Acute Hemodialysis Prescription

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<ul><li><p>25/1/2014 Acute hemodialysis prescription</p><p>;elapsedTimeMs=17&amp;source=search_result&amp;searchTerm= 1/15</p><p>Official reprint from UpToDate 2014 UpToDate</p><p>AuthorsPhillip Ramos, MD, MSCIMark R Marshall, MDThomas A Golper, MD</p><p>Section EditorsJeffrey S Berns, MDPaul M Palevsky, MDRichard H Sterns, MD</p><p>Deputy EditorAlice M Sheridan, MD</p><p>Acute hemodialysis prescription</p><p>Disclosures</p><p>All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Dec 2013. | This topic last updated: ene 9, 2013.</p><p>INTRODUCTION Acute renal failure (ARF) is a major cause of morbidity and mortality, particularly in the</p><p>hospital setting. Despite improvements in renal replacement therapy (RRT) techniques during the last several</p><p>decades, the mortality rate associated with ARF in critically ill patients remains above 50 percent. (See "Renal</p><p>and patient outcomes after acute tubular necrosis".)</p><p>RRT is ideally initiated in the acute setting prior to the dangerous accumulation of extravascular volume and/or</p><p>uremic toxins that can result in further multi-organ damage and failure. Once the decision to initiate RRT has</p><p>been made, the specific modality of dialytic support must be chosen. This consists of peritoneal dialysis,</p><p>intermittent hemodialysis (IHD) and its variations (eg, hemofiltration), and continuous RRT (CRRT). Once the</p><p>selection is made, the acute dialysis prescription can be determined.</p><p>An acute hemodialysis treatment is defined as a hemodialysis session specifically performed for ARF (also</p><p>known as acute kidney injury [AKI]) or in the setting of a hospitalized end-stage renal disease (ESRD) patient.</p><p>The choice of specific dialysis modality, particularly the choice between continuous or intermittent dialysis, is</p><p>discussed separately. (See "Continuous renal replacement therapy in acute kidney injury (acute renal failure)".)</p><p>The various components of the acute hemodialysis prescription will be described here. The use of peritoneal</p><p>dialysis in ARF is discussed separately (see "Use of peritoneal dialysis for the treatment of acute kidney injury</p><p>(acute renal failure)").</p><p>INDICATIONS The urgent indications for renal replacement therapy (RRT) in patients with acute renal failure</p><p>(ARF) generally include volume overload refractory to diuretics, hyperkalemia, metabolic acidosis, uremia, and</p><p>toxic overdose of a dialyzable drug. In an attempt to minimize morbidity, dialysis should be started prior to the</p><p>onset of overt complications of renal failure, whenever possible. This is discussed in detail separately. (See</p><p>"Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure) in adults: Indications, timing,</p><p>and dialysis dose", section on 'Indications for and timing of initiation of dialysis'.)</p><p>MODALITY Once the decision to initiate renal replacement therapy (RRT) has been made, the specific</p><p>modality of dialytic support must be chosen. The possibilities include peritoneal dialysis, intermittent</p><p>hemodialysis (IHD) and its variations (eg, hemofiltration), and continuous RRT (CRRT). Once this selection is</p><p>made, the acute dialysis prescription can be determined. The determining factors of which modality is chosen</p><p>include the catabolic state, hemodynamic stability, and whether the primary goal is solute removal (eg, uremia,</p><p>hyperkalemia), fluid removal, or both. This is reviewed elsewhere. (See "Renal replacement therapy (dialysis) in</p><p>acute kidney injury (acute renal failure) in adults: Indications, timing, and dialysis dose".)</p><p>VASCULAR ACCESS When acute hemodialysis is chosen as the dialytic support modality, vascular access</p><p>must be established prior to initiating treatment. Placement of the venous dialysis catheter must be considered</p><p>carefully, especially in the critically ill patient.</p><p>The location depends upon factors such as body habitus, whether the patient is ambulatory or bedridden,</p><p>presence of vascular disease or atypical anatomy, and the avoidance of specific complications in an at-risk</p></li><li><p>25/1/2014 Acute hemodialysis prescription</p><p>;elapsedTimeMs=17&amp;source=search_result&amp;searchTerm= 2/15</p><p>patient (eg, risk of pneumothorax while placing a subclavian venous dialysis catheter in a patient with severe</p><p>chronic obstructive pulmonary disease or history of deep vein thrombosis or other venous disease).</p><p>For hospitalized end-stage renal disease (ESRD) patients, daily reassessment of the existing angioaccess (eg,</p><p>arteriovenous graft or fistula) is appropriate. Many events during the hospitalization can jeopardize the existing</p><p>access (eg, hypotension). (See "Overview of central catheters for acute and chronic hemodialysis access".)