Cholecystitis

CHOLECYSTITIS, inflammation of the gallbladder. The anatomical and physiological features of the gallbladder (see), which is the primary site for the formation of gallstones (see Gallstone disease), create conditions conducive to the development of inflammation within it. Among these conditions, the most important is bile stasis in the gallbladder and bile ducts, which facilitates the penetration of infection into it. The latter can enter the gallbladder via various routes, of which the most frequent, according to the majority of authors (Ikonnikov), is the enterogenous route—from the lumen of the duodenum. The proximity of the latter to the bile ducts leads to the fact that their lower section—specifically the lower segment of the ductus choledochus—is constantly inhabited by bacteria [Bact. coli, B. typhi (Korte)], enterococci (Loewenberg), staphylococci (Gundermann and Huntemuller, Aschoff and Bacmeister), and streptococci. In isolated cases, anaerobes have been found. Another route of infection penetration into the gallbladder is the descending route—with the flow of bile, in which pathogenic agents that have entered the liver via the hematogenous route may be present. Some authors (Gundermann) believe that the infection enters the liver through the arterial trunks, while others (Langenbuch, Sozin) see the route of infection in the portal circulation. Finally, the lymphatic route is not excluded—e.g., the transfer of infection from an inflamed vermiform appendix or infected birth canals to the liver or directly to the gallbladder (Korte). Through the indicated routes, both streptococci and staphylococci, as well as tubercle bacilli (Simmonds) and others, can penetrate. Very interesting and practically important are the bacteriological studies of surgically removed gallbladders conducted by Gundermann. In 55% of the examined diseased gallbladders, he found staphylococcus, less frequently Bact. coli, streptococcus, and B. paratyphi. The same data were published by Huntemuller, Fuld, and Groninger; Fedorov, Konchalovsky, and others hold the same view. With free outflow of bile from the gallbladder, pathogenic agents, especially those of intestinal origin, carried along by this flow, do not have the opportunity to penetrate the gallbladder and remain in it for the time required for their development. However, in the case of bile stasis caused by various reasons, the conditions for the development of infection are present. In this respect, a complete analogy is observed in the gallbladder with all excretory or secretory organs that discharge their products by means of more or less long ducts (Fedorov). Bile stasis in the gallbladder depends mainly on mechanical causes; cases of stasis of functional origin (gallbladder dyskinesia) are less frequent. Among mechanical causes, the first place is occupied by obstruction of the ductus cysticus by a stone, less frequently by a plug of thickened bile and mucus, especially in the presence of edema of the ductus cysticus mucosa. A certain role in the occurrence of stasis can be played by conditions of intra-abdominal pressure changed due to the enlargement of the pregnant uterus or a growing intra-abdominal tumor. Sometimes bile stasis occurs from pressure on the ductus cysticus by a tumor growing in the vicinity, or by the enlargement of a lymph node located in the angle between the ductus cysticus and its entry into the ductus choledochus. Mechanical causes acting from the outside (pressure from inappropriate clothing) can also be a cause of stasis. Finally, the highly variable anatomical and functional features of the gallbladder and ductus cysticus, and the particular type of the latter's departure from the ductus choledochus (see Gallbladder), by creating difficulties in bile outflow, can under certain conditions also contribute to stasis or even to a complete (usually temporary) cessation of bile outflow from the gallbladder. These cases of the so-called stagnant gallbladder were described by Aschoff, Bacmeister, Schmieden, and subsequently by a number of other authors, and in our country by Fedorov, his student Talman, and others. Finally, inflammatory processes occurring in the vicinity of the gallbladder (perigastritis, periduodenitis, pericolitis) can lead to its deformations and displacements, as a result of which bile stasis may also occur. Inflammatory processes occurring in the gallbladder and caused by a combination of the various factors just listed can be divided pathologically, according to the classification of Aschoff, partially modified by Fedorov, into the following forms: 1. Acute primary cholecystitis: a) purulent cholecystitis, b) ulcerative cholecystitis, c) gangrenous cholecystitis. 2. Chronic uncomplicated recurrent cholecystitis. 3. Chronic complicated recurrent cholecystitis. 