therapeutic alternatives for the mallory-weiss tear

Therapeutic Alternatives for the Mallory-Weiss TearPedro Morales, MDAlex E. Baum, MD

AddressDepartment of Medicine, Section of Gastroenterology and Hepatology, SL-35, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA.E-mail: [email protected] Treatment Options in Gastroenterology 2003, 4:75–83Current Science Inc. ISSN 1092-8472Copyright © 2003 by Current Science Inc.

IntroductionThe Mallory-Weiss tear (MWT) is characterized bymucosal laceration of the gastric cardia or gastroesoph-ageal junction (GEJ); these anatomic lesions are usually3 to 20 mm long and 2 to 3 mm wide, and they areoriented along the longitudinal axis of the esophagus[1]. The MWT was initially described by Quincke [2],

who related the condition to repeated vomiting. About50 years later, Kenneth Mallory and Soma Weiss [3]described 15 patients, each of whom developed massivehematemesis after an alcoholic binge. The pathologicexamination of four cases described the classic mucosaltear in the GEJ.

Opinion statementThe Mallory-Weiss tear (MWT) is a frequent cause of upper gastrointestinal bleeding. It has been diagnosed more frequently since endoscopy was introduced. Once the diagnosis has been made, several treatment options are available. The treatment modality chosen depends on the type and location of the lesion, the patient’s comor-bid conditions, the availability of the different therapeutic modalities, and the experience of the endoscopist with each of these different modalities. In general, if the MWT is not actively bleeding at the time of endoscopy, no further treatment is needed owing to a low risk of rebleeding, unless a visible vessel is present. In the presence of a visible vessel or an actively bleeding vessel, then we recommend the use of any of the endoscopic treatment modalities discussed later in this article depending on the patient’s condition and clinical scenario. Our review of the literature suggests that multipolar electric coagulation (MPEC) is the treatment modality with better evidence-based support for safety and bleeding control. MPEC has been associated only with very few complications. It should be avoided when esophageal varices are suspected because it may precipitate and aggravate bleeding. In such instances, either polidocanol injection or endoscopic band ligation of the tear is recommended, which is emerging as a safe and effective treatment modality even in patients without varices. In addition, epinephrine injection is an effective first-line modality. However, it should be avoided in patients with history of coronary artery disease owing to the potential for systemic absorption. Endoscopic hemoclipping (EH) is another useful treatment option and is emerging as a first-line modality. However, it is not widely available in all endoscopy emergency units. If it is available, it is a great alternative. Finally, if bleeding continues or recurs despite endoscopic therapy, the patient should be referred for surgical treatment. However, if the patient is not a surgical candidate, then radiologic hemostasis with selective vasopressin or Gelfoam embolization represents a viable treatment alternative that may be used depending on availability of a specialized interventional radiologist.

76 Esophageal Disease

It is accepted that 5% to 15% of upper gastrointestinalbleeding (UGIB) is caused by MWT [4]. MWT occurs morecommonly in men than women, and 83% of tears arelocated just below the GEJ on the lesser curvature [5••].

PATHOGENESISMallory-Weiss tears are secondary to a sudden increasein intra-abdominal pressure, leading to the propulsionof the gastric cardia into the thoracic cavity through thehiatus. When this propulsion is forceful enough, a lacer-ation or tear may occur at the level of the GEJ. Nausea isassociated with closure of the pylorus, distention ofstomach, and forceful propulsion of gastric content intothe cardia, followed by retching and vomiting [6].

