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Partial Orthotopic Liver Transplantation in Combination With Two-stage Hepatectomy : a proof-of-concept explained by mathematical modelling
... Most notably, our model incorporates shunt behavior as liver disease progresses which has been theorized to contribute to the hemodynamic derangements of advanced portal hypertension (15,16). This is in comparison to past models that have omitted this major factor or maintained a fixed element to account for all cases (25,26,28,34,35). In this study, we propose that the portosystemic shunting can change as liver disease progresses and that shunt diameter increases as PSG increases. ...
... First, we do not use actual patient data in our study; however, our goal is not to simulate a specific patient's data but to ensure that the assumptions and physiology were self-consistent when integrated in a unifying model. Furthermore, creation of a digital twin requires invasive measurement of physiologic parameters and acquiring this level of data on the timescale needed to observe the natural history of cirrhosis is impractical (25,34). ...
Background and rationale for the studyAs liver disease progresses, scarring results in worsening hemodynamics ultimately culminating in portal hypertension. This process has classically been quantified via the Porto-Systemic pressure Gradient (PSG) which is clinically estimated by Hepatic Venous Pressure Gradient (HVPG), however PSG alone does not predict a given patient's clinical trajectory with regards to Baveno stage of cirrhosis. We hypothesize that a patient's 'PSG-sensitivity' to venous remodeling could explain disparate disease trajectories. We created a computational model of the portal system in the context of worsening liver disease informed by physiologic measurements from the field of portal hypertension. We simulated progression of clinical complications, HVPG and transjugular intrahepatic portosystemic shunt (TIPS) placement while only varying a patient's likelihood of portal venous remodeling.Main ResultsOur results unify hemodynamics, venous remodeling, and the clinical progression of liver disease into a mathematically consistent model of portal hypertension. We find that by varying how 'sensitive' patients are to create venous collaterals with rising PSG we can explain variation in patterns of decompensation for patients with liver disease. Specifically, we find that patients who have higher proportions of portosystemic shunting earlier in disease have an attenuated rise in HVPG, delayed onset of ascites, and less hemodynamic shifting after TIPS placement.Conclusion
This paper builds a computational model of portal hypertension which supports that patient level differences in venous remodeling may explain disparate clinical trajectories of disease.
... Le RAPID consiste en la succession de deux temps opératoires : le lobe gauche est d'abord implanté en position orthotopique auxiliaire, après que l'hémi-foie natif gauche a été retiré. L'hémi-foie natif droit restant fonctionne comme un "organe de réserve", compensant la fonction insuffisante du greffon immédiatement après la transplantation, avant d'être retiré lors d'une deuxième procédure (environ 1 mois plus tard) après hypertrophie satisfaisante du greffon (cf iconographie article N Golse et al. (66)). ...
... Le deuxième travail proposé ici s'intéresse à un type très spécifique de TH (dite « RAPID ») qui est à haut risque d'HTP (petit greffon transplanté) (66). Là encore, le modèle 0D adapté aux spécificités techniques du RAPID (deux interventions mêlant hépatectomie, transplantation, occlusion vasculaire) a montré sur une très petite cohorte norvégienne qu'il était possible de prédire le risque d'HTP, et donc d'anticiper le recours à des techniques de modulation du flux portal. ...
