Hepatic vagal branch preservation vs. division during fundoplication: a narrative review

Introduction

The hepatic branch of the vagus nerve arises from the anterior branch of the vagus, traversing the lesser curvature and pars flaccida region to innervate the biliary tree and gallbladder. Its fibers primarily supply the hepatobiliary system including the liver, extrahepatic biliary ducts, gallbladder, and associated structures with additional projections reaching the pylorus, proximal duodenum, and pancreas. Its integrity has been implicated in gallbladder motility function, and bile secretion (1).

During laparoscopic fundoplication for gastroesophageal reflux disease (GERD), surgical exposure and crural dissection may place this branch at risk. Definitive guidelines regarding hepatic branch preservation (HBP) or hepatic branch division (HBD) during fundoplication are not established, and there is no international consensus on this issue (2,3). Consequently, surgeons may exercise their own discretion in preserving or dividing the hepatic vagal branch. Although HBD may facilitate crural exposure and inferior mediastinal dissection, its preservation might maintain gallbladder motility with a theoretically reduce risk of gallstone formation in the long-term risk of. However, outcome data from clinical series and meta-analysis are unconclusive (4,5).

Hence our intent was to describe the current evidence onto this topic comparing outcomes for HBP vs. HBD during antireflux surgery. We reviewed clinical reports to synthesize existing evidence, assess study quality, and identify gaps. We present this article in accordance with the Narrative Review reporting checklist (available at https://aoe.amegroups.com/article/view/10.21037/aoe-25-27/rc).

Methods

An extensive literature search was conducted by all authors (A.A., D.B., L.B.) to identify all English-written published series reporting data on the effect of HBP vs. HBD during laparoscopic fundoplication. PubMed, Scopus, Web of Science, Cochrane Library, and Google Scholar databases were consulted matching the terms “GERD” and “fundoplication” and “hepatic nerve” with the Boolean operators “AND” or “OR” until 10th September 2025. The search was completed by consulting the listed references of each article. Articles reporting data for HBP vs. HBD in surgical context different than fundoplication were excluded to reduced heterogeneity. All the articles, case reports, and case series were included in this narrative review while abstracts were excluded. Two authors (A.A., D.B.) independently extracted data from eligible studies (Table 1). From each report we extracted study design, patient selection, operative approach, how hepatic-branch handling was decided (randomized vs. surgeon preference), sample size (when reported), follow-up duration, outcomes measured [gallbladder ejection fraction (GEF), fasting volume, gallbladder emptying time (GET), laboratory tests, symptoms], and the main findings. Data were synthesized narratively because of heterogeneity in design, outcomes, measurement methods, and reporting; no meta-analysis was performed (6). Specific approval was not necessary for this narrative review. Informed consent was not necessary for the literature review.

Results

Overall, three studies published after 2000 were included in this narrative review (Table 2). All included papers reported data for patients suffering from pathologic GERD undergoing laparoscopic Nissen fundoplication with HBP or HBD. Overall, 83 patients were included in data synthesis; HBD was reported in 51.8%. The age of the patient population ranged from 21 to 73 years, the majority were males (69%), and the preoperative body mass index ranged from 21.4 to 27.6 kg/m². None of the included studies reported preoperative pathophysiological GERD assessment data with either endoscopy, swallow study, manometry or pH-impedance testing.

The initial study addressing this topic was conducted by Morton et al. in 2002 (5). This prospective pre/post investigation assessed 19 patients who underwent laparoscopic Nissen fundoplication, with a subset re-evaluated postoperatively using cholecystokinin-stimulated technetium hepatobiliary (CCK-HIDA) scans. The primary endpoint was gallbladder GEF. Follow-up data were available for 12 patients. No significant differences were found for GEF for HBP vs. HBD [64.2% vs. 53%; P=not significant (NS)]. Interestingly, the authors found that 58% of patients had abnormal preoperative GEF values, which normalized after surgery.

Purdy et al. conducted a retrospective single-center analysis involving 38 patients (1). The study utilized a consecutive cohort comparison design, wherein the surgical approach shifted from HBP to HBD at a predetermined timepoint. Long-term follow-up (4–9 years) was obtained from a subset of participants using questionnaires and ultrasound. Outcomes included clinical symptoms, liver enzyme levels, plasma amylase concentrations, fasting gallbladder volume, and GEF. No differences were found in term of GEF (72.4% vs. 72%) however, HBD was associated with a trend toward reduced fasting gallbladder volumes (23.2 vs. 18.1 mL) and a modest increase in plasma amylase (46 vs. 58). The authors concluded that although decreased fasting gallbladder volume may represent a risk factor for symptomatic choledocholithiasis, its influence on cholelithiasis development and the broader clinical implications remain uncertain.

