Vascular compression of the duodenum

Vascular Compression

of the Duodenum*

Emphasis on Accurate

Diagnosis

ARLIE R. MANSBERGER, JR., M.D., JOHN B. HEARN, M.B., B.S., F.F.R., ROBERT M. BYERS, M.D., NORBERT FLEISIG, M.D., AND ROBERT W. BUXTON, M.D., Baltimore,

From the Departments of Surgery and Radiology, LJniversity of Maryland School of Medicine, Baltimore, Maryland.

C

OMP~SSIVE obstruction of the transverse or

ascending portions of the duodenum by the superior mesenteric vessels is a traditionally controversial entity. This unusual form of obstruction, first described by Rokitansky [I] over a hundred years ago, was reported with great frequency in the first three decades of this century. Several of the larger series [Z-P] were collected in relatively short periods of time, suggesting that the condition must have been considered prevalent. In recent years, only sporadic small series have been reported [5-131. Goin [14] in 1956 suggested that the disease seemed to be endemic in those areas where radiologists were aware of and trained in the procedures which would aid in the diagnosis. Although the initial diagnosis has been traditionally relegated to the sphere of the radiologist, very small and insignificant amounts of space are allocated to a discussion of this entity in recent radiologic texts. The so-called “classic” radiologic signs are apparently not always so since dilatation of the iirst and second portion of the duodenum, delay in barium passage with to and fro peristalsis, and an oblique extrinsic pressure defect are reported singly or in combination as normal variants in patients without symptoms and in patientswhoseduodenal obstruction is due to other etiologic factors [15-171. Further, there is a distressing lack of unaminity regarding the name of the syndrome and it has been reported

ikfuryhzd

in the literature under various headings, such as chronic duodenal ileus [18], vascular compression of the duodenum [19], superior mesenteric artery syndrome [IO], chronic intermittant arteriomesenteric occlusion of the duodenum [14], arteriomesenteric duodenal obstruction [6,13], Wilkes’ syndrome [19], and under the general heading of chronic duodenal stasis [4]. To further confuse the issue there are those who give it no name, for they question its existence as a valid clinical entity [16]. A variety of factors have been reported which may enhance tightening of the “pincer mechanism” and trigger the obstruction, including loss of weight, prolonged bed rest, various generalized systemic diseases, previous surgical procedures, acute inflammatory lesions of the bowel, increased lordosis (including application of body casts), and loss of muscle tone of the abdominal wall leading to visceroptosis [5,7,13, 20-Z]. The frequent association with other diseases which cause similar symptoms, including gastric and duodenal ulcer, cholelithiasis, cholecystitis, pancreatitis, duodenitis, and irritable colon has not enhanced the clarity of diagnosis [18,19,23-261. In fact those who accept this entity as valid report an average delay between onset of symptoms and definitive diagnosis of from seven to ten years [19,23]. We are of the opinion that although the entity has been labeled, mislabeled, over- and under-treated, over- and underdiagnosed, that it nevertheless does exist in fact. Our purpose, therefore, is to suggest a diagnostic technic which will aid in clarification of the etiology when radiologic

* Presentedat the Eighth Annual Meeting of the Societyfor Surgeryof the AlimentaryTract, Atlantic City, New Jersey,June 17 and 18, 1967. Vol. 115. January

1968

89

Mansberger et al.

90

TABLE MEASUREMENTS

DETERMINED

I BY

ANATOMIC

Author

No. of Dissections

Average Superior Mesenteric Artery-Aorta Take-Off Angle (degrees)

Derrick and Fadhli [27] Byers and Mansberger

64 31

41.65 30

DISSECTION

Range

(degrees)

Distance from Angle to Duodenal Midpoint (cm.)

20-70 18-60

10

Range (cm.)

4.5-16

1281

evidence of duodenal obstruction suggests that obstruction may be secondary to vascular compression. PERTINENT

