Predictors of Long-Term Rebleeding Risk in Cirrhotic Patients Undergoing Esophagogastric Devascularization and Splenectomy: Impact of Portal Vein Thrombosis and Hemoglobin Levels

Abstract

Background

Esophagogastric devascularization and splenectomy (EGDS) is widely used to treat patients with portal hypertension in China. This study aimed to determine risk factors that increase risk of rebleeding after EGDS and evaluate the effect of portal vein thrombosis (PVT) on rebleeding rates after EGDS.

Material/Methods

Clinical data of patients with cirrhosis (n=138) who underwent EGDS between December 2010 and January 2016 were retrospectively analyzed. Patients were assigned to rebleeding or non-rebleeding groups and followed up. Univariate and multivariate Cox regression analyses identified the independent predictors of 3-year and 5-year rebleeding.

Results

A total of 138 consecutive patients who underwent EGDS and met the inclusion criteria were enrolled. Total bilirubin (HR: 2.392, 95% CI 1.032–5.545, P=0.042) and PVT (HR: 3.345, 95% CI 1.477–7.573, P=0.004) predicted 3-year rebleeding during univariate analysis. Multivariate analysis revealed that PVT (HR: 3.967, 95% CI 1.742–9.035, P=0.001) was an independent predictor. Hemoglobin >87.5 g/L (HR: 3.104, 95% CI 1.283–7.510, P=0.012) and PVT (HR: 2.349, 95% CI 1.231–4.483, P=0.010) were predictors of 5-year rebleeding during multivariate analysis. Albumin >37.5 g/L was an independent predictor of rebleeding in patients with PVT at 3 and 5 years (HR: 3.964, 95% CI 1.301–9.883, P=0.008; HR: 3.193, 95% CI 1.275–7.997, P=0.013, respectively).

Conclusions

PVT is associated with increased 3-year and 5-year rebleeding rates after EGDS but not at 10 years. Also, hemoglobin >87.5 g/L predicted rebleeding at 5 years. Albumin has huge prospects as a predictor of rebleeding at 3 and 5 years in patients with PVT.

Background

Esophageal variceal hemorrhage is a serious complication of portal hypertension. Endoscopic therapy, such as endoscopic sclerotherapy and endoscopic variceal ligation, remains the mainstay of treatment for patients with esophagal varices. However, endoscopic therapy cannot alleviate portal hypertension or hypersplenism. Esophagogastric devascularization and splenectomy (EGDS) is a procedure for treating patients with esophagal varices and hypersplenism secondary to liver cirrhosis and portal hypertension, especially in patients with acute variceal bleeding. The underlying cause of portal hypertension is hepatitis-induced cirrhosis linked to reduced liver function. It is widely thought that EGDS plays an important role in portal hypertension treatment in China, given its relatively minimal impact on liver function [1–5].

While the benefits of using EGDS to manage portal hypertension in patients with liver cirrhosis have been widely documented in the literature [6–8], the drawback of EGDS lies in the potential risk of rebleeding, which can range from 1% to 31%[1,5,9–13]. Portal vein thrombosis (PVT) is another highly prevalent complication characterized by partial or total occlusion of the portal vein, with solid materials in the lumen [14]. Over the years, different models, including the portal vein diameter [15], Child-Pugh score [16], and model for end-stage liver disease (MELD) score [17] have been used to predict esophagal variceal rebleeding in patients with cirrhosis. However, they are not suitable for patients after EGDS [18–20]. In addition, few reports have discussed the risk factors of long-term postoperative rebleeding, especially the impact of PVT on rebleeding [19,20]. Also, the perioperative risk factors of rebleeding 3 and 5 years after EGDS remain unknown, warranting further research.

It is imperative to promptly evaluate risk factors to accurately categorize patients, determine the likelihood of rebleeding, and identify high-risk populations. In this retrospective study, we investigated routine laboratory parameters and their correlation with rebleeding. We aimed to determine the predictors of rebleeding in patients with liver cirrhosis after EGDS. Furthermore, we determined the effect of new-onset PVT postoperatively on long-term rebleeding in patients after EGDS. Finally, the perioperative and follow-up parameters and the rebleeding rate were analyzed.

