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Gastroenterology > Esophagus
Mallory-Weiss Tear
Article Last Updated: Apr 16, 2008
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Louis-Michel Wong Kee Song, MD, Assistant Professor, Department of Medicine, Division of Gastroenterology and Hepatology, Mayo Clinic
Louis-Michel Wong Kee Song is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Medical Association, and American Society for Gastrointestinal Endoscopy
Editors: Terence David Lewis, MBBS, FRACP, FRCPC, FACP, Program Director, Internal Medicine Residency, & Assistant Chairman, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, Loma Linda University Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Douglas M Heuman, MD, FACP, Director of Hepatology, McGuire Veterans Affairs Medical Center, Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine; Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine; Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Author and Editor Disclosure
Synonyms and related keywords:
MWT, gastroesophageal tears, Mallory-Weiss syndrome, Mallory-Weiss lesion, upper gastrointestinal hemorrhage, retching, vomiting, mucosal lacerations, intragastric pressure, gastric prolapse, straining, hiccuping, coughing, primal scream therapy, blunt abdominal trauma, cardiopulmonary resuscitation, iatrogenic tears, portal hypertension, gastroesophageal varices, hiatal hernia
Background
Mallory-Weiss syndrome is characterized by upper gastrointestinal bleeding secondary to longitudinal mucosal lacerations at the gastroesophageal junction or gastric cardia. The original description by Mallory and Weiss in 1929 involved patients with persistent retching and vomiting following an alcoholic binge. However, Mallory-Weiss syndrome may occur after any event that provokes a sudden rise in intragastric pressure or gastric prolapse into the esophagus.
Pathophysiology
A Mallory-Weiss tear (MWT) likely occurs as a result of a large, rapidly occurring, and transient transmural pressure gradient across the region of the gastroesophageal junction. Acute distension of the nondistensible lower esophagus can also produce a linear tear in this region. With a rapid rise in intragastric pressure due to precipitating factors, such as retching or vomiting, the transmural pressure gradient increases dramatically across the hiatal hernia, which abuts a low intrathoracic pressure zone. If the shearing forces are high enough, a longitudinal laceration eventually occurs. Within the hernia, the tear is more likely to involve the lesser curvature of the gastric cardia, which is relatively immobile compared to the remainder of the stomach. Another potential mechanism for MWTs is the violent prolapse or intussusception of the upper stomach into the esophagus, as can be witnessed during forceful retching at endoscopy.
Frequency
United States
MWTs account for 1-15% of cases of upper gastrointestinal bleeding.
International
Prevalence probably is similar to that in the United States.
Mortality/Morbidity
- Bleeding from MWTs stops spontaneously in 80-90% of patients. With conservative therapy, most tears heal uneventfully within 48 hours. Thus, a MWT can easily be missed if endoscopy is delayed.
- The degree of blood loss varies. Earlier studies reported that the proportion of patients requiring blood transfusions was 40-70%. These figures do not seem to be the trend today and are probably significantly lower.
- Hemodynamic instability and shock may occur in up to 10% of patients. In one series, mortality as high as 8.6% was attributed to MWTs. Current clinical experience suggests a significantly lower mortality rate from MWTs.
Race
MWTs have no racial predilection.
Sex
Most studies report a male predominance. Male-to-female ratios reportedly are 2-4:1.
Age
Patients usually present in their 40s or 50s, but the age range is quite wide.
History
- The classic presentation consists of an episode of hematemesis following a bout of retching or vomiting, although this presentation may be less common than previously thought. Graham and Schwartz found that a typical history was obtained in only about 30% of patients.1 In a study by Harris and DiPalma, hematemesis on first emesis was reported in 50% of patients.2
- Hematemesis is present in 85% of patients.
- Less common presenting symptoms include melena, hematochezia, syncope, and abdominal pain.
- Excessive alcohol use has been reported in 40-75% of patients, and aspirin use has been reported in up to 30% of patients.
- Attempt to identify a precipitating factor for the MWT (see Causes).
Physical
- MWTs do not elicit specific physical signs.
- Physical findings relate to the rate and the degree of gastrointestinal blood loss. Tachycardia, hypotension, orthostatic changes, or overt shock may be evident.
Causes
- The presence of a hiatal hernia is a predisposing factor and is found in 35-100% of patients with MWTs. During retching or vomiting, the transmural pressure gradient is greater within the hernia than the rest of the stomach, and it is the location most likely to sustain a tear. Precipitating factors include retching, vomiting, straining, hiccuping, coughing, primal scream therapy, blunt abdominal trauma, and cardiopulmonary resuscitation.
- Iatrogenic tears are uncommon, considering the frequency with which patients retch during endoscopy. The reported prevalence is 0.07-0.49%.
- In a few cases, no apparent precipitating factor can be identified. In one study, 25% of patients had no identifiable risk factor.
