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![Anterior cavoplasty (adapted from [1]). a The transverse incision line at the anterior sector of the orifice of the right hepatic vein (RHV) is marked in red. b Orifice has been incised and trimmed to create an anterior enlargement of the venous outflow tract](profile/Tung-Yu-Tsui/publication/49729616/figure/fig1/AS:277279360995328@1443119959269/Anterior-cavoplasty-adapted-from-1-a-The-transverse-incision-line-at-the-anterior.png)
Anterior cavoplasty (adapted from [1]). a The transverse incision line at the anterior sector of the orifice of the right hepatic vein (RHV) is marked in red. b Orifice has been incised and trimmed to create an anterior enlargement of the venous outflow tract
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![Fig. 1 Anterior cavoplasty (adapted from [1]). a The transverse...](profile/Tung-Yu-Tsui/publication/49729616/figure/fig1/AS:277279360995328@1443119959269/Anterior-cavoplasty-adapted-from-1-a-The-transverse-incision-line-at-the-anterior_Q320.jpg)
A common and serious problem after living donor liver transplantation (LDLT) of small grafts is small-for-size syndrome (SFSS). Although hyperdynamic portal inflow and portal hypertension are cornerstones in the development of SFSS, inadequate outflow may aggravate SFSS. Therefore, enlargement of the portal outflow tract by incision of the anterior...
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... syndrome (SFSS) injury is a major concern after living donor liver transplantation (LDLT) [1]. It manifests as coagulopathy, encephalopathy, intractable ascites, and prolonged jaundice [2]. SFSS may cause prolonged hospitalization and graft loss, and thus, survival rates of patients with small-for-size grafts are worse than those with adequate graft size [3]. SFSS is frequently encountered in small grafts, i.e., grafts with a graft weight- ratio below 0.8%, but may also be found in recipients of larger grafts [1, 4]. The initial mechanism of injury seems to be a hyperdynamic portal flow through a small liver graft, leading to excessive shear stress injury of sinusoidal cells [5]. Consequently, early attempts to avert SFSS in small grafts focused on the diversion or reduction of portal inflow, such as splenic artery ligation [6], splenectomy [7, 8], mesocaval shunt [9], or partial portocaval shunt [8, 10, 11]. But Fan and colleagues also suggest that a pivotal factor may also be a venous outflow of the graft, because “ in the absence of uniform and adequate outflow, the inflow impedance, graft hypoperfusion, and therefore, portal hypertension are aggravated ” [1]. Hence, in patients with outflow obstruction, portal hypertension rather reflects outflow obstruction and is not the cause of graft injury. It follows that in this situation, it may even be deleterious to mitigate portal pressure because it may reduce adequate portal flow that is also necessary for graft regeneration [12, 13]. Additionally, Boillot, who was one of the first to describe and widely adapt portal decompression to avoid SFSS, has retracted from advocating it in the general situation, because it may cause insufficient portal inflow and subsequent graft failure [14]. To address possible outflow obstruction in right liver grafts, Fan and colleagues [1] advocate anterior incision of the inferior vena cava (IVC) to enlarge the orifice of the right hepatic vein (RHV) and prevent outflow obstruction of the RHV (Fig. 1). But small grafts may also tilt laterodorsal into a large abdominal cavity, and this may lead to functional stenosis by choking on the outflow tract (Fig. 2). Therefore, we enlarged the orifice of the RHV by oval excision of the posterior sector of the orifice (Fig. 3) and compared our new technique of posterior cavoplasty to conventional end-to-end anastomosis of the RHV in a test- of-concept study. The study included 22 adult patients who underwent LDLT of the right hepatic lobe between March 2000 and May 2007, of which seven patients were allocated to the control group and 15 patients to the experimental group that received the new posterior cavoplasty. The first 14 patients underwent systematic allocation by alternate assignment to one of the two study groups in the sequence of their transplantation (pseudo-randomization). After the first interim analysis, there were strong indicators that patients receiving posterior cavoplasty had better clinical outcome, and we decided to allocate all further patients to the experimental