544395

research-article2014
PRF0010.1177/0267659114544395PerfusionLong et al.

Original Paper

Perfusion
2015, Vol. 30(1) 25­–32
Perfusionist techniques of reducing acute © The Author(s) 2014
Reprints and permissions:
kidney injury following cardiopulmonary sagepub.co.uk/journalsPermissions.nav
DOI: 10.1177/0267659114544395
bypass: an evidence-based review prf.sagepub.com

DM Long,1 E Jenkins2 and K Griffith2

Abstract
Cardiac surgery utilizing cardiopulmonary bypass has come a long way since its introduction nearly 60 years ago. In the
early days, end-organ damage was linked to contact of the blood with the extracorporeal circuit. One potential cardiac
surgery complication known to result in significant morbidity and mortality is acute kidney injury (AKI). Causes of AKI
are multifaceted, but most of them are associated with techniques that perfusionists employ during extracorporeal
circuit management. These can cause patients to either go on dialysis or renal replacement therapy. Patients with AKI
have longer lengths of stay and consume significant resources beyond those with normal kidney function. Few current
evidence-based markers determine if the kidneys are adequately protected during surgery. Most relevant literature does
not address perfusion-specific techniques that reduce the incidence of AKI. This paper reviews the pathophysiology of
the kidney and focuses on perfusion techniques that may reduce the incidence of AKI.

Keywords
cardiopulmonary bypass; acute kidney injury; perfusionist; cardiac surgery

Introduction
Over the last several decades, there has been an upsurge
in the use of medical technology. These advances have
revolutionized the practice of medicine and have resulted
in a marked improvement in outcomes. The practice of
cardiac surgery has been changed by the growth of these
new technologies and, by the late 1950s and early 1960s,
with the advent of the heart-lung machine (HLM), it
became possible to perform complex cardiac surgery
procedures without the high risks associated with these
procedures.1 Despite these advances, studies have shown
that there are detrimental effects to body systems when
the HLM is used during these procedures. As early as the
CPB using the HLM and postoperative renal dys-
function are correlated.5 The length of time on CPB is
an independent risk factor for AKI in the postopera-
tive setting.6 What occurs during the time on CPB
may have an effect on clinical outcomes. Perfusionists
can alter blood flow and mean arterial pressure
(MAP), control temperature, give fluids and adminis-
1Perfusion Services, NorthShore University Health System, Evanston,
IL, USA
2Cardiovascular Center-Perfusion Services, University of Michigan

Hospitals, Ann Arbor, MI, USA

1960s, it was noted that there was a change that occurs
with kidney function and cardiopulmonary bypass Corresponding author:
(CPB).2 As materials for CPB have decreased complica- Dennis M Long
tions, there remains significant morbidity that can occur Perfusion Services
during these procedures. These include a decrease in NorthShore University Health System
2650 Ridge Avenue
renal function as measured by postoperative changes in Evanston
glomerular filtration rate (GFR), renal blood flow, urine Illinois 60201
output, renal plasma clearance and serum creatinine.3 USA.
These complications have been associated with an Email: dlongccp@gmail.com
increased incidence of postoperative morbidity, mortal- Presented at the 35th Annual Seminar of The American Academy of
ity and length of hospital stay.4 Cardiovascular Perfusion, Orlando, Florida, 23-26 January, 2014
26 Perfusion 30(1)
ter medications via the CPB circuit. They also are
responsible for the selection and preparation of the
CPB circuit. Few studies clearly define the relation-
ships between perfusion-specific factors and AKI in
the adult population of patients undergoing CPB. This
review paper will examine the relationships between
CPB and AKI in order to determine the roles that
these relationships have on outcomes. Studies were
included based upon the relationship between CPB
and AKI with normal kidney function. Studies were
excluded in patients with pre-existing kidney disease
or if there was no clear CPB-related cause to AKI. The
review focuses on adult CPB-related management that
requires perfusionist intervention, including hemodi-
lution, systemic pump flow, pulsatile perfusion, MAP,
mannitol, furosemide, ultrafiltration, hemolysis and
mini-circuits.
