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cc
cAuthors
cMark R Marshall, MD
cJeffrey S Berns, MD
cPaul M Palevsky, MD
ccTheodore W Post, MD
Last literature review version 17.1: January 2009 | This topic last updated: June 10,
2008 (More
INTRODUCTION Ͷ 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 and
its variations (eg, hemofiltration), and continuous renal replacement therapy. Once the
selection is made, the acute dialysis prescription can be determined
c
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 Ͷ The urgent indications for RRT in patients with 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): Indications, timing, and dialysis dose", section on Indications
MODALITY Ͷ Once the decision to initiate RRT has been made, the specific modality of
dialytic support must be chosen. The possibilities include peritoneal dialysis, intermittent
hemodialysis and its variations (eg, hemofiltration), and continuous renal replacement
therapy. 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): Indications, timing, and dialysis dose
VASCULAR ACCESS Ͷ 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 bed-ridden, presence of vascular disease or atypical anatomy, and the avoidance of
specific complications in an at-risk 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
c
For hospitalized 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 "Acute hemodialysis vascular access"
for a more detailed discussion of this issue
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
cgenerate ultrapure dialysate
See "Renal replacement therapy (dialysis) in acute renal failure: Recovery of renal function
and effect of hemodialysis membrane", sections on Complement activation and High versus
low flux membranes and see "Maintaining water quality for hemodialysis", for a discussion
concerning water quality
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
chemodialysis
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 inter-dialytic period. A rapid rate of rise in serum
potassium may best be treated by daily hemodialysis rather than lowering the dialysate
potassium bath concentration
c
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 changes with hyperkalemia
are tall peaked T waves and shortened QT interval (show ECG 1). 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 AV nodal block, and ventricular fibrillation or asystole can
result. (See "Clinical manifestations and treatment of hyperkalemia
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 Ͷ If the predialysis serum potassium level is less than 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 Ͷ 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 Ͷ If patients have a predialysis serum potassium level greater than 5.5 meq/L and
less than 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 Ͷ 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
cshould 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
c[3
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 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 Ͷ 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
cpotassium 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
c
Complications with potassium removal Ͷ 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,
chypertension, and advanced age [6,7
In one study in chronic dialysis, for example, 23 stable 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
cpotassium concentration of 2.0 meq/L causes serious ventricular arrhythmias [4
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
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
c
Sodium modeling and hemodialysis hypotension Ͷ 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 3 to 4 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
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
c
Although sodium modeling has been studied mostly in the chronic hemodialysis population,
a randomized, cross-over study of 10 patients evaluated sodium modeling in acute renal
failure patients in the ICU [10] . The study used either a fixed dialysate sodium regimen (140
mEq/L) with a fixed ultrafiltration (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 to the fixed regimen. Significantly less
frequent interventions involving nursing and volume replacement was noted in the sodium
modeling and variable UF rate arm. Relative blood volume changes were less during sodium
cmodeling
The group concluded that sodium and ultrafiltration profiling may be the preferred dialysis
prescription for ARF patients in the ICU at risk for hemodynamic instability while undergoing
cintermittent hemodialysis [10
Several sodium modeling prescriptions exist. Multiple sodium modeling prescriptions are
programmed in most 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 intermittent hemodialysis (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 ultrafiltration rate is minimized or stopped. Ultrafiltration 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 pre-dialysis 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
ccmust 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
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
cc[13
As a result of all of these factors, a high sodium dialysate for the majority of patients would
be characterised 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 pre-dialysis
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
The overall dialysis strategy for the management of dysnatremias is the same as that in the
non-dialysis 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 intravenous 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 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 less than 10 meq/L in the first 24 hours and less
than 18 meq/L in the first 48 hours. (See "Treatment of hyponatremia
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
D5W. Hourly measurements of the serum sodium concentration during the course of dialysis
are mandatory. (See "Treatment of hyponatremia", section on rate of correction
Another possibility is to use continuous renal replacement therapy. This modality is far less
efficient at changing serum sodium concentrations, which may therefore change more
slowly than with the use of intermittent hemodialysis
Some authorities also favor the following approach [18] : Among patients with severe
chronic hyponatremia (predialysis serum sodium level less than 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
c "Treatment of hypernatremia
Buffer solutions Ͷ 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 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 decrease respiratory drive with higher
pH, and altered mental status, weakness, cramping, and lethargy due to acute metabolic
