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Acute hemodialysis prescription

Official reprint from UpToDate www.uptodate.com 2014 UpToDate

Acute hemodialysis prescription Authors Phillip Ramos, MD, MSCI Mark R Marshall, MD Thomas A Golper, MD Disclosures 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. INTRODUCTION Acute renal failure (ARF) is a major cause of morbidity and mortality, particularly in the hospital setting. Despite improvements in renal replacement therapy (RRT) techniques during the last several decades, the mortality rate associated with ARF in critically ill patients remains above 50 percent. (See "Renal and patient outcomes after acute tubular necrosis".) RRT is ideally initiated in the acute setting prior to the dangerous accumulation of extravascular volume and/or uremic toxins that can result in further multi-organ damage and failure. Once the decision to initiate RRT has been made, the specific modality of dialytic support must be chosen. This consists of peritoneal dialysis, intermittent hemodialysis (IHD) and its variations (eg, hemofiltration), and continuous RRT (CRRT). Once the selection is made, the acute dialysis prescription can be determined. An acute hemodialysis treatment is defined as a hemodialysis session specifically performed for ARF (also known as acute kidney injury [AKI]) or in the setting of a hospitalized end-stage renal disease (ESRD) patient. The choice of specific dialysis modality, particularly the choice between continuous or intermittent dialysis, is discussed separately. (See "Continuous renal replacement therapy in acute kidney injury (acute renal failure)".) The various components of the acute hemodialysis prescription will be described here. The use of peritoneal dialysis in ARF is discussed separately (see "Use of peritoneal dialysis for the treatment of acute kidney injury (acute renal failure)"). INDICATIONS The urgent indications for renal replacement therapy (RRT) in patients with acute renal failure (ARF) generally include volume overload refractory to diuretics, hyperkalemia, metabolic acidosis, uremia, and toxic overdose of a dialyzable drug. In an attempt to minimize morbidity, dialysis should be started prior to the onset of overt complications of renal failure, whenever possible. This is discussed in detail separately. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure) in adults: Indications, timing, and dialysis dose", section on 'Indications for and timing of initiation of dialysis'.) MODALITY Once the decision to initiate renal replacement therapy (RRT) has been made, the specific modality of dialytic support must be chosen. The possibilities include peritoneal dialysis, intermittent hemodialysis (IHD) and its variations (eg, hemofiltration), and continuous RRT (CRRT). Once this selection is made, the acute dialysis prescription can be determined. The determining factors of which modality is chosen include the catabolic state, hemodynamic stability, and whether the primary goal is solute removal (eg, uremia, hyperkalemia), fluid removal, or both. This is reviewed elsewhere. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure) in adults: Indications, timing, and dialysis dose".) VASCULAR ACCESS When acute hemodialysis is chosen as the dialytic support modality, vascular access must be established prior to initiating treatment. Placement of the venous dialysis catheter must be considered carefully, especially in the critically ill patient. The location depends upon factors such as body habitus, whether the patient is ambulatory or bedridden, presence of vascular disease or atypical anatomy, and the avoidance of specific complications in an at-risk
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Section Editors Jeffrey S Berns, MD Paul M Palevsky, MD Richard H Sterns, MD

Deputy Editor Alice M Sheridan, MD

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Acute hemodialysis prescription

patient (eg, risk of pneumothorax while placing a subclavian venous dialysis catheter in a patient with severe chronic obstructive pulmonary disease or history of deep vein thrombosis or other venous disease). For hospitalized end-stage renal disease (ESRD) patients, daily reassessment of the existing angioaccess (eg, arteriovenous graft or fistula) is appropriate. Many events during the hospitalization can jeopardize the existing access (eg, hypotension). (See "Overview of central catheters for acute and chronic hemodialysis access".) HEMODIALYZER MEMBRANES In the setting of acute renal failure (ARF), the choice of artificial membranes utilized may have a bearing on clinical outcome. Previously, it was postulated that non-complement-activating membranes may incur less inflammatory risk, with resultant decrease in infectious complications and possibly an increased probability of improved restoration of renal function. However, there are inconsistent findings concerning the effect of membrane biocompatibility on outcomes among patients with ARF, with several metaanalyses reporting disparate results. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Recovery of renal function and effect of hemodialysis membrane", section on 'Complement activation, membrane biocompatibility, renal recovery, and survival'.) Membranes can also be of low or high flux. High-flux membranes contain large pores that allow for enhanced permeability of larger molecules [1]. Although this property can enhance removal of putative toxins and improve outcome, it could also allow the back transport (from dialysate to blood) of potentially harmful water-borne molecules. This property is a factor that confounds some of the conclusions from previously performed studies. Certainly, having the purest dialysate water possible should be a goal when using these more porous membranes to utilize their positive attributes and to minimize their potential risks. Overall, there are theoretical advantages to high-flux biocompatible membranes that have not been consistently corroborated by often underpowered or flawed clinical studies. However, the effect of membrane biocompatibility on outcomes (when present) is consistently beneficial. In addition, since such membranes can now be obtained cheaply, cost has been eliminated as a deciding factor. We therefore suggest the following approach: If the water system used is high quality, high-flux biocompatible dialysis membranes should be used in the ARF setting. If the water system is not of high quality, low-flux biocompatible dialysis membranes should be used. Another option is the use of in-line membrane filtration devices on dialysis machines to generate ultrapure dialysate. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Recovery of renal function and effect of hemodialysis membrane", section on 'Complement activation, membrane biocompatibility, renal recovery, and survival' and "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Recovery of renal function and effect of hemodialysis membrane", section on 'Membranes' and "Maintaining water quality for hemodialysis".) DIALYSATE COMPOSITION The dialysate solution composition consists of potassium, sodium, bicarbonate buffer, calcium, magnesium, chloride, and glucose. Unlike chronic hemodialysis, the dialysate composition in acute hemodialysis is routinely altered each treatment to correct the metabolic abnormalities that can rapidly develop during acute renal failure (ARF). This is particularly true in the treatment of potassium and/or acid/base derangements. Thus, the dialysate potassium, sodium, bicarbonate, and calcium are routinely changed in this setting. Issues surrounding magnesium, chloride, and glucose include the following: The usual dialysate magnesium concentration is 0.5 to 1.0 mEq/L and is not usually different from that in the chronic setting. The amount of dialysate chloride is dependent upon the dialysate sodium and bicarbonate concentrations. The standard dialysate glucose concentration is 200 mg/dL, but may be decreased to more efficiently lower the serum potassium during hemodialysis.
