The Mallory-Weiss Syndrome: Evaluation by Early Endoscopy of its Clinical Picture and its Incidence in Upper Gastrointestinal Hemorrhage

DAVID KATZ, M.D., MOSHE FREUD, M.D., and ~¥ILLIAM M. P. McKINNON, M.D.

I N 1929, Mallory and Weiss 1 described.4 patients with histories of mas- sive hematemesis who were shown at autopsy to be bleeding f rom

linear tears in the nmcosa of the esophagogastric junction. T w o similal cases were noted by the same authors in 1932. 2 In 1963, a survey of the l i terature by Dobbins a revealed that a total of 54 cases of what has become known as the Mallory-Weiss syndrome had been reported to that date. Th i r ty addit ional cases have been reported in the past year. 4-s

In December 1961, a combined medical-surgical team was established at the New York Medical College-Metropoli tan Medical Center in order to initiate a prospective study of consecutive admissions for upper gastro- intestinal hemorrhage, utilizing early esophagogastroscopy in the diag- nosis of the bleeding source. Between December 1961 and May 1964, 297 cases of upper gastrointestinal bleeding were evaluated by this meth- od g, 10 Since all admissions for upper gastrointestinal bleeding were seen by the "bleeding team," we were afforded an oppor tuni ty to assess the in- cidence of the Mallory-'Weiss syndrome at a large municipal teaching in- stitute. Eight instances of esophageal and / o r gastric tears were encoun- tered.

I t is the purpose of this report to describe the varied types of the Mal- lory-Weiss syndrome, stressing the wide spectrum of the clinical picture, a fact which has not heretofore been generally recognized.

From the Section of Gastroenterology, Department of Medicine, and the Department of Surgery, New York Medical College-Metropolitan Hospital Medical Center, New York, N. Y.

Supported in part by Training Grant TI-AM-5237-0I from the National Institute of Arthritis and Metabolic Disease, N.I.H., U. S. Public Health Service, and Contract U-t373 from the Health Research Council of the City of New York.

*U. S. Public Health Service Trainee in Gastroenterology. Present address: Beilinson Hospital, Petah Tikvah, Israel.

314 Arner[can Journal of Digestive Diseases

K A T Z ET A L . : M A L L O R Y - W E I S S S Y N D R O M E

C A S E R E P O R T S

(/ase 1

J. G., a 52-year-old, white, male alcoholic was adnl i t ted because of vomit ing, hema t - cmcsis and epigastric pa in of 4-hr. dura t ion . His liver was greatly enlarged. On csophagoscopy the cardioesophageal junc t ion was encounte red at 37 em. f rom the in- (isor teeth, suggestive of a h ia tus hernia . Small 1- to 2-ram. nonb leed ing varices were noted. A rent was seen in the esophageal mucosa, the edges gap ing sonle 3 ram. im- mediately proximal to the ca,,'dia. T h e rent ex tended on the left wall of the esophagus th rough the cardia into the s tomach for a distance of 4 cm. T h e r e was no blood at the base of the tear, and its greatest dep th was es t imated to be 1.5 m m .

Gastroscopy disclosed n u m e r o u s aeute gastric erosions wi th active b leeding points and clots. U p p e r GI series demons t ra ted a sliding h ia tus hern ia and " m i n i m a l i r regular i ty of the duodena l cap."

Hemoglob in level on admission was 9,3 gm.%, and 3 uni t s of blood were t ransfused. T h e bleeding s topped soon after admission, and the hospi ta l course was o thmwise tmremarkable .

C O M M E N T

E n d o s c o p i c e x a m i n a t i o n r e v e a l e d a n o n b l e e d i n g g a s t r o e s o p h a g e a l t e a r ,

a n d f o u r a d d i t i o n a l p o t e n t i a l b l e e d i n g s o u r c e s ( e s o p h a g e a l v a r i c e s , h i a t u s

h e r n i a , a d e f o r m e d d u o d e n a l c a p , a n d g a s t r i c e r o s i o n s ) e x i s t e d . O f t h e s e ,

o n l y a c u t e g a s t r i c e r o s i o n s w e r e t h e b l e e d i n g s o u r c e . A l t h o u g h n o n b l e e d -

i n g g a s t r o e s o p h a g e a l t e a r s h a v e b e e n r e p o r t e d o n r a r e o c c a s i o n a t

n e c r o p s y , ~1 to o u r k n o w l e d g e t h i s is t h e f i r s t r e p o r t e d i n s t a n c e o f a n o n -

b l e e d i n g t e a r d i a g n o s e d i n v i v o .