CLINICAL AND ENDOSCOPIC RISK FACTORSThe combination of severe vomiting and alcohol intake iswell established as a cause of hematemesis in MWT. It ispresent in 75% of all patients, as reported by Michel et al.[7]. Other clinical risk factors reported in the literatureinclude recent ingestion of aspirin, anticoagulants, cough-ing paroxysm, uremia, pregnancy, heavy lifting, strainingat bowel movement, hiccoughing under anesthesia andblunt abdominal trauma [7], colonic lavage, and cardio-pulmonary resuscitation [6]. Increasing age has also beenreported as an associated factor. In addition, gastrointesti-nal endoscopy and transesophageal echocardiogram havebeen reported to cause MWT in 0.5% [8,9]. Portal hyper-tension has been recognized as a risk of unfavorable out-come. Paquet et al. [10] found that they are associated in16% of cases, and when stratified by Child-Pugh score,58% of the patients belong to class C. Other studies haveargued this conclusion, in which severity of bleeding mea-sured in units of red blood cells (RBCs) required was notstatistically significant among Child-Pugh class A, B, or C,but liver disease itself was the main factor for increasedmorbidity and mortality rates [11].

Endoscopically, the presence of hiatal hernia is vari-able. One series reported its presence in 52% of cases [12];other series reported the finding in 17% of patients [5••].However, it is accepted that the tears occurring within thegastric cardia are generally associated with the presence ofa hiatal hernia. However, the presence of a hiatal herniahas a higher impact on the location of the MWT than onthe incidence of MWT. The incidence of associated lesionssuch as superficial gastritis, duodenitis, esophagealvarices, and esophagitis (all of these lesions are alsorelated to ethanol ingestion) has been reported in approx-imately 83% of cases [5••,7].

Kortas et al. [13] proposed seven potentially predis-posing factors for developing MWT:

• Alcohol use (present in 44% of cases)• Recent binge• Vomiting• Anticoagulation• Other coagulopathies• Nonsteroidal anti-inflammatory drug use• The presence of hiatal hernia on endoscopy

(only present in 16% of cases).

These authors also propose 12 potential predictors of acomplicated course:

• Increasing age• Hematemesis• Melena• Hematochezia• Visible vessel on endoscopy• Adherent clot at endoscopy• Multiple tears, other pathology at endoscopy• Hypotension or orthostatic changes and

coagulopathy (PT > 14.5 s)• Active bleeding at endoscopy• A low hematocrit on admission

The latter two findings were statistically significant for acomplicated course.

DIAGNOSISEndoscopy is the diagnostic modality of choice to estab-lish the presence of a tear, allowing the possibility oftherapeutic interventions. It reveals a single tear in 80%to 90% of cases, which is most commonly located in thelesser curvature of the cardia (endoscopically between 2and 6 o’clock with the patient in left lateral decubitusposition [5••,6]. The endoscopic appearance of a MWTis that of a red longitudinal laceration in the mucosa orsometimes with extension into the muscularis mucosa,occasionally covered with a clot (Fig. 1).

It is well recognized that more than 90% of bleedingepisodes stop spontaneously and require only support-ive treatment. It has been reported that the incidence ofactive bleeding at the time of endoscopy is 25% [5••].These patients require a more aggressive treatment,because it has been associated with a poor outcomeincluding multiple blood transfusions, intensive caremonitoring, and therapeutic endoscopy.

Therapeutic Alternatives for the Mallory-Weiss Tear Morales and Baum 77

Treatment

• The management of MWT is for the most part supportive, because more than 90% of lesions stop bleeding spontaneously [5••]. Endoscopists have a wide variety of therapeutic options for patients with persistent bleeding. There are also interventional radiologic and surgical alternatives. We discuss these alternatives later. Finally, we propose an evidence-based treatment approach and an algorithm (Fig. 2) for treatment of the patient with MWT.

• Endoscopic therapy is the first-line treatment of actively bleeding lacera-tions. Several hemostatic methods have been used, all with great success.

• Injection therapy of various agents has been performed. In a randomized controlled trial, Llach et al. [14••] showed that injection of an active bleeding tear or a nonbleeding visible vessel with a total of 2 to 6 mL of epinephrine 1:10,000 and 4 to 12 mL of polidocanol 1%, a sclerosing agent, achieved hemostasis in all patients with a significant lower recurrent bleed of 6.2%, compared with 25.8% in the control group. The therapy also resulted in a shorter hospital stay. However, there was no significant reduction in units of blood transfused when these endoscopically treated bleeding lesions were

Figure 1. Actively bleeding Mallory-Weiss tear with oozing from a visible vessel.

