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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
Section Editors Jeffrey S Berns, MD Paul M Palevsky, MD Richard H Sterns, MD
Deputy Editor Alice M Sheridan, MD
with several metaanalyses reporting disparate results. section on 'Complement activation. bicarbonate. the dialysate potassium. membrane biocompatibility. high-flux biocompatible dialysis membranes should be used in the ARF setting.5 to 1. it could also allow the back transport (from dialysate to blood) of potentially harmful water-borne molecules. Many events during the hospitalization can jeopardize the existing access (eg. However. This is particularly true in the treatment of potassium and/or acid/base derangements. since such membranes can now be obtained cheaply.com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm=… 2/15 . with resultant decrease in infectious complications and possibly an increased probability of improved restoration of renal function. the effect of membrane biocompatibility on outcomes (when present) is consistently beneficial. sodium. Although this property can enhance removal of putative toxins and improve outcome. chloride. However. but may be decreased to more efficiently lower the serum potassium during hemodialysis. Certainly. it was postulated that non-complement-activating membranes may incur less inflammatory risk. 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). there are theoretical advantages to high-flux biocompatible membranes that have not been consistently corroborated by often underpowered or flawed clinical studies.25/1/2014 Acute hemodialysis prescription patient (eg. low-flux biocompatible dialysis membranes should be used. and glucose. ● The standard dialysate glucose concentration is 200 mg/dL. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Recovery of renal function and effect of hemodialysis membrane". Previously. the choice of artificial membranes utilized may have a bearing on clinical outcome. arteriovenous graft or fistula) is appropriate. renal recovery. daily reassessment of the existing angioaccess (eg. section on 'Membranes' and "Maintaining water quality for hemodialysis". cost has been eliminated as a deciding factor. there are inconsistent findings concerning the effect of membrane biocompatibility on outcomes among patients with ARF. and survival'. For hospitalized end-stage renal disease (ESRD) patients. renal recovery. We therefore suggest the following approach: ● If the water system used is high quality. magnesium. Issues surrounding magnesium. Overall. http://www. Thus. High-flux membranes contain large pores that allow for enhanced permeability of larger molecules .) DIALYSATE COMPOSITION — The dialysate solution composition consists of potassium. ● If the water system is not of high quality.0 mEq/L and is not usually different from that in the chronic setting. This property is a factor that confounds some of the conclusions from previously performed studies. 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). (See "Overview of central catheters for acute and chronic hemodialysis access". ● The amount of dialysate chloride is dependent upon the dialysate sodium and bicarbonate concentrations. hypotension). and calcium are routinely changed in this setting. chloride. sodium.uptodate. and survival' and "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Recovery of renal function and effect of hemodialysis membrane". 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. membrane biocompatibility. section on 'Complement activation. calcium. Another option is the use of in-line membrane filtration devices on dialysis machines to generate ultrapure dialysate.) HEMODIALYZER MEMBRANES — In the setting of acute renal failure (ARF). In addition. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Recovery of renal function and effect of hemodialysis membrane".) Membranes can also be of low or high flux. Unlike chronic hemodialysis. and glucose include the following: ● The usual dialysate magnesium concentration is 0. bicarbonate buffer.
The goal of an acute hemodialysis treatment is not necessarily to lower the total body potassium burden for general nutritional purposes. a dialysate potassium concentration of 1.25/1/2014 Acute hemodialysis prescription 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. (See "Clinical manifestations of hyperkalemia in adults". http://www.0 mEq/L if the predialysis serum potassium is between 4. if a rapid increase in extracellular potassium is anticipated prior to the next hemodialysis session (eg. (See "Treatment and prevention of hyperkalemia in adults". This is followed by progressive lengthening of the PR interval and QRS duration and then loss of the P wave. Although rarely recommended. the dialysate glucose concentration can be another determinant of the rate of potassium removal. the dialysate concentration should be increased to 2. Acute or severe hyperkalemia — Some patients with acute and/or severe hyperkalemia have muscle weakness and cardiac conduction abnormalities.com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm=… 3/15 .5 mEq/L. and ventricular fibrillation or asystole can result. a zero potassium bath has also been used to rapidly decrease the serum potassium in a short period of time [3.5 mEq/L.0 mEq/L).) Although there is no general consensus concerning the optimal strategy. and 3. potassium >8.5 mEq/L – If the predialysis serum potassium level is between 4.5 or 3. The first electrocardiographic (ECG) changes with hyperkalemia are tall peaked T waves (waveform 1) and shortened QT interval. However. due to marked rhabdomyolysis).5 to 5. such as normalizing the serum potassium level for the next 24 hours. >8. However.0 mEq/L should be used to ensure normokalemia in the lower range of normal.0 mEq/L in patients at risk for cardiac arrhythmia or those receiving digitalis .5 mEq/L and <8. medical management should be initiated immediately with continuous ECG monitoring. A rapid rate of rise in serum potassium may best be treated by daily hemodialysis rather than lowering the dialysate potassium bath concentration. Medical therapy is administered while emergency hemodialysis is being arranged.0 and 5. the dialysate potassium concentration should be varied based upon the pre-dialysis value . then a 2.0 mEq/L dialysate potassium bath should be used. then a dialysate potassium of 2.0 mEq/L – If the predialysis serum potassium level is <4.4].0 mEq/L. This is done to prevent the development of hypokalemia and its complications.0 mEq/L.0 to 4. We suggest using a dialysate potassium of 3.uptodate. As described below. (See 'Complications with potassium removal' below. the following is our general approach to the dialysate potassium concentration : ● Predialysis potassium <4. for example. The typical potassium concentration in the dialysate for acute hemodialysis ranges from 2.5 mEq/L.0 to 4.0 mEq/L. After four hours of hemodialysis in one study. ● Predialysis potassium >5. the goals are often more short term.0 to 4.0 mEq/L potassium dialysate bath in removing serum potassium. the typical potassium concentration in the dialysate for acute hemodialysis usually ranges from 2. we recommend that the dialysate potassium bath should be adjusted to 4.) If more advanced ECG features of hyperkalemia are present. with further prolongation of the QRS interval ("sine wave" pattern).0 and 5. Instead. and should be treated with more rapidly acting medical therapies prior to the initiation of dialysis.0 mEq/L bath and 46 percent more than a 1. removing 85 percent more potassium than a 2.0 mEq/L bath .5 mEq/L and <8. this should be done with a high degree of caution to avoid hypokalemia.0 mEq/L . However. Conduction delay can manifest as bundle branch or atrioventricular (AV) nodal block. a dialysate free of potassium was more effective than a 1.0 mEq/L – If patients have a predialysis serum potassium level >5.0 mEq/L can be used to rapidly decrease the serum potassium to a more tolerable level.5 mEq/L if the predialysis serum potassium is between 4.0 mEq/L – In cases of severe hyperkalemia (eg.0 or 2. The prescribed dialysate bath potassium is determined by both the absolute serum potassium and the rate of rise in the interdialytic period. 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.) ● Severe hyperkalemia. ● Predialysis potassium between 4.0 mEq/L. However.