Case 2

B. R., a 68-year~ohl, obese, white, male physician was admi t t ed because of severe vomi t ing after a heavy meal, followed by hematemes i s and me lena 8 hr. later. On admission he compla ined of diffuse abdomina l pain. A previous episode of vomi t ing and chest pain occurr ing 5 years before was diagnosed as "gastri t is ," bu t no endoscopy was pe r fo rmed at the time. T h e pa t ien t was known to be hyper tens ive and was being treated wi th reserpine. T h e r e was also a history of pept ic ulcer da t ing back 30 years. Physical examina t ion revealed relative hyper tens ion and epigastric tenderness.

T h e pa t ien t con t inued to bleed aetiveIy; hemoglob in level fell f rom 16.0 gm.~o to 11.5 gm.~o, and an adequate blood pressure could no t be m a i n t a i n e d in spite of the t ransfus ion of 10 un i t s of blood over a period of 24 hr. Endoscopy was deferred because of coronary artery disease suggested by electrocardiography. An emergency u p p e r GI series, technically unsatisfactory, was suggestive of h ia tus he rn i a and a lesser curva ture ulcer. Emergency distal gas t ro tomy and duodeno tomy, unde r t aken 30 hr, after admis- sion, revealed no source of bleeding. A second incision nea r the cardia and ex t end ing in to the esophagus, revealed two longi tudinal mucosal tears 2.5 and 5.0 era. in length , respectively, wi th gap ing edges located on the poster ior wall of the most distal esophagus. Both were actively bleeding. T h e s e were su tured . T h e h i a tus he rn i a was repaired. A vagotomy and pyloroplasty were added.

T h e pa t ien t developed peritonit is , mediast iui t is , congestive failure, and u r emia and

died on the sixth postoperat ive day.

New Series, Yol. 10, No. 4, 1965 315

N E W Y O R K M E D I C A L C O L L E G E ISSUE

Pos tmor t em e x a m i n a t i o n revealed tha t the esophagogas t ro tomy su tu re l ine had rup- tured, resul t ing in per i toni t i s and mediasf ini t is . I t was es tabl ished tha t the esophageal tears ex tended only t h r o u g h the mucosa into the submucosa . T h e y had n o t caused any f u r t h e r b leeding after h a v i n g been sutured.

C O M M E N T

Suspected coronary artery disease precluded emergency esophagogas- troscopy and delayed sm'gical exploration. The diagnosis of esophageal tears was established at surgery. Suture of the tears induced immediate hemostasis. Death was due to postoperative complications because oi anastomotic leak.

Case 3

E. S., a 32-year-old, white , male alcoholic wi th a history of duodena l ulcer and of r igh t u p p e r lobectoiny for tuberculosis, was admi t t ed because of three days of vomit- ing and several episodes of hematemes i s on the day of admission. He compla ined of epigastric pain. Physical examina t ion was unreveal ing. Esophagoscopy showed severe mucosal hyperemia and several superficial u lcerat ions of the distal 4 cm. of gullet . At 37.5 cm., a 2.5-cm. l inear mucosal tear commenced , ex t end ing to the cardia. T h e edges of the tear were gaping. No active bleeding or clots were seen at the base of the tear. Gastroscopy disclosed two superficial ulcers, 5 and 7 ram. in diameter , on the anter ior wall of pars med ia wi th a clot in the base of each.

Hemoglob in on admission was 9.5 gin.% and the pa t ien t was given 2 un i t s of blood. Bleeding s topped soon after admission. U p p e r GI series was m)t per formed because the pa t ien t left the hospital .

C O M M E N T

Esophagoscopy established the diagnosis of a nonbleeding esophageal tear, while gastroscopy demonstrated acute gastric lesions as the bleeding source in this heavy imbiber of alcohol. Without the performance of early esophagogastroscopy neither diagnosis could have been established.