group for ethical reasons. Sample size calculations showed that 1:2 allocations would not significantly increase the type II error while retaining the type I error at the predefined level. The patients (6 females and 16 males) had a median age of 46 (interquartile range (IQR) 41 – 54), a median body mass index of 24.7 kg/m2 (IQR 22.2 – 26.5), and a median graft-to-recipient weight ratio (percentage of recipient body weight) of 0.94% (IQR 0.83 – 1.1). Indication for liver transplantation included primary cancer of the liver (six patients), alcoholic liver disease (five patients), hepatitis B or C virus-related cirrhosis (five patients), cryptogenic cirrhosis (three patients), primary biliary cirrhosis (two patients), and acute-on-chronic autoimmune hepatitis (one patient). Most patients were severely ill, but some were transplanted primarily due to malignancy without reduced liver function (11 patients Child-Pugh class C, 3 patients class B, and 8 patients class A). Portal pressure was measured after exposure of the hepatoduodenal ligament by insertion of a 22-gauge needle into the portal vein. PVP and central vein pressure (CVP) were measured at the same time in millimeter of mercury (mmHg). After LDLT, PVP, and CVP were measured again in the same fashion just before abdominal closure. Graft function was assessed by daily measurements of total bilirubin, alanine (ALT), and aspartate transaminase (AST), gamma-glutamyl transferase (GGT), and prothrombin time (PT) in a standardized fashion. Measurements were taken from 24 h prior to LDLT until one of the following endpoints was reached: end of the predefined study time (20 days), discharge from hospital, re- transplantation, or death of the patient. For diagnosis of SFSS, the following criteria were used: prolonged hyperbilirubinemia (above 10 mg/dl at POD 14), no signs for biliary duct obstruction and no proof of rejection, therapy refractory ascites, coagulopathy ...
Citations
... All of them reported a significant reduction in PVF after PIM ( ). Seven of the 13 comparative studies monitored PVP (29)(30)(31)33,38,39). Only three of them clearly reported a cut-off value of more than 20 mmHg (29,31,36) and one reported a PVP more than 15 mmHg ( and ) (38). ...
... Meta-analysis was conducted using the data from the 13 comparative studies (27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39). There was no evidence of statistically significant differences in the demographic characteristics and ABO incompatibility between the donors and recipients. ...
... This finding supports the effectiveness of surgical techniques on the modulation of elevated PVP and/or PVF. In particular, four studies used only splenectomy (29,36,38,39), three used either SAL or splenectomy (34,35,37), two HPCS only (28,32), two splenectomies and/or portosystemic shunts (31,37), one study SAL and/or splenic artery embolisation (30), one only SAL (29), and one posterior cavoplasty (33). Recent guidelines by the international liver transplantation society recommend close monitoring of PVP, PVF, and hepatic artery haemodynamics to diagnose early occurrence of SFSS. ...
Introduction: Small-for-size graft and consequently small-for-size syndrome (SFSS) is an important issue for adult living donor liver transplantation (LDLT). The optimal intra- and postoperative prevention and management strategies for SFSS remain unclear. We aimed to analyse and compare the existing strategies of portal inflow modulation (PIM) and conduct a meta-analysis of studies comparing various PIMs. The primary outcome was the incidence SFSS. Methods: The Google Scholar, Embase, PubMed, and Cochrane Library databases were systematically searched. Both fixed-and random-effects models were used to perform the meta-analysis. Results: Twenty-five studies were selected from a pool of 830 studies, of which 13 compared available surgical techniques between cohorts with and without PIM, and 12 reported outcomes of patients who underwent LDLT and developed SFSS. The incidence rate of SFSS was significantly lower in the PIM cohort than in the non-portal inflow modulation (NPIM) cohort. One-year overall survival (OS) and the re-transplantation rate were significantly better in the PIM cohort than in the NPIM cohort. Conclusion: In LDLT patients diagnosed during the reperfusion period with increased portal venous pressure and/or flow, application of PIM significantly decreased the incidence rate of SFSS and demonstrated significantly better one-year OS.
