Monoethanolamine Oleate

Synonyms: Ethanolamine Oleate (USAN); Monoéthanolamine, Oléate de; Monoethanolamini Oleas; Oleato de monoetanolamina. 2-Hydroxyethylamine compound with oleic acid; 2-Aminoethanol compound with oleic acid.
Cyrillic synonym: Моноэтаноламина Олеат.

💊 Chemical information

Chemical formula: C2H7NO,C18H34O2 = 343.5.
CAS — 2272-11-9.
ATC — C05BB01.
ATC Vet — QC05BB01.

💊 Adverse Effects and Precautions

Monoethanolamine oleate is irritant to skin and mucous membranes. Local injection may cause sloughing, ulceration, and, in severe cases, necrosis. Pain may occur at the site of injection. Patients receiving treatment for oesophageal varices may develop pleural effusion or infiltration. Hypersensitivity reactions have been reported. Sclerotherapy should not be used to treat varicose veins of the legs in patients unable to walk, with obese legs, with thrombosis or a tendency to thrombosis, or with acute phlebitis, marked arterial, cardiac, or renal disease, local or systemic infections, or uncontrolled metabolic disorders such as diabetes mellitus. Monoethanolamine oleate should not be used in patients taking oral contraceptives.

Effects on the kidneys.

Acute renal failure, which cleared spontaneously within 3 weeks, occurred in 2 obese women given sclerosing injections of 15 to 20 mL of a solution containing monoethanolamine oleate 5% and benzyl alcohol 2%.1
1. Maling TJB, Cretney MJ. Ethanolamine oleate and acute renal failure. N Z Med J 1975; 82: 269–70.

💊 Uses and Administration

Monoethanolamine oleate is used as a sclerosant in the treatment of varicose veins and oesophageal varices. For sclerotherapy of varicose veins, 2 to 5 mL of a 5% solution of monoethanolamine oleate is injected slowly into empty isolated sections of vein, divided between 3 or 4 sites. Injection into full veins is also possible. For sclerotherapy of oesophageal varices, the dose is 1.5 to 5 mL of a 5% solution per varix to a maximum total dose of 20 mL per treatment session. Treatment may be given in the initial management of bleeding varices, then repeated at intervals until the varices are occluded.

Variceal haemorrhage.

