acute kidney injury - manipal university - one of the top most
TRANSCRIPT
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DR. RAVINDRA PRABHU A. MD, DM
DEPARTMENT OF NEPHROLOGYKasturba Medical College, Manipal
ACUTE KIDNEYINJURY
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TALK STRUCTURE Renal functionsRenal response to injury Acute kidney injury
DefinitionEtiology Clinical feature History, examLab investigations
PreventionTreatmentOutcome
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NORMAL RENAL FUNCTION
Excretion of waste products
Individual regulation of water and solute balance
Endocrine – EPO, VITD3, Renin, PGs etc
Glucose production, peptide catabolism
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NEPHRON
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WHY KIDNEY ?
Critically dependent on endothelial vasodilation
Undue sensitivity to vasoconstrictors
Medulla relatively ischemic normally
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Renal response to injury
Hypovolemia
Angiotensin 2 NE AVP
Vasoconstriction
↓ RBF, GFR
Autoregulation overwhelmed
Ischemic ATN
Sustained ↓ GFR → Recovery
EFF ART constriction,autoregulation, PG
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DEFINITION
Rapid decline in GFR – within 48 hours
Retention of Nitrogenous waste – Uremia
Extracellular fluid volume perturbed
Disturbed electrolytes, acid base balance
Mostly reversible
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Incidence and Mortality of AKI in the ICU
Setting (no. of patients)
AKI definition Incidence (% of study group)
Mortality (%)
General ICU (26,669)
Need for dialysis 27.6 56 (at hospital discharge)
Cardiothoracic ICU (58)
Need for dialysis N/A 67 (ARF)
75 (acute on CRF)
9 (ESRD)
CCU (2392) Complex 4.0 50
Postcardiopulmonary bypass (47)
Need for dialysis 2.0 53.8 (at ICU discharge)
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CAUSES
Prerenal 55%
Renal 40%Vessels, Glomeruli,
Tubules, Interstitium
Post renal 5%
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PRERENAL FAILURE
Acute decline in renal function reversed
rapidly by correction of perfusion
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PRERENALHypovolemia – Gastro enteritis Low cardiac output – CCFSystemic vasodilation- Sepsis, AnaesthesiaRenal vasoconstrictionCirrhosis with ascites - hepatorenalImpaired autoregulation- NSAIDS, ACE inhibitors
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RENAL
Large vessel obstruction
Small vessel obstruction
HUS, TTP, Toxemia of pregnancy, DIC, Malignant hypertension
Glomerulonephritis
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Renal….
Acute tubular necrosisIschemic
- Prerenal, obstetric, Post surgery, Multifactorial
PhasesInitiation - Hours to daysMaintainence - 1 – 2 weeksRecovery phase
Indicators – Hypotension, sepsis, dehydration
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ISCHEMIC ATN
Hypoperfusion causing acute decline in function sustained by aberrant hemodynamics, cell injury
Recovery – regeneration, repair
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AKI CAUSESToxinsExo - Contrast, Antibiotics (Aminoglycosides), ChemotherapyEndo - Hemolysis, Snake bite, Crush injuryIncreased risk in elderly, renal insufficiency, hypovolemia, concomitant toxins
Interstitial nephritisAllergy – AntibioticsInfection – Leptospirosis
Post renal Obstruction – Ureter, Bladder, Urethra
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SURGICAL AKI
Pre renal Volume depletion, nasogastric suction, GI bleed3rd space loss - burns, pancreatitis, peritonitisHemorrhage
