Endoscopic variceal sclerotherapy has become widely used to treat patients with portal hypertension and esophageal varices, either during acute variceal bleeding or as elective chronic therapy. But complications of sclerotherapy are not rare.¹⁾ This report deals with an esophageal intramulal hematoma, an unusual complication of endoscopic variceal sclerotherapy that is not previously described in Korea.

A 35-year-old man was admitted to the hospital because of hematemesis one month prior to admission. He had been treated with NPH insulin, 30 units daily, due to known diabetes mellitus for the past 2 years.

On admission, hemoglobin was 11.1 g/dl and alkaline phosphatase was 100 IU/l, but other liver function tests were within normal ranges. Serum HBs Ag was negative and alpha-fetoprotein was below 5 ng/ml. Bleeding time, prothrombin time, activated partial thromboplastin time and platlet counts were all normal.

Upper gastrointestinal fiberscopy revealed slightly bluish, beaded esophageal varices, located in the lower esophagus, with no sign of redness (Fig. 1). No evidence of recent bleeding was found. Sclerotherapy was started with 99.9% ethanol intravariceally. After discharge, 2 more sessions of sclerotherapy were done with intravariceal injections of 5% ethanolamine oleate in one week intervals. Two days after the third session, severe swallowing difficulty and retrosternal pain developed. On endoscopy, a huge submucosal bulge in the lumen of the esophagus 25 cm distal to the upper incisors was found with dark bluish mucosal discoloration (Fig. 2). The esophageal lumen was nearly occluded. Barium esophagogram revealed a large smooth filling defect in the lower two thirds of the esophagus with near total occlusion (Fig. 3). Because of the submucosal nature of the mass, an intramural hematoma was presumed as the cause. Supportive care with parenteral nutrition was given and liquids could be swallowed with mild discomfort on the seventh day after sclerotherapy. Two weeks after the third sclerotherapy, repeat endoscopy revealed that the hematoma had completely disappeared and was replaced with a longitudinal mucosal defect (Fig. 4).

Sclerotherapy of esophageal varices is commonly used to treat patients with portal hypertension. About 10–15% of the patients undergoing sclerotherapy may have significant complications.¹⁾ Minor complications such as retrosternal discomfort, fever, mild tachycardia, and ulceration of the esophageal wall as well as major complications such as bleeding, esophageal wall necrosis, perforation, empyema, mediastinitis, and late onset stenosis have been described.²⁾

Many causes of intramural hematoma have been described as resulting from emetics,³⁾ after ingestion of a foreign body and endoscopic instrumentation.⁴⁾ following remote trauma,⁵⁾ after medication,⁶⁾ or as spontaneous events in a patient with impaired hemostasis such as in thrombocytopenia,⁷⁾ in hemophiliacs⁸⁾ and in patients receiving anticoagulation therapy,⁴⁾ as well as in patients with normal hemostasis.⁹⁾

Only 4 cases of intramural hematoma of the esophagus after sclerotherapy have been described in the English literature^10–13) Harris et al.¹⁰⁾ reported a case of intramural hematoma after sclerotherapy with sodium tetradecyl sulphate and the patient died of bacteremia. Van Steenbergen et al.¹¹⁾ described a case after the fourth sclerotherpy session with 1 % polidocanol paravariceally and intravariceally in a 43-year-old woman with hematemesis and she recovered with conservative management. Korula¹²⁾ described a case after sclerotherapy with 1.5% sodium tetradecyl sulphate intravariceally in a 45-year-old man. Conservative treatment was done and no stricture or mucosal lesion was found 5 months later. Jones et al.¹³⁾ experienced a case after the second injection with 5% ethanolamine oleate intravariceally in a 50-year-old woman with alcoholic cirrhosis. After conservative management the hematoma spontaneously discharged into the lumen leaving a longitudinal ulcer. 4 weeks later, the ulcer had healed without stricture formation.

Coagulation profiles in Van Steenbergen’s case and ours were normal. In two cases^12,13) and ours intravariceal technique was used and in one case¹¹⁾ both intravariceal and paravariceal techniques were used. The intravariceal technique was found to cause less retrosternal pain than the paravariceal technique.¹⁴⁾ Even if intravariceal injection is attempted, extravasation of the sclerosant into the surrounding tissue has been noted.¹⁵⁾ It seems probale, therfore, that injection in the present case and in the others resulted in intramural extravasation of blood and sclerosant leading to mucosal dissection.

Diagnosis of esophageal hematoma can readily be made radiologically and endoscopically. On an esophagogram the unusual finding is an elongated radiolucent filling defect with smooth borders. Since posterior hematomas are relatively common, this appearance is often best shown on a lateral view.⁹⁾ From a review of 26 patients with esophageal hematoma, Shay et al.¹⁶⁾ found that in patients with normal hemostasis, the hematoma always presented radiologically as a single lesion involving the distal esophagus and in patients with impaired hemostasis, the hematoma either spared the distal esophagus or occured at multiple sites in 60% of the cases. Early fiberoptic endoscopy is useful in establishing the diagnosis. Intraluminal bulging of the mucosa with a characteristic dark bluish discoloration indicates the presence of a submucosal hematoma.^{6,11–13,16)}

The hematoma usually resolves spontaneously within 1 to 3 weeks,^4,9,11,13) So management of such lesion is preferably conservative, as is evident in our case. Resolution may occur without residual effects, such as stricture or dysmotility.