Variceal Sclerotherapy Research Articles

Mechanism of thrombosis caused by sclerotherapy of esophageal varices using sodium tetradecyl sulphate.

The mechanism of thrombosis following intravariceal injection of sodium tetradecyl sulphate (S.T.D.) was investigated with respect to effects on the vascular endothelium, the coagulation cascade, and platelet function. Using an umbilical cord model designed to simulate blood flow over the endothelium, it was found that S.T.D. is a potent toxin for endothelial cells in that brief exposure to even low concentrations of the agent were effective in stripping endothelium over a considerable distance, exposing highly thrombogenic endothelium in the process. Effects on coagulation and platelet function were found to be dependent on concentration. Diluted S.T.D. induced a hypercoagulable state, possibly in consequence of a selective inhibition of the physiological anticoagulant, protein C, and promoted platelet aggregation. Higher concentrations inactivated the coagulation cascade and lysed platelets completely. These results suggest that intravariceal infusion of S.T.D. at considerable dilution may be at least as effective in inducing thrombosis as standard dosage, and possibly more so.

A Complication following Endoscopic Injection Sclerotherapy for Esophageal Varices in Postoperative Congenital Biliary Atresia : A Case of Portal Vein Thrombosis

A Complication following Endoscopic Injection Sclerotherapy for Esophageal Varices in Postoperative Congenital Biliary Atresia : A Case of Portal Vein Thrombosis

Acute management of bleeding oesophageal varices.

The goals of therapy in acute variceal bleeding are to arrest haemorrhage and to prevent deterioration of liver function and complications related to bleeding. The measures used to stop acute bleeding should, ideally, also prevent the very early rebleeding that is frequently seen with bleeding varices. Variceal bleeding should be managed by a gastrointestinal bleeding team with intensive nursing care. Diagnostic endoscopy is mandatory once initial resuscitation has been achieved, and allows immediate injection sclerotherapy of varices. Drug therapy can be used as the first treatment in patients admitted with variceal bleeding since it can be given immediately. Of the available drugs, somatostatin has the least side effects and is as effective as vasopressin, terlipressin and the combination of vasopressin and an organic nitrate vasodilator. The role of drugs needs to be studied in combination with sclerotherapy. Sclerotherapy remains the mainstay of management as it achieves the twin goals of stopping active bleeding and preventing early rebleeding. Injection of tissue adhesive and endoscopic ligation or 'banding' are new endoscopic techniques that have shown promise in preliminary trials and are currently being assessed more widely. Balloon tamponade is a temporary measure used to prevent exsanguination. Surgery should be reserved for those patients in whom sclerotherapy is unsuccessful or cannot be carried out. Oesophageal staple transection is the most used operation. The new interventional radiological technique of transjugular intrahepatic portosystemic shunting will probably replace surgery in the future, but its role in acute variceal bleeding has yet to be fully defined.

The management of persistent or recurrent variceal bleeding after injection sclerotherapy by somatostatin.

Sixteen patients with persistent (n = 11) or recurrent (n = 5) variceal bleeding after injection sclerotherapy and balloon tamponade were treated with an intravenous infusion of somatostatin 250μg/ h. Somatostatin infusion successfully controlled the bleeding in 15 of the 16 patients but one rebled after 72 h of treatment. In one patient with poor liver function (Child’s C) bleeding was not controlled by somatostatin, further injection sclerotherapy or balloon tamponade of the oesophagus. The results of this study, although uncontrolled and with a small number of patients, suggest that somatostatin is a very effective treatment for the control of post-injection sclerotherapy variceal bleeding.