L’acte chirurgical est, par essence même, patient-spécifique. Pourtant, force est de constater que le chirurgien applique souvent des stratégies pré-établies en fonction de son expérience et de son ressenti, sans prise en compte rigoureuse et systématique de l’ensemble des éléments objectifs disponibles. Nous proposons ici un travail de modélisation numérique multi-échelles pour aider le chirurgien à planifier et réaliser une intervention hépatique:1/ Nous avons adapté à l’Homme un modèle électrique dit « 0D » permettant, via une analogie entre le système cardio-vasculaire et un circuit électrique, de prédire le risque d’hypertension portale post-hépatectomie, principal facteur de risque d’insuffisance hépatique postopératoire. Adapté puis validé chez 47 patients hépatectomisés par laparotomie, ce système, utilise actuellement des données d’entrée pré- et peropératoires, et permet d’anticiper la valeur de la pression porte et du gradient porto-cave post-résection. Cet outil pourrait permettre (en utilisant des données uniquement préopératoires) de récuser des chirurgies à haut risque de décompensation, ou inversement, de valider des gestes autrement récusés.2/ Nous avons mis au point un modèle mathématique permettant de prédire le risque de dysfonction précoce du greffon hépatique. Ce système quantifie la cinétique de montée du signal de la fluorescence parenchymateuse après injection systémique de vert d’indocyanine en fin de greffe. Il permet d’alerter le chirurgien face au risque de non-fonction primaire d’organe, et ainsi de planifier une surveillance armée et des mesures correctrices éventuelles.3/ Grâce à une modélisation de l’écoulement 3D du flux sanguin sus-hépatique post-hépatectomie droite, nous décrivons le lien entre régénération et modification de l’arbre vasculaire, et expliquons ainsi les observations de croissance hétérogène du parenchyme restant. Cet outil, applicable à d’autres situations cliniques, pourrait permettre au chirurgien de modifier la géométrie vasculaire pour favoriser l’écoulement et éviter l’outflow block, parfois infraclinique.4/ Nous avons mis au point un système de guidage peropératoire en temps réel par réalité augmentée permettant une navigation chirurgicale optimisée. La visualisation de l’anatomie réelle du patient, ajustée aux déformations, permettra un repérage plus sûre des structures internes et ainsi une amélioration des résultats oncologiques.
... Все параметры модели настраивались с учетом частоты сердечных сокращений (ЧСС) и массы доли, чтобы соответствовать шести основным гемодинамическим переменным пациента до операции: сердечный выброс, среднее артериальное давление, давление в полой вене, портальное давление, портальный кровоток и кровоток в печеночной артерии. Авторы смогли в модели количественно оценить гемодинамические изменения родной печени и пересаженной, что делает возможным перенести данный опыт на лечение гепатоцеллюлярной карциномы с циррозом печени, с высокой вероятностью портальной гипертензии [10]. ...
... The small graft used in the RAPID technique may be more susceptible to small-for-size syndrome, in which portal hyperperfusion leads to microvascular damage and subsequent liver failure (51,52). Outcomes may yet be improved by predictive models such as the one designed by Golse et al. (53). The RAPID procedure, while still experimental in nature, represents an exciting new option of expanding the donor pool for LT. ...
Background and Objective
Primary and metastatic liver tumors are a significant cause of mortality worldwide. Regardless of the etiology of the tumor, macro- and microscopically clear margins (R0) while preserving adequate function of the remaining organ are the main goals after liver resections. However, technically challenging procedures are required to achieve R0 resection. Currently, there is no consensus of which should be the ideal minimal safety margin for liver tumor resections, with contrasting reports in regards of safety, tumor recurrence and overall outcomes following R0. Therefore, we aim to review current worldwide surgical practices to achieve R0 resections for primary and metastatic liver tumors in challenging surgical techniques and their reported outcomes.
Methods
PubMed database, Google Scholar, and OVID Medline were searched for peer-reviewed original articles related to surgical techniques performed to achieve R0 resections in the setting of primary and/or metastatic liver tumors. An up-to-date review of English-language articles published between 2015 to July 2022 was performed.
Key Content and Findings
Primary and metastatic liver tumors can be effectively treated using hepatic resection. Current literature highlights that tumors involving major vascular structures are not uncommon. Surgical advances have allowed for vascular control techniques, as well as vascular resections to be performed in a feasible and safe manner to achieve R0 resections. Complex resections combining surgical techniques can be performed in certain population after a detailed evaluation. Liver transplantation (LT) have been used with varying degrees of success for treatment of patients with hepatocellular carcinoma, cholangiocarcinoma (CCA), colorectal liver metastases (CRLM), non-resectable CRLM and metastatic neuroendocrine tumors.
Conclusions
Safety and feasibility of R0 resections have been reported for multiple techniques. Technical complexity should not be a limitation to achieve or pursue R0 tumor resection. However, there has to be a balance between patient risk/benefit in attempting R0 resections. Adequate training of surgeons on implementation of complex techniques, as well as transplant oncology techniques applied to hepato-pancreato-biliary (HPB) surgery represents as a promising path to improve short and long-term outcomes for liver-related oncology patients.