1 mmol/L]) should be used in cases of mild to moderate hyperkalemia.5 mEq/L to avoid possibly life-threatening arrhythmias. and advanced age [6.0 mEq/L causes serious ventricular arrhythmias . 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). a lower dialysate glucose concentration may be used. which drives potassium into the cells. Second. Once the serum potassium is between 6 and 7 mEq/L. a dialysate potassium concentration of 2. Standard dialysate glucose concentration (200 mg/dL [11.7]. Additional issues http://www.0 mEq/L potassium bath and checking a serum potassium every 30 to 60 minutes. or bicarbonate either concurrently or prior to hemodialysis results in intracellular translocation of potassium.25/1/2014 Acute hemodialysis prescription However. It was concluded that a low dialysate potassium concentration can induce ventricular arrhythmias in hemodialysis patients on digoxin and with LVH. or heart disease). potassium rebound will be less by the same mechanism.0 mEq/L by using a dialysate potassium concentration no lower than 3. and potassium rebound. Dialysate glucose concentration — The dialysate glucose concentration is another factor that can modulate potassium removal since the glucose load enhances insulin secretion. beta-agonists. In patients with underlying cardiac disorders or those taking digoxin. Complications with potassium removal — The hemodialysis treatment can provoke ventricular arrhythmias.0 mEq/L) is present. Such patients warrant closer monitoring of the serum potassium. while rapid. >8.0 mEq/L for the remainder of the hemodialysis session. left ventricular hypertrophy (LVH).) The amount of potassium removal is proportional to the gradient between the serum and dialysate concentrations. To lower the risk of potentially life-threatening dialysis-induced arrhythmias among patients with underlying risk factors. If a rapid fall in serum potassium is desired because of severe hyperkalemia. The administration of insulin. with a postdialysis measurement at two to four hours. 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. First. digoxin. hypertension. the dialysate concentration can be changed to 3. the standard dialysate glucose concentration (200 mg/dL [11. with the postdialysis serum potassium goal of 4. Nine (39 percent) had ventricular tachycardia (VT) during and after hemodialysis performed with a dialysate potassium concentration of 2.0 mEq/L. we suggest using a 1. after dialysis. The immediate postdialysis value is generally the lowest. 23 stable end-stage renal disease (ESRD) patients were evaluated using a Holter monitor . this overall approach decreases the risk of hypokalemia and dialysis-induced arrhythmias. digoxin use. the dialysate potassium concentration can be changed to 2. the goal is to obtain a postdialysis serum potassium concentration of approximately 4.com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm=… 4/15 . particularly in patients with predisposing risk factors delineated below.uptodate. Poor perfusion states and underlying illnesses all affect potassium rebound. the degree of potassium rebound is highly variable. potassium removal during hemodialysis is associated with a larger reduction in serum potassium due to less potassium efflux from cells.6 mmol/L) if severe hyperkalemia (eg. (See 'Complications with potassium removal' below.0 mEq/L. to minimize the risk of hypokalemia and dialysis-induced arrhythmias. in cases of severe hyperkalemia where potassium removal is critical. depends upon the factors previously discussed. Poor systemic perfusion may have a potentially large impact in two ways. We do not use glucose-free dialysate because of the risk of hypoglycemia. intravenous (IV) glucose.0 mEq/L. in the absence of underlying risk factors (cardiac arrhythmias. depending upon many other prescriptive components discussed below. we do not recommend use of a zero potassium dialysate bath for the treatment of severe hyperkalemia. Although not studied in the acute setting. However. Periodic measurements of postdialysis potassium may be helpful. In one study in chronic dialysis. and therefore lower rates of potassium removal during dialysis.0 mEq/L once the serum potassium is approximately 5. in the presence of endogenous insulin.1 mmol/L]) results in significantly decreased potassium removal relative to glucose-free dialysate solution . lower serum levels. Thus. Thus. We suggest a dialysate glucose concentration of 100 mg/dL (5. for example. It is unknown if.