Material and Methods

Patients

This retrospective analysis included the data of consecutive patients with portal hypertension admitted to the Nanjing Second Hospital from December 2010 to January 2016. They all underwent EGDS. The eligibility criteria for the patients were as follows: (1) hypersplenism (platelet count <100×10⁹/L); (2) endoscopic evidence of gastroesophageal varices; (3) liver cirrhosis (diagnosed by clinical presentation, image examination, or liver biopsy) [21]; and (4) age above 18 years. The exclusion criteria were as follows: (1) hepatocellular carcinoma or other extrahepatic malignancy; (2) non-cirrhotic portal hypertension or myeloproliferative disease; (3) preoperative PVT; (4) severe organ dysfunction; (5) history of transjugular intrahepatic portosystemic shunt (TIPS); (6) patients with Child-Pugh class C; (7) incomplete clinical information; and (8) bleeding disorder. Before the operation, all patients provided written informed consent, and the investigation was performed in line with the principles of the Declaration of Helsinki (revised in Fortaleza, Brazil, in October 2013). The Ethics Committee of Nanjing Second Hospital approved the study protocol.

Clinical and Laboratory Data

The demographic data of the included patients, such as age, sex, primary cause of liver cirrhosis, body mass index (BMI), and history of upper gastrointestinal hemorrhage, were obtained. Blood samples were collected within 1 week for laboratory tests. Laboratory indexes, including liver function, renal function, coagulation parameters, and blood morphology, were measured in the clinical laboratory according to standard protocols. An upper gastrointestinal endoscopy, abdominal ultrasound, and contrast-enhanced spiral computed tomography were performed on each patient before the operation. The MELD score was calculated according to the United Network for Organ Sharing formula [22]. Moreover, 2 independent radiologists evaluated the width and velocity of the portal vein and the presence and extent of PVT of each patient using Doppler ultrasonography examination preoperatively and 7 days postoperatively. The diagnosis of PVT was based on the partial or complete absence of blood flow in the lumen of the splenoportomesenteric axis, with solid materials in the vein.

Surgical Procedure

An extended “L” incision was made in the left upper abdomen to access the spleen and stomach. A routine splenectomy was performed, followed by esophagogastric devascularization. The first step involved the disconnection of the gastric branch of the left gastric vein located near the gastric angular incisura and the small branches of the gastric coronary veins. The second step was to disconnect and suture-ligate the esophagal branches, such as the esophagal branches of the gastric coronary veins, high esophagal branches of the gastric coronary veins, and aberrant high esophagal branches of the gastric coronary veins, up to a length of 5 cm of the inferior esophagal segment. The posterior gastric veins, short gastric veins, and left subphrenic veins were also disconnected. Finally, the corresponding arteries were ligated, including the left gastric artery, left gastroepiploic artery, posterior gastric artery, and left subphrenic artery.

Follow-Up

The date of entry was the date of the operation. Follow-up data until December 2021 were acquired. Patients were regularly followed up until death or rebleeding, whichever came first. The primary outcome of this study was rebleeding. Rebleeding is defined as any significant upper gastrointestinal bleeding (GIB). In an ancillary study, we analyzed the influence of postoperative PVT on the evolution of variceal rebleeding.

Statistical Analysis

Quantitative data were presented as mean±SD and were compared using the t test. Categorical variables were evaluated using the chi-square test. The Kaplan-Meier analysis was used to estimate the cumulative risk of rebleeding, and the log-rank test was used to compare the differences. Univariate and multivariate Cox regression analyses were used to identify the independent predictors of 3-year and 5-year rebleeding. The potential risk factors in the univariate Cox regression analysis were included in the multivariate analysis when forward stepwise Cox regression was performed. The difference in 10-year rebleeding rates between the PVT and non-PVT groups was determined using the R programming language (v4.2.1, http://www.r-project.org/). Statistical analysis was performed with SPSS-V16.0 Software (IBM Corp, Armonk, NY, USA). P<0.05 was considered statistically significant.

