Cystitis

CYSTITIS (cystitis), inflammation of the urinary bladder, arises as a result of the penetration of infection into it. In individual cases, one can observe non-bacterial cystitis caused by chemical irritation of the bladder mucosa by urine that is very concentrated or contains impurities that act as irritants to the bladder mucosa (cantharidin, formaldehyde). The following pathways for the penetration of infection into the bladder are distinguished: 1) ascending from the urethra or prostate, 2) descending from the kidneys and ureters, 3) lymphogenous from the intestine (Vreden, Posner, Lewin), female reproductive organs, and the pelvic connective tissue. Furthermore, cystitis can be observed as a result of the direct introduction of infection into the bladder by instruments (catheter, bougie, cystoscope). In this case, the infection is usually introduced not from the outside, not as a result of insufficient sterility of the instruments used, but from the urethral mucosa, which, especially in women, constantly contains a significant quantity of various microorganisms (Escherichia coli, staphylococci, diplococci, streptococci, etc.). A sterile instrument, passing through a non-sterile urethra, carries pathogenic flora with it into the bladder (Melchior). Infection can penetrate from the urethra into the bladder even without any introduction of instruments into it per continuitatem, which is observed especially often in women. Inflammatory processes occurring in the urethra, especially the posterior urethra, facilitate the penetration of infection from there into the urinary bladder and the development of cystitis. The descending pathway of infection (urogenous) is observed mainly in inflammatory diseases of the kidneys and renal pelves, from where purulent urine, together with pathogenic microorganisms, penetrates into the cavity of the urinary bladder. In other cases, infection circulating in the blood is filtered through the renal glomeruli and, without causing damage to the renal tissue, penetrates with the urine into the bladder, where it causes inflammatory phenomena. If one introduces a pure culture of virulent microorganisms into the cavity of a healthy, well-functioning urinary bladder, then cystitis will not occur even with their prolonged presence there. This experiment (Rovsing) corresponds to clinical, everyday observations of cases of bacteriuria, cases of renal pyuria without phenomena of cystitis. But as soon as one traumatizes the wall of the urinary bladder simultaneously with the introduction of bacteria, or artificially causes urine retention, one can immediately observe the development of cystitis. The mucosa of the urinary bladder is extremely resistant to various external influences on it, and for the microorganisms that have penetrated into the bladder cavity to cause inflammatory phenomena of its walls, a number of precipitating factors are still necessary. Such are: 1) trauma to the bladder mucosa—single, caused by the rough introduction of a bougie, cystoscope, or catheter into the bladder, or prolonged, caused by a foreign body or stone lying in the bladder cavity. Mechanical trauma disrupts the integrity of the epithelial covering of the bladder and creates a gateway for the introduction of infection. 2) Acute or chronic urine retention, causing a disturbance of normal blood circulation; prolonged contact of the infection with the bladder wall, the tone of which is disturbed, creates favorable conditions for the decomposition of urine. 3) Changes in the walls of the urinary bladder in the form of diverticula or tumors, which cause reduced resistance of its walls to infection. 4) Chilling of the pelvic region, causing disturbances in the tone of the urinary bladder walls. 5) Diseases of the prostate in men, inflammatory processes of the uterus and its appendages, and their abnormal positions. The close connection of the vessels of the urinary bladder with the vessels of these organs entails constant congestive hyperemia of the mucosa in the area of the bladder outlet and stagnation of urine in the latter, which favors the development of cystitis. The most frequent causative agent of cystitis is Escherichia coli (colicystitis), followed by staphylococci and streptococci, the tubercle bacillus, diplococci, and Proteus Hauseri. In the last place is the gonococcus; some authors generally deny the possibility of gonococcal cystitis (Guyon). The stratified squamous epithelium of the bladder is an unfavorable soil for the development of gonococcal infection in it. Furthermore, urine, upon coming into contact with the gonococcus, destroys it before it can inoculate itself into the bladder mucosa (Fronshtein). By lowering the local resistance of the bladder mucosa through its action, the gonotoxin, which arrives here in abundance from the posterior urethra during gonorrhea of the latter, prepares a favorable soil in the bladder walls for the development of secondary infection (Pechersky). This explains the frequency of bladder