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Document Type:
Guideline
Unique Identifier:
CORP/GUID/014
Document Title:
Version Number:
1
Acute Kidney Injury (AKI)
Status:
Draft
Classification:
Organisational
Responsibility:
Medicine
Scope:
Trust Wide
Author / Title:
Dr Begho Obale
Replaces:
Medical Guidelines – Acute Renal Failure, page 197
Head of Department:
Validated By:
Divisional Governance and Assurance Group
Date:
DD/MM/YYYY
Ratified By:
Procedural Documents and Information Leaflet Group
Date:
DD/MM/YYYY
Review dates may alter if any significant changes
are made
Review Date:
01/07/2018
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CONTENTS
1
2
3
4
4.1
4.2
4.3
4.4
4.4.1
4.5
4.6
4.7.1-7
4.8
4.9.1
4.9.2
4.9.2.4
5.0-5.4
6.0-6.2
7.0
8.0
9.0
10.0
11.0
11.2
11.3-4
13.0
14.0
15.0
5
6
7
8
9
10
11
12
Appendix 1
Appendix 2
Appendix 3
Appendix 4
Background
PURPOSE
SCOPE
Guideline
Definition and Diagnosis
Patients at Increased Risk of AKI
Causes of AKI
AKI Staging
Importance of AKI Staging
AKI diagnosis documentation
Clinical Presentation of AKI
Management of AKI- History and Examination
Investigations AKI Staging
Treatments- Precipitating causes
Medication review
Pharmacist Review
Fluid Prescription
Fluid balance chart, urine output
Consultant review
Monitoring
Other investigations
Complications of AKI identification and management
Indication for Referral to nephrologist, and Guidance
Indications for Renal Replacement Therapy
Referral to Critical care, Urologist
AKI in special situations
Discharge and Follow Up
Summary
ATTACHMENTS
OTHER RELEVANT / ASSOCIATED DOCUMENTS
SUPPORTING REFERENCES / EVIDENCE BASED
DOCUMENTS
DEFINITIONS / GLOSSARY OF TERMS
CONSULTATION WITH STAFF AND PATIENTS
DISTRIBUTION PLAN
TRAINING
AMENDMENT HISTORY
AKI Care Bundle
Fluid Balance Chart
AKI Renal Referral Proforma
Equality & Diversity Impact Assessment Tool
University Hospitals of Morecambe Bay NHS Foundation Trust
ID No. Corp/Guid/014
Revision No: 1
Title: Acute Kidney Injury (AKI)
Next Review Date: 01/07/2018
Do you have the up to date version? See the intranet for the latest version
Page 2 of 26
Page
3
4
4
4
4
4
5
5
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6
6
7
8
9
9
10
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11
12-13
13
14
14
14
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17
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20-22
23
24-25
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1. Background
1.1 Acute Kidney Injury (AKI) is a sudden deterioration in kidney function over hours to
days, resulting in the inability of the kidneys to excrete wastes or maintain fluid and
electrolyte homeostasis (KDIGO 2012)1. It is a devastating medical problem affecting
about 1:5 of all emergency admissions to hospital ( Wang et al 2012)2; and accounts for
about 5-15% of all inpatients. (Kerr M et al 2014)3 The majority of patients with AKI have
no symptoms (KDIGO 2012)1. 35% of all AKI starts newly in hospitalised patients ( Selby
et al 2012)4. NICE CG 1695 lists patients at increased risk of AKI such as; the elderly,
patients presenting with sepsis, hypovolaemia, patients with known chronic kidney
disease, and other chronic conditions such as liver disease, heart failure or on some
“nephrotoxic” medications.
1.2 AKI is a “sick patient” problem; these patients tend to need more frequent monitoring of
vital signs, assessment of hydration status, fluid balance, treating precipitating cause such
as sepsis, correcting hypovolaemia, restore blood pressure, patient catheterisation in
urethral obstruction, stopping “nephrotoxic drugs”, patient education and monitoring in the
community on discharge (NICE CG 169 20135). Patients with AKI stay much longer in
hospital e.g 10 days compared to 4 days without AKI (Selby et al 20124, Challiner et al
2014)6.
1.3 AKI costs the NHS in England £1billion pounds on inpatient costs and a further 179
million on outpatient management of complications such as chronic kidney disease (CKD)
(Kerr et al, 2014)3.
Mortality link to AKI is about 25-30% of all patients in hospital with AKI (NICE CG 169)5,
and accounts for 100,000 inpatient deaths a year (NCEPOD 2009)7
Complications of AKI are associated with high mortality of up to 50% and need to be
managed promptly and escalated to the critical care team (Anaesthetists) (KDIGO 2012) 1.
1.4 The National Confidential Enquiry on Patients Deaths and Outcomes (NCEPOD
2009)7 identified that only 50% of patients who died received adequate care, and about
30% inpatient AKI deaths could have been prevented by early identification, assessment
and treatment of AKI. Challiner R et al 2014, assessed 743 inpatients admitted over a 14
day period with AKI, they suggested that a reduction of 10% in the incidence of AKI could
save around 3,000 bed days per annum in an acute hospitals with 900 – 1000 beds. This
will significantly improve patient outcome and reduction in morbidity and mortality.
Reduction in length of stay will be beneficial for the patient and the hospitals finances as
well. Such a reduction in the incidence of AKI would require a reliable method of early
identification of the ‘at risk’ patient, and management (Challiner R et al 2014) 6 .
(1042 inpatient cases of AKI in UHMB July 2015 – pathology data).
1.5 It is important to educate patients and relatives following a recent AKI to help prevent
recurrent episodes (NICE CG 169). Patients will need monitoring of their electrolytes and
urea on discharge as some patients may deteriorate further within the first month and
some patients may not have resolution of AKI and develop chronic kidney disease (CKD)
at 3 months, and some may progress to end stage renal disease needing dialyses. The
risk being highest in patients with severe AKI (AKI CQUIN 2015) (Coca SG et al 2012).
Patients and the GP are also to be informed of any medication alterations associated with
AKI (AKI CQUIN 2015).
University Hospitals of Morecambe Bay NHS Foundation Trust
ID No. Corp/Guid/014
Revision No: 1
Title: Acute Kidney Injury (AKI)
Next Review Date: 01/07/2018
Do you have the up to date version? See the intranet for the latest version
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2. PURPOSE
To improve the care of AKI in line with NICE guidelines and recommendations from the
NCEPOD 20097 with the ultimate goal of improving patients outcomes: reduce length of
hospital stay and reduced complications and mortality.
3. SCOPE
Covers recommendations of NICE CG1695 and NCEPOD 20097, as well as management
of complications of AKI and referral indications and protocols
Also includes learning resources for clinical staff, some for Nurses and Clinical Support
Workers and most of these for the doctors.
4. GUIDELINE
4.1 Definition and Diagnosis
4.1.1 Definition
Acute Kidney Injury ( AKI) is a sudden or rapid decline in kidney function that occurs within
hours to days in ill patients. Resulting in the inability to; maintain fluid balance, excretion of
wastes and toxins, impaired electrolytes and acid-base homeostasis. (KDIGO 2012)1
4.1.2 This diagnosis can be confirmed by;

