Esophageal Hematoma 

Updated: Dec 09, 2016
Author: Jennifer Lynn Bonheur, MD; Chief Editor: Philip O Katz, MD, FACP, FACG 

Overview

Background

Esophageal hematoma is a rare condition that can be spontaneous[1, 2, 3, 4, 5, 6, 7, 8, 9] or secondary to trauma, toxic ingestion, or medical intervention.[10, 11, 12, 13]

Marks and Keet reported a case of a spontaneous intramural hematoma of the esophagus in 1968.[14] This uncommon condition has now been well documented in the literature.

Pathophysiology

Vomiting can lead to increased intraesophageal pressure that may result in mucosal tears (Mallory-Weiss syndrome), transmural perforation (Boerhaave syndrome), or intramural hematoma of the esophagus. The hemorrhage occurs within submucosal tissues.[15, 16]

Intrinsic esophageal disease, such as achalasia, is rare in patients with esophageal hematoma.

Esophageal hematoma may occur at various sites of the esophagus. The mechanism producing the hematoma may determine the site. For example, a hematoma from vomiting would be in the region of the esophagogastric junction, and a hematoma from a caustic substance might be at points of narrowing.

Epidemiology

Sex- and Age-related demographics

Approximately 80% of intramural hematomas occur in women.

Primarily middle-aged women are affected. In a literature review of 31 patients, the mean age was 67 years.

Prognosis

Long-term results are very good with conservative and supportive treatment. Intermittent odynophagia usually subsides within 2 weeks after the primary event. Recurrence is extremely rare.

Mortality/Morbidity

If the hematoma is associated with a perforation of the esophagus, septic complications (eg, mediastinitis, abscess formation) are likely to occur.

The mortality rate associated with esophageal perforations is about 10-20%.[17]

 

Presentation

History

Spontaneous intramural hematoma of the esophagus usually presents initially with severe retrosternal or epigastric pain with or without radiation. The pain is described as abrupt in onset and is aggravated by swallowing.

In one meta-analysis, 32% of patients presented with the triad of chest pain, hematemesis, and dysphagia; 99% of patients had at least one of these symptoms.

Physical

A complete and thorough physical examination should be performed.

Asking a patient to take a sip of water as part of the general examination may help to unmask symptoms of dysphagia. This may help toward distinguishing between cardiac chest pain and an esophageal disorder causing chest pain.

Palpation looking for the presence of crepitus (suggesting the presence of air under the skin) along the neck, back, and chest can help to rule in or out the presence of an esophageal perforation.

Causes

Esophageal hematomas typically occur in the setting of vomiting or retching, although spontaneous hematomas (more commonly in patients with bleeding disorders) may also occur.

Precipitating or predisposing factors to esophageal hematoma include the following:

  • Coagulopathies, such as hemophilia, or treatment with anticoagulants or aspirin

  • Instrumentation, such as with endoscopy or variceal sclerotherapy

  • Foreign body ingestion

  • Chest trauma

  • Food-induced injury, as a result of abrasive trauma by foodstuffs

  • Cardioversion and subsequent anticoagulation

  • Toxin ingestion

  • Endotracheal intubation

One study reported on 3 patients who developed intramural esophageal hematoma while on hemodialysis. Onset was sudden and characterized by progressively worsening dysphagia and hematemesis. The patients were successfully managed conservatively, with the hematoma resolving within 2-3 weeks.[18]

A prospective study by Kumar et al indicated that transesophageal echocardiography (TEE)-guided atrial fibrillation (AF) is, in rare cases, associated with esophageal hematoma, a cause of significant morbidity. In the study, which involved 1110 TEE-guided AF ablation procedures, the procedural incidence of esophageal hematoma was 0.27% (three procedures). The patients’ predominant symptoms, which arose within 12 hours of the procedure, were hoarseness, odynophagia, and regurgitation. Long-term sequelae of esophageal hematoma included the formation of esophageal strictures, as well as persistent esophageal dysmotility (in association with midesophageal hematoma) and hoarseness caused by vocal cord paralysis (in association with upper esophageal hematoma).[19]

 

DDx

Diagnostic Considerations

Differentials to consider include dissection of the thoracic aorta and aortoesophageal fistula.

Differential Diagnoses

 

Workup

Laboratory Studies

The laboratory workup should include hemoglobin concentration and coagulation profile with platelet count.

Cardiac enzymes and troponin levels should be drawn to exclude a cardiac cause for the patient's chest pain.

Imaging Studies

Chest radiograph

Chest radiographs may reveal a broadened mediastinal mass or bilateral pleural effusions. Preliminary study helps to exclude a perforation and other pathologies included in the differential diagnosis of chest pain.

Barium swallow (esophagram)

Typically, this study helps to confirm the diagnosis, revealing a filling defect in the mid and lower esophagus, usually on the posterior wall, with luminal narrowing and sometimes with mucosal irregularity. Extravasation into the mediastinum is not observed unless a perforation has occurred.

A double barrel sign or a mucosal stripe sign may be demonstrated, that is, double columns of contrast medium separated by a radiolucent stripe and a large intramural mass that reflects a mucosal dissection that allows extravasation of contrast material into the hematoma.

