NIHR Clinical Lecturer in Nephrology University of Sheffield Acute Kidney Injury Tuesday 23 February 2016 Roslyn Simms NIHR Clinical Lecturer in Nephrology University of Sheffield

Overview of Acute Kidney Injury Importance Definition Epidemiology Causes Clinical Assessment Investigations Management Case Summary

Control blood pressure Control Calcium + Phosphate Acute Kidney Injury (AKI) – Importance? Filter 180L fluid daily Clear waste Control blood pressure Help to make blood Control Calcium + Phosphate

Acute Kidney Injury (AKI) – Importance? Associations with lots of Core Problems Cause associated with: Diarrhoea Haematuria Haemoptysis Hypotension Urine retention Consequence Fluid excess  SOB, Oedema

Definition of AKI Sudden, sustained decline in renal function assoc. nitrogenous waste, electrolyte (K, HCO3) and fluid balance disorders Based on: changes in serum Creatinine, urine output, need for dialysis

Measures of kidney function Blood tests: Creatinine eGFR – estimated glomerular filtration rate Urine output

AKI Definition - OLD International collaboration (ICU/Renal) 2004: Acute Dialysis Quality Initiative est. RIFLE: 3 severities, 2 outcomes (duration) OLD *End stage renal disease

AKI Definition modified Criticised – not recognising SMALL (Creat) changes Different definitions Timing? Size change? Challenged epidemiology NICE Guideline AKI (Aug 2013) inc. Detection

AKI – Early Identification NHS England Patient Safety Alert (July 2014) Biochem Lab software  AKI Stage 1-3 results e-alert KDIGO classification of AKI Standardised across England All patients (except dialysis units) Recognition AKI

Staging system (Blood or Urine results) AKI – Current definition Staging system (Blood or Urine results) Stage Serum Creatinine Urine output 1 (Early) >26.5µmol/l or 1.5-2 fold rise <0.5ml/kg/h >6h 2 (Moderate)  by 2-3 fold baseline <0.5ml/kg/h >12h 3 (Severe) >3 fold baseline or > 350µmol/l (>44µmol/l acute rise) or Start RRT <0.5ml/kg/h >24h or ≥ 12hr anuria KDIGO 2012 – Used in Sheffield Teaching Hospitals

Improve recognition & appropriate actions AKI - Definition Now – AKI Alert system Appear as lab result Link direct to online “AKI Care bundle” Step guidance on investigations/management Improve recognition & appropriate actions

AKI – Epidemiology AKI in 13-18% hospital admissions (esp. elderly) (incidence 480-630 pmp/yr) (NICE, UK 2013) Incidence AKI  dialysis 203pmp/yr (UK 2002) 20-60% critically ill patients have AKI (E, USA 2015) 4.9% AKI in ICU require CVVH (dialysis) (E 2002) AKI inpatient mortality ~ 25-30% (NICE, UK 2013) (UK) data, (E) European, USA data

AKI – Epidemiology £Lives Independent risk for morbidity, kidney failure mortality Comorbidities: bleeding (Plts/uraemic), sepsis (immunodeficient/drugs) cardiovascular risks Costs NHS (2º care) - £430-620million/yr (UK) Preventable…

National Confidential Enquiry Patient Outcomes & Death 2009 Deceased “AKI”: assoc. deficiencies in care Only 50% received “good care” Delays in recognition, Failures in prevention Recommendations (2009): All acute admissions – risk assess AKI (UEs) Consultant review within 12hrs Undergrad + Postgrad training: – detect, prevent, manage AKI request NICE guideline on AKI

AKI - Causes Often multiple causes/exacerbating factors Dehydration common Fluid balance assessment  helpful clues In hospital Interventions eg contrast scans, new drugs Sepsis Systemic disorder/renal limited

AKI - Causes Pre-renal – renal perfusion Intrinsic Renal renal parenchyma damaged Post Renal – outflow obstruction

AKI – Causes – Pre-renal - FIRST Commonest F - Failure-cardiac/liver/skin (burns) I - Infection/Sepsis + Intrarenal haemodynamics (NSAIDs, ACEi) R - Red cell haemorrhage Volume losses S - Sick –GI losses, Stenosis (RAS) - Poor perfusion T – Thrombosis