Case 4

W. F., a 53-year-old, Negro, male alcoholic was a dmi t t ed because of one day 's his- tory of vomit ing, retching, hematcmts i s , and melena. T h e r e were no o ther previous gast rointes t inal symptoms. Esophagoscopy demons t r a t ed no b leeding source in the gullet . Blood was seen to be coming from the s tomach. Gastroscopy disclosed n o r m a l a n t r u m and pars media. No blood was present in midd le o r distal s tomach. O n with- drawal of the gastroscope fresh blood was seen coming f rom the area a round the cardia, b u t the exact site of b leeding could not be identified.

H e m o g l o b i n level on admission was 12.5 gin./°7 o and the hlood pressure 60/30. Be- cause of con t inued uncont ro l led bleeding, r equ i r ing the t ransfusion of 10 uni t s of blood, emergency l aparo tomy was per formed 22 hr. after admission, Thro t lgh a gas- t ro tomy active bleeding was seen f rom two long i tud ina l tears of the mncosa on the lesser cu rva tu re 2.5 cm. distal to the cardioesophageal junc t ion . These were sutured. A n o n b l e e d i n g chronic duodena l ulcer was found in addi t ion, and subtotal gas t rectomy

316 American ,Journal of D|gesHve Diseases

KATZ ET AL. : MALLORY-~NEISS SYNDROME

, a s performed, The postoperative course was initially stormy, with the development (,[ hepatic coma and uremia. The patient gradually made a satisfactory recovery.

COMMENT

A l t h o u g h t h e a c t u a l d i a g n o s i s was e s t a b l i s h e d o n l y a t su rge ry , t h e en-

( l~scopis t d e m o n s t r a t e d t h e a r e a f r o m w h i c h b l e e d i n g e m a n a t e d a n d

M e r t e d t h e s u r g e o n to t h e p o s s i b i l i t y of a ga s t r i c t ea r . C o n s e q u e n t l y , a

c o r r e c t d i a g n o s i s of gas t r i c m u c o s a l tears was e s t a b l i s h e d at su rge ry . I n

:~ddi t ion, a c h r o n i c d t t o d e n a l u l ce r w h i c h was n o t b l e e d i n g was also

l e m o n s t r a t e d .

Case 5

M. H , a 50-year-old, white, male alcoholic was admitted because of vomiting, hematemesis, and melena of several hours' duration. There was a history of a bleeding duodenal nlcer t5 years prior to admission, with periodic episodes of recurrent epigas- tric pain, but with no recent relapse. Esophagoscopy demonstrated a 2.5-cm. superficial longitudinal tear just proximal to the cardioesophageal jtmction with active oozing of blood. Gastmscopy results were negative and the tipper GI series revealed a prepyloric ulcer.

The admission hemoglobin level was 9.0 gin.% and the patient was given 3 units of blood. Bleeding stopped promptly. Elective subtotal gastrectomy performed for per- sistent pain 2 weeks later, rc~ealed a duodenal ulcer with no evidence of recent bleeding.

COM~It;NT

In the face of a k n o w n d u o d e n a l u lcer , e a r l y e n d o s c o p y d e m o n s t r a t e d

a n e s o p h a g e a l tear , ac t ive ly b l e e d i n g , as t h e s o u r c e of h e m o r r h a g e . H a d

n o e n d o s c o p y b e e n p e r f o r m e d , t he u lcer w o u l d h a v e b e e n w r o n g l y con-

s i d e r e d the b l e e d i n g sou r (e .

Case 6

E. F., a mildly icteric 18 year-ohl, white female, was adnfitted to the hospital in her last month of pregnancy because of early separation of the placenta. A viable child was delivered. Massive postpartum bleeding occurred, mid the hemoglobin level fell to 8.5 gin.%, but rose to I5 gm.°/~ after the lransfusion of 3 traits of blood. Sixteen hours after an attack of retching, massive hematemesis occurred. A Levin tube was passed and 3000 co. of coffee-groined material was aspirated. Esophagoscopy results were negative, and gastroscopy disclosed a longitudinal 1.5-cm. tear of the mucosa just be- low the cardioesophageal junction with an active ooze of blood.

Bleeding slowed gradually, stopping after 30 hr. Three more units of blood were transfused. The jaundice, subsequently shown by liver biopsy to be due to acute fatty liver of pregnancy, was accompanied by signs of hepatic failure. The patient gradually made a satisfactory recmery on high-dose steroid therapy.

