Mallory-Weiss Syndrome in Perspective Jack L. Saylor, MD, and Francis J. Tedesco, MD
Nineteen patients with the Mallory-Weiss lesion diagnosed by panendoscopy are presented. This represents 10.5% of 180 acute upper-gastrointestinal bleeders. Only 36.8% of these 19 patients had a history of heavy ethanol intake and 26% had hiatus hernias. In addition to the Mallory-Weiss lesion, abnormalities in 63% were noted on endoscopy. None of the patients required surgery for control of the bleeding. Two patients were treated with selective arterial-vasopressin infusion. The importance of a high index of suspicion for this lesion in spite of the lack of a classical alcoholic or recurrent retching history and the value of intensive medical therapy, including early panendoscopy, is emphasized.
D e s p i t e excellent reviews o n t h e M a l l o r y W e i s s s y n d r o m e in t h e p a s t ten y e a r s ( 1 - 9 , 13), m a n y aspects of this s y n d r o m e h a v e received varying emphasis depending upon patient popu l a t i o n , t e c h n i c a l - e q u i p m e n t availability, a n d a p p r o a c h to t h e acute g a s t r o i n t e s t i n a l bleeder. A u n i v e r s a l l y a c c e p t a b l e incidence of o c c u r r e n c e h a s yet to be defined, m a n a g e m e n t h a s u n d e r gone s i g n i f i c a n t c h a n g e s , a n d e m p h a s i s on etiological events h a v e clearly shifted. T h i s s t u d y d e m o n s t r a t e s t h a t t h e etiological role of n o n a l c o h o l - r e l a t e d events r e q u i r e s increased e m p h a s i s a n d t h a t p r o m p t a n d t h o r o u g h p a n e n d o s c o p y is essential for o p t i m a l management.
MATERIALS AND METHODS The patients in this report represent those patients with the Mallory-Weiss lesion seen by the Gastroenterology Division at Barnes Hospital from July 1, 1972 to Oetober 15, From the Division of Gastroenterology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110. The opinions expressed herein are those of the authors and cannot be construed as reflecting the views of the United States Air Force. Address for reprint requests: Dr. Francis J. Tedesco, Department of Medicine, University of Miami School of Medicine, P.O. Box 875, Biscayne Annex, Miami, Florida 33152.
Digestive Diseases, Vol. 20, No. 12 (December 1975)
1974. This period represents 1,100 endoscopies with an end-view fiberoptic panendoscope (Olympus GIF-D, Olympus Corporation of American, New Hyde Park, New York), 287 of which were for upper-gastrointestinal (UGI) bleeding manifested by either melena or hematemesis. Of these 287 patients, 180 were classified as acute-UGI bleeders, defined as a history of hematemesis within 48 hours of endoscopy or a grossly bloody or coffee-ground guaiac positive-gastric aspirate within 24 hours of endoscopy. This study is a retrospective review of medical records, endoscopy reports, and photographs, and, where applicable, patient and/or attending physician follow-up questionnaires. The patients represent a cross section of a metropolitan and rural population served by a large private and teaching university hospital. Thorough gastric lavage was performed with iced saline or water prior to endoscopy. Each patient was examined by at least two endoscopists and all observations carefully recorded. Every attempt was made to examine the entire esophagus, stomach, duodenal bulb, and second portion of the duodenum consistent with the patient's status and technical feasibility. In those cases where a complete examination was not performed, notation as to the limiting factor was made. All patients with the MalloryWeiss lesion were managed medically, with two patients receiving selective vasopressin infusion (14, 17).
RESULTS O f t h e 180 acute U G I bleeders, 19 (10.5%) w e r e seen to h a v e the M a l l o r y - W e i s s lesion as t h e p r i m a r y etiology of t h e i r acute h e m o r r h a g e .
1131
SAYLOR & TEDESCO Table 1. Study Patients with Mallory-Weiss Lesions* Case no.
