prevention and nondialytic management of AKI.pptx

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1. Prevention and Nondialytic Management of AKI Dr Manoj Aryal DM-Resident Department of Nephrology NAMS (2081-05-11)

2. RISK ASSESSMENT

3. Avoid subclavian catheters if possible High Risk Discontinue all nephrotoxic agents when possible Consider invasive diagnostic workup Consider Renal Replacement Therapy 1 2 3 Non-invasive diagnostic workup Ensure volume status and perfusion pressure Check for changes in drug dosing Consider functional hemodynamic monitoring Monitor Serum creatinine and urine output Consider ICU admission Avoid hyperglycemia Consider alternatives to radiocontrast procedures AKI Stage

4. PRIMARY PREVENTIVE MEASURES Optimizing volume and hemodynamic status Assessing volume status in ICU patients can be challenging ½ of hemodynamically unstable ICU patients respond to fluid administration Passive leg raising test Fluid bolus test coupled with real time stroke volume monitoring Point of care USG Adverse outcomes of fluid overload Cardiopulmonary complications Delayed wound healing and kidney function recovery Increased mortality

5. Volume assessement

6. Volume assessement

7. Phases of fluid therapy Rescue implies the “administration of fluid for immediate management of life-threatening conditions associated with impaired tissue perfusion.” Optimization refers to the “adjustment of fluid type, rate, and amount based upon context to achieve optimization of tissue perfusion.” Fluid bolus typically includes 500ml of isotonic fluids over 15 minutes or less Fluid challenge with 250ml or 3ml/kg of isotonic fluids over 5-10 mins with stroke volume assessment(+response 10-15% increase in SV) Stabilization Achieving a neutral or slightly negative fluid balance De-escalation Minimization of fluid administration Mobilization of extra fluid to achieve fluid balance Oral or iv diuretics Fluid minimization Ultrafiltration

8. Controversy regarding choice of fluid for resuscitation Colloid vs Crystalloid solution

9. Physiologic Balanced Salt Solution Versus Normal Saline Solution

10. Blood pressure management NO DIFFERENCE between two group

11. Vasodilator therapy in AKI

12. Fenoldopam in AKI

13. ANP in AKI

14. Additional Therapies for AKI: Diuretics, Nutrition, and the Future Against the use of diuretics to treat AKI except in the setting of volume overload

15. Glycemic control in AKI

16. Pharmacotherapies in AKI At this time, there are no pharmacologic therapies for the prevention or treatment of AKI

17. Contrast associated AKI

18. N-acetylcysteine Multiple trials and meta analysis failed to give consensus on its use

19. Statins significant lower incidence of CIN in patients treated with high-dose rosuvastatin

20. September 2014, ARYA Atherosclerosis  10(5):252-258,Source: PubMed

21. Comprehensive Clinical Nephrology

22. Prevention of Drug-Induced and Nephrotoxin-Induced AKI Patient-related risk factors : Preventive measures correctly estimating the GFR before initiation of therapy adjusting the dosage monitoring renal function and drug dosage during therapy administration of intravenous saline before exposure if possible . Alternative non-nephrotoxic drugs should be used, and nephrotoxic drug combinations should be avoided whenever Older age (60 years or older) CKD Diabetes Heart failure Volume depletion Sepsis.

23. Angiotensin-Converting Enzyme Inhibitors, Angiotensin Receptor Blockers ACEI or ARBs should be discontinued: If creatinine increases by more than 30% bilateral renal artery stenosis stenosis of the renal artery in a solitary kidney diffuse intrarenal small-vessel disease It remains unclear whether withdrawing an ACE inhibitor or ARB before iodinated contrast administration is beneficial.

24. Nonsteroidal Antiinflammatory Drugs KDIGO 2012 guidelines provide the following recommendations for NSAIDs: eGFR 30 to <60 mL/minute/1.73 m 2 : Temporarily discontinue in patients with intercurrent disease that increases risk of acute kidney injury. eGFR <30 mL/minute/1.73 m 2 : Avoid use.

25. Aminoglycosides Usually occur 5 to 10 days after initiation of drug Non oliguric and associated with decreased urine concentrating ability Urinary magnesium wasting

26. Calcium channel blocker Drugs have been evaluated in the prevention of delayed graft function (DGF) Large multicenter RCT did not find any benefit on the incidence and severity of DGF. A systematic review did not find strong evidence for the routine use of CCBs to reduce the incidence of DGF after transplantation.

27. Emerging therapies Mesenchymal stromal cells

28. TREATMENT OF AKI COMPLICATIONS Fluid overload Morphine ,nitrates Diuretics Hemodialysis Potassium disorders Management of hyperkalemia Sodium disorders Management of hyper/hyponatremia

29. Calcium, phosphorus, magnesium disorders Hyperphosphatemia and hypocalcemia are common in AKI Hypocalcemia: skeletal resistance to PTH, low calcitriol production Mild hypermagnesemia is frequent in AKI and usually does not have clinical consequences Acid-base disorders Metabolic acidosis common Accumulation of phosphate and unexcreted unmeasured anions, such as sulfate, urate, Hippurate, hydroxy propionate, furan propionate, and oxalate, is contributory When metabolic acidosis is simply a complication of AKI, sodium bicarbonate can be administered if the serum bicarbonate concentrations fall below 15 to 18 mmol/l

30. Acid-base disorders

31. Nutrition Increased risk for protein-energy malnutrition because of poor nutrient intake and high catabolic rate Patients with AKI should receive a basic intake of 0.8 to 1.0 g of protein/kg/day if not catabolic and a total energy intake of 20 to 30 kcal/ kg/day, as recommended in the KDIGO guidelines. Patients on RRT, 1.0 to 1.5 g of protein/kg/day should be administered up to 1.7 g/kg/day in CRRT and hypercatabolic patients.

32. Thank you