Life-threatening haemorrhage from an ulcerated haemangioma: treatment by transcutaneous in-situ sclerosis.
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Human epidermal growth factor (EGF), a small polypeptide (6 kDa) with mitogenic properties, has been implicated in the protection of gastrointestinal mucosal integrity. The efficacy of EGF in the prevention and healing of sclerotherapy-induced esophageal lesions was investigated in 24 minipigs with surgically induced portal hypertension. In addition, the effect of EGF on intragastric acidity and pharmacokinetics was investigated as possible means to explain its protective mechanism of action. The animals underwent three weekly sessions of sclerotherapy with polidocanol 2% and were concomitantly and for an additional three weeks treated with either placebo or EGF administered paravenously in the esophagus and/or subcutaneously. The subcutaneous treatment with EGF significantly (P < 0.05) reduced esophageal stricture and scar formations associated with sclerotherapy. Gastric pH values were significantly (P < 0.01) elevated only in animals receiving subcutaneous injections of EGF. Furthermore, the subcutaneous administration of EGF was associated with unexpected prolonged plasma concentration of the peptide. These results suggest a possible clinical value of EGF as an adjunctive treatment with the sclerotherapy.
A case report of a patient who underwent submucosal injection sclerotherapy for hemorrhoids is presented. Subsequently developed necrotizing fascitis of the anorectum, perianal region, and scrotum necessitated emergency debridement and defunctioning colostomy. Postoperatively, the patient developed septicemia and renal failure requiring an extended hospital stay. Restoration of bowel continuity was done after three months. A brief review of known complications of this technique was made. It would appear that necrotizing fascitis can be added to this list.
We present a case of life-threatening retroperitoneal sepsis after injection sclerotherapy for first-degree hemorrhoids.
Endoscopic injection sclerotherapy is useful in stopping bleeding from esophageal varices. We compared the in vivo effects of sclerosants on thrombogenesis, hemostasis, and endothelial injury. We injected aethoxysclerol (AS) of ethanolamine oleate (EO) into the small veins of the rat intestine. The maximum thrombogenic index with AS was 30.7 and with EO was 9.2. The venous flow stopped sooner with EO than with AS. The thrombi caused by EO were mixed with red blood cells. Heparin pretreatment decreased the thrombogenic index with AS by 96.7%, but not that with EO. The area of the fluorescein-albumin conjugate that permeated from veins with AS was larger than that with EO. The fluorescent intensity with AS was lower than that with EO. We thus conclude that: (1) the size of thrombi is not necessarily proportional to the hemostatic efficacy; (2) change in a patient's coagulation may affect the potential of sclerosants; (3) the excellent hemostatic efficacy of EO is based on localized injury to the endothelium and the involvement of red blood cells aggregation; and (4) in vivo microscopy is useful in determining the rational selection of sclerosants.
We devised a transparent anorectoscope for internal hemorrhoidal sclerotherapy. Using this scope the grade of hemorrhoids of the patients can be evaluated accurately through the transparent wall of the scope, and the device facilitates easier and safer sclerotherapy under clear direct vision, compared to the conventional free-hand-style treatment. We conclude that sclerotherapy using this anorectoscope represents a minimally invasive treatment for low-grade internal hemorrhoids and is recommendable for outpatient therapy of internal hemorrhoids.
After excluding terminally all patients, we evaluated a total of 718 patients treated with endoscopic injection sclerotherapy. They involved 350 episodes of acute hemorrhage and 368 prophylactic procedures in patients with risky varices. The 1-year cumulative survival rate was significantly lower in the acute hemorrhage group than in the prophylactic group (P < 0.05). The difference in survival between the two groups was primarily due to the number of deaths in the first 2 months after sclerotherapy (20.1% vs 0.8%, P < 0.0005). Improvements in the sclerotherapy technique significantly reduced the number of deaths from bleeding (9.3% vs 3.4%, P < 0.05), but not those from liver failure following variceal hemorrhage. Prophylactic EIS is advantageous in the treatment of esophageal varices, i.e. it may prevent deaths from liver failure attributed to variceal hemorrhages. The present study shows that preliminary prevention of variceal hemorrhage provides favorable hemostatic efficacy in patients with risky varices.
