Variceal Sclerotherapy Research Articles

Endoscopic Sclerotherapy of Esophageal Varices. M. V. Sivak Jr. 240 × 160 mm. Pp. 157 + ix. Illustrated. 1984. New York: Praeger Publishers. £34.50

Journal Article Endoscopic Sclerotherapy of Esophageal Varices. M. V. Sivak Jr. 240 × 160 mm. Pp. 157 + ix. Illustrated. 1984. New York: Praeger Publishers. £34.50 Get access Endoscopic Sclerotherapy of Esophageal Varices. MV Sivak Jr. 240 × 160 mm. Pp. 157 + ix. Illustrated. 1984. New York: Praeger Publishers. £34.50 J L Dawson J L Dawson Search for other works by this author on: Oxford Academic Google Scholar British Journal of Surgery, Volume 72, Issue 4, April 1985, Page 331, https://doi.org/10.1002/bjs.1800720450 Published: 08 December 2005

Endoscopic sclerotherapy in the treatment of gastric varices.

Of 309 patients with portal hypertension, gastric varices were found in 48 (16 per cent). While the majority (88 per cent) of the patients had gastric varices in association with oesophageal varices, 6 (12 per cent) patients had 'isolated' gastric varices. Gastric varices were seen significantly (P less than 0.01) more often with grade 4 than with grade 3 varices. In 11 (28 per cent) of the 40 patients who completed sclerotherapy for oesophageal varices, gastric varices disappeared concurrently on eradication of oesophageal varices or during the following 6 months. Of the initial five patients with gastric varices who received direct intravariceal injections, four rebled; this technique was therefore replaced by combination (paravariceal + intravariceal) gastric variceal sclerotherapy. Emergency combination sclerotherapy successfully controlled bleeding from gastric varices in six of the eight treated patients. Thirty-two patients entered a programme of elective combination gastric variceal sclerotherapy. Variceal obliteration was achieved in 12 cases (38 per cent) and reduction in size was noted in another 7 patients (22 per cent) after a minimum of four courses. There were 11 (23 per cent) deaths, 8 due to uncontrolled bleeding from gastric varices and 3 due to hepatic coma. The other complications of gastric variceal sclerotherapy were minor and included retrosternal pain, fever and dysphagia. It is concluded that gastric varices often coexist with large oesophageal varices. If they persist for 6 months after eradication of oesophageal varices, a combination of paravariceal and intravariceal sclerotherapy should be attempted for their obliteration.

Mechanism of the haemostatic effect of ethanolamine oleate in the injection sclerotherapy for oesophageal varices.

Changes in coagulation and fibrinolysis were investigated in 20 patients with oesophageal varices, who underwent endoscopic injection sclerotherapy (EIS) with 5 per cent ethanolamine oleate (EO), by means of serial determination of plasma fibrinopeptide A (FPA) and fibrinopeptide B beta 15-42 (B beta 15-42). One hour after the completion of EIS, the value of FPA was significantly increased to 38.1 +/- 11.1 ng/ml (mean +/- s.e.m.) from a pre-EIS value of 7.1 +/- 1.4 ng/ml (P less than 0.01) and it gradually returned to normal range by 48 h after EIS. A very similar change was observed in the value of B beta 15-42 (P less than 0.01). These observations indicated that EIS provokes transient activation of coagulation and fibrinolysis. In vitro studies, however, revealed that EO inhibits fibrin clot formation because of the Ca2+-chelating ability of its constituent ethanolamine, although oleate or benzyl alcohol exhibited procoagulant activity in FPA formation in vitro. Nevertheless, an external application of EO or oleate over decapsulized kidney of rat resulted in a significant accumulation of 125I-labelled fibrin(ogen). From these results it was suggested that intravascular injection of EO, which exerts an inhibitory effect on coagulation in vitro, activates the local coagulation system. The activation may be accelerated by an acute inflammatory process provoked by oleate, which is supported by such clinical manifestations as mild fever, retrosternal pain leukocytosis and an increase in plasma fibrinogen level which was observed in all during the period.

Twenty-five years of injection sclerotherapy for bleeding varices.