... One study pseudo-randomised patients to posterior cavoplasty or standard surgical technique, but early indications supported the new posterior cavoplasty approach and this study subsequently allocated all patients to the experimental group. 15 The study designs were heterogenous; some studies compared patients with and without portal inflow modulation (PIM), others compared portal flow to graft-to-recipient weight ratio (GRWR), some compared PVP and SFSS whilst others compared the outcomes of right lobe (RL) and left lobe (LL) LDLT. ...
... All studies included data on the development of SFSS or PHLF (including SFSS), according to whether they were, [16][17][18][19][20][21][22][23] whilst six studies utilised the following; bilirubin >10 mg/dL on postoperative day (POD) 14 alongside intractable ascites (>1000 mls/day on POD14 or >500 mls/day on POD28). 3,15,[24][25][26][27] Three studies used a similar definition with bilirubin >5 mg/ dL 2,28,29 and one study increased the bilirubin cut off to >20 mg/ dL. 30 Two studies used definitions of prolonged cholestasis, coagulopathy and intractable ascites and did not state specific numerical cut offs. ...
... These studies have also shown that when PVP is reduced successfully following PIM, the survival of patients who underwent PIM to reduce their initially high PVP matched the survival of those who did not require PVP modulation (non PIM patients). 15,16,27 An interesting finding by one group was a survival benefit in the PIM group but they did not allocate PIM on the basis on initial high PVP. 34 Discussion SFSS is a well-recognised complication of liver transplantation. ...
... One study pseudo-randomised patients to posterior cavoplasty or standard surgical technique, but early indications supported the new posterior cavoplasty approach and this study subsequently allocated all patients to the experimental group. 15 The study designs were heterogenous; some studies compared patients with and without portal inflow modulation (PIM), others compared portal flow to graft-to-recipient weight ratio (GRWR), some compared PVP and SFSS whilst others compared the outcomes of right lobe (RL) and left lobe (LL) LDLT. ...
... All studies included data on the development of SFSS or PHLF (including SFSS), according to whether they were, [16][17][18][19][20][21][22][23] whilst six studies utilised the following; bilirubin >10 mg/dL on postoperative day (POD) 14 alongside intractable ascites (>1000 mls/day on POD14 or >500 mls/day on POD28). 3,15,[24][25][26][27] Three studies used a similar definition with bilirubin >5 mg/ dL 2,28,29 and one study increased the bilirubin cut off to >20 mg/ dL. 30 Two studies used definitions of prolonged cholestasis, coagulopathy and intractable ascites and did not state specific numerical cut offs. ...
... These studies have also shown that when PVP is reduced successfully following PIM, the survival of patients who underwent PIM to reduce their initially high PVP matched the survival of those who did not require PVP modulation (non PIM patients). 15,16,27 An interesting finding by one group was a survival benefit in the PIM group but they did not allocate PIM on the basis on initial high PVP. 34 Discussion SFSS is a well-recognised complication of liver transplantation. ...
Background:
Major hepatectomy (MH) and particular types of liver transplantation (LT) (reduced size graft, living-donor and split-liver transplantation) lead to a reduction in liver mass. As the portal venous return remains the same it results in a reciprocal and proportionate rise in portal venous pressure potentially resulting in small for size syndrome (SFSS). The aim of this study was to review the incidence, diagnosis and management of SFSS amongst recipients of LT and MH.
Methods:
A systematic review was performed in accordance with the 2010 Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) guidelines. The following terms were used to search PubMed, Embase and Cochrane Library in July 2019: ("major hepatectomy" or "liver resection" or "liver transplantation") AND ("small for size syndrome" or "post hepatectomy liver failure"). The primary outcome was a diagnosis of SFSS.