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). particularly in patients with an intact thirst mechanism and the ability to drink fluid based on their thirst. and dizziness. fatigue. particularly in the intensive care unit (ICU) setting. a randomized crossover study of 10 patients evaluated sodium modeling in ARF patients in the ICU . 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 . but can also have bearing in the acute setting. which varied dialysate sodium (160 mEq/L to 140 mEq/L) in a stepwise fashion. 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 remainder of the procedure. or bleeding complications. 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.) In addition. However.com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm=… 5/15 .25/1/2014 Acute hemodialysis prescription related to postdialysis rebound are discussed separately. infectious. with a fixed UF rate spread over the entire dialysis time. 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. vomiting. This approach can cause significant hypotension and discomfort in the form of nausea. interdialytic weight gain. the lower dialysate sodium level minimizes the development of hypertonicity and any resultant excessive thirst." Although sodium modeling has been studied mostly in the chronic hemodialysis population. During acute intermittent hemodialysis (IHD). we recommend that patients with underlying cardiac disorders who undergo acute hemodialysis should be placed on a cardiac rhythm monitor during the dialysis session. The hypotension that can develop during maximal rates of solute removal often compromises clearance and ultrafiltration (UF) targets. (See "Treatment and prevention of hyperkalemia in adults". hypotension is common since patients usually have compromised hemodynamic factors due to cardiac. or a variable dialysate sodium profile. fluid gain. the widespread use of these high-sodium solutions has caused dialysis salt loading with resultant postdialysis thirst. Since the early 1980s. However. The study used either a fixed dialysate sodium regimen (140 mEq/L). and hypertension in the interdialytic period. high-sodium bicarbonate-based dialysate has mostly eliminated hypotension and discomfort during hemodialysis. A concise mechanism describing sodium profiling is best described by the following quotation : "A high dialysate sodium concentration is used initially with a progressive reduction toward isotonic or hypotonic levels by the end of the procedure. when the reduction in osmolality accompanying urea removal is less abrupt. hepatic. and hypertension . To avoid hemodynamic instability during acute IHD. ● Relative blood volume changes were fewer during sodium modeling. section on 'Postdialysis potassium rebound'. low-dialysate sodium concentrations were routinely used to help decrease volume overload and hypertension.uptodate. muscle cramping. During the early days of hemodialysis. Multiple sodium modeling prescriptions are programmed in most http://www. Several sodium modeling prescriptions exist. 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. 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. The problem of postdialytic weight gain and hypertension is mostly seen in the chronic hemodialysis population.
● 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 .uptodate. the dialysate sodium level is then decreased in stepwise.com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm=… 6/15 . 130 mEq/L). 140 mEq/L). there is a subtly different relationship between the gradient and sodium ionic activity for each method used. Although uremia may provide some protection against osmotic demyelination. method of serum sodium measurement.) 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 [8.0 mEq/L below that of the predialysis serum sodium concentration [11. the diffusion gradient for sodium. Subsequently. We prefer either of the following two specific strategies: ● With one high/low-sodium modeling prescription. As a result of all of these factors. respectively.0 mEq/L). http://www. the time average concentration of dialysate sodium should be the same or marginally lower than the predialysis serum sodium concentration (approximately within 1. Thus. (See "Sustained low efficiency or extended daily dialysis". the dialysate sodium concentration that results in no net transfer of sodium has been estimated in various studies to be between 0. 140 mEq/L) is the dialysate sodium usually prescribed in hemodynamically stable patients with normal serum sodium levels. (See 'Dysnatremias' below and 'Sodium modeling and hemodialysis hypotension' above.1 to 3. For most patients with normal or near-normal serum sodium levels.0 to 2.12]. With a linear sodium profile. hemodynamic status. Other methods to treat hypotension are reviewed below. For individual patients.) Dialysate sodium concentration — The choice of dialysate sodium concentration depends upon the predialysis serum sodium concentration. The average of the high/low-sodium levels (eg.14-16]. 150 mEq/L) alternates with a low-dialysate sodium (eg. or linear decrements (depending on clinical effect) to a final low level (eg. a high sodium dialysate for the majority of patients would be characterized by a sodium concentration of approximately 141 mEq/L. Since laboratories use a variety of methods to measure serum sodium concentration (flame photometry. the UF rate is minimized or stopped. with each level set for an equal amount of time. Since lower blood flows through the dialyzer may result in less hemodynamic instability. ● Another sodium modeling prescription is to set the initial dialysate sodium at a high level (eg. UF only occurs during the high-sodium period to draw out intracellular water due to the extracellular hypernatremia. 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. 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. we use a sodium dialysate concentration of approximately 137 mEq/L. We recommend using combined sodium and UF profiling if hypotension occurs while on IHD in the acute setting. Patients may respond to only one or all available prescriptions. To maintain isonatremia. the duration (and degree) of dialysis spent below the isonatremic concentration must be approximately equal to that spent above it . case reports of this complication following dialysis of severely hyponatremic patients lead us to recommend a cautious approach in most patients. for example. a high-dialysate sodium (eg. The same sodium modeling principles used for intradialytic hypotension in the chronic hemodialysis population can also be used in ARF patients. trials are required to find the best sodium modeling prescription in ARF patients on hemodialysis. and a low sodium dialysate by a sodium concentration of approximately 137 mEq/L. exponential. indirect ionometry and direct ionometry).25/1/2014 Acute hemodialysis prescription hemodialysis machines. 150 to 160 mEq/L). and Gibbs-Donnan effect. During the low-sodium period. Issues surrounding dialysate sodium concentration in patients with dysnatremias or hemodynamic instability are discussed in the next and previous sections. Dysnatremias — Rapid correction of an abnormal serum sodium concentration should be avoided during dialysis to avoid neurologic complications .
