Critical care conference

Acute Kidney Injury: A Relevant Complication After Cardiac Surgery 2011 society of thoracic surgeons 主講人 : R2 顏介立

Introduction- Acute kidney injury (AKI) occurs in 40% patients

after cardiac surgery, 1% requires dialysis

- Poor outcome and high cost in AKI patient- AKI: consequence of interplay of different

pathophysiologic mechanism- Several biomarkers for acute kidney injury- Protective therapy for AKI

Acute kidney injury after cardiac surgery- Incidence of post-op AKI:

1%-30% of patient after cardiac surgery- Incidence of hemodialysis:

1%-6% of patient - Different type of cardiac operation:

@ CABG: lowest incidence 2%-5%

@ valvular disease or combied disease: 30%

- Different AKI definition

=>new classification critieria

Classification of AKI criteria

Pathology @ Post-op AKI: progressive course with different phase

- Vasomotor change : alteration in vaso-reactivity and renal perfusion- Prerenal azotemia, ATP depletion, oxidative injury => bone marrow/ endothelium: proinflammatory state- Inflammatory cells adhere peritubular capillaries=>

proximal tubule

- Proliferation of tubule cells=> function reconstitution

post-operative AKI is acute tubular necrosis

Pathogenesis- AKI is the consequence of different

mechanisms inerplay- Major cause: - 1. CPB (cardiopulmonary bypass)

2. patient-related factor( risk factor)

Pathogenesis- Cardiopulmonary bypass (CPB)- Kidney blood circulation

1. ischemia-reperfusion injury, low cardiac ouput

hemodilution, loss of pulsatile flow

2. Hypothermia

3. CPB induced systemic inflammation

4. CPB related emoblization

Risk Factor-many factor associated with AKI- pre-op renal function: baseline creatinine 2-4 =>10-20% hemodialysis

baseline creatinine > 4 =>30% hemodialysis- pre-op anemia- DM- Intravenous contrast and ACEi

Identified risk factor associated with AKI is

important

Pathogenesis

Biomarkers for AKI- Problem of conventional renal biomarker 1. become abnormal too late (urea, creatinine)

2. lack specificity (urine ouput)

- New biomarker of AKI ex. cystatin C, NGAL(neutrophil gelatinase associated

lipocalin), IL-6, IL-18, KIM-1( kidney injury molecule-1)

, L-FABP, NAG…….

Biomarkers for AKI- Neutrophil gelatinase-associated

lipocalin(NGAL) @Measure tubular stress, increase after tubular injury @precedes creatinine more than 24hrs!!

- Liver type FABP @ cell uptake fatty acid and promote metabolism @ increase within 4hr after surgery, accuracy of 81% of AKI development

- KIM-1(kidney injury molecular-1) @ predict AKI immediately after surgery=>than NGAL @ more specific to ischemic injury than NGAL

Strategies to prevent AKI- Difficulty of AKI prevention: complex AKI pathophysiology

1. Intravenous contrast

- vasoconstriction-mediated medullary

ischemia and direct cytotoxicity on glomerular

cells

- delay cardiac surgery beyond 24hrs of

exposure to contrast

Strategies to prevent AKI2. Drugs increasing blood flow

a. dopamine: no protective effect and even exacerbate renal tubular injury

b. Fenoldopam: increase renal blood flow in dose-dependent manner

Strategies to prevent AKIc. Atrial and brain natriuretic peptide increase GFR and inhibit sodium reabsorption

=> decrease renal dysfunction

d. Agent attenuating systemic inflammaatory

-Statins attenuate inflammation and oxidative

stress

- N-acetylcysteine, dexamethasone,…..

etc. (anti-inflammation agent)

Strategies to prevent AKI

Strategies to prevent AKIe. CPB use- The most relevant pathophysiologic mechanism- nonpulsatile flow

@ pulsatile perfusion =>improved renal protection

-Presta and colleagues research (2009)

- Poor oxygen availability to renal medulla when CPB

@ Hct<26% , oxygen delivery less than 272ml/kg/min

(Ranucci and collegue, 2005)

@pump flow > 3.0L /min/m2(von Heymann, 2006)

Strategies to prevent AKIe. CPB use- off-pump coronary bypass graft technique

@ controversial renal effect

Cost and Outcomes- post-op AKI has shown to be related to poor

prognosis- Relationship between In-hospital mortality

and post-op GFR (Thakear and colleagues, 2005)- Less than 30% decline GFR Mortality 0.4%- More than 30% decline Mortality 5.9%- Hemodialysis

=> Mortality 54%

Cost and Outcomes- AKI contributes to long- term mortality

@10years survival rate with RIFLE criteria

(Hobson and colleague 2009)

Risk: 51% Injury: 42% failure: 26%

Cost and Outcomes- Duration of AKI with long-term survival

@long term mortality is proportional to AKI duration

@importance of continuous monitoring of renal function

Cost and Outcomes post-op AKI mortality- Plausible mechanism :

. Fluid overloading, dialysis catheter insertion, impaired host immunity and infection

@ post-op infection: (Thaker and colleague 2003)

1.6% without AKI, 23.7% with AKI, 58.5 %

with hemodialysis

Cost and Outcomes- Hospital cost and length of stay increase

as AKI severity worsen

@ post- op AKI:

higher intensive care unit cost(1.7-fold)

pharmacy cost(2.3-fold)

laboratory cost (1.6-fold)

Conclusion- Acute kidney injury after cardiac surgery

-increase mortality and morbidity. Longer

hospitalization and increase cost

-consequence of interplay of different

mechanism

- patients who are at high risk

- novel renal biomarker

- protective strategies

Thank you for your attention !!

Any question????