Management of major complications after hepatectomy

The incidence of biliary leakage after hepatectomy remains controversial, ranging from 4 to 17% [6‐9]. It is defined by the ISGLS as a bilirubin concentration in the drain fluid ≥ three times the serum bilirubin concentration on the third postoperative day or later or as the necessity of intervention [10]. Biloma is defined as well-demarcated extra-biliary bile collection; however, the term is also used to describe any well-circumscribed intraabdominal collection of bile external to the biliary tract. Its contents are typically greenish yellow, although secondary infection with contents of blood and exudate may occur [11]. Encapsulation of the collection often develops due to the inflammatory response and fibrosis [12].

Large retrospective analyses have demonstrated that the most significant risk factors for bile leakage include repeat hepatectomy, a cut surface area of ≥ 57.5 cm², intraoperative blood loss of ≥ 775 ml, and an operation time of ≥ 300 min [8, 13]. Bile leakage is significantly associated with prolonged intensive care and hospital stay and mortality; however, no correlation of mortality with the severity of bile leakage was found [8]. The grading system of bile leakage as proposed by the ISGLS is shown in Table 1 [10].

There is evidence that certain intraoperative strategies such as reduction of the duration of Pringle maneuvers und performing the white test with biliary injected fat emulsion solution might reduce the risk of biliary leaks, especially after major and complex resections [14, 15]. Furthermore, in selected cases or after bile leak repair, the use of T‑tube drainages might reduce clinically relevant bile leakage [16].

Biloma might be asymptomatic and discovered incidentally. Most commonly, bilomas are located in the right upper quadrant, either in the right subphrenic or subhepatic region. Clinical symptoms include abdominal fullness and pain, nausea, vomiting, fever, and—in cases of external compression of the common bile duct—jaundice. In severe cases, bile leakage might cause biliary ascites and may lead to peritonitis and septic shock [12]. Figure 1 illustrates the various types of bile duct injuries. [17].

If bile leakage is suspected, further imaging with magnetic resonance cholangiopancreatography (MRCP) is indicated. The location and classification of leakage defines further management. The most common cause is transection of a distal bile duct within the liver remnant, followed by leakage at the bilioenteric anastomosis and iatrogenic surgical injury. The primary therapeutic approach is endoscopic retrograde cholangiopancreatography (ERCP), followed by percutaneous transhepatic cholangiography and drainage (PTCD), especially in cases of disconnected bile ducts where ERCP is not feasible. Surgical revision should be considered only as a last resort [18].

The efficacy of endoscopic biliary decompression in post-cholecystectomy biliary leakage has been reported at 87–100% [19]. Despite that, after major hepatic surgery, one of the major limitations in the endoscopic management of complications after hepatectomy is the altered anatomy after Roux-en‑Y bilioenteric reconstruction; therefore, percutaneous approaches have shown higher technical success rates. Disadvantages of external drainage include lower patient-reported quality of life and a relevant risk of persistent percutaneous biliary fistulas. Kokas et al. and Braunwarth et al. have identified perihilar tumor resection with bilioenteric reconstruction as a major risk factor for postoperative (anastomotic) bile leak. Patients with advanced comorbidities (ASA 3), elevated preoperative bilirubin levels, nondilated bile ducts, and cholangitis are associated with a higher leak rate [20, 21].

Current guidelines recommend conservative management of bile leakage if intraperitoneal drainages were placed during surgery, unless the patient exhibits high-output leakages or biliary peritonitis. According to the ISGLS criteria, a grade B bile leak is defined as “bile leak requiring treatment other than relaparotomy” or persistent drain output for more than a week [22]. Drainage output >100 ml on postoperative day 10 has been shown to be an independent predictor of conservative management failure [23]. In these clinical scenarios, endoscopic or percutaneous intervention is generally indicated. In cases of biliary peritonitis (grade C), reoperation is typically required.

Postoperative biliary interventions—whether endoscopic or percutaneous—always mandate a cholangiogram or fistulography to identify the site of the leak and distinguish between leakage from the biliary tree and from peripheral bile ducts, commonly at the resection surface. In biliary tree leaks, decompression alone is usually sufficient [20]. Complete ruptures with a disconnected duct should be bridged with a stent. If bridging is anatomically impossible, endoscopic drainage near the leak site is recommended to decompress biliary pressure [20].

