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To date, there are four randomized controlled trials that assess the effects of terlipressin versus placebo on
renal function in patients with HRS1
[8184]. Although the renal improvement effects of terlipressin is better
when coadministered with albumin
[85], these clinical trials encouraged but did not mandate the use of albumin.
All studies have confirmed that terlipressin is more efficacious than placebo in reversing HRS1 in 36%44% of
patients. The difference in the response rates may be related to different populations of patients being studied
and/or shorter duration of terlipressin treatment in the North American studies. A smaller proportion of patients
(29%) who reversed their HRS1 also survived for 10 days without the need for RRT
[84], thus allowing time for
these patients to wait for their liver transplant without having to deal with the downside of RRT. Although there
is no improvement in the overall survival of patients who received terlipressin versus placebo, the complete
reversal of HRS1 was associated with a significant better survival when compared to nonresponders
[86].Evena
partial response to terlipressin with a 20% decrease in the sCr is associated with an improved survival. In a
meta-analysis assessing the change in survival rate versus a change in sCr in response to treatment with vasocon-
strictors, there was a signifi cant correlation between the drop in sCr and the relative risk for mortality
[87].In
fact, for every 1 mg/dL drop in sCr with vasoconstrictor treatment, there was a 27% reduction in relative risk for
mortality.
Terlipressinisusuallygiveninbolusdosesrangingfrom1mgevery46 hours to a maximum dose of
12 mg/day
[8184]. More recently, a European study showed that a continuous infusion was able to achieve
the same efficacy with a lower total daily dose and less side effects
[88]. Common side e ffects are related to
ischemia, and therefore terlipressin is not recommended to patients with known ischemic conditions such as
ischemic heart disease or peripheral vascular disease. Known cardiovascular complications are angina, arrhyth-
mia, or digital ischemia. In the intestinal tract, terlipressin can stimulate intestinal motility, leading to abdomi-
nal pain and diarrhea.
In the latest North American study of terlipressin for HRS1
[84], there were more patients who received terli-
pressin with respiratory compromise, possibly related to an increase in afterload in patients with subtle cirrhotic
cardiomyopathy, in addition to the cardiac-depressing effects of terlipressin
[89,90]. Therefore, in addition to
ischemic conditions being known as contraindi cations to terlipressin use, clinicians should exercise caution when
ordering terlipressin for patients with known cardiac failure or underlying respiratory conditions. A recent study
showed that the combination of dobutamine could reverse the cardiac-depressing effects of terlipressin
[91],asit
reduces the peripheral vascular resistance and activates the renin-angiotensin system. However, it is the same
vasoactive properties of dobutamine that counteract the potential beneficial effects of terlipressin on the renal cir-
culation. Therefore, it is not surprising that the combination of terlipressin and dobutamine had no effects on
renal function on patients with HRS1
[91].
Norepinephrine
Norepinephrine is an alpha agonist and therefore its mode of action is to increase the mean arterial pressure,
and hence the renal perfusion pressure. Its administration usually requires the admission into a high-
dependency unit or intensive care unit as patients need constant hemodynamic monitoring. Its use also requires
a central line, adding to the complexity of its administration. The dose of norepinephrine is usually 0.53 mg/h,
targeting to end-organ perfusion. To date, there are no studies comparing the use of norepinephrine versus pla-
cebo for the treatment of HRS1. Rather, all the studies have compared the use of norepinephrine versus terlipres-
sin
[9295]. These trials are rather small in numbers, including 76 patients in the norepinephrine arm and 78
patients in the terlipressin arm. These all showed that norepinephrine was equal ly efficacious as terlipressin in
reversing HRS1. This has been confirmed in various meta-analyses
[9698]. However, these meta-analyses also
confirmed that all these trials were at high risk of bias and the evidence was of low quality. Despite this, the
meta-analyses agreed that terlipressin had overall more adverse events but less ischemia-type adverse events
when compared to norepinephrine.