A prospective controlled study of the risk of bacteremia in emergency sclerotherapy of esophageal varices

Reported incidences of bacteremia after endoscopy with esophageal variceal sclerotherapy are conflicting. A prospective controlled study was conducted to determine the frequency of bacteremia after emergency endoscopy with esophageal variceal sclerotherapy compared with frequency after elective esophageal variceal sclerotherapy and after emergency endoscopy in patients with upper gastrointestinal bleeding from nonvariceal sources. A total of 126 endoscopies were studied in 72 patients. Groups consisted of (a) emergency endoscopy without esophageal variceal sclerotherapy, 37 sessions with 36 patients; (b) elective esophageal variceal sclerotherapy, 33 sessions with 14 patients; and (c) emergency esophageal variceal sclerotherapy, 56 sessions with 36 patients. Blood cultures were obtained before and 5 and 30 minutes after endoscopy. There was a higher frequency of preendoscopic bacteremia in emergency esophageal variceal sclerotherapy (13%) than in emergency endoscopy alone (0%) (P = 0.02). Clinically significant bacteremia in emergency esophageal variceal sclerotherapy was observed in 7 of 56 (13%) sessions, compared with 0 of 33 in elective esophageal variceal sclerotherapy (P = 0.03) and 1 of 36 (3%) in emergency endoscopy alone (P = 0.45). Of these cases, 3 (5.4%) were potentially caused by emergency esophageal variceal sclerotherapy, but no clinically significant postendoscopic bacteremia was attributable to the procedure in the other groups.

Complications of Esophageal Variceal Sclerotherapy

The authors of this article provide a review of complications of esophageal variceal sclerotherapy, including their recognition, management, and prevention. They also discuss the safest possible performance of the procedure.

Portal colopathy: Prospective study of colonoscopy in patients with portal hypertension

Twenty patients with portal hypertension related to a variety of causes prospectively underwent colonoscopy for hematochezia (n = 10), hemoccult positive stool and anemia (n = 9), or polyp found with screening flexible sigmoidoscopy (n = 2) (includes 1 patient with anemia/heme-positive stool). Twelve patients (60%) had previously undergone a course of sclerotherapy, and 10 (50%) had endoscopie evidence of congestive gastropathy. Colonoscopic findings included mucosal abnormalities resembling multiple vascular ectasias in 14 (70%), 4 of whom also had endoscopic features suggesting a mild, chronic colitis. Neither signs of chronic liver disease nor stigmata suggestive of more severe portal hypertension correlated with the colonoscopic findings. Two patients required heater probe therapy for actively oozing lesions resembling vascular ectasias and an additional two patients sclerotherapy for bleeding midrectal varices. Although likely an over-estimate of the frequency, this study suggests that portal colopathy can occur in portal hypertension. Vascular ectasialike lesions in such settings may be associated with acute as well as chronic gastrointestinal bleeding and may require pharmacological, directed endoscopic, or portal decompressive therapy. Additional studies are required to determine not only the pathophysiology but also the true frequency of this entity.

Endoscopic sclerotherapy in the management of gastric variceal haemorrhage

The value of injection sclerotherapy in the management of active gastric variceal bleeding is unclear. A retrospective study was therefore performed of 46 episodes of acute variceal haemorrhage in 41 patients who were treated by endoscopic sclerotherapy. The site of gastric variceal haemorrhage was the lesser curve (Group 1) in 13, within a hiatus hernia (Group 2) in six, and fundal with or without associated oesophageal varices (Type 3) in 22 cases. Haemostasis was achieved by sclerotherapy in 54%, 71.4% and 26%, respectively. After additional measures including balloon tamponade or surgery 85% of the Group 1 cases had stopped bleeding significantly more frequently than was observed in Group 3 (44.4%). More patients in Group 3 died due to uncontrolled bleeding (41%) than in Group I (7.7%). Hospital mortality depended on the severity of the liver disease with 15% of Child's grade A and 56% of grade C cases dying. It is concluded that endoscopic sclerotherapy of gastric varices should be reserved only for lesser curve or hiatal varices and that early surgery (or sclerotherapy using tissue adhesive) be considered for variceal haemorrhage originating from fundal varices.

Prophylactic sclerotherapy increased mortality and did not prevent variceal esophageal hemorrhage in men with alcoholic liver disease

Source Citation The Veterans Affairs Cooperative Variceal Sclerotherapy Group. Prophylactic sclerotherapy for esophageal varices in men with alcoholic liver disease. A randomized, single-blind, multicenter clinical trial. N Engl J Med. 1991 Jun 20;324:1779-84.