Murata et al. demonstrated the efficacy and safety of endoscopic transpapillary drainage for postoperative biliary leakage by placing plastic stents, fully covered metal stents, or nasobiliary drainages. Body mass index was found to be a useful predictor of bile leaks refractory to endoscopic management [24]. Head-to-head studies comparing the endoscopic drainage strategies in the setting of major hepatic surgery are lacking. The selection of plastic, fully covered metal stents, or nasobiliary drainage is widely based on individual factors like the leakage site, common bile duct diameter, and personnel experience. Therefore, in small bile ducts or peripheral leaks, plastic stents are commonly used for bridging the papilla of Vater. The necessary mean duration of biliary stenting is 2–3 months; fully covered metal stents provide longer patency. Most available data on this topic focus on bile leakage after cholecystectomy, preferring fully covered metal stents over plastic stents for refractory bile leaks after cholecystectomy [25, 26]. Prospective head-to-head studies on stenting strategies are warranted in the future.

In clinical practice, biliary plastic stents are widely used for post-hepatectomy leakage. Data show an overall early clinical success rate of endoscopic drainage of 45% within a period of 28 days from primary endoscopic intervention to removal of all external drains (with regard to the altered anatomy). The post-ERCP complication rate was 9.5% for cholangitis, 5% for pancreatitis, and 5% for bleeding. The main proportion of leaks were localized intrahepatic and were treated with a near-leakage stent position [24].

Another study from Italy demonstrated the safety and efficacy of endoscopic management of post-surgery bile leaks via ERCP. Success rates of 96–100% for first or secondary biliary branch leaks and of 67% for main biliary duct leaks were reported. Use of a leak-bridging stent was associated with a higher probability of achieving clinical success compared to near-leak stenting (91% vs 53%). In this study, only 14% of patients had undergone hepatectomy (the others cholecystectomy, liver transplantation, and resection of the gall bladder bed) [27].

In general, if a non-anastomotic bile leak occurs after combined liver resection and bilioenteric reconstruction, evaluation of the anastomosis to rule out a stricture is mandatory, as approximately 30% may present with a concomitant stenosis [27].

A challenging situation arises when dealing with disconnected bile ducts. Studies propose ethanol insertion into the bile duct of disconnected ducts without communication with the biliary tree, although this strategy carries the risk of bile duct strictures [28]. This procedure should only be applied based on individual case evaluations after a multidisciplinary team discussion.

To manage chronic biloma secondary to bile leakage, advancements in interventional endosonography have enabled transmural transgastric drainage (EUS-TD) as an alternative for patients with biloma and altered postoperative anatomy. Lorenzo et al. showed a clinical success rate of 75%, with a 13% rate of procedure-related adverse events. In this study, transmural drainage was performed using direct puncture with a 19 G needle and a double-pigtail stent [29]. A case report has demonstrated the efficacy of novel lumen-apposing metal stents for this particular indication [30]. Despite widespread use of LAMS drainage in other indications like pancreatic pseudocysts or walled-off necrosis, data on safety and efficacy in the management of biloma are lacking—one major benefit may be avoidance of the risk of persisting percutaneous biliary fistulas, which can occur after percutaneous transhepatic approaches. Figure 2 illustrates an example of successful transgastric drainage for biloma.

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Due to the limited availability of randomized data on this topic, most existing data are derived from single-center retrospective analyses. We recommend an endoscopy-first strategy if feasible and a step-up procedure for patients with Roux-en‑Y reconstruction. Approximately 50% of patients with bile leaks following hepatectomy require a multidisciplinary approach involving both endoscopic and percutaneous drainage methods. For initial biloma drainage in patients with altered anatomy, EUS-TD is preferred. There is a lack of prognostic factors for failure of endoscopic management, with only BMI > 22 kg/m² appearing to have predictive value [24].

The reported incidence of PHH ranges from 1 to 8% and varies significantly across the literature. The ISGLS defines PHH as a postoperative drop in hemoglobin levels greater than 3 g/dL compared to the postoperative baseline, accompanied by the need of further intervention depending on the severity grade. Post-hepatectomy hemorrhage is classified into three grades (grades A, B, C) based on clinical symptoms and the grade directs subsequent clinical management [31]. Grading of PHH is presented in Table 2.

Identifying the bleeding site with contrast-enhanced multiphasic computed tomography (CECT) is recommended [2]. In most cases, PHH originates from the cut surface of the liver remnant and requires surgical management. However, if a localized, circumscribed arterial bleeding site is identified, immediate super-selective endovascular embolization should be considered [2, 18, 31]. Patient management for postoperative hemorrhage is shown in Fig 3 [2].