... Recent refinements in magnetic resonance imaging using hepatospecific contrast agents might be useful in this setting. 67 In the near future, 68,69 preoperative modelling of the post-LT hemodynamic status might help anticipate the need for portal flow modulation. ...
Background & aims:
The shortage of liver grafts continues to worsen. Because the expanded use of small-for-size grafts (SFSGs) would substantially alleviate this shortage, we aimed to analyse the available knowledge on auxiliary liver transplantation (ALT) with SFSGs in patients with chronic liver disease (CLD) to identify opportunities to develop ALT with SFSGs in patients with CLD.
Methods:
This is a systematic review on ALT using SFSGs in patients with CLD. The review was completed by updates obtained from the authors of the retained reports.
Results:
Heterotopic ALT was performed in 26 cases between 1980 and 2017, none for SFGS stricto sensu, and auxiliary partial orthotopic liver transplantation (APOLT) in 27 cases (from 1999 to 2021), all for SFSG. In APOLT cases, partial native liver resection was performed in most of cases, whereas the second-stage remnant native liver hepatectomy was performed in 9 cases only. The median graft-to-body weight ratio was 0.55, requiring perioperative or intraoperative portal modulation in 16 cases. At least 1 complication occurred in 24 patients following the transplant procedure (morbidity rate, 89%). Four patients (4/27, 15%) died after the APOLT procedure. At the long term, 19 (70%) patients were alive and well at 13 months to 24 years (median, 4.5 years) including 18 with the APOLT graft in place and 1 following retransplantation.
Conclusions:
Despite high postoperative morbidity, and highly reported technical variability, the APOLT technique is a promising technique to use SFSGs in patients with CLD, achieving satisfactory long-term results. The results need to be confirmed on a larger scale, and a standardised technique could lead to even better results.
Lay summary:
At the cost of a high postoperative morbidity, the long-term results of APOLT for small-for-size grafts are good. Standardisation of the procedure and of portal modulation remain needed.
Background & Aims
Despite improvements in medical and surgical techniques, post-hepatectomy liver failure (PHLF) remains the leading cause of postoperative death. High postoperative portal vein pressure (PPV) and portocaval gradient (PCG), which cannot be predicted by current tools, are the most important determinants of PHLF. Therefore, we aimed to evaluate a digital twin to predict the risk of postoperative portal hypertension (PHT).
Methods
We prospectively included 47 patients undergoing major hepatectomy. A mathematical (0D) model of the entire blood circulation was assessed and automatically calibrated from patient characteristics. Hepatic flows were obtained from preoperative flow MRI (n = 9), intraoperative flowmetry (n = 16), or estimated from cardiac output (n = 47). Resection was then simulated in these 3 groups and the computed PPV and PCG were compared to intraoperative data.
Results
Simulated post-hepatectomy pressures did not differ between the 3 groups, comparing well with collected data (no significant differences). In the entire cohort, the correlation between measured and simulated PPV values was good (r = 0.66, no adjustment to intraoperative events) or excellent (r = 0.75) after adjustment, as well as for PCG (respectively r = 0.59 and r = 0.80). The difference between simulated and measured post-hepatectomy PCG was ≤3 mmHg in 96% of cases. Four patients suffered from lethal PHLF for whom the model satisfactorily predicted their postoperative pressures.
Conclusions
We demonstrated that a 0D model could correctly anticipate postoperative PHT, even using estimated hepatic flow rates as input data. If this major conceptual step is confirmed, this algorithm could change our practice toward more tailor-made procedures, while ensuring satisfactory outcomes.
Lay summary
Post-hepatectomy portal hypertension is a major cause of liver failure and death, but no tool is available to accurately anticipate this potentially lethal complication for a given patient. Herein, we propose using a mathematical model to predict the portocaval gradient at the end of liver resection. We tested this model on a cohort of 47 patients undergoing major hepatectomy and demonstrated that it could modify current surgical decision-making algorithms.
