Stenosis Duodenum

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  • CALIFORNIA STATE JOURNAL OF MEDICINE VOL. XV, No. 3

    STENOSIS OF THE DUODENUM.By P. S. CAMPICHE,

    M. D., F. A. C. S., M. R. C. S. (Eng.), San Francisco.Case I. In September, 1913, Mrs. E. L., 34

    years old, was referred to me by Dr. Emil Schmoll.In childhood and as a girl she had always been

    in good health. At the age of 24 she sufferedfrom dysmenorrhea and was operated on (ventro-fixation and appendectomy). Soon after she be-gan to have frequent attacks of vomiting; in fact,for the last ten years she had been vomiting everyday, more or less. In 19I2 she married and hada normal confinement in July of the followingyear. While pregnant she felt much better, butsince the birth of her child her stomach becameworse than usual; during the three months priorto my seeing her she had managed to keep herbreakfast down but regularly vomited her lunchand her supper every day, together with a greatquantity of bile. In these attacks the food cameup first, then a gush of bile followed. She hadno appetite and was very constipated but did notcomplain of pain. The abdomen was never dis-tended, but was, in fact, rather retracted; theurine was normal. Her weight was 89 pounds.

    After keeping her under observation for a weekDr. Schmoll made a diagnosis of stenosis of theintestine, probably due to adhesions, and advisedoperation for the relief of the continuous vomiting.

    I operated on October 6, 19I3, making a medianlaparotomy incision. Exploration of the pelvisorgans revealed nothing abnormal, although theuterus was well attached to the anterior abdom-inal wall as a result of the previous ventro-fixation. The colon and sigmoid flexure appearedto be much under normal in size, but the smallintestine presented the most striking picture. Itwas quite empty and so much contracted that itscalibre was that of an ordinary lead pencil insome places.

    This suggested an obstruction at some higherlevel and the small intestine was followed up; thejejunum below the musculus suspensorius duodeni(Treitz' ligament) was somewhat wider thoughstill below normal in size, while the stomach andduodenum were found to be greatly dilated andmarkedly hypertrophied. The caliber of the duo-denum, in fact, was three times greater than nor-mal and its wall was thick and hypertrophied andin the third portion, or pars inferior, especiallywas embedded in shining white adhesions. I havetried to picture its condition in the accompanyingsketch.

    In spite of very thorough palpation no recentulcer of the duodenum or near the pylorus couldbe detected; the gall-bladder, apart from a fewadhesions, was normal and contained no stones.I concluded that there had been an ulcer theresome years previously which had healed and that,as a consequence, all these adhesions remained.Our diagnosis, based on the result of this longexploration, was stenosis of the duodeno-jejunalflexure due to peritoneal adhesions with secondarydilation and hypertrophy of the duodenum andthe stomach.

    Owing to the absence of a good serosa on theduodenum a direct anastamosis between the jeju-num and the duodenum would have been mostunsafe. Gastro-jejunostomy done in such instancesof stenosis below the papilla duodeni has the in-convenience that bile flows back into the stomach,

    ..e. '... ;:.|

    from which it escapes through the anastamosis.This could be prevented by closure of the pylorusif the duodeno-jejunal stenosis was incomplete, butin the case before me the stenosed part hardly ad-mitted the tip of the finger and for fear that astill greater contraction might develop later atthis point, I did not think it advisable to closethe pylorus. On the other hand, gall-stone opera-tions have shown in many cases of cholecysto-gas-trostomy that the patient becomes accustomed tothe continuous presence of bile in the stomachand does not suffer much discomfort or nausea.I therefore did a typical posterior no-loop gastro-jejunostomy with a very wide anastamosis; whenthe operation was completed I convinced myselfthat the new stoma readily admitted three fingers.