Age
Sex
History
UGI
Other endo findings
27
55
F
WNL
76
63
F
Edematous pylorus Esophagitis
149
47
M
151
49
M
Hypertension, nausea and vomiting for 1 week Labyrinthitis with tinnitus and vertigo, no vomiting Anorexia, nausea, and retching 1 day prior to admission Alcoholic, history unreliable
387
59
F
482
45
M
582
47
M
719 744
71 67
M M
755
47
F
791~
37
M
859
53
M
918
60
M
929
53
F
959
63
M
976
50
M
997w 1029
33 68
F F
1098
59
F
WNL WNL
Prepyloric edema and deformity Bulb deformity Erosive gastritis Acute distension of stomach with fluid, HHr HH no vomiting Psychogenic (?) nocturnal vomiting, Duodenitis Gastric ulcer, moderate singultus duodenitis Renal failure, home dialysis, WNL None vomited once Acute distension of stomach with food HH HH, duodenum not examined Hyperlipidemia, 11 months postWNL HH MI on Coumadin, protime 15%, no vomiting Viral gastroenteritis, 4 days WNL None of vomiting Heavy alcohol abuse, vomiting WNL HH, nodular antritis after alcohol debauch UGI bleed in 1952, nausea only, Mild esoStomach full of blood and adult diabetic phageal clots motility disturbances 12 hrs post-op TURP, no vomiting HH Antral gastritis, deformed antrum Behcet's disease, old MI on Coumadin, WNL None marked nausea, epigastric pain, no vomiting Heavy alcohol abuse, vomiting, Critically ill-Gastritis, gastric ulcer, and retching none duodenitis, duodenal diverticulum Heavy alcohol abuse, WNL Stomach full of blood and vomiting clots Psychogenic vomiting HH None Dysphagia, abdominal pain, retched HH, diffuse HH during endoscopy abnormal motility by cine Abdominal pain, past alcoholic Marked antral Severeantral diaphragm a b u s e - - n o n e recent--nausea and pyloric and vom iti ng deformity, ulcer (?)
*All patients were treated medically. Patients 719 and 1098 were treated with selective arterial infusion with vasopressin. All patients had an uneventful course with the exception of patient 959, who died. "i-Hiatal hernia. SThis is the second UGI bleed caused by a documented Mallory-Weiss lesion. w is the second UGI bleed caused by a documented Mallory-Weiss lesion.
1132
Digestive Diseases, Vol. 20, No. 12 (December 1975)
MALLORY-WEISS SYNDROME
Eight were female and 11 male, ranging in age from 33 to 71. Abnormalities other than the Mallory-Weiss lesion were noted in 9 of 18 patients examined by U G I barium-contrast roentgenography and in 13 of the 19 by endoscopy (68.4%). Hiatus hernia was identified in 7 (36.8%) and was the sole abnormality other than the mucosal tear(s) in 4 patients (Table 1). One patient sustained a Mallory-Weiss tear as a result of retching during panendoscopy for an unrelated problem. Careful alcohol-intake histories indicated that 7 (36.8%) had heavy alcohol intake (greater than 10 ounces per week), 1 had 4-10 ounces per week, 2 less than 4 ounces, 5 less than 2 ounces per month, and 3 no alcohol of any kind. An alcohol history was not obtained in 1 patient. 3 patients had been drinking heavily prior to the onset of hematemesis (15.8%). There was one death in this series (5%): an alcoholic admitted with sepsis, gastrointestinal bleeding, and pulmonary compromise. Although his bleeding stopped within 24 hours, he succumbed with overwhelming sepsis and a combination of pulmonary, hepatic, and renal failure, despite vigorous and intensive therapy. 10 (52.6%) patients did not receive blood replacement. Of the 9 patients receiving blood, the average replacement was 4.4 units. Of the nontransfused patients, 4 dropped their hemoglobin levels to 10 g. 6 (31.5%) patients, only one of whom was an alcoholic, did not have a history of vomiting or retching prior to hematemesis, and an accurate vomiting history was therefore questionable.