Comparative effects of 5% ethanolamine oleate versus 5% sodium morrhuate for sclerotherapy of oesphageal varices

Forty-five cirrhotic patients with oesophageal varices were randomized to receive endoscopic injection sclerotherapy with either 5% ethanolamine oleate (EO), or 5% sodium morrhuate (SM). In the EO group, there was a statistically significant higher rate of disappearance of red colour signs on the varices a week after the initial session of sclerotherapy than in the SM group (91.3% vs 45.5%, P less than 0.05). A jet-like bleeding from injection sites at the second session of sclerotherapy occurred in three patients in the SM group and they experienced blurred vision. There was no such occurrence in the EO group. Oesophageal bleeding requiring blood transfusion during the course of repeated sclerotherapy occurred only in the SM group (five patients): bleeding was from a partly thrombosed varix and in four was from oesophageal ulcers. We found that EO administered intravariceally is more efficacious than SM for sclerotherapy of oesophageal varices.

Endoscopic Sclerotherapy for Esophageal Varices After Surgical Procedures for Congenital Biliary Atresia

Abstract: The effectiveness of injection sclerotherapy for esophageal varices due to congenital biliary atresia has not yet been established. Sclerotherapy was performed to treat esophageal varices in four children with variceal bleeding who had received a hepatic portoenterostomy for congenital biliary atresia. Ethanolamine oleate was mixed with a contrast medium for the varicealography in order to determine the flow of the sclerosant by fluoroscopy. Varicealography which was conducted during the injection allowed us to stop the procedure so that mixture would fill up the varix and its feeders but would not enter the systemic circulation. Between 0.5 ml to 2.0 ml of sclerosant was injected at the variceal puncture. There was one case bleeding from the esophageal ulcer. However, it was resolved by conservative treatment. All four children experienced no rebleeding after the therapy. Therefore, injection sclerotherapy using varicealography with sclerosant–contrast medium mixture is recommended for children who develop esophageal varices after surgical procedures for congenital biliary atresia.

Efficacy of endoscopic sclerotherapy on long‐term management of oesophageal varices: A comparative study of results in patients with cirrhosis of the liver, non‐cirrhotic portal fibrosis (NCPF) and extrahepatic portal venous obstruction (EHO)*

A prospective study was conducted to compare the results of long-term endoscopic variceal sclerotherapy in patients with different aetiologies of portal hypertension. A total of 404 consecutive patients were included. There were 234 patients with hepatic cirrhosis, 83 with non-cirrhotic portal fibrosis (NCPF) and 87 with extrahepatic portal venous obstruction (EHO). The mean follow-up for patients with cirrhosis, NCPF and EHO was 25, 37 and 28 months. A total of 73 (31%) patients with cirrhosis, 19 (23%) with NCPF and 10 (11.5%) with EHO rebled (P less than 0.05) on follow-up, prior to eradication of varices. Irrespective of the aetiology, 40 (17%) patients of Child's A class, 42 (33%) of Child's B and 20 (50%) of Child's C class rebled (P less than 0.01). The median bleeding free period (BFP) was longer (P less than 0.05) in patients with EHO than in cirrhotics. Patients in Child's A class had significantly longer BFP than those in Child's B, and the latter had a longer BFP than those in Child's C class (P less than 0.01). The probability of 7-year survival was also better with EHO (97.5%) and NCPF (73.6%) than cirrhotics (41%). Survivals in patients with EHO and NCPF were comparable (P less than 0.1). Similarly 7-year survival irrespective of aetiology in Child's A patients (90.7%) was longer than in Child's B (28.8%), and longer in Child's B than Child's C patients (0%). Success of eradication was greater (P less than 0.05) in EHO (92%) and NCPF (87%) than cirrhotic patients (75%).(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of Endosonography in Sclerotherapy of Esophageal Varices

