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Acute Kidney InjuryFocus on Perioperative Setting
October 10, 2018
Banff, Alberta
Disclosures
Participate in a research group with funding from several sources including industry – funding is at arms length, no overlap with AKI
Disclosures
A lot of the data discussed today is population database derived- methodology varies , definitions vary, and analysis varies. I am aware of the issues but am not an expert in these methodologies.
Objectives
Increase awareness of the importance of AKI events and survivors
Review some aspects of diagnosis and management
Review some emerging processes in diagnosis and management
Mehta RL, et al. Lancet 2015; 385: 2616-2643 Susantitaphong P et al. Clin J Am Soc Nephrol 2013; 8: 1482-1493
RIFLE (2004), AKIN (2007), KD:IGO (2012)
Consensus Definitions for AKI criteria
Stage Serum Creatinine or eGFR Urine Output
RIFLE KD:IGO AKIN
RIFLE KD:IGOAKIN
Risk 1 Increased sCr ≥ 1.5 x baseline or GFR > 25%
Increased sCr 1.5 – 1.9 x baselinewithin prior 7 daysorIncreased sCr x 26.4 µmol/L [0.3 mg/dl]within 48 hours
< 0.5 ml/kg/h ≥ 6 h
Injury 2 Increased sCr ≥ 2 x baseline or GFR > 50% Increased sCr 2–2.9 x from baseline < 0.5 ml/kg/h ≥ 12 h
Failure 3 Increased sCr ≥ 3 x baseline or GFR > 75%, or≥ 354 µmol/L], with an acute ≥ 44 µmol/L
Increased sCr 3 x from baseline, or≥ 354 µmol/L, with an acute ≥ 44 µmol/Lor receiving RRT
< 0.3 ml/kg/h ≥ 24 horanuria ≥ 12 h
Bellomo R, et al. RIFLE. Crit Care 2004; 8(4): R204-12Mehta RL, et al. AKIN. Crit Care 2007; 11: R31-38KDOGI. KD:IGO. Kidney Int 2012; 2(suppl 1):19-36
Minjae K et al Anesthesia & Analgesia 2014; 119(5): 1121-1132
Susantitaphong P et al. Clin J Am Soc Nephrol 2013; 8: 1482-1493
Acute Kidney Injury – a continuum
Definition: “abrupt and sustained decrease in glomerular filtration, urine output, or both.”
Subclinical AKI
does not meet AKI criteria and Biomarker concentration increased AKI
Meets AKI criteria and rapid reversal within 48 hrs up to 7 days (renal recovery)
AKD
Sustained reduced renal function > 7 days CKD
Sustained reduced renal function > 90 days
KDIGO. Kid Int Supplements 2012; 2(Suppl 1): 19-36
Forni LG et al Intensive Care Med (2017) 43:855–866
AKI Outcomes
Dedhia P and Thakar CV. Core Concepts in Acute Kidney Injury. S. S. Waikar et al. (eds.) Springer Science+BusinessMedia, LLC 2018
DeathDeath Death?