Endoscopic therapy

Injection therapy


compared with those treated medically (ie, in the control group). In another prospective trial in which actively bleeding lesions were treated with injection of epinephrine and polidocanol [15] as opposed to nonactively bleeding

Figure 2. Treatment algorithm for patients with upper gastrointestinal bleeding secondary to Mallory-Weiss tear. *Avoid when coronary artery disease, cardiac arrhythmias, or congestive heart failure is suspected. †Preferred treatment modality in cases of patients with esophageal varices, portal hypertension, and coagulopathy. EBL—endoscopic band ligation; EGD—esophagogastroduodenoscopy; MPEC—multipolar electric coagulation; MWT—Mallory-Weiss tear.


lesions that were treated conservatively, a 100% success rate was achieved in the first group and no recurrence appeared in either arm of the trial. However, esophageal perforation was reported in 8% of patients, concluding that early endoscopy identifies those patients who will benefit from conservative management (those without active bleed). Several other case reports have been published on patients treated with isotonic saline injection and with epinephrine injection [16], and those treated with 98% dehydrated ethanol [17], with reported success rates higher than 95%. Minimal complications have been reported. Local epinephrine injection therapy diminishes arterial blood flow through a combination of vasocon-striction and edema. Hypertensive emergency and ventricular tachycardia have been reported when epinephrine injection was used [18].

• Multipolar electrocoagulation (MPEC) is a very effective, safe, and inexpen-sive treatment modality and one with which most endoscopists have had experience in the treatment of UGIB. In a randomized, controlled, prospec-tive trial, Laine [19] concluded that this modality has greater hemostatic effect (100% versus 13%), reduces the number of blood transfusions required, and decreases the rate of emergency surgery (0% versus 50%) when compared with medical therapy in patients with active bleeding from MWT. No complications were reported. It is recommended to use bipolar probe settings at 15 W with a mild tamponade force and noncontinuous 1-second pulses because of the smaller size of the underlying artery and minimal thickness of the GEJ mucosa (average size is 3 mm) to avoid perforations (Fig. 3). This modality should be avoided in patients with portal hypertension and esophageal varices, because it may precipitate or worsen the bleeding. Endoscopic band ligation (EBL) or sclerotherapy are recommended in these cases.

• Endoscopic band ligation has been compared with bipolar electrocoagula-tion in the control of nonvariceal upper gastrointestinal bleed [20]. In all patients with MWT with UGI bleeding, hemostasis was achieved with EBL and no recurrences were noted. Use of bipolar electrocoagulation achieved hemostasis in all cases, but there was one recurrent bleed. Based on a small subgroup of patients with MWT, the conclusions are that EBL can be performed easily, especially when the bleeding site has to be approached tangentially, which is difficult to achieve with other techniques. EBL is safe, simple, and fast. Once the bleeding site is fixed in the ligation hood, peristalsis is minimized, which makes the procedure easier. Perforation is extremely rare, as opposed to MPEC. A case report [21] of successful control of an active bleed secondary to MWT occurring during endoscopy, and two small series of cases reports [22,23] of successful treatment of active bleed-ing secondary to MWT using EBL were reported, all with a 100% success rate in achieving hemostasis and no complications.

• Endoscopic hemoclipping is emerging as another first-line alternative in the endoscopic treatment armamentarium against actively bleeding MWT. Yamaguchi et al. [24•] reported 26 patients in whom hemoclipping was

Multipolar electrocoagulation

Endoscopic band ligation

Endoscopic hemoclipping


technically successful and hemostasis was achieved in all without recur-rence of bleeding. Follow-up endoscopy 1 to 2 months later showed that in the majority of patients, the hemoclip had dislodged and passed in the feces without complications. In addition, complete tear healing and re-epithelialization was observed in all patients. They concluded that EH is safe, easy, and effective, even in the cases of active bleeding. In a prospective randomized clinical trial, Huang et al. [25•] compared the efficacy and safety of hemoclip placement with endoscopic epinephrine injection in actively bleeding lesions. They concluded based on 35 patients studied (18 in the epinephrine and 17 in the hemoclip group) that either method used is equally safe and effective for control of bleeding, spurting, or oozing lesions. Only one patient in each group experienced rebleeding and was successfully controlled by using the same modality as at random-ization. Therefore, either treatment modality can be used as a first-line therapy with actively bleeding MWT.

