P- Reviewer: Fernandez JM, Zosia K S- Editor: Yu J L- Editor: AmEditor E- Editor: Ma S
Published online Apr 7, 2015. doi: 10.3748/wjg.v21.i13.3888
Peer-review started: August 24, 2014
First decision: September 27, 2014
Revised: October 13, 2014
Accepted: December 5, 2014
Article in press: December 8, 2014
Published online: April 7, 2015
AIM: To explore the effect of in vitro porcine esophageal variceal pressure on complete ligation degree for polycyclic ligators.
METHODS: An in vitro model of experimental porcine venous vessels was used to test various venous pressures. Three treatment groups were designated according to the preset pressure range: P1 = 25-30 cmH2O; P2 = 35-40 cmH2O; P3 = 45-50 cmH2O. The effect of pressure on ligation was assessed and compared among the groups.
RESULTS: Complete ligation was achieved at a rate of 56.25% (18/32) in group P1, 37.5% (12/32) in group P2, and 33.33% (11/33) in group P3 (χ2 = 3.6126; P = 0.0573).
CONCLUSION: Higher variceal pressures impair the ligation completion rate. Therefore, measuring variceal pressure may help predict the effect of endoscopic ligation and guide treatment choice.
Core tip: This study aims to explore the factors influencing rebleeding after endoscopic variceal ligation, and provide the theoretic basis for prevention and reduction of rebleeding after the procedure.
- Citation: Li ZQ, LingHu EQ, Hu M, Li WM, Huang QY, Zhao YW. Esophageal variceal pressure influence on the effect of ligation. World J Gastroenterol 2015; 21(13): 3888-3892
- URL: https://www.wjgnet.com/1007-9327/full/v21/i13/3888.htm
- DOI: https://dx.doi.org/10.3748/wjg.v21.i13.3888
An increase in esophageal variceal pressure is a key factor leading to vascular rupture bleeding. Therefore, the measurement of esophageal variceal pressure is of great significance to evaluate and predict the risk of hemorrhage. Our previous in vitro preliminary work utilizing experimental ligation has shown that the ligation degree significantly differs among groups with various diameters of esophageal varices[1,2], though these experiments lacked evaluation of vascular pressure effects on the polycyclic ligator. Therefore, the aim of the present follow-up study was to explore the factors influencing rebleeding after endoscopic variceal ligation (EVL), in order to provide a theoretic basis for prevention and reduction of post-procedure rebleeding.
General surgical instruments were used in the procedures, including multi-band-ligators (Boston Scientific Corporation, Marlborough, MA, United States), glass column burettes, three-way stopcocks, and sodium chloride methylene blue solution. An Olympus GIF-Q260 gastroscope (Olympus Corporation, Tokyo, Japan) with a main engine and aspirator was also used.
The piglets were sacrificed, and exploratory laparotomy was performed to select the inferior vena cava, portal vein, and superior mesenteric vein as previously described. Three pressure groups were included in the in vitro study: group P1: 25-30 cm H2O; group P2: 35-40 cm H2O; and group P3: 45-50 cmH2O. The “0” point of the liquid level in the glass burette was calibrated before each reading (Figure 1).
The piglet was sacrificed, the chest cavity was opened, and a section the esophagus (40 cm long) was removed and divided into three segments. The esophageal inner membrane was inverted, and a blunt dissection of the submucosal soft tissue was performed with hemostatic forceps, forming the porcine esophageal submucosal tunnel (Figure 2). Hemostatic forceps were used to pull one end of a porcine vein through the esophageal submucosal tunnel, creating the model of esophageal varices with different pressures.
A Speedband Super 7 multiple band ligator was mounted on an Olympus upper endoscope aimed at a varicose vein with continuous negative pressure suction (0.03-0.05 MPa). When the endoscopic view was completely blue, the bands were released at the handle, the negative pressure suction was stopped, and a rubber band was firmly ligated on the lesion base. After cutting off the esophageal mucosa after band ligation, the submucosal ligated varix was stripped, and the effect of endoscopic variceal ligation was observed: complete ligation (100%) the ligation effect is reliable and complete, and bands do not easily fall off; partial or incomplete ligation (50%) indicates that the ligation effect is not reliable, and bands can fall off early; no ligation (0%) indicates that the ligation failed, and esophageal varices were not ligated (Figure 3).
