aki in the icu setting
DESCRIPTION
updates in management of AKI in ICUTRANSCRIPT
Outline
• A Paradigm Shift: ARF to AKI• Consensus Definition of AKI• Functional vs Structural Biomarkers • Risk Assessment• Prevention and Intervention Therapy• Future: The Way Forward
A Paradigm Shift
• Acute Renal Failure Versus Acute Kidney Injury
• Function Versus Injury
• Acute MyocardiaI Infarction (AMI)– Markers of function: EF
– Markers of injury: troponins
• In Acute Kidney Injury (AKI)– Markers of function: Creatinine
– Markers of injury: No gold standard
AKI Definition• Prior to 2004: > 35 different definitions for
AKI, comparisons between studies difficult
• Current consensus guidelines– ADQI (2004): RIFLE criteria (Bellomo Crit Care 2004,8:R204-12)
– AKIN (2007): AKIN criteria (Mehta Crit Care 2007,11:R31)
– KDIGO (2012) (KDIGO KI Supp 2012,2:19-36)
RIFLE
Risk
Injury
Failure
Loss
ESRD
Increased Cr x 1.5
End Stage Renal Disease
Creatinine Criteria Urine Output Criteria
UO < 0.3ml/kg/hx 24 hr or
Anuria x 12 hrs
UO < 0.5ml/kg/hx 12 hr
UO < 0.5ml/kg/hx 6 hr
Increased Cr x 2
Increased Crx 3 or
Cr 352 umol/l
HighSensitivity
HighSpecificity
Persistent ARF = complete loss of renal function > 4 weeks
Bellomo Crit Care 2004,8:R204-12
Lassnigg et al. J Am Soc Nephrol 15: 1597–1605, 2004
Chertow et al. J Am Soc Nephrol 16: 3365–3370, 2005
R (I)
I (II)
F (III)
Increased Cr x 1.5or > 26.4 umol/l
UO < 0.3ml/kg/hx 24 hr or
Anuria x 12 hrs
UO < 0.5ml/kg/hx 12 hr
UO < 0.5ml/kg/hx 6 hr
Increased Cr x 2
Increase Cr x 3 or
Cr 352 umol/l
AKIN Definition
RRT Started
Mehta Crit Care 2007,11:R31
48 hour window
Stage 1
Stage 2
Stage 3
Urine Output Criteria For AKI
• Consensus opinions amongst experts
AKI severity AKI by urine output
AKI definition < 0.5 ml/kg/h ≥ 6 h
Risk/Stage 1 < 0.5 ml/kg/h ≥ 6 h
Injury/Stage 2 < 0.5 ml/kg/h ≥ 12 h
Failure/Stage 3 < 0.3 ml/kg/h ≥ 24 h or
Anuria for ≥ 12 h
Functional vs Structural Injury Biomarkers
• Functional– Plasma Creatinine, Urine Output & GFR– Plasma Cystatin C
• Structural– Tubular enzymes: AP, GGT, α- & π-GST– NGAL, urinary CysC, KIM-1, IL-18
Risk Assessment
• Risk stratification of patients according to susceptibilities and exposures – Manage accordingly to reduce the risk of AKI.
• Monitor patients at increased risk for AKI– Individualize frequency and duration of
monitoring based on patient risk and clinical course.
KDIGO KI Supp 2012,2:19-36)
AKI Cause and Susceptibility
Exposure Susceptibility
Sepsis Dehydration or Volume Depletion
Critical Illness Advanced Age
Circulatory Shock Female Gender
Burns Black Race
Trauma CKD
Cardiac Surgery (especially with CPB) Chronic diseases (heart, lung, liver)
Major non-cardiac surgery Diabetes mellitus
Nephrotoxic Drugs Cancer
Radiocontrast Agents Anaemia
Poisonous Plants and Animals
Prevention and Treatment
• Monitor to stage AKI severity – Manage according to severity stage– Stage-based management of AKI
KDIGO KI Supp 2012,2:19-36)
Avoid subclavian catheters if possible
High Risk
Discontinue all nephrotoxic agents when possible
Consider invasive diagnostic workup
Consider Renal Replacement Therapy
1 2 3
Non-invasive diagnostic workup
Ensure volume status and perfusion pressure
Check for changes in drug dosing
AKI Stage
Consider functional hemodynamic monitoring
Monitor Serum creatinine and urine output
Consider ICU admission
Avoid hyperglycemia
Consider alternatives to radiocontrast procedures
Stage-Based Management of AKI
Pharmacological Prevention and Intervention in AKI
Doesn’t Work – Further RCTs NOT recommended
Might Work – RCTs Recommended
Works – Use Suggested in at risk patients*
Low Dose Dopamine ANP Isotonic Crystalloids
Diuretics Fenoldopam NAC for CI-AKI Prevention
IGF-1 EPO Isotonic Saline or Bicarbonate (for CI-AKI Prevention)
A1-Adenosine receptor antagonists
Theophylline x1 (for neonates with asphyxia for AKI prevention)
Goal Directed Therapy for early intervention or prevention
• Further RCTs recommended. NB all drugs recommended are investigational • and not FDA approved in AKI prevention or treatment
The Future: The Way Forward
• AKI Biomarkers– Will drive understanding of the pathophysiology
of AKI • Function vs Injury
– Will assist in AKI clinical trials of therapeutic intervention
• Triaging for AKI clinical trials
• Outcome measures
– Will facilitate risk stratification, diagnosis and intervention
Conclusions
• AKI complicates 30 to 40% of ICU patients, is associated with increased mortality and morbidity.
• Standardised definition allow for comparison between studies.
• Early identification would enable implementation of appropriate strategies to prevent and treat AKI.