muscle cramps. The main dialysate buffer currently used in IHD is bicarbonate. aggressive initial correction at a rate of 1. 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 . and extended duration of hemodialysis may be necessary. it may be impractical to avoid a rapid change solely by adjusting the dialysate sodium concentration. the minute ventilation (respiratory rate and/or tidal volume) may need to be reduced to avoid severe alkalemia as the metabolic acidosis is corrected http://www. the treatment during a single dialysis session should be adjusted to provide a rate of correction that does not exceed the generally recommended rate. Some authorities also favor the following approach : ● Among patients with severe chronic hyponatremia (predialysis serum sodium level <130 mEq/L). acetate is presently not routinely used because of associated cardiac and hemodynamic instability. The usual dialysate bicarbonate concentration in chronic hemodialysis is approximately 33 to 35 mEq/L. "Ecstasy") should ever be allowed to undergo aggressive initial correction of their serum sodium concentration. 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. and lethargy due to acute metabolic alkalosis .0 mEq/L per hour may be indicated for the first three to four hours or until the symptoms resolve.com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm=… 7/15 . In severe metabolic acidosis. Thus. disequilibrium syndrome. In addition. as a complication of marathon running or use of the drug.) Buffer solutions — Acetate was the predominant buffer used during the early days of hemodialysis. This modality is far less efficient at changing serum sodium concentrations.5 to 2. the concentration of the bicarbonate solution may be maximized (eg. in patients being mechanically hyperventilated to compensate for metabolic acidosis. Hourly measurements of the serum sodium concentration during the course of dialysis are mandatory.) In the vast majority of patients with more chronic dysnatremias. Subsequently. However." In contrast. The dialysate bicarbonate concentration should vary based upon the acid-base status of the patient.25/1/2014 Acute hemodialysis prescription The overall dialysis strategy for the management of dysnatremias is the same as that in the nondialysis general population. (See "Overview of the treatment of hyponatremia". This buffer is inexpensive and generally well tolerated. in patients being mechanically ventilated using low-tidal volume ventilation. ● In those with hypernatremia. an increased dialysate bicarbonate concentration may be required to compensate for the respiratory acidosis resulting from "permissive hypercapnea. 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 . The goal would be correction of the hyponatremia only after multiple hemodialysis sessions that are performed over a period of several days. 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. and. correction of the hypernatremia could be performed with the administration of hypotonic solutions. We suggest that this high-concentration bicarbonate solution be used in cases of moderate metabolic acidosis in ARF. which may therefore change more slowly than with the use of IHD. 40 mEq/L). with higher pH. If the serum sodium concentration is very high or very low. In addition. Large. Another possibility is to use CRRT. In many such patients. without the hemodynamic problems seen with acetate. 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). (See "Treatment of hypernatremia". possible side effects with bicarbonate include hypoxemia due to decreased respiratory drive.uptodate. 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. weakness. Only patients with hyperacute salt poisoning (eg. and altered mental status. for example. section on 'Rate of correction'. most importantly. cramping. In such patients with hyponatremia. However. rapid changes in the serum sodium concentration are very rarely indicated. the use of dialysate sodium concentrations more than 3 to 5 mEq/L below the plasma sodium concentration is associated with hypotension.
calcium administration to rodents with sepsis appears to be harmful [23. Hypocalcemia is fairly common in ICU patients. ● The improvements in blood pressure with high-dialysate calcium were not associated with similar reductions in symptoms or interventions for intradialytic hypotension. administering calcium to treat hemodynamic instability during acute IHD may be harmful to septic patients and should be considered carefully. Modern machines can adjust dialysate bicarbonate in 1 mEq/L increments (from 40 to 20 mEq/L). In addition.5 mEq/L) with low-dialysate calcium concentration (2.com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm=… 8/15 . the following results were reported: ● High-dialysate calcium significantly increased post-hemodialysis mean arterial pressure (MAP). Calcium — In chronic hemodialysis patients. the clinician must investigate whether there is ongoing generation versus a one-time insult causing the alkalosis. a higher dialysate calcium concentration used in the setting of predialysis hypocalcemia may prevent further worsening of hypocalcemia with the correction of acidosis .) Since total plasma calcium levels are poorly predictive of the ionized level. In addition to helping manage secondary hyperparathyroidism. http://www. A one-time insult can be resolved with a single hemodialysis treatment.24].0 to 3. Acute hemodialysis patients can also be alkalemic. the ionized plasma calcium level should be measured prior to hemodialysis in acutely ill patients with significant hypocalcemia or hypercalcemia. the dialysate calcium concentration may be chosen to treat the presence of either hypo. A higher dialysate calcium concentration can also improve intradialytic hypotension by improving cardiac performance.5 mEq/L.5 mEq/L) on hemodynamic stability in patients on IHD . If the predialysis serum bicarbonate level is >28 mEq/L or respiratory alkalosis is present.or hypercalcemia. (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". The patients in the study had a history of intradialytic hypotension and were also administered therapy with either midodrine. particularly those with sepsis .5 mEq/L. 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. sepsis) and changes in pH during dialysis and mechanical ventilation can affect ionized calcium levels independent of the total plasma calcium concentration. In particular. In this setting. but was not statistically significant. Thus. a lower bicarbonate dialysis concentration would be appropriate. considering the risk of developing hypocalcemia in the acute setting . cool dialysate. and the routine use of the standard concentration for chronic hemodialysis is inappropriate. one prospective crossover study compared the effect of high-dialysate calcium concentration (3. Compared with low-dialysate calcium. ● High-dialysate calcium improved the lowest intradialytic MAP.) In the acute hemodialysis setting. or a combination of these two therapies. However. Its administration may therefore be associated with higher mortality in critically ill patients with sepsis.25/1/2014 Acute hemodialysis prescription with dialysis. This combination is reportedly associated with increased mortality . The severity of the alkalemia and the process generating the alkalosis are the main issues to help determine the optimal dialysate bicarbonate concentration. This observation has led some to postulate that treatment of hypocalcemia in those with sepsis may improve outcomes. (See "Evaluation and management of severe sepsis and septic shock in adults". In addition. the dialysate calcium concentration for acute hemodialysis should be 3.uptodate. the standard dialysate calcium concentration is 2. According to some authorities. the usual dialysate bicarbonate concentration should not be used . As an example. whereas ongoing generation of alkalosis may require frequent and/or long hemodialysis sessions with a lower bicarbonate dialysate. This is particularly important since acute phase responses (eg. this level is used to avoid the development of hypercalcemia and elevated calcium-phosphorus product that can occur with higher dialysate calcium concentrations.