4. Sclerosis of the gallbladder. - Acute infectious cholecystitis (acute primary cholecystitis according to Fedorov). The inflammatory process here (unlike acute appendicitis) proceeds, for the most part, not only as a superficial catarrh of the mucous membrane, but with some infiltration of the wall, as a phlegmonous process (acute phlegmonous cholecystitis according to Fedorov). The inflammatory process quickly penetrates into the thickness of the gallbladder wall to its fibrous and subserous layers, which leads to thickening of the wall due to inflammatory edema of its layers. Macroscopically, the gallbladder is more or less enlarged, its walls are thickened. With the increase of inflammatory exudation from the wall into the cavity, the gallbladder becomes very tense. According to Mieczkowski, the pressure in such a gallbladder can reach 710 mm of mercury. Around such an inflamed gallbladder, loose adhesions form with neighboring organs (stomach, duodenum, colon—flexura hepatica, omentum), and fibrinous deposits appear on the reddened serous covering of the gallbladder (pericholecystitis). In the abdominal cavity in such cases, a serous effusion is sometimes found, which may turn out to be sterile. In the cavity of the gallbladder, purulent fluid with a significant admixture of bile and fibrin clots covering the mucous membrane are found. For the most part, gallstones are found in such gallbladders, sometimes obstructing the ductus cysticus, although even in so-called non-calculous cholecystitis, the course of the process, pathological-anatomical changes, and the general picture may not differ at all from that described (Bokastova). This similarity between the calculous and non-calculous forms naturally forced many authors to doubt the independence of the latter (non-calculous) form, which in their opinion is only one of the phases of cholecystitis with stones. However, the works of Riedel, Bokastova, and others provide grounds to still distinguish non-calculous cholecystitis as a separate form, although it is very close to cholecystitis with stones in its clinical manifestation. Such serous-purulent inflammation of the gallbladder can end in complete recovery to such an extent that it is sometimes difficult to find traces of inflammation even histologically later. Only accumulations of cellular elements or thickening of the connective tissue around the vessels of the fibrous and subserous layer may indicate a previously existing inflammatory process (Aschoff). A number of such cases were observed by Fedorov. However, such outcomes of an acute primary attack of cholecystitis are quite rare. In most cases, the process passes into a chronic stage, or progresses and leads to further stages of acute cholecystitis (ulcerative cholecystitis, gangrenous and diphtheritic cholecystitis). In the latter case, the accumulation of purulent exudate and purulent infiltration in the gallbladder increases. In the case of obstruction of the ductus cysticus by a stone, even greater distension of the gallbladder with pus occurs—acute empyema of the gallbladder is formed. Subsequently, ulcers form in the gallbladder wall, and a larger or smaller section of the gallbladder wall or even the entire gallbladder may undergo necrosis. If adhesions have not had time to form in its vicinity, then the resulting perforation of the wall and the emptying of the gallbladder contents into the free abdominal cavity lead to the development of general purulent peritonitis. Perforation can occur towards the gallbladder bed in the liver and subsequently lead to the formation of separate abscesses in the liver (see Cholangitis, Liver) or purulent inflammation of the entire liver. In the case of the formation of adhesions around the inflamed gallbladder, perforation leads to the formation of encapsulated abscesses in its vicinity, often containing stones. However, such a severe outcome of primary acute cholecystitis is observed relatively rarely. More often, the process passes into a chronic stage—into the so-called inflammatory dropsy of the gallbladder (hydrops vesicae felleae post cholecystitidem), which in its course gives more or less frequent exacerbations. Korte and other authors do not deny the possibility of the primary development of this chronic stage without a previously experienced acute attack. In most cases, however, it follows a previously experienced acute inflammation, especially in cases of complete obstruction of the gallbladder by a stone. In this process, the gallbladder is strongly distended and sometimes changes its shape, assuming a sausage-like or pear-like shape. This enlargement depends on a large accumulation of more or less transparent dropsical fluid, which sometimes turns out to be sterile upon examination. The latter circumstance is cited as proof of their correctness by proponents of the possibility of primary chronic cholecystitis (primary dropsy of the gallbladder, according to Fedorov). However, they are unable to provide other evidence, and the absence of attacks of acute cholecystitis in the history of such patients is also not conclusive.

