MALE GENITO – URINARY

TUBERCULOSISJAWAD ULLAH

GROUP 21st

SEMESTER 8th ISM IUK

INTRODUCTION young to middle-aged adults.

M/F ratio= 5:3

Uncommon in children

Approximately 20-30% of extra-pulmonary infection

Increase in incidence with HIV epidemic and multi drug resistant strains

Important to diagnose as non specific clinical presentation and progression to renal failure if undiagnosed and untreated.

The kidneys are the most common site of GUTB

Causative organism : Mycobacterium Tuberculosis.

history of previous clinical TB (25%) with a lag time

of 2- 20 years

SPREAD Hematogenous spread - from the

kidneys, the bacilli can spread to the renal tract, prostate and epididymis.

Lymphatic spread

Observed in two settings: commonly, as a late manifestation of

earlier clinical or subclinical pulmonary infection

rarely, as part of the multiorgan infection (miliary tuberculosis)

Rarely primary one—BCG Tt for Ca bladderTransplant recipient

CLINICAL FEATURES gross / microscopic hematuria sterile pyuria� Mild proteinuria urinary frequency, dysuria, ‘intractable’ UTI frequency, urgency, dysuria with involvement of bladder back, flank, or abdominal pain. : => extensive renal disease Constitutional symptoms such as fever, weight loss, fatigue,

and anorexia are less common haemospermia ‘acute epididymo-orchitis’ Hydrocele,discharging scrotal/perineal sinuses Infertility,spontaneous abortion,ectopic pregnancy. Menstrual irregularities

Three other major complications of renal tuberculosis:

hypertension (RAS axis mediated)super-infection (12 to 50%)nephrolithiasis (7 to 18%)

OTHER COMPLICATIONS: Perinephric inflammation Abscess formation :including psoas abscess Fistulae Sinus tract into adjacent tissues or viscera.

PATHOGENESIS

Progressive involvement of renal

parenchymacoalescence of

granulomas leading to unifocal or

multifocal mass lesions

Seen in advanced renal tuberculosis

Increase renal lengthIncrease thickness of

renal substanceDisplacement of

collecting system.Parenchymal surface scarring over retracted papillae or pelvis and dilated/ deformed calyces.

Associated calcification or calculiImpaired excretion of contrast

Erosion of pyramidCortical / papillary

necrosisCaliectasis

CavityDeformed calyx

Caseo – cavernous

type: enlarged sac filled with

caseous material, +/- calcification

Calcified shrunken non functioning of

kidney

Autonephrectomy : end stage d/s

Focal or diffuse involvement - fibrosis.

Following the drainage of a cavity into the collecting system, there is spread of infection to other parts of the urinary tract.

Stimulation of scirrhous reaction causes stenosis and obstruction of parts of the collecting system.

Common sites of stricture:

neck of a calyx – hydrocalyx, regional hydrocalycosis

pelvi – ureteric junction – generalised dilatation of pelvicalyceal system.

lower end of the ureter.

Imaging

High dose IVU – traditional gold standard CT – new standard Pyelography (ante/retrograde) – limited use Plain radiographs – important CXR,spine X-Ray,X-Ray KUB US – limited value Nuclear Perfusion Scan – function MRI – little application

Plain radiograph of abdomen

Renal Size: Small, enlarged or normal

Presence of scarring or focal bulge

Calcification

Calcification of ureter or urinary bladder : rare

Evidence of Skeletal Involvement : in hip, sacroiliac joint, spine, paraspinal abscess

calcification of lymph nodes, adrenal gland – 10%

Calcification : attempt to heal and limit the pathological processes – 50% - types

Dense punctate calcification representing healed tuberculoma.

Amorphous granular associated with granulomatous masses- autonephrectomy

Chest x ray

Abnormal in 50 %

Active pulmonary tuberculosis – 5- 10%

Sequelae of old tuberculosis of past infection.

Intravenous urography >70% cases- single kidney involved

IVP (abnormal in 85- 90%) though normal in initial stages.

Diagnosis can be made with certainity on urography only if lesion is ulcerated into calyx.

Miliary tubercles – involve both the kidneys.

globally poor renal function IVU-

assess the extent and severity of involvement To monitor response to treatment To look for complications

Imaging findings :

Parenchymal scars & Irregularity of the papillary tips - “moth-eaten” calices

Small cavities in the papillae

communicate with the collecting system

fibrotic reaction develops, stenosis and strictures of the caliceal infundibula - Infundibular strictures can lead to localized caliectasis

or phantom calyx.

Scarring of renal pelvis (Kerr kink)

Moth eaten appearance

Normal calices

Earliest abnormality –

an indistinct feathery outline

Irregularity of surface of one or more papillae or calyces with normal renal size and contour.

Fuzzy & irregular calices due to papillary necrosis.

Golf ball on a tee

On IVP :

Collecting system shows contrast material in a large papillary cavity, the “golf ball” (∗).

Blunted calyx, the “tee,” is adjacent (arrow).

Infundibular stenosis causing phantom calyx

Phantom calix

Infundibular stenosis

Phantom calyces

Decreased nephrographic opacity and nonfilling of the collecting system elements at the lower pole of left kidney – phantom calyces (ghost : exist, but not visualised, the same are visualized on RGP).