If a lower blood flow (or lower UF rate) is required because of hemodynamic instability due to rapid osmolar shifts. If the measured total plasma calcium level is used in this setting (although ionized plasma calcium is preferred).25/1/2014 Acute hemodialysis prescription (See "Relation between total and ionized serum calcium concentration". we use a dialysate calcium concentration of 2. For patients with chronic kidney disease (CKD) who are initiated on hemodialysis.0 mmol/L]). (See 'Ultrafiltration and blood pressure control' below and 'Dialysate sodium concentration' above.0 mmol/L]). promoting water movement into cells. (See "Overview of central catheters for acute and chronic hemodialysis access". We use a dialysate calcium concentration of 3. We do not use a dialysate calcium concentration >3.) We suggest the following concerning the dialysate calcium concentration: ● We favor adjusting the dialysate calcium concentration to avoid hypercalcemia or clinical hypocalcemia. However. (See "Dialysis disequilibrium syndrome".) Higher blood flows are necessary during IHD to provide sufficient overall solute clearance because of the relatively shorter duration of the session. thus reducing effective circulating volume. For patients with mild hypocalcemia. (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: http://www.0 mg/dL [>3. normocalcemia. and to evaluate the angioaccess. bleeding. given that the total plasma calcium concentration will change in parallel to the albumin concentration. which can lead to the development of the dialysis disequilibrium syndrome.0 mg/dL [2.5 mEq/L.) BLOOD FLOW RATE — Deciding upon the optimal blood flow rate through the dialyzer is determined by various factors. Left-sided internal jugular (IJ) and subclavian catheters tend to provide unreliable blood flow. or mild hypercalcemia (total plasma calcium level between 8. we use a dialysate calcium concentration of 2. the use of higher blood flows with IHD may result in rapid reduction in serum osmolality. there may be enough osmole accumulation in the central nervous system (CNS) to justify a slow removal for the first and second dialysis sessions.uptodate. ● To treat intradialytic hypotension. We use a dialysis blood flow rate of 400 mL per minute. However. the blood flow rate is increased incrementally over several sessions to avoid the rapid removal of accumulated blood solutes. Thus. If the patient has severe hypercalcemia (total plasma calcium level >12. smaller surface area dialyzers. particularly in critically ill patients suffering from septic shock. Until further data are available. and ultrafiltration (UF) control minimize the need to decrease blood flow rate.0 mmol/L]). The best blood flows are attained with femoral vein and right-sided IJ catheters. length. 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 . lower blood flow rates should be prescribed at the initiation of therapy in such patients.0 to 3. or hepatic insufficiency.5 mEq/L for this purpose.0 to 3. When this is not necessary. This may exacerbate intradialytic hypotension despite measures to treat intradialytic hypotension.0 to 12. Noncompliant dialyzers. if the blood urea nitrogen (BUN) has been >100 mg/dL for at least three days in the patient with ARF. where the venous blood flows are the highest.) Blood flow rate in acute hemodialysis is dependent upon temporary dialysis catheter performance. increasing the dialysate calcium may be used in combination with sodium profiling and a lower dialysate temperature.0 mg/dL [<2. the ideal level of ionized calcium in critically ill patients is not known and may not be the same as in normal subjects. The development of hypercalcemia must be avoided with this strategy. we suggest slower solute removal over 6 to 12 hours by sustained low-efficiency dialysis (SLED) or by CRRT. high blood flow rates can be initiated at the onset of acute intermittent hemodialysis (IHD) without fear of precipitating the disequilibrium syndrome.5 mEq/L in the patient with significant hypocalcemia (total plasma calcium level <8.5 mEq/L. it is important that this level is corrected based upon the serum albumin level and other factors. Dialysis catheters must be long enough to reach either the superior vena cava (SVC) or inferior vena cava. This issue and the correction formula are discussed separately (see "Relation between total and ionized serum calcium concentration"). particularly if the patient is symptomatic.) With acute renal failure (ARF). whereas lower blood flows are sufficient to achieve adequate clearance by continuous renal replacement therapy (CRRT) due to its continuous nature . cardiac decompensation. blood solutes have usually not had time to accumulate to the degree observed in the end-stage renal disease (ESRD) population. the best dialysis modality is unclear. and location. However.0 to 2. (See "Dialysis disequilibrium syndrome".com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm=… 9/15 .