The sterility of the gallbladder contents in such cases may be a consequence of so-called autosterilization, which occurs after a prolonged stay of bacteria in closed cavities, especially if these bacteria are of low virulence. For the most part, however, the dropsical fluid is turbid and contains bacteria, and to a greater or lesser degree, mucus, epithelial cells, and leukocytes. The presence of bacteria is the cause of exacerbations, which are characteristic of the course of chronic cholecystitis. The mucous membrane of the gallbladder at this stage has a velvety surface, its fine folding is lost, it is speckled with ulcers, and in old cases, with scars at the site of former ulcers. At the bottom of these ulcers, gallstones of various sizes may be found, and these ulcers themselves often form as a result of the pressure of gallstones on the altered wall, being essentially pressure sores. The muscular and fibrous layers of the wall are thickened, indurated, and in places contain islets of round-cell infiltration. Around the gallbladder at this stage, adhesions with neighboring organs and the omentum always form, which are more extensive the longer the process lasts. The described picture bears, according to Fedorov, the name uncomplicated chronic recurrent cholecystitis, and according to Aschoff—cholecystitis phlegmonosa simplex. Clinically, this is the most frequent form of chronic cholecystitis, proceeding with repeated attacks of colic, alternating with periods free from painful phenomena. With the passage of time, these free periods usually shorten, while the periods of exacerbation lengthen. Changes in the walls of the gallbladder progress, leukocytic infiltration increases, especially around the Luschka ducts, which are at the same time spreaders of infection into the depth of the gallbladder wall. The entire wall of the gallbladder is infiltrated and altered in all its layers, as a result of which it easily tears, breaks, and crumbles. Necrosis of the entire thickness of the gallbladder wall may occur. The contents of the gallbladder are thick pus, already without the slightest admixture of bile coloration (empyema of the gallbladder). Adhesions form around the gallbladder, sometimes resembling cartilage in density, thanks to which the necroses with subsequent perforation that often occur at this stage very rarely lead to general peritonitis. Perforations of the gallbladder into neighboring organs that have adhered to it during a long inflammatory process, accompanied by partial necrosis of the entire thickness of the wall, are often observed. Most often, perforation occurs into the duodenum, stomach, flexura hepatica, less often into the retroperitoneal space, with the formation of paranephritis, retroperitoneal phlegmon (see Retroperitoneal space), and also into the anterior abdominal wall, with subsequent formation of a fistula. Upon perforation into the lumen of the stomach or intestines, stones may exit the gallbladder through the formed fistulas, subsequently passing per vias naturales. In cases of large sizes of these stones, obstruction may develop, caused by the blockage of the intestinal lumen by the stone; in most cases, the small intestine is blocked slightly above the Bauhin valve. As a final stage of long-term chronic cholecystitis, a process of scarring of the gallbladder wall with an outcome in sclerosis is sometimes observed. Instead of leukocytic infiltration in the wall, especially in its fibrous and subserous layers, fibroblasts and angioblasts appear. The mucosa is replaced by scar tissue or granulations, gradually becoming covered with epithelium growing from the remnants of epithelium in the Luschka ducts, which are still preserved in some places. This epithelium is flatter compared to the normal one. However, in very chronic cases, the gallbladder wall gradually completely loses its structure and represents a homogeneous, dense, crunching scar tissue when cut. The gallbladder itself decreases sharply in size, sometimes taking the form of a small lump. Clinically, this stage may be equivalent to a complete recovery from any kind of seizures. The intimate proximity of the gallbladder to the liver, its connection with the liver through the vascular and lymphatic network, explain the frequency of changes in the liver of both a functional (see Liver) and morphological nature, occurring as a reaction to the inflammatory process in the gallbladder. Rufanov, who specifically investigated the liver parenchyma in cholecystitis, found in it a number of changes from mild degeneration to true necrosis with significant development of connective tissue. The same author, on extensive clinical and experimental material, proved that cholecystitis is the main cause of pancreatitis (see). Differential diagnosis between cholecystitis and cholelithiasis has no practical significance, but rather only theoretical interest, since in both cases we must reckon with the presence of infection in the gallbladder, without which gallstones, in the opinion of the