Gastric Endoscopic Mucosal Resection and Polypectomy among Patients with Liver Cirrhosis and Esophageal Varices in the setting of acute upper gastrointestinal bleeding

Background Gastric polyps are not infrequently reported among cirrhotic patients. Endoscopic resection of gastric polyps among patients with liver cirrhosis and esophageal varices carries the risk of post-polypectomy bleeding. This may explain why endoscopists are reluctant to its excision.


Introduction
Advanced liver disease with cirrhosis is complicated by portal hypertension and the formation of portosystemic collaterals and varices at different sites (esophageal, gastric, rectal, and ectopic sites) through the gastrointestinal tract. It may extend beyond the gastrointestinal tract, as in the retroperitoneal area. There is also splenomegaly complicated with thrombocytopenia [1]. Patients with liver cirrhosis (LC) tend to bleed due to a disruption of coagulation factor synthesis in the liver, and this disruption is often accompanied by thrombocytopenia and portal hypertension [2].
One critical study found that portal hypertensive polyposis is familiar in patients with portal hypertension and has benign characteristics [1].
Some studies suggested the management of portal hypertensive polyposis with APC, but the safety of polypectomy or band ligation of polyps has not been extensively investigated [3].
The incidence of gastric polyps increased; however, most polyps are asymptomatic and usually discovered incidentally during routine endoscopic interventions to manage acute GIT bleeding or follow-up [4]. Previous studies indicated that patients with LC are more prone to bleeding following an invasive procedure such as surgery or liver biopsy [5].
On the other side, the results of the study conducted by Winter et al. suggest that patients with portal hypertension are not at a higher risk of bleeding during polypectomy when compared to patients with healthy livers [6].
In cirrhotic patients, endoscopy is not only used to detect esophageal varices (OV). Still, we can see further gastrointestinal complications of portal hypertension, such as portal hypertensive gastropathy, gastric varices, and portal hypertensive polyps (PHP) [7].
With the increased and frequent use of endoscopy in cirrhotic patients with portal hypertension and varices, the detection of gastric polyps is increasing, as is the need for polyp removal to decrease the risk of recurrent spontaneous bleeding [8].
Gastric polyps are detected in 6 % to 8 % of all upper endoscopic examinations, with most polyps being classified as fundic gland polyps (77-80%) and hyperplastic polyps (17-19%)  Gastric hyperplastic polyps have been identified as a cause of transfusiondependent iron-deficiency anemia or obscure gastrointestinal bleeding.
They are more commonly seen in patients with chronic gastritis (e.g., Helicobacter-associated) [11]. Although endoscopic resection (ER) has  We reported the incidence of immediate (intraoperative) and delayed (within 30 days) follow-up post-procedure in these patients. Also, we studied the associated risk factors of polypectomy-related bleeding. Immediate (intraoperative) post-polypectomy bleeding is defined as developing bleeding from a polypectomy site during the endoscopic procedure. Delayed post-polypectomy bleeding is defined as the occurrence of GIT bleeding within 30 days of the endoscopic procedure [15].

Original research
The study included thirty-nine patients with LC with portal hypertension and varices presenting with GIT bleeding that had upper GI polyps during intervention for control bleeding or follow-up eradication of OV; in some cases, the polyps showed signs of bleeding or had a risk of bleeding.
All patients with LC and OV that had upper GI polyps in age > 18 years of both sexes presented with GIT bleeding that had upper GI polyps during intervention for control bleeding or follow-up for variceal eradication were included in this study. With informed consent from the patients included in the study, we excluded patients who refused to participate and those who were vitally unstable.

Tools and instruments:
The patient's laboratory workup, CBC, liver function tests, Creatinine, viral hepatitis markers (HCV Ab and HBs Ag), and blood glucose concentration were assessed by biochemical laboratory methods, abdominal ultrasound to determine liver status, esophagogastroduodenoscopy for upper GI to control variceal bleeding, and polypectomy in patients in whom polyps were discovered.