In order of efficacy. Although these systems can convincingly reduce the occurrence of intradialytic hypotension in ESRD patients . the estimation of target intravascular volume can be made in the usual fashion utilized for ESRD patients. ● The clinician should appreciate that the relationship between blood volume and hypotension is different in patients with ESRD and critically ill individuals with ARF. However. 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 http://www. no one specific test or parameter is sufficient in isolation. extracellular volume status in critically ill ARF patients is not necessarily an endpoint itself. which may be associated with symptoms. However. which is a biofeedback system that automatically adjusts UF rate and dialysate sodium content in response to a fall in circulating intravascular volume. it has not been evaluated in this setting. Blood temperature monitoring might conceivably allow for controlled cooling in critically ill acute renal failure (ARF) patients without the risk of hypothermic damage. UF during IHD can result in significant intradialytic hypotension. blood clotting. may be undesirable in critically ill patients due to adverse effects upon myocardial function.) 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). ULTRAFILTRATION AND BLOOD PRESSURE CONTROL — Determining optimal ultrafiltration (UF) requirements in critically ill acute renal failure (ARF) patients is challenging. Cool-temperature dialysate typically uses a temperature of 35. This can be illustrated by considering blood volume monitoring.0°C. pulse contour analysis [PiCCO]. The volume expansion that is frequently observed in such patients is often necessary to maintain optimal circulatory and oxygen transport status. and these factors are not comparable between the two groups. which can be treated by reducing or discontinuing UF. 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. end-organ perfusion. 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. and hemodynamic indices. Autonomic function and circulating humoral agents all mediate and mitigate this relationship.uptodate. and/or reducing the blood flow rate. however. and dialysis dose". It is effective in ameliorating hemodynamic instability for ESRD patients . or echocardiography) monitoring.25/1/2014 Acute hemodialysis prescription Indications. timing. section on 'CRRT versus intermittent hemodialysis'. but also in terms of the effect of intervention on the patient's broader clinical condition and hemodynamic status In hemodynamically stable patients. and possibly renal recovery . In addition to these maneuvers. cooling dialysate temperature and improving autonomic reflexes) can help deliver effective hemodialysis while optimizing UF and hemodynamic tolerance. laboratory values. In general.) Hypothermia. With blood-temperature monitoring.com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm… 10/15 . Our recommendations concerning the use of cold-temperature hemodialysis are presented in the next section. This is determined in part by physical examination. In contrast. they are ineffective for ameliorating hypotension in critically ill ARF patients . (See "Cool temperature hemodialysis: Hemodynamic effects". which should guide the UF goals for a given intermittent hemodialysis (IHD) session. in hemodynamically unstable patients. target intravascular volume should be titrated to invasive or noninvasive (bio-impedance analysis. the patients' blood temperature is maintained precisely at target value by a series of feedback loops controlling thermal transfer to and from the dialysate . modifying other dialysisdependent factors of intradialytic hypotension (eg.
and they answer the four or five key questions a patient might have about a given condition.25/1/2014 Acute hemodialysis prescription ● Cool-temperature dialysate ● Higher dialysate calcium concentration ● Midodrine (alpha-1 adrenergic agonist used in autonomic dysfunction). Despite the above-mentioned measures. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure) in adults: Indications. and in detail separately. with the vancomycin Vd 0. 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.uptodate. As an example. hypotension. easy-to-read materials. with monitoring of the delivered dose of therapy to ensure a minimum delivered Kt/V of 1. If measures to improve hemodynamic stability during IHD sessions are not successful. There have been some studies showing a relationship between acute IHD dose and mortality [33. vasodilatory. 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. “The Basics” and “Beyond the Basics. and dialysis dose". cardiogenic. The desired vancomycin peak level in this case is 30 mg/L. Based on the results of the ATN study.32].34]. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure) in adults: Indications. Drug monitoring — Therapeutic drug monitoring levels can be measured post-hemodialysis to help guide supplemental dosing. hyperkalemia. normal saline intravenous (IV) boluses given during hemodialysis can transiently increase blood pressure. we recommend that IHD be provided three times per week. Beyond http://www.Measured Level) where Vd is the volume of distribution of the drug and IBW is the ideal body weight. a patient with an IBW of 70 kg is receiving vancomycin. timing. as described elsewhere in UpToDate. 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. This is briefly reviewed in this section.” The Basics patient education pieces are written in plain language. In addition to these interventions. The calculated supplemental dose of vancomycin would be 945 mg after hemodialysis to achieve a peak level of 30 mg/L. etc). unless necessitated for specific indications (eg. (See "Hemodialysis anticoagulation". There is no evidence that more frequent hemodialysis is associated with improved outcomes.) PRE. 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.2 per treatment. ANTICOAGULATION — Issues surrounding anticoagulation in patients undergoing acute hemodialysis are presented separately. 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 : Supplemental dose = Vd * IBW * (Desired Peak Level . (See "Hemodynamic instability during hemodialysis: Overview". These articles are best for patients who want a general overview and who prefer short. DIALYSIS DOSE — Dialysis dose in acute renal failure (ARF) is increasingly recognized as an important issue.75 and the measured vancomycin level of 12 mg/L. or hypovolemic shock). volume excess. timing.) INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials. hemodynamic instability may still occur because of the various dialysis-independent causes of intradialytic hypotension present in the acute setting (eg. at the 5th to 6th grade reading level.) We recommend initially treating intradialytic hypotension with the first three measures listed above. However.AND POST-HEMODIALYSIS LABORATORY VALUE MONITORING — Specific laboratory values are usually required either before or after an acute hemodialysis session. and dialysis dose".com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm… 11/15 .) The delivered intermittent hemodialysis (IHD) dose tends to be low in critically ill ARF patients and lower than that prescribed [31.
