renal preservation and ARF management

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renal preservation and ARF management

  1. 1. RENAL PRESERVATION ARF AND ITS MANAGEMENT Dr.P.Narasimha Reddy M.D.,D.A. Professor and HOD Department of Anaesthesiology Kurnool Medical College Kurnool - A.P.
  2. 2. DEFINITION      ARF IS DEFINED AS A SUDDEN DECREASE IN RENAL FUNCTION THAT RESULTS IN INABILITY OF THE KIDNEY TO EXCRETE NITROGEN AND OTHER WASTES. THIS IS ASSOCIATED WITH PROLONGED HOSPITAL STAY AND MORTALITY (58%) ARF IN SURGICAL PATIENTS INVARIABLY CAUSED BY ISCHAEMIC INSULT. ATN IS THE MOST COMMON MECHANISM OF RENAL FAILURE. SCENARIO IS HIGH RISK SURGICAL PATIENTS WITH EXPOSURE TO ONE OR MORE NEPHROTOXIC DRUGS.S
  3. 3. BASIC CONCEPTS OF ANATOMY AND PHYSIOLOGY OF KIDNEY     CONTAINS OVER ONE MILLION NEPHRONS,MAJORITY ARE IN OUTER CORTEX ABOUT 15% IN JUXTAMEDULLARY REGION. JUXTA GLOMERULAR APPARATUS DISTAL CONVULUTED TUBULES PASS IN BETWEEN AFFERENT AND EFFERENT ARTERIOLES MACULA DENSA - TUBULAR EPITHELIAL CELLS AND SUBSET OF AFFERENT ARTERIOLAR EPITHELIAL CELLS. CONTAINS 8 - 10 LOBES. BLOOD FLOW: 20% OF COP (OR) 1 LITRE /MIN. KIDNEY WEIGHS ONLY 0.5% OF BODY WEIGHT. ARTERIO VENOUS OXYGEN DIFFERENCE 1.7 ml/dl 5ml/dl body). FLOW 75 TO 80% MEDULLA. EACH KIDNEY WEIGHS 150 grams.BLOOD GOES TO CORTEX REMAINING GOES TO
  4. 4. PATIENT FACTORS        PRE-OPERATIVE RENAL DYSFUNCTION PERIOPERATIVE CARDIAC DYSFUNCTION SEPSIS HEPATIC FAILURE, OBSTRUCTIVE JAUNDICE, ASCITES HYPOVOLEMIA ADVANCED AGE? MAJOR OPERATIONS
  5. 5. HIGH RISK SURGICAL PROCEDURES      TRAUMA AND BURN SURGERY: HIGH RISK, HYPOVOLEMIC SHOCK, PIGMENTURIA,EXO-NEPHROTOXINS OR SEPSIS. EARLY OLIGURIC FORM MORTALITY-90% CARDIAC SURGERY (CABG): MORTALITY-50%, PRESSURE AND TYPE OF BYPASS ARE LESS SIGNIFICANT DURATION AND HEMODYNAMIC INSTABILITY ARE IMPORTANT. VASCULAR SURGERY: AORTIC CROSS CLAMPING HAS BAD EFFECTS REGARDLESS OF LEVEL OF CLAMPING. SUPRARENALATN LIKE LESION, INFRA RENAL-SHORT TIME REDUCTION IN GFR, AORTIC SURGERY: ARF IS 25% END STAGE LIVER DISEASES AND CHOLESTASIS: HIGH INCIDENCE OF ARF (2/3 OF LIVER TRANSPLANTS. MOST OF THE TRANSPLANT PATIENTS HAVE OVERT HEPATO RENAL SYNDROME OR ASYMPTOMATIC RENAL DYSFUNCTION OR VASOSPASM, SUCH PTS IF EXPOSED TO MASSIVE BLOOD TRANSFUSION HEMODYNAMIC INSTABILITY OR NEPHROTOXINS THE RISK INCREASES .
  6. 6. NEPHROTOXINS       EXOGENOUS: ANTIBIOTICS:AMINOGLYCOSIDES,CEPHALOSPORINS, AMPHOTERICIN B, SULPHONAMIDES, TETRACYCLINS, VANCOMYCIN. ANAESTHETICS: METHOXYFLURANE, ENFLURANE. NSAIDS: ASPIRIN, IBUPROFEN, DICLOFENAC, KETOROLAC,INDOMETHACIN. CHEMOTHERAPEUTIC/IMMUNOSUPPRESIVE AGENTS: CISPLATIN, CYCLOSPORIN, METHOTREXATE, MITOMYCIN, NITROUREAS, TACROLINIUM. CONTRAST MEDIA .
