Tuberculosis of the genitourinary system

Tuberculosis By

of the Genitourinary RICHARD

M.

FRIEDENBERC,

System M.D.

D

ESPITE THE PRESENCE of many effective drugs for the treatment of genitourinary tuberculosis, the overall incidence does not appear to be decreasing.11 Many reports indicate that the GU tract is the most common extrapulmonary site of tuberculous involvement worldwide. With medical therapy, * there has been a decrease in the number of advanced lesions and a lessening of the need for surgical intervention.2,6,7,12 Surgery is usually limited to patients with the ulcerocavernous type of renal tuberculosis, strictures and proximal hydronephrosis, or progression and persistent positive urine cultures despite adequate medical therapy. Genitourinary tuberculosis is primarily a disease of young adults (predominantly male), the majority with previous or currently active pulmonary tuberculosis.10~14 Approximately a third of the patients do not have clinical or roentgen evidence of pulmonary lesions, the renal tuberculosis presumably having originated at an earlier date from active pulmonary lesions that subsequently regressed. Over 25% of patients dying of pulmonary tuberculosis have genitourinary tuberculosis,3,8,16 and in about a fifth of this group destructive renal involvement is present.12 Wechsler et al. noted that the majority of men with urinary tuberculosis, present with extrarenal symptoms, particularly epididymitis. The earliest symptom in the child is dysuria, occasionally hematuria.ls About 10%of patients are asymptomatic. Just as renal tuberculosis is usually secondary to pulmonary tuberculosis, tuberculosis of the ureter, bladder, and genital system is usually secondary to renal tuberculosis.16 Most patients with bladder or ureteral tuberculosis should, therefore, have detectable renal lesions. The definitive diagnosis is made by examining 24-hr urine specimens for the tubercle bacillus and by guinea pig inoculation. RENAL

TUBERCULOSIS

Prior to 1926, renal tuberculosis was considered a unilateral disease, and once diagnosed, nephrectomy was carried out. Medlar demonstrated in 1926 that renal tuberculosis is the result of hematogenous dissemination from a primary source elsewhere in the body. 15 Both kidneys are involved, although the tubercles may lie dormant for years. Clinically, only about 20% present with RICHARD M. FRIEDENBERG, M.D.: Professor and Chairman, Department of Radiology, New York Medical College-Metropolitan Hospital Center, New York, N.Y. 10029. ‘First-line drugs include streptomycin, para-aminosalicylic acid and isoniazid. Other somewhat more toxic drugs include ethionamide, cycloserine, and kanamycin. A minimal course of therapy should he 2 yr. Relapses occur in 15 to 20% and require another course of therapy. Recurrence is much greater in patients with bladder lesions. 310

SEMINARSINROENTGENOLOGY,

Vo~.6,No.3

(JULY),

1971

TUBERCULOSIS

OF GENITOURINARY

SYSTEM

Fig. l.-Early renal tuberculosis. Retrograde pyelogram. Communicating abscess in the lower pole of the kidnev (arrow) with blunting of the fomices df the adjacent calix. The remaining calices are normal.

bilateral disease.Heptinstall listed two main forms of renal tuberculosis, diffuse miliary lesions primarily in the cortex, as part of a generalized miliary tuberculosis, and caseous or ulcerative lesions which are usually progressively destructive.9 Progression may occur in one kidney or a portion of a kidney, categorizing renal tuberculosis as a focal asymmetric disease. The initial focus usually lies in the glomerulus. If tubercle formation progresses to tissue destruction, the organisms spill into the nephrons and are found in the urine. The bacilli enter the loop of Henle, forming tubercles which enlarge and produce tissue necrosis

Fig. 2.-Productive reaction granulomatous with fibrotic cicatrization obliterating the middle and lower caliceal complexes . Calcification is present in the lower pole. (Reproduced with permission of the publisher.17)

312

RICHARD

M.

