POSTGRAD. MED. J. (1965), 41, 243

PRIMARY CHRONIC INFLAMMATION OF THECYSTIC DUCT

G. LABO, M.D. L. ROSA, M.D.Cattedra di Semeiotica Medica, University of Bologna, Italy.

(Director: Prof. G. Labo)

WE WILL relate observations made during thelast ten years on primary chronic inflammationof the cystic duct: these observations willconcern only a few aspects of this interestingchapter in biliary pathology, long well known,but on whose theoretical and clinical meaningno full agreement has yet been reached.When we refer to the cystic duct, we include

also the neck and the infundibular portion ofthe gall bladder, which we consider an anatomi-cal unity.

Primary chronic inflammation of the cysticduct is, in our opinion, more frequent thangenerally supposed. The lack of pathologicalreports can be ascribed to the reluctance ofsurgeons to remove gall bladders which do notshow gross abnormalities on X-ray examination,and the tendency to consider this condition as amere functional disorder of the biliary tract.Our first observations were surgical surprises:

radiologically normal gall bladders, which achedwith an intensity that we thought due to thepresence of stones, appeared instead on micro-scopic examination as obstructive, hypertro-phic, chronic cystic duct inflammations, withno changes in the gall bladder itself or onlyminor ones.These findings induced us to study the pro-

blem further. We first tried to define betterthis clinical-pathological entity with researchesinto those clinical and laboratory signs thatwould differentiate this form from chroniccholecystitis and cholelithiasis.As a matter of fact, since cystic duct in-

flammation may present all the clinical featuresof other gall bladder diseases, the differentialdiagnosis by clinical signs presents remarkabledifficulties.

Furthermore, a primary cystic duct inflam-mation may arise at the same time as a chronicdiffuse gall bladder inflammation or be theinitial stage of it; or it may also be associatedwith cholelithiasis or with cholesterosis of thegall bladder. Usually, symptoms are subor-dinate to the gall bladder reaction to the cysticduct obstruction: they are highly painful, as in

cholelithiasis, when the gall bladder is tonic orhypertonic, that is when there is a conflict be-tween the force of contraction of the gallbladder and the obstacle to the evacuation ofbile; and dyspeptic, when the gall bladder ishypotonic.Between these two forms (painful and dys-

peptic) there exist others, such as the pseudo-ulcerous, which reveal the reflex and inflam-matory gastro-duodenal component of biliarypathology.

In colic caused by isolated primary cystic ductinflammation, the inflammatory signs, whichcharacterize the biliary colic of chronic cho-lecystitis and cholelithiasis, are usually not ob-served, while the slight paroxysmal painslocalized to the epigastric or to the subhepaticregion, which appear after meals or duringmenstruation, after physical or emotionalstress, are usually present.X-ray examination reveals evidence both

direct and indirect, while in cases of total ob-struction of the cystic duct the gall bladderis not filled.The direct features are the morphological

alterations of the cystic duct (thread-like duct,rigid duct, rosary-like duct or in the form of aswan-neck); equally important and more fre-quent is the indirect evidence, such as the delayin the gall bladder visualization time, the tonic-hypertonic as'ect with often rapid and efficientevacuation (s6metimes only partial or absent)and a large, hypotonic, gall bladder. Laboratoryfindings on bile can also supply importantevidence. We study, as a rule, the gall bladderconcentrating power by evaluating iodine con-tent of the cholecystic bile after intravenousinjection of iodated radiopaque substance. Nochanges in this concentration are observed inthe primary chronic cystic duct inflammation;while they are present in diffuse chronic chole-cystitis.

Electrophoretic studies on bile, according totechniques long-tested in our department, havesupplied other important data; among whichis the identification of typical inflammatory

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244 POSTGRADUATE MEDICAL JOURNAL May, 1965

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FIG. 1.-Atrophic chronic cysticitis. The width of thecystic duct, in oblique section, appears reduced.The mucous membrane is flattened, deficient ofepithelium and densely infiltrated by round cells.In the basement membrane are bundles of con-nective tissue, between the muscular fibres.(H. 4 E. x200).

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FIG. 2.-Atrophic chronic cysticitis. Detail of Fig. 1.(H. & E. x200).

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FIG. 3.-Normal gall bladder. Same case as in Fig.I and 2 (H. & E. x80).

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FIG. 4.-Hypertrophic chronic cysticitis. The width ofthe cystic duct is narrowed by large folds ofmucous membrane. (H. & E. x80).

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FIG. 5.-Hypertrophic chronic cysticitis. Large foldsof mucous membrane with a conspicuous infil-tration of neutrophils around their axes, projectforth in the duct. The muscular fibres areseparated by large connective tissue bundles.(H. & E. x80).

syndromes of chronic cholecystitis (with or with-out stones) characterized by the increase of pro-tein and glycoprotein materials, with particularincrease of the part with the most rapid migra-tion; non-inflammatory syndromes, which wehave defined as dysmetabolic, pure lithiasisdiathesis, are characterized by an increase ofsudanophilic material and in particular of anelectrophoretic inert component, composedmainly of cholesterol.The primary chronic cystic duct inflamma-

tions are characterized, instead, by an almostnormal electrophoretic pattern.Other diagnostic elements are offered by the

study of the biliary sediment and of the activat-ing capacity of bile on lipase. The former

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LABO' and ROSA: Inflammation of the Cystic Duct

FIG. 6.-Cholecystography in a case of cystic ductand cholecyst cholesterolosis. The gall bladder,in the shape of a sausage, is constricted by aninfundibular spasm. The gradation of the shadowis normal (A). After stimulation (B), a delayedcontraction, with an increase of the infundibularspasm, is perceived. Therefore we are here ob-serving a hypotonic cholecystostasis associatedwith alterations of the cystic-infundibular region.

