Bladder:
    • Acute urinary retention
    • Blocked catheter
  • Urethral:
    • Prostatic enlargement (BPH or malignancy)
    • Renal stones

Investigations

The investigations in acute kidney injury can be divided into bedside tests, blood tests, and imaging.

Bedside Tests

  • Examine the patient and assess their fluid status
    • Ensure to check the urine (dilute or concentrated? Blood stained?)
  • Urine dipstick (check for protein or blood)
    • Urine protein:creatinine ratio (PCR) if protein present, to quantify protein; consider nephrology referral if level is high and cause is undetermined

Bloods

  • Initial routine bloods (FBC, U&Es, CRP, LFTs, and Ca2+)
  • ABG (if possible sepsis or hypovolaemia) for assessment of acid-base balance and lactate levels.
  • Cultures (if possible sepsis)

Imaging

  • Ultrasound scan (USS) of the kidneys, ureters and bladder (USS-KUB) may be required if an obstructive causes is suspected
    • A hydronephrosis indicates a potential obstructive cause in the urinary tract
Fig 2 - Ultrasound scan of the kidney, showing marked hydronephrosis - caused by a left ureteral stone.

Fig 3 – Ultrasound scan of the kidney, showing marked hydronephrosis caused by a left ureteral stone.


Management

Acute kidney injury is a medical emergency and treatment should be instigated in a timely fashion. If the patient is critically unwell with AKI, resuscitate the patient as necessary and inform your senior, before attempting to treat the underlying cause.

Fluids

Fig 3 - IV fluid infusion is a conservative treatment for PONV

Fig 4 – Fluid assessment is an important part of management in a patient with acute kidney injury.

Assess the patient’s hydration status, looking predominantly for signs of hypovolaemia (dry mucous membranes, increased capillary refill time, reduced skin turgor, tachycardia, or hypotension (severe)).

Give a fluid bolus (250-500mL) STAT and re-assess their fluid status after 10-15 minutes. Give repeat fluid boluses until the patient is fluid repleted, before commencing maintenance fluids.

Involve your seniors if the patient appears fluid overloaded yet remains in AKI

Monitoring

Re-assess the patient clinically on a regular basis and ask the nurses to commence 4 hourly observations.

Start monitoring urine output, asking the nurses to start a fluid balance chart and consider catheterising the patient to permit more accurate assessment. If the patient is fluid overloaded (for example, the cause is cardiac failure), obtain medical input and begin monitoring daily weight.

Repeat twice daily bloods (especially U&Es) to monitor the progression of serum creatinine.

Drug Rationalisation

Medications can both affect and be affected by the kidneys; so its important that nephrotoxic medications are stopped and doses of medications are reviewed.

  • Drugs to be stopped:
    • ACEi and ARBs
    • NSAIDs
    • Aminoglycosides
    • Potassium-sparing diuretics (due to increased risk of hyperkalaemia)
  • Drugs to be altered or reduced:
    • Metformin (risk of lactic acidosis)
    • Diuretics (worsens hypovolaemia, if present)
    • Subcutaneous heparin
    • Aminoglycoside antibiotics
  • Drugs to be avoided:
    • IV radiological contrast

Quiz

Question 1 / 6
Which is NOT a definition of AKI...

Quiz

Question 2 / 6
Which of the following is NOT a cause of pre-renal AKI

Quiz

Question 3 / 6
Which of the following is NOT a nephrotoxic drug?

Quiz

Question 4 / 6
Which of the following is a cause of post-renal AKI?

Quiz

Question 5 / 6
Which is NOT a sign of hypovolaemia?

Quiz

Question 6 / 6
Why would you consider catheterisation in AKI? (most appropriate answer)

Results

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