Table 2. Incidence of Mallory-Weiss Lesion in Acute UG! Hemorrhage Author
Patients Incidence
Wells (1967) (5) St. John et al (1974) (8) Miller and Hirschowitz (1970) (9) Jones (1969) (10) Katz et al (1965) (13) Current study
25/170 16/121
14.7% 13.2%
23/712 8/297 8/297 19/180
3.2% 2.7% 2.7% 10.5%
The Mallory-Weiss lesion accounted for 13.2% of acute-UGI bleeding in the most review of this subject by St. John et al (8). In that study, it ranked second only to duodenal ulcers and equalled gastric ulcers as the etiology of acute bleeding. Although this study revealed a slightly lower incidence (10.5~ both patient populations are comparable, excluding the implied bias inherent in a military or Veterans
Administration hospital (2, 5, 7), and showed a significantly greater incidence than other previously reported series (Table 2). Prompt recognition of this entity has therefore become increasingly important. The original recognition and description of this syndrome (11) implicated alcohol, and many subsequent authors (2, 3, 5, 9) emphasized recent alcohol debauch or alcohol-induced retching as the sine q u a n o n for the suspicion or diagnosis of Mallory-Weiss lesions. However, several authors (1, 4, 6, 10, 18) have challenged this concept and have listed many events ranging from coughing paroxysms (6) to cardio-pulmonary resuscitation (12). Analysis of the 19 patients in this study shows that while vomiting was the most frequent event preceding the hematemesis (68%), alcohol-related events accounted for only 21% of these patients. 6 patients (31.5~ had hematemesis simultaneously with the first emesis as described by Holmes (3), and by Hinchey and Hreno (4). Panendoscopy revealed pathology other than the Mallory-Weiss lesion in 13 of 16 (81~ patients in whom a thorough and complete panendoscopic examination was possible. Of these, 9 patients had other lesions that could have been mistaken as the source of bleeding at surgery. It is our opinion that therein lies the importance of thorough panendoscopy in the early management of the acute-UGI bleeder. Stabler et al (15) and Etheridge (16) have described serious consequences when surgery is required in an emergency situation to control gastrointes-
Digestive Diseases, Vol. 20, No. 12 (December 1975)
1133
DISCUSSION
SAYLOR & TEDESCO
tinal hemorrhage and only incomplete preoperative knowledge is available. Stabler reported four patients (50%) who had more than the Mallory-Weiss lesion noted at surgery: a large antral ulcer; a massively bleeding duodenal ulcer in addition to two bleeding gastric tears; reoperation because of an overlooked tear due to obscuring gastric folds; and 1 patient who died after suture of gastric lacerations from an overlooked esophageal tear. Although none of our patients required surgery, it can be seen from Table 1 that significant abnormalities were seen that were not responsible for the U G I bleeding, but which might cause confusion in a patient at surgery who often stops actively bleeding concomitant with general anesthesia. All our patients were treated medically. 2 patients had selective angiography with vasopressin infusion resulting in rapid control of bleeding. It has been our experience that this newer procedure offers an effective, nonsurgical modality of therapy in the acute gastrointestinal bleeder. Thus, our approach is one of rapid stabilization, early panendoscopy and, if the rate of bleeding warrants, angiography. Surgical therapy is reserved for those patients in whom these intensive medical procedures fail to control the bleeding. We wish to emphasize the need to consider a Mallory-Weiss lesion in every acute-UGI bleeder, regardless of the lack of a "classical" history of recurrent retching prior to hematemesis. Our study also reiterates the value of thorough panendoscopy in these patients, particularly if surgery is contemplated. REFERENCES
1. Wychulis AR, Sasso A: Mallory-Weiss syndrome. Arch Surg 107:868-871, 1973 2. Dagradi AC, Broderick JT, Juler G, Wolinsky S, Stempien SJ: The Mallory-Weiss syndrome and lesion: A study of 30 cases. Am J Dig Dis 11:710-721, 1966 3. Holmes KD: Mallory-Weiss syndrome: Review of 20 cases and literature review. Ann Surg 164:810, 1966 1134
