acute renal failure
DESCRIPTION
Highlights the aetiopathogenesis, management and perioperative concerns of Acute Renal FailureTRANSCRIPT
AETIOPATHOGENESIS & MANAGEMENT OF ACUTE RENAL FAILURE
PRESENTER Dr Unnikrishnan PCOORDINATOR Dr SugandhaMODERATORS Dr Sheela Rani Dr Suneesh DEPT OF ANESTHESIOLOGY, MCH-TVM
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Human beings are essentially big bags of water, the volume of which must be kept under tight control, to prevent us from either drying out or drowning…..
Highlights…
FOLLOWING THE TRENDS….
CAPTURE THE KEYS TO OPEN THE DOOR
HOW TO PREVENT ARF [Anesthetist Rested during Failure]
NEVER ENDING CONTRAVERSIES
REPLACING KIDNEY […very difficult]
‘ACUTE KIDNEY INJURY’
Abrupt reduction [<48 hrs] in kidney function, defined as an absolute increase in S creatinine of ≥0.3 mg/dLA percentage increase in S creatinine of ≥ 50% [1.5 fold from baseline] or a reduction in urine output-- documented oliguria of < 0.5 ml/kg/hr, for more than six hours.
STAGING SYSTEM FOR A.K.I.STAGE S.CREATININE
CRITERIAURINE OUTPUT CRITERIA
1 INCREASE IN S.CREATININE ≥0.3mg/dL OR INCREASE TO ≥ 150-200% FROM BASELINE
<0.5 ml/kg/hr FOR >6HRS
2 INCREASE IN S.CREATININE TO >200-300%[2-3 FOLD] FROM BASELINE
<0.5 ml/kg/hr FOR >12 HRS
3 INCREASE IN S. CREATININE TO >300%[>3 FOLD] FROM BASELINE OR S.CREATININE OF ≥4mg/dL WITH AN ACUTE INCREASE OF ATLEAST 0.5 mg/dL
<0.3ml/kg/hr FOR 24 HRS OR ANURIA FOR 12 HRS
RIFLE criteria
CLASSIFICATION
AETIOPATHOGENESIS
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PRERENAL ARF
Most common
Renal hypo perfusion
Important form in perioperative period
. CAUSES-PRERENAL ARF
HYPOVOLEMIA>HEMORRHAGE>G-I LOSSES>DECREASED INTAKE>URINARY LOSSES>SKIN LOSSES>OTHERS:BURNS,PANCREATITIS,SEVERE HYPOALBUMINEMIA
ALTERED RENAL HEMODYNAMICS
LOW CARDIAC OUTPUT STATES>CHF >VALVULAR HEART DISEASE >PPV > REDUCED VENOUS RETURN
SYSTEMIC VASODILATION>SEPSIS >ANTIHYPERTENSIVES >VASODILATORS >ANAPHYLAXIS
RENAL VASOCONSTRICTION>CATECHOLAMINES >HYPERCALCEMIA
IMPAIREMENT OF RENAL AUTOREGULATION>NSAIDs >ACE-I >ARBs
HEPATORENAL SYNDROME
HYPOVOLEMIA- extrinsic
HYPOVOLEMIA- intrinsic
Tubuloglomerular feedback
Afferent arteriolar vasodilatation
Preferential efferent arteriolar vasoconstriction
Aim is to utilize the existing filtration reserve
maximally
In short….
EXTRINSIC INCREASE MAP, IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW, GFR & GLOMERULAR PRESSURE
When the insult cross the limits….
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ,i.e. away from cortex GFR decrease oliguria
“acute renal success” Increase perfusion pressure If we wait …..ATN
Hepatorenal syndrome
Unique form of prerenal ARF
Structurally normal
Profound renal vasoconstriction
Correction of liver disease resolution
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULAR>ATHEROEMBOLISM >MALIGNANT HTN > >HUS > DIC >PREECLAMPSIA
GLOMERULARGLOMERULAR>AGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIA>MAJOR CARDIOVASCULAR Sx >TRAUMA >HEMORRHAGE >HYPOVOLEMIA
TOXINSTOXINSExogenous: Radiocontrast dye,Antibiotics-Aminoglycosides,Chemotherapeutic agents-Cisplatin, Amphotericin-B, Ethylene glycolEndogenous: myoglobin,hemoglobin,calcium,bilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic: Antibiotics : b-lactam ,quinolone , rifampin NSAIDs B/L pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir, methotrexate , indinavir , myeloma proteins
Ischemic ATN
4 PHASES
INITIATION:GFR DECREASE , OBSTRUCTION BY DEBRIS , BACKLEAK
EXTENSION : CONTINUED….