Acute injection sclerotherapy has been used in Belfast for 25 years and the results are reviewed. During this period 264 patients had injection sclerotherapy for acute bleeding from oesophageal varices during 396 admissions; a rigid oesophagoscope was used and 447 injections were performed. The series includes 19 children who received 69 injections. Thirty-eight had extrahepatic portal venous hypertension and the remainder had intrahepatic disease. Overall, 81 were Child's grade A (including the 38 extrahepatics), 82 were grade B and 101 were grade C. Of the 396 admissions, acute injection sclerotherapy controlled bleeding in 362 instances (control rate 91.4 per cent); control rate in the children's group was 97.1 per cent and in the adults 90.2 per cent. The hospital mortality was 14.9 per cent (57 adults and 2 children). Nineteen deaths were due directly to bleeding oesophageal varices, two from bleeding gastric varices and seven directly or indirectly from oesophageal leaks. Most of the remaining deaths were due to liver failure. We consider that sclerotherapy is valuable in the control of variceal haemorrhage where bleeding is uncontrolled or recurs after vasopressin or tamponade in any admission.

Endoscopic and radiological appraisal of gastric varices

Of 104 patients with portal hypertension who were subjected to oesophageal variceal sclerotherapy, gastric varices were seen in 81 (78 per cent) at endoscopy and 69 (74 per cent) at splenoportography. In 50 (48 per cent) patients gastric varices were seen at the initial endoscopic examination and in 31 they developed during follow-up at intervals varying from 1 to 56 weeks. Gastric varices were seen significantly more often along the lesser curvature than in the gastric fundus and the left gastric vein was the main feeding vessel in 75 per cent of cases. Varices bled in nine of 81 patients and bleeding was seen significantly more often from fundal varices (30 per cent) than from lesser curve varices (5 per cent) (P less than 0.02). The incidence of gastric varices is high, and contrary to popular belief they are more often located along the lesser curvature of the stomach than in the gastric fundus.

Injection sclerotherapy for oesophageal varices in children.

Oesophageal varices in 21 children with portal hypertension (intrahepatic 13, extrahepatic 8) were treated with sclerotherapy using ethanolamine oleate injected via a fibreoptic endoscope. Repeat endoscopy confirmed variceal obliteration in 18 children with a mean of 3.5 (range 1-8) injections. No patient has bled since obliteration of varices. Complications were oesophageal stricture (2 patients), oesophageal ulcer (5 patients) and haemorrhage within 3 days of injection (5 patients). The early results suggest that this is a satisfactory method for the treatment of oesophageal varices in children.

The complications of injection sclerotherapy of bleeding oesophageal varices.

The complications of injection sclerotherapy were retrospectively studied in 122 patients with acute variceal bleeding. Initial control of bleeding was achieved in 72.5 per cent of patients and the final success rate of sclerotherapy was 86.1 per cent. The overall morbidity rate was 30.3 per cent. Minor complications occurred in 13.9 per cent of patients and major complications were recorded in 16.4 per cent. Twenty patients developed complications directly attributable to sclerotherapy: 14 minor and 6 major. The overall mortality rate was 21.3 per cent, and 7.4 per cent of the patients died due to complications. Pulmonary complications occurred in 15 patients and resulted in 3 deaths. Retrosternal pain developed in 8 patients, but dysphagia and oesophageal ulceration were rare. No stricture was recorded. The incidence of liver failure in 17 Child's grade C cases was almost certainly a complication of the underlying disease rather than the injection therapy. It is suggested that injection sclerotherapy is an effective and relatively safe treatment for variceal bleeding.

Eradication of oesophageal varices recurring after portal non-decompressive surgery by injection sclerotherapy

The results of injection sclerotherapy for oesophageal varices which recurred after portal non-decompressive surgery were analysed retrospectively to evaluate its efficacy. We treated 60 consecutive patients with portal hypertension; 19 were treated on an emergency basis, seven electively and 34 on a prophylactic basis. All acute bleeding was controlled with one session of sclerotherapy using a transparent overtube. After eradication by sclerotherapy, no bleeding episodes occurred and there was no recurrence of the varices, except in three uncompliant patients, during a mean follow-up period of 33.1 months. Bleeding from a gastric ulcer and gastritis occurred in one patient each. Oesophageal stenosis occurred in nine (15 per cent) patients and gastric varices developed in two (3 per cent) patients. Twelve patients died, five from liver failure and six with hepatoma, but there was no bleeding from the gastrointestinal tract. The overall 4-year survival rate was 80 per cent. We recommend the use of sclerotherapy as the primary treatment for recurrent oesophageal varices.

