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ken place in thater the duct opened with reten

that of a hickor externally or inthe only a loc

bladder with wax. Six intramural cysts are shown.

have been formed by the occlusion of the duct with retention of the secretions and later the duct opened, or rupture may have taken place in the gall bladder, permitting bile to enter. The size of the cysts vary from microscopic in size to that of a hickory nut. Rupture of the larger cysts may take place internally, externally or into the wall of the gall bladder. In the latter case there may be only a local edema which is later absorbed or an intramural abscess may develop. Trauma is a determining factor.

The wax cast (Fig. 2) was made from a gall bladder har. ing five intramural cysts connecting with its lumen. Thes

were not easily seen when the gall bladder was removed but upon emptying it, the cysts were seen as rounded rather firm masses. They were emptied into the gall bladder by pressure and then a

mixture of wax and paraffin inFig. 2. ('ast made by injecting galljected through the cystic duct.

"°****Soft stones made up of bile pig. ment sometimes form in these cysts.

(9) Adenomas: In adult life, whenever there is a proliferation of epithelium there is always the danger that the growth will continue into tumor formation. This occurs in the development of the glands of the gall bladder, producing either an adenoma or carcinoma.

Adenomata of the gall bladder are of three principal types: First, the adenomata which develop from Luschka's ducts or glands. These are intramural and are made up of tubules, separated by connective tissues. The tubules may be more or less distended and the epithelial lining may vary from tall, columnar epithelium, as is seen in the ducts, to flat epithelium lining the more distended tubules. Second, the fundus adenoma. These appear in the fundus of the gall bladder as small masses, often of a whitish color, and are made up of tubules, some of which may be distended into cysts as large as a pea or even larger. The lining epithelium is columnar in the tubule, but i nthe cysts it may be flat. Aschoff believes this condition to be congenital and reports finding it in about two-thirds of one per cent of all cases. In one hundred post mortem examinations on children under one month I failed to find a single case, although in adults I found it nearly as frequently as did Aschoff. I believe these adenomata develop similar to the Luschka ducts, but the growth continues until the condition is reached which we find. In one case I found a beginning growth of a mass of Luschka's ducts near the


proximal end of the gall bladder, which presented almost the same appearance as that seen upon section of one of these adenomata.

The third type of adenoma develops from the glands in the mucosa. They might be described by the term adenopapilloma, as they are peduculated tumors extending into the lumen of the gall bladder. The whole mass is covered with columnar epithelium continuous with that of the surface mucosa. The mass is made up of glands and connective tissue stroma with nutrient blood vessels. The gland consists either of a tubule, or it may be coiled upon itself to form a gland similar to those seen about the large bile ducts. The connective tissue is present as trabeculae or supporting frame work for the acini. The acini are lined with columnar or cuboidal epithelium and may lie singly or in groups surrounded by a capsule. This is not a true capsule, however, as its external fibers are continuous with those of the supporting frame work. It gives the appearance of having been formed by crowding back the connective tissue as the acini were developed. Although these tumors are usually pedunculated, sometimes the peduncle is so short that they appear sessile. In other instances the peduncle is long and narrow.

(10) Carcinoma: Just as any epithelium in the body may develop malignant changes, so may the epithelium of the glands of the gall bladder develop carcinoma. While some of the carcinomata show solid formation, many have a tubular structure indicating their origina. Carcinoma may develop from the glands by continuous growth. That is, the growth does not stop as it passes from benign to malignant, or the gland may have ceased to grow and malignant changes developed later. The solid, cylindrical-cell carcinoma may develop either from the surface epithelium or that of the glands.

The most important role played by the glands and ducts of the gall bladder is in harboring infection. When infection has once entered to the bottom of a Luschka gland, it may remain for a long time. If the duct remains open or if it opens at intervals, bacteria will be discharged into the gall bladder, thus serving to keep up infection or to cause recurrences. This explains why recurrence takes place after drainage of the gall bladder.

These organisms passing down into the intestines may be responsible for an enteritis, even when the gall bladder itself may not become infected. The patient may become immune to the organisms, so that they may be carried down and excreted with the feces without infecting the patient.

In the majority of the so-called typhoid carriers I believe

dder ise bottom oft remains into t1

S must be organisms a suspect

the infection lies in these glands and passes out with the feces without reinfecting the patient. The fact that infection is harbored in this manner explains the finding by Hunner of the typhoid bacillus in the gall bladder of a patient eighteen years after the primary infection, and in Droba's case where he found the organisms in the gall bladder seventeen years after the infection. It also explains why Halstead found a history of typhoid fever in 33 1-3 per cent of his cases of gall-stones.

As these glands may discharge periodically, it is not sufficient to examine the stools of a suspected typhoid carrier just once, unless the organisms should be found. Repeated examinations must be made.

Further, this buried infection undoubtedly serves frequently as the atrium from which infection enters the blood stream. Recent investigators have shown that rheumatism is in reality an infection, and probably the infection often comes from this source.

