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Approach to Acute renal failure.ppt
- 1. Acute renal failure KIU - series
- 2. Objective • Definition of ARF • Epidemiology • Etiology of ARF • Management of ARF – Diagnosis of ARF – Treatment of ARF
- 3. Definition; • Abrupt sustained decline in GFR resulting in impaired renal physiological function. • Diagnostic criteria1; – Abrupt(48hrs)absolute rise in serum cr.≥0.3mg/dl(from baseline<2mg/dl) – OR a % serum cr. rise ≥50% – OR oliguria <0.5mls/kg/hr > 6hrs 1) Acute Kidney Injury Network: report of an initiative to improve outcomes in AKI
- 4. AKIN stage Serum Creatinine Criteria Urinary Output Criteria Time 1 Cr ≥ 0.3 mg/dL or ≥ 150-200% from baseline < 0.5 mL/kg/hr > 6 hrs 2 Cr to > 200-300% from baseline < 0.5 mL/kg/hr > 12 hrs 3 Cr to > 300% from baseline or Cr ≥ 4mg/dL with an acute rise of at least 0.5 mg/dL < 0.5 mL/kg/hr or anuria X 24 hrs X 12 hrs *Patients needing RRT are classified stage 3 despite the stage they were before starting RRT Mehta R, Kellum J, Shah S, et al.: Acute kidney Injury Network: Report of an Initiative to improve outcomes in Acute Kidney Injury. Critical Care 2007; 11: R31.
- 5. Acute renal failure (ARF) or acute kidney injury (AKI) • Oliguria: <400 ml urine output in 24 hours • Anuria: <100 ml urine output in 24 hours
- 6. Epidemiology • It occurs in – 5% of all hospitalized patients and – 35% of those in intensive care units • Mortality is high: • up to 75–90% in patients with sepsis • 35–45% in those without
- 7. Non-Oliguric vs. Oliguric vs. Anuric • Oliguric renal failure. – Functionally, urine output less than that required to maintain solute balance (can’t excrete all solute taken in). – Defined as urine output < 400ml/24hr. • Anuric renal failure. – Defined as urine output < 100ml/24hr. – Less common – suggests complete obstruction, major vascular catastrophy, or more commonly severe ATN.
- 8. Non-Oliguric vs. Oliguric vs. Anuric • Classifying by urine output may help establish a cause. – Oliguria – more common with obstruction, prerenal azotemia – Nonoliguric – intrarenal causes – nephrotoxic ATN, acute GN, AIN. • More importantly, assists in prognosis. – Significantly higher mortality with oliguric renal failure. – 80% vs. 25% mortality in Oliguric vs. non-oliguric ARF – Nonoliguric renal failure may also suggest greater liklihood of recovery of function.
- 10. Pre-renal AKI – Volume depletion • Renal losses (diuretics, polyuria) • GI losses (vomiting, diarrhea) • Cutaneous losses (burns, Stevens-Johnson syndrome) • Hemorrhage • Pancreatitis – Decreased cardiac output • Heart failure • Pulmonary embolus • Acute myocardial infarction • Severe valvular heart disease • Abdominal compartment syndrome (tense ascites)
- 11. Post-renal AKI – Ureteric obstruction • Stone disease, • Tumor, • Fibrosis, • Ligation during pelvic surgery – Bladder neck obstruction • Benign prostatic hypertrophy [BPH] • Cancer of the prostate • Neurogenic bladder • Drugs(Tricyclic antidepressants, ganglion blockers, • Bladder tumor, • Stone disease, hemorrhage/clot) – Urethral obstruction (strictures, tumor)
- 12. Post-renal AKI
- 13. Renal – Glomerular • Anti–glomerular basement membrane (GBM) disease (Goodpasture syndrome) • Anti–neutrophil cytoplasmic antibody-associated glomerulonephritis (ANCA-associated GN) (Wegener granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis) • Immune complex GN (lupus, postinfectious, cryoglobulinemia, primary membranoproliferative glomerulonephritis) – Tubular • Ischemi • Toxic – Heme pigment (rhabdomyolysis, intravascular hemolysis) – Crystals (tumor lysis syndrome, seizures, ethylene glycol poisoning, megadose vitamin C, acyclovir, indinavir, methotrexate) – Drugs (aminoglycosides, lithium, amphotericin B, pentamidine, cisplatin, ifosfamide, radiocontrast agents)
