Perioperative AKI - white final

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Perioperative Acute Kidney Injury:

Perioperative Acute Kidney Injury Biomarkers, Physicians, and the Surgical Abdomen Dr. Andrew Ferguson Department of Anaesthetics & Intensive Care Medicine Craigavon Area Hospital

Disclosures:

Disclosures No conflicts of interest to declare

Outline:

Outline Why AKI matters to us Diagnostic and staging criteria for AKI AKI risk factors in perioperative patients Novel biomarkers – what do they offer? Clinical challenges – impact of fluid overload Take-home points

Perioperative AKI is NEVER benign!:

Perioperative AKI is NEVER benign!

PowerPoint Presentation:

“ Predictable and avoidable AKI should never occur ” “ Post-operative AKI is avoidable in the elderly and should not occur ”

How do we diagnose & stage AKI?:

How do we diagnose & stage AKI? Cruz DN et al. Critical Care 2009; 13 : 211

The grim reality of real world AKI:

Ng KP, et al. Q J Med 2011, advance access August 22 2011 The grim reality of real world AKI In 222 non-ICU AKI patients requiring RRT… 29% of patients died within 30 days 37.6% died within 90 days 51.4% died within one year 34.9% of survivors RRT dependent at 1 year 55% of survivors off RRT by 90d had eGFR < 60

All grades of AKI matter!:

All grades of AKI matter! Cruz DN, et al. Critical Care 2009; 13 : 211 Ricci Z, et al. Kidney International 2008; 73: 538-546 Clec ’ h C, et al. Crit Care 2011; 15 : R128 Mandelbaum T, et al. Crit Care Med 2011; 39 : Epub ahead of print AKIN

Scoring Perioperative AKI Risk:

Scoring Perioperative AKI Risk Age > 56 years Male gender Active CHF Ascites Hypertension Mild to moderate CKD Diabetes treated with OHA or insulin Emergency surgery Intra-peritoneal surgery Risk factors Hazard ratio 0-2 1 3 3.1 4 8.5 5 15.4 6 46.2 Kheterpal S, et al. Anesthesiology 2009; 110 : 505-515

Incidence - emergency surgery :

Incidence - emergency surgery N = 61, mean age 75, unpublished audit data

Incidence – elective surgery:

Incidence – elective surgery Study Population AKI definition AKI incidence Thakar 1 Retrospective 504 patients – gastric bypass > 50% rise in creatinine or need for HD 8.5% Kheterpal 2 Prospective , observational major non-cardiac surgery 15,102 patients creatinine clearance > 80 ml/min Creatinine clearance < 50 ml/min within 7 days of surgery 0.8% Abelha 3 Retrospective , 1,166 patients baseline creatinine < 140 major non-cardiac surgery AKIN stage 1 7.5% Kheterpal 4 Retrospective US national dataset 75,952 general surgery patients creatinine rise of > 167 m mol/L from baseline or need for HD 1% (6+ risk factors: 9%) Molnar 5 Retrospective database cohort Major elective surgery including cardiac in 213,347 over 65 ’ s Database coding as AKI 1.9% 1. Thakar CV, et al. Clin J Am Soc Nephrol 2007 ; 2 : 426-430 2. Kheterpal S, et al. Anesthesiology 2007 ; 107 : 892-902 3. Abelha FJ, et al. Crit Care 2009; 13 : R79 4. Kheterpal S, et al. Anesthesiology 2009; 110 : 505-515 5. Molnar AO, et al. J Am Soc Nephrol 2011; 22 : 939-946

Early diagnosis – the creatinine issue:

Early diagnosis – the creatinine issue Variation with muscle mass & age etc. Insensitive to rapid changes in renal function Insensitive to lesser degrees of dysfunction Frequently absent baseline Lag time – lost opportunity for therapy Altered by fluid shifts and fluid balance 1 Positive balance can “ hide ” AKI 1 Liu KD, et al. Crit Care Med 2011; 39 : Epub ahead of print (July 2011)

Biomarkers – the renal crystal ball?:

Biomarkers – the renal crystal ball?

Renal biomarker candidates:

Renal biomarker candidates Kidney injury molecule 1 (KIM-1) Cystatin C Interleukin 18 (IL-18) And others… Neutrophil gelatinase-associated lipocalin (NGAL)

NGAL - what is it?:

NGAL - what is it? 25kDa protein up-regulated in renal injury Present in urine and plasma in AKI Level rises as early as 2 hours after cell injury Falls with successful therapy (animal models) Predicts AKI Predicts poor outcomes (RRT/death) Allows monitoring of therapy Haase M, et al. Curr Opin Crit Care 2010; 16 : 526-532

Biomarker time-course:

Time (hours) 0 3-6 24 48 NGAL KIM - 1 Cystatin C Creatinine McIlroy DR, Wagener G, Lee HT. Anesthesiology 2010; 112 : 998-1004 Biomarker time-course   Therapeutic window  

NGAL and subclinical AKI:

NGAL and subclinical AKI NGAL rise only = similar outcomes to NGAL & creatinine rise Retrospective pooled design Haase M, et al. J Am Coll Cardiol 2011; 57 : 1752-1761 %

Biomarkers - unresolved issues:

Biomarkers - unresolved issues Bedside vs. laboratory testing Lack of “ real-world ” assay validation Timing/frequency of testing uncertain Lack of evidence for “ what ’ s best to do next? ” Impact of testing on outcomes unclear

Challenges in perioperative AKI:

Challenges in perioperative AKI Needs surgery NOW ! Can we keep up?

