O slideshow foi denunciado.
Utilizamos seu perfil e dados de atividades no LinkedIn para personalizar e exibir anúncios mais relevantes. Altere suas preferências de anúncios quando desejar.

Acute kidney injury

3.381 visualizações

Publicada em

Acute kidney Injury

Publicada em: Saúde e medicina
  • 1 Weird Diet Trick Heals Vitiligo Fast =>> https://j.mp/3kTNHDZ
       Responder 
    Tem certeza que deseja  Sim  Não
    Insira sua mensagem aqui
  • 1 Weird Diet Trick Heals Vitiligo Fast ☺☺☺ http://tinyurl.com/y4d5dqxj
       Responder 
    Tem certeza que deseja  Sim  Não
    Insira sua mensagem aqui
  • The "END OF GOUT" is a short, to the point guide on how to reverse gout symptoms without ever leaving your home. The guide goes into extensive detail on exactly what you need to do to safely, effectively and permanently get rid of gout, and you are GUARANTEED to see dramatic improvements in days if not hours. ♣♣♣ https://t.cn/A6AZCbfA
       Responder 
    Tem certeza que deseja  Sim  Não
    Insira sua mensagem aqui
  • I wouldn't have suffered three years of gout misery if I'd known that… Thousands of people are now gout-free simply from eating foods found in their local supermarket – now I'm one of them! No meds, doctors or procedures – three years of pain gone in weeks.  https://t.cn/A6AZCtO2
       Responder 
    Tem certeza que deseja  Sim  Não
    Insira sua mensagem aqui
  • Reverse Gout Pain? Can you really fix gout naturally? Yes you can. Click here to see how ◆◆◆ http://t.cn/A67DoaUo
       Responder 
    Tem certeza que deseja  Sim  Não
    Insira sua mensagem aqui

Acute kidney injury

  1. 1. ACUTE KIDNEY INJURY 1 DR Jayakrishnan M P PG Resident, Dept of Medicine MGM Medical College, Indore
  2. 2. DEFINITION • Increase in S.Cr by ≥ 0.3 mg/dl within 48 hours ; or • Increase in S. Cr to ≥ 1.5 times baseline, which is known and presumed to occur within the prior 7 days ; or • Urine volume < 0.5 ml/kg/h for 6 hours • AKI is not ATN, nor is it renal failure. KDIGO guidelines 2012 2
  3. 3. • Anuria - Urine output < 100ml/24hrs • Oliguria - Urine output < 400ml/24hrs • Polyuria - Urine output > 2.5 to 3 litres/24hrs 3
  4. 4. RIFLE CRITERIA(2004) 4
  5. 5. Staging of AKI – AKIN Criteria(2007) Stage Serum creatinine Urine output 1 1.5-1.9 times baseline or ≥ 0.3 mg/dl increase < 0.5 ml/kg/h for 6-12 hours 2 2-2.9 times baseline < 0.5 ml/kg/h for ≥ 12 hours 3 3.0 times baseline or Initiation of renal replacement therapy or In patients < 18 years, decrease in eGFR to < 35 ml/ min per 1.73 m2 < 0.3 ml/kg/h for ≥ 24 hours or Anuria for ≥ 12 hours 5
  6. 6. ETIOLOGY Causes of Prerenal AKI(40-55%): • Hemorrhage • GI Loss – diarrhoea,vomiting,NG tube loss • Renal loss – diuretics,DI • Burns,Hyperthermia • Nephrotic Syndrome,Cirrhosis • Reduced CO: Cardiogenic shock,CHF, pericardial diseases,vavular diseases. • Systemic vasodilatation – Sepsis,Cirrhosis,Anaphylaxis,Drugs • Renal Vasoconstriction – Early sepsis, HRS, Acute hypercalcaemia,Drugs-NE, vasopressin,NSAIDS,ACEIs,Calcineurin inhibitors, Iodinated contrast agents • Abdominal compartment syndrome. BRENNER AND RECTORS - THE KIDNEY 9TH EDITION 6