During intravariceal sclerotherapy of esophageal varices with polidocanol in 32 patients with portal hypertension due to liver cirrhosis of various etiologies, endosonographic assessment of both esophageal and gastric intramural vessels was carried out in order to evaluate the usefulness of endosonography in the follow-up of the variceal status. In all cases endosonography demonstrated esophageal and gastric varices; in contrast, only five cases of gastric varices could be demonstrated by endoscopy. Furthermore, different stages of variceal obliteration following sclerotherapy could be demonstrated by means of endosonography, and it was possible to identify incomplete obliteration in about one-third of the patients in whom inadequate sclerotherapy was suspected endoscopically. In addition, the status of gastric varices during sclerotherapy was demonstrated by means of endosonography. Only in cases of adequate sclerotherapy of esophageal varices, as assessed by both endoscopic and endosonographic criteria, were gastric varices plugged. On the basis of these findings endosonography would appear to be a useful technique for the diagnosis and follow-up of esophageal and gastric varices during intravariceal sclerotherapy.

Intramural Hematoma of the Esophagus after Variceal Sclerotherapy

Two patients with cirrhosis are presented who developed retrosternal pain and dysphagia immediately after sclerotherapy of esophageal varices. Extensive submucosal bleeding of the esophageal wall was demonstrated radiologically and endoscopically. Complete resolution occurred spontaneously and did not lead to residual complications such as strictures. Intramural hematoma of the esophagus is an unusual complication after endoscopic variceal sclerotherapy.

The effects of chronic endoscopic variceal sclerotherapy on portal pressure in cirrhotics

The effect of obliterating esophageal varices by endoscopic sclerotherapy on portal pressure was prospectively studied in 11 cirrhotic patients with variceal hemorrhage. Portal venous pressure gradient, determined as the difference between transhepatic portal and hepatic vein pressure, increased by a mean of 31.1% ± 14.5% in 8 (73%) and decreased by a mean of 30.1% ± 11.7% in 3 (27%) patients, with no statistically significant change overall (P = 0.1). These changes in portal venous pressure gradient occurred despite an improvement in the laboratory and clinical parameters of hepatic function. Deep abdominal sonography with color flow imaging at variceal obliteration showed patent paraumbilical veins in 6 (55%) patients, 3 of whom had decreases in portal venous pressure gradient (29%, 19%, 42.5%) at variceal obliteration. In 5 (45%) patients without patent paraumbilical veins, a statistically significant increase in portal venous pressure gradient between initial endoscopic variceal sclerotherapy and variceal obliteration was noted (P = 0.008). Rebleeding (single episode in all 4 patients, before obliteration in 3 patients) occurred in those with an increase in portal venous pressure gradient; all patients with portal venous pressure gradient decreases were nonbleeders. No correlation between changes in portal venous pressure gradient and time to variceal obliteration, number of sclerotherapy treatments, or rebleeding episodes was observed. Thus, an increase in portal venous pressure gradient was noted in the majority of patients at variceal obliteration. Although the portal venous pressure gradient decrease may be explained by a patent paraumbilical vein, the mechanism of portal venous pressure gradient increase is not clear. It is speculated that this portal venous pressure gradient increase may be caused by an increase in collateral resistance or flow or a combination of both, resulting from obliteration of esophageal varices by endoscopic sclerotherapy.

Unusual Presentation of a Case of Brain Abscess after Endoscopic Injection Sclerotherapy of Esophageal Varices

Although an increasing number and variety of complications of endoscopic injection sclerotherapy (EIS) of bleeding esophageal varices have been reported, infectious complications are rare. A case of brain abscess following EIS is reported which was characterised by an unusual clinical presentation in that there was no fever or leucocytosis. This presentation could have led to the abscesses being mistaken for brain metastases. The outcome of antimicrobial therapy was favorable which provided further evidence in support of the diagnosis.

Clinical evaluation of endoscopic injection sclerotherapy for bleeding esophageal varices in liver cirrhosis with hepatocellular carcinoma.