Portal hypertension may occur in many conditions that affect the liver, and leads to the development of collateral channels linking the portal and systemic circulations. Enlargement of such blood vessels beneath the oesophageal and gastric mucosa produces varices which have about a 30% risk of rupture and bleeding. Oesophageal varices are more often a cause of haemorrhage than gastric varices. Capillaries and veins in the gastric mucosa may also become swollen, a condition known as portal hypertensive gastropathy, and clinically important bleeding may occur in severe cases. Variceal haemorrhage is usually severe, with mortality as high as 50% for the initial episode; the recurrence rate may be as high as 100% in patients who survive without treatment. Bleeding may stop spontaneously, but in those who continue to bleed, control of haemorrhage is difficult and patients should be referred to a centre with appropriate specialist facilities. Treatment to stabilise the patient may be necessary before they can be safely transferred. Acute management. Initial treatment is supportive and requires measures to prevent aspiration and maintain a clear airway, and volume replacement with colloid and blood. Emergency endoscopy should be performed to establish the site of haemorrhage and exclude non-variceal sources of bleeding. The choice of treatment depends on the site of haemorrhage.1-9 Endoscopic methods have been favoured for initial management. Injection sclerotherapy or banding ligation are used for bleeding oesophageal varices but the optimum management of bleeding gastric varices remains to be defined; the value of injection sclerotherapy varies with their location. Intravariceal injection of bovine or human thrombin, or cyanoacrylate tissue adhesives, has been used in gastric varices. Where the source of haemorrhage is nonvariceal and due to gastropathy, portal decompressive surgery is effective, although it is associated with a high incidence of encephalopathy in cirrhotic patients. Small studies have shown propranolol to be effective in arresting haemorrhage.10 Injection sclerotherapy for variceal haemorrhage may be performed during the emergency endoscopy procedure. Intravariceal injection, paravariceal injection, or a combination of the two have been used. The most widely used sclerosants are monoethanolamine oleate and sodium tetradecyl sulfate for intravariceal injection and lauromacrogol 400 for paravariceal injection. Sclerotherapy controls bleeding in up to 95% of cases. Ulceration and stricture formation occur frequently following injection sclerotherapy. An alternative technique is endoscopic banding ligation, where elastic bands are placed around the varices. The tissue subsequently necroses to leave a superficial ulcer. This technique is more successful than injection sclerotherapy, but may be more difficult to perform if active bleeding is occurring. Procedures may be repeated if bleeding continues or restarts. Where endoscopy is unavailable, drug therapy or balloon tamponade may be used until the patient can be transferred to a specialist centre. These techniques may also have a role when sclerotherapy fails and some have suggested that initial drug therapy may be preferable to sclerotherapy11 or endoscopy.12 Drug therapy is aimed at controlling portal venous pressure, although it is ineffective in massive haemorrhage and its effects cease once the drug is stopped. Two meta-analyses11,13 have examined data from studies comparing drug therapy with endoscopic methods for the treatment of acute variceal bleeding. Sclerotherapy did not appear to be superior to vasoactive drugs as the first single treatment, and was associated with more frequent adverse effects.11 Adjunctive drug therapy improved the efficacy of endoscopic therapy (injection sclerotherapy or band ligation) compared with endoscopic methods alone, although overall mortality was not affected; severe adverse effects were similar in both groups.13 Drugs used include vasopressin and its analogue terlipressin and, more recently, somatostatin and its analogue octreotide. Vasopressin controls haemorrhage in about 50% of patients. It is given by continuous intravenous infusion, together with glyceryl trinitrate, which counteracts the adverse cardiac effects of vasopressin, while potentiating its reduction of portal pressure. Terlipressin has the advantage of a longer therapeutic action, enabling bolus doses to be given. A comparison14 of terlipressin and sclerotherapy found them to be equally effective for the control of acute variceal bleeding. A systematic review15 of studies comparing terlipressin with placebo, or other drugs or interventions, also gave favourable results. However, somatostatin,2 and particularly octreotide,2,16,17 which may be given by bolus injection, are now generally preferred as they are thought to have similar efficacy to vasopressin but fewer adverse effects. A metaanalysis18 of studies comparing somatostatin or its analogues octreotide and vapreotide with either placebo or no drug treatment suggested a small benefit in controlling bleeding; however, no mortality benefit has yet been shown. Clinical studies with recombinant factor VIIa to control acute variceal bleeding have produced beneficial results.12 Balloon tamponade controls bleeding by direct pressure on the varices. Although it is a very effective means of controlling haemorrhage, there is a high incidence of rebleeding once pressure is removed and the incidence of complications is high. It is useful in cases of massive haemorrhage when drug therapy is ineffective and sclerotherapy is difficult. Surgery, such as the formation of a shunt or oesophageal transection, may