vast majority of authors, do not manifest themselves in any way, and their carriers are subjectively healthy people. For prophylaxis, therapeutic and surgical treatment of cholecystitis, see Cholelithiasis, Gallbladder, surgery. The pathological anatomy of cholecystitis, according to what was stated above, largely coincides with the pathological-anatomical changes in appendicitis. When diagnosing acute cholecystitis, which in most cases does not present particular difficulties, one must exclude: an attack of renal colic, perforation of a gastric and duodenal ulcer, and an attack of acute appendicitis. Most often, acute cholecystitis is confused precisely with the latter disease, since the pains, which are the main subjective symptom, are by no means always localized by patients in accordance with the anatomical position of both organs, and the other symptoms characteristic of both diseases can also be very similar. An accurate anamnesis, a detailed, attentive examination of the patient, and a number of clinical studies (especially clinical blood analysis), performed without delay, and sometimes only laparotomy, clarify the nature of the disease. In the majority of cases, however, the differential diagnosis between acute cholecystitis and appendicitis is not very difficult. Differential diagnosis between chronic cholecystitis and chronic appendicitis is much more difficult. For the correct resolution of this task, long-term observation is necessary with the application of a number of clinical studies (examination of the stomach, duodenal juice, X-ray of the stomach, cholecystography, etc.). The comparative rarity of life-threatening complications of cholecystitis makes, in the opinion of many authors, the indications for its surgical treatment in most cases relative. They are absolute only in perforative processes that could lead to peritonitis. However, treatment of cholecystitis with internal remedies (see Cholelithiasis) in very many cases does not provide a complete cure. Unfortunately, the literature is not rich in statistics on a large number of cases treated therapeutically, in contrast to the statistics of surgeons who currently possess very large figures. Statistics of therapists (Naunyn, Binder, Jaguttis, Lowenberg, Tallquist, and many others) speak of a cure in the range of 50% to 85% of cases, however, this often does not result in a cure in the anatomical sense, but only a transition of the disease into a latent state. On the other hand, surgeons possessing large material (Mayo, Korte, Kehr, Fedorov, Martynov, Finkelstein, Chasovnikov) report mortality figures not exceeding 5-8% on average, and in the hands of some (Kment) even decreasing to 2.04% and lower. At the same time, it should be remembered that the most severe cases in their course are subjected to surgical treatment. The immediate results of surgical treatment of cholecystitis in the chronic stage, based on the cited figures, can be considered very good. Significantly inferior to them are the results of surgical treatment of cholecystitis in the acute stage, recently advocated by Riese, Nordmann, Kirschner, and in our country by Hesse and Yudin. According to the statistics of the named authors, mortality during surgery in the acute stage reaches 12-15% on average. Comparison of the indicated figures does not serve in favor of early operation. However, in acute cholecystitis accompanied by phenomena of severe intoxication, angiocholitis, one has to operate despite the more severe course of the postoperative period and outcomes, since waiting in these cases is dangerous. A large amount of material accumulated by surgeons and therapists has shown that the long-term results of surgical treatment of chronic cholecystitis are not always good. Approximately 10-15% of patients who tolerated the operation well subsequently suffer from recurrences of pain, which in intensity sometimes differ little from those before the operation. The clinical picture in these patients is also very similar to the preoperative one, with the exception of temperature, which in most cases remains normal. Pribram called these pains 'false recurrences'. Partly they can be caused by stones left during the operation in the bile duct, or most often by infection remaining in the bile ducts despite the removal of the main focus—the inflamed gallbladder. These pains appear especially often in patients who suffered from complications of cholecystitis (angiocholitis, pericholecystitis, periduodenitis). Hülsmann, Chiray, Navel, Fedorov, and others also attribute them to functional disorders of the autonomic nervous system, leading to spasmodic contractions of the ductus choledochus, causing pain.

Combating so-called false recurrences is very difficult and consists partly of therapeutic agents used during ordinary attacks of cholelithiasis, and partly of symptomatic agents, physiotherapeutic procedures, etc. Recurrences depending on unremoved, overlooked stones in the ductus choledochus are subject to repeated surgical intervention.