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RENAL FAILURE DR..M.H.MUMTAZ

RENAL FAILURE

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RENAL FAILURE. DR..M.H.MUMTAZ. TYPES. 1, REVERSIBLE DYSFUNTION (acute R.failure) 2, IRREVERSIBLE DYSFUNTION (Chronic R failure). ACUTE RENAL FAILURE. 1, PRE RENAL 2, RENAL - PowerPoint PPT Presentation

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  • RENAL FAILURE

    DR..M.H.MUMTAZ

  • TYPES1, REVERSIBLE DYSFUNTION (acute R.failure)2, IRREVERSIBLE DYSFUNTION (Chronic R failure)

  • ACUTE RENAL FAILURE 1, PRE RENAL 2, RENAL 3, POST RENAL

  • PRE RENAL FAILURECAUSES a,total body water depletion b,water redistribution ivs--------iss vasodilation,sepsis,anaphy. c,low CO--------low BP (S,M.D)

  • RENAL a, Interstitial nephritis b, A.T.N. hypoperfusion chemical trauma , toxins sepsis

  • PATHOLOGY T.obstruction T.damage

    T.backleakage

  • DIAGNOSIS a,History oligurea,concentrated U b,Tests lab. Serum,urine radiodiagnostics C.T. MRI. Ultrasount

  • ALTERNATIVE CLASS. Filteration failure Tubular dysfuntion

    Oliguric/non oliguric

  • RISK FACTORSAcute diseases sepsis SIRS jaundice I.A.P. renal trauma transfusion DIC

    Anaphylaxis muscle injury thermal burn electrocution

  • RISK FACTORS CHRONIC DISEASES advancing age diabetes mellitis renal disease vascular disease hyperuricaemia

  • RISK FACTORS Physiological changes 1. ^ age 2. ^ HR hypotension ^ CVP, lowRVPP high or low co,svr abnormal OER olig/polyurea

    3. Fluid balance Oedaema high/low protein intake

  • RISK FACTORS Chronic drug therapy NSAIDS Diuretics Cyclosporins

  • RISK FACTORSAcute drug therapyA. ATN aminoglycosides cephalosporins diuretics contra. rifampicin lithium cisplatin

    B. Interstitial nephritis cephalosporins diuretics aspirin,NSAIDS cemetidine captopril

  • RISK FACTORS Proceedures a. Aortic/renal cross clamping b.Transfusion c. Major surgery

  • RISK FACTORS IMPAIRED RBF hypotension/m.hypertension renal art. Occlosion hepatorenal failure endotoxaemia renal vein thrombosis renal venous hypertansion

  • RISK FACTORS Metaboic causes 1. Electrilytes hyper-cal hypo-k hyper-phosphate 2. High oncotic P.

    3. Metabolites Pigments bilirubin myoglobin haemoglobin

  • RISK FACTORS Post-renal urethral/blader obs. bil.ureter obs. stones/clot/tumur papillary necrosis

    Retroperitoneal fibrosisSurgical ligationBlader ruptureRenal pelvic traumaUrethral trauma

  • ACUTE TUBULAR NECROSIS PHASES

    a,Initiation phase

    b,Maintenance phase

  • INITIATION PHASEISCHAEMIA ^ symp.stimulation ^ renin activity PGE2 ANH inhibition ^ ADH ^ adenosine ^ endothelinNEPHROTOXINS

    Ischaemia increases the

    susceptibility to

    nephrotoxic agents

  • MANTENANCE PHASEFactors acting to maintain filteration failure 1,tubular obstruction 2,tubular backleak 3,vasodilatation of efferent art. 4,decreased GMP

  • Mechanism of oligurea a,glomerulo-tubular balance

    b,decreased GMP

    c,itratubular obstruction d,interstitial oedema e,cortical ischaemia

  • Complications of ARF/ATNA,oligurea

    absolute

    relativeB, azotaemia normal solute load maximum in catabolic states in ARF ^ urea/d ^ cr/d

  • ComplicationsC,Biochamical ^NaCl/water ^ K ^ HPO4 hypocalcaemia ^ Mg ^ uric acid M.acidosisD,Haematological Anaemia Thrombocytopaenia

    Leukocyte dysf.

  • ComplicationsE,Immunosupression Lumphopaenia Reduced IgG Reduced comple. Impaired PMN R.I.response Drug effects Infections

    F,C.V.S. CCF Hypertention Arrhythmias Pericarditis Effusion

  • ComplicationsG, G.I.T.

    Anorexia,Nausea, Ileus,Hmge.