  7. 7. ETIOLOGY Causes of intrinsic AKI: • Tubular injury: hypovolemia,sepsis,hemorrhage,cirrhosis,CHF toxins-Myoglobin,Haemoglobin,uric acid,paraproteinemia- antibiotics,chemotherapy,radio contrast agents,phosphate preparations • Tubulointerstitial injury: - AIN- NSAIDS,antibiotics - Infections, Infiltrations,Allograft rejection • Glomerular injury : Glomerular diseases, Haematological diseases • Renal microvasculature: Malignant HTN, PIH, radiocontrast agents,scleroderma,drugs • Large vessels : vasculitis,thrombosis,dissection,thromboembolism, atheroembolism,compression,trauma BRENNER AND RECTORS - THE KIDNEY 9TH Edtn 7
  8. 8. ETIOLOGY Causes of Postrenal AKI(<5%): • Extrinsic : - Upper urinary tract: pelvic tumours,retroperitoneal tumours or lymph nodes,fibrosis,surgical trauma - Lower urinary tract: prostate/ bladder/urethral pathologies,neurogenic. • Intrinsic : stone,stricture,malignancy,sloughed papillae,blood clots etc BRENNER AND RECTORS - THE KIDNEY 9TH Edtn 8
  9. 9. • Most likely causes in hospitalized patients – ATN (45%) – Prerenal (21%) – Acute on chronic kidney disease (13%) – Obstruction (10%) – Glomerulonephritis or vasculitis (4%) – Acute interstitial nephritis (2%) – Atheroemboli (1%) BRENNER AND RECTORS - THE KIDNEY 9TH Edtn 9
  10. 10. 10
  11. 11. Prerenal AKI • Most common cause of AKI in the outpatient setting – Look for patients with hemorrhage, GI and urinary fluid loss,severe burns – Decreased effective arterial blood volume ( CHF, Cirrhosis or nephrotic syndrome). – Drugs– NSAIDS,ACEIs,ARBs – O/E: tachycardia,signs of dehydration ,orthostatic hypotension,reduced JVP. CLINICAL EVALUATION BRENNER AND RECTORS - THE KIDNEY 9TH Edtn 11
  12. 12. Intrinsic kidney Diseases • ATN - Acute Tubular Necrosis – Usually occurs after an ischemic event or exposure to nephrotoxic agents. • AIN - Acute Interstitial Nephritis – Classic presentation is fever, rash, eosinophilia and Cr bump 7-10 days after drug exposure. • CIN - Contrast Induced Nephropathy – Increased Cr of 0.5mg/dl or 25% 48hrs after contrast administration. • Others – Glomerular Disease, Pigmented Nephropathy, Thrombotic Microangiopathy CLINICAL EVALUATION BRENNER AND RECTORS - THE KIDNEY 9TH Edtn 12
  13. 13. Postrenal diseases: • H/O of pelvic tumors, irradiation, congential abnormalities, kidney stones, genitourinary procedures or surgeries,spinal cord injury,DM • Nocturia,urinary frequency,urgency,hesistency,urinary retension • O/E Enlarged prostate on PR examination,Distended bladder CLINICAL EVALUATION BRENNER AND RECTORS - THE KIDNEY 9TH Edtn 13
  14. 14. INVESTIGATIONS Urine Analysis: • Specific gravity: > 1.01 -1.020 – Prerenal AKI 1.010(isosthenuria) - ATN • Haematuria – glomerulonephritis,urologic disease,interstitial nephritis,trauma,renal infarction,pigment nephropathy. • Urine sediment analysis: - Normal with hyaline casts- prerenal AKI - Pigmented granular casts- ischaemic or nephrotoxic ATN - RBC casts – acute glomerular disease - WBC & nonpigmented granular casts –interstitial nephritis - Broad granular casts – CKD BRENNER AND RECTORS - THE KIDNEY 9TH Edtn 14