ANATOMY

AND ANATOMICAL

STUDIES

The transverse and ascending segment of the duodenum is the most fixed portion of the alimentary canal. It is retroperitoneal, limited in its distal extreme by the ligament of Trietz and is, of course, bounded posteriorly by the vertebral bodies and abdominal aorta and is crossed anteriorly by the superior mesenteric neurovascular bundle. In many patients caudal descent of the transverse duodenum is limited by short vessels of supply originating from the inferior pancreaticoduodenal branch of the superior mesenteric artery. The usual anatomic description of the superior mesenteric artery directs it from its point of origin on the aorta toward the right lower quadrant so that it lies directly over the aorta only in its most proximal portion. Thus, it is apparent that “although the superior mesenteric artery-aortic angle may be quite acute in the saggital plane, the same angle in the frontal plane might allow ample room for the duodenum to pass behind the superior mesenteric artery and anterior to the vena cava” [13 1. It becomes apparent then that for duodenal obstruction to be caused by vascular compression either the duodenum must be fixed high in a narrow angle of superior mesenteric arterial origin by an unyielding ligament of Trietz as described by Strong [13] or that a narrow angled artery has continued its course abnormally and directly over the posterior structures capable of trapping the duodenum to a point beyond the duodenovetebral or duodenoaortic crossing. The important mechanical obstructing factors then would seem to be a combination of a narrow angle of origin with either an abnormally high positioned but fixed duodenum or an

anomalous arterial course directly over the posterior unyielding vertebral bodies and/or aorta to a point beyond the position at which the duodenum normally transverses one or both of these structures. Derrick and Fadhli [27] in a study of the surgical anatomy of the superior mesenteric artery from dissection of sixty-three specimens reported average angle of “take-off” of the superior mesenteric artery-aorta of 41.65 degrees with a range of 20 to 70 degrees and a standard deviation of 10.65 degrees. The median angle determined by frequency distribution was 40 degrees. In our own anatomic series to date collected from dissections of thirty autopsy specimens [28] the average angle of take-off has been 30 degrees with variation from 18 degrees to 60 degrees. (Table I.) The average distance from this angle to the midpoint of the duodenum at the vertebral aortic fissure was 10 cm. The shortest duodenal midpoint from the arterial angle was 4.5 cm., and the longest was 16 cm. In the patient whose duodenal midpoint was only 4.5 cm. from the arterial angle, the angle of take-off measured 56 degrees. RADIOGRAPHIC

STUDIES

In the past three years at the University of Maryland Hospital there have been twelve patients with partial obstruction of the duodenum attributed to vascular compression; nine of these patients have been treated surgically. (Table II.) In only one patient was the initial diagnosis thought to be obstruction due to vascular compression, and even then the surgeon consulted had the advantage of seeing a negative cholecystogram which the patient brought with her. In only two of the patients were associated diseases present which other authors have suggested might be primary causes of duodenal dilatation with an associated secondary vascular compression component. The paAmerican

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ofSurgery

Vascular Compression of Duodenum

91

TABLE II SUMMARY OF CASES

Age Case

(E. J., 2:.02.36)

(P. T., g-66-50)

III

(G. T., 29-67-45)

(G. K.,%14-15)

(F. M., ~1-66-39)

(D. J. F.::2-27.20)

“II

(T. H., 32-75-94)

Vol. 115. January

(r*.)

and Sex

symptoms

36, F

Two mo. history of upper abdominal distension after meals; no loss in weight

31, F

Epigastric pain and postprandial distension; symptoms intermittent over two yr. period with recent increase in frequency; no loss in weight Patient was admitted for investiaation of weight loss and iron deficiency anemia. In an attempt to perform jejunal biopsy with Quinton-Rubin biopsy tube, we found tube would pass through distal duodenum only if the patient was in a kneechest postiion. Patient lost 30 lb. in 2 mo. on self-prescribed diet; admitted for investigation of Reynaud’s phenomenon; for a few days after admission be vomited continuously

42, F

33, F

13, M

37, F

21, M

1968

Patient had body cast application after operation for congenital dislocation of hip; this WRBS followed shortly by intractable vomiting Initial symptoms of epigastric and left upper quadrant pain and distension after meals predate admission by 8 yr. TWO yr. prior to admission patient had nausea and B year later had B duodenal ulcer followed by occurrence of a gastric ulcer (both were successfully treated conservatively) Anorexia and abdominal fullness for several months; patient WBS a medical student with acanthosis nigricans and was concerned about cancer of the stomach

Roentgenographic Findings

Upper gastrointestinal series showed marked distention of duodenum, in transit barium delay, characteristic linear defect, and vigorous to and fro peristalsis; tine study performed Characteristic findings in upper gsstrointestinal tract with vigorous to and fro peristalsis

Upper gastrointestinal series showed duodenal distention with mild to and fro peristalsis but without significant delay in passage of barium

Gastrointestinal series demonstrated duodenal distention and to and fro peristalsis; there was s delay in barium passage and characteristic linear defect; tine study and angiograpby were performed All findings in upper gastrointestinal series were compatable with duodenal vascular compression; angiography performed

urpper gastrointestinal

series showed no evidence of duodenal or gastric ulcer, but there was LXdilated duodenum with delsyed emptying, to and fro oeristalsis. and line& defect; tine and angiography performed

occasions patient was accused of eating large meals before outpatient gastrointestinal series was performed; a large amount of residual gastric material necessitated suction prior to the series; findings classic for vascular compression of duodenum. Cine study performed

On two

Course and Treatment

Course Post Hospitalization

Conservative management (small meals, knee-chest position, sedation) for 2 mo. was unsuccessful; duodenojejunostomy was performed

Asymptomatic at 3 yr.