COM~IENT

T h i s p a t i e n t r e p r e s e n t s a r a r e i n s t a n c e of [ a t t y l i ve r o f p r e g n a n c y w i t h

s t t rv iva l of b o t h m o t h e r a n d ch i ld . I t wi l l b e r e p o r t e d in d e t a i l e l s e w h e r e

New Series, Vol. 10, No. 4, 1965 317

NEW YORK MEDICAL COLLEGE ISSUE

in this Jou rna l . A character is t ic gastric tear which was b leed ing was dem-

ons t ra ted gastroscopically. T h e endoscopic diagnosis of the b leed ing

source, in the absence of a pept ic ulcer, p e r m i t t e d the use of massive doses

of steroids, which p robab ly saved the life of the mothe r .

Case 7

K. W., a 39-year-old, white, female alcoholic was admitted to the hospital for vomit- ing of 2 days' duration and hematemesis on the day of admission. Portal cirrhosis had been diagnosed by liver biopsy 2 years previously. One year previously she had been hospitalized elsewhere for an episode of hematemesis of unknown etiology and for jaundice. Esophagoscopy showed a 2-cm. laceration with gaping edges, which extended across the cardioesophageal junction. Blood oozed from the laceration. No varices were seen. Gastroscopy results were negative, and an upper GI series disclosed extrinsic pressure on the lesser curvature of stomach from an enlarged liver.

Levin tube drainage remained bloody for 40 hr. Three units of blood were given during that period. Hemoglobin rose from 7.0 gin.% on admission to 11.6 gin.%. The patient developed hepatic eneephalopathy but made a slow and satisfactory recover}, with conservative therapy.

COMMENT

W i t h o u t early esophagogastroscopy, this k n o w n c i r rho t ic wou ld have

been considered to be a variceal b leeder . T h i s possibi l i ty was ru l ed ou t

at esophagoscopy and an actively b leed ing esophageal tear was demon-

s trated as the source of b leeding.

Case 8

F. j., a 24-year-old Negro in her third month of pregnancy was admitted because of three episodes of hematemesis in the 2 days prior to admission. She detailed repeated episodes of vomiting in the previous 2 weeks, Esophagoscopy results were negative, and gastroscopy disclosed a longitudinal 2.5-cm. clot at the cardioesophageal junction on the anterior wall. The admission hemoglobin level was 11.4 gm.%.

Bleeding stopped soon after admission and the patient's hospital course was unre- markable. No transfusions were required.

COMMENT

V o m i t i n g due to p regnancy resul ted in a gastr ic tear demons t r ab l e by

gastroscopy. T h e gastroscope (Eder-Palmer) was h e l p f u l in es tabl ish ing

the diagnosis by r e n d e r i n g visible the area abou t the cardia.

D I S C U S S I O N

T i l e assessment of the t rue inc idence of the Mallory-V(eiss syndrome

in a general hospi ta l has been impossible because repor t s were based on

cases d iagnosed by autopsy alone. On the o the r hand , repor t s dea l ing

with surgical r epa i r of the gas t roesophageal tears on ly encompass the

318 American Journal of Digesflve Diseases

KATZ ET A L , : M A L L O R Y - W E I S S S Y N D R O M E

,c~crely bleeding lesions which do not stop spontaneously. Our experi- ,nee suggests, however, that a far greater number of Mallory4¥eiss tesions ,h, not require surgical intervention for bleeding. Moreover, some pa- l icnts will develop the characteristic tear without manifest bleeding, as ,hown by our Cases 1 and 3, in which bleeding was from other acute gas- Eric lesions. It seems probable therefore that endoscopy of a large number ,,l patients vomiting acutely, but who had not bled, might disclose the Mallory-Weiss lesion in some.