KDIGO. Kid Int 2012; 2(Suppl 1): 19-36Ferenbach DA and Bonventre JV. Nephrologie & Therapeutique 2016; 12S: S41–S48Yang Y et al. Pharmacology and Therapeutics 2016;163: 58-73
AKI, Renal Recovery, CKD risk
Pannu N et al Clin J Am Soc Nephrol 2013; 8: 194–202Bucaloui ID et al Kidney Int 2012; 81: 477-485Heung M et al Am J of Kidney Dis 2015; 67(5):742-
No AKI
AKI - R
AKI- NR
Bihorac A et al Annals of Surgery 2009; 249 (5):851-858
Kork F et al Anesthesiology 2015; 123(6): 1301-1311
Summary
Normal kidneys with minimal risk can develop AKI
The more risk factors for AKI, the greater the risk for an AKI event
With AKI there is an increased risk of
Shorterm and longterm mortality,
repeat AKI, hospital readmission,
Incident CKD
progression to CKD and ESRD
CKD is a significant AKI risk factor
AKI Management – Moving to the 5Rs? Hx:
Co-morbidities, prior AKI events/CKD, FHx, acute clinical setting,
Medication exposure
Px: Hemodynamic status, infection, sepsis, anemia, hypovolemia, chronic organ dysfunction (Heart, Lung,
Liver), presence of 3rd spacing
Investigations:
urine dipstick/micro, +/- renal U/S, and as indicated
Management Stop Nephrotoxins, renal dose remaining medications
Volume resuscitate, do not volume overload
Serial follow-up; volume status, Cr/eGFR, manage associated complications
Treat hyperglycemia
Consult colleagues as required (Nephro, Cardio, hepatol, ICU)
Ultrasonography should be performed:
when there is no identified cause of acute kidney injury
when pts present with risk factors/symptoms of urinary tract obstruction
when an infected and obstructed kidney is suspected, or when they are at medium or high risk of obstruction based on the risk scoring system
Routine ultrasonography of the urinary tract is not required:
when a non-obstructive cause of the acute kidney injury has been identified
for patients without symptoms of obstruction, without risk factors
when at low risk of urinary tract obstruction based on the risk scoring system
Provincial Clinical Knowledge Topic Acute Kidney Injury, Adult – Inpatient V 2.0 December 2017, page 7
Hospital AKI
Incidence overall 2-23% (more recently 2-9%) (Alberta 20-30%)
Varies with setting – ICU, ward, surgery
ICU 22- 57%
Medical ward (18%)
Incidence of in-hospital (non-ICU/Surgical) AKI likely plateauing (4%)
mortality rates have generally fallen by 50% with and without dialysis
Bellomo R et al. Lancet 2012; 380: 756-766Hoste EA et al. Intensive Care Med 2015; 41: 1411-1423Finlay S et al. Clin Med 2013; 13(3): 233-238Bihorac A, et al. Crit Care Med 2013; 41(11): 2570-2583O’Neal JB et al. Crit Care 2016; 20: 187-195G ME t l A J Kid Di 2016 67(6) 872 880
Perioperative AKI
For general surgery 1-2% (7%)?
Higher risk surgeries:
Cardiac 15%
Trauma 26%
Transplant 71%
Neuro 13%
AKI is associated with higher rates of all postop complications, including CV
Bellomo R et al. Lancet 2012; 380: 756-766Hoste EA et al. Intensive Care Med 2015; 41: 1411-1423Finlay S et al. Clin Med 2013; 13(3): 233-238Bihorac A, et al. Crit Care Med 2013; 41(11): 2570-2583O’Neal JB et al. Crit Care 2016; 20: 187-195Grams ME et al. Am J Kid Dis 2016; 67(6): 872-880 Wang HE et al. Am J Nephrol. 2012;35:349–355
Case #1 - ED
64 yr old male, married, retired handyman, presenting with symptoms of bowel obstruction x 24 hours and 6 month hx of intermittent BRBPR) with progressive constipation.
PMHx – HTN, obesity, ex-smoker (age 57, 40+ pk yrs). Retired 7 years ago due to chronic low back pain. Had gained 10 kg since then but loss 5 kg recently. No prior Sx or hospitalizations.
FHx - Only child, mother 84 (T2DM, HTN, Chol, CAD, prior TIA). Father died of lung cancer remotely
Meds – perindopril 4/12.5, aodipine 2.5 mg (took yesterday) NKDA
Case #1-ED
ROS- sedentary, fatigued, denies CV symptoms or syncope, MRC class 2 dyspnea (true?), no obvious OSA, no oral intake last 24 hours
Non-drinker,
Vitals: 115/85 P 95 (reg) afebrile O2sat 93%
PX: conjunctiva pale, distended abdomen(BS ), JVP low, no S3S4, no carotid bruit, prolonged exp phase, no edema, no rash, no nodes, no hepatosplenomegaly
Lab: Cr 98, K 3.9, Na 132, CO2 21, Cl 96 ; Hgb 120, Plt 276, WBC 14, cholestatic liver profile, albumin 38, INR/PTT normal
Case #1
What do you think his risk is high, low, something else?