Computed tomography (CT) scanning with contrast

CT scanning reveals a nonenhancing, eccentric, well-defined, intramural esophageal mass that has the density of blood. It can help to better characterize esophagram findings, accurately define the extent of intramural dissection, and exclude esophageal perforation.

CT scanning is useful in excluding other conditions that may mimic esophageal hematoma, including mass lesions, aortic dissection, and pulmonary embolism.

Magnetic resonance imaging (MRI)

MRI can help demonstrate the extent of the hematoma in various planes and can help rule out additional mediastinal pathology. It is indicated for patients who cannot have a CT scan because of an allergy to iodinated contrast medium or renal impairment.

Endoscopic ultrasonography (EUS) 

An endoscopic ultrasound (EUS) shows an intramural hypoechoic submucosal mass.

Procedures

Upper endoscopy

It has been suggested that fiberoptic endoscopy is relatively contraindicated in the further evaluation of esophageal hematoma because many intramural hematomas are contained perforations that could be worsened by the insufflation of air. Others endorse the use of endoscopy in the initial evaluation once esophageal perforation has been ruled out.

Endoscopically, an esophageal hematoma is described as a bluish or purplish colored, submucosal mass protruding into the esophageal lumen.

Endoscopy can precisely identify the tear in the mucosa, but the risk of the procedure should be weighed against the need for this information and the generally uncomplicated course that these patients follow.

Flexible esophagoscopy

Flexible esophagoscopy may be a possible diagnostic tool in patients with traumatic esophageal injuries. Arantes et el evaluated the use of this technique in a retrospective (1998-2003) and prospective (2003-2005) study. One hundred sixty-three Findings from flexible esophagoscopy were compared with surgical findings or clinical follow-up in 163 patients with clinical suspicion of esophageal trauma (ie, laceration/perforation, hematoma, abrasion, hematin spots, ecchymosis) assessed.[20] No esophageal lesions were seen in 139 patients (85.3%), but 23 (14.1%) examinations demonstrated esophageal injuries, and 1 (0.6%) case was inconclusive (esophageal stricture).[20] There was surgical confirmation of lacerations in 14 patients. Of 9 patients with observed esophageal contusion, 5 underwent surgical exploration and 4 were managed nonoperatively. The investigators reported flexible esophagoscopy had 95.8% sensitivity, 100% specificity, 99.3% accuracy, 100% positive predictive value, and 99.2% negative predictive value in assessing esophageal injury.[20]

 

Treatment

Medical Care

For spontaneous intramural hematoma, conservative therapy leads to an excellent prognosis. Esophageal hematomas generally resolve within 2-3 weeks with no long-term sequelae.[21]  Note the following:

  • Nothing by mouth (NPO) for the first several days. Oral intake should be reintroduced gradually. A soft diet may be started in a stable patient on days 4-6. Parenteral feeding is generally not required, as most patients are able to swallow within a few days.

  • Provide intravenous fluids while the patient is NPO and transfusion of blood if needed. Acid suppression should also be considered to reduce the risk of esophageal ulceration. Antiemetics are indicated as needed.

  • Correction of any coagulation abnormalities is indicated.

  • Occasionally, extensive esophageal hematomas have been treated by sclerosant injections. Because this entity is so rare, a clear indication for this therapeutic approach has not yet been established. Complications during endoscopic sclerotherapy include rupture of the intramural hematoma.

Follow-up care after the acute event has resolved with either a barium swallow or endoscopy is necessary to rule out any additional esophageal disease not seen on the initial evaluation. This can be done prior to discharge or can be arranged to be done on an outpatient basis.

Surgical Care

Surgery is only indicated in patients with massive ongoing hematemesis. This occurred in 19% of patients, as reported in a literature review of 31 patients with esophageal hematoma.

Via a right thoracotomy, an esophagotomy may expose the bleeding tissue, which is then oversewn.

Consultations

Consultations with specialists in cardiology, gastroenterology, and thoracic surgery may be needed.

Complications

Full-thickness perforations of the esophageal wall have been reported during endoscopy of an esophageal hematoma.

 

Medication

Medication Summary

Acid suppression by histamine 2 (H2)-receptor antagonists or proton pump inhibitors is useful to treat or prevent esophageal ulcerations.

Proton pump inhibitors

Class Summary

Inhibit gastric acid secretion by inhibition of the H+/K+/ATP-ase enzyme system in the gastric parietal cells. These agents are used in cases of severe esophagitis and in patients not responding to H2-antagonist therapy.

Omeprazole (Prilosec)

Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATP pump.

Lansoprazole (Prevacid)

Inhibits gastric acid secretion. Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers.

Rabeprazole (Aciphex)

Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATP pump.

Esomeprazole magnesium (Nexium)

S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+ -ATP pump at secretory surface of gastric parietal cells.

Pantoprazole Sodium (Protonix)

Inhibits gastric acid secretion by inhibiting H+/K+ -ATP pump at secretory surface of gastric parietal cells.

H2-receptor antagonists

Class Summary

Reversible competitive blockers of histamine at the H2 receptors, particularly those in the gastric parietal cells where they inhibit acid secretion. The H2 antagonists are highly selective, do not affect the H1 receptors, and are not anticholinergic agents.

Ranitidine (Zantac)

Inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which in turn reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Famotidine (Pepcid)

Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Nizatidine (Axid)

Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Cimetidine (Tagamet)

Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.