Endoscopic injection sclerotherapy (EIS) for rupture of esophageal varices was carried out in 13 patients of liver cirrhosis with hepatocellular carcinoma (HCC). Sclerotherapy was performed by intravariceal injections of 5% ethanolamine oleate. According to the manual for the staging of cancer, these HCCs were classified as Stage I in 1 case, II in 1 case, III in 2 cases, and IV in 9 cases. There was no difference between post EIS prognosis and stage. Child's classification of these patients were class A in 1 case, B in 5 cases, and C in the remaining 7 cases. Only in 1 case of Child's A and 1 case of Child's B who were less advanced clinically and were free from icterus and ascites did EIS produce favorable results, it arresting esophageal variceal hemorrhage and led to a relatively good outcome. We suggest that emergency EIS for rupture of esophageal varices should be performed in patients with relatively good general conditions, irrespective of the stage of HCC.

Effects of Cyanoacrylate on the Gastric Mucosa of Dogs –Endoscopic and Histopathological Studies for Sclerotherapy of Gastric Varices–

Abstract: The effect of cyanoacrylate tissue adhesive (C. A.) on the gastric mucosa of dogs was investigated endoscopically and histopathologically. When C. A. was applied to the surface of the gastric mucosa, the endoscopic findings the next day showed local redness at the applied site (Fig. 1‐a) and histopathology revealed degenerative changes in the gastric mucosa (Fig. 1‐b). When C. A. was endoscopically injected into the gastric mucosa, the endoscopic findings revealed a submucosal tumor‐like lesion (Fig. 2‐a). One day after treatment, the endoscopic findings showed a hemorrhagic erosion on the surface of the lesion (Fig. 2‐b). An histopathological examination of the resected stomach revealed C. A. in the submucosal layer (Fig. 3‐a, 3‐b) and the lymph duct around the muscularis mucosa with severe acute inflammation (Fig. 4‐a, 4‐b). One week after treatment, a deep ulcer (Ul‐IV) was observed (Fig. 5, 6) and a histopathological examination of the resected specimen revealed C. A. at the site of the ulcer and inflammatory cell infiltration by fibroblasts and giant cells (Fig. 7‐a, 7‐b). One month after treatment, the ulcer had healed and was replaced by a scar (Fig. 8). Histopathological examination of the resected stomach revealed C. A. in both the muscularis mucosa and the submucosa and also inflammatory cell infiltration by giant cells in addition to the fibrosis (Fig. 9). When using endoscopic sclerotherapy with C. A., it should be kept in mind that there is the possibility of such a lesion occurring as demonstrated by our study.

Results of nonshunting operation and injection sclerotherapy for esophageal varices

The results of a total of 523 nonshunting operations performed at our institution from 1964 to 1990 were analyzed and compared to those of chronic sclerotherapy. Although the overall operative mortality rate of nonshunting operations was low (26/523:5.0%), it was relatively high in Child's C cirrhotic patients (22/129:17%) and in those who underwent surgery on an emergency basis (14/60:23%). Cumulative survival rates of Child's C cirrhotic patients at 5 and 10 years (37.4%, 13.0%) following nonshunting operations were much lower than those of Child's A (76.6%, 54.9%) or Child's B (71.6%, 35.5%). One- and three-year survival rates for patients treated with sclerotherapy were 90%, 72% in Child's A (22 patients), 82%, 49% in Child's B (47), and 56%, 30% in Child's C (50), while cumulative rebleeding rates at one and three years following sclerotherapy were 12%, 12% in Child's A, 18%, 27% in Child's B, and 35%, 55% in Child's C respectively. Our data indicated that nonshunting operations can be safely performed with a good long-term outcome in Child's A or B cases on an elective basis, and sclerotherapy may be the treatment of choice for emergency cases or for Child's C cases although the risk of rebleeding is high following sclerotherapy.

Squamous cell carcinoma after endoscopic injection sclerotherapy for esophageal varices : N. Kokudo, K. Sanjo, N. Umekita, et al. Am J Gastroenterol 85:861–864, (July), 1990

Squamous cell carcinoma after endoscopic injection sclerotherapy for esophageal varices : N. Kokudo, K. Sanjo, N. Umekita, et al. Am J Gastroenterol 85:861–864, (July), 1990