RGP

Hiked up pelvis => pulled up

Cephalic retraction of the inferior medial margin of the renal pelvis at the ureteropelvic junction (UPJ)

Kerr kink Cortical scarring with

dilatation & distortion of adjoining calyces coupled with strictures of the pelvicaliceal system.

Cause luminal narrowing either directly or by causing kinking of the renal pelvis at the UPJ.

If the ulcer or stricture extends to the renal pelvis or the pelvic ureteral junction, urine outflow obstruction may

occur.

IVUmay show delayed function, clubbed calyces, or absence of function.

Some show Hydronephrosis - irregular margins and filling defects owing to caseous debris.

If tuberculous infection extends directly to the rest of the kidney, the entire kidney becomes a bag of caseous

necrotic pus.

The kidney enlarges initially but subsequently may return to normal or become atrophic.

infection may extend into peri- / pararenal space + psoas

Some nonspecifically blunt calices in addition to a track leading to a cavity (arrow).

(A) ‘Cut-off’ upper pole infundibulum. No filling of calices in upper pole. Irregular cavitation in remainder of the kidney.

(B) Pathological specimen showing a fibrotic stricture of the upper infundibulum (black arrow) and a caseous pyonephrosis occupying the upper pole. Cavitation elsewhere.  

Putty kidney Autonephrectomy.

Diffuse, uniform, extensive parenchymalcalcifications forming a cast of the kidney with autonephrectomy.

End stage of GuTB.

URETER Almost always secondry to renal tuberculosis – 50% cases.

Spread of infection by bacilluria.

ureteral involvement is usually unilateral, bilateral changes are asymmetric when they occur.

The most common site of involvement is the lower third of the ureter.

Renal damage secondry to ureteral strictures may be more severe than the effect of original parenchymal involvement.

Dilatation and stenting of the ureter may restore ureteral patency and salvage a kidney.

dilatation resulting from atony and prolonged

bacilluria

PIPE STEM

URETER

irregular segments of ureter due to mucosal

ulcerations

necrosis of ureteral musculature is

accompanied by fibrosis - stricture formation- 50%.

severe thickening of the wall produces a rigid shortened ureter with narrow lumen

beaded or corkscrew

appearance.

Terminal segment

of the ureter

Saw tooth appearance

Ulcerations causingmucosal irregularity of ureter.

Beaded / Corkscrew ureter

Fusion of multiple strictures may create a long, irregular narrowing. Several nonconfluent strictures can produce a “beaded” or “corkscrew” ureter

Mucosal thickening of ureter

Pipe stem ureter Rigid ureter: irregular and lacks

normal peristaltic movement, fibrotic strictures noted.

Note the distortion, amputation and irregularity of the upper pole calices.

Old pipe stem

Urinary bladder Inv. in later course of d/s in 1/3 rd cases

Tubercular cystitis- edema of bladder

mucosa

Large tuberculomas in vesical wall – manifest

as filling defects

Advanced d/s – irregular contracture with thick walls

and reduction of bladder capacity – THIMBLE BLADDER.

Fibrosis in region of trigone produces gaping of the UV junction resulting in VUR.

Shrunken & calcification later

Genitourinary tract tuberculosis. Intravenous urography series in a man with renal tuberculosis shows marked irregularity of the bladder lumen due to mucosal edema and ulceration

Thimble bladder Diminutive and

irregular urinary bladder – simulating a thimble.

IVP film-The lower end of the right ureter demonstrates an irregular caliber with an irregular stricture at the right vesico-ureteric junction. Note the asymmetric contraction of the urinary bladder, with marked irregularity due to edema and ulceration.

Diffuse reflux nephropathy with multiple blunted calices.

Left kidney normal in size.

Shrunken right kidney.

Urethral tuberculosis Male urethra – uncommon, occurs secondry to renal infection.

The periurethral glands of Littre may become distended with bacteria and leukocytes and may lead to abscess formation.

Associated with prostatic abscess or fistula formation.

Result in non specific stricture in bulbo-membranous urethra.

Retrograde pyelography

Indicated in patients with non functioning kidney to demonstrate ureteric obstruction and cavitation in kidney.

Retrograde ureteropyelography showed an atrophic right kidney with diffuse caliceal dilatation, papillary necrosis, and infundibular narrowing.

mucosal irregularities and erosions of the ureter.

ultrasonography

Role of sonography : Guidance for interventional procedures of

percutaneouys nephrostomy (PCN) Antegrade dilatation of ureteral stricture Drainage of perinephric abscess.

Not a primary modality used for diagnosis: Unable to show early calyceal changes. No information about status of renal function.

Kidney Focal lesion of varying echogenecity. Early stages – papillary lesions as areas of hypoechogenicity or hypoechoic

foci with echogenic walls or echogenic non shadowing lesions. Sloughed calyx – echogenic flap separated from normal calyceal wall. Large liquefying conglomerate cavities or dilated calyces formed as a result

of infundibular stricture appear as hypoechoic nodules or masses. PCS- hydronephrosis or calyectasis.