  15. 15. INVESTIGATIONS • Eosinophiluria – drug induced AIN • Uric acid crystals – urate nephropathy • Oxalate crystals – ethylene glycol toxicity Proteinuria: • < 1g/day – ischaemic and nephrotoxic ATN • > 1g/day – glomerular diseases,multiple myeloma,drug induced AIN. BRENNER AND RECTORS - THE KIDNEY 9TH Edtn15
  16. 16. • Urine biochemical parameters: Diagnostic Index Prerenal AKI ATN FENa <1% >2% Urine Na <20 >40 U Cr/Pl Cr >40 <20 U urea N/Pl urea N >8 <3 Urine SG >1.018 1.010 Urine osmolality >500 300 Pl BUN/Cr >20 <10-15 Renal failure Index Una/(UCr/Pl Cr) <1 >1 Urine sediment Hyaline casts Muddy brown granular casts 16
  17. 17. INVESTIGATIONS Laboratory evaluation: • BUN : S Cr - >20:1 - prerenal AKI 10:1 - intrinsic AKI • Rhabdomyolysis –hyperkalemia,hyperuricemia hyperphosphatemia,hypocalcemia,elevated CPK • Tumor lysis syndrome/urate nephropathy –hyperkalemia, hyperuricemia hyperphosphatemia,elevated uric acid,normal CPK,Urine Uric acid/Cr ratio > 1 • Ethylene glycol poisoning – elevated serum anion gap and osmolal gap • Severe Anaemia – hemolysis,multiple myeloma,thrombotic angiopathy • Eosinophilia – Allergic interstitial nephritis BRENNER AND RECTORS - THE KIDNEY 9TH Edtn17
  18. 18. INVESTIGATIONS • Radiologic Evaluation : Xray KUB Renal Ultrasonography Noncontrast CT MRI • Renal biopsy: To assess the cause for intrinsic AKI after excluding pre and post renal AKI. BRENNER AND RECTORS - THE KIDNEY 9TH Edtn18
  19. 19. Acute Kideny Injury Prerenal Uosm > 5000 mosm/kg Una < 20meq/L FEna < 1% Microscopy - bland Intrinsic Renal Diseases Postrenal Uosm: variable Una: low early, high late FEna: variable Microscopy - bland Ischemic / Toxic ATN Uosm ~ 300 mosm/kg Una > 40meq/L FEna > 2% Microscopy – dark pigment cast Acute Interstitial Nephritis Uosm: variable, ~300 mosm.kg Una > 40 meq/L FEna > 2% Microscopy – leukocytes, erythrocyts, leukocyte casts Acute Glomerulonephritis Uosm: variable (>400 in early GN) Una: variable (<20meq/l in early GN) FEna: variable, <1% in early GN Microscopy – hematuria, proteinuria Erythrocyte casts (dysmorphic) 19
  20. 20. COMPLICATIONS OF AKI • Metabolic:Hyperkalemia,hyponatremia,hypocalcemia,hyperp hosphatemia,hypermagnesemia,hyperuricemia,metabolic acidosis. • Cardiovascular: Pulmonary oedema, arrhythmia, pericarditis,perricardial effusion,pulmonary embolism,hypertension,MI. • GI: Nausea,vomiting,malnutrition,haemorrhage. • Neurologic: irritability,asterixis,seizures,mental status changes. • Haematologic: anaemia,bleeding. • Infectious: pneumonia,septicemia,UTI • Others: Hiccoughs,elevated PTH,Low total T3 and T4. BRENNER AND RECTORS - THE KIDNEY 9TH 20
  21. 21. PREVENTION AND MANAGEMENT OF AKI – RECOMMENDATIONS KDIGO GUIDELINES 2012 21
  22. 22. PREVENTION AND MANAGEMENT OF AKI – RECOMMENDATIONS KDIGO GUIDELINES 2012 • Goals: - To facilitate recovery of kidney function - To prevent death - To minimize the risk of CKD • Patients be stratified& manage according to their susceptibilities and exposure to reduce the risk of AKI. • Test patients at increased risk for AKI with measurements of SCr and urine output. • Individualize frequency and duration of monitoring based on patient risk and clinical course. 22