  7. 7. NEPHROTOXINS  ENDOGENOUS:  HYPERCALCEMIA HYPERURICEMIA HYPERURICOSURIA RHABDOMYOLYSIS HAEMOLYSIS BILIRUBIN OXALATES PARAPROTIENS       
  8. 8. STRATEGIES TO PREVENT P.O. ARF PRE OP OPTIMIZATION: 1) EARLY IDENTIFICATION OF THE PROBLEM : INTRAVASCULAR VOLUME STATUS-MAINTAINANCE OF EFFECTIVE INTRAVASCULAR VOLUME, I.V. FLUIDS MAY BE STARTED ONE DAY BEFORE SURGERY, HEMODYNAMIC MONITORING-CVP, PA AND WEDGE PRESSURES, CI, SVR ARE HELPFUL IN OPTIMIZING THE FLUID VOLUME. CONTINOUS BP MONITORING AND MAINTAINING IT IN NORMAL RANGE. URINARY CATHETERIZATION (URINARY OUT PUT IS A POOR MONITOR OF KIDNEY FUNCTION). 2) ASSOCIATED MEDICAL, SURGICAL AND NEPHROTOXIC EXPOSURES: ASSOCIATED MEDICAL CONDITIONS TO BE ATTENDED, TIME OF SURGERY IS MINIMIZED, SPACING OF PROCEDURES AND AVOIDING NEPHROTOXIC AGENTS. 3) ANAESTHETIC PLAN THAT EMPHASISES RENAL PRESERVATION .
  9. 9. PHARMACOLOGICAL STRATEGIES    IN THE PAST IT WAS AIMED AT INCREASING GFR, PROMOTION OF TUBULAR FLOW AND REMOVAL OF TUBULAR DEBRIS. RECENTLY IT HAS BECOME APPARENT THAT MAINTAINANCE PHASE OF RENAL DYSFUNCTION IS PERPETUATED BY SEVERAL MECHANISMS THAT CAUSE CELLULAR INJURY. CURRENT CONCEPT IN RENAL INJURY IS “CELLULAR INJURY PARADIGM”.  SOME PHARMACOLOGICAL RENAL PRESERVATIVE AGENTS WILL ACT AT BOTH HEMODYNAMIC, HYDRAULIC LEVEL AND AT THE CELLULAR OR EVEN SUB CELLULAR LEVEL.
  10. 10. CALCIUM CHANNEL BLOCKERS     THEY INCREASE BLOOD FLOW BY INHIBITING VOLTAGE DEPENDENT CALCIUM CHANNEL MEDIATED VASOCONSTRICTION, HYPERTENSIVE PATIENTS TREATED WITH CCB- SLOW DECREASE IN SR.CR. CLEARANCE. IN TRANSPLANT PATIENTS THEY SHOWED MIXED RESULTS, TREATED WITH DILTEAZEM SHOWED INCREASED RBF, GFR AND URINEOUTPUT AND DECREASED REQUIREMENT OF DIALYSIS. IN MAJOR VASCULAR SURGERY THE EFFECTS ARE VARIABLE, INFRARENAL AORTIC SURGERY TREATED FELODIPINE FOR 5 DAYS BEFORE SURGERY THERE IS INCREASED GFR, IN FIRST 24 HOURS, AND IT IS NOT SUSTAINED. IN ANOTHER GROUP OF VASCULAR SURGERY TREATED WITH NIFEDIPINE HAD INCREASED POST CLAMP SR.CR. CLEARANCE AND LESS REDUCTION IN GFR COMPARED TO LOW DOSE DOPAMINE. NIFEDIPINE GROUP HAD DECREASED ENDOTHELN AFTER REMOVAL OF CLAMP AND HIGH RATIO OF PROSTAGLANDIN F-1 ALPHA TO THROMBOXANE B-2.