We report a case of Cruveihier-Baumgarten syndrome associated with portal vein thrombosis that developed, slowly during a 2-year period after endoscopic variceal sclerotherapy. The thrombosis led to the disappearance of the venous hum and the dilated abdominal wall veins characteristic of this syndrome. A 73-year-old woman was hospitalized for treatment of esophageal varices in April 1988. Her spleen was markedly enlarged, and the histologic findings of her liver were not consistent with hepatic cirrhosis, but with idiopathic portal hypertension. A venous hum was audible in the upper abdomen. Superior mesenteric angiography revealed a porto-systemic shunt vessel under the abdominal wall, originating from the umbilical vein. She was injected four times with a sclerosant, and this brought about disappearance of the esophageal varices. Two years after the first admission, the venous hum was no longer audible, but there was a recurrence of the esophageal varices. More than 2 years later (4 years after the first admission), ultasonographic study, computed tomography, and angiography showed a large thrombus, which completely obstructed the portal vein at the origin of the umbilical vein, and the development of collateral vessels, seen as a "cavernous transformation."
Between August 1983 and December 1991 at the Taichung Veterans General Hospital, Taiwan, 65 advanced hepatocellular carcinoma (HCC) patients with esophageal variceal bleeding received endoscopic injection sclerotherapy (EIS) and 60 such patients received conservative medical treatment without EIS. The rate of successful control of acute bleeding was 72.5% (27/40 patients) in the EIS group and 56.7% (34/60 patients) in the non-EIS group. The rebleeding rate was lower in the EIS group than in the non-EIS group (26.9% vs 73.5%). Thirty-one of the EIS and 44 of the non-EIS treatment patients, mainly Child's B and C patients, died within 2 months after the first bleeding. In the short term, EIS decreased the mortality due to esophageal variceal bleeding, but the survivors still had to face hepatic failure and tumor growth. Thus, benefits of EIS were noted on short- but not on long-term survival. The mean survival times were 2.38 months for the EIS group and 1.79 months for the non-EIS group. Since EIS had no beneficial effects on long-term survival it is doubtful whether sclerotherapy applied to esophageal variceal bleeding in patients with advanced HCC would be worthwhile, as the endoscopic procedure would only add to their suffering.
We report herein the case of a 46-year-old man in whom an esophageal hemangioma was successfully treated by endoscopic injection sclerotherapy (EIS). The patient was admitted to hospital after a routine upper gastrointestinal series demonstrated a filling defect in the esophagus. Endoscopy, computed tomography (CT) images, and magnetic resonance imaging (MRI) subsequently revealed a hemangioma in the middle esophagus. EIS was performed using 99% ethanol and 1% polydocanol, and 4 weeks later, the tumor had almost disappeared. This patient has since been followed up carefully with periodic endoscopy and barium studies and additional sclerotherapy will be performed if necessary.
A 74-year-old female with idiopathic myelofibrosis (IMF) was admitted to our hospital because of massive hematemesis and melena. Immediate upper gastrointestinal endoscopy revealed an intermittent spurting hemorrhage from extensive esophageal varices. Endoscopic injection sclerotherapy (EIS) was carried out and the bleeding ceased. After five courses of EIS, all the esophageal varices were eradicated. About 15 months later, the patient died, due to a cerebral hemorrhage, without further variceal bleeding. A postmortem examination was carried out and the portal hypertension was considered to be due not only to extramedullary hematopoiesis in the sinusoids, but also to increased splenic blood flow. We are confident that EIS is an effective therapeutic procedure for patients with IMF showing esophageal variceal hemorrhage. EIS should be the preferred choice of treatment for esophageal varices in patients with IMF, since it is less invasive than splenectomy.