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SURGICAL AKIRenal
Aortic dissection Drugs – NSAIDS, contrast, antibiotics
Post renal Uretero pelvic junction – stone, clotsUreter – Trauma, stone, papilla, clot, cancer RPF, tumor Bladder – Rupture Urethra – BPH, stone, FB, stricture, phimosis
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INCIDENCE
Highly prevalentPost operative 27%Trauma 20 – 40%Burns 15 – 30%
Risks: Cardiac surgeryJaundice
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REASONS
Comorbidity – DM, HTN, CHFAfferent art constriction
Second hitReoperationSepsis NephrotoxinsCirculatory / volume deficitHeart failure
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TRAUMAEarly – Hypovolemia, pigment induced Late – MOD, Sepsis
Risk factors for AKI: - Severe injury- Hypotension at arrival - Increased CPK- On mechanical ventilation- Mortality – creat < 4 – 71%
> 4 – 93%
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BURNS
3rd degree, > 10% BSAEarly – Vol. depletion
Hypotension↑ CPK
Late – NephrotoxinSepsis MOD
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AKI
PhasesInitiation- 2 daysMaintainence- 10 to 14 daysRecovery- 1 week
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PRESENTATIONAccording to cause
- Decreased urine oliguria/anuria- Uremia- Acidosis / Pulmonary edema
No reliable clinical indicator - Measure renal functions in all acutely ill
patients - Record fluid intake and output- Daily weighing - Postural BP recording
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SUSPECT AKI
HypertensionEdema/ DehydrationElectrolyte disturbanceUrinary abnormality Anemia, HypoalbuminemiaAbnormal RFT
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Risk factors for AKI
Diabetes mellitusHeart failureAge > 65 yearsNephrotic syndromeS. creat > 2IV contrast > 125 ml
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APPROACH
History
Physical exam
Urine analysis
RFT. Electrolytes
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DIAGNOSTIC APPROACH IN AKI
Establish whether acute or chronic - Look at previous records- Clinical features of CRF
Vague ill healthNocturia, pruritusAnemia, NeuropathyLongstanding hypertension, proteinuriaRenal size
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Diagnostic approach in AKI….Indicators of volume depletion
Low JVPPostural drop in BP > 10 mmHgPostural tachycardia > 10 /minFast thready pulse HypotensionCollapsed peripheral veinsCool peripheriesCVPFluid challenge
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Diagnostic approach in AKI….
Exclude urinary obstruction- Readily treatable
- Urological symptoms - Flank / suprapubic pain
- Prostatism – Nocturia, frequency, hesitancy
- Anuria, alternate polyuria / anuria
- Imaging
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Diagnostic approach in AKI….
Exclude AGN / AIN / Vasculitis- Oliguria / edema / HTN / active urine / fever /arthralgia / rash / multisystem disorder
- History of drug ingestion - Connective tissue work up
Exclude renal vascular event - Flank pain / Oligoanuria / Retinal change /digital ischemia / SC nodules
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URINALYSIS Prerenal Acellular, Hyaline castsPostrenal Pyuria, hematuriaRenal Muddy brown granular casts – ATN
RBC casts – AGNWBC / Nonpigment granular – AINBroad – CRFEosinophiluria – Allergic AIN, AtheroemboliCrystals – Uric acid, Oxalate, HippurateProteinuria –
> 1g/day – Glomerular> 1g – Tubular
Pigments – Hb, Myoglobin
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RENAL FAILURE INDICES
Prerenal ATN
UNA < 10 > 20
UOSM > 500 < 350
FENA < 1 > 2