  23. 23. PREVENTION AND MANAGEMENT OF AKI – RECOMMENDATIONS KDIGO GUIDELINES 2012 • Evaluate to determine the cause, with special attention to reversible causes. • Monitor with measurements of SCr and urine output to stage the severity. • Manage patients according to the stage and cause. • Evaluate patients 3 months after AKI for resolution, new onset, or worsening of pre-existing CKD. 23
  24. 24. PREVENTION AND MANAGEMENT OF AKI – RECOMMENDATIONS KDIGO GUIDELINES 2012 Prerenal AKI: • Volume resuscitation - Packed cell transfusion - Crystalloids prefered than colloids - Treat underlying cause • Use of vasopressors in conjunction with fluids in patients with vasomotor shock with, or at risk for AKI. 24
  25. 25. PREVENTION AND MANAGEMENT OF AKI – RECOMMENDATIONS KDIGO GUIDELINES 2012 • CHF: - Cautious use of diuretics - Ionotropes - Vasodilators to reduce afterload - Mechanical support – intra aortic balloon pumps,ventricular assist devices. • Liver failure and HRS: - Intravenous Albumin - Drugs: Terlipressin, Norepinephrine, Octreotide+Midodrine - Peritoneovenous shunts,Portosystemic shunts
  26. 26. PREVENTION AND MANAGEMENT OF AKI – RECOMMENDATIONS KDIGO GUIDELINES 2012 • Avoid using diuretics to prevent or treat AKI, except in the management of volume overload. • Avoid using low-dose dopamine to prevent or treat AKI. • Avoid using fenoldopam/ atrial natriuretic peptide (ANP)/ recombinant human (rh)IGF-1 to prevent or treat AKI. 26
  27. 27. PREVENTION AND MANAGEMENT OF AKI – RECOMMENDATIONS KDIGO GUIDELINES 2012 Intrinsic AKI : • Sepsis : - haemodynamic targets: MAP>65mmHg,CVP-10-12mmHg, Urine O/P-.5ml/kg/hr, central venous O2 saturation >70% - Use crystalloid solutions, RBC transfusion, Vasopressors - Intensive insulin therapy- Target glucose level 110- 149mg/dl • Correct intravascular volume depletion • Avoid nephrotoxic medications
  28. 28. PREVENTION AND MANAGEMENT OF AKI – RECOMMENDATIONS KDIGO GUIDELINES 2012 Aminoglycosides : • Avoid unless no suitable, less nephrotoxic, therapeutic alternatives are available. • Single daily doses are prefered. • Monitor drug levels if multiple daily dosing is used for more than 24 hours or single-daily dosing for more than 48 hours. • Use topical or local applications than i.v. application, when feasible and suitable. 28
  29. 29. PREVENTION AND MANAGEMENT OF AKI – RECOMMENDATIONS KDIGO GUIDELINES 2012 • Use lipid formulations of amphotericin B . • In the treatment of systemic mycoses or parasitic infections, azole antifungal agents and/or the echinocandins are prefered. 29
  30. 30. Contrast medium induced AKI: • Screening(S Cr,r/f questionnaire,Urine protein) • Use iso osmolar or low osmolar iodinated contrast media • Use lowest possible dose • Isotonic saline or sodium bicarbonate - 1 ml/kg/hr for 12 hours before and after procedure - OP settings – 3ml/kg/hr for 1hr before procedure f/b 1- 1.5ml/kg/hr for 6hrs after the procedure. • Oral N Acetyl cysteine 600 BD to 1200mg BD • Avoid Diuretics,Theophylline, Dopamine, Fenoldopam,CCBs,Mannitol, Prophylatic haemodialysis.