4. Hinchey EJ, Hreno A: Postemetic gastroesophageal laceration with hemorrhage. Surg Gyn Obstet 126:324-330, 1968 5. Wells RF: A common cause of upper gastrointestinal bleeding: The Mallory-Weiss syndrome. So Med J 60:1197-1201, 1967 6. Atkinson M, Bottrill MB, Edwards AT, Mitchell M, Peet BG, Williams RF: Mucosal tears at the oesophagogastric junction (the MalloryWeiss syndrome). Gut 2:1-11, 1961 7. Dobbins WP: Mallory-Weiss syndrome: A commonly overlooked cause of upper gastrointestinal bleeding. Gastroenterology 44:689-695, 1963 8. St. John DJB, Masterson JP, Yeomans ND, Dudley HAF: The Mallory-Weiss syndrome. Br Med J 1:140-143, 1974 9. Miller AC, Hirschowitz BI: Twenty-three patients with Mallory-Weiss syndrome. So Med J 63:441-444, 1970 10. James FA: Problems of alimentary bleeding. Br Med J 2:267-273, 1969 11. Mallory GK, Weiss S: Hemorrhages from laceration of the cardiac orifice of the stomach due to vomiting. Am J Med Sci 178:506-515, 1929 12. Lundberg GD, Mattei IR, Davis C J, Nelson DE: Hemorrhage from gastroesophageal lacerations following closed-chest cardiac message. J Am Med Assoc 202:123-126, 1967 13. Katz D, Freud M, McKinnon WMP: The Mallory-Weiss syndrome: Evaluation by early endoscopy of its clinical picture and its incidence in upper gastrointestinal hemorrhage. Am J Dig Dis 10:314-323, 1965 14. Baum S, Nusbaum M: The control of gastrointestinal hemorrhage by selective mesenteric arterial infusion of vasopressin. Radiology 98:497505, 1971 15. Stabler EV, Alder TM, Wichern WA: Massive hemorrhage from esophagogastric tears: Mallory-Weiss syndrome. Postrad Med 40:614620, 1966 16. Etheridge SN: The Mallory-Weiss syndrome. AmJ Surg 100:200, 1960 17. Koehler PR: New approaches to the radiological diagnosis of Mallory-Weiss syndrome. Br J Radiol 42:354-357, 1969 18. Weaver DH, Maxwell JG, Castleton KB: Mallory-Weiss syndrome. Am J Surg 118:887-892, 1969 Digestive Diseases, Vol. 20, No. 12 (December 1975)
Nineteen patients with the Mallory-Weiss lesion diagnosed by panendoscopy are presented. This represents 10.5% of 180 acute upper-gastrointestinal bleeders. Only 36.8% of these 19 patients had a history of heavy ethanol intake and 26% had hiatus hernias. In addition to the Mallory-Weiss lesion, abnormalities in 63% were noted on endoscopy. None of the patients required surgery for control of the bleeding. Two patients were treated with selective arterial-vasopressin infusion. The importance of a high index of suspicion for this lesion in spite of the lack of a classical alcoholic or recurrent retching history and the value of intensive medical therapy, including early panendoscopy, is emphasized.
D e s p i t e excellent reviews o n t h e M a l l o r y W e i s s s y n d r o m e in t h e p a s t ten y e a r s ( 1 - 9 , 13), m a n y aspects of this s y n d r o m e h a v e received varying emphasis depending upon patient popu l a t i o n , t e c h n i c a l - e q u i p m e n t availability, a n d a p p r o a c h to t h e acute g a s t r o i n t e s t i n a l bleeder. A u n i v e r s a l l y a c c e p t a b l e incidence of o c c u r r e n c e h a s yet to be defined, m a n a g e m e n t h a s u n d e r gone s i g n i f i c a n t c h a n g e s , a n d e m p h a s i s on etiological events h a v e clearly shifted. T h i s s t u d y d e m o n s t r a t e s t h a t t h e etiological role of n o n a l c o h o l - r e l a t e d events r e q u i r e s increased e m p h a s i s a n d t h a t p r o m p t a n d t h o r o u g h p a n e n d o s c o p y is essential for o p t i m a l management.
MATERIALS AND METHODS The patients in this report represent those patients with the Mallory-Weiss lesion seen by the Gastroenterology Division at Barnes Hospital from July 1, 1972 to Oetober 15, From the Division of Gastroenterology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110. The opinions expressed herein are those of the authors and cannot be construed as reflecting the views of the United States Air Force. Address for reprint requests: Dr. Francis J. Tedesco, Department of Medicine, University of Miami School of Medicine, P.O. Box 875, Biscayne Annex, Miami, Florida 33152.