No improvement with postural therapy, bland diet, frequent small feedings, and antacids; duodenojejunostomy was performed Malabsorption syndrome (Dredomiaantlv fats) proved and patient treated conservatively; biopsy of mucosa and submucosa with QuintonRubin tube ewe norma1 results; no operation was performed

Asymptomatic at 33 mo.

Duodenojejunostomy and duodenal bioosv (normal Auerbacf;s plexus) were performed. Studies for collagen disease including skin and muscle biopsy reveal no abnormalities to date Mobilization of ligament of Treitz; immediate postoperative course was complicated by some further vomiting which ceased by tenth postoperative day Conservative treatment (multiple small feedings, anticbolenergics, and position) unsuccessful,resection of the ligament of Treitz carried out, but duodenal mobiliz&ion abandoned because of short vessels from inferior pancreaticoduodenal artery, duodenojejuaostomy performed Duodenojejunostomy

At 24 mo. she has bad bilateral sympathectomy for Reynaud’s phenomenon; asymptomatic with respect to abdomen

At 31 mo. there are no symptoms suggesting vascular compression of duodenum

Asymptomatic at 21 mo.; weight gain of 10 lb. in first month

Asymptomatic at 16 mo.

Asymptomatic at 14 mo.; patient has gained 12 lb.

Mansberger et al.

92

TABLE II Continued SUMMARY OF CASES

CEWZ

Age c!J!Ji

Symptoms

Roentgenographic Findings

COllrX Post Hospitalization

Course and Treatment

Sex “III

(J. L., 31-75-91)

(A. L., g-52-97)

(E. C., 3x3-58-34)

(E. L., %-98-86)

x*1

(A. A., 16-76-24)

43.F

I ‘ostprandial,

29, M

I

18, M

On 7/27/66 patient sustained burn of 40 per cent of body surface area; on ?/27 he had sudden onset of persistent vomiting. On 9/15 he WBStransferreh to IJ. H. and on 9/20 had severe hypochloremic, hypokalemic alkslosis and elevated BUN; vomiting persisted after correction of Buid and electrolyte imbalance; patient WLScachectic on admission C lramplike postprandial pain, fullness, anorexia, nausea, and occasional vomiting for 5 mo.; patient was an operating room nllrse

20, F

42, F

intermittent, and episodic epigastric pain rsdiating to left chest and shoulder for 9 mo.; Masters two step test w*s positive

ntermittant pain, nausea, and vomiting for 12 yr. with increasing severity and frequency in recent months; patient is a hospital resident

Intermittent epigastric pain, nausea, and vomiting which was episodic and increasing; pain radiated to left shoulder and back

Gastrointestinal series showed gastric and duodenal dilatation with delayed emptying, to and fro peristalsis, and characteristic linear deformity; patient refused sngiography Previous wstrointestinal series reported as noncontributory but gastrointestinal series at U. H. showed all classic signs of v~scular compression of duodenum; tine studies performed. Patient WBSallergic to iodides Gastrointestinal series demonstrated gastric and duodenal distention, virorous to and fro duodenal peristalsis, and characteristic linear deformity

Gastrointestinal series showed findings suggesting vascular compression of duodenum, including characteristic linear deformity Gastrointestinal series showed findings suggesting vascular compression of duodenum including characteristic linear deformity

tient in case III was found to have a malabsorption syndrome of unknown etiology and the patient in case IV has progressive Reynaud’s phenomenon. As yet the cause of her vascular disease has not been clarified. Biopsy of the duodenum was unrevealing. The diagnosis was suggested in all patients by radiologic technics and all patients presented the aforementioned radiologic evidences of vascular compression of the duodenum. (Fig. 1.) It is noteworthy that with the patient supine it is often difficult to obtain a film which shows the