Defining the need for evidence-
based guidelines
Every year there are 800,000 cardiac surgical proce-
dures performed worldwide.7 It is estimated that AKI
occurs in as many as 40% of these patients.4 Patients
who develop AKI have twice the average intensive care
unit stay.8 Having to undergo dialysis after a heart oper-
ation can increase a patient’s mortality rate by as much
as 45%.9 Significant healthcare resources are spent on
patients who have AKI.10 Patients who develop AKI
after cardiac surgery are increasingly being discharged
to skilled nursing facilities, causing even more resource
consumption.9 If practitioners are to engage in strate-
gies that will help reduce the number of patients who
develop this complication after surgery, then healthcare
costs will decrease.8 The impetus to ensure healthcare
dollars are spent wisely is being felt throughout the
industry. Exceptional patient care with as little morbid-
ity as possible should be the goal. There is currently a
movement in medicine today towards evidence-based
practice guidelines.11 Perfusionists continue to be slow
at translating evidence-based research knowledge into
the clinical environment where it will affect patients
most.12 The use of evidence-based guidelines can
encourage research and allow practitioners to rely less
on instinct.
Renal function & physiology
The kidney is a complex organ based upon its design and
habitus in the body. It receives approximately 20% of the
cardiac output.13 It has unique oxygen requirements due
to how blood flows to the renal medulla.14 The renal
medulla, because of its design, functions at low oxygen
levels, but, during periods of ischemia, does not have the
capability to survive without some injury.15 The oxygen
tension inside the medulla is low and any alterations in
blood flow related to decreased hematocrit and pressure
may damage the kidney.16 The common problem post
CPB is acute tubular necrosis (ATN) and granular casts
are visible in damaged kidneys.4 The renal cortex is sensi-
tive to injury during the rewarming phase of a cardiac sur-
gical procedure due to hypoperfusion.17 The kidney
responds if the mean arterial blood pressures fall below 80
mmHg by reducing the glomerular filtration rate (GFR).18
Classification systems for acute
kidney injury
The definition of AKI was developed to ensure a stan-
dardized nomenclature for comparison. Thirty-five def-
initions of renal failure are mentioned in the literature.19
The Acute Dialysis Quality Initiative (ADQI), in 2004,
developed the RIFLE classification, which stands for
risk, injury, failure, loss of kidney function and end stage
renal failure.20 The first three classes are stages while the
final two classes are outcomes. This classification com-
pares the effect of serum creatinine values along with
glomerular filtration rate (GFR) and compares them to
decreases in urine output to grade the severity of renal
dysfunction as well as outcomes.20 Loss of kidney func-
tion is graded when a patient has been in the state for 4
weeks or more and end-stage kidney disease is observed
after three months.20 The term AKI was derived from
the ADQI and replaced the former use of the term acute
renal failure.20
The Acute Kidney Injury Network, in 2007, issued
the AKIN classification to allow for a rapid diagnosis.21
The changes in creatinine over a shorter timeframe are
believed to be prognostic of AKI. The first three stages
of the RIFLE classification correlate with three stages of
kidney injury.21 The AKIN classification measures renal
dysfunction in a 48-hour timeframe while the RIFLE
classification takes one week.21 The AKIN classification
also does away with the outcome-based final two meas-
ures of the RIFLE system. Instead of a patient winding
up on renal replacement therapy (RRT) or dialysis, they
are automatically assigned to the highest class in the
AKIN system, but that is not necessarily the case with
the RIFLE classification.22
The literature demonstrates the difficulty in coming to a
consensus before the AKIN classification. Research studies
did not have similar endpoints as to what defines kidney
injury.7 Some studies have examined the role of creatinine
and transient increases from preoperative levels as a marker
of kidney injury while other studies look at whether
patients end up on dialysis or RRT.3 Recent research has
focused on two new biomarkers which are sensitive to kid-
ney injury: neutrophil gelatinase-associated lipocalin
Long et al. 27
(NGAL) and cystatin C. These might be new and faster
ways to determine AKI following cardiac surgery.23 These
two markers have been found to be independent predictors
of AKI quicker than serum creatinine levels as well as being
predictive of the length of stay in the intensive care unit.23
Risk factors
A number of preoperative risk factors that predispose
patients to AKI include advanced age, preoperative ane-
mia, diabetes mellitus, increased body mass index (BMI)
and use of the intra-aortic balloon pump (IABP).24 The
duration of CPB correlates strongly with AKI.25 Also,
patients undergoing valve procedures as well as com-
bined procedures of coronary artery bypass grafting
(CABG) and valve surgery are at greater risk. 25
The use of CPB has been discovered to be an inde-
pendent risk factor for AKI.26 A retrospective study of
2199 patients by Stallwood et  al. of isolated CABG
patients without renal dysfunction found that surgery
with CPB was an independent risk factor for AKI in the