  11. 11. CALCIUM CHANNEL BLOCKERS (Cont’d)     IN CPB FELODIPINE DID NOT AFFECT RENAL RESISTANCE, PAH EXTRACTION IS HIGH DURING LOW AND HIGH FLOW CPB. IN RETROSPECTIVE STUDY WHERE DILTIAZEM USED FOR MYOCARDIAL PROTECTION EXPERIENCED HIGH SERUM CREATININE LEVELS AND INCIDENCE OF DIALYSIS WAS HIGH. THE FLUX OF CALCIUM ACROSS CELL MEMBRANES HAVE BEEN IMPLICATED IN REPERFUSION AND ISCHEMIC CELL DEATH. VERAPAMIL MODULATES NEUTROPHIL INFILTRATION INTO ISCHEMIC TISSUES AND TISSUE DAMAGE IS REDUCED. AT CELLULAR LEVEL CCB INCREASES GFR BY ALTERING RELAXATION PHASE OF MESANGIAL CELLS
  12. 12. CALCIUM CHANNEL BLOCKERS (Cont’d)  ROLE OF CCB IN CYTOPROTECTIVE RENAL ISCHEMIA IS COMPLEX. THEY HAVE EFFECT AND ANTIOXIDANT EFFECT.  GRIEF ET.AL., DEMONSTRATED IN RAT MODEL THAT INTERRUPTING THE CAL. CASCADE AT ANY OF THE THREE POINTS 1) CAL. INFLOW INTO CYTOSOL 2) MITOCHONDRIAL UPTAKE OF CAL. 3) CAL. DEPENDENT ACTIVATION OF CAL. CALMODIN COMPLEX IMPROVED SURVIVAL OF THE CELLS.  IN LONG TERM TREATMENT MANIDEPINE TUBULAR HYPERTROPHY IS SEEN. THE CLINICAL SIGNIFICANCE HAS TO BE EVALUATED.
  13. 13. PROSTAGLANDINS        IN NORMAL KIDNEY PG PLAY A HOMEOSTATIC AND PERMISSIVE ROLE, INHIBITION OF THEM CAN CAUSE DECREASE RENAL FUNCTION, PGS INCREASE GFR, RBF , NATREURISIS AND DECREASED OXYGEN CONSUMPTION AT THICK ASCENDING LOOP OF HENLE. IN RENAL DYSFUNCTION MODULATION OF PGS TO THROMBOXANE RATIO CAN HAVE FAVOURABLE EFFECTS. POST OP INFUSION OF PG-E2 (VASODIALATOR) MAY INCREASE RENAL FUNCTION. INFUSION OF ALPROSTADIL IMMEDIATELY AFTER GRAFT REVASCULARIZATION INCREASES RENAL FUNCTION. CIRRHOSIS PTS RESPOND DIFFERENTLY WITH PGS. PGS IN CARDIAC SURGERY INCREASED GFR. PGS CAN CAUSE SEVERE HYPOTENSION, MUST BE CAREFUL
  14. 14. ATRIAL NATRIURETIC PEPTIDE         ANALOGUES OF ANP HAS BEEN ISOLATED FROM ATRIA AND KIDNEYS. ANP FROM KIDNEY IS CALLED URODIALATIN. ACTIONS OF THIS PEPTIDES MEDIATED BY CYCLIC-GMP. ACTIVATION OF ANP RECEPTORS INCRESED GFR DUE TO DILATION OF AFFERENT AND VASOCONSTRICTION OF EFFERENT ARTERIOLE THEY ALSO CAUSE DECREASE SODIUM REABSORPTION. RELAXATION OF MESANGIAL CELLS CAUSE INCREASED FILTRATION FRACTION. ANP IS AN EFFICIENT ANTAGONIST OF ALL RENAL VASOCONSTRICTORS TESTED TO DATE. URODIALATIN IS A BETTER RENOPROTECTIVE AGENT THAN ANP BECAUSE OF IT S MORE NATRIURESIS AND DIURESIS.
  15. 15. ATRIAL NATRIURETIC PEPTIDE (Cont’d)        IT IS RESISTANT TO DEGRADATION BY ENDOPROTEASES. NO TACHYPHYLAXIS. LESS HYPOTENSIVE. CECEDI ET.AL., USED URODIALATIN AS A RESCUE THERAPY IN ARF PATIENTS AFTER TRANSPLANTATION FOR FIVE DAYS P O AND SHOWED IMPROVED RESULTS. FORSSMAN’S GROUP USED URODIALATIN IN CARDIAC PATIENTS AND SHOWED SIGNIFICANT DIURESIS. HERBERT ET. AL., USED URODIALATIN IN PTS OF ARF AFTER MAJOR ABDOMINAL SURGERIES. IN LIVER TRANSPLANTS URODIALATIN HAD GREATER REDUCTION IN SR. CR. LEVELS AND LESS REQUIREMENT OF FRUSEMIDE.