An Increase in Serum Creatinine of 26mmol/l within 48hours

Or
An increase in Serum Creatinine of >/=1.5x above base line value within 7 days

Or
Urine Output of <0.5ml/kg/h for over 6 hours
AKI encompasses a spectrum of illness whereby even small changes in creatinine of
26mmol/l indicate renal injury, which can be easily reversible if treated appropriately,
otherwise can progress to severe injury requiring haemofiltration.
4.2 Patients at Increased Risk of AKI include:
Elderly >65years
Sepsis
Hypovolaemia
Hypotension (BP<100mmhg systolic or 40mmhg drop in systolic BP compared to baseline)
due to; Hypovolaemia, Primary cardiac cause, Antihypertensive medication
Chronic Kidney Disease
Diabetes
University Hospitals of Morecambe Bay NHS Foundation Trust
ID No. Corp/Guid/014
Revision No: 1
Title: Acute Kidney Injury (AKI)
Next Review Date: 01/07/2018
Do you have the up to date version? See the intranet for the latest version
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Liver disease
Heart failure,
Emergency surgery,
Administration in past week of; iodinated contrast, “nephrotoxic drugs” e.g NSAIDs-e.g
ibuprofen, ACE-I e.g. Ramipril, ARB-losartan etc.
Oliguria urine output <0.5ml/kg/h over 2 hours
Deteriorating early warning scores (EWS) >/= 3
Neurological, cognitive impairment or disability e.g stokes, dementia which may mean a
limited access to fluids, or difficulties swallowing
4.3 Causes of AKI
Pre-Renal- 85% reduced
renal perfusion
1)Hypovolaemia due to
Bleeding
Sepsis
Dehydration
2) Hypotenison
3) Anaphylaxis
4)Shock
5) Acute severe Heart
Failure
6)Arrhythmias with reduced
Cardiac output
7) Hepatorenal syndrome
8) Drugs; NSAID, ACE-I,
ARB’s due to disruption in
the autoregulation of
intraglomerular pressures or
renal artery stenosis
Renal- 10%
Post renal 5%
Drugs; NSAID, ACE-I, ARB’s,
lithium, Gentamicin, Contrast
Sepsis
Glomerulonephritis
Acute Tubular necrosis(ATN)
Interstitial nephritis
Rhabdomyolysis
Vasculitis
Myeloma
Enlarged prostate
Renal Stones
Pelvic lesions
4.4 AKI Staging
There is the Trust pathology e-alert on AKI (creatinine) to help guide with staging,
Important to also consider urine output staging as changes in creatinine can be
delayed by up to 48hours
AKI


Serum Creatinine
Urine output
Stages
1
-Increase in Serum Creatinine >26mmol/l
from baseline over 48hours
< 0.5 mL/kg/hour for > 6
hours
-Increase in Creatinine of 1.5 to 1.9 times
baseline in past year
University Hospitals of Morecambe Bay NHS Foundation Trust
ID No. Corp/Guid/014
Revision No: 1
Title: Acute Kidney Injury (AKI)
Next Review Date: 01/07/2018
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2
- Increase in serum creatinine of 2 to 2.9
times baseline
< 0.5 mL/kg/hour for > 12
hours
3
-Creatinine >3 times baseline
or
Increase in serum creatinine to
>354mmol/L +/-with an acute increase of
at least 44 mmol/l
or
< 0.3 mL/kg/hour
for > 24 hours
or
no urine output > 12 hours
Initiation of renal replacement therapy
RRT
A rise in creatinine in patients with CKD may indicate AKI, a rise in Creatinine of
44mmol in a patient with CKD 3b, 4 or 5 may suggest severe AKI stage 3, hence
advisable to mention AKI 3 on background of CKD-, rather than acute on CKD.
Patients with CKD stage 3, 4, 5 could develop complications of AKI with rise in Cr less
than 50% of their baseline hence need for proactive management of these patients and
early consideration for referrals.
Endeavour to look at results and baseline(changes of 26mmol at 50hours or 40%
above baseline will not score but would have clinical significance)
4.4.1 Importance of Staging AKI
Stage 1 patients have a mortality of <10%, over 50% of patients present as stage 1.
Stage 2 mortality of 20-30%,
Stage 3 mortality 30-50%
Stage 2 and 3 patients have a high risk of developing complications and this pushes the
mortality to up to 80% in patients needing dialysis (RRT).
More frequent monitoring of patients with stage 2 or 3, look out for and treat complications
early. Prompt consideration for referral to anaesthetist or nephrology.
100,000 patients die in hospitals in the UK from AKI. About a third of these deaths are
preventable if patients are assessed for risks of AKI, identified and managed appropriately.
4.5 Diagnosis
AKI is “a syndrome not just a diagnosis”. Hence document cause of AKI and staging in
patient’s case note. As staging severity and cause will influence management plan
4.6 Clinical Presentation of AKI