Conservative positional treatment, antacids, anticholenergics, and sedation were unsuccessful; duodenojejunostomy and pyloroplasty were performed

At 1 yr. post operation patient is asymptomatic and has gained 25 lb. She now works as B volunteer hospital aid

Duodenojejunostomy

In the first 5 mo. since operation, the patient had three episodes of abdominal pain of a much milder nature; however, he has been asymptomatic for the past 4 months

Patient fed and turned semiprone on circaelectric bed: he WCultimately able to eat a 6,000 calorie diet and gained 14 lb. over a 17 day period. No operation was necessary

Asymptomatic

Six wk. trial on conservative management including multiple small feedings and position therapy was unsuccessful; duodenojejunostomy performed Section of ligament of Treitz; d&denal mobilization abandoned because of short vessels from inferior pancreatic duodenal artery to duodenum; duodenojejunostomy performed

At 6 mo. patient is asymptomatic and has regained lost weight

at 9 mo:

Patient asymptomatic 6 mo.

at

exact point of obstruction in the ascending portion of the duodenum. Because the proximal duodenum is dilated, the barium tends to fall back into the more dependent transverse portion and will only intermittently be propelled against the site of obstruction. Cinefluorography demonstrates this point to great advantage. Although anatomic studies of the aortomesenteric angle exist, to our knowledge, until recently, no in tivo demonstrations have been reported in the diagnosis of this entity. When the patients in cases III, IV, and v were American

Journal of Surgery

diagnosed as possibly having partial duodenal obstruction due to vascular compression, it was thought desirable to demonstrate the angle of take-off and the anatomic course and the aortasuperior mesenteric artery distances at the point of duodenal crossing by biplanar angiography. In one patient this technic was accomplished and then the superior mesenteric artery was selectively catheterized and outlined against the barium-filled duodenum. These technics not only allow for in viva measurements of both the arterial take-off angle and aortasuperior mesenteric artery distance at the point of duodenal crossing, but also enable the radiologist to detect aberrant vessels and aberrant TABLE III ROENTGENOGRAPHICMEASUREMENTS OF TAKE-OFF ANGLE

AND

AORTA

DISTANCE AND

AT DUODENAL

SUPERIOR

MESENTERIC

Take-Off Angie (degrees)

CROSSING

Distance at Duodenal Crossing

(mm.)

Aortograms in Normal Patients Patient 1 2 3 4

55 60 65 55

20

5

45

11

7 16 16

Aortograms in Patients with Vascular Compression of the Duodenum Case I II III

Vol. 115, January

12 10 22

1968

OF

ARTERY

3 2 2

courses of the parent superior mesenteric artery. The results of these studies are shown in Figures 2 and 3A, B, and C and in Table III. The measurements in Table III are compared with measurements obtained from biplanar aortography in five normal patients. (Fig. 2, Table III.) Although the series of patients on whom these studies were performed is much too small to warrant any final conclusions, comparison of measurements of the “normal” and “pathologic” groups disclosed rather remarkable differences between the in viva take-off angles and the distances from the aorta to superior mesenteric artery. It may well be significant that in each of the three instances the superior mesenteric artery was demonstrated to course directly over the posterior unyielding structures for a considerable distance. In any event we believe that the technics described are useful in advancement of the diagnosis of vascular compression of the duodenum. Further, we believe that when significant numbers of in erivomeasurements of this type have been accumulated and coupled not only with biospy of the duodenum immediately distal to the obstruction in every instance but also with complete studies to rule out other causes of the “big duodenum,” much progress will have been made toward the establishment and acceptance of vascular compression of the duodenum as a valid cause of partial duodenal obstruction. SUMMARY

AND CONCLUSIONS

1. Twelve patients with partial obstruction secondary to vascular compression of the duodenum are presented. 2. Emphasis has been placed on anatomic variations which enhance duodenal obstruction. 3. In viva demonstrations of the anatomic

Mansberger et al.

94

FIG. 2. Lateral aortograms

showing normal superior mesenteric-aortic

take-off angles.