SPSS 13.0 software (SPSS Inc., Chicago, IL, United States) was used for data management and statistical analysis. Using the linear trend χ2 test, P < 0.05 was considered as statistically significant.
A total of 97 in vitro models of esophageal varices were included in the study. For group P1, complete ligation was achieved 56.25% (18/32), whereas 6.25% (2/32) showed incomplete ligation and 37.50% (12/32) showed no ligation. In group P2, 37.50% (12/32) showed complete ligation, 12.50% (4/32) showed incomplete ligation, and 50.00% (16/32) showed no ligation. In group P3, complete ligation was achieved in 33.33% (11/33), incomplete ligation was observed in 3.03% (1/33), and 63.64% (21/33) showed no ligation. Univariate analysis revealed that variceal pressure is an interference factor in predicting the degree of ligation (χ2 = 3.6126, P = 0.0573).
Interest in esophageal variceal manometry has been increasing in recent years. This study indicates that variceal pressure, rather than hepatic venous pressure gradient, may more directly predict the risk of bleeding, as measuring esophageal variceal pressure is particularly important for determining the effect of bleeding prevention and treatment[6-9]. Nevens et al reported that variceal pressure is the most important predicting index of bleeding.
Normal portal vein pressure is 13-24 cmH2O (1.27-2.35 kPa), when portal hypertension occurs, the pressure can increase to 30-50 cmH2O (2.94-4.90 kPa). When the pressure exceeds 25 cmH2O (2.45 kPa), gastroesophageal varices are prone to rupture and hemorrhage. Currently, endoscopic sclerotherapy and ligation are the primary methods for treating variceal bleeding, which can be effective for emergency hemostasis and occlusion of varicose veins, though some patients still exhibit recurrent bleeding. Portal pressure and hepatic venous pressure gradient do not correlate well and do not accurately predict variceal bleeding[11,12]. Whether intravariceal pressure influences the effect of variceal ligation and correlates with the other suggested endoscopic predictors is not clearly known.
The purpose of the current study was to explore the hemostatic effect after EVL in an effort to reduce the incidence of rebleeding and improve the outcome from esophageal varices rupture or hemorrhage. Rebleeding after EVL may occur because the variceal surface of band ligation is not strong, which can easily lead to band dropping off early. Strict control of EVL indications and contraindications will help to reduce the incidence of postoperative bleeding. Moreover, gastroesophageal varices are significantly related with portal pressure; the higher the portal pressure, the more serious the esophageal gastric varices, and increased portal pressure is a necessary prerequisite for esophageal variceal bleeding. A highly significant positive correlation was seen between variceal pressure and bleeding, indicating that patients with higher pressures bled more often. Intravariceal pressure was the most important variable in predicting variceal bleeding[14,15].
The experiments in the current study demonstrate that venous pressure parameter variation in the model is similar to that in humans. We found that when the variceal pressure is within range of 25-30 cmH2O, the rate of complete ligation is the highest, whereas the efficacy is reduced with increasing pressures. Although the results did not achieve statistical significance, the marginal P value (P = 0.0573) indicates that venous pressure might be an interference factor in predicting the degree of complete ligation. Additional studies with larger sample sizes are needed to further confirm these findings. Therefore, the search for the mechanisms of variceal rupture and the factors influencing variceal bleeding continues[17-29]. In other words, there are other variables influencing variceal bleeding, such as the thickness of the variceal wall; the wall tension increases disproportionate to the rise in pressure in blood vessels. This is because a rise in the pressure causes an increase in the radius and a decrease in the wall thickness. Thus, measuring variceal pressure is expected to be helpful in correctly predicting the effect of variceal ligation; however, investigation of other variables influencing the effect of EVL should continue.
