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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 Which Principles of the NHS Constitution Apply? Which Staff Pledges of the NHS Constitution Apply? Please list from principles 1-7 which apply Please list from staff pledges 1-7 which apply Principles Staff Pledges Does this document meet the requirements of the Equality Act 2010 in relation to Race, Religion and Belief, Age, Disability, Gender, Sexual Orientation, Gender Identity, Pregnancy & Maternity, Marriage and Civil Partnership, Carers, Human Rights and Social Economic Deprivation discrimination? Yes / Please delete as appropriate Document for Public Display: *Yes / * Please delete as required Reference Check Completed by…………Frances Sim………..Date……27.7.15……. To be completed by Library and Knowledge Services Staff 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 5 6 6 7 8 9 9 10 10 11 11 11 11 12-13 13 14 14 14 15 15 16 17 17 17 18 18 18 18 20-22 23 24-25 26 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 Page 3 of 26 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 Page 4 of 26 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 Do you have the up to date version? See the intranet for the latest version Page 5 of 26 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 Do you have the up to date version? See the intranet for the latest version Page 6 of 26 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) Next Review Date: 01/07/2018 Do you have the up to date version? See the intranet for the latest version Page 7 of 26 • 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 Do you have the up to date version? See the intranet for the latest version Page 8 of 26 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 Do you have the up to date version? See the intranet for the latest version Page 9 of 26 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 Do you have the up to date version? See the intranet for the latest version Page 10 of 26 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 Do you have the up to date version? See the intranet for the latest version Page 11 of 26 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 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 12 of 26 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 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 13 of 26 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 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 14 of 26 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 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 15 of 26 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) 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 16 of 26 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) Next Review Date: 01/07/2018 Do you have the up to date version? See the intranet for the latest version 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 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 18 of 26 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 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 19 of 26 Review Date Appendix 1: AKI Care Bundle 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 20 of 26 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 21 of 26 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 22 of 26 Appendix 2: Fluid Balance Chart Appendix 3: AKI Renal Referral Proforma 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 25 of 26 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. 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 26 of 26