Week 6

Context

Acute kidney injury is defined as an abrupt loss of kidney function that develops over 7 days (NCPEOD, 2014). It is brought about by a loss of blood supply to the kidneys which leads to renal ischaemia. This eventually impedes the production and flow of urine through the kidneys. The result is oliguria and long term renal impairment, if not seen and managed effectively. AKI is common in deteriorating patients. Remember time is kidney function. Before commencing this section you may find it useful to review the structure and function of the kidney (see www.innerbody.com/image/urinov.html).

Content

Causes of Acute Kidney Injury (AKI)

There are a number of causes of AKI, both acute and chronic. They are spilt into three categories:

Pre-renal - Hypovolaemia (low blood volume in shock), hypotension, heart failure and liver cirrhosis
Intrinsic –damage to the glomeruli, renal tubules or glomerulonephritis
Post-renal – urinary tract obstruction. Stones, calculi and tumours can all be responsible for AKI.

Signs and symptoms of AKI

A patient showing signs of AKI will be acutely unwell. As the renal system begins to fail, nitrogen builds up in the blood stream. Signs ans symptoms include the following:

Metabolic acidosis (see Arterial Blood Gasses (ABGs) (Advanced))
General malaise and tiredness
Pain in loin regions around the flanks may be noted
Rash due to nephritis (inflammation of the kidneys)
Fluid overload in the patient
Diminished urine output

How a diagnosis is made

AKI is diagnosed from the patients history and blood investigations. Urea, nitrogen and creatinine all rise in the patients blood profile. AKI is defined as:

increase in Serum Creatinine (SCr) of 26 μmol/L within 48 hours OR an increase in SCr ≥1.5 times above baseline value within 1 week OR urine output of <0.5 ml/kg/hr for > 6 consecutive hours

AKI is staged for severity according to the following table (KIDGO, 2012)

Stage	Serum Creatinine	Urine Output
1	1.5–1.9 times baseline OR ≥ 0.3 mg/dl (≥ 26.5 mmol/l) increase	< 0.5 ml/kg/h for 6 -12 hours
2	2.0–2.9 times baseline	< 0.5 ml/kg/h for ≥ 12 hours
3	3.0 times baseline OR Increase in serum creatinine to ≥ 4.0 mg/dl (≥ 353.6 mmol/l) OR Initiation of renal replacement therapy OR, In patients < 18 years, decrease in eGFR to < 35 ml/min per 1.73 m²	< 0.3 ml/kg/h for ≥ 24 hours OR Anuria for > 12 hours

The Acute Dialysis Quality Initiative (ADQI) devised the 'RIFLE' criteria for staging AKI (Bellomo et al, 2004):

RISK – increase in serum creatinine by 1.5 fold. Decrease of glomerular filtration rate (GFR). Diminished urien output 0.5mls per KG per hour for 6 hours.
INJURY - two fold increase in serum creatinine or GFR decrease by 50%
FAILURE- threefold increase in serum creatinine or GFR decrease by 75%
LOSS – complete loss of kidney function for mor ethan 4 weeks
END STAGE RENAL DISEASE- complete loss of kidney function for more than 3 months.

Long term management: Renal Replacement Therapy

Once renal function is diminished, the patient will require dialysis. This can be in various forms; peritoneal dialysis, haemodialysis, or continuous venous haemofiltration. A recent patient safety alert (NHS England, 2014) highlights some factors for consideration in relation to the patient who is deteriorating. Knowing that your patient can experience AKI, enabling early detection, early management and long term planning of treatment options are imperative for patient with renal dysfunction.

Issues raised by the alert

It is estimated that 1 in 5 emergency admissions into hospital are associated with AKI, prolonging inpatient care and contributing to 100,000 deaths in secondary care. National Confidential Enquiry into Patient Outcome and Death (NCEPOD) estimated that one quarter to one third of cases have the potential to be prevented
Standardising the early detection of AKI is imperative. Complex long term medical conditions, medication and current illness are often complicated by AKI. Moves to promote early detection, immediate and long term management have been developed with some initiatives attempting to promote understanding of AKI.

The future of diagnosing AKI

A national algorithm, standardising the definition of AKI has now been agreed. This provides the ability to ensure that a timely and consistent approach to the detection and diagnosis of patients with AKI is taken across the NHS. This algorithm has been endorsed by NHS England and it is recommended that the algorithm is implemented across the NHS. When integrated into a Laboratory Information Management System (LIMS) the algorithm will identify potential cases of AKI from laboratory data in real time and produce a test result. The laboratory system will then send the test result, using existing IT connections to patient management systems.

The NICE Clinical Guideline 169 (2013) emphasises that early intervention is key to improve patient outcome. This should be based upon reviewing creatinine and urine output, and In acutely unwell patients, reviewing serum creatinine and comparing with baseline. Factors that might indicate a likelihood of AKI include:

Reduced Glomerular Filtration Rate (GFR), heart failure, diabetes, history of acute kidney injury, oliguiria, neurological or cognitive impairment or disability
Hypovolaemia
Drug intoxification of NSAIDs, ACE inhibitors
Iodinated contrasts agents within the past week
Sepsis
Deteriorating NEWS
Age 65 years and over

Signs of diminished urine output or oliguria causes concerns as this demonstrates signs of renal impairment. Left unmanaged the patient will deteriorate further. The patients history and blood profiles will assist in initial diagnosis but need to be compared to previous results. Ongoing blood profiles need to be carried out to ensure accurate patient management. In a deteriorating patient arterial blood gases may show evidence of metabolic acidosis. The urine output of less than 0.5 mls per kg per body weight over 6 hours may result in AKI.

Management during A to E assessment

Immediate

Continue to review National Early Warning Score (NEWS)
Monitor urine output 0.5 mls per kg per hour
ABGs
Blood profile
Ultrasound
Treat any urological obstruction ASAP
Refer to nephrology within 24 hours

Later considerations

Fluid balance charting is essential
Recording of NEWS should be ongoing
Fluid challenge use isotonic solutions not colloids unless haemorrhagic shock is seen.
In severe cases where renal impairment has progressed, sliding scale insulin with glucose monitoring should be performed
Avoid diuretics unless fluid overload is seen

Consider Gary's scenario: What signs and symptoms might Gary show if he showed signs of AKI ? What investigations might Gary need to determine AKI ?

References and Further Reading

Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P. (2004) Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Critical Care. Aug 2004;8(4):R204-12

Diehl-Oplinger, L. and Kaminski, M. (2004). Choosing the right fluid to counter hypovolemic shock . Nursing, 34 (3), 52-54

Hamilton, S. (2001). Detecting dehydration and malnutrition in the elderly. Nursing, 31 (12), 56-57.

NHS England (2014) Standardising the early indentification of Acute Kidney Injury. Leeds: NHS England

Young ME, and Flynn KT. (1988). Third spacing: When the body conceals fluid loss. Registered Nurse, 51 (8) , 46-48.

KIDGO (2012) Clinical Practice Guidelines.