  16. 16. DOPAMINE – 1 AGONISTS  FENOLDOPAM MESYLATE IS A NOVEL DOPAMINE ANALOGUE WITH SPECIFIC DOPAMINE-1 AGONIST ACTIVITY THAT STIMULATES POST SYNAPTIC PERIPHERAL DOPAMINE-1 RECEPTORS. NO ACTION ON DOPAMINE-2 ALPHA AND BETA RECEPTORS DOPAMINE FENOLDOPAM DOPAMINE-1 DOPAMINE-2 ALPHA BETA-1 BETA-2  +++ +++ ++ +++ + +++ NIL NIL NIL NIL THE EFFECTS OF FENOLDAPAM IS DOSE DEPENDENT, AT LOW DOSES RENAL VASODIALATION AND AT HIGHER DOSES PERIPHERAL VASODIALATION.
  17. 17. DOPAMINE – 1 AGONISTS (Cont’d)         SO IT CAUSES HYPOTENSION WITH INCREASED RENAL BLOOD FLOW. IT CAUSES INCREASED CARDIAC AND STROKE VOLUME INDICES IN CCF. END SYSTOLIC AND ENDDIASTOLIC VOLUMES ARE DECREASED. IT DECREASES B.P. IN HYPERTENSIVE PATIENTS WHEN COMPARED TO NORMOTENSIVES. REABSORPTION OF SODIUM , SODIUM AND POTASSIUM EXCHANGE FALL SIGNIFICANTLY. PATIENTS WITH CHRONIC RENAL INSUFFICIENCY RESPOND FAVOURABLY TO FENOLDAPAM. IT REVERSES REDUCTION IN RBF AND GFR DURING IPPV. PRELIMINARY REPORTS SAY THAT FENOLDAPAM MAY BE EFFECTIVE AS RENOPROTECTIVE AGENT IN HIGH RISK PATIENTS.
  18. 18. MODULATION OF COMPLEMENT SYSTEM       THERE IS CLEAR EVIDENCE THAT TERMINAL COMPLEMENT COMPLEX (C5-9) IS A MEDIATOR OF RENAL INJURY. COMPLEMENT ACTIVATION IS ASSOCIATED WITH IMMUNOLOGICALLY MEDIATED RENAL DISEASE SUCH AS LUPUS H S PURPURA, MEMBRANOUS NEPHROPATHY AND POST STREPTOCOCCAL G N. COMPLEMENT IS WIDELY ACTIVATED IN CPB, SEPSIS, TRAUMA AND AORTIC CROSS CLAMPING. UNDER NORMAL CIRCUMSTANCES COMPLEMENT ACTIVATION IS WELL REGULATED . MEMBRANE INHIBITORS OF COMPLEMENT (MIC) ARE PRESENT IN KIDNEY AND PLAY A VITAL ROLE. RENAL INJURY CAN BE AVOIDED BY DEPLETION OF COMPLEMENT OR BY INFUSION OF MIC.
  19. 19. 21 – AMINO STEROIDS (TIRILIZAD)  REACTIVE OXYGEN SPECIES CONTRIBUTE TO REPERFUSION INJURY THROUGH VARIOUS MECHANISMS.  21-AMINOSTERIODS INHIBIT LIPID PEROXIDATION BY SCAVENGING LIPID RADICALS AND INHIBITING LIPID RADICAL CHAIN REACTION.  IN ESTABLISHED CASE 21-AMINOSTERIOD IS BETTER THAN SUPER OXIDE DESMUTASE.  TRANSPLANTATION RELATED OXIDATIVE INJURY IS REDUCED BY 21AMINOSTERIODS AND ACCOMPANIED BY DECREASED EXPRESSIONOF CYTOKINES, MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGENS AND INDUCIBLE NITRIC OXIDE SYNTHASE.
  20. 20. ALPHA MELANOCYTE STIMULATING HORMONE          ISCHEMIA AND REPERFUSION INJURY IS ACCOMPANIED BY ILFLAMMATORY AND CYTOTOXIC CASCADE ACTIVATION. PREVENTION OF THIS CASCADE DEMONSTRATED TO PROTECT THE KIDNEY. ALPHA MELANOCYTE STIMULATING HARMONE REDUCES THE RENAL INJURY AFTER ISCHEMIA AND REPERFUSION. IT CAUSES REDUCTION IN BUN, SR. CR., AND HISTOLOGICAL CHANGES IN ANIMALS TREATED WITH THIS HARMONE. GROWTH HARMONE: THERE IS A GROWING INTEREST IN CELLULAR REPAIR AND REPLACEMENT OF ACUTE INJURY. KIDNEY CELLS ELOBARATE AND RESPOND TO VARIOUS GROWTH FACTORS. EPIDERMAL GROWTH FACTOR: CAUSES ENHANCED CELL REPAIR WITH REDUCTION IN BUN AND SR.CR. SOMATOMEDIN-C GIVEN UPTO 24 HOURS AFTER INJURY SHOWED SAME EFFECTS AS ABOVE. THYROXIN AND FIBROBLAST GROWTH FACTOR AND TRANFORMING GROWTH FACTOR-B ARE UNDER INVESTIGATION.