postoperative setting.26 Patients who had gone on CPB
had a 2.9% incidence of AKI versus 1.4% in the off-CPB
group.26 Patients in both groups were similar in terms of
comorbid conditions and the off-CPB group trended for
reoperation.26 Previous work at establishing CPB as an
independent risk factor in smaller cohorts did not show
the same effect.26
The evidence indicating CPB as a risk factor exists,
but the exact mechanism for AKI is complex. The exact
role of CPB-related AKI is hard to define and, while
there is an increase in mortality, it is hard to pinpoint
one factor that causes this. The systemic inflammatory
response syndrome (SIRS) is a potential problem of
CPB.27 The whole body inflammation that occurs dur-
ing SIRS subjects the kidneys to a potential insult from
the large foreign surface area of the bypass circuit.28
SIRS is a risk factor for the development of AKI postop-
eratively.6 Patients on CPB are at risk for receiving vari-
ous forms of emboli during surgery. Perfusionist
interventions, such as injections of medications into the
circuit, have been listed as a source of microemboli gen-
erated during CPB.29 Increased embolic load from per-
fusionist interventions during CPB has been correlated
to rising postoperative creatinine levels.30 Focus on
decreasing interventions through the sample manifold
and using larger bore syringes has been shown to
decrease, but not eliminate, the amount of emboli gen-
erated during CPB.31
Anemia & hemodilution
Anemia has been shown to be an independent risk factor
for AKI during cardiac surgery.32 Anemia potentially
primarily contributes to AKI by decreasing oxygen deliv-
ery, which can also lead to patients receiving homolo-
gous blood transfusions. The foreign surface of the CPB
circuit can cause coagulopathy to develop, leading to fur-
ther blood product administration. As the number of red
blood cell (RBC) transfusions increases, there is a ten-
dency for higher AKI rates.16 Swaminathan et al. made
the association between nadir hematocrit (Hct) and
renal outcomes in a retrospective study of isolated coro-
nary artery bypass graft (CABG) patients.33 As the nadir
Hct fell below 24%, renal failure increased.33 Patients
who received RBC transfusions to treat a low Hct had
increased renal injury as well.33 Habib et al. reported this
association in a retrospective study of isolated CABG
patients.32 A nadir Hct of less than 24%, RBC transfu-
sions and increased CPB time all played a role in renal
injury.32 The avoidance of hemodilution and maintain-
ing an Hct equal to or greater than 24% may be beneficial
as it can lead to less RBC transfusion during CPB.
Loor et  al. described the multiple hit phenomena,
which looked at anemia, transfusions or both. This ret-
rospective study of more than 8000 patients reported
that patients who experienced a hemoglobin level less
than 8 g/dl exhibited an increased tendency for AKI.34 If
RBCs were administered before this time, there was a
decreased likelihood of AKI.34 If the patient had received
both an RBC transfusion and experienced a hemoglobin
less than 8 g/dl during surgery, there was an increased
tendency for AKI to develop.34
Mehta et  al. retrospectively analyzed data on more
than 13,000 patients and found that, as Hct levels
decreased in both men and women, AKI increased. 35
Higher mortality was found in men at higher nadir Hct
levels than women.35 The implication is that different
genders may be able to tolerate different nadir Hct levels
during CPB.35 It is, however, difficult to make this asso-
ciation without prospective, randomized trials to delin-
eate what nadir Hct may injure patients.
The patient becomes hemodiluted in cardiac surgery
unless measures are taken to limit the volume of fluid
the patient receives.36 The perfusionist can limit the
degree of hemodilution during CPB by using retrograde
autologous priming (RAP).34 RAP is a technique in
which the patient’s own blood is used to displace the
crystalloid prime volume in the CPB circuit. RAP has
been shown to be a valuable technique to limit the
amount of fluid given during CPB and may cause
patients to receive less homologous blood transfusions.37
Other techniques of CPB circuit modification may
decrease prime volume and further reduce hemodili-
tion. Among them are vacuum-assisted venous drain-
age, mini-circuits and decreased circuit surface area.37
The degree of hemodilution and nadir hematocrit on
bypass are independent risk factors for postoperative
AKI.32,33
28 Perfusion 30(1)
Mini-circuits
Mini-circuits for CPB are closed systems without a venous
reservoir.38 These circuits dramatically decrease the for-
eign surface area the blood is exposed to during CPB.38
The use of mini-circuits has been shown to decrease the
incidence of AKI following CABG surgery.38 Less hemo-
dilution and concomitantly fewer RBC transfusions may
have contributed to the mechanism that lowered the inci-
dence of AKI.38A single-center, retrospective study of
more than 4600 patients looked specifically at the role
mini-circuits might play in renal outcomes.39 No differ-
ence was found between mini and conventional CPB cir-
cuits in preventing AKI.39 Asteriou et al. found, in high-risk
isolated CABG surgery, that mini-circuits decreased
adverse events, including renal failure.40 The limited appli-
cation of mini-circuits to use in isolated CABG surgery
makes it difficult to assess their role in decreasing AKI.