In 2013, Ozdogan et al. published the first and, to date, only clinical trial addressing this specific topic (7). The study enrolled 40 patients who were randomly assigned via sequentially numbered envelopes to either HBP or HBD during laparoscopic Nissen fundoplication. Although classified as a randomized controlled trial, the authors did not conduct a formal power analysis, nor did they provide details regarding postoperative blinding assessment. Of the initial cohort, 33 patients completed a 3-month follow-up evaluation. Outcomes assessed included fasting gallbladder volume (via ultrasound), GEF (measured by scintigraphy), and GET. The results demonstrated that both GEF and fasting volumes were similar between groups; however, HBD was associated with a significantly prolonged GET (24.7 vs. 34.7 minutes; P=0.02). The authors noted that while these early physiological changes were subclinical, the extended GET observed in HBD could pose a theoretical risk for increased long-term gallstone formation. Notably, baseline (preoperative) data were not collected, leaving the possibility that these findings may also reflect preexisting conditions. None of the included study provided clinical endpoints for symptomatic cholelithiasis or cholecystectomy rates.

Discussion

The surgical management of hiatus hernia and GERD primarily aims to achieve two objectives. The first is the proper relocation of the lower esophageal sphincter (LES) into an intra-abdominal position, which necessitates thorough dissection of the distal esophagus. The second goal is the repair of the hiatal defect to reconstruct the anti-reflux barrier and gastroesophageal junction mucosal flap valve (8,9). Key steps of a laparoscopic fundoplication include the dissection of the lesser omentum, exposure of the diaphragmatic crura, and extensive mediastinal dissection to obtain a minimum of 3 cm of intra-abdominal esophagus without traction, followed by creation of the fundoplication to increase LES pressure (10,11). Division of the hepatic branch of the vagus nerve may facilitate dissection along the lesser curvature and improve access to the right crus of the diaphragm, thereby aiding mediastinal esophageal mobilization. Nevertheless, data regarding the consequences of sacrificing this nerve on gallbladder function and gastrointestinal symptoms after fundoplication remain limited.

Gallbladder function is regulated by a complex interplay of hormonal peptides and neural components, including the hypothalamus, vagal nerves, sympathetic trunk, and right semilunar ganglion. Hormonal activation may occur through stimulation by autonomic nerves or directly via the gallbladder wall (1). Sympathetic innervation to the gallbladder and cystic duct is provided by the splanchnic nerves (nn. splanchnici, T8–9), while parasympathetic innervation arises from the vagus nerve (n. vagus, Cr10) with branches from both the anterior and posterior vagal trunk (7). These fibers initially form the celiac plexus before reaching the gallbladder through the hepatic plexus, which surrounds the ascending hepatic artery. The anterior division of the hepatic plexus supplies the cystic and hepatic ducts, whereas the posterior division innervates the choledochus. Sympathetic stimulation induces contraction of the sphincter of Oddi, facilitating bile accumulation within the gallbladder. Conversely, parasympathetic stimulation contracts the gallbladder and bile ducts. Parasympathetic activity promotes increased bile secretion, while sympathetic activity reduces bile secretion (12). It has been well established that truncal vagotomy negatively impacts gallbladder function. Johnson and Boyden were among the first to report that the gallbladder becomes dilated following truncal vagotomy (13). Further, in a prior study on hepatobiliary denervation, Csendes et al. indicated that selective hepatic vagotomy during open antireflux surgery results in gallbladder dilatation and a higher risk of cholelithiasis (14). The authors conducted a comparison between 26 subjects with normal gallbladders, who were re-evaluated after 3 to 5 years, and 22 patients diagnosed with GERD and esophagitis who underwent open posterior gastropexy combined with selective hepatic vagotomy. All participants underwent oral cholecystograms before and after surgery, revealing a lower incidence of gallstones in the non-operated group compared to the operated group (7.7% vs. 41%). While these findings are noteworthy, the outcome comparison lacks robustness due to the evaluation of two distinctly different patient populations.