Endoscopic variceal ligation is the primary method for the treatment of esophageal variceal bleeding. However, the effect of ligation on hemostasis in acute bleeding from esophageal varices was not been thoroughly investigated. The main problem for ligation in acute esophageal variceal bleeding is the accumulation of large amounts of blood in the gastrointestinal lumen, which may obscure endoscopic visualization. Therefore, the aims of this study were to understand the impact and the role of different degrees of variceal pressure on achieving complete ligations.
Using porcine veins and esophagus, in vitro ligation of esophageal varices, is an innovative method to evaluate efficacy of variceal ligation treatments.
This study evaluated porcine esophageal variceal pressure and complete ligation degree using an animal model to guide endoscopic variceal treatment. The article has better practicability, and there are currently no relevant reports.
Variceal pressure may provide a valuable predictor for variceal bleeding following endoscopic variceal ligation.
This manuscript about esophageal variceal pressure influence is very interesting. In this manuscript, the authors explored the effect of in vitro porcine esophageal variceal pressure on complete ligation degree for polycyclic ligator. Three groups were studied. The results are interesting. Based on the results, the authors concluded that when variceal pressure is higher, the effect on ligation is worse.
|1.||Lei YL, Wang Y, Wang LP. A Case-control Study on the Influencing Factors of Rebleeding after Esophageal Variceal Ligation. Xiandai Shengwu Yixue Jinzhan. 2013;12:2318-2320.|
|2.||Li ZQ, Linghu EQ, Li WM. Effects of different vascular diameter and pressure on complete ligation degree in vitro. Zhonghua Xiaohuaneijing Zazhi. 2014;31:93-96.|
|3.||Wang GF, Xie H. Nursing care in treatment of esophageal variceal ligation. Zhongguo Linchuang Yixue Yanjiu. 2007;13:1039.|
|4.||Liu M, Wang L, Pu LX. The clinical application of a new self-made of pneumatic ligator. Zhonghua Neijing Zazhi. 2002;8:48-49.|
|5.||Nevens F, Broeckaert L, Rutgeerts P, Van Steenbergen W, Fevery J. The long-term morbidity and mortality rate in a cohort of patients with liver cirrhosis and oesophageal varices. Hepatogastroenterology. 1995;42:979-984. [PubMed]|
|6.||Bosch J, Bordas JM, Rigau J, Viola C, Mastai R, Kravetz D, Navasa M, Rodés J. Noninvasive measurement of the pressure of esophageal varices using an endoscopic gauge: comparison with measurements by variceal puncture in patients undergoing endoscopic sclerotherapy. Hepatology. 1986;6:667-672. [PubMed] [DOI]|
|7.||Yu FF, Wang JG, He BB. A fiber-optic pressure sensor for measuring esophageal variceal pressure. Shijie Huaren Xiaohua Zazhi. 2014;22:221-226. [DOI]|
|8.||Kleber G, Sauerbruch T, Fischer G, Paumgartner G. Pressure of intraoesophageal varices assessed by fine needle puncture: its relation to endoscopic signs and severity of liver disease in patients with cirrhosis. Gut. 1989;30:228-232. [PubMed] [DOI]|
|9.||Hou MC, Lin HC, Kuo BI, Liao TM, Lee FY, Chang FY, Lee SD. Sequential variceal pressure measurement by endoscopic needle puncture during maintenance sclerotherapy: the correlation between variceal pressure and variceal rebleeding. J Hepatol. 1998;29:772-778. [PubMed] [DOI]|
|10.||Nevens F, Bustami R, Scheys I, Lesaffre E, Fevery J. Variceal pressure is a factor predicting the risk of a first variceal bleeding: a prospective cohort study in cirrhotic patients. Hepatology. 1998;27:15-19. [PubMed] [DOI]|