- 14. Renal – Interstitial • Drugs (penicillins, cephalosporins, NSAIDs, proton-pump inhibitors, allopurinol, rifampin, indinavir, mesalamine, sulfonamides) • Infection (pyelonephritis, viral nephritides) • Systemic disease (Sjogren syndrome, sarcoid, lupus, lymphoma, leukemia, tubulonephritis, uveitis
- 15. Acute Renal Failure Clinical Assessment (Volume Status, Urinalysis and Ultrasound) Pre-Renal Intra-Renal Post-Renal Absolute Decrease In ECF Volume GI losses Hemorrhage Decreased Renal Blood Flow Heart failure Renal artery stenosis Altered Intra-Renal Hemodynsmics Drug-induced NSAIDS/COX-2 Inhibitors Calcineurin inhibitors ACE inhibitors AII Receptor Blockers Sepsis Hypercalcemia Cirrhosis/Hepatorenal syndrome Abdominal compartment syndrome Tubulointerstitial Disorders Tubular Injury Ischemic Nephrotoxic Interstitial Nephritis Allergic-type NSAID-type Glomerular Disorders Glomerulonephritis Thrombotic microangiopathies Atheroembolic disease Anatomic Obstruction Bladder Outlet Prostate Pelvic Tumor Ureteral Tumor Stones Stricture Tubular Obstruction Crystals Calcium oxalate (Ethylene glycol poisoning) Drugs Indinovir Methotrexate Proteins Myeloma cast nephropathy Clinical Approach to Acute Renal Failure
- 16. 5 Key Steps in Evaluating Acute Renal Failure 1) Obtain a thorough history and physical; review the chart in detail 2) Do everything you can to accurately assess volume status 3) Always order a renal ultrasound 4) Look at the urine 5) Review urinary indices
- 17. Clinical feature-1 • Signs and symptoms resulting from loss of kidney function: – decreased or no urine output, flank pain, edema, hypertension, or colour of urine • Asymptomatic – elevations in the plasma creatinine – abnormalities on urinalysis
- 18. Evaluation of Renal Failure • Is the renal failure acute or chronic? – laboratory values do not discriminate between acute vs. chronic – oliguria supports a diagnosis of acute renal failure • Clues to chronic disease – Pre-existing illness – DM, HTN, age, vascular disease. – Uremic symptoms – fatigue, nausea, anorexia, pruritis, altered taste sensation, hiccups. – Small, echogenic kidneys by ultrasound.
- 19. Acute Renal FAilure • Symptoms: – Fever, rash, joint pains, myalgias • Concern for SLE, vasculitis, acute interstitial nephritis. – Dyspnea – heart failure. – Hemoptysis – Goodpasture’s, Wegener’s. – Preceding bloody diarrhea – HUS. – Preceding pharyngitis – post-Strep GN, post- infectious GN.
- 20. Acute Renal Failure • Urine output. – Abrupt anuria. • Acute obstruction, severe acute GN, sudden vascular catastrophe. – Slowly diminishing. • Ureteral stricture. • Prostatic enlargement. – Presence of hematuria • Painless – suggests GN. • Painful – suggest ureteral obstruction. Other symptoms - mental status changes and seizures
- 21. Acute Renal Failure • Physical Exam. – Skin – new rashes. • Livedo reticularis – atheroemboli, SLE, cryoglobulins. • Petechiae – HSP. • Malar rash – SLE. – Eye • Papilledema – malignant HTN. • Roth’s spots – endocarditis. – CV • Rub – suggestive of uremic pericarditis, lupus. • Gallop – suggesting CHF.
- 22. • BUN/Creatinine ratio. – > 20:1 – suggest prerenal or obstruction. – Can be elevated by anything leading to increased urea production/absorption. • GI bleed • TPN • Steroids • Drugs –.