Identification and preservation of the posterior vagus nerve is mandatory during fundoplication and is recognized as standard of care (2,3). However, the optimal management of the hepatic branch of the anterior vagus nerve remains unclear, with no definitive guidelines currently available. A recent systematic review evaluated the effects of HBD vs. HBP in upper gastrointestinal surgeries. HBP was reported to be associated with more favorable long-term outcomes, including reduced appetite loss, lower incidence of gallstone disease, decreased reflux symptoms, improved glycemic control, and a likely reduction in both esophagitis and dumping syndrome. However, conclusions were limited by the inclusion of various surgical techniques, including fundoplication, sleeve gastrectomy, subtotal gastrectomy, and total gastrectomy thus introducing significant heterogeneity. In our review, in attempt to reduce heterogeneity, we mainly focused on laparoscopic antireflux surgery for GERD. Morton et al. (5) evaluated the impact of HBD on gallbladder function using scintigraphy in the early postoperative period among 12 patients that underwent LNF. The authors found that HBD resulted in decreased gallbladder volume but did not alter GEF in the early postoperative phase. In a subsequent retrospective analysis, Purdy et al. (1) studied 38 patients who underwent LNF for GERD with HBP vs. HBD. Gallbladder motor function, assessed via ultrasound, revealed no significant postoperative gallbladder dilation, though mean gallbladder volume was reduced. These results are consistent with those of Morton et al. (5), and the authors suggested that preservation of the antral and prepyloric branches of the anterior vagus nerve along with the preservation of parasympathetic fibers originating from the posterior vagus may play a more pivotal and probably vicariant role in maintaining postoperative gallbladder function than preservation of the hepatic branch. Finally, the study by Ozdogan et al. (7) showed no statistically significant difference between the groups regarding the ultrasound (US)-determined fasting gallbladder volumes and GEF. The authors concluded a significantly higher GET (34.7 vs. 24.7 minutes) in patients that underwent selective anterior vagotomy. The exact clinical significance of such delays remains unclear, as gallstone formation is influenced by multiple factors. While it could be hypothesized that prolonged GET may promote bile stasis and subsequent crystal formation and aggregation, the impact of a 10-minute difference in emptying time appears unlikely to be decisive for gallstone development, even over the long term. Additionally, various other predisposing factors including dietary habits, cholesterol levels, bile salts, bilirubin supersaturation, excess mucin secretion, and inflammatory factors may play a more substantial role in stone formation. These variables were not addressed in the included studies; therefore, it is not possible to draw firm conclusions regarding whether an average 10-minute prolongation in GET affects gallstone formation. Notably, Morton et al. unexpectedly reported that nearly 60% of GERD patients exhibited preoperative baseline gallbladder motor dysfunction (5). Consequently, any postoperative evaluation of gallbladder function should take into account pre-existing conditions, which were not considered in the studies by Purdy et al. (1) and Ozdogan et al. (7).

Preserving the posterior and anterior vagus nerves remains a crucial step during fundoplication (15,16). However, the precise function of the hepatic branch of the anterior vagus nerve in pyloric regulation is not yet clearly understood. The influence of HBD on postoperative fundoplication outcomes including delayed gastric emptying, gastroparesis, gas bloat, and diarrhea remains uncertain. Although some studies suggest that hepatic branch collaterals play a significant role in maintaining proper pyloric homeostasis, it is widely recognized that pyloric function predominantly depends on the preservation of parasympathetic innervation from the Latarjet fibers (descending along the lesser curvature), parasympathetic fibers originating from the posterior vagus nerve, and intrinsic innervation from the myenteric plexus. Since the three studies reviewed primarily addressed gallbladder function, there was a lack of consistent data reporting on the resolution of GERD or gastrointestinal post-fundoplication symptoms when comparing HBP vs. HBD. Hence, conclusive evidence regarding the impact of HBP vs. HBD on post-fundoplication symptoms has yet to be established.

Given the lack of consistent short-term symptomatic harm, routine division of the hepatic vagal branch should not be categorically discouraged. However, considering the physiological changes discussed, it is appropriate for surgeons to evaluate individual patient factors such as preexisting gallbladder disease, the presence of gallstones or biliary symptoms, patient age, and baseline gallbladder function when deciding on HBP (2). Where technically feasible and not compromising fundoplication or esophageal mediastinal dissection, HBP may be justified; nonetheless, current evidence does not warrant a universal change in standard operative practice.

Limitations

Current evidence remains constrained by a limited number of comparative studies, with only a single randomized trial characterized by a small, likely underpowered sample size. This is further exacerbated by heterogeneous outcome measures and timing, reflecting variability in imaging modalities and protocols, as well as the absence of standardized measurement or blinded assessment in numerous reports. Furthermore, there is a paucity of long-term outcome data, with insufficient robust evidence addressing downstream clinical events such as gallstone formation and cholecystectomy. Additionally, the potential for publication bias exists, given that small negative or null studies may be underrepresented in the literature.

Conclusions

Current clinical evidence directly comparing HBP vs. HBD during fundoplication is sparse and highly heterogeneous. Short-term symptomatic outcomes appear similar across small series, but physiologic changes have been reported after division. The real clinical significance of these physiologic changes and their impact on gallstone formation remain unclear. Well designed and sufficiently powered multicenter prospective studies with extended follow-up, utilizing standardized physiologic assessments and clinical confirmation of cholelithiasis, are essential for informing surgical practice.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://aoe.amegroups.com/article/view/10.21037/aoe-25-27/rc

Peer Review File: Available at https://aoe.amegroups.com/article/view/10.21037/aoe-25-27/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://aoe.amegroups.com/article/view/10.21037/aoe-25-27/coif). L.B. serves as an unpaid editorial board member of Annals of Esophagus from October 2025 to September 2027. A.A. serves as an unpaid editorial board member of Annals of Esophagus from September 2025 to December 2027. The other author has no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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