FIG. 3A, B, and C. Lateral and posteroanterior aortograms with barium-filled duodenum depicting narrow superior mesenteric-aortic angles and aberrent course of the superior mesenteric artery over posterior unyielding structures. American

Journal of Surgery

Vascular Compression of Duodenum variations presented.

utilizing

biplanar

aortography

are

conditions

of the bowel. Radiology,

23. BOCKUS,H. L. Gastroenterology, vol. 2, 2nd ed.,

REFERENCES C. Lehrbuch der pathologischen 1. KOKITANSKY, anatomie. 1st ed. vol. III,p. 187. Wein, 1842, W. Barumuller. E. L. and KELLOGG, W. A. Chronic 2. KELLOGG, duodenal stasis. Radiology, 9: 23, 1927. appliquee a 3. WEISS, A. La duodeno-jejunostomie trentequatre cas de stenose chronique sousvaterienne du duodenum. Arch. mal. app. digest, 15: 318, 1925. 4. WILKIE, D. P. D. Chronic duodenal ileus. &it. J. Surg., 9: 205, 1921. 5. BERLEY, F. V. and BROWN, R. B. Arteriomesenteric obstruction of the duodenum. U.S. Armed Forces M. J., 5: 1044, 1954. 6. ENGLER, H. S., MANN, T. C., and MORETZ, W. H. Arteriomesenteric duodenal obstruction. J. M. A. Georgia, 52: 501, 1963. 7. JONES, S. A., CARTER, R., SMITH, L. L., and JOERGENSON, E. J. Arteriomesenteric duodenal compression. Am. J. Surg., 100: 262, 1960. 8. KAUFFMAN, R. R. and GERBODE, F. Arteriomesenteric duodenal ileus. Stanford M. Bull., 9: 262, 1951. 9. KELLY, T. R. and SWEENY, J. T. Vascular compression of the duodenum. Am. Surgeon, 32: 338,1966. 11. MCKINNON, D. A. and SPENCER, J. R. Superior mesenteric artery syndrome. Am. J. Suug., 106: 552,1963. 11. POSTMUS, R. and THIEME, E. T. The superior mesenteric artery syndrome. J. Michigan M. SOL, 61: 303,1962. 12. REESE, J. L. and HOLT, J. H. Duodenal obstruction. J. Kansas M. SOL, 67: 416, 1966. of arteriomesenteric 13. STRONG, E. K. Mechanics duodenal obstruction. Ann. Surg., 148: 725, 1958. 14. GOIN, L. S. and WILK, S. P. Intermittent arteriomesenteric occlusion of the duodenum. Radiology, 67: 729,1956. 15. CIMMINO, C. V. The status of the syndrome of arteriomesenteric occlusion of the duodenum. Virginia M. Month., 88: 192, 1961. 16. CIMMINO, C. V. Arteriomesenteric occlusion of the duodenum: an entity? Radiology, 76: 828, 1961. 17. FISCHER, H. W. The big duodenum. Am. J. Roentgenol., 83: 861, 1960. 18. WILICIE, D. P. D. Chronic duodenal ileus. Am. J. Med. Sci., 173: 643, 1927. 19. BARNER, H. B. and SHERMAN, D. C. Vascular compression of the duodenum. Surg. Gynec. 6 Obst., 117: 103,1963. 20. KAISER, G. J., MCCAIN, J. M., and SCHUMACKER, H. B. The superior mesenteric artery syndrome. SUIP. Gynec. & Obst.. 110: 133. 1960. 21. RABI;OVI&H, J., PINES, B., and FELTON, M. Superior mesenteric artery syndrome. J.A. M.A., 179: 257,1963. 22. SIMON, M. and LERNER, M. Duodenal compression of the mesenteric root in acute pancreatitis and Vol. Il5, January

inflammatory 79: 75,1962.

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pp. 102. Philadelphia, 1964. W. B. Saunders. 24. CODMANE. A. Chronic obstruction of the duodenum at the root of the mesentery. Boston M.

&if S. J., 158: 503, 1908. 25. DREILING, D. A., KIRSCHNER, P. A., and NEMSER, H. Chronic duodenal obstruction: a mechanovascular etiology of pancreatitis. Am. J. Digest. Dis., 5: 991, 1960. 26. WILLIAMS, L. F. and BOWERS, W. F. Arteriomesenteric duodenal obstruction associated with severe peptic ulcer disease. Ann. Surg., 153: 250,196l. 27. DERRICK, J. R. and FADHLI, H. A. Surgical anatomy of the superior mesenteric artery. Am. Surgeon, 31: 545, 1965. 28. BYERS, R. and MANSBERCER, A. R., JR. Unpublished data. 29. HEARNE, J. B. Duodenal ileus with special reference to superior mesenteric artery compression. Radiology, 86: 305, 1966.