As the liver plays a key role in maintaining hemostasis, hepatic dysfunction may lead to coagulopathy due to impaired synthesis of clotting factors, inhibitors, and regulatory proteins. Major hepatic resection, massive transfusion, prolonged vascular occlusion, and underlying hepatic disease have been identified as risk factors for abnormal postoperative coagulation profiles and PHH [32].

A retrospective study highlighted the role of interventional radiology (IR) and embolization in management of PHH. In 88.5%, technical success with IR could be achieved even though successful hemostasis did not directly lead to better survival, with a high mortality rate of 26.2%. The study suggests this might be due to the complexity of the initial surgery and complications following embolization, such as liver abscess, sepsis, or reduced arterial flow and impaired liver function [33].

Another retrospective analysis investigating morbidity and mortality after relaparotomy for PHH highlights the importance of early recognition and immediate treatment. In patients undergoing late surgery (> 6h after the index operation), mortality was significantly higher. This study suggests that relaparotomy should be performed if hemostasis with conservative agents cannot be reached. Hemodynamic instability increases injury to the remnant liver, and continued bleeding results in consumption of clotting factors and subsequent coagulopathy. Nonetheless, mortality in patients undergoing relaparotomy for PHH was high, with the leading cause of death being acute liver failure. Preventive measures such as avoiding hepatic vascular occlusion, preserving function of the remnant liver, and active management of acute liver failure should be carried out [34].

Most gastrointestinal bleeding results from stress ulcers, anastomotic bleeding after Y‑Roux reconstruction, portal hypertension, or congestion due to secondary portal hypertension. If intraluminal bleeding is suspected, endoscopy is the first-line treatment. In cases of non-intraluminal bleeding, CECT should be performed for further assessment [2].

Biliary tract hemorrhage is most commonly caused by iatrogenic injury during surgery, followed by trauma from T‑tube placement, mucosal erosion, ulcers, and inflammation. If active bleeding is detected on CECT, treatment options should be discussed based on the available expertise, with endovascular or surgical management being considered. In cases of uncontrolled hemorrhagic shock, surgical intervention is the treatment of choice [2, 18, 35].

Physiological functions of the liver include protein synthesis, bile production and endocrine control, detoxification, gluconeogenesis and other metabolic pathways, and blood volume regulation [36, 37]. Post-hepatectomy liver failure (PHLF) remains one of the most significant complications following liver resection, with an incidence of 10% [38] and a mortality rate up to 70% [39, 40], with the highest mortality of 25% after the first postoperative month [41]. Post-hepatectomy liver failure is the single most prevalent cause of 90-day fatality after major hepatectomy [42]. The incidence and risk of developing PHLF depends on patient-, liver-, and surgery-related risk factors. Patient-related risk factors include several anthropometric measures like male sex [41], comorbidities like hepatocellular carcinoma (HCC) [43], and sepsis [44]. Liver-related factors include steatosis, neoadjuvant chemotherapy, cholestasis, and portal hypertension [45‐48]. A selection of surgery-related factors include the size and volume of the future liver remnant (FLR), intraoperative blood loss, major hepatectomy (≥ 3 segments removed), and surgical techniques like intermittent inflow occlusion or total vascular occlusion (Pringle maneuver) due to ischemia–reperfusion injury [49‐52]. Table 3 illustrates the PHLF grading according to the ISGLS [38].

The pathophysiological background to PHLF is complex and primarily results from molecular disruptions due to a sudden lack of hepatocytes. This cellular deficit leads to an energy deficiency, which in turn stimulates mitotic activity, resulting in the release of nitric oxide to promote hepatocyte proliferation [53‐55]. Postoperatively increased portal vein flow in comparison to the residual liver volume leads to vascular shear stress and raised intravascular pressure, which may be followed by a reduction in liver cell regenerative potential [56]. These selected pathophysiological pathways have been renamed “small-for-flow” syndrome (SFFS) in analogy to “small-for-size” syndrome (SFSS), a prevalent complication in patients with liver failure after (orthotopic) liver transplantation (OLT) [57].