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Dialysate potassium concentration There is no standard dialysate potassium concentration in the acute hemodialysis prescription because of wide variability in serum potassium prior to initiating the hemodialysis session. It is crucial to know the predialysis serum potassium level at the start of the hemodialysis session to tailor the dialysate potassium so that normokalemia will be attained with avoidance of hypokalemia. The goal of an acute hemodialysis treatment is not necessarily to lower the total body potassium burden for general nutritional purposes. Instead, the goals are often more short term, such as normalizing the serum potassium level for the next 24 hours. The typical potassium concentration in the dialysate for acute hemodialysis ranges from 2.0 to 4.0 mEq/L. However, the dialysate potassium concentration should be varied based upon the pre-dialysis value [2]. As described below, the dialysate glucose concentration can be another determinant of the rate of potassium removal. The prescribed dialysate bath potassium is determined by both the absolute serum potassium and the rate of rise in the interdialytic period. A rapid rate of rise in serum potassium may best be treated by daily hemodialysis rather than lowering the dialysate potassium bath concentration. Acute or severe hyperkalemia Some patients with acute and/or severe hyperkalemia have muscle weakness and cardiac conduction abnormalities, and should be treated with more rapidly acting medical therapies prior to the initiation of dialysis. The first electrocardiographic (ECG) changes with hyperkalemia are tall peaked T waves (waveform 1) and shortened QT interval. This is followed by progressive lengthening of the PR interval and QRS duration and then loss of the P wave, with further prolongation of the QRS interval ("sine wave" pattern). Conduction delay can manifest as bundle branch or atrioventricular (AV) nodal block, and ventricular fibrillation or asystole can result. (See "Clinical manifestations of hyperkalemia in adults".) If more advanced ECG features of hyperkalemia are present, medical management should be initiated immediately with continuous ECG monitoring. Medical therapy is administered while emergency hemodialysis is being arranged. (See "Treatment and prevention of hyperkalemia in adults".) Although there is no general consensus concerning the optimal strategy, the following is our general approach to the dialysate potassium concentration [2]: Predialysis potassium <4.0 mEq/L If the predialysis serum potassium level is <4.0 mEq/L, we recommend that the dialysate potassium bath should be adjusted to 4.0 mEq/L [2]. This is done to prevent the development of hypokalemia and its complications. Predialysis potassium between 4.0 and 5.5 mEq/L If the predialysis serum potassium level is between 4.0 and 5.5 mEq/L, the typical potassium concentration in the dialysate for acute hemodialysis usually ranges from 2.0 to 4.0 mEq/L. We suggest using a dialysate potassium of 3.5 mEq/L if the predialysis serum potassium is between 4.0 to 4.5 mEq/L, and 3.0 mEq/L if the predialysis serum potassium is between 4.5 to 5.5 mEq/L. However, if a rapid increase in extracellular potassium is anticipated prior to the next hemodialysis session (eg, due to marked rhabdomyolysis), then a dialysate potassium of 2.0 mEq/L should be used to ensure normokalemia in the lower range of normal. Predialysis potassium >5.5 mEq/L and <8.0 mEq/L If patients have a predialysis serum potassium level >5.5 mEq/L and <8.0 mEq/L, then a 2.0 mEq/L dialysate potassium bath should be used. However, the dialysate concentration should be increased to 2.5 or 3.0 mEq/L in patients at risk for cardiac arrhythmia or those receiving digitalis [2]. (See 'Complications with potassium removal' below.) Severe hyperkalemia, potassium >8.0 mEq/L In cases of severe hyperkalemia (eg, >8.0 mEq/L), a dialysate potassium concentration of 1.0 mEq/L can be used to rapidly decrease the serum potassium to a more tolerable level. However, this should be done with a high degree of caution to avoid hypokalemia. Although rarely recommended, a zero potassium bath has also been used to rapidly decrease the serum potassium in a short period of time [3,4]. After four hours of hemodialysis in one study, for example, a dialysate free of potassium was more effective than a 1.0 or 2.0 mEq/L potassium dialysate bath in removing serum potassium, removing 85 percent more potassium than a 2.0 mEq/L bath and 46 percent more than a 1.0 mEq/L bath [3].
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However, to minimize the risk of hypokalemia and dialysis-induced arrhythmias, we do not recommend use of a zero potassium dialysate bath for the treatment of severe hyperkalemia. If a rapid fall in serum potassium is desired because of severe hyperkalemia, we suggest using a 1.0 mEq/L potassium bath and checking a serum potassium every 30 to 60 minutes. Once the serum potassium is between 6 and 7 mEq/L, the dialysate potassium concentration can be changed to 2.0 mEq/L for the remainder of the hemodialysis session, depending upon many other prescriptive components discussed below. In patients with underlying cardiac disorders or those taking digoxin, the dialysate concentration can be changed to 3.0 mEq/L once the serum potassium is approximately 5.5 mEq/L to avoid possibly life-threatening arrhythmias, with the postdialysis serum potassium goal of 4.0 mEq/L. Although not studied in the acute setting, this overall approach decreases the risk of hypokalemia and dialysis-induced arrhythmias, particularly in patients with predisposing risk factors delineated below. (See 'Complications with potassium removal' below.) The amount of potassium removal is proportional to the gradient between the serum and dialysate concentrations. The administration of insulin, intravenous (IV) glucose, beta-agonists, or bicarbonate either concurrently or prior to hemodialysis results in intracellular translocation of potassium, lower serum levels, and therefore lower rates of potassium removal during dialysis. Dialysate glucose concentration The dialysate glucose concentration is another factor that can modulate potassium removal since the glucose load enhances insulin secretion, which drives potassium into the cells. Thus, in the presence of endogenous insulin, the standard dialysate glucose concentration (200 mg/dL [11.1 mmol/L]) results in significantly decreased potassium removal relative to glucose-free dialysate solution [5]. Thus, in cases of severe hyperkalemia where potassium removal is critical, a lower dialysate glucose concentration may be used. We suggest a dialysate glucose concentration of 100 mg/dL (5.6 mmol/L) if severe hyperkalemia (eg, >8.0 mEq/L) is present. We do not use glucose-free dialysate because of the risk of hypoglycemia. Standard dialysate glucose concentration (200 mg/dL [11.1 mmol/L]) should be used in cases of mild to moderate hyperkalemia. Complications with potassium removal The hemodialysis treatment can provoke ventricular arrhythmias, which are related to dialysis-induced reductions in the serum potassium. Multiple studies have demonstrated that potentially life-threatening dialysis-induced arrhythmias with potassium removal are independently associated with risk factors such as coronary artery disease, left ventricular hypertrophy (LVH), digoxin use, hypertension, and advanced age [6,7]. In one study in chronic dialysis, for example, 23 stable end-stage renal disease (ESRD) patients were evaluated using a Holter monitor [7]. Nine (39 percent) had ventricular tachycardia (VT) during and after hemodialysis performed with a dialysate potassium concentration of 2.0 mEq/L. Episodes of frequent or complex ventricular arrhythmias were more likely in patients on digoxin (8/9 versus 1/14 without arrhythmias) and those with LVH (9/9 versus 7/14 without arrhythmias). It was concluded that a low dialysate potassium concentration can induce ventricular arrhythmias in hemodialysis patients on digoxin and with LVH. It is unknown if, in the absence of underlying risk factors (cardiac arrhythmias, digoxin, or heart disease), a dialysate potassium concentration of 2.0 mEq/L causes serious ventricular arrhythmias [4]. To lower the risk of potentially life-threatening dialysis-induced arrhythmias among patients with underlying risk factors, the goal is to obtain a postdialysis serum potassium concentration of approximately 4.0 mEq/L by using a dialysate potassium concentration no lower than 3.0 mEq/L. Periodic measurements of postdialysis potassium may be helpful. The immediate postdialysis value is generally the lowest, and potassium rebound, while rapid, depends upon the factors previously discussed. However, the degree of potassium rebound is highly variable. Poor perfusion states and underlying illnesses all affect potassium rebound. Poor systemic perfusion may have a potentially large impact in two ways. First, potassium removal during hemodialysis is associated with a larger reduction in serum potassium due to less potassium efflux from cells. Second, after dialysis, potassium rebound will be less by the same mechanism. Such patients warrant closer monitoring of the serum potassium, with a postdialysis measurement at two to four hours. Additional issues
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related to postdialysis rebound are discussed separately. (See "Treatment and prevention of hyperkalemia in adults", section on 'Postdialysis potassium rebound'.) In addition, we recommend that patients with underlying cardiac disorders who undergo acute hemodialysis should be placed on a cardiac rhythm monitor during the dialysis session. Sodium modeling and hemodialysis hypotension The choice of the dialysate sodium concentration can have a significant impact on the patient's volume and hemodynamic status. During the early days of hemodialysis, low-dialysate sodium concentrations were routinely used to help decrease volume overload and hypertension. However, a low-dialysate sodium during a three to four hour hemodialysis session acutely decreases the intravascular volume over a short period of time as the result of the net negative sodium balance that is produced by diffusion. This approach can cause significant hypotension and discomfort in the form of nausea, vomiting, muscle cramping, fatigue, and dizziness. Since the early 1980s, high-sodium bicarbonate-based dialysate has mostly eliminated hypotension and discomfort during hemodialysis. However, the widespread use of these high-sodium solutions has caused dialysis salt loading with resultant postdialysis thirst, interdialytic weight gain, and hypertension [8]. The problem of postdialytic weight gain and hypertension is mostly seen in the chronic hemodialysis population, but can also have bearing in the acute setting, particularly in patients with an intact thirst mechanism and the ability to drink fluid based on their thirst. During acute intermittent hemodialysis (IHD), particularly in the intensive care unit (ICU) setting, hypotension is common since patients usually have compromised hemodynamic factors due to cardiac, hepatic, infectious, or bleeding complications. The hypotension that can develop during maximal rates of solute removal often compromises clearance and ultrafiltration (UF) targets. To avoid hemodynamic instability during acute IHD, sodium modeling can be administered by utilizing a higher dialysate sodium concentration at the beginning of hemodialysis and progressively decreasing it throughout the session to avoid lowering the plasma osmolarity abruptly. A concise mechanism describing sodium profiling is best described by the following quotation [9]: "A high dialysate sodium concentration is used initially with a progressive reduction toward isotonic or hypotonic levels by the end of the procedure. This method allows for a diffusive sodium influx early in the session to prevent the rapid decline in plasma osmolality resulting from the efflux of urea and other small molecular weight solutes. During the remainder of the procedure, when the reduction in osmolality accompanying urea removal is less abrupt, the lower dialysate sodium level minimizes the development of hypertonicity and any resultant excessive thirst, fluid gain, and hypertension in the interdialytic period." Although sodium modeling has been studied mostly in the chronic hemodialysis population, a randomized crossover study of 10 patients evaluated sodium modeling in ARF patients in the ICU [10]. The study used either a fixed dialysate sodium regimen (140 mEq/L), with a fixed UF rate spread over the entire dialysis time, or a variable dialysate sodium profile, which varied dialysate sodium (160 mEq/L to 140 mEq/L) in a stepwise fashion. The group's UF profile was varied in a similar fashion to the sodium profiling prescription (half of the fluid being removed during the first third of the treatment and the remaining half over the last two thirds). The following results were observed: Sodium modeling with variable UF rate was associated with greater hemodynamic stability compared with the fixed regimen. Significantly fewer frequent interventions involving nursing and volume replacement were noted in the sodium modeling and variable UF rate arm. Relative blood volume changes were fewer during sodium modeling. The group concluded that sodium and UF profiling may be the preferred dialysis prescription for ARF patients in the ICU at risk for hemodynamic instability while undergoing IHD [10]. Several sodium modeling prescriptions exist. Multiple sodium modeling prescriptions are programmed in most
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hemodialysis machines. Patients may respond to only one or all available prescriptions. Thus, trials are required to find the best sodium modeling prescription in ARF patients on hemodialysis. The same sodium modeling principles used for intradialytic hypotension in the chronic hemodialysis population can also be used in ARF patients. We recommend using combined sodium and UF profiling if hypotension occurs while on IHD in the acute setting. We prefer either of the following two specific strategies: With one high/low-sodium modeling prescription, a high-dialysate sodium (eg, 150 mEq/L) alternates with a low-dialysate sodium (eg, 130 mEq/L), with each level set for an equal amount of time. The average of the high/low-sodium levels (eg, 140 mEq/L) is the dialysate sodium usually prescribed in hemodynamically stable patients with normal serum sodium levels. During the low-sodium period, the UF rate is minimized or stopped. UF only occurs during the high-sodium period to draw out intracellular water due to the extracellular hypernatremia. Another sodium modeling prescription is to set the initial dialysate sodium at a high level (eg, 150 to 160 mEq/L). Subsequently, the