How Best To Prevent & Manage Acute Renal failure


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How Best To Prevent & Manage Acute Renal failure

  1. 1. How Best to Prevent & Manage Acute Renal Failure ? Dr. T.R.Chandrashekar Director Critical Care, K.R. Hospital Bangalore
  2. 2. Some facts about ARF <ul><li>Incidence=1-25%. </li></ul><ul><li>Mortality =28-90% </li></ul><ul><li>High Attributable risk </li></ul><ul><li>35 different definitions have been used in the literature, creating confusion and making comparisons among the studies difficult. </li></ul><ul><li>This situation has impaired the study of ARF as well as the development of possible treatments. </li></ul><ul><li>Recent data indicates that a small change in SC influences outcome.(>0.3 increase in SC ). </li></ul><ul><li>A change from 1.5 mg/ml—1.8mg/dl is significant </li></ul>
  3. 3. Definition of ARF <ul><li>Acute renal failure (ARF) is defined as an abrupt and sustained decline in the glomerular filtration rate (GFR), which leads to accumulation of nitrogenous waste products and uremic toxins. </li></ul><ul><li>Few caveats </li></ul><ul><li>No consensus on </li></ul><ul><li>Assessment of renal function tests </li></ul><ul><li>The exact cutoffs values for the diagnosis </li></ul><ul><li>The degrees to which the process is “abrupt” or “sustained” are variable. </li></ul>
  4. 4. <ul><li>The term A cute kidney injury (AKI) has been put forth as the preferred nomenclature to replace acute renal failure with the understanding that the spectrum of AKI is broad and includes different degrees of severity </li></ul><ul><li>Because the most powerful tool to improve outcome of AKI is prevention , </li></ul><ul><li>The definition should have a high sensitivity, be multifaceted, and allow detection of patients who are at risk to develop kidney injury, as well as those with already established AKI and those with established ARF </li></ul>
  5. 5. Diagnostic criteria for acute kidney injury <ul><li>An abrupt (within 48 hrs) reduction in kidney function currently defined as </li></ul><ul><li>An absolute increase in serum creatinine of more than or equal to 0.3 mg/dl or A % increase in serum creatinine of more than or equal to 50% </li></ul><ul><li>or </li></ul><ul><li>A reduction in urine output ( documented oliguria of less than 0.5ml/kg per hour for more than 6 hrs). </li></ul>AKIN march 2007 To rule out Foley’s catheter block To correlate with clinical picture Does nor require baseline SC values Correct volume status Look for easily correctable causes for reduced UO
  6. 6. Acute Dialysis Quality Initiative (ADQI) -RIFLE classification of AKI. Three stages of increasing severity Two outcome variables
  7. 7. Modified RIFLE criteria for AKI Classification/Staging system for AKI <0.3ml/kg/hr for 24 hrs or Anuria for 12 hrs Increase to >= to 300% from baseline SC >= 4.0mg/dl with an acute increase of at least 0.5mg/dl 3 < 0.5ml/kg/hr for more than 12 hrs Increase to >= to 200%-300 % from baseline 2 < 0.5ml/kg/hr for more than 6 hrs Increase in SC of >= to 0.3 mg/dl or increase to >= to150-200% from baseline 1 U.O criteria Serum Creatinine criteria Stage