be necessary if the above measures fail to control the bleeding. However, such techniques have been associated with high mortality in some series. Formation of a transjugular intrahepatic portal-systemic shunt (TIPS) is now generally preferred.4It may be particularly useful in candidates for liver transplantation. Limited data suggest that the shunt may remain patent in the majority of patients for at least 3 years.19 Short-term antibacterial prophylaxis has been proposed20 for cirrhotic patients with gastrointestinal bleeding, including variceal bleeding, because reduced rates of infection and improved short-term survival have been reported in a few studies, although there is no benefit on overall mortality.21 Long-term management. Once the acute bleeding has been controlled measures are needed to prevent rebleeding. Endoscopic therapy is widely used, with injection sclerotherapy or banding ligation being repeated until the varices are obliterated. Banding ligation is now the treatment of choice; it eradicates varices in fewer treatment sessions than injection sclerotherapy and reduces the risk of ulceration and stricture formation.22,23 Sucralfate has been given following sclerotherapy as it may reduce the frequency of stricture formation and reduce bleeding from treatment-related ulcers. It seems to have no influence on ulcer healing following banding ligation.24 Some practitioners carry out regular endoscopic checks and repeat sclerotherapy or banding ligation when varices reappear, although this approach is no more effective in terms of improving survival than giving treatment once bleeding occurs. Drug therapy is an alternative to endoscopic methods.25 Beta blockers (mainly propranolol) reduce the incidence of recurrent variceal bleeding and may improve survival.23,26,27 A combination of nadolol with isosorbide mononitrate has been reported to reduce the risk of rebleeding more than repeated sclerotherapy, although there was no significant effect on mortality.28 Drug therapy has also been used as an adjunct to endoscopic methods to control rebleeding in the period before variceal obliteration has occurred, or for long-term management following endoscopic therapy. However, studies comparing endoscopic band ligation with combination drug therapy have produced variable results.29 Long-term octreotide therapy following sclerotherapy has also been investigated and may reduce recurrent variceal bleeding.30 Several studies31-33 have compared TIPS with endoscopic treatment, but no clear benefit has been demonstrated and there may be an increased risk of encephalopathy with the use of shunts. Surgery, including liver transplantation, should be considered in patients with recurrent life-threatening haemorrhage. Propranolol may also have a role in patients with portal hypertensive gastropathy. In a controlled study, propranolol reduced the incidence of recurrent bleeding from portal hypertensive gastropathy in patients with cirrhosis.34 Prophylaxis of a first bleed in patients with portal hypertension is controversial since about 70% of patients who have varices will never bleed, but should probably be given to patients with cirrhosis and varices thought to be at high risk of bleeding. A reliable system that will identify those at high risk of haemorrhage has yet to be devised. The NIEC (North Italian Endoscopic Club) system is probably the best so far,35,36 and is based on size of the varices, presence of red wale marks on the varices, and Child-Pugh class; amendments to improve the traditional index have been suggested.36 Sclerotherapy had been considered as a method of prophylaxis, but its value has not been clearly established. Studies show that beta blockers decrease the incidence of a first bleed27,37 and are probably the treatment of choice if prophylaxis is to be given. Banding ligation may be a suitable alternative for patients who are unable to take beta blockers.38Others consider banding ligation to be the standard therapy for prophylaxis.9 A meta-analysis39 of 9 randomised controlled studies concluded that variceal banding ligation was superior to beta blockers in preventing a first variceal bleed, whereas a systematic review40 of 16 randomised controlled studies found both treatments to be effective and suggested that the estimated effect of banding ligation in some studies may be biased and was associated with shorter duration of follow-up. It is postulated that a reduction in portal pressure to below 12 mmHg is necessary to reduce the incidence of variceal bleeding and that treatment with beta blockers alone does not achieve this. More effective drugs are being sought, and isosorbide mononitrate9,41,42 (as adjunctive therapy with a beta blocker) and clonidine43 have been investigated for the prophylaxis of a first bleed and prevention of recurrent haemorrhage in patients with portal hypertension.
1. Williams SGJ, Westaby D. Management of variceal haemorrhage. BMJ 1994; 308: 1213–17
2. Roberts LR, Kamath PS. Pathophysiology and treatment of variceal hemorrhage. Mayo Clin Proc 1996; 71: 973–83
3. Sung JJY. Non-surgical treatment of variceal haemorrhage. Br J Hosp Med 1997; 57: 162–6
4. Stanely AJ, Haynes PC. Portal hypertension and variceal haemorrhage. Lancet 1997; 350: 1235–9
5. McCormack G, McCormick PA. A practical guide to the management of oesophageal varices. Drugs 1999; 57: 327–35
6. Dagher L, et al. Management of oesophageal varices. Hosp Med 2000; 61: 711–17
7. Anonymous. Early management of bleeding oesophageal varices. Drug Ther Bull 2000; 38: 37–40
8. Krige JEJ, Beckingham IJ. ABC of diseases of liver, pancreas, and biliary system. Portal hypertension—1: varices. BMJ 2001; 322: 348–51