dialysate sodium level is then decreased in stepwise, exponential, or linear decrements (depending on clinical effect) to a final low level (eg, 140 mEq/L). To maintain isonatremia, the time average concentration of dialysate sodium should be the same or marginally lower than the predialysis serum sodium concentration (approximately within 1.0 to 2.0 mEq/L). With a linear sodium profile, for example, the duration (and degree) of dialysis spent below the isonatremic concentration must be approximately equal to that spent above it [11]. Other methods to treat hypotension are reviewed below. Since lower blood flows through the dialyzer may result in less hemodynamic instability, sustained low efficiency hemodialysis (SLED) over 6 to 12 hours or continuous renal replacement therapy (CRRT) can be used if sodium modeling on IHD does not improve the blood pressure. (See "Sustained low efficiency or extended daily dialysis".) Dialysate sodium concentration The choice of dialysate sodium concentration depends upon the predialysis serum sodium concentration, hemodynamic status, the diffusion gradient for sodium, method of serum sodium measurement, and Gibbs-Donnan effect. Issues surrounding dialysate sodium concentration in patients with dysnatremias or hemodynamic instability are discussed in the next and previous sections, respectively. (See 'Dysnatremias' below and 'Sodium modeling and hemodialysis hypotension' above.) With respect to the additional factors that affect the choice of the dialysate sodium concentration: The diffusion gradient for sodium lies between its ionic activity in dialysate and blood water [8,12]. Since laboratories use a variety of methods to measure serum sodium concentration (flame photometry, indirect ionometry and direct ionometry), there is a subtly different relationship between the gradient and sodium ionic activity for each method used. The Gibbs-Donnan effect denotes the reduced sieving coefficient of the dialysis membrane for sodium that arises as a result of negatively charged plasma proteins [13]. As a result of all of these factors, a high sodium dialysate for the majority of patients would be characterized by a sodium concentration of approximately 141 mEq/L, and a low sodium dialysate by a sodium concentration of approximately 137 mEq/L. For individual patients, the dialysate sodium concentration that results in no net transfer of sodium has been estimated in various studies to be between 0.1 to 3.0 mEq/L below that of the predialysis serum sodium concentration [11,14-16]. For most patients with normal or near-normal serum sodium levels, we use a sodium dialysate concentration of approximately 137 mEq/L. Dysnatremias Rapid correction of an abnormal serum sodium concentration should be avoided during dialysis to avoid neurologic complications [17]. Failure to adjust the dialysis prescription may lead to cerebral edema in the patient with severe chronic hypernatremia and osmotic demyelination (pontine and extrapontine myelinolysis) in the patient with severe chronic hyponatremia. Although uremia may provide some protection against osmotic demyelination, case reports of this complication following dialysis of severely hyponatremic patients lead us to recommend a cautious approach in most patients.
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The overall dialysis strategy for the management of dysnatremias is the same as that in the nondialysis general population. Large, rapid changes in the serum sodium concentration are very rarely indicated. Only patients with hyperacute salt poisoning (eg, due to the suicidal ingestion of sodium chloride or the inadvertent IV infusion of hypertonic saline during a therapeutic abortion) or hyperacute water intoxication (eg, as a complication of marathon running or use of the drug, "Ecstasy") should ever be allowed to undergo aggressive initial correction of their serum sodium concentration. In such patients with hyponatremia, for example, aggressive initial correction at a rate of 1.5 to 2.0 mEq/L per hour may be indicated for the first three to four hours or until the symptoms resolve. However, the plasma sodium concentration should probably be raised by <10 mEq/L in the first 24 hours and <18 mEq/L in the first 48 hours. (See "Overview of the treatment of hyponatremia", section on 'Rate of correction'.) In the vast majority of patients with more chronic dysnatremias, the treatment during a single dialysis session should be adjusted to provide a rate of correction that does not exceed the generally recommended rate. If the serum sodium concentration is very high or very low, it may be impractical to avoid a rapid change solely by adjusting the dialysate sodium concentration. In many such patients, it may be necessary to either cut the dialysis session short or to offset the effect of dialysis by concurrent infusions of hypertonic saline or 5 percent dextrose (D5W). Hourly measurements of the serum sodium concentration during the course of dialysis are mandatory. Another possibility is to use CRRT. This modality is far less efficient at changing serum sodium concentrations, which may therefore change more slowly than with the use of IHD. Some authorities also favor the following approach [18]: Among patients with severe chronic hyponatremia (predialysis serum sodium level <130 mEq/L), a cautious strategy is to set the dialysate sodium concentration at a level that is no higher than 15 to 20 mEq/L above the plasma level of the patient [18]. The goal would be correction of the hyponatremia only after multiple hemodialysis sessions that are performed over a period of several days. In those with hypernatremia, the use of dialysate sodium concentrations more than 3 to 5 mEq/L below the plasma sodium concentration is associated with hypotension, muscle cramps, and, most importantly, disequilibrium syndrome. Thus, a reasonable and safe approach would be to use a dialysate sodium concentration within 2 mEq/L of the plasma sodium concentration in the first dialysis session. Subsequently, correction of the hypernatremia could be performed with the administration of hypotonic solutions. (See "Treatment of hypernatremia".) Buffer solutions Acetate was the predominant buffer used during the early days of hemodialysis. However, acetate is presently not routinely used because of associated cardiac and hemodynamic instability. The main dialysate buffer currently used in IHD is bicarbonate. This buffer is inexpensive and generally well tolerated, without the hemodynamic problems seen with acetate. The main disadvantage of bicarbonate is that it precipitates as an insoluble salt when stored together with the divalent cations calcium and magnesium, thereby requiring the buffer and electrolytes to be stored separately prior to hemodialysis [19]. In addition, possible side effects with bicarbonate include hypoxemia due to decreased respiratory drive, with higher pH, and altered mental status, weakness, cramping, and lethargy due to acute metabolic alkalosis [9]. The dialysate bicarbonate concentration should vary based upon the acid-base status of the patient. The usual dialysate bicarbonate concentration in chronic hemodialysis is approximately 33 to 35 mEq/L. We suggest that this high-concentration bicarbonate solution be used in cases of moderate metabolic acidosis in ARF. In severe metabolic acidosis, the concentration of the bicarbonate solution may be maximized (eg, 40 mEq/L), and extended duration of hemodialysis may be necessary. In addition, in patients being mechanically ventilated using low-tidal volume ventilation, an increased dialysate bicarbonate concentration may be required to compensate for the respiratory acidosis resulting from "permissive hypercapnea." In contrast, in patients being mechanically hyperventilated to compensate for metabolic acidosis, the minute ventilation (respiratory rate and/or tidal volume) may need to be reduced to avoid severe alkalemia as the metabolic acidosis is corrected