Most patients with AKI may have no complaint
Thirst
Reduced urine production
University Hospitals of Morecambe Bay NHS Foundation Trust
ID No. Corp/Guid/014
Revision No: 1
Title: Acute Kidney Injury (AKI)
Next Review Date: 01/07/2018
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




Dark or concentrated urine
Urinary obstruction- frequency, oliguria, anuria, hesitancy, Suprapubic fullness,
Renal problem- dysuria, Urinary frequency, loin pains, rigours, haematuria
Non-specific- Lethargy, confusion, tiredness,nausea, vomiting, dizzy, falls, breathless
Features suggestive of precipitating illness e.g pneumonia, UTI, MI, Diarrhoea and
Vomiting, haemoptysis
4.7 Management of AKI (See appendix 1 AKI Care Bundle for inclusion in case notes)
4.7.1 Assessment- history and clinical examinination:
4.7.1.1 Clinical history:
Systemic symptoms e.g thirst, urinary symptoms, haematuria, fever, source of sepsis,
Increase fluid loss e.g Diarrhoea, vomiting, increased loss from stoma etc, limited intake,
haemoptysis, flu like illness, sore throat, rash
4.7.1.2 Recent Respiratory Infection
Haemoptysis or sore throat followed by Haematuria and AKI should alert possibility of a
vasculitic cause such as Anti-Glomerular Basement membrane disease, IgA nephropathy,
Post streptococcal glomerulonephritis, Lupus nephritis, ANCA positive vasculitis.
4.7.1.3 Falls
Prolonged stay on floor, Rhabdomyolysis, muscle crush releases myoglobin, this breaks
down to haem which is toxic to the tubules, fascilitates cast formation and obstruction in
the tubules, treat with IV fluids to encourage increased urine output.
4.7.1.4 Recent Diarrhoea
If anaemia, thrombocytopenia, +/- E.Coli 0157 positive, in addition to abnormal red cells
on blood film e.g. helmet cells suggests Haemolytic ureamic syndrome (HUS)
4.7.1.5 Drug history:
Recent use, introduction or increased dosages of; Contrast, ACE-I, ARB, NSAIDs,
Diuretics, PPI, Antibiotics, including over the counter medicines and herbal medicines
4.7.1.6 Past medical history of AKI, Chronic illness e.g CKD, DM, SLE, Liver disease,
Congestive cardiac failure.
4.7.1.7 Social History- recent travel with possible exposure to tropical diseases (e.g.
malaria), Occupation ( work in sewers) exposure to rodents (e.g. leptospirosis, hantavirus)
4.7.2 Examine
 4.7.2.1 Assess Hydration Status ,
Presence of some of these indicate patient likely to need fluids(Hypovolaemia)
• Dry mucus membranes,
• Loss of skin turgor
• Respiratory Rate >20/min
• Systolic BP<100mmhg
University Hospitals of Morecambe Bay NHS Foundation Trust
ID No. Corp/Guid/014
Revision No: 1
Title: Acute Kidney Injury (AKI)
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• Postural hypotension,-drop in BP>20mmhg on standing and increase in pulse rate
of 30/min
• ↓JVP
• Pulse >90/min
• CRT>2secs or cold peripheries to touch
• EWS>/=3
• 45◦ Straight leg raising responsiveness
• Oliguria, Urine output<0.5ml/kg/h x2h
Check temperature, if febrile- increased insensible water loss
4.7.3 Watch out for Fluid overload—bibasal crepitations, peripheral oedema, raised JVP
4.7.4 systemic examination

Lungs for features of pneumonia, pleural rub, heart failure – bibasal fine creps
 CVS- heart rate, rhythm, sounds, pericardial rub, BP- hypotension, low JVP
 Skin for vasculitis rash, pallor, cellulitis,

Joints for arthralgia,
 Renal angle for tenderness, masses
 Urinary obstruction- suprapubic fullness if retention
4.8














Investigations
Renal Function- U&E
Venous gases, Bicarbonate and Ph
ABG if EWS>3, or AKI 2-3, expecially if deteriorating
Full blood count(FBC)
CRP, Lactate, Cultures, if suspected sepsis
ESR
Bone profile- Calcium, Phosphate
Liver function test (LFT),
Glucose
Creatinine Kinase (CK)- if falls- Rhabdomyolysis
Blood film if suspected HUS or TTP,- often low platelets
INR, abnormal in sepsis, liver failure
ECG- Ischaemic heart disease, hyperkalaemia, tachyarrhythmia
CXR- if suspected pulmonary oedema or pneumonia, alveolar haemorrhage
4.8.1 Urinalysis
Document all urinalysis results in case notes
Normal- likely to be due to a pre-renal or post renal cause of AKI
Blood + protein+ no nitrites and no symptoms of UTI- AKI also possible inflammatory renal
University Hospitals of Morecambe Bay NHS Foundation Trust
ID No. Corp/Guid/014
Revision No: 1
Title: Acute Kidney Injury (AKI)
Next Review Date: 01/07/2018
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disease such as vasculitis, glomerulonephritis or interstitial nephritis.
Blood only- trauma, stone, malignancy, severe renal ischemia due to arterial or venous
thrombosis
Protein >2+ only- Intrinsic glomerular disease, amyloidosis, severe HT, Diabetic
nephropathy
Increased white cells +/-nitrites can suggest UTI, Pyelonephritis, Acute Interstitial nephritis
Send sample for MCS and protein/creatinine ratio if dipstick protein >/=2+
4.8.2 Renal USS within 6h if suspected acute obstruction and sepsis -Pyonephrosis.
USS within 12-24h if; unknown cause of AKI, suspected renal tract obstruction, AKI
stage 2/3 if deterioration or poor response to treatment
4.9 Treatments
4.9.1 Treat precipitating cause of AKI e.g







