Prevention of aki on icu


Published on

Published in: Health & Medicine
1 Like
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Prevention of aki on icu

  1. 1. Prevention of Acute Kidney Injury on ICU – Journal Review Dr James Hayward RSCH – ICU Teaching 2010
  2. 2. Acute Kidney Injury • Commonly occurs in the course of critical illness • Independent predictor of adverse outcomes • Common causes – Renal hypoperfusion – SIRS – Nephrotoxic drug – Contrast nephropathy
  3. 3. Critical Care Nephrology Working Group of the European Society of ICM • Volume expansion • Diuretics • Inotropes • Vasopressors/vasodilators • Hormonal interventions • Nutrition • Extracorporeal techniques
  4. 4. GRADE criteria • Grades of Recommendation, Assessment, Development, and Evaluation. • Quality of intervention – Strong = 1 - Intervention’s desirable effects clearly outweighs the undesirable effects – Weak = 2 - Balance between risk/benefit is unclear • Quality of evidence – A = high - Repeated large RCTs, and good meta- analyses – B – Small RCTs – C = Low grade – Case series
  5. 5. Volume Expansion • Mainstay for correction of extracellular volume depletion is isotonic crystalloids. – Increased chloride load may result in hyperchloraemic acidosis and renal vasoconstriction and altered organ perfusion. • Large volume replacement with colloids risks hyperoncotic impairment of glomerular filtration, as well as osmotic tubular damage particularly in sepsis.
  6. 6. Volume Expansion • HAS – no proven benefit – expensive • Gelatins – Unlikely to impair renal function – Remain intravascular longer than crystalloid but shorter than HES – May cause histamine release, coagulopathy, prion transmission • Dextrans – Good volume expanders – Anaphylaxis, coagulopathy and AKI may occur • HES – Prolonged volume effect – The polymers undergo hydrolytic cleavage and the products undergo renal elimination, which may be reabsorbed and contribute to osmotic nephrosis and possibly medullary hypoxia – May deposit in tissues and cause pruritis
  7. 7. Volume Expansion • Timely fluid resuscitation is a key aspect to the surviving sepsis campaign. • No one has compared fluid resuscitation with no fluid resuscitation. • CRYCO study – crystalloid vs colloid in ICU – colloid group had increased risk of AKI • VISEP study showed higher incidence of AKI, RRT and mortality in the group treated with HES vs Hartmann’s • Other RCTs have shown no difference.
  8. 8. Diuretics • Olig/anuria is the common herald of impending renal dysfunction and loop diuretics are commonly used in this context. • Theoretical basis is prevention of tubular obstruction, reduction in medullary oxygen consumption, increased renal blood flow.
  9. 9. Diuretics • 4 RCTs – no improvement. • Three meta-analyses showed diuretics do not alter outcome but do increase the risk of side- effects. • One international cohort study showed an increased risk of death and established renal failure.
  10. 10. Vasopressors and Inotropes • Increased cardiac output might equal increased renal perfusion • Various studies quote different targets • Those at greatest risk will need specific targeted pressures
  11. 11. Vasopressors and Inotropes • Low-dose dopamine – does not prevent, or ameliorate AKI and some studies have suggested that it may promote AKI. • Dobutamine and dopexamine have not been demonstrated as protective. • Noradrenaline is frequently used in septic shock and has been shown to increase diuresis and creatinine clearance. • RCT comparing dopamine and noradrenaline as the initial vasopressor showed no difference between renal function or mortality.
  12. 12. Vasodilators • Reduced tissue perfusion causes neurohumoral activation which will maintain systemic pressure at the expense of splanchnic and renal vasoconstriction. • In circumstances of persistent renal vasoconstriction, vasodilators might have a beneficial effect on kidney function. • Be careful!
  13. 13. Vasodilators - Fenoldopam • Fenoldopam = pure dopamine A1 agonist – Thee RCTs compared with placebo or dopamine • Fenoldopam reduced dialysis free survival and need for RRT • Fenoldopam caused a significant decrease in mild AKI and a non-significant decrease in severe AKI • Compared to dopamine fenoldopam significantly reduced serum creatinine – Two large meta-analyses • 1059 Cardiovascular surgical patients – reduced need for RRT and reduced in hospital mortality • 1290 Critical care and surgical patients – reduced incidence of AKI, need for RRT and hospital mortality. – No use in prevention of CIN