Results

Baseline Characteristics of Patients at Admission

The data of 178 consecutive patients who underwent EGDS were evaluated in this study. As shown in Figure 1, after excluding 40 patients, 138 patients were finally included. The baseline characteristics of the included patients are summarized in Table 1. All enrolled patients were classified into the rebleeding group or the non-rebleeding group.

Figure 1.

Flowchart. Retrospective selection process of patients (Photoshop CS6, Adobe).

Table 1.

Comparison of clinical characteristics in all patients stratified according to postoperative rebleeding within 3 and 5 years.

Variables	3-year follow up		p-value
	Bleeding (n=25)	Non-bleeding (n=113)
Age (Y)	48.76±11.25	48.46±10.21	0.896
Gender(male/female)	19/6	73/40	0.274
BMI	22.73±3.30	23.22±3.07	0.493
Etiology: hepatitis B/others	23/2	101/12	0.695
Emergency surgery (yes/no)	2/23	9/104	0.995
Previous bleeding (yes/no)	10/15	50/63	0.698
Velocity of portal blood flow (cm/s)	16.52±3.60	17.23±4.86	0.555
Diameter of portal vein (mm)	12.88±1.89	13.66±2.77	0.246
Thickness of spleen (mm)	60.97±14.63	58.73±15.12	0.551
Longitudinal diameter of spleen (mm)	180.05±30.81	173.55±27.42	0.352
Child-Pugh class, n (%)			0.851
A	17	79
B	8	34
Child-Pugh score	6.12±1.23	6.08±1.11	0.872
Meld score	11.32±2.43	10.76±2.46	0.305
Gastric varices, n (%)			0.684
GOV-1	5	15
GOV-2	2	9
GOV-3	18	89
Platelet count (109/L)	37.08±18.34	45.28±25.26	0.128
Haemoglobin (g/L)	107.44±22.89	98.36±21.28	0.059
TBIL (μmol/L)	27.38±13.75	22.63±11.22	0.069
ALB (g/L)	38.18±6.63	36.24±4.80	0.102
ALT (IU/L)	29.62±18.80	27.54±18.26	0.610
AST (IU/L)	35.87±15.59	32.85±28.18	0.606
ACE	4014.1±1172.85	3752.2±1209.36	0.336
BUN (mmol/L)	6.09±2.59	5.68±2.48	0.458
Cr (μmol/L)	65.84±14.20	64.92±17.30	0.805
PT (s)	15.61±1.95	15.70±2.32	0.866
INR	1.36±0.16	1.35±0.21	0.775
Portal vein thrombosis (yes/no)	16/9	35/78	0.002
Velocity of portal blood flow (cm/s)	15.15±4.67	15.48±4.76	0.792
Diameter of portal vein (mm)	12.43±1.93	12.64±2.20	0.684
Variables	5-year follow up		p -value
	Bleeding (n=38)	Non-bleeding (n=100)
Age (Y)	49.47±10.42	48.15±10.37	0.505
Gender(male/female)	30/8	62/38	0.059
BMI	23.10±2.98	23.12±3.17	0.949
Etiology: hepatitis B/others	33/5	91/9	0.470
Emergency surgery (yes/no)	3/35	8/92	0.984
Previous bleeding (yes/no)	18/20	42/58	0.570
Velocity of portal blood flow (cm/s)	15.99±3.19	17.48±5.03	0.142
Diameter of portal vein (mm)	13.31±3.62	13.61±2.26	0.596
Thickness of spleen (mm)	59.39±12.37	58.96±15.88	0.890
Longitudinal diameter of spleen (mm)	176.48±29.16	173.90±27.64	0.657
Child-Pugh class, n (%)			0.552
A	25	71
B	13	29
Child-Pugh score	6.11±1.16	6.08±1.13	0.907
Meld score	11.21±2.40	10.73±2.48	0.306
Gastric varices, n (%)			0.720
GOV-1	5	15
GOV-2	2	9
GOV-3	31	76
Platelet count (109/L)	39.84±21.95	45.29±25.08	0.241
Haemoglobin (g/L)	105.03±22.46	98.10±21.33	0.096
TBIL (μmol/L)	24.72±12.73	23.03±11.47	0.456
ALB (g/L)	37.47±5.82	36.26±4.94	0.224
ALT (IU/L)	29.33±17.65	27.38±18.61	0.579
AST (IU/L)	34.56±15.21	32.96±29.53	0.751
ACE	3816.6±1256.78	3792.9±1187.95
BUN (mmol/L)	5.81±2.52	5.74±2.50	0.877
Cr (μmol/L)	68.92±16.50	63.66±16.68	0.103
PT (s)	15.83±2.14	15.62±2.29	0.624
INR	1.38±0.18	1.35±0.21	0.402
Portal vein thrombosis (yes/no)	19/19	32/68	0.050
Velocity of portal blood flow (cm/s)	14.25±4.16	15.80±4.86	0.138
Diameter of portal vein (mm)	12.43±1.98	12.67±2.21	0.588