FRIEDENBERG

Fig. 3.-Advanced renal tuberculosis with multiple abscesses in a young woman. A. Retrograde pyelogram shows multiple abscesses communicating with the middle calices together with moderate scarring and obstruction of the lower calices. The patient was placed on therapy, but was lost to follow-up. B. Three years later. Severe ulcerocavemous tuberculosis affecting the entire kidney which was now nonfunctioning.

and a tuberculous abscess(ulcerative) in a papilla.la Abscessesmay also occur in the cortex. The subsequent course is variable, The host may control the infection, the tuberculous bacilluria may cease, and the urogram will remain normal. Coalescent lesions may erode into a minor calix and produce a communicating abscess (Fig. 1). Such caliceal destruction with abscess formation is one of the hallmarks of renal tuberculosis. Partial healing may result, particularly under the influence of antibiotics, with production of granulation tissue which may cicatrize and distort or, occasionally, obliterate an infundibulum or calixr (Fig. 2). If the coalescing lesion enlarges distal to the calix without eroding it, a tumor-like caseous mass, representing a tuberculoma may form. In far advanced disease, the lesion may destroy renal segments or the entire kidney and produce either a cavernous type of ulcer or a diffuse tuberculous renal empyema. (Figs. 3 to 5). Parenchymal calcifications are seen in about 10%and calculi are frequently present. Hydronephrosis is a frequent complication

TUBERCULOSIS

OF GENITOURINARY

SYSTEM

313

Fig. 4.-Advanced renal tuberculosis. Large communicating abscesses have eroded into and destroyed segments of the upper and lower calices. Marginal changes in the lower calices suggest caliectasis cystica. (Reproduced with permission of the publisher.17)

Fig. 5.-Advanced renal tuberculosis with parenchymal calcification on pIain film. The kidney is shrunken. The calcifications are in areas of necrosis and caseation.

314

RICHARD M. FRIEDENRERG

TUBERCULOSIS

OF GENITOURINARY

Table

l.-Roentgen

315

SYSTEM

Findings

in Renal Tuberculosis

Early Normal urogram Dilatation of calices or pelvis, localized or generalized Destruction of the fornix of the calix with communicating Advanced Localized stricture of the infundibula Multiple abscesses, frequently communicating Parenchymal calcifications Localized mass lesion (tuberculoma) Nonfunctioning kidney Tuberculous empyema Massive ulcerating cavernous tuberculosis

abscess

because of the tendency for ureteral strictures and calculi. Table 1 lists the roentgen findings seen in the various stages of tuberculosis of the kidney. These roentgen characteristics of renal tuberculosis are usually adequately visualized in routine studies ( urogram, pyelogram, nephrotomogram ) . Many authors believe that more precise information can be obtained by angiography.335 The vascular study may provide a better assessmentof the degree of hydronephrosis, the extent of cortical destruction (Fig. 6), and the sites of

Fig. S.-Early tuberculous ureteritis. Retrograde ureterography. A. Characteristic moth-eaten appearance of ulcerative ureteritis. B. Prompt antituberculous therapy produced complete healing without residual stricture formation. (Reproduced with permission of the publisher.17)

316

RICHARD

M.

FBIEDENBERG

Fig. 9.-Severe ulcerative ureter& in a patient with advanced renal tuberculosis. Alternating segments of stricture and dilatation are seen. Note the marked mucosal irregularity, characteristic of ulcerative tuberculous ureteritis. Retrograde pyelogram.

peripheral changes by delineating small vessel alteration. However, there are no specific angiographic characteristics that distinguish renal tuberculosis from other inflammatory diseases. URETERAL

TUBERCULOSIS

The mechanisms that theoretically produce tuberculosis of the ureter include:4 ( 1) A renal focus rupturing into a ‘calix, producing tuberculous bacilluria which infects the ureteral mucosa. (2) Tubercle bacilli extending from the renal parenchyma into the ureter via communicating blood vessels and lymphatics. (3) Extrarenal lesions, such as ovarian tuberculosis, involving the ureter by contiguity. (4) Primary involvement, without renal or genital involvement. If this occurs, it must be extremely rare. It has been described radiologically, but can only be con&n-red by histologic exclusion of tuberculosis in the kidney and bladder. (5) Tuberculosis of the kidney with reflux of infected bladder urine into the contralateral ureter. This is a possibility that has never been reported. In the early stages there may be ureteral dilatation. The entire ureter down to the ureterovesical junction may be involved. This may result from ureteral