There is a lack of a definition of PHLF, with symptoms like hyperbilirubinemia, uncontrolled ascites, and prolonged hospitalization in the context of hepatic functional insufficiency being the most frequently described diagnostic criteria [58]. Monitoring of lactate levels may be useful in the prediction of peri- and postoperative complications [59]. The current clinical grading of PHLF includes three categories (A–C) based on the severity of liver dysfunction and the need of invasive therapy [40, 60]. Insufficiency can be objectified by measuring the international normalized ratio (INR) and postoperative serum bilirubin concentration on or after postoperative day 5. Additionally, the ratio of remnant liver volume to body surface area (RLV/BSA ratio) can be used as a risk factor for developing PHLF [58]. Grade A requires no invasive therapy, grade B requires intensified individualized postoperative clinical management without invasive therapy, and grade C is defined by the indication for invasive therapy [40].

Small experimental studies to pre-assess the postoperative outcome of liver function in patients with liver cirrhosis using the hepatic venous pressure gradient (HVPG) have been conducted. These studies showed a correlation between increased HVPG and the PHLF risk. Indirect signs of portal hypertension (esophageal varices, splenomegaly, thrombocytopenia) did not show significant correlation to the rate of PHLF in all studies performed [61].

Further, more available preventive options for PHLF include anatomical, functional, and laboratory preoperative risk calculations. The risk of PHLF indirectly correlates with the postoperative organ size—a smaller liver remnant volume shows a greater risk of PHLF development [49]. Pre-interventional laboratory assessments for liver function include the aspartate aminotransferase/platelet ratio index (APRI) and the albumin–bilirubin grade (ALBI)—both have been validated for calculative predictions of patient-dependent liver synthesis [62]. Another noninvasive liver function test named FIB‑4 combines platelet count, transaminase levels, and age [63]. Tian et al. combined the ALBI score with FIB‑4 to maximize the value of laboratory preassessment to predict postoperative liver function [64]. The MELD 3.0 score generally reflects current liver synthesis and can be used both pre- and postoperatively to quantitatively depict the liver-related outcome, while direct postoperative prognostication using the MELD 3.0 score requires further research and validation [65].

Pre-procedural measurement of the liver volume using three-dimensional reconstruction to estimate the pre- and postoperative liver volume (future liver remnant, FLR) and mass is the standard anatomy-based PHLF risk evaluation [66]. The FLR includes the ratio of the remnant liver volume (RLV) and the total functioning liver volume (TFLV) [67].

Established functional preoperative evaluations of liver function include perfusion- and secretion-based tests like indocyanine green (ICG) clearance as well as metabolism-based analyses like the 13C-methacetin-breath (LiMAx) test, combined with volumetric evaluation [68, 69]. Indocyanine green is injected intravenously and secreted into bile; hence, this technique might be impaired by cholestatic processes [70]. The LiMAx test uses the CYP1A2 hepatic metabolism of intravenously injected 13C-methacetin, measuring exhaled 13CO₂ as a direct parameter of hepatic enzyme function. As tumor tissue usually shows very low CYP1A2 activity, LiMAx testing allows calculation of functioning liver tissue [69].

Treatment of PHLF is based on supporting organ function. Conservative options are limited to supportive treatment: enhanced recovery after surgery (ERAS) concepts have been shown to reduce the risk of postoperative infections [71]. Preemptive antibiotic treatment is not recommended and did not show a reduction of the rate of PHLF and mortality in patients undergoing hepatectomy; however, when PHLF is detected, antimicrobial treatment is advised, as infections and sepsis often occur in PHLF and increase the risk of adverse events and outcomes [72]. Lactulose is a common medication in the management of hepatic encephalopathy in patients with acute or chronic liver failure [73]. L‑ornithine L‑aspartate (LOLA) has been established for hepatic encephalopathy due to its stimulation of residual hepatocyte ammonia removal and promotion of extrahepatic ammonia detoxification; however, its suitability for PHLF encephalopathy needs to be proven [74]. Rifaximin acts as a reducing factor for gut production of ammonia and has its role in the treatment of hepatic encephalopathy [75]; evidence of efficacy in the setting of post-hepatectomy liver failure is, however, limited.