    For the first week after operation the patientwas kept on liquids and did fairly well; on thesixth day, after eating some toast and scrambledegg, she vomited bile in large quantities so thatthe liquid diet was continued a little longer untilabout the fourteenth day she was eating a regularsemi-solid diet. Her weight was 82 pounds.,

    I saw 'her lately, nearly three years after opera-tion; her weight is now io8 pounds. She consid-ers her condition greatly improved as evidencedby the fact that she can now eat three squaremeals a day and does not vomit more than once

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  • CALIFORNIA STATE JOURNAL OF MEDICINE

    at night and only bile, which, considering herprevious state of constant nausea, is indeed a vastchange for the better.

    I have been disappointed, however, because ofher not gaining more in weight since the opera-tion, although this may be attributed to the con-tinuous presence of bile and pancreatic juice inthe stomach which probably interferes to someextent with gastric digestion; but she is satisfiedto be able to keep her food down and to find thatshe is much stronger and much more active thanshe was before the operation.

    Case II. Mr. R. McH., 38 years old, wasreferred to me by Dr. M. Etcheverry in Septem-ber, 19I 1.The man had been ailing for several years and

    had been treated for gastric ulcer and afterwardsfor gall-stones; he was sent to me with a diag-nosis of gall-stones. In spite of a fairly goodappetite he was thin and anaemic and complainedof severe pain in the epigastrium occurring abouttwo hours after meals, accompanied with a sen-sation of hunger; the pain would occasionally ex-tend toward the shoulders and was relieved byfood. Although he always felt distressed andwas often nauseated he never vomited.When operated on in October, I9II, I found

    that the gall-bladder and the liver were slightlyadherent to the duodenum, but normal otherwise;the serosa showed no alteration. At the secondportion of the duodenum above the papilla duodenithere was a hard growth, three by three centi-meters in size, somewhat irregular and seeminglymore prominent on the anterior wall; a narrowchannel could be felt through the tumor whichexplained the absence of more serious symptoms,the obstruction being incomplete. My diagnosisat the time of operation was duodenal ulcer,though later I had to change it; I did a posteriorgastro-jejunostomy.The patient improved very much at first; his

    pains left him and in three months he gained 15pounds in weight. However, when I again sawhim in May, I912, he had a large, hard, irregulartumor in the liver and under the right costalmargin, evidently a cancerous metastasis. Thisshowed conclusively that the primary growth wasnot an ulcer but a carcinoma of the duodenum.Two months later, in July, 1912, he died.

    Stenosis of the duodenum may be congenital oracquired. A congenital form described by Terryand Kilgore 1 was, in reality, a malformation ofthe duodenum. As a consequence of faulty de-,velopment at the junction of the embryonic fore-gut and midgut the second part of the duodenumhad a very narrow canal; the general nutrition ofthe patient had suffered very much and the caseterminated fatally after a gastro-jejunostomy.

    In the cases described by Harris 2 the troublewas also congenital and consisted in abnormalfolds which caused constriction of an otherwisewell-developed duodenum. Harris called thesefolds abnormal remains of a perfectly normal em-bryologic structure. The symptoms were mild, re-sembling those of duodenal ulcer and with verylittle or no vomiting. In all his six cases divi-sion of the abnormal bands was sufficient to effecta cure.A third form of congenital constriction results

    from the so-called pancreas annulare, where thehead of the pancreas completely encircles theduodenum and compresses it.The duodenal stenosis in the acquired form may

    be due to several different causes, all of whichare fully enumerated in Anders' 3 paper, who hascollected reports of 262 cases, and gives a sum-marv of eighty of them. In his opinion the fac-tors most frequently responsible for stenosis areas follows, and though these conditions are some-what rare, each of us has probably seen them all,at least once:

    1. Carcinoma of the head of the pancreas andchronic pancreatitis, which are known to havebeen the cause of stenosis of the pars descendensof the duodenum, although they more ordinarilyproduce symptoms of papillary stenosis, such aschronic and progressive jaundice, with acholicstools and marked enlargement of the liver andgall-bladder. Such cases are common and all ofus have seen them, no doubt.