MAINTENANCE : GFR LOWEST , URINE O/P LOWEST, UREMIC COMPLICATIONS MAY OCCUR
RECOVERY : EPITHELIAL CELL REGENERATION , GFR RETURNS
The so called diuretic phase…
• Recovery phase• Filtration recovers early• Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxins….
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA & S CREATININE INCREASE
Atheroembolic ATN
After manipulation of aorta or renal arteries during surgery / angiography / traumaIn patients with atherosclerosisFrequently irreversible
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaB/L uretericU/L ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
• Anesthetic agents: no renal vasodilation per se ; effects by reducing CO & BP
• EDB & high spinal anesthesia reduce sympathetic tone
• PPV decrease renal blood flow• ACE-I cause significant reduction in perfusion
pressure during anesthesia• Narcotics can increase ADH response
Raised intra abdominal pressure
Normal 0-17mm of Hg>20 mm of Hg compression of pelvis anuria
Improvement occurs only after decompressionMay also cause false high CVP readings due to decreased venous return
SITUATIONS
EMERGENCY LAPAROTAMIES
LEAKING ABD AORTIC ANEURISMS
INTESTINAL DISTENSION
PARALYTIC ILEUS
ASCITES
Clinical features
Pre renal
vomiting , diarrhoea Intestinal obstruction….Carry over cases..NPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguria,edema,hypertension AGNIntake of nephrotoxic drugsh/o atrial fibrillation : renal artery thrombush/o vascular surgeries : atheroembolic ARFMuscle trauma : rhabdomyolysis
Post renal
AnuriaFlank painh/o prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CAST/PUS CELLS/HEMATURIA
ATN MUDDY BROWN GRANULAR/EPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs, RBC CASTS, NON-PIGMENTED GRANULAR CAST,EOSINOPHILS, LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mg/dL
Increased in dehydration , post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal: <1.5 mg/dLOverestimate GFRLags behind renal injury & recoveryRise by 1-2 mg/dL in ARF,>2mg/dL in rhabdomyolysisCritically ill patient: a “normal” value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs, peak in 3-5 days , reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings, 2hr samples[140-age] x body wt / / S.Creatinine x 7291-130 ml / min CrCl = U. Creatinine [mg/dL] x volume [mL/min] P Creatinine[mg/dL]S cystatin C
Assessment of tubular function
• Renal Failure IndicesPRERENAL INTRINSIC
FENa <1 >1
URINARY Na <20 >40
URINE OSM >400 250-300
URINE:PLASMA OSMOLALITY
1.4:1 1:1
Ur.Cr : P. Cr >50:1 <20:1
BUN/Cr >20 <10
SPECIFIC GRAVITY
>1.018 <1.015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa <1ATNNa absorption impaired FENa > 1CKD & diuretics also FENa >1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis , CRFNormal / large DM , AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography : localizationMRA/ Doppler US : arterial /venous obstruction
Others
renal biopsy Increased potassium ,phosphorus , CK-MM, Uric Acid, decreased Calcium rhabdomyolysis
Complications
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Complications
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Complications
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Also…
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Identify patients at riskPATIENT FACTORS TYPE OF SURGERY
CKD CARDIOPULMONARY BYPASS
ELDERLY AORTIC ANEURYSM SURGERY
NEPHROTOXINS HEPATIC/RENAL TRANSPLANTATION
HYPOVOLEMIA/HYPOTENSION SURGERY IN TRAUMA/BURNS
SEPSIS
HEMORRHAGE
LIVER DISEASE/JAUNDICE
DM,HTN
MULTIPLE MYELOMA
PREECLAMPSIA
MASSIVE BLOOD TRANSFUSION
ATHEROSCLEROTIC DISEASE
CARDIAC DYSFUNCTION
Adequate pre-intra & post op hydration
Large bore cannulaCalculate for deficit correction ,maintenance,3rd space lossesFluid challenge:250-500mL of NS over 10-15 minsIf CVP monitoring established:
small elevation[1-2mm]= need more
large increase[5mm] = be slowColloid Controversies over use