  8. 8. Modified RIFLE criteria for AKI <ul><li>The staging system proposed is highly sensitive and is based on recent data indicating that a small change in SC influences outcome. </li></ul><ul><li>One criteria either SC or UO has to be fulfilled to qualify for staging. </li></ul><ul><li>Patients receiving RRT are considered stage -3 irrespective of the stage they are in at the time of RRT. </li></ul>
  9. 9. Causes of AKI <ul><li>CASE-I </li></ul><ul><li>A 20yr old boy with H/o RTA with Hemoperitonium, Thready pulse 150/mt , sweating, restless, BP 70/40mm Hg, UO in last four hrs 30ml </li></ul><ul><li>PRE-RENAL- Low volume/ Hypoperfusion </li></ul><ul><li>CASE-II </li></ul><ul><li>A 40 yr old male with small bowel perfusion 2 days back comes with thready pulse 160/mt, cold extremities, restless, BP 80/ 50 mmHg,, Spo2 90% on 4l of O2. with anuria </li></ul><ul><li>ATN-ischemic/ toxic </li></ul><ul><li>CASE-III </li></ul><ul><li>A 40 yr old male with small bowel perfusion 2 days back comes with thready pulse 160/mt, cold extremities, restless, BP 80/ 50 mmHg, distended of abdomen which is very tense, spo2 90% on 4l of O2. with Anuria </li></ul><ul><li>Decreased renal perfusion –ACS </li></ul><ul><li>CASE-IV </li></ul><ul><li>A 70 yr old man with no urine output since 2 days, ultrasound shows BPH with distended bladder hydronephrosis and SC of 2.5 mg/dl </li></ul><ul><li>Post- Renal </li></ul>
  10. 10. Pre renal causes Low volume states NSAIDS,ACEI Renal artery stenosis Post renal causes Renal stones, ureteric stones Ca Cervix Prostate hypertrophy, tumors Renal papillary necrosis Renal causes Glomerular –Glomerularnephritis ATN Hypoperfusion and toxins Tubulointerstitial Drugs, Myeloma Causes of AKI
  11. 11. Etiology of ARF ATN is the cause in more than 90% Sepsis is the leading cause of ATN
  12. 12. DD of type of AKI <ul><li>Perform careful history, physical exam and urinalysis (sediment and chemistry) </li></ul><ul><li>If a patient has been hospitalized for some time prior to developing ARF, you must prepare a flow sheet of vital signs, weights, I/Os, labs, fluids and medications </li></ul><ul><li>Imaging- Ultrasound examination, C.T scan, IVP etc… </li></ul>
  13. 13. Laboratory Findings in Acute Renal Failure Cr improves with IVF Cr won’t improve much Response to volume ATN: muddy brown granular casts, cellular debris, tubular epithelial cells Bland Urinary Sediment >2% <1% Fractional excretion of sodium <350 >500 Urine osmolality, mosmol/L H 2 O >40 <20 Urine sodium (U Na ), meq/L 10-15:1 >20:1 BUN/P Cr Ratio Oliguric Acute Renal Failure (ATN) Prerenal Azotemia Index
  14. 14. <ul><li>Let us look at an Ex. 40 year old DM in ketosis due to vomiting </li></ul><ul><li>Urea 200, SC 5mg/dl </li></ul><ul><li>Ratio BUN/SC=40 </li></ul><ul><li>Urine Spot Na=15meq/l </li></ul><ul><li>Prerenal </li></ul><ul><li>Let us look at an EX. 40 year old DM in ketosis due to vomiting </li></ul><ul><li>Urea 200, SC 5mg/dl </li></ul><ul><li>Ratio BUN/SC=40 </li></ul><ul><li>Urine Spot Na=50meq/l </li></ul><ul><li>Prerenal + ATN </li></ul>DD of type of AKI Got a diuretic Prolonged hypoperfusion and ATN Prerenal azotemia and ischemic tubular necrosis represent a continuum. Azotemia progresses to necrosis when blood flow is sufficiently compromised to result in the death of tubular cells. Urine chemistries cannot be not relied on to rule out active renal injury
  15. 15. Mechanism of ATN Hypo-perfusion GFR Renal blood flow Cortical vasoconstriction Anuria Oliguric Renal failure Septic shock Volume depletion Drugs Low cardiac output Toxins Tubular malfunction Non-oliguric renal failure Cell shedding Death Tubular obstruction Medullary hypoxia Endothelial damage Back leak