• Arteriography in the diagnosis of gastrointestinal bleeding was first intro-duced in 1963 by Nusbaum and Baum [26]. Therapeutic angiography with selective infusion of vasopressin in the celiac or left gastric artery has been used successfully, although gastric arterial embolization, a more technically demanding procedure, may be needed when selective perfusion fails or the patient is a poor surgical candidate. Their goal is to reduce the blood supply to the bleeding vessel temporarily to allow the hemostatic mechanism to function through vasoconstriction (vasopressin) or by hemostatic plug formation with Gelfoam. Vessel recanalization occurs after several weeks.

Figure 3. Mallory-Weiss tear after treat-ment with multipolar electrocoagulation.

Radiologic therapy


• In general, angiographic evidence of diffuse gastric mucosal hemorrhage is best managed by vasopressin infusion as opposed to a specific arterial bleeding site that is amenable to control with selective embolization. Selective embolization is much more difficult to perform and therefore is done only at medical centers with highly skilled interventional radiologists.

• In a trial of 55 patients with UGIB, Robinette and Gerlock [27] reported on eight patients with MWT who were diagnosed by endoscopy and were treated with intra-arterial vasopressin at a rate of 0.2 to 0.5 U/min for 20 minutes using the left gastric artery and inferior phrenic artery catheteriza-tion. Successful control was achieved in four of the patients. Other trials implementing the same protocol [28] have reached 100% success with sim-ilar results and minimal complications. It is also recommended to continue the infusion for 12 hours to 5 days if complications are not present [27,28].

• Arterial embolization is not recommended for all patients with refractory UGIB. Furthermore, the procedure requires skilled angiographers who can perform superselective catheterization and should be performed only in patients who are poor surgical candidates, as stated earlier. In a small subset of patients with MWT, Lieberman et al. [29] obtained complete hemostasis in all five patients with embolization of the left gastric artery, and there were no complications. Other small series have shown similar results [30,31].

• Fisher et al. [32] reported on 15 patients of 18 with MWT who underwent angiotherapy, 13 with intra-arterial vasopressin and two with Gelfoam embolization. Hemostasis was permanent in eight patients in the vasopressin-treated group and in two patients in the group treated with Gelfoam. There were two cases of myocardial infarction in the vasopressin-treated group. These complications are related to the decrease in coronary artery flow, cardiac output, arterial PO2, as well as presence of cardiac arrhythmias. The two patients who underwent embolization had no complications. The lack of success in the patients in whom vasopressin was used is due to the misplace-ment of the catheter tip in the celiac axis instead of the left gastric artery (LGA), which emerges from the celiac axis at its origin.

• Multiple complications have been reported secondary to the acute cessation of blood flow to the organ supplied. If inadequate collateral circulation is present secondary to diffuse atherosclerosis or prior surgery that may have obliterated potential collaterals, then the organ supplied by the artery that is actively occluded may not survive the ischemic event, leading to ischemia and infarction.

• Either procedure may have complications related to the insertion of the catheter in the groin. These complications include a hematoma, gangrene, and amputation of the limb [32]. We want to emphasize that either modality is effective, but vasopressin infusion cannot be performed after embolization.

• Compression of the GEJ by the inflated gastric balloon of a Sengstaken-Blakemore tube was used in six patients with coagulation defect secondary to liver disease, leading to a satisfactory outcome in all of them [33]. Others have reported on the use of this procedure in four patients. The method was successful in only two of them [5••]. This finding is very controversial, especially because hiatal hernia is frequently found in patients with MWT, which makes this treatment modality inadequate and dangerous. In these patients, the asymmetric pressure within the hiatal hernia causes necrosis and perforation in and around the tear [7].