Operational design:
The entire history, considering age, sex, the etiology of liver disease, GIT symptoms, and medications.
Laboratory findings such as CBC, serum albumin, total bilirubin, prothrombin time, platelet counts, viral markers (HCV Ab and HBs Ag), and Histopathological examination of GI polyps that were removed by polypectomy or biopsy from the polyp Child-Pugh (CP) scores, number, Original research size, and location of the polyps, underlying diseases (diabetes mellitus, hypertension, dyslipidemia, coronary heart disease, cerebrovascular disease, and chronic kidney disease), and whether the patient was taking concomitant antiplatelet and anticoagulant medications Patients who received transfusions of fresh frozen plasma or platelet concentrates for coagulopathy before the procedures were included.
Generally, patients taking antiplatelet or anticoagulant agents were advised to hold the medication as follows: aspirin for seven days, clopidogrel for five days, heparin for 6 hours, low molecular weight heparin for 12 hours, warfarin for 3 to 5 days, and a new oral anticoagulant for 1 to 2 days before the procedures. Liver cirrhosis severity was classified into Child-Pugh classes A to C based on each patient's CP score (CP-A, 5-6 points; CP-B, 7-9 points; CP-C, 10-15 points).
General and Local examination: with special consideration of vital signs, oxygen saturation, and manifestations of liver cell failure.
Steps of performance and techniques: either snare polypectomy or endoscopic mucosal resection (including injection-assisted, cap-assisted, and ligation-assisted plans) according to the medical situation. In patients with small solitary polyps, either biopsy samples were obtained or polypectomy was performed so that the polyp was examined microscopically for histologic characterization, and most polyps were discarded after EMR by cap-or BL-assisted techniques.

Original research
The organization, tabulation, presentation, and data analysis were performed using SPSS IBM Chicago, version 23. Qualitative data were divided into categories and presented as frequency numbers and percentages, with the chi-square test used to determine the relationship between groups. Quantitative data were presented as mean ± SD, and the relationship between groups was done using an independent student t-test.
The level of significance adopted was p > 0.05.    .  Increased platelets count independently decreased the risk of early bleeding among the studied patients (Table 7).

Discussion
Little information is available regarding the feasibility and safety of gastric showed that most IPPB attacks were mild, self-limited, and easily controlled endoscopically, with no increase in morbidity or mortality.
The study conducted by Badar Hassan found that colonic EMR in cirrhotic patients has an acceptable bleeding risk. Immediate and delayed bleeding rates were 9.2% and 5.8%, respectively [17].

Original research
PPB was shown to occur in 7.5% of CLD patients, and patients in CPS classes B and C had more excellent rates of both IPPB and DPPB, according to SOH et al. [18].
About 14% of cirrhotic individuals had DPPB in a colon polyp, according to a study by Lee et al. [19].
According to a cohort study of elective endoscopy in cirrhotic patients, which revealed a 2% incidence of post-polypectomy bleeding in colon polypectomy, an elective procedure and good pre-procedural preparations of plasma, blood, or platelet transfusion in some cases may account for this difference [20].
According to Kwon et al., the study found no significant difference in the incidence of perforation between the CRF, LC, and control groups.
However, immediate bleeding tended to occur more frequently in the CRF + LC group than in the controls. [19]. Patients who bled in this study were statistically older than non-bleeders (P = 0.017), and there was no statistical significance about the sex of the patients [21].
In contrast, Kundumadam et al. found that patients who bled after polypectomy were younger than those who did not bleed [20].
About half of the patients in this study had Child-Pugh B and C, and about 46% had large-sized OV. 38.5% of patients had ascites. There is a statistically significant relationship between early post-polypectomy bleeding and CPS, OV grades, and marginally substantial with ascites (p = 0.06), and these parameters indicate advanced liver disease, so the In this study, the platelet count in the study population ranged between 46 and 263 *109 (with a mean of 124.0 ±56.7* 109), and a significant Original research association was found between the severity of thrombocytopenia (50* 109) and the risk of IPPB (p = 0.02).
In this study, we noticed that cirrhotic patients with portal hypertension who had IPPB also had significantly lower platelet counts than those who did not (P = 0.02), had more portal hypertension and large varices compared to patients without IPPB (P = 0.005), and also had relatively significant moderate ascites (p= 0.06).
Huang et al. found that the bleeding risk following polypectomy in cirrhotic patients was significantly increased with low platelet counts, increased ascites, and the presence of OV, which matched our results [17].
According to Kundumadam, 29% of patients who bled had a platelet count of 50 ×10 3 /mm 3 , compared to 6.3% of those who did not bleed, even though there was no statistically significant difference in platelet counts between patients with or without bleeding after polypectomy (mean 85 vs. 117; P = 0.17). (P 5 0.08) [18]. Also, SOH et al. found that platelet counts less than 50 ×10 3 were more vulnerable to PPB in cirrhotic patients [18].
In this study, PPB in cirrhotic patients did not significantly increase in patients receiving antiparticles (p = 0.127).
No noticeable difference was observed between patients with or without PPB regarding anti-platelets. Kundumadam noticed that antiplatelet and anticoagulant medications were not linked to bleeding, but his study contained only a small number (15 patients) receiving anticoagulants [20].
Increased platelet count and ALT independently decreased the risk of early bleeding among the studied patients.