AKI – Causes – Intrinsic Renal Renal parenchyma damaged Vascular Large: Renal artery/vein thrombosis Cholesterol emboli Small: Vasculitis, HUS/TTP, malignant Ht Glomeruli: Glomerulonephritis, Nephrotic syndrome Tubulointerstitium Acute interstitial nephritis (drugs), cast nephropathy (myeloma), contrast nephropathy, tumour lysis/urate, Ischaemia, acute tubular necrosis (ATN)

AKI – Causes – Intrinsic Renal Vasculitis: “inflammation” of blood vessels Renal limited/Primary eg Post infectious GN Systemic eg SLE Haemolytic Uraemic Syndrome (HUS): thrombotic microangiopathy: haemolytic anaemia, Plts, AKI. Diarrhoea +/- Glomerulonephritis: “inflammation of glomeruli”, infections, inherited, autoimmune Nephrotic syndrome: proteinuria (>3 g/24hrs), oedema, albumin, cholesterol

AKI – Causes – Intrinsic Renal Acute tubular necrosis (acute tubular injury) Very common, esp. in hospital patients Oliguric/non-oliguric Continuum from pre-renal Dx of exclusion Urine biochem: Una >40mmol/l FeNa>2 Ischaemic:   renal perfusion Nephrotoxic: Hb, myoglobin, myeloma casts, drugs, contrast 60% recover, 30% improve, 5-10% ESRF

AKI – Causes – Post-Renal Urinary tract obstruction – any site Ureter Bladder Prostate Intrinsic/extrinsic Stones Tumour Retroperitoneal fibrosis

AKI - Clinical Assessment - History History: patient/collateral Presenting symptoms (may be nonspecific – renal) Uraemic: lethargy, nausea, anorexia, itch, confusion Systemic: rash, joint pains, red eyes, nasal stuffiness /bleeding, haemoptysis Ask: if reduced urine output/adequate fluid intake PMH: comorbidites/risk factors eg DM, CKD, prostate cancer, elderly DH: current (dosing – may need to reduce/stop!), Recent change in meds, INCLUDE over-the-counter

AKI - Clinical Assessment - Examination Volume/haemodynamic status: Pulse, JVP, Blood pressure (postural), Oedema (sacral/peripheral), skin turgor Urine volumes (if available) Urinalysis Airways: O2 sats, RR, chest (haemoptysis) Pericardial rub (if very uraemic) Abdomen: suprapubic percussion dull Skin rash

AKI - Investigations Baseline UE, HCO3, bone, Glu, LFTs, CRP, FBC, Coag, ± blood film Urinalysis ± microscopy ± MSSU ± Urine:PCR Renal ultrasound (PRIORITY if anuric) ECG – hyperkalaemic changes? CXR If sick consider ABG (lactate, pH)

AKI – Investigations - ongoing History suggestive/no obvious cause eg Fall with “long lie”  CK (Rhabdo) Lymphoma, recent chemo  (Tumour lysis) GN screen: ANCA, Anti-GBM, Complement, ANA, ENA, Igs, ASO, Cryoglobulins Myeloma screen: serum+urine electrophoresis, serum+urine free light chains Renal referral  renal biopsy Ideally avoid imaging requiring CONTRAST

Consider renal referral AKI - Management Identify precipitating cause Stop nephrotoxins Optimise fluid balance/haemodynamic support Monitor UEs, urine output Senior review Print “AKI bundle” (checklist of investigations/management) & file in notes Consider renal referral

AKI - Management Consider renal referral AKI – poor response to management AKI – cause unknown Severe (stage 3) AKI (>3 fold baseline or > 350µmol/l (>44µmol/l acute rise) or 12hrs anuric) AKI in renal transplant patient AKI on CKD (stages 4-5) Need for dialysis

AKI – Management - Indications for dialysis Suggestions? K (resistant to med therapy) Fluid overload (resistant to diuretics) Metabolic acidosis (not responding to medical therapy) Complications of uraemia: (pericarditis, encephalopathy) Toxin removal – Li, ethylene glycol, salicylates