Boerhaave Syndrome
Esophagitis
Gastric Ulcers
Other Problems to be Considered
Cameron erosions
Lab Studies
- Hemoglobin and hematocrit studies are performed to assess the severity of the initial bleeding episode and to monitor patients.
- Platelet count, prothrombin time, and activated partial thromboplastin time are performed to assess for severe thrombocytopenia and coagulopathy as complicating issues. Coagulation studies are needed in patients on anticoagulants or with minimal or no oral intake while on antibiotics. Platelet count may be low because of alcohol use.
- BUN, creatinine, and electrolyte levels are measured to guide intravenous fluid therapy.
- Blood type and antibody screen are obtained for potential blood transfusions.
Imaging Studies
- Barium or Gastrografin studies should not be performed owing to their low diagnostic sensitivity and interference with endoscopic assessment and therapy.
Other Tests
- Electrocardiogram and cardiac enzymes (if indicated) - To assess for myocardial ischemia related to acute gastrointestinal blood loss, especially in patients with significant anemia, hemodynamic instability, cardiovascular disease, coexisting chest pain, and/or advanced age.
Procedures
- Perform endoscopy early in the clinical course. Endoscopy is the procedure of choice for both diagnosis and therapy.
- Endoscopic diagnosis of a MWT is readily made by identifying active bleeding, an adherent clot, or a fibrin crust over a mucosal split within or near the gastroesophageal junction (see Media file 1).
- On average, the split is 2-3 cm in length and a few millimeters in width. Most patients (>80%) present with a single tear.
- The usual location of the tear is just below the gastroesophageal junction on the lesser curvature of the stomach (between 2 and 6 o'clock on endoscopic viewing with the patient in the left lateral decubitus position).
- MWTs are usually associated with other mucosal lesions. In one study, 83% of patients had additional mucosal abnormalities potentially contributing to bleeding or actually causing retching and vomiting that would induce these tears.
- Several endoscopic modalities are effective for treating a bleeding MWT. The choice usually depends on the endoscopist's familiarity with a particular technique and on equipment availability. Patients with actively bleeding MWTs (ie, arterial spurting, streaming from focal point, diffuse oozing) are treated. Stigmata (eg, nonbleeding visible vessel, adherent clot) do not necessarily require treatment in MWTs as they do in peptic ulcers. Such stigmata usually are not treated unless they are rebleeding episodes from the same lesion or are associated with a coagulopathy. MWTs with a clean, fibrinous base or with flat, pigmented spots are not treated since the risk of rebleeding is minimal.
- A contact thermal modality, such as multipolar electrocoagulation (MPEC) or heater probe, with or without epinephrine injection, is typically used to treat an actively bleeding MWT. Effectiveness and safety have been established in only a few randomized, controlled trials. For example, Laine demonstrated greater hemostatic efficacy, fewer emergency interventions, and a trend toward decreased transfusion requirements in favor of MPEC versus sham MPEC.3
- The MPEC or heater probe is applied on the bleeding point with mild-to-moderate pressure.
- Suggested treatment parameters for MPEC include a power setting of 14-16 watts (W), 3-4 seconds per application, and 1-5 applications on average.
- Suggested treatment parameters for heater probe include 15- to 20-J pulses in a sequence of 2-3 pulses. The endpoint is cessation of bleeding and formation of a white coagulum.
- Epinephrine injection (1:10,000-1:20,000 dilution) reduces or stops bleeding via a mechanism of vasoconstriction and tamponade. It is usually combined with a more definitive therapy (eg, thermal therapy). Aliquots of 0.5-1 mL are injected around and into the bleeding point. No ceiling volume has been identified, and as much as 20 mL of epinephrine have been used. Careful monitoring is required, since submucosal esophageal injection of epinephrine may enter the systemic circulation without a protective first-pass effect, potentially causing serious cardiovascular complications. Epinephrine injection is best avoided in patients with active cardiovascular disease.
- Successful use of sclerosants, such as alcohol or polidocanol, has been reported. Safer alternatives exist, and sclerosant injection is not recommended by the author because of its potent tissue-damaging effects, risk of deep tissue necrosis, and potential for perforation.
- Reports on the use of the argon plasma coagulator (APC) in the treatment of bleeding MWTs are limited, but this noncontact device is gaining in popularity owing to its ease of use. In the thin-walled esophagus, the power output should be set at 40-45 W and with a relatively low argon gas flow rate (1 L/min). The APC probe should be maintained 1-2 mm from the target site, which may be difficult to accomplish in the setting of peristalsis.
- Endoscopic band ligation has been shown to be effective for treating bleeding MWTs. In a small, prospective, randomized study of 34 patients with actively bleeding MWTs, no difference was detected in the efficacy or safety of band ligation versus epinephrine injection. Band ligation should be particularly useful for bleeding MWTs associated with portal hypertension and gastroesophageal varices, in which thermal therapy is not recommended.