Ultrafiltration
The use of conventional ultrafiltration (CUF) during CPB
to remove excessive fluid is believed by some to have an
effect on kidney function. If the hemoconcentrator
removes fluid the kidneys are supposed to remove, then it
is believed that the kidneys may not function as efficiently.
A prospective, observational study looked at the effects of
CUF during CPB on kidney function postoperatively and
found no difference between the two groups. Non-CUF
patients tended to receive more fluid, but only produced
slightly more urine on CPB.41 During the 24-hour period
following surgery, the urine output of the non-CUF
patients increased; however, they still maintained a higher
fluid balance.41 Perez-Vela et al. also found no increase in
AKI in patients randomized to receive CUF during their
surgery.42 The limited evidence suggests that CUF does
not protect against AKI nor does it cause injury.
Pump flow
The role of the perfusionist during CPB is to ensure that
the physiologic and metabolic needs of the patients are
being met.1 The CPB circuit provides the cardiac output
during surgery and is an area where perfusionist man-
agement can cause harm.43 The typical pump flow for a
patient undergoing normothermic bypass is from 2.2 to
2.5 L/min/m2, but many factors play into whether this
pump flow is achieved:44 the type of surgery being per-
formed, collateral blood flow returning to the heart as
well as surgeon preference are all factors which can cause
the perfusionist to pump less than the targeted flow.1
The oxygen delivery (DO2) to the patient can be cal-
culated with information that is readily available dur-
ing the procedure. Ranucci et al. prospectively studied
the relationship between DO2, systemic pump flow and
Hct in a cohort of over 1400 patients.36 As a patient’s
DO2 decreased below the 272 ml/min/m2 threshold, the
tendency for AKI to develop increased.36 The perfu-
sionist can augment oxygen delivery by increasing the
pump flow, even in the presence of anemia. The DO2
should be considered another option to be examined
other than hematocrit alone.36 De Somer et  al. retro-
spectively studied the idea that DO2 values influence
AKI.45 Increased carbon dioxide production (VCO2)
and DO2 were studied and a ratio comparing their val-
ues was calculated (DO2/VCO2).45 As nadir DO2 values
decreased below 262 ml/min/m2 and DO2/VCO2 ratios
fell below 5.3 the odds of AKI developing increased.45
Additionally, when the hematocrit fell below 23.5%, the
incidence of AKI increased. The predictive value of the
DO2 and DO2/VCO2 models are more than 90% effec-
tive, with the nadir DO2 being the most predictive in
this setting. Although this study is retrospective, main-
taining higher DO2 values may very well mitigate the
development of AKI.
Mean arterial pressure
Kidneys are autoregulated over a range of mean arterial
blood pressures (MAP). It has been asserted that auto-
regulation is lost below a MAP of less than 80 mmHg.18
During CPB, the patient is exposed to extremes in terms
of MAP.46 Whether or not a low MAP at a normal cardiac
index on CPB can cause AKI is unknown. Similarly, what
the ideal MAP is during CPB to ensure adequate renal
protection is much debated. One study looked at differ-
ent MAP ranges during bypass and found no correlation
to AKI. 47 Kanji et al., on the other hand, in a prospective
observational study, found that a MAP variance of more
than 26 mmHg between preoperative and CPB values is
an independent risk factor for AKI development.46 This
so called delta MAP observation was noted in the pres-
ence of low systemic pump flows on CPB, further dem-
onstrating the need for adequate systemic pump flow
during CPB to protect the kidneys.46 In a retrospective
study with a small cohort, Fischer et al. found the devel-
opment of AKI was associated with a MAP of less than
60 mmHg, low systemic pump flow and long CPB time.48
Haase et al. reported that severe hypotension (MAP less
than 60 mmHg) occurring with a hemoglobin less than 8
g/dl predicted AKI.49 While no consensus exists regard-
ing the ideal MAP on CPB, a target MAP of at least 60
mmHg may reduce the risk of AKI.1
Temperature management
The link between temperature and CPB has been stud-
ied with a particular focus on neurologic events.