- 23. Acute Renal Failure Diagnosis • Blood urea nitrogen and serum creatinine • CBC, peripheral smear, and serology • Urinalysis • Urine electrolytes • U/S kidneys • Serology: ANA,ANCA, Anti DNA, HBV, HCV, Anti GBM, cryoglobulin, CK, urinary Myoglobulin
- 24. Acute Renal Failure Diagnosis • Urinalysis – Unremarkable in pre and post renal causes – Differentiates ATN vs. AIN. vs. AGN • Muddy brown casts in ATN • WBC casts in AIN • RBC casts in AGN – Hansel stain for Eosinophils
- 25. Renal failure Differentiation between acute and chronic renal failure Acute Chronic History Short (days- week) Long (month-years) Haemoglobin concentration Normal Low Renal size Normal Reduced Renal osteodystrophy Absent Present Peripheral neuropathy Absent Present Serum Creatinine concentration Acute reversible increase Chronic irreversible
- 26. Complications • ECF expansion • Hyperkalaemia • Metabolic acidosis • Hyperphosphataemia • Hypocalcaemia • Anaemia • Bleeding diasthesis • Infections • Uraemic syndrome • hypernatraemia
- 27. Treatment of AKI • Optimization of hemodynamic and volume status • Avoidance of further renal insults • Optimization of nutrition • If necessary, institution of renal replacement therapy
- 28. Replacement fluids • Ringers lactate - since contains K+ do not give to oliguric patient • ½ NS – avoid in hyponatremic patient • 0.9 NS resuscitation fluid of choice, but can worsen hyponatremia if SIADH
- 29. Initial Management • Correct hypovolaemia and hypotension • Management of hyperkalaemia • Avoid further nephrotoxins
- 30. Management priorities in AKI (I) • Detect as early as possible even minimal AKI • Exclude other renal causes of AKI, • Search for and correct prerenal and postrenal factors • Review medications and stop nephrotoxins • Optimize cardiac output and renal blood flow • Restore and/or increase urine flow • Monitor fluid intake and output, daily weight
- 31. - EMERGENCY THERAPY FOR HYPERKALEMIA - Ca gluconate - Insulin + Glucose - NaHCO3 ? - 2 -Adrenergics ? - Kayexalate Enema --slower
- 32. AKI - use of dopamine or diuretics • Low dose dopamine – does not reduce the incidence of AKI, the need for RRT or improve the outcome in AKI. Is associated with increased myocardial 02 demand and increased incidence of atrial fib • Diuretics - can sometimes convert oliguric to non oliguric but no data that shorten duration of AKI, reduce need for RRT, or improve overall outcomes. But can help control volume overload.
- 33. Treatment cont’d – Intrinsic renal AKI: • Glucocorticoids/alkylating agents/plasmapharesis in AGN/vasculitis • Aggressive BP control in malignant HT – Post renal AKI • Ealry US and Relief of obstruction – Supportive measures • Restriction of salt and water intake in hypervolaemia and diuretics • Ultrafiltration/dialysis in refractory cases • Hypernatraemia-free water,hypotonic saline/5%D • Ca resonium 15g QDS orally • If systolic BP<100mmHg despite optimal intravascular volume start ionotropes • Consider renal biopsy if features suggestive of multisystem disease • Look for sepsis
- 34. Supportive measures should be aimed to correct the following • Hyperkalaemia – start on hyperkelemic protocal • Metabolic acidosis - bicarbonate • Nutritional mgt • Anaemia - blood transfusion • Antiacids - • Avoid other nephrotoxins • Dialysis – check on indications
- 35. Indications for RRT • Refractory fluid overload • Hyperkalemia – eg, K+ >6.5 meq/L, rapidly rising levels, marked EKG changes especially if patient oliguric or can not take kayexalate • Marked metabolic acidosis in which are limited in giving NAHCO3 due to volume constraints • Signs of uremia, such as declining mental status, not eating, uremic pericarditis (rare)
- 36. Timing of initiation of RRT • Initiation of dialysis prior to the development of symptoms and signs of renal failure due to AKI is recommended. • It is unproven whether initiation of earlier or prophylactic dialysis offers any clinical or survival benefit. • If start RRT before symptoms is no concensus on what level of BUN or creatinine to start
- 37. prognosis • Depends on the underlying aetiology and severity of the AKI • Oliguria at presentation and cr>3mg/dl poor prognosis • Overall mortality ~50% • Older age-poor prognosis • 50% subclinical renal impairment • 5% never recover normal kidney function • 5% have progressive decline in GFR following initial recovery N.B. primary goal is to achieve optimal blood volume, urine flow is of secondary importance.
- 38. References • Harrisons 16th Ed. • Kellum et al. acute renal failure, aug 01/07 BMJ. Vol 76 No 3 • Uptodate 15.2 • Acute kidney injury network:report of an initiative to improve outcomes in AKI