1. Acute kidney injury and the anesthesiologist
Dr. S. Parthasarathy
MD., DA., DNB, Dip. Diab. DCA,
Dip. Software based statistics-
PhD ( physiology),
IDRA

2. Define ??
AKI is defined when any of the following three criteria are met;
an increase in serum creatinine by 50% in seven days,
an increase in serum creatinine>0.3 mg/dL in 48 hours
oliguria.

3. How will you grade ?? – simple !!
Risk - < 0.5 ml/ kg/ hour – 6 hours – 12
Injury - < 0.5 ml/ kg/ hour – 12 hours
Failure = < 0.3 ml/ kg/ hour hours – or anuria for 12 hours
Rise in Serum creatinine 2 time , 2.9 times or 3 times
RIFLE and AKIN – relax !!

4. Risk factors for AKI

5. Why do we want this ?? Upto two risk factors – 0.2 % AKI
But more than 6 factors – 9.5 % AKI
Cardiac surgery – mortality rises 5 fold almost
Non cardiac surgery – 30 day mortality – almost six times more

6. AKI is associated with Other organ dysfunction
Acid-Base, Electrolyte Disturbances
Fluid Overload
Wound infection
Post op Immobility
Delayed wound healing

7. Progression of kidney Injury
Three possible outcomes
1. Return to baseline function (recovery may be prolonged in elderly patients)
2. Development of chronic kidney disease in previously normal kidneys
3. Accelerated progression of disease in patients with pre-existing chronic kidney disease, and about a fivefold increased risk for end stage disease

8. Rise in creatinine – when will it take place ?
50 % of GFR should reduce
Can we wait ?
So we need some other biomarkers ?

9. Multiple evidences – not a single biomarker !!
Biomarkers of AKI ??
neutrophil gelatinase associated lipocalin (NGAL),
( children better , CPB – studied more , both urine and plasma levels , in a setting of CKD ?
kidney injury molecule − 1 (KIM-1), biopsy and urine
IL-18 – good marker post CPB for AKI but in sepsis !!
cystatin-C. filtration by glomerulus- secretion – nil but complete resorption
steroids, thyroid dysfunction, age, gender modify good marker
Multiple evidences – not a single biomarker !!

10. 30 – 60 % , 20 – 40 % ,, approx 10 % pre renal, renal and post renal

11. Pathophysiology Decreased renal perfusion leading to injury
But ischemia reperfusion injury is also there
Post mortem findings suggest – cytopathic hypoxia – more common than apoptosis

12. Management Preservation of renal function
Problem corrections(hyperkalemia, acidosis, volume overload)
Plan for long term RRT

13. Preventive measures Maintenance of hemodynamics
Over zealous fluid administration may decrease wound healing and increased mechanical ventilation in sick patients
0.9 % saline – increased incidence of AKI – decreased renal perfusion
Preoperative cardiac status stabilization volume correction and avoidance of nephrotoxic drugs
Nephrologist consultation

14. No HES especially in sepsis
Goal directed therapy
Goal directed therapy (GDT) is a strategy that involves the use of fluids, packed red cells and inotropes ( in boluses) to reach target hemodynamic parameters including cardiac output and oxygen delivery to prevent organ dysfunction.
To use cardiac output monitors
Soda bicarb is associated with less AKI in patients with CPB !!
No HES especially in sepsis

15. Avoidance of nephrotoxic agents
ARBs and ACEi may be discontinued
After major liver resections ,can continue to decrease AKI is debatable.
NSAIDs can cause interstitial nephritis
penicillins, quinolones and cephalosporins.
But aminoglycosides dangerous
IV contrast = low doses especially
non ionic iso osmolar

16. Preoperative anemia – AKI
RBC transfusion = increased AKI association
But preoperative erythropoietin in small studies found to be effective in decreasing AKI