Other nonsurgical modalities


• Only 3% of patients with MWT require surgery. The most common surgical tech-nique used is anterior gastrotomy and oversewing of the bleeding point [5••].

• Based on the literature reviewed, we suggest the following approaches when treating patients with MWT.

• In patients in whom bleeding has stopped and no visible vessel is observed at the time of endoscopy, there is no need for further endoscopic interven-tion. Their rebleeding rates are close to 0%. However, these patients need supportive care. Consequently, it is recommended that these patients be hospitalized for 24 hours.

• Patients with active bleeding or a visible vessel should be treated endo-scopically. Electrocoagulation, epinephrine, and polidocanol injection have been validated in a randomized controlled trials. Isotonic saline solution injection may be used in patients with severe hypertension or underlying cardiac arrhythmias. Other emergent modalities include band ligation and hemoclipping. Both procedures are locally effective and produce minimal side effects, but more data are needed to consider them as first-line treat-ment modalities. However, EBL in the case of MWT in patients with portal hypertension and esophageal varices has shown great results in case reports, case series, and one prospective study, indicating that EBL is a promising treatment modality in such cases. Thermal coagulation should not be performed in patients with portal hypertension and esophageal varices because it may precipitate or worsen the bleeding episode. Patients with active bleeding at endoscopy should be hospitalized for at least 48 hours because rebleeding generally occurs within 24 hours of the initial therapeutic endoscopy procedure. Portal hypertension and coagulopathy have been identified as major risk factors for rebleeding.

• If patients are poor surgical candidates, embolization should be attempted if endoscopic therapy failed to obtain hemostasis. Pharmacotherapy with selective vasopressin infusion in the LGA is very effective. If a skilled interventional radiologist is available, embolization of the LGA could be performed. Once embolization has been done, vasopressin should not be used.

• Patients who are fit for surgery and in whom endoscopic therapy has failed should undergo embolization because it is safe and highly successful. We do not recommend the use of a balloon owing to the high risk of perfora-tion. The use of H2 blockers, PPIs or sucralfate may be used to attempt faster healing rates. However, no trials have shown any benefit in their use in controlling active bleeding in patients with MWT.

• Based on the review of the literature, we propose a treatment algorithm (Fig. 2) to guide physicians in the management of patients with MWT.

Surgical treatment

Recommendations for the treatment of patients with a Mallory-Weiss tear


References and Recommended ReadingPapers of particular interest, published recently, have been highlighted as:• Of importance•• Of major importance

1. Katz P, Salas L: Less frequent causes of upper gastrointesti-nal bleeding. Gastroenterol Clin North Am 1993, 22:875.

2. Quincke H: Ulcus oesophagi ex digestion. Dtsch Arch Kin Med 1879, 24:72.

3. Mallory GK, Weiss S: Hemorrhages from lacerations of the cardiac orifice of the stomach due to vomiting. Am J Med Sci 1929, 178:506–512.

4. Harris J, Dipalma J: Clinical significance of Mallory-Weiss tears. Am J Gastroenterol 1986, 88:2056-2058.

5.•• Sugawa C, Nenishek D, Walt A: Mallory-Weiss syndrome: a study of 224 patients. Am J Surgery 1983, 145:30–33.

This is the largest series of patients with MWT published. It provides ample information on epidemiology, diagnosis, treatment, and outcomes in patients with MWT.6. Younes Z, Johnson D: The spectrum of spontaneous

and iatrogenic esophageal injury. J Clin Gastroenterol 1999, 29:306–317.