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Sclerotherapy is currently used to treat acute variceal bleeds and also in the long-term management after a variceal bleed. The technical variants and results of sclerotherapy in both settings are reviewed and compared with alternative surgical treatment options. Sclerotherapy has become an accepted therapy for acute variceal bleeding. In Cape Town it is used in combination with the Sengstaken tube. A preliminary analysis of an ongoing trial comparing a rigid scope technique with a fibreoptic scope technique provides support for the use of the rigid scope in acute variceal bleeding. The place of repeated sclerotherapy in long-term management has become controversial. Varices can be eradicated and repeated variceal bleeds markedly reduced, but its role in improving survival requires further clarification.
Injection sclerotherapy is one of the most effective treatments for esophageal varices. To investigate the fate of esophageal varices embolized with a sclerosant (ethanolamine oleate), we have examined at autopsy the esophageal wall of 14 patients with esophageal varices. When the sclerosant was injected into the varices, at first thrombi formed. After two weeks, granulation tissue appeared and the thrombi were gradually replaced. The granulation tissues were organized slowly after 3 months and in the organized granulation tissue, microscopic recanalization of vessels were seen in 8 out of 9 cases. There was no recurrence of the original varices and de novo varices occurred in one patient. These observations indicate that the varices embolized with ethanolamine oleate become organized in three months after the treatment, and accordingly the esophageal varices are cured. It became also clear that recurrence of the original varices did not occur after the organization.
This report describes our data regarding repeated injection sclerotherapy using a newly designed over-tube. We treated 17 consecutive patients with esophageal varices, (3 acute, 6 elective and 8 prophylactic). An intravariceal injection of 5 per cent ethanolamine oleate was administered, using a newly designed transparent over-tube containing a second lumen for a flexible injection needle. This over-tube provides an easier, safer, shorter-in-time method of sclerosing esophageal varices. One of the 17 patients died as a result of liver failure associated with advanced cirrhosis and a concomitant hepatoma. Eradication of esophageal varices was attained in the remaining 16 patients, after an average of 5.0 injections over an average period of 5.8 weeks (range: 3-7 injections during 3-11 weeks). No complications, such as esophageal perforation or aspiration pneumonia were encountered. Recurrent variceal bleeding has not occurred during the 9 months follow-up.
Although sclerotherapy is currently the most widely used treatment for the management of both acute variceal bleeding and the long-term management of patients with varices, its definitive role in the treatment of these patients has yet to be finally proven. Sclerotherapy appears to be the most effective treatment for the majority of patients with acute variceal bleeding. Failures require either a shunt or a transection and/or devascularisation procedure. Current evidence favours simple staple gun transection or a shunt (either a portacaval shunt or a side-to-side narrow diameter polytetrafluoroethylene graft between the portal vein and vena cava). In long-term management of patients after a variceal bleed the currently favoured treatment is repeated sclerotherapy. However, failures should be identified early. We define failures as patients who present with varices that are either difficult to eradicate by sclerotherapy or who have repeated life-threatening variceal bleeds during the course of repeated injection sclerotherapy. Such patients should have either a portal-to-systemic shunt or a transection and devascularisation operation. Further controlled trials are required to define the specific indications for the individual forms of therapy. Prophylactic treatment for varices that have not yet bled is unjustified at present.
Sclerotherapy of esophageal varices is an effective hemostatic treatment and may also prevent bleeding. In our study, we examined the effects of prophylactic sclerotherapy on esophageal motility in 15 patients with Child's A cirrhosis of the liver. All the patients underwent three manometric measurements, performed respectively before the sclerotherapy, 1 week after the eradication of varices, and 3 months later. The results of our study show that prophylactic sclerotherapy of esophageal varices does not significantly change the resting pressure and length of the lower esophageal sphincter. Neither the amplitude nor the duration of the postswallowing esophageal peristaltic waves is significantly influenced by sclerotherapy. However, sclerotherapy produces a significant increase in tertiary contractions in the distal esophagus, which could explain the onset of dysphagia among patients in whom postsclerotherapy stricture is not evident.