If the water system is of high quality. Here are the patient education articles that are relevant to this topic.) ● In the setting of ARF.com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm… 12/15 .) ● Once the decision to initiate RRT has been made. They are independently associated with numerous risk factors such as coronary artery disease.uptodate. vascular access must be established prior to initiating treatment. We suggest that biocompatible dialysis membranes be used in this setting. We encourage you to print or e-mail these topics to your patients. This includes peritoneal dialysis or hemodialysis and its variations (eg. systolic blood pressure.) ● The dialysate solution composition consists of potassium. The typical potassium concentration in the dialysate for acute hemodialysis ranges from 2. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest. The dialysate bath potassium is determined by both the absolute predialysis serum potassium and the rate of rise in the interdialytic period.25/1/2014 Acute hemodialysis prescription the Basics patient education pieces are longer. sodium. chloride. timing. hyperkalemia. the specific modality of dialytic support must be chosen. metabolic acidosis. We http://www. A rapid rate of rise of the serum potassium may best be treated by daily hemodialysis rather than lowering the dialysate potassium bath concentration. The dialysate composition in acute hemodialysis is routinely altered each treatment to correct the metabolic abnormalities that can rapidly develop during ARF.) ● 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. 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. the optimal choice of artificial dialysis membrane is unclear. Placement of the venous dialysis catheter must be considered carefully. and toxic overdose of a dialyzable drug. (See 'Sodium modeling and hemodialysis hypotension' above. more sophisticated. left ventricular hypertrophy (LVH). 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 dialysate bicarbonate concentration should vary based upon the acid-base status of the patient. digoxin use. (See 'Hemodialyzer membranes' above. high-flux biocompatible dialysis membranes should be used. (See 'Indications' above and "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure) in adults: Indications. and advanced age. (See 'Dialysate composition' above. (See 'Modality' above and "Continuous renal replacement therapy in acute kidney injury (acute renal failure)".) ● 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. (See 'Vascular access' above and "Overview of central catheters for acute and chronic hemodialysis access".0 mEq/L. and dialysis dose".) ● When acute hemodialysis is chosen as the dialytic support modality. By comparison. hemofiltration).0 to 4. and glucose. and the acute dialysis prescription determined. and more detailed. calcium. 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. which are related to dialysis-induced reductions in the serum potassium. uremia. magnesium.) ● The hemodialysis treatment can provoke ventricular arrhythmias. (See 'Dialysate potassium concentration' above. The usual dialysate bicarbonate concentration in chronic hemodialysis is approximately 33 to 35 mEq/L. bicarbonate buffer.) ● The choice of the dialysate sodium concentration can have a significant impact on the patient's volume and hemodynamic status.
Brown S. acid-base and potassium changes. If a lower blood flow rate is required because of hemodynamic instability due to rapid osmolar shifts. Morganroth J. 40 mEq/L) and extended duration of hemodialysis may be necessary. Zehnder C. Weisberg LS. Moreno L. Gutzwiller JP. http://www. McElroy PA. Hyperkalemia in dialysis patients. Hou S. Ward RA. p. Acute hemodialysis patients can also be alkalotic. Sandy D. Suh CK. Lippincott Williams & Wilkins. (See 'Dialysis dose' above. Daugirdas JT. Michelson EL. Morrison G. 7.) However. Am J Kidney Dis 2002. 17:279. Williams TE. Mechanism and prevention of cardiac arrhythmias in chronic hemodialysis patients. Use of UpToDate is subject to the Subscription and License Agreement. 11. we suggest slower solute removal over 6 to 12 hours by sustained low-efficiency dialysis (SLED) or by continuous renal replacement therapy (CRRT). 3. Am J Kidney Dis 1989. Ing TS.com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm… 13/15 . Philadelphia 2004. 14:348.) ● We use a dialysis blood flow rate of 400 mL per minute. such as intractable hyperkalemia. or severe hypotension. The severity of the alkalosis and the process generating the alkalosis are the main issues to help determine the optimal dialysate bicarbonate concentration.25/1/2014 Acute hemodialysis prescription recommend that this high-concentration bicarbonate solution be used in cases of moderate metabolic acidosis in ARF. et al. Taylor & Francis. Safety and efficacy of low-potassium dialysate. 17:811. Nephrol Dial Transplant 2001. 4. UF during IHD can result in significant intradialytic hypotension. 6. Until further data are available. Henrich WL. the concentration may be maximized (eg. Semin Dial 2004. Kim MJ. with monitoring of the delivered dose of dialysis to ensure delivery of a Kt/V of at least 1. (See 'Calcium' above. (See 'Ultrafiltration and blood pressure control' above. stratified. 13:137.) ● Determining the ultrafiltration (UF) goals in ARF patients can be challenging. Wathen RL. 10. 32:129. Nootens J. Paganini EP. and using cool-temperature dialysate.696. Kidney Int 1980. 2. 11 Suppl 8:32. Beach M. 16:78. Low-potassium and glucose-free dialysis maintains urea but enhances potassium removal. This can be treated by minimizing UF rate requirements by increasing frequency of treatments and/or increased duration of treatments. Philadelphia 2007. 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. 8. 4th ed. Murray P. (See 'Buffer solutions' above. Semin Dial 2001. Hall J (Eds). Time-averaged concentration of dialysate sodium relates with sodium load and interdialytic weight gain during sodium-profiling hemodialysis. randomized. Oxford 2005.) ● We recommend that IHD be provided at least three times per week (alternate days). 9. 3rd ed. Marshall MR. Intermittent Hemodialysis in Intensive Care in Nephrology. Lee SW. The estimation of target intravascular volume will guide the UF goals for a given intermittent hemodialysis (IHD) session. Golper TA. Brady H. Ahmed J. Blake PG. Dialysate composition and hemodialysis hypertension. et al. Nephrol Dial Transplant 1996. Song JH. Flanigan M. Hemodialysate composition and intradialytic metabolic. Harding GB. more frequent dialysis may be necessary for specific clinical scenarios. Handbook of dialysis. (See 'Blood flow rate' above. 40:291. Kidney Int 1987. Principles and practice of dialysis.uptodate. volume overload.) ● We recommend adjusting the dialysate calcium concentration to avoid hypercalcemia or clinical hypocalcemia. 5. REFERENCES 1. cross-over study. as well as sodium/UF profiling. the best dialysis modality is unclear and the subject of ongoing study. Lippincott Williams & Wilkins. In severe metabolic acidosis. Huber A.2 per treatment (Grade 1B).
