Predicting the risk of post-hepatectomy portal hypertension using a digital twin: A clinical proof of concept.


Journal

Journal of hepatology
ISSN: 1600-0641
Titre abrégé: J Hepatol
Pays: Netherlands
ID NLM: 8503886

Informations de publication

Date de publication:
03 2021
Historique:
received: 29 06 2020
revised: 25 10 2020
accepted: 28 10 2020
pubmed: 20 11 2020
medline: 21 1 2022
entrez: 19 11 2020
Statut: ppublish

Résumé

Despite improvements in medical and surgical techniques, post-hepatectomy liver failure (PHLF) remains the leading cause of postoperative death. High postoperative portal vein pressure (P 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 P 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 P 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. 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.

Sections du résumé

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 (P
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 P
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 P
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.

Identifiants

pubmed: 33212089
pii: S0168-8278(20)33761-2
doi: 10.1016/j.jhep.2020.10.036
pii:
doi:

Types de publication

Evaluation Study Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

661-669

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2020 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest The authors declare no conflicts of interest that pertain to this work. Please refer to the accompanying ICMJE disclosure forms for further details.

Auteurs

Nicolas Golse (N)

Department of Surgery, Paul-Brousse Hospital, Assistance Publique Hôpitaux de Paris, Centre Hépato-Biliaire, Villejuif, 94800, France; Université Paris-Saclay, INSERM, Physiopathogénèse et Traitement des Maladies du Foie, UMR-S 1193; INRIA, Centre de Recherche de Paris, 2 rue Simone Iff, Paris 75012, France. Electronic address: nicolas.golse@aphp.fr.

Florian Joly (F)

INRIA, Centre de Recherche de Paris, 2 rue Simone Iff, Paris 75012, France; Université de la Sorbonne, CNRS, Université de Paris, Laboratoire Jacques-Louis Lions (LJLL), F-75005 Paris, France.

Prisca Combari (P)

Department of Surgery, Paul-Brousse Hospital, Assistance Publique Hôpitaux de Paris, Centre Hépato-Biliaire, Villejuif, 94800, France.

Maïté Lewin (M)

Department of Radiology, Paul-Brousse Hospital, Assistance Publique Hôpitaux de Paris, Centre Hépato-Biliaire, Villejuif, 94800, France.

Quentin Nicolas (Q)

INRIA, Centre de Recherche de Paris, 2 rue Simone Iff, Paris 75012, France.

Chloe Audebert (C)

INRIA, Centre de Recherche de Paris, 2 rue Simone Iff, Paris 75012, France; Université de la Sorbonne, CNRS, Université de Paris, Laboratoire Jacques-Louis Lions (LJLL), F-75005 Paris, France; Université de la Sorbonne, CNRS, Institut de Biologie Paris-Seine (IBPS), Laboratoire de Biologie Computationnelle et Quantitative UMR 7238, F-75005 Paris, France.

Didier Samuel (D)

Department of Surgery, Paul-Brousse Hospital, Assistance Publique Hôpitaux de Paris, Centre Hépato-Biliaire, Villejuif, 94800, France; Université Paris-Saclay, INSERM, Physiopathogénèse et Traitement des Maladies du Foie, UMR-S 1193.

Marc-Antoine Allard (MA)

Department of Surgery, Paul-Brousse Hospital, Assistance Publique Hôpitaux de Paris, Centre Hépato-Biliaire, Villejuif, 94800, France; Université Paris-Saclay, INSERM, Physiopathogénèse et Traitement des Maladies du Foie, UMR-S 1193.

Antonio Sa Cunha (A)

Department of Surgery, Paul-Brousse Hospital, Assistance Publique Hôpitaux de Paris, Centre Hépato-Biliaire, Villejuif, 94800, France; Université Paris-Saclay, INSERM, Physiopathogénèse et Traitement des Maladies du Foie, UMR-S 1193.

Denis Castaing (D)

Department of Surgery, Paul-Brousse Hospital, Assistance Publique Hôpitaux de Paris, Centre Hépato-Biliaire, Villejuif, 94800, France; Université Paris-Saclay, INSERM, Physiopathogénèse et Traitement des Maladies du Foie, UMR-S 1193.

Daniel Cherqui (D)

Department of Surgery, Paul-Brousse Hospital, Assistance Publique Hôpitaux de Paris, Centre Hépato-Biliaire, Villejuif, 94800, France; Université Paris-Saclay, INSERM, Physiopathogénèse et Traitement des Maladies du Foie, UMR-S 1193.

René Adam (R)

Department of Surgery, Paul-Brousse Hospital, Assistance Publique Hôpitaux de Paris, Centre Hépato-Biliaire, Villejuif, 94800, France; INSERM, Unit 985, Villejuif, 94800, France.

Eric Vibert (E)

Department of Surgery, Paul-Brousse Hospital, Assistance Publique Hôpitaux de Paris, Centre Hépato-Biliaire, Villejuif, 94800, France; Université Paris-Saclay, INSERM, Physiopathogénèse et Traitement des Maladies du Foie, UMR-S 1193.

Irene E Vignon-Clementel (IE)

INRIA, Centre de Recherche de Paris, 2 rue Simone Iff, Paris 75012, France.

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