The communicating tract from a cavity appears as a sonolucent track entering the dilated calyx.

Heterogenous echotexture of the parenchyma or normal appearing parenchyma may be seen in diffuse involvement.

May demonstrate hydronephrosis, parenchymal calcification and perinephric abscess.

Sonogram of left kidney shows 1.5-cm hypoechoic nodule (arrowhead) in cortex

USGEarly findings may be missed

Pseudoureterocele

IVP: cobra head sign, the lucent halo is however thick, irregular and less well defined.

Usg is poor in assessing ureter but shows back pressure changes and adjacent retroperitoneal disease.

UB- focal irregular thickening with reduced capacity.

Deformed shape and focal abnormalities better appreciated following distension.

Computed tomography Indicated only in patients with strong clinical suspicion but

normal IVU and USG.

Uses :MDCT: Renal and extra renal spread of disease. Length of ureteric stricture Adjoining retroperitoneal disease Associated spinal or solid organ involvement.

excretory urography is sensitive in the detection of early urothelial mucosal changes

CT identifying renalcalcifications, Coalesced cortical granulomas containing either caseous or

calcified material Calices that are dilated and filled with fluid have an attenuation between 0 and 10 HU; debris and caseation, between 10 and 30 HU; putty-like calcification, between 50 and 120 HU; and calculi, greater than 120 HU. Cortical thinning is a common CT finding and may be either focal

or global. Parenchymal scarring is readily apparent at CT. Fibrotic strictures of the infundibula, renal pelvis, and ureters may

be seen at contrast-enhanced CT and are highly suggestive of tuberculosis.

Ureter : thickening of ureteral wall or pelvis with periureteric inflammation

Bladder Tuberculosis thickened bladder wall (= muscle hypertrophy + inflammatory

tuberculomas) filling defects (due to multiple granulomas) bladder wall ulcerations shrunken bladder - scarred bladder with diminished capacity -

thimble bladder.� bladder wall calcifications (rare)

CT urogram shows severe nonuniform caliectasis and multifocal strictures (arrowheads) involving renal pelvis and ureter.. Calcification (arrow) is noted in left distal ureter.

A, Contrast-enhanced CT scan obtained at level of right renal hilum shows wedge-shaped hypoperfused areas (arrowheads).

B, CT scan - hypoperfused areas (arrowheads) and focal caliectasis (arrows)

 (a) Contrast-enhanced excretory-phase CT scan shows dilated calices and narrowing of the infundibula (arrowheads). 

53-year-old man with tuberculosis involving collecting system. Contrast-enhanced CT scan of left kidney shows uneven caliectasis caused by varying degrees of stricture at various sites.

(a) Contrast-enhanced nephrographic-phase CT scan shows dilated calices and thinning of the renal cortex (arrow). (b) Magnified view from a contrast-enhanced nephrographic-phase CT scan obtained caudad to a shows mural enhancement and thickening of the proximal ureter (arrow).

Renal Tuberculosis. Coronal reformatted non-enhanced CT scan of the abdomen and pelvis demonstrates a small, left kidney containing globular calcifications (white circle) pathognomonic for renal tuberculosis.

CT scan shows dense calcification replacing right kidney, so-called “putty kidney.” in NCCT

The left kidney shows large, dense, oval calcifications. Low-density areas in the right kidney probably represent foci of caseous necrosis.

MRI

MR urography: evaluate poorly or non functioning kidney specially obstructive form for demonstration of ureteric involvement.

MR – renal parenchymal changes and details of PCS

Used for evaluation of ureteral peristalsis.

Genital tuberculosis

Male Genital Tuberculosis seeding from infected urine or via the bloodstream. The most common manifestation is tuberculous prostatitis, less

common is epididymo-orchitis

calcifications in 10% (diabetes more common cause)

Tuberculous epididymitis ascending / descending route of infection

Tuberculous orchitis direct extension from epididymal infection, rarely from hematogenous spread

Prostatic involvement : Plain radiographs-dense calcification within the prostatic bed Cavities/ abscesses--discharge into the surrounding tissues

sinuses or fistulae to the perineum or rectum ‘ watering-can perineum.’

Cystourethrography- early cases - filling of the prostatic ducts without evidence of cavitation, Advanced cases the ducts may be greatly dilated. Varying degrees of destruction of prostatic parenchyma with sloughing may produce

irregular cavities.

Tuberculous prostatitis / prostatic abscess: caseation, cavitation and fibrosis. hypoechoic irregular area in peripheral zone hypoattenuating prostatic lesion hypointense diffuse radiating streaky areas on T2WI (watermelon sign)� peripheral enhancement Occasionally fistulous formation

Prostatic tuberculosis. Contrast-enhanced CT scan shows a well-defined hypoattenuating lesion within the prostate gland (arrowhead). Scrotal tuberculosis. US image of a testis shows a nonspecific focal area of hypoechogenicity, which proved to represent caseous necrosis secondary to tuberculosis.

Watermelon skin

Prostatic abscess, T2-weighted MRI shows a peripheral enhancing cystic mass with radiating, streaky areas of low signalintensity.