Results:
Twenty-four articles met the inclusion criteria and could be included in this review. In total 2728 patients were included of whom 316 (12%) patients met criteria for SFSS or post hepatectomy liver failure (PHLF). Of these, 31 (10%) fulfilled criteria for PHLF following MH. 8 of these patients developed intractable ascites alongside elevated portal venous pressure following MH indicative of SFSS.
Conclusion:
SFSS is under-recognised following major hepatectomy and should be considered as an underlying cause of PHLF. Surgical and pharmacological therapies are available to reduce portal congestion and reverse SFSS.
... Intraoperatively, the inferior vena cava appeared narrowed due to liver compression, but after removing the liver, the cava lumen sufficiently expanded. In spite of this, we conducted posterior cavoplasty for enlargement of the hepatic venous outflow tract of the right lobe according to a technique published previously [16]. ...
BACKGROUND Acute-on-chronic liver failure was first defined within the last 10 years as acute decompensation of chronic liver disease accompanied by multiorgan failure and poor outcome. Budd-Chiari syndrome is a rare and potentially deadly hepatic condition. To the best of our knowledge, this is the first case report of a live liver donor recipient with antiphospholipid antibody syndrome. CASE REPORT A 47-year-old woman from Sudan with acute-on-chronic liver failure and subacute Budd-Chiari syndrome triggered by active pneumonia was evacuated to Amman, Jordan. In Amman, she was transferred to our hospital for liver transplant evaluation. She presented with progressive liver failure, acute kidney failure, acute respiratory failure, and encephalopathy stage IV. Multidisciplinary therapy was initiated with IV anti-infective drugs and optimizing mechanical ventilation. Clinically, we stopped her progressive deterioration after 48 h and she improved slightly in our ICU. Accelerated work-up for donors and recipient was completed and her daughter was selected as a medically appropriate donor despite the fact that she was found to have heterozygote factor V Leiden mutation and antiphospholipid antibody syndrome, similar to her mother. A lifesaving live-donor liver transplantation was carried out after 72 h. Donor and recipient were discharged in good condition with normal liver function and both were discharged on anticoagulant Rivaroxaban 20 mg. CONCLUSIONS We present the first case of a patient with acute-on-chronic liver failure with subacute Budd-Chiari syndrome, which was triggered by bacterial pneumonia and was successfully treated by live-donor liver transplantation from a donor with antiphospholipid antibody syndrome.
... Small-for-size syndrome (SFSS), including smallfor-size dysfunction (SFSD) and small-for-size nonfunction (SFSNF), is a concerning and life-threatening complication in patients receiving grafts with a GRWR < 0.8% [21,22] . The incidence of SFSS varies from 4.7% to 27.5% in different LT centers [23][24][25][26][27][28][29][30] . Specifically, the syndrome rate can be as high as 50%-75% in left-lobe LDLT or small-for-size grafts group and as low as 8.4% in right-lobe LDLT [31,32] . ...
... Hemi-portocaval shunt can decrease SFSS incidence RS Goralczyk et al [24] [27] (2012) NS 10%-20% Left lobe grafts predisposes the graft to SFSS RE Yi et al [28] (2008) 29 8 (27.5) Left lobe grafts predisposes the graft to SFSS RS Soejima et al [29] (2012) 312 43 (15.3) ...
... Botha et al [23] (2010) 21 Hemi-portocaval shunt can decrease SFSS incidence RS Goralczyk et al [24] (2011) 22 Posterior cavoplasty can decrease SFSS incidence RS Kim et al [47] (2017) 160 ...