Sepsis- treat with antibiotics promptly, as per Sepsis 6 protocol
Bleeding- Investigate and stop source of bleeding and transfuse as appropriate
Dehydration/ hypovolaemia- treat with fluids increased oral or intravenous- Give
intravenous boluses of 250-500ml of Chrystalloid fluids such as Hartmann’s or 0.9%
Sodium Chloride(Nacl) fluid every 15mins. Reassess to ensure features of
hypovolaemia such as tachycardia, tachypnoea, low JVP, CRT, EWS etc. are
improving, and evidenced by urine output >0.5ml/kg/h
Hypotension Stop antihypertensives. Treat with fluids as for hypovolaemia, treat
precipitating causes such as sepsis, haemorrhage. Give up to 30ml/kg fluids at 2 litres
maximum over 2 hours or longer if elderly or known heart failure.
Consider referral to critical care team for possible ionotropes if persistent hypotension
despite 2 litres of fluid, especially if associated oliguria or pulmonary oedema
Obstruction- catheterise if urethral obstruction
Stop nephrotoxins- Medication review
4.9.2 Medication Review- Temporarily stop drugs with“Nephrotoxic” potentials such as;
NSAID- Ibuprofen, Voltarol,etc
ACE-I - Ramipril, Lisinopril, Perindopril etc
ARB- Losartan, Irbesartan, Candesartan etc ,
Diuretics, - Furosemide, bendroflumethiazide, Bumetanide, Spironolactone
Antihypertensive especially if hypotensive or BP < 110mmhg systolic
PPI such as omeprazole and Lansoprazole as known cause of interstitial nephritis
Trimethoprim as can increase creatinine level by preventing secretion in kidneys
Metformin( if e-GFR<30 as risk of lactic acidosis), if severe AKI, or needing contrast
Long acting Opiate e.g Zomorph, Tramadol MR, replace with short acting opiates or ones
with low renal excretion such as oramorph, oxynorm, oxycodone, Fentanyl patches
University Hospitals of Morecambe Bay NHS Foundation Trust
ID No. Corp/Guid/014
Revision No: 1
Title: Acute Kidney Injury (AKI)
Next Review Date: 01/07/2018
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4.9.2.1 Reduce dose of some medication such as;
Enoxaparin to 20mg and antibiotics e.g augmentin depending on the severity of the AKI,
Give renal dose of Gentamicin 3mg/kg as stat dose if clinical need instead of 5mg/kg
Reduce dose of some antiarrythmics ( e.g Beta blockers etc),
Reduce dose of opiates, digoxin as to avoid toxicity due to impaired excretion,
Reduce dose of ACE-I and diuretics in case of AKI in known patient with heart failure
Reduce dose of metformin for some days till AKI improved
Avoid iodinated radiology contrast especially in patients with EGFR < 40ml/min/1.73/m2
4.9.2.2 Review of the above medication as AKI resolves, may be re- introduced at lower
levels, dose titrated and monitoring of renal function on a weekly basis. Or usual dose
restored
4.9.2.3 Some Medication may be stopped for good e.g AKI stage 3 in a person started
on ACE-1 or PPI weeks or a few months earlier indicating severe renal artery stenosis or
interstitial nephritis respectively. Zomorph if persistent AKI 3 on discharge
4.9.2.4 Pharmacist review of drugs within 24 hours if possible as list above is limited
and advise on other drugs and interactions is highly advisable
5.0 Fluids- Prescription
5.1 Prescribe Fluids appropriatesly to treat hypovolaemia as above, once hypovolaemia is
resolved and patient is making >0.5ml/kg/h, assess hydration status. If stable and no
excess loses from vomiting etc, prescribe maintenance fluids
5.2 Maintenance fluid at 30ml/kg/24hours ( 25ml/kg/24h in the elderly) preferable
balanced crystalloids e.g Hartmanns, or Dextrose saline 0.18/4%, 0.9% Nacl preferable in
patients with vomiting and diarrhoea.
5.3 Other fluid considerations Replacement Fluids = maintenance fluid + matched
excess volume lost from stoma, polyuria , diarrhoea or vomiting etc
5.4 Appropriate prescriptions in managing redistribution problems in patients with CCF,
Liver failure, Nephrotic syndrome, preeclampsia etc (e.g.needs lower volume boluses,
albumin, ionotopes etc) as per NICE CG 1748 with considered Critical care input.
5.5 Avoid potassium containing fluids in anuric patients. Caution in patients with AKI at
risk of hyperkalaemia, (Maximum potassium replacement of 20mmol on first day and 0.51mmol/kg /24 daily dependent on if patient is hypokalaemic) daily requirement for
Sodium and Chloride is 1mmol/kg/24h each hence caution with excessive 0.9% Nacl
containing 154mmol/l sodium and same of Chloride. Risk of hyperchloraemic Acidosis
and worsening of AKI
5.6 Weigh patient daily- to help prescribe iv fluids and assess minimum urine output of
0.5ml/kg/h. Daily weight to help identify issues with hypovolaemia and fluid overload early
University Hospitals of Morecambe Bay NHS Foundation Trust
ID No. Corp/Guid/014
Revision No: 1
Title: Acute Kidney Injury (AKI)
Next Review Date: 01/07/2018
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6.0 Fluid balance chart and urine output (See appendix 2)
6.1 Open a fluid balance Chart in all patients with AKI or at high risk of AKI