</p><p>HEMODIALYZER MEMBRANES In the setting of acute renal failure (ARF), the choice of artificial membranes</p><p>utilized may have a bearing on clinical outcome. Previously, it was postulated that non-complement-activating</p><p>membranes may incur less inflammatory risk, with resultant decrease in infectious complications and possibly</p><p>an increased probability of improved restoration of renal function. However, there are inconsistent findings</p><p>concerning the effect of membrane biocompatibility on outcomes among patients with ARF, with several meta-</p><p>analyses reporting disparate results. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute</p><p>renal failure): Recovery of renal function and effect of hemodialysis membrane", section on 'Complement</p><p>activation, membrane biocompatibility, renal recovery, and survival'.)</p><p>Membranes can also be of low or high flux. High-flux membranes contain large pores that allow for enhanced</p><p>permeability of larger molecules [1]. Although this property can enhance removal of putative toxins and improve</p><p>outcome, it could also allow the back transport (from dialysate to blood) of potentially harmful water-borne</p><p>molecules. This property is a factor that confounds some of the conclusions from previously performed studies.</p><p>Certainly, having the purest dialysate water possible should be a goal when using these more porous</p><p>membranes to utilize their positive attributes and to minimize their potential risks.</p><p>Overall, there are theoretical advantages to high-flux biocompatible membranes that have not been consistently</p><p>corroborated by often underpowered or flawed clinical studies. However, the effect of membrane biocompatibility</p><p>on outcomes (when present) is consistently beneficial. In addition, since such membranes can now be obtained</p><p>cheaply, cost has been eliminated as a deciding factor.</p><p>We therefore suggest the following approach:</p><p>(See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Recovery of renal function</p><p>and effect of hemodialysis membrane", section on 'Complement activation, membrane biocompatibility, renal</p><p>recovery, and survival' and "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure):</p><p>Recovery of renal function and effect of hemodialysis membrane", section on 'Membranes' and "Maintaining</p><p>water quality for hemodialysis".)</p><p>DIALYSATE COMPOSITION The dialysate solution composition consists of potassium, sodium, bicarbonate</p><p>buffer, calcium, magnesium, chloride, and glucose. Unlike chronic hemodialysis, the dialysate composition in</p><p>acute hemodialysis is routinely altered each treatment to correct the metabolic abnormalities that can rapidly</p><p>develop during acute renal failure (ARF). This is particularly true in the treatment of potassium and/or acid/base</p><p>derangements. Thus, the dialysate potassium, sodium, bicarbonate, and calcium are routinely changed in this</p><p>setting.</p><p>Issues surrounding magnesium, chloride, and glucose include the following:</p><p>If the water system used is high quality, high-flux biocompatible dialysis membranes should be used in the</p><p>ARF setting.</p><p>If the water system is not of high quality, low-flux biocompatible dialysis membranes should be used.</p><p>Another option is the use of in-line membrane filtration devices on dialysis machines to generate ultrapure</p><p>dialysate.</p><p>The usual dialysate magnesium concentration is 0.5 to 1.0 mEq/L and is not usually different from that in</p><p>the chronic setting.</p><p>The amount of dialysate chloride is dependent upon the dialysate sodium and bicarbonate concentrations.</p><p>The standard dialysate glucose concentration is 200 mg/dL, but may be decreased to more efficiently</p><p>lower the serum potassium during hemodialysis.</p></li><li><p>25/1/2014 Acute hemodialysis prescription</p><p>;elapsedTimeMs=17&amp;source=search_result&amp;searchTerm= 3/15</p><p>Dialysate potassium concentration There is no standard dialysate potassium concentration in the acute</p><p>hemodialysis prescription because of wide variability in serum potassium prior to initiating the hemodialysis</p><p>session. It is crucial to know the predialysis serum potassium level at the start of the hemodialysis session to</p><p>tailor the dialysate potassium so that normokalemia will be attained with avoidance of hypokalemia.</p><p>The goal of an acute hemodialysis treatment is not necessarily to lower the total body potassium burden for</p><p>general nutritional purposes. Instead, the goals are often more short term, such as normalizing the serum</p><p>potassium level for the next 24 hours.</p><p>The typical potassium concentration in the dialysate for acute hemodialysis ranges from 2.0 to 4.0 mEq/L.</p><p>However, the dialysate potassium concentration should be varied based upon the pre-dialysis value [2]. As</p><p>described below, the dialysate glucose concentration can be another determinant of the rate of potassium</p><p>removal.</p><p>The prescribed dialysate bath potassium is determined by both the absolute serum potassium and the rate of</p><p>rise in the interdialytic period. A rapid rate of rise in serum potassium may best be treated by daily</p><p>hemodialysis rather than lowering the dialysate potassium bath concentration.