  31. 31. Management of other causes of intrinsic AKI: • Urate nephropathy – Allopurinol, Rasburicase • Cisplatin induced nephropathy – Amifostine • Ethylene glycol toxicity – Fomepizole • Vasculitis and glomerular diseases – Steroids,Alkylating agents, Plasmapheresis. • TTP/HUS - Plasma exchange • Scleroderma – ACEIs • Multiple myeloma – Plasmapheresis with chemotherapy • Acute interstitial nephritis – Discontinue the offending drug. steroids,Mycophenolate mofetil.
  32. 32. • Use of Dopamine ,Fenoldopam,Natriuretic peptides,Mannitol are not recommended. • Avoid Loop diuretics for prevention and management of AKI except in case of fluid overload. Postrenal AKI: • PCN, Ureteric stents • Correction of underlying cause
  33. 33. DIALYSIS INTERVENTIONS FOR THE MANAGEMENT OF AKI • Indications for RRT  Absolute : - Volume overload unresponsive to diuretic therapy - Refractory hyperkalemia - Persistent metabolic acidosis - Overt uremic symptoms – Encephalopathy, Pericarditis, Uremic bleeding diathesis.  Relative: - Progressive azotemia without uraemic manifestations - Persistent oliguria 33
  34. 34. Modalities of RRT: • Intermittent Haemodialysis • Continuous renal replacement therapy - Continuous venovenous haemofiltration(CVVH) - Continuous venovenous haemodialysis(CVVHD) - Continuous venovenous haemodiafiltration(CVVHDF) • Hybrid therapies : - Sustained low efficiency dialysis(SLED) - Extended daily dialysis(EDD) - Sustained low efficiency daily diafiltration(SLEDD-f) • Peritoneal dialysis
  35. 35. DIALYSIS INTERVENTIONS FOR THE MANAGEMENT OF AKI • Initiate RRT emergently when life-threatening changes in fluid, electrolyte, and acid-base balance exist. • Consider the broader clinical context, the presence of conditions that can be modified with RRT, and trends of laboratory tests—rather than single BUN and creatinine thresholds alone. • Discontinue RRTwhen it is no longer required, either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs, or because RRT is no longer consistent with the goals of care. • Avoid using diuretics to enhance kidney function recovery, or to reduce the duration or frequency of RRT. 35
  36. 36. DIALYSIS INTERVENTIONS FOR THE MANAGEMENT OF AKI Anticoagulation: • In a patient with AKI requiring RRT, base the decision to use anticoagulation for RRT on assessment of the patient’s potential risks and benefits from anticoagulation. • Anticoagulation during RRT in AKI is recommended if a patient does not have an increased bleeding risk or impaired coagulation and is not already receiving systemic anticoagulation. 36
  37. 37. DIALYSIS INTERVENTIONS FOR THE MANAGEMENT OF AKI • For patients without an increased bleeding risk or impaired coagulation and not already receiving effective systemic anticoagulation: - In intermittent RRT, use either UF or LMW heparin. - In CRRT, use regional citrate anticoagulation rather than heparin in patients who do not have CIs for citrate. - In patients with contraindications for citrate, use either UF or LMW heparin. 37
  38. 38. • For patients with increased bleeding risk who are not receiving anticoagulation: - Regional citrate anticoagulation can be used, rather than no anticoagulation, during CRRT . - Avoid regional heparinization during CRRT . • In patients with heparin-induced thrombocytopenia (HIT), direct thrombin inhibitors (argatroban) or Factor Xa inhibitors (danaparoid or fondaparinux) are recommended rather than other or no anticoagulation during RRT. 38
  39. 39. • Initiate RRT via an uncuffed nontunneled dialysis catheter, rather than a tunneled catheter. • Vein for insertion of a dialysis catheter: - Right jugular vein > femoral vein > left jugular vein - Last choice: subclavian vein(dominant side). - use USG guidance for dialysis catheter insertion. • Take a CXR promptly after placement and before first use of an IJV or subclavian dialysis catheter. 39
