Acute Kidney Injury
Acute kidney injury (AKI) is a common, but often predictable and avoidable complication post-operatively. It should be considered a significant medical condition that warrants early diagnosis, investigation and management.
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
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
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)
- Dehydration (including pre-operative NBM or bowel preparation)
- 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.
- Nephrotoxins, such as NSAIDs, ACEi (or ARBs), antibiotics (such as aminoglycosides, or chemotherapy (such as cisplatin)
- Parenchymal Disease, such as glomerulonephritides, acute tubulointerstitial nephritis, rhabdomyolysis, Haemolytic Uraemic Syndrome (HUS), or multiple myeloma
- Retroperitoneal fibrosis
- Bilateral renal stones
- Tumours (either mural or extra-mural)
- Acute urinary retention
- Blocked catheter
- Prostatic enlargement (BPH or malignancy)
- Renal stones
Examine the patient and assess their fluid status, alongside a bladder scan for any evidence of retention, before reviewing the drug chart for any nephrotoxins that could be causing or confounding the condition.
A urine dip can aid in differentiating between pre-renal and intrinsic causes of AKI; the urine specific gravity and osmolality values will be higher in pre-renal causes and urine Na excretion will be lower*.
*This is due to the kidney actively conserving Na and water in pre-renal cases, compared to intrinsic causes
Initial bloods should be taken alongside U&Es, including FBC, CRP, LFTs, and Ca2+. A blood gas if useful in severe cases to ensure no significant acid-base disturbance secondary to renal dysfunction has occurred.
An ultrasound scan of the kidneys, ureters and bladder is required in severe cases of AKI, especially if there is no response to initial management, in order to evaluate for any obstructive causes.
Any hydronephrosis present can indicate a potential obstructive cause in the urinary tract that can be addressed accordingly if the underlying cause of the AKI
Acute kidney injury should be viewed as a medical emergency and treatment should be instigated in a timely fashion. The condition is associated with worse morbidity and mortality rates hence should be managed promptly.
If the patient is critically unwell with AKI, resuscitate the patient as necessary and inform your senior, before attempting to treat the underlying cause.
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)) or sepsis.
If suspected of pre-renal AKI, give a fluid bolus (250-500mL) STAT and re-assess their fluid status after 10-15 minutes, monitoring their urine output after the bolus. Give repeat fluid boluses until the patient is fluid repleted, before subsequently prescribing maintenance fluids if required.
Involve your seniors if the patient appears fluid overloaded yet remains in AKI
Re-assess the patient clinically on a regular basis and ensure to commence regular 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.
In those that do not respond to fluid therapy, consider intrinsic or post-renal aetiology as the underlying cause for the condition and manage accordingly
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
- Potassium-sparing diuretics (due to increased risk of hyperkalaemia)
- Drugs to be altered or reduced:
- Metformin (risk of lactic acidosis)
- Diuretics (in cases of intra-vascular fluid depletion)
- Subcutaneous heparin
- Aminoglycoside antibiotics
- AKI is associated with worse patient outcomes and needs to be managed promptly
- Causes can be divided into pre-renal, intrinsic, and post-renal causes
- Fluid status, bladder scan, urine dip, routine bloods, and ultrasound scans all form part of the work-up of cases of AKI
- Ensure to treat the underlying condition and monitor regularly for response