TUBERCULOSIS

OF GENITOURINARY

SYSTEM

317

Fig. lo.-Tuberculous ureteritis. Retrograde pyelograms in two different patients. A. Corkscrew configuration. B. Beaded pattern. (Reproduced with permission of the publisher.1’)

atony secondary to prolonged tuberculous bacilluria or to early stricture formation at the ureterovesical junction (Fig. 7). As the disease progresses, mucosal ulcerations occur which coalesce, ulcerate, and spread around the circumference of the ureter. The classical roentgen appearance is one of a ragged, moth-eaten, ulcerated segment of ureter. This differs from nonspecific ureteritis in its tendency to involve several centimeters of the ureter with irregular areas of dilatation and constriction. If ureteral involvement is superficial, more or less limited to the mucosa, prompt therapy may effect complete healing without stricture formation ( Fig. 8). Further necrosis of the ureteral musculature is accompanied by fibrosis. This results in cicatrization and stricture formation, with shortening of the ureter. Strictures are the most common abnormality seen in ureteral tuberculosis, occurring most often in the distal half of the ureter. The strictures vary in appearance. A single short stricture does not differ from that seen in nonspecific ureteritis. However, there is a tendency toward longer involvement. When the

318

RICHARD

M.

FRJEDENBERG

Fig. Il.-Late tuberculous ureteritis with nonfunctioning kidney and renal empyema. The wall of the ureter is markedly thickened, narrowing the lumen and producing a pipestem appearance.

Fig. 12.-End stage of tuberculous empyema. Plain film. Massive pelvocaliceal dilatation with marked calcification of the kidney and upper ureter. Such severe dilatation suggests the presence of distal obstructive lesion.

deeper ureteral tissues are invaded, a stricture may occur in one segment while a neighboring segment, more superficially involved, may heal without stricture formation. These alternate areas of healing and stricture formation produce a headed ureteral configuration and, in severe cases, a corkscrew appearance (Figs. 9 and 10). In the late stages of ureteral tuberculosis, severe thickening of the ureteral wall may produce a rigid narrow lumen, usually associated with tuberculous empyema in a nonfunctioning kidney (Fig. 11). Massive calcification of the kidney and ureter is sometimes seen with tuberculous empyema. The kidney may be large or small, depending on the degree of ureteral or pelvic obstruction (Fig. 12). Schistosomiasis also produces ureteral calcification, but this almost always coexists with bladder calcification and is most prominent in the distal ureter. Table 2 lists the roentgen signs of tuberculosis ureteritis.

TUBERCULOSIS

OF GENITOURINARY

SYSTEM

319

Fig. 13.-Early tuberculous cystitis. The irregularity of the bladder dome implies mucosal edema.

Fig. 14.-Late with a capacity

state of tuberculous cystitis. Reflux and a small contracted of less than 50 cc. The bladder wall is markedly thickened.

bladder

320

RICHARDM.FRIEDENBERG

Fig. KS.-Tuberculous abscessin a seminal vesicle. The contrast medium has remained in the abscess from a seminal vesiculogram performed with Ethiodol 2 yr earlier. The catheter in the left ureter shows its relation to the seminal vesicle abscess.

BLADDERANDGENITALTUBERCXJLOSIS

Tuberculosis produces one of the specific forms of interstitial cystitis. Again, tuberculosis of the bladder is most commonly secondary to renal tuberculosis. Occasionally, the renal structures may appear normal, suggesting that the process is secondary to genital tuberculosis or represents primary bladder involvement. In the early stages, the findings are nonspecific, with minor irregularities of the bladder contour and increased trabeculation (Fig. 13). As the disease progresses, the inflammation involves the whole thickness of the bladder, increasing the wall thickness and decreasing the bladder capacity. In the late stages, bladder capacity may be reduced to a volume of 25 to 50 cc (Fig. 14). Ureteral reflux is common. Occasionally, the thick bladder wall may constrict and obstruct the distal end of the ureter, producing hydronephrosis. Table 3 summarizes these signs. Tuberculosis of the seminal vesicles produces severe destruction of the convolutions, usually with abscessformation (Fig. 15). The ejaculatory ducts may become obstructed. The disease is more frequently bilateral. Tuberculosis and schistosomiasisare the major inflammatory lesions that produce calcification in the seminal vesicles.