    2. Carcinoma of the duodenum, frequently men-tioned by older authors, although it is now con-sidered a great rarity. The second case reportedabove is a typical example of this condition, aswas proved in the operation and by the subse-quent course of the disease, although the clinicalsymptoms were not truly typical, being obscuredby the fact that vomiting was absent owing tothe incompleteness of the obstruction.

    3. Duodenal ulcer is a condition which oftencauses narrowing of the duodenum, as is attestedby Moynihan,4 who had 43 such cases in his ownexperience; it is usually a cicatricial stenosis, butin some instances, as was also reported by theMayos,5 an hour-glass- duodenum was found. Moy-nihan further observed that stenosis may occurafter the suturing of a perforation of the duo-denum.

    4. Peritoneal adhesions, sometimes of unknownorigin, may cause stenosis, which is well illus-trated by the first case-above reported. The ulcer,originally the cause of the trouble, has probablyhealed spontaneously or cannot be found, but ithas left behind a trail of dense adhesions tocompress the duodenum and pave the way forfuture complications.

    5. Compression of the duodenum by gall-stonesor by an inflamed gall-bladder is not such a veryrare condition, and here the adhesions may also

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  • 78 CALIFORNIA STATE JOURNAL OF MEDICINE VOL. XV, No. 3

    be so dense that sometimes a gastro-jejunostomybecomes necessary.

    In November, 1912, I recall, Drs. D. Voor-sanger and Charles G. Levison's reported to thissociety a case of duodenal stenosis due to com-pression by a long adherent gall-bladder, andwhich was cured by cholecystectomy.

    6. Compression by the root of the mesenteryis given by Anders as a cause of stenosis and ithas been the subject of so many reports publishedin recent years that I do not need to insist uponit here.The symptoms of duodenal stenosis have been

    clearly stated already by Wilms,7 Kausch,8 andothers. If the construction lies above the papilla(suprapapillary stenosis), as it was in my case otcancer of the second portion of the duodenum,the clinical signs will be the same as those ofpyloric stenosis, such as vomiting of food withlittle or no bile, provided that the obstructionis complete.

    If the compression is in the region of thepapilla, especially if we have a papillary stenosis,the deep chronic jaundice with acholic stools andthe enlargement of the liver, all give a verydefinite picture.

    In cases of infrapapillary stenosis like the firstcase reported above, we will have two constantsymptoms, which are:

    1st. Abundant and oft-repeated vomiting of foodand bile, which, however, never becomes fecal incharacter; and,

    2nd. Absence of distention, and often retractionof the abdomen, even, which is attended with con-stipation, while the patient is often emaciated andin a state of complete exhaustion.

    In pumping out the stomach in such cases, orwhen the patient vomits, colorless mucus or food1emnants are seen first, followed by a gush of bileat the end of the procedure.Treatment varies both according to the cause

    of the condition and as to the site of the stenosis.In cases where bands, congenital or otherwise,exist, and are the cause of the constriction, divisionwill be necessary, and this will often be sufficientas is shown in the cases reported by Harris.

    In stenosis due to diseases of the gall-bladdercholecystectomy is indicated as the best meansof removing the compression and preventing, or atleast minimizing, the formation of new adhesions.

    If, in conditions of papillary stenosis, the duo-denum itself has remained fairly patent, as oftenoccurs in some cases of carcinoma of the head otthe pancreas or in chronic pancreatitis, cholecysto-gastrostomy may give the patient great relief.When the narrowing of the lumen is due to any

    disease of the wall of the duodenum proper, suchas cancer, ulceration, cicatrices, or to dense anddiffuse adhesions, gastro-j1ejunostomy is indicated;but while this operation has given complete satis-faction in suprapapillary stenosis, which closelyresembles pyloric stenosis, it is by no means idealin cases of infrapapillary stenosis, for the bile ancpancreatic juice will constantly flow backward fromthe duodenum into the stomach and certainly inter-fere to some extent with gastric digestion, so thatthe patient is unable to gain very much in weightor even attain first class health, as may be judgedfrom the first case here reported. Yet this pro-cedure may be the only available one that will besafe in such a condition.