AKI Triggers & Perpetuators:

AKI Triggers & Perpetuators

AKI hurts other organ systems:

AKI hurts other organ systems Grams ME, Rabb H. Kidney International 2011; advance online publication, 3 August 2011

General management:

General management Optimise haemodynamics Appropriate fluid challenges +/- inotrope/pressor (dobutamine/dopamine) Stop nephrotoxins & adjust drug doses Treat underlying sepsis/obstruction Physiological surveillance/management Escalate to HDU/ICU ? CRRT Nephrology consult ? IHD

Problem areas - fluid overload:

Problem areas - fluid overload Fluids do not reverse vasodilatory hypotension Associated with poor outcomes Causes organ/tissue oedema Causes venous congestion Worsens tissue perfusion Intra–abdominal hypertension

Fluid overload & adverse outcome:

Fluid overload & adverse outcome Population N Design Results ARDS + AKI 1 306 Retrospective analysis of RCT Strong association + ve balance and mortality Septic shock 2 778 Retrospective analysis of RCT + ve balance correlated with increased mortality AKI 3 297 Prospective cohort More + ve balance associated with mortality AKI 4 618 Prospective cohort More + ve balance associated with mortality ICU 5 1,120 Prospective cohort More + ve balance associated with mortality ARDS 6 1,000 RCT Conservative balance = shorter ventilation time Pancreatitis 7 247 Prospective cohort More + ve balance associated with increased organ failures 1 Grams ME, et al. Clin J Am Soc Nephrol 2011; 6 : 966-973 2 Boyd JH, et al. Crit Care Med 2011; 39 : 259-265 3 Sutherland SM, et al. Am J Kid Dis 2010; 55 : 316-325 4 Bouchard J, et al . Kidney Int 2009; 76 : 422-427 5 Payen D, et al. Crit Care 2008; 12 : R74 6 Wiedemann HP, et al. N Engl J Med 2006; 354 : 2564-2575 7 de-Madaria E, et al. Am J Gastroenterol 2011. Epub 30/08/2011

Fluid overload causes tissue oedema:

Fluid overload causes tissue oedema Cerebral Altered mental status Myocardial Arrhythmia, diastolic/systolic dysfunction Pulmonary Impaired gas exchange, increased work Hepatic Cholestasis Renal Decreased RBF & GFR, venous congestion Gut Ileus, anastomotic breakdown Tissue Poor healing, pressure ulcers, infections Prowle JR, et al. Nat Rev Nephrol 2010; 6 : 107-115

Fluid overload worsens tissue perfusion:

Fluid overload worsens tissue perfusion Shedding of endothelial glycocalyx Triggered by hypervolaemia (ANP) & inflammation 1 Loss of vascular integrity => leak Leukocyte/platelet adhesion => microthrombi 1 Bruegger D, et al. Basic Res Cardiol 2011; 19 th July Online First

Microvascular responses to fluid:

Microvascular responses to fluid Differs from the macro-haemodynamic response Improvement in CO and BP do not guarantee improvement in microvascular perfusion Positive microvascular response to fluid bolus diminishes significantly over time Pottecher J, et al. Intensive Care Med 2010; 36 : 1874 Ospina-Tascon G, et al. Intensive Care Med 2010; 36 : 949-955 Harrois A, et al. Curr Opin Crit Care 2011; 17 : 303-307

Intra-abdominal hypertension:

Intra-abdominal hypertension Normal I ntra- A bdominal P ressure < 7 mmHg Normal A bdominal P erfusion P ressure > 75 mmHg APP = Mean arterial pressure (MAP) – IAP Renal filtration gradient = MAP – 2*IAP Decreased RBF, increased venous pressures Impaired gut blood flow & gut translocation IAP > 20 + organ failure = compartment syndrome

So what should we do?:

So what should we do? THINK before fluids and MONITOR after Early fluid resuscitation is appropriate Usually leads to early positive balance Make the switch Even balance by 48 hours, negative beyond this Diuretics or UF Earlier move to inotropes/pressors Make it part of daily practice

Take-home points:

Take-home points Any degree of AKI = worse outcome Risk recognition and tailored journey More haemodynamic optimisation? Earlier recourse to HDU/ICU? Biomarkers = earlier intervention Fluid timing and balance are critical Renal rescue bundles?

PowerPoint Presentation:

“ Poison is in everything, and no thing is without poison. The dosage makes it either a poison or a remedy ” Philippus Aureolus Theophrastus Bombastus von Hohenheim “ Paracelsus ” (1493-1541)

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