Close monitoring of fluid input and urine output aim for urine >0.5ml/kg/h (e.g. 40ml/h in a
80kg patient) and adjust fluid input as appropriate,
Balance calculated as; total oral and intravenous fluids minus total output urine,(+
diarrhoea+vomiting, +stoma output if appropriate) +500ml insensible water loss. A positive
balance is expected as AKI is being corrected.
A large excess positive balance in a patient with oliguria should raise concerns of severe
dehydration, provided features of hypovolaemia otherwise consider severe AKI or
associated Acute Tubular necrosis and increase risk of fluid overload and pulmonary
oedema
Record hydration status and previous days fluid balance in case notes everyday and take
appropriate action
Fluid balance should be assessed 1-2hourly in unstable patient and at least 4hourly if
stable
6.1 Watch out for Polyuria due to; post relief of obstructed urinary tract, from recovering
AKI, recovering ATN. Significant negative balance. Prescribe more fluids as appropriate
(replacement), monitor E&U, hydration status
6.2 Consider urethral catheterisation in patients with urethral obstruction, very unwell,
severe sepsis or severe AKI e.gstage 3 and deteriorating***Avoid routine catheterisation
7.0 Senior review by Consultant within 12 hours of Admission
8.0 Monitoring
 1-2 hourly monitoring of vital signs and urine output if AKI 2 or 3, or EWS >/=3,
otherwise if stable,
 4hrly review of EWS, Hydration status, urine output, fluid balance
 Renal Function-U&E, bicarbonate, at least daily. Consider 6-12 hourly initially
especially if AKI stages 2-3, or if clinical deterioration or poor urine output
 Daily review ; previous days fluid balance, Renal function, bicarbonate, fluid and drug
prescriptions, clinical improvement, complications- at ward round
 Pharmacy review of Medication within 24 hours of admission
 Daily weights
9.0 Other Investigations as appropriate
9.1 Urine MicroscopyEosinophil / casts can suggest Interstitial nephritis(Antibiotics, PPI, NSAID), other causes
include rapidly progressive glomerulonephritis (RPGN), transplant rejection.
Red cell casts – Glomerulonephritis,
White cell casts-Pyelonephritis
University Hospitals of Morecambe Bay NHS Foundation Trust
ID No. Corp/Guid/014
Revision No: 1
Title: Acute Kidney Injury (AKI)
Next Review Date: 01/07/2018
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9.2 Urine sodium- <20mmol/l in pre-renal AKI, >40mmol/l in renal causes of AKI
9.3 “Renal Screen” – in patients with suspected vasculitis or Patients with AKI 3 or AKI 2
with proteinuria and haematuria without UTI, or unexplained AKI 3
- CK, Anti- GBM Ab, ANA, ANCA, connective tissue disease screen, immunoglobulin,
serum electrophoresis, Urine BJP, Urine ACR or PCR
9.4 If likelihood of dialysis soon, check Hepatitis B, C and HIV screen
9.5 Urgent CT
Need to be discussed with Radiologist if AKI stage 2/3, if eGFR < 40 or poor urine output
and deteriorating renal function, follow Policy for IV Contrast Examinations on use of
contrast in patients with CKD (see section 6).
10.0 Look out for complications of AKI- treat, and refer promptly if not responding
10.1 HyperkalaemiaPotassium 6.5mmol/l or more, or >6.0mmol/l with ECG changes -Peaked T waves,
widening QRS complexes, patient may have tachyarrhythmia.
Treat with Calcium gluconate 10ml of 10% over 10-15min to stabilise the heart muscles
against arrhythmias, and treat with 50ml of 50% Glucose + 10units of actrapid insulin over
20-30mins( or 125ml of 20% glucose +10units insulin), ECG monitoring
-Repeat electrolytes in 2 hours, if persistent, repeat above treatment
10.1.1 Consider Salbutamol nebuliser 5mg doses up to 20mg if HR<110b/min
10.1.2 Ensure any potassium sparing medication such as spironolactone ,ACE-I , ARBs
and NSAIDs, have been stopped
10.1.3 Referral- Discussion with critical care team if persistent hyperkalaemia despite
treatment- indication for haemofiltration
10.2 Metabolic acidosisABG persistent pH<7.25 despite adequate treatment with fluids and treatment of
precipitating cause.
Acidosis affects enzyme function in the body, can impair cardiac contractility
10.2.1Patient may present with vomiting, confusion, irritability, breathlessness, drowsy,
reduced GCS, arrythmias
10.2.3 Oral Sodium bicarbonate 1g tds can be considered if bicarbonate <22mmol/l
10.2.4 ***Do not give IV bicarbonate 1.26-1.4% 500ml over 4h except following advice
from nephrologist/anaesthetist, as can cause complications such as fluid overload
hypocalcaemia, hypokalaemia.
10.2.5 Failure to correct acidosis and improve urine output will require urgent RRT
10.2.6 Urgent referral to critical care team- anaesthetist or nephrologist for haemofiltration
10.3 Pulmonary oedema, Fluid overload.
Often results from overenthusiastic rehydration in a patient with poor urinary output
<0.5ml/kg/h or anuria, often as a result of severe AKI
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10.3.1 Fluid balance likely to show a significant positive fluid balance,
10.3.2 Monitor hourly urine output, Review IV fluid prescription