  21. 21. DOPAMINE      LOW DOSE DOPAMINE (LDD) HAS BEEN USED TO PREVENT OR TREAT ARF WITH OUT CONVINCING EVIDENCE. 2-5 MICS/KG/MIN IS USED TO AVOID SYSTEMIC CARDIOVASCULAR EFFECTS BY STIMULATING ONLY DOPAMINE RECEPTORS IN KIDNEY. LDD HAS BEEN SHOWN TO INCREASE URINE FLOW IN SICK POST-OPERATIVE PATIENTS. BUT IT FAILED TO DEMONSTRATE BENEFICIAL EFFECTS IN MAJOR SURGERIES. SIDE EFFECTS: TACHYCARDIA, ARRYTHMIAS, INCREASED RT AND LT VENTRICULAR AFTER LOAD, INCREASED MYOCARDIAL OXYGEN CONSUPTION, ANGINA, ISCHAEMIA, DECREASED HYPOXIC RESPIRATORY DRIVE, INCREASED PULMONARY SHUNT, INCREASED PCWP, HYPONATREMIA, HYPOKALEMIA, HYPOPHOSPHOTEMIA,AND DEPLETION OF VOLUME.
  22. 22. DOPAMINE (Cont’d) RECPTOR LOCATION ACTION DA-1 POST- SYNAPTIC V.DIL DA-2 PRESYNAPTIC DECREASEN.A.REL B-1 ADR POST- SYNAPTIC CARD. STIM. B-2 ADR POSTSYNAPTIC V.DIL ALPHA-1 POST- SYNAPTIC V. CONSTR. ALPHA-2 PRE- SYNAPTIC DECREASE N.A.
  23. 23. EFFECTS OF DOPAMINE ON RENAL PHYSIOLOGY STRUCTURE EFFECT WHOLE KIDNEY INCREASED RBF INCREASED GFR NATREURESIS DIURESIS GLO. HEMODYN. AFFER. ART. DIL. VARI. EFFECT EFF.ART. NO EFFECT ON FILT.CO-EFF JUXTA GLOM. APP. ALT.GLOM.FEED BACK DECREASED RENIN RELEAS PROX . TUBULE INHI. OF NA – KATP ASE NA-H-EXCHANGE, NA-PO4COTRANSPORT AND ANTA. OF ANGIOTENSIN-2 T.A.L. INHI. OF NA-K-ATP ASE COLLECT. DUCT ANTA. OF ADH.
  24. 24. FUROSEMIDE      IT IS REGULARLY USED WHEN THERE IS DECREASED URINE OUTPUT. IT MAY FLUSH THE TUBULAR DEBRIS INCREASE RBF, DECREASED OXYGEN CONSUMPTION AND DECREASED RENO-VASCULAR RESISTANCE. THERE IS NO CONVINCING EVIDENCE THAT IT PROTECTS FAILING KIDNEY. INSTEAD LARGE DOSES CAUSE –OTO TOXICITY, SEVERE HYPOVOLEMIA, ELECTROLYTE DISTURBANCE AND CAN CAUSE RENAL FAILURE. IF AT ALL IT SHOULD BE GIVEN EARLY WITH PROPER MONITORING.
  25. 25. MANNITOL              OSMOTIC DIURETIC DOES NOT ENTER CELLS FILTERED COMPLETELY BY GLOMERULI NO APPRECIABLE REABSORPTION BY RENAL TUBULES INCREASED URINARY EXCRETION OF WATER DECREASED SODIUM REABSORPTION FLUSHING OF DEBRIS DECREASED ENDOTHELIAL SWELLING MAINTAINS OPTIMAL INTRAMEDULLARY BLOODFLOW DECREASED 0-2 DEMAND SCAVENGES EXTRA CELLULAR FREE HYDROXYL RADICALS IN CLINICAL SETTING, MANNITOL ROLE IN RENO-PROTECTION IS NOT WELL ESTABLISHED DISADVANTAGES:SUDDEN INCREASE IN INTRAVASCULAR VOLUME, DEPLETION OF WATER AND HYPOVOLEMIA AND PULM.EDEMA.