~NCIDENCE

In the 27-month period extending from December 1961 through March 1964, there were 49,760 admissions to the Metropoli tan Hospital. Two hundred ninety seven bleeding episodes were evaluated and 8 mucosal lacerations were noted in the distal esophagus or proximal stomach. T h e incidence of admissions for upper gastrointestinal bleeding at our insti- tution when compared to all admissions was 1 in 168 (.59%); the inci- dence of gastroesophageal tears diagnosed during the same period, 1 in 6220 admissions (0.016~o); and of bleeding episodes, 1 in 37 (2 .7~) . Since only 6 of the 8 lesions accounted for a bleeding source, the corrected incidence for Mallory-Weiss syndrome as a bleeding source was 1 in 8293 hospital admissions (0.012%) and 1 in 49.5 bleeding episodes (2.09%). There were 81 episodes of massive bleeding established by criteria we have described previously2,10 The incidence of the Mallory-Weiss syn- drome in cases of massive bleeding in our group of patients was 9.8%. Since endoscopy was done on all consecutive admissions for upper gastro- intestinal bleeding, the possibility of missing a bleedirlg esophageal or gastric tear was remote, and our statistics would seem to be accurate.

ETIOLOGY

T h e possible etiological factors in the pathogenesis of the Mallory- PCeiss syndrome have been well reviewed in the literature, a, ~, 6, 1~, 12 Th e common denominator, as demonstrated clinically and experimentally, is a sudden increase in intra-abdominal pressure. Vomiting is the most com- mon etiologic factor. In a large percentage of reported cases, alcohoIism has consequently been implicated, with its resultant vomiting or retching. Pregnancy, coughing, status asthmaticus, straining, epileptic fits, gastric atrophy, and the presence of an hiatus hernia have also been reported as etiologic factors, a-5

CLINICAL FEATURES

T h e important clinical features manifested in our cases are summarized in Table 1. Three of the 8 patients admitted to high alcoholic intake and

New Series, Vol. I0, No. 4, J965 319

TA

BL

E

1.

DA

TA

F

RO

M

8 C

AS

ES

O

F

MA

LL

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S

(M-W

) S

YN

DR

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No.

of

Pos

sibl

e L

owes

t tr

ans-

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Sour

ce

Alc

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-W

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.) di

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rati

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blee

ding

he

rnia

P

ain

Pre

viou

s hi

stor

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ul

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The

rapy

1 52

M

+

+

V

om

itin

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9.3

3 E

sop

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osc

op

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E

Ero

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ga

s-

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2 68

M

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- V

om

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11.5

10

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urg

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E

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3 32

M

+

--

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rug

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9.

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K A T Z E T A L , : M A L L O R Y - ~ V E t S S S Y N D R O M E

2 others admitted to a his:ory of chronic alcoholism. All 8 vomited at least once, from a few hours to several clays prior to the onset of hemab cmesis. Five patients complained of epigastric pain on admission, and 4 had a history of previous peptic ulcer. An hiatus hernia was demonstrable in only 2 patients. Two patients had acute gastric erosions as a con- comitant lesion from which they bled, without any bleeding from the gastroesophageal tears.

in 4 patients treated by blood replacement the bleeding stopped spon- taneously without surgical intervention. In a fifth patient bleeding stopped promptly after transfusions; however, he underwent elective sur- gery 2 weeks later because of intractable pain due to a nonbleeding duo- denal ulcer. Two patients required surgical intervention at 22 and 30 hr. after admission for uncontrolled bleeding. One of the operated patients survived. In 1 patient bleeding was minimal and self-limited, requiring no transfusion.

DIAGNOSIS

A review of the other 8t reported cases in the literature a s reveals that 30 cases were diagnosed at necropsy, 35 at surgery, and only 7 by en- doscopy. In addition, Dagradi: has recentIy alluded to 12 cases of the Mallory-Weiss syndrome diagnosed by endoscopy among 100 episodes of massive gastrointestinal bleeding at a veterans' hospital. Six of our cases were similarly diagnosed endoscopically; 4 by esophagoscopy and 2 by gastroscopy. A seventh case was strongly suspected on the basis of gastro- scopic examination. Since the experienced observer finds little difficulty in determining the bleeding site even in the face of active bleeding, rot> tine early esophagogastroscopy should uncover all bleeding mucosal tears.

TREATMENT

Our therapeutic approach to the Mallory-Weiss syndrome consists of the following. A Levin tube is left in place as an assessment of bleeding. Blood is replaced as necessary. A 24-hr. trial of conservative therapy is commenced. If bleeding is torrential at any time during the 24-hr. pe- riod, surgical intervention is mandatory. If bleeding has not begun to abate at 24 hr., laparotomy is indicated. V~Te feel that tile use of the Sengstaken-Btakemore tube may increase esophageal bleeding and will have no beneficial effect on a gastric tear. An abdominal approach is best should surgery become necessary.

