Acute kidney injury (AKI) is frequently encountered in the hospital setting. It may be present on admission or may develop during the hospital stay. Early and consistent recognition of AKI has been a challenge. This has led to the development of RIFLE and AKIN criteria for the definition of AKI. Acute Kidney Injury Network (AKIN) defines AKI as an abrupt (within 48 hours), absolute increase in the serum creatinine concentration of [greater than or equal to]0.3 mg/dL from baseline; a percentage increase in the serum creatinine concentration of [greater than or equal to]50 percent; or oliguria of [less than]0.5 mL/kg per hour for more than six hours. Additionally, the definition should be applied after volume resuscitation and exclusion of urinary tract obstruction if oliguria was used as the sole criterion[1]

Malhotra, Kunal

University of Missouri: MOspace

5/30/2018 Dialysis in the Acute Settinghttps://www.printfriendly.com/p/g/S2HAcZ 1/7October 8, 2015Dialysis in the Acute Settingmedicine2.missouri.edu/jahm/dialysis-in-the-acute-setting/Kunal Malhotra, MDDivision of Nephrology, Department of Medicine, University of Missouri School of Medicine,Columbia, MO.Citation: Malhotra K, Dialysis in Acute Setting. Journal of Academic Hospital Medicine 2015, Volume7, Issue 4.Acute kidney injury (AKI) is frequently encountered in the hospital setting. It may be present onadmission or may develop during the hospital stay. Early and consistent recognition of AKI has beena challenge. This has led to the development of RIFLE and AKIN criteria for the definition of AKI.Acute Kidney Injury Network (AKIN) defines AKI as an abrupt (within 48 hours), absolute increase inthe serum creatinine concentration of ≥0.3 mg/dL from baseline; a percentage increase in theserum creatinine concentration of ≥50 percent; or oliguria of <0.5 mL/kg per hour for more than sixhours. Additionally, the definition should be applied after volume resuscitation and exclusion ofurinary tract obstruction if oliguria was used as the sole criterion[1].Acute tubular necrosis (ATN), sepsis and pre-renal causes account for majority of the cases of AKI[2, 3] in hospitalized patients. The recovery can be rapid or delayed depending on the severity ofinitial insult, its duration, hemodynamic status, comorbid conditions including pre-existing chronickidney disease, nephrotoxic agents and urinary output.  The management of AKI is usuallysupportive and includes volume optimization, management of potassium, calcium, acidosis andsigns of uremia. Renal replacement therapy (RRT) or dialysis is indicated in severe disease.Indications for Dialysis1. Refractory fluid overload2. Hyperkalemia- refractory to medical management, life threatening or rapidly rising3. Metabolic acidosis4. Dialyzable drug (medication, recreational or illicit)5. Signs of uremiaThe timing for initiation of dialysis is a controversial topic. While it is recommended that earlyinitiation of RRT has better outcomes, most studies have limitations like lack of randomization, lowpower, selection bias, non-standardization of definitions of AKI, modality of RRT and indication fordialysis. This has led to variation in clinical practice and lack of consensus. Clinical practiceguidelines for AKI[4] recommend1. Initiating RRT emergently when life-threatening changes in fluid, electrolyte, and acid-basebalance exist.2. Considering the broader clinical context, the presence of conditions that can be modified withRRT, and trends of laboratory tests rather than single BUN and creatinine thresholds alonewhen aking the decision to start RRT.5/30/2018 Dialysis in the Acute Settinghttps://www.printfriendly.com/p/g/S2HAcZ 2/73. Discontinuing RRT when it is no longer required.Acute hemodialysis prescriptionThis involves decision on the modality of dialysis, the choice of hemodialysis membrane, the choiceof dialysate, blood flow rate, ultrafiltration amount and rate, choice of anticoagulation, dialysis dose,and the length of dialysis.Dialysis accessArteriovenous (AV) – In patients with pre-existing