|11.||Lebrec D, De Fleury P, Rueff B, Nahum H, Benhamou JP. Portal hypertension, size of esophageal varices, and risk of gastrointestinal bleeding in alcoholic cirrhosis. Gastroenterology. 1980;79:1139-1144. [PubMed]|
|12.||Garcia-Tsao G. Current management of the complications of cirrhosis and portal hypertension: variceal hemorrhage, ascites, and spontaneous bacterial peritonitis. Gastroenterology. 2001;120:726-748. [PubMed] [DOI]|
|13.||Yun QZ, Cheng CS. Correlation between direct measurement of portal venous pressure and esophageal gastric varices and degrees of portal venous expansion. Chengduyixueyuan Xuebao. 2013;5:620-621.|
|14.||Sarin SK, Sethi KK, Nanda R. Measurement and correlation of wedged hepatic, intrahepatic, intrasplenic and intravariceal pressures in patients with cirrhosis of liver and non-cirrhotic portal fibrosis. Gut. 1987;28:260-266. [PubMed] [DOI]|
|15.||Staritz M, Poralla T, Meyer zum Büschenfelde KH. Intravascular oesophageal variceal pressure (IOVP) assessed by endoscopic fine needle puncture under basal conditions, Valsalva’s manoeuvre and after glyceryltrinitrate application. Gut. 1985;26:525-530. [PubMed] [DOI]|
|16.||Xia SX, Zhou SP, Gao XH, Zhu LZ, Wang JR. Esophageal variceal ligation of negative pressure suction experiment and clinical study. Shiejie Huaren Xiaohua Zazhi. 2000;8:106.|
|17.||Garcia-Tsao G, Groszmann RJ, Fisher RL, Conn HO, Atterbury CE, Glickman M. Portal pressure, presence of gastroesophageal varices and variceal bleeding. Hepatology. 1985;5:419-424. [PubMed] [DOI]|
|18.||Witzel L, Wolbergs E, Merki H. Prophylactic endoscopic sclerotherapy of oesophageal varices. A prospective controlled study. Lancet. 1985;1:773-775. [PubMed] [DOI]|
|19.||Reliability of endoscopy in the assessment of variceal features. The Italian Liver Cirrhosis Project. J Hepatol. 1987;4:93-98. [PubMed] [DOI]|
|20.||The general rules for recording endoscopic findings on esophageal varices. Jpn J Surg. 1980;10:84-87. [PubMed] [DOI]|
|21.||Dagradi AE, Stempien SJ, Owens LK. Bleeding esophagogastric varices. An endoscopic study of 50 cases. Arch Surg. 1966;92:944-947. [PubMed] [DOI]|
|22.||Spech HJ, Wördehoff D. [Classification of esophageal varices - endoscopic and clinical aspects (author’s transl)]. Leber Magen Darm. 1982;12:109-114. [PubMed]|
|23.||Bolondi L, Caletti G, Brocchi E, Ferrentino M, Calcamuggi G, Casanova P, Gasbarrini G, Labò G. Ultrasonographic findings in portal hypertension: correlation with the presence and size of oesophageal varices. Ultrasound Med Biol. 1983;Suppl 2:499-503. [PubMed]|
|24.||Beppu K, Inokuchi K, Koyanagi N, Nakayama S, Sakata H, Kitano S, Kobayashi M. Prediction of variceal hemorrhage by esophageal endoscopy. Gastrointest Endosc. 1981;27:213-218. [PubMed] [DOI]|
|25.||Buset M, Des Marez B, Baize M, Bourgeois N, Cremer M. Bleeding esophagogastric varices: an endoscopic study. Am J Gastroenterol. 1987;82:241-244. [PubMed]|
|26.||Fortune B, Garcia-Tsao G. Current Management Strategies for Acute Esophageal Variceal Hemorrhage. Curr Hepatol Rep. 2014;13:35-42. [PubMed] [DOI]|
|27.||Reding P, Urbain D, Grivegnee A, Frere D. Portal venous-esophageal luminal pressure gradient in cirrhosis. Hepatology. 1986;6:98-100. [PubMed] [DOI]|
|28.||Mosimann R. Nonaggressive assessment of portal hypertension using endoscopic measurement of variceal pressure. Preliminary report. Am J Surg. 1982;143:212-214. [PubMed] [DOI]|
|29.||Bützow GH, Novak D. Clinical value of hepatic vein catheterization. Improved pracability by balloon catheter technique. Gastrointest Radiol. 1977;2:153-161. [PubMed] [DOI]|
|30.||Groszmann RJ. Reassessing portal venous pressure measurements. Gastroenterology. 1984;86:1611-1614. [PubMed]|