Manzoni C. Ann Intern Med 1987. 16:351. 13.176. Tonelli M. et al. Kidney Int 2002. Am J Kidney Dis 2001. Basile C. 32:731. Trans Am Soc Artif Intern Organs 1985. 32. The effects of control of thermal balance on vascular stability in hemodialysis patients: results of the European randomized clinical trial. 15. Treatment of Severe Intradialytic Hypotension With the Addition of High Dialysate Calcium Concentration to Midodrine and/or Cool Dialysate. 12:S41. Evanson JA. et al. Acute hemodialysis Prescription. Gmur DJ. et al. Zaloga GP. Temperature and thermal balance in hemodialysis. November 2-5. SA (Eds). 37:226. Topic 1854 Version 13. 4th ed. Holaday JW. Sager A. Am J Kidney Dis 1997. Chernow B. 16:68. The diagnostic pitfalls of the McLean-Hastings nomogram. PG. Pedrini L. San Antonio. 28:S81. Lippincott Williams & Wilkins. Schneditz D. 29. Cook D. p. Malcolm DS.25/1/2014 Acute hemodialysis prescription 12. Hollenbeck M.com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm… 14/15 . et al. Prescribed versus delivered dialysis in acute renal failure patients. et al. Am J Kidney Dis 1998. Ann Surg 1985. Semin Dial 2003. Congestive heart failure as an indication for continuous renal replacement therapy. 17. 14. 107:36. Kidney Int Suppl 1999. 21. Zager RA. 346:305. Abu-Alfa AK. Semin Dial 1999. 62:1034.uptodate. 25. Flanigan MJ. Philadelphia 2007. 31. et al. Chernow B. Schiffl H. JT. Evans MC. Bredl CR. Texas. Gotch FA. 16. Himmelfarb J. Blake. Assessment of calcium homeostasis in the critically ill surgical patient. et al. 19. Daugirdas. 34. Measurement of the effective dialyzer Na diffusion gradient in vitro and in vivo. The multifactorial basis for hypocalcemia during sepsis. Ponti R. JT. Cruz D. multicenter controlled trial. Ing. Temperature effects on ischemic and hypoxic renal proximal tubular injury. et al. Blood volume controlled hemodialysis in hypotension-prone patients: a randomized. Zaloga GP. Lang SM. N Engl J Med 2002. 30. Zaloga GP. 20. 64:766. 38:174. Prielipp R. Am J Kidney Dis 2002. Establishing a dialysis therapy/patient outcome link in intensive care unit acute dialysis for patients with acute renal failure. 1997. Mancini E. Sodium balance in hemodialysis therapy. Dialysate sodium delivery can alter chronic blood pressure management. 29:383. 24. Di Filippo S. Andreou P. Blood volume monitoring in intermittent hemodialysis for acute renal failure. Alappan R. Locatelli F. Low dose calcium administration increases mortality during septic peritonitis in rats. Santoro A. 17:900. Semin Dial 2003. Zaloga GP.0 http://www. Locatelli F. Philadelphia 1999. Oo TN. Aronoff GR. J Am Soc Nephrol 1997. 26. Leunissen K. 62:1075. Kooman JP. Nephron 1984. 28. Lab Invest 1991. Paganini EP. Does uremia protect against the demyelination associated with correction of hyponatremia during hemodialysis? A case report and literature review. Studies of the parathyroid hormone-vitamin D axis. 18. Smith CL. 14:357. Lim VS. Wingard R. Daily hemodialysis and the outcome of acute renal failure. Abstracts. In: Handbook of Dialysis. Swan SK. Santoro A. Drug Prescribing in Renal Failure: Dosing Guidelines for Adults. Sodium kinetics across dialysis membranes. van der Sande F. Eng MJ. Keen ML. et al. Semin Dial 2001. Black KW. Pizzarelli F. Deppe CE. Calcium administration increases the mortality of endotoxic shock in rats. 31:354. Khairullah QT. Circ Shock 1992. Locatelli F. 37:294. Am J Kidney Dis 1996. Ross. 27. American College of Physicians. Braüse M. Daugirdas. et al. 40:280. 23. Sodium kinetics during dialysis. Kidney Int 2002. Maggiore Q. 33. 8:1A. Astephen P. Crit Care Med 1989. 202:587. :S95. 22. American Society of Nephrology 30th annual meeting. Fischer R.
http://www.uptodate.25/1/2014 Acute hemodialysis prescription 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.com/contents/acute-hemodialysis-prescription?topicKey=NEPH%2F1854&elapsedTimeMs=17&source=search_result&searchTerm… 15/15 .
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