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with dialysis. Acute hemodialysis patients can also be alkalemic. The severity of the alkalemia and the process generating the alkalosis are the main issues to help determine the optimal dialysate bicarbonate concentration. In particular, the clinician must investigate whether there is ongoing generation versus a one-time insult causing the alkalosis. A one-time insult can be resolved with a single hemodialysis treatment, whereas ongoing generation of alkalosis may require frequent and/or long hemodialysis sessions with a lower bicarbonate dialysate. If the predialysis serum bicarbonate level is >28 mEq/L or respiratory alkalosis is present, the usual dialysate bicarbonate concentration should not be used [2]. In this setting, a lower bicarbonate dialysis concentration would be appropriate. Modern machines can adjust dialysate bicarbonate in 1 mEq/L increments (from 40 to 20 mEq/L). In addition, the frequency and duration of the dialysis treatment(s) as well as the volume of ultrafiltrate must all be considered when determining the specific concentration of bicarbonate in the dialysate. Calcium In chronic hemodialysis patients, the standard dialysate calcium concentration is 2.5 mEq/L. In addition to helping manage secondary hyperparathyroidism, this level is used to avoid the development of hypercalcemia and elevated calcium-phosphorus product that can occur with higher dialysate calcium concentrations. (See "Management of secondary hyperparathyroidism and mineral metabolism abnormalities in adult predialysis patients with chronic kidney disease" and "Management of secondary hyperparathyroidism and mineral metabolism abnormalities in dialysis patients".) In the acute hemodialysis setting, the dialysate calcium concentration may be chosen to treat the presence of either hypo- or hypercalcemia. According to some authorities, the dialysate calcium concentration for acute hemodialysis should be 3.0 to 3.5 mEq/L, and the routine use of the standard concentration for chronic hemodialysis is inappropriate, considering the risk of developing hypocalcemia in the acute setting [2]. In addition, a higher dialysate calcium concentration used in the setting of predialysis hypocalcemia may prevent further worsening of hypocalcemia with the correction of acidosis [2]. A higher dialysate calcium concentration can also improve intradialytic hypotension by improving cardiac performance. As an example, one prospective crossover study compared the effect of high-dialysate calcium concentration (3.5 mEq/L) with low-dialysate calcium concentration (2.5 mEq/L) on hemodynamic stability in patients on IHD [20]. The patients in the study had a history of intradialytic hypotension and were also administered therapy with either midodrine, cool dialysate, or a combination of these two therapies. Compared with low-dialysate calcium, the following results were reported: High-dialysate calcium significantly increased post-hemodialysis mean arterial pressure (MAP). High-dialysate calcium improved the lowest intradialytic MAP, but was not statistically significant. The improvements in blood pressure with high-dialysate calcium were not associated with similar reductions in symptoms or interventions for intradialytic hypotension. Hypocalcemia is fairly common in ICU patients, particularly those with sepsis [21]. This combination is reportedly associated with increased mortality [22]. This observation has led some to postulate that treatment of hypocalcemia in those with sepsis may improve outcomes. However, calcium administration to rodents with sepsis appears to be harmful [23,24]. Its administration may therefore be associated with higher mortality in critically ill patients with sepsis. Thus, administering calcium to treat hemodynamic instability during acute IHD may be harmful to septic patients and should be considered carefully. (See "Evaluation and management of severe sepsis and septic shock in adults".) Since total plasma calcium levels are poorly predictive of the ionized level, the ionized plasma calcium level should be measured prior to hemodialysis in acutely ill patients with significant hypocalcemia or hypercalcemia. This is particularly important since acute phase responses (eg, sepsis) and changes in pH during dialysis and mechanical ventilation can affect ionized calcium levels independent of the total plasma calcium concentration.
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(See "Relation between total and ionized serum calcium concentration".) We suggest the following concerning the dialysate calcium concentration: We favor adjusting the dialysate calcium concentration to avoid hypercalcemia or clinical hypocalcemia. If the measured total plasma calcium level is used in this setting (although ionized plasma calcium is preferred), it is important that this level is corrected based upon the serum albumin level and other factors, given that the total plasma calcium concentration will change in parallel to the albumin concentration. This issue and the correction formula are discussed separately (see "Relation between total and ionized serum calcium concentration"). We use a dialysate calcium concentration of 3.0 to 3.5 mEq/L in the patient with significant hypocalcemia (total plasma calcium level <8.0 mg/dL [<2.0 mmol/L]), particularly if the patient is symptomatic. If the patient has severe hypercalcemia (total plasma calcium level >12.0 mg/dL [>3.0 mmol/L]), we use a dialysate calcium concentration of 2.0 to 2.5 mEq/L. For patients with mild hypocalcemia, normocalcemia, or mild hypercalcemia (total plasma calcium level between 8.0 to 12.0 mg/dL [2.0 to 3.0 mmol/L]), we use a dialysate calcium concentration of 2.5 mEq/L. To treat intradialytic hypotension, increasing the dialysate calcium may be used in combination with sodium profiling and a lower dialysate temperature. We do not use a dialysate calcium concentration >3.5 mEq/L for this purpose. The development of hypercalcemia must be avoided with this strategy. However, the ideal level of ionized calcium in critically ill patients is not known and may not be the same as in normal subjects. (See 'Ultrafiltration and blood pressure control' below and 'Dialysate sodium concentration' above.) BLOOD FLOW RATE Deciding upon the optimal blood flow rate through the dialyzer is determined by various factors. For patients with chronic kidney disease (CKD) who are initiated on hemodialysis, the blood flow rate is increased incrementally over several sessions to avoid the rapid removal of accumulated blood solutes, which can lead to the development of the dialysis disequilibrium syndrome, and to evaluate the angioaccess. (See "Dialysis disequilibrium syndrome".) With acute renal failure (ARF), blood solutes have usually not had time to accumulate to the degree observed in the end-stage renal disease (ESRD) population. However, if