7. Michel L, Serrano A, Malt R: Mallory-Weiss syndrome. Ann Surg 1980, 192:716–721.

8. Baker R, Spiro A, Trnka Y: Mallory-Weiss tear complicat-ing upper endoscopy. Gastroenterology 1982, 82:140–142.

9. Vries A, van der Maaten J, Laurens R: Mallory-Weiss tear following cardiac surgery: transesophageal echoprobe or nasogastric tube? Br J Anesth 2000, 84:646–649.

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11. Schuman B, Threadgill T: The influence of liver disease and portal hypertension on bleeding in Mallory-Weiss syndrome. J Clin Gastroenterol 1994, 18:10–12.

12. Bharucha A, Gostout C, Balm R: Clinical and endo-scopic risk factors in the Mallory-Weiss syndrome. Am J Gastroenterol 1997, 92:805–808.

13. Kortas D, Haas L, Simpson W, Nickl N, Gates L: Mallory-Weiss tear: predisposing factors and predictors of a com-plicated course. Am J of Gastroenterol 2001, 96:2863–2865.

14.••Llach J, Elizalde I, Guevara C, et al.: Endoscopic injection therapy in bleeding Mallory-Weiss syndrome: a randomized controlled trial. Gastrointest Endosc 2001, 54:679–681.

This is one of the few recent randomized control trial on a therapeutic option for MWT.15. Bataller R, Llach J, Salmero J, et al.: Endoscopic sclerother-

apy in upper gastrointestinal bleeding due to Mallory-Weiss syndrome. Am J Gastroenterol 1994, 89:2147–2150.

16. Peng C, Tung C, Chow W, et al.: Efficacy of Endoscopic isotonic saline epinephrine injection for the for the management of active MWT. J Clin Gastroenterol 2001, 32:119–122.

17. Sugawa C, Fujita Y, Ikeda T, Walt A: Endoscopic hemostasis of bleeding of the upper gastrointestinal tract by local injection of 98% dehydrated ethanol. Surg Gynecol Obstet 1986, 162:159–163.

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19. Laine L: Multipolar electrocoagulation in the treatment of active upper gastrointestinal tract hemorrhage. N Engl J Med 1987, 316:1613–1617.

20. Matsui S, Kamisako T, Kudo M, Inoue R: Endoscopic band ligation for control of nonvariceal upper GI hemorrhage: comparison with bipolar electro-coagulation. Gastrointest Endosc 2002, 55:214–218.

21. Myung S, Kim H, Moon Y: Severe Mallory-Weiss tear after endoscopy treated by endoscopic band ligation. Gastrointest Endosc 2000, 52:99–101.

22. Terada R, Ito S, Akama F, et al.: Mallory-Weiss syndrome with severe bleeding: treatment by endoscopic ligation. Am J Emerg Med 2000, 18:812–815.

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24.• Yamaguchi Y, Yamato T, Katsumi N, et al.: Endoscopic hemoclipping for upper GI bleeding due to Mallory-Weiss syndrome. Gastrointest Endosc 2001, 53:427–430.

This is the first trial that evaluated the use of endoscopic hemo-clipping as a new treatment modality in patients with MWT.25.• Huang S, Wang H, Lee Y, et al.: Endoscopic hemoclip

placement and epinephrine injection for Mallory-Weiss with active bleeding. Gastrointest Endosc 2002, 55:842–846.

This trial has been the largest to examine the use of endo-scopic hemoclipping.26. Nusbaum M, Baum S: Radiographic demonstration

of unknown sites of gastrointestinal bleeding. Surg Forum 1963, 14:374–375.

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31. Pezzulli F, Purnell F, Dillo E: The Mallory-Weiss syn-drome: case report on embolization versus intrarterial vasopressin result. N Y State J Med 1986, 866:312–314.

32. Fisher R, Schwartz J, Graham D: Angiotherapy with Mallory-Weiss tear. Am J Roentgengol 1980, 134:679–684.

33. Welch G, McArdle C, Anderson J: Balloon tamponade for the control of Mallory-Weiss haemorrhage in patients with coagulation defects. Br J Surg 1987, 74:610–611.

therapeutic alternatives for the mallory-weiss tear

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