10.3.3 Patient could present with shortness of breath on minimal exertion, orthopnoea,
raised JVP, bibasal creps, cough productive of frothy sputum
10.3.4 CXR- likely to show acute pulmonary oedema, also request ABG
10.3.5 Management- Sit patient upright, give 100% oxygen with non-rebreathing bag.
If haemodynamically stable, give IV furosemide boluses of 50mg, up to 150mg slowly over
10-20minutes, and assess response, Stop IV fluids, close monitoring of urine output,
Infusion of frusemide 10mg/hour may be needed
If haemodynamically stable, and BP adequate, consider i.v GTN infusion at 1-10ml/hr,
improves the situation by causing vasodilatation to offload excess fluid until RRT available.
Failure to respond by diuresis indicates likelihood of ATN . Urgent referral for RRT
10.3.6 Urgent Referral- Critical care team or Nephrologist if no diuresis despite i.v
furosemide of 100-150mg as patient likely to need haemofiltration
10.4 Uraemic pericarditis- Patient presents with severe chest pain worse on lying flat,
improved on sitting up, short of breath, ECG may show classic saddle shaped changes on
leads
10.4.1 Management – Oxygen, analgesia, urgent Anaesthetist input for haemofiltration,
urgent ECHO if possible, consider cardiology input.
10.4.2 Uraemic encephalopathy- Confusion, vomiting, drowsy GCS </=8Management- protect airway, put patient in recovery position,
10.4.3 Urgent referral to anaesthetist for Haemofiltration in patients with uraemic
pericarditis or Encephalopathy
11 Referrals:
11.1 Indication for Referral to Nephrologist
 AKI stage 3 refer within 12-24 hours of detection if non- response to treatment.
 If cause of AKI unknown
o
Intrinsic renal disease or multi-system disease suspected (e.g. vasculitis,
glomerulonephritis, tubulointerstitial nephritis, myeloma, pregnant women or
postpartum especially if concerns about preeclampsia, TTP or HUS),
 Recent renal transplant
 CKD stage 4 or 5
 Patients needing Renal replacement therapy (RRT) also known as haemofiltration. In
UHMB Discuss with anaesthetist urgently
11.2 Guidance on Referral to nephrologist (see appendix 3)
(Registrar on call) in Royal Preston Hospital on Mobile number- 07415229709 or through
switch board number 0
In the near future we will be using the NoRSE( National Online Referral System for
Emergencies) electronic referral system for nephrologist advise
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11.3 Indication for RRT
 If complications of AKI are present: (not responding to treatment)
 Hyperkalaemia K>6.5mmol/l,>6.0mmol/l with ECG changes
 Fluid overload, pulmonary oedema,
 Metabolic acidosis persistent pH<7.25
 Uraemic pericarditis or encephalitis
 Toxins such as ethylene glycol, etc
11.4 Other referrals
Critical Care (Anaesthetist in UHMB)
 Patients needing RRT- as above
 Circulatory failure requiring inotropes
 Multi-organ failure,
 CCF
 Liver failure
11.5 Urology – urgent referral if;
 Pyonephrosis
 Bilateral ureteral obstruction
 Obstructed single kidney
 Also refer for any renal tract obstruction
12 Other AKI Issues
 Increased Length of stay in hospital, longer duration in higher stages of AKI. Up to
twice the expected stay in patients without AKI
 Incomplete resolution of AKI with progression to Chronic Kidney Disease
 Long term dialysis
 X4 fold increase in mortality in patients with AKI compared to the general population
 Increased cost to the NHS
 Acute Tubular Necrosis (ATN) due to prolonged hypoxia caused by hypoperfusion of
the kidneys due to hypovolaemia. Longer duration of hypovolaemia can result in more
severe AKI, damage to the tubules, and recovery may be incomplete with resulting
need for haemofiltration or long term CKD.
 Acute interstitial nephritis, renal injury caused by drugs such as Proton Pump
Inhibitors, NSAID, antibiotics( penicillines, cephalosporins), onset could be 2-3 weeks
after starting drug, damage often reversible on stopping these drugs.
13 AKI in special situations
13.1 Radiology contrast use- assess if patient is at risk of / or has got AKI or chronic
Kidney disease and document in case note
Inform patient of possibility of developing AKI or deterioration of AKI
13.1.2 Prevent contrast induced AKI treat dehydration and continue with IV fluids x 12h
after contrast by giving 1ml/kg/h for at least 12h in patients at risk, monitor fluid balance
and renal function daily
13.1.3 Avoid contrast if eGFR <40, or AKI stage 2 or 3, discuss with radiologist if an
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emergency
13.1.4Stop some possible nephrotoxic medication such as metformin, ACE-I at least 24
hours before contrast and 24 to 48 hours post contrast
13.2 Surgery- In case of emergency surgery inform patient of possibility of AKI (+/- risk of
haemofiltration)
13.2.1 Assess patients risk of AKI and document in case note, also document if known
CKD as increased risk of developing AKI
13.2.2 Withhold nephrotoxic drugs, Close monitor of fluid balance to prevent inpatient AKI
14.0 After an Episode of AKI – Discharge and Follow Up