Digestive Diseases, Vol. 20, No. 12 (December 1975)
1974. This period represents 1,100 endoscopies with an end-view fiberoptic panendoscope (Olympus GIF-D, Olympus Corporation of American, New Hyde Park, New York), 287 of which were for upper-gastrointestinal (UGI) bleeding manifested by either melena or hematemesis. Of these 287 patients, 180 were classified as acute-UGI bleeders, defined as a history of hematemesis within 48 hours of endoscopy or a grossly bloody or coffee-ground guaiac positive-gastric aspirate within 24 hours of endoscopy. This study is a retrospective review of medical records, endoscopy reports, and photographs, and, where applicable, patient and/or attending physician follow-up questionnaires. The patients represent a cross section of a metropolitan and rural population served by a large private and teaching university hospital. Thorough gastric lavage was performed with iced saline or water prior to endoscopy. Each patient was examined by at least two endoscopists and all observations carefully recorded. Every attempt was made to examine the entire esophagus, stomach, duodenal bulb, and second portion of the duodenum consistent with the patient's status and technical feasibility. In those cases where a complete examination was not performed, notation as to the limiting factor was made. All patients with the MalloryWeiss lesion were managed medically, with two patients receiving selective vasopressin infusion (14, 17).
RESULTS O f t h e 180 acute U G I bleeders, 19 (10.5%) w e r e seen to h a v e the M a l l o r y - W e i s s lesion as t h e p r i m a r y etiology of t h e i r acute h e m o r r h a g e .
1131
SAYLOR & TEDESCO Table 1. Study Patients with Mallory-Weiss Lesions* Case no.
Age
Sex
History
UGI
Other endo findings
27
55
F
WNL
76
63
F
Edematous pylorus Esophagitis
149
47
M
151
49
M
Hypertension, nausea and vomiting for 1 week Labyrinthitis with tinnitus and vertigo, no vomiting Anorexia, nausea, and retching 1 day prior to admission Alcoholic, history unreliable
387
59
F
482
45
M
582
47
M
719 744
71 67
M M
755
47
F
791~
37
M
859
53
M
918
60
M
929
53
F
959
63
M
976
50
M
997w 1029
33 68
F F
1098
59
F
WNL WNL
Prepyloric edema and deformity Bulb deformity Erosive gastritis Acute distension of stomach with fluid, HHr HH no vomiting Psychogenic (?) nocturnal vomiting, Duodenitis Gastric ulcer, moderate singultus duodenitis Renal failure, home dialysis, WNL None vomited once Acute distension of stomach with food HH HH, duodenum not examined Hyperlipidemia, 11 months postWNL HH MI on Coumadin, protime 15%, no vomiting Viral gastroenteritis, 4 days WNL None of vomiting Heavy alcohol abuse, vomiting WNL HH, nodular antritis after alcohol debauch UGI bleed in 1952, nausea only, Mild esoStomach full of blood and adult diabetic phageal clots motility disturbances 12 hrs post-op TURP, no vomiting HH Antral gastritis, deformed antrum Behcet's disease, old MI on Coumadin, WNL None marked nausea, epigastric pain, no vomiting Heavy alcohol abuse, vomiting, Critically ill-Gastritis, gastric ulcer, and retching none duodenitis, duodenal diverticulum Heavy alcohol abuse, WNL Stomach full of blood and vomiting clots Psychogenic vomiting HH None Dysphagia, abdominal pain, retched HH, diffuse HH during endoscopy abnormal motility by cine Abdominal pain, past alcoholic Marked antral Severeantral diaphragm a b u s e - - n o n e recent--nausea and pyloric and vom iti ng deformity, ulcer (?)
*All patients were treated medically. Patients 719 and 1098 were treated with selective arterial infusion with vasopressin. All patients had an uneventful course with the exception of patient 959, who died. "i-Hiatal hernia. SThis is the second UGI bleed caused by a documented Mallory-Weiss lesion. w is the second UGI bleed caused by a documented Mallory-Weiss lesion.