BMI – body mass index; MELD – model for end-stage liver disease; TBIL – total bilirubin; ALB – albumin; ALT – alanine aminotransferase; AST – aspartate aminotransferase; ACE – choline esterase; BUN – urea nitrogen; INR – international normalized ratio; Cr – creatine; PT – prothrombin time.

Rebleeding After EGDS

Postoperative rebleeding was observed in 34.6% (n=25) and 27.5% (n=38) of patients at 3 and 5 years, respectively, and all patients were successfully treated with conservative therapy. No patients died from esophagogastric variceal rebleeding. Of the 25 patients who experienced rebleeding within 3 years after the procedure, 10 had previously experienced bleeding, and 16 developed PVT after the operation. Similarly, among the 38 patients who had rebleeding within 5 years, 18 had a history of preoperative bleeding, and 19 developed PVT postoperatively. The rebleeding rates for all patients at 3 and 5 years were 18.12% (25/138) and 27.54% (38/138), respectively, as shown in Table 2. Portal vein thrombosis was diagnosed in 51 patients (36.9%), and their rebleeding rates at 3 and 5 years were 31.37% (16/51) and 37.25% (19/51), respectively.

Table 2.

Rebleeding rate after esophagogastric devascularization with splenectomy.

Time	Total (n=138)	PVT (n=51)	Non-PVT (n=87)	p-value
1-year rebleeding, n (%)	10 (7.25%)	6 (11.76%)	4 (4.60%)	0.117
3-year rebleeding, n (%)	25 (18.12%)	16 (31.37%)	9 (10.34%)	0.002
5-year rebleeding, n (%)	38 (27.54%)	19 (37.25%)	19 (21.84%)	0.050

PVT – portal vein thrombosis.

The cumulative risks of rebleeding were significantly higher in the PVT group at 3 years (log-rank P=0.002) and 5 years (log-rank P=0.028) than at 10 years (log-rank P=0.057), as shown in Figure 2.

Figure 2.

Kaplan-Meier curves of variceal rebleeding. (A) 3-year rebleeding after esophagogastric devascularization with splenectomy (SPSS-V16.0 Software, IBM Corp, Armonk, NY, USA); (B) 5-year rebleeding after esophagogastric devascularization with splenectomy (SPSS-V16.0 Software); (C) 10-year rebleeding after esophagogastric devascularization with splenectomy (R programming language, v4.2.1, http://www.r-project.org/, R Development Core Team).

Risk Factors that Increased 3-Year and 5-Year Rebleeding Rates

During univariate analysis, total bilirubin level (HR: 2.392, 95% CI 1.032–5.545, P=0.042) and PVT (HR: 3.345, 95% CI 1.477–7.573, P=0.004) were identified as predictors of rebleeding at 3 years. The multivariate analysis revealed that PVT (HR: 3.967, 95% CI 1.742–9.035, P=0.001) was an independent predictor (Table 3). Hemoglobin >87.5 g/L (HR: 3.104, 95% CI 1.283–7.510, P=0.012) and PVT (HR: 2.349, 95% CI 1.231–4.483, P=0.010) were predictors of 5-year rebleeding during multivariate analysis (Table 4; Figure 3). PVT represented a risk factor for rebleeding at both 3 and 5 years.