  16. 16. MECHANISM OF ATN Prognosis in ATN
  17. 18. How best to prevent AKI ? <ul><li>No drugs are currently available to enhance or hasten renal recovery once ARF occurs </li></ul><ul><li>There is now clear evidence that ARF is associated with excess mortality, irrespective of whether the patient requires renal replacement therapy. </li></ul><ul><li>Hence prevention is the only powerful tool to improve outcome of AKI. </li></ul>
  18. 19. 24 – 48 hrs For Anaesthesiologist This is when and where prediction and prevention strategies must be applied Window of Opportunity
  19. 20. How best to prevent AKI ? <ul><li>Non pharmacological Rx </li></ul><ul><li>Ensuring adequate hydration (reversing dehydration), </li></ul><ul><li>Maintenance of adequate mean arterial pressure, </li></ul><ul><li>Minimizing exposure to nephrotoxins </li></ul><ul><li>Pharmacological Rx </li></ul><ul><li>Loop diuretics </li></ul><ul><li>Mannitol </li></ul><ul><li>Dopamine & Fenoldopam </li></ul><ul><li>Natriuretic Peptides </li></ul>Identification of patients at high risk to develop AKI-Elderly, DM, HT, Sepsis etc.. Renal replacement therapy
  20. 21. Hydration <ul><li>NS or RL </li></ul><ul><li>CVP = 8-12 cm H2O, MAP> 65mmHg </li></ul><ul><li>Optimal rate of infusion remain unclear and should be individualized. </li></ul><ul><li>Peripheral edema is of cosmetic concern in sepsis </li></ul><ul><li>The available experimental data are not supportive of a beneficial effect of additional fluid therapy on renal function, in the context where cardiac output is normal or increased and mean </li></ul><ul><li>arterial pressure is re-established. </li></ul>
  21. 22. Hydroxyethyl starch (HES) <ul><li>A recent multicenter German study, the Efficacy of Volume Substitution and Insulin Therapy in Severe Sepsis study, indicates that HES administration in patients with severe sepsis may be associated with an increased risk of acute renal failure. </li></ul><ul><li>( 27th International Symposium of Intensive Care and Emergency Medicine, Brussels, March 2006.) </li></ul><ul><li>Effects of hydroxyethyl starch administration on renal function in critically ill patients </li></ul><ul><li>The administration of HES had no influence on renal function or the need for RRT in the ICU. </li></ul>Br J Anaesth 2007; 98: 216–24
  22. 23. Maintain renal perfusion pressure <ul><li>Target MAP >=65 mmHg </li></ul><ul><li>Which vasopressors to be used ? </li></ul><ul><li>Role of low dose dopamine </li></ul>
  23. 24. Vasopressors <ul><li>Noradrenaline is the drug of choice in AKI in sepsis </li></ul><ul><li>Norepinephrine has been demonstrated to preserve splanchnic blood flow better than dopamine </li></ul><ul><li>Optimise fluid before starting vasopressors </li></ul><ul><li>Low dose dopamine should not be used for renal protection in severe sepsis </li></ul>
  24. 25. <ul><li>Conclusion: Low-dose dopamine offers transient improvements in renal physiology, but no good evidence shows that it offers important clinical benefits to patients with or at risk for acute renal failure </li></ul>Meta-Analysis: Low-Dose Dopamine Increases Urine Output but Does Not Prevent Renal Dysfunction or Death Ann Intern Med. 2005;142:510-524.