involvement during gonorrhea, with cystitis in these cases usually being caused not by the gonococcus. The aforementioned microbes can be detected in cystitis in isolation or, more often, in symbiosis with each other. It is very important to note that in different periods of the same cystitis, the flora can change, and the microorganisms of the initial period give way to others (Marion). Staphylococcus and streptococcus disappear from the bladder faster than other microorganisms. Escherichia coli and Proteus Hauseri are distinguished by particular persistence. The intensity of the phenomena of cystitis is not related to the infection. Tuberculous cystitis—see Urinary bladder. The inflammatory process can involve the entire bladder—total cystitis. One can also observe involvement of limited areas of the bladder wall, most often in the area of the urinary bladder outlet—trigonitis, cystitis colli (see separate plate, fig. 1). The latter form is encountered most frequently in women (Kholtsov). One sometimes has to observe inflammation of limited areas (more often lateral) of the urinary bladder wall, caused by some perivesical inflammatory process (paracystitis). Pathological changes in the acute stage of cystitis consist mainly of changes in the mucosa—hyperemia, edema, and partial necrosis. Microscopic changes consist of dilation and congestion of the vessels and round-cell infiltration of the mucosa. The subepithelial tissue is edematous and contains a number of purulent accumulations. In individual cases, focal hemorrhages are observed in the mucosa—cystitis haemorrhagica (see separate plate, fig. 2); in others, edema of the mucosa predominates—cystitis bullosa (see separate plate, fig. 3). The inflammatory infiltrate in places gives significant thickenings in the subepithelial layer, visible to the naked eye in the form of nodules—cystitis nodularis. Increased diapedesis of leukocytes, in the presence of significant lymph exudation, causes necrotic change of the epithelium down to its deep layers—cystitis membranacea (see separate plate, fig. 4). The sloughing of necrotic epithelium and the formation of more or less widespread ulcers on the surface of the epithelium is called cystitis ulcerosa. The ulcers are usually covered with purulent clots impregnated with calcium phosphate salts—cystitis incrustata. In individual, albeit rare cases caused by anaerobic infection, detachment of the necrotic bladder mucosa occurs (cystitis exfoliativa, cystitis gangraenosa). In the chronic stage of the disease, all three layers of the bladder wall are involved in the inflammation, and the process proceeds in the direction of hyperplasia. In the mucosa, a process of its proliferation is observed with the formation of bleeding granulations (cystitis polyposa). In individual areas of the mucosa, processes of keratinization of its surface layers occur—leukoplakia. In other areas, the bladder epithelium is transformed into mucous cells, and cystic formations are present on the surface of the urinary bladder—cystic cystitis (cystitis cystica, cystitis glandularis). Under the influence of bacteria from the Escherichia coli group, cysts filled with gas form in the thickness of the mucosa (cystitis emphysematosa). In the muscular layer, the usual inflammatory changes are observed. The connective tissue between the muscle fibers becomes sclerotic, which leads to a decrease in the capacity of the urinary bladder (microcystis). In other cases, the inflammatory process in the bladder wall turns into suppuration—cystitis phlegmonosa. The resulting abscess usually ruptures into the bladder cavity, but in individual cases, it can rupture into the tissue surrounding the bladder, causing its inflammation (paracystitis). The following three symptoms characterize cystitis: pain, frequency of urination, and pus in the urine. The intensity of pain sensations in cystitis does not always stand in direct proportion to the intensity of the inflammatory phenomena. The localization of the latter plays a significant role in this. Inflammation of the neck of the urinary bladder (trigonitis), due to the large number of nerve endings located here, causes significantly greater pain than inflammation of the body of the urinary bladder itself. Pain appears upon filling of the bladder and intensifies toward the end of it, radiating to the glans penis and the rectum. After urination, a feeling of satisfaction does not occur; on the contrary, urination ends with painful spasms (tenesmus) of the urinary bladder, which last for the time necessary for a certain amount of urine to accumulate in the bladder, preventing the inflamed walls of the bladder from touching each other. Patients instinctively do not empty the urinary bladder completely during its acute inflammation. In the intervals between urinations, patients complain of a feeling of heaviness above the pubis. Percussion of the urinary bladder and palpation of it through the abdominal wall or vagina are painful and cause a desire to urinate.