  40. 40. DIALYSIS INTERVENTIONS FOR THE MANAGEMENT OF AKI • Avoid topical antibiotics over the skin insertion site of a nontunneled dialysis catheter. • Avoid using antibiotic locks for prevention of catheter-related infections of nontunneled dialysis catheters. • Use dialyzers with a biocompatible membrane for IHD and CRRT . • Use continuous and intermittent RRT as complementary therapy. • Use CRRT for hemodynamically unstable patients. • Use CRRT for AKI patients with acute brain injury or increased ICP or generalized brain edema. 40
  41. 41. DIALYSIS INTERVENTIONS FOR THE MANAGEMENT OF AKI • Use bicarbonate as a buffer in dialysate and replacement fluid for RRT in patients with AKI and circulatory shock/ liver failure and/ lactic acidemia. • Dialysis fluids and replacement fluids in patients with AKI, at a minimum, should comply with American Association of Medical Instrumentation (AAMI) standards regarding contamination with bacteria and endotoxins. 41
  42. 42. DIALYSIS INTERVENTIONS FOR THE MANAGEMENT OF AKI • Provide RRT to achieve the goals of electrolyte, acid-base, solute, and fluid balance that will meet the patient’s needs. • A Kt/V of 3.9 per week is recommended when using intermittent or extended RRT in AKI. • An effluent volume of 20–25 ml/kg/h is recommended for CRRT in AKI. 42
  43. 43. Supportive management of AKI • Intravascular volume overload : - Salt and water restriction,diuretics,Ultrafiltration • Hyponatremia : - Restriction of oral and iv free water • Hyperkalemia: - Dietary restriction - Discontinue K+ supplements/K+ sparing diuretics - K+ binding resins, Loop diuretics - Glucose(50 ml 50%)+ Regular Insulin 10-15U IV - Sodium bicarbonate - Calcium gluconate - RRT
  44. 44. Supportive management of AKI • Metabolic Acidosis : - Restriction of dietary protein - Sodium bicarbonate, RRT • Hyperphosphatemia : - Diet restriction, - PO4- binding agents(Ca carbonate,ca acetate,Sevelamer) • Hypocalcemia : - Calcium Carbonate Hypermagnesemia : - Discontinuation of Mg containing Antacids
  45. 45. PREVENTION AND MANAGEMENT OF AKI – RECOMMENDATIONS KDIGO GUIDELINES 2012 Nutrition : • Total energy intake of 20–30 kcal/kg/d any stage of AKI. • Avoid restriction of protein intake. - 0.8–1.0 g/kg/d of protein in noncatabolic AKI patients without need for dialysis. - 1.0–1.5 g/kg/d in patients with AKI on RRT - up to a maximum of 1.7 g/kg/d in patients on CRRT and in hypercatabolic patients. • Enteral route is prefered for nutrition. 45
  46. 46. Supportive management of AKI • Drug dosage : - Adjustment of all dosages for GFR and renal replacement modality.
  47. 47. AKI Stage Discontinue all nephrotoxic agents when possible Ensure volume status and perfusion pressure Consider functional hemodynamic monitoring Monitor serum creatinine and urine output Avoid hyperglycemia Consider alternative to radiocontrast procedures Non invasive diagnostic work up Consider invasive diagnostic work up Check for changes in drug dosing Consider renal replacement therapy Consider icu admission Avoid subclavian catheters if possible High Risk Stage 1 Stage 2 Stage 3 47
  48. 48. • Identify AKI early on – Monitor serum Cr for at risk patients – Make sure I/Os are recorded correctly • Diagnose as Prerenal, Intrinsic or Postrenal – Detailed history – Order routine labs including UA, Uosm, Ucr, Una (Urine Urea if on diuretics) – Imaging studies as necessary • Begin appropriate treatment – Stop offending agent – Fluids if appropriate – Relieve obstruction – Renal dosing of medicines Take Home Points 48
  49. 49. THANK YOU 49

×