AV fistula or graft. Here the systemic bloodpressure drives the blood into the extracorporeal circuit via an arterial needle, which after dialysis isthen returned via a venous needle.Venovenous (VV) – Requires one double lumen catheter (occasionally two catheters are used) to beplaced in a vein. It requires an extracorporeal blood pump to circulate blood through the dialysismachine.Dialysis ModalityThere are many dialysis modalities available including peritoneal dialysis (if already being used as anoutpatient), intermittent hemodialysis (IHD), sustained low efficiency hemodialysis (SLED) andcontinuous renal replacement therapy (CRRT). CRRT includes continuous hemofiltration,hemodialysis or a combination of the two i.e. hemodiafiltration.Hemofiltration is a convective therapy in which hydrostatic transmembrane pressure (TMP) gradientforces plasma water across the membrane. Small and middle molecular weight solutes move in thesame direction across the membrane due to solvent drag, resulting in their removal. A replacementor substitution fluid is required to prevent excessive fluid removal and optimization of electrolytes.Hemodialysis involves diffusion of solutes from high concentration compartment to lowconcentration compartment across the dialysis membrane. The blood and the dialysate move inopposite direction across the membrane to maximize the concentration gradient. Toxins, urea,creatinine, potassium and phosphorus usually move from blood to dialysate and bicarbonate movesfrom dialysate into blood.General principles of diffusion that apply are1. Solutes diffuse across the dialysis membrane down the concentration gradient.2. Net diffusion stops when concentration is equal on both sides3. Greater the concentration gradient, greater is the rate of diffusion. As a result, as theconcentration gradient decreases over time, rate of diffusion decreases as well.Diffusion flux (Jx) is also influenced by –1. Surface area of membrane (A)2. Thickness of membrane (dx)3. Temperature of dialysate (T)4. Concentration gradient across membrane (dc)5. Diffusion coefficient of the solute (D)5/30/2018 Dialysis in the Acute Settinghttps://www.printfriendly.com/p/g/S2HAcZ 3/7Jx = D*T*A (dc/dx)[5]Hemodiafiltration is a combination of both convection and diffusion.Continuous replacement therapies1. Continuous arteriovenous hemofiltration (CAVH)2. Continuous venovenous hemofiltration (CVVH)3. Slow continuous ultrafiltration (SCUF)4. Continuous arteriovenous hemodialysis (CAVHD or CAVD)5. Continuous venovenous hemodialysis (CVVHD or CVVD)6. Continuous arteriovenous hemodiafiltration (CAVHDF)7. Continuous venovenous hemodiafiltration (CVVHDF)8. Continuous equilibrium peritoneal dialysis (CEPD)9. Continuous-flow peritoneal dialysis10. Sustained low efficiency(SLED) or extended daily dialysis (EDD)Dialysis membranesThe membrane can be low flux or high flux membranes. High flux membranes contain larger sizedpores that allow diffusion of large molecules. Low flux hemodialysis is defined as ultrafiltrationcoefficient of dialyzer less than 20 mL/h/mmHg whereas high flux hemodialysis is more than that.Studies have demonstrated no statistical significant difference in all-cause mortality between highflux versus low flux groups and in fact have shown a lower relative risk for mortality for patientundergoing dialysis with high flux membranes [6-8]. A Cochrane database systemic reviewconcluded that high flux hemodialysis may reduce cardiovascular mortality by about 15%[9] . Thishas been generally attributed to enhanced middle molecular clearance by the high flux membranes.The downside to high flux membranes is that they can also allow waterborne pathogens andendotoxins to come into blood, therefore it should be used with only ultrapure water [6]. When apatient with chronic kidney disease is initiated on dialysis for the first time, a rapid reduction inblood urea nitrogen (BUN) levels can cause dialysis disequilibrium syndrome. To prevent this thefirst few session admit to be deliberately less efficient for a gradual