Table S.-Roentgen Findings in Ureteral Tuberculosis Early Dilated ureter Ulcerative ureteritis Advanced Long segments of ulcerating ureteritis Strictures ( frequently multiple) Beaded or corkscrew ureter Pipestem ureter Calcified ureter

TUBERCULOSIS

OF GENITOURINARY

321

SYSTEM

16.-Tuberculous Fig. epididymitis. The large

calcifications in the region of the epididymes and testes indicate tuberculous abscesses. The bladder was also involved. Tuberculosis may involve the prostate and epididymis producing destruction and abscesses.The testes are only occasionally affected (Fig. 16). Tuberculosis of the urethra is uncommon; mucosal invasion may result in strictures.

Table

S.-Roentgen

Findings

in Bladder

Early Mucosal irregularity Trabeculation Late Reflux Distal ureteral constriction Fibrosis with thickening of bladder Decreased bladder capacity

Tuberculosis

wall

REFERENCES

1. Barrie, H. J., Kerr, W. K., and Gale, G. L.: The incidence and pathogenesis of tuberculous strictures of the renal pyelus. J. Ural. 98:584, 1967. 2. Campbell, M. F. (Ed.) : Urology, Vol. 1. Philadelphia, Saunders, 1963. 3. Dautrebande, J., Duckett, G., and Roy, P.: Arteriography in renal tuberculosis. J. Canad. Assoc. Radio]. 18:382, 1967. 4. Friedenberg, R. M., Ney, C., Stachenfeld, R. A.: Roentgenographic manifestations of tuberculosis of ureter. J. Ural. 99:25, 1968. 5. Fritjofsson, A., and Edsman, G.: Angionephrography in renal tuberculosis. Acta Chir. Stand. 118:60, 1959. 6. Gould, R. S.: Current concepts of renal tuberculosis. J. Urol. 100:124, 1968.

7. Gow, J.: Genitourinary tuberculosis. Lancet 2:261, 1963. 8. Greenberger, M. E., Wershub, L. P., and Auerbach, 0.: The incidence of renal tuberculosis in five hundred autopsies for pulmonary and extrapulmonary tuberculosis. JAMA 104:726, 1935. 9. Heptinstall, R. W.: Pathology of the Kidney. Boston, Little, Brown and Co., 1966. 10. Jameson, E. M.: Renal tuberculosis in patients with active pulmonary tuberculosis. Surg. Gynec. Obstet. 67:56, 1938. 11. Lattimer, J. K.: Renal tuberculosis. New Eng. J. Med. 273:208, 1965. 12. -, and Kohen, R. J.: Renal tuberculosis. Amer. J. Med. 17:533, 1954. 13. -, and Vasquez, G.: Renal tubercu-

322 losis in children. Postgrad. Med. 28:336, 1960. 14. Mangelson, N. L., Saunders, J. C., and Brosman, S. A.: Urogenital tuberculosis. J. Ural. 104:309, 1970. 15. Medlar, E. M.: Cases of renal infection in pulmonary tuberculosis: evidence of healed tuberculosis lesions. Amer. J. Path. 2:401, 1926. 16. -, Spain, D. M., and Holliday, R. W.: Post-mortem compared with clinical diagnosis of genito-urinary tuberculosis in adult males. J. Ural. 61:1078, 1949. 17. Ney, C., and Friedenberg, R. M.:

RICHARD

M. FRIEDENBERG

Radiographic Atlas of the Genitourinary System. Philadelphia, Lippincott, 1966. 18. Siegel, J., and Lattimer, J. K.: Renal tuberculosis: Has the incidence of advanced lesions decreased in past two decades? J. Ural. 91:330, 1964. 19. Strauss, M., and Well, L. G. (Eds.): Diseases of the Kidney. Boston, Little, Brown, 1963. 20. Wechsler, H., Westfall, M., and Lattimer, J, K.: The earliest signs aud symptoms in 127 male patients with genitourinary tuberculosis. J. Ural. 83:801, 1960.