1132
Digestive Diseases, Vol. 20, No. 12 (December 1975)
MALLORY-WEISS SYNDROME
Eight were female and 11 male, ranging in age from 33 to 71. Abnormalities other than the Mallory-Weiss lesion were noted in 9 of 18 patients examined by U G I barium-contrast roentgenography and in 13 of the 19 by endoscopy (68.4%). Hiatus hernia was identified in 7 (36.8%) and was the sole abnormality other than the mucosal tear(s) in 4 patients (Table 1). One patient sustained a Mallory-Weiss tear as a result of retching during panendoscopy for an unrelated problem. Careful alcohol-intake histories indicated that 7 (36.8%) had heavy alcohol intake (greater than 10 ounces per week), 1 had 4-10 ounces per week, 2 less than 4 ounces, 5 less than 2 ounces per month, and 3 no alcohol of any kind. An alcohol history was not obtained in 1 patient. 3 patients had been drinking heavily prior to the onset of hematemesis (15.8%). There was one death in this series (5%): an alcoholic admitted with sepsis, gastrointestinal bleeding, and pulmonary compromise. Although his bleeding stopped within 24 hours, he succumbed with overwhelming sepsis and a combination of pulmonary, hepatic, and renal failure, despite vigorous and intensive therapy. 10 (52.6%) patients did not receive blood replacement. Of the 9 patients receiving blood, the average replacement was 4.4 units. Of the nontransfused patients, 4 dropped their hemoglobin levels to 10 g. 6 (31.5%) patients, only one of whom was an alcoholic, did not have a history of vomiting or retching prior to hematemesis, and an accurate vomiting history was therefore questionable.
Table 2. Incidence of Mallory-Weiss Lesion in Acute UG! Hemorrhage Author
Patients Incidence
Wells (1967) (5) St. John et al (1974) (8) Miller and Hirschowitz (1970) (9) Jones (1969) (10) Katz et al (1965) (13) Current study
25/170 16/121
14.7% 13.2%
23/712 8/297 8/297 19/180
3.2% 2.7% 2.7% 10.5%
The Mallory-Weiss lesion accounted for 13.2% of acute-UGI bleeding in the most review of this subject by St. John et al (8). In that study, it ranked second only to duodenal ulcers and equalled gastric ulcers as the etiology of acute bleeding. Although this study revealed a slightly lower incidence (10.5~ both patient populations are comparable, excluding the implied bias inherent in a military or Veterans
Administration hospital (2, 5, 7), and showed a significantly greater incidence than other previously reported series (Table 2). Prompt recognition of this entity has therefore become increasingly important. The original recognition and description of this syndrome (11) implicated alcohol, and many subsequent authors (2, 3, 5, 9) emphasized recent alcohol debauch or alcohol-induced retching as the sine q u a n o n for the suspicion or diagnosis of Mallory-Weiss lesions. However, several authors (1, 4, 6, 10, 18) have challenged this concept and have listed many events ranging from coughing paroxysms (6) to cardio-pulmonary resuscitation (12). Analysis of the 19 patients in this study shows that while vomiting was the most frequent event preceding the hematemesis (68%), alcohol-related events accounted for only 21% of these patients. 6 patients (31.5~ had hematemesis simultaneously with the first emesis as described by Holmes (3), and by Hinchey and Hreno (4). Panendoscopy revealed pathology other than the Mallory-Weiss lesion in 13 of 16 (81~ patients in whom a thorough and complete panendoscopic examination was possible. Of these, 9 patients had other lesions that could have been mistaken as the source of bleeding at surgery. It is our opinion that therein lies the importance of thorough panendoscopy in the early management of the acute-UGI bleeder. Stabler et al (15) and Etheridge (16) have described serious consequences when surgery is required in an emergency situation to control gastrointes-
Digestive Diseases, Vol. 20, No. 12 (December 1975)
1133