Table 3.

Competing risk factors of 3-year rebleeding in all patients.

Variables	Univariate analysis HR (95% CI)	p-value	Multivariate analysis HR (95% CI)	p-value
Hb (g/L) (>91.5 vs ≤91.5)	2.466 (0.926–6.573)	0.071	2.555 (0.932–7.006)	0.068
TBIL (μmol/L) (>21.45 vs ≤21.45)	2.392 (1.032–5.545)	0.042	2.042 (0.865–4.824)	0.104
PVT	3.345 (1.477–7.573)	0.004	3.967 (1.742–9.035)	0.001

TBIL – total bilirubin; PVT – portal vein thrombosis; Hb – hemoglobin.

Table 4.

Competing risk factors of 5-year rebleeding in all patients.

Variables	Univariate analysis HR (95% CI)	p-value	Multivariate analysis HR (95% CI)	p-value
Hb (g/L) (>87.5 vs ≤87.5)	2.689 (1.124–6.433)	0.026	3.104 (1.283–7.510)	0.012
Gender	0.496 (0.228–1.083)	0.079	0.545 (0.249–1.191)	0.128
PVT	2.013 (1.065–3.806)	0.031	2.349 (1.231–4.483)	0.010

PVT – portal vein thrombosis; Hb – hemoglobin.

Figure 3.

Kaplan-Meier curves of 5-year rebleeding after esophagogastric devascularization with splenectomy stratified by hemoglobin (Hb) level (SPSS-V16.0 Software).

The patients who had variceal rebleeding within 5 years were categorized into 4 groups based on 2 predictors: hemoglobin and PVT: (1) PVT and hemoglobin >87.5 g/L; (2) PVT and hemoglobin ≤87.5 g/L; (3) no PVT and hemoglobin >87.5 g/L; and (4) no PVT and hemoglobin ≤87.5 g/L. Portal vein thrombosis and hemoglobin >87.5 g/L were selected as references. Cox regression analysis was performed, and the results showed that no PVT and hemoglobin ≤87.5 g/L yielded a protective value (Table 5).

Table 5.

Competing risk factors of 5-year rebleeding in all patients.

Variables	HR	95% CI	p-value
PVT and Hb >87.5 g/L
PVT and Hb ≤87.5 g/L	0.426	0.153–1.184	0.102
No PVT and Hb >87.5 g/L	0.470	0.233–0.947	0.035
No PVT and Hb ≤87.5 g/L	0.068	0.009–0.519	0.009

Hb – hemoglobin; PVT – portal vein thrombosis.

The characteristics of patients in the PVT group with 3-year rebleeding (n=16) and no rebleeding (n = 35) were further analyzed. An albumin level > 37.5 g/L was the only independent predictor of 3-year rebleeding in patients with PVT (Table 6). Further analysis of 5-year rebleeding (n=19) and no rebleeding (n=32) in the PVT group revealed that albumin >37.5 g/L was also the only independent predictor (Table 7).

Table 6.

Competing risk factors of 3-year rebleeding in PVT patients.

Variables	Univariate analysis HR (95% CI)	p-value	Multivariate analysis HR (95% CI)	p-value
Hb (g/L) (>91.5 vs ≤91.5)	2.074 (0.720–5.976)	0.176	1.499 (0.491–4.575)	0.477
TBIL (μmol/L) (>21.45 vs ≤21.45)	2.171 (0.788–5.978)	0.134	2.074 (0.716–6.013)	0.179
Albumin (g/L) (>37.5 vs ≤37.5)	3.585 (1.301–9.883)	0.014	3.964 (1.301–9.883)	0.008

TBIL – total bilirubin; Hb – hemoglobin.