decline in BUN levels. This isachieved by utilizing a low flux membrane, although surface area membrane, lower blood flows andshorter duration.Dialysate composition [5, 10, 11]The dialysate is made up of sodium, potassium, bicarbonate buffer, calcium, magnesium, chlorideand glucose. For the purpose of acute hemodialysis, dialysate composition can be customized tomeet the needs of a particular patient. Trace elements, including water-soluble metals,micronutrients, minor acids and folate are lost during dialysis since they are absent in the dialysate.Bicarbonate – The amount of bicarbonate added to dialysis depends on patient’s acid base status.If the predialysis plasma bicarbonate level is 28 mmol/L or higher, or if the patient has respiratoryalkalosis then the dialysis solution should contain an appropriately lower bicarbonate level, forexample 25-28 mmol/L, depending on the degree of alkalosis [10]. This is important since even mildmetabolic alkalosis can cause the blood pH to rise to a high level. In patients with severe metabolicacidosis and plasma bicarbonate level less than 10 mmol per liter the goal of treatment should be5/30/2018 Dialysis in the Acute Settinghttps://www.printfriendly.com/p/g/S2HAcZ 4/7to reach plasma bicarbonate level of 15-20 mmol per liter post dialysis. Excessive correction ofsevere metabolic acidosis can cause lowering of the ionized calcium level, paradoxical acidificationof cerebrospinal fluid and increased tissue production of lactic acid.Sodium- Sodium is generally kept at physiological concentration except when patient has hypo-orhypernatremia. If the patient has chronic hyponatremia then sodium shouldn’t be corrected rapidlyto prevent osmotic demyelination syndrome. The maximum safe rate of correction of serum sodiumis recommended to be in the range of 6-8 mmol per liter in 24 hours. This can be achieved by usingthe lowest possible dialysate sodium with or without other hypotonic solutions like 5% dextrose.Similarly in hypernatremic patients dialysate sodium should be set closer to plasma sodium withgradual administration of hyponatric fluids and then gradually decreasing dialysate sodium tonormal plasma level. In such cases the serum sodium should be monitored on an hourly basis. SinceCRRT is a slower treatment, it is safer than intermittent hemodialysis for such patients.Potassium- In patients with hyperkalemia and a potassium level of more than 5.5 mmol per liter,dialysis solution potassium level of 2.0 is appropriate in stable patients who are undergoingintermittent hemodialysis. In extended therapies, care should be taken to avoid life-threateninghypokalemia, especially in patients prone to arrhythmias. Dialysate solution potassium of 4 mmolper liter is appropriate for extended therapies. If the potassium level is more than 7.0 mmol per literthen it may be appropriate to use a lower potassium bath that can be raised later when the serumpotassium level is in safe range. The dialysate potassium of zero is extremely dangerous and shouldnot be prescribed.Calcium- The dialysate calcium concentration is usually 2.0-3.0 mEq per liter. Dialysis can be usedto lower the calcium level in acute hypercalcemia, with a 2.0-2.5 mEq per liter dialysate calcium levelto avoid rapid decrease in serum calcium level that can cause tetany or seizures. Serum ionizedcalcium concentration should be measured frequently, along with frequent clinical examination.Patients who undergo extended dialysis treatments with citrate anticoagulation need a calciumchloride drip that needs to be titrated to achieve desired normal serum calcium level. Citrate isinfused in the extracorporeal circuit and it chelates calcium thus anticoagulating the circuit.Phosphate- Patients who are on intermittent hemodialysis usually have high phosphate levelshowever hypophosphatemia can occur in extended dialysis treatments and is usually avoided bygiving phosphate as a supplement in the CRRT fluids or as a separate supplement by enteral orparenteral route.Magnesium- The usual dialysate magnesium