Randomized controlled trial of injection sclerotherapy for bleeding oesophageal varices—an interim report

Oesophageal varices are the commonest cause of acute upper gastrointestinal bleeding in Egypt, due to the prevalence not only of schistosomiasis but also chronic hepatitis. Poor results of conventional treatment and shunt surgery led us to evaluate injection sclerotherapy, using fibreoptic endoscopy. In a controlled trial, 108 patients were randomly allocated to injection sclerotherapy or to conventional treatment (medical measures, with modified splenectomy and oesophagogastric devascularization in selected cases). We report the results in the first 108 patients, with a follow-up of 1-35 months. Fifty-three patients received injection sclerotherapy; 5 died (2 of recurrent bleeding) and 5 others had recurrent bleeding but were controlled by further injections. Thirty-six of the 55 control patients underwent surgery; 5 died (2 of recurrent bleeding) and 2 others developed recurrent bleeding. Further bleeding occurred in 12 of the 19 patients who were managed by medical measures alone, with 7 dying. These early results indicate that injection sclerotherapy can be effective in urgent and elective situations and that it appears to have advantages over conventional medical and surgical treatments.

Platelet aggregability after endoscopic intravariceal injection of 5 per cent ethanolamine oleate into oesophageal varices.

Platelet aggregability and the coagulative and fibrinolytic systems were examined in 45 patients who underwent endoscopic injection sclerotherapy for oesophageal varices. Five per cent ethanolamine oleate, the sclerosant used, was injected into the oesophageal varices. There were significant increases in the concentrations of fibrinopeptide A, fibrinopeptide B-beta-15-42 and fibrin degradation products-E after the sclero-therapy. At 1 h after the sclerotherapy the mean(s.e.m.) platelet aggregation was significantly suppressed to 71.9(4.2) per cent of that before the treatment (P less than 0.01). There was a gradual recovery within 1 week to the same level seen before the sclerotherapy. Thromboxane B2 and 6-keto-prostaglandin F1 alpha, both stable products of thromboxane A2 and prostacyclin respectively, showed significant temporary increases after the sclerotherapy (P less than 0.01). The peak increase in the level of thromboxane B2 was noted within 1 h after the sclerotherapy and earlier than that for 6-keto-prostaglandin F1 alpha. This increased ratio of prostacyclin and thromboxane A2 may be related to the marked limitation in platelet aggregation.

Injection sclerotherapy for bleeding varices: Risk factors and complications

Risk factors for complications after injection sclerotherapy were studied in 163 patients undergoing 667 treatments for bleeding oesophageal varices. The overall mortality rate was 7 per cent per injection sclerotherapy session; 16 per cent per acute session and 2.4 per cent per elective session. Acute variceal bleeding was controlled by injection sclerotherapy in 91 per cent of patients. Complications occurred after 16 per cent of injection sclerotherapy sessions. Deaths and complications were significantly associated with poor modified Child's grading (P less than 0.001), the first variceal bleed (P less than 0.001), acute injection sclerotherapy (P less than 0.001) and the use of the rigid oesophagoscope (P less than 0.001).

Devascularization following endoscopic sclerotherapy of oesophageal varices: Dangers and difficulties

Twenty-three patients underwent devascularization operations for acute variceal bleeding. All had received endoscopic sclerotherapy, either long-term or just before surgery. The oesophagus and peri-oesophageal tissues showed either oedematous or fibrotic reaction depending on the number and duration of sessions of sclerotherapy. These changes in the oesophagus and surrounding tissues were responsible for intraoperative oesophageal perforation and postoperative anastomotic leaks. To obviate these problems, stapling of the anterior and posterior walls of the stomach was tried and found to be safer than stapled transection of the oesophagus. During follow-up, varices reappeared in over 75 per cent of patients and were managed by further sclerotherapy. Patients who did not receive sclerotherapy had a higher incidence of rebleeding.