SUNDIALS is a suite of advanced computational codes for solving large-scale problems that can be modeled as a system of nonlinear algebraic equations, or as initial-value problems in ordinary differential or differential-algebraic equations. The basic versions of these codes are called KINSOL, CVODE, and IDA, respectively. The codes are written in ANSI standard C and are suitable for either serial or parallel machine environments. Common and notable features of these codes include inexact Newton-Krylov methods for solving large-scale nonlinear systems; linear multistep methods for time-dependent problems; a highly modular structure to allow incorporation of different preconditioning and/or linear solver methods; and clear interfaces allowing for users to provide their own data structures underneath the solvers. We describe the current capabilities of the codes, along with some of the algorithms and heuristics used to achieve efficiency and robustness. We also describe how the codes stem from previous and widely used Fortran 77 solvers, and how the codes have been augmented with forward and adjoint methods for carrying out first-order sensitivity analysis with respect to model parameters or initial conditions.
This paper presents a novel evolutionary optimization strategy based on the derandomized evolution strategy with covariance matrix adaptation (CMA-ES). This new approach is intended to reduce the number of generations required for convergence to the optimum. Reducing the number of generations, i.e., the time complexity of the algorithm, is important if a large population size is desired: (1) to reduce the effect of noise; (2) to improve global search properties; and (3) to implement the algorithm on (highly) parallel machines. Our method results in a highly parallel algorithm which scales favorably with large numbers of processors. This is accomplished by efficiently incorporating the available information from a large population, thus significantly reducing the number of generations needed to adapt the covariance matrix. The original version of the CMA-ES was designed to reliably adapt the covariance matrix in small populations but it cannot exploit large populations efficiently. Our modifications scale up the efficiency to population sizes of up to 10n, where n is the problem dimension. This method has been applied to a large number of test problems, demonstrating that in many cases the CMA-ES can be advanced from quadratic to linear time complexity.
Live donor liver transplantation (LDLT) is an important surgical technique for treating children with end-stage liver diseases. Surgical complications may occur, e.g., due to thrombosis formed in hepatic arteries (HAs) or portal veins (PVs). From the hepatic circulation point of view, a hepatic arterial buffer response (HABR) mechanism, where the HA flow counteracts the changes in the PV flow, could play a role in graft dysfunction, yet this intricate mechanism has not been elucidated in LDLT procedures. In this short communication we simulate the HABR which may occur in an adult-to-child LDLT, where the left lateral lobe of an adult donor is transplanted to a child. Using an electrical analog model we show that the HABR could be triggered in both portal hyper-perfusion and venous obstruction scenarios, and this may be associated with arterial and/or venous thrombosis in the liver graft as reported in clinical studies. In conclusion, HABR could be important in adult-to-child LDLT and it should be considered in pre-surgical planning.
Objective:
to report the first case of resection and partial liver segment 2-3 transplantation with delayed total hepatectomy (RAPID) from living donor in a patient affected of irresectable colorectal liver metastases (i-CRLM) BACKGROUND:: A renaissance of liver transplantation (LT) for i-CRLM has been recently observed. The Norwegian SECA trial demonstrated a 5-year overall survival rate of approximately 60%, notwithstanding early tumor recurrence. The RAPID technique was recently introduced as alternative to whole deceased donor LT, but it is limited by poor availability of splittable organs and many organisational aspects. In this context left lateral living donor LT may be the ideal solution.
Methods:
Report about the technique and results of living donor RAPID procedure.
Technique:
A 49 years old woman affected with i-CRLM from adenocarcinoma of right colon, underwent a left hepatectomy with ligation of right portal vein maintaining the right hepatic artery patent. Subsequently, the left lateral lobe from her son was implanted as auxiliary partial orthotopic LT. Two weeks later completion of hepatectomy was performed.
Results:
The donor postoperative course was uneventful. The recipient developed postoperatively a slight small for size syndrome which spontaneously resolved. No graft dysfunction and no rejection were observed. At POM 5 micrometastases occurred in bones and lungs, which were treated with radiotherapy and chemotherapy, respectively. Almost 2 years later the patient is alive, in good general condition, although slight progression of bone and lung metastases.