DISCUSSION HARRY H. LEVEEN (Brooklyn, N. Y.): Dr. Mansberger has mentioned a number of conditions which can produce this vascular compression. I should like to add an iatrogenic mechanism for such compression. In one middle-aged patient typical compression of the duodenum by the superior mesenteric artery developed after Heineke-Mikulicz pyloroplasty and vagotomy for duodenal ulcer. We reasoned that the duodenal ileus had occurred because the duodenal incision was so long that when it was closed in the transverse direction, the first portion of the duodenum was shortened, producing the compression seen on roentgenogram. In this patient, the duodenal ileus was relieved by cutting the ligament of Treitz and bringing down the duodenum. We are not fond of this type of pyloroplasty, but it is often performed. It is surprising that this complication does not occur more frequently. SIDNEYA. ROSENBERG(Pittsburgh, Pa.): About ten years ago I was interested in this entity and reported ten cases. I want to point out that the results in these cases have to be accurately analyzed and the patients have to be followed up for quite a period of time before one can draw any conclusions. Today, after having followed them up for a considerable period of time, I can say that I would not have operated on eight of the ten patients because I was not impressed with the fact that all their symptoms were relieved. Also, many other symptoms developed in these patients, convincing me that their trouble was not due to the so-called SLIperior mesenteric artery syndrome. Our indications for operation were pretty much the same as those outlined. Of course, Dr. Mans-

Mansberger et al. berger has added a very nice facility in diagnosis, showing the narrowing of the angle with visualization of the superior mesenteric artery. This finding is not necessarily productive of symptoms which can be relieved by the operation. I finally came to the conclusion that unless the patient showed definite gastric retention and delay as a result of this compression, it was not worthwhile to perform the operation for relief of symptoms. In those patients with gastric retention, the relief of symptoms seemed to be very gratifying; in others it was not. HENRY N. HARKINS (Seattle, Wash.): Dr. Rosenberg, would you mind stating briefly what operation you performed in most cases? DR. ROSENBERG: We carried out duodenojejunal anastomosis, bypassing the so-called obstruction. RICHARD KENNEDY GILCHRIST (Chicago, Ill.) : My own experience has been exactly the opposite of Dr. Rosenberg’s We have performed a number of these operations and in all of them the walls have been extremely thin. I am sure this contributes to the patient’s trouble. The operation can be carried out using local anesthesia in the aged and poor-risk patient. An excellent result can be obtained by making a fairly sizable duodenojejunal lateral anastomosis; we use a double layer continuous silk stitch. The patients are able to eat in a week. After very careful review of these cases, I am afraid that we have waited too long in many patients because we were too reluctant to operate upon them earlier. This is a good operation. I am not sure that I would want to tackle anything other than a simple bypassing maneuver, and I would not want to wait until the obstruction caused blocking up of the stomach. DR. HENRY N. HARKINS: Dr. S. Austin Jones has been a great student of the comparative morphology of this condition. He noted that in the pig walking on four legs, the pedicle of the colon hangs

down so that there is no compression of the duodenum. In man, in the erect position, the “nutcracker” phenomenon exists. Dr. Jones has performed air insufflation studies at operation. He has indicated that decompression of the distended duodenal loop must be at both ends. The Billroth I or other type of resection is of no value and the Billroth II operation is essentially useless. Gastroenterostomy decompresses the stomach but not the loop. Duodenojejunostomy is the procedure of choice. ARLIE R. MANSBERGER, JR. (closing) : Dr. LeVeen, with respect to cutting the ligament of Treitz, I think that the choice of operation is dictated by the anatomy at the time of operation. Trying to straighten out the duodenum can create a problem with ischemia of the duodenum if there are a significant number of branches coming from the inferior pancreaticoduodenal artery in the area to be transected. The candidates for operation must be selected with extreme caution. Our neck is on the proverbial chopping block with respect to four of these patients since they are in a personal series. One is a medical student, the second is a resident, the third a scrub nurse, and the fourth is a nurse’s aid, and we see them daily. If their long-term results are not good, I am afraid we may be embarrassed. It is because of the need for careful screening and accurate diagnosis that we have suggested the technics just presented. One of the patients not operated upon was a boy with a severe burn who was referred to our hospital on the fifty-sixth day post burn with intractable nausea and vomiting. He had severe electrolyte imbalance. Even after hydration and correction of hypokalemic alkalosis he continued to vomit. We finally made the diagnosis of vascular compression and placed him on a circoelectric bed so that he could be put in a semiprone position after eating. He was ultimately able to ingest 6,000 calories a day, and he gained 14 pounds in sixteen days and was discharged without operation.

American

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