17. Dopamine and fenoldapam
Low doses of dopamine – so called renoprotective dose has been questioned and almost disproved -- ?
Fenoldopam is a selective DA-1 agonist – decreased need for RRT if used in cardiac surgeries
Initiate dosing at 0.01 to 0.3 mcg/kg/min by continuous IV infusion for target blood pressure

18. Actually used in hypertensive emergencies
fenoldapam
D1-dopamine receptor agonist: rapid-acting vasodilator; decreases peripheral resistance and increases renal blood flow; has minimal adrenergic effects
Also diuretic, natriuretic
Hypotension is a problem
Actually used in hypertensive emergencies

19. Diuretics
use of diuretics may improve urine output in the setting of acute kidney injury, again there is no evidence to support that they confer any improvement in outcomes measured (including need for RRT and mortality)
Volume status ?
Do they give rest to kidneys ?

20. Mannitol:
“Flush” the tubules and reduce the cellular swelling.
Increases renal tubular oxygen consumption because of increased solute delivery to the tubules.
Lot of studies – only volume repletion use – dangerous in contrast induced nephropathy

21. Intraoperative management of oliguria
Step 1:
In hypovolemia increase the urine output to greater than 0.5 ml/kg/hr ( 500 ml of normal saline in 30 min)
Ensure effective cardiac output and renal perfusion pressure (MAP > 80 mmHg)- dopamine after hydration

22. Intraoperative management of oliguria
Step 2 :
urine analysis before diuretics
Step 3:
Frusemide 80 – 100 mg, Mannitol 50 – 100 ml and low dose dopamine (1 -2 µg/kg/min)
Synergistic effect when used together
Effective only if started within 18 hrs from the onset of oliguria

23. Regional Analgesia
Suppress the sympathoadrenal stress response and release of catecholamines
Maintain adequate renal perfusion pressure
Careful titration of block
Hypotension will result in decrease in urine

24. Concerned anesthetist is the best judge
Choice of Anesthesia to prevent Renal Injury
Regional or General Anesthesia ?
Concerned anesthetist is the best judge

25. Other drugs ??

26. Atrial natriuretic peptide (ANP)
Opposite of aldosterone
Secreted by atria
Vasodilates and removes sodium and water from system
Cardiac surgery
Nesiritide in aortic vascular surgery

27. Other drugs ??
Theophylline, an adenosine antagonist, in theory is proposed to preserve renal blood flow by attenuating vasoconstriction of renal vessels… not much benefits
NAC – not useful except possible contrast nephropathy
tight glycemic control and showed improved outcomes in an Intensiv Therapy Unit setting, with a 41% reduction in AKI requiring RRT (2001) -- but other studies don’t repeat

28. Intraoperative danger signals and correction
In cardiac surgery intraoperative risk factors for postoperative renal failure include use of intra-aortic balloon pump,
the need for deep hypothermic circulatory arrest,
low-output syndrome,
low urine output during cardiopulmonary bypass (CPB), need for pressors ( even in non cardiac) before CPB,
number of blood transfusions during surgery
Off pump – ok ?

29. RRT Prophylactic RRT Not much useful
One study with contrast nephropathy – doubtful use ??
It can correct problems – acidemia, electrolytes
Volume overload – yes in liver surgeries and aortic vascular repair

30. POST-OPERATIVE MANAGEMENT
The aim is to maintain a warm, well-perfused patient
Fluid regimes are often variable, taking into account the previous hour’s urine volume and changes in CVP

31. Postop Pain relief Intra-operative bolus of fentanyl
Regular paracetamol and fentanyl
Patient Controlled Analgesia protocols, if available, are well tolerated in this group
Non-steroidal anti inflammatory drugs should be avoided

32. The essence- perioperative
Maintain normovolumia
adequate MAP
no further exposure to nephrotoxins
Cardiac output by inotropes SOS
Renal tract obstruction to be cleared
Expert opinion

33. Summary Definition Incidence Dangers Prevention Drugs RRT
Thank you all