  25. 26. <ul><li>CASE-III </li></ul><ul><li>A 40 yr old male with small bowel perfusion 2 days back comes with thready pulse 160/mt, cold extremities, restless, BP 80/ 50 mmHg, distended abdomen which is very tense, Spo2 89% on 6l of O2 with Anuria. </li></ul>ABDOMINAL COMPARTMENT SYNDROME
  26. 27. ACS <ul><li>Oliguria is one of the first visible signs of elevated IAP </li></ul><ul><li>“ Normal IAP is approximately 5-7 mmHg in critically ill adults.” </li></ul><ul><li>“ IAH is defined by a sustained or repeated pathological elevation in IAP ≥ 12mmHg.” </li></ul><ul><li>“ ACS is defined as a sustained IAP > 20mmHg (with or without an APP < 60mmHg) that is associated with new organ dysfunction/ failure.” </li></ul>
  27. 28. Monitoring & Management - ACS Surgical decompression or if the pt is sick put flank drains
  28. 29. Nephrotoxic drug exposure <ul><li>Minimizing nephrotoxin exposure is an important strategy to prevent ARF in the ICU setting </li></ul><ul><li>Aminoglycosides, </li></ul><ul><li>Amphotericin,- lipid forms of amphotericin B be used preferentially in patients with renal insufficiency or evidence of renal tubular dysfunction. </li></ul><ul><li>Radiocontrast </li></ul><ul><li>are the most commonly encountered nephrotoxins in the ICU </li></ul>
  29. 30. Aminoglycoside <ul><li>Once-daily dosing is postulated to decrease tubular cell toxicity by reducing the fraction of the cumulative dose of drug taken up by proximal tubular cells. </li></ul><ul><li>Once-daily aminoglycoside dosing schedules demonstrated that there were no differences in the efficacy of aminoglycosides & there was a trend toward lower nephrotoxicity </li></ul>
  30. 31. Radiocontrast agents <ul><li>Reduce renal function by altering renal hemodynamics </li></ul><ul><li>Exert direct toxic effects on tubular epithelium. </li></ul><ul><li>Renal free-radical production increases after contrast agent administration and may in part be responsible for the renal injury. </li></ul><ul><li>Lowest volume necessary of nonionic, </li></ul><ul><li>Iso-osmolar, contrast medium be used in conjunction with IV isotonic fluids in all high-risk patients. </li></ul>
  31. 32. Radiocontrast agents <ul><li>NS 1ml/kg/hr/24hrs </li></ul><ul><li>N-acetyl cysteine (NAC) 1200mg BD a day before and on the day of contrast administration </li></ul><ul><li>Administration of 200mg theophylline 30 min before the procedure in a high risk pt </li></ul><ul><li>Bicarbonate- Alkalinizing urine should reduce renal medullary damage </li></ul><ul><li>D5W with 3 amps HCO3; bolus </li></ul><ul><li>3.5 mL/kg 1 hour pre-procedure, </li></ul><ul><li>Then 1mL/kg/hour for 6 hours post-procedure </li></ul><ul><li>Insufficient evidence to support the use of prophylactic hemofiltration to prevent contrast nephropathy </li></ul>
  32. 33. Diuretics <ul><li>Belief – Converts oliguric renal failure into non oliguric which carries lower risk </li></ul><ul><li>Clearing tubular debris in ATN </li></ul><ul><li>One retrospective study showed diuretic use was associated with significantly increased risk of death or nonrecovery of renal function. </li></ul><ul><li>Diuretics are never a treatment for oliguria but are sometimes required for management of volume overload. </li></ul><ul><li>Mannitol should not be used to prevent or treat ARF from any cause. </li></ul>Mehta JAMA 2002
  33. 34. Treatment: Diuretics <ul><li>Diuretics: Effects on outcome (large observational studies) </li></ul><ul><ul><ul><li>4-center, retrospective analysis of patients referred for nephrology consults (1989 - 1995; n = 552) </li></ul></ul></ul><ul><ul><ul><li>With adjustments for co-variates and propensity score, diuretic use was associated with: </li></ul></ul></ul><ul><ul><ul><ul><li>Significantly increased risk of death or non-recovery of renal function (odds ratio 1.77; 95% CI 1.14 - 2.76) </li></ul></ul></ul></ul><ul><ul><ul><li>Mehta et al. JAMA. 2002;288:2547-53 . </li></ul></ul></ul><ul><ul><ul><li>52-center, prospective inception cohort of ICU patients (n = 1743) </li></ul></ul></ul><ul><ul><ul><li>No differences in mortality, or renal recovery, even after adjustment for the same co-variates and propensity score </li></ul></ul></ul><ul><ul><ul><ul><li>Odds ratio 1.22 (p = 0.15) </li></ul></ul></ul></ul><ul><ul><ul><li>However, no benefit associated with diuretics either! </li></ul></ul></ul><ul><ul><ul><li>Uchino et al. Crit Care Med. 2004;32:1669 –77. </li></ul></ul></ul>
