Rodica Ouatu-Lascar, Gayatri Bharadhwaj and George Triadafilopoulos  Gastroenterology Section, Palo Alto Veterans Affairs Health Care System, Palo Alto, California and Division of Gastroenterology, Department of Medicine, Stanford University, Stanford, California, USA
Rodica Ouatu-Lascar, MD, Department of Internal Medicine, Wayne State University, Detroit, Michigan, USA; Gayatri Bharadhwaj, M.D, Gastroenterology Division, University of California San Francisco, San Francisco, California, USA; George Triadafilopoulos, MD, Gastroenterology Division, Stanford University, Stanford, California, USA
Correspondence to: George Triadafilopoulos, M.D., Gastroenterology Section (111-GI), Palo Alto VA Health Care System, 3801 Miranda Avenue, Palo Alto, CA 94304, USA
Telephone: 650-4935000 Ext.64485, Fax. 650-856-8024
Email. vagt@leland.stanford.edu
Received: 2000-02-13 Accepted: 2000-03-01

Subject headings: esophagus; hematoma/etiology; endoscopy; gast rointestinal hemorrhage/diagnosis; hematoma/classification; wounds; injuries

Ouatu-Lascar R, Bharadhwaj G, Triadafilopoulos G. Endoscopic appearance of esophageal hematomas. World J Gastroenterol, 2000;6(2):307-309

INTRODUCTION
Esophageal hematomas develop from the dissection of the mucosa from the mu scular layers of the esophageal wall and represent an uncommon condition affecti ng all ages^［1-3］. Although the most common cause of esophageal hematoma s is iatrogenic mechanical injury-induced by prolonged nasogastric intubation, difficult or forceful endoscopic intubation, or the result of variceal injection sclerot herapy- some may be spontaneous, particularly in patients receiving anticoagula nts^［3-6］. Presenting symptoms most commonly include dysphagia, hemateme sis, and sub-sternal or epigastric pain^［5,9］.
      In this report, we present four cases of esophageal hematomas diagnosed en doscopically, describe their clinical and endoscopic characteristics and propose a classification. As our cases exemplify, therapy is conservative and a favorab le prognosis is the rule. Although the diagnosis has traditionally been made by barium esophagography^［1］or CAT scanning^［1,10］, the increased us e of endoscopy will allow increased recognition of esophageal hematomas even at a subclinical (asymptomatic) stage and ultimately lead to a better understanding of their etiopathogenesis and their prevention.

CASE REPORTS
Case 1 A 90-year-old man with a history of hypertension, con gestive heart failure, and mild aortic stenosis was refered for upper endoscopy to determine the cause of iron deficiency anemia. A colonoscopy had previously revealed diver ticular disease. Laboratory values included a hematocrit of 30%, iron of 90mg/L and a TIBC of 358. Coagulation studies were normal. Endoscopy rev ealed salmon-colored mucosa extending from 28cm-34cm from the incis ors, consistent with Barrett＇s esophagus. A densely red, elevated lesion, consi stent with a hematoma was noted at 19cm(Figure 1a). No therapy was given. A follow-up endoscopy, performed one week later, showed complete resolution of the hematoma. Because of its location, the hematoma was attributed to a difficult, possibly traumatic, endoscopic intubation.

Case 2 A 59-year-old man was referred for upper endoscopy b ecause of chronic reflux symptoms. His medications included omeprazole 20mg po- daily, and aspirin 325mg po- daily. Endoscopy revealed conflu ent esophageal erosions and ulcers consistent with Savary stage Ⅲ esophagitis f rom 36cm-33cm. Upon biopsy of the esophagus, a purple-red, elevated lesion, consistent with a hematoma was noted at 35cm(Figure 1b).Histologic examination of the biopsy sample revealed changes consistent with ref lux esophagitis. The hematoma was attributed to the mucosal biopsy obtained in the context of aspirin intake.

Case 3 A 90-year-old man with solid food dysphagia was refer ed for esophageal dilation. He had a history of metastatic (stage 4) squamous es ophageal cancer treated with radiation therapy and esophageal dilation. He had m ild anemia, but no thrombocytopenia or coagulation abnormalities. Endoscopy reve aled a mid-esophageal stricture at 5cm-29cm which was dilated with minimal resistance using Savary dilators over a guide wire. This resulted in a 1cm-long submucosal hematoma at 26cm(Figure 1c). No biopsy was obtained. Because the patient＇s dysphagia resolved, there was no follow-up endoscopy.

Case 4 A 51-year-old male with a history of rheumatic heart disease, status post aortic valve replacement, was hospitalized for mitral valve replacement. Because his postoperative course was complicated by enterococcal s epsis, a transesophageal echocardiogram was performed which excluded the presenc e of endocarditis. The following day, hematemesis was noted. Coagulation paramet ers were within the expected therapeutic range for prosthetic valves. An emerge ncy upper endoscopy revealed a 3cm-long, dark red esophageal mass at the GE junction, completely obliterating the esophageal lumen(Figure 1d). Biopsies obtained from the surface of the mass revealed organized clot and acute esophageal mucosal inflammation (not shown). Broad spectrum antibiotics and H₂ receptor antagonists were administered intravenously; effective anticoagul-ation was also continued. Although there was no more evidence of gastrointestinal hemorrhage, the patient eventually succumbed to sepsis ten days later. Autopsy revealed severe herpetic tracheobronchitis without any evidence of eso phageal injury.

