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. DEFINITION


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
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. 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. PATIENT FACTORS


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PRE-OPERATIVE RENAL DYSFUNCTION
PERIOPERATIVE CARDIAC DYSFUNCTION
SEPSIS
HEPATIC FAILURE, OBSTRUCTIVE
JAUNDICE, ASCITES
HYPOVOLEMIA
ADVANCED AGE?
MAJOR OPERATIONS

5. HIGH RISK SURGICAL PROCEDURES

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
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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. NEPHROTOXINS
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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. NEPHROTOXINS

ENDOGENOUS:

HYPERCALCEMIA
HYPERURICEMIA
HYPERURICOSURIA
RHABDOMYOLYSIS
HAEMOLYSIS
BILIRUBIN
OXALATES
PARAPROTIENS

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

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. PHARMACOLOGICAL STRATEGIES

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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. CALCIUM CHANNEL BLOCKERS

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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. 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. 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. PROSTAGLANDINS
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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. ATRIAL NATRIURETIC PEPTIDE
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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. ATRIAL NATRIURETIC PEPTIDE
(Cont’d)
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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. 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. DOPAMINE – 1 AGONISTS (Cont’d)
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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. MODULATION OF COMPLEMENT SYSTEM
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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. 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. ALPHA MELANOCYTE STIMULATING HORMONE
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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. DOPAMINE

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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. 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. 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. FUROSEMIDE

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


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. MANNITOL
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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. 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. 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. PATHOPHYSIOLOGY

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
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


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. 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. MANAGEMENT

PREVENTION OF DAMAGE

CONSERVATIVE LINE OF MANAGEMENT

RENAL REPLACEMENT THERAPY

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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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-