What are his risk factors for AKI?
What to do preop? Investigations
interventions
AKI Risk Factors
Hypovolemia
Hypoalbuminemia
Advanced age >60, >75
Female
Black
Prior AKI
CKD (with or without proteinuria)
DM
CHFrEF (35% cardiac Sx) (50% CIN)
COPD
Cirrhosis
Hypotension
MM
CTD
Cancer
Sepsis
CIN
Drugs
General Sx
ContrastCardiac Sx
Community AKI
Wilson T et al. Nephrol Dial Transplant (2016) 31: 231–240
Comparison of 3 perioperative AKI evaluations
Biteker M et al 2014 Bell S et al 2015 Keterpal S et al 2009
N = 1200 prospective single acute care facility2010-2012
N = 10,615 (6220 development cohort, 4395 validation cohort)
N = 15,102 from 65,043 cs retrospective single acute care facility 2003-2006
AKI 6.7% N = 80 AKI 10.8 and 6.7 % AKI 0.8% N = 121
Age Age Age
RCRI Male Sex Male
DM DM DM
ASA ASA CHF
NSAID/Cox-2 Renal insufficiency
Total #of drugs Intraperitoneal Sx
ACEI/ARB Ascites
Emergency Sx
Biteker M et al Am J of Surgery 2014; 207(1): 53-59Keterpal S et al Anesthesiology 2007; 107: 892-902Bell S et al BMJ 2015;351:h5639
Our patient
Age Male ACE-I Hypovolemic Intraperitoneal Sx Emergency Sx?
What we added: HgbA1C 6.3% Urine dispstick +1; ACR 22 Urinalysis
James MT et al Am J of Kidney Dis 2015 66(4): 602-612
Dipstick
ACR
Neg <10
Trace 10-29
+1 30-299
+2 300-999
≥ +3 ≥ 1000
Partridge JS et al Age and Ageing 2012; 41: 142–147
TJA Silva Clinics(Sao Paulo)2009 Jul; 64(7): 613–618
Preop NT-proBNP
Meas perioperative High-sensitivity TNT, TNI, CK-MB, and NT-proBNP in AKI high risk CV pts:
≥ 1 of emergency surgery, preop sCr >177 mmol/L, ejection fraction ≤35% or less or grade 3 or 4 left ventricular dysfunction, age > 70, diabetes mellitus, concomitant CABG and valve surgery, or repeat revascularization surgery.
NT-proBNP had the best prediction rate for postop AKI and 1 yr mortality.
Belley-Cote EP et al Journal of Thoracic and Cardiovascular Surgery 2016; 152(1): 245-251
Preop risk factors – be proactive
AKI risk assessment tools have not been externally validated and most have been focused on identifying severe AKI.
The largest group of AKI pts Stage 1, may be under appreciated and misdiagnosed
Post op AKI has significant short and longterm consequences on par with perioperative MIs
Identifying the AKI risk pt preop may help reduce postop incidence +/or severity, LOS and readmission rates.