Liver transplantation (LT) is one of the most effective treatments for end-stage liver disease caused by related risk factors when liver resection is contraindicated. Additionally, despite the decrease in the prevalence of hepatitis B virus (HBV) over the past two decades, the absolute number of HBsAg-positive people has increased, leading to an increase in HBV-related liver cirrhosis and hepatocellular carcinoma. Consequently, a large demand exists for LT. While the wait time for patients on the donor list is, to some degree, shorter due to the development of living donor liver transplantation (LDLT), there is still a shortage of liver grafts. Furthermore, recipients often suffer from emergent conditions, such as liver dysfunction or even hepatic encephalopathy, which can lead to a limited choice in grafts. To expand the pool of available liver grafts, one option is the use of organs that were previously considered "unusable" by many, which are often labeled "marginal" organs. Many previous studies have reported on the possibilities of using marginal grafts in orthotopic LT; however, there is still a lack of discussion on this topic, especially regarding the feasibility of using marginal grafts in LDLT. Therefore, the present review aimed to summarize the feasibility of using marginal liver grafts for LDLT and discuss the possibility of expanding the application of these grafts.
... Posterior cavoplasty was also described in right lobe AA-LDLT by extension of the RHV orifice laterally down the IVC [40]. Most recently, Goralczyk et al. [47] established that portal venous pressures (PVP) were lessened by this outflow strategy, which was associated with a sustained decrease in bilirubin levels compared with the non-plasty controls. ...
Living donor liver transplantation (LDLT) has arisen as a viable means to reduce waitlist mortality. However, its widespread embrace by the liver transplant community has been met with frustration, centered on donor morbidity and small-for-size syndrome. Focusing on the latter entity, we describe the initial recognition of this early graft dysfunction, the theorized pathophysiology and solutions to remedy its emergence.
... 1,26 Transplant surgeons have tried to prevent outflow obstructions in hepatic vein anastomoses by many procedures. [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] Posttransplant outflow obstructions are more frequent in children, and children occasionally experience a later onset than adults. [27][28][29][30][31] It has been suggested that the regeneration of the liver graft and the narrower caliber of the recipient's IVC are responsible for outflow obstructions in children. ...
... Many procedures have been reported for the prevention of hepatic vein outflow obstructions. [6][7][8][9][10][11][12][13][14][15][16][17][18][19] Sugawara et al., 18,36 Hwang et al., 19 and Goralczyk et al. 6 introduced V-or diamond-shaped patch plasty, quilt venoplasty, and posterior cavoplasty for RHV reconstruction, respectively. Suehiro et al. 9 and Takemura et al. 10 reported venoplasty with cavoplasty and patch plasty in left liver grafts, respectively. ...
... Many procedures have been reported for the prevention of hepatic vein outflow obstructions. [6][7][8][9][10][11][12][13][14][15][16][17][18][19] Sugawara et al., 18,36 Hwang et al., 19 and Goralczyk et al. 6 introduced V-or diamond-shaped patch plasty, quilt venoplasty, and posterior cavoplasty for RHV reconstruction, respectively. Suehiro et al. 9 and Takemura et al. 10 reported venoplasty with cavoplasty and patch plasty in left liver grafts, respectively. ...
An outflow obstruction of the hepatic vein is a critical complication after living donor liver transplantation (LDLT) and occasionally leads to hepatic failure. Here we introduce a simple method for preventing outflow obstructions by patch plasty in adult LDLT. Between September 2001 and May 2010, 468 adult LDLT procedures were performed at Kyoto University Hospital. We harvested each recipient's portal vein (PV) from the extirpated liver for a patch. We intended to re-form several orifices of the hepatic veins into a single, large orifice. The patch was attached to the anterior wall of the re-formed orifice on the bench. After we put in the liver graft, the procedure for the hepatic vein anastomosis to the inferior vena cava was simple enough that the warm ischemia time was reduced. Three of the 468 cases were diagnosed with an outflow obstruction. All 3 cases underwent hepatic vein reconstruction without patch plasty. In contrast, none of the 159 cases that underwent LDLT with patch plasty suffered from an outflow obstruction, regardless of the liver graft type. The procedure for hepatic vein plasty using a patch from the native PV is simple and elegant and results in excellent outcomes. We propose this as the standard procedure for hepatic vein reconstruction in adult LDLT.