calkalosis [20
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 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 on-
going generation versus a one-time insult causing the alkalosis. A one-time insult can be
resolved with a single hemodialysis treatment, whereas on-going generation of alkalosis may
require frequent and/or long hemodialysis sessions with a lower bicarbonate dialysate
c
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 [21] . In addition, a
higher dialysate calcium concentration used in the setting of predialysis hypocalcemia may
cprevent further worsening of hypocalcemia with the correction of acidosis [21
Compared with low-dialysate calcium, the following results were reported: High-dialysate
calcium significantly increased posthemodialysis 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
csimilar reductions in symptoms or interventions for intradialytic hypotension
c
Hypocalcemia is fairly common in ICU patients, particularly those with sepsis [23] . This
ccombination is reportedly associated with increased mortality [24
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 [25,26] . Its administration may therefore be associated with higher
mortality in critically ill patients with sepsis. Thus, administering calcium to treat
hemodynamic instability during acute intermittent hemodialysis may be harmful to septic
patients and should be considered carefully. (See "Management of severe sepsis and septic
shock in adults
Since total plasma calcium levels are poorly predictive of the ionized
plasma calcium concentration. (See "Relation between total and ionized plasma calcium
concentration
BLOOD FLOW RATE Ͷ Deciding upon the optimal blood flow rate through the dialyzer is
determined by various factors. For patients with chronic kidney disease who are initiated on
hemodialysis, the blood flow rate is increased incrementally over several sessions to avoid
the rapid removal of accumulated blood solutes that can lead to the development of the
dialysis disequilibrium syndrome and to evaluate the angioaccess. (See "Dialysis
Disequilibrium Syndrome
With ARF, blood solutes have usually not had time to accumulate to the degree observed in
the ESRD population. However, if the BUN has been >100 mg/dL for at least three days in
the patient with ARF, there may be enough osmole accumulation in the 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 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 [27] . The best blood flows are
attained with femoral vein and right-sided IJ catheters. (See "Acute hemodialysis vascular
access", for a detailed discussion of these issues
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 CRRT due to its continuous nature [27] .
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. Non-compliant dialyzers, smaller surface
area dialyzers, and ultrafiltration control minimize the need to decrease blood flow rate
c
We use a dialysis blood flow rate of 400 mL per minute. If a lower blood flow (or lower
ultrafiltration rate) is required because of hemodynamic instability, the best dialysis
modality is unclear. Until further data are available, we suggest slower solute removal over
six to 12 hours by sustained low-efficiency dialysis (SLED) or by continuous renal
replacement therapy (CCRT). (See "Continuous renal replacement therapy in acute kidney
injury (acute renal failure)" and see "Renal replacement therapy (dialysis) in acute kidney
injury (acute renal failure): Indications, timing, and dialysis dose", section on CRRT versus
intermittent hemodialysis
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
[28] . 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 [29] . It is effective in ameliorating hemodynamic instability for ESRD
cpatients [30
Blood temperature monitoring might conceivably allow for controlled cooling in critically ill
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
The following two over-riding principles should be recognized: The target weight in 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 end-point 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 ultrafiltration 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 [31] , they are ineffective for
ameliorating hypotension in critically ill ARF patients [32] . 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
cpatient's broader clinical condition and hemodynamic status
Ultrafiltration during IHD can result in significant intradialytic hypotension, which can be
treated by reducing or discontinuing ultrafiltration, and/or a reducing the blood flow rate. In
addition to these maneuvers, modifying other dialysis-dependent factors of intradialytic
hypotension (eg, cooling dialysate temperature and improving autonomic reflexes) can help
deliver effective hemodialysis while optimizing ultrafiltration 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/ultrafiltration profiling 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
cpharmacologic forms of pressor support
We recommend initially treating intradialytic hypotension with the first three measures
listed above. In addition to these interventions, normal saline intravenous boluses given
during hemodialysis can transiently increase blood pressure
c
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 SLED or CRRT
usually improves hemodynamics while maintaining an acceptable rate of ultrafiltration and
solute clearance
where Vd is the volume of distribution of the drug and IBW is the ideal body weight
The delivered IHD dose tends to be low in critically ill ARF patients, and lower than that
prescribed [34,35,35] . Two studies support a relationship between acute IHD dose and
mortality: A retrospective observational study showed that a delivered single pool Kt/V >1.0
per treatment was associated with significantly improved outcome in patients with
intermediate illness severity [36] . This study did not attempt to relate outcomes to the
frequency of IHD. A prospective controlled trial demonstrated substantially improved
outcomes with a cumulative single pool Kt/V of 6.0 per week versus 3.0 per week (by simple
addition), and daily versus alternate day treatments [37] . Despite initial concerns about the
study conduct and methods, there is now general acceptance of this result. However, the
time averaged BUN in the lower dose group (approximately 100 mg/dL) indicates under-
cdialysis by modern standards, probably exaggerating the benefit in the higher dose group
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
intermittent hemodialysis 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):
Indications, timing, and dialysis dose
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