DISCUSSION
SAYLOR & TEDESCO
tinal hemorrhage and only incomplete preoperative knowledge is available. Stabler reported four patients (50%) who had more than the Mallory-Weiss lesion noted at surgery: a large antral ulcer; a massively bleeding duodenal ulcer in addition to two bleeding gastric tears; reoperation because of an overlooked tear due to obscuring gastric folds; and 1 patient who died after suture of gastric lacerations from an overlooked esophageal tear. Although none of our patients required surgery, it can be seen from Table 1 that significant abnormalities were seen that were not responsible for the U G I bleeding, but which might cause confusion in a patient at surgery who often stops actively bleeding concomitant with general anesthesia. All our patients were treated medically. 2 patients had selective angiography with vasopressin infusion resulting in rapid control of bleeding. It has been our experience that this newer procedure offers an effective, nonsurgical modality of therapy in the acute gastrointestinal bleeder. Thus, our approach is one of rapid stabilization, early panendoscopy and, if the rate of bleeding warrants, angiography. Surgical therapy is reserved for those patients in whom these intensive medical procedures fail to control the bleeding. We wish to emphasize the need to consider a Mallory-Weiss lesion in every acute-UGI bleeder, regardless of the lack of a "classical" history of recurrent retching prior to hematemesis. Our study also reiterates the value of thorough panendoscopy in these patients, particularly if surgery is contemplated. REFERENCES
1. Wychulis AR, Sasso A: Mallory-Weiss syndrome. Arch Surg 107:868-871, 1973 2. Dagradi AC, Broderick JT, Juler G, Wolinsky S, Stempien SJ: The Mallory-Weiss syndrome and lesion: A study of 30 cases. Am J Dig Dis 11:710-721, 1966 3. Holmes KD: Mallory-Weiss syndrome: Review of 20 cases and literature review. Ann Surg 164:810, 1966 1134
4. Hinchey EJ, Hreno A: Postemetic gastroesophageal laceration with hemorrhage. Surg Gyn Obstet 126:324-330, 1968 5. Wells RF: A common cause of upper gastrointestinal bleeding: The Mallory-Weiss syndrome. So Med J 60:1197-1201, 1967 6. Atkinson M, Bottrill MB, Edwards AT, Mitchell M, Peet BG, Williams RF: Mucosal tears at the oesophagogastric junction (the MalloryWeiss syndrome). Gut 2:1-11, 1961 7. Dobbins WP: Mallory-Weiss syndrome: A commonly overlooked cause of upper gastrointestinal bleeding. Gastroenterology 44:689-695, 1963 8. St. John DJB, Masterson JP, Yeomans ND, Dudley HAF: The Mallory-Weiss syndrome. Br Med J 1:140-143, 1974 9. Miller AC, Hirschowitz BI: Twenty-three patients with Mallory-Weiss syndrome. So Med J 63:441-444, 1970 10. James FA: Problems of alimentary bleeding. Br Med J 2:267-273, 1969 11. Mallory GK, Weiss S: Hemorrhages from laceration of the cardiac orifice of the stomach due to vomiting. Am J Med Sci 178:506-515, 1929 12. Lundberg GD, Mattei IR, Davis C J, Nelson DE: Hemorrhage from gastroesophageal lacerations following closed-chest cardiac message. J Am Med Assoc 202:123-126, 1967 13. Katz D, Freud M, McKinnon WMP: The Mallory-Weiss syndrome: Evaluation by early endoscopy of its clinical picture and its incidence in upper gastrointestinal hemorrhage. Am J Dig Dis 10:314-323, 1965 14. Baum S, Nusbaum M: The control of gastrointestinal hemorrhage by selective mesenteric arterial infusion of vasopressin. Radiology 98:497505, 1971 15. Stabler EV, Alder TM, Wichern WA: Massive hemorrhage from esophagogastric tears: Mallory-Weiss syndrome. Postrad Med 40:614620, 1966 16. Etheridge SN: The Mallory-Weiss syndrome. AmJ Surg 100:200, 1960 17. Koehler PR: New approaches to the radiological diagnosis of Mallory-Weiss syndrome. Br J Radiol 42:354-357, 1969 18. Weaver DH, Maxwell JG, Castleton KB: Mallory-Weiss syndrome. Am J Surg 118:887-892, 1969 Digestive Diseases, Vol. 20, No. 12 (December 1975)