the blood urea nitrogen (BUN) has been >100 mg/dL for at least three days in the patient with ARF, there may be enough osmole accumulation in the central nervous system (CNS) to justify a slow removal for the first and second dialysis sessions. Thus, lower blood flow rates should be prescribed at the initiation of therapy in such patients. When this is not necessary, high blood flow rates can be initiated at the onset of acute intermittent hemodialysis (IHD) without fear of precipitating the disequilibrium syndrome. (See "Dialysis disequilibrium syndrome".) Blood flow rate in acute hemodialysis is dependent upon temporary dialysis catheter performance, length, and location. Dialysis catheters must be long enough to reach either the superior vena cava (SVC) or inferior vena cava, where the venous blood flows are the highest. Left-sided internal jugular (IJ) and subclavian catheters tend to provide unreliable blood flow, at a rate that is typically up to 100 mL/min lower than elsewhere because their tips abut the walls of either the SVC or innominate vein [1]. The best blood flows are attained with femoral vein and right-sided IJ catheters. (See "Overview of central catheters for acute and chronic hemodialysis access".) Higher blood flows are necessary during IHD to provide sufficient overall solute clearance because of the relatively shorter duration of the session, whereas lower blood flows are sufficient to achieve adequate clearance by continuous renal replacement therapy (CRRT) due to its continuous nature [1]. However, the use of higher blood flows with IHD may result in rapid reduction in serum osmolality, promoting water movement into cells, thus reducing effective circulating volume. This may exacerbate intradialytic hypotension despite measures to treat intradialytic hypotension, particularly in critically ill patients suffering from septic shock, cardiac decompensation, bleeding, or hepatic insufficiency. Noncompliant dialyzers, smaller surface area dialyzers, and ultrafiltration (UF) control minimize the need to decrease blood flow rate. We use a dialysis blood flow rate of 400 mL per minute. If a lower blood flow (or lower UF rate) is required because of hemodynamic instability due to rapid osmolar shifts, the best dialysis modality is unclear. Until further data are available, we suggest slower solute removal over 6 to 12 hours by sustained low-efficiency dialysis (SLED) or by CRRT. (See "Continuous renal replacement therapy in acute kidney injury (acute renal failure)" and "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure) in adults:
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Indications, timing, and dialysis dose", section on 'CRRT versus intermittent hemodialysis'.) DIALYSATE TEMPERATURE Vasoconstriction due to lower body temperatures has been used to increase vascular resistance and improve hemodynamic stability during intermittent hemodialysis (IHD) in end-stage renal disease (ESRD). Cool-temperature dialysate typically uses a temperature of 35.0C, which may be associated with symptoms. (See "Cool temperature hemodialysis: Hemodynamic effects".) Hypothermia, however, may be undesirable in critically ill patients due to adverse effects upon myocardial function, end-organ perfusion, blood clotting, and possibly renal recovery [25]. With blood-temperature monitoring, the patients' blood temperature is maintained precisely at target value by a series of feedback loops controlling thermal transfer to and from the dialysate [26]. It is effective in ameliorating hemodynamic instability for ESRD patients [27]. Blood temperature monitoring might conceivably allow for controlled cooling in critically ill acute renal failure (ARF) patients without the risk of hypothermic damage. However, it has not been evaluated in this setting. Our recommendations concerning the use of cold-temperature hemodialysis are presented in the next section. ULTRAFILTRATION AND BLOOD PRESSURE CONTROL Determining optimal ultrafiltration (UF) requirements in critically ill acute renal failure (ARF) patients is challenging. This is determined in part by physical examination, laboratory values, and hemodynamic indices. In general, no one specific test or parameter is sufficient in isolation. The following two overriding principles should be recognized: The target weight in end-stage renal disease (ESRD) patients undergoing chronic maintenance dialysis is usually determined empirically as the weight at which clinical signs of extracellular fluid expansion are absent and below which clinical signs of extracellular depletion arise. In contrast, extracellular volume status in critically ill ARF patients is not necessarily an endpoint itself. The volume expansion that is frequently observed in such patients is often necessary to maintain optimal circulatory and oxygen transport status. The clinician should appreciate that the relationship between blood volume and hypotension is different in patients with ESRD and critically ill individuals with ARF. Autonomic function and circulating humoral agents all mediate and mitigate this relationship, and these factors are not comparable between the two groups. This can be illustrated by considering blood volume monitoring, which is a biofeedback system that automatically adjusts UF rate and dialysate sodium content in response to a fall in circulating intravascular volume. Although these systems can convincingly reduce the occurrence of intradialytic hypotension in ESRD patients [28], they are ineffective for ameliorating hypotension in critically ill ARF patients [29]. This lack of a predictable relationship between volume status and hemodynamic stability means that UF goals for a given patient should be assessed not only in terms of fluid mass balance or the mandatory removal of obligatory fluid loads, but also in terms of the effect of intervention on the patient's broader clinical condition and hemodynamic status In hemodynamically stable patients, the estimation of target intravascular volume can be made in the usual fashion utilized for ESRD patients. However, in hemodynamically unstable patients, target intravascular volume should be titrated to invasive or noninvasive (bio-impedance analysis, pulse contour analysis [PiCCO], or echocardiography) monitoring, which should guide the UF goals for a given intermittent hemodialysis (IHD) session. UF during IHD can result in significant intradialytic hypotension, which can be treated by reducing or discontinuing UF, and/or reducing the blood flow rate. In addition to these maneuvers, modifying other dialysisdependent factors of intradialytic hypotension (eg, cooling dialysate temperature and improving autonomic reflexes) can help deliver effective hemodialysis while optimizing UF and hemodynamic tolerance. In order of efficacy, the following measures help prevent intradialytic hypotension during IHD in ARF: Minimize UF rate requirements by increasing frequency of treatments and/or increased duration of treatments Sodium/UF profiling