</p><p>Acute or severe hyperkalemia Some patients with acute and/or severe hyperkalemia have muscle</p><p>weakness and cardiac conduction abnormalities, and should be treated with more rapidly acting medical</p><p>therapies prior to the initiation of dialysis. The first electrocardiographic (ECG) changes with hyperkalemia are</p><p>tall peaked T waves (waveform 1) and shortened QT interval. This is followed by progressive lengthening of the</p><p>PR interval and QRS duration and then loss of the P wave, with further prolongation of the QRS interval ("sine</p><p>wave" pattern). Conduction delay can manifest as bundle branch or atrioventricular (AV) nodal block, and</p><p>ventricular fibrillation or asystole can result. (See "Clinical manifestations of hyperkalemia in adults".)</p><p>If more advanced ECG features of hyperkalemia are present, medical management should be initiated</p><p>immediately with continuous ECG monitoring. Medical therapy is administered while emergency hemodialysis</p><p>is being arranged. (See "Treatment and prevention of hyperkalemia in adults".)</p><p>Although there is no general consensus concerning the optimal strategy, the following is our general approach</p><p>to the dialysate potassium concentration [2]:</p><p>Although rarely recommended, a zero potassium bath has also been used to rapidly decrease the serum</p><p>potassium in a short period of time [3,4]. After four hours of hemodialysis in one study, for example, a dialysate</p><p>free of potassium was more effective than a 1.0 or 2.0 mEq/L potassium dialysate bath in removing serum</p><p>potassium, removing 85 percent more potassium than a 2.0 mEq/L bath and 46 percent more than a 1.0 mEq/L</p><p>bath [3].</p><p>Predialysis potassium 8.0 mEq/L), a</p><p>dialysate potassium concentration of 1.0 mEq/L can be used to rapidly decrease the serum potassium to</p><p>a more tolerable level. However, this should be done with a high degree of caution to avoid hypokalemia.</p></li><li><p>25/1/2014 Acute hemodialysis prescription</p><p>;elapsedTimeMs=17&amp;source=search_result&amp;searchTerm= 4/15</p><p>However, to minimize the risk of hypokalemia and dialysis-induced arrhythmias, we do not recommend use of a</p><p>zero potassium dialysate bath for the treatment of severe hyperkalemia. If a rapid fall in serum potassium is</p><p>desired because of severe hyperkalemia, we suggest using a 1.0 mEq/L potassium bath and checking a serum</p><p>potassium every 30 to 60 minutes. Once the serum potassium is between 6 and 7 mEq/L, the dialysate</p><p>potassium concentration can be changed to 2.0 mEq/L for the remainder of the hemodialysis session,</p><p>depending upon many other prescriptive components discussed below.</p><p>In patients with underlying cardiac disorders or those taking digoxin, the dialysate concentration can be</p><p>changed to 3.0 mEq/L once the serum potassium is approximately 5.5 mEq/L to avoid possibly life-threatening</p><p>arrhythmias, with the postdialysis serum potassium goal of 4.0 mEq/L. Although not studied in the acute</p><p>setting, this overall approach decreases the risk of hypokalemia and dialysis-induced arrhythmias, particularly in</p><p>patients with predisposing risk factors delineated below. (See 'Complications with potassium removal' below.)</p><p>The amount of potassium removal is proportional to the gradient between the serum and dialysate</p><p>concentrations. The administration of insulin, intravenous (IV) glucose, beta-agonists, or bicarbonate either</p><p>concurrently or prior to hemodialysis results in intracellular translocation of potassium, lower serum levels, and</p><p>therefore lower rates of potassium removal during dialysis.</p><p>Dialysate glucose concentration The dialysate glucose concentration is another factor that can</p><p>modulate potassium removal since the glucose load enhances insulin secretion, which drives potassium into the</p><p>cells. Thus, in the presence of endogenous insulin, the standard dialysate glucose concentration (200 mg/dL</p><p>[11.1 mmol/L]) results in significantly decreased potassium removal relative to glucose-free dialysate solution</p><p>[5].</p><p>Thus, in cases of severe hyperkalemia where potassium removal is critical, a lower dialysate glucose</p><p>concentration may be used. We suggest a dialysate glucose concentration of 100 mg/dL (5.6 mmol/L) if severe</p><p>hyperkalemia (eg, &gt;8.0 mEq/L) is present. We do not use glucose-free dialysate because of the risk of</p><p>hypoglycemia. Standard dialysate glucose concentration (200 mg/dL [11.1 mmol/L]) should be used in cases of</p><p>mild to moderate hyperkalemia.</p><p>Complications with potassium removal The hemodialysis treatment can provoke ventricular</p><p>arrhythmias, which are related to dialysis-induced reductions in the serum potassium. Multiple studies have</p><p>demonstrated that potentially life-threatening dialysis-induced arrhythmias with potassium removal are</p><p>independently associated with risk factors such as coronary artery disease, left ventricular hypertrophy (LVH),</p><p>digoxin use, hypertension, and advanced age [6,7].</p><p>In one study in chronic dialysis, for example, 23 stable end-stage renal disease (ESRD) patients...</p></li></ul>