Conclusions:
LT poses a valid treatment option for i-CRLM. In times of organ paucity, "living donor-RAPID" procedure may represent a paradigm shift in the management of i-CRLM.
Goal:
Cirrhosis is the common end-stage of any given chronic liver disease, developing after persistent destruction and regeneration of parenchymal liver cells. The associated architectural distortion increases the intrahepatic vascular resistance, leading to portal hypertension and systemic circulatory disorders. This study investigates the impact of the changing vascular resistances on the hepatic and global circulation hemodynamics during cirrhogenesis.
Methods:
Cirrhogenesis was revisited using the thioacetamide rat model (N = 20). Rats were sacrificed at weeks 0, 6, 12, and 18. For each time-point 3D vascular geometries were created by combining hepatic vascular corrosion casting with μCT imaging. Morphological quantification of the trees branching topology provided the input for a lobe-specific lumped parameter model of the liver that was coupled to a closed-loop model of the entire circulation of the rat. Hemodynamics were simulated in physiological and pathological circumstances.
Results:
The simulations showed the effect of the liver vascular resistances (driven by the hepatic venous resistance increase) on liver hemodynamics with portal hypertension observed after 12 weeks. The closed-loop model was further adapted to account for systemic circulatory compensation mechanisms and disorders frequently observed in cirrhosis and simulated their impact on the hepatic, systemic and pulmonary hemodynamics.
Conclusion:
The simulations explain how vascular changes due to cirrhosis severely disrupt both hepatic and global hemodynamics.
Significance:
This study is a priori the first to model the rat entire blood circulation during cirrhogenesis. Since it is able to simulate cirrhosis main characteristics, the model may be translated to humans for the assessment of liver interventions.
Measurement of hepatic venous pressure gradient (HVPG) is currently widely adopted to provide an estimate of portal pressure gradient (PPG) in the diagnosis and treatment of portal hypertension associated with liver cirrhosis. Despite the well-documented clinical utility of HVPG, it remains poorly understood how the relationship between HVPG and PPG is affected by factors involved in the pathogenesis and progression of cirrhosis. In the study, a computational model of the hepatic circulation calibrated to in vivo data was developed to simulate the procedure of HVPG measurement and quantitatively investigate the error of HVPG relative to PPG under various pathophysiological conditions. Obtained results confirmed the clinical consensus that HVPG is applicable to the assessment of portal hypertension caused by increased vascular resistance located primarily at the sinusoidal and postsinusoidal sites rather than at the presinusoidal site. On the other hand, our study demonstrated that the accuracy of HVPG measurement was influenced by many factors related to hepatic hemodynamics even in the case of sinusoidal portal hypertension. For instance, varying presinusoidal portal vascular resistance significantly altered the difference between HVPG and PPG, while an enhancement in portosystemic collateral flow tended to improve the accuracy of HVPG measurement. Moreover, it was found that presinusoidal and postsinusoidal vascular resistances interfered with each other with respect to their influence on HVPG measurement. These findings suggest that one should take into account patient-specific pathological conditions in order to achieve a better understanding and utilization of HVPG in the clinical practice.
The liver function may be degraded after partial liver ablation surgery. Adverse liver hemodynamics have been shown to be associated to liver failure. The link between these hemodynamics changes and ablation size is however poorly understood. This article proposes to explain with a closed-loop lumped model the hemodynamics changes observed during twelve surgeries in pigs. The portal venous tree is modeled with a pressure-dependent variable resistor. The variables measured, before liver ablation, are used to tune the model parameters. Then, the liver partial ablation is simulated with the model and the simulated pressures and flows are compared with post-operative measurements. Fluid infusion and blood losses occur during the surgery. The closed-loop model presented accounts for these blood volume changes. Moreover, the impact of blood volume changes and the liver lobe mass estimations on the simulated variables is studied. The typical increase of portal pressure, increase of liver pressure loss, slight decrease of portal flow and major decrease in arterial flow are quantitatively captured by the model for a 75% hepatectomy. It appears that the 75% decrease in hepatic arterial flow can be explained by the resistance increase induced by the surgery, and that no hepatic arterial buffer response (HABR) mechanism is needed to account for this change. The different post-operative states, observed in experiments, are reproduced with the proposed model. Thus, an explanation for inter-subjects post-operative variability is proposed. The presented framework can easily be adapted to other species circulations and to different pathologies for clinical hepatic applications.