  26. 26. VOLUME LOADING  VOLUME LOADING OPTIMALLY WITH ACCURATE MONITORING OF PCWP HAS DEFINITELY DECREASED MORTALITY OF ARF 33%-10% . INTRA OP URINE OUT PUT IS NOT A PREDICTOR OF POST OP. RENAL FUNCTION. MAINTAINANCE OF ADEQUATE VOLUME STATUS IS CORNER STONE OF PROPHYLAXIS AGAINST ARF. KIDNEY PERFUSATE  THE SOLUTION CONSISTS OF 2500 UNITS OF HEPARIN, 100 ML OF 20% MANNITOL IN 500 ML OF RL WHICH IS COOLED TO 4 DEGREES CELSIUS, IT IS PERFUSED INTO THE KIDNEY. HYPOTHERMIA IS ALSO USED TO PRESERVE HARVESTED ORGANS FOR TRANSPLANTATION. ENDO VASCULAR AORTIC STENTING  NISHIMURA ET. AL., SUGGESTED THAT ENDO VASCULAR STENTING CAN MINIMIZE RISK OF MAJOR SURGERY ON THE KIDNEY. THE PROCEDURE CAN BE DONE UNDER L A.
  27. 27. MANAGEMENT OF ARF IN THE POST-OPERATIVE PERIOD      ARF IN THE POST OPERATIVE PERIOD CARRIES HIGH MORTALITY 50-70% EARLY INVOLVEMENT OF NEPHROLOGIST IS CRUCIAL TREATMENT DIFFERS WITH TYPE OF RENAL FAILURE AND SINGLE OR MULTI ORGAN INVOLVEMENT ARF IS DIVEDED INTO 1) PRE 2) POST 3) INTRA - RENAL ARF IS DIAGNOSED BY INCREASED CREATININE LEVELS AND BUN DIFFERENCES BETWEEN PRE-RENAL AND ATN PRE RENAL URINE SODIUM 10 mmol FRAC.EXCRE.OF SODIUM <19% URINE/SERUM OSMO. >1.8 BUN/CR. RATIO >15 ATN >20mmol >19% <1.1 <10
  28. 28. PATHOPHYSIOLOGY         SEVERE PROLONGED SURGERIES, DELAYED CARDIAC RESUCITATION, SEVERE SEPSIS LEADS TO ATN. GLOMERULI ARE NORMAL. TUBULES ARE DAMAGED, DILATED. CELLULAR LOSS. AREAS OF DENUDED BASEMENT MEMBRANE. OTHER CELLS ARE FLATTENED. MITOSIS IS SEEN. CASTS MAY BE OBSERVED.
  29. 29. SEVERITY SCORING - ARF ( CLEVELAND CLINIC SCORING)           VARIABLE MALE GENDER INTUBATION /IPPV BLOOD STATUS PLATELETS<50,000 LEUCOCYTES<2500 BLEEDING DIATHESIS BILIRUBIN > 2 ABSECENCE OF SURGERY NO. OF ORGANS FAILURE 1 2-3 5-7 BUN < 50 BUN > 50 SR. CR. <2 2-5 >5 ODDS RATIO 2.4 2.5 SCORE 2 3 2.1 3 2.1 2 3 1 1 1.3 2.5 1.8 2 1 2 3 1 2 4.8 2.6 1 0 1 3
  30. 30. MANAGEMENT  PREVENTION OF DAMAGE  CONSERVATIVE LINE OF MANAGEMENT  RENAL REPLACEMENT THERAPY
  31. 31. MANAGEMENT (Cont’d…) PREVENTION OF DAMAGE: IDEAL WAY TO PREVENT RENAL DAMAGE AND ALLOW RENAL RECOVERY IS TO PROVIDE 1. ADEQUATE SUPPLY OF OXYGENATED BLOOD BY INOTROPES I.V.FLUIDS AND MECHANICAL VENTILATION. 2. AVOIDING AND PROMPT TREATMENT OF SEPSIS: ASEPTIC TECHNIQUES CARE OF INTRACATHS, URINARY CATHETERS ANTIBIOTIC THERAPY, IDENTIFYING OCCULT INFECTION BYINVASIVE METHODS . 3.NEPHROTOXIC MATERIALS: AVOID OR USE WITH CARE LIKE ACE INHIBITORS AND CONTRAST MEDIA. 4.PIGMENTURIA: RAPID DESTRUCTION OF MUSCLE LEADS TO NEPHROTOXIC MATERIALS, THIS MYOGLOBIN IS NON-ENZYMATICALLY CONVERTED TO FERRIHEMATE PREVENT MUSCLE DESTRUCTION AND PREVENT ACIDOSIS. 5.ETHYLENE GLYCOL USED IN SUICIDE IT IS CONVERTED INTO FORMALDEHYDE AND OXALATE. TREATED BY ETHANOL OR H.D.