in sepsis
Maintain renal perfusion pressure
• Maintain MAP at 70-100 mm of Hg• Catecholamines may help if there is a cause
for hypotension other than hypovolemia
Hemodynamic &urinary output monitoring
Blood pressureCVPPAWPUrine output ensure catheter is not compressed ensure good urine flow from start monitor output hourly ensure output >1ml/kg/hr
Avoid nephrotoxins• ACE-I & ARB• NSAIDs• AMINOGLYCOSIDES• AMPHOTERICIN-B• CISPLATIN• ASPIRIN• CYCLOSPORIN• LMW-DEXTRAN• ACYCLOVIR,INDINAVIR• METHOTREXATE
Aggressive fluid loading
TraumaCompartment syndromeLimb revascularization
….high chance for rhabdomyolysis
Adequate oxygenation
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema, intra renal vasoconstriction
Mannitol
• 6.25-12.5g is given 15 mins prior to the defined insult / repeated 4-6 hrs
• 24 hr cumulative dose not >1.5 mg/kg• Aortic surgeries• Renal transplantation• CABG• rhabdomyolysis
Frusemide
• Inhibit Na-K ATPase in mTAL• Renal vasodilation• Clear debris • oliguric to non oliguric conversion• segmental blockade with thiazide e.g.
metolazone 2.5-5.0mg po• Ototoxicity, interstitial nephritis• Shouldn’t be given if pt is not adequately
fluid loaded
Frusemide
• Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
• Contrast nephropathy [with saline]• May reverse medullary hypoxia induced by
toxins• 2-10 mg/kg for converting oliguric to non
oliguric renal failure• Continuous infusion 1-10mg/hr after a LD of
10-20mg
Dopamine
• Non specific DA1+DA2 agonist• “subpressor dopamine has proved
ineffective in clinical trials , may trigger arrhythmias and should not be used as a renoprotective agent in this setting”
• S/E: increased myocardial O2 consumption, decrease hypoxic drive, intestinal ischemia
Others
• Fenoldapam• Nor adrenaline• Dopexamine• CCBs• PGE1• ANP• ADENOSINE• AMINOSTEROIDS
ALSO NOTE…
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration , n-acetyl cystiene , theophylline/aminophyllin, bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
• regular insulin 10 u + glucose [50 mL 50% dextrose
• Ca gluconate 105 10 mliv• Inhaled salbutamol 5 mg nebulised• Kayexelate,Na polystyrene sulfonate• NaHCO3 50-100 mEq iv• dialysis
others
• Metabolic acidosis: NaHCO3 to keep its level >15mmol/L or pH >7.2
• Hyperphosphatemia :Ca carbonate, Al(OH)3• Hypocalcemia :Ca gluconate , CaCl2• Nutrition• Anemia• Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia >6.5mmol/LSevere acidemia <7.2Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyser,dialysate,blood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc. gradientConvection technique
similar to what happens in glomeruli. Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension: poor tolerance to fluid removal or due to acetate component. Treatment decrease blood flow rate , IVFsHypoxemia : loss of CO2 via dialyzer , bronchospasm ,Treatment:Adr / b-agonist / aminophyllineHemorrhage : 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome: headache, nausea, delirium, seizures
hemodialysis
• Intermittent HD: 3-4hrs per day,3-4 times per week
• Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
.better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar & electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter1.5-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
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“Recent evidence suggest that more intensive hemodialysis [e.g. daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF , once dialysis is required.”
References Harrisons principles of internal medicine,17th eAcute kidney injury network , akinet.orgPrinciples of critical care,2nd e Farokh Erach UdwadiaAcute renal failure, Dr Rebecca Jacob, IJA 2003;47(5)Anesthesia and coexisting disease,4th eccmtutorials.comPerioperative acute renal failure and its management, Dr D Mallikarjuna [isacon-2007
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