Preoperatively linking AKI risk assessment to risk reducing measures intra and post op requires communication and team work
Risk factors for AKI, MI, and frailty overlap in the elderly
Consider the usefulness of preop ACR , +/- your NT-proBNP level in the right patient
Intra-op
Hypotension
Anemia, Transfusion PRBCs
Protective measures
Intraop Hypotension and Risk of AKI
Time, MAP, BP sys thresholds
Valmasi
Accumulative time > 90 min at ≥ 20% drop from preop sys BP
If > 50% below preop sys BP for ≥ 5 min incr risk AKI/MI
Sun (retrospective)
MAP < 60 for > 20 min; MAP < 55 for 10 min
Walsh
MAP < 55 incr AKI/MI
< 55 for 1-5 6-10 11-20 AKI HR 1.18; > 20 min HR 1.51
Sun YS et al Anesthesiology 2015; 123: 515-523Salmasi V et al Anesthesiology 2017; 126: 47-65Walsh M et al Anesthesiology 2013; 119(3): 507-515Hallqvist L et al Eur J Anesthesia 2018;35: 273-279
Hgb
Preop anemia ≤ 80 assoc with post AKI risk
PRBCs during and after cardiac Sx (TAVI)(CABG) increase AKI risk
Also increases IL-18 and NGAL levels post op (≥ 2 units)
No evidence for protective medications or “ischemic preconditioning”
Thongprayoon C et al World J Nephrol 2016; 5(5): 82-88Tewari P et al J Cardiothoracic Surgery2015; 10(Suppl1): A168
Biomarkers More than 50, urine and/or serum
No funding for NGAL in Calgary
Intended to find the sub-clinical AKI, restratify AKI and understand it’s natural Hx.
More likely cost effective in the ICU
Molitoris BA and Reilly E, Semin Nephrol 2016; 36(1): 31-41
Forni LG et al Intensive Care Med (2017) 43:855–866
Ortega LM and Heung M Nefrologia 2018; 38(4): 361-367
The 5 Rs
Risk
Recognition
Response
Recovery
Rehabilitation
Ebah L et al BMJ Quality Improvement Reports 2017;6:u219176.w7476.
Ebah L et al BMJ Quality Improvement Reports 2017;6:u219176.w7476.
Outcomes: 2015 to date
31% reduction new AKI
23% reduction in LOS
40% reduction in time to AKI recovery
10% reduction in AKI deaths
Ebah L et al BMJ Quality Improvement Reports 2017;6:u219176.w7476.
Summary
Clinical approaches to Dx and manage AKI at risk pts will
Continue to evolve along pt “care bundles”
Be more multi-disciplinary than present
Introduce new technologies and types of information into the clinical spaces
Require more cooperation and teamwork in the spirit of proactiveness
For now
If you haven’t been, focus preop more specifically on perioperative AKI risk
Discuss ways to improve Dx and management with your colleagues
Ensure appropriate follow up
Case#1- on the ward
Day 1 post op
u/o down overnight, 300 ml over 10 hrs
IV running NS 150 hr for the last hr, overnight IV went interstitial
Clinically hypovolemic
Foley catheter in situ
sCr 155
What do you think is going on?
What are you going to do?
Alberta AKI QI project
E-alerts (KDIGO stage 1, 2, 3)
Clinical pathway based on pre-intra- and post- renal evaluation for AKI and initial response
Order sets – diet, monitoring laboratory (focus on day 2 & 3), diagnostic imaging and fluid therapies
Disposition planning
Rural considerations
Minjae K et al Anesthesia & Analgesia 2014; 119(5): 1121-1132
Support AKI Outcome measures
When to involve Nephrology?
A possible diagnosis that may need specialist treatment (eg., presence of proteinuria or hematuria on urinalysis can suggest kidney vasculitis or glomerulonephritis; white blood cell casts can suggest tubulointerstitial nephritis; anemia, hypercalcemia, and fractures can suggest multiple myeloma)
* Acute kidney injury of unclear etiology (no pre-renal or post-renal cause identified)
* Progressive AKI despite correction of pre-renal/post-renal factors
* A kidney transplant
* Pre-existing advanced chronic kidney disease, eGFR less than 30mL/min/1.73m2
* Complications associated with AKI which may require renal replacement therapy:
o Hyperkalemia refractory to medical therapy
o Metabolic acidosis refractory to medical therapy
o Symptoms or complications of uremia (pericarditis, encephalopathy)
o Fluid overload causing respiratory compromise (pulmonary edema)
Discharge
Calculate the pt’s “Advanced CKD after AKI Risk Index”
Refer to nephrology, as necessary