  32. 32. CONSERVATIVE /MEDICAL MANAGEMENT * 1) FLUID VOLUME: EUVOLEMIA IS ESSENTIAL, * HYPER-VOLEMIA AND DEHYDRATION AVOIDED, * ADULT INSENSIBLE LOSS PER DAY IS 1 LT, IN FEVER WITH EACH DEGREE RISE NEEDS EXTRA 500 ML, * * * REPLACEMENT OF FLUID LOST IN DRAINS, TREATMENT MAY BE ENTERAL OR PARENTERAL DEPENDING ON THE CONDITION OF THE PATIENT.
  33. 33. HYPERKALEMIA (MANAGEMENT Contd)     RESULTS IN DECREASED RENAL FUNCTION FROM DAMAGED CELLS, LEAKAGE FROM CELLS AS A RESULT OF OUBAIN LIKE UREMIC TOXINS AND ACIDOSIS. SERUM K+ >6.5 MEQ SHOULD BE REGARDED AS DANGEROUS , NEEDS PROMPT TREATMENT. HEART IS AT RISK, EKG SHOWS PROLONGED P-R INTERVAL, PEAK ‘T’ WAVES, WIDE QRS COMPLEXES, ‘P’ WAVE DISAPPEARS, BRADYCARDIA AND VENTRICULAR FIBRILLATION. TR: a) AVOID K+ SPARING AGENTS LIKE ACE INHIBITORS, SPIRONOLACTONE AND DARROW’S SOLUTION b) TREATING ACIDOSIS, c) G-I SOLUTIONS, d) I.V. CALCIUM, e) RECTAL OR ORAL RESINS, f)DIURETICS, g)I.V. SOLBUTAMOL AND h) FINALLY DIALYSIS.
  34. 34. UREMIA MANAGEMENT      UREMIA DEPENDS ON CATABOLISM. AVOID OR TREAT INFECTION. PROTECTION AGAINST GASTRIC BLEEDING AND SUBSEQUENT DIGESTION (STRESS ULCERS, PLATELET DYSFUNCTION) TREATED WITH H-2 BLOCKERS. H-2 BLOCKERS CAN CAUSE BACTERIAL COLONIOZATION DUE TO INCREASED PH. EARLY NUTRITION PREVENTS INFECTION, DECREASES CATABOLISM AND INCREASES WOUND HEALING.
  35. 35. HYPER / HYPOTENSION MANAGEMENT   HYPERTENSION IS NOT PROBLEMATIC TREATED ROUTINELY WITH ANTIHYPERTENSIVE DRUGS. HYPOTENSION MAY BE PROBLEMATIC DUE TO IMPAIRED CARDIAC FUNCTION AND PERIPHERAL VASODILATION.
  36. 36. METABOLIC ACIDOSIS MANAGEMENT  METABOLIC ACIDOSIS IS DUE TO INCREASED CATABOLISM, DECREASED EXCRETION BY KIDNEY.  ACIDOSIS IS DETREMENTAL TO BODY. IT LEADS TO INCREASE PROTEIN CATABOLISM, DEPRESSED MYOCARDIAC CONTRACTILITY AND MINERAL LOSS FROM BONE. SERUM BI-CARBONATE LEVELS <15 Meq / lt OR ARTERIAL PH < 7.2 DENOTE SEVERITY OF ACIDOSIS , TREATED WITH SODA BI-CARB. 
  37. 37. ANAEMIA  ANAEMIA IS DUE TO UREMIA, DECREASED ERYTHROPOIETIN, SEPSIS, SHORTENED RBC LIFE SPAN.  TREATED WITH ERYTHROPOIETIN AND BLOOD TRANSFUSION. BONE METOBOLISM  HYPOCALCEMIA, HYPERPHOSPHOTEMIA, INCREASED PARATHYROID HARMONE, DECREASED ACTIVATION OF VIT-D.  TREATED WITH DECREASED PHOSPHATE INTAKE AND ORAL PHOSPHATE BINDING AGENTS.