Long et al. 29
Boodwani et al. were the first to show the relationship
between extreme hypothermia and hyperthermia caus-
ing problems while on CPB.50 The study demonstrated
that increased AKI was with patients warmed to 37°C
or cooled below 32°C.50 Newland et al. retrospectively
found that perfusate exiting the oxygenator at 37.5°C
correlated to an increased incidence of AKI when com-
pared to perfusate that did not exceed 37.0°C.51
Additionally, the length of time at higher temperatures
during rewarming increased the risk of AKI postopera-
tively.51
Mannitol, furosemide, and sodium
bicarbonate
Urine output is one of the simplest ways to measure
kidney function in the operating room during sur-
gery.25 If a patient has an abrupt decrease in urine pro-
duction, it can be indicative of problems that can be
addressed. In many institutions, the perfusionist
administers one of two diuretics to promote urine out-
put. Mannitol is an osmotic diuretic, which increases
renal blood flow.52 Typically, mannitol is given in doses
from 10 to 50 grams. While it does increase urine out-
put, mannitol has not been shown to prevent AKI fol-
lowing surgery.53 A prospective, randomized,
double-blinded, clinical trial of patients with normal
kidney function found no evidence that mannitol pro-
tected against AKI.52 Carcona et al. found that manni-
tol use increased the excretion of β2-microglobulin
following open-heart surgery, which indicated poten-
tial damage to the kidney tubules.54 If mannitol was
administered along with dopamine during surgery,
kidney damage was increased.54 The routine use of
mannitol for cardiac surgery cannot be recommended
for preventing AKI because no evidence has demon-
strated decreased damage.14 Mannitol use has also
been examined prospectively in patients with existing
kidney dysfunction. Urine output increased in patients
who received mannitol, but did not provide any renal
protection against further damage.53
Furosemide is a diuretic that exerts its effect on the
loop of Henle by preventing sodium reabsorption, but
does not increase renal blood flow. Dosage ranges from
10 mg to 100 mg.55 Furosemide also increases urine out-
put, but, in higher doses, can cause renal dysfunction.55
Parolari et al. found that administration of furosemide
along with low urine output during CPB were inde-
pendent risk factors for developing AKI postoperatively.
The use of any drug to augment urine output during
CPB is to treat a symptom not a cause.3 Caution should
be exercised whenever mannitol or furosemide is
administered because their relationship to AKI has not
been established.
The use of sodium bicarbonate to alkalinize the urine
of patients at risk for AKI is routine following cardiac
catheterization. It is believed to help prevent damage to
the tubules by slowing free radical oxygen species gen-
eration. The use of sodium bicarbonate is believed to be
the best available drug to decrease the incidence of
AKI.56 A pilot study showed that sodium bicarbonate
may mitigate AKI following CPB.57 A prospective, rand-
omized, double-blinded, multicenter trial involving 350
patients at high risk of developing AKI showed no
decrease in AKI development between groups, but an
increased mortality in the sodium bicarbonate group.58
This caused early termination of the study as it was
deemed that the use of sodium bicarbonate was causing
harm.58 The neutrophil gelatinase-associated lipocalin
(NGAL) biomarker was increased in the sodium bicar-
bonate group and was predictive between 6- 24 hours at
diagnosing AKI.58 Alkalinizing a patient’s urine with
sodium bicarbonate as a routine measure in order to
prevent AKI cannot be recommended at this time in
light of this study.
Hemolysis
The use of any extracorporeal circuit is associated with
some degree of hemolysis.59 Subjecting red blood cells
to shear stress in any part of the CPB circuit can cause
hemolysis.39 This occurs when haptoglobin can no lon-
ger bind free hemoglobin in the circulation, leading to
the formation of plasma free hemoglobin. This can be
seen in the urine when it turns to a pink color. There has
been a prevalent belief that pink-colored urine is a nor-
mal by-product of CPB and may not lead to AKI.60 The
association between CPB-induced hemolysis was
recently examined in aortic surgery. Vermeuelen
Windsant et al. found an association between the forma-
tion of plasma free hemoglobin from CPB and injury to
the proximal kidney tubules.59
Cardiotomy suction is the primary source of plasma
free hemoglobin generated by the extracorporeal cir-
cuit.61 The air-blood interface caused by excessive cardi-
otomy suction increases red cell fragility. CPB time and
degree of hemolysis are also directly related. Vanek et al.