B. Urea / creat > 40 < 20 – 30
Urine sediment Bland Pigmented granular casts
U.S.Gr > 1.018 < 1.015
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AKI RIFLE SCORE
ClassGlomerular filtration rate criteria Urine output criteria
Risk Serum creatinine ×1.5
< 0.5 ml/kg/hour × 6 hours
Injury Serum creatinine × 2 < 0.5 ml/kg/hour × 12 hours
Failure Serum creatinine × 3, or serum creatinine ≥4 mg/dl with an acute rise > 0.5 mg/dl
< 0.3 ml/kg/hour × 24 hours, or anuria × 12 hours
Loss Persistent acute renal failure = complete loss of kidney function > 4 weeks
End-stage kidney disease
End-stage kidney disease > 3 months
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MODIFIED RIFLE
AKIstage I
Increase of serum creatinine by>/= 0.3 mg/dl orincrease to >/= 150% – 200% from baseline
Urine output < 0.5 ml/kg/hour for > 6 hours
AKIstage II
Increase of serum creatinine to> 200% – 300% from baseline
Urine output < 0.5 ml/kg/hour for > 12 hours
AKIstage III
Increase of serum creatinine to> 300% from baselineorserum creatinine >/= 4.0 mg/dl with an acute rise > 0.5 mg/dl
ortreatment with renal replacement therapy
Urine output < 0.3 ml/kg/hour for > 24 hoursoranuria for 12 hours
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LABORATORY FINDINGS Raised B. urea, S. creatininine Hyperkalemia – Increased in hypercatabolic statesMetabolic acidosisHypocalcemia, HyperphosphatemiaHyperuricemia, CKAnemia, LeucocytosisDICNon obvious causes to be considered HUS, multiple myeloma
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ESTIMATE GFR
100 / S creatCockroft gault - (140 – age) x wt.kg
72 x S. creatMDRD
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PREVENTION
Pharmacologic ↑ ECF↑ Urine flowMaintain MAP? Renal vasodilatorsPre op optimisation
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PREVENTION
Aggressive restoration of volume statusAvoid / adjust dose of nephrotoxinsAminoglycosides
Once daily useMonitor S – CreatAvoid in liver disease, advanced age, preexisting renal insufficiency
Radiocontrasthydration,sodabicarb,acetylcysteine
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PREVENTION
Avoid ≥ 2 nephrotoxinsConsider alternativesUse small doses brieflyFormulation / dose modification, monitor levels Measure RFT frequentlyHydration Computer surveillance
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PREVENTION
Minimize nosocomial infection Hand washCatheter careAntibioticsAvoid aspiration
- Elevate head - Gastric aspiration- ↓ sedation
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MANAGEMENT1st treat life threatening complications ↑K+, pulmonary edemaAssess volume status and resuscitate accordingly Establish acute Vs chronic renal failureEstablish cause or causes of ARFPrescribe treatment / refer to specialist unit
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SURGERY IN AKI
elective surgeryScrupulous attention to volumeAvoid nephrotoxins
S. creat > 2.5 – increases incidence of SepsisGI bleedfluid overload
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COMPLICATIONS
Hyperkalemia (N: 3.5 - 5 mEq/L)Tenting of T waves↓ size of p waves↑PR interval, widened QRSDisappearance of P waveSine wave formation
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Complications…. Increased K+ treatment
IV 10% Ca Gluconate 10 ml over 1 minIV Glucose 50%, 50 ml over 10 min + 10 units insulin ↓K+ 1 – 2 mmol/L over 30 – 60 minSalbutamol nebuliserCationic exchange resin 15G 6 hrly oral/rectalHemodialysis
Pulmonary edemaUpright position O2, Morphine IV frusemideHemodialysis
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Complications….