9. Sharara AI, Rockey DC. Gastroesophageal variceal hemorrhage. N Engl J Med 2001; 345: 669–81
10. Anonymous. Portal hypertensive gastropathy. Lancet 1991; 338: 1045–6
11. D’Amico G, et al. Emergency sclerotherapy versus medical interventions for bleeding oesophageal varices in cirrhotic patients. Available in The Cochrane Database of Systematic Reviews; Issu
1. Chichester: John Wiley; 2002 (accessed 08/02/06)
12. Abraldes JG, et al. Medical management of variceal bleeding in patients with cirrhosis. Can J Gastroenterol 2004; 18: 109–13
13. Bañares R, et al. Endoscopic treatment versus endoscopic plus pharmacologic treatment for acute variceal bleeding: a metaanalysis. Hepatology 2002; 35: 609–15
14. Escorsell À, et al. Multicenter randomized controlled trial of terlipressin versus sclerotherapy in the treatment of acute variceal bleeding: the TEST study. Hepatology 2000; 32: 471–6
15. Ioannou G, et al. Terlipressin for acute esophageal variceal hemorrhage. Available in The Cochrane Database of Systematic Reviews; Issu
1. Chichester: John Wiley; 2003 (accessed 08/02/06)
16. Erstad BL. Octreotide for acute variceal bleeding. Ann Pharmacother 2001; 35: 618–26
17. Corley DA, et al. Octreotide for acute esophageal variceal bleeding: a meta-analysis. Gastroenterology 2001; 120: 946–54
18. Gøtzsche PC, Hróbjartsson A. Somatostatin analogues for acute bleeding oesophageal varices. Available in The Cochrane Database of Systematic Reviews; Issu
1. Chichester: John Wiley; 2005 (accessed 08/02/06)
19. van Buuren HR, ter Borg PC. Transjugular intrahepatic portosystemic shunt (TIPS): indications and long-term patency. Scand J Gastroenterol 2003; 38 (Suppl 239): 100–104
20. Bernard B, et al. Antibiotic prophylaxis for the prevention of bacterial infections in cirrhotic patients with gastrointestinal bleeding: a meta-analysis. Hepatology 1999; 29: 1655–61
21. Hou M-C, et al. Antibiotic prophylaxis after endoscopic therapy prevents rebleeding in acute variceal hemorrhage: a randomized trial. Hepatology 2004; 39: 746–53
22. Laine L, Cook D. Endoscopic ligation compared with sclerotherapy for treatment of esophageal variceal bleeding: a metaanalysis. Ann Intern Med 1995; 123: 280–7
23. Wright AS, Rikkers LF. Current management of portal hypertension. J Gastrointest Surg 2005; 9: 992–1005
24. Nijhawan S, Rai RR. Does post-ligation oesophageal ulcer healing require treatment? Lancet 1994; 343: 116–17
25. Bosch J, Garcia-Pagan JC. Prevention of variceal rebleeding. Lancet 2003; 361: 952–4
26. Bernard B, et al. Beta-adrenergic antagonists in the prevention of gastrointestinal rebleeding in patients with cirrhosis: a metaanalysis. Hepatology 1997; 25: 63–70
27. Talwalkar JA, Kamath PS. An evidence-based medicine approach to beta-blocker therapy in patients with cirrhosis. Am J Med 2004; 116: 759–66
28. Villanueva C, et al. Nadolol plus isosorbide mononitrate compared with sclerotherapy for the prevention of variceal rebleeding. N Engl J Med 1996; 334: 1624–9
29. Groszmann RJ, Garcia-Tsao G. Endoscopic variceal banding vs. pharmacological therapy for the prevention of recurrent variceal hemorrhage: what makes the difference? Gastroenterology 2002; 123: 1388–91
30. Jenkins SA, et al. Randomised trial of octreotide for long term management of cirrhosis after variceal haemorrhage. BMJ 1997; 315: 1338–41
31. Sanyal AJ, et al. Transjugular intrahepatic portosystemic shunts compared with endoscopic sclerotherapy for the prevention of recurrent variceal hemorrhage: a randomized, controlled trial. Ann Intern Med 1997; 126: 849–57
32. Cello JP, et al. Endoscopic sclerotherapy compared with percutaneous transjugular intrahepatic portosystemic shunt after initial sclerotherapy in patients with acute variceal hemorrhage: a randomized, controlled trial. Ann Intern Med 1997; 126: 858–65
33. Rössle M, et al. Randomised trial of transjugular-intrahepaticportosystemic shunt versus endoscopy plus propranolol for prevention of variceal rebleeding. Lancet 1997; 349: 1043–9
34. Pérez-Ayuso RM, et al. Propranolol in prevention of recurrent bleeding from severe portal hypertensive gastropathy in cirrhosis. Lancet 1991; 337: 1431–4
35. The North Italian Endoscopic Club for the Study and Treatment of Esophageal Varices. Prediction of the first variceal hemorrhage in patients with cirrhosis of the liver and esophageal varices: a prospective multicenter study. N Engl J Med 1988; 319: 983–9
36. Merkel C, et al. Prognostic indicators of risk for first variceal bleeding in cirrhosis: a multicenter study in 711 patients to validate and improve the North Italian Endoscopic Club (NIEC) index. Am J Gastroenterol 2000; 95: 2915–20
37. Pagliaro L, et al. Prevention of first bleeding in cirrhosis: a meta-analysis of randomised trials of nonsurgical treatment. Ann Intern Med 1992; 117: 59–70
38. Burroughs AK, Patch D. Primary prevention of bleeding from esophageal varices. N Engl J Med 1999; 340: 1033–5
39. Tripathi D, et al. Variceal band ligation versus beta-blockers for primary prevention of variceal bleeding: a meta-analysis. Eur J Gastroenterol Hepatol 2007; 19: 835–45
40. Gluud LL, et al. Banding ligation versus beta-blockers as primary prophylaxis in esophageal varices: systematic review of randomized trials. Am J Gastroenterol 2007; 102: 2842–8
41. Angelico M, et al. Isosorbide-5-mononitrate versus propranolol in the prevention of first bleeding in cirrhosis. Gastroenterology 1993; 104: 1460–5
42. Merkel C, et al. Randomised trial of nadolol alone or with isosorbide mononitrate for primary prophylaxis of variceal bleeding in cirrhosis. Lancet 1996; 348: 1677–81
43. Blendis LM. Clonidine for portal hypertension: a sympathetic solution? Ann Intern Med 1992; 116: 515–17.