A recent study showed that in patients with acute-on-chronic liver failure (ACLF), terlipressin was more effica-
cious than norepinephrine in reversing HRS1 and improving 28-day survival
[99]. The explanation propose d by
the investigators was that terlipressin with its portal pressure-reducing effects could potentially reduce the extent
of bacterial translocation across the gut wall, and therefore reduce the extent of inflammation in these patients, as
well as improve the hemodynamics. As noted above, inflammation plays a significant role in the pathogenesis of
HRS1 in cirrhosis, and therefore in the context of ACLF, a therapy that can improve two aspects of the pathogen-
esis of HRS would be more efficacious in reversing the HRS1. This is akin to what has been observed in patients
284 17. Hepatorenal syndrome and acute kidney injury in cirrhosis
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with HRS1 and the systemic inflammatory response syndrome, whose heightened inflammation was as sociated
with a better response to terlipressin
[79]. It has to be emphasized that the def inition of ACLF used in this partic-
ular study was defined as per the Asian Pacific Association for the Study of the Liver, which included a bilirubin
of $ 5 mg/dL (85 μmol/L) and an international normalized ratio of $ 1.5 in the presence of ascites with or with-
out hepatic encephalopathy in the preceding 4 weeks
[100]. Therefore, whether the same results will hold true
for patients in other parts of the world where ACLF is defined differently
[101,102] will have to await further
studies.
Midodrine and octreotide
Midodrine is another alpha agonist. It is indicated for the treatment of postural hypotension. Because of its abil-
ity to increase the mean arterial pressure, it has been used in combination with octreotide, a nonspecific antagonist
to splanchnic vasodilators, to treat HRS1. This combination has been shown to be inferior to terlipressin as a treat-
ment for HRS1
[103]. However, the combination is popular in North America as terlipressin is not commercially
available. The dose is titrated from 7.5 to 12.5 mg three times a day to induce an increase in mean arterial pressure
of 15 mmHg. Octreotide can be given either as subcutaneous doses of 100 μg, increasing to 200 μg three times a
day
[104], or as a continuous infusion [105]. Octreotide alone is ineffective [106]. Midodrine should only be used
in situations where the blood pressure remains low despite fluid resuscitation. In this era of increasing prevalence
of obesity, diabetes, and nonalcoholic steatohepatitis among patients with cirrhosis and therefore rising prevalence
of systemic hypertension, this will become less and less likely. In patients who are on nonselective beta blockers
(NSBBs) for prophylaxis against variceal bleeding, response to midodrine will remain inadequate while patients
remain on NSBB. It is imperative that patients have their varices dealt with endoscopically before coming off
NSBB. The response to midodrine and octreotide is typically very slow, dropping the sCr by a few μmol/L
everyday. Patients who have responded to vasoconstrictor treatment with a reduction in their sCr, to say, below
1.5 mg/dL (133 μmol/L), and if there is adequate liver reserve and the major clinical issue is one of refractory
ascites, should be assessed for definitive treatment of the ascites such as insertion of a TIPS shunt
[105].
Predictors of response to vasoconstrictors
Because not all patients with HRS1 respond to vasoconstrictor therapy, various investigators have tried to
identify predictors of response to vasoconstrictors. These include markers of bette r liver function as indicated by
a bilirubin of # 10 mg/dL (170 μmol/L)
[58], better renal function by a sCr of # 5 mg/dL (440 μmol/L)
[58,86,107], an increase in the mean arterial pressure of $ 5 mmHg with treatment [58,107], and lower grades of
ACLF
[108]. There are currently no biomarkers that can predict the response to treatment.
Renal replacement therapy
The use of RRT in patients with cirrhosis and HRS1 has been controversial and is typically dependent on the sta-
tus of liver transplantation. In general, RRT is not recommended as a stand-alone therapy for patients with AKI
unless there is a reversible cause of the AKI. This is because various studies have shown that the initiation of RRT
among patients not listed for liver transplant was not associated with an improved survival but rather prolonging
hospitalization with median survival of 1521 days
[109,110]. Recent data suggest that if the renal failure is part of
a multiorgan failure syndrome or ACLF, reducing the number of organ failures may improve short-term survival
[110,111]. Therefore, the decision to institute RRT or not has to be individualized. However, RRT should not be sim-
ply started to prolong survival. In patients who are candidates for liver transplant, RRT may be used as a bridge
therapy, as extended RRT will have a negative impact on posttransplant renal outcomes
[112].