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Cool-temperature dialysate Higher dialysate calcium concentration Midodrine (alpha-1 adrenergic agonist used in autonomic dysfunction), which may be administered in the absence of more powerful pharmacologic forms of pressor support Further discussion concerning intradialytic hypotension in patients undergoing chronic IHD can be found separately. (See "Hemodynamic instability during hemodialysis: Overview".) We recommend initially treating intradialytic hypotension with the first three measures listed above. In addition to these interventions, normal saline intravenous (IV) boluses given during hemodialysis can transiently increase blood pressure. Despite the above-mentioned measures, hemodynamic instability may still occur because of the various dialysis-independent causes of intradialytic hypotension present in the acute setting (eg, cardiogenic, vasodilatory, or hypovolemic shock). If measures to improve hemodynamic stability during IHD sessions are not successful, switching to sustained low efficiency hemodialysis (SLED) or continuous renal replacement therapy (CRRT) usually improves hemodynamics while maintaining an acceptable rate of UF and solute clearance. ANTICOAGULATION Issues surrounding anticoagulation in patients undergoing acute hemodialysis are presented separately. (See "Hemodialysis anticoagulation".) PRE- AND POST-HEMODIALYSIS LABORATORY VALUE MONITORING Specific laboratory values are usually required either before or after an acute hemodialysis session. A predialysis basic metabolic profile should be reviewed prior to some acute hemodialysis sessions since electrolyte and acid/base status can profoundly change between treatments and require alterations to the dialysate bath. Drug monitoring Therapeutic drug monitoring levels can be measured post-hemodialysis to help guide supplemental dosing. The following equation can be used to calculate the supplemental dose that takes the patient from the measured level to the desired peak level of drug [30]: Supplemental dose = Vd * IBW * (Desired Peak Level - Measured Level) where Vd is the volume of distribution of the drug and IBW is the ideal body weight. As an example, a patient with an IBW of 70 kg is receiving vancomycin, with the vancomycin Vd 0.75 and the measured vancomycin level of 12 mg/L. The desired vancomycin peak level in this case is 30 mg/L. The calculated supplemental dose of vancomycin would be 945 mg after hemodialysis to achieve a peak level of 30 mg/L. DIALYSIS DOSE Dialysis dose in acute renal failure (ARF) is increasingly recognized as an important issue. This is briefly reviewed in this section, and in detail separately. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure) in adults: Indications, timing, and dialysis dose".) The delivered intermittent hemodialysis (IHD) dose tends to be low in critically ill ARF patients and lower than that prescribed [31,32]. There have been some studies showing a relationship between acute IHD dose and mortality [33,34]. However, as described elsewhere in UpToDate, the VA/NIH Acute Renal Failure Trial Network (ATN) study did not find a difference in mortality associated with a more intensive dosing strategy for renal replacement therapy. Based on the results of the ATN study, we recommend that IHD be provided three times per week, with monitoring of the delivered dose of therapy to ensure a minimum delivered Kt/V of 1.2 per treatment. There is no evidence that more frequent hemodialysis is associated with improved outcomes, unless necessitated for specific indications (eg, hyperkalemia, volume excess, hypotension, etc). (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure) in adults: Indications, timing, and dialysis dose".) INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The Basics and Beyond the Basics. The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond
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the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info and the keyword(s) of interest.) Basics topic (see "Patient information: Hemodialysis (The Basics)") Beyond the Basics topic (see "Patient information: Hemodialysis (Beyond the Basics)") SUMMARY AND RECOMMENDATIONS Indications for renal replacement therapy (RRT) in patients with acute renal failure (ARF) generally include volume overload refractory to diuretics, hyperkalemia, metabolic acidosis, uremia, and toxic overdose of a dialyzable drug. (See 'Indications' above and "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure) in adults: Indications, timing, and dialysis dose".) Once the decision to initiate RRT has been made, the specific modality of dialytic support must be chosen. This includes peritoneal dialysis or hemodialysis and its variations (eg, hemofiltration), and the acute dialysis prescription determined. (See 'Modality' above and "Continuous renal replacement therapy in acute kidney injury (acute renal failure)".) When acute hemodialysis is chosen as the dialytic support modality, vascular access must be established prior to initiating treatment. Placement of the venous dialysis catheter must be considered carefully. (See 'Vascular access' above and "Overview of central catheters for acute and chronic hemodialysis access".) In the setting of ARF, the optimal choice of artificial dialysis membrane is unclear. We suggest that biocompatible dialysis membranes be used in this setting. If the water system is of high quality, high-flux biocompatible dialysis membranes should be used. By comparison, low-flux biocompatible dialysis membranes or a prefilter added to the dialysis machine should be used if the water system is not of high quality. (See 'Hemodialyzer membranes' above.) The dialysate solution composition consists of potassium, sodium, bicarbonate buffer, calcium, magnesium, chloride, and glucose. The dialysate composition in acute hemodialysis is routinely altered each treatment to correct the metabolic abnormalities that can rapidly develop during ARF. (See 'Dialysate composition' above.) There is not a standard or fixed dialysate potassium concentration in the acute hemodialysis prescription because of wide variability in the serum potassium level prior to initiating the hemodialysis session. The typical potassium concentration in the dialysate for acute hemodialysis ranges from 2.0 to 4.0 mEq/L. The dialysate bath potassium is determined by both the absolute predialysis serum potassium and the rate of rise in the interdialytic period. A rapid rate of rise of the serum potassium may best be treated by daily hemodialysis rather than lowering the dialysate potassium bath concentration. (See 'Dialysate potassium concentration' above.) The hemodialysis treatment can provoke ventricular arrhythmias, which are related to dialysis-induced reductions in the serum potassium. They are independently associated with numerous risk factors such as coronary artery disease, left ventricular hypertrophy (LVH), digoxin use, systolic blood pressure, and advanced age. We therefore recommend that patients with underlying cardiac disorders who undergo acute hemodialysis should be placed on a cardiac rhythm monitor during the dialysis session. (See 'Complications with potassium removal' above.) The choice of the dialysate sodium concentration can have a significant impact on the patient's volume and hemodynamic status. (See 'Sodium modeling and hemodialysis hypotension' above.) The dialysate bicarbonate concentration should vary based upon the acid-base status of the patient. The usual dialysate bicarbonate concentration in chronic hemodialysis is approximately 33 to 35 mEq/L. We