    Discussion.Dr. C. G. Levison: This paper is of interest

    on account of the infrequency of stenosis of theduodenum in the infrapapillary region. As Dr.Campiche has stated, Anders has collected severalhundred cases and if I recall them correctly, mos;of them have been suprapapillary conditions.There have been comparatively few infrapapillarystenoses reported, and when one considers the

    frequency of pathological processes in the upperquadrant, it is extraordinary that so few cases ofthis kind have come to our notice.In the condition reported by Voorsanger and

    myself that Dr. Campiche was kind enough tomention, the patient vomited large quantities ofbile incessantly. There was no bile entering theintestinal tract, so that the diagnosis was compara-tively easy to make. At the operation an enlon-gated, indurated gall-bladder was found lying acrossthe descending part of the duodenum, producingcomplete obstruction. It is interesting when oneconsiders the adhesions, ulcerations, old gall-bladderconditions and carcinomata that are so frequentlypresent in this region, that this type of obstruc-tion occurs so seldom.

    Literature.1. Terry, W., and Kilgore, A.: Congenital Stenosis of

    the Duodenum in an Adult. The Journal A. M. A.,June 3, 1916, p. 1774.

    2. Harris, M. L.: Constriction of the Duodenum dueto Abnormal Folds of the Anterior Mesogastrium.The Journal A. M. A., April 18, 1914, p. 1211.

    3. Anders, J.: Report of a New Case of Stenosis ofthe Duodenum. Am. Jour. Med. Sc., 1912, p. 360.

    4. Moynihan, B. G. A.: Duodenal Ulcer, 1910. W. B.Saunders Co., Phila.

    5. Eusterman, G. B.: Hour-glass Stomach and Duode-num. Collected Papers of the Mayo Clinic, 1914,p. 20.

    6. Voorsanger, D., and Levison, C. G.: Stenosis of theDuodenum due to Compression of the Gall-bladder.

    Calif. State Med. Journ., Nov., 1912.7. Wilms, M.: Stenosis des Unteren Duodenuins, Bruns'

    Beitrage, 1897, p. 511.8. Kausch, W.: Handbuch der Praktischen Chirurgie,

    1913, vol. 3, p. 297.

    ABSTRACT OF MINUTES OF THE EIGHTY-NINTH MEETING OF THE COUNCIL OFTHE MEDICAL SOCIETY OF THE STATEOF CALIFORNIA, UNION LEAGUE CLUB,SAN FRANCISCO.

    February 3, 1917.The meeting was called to order by the chair-

    man, C. G. Kenyon, at 12:15 p. m.Present: Chairman C. G. Kenyon, Drs. Jayet,

    Ryfkogel, Bine, Ewer, Edwards, Hoisholt, Parkin-son and later Hamlin. Dr. H. M. Sherman andMr. Hartley F. Peart, attorney for the Society,were also present.Parkinson acting as secretary, the minutes of

    the eighty-eighth meeting were read and approved.Auditing Committee.

    Ryfkogel for the Auditing Committee reportedthat in accordance with instructions of the Coun-cil, he had employed the firm of McLaren, Goode& Co., certified accountants, to install a systemof bookkeeping. This had been started and abookkeeper employed.He then submitted a detailed statement of the

    financial condition of the Society. The followingabstract shows the position of the Society at theend of the years 1915 and 1916, respectively:

    COMPARATIVE BALANCE SHEET.Dec. 31, 1915 Dec. 31, 1916

    Assets:Cash .$ 995.29 $1179.46Accounts receivable 960.86 945.09Paper on hand... 512.80 1943.80Furniture and fixtures.. 897.60 1300.50

    $3366.55 $5368.85Liabilities:Loan Union Trust Co.. 1500.00Medical Defense........ 2483.55 721.25Sundry accounts payable 1189.94 641.11Medical Indemnity Fund 4979.00

    $5173.49 $6341.36Deficiency: End of 1915, $1806.94; 1916, $972.51

    Bine also for the Auditing Committee said thatat present no definite statement of expense was