Small-for-size syndrome (SFSS) following living donor liver transplantation is a complication that can lead to
devastating outcomes such as prolonged poor graft function and possibly graft loss. Because of the concern about the
syndrome, some transplants of mismatched grafts may not be performed. Portal hyperperfusion of a small graft and hyperdynamic
splanchnic circulation are recognized as main pathogenic factors for the syndrome. Management of established
SFSS is guided by the severity of the presentation with the initial focus on pharmacological therapy to modulate portal flow
and provide supportive care to the patient with the goal of facilitating graft regeneration and recovery. When medical management
fails or condition progresses with impending dysfunction or even liver failure, interventional radiology (IR) and/or
surgical interventions to reduce portal overperfusion should be considered. Although most patients have good outcomes
with medical, IR, and/or surgical management that allow graft regeneration, the risk of graft loss increases dramatically in
the setting of bilirubin >10 mg/dL and INR>1.6 on postoperative day 7 or isolated bilirubin >20 mg/dL on postoperative day
14. Retransplantation should be considered based on the overall clinical situation and the above postoperative laboratory
parameters. The following recommendations focus on medical and IR/surgical management of SFSS as well as considerations
and timing of retransplantation when other therapies fail.
Background:
Focusing on tenascin-C (TNC), whose expression is enhanced during the tissue remodeling process, the present study aimed to clarify whether plasma TNC levels after living donor liver transplantation (LDLT) could be a predictor of irreversible liver damage in the recipients with prolonged jaundice (PJ).
Methods:
Among 123 adult recipients who underwent LDLT between March 2002 and December 2016, the subjects were 79 recipients in whom we could measure plasma TNC levels preoperatively (pre-) and on postoperative days 1 to 14 (POD1 to POD14). Prolonged jaundice was defined as serum total bilirubin level >10 mg/dL on POD14, and 79 recipients were divided into 2 groups: 56 in the non-PJ (NJ) group and 23 in the PJ group.
Results:
The PJ group had significantly increased pre-TNC; smaller grafts; decreased platelet counts POD14; increased TB-POD1, -POD7, and -POD14; increased prothrombin time-international normalized ratio on POD7 and POD14; and higher 90-day mortality than the NJ group. As for the risk factors for 90-day mortality, multivariate analysis identified TNC-POD14 as a single significant independent prognostic factor (P = .015). The best cut-off value of TNC-POD14 for 90-day survival was determined to be 193.7 ng/mL. In the PJ group, the patients with low TNC-POD14 (<193.7 ng/mL) had satisfactory survival, with 100.0 % at 90 days, while the patients with high TNC-POD14 (≥193.7 ng/mL) had significantly poor survival, with 38.5 % at 90 days (P = .004).
Conclusions:
In PJ after LDLT, plasma TNC-POD14 is very useful for diagnosing postoperative irreversible liver damage early.
Introduction
We aimed to describe our procedure for vascular reconstruction and back table bench preparation for the right lobe live donor allograft. Live donor liver transplantation (LDLT) remains an important option for the expansion of the donor pool. The procedure has been widely used, and its success is dependent on a technically perfect operation with appropriate inflow and outflow of the allograft. Adequate preparation of the right lobe (RL) allograft prior to implantation remains a vital part of the procedure.
Methods
Our technique of back table vascular reconstruction of the RL allograft has been performed using a hepatic vein patch venoplasty, inferior hepatic vein inclusion, portal vein reconstruction, and segment V and VIII reconstruction for all of our LDLTs.
Results
Between March 2009 and January 2020, 321 consecutive adult LDLTs were performed and underwent back table reconstruction with the techniques described. During that time period, no patients had hepatic insufficiency. There was a single thrombosis of a superior mesenteric vein (SMV) to PV jump conduit.
Conclusions
Our technique of back table reconstruction of the LDLT right lobe graft remains a crucial part of the operative procedure. Our experience with RL grafts without middle hepatic vein (MHV) and our systematic approach for inflow and outflow reconstruction has yielded excellent results with no technical outflow issues and minimal inflow complications.
