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considers how very little of this anmsthetic is used percase, this objection cannot be upheld. I have foundthat 25 c.cm. will suffice for a thyroid operationtaking perhaps an hour, and this only costs 4s. 6d.

(retail price), which compares favourably with, forexample, open ether. For a partial gastrectomy in anelderly patient I recently used 50 c.cm. of vinestheneand 1 oz. of vinesthene mixture, the cost of whichcannot be considered prohibitive.

SUMMARY

In vinesthene and vinesthene mixture we have ananaesthetic of the greatest value to the generalpractitioner and well within his means. The use ofthis drug will facilitate the production and main-tenance of anaesthesia and assist both practitionerand patient.

REFERENCES

Hadfield, C. F. (1938) Brit. med. J. 1, 1175.Harris, T. A. B. (1938) Lancet, 1, 1338.Shipway, F. E. (1935) Ibid, 1, 82.

CONGENITAL DUODENAL DIVER-TICULUM

BY W. E. TANNER, M.S. bond., F.R.C.S.SURGEON TO THE PRINCE OF WALES’S HOSPITAL, TOTTENHAM ;

AND

T. H. C. BENIANS, F.R.C.S.PATHOLOGIST TO THE PRINCE OF WALES’S AND NORTH

MIDDLESEX COUNTY HOSPITALS

ONE of us (Tanner 1936) has previously recordedthe excision of a large duodenal diverticulum situatedin the head of the pancreas ; one attack of pain hasoccurred since the operation and was relieved withbelladonna. A barium meal and radiography duringthe attack of pain showed spasm of the duodenumat the site of excision ; this disappeared after theinjection of atropine gr. 1 ÕO’ . The case recordedbelow is another example of a duodenal diverticulum,but not connected with the head of the pancreas.

CASE-RECORD

The patient, a married woman aged 64, was admittedto the Prince of Wales’s Hospital on Jan. 25, 1938,with a history of " indigestion " of twenty years’

FIG. I-Radiograms of duodenal diverticulum : (a) anteroposterior view,showing residue of barium meal, with an air pocket above it, to the rightof the spine ; (b) lateral view.

duration. The symptoms were pain and discomfortin the epigastrium and right hypochondrium, comingon half an hour to an hour after food and followedalmost immediately by nausea and occasionally byvomiting, wfiieli seemed torelieve the pain. Duringthe last year the pain hadbeen severe, with loss of1 st. in weight.On examination it was

obvious that she had lostweight, though her colourwas good. She was tenderin the right epigastriumand hypochondrium.There was no rigidity, andno mass was palpable.There were no o t h e rphysical signs. A radio-logical examination was

made by the late Dr. A. C.Dixon, who reported:" The six-hour meal showsa residue to the right ofthe spine with an air

pocket above (fig. la).Duodenal cap of goodshape and not tender. Thesecond stage of theduodenum passes towardsthe right and upwards,joining the residuepreviously mentioned in alarge diverticulum orpossibly in the gall-bladder,though in the lateral viewthe diverticulum seems too posterior to be the gall-bladder (fig. lb). Twenty-four hours later there isstill a residue in the diverticulum."

Operation.-On Jan. 27, 1938, a right paramedianlaparotomy was performed under intratrachealanaesthesia administered by Dr. Douglas Belfrage.The gall-bladder was healthy. No ulcer was foundin the stomach, and the first part of the duodenumwas unusually long and mobile. The edge of thediverticulum (fig. 2) could be seen under the peri-toneum covering the posterior abdominal wall to theright of the foramen of Winslow. The peritoneumcovering the posterior sac was not thickened, andthere were no signs of old or recent inflammation.The peritoneum was incised and the empty saceasily dissected out. - The sac arose from the posterior

aspect of the second part of theduodenum 1 in. above the level ofthe ampulla of Vater and extendedupwards and outwards. It wasdetached from the duodenum, andthe opening in the duodenum 1 in.in diameter was closed with twolayers of continuous catgut. Theincision in the posterior peritoneumwas also sutured with catgut, andthe abdomen was closed withoutdrainage.The patient has made a good

recovery and is now free from

symptoms and putting on weighton an ordinary diet.

Pathological report.-The diverti-culum (fig. 3) measures 2 in. inlength and 1 in. in width at theopening, increasing to I in. at thefundus. It is thin-walled and showssome still thinner sacculated areasat the distal end.

Sections under the microscope(fig. 4) show a mucosa with thecharacters of the jejunum ratherthan duodenum. There are well-formed villi with numerous gobletcells in the epithelium of the cryptsof Lieberkuhn. The lamina propria

FiG. 2-Diagram of edgeof duodenal diverticu-lum seen under the

peritoneum coveringthe posterior abdominalwall to the right of theforamen of Winslow.