Include AKI staging and cause of the AKI in the discharge summary.
Comment if Creatinine resolved to within 20% of normal baseline or not
Discuss Medication alteration e.g Omeprazole stopped due to interstitial nephritis,
never to restart. Ramipril dose reduced from 10mg to 2.5mg due to AKI,
 Give clear plans to both the patient and the GP about restarting medications that
may have been stopped as a result of AKI, and any that has been stopped for good –
failure to do so can result in increased risk from long term conditions e.g CCF,
angina, diabetes etc
Advise as to how to re-introduce medication e.g restart Ramipril at 1.25mg and
weekly monitoring of U&E, increase dose by 1.25mg every week if Creatinine levels
stable to maximum of 5mg when reviewed at 4 weeks- date in clinic or by GP
 Give clear instructions to the GP if renal function needs to be checked after
discharge, and how often this needs to be done. E.g weekly E&U if unresolved AKI,
for 1month, or 2 weekly if resolved AKI on discharge for 1month. And give review
date e.g at 1month by GP
 Repeat E&U also at 3months in all partially resolved AKI to identify CKD early
 If the patient has significant residual kidney dysfunction e.g eGFR <30ml/min/1.73/m,
consider outpatient referral to nephrology clinic within 4 weeks, with U&E monitoring
weekly
 Request Nephrology review on follow up if recurrent AKI in patients with known CKD
e.g x 2 in past year
 Explanation to patient and family about what has happened and how to prevent this in
future- e.g avoid drugs with “nephrotoxic” potential if unwell with dehydration or sepsis
 AKI Patient advice sheet and sick day rule card
15.0 Summary
Acute Kidney Injury Is a common medical problem affecting 20% of all emergency hospital
admissions, with an inpatient mortality of 100,000/year in the UK. It is easily preventable,
treatable and reversible if identified early and managed appropriately. Diagnosed if urine
output <0.5ml/kg/h for >6h or Creatinie >1.5x baseline or acute rise of 26mmol/l over
48hours. Commonest causes of AKI being Sepsis and Hypovolaemia
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1) Assess- history, risk factors, clinical examination, with emphasis on hydration
status, EWS
2) Diagnose cause of AKI and record in notes, Record stage as marker of severity
3) Urinalysis- record all results, blood and protein indicate damage –AKI ,or nephritis
4) Investigations- E&U, bicarbonate, FBC, Sepsis screen, Lactate, CRP, ECG, CXR,
5) Renal USS within 12-24h if AKI 3, unknown cause, obstruction. Within 6h if
pyonephrosis
6) Stop nephrotoxic drugs, and reduce dose of some medicines
7) Treat cause of AKI e.g sepsis or urinary obstruction, hypovolaemia, hypotension
8) Closely monitor vital signs, EWS, urine output hourly initially, then 4 hourly if stable
9) Look out for complications of AKI and treat appropriately
10) Prompt referral to Critical care team or Nephrologist if unresolving AKI 3 or
complications
11) On discharge communication to patient and GP about cause of AKI, medication
alteration, and plans to restart or titrate medicines and investigations and followup
12) Patient AKI advice leaflet
5. ATTACHMENTS
Number
Title
1
Acute Kidney Injury Care Bundle
2
Fluid balance Chart
3
AKI Renal Referral Proforma
4
Equality and Diversity Impact Assessment Tool
6. OTHER RELEVANT / ASSOCIATED DOCUMENTS- e-learning for staff
Unique Identifier
Title and web links from the document library
Policy on IV Contrast Examination
(to be uploaded to Heritage)
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7. SUPPORTING REFERENCES / EVIDENCE BASED DOCUMENTS
References in full
N
o
1
2
3
4
5
6
7
8
References
KDIGO (2012) Kidney disease: improving global outcomes. Clinical practice guideline
for acute kidney injury. Kidney International Supplement. 2(1), pp.1-138. [Online]
Available from:
http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pd
f [Accessed 13/07/2015]
Wang HE et al (2012). Acute kidney injury and mortality in hospitalized patients.
American Journal of Nephrolology;35 pp.349-55. doi: 10.1159/000337487. [Online]
Available from: https://www.karger.com/Article/Pdf/337487 (accessed 27.7.15)
Kerr, M et al (2014) The economic impact of acute kidney injury in England.
Nephrology Dialysis Transplantation 29 pp: 1362-68 doi: 10.1093/ndt/gfu016. [Online]
Available from: http://ndt.oxfordjournals.org/content/29/7/1362.full.pdf (accessed
27.7.15)
Selby, N.M. et al. (2012) Use of electronic results reporting to diagnose and monitor
AKI in hospitalized patients. Clinical Journal of the American Society of Nephrology.
7, pp.533–540. [Online] Available from:
http://cjasn.asnjournals.org/content/7/4/533.full.pdf+html (accessed 27.7.15)
NICE Guidelines (CG169) (2013) Acute kidney injury: Prevention, detection and
management of acute kidney injury up to the point of renal replacement therapy.
[Online] Available from: https://www.nice.org.uk/guidance/cg169 (accessed 27.7.15)
Challiner, R et al (2014) Incident and consequence of acute kidney injury in
unselected emergency admissions to a large acute UK hospital trust. BMC
Nephrology. 2014;15 pp.84. doi:10.1186/1471-2369-15-84. [Online] Available from:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4046061/ (accessed 27.7.15)
National Confidential Enquiry into Patient Outcome and Death (NCEPOD) (2009)
Adding Insult ot Injury: A review of the care of patients who died in hospital with
primary diagnosis of acute kidney injury (acute renal failure). [Online] Availabe from:
http://www.ncepod.org.uk/2009report1/Downloads/AKI_report.pdf (accessed
27.7.15)
NICE Guidelines (CG174) (2013) Intravenous fluid therapy in adults in hospital.
[Online] Available from: https://www.nice.org.uk/guidance/cg174 (accessed 27.7.15)
Bibliography- eLearning resources
University Hospitals of Leicester NHS Trust (2013) Acute kidney injury eLearning
course [Online] Available from: http://www.uhl-library.nhs.uk/aki/ [Accessed