  14. 14. Vasopressors – other. • Clonidine – 2 RCTs looking and cardiothoracic patients showed some benefit. • Natriuretic peptides – looked at only in cardiothoracic patients – seem to work. • Phosphodiesterase inhibitors are vasodilators and inotropes and could modulate the inflammatory response. – 10 RCTs, 3 meta-analyses have been inconclusive. – Recent RCT showed reduction in the incidence of CIN by preprocedural administration of 200mg theophylline in critically ill patients • Levosimendan – RCT 80 heart failure patients showed short term improvement in GFR only. • Angiotensin blockers – two studies evaluating short term enalaprilat in cardiac surgical patients showed improved cardiac and renal function
  15. 15. Hormonal Manipulation and Activated Protein C • IGF-1, and thyroxine have been shown to accelerate recovery in animal models of AKI • EPO might reduce cell death and induce tubular proliferation • APC has numerate effects and animal studies have shown beneficial effects in ischaemia/reperfusion AKI
  16. 16. Glycaemic control • Large RCT (van de Berghe) in surgical patients showed that tight glycaemic control showed increased survival and a 41% reduction in RRT • On the medial ICU tight glycaemic control reduced newly acquired renal injury by 34%, but not in need for RRT • Meta-analysis suggests that benefit might be confined to surgical ICU • NICE-Sugar trial – showed higher mortality in patients with tight glycaemic control versus intermediate control.
  17. 17. Other • IGF – no strong evidence • Thyroxine – no effect • Steroids – no beneficial effect • APC – no effect on the resolution of renal dysfunction. • EPO – no effect
  18. 18. Metabolic Interventions • Starvation accelerates catabolism aqnd impairs protein synthesis in the kidney. • Selenium and other antioxidants might reduce reactive oxygen species damage
  19. 19. NAC • Extensively studied – – studies that have shown a benefit have been criticised for having heterogeneous groups and a higher incidence of CIN in control arm. – studies have looked at creatinine concentration as an end point not RRT or death. – Several studies looking at NAC to prevent renal dysfunction in other high-risk groups did not demonstrate a beneficial effect of NAC on renal function or need for RRT.
  20. 20. Extracorporeal Therapies • May protect the kidney by removal of substances, such as contrast, particularly in patients with chronic renal insufficiency. • Degree of contrast removed depends on the filter.
  21. 21. Extracorporeal therapies • Several studies have looked at RRT to limit contrast nephropathy. – Periprocedural haemodialysis showed variable benefit – RCT using 114 patients having cardiac intervention showed haemofiltration 4-8hrs before and 24hrs after showed reduced need for ongoing renal support – Same group then studied pre-hydration, post- filtration, and pre/post filtration. Those patients having pre and post filtration had a better outcome.
  22. 22. Conclusions • Difficult to evaluate because of definitions of AKI and outcome variables. • Prompt restoration of circulatory “normality”. – Volume expansion in true hypovolaemia, with avoidance of HAS, and high molecular weight HES preparations. – Then use a vasoconstrictor up to MAP of at least 60-65mmHg, with consideration of premorbidity. – Vasodilators if circulatory status are recommended.
  23. 23. Contrast Induced Nephropathy (1) • Prophylactic volume expansion has been extensively investigated in the prevention of CIN. Benefit is conferred in certain patient groups. – Reduced GFR – Heart failure – Diabetes • Isotonic bicarbonate solutions have been shown to significantly reduce the incidence of CIN but not ultimately RRT nor mortality. – Other RCTs have shown no difference but when all are combined in meta-analysis, bicarbonate still demonstrated a benefit.
  24. 24. Contrast Induced Nephropathy (2) • No protection against contrast nephropathy has been observed with diuretics. • Recent RCT showed reduction in the incidence of CIN by preprocedural administration of 200mg theophylline in critically ill patients • If a patient is at risk of AKI, then CVVH will confer the most benefit if used pre and post promptly.