Liver transplantation
Liver transplantation is the definitive treatment for HRS1, as it removes the liver dysfunction and portal hyperten-
sion, and the pivotal pathogenetic mechanism that underlie the development of HRS1. The sCr at the onset of HRS,
the duration of HRS, and the duration of RRT if required before liver transplant, all have an impact on the likelihood
285Liver transplantation
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of HRS reversal post liver transplant [50], which in turn also has an effect on the posttransplant patient outcomes
[50]. Indeed, the strongest predictor for renal recovery is the duration of the RRT pretransplant, with patients requir-
ing more than 14 days of RRT pretransplant being 9.2 times more likely to have renal nonrecovery posttransplant
[50]. Therefore, the goal of care for these patients is to assess for liver transplant as early as possible, once the diag-
nosis of HRS1 is established, and to provide a trial of vasoconstrictor preliver transplant, since response to vasocon-
strictor therapy pretransplant will reduce the need for RRT
[84]. There are concerns that treating the HRS1 and
therefore reducing the sCr will reduce the MELD score and also lower the priority for liver transplant. It has been
recommended that such patients should continue to use their pretreatment baseline sCr and to consider the pharma-
cological treatment of HRS as dialysis in the calculation of the MELD score
[113]. A recent publication has reported
that although response to vasoconstrictor therapy has resulted in a lowering the MELD score and a delay in receiv-
ing a liver transplant, the posttransplant outcomes were significantly improved with less patients needing RRT and
developing CKD at 1 year post liver transplant
[114]. Therefore the argument should favor patients with HRS1
receiving vasoconstrictor therapy, to increase the time to wait for a suitable donor organ and to improve their post-
transplant outcomes. Once transplanted, renal recovery is not universal, occurring in approximately 80% recipients
of liver transplant
[112]. Patients who reverse their HRS have excellent 1-year survival of 97% post liver transplant,
significantly better than that of 60% in those who do not
[50].
Combined liver kidney transplant
There is a lot of controversy as to whether patients with HRS1 should receive simultaneous liver kidney transplants
(SLKT), as this takes away an organ from patients on the kidney transplant waiting list, with questionable additional
graft and patient survival benefits
[115]. However, the guidelines for SLKT are evolving. This is because the prevalence
for CKD in the cirrhotic population is increasingly related to the rising prevalence of obesity, diabetes, and nonalco-
holic steatohepatitis, and therefore the AKI frequently is superimposed on CKD due to structural renal diseases, the
so-called acute-on-chronic renal disease. These patients will never recover normal renal function even after treatment
for their AKI. As Europe and North America have different definitions for renal nonrecovery, there are also different
guidelines for SLKT.
Table 17.3 outlines the indications for SLKT between Europe [116] and the United States
[117,118]. In general, patients with organic renal diseases such as diabetes or systemic hypertension tend to have lower
survival than those with HRS-AKI or ATN after SLKT
[119]. These factors should be considered in any future proposal
regarding risk assessment for renal recovery and organ allocation policies.
Prognosis
The prognosis of HRS1 is poor with a median survival of days to weeks if left untreated [56]. Patients who
receive terlipressin have a 90-day survival of 27%54.2%
[81,86]. For those who respond to terlipressin, the
TABLE 17.3 Indications for simultaneous liver kidney transplant.
European Association for the Study of the Liver criteria:
• AKI on RRT for $ 4 weeks, or AKI with eGFR # 35 mL/min or measured GFR # 25 mL/min $ 4 weeks
• CKD with eGFR # 40 mL/min or measured GFR # 30 mL/min
• CKD with proteinuria $ 2 g a day
• CKD with renal biopsy showing .30% global glomerulosclerosis or .30% interstitial fibrosis
• Presence of inherited metabolic disease, for example, hyperoxaluria
United States criteria (Organ Procurement and Transplant Network):
• AKI and 6 weeks of consecutive dialysis, or AKI for 6 weeks with an eGFR # 25 mL/min, or AKI and 6 weeks of a combination of both
• ESRD patients chronically administered dialysis
• CKD stage 3 for .90 days with an eGFR of 30 mL/min or less
• Presence of comorbid metabolic disease, for example, hyperoxaluria
AKI, acute kidney injury; CKD, chronic kidney disease; eGFR, estimated glomerular filtration rate; ESRD, end-stage renal disease; RRT, renal replacement therapy.