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recommend that this high-concentration bicarbonate solution be used in cases of moderate metabolic acidosis in ARF. In severe metabolic acidosis, the concentration may be maximized (eg, 40 mEq/L) and extended duration of hemodialysis may be necessary. Acute hemodialysis patients can also be alkalotic. The severity of the alkalosis and the process generating the alkalosis are the main issues to help determine the optimal dialysate bicarbonate concentration. (See 'Buffer solutions' above.) We recommend adjusting the dialysate calcium concentration to avoid hypercalcemia or clinical hypocalcemia. (See 'Calcium' above.) We use a dialysis blood flow rate of 400 mL per minute. If a lower blood flow rate is required because of hemodynamic instability due to rapid osmolar shifts, the best dialysis modality is unclear and the subject of ongoing study. Until further data are available, we suggest slower solute removal over 6 to 12 hours by sustained low-efficiency dialysis (SLED) or by continuous renal replacement therapy (CRRT). (See 'Blood flow rate' above.) Determining the ultrafiltration (UF) goals in ARF patients can be challenging. The estimation of target intravascular volume will guide the UF goals for a given intermittent hemodialysis (IHD) session. UF during IHD can result in significant intradialytic hypotension. This can be treated by minimizing UF rate requirements by increasing frequency of treatments and/or increased duration of treatments, as well as sodium/UF profiling, and using cool-temperature dialysate. (See 'Ultrafiltration and blood pressure control' above.) We recommend that IHD be provided at least three times per week (alternate days), with monitoring of the delivered dose of dialysis to ensure delivery of a Kt/V of at least 1.2 per treatment (Grade 1B). (See 'Dialysis dose' above.) However, more frequent dialysis may be necessary for specific clinical scenarios, such as intractable hyperkalemia, volume overload, or severe hypotension. Use of UpToDate is subject to the Subscription and License Agreement. REFERENCES 1. Marshall MR, Golper TA. Intermittent Hemodialysis in Intensive Care in Nephrology, Murray P, Brady H, Hall J (Eds), Taylor & Francis, Oxford 2005. 2. Daugirdas JT, Blake PG, Ing TS. Handbook of dialysis, 4th ed, Lippincott Williams & Wilkins, Philadelphia 2007. 3. Zehnder C, Gutzwiller JP, Huber A, et al. Low-potassium and glucose-free dialysis maintains urea but enhances potassium removal. Nephrol Dial Transplant 2001; 16:78. 4. Hou S, McElroy PA, Nootens J, Beach M. Safety and efficacy of low-potassium dialysate. Am J Kidney Dis 1989; 13:137. 5. Ward RA, Wathen RL, Williams TE, Harding GB. Hemodialysate composition and intradialytic metabolic, acid-base and potassium changes. Kidney Int 1987; 32:129. 6. Ahmed J, Weisberg LS. Hyperkalemia in dialysis patients. Semin Dial 2001; 14:348. 7. Morrison G, Michelson EL, Brown S, Morganroth J. Mechanism and prevention of cardiac arrhythmias in chronic hemodialysis patients. Kidney Int 1980; 17:811. 8. Flanigan M. Dialysate composition and hemodialysis hypertension. Semin Dial 2004; 17:279. 9. Henrich WL. Principles and practice of dialysis, 3rd ed, Lippincott Williams & Wilkins, Philadelphia 2004. p.696. 10. Paganini EP, Sandy D, Moreno L, et al. The effect of sodium and ultrafiltration modelling on plasma volume changes and haemodynamic stability in intensive care patients receiving haemodialysis for acute renal failure: a prospective, stratified, randomized, cross-over study. Nephrol Dial Transplant 1996; 11 Suppl 8:32. 11. Song JH, Lee SW, Suh CK, Kim MJ. Time-averaged concentration of dialysate sodium relates with sodium load and interdialytic weight gain during sodium-profiling hemodialysis. Am J Kidney Dis 2002; 40:291.
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12. Kooman JP, van der Sande F, Leunissen K, Locatelli F. Sodium balance in hemodialysis therapy. Semin Dial 2003; 16:351. 13. Locatelli F, Di Filippo S, Manzoni C. Sodium kinetics during dialysis. Semin Dial 1999; 12:S41. 14. Locatelli F, Ponti R, Pedrini L, et al. Sodium kinetics across dialysis membranes. Nephron 1984; 38:174. 15. Gotch FA, Evans MC, Keen ML. Measurement of the effective dialyzer Na diffusion gradient in vitro and in vivo. Trans Am Soc Artif Intern Organs 1985; 31:354. 16. Flanigan MJ, Khairullah QT, Lim VS. Dialysate sodium delivery can alter chronic blood pressure management. Am J Kidney Dis 1997; 29:383. 17. Oo TN, Smith CL, Swan SK. Does uremia protect against the demyelination associated with correction of hyponatremia during hemodialysis? A case report and literature review. Semin Dial 2003; 16:68. 18. Daugirdas, JT, Ross, et al. Acute hemodialysis Prescription. In: Handbook of Dialysis, Daugirdas, JT, Blake, PG, Ing, SA (Eds), Lippincott Williams & Wilkins, Philadelphia 2007. 19. Brase M, Deppe CE, Hollenbeck M, et al. Congestive heart failure as an indication for continuous renal replacement therapy. Kidney Int Suppl 1999; :S95. 20. Alappan R, Cruz D, Abu-Alfa AK, et al. Treatment of Severe Intradialytic Hypotension With the Addition of High Dialysate Calcium Concentration to Midodrine and/or Cool Dialysate. Am J Kidney Dis 2001; 37:294. 21. Zaloga GP, Chernow B, Cook D, et al. Assessment of calcium homeostasis in the critically ill surgical patient. The diagnostic pitfalls of the McLean-Hastings nomogram. Ann Surg 1985; 202:587. 22. Zaloga GP, Chernow B. The multifactorial basis for hypocalcemia during sepsis. Studies of the parathyroid hormone-vitamin D axis. Ann Intern Med 1987; 107:36. 23. Malcolm DS, Zaloga GP, Holaday JW. Calcium administration increases the mortality of endotoxic shock in rats. Crit Care Med 1989; 17:900. 24. Zaloga GP, Sager A, Black KW, Prielipp R. Low dose calcium administration increases mortality during septic peritonitis in rats. Circ Shock 1992; 37:226. 25. Zager RA, Gmur DJ, Bredl CR, Eng MJ. Temperature effects on ischemic and hypoxic renal proximal tubular injury. Lab Invest 1991; 64:766. 26. Schneditz D. Temperature and thermal balance in hemodialysis. Semin Dial 2001; 14:357. 27. Maggiore Q, Pizzarelli F, Santoro A, et al. The effects of control of thermal balance on vascular stability in hemodialysis patients: results of the European randomized clinical trial. Am J Kidney Dis 2002; 40:280. 28. Santoro A, Mancini E, Basile C, et al. Blood volume controlled hemodialysis in hypotension-prone patients: a randomized, multicenter controlled trial. Kidney Int 2002; 62:1034. 29. Tonelli M, Astephen P, Andreou P, et al. Blood volume monitoring in intermittent hemodialysis for acute renal failure. Kidney Int 2002; 62:1075. 30. Aronoff GR, et al. Drug Prescribing in Renal Failure: Dosing Guidelines for Adults, 4th ed, American College of Physicians, Philadelphia 1999. p.176. 31. Evanson JA, Himmelfarb J, Wingard R, et al. Prescribed versus delivered dialysis in acute renal failure patients. Am J Kidney Dis 1998; 32:731. 32. American Society of Nephrology 30th annual meeting. San Antonio, Texas, November 2-5, 1997. Abstracts. J Am Soc Nephrol 1997; 8:1A. 33. Paganini EP. Establishing a dialysis therapy/patient outcome link in intensive care unit acute dialysis for patients with acute renal failure. Am J Kidney Dis 1996; 28:S81. 34. Schiffl H, Lang SM, Fischer R. Daily hemodialysis and the outcome of acute renal failure. N Engl J Med 2002; 346:305. Topic 1854 Version 13.0

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GRAPHICS EKG showing peaked T waves in hyperkalemia

A tall peaked and symmetrical T wave is the first change seen on the ECG in a patient with hyperkalemia.

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