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

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.

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 - 24 hours – or anuria for 12 hours Rise in Serum creatinine 2 time , 2.9 times or 3 times RIFLE and AKIN – relax !!

Risk factors for AKI

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

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

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

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

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 !!

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

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

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

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

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

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

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

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

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

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 ?

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

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

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

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

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

Other drugs ??

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

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

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 ?

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

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

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

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

Summary Definition Incidence Dangers Prevention Drugs RRT Thank you all