A distinction should be made between the Mallory-Weiss syndrome, wherein the tears extend into the submucosa only, and spontaneous rup- ture of the gastroesophageal area, wherein the whole thickness of the wall is involved. Although the pathogenesis of both conditions is prob-

New Series, Vol. 10, No. 4, I965 ~2]

NEW YORK MEDICAL COLLEGE ISSUE

ably similar (sudden increase in intra-abdominal pressure, possibly vary- ing in degree) the therapeutic approach is entirely different. T h e Mal- lory-Weiss syndrome can often be treated conservatively in contrast to rupture at the gastroesophageal area, where emergency surgery is essential and delay may be disastrous. Bruno et al. 5 and others la have recently suggested the use of the term Boerhaave syndrome for rupture of the gas- troesophageal area, limiting the use of the term Mallory:Weiss syndrome to those cases where the laceration does not extend beyond the sub- mucosa.

SUMMARY

1. In a prospective study of upper gastrointestinal hemorrhage, 297 cases were examined endoscopically. Eight instances of gastric or esopha- geal tears were noted. Over the 29-month.period during which the study was carried out, there were 49,760 admissions to this municipal teaching hospital. T h e incidence of gastroesophageal tears was 2.7~o of all upper gastrointestinal bleeders and 0.016% of all admissions.

2. Early endoscopy was of great value in establishing a rapid and ac- curate diagnosis of the lesion.

3. In 2 instances bleeding did not result from the demonstrated tears, but was due to coexistent acute gastric erosions.

4. In 4 other cases, bleeding from the tear stopped spontaneously; one of these was operated electively for a nonbleeding duodenal ulcer. Sur- gical intervention for continued bleeding was necessary in 2 patients, one of whom died.

5. An initial conservative approach to therapy of the Mallory-Weiss syndrome is suggested, provided the diagnosis is ascertained by early esophagogastroscopy. Continued bleeding will obviously dictate surgical intervention.

ADDENDUM

In the 9-month period subsequent to preparat ion of this manuscript, 2 more patients with esophageal tears were encountered. In one, a 52-year- old white male alcoholic, a classic Boerhaave syndrome was diagnosed at surgery. T h e patient died postoperatively of pancreatitis. Conservative therapy was successful in the second patient, a 51-year-old white male alcoholic with esophageal tear due to retching. T h e tear was diagnosed by esophagoscopy.

New York Medical College Fifth Ave. de 106th St

New York, N. Y.

322 American Journal of Dicjestlve Diseases

KATZ ET AL. : MALLORY-'~VEISS SYNDROME

R E F E R E N C E S

1. MALLORY, G. K., and WLJss, S. Hemorrhages from lacerations of the cardiac orifice of the stomach due to vomiting. Am..[. M. Sc. /78:506, 1929.

2. WEISS, S., and MALLORY, G. K. Lesions of the cardiac orifice of the stomach pro- duced by vomiting. J.A.M.A. 98:1353, 1932.

3. DOBmNS, W. O., III. Mallory-Weiss Syndrome: a commonly overlooked cause of upper gastrointestinal bleeding: Report of three cases and review of the Literature. Gastroenterology 44:689, 1963.

4. BAUE, A. E. Bleeding from laceration of the cardia: The Mallory-Weiss Syndrome. J.A.M./I. 184:325, 1963.

5, BRtmO, M. S., GKIER, W. R. N., and OBER, XV. B. Spontaneous lacerations and rupture of esophagus and stomach: Mallory-Weiss syndrome, Boerhaave Syndrome, and their variants. Ann. Int. Med. 112:574, 1964.

6. LIoN-CACHET, J. Gastric fundal mucosal tears. Brit. J. Surg. 50:985, 1963. 7. DACRAOI, A. B., LEE, R., and STEMPlEN, S. Experience with esophagogastroscopy

during massive upper gastrointestinal hemorrhage. Presented at the Annual meet- ing of the American Society for Gastrointestinal Endoscopy, Dallas, Apr. 22, 1964.

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