Table 7.

Competing risk factors of 5-year rebleeding in PVT patients.

Variables	Univariate analysis HR (95% CI)	p-value	Multivariate analysis HR (95% CI)	p-value
Hb (g/L) (>87.5 vs ≤87.5)	2.23 (0.801–6.207)	0.125	2.018 (0.721–5.648)	0.181
Gender	0.646 (0.214–1.947)	0.438
Albumin (g/L) (>37.5 vs ≤37.5)	3.129 (1.254–7.807)	0.014	3.193 (1.275–7.997)	0.013

Hb – hemoglobin.

Discussion

The most life-threatening complication of portal hypertension is acute esophagal or gastric variceal bleeding, which accounts for 70% of upper GIB episodes [23] and represents a common cause of death in patients with cirrhosis. In recent years, significant progress has been achieved in treating acute variceal bleeding, including drug therapy, endoscopic treatment, surgical interventions, and TIPS [24,25]. Also, surgical interventions, including liver transplantation and EGDS, play a key role in the treatment process; however, liver transplantation is not widely used because of organ shortage and high medical costs. EGDS is a widely adopted surgical procedure in China, as it can address esophagogastric variceal bleeding and hypersplenism, common complications of portal hypertension. In contrast, EGDS is less commonly utilized in Western countries. In the light of the fact that the cases of liver cirrhosis in China are from mainly post-hepatitis B cirrhosis (different from European and American countries, where most of them are alcoholic cirrhosis), the liver reserve function is poor, and there is still a certain gap between the actual popularization degree of endoscopy and TIPS treatment in China and that in Western developed countries [26].

It is now understood that variceal rebleeding is a major cause of treatment failure. A previous study [27] revealed that EGDS was superior to TIPS in preventing rebleeding in patients with liver function in Child-Pugh class A or B. In addition, EGDS was superior to endoscopy therapy regarding variceal vein improvement and rebleeding rate [12]. The main branches of the stomach coronary vein were divided during devascularization, significantly decreasing the rebleeding rate.

Some postoperative prophylactic approaches, such as endoscopic eradication programs, have been advocated to minimize the chances of bleeding recurrence. However, not all patients are indicated for these approaches. It is crucial to identify high-risk patients and predict the occurrence of rebleeding following EGDS to significantly improve the prognosis of this patient population. Ferreira et al [13] presumed that patients with a portal flow velocity of >15.5 cm/s in the first postoperative year should be enrolled in an esophagogastric varices endoscopic eradication program to minimize the chances of recurrence. Liu et al [28] confirmed that liver stiffness was a predictor of rebleeding and could accurately predict the rebleeding events of hepatitis B liver cirrhosis.

PVT is a significant complication of EGDS, with reported incidence rates ranging from 6.3% to 39.0% [29]. According to a previous study, patients with portal vein thrombosis after esophagal variceal band ligation experience higher rebleeding rates at 14 days and 6 weeks than do those without PVT [30]. Additionally, 17.3% of patients with acute variceal bleeding experience PVT [31]. Reduced blood flow to the liver due to PVT can lead to intestinal edema, bacterial translocation, and liver dysfunction. Previous studies have documented that bacterial translocation can cause systemic inflammation [32] and liver failure [33], which are considered risk factors for higher rebleeding rates. To the best of our knowledge, this is the first study to comprehensively analyze the long-term effect of PVT on rebleeding in patients after EGDS. We found the 5-year rebleeding rates were comparable between patients with and without PVT. In contrast, there was a significant difference in the rebleeding-free period between the 2 groups at both 3 and 5 years. Also, the incidence of rebleeding at 3 years was higher in patients with PVT than in those without. Furthermore, we observed that the presence of PVT did not affect the 10-year rebleeding-free period. This could be attributed, in part, to the existence of portosystemic collaterals or venous collateralization. There is an increasing consensus that 30% to 50% of patients with PVT can achieve spontaneous partial recanalization [34,35]. Moreover, other intricate factors (hepatogenous diabetes [36], gastric mucosal lesions [37], severity of cirrhosis, and timing of surgical intervention [11]) can play a role in rebleeding with disease progression.

