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ACUTE RENAL FAILURE PowerPoint Presentation
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ACUTE RENAL FAILURE

ACUTE RENAL FAILURE

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ACUTE RENAL FAILURE

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  1. ACUTE RENAL FAILURE

  2. Kidney Function • Detoxify blood • Increase calcium absorption • calcitriol • Stimulate RBC production • erythropoietin • Regulate blood pressure and electrolyte balance • renin

  3. DEFENITION • Acute renal failure is defined as a decrease in GFR, generally occurring over hours to days sometimes over weeks that is associated with an accumulation of waste products including urea and creatinine , inability to concentrate urine, regulate fluid and electrolyte balance and maintain acid base homeostasis.

  4. CLASSIFICATION • Based on precipitating and etiological factors, ARF is classified as:- • Pre renal . • Intra renal. • Post renal. • Based on amount of urine produced per day , it can be classified as:- • Anuric ARF ( <50 ml / day) • Oliguric ARF (50 – 400 ml / day) • Non oliguric ARF (> 400 ml / day)

  5. STAGING - RIFLE CRITERIA

  6. EPIDEMEOLOGY • Acute kidney injury is common among hospitalized patients. • It affects some 3-7% of patients admitted to the hospital and approximately 25-30% of patients in the intensive care unit

  7. etiology • Pre renal – decreased renal perfusion in the setting of undamaged parenchymal tissue. • Intrisic – structural damage to the kidney • Post renal – obstruction to urine flow. Trauma, rhabdomylosis, vessel thrombosis & drugs (contrast media, NSAID’s,ACEI,ARB etc) are also culprits. other risk factors – age, male gender, acute infection. next

  8. Pre renal ARF • Decreased cardiac output. • CHF • Cardiomyopathy • MI • Hypovolemia • Major trauma • Burns • Hemorrhage • Increased renovascular resistance • Systemic vasodialation • Renovascular obstruction BACK

  9. Intrinsic ARF • Prolonged pre renal azotemia • Nephrotoxic agents • Ischemic events • massive hemorrhage • septic shock • arterial thrombosis • Glomerular • Tubulo interstitial BACK

  10. Post renal ARF • Bilateral ureteral obstruction • intraureteral • extraureteral • Pappilary necrosis • Bladder obstruction • Mechanical • Functional • Urethral obstruction BACK

  11. pathophysiology • CIRCULATORY DISTURBANCES – Reduction in renal blood flow lead to ischemia. In response to reduced RBF, PG I₂ & PG E₂ increase blood flow to kidney. NSAID’s inhibit this. Ischemia —> oxidative phosphorylation stops & depletion of ATP.

  12. TUBULAR & GLOMERULAR EVENTS Diminished renal function occur due to:- • back leak of glomerular filtrate into per tubular fluid . • tubular obstruction • decreased glomerularcappillary permeability.

  13. SIGNS AND SYMPTOMS • SIGNS:- edema, coloured or foamy urine, orthostatic hypotension in volume depleted patients & hypertension in volume overloaded patients. • SYMPTOMS:- change in urinary habits, sudden weight gain, flank pain.

  14. DIAGNOSIS • Introduced by the Acute Kidney Injury Network (AKIN), specific criteria exist for the diagnosis of ARF. • Rapid time course (less than 48 hours) • Reduction of kidney function • Rise in serum creatinine • Absolute increase in serum creatinine of ≥0.3 mg/dl (≥26.4 μ mol/l) • Percentage increase in serum creatinine of ≥50% • Reduction in urine output, defined as <0.5 ml/kg/hr for more than 6 hours

  15. Patient History & Physical examination. • Urinalysis. • physical & chemical properties. • pH • concentrating ability. • Protein content. • Cells and casts. • sodium excretion.

  16. LABORATORY DATA • GFR. • Creatinine clearance. • BUN. • Renal imaging & renal biopsy.

  17. COMPLICATIONS • Metabolic acidosis, hyperkalemia, and pulmonary edema may require medical treatment with sodium bicarbonate, antihyperkalemic measures, and diuretics.

  18. PREVENTION & TREATMENT • The goals of treatment for acute renal failureare to: • Correct or treat the cause of kidney failure. • Support the kidneys until they have healed and can work properly. • Prevent or treat any complications caused by acute renal failure.

  19. NONPHARMACOLOGICAL • Adequate hydration and sodium loading prior to radio contrast dye administration. • when nephrotoxic agent use cannot be avoided, there may be ways to administer them in a manner that reduces their nephrotoxic potential. • Preventive dialysis.

  20. PHARMACOLOGICAL • Diuretics. • Mannitol. • Loop diuretics. • Vaso active agents. • Dopamine • Fenoldopam • Calcium channel blockers. • ANP. • Acetylcysteine. • Glycemic control.

  21. MANAGEMENT • ARF should be managed with hemodynamic support and volume replacement. • If immune related, initiate immuno suppressive therapy. • Regardless of etiology, supportive care should be given.

  22. NONPHARMACOLOGICAL • Renal replacement therapy. • Intermittent hemodialysis. • Continuous renal replacement therapy.

  23. PHARMACOLOGICAL • Therapy to prevent further insults . • If sepsis , antibiotic therapy. • Loop diuretics.

  24. ELECTROLYTE MANAGEMENT • Hypernatrimia and fluid retention – complications of ARF. • Electrolytes are closely monitired. • Serum potassium monitored daily or twice daily. • Medication containing potassium should be avoided. • Hyperphosphatemia should be treated.

  25. NUTRITIONAL INTERVENTION Provision of enteral nutrition – improved outcome. Dextrose contained in CRRT replacement solutions contribute significant amount of calories to patients regimen.

  26. DRUG DOSING CONSIDERATION • Response to drug regimen include patient’s clearance, accumulation of fluids. • For drugs with narrow therapeutic index drugs serum concentration should be measured. • Reduction in cardiac output or liver function alter p’kinetic profile of the drug.

  27. TREATMENT ALGORITHM • PATIENT IN ICU DEVELOPS ACUTE ARF • PHY EXAM,HISTRY,LAB VALUES SUGESTING ARF • DETERMINE CAUSE • INSTITUTE DIURESIS- frusemide 80 mg iv. • EXCLUDE REVERSIBLE CAUSE,TOXIC AGENTS, • INSTITUTE DIURESIS- frusemide 80 mg iv.

  28. U.O> 1 ml/kg/hr NO YES • FUROSEMIDE 100 mg i.v. –u.o>1ml/kg/hr • FUROSEMIDE 400 MG IV • U.O> 1 ml/kg/hr YES • FUROSEMIDE 10mg/hr, u.o>1 ml/kg/hr until euvolemic. NO • FUROSEMIDE 400mg,chlrthiazide 500mg,metolazone 5 mg • U.O>1ml/kg/hr in 2 hr YES NO • CONT. CHLORTHIAZIDE 500mg i.v • CONSDR RRT

  29. REFERENCE • Myrna Y. Munar, Harleen Singh,Acute Renal Disease In Richard A Helms,DavidQuan,Eric t. Herfindal et al(eds), Textbook of Therapeutics:drugs and disease management,8 thedition,page no: 1107-1135. • William Dager, Anne Spencer, Acute renal failure in Joseph T.Dipiro,Robert L. Talbert,GaryC.Yee et al(eds),Pharmacotherapy –A Pathophysiologic approach ,7 thedition,pg no: 723 – 741. • J. Marriot,S. Smith,Acute renal failure In Roger Walker, Clive Edwards Clinical pharmacy and therapeutics ,3rd edition, pg no: 229- 245.