Adapted from Formica RN, Jr. Simultaneous liver kidney transplantation. Curr Opin Nephrol Hypertens. 2016;25:577582; Boyle G, Simultaneous liver kidney
(SLK) allocation policy. https://optn.transplant.hrsa.gov/media/1192/0815-12_SLK_Allocation.pdf; Cannon RM, Jones CM, Davis EG, Eckhoff DE. Effect of renal
diagnosis on survival in simultaneous liver-kidney transplantation. J Am Coll Surg. 2019;228536544.
286 17. Hepatorenal syndrome and acute kidney injury in cirrhosis
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transplant-free survival rate at 90 days is consistently better than nonresponders [81,86,114]. The presence of
ACLF with other organ failures adds to the poor prognosis of these patients
[120]. High lactate levels, a sign of
tissue ischemia, have also been identified as a sign of poor prognosis
[121].
Even in patients who recover from their AKI episode, long-term follow-up shows that these patients are pre-
disposed to the development of CKD
[122,123]. The presence of CKD renders these patients much more suscepti-
ble to the development of future episodes of AKI. When AKI is superimposed on CKD, the progression of the
AKI episode is much more rapid
[2]. The presence of CKD also predisposes the patients with cirrhosis to the
development of other organ failures. In fact, for every 10 mL/min drop in estimated GFR, there is a 10.5%
increased risk for circulatory failure, 7.0% for brain failure, and 5.8% for respiratory failure
[124]. When you add
in the risk for CKD acceleration in patients with predisposing conditions for renal dysfunction such as diabetes,
the risk for AKI is substantial. The presence of CKD, as indicated by proteinuria, provides 82.4% sensitivity and
80% specificity for the development of AKI when the urinary protein/creatinine ratio is .30
[125]. Therefore,
one of the interventions is to monitor renal function in these patients regularly, to vigorously treat any underly-
ing etiologies of CKD and to prevent repeat episodes of AKI.
Prevention
The mainstay of treatment for HRS1 is to prevent it from developing in the first place. Therefore, every effort
should be made not to disturb the already abnormal hemodynamics in these patients further. For patients who
have ascites and diuretic resistance, it is prudent to withdraw diuretics and start regular paracentesis. Patients
should receive albumin infusions for large-volume paracentesis of more than 5 L in order to prevent the develop-
ment of postparacentesis circulatory dysfunction
[126], which is associated with a high incidence of renal dys-
function of 20%
[127].
Bacterial infections are the most common cause of HRS1. For patients suspected of having a bacterial infection,
early administration of empirical antibiotics is recommended once all the cultures from appropriate sites have
been taken. For every hour of delay in the start of antibiotics, there is an increase in mortality by 1.86 times from
multiorgan failure including kidney failure
[128]. Patients who have acute gastrointestinal bleeds are at risk for
bacterial infections and therefore should also be given prophylactic antibiotics. If no infection is found, the antibi-
otic can be stopped. If a bacterial infection is confirmed, then the antibiotic therapy can be modified accordin g to
sensitivity. In patients with SBP, there is evidence that the use of albumin in conjunction with antibiotics can pre-
vent the development of renal dysfunction, especially in patients with high baseline sCr or with liver dysfunction
[129]. Finally, patients with advanced cirrhosis should avoid nephrotoxic drugs and nonsteroidal antiinflamma-
tory agents. Patients with cirrhosis and baseline renal dysfunction should also avoid radiographic dye which can
worsen the renal ischemia.
Conclusion
HRS1 is a form of AKI in cirrhosis. It is a diagnosis of exclusion. Recent changes in nomenclature of renal dys-
function and diagnostic criteria mean that HRS-AKI can now be diagnosed at a lower level of sCr, thereby allow-
ing earlier institution of treatment. Vasoconstrictors are the mainstay of treatment with terlipressin being the
most commonly used worldwide, but terlipressin is not yet available in most parts of North America.