concentration is 0.5-1.0 mEq per liter.Ultrafiltration [4, 10, 12, 13]In a critically ill patient with acute kidney injury, the estimation of volume status is challenging. It isdetermined by physical examination, laboratory values, vital signs and other hemodynamic indiceslike CVP.In ESRD patients undergoing chronic maintenance hemodialysis the determination of the ‘targetweight’ aka ‘dry weight’ is done empirically as the weight at which clinical sign of extracellular fluidexpansion (hypertension, edema and shortness of breath) are absent and when they develops signsof volume depletion (hypotension, tachycardia, symptoms of orthostatic hypotension and5/30/2018 Dialysis in the Acute Settinghttps://www.printfriendly.com/p/g/S2HAcZ 5/7cramping). These variables can change based on clinical acute events in the hospital. For example, ifthe patient undergoes limb amputation, the dry weight would have to be reestablished, or if thepatient is admitted for acute coronary syndrome then rapid removal of fluid may lead to worseningischemia.In patients who are critically ill and have acute renal failure, fluid removal goals have to be taken ina broader clinical picture that includes hemodynamic status that is necessary to maintain optimalcirculatory and oxygenation needs.Fluid overload is being increasingly recognized as an important factor associated withadverse outcomes.Anticoagulation[5]Anticoagulation is needed to prevent blood from clotting after contact with the plastic and artificialsurfaces in the extracorporeal dialysis circuit.Reasons for clot in the circuit1. Suboptimal or inadequate anticoagulation2. Poor quality vascular access3. Poor attention to optimal machine operation4. Sudden changes and patient positioning that can alter catheter function5. Decreased blood flow6. Induced clotting due to stasisIncreasing the dose of anticoagulation for all the causes other than the first one can be dangerous.Therefore every clotting episode should be analyzed and troubleshooted accordingly.Different options for anticoagulation are1. Heparin anticoagulation-2. Most commonly used3. May cause heparin induced thrombocytopenia4. Patient’s clotting time is less frequently monitored for the purpose of circuit anticoagulation.APTT is monitored to ensure adequate therapeutic anticoagulation.5. Regional Citrate anticoagulation-6. This involves infusion of citrate into the blood circuit which combines with ionized calcium toform citrate calcium complexes. This decreases the ionized calcium in the circuit and preventscoagulation of the blood. Calcium is then infused separately into patient in the form ofcalcium chloride.7. Some citrate leaks into the patient’s blood and is metabolized by the liver. Therefore, patientswith liver failure can develop citrate toxicity.8. Argatroban- this can be used in patients with heparin-induced thrombocytopenia9. Bivalirudin- this is an alternative to Argatroban in patients with both kidney and liver failure. Ithas a short half-life, reversible thrombin binding and extrarenal and extrahepatic clearancemechanism.10. No anticoagulation5/30/2018 Dialysis in the Acute Settinghttps://www.printfriendly.com/p/g/S2HAcZ 6/7Peritoneal dialysis[10, 14]ESRD patient already on PD can continue on their home prescription while they are admitted to thehospital. Although underutilized, PD is also a viable option for acute renal failure in patients whohave hemodynamic instability, coagulation issues or when other modalities are not readily available.PD requires a catheter the tip of which rests in peritoneal cavity in the pelvic region. The dialysatefluid is then delivered by the catheter into the peritoneal cavity and allowed to sit there for 1-4hours depending on clinical need and then drained subsequently. This is called and exchange andPD prescription may require multiple exchanges to achieve the goals. It salient features are asfollows-1. Acute PD requires long sessions since it’s a slower treatment. An average session may last for48-72 hours with multiple 1-2 hour exchanges.2. PD dialysate comes in standard solutions of 1.5, 2.5, 4.25% dextrose. 