The latter is frequent, especially during the day while moving, whereas with prostate hypertrophy, on the contrary, urination is frequent at night. The frequency of urination in cystitis is explained by the loss of the ability to stretch inherent in the inflamed walls of the urinary bladder. The frequency of urination is in direct proportion to the intensity of the inflammatory process in the bladder. In the most acute cases, the urge to urinate is so frequent that it does not give the patient a moment of rest. Patients are unable to restrain the urge, and false incontinence (inability to hold) of urine is observed. Cystitis is as a rule accompanied by changes in the urine in the form of the appearance of pus and blood in it, the content of which is greater in some cases and less in others. All portions of urine are turbid, the last one being more turbid than the first. Blood is usually mixed into the last portion of urine; sometimes urination ends with a few drops of pure blood (terminal hematuria). The general well-being of patients is poor. Two forms of cystitis are distinguished: acidic, when the reaction of the urine continues to remain acidic, and alkaline cystitis. The former are caused by colibacillary and tuberculous infections, the latter by all other microorganisms. Urine in cystitis always contains protein, however, its quantity is small: we have 'false' albuminuria, i.e., the presence of protein depending on the decay of pathological formed elements of urine—leukocytes, erythrocytes. In addition to pus and blood, in alkaline cystitis, a significant amount of calcium phosphate and ammonium magnesium crystals can be found in the urine, precipitating from the solution as a result of the decomposition of urine by microorganisms. The course of cystitis varies depending on its etiology, the conditions supporting its existence, and those pathological changes of the wall which are caused by the inflammation. If a previously completely healthy bladder is affected, then the disease is usually eliminated very quickly and without a trace, often even without any treatment. If the infection develops in bladder walls previously altered by one or another painful process, then the inflammatory process drags on for a long time and persistently despite treatment. This especially applies to persons suffering from prostate hypertrophy or urethral stricture, in whom the bladder is in a stretched, toneless state for a long period of time. Complete recovery from cystitis can be achieved only after the elimination of the moments predisposing to its development—tumors, stones, atony, diverticula. Otherwise, the disease will constantly recur, causing flare-ups of the inflammatory process. With the long-term existence of cystitis, there is a danger of the development of paravesical phlegmon—paracystitis, and the spread of infection to the overlying urinary organs—the renal pelvis, kidneys. The diagnosis of cystitis, especially in acute cases, if one remembers its characteristic symptoms, is very simple. One should accurately remember—without pus in the urine, there is no cystitis. In all cases of chronic pyuria, cystoscopy should be performed on patients, which not only provides an accurate diagnosis of the disease but in a number of cases also reveals the predisposing moments (diverticula, stone, tumor) which led to the occurrence of cystitis. In the acute stage, cystoscopy is not only not indicated but is directly contraindicated. The stretching of the urinary bladder cavity necessary for its performance is sharply painful and can cause an exacerbation of the inflammatory process. Cystoscopically, all stages of the inflammatory process are visible, starting from the dilation of vessels to diffuse hyperemia. In addition, the cystoscopic picture in individual cases gives indications of the nature of the inflammatory phenomena—encrusting or ulcerative cystitis—and of the etiological moment of the inflammation (tuberculosis). Having established the diagnosis of cystitis, one should always engage in identifying the bacterial flora of the disease, since therapy and prognosis are in direct connection with it. In the vast majority of cases, an exhaustive answer is obtained as a result of bacterioscopic examination of the urine sediment. The absence of bacteria in the latter should always arouse suspicion of the tuberculous nature of the disease (see Urinary bladder, tuberculosis of the U.B.). Prophylaxis should be directed toward preventing the possibility of infection penetrating into the bladder. It is necessary to maintain cleanliness of the external genitalia in women, eliminate constipation, ensure thorough asepsis when catheterization is necessary, and treat purulent diseases of the upper urinary tract. Treatment of acute cystitis should as a rule begin with complete rest (bed rest) and drug therapy. The diet should be non-irritating, with abundant drinking to increase diuresis, thereby reducing the irritating effect of concentrated urine and washing out the products of inflammation from the urinary bladder. For this purpose, diuretic infusions of Folia Uvae Ursi, Folia Fragariae, Herba Herniariae are prescribed (brew one tablespoon with a glass of boiling water and drink throughout the day). Internally, disinfectants (salol 0.5 three times a day for alkaline and urotropin 0.5 twice a day for acidic urine reaction) with narcotics (codeine, papaverine, belladonna) are used. Heat in the form of a hot water bottle on the bladder area, warm sitz baths. The indicated measures are quite sufficient for the disappearance of acute phenomena. If these do not subside within 7-10 days, then one should resort to injections into the bladder (instillations) through a thin catheter of 1/2-1% silver nitrate—10 cm3 (very painful) or 2-5% collargol solution in the same amount. In chronic cystitis, in addition to the above-mentioned drug treatment, the bladder should be washed through a catheter with solutions of silver nitrate or collargol (1:1,000-3,000) for staphylococcal infection and mercury oxycyanide (1:2,000-5,000) for colibacillary infection. In alkaline membranous cystitis, a good effect is obtained from washing with a 1/2% soda solution; in encrusting cystitis, scraping the bladder cavity with a sharp curette is indicated. It is extremely important not to stop the washings, even if all subjective phenomena have disappeared, until bacterial examination of the urine shows it is sterile, otherwise a relapse is guaranteed. At the same time, the cause supporting the cystitis (urinary retention, stone, constipation) should be eliminated.