Bleeding: Heparin effect
Treat anemia
Antacids / H2 blockers / sucralfate
Infection: Important cause of death
Prophylactic antibiotics not useful
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TREATMENT OF AKI
Loop diuretics: 1-4 mg/Kg/hour. Max 1G/day
- May change oliguric to nonoliguric
- Overall course unchanged
Mannitol – May be helpful in crush injury
Dopamine – 1-5 μg/kg/min
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No response
YesVol Repletion
ResponseContinue
No respStop
Frusemide infuse2-4 mg/min+ Dopamine
X 4 hrly
No response
Frusemide 80 mg
No
CVP<5 cm H2O
Treat cause, avoid nephrotoxins
ARF, Urine <30-40 ml/h
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SPECIFIC THERAPYPrerenal
Correction of hemodynamic insult, inotropesStop nephrotoxinsCareful fluid infusion, Large volume paracentesis in cirrhosis
RenalAGN / AIN: Steroids
ImmunosuppressiveBP control
Post renalRemoval of obstruction
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FLUID REQUIREMENTS
According to fluid lost
- Hemorrhage – Blood
- GI / Urinary loss – 0.45% saline
- Burns, pancreatitis – N saline
- K+, HCO3- Supplement
- Assess daily requirement
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SUPPORTIVE Maintain fluid balance – Urine +500 ml/dayTreat acidosis – if HCO3 < 15, pH ≤ 7.2IV bicarbonate = 0.6 x B wt x Bicarb deficit To be given over several hours, dialysis Hyperphosphatemia – Phosphate binders, restrict PO4
Hypocalcemia – Ca replacementDose modification of drugsAvoid nephrotoxins
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DIALYSIS
Refractory hyperkalemiaRefractory fluid overloadOvert uremia
- Encephalopathy- Pericarditis
Acidosis causing circ. compromiseB. Urea > 180 mg/dl, S. Creat > 8-10 mg/dlModality depends on patient, facilities
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RENAL REPLACEMENT THERAPY
IndicationsUraemic encephalopathy Uraemic pericarditisUraemic neuropathy/myopathySevere dysnatraemia ([Na] > 160 or <115 meq/l) Hyperthermia Drug overdose with a dialysable toxinOne criteria can be an indication for the initiation of RRT. Two or more criteria make RRT mandatory. Multiple criteria are a reason for early initiation of RRT.
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NON RENAL INDICATIONSMOST
Blood purification and renal support Temperature control Acid–base control Fluid balance control Cardiac support Protective lung support Cerebral protection Bone marrow protection Blood detoxification and liver support Septic therapy - immunomodulation and endothelial support
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RENAL REPLACEMENT THERAPY
OptionsHemodialysis
IntermittentContinuousExtended intermittent
Peritoneal dialysis
Tailored to time, hemodynamic, metabolic requirements, molecules.
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RENAL REPLACEMENT THERAPY – Classification
Time Driving force Operational characteristics
IntermittentExtended intermittentSlowContinuous
ArteriovenousPumped venovenous
DiffusionHDConvectionHF, UFBoth – HDF, High flux AdsorptionPheresis
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TREATMENT NOMENCLATURE
Hemodialysis
Hemofiltration
Hemodiafiltration
High flux dialysis
UltrafiltrationPlasmapheresisHemoperfusionSLEDHybrid
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ASSESSMENT
Therapeutic potential
Goals of management
Practicality of delivery of RRT
Likelihood of improving survival
When to start RRT
Costs involved
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GOALSIMMEDIATE
Improve fluid, acid baseHemodynamic stabilityTemporary support till renal recovery
ONGOINGFluid removalWeaning vasopressorSupport organ functionPrevent further renal insultPromote renal recovery
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NUTRITION
Nutrition enteral preferred35 Kcal/kg,1 to 1.5 g protein / kgPO4, Na, K+ restrictionWater soluble vitaminsTrace elements
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MOLECULAR BIOLOGY
PharmacologyMolecular biologyNew molecules
(ANP, IGF1)
Engineeringartificial kidney
Immunologyinflammation
Cell biology
Cell adhesionCytoskeleton
PhysiologyModels of ARF
BiostatisticsRisk identification
studies
ACUTE RENALFAILURE
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FACTORS AFFECTING AKI MORTALITY
Primary diagnosisCo-morbidityQuality of non specialist managementAppropriate site of careEarly referral to a nephrologistIntensity of intermittent dialysisHigher doses of CVVH
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OUTCOME
Depends on systems involvedObstetric 15%
Nephrotoxic 30%
Trauma / Major surgery – 60%
Oliguria, creat > 3mg/dl, elderly, MOF
5% CRF
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AKI - MORTALITY
ATN 60%
Prerenal 35%
Acute on CRF 35%
ARF+RS- 50%
Obstructive 27%
Other 26%
MOF 90-100%
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CONCLUSION
AKI is commonPreventable if attention is paid to volume,avoid or use nephrotoxins with careOnce established lasts for 10 to 14 days and has no specific treatmentConsiderable mortality, morbidity,costs and requirement of specialist support
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