Branched-chain amino acid supplementation during the endoscopic injection sclerotherapy for esophageal varices may be useful for maintenance of nutritional status in patients with liver cirrhosis

Branched-chain amino acid supplementation during the endoscopic injection sclerotherapy for esophageal varices may be useful for maintenance of nutritional status in patients with liver cirrhosis

Efficacy of argon plasma coagulation for gastric antral vascular ectasia associated with chronic liver disease

Gastric antral vascular ectasia (GAVE) is a rare cause of chronic gastrointestinal bleeding. The aim of this study was to evaluate the relationship between GAVE with cirrhotic patients and liver dysfunction, portal hypertension and the safety and efficacy of argon plasma coagulation (APC) in treating GAVE with cirrhotic patients. Eight cirrhotic patients with the characteristic endoscopic findings of GAVE were registered. In this study, APC was performed for GAVE in all eight patients. The patients-liver function was classified by Child-Pugh classification and classifications were: two class A, five class B and one class C (mean score: 7.8). Five patients had previously received prophylactic endoscopic injection sclerotherapy for esophageal varices and one had esophageal varices. Balloon-occluded retrograde transvenous obliteration (B-RTO) for gastric varices had been performed in other one patient. Portal hypertensive gastropathy (PHG) was recognized in only one case. APC was performed in all eight patients and one to three treatment sessions were needed (mean: 1.8 sessions). No complications were observed in the initial treatment. During follow-up, endoscopies revealed the recurrence of GAVE in two patients requiring further treatment by APC (recurrence rate: 25%). After APC treatment, the recurrence of GAVE was not observed with endoscopy in the other six patients. The results suggest that GAVE is related to severe liver damage and portal hypertension in cirrhotic patients. APC is a safe and effective treatment against GAVE.

Evolving Consensus in Portal Hypertension Report of the Baveno IV Consensus Workshop on methodology of diagnosis and therapy in portal hypertension

Portal hypertension is associated with the most severe complications of cirrhosis, including ascites, hepatic encephalopathy, and bleeding from gastro-esophageal varices. Despite the progress achieved over the last decades, the 6-week mortality associated with variceal bleeding is still in the order of 10–20%. Awareness of the difficulty inherent to the evaluation of diagnostic tools and the design and conduct of good clinical trials for the treatment of portalhypertensionhas led to theorganization, since1986,of a series of consensus meetings. The first one was organized by Andrew Burroughs in Groningen, The Netherlands [1]. After Groningen, other meetings followed, in Baveno in 1990 (Baveno I) [2] and in 1995 (Baveno II) [3,4], in Milan in 1992 [5], in Reston, USA, in 1996 [6], in Stresa in 2000 (Baveno III) [7,8], again in Baveno in 2005 (Baveno IV) [9,10], and in Atlanta in 2007 [11]. The aims of these meetings were to develop definitions of key events in portal hypertension and variceal bleeding, to review the existing evidence on the natural history, the diagnosis and the therapeutic modalities of portal hypertension, and to issue evidence-based recommendations for the conduct of clinical trials and the management of patients. All these meetings were successful and produced consensus statements on some important points, although some issues remained unsettled. To continue the work of the previous meetings, a Baveno V workshop was held on May 21–22, 2010. The workshop was attended by many of the experts responsible for most of the major achievements of the last years in this field. Many of them had attended the previous meetings as well. The main fields of discussion of the Baveno V workshop were the same as in Baveno I–IV, i.e. the definitions of key events concerning the bleeding episode and the therapeutic options in patients with portal hypertension. For each of these topics, a series of consensus statements were discussed and agreed upon. As in Baveno IV, whenever applicable, the level of existing evidence was evaluated and the recommendations were ranked according to the Oxford System [12] (i.e.: level of evidence from 1 = highest

Comparison of Esophageal Stenosis Produced By Endoscopic Sclerotherapy or Ligation of Varices

Variceal Ligation (VL) eradicates esophageal varices faster than Endoscopic sclerotherapy (ES) with a lower rebleeding rate and fewer secondary effects. However, the majority of studies are short term and late complications are probably not detected. Patients. We analyzed our database that included 253 cirrhotic patients treated endoscopically for variceal bleeding from 1988 till 2004 looking for the incidence and the characteristics of stenosis. The stenosis was considered slight when the esophageal size was more than 10 mm and severe when it was not possible to pass through the stricture with the endoscope.