  34. 35. Prevention of AKI summary Loop diuretics Dopamine and dopamine receptor agonists ANPs Prophylactic hemofiltration Strategies that are not effective NAC Theophylline Low-dose recombinant ANP (in cardiac surgical patients) Strategies of unknown efficacy Isotonic hydration (IV route) Once-daily dosing of aminoglycosides Use of lipid formulations of amphotericin B Use of iso-osmolar nonionic contrast media Strategies that are likely to be effective
  35. 36. Indications for RRT in AKI <ul><li>Volume overload </li></ul><ul><li>Hyperkalemia </li></ul><ul><li>Metabolic acidosis </li></ul><ul><li>Uremia signs or Symptoms </li></ul><ul><li>Progressive azotemia in the absence of uremia </li></ul><ul><li>Uremic encephalopathy </li></ul><ul><li>Uremic neuropathy/myopathy </li></ul><ul><li>Uremic pericarditis </li></ul><ul><li>Drug overdose with dialyzable toxin </li></ul>
  36. 37. Goals of RRT <ul><li>To maintain fluid and electrolyte, acid-base, and solute homeostasis </li></ul><ul><li>To prevent further insults to the kidney </li></ul><ul><li>To promote healing and renal recovery </li></ul><ul><li>To permit other support measures such as nutrition to proceed without limitation. </li></ul>
  37. 38. RRT <ul><li>IHD=CRRT </li></ul><ul><li>Daily dialysis in sepsis improves outcome </li></ul><ul><li>Most of the conventional assessment of dose of dialysis –underdosing </li></ul><ul><li>IHD- can be done without anticoagulants </li></ul><ul><li>More solute removal- severe hyperkalemia </li></ul><ul><li>CRRT-in hemodynamically unstable pts </li></ul><ul><li>Septic mediators removal ? </li></ul>
  38. 39. Renal Replacement therapy =
  39. 40. What do you think is the problem ? <ul><li>70 yr old gentleman with HT, DM IHD, has BPH posted for TURP, well preserved baseline BP 160/90 mm Hg on ACE-I, insulin, Asprin which was stopped 7 days back </li></ul><ul><li>Under epidural </li></ul><ul><li>During the procedure has increased bleeding, BP 130/90 mmHg post operatively on Inj Inac 50 mg tid/ 20mics fentanyl tid </li></ul><ul><li>Baseline SC 1.6 mg/dl increases to 2.5, next day what went wrong ? </li></ul>
  40. 41. Normotensive Ischemic Acute Renal Failure <ul><li>Normotensive ischemic acute renal failure may develop in pts with hypertension, chronic kidney disease, and old age, on some drugs like ACE-I, ARB, COX2 inhibitors all of which are associated with narrowing and blunted vasodilatory capacity of renal vessels </li></ul><ul><li>Treated quickly by replacing volume, treating infection, or stopping medications such as NSAIDs, diuretics, and antihypertensive agents, especially ACE inhibitors or angiotensin-receptor blockers. </li></ul>Normotensive Ischemic Acute Renal Failure, NEJM Volume 357(8), 23 August 2007, pp 797-805 Do not overlook a drop in systolic blood pressure to the low normal range in patients with increased risk of normotensive AKI
  41. 42. Take home thoughts <ul><li>Even a small rise in SC to the tune 0.3mg/dl can influence the outcome </li></ul><ul><li>Prevention is the only powerful tool available for managing AKI </li></ul><ul><li>Use standard definitions like AKI and Modified RIFILE classification in all studies. </li></ul><ul><li>AKI=ATN </li></ul>
  42. 43. Take home thoughts <ul><li>Time is important-EGDT </li></ul><ul><li>Energy failure may be due to primitive hemodynamic inade q uacy and/or mitoc h ondrial dysfunction </li></ul><ul><li>Prolonged energy failure leads to irreversible mitoc h ondrial d y sfunction (necrosis – apoptosis) </li></ul><ul><li>Once MMDS starts shock becomes irreversible </li></ul><ul><li>Source control, appropriate antibiotics, hemodynamic stabilisation, APC etc… </li></ul>
  43. 44. Thank you “ Back to basics&quot;: Optimise Volume and Defend Pressure. There are no magic bullets just high quality intensive care
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