observed increased hemolysis during heart valve sur-
gery which was associated with length of time on CPB.62
The type of systemic pump head has little effect on the
generation of hemolysis. A meta-analysis done by
Sachzowzki et  al. found no significant difference
between roller and centrifugal pumps in any variable
measured, including plasma free hemoglobin.63
Mechanisms to reduce CPB hemolysis and AKI are
not clear due to the lack of direct research. The choice
of centrifugal or roller pump does not make a differ-
ence. The normal treatment for hemolysis is clear fluid
30 Perfusion 30(1)
and alkalinizing the urine. A recent study questions
the practice of urine alkalization and the potential for
kidney damage.58 Since there is little that can be done
in the treatment for hemolysis, it should be the opera-
tive team’s goal to reduce the amount of intraoperative
hemolysis that occurs. Areas that will decrease hemol-
ysis include the avoidance of over-occlusion of roller
pumps and the avoidance of unnecessary cardiotomy
suction.
Pulsatile flow
The kidneys function physiologically with pulsatile
flow, but, in most institutions, CPB is carried out in a
non-pulsatile manner. A recent meta-analysis by Sievert
et  al. found that, of the studies examined, there was
increased creatinine clearance and decreased lactate lev-
els with pulsatile CPB.64 A prospective, randomized trial
by Mohammadezah et al. found that pulsatile CPB was
associated with better kidney protection.65 Adademir
et al. prospectively examined the effect of pulsatile CPB
and found low levels of interleukin-18 (IL-18) and
NGAL in the pulsatile group, which indicates kidney
protection.66 Pulsatile perfusion is not without contro-
versy. The means by which to generate a pulse with the
CPB equipment may result in increased hemolysis.
Conclusion
In recent years, researchers have become increasingly
focused on the relationship between CPB and AKI. The
development of evidence-based practice guidelines in
the perfusion community has been an area that has
been slow to be adopted.12 Bartels et al. noted that the
entire field of CPB is practiced more on experience
than evidence.67 Studies have been slow to define the
independent effect of particular techniques employed
during CPB.1 The growth of medical databases collect-
ing procedurally specific data may delineate causative
relationships to define the relationship between CPB
and AKI. Additional research through randomized
clinical trials will also allow for evidence-based practice
to grow in CPB1
AKI following cardiac surgery requiring CPB may be
reduced by the application of a coordinated prevention
plan by multidisciplinary teams preoperatively, intraop-
eratively and postoperatively. Techniques that avoid a
nadir Hct of less than 24% and RBC transfusion should
be applied throughout a patient’s hospital stay. In par-
ticular, elective operations on anemic patients should be
avoided until the condition is resolved. Any technique
that minimizes hemodilution during surgery should
also decrease the need for RBC transfusion, including
the avoidance of unnecessary preoperative crystalloid
fluid administration, the reduction of extracorporeal
circuit prime volume, the application of RAP and the
assiduous and appropriate usage of a cell saver and peri-
cardial suction. The perfusionist should select equip-
ment designed to cause less shear stress, thereby,
producing less plasma free hemoglobin. The literature
indicates that maximizing pump flow, as well as main-
taining a MAP of greater than 60 mmHg during the pro-
cedure, may reduce the incidence of postoperative AKI.
Further research needs to be done in new biomarkers
that can earlier identify those at risk of developing AKI.
The limitations of this review stem largely from its
reliance upon an all-adult patient population while
examining perfusionist interventions related to AKI.
Any analyses or conclusions cannot be applied to chil-
dren. Some studies that met inclusion criteria were ret-
rospective or lacked a control group. Several studies had
a very low number of patients enrolled and researchers
may have not been blinded in their analyses. This review
is wide in scope and, while every effort to ensure rele-
vant studies were included, some may have been
excluded based upon how they were cataloged in data-
bases.
In summary, AKI following cardiac surgery is a com-
plication that causes significant morbidity and mortal-
ity. It increases the resources used to care for these
patients by doubling their stay in the ICU. The long-
term implications of patients ending up on hemodialy-
sis or renal replacement therapy should guide
practitioners to new and better ways to care for these
patients. Knowledge is still growing in this area and pro-
spective studies need to be done to establish a direct
relationship between techniques and outcomes.
Declaration of conflicting interest
The authors declare that there is no conflict of interest.
Funding
This research received no specific grant from any funding
agency in the public, commercial or not-for-profit sectors.
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