Small-for-size syndrome (SFSS) is a feared complication of extended liver resection and partial liver transplantation. Swine models of extended hepatectomy have been developed for studying SFSS and its different treatment options. Although portal inflow modulation (PIM) by splenectomy or splenic artery ligation (SAL) has been proposed in humans to prevent SFSS, such procedures have not yet been evaluated in swine.
The present study was designed to evaluate modifications in splanchnic haemodynamics yielded by extended hepatectomy with and without PIM in swine.
Nineteen animals underwent 70% hepatectomy (H70, n = 7), 90% hepatectomy (H90, n = 7) or sham laparotomy (H0, n = 5). Haemodynamic measurements were performed at baseline, after hepatectomy and after PIM by SAL and splenectomy.
Portal vein flow increased after both H70 (273 ml/min/100 g versus 123 ml/min/100 g; P = 0.016) and H90 (543 ml/min/100 g versus 124 ml/min/100 g; P = 0.031), but the hepatic venous pressure gradient (HVPG) increased only after H90 (10.0 mmHg versus 3.7 mmHg; P = 0.016). Hepatic artery flow did not significantly decrease after either H70 or H90. In all three groups, neither splenectomy nor SAL induced any changes in splanchnic haemodynamics.
Subtotal hepatectomy of 90% in swine is a reliable model for SFSS inducing a significant increase in HVPG. However, in view of the relevant differences between swine and human splanchnic anatomy, this model is inadequate for studying the effects of PIM by SAL and splenectomy.
© 2015 International Hepato-Pancreato-Biliary Association.
Selected patients with nonresectable colorectal liver metastases benefit from liver transplantation and have acceptable 5-year survival rates. However, allocating full-sized grafts to this group of patients is difficult due to the scarcity of grafts. This could be improved by utilizing small partial grafts, which mandates effective strategies to overcome the problems regarding insufficient functional liver mass.
We have developed a protocol incorporating previously reported experiences from living donor transplantation and recent developments in liver surgery, facilitating transplantation of very small liver grafts. At the time of transplantation, segments 1 to 3 are resected in the recipient and orthotropically replaced by a segment 2 to 3 allograft. Portal inflow is modulated by redirecting the portal flow to the graft with concomitant focus on keeping the portal vein pressure below 20 mm Hg. A second-stage hepatectomy is performed as soon as the graft has regenerated to a sufficient volume.
A graft weighing 330 g was transplanted to a 50-year-old man weighing 92 kg, and the portal vein to the right remnant liver was closed. The volume of the liver graft was doubled 2 weeks after the first procedure, and it increased further after the second procedure, with extended right hepatectomy performed at day 23 after transplantation. There were no signs of liver failure or small-for-size syndrome.
The current protocol and ongoing study could represent a possible strategy to increase the availability of liver transplantation to patients with nonresectable liver tumors such as hepatocellular carcinoma and colorectal liver metastases.
Purpose:
Hypothermic machine perfusion (HMP) is reviving as a better preservation method for donor livers than the golden standard of cold storage, but still faces challenges such as the risk for endothelial damage and flow competition between the arterial and portal venous inflow. Therefore, we previously developed an electrical analog model to investigate the effect of HMP settings on the human liver hemodynamics. While the model provided plausible results, it is based on a number of assumptions and its performance was never subjected to experimental validation. To this end, we present a new methodology to validate and calibrate this model to a specific liver.
Methods and results:
HMP experiments were performed to capture the perfusion behavior of a human liver during varying perfusion settings. Simultaneous pressure and flow signals were acquired at the hepatic artery, portal vein, and vena cava inferior. The calculation of hydraulic input impedances enabled reduced Windkessel models to be fitted to the global hepatic perfusion properties as an intermediate step. Based on these Windkessel models, the extended electrical analog model was calibrated to the specific available liver. Results revealed that literature values of one of the critical model parameters (wall viscoelasticity) are a few orders of magnitude off, having important consequences for simulated (pulsatile) hemodynamic variables.