Future treatment options may include stem cell transplantation, which has not yet been approved in a clinical treatment setting [76, 77]. Extracorporeal liver support systems like the molecular adsorbent circulating system (MARS) to remove water-soluble and albumin-bound toxins as a bridge-to-transplant option have not yet shown a positive impact on survival in acute or chronic liver failure [78, 79]. Despite singular prospective studies proving the safety and viability of MARS in the setting of PHLF [80], Sparrelid et al. did not show a survival benefit of routine use of MARS in patients with PHLF [81]. Future extracorporeal treatment options may include bioartificial liver support systems, which have not yet been established in clinical routine [82]. Liver transplantation is the only definitive treatment option in patients with PHLF. However, considering organ shortages, evaluation of post-transplant benefit remains crucial in the selection of qualified patients [83].

Definition, early detection and treatment of PHLF in both non-cirrhotic and cirrhotic patients remain a significant challenge in modern hepatobiliary surgery. Careful preoperative patient selection and close postoperative clinical and laboratory monitoring should be considered central steps in determining the eligibility for liver resection.

Intrahepatic and perihepatic abscess (IPHA) is a severe but understudied complication after hepatectomy. The incidence was reported as 3.3% in a large multicenter cohort study from China. In this study, obesity, diabetes, portal hypertension, major hepatectomy, open surgery, and intraoperative diaphragmatic incision were identified as independent risk factors [84]. Intrahepatic and perihepatic abscess usually results from an intraabdominal fluid collection or a bile leak. The clinical features include fever, right upper quadrant pain, septicemia, and in some cases pleural effusion and/or pulmonary atelectasis [18].

If IPHA is clinically or serologically suspected, the diagnosis should be confirmed via CECT. Postoperative IPHA may be managed conservatively if its maximum diameter is between 3 and 5 cm; however, needle aspiration can help to identify the causative organism, determine antibiotic resistance, and rule out biloma. Larger collections should be treated with CT- or ultrasound-guided percutaneous drainage placement. Surgical intervention is rarely necessary. If bile is present in the collection, biliary disease or leakage should be ruled out using MRCP [85].

Recent advancements in laparoscopy and robotic surgery have led to a significant increase in minimally invasive liver surgeries. Despite previous concerns regarding oncological outcome and postoperative complications, minimally invasive hepatectomy is now well established and can be performed safely by experienced surgeons [86, 87].

In a review by Maegawa et al. with a total of 24,150 hepatectomies, the impact of frailty and MIS on postoperative complications was investigated. A total of 19,772 operations were performed open, 529 robotically, and 3849 laparoscopically. Severe postoperative complications (Clavien–Dindo IV) were less frequent in MIS compared to open procedures (OH), both for frail and non-frail patients. A reduced incidence of bile leaks and postoperative liver failure in MIS was observed in both frail and non-frail patients [88].

Minimally invasive hepatectomy for hepatocellular carcinoma patients resulted in fewer complications (32 vs. 54%) than open hepatectomy, even with a lower rate of postoperative liver failure (0 vs. 7%) [89].

Another study reviewed post-hepatectomy bile leak incidences. Open hepatectomy had a higher incidence (11.4%) compared to robotic hepatectomy (5.4%), while there was no difference between robotic and laparoscopic hepatectomy (5.4 vs. 5.3%) [90].

However, a recently published review showed no major difference in the incidence of complications between laparoscopic and open surgery for minor complications classified as Clavien–Dindo I and II (29.5 vs. 30.7%) or for major complications Clavien–Dindo > IIIA (14.5 vs. 16.9%), although the time to recovery and length of stay was shorter in the laparoscopic group [91].

Currently, no clear advantages of robotic surgery over laparoscopy in liver surgery have been prospectively demonstrated, which is essential considering the high costs associated with robotic technology [92, 93]. However, retrospective analyses consistently indicate that the benefits of laparoscopic liver surgery can be transferred to robotic techniques. A retrospective cohort study involving 10,075 patients who underwent liver resection at 34 hepatobiliary centers between 2009 and 2021 compared the outcomes of laparoscopic liver surgery (LLS; n = 1505) and robotic liver surgery (RLS; n = 1505). The study included minor and major resections. Robotic liver surgery was associated with higher rates of textbook outcome in liver surgery (TOLS; Table 4; P < 0.001) and TOLS+ (P = 0.026), fewer Pringle maneuvers (P < 0.001), reduced blood loss (P < 0.001), lower transfusion rates (P = 0.003), a lower conversion rate (P < 0.001), lower overall morbidity (P < 0.001), and shorter operative times (P = 0.015). In subgroup analyses, RLS showed a trend toward better TOLS rates for minor resections in posterior–superior segments (P = 0.184) and for major resections (P = 0.086) [94]. Minimally invasive surgery carries a risk of gas embolism due to the necessarily increased intraperitoneal pressure. In a randomized controlled trial with 141 patients, Luo et al. showed advantages of lowering intraperitoneal pressure from 15 to 10 mm Hg, leading to fewer severe gas embolisms (P = 0.003), fewer abrupt decreases in end-tidal carbon dioxide partial pressure, shorter severe gas embolism duration, less peripheral oxygen desaturation, and fewer increases in heart rate. Patients required less fluid administration and fewer vasoactive medications [95]. Lymph node harvest may be higher in robotic surgery compared to laparoscopic and open surgery. Aside from this, no significant differences were observed in short- or long-term outcomes [96].