The present study also revealed that 3-year rebleeding was associated with PVT and total bilirubin >21.45 μmol/L. PVT was also an independent predictor during multivariate Cox regression analysis. A study reported that the serum bilirubin level [38] was a predictor of bleeding and was significantly associated with prophylactic endoscopic variceal ligation in cirrhosis, which is not in accordance with our study. Furthermore, our study confirmed that PVT and hemoglobin >87.5 g/L were independent predictors of rebleeding within 5 years. In contrast, a previous study demonstrated that hemoglobin >10 g/L might be a protective factor for the 42-day and 1-year rebleeding risk [33]. Hearnshaw et al [39] reported that in patients transfused with an initial hemoglobin level of <8 g/dL, rebleeding occurred in 23%, mortality was 13% compared with a rebleeding rate of 15%, and a mortality of 13% was found in those not transfused. In patients transfused with hemoglobin >8 g/dL, rebleeding occurred in 24% and mortality was 11% compared with a rebleeding rate of 6.7% and mortality of 4.3% in those not transfused. A small trial in AUGIB which compared liberal transfusion with transfusion only if the hemoglobin concentration fell below 8 g/dL showed that the percentage of rebleeding was markedly lower in the restricted transfusion group [40]. In cirrhotic patients with variceal bleeding, a liberal approach to transfusion is associated with an increased risk of rebleeding, likely due to the exacerbation of pre-existing portal hypertension [41], such that consensus guidelines strongly recommend maintaining a hemoglobin level around 8 g/dL [42,43]. The exact causal relationship between preoperative red blood cell transfusion and rebleeding cannot be determined based on current data, which has been addressed in numerous well-designed studies [41,44]. Interestingly, limited RBC transfusion has been shown to reduce the incidence of rebleeding, and most studies have found no correlation between reduced RBC transfusion and poorer prognosis [45,46]. Therefore, for patients undergoing EGDS, preoperative hemoglobin levels ≤87.5 g/L may be recommended.

Upon further analysis, it was determined that only an albumin level greater than 37.5 g/L was an independent predictor for both 3-year and 5-year rebleeding in patients with PVT. High albumin levels could predict 3-year and 5-year rebleeding in patients with PVT after EGDS, which is inconsistent with the literature [47]. In this respect, Wang et al [47] found that albumin infusion was associated with a low risk of rebleeding in cirrhosis patients with acute GIB, but this beneficial effect was predominately observed in patients with Child-Pugh class C, who had relatively high portal pressure. High albumin levels can be a protective factor for the 14-day and 6-week rebleeding risk in patients after esophagal variceal band ligation [30]. Theoretically, abundant albumin infusion in patients with GIB can cause rebleeding due to increased portal pressure, similar to the liberal transfusion strategy [48]. The necessity of albumin infusion in patients without hypoproteinemia and the related dosage remains to be clarified. Also, the effect of albumin infusion on cirrhosis with GIB has not been systemically studied. Importantly, the present study provided a reference for future studies.

The limitations of the present study should be acknowledged. First, this was a single-center retrospective study, and all data were recorded in the patient data management system before being analyzed. Although efforts were made to minimize selection bias, it cannot be entirely excluded. Also, the number of enrolled patients was limited, which can reduce the statistical power. A multicenter prospective study with a larger dataset is warranted for further analysis.

Conclusions

In conclusion, PVT is associated with the risk of rebleeding within 3 and 5 years following EGDS, but not over a 10-year span. A hemoglobin level greater than 87.5 g/L serves as a predictor for rebleeding at 5 years, while albumin level exhibits significant predictive value at both 3 and 5 years among patients with PVT. By combining PVT status and hemoglobin levels, medical professionals can more effectively stratify patients into various risk groups, facilitating the identification of high-risk populations. Indeed, further investigation is warranted to explore the impact of albumin infusion on rebleeding risk, especially when administered with preoperative red blood cell infusion following EGDS.