AKI – Management Indications for Urology referral Infected, obstructed urinary tract - EMERGENCY Obstructed urinary tract Renal stones/urological malignancy Renal trauma Frank haematuria

AKI – Management Indications for Urology referral Infected, obstructed urinary tract - EMERGENCY Obstructed urinary tract Renal stones/urological malignancy Renal trauma Frank haematuria

AKI – Spot Diagnoses Management

Interpret…

Interpret…

Severe Hyperkalaemia (K8.5mmol/l)

AKI - Management of Hyperkalaemia Hyperkalaemic ECG changes (K>6.5mmol/l) 10ml 10% Calc gluconate (upto 40ml) 10U Actrapid + 50ml 50% dextrose 500ml 1.26% NaHCO3 (NOT if overloaded) 10-20ml Salbutamol nebuliser 15-30g rectal Calcium resonium Haemodialysis – ESPECIALLY if dialysis patient!

AKI - Management of Pulmonary oedema Diuretics (IV Furosemide) Nitrates (GTN infusion) Opiates (diamorphine 1.25-2.5mg) * Venesection (rare nowadays) Haemodialylsis ± Ventilatory support

AKI - Management – Other Features Nutrition – dietician (Low K, appropriate calories, watch volume) Sequelae & kidney function  recovery or CKD Prevention – further complications/insults Multidisciplinary team involvement – Critical care support/Urologists/Dieticians/Pharmacist/Nurse specialists, Physio, OT…

Case Discussion

65yr old man presents to A&E with son ~3/52 diarrhoea, vomiting after pub meal Last 1/52 symptoms settled but tired & SOB Fell in bathroom last night, some abdominal pain  son concerned PMH: DM2 (tablets  diet controlled) Hypertension (lost weight, off meds) DH: nil Reviewed by surgeons - Awaiting abdominal CT Anything you want to know?

On examination BP 150/80 P68 Afebrile O2 sats 94% air RR18 Chest clear No ankle oedema, HS pure Slightly tender abdomen assoc. fall? – nil specific Catheterised in AE ~40ml clear urine Urinalysis: 2+blood, 1+protein, 1+leucocytes Anything you want to know?

Preliminary Investigations K6.5 Urea 43 Creat 1050 (no previous biochem!) HCO3 14 Hb 120 WCC 14.2 Plts 350 CRP 120 Bone, LFTS normal Anything you want to know? ECG – Tall T waves CXR - clear

Differential Diagnosis? Initial Management Treat hyperkalaemia: Ca Cl, Ins/Dex, HCO3 IV fluid Hourly urine output IV Augmentin 1.2g bd (cover for UTI – NB dose reduction!) Differential Diagnosis?

Differential Diagnosis? Excluded Diarrhoea, BUT normal Plts, no anaemia (HUS) Differentials? Urosepsis & ATN (recent diarrhoea assoc. pre-renal insult) – need MSSU Rhabdomyolysis – need to check CK “Renal” cause – glomerulonephritis/renal limited vasculitis?

Bilateral hydronephrosis & ureteric stones Further results Non-contrast CT Abdomen Bilateral hydronephrosis & ureteric stones Urine output: 40/5/0/5/0/ml per hour Repeat UEs: K6.1 Ur 42 Creat 1080

AKI - Cause Often multiple causes interacting In this case: Pre-renal insult – recent diarrhoea/vomiting and low fluid intake, urosepsis Intrinsic renal – possibly degree of ATN Post-renal - bilateral ureteric obstruction

Management Any suggestions? Urology review Plan for bilateral nephrostomies (next day!) Anuric & obstructive AKI with hyperkalaemia Femoral dialysis line & Haemodialysis

Outcome Post nephrostomies Polyuric IV fluids maintained Renal function improved significantly within days Transfer to Urology for management of ureteric stones

AKI - Summary AKI abrupt decline in renal function identified by change in serum creatinine or urine output Associated high morbidity and mortality Guidelines now available for detection, investigations & management AKI alert system ongoing in all English hospitals Broad differential diagnosis – pre-renal insults commonest (careful Hx, PMH, DH, examination) Importance of K, HCO3, fluid balance, haemodynamics Exclude obstructive nephropathy

Thank you Any questions