Several difficulty scoring systems have been established for minimally invasive hepatectomy to guide training and clinical implementation [97]. The IWATE criteria are used to grade MIH by difficulty. Labadie et al. showed in a retrospective review including 225 robotic liver resections that most complications after robotic liver resection were directly correlated to advanced or expert-level resections according to the IWATE criteria [98]. The TAMPA difficulty score was specifically developed for robotic liver resections, taking into account tumor size and location, resection volume, portal lymphadenectomy, and the need for biliary resection and reconstruction. Sucandy et al. could show an impact of the difficulty level on postoperative mortality and morbidity; however, further prospective studies are necessary to validate these results [99].

The first ERAS guidelines for liver surgery were published in 2016 [102]. A meta-analysis of seven randomized controlled trials (RCTs) by Zhao et al. in 2017 showed that the ERAS protocol reduced postoperative complications, shortened the length of stay (LOS), and improved gastrointestinal motility (described as time to first flatus) in both open and laparoscopic liver surgery [103, 104]. Although LOS is easy to measure, it may not be an ideal parameter for assessing protocol success. In general, quality of life, physical performance, and early acceptance of adjuvant chemotherapy seem to be better outcome measures [105]. The implementation of ERAS has been particularly effective in reducing non-surgical complications and expediting functional recovery [106].

The 2022 update of the ERAS Society recommendations for perioperative care in liver surgery further consolidated the best available evidence to standardize patient management. The 25 recommendations, established through a modified Delphi method, emphasized high evidence and strong recommendation levels specifically for preoperative smoking and alcohol cessation, preoperative nutrition, analgesia, wound catheter and transversus abdominis TAP block, prophylactic nasogastric intubation, prophylactic abdominal drainage, early postoperative oral intake, glycemic control, PONV prophylaxis, and fluid management [107]. High compliance with ERAS pathways has been associated with improved postoperative outcomes.

A recent study published in 2025 by Oehring et al., which included 1049 patients following the 2022 ERAS Society recommendations, demonstrated a significant reduction in general complications [108]. Specifically, while no significant differences were observed in surgery-related complications, general (non-surgical) complications decreased from 27.6 to 16.3% (P = 0.033). This reduction was mainly driven by a decline in infection-associated complications, such as wound and urinary tract infections. Although the incidence of deep venous thrombosis showed a slight trend towards reduction in the ERAS group, the difference was not statistically significant [108]. In contrast, ERAS protocols have no positive impact on liver-specific complications. Patients classified as ASA ≥ 3 or with major resections are independently associated with ERAS failure [109]. Consequently, future refinement is required to address the needs of high-risk patients regarding surgery-related complications.

The findings supporting the ERAS concept and dedicated pre- and rehabilitation programs underscore the importance of integrating surgery into a holistic perioperative strategy to further minimize postoperative complications [110, 111].

Centralization plays a pivotal role in optimizing care and outcomes for patients planned for hepatectomies, especially regarding postoperative mortality and failure-to-rescue (FTR) rates, reflecting the healthcare system’s ability to adequately recognize and manage complications [112]. Hospital volume has a significant impact on FTR rates [113, 114], but also surgeon volume contributes to beneficial effects on outcomes [115]. Magnin et al. demonstrated that > 25 hepatic resections are needed to reduce in-hospital mortality and FTR, particularly regarding PHLF, biliary, and vascular complications, despite an overall higher postoperative complication rate in high-volume centers [116]. Successful management of postoperative complications depends on factors such as standardized operating procedures, early detection protocols, 24/7 availability of interventional expertise (radiology, endoscopy), and trained intensive care unit/postoperative recovery units. Patient selection and prehabilitation may contribute to improved FTR rates and reduced mortality [113].