Varicose veins.

Varicose veins are tortuous, protruding veins in the legs, that occur when weak vein walls and valve incompetence result in venous reflux and dilatation. Symptoms associated with varicose veins include heaviness, tension, aching, and itching of the legs. Complications include oedema, thrombophlebitis, deep venous thrombosis, lipodermatosclerosis, and venous ulceration. Risk factors for varicose veins include increasing age, pregnancy, and occupations that involve prolonged standing.1 The management of varicose veins has been reviewed.1-3 Conservative management using compression hosiery may be effective for relief of symptoms in some patients but longer-term compliance is poor.3 Surgery or sclerotherapy are other treatment options, depending on the veins affected. Surgical treatment, which is the gold standard for treatment of more severe varicose veins, may involve ligation of the affected vein, stripping of the affected stem vein, or avulsions of the varicosities.3 In sclerotherapy, which may be the treatment of choice for thread veins,2 a sclerosant is injected into the affected vein where it irritates and damages the lining of the vein causing local thrombosis, fibrosis, and stenosis. Detergent sclerosants include monoethanolamine oleate, sodium tetradecyl sulfate, lauromacrogol 400, and sodium morrhuate; osmotic sclerosants include hypertonic sodium chloride solutions, and hypertonic mixtures of sodium chloride and glucose; caustic sclerosants include chromated glycerol, and a mixture of iodine and sodium iodide. Graduated compression dressings are usually applied after sclerotherapy to minimise the time taken for the surrounding tissue to absorb the damaged segment of vein. Compression may also help to reduce complications of sclerotherapy including hyperpigmentation, oedema, aching, thrombophlebitis, and deep venous thrombosis. A systematic review4 of randomised controlled trials of injection sclerotherapy failed to determine its place in the overall management of varicose veins, since the type of sclerosant, formulation, local pressure dressing, or degree and length of compression do not appear to have a significant effect on efficacy. However, the evidence supports its current place in practice, which is in the treatment of recurrent varicose veins following surgery, and thread veins. In another systematic review,5 the use of surgery or sclerotherapy for the management of primary varicose veins was compared. There was a tendency for better early outcomes with sclerotherapy whereas surgery produced more long-term benefits. However, there was insufficient evidence to recommend the use of one form of treatment over the other, and the extent of the varicose veins ultimately governs the choice. New methods of treatment being tried include foam sclerotherapy, in which a detergent-like sclerosant is mixed with air to create a foam,2 ambulatory phlebectomy, endovenous laser therapy, and radiofrequency ablation.3,6
1. London NJ, Nash R. ABC of arterial and venous disease: varicose veins. BMJ 2000; 320: 1391–4
2. Rabe E, et al. German Society of Phlebology. Guidelines for sclerotherapy of varicose veins (ICD 10: I83.0, I83.1, I83.2, and I83.9). Dermatol Surg 2004; 30: 687–93
3. Beale RJ, Gough MJ. Treatment options for primary varicose veins—a review. Eur J Vasc Endovasc Surg 2005; 30: 83–95
4. Tisi PV, et al. Injection sclerotherapy for varicose veins. Available in The Cochrane Database of Systematic Reviews; Issu
4. Chichester: John Wiley; 2006 (accessed 04/06/08)
5. Rigby KA, et al. Surgery versus sclerotherapy for the treatment of varicose veins. Available in the Cochrane Database of Systematic Reviews; Issu
4. Chichester: John Wiley; 2004 (accessed 09/02/06)
6. Sadick NS. Advances in the treatment of varicose veins: ambulatory phlebectomy, foam sclerotherapy, endovascular laser, and radiofrequency closure. Dermatol Clin 2005; 23: 443–55.

💊 Preparations

BP 2008: Ethanolamine Oleate Injection.

Proprietary Preparations

Braz.: Ethamolin; Jpn: Oldamin; USA: Ethamolin.
Published May 08, 2019.