Vasoconstrictors are usually given in conjunction with album in, but care has to be taken not to overdose patien ts
with albumin. This is because albumin increases the cardiac preload by improving the volume status of the
patients while vasoconstrictors, by increasing the afterload, may cause cardiac failure with pulmonary edema in
these patients.
Timely assessment for liver transplant is necessary, as these patients still have a high mortality rate despite
response to pharmacotherapy because of their advanced liver dysfunction. RRT may be used as a bridging ther-
apy, but patients should not be maintained on long-term RRT while waiting for a liver transplant, as this has a
negative impact on posttransplant patient outcomes including nonreversal of HRS. Combined liverkidney
transplant should be considered in patients with underlying CKD or with prolonged pretransplant RRT. The
future will see the availability of biomarkers to identify the susceptibility for HRS development, progression of
HRS, and response to treatment. This will allow for personalized targeted treatment to improve patient
outcomes.
287Prevention
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CHAPTER
18
Cardiopulmonary considerations for the
anesthetic management of liver transplantation
Christopher L. Wray
1
and Ryan Chadha
2
1
Department of Anesthesiology, University of California Los Angeles, Los Angeles, CA, United States
2
Department of
Anesthesiology and Perioperative Medicine, Mayo Clinic, Jacksonville, FL, United States
Perioperative cardiovascular management in the liver transplant patient
Immediate preoperative evaluation, optimization, and planning
The preoperative assessment of the liver transplant (LT) candidate with underlying cardiac disease requires a
detailed evaluation of the cardiovascular system prior to transplant. In addition, the overall fitness of the patient
to safely undergo LT must be investigated. Risk factors such as severe deconditioning, immobility, sarcopenia,
morbid obesity, and multiorgan failure that significantly impact graft and patient survival must be considered in
the setting of the underlying cardiovascular conditions. Risk factors are additive, and those that may be tolerated
by candidates without cardiovascular disease may adversely impact the perioperative course of patients with
underlying cardiovascular conditions. Cardiac pathology may also evolve over time. In the United States, it is
not unusual for candidates to endure long durations on waitlists; many years may occur between initial listing
for LT and an eventual LT organ offer.
Current guidelines recommend that transplant centers identify a primary cardiology consultant for the evalua-
tion of cardiac conditions in LT candid ates
[1]. However, the frequency of reevaluation has not been defined and
protocols for cardiac reassessment are generally determined by individual centers. Patients with a significant
change in a cardiovascular condition may no longer be appropriate candidates without further evaluation or
therapies. Candidates with underlying cardiac disease that present immediately prior to LT require a comprehen-
sive rapid evaluation of their cardiac status. Likewise, LT candidates with cardiac disease who develop decom-
pensated end-stage liver disease (ESLD) requiring hospitalization need urgent reevaluation of their cardiac
status; the multiorgan manifestations of advanced ESLD may adversely impact an underlying cardiac condition.
Coronary artery disease (CAD) is the most common cardiovascular condition in adults. Prior to listing, the pretrans-
plant cardiac evaluation is largely focused on the diagnosis and treatment of occult CAD in prospective adult LT can-
didates (see
Chapter 10). Following the diagnosis and treatment of CAD, candidates may remain on waiting lists for
long durations prior to receiving an organ offer. Current guidelines recommend that candidates with multivessel CAD
should be referred to a cardiologist for long-term management, however, there is no consensus regarding the fre-
quency for repeat evaluation
[1]. Current guidelines also provide recommendations for initial ischemia testing in LT
candidates, however, there are no recommendations for long-term ischemia screening in LT candidates
[1].Candidates
with a history of known CAD require an expedited cardiac reassessment when the likelihood of LT is high. In some
scenarios, the LT anesthesiologist may be one of the first physicians to assess a transplant candidate with CAD imme-
diately prior to LT. A detailed history including new cardiac symptoms, changes in exercise tolerance, and medication
changes should be sought. Clinical assessment of new ischemia by symptomatology is challenging in LT candidates.
Cardiac symptoms may be of a multifactorial etiology and exercise tolerance may be diminished due to noncardiac
disease processes. All previous cardiac studies including stress-testing, echocardiography, and angiography should be
293
Cardio-Hepatology.
DOI:
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