The Heisterian valves are folds extending into the lumen of the upper portion of the cystic duct. They consist of mucous membrane with circular muscle fibers in the center. Although usually overlooked these valves are not rarely the seat of pathologic lesions. Undoubtedly they are subject to many pathologie processes, but I have observed only acute and chronic inflammatory changes, ulceration, atrophy and secondary carcinoma.

Chronic inflammatory changes are the most frequent Heisterian valve lesions causing recurrence of cholecystitis. This condition is manifest by a thickening of the valve due to either connective tissue proliferation or thickening of the mucosa. Chronic inflammatory changes of themselves produce, as a rule, only a partial obstruction; but an edema, due to exacerbation or congestive disturbances causes a complete obstruction, resulting often in the same type of colic seen gallstones. The pain is produced by the severe muscular contraction made in an attempt to empty the gall bladder. Drainage in a case of this type is followed by a shrinking of the valve so that the duct will again functionate, but it is subject to recurrences.

In acute inflammation the entire mucosa of the duct is involved. The process is usually a part of a general involvment of the gall bladder and ducts. Ulceration is most often due to pressure from a stone, but may be infective in origin. Atrophy occurs most frequently in conjunction with dilatation of the duct but may be independent of it.

Stricture of the gall bladder may be either congenital or

ts: Uleet of a gene the duct

and to infection and as being of com

Pletely thds of thSeptum


acquired. That some are congenital has been proved by finding them in the new-born and by the absence of all evidence of infection present or past in the adult. It is sometimes difficult in the adult to differentiate between acquired strictures and congenital strictures in which changes have taken place, due to infection and gall-stone formation. Longitudinal septa have been described as being of congenital origin, but traverse strictures and septa have been usually regarded as being acquired. Morton reports a case in which there was a septum at the junction of the middle and lower thirds of the gall bladder obstructing the lumen so completely that the opening could not be found with a probe. There were fifty stones lying in the sac distal to the obstruction and sixty-five in the proximal sac. Morton regarded the septum as being of congenital origin, but other authors have doubted this because the presence of the stones is believed to bear evidence of infection present. Moynihan speaks of deformities of the gall bladder without going into details as to their character or origin. Many references are to be found to the so-called hourglass contraction.

Congenital strictures predispose to infection and gall-stone formation, and these in turn to ulceration and scar formation.

Congenital strictures are of three types: 1. Annular strictures.

2. Those due to the projection of folds of the inner layers into the lumen. These usually occur in conjunction with the first or third type, but sometimes occur independently. These, properly speaking, are cepta, but I have classified them here owing to their obstructing the lumen.

3. The fundus stricture or elbow deformity (Fig. 3) in which the fundus is folded upon the body of the gall bladder.

The annular strictures extend entirely around the gall bladder but they do not produce the marked interference with the lumen seen in the elbow deformity. When the gall bladder is not distended, a stricture of the annular type may not be perceptible, but upon distention, either by compressing one end as previously

described or by the injection of Fig. 3. Gall bladder with two conge-fluid into the gall bladder, it is nital strictures and having a mesentery.brought out. Sometimes there is a fold of the inner layers of the gall bladder projecting into the lumen. This fold may involve the whole circumference of

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the gall bladder along the line of stricture or only a portion of it.

Strictures, or, more properly speaking, diminution in the size of the lumen due to folds of the inner lavers, may occur in conjunction with the annular strictures as just described, or in conjunction with the elbow deformity to be described shortly, or independent of either. Such a fold may take its origin from a narrow base extending entirely around the gall bladder on a line perpendicular to the axis of the gall bladder or from only a portion of such a line. The folds do not take their origin from a short base, but, instead, the mucous membrane is continuous for the whole length of the flap. In other words, the folds are rarely or never pedunculated, but instead, the base of the fold is usually longer than the margin. There are some cases, however, in which the flap is attached for the entire circumference of the gall bladder, the opening being rarely in the center, but more or less eccentric.

These folds may be so small as to be easily overlooked, or so extensive as to produce a complete obstruction, as seen in one of my cases in which there was a small sac at the upper end completely separately from the gall bladder and contain: ing a mucous fluid not stained with bile. In addition to the septum producing the complete obstruction, there was a narrow transverse, shelf-like projection near the middle of the gall bladder. A case with a complete obstruction, as in this case, has been described by Deve. These folds are made up of the mucous and muscular coats when small, but when extensive may contain a central fibrous layer.

The elbow deformity or third type is the most common congenital stricture. In this condition there is a bending of the fundus upon the gall bladder, together with a diminution in the size of the lumen by a fold similar to that described in the second type of stricture. The outer coats of the gall hladder appear too short for the inner coats, and in place of dipping down into the fissure, pass directly over, so that in some cases without careful inspection one might overlook the deformity. The serosa passes over the under surface of the gall bladder to the distal, acting as guy ropes to maintain the deformity. The fibrous layer may pass over but usually dips down into the fold, in which case there are connective tissue bands passing across the fissure from one side to the other. In one such case as this I carefully cut the serosa, subserosa. and these connecting bands, permitting the distal portion to straighten out; but a narrowing of the lumen was still present.

The fold extending into the lumen is usually made up of the three inner coats folded upon themselves in such a man.

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