Conclusions:
A novel methodology, based on HMP experiments, signal processing and unconstrained nonlinear optimization was developed to validate and calibrate the liver-specific extended electrical model. Future research may focus on extending this approach to other applications (e.g. liver pathologies such as cirrhosis).
In this paper we present an electrical analog model for the hepatic arterial buffer response (HABR), an intrinsic regulation mechanism in the liver whereby the arterial flow counteracts the changes in portal venous flow. The model itself is a substantial simplification of a previously published model, with nonlinear arterial and portal resistors introduced to account for the dynamic HABR effects. We calibrate the baseline model using published hemodynamic data, and then perform a virtual portal occlusion simulation where the portal vein is half or fully occluded. The simulation results, which suggest that the increased arterial flow cannot fully compensate lost portal perfusion, are consistent with clinical reports and animal model findings. Since HABR functions in both the whole liver and liver graft after transplantation, we also simulate blood flow in a virtual right-lobe graft by adjusting the electronic component parameters in the electric circuit, and our model is able to reproduce the portal venous hyperperfusion and hepatic arterial hypoperfusion conditions due to the HABR effects.
The liver is a parenchyma which contains many vessels. They are composed of two inflow vessels: the portal vein and the hepatic artery, and one outflow system represented by the hepatic veins. We will see in the chapter most of the abnormalities and their consequences due to decrease or an increase of the blood flow of these vessels. Many illustrations will be provided with a special focus on CT findings with multiphasic images.
Previous studies have shown poor outcome after living-donor liver transplantation (LDLT) as a result of excessive portal venous pressure (PVP), excessive portal venous flow (PVF), or inadequate PVF. We investigated optimal portal venous circulation for liver graft function after LDLT in adult recipients retrospectively.
Between June 2003 and November 2004, 28 adult patients underwent LDLT in our institution. We modulated PVP under 20 mmHg in these 28 cases by performing a splenectomy (n=4) or splenorenal shunt (n=1). The PVF and PVP were measured at the end of the operation. Compliance was calculated by dividing PVF by PVP.
PVF and compliance showed a significant inverse correlation with peak billirubin levels after LDLT (r = -0.63: r=-0.60, P<0.01), and with peak international normalized ratio after LDLT (r=-0.41: r=-0.51, P<0.05). Compliance was higher in right-lobe graft with middle hepatic vein cases (148+/-27 ml/min/mmHg), and lower in left-lobe graft cases (119+/-50 ml/min/mmHg).
Liver graft function was better when PVF and graft compliance were higher and PVP was maintained under 20 mmHg.
It has been reported that 30-40% of patients with aortic stenosis are hypertensive. In such patients, the left ventricle faces a double (i.e. valvular and vascular) pressure overload, which results in subsequent wall volume hypertrophy. From a clinical standpoint, it is difficult to separate the respective contributions of aortic stenosis and systemic hypertension to left ventricular burden and patient's symptoms and thus to predict whether valve replacement would be beneficial. The objective of this theoretical study was therefore to investigate the relative effects of valvular and vascular afterloads on left ventricular hypertrophy. We used a ventricular-valvular-vascular mathematical model in combination with the Arts' model describing the myofiber stress. Left ventricular wall volume was computed for different aortic blood pressure levels and different degrees of aortic stenosis severity. Our simulations show that the presence of concomitant systemic hypertension has a major influence on the development of left ventricular hypertrophy in patients with aortic stenosis. These results also suggest that mild-to-moderate aortic stenosis has a minor impact on left ventricular wall volume when compared with hypertension. On the other hand, when aortic stenosis is severe, wall volume increases exponentially with increasing aortic stenosis severity and the impact of aortic stenosis on left ventricular hypertrophy becomes highly significant.
Subtotal hepatectomy in swine for studying small-for-size syndrome and portal inflow modulation: is it reliable?
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Clinical Biomechanics 73 (2020) 195-200