  38. 38. RENAL REPLACEMENT THERAPY  CRITERIA FOR RENAL REPLACEMENT THERAPY INCLUDE 1) INABILITY TO CONTROL HYPERVOLEMIA 2) INABILITY TO CONTROL HYPERKALEMIA 3) INABILITY TO CONTROL ACIDOSIS 4) INABILITY TO CONTROL UREMIA.  THERE ARE THREE FORMS OF RRT 1) INTERMITTENT HAEMODIALYSIS 2) CONTINUOUS HEMOFILTRATION 3) PERITONEAL DIALYSIS
  39. 39. INTERMITTENT HEMODIALYSIS       BLOOD IS WITHDRAWN AT THE RATE OF ABOUT 200 ml/min MIXED WITH HEPARIN PASSED THROUGH A DIALYSER PERFUSED WITH DIALYSATE SOLUTION AT THE RATE OF 500 ml /min IN THE OPPOSITE DIRECTION TO BLOOD FLOW. THESE TWO ARE SEPARATED BY A SEMIPERMEABLE MEMBRANE. UREMIC TOXINS LEAVE THE BLOOD BY DIFFUSION, ELECTROLYTES EQUILIBRATE DEPENDING ON THEIR CON. DIFFERENCE. EACH SESSION LOSTS FOR 3-4 HOURS ONCE A DAY 3-TIMES A WEEK. ADVANTAGES: HIGH CLEARANCE OF UREMIC TOXINS, RAPID CORRECTION OF ELECTROLYTES, SHORT PERIOD OF EXPOSURE TO ANTI COAGULANTS. DISADVANTAGES :DEDICATED TRAINED PERSONNEL NEEDED, ANTICOAGULATION, RAPID SHIFTS OF ELECTROLYTES AND TOXINS, RAPID SHIFT OF FLUIDS IN TISSUE COMPARTMENTS, INTRACELLULAR FLUID SHIFTS CAUSING CEREBRAL EDEMA AND DECREASED CEREBRAL PERFUSION.
  40. 40. CONTINUOUS HEMOFILTRATION          CONTINUOUS ARTERIO VENOUS HEMOFILTRATION (CAVH). ARTERY AND VEIN ARE CANNULATED , ARTERIAL BLOOD IS HEPARINISED PASSED THROUGH A FILTER AND RETURN TO THE PATIENT. THE FLUID REMOVED IS 1 lt/Hr AND IS USUALLY REPLACED DOWNSTREAM THE FILTER WITH A COMMERCIAL PREPARATION. HERE THERE IS INCREASED PERMEABILITY, SO INFLAMMATORY MEDIATORS ARE CLEARED FASTER. FILTER LIFE LOSTS FOR 1-4 DAYS. CONSTANT SLOW CORRECTION OF ELECTROLYTES. DISADVANTAGES: NEEDS ARTERIAL CANNULATION, DEPENDS ON B.P., CONTINUED ANTI-COAGULATION. CVVH: CONTINUOUS VENO VENOUS HEMOFILTRATION. ADDITION OF PUMP IN CVVH, NO NEED OF ARTERIAL CANNULATION. CVVHD: CONTINUOUS VENO VENOUS HEMO DIALYSIS. DIALYSIS FLUID PASS THROUGH THE FILTER IN OPPOSITE TO BLOOD FLOW @ 1000ml /Hr.
  41. 41. PERITONEAL DIALYSIS  GANTER 1923 .  CONTROL ON FLUID BALANCE, NEEDS INTACT PERITONEUM .  THE DIALYSIS FLUID IS PLACED INTO THE PERITONEAL CAVITY THROUGH A CATHETER AND AFTER SPECIFIED TIME IT IS DRAINED.  FLUID BALANCE IS ACHIEVED BY VARYING THE OSMOLALITY OF THE DIALYSIS FLUID BY ADDING GLUCOSE.  THE PROCESS IS MACHINE DRIVEN OR MANUAL.  ADVANTAGES: SIMPLE, REMOVAL OF INFLAMMATORY MEDIATORS GOOD, NO NEED OF ANTI-COAGULATION.  DISADVANTAGES: NOT EFFICIENT IN LOW BLOOD PRESSURES, MORE OF DIALYSIS FLUID IS NEEDED, INFECTION, LESS TIGHT.
  42. 42. REFERENCES  1] ANAESTHESIOLOGY CLINICS OF NORTH AMERICA: Anesthesia and renal considerations by JEROME F. OHARA, VOL.18 No.4, Dec.2000.  2] CLINICS IN CHEST MEDICINE: Acute Renal Failure In Intensive Care Unit by ANDREW BRIGLIA, ANDS EMIL P. PEGANINI.Vol.20, No.2 , June.1999.  British Journal of Intensive Care, Vol.8, No.5, Oct.1998. Pages 163-

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