DISCUSSION
Esophageal hematomas appear as raised purplish-red lesions, mostly sub-muc osal in location, but occasionally obliterating the esophageal lumen. Depending on their etiology, they may be classified as spontaneous or traumatic. Based on the above observations, we propose that esophageal hematomas can be further clas sified according to the degree of involvement of the lumen in four stages(Table 1). Esophageal hematoma formation^［11,12］, is an uncommon con dition in which an intramural hemorrhage leads to a variable degree of submucosa l dissection of the esophageal wall ranging from single or multiple localized he matomas to complete dissection of the esophagus^［1］. Esophageal hematomas may be spontaneous, associated with sudden changes in the transmural wall press ures due to a variety of causes including coughing, retching or protracted vomiti ng^［13］, or may result from iatrogenic instrumentation, such as esophage al variceal sclerotherapy^{［3,14,15］}or transesophageal ultrasonogr aphy^［6］(Table 2). Hematomas may also be associated with direct trauma from abrasive foodstuffs such as taco shells^［16］, pill-induced esophageal injury^［17］, or with a coagulopathy, with little or no history of esopha geal barotrauma^［5］. Other probable causes include esophageal s tricture, diverticulum, esophageal arteriovenous malformation, and aspirin use^［18］. The majority of patients with esophageal hematomas are older than 70 yr, although isolated reports of patients as young as 21 yr have been made. In some studies, there seems to be a predilection for the female gender^［1］.

Table 1 Stages of esophageal hematomas

Figure 1 Endoscopic appearance of esophageal hematom as.-
a: Stage Ⅰ esophageal hematoma. There is no surrounding edema. Patient was asymptomatic. 
b. Stage Ⅱ esophageal hematoma after an esophageal biops y. Note the surrounding tissue edema. 
c. Stage Ⅲ hematoma induced by esopha geal dilation of a stricture. There is edema and separation of the surface mucos al layer that is partially obliterating the lumen. Patient was asymptomatic. 
d. Stage Ⅳ esophageal hematoma related to recent transesophageal echocardiogra phy. Edema and clot formation led to complete obliteration of the esophageal lum en and hematemesis.

Table 2 Causes of esophageal hematomas

      The clinical presentation is variable. Although mostly asymptomatic, esoph ageal hematomas may present with dramatic chest pain, severe dysphagia, and hema temesis. In such instances, they should be differentiated from Mallory-Weiss t ear and Boorhaave＇s syndrome, conditions which they may closely mimic^{［19-2 1］}. Typically barium swallow or CAT scan have been used for the diagnosis, sh owing intraluminal filling defects or a double-barrelled appearance of the eso phagus^［22］. More recently, endoscopy is the preferred investigation, es pecially when hematemesis is the presenting symptom^［23］.Because spontaneous resolution is the rule, the treatment of esophageal hematomas is conservative and consists of a regime n of nil by mouth, intravenous alimentation and antibiotics in severe cases^［1］. Surgery is reserved only for rare instances, to drain a hematoma and cl ose an esophageal mucosal tear^［24］.
      In our study, all four patients were male, the hematoma was visualized end oscopically, and was traumatic either from insertion of the scope (cases 1 and 4 ), or from endoscopic manipulation (cases 2 and 3). In 3 out of 4 of our patient s the hematomas were asymptomatic. Because of the increased utilization of endos copy for diagnosis and therapy, it is expected that esophageal hematomas will be encountered more frequently. This is particularly true in cases of esophageal d ilation of strictures, repetitive multiple biopsies for surveillance of Barret t＇s esophagus, esophageal variceal sclerotherapy, and transesophageal echoc ardiog raphy.
      Hematomas related sclerotherapy seem to occur 2d-4d after injection, when tissue necrosis that extends into the submucosa reaches its maximum. Contr ibuting factors include volume of sclerosant per injection, interval between tre atments, paravariceal versus intra-variceal injection, bleeding diathesis, and o ccurrence of retching or prolonged Valsalva during or shortly after the treatmen t^［3-5］. Early endoscopy is useful in establishing the diagnosis and rev eals an intraluminal bulge of the mucosa with dark blue discoloration.
      The blind insertion of a transesophageal endosonographic probe for diagnosis of valvular heart disease^［25］, and its increased utilization during cardiothoracic surgery^［6］represents an additional risk for esophageal hematoma formation, as exemplified in case 4 of this report. A recent review of the literature on the association of transesophageal echocardiography during car diac surgery and gastrointestinal bleeding revealed that the overall percentage of postoperative gastrointestinal complaints following the procedure was 11%, an d frank upper gastrointestinal bleeding was 2.1%^［6］. Another multicent er survey of 10419 examinations on the safety of transesophageal echocardi ography revealed only 2 patients who developed bleeding complications which neca ssitated interruption of the examination^［7］. Realising that the risk of gastrointestinal bleeding is small but present, most authors recommend careful review of upper digestive symptoms to rule out preexisting esophageal pathology , ample lubrication of the endosonographic tip, and avoidance of fixation of the probe in a flexed position for prolonged periods in order to avoid contact pres sure and esophageal mucosal damage^［8］.
      In conclusion, our study reviews the endoscopic features of esophageal hem atomas and classifies them in terms of etiology and appearance. With the widespr ead use of esophageal instrumentation, these lesions will be increasingly recogn ized endoscopically. Depending on their severity and endoscopic stage, esophagea l hematomas may or may not be associated with symptoms. Treatment is generally c onservative and favorable prognosis is the rule.

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