    H,Neurological Lethargy,somnolance Confusion, Convulsions ^ sensitivity to anaesthetics

  • ComplicationsI,causes of pulmonary infilterates in ARF 1,LVF/CCF 2,bacterial pmeumonia 3,Atypical pneumonia 4,Septicaemia 5,ARDS 6,Autoammune diseases

  • Causes of Acidosis in ARFA,Tubular dysfuntion

    B,Glomerular dysfuntion

    C,Other causes low C.O. Resp.F Starvation

    Rhabdomyolysis Hyperkalaemia Organic acids

  • INVESTIGATIONS IN ARFBiochemistry

  • INVESTIGATIONS

  • Investigations-1, Biochemistry

  • Definitions RFI=RENA FAILURE INDEX =urine(Na)/(U/P creatinine)

    FEna=%fractional excretio Na

    =(U/P Na).100/(U/P creatinine)

  • Abnormal urea/creatinine ratio

    Normal U:C ratio 100:1( R;70-150)

    Pre-renal disease >200:1

  • Abnormal urea/creatinine ratio

    High Ratio ^ urea .dehydration/hypovol. .GIT.bleeding .Catabolic state .Hyperalimentation .Drugs low creatinie .elderly,low m. mass

  • Abnormal urea/creatinine ratioLow Ratio low urea. Liver failure hepato-renal synd Malnutrition High creatinie rhabdomyolysis acute m.disease ketones,drugs

  • CREATININE CLEARANCE1, clearance(ml/min=(N-age[years])*BW(kg)/serum creat. N = 150 foe female N = 160 for male > 70 N = 170 for male < 70 2, clearance(ml/min)=UV*1000 /p*420 U=urine creatinine level V=urine volume (midnight &7 am) P= plasma creatinine level

  • 2. Urinary sediment.Cast types i,hyaline casts, fever,diuretics,RD ii,red cell casts glomerulonephritis iii,w.cell casts pyelonephritis iv,waxy casts chronic renal disease

  • 3,Imaging 1, Ultrasound 2, CT scan 3, IV pylogram 4, radio-isotope perfusion scan 5, renal angiogram

  • 4,Renal biopsy 1, glomerulonephritis 2, vasculitis 3, SLE 4, Goodpasture syndrome 5, TTP 6, Interstitial nephritis 7, oligurea lasting > 8 weeks

  • Renal failureprophylaxis&protectionMethods 1, physiological 2,physical 3,pharmacological 4,replacement therapies

  • Physiological methods a, normalise blood volume iv fluids,(Na containg) b,optimise cardiac output iv fluids.inotropes,vasopressors c, optimise O2 delivery Hb,Spo2,avoid acidosis d, high sodium excretion

  • Physical methods Detection/management of IOH Detection/management-post renal obs. Limitation of aortic clamp times Avoidance of embolisation Minimise direct trauma

  • Pharmacological methods Avoid nephrotoxins Avoid inhibitors of autoregulation Diuretics Renodilators Other agents free radical scavengers Ca channel blockers

  • Renal replacement methods Haemo- filtration

    Haemo-diafiltration

    Haemodialysis

    R. Transplant.

  • Renal failure---FrusemideBeneficial effects Increased tubular&urine flow Increase Na &osmolar clearance Decreased tubular O2 demand Stimulate vasodilator prostaglandinsDeleterious effects Hypovolaemia Hypokalamia,Hyponatraemia Ototoxicity

  • Uses in non renal failure Fluid overload Cerebral oedema Hyperkalaemia Renal protection ( decreased O2 demand)

  • Renal failure---Mannitol 1,Osmotic diuresis

    2,Anti sludging ,tubular protect.

    3,renal vasodilatory PG synthesis 4,Free radical scavenger 5,Decreased T. swelling

  • Renal failure---Dopamine Increases Fe Na excretion Increases urine out put Does not increase creatinine clearance Inotropic effect Doesnot prevent ac.renal failure Side effects, gastric stasis,inhibition of ant pit.hormones,hypoxic drive depression.

  • Renal failure---Nor-adrenaline

    Increases perfusion pressure by increase

    of efferent arteriolar resistance

    more than afferent art.resistance

  • Other therapies 1,Calcium channel blockers 2,Adenicine recepter antagonists 3,Oxypentifylline 4,Chlorpromazine 5,Clonidine 6,ATP-MgCl2 7,ANF

  • Conclusion,Renal rescue therapyNormalise;- Blood flow blood volume blood pressure O2 delivery COCI Blood Pressure, s,m,d.