FIG. 7.-Cystic duct cholesterolosis. Same as in Fig. 6.Mucous folds, projecting forth in the cystic ductand narrowing its width, are observed. Under-neath the epithelium, we observe groups ofhistiocytes, containing lipoids. In the deepestmucous layers sclerosis is present. (H. & E. x15).

shows a bile with some inflammatory elements,the latter is normal.The anatomical study of chronic bile-duct

infection has furnished data of great theoreticaland practical importance, not only in theseinflammations in particular but also in regardsto the pathogenesis and evolution of thelesions.There is almost always a noticeable dispro-

portion between a bladder wall that is almostnormal and the thickening of the cystic duct,which can extend to the neck and infundibulumof the gall bladder.

Histologically, in the initial stages we havepredominantly oedema, desquamation and nec-rosis of the mucosa. This is followed by a

FIG. 8.-Hypertrophic chronic cysticitis with fibrouspericysticitis. Cystic duct section, showing remark-ably thickened walls and fibro-sclerotic changes.(H. & E. x15).

FIG. 9.-Strawberry gall bladder. Same case as inFig. 8. Large amount of folds, club-like, withheaps of histiocytes containing lipoids. Coat ofepithelium normal. (H. & E. x80).

round-cell infilration which replaces the initialneutrophil infiltration; the proliferation of theconnective tissue, which leads to sclerosis andpermanent thickening of the wall, constitutesthe final phase.

Moreover, the chronic inflammatory processstimulates a hyperplastic alteration of themucosa, which leads to a restriction or acomplete obstruction of the cystic duct by theforming of big hypertrophic mucosa folds(hypertrophic cysticitis).

Besides those forms, which are more fre-quent, we observe also a primary atrophicchange, which is characterized by the thinnessof the mucosa and the lack of epithelium.

Frequently we find fibrous pericysticitis

May, 1965 245

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246 POSTGRADUATE MEDICAL JOURNAL May, 1965

which according to some researchers, consti-tutes the initial stage of chronic cysticitis. Theorigin of these cystic duct inflammations isattributed to a chronic low-grade bacteremia inwhich factors of local sensitization play a funda-mental role. This is confirmed by the fact thatwe can observe the coexistence of chronicfibrosclerotic inflammation, foci of necrosisand recent infiltrations; and by experiments inanimals, since we have been able to inducecysticitis and chronic cholecystitis by theSanarelli-Schwartzmann reaction.

Moreover, Albot has described cystic ductinflammations in which it is possible to observecongestive and edematous phenomena of hyper-ergic inflammatory processes: giant-celledsclero-necrotic cysticitis.

Beside the purely inflammatory forms, thereare also primary dysplastic types, in which theobstruction of the cystic duct is secondaryto hyperplasia of the mucosa, as it can beobserved in dysendocrine states, especially inhyperfolliculinism, which is the determiningcause. In these cases the inflammatory processcan appear subsequently. We have studied theseforms extensively, both clinically and experi-mentally.

Primary chronic cysticitis seldom remains

localized to the cystic duct, but extends slowlyand progressively toward the infundibulum andthe body of the gall bladder, by disseminatedparietal lesions (Albot).

Finally, we consider the possibility thatchronic cysticitis may be associated with cho-lesterosis of the body of the gall bladder. Ourfindings have demonstrated that an experiment-ally induced lesion of the cystic duct, followedby a hyperlipid diet, may produce cholesterosisin the animal. The diet alone is not sufficientto induce the lesion, nor the chronic cystic ductinflammation by itself.

REFERENCES

ALBOT, G., OLIVIER, C., LIBAUDE, H., and DRESSLER,H. (1950): Les v6scicules Fraises sont des CysticitesCompliqu6es de Lipoidose Vesciculaire, Bull. Soc.med. Paris, 67, 140.

ALBOT, G., OLIVIER, C., POILLEUX, F., and LIBAUDE,H. (1950): Les Formes de Debut des CholcysticitesChroniques non Lithiasiques. p. 3. Paris: Vigor.

ALBOT, G., POILLEUX, F. (1952): Les Voies Biliaires.Paris: Masson.

ALBOT, G., TOULET, J., and PINEAU, P. (1952): Cys-ticite Fibreuse et Dyskin6sie Cystique. ResultatsConcordants de la Cholcystographie de Face etde Profil, du Tubage Minut6 et de la Radiomano-metrie Biliaire, Actualite's. hepato-gastro-enterol.Hotel-Dieu, 50-52.

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