- Endoscopic hemoclipping is also effective for MWTs. The margins of the tear may be approximated, starting at the distal end of the tear and applying successive clips in a cephalad fashion. Alternatively, only the bleeding point can be targeted for hemoclip placement. Optimal deployment of clips may not be achievable because of the tangential location of the tear, or the tear may be too wide. In a study of 26 patients, however, hemoclipping was technically successful in all cases, and the average number of clips used was 2.8 + 1.6 (range, 1-8). In a randomized prospective study of 35 patients with actively bleeding MWTs, hemoclip placement and epinephrine injection were equally effective for achieving primary hemostasis. Whenever feasible, the author favors the use of hemoclips over thermal modalities, as the latter may cause excessive tissue injury leading to necrosis and perforation.
- Although earlier studies reported balloon tamponade to be beneficial, this technique should probably be avoided, as it recreates the forces that predispose patients to lacerations and may further widen the tear.
- Angiotherapy with either selective vasopressin infusion or embolization of the left gastric artery can be performed in patients who have failed to respond to endoscopic therapy or who are at high risk of endoscopic complications.
Medical Care
Initial management consists of implementing resuscitative measures as appropriate, performing endoscopy promptly, and triaging patients to intensive care, hospital inpatient, or outpatient management, depending on the severity of bleeding, comorbidities, and risk of rebleeding and complications.
- Most patients have stopped bleeding at the time of endoscopy.
- Five to 35% of patients require some form of intervention, mostly endoscopic. Specific endoscopic therapy for actively bleeding MWTs is described in Procedures.
- Otherwise, supportive care with volume and/or blood replacement, acid suppression (eg, omeprazole), and antiemetic drug therapy (eg, prochlorperazine) is sufficient in most patients presenting with a MWT.
Surgical Care
Surgical oversewing of the tear is reserved for the occasional bleeding case refractory to endoscopic therapy or angiotherapy.
Consultations
- Interventional vascular radiology: Attempt angiotherapy for bleeding uncontrolled by endoscopic means.
- Surgical consultation: Surgery may be needed as salvage therapy for failed endoscopic and/or radiologic intervention.
Diet
- Fasting is restricted to hemodynamically unstable patients and to those who require repeat endoscopic intervention within a short time because of uncertainty regarding the effectiveness of endoscopic therapy or possible complication of the initial therapy.
- Unless nausea or vomiting is an issue, patients can resume oral intake following endoscopy, starting with a clear- or full-liquid diet and advancing as tolerated to a regular diet within 48 hours.
An acid suppressant (eg, proton pump inhibitor) or a mucosal protectant (eg, sucralfate) is usually prescribed for 1-2 weeks to accelerate healing, although this practice is of unproven benefit. An antiemetic (eg, prochlorperazine) is useful for controlling nausea and vomiting, common precipitating factors to MWTs.
Drug Category: Gastrointestinal agents
Protect the gastrointestinal lining and promote faster healing of the mucosa.
| Drug Name | Sucralfate (Carafate) |
|---|
| Description | Forms a viscous adhesive substance that protects GI lining against pepsin, peptic acid, and bile salts. Used for short-term management of ulcers. |
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| Adult Dose | 1 g PO qid |
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| Pediatric Dose | Not established; 40-80 mg/kg/d PO divided q6h suggested |
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| Contraindications | Documented hypersensitivity |
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| Interactions | May decrease effects of ketoconazole, ciprofloxacin, tetracycline, phenytoin, warfarin, quinidine, theophylline, and norfloxacin |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | Caution in renal failure and conditions that impair excretion of absorbed aluminum |
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Drug Category: Antiemetic agents
Control precipitating factors of nausea and vomiting in initiating or aggravating the tears.
| Drug Name | Prochlorperazine (Compazine) |
|---|
| Description | May relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors through anticholinergic effects and depressing reticular activating system. In addition to antiemetic effects, it has the advantage of augmenting hypoxic ventilatory response, acting as a respiratory stimulant at high altitude. |
|---|
| Adult Dose | 5-10 mg PO/IM tid/qid; not to exceed 40 mg/d
2.5-10 mg IV q3-4h prn; not to exceed 10 mg/dose or 40 mg/d
25 mg PR bid |
|---|
| Pediatric Dose | 2.5 mg PO/PR q8h or 5 mg q12h prn, not to exceed 15 mg/d; IV dosing not recommended for children
0.1-0.15 mg/kg/dose IM; change to PO as soon as possible |
|---|
| Contraindications | Documented hypersensitivity; bone marrow suppression; narrow-angle glaucoma; severe liver or cardiac disease |
|---|
| Interactions | Coadministration with other CNS depressants or anticonvulsants may cause additive effects; coadministration with epinephrine may cause hypotension |
|---|
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
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| Precautions | Drug-induced Parkinson syndrome or pseudoparkinsonism occurs quite frequently; akathisia is most common extrapyramidal reaction in elderly patients; lowers seizure threshold; caution with history of seizures |
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Drug Category: Proton pump inhibitors
Reduce or eliminate acid secretion to allow faster healing of the mucosal tear.