Therapeutic efficacy of isosorbide dinitrate for dysphagia after endoscopic injection sclerotherapy for varices in cirrhotic patients

Background: Isosorbide dinitrate (ID) improves dysphagia of achalasia patients by lowering the low esophageal pressure. Dysphagia occurs in cirrhotic patients undergoing endoscopic injection sclerotherapy (EIS) for esophageal varices even with no structural abnormalities as its sequela. We tested whether ID can be therapeutic for dysphagia of this type.Methods: ID was given for 2–6 weeks to 13 patients with dysphagia lasting for longer than 4 weeks after EIS despite no esophagolumenal stricture on endoscopy and barium swallows. EIS was done three to six times as an injection series of ethanolamine oleate into the varices at intervals of 1–2 weeks until they were obliterated. The therapeutic efficacy of ID was evaluated by symptom severity four‐degree scorings. Esophageal transit time and emptying time were calculated from the time–activity curves on esophageal scintigraphy.Results: At 2 weeks after ID medication, dysphagia was decreased by one score in 12 of 13 patients, and by two scores in one patient. However, dysphagia at the same extent recurred in nine patients within 6 weeks after stopping ID medication, which was improved similarly by remedication. Two patients in whom dysphagia of one and two scores disappeared after ID medication dropped out because of headache. The remaining two patients remained asymptomatic for longer than 6 months after the first medication. Esophageal scintigraphy disclosed the shortening of the emptying time after ID administration in two patients.Conclusions: ID may be effective for relieving functional dysphagia after EIS for esophageal varices in cirrhotic patients.

Effect of splenectomy and ligature of the left gastric vein on portal hypertensive colopathy in carriers of surgical hepatosplenic schistosomiasis mansoni

Esophageal variceal sclerotherapy and band ligation seem not to affect the endoscopic findings of Portal Hypertensive Colopathy (PHC) of cirrhotic patients. The aim was to assess the effect of splenectomy and ligature of the left gastric vein on the PHC in carriers of hepatosplenic schistosomiasis mansoni who underwent this surgery when they were between 9 and 18 year-old. Fourteen patients, mean age of 19.1 +/- 3.1 years, were included in the postoperative group (GI). The follow-up was from 1 to 9 years. The preoperative group (GII) consisted of nine patients, mean age of 14.0 +/- 3.1 years. Full-length colonoscopy was carried out in all patients. Search was made for PHC lesions. Telangiectasy (GI 100% vs GII 100%), increased vascularisation (GI 57.1% vs GII 100%), focal and diffuse hyperemia (GI 14.3% vs GII 66.7%), angiodysplasia (GI 7.1% vs GII 33.3%), and rectal varix (GI 0% vs GII 55.6%) were the most frequent findings. It was observed that the patients of this series tended to exhibit fewer hemodynamic manifestations of the PHC after treatment (postoperative versus preoperative - chi2 = 8.155 - p = 0.004). Splenectomy and ligature of the left gastric vein tend to reduce the abnormal vascular findings of PHC in carriers of hepatosplenic schistosomiasis mansoni.

Intramural Duodenal Hematoma after Endoscopic Therapy for a Bleeding Duodenal Ulcer in a Patient with Liver Cirrhosis

We report a case of intestinal obstruction due to intramural hematoma of the duodenum following therapeutic endoscopy for a bleeding duodenal ulcer in a patient with liver cirrhosis. A 44-year-old man was admitted to our hospital with severe epigastralgia, nausea and tarry stool. Two years previously he had undergone endoscopic sclerotherapy for esophageal varices caused by alcoholic liver cirrhosis. Endoscopy revealed an open ulcer with a bleeding vessel in the duodenal bulb, and sclerotherapy was performed by clipping the vessel and injecting 20 ml of 0.2% epinephrine. His platelet count was 3.5x10(4)/mul. Twelve hours later, he again developed epigastralgia and hypotension. Emergency computed tomography and ultrasonography revealed an intramural hematoma, 15x18 cm in diameter, at the dorsal and lateral duodenum. Endoscopy and upper gastrointestinal series revealed severe stenosis of the duodenal lumen caused by intramural hematoma. He received parenteral feeding for 22 days and within 8 weeks the hematoma was gradually absorbed using conservative management. Intramural duodenal hematoma may be diagnosed as a complication of the endoscopic procedure in a patient with a bleeding tendency, such as liver cirrhosis.

Proximal Compression during Sclerotherapy of Great Saphenous Varices and Appropriate Compression Pressure

Proximal Compression during Sclerotherapy of Great Saphenous Varices and Appropriate Compression Pressure