4.25% dextrose achievesmaximum ultrafiltration because of higher dextrose gradient and is the fluid of choice forrapid fluid removal.3. PD solution should be warmed to body temperature to avoid discomfort andvasoconstriction.4. The usual volume or exchange is around 2 L in a 60 to 80 kg adult. It may be more in thepatient who is bigger in size or in a patient who is not achieving effective clearance. It may beless in a patient who is small in size or in patients with respiratory insufficiency, hernias orleakage.5. Heparin may be added to the dialysate to prevent fibrin clot formation that can obstruct theperitoneal catheter. It should be noted that heparin is not absorbed through peritoneal cavityso it does not cause systemic anticoagulation.6. Insulin can be administrator intraperitoneally in diabetic patients on PD.7. Standard PD solutions do not contain potassium but it can be added to the PD solution toprevent hypokalemia and to maintain normal serum potassium level.8. In ESRD patient who are undergoing regular PD and are using icodextrin solution, regularglucometer should not be used and serum glucose testing should be done in the lab or byspecial glucometers that are more specific for glucose. Absorbed icodextrin is metabolized tomaltose that reacts with GDH-PQQ test strips in point-of-care glucose meters [15]References1. Mehta, R.L., et al., Acute Kidney Injury Network: report of an initiative to improve outcomes inacute kidney injury. Crit Care, 2007. 11(2): p. R31.2. Mehta, R.L., et al., Spectrum of acute renal failure in the intensive care unit: the PICARDexperience. Kidney Int, 2004. 66(4): p. 1613-21.3. Liano, F. and J. Pascual, Epidemiology of acute renal failure: a prospective, multicenter,community-based study. Madrid Acute Renal Failure Study Group. Kidney Int, 1996. 50(3): p.811-8.4. Summary of Recommendation Statements. Kidney Int Suppl (2011), 2012. 2(1): p. 8-12.5. Kellum, J.A., R. Bellomo, and C. Ronco, Continuous renal replacement therapy. Pittsburghcritical care medicine. 2010, Oxford ; New York: Oxford University Press. xix, 265 p.6. Canaud, B., et al., Mortality risk for patients receiving hemodiafiltration versus hemodialysis:European results from the DOPPS. Kidney Int, 2006. 69(11): p. 2087-93.5/30/2018 Dialysis in the Acute Settinghttps://www.printfriendly.com/p/g/S2HAcZ 7/77. Eknoyan, G., et al., Effect of dialysis dose and membrane flux in maintenance hemodialysis. NEngl J Med, 2002. 347(25): p. 2010-9.8. Locatelli, F., et al., Effect of membrane permeability on survival of hemodialysis patients. J AmSoc Nephrol, 2009. 20(3): p. 645-54.9. Palmer, S.C., et al., High-flux versus low-flux membranes for end-stage kidney disease.Cochrane Database Syst Rev, 2012. 9: p. CD005016.10. Daugirdas, J.T., P.G. Blake, and T.S. Ing, Handbook of dialysis. Fifth edition. ed. 2015,Philadelphia: Wolters Kluwer Health. xviii, 826 pages.11. Henrich, W.L., Principles and practice of dialysis. 3rd ed. 2004, Philadelphia: Lippincott Williams& Wilkins. xii, 696 p.12. Tonelli, M., et al., Blood volume monitoring in intermittent hemodialysis for acute renal failure.Kidney Int, 2002. 62(3): p. 1075-80.13. Bouchard, J., et al., Fluid accumulation, survival and recovery of kidney function in critically illpatients with acute kidney injury. Kidney Int, 2009. 76(4): p. 422-7.14. Passadakis, P. and D. Oreopoulos, Peritoneal dialysis in acute renal failure. Int J Artif Organs,2003. 26(4): p. 265-77.15. Flore, K.M. and J.R. Delanghe, Analytical interferences in point-of-care testing glucometers byicodextrin and its metabolites: an overview. Perit Dial Int, 2009. 29(4): p. 377-83.Copyright © 2018 - The Curators of the University of Missouri System. All rights reserved. DMCA and other copyright information. An equal opportunity/affirmative actioninstitution.

Dialysis in the acute setting

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Dialysis in the acute setting

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