| Drug Name | Omeprazole (Prilosec) |
|---|
| Description | Decreases gastric acid secretion by inhibiting parietal cell H+/K+-ATPase pump. For short-term (4-8 wk) treatment of active benign gastric ulcer and active duodenal ulcer, treatment of H pylori infection in combination with antibiotics, short-term treatment of symptomatic GERD poorly responsive to customary medical treatment, maintenance of healing of erosive esophagitis, and pathological hypersecretory conditions. |
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| Adult Dose | 20 mg PO qd/tid |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity |
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| Interactions | May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
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| Precautions | Bioavailability may increase in elderly patients |
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| Drug Name | Esomeprazole (Nexium) |
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| Description | S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+-ATPase enzyme system at secretory surface of gastric parietal cells. |
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| Adult Dose | 20-40 mg PO qd for 4-8 wk |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity |
|---|
| Interactions | None reported |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
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| Precautions | Symptomatic relief with proton pump inhibitors may mask symptoms of gastric malignancy |
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Further Inpatient Care
- Patients without risk factors for rebleeding (eg, portal hypertension, coagulopathy), severe bleeding (eg, hematochezia, hemodynamic instability), or active bleeding at endoscopy can be managed conservatively with an extended observation or brief hospitalization period (approximately 24 h). Patients with actively bleeding MWTs should be hospitalized for at least 48 hours. Patients with clinical risk factors for rebleeding (about 10% of cases) and endoscopic stigmata of nonbleeding visible vessel, pigmented protuberance, or adherent clot should be observed for 48 hours. If rebleeding occurs, it usually takes place within that time period. In one study, the presence of shock at initial manifestation and active bleeding at endoscopy were found to be independent risk factors predicting the recurrent bleeding in patients with MWTs.
- Monitor vital signs, obtain serial hemoglobin and hematocrit values (q6h initially), watch for clinical signs of rebleeding, correct coagulopathy if possible, and maintain hemodynamic support with fluid and blood replacement.
- Transfuse, generally, for hemoglobin levels less than 8 g/dL (<10 g/dL for patients with cardiopulmonary disease).
- Control or eliminate precipitating factors, such as nausea and vomiting.
- Treat other associated lesions observed endoscopically as appropriate.
Further Outpatient Care
- Watch for recurrent symptoms or signs of rebleeding.
In/Out Patient Meds
- Proton pump inhibitor (eg, omeprazole 20 mg PO qd) or sucralfate (eg, 1 g PO qid) for 1-2 weeks - To reduce injurious factors, such as acid, pepsin, or bile, that impair the healing of the mucosal tear
- Specific therapy toward precipitating factors responsible for the MWT (eg, antiemetic for nausea and vomiting)
Deterrence/Prevention
- Recurrence is rare.
- Counsel patients who have had a MWT on precipitating factors (eg, alcoholic binge, excessive straining and lifting, violent coughing) that may lead to a recurrent MWT.
Complications
- Complications, such as myocardial ischemia or infarction, hypovolemic shock, and death, usually relate to the acuity and the severity of bleeding and to associated comorbidities. Fortunately, these complications are uncommon with the current standard of care.
- Perforation or aggravation of bleeding during endoscopic therapy is a potential complication.
- Organ ischemia and infarction is a potential complication of angiotherapy.
Prognosis
- Prognosis is generally good. Most patients usually stop bleeding spontaneously, and MWTs tend to heal rapidly (within 48-72 h).
Medical/Legal Pitfalls
- Perform endoscopy promptly when indicated. MWTs heal rapidly and may not be readily apparent when endoscopically evaluated 2-3 days later.
- Endoscopic examination should be thorough, since coexisting lesions are not uncommon. These lesions may be actual or potential bleeding sites or precipitants of the MWT.
| Media file 1:
Mallory-Weiss tear. Typical longitudinal mucosal tear with overlying fibrinous exudate extending from the distal esophagus to the gastric cardia. Courtesy of C.J. Gostout, MD. |
 |  View Full Size Image | |
Media type: Photo
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| Media file 2:
Mallory-Weiss tear. Retroflexed view of the cardia showing the typical location of the tear with a clean base. |
 | View Full Size Image | |
Media type: Photo
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| Media file 3:
Mallory-Weiss tear with a pigmented protuberance and active oozing. |
 | View Full Size Image | |
Media type: Photo
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Mallory-Weiss Tear excerpt Article Last Updated: Apr 16, 2008
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