13/07/2015]
London Acute Kidney Injury Network (2012) Online learning and videos [Online]
Available from: http://www.londonaki.net/academy/online-learning-videos/index.html
[Accessed 13/07/2015]
e-Learning for Healthcare (2011) e-Learning for renal medicine. London: e-LfH.
[Online] Available from: http://www.e-lfh.org.uk/programmes/renal-medicine/
[Accessed: 13/07/2015]
UK Renal Registry (2015) Think kidneys. [Online] Available from:
https://www.thinkkidneys.nhs.uk/ Accessed 13/07/2015]
NHS Kidney Care and the Royal College of Physicians of Edinburgh (2014) Acute
kidney injury (AKI) (1.1). [Mobile app]. [13/07/2015]
University Hospitals of Morecambe Bay NHS Foundation Trust
ID No. Corp/Guid/014
Revision No: 1
Title: Acute Kidney Injury (AKI)
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Page 17 of 26
Lewington, A. (2015) Communities at risk of developing acute kidney injury. Bristol:
UK Renal Registry. [Online] Available from: https://www.thinkkidneys.nhs.uk/wpcontent/uploads/2015/07/Communities-at-risk-of-developing-AKI-Think-Kidneys010715.pdf [Accessed 13/07/2015].
National Institute for Health and Clinical Excellence (2007) Clinical guideline 50:
acutely ill patients in hospital: recognition of and response to acute illness in adults in
hospital. London: NICE. [Online] Available from:
http://www.nice.org.uk/guidance/cg50/resources/guidance-acutely-ill-patients-inhospital-pdf [Accessed 13/07/2015]
http://elearning.nice.org.uk/ National Institute for Health and Clinical Excellence
(NICE) Acute Kidney injury; An e-learning module for non- renal registered nurses
and Health Care Support workers in all settings. March 2014
8. DEFINITIONS / GLOSSARY OF TERMS
Abbreviation Definition
or Term
ABG
Arterial blood gases
ACE- I
Angiotensin Converting Enzyme inhibitor
AKI
Acute Kidney Injury
ARB
Angiotensin Receptor Blocker
ATN
Acute Tubular Necrosis
CCF
Congestive Cardiac Failure
CKD
Chronic Kidney Disease
CVS
Cardiovascular system
eGFR
Estimated Glomerular Filtration Rate
E&U
Electrolytes and Urea
GTN
Glyceryl Trinitrate Infusion
NSAID
Non Steroidal Anti Infalmatory Drugs
PPI
Proton pump inhibitor e.g Omeprazole
SLE
Systemic Lupus Erythematosus
9. CONSULTATION WITH STAFF AND PATIENTS
Enter the names and job titles of staff and stakeholders that have contributed to the document
Name
Job Title
Dr Gill O’Connell
Associate Medical Director, Anaesthetist
Dr Dimitios Poulikakos and Dr Leonard Ebah Nephrologists, Manchester, North Lancashire and
South Cumbria Strategic AKI Network
Dr Nick Selby
Nephrologist, NHS England AKI, Royal Derby Hosp
Dr Rob Nipah
Acute Physician?Nephrologist, Salford Royal
Matron Sue Smith
Executive Chief Nurse, Executive lead AKI UHMB
Dr Pepetual Uwe
ST3 Rheumatology FGH
Dr Rajit Varia
Acute Physician, St Helens and Knowsley NHS
Dr Richard Lea
Acute Physician FGH
Sister Tanya Holme
Ward Manager Acute Medical Unit FGH
Matron Melanie Woolfall
Advanced Nurse Practitioner Acute Medicne RLI
Matron Helen Thompson
Matron Acute Medicine FGH
10. DISTRIBUTION PLAN
Dissemination lead:
Dr Ian Chadwick Enter the lead of the
development group
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10. DISTRIBUTION PLAN
Previous document already being used?
If yes, in what format and where?
Proposed action to retrieve out-of-date
copies of the document:
To be disseminated to:
Document Library
Proposed actions to communicate the
document contents to staff:
Yes (Please delete as appropriate)
PDF format, in the Medical Clinical Guidelines
Update should remove present guideline in
place
Medical Clinical Guidelines for use by a
Please detail how staff will be informed of
document contents and changes.
Include in the UHMB Weekly News – New
documents uploaded to the Document Library
11. TRAINING
Is training required to be given due to the introduction of this procedural document?
appropriate
Action by
/ No Please delete as
Action required
12. AMENDMENT HISTORY
Revision Date of
Page/Selection
No.
Issue
Changed
Implementation
Date
Description of Change
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Review Date
Appendix 1: AKI Care Bundle
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University Hospitals of Morecambe Bay NHS Foundation Trust
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Title: Acute Kidney Injury (AKI)
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Page 21 of 26
University Hospitals of Morecambe Bay NHS Foundation Trust
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Appendix 2: Fluid Balance Chart
Appendix 3: AKI Renal Referral Proforma
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Appendix 4: EQUALITY & DIVERSITY IMPACT ASSESSMENT TOOL
Yes/No
1.
Comments
Does the policy/guidance affect one group
less or more favourably than another on the
basis of:

Race
no

Ethnic origins (including gypsies and
travellers)
no

Nationality
no

Gender
no

Culture
no

Religion or belief
no

Sexual orientation including lesbian, gay
and bisexual people
no

Age
no

Disability - learning disabilities, physical
disability, sensory impairment and mental
health problems
no
2.
Is there any evidence that some groups are
affected differently?
no
3.
If you have identified potential
discrimination are there any exceptions valid, legal and/or justifiable?
no
4.
Is the impact of the policy/guidance likely to
be negative?
no
4a
If so can the impact be avoided?
no
4b
What alternative are there to achieving the
policy/guidance without the impact?
no
4c
Can we reduce the impact by taking
different action?
no
If you have identified a potential discriminatory impact of this procedural document, please refer it to the HR
Equality & Diversity Specialist, together with any suggestions as to the action required to avoid/reduce this
impact.
For advice in respect of answering the above questions, please contact the HR Equality & Diversity
Specialist, Extension 6242.
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