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shows the usual character of small-bowel structure, butno nodules of lymphoid tissue are seen. The cryptsrest directly on the muscularis mucosa;, the two layersof which are intact and not pierced by the ducts ofBrunner’s glands as in normal duodenal structure.Brunner’s glands, which should lie beneath the

muscularis mucosee, areentirely lacking. Sec-tions toward the base ofthe diverticulum showa true outer musclecoat separated from themuscularis mucosee byareolar tissue ; moredistally the muscle coatfades out, leaving themuscularis m u c o s seonly, and beyond thisin the saccular dilata-tions the wall consistsof the mucosa with athin layer of areolartissue outside it.The diverticulum

appears to be a largesuperficial congenitalheterotopia or aberrantportion of the jejunalmucosa, which in itsgrowth has produced a

sacculus of some size, almost a viscus. No macro-scopical or microscopical evidence of inflammationis seen.

COMMENTS

The wide opening and general appearance of thediverticulum suggest a portion of bowel produced bynormal growth processes rather than a pressurediverticulum developing through a weakened spot inthe muscularis proper of the bowel. The unusualmobility and length of the diverticulum noted at

operation further support the view that it is congenital.Aberrant portions of the mucosa are not uncom-

mon in the upper alimentary tract, though perhapsless common in the duodenum than elsewhere. Theymay also be associated with congenital diverticula,

FIG. 3-Duodenal diverticu-lum excised. Scale shows 2 in.

although these latter are usually very small and,though perforating the muscularis mucosse, do notpass through the proper muscular coat of the bowel.

Certain points in the embryological origin ofdiverticula are worth discussion. Taylor (1927)suggests that these arise in the congenital diverticulawhich have beennoted in the ven-tral aspect of thefore gut of earlymammalian em-

bryos. Twodiverticula whichpersist into adultlife-namely,those forming theliver and p a n -creatic ductsarise on the ven-tral aspect of thefore gut. Theyare moved in earlyfoetal life, partlyby the rotation ofthe gut to the rightand partly by irregular growth in the wall of theprimitive gut, to their adult site on the medianposterior aspect of the duodenum. Such a diverti.culum as that described above could therefore havebeen derived from a primitive pouch on the ventralaspect of the fore gut.

Of the constituent elements of the mucosa of thesmall gut the crypts of Lieberkuhn are formed in thethird month, Brunner’s glands in the fourth, and thelymphoid tissue in the fifth. Only the first of thesewas present in the diverticulum. It may thereforebe said to correspond to the adult form of a third-month fcetal mucosa.

FIG. 4-Microscopic section of duo-denal diverticulum.

REFERENCES

Tanner, W. E. (1936) Lancet, 2, 853.Taylor, A. L. (1927) J. Path. Bact. 30, 415.

RENAL CALCULI FOLLOWING ALKALI

THERAPY

BY THOMAS MOORE, M.S. Durh., F.R.C.S.CHIEF ASSISTANT TO A SURGICAL UNIT AND UROLOGICAL REGISTRAR,

MANCHESTER ROYAL INFIRMARY

ALTHOUGH many factors related to the causation ofurinary calculi are known, no exact aetiology is yetclear. It is important therefore to report anyobservation having a bearing on this matter.

All calculi may be grouped into primary, developingin a healthy urinary tract, and secondary, caused bypre-existing pathological lesions. Primary calculi

commonly consist of calcium oxalate, uric acid, urates,or cystine. Although phosphatic calculi are usuallysecondary and associated with urinary obstructionand sepsis, they are much more often primary than isgenerally admitted. During the last few years I haveobserved several such cases. In most of these nocause is apparent, but in some it is only too obvious-namely, excessive consumption of alkalis in the treat-ment of peptic ulcer. Such therapy is not onlydangerous but unnecessary, for the most importantpart of the medical treatment of peptic ulcer mustalways be small and oft-repeated meals. This factis unfortunately little recognised by medical prac-

titioners, who regard the alkaline mixture as thesine qua non of ulcer treatment. Even more un-

fortunate, however, is the popularity of such therapywith the lay public, who can obtain unlimited

quantities without medical supervision. Simplycolossal doses are thus often taken.

It is not my object to emphasise the danger ofalkalosis ; I am interested only in the more obviouseffects on the urinary tract. The urine passed bysome of these patients is thick with phosphaticdeposit. A medical colleague informs me that hehas seen numerous ulcer cases in which the urineresembled milk. In such circumstances it is not

surprising that phosphatic renal calculi develop. Itmust be presumed that the constant irritation of therenal calices by the phosphatic deposit leads to theexudation of a little fibrin, which cements thecalculus. These changes usually take place in theinferior calyx, to which most of the deposit gravitates.The bland diet with which these patients are alsoàffiicted has some 2etiological importance. It is analkaline ash diet and’thus contributes to the alkalinityof the urine ; also it may be deficient in vitamin A.The following two recent cases illustrate the

condition.CASE-RECORD

CASE l.-A man, aged 30, was admitted to theManchester Royal Infirmary on Feb. 25, 1939.Since Nov. 4, 1938, he had had several attacks of