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 ?
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
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
fenoldapam
• D1-dopamine receptor agonist: rapid-acting
vasodilator; decreases peripheral resistance and
increases renal blood flow; has minimal adrenergic
effects
• Also diuretic, natriuretic Actually used in
• Hypotension is a problem 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
• 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,
Off pump
• the need for deep hypothermic circulatory arrest, – ok ?
• 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
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
