ACUTE RENAL FAILTURE

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ACUTE RENAL FAILTURE. LIJI VINCENT. Acute renal failure (ARF) refers to a sudden and usually reversible loss of renal function, which develops over a period of days or weeks and is usually accompanied by a reduction in urine volume. Reversible Pre-Renal Acute Renal Failure. Pathogenesis. - PowerPoint PPT Presentation

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  • ACUTE RENAL FAILTURE

    LIJI VINCENT

  • Acute renal failure (ARF) refers to a sudden and usually reversible loss of renal function, which develops over a period of days or weeks and is usually accompanied by a reduction in urine volume.

  • Reversible Pre-Renal Acute Renal FailurePathogenesis

  • Clinical FeaturesHypotension and signs of poor peripheral perfusionPostural hypotension fall in SBP/DBP >20/10 mmHg early sign of hypovolaemia.The cause of reduced renal perfusion may be obvious or concealedMetabolic acidosis and hyperkalaemia may be (+)

  • ManagementEstablish and correct the underlying cause of the ARF.If hypovolaemia (+) replace with blood, plasma or isotonic salineOptimise systemic haemodynamics. Monitor CPU or pulmonary a wedge pressure.Correct metabolic acidosis- Restoration of blood volume will restore kidney function- Isotonic sodium bicarbonate

  • Established Acute Renal FailureFollowing severe or prolonged under perfusion of the kidney.Histology: Acute tubular necrosis Acute Tubular Necrosis:Cause(1)Ischaemia(2)Nephrotoxicity

  • Nephrotoxic ATNDirect toxicity of the causative agent to the tubular cells.

  • Recovery From ATNTubular cells can regenerateIf the patient is supported during the regeneration phase.Kidney function restoresRecovery phase-Diuretic phase

  • Other featureUraemic features- anorexia, nausea and vomiting drowsiness, apathy, confusion, muscle twitchingRespiratory rate increased Acidosis, pulmonary oedema, infection.Anaemia Blood loss, haemolysis disordered platelet function and disturbances of the coagulation cascade.

  • Clinical Features of Established ARFReflect the causal condition trauma, septicemia or systemic diseases +1.Alterations in urine volume Oliguric (
  • URINARY TRACTOBSTRUCTIONSUGGESTED BY LOIN PAIN, RENAL COLIC OR DIFFICULTY IN MICTURITIONINVES- USGPROMPT RELIEF OF OBSTRUCTION RESTORES KIDNEY FUNCTION

  • VASCULAR EVENT

    MAJOR VASCULAR OCCLUTION OR SMALL VESSEL DISEASEURINE SHOW MINIMAL ABNORMALITIESMAY BE PRECIPITATED BY ACE INHIBITORS

  • RPGNSIGNIFICANT DIP STICK HAEMATURIAASSOSIATED WITH SYSTEMIC FEATURES BLOOD TESTS-ANA, ANCA, ANTI-GBM ANTIBODIESDIAGNOSIS- RENAL BIOPSY

  • ACUTE INTERSTITIAL NEPHRITISCAUSED BY ADVERSE DRUG REACTIONSMALL AMOUNT OF BLOOD AND PROTIEN IN URINEKIDNEYS NORMAL IN SIZETt-CESSATION OF DRUG AND PREDNISOLONE

  • DRUGSHAEMODYNAMIC EFFECTS- NSAIDs , ACE INHIBITORSDIRECT TOXICITY TO THE TUBULES- AMINOGLYCOSIDES

  • Screening Tests

    HematologyFull blood countBlood filmClotting screen, Group and save

    BiochemistryUrea, electrolytes and creatinine calciumUrinalysisUrine MicrocopyQuantitative urinary protein measurement

  • 3.MicrobiologyBlood cultureCRPMid-stream urineOther cultures4.Imaging Renal USGChest X rayECG

  • Immunoglobulin and protein electrophoresisUrinary Bence Jones ProteinComplementANA and ds DNA Extractable nuclear Antigen (ENA)Rheumatoid factor

  • Management1.Emergency resuscitationHyperkalaemia treated immediatelyCirculating blood volume restorationAcidosis-Isotonic sodium bicarbonate2.Addressing the underlying causeUSG showing urnary tract obstruction.ATN - restoring renal perfusion.Postrenal obstruction :Due to Pelvic or ureteric dilatation Percutaneous nephrostomy

  • Fluid and electrolyte balanceDaily fluid intake should = prev. day urine output + 500ml to cover unsensible loss.Abnormal loses like diarrhea electrolyte replacement. Since Na+ and K+ are retained their intake should be restricted Protein and energy intakeIn patients where dialysis is avoided protein restriction to 40g/dayIn patients with dialysis more dietary protein

  • Infection controlRegular clinical examination and microbiological investigation required.DrugsVasoactive drugs NSAIDs & ACE inhibitors are to be avoided.Renal Replacement therapy This may be required as supportive management in ARF.

  • Increased Plasma urea andcreatinine urea >30mmol/lCreatinine >6.8mgdlAt lower level Progressive biochemical deterioration.Hyperkalaemia K+ >6mmolMetabolic acidosis raise the plasma potassium further.Fluid overload and pulmonary oedema Uraemic pericarditis/ uraemic encephalopathy.

  • Intermittent haemodialysis

    Best rate of small solute clearance.1 hour tt is prescribed. Subsequently when haemodyamically stable 3 4 hours 3 4 times a week.Haemodialysis 2 3 hrs every day severly catabolic

  • HaemofiltrationIntermittent 15 30 liters of plasma ultra filtrate exchanged for replacement fluid over 3 5 hours.Continuous1 2 liters of filtrate replaced higher rate of filtration MODS sepsis.

  • Intermittent haemodiafiltration

  • Peritoneal dialysisSeldom achieves adequate biochemical control

  • Difference BetweenHD&PD

    EfficientLess efficent4hours 3 times a week4 exchanges per day each 30 60 min. CAPD or 8 -10 hrs Automated PD2-3 day betweenFew hrs between ttRequires visit to hospitalPerformed at homeRequires adequate venous accesRequires an intact peritoneal cavity

  • Careful compliance to diet and fluid restrictionDiet & fluid less restrictedFluid removal compressed during tt period - haemody instabilitySlow continous fluid removal - asymptomaticInfection reld to vascular accessInfection Peritonitis,catheter reld infectionsPatients are, to some extent dependent on othersPatients can take full reponsibility of their tt

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